http://www.lexingtonpulmonary.com/index.htmlArticlesendelton@lexpcc.netCopyright 2009 Don Elton2009-12-05T19:45:24-05:00 hourly 1 2000-01-01T12:00+00:00 Sat, 05 Dec 2009 19:45:32 -0500delton@lexpcc.netSleep apnea2009-12-05T19:45:24-05:00http://www.lexingtonpulmonary.com/articles/files/4278263b1f81c374b3f0213e9247f5ff-19.php#unique-entry-id-19http://www.lexingtonpulmonary.com/articles/files/4278263b1f81c374b3f0213e9247f5ff-19.php#unique-entry-id-19Sleep Apnea
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Sleep apnea is by far the most common sleep disorder encountered in clinical practice. Patients are profoundly affected by this disorder that frequently goes undiagnosed for years. Non invasive therapy (usually nasal CPAP - Continuous Positive Airway Pressure during sleep) is effective in 90% of patients. Treated sleep apnea patients are among the most pleased patients you will encounter as treatment often results in a fast and dramatic improvement in quality of life and general health.


Why it happens
Most sleep apnea is obstructive and is caused when the normal relaxation of sleep causes a loss of upper airway muscle tone. This normally results in snoring which is a vibration of the tongue and soft palate that occurs when a person breathes against a partially obstructed airway. In patients with obstructive sleep apnea, the combination of upper airway collapse and loss of muscle tone in the chest and abdomen result in either a cessation or significant decrease in airflow. Hypoxia (lack of oxygen) from the resulting apnea (stopped breathing) or hypopnea (shallow breathing) leads to an arousal (usually too brief to be recalled by the patient) which allows for a return of muscle tone and thus breathing. After a breath or two, the hypoxia is reversed and the patient goes back to sleep. This cycle repeats throughout the night.


Consequences
The pathology of obstructive sleep apnea results from frequent awakenings (as many as 50 to 100 awakenings per hour) and from repeated episodes of hypoxia. The frequent awakenings cause sleep to be non-restorative and cause excessive daytime sleepiness (EDS). The episodic hypoxia results in headaches, increased risk of strokes and heart attacks, and when severe, in systemic and pulmonary hypertension and eventually right sided heart failure in the worst cases.


Recognition
The two key symptoms that should lead you to suspect sleep apnea are the combination of snoring and excessive daytime sleepiness. With this combination in an adult there is as much as an 80% chance that a sleep study will document a clinically important degree of obstructive sleep apnea. Daytime sleepiness can be scored using the standardized Epworth Sleepiness Scale. This allows the patient or significant other to rate the patient's likelihood of dozing in 8 specific circumstances with scores assigned from 0 (no chance) to 3 (high chance). The situations are: Sitting and reading, watching TV, sitting inactive in a public place, a passenger in a car for an hour, sitting and talking with someone, sitting quietly after lunch, and in a car stopped for a few minutes in traffic. Scores of 5 or under are considered normal. Scores over 10 are definitely abnormal. Note that a patient's spouse will usually rate the patient higher and perhaps more accurately than the patient.

Anatomical clues that sleep apnea may exist include obesity (though lack of obesity does not exclude sleep apnea), excessive soft tissue over the external neck, an elongated soft palate (one in which you can't easily see the tip of the uvula without a tongue blade), large tonsils, and a mandible that doesn't extend as far forward as the maxilla. Sleep apnea patients frequently are diagnosed as having depression, chronic fatigue syndrome, difficult to control hypertension, recurrent refractory headaches, unexplained edema (cor pulmonale), unexplained pulmonary hypertension, abnormal Holter monitoring (arrhythmias, tachycardia, bradycardia, heart block during sleep) and other disorders.


Testing
Patients are typically initially evaluated by the sleep consultant to gather historical information and to assess airway anatomy and potential medication related problems that can lead to sleep disorders or affect the effectiveness of various treatment options. Seeing the patient before the study results in a more meaningful study interpretation and makes it easier to recommend the right treatment for the patient. The initial office visit is also used to explain the pathophysiology and treatment options for sleep disorders to the patient and to make sure the patient understands the sequence of events in working up and treating his or her disorders if they are diagnosed.

Testing is normally done in a sleep laboratory under the supervision of a sleep technologist who can immediately correct technical problems such as misplaced leads etc and can make observations and interventions while the study is going on. Some studies can be performed in the home if there is clinically little doubt as to the diagnosis though the risk of having to repeat the study due to technical problems is higher in an unattended study. Home studies typically do not measure as many parameters as can be measured in the sleep laboratory but home studies are usually less expensive than lab based attended studies.

A preliminary report is made available to the sleep consultant within a day or two of the study with the full data report sent to the sleep consultant within a week. An interpretation report is then dictated and sent to the referring or personal physician. If intervention is needed, it may be initiated over the telephone before the patient returns for formal follow-up. This allows the follow-up visit to be used to evaluate the response to treatment in many cases.

If a patient has obvious significant sleep apnea, the sleep laboratory will interrupt the study and start a CPAP (continuous positive airway pressure) titration study where the patient is placed on the CPAP and allowed to go back to sleep while the technologist adjusts the pressure level while monitoring the patient's sleep to find the minimum pressure level needed to correct the sleep apnea and resultant hypoxia. If there isn't enough time to find the optimum level during the first night of study, a second night will be used for this purpose. If the patient is found to have significant abnormalities they may be started on CPAP at home empirically pending the formal CPAP titration study.


Treatment
In 90% of patients, nasal CPAP is the only treatment needed and results in dramatic improvement even after the first night of use. The worse the patient's initial disease, the more likely the clinical results will be dramatic as a minimally symptomatic patient might not see much subjective difference with treatment. Some patients require more time and work to get them used to using CPAP. There are a variety of masks and CPAP device programming issues that can get the difficult patient used to CPAP and once the patient gets a full night of sleep and sees the clinical effects they are highly motivated to continue. Some patients have obstruction so severe that CPAP isn't adequate treatment or loss off CPAP could be life threatening. In these cases, if their upper airway anatomy has a correctable defect, surgery to correct the defect may be appropriate and the sleep consultant would then refer the patient to an ENT for this purpose. After surgery the CPAP titration study would be repeated as CPAP requirements would likely be different. Unfortunately, surgery as primary therapy in unselected patients for sleep apnea is only about 50-60% effective and may only correct the snoring thus masking the actual severity of disease. By limiting surgery to those patients who fail CPAP and have an anatomical problem to correct, the effectiveness of surgery is much better.

Follow up
Once the patient is effectively treated, routine follow-up by the sleep physician is not normally required. Patients are advised they may need a repeat CPAP titration study if they gain or lose more than 25 lbs of weight or if they find they are again having symptoms of sleep apnea (perhaps medication related etc.) ]]>delton@lexpcc.netPhysiology2009-12-05T19:45:02-05:00http://www.lexingtonpulmonary.com/articles/files/620e8a6b26422ef4ed78d19a5c439861-18.php#unique-entry-id-18http://www.lexingtonpulmonary.com/articles/files/620e8a6b26422ef4ed78d19a5c439861-18.php#unique-entry-id-18Shunt & Deadspace
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
Shunt and dead space are terms used to describe extreme conditions where either blood flow or ventilation does not meet the other in the lung as it should for gas exchange to take place. While in their pure sense, the terms refer to the extreme conditions, they can also be used to describe areas or effects where blood flow and ventilation are not properly matched though both may be present to varying extents. Some refer to shunt-effect or dead space-effect to designate the ventilation/perfusion mismatch states that are less extreme than absolute shunt or dead space.

Shunt:
that part of the cardiac output that returns to the left heart without the benefit of exposure to ventilated alveoli.

The oxygen content of mixed arterial blood (CaO2) is determined by the content of oxygen in the blood that reached ventilated alveoli (CcO2), the content of oxygen in blood that bypassed ventilated alveoli (CvO2), and the proportion of the two. Thus the formula:

QS/QT = (CcO2 - CaO2) / (CcO2 - CvO2)

Normal shunt fraction (QS/QT) is less than 0.05 (<5%).

Remember CxO2="1.39" x Hb x SxO2 + 0.003 x PxO2

CcO2 is the content of oxygen in pulmonary capillary blood and is estimated by plugging in 100% as the saturation (1.00 for the math) since the PcO2 (pulmonary capillary PO2) can be assumed to be high enough to assure 100% saturation. The PcO2 itself cannot be directly measured so we use PAO2 (from the alveolar air equation) in its place. This means that CcO2="1.39" x Hb + 0.003 x PAO2

Dead space:
that part of inspired air that is exhaled without the benefit of exposure to perfused alveoli.
The carbon dioxide content of mixed exhaled gas (PECO2) is determined by the carbon dioxide content of the gas that came in contact with perfused alveoli (PACO2), the content of the gas that did not come in contact with perfused alveoli, and the proportion of the two. It can be assumed that there is no carbon dioxide in inspired air and thus no carbon dioxide in that part of the inspired volume that does not come in contact with perfused alveoli. One can also assume that gas that does contact perfused alveoli will equilibrate to the carbon dioxide content in the perfusing blood PACO2="PcCO2" or arterial blood PcCO2="PaCO2" since arterial carbon dioxide content is not greatly influenced by shunting). Thus the formula:

VD/VT="(PaCO2" PECO2) / (PaCO2 PICO2)

if one assumes that PICO2="0" the formula is simplified to:

VD/VT="(PaCO2" PECO2) / PaCO2

Normal VD/VT is less than 0.33 (<33%).

Example Calculations

Available data:

Hb 10 gm% PaO2 75 SaO2 97% Pb 750 mm Hg PvO2 33 SvO2 65% PaCO2 45 mm Hg PECO2 15 mm Hg FIO2 40%

Calculate the shunt & dead space from the above data.

The dead space is the easiest using

VD/VT="(PaCO2" PECO2) / PaCO2

VD/VT="(45" 15) / 45

VD/VT="30/45"

The shunt equation is more complicated and takes more steps to complete. We start by calculating the contents to plug into the shunt equation:

QS/QT="(CcO2" CaO2) / (CcO2 CvO2)

arterial content:

CaO2="Hb" x SaO2 x 1.39 + 0.003 x PaO2

CaO2="10" x .97 x 1.39 + 0.003 x 75

CaO2="13.48" + 0.225="13.705" Vol %

mixed venous content:

CvO2="Hb" x SvO2 x 1.39 + 0.003 x PvO2

CvO2="10" x .65 x 1.39 + 0.003 x 33

CvO2="9.035" + 0.099="9.134" Vol %

Before we can calculate the CcO2, we must calculate the PAO2:

PIO2="FIO2" x (PB 47)

PIO2="0.4" x 713="285.2" mm Hg

PAO2="PIO2" PaCO2 x 1.25

PAO2="285.2" 45 x 1.25

PAO2="285.2" 56.25="228.95" mm Hg

pulmonary capillary content:

(CcO2): CcO2="Hb" x 1.39 + 0.003 x PAO2

CcO2="10" x 1.39 + 0.003 x 229

CcO2="13.9" + 0.687="14.59" Vol %

We can now fill in the final shunt equation:

QS/QT="(CcO2" CaO2) / (CcO2 CvO2)

QS/QT="(14.6" 13.7) / (14.6 9.1) QS/QT="0.9" / 5.5="0.16" %

Example Cases
Joe Crisco: A 64 year old male presents to the emergency room with chest pain, shortness of breath, and nausea. Initially he only had pain upon heavy exertion but over the last week he's had episodes at rest. Today he has had the pain continuously for the past hour. On physical examination he is acutely dyspneic and cyanotic. His lung exam reveals crackles up to the shoulders bilaterally and his neck veins are distended. A blood gas is drawn on 60% oxygen by mask and reveals a pH of 7.34, a PaCO2 of 33, and a PaO2 44.

1. What is wrong with this patient?

2. Why is he hypoxic?

3. What can be done therapeutically?

Cathy Crush: A 32 year old woman is in the hospital recovering from a fractured hip which she suffered in a motor vehicle accident. At 3 am one morning she develops sharp right sided chest pain and becomes acutely short of breath. She's never had these symptoms before. On physical examination she appears anxious and tachypneic. Her lung examination reveals a pleural friction rub heard over the right lateral chest. A chest x-ray is essentially normal and an electrocardiogram is significant for right atrial enlargement and tachycardia. A blood gas on a 40% oxygen mask shows a pH of 7.35, a PaCO2 of 33, and a PaO2 58.

1. What is wrong with this patient?

2. Why is she hypoxic?

3. What can be done therapeutically?

Winston Salem: This 49 year old man had his right lung removed because of lung cancer 6 months ago. He presents today for a routine follow-up visit and room air blood gasses are drawn revealing a pH of 7.42, a PaCO2 of 35, and a PaO2 88.

1. Why are this man's blood gasses normal? ]]>delton@lexpcc.netChest2009-12-05T19:44:35-05:00http://www.lexingtonpulmonary.com/articles/files/f34fc57aa89d574179a3b13e9850153a-17.php#unique-entry-id-17http://www.lexingtonpulmonary.com/articles/files/f34fc57aa89d574179a3b13e9850153a-17.php#unique-entry-id-17Pulmonary Embolism
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
Pulmonary embolus is a common condition occurring in about 1 in 50 hospital admissions. Because of difficulties in positively ruling the diagnosis in or out, many physicians hesitate the raise the possibility that a pulmonary embolus may be present in a particular case though the mortality of an untreated pulmonary embolus may approach 30%.

Pathophysiology
95% of pulmonary emboli originate as lower extremity deep venous thrombi. A recent study demonstrated that about 50% of patients with DVT could be shown to have an unmatched perfusion defect by V/Q scan and of these 66% of these defects resolved after anticoagulation suggesting that these were acute pulmonary emboli. 10% of pulmonary emboli result in some degree of pulmonary infarction. It is not clear whether pulmonary embolic mortality is strictly related to pulmonary vascular obstruction (i.e. hemodynamic effects) or whether humoral or gas-exchange factors predominate. It would not be surprising if the dominate pathology varied among patients. Note that since normal patients are able to at least double their cardiac output (and thus their pulmonary blood flow) without significantly elevating their pulmonary artery pressure, that at least 50% of the pulmonary circulation would need to be obstructed by a pulmonary embolus before significant hemodynamic compromise resulting from mechanical obstruction would occur. This, of course, assumes that the pulmonary circulation is normal before the embolus occurs. Pulmonary embolic disease converts normal lung units into dead space units. This results in V/Q mismatches (i.e. areas of normal ventilation with reduced perfusion). This alteration in V/Q mismatching result in hypoxemia and results in a need for an increased minute volume to maintain the same PaCO2 level. If the mismatch is significant one would expect tachypnea and hypoxia to develop as a result of this mismatch.

Signs/Symptoms
Most symptoms of pulmonary embolus emanate directly from the pathophysiology. Some (hypoxia) relate from the creation of deadspace while others (right atrial enlargement on the EKG) result from increased pulmonary artery pressure from mechanical obstructive phenomena. Common findings in pulmonary embolus include:

hypoxia and respiratory alkalosis

EKG evidence of RV overload such as right ventricular hypertrophy or right atrial enlargement.

Increased deadspace as shown by Vd/Vt measurement (rarely measured).

Pleural effusion, frequently bloody.

Hypoperfusion on chest radiograph.

Unmatched perfusion defects on V/Q scan.

Positive pulmonary angiogram (gold standard).

Tachycardia (this is frequently the only objective finding).

Chest pain and dyspnea (very common).

Diagnostic Work-up
Once the possibility of pulmonary embolus has been raised, a diagnostic work-up must be conducted to either confirm or deny the diagnosis. Given the high rate of pulmonary embolus in patients with deep venous thrombosis, it could be argued that all patients with DVT should be worked up for PE as well. In most cases, the treatment for DVT will be the same as the treatment for PE therefore diagnosis of either will result in treatment though it would be useful in future management to know whether PE has occurred. The two main methods used to evaluate for PE are V/Q lung scanning and pulmonary arteriography. The pulmonary angiogram is the 'gold standard' for diagnosing or ruling out a pulmonary embolus. The risks are the risks of a central venous line plus the risk of IV contrast. The usual algorithm though is to start with a V/Q scan except in cases where the V/Q is non-diagnostic (this is frequent) or in cases where one would expect the V/Q scan to be difficult to interpret. The V/Q scan is really two tests, one to evaluate ventilation and one to evaluate perfusion. The ventilation test involves the patient breathing a radioactive tracer gas and sitting under the gamma camera to evaluate whether ventilation is normal in areas of the lung that may be shown to have abnormal perfusion on a perfusion scan. A high probability V/Q scan would be one that showed a segmental defect in perfusion without a matching defect in ventilation. V/Q scans in patients with significant ventilation defects are difficult to interpret and even in a low probability scan, the incidence of pulmonary embolus may be as high as 25%. A recent study demonstrated that V/Q scanning had a sensitivity of 98% with a specificity of only 10% if one considers low probability scans to be positive scans. If you decide that only high probability scans are positive then the sensitivity drops to 41% with a specificity of 97%. Because of this diagnostic uncertainty in ruling out PE (i.e. low sensitivity), a V/Q scan really needs to be very normal, not just low probability, to avoid doing a pulmonary arteriogram to rule out PE if clinical suspicion is high unless the plan is to just treat the patient emperically. If a V/Q scan is positive, however, treatment can begin. A recent studies (Hull) suggest that the combination of clinical suspicion (prior probability) and the V/Q scan agreeing with that clinical suspicion would be 95% sensitive and 95% specific. Unfortunately the basis of this estimate of clinical suspicion was not standardized or defined in the paper. Since 95% of pulmonary emboli originate from the legs, a venogram or venous doppler study can be used to detect the DVT and treatment can proceed if this is positive even though there is a possibility of a PE without a DVT (5%) and you could have a DVT without PE (around 50% of the time). The need for further work-up for PE in the patient with a DVT would depend on how seriously ill the patient was and whether further therapy specific for the PE was considered (i.e. thrombolytic therapy or embolectomy). The echocardiogram is frequently useful in evaluating the patient with suspected pulmonary embolus. In some cases residual clot can be imaged in the right ventricle or right atrium (a finding that suggests a high likelihood of another embolus soon) and right ventricular overload can be demonstrated if it is present.

Chemical Tests for PE
Recently there has been work done to try to develop assays for serum and urine markers of pulmonary embolic disease. So far, these tests have a fairly high degree of sensitivity but have a fairly low specificity which means that they can be used to rule out a pulmonary embolus but they cannot be used to confirm one. This is still very useful, however, as they tests can be used as evidence to avoid an expensive, and perhaps risky, work up in patients who fail to show the markers. One test, the D-dimer test, measures the level of a product of fibrin degradation. A serum D-dimer concentration of less than 500 ug/l has a negative predictive value of 98% meaning that less than 2% of persons with a D-dimer level below 500 will be later found to have a pulmonary embolus. The sensitivity of this test remained high even 3 and 7 days after presentation. The RMH laboratory (1991) provides the D-dimer test on demand for a cost of $42 (a CBC is $48) and a testing time of under one hour. A recent paper (Leitha et al) has cast some controversy on the utility of the D-dimer test showing a sensitivity closer to 50% for predicting a high-probability V/Q scan if 500 ng/ml is the cut-off and 84% if the cut-off is 120 ng/ml. It should be noted, however, that V/Q scans may remain abnormal for some time (perhaps months or longer in some cases) after an acute event so a study using a V/Q scan as the end-point might not be valid as a test of the accuracy of the D-dimer study as a screening test for pulmonary embolus. In any case, realized that this use of the D-dimer study is likely to be the subject of further study before its utility is generally accepted. There is more than one methodology of D-Dimer test in common use in laboratories. Only the quantitative measurement techniques are really sensitive enough to be of much utility in ruling out a PE.

Treatment
Most pulmonary emboli are treated with systemic anti-coagulation. This means IV heparin followed by coumadin. Note the table below on how to actually administer these drugs. There have been some trials of thrombolytic therapy and thus far the results are promising but it remains to be seen whether morbidity and mortality are improved by this therapy. Thrombolysis is probably indicated for patients with hemodynamic compromise from a pulmonary embolus in the absense of contraindications and will possibly gain acceptance as treatment for all symptomatic emoboli in the future. Embolectomy is a therapy of last resort and most patients who might benefit from it are very sick and many die before the diagnosis is even certain.

References
Hyers TM, Hull RD, Weg JG: Antithrombotic Therapy for Venous Thromboembolic Disease, Chest 95:2, February 1989 supplement.
The PIOPED investigators: Value of Ventilation/Perfusion Scan in Acute Pulmonary Embolism, Results of the Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED), JAMA 263:20, May 1990.
Bone RC: Ventilation/Perfusion Scan in Pulmonary Embolism, 'The Emperor is Incompletely Attired', JAMA 1990; 263:20.
Bell WR: The Clinical Features of Submassive and Massive Pulmonary Emboli, AM J MED 1977; Vol. 62.
Hull RD: Diagnostic Value of Ventilation-Perfusion Lung Scanning in Patients with Suspected Pulmonary Embolism, Chest 1991; 88:6.
Tulchinsky, M, Zeller JA, Reba RC: Urinary Fibrinopeptide A in Evaluation of Patients with Suspected Acute Pulmonary Embolism, Chest 1991; 100:394-98.
Bounameaux H, Cirafici P, De Moerloose P, et al: Measurement of D-dimer in plasma as diagnostic aid in suspected pulmonary embolism, Lancet 1991; 337:196-200.
Kelly MA, Carson JL, Palevsky HI, Schwartz JS: Diagnosing Pulmonary Embolism: New Facts and Strategies, Annals of Internal Medicine 1991; 114: 300-306.
Hull RD, Hirsch J, Carter CJ, et al: Diagnostic value of ventilation-perfusion lung scanning in patients with suspected pulmonary embolism, Chest 1985; 88: 819-28.
Hull RD, Hirsh J, Carter CJ, et al: Pulmonary angiography, ventilation lung scanning, and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan, Ann Intern Med 1983; 98: 891-9.
Leitha T, Speiser W, Dudczak R: Pulmonary Embolism, Efficacy of D-dimer and thrombin-antithrombin III complex determinations as screening tests before lung scanning, Chest 1991; 100:1536-41. ]]>delton@lexpcc.netChestPAH2009-12-05T19:43:48-05:00http://www.lexingtonpulmonary.com/articles/files/e1cb682ab858fb35bd76c99cbf7b4f5f-16.php#unique-entry-id-16http://www.lexingtonpulmonary.com/articles/files/e1cb682ab858fb35bd76c99cbf7b4f5f-16.php#unique-entry-id-16Pneumothorax
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Definition
A pneumothorax is a collection of gas that is in the pleural space within the chest but outside of the lungs. The pleural space is a potential space bounced by the visceral and parietal pleura. This potential space exists to allow the chest wall to exert a suction to oppose the normal elastic recoil of the lungs. If this potential space is filled by air, this opposition is lost and a collapse of the involved lung occurs.

Classification
A pneumothorax is called spontaneous if it occurs in the absence of any trauma to the chest. It is considered to be primary when there is no obvious lung disease. A traumatic pneumothorax is normally caused by penetrating chest trauma but could be a result of barotrauma from a ventilator. A tension pneumothorax is one in which there is positive pressure in the pleural space sufficient to cause patient compromise.

Etiology
There are many causes of pneumothorax. Air enters the pleural space either from outside the chest (penetrating trauma), from lung parynchyma, or from the esophagus in cases of perforation. Obstructive lung diseases, either intrinsic, or resulting from foreign body airway obstruction, can lead to pneumothorax by allowing for inadequate exhalation of inspired gas. This can start out as "Auto-PEEP" which may damage lung tissues resulting in air leaks or can result from a "ball-valve" effect where an obstruction can be bypassed by enlarging airway diameter on inspiration but cannot be bypassed during exhalation when airway diameter is smaller. Such an obstruction could be caused by mucus plugging or by a foreign body in an airway. Pleural diseases can cause a pneumothorax by direct disruption of the pleura. Marfan syndrome patients are more susceptible to pneumothorax possibly due to a combination of abnormal connective tissue and by greater pleural pressure changes during breathing that result from the Marfan body habitus. This occurs mostly in young tall thin males.

Tension Pneumothorax
A tension pneumothorax results from situations where air can enter the pleural space but cannot leave. An example might be a stab wound to the chest that punctures the lung. While there is a hole in the chest, a knife wound tends to seal itself in the chest wall thus trapping any air leaked from the lung injury in the chest cavity. A gun shot wound is less likely to result in a tension pneumothorax as the leaked air can exit the chest via the entry wound in the chest wall. Most tension pneumothoraces are traumatic and many of these are iatrogenic and occur on patients who are receiving mechanical ventilation where positive airway pressures facilitate leakage of air into the pleural space. A tension pneumothorax is life threatening because there is more complete collapse of the affected lung and because the positive pressure exerts several adverse effects on the cardiovascular system including tamponade of the mediastinal structures and kinking of the great vessels at their point of entry to the thorax caused by mediastinal shift.

Diagnosis
A pneumothorax by have either an insidious or dramatic onset. Typical symptoms include pleuritic chest pain and dyspnea. Tachycardia and severe hypotension are the only noticeable findings in a mechanically ventilated patient or a patient who is otherwise unable to provide a history. There may be evidence of tracheal deviation and a deviated PMI if there is tension with mediastinal shift. Breath sounds will normally be absent or diminished but you may be able to hear breath sounds transmitted from the contralateral lung in some patients. In some cases, transillumination of the chest with a bright light source will light up the hemithorax of a patient with a pneumothorax though this technique is limited to pediatric patients or those with a thin chest wall. A chest x-ray, preferably with a lateral view or one taken during exhalation is normally the most definitive test to diagnose a pneumothorax but in some cases of tension pneumothorax, a patient may succumb before there is time to obtain one so it is necessary to consider treating an as-yet unconfirmed pneumothorax if the clinical situation dictates.

Radiographic diagnosis
The classic finding of pneumothorax on a chest x-ray is to see a peripheral lung margin with lucency between the lung margin and the chest wall. With a tension pneumothorax there will be mediastinal shift away from the affected side. It must be remembered, however, that the chest is a 3-dimensional structure and that the free air of a pneumothorax may be loculated anterior or posterior to lung or even interposed between the diaphragm and the lung. For this reason, presence of lung markings on a single view chest x-ray does not rule out a pneumothorax. One should be suspicious of any unusual lucencies in the chest and additional views should be obtained, perhaps even including CT scans of the chest in some cases.

Treatment
Not all pneumothoraces require specific therapy. In asymptomatic or mildly symptomatic patients, serial chest x-rays can be obtained to allow for spontaneous resorption of a small pneumothorax. Resorption can be accelerated by placing a patient on 100% oxygen to wash nitrogen from the pleural space with a resultant decrease in the size of the collected free gas. There has been some success reported with needle thoracentesis of spontaneous pneumothoraces though recurrences of pneumothorax are not unusual with this technique and a repeat procedure or chest tube may be required. If a patient is being mechanically ventilated there is a higher risk of progression to a tension pneumothorax and in these cases a chest tube should be used to evacuate any free air and allow time for the original air leak to heal.

Chest Drainage Systems
In an emergency, the initial treatment of a pneumothorax, tension or otherwise, is to place a large bore IV needle into the pleural space to decompress any tension and/or to remove free air to allow the lung to re-expand. Free air will normally collect anteriorly in a supine patient so the needle would be placed into the chest, over a rib, normally in the 2-4th rib interspace between the anterior axillary and mid-clavicular lines. In many cases, a patient will improve as soon as tension is released with a needle procedure though some patients will not improve until their lung has been re-expanded. Once a chest tube has been inserted in the pleural space (anteriorly if possible) a system is needed that will allow air and fluids out of the chest without allowing air to leak back into the chest. In some cases, it may be desirable to allow for suction to be applied to the pleural space to facilitate removal of air or fluids. A Heimlich valve can be used to satisfy the first requirement and consists essentially of a one-way valve that is attached directly to a chest tube. A make shift Heimlich valve can be produced by attaching the finger of a surgical glove over the end of a chest tube and placing a small hole in the end of the glove finger. The glove finder would tend to allow gasses to escape but would collapse in response to negative pressure in the pleural space.

A 3-bottle or Atrium or Pleurovac drainage system can provide valuable information about the patient's pleural pressure and the presence of absence of an active air leak (bronchopleural fistula for example). The first chamber (White on a Pleurovac) is a simple trap to catch any fluids drained from the chest tube. The second chamber (Pink on a Pleurovac) is the underwater seal or water seal chamber. This chamber exists to provide the one-way valve that will allow air to exit the chest but not to enter it. Note that the tube from the drainage chamber is immersed under water about 2 cm deep. Any pressure in the pleural space greater than 2 cm H2O will result in bubbles forming in this chamber. If you see bubbles in this chamber then there is air coming from the chest tube or connecting tubing. Note that a hole in the chest tube that is outside of the chest will result in heavy bubbling in this chamber so not all leaks are from the pleural space. The third chamber (Blue on a Pleurovac) is the suction control chamber. If the "S" connection is attached to wall suction and there is bubbling from the vent tube, then the level of negative pressure applied to the pleural space is equal to the depth that the vent tube is placed under water. 20 cm H2O would be a typical level of suction. Some chest drainage systems substitute a needle valve suction regulator for the suction control chamber. To measure the pleural pressure, one can pinch off the suction tubing "S" and read the water level in the underwater seal chamber (second chamber).

Prevention
Iatrogenic pneumothoraces can be prevented in some but not all cases. If a thoracentesis is to be performed, use of ultrasound guidance can help in avoiding lung injury and avoidance of pleural adhesions which may be likely to result in a pneumothorax if punctured. The biggest danger in an iatrogenic pneumothorax is in not recognizing that one has occurred. Listening to breath sounds before an invasive procedure starts will make it much easier to tell if a pneumothorax exists afterwards. In high risk patients (i.e. high airway pressures and/or unstable hemodynamics) plan ahead by having large bore needles, stop cocks, and syringes available before the procedure is started so there will be minimal delay in draining a life-threatening pneumothorax.

References
Connors AF, Altose MD: Textbook of Pulmonary Diseases, p.1592, Little Brown, Boston, 1989.
Bevelaqua FA and Aranda C: Management of spontaneous pneumothorax with small lumen catheter manual aspiration. Chest 1982; 81:693-694.
Gustman P, Yerger L, Wanner A: Immediate Cardiovascular Effects of Tension Pneumothorax, ARRD 1983; 127:171-174.
Haake R, Schlichtig R, Ulstad DR: Barotrauma Pathophysiology, Risk Factors, and Prevention, CHEST 1987, 91:608-613.
Conces DJ et al: Treatment of Pneumothoraces Utilizing Small Caliber Chest Tubes, CHEST 1988, 94:55-60.
Jenkinson, SG: Pneumothorax, Clinics in Chest Medicine, 1985, 6:153-161.
Ohata M, Suzuki H: Pathogenesis of Spontaneous Pneumothorax, CHEST 1980, 77:771-776. ]]>delton@lexpcc.netPhysiology2009-12-05T19:43:21-05:00http://www.lexingtonpulmonary.com/articles/files/1add35e2acb566460522a28c52b5dc58-15.php#unique-entry-id-15http://www.lexingtonpulmonary.com/articles/files/1add35e2acb566460522a28c52b5dc58-15.php#unique-entry-id-15Oxygen - Hemoglobin Affinity
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
It is commonly thought that shifts in the oxyhemoglobin dissociation curve are important factors in adaptation to hypoxic conditions. In actual fact, the subject is more complex than is generally recognized and benefits (or detriments) resulting from changes in hemoglobin's affinity for oxygen can only be demonstrated under extreme conditions. Structure = Function Human hemoglobin exhibits a sigmoid relationship between PO2 and hemoglobin saturation. This shape of curve offers benefits in that almost complete saturation can be obtained over a wide range of oxygen partial pressures at the lung while large quantities of oxygen can be delivered to peripheral tissues once the oxygen partial pressure falls to lower levels than those normally encountered at the alveoli. Several factors can cause shifts of the curve but the sigmoidal shape of the curve is ordinarily preserved except in cases of carbon monoxide poisoning. The sigmoidal shaped curve results from steric interactions between adjacent heme molecules as they bind successively with oxygen.

P50
It is common to use the concept of P50 to describe the affinity of a given hemoglobin for oxygen. The P50 is the PO2 at which the hemoglobin becomes 50% saturated with oxygen. As the P50 decreases, oxygen affinity increases and visa verse. Normal adult Hemoglobin A has a P50 of 26.5 mm Hg while Fetal Hemoglobin F has a P50 of 20 mm Hg and sickle cell anemia Hemoglobin S has a P50 of 34 mm Hg.

Oxygen Pickup & Delivery
It is convenient to divide the function of hemoglobin into oxygen pickup and oxygen delivery. Oxygen is initially added to the circulation in the lungs in the form of dissolved gas and delivery to end tissue mitochondria is by the same mechanism. Movement of oxygen in the physically dissolved state is dependent upon movement across a short distance according to a partial pressure/concentration gradient. In the lungs, oxygen will move into blood if the oxygen partial pressure in the alveolus exceeds the partial pressure in the pre-alveolar capillary blood. Oxygen present in the dissolved state reversibly binds with available hemoglobin at a rate determined by the affinity of that hemoglobin for oxygen. Once the partial pressure in the capillary exceeds about 150 mm Hg, no more oxygen can be loaded onto hemoglobin and saturation is complete. In the tissues, as physically dissolved oxygen is removed from the circulation by mitochondria, the local PO2 falls. The oxygen removed in this manner is replaced by oxygen that dissociates from available hemoglobin until the hemoglobin has no more oxygen to give or until the oxygen delivery exceeds the consumption requirements of the mitochondrion. Oxygen can continue to move into functioning mitochondrion as long as there is at least a 1 mm Hg partial pressure gradient and mitochondrial function has been demonstrated at a local PO2 of 1 mm Hg.

Adaptation to Changes in Oxygen Affinity
There are several ways that tissues compensate for changes in hemoglobin's affinity for oxygen that prevent changes in oxygen delivery that might otherwise occur.

Oxygen Affinity at the Lung
If oxygen affinity is increased at the lung level, complete saturation will occur at lower ambient PIO2. This can result in the arterial content approaching nearly normal levels even at high altitude. A reduced oxygen affinity (rising P50) can result in reduced oxygen content and delivery potential at the lung level. Again, under most usual circumstances, these are negligible effects over the usual range of P50 values found with normal hemoglobins though there are animal and some abnormal human hemoglobins with P50 values ranging from as low as 10 to as high as 70 mm Hg. When these grossly abnormal human hemoglobins occur, they usually make up less than half of the total hemoglobin available. If oxygen affinity is decreased, then oxygen delivery can still be maintained either by an increased cardiac output or an increased hemoglobin concentration. Local factors such as pH and other chemical mediators can also influence the oxygen affinity back toward normal under some circumstances.

Oxygen Affinity at the Tissues
As hemoglobin's affinity for oxygen rises at the tissue level (P50 going down), oxygen extraction will fall if the PO2 and blood flow are held constant. In vivo, however, the PO2 falls and oxygen extraction and blood flow is constant. Only when the PO2 reaches very low levels will the local blood flow increase and severe anemia must frequently be present to actually demonstrate this effect when the P50 has been experimentally reduced.

Natural Models
There are several models that demonstrate effects of altered P50. Some are experimental models while others occur naturally in nature. In the human fetus, a reduced P50 aids in pickup of oxygen at the placenta owing to the increased oxygen affinity of fetal hemoglobin (which interestingly results from an alteration in fetal hemoglobin's sensitivity to levels of 2,3-DPG). So long as severe anemia or severely reduced blood flow to tissues is avoided, the effects of this reduced P50 at the tissue level is negligible. Llamas and humans who are chronically adapted to life at high altitudes have been shown to have reduced P50 levels which presumably offer benefits similar to those seen with fetal hemoglobin in the normal human fetus. The short-term effects of high altitude on two human subjects with a high oxygen affinity hemoglobin (inherited) were tested by Hebbel who found that in contrast to normal subjects, at 3,100 meters, the high affinity subjects had lesser increases in resting heart rate, minimal increases in erythropoietin, and no decrement in maximal oxygen consumption.

Experimental Models
In a study of the effects of increased oxygen affinity of hemoglobin in monkeys (caused by transfusions of blood lacking 2,3-DPG), Riggs found that mixed venous PO2's fell while cardiac output, A-V difference, and oxygen consumption remained constant. A study by Malmberg of rats exchange transfused with blood of differing oxygen affinity showed that rats with a normal P50 were more likely to survive experimental shock and anemia than those with a reduced P50. Summary Leftward shifts in the oxyhemoglobin dissociation curve (falling P50) would appear to have benefits in preserving oxygen delivery and extraction under circumstances of severe hypoxic stress such as might be found in cases of hypoperfusion, anemia, and ambient hypoxia. Under the vast majority of circumstances, however, these effects are minimal because of the human's large capacity for adaptive compensation by means of polycythemia, increased cardiac output, increased oxygen extraction, and regional changes in blood flow. It remains to be demonstrated whether there are any therapeutic benefits to be gained by attempting to artificially alter the P50 and attempts to do so would be complicated by the body's attempts to restore the P50 toward normal.

References
Hebbel RP, Eaton JW, Berger EM, Kronenberg RS, Zanjani ED, Moore LG: Hemoglobin oxygen affinity and adaptation to altitude: evidence for pre-adaptation to altitude in humans with left-shifted oxyhemoglobin dissociation curves. Trans Assoc Am Physicians, 91:212-28, 1978.
Klocke RA, Saltzman AR: Gas Transport, pp 173-94, in Textbook of Pulmonary Diseases, edited by Baum GL, Wolinsky E, Little Brown and Company, 1989.
Riggs, TE, Shafer, AW, Guenter, CA: Acute changes in oxyhemoglobin affinity: Effects on oxygen transport and utilization. J. Clin. Invest. 52:2660, 1973.
Malmberg PO, Hlastala MP, Woodson RD: Effect of increased blood-oxygen affinity on oxygen transport in hemorrhagic shock. J. Appl. Physiol. 47:889, 1979.
]]>delton@lexpcc.netPhysics2009-12-05T19:42:57-05:00http://www.lexingtonpulmonary.com/articles/files/20f732e4cded06cd4c8fc9640caf0ed9-14.php#unique-entry-id-14http://www.lexingtonpulmonary.com/articles/files/20f732e4cded06cd4c8fc9640caf0ed9-14.php#unique-entry-id-14Lung Mechanics & Mechanical Ventilation
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Who Cares?
Why do we care about lung mechanics during mechanical ventilation? We all should if we want to provide adequate ventilatory support with a minimum of adverse effects. It would be useful if we could easily measure lung compliance, airway resistance, functional residual capacity, and other pulmonary function parameters during mechanical ventilation. Unfortunately, it is difficult to conduct formal pulmonary function testing on critically ill patients who frequently require high airway pressures and flows and may be paralyzed or otherwise unable to cooperate with testing. This paper will explore the theory and application of a few simple bedside maneuvers that anyone can perform either with or without patient cooperation to assess lung mechanics.

Compliance
Compliance is a measurement of the distensibility of the lung. It is expressed as a change in volume divided by a change in pressure. The standard units of Liters/cm H20. The normal lung+thorax compliance of an adult is around 0.1 L/cm H20. When the compliance is low, more pressure will be need to deliver a given volume of gas to a patient. Disease states resulting in low compliance include the Adult Respiratory Distress Syndrome (ARDS), pulmonary edema, pneumonectomy, pleural effusion, pulmonary fibrosis, and pneumonia among others. Emphysema is a typical cause of increased lung compliance.

Airway Resistance
Resistance is the amount of pressure required to deliver a given flow of gas and is expressed in terms of a change in pressure divided by flow. The standard units of resistance are cm H20/L/second and the normal value for an adult is around 0.5 - 1.5 cm H20/L/sec while in states of disease this value may be 100.0 cm H20/L/sec or higher. There really aren't any diseases characterized by decreased airway resistance since normal values are so low but there are many disease states that result in increased airway resistance including use of artificial airways, asthma, emphysema with airway collapse, mucus plugging, vocal cord paralysis, and endobronchial obstruction either from tumors or foreign bodies.

Time Constant
The Time Constant of the lung (TC) is a concept borrowed from electrical engineering which describes the phenomenon whereby a given percentage of a passively exhaled breath of air will require a constant amount of time to be exhaled regardless of the starting volume given constant lung mechanics. That's quite a mouth-full of a definition but consider what determines how long it takes to exhale a tidal breath passively. At the start of exhalation, the initial flow of gas out of the lung depends upon the driving pressure (i.e. alveolar pressure - mouth pressure) and it depends on the airway resistance. For any given volume of gas, the alveolar pressure at the start of exhalation is only dependent upon the lung compliance. Mathematically, the time constant is defined as compliance multiplied by the airway resistance and the resulting value has units of seconds of time..

Airway Pressure & Alveolar Pressure
Airway pressure is the pressure measured at the patient's airway during mechanical ventilation. Airway pressure is determined by the sum of the alveolar pressure and the pressure required to deliver flow across the airways which is determined by the airway resistance. Alveolar pressure is the pressure in the distensible parts of the respiratory tract and is determined by the tidal volume and the lung/chest compliance. Airway pressure is equal to alveolar pressure when there is no flow occurring. At the end of a mechanical inspiration, flow to the distal parts of the lung continues even after inspiratory flow from the ventilator stops as time is required for gas to reach the periphery of the lung. To measure alveolar pressure, one must measure the airway pressure at a time when both pressures are equal, i.e. when there is no flow. Measuring Compliance To measure lung compliance one must know the delivered tidal volume and must also know the change in alveolar pressure that results from the addition of that known tidal volume. We normally assume that alveolar and airway pressure start out at atmospheric (our zero reference) before an inspiration starts. To equalize airway and alveolar pressures we only have to prevent exhalation after inspiration has ceased by utilizing an inspiratory hold maneuver. The actual calculation is to divide the delivered tidal volume by the plateau pressure where the plateau pressure is the steady-state pressure measured during an inspiratory hold maneuver. If precise measurement is necessary then the pressure should be the plateau pressure minus any end expiratory pressure (or the pleural pressure or Auto-PEEP if it is available) and the volume should be either measured at the airway itself or should be corrected for compressible volume loss. In most cases, approximate values are adequate for clinical use so the plateau pressure minus the end expiratory pressure is divided into the exhaled tidal volume as measured by the ventilator. This compliance measurement is sometimes called the static compliance since it is measured after an inspiratory hold such that there is no gas flow during its measurement.

Measuring Resistance
Airway resistance can be estimated by dividing the difference between peak and plateau airway pressures by the mean inspiratory flow rate. Some ventilators have an inspiratory flow rate setting such that you can read the control for an estimate of delivered flow rate while others give an inspiratory time setting where you have to divide the tidal volume by the inspiratory time to determine the inspiratory flow rate. An alternative way of following airway resistance is to calculate a nonsense parameter known as the dynamic compliance . The dynamic compliance is the result of dividing the delivered tidal volume by the peak airway pressure. Since peak airway pressure is determined by a combination of the lung compliance, the airway resistance, inspiratory flow rate, and the tidal volume, this value does not really give a quantitative estimate of airway resistance itself but can be used to detect changes in the airway resistance if all other factors are held constant. This makes the value useful for comparing measurements on a single patient over a short period of time but it is too much to ask to expect that all of the other variables affecting peak airway pressure will stay the same from day to day or certainly from patient to patient. Because of the limitations of dynamic compliance measurements, it makes more sense to just follow the peak pressure to plateau pressure gradient since it requires less math and is just as useful (or useless) as the dynamic compliance calculation. A third way to estimate airway resistance can be used if the patient is exhaling passively. This method works based on the time constant. The practitioner times how long it takes for the patient to exhale completely and then divides this result by 3 to estimate the time constant. The lung compliance is then measured and divided into the time constant to result in the airway resistance thus: Raw = Time Constant / Clung

Auto PEEP
Auto PEEP is the popular name used to describe increased alveolar pressure caused by gas trapping during mechanical ventilation. Gas trapping occurs when there is inadequate time to exhale the mechanical tidal volume. Recall that the time constant determines the length of time needed for a passive exhalation and that the time constant is the product of airway resistance and lung compliance. The lower the compliance, the higher the driving pressure pushing gas out of the lungs during exhalation; the lower the resistance, the higher the expiratory flow rate can be when driven by the alveolar pressure. If the time constant is known (or can be estimated) then the maximum mechanical respiratory rate that can be used before Auto PEEP results can be estimated. Consider that at least 3 time constants are required to exhale passively any volume of gas. The combination of inspiratory and expiratory time leads to a give respiratory rate such that:

Total Breath Time = Insp time + Exp time

Respiratory Rate = 60 / Total Breath Time

Maximum Rate = 60 / (Insp time + 3 x TC)

A patient with a compliance of 0.05 L/cm H20 and an airway resistance of 30 cm H20/L/sec. This would give a time constant of 1.5 seconds. A complete exhalation would take around 4.5 seconds. If inspiratory time is 1 second then total breath time is 5.5 seconds and the maximum respiratory rate without gas trapping would be 11 breaths per minute. When gas trapping occurs, the functional residual capacity (FRC) is increased. As the FRC increases, the alveolar pressure increases by an amount of pressure determined by the patient's lung compliance. As the FRC rises in relation to the total lung capacity (TLC), the lung compliance will decrease. This decrease in lung compliance shortens the time constant for the next breath and thus shortens the time required to exhale the next breath and lessens the amount of trapping that will occur with each subsequent breath until the time constant shortens enough that gas trapping no longer occurs. When this steady state is reached, the FRC is at its maximum and the auto-PEEP is also at its maximum. This fact gives us a way to measure how much auto-PEEP exists since we can serially measure exhaled tidal volumes and then interrupt ventilation (by turning the respiratory rate to zero for several seconds) and measuring how much gas the patient exhales as the patient exhales back to the FRC level that existed prior to ventilation. If we take the difference between the exhaled volume during ventilation and the exhaled volume after interrupting ventilation then we have the amount of gas that was trapped. If we divide this volume by the lung compliance we will have calculated the amount of auto-PEEP applied to the alveoli during ventilation. Normally we are more interested in avoiding auto-PEEP than in measuring it though there are many patients in whom it cannot be avoided so it is useful to be able to quantitate it. Another way to detect auto-PEEP is to watch a patient's chest movement and/or breath sounds during exhalation to see if exhalation stops prior to initiation of inspiration by the ventilator. If exhalation doesn't finish then auto-PEEP is occurring. When exhaled tidal volumes cannot be measured (which is seldom with modern ventilators) the level of auto-PEEP can be very roughly estimated by interrupting exhalation just prior to initiation of inspiration and watching to see if there is a pressure increase at the airway as exhalation continues into the circuit between the patient and the point of your interruption. This is not an accurate measurement since the interruption necessarily cuts exhalation shorter than it would normally be and because the circuit volume dampens the pressure measurement but this technique can be useful if you are unable to use the more reliable methods outlined above.

References
Shapiro BA, Harrison RA, Trout CA: Clinical Application of Respiratory Care, Year Book Medical Publishers, Inc, Chicago, 1982.
Tobin, MJ, Lodato, RF: PEEP, Auto-PEEP, and Waterfalls, Editorial, Chest 1989, 96:449-51.
Lain, DC, Chaudhary, BA et al: Auto-PEEP and Proximal Airway Pressure, Need for clarification, Editorial, Chest 1990, 97:771.
Duncan, SR, Rizk, NW, Raffin, TA: Inverse Ratio Ventilation, PEEP in Disguise?, Chest 1987, 92:390-1.
Wright, J, Gong, H: "Auto-PEEP": Incidence, magnitude, and contributing factors, Heart and Lung 1990, 19:352-7.
Hoffman, RA, Ershowsky, P, Krieger, P: Determination of Auto-PEEP During Spontaneous and Controlled Ventilation by Monitoring Changes in End-Expiratory Thoracic Gas Volume, Chest 1989, 96:613-6.

]]>delton@lexpcc.netChest2009-12-05T19:42:35-05:00http://www.lexingtonpulmonary.com/articles/files/ddce5c7c62ec2c995720c317714249b9-13.php#unique-entry-id-13http://www.lexingtonpulmonary.com/articles/files/ddce5c7c62ec2c995720c317714249b9-13.php#unique-entry-id-13Hemothorax
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Definition
A hemothorax is a collection of blood in the pleural space. It is classified according to the amount of blood. 350 ml or less is considered minimal, 350-1500 ml is moderate, and greater than 1500 ml is considered massive. In many cases, blood in the pleural cavity will be diluted by other pleural fluid. In these cases, the pleural fluid hematocrit can be used to diagnose a hemothorax using a hematocrit of greater than half the serum hematocrit as diagnostic of hemothorax.

Presentation
The presentation of hemothorax is related primarily to the acuity in that a chronic or slowly accumulating hemothorax may be asymptomatic while an acute hemothorax may present with shock, anemia, and respiratory compromise relating to compression of the lung and mediastinum by pressurized blood resembling the presentation of a tension pneumothorax.

Etiology
Trauma is an important cause of hemothorax. Hemothorax may result from either blunt or penetrating trauma of the chest but can also result from trauma to the abdomen such as from a ruptured spleen or liver. A ruptured ectopic pregnancy, bleeding from recent abdominal or pelvic surgery, or a ruptured abdominal aneurysm can also cause a hemothorax. Blood most commonly comes from systemic chest-wall vessels but can get to the pleural space from the pulmonary and/or bronchial vasculature. Other diagnostic considerations for hemothorax include malignancy (lung or pleural), or a pulmonary embolus or infarct. An unusual iatrogenic cause of hemothorax is from insertion of a central IV line through a vascular structure and into the pleural cavity.

Treatment
Chest tube drainage is the primary therapy for a hemothorax and 85% of cases will resolve spontaneously with only this treatment. If blood loss continues at a rate higher than 100-200 ml / hour then a thoracotomy should be considered remembering that a hemothorax could originate in the abdomen.

References
Lewis FR, Krupski WC, Trunkey DD: Management of the Injured Patient In Way LW (Ed.), Current Surgical Diagnosis & Treatment, Lange Medical Publications, 1983. Pp 194-5.
Conners AF, Altose MD: Pleural Anatomy, Pleural Fluid Dynamics, and the Diagnosis of Pleural Disease In Baum GL, Wolinsky E (Ed.), Textbook of Pulmonary Diseases, 4th edition, Little, Brown and Company, 1989. p 1569.
Ganji H, Vidrine A: Ectopic Pregnancy presenting as hemothorax, American Journal of Surgery 1970 December; 120(6) 807-9.
Pratt JH, Shamblin WR: Spontaneous hemothorax as a direct complication of hemoperitoneum, Annals of Surgery 1968 June; 167(6) 867-72.]]>delton@lexpcc.netGERD2009-12-05T19:42:14-05:00http://www.lexingtonpulmonary.com/articles/files/97afa8787a495d685211739eaf4c6fdb-12.php#unique-entry-id-12http://www.lexingtonpulmonary.com/articles/files/97afa8787a495d685211739eaf4c6fdb-12.php#unique-entry-id-12Gastroesophageal Reflux and Asthma
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care


One thing that is frequently overlooked in difficult to control asthma
is evaluation and/or treatment for gastroesophageal reflux. In some patients,
small amounts of stomach acid will make their way up the esophagus and into the
airways causing wheezing, coughing, hoarseness in some patients, chest pain or
back pain, and other symptoms. Some say that as much as half of all adult onset
asthma is really GERD (GastroEsophageal Reflux Disease). In my practice I
usually just give a few weeks of Prilosec or Prevacid (strong though expensive
antiacids) rather than going straight to testing. Many patients have nearly
complete relief of asthma symptoms after this trial thus clinching the
diagnosis. Testing is more involved and expensive than a trial of therapy in my
experience but may be required in difficult cases. I've had a few patients go
from 4 or 5 asthma drugs to Prilosec alone for this particular problem. There
may be no other symptoms aside from the wheezing to indicate that reflux is
going on so absense of acid taste etc is not enough to say you don't have GERD.

GERD is typically worse at night (when supine) while asthma is usually just
worse at night whether supine or not though post nasal drip and reflux can
worsen asthma when supine too.

GERD is worse if you eat within a few hours of going to bed.

GERD is worse if you sleep flat as opposed to having the head of the bed
elevated.

GERD is worse if you're obese or pregnant.

GERD is worse if you eat chocolate or mints (these can relax the esophagus
more).

Rarely someone will get surgery for reflux but the meds are pretty effective
in most cases even if they do run $3 a pill (once daily therapy is the norm). ]]>delton@lexpcc.nettherapy2009-12-05T19:41:53-05:00http://www.lexingtonpulmonary.com/articles/files/73e301c2250a3060938a35612bd3285a-11.php#unique-entry-id-11http://www.lexingtonpulmonary.com/articles/files/73e301c2250a3060938a35612bd3285a-11.php#unique-entry-id-11ECMO
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care


Introduction
Extracorporeal Membrane Oxygenation (ECMO) is a form of partial cardiopulmonary bypass used for long-term support of respiratory and/or cardiac function. This technology arose from cardiopulmonary bypass used for cardiac surgery. Initial systems used bubble oxygenators which were poorly suited for prolonged use because of their tendency to hemolyze blood. Membrane oxygenators made long-term use of ECMO possible. The first report of successful ECMO support of an adult was published by Hill in 1972.

Rationale
ECMO is primarily indicated for patients with such severe ventilation and/or oxygenation problems that they are unlikely to survive conventional mechanical ventilation. Examples of such patients would include those with the adult respiratory distress syndrome (ARDS) without major non-pulmonary organ failure who are failing mechanical ventilation or who are suffering from major barotrauma that makes adequate ventilation impossible. ECMO is only useful in cases where the primary lung insult is reversible in the absence of the usual oxygen toxicity and barotrauma caused by usual mechanical support. Since most patients who die of ARDS die of multi-system organ failure or sepsis, it would follow that most ARDS patients are not good candidates for ECMO. Another criteria often cited for qualifying a patient for ECMO treatment is a pre-treatment predicted mortality threshold, typically above 80-90%. Such a threshold makes ECMO, a new and as yet non-mainstream therapy, an ethically appealing option for otherwise hopeless cases. Unfortunately, the use of such a criteria preselects patients that may already be too sick to benefit from ECMO. If the pre-treatment mortality predictions are over-estimated, as they frequently are, then ECMO, as a treatment, may get more credit than it deserves in saving these patients' lives.

Techniques
ECMO currently comes in two varieties: venoarterial (VA), and venovenous (VV). VA ECMO takes deoxygenated blood from a central vein or the right atrium, pumps it past the oxygenator, and then returns the oxygenated blood, under pressure, to the arterial side of the circulation (typically to the aorta). This form of ECMO partially supports the cardiac output as the flow through the ECMO circuit is in addition to the normal cardiac output. VV ECMO takes blood from a large vein and returns oxygenated blood back to a large vein. VV ECMO does not support the circulation. VA ECMO helps support the cardiac output and delivers higher levels of oxygenation support than does VV ECMO. VA ECMO carries a higher risk of systemic emboli than does VV. VV ECMO systems may actually recirculate previously oxygenated blood depending on the placement of the inflow and outflow catheters. Another variant of VV ECMO is extracorporeal CO2 removal (ECCO2R). With this mode of support, oxygenation is provided by slow ventilation of the native lungs while CO2 removal is accomplished by the ECMO circuit. In all forms of ECMO, CO2 removal is more efficient than O2 addition because of the solubility and diffusion properties of CO2 relative to O2. In fact, CO2 normally has to be added to ECMO circuits to offset this efficiency at CO2 removal. The flow through the ECMO circuit is typically on the order of 100 mL/kg/minute. This would be from 25-75% of the cardiac output. This high flow requires the placement of large catheters into the circulation. For adults, the intravascular catheters may be 20 Fr or larger while 14 Fr catheters might be used in infants. These are generally placed by cut-down. Current circuits require the use of systemic anticoagulation with heparin to keep the systems patent. This anticoagulation is, in large part, responsible for bleeding complications that can be seen with the use of ECMO. Bleeding may occur either at the site of catheter insertion or at remote sites such as intracranial or the gastrointestinal tract. Future catheters with inpregnated heparin may obviate the need for systemic anticoagulation and would be expected to reduce bleeding complications. Once blood leaves the patient, it comes in contact with a gas-permeable membrane that allows gas exchange to occur between the blood and the gasses (oxygen and carbon dioxide) that are run into the oxygenator. Carbon dioxide levels leaving the oxygenator can be adjusted about as low as the physician wants while oxygen levels typically reach the 400-500 mm Hg level. Note that CO2 content varies fairly directly with partial pressure while O2 content follows the shape of the oxyhemoglobin dissociation curve. Under normobaric conditions, this limits the amount of oxygen that can be loaded into blood. If you were to try to predict the final mixed arterial oxygen content or partial pressure during VA ECMO, you would need to know the pulmonary venous oxygen content, the ECMO effluent oxygen content, and the % of cardiac output flowing through the ECMO circuit:

CaO2 = (EO x EF + NO x NF) / (EF + NF)
Where EO: ECMO oxygen content
EF: ECMO flow
NO: non-ECMO oxygen content
NF: non-ECMO flow

Predicting final arterial content during VV ECMO is more complex and cannot be easily calculated. During VV ECMO, the lungs may actually excrete oxygen rather than remove it from the inspired gas. Once ECMO has been started, the ventilator is typically reduced to minimal settings to prevent atelectasis and barotrauma. The FIO2 is lowered as much as possible, perhaps to room air. The ECMO flow rate is adjusted to the minimum needed to provide for adequate gas exchange and/or circulation support in the case of VA ECMO. ECMO is typically used for 7-12 days and is weaned when there is evidence of pulmonary improvement as indicated by compliance or radiologic appearance. ECMO can also be stopped if there are major complications or if the patient's condition is determined to be hopeless.

Complications
ECMO complications are those associated with cannulation (pneumothorax, vascular disruptions, bleeding, infection, emboli), those associated with systemic anticoagulation (GI bleeding, intracranial bleeding etc), and exsanguination resulting from circuit disruptions. These potential complications require that a trained ECMO technician be present at the bedside 24 hours per day in addition to the patient's usual nursing presence. As many as 30% of ECMO treated infants reported to the Extracorporeal Life Support Organization (ELSO) registry suffer some degree of CNS injury.

Patient Selection
As mentioned previously, usual ECMO criteria include patients with a severe reversible process that would result in a very high predicted mortality with conventional ventilatory support. The best candidates are those without multi-system organ failure that are otherwise considered to be salvageable. It would be expected, that once ECMO becomes safer and more accepted by physicians, that these criteria would be revised to eliminate the requirement for a very high predicted pre-treatment mortality. There are several ways to evaluate patients to determine if they are 'sick enough' for ECMO. APACHE and other scoring systems could be used to predict mortality. More frequently, indexes to assess refractory hypoxemia are used. The a:A ratio or A-a gradient can be used, but the oxygenation index (OI) is currently in more common use: OI = (FIO2) (MAP) / PaO2 An OI greater than 0.40-0.55 is thought to predict an 80% predicted mortality. Unfortunately, mortality predictors have been notoriously pessimistic since they are derived by looking at retrospective data and tend to do a poor job of predicting prospective results.

Evaluation of Results
ECMO is a difficult therapy to study and compare to conventional means of support. Ideally, a therapy like ECMO should be studied with a prospective randomized clinical trial where patients that meet an inclusion criteria are randomized to receive either ECMO or conventional therapy. Unfortunately, in such a study, the typical end-point would be the death of the patient and this is an end-point that most investigators and institutional review boards are uncomfortable with. As a result, studies comparing ECMO to conventional therapy typically include an escape clause of sorts that allows patients who are determined to have failed conventional therapy can get a trial of 'rescue' ECMO. The other main problem with studies of ECMO for adult patients are that there are very few patients who are sick enough to need ECMO that have reversible disease that ECMO might allow time for reversal of the process. Less than 20% of ARDS deaths are caused by respiratory failure while higher numbers of pediatric and neonatal deaths are caused by primary respiratory failure which would explain why ECMO would be more successful in pediatrics than it has proven to be in adult medicine.
In 1979 an NIH sponsored study compared ECMO with conventional support of patients with acute respiratory failure. Survival with ECMO was 9.5% while survival with conventional therapy was 8.3%. In this study, however, many of the included patients had end stage irreversible lung disease. Until recently, the above study all but stopped the use of ECMO in adults.
Today, there are about 85 ECMO centers worldwide and about 4,000 neonates have been treated (as of September 1990). All of these patients had predicted pre-ECMO mortality estimates greater than 80% (remember the problems with predicted mortality figures) and 83% survived with ECMO treatment. Infants with meconium aspiration syndrome had a 93% survival rate while patients with congenital diaphragmatic hernia had the lowest survival rate at 62%. In August 1986, Luciano Gattinoni reported the results of a study of 43 patients with an expected mortality of greater than 90%. He used ECCO2R (VV ECMO with low frequency ventilation) and had 21 survivors (48.8%). Lung function improved during ECMO in 72.8% of cases. His study was not controlled and again has the problem of the questionable validity of the 90% predicted mortality figure.

Conclusions
From the neonatal experience, it would appear that the key to making successful use of ECMO in adults is proper patient selection. The following indications and criteria are probably appropriate:
1. Primary reversible respiratory failure
VV ECMO: The patients should be failing conventional ventilatory support in that they have poor oxygenation and/or ventilation in spite of high ventilator settings that carry a high risk of lung damage from barotrauma and/or oxygen toxicity. These patients are rare but they do exist. ARDS with severe barotrauma might be an example of this indication if there is no multi-system organ failure.
2. Reversible cardiogenic shock
VA ECMO: This is a potential indication but reversible cardiogenic shock is a rare condition hence the fall in popularity of intra-aortic balloon pumps perhaps with the exception of being a bridge to transplant.
3. No multi-system organ failure
Patients with MSOF have a very high mortality rate even when ventilation and oxygenation are more than adequate. ECMO would not be expected to do more than prolong death.
4. No contraindications for anticoagulation
This may be obviated when heparin inpregnated ECMO circuits are available.

References
Hill JD, O'Brien TG, Murray JJ, et al. Prolonged extracorporeal oxygenation for acute post-traumatic respiratory failure (shock lung syndrome): Use of the Bramson membrane lung. N Engl J Med 1972;286;629-634. [First report of prolonged ECMO]
O'Rourke PP. ECMO: Where Have We Been? Where Are We Going? Resp Care 1991;36:7,683-694. [Good review article]
Gattinoni L, Pesenti A, Mascheroni D, et al. Low-Frequency Positive-Pressure Ventilation With Extracorporeal CO2 Removal in Severe Acute Respiratory Failure. JAMA 1986;256:881-886. [non-randomized, non-controlled report of results]
Gattinoni L, Pesenti A, Marcolin R, Damia G. Extracorporeal Support in Acute Respiratory Failure, Intensive Care World 1988;5:2,42-45. [another report of the above results basically]
Zapol WM, Snider MT, Hill JD, et al. Extracorporeal membrane oxygenation in severe respiratory failure: A randomized prospective study. JAMA 1979;242:2193-2196. [This is the NIH study mentioned in the text]
O'Rourke PP, Crone RK, Vacanti JP, et al. Extracorporeal membrane oxygenation and conventional medical therapy in neonates with persistent pulmonary hypertension of the newborn: A prospective randomized study. Pediatrics 1989;84:957-963. [This study is interesting as consent was obtained for ECMO only after randomization so parents of patients assigned to conventional therapy didn't know they were in a study] ]]>delton@lexpcc.netCardiovascular2009-12-05T19:41:23-05:00http://www.lexingtonpulmonary.com/articles/files/558bd786faabe1b0a1e582f8aad38986-10.php#unique-entry-id-10http://www.lexingtonpulmonary.com/articles/files/558bd786faabe1b0a1e582f8aad38986-10.php#unique-entry-id-10Cardiac Output Measurement
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
Cardiac output is the amount of blood ejected from the left ventricle in one minute and is measured in liters per minute. Under normal circumstances, the outputs of the left and right ventricles must be equal in the absence of abnormal shunts between the pulmonary and systemic circulatory systems.

Physiology
Along with left ventricular filling pressures (pulmonary capillary wedge pressure), the cardiac output is one of the few hemodynamic parameters that with today's technology requires the placement of a pulmonary artery catheter. Cardiac output is the product of heart rate and stroke volume. Heart rate is determined by both intrinsic pacemaker function and modulation by the autonomic nervous system. Stroke volume is dependent upon the degree of diastolic ventricular filling coupled with the degree of contraction sometimes expressed as ejection fraction. Disease states can alter all of these components of cardiac output. Normally, as heart rate increases, the cardiac output increases proportionately. As heart rate increases however, the time available for ventricular filling to occur decreases and in each patient, there is a heart rate, above which, ventricular filling will decrease enough that further increases in heart rate will result in a lowered cardiac output. In a normal person, this cut-off occurs somewhere between 180-200 beats per minute while in disease states such as congestive heart failure secondary to cardiomyopathy, this cut-off may be reached at rates as low as 120 beats per minute. Uncontrolled atrial fibrillation or atrial flutter frequently result in heart rates that are too high for adequate cardiac output and a major part of the treatment of these arrythmias is to give the patient digoxin to help slow the abnormally high heart rate.

Measurement Methods
Two main methods are used to measure cardiac output today. These are the Fick method and dilution methods (either dye or thermal).

Fick Method
The Fick method requires that you be able to measure the A-V oxygen content difference and requires that you be able to measure the oxygen consumption. An arterial blood gas from a peripheral artery provides the blood for the CaO2 measurement or calculation while blood from the distal PA port of a Swan-Ganz catheter provides the blood for the CvO2 measurement or calculation. Oxygen consumption is obtained by measuring the inspired oxygen concentration and the expired oxygen concentration along with the expired minute volume. Small errors in the oxygen concentration measurements can result in large mathematical errors therefore these measurements should be made with a calibrated blood gas machine equipped for measurement of gas samples (such as the ABL 300, IL, or Corning blood gas machines). Note the Fick cardiac output formula from a previous lecture. Fick cardiac outputs are infrequently used mainly because of the inconvenience of collecting and analyzing exhaled gas concentrations. It's not as difficult to do as one might think but nonetheless Fick cardiac outputs are seldom used today. You may see mention of an estimated Fick cardiac output method where you just assume that oxygen consumption is normal by plucking a value off of a nomagram corrected for weight and height but in patients in whom a cardiac output determination is really needed, the oxygen consumption is seldom normal and these estimated cardiac output measurements can do more harm than good.

Dilution Methods
Dilution methods mathematically calculate (using calculus) the cardiac output based on how fast the flowing blood can dilute a marker substance introduced into the circulation normally via a pulmonary artery catheter. The marker must be distinguishable from the blood and must be able to be measured quickly and with a high degree of accuracy. Early dilution methods used dye solutions which were administered upstream and then drawn off in blood samples downstream from the infusion port where they could be analyzed for concentration. Cardiac output was inversely related to the downstream dye concentration. Dye dilution cardiac outputs are seldom used today outside of cardiac catheterization labs and even most of them use the more automated thermal dilution method. In thermal dilution, cold or room temperature water or D5W is used as the marker solution and distal concentration is determined by measuring the temperature downstream from the infusion port. Since water is non-toxic, multiple measurements can be made as often as needed and the downstream concentration (i.e. temperature) can be measured in situ without having to withdraw any blood from the circulation for analysis.

Errors
Cardiac output measurement is not precise using today's technology. For clinical use, we don't need 100% accuracy to 5 significant digits but to avoid big errors it is important to know the limitations of the measurement techniques. Fick cardiac output errors result from leaky gas collection apparatus, from inaccuracies in the measurement of inhaled and exhaled oxygen concentrations (these are particularly common when high levels of oxygen are used), an from errors in the calculations and/or measurements of blood oxygen contents (such as might be caused by using a bogus hemoglobin level or assuming the absence of carbon monoxide affecting oxygen saturation). Thermal dilution cardiac outputs are affected by the phase of respiration, particularly during mechanical ventilation and should thus always be measured at the same point in the respiratory cycle (normally end-expiratory) where the effect of breathing (either spontaneous or mechanical) is least. Small errors can result from using the wrong fluid (something other than D5W) as the injectate. Variations in the speed of cold water injection can result in altered measurements and devices to automatically inject the fluid are available to eliminate this source of variation. While there are lots of things that can result in cardiac output measurements not exactly equaling the true cardiac output, the most important concept here is to make the measurements reproducible and the errors consistent from one measurement to the next. It is the change in cardiac output, up or down, that allows the practitioner to determine the effects of therapy and disease and not the absolute value but to accurately detect changes, the output measurement errors must be consistent.
]]>delton@lexpcc.nettoxic gasses2009-12-05T19:40:57-05:00http://www.lexingtonpulmonary.com/articles/files/7775c4e5043fb792d8330e76c76684ee-9.php#unique-entry-id-9http://www.lexingtonpulmonary.com/articles/files/7775c4e5043fb792d8330e76c76684ee-9.php#unique-entry-id-9Carbon Monoxide Poisoning
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
Carbon monoxide (CO) poisoning is primarily a diagnostic challenge. It is a diagnosis that is seldom made, primarily because it is seldom considered. The gas is insidious as inhaling as little as 0.1% CO can be fatal. The gas has no odor, color, taste, or irritating quality. CO poisoning accounts for about 3,500 deaths annually and is the mechanism of half of all suicides. The physician must be sensitized to the possibility of CO exposure in many patients if the diagnosis is to be made. It doesn't take a rocket scientist to consider CO exposure in fire victims but patients exposed via other mechanisms are easily missed.

Where does CO come from?
CO is a product of incomplete combustion (complete combustion producesCO2 and H2O.) This obviously includes exposures to fires by victims and fire fighters but also includes smokers (cigars produce more CO than cigarettes - up to 20% CO Hb possible). Exhaust fumes are a common source of CO exposure. A recent report detailed high levels of CO exposure in enclosed pickup truck beds from a backdraft of exhaust fumes into the back of the truck. This is particularly common in children. For this reason, passengers should not ride in the back of enclosed pickup trucks. A local case resulted when a local hospital's mammography truck parked too close to a building allowing the truck's exhaust to be entrained into the diagnostic area of the truck. A radiologic technician skipped lung, staying in the van because she didn't feel good. Her main symptoms were nausea and headache. She later collapsed and was taken to an ER where it took some time for the possibility of CO exposure to be considered. A few hours after removal from exposure she was found to have a CO Hb level exceeding 20%. Other less obvious sources of CO exposure are endogenous. Methylene Chloride, an ingredient of paint thinners, can be converted to CO by the liver during metabolism with a longer than normal half-life of excretion. Porphyrin breakdown accounts for a normal 1% CO Hb during normal turnover of hemoglobin.

Why is CO toxic?
Most of us were taught that CO is toxic because of its effect of displacing oxygen from hemoglobin thus causing hypoxia. This is probably not the primary mechanism of CO toxicity. In 1975, Goldbaum conducted a study where three groups of dogs were compared. One group was exposed to CO until their CO Hb saturation was 13% (leaving 87% available for oxygen). All dogs in this group died. A second group was made 68% anemic, reducing the oxygen carrying capacity to 32% of normal. All dogs in this group lived. A third group was transfused with CO exposed blood until their CO Hb saturation was 60% and all of these dogs survived. Another animal study by Geyer removed blood from rats and perfused them with an artificial solution capable of oxygen transport but that did not carry CO. Upon exposure to a 10% CO environment, the rats did well (remember that 0.1% CO would normally be fatal). This suggests that hemoglobin binding by CO is necessary but not sufficient to cause toxicity. Interference with oxygen transport by hemoglobin must play a minor role in CO's toxicity. One should not be surprised if measurement of COHb levels by co-oximetry is a poor method to quantify meaningful CO exposure as high levels may be survivable while low levels may result in serious injury. It is thought, that CO, in dissolved form, directly interferes with cellular metabolism by binding with cytochrome oxidase enzymes such as cytochrome a3, the terminal enzyme in the electron transport chain. CO has 200 to 250 times greater affinity for hemoglobin than oxygen but also shifts the oxyhemoglobin curve leftward which makes oxygen bind more tightly which makes it more difficult for oxygen to leave hemoglobin at the tissue level.

CO Exposure Physiology
CO levels (COHb%) have a time course of elimination from the body. The elimination half-life of CO while breathing room air is 320 minutes. This drops to 90 minutes while breathing 100% oxygen and to 23 minutes with 100% oxygen under 3 atmospheres pressure (hyperbaric chamber). A 1% CO atmosphere can allow lethal concentrations to develop within 10 minutes. Hemoglobin acts as a sink or vacuum that quickly removes any inhaled CO from the alveolar gas. Symptoms develop more quickly in children and the elderly. Sicker and/or more active patients also do worse. Exercise, stress, and anemia make individuals more susceptible. Higher atmospheric concentrations and longer durations of exposure are also factors to be considered. In CO exposure victims where the exposure is fire related, one must remember to consider the effects of other frequently fire-associated toxins such as cyanide. Because of their higher oxygen demands, the brain and heart are most sensitive to the hypoxic effects of CO exposure. CNS involvement accounts for many of the signs of CO exposure. COHb levels below 20% are usually associated with nausea, headache and mild dyspnea. From 20-40%, vomiting, poor judgement, and visual disturbances (including cortical blindness) develop. Above 40%, ataxia, confusion, syncope, coma, seizures and tachypnea are found. COHb levels are not, prognostic. Deaths have been reported with very low CO levels. About 12% of patients have delayed neurological deficits often following an initial asymptomatic period of several days. The onset of these delayed symptoms varies from 1 to 21 days with a mean of 6 days. These changes include memory impairment and personality changes as well as dementia, cerebellar ataxia and dystonias.

Clinical Diagnosis
As mentioned previously, a clinical suspicion is very important in diagnosing CO exposures. Symptoms are non-specific and include headache, dizziness, nausea and vomiting. CO exposures in the winter (when most accidental CO exposures occur) are frequently misdiagnosed as influenza, particularly when whole families are involved as they frequently are if there is a malfunctioning heater or fireplace.

Laboratory Diagnosis
The CO Hb level can be measured with co-oximetry. Remember that SaO2 levels from blood gas machines are normally calculated based on the pH and PO2 and will thus not reflect reduced levels in cases of CO poisoning. With routine blood gasses, PO2's and SaO2's will be normal (or very high if oxygen is being administered). If the exposure is significant, a metabolic acidosis will be present, reflecting tissue hypoxia. An anion gap will frequently be present and serum lactate levels may be elevated. CO Hb levels are frequently greater than 10% (up to 10% levels can be obtained from heavy smokers). CO Hb levels greater than 60% are almost always fatal but fatalities and severe brain damage can result from patients with normal CO levels. Remember that the damage may be done once levels have returned to normal from normal excretion. EKG's may show tachycardia and evidence of ischemia. Psychometric testing will frequently show mental deficits that resolve with treatment and may be the most sensitive method of detecting significant CO exposure and also provide for a means to evaluate the effects of therapy.

Therapy
Initially, all patients with suspected CO exposure should be treated with 100% oxygen delivered by a tight fitting mask (non-rebreather or demand valve device). Patients who are unconscious should be intubated. Associated conditions (burns, trauma, cyanide poisoning) should be treated. Hyperbaric oxygen therapy (HBO) is considered to be standard of care for patients with significant exposure defined as any patient who has been unconscious, neurological symptoms beyond simple headache, evidence of myocardial ischemia (symptoms or EKG), COHb levels greater than 25%, or unexpected abnormalities on psychometric testing. HBO therapy results in faster reductions in CO Hb levels (this is of uncertain importance), it increases tissue oxygen levels, and decreases cerebral edema. HBO therapy is normally given with 3 atmospheres of pressure using 100% oxygen for 90 minutes every 8 hours for 24 hours. HBO therapy almost totally eliminates the development of delayed neurologic sequelae. These effects are related to removal of CO from peripheral binding sites and not from reduction of CO Hb levels.

Follow-up
Part of treating CO poisoning is to prevent future exposures. It is not unheard of to treat a whole family for CO exposure from home and to have the family return to the same contaminated atmosphere because of a lack of understanding of the risks and need for corrective action. Follow-up must also be provided for to look for delayed results of CO exposure. Late treatment with HBO has been shown to reverse some symptoms in some cases.

References
Goldbaum LR, Ramirez RG, Absalon KB: What is the mechanism of carbon monoxide toxicity? Aviat Space Environ Med 1975; 46:1289-1291.
Myers RAM, Snyder SK, Emhoff TA: Subacute sequelae of carbon monoxide poisoning. AnnEmerg Med 1985; 14:1163-1167.
Norkool DM, Kirkpatrick JN: Treatment of acute carbon monoxide poisoning with hyperbaric oxygen: A review of 115 cases. Ann Emerg Med 1985; 14:1168-1171.
Turnbull, Timothy: Emergency Department Screening for Unsuspected Carbon Monoxide Exposure. Ann Emerg Med 17:478-489.
Stewart, RD: The Effect of Carbon Monoxide on Humans, J Occ Med 1976; 18:5.
Myers RAM: Are Arterial Blood Gases of Value in Treatment Decisions for Carbon Monoxide Poisoning? Crit Care Med 1989;17:139-142.]]>delton@lexpcc.netasthma2009-12-05T19:40:32-05:00http://www.lexingtonpulmonary.com/articles/files/65b90879c85261f4dcbcab26eea4ae02-8.php#unique-entry-id-8http://www.lexingtonpulmonary.com/articles/files/65b90879c85261f4dcbcab26eea4ae02-8.php#unique-entry-id-8Life Threatening Asthma
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
Asthma mortality has been increasing in recent years. Various experts have debated why this is so but several facts are apparent from the available data. First, most patients who die of asthma do not die in the hospital. Most do not die suddenly and have frequently been in the midst of an exacerbation for several days. Near fatal asthma is a risk factor for fatal asthma. Many, if not most, in-hospital asthma fatalities are a result of barotrauma. Clearly, outpatient asthma mortality could be improved by identifying those patient s at risk for fatal asthma and making sure they know when to seek medical care. Inpatient asthma mortality requires recognition, on the part of the care giver, of the causes and prevention of barotrauma.

Pathophysiology
Asthma has been called eosinophillic bronchitis which reflects the important role of eosinophils in mediating the asthmatic response. Everyone has some degree of airway reactivity which means that an inflammatory response will be elicited in anyone if the stimulus is strong enough. For some people it might take Clorox fumes, histamine, or methacholine to elicit this response while for others mere exposure to cold air could lead to the same result. Bronchial provocation testing is a pulmonary function test where a known airway irritant such as methacholine or histamine is aerosolized with pre and post exposure FEV1 measurements to determine the threshold dose necessary to bring about a given decrease in FEV1. A patient with severe asthma would require a small dose of the irritant while a patient with very non-reactive airways would require a higher dose to get the same decrease in lung function. Airway reactivity may be an inherited trait or it may result from a chemical or biological exposure, lasting long after the exposure has come and gone. Once a sufficient stimulus has reached the patient, a cascade of events takes place involving many chemical mediators of inflammation. These mediators result in inflammation (infiltration of tissues by inflammatory cells), edema, mucus hypersecretion, and smooth muscle contraction (bronchospasm).

Natural History
Just as airway reactivity, varies from person to person, the typical history of an asthmatic varies. Some patients will only be symptomatic as children while others will only become symptomatic in middle age, perhaps as a component of other chronic lung diseases. One important characteristic of asthma is that lung function should be essentially normal between exacerbations, unlike the emphysema patient, who always has abnormal lung function. This is why bronchial provocation testing is sometimes required to actually diagnose asthma since routine pulmonary function studies may frequently be normal when a patient is doing well. In a particular asthmatic attack, there are really two phases consisting of the early (histamine related) and late (inflammatory) reactions. The early reaction typically lasts for the first hour of treatment and results in an early response to therapy that may then relapse into the later, second phase reaction two to eight hours later. Because of this biphasic nature of a typical asthma attack, one must be careful not to discharge a patient from the emergency department too soon only to have a severe relapse occur away from the hospital. The initial reaction tends to respond well to inhaled bronchodilator agents while the late response requires the use of corticosteroids that have a delayed action thus they should be given early during the patient's ER visit to avoid the second stage relapse.

Initial Evaluation
The initial evaluation of the asthmatic patient should be intended to determine which patients are at risk for dying from their asthma but to prevent inappropriate ER discharges and to help determine the course of therapy to be used. The initial evaluation of an asthma attack consists of the physical examination and peak expiratory flow measurement. Breath sounds are an important part of the physical examination but it is easy to misjudge the severity of an attack using breath sounds. Many patients with severely reduced lung function will have fairly silent chests with little audible wheezing. As they improve with therapy, their wheezing may become much louder as wheezing is dependent upon airflow. Other physical findings associated with severe asthma include cyanosis (a very grim finding), altered mentation (time to intubate), increased use of accessory muscles of respiration, increased pulsus parodoxis, upright posture, and absence of breath sounds. Peak flow measurement is fairly simple and inexpensive and can objectively (within the limits of patient effort) stage airway obstruction much more accurately than physical examination and should be a part of every asthmatic's initial ER evaluation. PEFR (Peak Expiratory Expiratory Flow Rate) measurement is used not only to stage the disease but also to assess the response, or lack of response, to therapy. All patients with more than mild asthma should have their own PEFR meters that they keep at home so they will know their own normals and can give physicians and others objective information on the severity of a given attack over the telephone. For most of my adult asthmatic patients that have normal PEFR readings in the 300-400 LPM range, I advise them to notify me if their PEFR falls below 250 LPM with treatment and to expect that I'll probably put them on a tapering dose of oral steroids and I tell them that if their PEFR falls below 150 LPM they need to get to the ER, via the 911 system if possible as patients tend to develop respiratory failure at PEFR values below about 80 LPM. PEFR meters cost less than $20 and last until you step on them. Patients with severe asthma should have chest radiographs, primarily to look for evidence of infection (pneumonia) and barotrauma (pneumothorax or pneumomediastinum). These are not that useful in milder cases and rarely show more than mild hyperinflation. Blood gasses don't add much to acute asthma management prior to intubation since intubation should be based primarily on ability to oxygenate and altered mental status rather than any particular value for pH or PCO2.

Initial Treatment
The initial priority in asthma therapy is providing oxygen (there have been many malpractice suits lost because this step was skipped). Next comes the use of inhaled beta-2 agonist medications. Studies have been done that basically show little advantage of using nebulizers as opposed to repeated use of metered dose inhalers though most physicians tend to use nebulizers since the acutely dyspneic patient will frequently not be likely to be an expert at MDI use. On any ER patient presenting with asthma, I go ahead and establish IV access and give an initial high dose of steroid, typically Solu-medrol. Again, oral steroids work almost as quickly as IV but I tend to at least give the first dose IV as many of these patients will be borderline theophylline toxic and will be at risk of vomiting which will raise the question of whether the oral medication was actually delivered adequately. Inhaled anticholinergic drugs such as Atrovent or Atropine can be given but I've not been impressed with their efficacy in my experience (though I'll try most anything in the non-responding patient with severe asthma). Theophylline and Aminophylline are falling out of favor in the acute management of asthma as many studies in recent years have failed to show any additional benefit in terms of improved lung function or prevented hospital admission when theophylline products are added to beta-2 agonist therapy. There is some thought that these products might have some usefulness in the late response or perhaps used as anti-inflammatory agents but bottom line data is lacking. Theophylline products have a much higher toxicity and many patients presenting to the ER will already have toxic levels. Given the relative lack of efficacy when compared to beta-2 agonist agents, one should be very careful if they are used, and loading doses should generally be avoided in patients in whom a drug level measurement is not available prior to the bolus.

How to dose aerosolized medications
Aerosol therapy is a very inexact science. There is very little relationship between the amount of medication put in a nebulizer cup and the amount actually delivered to the site of action in a given patient. The percentage of a nebulized dose of a drug that is actually delivered to the site of action is influenced by patient size (smaller patients have smaller minute volumes and thus breath in less drug), airway size (smaller airways result in more rain out before the site of action), breathing pattern (higher inspiratory flows result in more inertial impaction of droplets before the site of action), nebulizer used (this influences particle size and aerosol density), flow rate of the driving gas, mask or mouthpiece type in use, mouth vs nose breathing, use of airways such as endotracheal tubes, use of ventilators to deliver the medications, placement of nebulizers in ventilator circuits, whether the ventilator is a volume ventilator or a continuous flow system and probably many other factors. Because of these problems, many of which are not controllable, dosage should be based on patient response, good and bad (i.e. give enough to get the effect you're looking for and back off when toxic effects become unmanageable). In pediatric patients (or smaller patients in general) it will be necessary to actually increase the amount of drug placed in the nebulizer to get similar therapeutic effects as they have several factors (smaller minute volumes and smaller airways) that result in their automatically getting less drug to the site of action. In the severe asthmatic, I typically use a standard concentration of drug (i.e. 0.5 cc in 2.5 cc of saline in the case of albuterol) and either give this aerosol continuously or via rapidly repeated doses until the patient responds with improved flow rates or gets unacceptable side effects (which are rarely encountered). I have given albuterol by continuous nebulization as long as 48 hours around the clock in a few severe patients with little trouble though electrolytes such as potassium and magnesium need to be monitored during therapy as beta-2 agonists will lower these.

When & Whether to Intubate
Why ask why? Remember that one of the largest causes of mortality in acute asthma in hospitalized patients is a result of barotrauma. Because of the very prolonged time constants in asthmatics (high airway resistance causing longer passive expiratory times), any mechanical ventilation using a respiratory rate much higher than 4 or so breaths per minute will result in a dangerous sequence of events. First, there will be air-trapping owing to inadequate expiratory time, this then leads to increased alveolar pressure and Auto-PEEP, which, in turn, leads to reduced venous return, a cardiac tamponade effect, and reduced cardiac output and blood pressure. It is not unusual for Auto-PEEP levels to exceed 30 cm H2O pressure in asthmatics, even those ventilated at respiratory rates less than 10 breaths per minute. Remember that in most asthmatics in respiratory failure, the problem is not one of muscle strength or even oxygenation but is one of respiratory mechanics, namely airway resistance, that is incompatible with effective ventilation at normal minute volumes. Because of these factors, it can be dangerous to put a patient with an acute severe asthma attack on a mechanical ventilator. The other side of this issue, of course, is that patients can die of respiratory failure and/or hypoxia thus one needs to know when the risks of respiratory failure exceed the risks of the treatment (ventilation). There are no absolute rules here but think about how respiratory failure results in death. The primary mechanism is hypoxia. Few patients die because their PaCO2 gets too high or because their pH gets too low. Hence, if adequate oxygenation can be maintained, there is still some time to direct therapy toward the underlying cause of respiratory failure, namely, the increased airway resistance. Again, all acute asthmatics should receive oxygen therapy. This buys time for other more definitive therapy to work. Watch for evidence of muscle fatigue and/or CO2 narcosis (which will eventually result in respiratory arrest). Typical signs are decreased respiratory effort in spite of increased loads, and altered mental status. My general method is to hold off on intubating an asthmatic until I'm unable to maintain adequate oxygenation or until the patient develops altered mental status (confusion, unresponsiveness, coma etc). Until these indicators are present, there is still time (though maybe not much time) to continue continuous inhaled beta-2 agonist therapy and steroids. Using this method I've had patients with CO2's transiently in the 90's stay awake and alert and wind up not needing the ventilator after another 15 minutes of aerosol therapy. This sort of approach, of course, requires constant monitoring by the physician at the bedside with frequent (if not continuous) assessment and re-assessment of the response to therapy.

After Intubation
Remember that as outlined above, intubation and mechanical ventilation are not a treatment for asthma but are only a treatment for respiratory failure and/or hypoxia. Once a patient is intubated, the treatment for asthma should be continued if not intensified with the use of continuous aerosolized bronchodilators and steroids, as well as IV steroids and optionally IV bronchodilators (usually Brethine (terbutaline)). The goals of mechanical ventilation in acute asthma are primarily to keep a patient alive while you wait on the asthma therapy to work, hopefully without killing the patient with the ventilator. Normal blood gasses are NOT the goal of mechanical ventilation in asthma. Adequate oxygenation with a minimum of barotrauma is the goal. It is frequently necessary to use very low respiratory rates (less than 6 breaths per minute in some cases) to avoid dangerous Auto-PEEP and its resultant sequelae. Patients, should in most cases, be pharmacologically sedated and paralyzed both to prevent dyssynchronous ventilation (bucking the vent) and to decrease the rate of metabolism and thus the requirement for ventilation and oxygenation. Fever should be treated to lower the metabolic rate if it is present. Auto-PEEP should be measured hourly initially and adjusted to a safe level (probably less than 10 in most patients though IV volume loading of the patient will make them more tolerant from a blood pressure stand-point). As Auto-PEEP decreases (signifying a reduced airway resistance) the respiratory rate can slowly be increased to correct the expected respiratory acidosis that most severe asthmatics on the ventilator will have when ventilated at low rates. Once breath sounds are clearing up, the continuous bronchodilator dosing can be made intermittent and sedation and paralysis can be weaned as can the ventilator itself in most cases. In most cases, mechanical ventilation will only be necessary for a few days (sometimes just a few hours will be adequate) though I've had some difficult cases require ventilation as long as two weeks with severe wheezing until right before weaning.

After Extubation
Patients who have been mechanically ventilated for asthma are in a very high risk group for mortality from asthma. They and their families should know this so they will take future attacks very seriously. They should be reminded that most asthma mortality occurs outside of the hospital and they should be very familiar with using a peak flow meter to monitor their progress.

References
Olsen GN: Asthma Concepts & Control in Olsen, GN: Basic Handouts in Pulmonary Medicine, 2/92.
Nowak RM, Pensler MI, Sarkar DD, et al. Comparison of peak expiratory flow and FEV1.0 admission criteria for acute bronchial asthma. Ann Emer Med 1982; 11:64-69.
Guidelines for the Diagnosis and Mangement of Asthma, National Heart, Lung, and Blood Institute, NIH, US Dept HHS, August 1991.
Miller TP: Identification, treatment of adults at increased risk of fatal asthma, Today in Medicine, Nov/Dec 1992.
Fish, JE: Status Asthmaticus in Current Therapy in Allergy, Immunology and Rheumatology. ]]>delton@lexpcc.netCardiovascular2009-12-05T19:39:56-05:00http://www.lexingtonpulmonary.com/articles/files/811624871d403cdeb4adaebff4fb6fb6-7.php#unique-entry-id-7http://www.lexingtonpulmonary.com/articles/files/811624871d403cdeb4adaebff4fb6fb6-7.php#unique-entry-id-7Aortic Dissection
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
Aortic dissection is a potentially lethal condition that is the most common acute catastrophe involving the Aorta. It occurs two to three times more frequently than rupture of abdominal aortic aneurysms.

Etiology
The pathogenesis of aortic dissection is not completely understood. It was once thought that a condition known as cystic medial necrosis, a pathological condition of uncertain cause, had to exist along with an intimal tear before a dissection could occur. It is now known that what was once called cystic medial necrosis is a normal part of aging of the Aorta. One thing that is clear is that hypertension is related to aortic dissection. The peak incidence is between 50 and 70 years of age. Dissections are slightly more common in men and in patients who have Marfan's syndrome. Pregnancy is a rare predisposing condition.

Classification
There are two major classification systems for aortic dissections and both are based upon the location of the dissection. The vast majority of aortic dissections occur either at the ascending aorta just above the aortic valve or occur just below the origin of the left subclavian artery. The DeBakey classification calls a Type I dissection one in which the tear originates in the ascending aorta and dissects into the descending aorta. A Type II dissection originates in and is limited to the ascending aorta. A Type III dissection originates in the descending aorta and may progress in either direction. More recently, the Austen and Shumway classification divides dissections into Type A and Type B for ascending and descending dissections respectively.

Pathophysiology
Aortic dissections cause death and morbidity by any or all of several mechanisms. Depending on the location of the dissection, there can be disruption of any of the major branches off of the aorta leading to ischemic injury in the area of distribution of the involved vessels such as the carotids, renals, or coronary arteries. Dissection of the ascending aorta can distort the aortic valve resulting in acute life-threatening aortic insufficiency with resultant congestive heart failure. Thrombi can form and result in distal arterial obstruction in the lower extremities. Exsanguination can occur if the false lumen of the Aorta bleeds into the pleural space or mediastinum and pericardial tamponade can occur if blood dissects into the pericardium. Frequently the systemic blood pressure, particularly proximal to a major aortic obstruction can be very high and very labile and this can result in cerebrovascular accidents.

Presentation
Severe acute chest pain occurs in 95% of patients with aortic dissection. The pain is typically sudden in onset and has a sharp tearing or throbbing quality. The pain is usually centered in the sub sternal region but may be felt in the jaw, precordium, neck, jaw, extremities, epigastrium, or back. Depending on complications there may be neurologic deficits and or evidence of ischemia elsewhere such as blindness or extremity pain. If aortic insufficiency occurs then evidence of acute heart failure may result leading to the appearance of an acute myocardial infarction. Of course, an acute myocardial infarction can also occur because of disruption of a coronary artery at its origin in the proximal aorta. Physical findings vary from shock, to hypertension, to heart failure. Sequential filling of the true and false lumens may produce "double" pulses and there may be unequal blood pressures in the extremities if compromise of the distal artery has ocurred.

Diagnosis
The chest x-ray frequently shows a widened superior mediastinum representing either a mediastinal hematoma or a widened aortic shadow. The initial x-ray may be normal. CT and MRI scanning are fairly specific for aortic dissection and echocardiography, particularly using an esophageal probe can confirm the diagnosis if the area of dissection can be visualized but a negative echocardiogram is not adequate to rule out dissection. Aortography is considered to be the gold standard.

Therapy
Because aortic dissections are life-threatening, specific therapy must be initiated very quickly in many cases. Therapy should not be delayed for aortography if the diagnosis is already apparent. Immediate therapy is aimed at both reducing the blood pressure and at reducing the pulsatile force of left ventricular ejection. Typically, a combination of nitroprusside (Nipride) and propranolol (Inderal) are used to accomplish both goals. Trimethophan camsylate (Arfonad), a ganglionic blocking agent can also be used both to lower the blood pressure and lower the force of left ventricular contraction. Blood pressure should be lowered to the lowest pressure that maintains cerebral and renal perfusion. Definitive surgical repair is indicated for all proximal dissections and for distal dissections with complications (i.e. bleeding, vascular obstruction) while medical therapy is preferred for uncomplicated acute or chronic distal dissections. Repair of proximal dissections may require repair and/or replacement of the aortic valve as well as coronary revascularization.

Outcome
Half of patients with untreated thoracic aortic dissections die within 48 hours and 90% do not survive 6 months. A compilation of the literature in 1983 revealed that for treated type A dissections, medical treatment had a 72% mortality while surgical treatment had a 32% mortality. For type B dissections, medical treatment had a 27% mortality while surgical treatment had a 32% mortality. Ten year survival is around 20% for either type of dissection.

References
Little AG, Anagnostopoulos CE: Aortic Dissections in Thoracic and Cardiovascular Surgery, 4th Edition, Editor W. Glenn, 1983, Appleton-Century-Crofts.
Thompson WL: Hypertensive Urgencies and Emergencies in Textbook of Critical Care, 2nd Edition, Editor Shoemaker et al, 1989, W. B. Saunders Company.
DeBakey ME, Cooley DA, Creech O Jr: Surgical consideration of dissecting aneurysm of the aorta. Ann Surg 142:586, 1955.
]]>delton@lexpcc.netPhysics2009-12-05T19:38:56-05:00http://www.lexingtonpulmonary.com/articles/files/f80b9a42b0ab00630c1efe70fb31ab98-6.php#unique-entry-id-6http://www.lexingtonpulmonary.com/articles/files/f80b9a42b0ab00630c1efe70fb31ab98-6.php#unique-entry-id-6Aerosol Therapy
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care


Introduction

An aerosol is a suspension of small particles of liquid or solid in a gas. The particles, synthetic or natural, fall within the size range of 0.005 to 50 in diameter. Those that are medically important are less than 3 in diameter. Gravity begins to lose its influence on particles at this mass size. Examples of aerosols include dusts, bacteria, yeast, water, and smoke.

Terminology

Stability of an aerosol is the ability to remain in suspension and maintain its integrity as an aerosol. Stability is dependent upon the size and nature of the particle, the concentration of particles, ambient humidity, and movement of the suspending gas. Instability is the propensity of a suspended particle to remove itself from suspension. For therapeutic aerosols, penetration refers to the depth to which an aerosol particle can be carried by a tidal breath. Deposition refers to the aerosol becoming unstable as particles rain-out or are retained within the respiratory tract. Clearance refers to removal of deposited particles by biologic mechanisms.

Aerosol Generation

There are two main types of aerosol generators in general clinical use today. They are jet nebulizers and ultrasonic nebulizers. A Jet nebulizer works by directing a high flow of gas over a capillary tube that is immersed into the fluid to be nebulized (made into an aerosol). The suction generated at the top of the capillary tube draws fluid up the tube and into the air. Particles of improper size (from a stability stand-point) are frequently directed against a baffle that will encourage rain-out such that the fluid to be nebulized is not wasted by the creation of unstable particles. The particles that rain-out fall back into the fluid reservoir so they can be nebulized again. Many nebulizers have an air intake or venturi to allow the entrainment of room air for dilution of the primary gas, usually oxygen.

An ultrasonic nebulizer consists of a power chamber and a nebulizing chamber. The power chamber includes a ceramic transducer that is described as piezoelectric because is changes electrical energy into pressure energy. The transducer vibrates at a very high frequency (that requires FCC certification) up to about 1.5 mHz. The transducer sits at the bottom of a water filled power chamber. The vibrational energy is transmitted through the water and focused on a flexible diaphragm that vibrates in sympathy. The diaphragm is in contact with the solution to be aerosolized and shakes the solution into particles. At low frequencies, waves are produced that may produce some larger aerosol particles. At high frequencies a fine mist is generated. At low power (amplitude) the particles are produced intermittently as waves break while at higher power settings the particles are liberated continuously. At very high power settings, the chemical makeup of some medications can be disrupted. Ultrasonic nebulizers tend to produce a more consistent particle size than do jet nebulizers and can produce very large volumes of respirable particles with much greater deposition into the lungs. There is some experimental evidence to suggest that long-term use of ultrasonic nebulization can result to disruption of surface tension stability in the lung, perhaps owing to the large amount of fluid deposited into the lungs. Ultrasonic nebulizers are limited in that they cannot aerosolize viscous solutions though this is not a problem clinically.

Aerosol Behavior

Once an aerosol is generated, there is initially quite a variety of particle sizes. As the aerosol ages, however, larger particles aggregate and become unstable, falling out of suspension. This results in a decrease in the size deviation of an aerosol such that the resulting aerosol tends to consist of particles close to 0.1 micron. The depth of penetration of an aerosol particle into the respiratory tract increases as the particle size decreases. The nose will completely filter particles down to 5 to 10 microns in diameter while particles of 1 micron and down can get past the upper airway and into the terminal alveoli. Particles of around 1 micron are retained in alveoli while particles much below this size do not deposit and are exhaled. The rate at which a particle will settle is related to physical properties such as gravity, mass, volume, density, and viscous resistance of air. For particles within the size range of 0.1 to 70 microns, the settling velocity of a particle is proportional to the product of its density and the square of its diameter: Settling rate = Density x Diameter squared. Particles, as they approach 0.1 micron in size, become almost molecular in character and are influenced greatly by the kinetic activity of the suspending gas to a greater extent than gravity. A smaller particle is actually kept in suspension by collisions with adjacent gas molecules as it has a high surface area to mass ratio compared to the larger, more massive particle which is more influenced by gravity. Below a given size (about 0.25 microns) particle deposition/retention is actually increased. Rain-out, or retention, of an aerosol can be facilitated by the inertia of a particle tending to keep the particle moving in a straight line when the flow of inspired air changes direction suddenly. Particles at the edge of a stream of gas are more likely to impact by this mechanism. Particle composition also influences particle stability. A hygroscopic particle will tend in accumulate water vapor and increase the size of itself while other particles might tend to dry out and decrease in size. This mechanism is influenced by the relative humidity of the suspending gas. Ventilatory patterns influence particle deposition and retention. Deposition and retention are directly related to inhaled tidal volume and inversely related to flow rate. These factors are only important in conducting airways and become less important as the inspired gas approaches the alveoli where there is little air movement. Aerosolized particles are cleared from the lung by means of ciliary mucus clearance and by means of pulmonary tissue clearance which is a combination of phagocytosis by macrophages and diffusion and dissolving into tissue fluids.

Medical Aerosols

The two main areas where aerosols are used therapeutically are for humidification therapy and medication delivery. Humidification therapy depends on both the bulk delivery of water or saline solutions to the airways and alveoli as well as the tendency of evaporating particles to increase the relative humidity of the suspending gas. Ultrasonic nebulizers, in particular, are very efficient at delivering large amounts of liquid to the respiratory tract. There is controversy regarding what fluid is best to deliver in this manner. Fluids that are very hypertonic or hypotonic tend to be irritating and lead to coughing and bronchospasm in susceptible individuals. The tonicity of aerosolized fluids also tends to change enroute to the alveoli depending on the humidity of the suspending gas. What starts out as an isotonic solution may be either hypertonic or hypotonic by the time it arrives as the site of deposition. There is also controversy as to whether delivery of liquids to the airways is of any therapeutic value in decreasing the viscosity of or increasing the clearance of mucus.

Medication Delivery

Aerosols are an attractive way to delivery drugs, particularly those whose site of action is the lungs themselves as relatively high doses are delivered to the site of action, sparing high systemic doses that might otherwise cause adverse systemic effects. Unfortunately, there are many problems with using aerosols to deliver medications to include inconsistent dose delivery, inadvertent gastrointestinal delivery, non-uniform distribution of medication in the lungs, and elicitation of bronchospasm. There are even those that theorize that the use of suspending gasses like fluorocarbons might be causing cardiac arrests secondary to cardiac toxicity in some asthmatics.

Dosage delivery

Aerosolized medications are inconsistently delivered to the patient. When one places a given amount of medication in a nebulizer, it is difficult, if not impossible, to predict how much of the medication will actually be delivered to the patient, much less to the site of action in the alveoli where it is theorized that most systemic absorption takes place. The initial site of lost medication is into the room as most aerosols are delivered without the benefit of a closed delivery system. Continuous aerosols such as those delivered by hand held, gas powered nebulizers deliver as much as 2/3 of their output during the patient's exhalation. Of the amount of aerosol produced during inspiration, some still leaks out of the mask or mouthpiece, some rains out in the nose and/or oropharynx and some is actually delivered to the lower airways and lungs. Metered dose inhalers are subject to many of the same limitations and those with very short ejection periods are even more susceptible to asynchronous delivery. Commercially available metered dose inhalers eject about 15cc of gas per actuation. Many text books recommend dosing aerosolized medications the way oral or parenteral medications are dosed, i.e. based on body weight. The problem with this is that patients of different sizes already have different deposition rates. For example, say you have a drug that you'd give to a patient at 1 mg/kg of body weight if given IV. If you are going to use a gas powered continuous nebulizer you would have to use at least 3 times this dose to just get the usual dose directed in the general direction of the patient during inspiration. Since deposition is also minute volume dependent, patients with smaller minute volumes (i.e. pediatric patients) will get less delivery of drug to the lungs than those with larger minute volumes. This means that if you put 2 mg of Terbutaline in a nebulizer for an adult that the same 2 mg of Terbutaline would give a proportionately smaller delivered dose to a newborn. Further complicating the picture is the fact that there is a greater tendency to trap the medication in the upper airway of an infant such that you really have to greatly increase the dose to the nebulizer to treat an infant so it might take 6 mg of Terbutaline in the nebulizer to give an infant the same dose per kg of body weight that an adult would receive with 2 mg of drug in the nebulizer. Basing the amount of medication you place in the nebulizer on the body weight of the patient in a linear fashion will not accurately predict dose delivery to the patient's lungs as they are really inversely related at best. Aerosolized medication dosing is further complicated by the variety of devices used to create the aerosol. There is no simple way to compare doses unless the same nebulizer is used. A case in point is the aerosolization of Pentamidine. There are plenty of recommendations as to what dose of medication to deliver but whatever dose you choose, you must use the same nebulizer used in the study you like or your dose delivery will be different than that which was recommended, perhaps more, perhaps less, perhaps not even close to what you thought you were delivering. Particle Size vs Site of delivery To further complicate matters, the particle size produced by various nebulizers, greatly influences where the aerosol will be deposited and also determines whether it will be retained or simply exhaled. Nebulizers are frequently called efficient if a large percentage of their delivered dose is retained but this usually means that they produce larger particles that are more likely to impact in the upper airway and not be delivered to the alveoli, if indeed, that is the intended target of delivery. In the case of Pentamidine, for example, it is recommended that the Respigard II be used. The retention of the 0.9 particles is only 5.3% meaning that only 5.3% of the dose from the nebulizer is retained. This sounds inefficient and is but if one of the other nebulizers were used then the particle size would result in more of the medication being delivered to airways instead of the alveoli where you want the medicine to go. Rain-out in airways is responsible for at least some of th e complications of therapy and is thus avoided by using a nebulizer producing smaller particles even if much of the aerosol is stable enough to be exhaled again. If one wanted to increase the delivered dose a rebreathing circuit could be used but this would increase the delivered dose to a level greater than what is recommended since the dosage recommendations are made assuming the intentional inefficiency of the the Respigard II.

Intubated patients

Nebulizers and metered dose inhalers have been used with intubated and mechanically ventilated patients. Factors influencing delivery include whether a continuous or inspiration-only nebulizer is used, where the nebulizer is placed in the circuit, and whether a nebulizer or a metered dose inhaler is used. Ventilator settings also influence drug delivery. In general, intubated patients will get less lung deposition and retention than non-intubated patients so dosing has to be adjusted accordingly. So what gives? If you've gotten the idea that it's a joke to pretend that medications can be precisely delivered by aerosol then you have the right idea. Given the many confounding factors influencing drug delivery, the only real ways to sensibly choose a dose is to use secondary indicators such as response to therapy (in the case of bronchodilators) or perhaps measurement of drug levels in serum or urine in the case of Pentamidine. Perhaps it would be more sensible if medications prepared for aerosol delivery were available in standard solutions with no particular dosage ordered and actual dose usage determined strictly on the basis of response.

References

Patel P, Mukai D, Wilson AF: Dose-response effects of two sizes of monodisperse isoproterenol in mild asthma. ARRD (1990 Feb) 141(2): 357-60.

Simonds AK, Newman SP, Johnson MA, Talaee N, Lee CA, Clarke SW: Alveolar targeting of aerosol pentamidine. Toward a rational delivery system. ARRD (1990 Apr) 141(4 Pt 1):827-9.

Kim CS, Trujillo D, Sackner MA: Size aspects of metered-dose inhaler aerosols. ARRD (1985 Jul) 132(1):137-42.

Ilowite JS, Baskin MI, Sheetz MS, Abd AG: Delivered dose and regional distribution of aerosolized pentamidine using different delivery systems. Chest (1991 May) 99(5):1139-44.

Hiller C, Mazumder M, Wilson D, Bone R: Aerodynamic size distribution of metered-dose bronchodilator aerosols. ARRD (1978 Aug) 118(2):311-7.

Peters JA: Humidity and Aerosol Therapy, in Spearman CB, Sheldon RL, Egan DF: Egan's Fundamentals of Respiratory Therapy, 4th edition, The C.V. Mosby Co., 1982.

Hess D, Daugherty A, Simmons M: The Volume of Gas Emitted from Metered Dose Inhalers, abstract, Resp Care, (1991 Nov), 36(11):1320.

ink JB, Cohen NH, Covington J, Mahlmeister MJ: Titration for Optimal Do se Response to Bronchodilators Using MDI and Spacer in Ventilated Adults, abstract, Resp Care, (1991 Nov), 36(11):1321.

Don Elton
Lexington, South Carolina
http://www.lexingtonpulmonary.com ]]>delton@lexpcc.netairway2009-12-05T19:38:40-05:00http://www.lexingtonpulmonary.com/articles/files/22d88cbef3c497a8dacb9930a43f2dff-5.php#unique-entry-id-5http://www.lexingtonpulmonary.com/articles/files/22d88cbef3c497a8dacb9930a43f2dff-5.php#unique-entry-id-5Airway Emergencies
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
The airway, consisting either of natural anatomy or a plastic tube, is arguably the most important part of the pulmonary system. Without an adequate airway, the remainder of the cardiopulmonary system is of little value. Because of this importance, loss of patency becomes the most urgent emergency that can be imagined in medicine. Rapid accurate recognition and treatment of airway emergencies are essential to the provision of emergency and critical care medicine.

Anatomy
The natural human airway consists of the nasopharynx and oropharynx, the larynx, and the trachea. Most airway emergencies result from obstruction to airflow. Obstruction can result from internal obstruction either by edema, spasm, or a foreign body, or from external compression or distortion. Airway obstructions can be congenital or acquired. Examples of congenital airway obstructions are tracheal atresia, laryngeal web, choanal atresia, and vascular ring with tracheal compression. These congenital obstructions, if severe enough, can result in death in the delivery room if immediate surgical intervention is not provided.

Foreign Body Aspiration
Foreign body aspiration normally occurs during eating, particularly when the patient has an impaired gag reflex such as might be caused by consuming alcohol or by anatomical neurological deficits as might be seen following a stroke. With a complete obstruction, there is no sound of air movement audible at the mouth and the patient is unable to speak. Sternal, suprasternal, costal, and infracostal retractions are also common in upper airway obstruction as is a piston-like motion of the trachea as seen in the neck with inspiratory efforts. Of course, these findings are very temporary if the obstruction is not treated so airway obstruction must be assumed to exist in any apneic patient until proven otherwise. Treatment consists of either removing the obstruction via the fingers or instruments (forceps and laryngoscope for example) or by moving the obstruction below the level of the carina such that a complete obstruction only blocks ventilation to one lung. Complete obstruction can also be treated by bypassing the obstruction with a tracheotomy or cricothyrotomy. Some obstructions will require urgent bronchoscopy and the use of a rigid scope, if available, may be more successful given the larger channel size. The Heimlich maneuver may also be used when other more definitive methods are not immediately available. In cases of partial obstruction, one must be careful not to convert the situation to a complete obstruction and the urgency of treatment must be titrated to the degree of obstruction with severe partial obstructions being treated like complete obstructions. One seldom available technique for buying time in cases of partial airway obstruction is the use of a helium-oxygen mixture since the helium has a lower density than nitrogen and thus can ventilate a patient with less pressure required. If a patient must be ventilated past a partial airway obstruction, the ventilation should be provided by a manual resuscitator instead of a mechanical ventilator and slow deep breaths should be delivered with attention given to providing adequate expiratory time. Using a manual resuscitator allows for immediate detection of changes in airway resistance and will tend to do a better job of ventilating the patient.

Angioedema
Angioedema is an allergic type reaction that results in any combination of lip, face, neck, tongue, uvula, palate, epiglootic, glottic, and tracheal edema. The most common causes are drugs (particular ACE inhibitors - angiotensin converting enzyme inhibitor antihypertensive medications like Vasotec (enalapril), Capoten (captopril) and others). Other causes include various foods (commonly shellfish), and an ideopathic form (hereditary angioedema). This problem is a little tricky as it may occur after months or even years of incident free use of ACE inhibitor drugs. Most cases present with painless lip swelling, sometimes one, sometimes both. Symptoms increase if exposure to the offending agent continues and this is common since the cause is frequently unsuspected by the patient since it may not be a new exposure. If there is swelling of anything inside the mouth or throat then airway obstruction can occur leading to death. Intubation via the oral route is frequently impossible and may be difficult via the nasal route as well. Once airway obstruction has reached a critical stage, manipulation of the airway could lead to worsening edema and lead to complete obstruction. Ideally a patient with angioedema should be intubated in the operating room with someone ready to perform an emergent tracheotomy or cricothyrotomy if needed. Patients with swelling of the lip, uvual, or who already have respiratory compromise need admission and anyone who has difficulty breathing, swallowing, or speaking should have an airway secured as soon as safely feasible. Other treatments include subcutaneous epinephrine (when not otherwise contraindicated), steroids, Benadryl (diphenhydramine), and histamine blocker anti-acid medications like Tagamet (cimetidine) etc. Recovery usually occurs within a few days provided the causative substance is removed.

Infectious airway obstruction
The two most common infectious causes of airway obstruction are laryngotracheobronchitis (croup) and epiglottitis. Both are more common in children but both can occur in adults. Croup is usually a viral illness that results in subglottic (tracheal) stenosis.. The onset is usually over 4-5 days at the end of an upper respiratory infection. Croup does not usually become life threatening but it can be if severe. Diagnosis can be made by a PA soft tissue neck x-ray which will show tracheal narrowing at the top of the tracheal air shadow (steeple sign). Patients with croup have a variable amount of respiratory distress and have a peculiar barking cough (at least infants do). Croup is normally treated with cool mist and sometimes steroids and/or aerosolized racemic epinephrine which acts as a topical vasoconstrictor. The most important thing to remember with croup is that you must be sure that the patient doesn't really have epiglottitis which is usually a more serious condition. Epiglottis usually results from a bacterial infection, frequently Haemophilus influenzae. The onset is rapid and can progress to severe airway obstruction within 6-8 hours in infants though usually it takes longer in adults. Stridor, dysphagia, odynophagia, and drooling (from inability to swallow) are typical symptoms. Patients with epiglottitis tend to be very anxious (not to mention their doctors). A lateral soft tissue neck x-ray is usually diagnostic but if obstruction is severe the patient should probably proceed to the operating suite for a controlled intubation by the most experienced person available rather than risking a complete airway obstruction in the radiology department. Laryngoscopy should ideally not be attempted unless personnel and equipment for an emergent tracheotomy is available. An abscess can also obstruct the upper airway. Symptoms may vary depending on the location but are usually similar to those of epiglottitis. Again, a lateral soft-tissue neck x-ray is helpful for diagnosis and a CT scan is useful if the airway can be protected.

Airway Trauma
Airway trauma can result from either blunt or penetrating injuries. Blunt trauma can cause a collapse of the trachea with intraluminal obstruction from the extrinsic pressure or there can be disruption of the trachea or major bronchi resulting in air leaks. Air leaks from the major airways can result in soft tissue and subcutaneous emphysema which can either be benign or can compress the airway or cause a pneumothorax or pneumomediastinum. If the history of injury suggests blunt or penetrating trauma to the chest or neck, then the soft tissues should be palpated for deformities or subcutaneous air and x-rays should be obtained to look for evidence of air leaks. Positive pressure applied to the airway should be avoided if possible or at least minimized to prevent the extension of air leaks that might otherwise be self limited.

Artificial airway emergencies
Artificial airways are normally tracheostomy tubes, and oral/nasal endotracheal tubes. Other airways would be tracheal buttons and the like. It is important that physicians caring for patients with artificial airways be very familiar with the construction and proper use of those airways as improper use can be life threatening. For example, it's a bad idea to inflate the cuff of a fenestrated tracheostomy tube when you have both the external and internal lumens occluded. Endotracheal tubes can become obstructed with mucus, particularly in cases where the mucus contains blood, secretions are thick, humidification is inadequate, and/or airways are small in diameter or have sharp bends that narrow the lumen. It is possible to have an endotracheal tube totally obstructed by mucus that a patient cannot breath around and yet be able to pass a section catheter through the viscid obstruction. Sometimes a partial obstruction of an endotracheal tube will cause musical breath sounds over the trachea. In mechanically ventilated patients you might note adequate breath sounds for mechanical breaths (albeit with high peak pressures) but note no air movement with weaker spontaneous efforts. If there is any doubt of airway patency then the airway should be replaced immediately. It is possible for an airway cuff, if overinflated or defective, to herniate over the end of the tube resulting in partial or total airway obstruction. If this happens the airway should be replaced as a cuff deformed in this way may be more likely to herniate again. Cuff trauma to the tracheal mucosa can result in edema and/or fibrotic scarring that will obstruct the trachea upon extubation. This will not usually be suspected until the patient develops respiratory distress upon extubation. For this reason, patients should never be extubated unless someone is present who can immediately reinsert an endotracheal tube, perhaps of a smaller diameter than the one removed. With longer term intubation, it is possible for a cuff to erode through the tracheal wall and into blood vessels. This is less common today with lower pressure cuffs but can still happen. Usually airway obstruction secondary to the bleeding is more important than the amount of blood loss so the initial goal of therapy is to protect the airway, usually by inserting the tube beyond the point of bleeding and inflating the cuff. Elevating the head of the bed will reduce the blood pressure in the bleeding vessel until surgical assistance is available. Cuffs that won't hold their air pressure usually result from leaks somewhere between the cuff itself and the syringe adapter. Cuffs frequently can be torn by teeth or nasal bones and tubes have to be replaced when this happens. If the leak is in the pilot line valve (where the syringe attaches) or the pilot line is accidentally cut you can try inserting a stop-cock where the syringe goes or alternatively can cut the pilot line and insert a blunt needle with a stop-cock attached to replace the valve that came with the tube.

Accidental Extubation
This can be an emergency if there is difficulty replacing the airway or if it just isn't detected in a reasonable amount of time. Everyone knows to listen for breath sounds to verify an endotracheal tube's position but many don't realize that you can get pretty good breath sounds with the endotracheal tube cuff above the vocal cords or even in the esophagus. Two fairly reliable signs of an extubated patient are the patient's ability to speak or large leaks of ventilator breaths around a properly inflated tube. One quick reliable method of verifying that a tube is in the trachea is to just use a laryngoscope to look at the tube going beyond the cords. An alternative but less desirable method is to get a PA and lateral chest x-ray. The lateral is most important as the trachea is an anterior structure while the esophagus is posterior. In the patient with a tracheostomy, particularly a fresh tracheostomy, there is a possibility that it will be difficult to find the stoma in the neck through which to replace an accidentally removed tube. Remember that most such patients still have lips through which you can pass an oral tracheal tube in an emergency. Also, remember that you can always use a plain endotracheal tube to replace a tracheostomy tube in cases where the proper size tracheostomy tube isn't available or where the upper airway has been damaged by trauma, infection, or is bleeding. Several years ago I saw a patient who had fallen on a running chain saw and had severed his trachea and esophagus. A paramedic at the scene saved his life by intubating the free end of his trachea with an endotracheal tube.

References
Elton DR, Berkowitz GP: Endotracheal tube obstruction in neonates, Perinatology-Neonatology, 5:5, pp 75-80, 1981.
Shapiro BA, Harrison RA, Trout CA: Airway care in Clinical Application of Respiratory Care, , 2nd ed., Year Book Medical Publishers, 1979.
Rowe LD: Otolaryngology in Way LW: Current Surgical Diagnosis & Treatment, Lange Medical Publications, 1981.

Don Elton delton@lexpcc.net
Lexington, South Carolina
]]>delton@lexpcc.netPhysics2009-12-05T19:38:09-05:00http://www.lexingtonpulmonary.com/articles/files/03011f5d975e316205302ffbce0f6081-4.php#unique-entry-id-4http://www.lexingtonpulmonary.com/articles/files/03011f5d975e316205302ffbce0f6081-4.php#unique-entry-id-4Pressure, Flow, and Resistance Measurement
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
To study hemodynamics, it is necessary that you understand what you are measuring. Most hemodynamic measurements are based upon measuring pressures, flows, and resistances.

Pressure
Pressure is defined by physicists as force divided by area. Force can be thought of as mass or weight in simple terms. A given force applied to a small area will result in more pressure than that same force applied over a larger area. This is the basis for using snow shoes that spread out the weight of a man or woman over a larger area of snow to decrease the pressure applied to the snow thus preventing the snow-walker from falling into the snow.

Typical units for pressure include cm H2O and mm Hg which refer to the amount of pressure necessary to raise a column of a given height of either water or mercury. Hemodynamic pressures can be measured by three methods, column methods, occlusion methods, or transducer methods. In a column method, a column of fluid with the top open to the atmosphere is attached to tubing that leads to the place where you want to measure pressure.

Blood pressure was first measured, for example, by sticking a hollow cane pole into the carotid artery of a horse and watching to see how high in the pole the blood rose. Such a blood pressure might be measured in units of feet of blood or cm of blood or whatever.
Central venous pressure can be measured by the column method by using a vertical tube filled with water or IV fluid and attaching it to a catheter that's inserted into the right atrium and seeing how high the water or IV fluid rises in the column which usually has marks for cm of water (cm H2O). The column method has the advantage of low cost but the disadvantage that it can normally only be used to measure things of low pressure so the column size can be limited to something that would fit in the room with the patient.
The occlusion method of pressure measurement is how a sphygmomanometer (blood pressure cuff) works. The cuff is pumped up until flow is stopped and you note the pressure required on a gauge and assume that the occlusion pressure equals the vascular pressure you're interested in.
A transducer is an electrical device that converts pressure into electricity or a measurable electrical resistance. They work by the pressure of interest bending or distorting a strain gauge that changes its electrical properties based upon the degree of distortion. These are more expensive than the other methods but offer the advantage of accuracy and can be used over a wide range of pressures. They must be calibrated frequently during use and must be calibrated correctly if correct data is to be obtained from them. Some transducers can be placed directly into the vessel where pressure is to be measured but most are positioned outside of the patient and the patient's pressures are transmitted to the transducer via fluid filled non-compressible tubing. An external transducer must be placed at the same height above the floor as the place where you want to measure pressure (i.e. at the level of the heart if that's where you want to measure pressure) so the weight of the fluid conduit does not influence the pressure measured at the transducer.

Flow
Flow describes the movement of a volume fluid (gas or blood for example) over a given time. Typical units would be liters per minute or barrels per hour etc. The flow we are most frequently interested in is the cardiac output, normally expressed in liters per minute. We sometimes divide this value by a patient's body surface area (BSA) to come up with the cardiac index which is cardiac output normalized for variations in patient size. The cheapest way to measure cardiac output is to open the patient's chest and let the aortic outflow pour into a bucket for one minute. At the end of a minute you measure the volume of blood in the bucket and call that the cardiac output. This method has fallen out of clinical use. Most cardiac outputs today are measured by thermal dilution. In this method, cool water is injected into the circulation while the temperature is measured downstream. If one knows the distance downstream and can do some calculus, you can relate the rate of cooling and warming at the downstream location to the flow of blood by the temperature measuring point such that the temperature will rise and fall more quickly if the cardiac output is high. Radioactive dyes can also be used in place of cool water but cool water is cheaper, safer, and is easier to find. There are some high-tech ways to measure blood flow that are not yet in widespread clinical use and include doppler techniques and inductive plethysmography.

Resistance
Resistance describes the change in pressure that results from a given flow and is expressed in units of pressure over flow. Airway resistance would be in units of cm H2O per liter per second where cm H2O is the pressure and liters per second is the flow. The pressure part of resistance is found by subtracting the downstream pressure from the upstream pressure so you need to know three things to calculate a resistance: upstream pressure, downstream pressure, and flow. When dealing with vascular (blood vessel) resistances we normally use units of dynes.sec/cm5 by convention. To make life interesting, we first calculate a vascular resistance by taking the upstream - downstream pressures in mm Hg and then divide this result by the flow (normally cardiac output) in liters per minute. This results in a value of units mm Hg / liter / minute. To get this into the standard units of dynes.sec/cm5 we multiply the result by 80. Resistances are not measured directly but are calculated based on pressures and flows that are measured directly.


]]>delton@lexpcc.netPhysiology2009-12-05T19:37:30-05:00http://www.lexingtonpulmonary.com/articles/files/c5fb6fe41bae8cc7232cab5323cb8c12-3.php#unique-entry-id-3http://www.lexingtonpulmonary.com/articles/files/c5fb6fe41bae8cc7232cab5323cb8c12-3.php#unique-entry-id-3Pulmonary & Systemic Circulation
By Donald R. Elton, MD, FCCP
Lexington Pulmonary and Critical Care

Introduction
We will concern ourselves with two main types of blood vessels: systemic and pulmonary. After birth, systemic vessels (arteries and veins) supply peripheral tissues, including the lung and other organs, with oxygen and nutrients and remove carbon dioxide. The pulmonary vessels are responsible for carrying deoxygenated blood to alveoli in the lungs where gas exchange with the atmosphere takes place. Note that the systemic arteries and pulmonary veins both carry oxygenated blood while the systemic veins and pulmonary arteries carry deoxygenated blood. Pulmonary tissues themselves are supplied partially by the relatively deoxygenated pulmonary arteries and partially by the systemic bronchial arteries. All systemic arteries arise from the left ventricle and aorta while all pulmonary arteries arise from the right ventricle. All systemic veins drain into the vena cava and right atrium while all pulmonary veins drain into the left atrium.

Systemic Circulation
The systemic circulation is a high pressure system. Pressures within systemic arteries in some disease states can be as high as 300 mm Hg though normal pressures are below 150 mm Hg. The Aorta, the body's largest systemic artery, arises from the left ventricle and provides branches that supply the entire body. The important coronary arteries arise from the aorta just above the aortic valve at the left ventricular outflow tract. Systemic blood pressure (and really all blood pressures) are determined at a basic level by flow and resistance, namely the cardiac output and systemic vascular resistance. Cardiac output, in turn, is determined by heart rate and stroke volume (the volume pumped by the left ventricle in a single contraction). The body regulates the systemic blood pressure both by regulating the cardiac output and the systemic vascular resistance. Cardiac output can be increased or decreased by changing contractility (which results in alterations in stroke volume) or by changing the heart rate. There are several feed-back mechanisms involving primarily the kidneys and brain that regulate blood pressure. The kidneys play an important role as a certain amount of renal perfusion is required for their proper function and the brain is involved as it has high oxygen demands with little energy storage capability. Systemic arteries subdivide into smaller and smaller vessels until they become capillaries capable of allowing only one red blood cell to pass at a time. These capillaries are where gas exchange occurs between the oxygenated systemic blood and peripheral tissues. Capillaries, then empty into systemic veins that lead back toward the vena cava and right atrium. Unlike arteries, the systemic veins frequently have valves that assist in preventing back flow away from the heart. These are necessary as veins are the low pressure end of the systemic circulation and in animals like the human or giraffe, the vertical distance the venous blood has to travel to reach the right heart requires more pressure to overcome than will normally exist in the veins. Muscular activity and negative intrathoracic pressure both help push and pull systemic venous blood back toward the heart but they are not continuous forces so the valves prevent blood that was recently pushed or pulled toward the heart from sliding back into the distal legs and arms. Typical systemic venous pressures are in the range of 0 to 10 mm Hg. While there are some variations in arterial anatomy (i.e. finding one artery replacing two) arteries are fairly constant from one individual to another. Veins are much more variable with only the larger ones being constant across individuals. Humans can regenerate veins or generate collateral veins with little difficulty while this is frequently not possible with arteries. One reason why it is serious to damage or obstruct an artery is that there may well be necrosis of the tissue supplied by the artery before any repair or replacement of vasculature can take place. Arteries that supply a tissue without any collateral (backup) artery are called end arteries. Coronary arteries are frequently end arteries. Loss or obstruction of an end artery results in tissue necrosis. Obstruction of a vein results in alternative veins becoming engorged and can result in edema in the affected area but these changes normally do not result in tissue necrosis.

Systemic Arterial Pressure Monitoring
Systemic arterial pressure measurement is done either with a manual or automatic blood pressure cuff (sphygmomanometer) or with an indwelling arterial catheter attached to a strain gauge pressure transducer via a fluid filled catheter. It is normally desirable to use the cuff method so long as pseudo-hypertension does not occur from hardening of arterial walls and so long as the blood pressure is not so low as to make the cuff readings unreliable (the cut-off varies from patient to patient but an arterial catheter would normally be used if the blood pressure is below 70 mm Hg). Arterial catheters are saved for life threatening conditions because they are frequently associated with complications such as bleeding (you can exsanguinate a patient in very short order if tubing disconnects inadvertently) and occlusion of the artery which can result in loss of the hand, fingers, or other distal structures. Clots can form on an arterial catheter which can embolize (break free) and the clots can travel downstream occluding distal arteries resulting in tissue necrosis. A less frequently recognized complication of arterial blood pressure monitoring that is particularly important when they are used in pediatric or neonatal patients but still valid in adults is the pressure that can be exposed to the circulation when flushing the catheter. Most monitoring systems use an IV bag pressurized to 300 mm Hg that is then regulated via a down-regulating device to allow a few ml's per hour of heparin-containing fluid to pass through the catheter to keep the catheter from clotting off. When blood is drawn through the catheter, there is a button or switch that will briefly allow the 300 mm Hg pressure to be applied directly to the catheter, bypassing the regulator. This can cause a rapid rise in arterial pressure depending on the diameter of the catheter in use and can dislodge clots from the catheter pushing them both downstream (their normal direction of travel) and upstream which could result in emboli being sent far from the artery where the catheter sits. This could even cause a stroke or blindness if clots were washed toward the head during a catheter flush. To improve the safety of arterial catheter usage, they should only be placed when absolutely necessary, they should not be used for routine blood draws (other than perhaps blood gasses), they should only be used in an intensive care unit setting where they can be closely watched, they should only be placed in vessels that have collaterals (i.e. not in femoral or brachial arteries), and they should be removed as soon as possible or as soon as any sign of a complication presents.

Systemic Arterial Oxygen Monitoring
In the absence of unusual shunts, arterial blood from any systemic artery will have the same oxygen content as blood from any other systemic artery.

Systemic Venous Pressure Monitoring
Venous pressure monitoring is only done in the large or central veins. This is to avoid local variations in limbs and to avoid the effect that valves have on the pressures. Normally this means a catheter must be placed into the vena cava or right atrium of the heart. Typical access sites would include the internal or external jugular veins or the subclavian veins or femoral veins. Because venous pressures are lower, they can be measured with a column or with a transducer like that used for arterial pressure monitoring. Columns are simpler and cheaper but are seldom used today because of the availability of transducers which are more accurate when used properly and offer continuous rather than intermittent monitoring. The central venous pressure (CVP) can be estimated by physical exam (see diagram above) by measuring the vertical distance between the top of the internal jugular venous pulsation in the neck and the sternal angle and adding 5 to the value to give you the CVP in units of cm H2O.

Systemic Venous Oxygen Monitoring
Systemic venous oxygen contents reflect the oxygenation of the tissues they drain. For this reason, if the practitioner needs to know the venous oxygen content, the blood must be drawn from an area where all of the systemic venous blood in the body has mixed. The only suitable location to find such blood is in the pulmonary artery. While mixing actually starts at the level of the vena cava, studies have shown that mixing is not complete until the pulmonary artery. Some Swan-Ganz pulmonary artery catheters have a built-in oximeter that can continuously monitor the oxygen saturation in the pulmonary artery.

Pulmonary Circulation
The pulmonary circulation is a low pressure system. Normal pressures are less than 30 mm Hg though in certain disease states the pulmonary artery pressure can be 70 mm Hg or more and may approach the systemic arterial pressure. There is very little blood flow through the pulmonary circulation before birth but after the first breath, the pulmonary vascular resistance falls rapidly allowing blood that previously passed through the patent ductus arteriosis and foramen ovale to pass through the lungs to pick up oxygen and lose carbon dioxide. Pressures are lower in the pulmonary circulation because the pulmonary vascular resistance is lower. In the absence of shunts, pulmonary and systemic blood flow are equal. The lower pressures are the reason why the right ventricle has a thinner wall than the muscular left ventricle which must deal with higher systemic blood pressures. The pulmonary vascular resistance is really never too low but it can be made too high by a variety of disease states.

Pulmonary Hypertension
Elevations in pulmonary vascular pressures result primarily from increases in vascular volume, increases in pulmonary vascular resistance, or from blockage or destruction of pulmonary vessels. Pulmonary vascular resistance can be increased by hypoxemia or acidemia or by some drug effects. The increase caused by hypoxemia or acidemia has a useful function as these are the conditions that exist when a part of the lung is underventilated. If you underventilate a part of the lung but do not change the pulmonary blood flow to that area then the blood going to the underventilated segment of lung will not be brought up to arterial oxygen levels and will be added to the oxygenated blood from the well ventilated segments as a shunt. By clamping down on vessels to underventilated areas, the lung prevents shunts from developing. Because the pulmonary circulation can handle large increases in cardiac output with minimal pressure elevations, shutting down blood flow to a segment or even lung usually does not result in significant pulmonary hypertension. However, if you globally reduce oxygenation or have acidosis, then all pulmonary vessels will clamp down resulting in an increase in the pulmonary vascular resistance and resultant pulmonary hypertension. This is an example of how a normal adaptive mechanism can cause pathology in some disease states. Obstruction of pulmonary vessels can occur as a result of pulmonary embolic disease or from destructive lung diseases such as emphysema or cystic fibrosis. Usually, 30-50% of the pulmonary circulation must be lost before significant pulmonary hypertension occurs. Pulmonary vascular pressure monitoring This will be covered during the lectures on the Swan-Ganz catheter.

Congenital Heart Disease
There are numerous congenital heart defects that result in alterations in normal anatomy and physiology of the pulmonary and systemic circulatory systems. Some defects result from abnormal shunts or openings between the two circulatory systems such as in atrial or ventricular septal defects or persistence of fetal circulation and other defects result in abnormal connections of normal vessels such as transposition of the great vessels or anomalous pulmonary venous return. Some of these defects cause right to left shunting (reduced pulmonary blood flow) and these defects result in severe hypoxia. Other defects cause left to right shunting (increased pulmonary blood flow) and these result in milder hypoxia resulting from pulmonary edema. It is important to have an idea of what sorts of defects can occur as many of these defects are barely symptomatic and can escape detection until adulthood and may be noted incidentally when a Swan-Ganz catheter is inserted for management of an unrelated condition but they can cause unexpected pressures and oxygen contents to be measured. ]]>delton@lexpcc.netSwine Flu2009-04-28T21:08:11-04:00http://www.lexingtonpulmonary.com/articles/files/swineflu.php#unique-entry-id-2http://www.lexingtonpulmonary.com/articles/files/swineflu.php#unique-entry-id-2Unless you’ve been living in a cave you know by now that there has been an outbreak of a novel influenza virus that potentially could cause a pandemic. In North America, the seasonal flu season is about over and here in South Carolina influenza cases have been relatively rare. The current H1N1 virus also known as Swine Flu seems to be a mutated flu with features of avian, human, and swine flu viruses. As of this writing (28 April 2009) there have been about 2,000 infections known in Mexico with about 152 deaths suspected from the flu in Mexico. Elsewhere there have been clusters of cases mostly among people who had recently travelled to Mexico with the largest cluster occurring among students of a private school in New York City where over 40 cases have been confirmed.

There have been no confirmed deaths from this virus outside of Mexico and many of the deaths within Mexico have not been fully confirmed to have been caused by the flu virus though some have been confirmed.

It is not yet known why almost all cases of this virus outside of Mexico have resulted in mild illnesses yet many of those in Mexico have been more severe. It may be that the epidemic just started earlier in Mexico and there could be far more cases in the community than have yet been reported and thus just statistically more deaths would naturally occur in that setting. Other possibilities may include genetic susceptibility or other unknown factors.

To date, the virus itself, seems identical between the cases in Mexico and those reported elsewhere in the world which would indicate that host or statistical factors are most likely the explanation for seemingly different mortality rates. Most experts believe there will be deaths outside of Mexico just as are seen every year with seasonal flu which is estimated to cause upwards of 30,000 deaths per year in the United States alone.

It should be noted that many people, including some healthcare workers use the word “flu” to describe a variety of minor illnesses that are not related to true influenza or flu infections. The real flu is spread through contact with respiratory secretions typically spread through coughs and physical contact with cough droplets that contain active virus. The virus can survive on surfaces for up to an hour and it is generally felt that you can catch the flu if you are within 6-7 feet (2 meters) of an infected person who is coughing.

The real flu causes a cough, sore throat, sinus pain, headaches, body aches, and fever typically to 102 F or higher. Patients become symptomatic within 48 hours of exposure to the virus and are felt to be contagious from the day before the onset of symptoms until about 7 days after symptom onset. Many patients keep a cough for up to a month after a flu infection and are profoundly weak and ill for the first week. Patients who die of the flu typically develop influenza pneumonia which is a life threatening infection that causes low oxygen levels and increased work of breathing and can frequently lead to respiratory failure and need for life support in an intensive care unit. The flu can kill even young healthy people but people with other cardiac or pulmonary illnesses are at increased risk of trouble or even death even if they do not develop the full influenza pneumonia.

Prevention of the flu typically includes taking a flu shot but the current and last year flu shots were not tuned to this new Swine flu virus and will not help in this case. Drug companies have started working on a new vaccine to protect against Swine flu but this will take months to develop and the shot must be administered about 4 weeks prior to exposure to be effective. Additional preventive measures are to stay at least 6 feet away from anyone who is infected and to use good hand washing technique including washing your hands after contact with anyone who might be sick or after coughing or sneezing.

Routine antibiotics do not help the flu as the flu is caused by a virus and antibiotics are not effective. There are two antiviral medications that can help prevent or shorten the course and severity of flu and they require a doctor’s prescription. They are fairly expensive but can help. When treating an actual infection with flu though, the antiviral medications must be started within 3 days of symptom onset to do any good and should be taken for a total course of 5 days.

For more information, check out the Centers for Disease control website at http://www.cdc.gov/swineflu.

Don Elton, MD]]>delton@lexpcc.netPAH, Pulmonary HTN, Clinical Trials2008-10-17T11:55:19-04:00http://www.lexingtonpulmonary.com/articles/files/PAHCenter.php#unique-entry-id-1http://www.lexingtonpulmonary.com/articles/files/PAHCenter.php#unique-entry-id-1
We also offer participation in several clinical trials to assure that our patients can receive the latest in State-of-the-art care right here in the Columbia/Lexington area that used to be available only at major medical centers.

As of today (October 17, 2008) we are actively following 199 patients with known or suspected pulmonary hypertension.

We have the following number of patients on the various approved therapy for pulmonary hypertension:

Tracleer (bosentan) 45
Letairis (ambrisentan) 16
Revatio (sildenafil) 39
Ventavis (iloprost) 9
Remodulin (treprostinil) 1

We are currently recruiting patients for the following clinical trials related to treatment of pulmonary arterial hypertension:

COMPASS-2 study - This is a drug study sponsored by Actelion Pharmaceuticals testing the combination of sildenafil and bosentan for treatment of Pulmonary Arterial Hypertension.

Athena-1 study - This is a drug study sponsored by Gilead pharmaceuticals to evaluate the safety and effectiveness of the combination of sildenafil and ambrisentan for treatment of Pulmonary Arterial Hypertension.

Aries-3 study - This is a drug study sponsored by Gilead pharmaceuticals to evaluate the safety and effectiveness of ambrisentan for treatment of Pulmonary Arterial Hypertension.

ABS-LT study - This is the long-term extension study for AIRES-3.

REVEAL registry - This is a registry study sponsored by Actelion Pharmaceuticals to record data on patients treated for pulmonary hypertension.

For referrals call our office at 803-520-5100 or send email to delton@lexpcc.net.

]]>delton@lexpcc.netSmokingPreventive Health2008-10-17T11:34:16-04:00http://www.lexingtonpulmonary.com/articles/files/smokingbad.php#unique-entry-id-0http://www.lexingtonpulmonary.com/articles/files/smokingbad.php#unique-entry-id-0
1 - Cancer - Lung Cancer kills more people than the next 4 cancers combined. You hear a lot about colon cancer, breast cancer, breast cancer, melanoma but compared to lung cancer these are insignificant in terms of mortality. Maybe they have better press agents but those other cancers don’t kill near as many people as lung cancer does. Part of the problem is that the cure rate for lung cancer has hovered around 11% for years. 75% of patients diagnosed with lung cancer already have metastatic disease and are thus not curable with surgery - still the only cure. This happens because the lungs are big and a cancer can grow for months if not years without causing any symptoms at all. There won’t be symptoms until the tumor either blocks an airway or interferes with a nerve or vascular structure or until the patient coughs up blood. Other than cutting down on smoking, the only way to have a meaningful improvement in the cure rate for lung cancer is to increase early detection. Various studies are being done to determine if there is a cost effective way to screen for lung cancer. In my practice, I recommend an annual chest x-ray for anyone who has ever smoked. This may not be cost effective but it saves lives in my experience as many lung cancers cured by surgery were actually discovered on randomly obtained chest x-rays in many cases done for other reasons like after a car accident.

How big a deal is smoking in causing lung cancer? As of 2008 I’ve been in this practice 11 years. During that time we have steadily discovered 1 or 2 new lung cancers per week or have found about 75-100 cancers per year. Multiply that times 11 years and it’s close to 1000 lung cancers we’ve diagnosed. Of those, only 4 had never been smokers. Some had quit 20 years before the diagnosis (unfortunately the risk never totally goes away even though it gets smaller with each year away from smoking). Lung cancer in non-smokers is so rare that in many cases the cancer isn’t lung cancer at all but is a cancer of some other organ that just happened to spread to the lungs.

Finally, other cancers such as bladder cancer also occur more frequently in smokers.

Bottom line - not all smokers get lung cancer but almost all lung cancer occurs in smokers or former smokers.

2- Lung disease - it’s widely known that in many (though not all) patients, smoking leads to chronic bronchitis, emphysema, and chronic obstructive pulmonary disease. So far as second hand smoke the only proven bad effect other than the fact that you smell bad is that children who grow up in the house of a smoker are more likely to develop asthma and are more likely to miss time from school due to various illnesses.

3- Vascular disease - This includes coronary artery disease (leading to heart attacks), cerebrovascular disease (leading to strokes), and peripheral vascular disease (leading to amputations). In fact, with severe peripheral vascular disease it’s rare to see the disease in a patient who has never smoked.

Don Elton, MD]]>