Pulmonary & 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.