Pulmonary Circulation And Anatomical Right-To-Left Shunts.
Pulmonary circulation compared with the systemic circulation (Fig. 13a)
The pulmonary circulation is in series with the systemic circulation, and pulmonary blood flow nearly equals aortic blood flow. Pulmonary vascular resistance is only about one-sixth of systemic resistance, and the thin-walled right ventricle needs only to generate a mean pulmonary artery pressure of about 15 mmHg to drive the cardiac output through the lungs. Systemic pressures are higher (Fig. 13a), dropping steeply across the main resistance vessel, the arteriole, to give a capillary flow which is usually non-pulsatile. Pulmonary vascular resistance is more evenly distributed in the microcirculation and pulmonary capillary flow remains pulsatile.
Local systemic resistance and blood flow are controlled by sympathetic nerves, metabolites and other substances acting on arterioles. Both sympathetic and parasympathetic nerves innervate pulmonary vessels, but their influence is weak in most circumstances. Systemic arterioles dilate in response to hypoxia, increasing flow and hence oxygen delivery to hypoxic tissues. In contrast, hypoxic pulmonary vasoconstriction occurs in the pulmonary circulation. This response, which is accentuated by high Pco2, improves gas exchange by diverting blood from underventilated to well-ventilated regions (Chapter 14). The response is unhelpful in the presence of global lung hypoxia, at altitude or in respiratory failure, where it may contribute to the development of pulmonary hypertension and right-sided heart failure.
Systemic vascular beds (especially the renal and cerebral) respond to changes in perfusion pressure by constricting or dilating to hold blood flow fairly constant. This autoregulation does not occur in the pulmonary circulation. As cardiac output increases in exercise, pulmonary vascular resistance falls, as vessels are recruited and distended and the rise in pulmonary arterial pressure is small. The pulmonary circulation acts as a blood reservoir and the volume it contains varies, being about 450 mL when upright and 800 mL when lying down. Inspiration also increases pulmonary vascular volume.
Fluid balance across capillaries is determined by hydrostatic and oncotic pressures (the Starling forces; see The Cardiovascular System at a Glance) across capillary walls. Capillary oncotic pressure opposes filtration and is about 27 mmHg in both circulations. Although hydrostatic pressure is low in the pulmonary capillaries ( 10 mmHg), net filtratio of fluid occurs in pulmonary capillaries as it does in systemic capillaries. Other factors favouring filtration are interstitial oncotic pressure, which is relatively high in the lungs (about 18 mmHg) and interstitial hydrostatic pressure, which is negative (about 4 mmHg). Pulmonary oedema occurs when these forces are altered to increase net filtration above the rate that can be cleared by the pulmonary lymphatics. For example, it may occur when pulmonary capillary pressure is increased in mitral stenosis and left ventricular failure. Inspiratory crepitations (crackles) on auscultation in these conditions are probably caused by popping open of airways in lungs stiffened by congestion with blood. They are most obvious at the bases, where hydrostatic pressure is highest. Pulmonary congestion and oedema (and hence breathlessness in these conditions) are worsened by the increase in pulmonary blood volume lying down.
Anatomical or true right-to-left shunts Ideally, all venous blood emerging from tissues would return to the right side of the heart to be pumped through the gas-exchanging lung. In fact, part of the blood draining the bronchial circulation joins the pulmonary vein. This part results in deoxygenated blood from the airways contaminating blood returning from alveoli (Fig. 13a). In addition, a small amount of the coronary venous blood drains directly into the left ventricular cavity via the venae cordis minimae (Thebesian veins). These additions of deoxygenated (right-sided) blood to oxygenated (left-sided) blood are known as anatomical right-to-left shunts. In healthy people, they are equivalent to 2% or less of the cardiac output, but they explain why arterial Po2 is less than alveolar Po2 even though pulmonary capillary blood equilibrates with alveolar gas.
In disease, right-to-left shunting of blood may be much larger. Atelectasis (airless lung) or consolidation in pneumonia will result in pulmonary arterial blood supplying the affected region failing to undergo gas exchange. Right-to-left shunts are also the cause of reduced arterial oxygenation in cyanotic congenital heart disease such as tetralogy of Fallot. Atrial or ventricular septal defects do not usually cause impaired gas exchange and cyanosis, as the higher left-sided pressures give rise to left-to-right shunts in which some oxygenated blood is pumped again through the lungs. If a large left-to-right shunt remains untreated, eventually the excessive pulmonary blood flow leads to pulmonary hypertension. As right ventricular pressure increases, the shunt through the atrial or ventricular septal defect may then reverse to give a right-to-left shunt and cyanosis (Eisenmenger's syndrome).
Effect of right-to-left shunts on arterial blood gases
In the right-to-left shunt, shown schematically in Fig. 13b, 20% of blood fails to pass through functioning alveoli and its O2 and CO2 contents remain at mixed venous levels of 150 and 520 mL/L, respectively. Eighty per cent of the blood undergoes normal gas exchange, emerging with normal O2 and CO2 contents of 200 and 480 mL/L, respectively. The initial effect on arterial gas contents is calculated from a weighted average of the contents in these two bloodstreams. This gives an arterial O2 content 10 mL/L below normal and CO2 content 8 mL/L above normal. From the f at part of the oxygen dissociation curve, it can be seen that the resulting arterial Po2 is about 9 kPa (68 mmHg) compared with the normal 13 kPa (97 mmHg). The much steeper CO2 dissociation curve means the rise in Pco2 is small, from the normal value of 5.3 kPa (40 mmHg) to about 5.5 kPa (41 mmHg).
If the respiratory system is otherwise normal, the reduced Pao2 and increased Paco2 simulate ventilation via the chemoreceptors and the CO2 washed-out of the functioning areas restores arterial CO2 content and Paco2 to normal. In contrast, increased ventilation has little effect on arterial oxygen content and Po2, as blood draining the ventilated areas of the lung was already saturated. If hypoxia is severe, the stimulation in ventilation is often great enough to reduce Paco2 below normal. Typically, in a right-to-left shunt, there is a low Pao2 with a normal or low Paco2.