Hypoxia-Induced Pulmonary Hypertension
Hypoxia has opposite effects on the pulmonary and systemic circulations. Hypoxia relaxes vascular smooth muscle in systemic vessels and elicits vasoconstriction in the pulmonary vasculature. Hypoxic pulmonary vasoconstriction is the major mechanism regulating the matching of regional blood flow to regional ventilation in the lungs. With regional hypoxia, the matching mechanism automatically adjusts regional pulmonary capillary blood flow in response to alveolar hypoxia and prevents blood from perfusing poorly ventilated regions in the lungs. Regional hypoxic vasoconstriction occurs without any change in pulmonary arterial pressure. However, when hypoxia affects all parts of the lung (generalized hypoxia), it causes pulmonary hypertension because all of the pulmonary vessels constrict. Hypoxia-induced pulmonary hypertension affects individuals who live at a high altitude (8,000 to 12,000 feet) and those with chronic obstructive pulmonary disease (COPD), especially patients with emphysema.
With chronic hypoxia-induced pulmonary hypertension, the pulmonary artery undergoes major remodeling during several days. An increase in wall thickness results from hypertrophy and hyperplasia of vascular smooth muscle and an increase in connective tissue. These structural changes occur in both large and small arteries. Also, there is abnormal extension of smooth muscle into peripheral pulmonary vessels where muscularization is not normally present; this is especially pronounced in precapillary segments. These changes lead to a marked increase in pulmonary vascular resistance. With severe, chronic hy-poxia-induced pulmonary hypertension, the obliteration of small pulmonary arteries and arterioles, as well as pulmonary edema, eventually occur. The latter is caused, in part, by the hypoxia-induced vasoconstriction of pulmonary veins, which results in a significant increase in pulmonary capillary hydrostatic pressure.
A striking feature of the vascular remodeling is that both the pulmonary artery and the pulmonary vein constrict with hypoxia; however, only the arterial side undergoes major remodeling. The postcapillary segments and veins are spared the structural changes seen with hypoxia. Because of the hypoxia-induced vasoconstriction and vascular remodeling, pulmonary arterial pressure increases. Pulmonary hypertension eventually causes right heart hypertrophy and failure, the major cause of death in COPD patients.
pressure, capillary permeability, or alveolar surface tension or by a decrease in plasma colloid osmotic pressure. Increased capillary hydrostatic pressure is the most frequent cause of pulmonary edema and is often the result of an abnormally high pulmonary venous pressure (e.g., with mitral stenosis or left heart failure).
The second major cause of pulmonary edema is increased capillary permeability, which results in excess fluid and
'Fluid movement in and out of capillaries depends on the net difference between hydrostatic and colloid osmotic pressures. Two additional factors involved in pulmonary fluid exchange are alveolar surface tension, which enhances filtration, and alveolar pressure, which opposes filtration. The relatively low pulmonary capillary hydrostatic pressure helps keep the alveoli "dry" and prevents pulmonary edema.
plasma proteins flooding the interstitial spaces and alveoli. Protein leakage makes pulmonary edema more severe because additional water is pulled from the capillaries to the alveoli when plasma proteins enter the interstitial spaces and alveoli. Increased capillary permeability occurs with pulmonary vascular injury, usually from oxidant damage (e.g., oxygen therapy, ozone toxicity), an inflammatory reaction (endotoxins), or neurogenic shock (e.g., head injury). High surface tension is the third major cause of pulmonary edema. Loss of surfactant causes high surface tension, lowering interstitial hydrostatic pressure and resulting in an increase of capillary fluid entering the interstitial space. A decrease in plasma colloid osmotic pressure occurs when plasma protein concentration is reduced (e.g., starvation).
Pulmonary edema is a hallmark of adult respiratory distress syndrome (ARDS), and it is often associated with abnormally high surface tension. Pulmonary edema is a serious problem because it hinders gas exchange and, eventually, causes arterial Po2 to fall below normal (i.e., Pao2 < 85 mm Hg) and arterial Pco2 to rise above normal (Paco2 > 45 mm Hg). As mentioned earlier, abnormally low arterial Po2 produces hypoxemia and the abnormally high arterial Pco2 produces hypercapnia. Pulmonary edema also obstructs small airways, thereby, increasing airway resistance. Lung compliance is decreased with pulmonary edema because of interstitial swelling and the increase in alveolar surface tension. Decreased lung compliance, together with airway obstruction, greatly increases the work of breathing. The treatment of pulmonary edema is directed toward reducing pulmonary capillary hydrostatic pressure. This is accomplished by decreasing blood volume with a diuretic drug, increasing left ventricular function with digitalis, and administering a drug that causes vasodilation in systemic blood vessels.
Although fresh-water drowning is often associated with aspiration of water into the lungs, the cause of death is not pulmonary edema but ventricular fibrillation. The low capillary pressure that normally keeps the alveolar-capillary membrane free of excess fluid becomes a severe disadvantage when fresh water accidentally enters the lungs. The aspirated water is rapidly pulled into the pulmonary capillary circulation via the alveoli because of the low capillary hydrostatic pressure and high colloid osmotic pressure. Consequently, the plasma is diluted and the hypotonic environment causes red cells to burst (hemolysis). The resulting elevation of plasma K+ level and depression of Na+ level alter the electrical activity of the heart. Ventricular fibrillation often occurs as a result of the combined effects of these electrolyte changes and hypoxemia. In salt-water drowning, the aspirated seawater is hypertonic, which leads to increased plasma Na+ and pulmonary edema. The cause of death in this case is asphyxia.
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Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...