Page 85 - Cardiac Nursing

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C HAPTER 2 / Systemic and Pulmonary Circulation and Oxygen Delivery 61
vasodilation, any of these conditions in the pulmonary circula- Causes of Arterial Hypoxemia
tion may cause arteriolar vasoconstriction. In well-ventilated re- There are six sources of arterial hypoxemia:
gions, there is little vasoconstriction in response to deoxygenated
■ Decreased partial pressure of inspired oxygen
blood. In poorly ventilated areas where the amount of alveolar
■ Decreased percentage of inspired oxygen (decreased fraction of
oxygen is less than normal, such as when a bronchus is ob-
structed, vasoconstriction occurs and blood is shunted to other inspired oxygen, FI O )
2
■ Diffusion limitation
lung areas.
■ Hypoventilation
Distribution of pulmonary blood flow in normal adults is
˙ ˙
■ V/Q mismatch
normally controlled to a greater extent by the hydrostatic pressure
■ Shunt
gradient discussed earlier. Active control of pulmonary circula-
tion, for example hypoxic vasoconstriction, serves a useful role in Decreases in the atmospheric pressure related to higher alti-
diverting blood flow to areas of the lung with more abundant oxy- tude result in a proportional decrease in the partial pressure of
gen, thus improving gas exchange. In contrast to peripheral vas- inspired oxygen (PI O ). These conditions are common to high-
2
culature, which vasodilates in response to hypoxia, pulmonary altitude locations and air travel; however, they are rarely encoun-
vessels constrict (e.g., HPV) to shunt blood away from poorly tered in the clinical setting. Decreased percentage of inspired oxygen
ventilated areas to match perfusion and ventilation. 167 HPV oc- (FI O ) occurs in situations in which other gases may displace oxy-
2
curs within seconds in response to alveolar hypoxia and decreased gen and lower the overall percentage of oxygen below 21% (e.g.,
mixed venous (pulmonary arterial) PO 2 , with alveolar PO 2 exert- diagnostic testing, fire). Diffusion limitation can potentially cause
ing a greater effect. 156 The exact mechanism of HPV is unknown; abnormal diffusion of oxygen across the alveolar–capillary mem-
however, the most likely cause is hypoxia-induced vascular brane. Diffusion limitation can be caused by increases in the
smooth muscle hyperpolarization, which leads to increased intra- thickness of the diffusion pathway and/or decreased transit time
cellular calcium and subsequent vasoconstriction. 168–170 Other through the pulmonary circulation. Hypoventilation can result in
factors that are endothelium dependent, and may modulate hy- a decrease in alveolar PO 2 caused by insufficient gas exchange be-
poxic vasoconstriction and cause vascular remodeling, include tween the external environment and the alveoli. Hypoventilation
inhibition of NO production, decreased effect of prostacyclin and can result from trauma to the chest wall, paralysis of the respira-
increased endothelin. 156,171 Of clinical importance, while inhaled tory muscles, and medications such as morphine sulfate and bar-
NO has been used to acutely treat pulmonary hypertension, its ef- biturates, which depress the respiratory center. 179
fectiveness is equivocal, 172 and a recent meta-analysis recom- Matching ventilation of the alveoli with perfusion of the pul-
˙ ˙
mended that NO not be used for the treatment of acute respira- monary capillary bed is a delicate balance. V/Q matching is a dy-
tory distress syndrome. 173 In contrast, phosphodiesterase namic process with different distributions occurring simultane-
inhibitors, which enhance NO-mediated vasodilation have been ously within the regions of the lungs. In disease, there are a myriad
˙ ˙
found to improve outcomes. 174,175 In addition, endothelin recep- of V/Q relationships exemplified by regions receiving excessive
tor antagonists have become first-line therapy for pulmonary ar- ventilation (dead space), normal ventilation and perfusion (ideal),
terial hypertension 176 and intravenous prostacylin is reserved for and excessive perfusion (shunt).
severely ill patients. 175,177 Shunt refers to the condition when blood passes into the sys-
When blood flow to a region of the lung is decreased, there is temic circulation without passing through a ventilated region of
also a decrease in alveolar CO 2 . The bronchial smooth muscle re- the lung. Under normal conditions, there exists a small physio-
sponds to the decreased alveolar CO 2 levels by constricting; thus, logical shunt because of the difference in PO 2 between alveolar gas
shifting ventilation away from a poorly perfused area. This re- and end-capillary blood. Physiologically, mixed venous blood
sponse occurs in conditions such as prolonged high altitude or in from the pulmonary arterial bed mixes with capillary blood from
patients with chronic obstructive pulmonary disease or prolonged pulmonary venous beds, thereby lowering the end-capillary PO 2 .
pulmonary hypertension. 178 This difference can become larger in conditions such as ventricu-
Ventilation and perfusion must occur in equal proportion in lar septal defect, in which greater amounts of venous blood are
the various regions of the lung to achieve adequate gas exchange. added to arterial blood across the defect, resulting in a lower Pa O .
2
Gas exchange determines the levels of alveolar oxygen partial pres- An important clinical characteristic of a shunt is that the hy-
sure (PA O ) and carbon dioxide partial pressure (PA CO ). An ade- poxemia cannot be completely resolved by placing the patient on
2 2
quate alveolar PO 2 depends on a balance of two factors: the rate of an inspired oxygen fraction (FI O ) of 100%. Because the shunt
2
removal of oxygen by the pulmonary arterial blood and the rate of blood bypasses the ventilated regions of the lung, it is not exposed
replenishment of oxygen by alveolar ventilation. An adequate to the higher alveolar PO 2 . In patients with shunt, the arterial
PA CO depends on the rate of removal of carbon dioxide by alve- PCO 2 may be low, normal, or high, depending on the capacity to
2
olar ventilation. A key concept used to understand pulmonary gas increase respiratory drive in response to hypoxemia.
˙ ˙
exchange is the ventilation–perfusion ratio (V/Q).The concen-
tration of gases (i.e., oxygen, carbon dioxide, nitrogen) in the Gas Transport
various regions of the lung is determined by the ratio of the rate
of ventilation to the rate of perfusion (blood flow). Obstruction Gas Exchange
to ventilation or perfusion leads to alteration in this ratio and, con- In the lungs, oxygen and carbon dioxide equilibrate across the
sequently, the composition of gases. Inequality in ventilation– alveolar–capillary membranes by simple passive diffusion, mov-
perfusion hinders the lungs’ ability to replenish oxygen and ing from an area of greater partial pressure to a region of lesser
remove carbon dioxide. Impairment of gas exchange can result in partial pressure. The partial pressure of oxygen in pulmonary
and an increase in tissue PCO 2 . Clinically, these arterial blood (venous blood from the body) is approximately
a decrease in Pa O 2
conditions can result in hypoxemia. 40 mm Hg, whereas pulmonary alveolar partial pressure of