Page 417 - Clinical Small Animal Internal Medicine

39 Acute Respiratory Failure 385

with anatomic shunting, physiologic shunting, when blood encounters atypically low alveolar oxygen tensions
VetBooks.ir excessive, can result in hypoxemia that is unresponsive and saturation is submaximal. The mixing of this poorly
arterialized blood with the blood draining high and nor-
to oxygen supplementation. In this setting, the clinical
priority is to restore ventilation to the nonventilated
shape of the oxyhemoglobin equilibrium curve precludes
alveoli, which often mandates mechanical ventilation mal V–Q regions results in systemic hypoxemia. The
with positive end‐expiratory pressure (PEEP). the high V–Q regions from “compensating” for the low
Ventilation–perfusion (V–Q) mismatch is perhaps the V–Q regions. The flat portion observed at high PO 2 val-
most common cause of hypoxemic respiratory failure in ues prevents an increase comparable to the decrease
small animal practice. Aspiration pneumonia, cardio- observed at lower PO 2 values (the steep portion).
genic edema, and noncardiogenic edema are commonly Moreover, the low V–Q regions may be of that nature
encountered causes of hypoxemia in small animal because of high flow (not just low ventilation) and are
patients and can each result in respiratory failure. Pleural thus contributing a disproportionately high volume to the
filling disorders can result in V–Q mismatch as well as final mixture. Likewise, the high V–Q regions may repre-
hypoventilation. Atelectasis and pulmonary thrombo- sent areas with normal ventilation but lower perfusion
embolism each result in V–Q mismatch as well, albeit by and are thus contributing relatively less volume to the
vastly different mechanisms. Pulmonary hypertension is final mixture.
increasingly recognized as a major health concern in vet- As with physiologic shunting, V–Q mismatch may be
erinary species and can result in substantial V–Q abnor- considered a failure of hypoxic pulmonary vasoconstric-
malities. Figure 39.1 illustrates the basic concepts of tive responses in many settings. Whether the problem
V–Q matching and mismatching. arose due to a reduction in ventilation or an increase in
In the ideal lung, ventilation and blood flow would be perfusion, adaptive compensatory adjustments would be
delivered proportionally to alveoli. An increase in ventila- expected in any otherwise healthy animal. In other cir-
tion relative to blood flow (high V:Q ratio) is akin to dead cumstances, inadequate hypoxic pulmonary vasocon-
space ventilation and does not directly cause hypoxemia striction may not be primarily responsible for the V–Q
since blood flowing to such alveoli encounters alveolar inequality. In massive pulmonary thromboembolism
oxygen tensions that are normal or slightly above typical (PTE), the portion of the lung to which blood flow is
values. Perfect one‐to‐one matching likewise produces compromised is now a high V–Q region. It has become
conditions that are favorable for pulmonary capillary and physiologic dead space and is not directly responsible for
alveolar oxygen tensions to reach equilibrium, assuming hypoxemia (high V–Q regions provide well‐oxygenated
blood flow rates are not excessive (and they rarely are blood). In this setting, if cardiac output does not fall sub-
except in extreme circumstances). It is in those alveolar stantially then the remaining lung is now overperfused
units where perfusion is disproportionately high relative and represents a large region of low V–Q alveolar units.
to ventilation that hypoxemia develops. In this setting, In this way, hypoxemia can result indirectly.

Figure 39.1 Ventilation–perfusion Room Air Ventilation
mismatching. Partial pressure values are in P O =150
2
I
units of mmHg. Flow to normal and high V–Q
regions produces appropriately arterialized
blood. The blood perfusing the region with
reduced alveolar ventilation (far left alveolus)
produces hypoxemic blood. The final mixture
is hypoxemic due to the disproportionate
decrease in saturation in the blood (70% vs PO =144
97%) from the low V–Q regions and the 2 =10.7
minimal increase (99.4% vs 97%) in saturation V/Q V/Q PCO 2
Sat=99.4%
in the blood from the high V–Q regions. =0.05 V/Q =1 =20 Content=19.8
Moreover, the low V–Q region has Mixed Arterial blood
disproportionately high flows relative to the venous 3.95 L/min 0.05 L/min PaO =64.6
2
high V–Q regions (1.0 L/min vs 0.05 L/min). blood 1 .0 L/min PaCO =42.2
2
Sat=91.5%
Content=18.0
PVO =37.8
2
PVCO =47.9
2
Sat=66% PO =40.2 PO =101
2
2
Content=13.0 PCO =47.7 PCO =40.6
2
2
Sat=70% Sat=97%
Content=13.7 Content=19.2