Page 573 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice

Shock Syndromes 561

feline patients with circulatory shock, raising the the compensatory responses to this abnormality will be
possibility that body temperature could play a role in this similar to those seen in hypovolemic shock, with increases
phenomenon. 107 in systemic vascular resistance and tachycardia. Hence the
clinical signs of cardiogenic shock will be similar to those
Chemoreceptors of hypovolemic shock, namely, pale mucous membranes,
The chemoreceptors are specialized cells that sense prolonged capillary refill time, poor pulse quality, and
decreases in oxygen, increases in carbon dioxide, and differences between extremity and core temperature.
increases in hydrogen ion concentration. The peripheral Causes of cardiogenic shock include myocardial failure
chemoreceptors are found in the carotid body and aortic as may occur with dilated cardiomyopathy or end
arch adjacent to the baroreceptors. When ECV decreases stage valvular regurgitation. Cardiogenic shock
to a critical level, these cells are stimulated by the lack of secondary to decreased diastolic filling can occur with
oxygen and the accumulation of carbon dioxide and tachyarrhythmias, hypertrophic cardiomyopathy, or peri­
hydrogen ions. They transmit signals to the central vaso­ cardial tamponade. 147 Patients presenting in cardiogenic
motor center in a manner similar to the baroreceptors, shock may or may not have concurrent congestive heart
causing increases in sympathetic tone and vasopressin failure typified by pulmonary edema, pleural effusion,
levels. They also stimulate the respiratory center, leading or ascites. For example end-stage valvular regurgitation
to increases in alveolar ventilation that maybe evident as cases are likely to have significant morbidity associated
tachypnea in the patient with circulatory shock. These with their congestive heart failure and are now
receptors contribute to the maintenance of blood demonstrating evidence of poor perfusion. In contrast
pressure in the face of severe decreases in ECV and are patients with malignant tachyarrhythmias may have no
not thought to contribute to the regulation of MAP in evidence of congestive heart failure at the time of
the face of mild to moderate insults. 11 presentation for cardiogenic shock.
Starling Forces Distributive Shock
Hemorrhagic shock will also lead to alterations in When regulation of vasomotor tone is abnormal it can
Starlings forces. Following acute hemorrhage there is a cause circulatory shock despite an adequate blood volume
sudden drop in capillary hydrostatic pressure that and normal cardiac function (see Table 23-2). Global
promotes the movement of fluid from the interstitium decreases in arteriolar tone will cause decreases in ECV
to the intravascular space. Interstitial fluid can replace that is sensed by the baroreceptors, as described for hem­
up to 75% of the shed blood volume. 10 This process is orrhagic shock. But in this scenario there is a failure of
known as transcapillary refill or autotransfusion. As the compensatory vasoconstriction in response to increases
protein concentration (and red blood cell concentration) in sympathetic tone and tachycardia is the sole compensa­
of interstitial fluid is lower than that of blood, this tory response. Global vasodilatation is marked by hypo­
response causes a decrease in both hematocrit and total tension that is unresponsive to fluid administration. On
plasma protein. In dogs and cats splenic contraction physical examination these patients can have red mucous
can supplement hematocrit and the end result may be a membranes, rapid capillary refill times, tachycardia,
proportionally greater drop in the total protein than that bounding pulses, and warm extremity temperatures
of the packed cell volume following hemorrhage. 22 reflecting vasodilatation. 61 Some causes of distributive
shock such as sepsis can cause heterogenous changes in
Hypovolemic Shock microcirculatory vasomotor tone leading to inadequate
Hypovolemic shock can occur without hemorrhage; for, perfusion of some tissue beds while there is normal or
example severe dehydration or third-space losses can possibly excessive perfusion of others. If microcirculatory
cause significant decreases in blood volume. Increased abnormalities occur in the absence of generalized vasodi­
vascular permeability as may occur with severe systemic latation the patient may have normal global hemody­
inflammation or anaphylaxis can also cause significant namic parameters while some tissue beds are suffering
blood volume loss. The responses to hemorrhagic shock, from hypoperfusion and inadequate cellular energy pro­
as described previously, are equally applicable to other duction (also known as cryptic shock). 38 This is another
causes of hypovolemia. form of distributive shock.
Cardiogenic Shock PATHOLOGIC CONSEQUENCES OF
SHOCK
Cardiogenic shock causes decreases in effective
circulating volume despite a normal, or frequently Shock of any cause will result in a common pathway of cell
increased blood volume (see Table 23-2). A decrease in injury and tissue damage. The pathogenesis of circulatory
cardiac contractility or diastolic filling will impair stroke shock includes cellular hypoxia, inflammatory mediator
volume. From Figure 23-1 it can be appreciated that generation, and free radical mediated damage.