Early Septic Shock

Septic shock, by definition, implies arterial hypotension and circulatory failure despite adequate intravascular volume resuscitation. It is the final and most extreme stage in the continuum between sepsis and septic shock. Earlier in the course of sepsis, clinical signs result from SIRS, and these patients may appear hemodynamically stable.^3,4,7 Neurohumoral responses that contribute to physiologic compensation during early septic shock include a baroreceptor-mediated release of catecholamines which, in turn, leads to production of counterregulatory hormones such as glucagon, adrenocorticotropic hormone, and cortisol.

Unlike cats in the early stages of sepsis, dogs manifest a hyperdynamic and hypermetabolic response that is typified by tachycardia, tachypnea, hyperemia, decreased capillary refill time, and pyrexia.^3,4,7,8 Cats, on the other hand, are more likely to be lethargic, bradycardic, hypothermic, and pale, with weak pulses.⁸

Early Decompensated Sepsis

During this phase of septic shock, compensatory responses fail and the patient develops hypotension and hypoperfusion. Indirect indicators of tissue hypoperfusion are hyperlactatemia and decreased central (or mixed) venous oxygen saturation.^9,10 Central venous oxygen saturation of less than 70% suggests that oxygen delivery is in a supply-dependent state and may result in anaerobic metabolism and consequently lactate production.⁹

Sepsis results in maldistribution of blood flow. Preferential distribution of blood flow to the heart and brain may lead to poor perfusion to the kidneys, GI, liver, and skin. Heterogenous flow within organs also occurs. In addition, endothelial dysfunction, activation of white blood cells, and coagulation can lead to microthromboses and capillary obstruction, interfering with perfusion of tissues and organs. Oxygen delivery is further compromised by interstitial tissue edema secondary to increased capillary permeability.

Clinically, the mucous membranes become pale, pulse quality is poor, and the patient is mentally depressed. Clinicopathologic changes suggestive of organ dysfunction or failure may start to appear (azotemia, oligoanuria, hyperbilirubinemia, disseminated intravascular coagulopathy [DIC]).

Late Decompensated Septic Shock

As the patient makes the transition into late decompensated septic shock, refractory hypotension and multiple organ failure may develop and lead to death. The brain and heart lose their preferential blood flow, and a complete loss of vasomotor control and severe impairment of cardiac contractility occur. Renal hypoperfusion causes oligoanuria; acute respiratory distress syndrome (ARDS) and pulmonary edema cause respiratory failure. Clinically, the patient becomes hypothermic, stuporous or comatose, has pale mucous membranes with slow or no capillary refill time, and pulses are waning.

Cardiovascular Dysfunction

The cardiovascular system can be affected by the circulating cytokines associated with sepsis in three important ways: (1) the vasculature becomes more permeable, allowing for fluid transudation across the endothelium into extravascular spaces, leading to hypovolemia and tissue edema, (2) the contractility of the heart becomes impaired leading to poor cardiac output, and (3) the vasculature becomes incapable of maintaining tone, causing maldistribution of blood flow. At one time the impaired cardiac performance seen in septic animals and humans was thought to be due to a single “myocardial depressant factor,” but the effects on cardiac performance are thought to be due to the actions of not one, but many, circulating cytokines (e.g., tumor necrosis factor-α, interleukin (IL)-1β, IL-2, and IL-6).¹⁷

Respiratory Dysfunction

Acute lung injury (ALI) and the more severe condition, ARDS, are manifestations of lung injury that occur during sepsis and SIRS (see Chapter 24, Acute Lung Injury and Acute Respiratory Distress Syndrome). ALI and ARDS are labels that describe the syndrome of SIRS-associated or sepsis-associated lung injury, rather than disease processes themselves. The distinction between the two is merely the severity of compromise in gas exchange. The pathogenesis of impaired gas exchange in ALI and ARDS involves endothelial and epithelial injury, neutrophil-dependant lung injury, proinflammatory cytokines, abnormalities of the coagulation system, and abnormalities in the production, composition, and function of surfactant.¹⁸ Ultimately there is an accumulation of protein-rich fluid in the alveoli and infiltration of the alveolar interstitial space with inflammatory cells, fluid, and debris that may be seen radiographically as alveolar infiltrates. The lungs are the “shock organ” in cats and are especially vulnerable to injury during sepsis; tachypnea was a common finding in one study looking at cats with severe sepsis and, although only 11 of 29 cats had an underlying respiratory cause (pneumonia or pyothorax), 17 of 29 had clinical or radiographic signs of respiratory disease.⁸ Septic cats commonly are fluid intolerant and quite susceptible to fluid overload.