INTRODUCTION

Shock is defined as inadequate cellular energy production. It most commonly occurs secondary to poor tissue perfusion from low or unevenly distributed blood flow that causes a critical decrease in oxygen delivery (DO₂) in relation to oxygen consumption (VO₂). Although metabolic disturbances (e.g., cytopathic hypoxia, hypoglycemia, toxic exposures) and hypoxemia (e.g., severe anemia, pulmonary dysfunction, methemoglobinemia) can lead to shock, it most commonly results from a reduction in DO₂ secondary to one of three major mechanisms: loss of intravascular volume (hypovolemic shock), maldistribution of vascular volume (distributive shock), or failure of the cardiac pump (cardiogenic shock). Box 10-1 lists all of the functional classes of shock. An index of suspicion based on signalment and a brief history may help differentiate between these various causes of shock. Early recognition of cardiovascular instability, along with a combination of physical examination findings and point of care testing suggestive of reduced perfusion are all that is necessary to initiate therapy. Rapid, aggressive therapy and appropriate monitoring, along with the removal of any underlying causes, are necessary to optimize the chance for a successful outcome.

CLINICAL PRESENTATION

Hypovolemic shock is commonly associated with internal or external blood loss, or excessive loss of other body fluids (severe vomiting, diarrhea, polyuria, burns). In hypovolemic states, reduced cardiac output due to diminished venous return triggers compensatory mechanisms that attempt to raise the circulating blood volume. An increase in sympathetic activity causes vasoconstriction, increased cardiac contractility, and tachycardia with a resultant rise in cardiac output. Extreme vasoconstriction and microvasculature alterations induce mobilization of fluid from the interstitial and extracellular spaces to the intravascular space. Additionally, a reduction in renal blood flow activates the renin-angiotensin-aldosterone system, which further upregulates the sympathetic nervous system and causes sodium and water retention via the production of both aldosterone and antidiuretic hormone, respectively. Since the net effect of these responses is to increase intravascular volume, clinical signs of shock may be subtle initially, characterized by mild to moderate mental depression, tachycardia with normal or prolonged capillary refill time, cool extremities, tachypnea, and a normal blood pressure. Pulse quality is often normal, and this stage is generally referred to as “compensated shock.” With ongoing compromise of systemic perfusion, compensatory mechanisms are inadequate and often begin to fail. Pale mucous membranes, poor peripheral pulse quality, depressed mentation, and a drop in blood pressure become apparent as the animal progresses to decompensated shock. Ultimately, reduced organ perfusion results in signs of end organ failure (e.g., oliguria) and ultimately death.

Rather than causing an absolute reduction in circulating blood volume/hypovolemia, diseases such as sepsis and gastric dilatation and volvulus lead to maldistribution of blood flow and result in distributive shock. Dogs with sepsis or a systemic inflammatory response syndrome (SIRS) can show clinical signs of hyperdynamic or hypodynamic shock (see Chapters 11 and 107, Systemic Inflammatory Response Syndrome and Septic Shock, respectively). The initial hyperdynamic phase of sepsis or SIRS is characterized by tachycardia, fever, bounding peripheral pulse quality and hyperemic mucous membranes secondary to cytokine (e.g., nitric oxide)-mediated peripheral vasodilatation. This is often referred to as vasodilatory shock. If septic shock or SIRS progresses unchecked, a decreased cardiac output and signs of hypoperfusion often ensue due to cytokine effects on the myocardium or myocardial ischemia. Clinical changes may then include tachycardia, pale (and possibly icteric) mucous membranes with a prolonged capillary refill time, hypothermia, poor pulse quality, and a dull mentation. Hypodynamic septic shock is the decompensatory stage of sepsis, and without intervention will result in organ damage and death. Lastly, the gastrointestinal tract is the shock organ in dogs, so shock often leads to ileus, diarrhea, or melena.

The hyperdynamic phase of shock is rarely recognized in cats. Also, in contrast to dogs, changes in heart rate in cats with shock are unpredictable; they may exhibit tachycardia or bradycardia. In general, cats typically present with pale mucous membranes (and possibly icterus), weak pulses, cool extremities, hypothermia, and generalized weakness or collapse. In cats, the lungs seem to be the organ most vulnerable to damage during shock or sepsis and signs of respiratory dysfunction are common.^1-3

Dogs with gastric dilatation-volvulus may have normal circulating blood volume; however, compression of the major vessels secondary to severe gastric dilatation causes decreased venous return and reduced cardiac output. This is a form of relative hypovolemia. Although the classifications of shock are useful in understanding the underlying mechanism of cardiovascular instability, it is important to remember that different forms of shock can occur simultaneously in the same patient. A dog with gastric dilatation-volvulus, for example, will often have a component of hypovolemic shock secondary to blood loss associated with rupture of the short gastric vessels. Dogs with septic peritonitis may experience tissue hypoxia due to reduced of systemic vascular resistance, but likely suffer from hypovolemia as well if severe cavitary effusions or protracted vomiting are present.