Learning Objectives

Discuss evidence base information related to the shock in small animal with specific emphasis on definitions, classification and staging. Shock is defined as a state of inadequate tissue oxygenation and lack of vital energy due to poor volume, distribution o quality of the bloods components. There are multiple types of shocks described in different ways. Every kind of shock has the same underlying problem, which is impairment of oxygen delivery to the tissues. Decrease supply or maldistribution can limit oxygen utilization. Severe tissue hypoxia leads to metabolic and structural changes that will be irreversible if it isn't managed properly.

In a very accurate description, Haskin remark how important is semantics in shock discussions: To describe an animal as being "in shock" says that the animal is "very sick". One should always use adjective such as hypovolemic, cardiogenic, traumatic, etc., to more clearly assign the underlying cause of the shock. In addition, animals can, for instance, be hypovolemic, but not in shock. The animal is not normal, but is compensating for the problem in all of the appropriate ways and is not in imminent danger of dying. Such patients should be described simply as hypovolemic.

When the disease has progressed to the point that compensatory mechanisms can no longer maintain adequate tissue perfusion and oxygenation, and there is laboratory or physical evidence of organ dysfunction, the condition should be described as hypovolemic shock.

The same would apply to sepsis vs. septic shock, and heart dysfunction vs. cardiogenic shock. These words describe points on a disease continuum, however, and the exact spot where the condition stops being just hypovolemia and starts being hypovolemic shock is admittedly quite fuzzy; do the best you can. The reason to worry about such terminology at all is to provide prognostic and therapeutic implications of the animal's condition so that both the veterinarian and the owner know what they are getting themselves into.

Categorical definitions of shock provide a framework upon which one may organize their thoughts on the issue. All such categorization schemes are somewhat arbitrary since there are overlapping mechanisms, but they do provide some therapeutic direction. Such categories are not distinct entities and a single patient may suffer multiple shock mechanisms. Gradations of severity are also somewhat arbitrary and in the end, based upon a thorough physical, physiologic, and laboratory evaluation, one must construct a list of the patient current problems which must be addressed in the therapy plan.

Cardiogenic Shock

Cardiogenic shock is a low forward flow state due to heart-specific related problems. Low forward flow states secondary to low preload are considered hypovolemic in nature. Cardiogenic shock may be due to poor diastolic function (hypertrophic cardiomyopathy, pericardial tamponade, fibrosis, arrhythmias), poor systolic function (dilative cardiomyopathy, general anesthetics, arrhythmias), or valvular limitations (outflow stenosis; backflow regurgitation).

Distributive Shock

Distributive shock encompasses a potpourri of problems generally associated with an inappropriate distribution of cardiac output and includes hypovolemia. Hypovolemia may be due to whole blood loss, hypoproteinemia, increased vascular permeability or severe dehydration. Arteriovenous shunts reduce the net cardiac output and tissue blood flow. Vessel occlusion from external sources (intestinal torsion, masses, or foreign bodies) interfere with blood flow to the involved organ. Thromboembolism interferes with blood flow to the involved organs and severe pulmonary thromboembolism can cause cor pulmonale and right heart failure.

Hypoxic Shock

Hypoxic shock implies that the tissues are being perfused (to differentiate it from distributive shock) but that there is a problem with the oxygen content or unloading. Hypoxemia (low partial pressure of oxygen or low hemoglobin saturation due to pulmonary pathology) or anemia (low oxygen content) are the two common examples. Methemoglobinemia (oxidized, ferric, hemoglobin) and carboxyhemoglobin (carbon monoxide poisoning) decrease the oxygen carrying capacity of the hemoglobin.

Metabolic Shock

Even though the tissues are being adequately perfused and oxygenated, there may be intracellular problems which interfere with energy production. Sepsis, in addition to all of its vasoactive intermediates and cell-mediated injury, interferes with intermediary metabolism. Cyanide intoxication interferes with mitochondrial function.

Heat stroke is a form of metabolic shock wherein the metabolic rate exceeds the animal's ability to deliver energy substrates. Hypoglycemia, as a cause of inadequate energy substrate for cerebral metabolism, is another form of metabolic shock.

Hemodynamic Mechanisms in Shock

There are several important mechanisms related to shock developing which are the following:

1.  Intravascular volume which regulates mean circulatory pressures and venous return to the heart, any important decrease will be the main factor in noncardiac forms of shock.

2.  Heart, cardiac dysfunction is the main abnormality in cardiogenic shock and it contributes to hypoperfusion in another forms of shock. Heart rate, contractility and balance between preload and afterload determine cardiac output.

3.  Resistance circuit. Ventricular loading, arterial blood pressure and distribution of systemic blood flow are affected by alterations in arteriolar tone. Increases impedes cardiac ejection and compromises blood flow, decreases will provoke hypotension and limit organ perfusion. Maldistribution of blood flow produced by differences in arteriolar tone will impair oxygen demand and supply.

4.  Capillary exchange network represents the largest area of the circulatory tree. Capillaries are the sites of nutrient and fluid exchange between the intra and extravascular space. Capillary occlusion or increases in nonnutritional flow will compromise organ metabolic functions.

5.  Venules represent 10 to 15% of total vascular resistance. Because the lowest flow rates happens here, they are usually the initial sites of vascular occlusion.

6.  Arteriovenous connections the opening of these connections will lead to bypasses in the capillary network that will result in tissue hypoxia and ineffective nutritional exchange.

7.  Venous capacitance contains 80% of total blood volume, any increase or decrease in tone or venous capacitance will decrease effective circulating volumes limiting venous return to the heart. It will also redirect the blood volume to the central circulation acting as an initial compensatory mechanism to maintain cardiac output.

8.  Mainstream vascular patency determines adequate ventricular ejection and tissue perfusion. Any obstruction may critically limit venous return.

Frequently one or more type of shock is present, this can be easily demonstrated with septic shock where distributive abnormalities of blood volume, systemic and microvascular blood flow are the main factors that lead to hypoperfusion. However, hypovolemia and cardiac dysfunction are two major features of septic shock.

Shock can also be classified into mechanical and mediator syndromes. Mechanical syndromes such as massive pulmonar embolism and acute gastrointestinal hemorrhage resolve rapidly if the underlying injury is successfully handled. The severity of these syndromes can be directly correlated with the extent of the injury or damage suffered by the patient. They are characterized by circulatory states where the primary mechanism of tissue injury is global hypoperfusion and ischemia, because a decrease in cardiac output.

On the other hand, mediator syndromes such as septic shock are caused by the massive release of biological mediators into the blood stream. The severity of the syndrome is proportional to the degree of mediator activation and of its regulation, therefore we can find SIRS, CARS and MODS. In these type of syndrome organ dysfunction are due to ischemia and mediator related injury.

Reperfusion Injury

Tissue injury during reperfusion results directly from the release of mediators and indirectly from microvascular dysfunction that compromises the restoration of blood flow to normal levels.

Oxygen-free radicals and increased intracellular calcium, sodium and water produce organic damage. The most affected organs are kidneys, brain and heart; therefore they must be aggressively monitored and treated at the first sign of compromise. Capillary stasis and tissue hypoxia predispose to sludging of blood, increase capillary permeability and platelet aggregation, if clotting factors are depleted DIC can develop.