5 Secretos en el Shock

Learning Objectives

Provide some specific information about the mechanisms, types, stages and classification of the shock in small animals.

Definition(S)

Many definitions has been provided for this complex syndrome: impairment of oxygen delivery to the tissues, reduced cellular energy due to decreased supply or maldistribution of oxygen, inadequate cellular energy production or the inability of the body to supply cells and tissues with oxygen and nutrients and remove waste products.

Mechanisms of Shock

Some important mechanisms related to shock developing 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 non-cardiac forms of shock.

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

3.  Vascular resistance, ventricular loading, arterial blood pressure and distribution of systemic blood flow are affected by alterations in arteriolar tone. Increased tone impedes cardiac ejection and compromises blood flow. Decreased tone will lead to hypotension and limited 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 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.

Classification of Shock

 Hypovolemic: Hypovolemic shock results from a decreased intravascular volume, and causes commonly include hemorrhage, severe dehydration, and hypoproteinemia. It occurs when there is blood volume deficit of at least 15–25%, hypotension and decrease cardiac output is present. Commonly cardiac output and pulmonary capillary wedge pressure (PCWP) are decreased and peripheral vascular resistance is increased.

 Cardiogenic: occurs with failure of the heart as a pump associated with a normal to increased intravascular volume, leading to decreased cardiac output. Frequent etiologies include cardiac failures, pulmonary emboli, cardiac tamponade, valvular rupture and cardiac contusions. There are increased PCWP, peripheral vascular resistance and decreased cardiac output.

 Distributive, septic or vasogenic: Distributive shock is often seen as a relative hypovolemia, resulting from a maldistribution of blood flow despite adequate total body fluid volume. Causes of distributive shock include systemic inflammatory response syndrome (SIRS), sepsis, and anaphylaxis. The release of cytokines, vasoactive peptides and arachidonic acid metabolites, increase the vascular permeability and increase vascular capacity. There is increased or decreased cardiac output, decreased PCWP and decreased peripheral vascular resistance.

 Hypoxic shock: Hypoxic shock is seen with normal tissue perfusion but decreased oxygen content of arterial blood. The equation for oxygen content is: CaO₂ = Hb (gm/dl) x 1.34 ml O₂/gm Hb x SaO₂ + PaO₂ x (0.003 ml O₂/mm Hg/dl), the value in understanding this equation and its relationship with hypoxic shock is that tissues need a requisite amount of oxygen for normal metabolism. Neither the PaO₂ nor the SaO₂ provide information on the number of oxygen molecules in the blood. Of the three values used for assessing blood oxygen levels (i.e., CaO₂, PaO₂, and SaO₂), CaO₂ is the only value that has a measure of units, notably O₂/dl. This is because CaO₂ is the only value that incorporates the hemoglobin content. The most common causes of hypoxic shock include pulmonary disease resulting in a low partial pressure of arterial oxygen and anemia resulting in low levels of hemoglobin, impairing oxygen delivery to the tissues.

 Metabolic shock: Metabolic shock is observed when the tissues receive the appropriate perfusion, nutrients, and oxygen delivery, but the cells are incapable to utilize these resources. Causes for metabolic shock include cyanide toxicity, cytopathic hypoxia of sepsis, and hypoglycemia.

Shock can also be classified into mechanical and mediator syndromes. Mechanical syndromes are represented by pulmonary embolism while mediator syndromes such as septic shock are caused by the massive release of biological mediators into the blood stream.

Reperfusion Injury

A common complication of all types of shock, the 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.

Stages

Clinically shock progress through different stages. Often there is an overlapping of these stages, and in cats is much more difficult to recognize them. The signs and symptoms can help to direct a more adequate therapy.

Early stages

 Tachycardia

 Anxious behavior

 Bright red MM

 Shallow and rapid breathing

 Femoral and tarsal pulse are easy to find

Middle stages

 Heart rate rises further

 MM turn pale or blue

 Pulse is difficult to find

 Dog are less responsive and appears lethargic

 Respiration becomes rapid and shallow

 Temperature decrease

Late stages

 MM appears white or may be mottled

 Heart rate normally elevates and appears irregular

 The pulse is difficult, if not impossible, to locate

 Change in respiration; may be slow and shallow or rapid and deep

 The eyes appear to glaze over and become unfocused

 The dog slips from lethargy to stupor to coma

 Rectal temperature drops to a critical low

References

References are available upon request.