Etiology And Epidemiology

Practitioners must have a good understanding of cardiovascular physiology to diagnose, treat, and monitor circulatory problems in critically ill patients. The interrelationships between the major hemodynamic variables are depicted in Figure 13-1.1 These variables include: arterial BP, cardiac output (CO), systemic vascular resistance (SVR), heart rate (HR), stroke volume (SV), left ventricular size, afterload, myocardial contractility, and preload. While an oversimplification, Figure 13-1 is beneficial in conceptualizing where the major abnormalities occur in patients with circulatory shock as well as predicting the body's compensatory responses.

Shock can be effectively categorized by etiology into four major types: hypo-

volemic, obstructive, cardiogenic, and distributive (Table 13-1). ' As noted, all patients with shock have profound decreases in arterial BP. Understanding the primary cause of the circulatory abnormality in these respective shock states is invaluable to their management. Hypovolemic shock is caused by a loss of intravascular volume either by hemorrhage or fluid loss (e.g., dehydration). Obstructive shock is caused by an obstruction that directly compromises inflow or outflow of blood from the heart. Cardiogenic shock is caused by diminished myocardial contractility which results in decreased CO with an increase in SVR. Lastly, distributive shock is caused by a major decrease in SVR with an increase in CO. Differentiating between the underlying abnormality and the associated compensatory response is also essential in terms of treatment and monitoring. Hypovolemic shock is considered to be essentially a profound deficit in preload. Preload is defined as the volume in the left ventricle at the end of diastole. Decreased preload results in subsequent decreases in SV, CO, and eventually, mean arterial pressure (MAP). As such, restoration of preload becomes an over-riding goal in the management of hypovolemic shock.

The prognosis of shock patients depends on several variables including severity, duration, underlying etiology, pre-existing organ dysfunction, and reversibility.4 Data are not readily available as to the incidence of hypovolemic shock, although hypo-volemia due to hemorrhage is a major factor in 40% to 50% of trauma deaths annually.5

FIGURE 13-1. Hemodynamic relationships among key cardiovascular parameters (A). Solid lines represent a direct relationship; the broken line represents an inverse relationship. In B, the alterations typically observed in hypovolemic shock are highlighted with arrows depicting the likely direction of the alteration. (From Ref. 1.)

FIGURE 13-1. Hemodynamic relationships among key cardiovascular parameters (A). Solid lines represent a direct relationship; the broken line represents an inverse relationship. In B, the alterations typically observed in hypovolemic shock are highlighted with arrows depicting the likely direction of the alteration. (From Ref. 1.)

Table 13-1 Major Shock Classifications and Etiologies

I. Hypovolemic

Hemorrhagic Trauma Gl

Abdominal aortic aneurysm Nonhemorrhagic (dehydration)

Vomiting

Diarrhea

Third spacing

II. Cardiogenic

Myocardial infarction

Septal wall rupture

Acute mitral valve regurgitation

Myocarditis

Arrhythmias

III. Obstructive

Pericardial tamponade Pulmonary embolism Amniotic fluid embolism

Tumor embolism IV. Distributive

Sepsis

Anaphylactic Spinal cord injury From Refs. 2, 3.

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