Pathophysiology and classification of shock states

Mechanisms underlying impaired cardiovascular performance

The development of shock is related to alterations in the components of the circulatory system that regulate cardiovascular performance. The first component is intravascular volume, which regulates mean circulatory pressures and venous return to the heart. Decreases in intravascular volume limit venous return to the heart and cardiac output. The heart is the second component. Cardiac output is determined by heart rate, contractility, and loading conditions. Abnormalities in rhythm and heart rate may limit cardiac output. Impaired cardiac contractility decreases effective ventricular ejection and compromises stroke volume. Abnormalities in valvular function may also limit cardiac output. The third component is the resistance circuit; it consists of the arteriolar bed, where the major decreases in vascular resistance occur. Arteriolar tone plays an important role in ventricular loading conditions, arterial pressure, and distribution of systemic blood flow. Excessive decreases in arteriolar tone lead to hypotension and limit effective organ perfusion, whereas excessive increases in arteriolar tone impede cardiac ejection by increasing ventricular afterload. Differences in arteriolar tone between organs can result in maldistribution of blood flow and mismatching of blood supply with tissue metabolic demands. The capillaries are the fourth component. They are the site of nutrient exchange and fluid flux between the intravascular and extravascular spaces. Increases in capillary permeability result in tissue edema and loss of intravascular volume. Decreases in capillary cross-sectional area, secondary to either obstruction or impairment in endothelial cell function, compromise nutrient blood flow. The opening of arteriovenous connections, which bypass the capillary network, may play a role in tissue hypoperfusion. The venules are the fifth component. They are the site of the lowest shear stress in the circulatory system and are thus the site most prone to occlusion from alterations in cell rheology. Venular resistance contributes 10%–15% of total vascular resistance. Increases in venular tone increase capillary hydrostatic pressures, thereby promoting the extravascular movement of fluid. The sixth component is the venous capacitance circuit. More than 80% of the total blood volume resides in large-capacitance vessels. Increases in venous tone decrease venous capacitance, redistributing blood volume centrally and thereby increasing venous return to the heart. Decreases in venous tone increase venous capacitance and decrease effective arterial blood volume and venous return. The seventh component is mainstream patency. Obstruction of the systemic or pulmonary circuit impedes ventricular ejection, and venous obstruction limits venous return to the ventricles.

Hemodynamic assessment

Circulatory performance can be assessed from hemodynamic parameters. A low heart rate may limit cardiac output, whereas an increased heart rate can compromise stroke volumes by limiting ventricular filling times. Bradyarrhythmias indicate structural abnormalities, effects of drugs, hypoxia, or other metabolic stimuli. Severe bradyarrhythmias can also represent reflex-mediated responses, as occurs in cases of severe hemorrhagic shock and acute inferior wall myocardial infarction. Tachyarrhythmias may be the result of underlying cardiac disease or pharmacologic or environmental stimuli. Alternatively, increases in the heart rate may reflect compensatory responses to maintain cardiac output.

In patients with circulatory shock, blood pressure should be monitored using intravascular measurements. Vasoconstriction related to compensatory mechanisms to maintain arterial pressure and the use of pharmacologic agents limits the accuracy of noninvasive measurements. This is particularly true in hypodynamic forms of circulatory failure.

For most vital organs, autoregulatory and neuronal mechanisms maintain blood flow independent of blood pressure at a mean arterial pressure of 60–130 mm Hg. At either higher or lower levels of pressure, blood flow becomes linearly dependent on blood pressure. Diseases such as hypertension can shift this relationship and increase the critical level of arterial pressure required for organ perfusion. Similarly, impaired autoregulatory mechanisms present in a variety of pathologic states expand the range of pressure-dependent blood flow.

The level of arterial pressure is not a reliable indicator of circulatory performance and tissue perfusion. ^, In states of hypodynamic circulatory shock such as traumatic injury, cardiac failure, and obstructive shock, hypotension is a late marker of critical hypoperfusion. As cardiac output falls, blood pressure is initially maintained by increases in peripheral vascular resistance largely mediated by the sympathoadrenal system. It is only after these mechanisms have been exhausted that hypotension develops. Accordingly, tissue hypoperfusion may be present despite normal levels of blood pressure as blood flow is redirected toward more vital organs. Conversely, hypotension may exist without evidence of organ hypoperfusion. In some vasodilated states, increases in cardiac output maintain vital organ blood flow despite decreased levels of arterial pressure.

Filling pressures have traditionally been used as measures of ventricular preload and to guide fluid resuscitation. However these measurements correlate poorly with blood volume, end-diastolic volumes, and fluid responsiveness. Echocardiographic techniques can provide an alternative assessment of chamber size and end-diastolic volumes, whereas fluid responsiveness is best assessed with dynamic measurements that reflect the response of stroke volume to changes in loading conditions. Examples include respiratory variations in pulse pressure, velocity time integral, and stroke volume on mechanical ventilation. Alternatively, changes in stroke volume may be assessed during passive leg raising or after volume challenge.

Cardiac output can be measured by multiple techniques. ^, Pulmonary artery thermodilution has been supplanted by less-invasive techniques, including lithium dilution, bioreactance, echocardiography, esophageal Doppler, and arterial pulse contour analysis. Echocardiographic measurements and esophageal Doppler can be used to assess ventricular ejection and provide diagnostic information regarding the presence of pericardial tamponade and valvular function. The response of stroke volume to changes in ventricular loading during fluid infusion is also useful to assess cardiac function. A good response indicates preserved cardiac function, whereas lack of response may be related to either cardiac dysfunction or inadequate fluid volumes. However, the adequacy of cardiac output in meeting tissue metabolic demands must be assessed independently by monitoring indices of tissue perfusion and oxygen metabolism. A low cardiac output may be adequate when metabolic requirements are decreased—for example, in deep sedation or hypothermia. In contrast, an increased cardiac output may not be adequate when metabolic requirements are increased or maldistribution of blood flow exists, such as in septic shock.

Systemic vascular resistance is an indicator of arterial tone; it is calculated from cardiac output and arterial pressure. Increases in systemic vascular resistance are the result of vasoconstriction and represent compensatory mechanisms directed at maintaining blood pressure in the setting of a decreased cardiac output. Excessive increases in vascular resistance increase ventricular afterload and the impedance to ejection. Decreases in vascular resistance are the result of vasodilation, decreases in blood viscosity, or presence of arteriovenous connections. Vasodilation may be pathologic, as occurs in septic shock and liver disease, or it may be adaptive, as occurs in hyperdynamic stress after major surgery and traumatic injury. Venous tone is much harder to assess clinically. In most cases, changes in venous tone parallel changes in arterial tone. Modest increases in central venous pressures in the setting of large-volume infusion and the absence of intravascular volume loss suggest decreased venous tone.