Shock Syndromes II

In impaired diastolic filling, RV preload is significantly decreased because of the inhibition of

venous return.

In cardiac tamponade, an accumulation of fluid in the pericardium leads to an increase in

pericardial pressure.

ii.

This increases and equalizes diastolic pressures between the left and right heart (equalization of

central venous pressure [CVP], pulmonary artery diastolic pressure, and pulmonary capillary

wedge pressure [PCWP] and impaired ventricular filling). CVP and PCWP elevations should

not be mistaken as representing an increase in ventricular volume (preload).

In impaired systolic function, ventricular afterload is acutely increased, leading to ventricular

failure.

This typically occurs in an acute RV afterload (pulmonary vascular resistance) increase caused

by a massive PE or in acute PH.

ii.

An acute increase in LV afterload does not typically lead to shock.

iii.

An acute rise in RV afterload leads to reduced RV CO and a subsequent decrease in LV

CO. Subsequently, systemic hypotension develops, leading to reduced RV tissue perfusion

(decreased right coronary artery perfusion), RV free wall ischemia, reduced RV free wall

contractility, and further impairment of RV CO (a vicious cycle).

iv.

In addition, acute RV pressure overload leads to a shift of the intraventricular septum toward

the LV, impairing LV diastolic filling (because of intraventricular dependence) and further

decreasing in LV CO.

Fluid administration and vasoactive medications may be used as a temporizing measure to increase

tissue perfusion.

Intravenous fluids (typically crystalloids) are usually recommended, but they may not improve CO.

Cardiac tamponade: Patients with preexisting hypovolemia may respond to fluids, but in

general, hemodynamics may not improve with fluid administration. Despite this finding, fluid

administration is usually recommended in cardiac tamponade.

ii.

Massive PE: Initial fluid administration improves CO, but care should be taken because

excessive fluid administration can lead to further RV dilation and impaired LV CO from

worsened septal shifting and decreased LV filling (because of intraventricular dependence).

iii.

Acute or chronic PH: Optimization of fluids in patients with acute or chronic PH is challenging.

Some patients, such as those with signs of intravascular volume depletion, may require

fluids. Others may require diuretics to reduce RV dilation and improve LV filling, even with

vasoactive medication administration.

Vasopressors should be initiated to increase MAP and maintain an adequate perfusion pressure.

This is particularly important in a massive PE because adequate right coronary artery perfusion

is of greatest importance to prevent/reduce RV free wall ischemia.

ii.

Caution must be used because catecholamine vasopressors may increase pulmonary vascular

resistance, which may worsen RV dysfunction.

Inotropes may increase RV CO in a massive PE or acute or chronic PH but are likely ineffective in

tamponade.

chronic PH, but neither therapy is likely effective for massive PE or cardiac tamponade.

Impaired diastolic filling

Cardiac tamponade: Pericardiocentesis or surgical evacuation and potential drain placement

ii.

Tension pneumothorax: Needle decompression and potential chest tube thoracostomy