RV contraction is functionally different from LV contraction [19]. LV contraction causing decreases in LV volume primarily results from combined cross-sectional area reductions due to circumferential fiber shortening and twisting or “wringing” owing to oblique fiber shortening with longitudinal axis shortening. RV contraction on the other hand primarily occurs by longitudinal shortening and occurs in a peristaltic fashion starting with inflow track contraction and proceeding to RV mid-wall then RV outflow track (infundibulum) contraction with a timing difference of approximately 25–50 ms [20]. Thus, measures of RV peak systolic strain by echocardiography reflect a sensitive measure of RV systolic performance [21].

Contractile function can be assessed in a variety of ways. One can measure stroke volume, stroke work, ejection fraction, and velocity of circumferential fiber shortening. However, the most accurate measure of systolic function is time-varying elastance and end-systolic elastance, as a measure of the progressively increasing stiffness that the heart undergoes during contraction [22]. LV end-systolic elastance (Ees) is the slope of the end-systolic pressure–volume relationship and is approximated by the maximal LV systolic pressure to volume ratio at end-ejection. It is highly correlated with contractility and though the actual end-systolic pressure and volume will be a function of both LV preload and afterload, the slope of the line is independent of these variables. Although RV Ees can also be measured if one knows end-systolic RV pressure and volume, it does not describe RV contractility as much as systolic ventricular interdependence [23] because more than half of RV developed pressure comes from LV free wall contraction [24]. This explains why insertion of a LV assist device in a patient with combined acute LV failure and mild pulmonary hypertension often induces acute RV failure [25]. When pulmonary vascular reserve is compromised, as in pulmonary hypertension and LV failure, RV ejection is also compromised, initially causing right atrial pressure to rise in response to increased venous return and eventually to remain elevated even at rest. RV ejection is also compromised, initally causing right atrial pressure to rise in response to the decreased RV stroke volume and increased RV end-diastolic volume, causing venous return to decrease. If sustained, right atrial pressure will remain elevated at rest. This combined impaired RV ejection and increased right atrial pressure is also associated with a markedly decreased maximal cardaic output in response, limiting exercise tolerance and causing fluid retention.

Acute increases in RV outflow resistance, as may occur with acute pulmonary embolism and hyperinflation, will cause acute RV dilation and, by ventricular interdependence, markedly decreased LV diastolic compliance, decreasing LV stroke volume, cardiac output, and arterial blood pressure and rapidly spiraling to acute cardiogenic shock and death. Coupled with these findings is the reality that RV ejection is exquisitely dependent on RV ejection pressure [26]. Presumably, this is also the cause of backward LV failure causing RV failure. As LV systolic function deteriorates, stroke volume decreases owing to an increase in LV end-systolic volume. Clearly this must increase LV end-diastolic volume and filling pressures. If pulmonary vascular resistance is unchanged, the increase in left atrial pressure will be reflected back to pulmonary artery pressure, increasing RV afterload. Thus, the combined decreased LV contraction coupled with the increased pulmonary arterial pressure may lead to the commonly seen biventricular failure. Since this process usually happens gradually, fluid retention concomitantly occurs, producing peripheral edema as right atrial pressure rises. If LV failure occurs rapidly, as may occur with an acute coronary syndrome, then the pooling of blood in the lungs associated with acute cardiogenic pulmonary edema will also be associated with a relative hypovolemia. It is unclear if mean systemic filling pressure, the equilibrium stop flow pressure in the circulation, will also decrease in this scenario of acute LV failure despite the shift of blood from the peripheral to the central compartment. Concomitant with the induction of acute heart failure, profound increases in sympathetic tone also occur, increasing arterial resistance and decreasing venous capacitance. Thus, patients presenting with an acute coronary syndrome often display systemic hypertension, tachycardia, and pulmonary edema with elevated left- and right-sided filling pressures. The common clinical mistake is to interpret these findings as general volume overload and treat the pulmonary edema with a diuretic as opposed to an afterload-reducing agent. The diuretic will worsen the circulatory shock whereas the afterload-reducing agent will not. Examples of afterload reduction include using continuous positive airway pressure to abolish the negative swings in ITP, narcotics as sympathetolitics, and pharmacologic vasodilators (e.g., nitroglycerine).

Furthermore, most of the RV coronary blood flow occurs during systole, unlike LV coronary blood flow, which primarily occurs in diastole [27]. Thus, systemic hypotension or relative hypotension where pulmonary artery pressures equal or exceed aortic pressure must cause RV ischemia. Treatments here include not only reversing the causes of pulmonary hypertension but efforts to sustain mean arterial pressure higher than pulmonary artery pressure to maximal RV coronary blood flow. Clinically, this is usually done by the infusion of potent vasoconstrictor agents (e.g., norepinephrine).

Clinically, these findings carry a common end result. For cardiac output to increase, RV volumes must increase. If increasing RV volumes also results in increased filling pressures, then RV over-distention may occur, causing RV free wall ischemia. It is not clear at what pressure RV volumes become limited but this probably occurs at relatively low transmural pressures of ~10–12 mmHg. As mentioned above, however, if pericardial pressure is also increased, then right atrial pressure may be quite high without RV dilation. If relative systemic hypotension co-exists, then selective increases in arterial pressure will improve RV systolic function. Accordingly, fluid resuscitation, if associated with rapid increases in right atrial pressure, should be stopped until evidence of acute cor pulmonale is excluded [28]. Acute cor pulmonale is treated by improving LV systolic function, maintaining coronary perfusion pressure, or reducing pulmonary artery outflow impedance. Since more than half of RV systolic force is generated by LV contraction, through the free wall interconnection of fibers and not through stiffening or thickening of the intraventricular septum [24], efforts to increase LV contractility independent of maintaining coronary perfusion pressure are important. Since RV coronary perfusion primarily occurs during systole, maintaining coronary perfusion pressure greater than pulmonary artery pressure by the use of systemic vasopressor therapy is also indicted [27]. Finally, since increased RV afterload is a major limitation to RV ejection, efforts to minimize pulmonary vascular resistance and increase pulmonary vascular compliance are also beneficial.