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.