The distribution of blood volume in the two vascular systems is altered by any change in contractility that affects the two ventricles differently. When a coronary artery to the left ventricle becomes blocked, it impairs left ventricular contractility and leads to acute left ventricular failure. Initially, the left atrial pressure remains unchanged, but the left ventricle starts pumping blood at a diminished rate. If the right ventricle is not affected by the occlusion, it continues to pump blood normally. This results in a progressive increase in left atrial pressure and a progressive decrease in right atrial pressure. Eventually, the output of the two ventricles becomes equal again, but at an abnormal level. The elevation in left atrial pressure is accompanied by an equal elevation in pulmonary venous pressure, which can have serious clinical consequences. The high pulmonary venous pressure can increase lung stiffness and cause respiratory distress by increasing the mechanical work of pulmonary ventilation. Additionally, it can lead to the transudation of fluid from the pulmonary capillaries to the pulmonary interstitium or alveoli, causing pulmonary edema which can be lethal.

Two important principles to remember about ventricular function are that the left ventricle pumps blood through the systemic vasculature, while the right ventricle pumps blood through the pulmonary vasculature. However, this doesn't necessarily mean that both ventricles are essential for adequate perfusion of the systemic and pulmonary vascular beds. To better understand the relationships between the ventricles and vascular beds, let's examine the function of the right ventricle in more detail.

In the circulatory system model shown in Fig. 19.12, let's consider the hemodynamic consequences if the right ventricle suddenly stops pumping and instead acts as a passive conduit between the systemic veins and pulmonary arteries. In this scenario, the left ventricle becomes the only functional pump, responsible for pumping blood through both the systemic and pulmonary resistances (assuming negligible resistance through the inactive right ventricle).

Normally, pulmonary vascular resistance is approximately 10% of systemic vascular resistance. Since these resistances are in series, the total resistance would be 10% higher than systemic resistance alone. In a normal cardiovascular system, a 10% increase in left ventricular afterload would not significantly affect its function. However, under certain conditions, this increase in afterload could have a significant impact on cardiovascular function. If the 10% increase in total resistance is achieved by adding a small degree of resistance (pulmonary vascular resistance) to the much larger systemic resistance, and if there is a large degree of compliance separating pulmonary vascular resistance from systemic resistance (combined systemic venous and pulmonary arterial compliance), the cardiovascular system's operation could be drastically impaired.

The effects of inactivating the pumping action of the right ventricle in a hydraulic analogue of the circulatory system are simulated in [figure].
Anychangeincontractilitythataffectsthetwoventriclesdifferentlyaltersthedistributionofbloodvolumeinthetwovascularsystems.Ifacoronaryarterytotheleftventriclebecomesoccluded,leftventricularcontractilityisimpaired,andacute left ventricular failure ensues.Intheinstantafterocclusion,leftatrialpressuredoesnotchange,andtheleftventriclebeginstopumpatadiminishedrateofflow.Iftherightventricleisnotaffectedbytheacutecoronaryarteryocclusion,therightventricleinitiallycontinuestopumpthenormalflow.Thedisparaterightandleftventricularoutputsresultinaprogressiveincreaseinleftatrialpressureandaprogressivedecreaseinrightatrialpressure.Therefore,leftventricularoutputincreasestowardthenormalvalue,andrightventricularoutputfallsbelowthenormalvalue.Thisprocesscontinuesuntiltheoutputsofthetwoventriclesagainbecomeequal.Atthisnewequilibrium,theoutputofthetwoventriclesissubnormal.Theelevationinleftatrialpressureisaccompaniedbyanequalelevationinpulmonaryvenouspressure,whichcanhaveseriousclinicalconsequences.Thehighpulmonaryvenouspressurecanincreaselungstiffnessandleadtorespiratorydistressbyincreasingthemechanicalworkofpulmonaryventilation(see ).Furthermore,thehighpulmonaryvenouspressurecausesanelevatethehydrostaticpressureinthepulmonarycapillariesandmayleadtothetransudationoffluidfromthepulmonarycapillariestothepulmonaryinterstitiumorintothealveoli(pulmonary edema), whichmaybelethal.
Two basic principles to remember about ventricular function are that (1) the left ventricle pumps blood through the systemic vasculature, and (2) the right ventricle pumps blood through the pulmonary vasculature. However, these principles do not necessarily imply that both ventricles are essential to perfuse the systemic and pulmonary vascular beds adequately. To better understand the relationships between the two ventricles and the two vascular beds, the right ventricular function is examined in more detail as follows.
In the circulatory system model shown in
Fig. 19.12, consider the hemodynamic consequences that would occur if the right ventricle suddenly ceased its pump function but instead served merely as a passive, low-resistance conduit between the systemic veins and the pulmonary arteries. Under these conditions, the only functional pump would be the left ventricle, which would then be required to pump blood through both the systemic and pulmonary resistances (for the purposes of this discussion, consider the resistance to the flow of blood through the inactive right ventricle to be negligible).
Normally, pulmonary vascular resistance is approximately 10% as great as systemic vascular resistance. Because the two resistances are in series with one another, total resistance would be 10% greater than systemic resistance alone (see ). In a normal cardiovascular system, a 10% (and hence left ventricular afterload) by approximately 10%. This increase would not drastically affect left ventricular function. Under certain conditions, however, this increase in Pa could significantly alter the function of the cardiovascular system. If the 10% increase in total resistance is achieved by adding a small degree of resistance (i.e., pulmonary vascular resistance) to that of the much larger systemic resistance, and if the pulmonary vascular resistance is separated from the systemic resistance by a large degree of compliance (the combined systemic venous and pulmonary arterial compliance), the 10% increase in total resistance could drastically impair operation of the cardiovascular system.
The simulated effects of inactivating the pumping action of the right ventricle in a hydraulic analogue of the circula tory system are shown in