Right ventricular performance

The right ventricle receives systemic and coronary venous return and pumps it into the left ventricle across the pulmonary vascular bed. The right and left ventricles can be described as two pumps in series coupled by the lungs and operating as one functional unit. Both parts of this unit have a common blood supply, a common muscular septum separating both cavities, and common intertwining myocardial bundles. Moreover, both ventricles are confined within the common pericardium and exposed to the same changes in intrathoracic pressure and lung volume. There are, however, important differences between both ventricles. Anatomically, the right ventricle consists of the free wall and septum arranged into the inflow tract (sinus) and the outflow tract (conus); the conus represents the phylogenic relic of the bulbus cordis.98 The right ventricular outflow tract contracts after the inflow tract with a delay of up to 25-50 ms; this asynchrony causes the outflow tract to expand during the contraction of the inflow tract and to maintain right ventricular ejection by the time the inflow tract is beginning to relax. Under intense sympathetic stimulation, significant pressure gradients between inflow and outflow tracts can occur.99-101

Wall thickness and myocardial mass of the right ventricle are considerably less than those of the left ventricle, reflecting the lower external work of the former. Although the right ventricle pumps the same amount of blood (cardiac output) as the left ventricle, it does so into the low pressure pulmonary vascular bed with low resistance to flow. Pulmonary arteries are much more distensible than systemic arteries, and the pulse wave velocity in the pulmonary arteries is lower than in the systemic arterial tree. This causes the reflected pressure waves to return after the closure of the pulmonic valve. The pulmonary input impedance, representing the external load of the right ventricle, differs from the aortic impedance in that the oscillatory component (characteristic impedance) is relatively greater and makes up to 25-30% of the total pulmonary resistance.102 The right ventricular ejection into the low impedance pulmonary vascular bed, together with the delayed return of the reflected waves, affect the right ventricular pressure waveform. There is a very short isovolumic contraction period, lower right ventricular dP/dt, and systolic peak pressure occurs early during the ejection. Furthermore, the ejection continues despite the rapid and marked decline in pressure.103

As a result of the low intraventricular and, consequently, low intramural pressure, the coronary blood flow in the right ventricle is continuous throughout the cardiac cycle. In spite of these differences, the mechanical behaviour of the right ventricle closely resembles that of its left companion. An increase in right ventricular filling (reflected by increases in end diastolic volume and pressure, and related to an increase in resting fibre length) leads to an augmentation of right ventricular stroke volume and stroke work according to the Frank-Starling law. Similar to the left ventricle, there is an inverse relationship between the impedance opposing ejection and the right ventricular function expressed as either ejection fraction or stroke volume.

An augmentation of right ventricular preload and positive inotropic stimulation will improve right ventricular performance.99 101 The right ventricle is more sensitive to increases in afterload than the left one. With increasing resistance to ejection (for example, in pulmonary hypertension), the right ventricle readily uses up its preload reserve and dilates. As a result of the high chamber compliance of the thin walled right ventricle, the increase in end diastolic volume can be more pronounced than the increase in filling pressure. Thus, the right ventricle is able to maintain normal pulmonary blood flow and left ventricular filling without an undue increase in central venous pressure. The right ventricular ejection fraction will, however, exhibit a linear decrease with increasing afterload.99 101 A prerequisite to the maintenance of flow is an adequate preload reserve. Yet, there is a limitation to right ventricular performance, as a normal, non-hypertrophied right ventricle will not sustain an acute increase in peak systolic pressure of more than 7080 mm Hg without failing.101

Similar to the left ventricle and the systemic circulation, the coupling of the right ventricle and the pulmonary vasculature was studied by means of the time varying elastance model, which revealed an optimal matching between the right ventricle and its load under physiological conditions.102 The right ventricular P/V loop reflects its ejection characteristics. Isovolumic contraction is almost absent, and there is a continuous decrease in ventricular volume after the end systolic point. The slope of the end systolic P/V relationship (right ventricular Emax) is lower and the volume intercept (Vo) is higher in the right than in the left ventricle.103

The right ventricle appears to have better tolerance of acute decreases in pulmonary compliance (for example, occlusion of a central pulmonary artery branch) than of increases in resistance (for example, peripheral pulmonary embolisation or lung hyperinflation).104 105

Considering the close anatomical relationship between both ventricles, it is not surprising that changes in geometry, pressure, and volume of one ventricle directly affect the function of the other. This is known as ventricular cross talk or interdependence, and occurs in both diastole and systole.106 107 An increase in filling volume of one ventricle causes an upward shift of the diastolic P/V relationship, a decrease in diastolic chamber compliance, and impaired filling of the other ventricle. For instance, an increase in right ventricular diastolic volume and pressure leads to an inversion of the diastolic trans-septal pressure gradient, flattening of the ventricular septum curvature, and a leftward shift of the septum during diastole; these effects increase the stiffness of the left ventricle and limit its filling. In patients with an overloaded and failing right ventricle, right ventricular filling pressure (right atrial pressure) exceeds left sided filling pressure (left atrial pressure or wedge pressure). Diastolic ventricular interdependence is more pronounced with the pericardium intact.108 109

The term "systolic interdependence'' describes the observation that an increase in pressure in one ventricle leads to an immediate pressure increase in the other ventricle. The contribution of the left ventricle to pressure generation in the right ventricle exceeds the contribution of the right to the left ventricle and is estimated to be about one third of the right ventricular systolic pressure.110 Although ventricular interdependence operates primarily through the interventricular septum, the free walls of both ventricles are also involved: in the case of the right ventricle, this is accomplished by pulling the right ventricular free wall against the septum during contraction of the intertwining muscle bundles shared by both ventricles.108 111 This mechanism of "left ventricular assistance", combined with the force acting from behind ("vis a tergo") imparted by left ventricular contraction, explains why there is only a modest depression of haemodynamic function after total exclusion of the right ventricular free wall, provided that there is low pulmonary vascular resistance.112

The diastolic and systolic interdependence plays an important role in clinical conditions such as right ventricular volume or pressure overload and right ventricular ischaemia. In these conditions, both diastolic filling and systolic performance of the left ventricle are compromised and left ventricular support of the right ventricle reduced. Therapy aimed at improved left ventricular function and developed pressure will result in enhanced right ventricular function. That will result partly from the interdependence mechanism, and partly from the increase in right ventricular coronary perfusion pressure.

The right ventricle plays an important role in the perioperative period and critical care medicine where acute changes in loading conditions, gas exchange, ventilatory patterns, and coronary blood flow can often eventually lead to right ventricular failure. To assess the right ventricular function properly, to detect its dysfunction in time, and to treat it correctly, the measurement of pressures and flows in the right heart and lesser circulation is necessary (Table 2.2).18 113

The use of fast thermistor pulmonary catheters and the thermodilution method for assessment of right ventricular ejection fraction and volumes can provide additional useful information. The most valuable information on the structure and function of the right ventricle at the bedside is now obtained by transthoracic and transoesophageal echocardiography. With the help of echocardiography, and the end diastolic and end systolic size of the right ventricle, its ejection fraction, regional wall motion, septum shifts, and presence of tricuspid and pulmonic valve regurgitation can be evaluated. By means of Doppler measurements of forward and regurgitant

Table 2.2 Right ventricular pump function18113

Normal values

Right atrial pressure

5 mm Hg

Right ventricular pressure (systolic/diastolic)

25/5 mm Hg

Pulmonary artery pressure (systolic/diastolic)

25/9 mm Hg

Pulmonary artery pressure (mean)

15 (10-20) mm Hg

Right ventricular end diastolic volume index

65-100 ml/m2

Right ventricular ejection fraction

48-66%

Right ventricular stroke work index

5-10 gm/m2

blood flow velocities across the tricuspid and pulmonic valve, estimates of right ventricular and pulmonary artery pressures can be made.

Your heart pumps blood throughout your body using a network of tubing called arteries and capillaries which return the blood back to your heart via your veins. Blood pressure is the force of the blood pushing against the walls of your arteries as your heart beats.Learn more...