François Jardin
Ventricular interdependence:
how does it impact on hemodynamic evaluation in clinical practice?
The left (LV) and right ventricles (RV) are enclosed in a stiff envelope, the pericardium. They have similar end- diastolic volumes, and there is no free space for acute ventricular dilatation within a normal pericardial space.
Thus, when RV end-diastolic volume increases owing to increased RV loading, it can only occur at the expense of the space devoted to the left ventricle, which is prevent- ed from dilating to as large an end-diastolic volume as it would otherwise given its distending pressure. From a practical point of view this reduced LV end-diastolic vol- ume is accompanied by decreases in LV diastolic com- pliance, such that for the same LV distending pressure LV end-diastolic volume is less. This point was de- scribed in a previous Physiological Note [1]. LV im- paired relaxation by RV enlargement is evidenced by Doppler examination of mitral flow velocity (Fig. 1).
Such competition for end-diastolic volume between the right and left ventricles is enhanced when mediasti- nal pressure (i.e., pleural, pericardial, or both) or lung volume are increased. Moreover, relative ventricular compliance, that is, the relation between LV end-diastol- ic pressure and LV end-diastolic volume, is markedly af- fected by pericardial pressure. If pericardial pressure were to increase but not accounted for in the calculation of LV distending pressure, LV diastolic compliance would appear to be decreased. Often esophageal pressure is used to estimate intrathoracic pressure and, by exten- sion, pericardial pressure. Importantly, many processes
can alter pericardial pressure independent of esophageal pressure, such as hyperinflation, pericardial effusions and acute RV dilation
Another aspect of ventricular interdependence relates to the fact that both ventricles are arranged in series.
Since LV filling requires RV output, adequate left ventricular filling can be only supplied by adequate RV output. In turn, adequate RV output requires adequate venous return, and nonobstructed pulmonary circulation.
The “age of oil lamps”: ventricular interdependence renders inaccurate the classical hemodynamic evalua- tion by a pulmonary artery catheter. For a long time, fluid management in critically ill patients requiring me- chanical ventilation was guided by measurement of both RV and LV filling pressures. Moreover, evidence of de-
Fig. 1 Illustration of left ventricular (LV) relaxation impairment by right ventricular (RV) dilatation, in a mechanically ventilated patient with acute respiratory distress syndrome. During the first day of mechanical ventilation (left) a normal right ventricular size, observed in the two-dimensional view, was associated with a nor- mal pattern of Doppler mitral flow velocity, with a preeminent peak velocity of the E wave (early filling) and a less marked peak velocity of the A wave (atrial systole). After 48 h of respiratory support (right) right ventricular dilatation, observed on the two-di- mensional view, was associated with a modified pattern of Dopp- ler mitral flow velocity, with equalization of peak velocities
pressed systolic ventricular function was based upon ob- servational changes in filling pressure related to changes in cardiac output during a fluid challenge. Pulmonary arterial catheterization is commonly used to assess these parameters. Direct measures of right atrial (or central venous, CV) pressure (P) and pulmonary artery occlu- sion pressure (Ppao) can be made from a pulmonary ar- terial catheter. And using a distal tip thermistor, pulmo- nary blood flow as a surrogate of cardiac output can be measured. Clinically CVP is used to reflect RV filling pressure and Ppao LV filling pressure. This allows the construction of RV and LV “Frank-Starling curves”
when filling pressures are plotted against stroke volume or cardiac output. It is theoretically possible to discrimi- nate between an insufficient preload (requiring volume expansion) and a contractile defect (requiring inotropic support) in the hemodynamically unstable patient using this analysis.
A major drawback of the above method results from the lack of measurement of ventricular volume. Since RV and LV diastolic compliance can and do vary rapidly in unstable patients, filling pressures or their changes in response to therapy may poorly reflect preload. Regretta- bly, at the present time it is not possible to measure diastolic compliance at the bedside. As a result a high filling pressure may coexist with a reduced preload if ventricular compliance is low, and a low filling pressure may coexist with a normal preload if ventricular compli- ance is high [2]. This drawback characterizes particularly patients with acute respiratory distress syndrome, in whom a progressive increase in PEEP produces a pro- gressive increase in measured LV end-diastolic pressure, associated with a progressive decrease in LV end-diastol- ic size [3].
The “age of electricity”: ventricular interdependence does not affect the accuracy of hemodynamic evaluation by bedside echocardiography. Whereas knowledge of ventricular diastolic compliance is fundamental in inter- preting ventricular intracavitary pressure, it is less im- portant with the use of echocardiography, which permits direct visualization of venous distention, biventricular maximal chamber size, and a rough approximation of systolic function.
In clinical practice, the adequacy of venous return un- der respiratory support can be evaluated by inspection of respiratory changes in the superior vena caval diameter (Fig. 2). In particular, a high collapsibility index (i.e., major expiratory diameter minus minor inspiratory diam- eter divided by major expiratory diameter) of the superi- or vena cava identified potential differences between measured CVP and actual RV filling pressure, because the external pressure for the vessel, which is pleural pressure, causes vascular collapse. Such a condition in a hemodynamically unstable person denotes a need for volume expansion [4].
RV and LV end-diastolic dimensions can be obtained by bedside echocardiography. These measurements are particularly relevant in the clinical setting of acute cor pulmonale, where hemodynamic impairment resulting from ventricular interdependence has been documented (Fig. 3) [5]. Echocardiographic measurements of LV size has documented an inability of the left ventricular of septic patients to dilate [6].
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Fig. 2 Illustration of the gauge for central blood volume constitut- ed by vena caval collapsibility. Before volume expansion (left) the patient exhibited a marked reduction in superior vena caval diame- ter during tidal ventilation. After volume expansion (right) inspi- ratory reduction in vena caval diameter was minimized
Fig. 3 Two illustrations of ventricular interdependence, where acute right ventricular dilatation is associated with a reduced size of the left ventricular cavity. This interdependence was observed by a long-axis view, in a patient with massive pulmonary embo- lism (left, transthoracic examination) and in a patient with acute respiratory distress syndrome (right, transesophageal examination) 62
References
1. Pinsky MR (2003) Significance of pulmonary artery occlusion pressure. Intensive Care Med 29:19–22 2. Jardin F, Bourdarias JP (1995) Right
heart catheterization at bedside:
a critical view. Intensive Care Med 21:291–295
3. Jardin F, Farcot JC, Boisante L, Curien N, Margairaz A, Bourdarias JP (1981) Influence of positive end- expiratory pressure on left ventricular performance. N Engl J Med
1981:304:387–392
4. Vieillard-Baron A, Augarde R, Prin S, Page B, Beauchet A, Jardin F (2001) Influence of superior vena caval zone condition on cyclic changes in right ventricular outflow during respiratory support. Anesthesiology 95:1083–1088 5. Vieillard-Baron A, Prin S, Chergui K,
Dubourg O, Jardin F (2002) Echo-Doppler demonstration of acute cor pulmonale at the bedside in the medical intensive care unit. Am J Respir Crit Care Med 166:1310–1319
6. Vieillard-Baron A, Schmitt JM, Beauchet A, Augarde R, Prin S, Page B, Jardin F (2001) Early preload adaptation in septic shock? A transesophageal echocardiographic study. Anesthesiology 94:400–406
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