The Right Ventricle-You May Forget it, but It Will Not Forget You

Abstract

Right ventricular (RV) dysfunction and failure are common and often overlooked causes of perioperative deterioration and adverse outcomes. Due to its unique pathophysiologic underpinnings, RV failure often does not respond to typical therapeutic measures such as volume resuscitation and often worsens when therapy is escalated and mechanical ventilation is begun, with a danger of irreversible cardiovascular collapse and death. The single most important factor in improving outcomes in the context of RV failure is anticipating and recognizing it. Once established, a vicious circle of systemic hypotension, and RV ischemia and dilation is set in motion, rapidly spiraling down into a state of shock culminating in multi-organ failure and ultimately death. Therapy of RV failure must focus on rapidly reestablishing RV coronary perfusion, lowering pulmonary vascular resistance and optimizing volemia. In parallel, underlying reversible causes should be sought and if possible treated. In all stages of diagnostics and therapy, echocardiography plays a central role. In severe cases of RV dysfunction there remains a role for the use of the pulmonary artery catheter. When these mostly simple measures are undertaken in a timely fashion, the spiral of death of RV failure can often be broken or even prevented altogether.

Keywords: dysfunction; failure; management; perioperative; postoperative; prevention; right ventricle; right ventricular; shock.

Figure 1

The progression from right ventricular (RV) dysfunction to failure is a continuum marked by progressive RV dilation and increases in heart rate to maintain cardiac index. When the compensatory mechanisms are exhausted, ventriculo-arterial uncoupling occurs with a drop in cardiac index and pulmonary pressures as well as a rise in central venous pressure, late markers of RV failure and imminent cardiovascular demise. Abbreviations: CI, cardiac index; CVP, central venous pressure; PAP, pulmonary artery pressure; PVR, pulmonary vascular resistance; RV, right ventricular; RVV, right ventricular volume; SV, stroke volume. Modified from Haddad et al. [8] Vonk Noordegraaf et al. [11] and Wanner PM & Filipovic M. (Der rechte Ventrikel—das Wichtigste für den Intensivmediziner. In: Eckart, Forst, Briegel, eds.: Intensivmedizin. Kompendium und Repetitorium zur interdisziplinären Weiter- und Fortbildung. ecomed Verlagsgesellschaft AG & Co., Landsberg. 2018) [12].

Figure 2

Vicious circle of right ventricular failure. Abbreviations: CI, cardiac index; IVS, interventricular septum; LV, left ventricular; MAP, mean arterial pressure; mPAP, mean pulmonary artery pressure; P_it, intrathoracic pressure; PVR, pulmonary vascular resistance; RV, right ventricular; SVR, systemic vascular resistance. Modified from Wanner PM & Filipovic M. (Der rechte Ventrikel—das Wichtigste für den Intensivmediziner. In: Eckart, Forst, Briegel, eds.: Intensivmedizin. Kompendium und Repetitorium zur interdisziplinären Weiter- und Fortbildung. ecomed Verlagsgesellschaft AG & Co., Landsberg. 2018) [12].

Figure 3

Transthoracic echocardiogram (parasternal short axis view) showing massive D-shaping of the interventricular septum.

Figure 4

Transthoracic echocardiogram (apical 4-chamber view) showing massive right ventricular dilation (RV diameter > LV diameter).

Figure 5

Transthoracic echocardiogram (apical 4-chamber view) showing severe tricuspid regurgitation due to massive RV dilation.

Figure 6

Measurement of tricuspid annular plane systolic excursion (TAPSE) as a measure of RV systolic function. Values < 17 mm are considered pathological (here 10 mm).

Figure 7

Transesophageal echocardiogram (midesophageal 4-chamber view) showing severe dilation of the right-sided cardiac chambers, bowing of the interatrial septum into the LV due to elevated right atrial pressures and a hyperechogenic structure in the RA and RV, in this case a clot in transit.