Management of Right Ventricular Failure in the Critically Ill
April 1, 2022 16 minutes read
By Vibhu Sharma, MD, MS
Associate Professor of Medicine, University of Colorado, Denver
This review will outline the management of right ventricular failure in the critically ill. Specialized discussion of right ventricular assist devices (RVADs) is outside the scope of this review. Dilation of the right ventricle (RV) as a consequence of RV systolic failure relating to either pressure or volume overload necessarily infringes on function of the left ventricle (LV). This is a result of the ventricles occupying the same space and being cradled inside a relatively inelastic pericardium. A dilated RV will lead to underfilling of the LV and a reduction in cardiac output. A dilating, failing RV, therefore, begets a failing LV in the setting of an intact pericardium and septal shift, the oft-described “death spiral.” This effect is attenuated with experimental pericardiectomy.1 In a hypotensive patient with echocardiogram evidence of RV failure, therapeutic decision-making hinges on the etiology of the RV failure. The potential etiologies can conceptually be thought of as an imposition of afterload (e.g., acutely in pulmonary embolism [PE], chronically in pulmonary vascular disease), failure of the pump (e.g., RV ischemia/infarction), or imposition of preload (e.g., congenital heart disease such atrial septal defects/shunts or valvular insufficiency due to pulmonic or tricuspid valve pathologies).
Clinical Assessment
It is important to image the RV at the bedside in any patient with hypotension, primarily because diagnoses like sepsis, pulmonary embolism, and left ventricular valvular insufficiency may complicate previously undetected RV dysfunction and impose an additional load that may lead to failure of a previously compensated RV. Therapy based on clinical assessment alone may completely miss a dilated, failing RV as the proximate cause of shock. With a previously compensated RV, mean arterial pressure may be maintained with a narrow pulse pressure and prolonged capillary refill time; a rising lactate may be the only clue to occult cardiogenic shock. Jugular venous pressure (JVP) may be difficult to evaluate clinically in an individual with a short and thick neck. An example from clinical practice is a patient with sepsis accompanied by worsening renal and liver function with a rising serum lactate that is falsely interpreted to be related to a need for more fluid resuscitation. Fluid therapy in this setting may be counterproductive, leading to the previously described “death spiral.” On the opposite end of the spectrum is a patient with preexisting RV failure presenting with shock related to severe diarrhea and hypovolemia. In this setting, small fluid boluses may be warranted, and the inferior vena cava may go from collapsible to non-collapsible with relatively small volumes of fluid.
Ultrasound-assessed JVP and inferior vena cava (IVC) collapsibility may be used as surrogates of RV filling pressures in both of these scenarios. Point-of-care ultrasound (POCUS) is invaluable in following patients with complex physiology, with multiple assessments over time enabling measurements that may indicate improvement with or worsening despite treatment. An ultrasonographically assessed normal or low JVP strongly argues against RV failure as the proximate cause of shock. The following parameters define RV failure echocardiographically: a dilated RV (RV/LV end diastolic area ratio > 0.6), reduced systolic function (tricuspid annular plane systolic excursion, or TAPSE) < 17 mm, tissue Doppler imaging-assessed tricuspid annular systolic velocity < 10 cm/s, and an RV systolic pressure > 50 mmHg. A caveat here is that an RV that has dilated to the point of equalization of RV and right atrial pressures may be associated with falsely low echo-estimated RV systolic pressures (RVSPs) due to a wide-open tricuspid valve. These quantitative measures of RV failure are qualitatively associated with septal flattening that progresses with volume and pressure overload of the RV. Absence of septal flattening and a hypertrophied RV suggest compensated chronic RV pressure overload. An RV that has failed in the setting of severe and advanced pulmonary hypertension can appear identical to an RV that has failed as a result of acute PE.2 The 60/60 sign and the McConnell sign can be helpful in distinguishing these two entities. A pulmonary artery acceleration time of ≤ 60 ms when accompanied by a pressure gradient across the tricuspid valve of ≤ 60 mmHg supports a diagnosis of acute PE rather than a failed RV in the setting of severe pulmonary hypertension (PH) with a high positive likelihood ratio. A similar high positive likelihood ratio was noted for McConnell’s sign, defined by RV free wall hypokinesis with apical sparing. Neither sign has adequate negative predictive value.3 A normal RV does not exclude acute PE, although in one study all PE patients with hemodynamic instability had an enlarged hypokinetic RV.4
Treatment
Efforts to optimize afterload may include delivery of inhaled vasodilators and treatment of a hemodynamically significant PE with thrombolytics or catheter-based therapies, for example. Correction of acidosis and hypoxia to allow for optimal vasodilation and optimizing positive end-expiratory pressure (PEEP) and plateau pressures allows for optimal West lung zone perfusion. Decompensated pulmonary hypertension without pulmonary pathology typically is treated in consultation with a pulmonary hypertension service. Efforts to optimize preload may include diuresis or continuous renal replacement therapy in patients with borderline hemodynamics, volume overload, and acute kidney injury related to cardiorenal syndrome. On occasion, optimization of preload may require intravenous fluid therapy; this ought to be done cautiously and with careful deliberation of end points, which often are monitored with a Swan-Ganz catheter. A right heart catheterization in a steady state as an outpatient may provide a central venous pressure (CVP) target for diuresis.
Special Scenarios
RV Infarction and Ischemia
RV myocardial infarction (RVMI) is suspected in an at-risk patient with chest pain and clinical signs of RV failure but no pulmonary edema. The proximal right coronary artery is always the culprit lesion.5 Imaging typically demonstrates severe RV free wall dysfunction and severe RV dilation at end diastole. Clinical signs (e.g., increased JVP without pulmonary edema) are magnified in the presence of preexisting high pulmonary vascular resistance (PVR). Management hinges on coronary reperfusion with catheter-based therapies or thrombolysis. Volume expansion in the setting of RVMI is controversial, but an initial bolus of crystalloid (500 mL of normal saline)6 may be appropriate if estimated CVP is < 15 mmHg5; it typically is recommended that a CVP of 20 mmHg not be exceeded.7 Invasive hemodynamic monitoring is essential if further volume challenges are being considered, with consideration for inotropic support with dobutamine and RVAD initiation in quick succession in the setting of refractory shock.7 Pulmonary vasodilators typically are not indicated unless PVR is known to be elevated.
Peri-Intubation Management
Patients with a failed RV are at high risk for peri-intubation cardiac arrest; it is, therefore, important to avoid rapid sequence intubation, if at all possible. Awake intubation with the patient sitting up and breathing spontaneously may be the safest technique; topical lidocaine and small doses of opiates/benzodiazepines if needed can be given with bronchoscopic delivery of the endotracheal tube.
Optimization of volume status and pulmonary vasodilation with nebulized therapies (e.g., inhaled nitric oxide [iNO]) prior to intubation should be considered. Set-up of the iNO delivery system may take up to 30 minutes; it is important to plan in advance for intubation timed for maximal pulmonary vasodilation. Heated high flow nasal cannula (HHFNC) oxygen to maximize PaO2 is ideal, and iNO can be delivered via an HHFNC device.8 Noninvasive administration of iNO has been associated with hemodynamic improvements in acute RV failure.9
Vasopressors and inotropes should be available, with infusion lines primed and central access available, if possible, prior to elective intubation. In the scenario of borderline hemodynamics, it is prudent to begin a low-dose norepinephrine and vasopressin infusion to prevent hypotension with instrumentation for intubation. Epinephrine and atropine should be available in the scenario of hypotension relating to removal of sympathetic tone with medications and increased vagal tone with intubation. Etomidate is the hypnotic of choice, given its hemodynamically neutral characteristics. Ketamine typically is avoided in settings of RV failure because of pulmonary arterial hypertension relating to physiologic effects of augmentation of PVR.10 It is critical to identify patients who may not tolerate any positive pressure ventilation or attempts at intubation. For these patients, awake cannulation for venoarterial extracorporeal membrane oxygenation (VA ECMO) may be the safest intervention. Mechanical ventilation is discussed in more detail later.
Acute Pulmonary Embolism/Cardiac Arrest
Acute PE may complicate preexisting PH, but PE also may be the sole cause of acute cor pulmonale. Shock in a patient presenting with acute PE is an indication for thrombolytic therapy; however, borderline hemodynamics and near-arrest situations are common. Volume expansion with crystalloids in these settings is controversial. Experimental studies in dogs have demonstrated that LV compliance and contractility are maintained in acute PE, but LV preload is reduced because of septal shift and pericardial constraint.11 Experimental volume loading in this dog model of acute PE demonstrated marked adverse changes in LV area and function, especially in animals subjected to repeated experimental embolism. This was accompanied by significant reductions in LV systolic pressure.12 Another study compared vasopressors to volume expansion in an experimental animal model of acute PE with the finding that volume expansion led to RV dysfunction while vasopressor therapy led to an improvement in both RV and LV hemodynamics.13
Multiple studies suggest a benefit to diuresis rather than volume loading of normotensive patients with acute PE.14,15 Investigators for the DiPER trial recently reported outcomes of a single 80-mg dose of furosemide compared to placebo in intermediate-risk PE.16 Furosemide was associated with a greater probability of normalization of respiratory and hemodynamic status at 24 hours compared with placebo. Fluid therapy in acute PE, therefore, may be harmful, and careful baseline and serial assessments of ultrasound parameters (i.e., JVP, RV end diastolic volume, RV ejection fraction) are necessary prior to fluid therapy. Small boluses of 500 mL of crystalloids may be appropriate therapy if relative hypovolemia is suspected based on history and consistent with JVP or IVC collapsibility. Patients with intermediate-risk PE require the clinician to be at the bedside to direct diagnostics and therapeutic interventions.
iNO reduces pulmonary artery pressure (PAP) and PVR in animal models of massive PE; it has been used to stabilize hemodynamics and is safe to use in this setting.17-19 Intravenous pulmonary vasodilators typically are not used in acute PE.20 When vasopressors are needed, norepinephrine is the vasopressor of choice, with low-dose vasopressin added as indicated.21 Inhaled nitric oxide and inhaled epoprostenol have been used as a bridge to definitive therapy in acute PE. Other nebulized therapies (as described in the section on decompensated pulmonary arterial hypertension [PAH]) may be used synergistically as a bridge to definitive therapy in scenarios where first-line therapies (e.g., thrombolysis or catheter-based therapies) have failed.
Discovery of a dilated RV during cardiac arrest does not imply that acute PE is the proximate cause of the arrest. RV dilation has been demonstrated in cardiac arrests related to ischemia, hemorrhagic shock, and hyperkalemia.22 However, a high suspicion for acute PE must be maintained in a patient with cardiac arrest. An estimated 5% to 9% of in-hospital cardiac arrests are related to acute PE, and one-third have no risk factors.23 A persistently dilated RV with return of spontaneous circulation (ROSC), repeated ROSC with sinus tachycardia, persistently low end-tidal CO2 despite good-quality cardiopulmonary resuscitation (CPR), detection of deep vein thrombosis during CPR, or detection of a clot in transit on echocardiographic assessment during CPR may prompt administration of tissue plasminogen activator (tPA), although none of these findings are specific for acute PE. If PE is suspected, it is recommended that tPA be given early and CPR continue for 60-90 minutes after administration, since late ROSC has been described.24 Depending on institutional availability and appropriateness, VA ECMO or surgical thrombectomy may be considered if PE is discovered during CPR. Outcomes of CPR in the setting of PH are uniformly poor unless a reversible cause can be identified and quickly corrected. In one multicenter study, resuscitation efforts were unsuccessful in 80% of patients.25
Mechanical Ventilation
RV failure may be the result of severe acute respiratory distress syndrome (ARDS) or may be previously unrecognized in a patient who presents with ARDS. Invasive mechanical ventilation is associated with a high rate of mortality in patients with PH.26 Acute cor pulmonale, as defined as a dilated RV and septal dyskinesia, occurs in up to one-quarter of patients with ARDS.27 Severe cor pulmonale was associated with increased mortality, but mild to moderate RV dilation and cor pulmonale was not.27 Prone positioning unloads the RV, and while an arterial partial pressure of oxygen to fractional inspired oxygenation (P/F) ratio of < 150 typically is defined as an indication to prone in the setting of ARDS, evidence of RV dysfunction may prompt earlier proning.28 Hypercapnia resulting from low tidal volume (Vt) ventilation results in an adverse effect on RV hemodynamics. This holds even if plateau pressures remain unchanged and oxygenation improves with addition of PEEP.29 Further, application of extrinsic PEEP may reduce RV stroke index and contribute to hypotension.30 Based on one study, PEEP targeting optimal lung compliance may have a smaller impact on RV hemodynamics compared to a PEEP that targets the lower inflection point of the pressure volume curve.30 Inhaled nitric oxide may have some role in the treatment of acute RV failure in the setting of respiratory failure, with 85% of favorable responses (i.e., reduction in PASP and PVR) occurring with doses of < 40 ppm.31 In the absence of ARDS, the mode of mechanical ventilation does not affect relevant outcomes whether the patient has LV, RV, or biventricular failure. It is recommended that synchronized intermittent mandatory ventilation (SIMV) be avoided because of the potential for swings in intrathoracic pressure adversely affecting RV hemodynamics.32 Lower Vt (less than 9 mL/kg predicted body weight) is associated with improved survival across all etiologies of heart failure and, therefore, low Vt ventilation should be targeted even in the absence of ARDS.33
Decompensated Pulmonary Arterial Hypertension
In this scenario, the first step is identification and reversal of exacerbating factors. Patients with compensated PAH may deteriorate because of sepsis, fever, hypoxia, RV infarction, acute PE, and hemorrhagic or hypovolemic shock. Among various reversible factors, sepsis imposes the highest odds of mortality in the critically ill patient with pulmonary hypertension.34 Abrupt discontinuation of pulmonary vasodilator therapy because of catheter malfunction or dislodgement may lead to cardiogenic shock, and restarting these therapies immediately via peripheral access is indicated.35 New-onset atrial fibrillation or other supraventricular tachycardias worsen RV function and are associated with increased mortality.36 Attempts to maintain sinus rhythm are indicated since rapid ventricular rates are poorly tolerated. An amiodarone drip and immediate cardioversion, if needed, for new-onset atrial fibrillation should be considered. Intravenous adenosine to interrupt an atrioventricular nodal reentry tachycardia (AVNRT) would be indicated because of rapid onset and offset of action. Calcium channel blockers and beta-blockers typically are avoided in the setting of decompensated PH and RV failure.37,38 Consultation with an electrophysiology service to assess suitability for ablation of AVNRTs and atrial flutter is prudent in an attempt to avoid recurrence. A temporary transvenous pacemaker is indicated in the setting of a high-grade atrioventricular (AV) block.
Patients with known PAH admitted to the intensive care unit (ICU) with mixed or vasodilatory shock may require a reduction in dosing of preexisting intravenous pulmonary vasodilator therapies. Dose adjustments typically are guided by placement of a Swan-Ganz catheter in an attempt to carefully modulate systemic vascular resistance (SVR) while simultaneously optimizing PVR. In this setting, the goal is to maintain SVR > PVR and maintain perfusion to the coronary arteries. In the setting of shock due to RV failure, the goal remains to augment RV function and maintain coronary perfusion with vasopressors and inotropes as indicated. Vasopressin typically is more selective for systemic circulation at doses of 0.01 U/min to 0.03 U/min, with higher doses affecting PVR adversely. Low doses of norepinephrine improve RV and pulmonary artery (PA) coupling; however, higher doses may adversely increase mean PAP (mPAP) and PVR.
Inhaled epoprostenol (50 mcg/min) is less costly than iNO and has similar hemodynamic effects.39 Inhaled pulmonary vasodilators may be used to synergistically reduce PVR with iNO as well. One report described the use of continuous nebulized milrinone (4 mg/hour delivered via a MiniHEART nebulizer) in a patient with PAH failing intravenous treprostinil and iNO and subsequently via a ventilator circuit.40 In the absence of availability of either iNO or nebulized prostacyclins, small reports describe the use of nebulized nitroglycerin being effective in reducing PVR. Nitroglycerin is dosed at 50 mcg/kg (~5 mg in adult patients) nebulized over 15 minutes.41 Note that data for the use of nebulized milrinone and nitroglycerin are sparse and on the level of case reports in the cardiac population only.
PH related to valvular disease requires specialized care in the postoperative period. In this setting, iNO reduces RV afterload and stroke work.42 Others have described the use of 2 mg to 3 mg of milrinone nebulized over 10 minutes to augment reductions in PVR obtained with nebulized prostacyclins in patients after cardiac surgery.43 Nebulized therapies typically are used as a bridge to more definitive therapies (i.e., ECMO), if needed. AV sequential pacing is critical to maintaining RV function in cardiac surgery patients.44
In summary, three options for alternatives/additions to iNO for decompensated PAH exist: milrinone, nitroglycerin, or prostacyclins (mnemonic: MNoP). Nebulized nitroglycerin typically is indicated if either iNO or inhaled prostacyclins are unavailable or will take extended periods of time to set up.
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