Ask The Expert: Acute Right Ventricular Failure in the ED


Author: Quentin Reuter, MD (EM Resident Physician, PGY-3, NUEM) // Edited by: Alison Marshall, MD (EM Resident Physician, PGY-4, NUEM) // Expert Review: James Walter, MD

Citation: [Peer-Reviewed, Web Publication] Reuter Q , Marshall A (2016, November 15). Ask The Expert: Acute Right Heart Failure In The ED [NUEM Blog. Expert Commentary By Walter J]. Retrieved from


Let’s be honest, patients with right ventricular (RV) failure terrify us as emergency medicine (EM) physicians, particularly when they are acutely decompensating. There are limited therapeutic options, they are brittle in their response to interventions, and they are usually on a spectrum of vasodilators that we have to reference on Up-To-Date

But, fear not (okay still fear a little); this post will introduce key concepts regarding the pathophysiology of RV failure and provide you with answers to high yield questions in management of these difficult patients. 


To make intelligent management decisions, you must first understand several key pathologic pathways in RV failure: 

  • RV response to increased PVR (i.e. RV afterload)
  • RV pressure/volume overload causing bowing of the interventricular septum
  • RV ischemia

RV response to increased PVR (i.e. RV afterload)

The RV is thin-walled, poorly contractile, and typically ejects blood against a vascular resistance only 1/5th that of the systemic circulation.  As a result, it does not handle increases in RV afterload well (such as PE or rapidly progressive pulmonary artery hypertension (PAH)).  In chronic pressure overload, the RV hypertrophies and dilates in response to increased mean pulmonary artery pressure (mPAP measured by RHC that is >25 defines pulmonary hypertension). However, even in patients with chronic disease, sudden increases in mPAP can lead to ↓RV ejection fraction, ↓RV stroke volume, and subsequent RV pressure- and volume-overload. Hypoxia (due to V/Q mismatch, loss of pulmonary vascular bed volume, decreased CO, PNA, altelectasis, or thrombus) leads to further increases in PVR through hypoxic vasoconstriction.

RV pressure/volume overload causing bowing of the interventricular septum

In response to increases in RV pressure and volume, the interventricular septum (IVS) bows into the left ventricle (LV).  This compresses the LV cavity and decreases LV filling leading to decreased cardiac output & subsequently decreased systemic blood pressure.  Bowing of the IVS is what causes the characteristic “D-sign” seen on a parasternal short-axis view in a patient with a failing RV and provides a nice visual representation of how compression of the LV cavity can impede filling.   


Figure 1 The D-sign: Parasternal short axis view demonstrating a significantly enlarged right ventricle with bowing of the interventricular septum into the LV resulting in a "D" shape appearance. 


RV Ischemia

RV ischemia is another major issue: there is a need for increased coronary perfusion to the strained right heart, but right coronary artery flow (which occurs during both systole and diastole) is especially compromised during systole by decreased systemic MAP and by increased RV pressure.  This is really important and the reason why avoiding hypotension is so critical in patients with right heart failure. 

The Pulmonary Arterial Hypertension Death Spiral

Putting these pathways together explains the potential for rapid clinical deterioration in acute right heart failure (aka the PAH “death spiral”). The flow chart below from a review in Chest provides a nice visual summary [4] 


Figure 2 The PAH Death Spiral


Understanding the pathological derangements in acute right sided heart failure will help lead you to choosing the appropriate management strategy. While most therapy in these patients will be dictated by a specialist consulted from the ED, the focus should be on diagnostic testing to determine the cause of a patient’s deterioration including the use of bedside ultrasound, laboratory evaluation, careful assessment and monitoring of markers of end-organ perfusion (mental status, skin tone, lactate, renal function, urine output), initial hemodynamic stabilization, consideration of mechanical ventilation if necessary, consultation with necessary specialists and expediting transfer to an ICU.  Below you will find a list of answers to questions that will assist with optimizing your initial management of these patients in the ED.

Right Ventricular Failure Q & A


1. What do we need to know about RV failure patients presenting on pulmonary arteriolar vasodilators?  

You should be familiar with the general categories of chronic therapy for patients with pulmonary hypertension if you see these patients often in your emergency department:

  • Prostacyclins
    • Names: Epoprostenol (Flolan), Treprostinil (Remodulin or Tyvaso), Ilosprost
    • Mechanism of action: binds to prostaglandin receptor and activates cGMP -> vasodilation
  • Endothelial receptor antagonists
    • Name: Bosentan (Tracleer), ambrisentan (Letairis), macitentan (Opsumit)
    • Mechanism of action: Attenuates the effects of elevated endothelin-1 which contributes to vasoconstriction and smooth muscle proliferation.
    • Important side effect is hepatotoxicity
  • PDE-5 inhibitors
    • Names: Sildenafil (Revatio), Tildalafil (Adcirca)
    • Mechanism of action: Blocks degradation of cGMP
  • Soluble Guanylate Cyclase Stimulators
    • Names: Riociguat (Adempas)
    • Mechanism of action: Sensitizes soluble guanylate cyclase to endogenous NO and directly stimulates soluble guanylate cyclase leading to vasodilation

CLINICAL PEARL:  Epoprostenol and treprostinil are given via continuous infusion. Abrupt discontinuation (i.e., catheter malfunction) can cause acute RV failure.  This is critical to recognize in the emergency department.  If there is a concern regarding catheter malfunction of a patient on a continuous infusion, the patient’s PAH specialist should be consulted immediately and the medication restarted through a peripheral line. These patients are also at high risk for line infection. Sepsis should always be on the differential for a patient on infusion therapy who presents with an acute decompensation.  

2. What is the best echocardiographic view and key findings associated with RV failure? 

A bedside ultrasound can be very difficult to interpret in a patient with severe underlying PH as they often have a dilated, poorly functioning RV with septal bowing at baseline.  Reviewing a formal transthoracic echo with a cardiologist who has access to a patient’s prior echo imaging is much more helpful (although unrealistic in the acute setting).

For a patient without a history of PH, bedside US should follow a structured protocol for focused bedside US in shock (i.e. the RUSH exam or similar). Documenting a D-shaped LV on the parasternal short axis view, an increased RV/LV ratio or McConnell’s Sign on an apical 4-chamber view, or a dilated IVC on a subcostal view are all helpful findings.

3. Is there a role for a fluid bolus in a patient presenting with right ventricular failure?

Especially for patients with underlying PAH, clinical deterioration is much more commonly caused by worsening right heart function and falling cardiac output (via bowing of the IVS into the LV and progressive RV ischemia) than true hypovolemia.  For a patient with a convincing story for dehydration, a small volume challenge (I would start with 250 cc is a patient with severe underlying PAH) can be considered but this should be done cautiously and with close monitoring.  I would caution against empiric 500 cc volume challenges in patients with acute on chronic right heart failure.  Excessive IVF risks the vicious cycle:


Figure 3 Cycle of iatrogenic decompensation in acute right heart failure with liberal use of IVFs


Far more often than fluids, these patients require inotropes/pressors + diuretics to offload a distended failing RV. In my view, the above physiology explaining why excessive IVF can precipitate cardiovascular collapse in patients with PAH is a critical concept to grasp. 

4. What is the best pressor in right sided heart failure?

In my view, the specific vasoactive agent used is much less important than attentive bedside care, a thorough evaluation to determine the cause of a patient’s decompensation (i.e. indwelling line infection, pulmonary embolism, etc.) and expedited consultation with specialists when indicated.

For the hypotensive patient, norepinephrine is a nice drug as it has both inotropic and vasoconstrictive effects.  It can, however, induce arrhythmias and therefore requires attentive bedside management.

Phenylephrine may increase mPAP and decrease cardiac output so it is avoided by some providers although others find it appealing as it may avoid dangerous tachyarrhythmias seen with other agents while raising MAP and increasing RV perfusion.

Data suggests that dopamine may worsen outcomes in patients with cardiogenic shock (RV or LV) and cause more adverse events than norepinephrine [5]. In Hall, Schmidt, and Wood’s Principles of Critical Care, they note “we avoid the use of dopamine because of its highly variable pharmacokinetics and concern for disproportionate splanchnic vasoconstriction even in relatively low doses.”

Dobutamine or milrinone are appropriate choices if a patient is not yet hypotensive. 

In short, there is little definitive data to guide vasopressor choice. Agents that raise BP without significantly raising heart rate will work.  

5. What are your thoughts about HFNC vs NIPPV for these patients?

Any oxygen delivery device that corrects hypoxemia (and subsequent hypoxic vasoconstriction) is a step in the right direction.  There is increasing evidence that HFNC may improve outcomes for patients with hypoxemic respiratory failure, aid secretion clearance (especially helpful in patients with pneumonia), and increase device tolerance so I have been moving more to that as a first-line therapy for acutely hypoxemic patients without hypercarbia or cardiogenic edema (where there is a clear benefit for NIPPV).  There is no high-quality data I am aware of that compares devices in patients with RV failure.  As with most things, whatever management strategy you choose, attentive bedside monitoring for tolerance or further decompensation is probably what matters most. 

6. Should Intubation be a Last Resort? 

It is important to emphasize that while the initiation of invasive mechanical ventilation has significant hemodynamic effects on a patient with right heart failure, it is often needed and not something that should be avoided or delayed in critically ill patients. 

It is important to understand the impact of mechanical ventilation on the right heart.

  • Increased mean airway pressure decreases the gradient for venous return and decreases RV preload.  
  • This increase in right atrial pressure may also cause or worsen right-left shunt across a patent foramen ovale. The presence of a patent PFO is worth considering in any patient with right heart failure who suddenly develops refractory hypoxemia (would confirm with a bubble study).
  • Excessive tidal volumes may increase pulmonary vascular resistance by compressing intra-alveolar vessels.  There is nice summary in the Annals of the American Thoracic detailing this physiology [6].
  • Hypercapnia (which is often seen as a result of low-tidal volume ventilation) increases pulmonary artery pressures.

How each of these factors impact a particular patient is incredibly variable.  In general, a strategy focused on low-tidal volumes, the “least PEEP” which maximizes alveolar recruitment but limits impairment of venous return and shunting across a PFO, and avoidance of significant hypercapnia is a reasonable initial strategy.  As always, attentive bedside monitoring is essential. 

Big picture principles for ventilator management in RV failure:

  • Avoid huge tidal volumes (i.e., start around 8cc/kg/IBW and slowly drop to around 6cc if you can).
    • This should not differ much from your typical approach to any patient with hypoxemic respiratory failure
  • Be careful with PEEP    
    • This is where things differ a little.  In ARDS, we often move to a “high-PEEP” strategy to maximize alveolar recruitment.  In a patient with RV failure, I would be much more careful with PEEP.  I would start at 5 and slowly increase. If FiO2 starts to drop at all, I would quickly drop back to my previous level.
  • Be “less permissive” with PaCO2.  
    • In ARDS, a rise in PaCO2 is a tolerable consequence of dropping TVs to 6cc/kg/IBW.  With RV failure, I would be worried if the PaCO2 rises too high given the impact of hypercapnia on PA pressures and I would liberalize my TVs a bit.  There is no data to guide what level of PaCO2 is “too high.”   

Final Thoughts

While knowing all the causes of acute right heart failure is important, it’s more important to understand how right heart physiology informs acute management. Remember the three key pathologic forces at play: RV response to increased PVR (i.e. RV afterload), RV pressure/volume overload causing bowing of the interventricular septum and RV ischemia.

Key ED Management Principles in RV Failure: 

  • Early and aggressive care: Patients with acute on chronic right heart failure can crash within minutes. They require attentive bedside monitoring and should be treated with the same urgency as a patient with septic shock. These are not patients to put in a corner room and check on every few hours.  
  • Rapid evaluation for end-organ dysfunction: mental status and skin exam, oxygenation, creatinine/UOP, lactate.  
  • Thorough work-up for reversible causes of decompensation especially 
    • Line infection/catheter malfunction for patients on IV prostacyclin therapy
    • PNA
    • VTE
  • Use caution when considering IVF in patients with known PAH.  Typically, these patients require early diuretics + inotropes (dobutamine) if normotensive or vasopressors (norepinephrine) if hypotensive rather than IVF
  • Correct hypoxemia (to prevent hypoxic vasoconstriction from further raising PVR), consider HFNC as first line, but do not delay intubation when necessary.
  • Early specialist consultation and ICU transfer

As interns none of us appreciated how sick and brittle these patients are. These are concepts that should be emphasized to new housestaff, just as we emphasize the importance of early and aggressive care in sepsis.

James Walter, MD

Clinical Fellow; Division of Pulmonary and Critical Care; Northwestern University Feinberg School of Medicine 


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