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Right Ventricular Failure 

Right Ventricular Failure
Chapter:
Right Ventricular Failure
Author(s):

John W. Kreit

DOI:
10.1093/med/9780190670085.003.0014
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date: 03 July 2020

Right ventricular (RV) failure is common in the ICU. Chronic RV failure is most often due to long-standing pulmonary hypertension. Acute RV failure can result from massive pulmonary embolism, ARDS, RV infarction, and acute LV failure. Finally, acute-on-chronic RV failure can be precipitated by any disorder that leads to an abrupt rise in pulmonary vascular resistance (PVR) and RV afterload. Common causes include pneumonia, exacerbation of chronic lung disease, and pulmonary embolism. As discussed in Chapter 3, mechanical ventilation and PEEP also increase RV afterload, so it’s not surprising that they can trigger acute or acute-on-chronic RV failure. This chapter reviews the pathophysiology of RV failure, highlights the effects of mechanical ventilation and PEEP on the pulmonary circulation and RV, and provides physiology-based mechanical ventilation guidelines for patients with, or at risk for, RV failure.

Pathophysiology of RV Failure

In the absence of acute RV infarction, acute or acute-on-chronic RV failure (which I will refer to collectively as “acute RV failure”) is most commonly precipitated by an abrupt increase in afterload. That’s because neither the normal right ventricle, nor one that is hypertrophied due to chronic pulmonary hypertension, is capable of generating sufficient additional pressure to overcome even a relatively small increase in PVR.

Acute RV failure causes ventricular dilation and a rise in RV end-diastolic pressure and volume. This triggers a sequence of events that leads to further impairment of RV function and may progress to cardiogenic shock (Figure 14.1). Since both ventricles share a common wall (the septum), and their combined volume is limited by the pericardium, RV dilation causes the septum to flatten and shift toward the LV (Figure 14.2). This reduces LV size and compliance, which impairs diastolic filling. RV dilation may also cause or worsen tricuspid regurgitation. The combination of reduced RV systolic function and tricuspid regurgitation decreases RV stroke volume. This, in combination with impaired LV diastolic filling, decreases LV stroke volume, which, if sufficiently severe, leads to hypotension. At the same time, increased pressure-generation by the RV augments wall stress and oxygen demand while reducing coronary blood flow. This leads to RV ischemia, which reduces contractility and worsens RV dilation, RV systolic and LV diastolic function, and LV stroke volume. Systemic hypotension worsens this vicious cycle by further reducing coronary blood flow.

Figure 14.1 An acute rise in RV afterload may precipitate a series of events that ultimately leads to cardiogenic shock.

Figure 14.1 An acute rise in RV afterload may precipitate a series of events that ultimately leads to cardiogenic shock.

Figure 14.2 Representation of a short-axis, parasternal view from a transthoracic echocardiogram in a patient with (A) normal right ventricle (RV) and left ventricle (LV) and (B) severe RV dilation. RV pressure and volume overload causes the interventricular septum to shift toward the left ventricle.

Figure 14.2 Representation of a short-axis, parasternal view from a transthoracic echocardiogram in a patient with (A) normal right ventricle (RV) and left ventricle (LV) and (B) severe RV dilation. RV pressure and volume overload causes the interventricular septum to shift toward the left ventricle.

Mechanical Ventilation and the RV

The effects of mechanical ventilation and PEEP on PVR and RV afterload were reviewed in Chapter 3. Here, I will only summarize the important points.

  • RV afterload is proportional to PVR.

  • PVR is proportional to lung transmural pressure (PlTM), which is alveolar pressure (PALV) minus pleural pressure (PPL).

  • By increasing PlTM, mechanical ventilation causes a cyclical increase in PVR and RV afterload.

  • Extrinsic and intrinsic PEEP cause continuous elevation of end-expiratory and end-inspiratory PlTM, which further increases PVR and RV afterload.

  • The hemodynamic significance of these changes depends on the extent to which tidal ventilation and PEEP increase PlTM, and on baseline ventricular function.

    • The change in PlTM varies directly with the delivered tidal volume and the level of total PEEP, and inversely with lung compliance (Figure 14.3). In other words, a mechanical breath and PEEP will have a greater effect on RV afterload in a patient with low lung compliance (e.g., from pulmonary fibrosis).

    • The hemodynamic effect of a given rise in PlTM will be greater in patients with impaired RV contractility or elevated RV afterload.

Figure 14.3 The relationship between lung volume and alveolar (PALV), pleural (PPL), and lung transmural (PlTM) pressure in a patient with normal (A) and decreased (B) lung compliance. The increase in lung transmural pressure (∆PlTM), pulmonary vascular resistance, and RV afterload varies directly with tidal volume (VT) and PEEP and inversely with lung compliance.

Figure 14.3 The relationship between lung volume and alveolar (PALV), pleural (PPL), and lung transmural (PlTM) pressure in a patient with normal (A) and decreased (B) lung compliance. The increase in lung transmural pressure (∆PlTM), pulmonary vascular resistance, and RV afterload varies directly with tidal volume (VT) and PEEP and inversely with lung compliance.

Guidelines for Mechanical Ventilation

Because of its adverse effects on RV afterload, mechanical ventilation should be avoided in patients with acute or chronic RV failure. If mechanical ventilation is absolutely necessary, the following recommendations are based on reducing the physiological effects listed previously.

  • Non-invasive ventilation (Chapter 16) may be preferable to intubation because of the decreased need for sedating drugs, which may cause or worsen hypotension.

  • Use low tidal volume ventilation; 6 ml/kg of ideal body weight is an appropriate target.

  • Maintain a low plateau pressure (PPLAT). Remember that PPLAT is alveolar pressure at end-inspiration, so it’s directly related to lung transmural pressure (PALV - PPL) and PVR. Studies in ARDS patients suggest that the risk of acute RV failure is minimized when PPLAT is maintained ≤27 mmHg.

  • Since PlTM (and PVR) falls as compliance increases, PEEP should be titrated to maximize alveolar recruitment in patients with ARDS (Chapter 12).

  • PEEP should be set at zero in patients without ARDS.

  • Assess for and minimize intrinsic PEEP (Chapter 10).

  • Correct hypoxemia, hypercapnia, and acidemia. All three conditions cause pulmonary vasoconstriction, which increases PVR and RV afterload.

Of course, it may be difficult to simultaneously achieve all of these goals. In particular, maintaining low tidal volume ventilation at a low PPLAT is likely to precipitate or worsen arterial hypoxemia, hypercapnia, and acidemia. These abnormalities can often be at least partially corrected by increasing the FIO2, the set respiratory rate, or both.

Other Therapies

The following therapies are logical and often recommended, although no studies have been performed to evaluate their efficacy.

Optimize RV Preload

With the possible exception of patients with RV infarction, acute or acute-on-chronic RV failure is almost always accompanied by elevated RV preload. The magnitude of pressure and volume overload can be assessed by point-of-care cardiac ultrasound and by measuring central venous pressure (CVP). When confirmed, excessive RV preload should be treated with diuresis in an effort to reduce LV compression and improve LV diastolic filling. Serial ultrasound imaging and CVP measurements are essential to avoid over-diuresis and a significant drop in RV stroke volume. In many cases, right heart catheterization provides additional information that helps optimize RV preload, LV stroke volume, and cardiac output.

Vasopressors and Inotropes

Systemic blood pressure must be maintained to provide adequate blood flow to the heart and other vital organs. Norepinephrine is most often used in patients with acute RV failure because it increases cardiac contractility and systemic vascular resistance (SVR), with relatively little increase in heart rate or PVR.

If blood pressure is adequate, inotropes such as dobutamine or milrinone may improve hemodynamics by increasing RV contractility. The downside of both drugs is that they cause systemic vasodilation, which often leads to hypotension.

Pulmonary Vasodilators

Nebulized nitric oxide (NO) and epoprostenol are potent vasodilators that can rapidly and significantly reduce PVR in patients with RV failure. Because they are administered by inhalation and have a very short half-life, these drugs do not cause systemic vasodilation and hypotension.

Additional Reading

Harjolal VP, Mebazaa A, Celutkiene J, et al. Contemporary management of acute right ventricular failure: A statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology. Eur J Heart Fail. 2016;18:226–241.Find this resource:

Krishnan S, Schmidt GA. Acute right ventricular dysfunction. Chest. 2015;147:835–846.Find this resource: