CONTENTS
- Rapid Reference: Approach to RV failure 🚀
- Preamble: Don't forget the right ventricle!
- Pathophysiology of RV failure
- Diagnosis of RV failure
- Causes of right ventricular failure
- Treatment
- 1st Tier: Core treatments for all RV failure patients:
- 2nd Tier: Often needed:
- 3rd Tier:
- Podcast
- Questions & discussion
- Pitfalls
correct any precipitating factors 📖
- D/C negative inotropes (e.g., beta-blockers).
- D/C systemic vasodilators (if hypotensive).
- Manage arrhythmia (e.g., cardioversion of new AF).
- Manage acidosis.
- Treat other active processes (e.g., infection, pulmonary embolism).
optimize the lungs 📖
- Aggressive oxygenation (O2 is a pulmonary vasodilator).
- Consider drainage of any substantial pleural effusions.
- Treat hypercapnia (but avoid intubation).
- If intubated: avoid excess PEEP.
volume management 📖
- Most patients require diuresis (even if on vasopressors).
- If CVP >>12, may diurese to a target CVP of ~8-12 mm.
- Avoid fluid administration unless there is unequivocal hypovolemia.
establish an adequate MAP 📖
- Target a MAP >65 mm, or perhaps >(60 + CVP).
- Choice of agent?
- Vasopressin may be preferred, if central access is available.
- Mildly unstable: norepinephrine is often effective.
- Sickest patients: consider 🏆 epinephrine.
inhaled pulmonary vasodilators PRN 📖
- Indications may include:
- Refractory hypoxemia (especially with R ➡️ L shunt).
- High risk of death (e.g., peri-intubation stabilization).
- Poor perfusion.
- Main contraindication: Left ventricular failure.
inotrope PRN 📖
- Consider for:
- RV systolic failure.
- Poor perfusion.
- Bradycardia or inappropriately low heart rate.
- Options include:
- Dobutamine.
- Epinephrine.
The right ventricle is sometimes called the forgotten ventricle. Many textbooks on critical care cardiology are written almost entirely about left ventricular failure. Likewise, nearly all evidence surrounding heart failure is with regards to the left ventricle. There is nearly no high-quality evidence regarding the management of right ventricular failure in the ICU.
Nonetheless, right ventricular failure is quite common in the ICU, occurring in perhaps about a third of patients with ARDS or septic shock. Our most important task in the ICU is identifying patients with RV failure and providing them with a basic RV-friendly resuscitation. Simple interventions can go a long way in these patients, if we can merely understand their precarious physiology.
Four concepts are especially useful clinically.
vicious spirals of RV failure
- RV failure tends to produce a set of vicious spirals, which tend to cause progressively worse failure (figure above). This is extremely dangerous, because if left untreated RV failure will tend to spiral out of control.
- These spirals explain why patients with RV failure can sometimes suddenly die (a phenomenon often seen in patients with massive pulmonary embolism or following intubation).
- A central feature of RV failure is RV dilation that causes shifting of the interventricular septum, as well as functional tricuspid regurgitation.
RV myocardial perfusion
RV systolic perfusion pressure = (Systolic Bp) – (Pulmonary Artery Systolic Pressure)
- Unlike the left ventricle, the RV is normally perfused during both systole and diastole. Since the RV pressure is relatively low, the systemic pressure is greater than the RV pressures throughout the cardiac cycle – allowing perfusion to occur continuously.(32284101)
- Systolic perfusion of the right ventricle depends on the pressure gradient between the coronary arteries (the systolic blood pressure) and the right ventricle pressure (which is equal to the pulmonary artery systolic pressure) – as shown above.
- In RV failure, systemic hypotension may cause the systolic Bp to fall to levels close to the pulmonary artery systolic pressure. This will impair RV perfusion during diastole.
- Defending the RV myocardial perfusion depends on maintaining the RV systolic perfusion pressure as shown above. This requires interventions that increase the systolic Bp and decrease the pulmonary artery systolic pressure.
RV failure patients can fall off the Starling curve
- Traditionally, it has been taught that excess volume administered to patients with heart failure may cause ventricular dilation, leading to ineffective systolic contraction and a reduction in cardiac output. This is referred to as “falling off the Starling curve.”
- This phenomenon probably doesn't really occur acutely in patients with isolated left ventricular failure, because the left ventricle is a thick-walled chamber with a fairly fixed volume. Thus, the left ventricle doesn't dilate acutely in response to volume overload.
- The phenomenon of falling off the Starling curve does occur in patients with right ventricular failure:
- (1) Excess volume loading can cause acute dilation of the thin-walled right ventricle that leads to impaired right ventricular function and functional tricuspid regurgitation.
- (2) RV dilation may compress the LV, leading to left-sided diastolic dysfunction. In extreme cases, this may induce LV outflow tract obstruction (LVOTO).
- (3) Systemic congestion impairs systemic organ perfusion (discussed in the section below).
occult systemic hypoperfusion
Systemic Perfusion Pressure = (MAP – CVP)
- In isolated left ventricular failure, volume overload results in pulmonary edema. This causes overt hypoxemia, dyspnea, and pulmonary edema on chest X-ray – an obvious problem which demands immediate attention.
- In right ventricular failure, volume overload instead results in systemic congestion (with an elevated central venous pressure). Since systemic congestion doesn't result in any vital sign abnormality or dramatic symptomatology, it is often ignored until it is profound (leading to anasarca).
- Systemic congestion with elevated central venous pressure may lead to organ malperfusion, because it reduces the systemic perfusion pressure (formula above). For example, a patient with a MAP of 60 mm and a CVP of 25 mm may have an extremely low systemic perfusion pressure (35 mm). This cannot be detected based on usual vital signs, so it may lead to occult organ failure. Organs which are particularly affected include the kidneys, liver, brain, and bowel.
- If patients deteriorate further and develop overt hypotension, visceral organs will suffer a “double hit” due to both the reduced MAP plus the elevated central venous pressure.
defining RV failure
getting started
- There is no universal definition of RV failure.(29744563)
- Technically, the RV could fail in two ways:
- “Forwards failure” – RV fails to generate an adequate cardiac output, leading to cardiogenic shock.
- “Backwards failure” – RV fails to decongest the systemic venous system, leading to an excessively high central venous pressure with systemic congestion.
- Physiologically, RV failure nearly always involves systemic congestion. (Isolated “forwards failure” of the RV is extremely rare, in the absence of marked hypovolemia.)
stages of RV failure
- (1) Systemic congestion (“backwards failure” of the RV):
- Markedly elevated CVP (central venous pressure) usually indicates RV failure, in the absence of an obvious alternative explanation (e.g., severe hypervolemia, intubation with high airway pressures, abdominal compartment syndrome, pericardial tamponade).
- Initially systemic congestion may cause tissue edema, without hypoperfusion.
- (2) Hypoperfusion without frank hypotension (“occult systemic hypoperfusion”)
- Severe congestion can cause organ hypoperfusion without obvious hypotension.
- The systemic perfusion pressure equals (MAP – CVP). Patients with markedly elevated CVP and borderline reduced MAP may develop organ hypoperfusion. For example:
- Congestive encephalopathy (delirium with agitation, confusion, or drowsiness).
- Congestive nephropathy, with reduced urine output.
- (3) Frank hypotension with shock.
- This is extremely dangerous because it causes a “double hit” to the systemic perfusion (MAP-CVP), in terms of both an elevated CVP and a reduced MAP.
- Bowel wall edema may promote bacterial translocation and systemic inflammation, adding a component of vasodilatory shock.(30545979)
history & physical examination findings
history elements that may suggest RV failure
- Very substantial weight gain.
- Increasing peripheral edema.
- Early satiety, abdominal fullness, right upper quadrant tenderness.
- Exercise intolerance, dyspnea on exertion. (36947468)
systemic congestion is usually present (unless RV failure is extremely acute)
- Peripheral edema.
- Ascites.
- Hepatic distension may cause right upper quadrant pain.(32284101)
- Jugular vein distension.
shock with hypoperfusion eventually occurs
- Cool and clammy extremities, with poor capillary refill.
- Reduced urine output is an early finding (due to congestive nephropathy).
- Congestive encephalopathy may cause delirium.
laboratory findings in RV failure may include:
- Congestive nephropathy with elevated creatinine.
- Congestive hepatopathy: The combination of reduced cardiac output plus systemic congestion may promote malperfusion with markedly elevated transaminases (shock liver). This can occur despite the absence of frank hypotension.
- BNP (brain natriuretic peptide) may be elevated, but this is nonspecific.
- Lactate elevation may occur.
radiological findings in RV failure may include:
RV failure on CT scan
- CT scans provide snapshots of the heart, yielding a wealth of information (which is often overlooked). Chest CT scans are ideal for imaging the heart, but abdominal scans are often sufficient to reveal right ventricular enlargement. Review of archival CT images can also help sort out acute versus chronic pathology. Findings may include the following:
- RV dilation is suggested by an RV/LV diameter ratio >1.
- Pulmonary artery dilation to a size greater than the aorta suggests chronic pulmonary hypertension.
- Contrast reflux into the inferior vena cava and hepatic veins suggests right ventricular insufficiency (analogous to the Kussmaul's sign above, the right ventricle is unable to handle additional preload).
electrocardiographic findings
Findings of acute and chronic right ventricular strain can be quite similar. Prior EKGs and clinical context may be needed to differentiate between these two possibilities.
(1) Acute right ventricular strain (usually due to PE, but may be due to any cause of acute pulmonary hypertension – such as acute asthma)
- Right bundle branch block (complete or in complete).
- Terminal right-axis deviation:
- Prominent terminal S-wave in Lead I.
- Prominent S-wave in V6 (normally V6 has no S-wave).
- T-wave inversion:
- Right precordial leads.
- Inferior leads (III > aVF).
- Severe cases may cause ST changes, in various patterns:
- STE in III and aVF, +/- anteroseptal leads.
- Diffuse ST depression with ST elevation in aVR.
- Right precordial ST depression can mimic a posterior MI.
(2) Chronic right ventricular hypertrophy (RVH)
- Tall R-wave in V1:
- Most classic finding of RVH.
- Defined in terms of R>S, or R>7 mm.
- Highly specific for RVH, but insensitive.
- Terminal right-axis deviation:
- Prominent terminal S-wave in Lead I (in some cases, S>R).
- Prominent S-wave in V6 (normally V6 has no S-wave).
- RV strain pattern: ST depression +/- T-wave inversion in V1-V4, and to a lesser degree in the inferior leads.
- Right atrial abnormality (especially increased P-wave amplitude in Lead II).
echocardiography
RV dilation
- This is best appreciated in subcostal four-chamber view, in diastole.
- Normally the RV is <~60% the size of the LV.
- Moderate RV dilation: RV is ~60-100% the size of the LV.
- Severe RV dilation: RV is larger than the LV.
RV septal flattening (“D” sign)
- The D-sign refers to septal flattening observed in short-axis views of the heart (either via the parasternal or subcostal window).
- D-configuration in diastole suggests volume overload.
- D-configuration in systole suggests pressure overload (i.e., pulmonary hypertension).
- D-configuration throughout the cardiac cycle suggests a combination of both volume and pressure overload (as is often seen in advanced pulmonary hypertension).
TAPSE (tricuspid annular plane systolic excursion)
- TAPSE is the best single indicator of RV systolic function at the bedside.
- TAPSE is most precisely assessed via M-mode from apical four chamber (if possible). However, visual estimation from other views may be used as well (e.g., subcostal).
- Grading:
- Normal TAPSE: >17 mm.(33853435)
- Mild RV dysfunction: 10-17 mm.
- Moderate RV dysfunction: 5-10 mm.
- Severe RV dysfunction: <5 mm.
central venous pressure (CVP)
- (1) Based on inferior vena cava:
- IVC >2 cm with lack of respirophasic variation suggests CVP is elevated.
- IVC <2 cm with respirophasic variation suggests CVP is ~0-5 mm (which is normal).
- (2) Based on examination of the right internal jugular vein:
- This is a more accurate way to measure jugular venous pressure (JVP) at the bedside. With minimal pressure, scan along the neck to detect the height of jugular distension.
- The sternal angle of Louis corresponds to 5 cm of water pressure. Add the height above the Sternal Angle to this, to obtain the jugular vein pressure in cm. To convert from cm water to mm mercury, multiply by 0.7.
PA systolic pressure (PASP)
PASP = CVP + 4(max TR jet in m/s)2
- PA systolic pressure (PASP) can be estimated based on the central venous pressure plus the maximal tricuspid regurgitant (TR) jet velocity, as shown above. The tricuspid regurgitant jet can be measured by using continuous wave doppler (CW) placed across the tricuspid valve.
- PA systolic pressure >35 mm suggests pulmonary hypertension.(26342901)
- Pulmonary hypertension is highly likely if the peak TR regurgitant jet velocity is ≧3.4 m/s, or if the TR jet is 2.9-3.4 m/s in the context of other echocardiographic features of right ventricular dysfunction.(33853435)
- In one ICU study, PA systolic pressure could be estimated in only 60% of patients due to technical limitations.(33853435) In the absence of transesophageal echocardiography, this technique cannot be relied upon to be helpful in all patients.
signs of chronic pulmonary hypertension
- (1) RV wall thickening (>~5 mm measured at end-diastole) suggests chronic pulmonary hypertension. This is best measured via parasternal long axis or subcostal windows. However, wall thickening may increase within 48 hours, so this can develop rapidly in the context of acute pulmonary hypertension. RV wall thickening >10 mm suggests that the PA pressure may be approaching systemic pressures.(28024557)
- (2) PA systolic pressure >60 mm suggests chronicity, since a hypertrophied right ventricle is required to generate this much pressure (an acute increase in PASP >60 mm in an unconditioned right ventricle is probably inconsistent with survival).
- (3) A pericardial effusion is often an indicator of severe, chronic pulmonary hypertension.(36116812)
bedside echo bubble study to evaluate severe hypoxemia
- Patients with pulmonary hypertension may suddenly develop severe hypoxemia due to opening up a patent foramen ovale (PFO), with subsequent intracardiac shunting of deoxygenated blood into the systemic circulation.
- Echocardiography during injection of agitated saline may rapidly evaluate for a right-to-left shunt in patients with right ventricular failure and severe hypoxemia. Appearance of bubbles in the left ventricle within <6 beats after appearance of bubbles in the right ventricle indicates an intracardiac shunt (whereas delayed shunting may result from pulmonary arteriovenous malformations).(33853435)
- The presence of a right-to-left shunt should serve as a stimulus for more aggressive reduction of pulmonary artery pressures (e.g., inhaled pulmonary vasodilators, vasopressors to increase the systolic/pulmonary pressure gradient, diuresis).
Causes of right ventricular failure can be divided into three general groups:
- Causes of chronic pulmonary hypertension.
- Causes of acute pulmonary hypertension.
- Causes of right ventricular myocardial dysfunction/decompensation.
Right ventricular failure is usually partially or entirely due to pulmonary hypertension (#1-2 above). However, an individual patient will often have several of these factors together. Identifying and treating all causative factors is important. Review of prior right ventricle imaging (if available) may help clarify whether there is a substantial component of chronic pulmonary hypertension.
#1/5: causes of chronic pulmonary hypertension
- Group 1: Pulmonary Arterial Hypertension (PAH)
- 1.1 Idiopathic.
- 1.2 Hereditary.
- 1.3 Drug and toxin induced (e.g., anorexigens, cocaine, chemotherapy).
- 1.4 Pulmonary Arterial Hypertension associated with:
- 1.4.1 Connective tissue disease (e.g., SLE, scleroderma).
- 1.4.2 HIV.
- 1.4.3 Portal hypertension.
- 1.4.4 Congenital right-to-left shunt (e.g., atrial septal defect).
- 1.4.5 Schistosomiasis.
- 1.5 Long-term responders to calcium channel blockers.
- 1.6 Pulmonary veno-occlusive disease / pulmonary capillary hemangiomatosis.
- Group 2: Left heart disease (e.g., systolic failure, diastolic failure, valvular disease).
- Group 3: Lung disease and/or hypoxemia (e.g., COPD, interstitial lung disease, obesity hypoventilation syndrome).
- Group 4: Pulmonary artery obstruction.
- 4.1 Chronic thromboembolic pulmonary artery hypertension (CTEPH).
- 4.2 Other pulmonary artery obstructions.
- Group 5: Unclear/multifactorial:
#2/5: causes of acute pulmonary hypertension
- Pulmonary embolism (PE)
- Massive PE can cause acute-onset pulmonary hypertension. 📖
- Moderate-size PE may cause decompensation among patients with chronic pulmonary hypertension.
- Essentially any lung disease (e.g., any cause of hypoxemia and/or hypercapnia).(28024557)
- ARDS
- Pneumonia.
- Lung overdistension: excessive PEEP or autoPEEP.
- Lung underdistention: atelectasis, pleural effusion, pneumothorax.
- Sickle cell acute chest syndrome (~20% incidence of RV failure).(29744563)
- Alpha-agonists:
- Excessive doses of phenylephrine or norepinephrine.
- oral decongestants (e.g., neosynephrine) may exacerbate chronic PH.
- Nonadherence with pulmonary hypertension therapy.
#3/5: causes of right ventricular myocardial dysfunction
- Negative inotropic medications:
- Beta-blockers.
- Diltiazem, verapamil.
- Arrhythmia, e.g.:
- Atrial fibrillation is especially problematic, as this causes a loss of atrial kick. When possible, the optimal treatment may be restoration of normal sinus rhythm. Beta-blockers or diltiazem should be avoided, given their negative inotropic properties. For patients who cannot be cardioverted, digoxin may be a good option for providing rate control and positive inotropy. More on the management of critical AF here.
- Bradycardia is often very poorly tolerated and suggestive of imminent death in some contexts. This must be treated aggressively (as discussed here).
- Septic cardiomyopathy
- Cytokine release may increase the pulmonary vascular resistance and reduce right ventricular contractility.(33541609, 32740380)
- Roughly a third of patients may have RV dysfunction.
- Recognition of RV dysfunction may be especially important, because this may be exacerbated by many treatments of septic shock (e.g., large-volume fluid administration).
- Post-cardiac arrest myocardial dysfunction.
- Right ventricular myocardial infarction (RVMI). 📖
- Status post cardiac surgery.
- Rare:
#4/5: excessive preload
- Hypervolemia is a common precipitant of RV failure.
- Tricuspid regurgitation (e.g., tricuspid endocarditis); pulmonic regurgitation.
- Arteriovenous shunts/fistulas.
#5/5: increased cardiac demand: any cause of systemic vasodilation
- Medications that cause systemic vasodilation.
- Severe systemic inflammation:
- Septic shock.
- Pancreatitis.
- Post-cardiac arrest SIRS.
- Post-MI SIRS.
- Anaphylaxis.
- Endocrine:
- Adrenal crisis.
- Thyroid storm.
- Neurogenic shock:
- Trauma.
- Spinal anesthesia.
- Liver failure.
- Beri-beri (thiamine deficiency).
Any factors promoting pulmonary hypertension should be treated if possible, for example:
- Discontinuing medications (e.g., negative inotropes, systemic vasodilators, alpha-agonists).
- Control of atrial fibrillation.
- Treat any metabolic acidosis.
Any pulmonary dysfunction will increase the pulmonary vascular resistance, thereby increasing the afterload on the right ventricle.
(#1) liberal oxygen
- Oxygen is the original pulmonary vasodilator.
- Aggressive oxygen may reduce pulmonary vascular resistance and improve cardiac output.
(#2) optimize lung function, for example:
- Drainage of moderate/large pleural effusion.
- CPAP/BiPAP for management of atelectasis, COPD, or OHS (obesity hypoventilation syndrome).
(#3a) if not intubated: avoid intubation
- Avoid intubation if possible, as this is an extremely high-risk procedure in the context of right ventricular failure (more on the intubation procedure below).
- High flow nasal cannula may be a safe and noninvasive strategy to improve oxygenation and ventilation (among patients who don't have an indication for CPAP or BiPAP).
(#3b) if intubated: optimize ventilator settings
- (a) Maintain an adequate oxygen saturation, with generous oxygen administration as above.
- (b) Avoid hypercapnia as able:
- CO2 is a pulmonary vasoconstrictor.
- Hypercapnia should be treated if possible, with a goal of normocapnia.
- (c) Avoid using excessive PEEP or mean airway pressure. However, using adequate PEEP to prevent atelectasis remains beneficial, as this will recruit lung tissue and thereby reduce the pulmonary vascular resistance.
optimizing volume status in RV failure
- Patients with RV failure are rarely hypovolemic. Fluid should not be administered unless there is an especially good reason (e.g., severe diabetic ketoacidosis plus echocardiographic evidence of a low CVP).
- Hypervolemia is generally present and usually requires diuresis (physiology above: 📖).
- 🛑 Beware that right ventricular dysfunction may cause many tests of fluid responsiveness to fail (e.g., pulse pressure variability).
central venous pressure (CVP) as a diuresis target
- CVP is generally not very helpful in the ICU, because we're often trying to use CVP as a surrogate for left-sided filling pressures (something the CVP is awful at). However, in right heart failure, we are actually interested in right-sided filling pressures – so the CVP actually measures what we need.
- Consensus suggests that a reasonable target might be a CVP of ~8-12 cm (i.e., slightly elevated filling pressures).(32740380, 32411259, 24828526, 30190155) The optimal role of the CVP here is as a tool to encourage diuresis (rather than to stimulate fluid administration).
- 💡 If the CVP is >>12, this may provide reassurance that diuresis is likely safe.
why maintaining an adequate MAP is important:
- An adequate MAP will promote adequate perfusion of the right ventricular myocardium.
- An adequate MAP is necessary to perfuse the kidneys (allowing for diuresis, if needed).
- A higher MAP will increase the LV afterload, which may counteract septal flattening and thereby promote normal cardiac geometry.(33541609)
- Among patients with a patent foramen ovale and right-to-left shunting, elevation of left-sided pressures may help reduce the amount of shunting.
optimal target MAP?
- MAP >65 mm is a reasonable place to start.
- MAP >(60 mm + CVP)
- Patients with markedly elevated CVP might need a higher MAP target to achieve adequate systemic perfusion pressures.
- A reasonable target MAP might be >(60 mm + CVP).
- Patients with systemic congestion and low MAP may require a combination of simultaneous vasoconstrictors plus diuresis (to promote decongestion and optimization of right ventricular preload).
- When in doubt, it may be reasonable to trial an elevated MAP to determine if this causes clinical improvement (e.g., improved urine output)(figure below).
- Once the patient has been adequately decongested, vasoconstrictors can often be weaned. At this point, the patient may be able to clinically tolerate a lower MAP without hypoperfusion (because, due to the lower CVP, the systemic perfusion pressure is now adequate at a lower MAP).
- SBP > RVSP
- To ensure RV perfusion, the systemic systolic blood pressure should be kept well above the RV systolic blood pressure (SBP >> RVSP).
- This usually isn't difficult to achieve, but for patients with chronic, severe pulmonary hypertension it may be an issue.(32284101)
choice of agent
- Vasopressin is arguably the ideal agent, since it offers the ability to increase MAP while simultaneously reducing pulmonary vascular resistance.(33541609) The limitations of vasopressin include that it is difficult to titrate, it is not safe for peripheral administration, and it will often be insufficient among patients with profound hypotension (because it is typically not titrated above 0.06 units/min).
- Epinephrine is a good choice among the sickest patients. At lower doses, epinephrine may function more as an inotrope, whereas at increasing doses it will function more as a vasoconstrictor. The beta-agonist activity of epinephrine will reduce the pulmonary vascular resistance and support right ventricular function, thereby improving the MAP without worsening RV afterload.
- Norepinephrine is a reasonable choice which is commonly used. Norepinephrine is easy to titrate and it is safe for peripheral administration. It is immediately available in most contexts. However, norepinephrine does function predominantly as an alpha-agonist, so it may increase the pulmonary vascular resistance (especially at higher doses).(32740380)
inhaled pulmonary vasodilators offer numerous benefits:
- (1) Improvement in oxygenation and ventilation, due to improved ventilation-perfusion matching.
- (2) Reduced pulmonary vascular resistance, which improves right ventricular failure.
- (3) Administration via inhalation generally doesn't cause systemic vasodilation or systemic hypotension (because the drug selectively vasodilates the pulmonary vasculature).
- With the exception of patients with substantial LV failure, pulmonary vasodilators offer several physiological benefits with very little downside (aside from cost and logistic considerations).
indications & contraindications
- The main contraindication to inhaled pulmonary vasodilators is severe left ventricular failure or pulmonary veno-occlusive disease. By increasing blood flow through the right ventricle, pulmonary vasodilators may increase the left ventricular preload. This could precipitate cardiogenic pulmonary edema among patients with left ventricular dysfunction.
- The exact indication for pulmonary vasodilators in right ventricular failure is unknown. Potential indications include:
- (1) Refractory hypoxemia (especially in the presence of a right-to-left shunt due to a patent foramen ovale).
- (2) Stabilization in the peri-intubation period.
- (3) RV failure patients with high risk of mortality.
- (4) Failure to respond to less aggressive treatments, as listed above.
- In the most dire situations, multiple different pulmonary vasodilators may be used simultaneously, to utilize different mechanisms of action on the pulmonary vasculature (e.g., nitric oxide plus epoprostenol).
For further discussion see the chapter on inhaled pulmonary vasodilators.
benefits:
- (1) Positive inotropy may improve RV function.
- (2) Vasodilation of the pulmonary vasculature may reduce the RV afterload.
risks/contraindications:
- (1) There may be a risk of tachyarrhythmia (especially atrial fibrillation).
- (2) Increasing contractility may exacerbate relative ischemia of the right ventricle.
- (3) Systemic vasodilation may promote hypotension.
clinical indications to consider inotropic therapy may include:
- (1) Systolic failure of the right ventricle (e.g., reduced TAPSE).
- (2) Inadequate systemic perfusion (especially if this occurs despite other measures – such as pulmonary vasodilators, volume optimization, and/or vasoconstrictor support).
- (3) Bradycardia, or a heart rate which seems inappropriately low (given the current level of physiological stress).
two options to add inotropy
- Epinephrine:
- Epinephrine functions largely as an inotrope, especially at lower doses. However, epinephrine does have enough alpha-activity to prevent hypotension. This makes it an attractive single agent for patients who require substantive inotropy and also vasoconstriction.
- For patients on norepinephrine who require inotropic activity, the norepinephrine may be switched to epinephrine. Using epinephrine as a single agent may be a simple and effective approach. This makes dose-titration easy (as opposed to using a combination of norepinephrine plus dobutamine, which can sometimes get combined in bizarre ratios).
- Epinephrine stimulates cardiac beta-1 and beta-2 receptors, which may allow it to be a more powerful inotrope than dobutamine (which selectively affects beta-1 receptors).
- Dobutamine:
- The usual dose range is 2-10 mcg/kg/min (at higher doses, there may be greater systemic vasodilation causing hypotension).(33541609)
- Dobutamine is generally favored over milrinone, since dobutamine is easier to titrate and supported by greater experience in pulmonary hypertension.
sildenafil
- Enteral sildenafil appears to be safe and effective in reducing pulmonary pressures. It has predominantly been investigated following cardiothoracic surgery.(30685151, 24987174, 24613188, 22057829, 21513610) The dose studied has often been ~20 mg q8hr.
- Sildenafil has not been well studied among a general ICU population. Currently, this might be considered in a context where all other therapies are failing. There is a risk that nonspecific pulmonary vasodilation could worsen ventilation/perfusion matching and thereby exacerbate hypoxemia.(20130830)
intravenous pulmonary vasodilators
- Intravenous pulmonary vasodilators (e.g., epoprostenol) should always be continued for patients who were previously on them.
- Rarely, IV epoprostenol might be initiated in the ICU for a patient with known pulmonary arterial hypertension (Type-1 pulmonary hypertension). The use of intravenous pulmonary vasodilators is trickier than inhaled pulmonary vasodilators, for three reasons:
- (1) Intravenous pulmonary vasodilators may cause systemic vasodilation, reducing the systemic blood pressure.
- (2) Intravenous pulmonary vasodilators will impair ventilation-perfusion matching, which may worsen oxygenation and ventilation.
- (3) Intravenous pulmonary vasodilators may function as a bridge to long-term intravenous pulmonary vasodilator use. Thus, they may be most suitable for patients who are candidates for long-term intravenous pulmonary vasodilator therapy.
- For these reasons, initiation of IV pulmonary vasodilator therapy should usually be performed in conjunction with a specialist in pulmonary hypertension.
ECMO
- VA ECMO offers the ability to support both circulation and gas exchange. However, VV ECMO could be used in situations where hypoxemia/hypercapnia was a primary driver of instability.(28979557)
- Precise indications are unclear, but would generally encompass the failure of less invasive therapy, as well as the presence of reversible pathology or transplant options (such that ECMO can function as either a bridge to recovery or as a bridge to transplant).
Intubation is fraught with peril for the patient with substantial RV failure. Patients may respond poorly to hypoxemia, hypercapnia, positive pressure, and sedation. When possible, patients and families should be informed regarding these risks and participate in informed consent. However, in the context of critical illness, this is often not possible.
There are a variety of different ways to approach this. The ideal way is arguably a hemodynamically neutral intubation, but this may be difficult to achieve on an emergent basis in many units.
A more accessible strategy is roughly as follows:
- The more you can optimize the patient prior to intubation, the better. If there are fixable processes, it's ideal to fix these prior to intubation. For example:
- Chest tube to drain a pneumothorax or pleural effusion.
- Systemic thrombolysis for a submassive or massive PE.
- Management of DKA (try to delay intubation as long as possible, to allow more time for this).
- Stabilize the blood pressure with RV-friendly agents (e.g., vasopressin plus epinephrine). Target a moderately elevated MAP prior to intubation (e.g. ~80 mm) if possible, with the anticipation that the MAP will decrease following intubation.
- Consider insertion of an arterial catheter.
- Plan the insertion depth of your endotracheal tube, using MDCalc here.
- Place the patient on BiPAP with 100% FiO2. Gradually increase the BiPAP settings to a moderate amount of support (e.g., 18 cm/12 cm). Follow hemodynamics carefully and titrate vasoactives as needed to maintain a healthy blood pressure. BiPAP allows you to ease the patient onto positive pressure ventilation slowly and in a reversible fashion. BiPAP is also a great modality to preoxygenate the patient and avoid derecruitment during intubation.
- Consider administration of a nebulized pulmonary vasodilator prior to intubation. Also, have a pulmonary vasodilator at the bedside ready to administer through the endotracheal tube as soon as the patient is intubated.
- Induce the patient with hemodynamically stable agents (e.g., ketamine plus rocuronium). Set the BiPAP device to provide apneic ventilation as the patient begins to become sedated, until you are about to insert the endotracheal tube (e.g., as described here).
- Intubate the patient as quickly as possible and immediately connect the patient to the ventilator. Provide cautious, lung-protective ventilation. Avoid aggressively bagging the patient, as this may increase intrathoracic pressure and precipitate cardiac arrest.
- Insert the ETT to the preplanned depth. Verify that it is not in the right mainstem bronchus.
- Immediately following intubation, initiate a pulmonary vasodilator at maximal dosage.
- Follow the patient's hemodynamics and capnographic waveform very closely for the following 15-30 minutes. This is a critical juncture when many patients may insidiously slip into an RV death spiral. Don't hesitate to aggressively escalate the epinephrine infusion if the blood pressure is falling.
- Check a blood gas and avoid hypercapnia (if possible).
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- Don't leave the room within 10 minutes of intubating a patient with pulmonary hypertension. This is when they usually crash: once the ETT is in, when everyone thinks that they're all set.
- Don't give fluid to a pulmonary hypertension patient unless you have an exceptionally good reason.
- If a pulmonary hypertension patient is chronically on intravenous vasodilator, ensure that this is never interrupted.
- Don't ignore pulmonary hypertension. You don't need to be a rocket scientist to treat this, but you do need to try.
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https://pubmed.ncbi.nlm.nih.gov/35953215/