Right Ventricular Dysfunction

Right Ventricular (RV) Failure: Questions and Answers

Pathophysiology of Right Ventricular Failure

What are the key features of normal RV function?
- Governed by systemic venous return, pulmonary artery pressure, pericardial compliance, and RV free wall/interventricular septum contractility.
- RV is volume-adapted: handles volume changes well but is sensitive to increases in afterload.
How does acute RV failure differ from chronic RV failure?
- Acute RV Failure:
  - Caused by increased RV afterload (e.g., PE, hypoxia, acidemia), increased RV preload (e.g., left-to-right shunt, tricuspid valve disease), or reduced RV contractility (e.g., MI, myocarditis).
  - Leads to RV wall stress, ischemia, and subsequent LV failure through:
    1. Decreased LV preload (RV output = LV preload).
    2. Septal bowing into LV, impairing diastolic filling.
- Chronic RV Failure:
  - Gradual increase in RV afterload due to pulmonary hypertension, pulmonic stenosis, or tricuspid regurgitation.
  - Progresses to the "RV death spiral" with ventricular dilatation, increased wall stress, and failure.

Clinical Features and Workup

What are the hallmark clinical signs of RV failure?
- Increased jugular venous pressure (JVP).
- Peripheral edema.
- RV heave and pulsatile liver.
- Split S2 with possible new tricuspid regurgitation murmur (holosystolic at LLSB).
What imaging and diagnostic tools are useful in RV failure?
- Imaging:
  - Chest X-ray: Look for RV enlargement (RV/LV ratio >0.9 suggests RV strain).
  - Echocardiogram: Assess RV size, function, and RVEF using parameters like TAPSE (≥17 mm indicates normal RV function).
- Invasive Monitoring:
  - Right heart catheterization (RHC): Gold standard to measure ventricular filling pressures, cardiac output, and PA pressures.
  - Key metrics include:
    - CVP/PCWP ratio (normal = 0.5; elevated in RV failure).
    - Pulmonary artery pulsatility index (PAPi): <0.9 suggests RV failure.
    - RV stroke work index.

Management Principles

How should preload be managed in RV failure?
- Volume depletion (e.g., in PE, tamponade, RVMI):
  - Use judicious IV fluid boluses (500–1000 mL) to optimize RV preload (goal CVP 10–14 mmHg in RVMI).
- Volume overload:
  - Initiate IV diuretics to reduce RV filling pressures and improve LV output.
What are the key strategies for afterload management?
- Systemic Afterload:
  - Avoid systemic hypotension; use vasopressors like vasopressin or norepinephrine.
  - Norepinephrine is preferred in profound hypotension; vasopressin has less impact on pulmonary vascular resistance (PVR).
- Pulmonary Afterload:
  - Remove factors that increase pulmonary vascular tone (e.g., correct hypoxemia, acidemia).
  - Consider pulmonary vasodilators (inhaled preferred over systemic) for pulmonary arterial hypertension:
    - Agents: Inhaled nitric oxide (iNO), prostacyclin agonists, endothelin receptor antagonists (e.g., bosentan), PDE-5 inhibitors (e.g., sildenafil).
When are inotropes indicated?
- Use dobutamine or milrinone to improve RV contractility and reduce pulmonary vascular resistance.
- Monitor for hypotension, especially with milrinone.
What are advanced interventions for refractory RV failure?
- Consider mechanical circulatory support:
  - Impella RP for RV support.
  - VA-ECMO for biventricular or severe cardiogenic shock.

Intubation Considerations

What precautions are needed for intubation in RV failure?
- Intubation can worsen RV afterload due to increased intrathoracic pressure, risking hemodynamic collapse.
- Use rapid sequence induction with agents like etomidate.
- Anticipate hypotension; prepare push-dose vasopressors (e.g., phenylephrine, epinephrine) and maintain low PEEP (<12 cm H2O) and moderate tidal volumes (~8 mL/kg).

Key Additional Points on Right Ventricular (RV) Failure Management

Advanced Hemodynamic Considerations

Perfusion Pressure vs. MAP Alone:
- Effective perfusion pressure is MAP minus CVP. A CVP of 20 mmHg with MAP of 65 results in a perfusion pressure of only 45 mmHg, which is insufficient.
- Optimize perfusion by maintaining MAP >65 mmHg and considering even higher targets in high CVP states.
Volume Responsiveness:
- Traditional markers (e.g., pulse pressure variation) may be misleading due to reverse pulsus paradoxus in RV failure.
- Early echocardiography is crucial to assess volume status:
  - Hypovolemia (e.g., RVMI): May need careful fluid boluses.
  - Volume overload (e.g., RV failure due to PE or pulmonary hypertension): Avoid fluids; consider aggressive diuresis.

Pharmacologic Management

Vasopressors:
- Preferred Agents: Norepinephrine or vasopressin to support systemic pressures without increasing pulmonary vascular resistance.
- Avoid Phenylephrine: Pure alpha agonist; worsens pulmonary afterload.
Inotropes:
- First-line: Dobutamine or epinephrine.
- Alternative: Milrinone (use cautiously as it is harder to titrate and may exacerbate hypotension).
- Monitor response with echocardiography; switch agents if needed.
Pulmonary Vasodilators:
- Inhaled nitric oxide or prostacyclin analogs (e.g., epoprostenol).
- Effective in isolated RV afterload problems such as massive PE.
- Delivery: High-flow nasal cannula, ventilator, or non-invasive setups.

Oxygenation and Acid-Base Balance

Oxygenation Targets:
- Maintain SpO₂ ≥95% to reduce hypoxia-induced pulmonary vasoconstriction.
- Prioritize high-flow nasal cannula or non-invasive ventilation.
Acidosis Management:
- Metabolic acidosis (pH <7.2) worsens pulmonary vascular resistance.
- Bicarbonate: Use judiciously in severe acidosis to increase pH >7.2.
  - Be cautious with volume-overloaded patients, as bicarbonate can increase intravascular volume.

Advanced Therapies

Pulmonary Vasodilator Access:
- Check availability of inhaled therapies in specialized hospital units (NICU, PICU, cardiovascular ICUs).
- Discuss logistical and setup requirements with pharmacy or critical care teams in advance.

Practical Application

Early Echo Use:
- Essential for volume assessment and guiding therapy.
- Monitor TAPSE (<10 mm indicates severe dysfunction) and treatment response.
Multidisciplinary Collaboration:
- Coordinate with ICU teams, cardiology, and respiratory therapy for seamless implementation of advanced therapies.

Intubation in Right Ventricular (RV) Failure: Practical Guidance and Key Considerations

When to Intubate

Avoid intubation unless absolutely necessary, as it poses a high risk of peri-intubation cardiovascular collapse.
Situations requiring intubation:
- Refractory respiratory failure (e.g., pneumonia with interstitial lung disease).
- Intractable vomiting or aspiration.
- Severe ventilatory failure where non-invasive measures fail.

Preparation for Intubation

Optimize Physiology Beforehand:
- Preoxygenation:
  - Use high-flow nasal cannula or BiPAP through a ventilator.
  - Start positive pressure early to assess hemodynamic response.
- Hemodynamic Support:
  - Ensure vasopressors (e.g., norepinephrine, vasopressin) are running before intubation.
  - Push MAP to 75 mmHg in severely ill pulmonary hypertensive patients.
- Medications:
  - Use lower doses of sedatives (e.g., ketamine) in shock.
  - High doses of paralytics (e.g., rocuronium) to ensure adequate paralysis.
Team and Equipment Ready:
- Ensure the availability of post-intubation support (e.g., ECMO team or cardiology consultation for circulatory collapse).

Ventilator Strategy Post-Intubation

PEEP Considerations:
- Avoid excessive PEEP, but do not allow lung derecruitment.
- Adjust to achieve lung recruitment (clear chest X-ray with smooth diaphragms) without over-distension.
Avoiding Hypoxia and Hypercarbia:
- Maintain SpO₂ >92%, ideally ≥95% to prevent hypoxia-induced pulmonary vasoconstriction.
- Manage ventilation to prevent hypercapnia and acidosis.
Post-Intubation Monitoring:
- Stay at bedside for extended monitoring of perfusion, BP, oxygenation, and end-tidal CO₂.

Advanced Interventions

Mechanical Circulatory Support:
- VA-ECMO for profound shock unresponsive to medical therapy.
- Coordinate with perfusion and cannulation teams in advance.
Specialty Medications:
- Continue pulmonary vasodilators like prostacyclin analogs for known pulmonary arterial hypertension patients.
- Rapidly reinstate continuous infusions of critical medications (e.g., epoprostenol) if previously interrupted.

Key Takeaways

Intubation is a high-risk intervention in RV failure but unavoidable in some situations.
Meticulous preparation, peri-intubation hemodynamic support, and careful ventilator settings are critical to minimizing risks.
Leverage institutional resources (e.g., ECMO, pulmonary hypertension specialists) for complex cases.

This comprehensive approach aims to stabilize critically ill patients while mitigating the significant risks associated with intubation in the setting of RV failure.

Comparison of the Right Ventricle (RV) vs. Left Ventricle (LV)

Anatomical Differences

Feature	Right Ventricle (RV)	Left Ventricle (LV)
Wall Thickness	Thin (~3-5 mm)	Thick (~10-15 mm)
Chamber Shape	Crescent-shaped; wraps around the LV	Conical and elliptical
Structure	Composed of inflow tract, apex, and outflow tract	Consists of inflow and outflow chambers
Fiber Orientation	Longitudinal fibers; less overlap	Concentric fibers; high overlap for strong contraction

Physiological Differences

Feature	Right Ventricle (RV)	Left Ventricle (LV)
Primary Role	Pumps deoxygenated blood to low-resistance pulmonary circulation	Pumps oxygenated blood to high-resistance systemic circulation
Pressure Tolerance	Designed for low-pressure environment (15-25 mmHg systolic)	Handles high-pressure environment (90-140 mmHg systolic)
Compliance	Highly compliant; tolerates large volume changes	Less compliant; better suited for high pressures
Stroke Volume Dependency	Highly sensitive to preload (volume changes)	Sensitive to both preload and afterload
Perfusion Timing	Continuous perfusion throughout the cardiac cycle	Perfused primarily during diastole due to high systolic wall tension

Pathophysiology and Failure Modes

Feature	Right Ventricle (RV)	Left Ventricle (LV)
Response to Afterload	Highly sensitive to afterload: even moderate increases (e.g., PA pressure >20 mmHg) can reduce output significantly	More resilient to afterload changes due to thicker walls
Failure Mechanisms	Fails primarily due to increased afterload (e.g., pulmonary hypertension, PE)	Fails due to ischemia, increased afterload (e.g., systemic hypertension)
Clinical Presentation of Failure	Systemic venous congestion (JVD, ascites, peripheral edema)	Pulmonary congestion (dyspnea, pulmonary edema)

Functional Adaptations

Feature	Right Ventricle (RV)	Left Ventricle (LV)
Energy Efficiency	Highly efficient pump; optimized for low energy demand	High-energy pump; optimized for forceful ejection
Contractile Dynamics	Primarily longitudinal contraction	Both longitudinal and radial contraction for efficient output
Coupling with Circulation	Designed to work with low-resistance pulmonary circulation	Adapts to systemic circulation with high resistance

Clinical Implications

RV Failure:
- Caused by increased afterload (e.g., pulmonary hypertension, PE), decreased preload (e.g., tamponade), or reduced contractility (e.g., RVMI).
- Leads to systemic venous congestion.
- Management focuses on reducing afterload and optimizing preload without excessive fluids.
LV Failure:
- Driven by ischemic damage, pressure overload (e.g., hypertension), or volume overload (e.g., valvular regurgitation).
- Leads to pulmonary congestion and systemic hypoperfusion.
- Treatment targets reducing afterload and improving contractility.

Summary

The RV is a low-pressure, high-compliance pump optimized for volume handling, while the LV is a high-pressure, high-force pump designed for systemic circulation. These structural and functional differences underlie distinct failure mechanisms and guide tailored management strategies for conditions involving the right vs. left heart.

Right Ventricular (RV) Failure: Clinical Overview and Key Management Principles

Clinical Recognition

Key symptoms and signs:
- Hypotension and shock without clear lung findings.
- Abdominal discomfort, peripheral edema, increased jugular venous pressure (JVP).
- Clear lungs in acute conditions like pulmonary embolism (PE).
- Contributing factors:
  - Chronic lung disease, pneumonia, arrhythmias.
  - Acute triggers: Massive PE, myocardial infarction (MI), lung collapse, post-cardiac arrest states.
Diagnostics:
- ECG Findings:
  - Right axis deviation, anterior ST depression, S1Q3T3 pattern (non-specific).
- Imaging:
  - Chest X-ray: Enlarged right heart border or clear lungs.
  - CT scan:
    - RV
      ratio >0.9 indicates RV strain.
    - Septal flattening and reflux of contrast into the IVC/hepatic veins.
- Echocardiogram (POCUS):
  - TAPSE (<17 mm indicates RV dysfunction).
  - Dilated RV, flattened septum, reduced tricuspid annular motion.
  - IVC dilation >2 cm: Suggests fluid overload; avoid fluid boluses.

Management Framework

Stabilization Goals:
- Defend oxygenation/ventilation:
  - Use high-flow nasal cannula.
  - Liberal oxygen supplementation to avoid hypoxia-induced pulmonary vasoconstriction.
- Defend mean arterial pressure (MAP ≥ 65 mmHg):
  - Consider higher MAP targets in the presence of elevated central venous pressure (CVP).
- Maintain sinus rhythm:
  - Early cardioversion for arrhythmias to optimize RV filling and output.
Volume Management:
- Avoid aggressive IV fluids:
  - Patients with dilated IVC are likely to worsen with fluids.
- Diuretics for congestion:
  - IV furosemide or equivalent to reduce systemic congestion and relieve RV overload.
Hemodynamic Support:
- Inotropes:
  - Dobutamine or milrinone to enhance RV contractility and reduce pulmonary vascular resistance.
- Vasopressors:
  - Norepinephrine preferred for systemic hypotension.
  - Avoid pure alpha-agonists like phenylephrine due to their potential to worsen pulmonary hypertension.
Pulmonary Vasodilation:
- Selective Pulmonary Vasodilators:
  - Inhaled nitric oxide or epoprostenol for pulmonary arterial hypertension.
- Ensure continuation of chronic therapies (e.g., sildenafil, bosentan, prostacyclins).
Intubation and Mechanical Ventilation:
- Avoid intubation if possible:
  - Increases intrathoracic pressure and worsens RV afterload.
- If necessary:
  - Use rapid sequence induction with agents like etomidate.
  - Apply low PEEP and moderate tidal volumes to minimize afterload impact.

Monitoring and Advanced Interventions

Monitor RV response to therapies via serial echocardiograms and invasive hemodynamic measurements.
Consider mechanical circulatory support for refractory cases:

Impella RP for isolated RV support.
VA-ECMO for biventricular failure.

https://www.youtube.com/watch?v=KudZpzw53Cw&ab_channel=umemergencymed%E2%80%9CUMEM%E2%80%9D

Crashing PE and Right Ventricular (RV) Failure: Q&A Breakdown

Understanding the Problem

What makes the right ventricle (RV) vulnerable to strain in acute pulmonary hypertension (PH)?
- The RV is thin-walled and designed for low-pressure pulmonary circulation.
- It relies on efficiency, not force, making it sensitive to even small increases in pulmonary vascular resistance (PVR).
- Conditions like hypoxemia, hypercapnia, acidosis, and pulmonary edema exacerbate PVR, causing RV strain.

Recognizing RV Dysfunction

What are the early signs of RV dysfunction in acute pulmonary hypertension?
- RV dilation is the first sign as the ventricle adapts to afterload stress.
- Echocardiogram findings include:
  - RV
    ratio ≥1:1.
  - Decreased tricuspid annular plane systolic excursion (TAPSE).
  - Septal flattening (D-shaped septum on imaging).
What common interventions exacerbate RV dysfunction?
- Intubation and mechanical ventilation:
  - Overdistension of alveoli compresses peri-alveolar vessels, worsening PVR.
  - Mismanagement of tidal volume and PEEP increases RV afterload.

Physiologic Principles of Management

Why does the RV respond differently from the LV under stress?
- The LV’s concentric fibers and thick walls make it adept at handling high afterload.
- The RV’s helical fibers and thin walls prioritize compliance, limiting its ability to handle increased pressure.
What is the priority in managing RV dysfunction?
- Avoid interventions that increase PVR:
  - Maintain oxygenation to prevent hypoxemia-induced vasoconstriction.
  - Correct acidosis and hypercapnia to reduce vasoconstriction.
  - Use low tidal volume and appropriate PEEP during ventilation.

Management Strategies for Crashing PE

What are the initial steps in resuscitating a crashing PE patient?
- Oxygenation: Target SpO₂ ≥95% to prevent hypoxemia.
- Hemodynamics:
  - Use vasopressors like norepinephrine to support systemic pressure.
  - Avoid pure alpha agonists like phenylephrine, which can increase PVR.
- Echocardiography:
  - Use bedside ultrasound to assess RV dilation and septal motion.
What ventilator settings should be used if intubation is unavoidable?
- Low tidal volume (4-6 mL/kg predicted body weight).
- Minimize PEEP to avoid alveolar overdistension.
- Monitor driving pressures to ensure efficient airflow distribution.

Advanced Therapies

When should mechanical circulatory support be considered?
- Use VA-ECMO in profound RV failure unresponsive to medical therapy.
- Consider thrombolytics for massive PE with hemodynamic instability.
What is the role of inhaled pulmonary vasodilators?
- Inhaled nitric oxide or prostacyclins can reduce PVR without systemic side effects.
- Consider in settings of acute RV failure, such as massive PE.

Key Pearls and Pitfalls

Key pearls:
- Think size before function: RV dilation is the earliest sign of dysfunction.
- Optimize oxygenation and ventilation; avoid hyperoxia or hypercapnia.
- Use bedside echocardiography early and often to guide interventions.
- Ensure appropriate vasopressor and inotrope selection.
Common pitfalls:
- Aggressive fluid resuscitation worsens RV strain in most cases.
- Poorly managed intubation and ventilation can precipitate RV collapse.
- Ignoring early signs of RV dysfunction (e.g., RV dilation on imaging).

This structured approach emphasizes early recognition and targeted management strategies to stabilize the crashing PE patient and minimize the risk of RV collapse.

SamuelYHuang

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