3.3 Pulmonary Hypertension & Right Ventricular Failure in the ICU

ABIM Critical Care Medicine Study Guide Exam

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1 Chapter 1: Exam Orientation: Format, Blueprint & Study Strategy

1.1 ABIM Critical Care Medicine Exam: Format, Blueprint & Study Strategy

2 Chapter 2: Acute Respiratory Failure & ARDS

2.1 ARDS Definition, Pathophysiology & Phenotypes 2.2 Lung-Protective Mechanical Ventilation 2.3 Refractory ARDS: Prone Positioning, Neuromuscular Blockade & VV-ECMO

3 Chapter 3: Obstructive Airways, Pulmonary Vascular & Pleural Emergencies

3.1 Severe Asthma & COPD Exacerbations in the ICU 3.2 Massive & Submassive Pulmonary Embolism 3.3 Pulmonary Hypertension & Right Ventricular Failure in the ICU 3.4 Massive Hemoptysis, Complex Pleural Effusions & Thoracic Drainage

4 Chapter 4: Airway, Parenchymal & Nonthrombotic Pulmonary Emergencies

4.1 Airway Management, Upper-Airway Obstruction & Artificial-Airway Complications 4.2 Diffuse Alveolar Hemorrhage, Interstitial Lung Disease, Pulmonary Vasculitis & Noncardiogenic Edema 4.3 Severe Community-Acquired & Viral Pneumonia 4.4 Nonthrombotic Embolism (Air, Fat, Amniotic Fluid, Tumor, Septic) & Acute Chest Syndrome

5 Chapter 5: Mechanical Ventilation Modes, Dyssynchrony & Liberation

5.1 Mechanical Ventilator Modes & Advanced Breath Delivery 5.2 Patient-Ventilator Dyssynchrony & Waveform Analysis 5.3 Ventilator Liberation, Spontaneous Breathing Trials & Post-Extubation Support

6 Chapter 6: Shock Syndromes & Hemodynamic Principles

6.1 Shock Classification, Cellular Pathophysiology & Biomarkers 6.2 Hemodynamic Monitoring: Arterial Lines, CVP & Pulmonary Artery Catheter 6.3 Dynamic Assessment of Fluid Responsiveness & Resuscitation Targets

7 Chapter 7: Vasoactive Therapies & Mechanical Circulatory Support

7.1 Vasopressors & Inotropes: Pharmacology & Clinical Titration 7.2 Temporary Mechanical Circulatory Support: IABP, Impella & TandemHeart 7.3 Venoarterial ECMO (VA-ECMO) & Differential Hypoxemia 7.4 Post-Cardiac Arrest Care, Targeted Temperature Management & Neuroprognostication

8 Chapter 8: Acute Kidney Injury & Renal Replacement Therapy

8.1 KDIGO AKI Classification, Etiologies & Diagnostic Evaluation 8.2 Continuous Renal Replacement Therapy (CRRT) vs Intermittent Hemodialysis 8.3 Indications & Timing for RRT in Critical Illness: AKIKI & STARRT-AKI

9 Chapter 9: Electrolyte, Acid-Base & Endocrine Emergencies

9.1 Severe Dysnatremias: Hyponatremia, Hypernatremia & Osmotic Demyelination 9.2 Potassium, Calcium, Magnesium & Phosphate Disorders 9.3 Complex & Mixed Acid-Base Disorders: Boston vs Copenhagen vs Stewart 9.4 Endocrine Crises: DKA, HHS, Thyroid Storm, Myxedema Coma & Adrenal Crisis

10 Chapter 10: Glycemic Control, Hyperammonemia, Pituitary & Adrenal Disorders

10.1 ICU Glycemic Control & Severe Hypoglycemia 10.2 Non-Hepatic Hyperammonemia & Metabolic Encephalopathy 10.3 Pituitary Emergencies, Adrenal Excess & Critical Illness-Related Corticosteroid Insufficiency

11 Chapter 11: Acute Coronary Syndromes & Cardiac Arrhythmias

11.1 Acute Coronary Syndromes & Mechanical Complications of Myocardial Infarction 11.2 Critical Tachyarrhythmias: Atrial Fibrillation with RVR, VT & VF 11.3 Critical Bradyarrhythmias, Conduction Blocks & Temporary Cardiac Pacing

12 Chapter 12: Acute Heart Failure, Valvular & Pericardial Emergencies

12.1 Acute Decompensated Heart Failure & Cardiogenic Pulmonary Edema 12.2 Acute Valvular Regurgitation & Prosthetic Valve Emergencies 12.3 Pericardial Tamponade & Acute Aortic Syndromes

13 Chapter 13: Myocardial Disease, Hypertensive & Cardiac Device Emergencies

13.1 Fulminant Myocarditis, Stress & Peripartum Cardiomyopathy, and Hypertrophic Cardiomyopathy 13.2 Hypertensive Emergencies & Ruptured Abdominal Aortic Aneurysm 13.3 Implanted Cardiac Devices, LVAD Emergencies & Electrical Storm

14 Chapter 14: Sepsis & Systemic Infectious Diseases

14.1 Sepsis-3 Definitions & Surviving Sepsis Campaign 2026 Guidelines 14.2 Refractory Septic Shock & Adjunctive Therapies 14.3 Multidrug-Resistant Pathogens & Antimicrobial Stewardship in the ICU

15 Chapter 15: ICU-Acquired & Severe Focal Infections

15.1 Hospital-Acquired & Ventilator-Associated Pneumonia 15.2 Central Line-Associated Bloodstream Infections & Catheter-Associated UTIs 15.3 Intra-Abdominal Sepsis, Necrotizing Soft Tissue Infections & CNS Infections

16 Chapter 16: Focal, Special-Host & Systemic Infections

16.1 CNS Infections Beyond Bacterial Meningitis: Encephalitis, Brain Abscess & Epidural Abscess 16.2 Infections in the Immunocompromised Host, Tropical & Bioterror Infections 16.3 Infective Endocarditis, Device Infections & Other Focal Cardiovascular Infections 16.4 Antimicrobial Pharmacokinetics, Allergy, Toxicity & Infection Prevention 16.5 Gastrointestinal & Hepatobiliary Infections: Fulminant C. difficile, Typhlitis, CMV Colitis & Abscesses

17 Chapter 17: Neurocritical Care & Coma

17.1 Coma, Altered Mental Status & Acute Delirium in the ICU 17.2 Status Epilepticus & Non-Convulsive Status Epilepticus 17.3 Acute Ischemic Stroke & Intracranial Hemorrhage

18 Chapter 18: Cerebrovascular Syndromes, Encephalopathy & Withdrawal States

18.1 Cerebral Venous Sinus Thrombosis, PRES & Reversible Cerebral Vasoconstriction Syndrome 18.2 Alcohol & Sedative Withdrawal, Wernicke Encephalopathy & Drug-Induced Encephalopathy

19 Chapter 19: Intracranial Hypertension & Neuromuscular Weakness

19.1 Intracranial Pressure Monitoring, Cerebral Perfusion & Tiered ICP Management 19.2 Acute Neuromuscular Respiratory Failure, ICU-Acquired Weakness & Brain Death Determination

20 Chapter 20: Traumatic Brain Injury, Spinal Cord Injury & Toxin-Mediated Paralysis

20.1 Traumatic Brain Injury Management & Paroxysmal Sympathetic Hyperactivity 20.2 Acute Spinal Cord Injury, Neurogenic Shock & Autonomic Dysreflexia 20.3 Toxin-Mediated Paralysis & Neuromuscular Crises: Botulism, Tetanus, Tick Paralysis & Myasthenic Crisis

21 Chapter 21: Gastrointestinal, Hepatic & Abdominal Emergencies

21.1 Acute Upper & Lower Gastrointestinal Bleeding in the ICU 21.2 Acute Liver Failure & Severe Acute Pancreatitis 21.3 Abdominal Compartment Syndrome & Acute Mesenteric Ischemia

22 Chapter 22: Luminal GI Emergencies & Complications of Cirrhosis

22.1 Esophageal, Gastric & Bowel Emergencies: Perforation, Obstruction, Ogilvie Syndrome & Colonic Ischemia 22.2 Complications of Cirrhosis: Alcohol-Associated Hepatitis, Hepatorenal Syndrome & Pulmonary Vascular Syndromes

23 Chapter 23: Trauma, Burns & Perioperative Critical Care

23.1 Polytrauma Resuscitation, Damage Control & Massive Transfusion 23.2 Severe Burn Injury, Inhalation Injury & Environmental Emergencies 23.3 Perioperative Critical Care for High-Risk Surgical Patients

24 Chapter 24: Thoracic Trauma, Environmental Injury & Obstetric Critical Care

24.1 Thoracic Trauma: Flail Chest, Pulmonary Contusion, Great Vessel & Tracheobronchial Injury 24.2 Environmental Injury: Drowning, Diving, Altitude, Heat, Cold, Electrical & Radiation 24.3 Obstetric & Genitourinary Emergencies and the Physiology of Pregnancy

25 Chapter 25: Transplantation, Donor Management & Post-Cardiac Surgery Care

25.1 Solid Organ Transplant Recipients & Deceased Donor Management 25.2 Post-Cardiac Surgery Critical Care: Bleeding, Tamponade, Low Output & Vasoplegia

26 Chapter 26: Hematologic Emergencies, Toxicology, Critical Ultrasound & ICU Liberation

26.1 Hematologic Emergencies in the ICU: HIT, DIC, TMA & Anticoagulant Reversal 26.2 Critical Care Toxicology, Toxidromes & Specific Antidotes 26.3 Critical Care Point-of-Care Ultrasound (POCUS) 26.4 ICU Liberation, Analgosedation, Goals of Care & Critical Care Ethics

27 Chapter 27: Transfusion Medicine, Hematologic & Oncologic Disorders

27.1 Transfusion Medicine: Products, Thresholds, Reactions & Apheresis 27.2 Red and White Cell Disorders, Hemoglobinopathies, Factor Deficiencies & Hypercoagulable States 27.3 Oncologic Emergencies, Hematopoietic Cell Transplant Complications & Cellular Therapy Toxicity

28 Chapter 28: Clinical Pharmacology, Adverse Drug Reactions & Specific Poisonings

28.1 Pharmacokinetic Principles, Dose Adjustment & Drug Interactions in Critical Illness 28.2 Adverse Drug Reactions: Anaphylaxis, Severe Cutaneous Reactions & Hyperthermic Syndromes 28.3 Specific Poisonings: Sodium-Channel Blockers, Lithium, Valproate, Theophylline, Iron, Sulfonylureas & Methemoglobinemia

29 Chapter 29: Ethics, Research Methods, Administration & Abdominal Ultrasound

29.1 Advance Care Planning, Nonbeneficial Treatment, Informed Consent & Confidentiality 29.2 Critical Care Research Methods, Statistics, IRB Oversight & Quality Improvement 29.3 Abdominal, Vascular & Procedural Point-of-Care Ultrasound

3.3 Pulmonary Hypertension & Right Ventricular Failure in the ICU

Key Takeaways Explain This Topic AI

Pulmonary hypertension is defined hemodynamically by a resting mean pulmonary artery pressure (mPAP) >20 mmHg on right heart catheterization, classified across five clinical WHO categories.

The 'RV death spiral' is driven by ventricular interdependence: acute afterload spikes dilate the thin-walled RV, inducing functional tricuspid regurgitation and shifting the interventricular septum leftward, which compromises LV filling, drops cardiac output, and obliterates right coronary artery perfusion.

Fluid resuscitation must be strictly restricted; the failing RV is on the flat or descending limb of the Frank-Starling curve, and over-resuscitation worsens tricuspid regurgitation and septal bowing.

Systemic perfusion pressure must be aggressively maintained with norepinephrine or vasopressin to ensure MAP > mPAP, preserving right coronary perfusion pressure.

Inhaled selective pulmonary vasodilators (inhaled epoprostenol or inhaled nitric oxide) lower pulmonary vascular resistance and improve V/Q matching without precipitating systemic arterial hypotension.

Last updated: October 2026

Acute right ventricular (RV) failure is a catastrophic hemodynamic syndrome characterized by the inability of the right ventricle to generate adequate forward stroke volume to maintain left ventricular filling, leading to systemic venous congestion, tissue hypoperfusion, and cardiogenic shock. In the intensive care unit, acute RV failure may occur as de novo decompensation (e.g., massive pulmonary embolism, acute respiratory distress syndrome) or as an acute-on-chronic crisis in patients with underlying pulmonary arterial hypertension (PAH).

Classification & Hemodynamics of Pulmonary Hypertension

Pulmonary hypertension (PH) is defined hemodynamically by a resting mean pulmonary artery pressure (mPAP) > 20 mmHg >20\text{ mmHg} > 20 mmHg measured via right heart catheterization.

Hemodynamic Phenotypes

Pre-Capillary PH: Defined by mPAP > 20 mmHg \text{mPAP} > 20\text{ mmHg} mPAP > 20 mmHg , Pulmonary Arterial Wedge Pressure ( PAWP ≤ 15 mmHg \text{PAWP} \le 15\text{ mmHg} PAWP ≤ 15 mmHg ), and Pulmonary Vascular Resistance ( PVR > 2 Wood Units \text{PVR} > 2\text{ Wood Units} PVR > 2 Wood Units ; 2022 ESC/ERS). Typical of WHO Groups 1, 3, 4, and 5.

Post-Capillary PH: Defined by mPAP > 20 mmHg \text{mPAP} > 20\text{ mmHg} mPAP > 20 mmHg and PAWP > 15 mmHg \text{PAWP} > 15\text{ mmHg} PAWP > 15 mmHg . Driven by elevated left-sided filling pressures (WHO Group 2). Subdivided into:

Isolated Post-Capillary PH (IpcPH): PVR ≤ 2 Wood Units \text{PVR} \le 2\text{ Wood Units} PVR ≤ 2 Wood Units .

Combined Post- and Pre-Capillary PH (CpcPH): PVR > 2 Wood Units \text{PVR} > 2\text{ Wood Units} PVR > 2 Wood Units , indicating reactive vascular remodeling.

The Five WHO Diagnostic Groups WHO Pulmonary Hypertension Diagnostic Classification:

├── Group 1: Pulmonary Arterial Hypertension (PAH)

│ └── Idiopathic, heritable, drug/toxin-induced, connective tissue disease (scleroderma), HIV, portal hypertension

• ├── Group 2: PH Secondary to Left Heart Disease (Most Common)
• │ └── Heart failure with preserved ejection fraction (HFpEF), HFrEF, mitral/aortic valvular disease
• ├── Group 3: PH Secondary to Lung Diseases and/or Hypoxia
• │ └── COPD, interstitial lung disease (ILD), obstructive sleep apnea, chronic high-altitude exposure
• ├── Group 4: Chronic Thromboembolic Pulmonary Hypertension (CTEPH)
• │ └── Recurrent/unresolved pulmonary thromboemboli, amenable to pulmonary thromboendarterectomy (PTE)
• └── Group 5: PH with Unclear or Multifactorial Mechanisms
• └── Hematologic disorders (myeloproliferative diseases), sarcoidosis, histiocytosis X, chronic renal failure
• The Biomechanics of the RV & the "Death Spiral"
• Unique RV Anatomy and Physiology

The right ventricle is a thin-walled, compliant, crescent-shaped pump wrapped around the muscular, conical left ventricle. Under normal physiological conditions:

The RV operates against a low-pressure, highly distensible pulmonary vascular bed with a resistance approximately one-tenth that of the systemic circulation.

Unlike the left ventricle (which is perfused by coronary flow almost exclusively during diastole), the thin-walled RV is perfused by the right coronary artery (RCA) during both systole and diastole because normal RV peak systolic pressure ( 20 – 25 mmHg 20–25\text{ mmHg} 20–25 mmHg ) is far below systemic aortic systolic pressure ( 100 – 120 mmHg 100–120\text{ mmHg} 100–120 mmHg ).

The RV adapts poorly to acute spikes in afterload. An acute elevation in PVR rapidly overpowers the contractile reserve of the non-hypertrophied RV.

• The Pathophysiologic Cascade of the RV Death Spiral Acute Increase in RV Afterload (PVR)
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• Acute RV Dilation & Wall Tension Spikes
• (Laplace's Law: σ = P·r / 2h)
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• Severe Functional Tricuspid Regurgitation
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• Ventricular Interdependence
• (Septum shifts leftward into LV → "D-shaped" LV)
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• Impaired LV Diastolic Filling & Preload
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• Marked Fall in Cardiac Output & SBP (MAP)
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• Severe Drop in RV Coronary Perfusion Pressure
• (CPPRV = MAP - RVSP ≤ 0)
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• RV Subendocardial Myocardial Ischemia
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• Worsening RV Contractile Failure → PEA Arrest

Afterload Spike: Acute increases in PVR (from PE, hypoxia, hypercapnia, acidosis, or high intrathoracic ventilator pressure) cause acute RV afterload mismatch.

Chamber Dilation & Tricuspid Regurgitation: The RV dilates to recruit preload via the Frank-Starling mechanism. However, as it dilates, the tricuspid valve annulus widens, producing severe, functional tricuspid regurgitation. Blood regurgitates into the right atrium, driving central venous pressure (CVP) upwards of 18 – 25 mmHg 18–25\text{ mmHg} 18–25 mmHg and causing end-organ venous congestion.

Ventricular Interdependence: Because both ventricles share common circumferential myocardial fibers, the interventricular septum, and a non-distensible pericardium, RV dilatation shifts the interventricular septum toward the left ventricular cavity. On short-axis echocardiography, the LV assumes a characteristic "D-shaped" morphology in diastole , restricting LV volume, lowering LV compliance, and drastically reducing LV end-diastolic volume (preload).

Cardiogenic Shock & Ischemia: Compromised LV filling causes systemic cardiac output and mean arterial pressure (MAP) to plummet. Concurrently, RV systolic pressure (RVSP) rises to equal or exceed systemic pressure. The perfusion pressure of the right ventricle is governed by:

CPP RV = MAP − RVSP \text{CPP}_{\text{RV}} = \text{MAP} - \text{RVSP} CPP RV ​ = MAP − RVSP

When RVSP approaches MAP, RCA flow during systole ceases entirely; perfusion is restricted to a brief diastolic window. This produces profound RV subendocardial ischemia , culminating in fatal electromechanical dissociation.

Principles of RV-Directed Resuscitation in the ICU

Management of the failing right ventricle requires a strict, physiologically driven resuscitation protocol anchored on four therapeutic goals: Four Pillars of RV Resuscitation:

• ├── 1. Preload Optimization: Strict volume limitation; judicious diuresis for congestion
• ├── 2. Systemic Perfusion: Maintain MAP > mPAP (target MAP 65–75 mmHg) with norepinephrine/vasopressin
• ├── 3. Inotropy: Augment RV contractility with low-dose dobutamine or milrinone (paired with vasopressor)
• └── 4. Afterload Reduction: Inhaled epoprostenol or inhaled nitric oxide (avoid systemic vasodilators)
• Pillar 1: Preload Optimization

Caution

The knee-jerk administration of intravenous crystalloid boluses in acute RV shock is frequently fatal. While hypovolemia should be corrected, an already dilated RV is positioned on the flat or descending limb of the Frank-Starling curve. Excess fluid worsens tricuspid regurgitation, exacerbates septal displacement into the LV, and further crushes cardiac output.

Fluid Challenge: Only indicated if the patient has unambiguous evidence of hypovolemia (e.g., CVP < 8 mmHg <8\text{ mmHg} < 8 mmHg , flat non-distended IVC). If attempted, volume should be administered in small, monitored aliquots of 250 mL 250\text{ mL} 250 mL crystalloid.

Volume Overload Decompression: When CVP is elevated ( > 12 – 15 mmHg >12–15\text{ mmHg} > 12–15 mmHg ) and physical exam confirms systemic congestion (hepatomegaly, ascites, peripheral edema), careful diuresis with intravenous loop diuretics (furosemide) or continuous venovenous ultrafiltration (CRRT) is paradoxically life-saving. Decompressing the RV relieves interventricular septal flattening, restores LV diastolic filling, and augments systemic cardiac output.

Pillar 2: Restoring Systemic Perfusion Pressure

To restore right coronary artery perfusion, mean arterial pressure must be vigorously defended to ensure MAP > mPAP \text{MAP} > \text{mPAP} MAP > mPAP (typically targeting MAP ≥ 65 – 75 mmHg \text{MAP} \ge 65–75\text{ mmHg} MAP ≥ 65–75 mmHg ):

Norepinephrine: The first-line vasopressor in acute RV failure. By stimulating vascular α 1 \alpha_1 α 1 ​ receptors, it elevates systemic vascular resistance (SVR) and aortic diastolic pressure, immediately restoring RCA perfusion. Concomitant β 1 \beta_1 β 1 ​ stimulation provides inotropic support to the RV without causing disproportionate increases in PVR.

Vasopressin: An ideal second-line adjunct dosed at 0.01 – 0.03 units/min 0.01–0.03\text{ units/min} 0.01–0.03 units/min . Vasopressin constricts systemic arterioles via vascular V 1 V_1 V 1 ​ receptors while causing selective pulmonary vasodilation at low doses through endothelial nitric oxide release, effectively raising MAP without elevating PVR.

Agents to Avoid: Pure α 1 \alpha_1 α 1 ​ agonists like phenylephrine are generally avoided as sole agents because they can raise PVR and provide no inotropy; vasopressin or norepinephrine is preferred to support systemic pressure.

Pillar 3: Augmenting RV Inotropy

Dobutamine: Initiated at low doses ( 2 – 5 μ g/kg/min 2–5\ \mu\text{g/kg/min} 2–5 μ g/kg/min ). Stimulates myocardial β 1 \beta_1 β 1 ​ receptors, augmenting RV contractility and reducing PVR via mild β 2 \beta_2 β 2 ​ vasodilation. Doses above 10 μ g/kg/min 10\ \mu\text{g/kg/min} 10 μ g/kg/min should be avoided due to tachycardia and peripheral vasodilation.

Milrinone: A phosphodiesterase-3 (PDE-3) inhibitor. It prevents cAMP degradation, providing powerful combined inotropy and pulmonary afterload reduction ("inodilator"). However, milrinone has a long elimination half-life ( 2 – 4 hours 2–4\text{ hours} 2–4 hours ), is eliminated renally, and causes substantial systemic arterial vasodilation. Milrinone must always be paired with norepinephrine to prevent systemic hypotension. Inhaled milrinone can be considered to deliver selective pulmonary vasodilation without systemic hypotension.

Pillar 4: Selective Pulmonary Vasodilation

Systemic vasodilators (calcium channel blockers, intravenous nitroglycerin, intravenous hydralazine, and newly started oral sildenafil) should be avoided in hypotensive acute RV failure because they lower systemic pressure, and therefore RV coronary perfusion, before producing meaningful pulmonary vasodilation. Therapy must rely on inhaled agents that selectively target ventilated pulmonary segments:

Inhaled Epoprostenol (Prostacyclin / PGI2): Delivered via continuous vibrating-mesh nebulizer at 10 – 50 ng/kg/min 10–50\text{ ng/kg/min} 10–50 ng/kg/min . It activates smooth muscle adenylate cyclase, increasing intracellular cAMP and dilating intra-alveolar pulmonary vessels. It significantly improves ventilation-perfusion matching and reduces RV afterload.

Inhaled Nitric Oxide (iNO): Delivered at 10 – 40 ppm 10–40\text{ ppm} 10–40 ppm . It activates soluble guanylyl cyclase to increase cGMP. It has an ultra-short half-life (several seconds) because it is immediately inactivated upon entering the bloodstream by binding to hemoglobin, preventing any systemic vasodilation.

Mechanical Ventilation in the Failing RV

Endotracheal intubation is an exceptionally high-risk event in severe RV failure. The combination of sedative-induced loss of sympathetic tone and positive-pressure mechanical ventilation can trigger instantaneous circulatory arrest.

The "Killers of the Right Ventricle"

Physiological Stressor Mechanism of Harm on RV Ventilator / ICU Strategy

Hypoxia ( PaO 2 < 60 mmHg \text{PaO}_2 < 60\text{ mmHg} PaO 2 ​ < 60 mmHg ) Triggers potent hypoxic pulmonary vasoconstriction (HPV), doubling PVR Titrate FiO 2 \text{FiO}_2 FiO 2 ​ to maintain PaO 2 ≥ 65 – 70 mmHg \text{PaO}_2 \ge 65–70\text{ mmHg} PaO 2 ​ ≥ 65–70 mmHg ( SpO 2 ≥ 92 – 94 % \text{SpO}_2 \ge 92–94\% SpO 2 ​ ≥ 92–94% )

Acidosis & Hypercapnia ( pH < 7.30 , PaCO 2 > 45 \text{pH} < 7.30, \text{PaCO}_2 > 45 pH < 7.30 , PaCO 2 ​ > 45 ) Directly constricts pulmonary arterial vascular smooth muscle Maintain normal ventilation; target pH 7.35 – 7.45 \text{pH } 7.35–7.45 pH 7.35–7.45 and PaCO 2 35 – 40 mmHg \text{PaCO}_2\ 35–40\text{ mmHg} PaCO 2 ​ 35–40 mmHg

Excessive PEEP ( > 10 – 12 cmH 2 O >10–12\text{ cmH}_2\text{O} > 10–12 cmH 2 ​ O ) Compresses intra-alveolar vessels, shifting lung to West zone 1 and spiking PVR Set lowest PEEP compatible with oxygenation (typically 5 – 8 cmH 2 O 5–8\text{ cmH}_2\text{O} 5–8 cmH 2 ​ O )

Lung Hyperinflation ( V T > 8 mL/kg PBW V_T > 8\text{ mL/kg PBW} V T ​ > 8 mL/kg PBW ) Overdistension stretches intra-alveolar capillaries, increasing resistance Use lung-protective low tidal volume ( 6 – 8 mL/kg PBW 6–8\text{ mL/kg PBW} 6–8 mL/kg PBW )

Alveolar Atelectasis Hypoxia and extra-alveolar capillary collapse increase resistance Prevent derecruitment without overdistending alveoli (target FRC)

Important

High driving pressure ( > 15 cmH 2 O >15\text{ cmH}_2\text{O} > 15 cmH 2 ​ O ) and high transpulmonary pressures directly correlate with acute cor pulmonale in ARDS. Ventilate to maintain plateau pressure ≤ 28 – 30 cmH 2 O \le 28–30\text{ cmH}_2\text{O} ≤ 28–30 cmH 2 ​ O and driving pressure ≤ 14 cmH 2 O \le 14\text{ cmH}_2\text{O} ≤ 14 cmH 2 ​ O .

Mechanical Circulatory Support for Refractory RV Failure

When medical management fails to arrest the RV death spiral, advanced mechanical circulatory support must be deployed rapidly:

Percutaneous Right Ventricular Assist Device (RVAD): Systems such as the Impella RP or ProtekDuo with TandemHeart drain venous blood directly from the right atrium or inferior vena cava and pump it directly into the main pulmonary artery, actively bypassing the failing right ventricle and restoring left-sided filling.

Venoarterial Extracorporeal Membrane Oxygenation (VA-ECMO): Provides complete circulatory and respiratory support. Blood is withdrawn from the right atrium via a femoral venous cannula, passed through an extracorporeal membrane oxygenator, and returned under high pressure into the femoral artery. VA-ECMO fully decompresses the right heart, restores systemic organ perfusion, and provides an immediate bridge to recovery, lung transplantation, or pulmonary thromboendarterectomy.