#70 The People’s Ventricle with Dr Matt Siuba

Buckle up because on this week's episode of Critical Care Time we are treated to a master class on Right Heart Failure with world-class educator Dr. Matt Siuba. We are taking a deep dive on diagnosis, management and of course, sharing our love for the PAC! Make sure you clear your schedule and take notes for this one because as far as we are concerned, this is required listening for anyone who cares for the critically ill!

Dr. Matt Siuba

Intensivist, Cleveland Clinic

@msiuba (twitter)

zentensivist (bksy)

Website

“The RV is the ventricle of the downtrodden”

— Matt Siuba

Part 1 — Why the Right Ventricle Is the “People’s Ventricle”

• “The People’s Ventricle” is a nod to A People's History of the United States by Howard Zinn — and yes, a subtle wink to Good Will Hunting.

  • The right ventricle (RV) is the overlooked chamber. It doesn’t get the glamour of the LV. It runs low pressures. It operates quietly. But when it fails, it can bring down the entire circulation with astonishing rapidity.

• Key physiological differences between RV and LV:

  • Pressure: The RV/pulmonary circulation is a low pressure circuit, high compliance circuit (in contrast to the LV)

    • The RV wall normally < 5 mm; it cannot acutely generate high pressure —> the acutely injured RV rarely sustains RVSP > 60 mmHg

  • Contractility: The RV has 1/3 to 1/5 the contractility of the LV → thus the RV has less physiological reserve

  • Fiber orientation: 80% of the RV cardiac output is via lengthwise contraction (in contrast to primarily concentric contraction in the RV)

  • Perfusion: The RCA perfuses the RV in systole and diastole (unlike the LV which is perfused only in diastole but multiple coronary vessels); RV perfusion is heavily dependent upon MAP and has little redundancy.

• Understanding the RV Death Spiral:

  • Increased afterload → RV dilation → septal shift → ↓ LV preload → worsening shock

  • RV dilates to maintain stroke volume (Frank–Starling adaptation)

  • Stretch is initially adaptive, however Progressive dilation is maladaptive

  • Septal bowing causes intraventricular dependence, reducing LV stroke volume.

    • Impaired LV filling → systemic hypotension → worsened RV ischemia

  • This is why RV dysfunction is uniquely catastrophic.

What Causes RV Failure in the ICU?

• Assume RV dysfunction until proven otherwise in:

  • Pulmonary Vascular Stressors

    • Acute PE

    • ARDS

    • Hypoxemia

    • Hypercapnia

    • Acidemia

    • Sepsis

    • Pulmonary hypertension (PH)

      • Definition update: Mean PAP > 20 mmHg defines PH (2022 ESC/ERS Guidelines)

  • Ischemic Causes

    • Isolated RV MI (RCA territory)

    • Larger infarcts involving the inferior wall (RV often neglected, initially)

  • PH Triggers in ICU

    • Hypoxia

    • Hypercapnia

    • Sepsis

    • Tachyarrhythmias

    • PE

RV and Ventilator Interactions

U-shaped relationship between Pulmonary Vascular Resistance (PVR) and Tidal Volume (TV); note the rising PRV with lung volumes either above or below FRC.

• Positive pressure ventilation increases RV afterload by:

  • Increasing transpulmonary pressure

  • Compressing pulmonary capillaries

  • Increasing PVR

  • PVR vs lung volume is U-shaped.

    • Too little PEEP → atelectasis → ↑ PVR

    • Too much PEEP → overdistension → ↑ PVR

  • Practical Targets

    • Driving pressure < 15 cmH₂O (ideally < 12–13)

    • Avoid severe hypercapnia (can increase PVR)

    • In obesity: plateau pressure may be higher but driving pressure still safe

    • Hypercapnia + rising dead space may signal overdistension.

Part 2 — Monitoring the RV

• Two Core Questions:

  • 1. How invasive?

  • 2. How repeatable?

• Least invasive → Most invasive:

  • Transthoracic Echo (TTE)

  • Tranesophageal Echo (TEE)

  • Central Venous Pressure (CVP)

  • Pulmonary Artery Catheter (PAC)

• Bedside Echocardiogram for assessing RV size and function

  • 1. Size (Apical 4-chamber)

    • Normal LV:RV ≈ 2:1

    • RV = LV → dilated

    • RV > LV → severely dilated

  • 2. Squeeze

    • TAPSE normal > 1.7 cm (often simplified > 2 cm)

    • RV fractional area change

    • Tissue Doppler S’

  • 3. Septal Kinetics

    • Flattened septum in systole → pressure overload

    • Flattened septum in diastole → volume overload

• When Is a PAC Helpful?

  • Unselected ICU patients do NOT benefit from routine use of a PAC (PAC-MAN trial) however it can be immensely useful in the right patient.

  • Ask:

    • How uncertain am I?

    • How sick is the patient?

    • Will the data change management?

  • But:

    • “A PAC is useless if you only look at one number.”

    • Use it as a Starling curve generator.

    • Key Metrics

      • CO/CI (must use!)

      • PVR = (Mean PAP – PCWP) / CO

    • Distinguish:

      • Pre-capillary PH → PVR ≥ 2 Wood units

      • Post-capillary PH → PCWP elevated

    • Thermodilution remains reasonably accurate even with TR

    • Continuous vs Intermittent CO

      • CCO PAC allows trending

      • Direct Fick = gold standard but impractical in ICU

      • Indirect Fick assumes estimated VO₂ which is often wrong.

• Role of the pulmonary artery catheter (PAC) in 2026:

“I gottah numba! How ‘bout them apples?”

“Zentensivism” vs ICU Nihilism

• Zentensivism is:

  • Minimally invasive

  • Maximally attentive

  • Uses no crystals except the ultrasound ones

  • Elevates the humanity of the patient

  • Never involves placing devices without purpose

• Thoughtfully choosing interventions based on your patients goals and physiology is the essence of Zentensivism. It requires a deep understanding of the literature and the reason you are performing an intervention.

• In contracts, ICU Nihilism is a misunderstanding of physiology and the evidence. It often manifests with blanket statements like:

  • “PACs don’t improve survival” (PAC-MAN)

  • “Art lines aren’t beneficial in sepsis” (EVERDAC)

  • “No one should be checking CVP and ScvO2 anymore”

• How does a Zentensivist respond to ICU Nihilism:

  • PAC-MAN showed no survival benefit in unselected patients, mostly with sepsis and when placed without ultrasound. That doesn’t inform contemporary placement in carefully selected patients with RV failure.

  • EVERDAC showed routine placement of art lines in all ICU patients on vasopressors didn’t improve mortality. It was underpowered. Most ICU patients on low dose vasopressors don’t need an art line.

  • CVP has been demonstrated not to be an effective resusciation target in septic shock. It can provide useful information when evaluating other etiologies of shock such as RV failure.It means: use thoughtfully.

• Be an Zentensivist not an ICU Nihilist

• We discuss several of these trials - and their limitations - at greater length in other episodes:

Part 3 — Managing RV Failure

• Therapeutic schema:

  • Lower afterload

  • Optimize preload

  • Support contractility

  • Maintain oxygenation

  • Support systemic perfusion

Afterload: “The Most Energetically Favorable Target”

• Lowering PVR is “free cardiac output.”

• Oxygen

  • Even 6 L/min NC vs room air can improve RV function in PH patients (Rich et al., CHEST 1982).

  • Avoid:

    • Hypoxemia

    • Hypercapnia

    • Acidemia

• Pulmonary Vasodilators

  • Inhaled nitric oxide (iNO)

    • iNO → U-shaped PVR response

  • Inhaled epoprostenol (EPO)

    • EPO → more linear

  • Both:

    • Delivered via ventilator or HFNC

    • Reduce PVR

    • Must reassess: CO ↑, mean PAP ↓

  • Be cautious in the presence of shunt physiology.

Preload: “The RV Is Preload Intolerant”

• When you meet a sick RV, it’s usually volume overloaded.

• Goals:

  • Normalize geometry

  • Reduce septal shift

• Clues:

  • CVP waveform without respiratory variation → volume overloaded

  • Large Y descents → volume overload

• Portal vein pulsatility and VExUS can help.

• Avoid BNP to manage critically ill RV failure.

• Monitor perfusion: B-U-S

  • Brain —> are they mentating?

  • Urine —> are they peeing?

  • Skin —> cap refill?

Contractility

• After optimizing preload and afterload, consider enhancing RV contractility

• Inotropes

  • Dobutamine

    • Rapid onset/offset

    • Can lower SVR

  • Milrinone

    • Prominent pulmonary vasodilator effect

    • Longer half-life, especially in renal failure

    • More systemic hypotension

  • Epinephrine

    • Strong inotropy

    • May raise lactate

  • DORAME study (n=16 isolated RV failure) suggests dobutamine improves hemodynamics (Haddad et al., Crit Care Med 2009).

Vasopressors: Choose Carefully

• Goal:

  • Maintain systemic pressure > RV systolic pressure

  • Preserve RCA perfusion

• Preferred

  • Vasopressin

  • Norepinephrine

• Physiologically appealing: Angiotensin II (limited data)

• Avoid: Phenylephrine (↑ PVR)

• Always consider:

  • MAP target relative to RVSP

  • Renal perfusion pressure = MAP – CVP

Mechanical Circulatory Support

• Consider when still failing despite:

  • Afterload optimized

  • Preload corrected

  • Inotrope initiated

• MCS options in RV failure:

  • VA-ECMO

  • RVAD

  • RV Impella (e.g., Impella RP)

• Device choice depends on:

  • Isolated RV failure?

  • Biventricular failure?

  • Transplant candidate?

High-Yield Takeaways

1. RV failure kills by geometry and perfusion collapse.

2. Ventilators can worsen RV afterload — lung volume matters.

3. Lower afterload first. It’s free cardiac output.

4. The RV is not preload dependent. It is preload intolerant.

5. Use PAC thoughtfully — not nihilistically.

6. Maintain systemic pressure above RV systolic pressure.

7. Optimize oxygenation and avoid hypercapnia.

• Clinical Trials Discussed

  ANDROMEDA-SHOCK-2

  EVERDAC

  SuDDICU

  BICAR-ICU-2

• Related Episodes

• References