Allison Clemens
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2025 PACUPrep BCCCP Preparatory Course Pulmonary Hypertension (Acute and Chronic severe pulmonary hypertension) Hemodynamic and Imaging-Based Severity Assessment in Critical Pulmonary Hypertension

Lesson 8, Topic 2

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Hemodynamic and Imaging-Based Severity Assessment in Critical Pulmonary Hypertension

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Hemodynamic and Imaging Assessment of Pulmonary Hypertension in the Critically Ill

Lesson Objective

Apply diagnostic strategies and severity assessment for pulmonary hypertension (PH) in the critically ill.

Key Learning Points:

Confirm and characterize PH hemodynamics with right heart catheterization (RHC).
Assess right ventricular (RV) structure and function via echocardiography and CT/MRI.
Integrate risk scores (REVEAL, COMPERA) and biomarkers (NT-proBNP, troponin, lactate) for prognostication.
Identify reversible precipitants (PE, sepsis, acidosis) versus chronic PH progression.
Determine when to escalate to invasive monitoring or transfer to a specialized PH center.

I. Right Heart Catheterization (RHC)

Summary: RHC is the gold standard for diagnosing and subtyping PH in unstable patients. Prompt, accurate measurements guide therapy and risk stratification.

A. Indications and Timing

Diagnostic confirmation when noninvasive data are inconclusive or inconsistent with clinical presentation.
Guidance of acute therapies: vasodilator challenge, inotrope/vasopressor titration.
Timing considerations:
- Perform early in ICU if PH contributes to shock or RV failure.
- Decongest left heart–failure patients before RHC to avoid misclassification.

Key Pearl

Early RHC in unexplained hemodynamic instability improves diagnostic accuracy and aids rapid treatment decisions.

B. Hemodynamic Parameters

Mean pulmonary artery pressure (mPAP) ≥20 mmHg defines PH.
Pulmonary artery wedge pressure (PAWP) ≤15 mmHg indicates pre-capillary PH; >15 mmHg indicates post-capillary PH.
Pulmonary vascular resistance (PVR) = (mPAP – PAWP)/cardiac output; >2 WU signifies pre-capillary PH.
Cardiac output/index: low values (<2.5 L/min/m²) correlate with worse outcomes.

Hemodynamic Classification:

Hemodynamic Classification of Pulmonary Hypertension
Profile	mPAP (mmHg)	PAWP (mmHg)	PVR (WU)
Pre-capillary PH	>20	≤15	>2
Isolated post-capillary PH	>20	>15	≤2
Combined pre- and post-capillary	>20	>15	>2

Key Pearl

Even mild elevations in mPAP/PVR are linked to increased mortality—detect early and intervene.

C. Procedural Pitfalls

Zero‐reference at mid‐thoracic level; record pressures at end-expiration.
Adjust for positive-pressure ventilation: high PEEP can overestimate PAWP/mPAP.
Distinguish true PAWP from pulmonary artery dicrotic notches and v-waves.

Clinical Pearl

Misplaced transducer or failure to account for respiratory swings can lead to misclassification and inappropriate therapy.

II. Echocardiography and CT/MRI Assessment

Summary: Noninvasive imaging complements RHC, offering rapid RV functional and vascular insights.

A. Transthoracic Echocardiography (TTE)

TAPSE <17 mm: impaired RV longitudinal systolic function.
RV fractional area change (FAC) <35%: reduced RV contractility.
Tissue Doppler S′ <9.5 cm/s: abnormal systolic velocity.
Estimated RV systolic pressure from TR jet >35–40 mmHg suggests PH.
RA area enlargement and pericardial effusion signal advanced disease.

Key Pearl

Subtle drops in TAPSE or FAC, even with borderline pressures, predict worse survival.

B. Advanced Imaging (CT/MRI)

CT metrics:

Main PA diameter >29 mm or PA/Ao ratio >1.
Vascular pruning (loss of small vessels) correlates with mortality.
Detection of acute or chronic thromboembolic lesions.

MRI metrics:

RV end-diastolic/systolic volumes and ejection fraction (RVEF).
Late gadolinium enhancement indicates fibrosis and adverse prognosis.
Perfusion sequences for regional hypoperfusion (CTEPH workup).

Key Pearl

CT vascular pruning independently predicts mortality and guides consideration for CTEPH evaluation.

C. Advantages and Limitations

TTE: bedside, repeatable, no contrast—but operator and window dependent.
CT/MRI: high spatial resolution and quantification but require transport, contrast/radiation, and have contraindications (e.g., MRI with implants).

Clinical Pearl

Use TTE for screening and follow-up; reserve CT/MRI for detailed anatomical or tissue characterization when stable.

III. Clinical Risk Stratification Tools

Summary: Multi-parametric scores plus biomarkers refine prognosis and triage in ICU PH.

A. REVEAL and COMPERA Risk Models

REVEAL: integrates demographics, functional class, 6MWD, BNP/NT-proBNP, echo, RHC data; stratifies 1-year mortality risk.
COMPERA 2.0: four-strata model using continuous clinical, lab, and hemodynamic variables; improved discrimination.
ICU limitations: functional assessments (6MWD, WHO FC) often not feasible.

Key Pearl

Serial application highlights treatment response; use available surrogates if walk tests are unavailable.

B. Biomarker Integration

NT-proBNP: high risk when >1,400 pg/mL; reflects RV wall stress.
High-sensitivity troponin: signals RV ischemia; any detectable elevation indicates poor prognosis.
Lactate: marker of global hypoperfusion; clearance >10–20% over 6 hours predicts survival.

Clinical Pearl

Combine trends in lactate, troponin, and NT-proBNP with hemodynamics to guide escalation.

IV. Laboratory and Biomarker Data in Acute Decompensation

Summary: Serial labs provide a dynamic picture of RV performance and systemic perfusion.

A. Lactate

Elevated in low-output states; aim for clearance ≥10% in first 6 hours.

B. Cardiac Troponins

Elevated troponin I/T correlates with RV strain; portends increased mortality.

C. Natriuretic Peptides

BNP vs NT-proBNP: NT-proBNP less affected by renal dysfunction; interpret in context of sepsis and volume status.

Key Pearl

Rising lactate with unchanged hemodynamics may signal occult RV ischemia—consider early invasive monitoring.

V. Differentiating Acute Precipitants vs Chronic Progression

Summary: Rapid identification and treatment of reversible causes prevent irreversible RV injury.

A. Acute Pulmonary Embolism

Age-adjusted D-dimer rule‐out; CT pulmonary angiography for definitive diagnosis; V/Q scan if contrast contraindicated.
Distinguish new central/lobar defects from chronic webs or bands.

B. Infection and Sepsis

Sepsis increases RV afterload and depresses contractility.
Use cultures and procalcitonin to guide antimicrobial therapy; prioritize source control.

C. Metabolic Acidosis and Other Triggers

ABG: pH <7.35 exacerbates pulmonary vasoconstriction.
Correct electrolytes (K+, Mg2+) and optimize volume status.

Clinical Pearl

Address reversible triggers before initiating or escalating PH-specific therapies.

VI. Indications for Advanced Monitoring and Transfer

Summary: Escalate to invasive monitoring or PH center referral when standard care fails.

A. When to Use Invasive Monitoring

Persistent shock or hypotension on vasopressors/inotropes.
SvO₂ <60% despite optimization suggests low cardiac output.
Unexplained RV deterioration.

B. Criteria for PH Center Transfer

Refractory PH crisis requiring ECMO or atrial septostomy.
Consideration for lung transplantation.
Need for multidisciplinary expertise (surgical, advanced therapies).

Key Pearl

Early transfer to a PH center with ECMO/septostomy capability reduces mortality in refractory cases.

References

Humbert M, Kovacs G, Hoeper MM, et al. 2022 ESC/ERS guidelines for the diagnosis and treatment of pulmonary hypertension. Eur Heart J. 2022;43(36):3618–3731.
Johnson S, Sommer N, Cox-Flaherty K, et al. Pulmonary hypertension: a contemporary review. Am J Respir Crit Care Med. 2023;208(5):528–548.
Maron BA. Revised definition of pulmonary hypertension and approach to management: a clinical primer. J Am Heart Assoc. 2023;12:e029024.
Chai T, Qiu C, Xian Z, et al. Research advances in hypoxic pulmonary hypertension. Ann Transl Med. 2022;10(4):230.
Brener MI, Masoumi A, Ng VG, et al. Invasive right ventricular pressure-volume analysis: principles and clinical applications. Circ Heart Fail. 2022;15(1):e009101.
Maron BA, Brittain EL, Hess E, et al. Pulmonary vascular resistance and clinical outcomes in pulmonary hypertension. Lancet Respir Med. 2020;8(9):873–884.
Huston JH, Maron BA, French J, et al. Association of mild echocardiographic PH with mortality and RV function. JAMA Cardiol. 2019;4(11):1112–1121.
Aluja Jaramillo F, Gutierrez FR, Díaz Telli FG, et al. Approach to PH: From CT to clinical diagnosis. Radiographics. 2018;38(2):357–373.
Ley S, Kreitner KF, Fink C, et al. Assessment of PH by CT and MR imaging. Eur Radiol. 2004;14(2):359–368.
Synn AJ, Li W, San José Estépar R, et al. Pulmonary vascular pruning on CT and risk of death. Am J Respir Crit Care Med. 2021;203(2):251–254.
Benza RL, Gomberg-Maitland M, Miller DP, et al. The REVEAL risk score calculator in PAH. Chest. 2012;141(2):354–362.
Hoeper MM, Pausch C, Olsson KM, et al. COMPERA 2.0: a four-stratum risk model for PAH. Eur Respir J. 2022;60(2):2102311.
Yogeswaran A, Tello K, Lund J, et al. Risk assessment in PH based on laboratory parameters. J Heart Lung Transplant. 2022;41(3):400–410.
Rodriguez-Gonzalez M, Benavente-Fernandez I, Castellano-Martinez A, et al. NT-proBNP plasma levels as biomarkers in PH. Biomark Med. 2019;13(7):605–614.

2025 PACUPrep BCCCP Preparatory Course

Pulmonary

Participants 432

Hemodynamic and Imaging-Based Severity Assessment in Critical Pulmonary Hypertension

Lesson Objective

Key Learning Points:

I. Right Heart Catheterization (RHC)

A. Indications and Timing

B. Hemodynamic Parameters

Hemodynamic Classification:

C. Procedural Pitfalls

II. Echocardiography and CT/MRI Assessment

A. Transthoracic Echocardiography (TTE)

B. Advanced Imaging (CT/MRI)

CT metrics:

MRI metrics:

C. Advantages and Limitations

III. Clinical Risk Stratification Tools

A. REVEAL and COMPERA Risk Models

B. Biomarker Integration

IV. Laboratory and Biomarker Data in Acute Decompensation

A. Lactate

B. Cardiac Troponins

C. Natriuretic Peptides

V. Differentiating Acute Precipitants vs Chronic Progression

A. Acute Pulmonary Embolism

B. Infection and Sepsis

C. Metabolic Acidosis and Other Triggers

VI. Indications for Advanced Monitoring and Transfer

A. When to Use Invasive Monitoring

B. Criteria for PH Center Transfer

References