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:
| 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
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