Right Heart Catheterization: Best Practices and Specific Considerations

Abstract

Right heart catheterization (RHC) remains the gold standard for the invasive assessment of cardiovascular hemodynamics, enabling direct measurement of right atrial, right ventricular, pulmonary artery, and pulmonary arterial wedge pressures, as well as cardiac output and mixed venous oxygen saturation. Although earlier randomized trials questioned the routine use of pulmonary artery catheters in critically ill patients, RHC continues to play a crucial role in the diagnosis and management of pulmonary hypertension, advanced heart failure, cardiogenic shock, and complex structural or valvular heart disease. The clinical value of RHC, however, depends not only on performing the procedure but also on obtaining accurate and physiologically meaningful measurements. This review summarizes contemporary best practices for performing RHC in routine clinical practice. Key procedural considerations include defining the clinical objective prior to catheterization, selecting appropriate vascular access, ensuring correct transducer leveling and signal fidelity, and accounting for respiratory variation and hemodynamic conditions during pressure acquisition. The review also discusses methodological aspects of measuring pulmonary arterial wedge pressure, cardiac output, and intracardiac shunts, and highlights common technical pitfalls that may lead to misinterpretation of hemodynamic data. In addition, the evolving role of RHC in clinical decision-making is reviewed, including its application in the hemodynamic classification of pulmonary hypertension, vasoreactivity testing, exercise hemodynamics for suspected heart failure with preserved ejection fraction, and differentiation of constrictive pericarditis from restrictive cardiomyopathy. Standardized acquisition and careful interpretation of hemodynamic data are essential to maximize the diagnostic and therapeutic value of RHC in contemporary cardiovascular practice.

Graphical Abstract

INTRODUCTION

Right heart catheterization (RHC) remains a cornerstone of invasive cardiovascular assessment because it directly quantifies intracardiac and pulmonary hemodynamics, including right atrial and pulmonary artery pressures (PAPs), pulmonary arterial wedge pressure (PAWP), cardiac output (CO), and mixed venous oxygen saturation. These measurements provide diagnostic and prognostic information that cannot always be replaced by non-invasive imaging, particularly when a definitive hemodynamic diagnosis is required or when treatment decisions depend on precise pressure and flow estimates.¹,²,³,⁴⁾

Over the past 2 decades, RHC practice has evolved within a broader shift in the cardiac catheterization laboratory. However, the previous PAC-Man study showed that the routine use of pulmonary artery catheter (PAC) showed no significant clinical benefit for critically ill patients in terms of mortality.⁵⁾ Additionally, the ESCAPE study also demonstrated that PAC-guided therapy for patients with severe heart failure did not significantly affect the primary end point of days alive and out of the hospital during the first 6 months.⁶⁾ Contemporary hemodynamic assessment has regained relevance because of the increase in complex structural and valvular interventions, along with advanced heart failure therapies.⁴⁾ More importantly, in the multicenter observational data, PAC-guided treatment in the cardiac intensive care unit was associated with lower mortality for all shock patients.⁷⁾ The ongoing PACCS randomized clinical trial is planned to test whether early invasive hemodynamic assessment and further management with PAC can decrease in-hospital mortality for cardiogenic shock due to acutely decompensated heart failure (ClinicalTrials.gov, NCT05485376). Furthermore, in pulmonary hypertension (PH), RHC remains the definitive test for confirming diagnosis and classifying the hemodynamic phenotype, and it is also increasingly used to guide therapy and provide prognostic information because of the increase in complex structural and valvular interventions.⁸⁾

The limitations of “routine” or non-standardized hemodynamic measurements have become more apparent, reinforcing that the utility of RHC depends on meticulous technique, reproducibility, and interpretation anchored in physiology. In this regard, the current review summarizes “how to do” RHC correctly and consistently in the daily clinical practice (Tables 1 and 2).

Table 1. RHC: best practices and specific considerations.

Aspect	Best practice (what to do)	Specific considerations/common pitfalls
Clinical question & Study design	Define a prespecified diagnostic/management question and tailor the protocol (required pressures, CO method, oximetry run, provocative testing) to that question.	“Routine” RHC without a defined question risks incomplete datasets and misclassification (e.g., omitting oximetry or provocative maneuvers when clinically indicated).
Patient position	Perform RHC in a fully supine position and document any deviation.	Even semi-supine positioning or leg raise can materially change pressures and CO; interpret values in context of positioning.
Vascular access	Prefer ultrasound-guided right internal jugular venous access and full sterile technique.	Femoral access may increase infection risk and often require fluoroscopy and post-procedure bedrest; consider alternatives (e.g., upper-extremity veins) in selecting patients who cannot tolerate supine positioning.
Anticoagulation planning	Individualize anticoagulation management (bleeding vs. thrombotic risk).	Not accounting for anticoagulants increases access-site bleeding; conversely, unnecessary interruption increases thromboembolic risk.
Transducer levelling & zeroing	Zero to atmospheric pressure and level to a reproducible anatomic reference (mid-thoracic/phlebostatic axis).	A 1 cm error changes pressure by ~0.8 mmHg—clinically relevant for PAWP thresholds and PH classification.
Signal quality (damping/flush test)	Perform a flush test and ensure an optimally damped waveform before recording values.	Overdamping blunts systolic peaks and distorts contours; underdamping exaggerates systolic pressure with oscillations, causes include kinking.
Catheter advancement & waveform monitoring	Advance the PAC with continuous waveform monitoring and confirm sequential chamber waveforms (RA→RV→PA→PAWP).	Catheter whip can cause a sharp systolic upstroke and spuriously high systolic readings; reduce by repositioning and/or increasing damping.
Respiratory timing for pressures	Measure pressures at end-expiration without breath-holding or Valsalva; if respiratory swings are large, average over 3–4 cycles.	COPD, obesity, mechanical ventilation, or hyperventilation can cause large intrathoracic pressure effects; “electronic mean” values across the respiratory cycle may mislead.
PAWP acquisition	Obtain PAWP deliberately and briefly; stop balloon inflation once a wedge waveform is achieved; avoid prolonged wedging and never flush while wedged.	Repeated wedging or inflations/deflations at the wedge position increases risk of pulmonary infarction/rupture; repeat only when essential for diagnostic clarity.
Volume status & provocative testing	Aim for euvolemia; interpret PAWP with awareness of diuresis/decongestion; consider provocative testing (fluid challenge/exercise) when HFpEF is suspected.	Major diuresis can yield “false-low” PAWP (PVR overestimation); severe RV failure/pericardial restraint can yield “false-high” PAWP.
CO measurement	Prefer direct Fick (measured VO2) or thermodilution with 3–5 injections and <10% variability; clearly report the method used.	Indirect Fick (assumed VO2) is less reliable; thermodilution becomes unreliable with shunts and may be affected by severe TR.
Oximetry run & shunt assessment	Perform stepwise oximetry run when shunt is suspected; consider complete assessment when SvO2 is high (e.g., >75%).	In complex congenital physiology, standard assumptions for Qp/Qs may not hold; consider specialized center interpretation and, when needed, left-sided sampling.

RHC = right heart catheterization; CO = cardiac output; PAC = pulmonary artery catheter; RA = right atrium; RV = right ventricle; PA = pulmonary artery; PAWP = pulmonary arterial wedge pressure; COPD = chronic obstructive pulmonary disease; HFpEF = heart failure with preserved ejection fraction; PVR = pulmonary vascular resistance; VO₂ = oxygen consumption; TR = tricuspid regurgitation; SvO₂ = mixed venous oxygen saturation.

Table 2. Normal hemodynamic values.

Variables		Normal values
Measured variables
	RA (mmHg)	1–6
	RV (mmHg)	Systolic: 15–25
		Diastolic: 1–8
	PA pressure (mmHg)	Systolic: 15–25
		Diastolic: 4–12
		Mean: 8–20
	PAWP (mmHg)	≤13
	CO (L/min)	4–8
Calculated variables
	CI (L/min/m2)	2.5–4.0
	DPG (mmHg)	<7
	PVR (WU)	0.3–2.0
	RA pressure/PAWP ratio	<0.5
	SVR index (WU)	10–15
	CPO (Watts)	0.8–1.1
	RVSWI (g·m/m2/beat)	5–10
	PAPi	>2.0

RA = right atrium; RV = right ventricle; PA = pulmonary artery; PAWP = pulmonary arterial wedge pressure; CO = cardiac output; CI = cardiac index; DPG = diastolic pressure gradient; PVR = pulmonary vascular resistance; SVR = systemic vascular resistance; CPO = cardiac power output; RVSWI = right ventricular stroke work index; PAPi = pulmonary artery pulsatility index.

GENERAL PRINCIPLES OF RHC

Start with a specific clinical question and design the hemodynamic study

RHC should be performed to answer a pre-defined diagnostic or management question, rather than as a “routine” evaluation.²⁾ The guidelines and scientific statements emphasize tailoring the RHC to the clinical scenario, such as confirming PH, clarifying valve hemodynamics, guiding treatment decisions for congenital heart disease, or differentiating constrictive pericarditis (CP) from restrictive cardiomyopathy (RCM), while integrating findings with non-invasive data.⁸,⁹,¹⁰⁾ Specialized interpretation is essential when standard assumptions for hemodynamic calculations are unreliable, as seen in complex congenital physiology, multilevel shunts, or questionable oxygen consumption estimates, making this principle especially crucial. Practically, the “study design” includes pre-specifying which pressures must be obtained, whether a complete oximetry run is needed, and whether adjunctive maneuvers (e.g., fluid challenge, vasodilator challenge test, exercise hemodynamics) are being considered for specific diagnostic dilemmas such as severe PH or heart failure with preserved ejection fraction (HFpEF).

Patient preparation and access

Patients should be informed of the indication and procedural risks. Based on the previous study, serious adverse event rates are low but non-trivial (on the order of ~1%), with rare procedure-related mortality.¹,²⁾ Sedation is rarely required for diagnostic RHC and local anesthesia is generally sufficient. Minimizing sedation is particularly crucial when hemodynamics may be sensitive to respiratory mechanics and changes in preload/afterload. Although the right internal jugular vein is a preferable site for a direct route to the right atrium, the choice of venous access, including internal jugular, femoral, antecubital, or arm proximal vein, should be dictated by the operator experience, the necessity for simultaneous left-heart catheterization, and patient-specific factors (e.g., medical devices, prior venous access history). The application of ultrasound guidance improves the success and reduces complications for internal jugular cannulation. Routine systemic anticoagulation is not required to perform diagnostic RHC itself. In patients already receiving anticoagulants, periprocedural management should be individualized according to bleeding risk, thromboembolic risk, access site, and local expertise. Simple diagnostic RHC can be performed safely without interruption of anticoagulation in selected patients,¹¹⁾ although supporting evidence remains limited.

Secure the right position of pressure transducer

Inaccurate waveforms lead to incorrect diagnoses and poor clinical decisions; therefore, troubleshooting artifacts and preventing measurement error are core competencies rather than technical issues.

Leveling/zeroing

Transducers must be zeroed to atmospheric pressure and leveled to a reproducible anatomic reference. A commonly used approach is to level the transducer at the mid-thoracic level, which corresponds to left atrial level in the most patients.⁸⁾ Even small errors in height (1 cm) materially affect measured pressures, with ≈0.8 mmHg change per centimeter of vertical displacement.¹²⁾ However, “one-size” leveling can be imperfect when patients are not in the standard supine position; therefore, standard reference points may be inaccurate in non-supine postures, and it is recommended to maintain consistent institutional practice with awareness of these limitations.

Signal quality

A flush test and assessment of under- or over-damping are essential. Overdamping can blunt systolic peaks and distort pressure contours; underdamping can exaggerate systolic pressure (often with multiple oscillations) and mislead interpretation.

Respiratory and rhythm considerations

Intrathoracic pressure changes during respiration can significantly influence measured pressures (particularly PAWP), so clinicians should specify how pressures are recorded and reported. Contemporary guidance recommends measuring PAWP at end-expiration without breath-holding and averaging across several respiratory cycles, rather than relying on a single beat or a computer-generated respiratory mean that may obscure clinically meaningful variability.³⁾ Automated or digitized averaging can be misleading in some settings; for example, computer-averaged “mean” PAWP may not correspond to the desired end-expiratory value and can create substantial interpretation errors. For patients with atrial fibrillation, wedge pressure may be overestimated.⁴⁾ Accuracy of PAWP may be improved when averaged over 3–5 beats in this case.³⁾ Additionally, exaggerated intrathoracic pressure fluctuations (e.g., morbid obesity or advanced lung disease) can confuse interpretation and may even contribute to diagnostic misclassification depending on whether end-expiratory or respiratory-mean PAWP is used.¹⁾

Pressure acquisition

A complete diagnostic RHC typically includes right atrial pressure, right ventricular (RV) pressure, PAP, PAWP, CO, and mixed venous oxygen saturation.¹,²,³,⁴⁾ The PAC should be advanced with continuous waveform monitoring. Once the balloon is inflated, counterclockwise rotation allows for passage in the right atrium to the right ventricle across the tricuspid valve.¹³⁾ Although continuous waveform monitoring during catheter advancement is essential for safe chamber-to-chamber passage, in routine practice pressure and oximetry measurements are often recorded during catheter withdrawal after the catheter has been advanced to the pulmonary artery (PA) or wedge position, which may reduce ventricular ectopy and limit hemodynamic perturbation from prolonged manipulation. Waveform artifact due to the whipping motion of the PAC in the pulmonary artery causes a sharp upsloping wave at the beginning of the systolic phase.³⁾ This artifact can be reduced by re-positioning of PAC or increasing dampening. Wedge pressure measurement should be deliberate and brief, and avoid prolonged balloon inflation at the wedge position because of the risk of pulmonary infarction or rupture.²,³,⁴⁾ Practical recommendations include slow inflation with continuous monitoring, stopping inflation once a wedge waveform is achieved, minimizing time in wedge, and never flushing while wedged. Pulmonary artery rupture is the most fatal complication that occurs during overinflating the balloon. The overall complication rate has been reported as 1.1% (0.8–1.3%) with 0.06% fatality rate.¹⁴⁾ Therefore, repeat wedging should be limited to situations where it is essential for diagnostic clarity.

In patients with markedly elevated pulmonary vascular resistance or atypical wedge morphology, wedge oxygen saturation may help confirm an adequate catheter position; a wedge oxygen saturation approximating systemic arterial oxygen saturation, or within approximately 5% of SpO₂/SaO₂, supports appropriate wedging and allows the mean PAWP to be interpreted with greater confidence. Since PA diastolic pressure closely tracks PAWP (commonly within ~6 mmHg), PA diastolic pressure may serve as a substitute for repeated wedge measurements in follow-up assessments.¹⁵⁾ However, although PA diastolic pressure approximates PAWP under normal pulmonary vascular conditions, this relationship may be disrupted in states of elevated pulmonary vascular resistance, RV failure, or low CO, limiting the reliability of PA diastolic pressure as a surrogate of left-sided filling pressure in cardiogenic shock (Figure 1).

Figure 1. Catheter positioning and pressure waveform during right heart catheterization. Representative fluoroscopic images and invasive pressure tracings obtained during sequential catheter advancement through the RA, RV, PA, and PAWP positions.

RA = right atrium; RV = right ventricle; PA = pulmonary artery; PAWP = pulmonary arterial wedge pressure.

Cardiac output

CO can be measured using thermodilution or the Fick principle. The direct Fick (with measured oxygen consumption) is the gold standard, while indirect Fick (with assumed oxygen consumption) is frequently used but can be inaccurate.⁴,⁸⁾ There was a significant discrepancy between the directly measured and estimated values (e.g., >25% differences) in 17–25% of patients.¹⁶⁾ Thermodilution also has limitations. It is recommended to use an average of 3–5 thermodilution CO measurements with less than 10% variability.³⁾ Earlier methodological work reported that thermodilution becomes unreliable in settings such as significant tricuspid regurgitation (TR), intracardiac shunts, or very low CO states.¹⁷⁾ Therefore, the RHC report should clearly specify the CO method used and, whenever possible, incorporate internal quality checks such as verifying consistency across repeated thermodilution injections and ensuring coherence with oxygen saturations and hemodynamic phenotype. Interpretation of measured CO should extend beyond cardiac index thresholds alone and should be integrated with the overall Fick framework and hemodynamic phenotype. A numerically “normal” CO may still be inappropriate when considered relative to oxygen delivery, filling pressures, systemic or pulmonary vascular resistance, mixed venous oxygen saturation, and the clinical state. Accordingly, CO should be interpreted in conjunction with oxygen saturation data and the broader clinical context rather than by a single threshold alone.

Oximetry run and shunt assessment

RHC can assess intracardiac shunts using oximetry runs. This includes measuring oxygen saturations in venous and right-sided heart chambers (such as the PA, RV, right atrium, and superior vena cava) and identifying a step-up pattern to localize the level of shunting.¹⁾ Under standard conditions, mixed venous oxygen saturation is typically obtained from the PA, where venous return from the superior vena cava, inferior vena cava, and coronary sinus have mixed. In suspected shunt physiology, however, true mixed venous saturation may be difficult to define, and interpretation should rely on a complete stepwise oximetry run rather than a single value alone. In addition to an unexpectedly high PA saturation (e.g., >75%),⁸⁾ step-ups in oxygen saturation between adjacent chambers or vessels should raise suspicion for intracardiac or extracardiac shunting and may help localize the lesion. For the confirming diagnosis of PH phenotypes or shunt localization and quantification, sampling of left-sided heart (including left ventricle (LV), ascending, and descending aorta) is needed. In complex congenital lesions, the usual assumptions for Qp/Qs calculations might not be valid; these cases require evaluation by specialized centers with experienced interpretation.

The importance of standardization in RHC

Even when procedural complications are uncommon, diagnostic harm can arise from either omitting RHC when it is indicated or performing it without standardized acquisition and rigorous interpretation. Non-standardized measurement or interpretation can increase diagnostic inaccuracies and lead to inappropriate treatment.¹⁾ There are substantial rates of diagnostic revision after experienced center evaluation, and concerns have been raised about non-guideline-supported treatment in patients misclassified prior to referral.¹⁸⁾ Accordingly, we emphasize standardization across centers and within laboratories, particularly for transducer levelling, respiratory timing, wedge acquisition, and CO methodology, to ensure hemodynamics reliably inform diagnosis, risk stratification, and longitudinal management.

HEMODYNAMIC ASSESSMENT AND CLASSIFICATION OF PH

RHC remains the gold standard for the definitive diagnosis, classification, and management of PH.⁸,¹⁹⁾ It provides direct measurements of pulmonary hemodynamics that are essential for differentiating between the various clinical groups of PH, which have distinct pathophysiological mechanisms and therapeutic strategies.²⁰⁾

The hemodynamic definition of PH has evolved significantly in recent years. The 6th World Symposium on Pulmonary Hypertension in 2019 proposed revising the definition of PH from a mean PAP ≥25 mmHg to >20 mmHg.²¹⁾ This change was subsequently adopted by the 2022 European Society of Cardiology (ESC)/European Respiratory Society guidelines for the diagnosis and treatment of PH. Currently, PH is defined as a mean PAP >20 mmHg at rest.

DIFFERENTIATION OF PH GROUPS

Group 1: Pulmonary arterial hypertension (PAH) vs. Group 2: PH due to left heart disease

Distinguishing between Group 1 and Group 2 PH is one of the most common and critical challenges in the cardiac catheterization laboratory.¹⁾ While a resting PAWP >15 mmHg indicated a post-capillary component, many patients with left heart disease, particularly those with HFpEF or those treated with diuretics, may present with a resting PAWP between 13 and 15 mmHg. In these borderline cases, accurate classification is paramount because therapies for PAH can be harmful to patients with pulmonary venous hypertension. To unmask occult left heart disease, provocative maneuvers are recommended. A fluid challenge, typically involving the infusion of 500 mL of normal saline over 5–10 minutes, can be performed. In patients with Group 2 PH, the compromised compliance of the LV leads to a disproportionate rise in PAWP (typically to >18 mmHg) in response to the volume load. In contrast, patients with Group 1 PAH generally maintain a stable PAWP or show only a minimal increase. Alternatively, exercise hemodynamics can be utilized; a significant rise in PAWP during exercise (≥25 mmHg) confirms a diagnosis of HFpEF and Group 2 PH.²²⁾

Group 3: PH due to lung disease

In patients with suspected Group 3 PH, RHC typically reveals precapillary hemodynamics like PAH. However, the differentiation relies on the clinical context of significant respiratory disease. Diagnostic criteria include the presence of severe parenchymal lung disease (e.g., chronic obstructive lung disease, interstitial lung disease) or hypoxia. The severity of PH in Group 3 usually correlates with the severity of the lung disease, although some patients exhibit “out-of-proportion” PH. Key differentiation points include pulmonary function tests and high-resolution computed tomography imaging. If pre-capillary PH is confirmed but lung disease is mild, the patient may be classified as Group 1 PAH; however, if significant hypoxia or restrictive/obstructive patterns are present, Group 3 is the appropriate classification.

Group 4: Chronic thromboembolic PH

Group 4 PH also presents with a precapillary hemodynamic profile. The differentiation from Group 1 PAH is not solely hemodynamic but requires imaging evidence of chronic thromboembolism. A ventilation-perfusion (V/Q) scan is the screening test of choice, followed by pulmonary angiography to confirm chronic thromboembolic occlusion. RHC is essential not only for confirming the diagnosis but also for assessing the feasibility of pulmonary endarterectomy or balloon pulmonary angioplasty by quantifying the pulmonary vascular resistance and ruling out significant left heart disease.²³⁾

Vasoreactivity testing

Vasoreactivity testing is a specific component of RHC indicated for a subset of patients with Group 1 PAH-specifically those with idiopathic PAH, heritable PAH, or drug-induced PAH. The primary purpose is to identify the rare patients (approximately 10–15%) who have a significant acute vasodilator response and may benefit from high-dose calcium channel blocker therapy.²⁴⁾ It is generally not recommended for other forms of PH or Group 2 PH, although it may be considered in selected candidates for heart transplantation. The testing involves the administration of a short-acting, selective pulmonary vasodilator (Table 3).²⁵,²⁶,²⁷,²⁸⁾ Patients who meet these criteria are candidates for a trial of high-dose calcium channel blockers (e.g., amlodipine, diltiazem, nifedipine). It is crucial to note that only about half of the acute responders typically show a sustained long-term clinical response to calcium channel blockers.²⁹⁾ Therefore, close clinical follow-up is mandatory.

Table 3. Pharmacological agents for vasoreactivity testing and positive response criteria.

Agent	Administration & protocol	Clinical consideration & side effect
Inhaled nitric oxide	10–20 ppm (up to 40 ppm) via inhaled for 5–10 minutes.	Gold standard agent; measure hemodynamics at baseline and the end of inhalation.
IV epoprostenol	Incremental infusion starting at 2 ng/kg/min; increase every 10–15 minutes.	Less commonly used for screening due to the risk of systemic side effects.
IV adenosine	Start at 50 mcg/kg/min; increase by 50 mcg/kg/min every 2 minutes (maximum 250–350 mcg/kg/min).	Use may be limited by bradycardia, heart block, and hypotension.
Inhaled iloprost	Nebulize 2.5 mcg (diluted in saline); may increase to 5 mcg.	Measurements are taken immediately after the inhalation period.
Positive response criteria	1. Absolute mPAP ≤40 mmHg	Cardiac output must be increased or unchanged to be considered positive.
	2. Reduction in mPAP ≥10 mmHg

IV = intravenous; mPAP = mean pulmonary artery pressure.

DIAGNOSIS OF HFpEF AND EXERCISE HEMODYNAMICS

HFpEF accounts for approximately half of all heart failure cases.³⁰⁾ It poses a significant diagnostic challenge because patients often present with non-specific symptoms like exertional dyspnea, and resting echocardiography may be unrevealing.³¹⁾ In this context, RHC, particularly with exercise provocation, has emerged as a cornerstone for definitive diagnosis.³²⁾

Before proceeding to invasive testing, non-invasive risk stratification is performed using scoring systems like the H₂FPEF and HFA-PEFF scores. The H₂FPEF score aggregates clinical and echocardiographic variables. A score of 0–1 implies low probability, 6–9 implies high probability, and an intermediate score of 2–5 suggests the need for further testing, such as diastolic stress echocardiography or RHC. The HFA-PEFF score is a more comprehensive algorithm proposed by the ESC Heart Failure Association. A total score of ≥5 confirms HFpEF, while a score of 2–4 indicates an intermediate probability, necessitating Step 3 (diastolic stress test or invasive hemodynamics).

The gold standard for diagnosing HFpEF is the demonstration of elevated left ventricular filling pressures. A resting PAWP ≥15 mmHg or LV end-diastolic pressure ≥16 mmHg is diagnostic for HFpEF. This finding confirms that the patient’s symptoms are due to cardiac congestion. However, resting hemodynamics have limited sensitivity (approximately 60%) because many patients with early-stage HFpEF have normal filling pressures at rest that only rise to pathological levels during physical exertion.³³⁾ Therefore, a normal resting RHC does not rule out HFpEF.

For patients with unexplained dyspnea and normal resting pressure (PAWP <15 mmHg), exercise RHC is the definitive test. It assesses the hemodynamic response to physiological stress, unmasking impairments in diastolic reserve. The preferred method is a symptom-limited, multistage exercise test using a supine bicycle ergometer.³⁴⁾ The supine position facilitates continuous hemodynamic monitoring and catheter stability.

• 1. Preparation: A Swan-Ganz catheter is inserted, typically via the right internal jugular vein to allow free movement of the legs. A radial arterial line is often placed for systemic blood pressure and arterial blood gas monitoring.

• 2. Resting measures: Baseline pressure, CO (Fick and/or thermodilution), and mixed venous oxygen saturation.

• 3. Exercise stages: The patient begins cycling at a low workload (e.g., 20 Watts). The workload is increased incrementally (e.g., by 10 Watts or 20 Watts) every 3 minutes to achieve a steady state at each stage.

• 4. Measurements: At the end of each stage, and particularly at peak exercise, hemodynamics are re-measured. It is critical to measure PAWP at end-expiration to minimize respiratory artifacts, which are exaggerated during the hyperpnea of exercise.³⁵⁾

The diagnostic hallmark of HFpEF during exercise is a disproportionate rise in filling pressures relative to the increase in CO (Table 4).³⁶,³⁷,³⁸⁾

Table 4. Hemodynamic criteria for HFpEF diagnosis: exercise and provocation testing.

Diagnostic parameter/method	Criteria & thresholds	Clinical interpretation
Peak exercise PAWP	≥25 mmHg	Primary diagnostic hallmark; effectively distinguishes cardiac dyspnea from non-cardiac causes or healthy controls.
△mPAWP/△CO slope	>2 mmHg/L/min	Confirms a post-capillary etiology; specifically suggests HFpEF rather than primary pulmonary vascular disease.
Peak VO2	<14 mL/kg/min	Supportive of HFpEF diagnosis in the setting of normal systolic function; requires RER ≥1.10 to ensure maximal effort.
Passive leg raise	PAWP ≥18–19 mmHg	Simple alternative for patients unable to exercise; increases venous return, although less sensitive than active exercise testing.
Fluid challenge	PAWP ≥18 mmHg	Represents a pure preload stress test; lacks the neurohumoral and chronotropic components of actual exertion.

HFpEF = heart failure with preserved ejection fraction; PAWP = pulmonary arterial wedge pressure; CO = cardiac output; RER = respiratory exchange ratio; VO₂ = oxygen consumption.

DIFFERENTIATION OF CONSTRICTION, RESTRICTION, AND SEVERE TR

In advanced hemodynamic assessment, differentiating CP from RCM and accurately assessing severe TR are complex tasks where RHC provides unique insights unavailable from non-invasive imaging.³⁹⁾

Constrictive pericarditis vs. restrictive cardiomyopathy

CP and RCM share a similar clinical presentation of predominant right heart failure (edema, ascites, elevated jugular venous pressure) with preserved ejection fraction, making differentiation difficult.⁴⁰⁾ Both conditions are characterized by impaired diastolic filling, leading to elevated filling pressures. Both show high right atrial and left atrial pressures.⁴¹⁾ And the ventricular pressure waveforms exhibit a rapid early diastolic dip followed by a plateau (square root sign).⁴²⁾ This reflects rapid early filling that is abruptly halted by the rigid pericardium or stiff myocardium. Finally, a paradoxical rise or lack of fall in right atrial pressure, as assessed by jugular venous pressure during inspiration, indicating impaired right heart filling, can be seen in both, though historically associated with CP.

The fundamental difference lies in the transmission of intrathoracic pressure. In RCM, the myocardium is stiff, but the pericardial space is normal; therefore, changes in intrathoracic pressure during respiration are transmitted equally to the cardiac chambers. In CP, the rigid, thickened pericardium isolates the heart from intrathoracic pressure changes (dissociation of intrathoracic and intracavitary pressure), but the fixed total cardiac volume creates exaggerated interaction between the ventricles.

In CP, inspiration lowers intrathoracic and pulmonary venous pressure, but this fall is not fully transmitted to the cardiac chambers because the rigid pericardium functionally insulates the heart from intrathoracic pressure change. The reduction in pulmonary venous-to-left atrial driving pressure decreases left atrial and left ventricular filling. At the same time, systemic venous return to the right heart increases, particularly from the extrathoracic vena cava, augmenting RV filling. Because total intrapericardial cardiac volume is constrained, the interventricular septum shifts toward the LV, further reducing LV filling and stroke volume while RV stroke volume increases.⁴³⁾ This produces the characteristic inspiratory discordance of LV and RV systolic pressures and contributes to near-equalization of diastolic pressures across the chambers. During expiration, the reverse occurs (Figure 2). Whereas, In RCM, the inspiratory drop in intrathoracic pressure is transmitted to all chambers. Thus, filling pressures and systolic pressures of both the LV and RV fall together during inspiration and rise together during expiration (Concordance).

Figure 2. Ventricular interdependence in constrictive pericarditis. Simultaneous intracardiac pressure tracings obtained from the LV (pink) and RV (green) are shown together with surface electrocardiography and respiratory monitoring. During inspiration, LV systolic pressure-volume decreases slightly, accompanied by reciprocal changes in RV pressure-volume, reflecting ventricular interdependence. Inspiratory equalization of LV and RV diastolic pressures is also observed.

LV = left ventricle; RV = right ventricle.

In CP, the constraint is external and affects all chambers equally, often leading to equalization of LV end-diastolic pressure and RV end-diastolic pressure (within 5 mmHg). In RCM, LV end-diastolic pressure is often significantly higher than RV end-diastolic pressure due to the inherently higher stiffness of the LV, particularly in conditions like amyloidosis, although this is less specific than respiratory variation. However, relying solely on hemodynamic findings from catheterization for differentiation has become challenging in certain mixed clinical scenarios. For instance, in patients who develop concurrent pericardial disease and myocardial fibrosis following radiation therapy for lung or breast cancer, or in those with coexisting postoperative pericarditis and myocardial dysfunction following cardiac surgery, integrating hemodynamic data with a comprehensive assessment of the patient’s clinical context has become increasingly crucial.⁴⁴,⁴⁵⁾

Hemodynamic assessment of severe TR

Severe TR presents unique hemodynamic challenges. In the setting of torrential TR with a massive regurgitant orifice, Doppler-based estimation of PA systolic pressure may be unreliable because rapid RV-right atrial pressure equalization can generate a low-velocity, laminar regurgitant signal and lead to underestimation of PA systolic pressure.⁴⁶⁾ Conversely, PA systolic pressure may also be overestimated when TR velocity or right atrial pressure is inaccurately assessed, or when forward flow is increased in high-output states. Therefore, invasive hemodynamic assessment is often required when concomitant PH or candidacy for valve intervention must be defined.

The hallmark of severe TR on RHC is a ventricularization of the right atrial pressure waveform. A large, fused c-v wave is observed, resembling the RV pressure trace. The presence of a prominent V-wave indicates that the highly compliant right atrium is being pressurized by the RV systole. RHC is mandatory to directly measure PAP and pulmonary vascular resistance in these patients to guide decisions regarding valve intervention (e.g., tricuspid valve surgery or tricuspid transcatheter edge-to-edge repair). Excluding severe PH is often a prerequisite for intervention. Measuring CO in severe TR is technically difficult. Measuring CO in severe TR can be technically challenging. Thermodilution may be less reliable because regurgitant recirculation can distort the injectate curve and lead to underestimation in some patients,⁴⁷⁾ although more recent data suggest acceptable agreement with direct Fick in selected cases.⁴⁸⁾ When a reference standard is needed and available, direct Fick remains the preferred method. Indirect Fick should be interpreted cautiously because it relies on assumed oxygen consumption.

CONCLUSION

In an era of rapidly evolving non-invasive imaging technologies, RHC remains the reference standard for definitive hemodynamic assessment. The clinical value of RHC, however, lies not merely in performing the procedure but in obtaining accurate, standardized, and physiologically interpretable measurements. Rigorous attention to methodological details—including transducer leveling, respiratory timing, wedge pressure acquisition, and CO determination—is essential to ensure diagnostic accuracy and prevent hemodynamic misclassification. When applied with these principles, RHC continues to provide critical insights into the pathophysiology of PH, heart failure, and complex cardiopulmonary disorders, thereby guiding optimal clinical decision-making.