The history of right heart catheterization (RHC) began in 1929, when Dr. Werner Forssmann, as a surgical trainee in Germany, advanced a 4 French urinary tract catheter from the antecubital fossa to the right atrium and confirmed the position by fluoroscopy [1]. Decades later, Drs. Cournand and Richards won the Nobel Prize in medicine for describing the concept of invasive hemodynamics using RHC [2]. In 1970, a case series of 100 consecutive pulmonary catheterizations with the flow-directed catheter was published [3], validating modern-day RHC developed by Drs. Ganz and Swan [3] (Fig. 1). Since then, RHC has been utilized in many clinical scenarios and endorsed by many societal guidelines (Tables 1,2). It is the objective of this review to summarize the current understanding and indications of RHC.

Fig. 1.

The development of the pulmonary artery catheter. (A) Drs. Swan and Ganz. (B) Swan-Ganz catheter and waveforms generated after floated from the right atrium to the pulmonary arteries. (Figure courtesy of Dr. Peter Ganz, San Francisco General Hospital, University of California, San Francisco).

The utility of invasive hemodynamic evaluation via RHC in patients with acute decompensated heart failure is still under debate. Before the 1970s, an invasive hemodynamic assessment was essential in the diagnosis of structural heart disease [4]. In the late 1970s, however, significant advancements were made in echocardiography. Specifically, Doppler echocardiography permitted the estimation of pressure gradients across stenotic valves and of intracardiac chamber pressures with a good correlation between invasive measurements and Doppler estimations in most circumstances [5, 6]. The use of full Doppler echocardiographic examination has been proposed as a complete, viable replacement to RHC in stable patients with heart failure. Temporelli et al. [7] found an excellent correlation between Doppler echocardiographic results and direct hemodynamic values obtained from RHC. However, RHC remains a crucial tool in the hemodynamic evaluation due to known limitations of echocardiography. Right heart filling pressures are hampered in patients with mechanical ventilation, indwelling cardiac devices can generate artifacts, and patient habitus or dressings after cardiac surgery may make correct alignment of Doppler waveforms impossible and hemodynamic calculations inaccurate. Complex hemodynamic scenarios with multiple high-velocity jets can also render isolating the correct waveform challenging. Furthermore, continuous echocardiography over hours and days to provide real-time hemodynamic data in response to interventions is not feasible in the same manner that continuous hemodynamic monitoring with RHC is feasible.

Despite the advances in technology, physical examination remains crucial in the management of heart failure patients. Thus, it is important to recognize the strengths and limitations of the clinical examination in these patients. In general, the ability to estimate congestion by physical examination is superior to the recognition of an inadequate perfusion status [8]. The physical examination is accurate in the assessment of elevated cardiac filling pressures in only 60–70% of cases, mostly due to elevation in jugular venous pressure [9]. Drazner et al. [10] demonstrated a concordant relationship between elevated right atrial pressure and pulmonary capillary wedge pressure in approximately 80% of patients with decompensated heart failure. Thus, the role of RHC in the clinical scenarios of a patient with elevated right-side pressures that are not correlated with elevated left-sided filling pressures (e.g., in patients with advanced lung disease and pulmonary hypertension), remains invaluable.

The widespread use of RHC has been called into question by some clinicians, primarily because of the Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) trial [11]. That randomized controlled study included nearly 400 patients with heart failure comparing RHC to clinical assessment alone. The study excluded patients for whom RHC may have been warranted by significant renal dysfunction (serum creatinine $>$3.5 mg/dL), prior use of moderate dose inotropes, or pulmonary hypertension. In addition, the ESCAPE trial did not study patients with cardiogenic shock in whom inotropic and vasopressor therapy is frequently used. The study concluded that the use of RHC did not demonstrate a mortality benefit or shorter hospitalization in stable, hospitalized patients. Therefore, the use of RHC should be restricted to complex and severe cases.

The American College of Cardiology Foundation (ACCF)/American Heart Association (AHA) [12] and European Society of Cardiology (ESC) [13] guidelines for the management of heart failure outline the clinical conditions in which the use of RHC should be considered (Table 1). The guidelines emphasize that RHC is not routinely recommended for all patients with decompensated heart failure. Rather, invasive hemodynamic monitoring should be considered in patients with decompensated heart failure refractory to the initial therapy, for patients with unclear volume status and ongoing hypoperfusion, or patients being considered for advanced therapies.

Cardiogenic shock (CS) is the most severe form of heart failure with significant mortality and morbidity [14]. CS is a consequence of myocardial muscle dysfunction either due to ischemic or non-ischemic culprit event, manifested by detrimental organ perfusion and could progress into multiorgan failure.

CS, defined by clinical presentation and invasive hemodynamic criteria, is characterized by a state of tissue hypoperfusion secondary to inadequate cardiac output (CO) in the absence of hypovolemia [15] (Table 3). Within this context, the utility of RHC in the diagnosis, staging, phenotyping, and monitoring of patients in CS is invaluable, especially in the presence of complex hemodynamic interplays such as valvular disease and/or pulmonary hypertension. In 2019, the Society for Cardiovascular Angiography and Interventions released a consensus statement on the classification of CS, which stratifies patients in five stages (A through E in ascending levels of severity) (Table 4, Ref. [15]). While physical exam findings and laboratory biomarkers figure into the schematic, invasive hemodynamic parameters from RHC become a crucial addition to the assessment, especially at the more advanced (C–E) stages of CS (Table 5).

The classical CS invasive hemodynamic profiling is “cold and wet” when low CO is associated with and with elevated systemic vascular resistance (SVR), however, there are several other CS profiling we recognized only with the use of invasive hemodynamic assessment (Table 6, Ref. [14]). Other less frequent subtypes of CS are normotensive and right ventricular (RV) CS. Normotensive CS patients have falsely ‘normal’ systemic blood pressure due to an elevated SVR but in the presence of low CO. In a post-MI CS registry of over 1000 patients, 5% of those had evidence of hypoperfusion with a systolic blood pressure of more than 90 mmHg [16]. RV shock is present in approximately 5% of patients with post-myocardial infarction CS. Several invasive hemodynamic calculations can be crucial in the determination of right ventricular (RV) versus left ventricular (LV) CS: right atrial pressure (RAP) more than 15 mmHg (mostly validated in post LV assist device (LVAD) patients), the ratio of the RAP and PCWP more than 0.8, pulmonary artery pulsatility index (PAPI) lower than 1.0, and RV stroke work index (RVSWI) 600 mmHg $\times$ mL/m${}^2$ are present in RV failure [17, 18].

Cardiac power output (CPO) calculated as mean arterial pressure multiplied by CO and divided by 451 is a strong parameter to assess LV systolic function, especially for patients with chronic systolic heart failure with acute decompensation and a strong predictor of morbidity and mortality [19].

Given the high mortality rate of CS, several institutions have begun deploying ‘shock teams’ to streamline the expedient diagnosis and management of CS patients. Ideally formed by an advanced heart failure, an interventional cardiologist, intensivist, and cardiovascular surgeon, a cardiogenic shock would take time-sensitive decisions, execute a treatment and choose the most appropriate intervention depending on the patient’s status in a multidisciplinary approach, from the escalation of vasoactive drugs to temporary mechanical circulatory support (TMCS) devices in the acute shock phase. Decided which patients might need escalation on therapy for potential recovery or advanced heart failure candidacy, like heart transplantation, needs to be taken into account. Tehrani et al. [20] published a framework for the design and implementation of shock teams and protocols for both post-acute myocardial infarction CS (AMI-CS) and acute or chronic non-ischemic CS (non-AMI-CS). RHC after suspected CS helps to stratify the need for escalation of shock therapy and earlier utilization of TMCS. Survival of CS at their institution increased from 47% to 77% after implementation of risk scores based on invasive hemodynamic parameters and other clinical markers, with a 39% absolute increase in survival. The authors also developed a multifaceted risk score for CS that included the CPO and PAPI for the 30-day risk of mortality [20]. Similarly, the National Cardiogenic Shock Initiative implemented an algorithm designed to address AMI-CS. This algorithm uses invasive hemodynamic assessment and has changed the paradigm from solely “door-to-balloon” to “door-to-support” with the placement of TMCS before coronary revascularization if the cardiac index (CI) is 2.2 L/min/m${}^2$ and LV end-diastolic pressure is $>$15 mmHg [21].

Invasive hemodynamic assessment remains essential in patients who are in CS when the etiology is unknown or not well clarified. Moreover, continuous hemodynamic monitoring of the response to therapeutic regimens may help guide medical therapy. Several observational studies have shown that “tuning up” the hemodynamics in circulatory shock patients (i.e., target a PCWP less or equal than 15 mmHg and a RAP less or equal than 8 mmHg while avoiding systemic hypotension and progressive renal insufficiency) has led to a significant change in the critical care management and is associated with improved outcomes [22].

Invasive hemodynamic assessment is recommended by both American and European heart failure guidelines for the management of heart failure patients being considered for durable LV assist device (LVAD) or cardiac transplantation. In addition, to evaluate the reversibility of pulmonary hypertension, the use of RHC may have important prognostic implications and may help clinicians in their decision to implant an LVAD or to transplant [23]. For example, a study of 657 consecutive heart transplant recipients in Italy from 2000–2018 found that right heart failure (RHF) defined by low PAPI (1.68) was associated with the need for renal replacement therapy and primary graft dysfunction [24]. For both LVAD and transplant patients, in an analysis of the previously described ESCAPE trial, the authors found that an increased RAP/PCWP ratio was associated with adverse clinical outcomes [25].

Pulmonary hypertension occurs frequently in patients with heart failure and has important therapeutic and prognostic implications in both inpatient and outpatient management [26]. The gold standard for diagnosis and monitoring of pulmonary hypertension is right heart catheterization. With the publication of proceedings from the 2018 6th World Symposium on Pulmonary Hypertension, updated definitions and subtypes of pulmonary hypertension were elaborated. Most conspicuously, the threshold for mean pulmonary artery pressure was established at 20 mmHg from the prior cutoff of 25 mmHg [27]. The traditional classification into WHO groupings 1–5 remained unchanged, with WHO group 2 defined as PH due to left heart disease. In addition to etiological groupings, the proceedings defined 3 different hemodynamic profiles: isolated pre-capillary pulmonary hypertension, combined pre-/post-capillary hypertension, and isolated post-capillary pulmonary hypertension [27] (Table 7). Of these profiles, combined pre-/post-capillary PH and isolated post-capillary PH are found in patients with left heart disease. Typically, a transpulmonary gradient (mPA-PCWP) greater than 12 mmHg with a diastolic pulmonary gradient (diastolic PA pressure–PCWP) below 3 mmHg is seen in these patients.

In addition to the standard collection of hemodynamic data, vasoreactivity testing and exercise testing are sometimes important in the evaluation of this patient population. For example, vasoreactivity testing (preferably with inhaled nitric oxide at 10–20 ppm) is performed in patients with PAH (WHO group 1 PH) wherein an absolute drop in mPA by 10 mmHg to an absolute value of less than 40 mmHg while maintaining cardiac output. In advanced HF patients with WHO group 2 PH being considered for transplantation, vasoreactivity testing may be used to assess for fixed PH and prognosticate before transplantation [42]. Exercise testing or fluid challenge during RHC can also be used to unmask pulmonary hypertension in patients with borderline hemodynamic profiles [28].

Finally, precise diagnosis with meticulous attention to detail is crucial when evaluating the heart failure patient with PH for several reasons. Administration of therapies directed towards PAH (WHO group 1 PH) has met with mostly negative results including worsening of HF and increased mortality across a range of PAH therapies [26]. Furthermore, the degree, presence of, and vasoreactivity of PH in patients with advanced HF can have important prognostic consequences when considering the placement and adjustment of advanced therapies including temporary and durable mechanical circulatory support as well as transplantation.

For patients with advanced heart failure, RHC will remain an important standard of care for diagnostic and prognostic purposes as well as for long-term management.

Authors AA and JMC contributed equally. CYGM contributed substantially. Each author was involved in every step of the writing process.

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This research received no external funding.

The authors declare no conflict of interest.