key: cord-0060475-v2l8zlp6
authors: Isseh, Iyad N.; Lee, Ran; Khedraki, Rola; Hoffman, Karlee
title: A Critical Review of Hemodynamically Guided Therapy for Cardiogenic Shock: Old Habits Die Hard
date: 2021-03-23
journal: Curr Treat Options Cardiovasc Med
DOI: 10.1007/s11936-021-00903-8
sha: 79936b36601008c9b1f7d73db6f8152d76b3db9c
doc_id: 60475
cord_uid: v2l8zlp6

PURPOSE OF REVIEW: Here, we review the importance of using hemodynamic data to guide therapy and risk stratification in cardiogenic shock as well as the various definitions of this syndrome that have been used in prior studies. Furthermore, we provide perspective regarding the controversy surrounding pulmonary artery (PA) catheter use as well as current society guidelines and scientific statements. Lastly, we review the technical aspects for accurate interpretation of data of cardiogenic shock. RECENT FINDINGS: More recent studies specifically evaluating cardiogenic shock patients have shown higher mortality when PA catheters were not used. Furthermore, initiatives are underway to develop more standardized definitions of cardiogenic shock, including the SCAI Shock Classification Scheme. Only by having a standardized fashion of conveying severity of shock will we be able to more systematically study this patient population and improve outcomes moving forward. SUMMARY: PA catheters are critical to the prognostication and management of a subset of patients with cardiopulmonary disease, particularly in those with pulmonary hypertension, cardiogenic shock, or requiring mechanical circulatory support or undergoing evaluation for advanced heart failure therapies.

When the Swan-Ganz catheter was introduced in 1970, it was considered revolutionary in the then nascent era of cardiac catheterization [1] . Up until then, pulmonary artery catheterization was cumbersome and required significant technical skill to manipulate stiff catheters which often caused ectopy and required the use of fluoroscopy for correct positioning [2] . However, the inspiration for using a balloon-tipped catheter to "flow" into the pulmonary artery (PA) position using the natural fluid mechanics of cardiac circulation serendipitously came to Dr. H.J.C. Swan while watching sailboats progress on a calm sea in Santa Monica [3] . He then began work with his colleague, Dr. William Ganz, to develop a novel flexible catheter with an inflatable balloon tip. This invention suddenly facilitated the transfer of hemodynamic monitoring from the confines of the catheterization laboratory to the bedside without the use of fluoroscopy and with minimal ectopy.

Questions about the utility of PA-guided therapy have since emerged after several randomized controlled trials cast doubt regarding benefit in the routine management of critically ill patients [3] . Although swan guided therapy has stimulated controversy in some academic circles, there is no question that the PA catheter is an essential tool among most cardiac intensive care units in the management of cardiogenic shock. Here, we review the utility of invasive hemodynamic monitoring in cardiogenic shock. We also provide a review of contemporary literature in light of significant advances in therapy and an increasing repertoire of therapeutic tools for management of cardiogenic shock in the modern era, including temporary mechanical circulatory support devices (MCS).

Cardiogenic shock: classic definitions, novel parameters, and evolving paradigms Essential to the evaluation and management of cardiogenic shock is the establishment of standard definitions for this high-acuity disease state. Shock is defined as a state of hypotension which results in tissue hypoperfusion. Cardiogenic shock is a state of diminished cardiac output leading to inadequate end-organ perfusion, with the primary insult coming from a reduction in myocardial contractility. This can occur from a variety of etiologies affecting the myocardium, endocardium, pericardium, or electrical conduction system. Subsequently, compensatory mechanisms of peripheral vasoconstriction and fluid retention lead to a rise in biventricular filling pressures. Coupled with ongoing hypotension which diminishes primary coronary perfusion pressure and mediates ongoing cardiac ischemia, a vicious downward spiral of cardiac dysfunction ensues [4] .

Historically, the standard definitions of cardiogenic shock have been described by landmark clinical trials such as SHOCK (Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock) and IABP-SHOCK II (Intraaortic Balloon Pump in Cardiogenic Shock II) [5] [6] [7] . In the SHOCK trial, the definition of cardiogenic shock was any cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion. It was further clinically defined as a systolic blood pressure (SBP) G 90 mmHg for ≥30 min or support to maintain SBP ≥ 90 mmHg and markers of organ hypoperfusion such as urine output G 30 mL/h or cool extremities. Hemodynamic criteria were defined as a cardiac index of ≤ 2.2 L/min/m 2 and a pulmonary capillary wedge pressure (PCWP) ≥ 15 mmHg. The IABP-SHOCK II trial further refined these definitions by clarifying utilization of catecholamines to maintain SBP 9 90 mmHg, while delineating further signs of impaired end-organ perfusion to include altered mental status, and lactate level 9 2.0 mmol/L (Table 1) .

Over the last several years, further nuance has been provided to these classic definitions. A recent American Heart Association Scientific Statement on Cardiogenic Shock outlined four classic phenotypes of shock based on volume status and peripheral circulation [8] . Classic "cold and wet" cardiogenic shock is defined as a state of diminished cardiac index with concomitant elevated systemic vascular resistance (SVR) and pulmonary congestion, while "cold and dry" euvolemic cardiogenic shock was defined as reduced cardiac index and elevated SVR, but with a normal PCWP.

These classic definitions of shock have traditionally been applicable for left-sided cardiogenic shock, in which the patient has clinical signs including rales, an S3, and a displaced apical impulse, and hemodynamics using a PA catheter reveal elevated SVR, PCWP, and reduced cardiac index. A novel hemodynamic parameter, the cardiac power output (CPO), was tested in a sub-study of patients from the SHOCK trial and found to correlate strongest with inhospital mortality [9] . Defined as mean arterial pressure × cardiac output / 451, CPO in units of watts (W) was calculated in 181 out of 541 patients included with NCSI [10] 2019 AMICS Prolonged hypotension (SBP G 90 mmHg, or inotropes/vasopressors to maintain SBP 9 90 mmHg) Signs of end-organ hypoperfusion (cool extremities, oliguria or anuria, or elevated lactate levels) Hemodynamic criteria represented by CI G 2.2 L/min/m 2 or CPO G 0.6 W SCAI [29] 2017 ALL CS CS patients staged based on severity of shock: A: "At risk" for CS. A patient who is not experiencing signs or symptoms of CS but is at risk for its development. B: "Beginning" CS (pre-shock/compensated shock). A patient who has clinical evidence of relative hypotension or tachycardia (SBP G90 mmHg, MAP G60 mmHg or 9 30 mmHg drop from baseline) without hypoperfusion (cold, clamped extremities, poor UOP, mental confusion, etc). Laboratories may be normal. C: "Classic" CS. A patient with hypoperfusion that requires an initial set of interventions (inotropes, pressor, MCS, or ECMO) beyond volume resuscitation to restore perfusion. These patients typically present with the classic shock phenotype of hypotension along with hypoperfusion. Laboratory findings may include impaired kidney function, elevated lactate, BNP, and/or liver enzymes. Invasive hemodynamics demonstrates depressed CI. D: "Deteriorating" CS. A patient who has failed to stabilize despite intense initial efforts and further escalation is required. Classification in this stage requires that the patient has had some degree of appropriate treatment and medical stabilization. In addition, at least 30 min has elapsed but the patient has not responded. Escalation is an increase in the number or intensity of intravenous therapies to address hypoperfusion, or addition of MCS. E: "Extremis" CS. A patient with circulatory collapse, frequently (but not always) in refractory cardiac arrest with ongoing CPR or ECMO-facilitated CPR.

CSWG [24] Established 2017 ALL CS Sustained episode of SBP G 90 mmHg for at least 30 min CI G 2.2 L/(min m 2 ) determined to be secondary to cardiac dysfunction Requirement for either pharmacological support (vasopressors or inotropes) or short-term MCS (i.e., IABP, Impella, VAECMO) EURO SHOCK [46] Study start 2019 AMICS SBP G 90 mmHg 9 30 min, or a requirement for a continuous infusion of vasopressor or inotropic therapy to maintain SBP 9 90 mmHg Clinical signs of pulmonary congestion, plus signs of impaired organ perfusion with at least one of the following: Altered mental status Cold and clammy skin and limbs Oliguria with a UOP G 30 mL/h Elevated lactate of 9 2.0 mmol/L DANGER SHOCK [47] Study start 2012 AMICS Peripheral sign of tissue hypoperfusion with lactate ≥2.5 mmol/L Persistent (9 30 min) SBP G 100 mmHg and/or need for vasoactive therapy LVEF G 45% on echocardiography CS cardiogenic shock, CI cardiac index, IABP intra-aortic balloon pump, LVEF left ventricular ejection fraction, MAP mean arterial blood pressure, MCS mechanical circulatory support, PCWP pulmonary capillary wedge pressure, SBP systolic blood pressure, UOP urine output, VAECMO venoarterial extracorporeal membrane oxygenation predominant left-sided failure in the setting of acute myocardial infarction-cardiogenic shock. In multivariate analysis, CPO (OR 0.60 (0.44-0.83 CI), p = 0.002) was strongly associated with in-hospital mortality, independent of other significant variables such as age or history of hypertension. A CPO cutoff of 0.53 W was found to most accurately predict in-hospital mortality (c-statistic 0.69) [9] . In more recent analysis from the National Cardiogenic Shock Initiative, a CPO G 0.6 W and a serum lactate 9 4 were independent predictors of mortality, further validating the utility of this novel hemodynamic calculation in monitoring patients with this highly complex disease state [10] .

Other shock profiles exist outside of left-sided cardiogenic shock. Predominant right-sided cardiogenic shock can occur in right ventricular myocardial infarction, in acute pulmonary embolism, in acute-on-chronic right-sided valvulopathy including tricuspid regurgitation and pulmonary regurgitation, in acute-on-chronic pulmonary arterial hypertension, as sequelae after left ventricular assist device (LVAD) implantation, or as a result of complex congenital cardiac lesions. Specific evaluation of right heart failure requires hemodynamic parameters provided by real-time PA catheter monitoring, including right atrial pressure (RAP) to PCWP ratio, RV stroke work index, and pulmonary artery pulsatility index (PAPi). Calculated by subtracting the pulmonary artery diastolic pressure from the pulmonary artery systolic pressure and dividing by the RAP, the PAPi has been utilized primarily to predict RV failure after LVAD surgery [11] . However, it has also been utilized in patients presenting with RV myocardial infarction, proving to have the highest sensitivity and specificity to predict in-hospital mortality among this high-risk cohort [12] .

In 2019, the Society for Cardiovascular Angiography & Interventions (SCAI), in combination with other major societies encompassing both cardiovascular medicine and critical care medicine along with cardiothoracic surgery, published a clinical expert consensus statement on the classification of cardiogenic shock [13••] , placing a clear emphasis on early recognition of these disease states, as well as demonstrating the spectrum of clinical presentation. In creating a five-step pyramid scheme for cardiogenic shock, the consensus document defines clinical description, clinical exam, biochemical markers, and hemodynamic evaluation along the continuum of cardiogenic shock, from Stage A (at risk) to Stage B (beginning) to Stage C (classic) to Stage D (deteriorating) to Stage E (extremis). The new schema emphasizes that shock is a progressive state. There is inherent emphasis made on time to recognition, time to evaluation, and ultimately time to perfusion, whether that is with pharmacologic or MCS, to prevent the progression from Stage A to Stage E. This classification scheme has been applied in different studies, both retrospective and prospective, to accurately stratify the risk of in-hospital mortality [14, 15] . In the retrospective Mayo Clinic study, each progressive SCAI shock stage was associated with increased hospital mortality irrespective of cause of cardiogenic shock. In the prospective study by Baran et al. , the initial SCAI stage predicted survival, further emphasizing the need for accurate and early hemodynamic monitoring. In a recent "State-of-the-Art Review: a Standardized and Comprehensive Approach to the Management of Cardiogenic Shock," a multidisciplinary approach utilizing standardized protocols was advocated that emphasizes early invasive hemodynamics with the aim of early diagnosis, early classification of shock severity using common nomenclature (SCAI CS staging system), and early phenotyping of CS type [16] .

The increasing heterogeneity and phenotyping of different cardiogenic shock states, along with the clear recognition that time to perfusion is paramount to prevent the further downward spiral of organ hypoperfusion, highlights the need for accurate hemodynamic monitoring early in patients who are at risk for the development of shock or in beginning stages according to the SCAI Shock Classification. These recent advances in our knowledge of cardiogenic shock, along with scientific societal impetus to improve systems of care to reduce the associated high mortality, have the potential to improve the care delivery of this critically ill population. However, previous studies regarding the utility of invasive hemodynamic monitoring continue to pose challenges to contemporary care of cardiogenic shock.

In 1996, the SUPPORT trial investigators analyzed a critically ill adult population from ICUs across multiple academic medical centers in an observational study, finding via case-matching analysis that use of right heart catheterization (RHC) in the first 24 h of care was associated with higher 30-day mortality (OR 1.24; 95% CI 1.03-1.49), in addition to an increase in mean length of stay and cost per hospital stay [17] . However, the percentage of patients with "congestive heart failure" as disease category was only 7% in the group without RHC and 10% in the group with RHC, suggesting that widespread use of RHC in patients with respiratory failure or undifferentiated multisystem organ dysfunction may not be appropriate. This led to further analysis with the landmark Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheterization Effectiveness (ESCAPE) Trial in 2005, which was a randomized controlled trial of 433 patients at 26 institutions assigned to receive PA catheter-guided therapy vs. therapy by clinical assessment alone [3] . In a population of patients with acute-on-chronic decompensated heart failure without cardiogenic shock, the routine use of PA catheter-guided therapy in addition to clinical assessment had no difference on the primary end point of days alive and out of the hospital during the first 6 months (133 days vs. 135 days, HR 1.00 95% CI 0.82-1. 21 [19, 20] and societal guidelines [21] , both tested the use of PA catheter in patients with acute decompensated heart failure and recommend against routine use in heart failure hospitalizations. However, patients with cardiogenic shock have been excluded from the above trials investigating all-comer critically ill states or in routine admissions for decompensated heart failure. A recent retrospective study utilizing the National Impatient Sample investigating the use of PA catheter in patients who developed CS during index hospitalization showed that PA catheter use was associated with lower mortality (35.1% vs. 39.2%, p G 0.001) which remained lower in the PA catheter group after propensity matching. By the end of the study period (final year), mortality for CS patients with PA catheter was 29.7% compared with 38.1% in those without it [22] . In a subspecified group of patients with acute myocardial infarction-related cardiogenic shock being supported with temporary percutaneous ventricular assist device therapy, another study utilizing the National Inpatient Sample found that the use of PA catheter was associated with improved outcomes [23] . More recently, the Cardiogenic Shock Working Group, a large multicenter registry representing real-world patients with CS in the contemporary MCS era, found that complete PA catheter-derived hemodynamic data prior to MCS initiation is associated with survival from CS across all SCAI CS stages and having no PA catheter assessment was associated with higher inhospital mortality than complete PA catheter assessment [ [26] . The 2012 Surviving Sepsis Campaign: international guidelines for management of septic shock recommends against the routine use of PA catheters in patients with sepsis-induced acute respiratory distress syndrome (I, A) [27] . For routine management of heart failure without evidence of tissue hypoperfusion, the ACC/AHA 2013 guidelines for management of heart failure recommend against the routine use of PA catheters in acute decompensated heart failure patients who are normotensive and responding to medical therapy. However, they recommend monitoring with a PA catheter only in patients with respiratory distress or impaired systemic perfusion when clinical assessment is inadequate (I, C) or in patients who have unclear fluid status, low systemic systolic pressure, worsening of renal function with therapy, and requirement of parenteral vasoactive agents, or who are being considered for advanced heart therapies (durable left ventricular assist device or transplantation) (IIa, C) [21] . Similarly, the 2013 ISHLT guidelines for MCS recommend PA catheter utilization in the following clinical situations: after MCS if persistent or recurrent HF symptoms to evaluate for evidence of RV failure or device malfunction (I, B); after MCS placement when evaluating for myocardial recovery before pump explantation (IIa, C); and at regular intervals in patients being evaluated for or listed for heart transplant for evaluation of irreversible pulmonary hypertension (I, A), which is the only Class IA indication listed in any society guidelines [28] . However, in light of recent evidence showing potential benefit of invasive hemodynamic monitoring in CS with tissue hypoperfusion, there has been recent updates to scientific statements regarding the use of the PA catheter in CS and MCS. The 2017 AHA scientific statement on contemporary management of cardiogenic shock states to consider PA catheter utilization early in the treatment course in patients not responsive to initial therapy or in case of diagnostic or therapeutic uncertainty [8] . Similarly, the 2017 SCAI/HFSA clinical expert consensus document on the use of invasive hemodynamics for the diagnosis and management of cardiovascular disease recommended invasive hemodynamic assessment for diagnosis of cardiogenic shock; continuous hemodynamic monitoring with a PA catheter in patients with MCS; to guide weaning of MCS; and to assess candidacy for and transition to advanced heart failure therapies (durable left ventricular assist device or transplantation) [29] .

While there are no recommendations to apply PA catheters routinely to heterogeneous populations of critically ill patients or all patients with acute decompensated heart failure, growing evidence is supporting the benefit of early invasive hemodynamic monitoring in patients with CS who have signs of tissue hypoperfusion such as elevated lactate levels or markers of end-organ dysfunction. Potential benefit of early use of MCS is prevention of multi-organ failure and improved outcomes [30] . Early implementation of PA catheters in CS leads to rapid diagnosis and identification of shock phenotype which can allow for early escalation of therapy. Once MCS is initiated, PA catheter hemodynamics determine the efficacy of the initially chosen form of MCS and the need for MCS escalation. Table 2 summarizes most common forms of percutaneous mechanical circulatory support.

There is also data supporting invasive hemodynamic monitoring in acute myocardial infarction complicated by CS. The National Cardiogenic Shock Initiative demonstrated that adherence to a protocol-based approach emphasizing "best practices" including utilization of a PA catheter (92% of patients had PA catheter monitoring) was associated with improved outcomes [10] . Similarly, in a retrospective registry of acute myocardial infarction complicated by CS treated with Impella, survival improved when a PA catheter was used (49% vs 63%, p G 0.0001) [31] .

Hemodynamic data provided by a PA catheter can help with early identification of univentricular vs biventricular failure in CS, thus guiding appropriate therapies. Masked right ventricular failure frequently complicates left ventricular failure, and availability of PA catheter data before device selection would alert the clinician to the potential need for early initiation of right ventricular MCS [11, 12, 32, 33] .

Escalation of support can also be considered when the use of an initial support device results in unintended hemodynamic effects. It is now well recognized that LV distention and pulmonary edema can be deleterious consequences of venous-arterial extracorporeal membrane oxygenation. Routine use of LV unloading devices in venous-arterial extracorporeal membrane oxygenation is controversial, but recent evidence has emerged recommending its use [34] . Invasive hemodynamic monitoring can identify scenarios where LV unloading is needed (e.g., lack of arterial line pulsatility, elevated PCWP) by a continuous axial flow device.

The impact of systemic inflammatory response syndrome (SIRS) in CS is significant. In later stages of CS, a paradoxical vasodilatory phase of CS can occur due to SIRS secondary to endogenous cytokine release [35, 36] . Clinical SIRS as evidenced by fever, elevated white blood cell count, and low SVR was observed in many patients with confirmed CS complicating acute myocardial infarction in the randomized SHOCK trial and often led to a secondary clinical diagnosis of suspected sepsis. However, out of the 54 patients in the SIRS group, 14 were "culture-negative" and had no source of infection identified [37] . PA catheter utilization in this subset of CS patients is important to identify this "mixed picture," guide therapy, and avoid mismanagement in acute care of the critically ill patient.

Adequately acquiring hemodynamic data from a PA catheter along with accurate interpretation is important for appropriate decision-making in CS, and clinical decisionmaking based on inaccurate information from PA catheters can have unfavorable outcomes (Fig. 1) . Trottier and Fig. 1 . Normal pulmonary artery catheter pressure waveform tracing. RA (blue waveform): "a" atrial systole/contraction, "c" closure of tricuspid valve, "x" atrial relaxation, "v" ventricular systole/contraction (and atrial diastole), "y" passive filling of RV. RV (yellow waveform): "S" systole, "D" diastole, "ED" end diastole. PA (red waveform): "S" systole, "D" diastole, "Di" dicrotic notch, mean PA pressure is PAS + (PAD × 2) / 3. PCW (green waveform): "a" atrial contraction, "v" ventricular contraction, mean PCW pressure is mean of "a" descent. RA, right atrium; RV, right ventricle; PA, pulmonary artery; PCW, pulmonary capillary artery wedge. 

Pulmonary capillary wedge pressure tracings during different modes of respiration during a normal respiration: PCWP measured at end expiration; b PVV: in a typical patient under mechanical ventilation, positive-pressure ventilation increases intrathoracic pressures. Usual hemodynamic tracings during positive-pressure ventilation rise during inhalation and fall during exhalation, and typical PCWP measurements are made in the troughs of the respiratory cycle. c PVV: note here that there is more significant negative intrathoracic pressure generated by the patient's respiratory muscles (Pmus) compared to the contribution from the ventilator positive pressure (Pvent). As a result, the PCWP tracing at end-tidal CO 2 , which signifies end expiration (top right of the shark fin), is measured similarly in this ventilated patient as it would be in a spontaneously breathing patient just prior to the onset of the negative waveform deflection. Red circles indicate end expiration. Therefore, the accurate measurement of pulmonary wedge pressure is~30. PCWP, pulmonary capillary wedge pressure; PVV, positive-pressure ventilation. Taylor found that one-third of critical care physicians participating in a study incorrectly identified PCWP tracings [38] . Detailed attention to several factors when performing a right heart catheterization is required. In a prospective study, a standard-of-care clinical protocol was instituted where if PCWP saturation suggested incomplete occlusion (i.e., G 90% or not within 5% of systemic arterial saturation), up to 2 additional attempts are made to obtain an occlusive PCWP saturation. Utilization of this protocol resulted in significantly lower PCWP, higher PVR, and clinically relevant pulmonary hypertension reclassification of 11.8% of patients [39••] . A systematic approach to PA catheter insertion and waveform measurement is essential [40] . The pressure transducer should be zeroed to atmospheric pressure at the level of the left atrium (usually located in the midthorax level). The pressure tracing quality should be examined. Any signs of signal dampening should be investigated and corrected. All measurements should be made at end expiration, irrespective of the mode of ventilation (Fig. 2a) . During normal spontaneous ventilation (negative pressure), all pressures should be measured at the peak of the waveform. However, measurements during positivepressure ventilation should be made at the troughs of the respiratory cycle ("end of the valley") (Fig. 2b) . However, there are certain scenarios where mechanically ventilated patients can still generate negative-pressure ventilation which could be misleading when measuring PCWP. Waveform capnography and end-tidal CO 2 monitoring can be useful adjuncts to accurate hemodynamic monitoring in mechanically ventilated patients (Fig. 2c) . Additionally, under the conditions of labored respiration or wide respiration variation, the best signal quality may be obtained by measurements during controlled respiration and selection of hemodynamic monitor signal averaging routines [41••] . Different hemodynamic parameters obtained from the PA catheter are summarized in Table 3 .

The modern era has seen substantial progress in defining different hemodynamic parameters and modules to aid in the diagnosis, prognosis, and treatment of cardiopulmonary disease. While the PA catheter remains the cornerstone of invasive hemodynamic monitoring in current clinical practice, the introduction of the left ventricular conductance catheter and subsequently derived left ventricular pressure-volume loop (PVL) by Baan et al. in 1984 is increasingly being studied to evaluate hemodynamics of MCS [42] . Left ventricular conductance catheters measure instantaneous conductance in the left ventricle, which is then converted to ventricular blood volume using complex formulas. More recently, non-invasive PVL methods have been evaluated in vivo and have shown to be feasible in patients with a durable left ventricular assist device [43] . Under normal conditions, the PVL is roughly trapezoidal. The 4 sides of the loop represent phases of the cardiac cycle: (1) isovolumic contraction; (2) ejection; (3) isovolumic relaxation; and (4) filling (Fig. 3a) . The shape of the loop depends on ventricular preload and afterload. Although PVL utilization in current clinical practice is limited, PVL-derived data can be additive to PA catheter hemodynamics in an increasingly complex subset of CS patients requiring temporary MCS. PVLs can be useful for demonstrating the hemodynamics of different MCS devices and confirming favorable hemodynamic impact. Left ventricular unloading reduces myocardial oxygen demand, optimizes myocardial energetics, and may facilitate myocardial recovery. Left ventricular pressure-volume area provides the strongest index of myocardial oxygen consumption (Fig. 3b) . It is equivalent to the total mechanical energy performed by the heart on each beat and is represented on the PVL by the area bounded by the end-systolic and end-diastolic pressure-volume relationship curves and the systolic portion of the pressure-volume curve. Direct LV unloading with a continuous axial flow pump leads to reduction of the pressure-volume area due to a reduction in end-diastolic volume and end-diastolic pressure (preload) (Fig. 3c) . It also contributed to the overall reduction of the pressure-volume area since the isovolumic periods of ejection and relaxation no longer exist due to continuous pumping of volume from the left ventricle to the aorta [43] .

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patients with acute decompensated heart failure. However, in current clinical practice and moving forward, PA catheters should be utilized in the evaluation and management of cardiogenic shock and temporary MCS. Invasive hemodynamics are critical for diagnosis and treatment of this subset of patients with cardiopulmonary disease.

Iyad N. Isseh, Ran Lee, Rola Khedraki, and Karlee Hoffman declare that they have no conflict of interest.

All authors report no disclosures.

All reported studies/experiments with human or animal subjects performed by the authors have been previously published and complied with all applicable ethical standards (including the Helsinki declaration and its amendments, institutional/national research committee standards, and international/national/institutional guidelines).