Initial Management of Cardiogenic Shock: History
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Contributor:
Effie Polyzogopoulou
,
Sofia Bezati
,
Grigoris Karamasis
,
Antonios Boultadakis
,
John Parissis

Cardiogenic shock (CS) is a complex syndrome manifesting with distinct phenotypes depending on the severity of the primary cardiac insult and the underlying status. As long as therapeutic interventions fail to divert its unopposed rapid evolution, poor outcomes will continue challenging health care systems. CS represents a life-threatening condition equated to a dismal prognosis. Since the introduction of the fundamental mechanisms of shock in 1972, CS has been universally defined as a state of severe end-organ hypoperfusion and tissue hypoxia resulting primarily from cardiac pump failure.

  • cardiogenic shock
  • risk stratification
  • risk scores
  • management

1. Symptom Relief

Pain and anxiety should be cautiously managed with the administration of morphine in selected patients with intense insisting pain not resolving with supportive treatment. Routine use of opiates is not recommended [1], as morphine has been associated with increased need for mechanical ventilation support, prolonged hospitalization and worse prognosis [2].

2. Fluid Resuscitation

In the absence of signs of congestion and in patients with preload-dependent phenotypes, fluid resuscitation should be considered with boluses of normal saline or Ringer’s lactate, 250 mL over 15–30 min and under close monitoring with POCUS [3]. POCUS is a dynamic tool for the real-time and serial assessment of volume status and systematic congestion in order detect volume overload and to guide fluid administration. Valuable parameters for optimizing and monitoring fluid resuscitation include the IVC respiratory variation and collapsibility index, the presence of a B-line profile in the lungs, LV and RV diastolic diameters, LV filling pressure (e/e’) and RV filling pressure [3][4], as well as VExUS score [5]. Passive leg raising (PLR) could be reliably used in order to assess fluid responsiveness [6][7]. Fluid responsiveness is the increase in cardiac output of greater than 10% following a 500 mL fluid bolus [8]. PLR, acting as an endogenous fluid challenge, augments venous return, central venous pressure and biventricular preload, and the eventual rise in cardiac output indicates the need for volume expansion. Performance of the test in the ED setting could be aided by the use of echocardiography, estimating changes in the CO through the measurement of the left ventricular outflow tract velocity time integral (LVOT VTI) [9][10].
Currently, data on crystalloid type remain controversial for use in sepsis and shock. There is lack of robust data in the literature specifying the appropriate type of crystalloid fluid for CS patient resuscitation. There is a relative concern regarding the use of saline solutions, as they may cause hyperchloremic metabolic acidosis and acute kidney injury (AKI) [11], and since cardiorenal syndrome is a common complication of CS [12], selection of the least harmful fluid retains a significant importance. Studies on critically ill ICU patients have shown a favorable effect of balanced crystalloid (plasmalyte or Ringer’s lactate) versus saline administration with respect to the need for renal replacement therapy (RRT), AKI and mortality [13][14]. Hammond et al. showed in a metanalysis that administration of balanced crystalloids resulted in a relative reduction in the risk of death at 90 days, ranging from a 9% to 1% relative increase [15]. However, two other metanalyses concluded that there was no statistically significant difference between administration of balanced crystalloid solutions and saline in terms of mortality, incidence of AKI and RRT [16][17]. Given the rather contradictory results, and as critically ill ICU patients represent fairly heterogeneous populations, more studies are needed in order to elucidate which is the appropriate fluid therapy for such high-risk patients, especially those with CS.

3. Oxygenation Support

The need for immediate intubation and mechanical ventilatory support must be addressed on arrival on a patient-to-patient basis [1]. Clinical presentation and point-of-care-acquired data will define the choice of noninvasive ventilatory support (NIV) versus invasive mechanical ventilatory support (IMV) [18]. The majority of patients with signs of congestion and without signs of acute RV failure will benefit from positive pressure ventilation both in respiratory and hemodynamic features, since the mechanical-ventilation-related decrease in left ventricular (LV) preload and afterload can reduce the workload of the failing LV [19][20]. Special caution must be taken with hemodynamically unstable patients who are not responding to initial therapy with vasopressors and inotropes and with those with signs of acute RV failure, where the reduction in the preload of the RV and increase in pulmonary vascular resistance caused by positive intrathoracic pressures may lead to further hemodynamic deterioration [20][21]. In this context, in most of the patients with CS, an early NIV trial of 30 min to 1 h will be beneficial, along with initial hemodynamic stabilization, and may help to avoid endotracheal-intubation-related risks such as airway complications, further destabilization due to anesthesia induction and the need for ongoing sedation [19]. Furthermore, IMV is associated with complications such as ventilator-acquired pneumonia, increased length of ICU stays, and increased in-hospital mortality [22]. Major contraindications to NIV are altered mental status on presentation, refractory hypotension, acute RV failure, facial deformities, secretions and vomiting, as well as an uncooperative patient [20][21][23]. The choice of NIV mode (C-PAP vs. Bi-PAP) depends mainly on the presence of hypercapnia, which outlines the need to support both oxygenation and ventilation [18]. Nevertheless, in patients scheduled for primary coronary intervention, the choice of IMV with early intubation and stabilization during the ED stay may be preferential, considering patient control, safety and positioning in the cath-lab. The indications and initial settings for both NIV and IMV are presented in Table 1.
Table 1. Indications and initial settings for both noninvasive ventilation (NIV) and invasive mechanical ventilation (IMV) [18][19].
Mechanical Ventilation
  Noninvasive Ventilation Intubation and Invasive Ventilation
  C-PAP Bi-PAP Intubation
Indications Hypoxia without hypercapnia Hypoxia + hypercapnia Failed NIV trial
Refractory shock
Altered mental status
Severe acid–base disorder
Scheduled PCI and concomitant respiratory failure
Initial Settings Initial Pressure:
5–10 cm H2O
Increase by 2 cm H2O to target oxygenation
Target SPO2 ≥ 92%		 Initial IPAP: 10 cm H2O
Increase by 2 cm H2O up to 20 cm H2O
Avoid IPAP > 20 cm H2O
Initial EPAP: 5 cm H2O
Increase by 2 cm H2O to target oxygenation		 MV in non-RV failure patients
Initial FiO2 = 100%, VT = 6–10 mL/kg of IBW, RR = 10–20 breaths/min
Maintain Ppl < 30 cm H2O, monitor auto-PEEP
PEEP = 5–10 cm H2O, Increase by 2 cm H2O to target SPO2
MV in RV failure patients
Avoid PPV if possible
Optimize hemodynamics
Maintain normovolemia
Induction agents of choice:
Ketamine (1–2 mg/kg) or Etomidate (0.1–0.3 mg/kg)
Opioids
Benzodiazepines
Avoid Propofol
Administer all induction agents at lowest necessary dose
Drug combinations may be preferable
Initial PEEP 2–5 cm H2O—maintain low PEEP
Abbreviations: Bi-PAP = bilevel positive airway pressure; C-PAP = continuous positive airway pressure; EPAP = expiratory positive airway pressure; FiO2 = fraction of inspired oxygen; IBW = ideal body weight; IPAP = inspiratory positive airway pressure; MV = mechanical ventilation; NIV = noninvasive ventilation; PCI = percutaneous coronary intervention; PEEP = positive end-expiratory pressure; Ppl = plateau pressure; PPV = positive pressure ventilation; RR = respiratory rate; RV = right ventricular; SPO2 = peripheral capillary oxygen saturation; VT = tidal volume.

4. Vasoactive Agents

Inotropes and vasopressors represent a necessary evil in the initial management of patients on the verge of circulatory compromise. They are indispensable and promptly available pharmacological agents, but they should be used at the lowest possible dose and for the lowest possible duration [24][25][26], since prolonged administration is associated with increased oxygen demand (further aggravating myocardial ischemia), increased afterload, impaired microcirculation, arrhythmogenesis [27] and mortality [28]. Their hemodynamic effects may vary, and selection of the appropriate agent should be based on CS etiology, hemodynamic profile and shock severity [27][29][30].
Use of vasopressors and inotropes should be individualized based on patient fluid status and CS etiology and should be adjusted based on clinical judgement. In fluid-responsive patients with signs of hypoperfusion (tachycardia and vasoconstriction) but without hypotension (compensated CS), inotropes (dobutamine or levosimendan) may be cautiously started after first the bolus of fluids has failed to restore peripheral organ perfusion. Attention is required in patients with RV dysfunction who may not tolerate fluid administration or in patients with signs of congestion. When hypotension is also present, concomitant administration of an inotropic agent and a vasopressor (preferably norepinephrine) should be initiated and titrated until perfusion is restored. In patients with refractory shock, escalation of therapy is required with the addition of a second vasopressor (vasopressin) or MCS [30].
Norepinephrine is recommended as a first-line vasopressor (Class IIb/B recommendation) [1] to restore end-organ perfusion and maintain systolic blood pressure [3][27]. Additionally, through cardiac β1 adrenergic stimulation, it enhances cardiac contractility and ventricular–arterial coupling [31]. The exact target of SBP is not fully clarified, but an initial goal of SBP > 90 mmHg and/or MAP of 55–75 mmHg in conjunction with other clinical markers of end-organ perfusion is advised [32]. Compared to epinephrine, norepinephrine had similar hemodynamic effects on mean arterial pressure (MAP) and CI, but epinephrine was associated with higher rates of refractory shock, tachycardia, lactic acidosis [33] and mortality [34][35]. Moreover, compared to dopamine, norepinephrine had a safer profile in patients with CS, due to a lower trend for arrhythmic events and mortality [36]. Vasopressin lacks inotropic properties and may be used as a second-line vasoactive agent, concomitantly to norepinephrine, if hemodynamic status does not improve with single use of norepinephrine [3][30][37]. Its administration may be appealing in special circumstances, like in patients with right ventricular failure, as it does not affect pulmonary arterial pressure [23][27][38], or in combination with milrinone in order to counteract its vasodilatory effect [3], but evidence is lacking [23].
Inotropes may be considered in addition to vasopressors in order to augment cardiac output and end-organ perfusion (Class IIb/C recommendation) [1]. Dobutamine is recommended over other inotropic agents if signs of hypoperfusion persist despite first-line vasopressor therapy [3]. However, a systematic review failed to show any benefit of dobutamine over levosimendan for short- and long-term survival [39]. Levosimendan and milrinone may be preferable over dobutamine in special cases such as long b-blockade, right ventricular dysfunction, pulmonary hypertension, or Takotsubo cardiomyopathy [1][3][40].
In CS patients with refractory hypotension, vasopressin may aid in preserving arterial blood pressure, as a third vasoactive agent, in conjunction with norepinephrine and dobutamine [30].

5. Short-Term Mechanical Circulatory Support

Patients who present with deteriorating or extremis CS, or those who fail to stabilize hemodynamically with two vasoactive agents may benefit from devices for temporary MCS in an individualized manner (Class IIa/C recommendation) [1][29]. Early initiation of MCS may provide univentricular or biventricular support by improving cardiac contractility, reducing left/right ventricular end-diastolic pressures, enhancing coronary perfusion and decreasing myocardial oxygen demand [41][42], resulting in effective weaning from cardiotoxic vasoactive agents [43]. However, controversial results with respect to mortality [44][45][46][47] incite the consideration of challenging issues regarding their application in practice, such as patient selection, type of device, appropriate timing, and prognostic impact. A characteristic recent example is the ECMO-CS randomized controlled trial where patients with deteriorating CS were randomized to immediate ECMO or early conservative therapy (with the ECMO kept as a bailout option at a later stage). The study did not show a benefit for the early ECMO approach. Despite having several limitations (i.e., relatively small sample size, mixed cohort of AMI- and non-AMI-related CS, and significant crossover rate (39% crossover to VA-ECMO in early conservative arm)), the study provides important data for the CS population.
Available choices for left ventricular assistance include the intra-aortic balloon pump (IABP), microaxial flow pumps (Impella CP, Impella 5), or the left-atrium-to-femoral-artery system device (Tandem Heart), while right ventricular assistance may be supported by the Impella RP, Tandem Heart RA-PA and Protek Duo devices. Venous–arterial extracorporeal membrane oxygenation (VA-ECMO) may reinforce biventricular performance and improve oxygenation [3][42][48]. Regarding the down-side of advanced percutaneous left ventricular devices, IABP use has subsided, taking into account no proven survival benefit for patients with AMI-CS [44], and currently its implementation may be considered for patients with refractory CS of non-AMI etiology (class IIb/C recommendation) [1] or for AMI-CS patients with mechanical complications as a bridge to more advanced MCS devices (class IIa/C recommendation) [49]. Even if Impella devices seem like promising approaches, data regarding their beneficial effect on mortality are scarce [45][46][50]. Although ECMO may ensure hemodynamic stabilization in cardiopulmonary resuscitation [51], it may also increase LV afterload, making its use reasonable with concomitant LV unloading (IABP, Impella, septostomy and hybrid circuit configuration) [3][42][52]. It must be emphasized that devices like Impella and ECMO necessitate the insertion of large-bore cannulas into major vessels and carry a high risk of complications, including vascular and bleeding complications. Characteristically, for Impella used in AMI-related CS, the rate of severe bleeding reported in the literature ranged from 8.5% to 31% [53][54]. Thus, to improve the efficacy of advanced MCS devices and increase the chances of positive studies in the CS field, specific measures should be taken to reduce complications. Such measures include comprehensive training in device insertion and maintenance, formation of dedicated teams (e.g., ECMO team including perfusionists), ultrasound guided vascular access, use of vascular closure systems, etc.
The uniqueness of each device, indicated by distinct hemodynamic effects, favorable profiles, contraindications and complications, limits their use to selected patients and under the supervision of expert teams [55]. The comprehensive approach by multidisciplinary teams in the context of a shock network emerges as an ultimate but not impossible goal to improve survival. Interestingly, recent data support that early initiation of MCS in the initial stages of CS, even before the administration of inotropes or the PCI strategy, is significantly associated with increased survival rates in patients presenting with AMI-CS [56], supporting the need to achieve shorter “door to support” intervals, so as to anticipate the deleterious effects of the fatal spiral of cardiac compromise [57].

This entry is adapted from the peer-reviewed paper 10.3390/jcm12072643

References

  1. McDonagh, T.A.; Metra, M.; Adamo, M.; Gardner, R.S.; Baumbach, A.; Böhm, M.; Burri, H.; Butler, J.; Čelutkienė, J.; Chioncel, O.; et al. 2021 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure. Eur. Heart J. 2021, 42, 3599–3726.
  2. Gil, V.; Domínguez-Rodríguez, A.; Masip, J.; Peacock, W.F.; Miró, Ò. Morphine Use in the Treatment of Acute Cardiogenic Pulmonary Edema and Its Effects on Patient Outcome: A Systematic Review. Curr. Heart Fail. Rep. 2019, 16, 81–88.
  3. Chioncel, O.; Parissis, J.; Mebazaa, A.; Thiele, H.; Desch, S.; Bauersachs, J.; Harjola, V.; Antohi, E.; Arrigo, M.; Ben Gal, T.; et al. Epidemiology, Pathophysiology and Contemporary Management of Cardiogenic Shock—A Position Statement from the Heart Failure Association of the European Society of Cardiology. Eur. J. Heart Fail. 2020, 22, 1315–1341.
  4. For the Acute Heart Failure Study Group of the European Society of Cardiology Acute Cardiovascular Care Association; Price, S.; Platz, E.; Cullen, L.; Tavazzi, G.; Christ, M.; Cowie, M.R.; Maisel, A.S.; Masip, J.; Miro, O.; et al. Echocardiography and Lung Ultrasonography for the Assessment and Management of Acute Heart Failure. Nat. Rev. Cardiol. 2017, 14, 427–440.
  5. Soliman-Aboumarie, H.; Denault, A.Y. How to Assess Systemic Venous Congestion with Point of Care Ultrasound. Eur. Heart J. Cardiovasc. Imaging 2023, 24, 177–180.
  6. Cherpanath, T.G.V.; Hirsch, A.; Geerts, B.F.; Lagrand, W.K.; Leeflang, M.M.; Schultz, M.J.; Groeneveld, A.B.J. Predicting Fluid Responsiveness by Passive Leg Raising: A Systematic Review and Meta-Analysis of 23 Clinical Trials*. Crit. Care Med. 2016, 44, 981–991.
  7. Monnet, X.; Marik, P.; Teboul, J.-L. Passive Leg Raising for Predicting Fluid Responsiveness: A Systematic Review and Meta-Analysis. Intensive Care Med. 2016, 42, 1935–1947.
  8. Monnet, X.; Teboul, J.-L. Assessment of Fluid Responsiveness: Recent Advances. Curr. Opin. Crit. Care 2018, 24, 190–195.
  9. Blanco, P. Rationale for Using the Velocity–Time Integral and the Minute Distance for Assessing the Stroke Volume and Cardiac Output in Point-of-Care Settings. Ultrasound J. 2020, 12, 21.
  10. Ashley, M.; Justin, M. Predicting and Measuring Fluid Responsiveness with Echocardiography. Echo Res. Pract. 2016, 3, G1–G12.
  11. Kellum, J.A. Abnormal Saline and the History of Intravenous Fluids. Nat. Rev. Nephrol. 2018, 14, 358–360.
  12. Lauridsen, M.D.; Gammelager, H.; Schmidt, M.; Rasmussen, T.B.; Shaw, R.E.; Bøtker, H.E.; Sørensen, H.T.; Christiansen, C.F. Acute Kidney Injury Treated with Renal Replacement Therapy and 5-Year Mortality after Myocardial Infarction-Related Cardiogenic Shock: A Nationwide Population-Based Cohort Study. Crit. Care 2015, 19, 452.
  13. Semler, M.W.; Self, W.H.; Wanderer, J.P.; Ehrenfeld, J.M.; Wang, L.; Byrne, D.W.; Stollings, J.L.; Kumar, A.B.; Hughes, C.G.; Hernandez, A.; et al. Balanced Crystalloids versus Saline in Critically Ill Adults. N. Engl. J. Med. 2018, 378, 829–839.
  14. Zampieri, F.G.; Ranzani, O.T.; Azevedo, L.C.P.; Martins, I.D.S.; Kellum, J.A.; Libório, A.B. Lactated Ringer Is Associated with Reduced Mortality and Less Acute Kidney Injury in Critically Ill Patients: A Retrospective Cohort Analysis*. Crit. Care Med. 2016, 44, 2163–2170.
  15. Hammond, N.E.; Zampieri, F.G.; Di Tanna, G.L.; Garside, T.; Adigbli, D.; Cavalcanti, A.B.; Machado, F.R.; Micallef, S.; Myburgh, J.; Ramanan, M.; et al. Balanced Crystalloids versus Saline in Critically Ill Adults—A Systematic Review with Meta-Analysis. NEJM Evid. 2022, 1, EVIDoa2100010.
  16. Dong, W.-H.; Yan, W.-Q.; Song, X.; Zhou, W.-Q.; Chen, Z. Fluid Resuscitation with Balanced Crystalloids versus Normal Saline in Critically Ill Patients: A Systematic Review and Meta-Analysis. Scand. J. Trauma Resusc. Emerg. Med. 2022, 30, 28.
  17. Zayed, Y.Z.M.; Aburahma, A.M.Y.; Barbarawi, M.O.; Hamid, K.; Banifadel, M.R.N.; Rashdan, L.; Bachuwa, G.I. Balanced Crystalloids versus Isotonic Saline in Critically Ill Patients: Systematic Review and Meta-Analysis. J. Intensive Care 2018, 6, 51.
  18. Alviar, C.L.; Miller, P.E.; McAreavey, D.; Katz, J.N.; Lee, B.; Moriyama, B.; Soble, J.; van Diepen, S.; Solomon, M.A.; Morrow, D.A. Positive Pressure Ventilation in the Cardiac Intensive Care Unit. J. Am. Coll. Cardiol. 2018, 72, 1532–1553.
  19. Alviar, C.L.; Rico-Mesa, J.S.; Morrow, D.A.; Thiele, H.; Miller, P.E.; Maselli, D.J.; van Diepen, S. Positive Pressure Ventilation in Cardiogenic Shock: Review of the Evidence and Practical Advice for Patients with Mechanical Circulatory Support. Can. J. Cardiol. 2020, 36, 300–312.
  20. Masip, J.; Peacock, W.F.; Price, S.; Cullen, L.; Martin-Sanchez, F.J.; Seferovic, P.; Maisel, A.S.; Miro, O.; Filippatos, G.; Vrints, C.; et al. Indications and Practical Approach to Non-Invasive Ventilation in Acute Heart Failure. Eur. Heart J. 2018, 39, 17–25.
  21. Harjola, V.-P.; Lassus, J.; Sionis, A.; Køber, L.; Tarvasmäki, T.; Spinar, J.; Parissis, J.; Banaszewski, M.; Silva-Cardoso, J.; Carubelli, V.; et al. Clinical Picture and Risk Prediction of Short-Term Mortality in Cardiogenic Shock: Clinical Picture and Outcome of Cardiogenic Shock. Eur. J. Heart Fail. 2015, 17, 501–509.
  22. Berbenetz, N.; Wang, Y.; Brown, J.; Godfrey, C.; Ahmad, M.; Vital, F.M.; Lambiase, P.; Banerjee, A.; Bakhai, A.; Chong, M. Non-Invasive Positive Pressure Ventilation (CPAP or Bilevel NPPV) for Cardiogenic Pulmonary Oedema. Cochrane Database Syst. Rev. 2019, 4, CD005351.
  23. Harjola, V.-P.; Mebazaa, A.; Čelutkienė, J.; Bettex, D.; Bueno, H.; Chioncel, O.; Crespo-Leiro, M.G.; Falk, V.; Filippatos, G.; Gibbs, S.; et al. Contemporary Management of Acute Right Ventricular Failure: A Statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology: Contemporary Management of Acute RV Failure. Eur. J. Heart Fail. 2016, 18, 226–241.
  24. Mebazaa, A.; Combes, A.; van Diepen, S.; Hollinger, A.; Katz, J.N.; Landoni, G.; Hajjar, L.A.; Lassus, J.; Lebreton, G.; Montalescot, G.; et al. Management of Cardiogenic Shock Complicating Myocardial Infarction. Intensive Care Med. 2018, 44, 760–773.
  25. Klein, T.; Ramani, G.V. Assessment and Management of Cardiogenic Shock in the Emergency Department. Cardiol. Clin. 2012, 30, 651–664.
  26. Thiele, H.; Ohman, E.M.; Desch, S.; Eitel, I.; de Waha, S. Management of Cardiogenic Shock. Eur. Heart J. 2015, 36, 1223–1230.
  27. Levy, B.; Buzon, J.; Kimmoun, A. Inotropes and Vasopressors Use in Cardiogenic Shock: When, Which and How Much? Curr. Opin. Crit. Care 2019, 25, 384–390.
  28. Delmas, C.; Roubille, F.; Lamblin, N.; Bonello, L.; Leurent, G.; Levy, B.; Elbaz, M.; Danchin, N.; Champion, S.; Lim, P.; et al. Baseline Characteristics, Management, and Predictors of Early Mortality in Cardiogenic Shock: Insights from the FRENSHOCK Registry. ESC Heart Fail. 2022, 9, 408–419.
  29. Baran, D.A.; Grines, C.L.; Bailey, S.; Burkhoff, D.; Hall, S.A.; Henry, T.D.; Hollenberg, S.M.; Kapur, N.K.; O’Neill, W.; Ornato, J.P.; et al. SCAI Clinical Expert Consensus Statement on the Classification of Cardiogenic Shock: This Document Was Endorsed by the American College of Cardiology (ACC), the American Heart Association (AHA), the Society of Critical Care Medicine (SCCM), and the Society of Thoracic Surgeons (STS) in April 2019. Catheter. Cardiovasc. Interv. 2019, 94, 29–37.
  30. Polyzogopoulou, E.; Arfaras-Melainis, A.; Bistola, V.; Parissis, J. Inotropic Agents in Cardiogenic Shock. Curr. Opin. Crit. Care 2020, 26, 403–410.
  31. Levy, B.; Klein, T.; Kimmoun, A. Vasopressor Use in Cardiogenic Shock. Curr. Opin. Crit. Care 2020, 26, 411–416.
  32. Mathew, R.; Fernando, S.M.; Hu, K.; Parlow, S.; Di Santo, P.; Brodie, D.; Hibbert, B. Optimal Perfusion Targets in Cardiogenic Shock. JACC Adv. 2022, 1, 100034.
  33. Levy, B.; Clere-Jehl, R.; Legras, A.; Morichau-Beauchant, T.; Leone, M.; Frederique, G.; Quenot, J.-P.; Kimmoun, A.; Cariou, A.; Lassus, J.; et al. Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction. J. Am. Coll. Cardiol. 2018, 72, 173–182.
  34. Léopold, V.; Gayat, E.; Pirracchio, R.; Spinar, J.; Parenica, J.; Tarvasmäki, T.; Lassus, J.; Harjola, V.-P.; Champion, S.; Zannad, F.; et al. Epinephrine and Short-Term Survival in Cardiogenic Shock: An Individual Data Meta-Analysis of 2583 Patients. Intensive Care Med. 2018, 44, 847–856.
  35. For the CardShock Study Investigators; Tarvasmäki, T.; Lassus, J.; Varpula, M.; Sionis, A.; Sund, R.; Køber, L.; Spinar, J.; Parissis, J.; Banaszewski, M.; et al. Current Real-Life Use of Vasopressors and Inotropes in Cardiogenic Shock—Adrenaline Use Is Associated with Excess Organ Injury and Mortality. Crit. Care 2016, 20, 208.
  36. De Backer, D.; Biston, P.; Devriendt, J.; Madl, C.; Chochrad, D.; Aldecoa, C.; Brasseur, A.; Defrance, P.; Gottignies, P.; Vincent, J.-L. Comparison of Dopamine and Norepinephrine in the Treatment of Shock. N. Engl. J. Med. 2010, 362, 779–789.
  37. Jolly, S.; Newton, G.; Horlick, E.; Seidelin, P.H.; Ross, H.J.; Husain, M.; Dzavik, V. Effect of Vasopressin on Hemodynamics in Patients with Refractory Cardiogenic Shock Complicating Acute Myocardial Infarction. Am. J. Cardiol. 2005, 96, 1617–1620.
  38. Wallace, A.W.; Tunin, C.M.; Shoukas, A.A. Effects of Vasopressin on Pulmonary and Systemic Vascular Mechanics. Am. J. Physiol.-Heart Circ. Physiol. 1989, 257, H1228–H1234.
  39. Uhlig, K.; Efremov, L.; Tongers, J.; Frantz, S.; Mikolajczyk, R.; Sedding, D.; Schumann, J. Inotropic Agents and Vasodilator Strategies for the Treatment of Cardiogenic Shock or Low Cardiac Output Syndrome. Cochrane Database Syst. Rev. 2020, 2020.
  40. Mebazaa, A.; Nieminen, M.S.; Filippatos, G.S.; Cleland, J.G.; Salon, J.E.; Thakkar, R.; Padley, R.J.; Huang, B.; Cohen-Solal, A. Levosimendan vs. Dobutamine: Outcomes for Acute Heart Failure Patients on β-Blockers in SURVIVE†. Eur. J. Heart Fail. 2009, 11, 304–311.
  41. Burkhoff, D.; Sayer, G.; Doshi, D.; Uriel, N. Hemodynamics of Mechanical Circulatory Support. J. Am. Coll. Cardiol. 2015, 66, 2663–2674.
  42. Salter, B.S.; Gross, C.R.; Weiner, M.M.; Dukkipati, S.R.; Serrao, G.W.; Moss, N.; Anyanwu, A.C.; Burkhoff, D.; Lala, A. Temporary Mechanical Circulatory Support Devices: Practical Considerations for All Stakeholders. Nat. Rev. Cardiol. 2022, 20, 263–277.
  43. Tongers, J.; Sieweke, J.-T.; Kühn, C.; Napp, L.C.; Flierl, U.; Röntgen, P.; Schmitto, J.D.; Sedding, D.G.; Haverich, A.; Bauersachs, J.; et al. Early Escalation of Mechanical Circulatory Support Stabilizes and Potentially Rescues Patients in Refractory Cardiogenic Shock. Circ. Heart Fail. 2020, 13, e005853.
  44. Thiele, H.; Zeymer, U.; Neumann, F.-J.; Ferenc, M.; Olbrich, H.-G.; Hausleiter, J.; Richardt, G.; Hennersdorf, M.; Empen, K.; Fuernau, G.; et al. Intraaortic Balloon Support for Myocardial Infarction with Cardiogenic Shock. N. Engl. J. Med. 2012, 367, 1287–1296.
  45. O’Neill, W.W.; Kleiman, N.S.; Moses, J.; Henriques, J.P.S.; Dixon, S.; Massaro, J.; Palacios, I.; Maini, B.; Mulukutla, S.; Džavík, V.; et al. A Prospective, Randomized Clinical Trial of Hemodynamic Support with Impella 2.5 Versus Intra-Aortic Balloon Pump in Patients Undergoing High-Risk Percutaneous Coronary Intervention: The PROTECT II Study. Circulation 2012, 126, 1717–1727.
  46. Ouweneel, D.M.; Eriksen, E.; Sjauw, K.D.; van Dongen, I.M.; Hirsch, A.; Packer, E.J.S.; Vis, M.M.; Wykrzykowska, J.J.; Koch, K.T.; Baan, J.; et al. Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic Shock After Acute Myocardial Infarction. J. Am. Coll. Cardiol. 2017, 69, 278–287.
  47. Basir, M.B.; Kapur, N.K.; Patel, K.; Salam, M.A.; Schreiber, T.; Kaki, A.; Hanson, I.; Almany, S.; Timmis, S.; Dixon, S.; et al. Improved Outcomes Associated with the Use of Shock Protocols: Updates from the National Cardiogenic Shock Initiative. Catheter. Cardiovasc. Interv. 2019, 93, 1173–1183.
  48. Vahdatpour, C.; Collins, D.; Goldberg, S. Cardiogenic Shock. JAHA 2019, 8, e011991.
  49. Ibanez, B.; James, S.; Agewall, S.; Antunes, M.J.; Bucciarelli-Ducci, C.; Bueno, H.; Caforio, A.L.P.; Crea, F.; Goudevenos, J.A.; Halvorsen, S.; et al. 2017 ESC Guidelines for the Management of Acute Myocardial Infarction in Patients Presenting with ST-Segment Elevation. Eur. Heart J. 2018, 39, 119–177.
  50. Burkhoff, D.; Cohen, H.; Brunckhorst, C.; O’Neill, W.W. A Randomized Multicenter Clinical Study to Evaluate the Safety and Efficacy of the TandemHeart Percutaneous Ventricular Assist Device versus Conventional Therapy with Intraaortic Balloon Pumping for Treatment of Cardiogenic Shock. Am. Heart J. 2006, 152, 469.e1–469.e8.
  51. Tsangaris, A.; Alexy, T.; Kalra, R.; Kosmopoulos, M.; Elliott, A.; Bartos, J.A.; Yannopoulos, D. Overview of Veno-Arterial Extracorporeal Membrane Oxygenation (VA-ECMO) Support for the Management of Cardiogenic Shock. Front. Cardiovasc. Med. 2021, 8, 686558.
  52. Schrage, B.; Becher, P.M.; Bernhardt, A.; Bezerra, H.; Blankenberg, S.; Brunner, S.; Colson, P.; Cudemus Deseda, G.; Dabboura, S.; Eckner, D.; et al. Left Ventricular Unloading Is Associated with Lower Mortality in Patients with Cardiogenic Shock Treated with Venoarterial Extracorporeal Membrane Oxygenation: Results from an International, Multicenter Cohort Study. Circulation 2020, 142, 2095–2106.
  53. Dhruva, S.S.; Ross, J.S.; Mortazavi, B.J.; Hurley, N.C.; Krumholz, H.M.; Curtis, J.P.; Berkowitz, A.; Masoudi, F.A.; Messenger, J.C.; Parzynski, C.S.; et al. Association of Use of an Intravascular Microaxial Left Ventricular Assist Device vs. Intra-Aortic Balloon Pump with In-Hospital Mortality and Major Bleeding among Patients with Acute Myocardial Infarction Complicated by Cardiogenic Shock. JAMA 2020, 323, 734.
  54. Schrage, B.; Ibrahim, K.; Loehn, T.; Werner, N.; Sinning, J.-M.; Pappalardo, F.; Pieri, M.; Skurk, C.; Lauten, A.; Landmesser, U.; et al. Impella Support for Acute Myocardial Infarction Complicated by Cardiogenic Shock: Matched-Pair IABP-SHOCK II Trial 30-Day Mortality Analysis. Circulation 2019, 139, 1249–1258.
  55. Tehrani, B.N.; Truesdell, A.G.; Psotka, M.A.; Rosner, C.; Singh, R.; Sinha, S.S.; Damluji, A.A.; Batchelor, W.B. A Standardized and Comprehensive Approach to the Management of Cardiogenic Shock. JACC Heart Fail. 2020, 8, 879–891.
  56. Basir, M.B.; Schreiber, T.L.; Grines, C.L.; Dixon, S.R.; Moses, J.W.; Maini, B.S.; Khandelwal, A.K.; Ohman, E.M.; O’Neill, W.W. Effect of Early Initiation of Mechanical Circulatory Support on Survival in Cardiogenic Shock. Am. J. Cardiol. 2017, 119, 845–851.
  57. Esposito, M.L.; Kapur, N.K. Acute Mechanical Circulatory Support for Cardiogenic Shock: The “Door to Support” Time. F1000Research 2017, 6, 737.
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