Cardiogenic shock medical therapy

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Cardiogenic shock is considered an emergency and irrespectively to the therapeutic approach, the target goal of any therapy is prompt revascularization of ischemic myocardium. This should be achieved in the shortest timespan possible. There are two major categories of treatment for cardiogenic shock, the medical/conservative approach and the interventional approach. The ideal treatment combines both techniques, in which medical therapy, after restored filling pressures, allows hemodynamical stabilization of the patient, until interventional methods, that contribute to the reversal of the process leading to the shock state, may performed. The interventional approach may include PCI or coronary artery bypass graft surgery (CABG) and in both techniques the goal is not only to reestablish perfusion of the occluded coronary artery, but also to prevent vessel reoclusion. If there is no access to a cardiac catheterization facility, nor the possibility of transferring the patient to one within 90 minutes, then immediately thrombolytic therapy should be considered.[1] Other important factors to increase the chances of a better outcome are: mechanical ventilation, in order to improve tissue oxygenation, and close monitoring of the therapeutic dosages, particularly of vasoactive drugs, since these have been associated with excess mortality due to toxicity effects.[2][3] Also, it is recommended invasive hemodynamic monitoring, in order to monitor and guide the effects of the therapy as well as the overall status of the patient. The success of reperfusion is usually suggested by the relief of symptoms, restoration of hemodynamic parameters and electrical stability, as well as the reduction of at least 50% in the ST-segment on the EKG, in the case of a STEMI.[1][4]

Medical Therapy

Cardiogenic shock is considered a medical emergency and therefore resuscitative therapy is mandatory before permanent damage to vital organs has settled in. In order to improve chances of a better outcome, prompt diagnosis, adequate filling pressure and pharmacological therapy, to insure maintenance of adequate hemodynamic parameters, should be started within the shortest timespan possible.

Irrespectively to the therapeutic approach, the target goal of any therapy is prompt revascularization of ischemic myocardium. In order to do so and depending on the underlying cause of shock, the therapeutic approach, along with the class of drugs needed, might be different.

Depending on the underlying cause for the cardiogenic shock, the approach of treatment will change. Knowing that myocardial infarction is the most common cause for this condition, prompt revascularization of the ischemic myocardium is gold standard. However, other causes may require more invasive interventions, such as heart valve repair or even heart transplant. It is also important to address metabolic, electrolyte and acid-base abnormalities that may be present. Throughout this process it is important to keep a constant a constant invasive hemodynamic monitoring, such as a central line, in order to have as accurate values as possible as well as to facilitate some techniques, such as volume resuscitation.

Urgent Revascularizaiton

If the patient has an ST elevation myocardial infarction, then primary angioplasty should be considered to restore flow to the culprit artery. Consideration should also be given to restoration of flow in the non-culprit territories in the setting of cardiogenic shock.

Administration of streptokinase therapy to patients with cardiogenic shock has not been associated with an improvement in survival.[5] These studies, however, are older and are limited by the infrequent use of adjunctive PCI. If a patient is not deemed a candidate for primary angioplasty, then consideration should be given to fibrinolyitc administration.

Volume Management

The goal of managing the patient with cardiogenic shock is to optimize the filling of the left ventricle so that the starling relationship and mechanical performance and contractility of the heart is optimized. In the setting of acute MI, a pulmonary capillary wedge pressure of 18 to 20 mm Hg may optimize left ventricular filling. Filling pressures higher than this may lead to LV dilation, and poorer left ventricular function.

Pharmacologic Hemodynamic Support

If hypotension persists, despite adequate left ventricular filling pressures, then the addition of vasoconstrictors and/or inotropes is suggested. Hemodynamic monitoring is essential to assure that a target mean arterial pressure (MAP) of 60 to 65 mmHg is achieved, in order to maintain perfusion to vital organs, such as the brain, kidney and heart, as well as to monitor and guide the effect and doses of the treatment drugs. The main purpose of these vasoactive drugs is to maintain adequate perfusion to peripheral tissues. However, due to the significant toxicity of these drugs, they should be given in doses as minimal as possible.[6]

Selection of a Vasopressor or an Inotrope

  • Systolic Blood Pressure (SBP) > 80 mm Hg

Dobutamine may be preferable over dopamine at this blood pressure. Dopamine increases contractility and heart rate and thereby increases myocardial oxygen demand. Dobutamine reduces the systemic vascular resistance and may not increase oxygen demands as much as dopamine, and is preferable at this systolic blood pressure. Phosphodiesterase inhibitors (PDIs) such as milrinone and inamrinone (formerly known as amrinone) are not dependent upon the adrenoreceptor activity and patients may not develop tolerance, and they may be less likely to increase myocardial oxygen demands. However, the addition of a vasopressor is often required as these agents reduce preload and afterload. PDIs are more likely to be associated with tachyarrhythmias than dobutamine.

  • Systolic Blood Pressure (SBP) < 80 mm Hg

At systolic blood pressures < 80 mm Hg dopamine should be initiated first. The patient may not tolerate the vasodilating effects of dobutamine at this blood pressure. The initial dose of dopamine is 5 to 10 mcg/kg/min.

If the dopamine at doses of 20 mcg/kg/min does not achieve a MAP of 60-65 mm Hg, then norepinephrine can be added at an initial dose of 0.5 mcg/kg/min which can then be titrated up to 3.3 mcg/kg/min. Norepinephrine is avoided as a first line agent because of its adverse impact upon renal perfusion.

If norepinephrine does not generate a MAP of 60 mm Hg, then epinephrine can be added. Epinephrine increases both the stroke volume and heart rate, but is associated with lactic acidosis.

Mechanical Support

Intra-aortic Balloon Placement

In the setting of acute MI, the placement of an intra-aortic balloon pump (which reduces workload for the heart, and improves perfusion of the coronary arteries) should be considered.

A recent meta-analysis of randomized trial data, however, challenges this common practice and class 1B recommendation.[7] In a meta-analysis of seven randomized trials enrolling 1009 patients, IABP placement in STEMI was not associated with an improvement in mortality or in left ventricular function but was associated with a higher rate of stroke and bleeding. When data from non-randomized cohort studies were evaluated in a meta-analysis (n=10,529 STEMI patients with cardiogenic shock), IABP placement was associated with an 18% relative risk reduction in 30 day mortality among patients treated with a fibrinolytic agent. This particular analysis is confounded by the fact that those patients in whom an IABP was placed underwent adjunctive percutaneous intervention (PCI) more frequently. In this non-randomized cohort analysis, IABP placement in patients undergoing primary angioplasty was associated with a 6% relative increase in mortality (p<0.0008). Thus, neither randomized nor observational data support IABP placement in the setting of primary PCI for cardiogenic shock, and careful consideration should be given to the risk of stroke and bleeding prior to IABP placement in this population.

Left Ventricular Assist Device Placement

In the setting of pronounced hypotension despite medical therapy and IABP placement, placement of a left ventricular assist device (which augments the pump-function of the heart) should be considered. A ventricular assist device should only be placed in those patients in whom the cardiogenic shock is deemed to be reversible or if it is being used as a bridge option.[8]

Percutaneous left ventricular assist devices (PLVADs) such as Tandem heart, Impella, ECMO can be used as a bridge to transplant, left ventricular assist device (LVAD) or decision making. They provide improved hemodynamics in patients with cardiogenic shock.

Coronary Artery Bypass Graft (CABG) Placement

CABG in this setting is associated with high rates of mortality and morbidity and is generally not performed if primary angioplasty can be performed.

Invasive Hemodynamic Monitoring

Considering the importance of proper blood pressure assessment in patients in shock, along with the fact that peripheral vasoconstriction may jeopardize blood pressure assessment through common manual sphygmomanometry, all patients should have an indwelling arterial pressure catheter placed in order to gather more accurate measurements.[9][10] This method not only supplies continuous hemodynamic data, unlike other manual methods, but also allows for the collection of arterial blood gas samples. The most commonly used catheter is the flow-directed balloon-tipped pulmonary artery catheter, which not only allows for cardiac output determination, as it is a good method for hemodynamic assessment of these patients, as well as continuous monitoring of pulmonary artery and central venous pressure and waveforms.[11] With this device is also possible to collect blood from the pulmonary artery, therefore enabling determination of MVO2, to verify oxygen delivery and it also helps in the diagnosis of left-to-right shunts, associated with anatomic abnormalities. All these features make the flow-directed balloon-tipped pulmonary artery catheter a good tool for diagnosis, management and monitoring of therapy of cardiogenic shock patients.[12]

Other monitoring techniques include:[13]

Mechanical Ventilation

Mechanical ventilation is often required in patients with cardiogenic shock to assure adequate oxygenation.

2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)[25]

Treatment of Cardiogenic Shock in Patients with STEMI (DO NOT EDIT)[25]

Class I
"1. Emergency revascularization with either PCI or CABG is recommended in suitable patients with cardiogenic shock due to pump failure after STEMI irrespective of the time delay from MI onset.[26][27][28] (Level of Evidence: B)"
"2. In the absence of contraindications, fibrinolytic therapy should be administered to patients with STEMI and cardiogenic shock who are unsuitable candidates for either PCI or CABG.[29][30][31] (Level of Evidence: B)"
Class IIa
"1. The use of intra-aortic balloon pump counterpulsation can be useful for patients with cardiogenic shock after STEMI who do not quickly stabilize with pharmacological therapy.[32][33][34][7][35] (Level of Evidence: B)"
Class IIb
"1. Alternative left ventricular (LV) assist devices for circulatory support may be considered in patients with refractory cardiogenic shock. (Level of Evidence: C)"

References

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  7. 7.0 7.1 Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J, Koch KT, de Winter RJ, Piek JJ, Tijssen JG, Henriques JP (2009). "A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines?". European Heart Journal. 30 (4): 459–68. doi:10.1093/eurheartj/ehn602. PMID 19168529. Unknown parameter |month= ignored (help)
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  25. 25.0 25.1 O'Gara PT, Kushner FG, Ascheim DD; et al. (2012). "2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction: Executive Summary: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines". Circulation. doi:10.1161/CIR.0b013e3182742c84. PMID 23247303. Unknown parameter |month= ignored (help)
  26. Hochman JS, Sleeper LA, Webb JG; et al. (1999). "Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock". N. Engl. J. Med. 341 (9): 625–34. doi:10.1056/NEJM199908263410901. PMID 10460813. Unknown parameter |month= ignored (help)
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  29. "Indications for fibrinolytic therapy in suspected acute myocardial infarction: collaborative overview of early mortality and major morbidity results from all randomised trials of more than 1000 patients. Fibrinolytic Therapy Trialists' (FTT) Collaborative Group". Lancet. 343 (8893): 311–22. 1994. PMID 7905143. Unknown parameter |month= ignored (help)
  30. Morrow DA, Antman EM, Charlesworth A; et al. (2000). "TIMI risk score for ST-elevation myocardial infarction: A convenient, bedside, clinical score for risk assessment at presentation: An intravenous nPA for treatment of infarcting myocardium early II trial substudy". Circulation. 102 (17): 2031–7. PMID 11044416. Unknown parameter |month= ignored (help)
  31. French JK, Feldman HA, Assmann SF; et al. (2003). "Influence of thrombolytic therapy, with or without intra-aortic balloon counterpulsation, on 12-month survival in the SHOCK trial". Am. Heart J. 146 (5): 804–10. doi:10.1016/S0002-8703(03)00392-2. PMID 14597928. Unknown parameter |month= ignored (help)
  32. Barron HV, Every NR, Parsons LS; et al. (2001). "The use of intra-aortic balloon counterpulsation in patients with cardiogenic shock complicating acute myocardial infarction: data from the National Registry of Myocardial Infarction 2". Am. Heart J. 141 (6): 933–9. doi:10.1067/mhj.2001.115295. PMID 11376306. Unknown parameter |month= ignored (help)
  33. Chen EW, Canto JG, Parsons LS; et al. (2003). "Relation between hospital intra-aortic balloon counterpulsation volume and mortality in acute myocardial infarction complicated by cardiogenic shock". Circulation. 108 (8): 951–7. doi:10.1161/01.CIR.0000085068.59734.E4. PMID 12912817. Unknown parameter |month= ignored (help)
  34. Sanborn TA, Sleeper LA, Bates ER; et al. (2000). "Impact of thrombolysis, intra-aortic balloon pump counterpulsation, and their combination in cardiogenic shock complicating acute myocardial infarction: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK?". J. Am. Coll. Cardiol. 36 (3 Suppl A): 1123–9. PMID 10985715. Unknown parameter |month= ignored (help)
  35. Ohman EM, Nanas J, Stomel RJ; et al. (2005). "Thrombolysis and counterpulsation to improve survival in myocardial infarction complicated by hypotension and suspected cardiogenic shock or heart failure: results of the TACTICS Trial". J. Thromb. Thrombolysis. 19 (1): 33–9. doi:10.1007/s11239-005-0938-0. PMID 15976965. Unknown parameter |month= ignored (help)


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