The management of cardiogenic shock

This is a free full text review the need for which is outlined in the opening of the paper:

Contrary to septic shock, there are no international recommendations regarding the management of cardiogenic shock (CS) in intensive care. Reasons include the rarity of the disease, but also the fact that patients with CS often solely receive care in cardiology. Recent European Society of Cardiology (ESC) guidelines on the management of acute heart failure include a section on CS [1]. However, these guidelines are vague for the intensivist and at times obsolete (with regard to vasopressors, for example). The lack of a specific approach to the management of severe forms of CS in the latest international guidelines led our group to draw the following recommendations.

There is a wealth of information here which should be read in the original. I will highlight only a few points of particular interest below.

Cardiogenic shock definition

Cardiogenic shock (CS) is defined as a state of critical end-organ hypoperfusion due to reduced cardiac output. Notably, CS forms a spectrum ranging from mild hypoperfusion to profound shock…

Area 1: epidemiology

In cardiogenic shock, a coronary cause should routinely be sought (strong agreement).

In over 70 % of cases, CS is related to acute myocardial infarction (MI) with ST-segment elevation, with or without mechanical complications (rupture of the septum, of the ventricular wall or of chordae tendineae). However, shock rarely occurs during MI (4.2 to 8.6 % of cases, depending on the study) and is declining…

Area 2: cardiogenic shock in acute myocardial infarction

Predictors of progression to cardiogenic shock, in particular a heart rate >75 beats/min and signs of heart failure, should be sought in all patients with myocardial infarction (strong agreement)….

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Coronary angiography, followed by coronary revascularization using angioplasty or exceptionally coronary artery-bypass surgery, is required in cardiogenic shock secondary to acute myocardial infarction irrespective of the time interval since the onset of pain (strong agreement)…

Plasma lactate should be assayed repeatedly (in the absence of epinephrine therapy) to assess the persistence or correction of shock during treatment (strong agreement).

Here the exception of epinephrine use for lactate monitoring is based on the fact that epinephrine causes lactic acidosis by non ischemic mechanisms (type B lactic acidosis) and thus would confound the interpretation of lactate levels.

The recommendations for hemodynamic monitoring and invasive access are based more on expertise. In the case of CVP monitoring they run counter to the latest evidence applied to septic shock:

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A central venous catheter placed in the superior vena cava should be used for intermittent (blood sample) or continuous (fiber optic) measurement of central venous oxygen saturation (ScvO2) (strong agreement).

Inasmuch as central venous catheterization is mandatory in shock, particularly in cardiogenic shock, use of this catheter is recommended for intermittent (blood sample) or continuous (fiber optic) measurement of central venous oxygen saturation (ScvO2), which indicates whether cardiac output is appropriate to the metabolic conditions and provides useful information for adaptation of treatment.

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Central venous pressure should not be measured because of the constraints of measurement and its limits as a marker of preload and of preload dependency (weak agreement).

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In shock refractory to empirical treatment, cardiac output as well as mixed venous oxygen saturation (SvO2) or ScvO2 should be continuously monitored (strong agreement).

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We suggest pulmonary artery catheterization in patients with refractory cardiogenic shock and right ventricular dysfunction (weak agreement).

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We suggest the use of a transpulmonary thermodilution monitor/pulse wave analysis plus measurement (continuous or intermittent) of mixed venous oxygen saturation (SvO2) or ScvO2 when cardiogenic shock is refractory to initial treatment, in the absence of mechanical assistance and of predominant right ventricular dysfunction (weak agreement)…

Concerning the use of vasoactive agents, the authors recommend norepinephrine for raising perfusion pressure and dobutamine for inotropic support, to raise cardiac output. Although epinephrine could be used to achieve both objectives with one drug the authors prefer the combination of dubutamine and norepinephrine. Dopamine is not recommended.

This recommendation implies that norepinephrine could be infused without a central line:

In prehospital and emergency care, the vasopressor of choice is norepinephrine (weak agreement).

The authors did not elaborate and whether they had in mind interaosseous or peripheral access is not clear.

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In proven post-cardiac arrest cardiogenic shock, especially in shockable rhythms, routine coronary angiography is recommended (strong agreement)…

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The existence or onset of post-cardiac arrest cardiogenic shock is not a contraindication to therapeutic hypothermia (strong agreement)…

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If temporary circulatory support is needed, the use of peripheral extracorporeal membrane oxygenation is preferred (strong agreement)…

In cardiogenic shock, ventricular resynchronization is possible in cases of left-bundle branch block with wide QRS complex (weak agreement).

ESC recommendations do not mention CS as an indication for resynchronization. Resynchronization has enabled improvement of clinical condition and weaning from inotropic agents in patients with severe acute heart failure (NYHA class III-IV). In 15 CS patients with left-bundle branch block, a German team showed that temporary resynchronization of the left ventricle using a lead placed in the coronary sinus (while maintaining atrioventricular synchronous contraction using a right atrial lead) optimized macrocirculatory parameters and reduced blood-lactate concentration [31]. However, because of the absence of literature data of high level of proof, its routine use in CS patients cannot be recommended, because of the risk of infectious and mechanical complications associated with pacemaker implantation.

Here's a recommendation that's bound to be controversial:

In ischemic cardiogenic shock, the hemoglobin level should be maintained at around 10 g/dL

During the very acute phase of cardiogenic shock in which oxygen delivery is low and cardiac output is insufficient to meet metabolic demand, it may be useful to increase hemoglobin levels. Nevertheless, as soon as cardiogenic shock is resolved, the transfusion trigger should to 7 g/dL.

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When cardiogenic shock is not ischemic in origin, the hemoglobin level should be maintained above 8 g/dL (weak agreement).

For cardiogenic shock caused by drug overdoses early use of ECMO is advised. In addition:

Adjuvant treatments such as glucagon (beta-blockers), insulin therapy (calcium inhibitors), and lipid emulsion (lipid-soluble cardiotoxic local anesthetic) should be initially used in association with vasopressor/inotrope agents (strong agreement). Medical supportive treatment should not delay use of ECMO in case of refractory shock (weak agreement).

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The administration of molar sodium bicarbonate (doses fractionated from 100 to 250 mL up to a maximum total dose of 750 mL) is indicated in toxic shock with intraventricular conduction abnormalities (wide QRS complex), together with other treatments (strong agreement).

during the acute phase (weak agreement).

It goes on to say:

During the very acute phase of cardiogenic shock in which oxygen delivery is low and cardiac output is insufficient to meet metabolic demand, it may be useful to increase hemoglobin levels. Nevertheless, as soon as cardiogenic shock is resolved, the transfusion trigger should to 7 g/dL.

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When cardiogenic shock is not ischemic in origin, the hemoglobin level should be maintained above 8 g/dL (weak agreement).

For cardiogenic shock caused by drug overdoses early use of ECMO is advised. In addition:

Adjuvant treatments such as glucagon (beta-blockers), insulin therapy (calcium inhibitors), and lipid emulsion (lipid-soluble cardiotoxic local anesthetic) should be initially used in association with vasopressor/inotrope agents (strong agreement). Medical supportive treatment should not delay use of ECMO in case of refractory shock (weak agreement).

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The administration of molar sodium bicarbonate (doses fractionated from 100 to 250 mL up to a maximum total dose of 750 mL) is indicated in toxic shock with intraventricular conduction abnormalities (wide QRS complex), together with other treatments (strong agreement).

For end stage heart disease progressing to CS:

Area 12: cardiogenic shock complicating end-stage heart disease

Patients with severe chronic heart disease should be assessed for their heart transplant eligibility in a center equipped for this intervention (strong agreement).

A patient with end-stage decompensated heart failure considered eligible for heart transplantation should be rapidly managed in the expert center that conducted the assessment (strong agreement).

ECMO/extracorporeal life support is indicated as first-line treatment in the case of progressive or refractory shock (persistent lactic acidosis, low cardiac output, high doses of catecholamines, kidney and/or liver failure) and of cardiac arrest without “no flow” in patients with advanced chronic heart disease with no contraindication for heart transplantation (strong agreement).

In progressive or refractory cardiogenic shock in a patient hospitalized for decompensated heart failure in a center without circulatory support, prompt use of a circulatory support mobile unit to implement veno-arterial ECMO followed by transfer of the patient on ECMO to an expert center is recommended (strong agreement).

Miscellaneous etiologies:

Area 14: other etiologies

Patients with acute heart failure or cardiogenic shock associated with myocarditis should be transferred to an expert center, on ECMO if necessary (strong agreement).

Bromocriptine treatment should be considered in cardiogenic shock complicating peripartum cardiomyopathy after discounting pre-existing or genetic heart disease (weak agreement).

For stress cardiomyopathy the authors recommend minimizing or, if possible, discontinuation of inotropic agents.