Cardiogenic shock medical therapy: Difference between revisions

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=====Low Output with Shock=====
=====Low Output with Shock=====


=====Systolic blood pressure (SBP) > 80 mm Hg=====
=====Systolic blood pressure (SBP) > 70 or 80 mm Hg=====
[[Dobutamine]] may be preferable over [[dopamine]] at this blood pressure. Dopamine increase 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]] ([[PDI]]s) 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]].
[[Dobutamine]] is preferred over [[dopamine]] when the patient does not have symptoms:
* Usual dose: 2.0–20 μg/kg/min
* Maximum dose: 40 μg/kg/min
* Avoid ↑ HR by >10% of baseline


=====Systolic blood pressure (SBP) < 80 mm Hg=====
[[Dopamine]] should be administered among symptomatic patients:
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.
* Cardiac dose: 5.0–10 μg/kg/min
* Pressor dose: 10–20 μg/kg/min
* Maximum dose: 20–50 μg/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.
[[Phosphodiesterase inhibitors]] ([[PDI]]s) 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) < 70 or 80 mm Hg=====
Norepinephrine is indicated among patients with severe hypotension:
* Initial dose: 0.5–1.0 μg/min
* Maximum dose: 30–40 μg/min
* Titrate to [[SBP]] >90 mm Hg


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]]
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]]

Revision as of 17:34, 9 February 2015

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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 a medical emergency, rescusitive measures should be initiated immediately while the underlying etiology of the cardiogenic shock is promptly investigated. Myocardial infarction is the most common cause of cardiogenic shock, and when present, prompt revascularization should be performed. Other causes, such as free wall rupture, acute valvular abnormality, or left ventricular septum rupture, may require more invasive interventions.

Goals of Therapy

Cardiogenic shock is characterized by low cardiac output, high left ventricular filling pressure, and decreased blood pressure with organ hypoperfusion. Goals of therapy:

  • Increase coronary blood flow
  • Decrease myocardial energy consumption
  • Increase systemic blood flow

Management Plan

  • Resuscitation and general measures
  • Optimization of the blood pressure
    • Pharmacological therapy
    • Mechanical therapy
  • Reperfusion or revascularization
  • Hemodynamic monitoring and stabilization

Resuscitation and General Measures

Resuscitation measures should be IMMEDIATELY initiated:

Optimization of the Blood Pressure

The goal of blood pressure optimization are to:

  • Improve coronary blood flow
  • Improve systemic reperfusion

The first line treatment to increase blood pressure in cardiogenic shock is the administration of pharmacological therapy with either ionotropes or vasopressors,[5] the main choices being dopamine, dobutamine, and norepinephrine. If pharmacological therapy fails to stabilize the patient's blood pressure, mechanical support must be provided.

Pharmacological Therapy

The appropriate choice of an inotrope or vasopressor requires the assessment of the balance between its desired and undesired effects:

  • Desired effects: ↑ cardiac output and ↓ left ventricular pressure
  • Undesired effects: ↑ myocardial energy consumption

All inotropes and vasopressors increase myocardial oxygen consumption to a certain extent. However, the benefit of their administration in the setting of a cardiogenic shock is achieved through counteracting the deleterious effects of hypotension. In cardiogenic shock, hypotension decreases myocardial perfusion and leads to compensatory elevation in LV filling pressure which in turn increases myocardial energy consumption. Therefore, the balance between desired and undesired effects of these agents necessitate their administration at the minimum efficacious dose.[6] There is no robust data that compares the efficacy of inotropes and vasopressors in improvement of cardiovascular outcomes and reduction in mortality.[7]

The two main agents used to optimize the blood pressure are:

Alternative agents include dobutamine (mainly in non-sick patients) and phosphodiesterase inhibitors (amrinone or milrinone).

Selection of a Vasopressor or an Inotrope

The choices of pharmacological agents is guided by the blood pressure and clinical status of the patient. There is no clear cut regarding the choice of the agents, combinations of moderate doses of different medications are commonly used instead of the administration of the maximal dose of any individual drug.[8]

Low Output without Shock

Patients presenting in this setting should be started on an inotrope, such as dobutamine.

Low Output with Shock
Systolic blood pressure (SBP) > 70 or 80 mm Hg

Dobutamine is preferred over dopamine when the patient does not have symptoms:

  • Usual dose: 2.0–20 μg/kg/min
  • Maximum dose: 40 μg/kg/min
  • Avoid ↑ HR by >10% of baseline

Dopamine should be administered among symptomatic patients:

  • Cardiac dose: 5.0–10 μg/kg/min
  • Pressor dose: 10–20 μg/kg/min
  • Maximum dose: 20–50 μg/kg/min

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) < 70 or 80 mm Hg

Norepinephrine is indicated among patients with severe hypotension:

  • Initial dose: 0.5–1.0 μg/min
  • Maximum dose: 30–40 μg/min
  • Titrate to SBP >90 mm Hg

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

Mechanism of Action of Ionotropes and Vasopressors

Shown below is a table summarizing the different inotrope or vasopressor agents used in the setting of cardiogenic shock.[9][6]

Drug Alpha 1 Beta 1 Beta 2 Dopamine Effects
Norepinephrine +++ ++ + -
  • Minimal to moderate inotropic effect
  • Minimal chronotropic effect
  • Increase systolic and diastolic BP
  • Minimal impact on CO
  • Potent vasoconstriction
  • Increase coronary blood flow (increase diastolic BP)
Dopamine (dose---) ++ ++ - ++
  • Increase CO
  • Increase BP and SVR
  • Increase myocardial consumption
  • Increase renal perfusion and urine output
  • Peripheral vasoconstriction
  • Increases PCWP
Dobutamine + +++ ++ -
  • Increase CO
  • Increase myocardial contractility
  • Decrease LV filling pressure
  • Increase coronary flow during diastole
  • Increase collateral blood flow to ischemic regions
  • Vasoconstriction
  • Less arrythmogenic
Isoprotenerol - +++ +++ -
  • Positive inotrope
  • Positive chronotrope
  • Decrease coronary reperfusion
  • No effect of CO
  • Arrhythmogenic
  • Consider ONLY in patients with bradyarrhythmia as a bridge to temporary pacemaker
Phenylephrine +++ - - -
  • Reflex bradycardia
  • Vasoconstriction
Epinephrine +++ +++ ++ -
  • Arrythmogenic
  • Increase myocardial contractility

Phosphodiesterase inhibitors (milrinone, amrinone)

  • Potent ionotrope
  • Potent chronotrope
  • Vasodilation
  • Increase myocardial contractility

Vasopressin:

  • Act on V1 (vascular smooth muscle cells) and V2 (renal collecting duct system) receptors
  • May cause cardiac ischemia
  • Severe peripheral and splanchnic vasoconstriction

Levosimendan:

  • Ussed in decompensated heart failure

Mechanical Therapy

Intra-aortic balloon placement

As per the recommendation of the 2013 AHA/ACC guidelines, in the setting of acute MI, the placement of an intra-aortic balloon pump (IABP) (which reduces workload for the heart, and improves perfusion of the coronary arteries) should be considered.[10]

A meta-analysis of randomized trial data, however, challenges this common practice and class 1B recommendation.[11] In a meta-analysis of seven randomized trials enrolling 1009 patient, 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

As per the recommendation of the 2013 AHA/ACC guidelines, 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.[10] 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. [12]

Urgent Revascularization

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.

Urgent revascularization can be achieved through one of the following:

Urgent revascularization is a priority over hemodynamic monitoring in MI patients and should not be delayed. PCI or CABG are indicated among MI patients with cardiogenic shock. When PCI or CABG can not be perfomed, fibrinolytic therapy is indicated in the absence of any contraindications.[10][13] [14][15] Administration of streptokinase therapy to patients with cardiogenic shock has not been associated with an improvement in survival.[16] Yet, these studies are old and 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. CABG in the setting of cardiogenic shock is associated with high rates of mortality and morbidity, therefore if primary angioplasty can be performed successfully, CABG is preferably avoided.

Hemodynamic Monitoring and Stabilization

Hemodynamic Monitoring

The aims of hemodynamic monitoring are:

The response to the treatment is determined through the assessment of whether the mean arterial pressure reached the target value, an increase in blood pressure, and bed-side clinical assessment by evaluating indices of organ perfusion, such as physical exam, urine output, and lactate levels,

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.

Even though, there is adequate intravascular volume in cardiogenic shock, fluid administration should be considered in patients with cardiogenic shock following acute MI because patients are often diaphoretic with subsequent relative hypovolemia.[17][18]

Volume Management

Even though, by definition cardiogenic shock's etiology resides in a heart problem with adequate intravascular volume, fluid administration should be considered in patients with CS following acute MI, since these are often diaphoretic and relative hypovolemia may be present.[17][18] The goal of managing the patient with cardiogenic shock is to optimize the filling of the left ventricle so that the starling relationship, mechanical performance and contractility of the heart are 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 LV function.

There are different approaches to volume management, yet some critical elements should be present in every one of them, such as: constant deliverance of oxygen, thereby ensuring adequate arterial oxygen saturation at all times; titration of the treatment to specific clinical endpoints of volume repletion and therapy guided by parameters that represent tissue and organ perfusion.[17]

Pharmacologic Hemodynamic Support

According to the recommendations of the AHA/ACC guidelines, in the case of cardiogenic shock complicating acute MI, the most common cause of CS, pharmacological therapy with vasopressor and inotropic drugs, stands as a mainstay in the management of these patients.[5] 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 of vital organs, such as the brain, kidney and heart, as well as to monitor and guide the effects and doses of the treatment drugs. The main purpose of this hemodynamic therapy is to restore adequate tissue perfusion and to normalize the cellular metabolism.[17] However, due to the significant toxicity of these drugs, they should be given in doses as minimal as possible. This toxicity may be translated into short and long-term adverse effects, such as activation of pro-apoptotic signaling cascades, mitochondrial damage or membrane disruption and necrosis, following increases of already elevated cytosolic calcium levels in postischemic cardiac myocytes, after administration of dopamine.[19] When choosing the dosages and medications to use, it is better to choose combinations of moderate doses of different medications, than to use the maximal dose of any individual drug.[8]

Although a definitive approach to evaluate the adequacy of global perfusion and determine the adequate administration and titration of certain vasoactive medications, and proper volume manipulation, are yet to be established, this evaluation may be done by targeting:[20][17]

  • Selection of a Vasopressor or an Inotrope - In the clinical setting, patients are usually treated with a combination of vasopressors and inotropes. However, generally and according to the AHA/ACC guidelines:[21]

Attending to the fact that many vasoactive drugs have both inotropic and vasopressor actions, the selection of the adequate drug will depend on the target parameters to approach in each patient, since different drugs will work on different receptors and locations, therefore resulting in different actions. Vasoconstrictive drugs commonly aim at restoration of adequate arterial pressure, while inotropic drugs aim at increasing the cardiac output. The individual patient scenario is of extreme importance, since for instance: tissue hypoperfusion may occur in different settings, such as abnormal shunting of blood within organs, decreased perfusion or inability to deliver substrates to peripheral cells, which may justify the failure of certain therapies that aim for global hemodynamics.[17][22][23][24]

Vasopressors

The main goal of vasopressor therapy is to reach an adequate arterial pressure in order to maintain perfusion to vital organs, when in the presence of severe hypotension with shock. It is important to notice that hypotension alone may not require vasopressor therapy. Treatment should be initiated once fluid administration is shown to be insufficient to reach adequate pressures.[17][25] Vasopressors have different funtions in the different types of shock, however, in the cardiogenic type, since hypotension may exacerbate the underlying myocardial ischemia, vasopressors should be administered in order to maintain capable coronary perfusion pressure. [17] Potential vasopressor drugs include:

However, especially in critically ill patients, these effects may overlap. Other adverse effects include: immunosuppression from lymphocyte apoptosis; common arrhythmic effects of catecholamines that appear to be more prominent with the use of dopamine; and potential decrease in prolactin release.[41][42]

Inotropes

Inotropic therapy targets the improvement of myocardial contractility and therefore the increase of cardiac output. The best way to monitor its effect is to evaluate the changes in cardiac output, following a certain dosage of the drug. It is important to notice that many catecholamines have both inotropic and vasopressor effects. In the particular case of cardiogenic shock, hypoperfusion of peripheral tissues is a consequence of impaired cardiac output, therefore inotropic treatment should only be given once the etiology of shock has been established. It may be necessary to use a vasopressor drug in order to insure adequate coronary perfusion pressure.[17]

  • Levosimendan - new drug with both inotropic and vasodilatory properties that has the benefit of not increasing myocardial oxygen consumption. This is achieved by an increase of cardiac muscle calcium responsiveness, as well as the opening of ATP-dependent K+ channels. It has the possible adverse effect of causing hypotension, hence it should be carefully used in cardiogenic shock patients.[17]

Mechanical Support

Intra-aortic Balloon Placement

According to the AHA/ACC guidelines, IABP may be indicated in patients left ventricular failure, following STEMI, complicated by cardiogenic shock (under a level of evidence B) who fail to respond to pharmacological therapy.[10] In the setting of acute MI, the placement of an IABP (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.[11] In a meta-analysis of seven randomized trials enrolling 1009 patients, IABP placement in STEMI patients was not associated with a decrease in mortality nor improvement 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

According to the AHA/ACC guidelines, alternative LV assist devices may be indicated in patients with refractory cardiogenic shock for circulatory support (under a level of evidence C).[10] In the setting of pronounced hypotension, despite medical therapy and IABP placement, LV assist devices, which augment the pump-function of the heart, should be considered. A ventricular assist device should only be placed in those patients in whom cardiogenic shock is deemed to be reversible or if it is being used as a bridge option.[52]

Percutaneous LV assist devices (PLVADs) such as Tandem heart, Impella, ECMO may be used until cardiac recovery occurs, as a temporary procedure during high-risk coronary interventions, or as a bridge to definitive therapy, such as heart transplant, left ventricular assist device (LVAD) or decision making. They provide improved hemodynamics in patients with cardiogenic shock.[53]

Coronary Artery Bypass Graft (CABG) Placement

CABG in this setting is associated with high rates of mortality and morbidity, therefore if primary angioplasty can be performed successfully, CABG is preferably avoided.

Mechanical Ventilation

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

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.[54][55] This method not only supplies continuous hemodynamic data, therefore allowing a beat-to-beat analysis, useful in evaluating the response to therapy, unlike other manual methods, but also allows for the collection of arterial blood gas samples.[17][56] 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.[57] With this device it is also possible to collect blood from the pulmonary artery, therefore enabling determination of MVO2, in order to evaluate oxygen delivery to peripheral tissues and at the same time also helping in the diagnosis of left-to-right shunts, usually 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.[58]

Other monitoring techniques include:[59]

Contraindicated Medications

Cardiogenic shock is considered an absolute contraindication to the use of the following medications:

2013 Revised ACCF/AHA Guidelines for the Management of ST-Elevation Myocardial Infarction (DO NOT EDIT)[10]

General and Specific Considerations (DO NOT EDIT)[10][71]

Class I
"1. Primary PCI should be performed for patients less than 75 years old with ST elevation or presumably new left bundle-branch block who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock, unless further support is futile because of the patient’s wishes or contraindications/unsuitability for further invasive care. (Level of Evidence: A)"
"7. Primary PCI should be performed in patients with STEMI and cardiogenic shock or acute severe HF, irrespective of time delay from myocardial infarction (MI) onset.[72][73][74] (Level of Evidence: B)"


Class IIa
"1. Primary PCI is reasonable for selected patients 75 years or older with ST elevation or left bundle-branch block or who develop shock within 36 hours of MI and are suitable for revascularization that can be performed within 18 hours of shock. Patients with good prior functional status who are suitable for revascularization and agree to invasive care may be selected for such an invasive strategy. (Level of Evidence: B)"

Treatment of Cardiogenic Shock in Patients with STEMI (DO NOT EDIT)[10]

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.[72][75][76] (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.[77][78][15] (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.[79][80][81][11][82] (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

  1. ↑ 1.0 1.1 Ng, R.; Yeghiazarians, Y. (2011). "Post Myocardial Infarction Cardiogenic Shock: A Review of Current Therapies". Journal of Intensive Care Medicine. 28 (3): 151–165. doi:10.1177/0885066611411407. ISSN 0885-0666.
  2. ↑ TRIUMPH Investigators. Alexander JH, Reynolds HR, Stebbins AL, Dzavik V, Harrington RA; et al. (2007). "Effect of tilarginine acetate in patients with acute myocardial infarction and cardiogenic shock: the TRIUMPH randomized controlled trial". JAMA. 297 (15): 1657–66. doi:10.1001/jama.297.15.joc70035. PMID 17387132.
  3. ↑ Sakr Y, Reinhart K, Vincent JL, Sprung CL, Moreno R, Ranieri VM; et al. (2006). "Does dopamine administration in shock influence outcome? Results of the Sepsis Occurrence in Acutely Ill Patients (SOAP) Study". Crit Care Med. 34 (3): 589–97. doi:10.1097/01.CCM.0000201896.45809.E3. PMID 16505643.
  4. ↑ Hochman, Judith (2009). Cardiogenic shock. Chichester, West Sussex, UK Hoboken, NJ: Wiley-Blackwell. ISBN 9781405179263.
  5. ↑ 5.0 5.1 Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M; et al. (2004). "ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction)". Circulation. 110 (5): 588–636. doi:10.1161/01.CIR.0000134791.68010.FA. PMID 15289388.
  6. ↑ 6.0 6.1 Overgaard CB, Dzavík V (2008). "Inotropes and vasopressors: review of physiology and clinical use in cardiovascular disease". Circulation. 118 (10): 1047–56. doi:10.1161/CIRCULATIONAHA.107.728840. PMID 18765387.
  7. ↑ Unverzagt S, Wachsmuth L, Hirsch K, Thiele H, Buerke M, Haerting J; et al. (2014). "Inotropic agents and vasodilator strategies for acute myocardial infarction complicated by cardiogenic shock or low cardiac output syndrome". Cochrane Database Syst Rev. 1: CD009669. doi:10.1002/14651858.CD009669.pub2. PMID 24385385.
  8. ↑ 8.0 8.1 Richard C, Ricome JL, Rimailho A, Bottineau G, Auzepy P (1983). "Combined hemodynamic effects of dopamine and dobutamine in cardiogenic shock". Circulation. 67 (3): 620–6. PMID 6821904.
  9. ↑ Francis GS, Bartos JA, Adatya S (2014). "Inotropes". J Am Coll Cardiol. 63 (20): 2069–78. doi:10.1016/j.jacc.2014.01.016. PMID 24530672.
  10. ↑ 10.0 10.1 10.2 10.3 10.4 10.5 10.6 10.7 O'Gara PT, Kushner FG, Ascheim DD, Casey DE, Chung MK, de Lemos JA; et al. (2013). "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. 127 (4): 529–55. doi:10.1161/CIR.0b013e3182742c84. PMID 23247303.
  11. ↑ 11.0 11.1 11.2 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)
  12. ↑ Farrar DJ, Lawson JH, Litwak P, Cederwall G. Thoratec VAD system as a bridge to heart transplantation. J Heart Transplant. Jul-Aug 1990;9(4):415-22; discussion 422-3.
  13. ↑ Fath-Ordoubadi, F.; Beatt, Kj; Davis, R.C.; Carlsson, Jörg; Rahlf, Günther; Tebbe, Ulrich (1994). "Fibrinolytic therapy in suspected acute myocardial infarction". The Lancet. 343 (8902): 912–913. doi:10.1016/S0140-6736(94)90029-9. ISSN 0140-6736.
  14. ↑ Morrow, D. A.; Antman, E. M.; Charlesworth, A.; Cairns, R.; Murphy, S. A.; de Lemos, J. A.; Giugliano, R. P.; McCabe, C. H.; Braunwald, E. (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): 2031–2037. doi:10.1161/01.CIR.102.17.2031. ISSN 0009-7322.
  15. ↑ 15.0 15.1 French JK, Feldman HA, Assmann SF, Sanborn T, Palmeri ST, Miller D; 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.
  16. ↑ "Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI)". Lancet. 1 (8478): 397–402. 1986. PMID 2868337. Unknown parameter |month= ignored (help)
  17. ↑ 17.00 17.01 17.02 17.03 17.04 17.05 17.06 17.07 17.08 17.09 17.10 17.11 17.12 17.13 17.14 Hollenberg, Steven M. (2011). "Vasoactive Drugs in Circulatory Shock". American Journal of Respiratory and Critical Care Medicine. 183 (7): 847–855. doi:10.1164/rccm.201006-0972CI. ISSN 1073-449X.
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  72. ↑ 72.0 72.1 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)
  73. ↑ Hochman JS, Lamas GA, Buller CE; et al. (2006). "Coronary intervention for persistent occlusion after myocardial infarction". N. Engl. J. Med. 355 (23): 2395–407. doi:10.1056/NEJMoa066139. PMC 1995554. PMID 17105759. Unknown parameter |month= ignored (help)
  74. ↑ Thune JJ, Hoefsten DE, Lindholm MG; et al. (2005). "Simple risk stratification at admission to identify patients with reduced mortality from primary angioplasty". Circulation. 112 (13): 2017–21. doi:10.1161/CIRCULATIONAHA.105.558676. PMID 16186438. Unknown parameter |month= ignored (help)
  75. ↑ Babaev A, Frederick PD, Pasta DJ, Every N, Sichrovsky T, Hochman JS (2005). "Trends in management and outcomes of patients with acute myocardial infarction complicated by cardiogenic shock". JAMA. 294 (4): 448–54. doi:10.1001/jama.294.4.448. PMID 16046651. Unknown parameter |month= ignored (help)
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  77. ↑ "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)
  78. ↑ 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)
  79. ↑ 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)
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  82. ↑ 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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