eMedicine Specialties > Cardiology > Myocardial Disease and Cardiomyopathies

Cardiogenic Shock: Treatment & Medication

Author: Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Coauthor(s): Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Contributor Information and Disclosures

Updated: Aug 20, 2008

Treatment

Medical Care

Initial management includes fluid resuscitation to correct hypovolemia and hypotension, unless pulmonary edema is present. Central venous and arterial lines are often required. Swan-Ganz catheterization and continuous percutaneous oximetry are routine. Oxygenation and airway protection are critical; intubation and mechanical ventilation are commonly required. Correction of electrolyte and acid-base abnormalities, such as hypokalemia, hypomagnesemia, and acidosis, are essential.

  • Patients with MI or acute coronary syndrome are given aspirin and heparin. Both of these medications have been shown to be effective in reducing mortality in separate studies.
  • The glycoprotein IIb/IIIa inhibitors improve the outcome of patients with NSTACS. Their benefit has been proven in reducing recurrent MI following percutaneous coronary intervention (PCI) and in cardiogenic shock.
  • All patients with cardiogenic shock require close hemodynamic monitoring, volume support to ensure adequate sufficient preload, and ventilatory support as discussed in Respiratory Failure.
  • Hemodynamic support
    • Dopamine, norepinephrine, and epinephrine are vasoconstricting drugs that help maintain adequate blood pressure during life-threatening hypotension and help preserve perfusion pressure for optimizing flow in various organs. The mean blood pressure required for adequate splanchnic and renal perfusion (mean arterial pressure [MAP] of 60 or 65 mm Hg) is based on clinical indices of organ function.
    • In patients with inadequate tissue perfusion and adequate intravascular volume, initiation of inotropic and/or vasopressor drug therapy may be necessary. Dopamine increases myocardial contractility and supports the blood pressure; however, it may increase myocardial oxygen demand. Dobutamine may be preferable if the systolic blood pressure is higher than 80 mm Hg and has the advantage of not affecting myocardial oxygen demand as much as dopamine. However, the resulting tachycardia may preclude the use of this inotropic agent in some patients.
    • Dopamine is usually initiated at a rate of 5-10 mcg/kg/min intravenously, and the infusion rate is adjusted according to the blood pressure and other hemodynamic parameters. Often, patients may require high doses of dopamine (as much as 20 mcg/kg/min). If the patient remains hypotensive despite moderate doses of dopamine, a direct vasoconstrictor (eg, norepinephrine) should be started at a dose of 0.5 mcg/kg/min and titrated to maintain an MAP of 60 mm Hg. The potent vasoconstrictors (eg, norepinephrine) have traditionally been avoided because of their adverse effects on cardiac output and renal perfusion.
  • Vasopressor supportive therapy: The following is a brief review of the mechanism of action and indications for drugs used for hemodynamic support of cardiogenic shock.
    • Dopamine is a precursor of norepinephrine and epinephrine and has varying effects according to the doses infused. A dose of less than 5 mcg/kg/min causes vasodilation of renal, mesenteric, and coronary beds. At a dose of 5-10 mcg/kg/min, beta1-adrenergic effects induce an increase in cardiac contractility and heart rate. At doses of approximately 10 mcg/kg/min, alpha-adrenergic effects lead to arterial vasoconstriction and an elevation in blood pressure. The blood pressure increases primarily as a result of inotropic effect, and the undesirable effects are (1) tachycardia and increased pulmonary shunting and (2) the potential to decrease splanchnic perfusion and increase pulmonary arterial wedge pressure.
    • Norepinephrine is a potent alpha-adrenergic agonist with minimal beta-adrenergic agonist effects. Norepinephrine can increase blood pressure successfully in patients who remain hypotensive following dopamine. The dose of norepinephrine may vary from 0.2-1.5 mcg/kg/min, and large doses, as high as 3.3 mcg/kg/min, have been used because of the alpha-receptor down-regulation in persons with sepsis.
    • Epinephrine can increase the MAP by increasing the cardiac index and stroke volume, along with an increase in SVR and heart rate. Epinephrine may increase oxygen delivery and consumption and decreases the splanchnic blood flow. Administration of this agent is associated with an increase in systemic and regional lactate concentrations. The use of epinephrine is recommended only in patients who are unresponsive to traditional agents. The undesirable effects are an increase in lactate concentration, a potential to produce myocardial ischemia, the development of arrhythmias, and a reduction in splanchnic flow.
  • Inotropic supportive therapy
    • Dobutamine (sympathomimetic agent) is a beta1-receptor agonist, although it has some beta2-receptor and minimal alpha-receptor activity. Intravenous dobutamine induces significant positive inotropic effects with mild chronotropic effects. It also induces mild peripheral vasodilation (decrease in afterload). The combined effect of increased inotropy and decreased afterload induces a significant increase in cardiac output. In the setting of acute MI, dobutamine use could increase the size of the infarct because of the increase in myocardial oxygen consumption that may ensue. In general, avoid dobutamine in patients with moderate or severe hypotension (eg, systolic blood pressure <80 mm Hg) because of the peripheral vasodilation.
    • Phosphodiesterase inhibitors (PDIs), currently inamrinone (formerly amrinone) and milrinone, are the PDI inotropes that have proved valuable.
      • These are inotropic agents with vasodilating properties, and each has a long half-life. The hemodynamic properties of PDIs are (1) a positive inotropic effect on the myocardium and peripheral vasodilation (decreased afterload) and (2) a reduction in pulmonary vascular resistance (decreased preload).
      • PDIs are beneficial in persons with cardiac pump failure, but they may require concomitant vasopressor administration. Unlike catecholamine inotropes, these drugs are not dependent on adrenoreceptor activity; therefore, patients are less likely to develop tolerance to these medications.
      • PDIs are less likely than catecholamines to cause adverse effects known to be associated with adrenoreceptor activity (eg, increased myocardial oxygen demand, myocardial ischemia). They are also associated with less tachycardia and myocardial oxygen consumption. However, the incidence of tachyarrhythmias is greater with PDIs compared to dobutamine.
  • Thrombolytic therapy
    • Although thrombolytic therapy (TT) reduces mortality rates in patients with acute MI, its benefits for patients with cardiogenic shock secondary to MI are disappointing. When used early in the course of MI, TT reduces the likelihood of subsequent development of cardiogenic shock after the initial event.
    • In the Gruppo Italiano Per lo Studio Della Streptokinase Nell'Infarto Miocardio trial, 30-day mortality rates were 69.9% in patients with cardiogenic shock who received streptokinase, compared to 70.1% in patients who received a placebo. Similarly, other studies with a tissue plasminogen activator did not show any benefit in mortality rates from cardiogenic shock. Lower rates of reperfusion of the infarct-related artery in patients with cardiogenic shock might help explain the disappointing results from TT. The other reasons for the decreased efficacy of TT are the presence of hemodynamic, mechanical, and metabolic factors causative of cardiogenic shock; these factors are unaffected by TT.
    • A recent prospective study investigated the potential benefit of TT and intra-aortic balloon pump (IABP) counterpulsation on in-hospital mortality rates of patients with MI complicated by cardiogenic shock.
      • Out of 1190 patients enrolled, the treatments were (1) no TT and no IABP counterpulsation (33%, n = 285), (2) IABP counterpulsation only (33%, n = 279), (3) TT only (15%, n = 132), and (4) TT and IABP counterpulsation (19%, n = 160).
      • Patients in cardiogenic shock treated with TT had lower in-hospital mortality rates compared to those who did not receive TT (54% vs 64%, P = .005), and those selected for IABP counterpulsation had lower in-hospital mortality rates compared to those who did not receive IABP counterpulsation (50% vs 72%, P <.0001).
      • Furthermore, a significant difference was noted in in-hospital mortality rates among the 4 treatment groups, ie, TT plus IABP counterpulsation (47%), IABP counterpulsation only (52%), TT only (63%), no TT and no IABP counterpulsation (77%) (P <.0001).
      • Revascularization influenced in-hospital mortality rates significantly (39% with revascularization vs 78% without revascularization, P <.0001).
    • Patients who are unsuitable for invasive therapy should be treated with a thrombolytic agent in the absence of contraindications. This is a class I recommendation by American College of Cardiology (ACC)/American Heart Association (AHA) guidelines.
  • Intra-aortic balloon pump
    • The use of the IABP reduces systolic left ventricular afterload and augments diastolic coronary perfusion pressure, thereby increasing cardiac output and improving coronary artery blood flow. The IABP is effective for the initial stabilization of patients with cardiogenic shock. However, an IABP is not definitive therapy; the IABP stabilizes the patients so that definitive diagnostic and therapeutic interventions can be performed.
    • The IABP also may be a useful adjunct to thrombolysis for initial stabilization and transfer of patients to a tertiary care facility. Some studies have shown lower mortality rates in patients with MI and cardiogenic shock treated with an IABP and subsequent revascularization, as previously mentioned.
    • Complications may be documented in up to 30% of patients who undergo IABP therapy and mainly relate to local vascular problems, embolism, infection, and hemolysis. The impact of an IABP on long-term survival is controversial and depends on the hemodynamic status and etiology of the cardiogenic shock. Patient selection is the key issue; early insertion of the IABP may result in clinical benefit, rather than waiting until full-blown cardiogenic shock has developed.
  • Ventricular assist devices
    • In recent years, left ventricular assist devices (LVADs) capable of providing complete short-term hemodynamic support have been developed. The application of LVAD during reperfusion, after acute coronary occlusion, causes reduction of the left ventricular preload, increases regional myocardial blood flow and lactate extraction, and improves general cardiac function. The LVAD makes it possible to maintain the collateral blood flow as a result of maintaining the cardiac output and aortic pressure, keeping wall tension low, and reducing the extent of microvascular reperfusion injury.
    • The pooled analysis from 17 studies showed that the mean age of this group of patients was 59.5 ± 4.5 years, mean support duration was 146.2 ± 60.2 hours. In 78.5% of patients (range, 53.8-100%), adjunctive reperfusion therapy, mainly PTCA, was used. Mean weaning and survival rates were 58.5% (range, 46-75%) and 40% (range, 29-58%), respectively. In any case, comparing studies is difficult because important data are usually missing, patients were younger, and time to treatment is not standardized. Hemodynamic presentation seems to be worse compared with data reported in the SHOCK trial, with lower cardiac index, lower systolic aortic pressure, and higher serum lactates. Taking these considerations into account, LVAD support seems to give no survival improvement in patients with CS complicating acute MI, compared with early reperfusion alone or in combination with IABP.
    • One randomized controlled trial assigned 129 patients with end-stage heart failure who were ineligible for cardiac transplantation to receive a left ventricular assist device (68 patients) or optimal medical management. Survival analysis that received left ventricular assist devices as compared with the medical therapy group (relative risk, 0.52; 95% confidence interval, 0.34-0.78; P=0.001). The rates of survival at 1 year were 52% in the device group and 25% in the medical therapy group (P=0.002), and the rates at 2 years were 23% and 8% (P=0.09), respectively. The quality of life was significantly improved at 1 year in the device group.49
    • Implantable LVAD is being used as a bridge-to-heart transplantation for patients with acute MI and CS. Farrar and colleagues reported the best outcome in a multicenter trial that included 17 patients in CS from acute MI.48 Thirteen patients (76%) underwent HTx and all were discharged after support with the Thoratec LVAD. According to the HeartMate Data Registry50 , from 1986-1998, 41 patients (5% of the total number of HeartMate IP patients) were supported with this implantable pneumatic device for acute MI and 25 (61%) were successfully bridged to heart transplantation. However, LVADs as a bridging option for patients with CS must be considered cautiously and must be avoided in patients unlikely to survive or unlikely to be transplant candidates. Further investigations are required to better define indications, support modalities, and outcomes.
    • The indications for insertion of a ventricular assist device are controversial. Such an aggressive approach to support the circulatory system in cardiogenic shock is appropriate (1) after the failure of medical treatment and the IABP and (2) when the cause of cardiogenic shock is potentially reversible or as a bridging option.

Surgical Care

The retrospective and prospective data favor aggressive mechanical revascularization in patients with cardiogenic shock secondary to MI.

  • Percutaneous transluminal coronary angioplasty
    • Reestablishing blood flow in the infarct-related artery may improve left ventricular function and survival following MI. In acute MI, studies show that percutaneous transluminal coronary angioplasty (PTCA) can achieve adequate flow in 80-90% of patients, compared with 50-60% of patients after TT.
    • Several retrospective clinical trials have shown that patients with cardiogenic shock due to myocardial ischemia benefitted (reduction in 30-d mortality rates) when treated with angioplasty. A recent study of direct (primary) PTCA in patients with cardiogenic shock reports lower mortality rates in patients treated with angioplasty combined with the use of stents, compared to medical therapy.
    • To study the relationship of time to treatment and mortality in patients with acute MI, a series of 1336 patients who underwent successful primary PTCA were stratified into low-risk and not low–risk patient groups. The 6-month mortality rate was 9.3% for not low–risk patients and 1.3% for the low-risk patients (P <.001). An increase in the mortality rate from 4.8% to 12.9% with increasing time to reperfusion was observed in the not low–risk group. A delay from symptom onset to treatment resulted in higher mortality rates for the not low–risk patients.4
  • Coronary artery bypass grafting
    • Critical left main artery disease and 3-vessel coronary artery disease are common findings in patients who develop cardiogenic shock. The potential contribution of ischemia in the noninfarcted zone contributes to the deterioration of already compromised myocardial function.
    • Coronary artery bypass grafting (CABG) in the setting of cardiogenic shock is generally associated with high surgical morbidity and mortality rates. Because the results of percutaneous interventions can be favorable, routine bypass surgery is often discouraged for these patients.
    • A 2004 task force of the ACC and the AHA gave a class I recommendation to the performance of primary PCI or emergent CABG in patients younger than 75 years who have STEMI and who develop shock within 36 hours of MI and can be treated within 18 hours of onset of shock. Performance of primary PCI or emergent CABG was considered reasonable in patients older than 75 years (class IIa recommendation).
  • SHOCK trial
    • A recent study known as the SHOCK (ie, SHould we emergently revascularize Occluded Coronaries in cardiogenic shocK) trial addressed the question of revascularization in patients with cardiogenic shock. Patients were assigned to receive either optimal medical management, including an IABP and TT, or cardiac catheterization followed by revascularization using PTCA or CABG.18
    • The 1-month and 6-month survival rates were reported from the SHOCK Trial.19 The mortality rates at 30 days were 46.7% in the early intervention group and 56% in patients treated with optimal medical management. Although this did not reach a statistical significance at 1 month, the mortality rate at 6 months was significantly lower in the early intervention group (50.3% vs 63.1%, P = .027). The results of this study support the superiority of a strategy that combines early revascularization with medical management in patients with cardiogenic shock.
    • The 1-year survival rates were also reported from the SHOCK Trial.20 The survival rate at 1-year was 46.7% for patients in the early revascularization group and was 33.6% in the conservative management (absolute difference in survival, 13.2%; 95% confidence interval, 2.2-24.1%; P <.03; relative risk for death, 0.72; 95% confidence interval, 0.54-0.95) group. The treatment benefit was apparent only for patients younger than 75 years (51.6% survival rate in early revascularization group vs 33.3% in patients treated with optimal medical management). Based on the outcome of this study, the recommendation is that patients with acute MI complicated by cardiogenic shock, particularly those younger than 75 years, should be rapidly transferred to a center with personnel capable of performing early angiography and revascularization procedures.

Consultations

Consultation with a cardiologist and/or an intensivist should be sought early in the patient's clinical course. The patient is usually admitted to a coronary care unit or intensive care unit. All patients with cardiogenic shock should be cared for in a facility at which right heart catheterization, coronary arteriography, and revascularization facilities are readily available.

Medication

Vasopressors augment the coronary and cerebral blood flow during the low-flow state associated with shock. Sympathomimetic amines with both alpha- and beta-adrenergic effects are indicated for persons with cardiogenic shock. Dopamine and dobutamine are the drugs of choice to improve cardiac contractility, with dopamine the preferred agent in patients with hypotension.

Vasodilators relax vascular smooth muscle and reduce the SVR, allowing for improved forward flow, which improves cardiac output. Adequate pain control is essential for quality patient care and patient comfort. Diuretics are used to decrease plasma volume and peripheral edema. The reduction in extracellular fluid and plasma volume associated with diuresis may initially decrease cardiac output and, consequently, blood pressure, with a compensatory increase in peripheral vascular resistance. With continuing diuretic therapy, the plasma volume and peripheral vascular resistance usually return to pretreatment values.

Vasopressors/inotropic agents

Augment coronary and cerebral blood flow during low-flow state associated with cardiogenic shock.


Dopamine (Intropin)

Stimulates adrenergic and dopaminergic receptors. Hemodynamic effect depends on dose. Lower doses stimulate mainly dopaminergic receptors that produce renal and mesenteric vasodilation. Higher doses produce cardiac stimulation and vasoconstriction.

Adult

5-20 mcg/kg/min IV continuous infusion; dose may be increased by 1-4 mcg/kg/min q10-30min until optimal response is achieved; >50% of patients are maintained satisfactorily on doses <20 mcg/kg/min

Pediatric

Administer as in adults

Phenytoin, alpha- and beta-adrenergic blockers, general anesthesia, and MAOIs increase and prolong effects

Documented hypersensitivity; pheochromocytoma; ventricular fibrillation

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Must be administered via central vein; closely monitor urine flow, cardiac output, pulmonary wedge pressure, and blood pressure during infusion; prior to infusion, correct hypovolemia with either whole blood or plasma, as indicated; monitoring central venous pressure or left ventricular filling pressure may be helpful for detecting and treating hypovolemia


Dobutamine (Dobutrex)

Sympathomimetic amine with stronger beta than alpha effects. Produces systemic vasodilation and increases the inotropic state. Higher doses may cause increase in heart rate, exacerbating myocardial ischemia.

Adult

5-20 mcg/kg/min IV continuous infusion, titrate to desired response; not to exceed 40 mcg/kg/min

Pediatric

Administer as in adults

Beta-adrenergic blockers antagonize effects; general anesthetics may increase toxicity

Documented hypersensitivity; hypertrophic cardiomyopathy, atrial fibrillation or flutter, severe tachycardia

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Following MI, use with extreme caution; correct hypovolemic state before using; may exacerbate hypotension; use with caution when ventricular or life-threatening tachyarrhythmias present

Phosphodiesterase enzyme inhibitors

Induce peripheral vasodilation and provide inotropic support.


Milrinone (Primacor)

Positive inotrope and vasodilator with little chronotropic activity. Different in mode of action from either cardiac glycosides (digoxin) or catecholamines.

Adult

50 mcg/kg IV loading dose over 10 min, followed by 0.375-0.75 mcg/kg/min continuous IV infusion

Pediatric

Administer as in adults; although DOC in many pediatric ICUs, safety and efficacy are not well established

May precipitate if infused in same IV line as furosemide

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor fluid, electrolyte changes, and renal function during therapy; excessive diuresis may cause increase in potassium loss and predispose digitalized patients to arrhythmias (correct hypokalemia by potassium supplementation prior to treatment); slow or stop infusion in patients showing excessive decreases in blood pressure; if vigorous diuretic therapy causes significant decreases in cardiac filling pressure, cautiously administer drug and monitor blood pressure, heart rate, and clinical symptomatology


Inamrinone (Inocor)

Formerly known as amrinone. Phosphodiesterase inhibitor with positive inotropic and vasodilator activity. Produces vasodilation and increases inotropic state. More likely to cause tachycardia than dobutamine and may exacerbate myocardial ischemia.

Adult

Initial dose: 0.75 mg/kg IV bolus slowly over 2-3 min
Maintenance infusion: 5-10 mcg/kg/min; not to exceed 10 mg/kg; adjust dose according to patient response

Pediatric

Administer as in adults; safety and efficacy not well established

Diuretics may cause significant hypovolemia and a decrease in filling pressure; has additive effects with cardiac glycosides

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Causes thrombocytopenia in 2-3% of patients; hypotension may occur following a loading dose; requires adequate preload; ventricular dysrhythmias may occur but may be related to underlying condition; do not use in patients with cardiac outlet obstruction (eg, aortic stenosis, pulmonic stenosis, hypertrophic cardiomyopathy); discontinue therapy if clinical symptoms of liver toxicity occur; correct hypokalemic states before using

Vasodilators

Decrease preload and/or afterload.


Nitroglycerin (Nitro-Bid)

Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in preload and blood pressure (ie, afterload).

Adult

10-200 mcg/min IV continuous infusion

Pediatric

0.1-1 mcg/kg/min IV infusion

Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary)

Documented hypersensitivity; severe anemia, shock, postural hypotension, head trauma, closed-angle glaucoma, cerebral hemorrhage

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in 3-vessel, left main coronary artery disease, aortic stenosis, or low systolic blood pressure

Analgesics

Reduce pain, which decreases sympathetic stress, in addition to providing some preload reduction.


Morphine sulfate (Duramorph, Astramorph, MS Contin)

DOC for narcotic analgesia due to its reliable and predictable effects, safety profile, and ease of reversibility with naloxone. Various IV doses are used, commonly titrated until desired effect is achieved.

Adult

Initial dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC, reassess hemodynamic effects of dose

Pediatric

0.1-0.2 mg/kg/dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; may initiate at 0.05 mg/kg/dose

Phenothiazines may antagonize analgesic effects of opiate agonists; TCAs, MAOIs, and other CNS depressants may potentiate adverse effects

Documented hypersensitivity; hypotension, potentially compromised airway in patient in whom establishing rapid airway control would be difficult

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate

Diuretics

Decrease plasma volume and peripheral edema. Excessive reduction in plasma volume and stroke volume associated with diuresis may decrease cardiac output and, consequently, blood pressure.


Furosemide (Lasix)

Increases excretion of water by interfering with chloride-binding cotransport system, which, in turn, inhibits sodium and chloride reabsorption in ascending loop of Henle and distal renal tubule.
Individualize dose to patient. Depending on response, administer at increments of 20-40 mg no sooner than 6-8 h after previous dose, until desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg/dose until satisfactory effect is achieved.

Adult

20-80 mg/d PO/IV/IM; titrate up to 600 mg/d for severe edematous states; also may be administered as continuous infusion

Pediatric

1 mg/kg IV/IM slowly under close supervision; not to exceed 6 mg/kg

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle-relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently; increased plasma lithium levels and toxicity are possible when taken concurrently

Documented hypersensitivity, hepatic coma, anuria, and a state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Observe for blood dyscrasias, liver or kidney damage, or idiosyncratic reactions; perform frequent serum electrolyte, carbon dioxide, glucose, uric acid, calcium, creatinine, and BUN determinations during first few months of therapy and periodically thereafter; loop diuretics may increase urinary excretion of magnesium and calcium

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References
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Further Reading

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Keywords

cardiogenic shock, cardiac failure, heart failure, myocardial infarction, MI, ST-elevation MI, ST-elevation myocardial infarction, STEMI, non–ST-elevation acute coronary syndrome, NSTEMI, unstable angina, myocardial ischemia, heart attack, cardiac dysfunction, acute myocarditis, sustained arrhythmia, acute valvular catastrophe, end-stage cardiomyopathy, coronary artery disease, CAD, myocardial pathology, myocardial stunning, hibernating myocardium, systolic dysfunction, diastolic dysfunction, valvular dysfunction, cardiac arrhythmias, mechanical heart complications, left ventricular end-systolic pressure-volume curve, curvilinear diastolic pressure-volume curve, shock state, hemodynamic support, vasopressor supportive therapy, inotropic supportive therapy, thrombolytic therapy, intra-aortic balloon pump, ventricular assist device, percutaneous transluminal coronary angioplasty, coronary artery bypass grafting, coronary artery bypass grafting, shock trial

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Contributor Information and Disclosures

Author

Sat Sharma, MD, FRCPC, Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital
Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College
Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Ronald J Oudiz, MD, FACP, FACC, Associate Professor of Medicine, Division of Cardiology, The David Geffen School of Medicine at UCLA; Director, Liu Center for Pulmonary Hypertension, LA Biomedical Research Institute at Harbor-UCLA Medical Center
Ronald J Oudiz, MD, FACP, FACC is a member of the following medical societies: American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Heart Association, and American Thoracic Society
Disclosure: Actelion Grant/research funds Clinical Trials + honoraria; Encysive Grant/research funds Clinical Trials + honoraria; Gilead Grant/research funds Clinical Trials + honoraria; Pfizer Grant/research funds Clinical Trials + honoraria; United Therapeutics Grant/research funds Clinical Trials + honoraria; Lilly Grant/research funds Clinical Trials + honoraria; LungRx  Clinical Trials + honoraria

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Thomas G Di Salvo, MD, Associate Professor of Medicine, Medical Director, Vanderbilt Heart and Vascular Institute, Vanderbilt University Medical Center
Disclosure: Nothing to disclose.

 
 
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