1. Cardiogenic Shock in Emergency Medicine http://emedicine.medscape.com/article/759992-overview
Author: Ethan S Brandler, MD, MPH; Chief Editor: David FM Brown, MD more...
Updated: Nov 2, 2010
Background
Cardiogenic shock is characterized by a decreased pumping ability of the heart that causes a shocklike state (ie,
global hypoperfusion). It most commonly occurs in association with, and as a direct result of, acute myocardial
infarction (AMI).
Similar to other shock states, cardiogenic shock is considered to be a clinical diagnosis characterized by decreased
urine output, altered mentation, and hypotension. Other clinical characteristics include jugular venous distension,
cardiac gallop, and pulmonary edema. The most recent prospective study of cardiogenic shock defines cardiogenic
shock as sustained hypotension (systolic blood pressure [BP] less than 90 mm Hg lasting more than 30 min) with
evidence of tissue hypoperfusion with adequate left ventricular (LV) filling pressure.[1] Tissue hypoperfusion was
defined as cold peripheries (extremities colder than core), oliguria (< 30 mL/h), or both.
For related information, see Medscape's Cardiology Resource Centers.
Pathophysiology
The most common initiating event in cardiogenic shock is AMI. Dead myocardium does not contract, and classical
teaching has been that when more than 40% of the myocardium is irreversibly damaged (particularly, the anterior
cardiac wall), cardiogenic shock may result. On a mechanical level, a marked decrease in contractility reduces the
ejection fraction and cardiac output. These lead to increased ventricular filling pressures, cardiac chamber dilatation,
and ultimately univentricular or biventricular failure that result in systemic hypotension and/or pulmonary edema. The
SHOCK trial, however, demonstrated that left ventricular ejection fraction is not always depressed in the setting of
cardiogenic shock. Additional surprising findings included nonelevated systemic vascular resistance on vasopressors
and that most survivors have only New York Heart Association (NYHA) class I congestive heart failure.
A systemic inflammatory response syndrome–type mechanism has been implicated in the pathophysiology of
cardiogenic shock. Elevated levels of white blood cells, body temperature, complement, interleukins, and C-reactive
protein are often seen in large myocardial infarctions. Similarly, inflammatory nitric oxide synthetase (iNOS) is also
released in high levels during myocardial stress. iNOS induces nitric oxide production, which may uncouple calcium
metabolism in the myocardium resulting in a stunned myocardium. Additionally, iNOS leads to the expression of
interleukins, which may themselves cause hypotension.
Myocardial ischemia causes a decrease in contractile function, which leads to left ventricular dysfunction and
decreased arterial pressure; these, in turn, exacerbate the myocardial ischemia. The end result is a vicious cycle that
leads to severe cardiovascular decompensation. Other pathophysiological mechanisms responsible for cardiogenic
shock include papillary muscle rupture leading to acute mitral regurgitation (4.4%); decreased forward flow, ejection
fraction, and ventricular septal defect (1.5%); and free wall rupture (4.1%) as a consequence of AMI.
Right ventricular (RV) infarct, by itself, may lead to hypotension and shock because of reduced preload to the left
ventricle. The management of RV infarcts is discussed elsewhere but should be considered in the setting of inferior
wall MI.
Cardiac tamponade may result as a consequence of pericarditis, uremic pericardial effusion, or in rare cases systemic
lupus erythematosus.
Whenever patients who present in shock have been exposed to medications that may cause hypotension, these drugs
should be considered as possible culprits in the disease. Calcium channel blockers may cause profound hypotension
with a normal or elevated heart rate. Beta-blocking agents may also cause hypotension. Hypotension can be seen with
or without bradycardia, or AV node block can be seen with either of these types of medications. If these medications
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2. Cardiogenic Shock in Emergency Medicine http://emedicine.medscape.com/article/759992-overview
are the culprits, therapy directed at these toxicities is beneficial. Nitroglycerin, angiotensin-converting enzyme
inhibitors, opiate, and barbiturates can all cause a shock state and may be difficult to distinguish from cardiogenic
shock.
Initiating events other than AMI and ischemia include infection, drug toxicity, and pulmonary embolus.
For children, the causes of cardiogenic shock are vastly different. The 3 primary causes of cardiogenic shock in
children and infants are viral myocarditis, congenital heart disease, and toxic ingestions. For details, see eMedicine's
Pediatric Critical Care Medicine article on Shock.
Epidemiology
Frequency
United States
Cardiogenic shock occurs in 8.6% of patients with ST-segment elevation MI with 29% of those presenting to the
hospital already in shock. It occurs only in 2% of patients with non–ST-segment elevation MI.
Mortality/Morbidity
Cardiogenic shock is the leading cause of death in acute myocardial infarction (AMI).
The overall in-hospital mortality rate is 57%. For persons older than 75 years, the mortality rate is 64.1%. For
those younger than 75 years, the mortality rate is 39.5%.
Outcomes significantly improve only when rapid revascularization can be achieved. The SHOCK trial
demonstrated that overall mortality when revascularization occurs is 38%. When rapid revascularization is not
attempted, mortality rates approach 70%.
Rates vary depending on the procedure (eg, percutaneous transluminal coronary angioplasty, stent placement,
thrombolytic therapy), but they have been reported to be as low as 30-50%.
Mortality rates have declined over time. In the National Registry of Myocardial Infarction covering the period
from 1995-2004, in-hospital mortality declined from 60.3% to 47.9%.[2] This improvement has been attributed
to the increasing frequency of the use percutaneous coronary intervention (PCI) and other revascularization
procedures. Mortality rates attributable to cardiogenic shock are also thought to be due to the increased
frequency of use of PCI, antiplatelet therapies, and lipid-lowering agents in patients with acute coronary
syndromes. This has decreased the incidence of cardiogenic shock developing in the hospital due to acute
coronary syndromes. The incidence of cardiogenic shock on arrival to the hospital has not changed
significantly.[3, 4]
Race
Race-stratified mortality rates are as follows: Hispanics, 74%; African Americans, 65%; whites, 56%; and
Asians/others, 41%.
Race-based differences in mortality disappear with revascularization.
Sex
Women comprise 42% of all patients with cardiogenic shock.
Age
Median age for cardiogenic shock mirrors the bimodal distribution of disease. For adults, the median age ranges from
65-66 years. For children, cardiogenic shock presents as a consequence of fulminant myocarditis or congenital heart
disease.
Contributor Information and Disclosures
Author
Ethan S Brandler, MD, MPH Clinical Assistant Professor, Attending Physician, Departments of Emergency
Medicine and Internal Medicine, University Hospital of Brooklyn, Kings County Hospital
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3. Cardiogenic Shock in Emergency Medicine http://emedicine.medscape.com/article/759992-overview
Ethan S Brandler, MD, MPH is a member of the following medical societies: American College of Emergency
Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Coauthor(s)
Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine,
Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency
Medicine, Kings County Hospital Center
Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society
for Academic Emergency Medicine
Disclosure: Nothing to disclose.
Specialty Editor Board
Daniel J Dire, MD, FACEP, FAAP, FAAEM Clinical Professor, Department of Emergency Medicine, University of
Texas-Houston; Clinical Professor, Department of Pediatrics, University of Texas Health Sciences Center, San
Antonio, Texas
Daniel J Dire, MD, FACEP, FAAP, FAAEM is a member of the following medical societies: American Academy of
Clinical Toxicology, American Academy of Emergency Medicine, American Academy of Pediatrics, American
College of Emergency Physicians, and Association of Military Surgeons of the US
Disclosure: Talecris Biotherapeutics Honoraria Speaking and teaching
Francisco Talavera, PharmD, PhD Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
A Antoine Kazzi, MD Chair and Medical Director, Department of Emergency Medicine, American University of
Beirut, Lebanon
A Antoine Kazzi, MD is a member of the following medical societies: American Academy of Emergency Medicine
Disclosure: Nothing to disclose.
John D Halamka, MD, MS Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess
Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending
Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency
Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency
Medicine
Disclosure: Nothing to disclose.
Chief Editor
David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice
Chair, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians
and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.
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