|
|
| (23 intermediate revisions by 10 users not shown) |
| Line 1: |
Line 1: |
| __NOTOC__ | | __NOTOC__ |
| | {| class="infobox" style="float: right;" |
| | | style="vertical-align: middle; padding: 5px;" align=center | [[File:Siren.gif|30px|link=Cardiogenic shock resident survival guide]] |
| | | style="vertical-align: middle; padding: 5px;" align=center | [[Cardiogenic shock resident survival guide|'''Resident'''<br>'''Survival'''<br>'''Guide''']] |
| | |} |
| {{Cardiogenic shock}} | | {{Cardiogenic shock}} |
| '''For patient information click [[Heart attack (patient information)|here]]''' | | '''For patient information, click [[Cardiogenic shock (patient information)|here]].''' |
|
| |
|
| {{CMG}} | | {{CMG}}; {{AE}} {{JS}} {{AEL}}, {{sali}} |
| ==Overview==
| |
|
| |
|
| '''Cardiogenic shock''' is defined as an insufficient forward [[cardiac output]] to maintain adequate perfusion of vital organs to meet ongoing demands for oxygenation and metabolism. Cardiogenic shock is due to either inadequate left ventricular pump function (such as in [[congestive heart failure]]) or inadequate left ventricular filling (such as in [[cardiac tamponade]] or [[mitral stenosis]] with tachycardia). In so far as the course of treatment differs substantially, cardiogenic shock should be distinguished from other forms of [[shock]] such as [[septic shock]], [[distributive shock]], [[hypovolemic shock]] and [[neurogenic shock]].
| | ==[[Cardiogenic shock overview|Overview]]== |
|
| |
|
| == Definition == | | ==[[Cardiogenic shock historical perspective|Historical Perspective]]== |
| Cardiogenic shock is defined as sustained [[hypotension]] (>30 minutes) with evidence of tissue hypoperfusion despite adequate left ventricular filling pressure. Signs of tissue hypoperfusion include [[oliguria]] (<30 mL/h), cool extremities, cyanosis and altered mentation. | |
|
| |
|
| The pathophysiology of cardiogenic shock is complex and multifactorial. Furthermore, there are a variety of compensatory mechanisms in response to the pathophysiology that can mask the underlying hemodynamic derangements that may be present. As a result, the diagnostic criteria for cardiogenic shock are complex and have been debated.
| | ==[[Cardiogenic shock classification|Classification]]== |
|
| |
|
| Given that the condition is a form of "shock", many clinicians argue that by definition "shock" must therefore be present. However, some clinicians argue that [[hypotension]] alone should not be the key criteria in so far as compensatory tachycardia and vasoconstriction may compensate for the reduced [[cardiac output]] to yield only a mildly depressed [[systolic blood pressure]]. These clinicians advocate a hemodynamic definition with greater reliance placed on hemodynamic measures and interpretation of the [[cardiac output]] in the context of left ventricular filling pressure as often gauged by the [[pulmonary capillary wedge pressure]]. For instance, a patient who has a history of hypertension who now has a blood pressure of 100 mm Hg with a markedly elevated [[systemic vascular resistance]] ([[SVR]]) and pronounced [[tachycardia]] with a markedly reduced [[cardiac output]], would be in cardiogenic shock in the judgement of some clinicians despite the absence of [[hypotension]]. Some definitions require a drop in systolic blood pressure of 30 mm Hg.
| | ==[[Cardiogenic shock pathophysiology|Pathophysiology]]== |
|
| |
|
| In clinical trials, cardiogenic shock has been defined as follows by the SHOCK investigators: <ref>Hochman JS, Sleeper LA, Webb JG, et al. 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 1999; 341 (9) : 625–34.</ref>
| | ==[[Cardiogenic shock causes|Causes]]== |
|
| |
|
| ===Clinical criteria=== | | ==[[Cardiogenic shock differential diagnosis|Differentiating Cardiogenic shock from other Diseases]]== |
| # Systolic blood pressure <90 mm Hg for at least 30 minutes
| |
| # Evidence of hypoperfusion
| |
| # Cool, clammy periphery
| |
| # Decreased urine output
| |
| # Decreased level of consciousness
| |
|
| |
|
| ===Hemodynamic criteria=== | | ==[[Cardiogenic shock epidemiology and demographics|Epidemiology and Demographics]]== |
| # Left ventricular end diastolic pressure or pulmonary capillary wedge pressure >15 mm Hg
| |
| # Cardiac index <2.2 L/min/m2
| |
|
| |
|
| == Pathophysiology of Cardiogenic Shock == | | ==[[Cardiogenic shock risk factors|Risk Factors]]== |
| ===Basic hemodynamic derangements===
| |
| Cardiogenic shock is due to inadequate forward output of the heart. This can be due to the following (either alone or often in combination):
| |
| *Systolic left ventricular dysfunction (e.g. acute MI, [[CHF]], [[Cardiomyopathy]], [[coronary artery bypass grafting]], [[myocarditis]], [[myocardial contusion]],[[hypophosphatemia]] as can be seen in the [[refeeding syndrome]]). It is often said that 40% of the left ventricle must be infarcted to have cardogenic shock.
| |
| *Diastolic left ventricular dysfunction (e.g. ischemia)
| |
| *Obstruction of left ventricular outflow and increased after load (e.g. [[aortic stenosis]], [[HOCM]], [[coarctation of the aorta]], [[malignant hypertension]])
| |
| *Reversal of flow into the left ventricle (e.g. acute [[aortic insufficiency]], [[endocarditis]])
| |
| *Inadequate left ventricular filling due to mechanical causes (e.g. [[tamponade]], [[pulmonary embolism]]). This has also been called [[obstructive shock]] in the past.
| |
| *Inadequate left ventricular filling due to inadequate filling time (e.g. [[tachycardia]], tachycardia mediated cardiomyopathy)
| |
| *Conduction abnormalities (e.g. [[atrioventricular block]], [[sinus bradycardia]])
| |
| *A mechanical defect (e.g. a [[VSD]], myocardial rupture of the left ventricular free wall)
| |
| *Right ventricular failure (e.g. [[Pulmonary embolism]], hypoxic pulmonary vasoconstriction)
| |
|
| |
|
| ===The impact of cardiogenic shock on the [[pressure-volume loop]]=== | | ==[[Cardiogenic shock natural history, complications and prognosis|Natural History, Complications and Prognosis]]== |
| Cardiogenic shock shifts the pressure volume loop to the right: that is to say at a given pressure, the heart is able to eject less blood per heart beat, and [[stroke volume]] is reduced. Diastolic compliance is reduced, and left ventricular volumes are increased. This leads to the classic observation that an increased left ventricular end diastolic pressure is required to maintain adequate [[cardiac output]]. The rise in end diastolic pressure increases the wall stress and oxygen demands of the myocardium. These hemodynamic abnormalities contributes to the pathophysiologic spiral described below. | |
|
| |
|
| ===The pathophysiologic "spiral" of cardiogenic shock=== | | ==Diagnosis== |
| Among patients with acute MI, there is often a downward spiral of hypoperfusion leading to further ischemia which leads to a further reduction in cardiac output and further hypoperfusion. The [[lactic acidosis]] that develops as a result of poor systemic perfusion can further reduce cardiac contractility. Reduced cardiac output leads to activation of the sympathetic nervous system, and the ensuing [[tachycardia]] that develops further exacerbates the myocardial ischemia. The increased left ventricular end diastolic pressures is associated with a rise in wall stress which results in further myocardial ischemia. [[Hypotension]] reduces epicardial perfusion pressure which in turn further increases myocardial ischemia.
| |
|
| |
|
| Patients with cardiogenic shock in the setting of [[STEMI]] more often have multivessel disease, and myocardial ischemia may be present in multiple territories. It is for this reason that multivessel angioplasty may be of benefit in the patient with cardiogenic shock. Non-culprit or remote territories may also exhibit [[myocardial stunning]] in response to an ischemic insult which further reduces myocardial function. The pathophysiology of myocardial stunning is multifactorial and involves calcium overload in the sarcolemma and "stone heart" or [[diastolic dysfunction]] as well as the release of myocardial depressant substances. Areas of stunned myocardium may remain stunned after revascularization, but these regions do respond to inotropic stimulation. In contrast to stunned myocardium, [[hibernating myocardium]] does respond earlier to revascularization. <ref>http://emedicine.medscape.com/article/152191-overview</ref>
| | [[Cardiogenic shock diagnostic evaluation|Diagnostic Evaluation]] | [[Cardiogenic shock history and symptoms|History and Symptoms]] | [[Cardiogenic shock physical examination|Physical Examination]] | [[Cardiogenic shock laboratory findings|Laboratory Findings]] | [[Cardiogenic shock electrocardiogram|Electrocardiogram]] | [[Cardiogenic shock chest x ray|Chest X Ray]] | [[Cardiogenic shock CT|CT]] | [[Cardiogenic shock MRI|MRI]] | |
| | [[Cardiogenic shock echocardiography or ultrasound|Echocardiography or Ultrasound]] | [[Cardiogenic shock other imaging findings|Other Imaging Findings]] | [[Cardiogenic shock other diagnostic studies|Other Diagnostic Studies]] |
|
| |
|
| The multifactorial nature of cardiogenic shock can also be operative in the patient with critical [[aortic stenosis]] who has "spiraled": There is impairment of left ventricular outflow, with a drop in [[cardiac output]] there is greater [[subendocardial]] ischemia and poorer flow in the coronary arteries, this leads to further [[left ventricular systolic dysfunction]], given the subendocardial ischemia, the left ventricle develops [[diastolic dysfunction]] and becomes harder to fill. Inadvertent administration of [[vasodilator]]s and [[venodilator]]s may further reduce cardiac output and accelerate or trigger such a spiral.
| | ==Treatment== |
|
| |
|
| ===Pathophysiologic mechanisms to compensate for cardiogenic shock===
| | [[Cardiogenic shock medical therapy|Medical Therapy]] | [[Cardiogenic shock surgery|Surgery]] | [[Cardiogenic shock primary prevention|Primary Prevention]] | [[Cardiogenic shock secondary prevention|Secondary Prevention]] | [[Cardiogenic shock cost-effectiveness of therapy|Cost-Effectiveness of Therapy]] | [[Cardiogenic shock future or investigational therapies|Future or Investigational Therapies]] |
| [[Cardiac output]] is the product of [[stroke volume]] and heart rate. In order to compensate for a reduction in stroke volume, there is a rise in the heart rate in patients with cardiogenic shock. As a result of the reduction in [[cardiac output]], peripheral tissues extract more oxygen from the limited blood that does flow to them, and this leaves the blood deoxygenated when it returns to the right heart resulting in a fall in the mixed venous oxygen saturation. | |
|
| |
|
| ===Pahtophysiology of multiorgan failure=== | | ==Case Studies== |
| The poor perfusion of organs results in [[hypoxia]] and [[metabolic acidosis]]. Inadequate perfusion to meet the metabolic demands of the brain, kidneys and heart leads to multiorgan failure.
| |
|
| |
|
| ==Epidemiology and demographics of cardiogenic shock==
| | [[Cardiogenic shock case study one|Case #1]] |
| The incidence of cardiogenic shock among patients with [[acute MI]] is approximately 5% to 10% <ref>Goldberg RJ, Samad NA, Yarzebski J, et al. Temporal trends in cardiogenic shock complicating acute myocardial infarction. N Engl J Med. Apr 15 1999;340(15):1162-8.</ref><ref>Hasdai D, Holmes DR, Topol EJ, et al. Frequency and clinical outcome of cardiogenic shock during acute myocardial infarction among patients receiving reteplase or alteplase. Results from GUSTO-III. Global Use of Strategies to Open Occluded Coronary Arteries. Eur Heart J. Jan 1999;20(2):128-35.</ref>
| |
|
| |
|
| Because [[atherosclerosis]] and [[myocardial infarction]] are both more frequent among men, the number of men developing cardiogenic shock exceeds that of women. However, because women present with acute myocardial infarction at a later age than men, and because they may have more multivessel disease when they do present at a later age, a greater proportion of women with acute MI develop cardiogenic shock.<ref>Hasdai D, Califf RM, Thompson TD, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol. Jan 2000;35(1):136-43.</ref>
| | ==Related Chapters== |
|
| |
|
| ==Differential diagnosis of underlying causes of cardiogenic shock==
| |
| The causes of cardiogenic shock can be classified on the basis of the underlying pathophysiologic mechanism:
| |
|
| |
| ===Systolic left ventricular dysfunction===
| |
| *[[Acute MI]]
| |
|
| |
| *[[Congestive heart failure]] ([[CHF]])
| |
|
| |
| *[[Cardiomyopathy]]
| |
|
| |
| *[[Coronary artery bypass grafting]]
| |
|
| |
| *[[Myocarditis]]
| |
|
| |
| *[[Myocardial contusion]]
| |
|
| |
| *[[Hypophosphatemia]] as can be seen in the [[refeeding syndrome]])
| |
|
| |
| ===Diastolic left ventricular dysfunction===
| |
| *Subendocardial [[ischemia]]
| |
|
| |
| *Excess wall stress
| |
|
| |
| *[[Valvular heart disease]]
| |
|
| |
| *[[Hypertensive crisis]]
| |
|
| |
| ===Obstruction of left ventricular outflow and increased after load===
| |
| *[[Aortic stenosis]]
| |
|
| |
| *[[Coarctation of the aorta]]
| |
|
| |
| *[[Hypertrophic obstructive cardiomyopathy]] ([[HOCM]])
| |
|
| |
| *[[Malignant hypertension]]
| |
|
| |
| ===Reversal of flow into the left ventricle===
| |
| *[[Aortic insufficiency]]
| |
|
| |
| *[[Endocarditis]]
| |
|
| |
| *[[Aortic dissection]]
| |
|
| |
| ===Inadequate left ventricular filling due to mechanical causes===
| |
| *[[Tamponade]]
| |
|
| |
| ===Inadequate left ventricular filling due to inadequate filling time===
| |
| *[[Tachycardia]]
| |
|
| |
| *Tachycardia mediated [[cardiomyopathy]]
| |
|
| |
| ===Conduction abnormalities===
| |
| *[[Atrioventricular block]]
| |
|
| |
| *[[Sinus bradycardia]]
| |
|
| |
| ===Mechanical defect===
| |
| *[[Ventricular septal defect]] ([[VSD]])
| |
|
| |
| *Myocardial rupture of the left ventricular free wall
| |
|
| |
| ===Right ventricular failure===
| |
| *[[Pulmonary embolism]]
| |
|
| |
| *[[Hypoxic pulmonary vasoconstriction]]
| |
|
| |
| ===Iatrogenic===
| |
| *Iatrogenic due to excess administration of vasodilators and venodilators
| |
|
| |
| == Diagnosis ==
| |
|
| |
| === Symptoms ===
| |
| * [[Anxiety]], agitation, restlessness, and an [[Glasgow Coma Scale|altered mental state]] including flacid [[coma]] may be present due to decreased cerebral perfusion and ensuing [[hypoxia (medical)|hypoxia]].
| |
| * [[Fatigue]] may be present due to the work of breathing and [[hypoxia]].
| |
|
| |
| ===Physical Examination===
| |
| ====Vitals====
| |
| * [[Hypotension]] may be present due to a decrease in [[cardiac output]].
| |
| * [[Tachycardia]] with a rapid, weak, thready rapid pulse is present.
| |
| *[[Pulse pressure]] is reduced
| |
|
| |
| ====Neck====
| |
| * Distended [[jugular vein]]s due to increased [[jugular venous pressure]].
| |
| ====Skin====
| |
| * [[Cyanosis]], cool, clammy, and mottled skin ([[cutis marmorata]]), due to vasoconstriction and subsequent hypoperfusion of the skin are often present.
| |
|
| |
| ====Lungs====
| |
| * Rapid and deep respirations (hyperventilation) due to sympathetic nervous system stimulation by stretch receptors and as compensation for [[metabolic acidosis]].
| |
|
| |
| * [[Pulmonary Edema]] (fluid in the lungs) due to insufficient pumping of the heart, fluid backs up into the lungs.
| |
|
| |
| ====Genitourinary====
| |
| * [[Oliguria]] (low urine output) due insufficient renal perfusion is present if the condition persists.
| |
|
| |
| ==Laboratory findings==
| |
|
| |
| ===Markers of Myonecrosis===
| |
| An elevation of troponin and CK MB are diagnostic of myonecrosis. This would suggest either [[ST elevation MI]], [[myocarditis]], or [[myopericarditis]], or [[myonecrosis]] due to profound [[hypophosphatemia]].
| |
|
| |
| ===Complete Blood Count===
| |
| An elevated [[white blood cell count]] ([[WBC]]) may suggest an alternate diagnosis of [[septic shock]], however, it should be noted that the [[WBC]] can be elevated in [[STEMI]] due to demarginization. A reduced hemoglobin may suggest an alternate diagnosis of [[hypovolemic shock]]. A reduced platelet count may suggest an alternate diagnosis of [[septic shock]].
| |
|
| |
| ===Serum electrolytes===
| |
| [[Hypophosphatemia]] should be excluded as an underlying cause. [[Hypophosphatemia]] mediated [[myonecrosis]] can be observed with the [[refeeding syndrome]] as phosphate is used to convert glucose to glycogen.
| |
|
| |
| ===Serum lactate===
| |
| The magnitude of [[lactic acidosis]] is a maker of the extent of hypoperfusion and is valuable in gauging a patient's prognosis.
| |
|
| |
| === Electrocardiogram ===
| |
| An [[ECG|electrocardiogram]] may be useful in distinguishing cardiogenic shock from [[septic shock]] or [[neurogenic shock]]. A diagnosis of cardiogenic shock is suggested by the presence of [[ST segment changes]], new [[left bundle branch block]] or signs of a [[cardiomyopathy]]. [[Cardiac arrhythmia]]s may also be present.
| |
|
| |
| === Radiology ===
| |
| The [[chest x ray]] will show [[pulmonary edema]], pulmonary vascular redistribution, enlarged hila, Kerley's B lines, and bilateral [[pleural effusions]] in patients with [[left ventricular failure]]. In contrast, a [[pneumonia]] may be present in the patient with [[septic shock]].
| |
|
| |
| The heart may be enlarged ([[cardiomegaly]]) in the patient with [[tamponade]]. A [[widened mediastinum]] may be present in the patient with [[aortic dissection]].
| |
|
| |
| The chest x ray may also be useful in excluding a [[tension pneumothorax]] that may be associated with [[hypotension]]
| |
|
| |
| ===Echocardiography===
| |
| [[Echocardiography]] is important imaging modality in the evaluation of the patient with cardiogenic shock. It allows the clinician to distinguish cardiogenic shock from [[septic shock]] and [[neurogenic shock]]. In cardiogenic shock due to acute MI, poor wall motion will be present. In [[septic shock]], a hypercontractile ventricle may be present. Mechanical complications such as [[papillary muscle rupture]], pseudoaneurysm, and a [[ventricular septal defect]] may also be visualized. [[Valvular heart disease]] such as [[aortic stenosis]], [[aortic insufficiency]] and [[mitral stenosis]] can also be assessed. Dynamic outflow obstruction such as [[HOCM]] can also be indentified and quantified. The magnitude of left ventricular dysfunction in patients with cardiomyopathy can be evaluated.
| |
|
| |
| === Swan-ganz catheter ===
| |
| The [[Swan-ganz catheter]] or [[pulmonary artery catheter]] may be helpful in distinguishing cardiogenic shock from [[septic shock]] and in optimizing the patient's left ventricular filling pressures (see section on [[Cardiogenic shock#Treatment|Treatment below)]]. The presence of significant V waves (greatly exceeding the pulmonary [[capillary wedge pressure]]) on the [[pulmonary artery]] tracing suggests either acute [[mitral regurgitation]] or a [[ventricular septal defect]].
| |
|
| |
| === Biopsy ===
| |
| In case of suspected cardiomyopathy a [[biopsy]] of heart muscle may be of benefit in establishing a definitive [[diagnosis]].
| |
|
| |
| == Treatment ==
| |
| ===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.<ref name="pmid2868337">{{cite journal |author= |title=Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico (GISSI) |journal=Lancet |volume=1 |issue=8478 |pages=397–402 |year=1986 |month=February |pmid=2868337 |doi= |url=}}</ref> These studies, however, oare 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 vasconstrictors and/or inotropes is suggested. Hemodynamic monitoring is essential to assure that a target [[mean arterial pressure]] ([[MAP]]) of 60 to 65 mmHg is acheived to maintain perfusion to vital organs (brain, kidney, heart).
| |
|
| |
| ====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 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]].
| |
|
| |
| =====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 [[afterload|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.<ref name="pmid19168529">{{cite journal |author=Sjauw KD, Engström AE, Vis MM, van der Schaaf RJ, Baan J, Koch KT, de Winter RJ, Piek JJ, Tijssen JG, Henriques JP |title=A systematic review and meta-analysis of intra-aortic balloon pump therapy in ST-elevation myocardial infarction: should we change the guidelines? |journal=European Heart Journal |volume=30 |issue=4 |pages=459–68 |year=2009 |month=February |pmid=19168529 |doi=10.1093/eurheartj/ehn602 |url=http://eurheartj.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=19168529}}</ref> 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====
| |
| 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. <ref>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.</ref>
| |
|
| |
| ====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.
| |
|
| |
| ===Mechanical ventilation===
| |
| [[Mechanical ventilation]] is often required in patients with cardiogenic shock to assure adequate oxygenation.
| |
|
| |
| ==Complications==
| |
| Complications of cardiogenic shock include:
| |
| ===Cardiac===
| |
| A downward spiral of hypotension leading to reduced coronary perfusion leading to further hypotension and a further reduction in coronary perfusion
| |
| ===Neurologic===
| |
| Coma
| |
| ===Renal===
| |
| Oligurin [[renal failure]]
| |
| ===Pulmonary===
| |
| Cardiogenic [[pulmonary edema]]
| |
|
| |
| ==Prognosis==
| |
| Cardiogenic shock carries a very poor prognosis, particularly in the elderly. In the GUSTO 1 trial, the following were identified as correlates of higher mortality among patients with cardiogenic shock:<ref>Hasdai D, Califf RM, Thompson TD, et al. Predictors of cardiogenic shock after thrombolytic therapy for acute myocardial infarction. J Am Coll Cardiol. Jan 2000;35(1):136-43.</ref>
| |
| *Older age
| |
| *Prior MI
| |
| *Signs of hypoperfusion including cold, clammy skin
| |
| *[[Altered mental state]]
| |
| *[[Oliguria]]
| |
|
| |
| ==ACC/AHA Guidelines (DO NOT EDIT)<ref name="pmid15339869">{{cite journal |author=Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK |title=ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction) |journal=Circulation |volume=110 |issue=9 |pages=e82–292 |year=2004 |month=August |pmid=15339869 |doi= |url=http://circ.ahajournals.org/cgi/pmidlookup?view=long&pmid=15339869}}</ref>==
| |
|
| |
| {{cquote|
| |
| ===Class I===
| |
|
| |
| 1. [[Intra-aortic balloon counterpulsation]] is recommended for [[STEMI]] patients when [[cardiogenic shock]] is not quickly reversed with pharmacological therapy. The [[IABP]] is a stabilizing measure for [[angiography]] and prompt [[revascularization]]. ''(Level of Evidence: B)''
| |
|
| |
| 2. Intra-arterial monitoring is recommended for the management of [[STEMI]] patients with [[cardiogenic shock]]. ''(Level of Evidence: C)''
| |
|
| |
| 3. Early [[revascularization]], either [[PCI]] or [[CABG]], is recommended for patients less than 75 years old with ST elevation or [[LBBB]] who develop shock within 36 hours of [[MI]] and who 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)''
| |
|
| |
| 4. [[Fibrinolytic therapy]] should be administered to [[STEMI]] patients with [[cardiogenic shock]] who are unsuitable for further invasive care and do not have contraindications to [[fibrinolysis]]. ''(Level of Evidence: B)''
| |
|
| |
| 5. [[Echocardiography]] should be used to evaluate mechanical complications unless these are assessed by invasive measures. ''(Level of Evidence: C)''
| |
|
| |
| ===Class IIa===
| |
|
| |
| 1. Pulmonary artery catheter monitoring can be useful for the management of [[STEMI]] patients with [[cardiogenic shock]]. ''(Level of Evidence: C)''
| |
|
| |
| 2. Early [[revascularization]], either [[PCI]] or [[CABG]], is reasonable for selected patients 75 years or older with ST elevation or [[LBBB]] who develop shock within 36 hours of [[MI]] and who are suitable for [[revascularization]] that can be performed within 18 hours of [[shock]]. Patients with good prior functional status who agree to invasive care may be selected for such an invasive strategy. ''(Level of Evidence: B)''}}
| |
|
| |
| == See also ==
| |
| * [[Intra-aortic balloon pump]] | | * [[Intra-aortic balloon pump]] |
| * [[Ventricular assist device]] | | * [[Ventricular assist device]] |
|
| |
| == Sources ==
| |
| *Irwin, R.S., Rippe, J.M., Curley, F.J., Heard, S.O. (1997) Procedures and Techniques in Intensive Care Medicine (3rd edition). Boston: Lippincott, Williams and Wilkins.
| |
| *Marino, P. (1997) The ICU Book. (2nd edition). Philadelphia: Lippincott, Williams and Wilkins.
| |
|
| |
| ==References==
| |
| {{reflist|2}}
| |
|
| |
|
| [[Category:Cardiology]] | | [[Category:Cardiology]] |
| [[Category:Cardiovascular diseases]] | | [[Category:Cardiovascular diseases]] |
| | [[Category:Emergency medicine]] |
| | [[Category:Intensive care medicine]] |
| [[Category:Medical emergencies]] | | [[Category:Medical emergencies]] |
| [[Category:Intensive care medicine]]
| |
| [[Category:Emergency medicine]]
| |
| [[Category:Disease]]
| |
|
| |
| [[de:Kreislaufstillstand]]
| |
| [[es:Parada cardiorrespiratoria]]
| |
| [[fr:Arrêt cardio-circulatoire]]
| |
| [[id:Gagal jantung]]
| |
| [[he:דום לב]]
| |
| [[nl:Hartstilstand]]
| |
| [[ja:心停止]]
| |
| [[pl:Asystolia]]
| |
| [[pt:Choque cardiogênico]]
| |
| [[sr:Кардиогени шок]]
| |
|
| |
| {{WikiDoc Help Menu}}
| |
| {{WikiDoc Sources}}
| |
