Cardiogenic shock

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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.

Definition
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.

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.

In clinical trials, cardiogenic shock has been defined as follows by the SHOCK investigators:

Clinical criteria

 * 1) Systolic blood pressure <90 mm Hg for at least 30 minutes
 * 2) Evidence of hypoperfusion
 * 3) Cool, clammy periphery
 * 4) Decreased urine output
 * 5) Decreased level of consciousness

Hemodynamic criteria

 * 1) Left ventricular end diastolic pressure or pulmonary capillary wedge pressure >15 mm Hg
 * 2) Cardiac index <2.2 L/min/m2

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 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
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.

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 vasodilators and venodilators may further reduce cardiac output and accelerate or trigger such a spiral.

Pathophysiologic mechanisms to compensate for cardiogenic shock
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
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
The incidence of cardiogenic shock among patients with acute MI is approximately 5% to 10%

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.

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

Symptoms

 * Anxiety, agitation, restlessness, and an altered mental state including flacid coma may be present due to decreased cerebral perfusion and ensuing hypoxia.
 * Fatigue may be present due to the work of breathing and hypoxia.

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 veins 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.

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 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 arrhythmias 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 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.

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. 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).

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 (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) < 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

Intra-aortic balloon placement
In the setting of acute MI, the placement of an intra-aortic balloon pump (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. 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.

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:
 * Older age
 * Prior MI
 * Signs of hypoperfusion including cold, clammy skin
 * Altered mental state
 * Oliguria

==ACC/AHA Guidelines (DO NOT EDIT) ==

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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)}}