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

Pathophysiology of Cardiogenic Shock

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

Diagnosis

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.

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 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.

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 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.

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.

If primary angioplasty cannot restore flow within 90 minutes of the patients presentation, then consideration should be given to administration of fibrinolytic therapy.

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.

Inotropic support

If hypotension persists in the presence of adequate left ventricular filling pressures, then the addition of positive inotropic agents to improve contractility may be required.

Mechanical support

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. In the setting of pronounced hypotension, placement of a left ventricular assist device (which augments the pump-function of the heart) should be considered.

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

See also

• Intra-aortic balloon pump
• 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.

External links

• Cardiogenic Shock by eMedicine