Cardiogenic shock

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Overview

Cardiogenic shock is defined as an inadequate cardiac output to maintain adequate perfusion of vital organs to meet ongoing demands for oxygenation and metabolic demands. 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 and neurogenic shock.

Definition

Cardiogenic shock is defined by sustained hypotension with tissue hypoperfusion despite adequate left ventricular filling pressure. Signs of tissue hypoperfusion include oliguria (<30 mL/h), cool extremities, and altered mentation.

The pathophysiology of cardiogenic shock is complex and multifaceted, and as a result, diagnostic criteria for cardiogenic shock have been debated. 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 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.

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, myocarditis). 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 (e.g. aortic stenosis, HOCM)
• Reversal of flow into the left ventricle (e.g. acute aortic insufficiency)
• Inadequate left ventricular filling due to mechanical causes (e.g. tamponade)
• Inadequate left ventricular filling due to inadequate filling time (e.g. tachycardia)
• A mechanical defect (e.g. a VSD)

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, and this further reduces cardiac contractility. Reduced cardiac output leads to activation of the sympathetic nervous system, and the ensuing tachycardia that develops further exacerbates the myocardial ischemia.

Patients with cardiogenic shock in the setting of STEMI more often have multivessel disease, and there may be ischemia 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 demonstrated in a 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 function, given the subendocardial ischemia, the left ventricle developes diastolic dysfunction and becomes harder to fill. Inadvertent administration of vasodilators and venodilators may further reduce cardiac output and accelarate 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

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

Cardiogenic shock can be a complication of the following conitions:

• Acute MI, more often ST elevation MI than non ST elevation MI (NSTEMI) or unstable angina. Anterior MI with pronounced left ventricular dysfunction, posterior MI with acute mitral regurgitation or papillary muscle rupture, and inferior MI with right ventricular infarct physiology can be associated with cardiogenic shock.
• Tachyarrhythmias resulting in inadequate ventricular filling times and inadequate forward cardiac output
• Congestive heart failure
• Cardiomyopathy, particularly in its end stages
• Valvular heart disease including aortic stenosis, acute aortic insufficiency or mitral stenosis with tachycardia and inadequate diastolic filling time.
• Aortic dissection
• Hypertrophic obstructive cardiomyopathy with systolic anterior motion (SAM)
• Ventricular septal defect
• Cardiac tamponade
• Myocarditis
• 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.

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

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 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.

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).

Biopsy

In case of suspected cardiomyopathy a biopsy of heart muscle may be of benefit in establishing a definitive diagnosis.

Treatment

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

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.

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