Cardiogenic shock: Difference between revisions

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=== Symptoms ===
=== Symptoms ===
* [[Anxiety]], restlessness, and an [[Glasgow Coma Scale|altered mental state]] may be present due to decreased cerebral perfusion and ensuing [[hypoxia (medical)|hypoxia]].
* [[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]].
* [[Fatigue]] may be present due to the work of breathing and [[hypoxia]].



Revision as of 15:36, 17 May 2009

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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: [1]

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

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 multifactorial nature of cardiogenic shock can 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, and inadvertent administration of vasodilators and venodilators may further reduces cardiac output.

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. 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.

Differential diagnosis of underlying causes of cardiogenic shock

Cardiogenic shock can be a complication of the following conitions:

History of Cardiogenic Shock

It was not until the late 20th century when cardiologists began to fully investigate the pathophysiology of cardiogenic shock and came to define it as a state of low cardiac output secondary to extensive left ventricular dysfunction (usually acute MI) or secondary to the development of a mechanical defect such as a ventricular septal defect or papillary muscle rupture or under filling of the left ventricle due to right ventricular (RV) infarction. [2]

Diagnosis

Symptoms

Physical Examination

Vitals

Neck

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 and 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.

Electrocardiogram

An Electrocardiogram is 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

Echocardiography may show arrhythmia, signs of PED, ventricular septal rupture (VSR), an obstructed outflow tract or cardiomyopathy.

Swan-ganz catheter

The Swan-ganz catheter or Pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics.

Biopsy

In case of suspected cardiomyopathy a biopsy of heart muscle may be needed to make a definite 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.

Prognosis

Cardiogenic shock carries a very poor prognosis, particularly in the elderly.

See also

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

  1. 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.
  2. http://emedicine.medscape.com/article/152191-overview

External links

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