Cardiogenic shock pathophysiology: Difference between revisions
No edit summary |
Joao Silva (talk | contribs) No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Cardiogenic shock}} | {{Cardiogenic shock}} | ||
{{CMG}} | {{CMG}}; {{AE}} {{JS}} | ||
==Overview== | ==Overview== | ||
Revision as of 18:07, 9 May 2014
|
Cardiogenic Shock Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cardiogenic shock pathophysiology On the Web |
|
American Roentgen Ray Society Images of Cardiogenic shock pathophysiology |
|
Risk calculators and risk factors for Cardiogenic shock pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]
Overview
Cardiogenic shock is inadequate cardiac output due to myocardial depression caused by various factors. Inflammatory mediators generated due to infarction or ischemia cause myocardial muscle depression causing a loss in the contractile ability of the heart and in turn hypotension. Lactic acidosis that develops as a result of poor systemic perfusion also depresses the myocardium.
Pathophysiology
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.
Cardiogenic shock and Inflammatory Mediators
Myocardial infarction or ischemia lead to production of superoxide radicals which combine with nitrous oxide to form perioxinitrite which in turn causes myocardial depression and hypotension.
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.
Pathophysiology 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.