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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. | 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. | ||
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Differential Diagnosis | Differential Diagnosis | ||
Revision as of 18:56, 11 May 2014
Pathophysiology
Inflammation and Hemodynamics
- (SIRS, iNOS, LV DYSFUNCTION)
Pathology
Myocardium
- INFARCT EXTENSION AND EXPANSION
- REMOTE ISCHEMIA
- DIASTOLIC DYSFUNCTION
- VALVULAR ABNORMALITIES
Cellular
- ENERGY METABOLISM
- ION PUMPS
- NECROSIS
- APOPTOSIS
Myocardial dysfunction
- STUNNING
- HIBERNATING
Reperfusion Injury
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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.
Differential Diagnosis
Type of Shock | Etiology | CO | SVR | PCWP | CVP | SVO2 | RVS | RVD | PAS | PAD |
Cardiogenic | Acute Ventricular Septal Defect | ↓↓ | ↑ | N — ↑ | ↑↑ | ↑ — ↑↑ | N — ↑ | ↑ | N — ↑ | N — ↑ |
Acute Mitral Regurgitation | ↓↓ | ↑ | ↑↑ | ↑ — ↑↑ | ↓ | ↑ | N — ↑ | ↑ | ↑ | |
Myocardial Dysfunction | ↓↓ | ↑ | ↑↑ | ↑↑ | ↓ | N — ↑ | N — ↑ | N — ↑ | ↑ | |
Right Ventricular Infarction | ↓↓ | ↑ | N — ↓ | ↑↑ | ↓ | ↓ — ↑ | ↑ | ↓ — ↑ | ↓ — ↑ | |
Obstructive | Pulmonary Embolism | ↓↓ | ↑ | N — ↓ | ↑↑ | ↓ | ↓ — ↑ | ↑ | ↓ — ↑ | ↓ — ↑ |
Cardiac Tamponade | ↓ — ↓↓ | ↑ | ↑↑ | ↑↑ | ↓ | N — ↑ | ↑ | N — ↑ | N — ↑ | |
Distributive | Septic Shock | N — ↑↑ | ↓ — ↓↓ | N — ↓ | N — ↓ | ↑ — ↑↑ | N — ↓ | N — ↓ | ↓ | ↓ |
Anaphylactic Shock | N — ↑↑ | ↓ — ↓↓ | N — ↓ | N — ↓ | ↑ — ↑↑ | N — ↓ | N — ↓ | ↓ | ↓ | |
Hypovolemic | Volume Depletion | ↓↓ | ↑ | ↓↓ | ↓↓ | ↓ | N — ↓ | N — ↓ | ↓ | ↓ |
References
- ↑ Parrillo, Joseph E.; Ayres, Stephen M. (1984). Major issues in critical care medicine. Baltimore: William Wilkins. ISBN 0-683-06754-0.
- ↑ Judith S. Hochman, E. Magnus Ohman (2009). Cardiogenic Shock. Wiley-Blackwell. ISBN 9781405179263.