Cardiogenic shock is decreased cardiac output state and occurrence of tissue hypoxia as a result of inadequate intravascular volume contractility disturbances caused by hemodynamic criteria continuous hypotension with systolic blood pressure less than 90 mm Hg, cardiac index decreased less than 2.2 liters per minute and increased pulmonary wedge pressure ( PCWP) over 15 mmHg, and most of the events due to acute myocardial infarction (Hollenberg, 2004)
Etiology
1. Impaired myocardial function: an extensive acute myocardial infarction (> 40%), right ventricular infarction, arteriosklerotik heart disease, cardiomyopathy.
2. Mechanical: Mitral regurgitation, aortic regurgitation, septal rupture interventrikuler, anurisma massif ventricle, atrium stenosis, mitral stenosis, left atrial thrombus, pericarditis or pleural pericardium.
3. Arrhythmia: bradiaritmia, takhiaritmia
Sign And Symtomps
1. Changes in mental status (decreased perfusion cerebri): confusion, disorientation, anxiety and restlessness.
2. Pale, cool, moist (vasoconstriction and hypoperfusion)
3. Tachycardi / bradicardy.
4. Jugular venous distension.
5. Oliguria, urine production of less than 20 ml / hour.
6. Takhypnea, dyspnea
7. Fatique
8. Pulmonary edema
Pathophysiology
Decreased left ventricular function resulting in decreased ability of the left ventricle to pump blood, causing a decrease in stroke volume and cardiac output and blood pressure. Decrease in cardiac output resulting in decreased perfusion to the peripheral terjdinya and reduced supply of O2 to the tissues resulting in vital organ dysfunction such as brain, kidney and heart problems that occur in mental status, decreased urine production, and other cardiac arrhythmias.
The decrease in stroke volume will increase the end left ventricular diastolic pressure (LVEDP) and result in increased pressure in the left atrium and pulmonary veins. These conditions increase the hydrostatic pressure in the pulmonary veins, causing the occurrence of pulmonary edema which would interfere with gas exchange and tissue hypoxia.
Etiology
1. Impaired myocardial function: an extensive acute myocardial infarction (> 40%), right ventricular infarction, arteriosklerotik heart disease, cardiomyopathy.
2. Mechanical: Mitral regurgitation, aortic regurgitation, septal rupture interventrikuler, anurisma massif ventricle, atrium stenosis, mitral stenosis, left atrial thrombus, pericarditis or pleural pericardium.
3. Arrhythmia: bradiaritmia, takhiaritmia
Sign And Symtomps
1. Changes in mental status (decreased perfusion cerebri): confusion, disorientation, anxiety and restlessness.
2. Pale, cool, moist (vasoconstriction and hypoperfusion)
3. Tachycardi / bradicardy.
4. Jugular venous distension.
5. Oliguria, urine production of less than 20 ml / hour.
6. Takhypnea, dyspnea
7. Fatique
8. Pulmonary edema
Pathophysiology
Decreased left ventricular function resulting in decreased ability of the left ventricle to pump blood, causing a decrease in stroke volume and cardiac output and blood pressure. Decrease in cardiac output resulting in decreased perfusion to the peripheral terjdinya and reduced supply of O2 to the tissues resulting in vital organ dysfunction such as brain, kidney and heart problems that occur in mental status, decreased urine production, and other cardiac arrhythmias.
The decrease in stroke volume will increase the end left ventricular diastolic pressure (LVEDP) and result in increased pressure in the left atrium and pulmonary veins. These conditions increase the hydrostatic pressure in the pulmonary veins, causing the occurrence of pulmonary edema which would interfere with gas exchange and tissue hypoxia.
