Zusammenfassung der Ressource
Cardiogenic Shock
- Etiology
- Impaired blood flow, oxygen, nutrients to cardiac muscle
cells
- Right or left ventricular dysfunction
- End-stage
cardiomyopathy
- Papillary muscle dysfunction
- Free wall
rupture
- Congenital Heart Defect
- Myocardial
Infraction (most common)
- Cardiac tamponade
- Pathogenesis
- Low cardiac
output
- Decreased peripheral perfusion
- Sympathetic Nervous System
Response
- Catecholamine
Release
- Activation of renin-angiontensin-aldosterone
system
- Increases preload, stroke
volume, and heart rate.
Sodium and water retention
by the kidneys due to RAAS
causes intravascular volume
to increase along with blood
pressure. Increased systemic
vascular resistance occurs
due to the release of
hormones (catecholamines)
increasing heart rate and
afterload. Cardiac muscles
have to work harder to pump
and subsequently the heart's
oxygen demand increases.
- Cardiac tissue necrosis and ischemia increases
- Cyanosis, cool clammy
skin, decreased
cap-refill
- High left ventricular preload
- Increase left ventricular end diastolic pressure
- Diagnosis
- Assessment Findings
- Hypoxemia
- Altered LOC. Anxiety, confusion, and
agitation from decreased
cerebral perfusion
- Decreased Urine Output
due to RAAS
- Narrow pulse pressure
- Decrease systolic
pressure due to low
stroke volume