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