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Perfusion: Acute Heart Failure - Coggle Diagram
Perfusion: Acute Heart Failure
Pathophysiology
BP increases
Contractility and force and force increase to overcome the resulting increase in afterload
Cardiac output (CO) reduces as a result of injury - stimulating release of vasoconstrictors (epinephrine) and vasopressin (an anti-diuretic, increasing blood volume)
Increased myocardial workload causes cell death (cardiac injury)
Myocardial injury happens
Cycle continues and worsens CO
Renin-angiotensin-aldosterone system is stimulated
Increase blood volume increases preload
BP and blood vloume increases resulting from Na+ and water retention
More force is required to shift preload into ventricles
myocardial death results from continuous increased workload feeding into the above mechanism
Symptoms
Dizziness
Shortness of breath
Peripheral edema
Acute pulmonary edema
Cheyne-Stokes resp
Cyanosis
Fatigue and weakness
Diminished LOC
Arrhythmias
A Fib most common
Sudden cardiac death
Risks
Family hx
Smoking hx
Sedentary lifestyle
Obesity
HTN
Stress
Alcohol
Hyperlipidemia
Dilated cardiomyopathy
CAD
Valvular heart disease
Labs and Diagnostics
ECG
Chest radiography
Echocardiography
BNP
NT-proBNP
Invasive hemodynamic monitoring
Ejection fraction
Collaborative Treatment
Drugs
Cardiac output and blood pressure
Calcium channel blockers
Beta blockers
ACE Inhibitors
Diuretics
ARBs
Digoxin
O2 therapy
Diet (low sodium, fluid restriction, weight management)
Exercise
Pacemaker
Complications
Arrhythmias
Myocardial hypertrophy
Sudden cardiac death
CKD
Pulmonary HTN
Stroke