Pathophysiology and Treatment Introdruction of Chronic Heart Failure Flashcards
What is heart failure
Clinical syndrome caused by the inability of the heart to pump enough blood to meet the metabolic demands of the body
What are symptoms of heart failure
dyspnea, fatigue, fluid retention
T/F: Heart failure will get worse if not treated or is on medication than taken off
True
What is preload, afterload
End diastolic volume that stretches the left ventricle to the most, pressure against which the heart must work to eject blood during systole
What ejection fraction
Portion of the total ventricular blood volume that is ejected during each contraction
What is a normal ejection fraction, what is the most accurate way to find the ejection fraction
50% or more, echocardiogram and cardiac MRI
What are the two types reduced ejection fraction and how are they caused
Heart Failure Reduced Ejection Fraction: Results from loss of muscle mass, pressure or volume overload (systolic dysfunction)/ Heart Failure preserved Ejection Fraction: Results from increased ventricular stiffness
T/F: Any type of heart failure has a ejection fraction less than 50%
False: HF-Reduced has an EF less than or equal to 40% while HF-Preserved has an EF greater than or equal to 50%
What is the most common cause of HF-Preserved
Left Ventricular Hypertrophy due to longstanding hypertension
What causes HF-Reduced
Initial cardiac insult -> primary damage-> activation of compensatory mechanisms -> secondary damage mediated by neurohormones
What are the two most common initial cardiac insults that could cause primary damage leading to HF-reduced
Myocardial infarction and Hypertension
What are the compensatory mechanisms that can cause secondary damage mediated by neurohormones
Increased preload, vasoconstriction, tachycardia, ventricular remodeling
How is compensating for cardiac output increasing the preload therefore contributing to HF-Reduced
Increased preload-> less cardiac output-> reduced renal perfusion-> kidney interprets this as ineffective blood volume-> activation of the RAAS system leading to H2O and NA retention: chronic volume overload and increased myocardial demand
How is compensating for cardiac output increasing the afterload therefore contributing to HF-Reduced
Increased afterload-> less cardiac output-> reduced Mean Arterial Blood Pressure-> activation of the RAAS system and SNS leads to VASOCONSTRICTION: increase myocardial demand and the heart become to week to overcome
How is compensating for cardiac output causing tachycardia that contributes to HF-REduced
ess cardiac output-> reduced O2 supply to tissues-> activation of SNS leads to increased HR: Decreased disatolic filling time, increased myocardial demand, precipitation of arrhythmias, down regulation of beta receptors