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Clinical Medicine (CHF)47 cards
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“A heterogeneous syndrome in which an abnormality of cardiac function is responsible for the inability of the heart to pump blood at an output sufficient to meet the requirements of metabolizing tissues and/or to do so only at abnormally elevated dia
Intravascular and interstitial volume overload, and manifestations of inadequate tissue perfusion
SOB, rales, edema
Impaired exercise tolerance, fatigue, renal dysfunction
5 million people
Impaired systolic function, diastolic dysfunction, mechanical abnormalities, Disorder of Rate and Rhythm, Pulmonary Heart Disease, High Output states
-Ischemic damage or dysfunction (MI, shock) -Chronic pressure overload (HTN, Obstructive VHD-aortic stenosis -Chronic volume overload (Regurgitant VHD, Intracardiac right to left shunting) -Non-ischemic dilated cardiomyopathy (Infectious agents, Inf
– Contractile state of the myocardium – Preload of the ventricle – Afterload of the ventricle – Heart Rate
end-diastolic volume or pressure
The amount of pressure the LV is pumping against
Vasodilators (improves CO and CHF)
Since the SV is less with HF than with a normal heart, but if you give inotropic drug to pt. then the SV increases
Heart Rate (HR) x Stroke Volume(SV) = CO
CO can be affected by HR, SVR, and the degree of LV dilation
? Heart Rate – Increasing rate increases the inotropic state – Increased rate increases cardiac output, especially in CHF with fixed stroke volume – However, chronic tachycardia inhibits cardiac function ? Rhythm – Coordinated atrial and ventricular
-Pathologic hypertrophy of cardiac myocardium LVH- LV hypertrophy (“stiff”) -Aging -Ischemic fibrosis -Restrictive cardiomyopathy (Amyloidosis, Sarcoidosis, hemochromatosis)-decr. LV complaince
Stiff ventricle does not allow normal filling to occur. Atrial kick provides most of the filling, which is caused by diastolic dysfunction.
– Regurgitant VHD (MR, AI) – Intracardiac shunts (VSD, ASD) – Congenital abnormalities
– Obstructive (Coarctation) – Left-to-right shunting (patent ductus)
– Right sided heart failure due to increased pulmonary artery pressures
High Output Failure
Left-sided heart failure
Acute CHF – Acute pulmonary edema – Sudden onset of symptoms – Hypotension – Significant hypoxia – Peripheral edema often not found – Tachycardia, diaphoresis, cyanosis more common Chronic CHF – Pt may have some element of chronic pleural effusions –
B-type natriuretic peptide; indicates myocardial stretch
Anemia. Anemia may be a cause of high output failure.
– Case management, diet, & exercise training – Coronary revascularization – Biventricular pacing (resynchronization) – Implantable Cardiac Defibrillators (ICD) – Cardiac transplantation, valve repair or replacement
– Correct reversible causes- CAD, VHD – Decrease preload – Decrease afterload – Increase systolic function
Positive Inotropic Agents
Severe LV dysfunction, especially after an anterior MI
A patient is weighing themselves at home, in the AM, and has gained 4 pounds compared to yesterday at the same time. What should they do?
Contact practitioner if more than 3 lbs is gained in 48 hrs
May be beneficial in pts with cardiomyopathy and left bundle branch block
You have a patient who has chronic CHF, he asks you what the prognosis looks like now (even though he continues to consume high NA+ diet, no exercise, etc). What do you tell him?
Poor prognosis and currently studies show a 5 yr survival rate is less than 50%
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