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Flashcards in CHF Deck (46)
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LV failure

Symptoms due to low cardiac output and congestion, including dyspnea


Optimal management for LV failure includes

ACE-I/ARB, BB, aldosterone inhibitors


RV failure

cor pulmonale or more likely due to LV failure

symtoms: peripheral congestion


High-output heart failure is a heart condition that occurs when the cardiac output is higher than normal, examples are:

beri beri (nutritional deficit in vitamin B1 (thiamine), and hyperthyroidism


Causes of systolic CHF

-Ischemic cardiomyopathy
-infectious (Chagas)
-sarcoid, amyloid


Causes of diastolic CHF

-pericardial disease
-aging (causes diastolic heart failure)


Neurohormonal activation is partially responsible for ________

mechanical changes in heart failure


Vasopressin secretion-

promotes water absorption by kidney


Renin-angiotensin-aldosterone axis (RAAS)

-maintains cardiac output (CO) and tissue perfusion
-stimulates arterial vasoconstriction with angiotensin II
-expands intravascular volume with Na+ and water retention


Left ventricular end diastolic pressure (preload right before cardiac output) is important when patient may have heart failure and is presenting with


-Need to know if LVEDP is high or low
-LVEDP is the last pressure right before it pumps blood out to body


If LVEDP is high, _______

will have congestion and backing up into lungs

LVEDP is about the same as central venous pressure and jugular venous pulsation
Need to know if they’re “wet” (congested, fluid overload) or “dry” (Euvolemic, fluid status is stable, SOB from lung problems)


Decreased CO leads to increased HR, increased contractility, vasoconstriction (all raise bp, increase CO)
Low CO also causes increased renin angiotensin, increased ADH and blood volume
Problem with this, you’ll have __________

pulmonary edema


Classification by

stages A-D

(NYHA uses FC class 1-4)


general S/S and physical exam findings

Tachycardia, Palpations, S3/S4, S3 indicates systolic dysfunction, murmurs, HJR (hepatojugular reflex, press on liver, may see increase in jugular venous pressure), JVP, edema



-BNP (BNP becomes physiologically elevated, increases in response to left vent wall stress increase, triggers atrium to release ANP)


What do you use to assess LV function?

Echo (best way overall, no radiation, easy), MUGA (Multi Gated Acquisition Scan-BEST WAY to look at EF, intervention), angiogram



Target any potential reversible causes (CAD, tachycardia, ETOH, etc..)


When do you biopsy?

-if pt has acute fulminant myocarditis (pt comes in with flu like illness and then crash, have arrhythmias, pt needs biopsy to rule out giant cell myocarditis, worst type but is treatable)

-Acute presentation (symptoms are new and just started), hemodynamic compromise at initial presentation, new AVB, VT


S/S of CHF caused by venous congestion (right sided)

-pleural effusion--> edema, jugular venous distension


S/S of CHF caused by low cardiac output

-fatigue/low energy
-cool extremities
-poor growth
-altered consciousness
-tachypnea, nasal flaring/grunting (indicates left sided)
-retractions; pulmonary edema


Other etiologies of CHF

-Infectious myocarditis
-Dilated cardiomyopathy
-Tako-Tsubo (apical ballooning)
-Drug induced (chemo/toxic)


Dilated cardiomyopathy

ARVD (arrhythmiogenic RV dysplasia also called Uhl Cardiomyopathy; fattiness of R vent and can lead to death in young people), non-compaction (massive trabeculation;
tx: defibrillator)


Tako-Tsubo (apical ballooning)

Stress cardiomyopathy; typically in females, older, emotional stress can trigger sympathetic surge, hypercontratility of base of left vent and base will dilate (balloon), must rule out coronary disease; usually reversible


Hypertrophic heart

CHF and risk of sudden death (at risk for myopathy, put defibrillator on heart); hypertrophy of left vent, blood cant get out


Diastolic heart

-“little old lady heart”; very small, has low volume
-SOB; LVEDV is low; JV distension; edema (reflected with elevated central vein pressures)
-BNP increases (EF is greater than 45)

*NOTHING REDUCES MORTALITY- NO MEDS TO IMPROVE MORTALITY FOR DIASTOLIC; little bit of lasix, try and lower BP, but still wont decrease mortality*


Systolic heart

-heart is dilated, it’s very big; has many liters of volume
-SOB; LVEDP is low; JV distension; edema (reflected with elevated central vein pressures)
-BNP increases because of stretch, wall tension, vol or P, whatever makes left V work harder; If you hear S3 its systolic (EF is less than 45)

*LOWER MORTALITY FOR SYSTOLIC: ACE inhibitors, ARBs, beta blockers (metropalol or carbatolol only); aldosterone antagonists*


If you hear an S3 the problem is

systolic (Not diastolic)


EF, ejection fraction is less than _______ you GET A DEFRIBILATOR, ICD (implantable cardioverter defibrillator)



What can be used in African Americans to reduce mortality?

hydrolazine nitrate combo reduces mortality


Besides S3, only way you can tell the difference (systolic vs diastolic) is _______

from an Echo (can’t rely on S/S because they’re the same)