HF lecture Flashcards
A pathophysiologic state in which an abnormality of cardiac function is responsible for failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues and/or can do so only from an abnormally elevated diastolic volume/pressure.
Heart failure
Coronary heart dz Primary pump failure Valvular heart dz Congenital heart dz Uncontrolled HTN
can all cause…
Heart failure
Primary contraction abnormality; inadequate delivery of O2 to tissues and associated symptoms; e.g: large or multiple MI(s), dilated cardiomyopathy, chronic AR, MR.
Systolic failure (or dysfunction)
Impaired ventricular relaxation- elevation of ventricular filling pressures and associated symptoms; e.g: long standing hypertension (with LVH), hypertrophic cardiomyopathy, acute ischemia, prior infarcts, restrictive cardiomyopathy.
Diastolic failure (or dysfunction)
Can diastolic and systolic failure occur together?
YES
Most common cause of R sided failure?
L sided failure/dysfunction
Inadequate ventricular emptying; pressures in the atrium and venous system behind the failing ventricle rise resulting in transudation of fluid into interstitial spaces.
Backward failure
Inadequate forward CO; Na and water retention result from diminished renal perfusion and activation of renin-angiotensin-aldosterone system.
Forward failure
Compensatory mechanisms of HF?
- Redistribution of CO
- Na and H20 retention
Increase levels of norepinephrine result in increase HR, contractility and SVR- helps maintain arterial perfusion pressure (BP) in presence of decreased CO.
Adrenergic Nervous System
Long term elevation of catecholamines leads to progressive myocardial damage and….
fibrosis
extremely potent vasoconstrictor- leads to arteriolar constriction and increase in SVR, raising BP.
Angiotensin II
Angiotensin II stimulates adrenal gland to secrete…
Aldosterone
a mineralocorticoid hormone that ↑’s renal Na and H2O reabsorption; contributes to edema formation.
Aldosterone
Long term activation of angiotensin II and aldosterone lead to myocardial thinning and..
fibrosis (remodeling)
Which NYHA classification of Heart dz:
No limitation of physical activity. No symptoms of SOB, CP dizzyness, etc.
I
Which NYHA classification of Heart dz:
Slight limitation of physical activity. Some (ordinary) activities (exercise, exertion, etc) cause symptoms.
II
Which NYHA classification of Heart dz:
Marked limitation of physical activity. Less than ordinary activities (walking, dressing, etc.) cause symptoms.
III
Which NYHA classification of Heart dz:
Symptomatic at rest or minimal activity; unable to engage in any physical activity.
IV
3 common manifestations of HF
Dyspnea
Orthopnea
Paroxysmal Nocturnal Dyspnea
Severe dyspnea at rest as pulmonary congestion progresses; accompanied by marked elevation of pulmonary capillary pressure (PCP) leading to interstitial, then alveolar edema. A medical emergency usually addressed in ED.
Acute pulmonary edema
How can you measure pulmonary pressure?
Right heart cath
can get Capillary Wedge pressure
PCW greater than 20 mmHg
Interstitial edema
PCW greater than 25 mmHg
Alveolar edema
moist inspiratory crackles, begin at bases and progress upwards through the lungs; wheezes occasionally heard.
Crackles
- Increased systemic venous pressure; JVD reflects ↑JVP
- Hepato-Jugular Reflux.
- Congestive hepatomegaly- enlarged, tender, pulsatile liver.
Acute pulmonary edema
“Wasted appearance” occurs with severe chronic heart failure→weight loss, anorexia, nausea; correlates with increased levels of cytokines like circulating tumor necrosis factor.
Cardiac cachexia
findings unique to pathology responsible for HF; best non-invasive tool. Identifies ventricular dysfunction and EF.
Echo-doppler
hormone produced by heart (ventricle) in response to wall stress- marker of decompensated heart failure in blood
beta-type natriuretic peptide (BNP)
- Blood test for acute ventricular dysfunction → symptomatic heart failure.
- Useful in diagnosis of HF in patients presenting with SOB of uncertain (Cardiac vs Pulm) etiology and confirming HF when suspected clinically.
BNP
Has vasodilator (a&v) and diuretic properties. Normal is 100pg/ml common with HF.
BNP
What do you want to start right way in HF patients?
ACEi/ARBs
Must monitor renal function (BUN, Cr.) serum electrolytes (esp. K), uric acid and glucose
**can cause hypokalemia, and hyperuricemia as well as metabolic alkalosis.
Loop diuretics
Which drugs decrease remodeling of the LV post MI and in HF by reducing wall thinning, fibrosis and interfering with programmed cell death (apoptosis) result is ↓ mortality
ACE inhibitors
Do ARBs increase bradykinin (and therefor cause a cough)?
NO!
Drug class of Valsartan
ARB
MUST!!! check K levels in these patients, because this drug is potassium sparing
Aldosterone Antagonist
Prolongs refractory period of AV node (vagal tone increased): slows rate of Atrial fibrillation and flutter.
Modest improvement in cardiac function in patients with LV dilatation and dysfunction.
Falling out of favor for Rx of CHF; improves symptom but not mortality.
Digoxin
Sympathomimmetic amines are given via…
IV
Potent inotropes administered IV for…
short term use
- Secondary: Rescusitated cardiac arrest/Vfib or hemodynamically unstable Vtach
- Primary: EF ≤ .35 + mild to moderate HF symptoms
indications for….
implantable cardioverter defibrillators (ICD)
low pitched sound in early diastole. (best heard with the bell bc it is low pitched)
S3 gallop
Useful in diagnosis of HF in patients presenting with SOB of uncertain (Cardiac vs Pulm) etiology and confirming HF when suspected clinically.
BNP
ACE inhibitors
Beta blockers
Spironolactone
all prevent…
Remodeling
Once HF is symptomatic, prognosis is..
poor
severe failure (class IV) has ____% mortality in 12 months
40-50%
Moderate failure (class III)- 40-50% mortality in…
3-4 years
30-40% of HF patients die suddenly due to…
an arrhythmia
ow many grams of Na should you try to stay under with a low sodium diet
4 gm
Cramping and constipation could be indicative of…
HYPOkalemia
In patients with acute and chronic HF, treatment with _______ results in: decreasing SVR, increasing CO, decreasing PCW, and relief of symptoms; also decreases mortality.
vasodilators
Reduce mortality by >25%.
Long term, has natriuretic effects resulting in improved diuresis (↓ production of aldosterone).
ACE inhibitors
these decrease remodeling of the LV post MI and in HF by reducing wall thinning, fibrosis and interfering with programmed cell death (apoptosis) result is ↓ mortality.
ACE inhibitors
Elevation of _____ from ACE inhibition may also have beneficial effects on hemodynamics (vasodilation) and remodeling
kinins
increased levels of prostaglandins and nitric oxide may lead to…
vasodilation
Drug related persistent cough resulting from elevated bradykinin levels; occurs in up to 15-20% of patients, but only 5% need to DC the drug.
ACE inhibitor
Must monitor renal function; Cr and BUN often increase mildly (and expectedly) with..
ACE inhibitor
Beneficial for all classes of heart failure with up to 30% decrease in mortality.
Beta blockers
What MUST you check in aldosterone antagonists
potassium levels!!!
these are K sparing, may have HYPERkalemia
only oral inotropic agent available; improves cardiac contractility.
Increases automaticity of cardiac electrical tissue - can induce arrhythmias.
Digoxin
