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Clin Med-Cardio pt 2 > HF lecture > Flashcards

HF lecture Flashcards

1
Q

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.

A

Heart failure

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2
Q 
Coronary heart dz
Primary pump failure
Valvular heart dz
Congenital heart dz
Uncontrolled HTN

can all cause…

A

Heart failure

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3
Q

Primary contraction abnormality; inadequate delivery of O2 to tissues and associated symptoms; e.g: large or multiple MI(s), dilated cardiomyopathy, chronic AR, MR.

A

Systolic failure (or dysfunction)

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4
Q

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.

A

Diastolic failure (or dysfunction)

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5
Q

Can diastolic and systolic failure occur together?

A

YES

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6
Q

Most common cause of R sided failure?

A

L sided failure/dysfunction

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7
Q

Inadequate ventricular emptying; pressures in the atrium and venous system behind the failing ventricle rise resulting in transudation of fluid into interstitial spaces.

A

Backward failure

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8
Q

Inadequate forward CO; Na and water retention result from diminished renal perfusion and activation of renin-angiotensin-aldosterone system.

A

Forward failure

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9
Q

Compensatory mechanisms of HF?

A
  • Redistribution of CO

- Na and H20 retention

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10
Q

Increase levels of norepinephrine result in increase HR, contractility and SVR- helps maintain arterial perfusion pressure (BP) in presence of decreased CO.

A

Adrenergic Nervous System

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11
Q

Long term elevation of catecholamines leads to progressive myocardial damage and….

A

fibrosis

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12
Q

extremely potent vasoconstrictor- leads to arteriolar constriction and increase in SVR, raising BP.

A

Angiotensin II

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13
Q

Angiotensin II stimulates adrenal gland to secrete…

A

Aldosterone

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14
Q

a mineralocorticoid hormone that ↑’s renal Na and H2O reabsorption; contributes to edema formation.

A

Aldosterone

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15
Q

Long term activation of angiotensin II and aldosterone lead to myocardial thinning and..

A

fibrosis (remodeling)

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16
Q

Which NYHA classification of Heart dz:

No limitation of physical activity. No symptoms of SOB, CP dizzyness, etc.

A

I

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17
Q

Which NYHA classification of Heart dz:

Slight limitation of physical activity. Some (ordinary) activities (exercise, exertion, etc) cause symptoms.

A

II

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18
Q

Which NYHA classification of Heart dz:

Marked limitation of physical activity. Less than ordinary activities (walking, dressing, etc.) cause symptoms.

A

III

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19
Q

Which NYHA classification of Heart dz:

Symptomatic at rest or minimal activity; unable to engage in any physical activity.

A

IV

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20
Q

3 common manifestations of HF

A

Dyspnea
Orthopnea
Paroxysmal Nocturnal Dyspnea

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21
Q

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.

A

Acute pulmonary edema

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22
Q

How can you measure pulmonary pressure?

A

Right heart cath

can get Capillary Wedge pressure

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23
Q

PCW greater than 20 mmHg

A

Interstitial edema

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24
Q

PCW greater than 25 mmHg

A

Alveolar edema

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25
Q

moist inspiratory crackles, begin at bases and progress upwards through the lungs; wheezes occasionally heard.

A

Crackles

26
Q
  • Increased systemic venous pressure; JVD reflects ↑JVP
  • Hepato-Jugular Reflux.
  • Congestive hepatomegaly- enlarged, tender, pulsatile liver.
A

Acute pulmonary edema

27
Q

“Wasted appearance” occurs with severe chronic heart failure→weight loss, anorexia, nausea; correlates with increased levels of cytokines like circulating tumor necrosis factor.

A

Cardiac cachexia

28
Q

findings unique to pathology responsible for HF; best non-invasive tool. Identifies ventricular dysfunction and EF.

A

Echo-doppler

29
Q

hormone produced by heart (ventricle) in response to wall stress- marker of decompensated heart failure in blood

A

beta-type natriuretic peptide (BNP)

30
Q
  • 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.
A

BNP

31
Q 
Has vasodilator (a&v) and diuretic properties.
Normal is 100pg/ml common with HF.
A

BNP

32
Q

What do you want to start right way in HF patients?

A

ACEi/ARBs

33
Q

Must monitor renal function (BUN, Cr.) serum electrolytes (esp. K), uric acid and glucose
**can cause hypokalemia, and hyperuricemia as well as metabolic alkalosis.

A

Loop diuretics

34
Q

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

A

ACE inhibitors

35
Q

Do ARBs increase bradykinin (and therefor cause a cough)?

A

NO!

36
Q

Drug class of Valsartan

A

ARB

37
Q

MUST!!! check K levels in these patients, because this drug is potassium sparing

A

Aldosterone Antagonist

38
Q

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.

A

Digoxin

39
Q

Sympathomimmetic amines are given via…

A

IV

40
Q

Potent inotropes administered IV for…

A

short term use

41
Q
  • Secondary: Rescusitated cardiac arrest/Vfib or hemodynamically unstable Vtach
  • Primary: EF ≤ .35 + mild to moderate HF symptoms

indications for….

A

implantable cardioverter defibrillators (ICD)

42
Q

low pitched sound in early diastole.
(best heard with the bell bc it is low pitched)

A

S3 gallop

43
Q

Useful in diagnosis of HF in patients presenting with SOB of uncertain (Cardiac vs Pulm) etiology and confirming HF when suspected clinically.

A

BNP

44
Q

ACE inhibitors
Beta blockers
Spironolactone

all prevent…

A

Remodeling

45
Q

Once HF is symptomatic, prognosis is..

A

poor

46
Q

severe failure (class IV) has ____% mortality in 12 months

A

40-50%

47
Q

Moderate failure (class III)- 40-50% mortality in…

A

3-4 years

48
Q

30-40% of HF patients die suddenly due to…

A

an arrhythmia

49
Q

ow many grams of Na should you try to stay under with a low sodium diet

A

4 gm

50
Q

Cramping and constipation could be indicative of…

A

HYPOkalemia

51
Q

In patients with acute and chronic HF, treatment with _______ results in: decreasing SVR, increasing CO, decreasing PCW, and relief of symptoms; also decreases mortality.

A

vasodilators

52
Q

Reduce mortality by >25%.

Long term, has natriuretic effects resulting in improved diuresis (↓ production of aldosterone).

A

ACE inhibitors

53
Q

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.

A

ACE inhibitors

54
Q

Elevation of _____ from ACE inhibition may also have beneficial effects on hemodynamics (vasodilation) and remodeling

A

kinins

55
Q

increased levels of prostaglandins and nitric oxide may lead to…

A

vasodilation

56
Q

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.

A

ACE inhibitor

57
Q

Must monitor renal function; Cr and BUN often increase mildly (and expectedly) with..

A

ACE inhibitor

58
Q

Beneficial for all classes of heart failure with up to 30% decrease in mortality.

A

Beta blockers

59
Q

What MUST you check in aldosterone antagonists

A

potassium levels!!!

these are K sparing, may have HYPERkalemia

60
Q

only oral inotropic agent available; improves cardiac contractility.
Increases automaticity of cardiac electrical tissue - can induce arrhythmias.

A

Digoxin

Clin Med-Cardio pt 2 (11 decks)

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