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Clinical 2.0 > Chronic Heart Failure > Flashcards

Chronic Heart Failure Flashcards

1
Q

what is heart failure

A

clinical syndrome with subsets of conditions due to cardiac dysfunction
occurs when heart is unable to deliver adequate supply of oxygenated blood to meet metabolic demands of the organ

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2
Q

what causes decreased contractility

A

rheumatic heart disease
cardiomyopathy
coronary heart disease/mi

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3
Q

what causes increased afterload

A

hypertension

aortic stenosis

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4
Q

what causes increase preload

A

increased sodium/water retention
malfunction of aortic valve
drugs - nsaids

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5
Q

causes of heart failure

A 
decreased contractility 
increased afterload 
increased preload
direct cardiotoxic drugs
high output failure
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6
Q

what is cardiac output

A

SV x HR

volume of blood pumped by the heart per minute

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7
Q

what is ejection fraction

A

fraction of blood ejected from LV

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8
Q

define preload

A

degree of filling from the left atrium (venous return)

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9
Q

define afterload

A

arteriolar resistance the heart must pump against to eject stroke volume

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10
Q

describe contractility

A

intrinsic ability of cardiac myocytes to contract

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11
Q

what are the 3 general patterns of remodeling

A

concentric ventricular remodeling (thickening)
eccentric left ventricular hypertrophy (sacromeres being stretched)
mixed

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12
Q

how does the body maintain CO and BP

A

increase preload
vasoconstriction
tachycardia and increased contractility
neurohormonal activation- renin, NE

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13
Q

how does the body increase preload

A

increase venous return
sodium water retention
activation of renin angiotensin

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14
Q

how does vasoconstriction help in heart failure

A

increases afterload

increases systemic vascular resistance

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15
Q

describe heart failure with reduced ejection fraction

A 
low output 
hypofunctioning left ventricle, decreased contractility 
ejection fraction <40%
ventricles enlarge  
systolic heatr failure
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16
Q

describe hert failure with preserved ejection fraction

A

diastolic heart failure
normal contractility and heart size
impaired LV filling during diastole
thickened LV or stiff ventricle

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17
Q

what can be the result of a LV stiffness and inability to relax during diastole

A

increased resting pressure within the ventricle

increased pressure impedes ventricular filling therefore reducing stroke volume

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18
Q

what is hpertrophic cardiomyopathy

A

thickened LV

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19
Q

what is restrictive cardiomyopathy

A

stiff ventricle

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20
Q

bad effects of the following compensatory mechanisms
vasoconstriction:
increased HR:
increased preload:

A

vaso - decreased cardiac output
hr - increased oxygen utilization
preload - peripheral and pulmonary edema

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21
Q

signs of left sided heart failure (pulmonary congestion)

A

dyspnea (difficult breathing) on exertion
orthopnea (SOB when lying down)
paroxysmal nocturnal dyspnea (SOB that awakens the patient)
pulmonary edema

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22
Q

signs of right sided heart failure (systemic venous congestion)

A

organomegaly
jugular venous distention
hepatojugular reflex
lower extremity peripheral edema

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23
Q

other signs of heart failure

A 
weakness 
exercise tolerance 
fatigue 
cns
cold, pale, clammy skin
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24
Q

nyha class 1

A

cardiac function uncompromised

able to perform ordinary physical activity

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25
Q

nyha class 2

A

slightly compromised cardiac function

ordinary physical activity results in symptoms

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26
Q

nyha class 3

A

moderately compromised cardiac function

less than ordinary physical activity results in symptoms

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27
Q

nyha class 4

A

severely compromised cardaic function

symptoms may be present at rest

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28
Q

acc/aha class a

A

at righ for hf but without structural heart disease of symptoms of hf
ex. diabetes

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29
Q

acc/aha stage b

A

structural heart disease without signs or symptoms of HF

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30
Q

acc/aha stage c

A

structural heart disease with prior or current symptoms of HF

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31
Q

acc/aha stage d

A

refractory HF requiring specialized intervention

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32
Q

signs on clinical exams of HF

A 
auscultation of heart and lung - rales, S3 gallop
edema 
jugular vein distention 
hepatojugular reflux
dyspnea
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33
Q

goals of therapy

A 
minimize disabling symptoms 
decrease hospitalization 
improve quality of life
minimize disease complications 
slow progression of disease
improve survival
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34
Q

what are some medical management strategies

A 
elminate exacerbating factors
control associated diseases 
restrict activity when acute 
sodium resticted diet 
exercise condition when stabilized 
drug therapy
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35
Q

what are the four types of drugs used in hf

A

diuretics - excrete excess water
inotropic agents - increase myocardial contractility
vasodilators - decrease cardiac work
acei - neurohormonal modulators

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36
Q

how do diuretics help in hf, any evidence

A

relieve breathlessness and edema in patients with congestion

no evidence for reduced mortality

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37
Q

use of diuretics in hf

A

use loop
start with low dose and adjust to achieve body weight reduction of .75-1kg until euvolemia (normal water volume)
try to maintain ppatients dry weight with the lowest possible dose
can alter dose based on volume status

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38
Q

furosemide dosing

A

20-40 daily then increase to acheive edema free state, once symptoms relieved use lowest possible maintenance dose

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39
Q

when would you initiate metolazone

A

in combo with loop diuretic if not enough, given 30 min before furosemide

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40
Q

metoalzone dosing

A

start 2.5 mg, usual dose 2.5-10mg/d

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41
Q

AE of diuretics

A

volume depletion - dehydration, reduced bp and co
loss of K and Mg
renal impairment

42
Q

do thiazides work in renal impairment

A

no

43
Q

monitoring of diuretics

A

signs of hypovolemia, symptomatic hypotension
electrolytes K>4
renal function before initiating, SCr, eGFR
check renal function and electrolytes 1-2 weeks after initiation or dose increase

44
Q

how to monitor the efficacy of diuretics

A 
daily weight 
input/output
jugular venous distention 
peripheral edema
HR/BP
organ congestion
45
Q

which hf are beta blockers along with acei indicated for

A

HFrEF

46
Q

metoprolol SR dosing

A

12.5mg daily target 200

47
Q

bisoprolol dosing

A

1.25 daily

target 10mg

48
Q

carvediol dosing

A

3.125mg bid

target 25 bid

49
Q

when and how do you initiate beta blockers

A

when stable not in acute decompensated HF
start with very low dose, increase every 2 weeks to attain target dose or highest tolerated
avoid abrupt withdrawal

50
Q

AE of beta blockers

A 
postural hypotension 
headache 
dizzines
bradycardia
bronchospasm 
fatigue 
decreased exercise tolerance 
insomnia 
sexual dysfunction
PAD, cold extremities
caution in diabetic
51
Q

monitoring fo rbeta blockers

A

BP
HR
worsening symptoms

52
Q

hemodynamic effects of acei

A

increase co
decrease preload
decrease systemic vascular resistance
decrease BP

53
Q

hormonal effects of acei

A

inhibit raas
decrease angiotensin II
decreases aldosterone
slow ventricularremodelling

54
Q

ramipril dosing

A

1.25-2.5 bid

target 5 bid

55
Q

perindopril dosing

A

2mg daily

target 4

56
Q

lisinopril dosing

A

2.5-5 daily

target 20-40

57
Q

adverse effects of acei

A 
hypotension 
renal impairment 
hyperkalemia 
cough 
rash 
taste alteration 
angioedema
58
Q

why do you caution low salt subs

A

have high K content

59
Q

monitoring of acei

A

check renal function and electrolytes at baseline
monitor blood chemistry 1-2 weeks after initiation and final dose titration then every 3-4 months after
new cough
efficacy

60
Q

what does aldosterone do

A

sodium/water retention
sympathetic activation
myocardial and vascualr fibrosis

61
Q

what are mras indicated in

A

HFrEF nyha class 2-4 in addition to acei and bb

62
Q

spironolactone dosing

A

start 25mg daily

target 50

63
Q

dosing of eplerenone and advantage

A

25mg
target 50
has less hormonal side effects

64
Q

who should you caution the use of mras in

A

hyperkalemia
renal failure
digoxin (hyperkalemia precipitates digoxin toxicity)
male may develop gynecomastia

65
Q

when do you use arb should you use it in combo with acei

A

alternative if acei cough

no more adr

66
Q

valsartan dosing

A

40 bid

target 160 bid

67
Q

candesartan

A

4 daily

target 32

68
Q

when is hydralazine/nitrate combo recommended

A

in african americas
add on wiht acei
other patients unable to tolerate acei and BB

69
Q

what is the rationale for using hydralazine(vasodilator) and nitrate combo in heart failure

A

vasodilation decreased cardiac work, afterload reduction

nitrates reduce preload

70
Q

target dose for hydralazine/nitrate combo

A

hyd 75mg / isdn 40 mg tid-qid

71
Q

how does an angiotensin receptor neprilysin inhibitor (sacubitril) work

A

inhibit neprilysin which is an enzyme that breaks down anp and bnp to increase the circulation of ANP and BNP
anp and bnp enhance diureses, natriureses, mayocardial relaxation, antiremodeling, and inhibit RAAS

72
Q

is there any evidence of a sacubitril/valsartan combo, when should it be used

A

reduction in mortality, higher symptomatic hypotension

replacement for acei in people with HFrEF who are still symptomatic on acei, BB, and mra

73
Q

sacubitril/valsartant (entresto) dosing

A

starting 49-51 bid
target 97/103 bid
(higher bioavalabilty of valsartan in the form)

74
Q

entresto should not be given with acei or within how many hours of the last dose of an acei

A

36

75
Q

ivabradine moa

A

inhibit f channels within sa node resulting in disruption of If ion current flow prolonging diastolic depol and reducing heart rate
no effects on BP, myocardial contractility or AV conduction

76
Q

in what patients did ivabradine decrease heart rate but not affect mortality

A

HFEF with LVEF <35 in normal sinus rthym, nyha class 2-4, hospirtalized in the past 12 months

77
Q

ivabradine dosing

A

5mg big up to 7.5 bid

78
Q

digitalis glycosides- digoxin moa

A

increase force and velocity of contraction through inhibition of NAKATPase
decrease av conduction

79
Q

when is digoxin used

A

heart failure with fast atrial rate, severe, S3 gallop, low EF, enlarged heart size
improves the quality of life not mortality
persistent symptoms despite maximized meds

80
Q

distribution of digoxin adn when you should collect samples

A

50% in skeletal muscle, dependent of body weight
long distribution time
have to collect samples >6 hours post dose

81
Q

digoxin elimination and half life

A

renal so normal half life 1.5 days and with kidney failure increase to >5 days

82
Q

target digoxin concentration

A

<1mcg/L to gain neurohormonal modulating effects without enhancing adverse outcome

83
Q

digoxin dosing

A

.125mg/day

CRCL<20 or weight <40kg give .0625mg/day

84
Q

signs of digoxin toxicity

A 
NV 
confusion 
altered color vision 
weakness
dizziness
av conduction disturbances - arrthymia
85
Q

factors affecting digoxin activity/toxicity

A

electrolyte disturbances - potassium
renal function -decreased elimination
elderly
hypothyroidism

86
Q

digoxin drug interaction

A

increase bioavail-tetracycline, erythromycin
decrease bioavil - antacids, cholestyramine, metoclopramide
decrease elimination - quinidine, verapamil, spironolactone, amiodarone
drugs that increase K Mg - diuretics

87
Q

treatment of digoxin toxicity

A 
withdrawal of digoxin 
correction of electrolyte abnormalities
antiarrhythmic agents 
pacemake 
digoxin specific antibodies 
oral activated charcoal
88
Q

properties and evidence of hawthorn extract

A

inotropic, vasodilating, lipid lowering, antioxidant, antiinflammatory
modest increase in exercise tolerance but not really good trials

89
Q

Lcarnitine role in myocardial energy production

A

chronic replacement to increase exercise tolerance and decrease cardiac dimensions
improved 3 yr survival in dilated cardiomyopathy

90
Q

fish oild for heart failure

A

small but sig mortality benefit

91
Q

coenzyme Q10 properties and evidence

A

component of the electron transport chain
decreased levels in heart failure
mixed results

92
Q

why avoid antiarrhythmic agents in HF

A

proarrhythmia
negative inotropic effects
increased mortality

93
Q

why avoid nonDHP calcium antagonists in HF

A

direct negative inotropic agents

CI in systolic heart failure

94
Q

why avoid tricyclic antidepressants in HF

A

proarrhythmic potential

95
Q

why avoid nsaids in HF

A

inhibit effects of diuretics and acei
cause salt and water retention
can worsen cardiac and renal function

96
Q

why avoid corticosteroids in HF

A

AE on salt and water retention

97
Q

why avoid doxorubicin and tratuzamab in HF

A

dose dependent cardio toxicity

can cause HF

98
Q

exercise recommendation in HF

A 
aerobic 3-5x per week 
30-45 min for class 1-3
99
Q

salt and fluid restriction in HF

A

no added salt diet
<2g per day
limit fluid intake to 1.5L-2L per day
include jello, soup….

100
Q

non pharms for HF

A 
exercise
limit salt and fluids 
monitor daily morning weight
no more than 1 alcoholic drink a day 
smoking cessation 
influenza and pneumococcal vaccine
101
Q

when is left ventricular assist device used

A

end stage HF or as bridging to heart transplant

Clinical 2.0 (24 decks)

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