Chronic Heart Failure Flashcards
what is heart failure
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
what causes decreased contractility
rheumatic heart disease
cardiomyopathy
coronary heart disease/mi
what causes increased afterload
hypertension
aortic stenosis
what causes increase preload
increased sodium/water retention
malfunction of aortic valve
drugs - nsaids
causes of heart failure
decreased contractility increased afterload increased preload direct cardiotoxic drugs high output failure
what is cardiac output
SV x HR
volume of blood pumped by the heart per minute
what is ejection fraction
fraction of blood ejected from LV
define preload
degree of filling from the left atrium (venous return)
define afterload
arteriolar resistance the heart must pump against to eject stroke volume
describe contractility
intrinsic ability of cardiac myocytes to contract
what are the 3 general patterns of remodeling
concentric ventricular remodeling (thickening)
eccentric left ventricular hypertrophy (sacromeres being stretched)
mixed
how does the body maintain CO and BP
increase preload
vasoconstriction
tachycardia and increased contractility
neurohormonal activation- renin, NE
how does the body increase preload
increase venous return
sodium water retention
activation of renin angiotensin
how does vasoconstriction help in heart failure
increases afterload
increases systemic vascular resistance
describe heart failure with reduced ejection fraction
low output hypofunctioning left ventricle, decreased contractility ejection fraction <40% ventricles enlarge systolic heatr failure
describe hert failure with preserved ejection fraction
diastolic heart failure
normal contractility and heart size
impaired LV filling during diastole
thickened LV or stiff ventricle
what can be the result of a LV stiffness and inability to relax during diastole
increased resting pressure within the ventricle
increased pressure impedes ventricular filling therefore reducing stroke volume
what is hpertrophic cardiomyopathy
thickened LV
what is restrictive cardiomyopathy
stiff ventricle
bad effects of the following compensatory mechanisms
vasoconstriction:
increased HR:
increased preload:
vaso - decreased cardiac output
hr - increased oxygen utilization
preload - peripheral and pulmonary edema
signs of left sided heart failure (pulmonary congestion)
dyspnea (difficult breathing) on exertion
orthopnea (SOB when lying down)
paroxysmal nocturnal dyspnea (SOB that awakens the patient)
pulmonary edema
signs of right sided heart failure (systemic venous congestion)
organomegaly
jugular venous distention
hepatojugular reflex
lower extremity peripheral edema
other signs of heart failure
weakness exercise tolerance fatigue cns cold, pale, clammy skin
nyha class 1
cardiac function uncompromised
able to perform ordinary physical activity
nyha class 2
slightly compromised cardiac function
ordinary physical activity results in symptoms
nyha class 3
moderately compromised cardiac function
less than ordinary physical activity results in symptoms
nyha class 4
severely compromised cardaic function
symptoms may be present at rest
acc/aha class a
at righ for hf but without structural heart disease of symptoms of hf
ex. diabetes
acc/aha stage b
structural heart disease without signs or symptoms of HF
acc/aha stage c
structural heart disease with prior or current symptoms of HF
acc/aha stage d
refractory HF requiring specialized intervention
signs on clinical exams of HF
auscultation of heart and lung - rales, S3 gallop edema jugular vein distention hepatojugular reflux dyspnea
goals of therapy
minimize disabling symptoms decrease hospitalization improve quality of life minimize disease complications slow progression of disease improve survival
what are some medical management strategies
elminate exacerbating factors control associated diseases restrict activity when acute sodium resticted diet exercise condition when stabilized drug therapy
what are the four types of drugs used in hf
diuretics - excrete excess water
inotropic agents - increase myocardial contractility
vasodilators - decrease cardiac work
acei - neurohormonal modulators
how do diuretics help in hf, any evidence
relieve breathlessness and edema in patients with congestion
no evidence for reduced mortality
use of diuretics in hf
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
furosemide dosing
20-40 daily then increase to acheive edema free state, once symptoms relieved use lowest possible maintenance dose
when would you initiate metolazone
in combo with loop diuretic if not enough, given 30 min before furosemide
metoalzone dosing
start 2.5 mg, usual dose 2.5-10mg/d
AE of diuretics
volume depletion - dehydration, reduced bp and co
loss of K and Mg
renal impairment
do thiazides work in renal impairment
no
monitoring of diuretics
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
how to monitor the efficacy of diuretics
daily weight input/output jugular venous distention peripheral edema HR/BP organ congestion
which hf are beta blockers along with acei indicated for
HFrEF
metoprolol SR dosing
12.5mg daily target 200
bisoprolol dosing
1.25 daily
target 10mg
carvediol dosing
3.125mg bid
target 25 bid
when and how do you initiate beta blockers
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
AE of beta blockers
postural hypotension headache dizzines bradycardia bronchospasm fatigue decreased exercise tolerance insomnia sexual dysfunction PAD, cold extremities caution in diabetic
monitoring fo rbeta blockers
BP
HR
worsening symptoms
hemodynamic effects of acei
increase co
decrease preload
decrease systemic vascular resistance
decrease BP
hormonal effects of acei
inhibit raas
decrease angiotensin II
decreases aldosterone
slow ventricularremodelling
ramipril dosing
1.25-2.5 bid
target 5 bid
perindopril dosing
2mg daily
target 4
lisinopril dosing
2.5-5 daily
target 20-40
adverse effects of acei
hypotension renal impairment hyperkalemia cough rash taste alteration angioedema
why do you caution low salt subs
have high K content
monitoring of acei
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
what does aldosterone do
sodium/water retention
sympathetic activation
myocardial and vascualr fibrosis
what are mras indicated in
HFrEF nyha class 2-4 in addition to acei and bb
spironolactone dosing
start 25mg daily
target 50
dosing of eplerenone and advantage
25mg
target 50
has less hormonal side effects
who should you caution the use of mras in
hyperkalemia
renal failure
digoxin (hyperkalemia precipitates digoxin toxicity)
male may develop gynecomastia
when do you use arb should you use it in combo with acei
alternative if acei cough
no more adr
valsartan dosing
40 bid
target 160 bid
candesartan
4 daily
target 32
when is hydralazine/nitrate combo recommended
in african americas
add on wiht acei
other patients unable to tolerate acei and BB
what is the rationale for using hydralazine(vasodilator) and nitrate combo in heart failure
vasodilation decreased cardiac work, afterload reduction
nitrates reduce preload
target dose for hydralazine/nitrate combo
hyd 75mg / isdn 40 mg tid-qid
how does an angiotensin receptor neprilysin inhibitor (sacubitril) work
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
is there any evidence of a sacubitril/valsartan combo, when should it be used
reduction in mortality, higher symptomatic hypotension
replacement for acei in people with HFrEF who are still symptomatic on acei, BB, and mra
sacubitril/valsartant (entresto) dosing
starting 49-51 bid
target 97/103 bid
(higher bioavalabilty of valsartan in the form)
entresto should not be given with acei or within how many hours of the last dose of an acei
36
ivabradine moa
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
in what patients did ivabradine decrease heart rate but not affect mortality
HFEF with LVEF <35 in normal sinus rthym, nyha class 2-4, hospirtalized in the past 12 months
ivabradine dosing
5mg big up to 7.5 bid
digitalis glycosides- digoxin moa
increase force and velocity of contraction through inhibition of NAKATPase
decrease av conduction
when is digoxin used
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
distribution of digoxin adn when you should collect samples
50% in skeletal muscle, dependent of body weight
long distribution time
have to collect samples >6 hours post dose
digoxin elimination and half life
renal so normal half life 1.5 days and with kidney failure increase to >5 days
target digoxin concentration
<1mcg/L to gain neurohormonal modulating effects without enhancing adverse outcome
digoxin dosing
.125mg/day
CRCL<20 or weight <40kg give .0625mg/day
signs of digoxin toxicity
NV confusion altered color vision weakness dizziness av conduction disturbances - arrthymia
factors affecting digoxin activity/toxicity
electrolyte disturbances - potassium
renal function -decreased elimination
elderly
hypothyroidism
digoxin drug interaction
increase bioavail-tetracycline, erythromycin
decrease bioavil - antacids, cholestyramine, metoclopramide
decrease elimination - quinidine, verapamil, spironolactone, amiodarone
drugs that increase K Mg - diuretics
treatment of digoxin toxicity
withdrawal of digoxin correction of electrolyte abnormalities antiarrhythmic agents pacemake digoxin specific antibodies oral activated charcoal
properties and evidence of hawthorn extract
inotropic, vasodilating, lipid lowering, antioxidant, antiinflammatory
modest increase in exercise tolerance but not really good trials
Lcarnitine role in myocardial energy production
chronic replacement to increase exercise tolerance and decrease cardiac dimensions
improved 3 yr survival in dilated cardiomyopathy
fish oild for heart failure
small but sig mortality benefit
coenzyme Q10 properties and evidence
component of the electron transport chain
decreased levels in heart failure
mixed results
why avoid antiarrhythmic agents in HF
proarrhythmia
negative inotropic effects
increased mortality
why avoid nonDHP calcium antagonists in HF
direct negative inotropic agents
CI in systolic heart failure
why avoid tricyclic antidepressants in HF
proarrhythmic potential
why avoid nsaids in HF
inhibit effects of diuretics and acei
cause salt and water retention
can worsen cardiac and renal function
why avoid corticosteroids in HF
AE on salt and water retention
why avoid doxorubicin and tratuzamab in HF
dose dependent cardio toxicity
can cause HF
exercise recommendation in HF
aerobic 3-5x per week 30-45 min for class 1-3
salt and fluid restriction in HF
no added salt diet
<2g per day
limit fluid intake to 1.5L-2L per day
include jello, soup….
non pharms for HF
exercise limit salt and fluids monitor daily morning weight no more than 1 alcoholic drink a day smoking cessation influenza and pneumococcal vaccine
when is left ventricular assist device used
end stage HF or as bridging to heart transplant
