HF Flashcards
ventricular filing –
diastolic dysfunction
myocardial contractility
systolic dysfunction
current understanding of HF Is described by:
neurohormonal model
neurohormone activation:
norepinephrine
angiotensin II
aldosteorne
proinflammatory cytokines
HF targeted pharmacotherapy taht antagonized ___
neurohormonal activation
diastolic dysfunction =
HF w/ preserved EF (HFpEF)
systolic dysfunction:
HF w/ reduced EF (HFrEF)
most trials include patients w/ ___
HFrEF
NYHA classification I
patients with cardiac disease but without limitations of physical activity
NYHA II
patients with cardiac disease that results in slight limitations of physical activity
NYHA III
patients with cardiac disease that result in marked limitation of physical activity
NYHA IV
short timepatients with cardiac disease that result in inability to carry on physical activity w/o discomfort
NYHA states that symptoms may change over ___
short time
ACC/AHA stage A
patients at risk for developing HF
ACC/AHA B
patients w/ structural heart disease but no HF signs of sx
ACC/AHA C
patients with structural heart disease and current or previous symptoms
ACC/AHA D
refractory HF requiring specialized interventions
in ACC/AHA stage will not change. – consistent with
progressive nature of HF
majority of trials have been geared toward
systolic dysfunction patients
new medications for systolic dysfunction
ivabradine (coplanar)
sacubitril/valsartan (Entresto)
Diuretics are indicated in all patients with ___
evidence of h/o fluid retention
monitor effect of diuretics by ___
daily morning weight measurements
thiazide diuretics are __ diuretics
weak
metolazone may be a dded to loops for ___
diuretic resistance
2.5-19mg once daily PLUS loop diuretic
most potent diuretic
loop
ceiling effect of loop diuretics
give ceiling dose more frequently rather than increasing dose
torsemide is preferred in patients with ___
persistent fluid retention despite high doses of other loops
___mg lasix = ___ mg torsemide = ___ mg bumetanide
40; 20; 1
dose of chlorthalidone and metolazone
daily
cornerstone of HF therapy
ACEI
first line therapy in patients with systolic HF
ACEI
ACEI in HF reduces mortality by ___
20-30% vs placebo
for HF, use ACEI w/ ___
beta blocker unless contraindicated
add beta blocker after ___
titrating maximal ACEI dose
even if ACEI dose is < recommended max
with ACEI, monitor ___
serum K and renal function
abrupt withdrawal of ACEI may precipitate ___
decompensation
ACEI adverse effects
hypotension
functional renal insufficiency
cough (dry, hacking)
angioedema
to combat ACEI induced hypotension:
spread other vasoactive meds throughout the day (not all at once)
to combat ACEI induced hypotension, start on
catopril, titrate to max, then switch to ACEI w/ once daily dosing
if cough using ACEI, consider ___
substituting ARB
if angioedema with ACEI,
lifetime avoidance of ACEI
use beta blockers in all ___
stable HF pts unless intolerant or contraindicated
BBs that have demonstrated decreased mortality in HF
bisoprolol
carvedilol
metoprolol succinate (not IR metoprolol tartare)
carvedilol blocks ____
b1, b2 and a1 receptors (nonselective)
carvedilol may be preferred in patients with ___
poorly controlled BP (due to a and b1 blockade)
avoid carvedilol in ___
asthmatics (because they use beta 2 agonists)
begin beta blockers at very low doses with ____
gradual titration to max doses
delay dose increase of BB until ___ have disappeared
AEs
continue long term treatment with BB , even ____
if symptoms do not improve
abrupt withdrawal of BB may cause ___
acute decompensation
taper if discontinued
BBs used for HF
bisoprolol
carvedilol
metoprolol
benefits of BB in pts with HF and reduced ejection fraction seem to be mainly due to ___
class effect
Major AE of BB used for HF
fluid retention
fatigue
bradycardia
hypotension
Minor AE of BB used for HF
bronchospasm (in asthma pts)
worsening glucose tolerance
sexual dysfunction in males
BB worsen glucose tolerance in diabetics and may mask sx of
tachycardia
tremor
BUT NOT SWEATING
ARBs inhibit ___ at its receptor
angiotensin II
ARBs do not inhibit _____
bradykinin metabolism (so no increase in bradykinin)
ARBs produce less ___ and __
cough and angioedema
combined use of ace and arb is potentially ___
harmful – no longer recommended
when using ARBs, ___ may still occur but less than with ACEs
angioedema
angioedema using ARBs happens more frequently in ___
blacks
as with ACEI’s, start ___ before reaching max ARB dose
BB
starting requirement for an aldosterone receptor antagonist (ARA)
SCr of <2.5 mg/dl (M)
SCr <2 mg/dl (F)
CrCl >30
Serum K <5
Aldosterone Receptor Antagonists (ARA)
spironolactone (aldactone)
Eplerenone (Inspra)
discotinue ___ after starting an ARA
potassium supplements
counsel patients to stop ARAs during episodes of:
diarrhea
dehydration
interruptions of diuretic therapy
AE of Spironolactone
gynecomastia
hyperkalemia
up t o 35% of patients in the general population are
hyperkalemic
AE of epleronone
hyperkalemia
gynecomastia
serious hyperkalemia using epleronone
serum k >6 (discontinue ARA)
mild hyperkalemia using
serum K >5.5 (discontinue ARA or decrease dose)
only orally active positive cardiac inotrope
digoxin
digoxin does not ____
decrease mortality in HF
digoxin may improve:
LVEF
quality of life
exercise tolerance and
HF sx
loading dose of ___ for A-fib is not recomended
digoxin
target plasma levels when using digoxin
0.5-1.0 ng/mL
higher levels off plasma increase mortality
toxicity with digoxin occur earlier with :
hypokalemia, hypomagnesemeia, hypothyroidism
obtain first dose of digoxin ____
3-5 days after starting therapy
check plasma levels _____ after dosage of digoxin changes
5-7 days
draw plasma levels ___ after previous dose of digoxin
6-8 hours
adverse effects of digoxin for HF
cardiac arrythmias
GI sx
neurological coplaints
neurological complaints using digoxin
visual disturbance
altered color perception (blue/green & yellow halos)
hydralazine is a potent ____
arterial vasodilator
hydralazine is an ___
afterload reducer
isosorbide dinitrate is a potent ___
venous vasodilator
isosorbide dinitrite is an ___
preload reducer
H/ISDN is demonstrated to be especially useful in ___
AA with HF
start H/IDSN on all ___
AA on optimum therapy w/ ACEI & BB unless contraindicated
start H/ISDN on non AA’s intolerant to/ or contraindicated for ___
ACEI/ARB
unique MOA for Ivabradine
deceases HR by inhibiting If pacemaker current in SA Node
Ivabradine reduces risk fo ___
hospitalization for worsening HF
class for Sacubitril/Valsartan
new class – angiotensin receptor-Neprilysin inhibitor (ARNI
entrust lowered CV mortality by ___
20%
AMI medications
Oxygen Nitrates Analgesia BB CCB Other anti-ischemic cholesterol lowering agents RAAS inhibitors anti-platelet agents parenteral anticoagulation
administer supplemental o2 to AMI patients with
o2 sat <90%
respiratory distress
other high-risk features of hypoxemia
oxygen may have negative effects in ___
coronary patients
oxygen can cause ___ in coronary patients
increased coronary vascular resistance
reduced coronary blood flow
increased risk of mortality
significantly LARGER infarct sizes than non-oxygen group
administer supplemental o2 to AMI pts with ___
o2 sat <90%
respiratory distress
other high-risk features of hypoxemia
oxygen may have negative effects in ___
coronary patients
o2 can cause increased ___
coronary vascular resistance
o2 can cause reduced ___`
coronary blood flow
o2 has increased risk of mortality in ___
coronary patietns
o2 can cause significantly larger ___
infarct sizes
MOA of nitrates
dilate capacitance vessels (decrease preload)
for continued chest pain, administer
SL nitroglycerin
0.3-0.4 mgQ5 min x 3
then assess for IV NTG
do not give nitrates if pt is on ___
phosphodiesterase inhibitors (ED med)
do not give nitrates if pt was on ____ over the last 24 hours
sildenafil, vardeniafil
do not give nitrates if pt was on ___ over last 48 hrs
tadalafil
reason you cannot give nitrates to patients on phosphodiesterase inhibitors
potential marked decrease in BP
____ may be given IVP for continued chest pain if already on max tolerated NTG
morphine sulfate
analgelsia for HF
morphine sulfate traditional NSAIDs (NOT aspirin) & COX-2 inhibitors
NSAIDs actually enhance platelet aggregation by ___
inhibiting PG synthesis
NSAIDs should be ___ in AMI patients
avoided
__ is ok for anti-platelet effects in AMI pts
aspirin (low-dose)
begin ___ within 24h in all AMI pts
BBs PO
AMI pts with stable HF should be continued on:
metoprolol succinate, carvedilol, bisprolol
why avoid IV BBs?
may increase risk of shock
give CCB to ischemic patients:
with contraindications to BB
unacceptable side-effects of BBs
with continued pain after appropriate use of BBs and nitrates
use non-dihydropyridin CCBs as initial therapy
ORAL verapamil
ORAL diltiazem
Immediate release nifedipine should nOT be used due to ___
causes dose-related increase in mortality in CAD and harm in ACS pts
abtianginal with minimal effects on HR and BP
ranolazine
A/E of Ranolazine
constipation
dose-related QT prolongation (not sufficient for dose reduction in RCTs)
high intensity statin therapy
atorvastatin titrate 10-80mg PO once daily
rosuvastatin titrate 5-40mg PO once daily
start ACE-I in all pts w/ LVEF < __
40% – continue indefinitely
start ACEI in hospital with __ or ___ and switch to long acting ACE-I at max
catopril (TID)or enalapril (BID)
use ___ in those intolerant or those with c/I to ACEI
ARB
use ___ to those on therapeutic doses of ACE-I and BB
ARAs
acute need for anti-platelet agents:
give non-enteric-coated chewable aspirin (162-324mg)
do not order enteric-coated ASA acutely because…
delays absorption
in patients who acutely need anti-platelt therapy and are intolerant to aspirin, give:
clopidogrel
for chronic anti platelet:
give aspirin 81-325mg PO daily indefinitely PLUS
up to 12 mo, either p2y12 aspirin receptor inhibitor
p2y12 aspirin receptor inhibitors
clopidogrel (daily)
ticagrelor (BID)
___ is not recommended for chronic anti-platelet therapy
prasugrel
prasugrel increases risk of :
spontaneous bleeding, life -threatening bleeding and fatal bleeding
parenteral anticoag
in addition to anti platelet therapy, anticoagulation is recommended for all pts
enoxaprin is preferred ___
LMWH for ACS
avoid LMWH in ___
dialysis pts w/ ACS
bivalrudin is usually used in ___
Cath labs
potential advantages of bivalrudin
will bind to clot - bound thrombin
no significant protein binding (more predictable anticoagulant response)
synthetic pentasaccharide (selective xa inhibitor)
fondaparinux
fondaparinux shows little risk for __
HITT
fondaparinux is c/I for ___
CrCl <30 mL/min (increased risk of bleeding)
use w/ caution for CrCl 30-50 mL/min
UFH has a relatively short half life:
~1.5h
can d/c IV heparin for ___
urgent interventions
____ recommended over fixed dose of heparin
weight-based regimen
max initial bolus of IV heparin
4,000 units
max initial maintenance infusion of heparin
1,000 units/h
parenteral anticoagulation used in pts w h/o HITT undergoing PCI
argatroban
