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SPP2 CHF and AFib > exam > Flashcards

exam Flashcards

1
Q

force tension curve

A

after load and SV relationship

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2
Q

NYHA I

A

cardiac disease with no symptoms

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3
Q

NYHA II

A

slight limitations of physical activity

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4
Q

NYHA III

A

limitations of physical activity

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5
Q

NYHA IV

A

inability to carry on any physical activity without discomfort

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6
Q

CHF stage A

A

High risk of developing HF, no abnormalities, HTN, CAD, DM, etc

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7
Q

CHF stage B

A

structural disease but no signs or symptoms of HF, NYHA I

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8
Q

CHF stage C

A

current or prior symptoms of HF, NYHA II or III

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9
Q

CHF stage D

A

advanced structural heart disease and marked symptoms of HF at rest, NYHA IV

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10
Q

summary of stage A treatment

A

ACEIs or ARBs

if atherosclerotic disease is present

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11
Q

summary of stage B treatment

A

ACEIs
BB
if previous MI or asymptomatic rEF

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12
Q

stage C treatment summary

A

routine use: diuretics, ACEIs, BBs
selected patients: ARBs, aldosterone antagonists, valsartan/sacubitril, ISDN/hydralazine, digoxin, amlodipine/felodipine, ICD/cardiac resynchronization

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13
Q

___ may be used in patients with mild HF and small amounts of fluid retention

A

thiazides

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14
Q

thiazide use in decreased renal function

A

lose effectiveness, higher doses are generally necessary

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15
Q

starling curve

A

preload and SV relationship

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16
Q

loop diuretic equivalent doses

A

furosemide 40 = bumetanide 1 = torsemide 10-20 = ethacrynic acid 50

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17
Q

furosemide dosing in HF

A

start: 20-40 mg QD or BID
Max with CrCl greater than 50: 80-160
max with CrCl 20-50: 160
max with CrCl less than 20: 400

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18
Q

bumetanide dosing in HF

A

start: 0.5-1 mg QD or BID
Max with CrCl greater than 50: 1-2
max with CrCl 20-50: 2
max with CrCl less than 20: 8-10

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19
Q

torsemide dosing in HF

A

start: 10-20 mg QD or BID
Max with CrCl greater than 50: 20-40
max with CrCl 20-50: 40
max with CrCl less than 20: 100-200

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20
Q

ethacrynic acid dosing in HF

A

start: 25-50 mg QD or BID

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21
Q

enalapril dosing in HF

A

start: 2.5-5 mg BID
target: 10 mg BID

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22
Q

captopril dosing in HF

A

start: 6.25-12.5 mg TID
target: 50 mg TID

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23
Q

lisinopril dosing in HF

A

start: 2.5-5 mg QD
target: 20-40 mg QD

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24
Q

ramipril dosing in HF

A

start: 1.25-2.5 mg QD
target: 5 mg BID - 10 mg QD

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25
Q

ACEI dosing in CKD

A

if CrCl is less than 30, the target dose is 1/2 normal

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26
Q

ACEI CI

A

pregnancy
hx of angioedema or hypersensitivity
bilateral renal artery stenosis
history of well-documented intolerance due to symptomatic hypotension, decline in renal fxn, hyperkalemia or cough

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27
Q

ACEI AE

A 
hypotension
functional renal insufficiency
hyperkalemia (monitor)
cough
rash and dysgeusia
angioedema
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28
Q

use ACEI with caution if:

A

volume depleted
SBP less than 80 mmHg
serum K over 5
SCr over 3

K-sparing diuretics and K supplements should be used with extreme caution and monitored very closely

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29
Q

losartan dosing in HF

A

start: 25-50 mg QD
target: 50-150 mg QD

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30
Q

valsartan dosing in HF

A

start: 20-40 mg QD
target: 160 mg BID

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31
Q

candesartan dosing in HF

A

start: 4-8 mg QD
target: 32 mg QD

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32
Q

patient selection to start a BB

A

stable and euvolemic (no pitting or angioedema)
on heart failure drug regimens (ACEI, diuretic)
caution with bronchospasm and bradycardia
do not abruptly DC
don’t need to reach target ACEI before initiating BB, if we can only maximize one chose the BB

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33
Q

carvedilol dosing in HF

A

start: 3.125 mg BID for 2 weeks
target: under 85 kg, 25 mg BID
over 85 kg, 50 mg BID

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34
Q

coreg CR dosing in HF

A

start: 10 mg QD for 2 weeks
target: 80 mg QD

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35
Q

metoprolol XL dosing in HF

A

start: 12.5-25 mg QD
target: 200 mg QD

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36
Q

BB titration in HF

A

double the dose every 2 weeks and monitor closely vital signs and symptoms
planned dose increases can be slowed if necessary to manage
aim for target dose in 8-12 weeks or highest tolerated dose

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37
Q

BB monitoring

A

BP and HR (1-2 weeks)
reduce dose 50% if experiencing systomatic hypotension, bradycardia and dizziness
if hypotension only.. reduce other drugs first
edema and fluid retention (1-2 weeks)
fatigue or weakness

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38
Q

eplerenone dosing in HF

A

only if K is less than 5
if CrCl over 50: start 25 mg QD and target 50 mg QD
if CrCl 30-49: start 25 mg QOD and target 25 mg QD

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39
Q

spironolactone dosing in HF

A

only used if K is less than 5
if CrCl is over 50: start 12.5-25 mg QD and target 25 mg QD
if CrCl is 30-49: start 12.5 mg QD or QOD and target 12.5-25 mg QD

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40
Q

ISDN/hydralazine use in HF

A

venous vasodilator/arterial vasodilator

treatment of HF in black patients as an adjunct to standard therapy

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41
Q

digoxin use in HF

A

inhibits Na+/K+ ATPase altering excitation contraction coupling. this ultimately increases intra ellipse Ca2+ which enhances the force of contraction
efficacy in HF with Afib is well established

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42
Q

digoxin dosing in HF

A

0.125-0.25 mg QD with 0.5-0.9 Ng/ml as the goal SDC
lower doses used in patients over 70, impaired renal function, low weight
main AE at normal dose is sinus bradycardia

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43
Q

digoxin drug interactions

A

many

amiodarone, itra/ketoconazole, verapamil require decrease in dig dose (1/2)

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44
Q

sacubitril/valsartan dosing

A

49/51 mg BID, doubled in 2-4 weeks to 97/103 BID

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45
Q

sacubitril/valsartan AE

A

hypotension (more than enalapril)
elevated SCr and K (less than enalapril)
angioedema rare

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46
Q

Ivabradine dosing

A

5 mg BID, adjust q 2 weeks based on HR
heart rate over 60: increase 2.5 (BID) to a max of 7.5
HR 50-60: maintain dose
HR less than 50 or s/sx bradycardia: decrease dose by 2.5 (BID)

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47
Q

Ivabradine AEs

A

fetal toxicity
AFib
Bradycardia and conduction disturbances

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48
Q

nonpharm therapies for HFrEF

A

ICD (implantable cardio defibrillator)

cardiac resynchronization therapy

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49
Q

antiplatelet therapy in HF

A

aspirin recommended in patients with HF and CAD

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50
Q

anitcoag therapy in HF

A

NOT RECOMMENDED

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51
Q

CCB in HF

A

diltiazem, verapamil and nifedipine should not be routinely used
felodipine and amlodipine may be useful in managing angina and/or HTN if not effectively managed with HF therapies

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52
Q

guide-line based drug therapy of HFpEF

A

SBP/DBP control (I)
reduce volume overload with diuretics (I)
manage AFib (IIa)
use of BB, ACEI, ARBs are reasonable in patients with HTN (IIa)
use of ARBs may decrease hospitalizations (IIb)

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53
Q

decompensated HF precipitation

A

CV causes: ischemia, arrhythmiz, valvular disease, uncontrolled HTN, pulmonary embolism, progressive HF
metabolic causes: infection, anemia, thyroid disorders, renal insufficiency
toxins and drugs: negative ionotropes, cardiotoxins, Na an water retention
drug nonadherance and diet

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54
Q

hospitalization recommended in HF

A

evidence of severly DHF
dyspnea at rest
hemodynamically significant arrhythmia
ACS

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55
Q

hospitalization considered

A 
worsened congestion
s/s of pulmonary or systemic congestion
major electrolyte disturbance
comorbid conditions
repeated ICD firings
undiagnosed HF with s/s of systemic or pulmonary congestion
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56
Q

clinical manifestations and classification of ADHF

A

warm and dry: normal I
warm and wet: pulmonary congestion II
cool and dry: hypoperfusion III
cool and wet: pulmonary congestion and hypoperfusion IV

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57
Q

chronic therapy while hospitalized

A

should be continued and maximized in the absence of hemodynamic instability or CIs

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58
Q

initiation of BB while hospitalized

A

after optimization of volume status and successful DC of IV diuretics, VDs and inotropes

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59
Q

diuretics while hospitalized

A

significant fluid overload: IV diuretics

dosing: initial IV dose should equal or exceed the chronic daily dose and give as intermittent bolus or C infusion

60
Q

parenteral therapy in AHF

A

vasodilators and positive inotropes

61
Q

vasodilators used in AHF

A

nitroprusside, nitroglycerin, nesiritide, morphine, enalaprilat, hydralazine

62
Q

positive inotropes used in AHF

A

helps when patients are cold and wet or cold and dry while adequately hydrated
dobutamine, milrinone, dopamine(used when hypotension)

63
Q

Tx for warm and wet

A

no immediate interventions necessary except optimizing oral tx

64
Q

Tx warm and wet

A

reduce congestion

loop diuretics

65
Q

tx cool and dry

A

increase output and perfusion with positive inotropes +/- IV fluids

initial: fluids until BP maximized
following: if still “Cool”, inotrope may be required

66
Q

Tx cool and wet

A

reduce preload and congestion and increase perfusion to restore delivery of adequate oxygen to the tissues
many require BP support
combination therapy of diuretics and/or vasodilators and inotropes
vasopressors may be requires to maintain BP support

67
Q

pacemaker action potentials

A

“upstroke” mediated by Ca2+ cells
repolarization mediated by K+
depolarization or “pacemaker current” mediated by HCN and ACh-gated K+ channels

68
Q

myocyte action potentials

A

“upstroke” involves a rapid increase in conductance due to opening of sodium channels
“notch” brief repolarization
plateau phase: inward Ca2+ currents with some contribution from Na and K
repolarization: K curretns dominate and serve to return the membrane potential back to resting

69
Q

the refractory period between action potentials

A

as you move later toward the end of a refractory period, a stimulus of the same strength results in a stronger and stronger depolarization

70
Q

bAR signaling in pacemaker cells

A

bAR stimulation leads to cAMP formation which increases the activity of HCN channels. this results in increased depolarizing currents during phase 4 and helps return the cell to firing threshold sooner
bAR stimulation and cAMP formation also increases protein kinase A activity, which increases phosphorylation of Ca channels, this increases the amount of current these channels can pass and allows them to open at a more negative membrane potential

71
Q

bAR blockers used as antiarrhythmics

A

esmolol (IV), acebutolol, propranolol
used when there is increased sympathetic tone or when sensitivity to catecholamines has increased
often used in atrial arrythmias to protect ventricular rate
used post-MI to prevent ventricular arrhythmias

72
Q

CCBs used as antiarrhythmics

A

verapamil and diltiazem
exhibit frequency-dependent blockade thus the Ca channels that are opening and closing more are susceptible to block
chiefly used to protect ventricular rate in atrial flutter and fibrilation

73
Q

class I antiarrythmic drugs

A

1A: quinidine, procainamide, disopyramide
1B: lidocaine (IV only, rapid control of ventricuar arrhythmias), tocainide, mexilitine
1C: propafenone, flecainide

74
Q

class 3 antiarrhythmics MOA

A

block K channels and effect repolarization
prolong the action potential, making the cell dwell longer at voltages that favor sodium channel inactivation, this delays its ability to support a subsequent action potential

75
Q

torsade de pointes

A 
can develop due to administration of class 3 agents
occurs when cells dwell too long in the depolarized range and inward currents start to be greater than outward K currents and early afterdepolarization can develop
76
Q

class 3 antiarrhythmic drugs

A

amiodarone, dronedarone, ibutilide, sotalol, dofetilide

77
Q

questions to determine if an ECG is normal sinus rhythm

A

is there a P wave in front of every QRS complex?
is there a QRS complex after every p wave?
is the interval between the R waves equal (regular rhythm)?
is the heart rate between 60-100 bpm?

78
Q

numbers when reading HR on an ECG

A

300, 150, 100, 75, 60

79
Q

normal values for an ECG

A

PR: 0.12-0.20 seconds (begining of P until Q; AV nodal conduction time)
QRS: 0.08-0.12 seconds
QT: 0.38-0.46 seconds (Q until end of T)
QTc men: 0.36-0.47 seconds (worry at 0.5)
QTc women: 0.36-0.48 seconds (worry at 0.5)

80
Q

if PR interval is longer than ___…

A

0.2 seconds = 1st degree AV block

81
Q

QTc =

A

QTc = QT interval / (square root (time between R waves (sec))

82
Q

examples of supraventricular arrhythmias

A 
sinus bradycardia
AV block
sinus tachycardia
Afib
paroxysmal supraventricular tachycardia
83
Q

examples of ventricular arrhythmias

A

ventricular premature depolarizations
ventricular tachycardia
ventricular fibrillation

84
Q

sinus bradycardia features

A

HR less than 60 bpm due to decreased automaticity of SA node

impulses originate in SA node

85
Q

sinus bradycardia risk factors/etiologies

A

MI, abnormal sympathetic tone, electrolyte abnormalities
drugs: digoxin, BB, diltiazem/verapamil, amiodarone, dronedarone
idiopathic (sick sinus syndrome)

86
Q

sinus bradycardia symptoms

A

hypotension, dizziness, fainting (syncope)

87
Q

sinus bradycardia treatment

A

ONLY necessary if patient is symptomatic
atropine 0.5 mg IV q5m up to 3 doses
unresponsive? dopamine, epinephrine
some patients may require a pacemaker

88
Q

atropine AE

A

tachycardia , urinary retention, blurred vision, dry mouth, mydriasis

89
Q

Afib features

A

atrial: chaotic and disorganized depolarizations (quivering)
ventricular rate: 120-180 bpm
rhythm: irregularly irregular
p waves: absent

90
Q

paroxysmal Afib

A

episodes start suddenly and spontaneously and resolve suddenly

91
Q

persistent Afib

A

continuous episode of Afib that does not terminate spontaneously, may last over 7 days

92
Q

long-standing persistent Afib

A

continuous afib lasting over 12 months

93
Q

permanent Afib

A

patient is never in NSR and Afib cannot be terminated

94
Q

nonvalvular Afib

A

absence of rheumatic mitral valve stenosis, a mechanical or bioprosthetic heart valve or mitral valve repair

95
Q

Afib risk factors

A

HTN, CAD, HF, valvular heart disease

96
Q

etiologies of reversible Afib

A

hyperthyroidism, pulmonary embolism, thoracic surgery, alcohol binging

97
Q

Afib symptoms

A

palpations, dizziness, fatigus, lightheaded, SOB, hypotension, syncope, angina, exacerbation of HF sx

98
Q

Afib morbidity/mortality

A

inc risk of stroke, HF, dementia and mortality

99
Q

Afib treatment goals of therapy

A

ventricular rate control, convert Afib to NSR, maintain sinus rhythm, prevent strokes

100
Q

all types of Afib have 2 treatment goals

A

rate control and stroke prevention

101
Q

persistent AFib specific goal

A

conversion to NSR

102
Q

paroxysmal Afib specific goal

A

maintenance of sinus rhythm if ventricular rate control is not sufficient to control symptoms

103
Q

diltiazem in Afib

A

direct AV node inhibition

AE: hypotension, bradycardia, HF exacerbation, AV block

104
Q

verapamil in Afib

A

direct AV node inhibition

AE: hypotension, bradycardia, HF exacerbation, AV block, constipation

105
Q

B blockers in Afib

A

direct AV node inhibition
notably: esmolo, propranolol, metoprolol
AE: hypotension, bradycardia, HF exacerbation (IV), AV block

106
Q

digoxin use in Afib

A

vagal stimulation and direct AV node inhibition
AE: N/V, anorexia, ventricular arrhythmias
interactions: amiodarone (USE HALF DOSE OF DIG)

107
Q

amiodarone use in Afib

A

AE: hypotension, bradycardia, blue-grey skin, photosensitivity, conreal microdeposits, PULMONARY FIBROSIS, hepatotoxicity, hypo/hyperthyroidism

108
Q

hemodynamically unstable

A 
any of the following:
SBP less than 90
HR over 150
ischemic chest pain
unconscious
109
Q

persistent Afib acute rate control algorithm

A

MUST BE hemodynamically stable
no HF: IV CCB/BB
HF: IV amiodarone
assess HR; goal less than 110; if symptomatic of HFrEF, goal less than 80
goal met: change to oral
goal not met: increase dose or add a second derug

110
Q

paroxysmal or persistent Afib long-term ventricular rate control

A 
no HF (LVEF over 40): CCB/BB,  then CCB and dig OR BB and dig, then amiodarone (generally by itself)
HF (LVEF under 40): BB (inc to HF dose), then BB and dig, then amiodarone (BB may be kept for HF)
with each therapy/dose change: assess HR control; goal less than 80 with sx relief. if goal not met, move to next step in algorithm
111
Q

Afib conversion to NSR

A

if Afib has been present less than 48 hours, conversion is safe
if Afib has been present over 48 hours, conversion should not be performed until patient has been anticoagulated for 3 weeks or TEE has been performed to rule out a clot in the atrium

112
Q

conversion to NSR treatments

A

synchronized direct current cardioversion (DCC), amiodarone, dofetilide (risk of Tdp, must adjust for CrCl), ibutilide (risk of Tdp), propafenone, flecainide (HF exacerbations)

113
Q

synchronized DCC

A

chest paddles
automatic for hemodynamically unstable
simultaneously depolarizes all myocardial cells, allowing the SA node to take over as pacemaker

114
Q

persistent Afib conversion algorithm

A

less than 48 hours = DCC (requires sedation unless pt has eaten that day); otherwise use: no HF: dofetilide, flecainide, ibutlide, propafenone; HF: amiodarone, dofetilide, ibutilide
over 48 hours or unknown: delayed conversion after 3 weeks of warfarin therapy, early conversion by heparin IV and TEE to rule out atrial clot; no atrial clot = DCC, atirial clot = anticoag

115
Q

maintenance of NSR (paroxysmal only)

A 
amiodarone
dofetilide
dronedarone (advantages: no thyroid toxicity, shorter half life, less pulmonary toxicity, no interaction with warfarin; disadvantages: not as effective as amiodarone, increases mortality in HF; AE: bradycardia, diarrhea, nausea)
sotalol
propafenone
felcainide
116
Q

maintenance of NSR following conversion to NSR with paroxysmal algorithm

A

no heart disease (IHD, CAD, HF): dofetilide, dronedarone, flecainide, propafenone, sotalol then amiodarone then catheter ablation
catheter ablation is first line in paroxysmal
heart disease:
CAD: dofetilide, dronendarone, sotalol, (then amiodarone), then catheter ablation
HFrEF: amiodarone, dofetilide, the catheter ablation

117
Q

prevention of embolization/stroke in nonvalvular Afib

A

CHA2DS2VASc score
0=no antithrombic/anticoag
1= no treatment, oral anticoag or aspirin considered
over 2= oral anticoag is recommended with warfarin (INR goal 2-3), edoxaban, dabigatran, rivaroxaban, apixaban
warfarin is the agent of choice for valvular disease, hemodialysis, ESRD

118
Q

dabigatran

A

150 mg BID
75 mg BID (CrCl 15-30)
idarucizumab is antidote

119
Q

rivaroxaban

A

20 mg with evening meal
15 mg with evening meal (CrCl 15-50)
no antidote right now

120
Q

apixaban

A

5 mg or 2.5 mg BID
not recommended in severe kidney disease
no antidote
use 2.5 if 2 of theseL over 80, SCr over 1.5, weight under 60

121
Q

edoxaban

A

60 mg QD (CrCl 50-95)
30 mg QD (CrCl 15-50)
no antidote

122
Q

warfarin

A

goal INR 2-3; 2.5-3.5 for artifical valve

INR should be determined weekly at initiation of therapy

123
Q

paroxysmal supraventricular tachycardia features

A

regular rate and rhythm, narrow QRS

124
Q

paroxysmal supraventricular tachycardia risk factors

A

heart disease, fever or infection, electrolyte abnormalities

125
Q

paroxysmal supraventricular tachycardia symptoms

A

palpations, dizziness/weakness, syncope, angina, HF

126
Q

paroxysmal supraventricular tachycardia goals

A

terminate paroxysmal supraventricular tachycardia, restore NSR

127
Q

paroxysmal supraventricular tachycardia drugs

A

adenosine: inhibits conduction through AV node
verapamil: direct AV nodal inhibition
diltiazem: direct AV nodal inhibition
digoxin: negative chronitropic activity, vagal stimulation, direct AV nodal inhibition
amiodarone: direct AV nodal inhibition

128
Q

termination of hemodynamically stable paroxysmal supraventricular tachycardia algorithm

A

vagal maneuvers, then adenosine, then…
no HF: diltiazem/verapamil or BB, then amidarone or DCC
HF: amiodarone or DCC

129
Q

for hemodynamically unstable paroxysmal supraventricular tachycardia…

A

DCC should be used

130
Q

prevention of recurrent paroxysmal supraventricular tachycardia algorthim

A

symptomatic = catheter ablation
if patient does not prefer CA…
no HF = BB, verapamil, diltiazem, then flecainide or propafenone, then CA
HF = amiodarone, digoxin, dofetilide, sotalol, then CA
asymptomatic = f/u w/o tx

131
Q

ventricular premature depolarization features

A

wide QRS, variable frequency

132
Q

ventricular premature depolarization risk factors

A

CAD, MI, drugs, anemia, hypoxia, cardiac surgery

133
Q

ventricular premature depolarization symptoms

A

often asymptomatic, palpations, syncope

134
Q

ventricular premature depolarization treatment

A

asymptomatic VPDs should not be treated

symptomatic VPDs should be treated with BB

135
Q

ventricular tachycardia features

A

regular rhythm (150-200 bpm), wide QRS, series of consecutive VPDs

136
Q

ventricular tachycardia risk factors

A

CAD, MI, HF, electrolyte abnormalities, drugs

137
Q

ventricular tachycardia symptoms

A

may be asymptomatic, hypotension, palpations

138
Q

ventricular tachycardia prognostic significance

A

sustained VT may progress to Vfib; some patients with VT are at a risk for the syndrome of sudden cardiac death

139
Q

ventricular tachycardia goals

A

terminate VT, restore NSR, prevent recurrance, reduce risk of sudden cardiac death

140
Q

ventricular tachycardia termination

A

procainamide: risk of Tdp
amiodarone
no HF: procainamide then amiodarone
HF: amiodarone then DCC

141
Q

prevent reccurance of VT and prevention of sudden cardiac death

A

ICD
amiodarone
sotalol; risk of Tdp

142
Q

ventricular fibrillation features

A

irregular disorganized ventricular rhythm. no QRS complexes

143
Q

ventricular fibrillation risk factors

A

MI, HF, CAD

144
Q

ventricular fibrillation symptoms

A

sudden cardiac death

145
Q

ventricular fibrillation goal and treatment

A

terminate Vfib, restore NSR
Only effective treatment is defibrillation, drugs can help facilitate but will not help alone
Primary ABCD survey (airway, breathing, circulation, defibrillation), then Defibrillation x 3 attempts, if VF still present, Epinephrine every 3-5 minutes, alternate Amiodarone (defibrillation done after every dose of drug)
VF, CPR, shock, CPR, epi, shock, CPR, ami, shock, CPR, epi, shock, CPR, ami, shock, CPR, epi, continue or terminate

SPP2 CHF and AFib (1 decks)

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