exam Flashcards
force tension curve
after load and SV relationship
NYHA I
cardiac disease with no symptoms
NYHA II
slight limitations of physical activity
NYHA III
limitations of physical activity
NYHA IV
inability to carry on any physical activity without discomfort
CHF stage A
High risk of developing HF, no abnormalities, HTN, CAD, DM, etc
CHF stage B
structural disease but no signs or symptoms of HF, NYHA I
CHF stage C
current or prior symptoms of HF, NYHA II or III
CHF stage D
advanced structural heart disease and marked symptoms of HF at rest, NYHA IV
summary of stage A treatment
ACEIs or ARBs
if atherosclerotic disease is present
summary of stage B treatment
ACEIs
BB
if previous MI or asymptomatic rEF
stage C treatment summary
routine use: diuretics, ACEIs, BBs
selected patients: ARBs, aldosterone antagonists, valsartan/sacubitril, ISDN/hydralazine, digoxin, amlodipine/felodipine, ICD/cardiac resynchronization
___ may be used in patients with mild HF and small amounts of fluid retention
thiazides
thiazide use in decreased renal function
lose effectiveness, higher doses are generally necessary
starling curve
preload and SV relationship
loop diuretic equivalent doses
furosemide 40 = bumetanide 1 = torsemide 10-20 = ethacrynic acid 50
furosemide dosing in HF
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
bumetanide dosing in HF
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
torsemide dosing in HF
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
ethacrynic acid dosing in HF
start: 25-50 mg QD or BID
enalapril dosing in HF
start: 2.5-5 mg BID
target: 10 mg BID
captopril dosing in HF
start: 6.25-12.5 mg TID
target: 50 mg TID
lisinopril dosing in HF
start: 2.5-5 mg QD
target: 20-40 mg QD
ramipril dosing in HF
start: 1.25-2.5 mg QD
target: 5 mg BID - 10 mg QD
ACEI dosing in CKD
if CrCl is less than 30, the target dose is 1/2 normal
ACEI CI
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
ACEI AE
hypotension functional renal insufficiency hyperkalemia (monitor) cough rash and dysgeusia angioedema
use ACEI with caution if:
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
losartan dosing in HF
start: 25-50 mg QD
target: 50-150 mg QD
valsartan dosing in HF
start: 20-40 mg QD
target: 160 mg BID
candesartan dosing in HF
start: 4-8 mg QD
target: 32 mg QD
patient selection to start a BB
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
carvedilol dosing in HF
start: 3.125 mg BID for 2 weeks
target: under 85 kg, 25 mg BID
over 85 kg, 50 mg BID
coreg CR dosing in HF
start: 10 mg QD for 2 weeks
target: 80 mg QD
metoprolol XL dosing in HF
start: 12.5-25 mg QD
target: 200 mg QD
BB titration in HF
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
BB monitoring
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
eplerenone dosing in HF
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
spironolactone dosing in HF
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
ISDN/hydralazine use in HF
venous vasodilator/arterial vasodilator
treatment of HF in black patients as an adjunct to standard therapy
digoxin use in HF
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
digoxin dosing in HF
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
digoxin drug interactions
many
amiodarone, itra/ketoconazole, verapamil require decrease in dig dose (1/2)
sacubitril/valsartan dosing
49/51 mg BID, doubled in 2-4 weeks to 97/103 BID
sacubitril/valsartan AE
hypotension (more than enalapril)
elevated SCr and K (less than enalapril)
angioedema rare
Ivabradine dosing
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)
Ivabradine AEs
fetal toxicity
AFib
Bradycardia and conduction disturbances
nonpharm therapies for HFrEF
ICD (implantable cardio defibrillator)
cardiac resynchronization therapy
antiplatelet therapy in HF
aspirin recommended in patients with HF and CAD
anitcoag therapy in HF
NOT RECOMMENDED
CCB in HF
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
guide-line based drug therapy of HFpEF
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)
decompensated HF precipitation
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
hospitalization recommended in HF
evidence of severly DHF
dyspnea at rest
hemodynamically significant arrhythmia
ACS
hospitalization considered
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
clinical manifestations and classification of ADHF
warm and dry: normal I
warm and wet: pulmonary congestion II
cool and dry: hypoperfusion III
cool and wet: pulmonary congestion and hypoperfusion IV
chronic therapy while hospitalized
should be continued and maximized in the absence of hemodynamic instability or CIs
initiation of BB while hospitalized
after optimization of volume status and successful DC of IV diuretics, VDs and inotropes
diuretics while hospitalized
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
parenteral therapy in AHF
vasodilators and positive inotropes
vasodilators used in AHF
nitroprusside, nitroglycerin, nesiritide, morphine, enalaprilat, hydralazine
positive inotropes used in AHF
helps when patients are cold and wet or cold and dry while adequately hydrated
dobutamine, milrinone, dopamine(used when hypotension)
Tx for warm and wet
no immediate interventions necessary except optimizing oral tx
Tx warm and wet
reduce congestion
loop diuretics
tx cool and dry
increase output and perfusion with positive inotropes +/- IV fluids
initial: fluids until BP maximized
following: if still “Cool”, inotrope may be required
Tx cool and wet
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
pacemaker action potentials
“upstroke” mediated by Ca2+ cells
repolarization mediated by K+
depolarization or “pacemaker current” mediated by HCN and ACh-gated K+ channels
myocyte action potentials
“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
the refractory period between action potentials
as you move later toward the end of a refractory period, a stimulus of the same strength results in a stronger and stronger depolarization
bAR signaling in pacemaker cells
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
bAR blockers used as antiarrhythmics
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
CCBs used as antiarrhythmics
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
class I antiarrythmic drugs
1A: quinidine, procainamide, disopyramide
1B: lidocaine (IV only, rapid control of ventricuar arrhythmias), tocainide, mexilitine
1C: propafenone, flecainide
class 3 antiarrhythmics MOA
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
torsade de pointes
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
class 3 antiarrhythmic drugs
amiodarone, dronedarone, ibutilide, sotalol, dofetilide
questions to determine if an ECG is normal sinus rhythm
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?
numbers when reading HR on an ECG
300, 150, 100, 75, 60
normal values for an ECG
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)
if PR interval is longer than ___…
0.2 seconds = 1st degree AV block
QTc =
QTc = QT interval / (square root (time between R waves (sec))
examples of supraventricular arrhythmias
sinus bradycardia AV block sinus tachycardia Afib paroxysmal supraventricular tachycardia
examples of ventricular arrhythmias
ventricular premature depolarizations
ventricular tachycardia
ventricular fibrillation
sinus bradycardia features
HR less than 60 bpm due to decreased automaticity of SA node
impulses originate in SA node
sinus bradycardia risk factors/etiologies
MI, abnormal sympathetic tone, electrolyte abnormalities
drugs: digoxin, BB, diltiazem/verapamil, amiodarone, dronedarone
idiopathic (sick sinus syndrome)
sinus bradycardia symptoms
hypotension, dizziness, fainting (syncope)
sinus bradycardia treatment
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
atropine AE
tachycardia , urinary retention, blurred vision, dry mouth, mydriasis
Afib features
atrial: chaotic and disorganized depolarizations (quivering)
ventricular rate: 120-180 bpm
rhythm: irregularly irregular
p waves: absent
paroxysmal Afib
episodes start suddenly and spontaneously and resolve suddenly
persistent Afib
continuous episode of Afib that does not terminate spontaneously, may last over 7 days
long-standing persistent Afib
continuous afib lasting over 12 months
permanent Afib
patient is never in NSR and Afib cannot be terminated
nonvalvular Afib
absence of rheumatic mitral valve stenosis, a mechanical or bioprosthetic heart valve or mitral valve repair
Afib risk factors
HTN, CAD, HF, valvular heart disease
etiologies of reversible Afib
hyperthyroidism, pulmonary embolism, thoracic surgery, alcohol binging
Afib symptoms
palpations, dizziness, fatigus, lightheaded, SOB, hypotension, syncope, angina, exacerbation of HF sx
Afib morbidity/mortality
inc risk of stroke, HF, dementia and mortality
Afib treatment goals of therapy
ventricular rate control, convert Afib to NSR, maintain sinus rhythm, prevent strokes
all types of Afib have 2 treatment goals
rate control and stroke prevention
persistent AFib specific goal
conversion to NSR
paroxysmal Afib specific goal
maintenance of sinus rhythm if ventricular rate control is not sufficient to control symptoms
diltiazem in Afib
direct AV node inhibition
AE: hypotension, bradycardia, HF exacerbation, AV block
verapamil in Afib
direct AV node inhibition
AE: hypotension, bradycardia, HF exacerbation, AV block, constipation
B blockers in Afib
direct AV node inhibition
notably: esmolo, propranolol, metoprolol
AE: hypotension, bradycardia, HF exacerbation (IV), AV block
digoxin use in Afib
vagal stimulation and direct AV node inhibition
AE: N/V, anorexia, ventricular arrhythmias
interactions: amiodarone (USE HALF DOSE OF DIG)
amiodarone use in Afib
AE: hypotension, bradycardia, blue-grey skin, photosensitivity, conreal microdeposits, PULMONARY FIBROSIS, hepatotoxicity, hypo/hyperthyroidism
hemodynamically unstable
any of the following: SBP less than 90 HR over 150 ischemic chest pain unconscious
persistent Afib acute rate control algorithm
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
paroxysmal or persistent Afib long-term ventricular rate control
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
Afib conversion to NSR
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
conversion to NSR treatments
synchronized direct current cardioversion (DCC), amiodarone, dofetilide (risk of Tdp, must adjust for CrCl), ibutilide (risk of Tdp), propafenone, flecainide (HF exacerbations)
synchronized DCC
chest paddles
automatic for hemodynamically unstable
simultaneously depolarizes all myocardial cells, allowing the SA node to take over as pacemaker
persistent Afib conversion algorithm
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
maintenance of NSR (paroxysmal only)
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
maintenance of NSR following conversion to NSR with paroxysmal algorithm
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
prevention of embolization/stroke in nonvalvular Afib
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
dabigatran
150 mg BID
75 mg BID (CrCl 15-30)
idarucizumab is antidote
rivaroxaban
20 mg with evening meal
15 mg with evening meal (CrCl 15-50)
no antidote right now
apixaban
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
edoxaban
60 mg QD (CrCl 50-95)
30 mg QD (CrCl 15-50)
no antidote
warfarin
goal INR 2-3; 2.5-3.5 for artifical valve
INR should be determined weekly at initiation of therapy
paroxysmal supraventricular tachycardia features
regular rate and rhythm, narrow QRS
paroxysmal supraventricular tachycardia risk factors
heart disease, fever or infection, electrolyte abnormalities
paroxysmal supraventricular tachycardia symptoms
palpations, dizziness/weakness, syncope, angina, HF
paroxysmal supraventricular tachycardia goals
terminate paroxysmal supraventricular tachycardia, restore NSR
paroxysmal supraventricular tachycardia drugs
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
termination of hemodynamically stable paroxysmal supraventricular tachycardia algorithm
vagal maneuvers, then adenosine, then…
no HF: diltiazem/verapamil or BB, then amidarone or DCC
HF: amiodarone or DCC
for hemodynamically unstable paroxysmal supraventricular tachycardia…
DCC should be used
prevention of recurrent paroxysmal supraventricular tachycardia algorthim
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
ventricular premature depolarization features
wide QRS, variable frequency
ventricular premature depolarization risk factors
CAD, MI, drugs, anemia, hypoxia, cardiac surgery
ventricular premature depolarization symptoms
often asymptomatic, palpations, syncope
ventricular premature depolarization treatment
asymptomatic VPDs should not be treated
symptomatic VPDs should be treated with BB
ventricular tachycardia features
regular rhythm (150-200 bpm), wide QRS, series of consecutive VPDs
ventricular tachycardia risk factors
CAD, MI, HF, electrolyte abnormalities, drugs
ventricular tachycardia symptoms
may be asymptomatic, hypotension, palpations
ventricular tachycardia prognostic significance
sustained VT may progress to Vfib; some patients with VT are at a risk for the syndrome of sudden cardiac death
ventricular tachycardia goals
terminate VT, restore NSR, prevent recurrance, reduce risk of sudden cardiac death
ventricular tachycardia termination
procainamide: risk of Tdp
amiodarone
no HF: procainamide then amiodarone
HF: amiodarone then DCC
prevent reccurance of VT and prevention of sudden cardiac death
ICD
amiodarone
sotalol; risk of Tdp
ventricular fibrillation features
irregular disorganized ventricular rhythm. no QRS complexes
ventricular fibrillation risk factors
MI, HF, CAD
ventricular fibrillation symptoms
sudden cardiac death
ventricular fibrillation goal and treatment
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
