-
Amiodarone (Pacerone, Cordarone)
Considered class III but has properties of all three classes
-
Digoxin (Lanoxin)
Inhibits the sodium potassium ATPase pump
-
A system of classifying antiarrhythmic medications based on simplified electrophysiologic actions
Vaughan-Williams
-
Procainamide (Procan SR, Procanabid)
Vaughan-Williams Type IA
-
Modulation/blockade of sodium channels
Vaughan-Williams Type I antiarrhythmics
-
The class that exhibits slow conduction velocity and prolongs action potential duration
Vaughan-Williams Type IA
-
Quinidine (Quinidex)
Vaughan-Williams Type IA
-
Disopyramide (Norpace)
Vaughan-Williams Type IA
-
Lidocaine (Xylocaine)
Vaughan-Williams Type IB
-
Mexiletine
Vaughan-Williams Type IB
-
Class that has no effect on conduction velocity, May shorten action potential duration
Vaughan-Williams Type IB
-
Flecainide (Tambocor)
Vaughan-Williams Type IC
-
Propafenone (Rhythmol)
Vaughan-Williams Type IC
-
Moricizine
Vaughan-Williams Type IC
-
Slows coduction velocity and may prolong action potential duration (mildly)
Vaughan-Williams Type IC
-
Mexiletine
Oral analog of Lidocaine
-
Lidocaine
unlike other class I antiarrhytmics it can be used in patients with active ischemia
-
Beta blockers
Vaughan-Williams Type II
-
Beta blockers
Inhibit phase IV (depolarizing current) and prolong repolarization
-
Beta blockers
decrease sympathetic stimulation of myocardium
-
Beta blockers
slow the sinus rate
-
Amiodarone (Pacerone, Cordarone)
Vaughan-Williams Type III
-
Sotalol (Betapace)
Vaughan-Williams Type III
-
Dofetilide (Iikosyn)
Vaughan-Williams Type III
-
Ibutilide
Vaughan-Williams Type III
-
Blockade of potassium channel
Vaughan-Williams Type III
-
Prolongation of action potential plateau, repolarization, and refractor period
Vaughan-Williams Type III
-
Verapamil
Vaughan-Williams Type IV
-
Diltiazem
Vaughan-Williams Type IV
-
Calcium channel blockers
Vaughan-Williams Type IV
-
Blockade of calcium channel
Vaughan-Williams Type IV
-
slows conduction velocity through AV node and prolongs refractory period
Vaughan-Williams Type IV
-
Sets of the initial depolarization
Phase IV
-
Does not increase mortality in high risk patients-has a higer safety level than the other classes
Type III
-
Ibutilide
IV administration only -one time use for conversion-no long term treatment
-
Anticipated ECG change for this type is prolongation of the QT interval
Type IA
-
Usually no ECG changes in therapeutic doses
Type IB
-
Anticipated ECG changes for this type is prolongation of the PR and QRS intervals
Type IC
-
Anticipated ECG change for this type is prolongation of the QT interval
Type III
-
This type is used for atrial and ventricular tachyarrhythmias
Type IA
-
This type is used for ventricular arrhythmias
Type IB
-
This type is used for atrial and ventricular arrhythmias
Type IC
-
Procainamide (Procan SR, Procanabid)
Used for WPW
-
This type is used for atrial and ventricular arrhythmias
Type II
-
This type is used for atrial and ventricular arrhythmias
Type III
-
This type is used for atrial arrhthmias
Type IV
-
Procainamide (Procan SR, Procanabid)
SE-lupus like syndrome, torsades
-
Disopyramide (Norpace)
SE-anticholinergic symptoms, heart failure, torsades (QT prolongation)
-
Lidocaine (Xylocaine)
SE-seizures, CNS
-
Amiodarone (Pacerone, Cordarone)
SE-many toxic side effects (Pulmonary fibrosis, hypo/hyperthyroidism, photophobia, liver toxicity, blue staining of skin.
-
Amiodarone (Pacerone, Cordarone)
Has a very large volume of distribution
-
Amiodarone (Pacerone, Cordarone)
Has a half life of 15-180 days
-
Amiodarone (Pacerone, Cordarone)
If patient is on Warfarin at the time of prescription, cut the Warfarin dose by 30-50%
-
Procainamide (Procan SR, Procanabid)
Used for hemodynamically stable VT
-
Procainamide (Procan SR, Procanabid)
Limited role in a-fib/a-flutter
-
Quinidine (Quinidex)
SE-include chinchonism, hypotension, torsades, hemolytic anemia
-
Quinidine (Quinidex)
Use with digoxin leads to increased digoxin concentration
-
Disopyramide (Norpace)
Indicated for conversion/maintenance of sinus rhythm in patients with a-fib/a-flutter
-
Lidocaine (Xylocaine)
Used for management of VT or pulseless VT/Vfib
-
Lidocaine (Xylocaine)
Dose determined by liver function
-
Flecainide (Tambocor)
used in a-fib/a-flutter for maintenance of sinus rhythm
-
Flecainide (Tambocor)
Avoid in patients with structural heart disease or history of CAD
-
Propafenone (Rhythmol)
Indicated for conversion/maintenance of sinus rhythm in patients with a-fib/a-flutter
-
Dofetilide (Tikosyn)
Indicated for conversion/maintenance of sinus rhythm in patients with a-fib/a-flutter
-
Dofetilide (Tikosyn)
Starting dose based on estimated creatinine clearance. Contraindicated in patients with CrCl <20 ml/min.
-
Sotalol (Betapace)
used in a-fib/a-flutter for maintenance of sinus rhythm
-
Stroke risk index based on a point system, integrating risk based on various co-morbidities
CHADS2
-
The C in CHADS2 stands for
Cardiac failure (one point)
-
The H in CHADS2 stands for
Hypertension (one point)
-
The A in CHADS2 stands for
Age >75 years (one point)
-
The D in CHADS2 stands for
Diabetes (one point)
-
The S2 in CHADS2 stands for
Sroke or TIA (you get 2 points for this one)
-
CHADS2 score of 0-1
Low risk-treat with full dose asa
-
CHADS2 score of 2 and above
High risk-treat with Warfarin
-
Most common arrhythmia
A-fib
-
Characterized by rapid and disorganized atrial activation with ventricular responses of 120-180 bpm
A-fib
-
A-fib management in the hemodynamically stable patient
Ventricular rate control with beta blocker, calcium channel blocker, or digoxin
-
A-fib management in the hemodynamically stable patient
Anticoagulation therapy
-
A-fib management in the hemodynamically unstable patient
Cardioversion
-
When a-fib is symptomatic, recurrent and failed response of greater than or equal to 1 AAD plus rate contrel
consider ablation
-
Beta blockers
safe and effective treatment for Ventricular Premature Beat suppression
-
Lidocaine (Xylocaine)
Sustained monomorphic V-tach with LVEF <40% and expected ischemia/MI
-
Movement of ions across the cell membrane resulting in activation of cardiac cells and a transient depolarization.
Action Potential
-
Impulse generation; the property of a cardiac cell that causes it to depolarize spontaneously during phase 4 of the AP
Automaticity
-
The speed of impulse propagation through cardiac tissue.
Conduction Velocity
-
the period of recovery cells require after being discharged before they can be re-excited by a stimulus.
Refractory Period
-
All antiarrhythmic agents have the potential to cause arrhythmias
Proarrhythmic
-
Risk factors including ischemic heart disease, left ventricular dysfunction and underlying ventricular arrhythmias
predispose patients to proarrhythmia
-
Procainamide; Quinidine; Disopyramide
IA
-
Modulation/blockade of Na+ channels inhibiting phase 0 depolarization
IA; IB & IC
-
Slow conduction velocity and prolongs action potential duration (APD). Intermediate association/dissociation
IA
-
No effect on conduction velocity; may shorten APD. Fast association/ dissociation
IB
-
Slow conduction velocity and may prolong APD (mildly). Slow association/dissociation
IC:
-
-
Flecainide; Propafenone; Moricizine
IC
-
Inhibition of phase IV (depolarizing current) and prolongation of repolarization; ↓ sympathetic stim, slow sinus rate
Beta blockers (type II)
-
Blockade of potassium channelProlongation of action potential plateau, repolarization, and refractory period
Type III: Amiodarone; Sotalol; Dofetilide; Ibutilide; Dronedarone
-
Blockade of calcium channel; slows conduction velocity through AV node and prolongs refractory period
Type IV:Verapamil; Diltiazem
-
Prolongation of the QT interval
Type IA: Procainamide; Quinidine; Disopyramide
-
None (Possible increased QRS and PR intervals with toxic concentrations)
Type IB: Lidocaine; Mexiletine
-
Prolongation of the PR and QRS intervals
Type 1C: Flecainide; Propafenone
-
Prolongation of the QT interval
Type III: Amiodarone; Sotalol; Dofetilide; Ibutilide; Dronedarone
-
Atrial and ventricular tachyarrhythmias
Type IA: Procainamide; Quinidine; Disopyramide: Use/Indication
-
Ventricular arrhythmias
Type IB: Lidocaine; Mexiletine; Use/Indication
-
Atrial and ventricular arrhythmias
Use/Indication: Type IC: Flecainide; Propafenone
-
Atrial and ventricular arrhythmias
Use/Indication: Beta blockers
-
Atrial and ventricular arrhythmias
Use/Indication: Type III:Amiodarone; Sotalol; Dofetilide; Ibutilide; Dronedarone
-
Atrial arrhythmias
Use/Indication: Type IV: Verapamil; Diltiazem
-
Fatigue, bradycardia, exercise intolerance, erectile dysfunction, exacerbation of pulmonary d/o’s
AE Beta blockers: Type II
-
AV block, bradycardia, HF exacerbation, hypotension
Verapamil; Diltiazem: Type IV
-
Limited role in management of afib/flutterRole in WPW, hemodynamically stable VT
Procainamide
-
Elimination/metabolismHepatic: acetylation forms less active (but toxic) metabolite NAPARenal: NAPA primarily elim. Renally
Procainamide
-
Side effects include drug-induced lupus, torsades, vent arrhythmias, aggravation of underlying heart failure
Procainamide
-
Side effects include GI, cinchonism, hypotension (IV), torsades, vent arrhythmias, hemolytic anemia
Quinidine
-
Eliminated by hepatic metabolism (3A4) and renal elimination
Quinidine
-
Indicated for conversion/maintenance of sinus rhythm in patients with afib/flutter.
Disopyramide
-
Significant negative inotropic effects
Disopyramide
-
Side Effects include: GI, anticholinergic symptoms, heart failure, worsening of underlying conduction abnormalities, ventricular arrhythmias, torsades (QT prolongation)
Disopyramide
-
Class 1B antiarrhythmic agent; Used in management of ventricular tach or pulseless VT/Vfib; Dose determined by hepatic function/cardiac output (LVEF)
Lidocaine
-
Normal half-life extends to up to 12 hrs in patients with cirrhosis/CHF; Side-effects include CNS (confusion,tremor,paresthesias), seizures
Lidocaine
-
Used to manage ventricular arrhythmias; esp when responsive to lidocaine. Significantly hepatically metabolized, 1º to inactive metabolites
Mexiletine
-
Substrate for CYP 2D6 and 1A2; Inhibitor of CYP 1A2; Half-life 8-15 hours
Mexiletine
-
Side-effects: CNS, psychosis, GI, aggravation of underlying conduction disturbances or ventricular arrhythmias, rarely blood dyscrasias
Mexiletine
-
Used in afib/flutter for maintenance of sinus rhythmAvoid in patients with structural heart disease or history of CAD
Flecainide
-
Side-effects: EKG (prolongation of QRS and PR), ventricular arrhythmias, GI, blurred vision; Elimination: renal and hepatic (CYP2D6)
Flecainide
-
Used for conversion/maintenance of sinus rhythm in patients with afib/flutter.Potent negative inotropic agent (avoid in patients with systolic dysfunction)
Propafenone
-
Side-effects: GI, worsening of underlying CHF, ventricular arrhythmias; Elimination: hepatic metabolism
Propafenone
-
Prescribers must complete training program; Requires hospitalization for at least 3 days to initiate (due to risk of proarrhythmias)
Dofetilide
-
Baseline QTc should be less than 440 msec (500 msec if baseline ventricular conduction abnormalities)
Dofetilide
-
Class III antiarrhythmic with beta-blocking activity. Indicated for maintenance of sinus rhythm. May chemically convert patientsContraindicated if baseline QTc > 450 msecCareful monitoring of electrolytes
Sotalol (Betapace®, Betapace AF®
-
Mechanism of Action: Class III anti-arrhythmic with properties of all classes:inhibition of adrenergic stimulation; decreased AV node conduction and sinus node function; prolongation of action potential and; refractory period of myocardial tissue
Amiodarone
-
Cardiac: QT prolongation, monitor EKG daily during initiation and q 3 months
Amiodarone Side Effects
-
Pulmonary toxicity: Pulmonary fibrosis (3-10%), check baseline pulmonary function tests
Amiodarone Side Effects
-
Thyroid disturbances: hypothyroidism (~20%), hyperthyroidism (~5-10%), monitor thyroid function tests at baseline and q 6 months
Amiodarone Side Effects
-
Ocular: optic neuritis (1%), photophobia (75-90%) eye exam at baseline and every year thereafter
Amiodarone Side Effects
-
Liver: elevated hepatic transaminases (5-20%), monitor liver function at baseline and q 6 m
Amiodarone Side Effects
-
Indicated to reduce CV hospitalization in patients with PAF or AF or aflutter with recent episode and associated risk factors who are in sinus rhythm or who will be cardioverted.
Dronedarone
-
Effective for both conversion and maintenance of NSR in Afib pts. Use only in persons without coronary artery disease or left ventricular dysfunction.
Propafenone and Flecainide
-
Symptoms precede LV dysfunctionTypically, intervene for symptoms
Stenosis
-
LV dysfunction may precede symptomsMonitor LV functionIntervene for symptoms AND to preserve cardiac function
Regurgitation
-
Narrowing or obstruction to forward flow while valve is openChronic – slow progression of disease
Stenosis
-
Backward leakage during time when valve is closedAcute vs chronic
Regurgitation / Insufficiency
-
thickness is < 12 mm
Normal LV wall
-
Who: Older, calcific or younger, bicuspid
Aortic Stenosis
-
Sx: Angina, syncope, CHF
Aortic Stenosis
-
PE findings: Harsh, systolic ejection murmur at RUSB with radiation to neck, subclavian; sit patient forward, exhalation
Aortic Stenosis
-
Dx: Echo, cardiac cath
Aortic Stenosis
-
Management: Surgery for symptoms
Aortic Stenosis
-
Marfan syndrome, syphilis, ankylosing spondylitis, cystic medial necrosis, aortic dissection, trauma
Aortic root disease
-
Wide pulse pressureLarge difference between systolic and diastolic pressuresDiastolic murmur – soft, high pitched and localized to left sternal border‘Water-hammer’ or ‘Corrigan’s’ pulseQuincke’s pulse – nail bedMusset’s sign – head bob
- Chronic Aortic Regurgitation--
- Physical Findings
-
-
-
Who: No classic patient, think bicuspid or Marfan syndrome
Aortic Regurgitation
-
Sx: CHF symptoms – dyspnea, fatigue
Aortic Regurgitation
-
PE findings:Wide pulse pressureSoft, decrescendo diastolic murmurBounding pulses - ‘Water-hammer’, Musset’s head bob, Quincke’s pulse
Aortic Regurgitation
-
Dx: Echo
Aortic Regurgitation
-
Management: Medical therapy; surgery for acute AI, symptoms, or evidence of LV changes
Aortic Regurgitation
-
Think rheumatic heart disease first
Mitral Stenosis
-
PathophysiologyFibrosis, scarring and thickeningCommissural fusionChordae fusion and shorteningDecrease in orifice size
Mitral Stenosis
-
Who: History of rheumatic fever
Mitral Stenosis
-
Symptoms: Dyspnea/orthopnea and fatigue
Mitral Stenosis
-
PE findings: Low pitched, diastolic rumble near apex with opening snapHeard best in left lateral decubitus position
Mitral Stenosis
-
Diagnosis: Echo
Mitral Stenosis
-
Management: Intervene for symptoms – balloon valvuloplasty or mitral valve replacement
Mitral Stenosis
-
Who: Myxomatous valve or post-MI
Mitral Regurgitation
-
Symptoms: CHF
Mitral Regurgitation
-
PE: Holosystolic murmur at apex
Mitral Regurgitation
-
Diagnosis: Echo or cardiac cath
Mitral Regurgitation
-
Management: Medical mgt., Surgical for symptoms or decrease in LV function
Mitral Regurgitation
-
Who: Young, female
Mitral valve prolapse
-
Symptoms: Atypical chest pain, palpitations
Mitral valve prolapse
-
PE: Mid-systolic click +/- MR
Mitral valve prolapse
-
Diagnosis: Echo – assess MR
Mitral valve prolapse
-
Management: Supportive, SBE prophylaxis
Mitral valve prolapse
-
Pathology: Narrowing and calcification of TV causing diastolic pressure gradient (5 mmHg) between RA and RV
Tricuspid Valve Stenosis
-
Symptoms: Related to elevated RA pressuresEdema, hepato-splenomegaly / ascites, fatigue, weakness
Tricuspid Valve Stenosis
-
Exam: Jugular veinous distension with giant venous A wavesDiastolic murmur at left sternal border which increases with inspiration
Tricuspid Valve Stenosis
-
Therapy: Balloon Valvuloplasty or Surgical valve replacement if symptoms and mean valve gradient > 5 mm Hg
Tricuspid Valve Stenosis
-
Small degrees present in normal individual; Causes of mod/severe TR; Usually functional – related to RV dilatation or increases in pulmonary artery pressure; Ebstein’s anomaly; Rheumatic disease; Carcinoid, endocarditis, trauma
Tricuspid Regurgitation
-
Symptoms: Identical to those of RV failure
Tricuspid Regurgitation
-
Physical exam findings: C-V waves of the jugular veins with venous congestion; Pulsatile liver; Hepatojugular refluxHolosystolic murmur at LSB; Increases with inspiration
Tricuspid Regurgitation
-
Symptoms: Exertional dyspnea; Fatigue; Pre-syncope; Cyanosis
Pulmonic Stenosis
-
Signs on ECHO: RV hypertrophy; Systolic doming of PV; Transpulmonic gradient
Pulmonic Stenosis
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