Cardiology 1

Amiodarone (Pacerone, Cordarone)

Digoxin (Lanoxin)

A system of classifying antiarrhythmic medications based on simplified electrophysiologic actions

Procainamide (Procan SR, Procanabid)

Modulation/blockade of sodium channels

The class that exhibits slow conduction velocity and prolongs action potential duration

Quinidine (Quinidex)

Disopyramide (Norpace)

Lidocaine (Xylocaine)

Mexiletine

Class that has no effect on conduction velocity, May shorten action potential duration

Flecainide (Tambocor)

Propafenone (Rhythmol)

Moricizine

Slows coduction velocity and may prolong action potential duration (mildly)

Mexiletine

Lidocaine

Beta blockers

Beta blockers

Beta blockers

Beta blockers

Amiodarone (Pacerone, Cordarone)

Sotalol (Betapace)

Dofetilide (Iikosyn)

Ibutilide

Blockade of potassium channel

Prolongation of action potential plateau, repolarization, and refractor period

Verapamil

Diltiazem

Calcium channel blockers

Blockade of calcium channel

slows conduction velocity through AV node and prolongs refractory period

Sets of the initial depolarization

Does not increase mortality in high risk patients-has a higer safety level than the other classes

Ibutilide

Anticipated ECG change for this type is prolongation of the QT interval

Usually no ECG changes in therapeutic doses

Anticipated ECG changes for this type is prolongation of the PR and QRS intervals

Anticipated ECG change for this type is prolongation of the QT interval

This type is used for atrial and ventricular tachyarrhythmias

This type is used for ventricular arrhythmias

This type is used for atrial and ventricular arrhythmias

Procainamide (Procan SR, Procanabid)

This type is used for atrial and ventricular arrhythmias

This type is used for atrial and ventricular arrhythmias

This type is used for atrial arrhthmias

Procainamide (Procan SR, Procanabid)

Disopyramide (Norpace)

Lidocaine (Xylocaine)

Amiodarone (Pacerone, Cordarone)

Amiodarone (Pacerone, Cordarone)

Amiodarone (Pacerone, Cordarone)

Amiodarone (Pacerone, Cordarone)

Procainamide (Procan SR, Procanabid)

Procainamide (Procan SR, Procanabid)

Quinidine (Quinidex)

Quinidine (Quinidex)

Disopyramide (Norpace)

Lidocaine (Xylocaine)

Lidocaine (Xylocaine)

Flecainide (Tambocor)

Flecainide (Tambocor)

Propafenone (Rhythmol)

Dofetilide (Tikosyn)

Dofetilide (Tikosyn)

Sotalol (Betapace)

Stroke risk index based on a point system, integrating risk based on various co-morbidities

The C in CHADS2 stands for

The H in CHADS2 stands for

The A in CHADS2 stands for

The D in CHADS2 stands for

The S2 in CHADS2 stands for

CHADS2 score of 0-1

CHADS2 score of 2 and above

Most common arrhythmia

Characterized by rapid and disorganized atrial activation with ventricular responses of 120-180 bpm

A-fib management in the hemodynamically stable patient

A-fib management in the hemodynamically stable patient

A-fib management in the hemodynamically unstable patient

When a-fib is symptomatic, recurrent and failed response of greater than or equal to 1 AAD plus rate contrel

Beta blockers

Lidocaine (Xylocaine)

Movement of ions across the cell membrane resulting in activation of cardiac cells and a transient depolarization.

Impulse generation; the property of a cardiac cell that causes it to depolarize spontaneously during phase 4 of the AP

The speed of impulse propagation through cardiac tissue.

the period of recovery cells require after being discharged before they can be re-excited by a stimulus.

All antiarrhythmic agents have the potential to cause arrhythmias

Risk factors including ischemic heart disease, left ventricular dysfunction and underlying ventricular arrhythmias

Procainamide; Quinidine; Disopyramide

Modulation/blockade of Na+ channels inhibiting phase 0 depolarization

Slow conduction velocity and prolongs action potential duration (APD). Intermediate association/dissociation

No effect on conduction velocity; may shorten APD. Fast association/ dissociation

Slow conduction velocity and may prolong APD (mildly). Slow association/dissociation

Lidocaine; Mexiletine

Flecainide; Propafenone; Moricizine

Inhibition of phase IV (depolarizing current) and prolongation of repolarization; ↓ sympathetic stim, slow sinus rate

Blockade of potassium channelProlongation of action potential plateau, repolarization, and refractory period

Blockade of calcium channel; slows conduction velocity through AV node and prolongs refractory period

Prolongation of the QT interval

None (Possible increased QRS and PR intervals with toxic concentrations)

Prolongation of the PR and QRS intervals

Prolongation of the QT interval

Atrial and ventricular tachyarrhythmias

Ventricular arrhythmias

Atrial and ventricular arrhythmias

Atrial and ventricular arrhythmias

Atrial and ventricular arrhythmias

Atrial arrhythmias

Fatigue, bradycardia, exercise intolerance, erectile dysfunction, exacerbation of pulmonary d/o’s

AV block, bradycardia, HF exacerbation, hypotension

Limited role in management of afib/flutterRole in WPW, hemodynamically stable VT

Elimination/metabolismHepatic: acetylation forms less active (but toxic) metabolite NAPARenal: NAPA primarily elim. Renally

Side effects include drug-induced lupus, torsades, vent arrhythmias, aggravation of underlying heart failure

Side effects include GI, cinchonism, hypotension (IV), torsades, vent arrhythmias, hemolytic anemia

Eliminated by hepatic metabolism (3A4) and renal elimination

Indicated for conversion/maintenance of sinus rhythm in patients with afib/flutter.

Significant negative inotropic effects

Side Effects include: GI, anticholinergic symptoms, heart failure, worsening of underlying conduction abnormalities, ventricular arrhythmias, torsades (QT prolongation)

Class 1B antiarrhythmic agent; Used in management of ventricular tach or pulseless VT/Vfib; Dose determined by hepatic function/cardiac output (LVEF)

Normal half-life extends to up to 12 hrs in patients with cirrhosis/CHF; Side-effects include CNS (confusion,tremor,paresthesias), seizures

Used to manage ventricular arrhythmias; esp when responsive to lidocaine. Significantly hepatically metabolized, 1º to inactive metabolites

Substrate for CYP 2D6 and 1A2; Inhibitor of CYP 1A2; Half-life 8-15 hours

Side-effects: CNS, psychosis, GI, aggravation of underlying conduction disturbances or ventricular arrhythmias, rarely blood dyscrasias

Used in afib/flutter for maintenance of sinus rhythmAvoid in patients with structural heart disease or history of CAD

Side-effects: EKG (prolongation of QRS and PR), ventricular arrhythmias, GI, blurred vision; Elimination: renal and hepatic (CYP2D6)

Used for conversion/maintenance of sinus rhythm in patients with afib/flutter.Potent negative inotropic agent (avoid in patients with systolic dysfunction)

Side-effects: GI, worsening of underlying CHF, ventricular arrhythmias; Elimination: hepatic metabolism

Prescribers must complete training program; Requires hospitalization for at least 3 days to initiate (due to risk of proarrhythmias)

Baseline QTc should be less than 440 msec (500 msec if baseline ventricular conduction abnormalities)

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

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

Cardiac: QT prolongation, monitor EKG daily during initiation and q 3 months

Pulmonary toxicity: Pulmonary fibrosis (3-10%), check baseline pulmonary function tests

Thyroid disturbances: hypothyroidism (~20%), hyperthyroidism (~5-10%), monitor thyroid function tests at baseline and q 6 months

Ocular: optic neuritis (1%), photophobia (75-90%) eye exam at baseline and every year thereafter

Liver: elevated hepatic transaminases (5-20%), monitor liver function at baseline and q 6 m

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.

Effective for both conversion and maintenance of NSR in Afib pts. Use only in persons without coronary artery disease or left ventricular dysfunction.

Symptoms precede LV dysfunctionTypically, intervene for symptoms

LV dysfunction may precede symptomsMonitor LV functionIntervene for symptoms AND to preserve cardiac function

Narrowing or obstruction to forward flow while valve is openChronic – slow progression of disease

Backward leakage during time when valve is closedAcute vs chronic

thickness is < 12 mm

Who: Older, calcific or younger, bicuspid

Sx: Angina, syncope, CHF

PE findings: Harsh, systolic ejection murmur at RUSB with radiation to neck, subclavian; sit patient forward, exhalation

Dx: Echo, cardiac cath

Management: Surgery for symptoms

Marfan syndrome, syphilis, ankylosing spondylitis, cystic medial necrosis, aortic dissection, trauma

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

nail bed

head bob

Who: No classic patient, think bicuspid or Marfan syndrome

Sx: CHF symptoms – dyspnea, fatigue

PE findings:Wide pulse pressureSoft, decrescendo diastolic murmurBounding pulses - ‘Water-hammer’, Musset’s head bob, Quincke’s pulse

Dx: Echo

Management: Medical therapy; surgery for acute AI, symptoms, or evidence of LV changes

Think rheumatic heart disease first

PathophysiologyFibrosis, scarring and thickeningCommissural fusionChordae fusion and shorteningDecrease in orifice size

Who: History of rheumatic fever

Symptoms: Dyspnea/orthopnea and fatigue

PE findings: Low pitched, diastolic rumble near apex with opening snapHeard best in left lateral decubitus position

Diagnosis: Echo

Management: Intervene for symptoms – balloon valvuloplasty or mitral valve replacement

Who: Myxomatous valve or post-MI

Symptoms: CHF

PE: Holosystolic murmur at apex

Diagnosis: Echo or cardiac cath

Management: Medical mgt., Surgical for symptoms or decrease in LV function

Who: Young, female

Symptoms: Atypical chest pain, palpitations

PE: Mid-systolic click +/- MR

Diagnosis: Echo – assess MR

Management: Supportive, SBE prophylaxis

Pathology: Narrowing and calcification of TV causing diastolic pressure gradient (5 mmHg) between RA and RV

Symptoms: Related to elevated RA pressuresEdema, hepato-splenomegaly / ascites, fatigue, weakness

Exam: Jugular veinous distension with giant venous A wavesDiastolic murmur at left sternal border which increases with inspiration

Therapy: Balloon Valvuloplasty or Surgical valve replacement if symptoms and mean valve gradient > 5 mm Hg

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

Symptoms: Identical to those of RV failure

Physical exam findings: C-V waves of the jugular veins with venous congestion; Pulsatile liver; Hepatojugular refluxHolosystolic murmur at LSB; Increases with inspiration

Symptoms: Exertional dyspnea; Fatigue; Pre-syncope; Cyanosis

Signs on ECHO: RV hypertrophy; Systolic doming of PV; Transpulmonic gradient