AntiArrhythmics | 暗記メーカー

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4 mechanisms of arrhythmias:

1. altered automaticity 2. delayed after depolarization 3. re-entry 4. conduction block

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latent pacemaker cells take over SA node role- escape beats

altered automaticity

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normal AP of cardiac cell triggers train of abnormal depol

delayed after depol

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refractory tissue reactivated repeatedly and rapidly due to unidirectional block and causes abnormal circuit (WPW, a fib, a flutter)

re-entry

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impulse fails to propagate in non conductive tissue

conduction block

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factors of arrhythmias

arterial hypoxemia electrolyte acid base MI- ST elevation altered SNS- anxiety bradycardia enlarged failing ventricle certain drugs alkalosis> acidosis

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atrial depolarization wave:

p wave

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ventricle depolarization wave

QRS

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ventricle repolarization wave

t wave

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class 1A antiarrymthmics:

quinidine, procainamide, disopryramide

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class 1B antiarrhythmics

lidocaine, mexiletine

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most potent Na+ channel blocker

class 1C

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inhibits conduction rate by HIS-purkinje

class 1C

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inhibits conduction rate by HIS-purkinje

class 1C: flecainide and propafenone most potent Na+ blockers slows depol rate: depress slope of phase 0 AP same inhibits conduction rate by HIS-purkinje suppress: WPW atrial and ventricular tachyarrythmia- a fib a flutter PVCs caution: 1.MI 2.LV dysfunction 3.HF 4. CAD

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no change to action potential

class 1C: flecainide and propafenone most potent Na+ blockers slows depol rate: depress slope of phase 0 AP same inhibits conduction rate by HIS-purkinje suppress: WPW atrial and ventricular tachyarrythmia- a fib a flutter PVCs caution: 1.MI 2.LV dysfunction 3.HF 4. CAD

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class 1C drugs

class 1C: flecainide and propafenone most potent Na+ blockers slows depol rate: depress slope of phase 0 AP same inhibits conduction rate by HIS-purkinje suppress: WPW atrial and ventricular tachyarrythmia- a fib a flutter PVCs caution: 1.MI 2.LV dysfunction 3.HF 4. CAD

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class 1C caution with:

class 1C: flecainide and propafenone most potent Na+ blockers slows depol rate: depress slope of phase 0 AP same inhibits conduction rate by HIS-purkinje suppress: WPW atrial and ventricular tachyarrythmia- a fib a flutter PVCs caution: 1.MI 2.LV dysfunction 3.HF 4. CAD

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strongest

class 1C

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inhibits conduction rate by HIS Purkinje

class 1C

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depresses phase 0 with no AP change

class 1C

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caution: MI, LV dysfunction, HF, CAD

class 1C

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moderate Na+ blocker

class 1A: quinidine, procainamide, disopryramide depress slope of phase 0 decrease depol rate decrease conduction velocity, decrease pacemaker rate direct depression on AV/SA node prolong AP and refractory > prolong QRS (torsades risk) suppress: arterial and ventricular arrhythmias- a fib, a flutter, SVT, WPW caution: torsades myocardial depression > CHF and hypotension toxicity > heart failure LV dysfunction adverse: lupus like syndrome

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direct depression on AV/SA node

class 1A: quinidine, procainamide, disopryramide depress slope of phase 0 decrease depol rate decrease conduction velocity, decrease pacemaker rate direct depression on AV/SA node prolong AP and refractory > prolong QRS (torsades risk) suppress: arterial and ventricular arrhythmias- a fib, a flutter, SVT, WPW caution: torsades myocardial depression > CHF and hypotension toxicity > heart failure LV dysfunction adverse: lupus like syndrome

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prolongs AP and refractory

class 1A: quinidine, procainamide, disopryramide depress slope of phase 0 decrease depol rate decrease conduction velocity, decrease pacemaker rate direct depression on AV/SA node prolong AP and refractory > prolong QRS (torsades risk) suppress: arterial and ventricular arrhythmias- a fib, a flutter, SVT, WPW caution: torsades myocardial depression > CHF and hypotension toxicity > heart failure LV dysfunction adverse: lupus like syndrome

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prolongs QRS (class 1:)

class 1A: quinidine, procainamide, disopryramide depress slope of phase 0 decrease depol rate decrease conduction velocity, decrease pacemaker rate direct depression on AV/SA node prolong AP and refractory > prolong QRS (torsades risk) suppress: arterial and ventricular arrhythmias- a fib, a flutter, SVT, WPW caution: torsades myocardial depression > CHF and hypotension toxicity > heart failure LV dysfunction adverse: lupus like syndrome

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lupus like syndrome

class 1A: quinidine, procainamide, disopryramide depress slope of phase 0 decrease depol rate decrease conduction velocity, decrease pacemaker rate direct depression on AV/SA node prolong AP and refractory > prolong QRS (torsades risk) suppress: arterial and ventricular arrhythmias- a fib, a flutter, SVT, WPW caution: torsades myocardial depression > CHF and hypotension toxicity > heart failure LV dysfunction adverse: lupus like syndrome

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myocardial depression > CHF and hypotension

class 1A: quinidine, procainamide, disopryramide depress slope of phase 0 decrease depol rate decrease conduction velocity, decrease pacemaker rate direct depression on AV/SA node prolong AP and refractory > prolong QRS (torsades risk) suppress: arterial and ventricular arrhythmias- a fib, a flutter, SVT, WPW caution: torsades myocardial depression > CHF and hypotension toxicity > heart failure LV dysfunction adverse: lupus like syndrome

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lupus syndrome

class 1A

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direct depression on AV/SA node

class 1A

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prolongs AP and refractory

class 1A

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weakest Na+ channel blocker

class 1B: lidocaine and mexiletine (oral) weakest effect on Na+ channel, rapidly binds Shortens AP duration and refractory depolarization depression of phase 0 decrease max velocity depression rate (height) decrease rate of spontaneous phase 4 depol decreased automaticity lidocaine: 1st line ventricular tach associated with MI vtach, vfib, PVCs drug interactions: slow metabolism of lidocaine by: GA, cimetidine, propranolol, CHF, acute MI, liver dysfunction, potentiate: barbiturates, phenytoin, rifampin dose: bolus: 2mg/kg gtt: 1-4mg/min active metabolite prolongs E12t adverse: elderly seizure tinnitus hypotension Brady CNS depression dizzy drowsy myocardial depression potentiate NMB

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shortens AP duration and depresses phase 0

class 1B: lidocaine and mexiletine (oral) weakest effect on Na+ channel, rapidly binds Shortens AP duration and refractory depolarization depression of phase 0 decrease max velocity depression rate (height) decrease rate of spontaneous phase 4 depol decreased automaticity lidocaine: 1st line ventricular tach associated with MI vtach, vfib, PVCs drug interactions: slow metabolism of lidocaine by: GA, cimetidine, propranolol, CHF, acute MI, liver dysfunction, potentiate: barbiturates, phenytoin, rifampin dose: bolus: 2mg/kg gtt: 1-4mg/min active metabolite prolongs E12t adverse: elderly seizure tinnitus hypotension Brady CNS depression dizzy drowsy myocardial depression potentiate NMB

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first line vtach with MI

class 1B: lidocaine and mexiletine (oral) weakest effect on Na+ channel, rapidly binds Shortens AP duration and refractory depolarization depression of phase 0 decrease max velocity depression rate (height) decrease rate of spontaneous phase 4 depol decreased automaticity lidocaine: 1st line ventricular tach associated with MI vtach, vfib, PVCs drug interactions: slow metabolism of lidocaine by: GA, cimetidine, propranolol, CHF, acute MI, liver dysfunction, potentiate: barbiturates, phenytoin, rifampin dose: bolus: 2mg/kg gtt: 1-4mg/min active metabolite prolongs E12t adverse: elderly seizure tinnitus hypotension Brady CNS depression dizzy drowsy myocardial depression potentiate NMB

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decrease rate of spontaneous phase 4 depol

class 1B: lidocaine and mexiletine (oral) weakest effect on Na+ channel, rapidly binds Shortens AP duration and refractory depolarization depression of phase 0 decrease max velocity depression rate (height) decrease rate of spontaneous phase 4 depol decreased automaticity lidocaine: 1st line ventricular tach associated with MI vtach, vfib, PVCs drug interactions: slow metabolism of lidocaine by: GA, cimetidine, propranolol, CHF, acute MI, liver dysfunction, potentiate: barbiturates, phenytoin, rifampin dose: bolus: 2mg/kg gtt: 1-4mg/min active metabolite prolongs E12t adverse: elderly seizure tinnitus hypotension Brady CNS depression dizzy drowsy myocardial depression potentiate NMB

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bolus dose of lidocaine

2mg/kg

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gtt lidocaine

1-4 mg/min

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adverse effects of lidocaine

class 1B: lidocaine and mexiletine (oral) weakest effect on Na+ channel, rapidly binds Shortens AP duration and refractory depolarization depression of phase 0 decrease max velocity depression rate (height) decrease rate of spontaneous phase 4 depol decreased automaticity lidocaine: 1st line ventricular tach associated with MI vtach, vfib, PVCs drug interactions: slow metabolism of lidocaine by: GA, cimetidine, propranolol, CHF, acute MI, liver dysfunction, potentiate: barbiturates, phenytoin, rifampin dose: bolus: 2mg/kg gtt: 1-4mg/min active metabolite prolongs E12t adverse: elderly seizure tinnitus hypotension Brady CNS depression dizzy drowsy myocardial depression potentiate NMB

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chronic supraventriuclar vent. arrhythmia treatment

class 1B: lidocaine and mexiletine (oral) weakest effect on Na+ channel, rapidly binds Shortens AP duration and refractory depolarization depression of phase 0 decrease max velocity depression rate (height) decrease rate of spontaneous phase 4 depol decreased automaticity lidocaine: 1st line ventricular tach associated with MI vtach, vfib, PVCs drug interactions: slow metabolism of lidocaine by: GA, cimetidine, propranolol, CHF, acute MI, liver dysfunction, potentiate: barbiturates, phenytoin, rifampin dose: bolus: 2mg/kg gtt: 1-4mg/min active metabolite prolongs E12t adverse: elderly seizure tinnitus hypotension Brady CNS depression dizzy drowsy myocardial depression potentiate NMB

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shortens AP

class 1B

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weakest Na+ channel blocker

class 1B

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decrease max velocity depol rate

class 1B

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decreases rate of spontaneous phase 4 depol

class 1B

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lidocaine

class 1B

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flecainide

class 1C

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propafenone

class 1C

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lidocaine

class 1B

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class II:

beta Adrenergic antagonists depress spontaneous phase 4 depol > decrease SA node discharge slow conduction (repol) through AV node > prolong PR interval prolong AP duration in atria decrease automaticity drug induces slowing of heart rate decrease myocardial oxygen requirements (good for CAD) treat: SVT prophylaxis atrial and vent arry- a fib a flutter PVCs suppress and treat vent arrhythmias during MI and reperfusion tachyarry due to digoxin toxicity Propranolol B1=B2: prevent reoccurrence of tachy arrhythmia due to sympathetic stimuli: 1-10mg Metoprolol B1>>>B2: 5mg Esmolol B1>>>B2: 10-100mg, last 9 min, met by plasma esterase

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this drug prevetns reoccurnace of tachy arrhythmias due to sympathetic stimuli:

propranolol class II beta antagonist B1=B2 1-10mg

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class III effects what phase:

K blockers: phase 3: prolongs repolarization, prolongs refractory (in all tissues) but also phase 1, 2, 3 slows the K efflux which decreases re-entry has properties of class I, II, IV because it affects phase 1,2,3 treats: supraventricular and vent arry prophylaxis before heart surgery to prevent a fib preventative with post cardiac death with no ICD AFIB Amiodarone: afib aflutter refractory SVT, VT, VF post MI (unlike class I) 1st line for VT/VF (not due to MI) and defibrillator didn’t help bolus: 150-300 mg over 2-5 min gtt: 1mg/hr 6 hours, .5mg/hr 18 hours E12t: 29 days and 96% protein bound high VOD active metabolite: desethylamiodarone biliary/intestinal excretion therapeutic plasma level: 1.0-3.5 mcg/ml adverse: Pulm toxitiy Pulm edem ARDS photosentive rash grey/blue skin torsades inhibits p450 thyroid issue and iodine hepatotoixivty

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1st line drug to VT/VF when defib unsuccessful (and not due to MI)

amiodarone

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dose of Amiodarone:

bolus 150-300mg over 2-5 min gtt: 1mg/hr 6 hours .5mg/hr 18 hours

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Amiodarone active metabolite

desethylamiodarone

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excretion of Amiodarone

met liver excreted biliary intestine

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adverse effects of Amiodarone:

K blockers: phase 3: prolongs repolarization, prolongs refractory (in all tissues) but also phase 1, 2, 3 slows the K efflux which decreases re-entry has properties of class I, II, IV because it affects phase 1,2,3 treats: supraventricular and vent arry prophylaxis before heart surgery to prevent a fib preventative with post cardiac death with no ICD AFIB Amiodarone: afib aflutter refractory SVT, VT, VF post MI (unlike class I) 1st line for VT/VF (not due to MI) and defibrillator didn’t help bolus: 150-300 mg over 2-5 min gtt: 1mg/hr 6 hours, .5mg/hr 18 hours E12t: 29 days and 96% protein bound high VOD active metabolite: desethylamiodarone biliary/intestinal excretion therapeutic plasma level: 1.0-3.5 mcg/ml adverse: Pulm toxitiy Pulm edem ARDS photosentive rash grey/blue skin torsades inhibits p450 thyroid issue and iodine hepatotoixivty

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class IV:

class IV: CCB site: AV node: rate control blocks L type Ca++ = slows conduction shortens phase 2 (per her slides but UNTRUE) decrease contractility tx: SVT prophylaxis- prevent reoccurrence ventricular rate control: afib a flutter ***not with ventriclular arrhythmias: vtach, vfib…*** 1. Verapamil (class I CCB prototype) and class IV antriarrhythmic dose: 2.5-10mg over 1-3 min (max 20mg) gtt: 5mcg/kg/min do not use with BB metabolite: norverapamil 2. Diltiazem dose: 5-10mg over 2 min gtt: 10mg/hr contra: decompensated HR Adverse: myocardial depression hypotension constipation n potentiate NMB increase locals toxicity with dantrolene will cause hyperkalemia decrease clearance of digoxin- dig toxicity

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verapamil dose:

1. Verapamil (class I CCB prototype) and class IV antriarrhythmic dose: 2.5-10mg over 1-3 min (max 20mg) gtt: 5mcg/kg/min

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diltiazem dose and gtt:

class IV: CCB site: AV node: rate control blocks L type Ca++ = slows conduction shortens phase 2 (per her slides but UNTRUE) decrease contractility tx: SVT prophylaxis- prevent reoccurrence ventricular rate control: afib a flutter ***not with ventriclular arrhythmias: vtach, vfib…*** 1. Verapamil (class I CCB prototype) and class IV antriarrhythmic dose: 2.5-10mg over 1-3 min (max 20mg) gtt: 5mcg/kg/min do not use with BB metabolite: norverapamil 2. Diltiazem dose: 5-10mg over 2 min gtt: 10mg/hr contra: decompensated HR Adverse: myocardial depression hypotension constipation n potentiate NMB increase locals toxicity with dantrolene will cause hyperkalemia decrease clearance of digoxin- dig toxicity

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adenosine MOA:

binds to adenosine 1 receptor open K channel to increase K currents efflux and hyperpolarize slow AV conduction decrease AP duration acute suppression of AV node acute RX only - SVT dose: 6mg rapid 3 min: 6-12mg t12t: under 10 seconds met: plasma and vascular cell enzymes adverse: bronchospasm- contra with asthma COPD heart block face flushing headache chest pain dyspnea

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adenosine dosing:

6mg then 3 min then 6-12 mg

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adenosine metabolized:

plasma and vascular cell enzymes

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digoxin MOA

cardiac glycoside increase fatal activity and decrease SA node action prolong conduction impulse to AV node and increase AV refractory decrease: HR, afterload, preload positive inotropy (good for CHF) inhibits NA/K pump in cardiac cells treat: afib aflutter dose: 0.5-1mg divided dose over 12-24 hours onset: 30-60 min e12t: 36 hours narrow therapeutic level: 0.5-1.2ng/ml met: RENAL adverse: toxicity: bigemity heart block anorexia, NV confusion - all potentiated with hypokalemia and hypomagnesium toxic: digibind phenytoin pacing atropine

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cardiac glycoside:

digoxin

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dose of digoxin:

0.5-1mg divided over 12-24 hours

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digoxin therapeutic level:

0.5-1.2ng/ml

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will potentiate side effects of this drug if hypokalemic or hypomagniusm

digoxin toxic bigemity anorexia nV heart block confusion

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decrease HR, afterload and preload

digoxin

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digoxin metabolism

renal

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effects resemble lidocaine

phenytoin used when not responsive to other drugs class 1A effects resemble lidocaine treat: digoxin toxicity - vent arrhythmia vent tachy torsades therapeutic level: 10-18 mcg/ml adverse: CNS disturbance inhibit insulin bone marrow depression N

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phenytoin therapeutic level

10-18 mcg/ml

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phenytoin treats:

digoxin toxicity vent tachy torsades