Cardiac ArrhythmiasCardiac Arrhythmias

Andrea SzékelyAndrea Székely

ObjectivesObjectives

• Identify common arrhythmias Identify common arrhythmias encountered by the family physicianencountered by the family physician

• Discuss arrhythmia etiologiesDiscuss arrhythmia etiologies

• Discuss initial primary care work-up Discuss initial primary care work-up and treatmentand treatment

• Practice questionsPractice questions

Physiology of cardiac rate Physiology of cardiac rate and rhythmand rhythm• Cardiac myocytes are Cardiac myocytes are electrically electrically

excitableexcitable• Resting intracellular voltage of myocardial Resting intracellular voltage of myocardial

cells is negative -90mV (SA node is -40mV)cells is negative -90mV (SA node is -40mV)• Resting state - KResting state - K+ + inside and Nainside and Na++ outside cell outside cell

(Na(Na++/K/K+ + pump)pump)• Action potentialAction potential occurs when Na occurs when Na++ enters enters

the cell and sets up a depolarising currentthe cell and sets up a depolarising current• Stimulation of a single muscle fibre causes Stimulation of a single muscle fibre causes

electrical activity to spread across the electrical activity to spread across the myocardiummyocardium

Phases of action potential of Phases of action potential of cardiac cellscardiac cells• Phase 0Phase 0 rapid depolarisation rapid depolarisation

(inflow of Na(inflow of Na+)+)

• Phase 1Phase 1 partial repolarisation partial repolarisation (inward Na(inward Na++ current current deactivated, outflow of Kdeactivated, outflow of K++))

• Phase 2Phase 2 plateau (slow inward plateau (slow inward calcium current)calcium current)

• Phase 3Phase 3 repolarisation repolarisation (calcium current inactivates, K(calcium current inactivates, K++ outflow)outflow)

• Phase 4Phase 4 pacemaker potential pacemaker potential (Slow Na(Slow Na++ inflow, slowing of K inflow, slowing of K++ outflow) ‘autorhythmicity’outflow) ‘autorhythmicity’

• Refractory periodRefractory period (phases 1- (phases 1-3)3)

Phase 4

Phase 0

Phase 1

Phase 2

Phase 3

0 mV

-80mV

II

IIII

IV

Mechanisms of arrhythmia Mechanisms of arrhythmia productionproduction• Re-entryRe-entry (refractory tissue reactivated due (refractory tissue reactivated due

to conduction block, causes abnormal to conduction block, causes abnormal continuous circuit. eg accessory pathways continuous circuit. eg accessory pathways linking atria and ventricles in Wolff-linking atria and ventricles in Wolff-Parkinson-White syndrome) Parkinson-White syndrome)

• Abnormal pacemaker activityAbnormal pacemaker activity in non- in non-conducting/conducting tissue (eg ischaemia)conducting/conducting tissue (eg ischaemia)

• Delayed after-depolarisationDelayed after-depolarisation (automatic (automatic depolarisation of cardiac cell triggers ectopic depolarisation of cardiac cell triggers ectopic beats, can be caused by drugs eg digoxin)beats, can be caused by drugs eg digoxin)

Normal Sinus RhythmNormal Sinus Rhythm

Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.

EKG Characteristics: Regular narrow-complex rhythm

Rate 60-100 bpm

Each QRS complex is proceeded by a P wave

P wave is upright in lead II & downgoing in lead aVR

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Sinus BradycardiaSinus Bradycardia

• HR< 60 bpm; every QRS narrow, preceded by p HR< 60 bpm; every QRS narrow, preceded by p wavewave

• Can be normal in well-conditioned athletesCan be normal in well-conditioned athletes

• HR can be<30 bpm in children, young adults HR can be<30 bpm in children, young adults during sleep, with up to 2 sec pausesduring sleep, with up to 2 sec pauses

Sinus bradycardia--Sinus bradycardia--etiologiesetiologies• Normal agingNormal aging

• 15-25% Acute MI, esp. affecting inferior wall15-25% Acute MI, esp. affecting inferior wall

• Hypothyroidism, infiltrative diseasesHypothyroidism, infiltrative diseases

(sarcoid, amyloid)(sarcoid, amyloid)

• Hypothermia, hypokalemiaHypothermia, hypokalemia

• SLE, collagen vasc diseasesSLE, collagen vasc diseases

• Situational: micturation, coughingSituational: micturation, coughing

• DrugsDrugs: beta-blockers, digitalis, calcium : beta-blockers, digitalis, calcium channel blockers, amiodarone, cimetidine, channel blockers, amiodarone, cimetidine, lithiumlithium

Sinus bradycardia--Sinus bradycardia--treatmenttreatment• No treatment if asymptomaticNo treatment if asymptomatic• Sxs include chest pain (from coronary Sxs include chest pain (from coronary

hypoperfusion), syncope, dizzinesshypoperfusion), syncope, dizziness• OfficeOffice: Evaluate medicine regimen—stop all : Evaluate medicine regimen—stop all

drugs that may causedrugs that may cause• Bradycardia associated with MI will often Bradycardia associated with MI will often

resolve as MI is resolving; will not be the resolve as MI is resolving; will not be the sole sxs of MIsole sxs of MI

• ERER: Atropine if hemodynamic compromise, : Atropine if hemodynamic compromise, syncope, chest painsyncope, chest pain

• PacingPacing

Sinus tachycardiaSinus tachycardia

• HR > 100 bpm, regularHR > 100 bpm, regular

• Often difficult to distinguish p and t wavesOften difficult to distinguish p and t waves

Sinus tachycardia--Sinus tachycardia--etiologiesetiologies• FeverFever• Hyperthyroidism Hyperthyroidism • Effective volume Effective volume

depletion depletion • Anxiety Anxiety • Pheochromocytoma Pheochromocytoma • Sepsis Sepsis • Anemia Anemia • Exposure to stimulants Exposure to stimulants

((nicotinenicotine, , caffeinecaffeine) or ) or illicit drugsillicit drugs

• Hypotension and Hypotension and shock shock

• Pulmonary embolism Pulmonary embolism • Acute coronary Acute coronary

ischemia and ischemia and myocardial infarction myocardial infarction

• Heart failure Heart failure • Chronic pulmonary Chronic pulmonary

disease disease • Hypoxia Hypoxia

Sinus Tachycardia--Sinus Tachycardia--treatmenttreatment

• OfficeOffice: evaluate/treat potential : evaluate/treat potential etiology :check TSH, CBC, optimize etiology :check TSH, CBC, optimize CHF or COPD regimen, evaluate CHF or COPD regimen, evaluate recent OTC drugsrecent OTC drugs

• Verify it is Verify it is sinussinus rhythm rhythm

• If no etiology is found and is If no etiology is found and is bothersome to patients, can treat bothersome to patients, can treat with beta-blockerwith beta-blocker

Sinus ArrhythmiaSinus Arrhythmia

• Variations in the cycle lengths between p waves/ Variations in the cycle lengths between p waves/ QRS complexesQRS complexes

• Will often sound irregular on examWill often sound irregular on exam• Normal p waves, PR interval, normal, narrow QRSNormal p waves, PR interval, normal, narrow QRS

Sinus arrhythmiaSinus arrhythmia

• Usually respiratory--Increase in heart rate Usually respiratory--Increase in heart rate during inspirationduring inspiration

• Exaggerated in children, young adults and Exaggerated in children, young adults and athletes—decreases with ageathletes—decreases with age

• Usually asymptomatic, no treatment or Usually asymptomatic, no treatment or referralreferral

• Can be non-respiratory, often in normal or Can be non-respiratory, often in normal or diseased heart, seen in digitalis toxicitydiseased heart, seen in digitalis toxicity

• Referral may be necessary if not clearly Referral may be necessary if not clearly respiratory, history of heart diseaserespiratory, history of heart disease

Sick Sinus SyndromeSick Sinus Syndrome

•All result in bradycardia

•Sinus bradycardia (rate of ~43 bpm) with a sinus pause

•Often result of tachy-brady syndrome: where a burst of atrial tachycardia (such as afib) is then followed by a long, symptomatic sinus pause/arrest, with no breakthrough junctional rhythm.

Sick Sinus Syndrome--Sick Sinus Syndrome--etiologyetiology• Often due to sinus node fibrosis, SNode Often due to sinus node fibrosis, SNode

arterial atherosclerosis, inflammation arterial atherosclerosis, inflammation (Rheumatic fever, amyloid, sarcoid)(Rheumatic fever, amyloid, sarcoid)

• Occurs in congenital and acquired heart Occurs in congenital and acquired heart disease and after surgerydisease and after surgery

• Hypothyroidism, hypothermiaHypothyroidism, hypothermia• DrugsDrugs: digitalis, lithium, cimetidine, : digitalis, lithium, cimetidine,

methyldopa, reserpine, clonidine, methyldopa, reserpine, clonidine, amiodaroneamiodarone

• Most patients are elderly, may or may not Most patients are elderly, may or may not have symptomshave symptoms

Sick sinus syndrome--Sick sinus syndrome--treatmenttreatment

• Address and treat cardiac conditionsAddress and treat cardiac conditions

• Review med list, TSHReview med list, TSH

• Pacemaker for most is requiredPacemaker for most is required

Paroxysmal Supraventricular Paroxysmal Supraventricular TachycardiaTachycardia

• Refers to supraventricular tachycardia Refers to supraventricular tachycardia other than afib, aflutter and MATother than afib, aflutter and MAT

• Occurs in 35 per 100,000 person-yearsOccurs in 35 per 100,000 person-years

• Usually due to reentry—AVNRT or AVRTUsually due to reentry—AVNRT or AVRT

PSVTPSVT

• Initial eval: Is the patient stable?Initial eval: Is the patient stable?• Determine quickly if sinus rhythmDetermine quickly if sinus rhythm• If not sinus and unstable, cardioversionIf not sinus and unstable, cardioversion• Unstable sinus tachycardia---IV beta-Unstable sinus tachycardia---IV beta-

blocker, and treat cause blocker, and treat cause

• Sxs of instability would include: chest pain, Sxs of instability would include: chest pain, decreased consciousness, short of breath, decreased consciousness, short of breath, shock, hypotension—unstable sxs shock, hypotension—unstable sxs require require shockshock

PSVTPSVT

• If stable, determine whether If stable, determine whether regularregular rhythm (sinus or PSVT) vs rhythm (sinus or PSVT) vs irregularirregular (afib/flutter, MAT)? p waves (MAT vs. (afib/flutter, MAT)? p waves (MAT vs. AF)?AF)?

• If If regularregular, determine whether p waves , determine whether p waves are present, if can’t see---administer are present, if can’t see---administer adenosine (6mg, can give 2 doses) or adenosine (6mg, can give 2 doses) or CSM or other vagal maneuvers)CSM or other vagal maneuvers)

PSVTPSVT

• CSM or adenosine commonly CSM or adenosine commonly terminate the arrhythmia, esp, AVRT terminate the arrhythmia, esp, AVRT or AVNRTor AVNRT

• Can also use CCB or beta blockers to Can also use CCB or beta blockers to terminate, if availableterminate, if available

• Counsel to avoid triggers, caffeine, Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stressEtoh, pseudoephedrine, stress

PSVTPSVT

• No p wavesNo p waves —junctional tachycardia, —junctional tachycardia, AVRT or AVNRT, AfibAVRT or AVNRT, Afib

• AVRT and AVNRT: can have AVRT and AVNRT: can have retrograde pretrograde p waves and short RP waves and short RP intervalinterval

• Abnormal p wavesAbnormal p waves morphology: MAT morphology: MAT

Atrial FibrillationAtrial Fibrillation

• Irregular rhythm Irregular rhythm • Absence of definite p wavesAbsence of definite p waves• Narrow QRSNarrow QRS• Can be accompanied by rapid ventricular responseCan be accompanied by rapid ventricular response

Atrial Fibrillation—causes and Atrial Fibrillation—causes and associationsassociations

• HypertensionHypertension

• Hyperthyroidism and Hyperthyroidism and subclinical subclinical hyperthyroidismhyperthyroidism

• CHF (10-30%), CADCHF (10-30%), CAD

• Uncommon Uncommon presentation of ACSpresentation of ACS

• Mitral and tricuspid Mitral and tricuspid valve diseasevalve disease

• Hypertrophic Hypertrophic cardiomyopathycardiomyopathy

• COPDCOPD

• OSAOSA

• ETOHETOH

• CaffeineCaffeine

• DigitalisDigitalis

• FamilialFamilial

• Congenital (ASD)Congenital (ASD)

Atrial fibrillation--Atrial fibrillation--assessmentassessment• H & P—assess heart rate, sxs of SOB, H & P—assess heart rate, sxs of SOB,

chest pain, edema (signs of failure)chest pain, edema (signs of failure)• If unstable, need to cardiovertIf unstable, need to cardiovert• Echocardiogram to evaluate valvular and Echocardiogram to evaluate valvular and

overall functionoverall function• Check TSHCheck TSH• Assess for RVRAssess for RVR• Assess onset of sxs—in the last 24-48 Assess onset of sxs—in the last 24-48

hours? Sudden onset? Or no sxs?hours? Sudden onset? Or no sxs?

Atrial fibrillation--Atrial fibrillation--managementmanagement• Rhythm vs Rate control—if onset is within last Rhythm vs Rate control—if onset is within last

24-48 hours, may be able to arrange 24-48 hours, may be able to arrange cardioversion—use heparin around procedurecardioversion—use heparin around procedure

• Need TEE if valvular disease (high risk of Need TEE if valvular disease (high risk of thrombus)thrombus)

• If unable to If unable to definitely definitely conclude onset in last conclude onset in last 24-48 hours: need 4-6 weeks of 24-48 hours: need 4-6 weeks of anticoagulation prior to cardioversion, and anticoagulation prior to cardioversion, and warfarin for 4-12 weeks afterwarfarin for 4-12 weeks after

Atrial FibrillationAtrial Fibrillation

• CardioversionCardioversion: synchronized (w/QRS) : synchronized (w/QRS) delivery of current to heart; delivery of current to heart; depolarizes tissue in a reentrant depolarizes tissue in a reentrant circuit; afib involves more cardiac circuit; afib involves more cardiac tissue, but cardioverttissue, but cardiovert

• DefibrillationDefibrillation: non-synchronized : non-synchronized delivery of currentdelivery of current

Atrial fibrillation--Atrial fibrillation--managementmanagement• Rate controlRate control with chronic anticoagulation is with chronic anticoagulation is

recommended for first line approach for recommended for first line approach for majority of patients; overall Afib is a stable majority of patients; overall Afib is a stable rhythmrhythm

• Beta-blockers (atenolol and metoprolol) or Beta-blockers (atenolol and metoprolol) or calcium channel blockers (verapamil or calcium channel blockers (verapamil or diltiazem) recommended. Digoxin not diltiazem) recommended. Digoxin not recommended for rate controlrecommended for rate control

• Anticoagulation: LMWH and then warfarin; Anticoagulation: LMWH and then warfarin; can use aspirin for anticoagulation if CI to can use aspirin for anticoagulation if CI to warfarin, not as effectivewarfarin, not as effective

Atrial fibrillation--Atrial fibrillation--managementmanagement

• Goal INR of 2.5 (2.0-3.0)Goal INR of 2.5 (2.0-3.0)

• Rhythm control-Rhythm control---second line --second line approach, if unable to control rate or approach, if unable to control rate or pt with persistent sxspt with persistent sxs

• Can also consider radiofrequency Can also consider radiofrequency ablation at pulm veinsablation at pulm veins

PACPAC

• P wave from another atrial focusP wave from another atrial focus• Occurs earlier in cycleOccurs earlier in cycle• Different morphology of p waveDifferent morphology of p wave

PACPAC

• Benign, common cause of perceived Benign, common cause of perceived irregular rhythmirregular rhythm

• Can cause sxs: “skipping” beats, Can cause sxs: “skipping” beats, palpitationspalpitations

• No treatment, reassuranceNo treatment, reassurance• With sxs, may advise to stop smoking, With sxs, may advise to stop smoking,

decrease caffeine and ETOHdecrease caffeine and ETOH• Can use beta-blockers to reduce Can use beta-blockers to reduce

frequencyfrequency

11stst Degree AV Block Degree AV Block

• PR interval >200msPR interval >200ms

• If accompanied by wide QRS, refer to cardiology, If accompanied by wide QRS, refer to cardiology, high risk of progression to 2high risk of progression to 2ndnd and 3 and 3rdrd deg block deg block

• Otherwise, benign if asymptomaticOtherwise, benign if asymptomatic

22ndnd Degree AV Block Mobitz Degree AV Block Mobitz type I (Wenckebach)type I (Wenckebach)

• Progressive PR longation, with eventual Progressive PR longation, with eventual non-conduction of a p wavenon-conduction of a p wave

• May be in 2:1 or 3:1 May be in 2:1 or 3:1

Wenckebach, Mobitz type IWenckebach, Mobitz type I

• Usually asymptomatic, but with accompanying Usually asymptomatic, but with accompanying bradycardia can cause angina, syncope esp in bradycardia can cause angina, syncope esp in elderly—will need pacing if sxselderly—will need pacing if sxs

• Also can be caused by drugs that slow conduction Also can be caused by drugs that slow conduction (BB, CCB, dig)(BB, CCB, dig)

• 2-10% long distance runners2-10% long distance runners• Correct if reversible cause, avoid meds that block Correct if reversible cause, avoid meds that block

conductionconduction

22ndnd degree block Type II degree block Type II (Mobitz 2)(Mobitz 2)

• Normal PR intervals with sudden failure of a p wave to Normal PR intervals with sudden failure of a p wave to conductconduct

• Usually below AV node and accompanied by BBB or Usually below AV node and accompanied by BBB or fascicular blockfascicular block

• Often causes pre/syncope; exercise worsens sxsOften causes pre/syncope; exercise worsens sxs• Generally need pacing, possibly urgently if symptomaticGenerally need pacing, possibly urgently if symptomatic

33rdrd Degree AV Block Degree AV Block

• Complete AV disassociation, HR is a ventricular rateComplete AV disassociation, HR is a ventricular rate

• Will often cause dizziness, syncope, angina, heart failureWill often cause dizziness, syncope, angina, heart failure

• Can degenerate to Vtach and VfibCan degenerate to Vtach and Vfib

• Will need pacing, urgent referralWill need pacing, urgent referral

PVCPVC

• Extremely common throughout the population, Extremely common throughout the population, both with and without heart diseaseboth with and without heart disease

• Usually asymptomatic, except rarely dizziness or Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and fatigue in patients that have frequent PVCs and significant LV dysfunctionsignificant LV dysfunction

PVCPVC

• No treatment is necessary, risk No treatment is necessary, risk outweighs benefitoutweighs benefit

• ReassuranceReassurance

• Optimize cardiac and pulmonary Optimize cardiac and pulmonary disease managementdisease management

Non-sustained Ventricular Non-sustained Ventricular tachycardiatachycardia

• Defined as 3 or more consecutive ventricular beatsDefined as 3 or more consecutive ventricular beats

• Rate of >120 bpm, lasting less than 30 secondsRate of >120 bpm, lasting less than 30 seconds

• May be discovered on Holter, or other exercise May be discovered on Holter, or other exercise testingtesting

Non-sustained ventricular Non-sustained ventricular tachycardiatachycardia

• Need to exclude heart disease with Echo Need to exclude heart disease with Echo and stress testingand stress testing

• If normal, there is no increased risk of If normal, there is no increased risk of deathdeath

• May need anti-arrhythmia treatment if sxsMay need anti-arrhythmia treatment if sxs

• In presence of heart disease, increased risk In presence of heart disease, increased risk of sudden deathof sudden death

• Need referral for EPS and/or prolonged Need referral for EPS and/or prolonged Holter monitoringHolter monitoring

Ventricular fibrillationVentricular fibrillation

• DefibrillationDefibrillation

Pulseless Electrical ActivityPulseless Electrical Activity

Sinus Tachycardia Sinus Tachycardia With No PulseWith No Pulse

PEA? Asystole?PEA? Asystole?

Pulseless Electrical Activity?Pulseless Electrical Activity?

Pulseless Electrical Activity?Pulseless Electrical Activity?

Pulseless Electrical Pulseless Electrical ActivityActivity

Atropine 1 mg IV (if PEA rate is slow),repeat every 3 to 5 minutes as needed, to a totaldose of 0.04 mg/kg

• Hypovolemia• Hypoxia• Hydrogen ion—acidosis• Hyper-/hypokalemia• Hypothermia

• “Tablets” (drug OD, accidents)• Tamponade, cardiac• Tension pneumothorax• Thrombosis, coronary (ACS)• Thrombosis, pulmonary (embolism)

Review for most frequent causes

3

1

Epinephrine 1 mg IV push,repeat every 3 to 5 minutes

2

Vaughan Williams Vaughan Williams classification of antiarrhythmic classification of antiarrhythmic drugsdrugs

• Class IClass I: : block sodium channels block sodium channels – Ia (quinidine, procainamide, Ia (quinidine, procainamide,

disopyramide) disopyramide) APAP– Ib (lignocaine) Ib (lignocaine) APAP– Ic (flecainide) Ic (flecainide) APAP

• Class IIClass II: : ß-adrenoceptor ß-adrenoceptor antagonists (atenolol, sotalol)antagonists (atenolol, sotalol)

• Class IIIClass III:: prolong action prolong action potential and prolong refractory potential and prolong refractory period (suppress re-entrant period (suppress re-entrant rhythms) (amiodarone, sotalol)rhythms) (amiodarone, sotalol)

• Class IVClass IV:: Calcium channel Calcium channel antagonists. Impair impulse antagonists. Impair impulse propagation in nodal and propagation in nodal and damaged areas (verapamil)damaged areas (verapamil)

Phase 4

Phase 0

Phase 1

Phase 2

Phase 3

0 mV

-80mV

II

IIII

IV

Management of arrhythmiasManagement of arrhythmias

• Acute management (clinical Acute management (clinical assessment of patient and diagnosis)assessment of patient and diagnosis)

• ProphylaxisProphylaxis

• Non-pharmacologicalNon-pharmacological

• Pharmacological (some antiarrhythmics Pharmacological (some antiarrhythmics are also proarrhythmic)are also proarrhythmic)

Non-pharmacological Non-pharmacological treatmenttreatment• AcuteAcute

– Vagal manoeuvresVagal manoeuvres– DC cardioversionDC cardioversion

• ProphylaxisProphylaxis– Radiofrequency ablationRadiofrequency ablation– Implantable defibrillatorImplantable defibrillator

• PacingPacing (external, temporary, (external, temporary, permanent)permanent)

Pharmacological treatment-Pharmacological treatment-Lignocaine (Lidocaine) Lignocaine (Lidocaine) • Class IbClass Ib (blocks Na (blocks Na++ channels, reduces AP channels, reduces AP

duration)duration)• Ventricular arrhythmias (acute Rx)Ventricular arrhythmias (acute Rx)• IV infusion only (2 hour half life, high first IV infusion only (2 hour half life, high first

pass metabolism)pass metabolism)• Hepatic metabolism (inhibited by Hepatic metabolism (inhibited by

cimetidine, propranolol)cimetidine, propranolol)• SE mainly CNS - drowsiness, SE mainly CNS - drowsiness,

disorientation, convulsions, hypotensiondisorientation, convulsions, hypotension

FlecainideFlecainide

• Class IcClass Ic (block Na (block Na++ channels, no change to channels, no change to AP)AP)

• Slows conduction in all cardiac cellsSlows conduction in all cardiac cells• Acute Rx /prophylaxisAcute Rx /prophylaxis• Supraventricular tachycardiasSupraventricular tachycardias• Paroxysmal atrial fibrillationParoxysmal atrial fibrillation• Ventricular tachycardiasVentricular tachycardias• Oral/IVOral/IV• Long acting (T1/2 14 hours)Long acting (T1/2 14 hours)• Hepatic metabolism, urinary eliminationHepatic metabolism, urinary elimination

FlecainideFlecainide

• CAST (Cardiac Arrhythmia CAST (Cardiac Arrhythmia Suppression Trial) 1989 – increased Suppression Trial) 1989 – increased mortality post MI (VF arrest)mortality post MI (VF arrest)

• SE- cardiac failure, ventricular SE- cardiac failure, ventricular arrhythmias, blurred vision, arrhythmias, blurred vision, abdominal discomfort, nausea, abdominal discomfort, nausea, paraesthesia, dizzyness, tremor, paraesthesia, dizzyness, tremor, metallic tastemetallic taste

AmiodaroneAmiodarone• Class IIIClass III - increases refractory period and AP - increases refractory period and AP• Major effect acutely is depression of AV nodeMajor effect acutely is depression of AV node• Acute Rx/prophylaxisAcute Rx/prophylaxis• Atrial and ventricular arrhythmiasAtrial and ventricular arrhythmias• Oral or IV (central line)Oral or IV (central line)• Loading and maintenance dosesLoading and maintenance doses• T1/2 54 daysT1/2 54 days• Large volume of distributionLarge volume of distribution• AccumulatesAccumulates• Hepatic metabolism- biliary and intestinal Hepatic metabolism- biliary and intestinal

excretionexcretion

Amiodarone – adverse Amiodarone – adverse effectseffects• Photosensitive rashesPhotosensitive rashes• Grey/blue discolouration of skinGrey/blue discolouration of skin• Thyroid abnormalities 2%Thyroid abnormalities 2%• Pulmonary fibrosisPulmonary fibrosis• Corneal depositsCorneal deposits• CNS/GI disturbanceCNS/GI disturbance• Pro-arrhythmic effects (torsade de pointe)Pro-arrhythmic effects (torsade de pointe)• Heart blockHeart block• Nightmares 25%Nightmares 25%• Abnormal LFT 20%Abnormal LFT 20%• Interacts with digoxin, warfarin (reduces clearance)Interacts with digoxin, warfarin (reduces clearance)

AdenosineAdenosine

• Not in Vaughan Williams classNot in Vaughan Williams class

• Purine nucleotide (activates adenosine Purine nucleotide (activates adenosine receptors)receptors)

• Slows AV nodal conductionSlows AV nodal conduction

• Acute RxAcute Rx

• Termination of SVT/ diagnosis of VTTermination of SVT/ diagnosis of VT

• Given IV only (rapid bolus)Given IV only (rapid bolus)

• T1/2 < 2secondsT1/2 < 2seconds

Adenosine- adverse effectsAdenosine- adverse effects

• Feeling of impending doom!Feeling of impending doom!

• Flushing, dyspnoea, chest pain, Flushing, dyspnoea, chest pain, transient arrhythmiastransient arrhythmias

• Contraindicated in asthma, heart Contraindicated in asthma, heart blockblock

VerapamilVerapamil

• Class IVClass IV (calcium channel blocker) (calcium channel blocker)• Prolongs conduction and refractoriness in AV Prolongs conduction and refractoriness in AV

node, slows rate of conduction of SA nodenode, slows rate of conduction of SA node• Acute Rx /prophylaxisAcute Rx /prophylaxis• Used IV/oralUsed IV/oral• SUPRAVENTRICULAR NOT VENTRICULAR SUPRAVENTRICULAR NOT VENTRICULAR

ARRHYTHMIAS (cardiovascular collapse)ARRHYTHMIAS (cardiovascular collapse)• Do not use IV verapamil with ß- blocker (heart Do not use IV verapamil with ß- blocker (heart

block)block)• T1/2 6-8 hoursT1/2 6-8 hours

Verapamil- adverse effectsVerapamil- adverse effects

• Heart failureHeart failure

• ConstipationConstipation

• BradycardiaBradycardia

• NauseaNausea

DigoxinDigoxin

• Not in Vaughan Williams class Not in Vaughan Williams class

• Cardiac glycoside (digitalis, foxglove)Cardiac glycoside (digitalis, foxglove)

• Act on Na/K-ATPase of cell membrane Act on Na/K-ATPase of cell membrane (inhibits Na(inhibits Na++/K/K++ pump, increases pump, increases intracellular Naintracellular Na++ and calcium)/ increases and calcium)/ increases vagal activityvagal activity

• Increase cardiac contraction and slows AV Increase cardiac contraction and slows AV conduction by increasing AV node conduction by increasing AV node refractory periodrefractory period

DigoxinDigoxin• Atrial fibrillation or flutter (controls Atrial fibrillation or flutter (controls

ventricular rate)ventricular rate)• Acute Rx/prophylaxisAcute Rx/prophylaxis• Oral/IVOral/IV• Loading and maintenance dosesLoading and maintenance doses• T1/2 36 hoursT1/2 36 hours• Excreted by kidneysExcreted by kidneys• Narrow therapeutic indexNarrow therapeutic index• Therapeutic drug monitoringTherapeutic drug monitoring• Reduce dose in elderly/renal impairmentReduce dose in elderly/renal impairment

Digoxin – adverse effectsDigoxin – adverse effects

• Arrhythmias, heart block, anorexia, Arrhythmias, heart block, anorexia, nausea, diarrhoea, xanthopsia, nausea, diarrhoea, xanthopsia, gynaecomastia, confusion, agitation gynaecomastia, confusion, agitation

• AE potentiated by hypokalaemia and AE potentiated by hypokalaemia and hypomagnesaemiahypomagnesaemia

• Overdose –Digibind (digoxin binding Overdose –Digibind (digoxin binding antibody fragments), phenytoin for antibody fragments), phenytoin for ventricular arrhythmias, pacing, ventricular arrhythmias, pacing, atropine atropine

Clinical casesClinical cases

36 year old woman with 36 year old woman with asthma has ‘thumping in chest’asthma has ‘thumping in chest’

76 year old man with 76 year old man with breathlessnessbreathlessness

54 year woman collapses 24 54 year woman collapses 24 hours post MIhours post MI

60 year old man with recurrent 60 year old man with recurrent blackoutsblackouts

SummarySummary• Anti-arrhythmic drugs are classified by their Anti-arrhythmic drugs are classified by their

effect on the cardiac action potentialeffect on the cardiac action potential• Not all drugs fit this classificationNot all drugs fit this classification• In clinical practice treatment of arrhythmias In clinical practice treatment of arrhythmias

is determined by the type of arrhythmia is determined by the type of arrhythmia (SVT, VT) and clinical condition of the (SVT, VT) and clinical condition of the patientpatient

• Anti-arrhythmic drugs are efficacious but Anti-arrhythmic drugs are efficacious but may have serious adverse effectsmay have serious adverse effects

• Not all arrhythmias are treated with drug Not all arrhythmias are treated with drug therapy alonetherapy alone

Practice Questions—Case 1Practice Questions—Case 1

• 37-year old male comes to office for 37-year old male comes to office for “skipping heart beats.” Going on “skipping heart beats.” Going on over last 8 months, no other sxs: no over last 8 months, no other sxs: no sweating, palpitations, wt loss, chest sweating, palpitations, wt loss, chest pain, anxiety or pleuritic chest pain.pain, anxiety or pleuritic chest pain.

On PE, BP is 100/70, normal S1S2, On PE, BP is 100/70, normal S1S2, no murmurs/gallops. You hear about no murmurs/gallops. You hear about 5 premature beats.5 premature beats.

Practice QuestionsPractice Questions

1.1. What is the most commonly What is the most commonly encountered “premature encountered “premature contraction?”contraction?”

a. a ventricular premature beata. a ventricular premature beat

b. an atrial premature beatb. an atrial premature beat

c. atrial flutterc. atrial flutter

d. atrial fibrillationd. atrial fibrillation

e. none of the abovee. none of the above

Practice questionsPractice questions

Answer B: atrial premature beatsAnswer B: atrial premature beats

• Most common premature beat in Most common premature beat in adultsadults

• Almost always asxsAlmost always asxs

• Often patients c/of sxs during stress, Often patients c/of sxs during stress, or while laying quietlyor while laying quietly

Practice QuestionsPractice Questions

2. Most atrial premature beats discovered 2. Most atrial premature beats discovered on clinical examination are:on clinical examination are:a. associated with COPDa. associated with COPDb. completely benignb. completely benignc. associated with valvular heart c. associated with valvular heart diseasediseased. associated with an increase in d. associated with an increase in cardiovascular mortalitycardiovascular mortalitye. None of the abovee. None of the above

Practice QuestionsPractice Questions

Answer B: completely benignAnswer B: completely benign

• require no treatment except require no treatment except reassurancereassurance

Practice QuestionsPractice Questions

3. Most ventricular premature beats 3. Most ventricular premature beats discovered on clinical exam are:discovered on clinical exam are:a. associated with COPDa. associated with COPDb. completely benignb. completely benignc. associated with valvular heart c. associated with valvular heart diseasediseased. associated with increased d. associated with increased cardiovascular mortalitycardiovascular mortalitye. none of the abovee. none of the above

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Answer B: completely benignAnswer B: completely benign

• Patients need reassurancePatients need reassurance

• Usually asymptomaticUsually asymptomatic

• Occasionally can be associated with Occasionally can be associated with severe heart disease with multiple severe heart disease with multiple PVCs in a row---Vtach---which can PVCs in a row---Vtach---which can cause syncope, chest pain, dyspnea cause syncope, chest pain, dyspnea and cardiac arrestand cardiac arrest

Practice Questions—Case 2Practice Questions—Case 2

A 51 year old male presents to the A 51 year old male presents to the emergency room with an acute emergency room with an acute episode of chest pain. He has a episode of chest pain. He has a history of afib. On exam BP is 70/50, history of afib. On exam BP is 70/50, and ventricular rate is 160. He is in and ventricular rate is 160. He is in acute distress. His resp rate is 32. acute distress. His resp rate is 32. ECG shows afib with rapid ventricular ECG shows afib with rapid ventricular response. response.

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4. What should your first step in 4. What should your first step in management be?management be?

a. digitalize the patienta. digitalize the patient

b. give the patient IV verapamilb. give the patient IV verapamil

c. give the patient IV adenosinec. give the patient IV adenosine

d. start synchronized cardioversiond. start synchronized cardioversion

e. start rapid IV hydratione. start rapid IV hydration

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Answer D: this Answer D: this patient has an acute onset afib with RVR, with chest pain and hypotension. Treatment of choice per ACLS protocol is cardioversion.

Practice Questions—Case 3Practice Questions—Case 3

A 44 year old male comes to your ER A 44 year old male comes to your ER saying he has palpitations. Denies chest saying he has palpitations. Denies chest pain or SOB. No known history of CAD or pain or SOB. No known history of CAD or risk factors except mild obesity. Does risk factors except mild obesity. Does admit to drinking heavily the night admit to drinking heavily the night before.before.

On PE, BP is 120/80 and heart rate is On PE, BP is 120/80 and heart rate is 160. ECG confirms afib with rapid 160. ECG confirms afib with rapid ventricular response.ventricular response.

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5. What should you do at this time?5. What should you do at this time?

a. digitalize the patienta. digitalize the patient

b. treat the patient with IV verapamilb. treat the patient with IV verapamil

c. treat the patient with IV procainamidec. treat the patient with IV procainamide

d. cardiovert the patientd. cardiovert the patient

e. have him perform a Valsalva e. have him perform a Valsalva maneuver by rebreathing into a paper maneuver by rebreathing into a paper bagbag

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Answer B: this patient has the same Answer B: this patient has the same condition but is hemodynamically condition but is hemodynamically stable. His afib is following Etoh stable. His afib is following Etoh ingestion, not uncommon after ingestion, not uncommon after holidays and weekends.holidays and weekends.

Initial management would be rate Initial management would be rate controlcontrol

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6. What is the recommended treatment 6. What is the recommended treatment for PSVT with hemodynamic for PSVT with hemodynamic compromise?compromise?

a. synchronized cardioversiona. synchronized cardioversion

b. direct-current counter shockb. direct-current counter shock

c. IV adenosinec. IV adenosine

d. IV verapamild. IV verapamil

e. IV digoxine. IV digoxin

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Answer A: cardioversion. If a patient Answer A: cardioversion. If a patient presents with stable PSVT, start with presents with stable PSVT, start with vagal maneuvers or adenosine. Vagal vagal maneuvers or adenosine. Vagal maneuvers can help diagnosis, by maneuvers can help diagnosis, by slowing rate, and treat arrhythmia. slowing rate, and treat arrhythmia. CSM, ice pack, Valsalva are all possible CSM, ice pack, Valsalva are all possible maneuvers. Pressing eyeballs---not maneuvers. Pressing eyeballs---not recommended. This patient however is recommended. This patient however is unstable--shock unstable--shock

Practice QuestionsPractice Questions

Which of the following statements about Which of the following statements about treatment of atrial premature beats is true?treatment of atrial premature beats is true?

a. the benefit outweighs the riska. the benefit outweighs the risk

b. the risk outweighs the benefitb. the risk outweighs the benefit

c. the risk and benefit are equalc. the risk and benefit are equal

d. the risk and benefit depend on the d. the risk and benefit depend on the patientpatient

e. nobody really knows for suree. nobody really knows for sure

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Answer B: risk outweighs benefitAnswer B: risk outweighs benefit

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Which of the following statements about Which of the following statements about treatment of ventricular premature beats is treatment of ventricular premature beats is true?true?

a. the benefit outweighs the riska. the benefit outweighs the risk

b. the risk outweighs the benefitb. the risk outweighs the benefit

c. the risk and benefit are equalc. the risk and benefit are equal

d. the risk and benefit depend on the d. the risk and benefit depend on the patientpatient

e. nobody really knows for suree. nobody really knows for sure

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Answer B: risk outweighs benefit.Answer B: risk outweighs benefit.

For both PACs and PVCs, unless For both PACs and PVCs, unless circumstances are unusual and circumstances are unusual and documented by EPS studies, multiple documented by EPS studies, multiple trials have shown that the risk trials have shown that the risk outweighs the benefit for both.outweighs the benefit for both.

Practice questionsPractice questions

• A 50 year old male is brought to the A 50 year old male is brought to the emergency department via EMS c/of emergency department via EMS c/of severe substernal chest pain, severe substernal chest pain, w/nausea, diaphoresis. BP is 90mm w/nausea, diaphoresis. BP is 90mm Hg systolic, HR 120 bpm. Pulse Hg systolic, HR 120 bpm. Pulse disappears on arrival and monitor disappears on arrival and monitor shows Vtach. Venous access is shows Vtach. Venous access is established and he has O2 via mask.established and he has O2 via mask.

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True or false, the appropriate True or false, the appropriate management at this time includes:management at this time includes:

1.1. Lidocaine 1 mg/kg IV pushLidocaine 1 mg/kg IV push

2.2. Procainamide, 20mg/min IV infusionProcainamide, 20mg/min IV infusion

3.3. DefibrillationDefibrillation

4.4. Transvenous pacemakerTransvenous pacemaker

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• 1. False, 2. False, 3. True, 4. False1. False, 2. False, 3. True, 4. False

The patient is having an MI. Unstable, The patient is having an MI. Unstable, pulseless pulseless Vtach is treated with Vtach is treated with defibrillation---unstable pts with Vtach defibrillation---unstable pts with Vtach include those with sxs (chest pain, SOB), include those with sxs (chest pain, SOB), hypotension, CHF, ischemia or hypotension, CHF, ischemia or infarction, if still with pulse—infarction, if still with pulse—cardioversion first, then defibrillate if cardioversion first, then defibrillate if necessary.necessary.

Practice QuestionsPractice Questions

His rhythm stabilizes and you note His rhythm stabilizes and you note evidence of acute MI on EKG. Which of evidence of acute MI on EKG. Which of the following should be taken into the following should be taken into account when considering thrombolytic account when considering thrombolytic therapy?therapy?

5. Degree of coronary occlusion5. Degree of coronary occlusion

6. Whether the patient has a hx of stroke6. Whether the patient has a hx of stroke

7. Time interval from onset of sxs7. Time interval from onset of sxs

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5. false, 6. true, 7. true5. false, 6. true, 7. true tPa is contraindicated in persons with tPa is contraindicated in persons with

recent (<3 months) hx of internal bleeding; recent (<3 months) hx of internal bleeding; known hemorrhagic diathesis; hx of stroke, known hemorrhagic diathesis; hx of stroke, intracranial AV malformation, neoplasm, intracranial AV malformation, neoplasm, aneurysm; severe, uncontrolled htn just aneurysm; severe, uncontrolled htn just prior to administration; recent intracranial, prior to administration; recent intracranial, intraocular, intraspinal surgery; recent intraocular, intraspinal surgery; recent trauma or cpr; recent tPa. Thrombolytics are trauma or cpr; recent tPa. Thrombolytics are considered appropriate up to 12 hours after considered appropriate up to 12 hours after sxs onset.sxs onset.