Case presentationCase presentationAtrial fibrillationAtrial fibrillation

Presented by Ri Presented by Ri 顏廷珊、顏廷珊、 Ri Ri 江易穎江易穎Directed by Dr. Directed by Dr. 蕭柏妮蕭柏妮

Admission summaryAdmission summary

林林 XX, 51y/o, male, 75kgXX, 51y/o, male, 75kgUrge incontinence in 2001-8Urge incontinence in 2001-8– 外院，外院， treated as UTItreated as UTI

Painless gross hematuria in 2002-9Painless gross hematuria in 2002-9– 馬偕，馬偕， urine cytology= TCC, Af notedurine cytology= TCC, Af noted– IVP= bladder tumor (multiple)IVP= bladder tumor (multiple)– Bladder TCCBladder TCC TUR-BT & MMC*1 in 2002-1 TUR-BT & MMC*1 in 2002-1

00

Transferred to NTUHTransferred to NTUH– Severe dysuriaSevere dysuria– Patho= bladder TCC with muscle invasionPatho= bladder TCC with muscle invasion– Admission on 11/3, Arrange radical cystectomAdmission on 11/3, Arrange radical cystectom

yy

Past historyPast historyAdmission EKG = Admission EKG = AfAf + VPC + VPCAdmission CXRAdmission CXRLab dataLab data

Lab data 911103Lab data 911103

RBC 4.54 Na 137.7HGB 14.3 K 4.37HCT 41.4 Cl 102MCV 91.2 Ca 2.28PLT 371WBC 12240 Bleeding time 5.5

PT 12.2T-Bil 0.9 PT control 12.2GOT 29 inr 1BUN 18.5 APTT 28.1

Creatinine 1.34 APTT control 35.5

Preparation for 1Preparation for 1stst OP on 11-05 OP on 11-05

CV consultation report on 11-04CV consultation report on 11-04– Af, abberant QRS, no specific ST-T changeAf, abberant QRS, no specific ST-T change– HR= 75~85 ;BP= 110/70; RR= 8HR= 75~85 ;BP= 110/70; RR= 8– AsymptomaticAsymptomatic ， ， NYHA I NYHA I （（ 6F6F ））– Goldman multifactorial cardiac risk indexGoldman multifactorial cardiac risk index

Multi-factorial Cardiac Risk Index (Goldman)Multi-factorial Cardiac Risk Index (Goldman)Ref: Goldman M, Caldera D, Southwick, et al: Multifactorial index of cardiac risk in non-cardiac surgRef: Goldman M, Caldera D, Southwick, et al: Multifactorial index of cardiac risk in non-cardiac surg

ical procedures. N Engl J Med Oct 1977ical procedures. N Engl J Med Oct 1977..

index of cardiac risk in the non-cardiac surgeryindex of cardiac risk in the non-cardiac surgery

CV Suggestion (11/4):CV Suggestion (11/4):– Digoxin 1# qd (11/6), F/U digoxin level (11/13)Digoxin 1# qd (11/6), F/U digoxin level (11/13)– EKG qd (11/6)EKG qd (11/6)– TTE (11/7)TTE (11/7)

life threatening (>25% cardiac death)•pulmonary edema•MI•observed VT

Multi-factorial Cardiac Risk Index (Goldman)Multi-factorial Cardiac Risk Index (Goldman)Ref: Goldman M, Caldera D, Southwick, et al: Multifactorial index of cardiac risk in non-cardiac surgicRef: Goldman M, Caldera D, Southwick, et al: Multifactorial index of cardiac risk in non-cardiac surgic

al procedures. N Engl J Med Oct 1977al procedures. N Engl J Med Oct 1977..

11stst OP on 11-05 OP on 11-05

Diagnosis: bladder TCC with muscle invasionDiagnosis: bladder TCC with muscle invasion

Operation: TUR-BT, TRUSP BxOperation: TUR-BT, TRUSP Bx

ASA III, ASA III, AfAf (Dr. (Dr. 黃謙琳黃謙琳))

麻醉紀錄麻醉紀錄

HistoryHistory

AfAf– Acute & ChronicAcute & Chronic

Af noted at Af noted at 馬偕 馬偕 in 2002-09, unknown previous Hxin 2002-09, unknown previous HxRecent onset of Af Recent onset of Af RVR (>100) RVR (>100)In this case, VR usually < 100In this case, VR usually < 100 Chronic Af Chronic Af

– Asymptomatic, NYHA class IAsymptomatic, NYHA class I （（ 6F6F ））– PE: No Signs of heart failurePE: No Signs of heart failure– TTE: no chamber dilatation, no thrombus, fair contrTTE: no chamber dilatation, no thrombus, fair contr

atilityatility– CXR: no cardiomegaly, no pulmonary congestionCXR: no cardiomegaly, no pulmonary congestion

type and frequency, medicationsymptoms (palpitations, dizziness,

syncope)precipitating factors and aggravating

factors

Patient with arrhythmia for OPPatient with arrhythmia for OP-- On Pre-Operative Evaluation-- On Pre-Operative Evaluation

Patient with arrhythmia for OPPatient with arrhythmia for OP-- On Pre-Operative Evaluation-- On Pre-Operative Evaluation

Goldman risk index Goldman risk index

EKG: ischemic disease, E’, QT changeEKG: ischemic disease, E’, QT change

LAB: K, Mg, (digilatis…), drug levelLAB: K, Mg, (digilatis…), drug level

Continue antiarrhythmic medicationsContinue antiarrhythmic medications

anxiety control, sedative hypnoticsanxiety control, sedative hypnotics

Anticoagulant therapyAnticoagulant therapy– Coumadin (II VII IX X C S, PT>aPTT)Coumadin (II VII IX X C S, PT>aPTT)

Onset time= 24hr; Max effect achieved = 3~4dOnset time= 24hr; Max effect achieved = 3~4dHalf life= 40hr (duration 2~5d) (liver function)Half life= 40hr (duration 2~5d) (liver function)

– Heparin (Antithrombin III X, aPTT>all)Heparin (Antithrombin III X, aPTT>all)Total Clearance within 6hrs (liver, BT, shock)Total Clearance within 6hrs (liver, BT, shock)Protamine 1mg = heparin 100UProtamine 1mg = heparin 100U

– Aspirin & NSAIDs (platelet aggregation, BT)Aspirin & NSAIDs (platelet aggregation, BT)irreversible acetylation of cyclo-oxygenaseirreversible acetylation of cyclo-oxygenaselife of that platelet (7-10 days)life of that platelet (7-10 days)

Patient with arrhythmia for OPPatient with arrhythmia for OP-- On Pre-Operative Evaluation-- On Pre-Operative Evaluation

Peri-operative Af with RVR was notedPeri-operative Af with RVR was noted

HR= 120~175HR= 120~175

BP= 100~120/60~70BP= 100~120/60~70

•Tachycardia subsided after returning to ward

Preparation for 2Preparation for 2ndnd OP on 11-12 OP on 11-12

CV consultation report (11/6):CV consultation report (11/6):– Digoxin 1# qd (11/6), F/U digoxin level (11/13)Digoxin 1# qd (11/6), F/U digoxin level (11/13)– EKG qd (11/6) , EKG qd (11/6) , monitor QTc intervalmonitor QTc interval– Add Propafenone (11/6) 1# tidAdd Propafenone (11/6) 1# tid– TTE (11/7)TTE (11/7)

Lab Data 911111Lab Data 911111

911103 911111 911103 911111RBC 4.54 4.54 Na 137.7 137HGB 14.3 13.9 K 4.37 4.2HCT 41.4 40 Cl 102 100MCV 91.2 88.1 Ca 2.28PLT 371 292 Mg 0.83

WBC 12240 9840 Bleeding time 5.5PT 12.2 11.6

Bil (T/D) 0.9 0.5/0.2 PT control 12.2 12.4GOT 29 73 inr 1 1GPT - 56 APTT 28.1 31BUN 18.5 15.4 APTT control 35.5 36..5

Creatinine 1.34 1.1

22ndnd OP on 11-12 OP on 11-12

Diagnosis: bladder TCC with muscle invasionDiagnosis: bladder TCC with muscle invasion

Operation: Radical cystectomyOperation: Radical cystectomy

ASA III, AfRVR, LVEF=54% (Dr. ASA III, AfRVR, LVEF=54% (Dr. 蕭柏妮蕭柏妮 ))

麻醉紀錄麻醉紀錄

• Hx of intra-op AfRVRHx of intra-op AfRVR• Heart EchoHeart Echo

• Af (borderline LA size, no thrombus formation)Af (borderline LA size, no thrombus formation)

• LVEF= 54% (borderline), normal LV sizeLVEF= 54% (borderline), normal LV size

• mild MR, TR (susp. Small chordae tendinae rupture)mild MR, TR (susp. Small chordae tendinae rupture)

• EKG: Af with irregular VR, AFEKG: Af with irregular VR, AF

Patient with arrhythmia for OPPatient with arrhythmia for OP-- On Pre-Operative Evaluation-- On Pre-Operative Evaluation

• Af with RVR

•HR upto 170

•BP down to 90~100/60~65

•OP DC

Later on…Later on…

Digoxin 1.5# QD (11/14)Digoxin 1.5# QD (11/14)

CV consultation (11/18)CV consultation (11/18)– Add Add Isoptin (verapamil) 1#Isoptin (verapamil) 1#– Control Digoxin level (0.8~2.0)Control Digoxin level (0.8~2.0)– Perioperative AF+RVR, BP downPerioperative AF+RVR, BP down control RVR and BP control RVR and BP 即可即可P’t discharged on 11/18P’t discharged on 11/18

911113 911118Digoxin (RIA) 0.83~3.0 0.32 0.98

DiscussionDiscussion

Anesthesia & Atrial FibrillatAnesthesia & Atrial Fibrillationion

Why is A. Fib Important to the Why is A. Fib Important to the Anesthesiologist?Anesthesiologist?

1.1. It is an indicator of It is an indicator of significant systemic diseasesignificant systemic disease (e.g. un (e.g. undiagnosed thyrotoxicosis).diagnosed thyrotoxicosis).

2.2. The loss of the atrial component to systole may lead to The loss of the atrial component to systole may lead to a decrease in cardiac output.a decrease in cardiac output.

3.3. An excessive ventricular rate may lead to An excessive ventricular rate may lead to angina, ischeangina, ischemia, hypotension, pulmonary edemamia, hypotension, pulmonary edema..

4.4. Development of left atrial thrombus leads to Development of left atrial thrombus leads to systemic esystemic embolism.mbolism.

5.5. The patient may develop The patient may develop anxietyanxiety secondary to palpitatio secondary to palpitations.ns.

6.6. Treatment with digoxin may cause Treatment with digoxin may cause toxicitytoxicity, particularly i, particularly in the presence of n the presence of hypokalemia.hypokalemia.

7.7. Treatment with warfarin may lead to Treatment with warfarin may lead to bleeding complicatibleeding complicationsons

The "Atrial Kick" The "Atrial Kick"

In patients with ischemic heart disease, thIn patients with ischemic heart disease, the loss of the atrial component may lead to e loss of the atrial component may lead to a 50% decrease in cardiac output & blood a 50% decrease in cardiac output & blood pressure. pressure. If there is impaired LV function, then the hIf there is impaired LV function, then the heart may be more dependent than normal eart may be more dependent than normal on the atrial component. on the atrial component. The loss of the atrial kick may only be appThe loss of the atrial kick may only be apparent during exercise. arent during exercise.

Irregular Ventricular Response Irregular Ventricular Response

The irregularity, per se, of the ventricular rThe irregularity, per se, of the ventricular response, does esponse, does notnot cause any problems. cause any problems.

The ventricular rate, however, is critical:The ventricular rate, however, is critical:

1.1. Rapid ventricular ratesRapid ventricular rates are associated with are associated with decreased ventricular filling, and consequedecreased ventricular filling, and consequently reduced cardiac output. ntly reduced cardiac output.

2.2. In Mitral StenosisIn Mitral Stenosis – ventricular filling time i – ventricular filling time is critical, onset of AF causes a sudden dets critical, onset of AF causes a sudden deterioration in the disease process. erioration in the disease process.

HOW IS ATRIAL FIBRILLATION HOW IS ATRIAL FIBRILLATION MANAGED?MANAGED?

Up to Up to 50%50% of cases of perioperative onset of cases of perioperative onset atrial fibrillation revert atrial fibrillation revert spontaneouslyspontaneously to sin to sinus rhythm. us rhythm.

Treatment plan:Treatment plan:

1. Treat the cause.1. Treat the cause.

2. Return to sinus rhythm.2. Return to sinus rhythm.

3. Control the ventricular rate.3. Control the ventricular rate.

4. Prevent thromboembolism4. Prevent thromboembolism

Step 1: treat the causeStep 1: treat the cause

Correct any electrolyte imbalance:Correct any electrolyte imbalance: check Potassium and Magnesium level check Potassium and Magnesium level

Acid-base imbalanceAcid-base imbalance

HypovolemiaHypovolemia

Step 2: Consider cardioversion Step 2: Consider cardioversion

Synchronized direct current cardioversion (SDDC) is the gold standSynchronized direct current cardioversion (SDDC) is the gold standard for management of acute onset AF. ard for management of acute onset AF. SDDCSDDC is the treatment of choice in acute onset AF with cardiovascul is the treatment of choice in acute onset AF with cardiovascular compromise. ar compromise. A DC current of A DC current of 25 to 100J25 to 100J is usually required (synchronized with th is usually required (synchronized with the QRS complex to prevent V. Fib). e QRS complex to prevent V. Fib). The success rate depends on the duration of the arrhythmia; The success rate depends on the duration of the arrhythmia; shortershorter=better=better.. Large left atrial sizeLarge left atrial size (on TOE) >4.5cm suggests difficulty in cardiover (on TOE) >4.5cm suggests difficulty in cardioversion. sion. AF secondary to AF secondary to rheumatic heart diseaserheumatic heart disease rarely cardioverts. rarely cardioverts.

The risk of The risk of thromboembolismthromboembolism is high: if the AF is of >48 hrs duration, is high: if the AF is of >48 hrs duration, the patient should be anticoagulated for 3 weeks before cardioversiothe patient should be anticoagulated for 3 weeks before cardioversion is attempted. n is attempted.

Pharmacologic cardioversionPharmacologic cardioversion can be attempted can be attempted with a number of agents, class Ia (disopyramide),with a number of agents, class Ia (disopyramide), class Ic ( class Ic (propafenonepropafenone) or class III (amiodarone). ) or class III (amiodarone). These are, at best, only partially effective, but mThese are, at best, only partially effective, but may be efficacious in the maintenance of sinus rhyay be efficacious in the maintenance of sinus rhythm thm post cardioversion post cardioversion Moreover, conversion to and maintenance of sinMoreover, conversion to and maintenance of sinus rhythm with antiarrhythmic drug therapy has nus rhythm with antiarrhythmic drug therapy has not shown any improvement in mortality. ot shown any improvement in mortality. For most patients, For most patients, control of the ventricular respcontrol of the ventricular responseonse is the most effective therapy. is the most effective therapy.

Step 3: control the ventricular Step 3: control the ventricular response response

A variety of agents have been used, but thA variety of agents have been used, but the most effective are e most effective are digoxin, calcium chandigoxin, calcium channel blockers( class IV), beta blockers (clasnel blockers( class IV), beta blockers (class II) and amiodarone( class III) s II) and amiodarone( class III)

Vaughan Williams Classification Vaughan Williams Classification of Antiarrhythmic Drugsof Antiarrhythmic Drugs

ClassClass ActionAction DrugDrug

II Sodium channel blockade Sodium channel blockade

IaIa Prolong repolarizationProlong repolarization QuinidineQuinidine, procainamide, procainamide, dis, disopyramideopyramide

IbIb Shorten repolarizationShorten repolarization LidocaineLidocaine, mexiletine, tocain, mexiletine, tocainide, phenytoinide, phenytoin

IcIc Little effect on repolarizationLittle effect on repolarization Encainide, flecainide, Encainide, flecainide, propafpropafenoneenone, moricizine(?) , moricizine(?)

IIII Sympatholysis: beta blockerSympatholysis: beta blocker Propanolol, Propanolol, esmololesmolol, acebut, acebutolol olol

IIIIII Prolong repolarizationProlong repolarization Ibutilide, dofetilide, sotalol, Ibutilide, dofetilide, sotalol, aamiodaronemiodarone, bretylium , bretylium

IVIV Ca channel blockerCa channel blocker VerapamilVerapamil, diltiazem, bepridi, diltiazem, bepridil l

nonenone Adenosine, digitalisAdenosine, digitalis, magne, magnesium sium

Class Toxicities of Class Toxicities of Antiarrhythmic DrugsAntiarrhythmic Drugs

Class IClass I Class IIClass II

( beta-blocker)( beta-blocker)

Class IIIClass III Class IVClass IV

(Ca channel (Ca channel blocker)blocker)

Proarrhythmic efProarrhythmic effects:fects:

IA- IA- TorsadesTorsades de pointes de pointes

IC- IC- CAST CAST proarrhythmiaproarrhythmia

Negative inotropNegative inotropic effectic effect

Infranodal condInfranodal conduction block uction block

Sinus bradycardSinus bradycardiaia

AV blockAV block

Depression of LDepression of LV function (adreV function (adrenergic-dependenergic-dependent) nt)

Sinus bradycardSinus bradycardiaia

Torsades de poiTorsades de pointes ntes

Sinus bradycardSinus bradycardiaia

AV blockAV block

Negative inotropNegative inotropic effect ic effect

BETA BLOCKERS BETA BLOCKERS

These agents are These agents are ineffectiveineffective in terminating atrial fibrillatio in terminating atrial fibrillation. n. They are, however, useful for They are, however, useful for slowing the ventricular resslowing the ventricular responseponse, used alone or , used alone or in combination with digoxinin combination with digoxin. . Most effective agents in slowing the ventricular response Most effective agents in slowing the ventricular response in in hyperadrenergic stateshyperadrenergic states (thyrotoxicosis). (thyrotoxicosis). b -Blockers have b -Blockers have a negative inotropic effect. a negative inotropic effect. EsmololEsmolol is an ultrashort acting agent, with rapid onset ti is an ultrashort acting agent, with rapid onset time to control the rate, although it may cause hypotensiome to control the rate, although it may cause hypotension. The theraputic effect is lost within 30 mins of stopping n. The theraputic effect is lost within 30 mins of stopping the infusion. the infusion. Withdrawl of b -Blockers post operatively is associated wWithdrawl of b -Blockers post operatively is associated with a higher incidence of tachyarrhythmias. ith a higher incidence of tachyarrhythmias.

   

EsmololEsmolol

Dosage- supraventricular and postoperativDosage- supraventricular and postoperative tachycardia load 500mcg/kg x 1min then e tachycardia load 500mcg/kg x 1min then 50mcg/kg/min x 4min, maintenance 50-2050mcg/kg/min x 4min, maintenance 50-200mcg/kg/min 0mcg/kg/min

Side effect- hypotension, dizziness, asthenSide effect- hypotension, dizziness, asthenia ia

AMIODARONE AMIODARONE

Complex potent antiarrhythmic agent with class I, II, III, IComplex potent antiarrhythmic agent with class I, II, III, IV activity and antifibrillatory effects. Effective against supV activity and antifibrillatory effects. Effective against supra- and ventricular- tachyarrhythmias. In atrial fibrillation ira- and ventricular- tachyarrhythmias. In atrial fibrillation its main action is to ts main action is to decrease nodal conduction. decrease nodal conduction. Amiodarone is more effective than quinidine & flecainide Amiodarone is more effective than quinidine & flecainide for maintaining sinus rhythm for maintaining sinus rhythm post DC cardioversionpost DC cardioversion. . Amiodarone Amiodarone increases ejection fractionincreases ejection fraction in patients with c in patients with congestive heart failure and arrhythmias (probably from it’ongestive heart failure and arrhythmias (probably from it’s vasodilatory effect). s vasodilatory effect). The onset of action for Amiodarone compared to digoxin The onset of action for Amiodarone compared to digoxin is more is more rapidrapid, assuming adequate loading doses of each , assuming adequate loading doses of each are given.are given.

   

AMIODARONEAMIODARONE

Dosage- IV load 15mg/min x 10min then 1Dosage- IV load 15mg/min x 10min then 1mg/min x 6hr, IV maintenance 0.5mg/min mg/min x 6hr, IV maintenance 0.5mg/min (720mg/24hr) (720mg/24hr)

Side effects: arrhythmias, lung dysfunction,Side effects: arrhythmias, lung dysfunction, thyroid dysfunction, hepatotoxicity, poor c thyroid dysfunction, hepatotoxicity, poor coordination, tremoroordination, tremor

CALCIUM CHANNEL BLOCKERSCALCIUM CHANNEL BLOCKERS

Ca channel blockers block the inward movement of calCa channel blockers block the inward movement of calcium into the cells of the conducting system, thereby thcium into the cells of the conducting system, thereby they: ey:

1.1. Reduce automaticity Reduce automaticity 2.2. Reduce conduction velocity Reduce conduction velocity 3.3. Increase the refractory period Increase the refractory period 4.4. These agents do not promote conversion to sinus rhythThese agents do not promote conversion to sinus rhyth

m, but merely m, but merely control the ventricular ratecontrol the ventricular rate. . 5.5. Negative inotropic effect. Negative inotropic effect. 6.6. May be effectively combined for May be effectively combined for synchronous activity wsynchronous activity w

ith digoxinith digoxin, but , but should not be combined with beta blockshould not be combined with beta blockersers. .

   

VerapamilVerapamil

Dosage- IV loading 5-10 mg over 1-2 min, Dosage- IV loading 5-10 mg over 1-2 min, maintenance 0.005 mg/kg/minmaintenance 0.005 mg/kg/min

Side effects- AV block, constipation, Side effects- AV block, constipation, headache, symptomatic hypotension headache, symptomatic hypotension

DIGITALISDIGITALIS

Digoxin has two effects:Digoxin has two effects:1. Stimulation of activity in vagal tissue / baroreceptors lead1. Stimulation of activity in vagal tissue / baroreceptors lead

ing to ing to an increase in vagal tone:an increase in vagal tone:(1)Decreased automaticity in the sinoatrial node. (1)Decreased automaticity in the sinoatrial node. (2)Increased refractory period and decreased conduction in (2)Increased refractory period and decreased conduction in

the AV node. the AV node. (3)Decreased refractory period in atrial muscle (3)Decreased refractory period in atrial muscle 2. Digoxin inhibits the Na-K ATPase on the membrane of th2. Digoxin inhibits the Na-K ATPase on the membrane of th

e myocyte; to maintain electical neutrality the Na-Ca pue myocyte; to maintain electical neutrality the Na-Ca pump reverses its flow, thereby increasing the intracellular mp reverses its flow, thereby increasing the intracellular concentration of calcium. concentration of calcium. This has an inotropic and proarThis has an inotropic and proarrhythmic effect.rhythmic effect.

Digoxin is relatively Digoxin is relatively ineffectiveineffective in controlling the in controlling the ventricular response in situations where the ventricular response in situations where the symsympathetic tone is highpathetic tone is high (thyrotoxicosis, sepsis). (thyrotoxicosis, sepsis).

Digoxin has a narrow theraputic window, and Digoxin has a narrow theraputic window, and toxtoxicityicity can cause every known arrhythmia. can cause every known arrhythmia.

Theraputic onset time is Theraputic onset time is slowslow, requiring several , requiring several hours to control vent. rate. hours to control vent. rate.

ECG: flattened or inverted T waves ECG: flattened or inverted T waves

Dosage- IV loading 0.5-1.0 mg, maintenance Dosage- IV loading 0.5-1.0 mg, maintenance 0.125-0.25 mg q.d.0.125-0.25 mg q.d.Side EffectsSide Effects

1.1. CARDIAC: all forms of dysrhythmias, particularCARDIAC: all forms of dysrhythmias, particularly ectopics / heart block ly ectopics / heart block

2.2. GASTROINTESTINAL: anorexia and vomiting GASTROINTESTINAL: anorexia and vomiting 3.3. VISUAL: blurring, and abnormalities of colour vVISUAL: blurring, and abnormalities of colour v

ision (yellow vision) ision (yellow vision) 4.4. MENTAL: confusion, nightmares MENTAL: confusion, nightmares 5.5. OTHER: gynecomastia in males OTHER: gynecomastia in males

Step 4: Anticoagulation Step 4: Anticoagulation

Risk of embolic stroke is increased with:Risk of embolic stroke is increased with:1.1. Large left atrial size (>4.5 cm) Large left atrial size (>4.5 cm) 2.2. Valvular heart disease Valvular heart disease 3.3. Congestive cardiac failure. Congestive cardiac failure. 4.4. With With warfarin warfarin anticoagulation, the risk of stroke is anticoagulation, the risk of stroke is reduredu

ced by about 60%ced by about 60% ( (3%3% vs 8%) vs 8%) 5.5. The risk of intracranial hemorrhage is about 0.3% per yThe risk of intracranial hemorrhage is about 0.3% per y

ear. ear. 6.6. Patients Patients <65y<65y with lone a. fib have a low incidence of t with lone a. fib have a low incidence of t

hromboembolism, and hromboembolism, and aspirinaspirin is recommended. is recommended. 7.7. Patients Patients >75y>75y with a. fib & diabetes, previous CVA/TIA/ with a. fib & diabetes, previous CVA/TIA/

RIND, hypertension, should be anticoagulated, unless RIND, hypertension, should be anticoagulated, unless hemorrhagic risks are deemed unacceptably high. hemorrhagic risks are deemed unacceptably high.

ACC/AHA Guidelines 2002 Update for Perioperative CardioACC/AHA Guidelines 2002 Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgeryvascular Evaluation for Noncardiac Surgery

Cardioversion of atrial fibrillation/flutter is generally not Cardioversion of atrial fibrillation/flutter is generally not recommended for asymptomatic or minimally symptomrecommended for asymptomatic or minimally symptomatic arrhythmias until correction of the atic arrhythmias until correction of the underlying problunderlying problemsems has occurred, which frequently leads to a return to has occurred, which frequently leads to a return to normal sinus rhythm. normal sinus rhythm. Also, cardioversion is unlikely to result in long-term norAlso, cardioversion is unlikely to result in long-term normal sinus rhythm if the underlying problem is not correcmal sinus rhythm if the underlying problem is not corrected. ted. The avoidance of an The avoidance of an electrolyte abnormalityelectrolyte abnormality, especially , especially hypokalemia and hypomagnesemiahypokalemia and hypomagnesemia, may reduce the per, may reduce the perioperative incidence and risk of arrhythmias, although aioperative incidence and risk of arrhythmias, although acute preoperative repletion of potassium in an asymptocute preoperative repletion of potassium in an asymptomatic individual may be associated with greater risk thamatic individual may be associated with greater risk than benefitsn benefits

ACC/AHA Guidelines 2002 Update for Perioperative CardiACC/AHA Guidelines 2002 Update for Perioperative Cardi

ovascular Evaluation for Noncardiac Surgeryovascular Evaluation for Noncardiac Surgery In the perioperative setting: In the perioperative setting:

Supraventricular arrhythmias may require either electricaSupraventricular arrhythmias may require either electrical or pharmacological cardioversion l or pharmacological cardioversion if they produce symptif they produce symptoms or hemodynamic compromiseoms or hemodynamic compromise. . If cardioversion is not possible, satisfactory heart rate coIf cardioversion is not possible, satisfactory heart rate control should be accomplished with oral or ntrol should be accomplished with oral or intravenous digintravenous digitalis, beta-adrenergic blockers, or calcium channel blockitalis, beta-adrenergic blockers, or calcium channel blockersers. Among these three types of medications, digitalis is t. Among these three types of medications, digitalis is the least effective agent, and he least effective agent, and beta blockersbeta blockers are the most are the most effective agent for controlling the ventricular response dueffective agent for controlling the ventricular response during atrial fibrillation ring atrial fibrillation An additional benefit of beta blockers is that they have bAn additional benefit of beta blockers is that they have been shown to een shown to accelerate the conversion of postoperative accelerate the conversion of postoperative supraventricular arrhythmias to sinus rhythmsupraventricular arrhythmias to sinus rhythm as compare as compared with diltiazem d with diltiazem

ACC/AHA Guidelines 2002 Update for Perioperative CardioACC/AHA Guidelines 2002 Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgeryvascular Evaluation for Noncardiac Surgery

In patients with atrial fibrillation who are taIn patients with atrial fibrillation who are taking oral anticoagulation therapy, it may bking oral anticoagulation therapy, it may be necessary to discontinue the anticoagulae necessary to discontinue the anticoagulant nt several daysseveral days before surgery. If time doe before surgery. If time does not allow and it is important that the paties not allow and it is important that the patient not be on anticoagulants, the effect of wnt not be on anticoagulants, the effect of warfarin can be arfarin can be reversed by parenteral vitareversed by parenteral vitamin K or fresh frozen plasma min K or fresh frozen plasma

KEY POINTS KEY POINTS Atrial fibrillation is a common cardiac arrhythmia characterised by an atrial rate >400bAtrial fibrillation is a common cardiac arrhythmia characterised by an atrial rate >400beats/min, and a variable ventricular response. eats/min, and a variable ventricular response. There is loss of atrial mechanical activity leading to reduced cardiac output . This is mThere is loss of atrial mechanical activity leading to reduced cardiac output . This is more apparent on exercise, in LV dysfunction and in mitral stenosis. ore apparent on exercise, in LV dysfunction and in mitral stenosis. In most cases atrial fibrillation signifies significant systemic disease. In most cases atrial fibrillation signifies significant systemic disease. There is a history of palpitations, an irregularly irregular pulse, and varying pulse presThere is a history of palpitations, an irregularly irregular pulse, and varying pulse pressure, leading to an apex-radial pulse deficit. sure, leading to an apex-radial pulse deficit. Treatment is necessary to control the ventricular rate and maintain cardiac output, anTreatment is necessary to control the ventricular rate and maintain cardiac output, and prevent systemic embolisation of thrombus. d prevent systemic embolisation of thrombus. Treatment involves correcting the cause, cardioverting to sinus rhythm, controlling the Treatment involves correcting the cause, cardioverting to sinus rhythm, controlling the ventricular rate and anticoagulation. ventricular rate and anticoagulation. The ideal ventricular rate is 90 beats/min The ideal ventricular rate is 90 beats/min Cardioversion is indicated for acute onset AF (<3 days). If the duration is longer, anticCardioversion is indicated for acute onset AF (<3 days). If the duration is longer, anticoagulation is essential. Mechanical activity may take weeks to normalize. Cardioversioagulation is essential. Mechanical activity may take weeks to normalize. Cardioversion may be ineffective in rheumatic AF or if the LA size >4.5cm on may be ineffective in rheumatic AF or if the LA size >4.5cm The ventricular response may be controlled with digoxin, beta blockers, calcium chanThe ventricular response may be controlled with digoxin, beta blockers, calcium channel blockers, amiodarone, or other antiarrhythmics. nel blockers, amiodarone, or other antiarrhythmics. Digoxin remains the gold standard, but is limited by it’s narrow theraputic range, slow Digoxin remains the gold standard, but is limited by it’s narrow theraputic range, slow onset time and potential toxicity onset time and potential toxicity

Digoxin is ineffective in controlling the ventricular response in thyrotoxicosis (where sympathetic tDigoxin is ineffective in controlling the ventricular response in thyrotoxicosis (where sympathetic tone is high) and probably in sepsis. one is high) and probably in sepsis. Beta blockers and calcium channel blockers are effective for slowing the ventricular response, buBeta blockers and calcium channel blockers are effective for slowing the ventricular response, but they do not restore sinus rhythm and are negatively inotropic. t they do not restore sinus rhythm and are negatively inotropic. Amiodarone has rapid onset time, has negligable effect on the myocardium, and is useful for maiAmiodarone has rapid onset time, has negligable effect on the myocardium, and is useful for maintaining NSR post cardioversion.A loading dose is required, and long term therapy is associated ntaining NSR post cardioversion.A loading dose is required, and long term therapy is associated with a myriad of complications. with a myriad of complications. Anticoagulation significantly reduces the incidence of stroke in patients >65 years with AF. Anticoagulation significantly reduces the incidence of stroke in patients >65 years with AF. When assessing a patient with AF for theatre, it is essential to examine the patient looking for the When assessing a patient with AF for theatre, it is essential to examine the patient looking for the potential cause of the disease. potential cause of the disease. Watch out for the undiagnosed thyrotoxic patient. Watch out for the undiagnosed thyrotoxic patient. Volatile agents, with the exception of Halothane, have anti fibrillatory properties. Vagolytics and sVolatile agents, with the exception of Halothane, have anti fibrillatory properties. Vagolytics and sympathomimetics may drive up the ventricular response ympathomimetics may drive up the ventricular response New onset AF is associated with cardiothoracic surgery and ECT. New onset AF is associated with cardiothoracic surgery and ECT. AF occurs at a rate of 11-40% following CABG, >50% following valvular surgery, and insreases wAF occurs at a rate of 11-40% following CABG, >50% following valvular surgery, and insreases with age. ith age. Most of these cases are self limiting. Most of these cases are self limiting. Initial treatment with magnesium and normalisation of serum potassium is indicated. Initial treatment with magnesium and normalisation of serum potassium is indicated. Diltiazem, Beta blockers and Amiodarone probably have a protective effect (reducing the incidenDiltiazem, Beta blockers and Amiodarone probably have a protective effect (reducing the incidence of AF). The significance of this is unknown. Preoperative digitalisation is ineffective. ce of AF). The significance of this is unknown. Preoperative digitalisation is ineffective.

referencesreferences

www.4um.com/tutorialwww.4um.com/tutorial

www.acc.orgwww.acc.org : ACC/AHA Guideline 2002 : ACC/AHA Guideline 2002 Update for Perioperative Cardiovascular EUpdate for Perioperative Cardiovascular Evaluation for Noncardiac Surgeryvaluation for Noncardiac Surgery

Textbook of cardiothoracic anesthesiology, Textbook of cardiothoracic anesthesiology,