Case presentation Atrial fibrillation

1. Case presentationAtrial fibrillation Presented by Ri 顏廷珊、Ri 江易穎 Directed by Dr. 蕭柏妮

2. Admission summary • 林XX, 51y/o, male, 75kg • Urge incontinence in 2001-8 • 外院，treated as UTI • Painless gross hematuria in 2002-9 • 馬偕，urine cytology= TCC, Af noted • IVP= bladder tumor (multiple) • Bladder TCC TUR-BT & MMC*1 in 2002-10

3. Transferred to NTUH • Severe dysuria • Patho= bladder TCC with muscle invasion • Admission on 11/3, Arrange radical cystectomy • Past history • Admission EKG = Af + VPC • Admission CXR • Lab data

7. Lab data 911103

8. Preparation for 1st OP on 11-05 • CV consultation report on 11-04 • Af, abberant QRS, no specific ST-T change • HR= 75~85 ;BP= 110/70; RR= 8 • Asymptomatic，NYHA I （6F） • Goldman multifactorial cardiac risk index

9. Multi-factorial Cardiac Risk Index (Goldman)Ref: Goldman M, Caldera D, Southwick, et al: Multifactorial index of cardiac risk in non-cardiac surgical procedures. N Engl J Med Oct 1977. • index of cardiac risk in the non-cardiac surgery

10. Multi-factorial Cardiac Risk Index (Goldman)Ref: Goldman M, Caldera D, Southwick, et al: Multifactorial index of cardiac risk in non-cardiac surgical procedures. N Engl J Med Oct 1977. • CV Suggestion (11/4): • Digoxin 1# qd (11/6), F/U digoxin level (11/13) • EKG qd (11/6) • TTE (11/7) • life threatening (>25% cardiac death) • pulmonary edema • MI • observed VT

11. 1st OP on 11-05 • Diagnosis: bladder TCC with muscle invasion • Operation: TUR-BT, TRUSP Bx • ASA III, Af (Dr. 黃謙琳) • 麻醉紀錄

12. Patient with arrhythmia for OP-- On Pre-Operative Evaluation • History • Af • Acute & Chronic • Af noted at 馬偕 in 2002-09, unknown previous Hx • Recent onset of Af  RVR (>100) • In this case, VR usually < 100 Chronic Af • Asymptomatic, NYHA class I（6F） • PE: No Signs of heart failure • TTE: no chamber dilatation, no thrombus, fair contratility • CXR: no cardiomegaly, no pulmonary congestion type and frequency, medication symptoms (palpitations, dizziness, syncope) precipitating factors and aggravating factors

13. Patient with arrhythmia for OP-- On Pre-Operative Evaluation • Goldman risk index • EKG: ischemic disease, E’, QT change • LAB: K, Mg, (digilatis…), drug level • Continue antiarrhythmic medications • anxiety control, sedative hypnotics

14. Patient with arrhythmia for OP-- On Pre-Operative Evaluation • Anticoagulant therapy • Coumadin (II VII IX X C S, PT>aPTT) • Onset time= 24hr; Max effect achieved = 3~4d • Half life= 40hr (duration 2~5d) (liver function) • Heparin (Antithrombin III X, aPTT>all) • Total Clearance within 6hrs (liver, BT, shock) • Protamine 1mg = heparin 100U • Aspirin & NSAIDs (platelet aggregation, BT) • irreversible acetylation of cyclo-oxygenase • life of that platelet (7-10 days)

15. Peri-operative Af with RVR was noted • HR= 120~175 • BP= 100~120/60~70 • Tachycardia subsided after returning to ward

16. Preparation for 2nd OP on 11-12 • CV consultation report (11/6): • Digoxin 1# qd (11/6), F/U digoxin level (11/13) • EKG qd (11/6) , monitor QTc interval • Add Propafenone (11/6) 1# tid • TTE (11/7)

21. Lab Data 911111

22. 2nd OP on 11-12 • Diagnosis: bladder TCC with muscle invasion • Operation: Radical cystectomy • ASA III, AfRVR, LVEF=54% (Dr. 蕭柏妮) • 麻醉紀錄

23. Patient with arrhythmia for OP-- On Pre-Operative Evaluation • Hx of intra-op AfRVR • Heart Echo • Af (borderline LA size, no thrombus formation) • LVEF= 54% (borderline), normal LV size • mild MR, TR (susp. Small chordae tendinae rupture) • EKG: Af with irregular VR, AF

24. Af with RVR • HR upto 170 • BP down to 90~100/60~65 • OP DC

25. Later on… • Digoxin 1.5# QD (11/14) • CV consultation (11/18) • Add Isoptin (verapamil) 1# • Control Digoxin level (0.8~2.0) • Perioperative AF+RVR, BP down •  control RVR and BP 即可 • P’t discharged on 11/18

26. Discussion Anesthesia & Atrial Fibrillation

27. Why is A. Fib Important to the Anesthesiologist? • It is an indicator of significant systemic disease (e.g. undiagnosed thyrotoxicosis). • The loss of the atrial component to systole may lead to a decrease in cardiac output. • An excessive ventricular rate may lead to angina, ischemia, hypotension, pulmonary edema. • Development of left atrial thrombus leads to systemic embolism. • The patient may develop anxiety secondary to palpitations. • Treatment with digoxin may cause toxicity, particularly in the presence of hypokalemia. • Treatment with warfarin may lead to bleeding complications

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

29. Irregular Ventricular Response • The irregularity, per se, of the ventricular response, does not cause any problems. • The ventricular rate, however, is critical: • Rapid ventricular rates are associated with decreased ventricular filling, and consequently reduced cardiac output. • In Mitral Stenosis – ventricular filling time is critical, onset of AF causes a sudden deterioration in the disease process.

30. HOW IS ATRIAL FIBRILLATION MANAGED? • Up to 50% of cases of perioperative onset atrial fibrillation revert spontaneously to sinus rhythm. • Treatment plan: 1. Treat the cause. 2. Return to sinus rhythm. 3. Control the ventricular rate. 4. Prevent thromboembolism

31. Step 1: treat the cause • Correct any electrolyte imbalance: check Potassium and Magnesium level • Acid-base imbalance • Hypovolemia

32. Step 2: Consider cardioversion • Synchronized direct current cardioversion (SDDC) is the gold standard for management of acute onset AF. • SDDC is the treatment of choice in acute onset AF with cardiovascular compromise. • A DC current of 25 to 100J is usually required (synchronized with the QRS complex to prevent V. Fib). • The success rate depends on the duration of the arrhythmia; shorter=better. • Large left atrial size (on TOE) >4.5cm suggests difficulty in cardioversion. • AF secondary to rheumatic heart disease rarely cardioverts. • The risk of thromboembolism is high: if the AF is of >48 hrs duration, the patient should be anticoagulated for 3 weeks before cardioversion is attempted.

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

34. Step 3: control the ventricular response • A variety of agents have been used, but the most effective are digoxin, calcium channel blockers( class IV), beta blockers (class II) and amiodarone( class III)

35. Vaughan Williams Classification of Antiarrhythmic Drugs

36. Class Toxicities of Antiarrhythmic Drugs

37. BETA BLOCKERS • These agents are ineffective in terminating atrial fibrillation. • They are, however, useful for slowing the ventricular response, used alone or in combination with digoxin. • Most effective agents in slowing the ventricular response in hyperadrenergic states (thyrotoxicosis). • b -Blockers have a negative inotropic effect. • Esmolol is an ultrashort acting agent, with rapid onset time to control the rate, although it may cause hypotension. The theraputic effect is lost within 30 mins of stopping the infusion. • Withdrawl of b -Blockers post operatively is associated with a higher incidence of tachyarrhythmias.

38. Esmolol • Dosage- supraventricular and postoperative tachycardia load 500mcg/kg x 1min then 50mcg/kg/min x 4min, maintenance 50-200mcg/kg/min • Side effect- hypotension, dizziness, asthenia

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

40. AMIODARONE • Dosage- IV load 15mg/min x 10min then 1mg/min x 6hr, IV maintenance 0.5mg/min (720mg/24hr) • Side effects: arrhythmias, lung dysfunction, thyroid dysfunction, hepatotoxicity, poor coordination, tremor

41. CALCIUM CHANNEL BLOCKERS • Ca channel blockers block the inward movement of calcium into the cells of the conducting system, thereby they: • Reduce automaticity • Reduce conduction velocity • Increase the refractory period • These agents do not promote conversion to sinus rhythm, but merely control the ventricular rate. • Negative inotropic effect. • May be effectively combined for synchronous activity with digoxin, but should not be combined with beta blockers.

42. Verapamil • Dosage- IV loading 5-10 mg over 1-2 min, maintenance 0.005 mg/kg/min • Side effects- AV block, constipation, headache, symptomatic hypotension

43. DIGITALIS • Digoxin has two effects: 1. Stimulation of activity in vagal tissue / baroreceptors leading to an increase in vagal tone: (1)Decreased automaticity in the sinoatrial node. (2)Increased refractory period and decreased conduction in the AV node. (3)Decreased refractory period in atrial muscle 2. Digoxin inhibits the Na-K ATPase on the membrane of the myocyte; to maintain electical neutrality the Na-Ca pump reverses its flow, thereby increasing the intracellular concentration of calcium. This has an inotropic and proarrhythmic effect.

44. Digoxin is relatively ineffective in controlling the ventricular response in situations where the sympathetic tone is high (thyrotoxicosis, sepsis). • Digoxin has a narrow theraputic window, and toxicity can cause every known arrhythmia. • Theraputic onset time is slow, requiring several hours to control vent. rate. • ECG: flattened or inverted T waves

45. Dosage- IV loading 0.5-1.0 mg, maintenance 0.125-0.25 mg q.d. • Side Effects • CARDIAC: all forms of dysrhythmias, particularly ectopics / heart block • GASTROINTESTINAL: anorexia and vomiting • VISUAL: blurring, and abnormalities of colour vision (yellow vision) • MENTAL: confusion, nightmares • OTHER: gynecomastia in males

46. Step 4: Anticoagulation • Risk of embolic stroke is increased with: • Large left atrial size (>4.5 cm) • Valvular heart disease • Congestive cardiac failure. • With warfarin anticoagulation, the risk of stroke is reduced by about 60% (3% vs 8%) • The risk of intracranial hemorrhage is about 0.3% per year. • Patients <65y with lone a. fib have a low incidence of thromboembolism, and aspirin is recommended. • Patients >75y with a. fib & diabetes, previous CVA/TIA/RIND, hypertension, should be anticoagulated, unless hemorrhagic risks are deemed unacceptably high.

47. ACC/AHA Guidelines 2002 Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery • Cardioversion of atrial fibrillation/flutter is generally not recommended for asymptomatic or minimally symptomatic arrhythmias until correction of the underlying problems has occurred, which frequently leads to a return to normal sinus rhythm. • Also, cardioversion is unlikely to result in long-term normal sinus rhythm if the underlying problem is not corrected. • The avoidance of an electrolyte abnormality, especially hypokalemia and hypomagnesemia, may reduce the perioperative incidence and risk of arrhythmias, although acute preoperative repletion of potassium in an asymptomatic individual may be associated with greater risk than benefits

48. ACC/AHA Guidelines 2002 Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery In the perioperative setting: • Supraventricular arrhythmias may require either electrical or pharmacological cardioversion if they produce symptoms or hemodynamic compromise. • If cardioversion is not possible, satisfactory heart rate control should be accomplished with oral or intravenous digitalis, beta-adrenergic blockers, or calcium channel blockers. Among these three types of medications, digitalis is the least effective agent, and beta blockers are the most effective agent for controlling the ventricular response during atrial fibrillation • An additional benefit of beta blockers is that they have been shown to accelerate the conversion of postoperative supraventricular arrhythmias to sinus rhythm as compared with diltiazem

49. ACC/AHA Guidelines 2002 Update for Perioperative Cardiovascular Evaluation for Noncardiac Surgery • In patients with atrial fibrillation who are taking oral anticoagulation therapy, it may be necessary to discontinue the anticoagulant several days before surgery. If time does not allow and it is important that the patient not be on anticoagulants, the effect of warfarin can be reversed by parenteral vitamin K or fresh frozen plasma

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