Dysrhythmias and Blocks

1. Dysrhythmias and Blocks BKN 1/24/02

2. How to crack a rhythm • What is the atrial rate and what is the source? • What is the ventricular rate and what is the source? • What is the relationship between the atria and the ventricles? (Who’s in charge here?) • Is there conducting system blockade?

3. And after you crack it • What is the underlying cause? • Is the the rhythm hurting the patient? • What should be done?

4. Rules of the road • No arrests, you’ve all taken ACLS, you know how to treat VF. Asystole and PEA are dead people • “It’s 2 a.m., there’s noone in the place. . .” • PG1 or 2 assigned as senior resident • PG3 assigned assigned as attending • No kibbutzing from the crowd until I ok it.

5. Case 1: Dr. Nelson’s Happy New Year • 51 y/o M complaining of palpitations • Drunk on homemade wine (ETOH = 225) • PE unremarkable • Intermittent episodes of rapid pulse and pallor with BP 95/60 lasting up to 1/2 minute • Rhythm strips follow; not continuous

7. Happy New Year! What to do? • At next episode, cardiovert with 50j (YES!) • Amiodoarone or Lidocaine • Magnesium sulfate 4 gm • BAL 5 mg/kg • Adenosine 12 mg IVB • Leave him alone, we never liked him much anyway and we see a possible end to pimping

8. Happy New Year • What’s the rhythm? • Is it hurting him? • What’s the cause?

9. V tach vs SVT with aberrancy • Clinical features • Physical • EKG • Specific QRS patterns • Brugada’s Criteria for 4 step quick process • MANY PATIENTS IN VT HAVE NORMAL BP AND MENTATION. DX OF SUSTAINED VT REQUIRES >30 SEC OF RHYTHM

10. Clinical Features

11. Physical Exam

12. EKG

13. Specific QRS patterns

14. Brugada’s criteria: any Yes = VT • 1. Absence of RS complex in all precordial? • 2. R to S interval >100 ms in one precordial? • 3. Atrioventricular Dissociation? • 4. Morphology criteria for VT present in both leads V1-2 and V6?

15. Is there anything wrong with. . .? • Cardioversion if in sustianed wide complex tachycardia? Go ahead if patient metastable or worse. Be sure you reassure the patient that it doesn’t mean he’s dieing (if he’s not) • Adenosine? Probably safe, has a very short 1/2 life

17. Holiday Heart • Supraventricular tachycardias (most often Atrial Fibrillation) • Transient Ventricular Tachycardia • Seen in chronic alcoholics on a binge

18. Alcoholic Heart Disease • Holiday Heart • Alcoholic Cardiomyopathy • Acute intoxication has cardiodepressant, vasodilatory and diuretic effects even in those with a normal heart (keep in mind for that drunk mildly hypotensive trauma victim) • In those with coronary disease, >2 oz can decrease exercise tolerance and increase ST depression after angina

19. Treating Dr. Nelson • Abstinence will lead to conversion to sinus • Do not treat unless hemodynamically unstable

20. Case 2: Aunt Jane ain’t right • 76 y/o F noted to be increasingly confused by family over last several days • Her Doctor is not available • Family doesn’t know details of medical history • Patient complains of being weak

21. Aunt Jane’s physical • Elderly female, oriented x 1, mod respiratory distress • BP 80/p, P 150, T 97 R, RR 24, SaO2 88% RA • JVD, Rales in bases • ECG follows

23. Case 2: Aunt Jane ain’t right • What’s the rhythm? • What’s the underlying cause? • Is it hurting her? • What to do?

24. What’s the rhythm? • Atrial rate 180, probably sinus • Ventricular rate 150, alternates between ventricles (LBBB pattern, RBBB pattern) • Complete AV dissociation • Apparent complete heart block • Complete rhythm diagnosis: atrial tachycardia, bi-directional V Tach, AVdissociation

25. Aunt Jane’s rhythm problems • PAT with AVB and Bidirectional V Tach are both almost pathognomonic of Digitalis toxicity • Is it hurting her? Clearly yes, we probably need to treat while waiting for the Fab frags to arrive, be administered and take effect • What to do? Cardiovert her? Overdrive pacing? Diurese her? Use antidysrhythmics?

26. Cardiovert? • Cardioversion generally considered contraindicated for Dig toxic rhythms. The heart is irritable due to increased catecholamine sensitivity • Fear cardioversion to refractory VF, VT and asystole • Most of that literature is very old and is talking about cardioverting AF. Applicability to VT unclear. • Is Aunt Jane an exception because she’s so sick we don’t think we’ll make her worse?

27. Overdrive Pacing? • Transvenous pacing in dig toxicitycarries same dangers as cardioversion (Induces ventricular dysrhymias, mortality 13%) • Transthoracic pacing may be safer, but the pacer would need to be capable of higher rates than the intrinsic rhythm

28. Diuresis? • Most patients in chronic dig toxicity are already on diuretics and hypokalemic. Hypokalemia worsens Dig toxicity.Must check K and supplement as necessary if going to diurese

29. Antidysrhythmics • Most antidysrhythmics are contraindicated in Dig toxicity • Magnesium indicated for dig induced tachydysrhythmias. 1-2 gm over 2 minutes then 1-2 gm/hr • Lidocaine or phenytoin are considered safest

30. Anti digitalis Fab fragments • Expensive • Indicated for severe ventricular dysrhythmias, atropine refractory progessive hemodynamically sig bradydysrhythmias, severe hyperkalemia, rapidly progressive dysrhythmias, cardiotoxic coingestants, plant cardiac glycosides + severe dysrhythmias, high levels plus any of the above

31. Case #3: Bloody Awful • A 52 yo male presents with weakness, melena, and palpitations. H/O heavy ETOH intake chronically. • BP 80-100 P fast and weak, monitor heart rate 205, SaO2 = 78%, patient stuporous, no ETOH odor • Heart: very fast Abdomen soft, stool black, NG grossly bloody

32. Bloody awful • Initial lab: • Glucometer = 500 • ABGs =7.25/20/55, BE = -15, Hgb = 7,

34. Wassup? • What’s the rhythm? • What’s the underlying cause? • Do we need more info? • Is it hurting him?

35. Wassup? • Rhythm Atrial fibrillation with rapid ventricular response • Underlying causes: hypovolemic shock, alcoholic heart disease, possible DKA • Addl info: CXR borderline cardiomegaly without failure • Is it hurting him? In this clinical scenario, of course. Combination of rate, blood loss, base deficit, anemia suggest that cardiac arrest is imminent

36. What to do? • Define possible strategies

37. What to do? • Cardiovert? (electrically or chemically) • Slow Vent Response? • Correct hypovolemia, anemia, DKA and hope he gets better from this alone?

38. Cardioversion • Pro: rapid return to a rate allowing ventricular filling, adequate cardiac output • Con: In presence of chronic AF, atrial thrombus may exist. Cardioversion may lead to arterial embolism (stroke, mesenteric infarct, etc) • Do we think this is acute or chronic AF?

39. Acute or chronic? • The rate and the clinical scenario suggests acute, but you never really know. • How to do it? Electrical or chemical?

40. Electrical or Chemical • Electrical is quick and except in the dig toxic is unlikely to have side effects. However, the underlying condition leading to AF is unchanged. The heart may go right back into the rhythm • Chemical conversion is slower, but leads to conditions more likely to allow permanent conversion. However the drugs used (class 1a and 3) can all cause major dysrhythmias and cardiodepression. Digoxin is slower but won’t cause cardiodepression

41. Summary of recs (most pts hemodynamically stable) • For acute AF in patient without failure or cardiomyopathy: use class 3 agent (Ibutilide has highest success rate and quickest action, but can cause dysrhythmias after single dose) • Chronic AF usually with cardiomyopathy: rate control, anticoagulation for 3 weeks (or TEE) followed by electrical cardioversion

42. Slow ventricular rate • Calcium channel blockers are preferred for the patient in absence of ventricular dysfunction. • Digoxin for the hemodynamically unstable may take longer to have effect. • Note reading the studies, it appears that the differentiation between “rate-control” and “cardioversion” is probably not real

43. Correct conditions: always • MI, Ischemia, valvular disease, pericarditis, hyperthyroidism, SSS, contusion, holiday, idiopathic, hypertensive heart, cardiomyopathy, cardiac surgery, catecholamine excess, PE, CHF, WPW

44. For this patient • It was felt that arrest was imminent and acute AF was most likely, The patient was cardioverted with 200 j. He converted to sinus and within 3 seconds reverted to AF • Class 1a, 3, and Ca blockers were rejected because of patient’s probable cardiomyopathy and hypotension/shock

45. For this patient • O2 and fluid resuscitation were started • Type specific blood was ordered • Digoxin 0.5 mg was given IV • Within 5 minutes the patient converted spontaneously to sinus tach. Blood and octriatide started, Pt admitted to ICU, GI consulted.

46. Case 4: I fainted (4 p.m.) • 14 y/o female brought by mother and teacher. Child reportedly was in Biology lab, dissecting a frog which upset her • The biology teacher reports she fell to the ground suddenly, had few jerks of extremities, and awoke, fully concious in about a minute. • Child has no memory of falling and had no prodromal sympotoms

47. I fainted • Child is awake and alert • VS are normal, glucometer is 110, SaO2=98% • Complete neuro exam is normal • General physical exam is normal • Should we quit? If not, what would you like to do?

48. I might quit, but • You could easily argue for a b-hcg, bmp, cbc, and a CT/EEG to r/o pregnancy/ectopic, anemia, seizure disorder and subarachnoid bleed • An ECG is harder to justify, but this is a cardiology lecture, so:

50. What to do? • Is there a problem? • What will you recommend?