Cardiovascular Dysfunction

1. Cardiovascular Dysfunction Arrythmias in the Critically Ill S. Mountain Sept. 25, 2008

2. For each case, please answer the following 4 questions: • 1. What is the rhythm? Why do you think so? What is your approach to the diagnosis of this rhythm? • 2. What are some likely causes/risk factors? • 3. What is the potential impact of this rhythm in the ICU patient? What are the risks of not treating this rhythm? • 4. How do you treat this rhythm? What are some of the risks of treating? How efficacious are the various treatments?

3. Case 1. (Todd) *  Difficulty rating. See EKG 1, below. You are called to see a 78 year old man in emerg. regarding hypotension and tachycardia. His wife noted he had a fever and was more difficult to rouse this morning. You quickly interpret the EKG, and for the benefit of your med student, you delineate the answers to the 4 questions above.

5. Sinus Tachycardia • …With 1st-degree bock and left atrial enlargement • Why? It’s a regular rhythm at about 100 bpm, with a narrow QRS, prolonged PRI (driven by wide P wave, but that’s the way it goes), normal axis, and no evidence of intraventricular conduction delay. There are no ST or T-wave abnormalities, nor Q waves. • Approach is systematic, or something will be missed. The computer on the ECG cannot be trusted.

6. Sinus Tachycardia Likely cause? • Sinus tachycardia is the heart’s response to stress. In this case, an elderly gentleman with a likely clinical presentation of sepsis may have sinus tachycardia for several reasons: • Fever • Vasodilation • Intravascular volume depletion • Acidosis • Anxiety/fear/discomfort

7. Sinus Tachycardia • Why might this be bad? What’s the worst that can happen? • Increased myocardial oxygen demand • Degeneration into other arrhythmias, including interventricular conduction delays • CHF (tachycardia-mediated cardiomyopathy) • Hypotension (decreased diastolic filling time, although this is rare with sinus rhythm, as atrial component is preserved, and rate is usually slow enough) • On the plus side, it is a diagnostic clue (i.e. SIRS criteria, Wells criteria, early sign of hemorrhage, etc) • Treatment: Underlying cause.

8. Case 2. (Neil)* *  Difficulty rating. While your junior medicine resident is writing up the E.R. patient, you are paged back to the ICU to see one of your patients. She is a 79-year-old woman who is admitted to the unit with heart failure, and was intubated yesterday. She was stable until a few minutes ago when her EKG tracing changed, and her sats dropped. Previous physical exam had revealed a systolic murmur loudest at the apex radiating to the axilla. An EKG was done while you were on the way up from the E.R. and is available for your interpretation. Your med student wonders what the diagnosis is, and what it’s significance is to your patient.

10. Atrial Fibrillation w/ rapid Ventricular response NO P waves Usually Narrow complex Irregularly irregular ventricular response Fibrillary waves of irregular atrial activation may be seen (inferior or V1)

11. Causes/Risk Factors Ischemic Heart Disease Valvular disease (esp. Mitral) Pericarditis Sick Sinus Myocardial contusion Hypertensive Heart disease Cardiomyopathy Cardiac Surgery CHF Accessory pathway (WPW) PE Catecholamine excess Acute Ethanol ingestion (Holiday heart) Idiopathic Hyperthyroidism SAH

12. Potential Impact of this rhythm • Can cause hemodynamic instability • Worsens NYHA class • Especially MS or HOCM • Loss of atrial systole can decrease LVEDP by 20-35% • AF in the ICU • Increase in stroke, heart failure, all cause mortality • W>M

13. Risks CHADS2 score

14. Treatment • Stable vs. Unstable • Hemodynamically • Pulm edema • Chest pain • DC Cardioversion vs. Chemical • Electrical • Conversion rates reported high(67-94%), but one reported 35% in surgical ICU patients • Recommended for AF 50-100J

15. When is it safe to cardiovert?HD stable • AHA Class I • <48 hours • Anticoagulated > 3 weeks (INR 2-3) • No atrial clot on TEE

16. Which drug to use? • AFFIRM (2002) • Rate control = rhythm control in mortality • Less ADR’s in rate control • Not our population (ie. Not stressed or hypotensive)

17. Which drug to use?Rate control • AHA Class I • B-blockers • Calcium channel blockers • AHA Class I in Heart Failure • Digoxin • Amioderone

18. Which drug to use?Rhythm control • AHA Class I • Flecanide • Propafenone • Dofetilide • ibutilide • AHA Class IIb • amioderone

19. Which drug to use?Rhythm control

21. Case 3. (Todd)* *  Difficulty rating . See EKG 3. Just as you have finished making your diagnosis and educating your student about the last patient, the alarm goes off on the patient’s monitor across the hall. He is an 80 year old man with a remote history of an MI. He is in the ICU post abdominal surgery, and has been recovering from intra-abdominal sepsis, but is nearly ready for the ward. His BP has dropped with this new rhythm. You call for an EKG, interpret it, and make a diagnosis and management plan. What are they?

23. Supraventricular tachycardia; AVRT • How do we know what it is? It’s a rapid, regular rhythm with a narrow QRS. There are small P waves before every QRS (best seen in lead II here, but look also in II, aVF and V1), with a short PR interval. • The R wave has a slight slur to it (delta wave), indicating a bypass tract (classically associated with Wolff Parkinson White Syndrome, but not pathognomonic)and ventricular preexcitation • WPW: short PR, wide QRS, secondary repolarization abnormalities, and PSVT

24. Accessory Pathway

26. Differential diagnosis includes: • Atrial flutter. The ventricular rate is often a factor of 300 (“classic” is 150 bpm), indicating 2:1 conduction of… • Flutter waves. These are the “sawtooth” waves between the QRS complexes, which often look like T-waves. 250-350 bpm. • A reentry circuit in the right atrium, which usually runs counterclockwise, with a well-known path between the IVC and TV annulus • Classic flutter: negative F waves in II, III, aVF, positive in V1. Clockwise flutter is the opposite.

27. Atrial FlutterLikely cause? • Usually associated with organic heart disease, and is most commonly seen in post-bypass patients. Like atrial fibrillation, may be associated with physiologic stress, including sepsis, myocardial ischemia, fever, etc. • Atypical (clockwise) atrial flutter may be a transition between sinus rhytm and atrial fibrillation, according to animal models.

28. Supraventricular Tachycardia • Why might this be bad? What’s the worst that can happen? • Ventricular rate of 150 leaves little time for diastolic filling for patients who need it… • Hypotension • Stroke risk thought to be similar to that of atrial fibrillation • In case of atrial flutter, 1:1 conduction is rare, but the resulting HR would be 250-300 bpm. • May degenerate to a-fib, as evidenced by common presentation of atrial fib/flutter on rhythm strips.

29. Supraventricular arrhythmias in the ICU • Very common between 03:00 and 07:30… • Goodman, Shirov, et al Critical Care and Trauma 104 (4) 2007: • Patients with new-onset supraventricular arrhythmia (SVA) had higher APACHE II scores, sepsis/SIRS, ARF, catecholamine infusions, and longer LOS (ICU and hosp) compared to those without SVA. • Risk factors for new-onset supraventricular arrhythmia: • Sepsis/SIRS (OR 50), (LD) dopamine or other catecholamines, hypothyroidism, pulmonary disease • In ICU, ischemia, ARF and hemorrhagic shock in the setting of new-onset SVA were associated with in-hospital mortality

30. SVA: bottom line • According to this paper, mortality in hospital, ICU and after discharge was statistically significantly higher (38%, 36%, 16%) in the new onset SVA group compared to those who had no SVA • SVA included atrial fibrillation, atrial flutter, “other”/paroxysmal supraventricular tachycardias

31. SVA: Treatment • If hemodynamically unstable: synchronized cardioversion (often responds to lower energy than VT, i.e. 120 J biphasic ); 95% effective • Save the patient now, chin-scratch over the ECG later • If diagnosis is in doubt, may try to slow A-V conduction to either diagnose the origin or terminate the rhythm, whichever occurs first • Vagal maneuver • Adenosine • Rapid atrial pacing, usually done with endocardial electrodes (such as those left in post CABG)

32. SVA: Pharmacologic Treatment • Adenosine (6 mg, proceed to 12 mg if unsuccessful, rapid IV push with saline chaser) • Diltiazem or verapamil may also be used UNLESS a bypass tract (AVRT) is suspected • They may accelerate conduction over the bypass tract! • Beta blockers, amiodarone • Procainamide (long infusion time), propafenone, flecanide • Ibutilide (Class III antiarrhythmic. Takes about 30 minutes, may cause Torsades de Pointes)

33. Case 4. (Yoan)* *  Difficulty rating. See EKG 4. Just as you finish with the man in case 3, you are paged back to emerg. You are asked to see a 23 year old woman, who has presented with a rapid heart rate, and is complaining of shortness of breath. Please diagnose the arrhythmia, and answer the 4 questions.

35. Case 5 Naisan “not a cardiologist” Garraway

36. The case As you are finishing in the E.R. you are called back to see the man from case 3 (above). He has gone into a new rhythm, and his blood pressure has dropped significantly. He is complaining of chest pain. What do you make of his EKG now?

38. VT or not? • In 1991 the Brugada Criteria were published • 4 criteria established by the authors, which were prospectively analyzed in a total of 554 tachycardias with a widened QRS complex (384 ventricular and 170 supraventricular). The sensitivity of the four consecutive steps as 0.987, and the specificity was 0.965. • Pedro Brugada,et al. Circulation 1991;83:1649-1659

39. Step 1: Lack of RS Complex An RS complex was present in at least one precordial lead in all SVTs with aberrant conduction But only 26% of VTs did not have an RS complex in any precordial lead. 100% specific for the diagnosis of ventricular tachycardia.

40. Step 2: Whether the R to S interval in any precordial lead is greater than 100 ms RS interval greater than 100 msec was not observed in any SVT with aberrant conduction. Half of the VTs which did have an RS complex in at least one precordial lead had an RS interval less than 100 msec RS interval of more than 100 msec in any precordial lead when an RS complex was present were each 100% specific for the diagnosis of VT

41. Step 3: AV Dissociation When looking at an EKG of a wide complex tachycardia it is always nice to see AV dissociation because it is 100% specific for the diagnosis of VT

42. Step 4: Morphology Criteria the morphology criteria are analyzed in leads V1 and V6 If both leads have a morphology compatible with the diagnosis of VT, the diagnosis of VT is made

43. Tachycardia with a right bundle branch block-like QRS Lead V1 Monophasic R or QR or RS favors VT Triphasic RSR' favors SVT Lead V6 R to S ratio <1 (R wave smaller than S wave) favors VT QS or QR favors VT Monophasic R favors VT Triphasic favors SVT R to S ratio >1 (R wave larger than S wave)favors SVT

44. Tachycardia with a left bundle branch block-like QRS Lead V1 or V2 Any of following R >30 msec, >60 msec to nadir S, notched S favors VT Lead V6 Presence of any Q wave, QR or QS favors VT The absence of a Q wave in lead V6 favors SVT

45. So lets see…..Step 1

46. Step 2 110 MS V1

47. For Fun Step 3 Not sinus, looks like afib

48. Afib

49. Step 4 Morphology • Tachycardia with a left bundle branch block-like QRS • Lead V1 or V2 • Any of following R >30 msec, >60 msec to nadir S, notched S favors VT • R is 40 msec, 70 msec to nadir S • Lead V6 • Presence of any Q wave, QR or QS favors VT The absence of a Q wave in lead V6 favors SVT

50. Another Algorythm