1. Cardiac Arrhythmias A Guide For Medical Students
William Beaumont Hospital
Department of Emergency Medicine

2. Evaluating Arrhythmias
Rate – Is it fast or slow?
If slow, is there group to group beating?
Rhythm – Is it regular, irregular or irregularly irregular?
P waves – Are they present?
QRS – Is it narrow or wide?

3. Sinus Bradycardia What is it? What causes it? When do you treat it?
How do you treat it?
Answers in next slide

4. Sinus Bradycardia Characteristics: Etiology: Sinus rhythm
Normal intervals
Rate less than 60 bpm
Etiology:
Normal variant
Beta blocker overdose
Digoxin overdose
Hypothermia
Hypothyroidism
Brady-tachy syndrome
SA node ischemia

5. Sinus Bradycardia Treatment:
Requires treatment only if there is evidence of hypoperfusion
Two treatment options:
Pacing: transvenous or transcutaneous
Atropine 0.5 mg IVP

6. Sinus Tachycardia Characteristics: Etiology: Treatment: Sinus rhythm
Faster than 100 bpm
Etiology:
Usually a physiologic response to a stressor
Volume depletion / low stroke volume
Hypoxia
Systemic pathology: fever, anemia, hyperthyroidism
Drugs
Treatment:
Treat the underlying cause

7. Atrial Arrhythmias Premature Atrial Contraction (PAC)
Multifocal Atrial Tachycardia (MAT)
Atrial Fibrillation (A-fib)
Atrial flutter (A-flutter)
Supraventricular Tachycardia (SVT)
Pre-excitation Syndromes (WPW)

8. Multifocal Atrial Tachycardia
Three distinct p waves in a narrow complex tachycardia
Causes:
Almost always associated with pulmonary disease (hypoxia)
Less often due to hypokalemia or hypomagnesemia
Treatment:
Treat the underlying disorder – usually hypoxia
Unlike the other atrial tachyarrhythmias, cardioversion is of no value in MAT

9. MAT Rule of Threes
3 different p waves, 3 different pr intervals and 3 different r to r intervals

10. Atrial Fibrillation: Causes
Cardiovascular – CAD, HTN, CHF, myopathy, myo-, endo- and pericarditis, infiltrative disease, valvular, congenital
Metabolic – thyroid, electrolytes
Pulmonary – pulmonary HTN, PE
Toxic – cocaine, ETOH (holiday heart), beta agonists
Sepsis
Idiopathic

11. Atrial Fibrillation: EKGs
Regularity – irregularly irregular
Rate – atrial rate usually > 350
Controlled – ventricular rate < 100
RVR – ventricular rate > 100
P wave – none discernable, may be flutter waves
QRS
Less that 0.12 seconds
If > 0.12 sec must rule out VT (which is usually more regular)

12. Atrial Fibrillation with RVR
Ventricular rate > than bpm
Patients usually symptomatic requiring rapid treatment
Unstable – cardioversion
Stable – control rate with calcium channel blockers, beta blockers or digitalis

13. Atrial Fibrillation Treatment
Recognize the underlying cause
A rate under 120 in an asymptomatic patient generally requires no emergent treatment
Unstable patients with acute rapid a-fib should receive synchronized cardioversion with J
Treatment otherwise depends on the duration

14. Atrial Fibrillation Treatment
Less than 48 hours duration
Unstable – Cardiovert, synchronized if possible, with J
May also cardiovert electively in symptomatic, stable patients
Pharmacologic cardioversion
Procainamide
Amiodarone
Ibutilide

15. Atrial Fibrillation Treatment
Longer duration predisposes the patient to atrial clot formation and failure of conversion
Greater than 48 hours duration
Rate control with diltiazem, beta blockers or digitalis
Do not attempt cardioversion unless emergently indicated
Anticoagulation and arrangement for echo

16. Atrial Flutter Patients usually with cardiac or pulmonary disease
Conduction through the AV node may be at a 2,3, 4, or 5:1 rate
If you see a ventricular rate close to 150, consider atrial flutter
Frequently is a transient rhythm which may degenerate into atrial fibrillation or convert to sinus

17. Treatment of Atrial Flutter
Unstable – immediate synchronized cardioversion
Stable
Vagal manuevers – if no carotid bruits
Adenosine – will not terminate the atrial tachycardia, but may allow flutter waves to become more apparent
Dig, beta blockers or calcium channel blockers for AV nodal blockade to slow the ventricular rate

18. Supraventricular Tachycardia (SVT)
AV nodal reentrant tachycardia
Usually regular, narrow complex tachycardia without p waves
Treatment
Adenosine
Beta blockers
Calcium channel blockers
Digoxin

19. Is it SVT, a-fib, a-flutter, sinus tach?
SVT – HR around 150s
Is it SVT, a-fib, a-flutter, sinus tach?

20. Wolf-Parkinson-White Syndrome
Pre-excitation Syndrome
AV re-entrant tachycardia (accessory pathway)
Short PR interval, delta waves
Treatment:
Treat like SVT if the QRS is narrow
If the QRS is wide or if afib is present, use amiodarone or procainamide
Slow the atrial rate and increase conduction through the AV node
Avoid ABCD – adenosine, beta blockers, calcium channel blockers, digoxin if wide QRS

21. Narrow complex WPW

22. Wide complex WPW

23. Atrioventricular Blocks
First Degree
Second Degree - Type I
Second Degree - Type II
Third Degree

24. Second Degree AV Blocks
Group to group beating
Second degree blocks are partial blocks
Two types
Type I, Mobitz I or Wenckebach – transient
Type II, Mobitz II or Classic – often degenerates into 3rd degree heart block

25. Second Degree: Mobitz Type I
Decremental conduction: grouped beats with progressively longer PR intervals until an impulse is not conducted (a p without a QRS)
Usually narrow QRS
May be associated with inferior MI
Treatment:
Generally requires no treatment
Atropine, temporary pacing if symptomatic

26. Second Degree, Mobitz Type II
Conduction fails suddenly, no change in the PR interval
This is NOT a benign rhythm
Often progresses to a complete heart block
Associated with anteroseptal MI
May have wide QRS

27. Second Degree, Type II: Treatment
No pharmacologic treatment
Atropine has no effect on the His-Purkinje system and may worsen the conduction ratio
Emergency treatment – transcutaneous or transvenous pacing

28. Third Degree Block Complete block – there is total AV Dissociation
None of the atrial impulses are conducted through to the ventricles
P and QRS are independent, P-P and R-R intervals constant
An escape rhythm will drive the ventricles
If the escape rhythm originates in the AV junction, the ventricular rate will be in the range of with a narrow QRS
If the escape rhythm originates in the ventricles, the ventricular rate will be in the range of with a wide QRS

29. Third Degree Block: Treatment
Although patients may be asymptomatic, transcutaneous or transvenous pacing is warranted
Autonomic drugs such as atropine will have no effect on ventricular rate
Type I anti-arrhythmics should be avoided as they may suppress the escape rhythm

30. Ventricular Arrhythmias
Premature Ventricular Contraction (PVC)
Ventricular tachycardia (VT)
Ventricular fibrillation (V-fib)

31. PVCs: Causes Generally benign
May be a consequence of a pathology, especially if multifocal
More concerning causes including hypoxia, ischemia, MI, toxins/drugs, acidosis or alkalosis, hypokalemia

32. Ventricular Tachycardia
Results from a dysrhythmia originating at or below the bundle of His
Has a wide QRS complex (>0.12 second)
May be monomorphic or polymorphic

33. Monomorphic V-tach Morphologically consistent QRS complexes
Most common form of V-tach
Seen primarily with cardiac ischemia
Also seen in cardiomyopathy, valvular disease, electrolyte imbalance, myocarditis

34. Polymorphic V-tach QRS complexes vary in structure and amplitude
Predominantly caused by CAD
Associated with more severe disease

35. Torsades de Pointes A specific form of polymorphic v-tach
Associated with prolonged QT
May be due to drugs (tricyclics), electrolyte imbalance (hypo K, Mg or Ca), or subarachnoid hemorrhage

36. V-Tach: Treatment Unstable: Stable:
Immediate unsynchronized cardioversion
100J, 200J, 300J, 360 J
Stable:
Amiodorone 150 mg IVP or lidocaine 1 mg/kg
Prepare for elective synchronized cardioversion
Torsades de Pointes: magnesium sulfate 1-2g IV

37. Ventricular Fibrillation
An irregularly irregular rhythm with no p waves or definite QRS complexes

38. Treatment of V Fib Defibrillate
Adult: 360/360/360 joules
Children: 2 J/kg
Epinephrine 1 mg IVP q 3-5 min (0.01 mg/kg)
Amiodarone
Lidocaine
Magnesium

39. Other EKG Abnormalities
Osborne Waves
Brugada Syndrome

40. Osborne Waves
Not a true arrhythmia, but an EKG abnormality suggestive of underlying pathology
Seen primarily in hypothermia, < 35.6 degrees
May also be seen in other conditions, such as hypercalcemia or brain injury
Also called J-waves, Camel backs, hathooks

41. Osborne Waves – Hypothermia

42. Osborne Waves – Hypercalcemia

43. Brugada Syndrome Genetic disease – autosomal dominant
Mutation in the gene that controls the Na channel
Prevalence for Asians
Characteristic ECG:
ST segment elevation V1-V3
No signs of ischemia
Short QT interval
Most common cause of sudden death in young
males with no underlying cardiac disease
Cause of death – polymorphic V-tach or V-fib
Treatment:
AICD to abort lethal arhythmias

44. Brugada Syndrome: Diagnostic Criteria
Type I is the only ECG criterion that is diagnostic of Brugada (see figure).
Definitive diagnosis – Type 1 ST-segment is observed in greater than one right precordial lead (V1 to V3) PLUS one of the following:
Documented V-fib
Polymorphic VT
Family history of sudden cardiac death at <45 yo
Inducibility of VT with electrical stimulation
Coved-type ECGs in family members
syncope
nocturnal agonal respiration.

45. Brugada Syndrome

46. The End
Any Questions?