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Cardiac Arrhythmias

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  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?

  4. Sinus Bradycardia • Characteristics: • 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: • 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 3different p waves, 3different 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 100-120 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 50-100 J • Treatment otherwise depends on the duration

  14. Atrial Fibrillation Treatment • Less than 48 hours duration • Unstable – Cardiovert, synchronized if possible, with 50-100 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. 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 40-60 with a narrow QRS • If the escape rhythm originates in the ventricles, the ventricular rate will be in the range of 20-40 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: • 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?