Life Threatening Dysrhythmias

1. Life Threatening Dysrhythmias

2. Life Threatening Dysrhythmias • A life-threatening dysrhythmia is any rhythm that is associated with cardiac compromise and potential drop in cardiac output. Ventricular dysrhytmias, V-Tach and V-Fib are considered the most lethal but any abnormal beat can propagate the lead to compromise cardiac output state. Rhythm disturbance is considered the primary cause of sudden cardiac death (SCD).

3. Sudden Cardiac Death • Defined by AHA as death resulting from the sudden, abrupt loss of heart function in a person who may or may not have been previously diagnosed with heart disease. • 400,000 deaths per year • 1,000 deaths per day • 80-90% of SCD victims have CAD • Rhythm disturbance is the primary cause of SCD • Left Ventricular Dysfunction is the 2nd leading cause of SCD • Previous cardiac arrest is 3rd leading cause of SCD

4. Cardiac Electrophysiology • Automaticity: is the ability of each cardiac cell to generate a spontaneous impulse. The Sinoatrial (SA) node is the primary pacemaker of the heart because of the principles of: Lack of Competition and Frequency Dependent Inhibitions • Conductivity: is the transmission of the electrical impulse to adjacent cells, creating a depolarizing wave and subsequent myocardial contraction.

5. Impulse Conduction & Pathways • SA Node  Internodal pathways (atrial conduction)  AV Node (delay)  Bundle of His-Purkinje System (ventricular Contraction)

6. Action Potential • The depolarization wave occurs because of Ion changes across the cell membrane. • Alter the polarity (because ions have and electrical charge).

7. Fast Action Potential • Fibers of the atrial and ventricular tissue and His-Purkinje System. • Electrical impulse transmitted rapidly in these areas also called fast response tissue. • Resting is -90mV

8. Fast Action Phases • Phase 0: Rapid depolarization Na+ Channels open & Na- influx. • Phase 1: Brief Rapid Repolarization Termination of Na+ influx • Phase 2: Plateau (membrane stable) Ca++ enters the cell promoting contraction • Rapid depolarization K+ moves out Effective Refractory Period • Phase 4: Resting potential for depolarization.

9. For those who need pretty pictures Ca++ enters K+ leaves the cell Na+ Rushes in

10. Slow Action Potential • Resting is -60  70mV • Phase 0: Slow depolarization of SA & AV slow influx of Ca++ • Phase 1: There is no phase 1 • Phase 2: Insignificant in relationship to depolarization • Phase 3: Insignificant in relationship to depolarization • Phase 4: Spontaneous (rapid) repolarization

11. Slow Action Potentials Influx of Ca++

12. Pathophysiology • Arrhythmias develop for many reasons and are classified in many ways. • Primary cause: disturbance with the impulse formation or disturbance in conduction • Named according to where the Foci began/originated and whether the rhythm is fast, slow, early, or late.

13. Some Causes of Arrhythmias • Decreased Coronary Profusion (CAD) • Impaired Myocardial O2 Delivery (Hypoxia) • Electrical disturbances • Cardiac Muscle Injury • Ischemia or infarction • Defects in the Heart Muscle or Electrical System • Cardiac Surgery • Electrical Stimulation to the Heart Muscle • Medication • Wife’s Shopping Bill

14. Disturbance with Impulse Formation • Abnormal Automaticity: when a cell outside of the normal pathway fires. Happens with ischemia, acidosis, potassium shifts and catecholamine release. • Triggered Activity: The initiation of an abnormal depolarization that is ‘triggered’ by a normal depolarization. During repolarization (phase 1-4) there is an alteration which starts another depolarization (afterdepolarization). There are two types: Early Afterdepolarization and Delayed Afterdepolarizations

15. Early Afterdepolarization (EAD) • EAD occurs during phase 2 & 3 of the action potential. • Causes: Hypoxemia!, ischemia, electrolyte imbalances (Mg+), catecholamines, and antidysrhythmic agents. • Results: Polymorphic reentry VT better known as Torsde De Pointes

16. Early Afterdepolarization

17. Delayed Afterdepolarizations (DADs) • Occur during phase 4, after the repolarization is complete, but BEFORE the next ‘normal’ beat. • Dig Toxicity is associated with this type of depolarization.

18. Disturbance with Conduction • Reentry: Impulse transmission or depolarization typically travels in a unidirectional fashion. • When there is an impulse with varying degree of refractoriness it can cause a retrograde depolarization. • Causes: BBB, Ischemia, Infarction, and accessory pathways. • Notice it is all mechanical

19. Atrioventricular Nodal Blocks • A slowing or complete disruption in conduction of the impulse between the atria and the ventricle. • Cause: Electrical or Anatomical block of the impulse or decreased profusion to the node.

20. Treatment Options • Identify and treat the underlying cause!! • Electricity..Defibrilation /cardioversion: The passage of electrical current through the cardiac muscle (dells) causes massive depolarization.

21. What might get in your way? • Transthoracic Impedance: is the resistance to the current (from the defibrillator) from getting to the heart • Impedance is determined by: • Chest Size • Presence of Chest Hair • Size of Paddles • The Phase of Ventilation

22. Monophasic Verses Biphasic Waveform Defibrillators • Monphasic: One direct current • Biphasic: Directed with Redirected current shown to be superior…but expensive!

23. Pacing • For bradycardic Rhythms, electrical stimulation of the heart might be necessary with a transcutaneous, transvenous or permanent pacemaker. • Please be kind and sedate if possible.

24. Antidysrhythmic Agents • Drugs are SECONDARY to other interventions. • Sodium Channel Blockers (slow conduction velocity, negative Inotrope): Procainamide, Lidocaine, Dilantin • Beta Blockers (inhibit SNS): Inderal, Esmolol • Potassium Channel Blockers (delay repolarization, Prolong Q-T interval): Cordarone, Corvert (SVT) • Calcium Channel Blockers (Decrease SA node firing, decrease O2 demand and contractility) Cardizem, Verapamil

25. Specific Dysrhythmias • Tachycardias: The majority of the problem is decreased filling time. (A-Fib, V-Tach) decrease cardiac kick and up to 30% of cardiac output.

26. Narrow QRS Complex (SVT) Tachycardias • Rhythm: • Sinus Tachycardia (ST) • A-Fib, A-Flutter • Atrial Tachy (reentry) • Multifocal Atrial Tachycardia (AT) • Junctional Tachycardia (JT) • Accessory Pathway-Mediated  AT with accessory pathways, AV reentry Tachy.

27. Treatment (stable) • Evaluate Ventricular Function= is the patient stable? • A-Fib or AF: The length and time of with rhythm. Consider WPW and LV impairment before determining Tx. • Control rate • Convert Rhythm • Provide Anticoagulation • Vagal Stimulation • Adenosine • PSVT: B-Blockers, Ca++ Channel Blockers, Dig, Antiarrythmics and Cardioversion, If EF <40% Start with cardioversion. • JT: B-Blockers, CCB, Amiodorone, NO CARDIOVERSION!! • MAT: B-Blockers, CCB, Amiodorone, NO CARDIOVERSION!!

28. Unstable? • IMMEDIATE CARDIOVERSION!! • Then open your drug box.

29. Wide QRS Complex Tachycardias • Criteria for Wide QRS: • Rate >120bpm • Uniform QRS > 120ms

30. Rhythms • V-Tachycardia (VT) • V-Fib (VF) • SVT with aberrancy (identify and tx as SVT)

31. Treatments • Remember to evaluate ventricular function • V-Tach Stable with a pulse: • Monomorphic: Procanamide, Amiodorone, Lidocaine, (Amiodorone 1st if Ventricle impared) • Polymorphic: Normal QT – B-Blockers, Lidocaine, Amiodorone, Procainamide, (Amiodorone 1st if ventricularly impared) Long QT – Mg, Override pacing

32. Treatments (cont.) • V-Tach Unstable with a Pulse: • IMMEDIATE CARDIOVERSION!! • V-Tach without a Pulse – Treat as VF • V-Fib/Pulseless VT: • Assess ABC’s • BLS • Defibrillation:200, 300, 360j or equivalent with Biphasic • VASOPRESSIN or Epinephrine • Defibrillation 360j • Antiarrhythmics: Amiodorone, Lidocaine, Magnesium, Procainamide • Defibrillation 360j

33. Distinguishing VT from SVT with Aberrancy • VT: • Typically 110-250bpm • Usually regular • Stable or Unstable • AV dissociation • QRS .0.12 & maybe >0.14sec • QRS Configuration • Fusion & Capture If present = VT If absent = VT or SVT • Varying Systolic Blood Pressure

34. Distinguishing VT from SVT with Aberrancy • SVT with Aberrancy • May be >250bpm • Regular or Irregular • Stable or Unstable • AV Disassociation NOT PRESSENT • QRS Duration >0.12 & Usually <.14sec • Fusion & Capture NOT PRESSENT • Blood Pressure Consistent Systolic BP

35. Other Helpful Tips • History or Structural Heart Disease-Likely VT • ECG Reflects Old MI-Likely VT • Low LV EF-Likely VT • Elderly Patients-Likely VT • VT occurs More Frequently Than SVT with Aberrancy

36. Good Rule of Thumb • SVT: V1(usually)has a negative deflection V6 (usually) has a positive deflection • VT: V1 (usually) has a positive deflection V6 (usually) has a negative deflection • Look at all the other criteria to be sure: P waves, complex with, regularity…etc.

37. Enough with the chatter…Let’s Play! AV Dissociation = VT

38. Round TWO!! Sinus Tachycardia

39. This one is a tricky one…any brave souls? Ventricular Tachycardia = AV Dissociation

40. Exceptions to the rule Sinus Tachycardia

41. Last one…I promise! Atrial-Fib

42. Long QT Syndrome • QT is the repolarization of the ventricle • VT will be the outcome if the next R wave were to fall on the T wave. • Prolonged QT will increase the probability that an R on T can occur

43. Conditions that Lead to Long QT Syndrome • Congenital Long QT Syndrome • Exercise Induced QT Syndrome • Drug Induced QT Syndrome (Many drugs lenghten QT) • Antiarrhythmics • Tricyclic Antidepressants • Antimicrobials (Erythromycin) • Cardene • Propulsid • Haldol

44. Bradycardias • The major problem with slow rhythms is a lack of stroke volume to sustain adequate C.O. C.O. = HR X SV

45. Unstable Patient with Bradycardia • ABCs & BLS • Atropine • Transcutaneous Pacing • Dopamine • Epinephrine • Isoproterenol • If the Rhythm is Type II 2nd Degree or 3rd Degree HB and the patient is UNSTABLE pace ASAP

46. Any Questions?