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Ventricular Dysrhythmias

14. Ventricular Dysrhythmias. Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program. Ventricular Dysrhythmias. Premature ventricular complex (PVC) Ventricular escape complexes or rhythm Ventricular tachycardia Ventricular fibrillation Asystole. Ventricular Dysrhythmias.

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Ventricular Dysrhythmias

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  1. 14 Ventricular Dysrhythmias Fast & Easy ECGs, 2nd E – A Self-Paced Learning Program

  2. Ventricular Dysrhythmias • Premature ventricular complex (PVC) • Ventricular escape complexes or rhythm • Ventricular tachycardia • Ventricular fibrillation • Asystole

  3. Ventricular Dysrhythmias • Key features: • Wide (> 0.12 seconds in duration), bizarre QRS complexes • T waves in the opposite direction of the R wave • Absence of P waves

  4. Ventricular Dysrhythmias • Occur when: • The atria, AV junction, or both, are unable to initiate an electrical impulse • There is enhanced automaticity of the ventricular myocardium

  5. Ventricular Dysrhythmias • Can be benign or they can be potentially life-threatening (because the ventricles are ultimately responsible for cardiac output) I

  6. Premature Ventricular Complexes (PVCs) • Early ectopic beats that interrupt the normal rhythm • Originate from an irritable focus in the ventricular conduction system or muscle tissue Note: A PVC is not an entire rhythm—it is a single beat I

  7. Causes of PVCs • Enhanced automaticity or reentry, brought about by disruption of the normal electrolyte shifts during cell depolarization and repolarization • Causes include:

  8. Appearance of PVCs • PVCs are typically followed by a compensatory pause Q

  9. Appearance of PVCs • PVCs that look the same are called uniform (unifocal) • PVCs that look different from each other are called multiform (multifocal) Uniform Note: “Uni” means single, “multi” means many I Multiform

  10. Groupings of PVC • PVCs that appear after every • other normal beat are called bigeminal PVCs • second normal beat are called trigeminal PVCs • third normal beat are called qudrigeminalPVCs Bigeminal Trigeminal Quadrigeminal

  11. Couplets of PVCs • Two PVCs in a row are called a couplet and indicate extremely irritable ventricles

  12. Interpolated PVCs • PVCs that fall between two regular complexes and do not disrupt the normal cardiac cycle are called interpolated PVCs Q

  13. Run of PVCs • Three or more PVCs in a row are called a run of ventricular tachycardia or a run of PVCs Note: it may also be called a salvo, run, or burst of VT

  14. R-on T PVCs • PVCs occurring on or near the previous T wave (R-on-T PVCs) may precipitate ventricular tachycardia or fibrillation I

  15. Effects of PVCs • PVCs can be significant for two reasons • they can precipitate more serious dysrhythmias such as VT or VF • they can result in decreased cardiac output due to reduced diastolic filling time and a loss of atrial kick Note: When no pulse is felt during a PVC, it is called a nonperfusing PVC I

  16. Treatment of PVCs • Asymptomatic patients seldom require treatment • Patients with myocardial ischemia, treatment of frequent PVCs includes: • administration of oxygen and placement of an IV line • identifying and correcting the underlying factor causing the PVCs • in some settings, administering lidocaine or other antidysrhythmics (e.g., amiodarone) by IV push and a continued maintenance infusion • administering potassium chloride intravenously to correct hypokalemia or magnesium sulfate intravenously to correct hypomagnesemia; adjusting drug therapy; or correcting acidosis, hypothermia, and/or hypoxia

  17. Ventricular Escape Beats • Occur when there is temporary cessation of the heartbeat such as with sinus arrest or when the rate of the underlying rhythm falls to less than that the inherent rate of the ventricles

  18. Causes of Ventricular Escape Beats • Are compensatory in nature, occur when a higher pacemaker fails to initiate a heartbeat • Meant to preserve cardiac output • Can occur in sinoatrial pause/arrest, by a failure of the conductivity from the SA node to the AV node, or by AV (especially 3rd degree AV block)

  19. Effects of Ventricular Escape Beats • Low heart rate associated with the event leading up to the appearance of ventricular escape beats can result in a drop in blood pressure and syncope • Ventricular escape beats should be temporary as the heart should resume its normal electrical activity

  20. Treatment of Ventricular Escape Beats • Centers on treating the underlying condition • Support circulation, airway, and breathing; deliver oxygen; monitor the ECG, blood pressure and pulse oximetry; and establish an IV infusion • Continually reassess the clinical status and correct any reversible conditions • A primary goal of treatment is to maintain a ventricular rate sufficient to produce adequate cardiac output • Atropine or transcutaneous pacing can be used to treat the symptomatic patient • Drugs used to suppress ventricular activity such as lidocaine and amiodarone are contraindicated and may be lethal

  21. Idioventricular Rhythm • Slow dysrhythmia (rate of 20 to 40 BPM) with wide QRS complexes that arise from the ventricles Q I

  22. Causes of Idioventricular Rhythm • Massive myocardial ischemia or MI, digoxin toxicity, pacemaker failure, and metabolic imbalances • Other causes include:

  23. Effects of Idioventricular Rhythm • Slow ventricular rate and loss of atrial kick can significantly decrease cardiac output • resultant decreased cardiac output will likely cause patient to be symptomatic • Signs of decreased cardiac output such as disorientation, unconsciousness, hypotension, and/or syncope, and the patient may complain of dizziness, chest pain, and/or shortness of breath • In extreme cases, patient is pulseless I

  24. Treatment of Idioventricular Rhythm • For symptomatic patients: • Support the airway and breathing • Deliver oxygen, perform an ECG, monitor the blood pressure and pulse oximetry, and place an IV infusion • Continually reassess the clinical status, and correct any reversible conditions • Maintain a ventricular rate sufficient to produce adequate cardiac output • Administer atropine or deliver transcutaneous pacing • In unresolved idioventricular rhythm, the atropine dose may be repeated • Lidocaine and amiodarone are contraindicated • If there is no pulse, treat the dysrhythmia as if it is pulseless electrical activity (PEA)

  25. Accelerated Idioventricular Rhythm • Idioventricular rhythm that exceeds the inherent rate of the ventricles (60 to 100 BPM)

  26. Causes of Accelerated Idioventricular Rhythm • Same conditions that lead to idioventricular rhythm • Also, it is very common following acute MI • Further, it is often seen after administering thrombolytic medications • For that reason, it is considered a reperfusion dysrhythmia

  27. Effects of Accelerated Idioventricular Rhythm • While accelerated idioventricular rhythm is usually short lived and because the heart rate is close to normal, no ill effect may be seen • However, with accelerated idioventricular rhythm there may be decreased cardiac output, particularly when the rate is slower Q I

  28. Treatment of Accelerated Idioventricular Rhythm • Depends on whether the rhythm is sustained and whether or not cardiac output is diminished • For the symptomatic patient, transcutaneous pacing or atropine can be used • In unresolved idioventricular rhythm, the atropine dose may be repeated • Apermanent pacemaker may be required in sustained symptomatic accelerated idioventricular rhythm • Lidocaine and amiodarone are contraindicated and may be lethal • If there is no pulse, treat the dysrhythmia as if it were pulseless electrical activity (PEA)

  29. Ventricular Tachycardia (VT) • Fast dysrhythmia (100 to 250 BPM) that arises from the ventricles I

  30. Ventricular Tachycardia • Present when there are 3 or more PVCs in a row • May come in bursts of 6 to 10 complexes or may persist (sustained VT)

  31. Causes of Ventricular Tachycardia • Increased myocardial irritability that may be triggered by: • enhanced automaticity, • PVCs that occur during the downstroke of the preceding T wave, • reentry in the Purkinje system • Other causes include:

  32. Effects of Ventricular Tachycardia • Always significant • May be perfusing or nonperfusing • Even if the rhythm produces a pulse, it should be considered as potentially unstable because patients are likely to develop more life-threatening rhythms which progress into cardiac arrest • The rapid rate and concurrent loss of atrial kick associated with VT results in compromised cardiac output and decreased coronary artery and cerebral perfusion • Severity of symptoms varies with the rate of the VT and the presence and degree of underlying myocardial dysfunction I

  33. Treatment of Ventricular Tachycardia • Maintain a patent airway, administer oxygen, and place an IV line • Stable patient can be treated with antidysrhythmics (such as procainamide, amiodarone, or sotalol) • Unstable patients are managed with immediate synchronized cardioversion (100 J) • Energy level may be increased if the tachycardia does not convert with initial treatments (100, 200, 300, 360 J or the biphasic equivalent) • Contributing causes should be considered and treated • Patients with pulseless VT should be treated as though they are in VF I

  34. Ventricular Tachycardia • Monomorphic - appearance of each QRS complex is similar • Polymorphic - appearance varies considerably from complex to complex

  35. Causes of Torsades de Pointes • Associated with long QT syndrome, a condition whereby prolonged QT intervals are visible on the ECG • Causes include:

  36. Effects of Torsades de Pointes • Depends on the rate and duration of tachycardia and the degree of cerebral hypoperfusion • Findings include rapid pulse, low or normal blood pressure, or syncope or prolonged loss of consciousness • Pallor and diaphoresis may be noted, especially with a sustained episode • Can degenerate into VF

  37. Treatment of Torsades de Pointes • Cannot be reliably synchronized and should be managed like ventricular fibrillation (VF), with an initial unsynchronized shock • Standard antidysrhythmic drugs (such as procainamide) can worsen the condition, leading to cardiac arrest • Amiodarone may be effective in stable patients with normal QT interval • Magnesium sulfate should be administered in stable patients with prolonged QT interval • Offending drug(s) should be discontinued and electrolyte imbalance corrected • Patients with pulseless VT should be treated as though they are in VF, with the treatment of choice being prompt defibrillation

  38. Ventricular Fibrillation (VF) • Results from chaotic firing of multiple sites in the ventricles • Causes heart muscle to quiver rather than contract efficiently, producing no effective muscular contraction and no cardiac output I

  39. Ventricular Fibrillation • Most commonly associated with significant cardiovascular system disease • Causes include:

  40. Ventricular Fibrillation • Death occurs if patient not promptly treated (defibrillation) • Most common cause of prehospital cardiac arrest in adults

  41. Treatment of Ventricular Fibrillation • Prompt delivery of CPR and defibrillation • Organize ACLS actions around uninterrupted periods of CPR • Initiate securing the airway and placing an IV line in the course of treatment • After one shock and a 2-minute period of CPR, administer epinephrine or vasopressin • Amiodarone may be considered when VF/VT is unresponsive to CPR, defibrillation, and vasopressor therapy • If amiodarone is unavailable, lidocaine may be considered if allowed by local protocol • Continue CPR, stopping only to defibrillate and reassess rhythm. • Minimize interruptions in chest compressions before and after shock; resume CPR beginning with compressions immediately after each shock I

  42. Treatment of Ventricular Fibrillation • If the rhythm is successfully converted to an effective electromechanical rhythm (with a pulse and good perfusion): • assess vital signs, support airway and breathing, • provide medications to support blood pressure, heart rate, and rhythm and to prevent reoccurrence

  43. Asystole • Absence of any cardiac activity • Appears as a flat (or nearly flat) line • Complete cessation of cardiac output I

  44. Ventricular Standstill • Called ventricular standstill when the atria continue to beat but the ventricles have stopped • Seen as the presence of only P waves

  45. Asystole • Terminal rhythm • Chances of recovery extremely low I

  46. Treatment of Asystole • Promptly initiate CPR, deliver high-concentration oxygen, place an IV line, and secure the airway • Administer epinephrine, repeating its administration every 3 to 5 minutes • One dose of vasopressin may replace either the first or second dose of epinephrine • Continue CPR throughout the resuscitation effort, stopping periodically to reassess for a change in rhythm and to check for presence of a pulse • Follow local protocols for terminating resuscitation efforts • Always verify the presence of asystole in two leads prior to initiating treatment • Misplacement of an ECG lead or a loose wire can mimic asystole (or VF) on the monitor

  47. Pulseless Electrical Activity (PEA) • Condition that has an organized electrical rhythm on the ECG monitor (which should produce a pulse) but patient is pulseless and apneic I

  48. Treatment of PEA • Includes prompt initiation of CPR, high-concentration oxygen, placing an IV line, securing the airway and confirming placement • Administer epinephrine, repeating its administration every 3 to 5 minutes • One dose of vasopressin may replace either the first or second dose of epinephrine • Continue CPR throughout the resuscitation effort, stopping periodically to reassess for a change in rhythm and to check for a pulse

  49. Practice Makes Perfect • Determine the type of dysrhythmia I

  50. Practice Makes Perfect • Determine the type of dysrhythmia I

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