Arrythmias in ICCU


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Cardiac arrhythmias occur frequently in ICU patients.
12% incidence of ventricular plus supra ventricular arrhythmias for a general icu population.
The most common arrhythmia is sinus tachycardia. Atrial arrhythmias also occur with some frequency , where as ventricular arrhythmias are less common but usually more ominous.
Not all arrhythmias seen in the ICU are of new onset , some patients have preexisting arrhythmias that can be exacerbated by their critical illness

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Arrythmias in ICCU

  2. 2.  Cardiac arrhythmias occur frequently in ICU patients.• 12% incidence of ventricular plus supra ventricular arrhythmias for a general icu population. The most common arrhythmia is sinus tachycardia. Atrial arrhythmias also occur with some frequency , where as ventricular arrhythmias are less common but usually more ominous.• Not all arrhythmias seen in the ICU are of new onset , some patients have preexisting arrhythmias that can be exacerbated by their critical illness .
  3. 3. • Arrhythmias are most likely (90%) to occur in patients with structural heart disease, the inciting factor for an arrhythmia in a given patient may be a transient imbalance.• Management includes correction of these imbalances as well as medical therapy directed at the arrhythmia itself.• The urgency and type of treatment is determined by the physiologic impact of the arrhythmia as well as by underlying cardiac status.• Arrhythmias in the ICU represent a major source of morbidity and increased length of stay.
  4. 4. ARRHYTHMIASBrady (HR < 60/mt) Tachy (HR> 100/mt) SND AVND Narrow QRS(<120ms) Wide QRS(≥120ms) IVCD ASYSTOLE
  6. 6. Sinus node dysfunction1 . Sinus bradycardia:2 . Sinus pause or sinus arrest. 3 . Sino atrial Exit Block.
  7. 7. • 3 . Sino atrial Exit Block.  First-degree SA exit block cannot be recognized on the ECG because SA nodal discharge is not recorded  During type I (Wenckebach) second-degree SA exit block, the P-P interval progressively shortens prior to the pause, and the duration of the pause is less than two P-P cycles  An interval without P waves that equals approximately two, three, or four times the normal P-P cycle characterizes type II second-degree SA exit block  Third-degree SA exit block can be manifested as a complete absence of P waves and is difficult to diagnose with certainty without sinus node electrograms.
  8. 8. 4 . Sick Sinus SyndromeSyndrome encompassing a number of sinus nodalabnormalities(1) persistent spontaneous sinus bradycardia not caused bydrugs and inappropriate for the physiological circumstance(2) sinus arrest or exit block(3) combinations of SA and AV conduction disturbances(4) alternation of paroxysms of rapid regular or irregularatrial tachyarrhythmias and periods of slow atrial andventricular rates (bradycardia-tachycardia syndrome)
  9. 9. Extrinsic Intrinsic Drugs Sick sinus syndrome (SSS) Beta blockers,Digoxin, Coronary artery disease Adenosine Calcium channel blockers Inflammatory Antiarrhythmics (class I and Pericarditis, Myocarditis, RHD,CTD III) Hypothyroidism, Hypothermia Lyme disease Sleep apnea, Hypoxia Senile amyloidosis Increased intracranial pressure Congenital heart disease Autonomic TGA/Mustard and Fontan repairs• Endotracheal suctioning Diagnosis Iatrogenic The combination of findings are indicator of intrinsic SA node disease. cSNRT -525ms , SACT -125ms IHR - 117.2 – (0.53 x age) in beats/min (0.2 mg/kg propranolol and 0.04 mg/kg atropine)
  10. 10. Indications for Pacing in Sinus Node Dysfunction Class I 1. symptomatic bradycardia or sinus pauses.essential long-term drug. 2. Symptomatic chronotropic incompetence . Class IIa 1. Sinus node dysfunction occurring spontaneously or d/tnecessary drug therapy, with hr <40 beats/min when a clearassociation between significant symptoms consistent withbradycardia and the actual presence of bradycardia has not beendocumented 2. Syncope of unexplained origin when major abnormalities ofsinus node function are discovered in eps studies. Class IIb 1. Minimally symptomatic patients, chronic hr <40 bpm whileawake
  11. 11. Atrioventricular block1. First-Degree AV Block 2 .Second-Degree AV Block Mobitz type I
  12. 12. 3 .Second-Degree AV Block Mobitz type 2 Type 2 second-degree AV block is characterized4 . Third-degree AV by intermittent failure of conduction of the P wave without changes in the preceding PR or RR Block intervals
  13. 13. Mobitz type I Mobitz type 2Progressive prolongation of the Constant P-R intervals prior to A P-R interval prior to A nonconducted P wave nonconducted PProgressive shortening of R-R Constant R-R intervals intervals P-R interval prolongation at Constant P-P intervals progressively decreasing increments the last conducted P-R interval the last conducted P-R interval prior to the blocked P wave prior to the blocked P wavelonger than the next conducted equal to the next conducted P-R P-R interval interval
  14. 14. • Etiologies of Atrioventricular Block Metabolic Hyperkalemia , Hypermagnesemia Coronary artery disease Acute MI Drug-related Beta blockers , Adenosine ,Calcium channel blockers , Antiarrhythmics (class I & III) ,Digitalis, Lithium Infectious Endocarditis , Lyme disease, Diphtheria, Chagas Heritable/congenital Inflammatory Infiltrative Neoplastic/traumatic Degenerative
  15. 15. Indications for Pacing in Acquired Atrioventricular Block in AdultsClass I 1. 3rd & advanced 2nd-degree AV block at any anatomic level, associated with symptoms , essential drugs , after catheter abltion , post operative , neuromuscular diseases , periods of asystole 3.0 sec or any escape rate <40 beats/min in awake 2. mobitz type 2 AV block asymptomatic with broad QRS Class IIa 1. Asymptomatic AV block third-degree at any anatomic site rates if cardiomegaly or LVD is present type II second-degree AV block with a narrow QRS. type I second-degree AV block at intra- or infra-His levels found at EPS 2. 1st degree AV block with symptoms like pacemaker syndromeClass IIb 1. Marked 1st-degree AV block (>0.30 sec) with LVD and symptoms of CHF 2. Neuromuscular diseases with any AV block (including 1st-degree AV block)
  18. 18. Guidelines for Permanent Pacing in ChronicBifascicular and Trifascicular Block Class I Intermittent third-degree AV block Type II second-degree AV block Alternating bundle branch block Class IIa HV interval ≥100 msec in asymptomatic EPS of pacing-induced infra-His block that is notphysiological Class IIb Neuromuscular diseases with any degree offascicular block
  19. 19. Asystole• Patients who have a bradyarrhythmia or asystole at initial contact  Are less common presentation of cardiac arrest(10- 30%)  Have the worst prognosis  Only 9 % of such patients were admitted to hospital alive  None was discharged  Brady arrhythmias also have adverse prognostic implications after defibrillation from VF in the field Children had a higher probability of asystole as the initial documented rhythm but had a better overall survival rate because they had better outcomes of interventions for these rhythms than adults.
  20. 20. Bradyarrhythmia/ Asystole Maintain continuous CPR , Intubate Identify and treat reversible causes Continue CPR • Hypoxia • Hyper/Hypokalemia • Severe acidosis Pacing :external • Drug overdose or pacing wire • Hypothermia Epinephrine -------Atropine ------- Sodium Paced rhythm bicarbonate and pulse1 mg Iv 1 mg Iv 1 mEq/kg Iv
  22. 22. Atrial FibrillationECG : Absent p wave with irregularly irregular R-R interval Coarse fib waves (differentiate from AFL) Regular R-R intervals in AF Prolonged QRS duration in AF ventricular rates controlled – 60-90 at rest and 90-115 atexertion slow < 60 – sick sinus syndrome very fast > 200 – accessory pathway
  23. 23. The estimated prevalence of AF is 0.4% to 1% in the general population ,increasing with ageAtrial pressure elevation, atrial ischemia, Inflammatory or infiltrative atrial disease, Drugs, Endocrine disorders, Post operative, Congenital heart disease, Neurogenic , loneAF
  24. 24. • Anti thrombotic management in AF :
  25. 25. • Rhythm control in AF: Disabling symptoms of heart failure with recurrent paroxysmal and persistent AF PAROXYSMAL AF ( <7 DAYS) PERSISTANT AF ( >7 DAYS)
  26. 26. • Rhythm control in AF :Cardiac First line drug Second line drugconditionStructurally normal Flecainide Sotalol, amidaroneheart with outCADAdrenergic AF Beta blockers Sotalolwith out structuralHDCAD with Dofetilide , sotalol Amidaronepreserved LVfunctionHeart failure Amidarone , -- dofetilideHTN with LV wall Flecainide Amidarone
  27. 27. • Rate control in AF: 1. Minimal or no symptoms of heart failure with paroxysmal and persistent AF 2. Permanent AF 3. PIAF(2000), RACE(2002) ,STAF(2002) , AFFIRM(2002) , HOTCAFÉ(2004) showed no difference in rate and rhythm control With accessory pathway Amidarone (IIa) With out accessory Metaprolol , proponolol , pathway esmolol, diltiazem, verapamil(I) Heart failure with out Digoxin (I) accessory pathway Amidarone(IIa)
  28. 28. • Cardio version in AF
  29. 29. Multifocal atrial tachycardia The atrial rhythm is characterized by at least three distinct P wave morphologies at least three different PR intervals atrial and ventricular rates are typically between 100 and 150beats/min Presence of an isoelectric baseline distinguishes this arrhythmiafrom AF The absence of any intervening sinus rhythm distinguishes fromnormal sinus rhythm with frequent multifocal APCs Common in older pts with COPD and CHF , Digitalis,theophylline . Management is primarily directed toward the underlying disease
  30. 30. Atrial flutter• Atrial flutter is the most common type of macro reentrant atrialtachycardia.• Typical atrial flutter (counterclockwise flutter)• Atypical flutter (clockwise, or reverse flutter)• Atrial flutters originating in the left atrium
  31. 31. • Management Of Atrial Flutter Cardio version Synchronous DC low energies 50J IV ibutilide(convert 60-90% but inc QTc) IV Procainamide Rapid atrial pacing with a catheter in the esophagus or the right atrium Slow the ventricular rate Verapamil , adenosine , esmolol , digitalis, amidarone AFL is much more difficult to rate-control than AF Class IA , IC ,III RFAIndications for anticoagulation in patients with atrial flutter are similar to those with atrial fibrillation.
  32. 32. Tachycardia Involving AV Junction• AVNRT• AVRT
  33. 33. • Treatment of PSVTHemodynamic Vagal maneuverscompromise Carotid sinus massage Valsalva maneuver Exposure of the face to ice water Adenosin DC shock Verapamil Or Diltiazem Competitive pacing Long-acting calcium antagonist Long-acting beta- blocker, Digitalis , RFA
  34. 34. Focal Atrial Tachycardia Generally have atrial rates of 150 to 200 beats/min P wave contour different from that of the sinus P wave Characteristic isoelectric intervals between P waves Analysis of P wave configuration during tachycardiaindicates atrial focus The distinction between AT with block and AFL can bedifficult Atrial tachycardia Significant structural heart disease such as CAD with orwith out MI Cor pulmonale , Digitalis intoxication Atrial tachycardia in a patient not receiving digitalis istreated in a manner similar to the treatment of other atrialtachyarrhythmias If atrial tachycardia appears in a patient receiving digitalis,therapy includes cessation of digitalis and administration of
  35. 35. Focal AtrialTachycardia
  36. 36. PJR TSVT with a long RP interval that exceeds the PR intervalTachycardia is maintained by anterograde AV nodal conduction and retrograde conduction over the accessory pathwayPosteroseptal accessory pathway (most often right ventricular, but other locations as well) that conducts very slowly, possibly because of a long and tortuous route, appears responsibleElectrocardiographic manifestations of accessory pathway conduction during sinus rhythm are absent.Incent tachycardia with treatment similar to PSVT
  37. 37. Sinus tachycardia The sinus node exhibits a discharge frequency between100 and 180 Sinus tachycardia is common in infancy and earlychildhood and is the normal reaction to various physiologicalor patho physiological stresses and drugs Treat the underlying disorder
  38. 38. SVT with aberrancy & AF with WPW  Drugs That Slow Conduction in, and Prolong Refractoriness Affected Tissue Drugs Accessory Class IA pathway AV node Class II , Class IV , Adenosine, Digitalis  Patients with a history of recurrent symptomatic Both Class IC , Class III (amiodarone) SVT episodes, incessant SVT, and heart rates >200 beats/min with SVT should be given strong consideration for undergoing catheter ablation
  39. 39. Ventricular tachycardia• QRS contours during the VT can be Monomorphic , polymorphic, torsades de pointes, bidirectional VT• Ischemic heart disease , cardiomyopathy , ion channel abnormalities , mitral valve prolapse , valvular heart disease, congenital heart disease , LVH , Coronary artery spasm , after coronary artery bypass grafting
  40. 40. • Ventricular tachycardia classificationNonsustainedVT Three or more beats in duration , terminating spontaneously in less than 30s SustainedVT VT greater than 30s in duration and / or requiring termination due to Hemodynamic compromise in less than 30s. Monomorphic VT with a stable single QRS morphology. Polymorphic VT with a changing or multiform QRS morphology at cycle length Between 600 and 180 ms.
  41. 41. • Acute Management of Sustained Ventricular TachycardiaHemodynamic Decompensation No hemodynamic decompensation Cardio version  Acute termination by DC cardio version administering IV Amiodarone, Thump version Lidocaine, Or Procainamide Ventricular pacing  Amiodarone, sotalol, and procainamide appear to be TYPE OF VT SPECIFIC DRUG lidocaine superior to CPVT Beta blocker OUT FLOW Vagal maneuvers, adenosine, beta TRACT VT blockers and verapamil FASICULAR VT IV verapamil BB Reentrant Pace termination VT
  42. 42. • Bidirectional ventricular tachycardia Regular rhythm with ventricular rate is between 140 and 200beats/min Alternating polarity in the frontal plane from -60 to -90 to+120 to +130 Digitalis excess and CPVT Digitalis excess 1. Typically in older patients and with severe myocardial disease 2. The extent of toxicity is often advanced, with a poor prognosis
  43. 43. • Polymorphic ventricular tachycardia • VT with a changing or multiform QRS morphology at cycle length Between 600 and 180 ms. • Causes of 1) Ischemia , Myocarditis 2) Long & short QT syndrom 3) Brugada syndrome 4) Familial catecholaminergic polymorphic VT.
  44. 44. • Torsades de PointesVT characterized by QRS complexes of changing amplitude that appear to twist around the isoelectric line and occur at rates of 200 to 250/mincharacterized by prolonged ventricular repolarization, with QT intervals generally exceeding 500 millisecondsThe abnormal repolarization need not be present or at least prominent in all beats, but may be apparent only on the beat prior to the onset of torsades de pointesLong-short R-R cycle sequences commonly precede the onset of torsades de pointes from acquired causesTorsades de pointes can terminate with progressive prolongation in cycle length and larger and more distinctly formed QRS complexes and culminate in a return to the basal rhythm, a period of ventricular standstill, and a new attack of torsades de pointes or ventricular fibrillation.
  45. 45. • Torsades de Pointes The upper limit for duration of the normal QT interval correctedfor heart rate (QTc) is often given as 0.44 second 0.46 second for men and 0.47 second for womenWomen, perhaps because of a longer QT interval, are atgreater risk for torsades de pointes than men.
  46. 46. • Torsades de Pointes causesAntibiotics : antimalarials , erythromycin , quinalones , ketaconazoleAntihistaminics : astemazole , terfenidineAntidepressants : tricyclicAntiarrythmics : class IA , III , ICAntiemetics : cisaprideAntipsychotics : phenothiazinesStructural lesions : MVP , cardiac ganglionitis , CNS lesionsOthers : liquid protein diet , starvationCongenital
  47. 47. • Torsades de pointes treatmentIV magnesium is the initial treatment of choice for torsades de pointes from an acquired causeTemporary ventricular or atrial pacing.Isoproterenol can be used to increase the rate until pacing is institutedLidocaine, mexiletine, or phenytoin can be triedThe cause of the long QT should be determined and corrected, if possibleTorsades de pointes resulting from congenital long-qt syndrome is treated with beta blockade, surgical sympathetic interruption, pacing, and ICD.
  48. 48. Ventricular flutter / fibrillationVentricular flutter is manifested as a sine wave inappearance—regular large oscillations occurring at arate of 150 to 300/min .Ventricular fibrillation is recognized by the presence ofirregular undulations of varying contour and amplitudeDistinct QRS complexes, ST segments, and T wavesare absent.Fine-amplitude fibrillatory waves (0.2 mV) are presentwith prolonged ventricular fibrillation. These fine wavesidentify patients with worse survival rates and are
  49. 49. • Ventricular fibrillation Ventricular fibrillation occurs in various clinical situations but is most commonly associated with coronary artery disease and as a terminal event Ventricular fibrillation can occur during Antiarrhythmic drugs, Hypoxia, Ischemia , Atrial fibrillation Very rapid ventricular rates in the preexcitation syndrome Electrical shock administered during cardioversion Accidentally by improperly grounded equipment During competitive ventricular pacing to terminate VT In patients resuscitated from out-of-hospital cardiac arrest, 75 percent have ventricular fibrillation Of such patients, 40 percent were successfully resuscitated and admitted to the hospital alive and 23 percent were ultimately discharged alive.
  50. 50. •Ventricular fibrillation / tachycardia prevention Patients at continued risk for ventricular fibrillation or VT from nonreversible causes
  51. 51. •Misinterpretations
  52. 52.  Intensive care unit (ICU) monitors generate a high rate offalse alarms when physiological signals are severely corruptedby noise. To suppress the false life-threatening heart rate (HR)-relatedelectrocardiogram arrhythmia alarms, data derived from arterialblood pressure (ABP) signal were used. A new ABP signal quality index (SQI) was designed basedupon the combination of two previously reported signal qualitymeasures. HR was then tracked based on beat detection fromABP and a Kalman filter with a SQI-modified update sequence The false alarm reduction rate was 74.13% and 53.81%, andthe corresponding true alarm acceptance rate was 99.60% and99.58% for extreme bradycardia and extreme tachycardiarespectively.Combining ECG and ABP information therefore provides asignificant reduction in false alarms with minimal impact on truealarms.
  53. 53. Thank you