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Arrythmias in ICCU
Cardiac arrhythmias occur frequently in ICU patients, with the most common being sinus tachycardia. Arrhythmias are often seen in patients with structural heart disease and can be exacerbated by critical illness. Management involves treating any imbalances that may be triggering the arrhythmia as well as directed medical therapy. Arrhythmias in the ICU represent a major source of morbidity and increased length of stay.
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Arrythmias in ICCU
- 1. ARRHYTHMIAS IN ICU MSN Pavan ,DM. NIMS’HYDERABAD,AP.
- 2. Cardiac arrhythmiasoccur 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. • Arrhythmias aremost 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. ARRHYTHMIAS Brady (HR <60/mt) Tachy (HR> 100/mt) SND AVND Narrow QRS(<120ms) Wide QRS(≥120ms) IVCD ASYSTOLE
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- 6. Sinus node dysfunction 1. Sinus bradycardia: 2 . Sinus pause or sinus arrest. 3 . Sino atrial Exit Block.
- 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. 4 . SickSinus Syndrome Syndrome encompassing a number of sinus nodal abnormalities (1) persistent spontaneous sinus bradycardia not caused by drugs 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 irregular atrial tachyarrhythmias and periods of slow atrial and ventricular rates (bradycardia-tachycardia syndrome)
- 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. Indications for Pacingin 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/t necessary drug therapy, with hr <40 beats/min when a clear association between significant symptoms consistent with bradycardia and the actual presence of bradycardia has not been documented 2. Syncope of unexplained origin when major abnormalities of sinus node function are discovered in eps studies. Class IIb 1. Minimally symptomatic patients, chronic hr <40 bpm while awake
- 11. Atrioventricular block 1. First-DegreeAV Block 2 .Second-Degree AV Block Mobitz type I
- 12. 3 .Second-Degree AVBlock Mobitz type 2 Type 2 second-degree AV block is characterized 4 . Third-degree AV by intermittent failure of conduction of the P wave without changes in the preceding PR or RR Block intervals
- 13. Mobitz type I Mobitz type 2 Progressive prolongation of the Constant P-R intervals prior to A P-R interval prior to A nonconducted P wave nonconducted P Progressive 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 wave longer than the next conducted equal to the next conducted P-R P-R interval interval
- 15. • Etiologies ofAtrioventricular 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
- 16. Indications for Pacingin Acquired Atrioventricular Block in Adults Class 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 syndrome Class 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)
- 17. IVCD RBBB WITH LAFB RBBB WITH LPFB
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- 19. Guidelines for PermanentPacing in Chronic Bifascicular 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 not physiological Class IIb Neuromuscular diseases with any degree of fascicular block
- 20. Asystole • Patients whohave 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.
- 21. 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 pulse 1 mg Iv 1 mg Iv 1 mEq/kg Iv
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- 24. Atrial Fibrillation ECG : 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 at exertion slow < 60 – sick sinus syndrome very fast > 200 – accessory pathway
- 25. The estimated prevalenceof 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
- 26. • Anti thromboticmanagement in AF :
- 27. • Rhythm controlin AF: Disabling symptoms of heart failure with recurrent paroxysmal and persistent AF PAROXYSMAL AF ( <7 DAYS) PERSISTANT AF ( >7 DAYS)
- 28. • Rhythm controlin AF : Cardiac First line drug Second line drug condition Structurally normal Flecainide Sotalol, amidarone heart with out CAD Adrenergic AF Beta blockers Sotalol with out structural HD CAD with Dofetilide , sotalol Amidarone preserved LV function Heart failure Amidarone , -- dofetilide HTN with LV wall Flecainide Amidarone
- 29. • Rate controlin 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)
- 30. • Cardio versionin AF
- 31. 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 150 beats/min Presence of an isoelectric baseline distinguishes this arrhythmia from AF The absence of any intervening sinus rhythm distinguishes from normal sinus rhythm with frequent multifocal APCs Common in older pts with COPD and CHF , Digitalis, theophylline . Management is primarily directed toward the underlying disease
- 32. Atrial flutter • Atrialflutter is the most common type of macro reentrant atrial tachycardia. • Typical atrial flutter (counterclockwise flutter) • Atypical flutter (clockwise, or reverse flutter) • Atrial flutters originating in the left atrium
- 33. • Management OfAtrial 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 RFA Indications for anticoagulation in patients with atrial flutter are similar to those with atrial fibrillation.
- 34. Tachycardia Involving AVJunction • AVNRT • AVRT
- 35. • Treatment ofPSVT Hemodynami c Vagal maneuvers compromise 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
- 36. 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 tachycardia indicates atrial focus The distinction between AT with block and AFL can be difficult Atrial tachycardia Significant structural heart disease such as CAD with or with out MI Cor pulmonale , Digitalis intoxication Atrial tachycardia in a patient not receiving digitalis is treated in a manner similar to the treatment of other atrial tachyarrhythmias If atrial tachycardia appears in a patient receiving digitalis, therapy includes cessation of digitalis and administration of
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- 38. 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
- 39. Sinus tachycardia The sinus node exhibits a discharge frequency between 100 and 180 Sinus tachycardia is common in infancy and early childhood and is the normal reaction to various physiological or patho physiological stresses and drugs Treat the underlying disorder
- 41. 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
- 42. 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
- 43. • Ventricular tachycardiaclassification NonsustainedVT 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.
- 44. • Acute Managementof Sustained Ventricular Tachycardia Hemodynamic 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
- 45. • Bidirectional ventriculartachycardia Regular rhythm with ventricular rate is between 140 and 200 beats/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
- 46. • Polymorphic ventriculartachycardia • 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.
- 47. • Torsades dePointes 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.
- 48. • Torsades dePointes The upper limit for duration of the normal QT interval corrected for 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 at greater risk for torsades de pointes than men.
- 49. • Torsades dePointes 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
- 50. • Torsades depointes 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.
- 51. Ventricular flutter /fibrillation Ventricular flutter is manifested as a sine wave in appearance—regular large oscillations occurring at a rate of 150 to 300/min . Ventricular fibrillation is recognized by the presence of irregular undulations of varying contour and amplitude Distinct QRS complexes, ST segments, and T waves are absent. Fine-amplitude fibrillatory waves (0.2 mV) are present with prolonged ventricular fibrillation. These fine waves identify patients with worse survival rates and are
- 52. • 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.
- 54. •Ventricular fibrillation /tachycardia prevention Patients at continued risk for ventricular fibrillation or VT from nonreversible causes
- 55.
- 56. Intensive careunit (ICU) monitors generate a high rate of false alarms when physiological signals are severely corrupted by noise. To suppress the false life-threatening heart rate (HR)-related electrocardiogram arrhythmia alarms, data derived from arterial blood pressure (ABP) signal were used. A new ABP signal quality index (SQI) was designed based upon the combination of two previously reported signal quality measures. HR was then tracked based on beat detection from ABP and a Kalman filter with a SQI-modified update sequence The false alarm reduction rate was 74.13% and 53.81%, and the corresponding true alarm acceptance rate was 99.60% and 99.58% for extreme bradycardia and extreme tachycardia respectively. Combining ECG and ABP information therefore provides a significant reduction in false alarms with minimal impact on true alarms.
- 57.