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Transcript of Bhubaneswar / 15.10.06. Cardiac Arrhythmias in ICU Dr. P.K.Sahoo Cardiologist Kalinga Hospital...
Bhubaneswar / 15.10.06
Cardiac Arrhythmias in ICU
Dr. P.K.SahooCardiologistKalinga HospitalBhubaneswar
Cardiac arrhythmias do not necessarily mean structural
heart disease
Conditions provoking arrhythmias
CARDIAC• Myocardial Ischaemia• Valvular problems• CHF
NON CARDIAC• Hypoxemia• Hypercapnia• Hypotension• Electrolyte imbalance
(K;Ca;Mg)• Drug toxicity
When you suspect arrhythmia in ICU
• 12 lead ECG
• Long rhythm strip II;aVf or V1
• Double ECG voltage
• ↑ paper speed to 50mm/s
Arrhythmias in ICU
• Tachyarrhythmias (>100/min)
# Narrow QRS complex
# Wide QRS complex
• Bradyarrhythmias ( <60/min)
Clinical classification of arrhythmias
• Heart rate (increased/decreased)
• Heart rhythm (regular/irregular)
• Site of origin (supraventricular / ventricular)
• Complexes on ECG (narrow/broad)
Narrow QRS complex tachycardias
• Atrial premature beats
• Sinus Tachycardia (100-150)
• PSVT (150-250)
• Atrial tachycardia with blocks (150-250)
• Atrial flutter (250-350)
• Atrial fibrillation (>350)
• Multifocal atrial tachycardia
36 year old woman with asthma has ‘thumping in chest’
48yr.M; febrile
• Sinus tachycardia• Remove precipitating cause• BB if symptomatic
60yr. F. COPD; Resp. failure
• More than 3 different P wave shapes with varying PR interval
60yr. F. COPD; Resp. failure
Multifocal Atrial Tachycardia (Chaotic Atrial Tachycardia)
• Treat underlying lung disease
• Verapamil
ECG in Supraventricular Tachycardia
Atrial Flutter
Atrial Fibrillation
Relationship between P & QRS in supraventricular Tachycardia
(PR & RP interval)
AVNRT AVRT
Typical (Slow-Fast) Re-entry : PR > RP,
Atypical reentry (Fast-Slow), Sinus & Atrial tachycardias : PR < RP
ECG in AV Nodal Reentrant Tachycardia (AVNRT)
QRS is
•Regular (180-200/min)
•Narrow (<120ms),
•No distinct P wave or retrograde P just after QRS
WPW Syndrome
Sinus Rhthm Short PR, Delta wave. Wide QRS, Normal terminal QRS, Secondary ST/T changes
AVRTQRS is Regular (180-200/min)
Narrow (<120ms), Distinct retrograde P wave after QRS (RP<PR)
AF with Accessory pathway
Non- Paroxismal Junctional Tachycardia
Increased automaticity of a focus in AV junction (70 – 130 /min)
Retrograde P may precede QRS (High Junctional/Coronary sinus rhythm)
may coincide or may folow QRS (low junctional rhythm)
Wide QRS Tachycardia
Underlying Arrhythmia of Sudden Cardiac Death
VT62% Bradycardia
17%
Torsadesde Pointes
13%
PrimaryVF8%
Bayés de Luna A. Am Heart J. 1989;117:151-159.
Underlying Causes of Fatal Arrhythmias
15%
5%
Coronary Artery Disease
Cardiomyopathy
Other*
*ion-channel abnormalities, valvular or congenital heart disease, other causes
80%
Rhythm Strip During Episodeof Sudden Death
6:02 AM
6:05 AM
6:07 AM
6:11 AM
• VT degenerates into VF in 30 sec to 3 minutes
• 4 minutes into collapse,VF is identified in 90%, asystole identified in 10%
• As more time elapses,asystole and EMD areidentified in 60% of victims
The The
‘Dying ‘Dying
Heart’Heart’ !! !!
Wide QRS Tachycardia
• Ventricular Premature beats
• Ventricular Tachycardia
• Ventricular Fibrillation
• Torsades de pointes
• SVT with aberrancy
Cardiac ArrhythmiaPremature Ventricular Contraction
50 yr. M. post CABG presents with palpitations ;
(haemodynamically stable)
Misconceptions about VTMisconceptions about VT
MISDIAGNOSIS MISDIAGNOSIS
Haemodynamic stable wide QRS Haemodynamic stable wide QRS tachycardia cannot be VTtachycardia cannot be VT
UNDERDIAGNOSISUNDERDIAGNOSIS
Unexplained syncope : Unexplained syncope : ? Bradyarrhthmia / ??VT ? Bradyarrhthmia / ??VT
80% of wide QRS 80% of wide QRS tachycardias are VTtachycardias are VT
VT : manifestationsVT : manifestations
Syncope / Near syncopeSyncope / Near syncope
Wide QRS tachycardiaWide QRS tachycardia
Sudden Cardiac Death ( VF)Sudden Cardiac Death ( VF)
ECG ECG diagnosis of diagnosis of
VTVT
VT : Morphological typesVT : Morphological types
UNCHANGINGUNCHANGING : Monomorphic : Monomorphic
CHANGING :CHANGING : Polymorphic Polymorphic
# Repetitive – Torsades de Pointes# Repetitive – Torsades de Pointes
# Alternate complexes – Bidirectional VT# Alternate complexes – Bidirectional VT
# Stable but changing : RBB # Stable but changing : RBB LBB LBB
Monomorphic VT:Monomorphic VT:uniform QRS for all complexesuniform QRS for all complexes
Polymorphic VT:Polymorphic VT:beat to beat variation in QRS beat to beat variation in QRS
morphologymorphology
VT : common causesVT : common causes
MONOMORPHICMONOMORPHIC
CADCAD
DCMDCM
RV dysplasiaRV dysplasia
No structural diseaseNo structural disease
# RBB pattern# RBB pattern
# LBB pattern# LBB pattern
POLYMORPHICPOLYMORPHIC
Prolonged QTProlonged QT ( Torsades de ( Torsades de pointes)pointes)
# Congenital# Congenital
# Acquired# Acquired
Normal QTNormal QT
# Ischaemic (Acute)# Ischaemic (Acute)
# Others# Others
VT : How long does it last ?VT : How long does it last ?
SUSTAINED :SUSTAINED :
# >30sec.# >30sec.
# Requiring termination due to # Requiring termination due to haemodynamic instabilityhaemodynamic instability
NON SUSTAINED :NON SUSTAINED :
# <30 secs# <30 secs
# Stops spontaneously# Stops spontaneously
ECG in Ventricular Tachycardia (VT)ECG in Ventricular Tachycardia (VT)
Non-sustained VT (< 30 sec)Non-sustained VT (< 30 sec)
Sustained VT (≥ 30 sec)
Non sustained polymorphic VTNon sustained polymorphic VT
Polymorphic VT degenerating to Polymorphic VT degenerating to VFVF
Polymorphic VT in ICU :Polymorphic VT in ICU : search for a cause of prolonged search for a cause of prolonged
QT intervalQT interval
Polymorphic VT : prolonged QTPolymorphic VT : prolonged QT
PHARMACOLOGICAL AGENTSPHARMACOLOGICAL AGENTS
Quinidine, Erythromycin,Chloroquine, Quinidine, Erythromycin,Chloroquine, Amantadine,TCA,phenothiazines, Amantadine,TCA,phenothiazines, Organophosporous insecticides, Organophosporous insecticides, Antihistaminics ( astemizole, terfenadine)Antihistaminics ( astemizole, terfenadine)
ELECTROLYTE ABNORMALITIESELECTROLYTE ABNORMALITIES
Hypo Mg;K;CaHypo Mg;K;Ca
Is it Ventricular Tachycardia (VT)
or Supraventricular tachycardia with abberrancy (SVTab) ?
Wide QRS Tachycardia
Supraventricular Tachycardia with Aberration,BBB, Accessory pathway
Ventricular tachycardia Capture & Fusion beats, AV Dissociation / VA associationQRS > 140 msec, Superior QRS axis, Concordant pattern of QRS
AV Dissociation
Capture & Fusion beats
2:1 VA block
Bed side approach : VT vs SVTabBed side approach : VT vs SVTab
In an ICU setting In an ICU setting assume it to beassume it to be
VT rather than SVTab VT rather than SVTab
Specific Types of VT
Verapamil sensitive VT RBBB,LAD, Normal Heart
Arrhythmogenic RV DysplasiaVT with LBBB morphology
Specific Types of VT
Long QT Syndromes
Drugs, Electrolyte,
Genetic
(Jarvell & Lange-Nielsen
syndrome,
Romano-Ward Syndrome)
Brugada SyndromeRisk of MalignantVentricularArrhythmia & Sudden death
Torsades de pointes
60 year old man with recurrent blackouts
Malignant Ventricular Arrhythmia
Ventricular Flutter
Ventricular Fibrillation
Finally : a bad one !!!
Rhythm Management.
Acute Treatment of Regular Tachycardia
Haemodynamic Status
BP > 90/60
Narrow QRS DC Cardiovertion
Vagal Maneuvers
IV Adenosine/Verapamil/Diltiazem/esmolol
Vagal Maneuvers IV Adenosine
IV Lidocaine/Procainamide/Amiodarone
Refractory
IV Adenosine IV rocainamide/AmiodaroneAtrial PacingDC Cardioversion
Atrial PacingDC Cardioversion
BP < 90/60
Wide QRS
Refractory
Vagal Manoeuvres
• Carotid Sinus Pressure : # ? Carotid bruit # Firm pressure over carotid artery upper thyroid
cartilage # 5 secs. # One side at a time• Valsalva manoeuvre• Diving reflex : immerse face in ice cold water• Eyeball pressure: do not use
IV Adenosine
• ? Asthmatic • Warn patient : chest tightness/ pain;
flushing; feeling of panic ( ~20 secs)• Use large vein : Bolus; Rapid; flush
10ml.saline• Dose :3mg6mg9mg12mg till AV
block / termination• Low dose (0.5mg -1mg) in transplant
pts; pts. on dipyridamole
Arrhythmias post MI
Contain ischaemia
Beta-blockers calcium
antagonists
ACE inhibitors antiarrhymics
Preserve LV function
Prevent ventricular
dysrhythmias
Myocardial
infarction
CARDIAC DYSRHYTHMIAS &LVDYSFUNCTION IN MI
SURVIVORSMortality and
ventricular dysrhythmiaMortality and
LV dysfunction
LVEF %VPDs / hour
Tw
o-y
ear
mo
rtal
ity
Tw
o-y
ear
mo
rtal
ity
30
20
10
0 0.1 1 10 100 1000
60
50
40
30
20
10
0> 60 50-59 40-49 30-39 20-29 < 20
Acute termination of VTAcute termination of VT
PharmacotherapyPharmacotherapy
# Lidocaine# Lidocaine
# Procainamide# Procainamide
# Amiodarone# Amiodarone
# Betablockers# Betablockers
DefibrillationDefibrillation
Overdrive pacingOverdrive pacing
LidocaineLidocaine
Lidocaine DosingLidocaine Dosing– Suppression of ventricular ectopySuppression of ventricular ectopy
1.0 to 1.5 mg/kg may repeat every 5 minutes at 1.0 to 1.5 mg/kg may repeat every 5 minutes at half dose to a max of 3.0 mg/kghalf dose to a max of 3.0 mg/kg
– V-fib pulseless V-TachV-fib pulseless V-Tach1.5 mg/kg Q 3-5 min to a max of 3.0 mg/kg1.5 mg/kg Q 3-5 min to a max of 3.0 mg/kg
– Drip doseDrip dose2 to 4 mg/minute2 to 4 mg/minute
Lignocaine more effective Lignocaine more effective for acute coronary for acute coronary
syndromesyndrome
30% cases terminated30% cases terminated
Why Amiodarone ?Why Amiodarone ?
Terminates acute eventTerminates acute event
(may not be instantaneous)- (may not be instantaneous)- time to act !! time to act !!
Prevents recurrences after Prevents recurrences after cardioversioncardioversion
Amiodarone : First choice in VT ?Amiodarone : First choice in VT ?
ALIVEALIVE
ARRESTARREST
ALIVE STUDYALIVE STUDYAmiodarone As Compared With Lidocaine
For Shock-Resistant Ventricular Fibrillation (Dorian et al; NEJM, 2002)
Aim
To compare IV amiodarone and IV lidocaine in management of out-of-hospital ventricular fibrillation
347 pts of out-of-hospital VF resistant to either of 3 DC shocks followed by IV epinephrine & 4th DC shock
Persistent or recurrent VF after initial restoration of NSR
ALIVE ALIVE : DESIGN: DESIGN
Dosage regimen
5 mg/kg IV amiodarone in 5% dextrose by rapid infusion, or
1.5 mg/kg IV lidocaine rapidly infused
Followed with DC shock if necessary
If VF persistent, 2nd dose of amiodarone (5 mg/kg) or lidocaine (1.5 mg/kg)
Primary Outcome Criteria
Survival to hospital ICCU
ALIVEALIVE : RESULTS : RESULTSMedian duration from dispatch of paramedics to drug administration was 24 min for both drug
Su
rviv
al t
o A
dm
issi
on
22.8
12
24.8
14.2
0
5
10
15
20
25
AmiodaroneLidocaine
All pts Initial VF/ pulseless VT
p=0.009%
90% relative improvement in survival to hosp admission with amiodarone as compared to lidocaine
0
5
10
15
20
25
30
AmiodaroneLidocaine
Early Latetreatment treatment
193*
%
194*327*
325*
* time in min
p=0.05
ARRESTARREST((AAmiodarone in Out-of-Hospitalmiodarone in Out-of-Hospital R Resuscitation of esuscitation of ReRefractory fractory
SSustained Ventricular ustained Ventricular TTachyarrhythmias)achyarrhythmias) Non-traumatic Out-of-Hospital Cardiac Arrest (n=504)
VF or Pulseless VT
Shocks x 3
Persistent or Recurrent
VF/VT
Stable Rhyth
m
Asystole or PEA (Pulseless electrical
activity)
Study Drug
Standard ACLS Care
Excluded
ETT, IV, EPI
Placebo
Amiodarone
ARRESTARREST - Alive to hospital - Alive to hospital
4449
17
3439
120
10
20
30
40
50
60
All Rhythms VF Asystole/PEA
% o
f P
atie
nts
AmiodaronePlacebo
p=0.03p=0.03
29%26%
AmiodaroneAmiodarone
– Primary V-FibPrimary V-Fib300 mg bolus 300 mg bolus
– V-TachV-TachLoading dose 150 mg over 10 mins.Loading dose 150 mg over 10 mins.
1 mg/kg over next 6 hrs.1 mg/kg over next 6 hrs.
0.5mg/kg mg. maintainance 0.5mg/kg mg. maintainance
AmiodaroneAmiodarone
WATCH OUT !!!!WATCH OUT !!!!– Contraindicated in:Contraindicated in:
Second or third degree A-V blockSecond or third degree A-V block
Severe bradycardiaSevere bradycardia
PregnancyPregnancy
CHFCHF
HypokalaemiaHypokalaemia
Liver dysfunctionLiver dysfunction
Consider
• Lignocaine 100mg IV- can repeat once; then 2-4mg IV
• Different paddle position- antero-posterior• Bretylium tosylate- 5mg/ kg IV- continue
CPR for 20 mins• Procainamide 100 mg IV over 2 min.
Resistant VT / VFResistant VT / VF
Unresponsive VTUnresponsive VT
Rule outRule outAcidosisAcidosis
HypoxiaHypoxia
Electrolyte abnormalitiesElectrolyte abnormalities
? Drugs? Drugs
Magnesium SulphateMagnesium Sulphate
Polymorphic VT due toPolymorphic VT due to
# Hypokalemia ( CHF; Overdiuresis; # Hypokalemia ( CHF; Overdiuresis; Alcoholics)Alcoholics)
# Drug induced long QT# Drug induced long QT
DoseDose : Bolus 1-2gm/1-2 min : Bolus 1-2gm/1-2 min
Maintain 1-4gm/hr.Maintain 1-4gm/hr.
Beta Blockers ( Metoprolol)Beta Blockers ( Metoprolol)
Exercise induced VTExercise induced VT
Post Ischaemic VTPost Ischaemic VT
? Choice of Esmolol over Metoprolol? Choice of Esmolol over Metoprolol
No pharmacological No pharmacological cocktails please !!cocktails please !!
Automated External Defibrillator (AED)
EARLY DEFIBRILLATIONTo reestablish a normal spontaneous rhythm in the heart
Do not Do not hesitate to hesitate to defibrillate defibrillate
Defibrillation: ‘the single most important Defibrillation: ‘the single most important determinant of survival’determinant of survival’
(Cobbe et al 1992: ‘Heartstart Scotland’)(Cobbe et al 1992: ‘Heartstart Scotland’)
N=602
VTs to be defibrillatedVTs to be defibrillated(Unstable VTs)(Unstable VTs)
HypotensionHypotension
Chest Pain + SOBChest Pain + SOB
Pulmonary OedemaPulmonary Oedema
Location of paddlesLocation of paddles
Procedure of defibrillationProcedure of defibrillation
• Place paddles (with conducting paste or moist saline pads beneath them) over
• 2nd Intercostal space along right sternal border
• 5th or 6th Intercostal space at the apex of the heart
• Countershock of 200 joules - immediately
• If unsuccessful - 2nd countershock of 200 - 300 joules
• If VF still persists - 3rd countershock of 360 joules
• All 3 shocks - consecutively without interruption for CPR or drug therapy
Procedure of defibrillationProcedure of defibrillation
Energy selectionEnergy selection
ArrhythmiaArrhythmia initialinitial subsequentsubsequent maximummaximum
VFVF 200 J200 J 300J300J 360J360J
AFAF 100J100J 200J/300J200J/300J 360J360J
A FlA Fl 20-50J20-50J 100J100J 200J200J
ATAT 50J50J 100J100J 200J200J
VTVT 100J100J 200J/300J200J/300J 360J360J
0 2 4 6 8 10 12 14 16 18 20
Arrest Time (min)
CirculatoryPhase
ElectricalPhase
MetabolicPhase
Shock CPR ?
Importance of CPRImportance of CPRThree-Phase ModelThree-Phase Model
The 5 major changes in the 2005 guidelines:The 5 major changes in the 2005 guidelines:
1.1. improve delivery of effective chest compressionsimprove delivery of effective chest compressions
2.2. single compression-to-ventilation ratio (30:2) single compression-to-ventilation ratio (30:2) (except newborns)(except newborns)
3.3. each rescue breath should be given over 1 second each rescue breath should be given over 1 second to produce visible chest riseto produce visible chest rise
4.4. single shock followed by immediate CPR without single shock followed by immediate CPR without pulse or rhythm check for VF/ PVT cardiac arrestpulse or rhythm check for VF/ PVT cardiac arrest
5.5. AED use in children (1-8 years)AED use in children (1-8 years)
Important PointsImportant PointsImportant PointsImportant Points
RateRate
DepthDepth
ReleaseRelease
Five key aspectsto Great CPR
Five key aspectsto Great CPR
!!
UninterruptedUninterrupted
VentilationVentilation
Defibrillation (VF/ PVT): 1 Shock, Then Defibrillation (VF/ PVT): 1 Shock, Then Immediate CPR (NO pulse check, NO Immediate CPR (NO pulse check, NO
rhythm check)rhythm check)
SINGLE SHOCK = MORE CPRSINGLE SHOCK = MORE CPR
CONTINUE CPR WHILE MACHINE CONTINUE CPR WHILE MACHINE CHARGESCHARGES
Rationale - 1 Shock followed by Immediate Rationale - 1 Shock followed by Immediate CPRCPR
1.1. The rhythm analysis by current AEDs after The rhythm analysis by current AEDs after each shock typically results in each shock typically results in ≥ 37 sec≥ 37 sec delay delay in CPR in CPR
2.2. first shock eliminates VF in more than 85% of first shock eliminates VF in more than 85% of cases. If first shock fails, resumption of CPR is cases. If first shock fails, resumption of CPR is likely more beneficial likely more beneficial
3.3. it takes several minutes for a normal heart it takes several minutes for a normal heart rhythm to return and more time for the heart to rhythm to return and more time for the heart to create blood flow after VF is eliminated. CPR create blood flow after VF is eliminated. CPR can bridge that gap. can bridge that gap.
4.4. Immediate CPR after defibrillation is not Immediate CPR after defibrillation is not harmful.harmful.
1 shock versus 3 stacked shocks1 shock versus 3 stacked shocksBIPHASIC eliminates VF after first shock BIPHASIC eliminates VF after first shock >90%>90%AED requires 90 secs for 3 shocks (i.e. NO AED requires 90 secs for 3 shocks (i.e. NO CPR FOR 90 SECONDS)CPR FOR 90 SECONDS)Interruptions in chest compressions are Interruptions in chest compressions are harmfulharmful1 Shock strategy may be preferable1 Shock strategy may be preferable
Defibrillation – Energy setting Defibrillation – Energy setting
For adult defibrillation: For adult defibrillation:
– monophasic manual defibrillator 360J; monophasic manual defibrillator 360J;
– biphasic with truncated exponential biphasic with truncated exponential waveform 150-200J; waveform 150-200J;
– biphasic with rectilinear waveform 120J; biphasic with rectilinear waveform 120J;
– biphasic unknown type 200J.biphasic unknown type 200J.
Drug AdministrationDrug Administration
IV drug administration is preferred to ETT routeIV drug administration is preferred to ETT route
Drugs should be delivered during CPR as soon as Drugs should be delivered during CPR as soon as possible after rhythm checks.possible after rhythm checks.
timing of drug administration is less important than timing of drug administration is less important than the need to minimize interruptions in chest the need to minimize interruptions in chest compressionscompressions
Major changes in ACLS drugsMajor changes in ACLS drugs
VF/ pVT/ asystole/ PEA VF/ pVT/ asystole/ PEA – epinephrine q3-5 minepinephrine q3-5 min– Vasopressin X 1 may replace either the first or Vasopressin X 1 may replace either the first or
second dose of epinephrine.second dose of epinephrine.
VF/ pVTVF/ pVT– Amiodarone (Class IIb)Amiodarone (Class IIb)– Lidocaine (indeterminate)Lidocaine (indeterminate)
Bradycardia with recurrent Bradycardia with recurrent syncopesyncope
Atrioventricular (AV) Blocks in ICU
• First degree AV block
• Second degree AV block
• Third degree (complete) AV block
• Bifascicular and trifascicular block
1st Degree AV Block
EKG Characteristics: Prolongation of the PR interval, which is constant
All P waves are conducted
The Alan E. Lindsay ECG Learning Center ; http://medstat.med.utah.edu/kw/ecg/
2nd Degree AV Block
Type 1 (Wenckebach)
EKG Characteristics: Progressive prolongation of the PR interval until a P wave is not conducted.
As the PR interval prolongs, the RR interval actually shortens
EKG Characteristics: Constant PR interval with intermittent failure to conduct
Type 2
3rd Degree (Complete) AV Block
EKG Characteristics: No relationship between P waves and QRS complexes
Relatively constant PP intervals and RR intervals
Greater number of P waves than QRS complexes
www.uptodate.com
Bundle branch Blocks
Only reserved for acute situations.
1. ATROPINE 0.5 to 2mg IV
Vagolytic or Parasympatholytic
2. ISOPRENALINE 1 to 4g/min IV
Sympathomimetic, -receptor agonist Helpful in increasing HR when lesion upto
AV node. Insignificant effect on lower pacemaker.
PHARMACOLOGIC THERAPY OF BRADY ARRHYTHMIA
Non Invasive Non Invasive pacemakerpacemaker
Transvenous PacingTransvenous Pacing
Indications of Temporary pacing in Indications of Temporary pacing in ICUICU
AMI : AMI : # LBBB with 1# LBBB with 1stst degree HB degree HB # Mobitz type 2 / CHB# Mobitz type 2 / CHB # RVMI & bradyarrhythmias# RVMI & bradyarrhythmias Symptomatic blocks : Drug / Electrolyte Symptomatic blocks : Drug / Electrolyte
induced / poisoinings( oleander)induced / poisoinings( oleander) Overdrive pacing to terminate tachycardiasOverdrive pacing to terminate tachycardias Myocarditis with Heart blocksMyocarditis with Heart blocks VT : brady dependant / LQTS VT : brady dependant / LQTS
Disoriented male with low urine Disoriented male with low urine outputoutput
Sr. K = 7.6 meq / LSr. K = 7.6 meq / LUrea / Creatinine : Urea / Creatinine :
mildly elevatedmildly elevated
Post treatmentPost treatment
Hyper K ( 5.5 - 7.5)Hyper K ( 5.5 - 7.5)
Tall T (Earliest sign of Hyper K)Tall T (Earliest sign of Hyper K)Features to note in tall T Features to note in tall T
Peaking Peaking Narrow base Narrow base Directional change Directional change Best seen in II,III,V2-V5Best seen in II,III,V2-V5
Hyper K ( 7.5 - 10)Hyper K ( 7.5 - 10)
Flat / wide PFlat / wide PPR prolongationPR prolongationST depressionST depressionDisappearance of PDisappearance of PDecrease in R wave heightDecrease in R wave height
Hyper K ( > 10)Hyper K ( > 10)
QRS wideningQRS wideningVT/ VFVT/ VFBlocksBlocks
Arrhythmias in ICU:Arrhythmias in ICU:Do not be panickyDo not be panicky
you may lose the battle before you may lose the battle before fighting it !fighting it !
( but just don’t relax !!)( but just don’t relax !!)