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 !!)