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.

1. ARRHYTHMIAS IN
ICU
MSN
Pavan ,DM.
NIMS’HYDERABAD,AP.

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. • 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. ARRHYTHMIAS
Brady (HR < 60/mt) Tachy (HR> 100/mt)
SND
AVND Narrow QRS(<120ms) Wide QRS(≥120ms)
IVCD
ASYSTOLE

5. BRADYARRYTHMIAS

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 . Sick Sinus 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 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/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-Degree AV
Block
2 .Second-Degree AV Block Mobitz
type I

12. 3 .Second-Degree AV Block 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 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

16. Indications for Pacing in 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

18. TRIFASICULAR
BLOCK

19. Guidelines for Permanent Pacing 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 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.

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

22. TACHYARRYTHMIA
S

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 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

26. • Anti thrombotic management in AF :

27. • Rhythm control in AF:
Disabling symptoms of heart failure with recurrent
paroxysmal and persistent AF
PAROXYSMAL AF ( <7 DAYS)
PERSISTANT AF ( >7 DAYS)

28. • Rhythm control in 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 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)

30. • Cardio version in 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
• Atrial flutter 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 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
RFA
Indications for anticoagulation in patients with atrial flutter
are similar to those with atrial fibrillation.

34. Tachycardia Involving AV Junction
• AVNRT
• AVRT

35. • Treatment of PSVT
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

37. Focal Atrial
Tachycardia

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 tachycardia classification
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 Management of 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 ventricular tachycardia
 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 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.

47. • 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.

48. • Torsades de Pointes
 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 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

50. • 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.

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. •Misinterpretations

56.  Intensive care unit (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. Thank you