ETIOLOGY, DIAGNOSIS AND MANAGEMENT

1.  PRESENTERS:DR.SHARATH
DR.DHEERAJ
 MODERATOR: DR.GOPINATH
 DR.PRATHYUSHA
DEPARTMENT OF ANAESTHESIOLOGY
ESIC MEDICAL COLLEGE
HYDERABAD

2. 1)GROSS ANATOMY
2)PHYSIOLOGY
3)CLASSIFICATION
4)MECHANISM
5)ETIOLOGY
6)MANAGEMENT

5.  HEART RATE
TACHYDYSRHYTHMIAS: >100 bpm
BRADYDYSRHYTHMIAS: <60 bpm
 SITE OF THE ABNORMALITY
ATRIAL
JUNCTIONAL
VENTRICULAR

6. Mechanisms of Cardiac Arrhythmias
Mechanisms of bradycardias:
Sinus bradycardia is a result of abnormally slow
automaticity, while bradycardia due to AV block is caused
by abnormal conduction within the AV node or the distal AV
conduction system.
Mechanisms generating tachycardias include:
- Accelerated automaticity.
- Triggered activity
- Re-entry (or circus movements)

7.  SA node
 60 to 100 bpm
 AV node
 40 to 60 bpm
 Ventricular specialized conduction tissue
 30-45 bpm

8.  Abnormal automaticity can occur in virtually
all cardiac tissues and may initiate
dysrhythmias called ectopic rhythm.
 Automaticity of cardiac tissue changes when
the slope of phase 4 depolarization shifts or
RMP changes.
 Such changes are thought to produce sinus
tachycardia, escape rhythms and accelerated
AV nodal (junctional) rhythms.

9.  The majority of regular paroxysmal tachycardias,
premature beats are produced by this mechanism.

10. Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Reentry Requires…
Electrical Impulse
Cardiac
Conduction
Tissue
1. 2 distinct pathways that come together at
beginning and end to form a loop.
2. A unidirectional block in one of those pathways.
3. Slow conduction in the unblocked pathway.

11. Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Premature Beat Impulse
Cardiac
Conduction
Tissue
1. An arrhythmia is triggered by a premature beat , in a reentry
circuit there will be forward conduction over slow pathway and
backward conduction in fast accessory pathway
2. The fast conducting pathway is blocked because of its long
refractory period so the beat can only go down the slow conducting
pathway
Repolarizing Tissue
(long refractory period)
Reentry Mechanism

12. 3. The wave of excitation from the premature beat
arrives at the distal end of the fast conducting
pathway, which has now recovered and therefore
travels retrogradely (backwards) up the fast pathway
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
Reentry Mechanism

13. 4. On arriving at the top of the fast pathway it finds the
slow pathway has recovered and therefore the wave of
excitation ‘re-enters’ the pathway and continues in a
‘circular’ movement. This creates the re-entry circuit
Fast Conduction Path
Slow Recovery
Slow Conduction Path
Fast Recovery
Cardiac
Conduction
Tissue
Reentry Mechanism

14. Atrial Reentry
• atrial tachycardia
• atrial fibrillation
• atrial flutter
Atrio-Ventricular
Reentry
• WPW
• SVT
Ventricular Re-entry
• ventricular tachycardia
AV Nodal Reentry
•SVT
Reentry Circuits
SA Node

15. ◦ Myocardial damage can result in oscillations of the
transmembrane potential at the end of the action potential.
◦ These oscillations, which are called 'after depolarizations',
may trigger a complete depolarization.
◦ Can occur early during repolarization phase of
(Early afterdepolarization)
or
◦ After completion of repolarization phase
(Delayed afterdepolarization

16. • So when triggered it results in self sustained
dysrhythmias.
• Triggered dysrhythmias associated with early
afterdepolarization are enhanced by slow HR and
are treated by accelerating HR.
• The abnormal oscillations can be exaggerated by
pacing, catecholamines, electrolyte disturbances,
drugs.
• Examples :atrial tachycardias produced by digoxin
toxicity and the initiation of ventricular arrhythmia in
the long QT syndrome.

17. 1)ANAESTHETIC AGENTS
2)ELECTROLYTE ABNORMALITIES
3)TEMPERATURE
4)AUTONOMIC DISTURBENCES
5)ACID BASE BALANCE
6)ENDOCRINE ABNORMALITIES
7)CONGESTIVE CARDIAC FAILURE
8)MECHANICAL AND ELECTRICAL CAUSES

18.  Inhalational agents of halogenated nature
potentiate the dysrhythmogenic effect of
circulating catecholamines, either independently
or through interactions with drugs.
 Alpha and beta-adrenergic receptors are involved
in the halothane-epinephrine interaction.
 Sensitization to catecholamine-induced
dysrhythmias is greatest with halothane and least
with enflurane.
 Inhalational anaesthetic reduce the incidence of
myocardial ischemia and may reduce the incidence
of ventricular fibrillation during ischemia.

19. POTASSIUM:
Because of the close relationship between extracellular pH
and potassium, the primary mechanism of pH induced
dysrhythmias may be alteration of potassium
concentration.
hypokalemia decreases cellular permeability to
potassium. This prolongs the action potential by
slowing depolarization
slows conduction and increases the dispersion of
recovery of excitability and predisposes to the
development of dysrhythmias:
most common of these are premature
atrial contractions, atrial tachycardia,
and supraventricular tachycardia.

20. Moderate hyperkalemia increases membrane permeability to
potassium, which increases the speed of repolarization and
decreases the action potential duration, thereby decreasing the
tendency to dysrhythmias.
The increased potassium permeability caused by hyperkalemia
decreases the rate of spontaneous diastolic depolarization, which
slows the heart rate and, in the extreme case, can produce asystole.
Both atrioventricular and interventricular conduction
abnormalities are seen from the slowed conduction and uneven
repolarization.

21. Dysrhythmias induced by magnesium deficiency may be refractory to treatment with
drugs and either electrical cardioversion or defibrillation.
Thus, deficiency states of Magnesium mimic ECG findings like those seen with
hyperkalemia.
Functionally, magnesium is required for the membrane bound Na/K–ATPase, which is
the principal enzyme that maintains normal intracellular potassium concentrations.
Hypomagnesaemia is associated with a variety of cardiovascular disturbances
including dysrhythmias.

22.  Although transmembrane flux of sodium is frequently
important to the electrical activity of the heart, there is
little information regarding clinically significant
dysrhythmias produced by abnormal serum sodium
concentrations.

23. In hypercalcemia, premature ventricular contractions and ventricular
fibrillation or tachycardia can be seen and the synergistic interaction
with cardiac glycosides should be kept in mind.
Clinically significant dysrhythmias are much less common.
Because of the ubiquitous role in excitation and contraction of cardiac
muscle, calcium balance would be expected to be significantly
associated with cardiac rhythm.

24. . The cardiac action for lithium is related to its
substitution for other actions, notably sodium
and potassium.
Lithium displaces some intracellular
potassium and its ECG effects may resemble
those of hypokalemia and increases SAnode
recovery time.
Reported dysrhythmias include ventricular
dysrhythmias and paroxysmal left
bundlebranch block.

25. VF becomes increasingly likely with temperatures approximating 30 ºC.
Ventricular fibrillation threshold is decreased with hypothermia
Bradycardia is a progressive response to hypothermia.
Hypothermia decreases conduction velocity in all areas of the conduction
system, which increase the PR and QT intervals and QRS duration.

26. Sinus tachycardia is the earliest indicator of the increased
metabolic state associated with hyperthermia.
increase in plasma catecholamines may exacerbate the
development of dysrhythmias, in conjunction with inhalation
agents.
Anesthetic problems caused by dysrhythmias are likely in the case
of severe temperature elevation, as may be seen with malignant
hyperthermia or with more moderate hyperthermia associated
with cardiac pathology.

27. The occulocardiac reflex and the various
prolonged QT interval syndromes.
The oculocardiac reflex is manifested by profound
bradycardia, sinus arrest or asystole, all of which are
produced by stimulation of the eye or the extraocular
muscles.
Preventive treatment of the reflex is by adequate
regional anesthesia in the case of retro bulbar block
and by the preoperative use of vagolytic drugs.
Eliminating the stimulus and administration of
vagolytic drugs are the recommended treatment.

28.  Profound hypoxemia is associated with an
increased incidence of ventricular
dysrhythmias, pronounced bradycardia and
asystole.
 In this regard, both hypoxia and ischemia have
different cardiac effects because, although both
impede oxidative metabolism, ischemia has the
additive effects of decreasing both supply of
metabolites and remove of waste products.

29.  Hypo and hypercarbia are associated with
increased frequency of dysrhythmias.
 Respiratory acidosis is a potent stimulus for
sympathetic activation and the resulting
catecholamine release potentiates dysrhythmic
effects of hypercarbia.
 Hypocarbia produces a respiratory alkalosis,
which in turn decreases extra cellular
potassium concentration

30. Hypothyroid causes bradycardia and low voltage complex in ECG
Hyperthyroidism is often associated with a resting sinus tachycardia.
More serious supraventricular dysrhythmias (AF) and ventricular forms
are well recognized especially during thyroid storm.
Adrenal corticosteroid excess causes hypokalaemia which results to
dysrhythmias
Diabetes mellitus causes autonomic dysfunction and accelerated
coronary atherosclerosis

31. Cardiac dysrhythmias are a prominent feature of CHF and may be
one of the most common causes of sudden death.
Ventricular dysrhythmias including conduction blocks, VT and
other complex changes as well as atrial flutter and fibrillation can be
seen.
The etiology is not understood but sympathetic activation is thought
to have a role.
Hypokalemia secondary to diuretic therapy is another common
cause of rhythm changes in these patients.

32.  The potential for micro shock to precipitate
serious or lethal dysrhythmias is significant;
 Injudicious use of pacemakers can easily
trigger VT or VF.

33. CLASS ACTION DRUGS
I. Sodium Channel Blockers
1A. Moderate phase 0 depression and
slowed conduction (2+); prolong
repolarization
Quinidine,
Procainamide,
Disopyramide
1B. Minimal phase 0 depression and slow
conduction (0-1+); shorten
repolarization
Lidocaine
1C. Marked phase 0 depression and slow
conduction (4+); little effect on
repolarization
Flecainide
II. Beta-Adrenergic Blockers Propranolol, esmolol
III. K+ Channel Blockers
(prolong repolarization)
Amiodarone, Sotalol,
Ibutilide
IV. Calcium Channel Blockade Verapamil, Diltiazem
V MISCELLANEUOS Adenosine, magnesium
sulphate, digoxin

34. Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
R.M.P
(Plateau Phase)
Class I:
Na + channel blockers.
- Pacemaker potential
-
-
-
Class III:
K + channel blockers
-
Class IV:
Ca ++ channel blockers
Class II:
Beta blockers
Classification of Anti-Arrhythmic Drugs

35.  Class I: retards conduction enough so that beat still
gets through normal cardiac tissue but not through
any weakened tissue
 The class I drugs can completely block
conduction through the weakened tissue.
Since the weakened tissue isn’t going to
block an entire pathway through the heart,
just enough of one to cause some mischief,
the wavefront will still be able to propogate
in the surrounding normal tissue
 Class III: prolongs refractoriness
 The Class III drugs prolong repolarization
so the re-entry circuit will still begin to
develop, but since only one side will have
the issue, when the wave has circled all the
way back around the cells that are slowed
down still will not have recovered, so the
wave front is just going to die out—it won’t
just keep propogating.

36. Class IA drugs are of
moderate strength; they
also have some action at K+
channels
• Block the fast sodium
channel
• This prolongs the phase 0
thereby slowing
conduction
• This group includes drugs
such as quinidine,
procainamide, and
disopyramide
• Indicated for the
treatment of ventricular
tachycardias and
symptomatic premature
ventricular beats
Class IB drugs are the
weakest of the class I drugs
• Effect sodium channels
• Little or no effect at slow
heart rates—more
effective at higher HRs
• Shorten the action
potential and reduce
refractoriness (speeds up
phase 3)
• Include lidocaine, and
mexiletine (oral lidocaine
analog)
• Indicated for the
treatment of ventricular
tachycardia, symptomatic
premature ventricular
beats, and to prevent
ventricular fibrillation
Class IC drugs are the
newest and the strongest of
class I drugs
• Cause a strong depression
of the slope of phase 0 of
the cardiac action
potential
• Decrease conductivity but
have a minimal effect on
action potential duration
• Includes flecainide, and
propafenone
• Indicated for the
treatment of life-
threatening ventricular
tachycardia or ventricular
fibrillation, or
symptomatic PVCs

38. Metabolized into NAPA in the liver
NAPA only blocks potassium channels
Has an cardioactive metabolyte (can also work as produg), procainamide and N-acetyl procainamide
Blocker of open Na+ channels only
Long term oral treatment poorly tolerated (can cause lupus syndrome)
Analog of the local anesthetic procaine

39. The IB drugs blunt the upstroke slightly because it is a weak sodium channel blocker,
but it also has action at potassium channels which is why it shortens the action potential
duration

40. Local anesthetic also used in the acute intravenous
therapy of ventricular arrhythmias
Blocks both open and inactivated cardiac Na+
channels
Exerts greater effects in ischemic or rapidly driven
tissues
Decreases automaticity by reducing the slope of
phase 4 and altering the threshold for excitability
Action potential duration either unaffected or
shortened

42. • Given as flecainide acetate
• Can create re-entrant circuit
• Very long recovery from Na+ channel block which
• Blocks Na+ current and delayed rectifier K+
current
• Also blocks Ca2+ currents (K+ and Ca2+ blockage
has not been demonstrated to be clinically
revelent)
• Noncardiac side effects:
• Dose-related blurred vision and headache
• Originally marketed as Tambocor, but went off
patent and is now available generically

43. •POTENTIAL RE-ENTRANT CIRCUIT
CAN BE TURNED INTO AN ACTUAL
RE-ENTRANT CIRCUIT
 Increased incidence of death
in the case of myocardial
infarction

44.  Beta Blockers – Decrease Conduction
Velocity, Automaticity And Recovery Time (
Refractory Period) – Propranolol, Acebutolol

46.  Prolong Repolarization- Are Used In The
Emergency Treatment Of Ventricular
Dysrhythmias When Other Antidysrhythmics
Are Not Effective – Bretylium, Amiodarone

47.  Given as a racemic mixture
 D-pure potassium channel blocker
 L-beta blocker and potassium channel blocker
 Rx of VT, AF, Afl, in pt with WPWsyndrome.
 Major side effect are bradycardia,
hypotension, torsade which initiates a
triggered arrhythmia (functional type) that is
very dangerous and life-threat

48.  Calcium Channel Blockers – Blocks Calcium
Influx, Decreasing The Excitability And
Contractility Of The Myocardium –
Verapamil, Diltiazem

49.  RANOLAZINE
 VERNAKALANT
 IVABRADINE
 CELIVARONE
 BUDIADARONE
 TECADENOSON

50.  1)ECG ASSESSMENT
 2)IDENTIFICATION OF IMPORTANT
DYSRHYTHMIAS
 3)ANTI-ARRHYTHMIC DRUGS
 4)ALTERNATIVE METHODS

52.  1. Is the rate slow (<60 bpm) or fast (>100 bpm)?
 Slow
Suggests sinus bradycardia, sinus arrest or conduction block
 Fast
Suggest increased/abnormal automaticity or reentry
 2. Is the rhythm irregular?
 Irregular
Suggests atrial fibrillation, 2nd degree AV block, multifocal
atrial tachycardia, or atrial flutter with variable AV block
 3. Is the QRS complex narrow or wide?
 Narrow
Rhythm must originate from the AV node or above
 Wide
Rhythm may originate from anywhere

53.  4. Are there P waves?
 Absent P waves a indicates atrial fibrillation, ventricular
tachycardia, or rhythms originating from the AV node
 5. What is the relationship between the P waves and
QRS complexes?
 More P waves than QRS complexes a Suggests 2nd or 3rd
degree AV block.
 More QRS complexes than P waves a Suggests an
accelerated junctional or ventricular rhythm.
 6. Is the onset/termination of the rhythm abrupt or
gradual?
 Abrupt -Suggests reentrant rhythm
 Gradual- Suggests altered automaticity

54.  1)SINUS RHYTHM
 2)SUPRAVENTRICULAR RHYTHM
 3)VENTRICULAR RHYTHM

55. Heart Rate will be usually 60-100 bpm, irregular rhythm and characterized by more
than 10% variation in the P-P interval. P wave before each QRS identical and QRS <
0.12 sec.
Treatment
Sinus dysrhythmia may not be clinically significant most of the time and patients
remain asymptomatic. An increase in heart rate during inspiration and decrease
during expiration is noted in these patients. Most of the time, it is detected when the
heart rate is on lower side.
Asymptomatic patients do not require any specific treatment for sinus dysrhythmia.
But when the condition is a non-phasic variant, underlying condition requires to be
treated for giving symptomatic relief. Treatment with anticholinergic agents
improves the condition in 75% of the patients.

56. Heart Rate will be usually 40-100 bpm, regular rhythm, P wave identical before each
QRS; P to P interval may be fixed before and after the pause, PR interval 0.12 to 0.20
sec and QRS < 0.12 sec.
Treatment
This may occur in individuals with normal cardiac functions. Other causes of sinus
arrest include increased vagal tone, myocardial infarction, myocarditis and digitalis
toxicity. The underlying cause needs to be treated to control of this type of
dysrhythmia. When the patient is symptomatic and bradycardia is due to increased
vagal tone, it can be treated with atropine.

57. Heart Rate will be usually 100 bpm, regular rhythm, and P wave identical before each
QRS, PR interval 0.12 to 0.20 sec and QRS < 0.12 sec.
Treatment
The underlying cause (hypovolemia, dehydration, hypoxia, anxiety, inadequate
analgesia, fever etc.) have to be recognised and needs to be treated.

58. Heart Rate will be usually <60 bpm, regular rhythm, P wave identical before each QRS,
PR interval 0.12 to 0.20 sec and QRS < 0.12 sec.
Treatment
All patients with symptomatic bradycardia (haemodynamic compromise i.e., systemic
hypotension, signs of cerebral hypoperfusion, progressive heart failure or angina)
should be treated immediately. Inj. Atropine 0.5 mg IV should be given immediately
and may be repeated to a total dose of 3 mg. In patients not responding to medical
therapy, temporary transvenous pacing is advised. As a temporary measure,
transcutaneous pacing may be started.
Other drugs that may be considered are epinephrine infusion (2-10 mcg/min) or
dopamine infusion (2-10 mcg/ kg/min). In advanced prolonged AV block, permanent
pacing should be considered.

59. Heart Rate will be unpredictable may be too fast or too slow, irregular
rhythm, P wave premature, abnormal and may be hidden, PR interval 0.12 to
0.20 sec and QRS < 0.12 sec.
Causes of PACs include stress, caffeine, tobacco, alcohol, hypertension,
valvular cardiac disorders, old myocardial infarcts, digitalis toxicity, abnormal
blood levels of magnesium and potassium.
Treatment
PACs most of the time do not require any treatment. Proper cardiac
evaluation should be done to rule out any underlying cardiac cause. PACs
may change into flutter.

60. Heart Rate will be 140-250 bpm, regular rhythm, P wave abnormal before each QRS and
difficult to see, PR interval 0.12 to 0.20 sec and QRS < 0.12 sec.
Treatment
The primary treatment is to control the rate using beta-blockers and calcium channel
blockers alone or in combination.Atrial tachycardia from triggered activity are most
commonly found in case of digitalis toxicity and is sensitive to verapamil, beta-blockers,
and adenosine. Atrial tachycardia from enhanced automaticity is treated with Beta-
blockers. Atrial tachycardias which are refractory and recurrent are treated with Class Ic
anti-arrhythmic drugs and for maintenance of sinus rhythm. For patients in whom rate-
control drugs are ineffective or contraindicated,cardioversion is to be done. Patients
who are refractory to the medical treatment, radiofrequency catheter ablation is the
choice. Patients with complex congenital heart disease require surgical ablation.

61. Atrial rate usually 240-350 bpm, saw tooth pattern between QRST complexes, rhythm
regular, Ventricular rate 150 (due to 2:1 conduction and varies with conduction ratio),
QRS <0.12.
Treatment
AV nodal blocking agents like Diltiazem, Verapamil, Metoprolol, Digoxin, Amiodarone,
and Procainamide should be used for rate control. In patients with ejection fraction
<40%, consider digoxin or amiodarone should be used.
For Rhythm control – Amiodarone, Procainamide, Ibutilide, Flecainide, Propafenone
may be given. Rhythm control should be avoided if dysrhythmia is more than 48 hours
as conversion to sinus rhythm may cause embolization.
Anticoagulation is to be considered if dysrhythmia had lasted more than 48 hours or left
atrial clot is detected on echo. An acute paroxysm should be treated by electrical
cardioversion.

62. AF is more commonly seen in patients with advanced age, pre-existing cardiac disease,
COPD, alcoholics and caffeine addicts.
The ECG shows- P waves not clear, fine oscillations of the baseline. The QRS rhythm is
usually 160-180/min. AF may be acute (<48 hrs) and chronic.
Treatment
In the acute onset AF, precipitating factor should be treated. Ventricular response rate is
controlled by blocking AV node conduction with the use of intravenous beta blockers or
calcium channel blockers.
DC cardioversion is the most effective method in hemodynamically-compromised
patients. Chronic is commonly seen in patients with rheumatic heart disease undergoing
cardiac Surgery. The most useful drug for controlling ventricular rate in these patients is
digoxin. In patients of AF undergoing noncardiac surgery, presence of any atrial clot
should be ruled out

63. Heart rate 40-60 bpm , rhythm regular, p waves inverted in inferior leads,
before during or after the QRS or may be absent, PR Interval <0.12 sec and
QRS <0.12 sec.
Treatment
Asymptomatic patients with junctional rhythm no pharmacologic therapy
is required. But a permanent pacemaker may be required in patients with
complete AV block, high-grade AV block or symptomatic sick sinus
syndrome.

64. Heat rate is usually <140bpm, rhythm regular, P wave inverted, absent or
after QRS, PR interval <0.12 sec, QRS <0.12 sec.
Treatment
Underlying cause should be diagnosed and treated. Other modalities are
vagal maneuvers, verapamil and cardioversion.

65. It is supraventricular dysrhythmia characterized by narrow QRS complex and
atrioventricular (AV) dissociation or retrograde atrial conduction in a 1:1 pattern. JET
can occur immediately after surgical correction of congenital heart defects (post
operative) or a primary idiopathic form presenting in infancy during first six months of
life (congenital). Postoperative JET is usually a self-limiting disorder and resolves within
one week. However, it can be a potentially serious arrhythmia, associated with
hemodynamic compromise and a high morbidity and mortality.
Mortality with congenital JET has also been reported to be high. Congenital JET is rare
and associated with high mortality. It requires to be treated with multiple
antiarrhythmic medications, ablation and even pacemaker insertion may be needed due
to resultant complete AV node block.

66. Rate is variable; rhythm may be regular or irregular, P wave identical before
each QRS, PR interval 0.12-0.20 sec, QRS ≥0.12 sec and RSR pattern in V1.
Treatment
Right bundle branch block may not require treatment always but artificial
pacing or require cardiac resynchronization therapy (CRT) is needed for a
bifasicular block.

67. Rate is variable, rhythm may be regular or irregular, P wave identical before each
QRS, PR interval 0.12-0.20 sec, QRS ≥0.12 sec and QS or rS in V1, ST elevation in V2
and notched (‘M’-shaped) R wave in lead V6. The heart rhythm should be
supraventricular in origin.
Left bundle branch block is more threatening than right bundle branch block
because it usually is seen in diseased hearts. Causes of LBBB may be Aortic stenosis,
Ischaemic heart disease, Hypertension, Dilated cardiomyopathy,
Anterior MI, Primary degenerative disease (fibrosis) of the conducting system
(Lenegre disease), Hyperkalaemia and Digoxin toxicity.
Treatment
Artificial pacing is required to regulate the heart beats at the proper rate. Patients
with cardiac failure and left bundle branch block may even require cardiac
resynchronization therapy or CRT.

68. Rate is variable, rhythm regular, Identical P wave before each QRS, PR interval >0.20
sec, QRS <0.12 sec. This is the commonest conduction disorder. It may occur even in
healthy hearts as well as in people with preexisting cardiac disease. Causes of First
degree AV block may include increased vagal tone, inferior wall MI, myocarditis,
digitalis toxicity, acute rheumatic fever and hyperkalemia.
Treatment
Is of underlying cause and should be monitored carefully as may progress to
advanced AV block.

69. Rate is variable, rhythm irregular with intermittent conduction of P wave, PR
interval increasingly prolonged until one P wave is blocked, QRS <0.12 sec.
Treatment
Most of the time patients are asymptomatic and do not require any treatment.

70. Rate variable, P wave normal with constant P-P intervals, QRS broad ≥ 0.012
sec, P-R interval may be normal or prolonged, but it is constant until one P
wave is blocked and not conducted to the ventricles. This block usually
occurs below the Bundle of His and more likely to progress to complete heart
block.

71. P wave is normal but AV dissociation, with atrial rate (P wave) greater than QRS,
with no relation between these two. Ventricular escape rate is usually 25-45 per
minutes. Usually symptomatic and require treatment.
Treatment
Acute symptomatic episodes should be treated atropine and external pacing.
Permanent pacing is needed for chronic complete heart block.

72. Rhythm is irregular with PVCs (unifocal- similar shape, multifocal
different shapes), broad QRS complex (≥ 120 ms) with abnormal
morphology. Discordant ST segment and T wave changes.

73. Treatment of PVCs
Asymptomatic patients with occasional PVCs do not need any treatment. Reducing
or eliminating caffeine, tobacco and alcohol intake and reducing stress and anxiety
may be considered. Pharmacological management include radiofrequency ablation
is the option for patients with frequent or prolonged PVCs. Patients with cardiac
disease with frequent PVCs or when PVCs increase during exercise, angioplasty or
bypass surgery may be required.

74. Heart Rate 100- 220 bpm, rhythm three or more ventricular beats in a row; may be
regular or irregular, P wave absent before each QRS and obscured if present, QRS wide
and bizarre. Ventricular tachycardia always occurs in diseased hearts.
Common causes include coronary artery disease, acute myocardial infarction, digitalis
toxicity, CHF and ventricular aneurysms. Ventricular tachycardia can quickly progress
to ventricular fibrillation.
Treatment
Symptomatic VT with detectable pulse should be managed with urgent synchronized
cardioversion. In hemodynamically stable patient consider amiodarone, lidocaine or
procainamide. For pulseless VT, ACLS protocol should be followed.

75. Rate 150 to 220/bpm, P wave obscured if present, QRS wide and bizarre with
upward and downward deflection around the baseline, rhythm irregular.
Causes include electrolyte imbalances, particularly hypokalemia myocardial
ischemia, drugs which lengthen the QT interval such as quinidine
Treatment
In unstable patients synchronized cardioversion is indicated. Electrolyte
imbalance to be corrected using IV magnesium or IV potassium.

76. Heart Rate will be 300-600 bpm, extremely irregular rhythm, P wave
absent, PR interval absent and QRS absent.
This dysrhythmia results in the absence of cardiac output, it occurs in
preexisting severe cardiac disease or acute myocardial infarction.
Treatment
Immediate defibrillation and ACLS protocols should be followed.

77.  Ablation : physically
destroys the re-entrant
circuit by burning out
the tissue
 Implanantable Cardioverter
Defibrillators (ICDs): the
arrhythmia can be
terminated by pacing or
by electrical shock
.

78. ICD Placement In the Heart
It has a battery back / pacing machine that is going to go outside your ribcage and
under the skin, with leads coming out of it that will be embedded into some of the
tissues to the heart to give it the ability to pace it and to shock it if needed.

79.  It can be pharmacological with antiarrhythmic
drugs or giving electric shock to the heart.
 Cardiac dysrhythmias associated with
hypotension,loss of consciousness,chesth pain and
breathlessness require emergency cardioversion.
DYSRHYTHMIA MONOPHASIC BIPHASIC
ATRIAL
FIBRILLATION
200 120-200
ATRIAL FLUTTER 100 50-100
VENTRICULAR
TACHYCARDIA
200 100
VENTRICULAR
FIBRILLATION
360 120-200

80. THANK
YOU