A clear and precise presentation for medical students

1. BRADYARRHYTHMIA
Dr. Haimanot Tessema
Assistant professor,EMCC
March 2022

3. Measurements

4. ●Origin of depolarization
 sinoatrial (SA) node
●Transfer of depolarization
 Conduction system
■Atrial
■Atrioventricular (AV) node
■Intraventricular

5.  The P wave represents atrial activation
 The PR interval is the time from onset of atrial
activation to onset of ventricular activation.
 The QRS complex represents ventricular activation.
 The QRS duration is the duration of ventricular
activation.

6.  The ST-T wave represents ventricular repolarization.
 The QT interval is the duration of ventricular
activation and recovery.
 The U wave probably represents "after
depolarizations" in the ventricles.

7.  Measurements
 Rhythm Analysis
 Conduction Analysis
 Waveform Description
 ECG Interpretation
 Comparison with Previous ECG (if any)

8.  Heart rate 60-90 bpm
 PR interval (from beginning of P to beginning of
QRS) =0.12-0.20 sec
 QRS duration (width of most representative QRS)
<0.12 sec
 QT interval (from beginning of QRS to end of T)
= 0.42 sec

10.  Basics
 Arrhythmia/dysrhythmia = deviation from
physiologic heart rhythm

13.  INITIALAPPROACH TO THE STABLE
PATIENT
 The focused evaluation of the patient:
 Determining the presenting complaint(s)
 Obtaining the medical history
 Identifying medication use

14.  Performing a physical examination
 Initiating continuous cardiac rhythm monitoring,
reviewing the 12-lead ECG
 Analyzing the cardiac rhythm on the rhythm monitor,
a printer strip, or the ECG.

15.  Symptoms may include:
 palpitations
 lightheadedness
 Fatigue or weakness
 Ischemic symptoms:
-chest pain
-nausea
-dyspnea
-lightheadedness, may be due to dysrhythmia-
induced ischemia.

16.  INITIAL APPROACH TO THE UNSTABLE
PATIENT
 An unstable patient needs rapid assessment
and treatment to prevent cardiovascular
collapse.
 Establish an IV line, initiate cardiac rhythm
monitoring, obtain an ECG, and be prepared
for drug or electrical therapy.

17.  Hypotension (Systolic BP <90MMMHG)
 Systemic hypoperfusion
 Altered mentation
 Ischemic chest pain
 Respiratory distress
 Extremely rapid rate ( >200 in adults)

18.  Bradydysrhythmia describes rhythms with a
ventricular rate slower than 60 beats/min in the
adult.
 Categorized as :
 -Bradycardias:
 sinus bradycardia
 junctional rhythm
 idioventricular rhythm
 hyperkalemia-related sinoventricular rhythm.
 -Atrioventricular (AV) blocks /Bradydysrhythmias.

19. ●Depolarization origination defect
 Sinoatrial (SA) node
-SA node desfunction
●Depolarization transfer defect
 In atrias
- SA node desfunction
 AV node
-AV block
 Intraventricular conduction system
-Intraventricular conduction blocks

20.  Sinus node dysfunction
 many forms
-sinus bradycardia
-sinus arrest
-sinoatrial (SA) blocks
-brady - tachy form (switching between
bradycardia and tachycardia)
 If symptoms are present, we are talking about
sick sinus syndrome (SSS)

21.  ECG
 Long term ECG monitoring
 Holterovská monitoration (24 h. to 7 days)
 Telemetry
 Loop recorder (external or implantable)

22.  Stress ECG
 Head up tilt table test
 Carotid sinus massage
 Electrophysiology study (EPS)

23.  Emergent treatment of bradydysrhythmia is not
required unless :
 (1) the heart rate is slower than 50 beats/min
accompanied by hypotension or hypoperfusion
-requires resuscitative treatment while evaluating
the cause.
 (2) the bradydysrhythmia is due to structural
disease of the infranodal conduction system.
-does not require immediate treatment but
should be closely monitored, with pacing readily
available while arranging definitive care

24.  Medications used to increase heart rate in
symptomatic bradycardias include atropine,
β-adrenergic agonists, and glucagon
 Atropine 0.5-milligram IV push, may repeat
every 3–5 min until desired heart rate is
achieved or to total dose of 3 milligrams
(0.04 milligram/kg)
 Most effective for bradydysrhythmias due to
sinus and AV nodal disease.

25.  Dopamine IV infusion at rate 2–20
micrograms/kg/ min, titrate to desired heart
rate
 May precipitate myocardial ischemia and
ectopy
 Epinephrine IV infusion at rate 2–10
micrograms/min, titrate to desired heart rate
 May precipitate myocardial ischemia and
ectopy

26.  Glucagon 3–10 milligrams IV infused over 1–2
min, followed by an IV continuous infusion of
1–5 milligrams/h
 Used for cardiotoxicity associated with β-
blocker and calcium channel blocker
overdose
 Nausea and vomiting are often limiting side
effects
 Tachyphylaxis may develop during infusion

27.  Transcutaneous pacing can be applied quickly
and is the most appropriate pacing method
for the acutely symptomatic patient.
 Transvenous pacing requires physician
expertise and specialized equipment for
insertion and proper placement

28.  Disease-specific therapies for bradycardia:
 Treatment of hyperkalemia
 Treatment of toxicity from:
 calcium channel blockers
 β-blockers
 digitalis.

29.  A 45 years old man who is on nifidipine
20mg PO BID presented with chest pain.
PR=45/MIN BP=80/40MMHG, SPO2-95%WRA…
???

32. SINUS BRADYCARDIA

33. ECG features of sinus bradycardia:
 Normal SA node initiated P waves
morphoolgy with upright P waves in leads I,II
and III
 PR 120- 200ms
 1:1 atrioventricular conduction
 Rate<60 bpm

34.  Clinical Significance
 represents a reduction of the SA node discharge
rate.
-Sinus bradycardia can be:
(1) physiologic (in well-conditioned athletes, during
sleep, or with vagal stimulation),
(2) pharmacologic (β-blockers, digoxin, opioids,
calcium channel blockers),
(3) pathologic (hypoxia, acute inferior wall
myocardial ischemia or infarction, increased
intracranial pressure, carotid sinus
hypersensitivity, hypothyroidism).

35.  Treatment
 usually does not require specific treatment
unless the heart rate is slower than 50
beats/min and there is evidence of
hypoperfusion
 Correct underlying causes.
 Use atropine in the unstable patient, followed
by transcutaneous cardiac pacing and
infusions of dopamine or epinephrine if there
is no response to atropine.

36.  JUNCTIONAL RHYTHM
 If SA node discharges slow or fail to reach the
AV node, junctional escape beats will produce
a rhythm usually at a rate between 40 and 60
beats/min.
 If the junctional beats continue in sequence,
then a junctional rhythm is present.
 In most cases, junctional escape beats do not
conduct retrograde into the atria, so a QRS
complex without a P wave is usually seen.

37.  At times, enhanced AV nodal automaticity
overrides the sinus node and produces:
 Accelerated junctional rhythm with a rate of
60 to 100 beats/min or
 Junctional tachycardia with a rate greater than
100 beats/min.
 Usually, the enhanced junctional pacemaker
captures both the atria and ventricles.

38. Features of junctional rhythm
 Absence of SA node mediated P wave with
normal PR interval
 Rarely retrograde P wave immediately
adjacent to QRS (pre or post).
 Narrow QRS
 Regular rate
 Ventricular rate 40-60 (junctional rhythm)
 60-100 (accelerated junctional rhythm)
 >100 (junctional tachycardia)

39.  ??
 Rate?

40.  ??
 Rate?

41.  Clinical Significance
 Junctional escape beats may occur whenever
there is a long enough pause in the impulses
reaching the AV node, as with sinus
bradycardia, slow phase of sinus arrhythmia, or
during the pause after premature beats
 Sustained junctional escape rhythms may
be seen with heart failure, myocarditis,
hypokalemia, or digitalis toxicity.

42.  Treatment Isolated, infrequent junctional escape
beats usually do not require specific treatment.
 If sustained junctional escape rhythms are
producing symptoms, the underlying cause
should be treated.
 Atropine can be used to accelerate the SA node
discharge rate and enhance AV nodal conduction.
 Accelerated junctional rhythm and junctional
tachycardia usually do not produce significant
symptoms.

43.  IDIOVENTRICULAR RHYTHMS
 Idioventricular rhythms are of ventricular
origin manifesting as regular widened QRS
complexes without evidence of atrial activity.
 An idioventricular rhythm has a ventricular
rate of 30 to 50 beats/min, and the
 Accelerated idioventricular rhythm has a
ventricular rate of 50 to 75 beats/min.

44.  Clinical Significance
 Most commonly seen in the setting of an ST-
segment elevation myocardial infarction.
 An accelerated idioventricular rhythm that
appears during successful fibrinolysis of an
occluded coronary artery is termed a
reperfusion dysrhythmia.
 The slower versions, can produce dizziness,
weakness, syncope, chest pain, and dyspnea;
profound hypoperfusion may occur.

45.  Treatment
 If hypoperfuson, drugs to increase the heart
rate are appropriate.
 Atropine is recommended, although the
likelihood of successful treatment is low.
 Cardiac pacing is often needed, starting via
the transcutaneous route.
 In most cases of accelerated idioventricular
rhythm, treatment is not necessary.

46.  First-degree AV block is characterized by a delay
in AV conduction manifested by a prolonged PR
interval.
 Second-degree AV block is characterized by
intermittent AV conduction: some atrial impulses
reach the ventricles, and others are blocked.
 Third-degree AV block is characterized by the
complete blockage of atrial impulses to the
ventricles.
 AV blocks are divided into nodal and infranodal
blocks.

47.  1st degree
-Prolonged AV conduction (PR > 200ms)
-Every atrial depolarization is conducted to
ventricles

49.  There is progressive prolongation of the PR
interval until an atrial impulse is completely
blocked
 After the dropped beat, the AV conduction
returns to normal, and the cycle usually
repeats
 This type of block almost always occurs at the
level of the AV node and is often due to
reversible depression of AV nodal conduction

50.  Block occurs because each successive
depolarization produces prolongation of the
refractory period of the AV node.
 This process is progressive until an atrial
impulse reaches the AV node during the
absolute refractory period, and conduction is
blocked altogether.

51.  Clinical Significance This block is often
transient and usually associated with an
inferior myocardial ischemia, medication
toxicity, or myocarditis, or after cardiac
surgery.
 It may occur when a normal AV node is
exposed to very rapid atrial rates.
 This block can also be a normal variant, not
indicative of acute or chronic heart disease.
 Treatment Specific treatment is usually not
necessary

52.  Grade II
- Some of atrial depolarizations are
conducted to ventricles but some are not.
-Type 1 - gradual prolongation of PR
interval until one atrial depolarization is not
conducted to ventricles. After that PR interval
shortens again
-Type 2 - atrial depolarizations are
conducted to ventricles every 2nd, 3rd (n-th)
atrial depolarization

55.  •
The PR interval remains constant across the
rhythm strip, both before and after the
nonconducted atrial beats.
 Each P wave is associated with a QRS complex
until a nonconducted atrial depolarization.
 Even if the QRS complexes are narrow, the
block is generally in the infranodal system.
 High-grade AV block is noted when more
than one consecutive P wave is not conducted

56.  If it occurs with a fixed conduction ratio of 2:1, it
is not possible to differentiate between type I
(Wenckebach) or type II block.
 If the QRS complex is wide, the block is more
likely to be in the infranodal system.
 If the QRS complex is narrow, then the block is in
the AV node or infranodal system with about
equal incidence
 Clinical Significance :structural damage to the
infranodal conducting system, are usually
permanent, and may progress suddenly to
complete heart block, notably with concomitant
acute myocardial ischemia.

57.  Treatment
 Patients should have transcutaneous cardiac
pacing pads applied in the ED in anticipation
of possible need.
 Start emergent pacing when slow ventricular
rates produce symptoms of hypoperfusion.
 Atropine can be tried but the effect is
inconsistent.

59.  Grade III
-Complete heart block between atrias and
ventricles
 Advanced heart block
- Several atrial depolarization are not
conducted to ventricles

60.  There is no AV conduction
 An escape pacemaker (manifested by the QRS
complex) paces the ventricles at a rate slower
than the atrial rate manifested by the P wave.
 When block occurs in the AV node, a
junctional escape pacemaker takes over with
a ventricular rate of 40 to 60 beats/min.
 The QRS complexes are narrow because the
rhythm originates above the bifurcation of
the bundle of His.

61.  When third-degree AV block occurs at the
infranodal level, the ventricles are driven by a
ventricular escape rhythm at a rate slower
than 40 beats/min.
 Third degree AV blocks at the His bundle
level can have a narrow or wide QRS complex,
 When block occurs in the bundle branches or
elsewhere in the Purkinje system invariably
have escape rhythms with wide QRS
complexes.

62.  No association of P wave with QRS complexes
 Atrial rate greater than ventricular rate
 QRS complexes are usually widened
occasional narrow QRS complexes are seen
 Ventricular rate is regular

63.  Intraventricular conduction defects
 Bundle branch blocks
o Complete or incomplete
o Left bundle branch block (LBBB)
o Right bundle branch block (RBBB)
 Fascicular blocks (hemiblocks)
o Left anterior hemiblock (LAH)
o Left posterior hemiblock (LPH)

64.  Bifascicular block
o RBBB + LAH
o RBBB + LPH
 Trifascicular block
o Bifascicular block + 1st grade AV block

65.  Structural defect
 Myocardial infarction, myocarditis, cardiac
storage diseases, heart tumors, sarcoidosis
 Iatrogenic (alcohol septal ablation, cardiac
valve surgery/implantation, heart surgery,
catheter ablation)
 Idiopathic (degeneration, fibrosis)

66.  Functional defect
○Mineral dysbalance, pharmacotherapy,
hypothermia, autonomic nervous system
dysfunction

67.  Nodal third-degree AV block develops in up to
8% of inferior acute myocardial infarction
patients and may last for several days.
 Infranodal third-degree AV blocks indicate
structural damage to the infranodal conducting
system, as seen with an extensive anterior acute
myocardial infarction.
 The ventricular escape pacemaker is usually
inadequate to maintain cardiac output and the
patient is unstable, with periods of ventricular
asystole.
 When third-degree block is seen in acute
myocardial infarction, mortality is increased even
with pacing.

68.  Patients require monitoring and admission.
 Manage with either medication and/or pacing.
 Nodal blocks may respond to atropine.
 Infranodal blocks are unlikely to respond to atropine or other
medications that can enhance AV nodal conduction.
 Patients should have transcutaneous cardiac pacer pads
applied in the ED.

76.  Tintinallis text book of emergency medicine
9th edition
 Rosen’s text book of emergency medicine
9th edition
 Internet

77. THANK YOU