CASE 2: ARRYTHMIA AV bundle (Bundle of His)
- Connects atrial & ventricular
1) Anatomy of Heart (refer case 1)
2) Innervation of Heart
By cardiac plexus
i. Sympathetic
Presynaptic: T5/T6 spinal cord
Postsynaptic: Cervical & superior
thoracic paravertebral ganglia
cardiopulmonary splanchnic nerve
cardiac plexus ends at SA node &
AV node.
ii. Parasympathetic
Presynaptic: Vagus nerve
Postsynaptic: Intrinsic ganglia at
atrial wall & interatrial septum near
SA, AV node and along coronary
artery.
3) Heart conducting system
SA node atrial muscle AV node
AV bundles Bundle branches
Purkinje fibres Ventricular muscles
4) Histology of conducting system
SA node
- Small mass of specialized cardiac
muscle fibres
- Located anterolaterally, at the
junction of SVC & RA
- Pacemaker of heart; initiates &
regulates impulses for heart
contraction
AV node
- Smaller than SA node
- gap junctions
- Located at posteroinferior region
of interatrial septum
Phase O
opened, Na+ influx spike
myocardium
- At the junction of membranous &
muscular part of IVS septum, it
divides into right & left bundles.
Subendocardial branches (Purkinje
fibres)
- Have 1/2 central nuclei
- mitochondria & glycogen
- myofibrils restricted at
periphery of cytoplasm
- Extends at ventricular wall,
penetrate 1/3 endocardium.
5) Action potential (AP)
Pacemaker
cells
Phase O Depolarization, Ca2+ channel
opened, Ca2+ influx
Phase 3 Repolarization, K+ efflux
from cell
Phase 4 Resting potential, upward
slope (Na+ leakage)
Cardiac
muscle
cells
Depolarization, Na+ channel 7) Control of excitation & conduction
of heart
Phase 1 Rapid repolarization, Na+
Discharges
channel closed, K+ efflux
SA node: 60 -100x/min
Phase 2 Slow repolarization,
AV node: 40-60x/min
balance of K+ efflux &
Purkinje fibres: 15-40x/min
Ca2+ influx plateau
Pacemaker
Phase 3 Final phase of repolarization,
further K+ efflux. Normal: SAN
Ca is removal - Na+/Ca2+
2+ Latent: other than SAN
exchanger Ectopic: when SA node cant
Na+ is removed- Na+/K+ ATPase initiate impulse, latent
Phase 4 Resting potential pacemaker take over & produce
weaker discharges.
6) Cardiac rhythmical excitation Controlled by ANS
Specialized excitatory & conductive 8) ECG
system of heart Def: Recording of the electrical
- Initiate impulse & cardiac muscle activity of cardiac cells that
contracts rhythmically, conduct reaches the body surface.
impulse in normal pathway. Functions
- SA node intermodal pathway - Enlargement of chambers
AV node AV bundle R&L bundle - Arrhythmias
branch Purkinje fibre - Electrolyte abnormality
Normal ECG characteristics
Mechanism
i. SA node
- Self-excitation ability
- Rhythmical period is determined by
AP voltage (ion transport)
ii. AV node
- Control impulse by delay the AP to
allow blood fills efficiently into
ventricles.
- SA node(0.03s) AV node (0.09s) Vertical axis: voltage
AV bundle (0.04s) Purkinje Horizontal axis: time
Fibres (0.06s) ventricular muscles
- P wave : Atrial depolarization
iii. Purkinje fibres
- QRS complex : Ventricular
- Faster, via intercalated disks
depolarization
 I Block fast Na+ channel
- T wave : Ventricular repolarization ii. Disturbed impulse conduction IA : Qunidine, Disopyramide Adverse effect :
- ST segment : Early ventricular - Conduction block IB : Lidocaine Hypertension,
repolarization - Unidirectional block & Re-entry IC: Flecainide Arrhythmia
- QT interval : Ventricular - Accessory pathway & WPWS II adrenergic receptor v. Lidocaine
depolarization + repolarization Bundle of Kent agonists MOA: Class IA Block
Method to record ECG Classification III K+ channel blocker fast Na+ channel
Placement of 4 basic limb Ex : Amiodarone during phase 0 AP
1. Bradyarrhythmia (<60 bpm)
electrodes IV Block L-type Ca2+ channel Adverse effect: Slurred
- Sinus bradycardia
- Right & left arm Ex : Verapamil speech, dizzy
- Right & left leg - Junctional bradycardia (heart
vi. Propanolol
ECG leads block)
10) PP MOA: Class II - adrenergic
i. Standard limb leads a) 1st degree receptor agonists HR,
i. Amiodarone
I, II, III b) 2nd degree myocardial contractility & BP
MOA: Class III prevent K+
ii. Augmented unipolar leads Mobitz I O2
efflux during repolarization
aVR, aVL, aVF Mobitz II Adverse effect : Bradycardia
prolong AP & effective
iii. Precordial leads c) 3rd degree / complete vii. Verapamil
refractory period.
V1 ICS4, right sternal margin 2. Tachyarrhythmia (>100 bpm) MOA: Ca2+ channel
Adverse effect : bradycardia, blocker arterial
V2 ICS4, left sternal margin - Sinus tachycardia
heart block vasodilation
V3 Midway between V2 & V4 - Atrial/Ventricular
a) Tachycardia Amiodarone + Digoxin cardiac workload
V4 ICS5, midclavicular line, left
b) Flatter 250-350 level/effect of digoxin Adverse effect:
V5 Left anterior axillary line
c) Fibrillation >350 ii. Digoxin Headache,
V6 Left mid axillary line
MOA: Inhibits Na+/K+ ATPase hypotension
- Junctional tachycardia
intracellular Na+ Verapamil + Digoxin
9) Arrhythmia Management
Ca2+ efflux intracellular toxicity digoxin
Def : Abnormality of heart 1. Bradyarrhythmia Ca2+ stored in SR clearance &
electrical rhythm Anticholinergic drugs contraction force distribution volume,
Mechanism B1 receptor agonist Adverse effect : Severe GI tract absorption
i. Altered impulse formation Electronic pacemaker arrhythmias
- Altered automaticity 2. Tachyarrhythmia iii. Disopyramide BHP Beneficence & Non
* SA node automaticity Anti-arrhythmia (table) MOA: Class IA Block maleficence: Choose patients
Na+ medication wisely
(/) Vagotonic manuever fast channel
* automaticity of latent Electric cardioversion & during phase 0 AP
PHOP Educate patient to
pacemaker defibrillation Adverse effect : take medication given
- Abnormal automaticity Urinary retention regularly.
- Triggered activity iv. Epinephrine
MOA: Stimulate - CRP Research about
adrenergic receptor therapeutic window of
digoxin efficacy for treatment.