CONDUCTION

SYSTEM OF
HEART
Presenter – Dr.Diksha Sao
Guide – Dr. Leena ma’am
CONTENTS

 Overview of heart
 Anatomy and functions of heart
 Electrical events of cardiac cycle
 Waves and intervals
 Cardiac action potential
 Mechanical events of cardiac cycle
 Cardiac cellular physiology
 Neural control of heart
 ECG
 Conduction abnormalities
 Take home message
 References
THE HEART- OVERVIEW

 Functionally divided into left and right pumps each

consisting of atria and ventricles .
 Atria – conduits and priming pump
 Ventricles –major pumping chambers
 Right ventricle receives systemic venous deoxygenated
blood , pumps into pulmonary circulation
 Left ventricle receives pulmonary venous oxygenated
blood and pumps it into systemic circulation .
 4 valves normally ensure unidirectional flow through each chamber .
 Heart consist of specialized striated muscle in connective tissue
skeleton .
 Cardiac muscle -------
 Atrial
 Ventricular
 Specialized pacemaker
 Conducting cells
 Pumping action of heart is due to complex series of electrical and
mechanical events
 Electrical events precede mechanical ones .
FUNCTIONS OF HEART

• Cardiac cycle is sequence

of electrical and
mechanical activities during
the single heartbeat.

• Electrical Events of single

cardiac cycle is represented
by ECG with corresponding
mechanical events.
ELECTRICAL EVENTS AND
ECG
WAVES AND INTERVALS
CARDIAC ACTION POTENTIAL
ELECTRIC CONDUCTION IN THE
HEART
MECHANICAL EVENTS OF
HEART
• Artial systole = depolarisation of SA
node and P wave.

• Ventricular systole = iso-volumic

contraction.

• Rapid Ejection= Pulmonary artery

and aortic pressure is maximum.

• Reduced Ejection= Great artery

pressures taper.

• Iso-volumic relaxation= closure of

pulmonic and aortic valve= T wave.

• Ventricular filling = AV valves

reopens.
CELLULAR CARDIAC
PHYSIOLOGY
Excitation-contraction coupling
 Action potential causes the myofibrils of
muscle to contract
 Action potential spreads into each
cardiac muscle fiber along the transverse
(T) tubules
 Longitudinal sarcoplasmic tubules
release calcium ions into the sarcoplasm
T-tubules contain large amounts of Ca2+
released during action potential
 T tubules also open directly into the
extracellular fluid .
 Ca2+ content highly depends on ECF
[Ca2+] .
At the end of the plateau of the action
potential Influx of Ca2+ into the muscle fiber
abruptly stops Ca2+ is pumped back actively
into the SR and T tubules.
CARDIAC MUSCLE FIBRE
 Left Ventricular Rotation (Twist) Aids
Left Ventricular Ejection and Relaxation.
• Subepicardial layer spirals - leftward
direction
• Subendocardial layer spirals - rightward
direction
 During systole
• Clockwise rotation of apex
• Counterclockwise rotation of base
• Wringing motion pulling the base downward
toward the apex during systole
 At the end of systole
• LV similar to loaded spring - recoils or
untwists
• Blood enters rapidly
NEURAL CONTROL OF
CARDIOVASCULAR SYSTEM
Innervation of the heart
 Postganglionic sympathetic
nerves activates β1 -
adrenoceptors - Sinoatrial (SA)
node and Atrioventricular (AV)
node (↑ Heart rate or
+chronotropy)
 His-Purkinje conductive tissue
(↑ Conduction +dromotropy)
 Atrial and ventricular
contractile tissue (↑ Force of
ventricular contraction or
+inotropy)
 Postganglionic parasympathetic (vagus) nerves activates
muscarinic receptors
a. SA and AV nodes and atrial muscle --Reduces the heart rate
b. Rate of transmission through the AV node
c. Atrial contractility
 Adrenergic and cholinergic receptors on autonomic nerve
terminals that modulate transmitter release from nerve endings
 Release of acetylcholine from vagal nerve terminals inhibits the
release of norepinephrine from sympathetic nerve terminals
 Enhance the effects of vagal nerve activation on the heart.
PLACEMENT OF CHEST LEADS

V1 and V2: either side of

the sternum on the fourth
rib (count down from the
sternal angle, the second
rib insertion)
V4: on the apex of the
heart (feel for it)
V3: halfway between V2
and V4
V5 and V6: horizontally
laterally from V4 (not up
towards the axilla)
 Limb leads
 Three bipolar leads and three unipolar leads are obtained from three
electrodes attached to the left arm, the right arm, and the left leg,
respectively. (An electrode is also attached to the right leg, but this
is an earth electrode.) The bipolar limb leads reflect the potential
difference between two of the three limb electrodes:
 lead I: right arm–left arm
 lead II: right arm–left leg
 lead III: left leg–left arm
 The unipolar leads reflect the potential difference between one of
the three limb electrodes and an estimate of zero potential – derived
from the remaining two limb electrodes. These leads are known as
augmented leads. The augmented leads and their respective limb
electrodes are:
 aVR lead: right arm
 aVL lead: left arm
 aVF lead: left leg
 ECG GRAPH PAPER

 Speed of paper -25mm/sec

 1 horizontal small box – 0.04
sec
 1 horizontal large box -0.2 sec
 1 vertical small box -0.1 Mv
Heart rate calculation

Heart rate = 1500/no.of small squares in between RR

(0.04 x 1500 = 60 secs)
= 300/ no.of large squares in between RR
( 300 x 0.2 = 60 secs )
Standardization

 Beginning or end of ECG paper

 Voltage should always be 1mV
 1mm -0.1mV so 10mm –properly standardized to 1 mV
 Overdamping –when the pressure of the stylus is too
firm on the paper so its movement is retarded –
deflection fractionally wider and diminished amplitude
 WPW syndrome
 Underdamping –when the writing
stylus is not pressed firmly enough
against the paper –sharp spikes at the
corners
 Ischaemia
 Strain
 Prolonged QT
CARDIAC AXIS

 Leads VR and II look at the

heart from opposite
directions.
 When seen from the front,
the depolarization wave
normally spreads through
the ventricles from 11
o’clock to 5 o’clock, so the
deflections in lead VR are
normally mainly downward
(negative) and in lead II
mainly upward (positive)
 The presence of axis
deviation should alert you
to look for other signs of
right and left ventricular
hypertrophy
 A change in axis to the
right may suggest a
pulmonary embolus, and a
change to the left indicates
a conduction defect
Normal sinus rhythm
(sinus with 1:1 AV Conduction )
For Practical Examination

BRADYARRHTHMIAS
TACHYARRHYTHMIAS
 Sinus tachycardia  Sinus bradycardia
 SVT  A-V blocks
 AF ,AFL  Bundle brach blocks –
 Junctional tachycardia RBBB ,LBBB

 VT
 VF
 APC ,VPC
SINUS ARRHYTHMIA

 In sinus arrhythmia ,the impulses arise from the SA node

 The PR interval is normal as is the QRS complex
 The rate increases with inspiration and decreases with expiration
 This arrhythmia occurs more often in children than in adults
CAUSES OF INTRAOP
DYSRRYTHMIAS
 Lighter plane of anaesthesia
 Hypoxia
 Hypercarbia
 Hypocarbia
 Preexisting cardiac diseases
 Endocrine diseases
 Electrolyte disturbances
 Drugs
SINUS TACHYCARDIA

 HR > 100bpm – adult patient may be as high as 150 bpm

 Rhythm : is regular
 P/ QRS : the ratio of P waves to the QRS complexes is
1:1
 QRS complex : is normal
 Dangerous – IHD ,MS ,AS , Obstructive cardiomyopathy
 CAUSES
 Physiologic : excitement ,exertion ,pregnancy ,pain ,fever
 Surgical stimulation under lighter planes of anaesthesia
 Drugs : cardiac vagal tone blockers (eg.atropine and other
anticholinergic agents )
 Sympathetitone stimulants
(eg.norepinephrine ,epinephrine ,dopamine ,cocaine ,amphet
amine)
 Ketamine ,pancuronium ,ether ,cyclopropane
 Hypotension
 Hyperthyroidism
 Phaeochromocytoma
MANAGEMENT

 The underlying cause should be treated

 Hypovolemia and lighter planes of anaesthesia are the
most common causes
 In patients with ischaemic or stenitic valvular heart
disease
 Beta adrenergic blockers
 Supraventricular Tachycardia
 Rate -150 -250 beats /min
 Rhythm –regular
 P wave may be difficult to differentiate
 QRS narrow
 Therapy – depends on the degree of
haemodynamic compromise
 Vagal maneuvers – carotid sinus massage
 Adenosine 6mg IV ,repeat 12 mg IV
 Cardioversion
 ATRIAL FLUTTER

 Rate -150-200 bpm

 Rhythm regular
 Absent P waves – flutter
waves
 ATRIAL FIBRILLATION

 Rate variable – 150- 250 /min

 Rhythm – irregularly irregular
 P waves absent
 QRS complex – narrow and irregularly placed
Conditions :
 Mitral stenosis
 Hyperthyroidism
 Hypertension
 Old age and collagen disorders
Management :
 If haemodynamically stable –pharmacological management
 If unstable –cardioversion
 Chronic AF – require anticoagulation –CHA2DS2 VASe scoring
PREMATURE ATRIAL
CONTRACTION
 Origin is from a site in the atria other than SA node
 Rate <100/min
 Rhythm – irregular
 P wave – abnormal
 PR interval variable
 QRS – normal configuration
 Incomplete compensatory pause
VENTRICULAR PREMATURE
CONTRACTIONS
 Usually < 100 beats/min
 Rhythm –irregular
 P wave absent
 QRS wide bizarre
 T wave opposite to QRS
 Complete compensatory pause
When to treat ?

 Multiple in number > 6 /min

 Multifocal in origin
 Bigeminy or trigeminy
 R or T phenomenon
 Runs of > 3 mimicking VT
MONOMORPHIC VENTRICULAR
TACHYCARDIA
 Rate > 100- 250
 Rhythm ventricular – regular
 Wide bizarre QRS complexes
 Mangement :
1. Hemodynamically stable then amiodarone in one or
more doses of 150 mg given IV in 100 ml NS or D5W
over 10 min ,followed by an IV infusion of 1mg / min
for 6 hrs and 0.5 mg/min
2.Hemodynamically unstable – synchronized cardioversion ( 200 J )
POLYMORPHIC VT – Torsades
de pointis
 A form of polymorphic VT
 Rate 150-200
 Rhythm may be irregular
 P wave absent
 QRS COMPLEXES – wide appears twisting around a
central axis
 Responds to IV magnesium
 If unstable – electrical defibrillation
VENTRICULAR FIBRILLATION

 Rate absent
 Rhythm none
 Bizarre wave form
 Management CPCR and defibrillation
SINUS BRADYCARDIA

 Rate < 60 beats

/min
 Other waves and
intervals will be
normal
Physiologic variants :
 Healthy people – resting pulse rate < 60 /min
 Trained athletes – resting pulse rate as low as 35 beats / min

Drugs :
 Increasing cardiac vagal tone ( eg. Digitalis , edrophonium )
 Decreasing sympathetic tone (eg. Beta blockers ,amiodarone )
 Decreasing sinus node automaticity via calcium channel blockade
(eg,verapamil , diltiazem )
 Halothane , succinyl choline .
FIRST DEGREE HEART BLOCK

 Common if asymptomatic – no specific investigation or treatment

 if symptomatic – will need preoperative pacing
 Implication – can rarely progress to second degree block , usually Mobitz
type 1
SECOND DEGREE AV BLOCK
Mobitz type 1 – Wenckeback
 Rhythm – atrial regular and ventricular irregular
 Gradually increasing PR interval with a drop of QRS
complex
 QRS complex is normal
SECOND DEGREE AV BLOCK-
Mobitz type 2

 Rhythm irregular
 PR interval normal
 Some P waves are not followed by QRS complex
 Atrial rate regular
 Ventricular irregular
THIRD DEGREE HEART
BLOCK
 COMPLETE HEART BLOCK

 Rate < 45 beats /min

 Rhythm – atrial regular
 Ventricular – regular
 No association between P waves and QRS complexes .
Pacemaker ECG

 Atrial pacing , ventricular pacing ,atrial and

ventricular pacing
RBBB

 Can be a normal variant

 Rhythm regular
 Wide QRS complex – r SR pattern - M pattern
 V 5 – 6 presence of an S wave
LBBB

 Wide QRS complexes

 V1 – negative RS complex
 V 5-6 positive R wave without an S wave
 Always pathological
WPW SYNDROME

 Short PR interval ,wide QRS complex

 Delta wave
 Avoid sympathomimetic ,atropine
RIGHT VENTRICULAR
HYPERTROPHY
LEFT VENTRICULAR
HYPERTROPHY
 S in V1 + R in V5
 => 35 small squares
MYOCARDIAL INFARCTION
HYPERKALEMIA
DEXTROCARDIA
BIFASCICULAR AND
TRIFASCICULAR BLOCKS
 Bifascicular block
RBBB + LAD –right bundle branch block with left anterior
hemiblock

Trifascicular block --- RBBB + LAD + first degree AV block

Periop complete heart block
TAKE HOME MESSAGE

 Read an ECG systematically

 Look for standardization
 Rhythm and rate
 Presence and morphology of p wave
 Look for PR interval – any abnormality
 Presence of significant Q qave
 QRS complex – width ,hypertrophy
 ST segment – elevated ,depressed ,flat ,sagging .
 T wave – upright ,peaked ,inverted
 QT interval – normal /prolonged
REFERENCES

 Guyton & Hall Textbook of Medical Physiology 3rd SAE. Elsevier

Health Sciences.
 Barash, Paul G.. Clinical Anesthesia, 8/e. Lippincott Williams &
Wilkins.
 Gropper, Michael A.; Miller, Ronald D. Miller's Anesthesia, 2-
Volume Set E-Book. Elsevier Health Sciences.
 ECG made easy ||John R. Hampton (DM MA DPhil FRCP FFPM
FESC) Emeritus Professor of Cardiology University of Nottingham,
UK
 Morgan & Mikhail's Clinical Anesthesiology
Book by David C. Mackey, John D. Wasnick, and John F.
Butterworth
THANKYOU !