Download PHYSIOLOGY OF HEART

ECG BASICS
&
PHYSIOLOGY
OF
HEART
Heart is a pumping organ
How heart keeps pumping?
1.special structure of cardiac muscle
 syncytial nature
 both resting membrane potential & action
potential are different form skeletal muscle
2.auto rhythmicity of heart
Action potential of heart muscle
Factors affecting action potential
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1 K+ concentration
2 Ca++ concentration
3Na+ concentration
4 temperature
Excitation contraction coupling
Excitation contraction coupling
Duration of contraction
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Atria 0.2sec
Ventricle 0.3 sec
Normally contraction time is 40% of cardiac
cycle. When heart rate increases 3 times it is
65% of cardiac cycle.
Relaxation decreases
Ventricular filling decreases
Cardiac cycle
Atrial systole
IMC
ejection phase
IMR
Heart sounds
Regulation of pumping
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1Frank Starling mechanism
2 autonomic innervation
Within physiological limit heart pumps all the
blood that comes to it without allowing
excessive pooling of blood in the veins
Parasympathetic innervation
Effects of autonomic stimulation
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Chronotropic effect
Dromotropic effect
Bathmotropic effect
Inotropic effect
Effects of autonomic stimulation
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Sympathetic stimulation: HR can go upto 250
bpm in young individual.
Parasympathetic stimulation: HR can go down
to zero. Although vagal escape follows.
Both Sympathetic and parasympathetic system
maintain a low level firing at resting condition.
Energy considerations
Source: oxidative respiration
 FA- biggest source
 glucose/ lactate also used
 Energy efficiency max 20-25%, rest is converted
to heat (HF: 5-10% )
 Expenditure increases when
ventricles are dialated
BP is elevated
Energy expenditure is measured by oxygen
comsumption
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Special conductive system
Rate of discharge
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SA node 70-80 bpm
AVnode 40-60 bpm
AV bundle 15-40 bpm
Autorhythmicity of SA node
Autorhythmicity of SA node
Autorhythmicity of SA node
Autorhythmicity of SA node
Autorhythmicity of SA node
Special conductive system
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Nodal delay
.09sec AV node
.04 sec penetrating
portion
Additional .03 sec
internodal pathway
Ectopic pacemaker
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Heart block
Stokes Adams syndrome
ECG
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Heart muscle wraps around heart like a double
spiral with a fibrous septa between the spiral
layers.
Flow of current
leads
Other leads
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Chest leads 6 in no.
+ pole connected to chest, -ve to all 3 limbs
Infrequently 7th & 8th chest leads & esophageal
leads used.
aVR- Rt +ve
aVF- Lt leg +ve
aVL- Lt arm +ve
Recording of V1 V2 upside down as it is more
closer to base rather than apex
Axis of leads
Vector
Instantaneous mean vector:
At any given instance the total amount of current
flowing in the heart is represented in magnitude
and direction by the vector. Current flows from
DEPOLARISED to POLARISED area i.e.
NEGATIVE to POSITIVE
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Vector analysis
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Closer the angle higher is the component
+ve vector: reading above the baseline
- ve vector: reading below the baseline
Mean vector
Axis deviation
1Normal:
20degree to left, 100 degree to right
Lt
Rt
Expiration
Inspiration
Supine
Standing
Fat
Tall/ lean
2Hypertrophy / conduction block
Left Deviation : pathological
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Hypertension
Aortic valve stenosis
Regurgitation
LBBB
LBBB Left Deviation
Right Deviation
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Pulmonary stenosis
Fallots tetralogy
VSD
Pulmonary hypertension
RBBB
Right Deviation
Vector analysis: axis deviation
High voltage ECG
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Normally peak of R to bottom of S: 0.5 to 2 mv
Abnormally large: summation of all 3 leads
>4mv
Cause :hypertrophy
Low voltage ECG
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1 decreased current production
low muscle mass: common in old MI
propagation also slowed- prolongation
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2 reduced conduction
A. pericardial effusion
B. pulmonary emphysema
3 flow in AP axis
rotation of axis
Prolonged QRS complex
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Normal : 0.06- 0.08 sec
Hpertrophy or dilatation of ventricles:
conduction prolonged .09- .12sec
Prolongation in BBB- propagation through
muscle:
>.09 sec abnormal
>.12- almost certain to be pathological block in
ventricular conduction system
>.14 – complete block
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Bizzare QRS complex
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1 scar tissue
2 Multiple block
Current of injury
Current of injury
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Injured area: depolarised- emits –Ve charge.
Injury: mechanical/ infection/ ischemia
As the area remains continuously depolarised a
current flow in the ventricle even before QRS
starts. This is Current of injury.
Axis deviation also present
Current of injury
J point
No current flows when the ventricles are fully
depolarised. So the iso electric point is seen at
the end of QRS complex.this is called J point.
 ST segment shift
As the Current of injury is present the TP
segment is shifted. But in common practice it is
considered TP is in iso electric line. So this
phenomenon is usually termed as ST segment
shift
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Current of injury
Current of injury
T WAVE ABNORMALITY
Arrhythmias
1 tachycardia
>100bpm, normal but shorter waves
Causes:
Temperature- 10beats/degree F upto 105degree
Sympathetic stimulation
toxicity
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2 bradycardia:
<60 bpm
Athletes, carotid sinus syndrome
Due to increased vagal stimulation
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Sinus arrhythmia
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Can result from any circulatory reflex that alters
the strength of the autonomic signal to SA node
Respiratory type results from spill over of
signals from the medullary respiratory centre to
vasomotor centre.
Normal 5% variation in inspiration and
expiration.
Deep breathing: 10%
Sinoatrial block
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Block in SA node
No P wave
AV nodal rhythm
Normal QRS-T
Slow
AV Blocks
Ischemia of AV node/ bundle
 Compression of bundle: scar/ calcified portion
 Inflammation of AV node/ bundle
myocarditis/ diptheria/ rheumatic fever
 Extreme vagal stimulation:
carotid sinus syndrome
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AV block
A.
Incomplete
1. first degree: prolonged PR interval (>.20
sec). Conduction is delayed but no actual
blockage.
May prolong upto .35-.45 sec
The measurement of duration gives
estimate of severity.
2. second degree
here also PR prolonged. Some beats strong
enough to go through block some are not. So
for some P wave QRS complex is present
whereas for some it is absent.
2:1/3:2/3:1 rhythms are present sometimes
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Third degree
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No impulse propagation to AV node
Atrioventricular dissociation
Atria 100 bpm ventricle 40 bpm
Bundle branch block
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A branch of the bundle delays propagation
Normal side contracts first
Duplication of 1st heart sound
Prolonged QRS
More severe when on the left side
Arborisation block
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Purkinje fibre dysfunction due to chronic
myocardial damage
Other abnormalities
Stokes Adams syndrome
Borderline ischemia of conductive tissue
 Electrical alternans
tachycardia
Ischaemia
Myocarditis
Digitalis toxicity
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Premature beats
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Extrasystole & compensatory pause
Local areas of ischemia
Small calcified plaques at different points of
heart- irritating
Mechanical stimulation during cardiac
catheterisation
Toxic irritation nicotine, caffeine, drugs
Pulse deficite & bigeminal pulse
AV nodal/ bundle premature contraction
P wave not distinct, atria & ventricles depolarises
at the same time
 Ventricular premature contraction
prolonged QRS due to volume conduction
High voltage as one voltage depolarises before
another
Inverted t wave
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Ventricular fibrillation
Contraction of ventricular muscle mass without
coordination and at a high rate
 Some of muscle fibres contract at any given time and
others relax so heart is neither in systole nor diastole
 Caused by reentry, facilitated by:
Long pathway – dilated heart
Decreaesd conduction speed: high K+, ischemia,
purkinje block
Low refractory period: repeated stimulant/ epinephrine
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