4. 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
9. Duration of contraction
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
17. Regulation of pumping
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
20. Effects of autonomic stimulation
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.
21. 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
42. Other leads
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
44. 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
45. Vector analysis
Closer the angle higher is the component
+ve vector: reading above the baseline
- ve vector: reading below the baseline
59. High voltage ECG
Normally peak of R to bottom of S: 0.5 to 2 mv
Abnormally large: summation of all 3 leads
>4mv
Cause :hypertrophy
60. Low voltage ECG
1 decreased current production
low muscle mass: common in old MI
propagation also slowed- prolongation
61.
62. 2 reduced conduction
A. pericardial effusion
B. pulmonary emphysema
3 flow in AP axis
rotation of axis
63. Prolonged QRS complex
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
66. Current of injury
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
67. 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
71. Arrhythmias
1 tachycardia
>100bpm, normal but shorter waves
Causes:
Temperature- 10beats/degree F upto 105degree
Sympathetic stimulation
toxicity
72. 2 bradycardia:
<60 bpm
Athletes, carotid sinus syndrome
Due to increased vagal stimulation
73. Sinus arrhythmia
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%
74. Sinoatrial block
Block in SA node
No P wave
AV nodal rhythm
Normal QRS-T
Slow
75. 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
76. 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.
77. 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
78.
79. Third degree
No impulse propagation to AV node
Atrioventricular dissociation
81. Bundle branch block
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
82. Arborisation block
Purkinje fibre dysfunction due to chronic
myocardial damage
83. Other abnormalities
Stokes Adams syndrome
Borderline ischemia of conductive tissue
Electrical alternans
tachycardia
Ischaemia
Myocarditis
Digitalis toxicity
84. Premature beats
Extrasystole & compensatory pause
o Local areas of ischemia
o Small calcified plaques at different points of
heart- irritating
o Mechanical stimulation during cardiac
catheterisation
o Toxic irritation nicotine, caffeine, drugs
o Pulse deficite & bigeminal pulse
85. 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
86. 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