Download Cardiovascular Physiology Today

Cardiovascular Physiology
Today

Anatomy

Requirements of an effective heart

ECG’
ECG’s

Arrhythmias in the normal heart

Abnormal arrhythmias
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The Heart
Aorta
Pulmonary artery
Superior vena cava
Pulmonary veins
Pulmonary veins
Left atrium
Right atrium
Right ventricle
Left ventricle
Interventricular septum
Inferior vena cava
Sherwood Fig. 9-4a, p. 303
The Heart Wall

Endocardium (inner)


Myocardium (middle)


Cardiac muscle
Epicardium (outer)


Layer of endothelial cells
External membrane
Pericardium
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Cardiac Muscle (myocardium)

99% contractile cells

1% autorhythmicity cells


Aerobic muscle


Self-excitate
Properties of skeletal and smooth muscle
Intercalated discs


Gap junctions
Desmosomes
Electrical activity of the heart
Autorhythmicity
the ability to generate own rhythm

Pacemaker/autorhythmic cells
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Conductive system (fibers)

spreads excitation throughout heart
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Anatomy of
conduction
system
Interatrial
pathway
Atrioventricular
(AV) node
Sinoatrial
(SA) node
Right
atrium
Left
atrium
Internodal
pathway
Left
branch
of bundle
of His
Right
branch
of bundle
of His
Left
ventricle
Right
ventricle
Purkinje
fibers
Sherwood Fig. 9-8, p. 306
Delay between Atrial and
Ventricular contractions

Impulse does not travel from to ventricles
before atria contract




Atria must empty contents into ventricles
before ventricular contraction
AV valves
If both contracted together – not efficient
AV nodal delay (at least .1s)
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Electrical Activity in Pacemaker Cell
(SA nodal fibre)
Sherwood Fig. 9-15, p. 313
Pacemaker cells




SA node = pacemaker of the heart
If SA node is damaged, other cardiac cells
can take over
Latent pacemakers- AV node and purkinje
fibers
Action potentials can be changed
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Electrical Activity in Contractile Cells
Sherwood Fig 9.15, p.279
Comparison of nodal fibre and
cardiac muscle fibre
Guyton & Hall Fig. 10-2, pg.122
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Coordination and pressure generation
for left and right outputs



Both members of a pair contact
simultaneously
Each atria and ventricle contract as a
syncytium
Pressure generation determined by force
of contraction
Guaranteed time for filling
Refractory period
Tetanus cannot
occur
Ventricle .25.30sec
Atria .15sec
Sherwood Fig. 9-17, p. 281
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Electrocardiogram

Non-invasive

Body fluids are conductors



Comparison of voltages detected by electrodes at
two points
SUM of activity in ALL cardiac muscle
Exact pattern of activity depends on orientation of
electrodes
ECG diagram
R
T
P
Q
PR
P
S
ST
TP interval
Sherwood Fig. 9-15, p. 313
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Normal ECG
Heart beat
reciprocal of time
interval between
two successive
beats
??? Shape/
organization of heart
http://library.med.utah.edu/kw/ecg/image_index/index.html
Athletes ECG’s
1 horizontal box= .2s (small box 0.04s), 5 boxes = 1sec
10 small division upward or downward= 1millivolt
Respiratory Sinus Arrhythmia
Normal phenomom
HR ↑ with inspiration
HR ↓ with expiration
Expressed more in
young and fit
Marquette Electronics Copyright 1996
http://library.med.utah.edu/kw/ecg/image_index/index.html
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Bradycardia & Tachycardia
Bradycardia
≤60bts/min
Tachycardia ≥ 100
bts/min
Timing of P-QRS-T
same but more/less
frequent
Guyton & Hall fig. 13-1 & 13-2, pg. 150
Abnormal Arrhythmias

Abnormal rhythmicity of pacemaker

Shift of pacemaker from SA node

Blocks during transmission of impulse

Abnormal transmission pathways

Spontaneous generation of abnormal
impulses
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Breakdown of SA node
Pacemaker Authority
152
Guyton & Hall fig. 13-4 pg.152
Impulse from SA node is blocked before it enters atria
Latent pacemakers pick up authority
No/small p-waves clue: Atrial fibrillation
Breakdown of AV coupling
Causes: ischaemia,
compression, inflammation,
extreme stimulation
1st degree: delay in
conduction, prolonged P-R
interval 0.2s, QRS same
2nd degree: incomplete heart
block, P-R interval between
.25-.45sec, atria beating
faster than ventriclesdropped beats
Compete AV block: P-wave
regular frequency completely
unrelated to ventricular
firing, Ventricular QRS
followed by T wave normal.
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Breakdown of ventricular
coupling and refractory period

Breakdown of left/right ventricular
coupling


Same mechanisms that cause AV block
QRS may be considerable abnormal
Breakdown of refractory safety period

Hypertrophy can cause different refractory
periods in epicardium & endocardium
Left Ventricular Hypertrophy
In exerciseadaptation to
increased
preload/afterload
Enhances pumping
capacity
http://library.med.utah.edu/kw/ecg/image_index/index.html
Increased QRS
amplitude
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Exercise Hyperkalaemia
Elevated potassiumspeeds recovery of
action potentials
Tall peaked T-wave
with narrow base
http://library.med.utah.edu/kw/ecg/image_index/index.html
Widened QRS
complex
Review: Cardiac Pumping

Efficient cardiac pumping requires:



Atrial excitation and contraction to be
complete before onset of ventricular
contraction
Each heart chamber to contract as a unit
Both atria to contract simultaneously and both
ventricles to contract simultaneously
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