ELEMENTS OF CARDIAC EXCITATION

I) CARDIAC ACTION POTENTIAL

PHAS
E
4

FAST RESPONSE

SLOW RESPONSE

Resting membrane potential

due to outward diffusion of
potassium

Depolarization due to influx

of sodium via fast sodium
channels
Initial repolarization due to
transient efflux of potassium
Plateau due to entry of
calcium
Repolarization due to efflux
of potassium

Slow
depolarization/automaticity
due to inward movement of
sodium (via funny channels)
and Ca (via T channels)
Depolarization caused by
increased inward calcium
current
None

1
2
3

None
Repolarization due to efflux
of potassium

** RESTORATION OF IONIC CONCENTRATIONS via Na-K-ATPse pump

and 3Na-1Ca antiporter
** Check out Figures 16-1 and 16-3, Berne and Levy
CLINICAL CORRELATION:
1. Class Ia antiarrhythmics control heart rate by blocking Na
influx
2. Class II (beta blockers) and Class IV (calcium-channel blockers
like verapamil and diltiazem) antiarrhythmics block calcium
entry
3. With myocardial ischemia or infarction, activity of Na-K-ATPse
pump is impaired
FACTORS AFFECTING CONDUCTION VELOCITY
1. Amplitude of action potential: the greater the action potential
amplitude, the more rapidly is the wave of depolarization
propagated
2. Rate of change of potential during phase 0: the more gradual the
rate of change of potential in phase 0, more time required to reach
threshold, slower conduction velocity
3. resting membrane potential (RMP): the more negative the RMP,
the harder it is to reach threshold, decreases amplitude of action
potential and slope of upstroke, slower conduction velocity
CARDIAC EXCITABILITY
1. Absolute or effective refractory period: another action
potential cannot be generated; prevents sustained, tetanic
contraction of cardiac muscle

2. Relative refractory period (RRP): another action potential can

be generated in presence of stronger stimulus; the later in the
RRP that the fiber is stimulated, the greater the increase in
amplitude of response and slope of upstroke, thus the
propagation velocity also increases
** Check out Figure 16-15
II) CARDIAC CONDUCTION
- one-way conduction: SA node to AV node to AV bundle to right
and left bundle branches to Purkinje fibers
- Spread of depolarization is from endocardium to epicardium,
apex to base
- Automaticity self-excitation; ability to initiate its own beat
- Rhythmicity regularity of pacemaking activity
1. SA node
a. Pacemaker of the heart- controls rate of beating of the
entire heart
b. With greatest automaticity and rhythmicity
2. AV node: Delay in impulse conduction at the AV node to allow
complete emptying of blood from atria to ventricles; with
constant ERP protecting ventricle from excessive firing even in
the presence of premature excitations of atria
3. Ventricular conduction: via bundle branches and Purkinje
fibers; rapid transmission of action potential for synchronized
and immediate contraction of thick-walled ventricles
CLINICAL CORRELATION
1.Sympathetic effect: increased permeability to Na and Ca thus
increasing slope of slow diastolic depolarization
- More positive RMP of SA node
- Increased rate of SA node discharge
- Increased rate of conduction and excitability of A-V node
- Increased force of contraction
2. Parasympathetic effect/ increased vagal activity: increased
permeability to potassium thus hyperpolarizing pacemaker cell
membrane and reducing slope of slow diastolic depolarization
3. Quinidine and procainamide (antiarrhythmics) raise threshold
value to less negative values
** Check out Figure 16-18
ECTOPIC PACEMAKERS
- regions in the heart other than SA node initiating beats
-Mechanisms:
1. Enhanced own rhythmicity
2. Depressed rhythmicity of higher-order pacemakers

3. Block in pathways between ectopic focus and pacemaker

III) ELECTROCARDIOGRAPHY
1. P wave - atrial depolarization
2. PR interval: measures time from onset of atrial activation to onset
of ventricular activation
3. QRS ventricular depolarization
4.QT interval: time it takes for impulse to spread through ventricles
and for repolarization to occur; electrical systole of ventricles
5. T wave ventricular repolarization
6. J point point at which all parts of the ventricles are depolarized
CARDIAC VECTOR
- vector sum of all cardiac electrical activity at any moment
- orientation of vector represents mean electrical axis of the heart in
the frontal plane
AXIS

QRS in LEAD I

QRS in
LEAD II

QRS in
LEAD III

Normal axis ( -30 to

+100)
Left axis deviation (more
negative than -30)
Right axis deviation
(more positive than
+100)

CLINICAL CORRELATION: Ventricular hypertrophy shifts the axis

towards the hypertrophied side
IV) ARRHYTHMIAS
Arrhythymia
Sinus bradycardia

Pathophysiology
decreased SA node firing

Sinus tachycardia

increased SA node firing

First Degree AV
block
Second-degree AV
block

prolonged PR interval

Third degree AV
block/complete
heart block
Premature
depolarizations
(atrial/ventricular)
Fibrillation (Atrial

atria are depolarized at a high rate but only a

fraction of the atrial impulses are conducted to
ventricles; protects ventricles from excessive
contraction
none of the atrial impulses reaches ventricle;
atrial and ventricular rhythms are entirely
independent
excitation occurs at some ectopic focus
reentry phenomenon; premature impulse

or ventricular)

arrives during vulnerable period of cardiac

cycle ( downslope of T wave); during this
period, excitability of cardiac cells varies
( some in ERP, others fully recovered, others
able to conduct impulses). As region of cardiac
cells becomes excitable again, it is ultimately
reentered by one of the wave fronts travelling
around chamber, hence process is selfsustaining

V) CARDIAC CYCLE
Ventricular Filling
1. Rapid ventricular filling: AV valves open due to higher pressures
in atria; ventricular volumes start to increase rapidly
2. Diastasis or reduced ventricular filling: reduced ventricular filling
since increasing volume in ventricles results to equilibrating
pressures in atria and ventricles
3. Atrial systole: ventricular pressures start to increase greater than
atrial pressures, thus atria have to contract to empty remaining
blood in atria into ventricles
Isovolumic Contraction
- Increasing ventricular pressure
- Closure of A-V valves
- Tension is increasing but there is no emptying (WHY???)
- Ventricular volume remains constant (isovolumic, same volume)
Period of Ejection
- LV pressure is at its maximum
- Semilunar valves open
- Blood pours out of ventricles
Isovolumic Relaxation
- Decreasing intraventricular pressure
- Increased pressure in large arteries
- Closure of semilunar valves
- Ventricles relax, no change in ventricular volume
- Atria start to fill with blood
Left atrial pressure curve
1. a wave rise in pressure caused by atrial contraction
2. c wave - caused by impact of common carotid artery with
adjacent jugular vein and to some extent by abrupt closure of
the tricuspid valve in early ventricular systole
3. v wave rise in pressure associated with atrial filling
** Check out Figure 16-40

**Check out the following websites for Cardiac Cycle animations:

1.
http://highered.mcgrawhill.com/sites/0072495855/student_view0/ch
apter22/animation_the_cardiac_cycle_quiz_1_.html
2. http://anatimation.com/cardiac/intro.html
3. http://library.med.utah.edu/kw/pharm/hyper_heart1.html
DETERMINANTS OF Myocardial Contractility
1. Preload force that stretches relaxed muscle fibers
2. Afterload force against which contracting muscle must
overcome
*INDEX OF CONTRACTILITY: Ejection fraction