Accept responsibility for

your life. Know that it is you

who will get you where
you
[PHYSIOLOGY
LECTURE DR. DOMINGUEZ]

MECHANISMS OF ARRHYTHMIAS
I.

Alterations in impulse initiation

slow

Ectopic pacemakers:
a. Enhanced own rhythmicity: e.g. sinus
tachycardia (automaticity of the SA
node, P-waves are present)
b. Depressed rhythmicity of higher-order
pacemakers
c. Block in pathways between ectopic
focus and pacemaker (e.g. 3rd degree
AV block, COMPLETE AV block. There is
a P wave but the QRS do not follow.
The QRS is fired by the purkinje fibers,
so there are more P-waves than
QRSs.)

fast

NORMAL
REENTRY
impulses cannot
travel going down, but can go up.
Short effective refractory period
Results in AV node reentry in circuit.
Prolonged conduction time

Triggered automaticity:
-dependent on ATP
2mechanisms:
a. Early After Depolarization: occurs
midway between plateau phase and
initial part of phase 3 of the ventricular
action potential. Pathophysiology:
reactivation of calcium channels. Usually
in ischemias due to calcium overload.
When heart rate is slow.
b. Delayed after depolarization: occurs
after phase 3, delayed calcium entry,
occurs in patients with tachycardia.
II.

uni-directional block: meaning

e.g. of reentry is when there is an

accessory pathway e.g. bundle of
Kent/bypass tract.
Ectopic tachycardias treatment
Shock: ventricular fibrillation
Antiarrhythmics: atrial fibrillation
Antiarrhytmics:
Class 1: block sodium channels
depolarization or phase 0 upstroke
decreases
conduction decreases
action potential prolonged
increased effective refractory
period
raised the threshold for firing
decreased automaticity
Class 3: e.g. amiodarone, Beta
blockers
blocks potassium channels
delayed repolarization; prolonged
absolute refractory period

Abnormal Impulse Conduction:

Reentry
AV node - fast and slow branch.
Fast branch - has fast depolarization and
repolarization.
Slow branch - has slow depolarization
but fast repolarization.
NORMALLY:
impulse from AV node goes to fast
branch - trigger the ventricles goes
to slow branch
*In fast branch, some may conduct
retrograde through the slow branch
* when the fast and slow braches
meet, they extinguish each other =
normal sinus rhythm

Danger: anti-arrhythmics are also proarrhythmics

- may have triggered activity
*beta blockers, amiodarone, metoprolol

REENTRY

Arrhythymia
Sinus bradycardia

Pathoph
decreased SA node firi

Sinus tachycardia

increased SA node firin

Accept responsibility for

your life. Know that it is you
who will get you where
you
[PHYSIOLOGY
LECTURE DR. DOMINGUEZ]
- Tension is increasing but there is no
prolonged PR intervalemptying since all valves are closed
remains constant
atria are depolarized -atVentricular
a high ratevolume
but only
(isovolumic,
same
volume)
Left
a fraction of the atrial impulses are
Ventricular
End
Diastolic
Volume
conducted to ventricles; protects ventricles
(LVEDV)
from excessive contraction
Third degree AV
none of the atrial impulses reaches
Period of Ejection [Systole]
block/complete heart block
ventricle; atrial and ventricular rhythms are
- LV pressure is at its maximum
entirely independent; ATRIAL >
- Semilunar valves open
VENTRICULAR RATE - Blood pours out of ventricles
Premature depolarizations
excitation occurs at ectopic focus aside from
(atrial/ventricular)
SA node
Isovolumic Relaxation [Diastole]
Fibrillation (Atrial or
reentry phenomenon;- premature
impulse
R wave
ventricular)
arrives during vulnerable
period ofintraventricular
cardiac
- Decreasing
pressure
cycle ( downslope of T- Increased
wave); during
this
pressure in large arteries
Closurecells
of semilunar
valves: s2 dubb
period, excitability of -cardiac
varies
Ventricles
relax,others
no change in ventricular
( some in ERP, others-fully
recovered,
volume
able to conduct impulses).
As region of
Atria startagain,
to fill with
cardiac cells becomes- excitable
it is blood
ultimately reentered by one of the wave
Leftchamber,
atrial pressure
fronts travelling around
hence curve
1. a wave rise in pressure caused by
process is self-sustaining
atrial contraction (seen in jugulars)
*tricuspid stenosis - atrial
Cardiac cycle: from 1 heart beat to the
contraction - a wave (cannon anext heartbeat.
waves/ giant a-waves)
Contraction: systole
2. c wave - caused by impact of common
Relaxation: diastole
carotid artery with adjacent jugular
vein and to some extent by abrupt
CARDIAC CYCLE
closure of the tricuspid valve in early
ventricular systole
Ventricular Filling [Diastole]
3. v wave rise in pressure associated
1. Rapid ventricular filling:
with atrial filling
AV valves open due to higher
pressures in atria; ventricular volumes
Determinants of Myocardial Contractility
start to increase rapidly
1. Preload force that stretches relaxed
2. Diastasis or reduced ventricular filling:
muscle fibers
Reduced ventricular filling since
force = Stroke volume/Cardiac output
increasing volume in ventricles results to
2. Afterload force against which contracting
equilibrating pressures in atria and
muscle must overcome
ventricles
- in aorta/arterial system: afterload =
3. Atrial systole:
force INITIALLY; CHRONIC lose contractility
Ventricular pressures start to increase
(hypertrophy)
greater than atrial pressures, thus atria
have to contract to empty remaining
*Stroke volume = amount of blood pumped
blood in atria into ventricles
per beat
*IMPORTANT: adds 30% blood during
*Cardiac output = stroke volume/minute
heart failure
(multiply with heart rate)
First Degree AV block
Second-degree AV block

Isovolumic Contraction [Systole]

- Increasing ventricular pressure
- Closure of A-V valves: s1, lubb

*INDEX OF CONTRACTILITY: Ejection fraction

Measured through 2D echo
ejection fraction: failure
2

Accept responsibility for

your life. Know that it is you
who will get you where
you
[PHYSIOLOGY
LECTURE DR. DOMINGUEZ]

Cardiac Cycle animations:

1.
http://highered.mcgrawhill.com/sites/007249
5855/student_view0/chapter22/animation_th
e_cardiac_cycle_quiz_1_.html
2. http://anatimation.com/cardiac/intro.html
3.
http://library.med.utah.edu/kw/pharm/hyper_
heart1.html

Note takers:
Dumaup, David
Pagbilao, Vic
Tulas,
Ulysses