Challenge yourself with something

you know you could never do, and

what youll find out is that you can
overcome anything. [PHYSIOLOGY

LECTURE DR. DOMINGUEZ]

CARDIAC CONDUCTION

*no P wave- SA node not firing

*if SA node not functioning, AV node takes
over (40-59 bpm)
*if AV node not functioning, Purkinje fibers
take over (15-30 bpm)

1. SA node
a. Pacemaker of the heart- controls
rate of beating of the entire
heart; highest firing rate (60-100
bpm)
b. With greatest automaticity and
rhythmicity

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

Pacemaker Activity Determinants:

Determinant
Sympathetic Parasympath
etic
Rate of
SA node is
SA node
Depolarizatio
more
more
n (phase 4)
permeable
permeable to
to Na and Ca K (slower)
(faster)
Maximal
Less
More
Negativity
negative
negative
(phase 4)
(faster)
(slower)
Threshold
Potential
*Increased
threshold =
slower firing
Beta
Beta blockers
agonists
(-olols)
(salbutamol)

ELECTROCARDIOGRAPHY

2. AV node via AV Node and Bundle of

His
- Physiologic delay in impulse
conduction at the AV node to allow
complete emptying of blood from
atria to ventricles; most constant
ERP protecting ventricle from
excessive firing even in the
presence of premature excitations
of atria
- Allow complete emptying of blood
from atria to ventricles

1. P wave - atrial depolarization

- Impulses from SA node
- First upward deflection
2. PR interval - measures time from onset
of atrial activation to onset of
ventricular activation
- Time it takes for impulse to travel
from SA to AV node
3. QRS ventricular depolarization (+
atrial repolarization)

3. Ventricular conduction - via bundle

branches and Purkinje fibers; most
rapid transmission of action potential
for synchronized and immediate
contraction of thick-walled (muscular)
ventricles
PROBLEM: Long refractory period:
predispose to arrhythmias
1

Challenge yourself with something

you know you could never do, and
what youll find out is that you can
overcome anything. [PHYSIOLOGY

LECTURE DR. DOMINGUEZ]

-q wave- septal depolarization (Q

infarction)
-R- ventricular apex
-S- ventricular base
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

Extremity Limb Leads - record potentials in

frontal plane
Bipolar Leads
I - right arm to left arm (0o)
II right arm to left foot (+60o)
III left arm to left foot (+120o)
Unipolar Leads
aVR to right arm(-150o)
aVL to left arm(-30o)
aVF to left foot (+90o)

QRS-T cycle and ventricular action potential

>QRS= phase 0 (depolarization)
>ST= phase 2 (plateau)
>T wave= phase 3 (repolarization)
*QT prolonged - affects phase 0-3;
action potential becomes longer
CLINICAL CORRELATION
atrial hypertrophy- big P wave
ventricular hypertrophy- QRS
wider/prolonged
hyperkalemia- T wave peaked,
tenting
hypokalemia- flat/inverted T wave;
U wave

Chest/precordial leads record potentials in

horizontal plane
Einthovens triangle- determine axis of the
heart
Axis sum of all electrical activities of the
heart (vectors)
Normal: -30 to 100

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

normal cardiac vector - downward and to the

left

Challenge yourself with something

you know you could never do, and
what youll find out is that you can
overcome anything. [PHYSIOLOGY

LECTURE DR. DOMINGUEZ]

AXIS
Normal axis
( -30 to
+100)
Left axis
deviation
(more
negative
than -30)
Right axis
deviation
(more
positive
than +100)
extreme
right angle
deviation
(-91 to
180)

QRS in
LEAD I
^

QRS in
LEAD II
^

QRS in
LEAD III
^

small ^
/v

CLINICAL CORRELATION: Ventricular

hypertrophy shifts the axis towards the
hypertrophied side
Left Ventricular Hypertrophy Left axis
deviation
Right Ventricular Hypertrophy Right
axis deviation
NOTE TAKERS:
Magnaye, Seth; Gomez, Kenneth; Rimando;
Janelle