PHYSIOLOGY SGD 12-15

HEART I
Sequence and Direction of Depolarization from SA node till ventricular free
wall

Physiological Basis for Difference in Recording of Leads AVR/AVF

Types Sub Types Location of (+) Perspective Directions Derived
electrode in relation
to center of heart
Limb Leads Standard I 0 (R arm, L arm) Frontal axis Superior/ Inferior
II +60 (R arm, L leg) Right/Left
III +120 (L arm, L leg)
Augmented aVF +90 (L foot +)
aVL -30 (L arm +)
aVR -150 (R arm +)
Chest 4th ICS, R sternal V1 Right/ Anterior Horizontal Anterior/Posterior
Leads 4th ICS, L sternal V2 Right/ Anterior axis Right/Left
Halfway bet V2 and V4 V3
5th ICS, L midclavicular V4
5th ICS, L ant axillary V5 Left/Posterior
5th ICS, L midaxillary V6 Left/Posterior

Created by making: Created by making:

Right Arm positive (+)
All other extremities negative (-)
Angle of orientation: -150
Looks across the heart from the left hip up
through the right shoulder along the -150
axis of the frontal plane
Looks toward the right side of the heart and
is considered to be a lead in no mans land
Offers no specific view of the left ventricle
but rather, it views the inside of the
endocardial wall to the surface of the right
atrium, from its perspective on the right
shoulder
Legs positive (+)
All other extremities negative (-)
Angle of orientation: +90
Looks through the heart from the chin down to
the feet along the +90 axis in the frontal plane
Looks at the inferior portion of the heart
Can detect the presence of vessel obstructions
and MIs in the inferior wall of the heart
Right Ventricular Hypertrophy
o Right Axis Deviation
o Due to the overpowering current generated by a hypertrophied right
ventricle
o V1/V2: Tall R
o This is because increased right ventricular muscle mass (higher
amplitude) causes the net ventricular depolarization current to move
towards this right chest lead
o V5/V6: Deep S
o Affecting the right ventricle (great pressure on RV because of abnormality on
pulmonary valve)
o Right atrial abnormality results from the right atrium having to pump blood
into a thick-wall non-compliant hypertrophied right ventricle.

Left Bundle Branch Block

o Left cant depolarize so right depolarizes
o Muscle to muscle
o QRS is longer and wider in V1/V2
o Rabbit ear pattern in V5/V6
o Left Axis Deviation

In BBB, irrespective of whether it is right or left,

activation of the ventricles becomes asynchronous:
Depolarization of the ventricle on the blocked side
is delayed. This delay causes the individual QRS
complex of the blocked ventricle to be wider than
normal and appear after the individual QRS
complex of the not-blocked ventricle. As a result,
the composite QRS complex is > 120 ms wide and has RSR waves: the R wave
belongs to the individual QRS of the not-blocked ventricle and the R wave to the
individual QRS of the blocked ventricle (rabbit ear pattern)

If the left bundle-branch is defective so that the electrical impulse cannot travel
through it to the left ventricle, activation reaches the left ventricle by proceeding
from the right ventricle.

Ischemic Myocardium in Right Ventricle as Hearts Pacemaker

Sequence of Heart Depolarization
Ischemia lack of oxygen
ST segment depression occurs because when the ventricle is at rest and repolarized
states, the depolarized, ischemic region generates electrical currents that are
recorded by an overlying electrode. If the depolarizing currents are traveling toward
the positive electrode, the baseline voltage prior to the QRS complex (which is
normally isoelectric - i.e., zero volts) will be elevated. In contrast, when the ventricle
becomes depolarized, all the muscle is depolarized so that zero voltage is recorded
by the electrode as usual. Therefore, the net effect of the elevated baseline voltage
is that the ST segment appears to be depressed relative to the baseline.

Lead II Tracing
o ST segment depression (myocardial ischemia)

Ionic Basis of Slow and Fast Response

Compared to a fast response, a slow response has the ff features

Slow
Phase 0 slope Less steep (opening of Ca channels)
Overshoot (amplitude) Lower
Phase 1 Absent
Phase 2 (plateau) Less sustained
Phase 3 Less steep
Negativity of Phase 4 Less
Phase 4 diastolic depolarization Present
Refractory period Longer
Blood Flow between Atrium and Ventricles
- Isovolumetric Contraction
o AV valves bulge into atrium
- Rapid Ejection
o AV valves are retracted into ventricular chamber
- Slow Ejection
o Blood flows into atrial chamber
- Isovolumetric Relaxation
o Blood continues to flow into atrial chamber
- Rapid Filling
o Blood flows from atrium to ventricles
- Slow Filling
o Blood slightly accumulates in atrium
o Inflow of blood from vena cava and pulmonary veins > outflow from
atrium to ventricle
- Atrial Systole
o Variable blood flow

Blood Flow between Ventricles and Great Vessels

- Isovolumetric Contraction
o Blood flows from aorta to peripheral
- Rapid Ejection
o Blood flow from ventricles to aorta > Blood flow from aorta to
peripheral
- Slow Ejection
o Blood flow from aorta to peripheral > Blood flow from ventricles to
aorta
- Isovolumetric Relaxation
o Elastic recoil of aorta propels blood to flow bidirectionally
o Increased volume due to temporary reversal of flow
o Leads to formation of dicrotic notch or incisure

Phase Aortic Blood Flow

Isovolumetric Contraction None
Rapid Ejection Rapid Increase
Reduced Ejection Declines
*Despite greater P, there is no
cessation of flow because of
inertia
Isovolumetric Relaxation Further decline to negative
*Due to elastic recoil of aorta,
theres bi-directional flow
Rapid Filling None
Reduced Filling None
Atrial Systole None
Heart Sounds
- First Heart Sound (S1) and Second Heart Sound (S2)
o S1: closure of AV valves (isovolumetric contraction)
Because of sudden tension in AV Valves leaflet
Vibrations in adjacent ventricular wall
o S2: closure of SL valves (isovolumetric relaxation)
Because of vibration in large blood vessels
Because of vibration from column of blood
o Between S1 and S2: systolic period
o Between S2 and S1: diastolic period

- Third Heart Sound (S3) and Fourth Heart Sound (S4)

o S3: rapid ventricular filling
Because of recoil of ventricular wall
Usually heard in children because walls are compliant
Pathologic condition may cause overfilling of ventricles
(congestive heart failure)
Ventricles operate in less compliant curve (S2)
o S4: atrial systole
Not heard in adults because additional ventricle filling is usually
negligible
Pathologic condition where additional ventricular filling becomes
significant
Ventricles operate in less compliant curve (S4)
o S3 and S4: diastolic period
o Sequence: S1-S2-S3-S4-S1
Heart Murmur
1. Simultaneous with carotid pulsation: S1 (isovolumetric contraction)
2. Between S1 and S2: Systolic
3. Between S2 and S1: Diastolic

Venous Pulse Tracing

A Wave: atrial systole
right atrial contraction

C Wave: Isovolumetric Contraction

bulging of tricuspid valve into atrium

V Wave: Isovolumetric Relaxation

increase in blood volume in atrium
while tricuspid valve is closed

Changes during Tricuspid stenosis

Obstruction to right ventricular flow
Elevated pressure (high A, low C)
Flatter descent after v

Changes during Tricuspid

regurgitation
Tricuspid valve does not close
properly, causing blood to flow
backward (leak) into the right atrium
when the right ventricle contracts
No depression after c wave, wave
becomes positive from negative
Single large positive v wave
Deep descent after v wave
Determinants of Stroke Volume and effects on Cardiac Output
Factors that influence CO
1. Stroke Volume
a. Force of Contraction
i. Preload
Increased preload Increased EDV Increased SV
Increased CO
ii. Contractility
Increased contractility Increased SV Increased CO
iii. Afterload
Increased afterload Decreased SV Decreased CO
2. Heart rate
Within 50-100
Increase in HR Increase in CO
Increase in HR > Decrease in SV

Within 100-200
Increase in HR Consistent CO
Increase in HR = Decrease in SV

Above 200
Increase in HR Decrease in CO
Increase in HR < Decrease in SV

Very low HRs

The increase in filling during diastole
cannot compensate for the small
number of cardiac contractions

Very high HRs

Large number of contractions cannot
compensate for inadequate filling
time

Frank Starlings Law of the Heart

1. Increased contractility
a. Increase in CO for any level of right atrial pressure or EDV
b. Curve shifted upward
c. Example: Increased sympa activity, cardiac glycosides
2. Decreased contractility
a. Decrease in CO for any level of right atrial pressure or EDV
b. Curve shifted downward
c. Example: Heart failure

Venous Return Curve

 a. CVP/RAP & CO
i. CVP is dependent; CO is independent
ii. CVP varies inversely with CO
iii. As CO increases, RAP falls because blood is sequestered in
atrial compartment
b. Venous return & RAP
i. Venous return is dependent; RAP is independent
ii. Venous return varies inversely with RAP
iii. As RAP decreases, venous return increases
iv. However, vascular function curve plateaus as RAP becomes
more negative because transmural pressure of large veins
becomes negative, collapses and no further increase in VR can
occur
c. Mean systemic filling pressure
i. Redistribute pressure evenly
d. Resistance to blood flow
i. If resistance increases, SV decreases, CO decreases
ii. If resistance decreases, SV increases, CO increases

Changes in TPR change both CO and VR curves

a. Increase TPR decrease in both CO and VR counterclockwise
rotation of VR curve
i. Decreased VR as blood is retained on atrial side
ii. Downward shift of CO curve increased aortic
pressure/afterload as heart pumps against a higher pressure
iii. New equilibrium point where both CO and VR are decreased,
but RAP is unchanged
b. Decrease TPR increase in both CO & VR clockwise rotation of VR
curve
iii. Increased VR as more blood is allowed to flow back to heart
from arterial side
iv. Upward shift of CO curve is caused by decreased aortic
pressure/afterload as heart pumps against a lower pressure
i. New equilibrium point where both CO and VR are increased, but
RAP is unchanged.

Combined CO and VR curves

As a function of RAP or EDV
Equilibrium (steady state point) is point where CO and VR intersect at a single
value of RAP
Only transient deviations are possible UNLESS either or both function curves
change in shape
o If RAP increases from 2-4mmHg
Ventricular filling will increase which increases CO from 5-7
o If driving pressure for VR decreases; this decreases VR
Imbalance is transient because increased CO will suck RA dry decreasing RAP.
Will also increase CVP because of pumping blood into veins
o Results in a gradual increase in VR, gradual decrease in CO, gradual
decrease in RAP until balanced