REGULATION OF

CARDIAC FUNCTION
 A. INTRINSIC
REGULATION

• The amount of blood pumped by

the heart each minute (cardiac
output) is determined by the rate
of blood flow into the heart from
the veins (venous return)
 STARLING’S LAW OF THE
HEART
• “ The mechanical energy set free on
passage from the resting to the contracted
state is a function of the length of the
muscle fiber..”
• Increasing the resting muscle fiber length, as with
increasing end-diastolic volume, will result in an
increased force of contraction manifested as an
increased peak pressure and increased stroke
volume
• The reverse will be true if fiber length or end-
diastolic volume is decreased
• Also called Heterometric Autoregulation or
intrinsic regulation due to changing length of
cardiac muscle fiber
 CARDIAC OUTPUT
• Quantity of blood pumped by the heart into the aorta per minute.
• Quantity of blood that flows through the circulation per minute
• Average cardiac output in adults: 5 liters per minute (5.6
liters/minute in young adult male)
• Factors which affect cardiac output:
1. Level of activity of the body
2. Sex - C.O. in women is 10-20 % less than men
3. Age - C.O. decreases with increasing age due to a
progressive
decrease in activity
4. Body size - C.O. increases in approximate proportion to the
surface area of the body
Cardiac Index
- C.O. per square meter body surface area
- normal average: 3 liters/m2 BSA
 VENOUS RETURN
• Quantity of blood flowing from the veins into the right
atrium each minute.
• Sum of all local blood flows from the individual
segments of the peripheral circulation
• Primary controller of cardiac output
• Mechanism by which venous return controls
cardiac output:
1. Frank-Starling’s Law of the heart
- increased venous return will increase stretch of
cardiac
muscles thereby increasing force of contraction
2. Increase stretch of the sinus node in the wall of the
right
atrium which increases the heart rate by 10-15%
3. Bainbridge Reflex
- increase in heart rate induced by increased stretch
of
the right atrium
 B. AUTONOMIC NERVOUS
SYSTEM REGULATION
• 1.Sympathetic Stimulation
- discharge continuously at a slow rate under normal
conditions
- to maintain pumping at about 30% above that with
no sympathetic stimulation
EFFECTS: 1.1 Increase heart rate
1.2 Increase force of contraction
1.3 Increase cardiac output
• 2. Parasympathetic Stimulation
- direct effect on strength of ventricular contraction
is not great
- can decrease cardiac output by 50% or more due
to its combined
effect on HR and force of contraction
EFFECTS: 2.1 Decrease heart rate
2.2 Decrease force of contraction
(~20-30 %)
2.3 Decrease cardiac output
 C. EFFECT OF HEART RATE
• In general, the more times the heart
beats per minute, the more blood it
can pump,
up to a certain limit.
• As heart rate increases above a
critical level, the heart strength
decreases due to:
1. Overuse and depletion of
metabolic
substrate
2. Decreased ventricular filling due
to
 D. EFFECT OF POTASSIUM AND
CALCIUM IONS
• 1. EFFECT OF POTASSIUM IONS
- increase ECF [K+] decreases the resting membrane potential
decrease the intensity of action potential weaker
contraction
Effects of increased ECF [K+]:
1. Dilatation and flaccidity of the heart
2. Decrease heart rate
3. Blocks conduction of impulses through the AVN
• 2. EFFECT OF CALCIUM IONS
- excess Ca2+ causes effects that are almost exactly opposite
those
of increased K+ it cause the heart to go into spastic
contraction
due to the direct effect of of Ca2+ in exciting the cardiac
contractile process.
- deficiency of Ca2+ causes effects similar to those of increased
K+
cardiac flaccidity or weakness
E. EFFECT OF TEMPERATURE
• Increased temperature will increase heart
rate presumably due to increased
permeability of muscle membrane to ions
• Increase in heart rate will be about 10 beats
per minute for each degree Fahrenheit
increase in temperature or 18 beats per
minute per degree Celcius rise in
temperature
• Contractile strength of the heart is often
enhanced by a moderate increase in
temperature but prolonged increase in
temperature can exhaust the metabolic
system and cause weakness of the heart
 Factors that can cause
hypereffectivity
• 1. Nervous stimulation
- combination of sympathetic stimulation
and parasympathetic
inhibition will increase pumping
effectiveness of the heart via 2
mechanisms:
a. Increased heart rate
b. Increased strength of contraction
• 2. Hypertrophy of heart muscle
- increase in mass and contractile
strength due to increased workload
- can increase the plateau level of the
C.O. curve up to 50-100%
 Factors that can cause
hypoeffectivity
• 1. Inhibition of nervous excitation
• 2. Abnormal rhythm or rate
• 3. Valvular heart disease
• 4. Hypertension
• 5. Congenital heart disease
• 6. Myocarditis
• 7. Cardiac anoxia
• 8. Myocardial damage or toxicity
 Effect of changes in arterial
pressure load on cardiac
output
• Within reasonable limits, changes in
the arterial pressure against which the
heart pump have almost no effect on
cardiac output
• A consequence of Frank-Starling’s
mechanism
• Significance: regardless of the arterial
pressure load up to a certain limit, the
important factor that determines the
cardiac output is still the venous
return
Effect of arterial pressure load
on cardiac output
Cardiac Output (L / min)

5
4
3
2

50 100 150 200 250

Arterial Pressure (mmHg)
 Effect of total peripheral
resistance on long-term cardiac
output level

• When the arterial pressure is

controlled normally, the long-term
cardiac output level varies inversely
with the change in total peripheral
resistance:
• Total peripheral resistance
C.O.
• Total peripheral resistance
C.O.
Effect of total peripheral resistance on
long-term cardiac output level

200
Cardiac Output (% of Normal)

150

Normal
High CO
State

100 %

Low CO State

50

50 100 % 150
Total Peripheral resistance (% of Normal)
Pathological Cardiac Output
States
High C.O. States Low C.O. States
• 1. Beri-beri • 1. Severe heart disease
• 1.1 Severe MI
• 2. AV fistula
• 1.2 Severe valvular dse
• 3. • 1.3 Myocarditis
Hyperthyroidism • 1.4 Cardiac tamponade
• 4. Anemia • 2. Decrease blood volume
• 5. Pulmonary • 3. Acute venous dilatation
disease • 4. Obst. of large vein
• 6. Paget’s Disease
• Pathological high cardiac output
states are almost always caused by
a chronic decrease in total
peripheral resistance
• Pathological low cardiac output
states fall into 2 categories:
• 1. those that decrease the pumping
effectiveness of the heart
(cardiac factors)
• 2. those that decrease venous
return
(peripheral factors)
 VENOUS RETURN CURVE
• Relates venous return to right atrial
pressure
• Normal venous return (VR): 5 L / minute
• 3 Factors that affect venous return to the
heart:
1. Right Atrial Pressure ( PRA )
- normal: 0 mmHg
2. Mean Systemic Filling Pressure ( PSF )
- normal: 7 mmHg
3. Resistance to venous return ( RVR)
- normal: 1.4 mmHg / L of blood flow
 Venous Return

PSF - PRA
VR =
RVR
 1. Effect of Right Atrial
Pressure on Venous Return
VenousReturn (L / min)

0
-8 -4 0 +4 +8
Right Atrial Pressure (mmHg)
2. Effect of Mean Circulatory
Filling Pressure on Venous
Return
Venous Return

PSF = 3.5 PSF = 7 PSF =14

0 Right Atrial Pressure

Effect of Resistance to Venous
Return on Venous Return

1/2 resistance
Venous Return

Normal resistance

2x resistance

Right Atrial Pressure

Effect of Right Atrial Pressure
on Venous Return
• Increased right atrial pressure will exert a
backward force on the veins thereby
impeding the flow of blood into the right
atrium and decreasing venous return.
• When right atrial pressure falls below zero,
further increase in venous return ceases
rapidly producing a plateau in the venous
return curve.
- explained by the collapse of veins
entering
the chest due to the sucking effect of
negative
PRA on the walls of the veins.
 Effect of Mean Circulatory or Systemic
Filling pressure on Venous Return
• Equilibrated pressure everywhere in the circulation when blood
flow is stopped.
• Factors which affect Mean Systemic FillingPressure:
1. Blood Volume
- the greater the blood volume, the greater the distending
pressure
or stress on the walls of the vasculature, the greater the PSF
2. Sympathetic Stimulation
- causes vasoconstriction which decreases the capacity of the
vasculature thereby increasing wall stress and increasing PSF
• The greater the PSF, the greater the “tightness” with which the
circulatory system is filled with blood, the easier it is for blood to
flow into the heart
Effect of Resistance to Venous
Return on Venous Return
• 2/3 of the resistance to venous
return occurs in the veins and 1/3 in
the arterioles and small arteries
• Increased resistance to venous
return will decrease venous return
because the high distensibility of the
veins will prevent it from generating
enough pressure to overcome the
resistance
Pressure Gradient for Venous
Return
• Diffference between mean systemic filling
pressure and right atrial pressure: (PSF -
PRA)
• The greater the difference, the greater the
venous return
• When gradient is zero, venous return is zero
• When PRA increases, gradient will decrease
and venous return will also decrease
• When PRA decreases, gradient will increase
and venous return will also increase
 NORMAL
ELECTROCARDIOGRAM
 THE ELECTROCARDIOGRAM
• Records the electrical impulses of the
heart through electrodes place on
the skin
• The normal ECG is composed of
three waves:
– P wave – atrial depolarization
– QRS complex – ventricular
depolarization
– T wave – ventricular repolarization
DEPOLARIZATION AND
REPOLARIZATION
• During depolarization the
normal negative
potential inside the cell
reverses and it becomes
positive
• The part that is
depolarized becomes
negative with respect to
the part not yet
depolarized
• Once the whole fiber has
been depolarized the
recording returns to
baseline
• During repolarization,
positivity returns to the
outside of the cell
THE MONOPHASIC ACTION POTENTIAL IN
RELATION TO QRS AND T WAVES
• The upsweep of the
action potential is the
depolarization and is
reflected as the QRS
complex in the ECG
• The downsweep of the
action potential is
repolarization and is
reflected as the T
wave in the ECG
• No potential is
recorded in the ECG
when the tissue is
either completely
depolarized or
repolarized
HOW THE ECG WORKS
ELECTROCARDIOGRAPHIC
LEADS
 ECG Electrodes &
Color Coding
Tip Color Symbol Electrode Position

Red RA Right arm

Yellow LA Left Arm
Green LF Left Foot
Black RF Rightfoot
White/Red C1 V1
White/Yellow C2 V2
White/Green C3 V3
White/Brown C4 V4
White/Black C5 V5
White/Violet C6 V6
 LEAD SYSTEMS
• Bipolar Limb Leads – the
electrocardiogram is recorded from
two electrodes on the body
– Lead I – (-) = (R) Arm, (+) = (L) arm
– Lead II – (-) = (R) Arm, (+) = (L) leg
– Lead III – (-) = (L) Arm, (+) = (L) leg
• Einthoven’s Law – The electrical
potential of a limb lead is the
summation of the electrical potential
of the two other leads
LEAD SYSTEMS
• Chest leads – electrodes
are placed in the
anterior chest at one of
six points.
• Each chest lead records
electrical potential of
the cardiac musculature
immediately beneath it.
It can detect minute
abnormalities especially
in the ventricles.
 LEAD SYSTEMS

• Augmented Limb leads – two of the

terminals are connected together
to the negative terminal and the
third is connected to the positive
terminal.
– AVR – R arm is positive
– AVL – L arm is positive
– AVF – L foot is positive
• Similar to standard lead but AVR is
inverted
 Guide in Reading ECG
• Rhythm
• Rate: atrial & ventricular
• P wave morphology & duration
• P-R interval
• QRS complex morphology & duration
• ST segment
• T-wave
• U wave
• Q-T interval
• Standardization & technique
ECG Graph paper
Intervals
Normal duration of conduction
Normal Range of intervals (sec.)
P-R QRS Rate Q-T ST
Adult 0.18-0.20 0.07-0.10 60 0.33-0.43 0.14-0.16

Children 0.15-0.18 70 0.31-0.41 0.13-0.15

80 0.29-0.38 0.12-0.14

90 0.28-0.36 0.11-0.13

100 0.27-0.35 0.10-0.11

120 0.25-0.32 0.06-0.07

Det erminatio n of Heart
Rate

Heart rate assessment by “rule of 300”

 Measurement of Rate
• Formula 1:____________300__________
# big squares between R-R

• Formula 2: ___________1500__________
# small squares between R-R
Determ inat ion of Axi s:

Hexaxial System
QRS axis
 ABNORMAL ECG
• Abnormal rhythm
• Abnormal morphology
– Axis deviation
– Chamber hypertrophy
– Ischemia and infarction
– Effect of drugs and electrolyte
abnormalities
– Myocarditis, pericarditis
ABNORMAL VENTRICULAR CONDITIONS
CAUSING AXIS DEVIATION
• Change in the position of the heart
– Can be due to respiration, body habitus,
pregnancy, etc.
• Hypertrophy of one ventricle
– The axis of the heart shifts towards the
hypertrophied ventricle
• Bundle branch blocks
– Delay in depolarization on one ventricle
prevents the potentials of the two ventricles
from neutralizing each other
INCREASED VOLTAGES IN THE ECG
• Voltage in the limb
lead normally
varies from 0.5 to 2
mv.
• Most common
cause of increased
voltage is
ventricular
hypertrophy due to
increased quantity
of electricity
generated by
increased muscle
 DECREASED VOLTAGES IN THE ECG

• Myopathies – caused by decreased

muscle mass (i.e AMI)
• Pericardial effusion – presence of
fluid ‘shorts out’ the currents
generated by the heart.
• Pulmonary emphysema – excessive
air in the lung serves as ‘insulator’
and diminishes current reaching the
surface.
PROLONGED QRS COMPLEX
• Cardiac hypertrophy or dilatation –
the increased distance that the
current needs to travel to depolarize
the ventricle causes prolonged QRS
complex (0.09 – 0.12 s)
• Purkinje system blocks
• Scar tissue or local blocks in purkinje
system causing bizarre QRS complex
 CURRENT OF INJURY
• Damage to the cardiac muscle cause
part of the heart to become partially
or fully depolarized all the time.
• This can be caused by mechanical
trauma, infectious process or
ischemia.
• Current flows from the injured part of
the heart (-) to the normal non-
depolarized tissues. (+)
 Effect of the Current of Injury
to the QRS complex
• The injured part of the heart is
negative and emits electrons
• The current of injury causes
displacement of the TP segment in
relation to the baseline
 T WAVE ABNORMALITY
• Repolarization normally proceeds
from the endocardium to the walls of
the ventricle producing upright t-
wave
• T-wave become abnormal when this
normal sequence of repolarization
does not occur
• Prolonged depolarization caused by
ischemia, conduction blocks or
premature contraction will produce
abnormal t-waves
 ARHYTHMIAS
• Cause of arrhythmia is usually one or
a combination of the following
– Abnormal rhythmicity of the pacemaker
– Shift of the pacemaker to other part of
the heart
– Blocks in the transmission of impulses
– Abnormal pathways of impulse
transmission
– Spontaneous generation of abnormal
impulses in any part of the heart
 ABNORMAL SINUS RHYTHM
• Sinus tachycardia
– Sinus rate greater than 100 beats/min
– Usually caused by increased body
temperature, sympathetic stimulation and
toxic conditions of the heart
• Sinus bradycardia –
– Rate less than 60 beats/min
– Common in athletes, also caused by vagal
stimulation
• Sinus arrhythmia – irregular rhythm from
the sinus node
 ATRIOVENTRICULAR BLOCKS
• Decrease or block in transmission of
impulse through the AV bundle
– Ischemia of the A-V nodal or A-V bundle
fibers
– Compression of the A-V bundle by scar
tissue
– Inflammation of the A-V node in
myocarditis
– Extreme stimulation of the heart by the
vagus nerve
COMPLETE HEART BLOCK
 PREMATURE CONTRACTIONS
• Also called extrasystole, premature
beat or ectopic beat
• Most come from ectopic foci in the
heart
• Causes include local areas of
ischemia, small calcified portions of
the heart irritating some of the
cardiac fibers or toxic irritation of the
AV node
• May occur in healthy people
 PAROXYSMAL TACHYCARDIA
• Rapid rhythmical discharge of impulses
spreading in all directions throughout the
heart.
• Usually caused by reentrant pathways that
set up a repeated self re-excitation
• Paroxysmal meaning the heart rate
becomes rapid suddenly lasting for a few
seconds, minutes or longer and normalize
just as suddenly
• Can often be stopped by eliciting a vagal
reflex
 VENTRICULAR FIBRILLATION
• Disordered activation within the ventricle
resulting in uncoordinated conractions of
different portions of the ventricular
musculature. The result is that the
ventricle neither enlarges or contracts and
pumps negligible amount of blood to the
circulation
• This condition results in unconsciousness
within 4-5 seconds and is invariably fatal if
not corrected