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
decreased duration of diastole
 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
 2. AV fistula
 1.1 Severe MI
 1.2 Severe valvular dse
 3. Hyperthyroidism
 1.3 Myocarditis
 4. Anemia  1.4 Cardiac tamponade
 5. Pulmonary  2. Decrease blood volume
disease  3. Acute venous dilatation
 6. Paget’s Disease  4. Obst. of large vein
 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)
 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
 Diffferencebetween 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
 BipolarLimb 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
 Similarto 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
Det ermi nati on of Ax is:

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
mass
 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
 Causeof 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
 Sinusarrhythmia – 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