SAN BEDA COLLEGE OF MEDICINE

CARDIAC PHYSIOLOGY HANDOUT PART 1 BY EDME MARTINEZ, MD

CARDIAC PHYSIOLOGY
By Edme Martinez, MD
EDUCATIONAL OBJECTIVES
1. De#ine cardiac cycle.
2. Name the phases of the cardiac cycle.
3. Describe the events that take place during each phase.
4. Name and describe the four heart sounds.
5. Discuss the pressure changes in the atria, ventricles, and aorta during the different phases of the cardiac cycle.
6. Discuss the volume changes in the ventricle during the different phases of the cardiac cycle.
7. Draw and explain the Wiggers Diagram.

THE CARDIAC CYCLE

CARDIAC CYCLE
PHASES:
1. Period of Atrial Systole/Pre-systole
2. Isovolumic contraction period
3. Rapid/Maximum Ejection
4. Reduced Ejection
5. Protodiastole
6. Isovolumic Relaxation
7. Rapid Filling
8. Reduced #illing/Diastasis

TIMING
Events on the 2 sides of the heart are similar
but somewhat asynchronous.
Right atrial systole precedes left atrial systole
Contraction of right ventricle starts after that of left ventricle
Right ventricle ejection begins before the left. Because pulmonary pressure is lower than aortic pressure.
During inspiration, aortic valve closes slightly before the pulmonary valve. Due to the lower impedance and distensibility
of the pulmonary vascular bed

These concurrent electrical and mechanical events occurring during the cardiac cycle are plotted and shown in a diagram, the
WIGGERS DIAGRAM.

ATRIAL PRESSURE PULSE

Normally between 0-4 mmHg
PEAKS
A Wave - A TRIAL CONTRACTION
C Wave - C ONRACTION OF VENTRICLES OVERBULGING OF AV VALVES
V Wave V ENOUS BLOOD GOING TO THE ATRIUM
AORTIC PRESSURE PULSE
We plot this curve at 80 mm Hg level because aortic pressure is always high.
Remember that:
1. Blood Vessels are always in a condition or state of being slightly #illed with blood
2. Aorta made up of elastic tissues therefore can be stretched within limits
3. If remove stretch --- recoils

The rise and fall of Aortic Pressure Pulse re#lects the balance between:
2. The volume of blood entering the aorta from the heart
3. The volume of blood leaving the aorta and draining into the periphery, called PERIPHERAL RUN-OFF

When ejection exceeds run-off

Aortic Pressure increases
When run-off exceeds ejection
Aortic Pressure goes down or decreases

Atrial Contraction
} Occurs during the distal third of diastole
} Preceded by p-wave in the ECG
} Slight increase in atrial pressure, ventricular pressure and ventricular volume
} NOT essential for ventricular #illing
Isovolumic Contraction
} Preceded by QRS complex in the ECG
} First Heart Sound (S1) is heard
} Increase in ventricular pressure BUT ventricular volume remains the same

Ventricular Pressure < Aortic Pressure

All Heart Valves are closed

Rapid Ventricular Ejection
} Ventricular Pressure > Aortic Pressure

Semilunar valves open

} Rapid Increase in Ventricular Pressure, Decrease in Ventricular Volume
Reduced Ventricular Ejection
} T-wave occurs in the ECG
} Decrease in ventricular pressure, decrease in ventricular volume
Isovolumic Relaxation
} Ventricular Pressure < Aortic Pressure

Semilunar valves are closed

} Ventricular Pressure > Atrial Pressure

AV valves are still closed

} Decrease in ventricular pressure BUT ventricular volume remains the same
} Second Heart Sound Heard (S2)
Rapid Ventricular Filling
} Ventricular Pressure < Atrial Pressure

Opening of the AV valves

} Rapid increase in ventricular volume
} First 1/3 of diastole
Reduced Ventricular Filling
} Reduced increase in ventricular volume
} Middle 1/3 of diastole

HEART SOUNDS
are vibrations caused by turbulent #low of blood and contraction of ventricular muscle, which are transmitted through the
supporting tissues and to the chest wall
FIRST HEART SOUND (S1) LUB
associated with the closure of the AV valves at the onset of systole and isovolumetric ventricular contraction
Soft closure
slightly prolonged, soft, low-pitched
duration of 0.15 seconds
splitting when mitral valve closes before tricuspid valve
heard best at mitral and tricuspid area
SECOND HEART SOUND (S2)DUP
occurs at the end of systole as the pulmonary and aortic valves closed
Snapping closure
shorter, louder, high-pitched
duration of 0.12 secs
inspiration causes splitting of 2nd HS because aortic valve closes slightly before pulmonary valve
heard best at pulmonic and aortic area
THIRD HEART SOUND (S3)
associated with the rapid in rush of blood during rapid ventricular #illing
soft, low-pitched, duration of 0.1 sec
recordable in from 26 to 85% of normal person
maybe present 0.04 to 0.12 seconds after the onset of the second sound
is most common in the presence of mitral stenosis
normal in children
FOURTH HEART SOUND (S4)
associated with the atrial systole / contraction of the atrium #illing of ventricle
recorded in 25% of normal person
sometimes heard immediately before 1st heart sound
not audible in normal adults
audible in persons with left ventricular hypertrophy associated with hypertension
present also when atrial pressure is high
MURMURS
are abnormal heart sounds which can be produced by:
2. blood #lowing rapidly in the usual direction through an abnormally narrowed valve (STENOSIS)
3. blood #lowing backward through a damaged, leaky valve (INSUFFICIENCY)
4. blood #lowing between the 2 atria or 2 ventricles through a small hole in the wall separating them.

The exact timing and location of murmur important in diagnosis:

A murmur heard throughout systole

suggest stenotic sl valve or insuf#icient AV valve

A murmur heard during diastole

suggests stenotic AV valve or an insuf#icient sl valve

Occasionally, a 3rd heart sound is heard which give rise to a triple beat that resembles the hoof beats of a galloping horse, called
GALLOP RHYTHM. Most frequently associated with congestive heart failure.
CARDIODYNAMICS

CARDIODYNAMICS
The function of the ventricles is described
by three parameters
1. Stroke volume
2. Ejection Fraction
3. Cardiac output
STROKE VOLUME
The volume of blood ejected on one ventricular contraction or the volume ejected on one beat (ml/beat)
The difference between the volume of blood in the ventricle before each ejection and the volume remaining in the ventricle after
each ejection
SV = EDV ESV

EJECTION FRACTION
The fraction (percent) of the EDV that is ejected in each stroke volume
The ratio of SV to EDV and normally 60% to 65%
Expressed by the ff equation:
EF = SV

EDV

A valuable index of ventricular function (contractility)

When strength of contraction increases without an increase in #iber length, more blood in the ventricle is expelled, thus, EF
increases and ESV decreases
Increases in EF re#lects an increase in contractility
Decreases in EF re#lects a decrease in contractility

Cardiac Output
The total volume of blood ejected per minute
CO (ml/min) = SV (ml/beat) x HR (beats/min)
Direct proportionality true within limits
If HR remains constant, CO increases in proportion to SV. Thus factors that increases SV can increase CO
If SV remains constant, CO increase in proportion to HR up to about 180 beats/min
HR and SV do not always change in the same direction
Ex. Following blood loss, SV decreases while HR increases to raise ABP
Average CO = 5L/min
Normal Blood Volume = 5 liters
This means that essentially all blood is pumped around the circuit each minute
Determinants of cardiac output

Factors that affect cardiac output

Heart Rate (100 beats/min) 70 beats/min
respiration
- body temp.

- electrolyte concentration
- exercise
- emotions
EFFECT OF RESPIRATION ON HEART RATE
Inspiration heart rate
Expiration heart rate
Bainbridge Re_lex
Inspiration ITP venous return (right atrium) atrial volume (+) atrial stretch receptors heart rate

Factors Affecting SV
1. PRELOAD

The load that stretches the cardiac muscle before contraction

The degree of tension on the muscle when it begins to contract.

Considered to be the end diastolic pressure, when the ventricle has been #illed

2. AFTERLOAD

Degree of vascular resistance to ventricular contraction

The load against which the muscle exerts its contractile force

Importance of the concepts of Preload and afterload is that in many abnormal functional states of the CVS, the pressure during
ventricular #illing and the arterial pressure against which the ventricle must contract are severely altered from normal

3. Inotropic State Myocardial Contractility

FACTORS THAT INCREASE CONTRACTILITY (POSITIVE INOTROPISM)
1. Increased heart rate
more APs per unit time
more Ca++ enters myocardial cell during plateau of AP
more Ca++ released from SR
greater tension produced during contraction
Control of Stroke Volume
A) HETEROMETRIC
regulation of SV as a result of changes in cardiac muscle #iber length
(Frank Starlings Principle)
B) HOMEOMETRIC
not dependent on muscle length
HOMEOMETRIC REGULATION
A) Nervous Control (autonomic nervous system)
sympathetic distensibility and force of
ventricular contraction

 ventricular contraction
parasympathetic atrial force of
contraction
B) Hormonal Control

catecholamines distensibility and force of

ventricular contraction
( cAMP on B1 adrenergic

receptors)
acetylcholine atrial force of contraction
(acting on muscarinic receptors )
thyroxine
glucagon increases cAMP
3) other factors

respiration
agents
caffeine
theophylline ( cAMP)
digitalis
temperature
If the heart is to be an effective pump, it must have an adequate EDV.
Factors that determine an adequate EDV:
1. Filling time of Ventricle

dependent on cardiac rate

2. Distensibility of Ventricle (Vent Compliance)

Increase in ventricular stiffness produced by M.I.

in heart failure, there must be a greater stretch of myocardium to achieve the needed CO

attained by administration of + inotropes

3. Stronger Atrial Contraction

a minor factor

not very essential for ventricular #illing WHY:

adequate #illing is often observed in patients with atrial #ibrillation, despite absence of atrial contraction

severe Tachycardia period of ventricular systole becomes markedly shortened ventricular #illing is seriously impaired despite the
contribution of atrial contraction
}

However, contribution of Atrial Contraction is governed by:

Heart rate

Moderate Tachy diastasis shortened therefore atrial contraction becomes substantial

Stenotic AV Valve

Atrial contraction is important in ventricular #illing

4. INTRAPERICARDIAL PRESSURE
} when increased, limits the extent in which the ventricle can #ill decreased EDV decreased CO

ex. Pericardial effusion heart muscle

} cannot stretch enough
5. Adequate Venous Return VR

#low of blood from periphery back to right atrium

main determinant of cardiac output

The degree of myocardial stretch created by venous return is called the PRE-LOAD on the heart
Factors that in_luences VR:
1. Total Blood Volume
2. Increased Venous Tone (constriction of veins)(Sympathetic Tone)

venoconstriction

reduces the size of venous reservoir

decreases venous pooling

increases VR
3. Posture

gravitational force causes pooling of blood in the legs (venous pooling)

standing decreases VR

decrease CO because of pooling of blood in lower limbs

4. Skeletal Muscle Pump
5. Respiratory / Thoraco Abdominal Pump Practical Application : Cardiac patients refrain from Valsalvas maneuver

END SYSTOLIC VOLUME

determined primarily by the balance between the
force of contraction of the ventricle and aortic
pressure.
a) force of myocardial contraction

b) aortic pressure load ( afterload )

ESV Determined by:

1. AFTER LOAD

In the left ventricle, afterload is equal to all the forces the muscle must overcome to eject at given volume of blood

Dependent upon:

Aortic pressure the major contributor to afterload in the heart

State of sl valves
2. CONTRACTILITY

Increased myocardial contraction decreased ESV

Severely dilated heart (heart failure) ESV can become much greater than SV
ESV

Decreased by increases in myocardial contractility and heart rate

Increased whenever heart is weakened (heart failure)
Increased with increased out#low resistance (aortic valve stenosis, increased aortic pressure)
Examination of ESV is clinically useful as an indicator of conditions affecting the heart

Cardiac Output Varies According to:

1. Level of activity of the body
Strenuous exercise: CO = 35 L/min

Entire blood volume pumped around the circuit seven times per minute
CARDIAC RESERVE the difference
etween CO at rest and the maximum volume of blood the heart is capable of pumping per
b
minute

The maximum amount of blood that can be pumped out by the heart above normal value

Essential to withstand the stress of exercise

Expressed in percentage
Normal Young Adult = 300 - 400%
Old Age
= 200 250%

Athletes
Cardiac diseases

= 500 600%
= minimum or nil

2. Size of Body (Surface Area)

CO increases in proportion to the surface area of the body, stated in terms of CARDIAC INDEX

The amount of blood pumped out of the ventricle per minute per square meter of body surface area

CI = CO divided by body surface

area

Normal adults = 3 L/min/ sq.m.

10 yrs age = 4 L/min/ sq.m.
80 yrs age = 2.4 L/min/ sq.m.
STROKE WORK
Work the heart performs on each beat
} Is equal force (aortic pressure) x Distance (SV)
SW = AP x SV

SW = AP x SV
}

Cardiac work = ABP x SV

Stroke Work amount of work done by right heart < left heart
The ff will increase the work of the heart

increase CO & aortic pressure

DISTRIBUTION of CO by LEFT VENTRICLE

Liver
1,500ml
0%
3
Kidneys
Skeletal M

Brain
Skin
Bone
GIT
Heart
Total:

,300
1
900
800
300
300
300
200
5,000ml

6
2
18
16
06
6
0
06
04
100%

DISTRIBUTION of CO by RIGHT VENTRICLE

Lungs
5,000ml
100%

Variations in CO
Physiological Variations
} Sleep- no change
} Age
} Sex
} Body build
} Diurnal condition low early morning
} Environmental conditions - Temperature above 37 degrees centigrade raises CO
} Emotional conditions anxiety, excitement increases CO to 50%
} After meals increased during #irst hour after meal to 30 %
} Exercise increases up to 700%
} Pregnancy increased by 45 to 60 % during later pregnancy
} Posture recumbent to upright, decreases CO because of pooling of blood in the lower limb
PATHOLOGICAL VARIATIONS
} CO increased in

Fever due to oxidative process

Anemia due to hypoxia

Hyperthyroidism increased basal metab

} CO decreased in

Hypothyroidism

Atrial #ibrillation

Congestive heart failure

Heart block

Hemorrhage

Valvular lesions (insuf#iciency)

Measurement of Cardiac Output
Direct Method

Use of cardiometer

Use of #lowmeter

Mechanical #lowmeter

Electromagnetic #lowmeter

Ultrasonic doppler #lowmeter

Indirect Method
} Using FICKs principle
} CO = 0 consumed (in ml/min)

Arteriovenous 0 difference
SOURCES:
1. Guyton & Hall Textbook of Medical Physiology 12th Edition by Hall, John &, Guyton, Arthur C. , , Published in Philadelphia,
Pensylvania: Saunders/Elsevier, 2011
2. Berne & Levy Physiology 6th Edition bby Berne, Robert M., 1918-2001., Koeppen, Bruce M., Published: Philadelphia :
Mosby/Elsevier, 2008
3. Ganong Review of Medical Physiology, 23rd Edition, by Barrett, Kim , Barrett, Kim E., Barman, Susan, Boitano, Scott, Brooks,
Heddwen, Published: New York : McGraw-Hill Medical, 2010
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CARDIAC PHYSIOLOGY HANDOUT BY EDME MARTINEZ, MD