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Cardiovascular Physiology
I: Physiology of the Heart &
The Cardiac Cycle
References:
Seeley, R., Stephens, T., and Tate, P.,
Anatomy & Physiology. 8th ed. McGraw
Hill Company Inc., (2008)
 Guyton, A., Hall, J., Textbook of Medical
Physiology. 11th ed. WB Saunders Co.
(2006)
• Martini, F., Fundamentals of
Anatomy & Physiology. 6th ed.
Benjamin Cummings Inc (2003)

Part I
FUNCTIONS OF THE
CARDIOVASCULAR SYSTEM
Function of the CV System:
Blood
 Transport
 Protection
 Regulation
Function of the CV System:
Heart

Generating BP

Blood routing

Ensuring one-way blood flow

Regulating blood supply
Function of the CV System:
Blood Vessels
Carry blood
 Gas & nutrient
exchange
 Transport
 BP regulation
 Direct blood flow

Part II
THE CARDIAC CYCLE
Cardiac cycle
 Events
occurring from the
beginning of one heartbeat to the
beginning of the next
 Consists
of 2 periods as to the
activity of the ventricles
Cardiac Cycle
Systole – period of contraction
 Isovolumetric contraction
 Ejection
 Diastole – period of relaxation
 Isovolumetric Relaxation
 Passive Ventricular filling
 Atrial Contraction

Isovolumetric Contraction

Ventricular contraction
causing abrupt ↑ Po

AV valves close

Continuous contraction
to overcome aortic &
pulmonary arterial Po
and open SL valves
Ejection
(L) ventricular Po
reaches 80 mmHg & ®
ventricular Po reached
8 mmHg
• SL valves open, then close
•70% ejected in the 1st 1/3 of the
period: rapid ejection
• 30% ejected in the next 2/3 of the
period: slow ejection

Isovolumetric Relaxation
Ventricular relaxation
causes rapid ↓ of
intraventricular Po
 SL valves close d/t Po
increase in the large
arteries
 Further ↓ in
intraventricular Po would
cause opening of AV
valve.

Passive Filling
~75% of the blood
from the great veins
 AV valves are open
and semilunar valves
closed
 ↑ intraventricular Po relative to the
atrium would slow down filling:
Diastasis

Atrial Contraction

Contraction of atria will eject the
remaining 25% into the ventricles
Ventricular Volumes Relative to
Systolic and Diastolic contractions
Volume of Blood in the
Ventricle
END-DIASTOLIC
VOLUME
STROKE VOLUME
OUTPUT
END SYSTOLIC
VOLUME
EJECTION FRACTION
(110-120mL)
(-70mL)
What remains after
systole (40-50mL)
Usually 60%
Pressure-Volume
Relationships during the
cardiac cycle
Summary of Pressure
Volume Relationships

CARDIAC CYCLE TABLE SUMMARY.pdf
Heart Valves

Atrioventricular valves


Prevent back flow of blood between
ventricles and atria
Semilunar valves

Prevent back flow of blood between
aorta (and pulmonary artery) and
ventricles
Heart Valves

Papillary mm
 Pull on the cusps of
the AV valves
during systole
 Do not help valve
closure
 Prevent bulging into
the atria
Heart Valves and Heart
Sounds

1st heart sound:
Lub
 closure of the
AV valves
 Heard during
systole
 Relatively low
in pitch and
long

2nd heart sound:
Dup
 Closure of the
SL valves
 Heard during
diastole
 Rapid snap
 Shorter
Heart Valves and Heart
Sounds

3rd heart sound
 Mid-diastole
 Blood
oscillation as it
rushes from
the aorta
 Weak rumbling
sound

4th heart sound
 Atrial
contraction
 Inrush of blood
into the
ventricles
 Low frequency
sound
Heart Valves and Abnormal
Heart Sounds

Murmurs: Abnormal Heart Sounds
 Valvular Stenosis: Opening is too
small
 Valvular Regurgitation: Valve does
not close completely
Heart Valves and Abnormal
Heart Sounds
SL Valve
AV Valve
Regurgitation
Diastole
High pitch,
swishing
Systole
High pitch,
swishing
Stenosis
Systole
Loud and
harsh
Diastole
Weak and
low
frequency
Part III
CARDIAC
ELECTROPHYSIOLOGY
Let’s review!
Cardiac Muscle Action
Potential
Cardiac Muscle Action
Potential
 RMP
of cardiac muscle: -90 mV
 Overshoots until ~+20 mV
Phase 0: Rapid
Depolarization
opening of fast
acting Na
channels and
slow acting Ca
channels
 Fast Na channels
immediately close

Phase 1: Partial
Repolarization
Closed Na
channels
 Partially
repolarized d/t
efflux of K

Phase 2: Plateau
Full opening of
Ca channels
counteracting K
efflux
 Ca influx is
involved in
excitationcontraction

Phase 3: Rapid
Repolarization
Gradual  in K
efflux
 Ca channels close


Phase 4: Return to
Resting
Membrane
Potential
Cardiac Muscle ExcitationContraction Coupling

Phase 2
 Action potential spreads to interior
via T-tubules
 Excitation of T-tubules promote Ca
release from sarcoplasmic reticulum
adding to Ca influx
 Actin-Myosin binding
Cardiac Muscle Excitation –
Contraction Coupling

Phase 3
 Ca influx is cut
 Ca ions are pumped back into the
sarcoplasmic reticulum
 relaxation
Part IV
CONDUCTING SYSTEM OF
THE HEART
Conducting System of the
Heart

Sinoatrial Node
 Superior posterolateral wall of ®
atrium, below and lateral to SVC
opening
 Non-contractile
 Self excitatory
Conducting System of the
Heart

Sinoatrial node
 RMP of -55 to -60 mV
 Firing level of -40 mV
 Depolarization only by opening of
slow Na-Ca channels
Conducting System of the
Heart
Conducting System of the
Heart
Internodal pathways
 Anterior Tract of Bachman
 Middle Tract of Wenckebach
 Posterior Tract of Thorel
 Impulses converge on the
Atrioventricular node

Conducting System of the
Heart

Atrioventricular Node
 Posterior wall of ®
atrium, adjacent to
coronary sinus
 Delay of impulse
conduction allows
full contraction of
atrium
Conducting System of the
Heart

Bundle of His
 Located on either
side of
interventricular
septum
 Conducts
impulses from
atria to ventricles
Conducting System of the
Heart

Purkinje Fibers
 Conducting tissues of the ventricles
Conducting System of the
Heart


Why is the SA node the pacemaker of the
heart?
Frequency of impulse production is faster
Structure
Impulses/min
SA
70-80
AV
40-60
Purkinje Fibers
15-40
Greater rhythmicity depresses other potential
pacemakers
The Electrocardiogram

a graphic representation of the
electrical activity generated by the
atria and ventricles.
The Electrocardiogram
Strip
Small block =
1mm
TIME (x-axis)
Small block =
0.04 second
Bold block =
0.20 second
The Electrocardiogram
Strip

AMPLITUDE (yaxis)
Small block = 0.1
mV

Rate:
22mm/second
The Electrocardiogram:
Einthoven’s Triangle
The Electrocardiogram:
Precordial Leads
The Electrocardiogram
When a positive wave of
depolarization within the heart
cells moves toward a positive skin
electrode, there is an upward
deflection on the ECG
The Electrocardiogram
The Electrocardiogram
The Electrocardiogram
P-WAVE
 The first positive
deflection on the
ECG.
 Atrial
depolarization
The Electrocardiogram
PR INTERVAL
 time required for
the impulse to
travel from the
SA node through
the conduction
system to the
Purkinje fibers
The Electrocardiogram
QRS Complex
 Ventricular
depolarization
 Atrial
repolarization is
not seen
The Electrocardiogram
ST SEGMENT
 represents the
beginning of
ventricular
muscle
repolarization
The Electrocardiogram
T WAVE
 representing
ventricular
repolarization
The Electrocardiogram
Interpreting the
Electrocardiogram

Heart Rate


# of QRS complexes is a 6 second strip x 10
# of QRS complexes in a 3 second strip x 20
Interpreting the
Electrocardiogram

Heart Rate = 300 / # of big squares
between 2 QRS complex

Triplicate system
300 – 150 – 100 – 75 – 60 - 50
Anatomic Representation
in the ECG

Inferior wall
 II, III, AVF

Anterior Wall
 V1, V2, V3, V4

Lateral Wall
 I, AVL, V5, V6

Superior Wall
 AVR
Part V
CARDIAC REGULATION
Intrinsic Cardiac
Regulation

Largely determined by Preload
 The degree to which the ventricular
walls are stretched at the end of
diastole
 Determined by venous return
(amount of blood returning to the
heart)
Intrinsic Cardiac
Regulation

Starling’s Law of the Heart
 Relationship between preload and
force of cardiac contraction
  preload =  contraction force = 
SV
Intrinsic Cardiac
Regulation

Starling’s Law of the Heart
 Major influence on stroke volume
(amount of blood ejected by the heart
every cardiac cycle) and cardiac output
(amount of blood ejected by the heart in
one minute)
CO = SV x HR
= 5* L/min
Stroke Volume and
Inotropic regulation

Inotropic effects
 Force of Contraction
 ↑ inotropic effect = ↑ force of
contraction = ↑ amount of blood
ejected
Intrinsic Cardiac
Regulation
Intrinsic Cardiac
Regulation

Afterload
 pressure against which the
ventricles must pump blood
  afterload=  work of cardiac mm =
 SV
Extrinsic Cardiac
Regulation

Hormonal
 Catecholamines

Neuronal
 Autonomic nervous system
 Cardiorespiratory centers of the
medulla
Extrinsic Cardiac
Regulation

Other control mechanisms
 Barorecpetor and chemoreceptor
 Temperature
 Electrolyte levels (K, Na, Ca)
Extrinsic Cardiac
Regulation: Neuronal
influences

Sympathetic


Cardioaccleratory center
 stimulation =  HR and contractility (SV)
Extrinsic Cardiac
Regulation: Neuronal
Influences

Parasympathetic


Cardioinhibitory center
 stimulation =  HR and contractility (SV)
Extrinsic Cardiac
Regulation: Hormonal
influences

Catecholamines
 Norepinephrine and Epinephrine :
 sympathetic stimulation
Extrinsic Cardiac
Regulation: Reflex
Mechanisms

Baroreceptor & Chemoreceptor reflex
Extrinsic Cardiac
Regulation: Other Control
Mechanisms

Na & Ca levels
 Direct relation with HR

K levels
 Inverse relation with HR
Extrinsic Cardiac
Regulation: Other Control
Mechanisms

Temperature
  1 oC =  4 bpm

Coronary blood flow
  coronary blood flow
=  contractility
Extrinsic Cardiac
Regulation: other Control
Mechanisms

Bainbridge reflex
 relationship of venous return with
heart rate
  VR = HR
Heart Rate and
Chronotropic Regulation

Chronotropic effects
 Speed of contraction
 ↑ chronotropic effects = ↑ speed of
contraction = ↑ amount of blood
ejected
Ejection Fraction and Heart
Function

Determines how much of the blood
entering the ventricles is pumped
(End-Diastolic ventricular Volume - Endsystolic ventricular volume)
End diastolic ventricular volume

(N) 63-77% for males and 55-75% for
females
The Hypoeffective Heart
Inhibition of nervous excitation
 AbN heart rhythm
 Valvular heart disease
 Hypertension
 Cardiac anoxia
 Myocardial damage

THE END