Chapter 14

Part B

Cardiovascular
Physiology

Lecture Presentation by
Myriam Alhadeff Feldman
Lake Washington Institute of
Technology

2016 Pearson Education, Inc.

 Electrical Conduction

Sinoatrial (SA) node

Sets the pace of the heartbeat at 70 bpm
AV node (50 bpm) and Purkinje fibers (2540 bpm)
can act as pacemakers under some conditions
Internodal pathway from SA to atrioventricular (AV)
node
Routes the direction of electrical signals so the heart
contracts from apex to base
AV node delay is accomplished by slower
conductional signals through nodal cells
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 Electrical Conduction

Purkinje fibers transmit electric signals down the

atrioventricular bundle (bundle of His) to left and
right bundle branches.

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Figure 14.13 Electrical conduction in myocardial cells

Action potentials
of autorhythmic cells
Cells of
SA node

Electrical Action potentials

current of contractile cells

Contractile cell

Intercalated disk
with gap junctions

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 Cardiac Action Potential

Interactive Physiology Animation: Cardiovascular

Physiology: Cardiac Action Potential

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Figure 14.14 The conducting system of the heart Slide 1

SA node depolarizes.
SA node Purple shading in
steps 25 represents
AV node depolarization.

Electrical activity goes

rapidly to AV node via
internodal pathways.

Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART

Depolarization moves
rapidly through ventricular
conducting system to the
SA node apex of the heart.

Internodal
pathways Depolarization wave
spreads upward from
the apex.

AV
node

AV
bundle
Bundle
branches
Purkinje
fibers

FIGURE QUESTION
What would happen to conduction
if the AV node malfunctioned and
could no longer depolarize?

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Figure 14.14 The conducting system of the heart Slide 2

SA node depolarizes.
SA node

AV node

THE CONDUCTING SYSTEM

OF THE HEART

SA node

Internodal
pathways

AV
node

AV
bundle
Bundle
branches
Purkinje
fibers

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Figure 14.14 The conducting system of the heart Slide 3

SA node depolarizes.
SA node Purple shading in
steps 25 represents
AV node depolarization.

Electrical activity goes

rapidly to AV node via
internodal pathways.

THE CONDUCTING SYSTEM

OF THE HEART

SA node

Internodal
pathways

AV
node

AV
bundle
Bundle
branches
Purkinje
fibers

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Figure 14.14 The conducting system of the heart Slide 4

SA node depolarizes.
SA node Purple shading in
steps 25 represents
AV node depolarization.

Electrical activity goes

rapidly to AV node via
internodal pathways.

Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART

SA node

Internodal
pathways

AV
node

AV
bundle
Bundle
branches
Purkinje
fibers

2016 Pearson Education, Inc.

Figure 14.14 The conducting system of the heart Slide 5

SA node depolarizes.
SA node Purple shading in
steps 25 represents
AV node depolarization.

Electrical activity goes

rapidly to AV node via
internodal pathways.

Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART

Depolarization moves
rapidly through ventricular
conducting system to the
SA node apex of the heart.

Internodal
pathways

AV
node

AV
bundle
Bundle
branches
Purkinje
fibers

2016 Pearson Education, Inc.

Figure 14.14 The conducting system of the heart Slide 6

SA node depolarizes.
SA node Purple shading in
steps 25 represents
AV node depolarization.

Electrical activity goes

rapidly to AV node via
internodal pathways.

Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART

Depolarization moves
rapidly through ventricular
conducting system to the
SA node apex of the heart.

Internodal
pathways Depolarization wave
spreads upward from
the apex.

AV
node

AV
bundle
Bundle
branches
Purkinje
fibers

FIGURE QUESTION
What would happen to conduction
if the AV node malfunctioned and
could no longer depolarize?

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 The Waves of Electrocardiogram (ECG)

Waves and segments two major components of an

ECG
Three waves
P depolarization of the atria
QRS complex: wave of ventricular depolarization
T repolarization of the ventricle
Atrial repolarization is part of QRS

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Figure 14.15f The Electrocardiogram

5 mm 25 mm = 1 sec

An electrocardiogram is divided into waves (P, Q, R, S, T),

segments between the waves (the P-R and S-T segments,
for example), and intervals consisting of a combination of
waves and segments (such as the PR and QT intervals).
This ECG tracing was recorded from lead I.

P wave: atrial depolarization

P-R segment: conduction through AV

node and AV bundle

QRS complex: ventricular +1 R R

depolarization

T wave: ventricular repolarization

Millivolts

P-R S-T
segment segment
Q S
P wave T wave

FIGURE QUESTION
0
1. If the ECG records at a speed of
25 mm/sec, what is the heart
rate of the person?
(1 little square = 1 mm) PR interval* QT interval QRS complex

*Sometimes the Q wave is not seen in the ECG. For this reason, the segments and intervals are
named using the R wave but begin with the first wave of the QRS complex.

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 The Electrical Events of the Cardiac
Cycle
Mechanical events lag behind electrical events:
contraction follows action potential
ECG begins with atrial depolarization, atrial
contraction at the end of P wave
P-R segment signal goes through AV node and AV
bundle
Q wave end: ventricular contraction begins and
continues through T wave
ECG analysis

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 The Electrical Events of the Cardiac
Cycle
Heart rate: time between two P waves or two Q
waves
Rhythm: regular pattern
Waves analysis: presence and shape
Segment length constant

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Figure 14.16 Correlation between an ECG and electrical events in the heart

START
P wave: atrial
depolarization
P

End

P-Q or P-R segment:

conduction through
T AV node and AV
P
bundle

QS
P

Atria contract

T wave:
ventricular
repolarization

R ELECTRICAL EVENTS
OF THE
Ventricular CARDIAC CYCLE
T repolarization
P

QS

Q wave
P
Atrial
repolarization
S-T segment Q

R wave
P
R
QS

Ventricles contract R
P

P S wave

QS

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Figure 14.15h The Electrocardiogram

Normal and abnormal ECGs. All tracings represent 10-sec recordings.

10 sec
R R
P T P T

(1) Normal ECG

R R R R
P P P P P P P P P P P P P P

(2) Third-degree block

(3) Atrial fibrillation

FIGURE QUESTIONS
2. Three abnormal ECGs are shown at right.
Study them and see if you can relate the
ECG changes to disruption of the normal (4) Ventricular fibrillation
electrical conduction pattern in the heart.
3. Identify the waves on the ECG in part (5).
Look at the pattern of their occurrence and
describe what has happened to electrical
conduction in the heart.

(5) Analyze this abnormal ECG.

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 The Mechanical Events of the Cardiac
Cycle
Diastole: cardiac muscle relaxes
Systole: cardiac muscle contracts
Beginning of cycle: the heart at rest: atrial and
ventricular diastole
The atria are filling with blood from the vein
AV valves open ventricles fill
Atrial systole: atria contract
Early ventricular contraction and AV valves close
first heart sound

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 The Mechanical Events of the Cardiac
Cycle
Atrial diastole: all valves shut, isometric contraction of
the heart, atria relax and blood flows in the atria
Ventricular systole: ventricles finish contracting
pushing semilunar valves open and blood is ejected in
arteries: ventricular systole
Ventricular diastole: ventricular relaxation and
pressure drops, still higher than atrial pressure
Arterial blood flows back pushing semilunar valves
shut second heart sound

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 The Mechanical Events of the Cardiac
Cycle
Isovolumic ventricular relaxation, volume of blood in
ventricles not changing
AV valves open when ventricular pressure drops
below atrial pressure

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Figure 14.17a Mechanical events of the cardiac cycle Slide 1

The heart cycles between contraction (systole)

and relaxation (diastole). Late diastoleboth sets of
chambers are relaxed and
ventricles fill passively.

START

Isovolumic ventricular
relaxationas ventricles Atrial systoleatrial contraction
relax, pressure in ventricles forces a small amount of
falls. Blood flows back into additional blood into ventricles.
cusps of semilunar valves
and snaps them closed.

S1

S2

Isovolumic ventricular contraction

Ventricular ejectionas first phase of ventricular contraction
ventricular pressure rises pushes AV valves closed but does
and exceeds pressure in not create enough pressure to open
the arteries, the semilunar semilunar valves.
valves open and blood is
ejected.

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Figure 14.17a Mechanical events of the cardiac cycle Slide 2

The heart cycles between contraction (systole)

and relaxation (diastole). Late diastoleboth sets of
chambers are relaxed and
ventricles fill passively.

START

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Figure 14.17a Mechanical events of the cardiac cycle Slide 3

The heart cycles between contraction (systole)

and relaxation (diastole). Late diastoleboth sets of
chambers are relaxed and
ventricles fill passively.

START

Atrial systoleatrial contraction

forces a small amount of
additional blood into ventricles.

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Figure 14.17a Mechanical events of the cardiac cycle Slide 4

The heart cycles between contraction (systole)

and relaxation (diastole). Late diastoleboth sets of
chambers are relaxed and
ventricles fill passively.

START

Atrial systoleatrial contraction

forces a small amount of
additional blood into ventricles.

S1

Isovolumic ventricular contraction

first phase of ventricular contraction
pushes AV valves closed but does
not create enough pressure to open
semilunar valves.

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Figure 14.17a Mechanical events of the cardiac cycle Slide 5

The heart cycles between contraction (systole)

and relaxation (diastole). Late diastoleboth sets of
chambers are relaxed and
ventricles fill passively.

START

Atrial systoleatrial contraction

forces a small amount of
additional blood into ventricles.

S1

Isovolumic ventricular contraction

Ventricular ejectionas first phase of ventricular contraction
ventricular pressure rises pushes AV valves closed but does
and exceeds pressure in not create enough pressure to open
the arteries, the semilunar semilunar valves.
valves open and blood is
ejected.

2016 Pearson Education, Inc.

Figure 14.17a Mechanical events of the cardiac cycle Slide 6

The heart cycles between contraction (systole)

and relaxation (diastole). Late diastoleboth sets of
chambers are relaxed and
ventricles fill passively.

START

Isovolumic ventricular
relaxationas ventricles Atrial systoleatrial contraction
relax, pressure in ventricles forces a small amount of
falls. Blood flows back into additional blood into ventricles.
cusps of semilunar valves
and snaps them closed.

S1

S2

Isovolumic ventricular contraction

Ventricular ejectionas first phase of ventricular contraction
ventricular pressure rises pushes AV valves closed but does
and exceeds pressure in not create enough pressure to open
the arteries, the semilunar semilunar valves.
valves open and blood is
ejected.

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 Heart Sounds

First heart sound

Vibrations following closure of the AV valves
Lub
Second heart sound
Vibrations created by closing of semilunar valve
Dup
Auscultation is listening to the heart through the
chest wall through a stethoscope.

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 Cardiac Cycle

Interactive Physiology Animation:

Cardiovascular Physiology: Cardiac Cycle

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 Stroke Volume and Cardiac Output

End diastolic volume (EDV)

End systolic volume (ESV)
Stroke volume
Amount of blood pumped by one ventricle during a
contraction
Volume of blood before contraction-volume of blood
after contraction = stroke volume
EDV ESV = stroke volume
Average = 70 mL

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 Stroke Volume and Cardiac Output

Cardiac output (CO)

Volume of blood pumped by one ventricle in a given
period of time
Cardiac output = heart rate stroke volume
Average = 5 L/min

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 Stroke Volume

Force of contraction is affected by

Length of muscle fiber
Determined by volume of blood at beginning of
contraction
Contractility of heart
As stretch of the ventricular wall increases, so does
stroke volume
Preload is the degree of myocardial stretch before
contraction

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 Stroke Volume

Sympathetic activity speeds heart rate

1-adrenergic receptors on the autorhythmic cells
Parasympathetic activity slows heart rate

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Figure 14.19a-b Autonomic control of heart rate

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Figure 14.19c Autonomic control of heart rate

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Figure 14.19d Autonomic control of heart rate

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Figure 14.19e Autonomic control of heart rate

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 Stroke Volume

Frank-Starling law states

Stroke volume increases as EDV increases
EDV is determined by venous return
Venous return is affected by
Skeletal muscle pump
Respiratory pump
Sympathetic innervation of veins

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Figure 14.20a Length-tension relationships

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Figure 14.20b Length-tension relationships

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 Contractility

Any chemical that affects contractility is an inotropic

agent
Epinephrine, norepinephrine, and digitalis have
positive inotropic effects
Chemicals with negative inotropic effects decrease
contractility

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Figure 14.20c Length-tension relationships

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 Cardiac Output

Interactive Physiology Animation:

Cardiovascular Physiology: Cardiac Output

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Figure 14.21 Catecholamines increase cardiac contraction

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 Afterload and Ejection Fraction

Afterload is the combined load of EDV and arterial

resistance during ventricular contraction
Ejection fraction is the percentage of EDV ejected
with one contraction
Stroke volume/EDV
Average = 52%

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Figure 14.22 Stroke volume and heart rate determine cardiac output

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 Summary

Overview of the cardiovascular system

Pressure, volume, flow, and resistance
Cardiac muscle and the heart
The heart as a pump

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