Chapter 14b

Cardiovascular Physiology

Figure 14-15

Action Potentials in Cardiac Autorhythmic Cells• Pacemaker potential - no resting• -60mV drifts to -40 to action potential• Spread through connections to contractile fibers• If channels are permeable to both K+ and Na+

Time Time

Ca2+ in

Ca2+ in

K+ out

Net Na+ in

Lots of Ca2+

channelsopen

Ca2+ channels close,K+ channels open

Some Ca2+

channels open,If channels close

If channelsopen K+ channels close

If channelsopen

(b) Ion movements during an actionand pacemaker potential

(c) State of various ion channelsTime

Threshold

Pacemakerpotential

Actionpotential

20

0

–20

–40

–60

(a) The pacemaker potentialgradually becomes less negativeuntil it reaches threshold,triggering an action potential.

Mem

bran

e po

tent

ial (

mV)

Action Potentials in Cardiac Autorhythmic Cells

PLAY Interactive Physiology® Animation: Cardiovascular System: Cardiac Action Potential

Modulation of Heart Rate by the Autonomic Nervous System

Figure 14-16

Normal Parasympathetic stimulationNormal Sympathetic stimulation

Hyperpolarized Slower depolarization

Time (sec)Time (sec)

20

0

–60

0.8 1.6 2.40.8 1.6 2.4

(b)(a)

Depolarized More rapid depolarization

20

–20

–40

–60

0

Mem

bran

e po

tent

ial (

mV)

Mem

bran

e po

tent

ial (

mV)

Action Potentials

Table 14-3

Electrical Conduction in Myocardial Cells

Figure 14-17

Membrane potentialof autorhythmic cell

Membrane potentialof contractile cell

Contractile cell

Cells ofSA node

Depolarizations of autorhythmic cellsrapidly spread to adjacent contractilecells through gap junctions.

Intercalated diskwith gap junctions

Electrical Conduction in the Heart

Figure 14-18

1

2

3

4

5

5

4

3

2

1

THE CONDUCTING SYSTEMOF THE HEART

SA node

AV node

Purkinjefibers

Bundlebranches

AV bundle

AV node

Internodalpathways

SA node

SA node depolarizes.

Electrical activity goesrapidly to AV node viainternodal pathways.

Depolarization spreadsmore slowly acrossatria. Conduction slowsthrough AV node.

Depolarization movesrapidly through ventricularconducting system to theapex of the heart.

Depolarization wavespreads upward fromthe apex.

Electrical Conduction

• SA node• Sets the pace of the heartbeat at 70 bpm• AV node (50 bpm) and Purkinje fibers (25-40

bpm) can act as pacemakers under some conditions

• AV node• Routes the direction of electrical signals • Delays the transmission of action potentials

Einthoven’s Triangle

Figure 14-19

Electrodes areattached to theskin surface.

A lead consists of twoelectrodes, one positiveand one negative.

Right arm Left arm

Left leg

I

II III

The Electrocardiogram

• Three major waves: P wave, QRS complex, and T wave

Figure 14-20

Electrical Activity

• Correlation between an ECG and electrical events in the heart

Figure 14-21

P

Q

R

T

S P

T wave:ventricularrepolarization

PQ or PR segment:conduction throughAV node and AVbundle

P wave: atrialdepolarization

ELECTRICALEVENTSOF THE

CARDIACCYCLE

Repolarization

START

P

Q

P

Q

R

P

Q

R

T

S

R waveP

Q

R

S

S wave

Q

R

P

Q wave

Ventricles contract

ST segment

The end

P

Atria contract

S

Electrical Activity

Figure 14-21 (9 of 9)

P

Q

R

T

S P

T wave:ventricularrepolarization

PQ or PR segment:conduction throughAV node and AVbundle

P wave: atrialdepolarization

ELECTRICALEVENTSOF THE

CARDIACCYCLE

Repolarization

START

P

Q

P

Q

R

P

Q

R

T

S

R waveP

Q

R

S

S wave

Q

R

P

Q wave

Ventricles contract

ST segment

The end

P

Atria contract

S

Electrical Activity

• Comparison of an ECG and a myocardial action potential

Figure 14-22

(a) The electrocardiogram represents the summedelectrical activity of all cells recorded from thesurface of the body.

(b) The ventricular action potential is recorded froma single cell using an intracellular electrode.Notice that the voltage change is much greaterwhen recorded intracellularly.

110mV

1 mV

1 sec

1 sec

Electrical Activity

• Normal and abnormal electrocardiograms

Figure 14-23

Mechanical Events

• Mechanical events of the cardiac cycle

Figure 14-24

5

43

2

1 Late diastole—both sets ofchambers are relaxed andventricles fill passively.

Atrial systole—atrial contractionforces a small amount ofadditional blood into ventricles.

Isovolumic ventricularcontraction—first phase ofventricular contraction pushes AVvalves closed but does not createenough pressure to open semilunarvalves.

START

Ventricular ejection—as ventricular pressurerises and exceeds pressurein the arteries, the semilunarvalves open and blood isejected.

Isovolumic ventricularrelaxation—as ventriclesrelax, pressure in ventriclesfalls, blood flows back intocusps of semilunar valvesand snaps them closed.

S1

S2

Cardiac Cycle

PLAY Interactive Physiology® Animation: Cardiovascular System: Cardiac Cycle

Cardiac Cycle

• Left ventricular pressure-volume changes during one cardiac cycle

Figure 14-25

120

80

40

0 65 100 135Left ventricular volume (mL)

AB

C

EDV

ESVD

Stroke volume

Onecardiaccycle

EDV = End-diastolicvolumeESV = End-systolicvolume

KEY

Left

vent

ricul

ar p

ress

ure

(mm

Hg)

Wiggers Diagram

Figure 14-26

P PT

0 100 200 300 400 500 600 700 800

120

A

B

60

90

Time (msec)

Electro-cardiogram

(ECG)

Pressure(mm Hg)

Dicrotic notch

QRScomplex

QRScomplex

Leftventicularpressure

135

0 C

D

E

F

S1 S2

65

Heart sounds

Leftventricular

volume (mL)

Atrialsystole

Atrialsystole

Atrialsystole

Atrialsystole

Ventricularsystole

Ventricularsystole

Ventriculardiastole

Isovolumicventricularcontraction

Earlyventricular

diastole

Lateventricular

diastole

Left atrialpressure

30

Aorta

Wiggers Diagram

Figure 14-26 (13 of 13)

P PT

0 100 200 300 400 500 600 700 800

120

A

B

60

90

Time (msec)

Electro-cardiogram

(ECG)

Pressure(mm Hg)

Dicrotic notch

QRScomplex

QRScomplex

Leftventicularpressure

135

0 C

D

E

F

S1 S2

65

Heart sounds

Leftventricular

volume (mL)

Atrialsystole

Atrialsystole

Atrialsystole

Atrialsystole

Ventricularsystole

Ventricularsystole

Ventriculardiastole

Isovolumicventricularcontraction

Earlyventricular

diastole

Lateventricular

diastole

Left atrialpressure

30

Aorta

Stroke Volume and Cardiac Output

• Stroke volume• Amount of blood pumped by one ventricle

during a contraction• EDV – ESV = stroke volume

• Cardiac output• Volume of blood pumped by one ventricle in a

given period of time• CO = HR SV• Average = 5 L/min

Na+ and Ca2+ influx

Sympathetic neurons(NE)

Rate of depolarization

Heart rate

Muscarinic receptorsof autorhythmic cells

K+ efflux; Ca2+ influx

Parasympatheticneurons (Ach)

Hyperpolarizes cell and rate of depolarization

Heart rate

1-receptors ofautorhythmic cells

Integrating center

Efferent path

Effector

Tissue response

Cardiovascularcontrol

center in medullaoblongata

KEY

Autonomic Neurotransmitters Alter Heart Rate

Figure 14-27

Stroke Volume

• Frank-Starling law states• Stroke volume increase as EDV (ending diastolic

volume) increases – stretch -> more force• EDV is affected by venous return• Venous return is affected by• Skeletal muscle pump• Respiratory pump• Sympathetic innervation of vessels

• Force of contraction is affected by• Stroke volume• Length of muscle fiber and contractility of heart

Stroke Volume

• Length-force relationships in intact heart: a Starling curve

Figure 14-28

Inotropic Effect

• The effect of norepinepherine on contractility of the heart

Figure 14-29

Cardiac Output

PLAY Interactive Physiology® Animation: Cardiovascular System: Cardiac Output

bind to

that activate

resulting in phosphorylation of

1-receptors

Epinephrineand

norepinephrine

cAMP secondmessenger system

Ca2+ removed from cytosol faster

Shortens Ca-troponinbinding time

Ca2+ stores in SR

Shorterduration

of contractionMore forcefulcontraction

Phospholamban

Ca2+-ATPase on SR

Ca2+ released

Ca2+ entry from ECF

Open time increases

SR = Sarcoplasmicreticulum

ECF = Extracelllularfluid

Voltage-gated Ca2+ channels

KEY

Catecholamines Modulate Cardiac Contraction

Figure 14-30

Stroke Volume and Heart Rate Determine Cardiac Output

Figure 14-31

determined by

is influenced by

which varies with

is a function of

increases

increases

determined by

CARDIAC OUTPUT

aided by

Heart rate

Due toparasympathetic

innervation

Sympatheticinnervation and

epinephrine

Venous returnVenous constriction

End-diastolicvolume

Rate of depolarizationin autorhythmic cells

Stroke volume

Contractility

Respiratorypump

Skeletal musclepump

Decreases Increases

Force of contraction inventricular myocardium

Summary

• Cardiovascular system—anatomy review• Pressure, volume, flow, and resistance• Pressure gradient, driving pressure, resistance,

viscosity, flow rate, and velocity of flow• Cardiac muscle and the heart• Myocardium, autorhythmic cells, intercalated

disks, pacemaker potential, and If channels

• The heart as a pump• SA node, AV node, AV bundle, bundle

branches, and Purkinje fibers

Summary

• The heart as a pump (continued)• ECG, P wave, QRS complex, and T wave

• The cardiac cycle• Systole, diastole, AV valves, first heart sound,

isovolumic ventricular contraction, semilunar valves, second heart sound, and stroke volume

• Cardiac output• Frank-Starling law, EDV, preload, contractility,

inotropic effect, afterload, and ejection fraction