The cells of the heart

Copyright © 2010 Pearson Education, Inc.

The cells of the heart• Two types of cardiac muscle cells that are involved in

a normal heartbeat:• Specialized muscle cells of the conducting system• Contractile cells

• The heart is an autonomic system that can work without neural stimuli – an intrinsic conduction system.

• The autonomic function of the heart results from:• The pacemaker function – Autorhythmic cells• The conductive system that transfer those impulses

throughout the heart


Properties of Cardiac Muscle

• Aerobic muscle

• No cell division after infancy - growth by hypertrophy

• 99% contractile cells (for pumping)

• 1% autorhythmic cells (set pace)


Electrical Conduction in Myocardial Cells

Figure 14-17

Membrane potentialof autorhythmic cel

Membrane potentialof contractile cell

Contractile cell

Cells ofSA node

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

Intercalated diskwith gap junctions


Intrinsic cardiac conduction system – autorhythmic cells

• Have unstable resting potentials/ pacemaker potentials

• constantly depolarized slowly towards AP

• At threshold, Ca2+ channels open

• Ca2+ influx produces the rising phase of the action potential

• Repolarization results from inactivation of Ca2+ channels

and opening of voltage-gated K+ channels

Copyright © 2010 Pearson Education, Inc. Figure 18.13

1 2 3 Pacemaker potentialThis slow depolarization is due to both opening of Na+

channels and closing of K+

channels. Notice that the membrane potential is never a flat line.

Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca2+

influx through Ca2+ channels.

Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which brings the membrane potential back to its most negative voltage.

Actionpotential

Threshold

Pacemakerpotential

1 1

2 2

3


Conduction System of Heart


Autorhythmic Cells

Location Firing Rate at Rest

SA node 70–80 APs/min*

AV node 40–60 APs/min

Bundle of His 20–40 APs/min

Purkinje fibers 20–40 APs/min

• Cardiac cells are linked by gap junctions

• Fastest depolarizing cells control other cells

• Fastest cells = pacemaker = set rate for rest of heart* action potentials per minute


Cardiac Electrical Connections


Cardiac contractile cells

• Depolarization opens voltage-gated fast Na+ channels in the sarcolemma

• Depolarization wave causes release Ca2+ that causes the cell contraction

• Depolarization wave also opens slow Ca2+ channels in the sarcolemma

• Ca2+ surge prolongs the depolarization phase (plateau)


Electrical Activity: Contractile Cell


Absoluterefractoryperiod

Tensiondevelopment(contraction)

Plateau

Actionpotential

Time (ms)

1

2

3

Depolarization isdue to Na+ influx throughfast voltage-gated Na+

channels. A positivefeedback cycle rapidlyopens many Na+

channels, reversing themembrane potential.Channel inactivation endsthis phase. Plateau phase isdue to Ca2+ influx throughslow Ca2+ channels. Thiskeeps the cell depolarizedbecause few K+ channelsare open.

Repolarization is due to Ca2+ channels inactivating and K+

channels opening. This allows K+ efflux, which brings the membranepotential back to itsresting voltage.

1

2

3

Tens

ion

(g)

Mem

bran

e po

tent

ial (

mV)


Action Potentials

Table 14-3


Conduction System of Heart


Electrical Conduction in the Heart

Figure 14-18, steps 1–5

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.


Cardiac Cycle• Cardiac cycle - The period between the start of one heartbeat and the

beginning of the next.

• refers to all events associated with blood flow through the heart• During the cycle, each of the four chambers goes through

• Systole – contraction of heart muscle

• Diastole – relaxation of heart muscle

• An average heart beat (HR)/cardiac cycle is 75 bpm. That means that a cardiac cycle length is about 0.8 second.

• Of that 0.1 second is the atrial contraction, 0.3 is the atrial relaxation and ventricular contraction.

• The remaining 0.4 seconds are called the quiescent period which represent the ventricular relaxation


RelaxationAtria contract Ventricles contractRelaxation

The sequence of events during a single heartbeat

Figure 18 Section 2 2


Phases of the Cardiac Cycle

1. Ventricular filling — takes place in mid-to-late diastole

• AV valves are open • 80% of blood passively flows into ventricles• Atrial systole occurs, delivering the remaining

20%• End diastolic volume (EDV): volume of blood in

each ventricle at the end of ventricular diastole


Phases of the Cardiac Cycle2. Ventricular systole

• Atria relax and ventricles begin to contract • Rising ventricular pressure results in closing of AV

valves• Isovolumetric contraction phase (all valves are

closed)• In ejection phase, ventricular pressure exceeds

pressure in the large arteries, forcing the SL valves open

• End systolic volume (ESV): volume of blood remaining in each ventricle



3. Isovolumetric relaxation occurs in early diastole

• Ventricles relax

• Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure)



Figure 20.16


Cardiodynamics

• Movements and forces generated during cardiac contractions

• End-diastolic volume (EDV) – the amount of blood in each ventricle at the end of ventricular diastole (before contraction begins)

• End-systolic volume (ESV) - the amount of blood remains in each ventricle at the end of ventricular systole


Cardiodynamics• Stroke volume (SV) – The amount of blood that leaves the

heart with each beat or ventricular contraction; EDV-ESV=SV

• Not all blood ejected

• Normal Adult 70 ml / beat• Ejection fraction – The percentage of end-diastole blood

actually ejected with each beat or ventricular contraction.

• Normal adult 55-70% (healthy heart)


• Cardiac output (CO) – the amount of blood pumped by each ventricle in one minute.

• Physiologically, CO is an indication of blood flow through peripheral tissues

• Cardiac output equals heart rate times stroke volume; Normal CO: Approximately 4-8 liters/minute

Stroke Volume and Cardiac Output

COCardiac output

(ml/min)=

HRHeart rate(beats/min)

X

SVStroke volume

(ml/beat)


Figure 18.8 2

Time (msec)

00 100 200 300 400 500 600 700 800

30

60

90

120

Left AVvalve closes.

Aortic valveopens.

Aortic valve closes.

Left AV valve opens.

Dicrotic notch

Pres

sure

(mm

Hg)

The correspondence of the heart sounds with events during the cardiac cycle

Heart soundsS4

S1 S2S3

S4

“Dubb”“Lubb”

KEYAtrial contraction begins.Atria eject blood into ventricles.Atrial systole ends; AV valves close.Isovolumetric contraction.Ventricular ejection occurs.Semilunar valves close.Isovolumetric relaxation occurs.AV valves open; passive ventricularfilling occurs.

Leftventricle

Left atrium

The pressure changes within the aorta, left atrium, and left ventricle during the cardiac cycle

ATRIALDIASTOLE

ATRIALSYSTOLE ATRIAL DIASTOLE

VENTRICULARDIASTOLE

VENTRICULARSYSTOLE VENTRICULAR DIASTOLE

ATRIALSYSTOLE

Aorta


1 2a 2b 3

Atrioventricular valvesAortic and pulmonary valves

Open OpenClosed

Closed ClosedOpenPhase

ESV

Left atriumRight atriumLeft ventricleRight ventricle

Ventricularfilling

Atrialcontraction

Ventricular filling(mid-to-late diastole)

Ventricular systole(atria in diastole)

Isovolumetriccontraction phase

Ventricularejection phase

Early diastole

Isovolumetricrelaxation

Ventricularfilling

11 2a 2b 3

Electrocardiogram

Left heart

P

1st 2nd

QRSP

Heart sounds

Atrial systole

Dicrotic notch

Left ventricle

Left atrium

EDV

SV

Aorta

T

Vent

ricul

arvo

lum

e (m

l)Pr

essu

re (m

m H

g)


Factors Affecting Cardiac Output

Figure 20.20


Extrinsic Innervation of the Heart

• Heartbeat is modified by the ANS

• Cardiac centers are located in the medulla oblongata

• Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons

• Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves


Autonomic Inputs to Heart


• Effect inotropy – (from Greek, meaning fiber) effect on contractility of the heart

• Effect chronotropy – effect on HR

• Effect dromotropy – Derives from the Greek word "Dromos", meaning running.

• A dromotropic agent is one which affects the conduction speed in the AV node

• Sympathetic stimuli has a positive effect (increase) all

• Parasympathetic stimuli has a negative effect (decrease) all


Autonomic Nervous System Regulation

• In healthy conditions, parasympathetic effects dominate and slows the rate of the pacemaker from 80-100 bpm to a 70-80 bpm.• The binding of Ach to muscarinic receptors (M2) inhibit NE

release (mechanism by which vagal stimulation override sympathetic stimulation)

• Sympathetic nervous system is activated by emotional or physical stressors• Norepinephrine causes the pacemaker to fire more rapidly (and

at the same time increases contractility) • Parasympathetic nervous system opposes sympathetic effects

• Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels

• The heart at rest exhibits vagal tone (parasympathetic)


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


Figure 18.11 1

Heart rate under three conditions: at rest, under parasympatheticstimulation, and under sympathetic stimulation

A prepotential or pacemaker potentialin a heart at rest

+20

0

–30

–60

Threshold

Heart rate: 75 bpm

Membranepotential

(mV)

Normal (resting) Prepotential(spontaneous

depolarization)

Time (sec)2.41.60.8


Figure 18.11 2

Increased heart rate resulting whenACh released by parasympatheticneurons opens chemically gated K+

channels, thereby slowing the rateof spontaneous depolarization

Threshold

+20

–30

0

–60

Heart rate: 40 bpm

Membranepotential

(mV)

Slower depolarization

Hyperpolarization

Parasympathetic stimulation


A prepotential or pacemaker potentialin a heart at rest

2.41.60.8Time (sec)


Figure 18.11 3

Decreased heart rate resulting whenNE released by sympathetic neuronsleads to the opening of ion channels,increases the rate of depolarizationand shortens the period ofrepolarization

More rapiddepolarization

2.41.60.8Time (sec)

Heart rate: 120 bpm

Reduced repolarization

Threshold–30

+20

0Membrane

potential(mV)

Sympathetic stimulation


–60


Chemical Regulation of Heart Rate

1. Hormones

• Epinephrine from adrenal medulla enhances heart rate and contractility

• Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine

2. Intra- and extracellular ion concentrations (e.g., Ca2+ and K+) must be maintained for normal heart function


Homeostatic Imbalances

• Tachycardia: abnormally fast heart rate (>100 bpm)

• If persistent, may lead to fibrillation

• Bradycardia: heart rate slower than 60 bpm

• May result in grossly inadequate blood circulation

• May be desirable result of endurance training


Factors Affecting Stroke Volume

Figure 20.23


Regulation of Stroke Volume

• SV = EDV – ESV

• Three main factors affect SV

• Preload

• Contractility

• Afterload


Regulation of Stroke Volume• Preload• The amount of tension on a muscle before it begins to

contract. The preload of the heart is determined by the EDV.

• In general, the greater the EDV the larger is the stroke volume : EDV-ESV=SV

• These relationships is known as the Frank-Starling principle/Sterling’s law of the heart :• The force of cardiac muscle contraction is

proportional to its initial length• The greater the EDV the larger the preload


Preload and Stroke Volume

• Frank-Starling law states

• Stroke volume increase as EDV increases• EDV is affected by venous return

• Venous return is affected by

• Skeletal muscle pump

• Respiratory pump

• Sympathetic innervation


• Stroke volume is the difference between the EDV and ESV. Changes in either one can change the stroke volume and cardiac output:

• The EDV volume is affected by 2 factors:

• The filling time – duration of ventricular diastole; depends on HR – the faster the HR the shorter is the available filing time

• The venous return – changes in response to several changes: cardiac output, blood volume, peripheral circulation.

Factors Affecting stroke volume - Preload/EDV


Reminder - Length-tension relationship

• The force of muscle contraction depends on the length of the sarcomeres before the contraction begins

• On the molecular level, the length reflects the overlapping between thin and thick filaments

• The tension a muscle fiber can generate is directly proportional to the number of crossbridges formed between the filament


Preload = Contractility (to a point)


Stroke Volume

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

Figure 14-28


Diastolic filling increased

EDV increase (preload increased)

Cardiac muscle stretch increased

Force of contraction increased

Ejection volume increased


Regulation of Stroke Volume - Afterload

• The amount of resistance the ventricular wall must overcome to eject blood during systole (influenced by arterial pressure).

• The greater is the afterload, the longer is the period of isovolumetric contraction (ventricles are contracting but there is no blood flow), the shorter the duration of ventricular ejection and the larger the ESV – afterload increase – stroke volume decrease

• Hypertension increases afterload, resulting in increased ESV and reduced SV


Regulation of Stroke Volume - Contractility

• Force of ventricular contraction (systole) regardless of EDV

• Positive inotropic agents increase contractility

• Increased Ca2+ influx due to sympathetic stimulation

• Hormones (thyroxine and epinephrine)

• Negative inotropic agents decrease contractility

• Increased extracellular K+ (hyperpolarization)

• Calcium channel blockers (decrease calcium influx)


Congestive Heart Failure (CHF)• Progressive condition where the CO is so low that blood

circulation is inadequate to meet tissue needs

• Caused by

• Coronary atherosclerosis

• Persistent high blood pressure

• Multiple myocardial infarcts (decreased blood supply and myocardial cell death)

• Dilated cardiomyopathy (DCM) – heart wall weakens and can not contract efficiently. Causes are unknown but sometimes associated with toxins (ex. Chemotherapy), viral infections, tachycardia and more


Electrocardiography (ECG or EKG)

• Body fluids are good conductors which allows the record of the myocardial action potential extracellularly

• EKG pairs of electrodes (leads) one serve as positive side of the lead and one as the negative

• Potentials (voltage) are being measured between the 2 electrodes

• EKG is the summed electrical potentials generated by all cells of the heart and gives electrical “view” of 3D object (different from one action potential)

• EKG shows depolarization and repolarization


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 of Heart

• P wave: atrial depolarization

• QRS complex: ventricular depolarization and atrial repolarization

• T wave: ventricular repolarization

• PQ segment: AV nodal delay

• QT segment: ventricular systole

• QT interval: ventricular diastole


Electrical Activity of Heart – normal values


Correlation between an ECG and electrical events in the heart


Electrical Activity

Figure 14-21 (1 of 9)

P wave: atrialdepolarization

ELECTRICALEVENTSOF THE

CARDIACCYCLE

START

P


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



• Defects in the intrinsic conduction system may result in

1. Arrhythmias: irregular heart rhythms

2. Uncoordinated atrial and ventricular contractions (heart block)

3. Fibrillation: rapid, irregular contractions; useless for pumping blood


Figure 18.14 2

Atrial Fibrillation (AF)

Paroxysmal Atrial Tachycardia (PAT)

Premature Atrial Contractions (PACs)

Important examples of cardiac arrhythmias

Premature atrial contractions (PACs) often occur in healthy individuals. In aPAC, the normal atrial rhythm is momentarily interrupted by a “surprise” atrialcontraction. Stress, caffeine, and various drugs may increase the incidence ofPACs, presumably by increasing the permeabilities of the SA pacemakers. Theimpulse spreads along the conduction pathway, and a normal ventricularcontraction follows the atrial beat.

In paroxysmal (par-ok-SIZ-mal) atrial tachycardia, or PAT, a premature atrialcontraction triggers a flurry of atrial activity. The ventricles are still able to keeppace, and the heart rate jumps to about 180 beats per minute.

During atrial fibrillation (fib-ri-LĀ-shun), the impulses move over the atrialsurface at rates of perhaps 500 beats per minute. The atrial wall quivers insteadof producing an organized contraction. The ventricular rate cannot follow theatrial rate and may remain within normal limits. Even though the atria are nownonfunctional, their contribution to ventricular end-diastolic volume is so smallthat the condition may go unnoticed in older individuals.

P P P P P P

P P P


Figure 18.14 2

Ventricular Fibrillation (VF)

Ventricular Tachycardia (VT)

Premature Ventricular Contractions (PVCs)

Premature ventricular contractions (PVCs) occur when a Purkinje cell orventricular myocardial cell depolarizes to threshold and triggers a prematurecontraction. Single PVCs are common and not dangerous. The cell responsibleis called an ectopic pacemaker. The frequency of PVCs can be increased byexposure to epinephrine, to other stimulatory drugs, or to ionic changes thatdepolarize cardiac muscle cell membranes.

Ventricular tachycardia is defined as four or more PVCs without interveningnormal beats. It is also known as VT or V-tach. Multiple PVCs and VT mayindicate that serious cardiac problems exist.

Ventricular fibrillation (VF) is responsible for the condition known as cardiacarrest. VF is rapidly fatal, because the ventricles quiver and stop pumping blood.

P

PPP T T T

Important examples of cardiac arrhythmias

Copyright © 2010 Pearson Education, Inc. Figure 13.17 (4 of 4)

ECG Arrhythmias: Fibrillation

Ventricular Fibrillation

• Loss of coordination of electrical activity of heart

• Death can ensue within minutes unless corrected



• Defective SA node may result in

• Ectopic focus: abnormal pacemaker takes over

• If AV node takes over, there will be a junctional rhythm (40–60 bpm)

• Defective AV node may result in

• Partial or total heart block

• Few or no impulses from SA node reach the ventricles


First and second degree Heart Block• Slowed/diminished conduction through AV node occurs in

varying degrees

• First degree block• Increases duration PQ segment

• Increases delay between atrial and ventricular contraction

• Second degree block • Lose 1-to-1 relationship between P wave and QRS

complex

• Lose 1-to-1 relationship between atrial and ventricular contraction


Third Degree Heart Block

Third degree block

• Loss of conduction through the AV node

• P wave becomes independent of QRS

• Atrial and ventricular contractions are independent

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The cells of the heart

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