copyright © 2010 pearson education, inc. cardiovascular system – the heart

Copyright © 2010 Pearson Education, Inc.

Cardiovascular system – the heart


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


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


Autorythmic cells - ectopic pacemakers

• Autorythmic cells of the SA node (pacemaker) may be replaced by ectopic pacemakers

• Ectopic pacemakers – other parts in the heart that can induce beating

• The ectopic pacemakers may become dominant:

• If their rythmicity increased

• The pacemaker is inhibited/blocked

• The conduction system pathways are blocked

• First to take over will be the AV node


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


Action Potentials

Table 14-3


Heart Physiology: Sequence of Excitation


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.


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


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 (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


Homeostatic Imbalances

• 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

Copyright © 2010 Pearson Education, Inc. Figure 13.17 (1 of 4)

ECG Arrhythmias: Abnormal Rates

• Sinus rhythm = pace generated by SA node

• Abnormal rates shown

• Tachycardia = fast rhythm

• Bradycardia = slow rhythm



• 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

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


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


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

CO

Cardiac output

(ml/min)=

HR

Heart rate

(beats/min)X

SV

Stroke volume

(ml/beat)


Factors Affecting Cardiac Output

Figure 20.20


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


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


• 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


Heart Rate — Determined by SA Node Firing Rate

• SA node intrinsic firing rate = 100/min

• No extrinsic control on heart, HR = 100

• SA node under control of ANS and hormones

• Rest: parasympathetic dominates, HR = 75

• Excitement: sympathetic takes over, HR increases


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


Autonomic Nervous System Regulation

• Atrial (Bainbridge) reflex: a sympathetic reflex initiated by increased venous return

• Stretch of the atrial walls stimulates the SA node

• Also stimulates atrial stretch receptors activating sympathetic reflexes


Pacemaker Function

Figure 20.22


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



• 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


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 - 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)


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


Factors Influencing Stroke Volume


Regulation of Cardiac Output


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

copyright © 2010 pearson education, inc. cardiovascular system – the heart

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