marieb chapter 18 part b: the heart

Copyright © 2010 Pearson Education, Inc.

Marieb Chapter 18 Part B: The Heart


Cardiac Muscle Contraction• Depolarization of the heart is rhythmic and

spontaneous (autorhythmic)

• About 1% of cardiac cells have automaticity— (are self-excitable)

• Gap junctions ensure the heart contracts as a unit

• Long absolute refractory period (250 ms); muscle fibers can’t go into sustained contraction with no relaxation

Copyright © 2010 Pearson Education, Inc. Figure 18.12

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 Potential in Myocardium


Heart Physiology: Electrical Events

• Intrinsic cardiac conduction system

• A network of non-contractile (autorhythmic) cells that initiate and distribute impulses to coordinate the depolarization and contraction of the heart


Autorhythmic Cells

• Have unstable resting potentials (pacemaker potentials) due to open slow Na+ channels

• At threshold, Ca2+ channels open

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

• Repolarization results from closure of Ca2+ channels and opening of voltage-gated K+ channels


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

Action Potential in Conduction System Cells


Heart Physiology: Sequence of Excitation

1. Sinoatrial (SA) node (pacemaker)

• Generates impulses about 75 times/minute (sinus rhythm)

• Depolarizes faster than any other part of the myocardium



2. Atrioventricular (AV) node

• Delays impulses approximately 0.1 second; gives the atria

• Depolarizes at 50 times per minute in absence of SA node input

• Is this fast enough to stay alive?



3. Atrioventricular (AV) bundle (bundle of His)

• Only electrical connection between the atria and ventricles

• Fibrous skeleton (fibrous trigone)



4. Right and left bundle branches

• Two pathways in the interventricular septum that carry the impulses toward the apex of the heart



5. Purkinje fibers

• Complete the pathway into the apex and ventricular walls

• AV bundle and Purkinje fibers depolarize only 30 times per minute in absence of AV node input

• Is this fast enough to keep you alive?

Copyright © 2010 Pearson Education, Inc. Figure 18.14a

(a) Anatomy of the intrinsic conduction system showing the sequence of electrical excitation

Internodal pathway

Superior vena cavaRight atrium

Left atrium

Purkinje fibers

Inter-ventricularseptum

1 The sinoatrial (SA) node (pacemaker)generates impulses.

2 The impulsespause (0.1 s) at theatrioventricular(AV) node. The atrioventricular(AV) bundleconnects the atriato the ventricles.4 The bundle branches conduct the impulses through the interventricular septum.

3

The Purkinje fibersdepolarize the contractilecells of both ventricles.

5


Homeostatic Imbalances

• Defects in the intrinsic conduction system may result in

1. Arrhythmias/dysrhythmias: irregular heart rhythms

2. Uncoordinated atrial and ventricular contractions

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


Homeostatic Imbalances• Defective SA node may result in• Ectopic focus: abnormal pacemaker

somewhere else takes over

• If the 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


Extrinsic Innervation of the Heart and Blood Vessels

• Heartbeat is modified by the ANS

• Cardiac centers are located in the medulla oblongata

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

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

• A vasomotor center (VMC;) is also in the medulla; it sends sympathetic fibers to blood vessels


Thoracic spinal cord

The vagus nerve (parasympathetic) decreases heart rate.

Cardioinhibitory center

Cardio-acceleratorycenter

Sympathetic cardiacnerves increase heart rateand force of contraction.

Medulla oblongata

Sympathetic trunk ganglion

Dorsal motor nucleus of vagus

Sympathetic trunk

AV nodeSA node

Parasympathetic fibersSympathetic fibersInterneurons


ANS Effects on HR


Electrocardiography• Electrocardiogram (ECG or EKG): a composite of

all the action potentials generated by all cardiac cells at a given time

• THIS IS NOT AN OSCILLOSCOPE TRACING!!!!!

• Three waves

1. P wave: depolarization of SA node

2. QRS complex: ventricular depolarization

3. T wave: ventricular repolarization

See the next two figures…


Sinoatrialnode

Atrioventricularnode

Atrialdepolarization

QRS complex

Ventriculardepolarization

Ventricularrepolarization

P-QInterval

S-TSegment

Q-TInterval


ECG


Atrial depolarization, initiatedby the SA node, causes theP wave.

P

R

T

QS

SA node

AV node

With atrial depolarizationcomplete, the impulse isdelayed at the AV node.

Ventricular depolarizationbegins at apex, causing theQRS complex. Atrialrepolarization occurs.

P

R

T

QS

P

R

T

QS

Ventricular depolarizationis complete.

Ventricular repolarizationbegins at apex, causing theT wave.

Ventricular repolarizationis complete.

P

R

T

QS

P

R

T

QS

P

R

T

QS

Depolarization Repolarization

1

2

3

4

5

6

Copyright © 2010 Pearson Education, Inc. Figure 18.17, step 1

Atrial depolarization, initiated bythe SA node, causes the P wave.

P

R

T

QS

SA node DepolarizationRepolarization

1



P

R

T

QS

SA node

AV node

With atrial depolarization complete,the impulse is delayed at the AV node.

P

R

T

QS

DepolarizationRepolarization

1

2



P

R

T

QS

SA node

AV node

With atrial depolarization complete,the impulse is delayed at the AV node.

Ventricular depolarization beginsat apex, causing the QRS complex.Atrial repolarization occurs.

P

R

T

QS

P

R

T

QS


1

2

3


Ventricular depolarization iscomplete.

P

R

T

QS


4



Ventricular repolarization beginsat apex, causing the T wave.

P

R

T

QS

P

R

T

QS


4

5



Ventricular repolarization beginsat apex, causing the T wave.

Ventricular repolarization iscomplete.

P

R

T

QS

P

R

T

QS

P

R

T

QS


4

5

6


Atrial depolarization, initiatedby the SA node, causes theP wave.

P

R

T

QS

SA node

AV node

With atrial depolarizationcomplete, the impulse isdelayed at the AV node.

Ventricular depolarizationbegins at apex, causing theQRS complex. Atrialrepolarization occurs.

P

R

T

QS

P

R

T

QS

Ventricular depolarizationis complete.

Ventricular repolarizationbegins at apex, causing theT wave.

Ventricular repolarizationis complete.

P

R

T

QS

P

R

T

QS

P

R

T

QS

Depolarization Repolarization

1

2

3

4

5

6


(a) Normal sinus rhythm.

(c) Second-degree heart block. Some P waves are not conducted through the AV node; hence more P than QRS waves are seen. In this tracing, the ratio of P waves to QRS waves is mostly 2:1.

(d) Ventricular fibrillation. These chaotic, grossly irregular ECG deflections are seen in acute heart attack and electrical shock.

(b) Junctional rhythm. The SA node is nonfunctional, P waves are absent, and heart is paced by the AV node at 40 - 60 beats/min.


Pacemakers


Heart Sounds

• Two sounds (lub-dup) associated with closing of heart valves

• First sound occurs as AV valves close and signifies beginning of systole

• Second sound occurs when SL valves close at the beginning of ventricular diastole

• Heart murmurs: abnormal heart sounds most often occur because of valve problems


Mechanical Events: The Cardiac Cycle• Cardiac cycle: all events associated with

blood flow through the heart during one complete heartbeat

• Systole—contraction

• Diastole—relaxation


Phases of the Cardiac Cycle1. Ventricular filling—takes place in mid-to-late

diastole

• AV valves are open; SL valves are closed

• 80% of blood passively flows into ventricles (Drips!)

• 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


Phases of the Cardiac Cycle3. Isovolumetric relaxation occurs in early

diastole

• Ventricles relax

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


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)


Cardiac Output (CO)

• Volume of blood pumped by each ventricle in one minute

• CO = heart rate (HR) x stroke volume (SV)

• HR = number of beats per minute

• SV = volume of blood pumped out by a ventricle with each beat


Cardiac Output (CO)• At rest• CO (ml/min) = HR (75 beats/min) SV (70

ml/beat)

= 5.25 L/min

• Maximal CO is 4–5 times resting CO in nonathletic people

• Maximal CO may reach 35 L/min in trained athletes

• What’s the resting CO in athletes?


Cardiac Output (CO)

•Why do athletes have a low HR? (bradycardia)


Regulation of Stroke Volume

• SV = EDV – ESV

• Three main factors affect SV

• Preload

• Contractility

• Afterload



• Preload: degree of stretch of cardiac muscle cells before they contract (Frank-Starling law of the heart)

• Cardiac muscle exhibits a length-tension relationship

• At rest, cardiac muscle cells are shorter than optimal length

• Slow heartbeat and exercise increase venous return

• Increased venous return ( ) stretches the ventricles and increases contraction force (SNAP!)


Regulation of Stroke Volume• Contractility: contractile strength at a given muscle

length, independent of muscle stretch and EDV

• Dependent on the activity of the sympathetic NS

• Positive inotropic agents increase contractility• Increased Ca2+ influx due to sympathetic stimulation

• Hormones (thyroxine, glucagon, and epinephrine)

• Negative inotropic agents decrease contractility• Acidosis

• Increased extracellular K+

• Calcium channel blockers



• Afterload: pressure that must be overcome for ventricles to eject blood

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

• What else could increase afterload?


Autonomic Nervous System Regulation

• 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)


Autonomic Nervous System Regulation

• The parasympathetic nervous system opposes sympathetic effects

• Acetylcholine hyperpolarizes pacemaker cells by opening K+ channels

• The heart at rest exhibits parasympathetic tone; it is slowed down to 70-80 bpm from 100 bpm.


Venousreturn Contractility Sympathetic

activityParasympathetic

activity

EDV(preload)

Strokevolume

Heartrate

Cardiacoutput

ESV

Exercise (byskeletal muscle andrespiratory pumps;

see Chapter 19)

Heart rate(allows more

time forventricular

filling)

Bloodborneepinephrine,

thyroxine,excess Ca2+

Exercise,fright, anxiety

Initial stimulus

ResultPhysiological response


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


Other Factors that Influence Heart Rate

• Age

• Gender

• Exercise

• Body temperature


Homeostatic Imbalances

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

• If persistent, may lead to fibrillation

• Bradycardia: heart rate < 60 bpm

• May result in grossly inadequate blood circulation

• May be a desirable result of endurance training


Congestive Heart Failure (CHF)

• Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs

• Some possible causes of this condition:

• Coronary atherosclerosis

• Persistent high blood pressure

• Multiple myocardial infarcts

marieb chapter 18 part b: the heart

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