2402 Lecture02 Ch 18 Heart

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Anatomy & Physiology II -2402

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Heart Physiology:

Intrinsic Conduction System

Autorhythmic cells: Initiate action potentials

Have unstable resting potentials called pacemakerpotentials

Use calcium influx (rather than sodium) for rising phase of

the action potential

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Cardiac Muscle Contraction

Heart muscle: Is stimulated by nerves and is self-excitable

(automaticity)

Contracts as a unit Has a long (250 ms) absolute refractory period

Cardiac muscle contraction is similar toskeletal muscle contraction

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Heart Physiology:

Sequence of Excitation

Sinoatrial (SA) node generates impulses about 75times/minute

Atrioventricular (AV) node delays the impulseapproximately 0.1 second

Impulsepasses from atria to ventricles via theatrioventricular bundle (bundle of His)

AV bundle splits into two pathways in the interventricularseptum (bundle branches)

Bundle branches carry the impulse toward the apexof the heart

Purkinje fibers carry the impulse to the heart apexand ventricular walls

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Cardiac Intrinsic Conduction

Figure 18.14a

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Action Potential Sequence in the Heart

1

2

3

4

Conducting System of the Heart
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Conduction System & Action Potential

One Heart Beat

1. Pacemaker potential produced by the SA node

2. Action potential as is goes through the atrial muscle

3. Action potential as is passes through the AV node

4. Action potential of the contractile cardiac cells of the ventricles

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Extrinsic Innervation

of the Heart

Heart is stimulated by the

sympatheticcardioacceleratory center

Heart is inhibited by the

parasympatheticcardioinhibitory center

Figure 18.15

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Electrocardiography

Figure 18.16

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Electrocardiography

Electrical activity is recorded by electrocardiogram (ECG)

P wave corresponds to depolarization ofSA node

QRS complex corresponds to ventricular depolarization

T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the largerQRS

complex

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Heart Excitation Related to ECG

SA node generates impulse;atrial excitation begins

Impulse delayedat AV node

Impulse passes toheart apex; ventricular

excitation beginsVentricular excitation

complete

SA node AV nodePurkinj

efibers

Bundlebranches

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ECG Tracings

Figure 18.18

Normal Sinus Rhythm Second Degree Heart Block

Junctional Rhythm Ventricular Fibrillation

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Electrocardiogram Tracings

Normal Sinus Rhythm

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Junctional Rhythm (Nodal Rhythm) The SA node is nonfunctional

P waves are absent

Heart rate is paced by the AV node, 40-60 beats/min

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Second Degree Heart Block Some P waves areNOTconducted through the AV

node consequently more P waves than QRS wavesare present.

Ratio of P waves to QRS waves is 2:1

PPPP

QRS QRSQRS

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Figure 18.18

Ventricular Fibrillation Chaotic grossly irregular ECG deflections as seen in

acute heart attack and electrical shock

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Atrial Fibrillation

Atrial fibrillation is an abnormal heart rhythmoriginating in the atria. This causes a rapid anddisorganized heartbeat.
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Heart Sounds Sounds produced by the heart LUBB-dupp

First heart sound orLUBB

LUBB sound is created by the closure of the AV valves

Second heart sound ordupp

dupp sound is created by the closure of the aortic andpulmonary semilunar valves at the beginning of theventricular diastole, lasts longer.

Third heart sound (occasional)

Caused by turbulent blood flow into ventricles anddetected near end of first one-third of diastole.

Peculiar or abnormal heart sounds are called murmurs.

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Mechanical Events of the Cardiac Cycle

Cardiac cycle refers to all events associated with blood flowthrough the heart during one complete heartbeat

Systole contractionof heart muscle

Diastole relaxationof heart muscle

Heart Beats ~ 75 times per minute

Complete Cardiac Cycle = 0.8 seconds

Mechanical events always follow the electrical events as seen

in the ECG

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Figure 18.20

Summary

of Events

Cardiac

Cycle

(End of Systolic Vol)

(End of Dystolic Vol)

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Phases of the Cardiac Cycle:

1. Ventricular filling mid-to-late diastole

Ventricular filling mid-to-late diastole

Heart blood pressure

is low as blood enters

atria and flows intoventricles

AV valves are open,then atrial systole

occurs

Ph f th C di C l

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2. Ventricular systole

Ventricular systole

Atria relax

Rising ventricular

pressure results inclosing of AV valves

Isovolumetriccontraction phase

Ventricular ejectionphase opens semilunarvalves

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3. Isovolumetric relaxation

Isovolumetric relaxation early diastole

Ventricles relax

Backflow of blood inaorta and pulmonary

trunk closes semilunar

valves

Dicrotic notch brief risein aortic pressure caused

by backflow of blood

rebounding off semilunar

valves

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Cardiac Output (CO) and Reserve

CO is the amount of blood pumped by each ventricle in one minute

CO is the product of heart rate (HR) and stroke volume (SV)

HR is the number of heart beats per minute

SV is the amount of blood pumped out by a ventricle with each beat

Cardiac Output (ml/min) =

Heart Rate (75 beats/min) x Stroke Volume (70 ml/beat)

Cardiac Output = 5250 ml/min (5.25 L/min)

Cardiac reserve is the difference between resting and maximal CO

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Regulation of Stroke Volume

Stroke Volume = End diastolic volume (EDV) minus Endsystolic volume (ESV)

EDV = amount of

blood collectedin a ventricleduring diastole

ESV = amount ofblood remainingin a ventricleafter contraction

(End of Systolic Vol)

(End of Dystolic Vol)

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Factors Affecting Stroke Volume

Preload amount ventricles are stretched by containedblood

Contractility cardiac cell contractile force due to factorsother than EDV

Afterload back pressure exerted by blood in the largearteries leaving the heart

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Preload and Afterload

Figure 18.21

Preload is proportional to the amount of ventricular myocardial fiberstretchjust before systole.

Afterload is the pressure that the ventricles must overcome to forceopen the aortic and pulmonary valves.

Direction ventricularwalls are moving.

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Frank-Starling Law of the Heart

is the relationship between Preload and Stroke Volume

Preload, or degree of stretch of cardiac muscle cells beforethey contract is the critical factor controlling stroke volume

Slow heartbeat and exerciseincrease venous return tothe heart, increasing SV

Blood loss and extremely rapid heartbeat decrease SV

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Intrinsic & Extrinsic Factors & Contractility

End diastolic volume (EDV) is the majorintrinsic factorinfluencing Stroke Volume

Extrinsic factors can also influence Stroke Volume

E t i i F t I fl i St k V l

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Extrinsic Factors Influencing Stroke Volume

Contractility is the increase in contractile strength,

independent of stretch and EDV Increase in contractility comes from:

Increased sympathetic stimuli

Certain hormones positive inotropic agents

Ca2+ and some drugs (increase contractility)

Agents/factors that decrease contractility include:

Acidosis (high [H+

] low pH) Increased extracellular K+ negative inotropic agents

Calcium channel blockers (decrease contractility)

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Sympathetic nervous system (SNS) stimulation isactivated by stress, anxiety, excitement, or exercise

Parasympathetic nervous system (PNS) stimulation ismediated by acetylcholine and opposes the SNS

PNS dominates the autonomic stimulation, slowing heartrate and causing vagal tone (inhibition of the heartbeat)

Regulation of Heart RateAutonomic Nervous System

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Chemical Regulation of the Heart

The hormones epinephrine and thyroxine increaseheart rate

Intracellular & extracellular ion concentrations must be

maintained for normal heart function

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Figure 18.23

FactorsInvolved in

the Regulation

of CardiacOutput

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Congestive Heart Failure (CHF)

Congestive heart failure (CHF) is caused by:

Coronary atherosclerosis

Persistent high blood pressure

Multiple myocardial infarcts Dilated cardiomyopathy (DCM)

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Developmental Aspects of the Heart

Fetal heart structures that bypass pulmonary circulation

Foramen ovale connects the two atria

Ductus arteriosus connects pulmonary trunk & the aorta

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2402 Lecture02 Ch 18 Heart