2402 lecture02 ch 18 heart
TRANSCRIPT
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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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Electrocardiogram Tracings
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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Electrocardiogram Tracings
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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Electrocardiogram Tracings
Figure 18.18
Ventricular Fibrillation Chaotic grossly irregular ECG deflections as seen in
acute heart attack and electrical shock
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Electrocardiogram Tracings
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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Phases of the Cardiac Cycle:
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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Phases of the Cardiac Cycle:
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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