Cardiac Muscle Contraction
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Cardiac Muscle ContractionCardiac Muscle Contraction
Heart muscle:Heart muscle: Is stimulated by nerves and is self-excitable Is stimulated by nerves and is self-excitable
(automaticity)(automaticity) Contracts as a unitContracts as a unit Has a long (250 ms) absolute refractory periodHas a long (250 ms) absolute refractory period
Cardiac muscle contraction is similar to Cardiac muscle contraction is similar to skeletal muscle contractionskeletal muscle contraction
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Heart Physiology: Intrinsic Heart Physiology: Intrinsic Conduction SystemConduction System
Autorhythmic cells:Autorhythmic cells: Initiate action potentials Initiate action potentials Have unstable resting potentials called pacemaker Have unstable resting potentials called pacemaker
potentialspotentials Use calcium influx (rather than sodium) for rising Use calcium influx (rather than sodium) for rising
phase of the action potentialphase of the action potential
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Cardiac Membrane PotentialCardiac Membrane Potential
Figure 18.12
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Heart Physiology: Sequence of Heart Physiology: Sequence of ExcitationExcitation
Sinoatrial (SA) node generates impulses about Sinoatrial (SA) node generates impulses about 75 times/minute75 times/minute
Atrioventricular (AV) node delays the impulse Atrioventricular (AV) node delays the impulse approximately 0.1 secondapproximately 0.1 second
Impulse passes from atria to ventricles via the Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)atrioventricular bundle (bundle of His)
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Heart Physiology: Sequence of Heart Physiology: Sequence of ExcitationExcitation
AV bundle splits into two pathways in the AV bundle splits into two pathways in the interventricular septum (bundle branches)interventricular septum (bundle branches) Bundle branches carry the impulse toward the apex Bundle branches carry the impulse toward the apex
of the heartof the heart Purkinje fibers carry the impulse to the heart apex Purkinje fibers carry the impulse to the heart apex
and ventricular wallsand ventricular walls
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Cardiac Intrinsic ConductionCardiac Intrinsic Conduction
Figure 18.14a
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SA node generates impulse;atrial excitation begins
Impulse delayedat AV node
Impulse passes toheart apex; ventricular
excitation begins
Ventricular excitationcomplete
SA node AV node Purkinjefibers
Bundlebranches
Figure 18.17
Heart Excitation Related to ECGHeart Excitation Related to ECG
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Extrinsic Innervation of the Extrinsic Innervation of the HeartHeart
Heart is stimulated Heart is stimulated by the sympathetic by the sympathetic cardioacceleratory cardioacceleratory center center
Heart is inhibited by Heart is inhibited by the parasympathetic the parasympathetic cardioinhibitory cardioinhibitory centercenter
Figure 18.15
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ElectrocardiographyElectrocardiography
Electrical activity is recorded by Electrical activity is recorded by electrocardiogram (ECG)electrocardiogram (ECG)
P wave corresponds to depolarization of SA nodeP wave corresponds to depolarization of SA node QRS complex corresponds to ventricular QRS complex corresponds to ventricular
depolarizationdepolarization T wave corresponds to ventricular repolarizationT wave corresponds to ventricular repolarization Atrial repolarization record is masked by the Atrial repolarization record is masked by the
larger QRS complexlarger QRS complex
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Heart SoundsHeart Sounds
Figure 18.19
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Heart SoundsHeart Sounds
Heart sounds (lub-dup) are associated with Heart sounds (lub-dup) are associated with closing of heart valvesclosing of heart valves First sound occurs as AV valves close and First sound occurs as AV valves close and
signifies beginning of systolesignifies beginning of systole Second sound occurs when SL valves close at the Second sound occurs when SL valves close at the
beginning of ventricular diastolebeginning of ventricular diastole
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Cardiac CycleCardiac Cycle
Cardiac cycle refers to all events associated Cardiac cycle refers to all events associated with blood flow through the heartwith blood flow through the heart Systole – contraction of heart muscleSystole – contraction of heart muscle Diastole – relaxation of heart muscleDiastole – relaxation of heart muscle
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Phases of the Cardiac CyclePhases of the Cardiac Cycle
Ventricular filling – mid-to-late diastoleVentricular filling – mid-to-late diastole Heart blood pressure is low as blood enters atria Heart blood pressure is low as blood enters atria
and flows into ventriclesand flows into ventricles AV valves are open, then atrial systole occursAV valves are open, then atrial systole occurs
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Phases of the Cardiac CyclePhases of the Cardiac Cycle
Ventricular systoleVentricular systole Atria relax Atria relax Rising ventricular pressure results in closing of Rising ventricular pressure results in closing of
AV valvesAV valves Ventricular ejection phase opens semilunar valvesVentricular ejection phase opens semilunar valves
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Phases of the Cardiac CyclePhases of the Cardiac Cycle
Isovolumetric relaxation – early diastoleIsovolumetric relaxation – early diastole Ventricles relaxVentricles relax Backflow of blood in aorta and pulmonary trunk Backflow of blood in aorta and pulmonary trunk
closes semilunar valvescloses semilunar valves Dicrotic notch – brief rise in aortic pressure Dicrotic notch – brief rise in aortic pressure
caused by backflow of blood rebounding off caused by backflow of blood rebounding off semilunar valvessemilunar valves
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Cardiac Output (CO) and Cardiac Output (CO) and ReserveReserve
CO is the amount of blood pumped by each CO is the amount of blood pumped by each ventricle in one minuteventricle in one minute
CO is the product of heart rate (HR) and stroke CO is the product of heart rate (HR) and stroke volume (SV)volume (SV)
HR is the number of heart beats per minuteHR is the number of heart beats per minute SV is the amount of blood pumped out by a SV is the amount of blood pumped out by a
ventricle with each beatventricle with each beat Cardiac reserve is the difference between Cardiac reserve is the difference between
resting and maximal COresting and maximal CO
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Cardiac Output: ExampleCardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70 CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)ml/beat)
CO = 5250 ml/min (5.25 L/min)CO = 5250 ml/min (5.25 L/min)
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Regulation of Stroke VolumeRegulation of Stroke Volume
Defined as the amount of blood pumped out of Defined as the amount of blood pumped out of one ventricle in a single beat.one ventricle in a single beat.
SV = end diastolic volume (EDV) minus end SV = end diastolic volume (EDV) minus end systolic volume (ESV)systolic volume (ESV)
EDV = amount of blood collected in a EDV = amount of blood collected in a ventricle during diastoleventricle during diastole
ESV = amount of blood remaining in a ESV = amount of blood remaining in a ventricle after contractionventricle after contraction
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Factors Affecting Stroke VolumeFactors Affecting Stroke Volume
Preload – amount ventricles are stretched by Preload – amount ventricles are stretched by contained blood contained blood
Contractility – cardiac cell contractile force Contractility – cardiac cell contractile force due to factors other than EDVdue to factors other than EDV
Afterload – back pressure exerted by blood in Afterload – back pressure exerted by blood in the large arteries leaving the heartthe large arteries leaving the heart
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Frank-Starling Law of the HeartFrank-Starling Law of the Heart
Preload, or degree of stretch, of cardiac muscle Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor cells before they contract is the critical factor controlling stroke volumecontrolling stroke volume
Slow heartbeat and exercise increase venous Slow heartbeat and exercise increase venous return to the heart, increasing SVreturn to the heart, increasing SV
Blood loss and extremely rapid heartbeat Blood loss and extremely rapid heartbeat decrease SVdecrease SV
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Preload and AfterloadPreload and Afterload
Figure 18.21
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Extrinsic Factors Influencing Extrinsic Factors Influencing Stroke VolumeStroke Volume
Contractility is the increase in contractile Contractility is the increase in contractile strength, independent of stretch and EDVstrength, independent of stretch and EDV
Increase in contractility comes from: Increase in contractility comes from: Increased sympathetic stimuliIncreased sympathetic stimuli Certain hormonesCertain hormones CaCa2+2+ and some drugs and some drugs
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Extrinsic Factors Influencing Extrinsic Factors Influencing Stroke VolumeStroke Volume
Agents/factors that decrease contractility Agents/factors that decrease contractility include:include: AcidosisAcidosis Increased extracellular KIncreased extracellular K++
Calcium channel blockersCalcium channel blockers
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Regulation of Heart RateRegulation of Heart Rate
Positive chronotropic (affects rate or timing) Positive chronotropic (affects rate or timing) factors increase heart ratefactors increase heart rate
Negative chronotropic factors decrease heart Negative chronotropic factors decrease heart raterate
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Sympathetic nervous system (SNS) stimulation is Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation is Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone (used to describe the heart rate and causing vagal tone (used to describe the vagus nerve’s involvement of the inhibition of heart vagus nerve’s involvement of the inhibition of heart beat)beat)
Regulation of Heart Rate: Regulation of Heart Rate: Autonomic Nervous SystemAutonomic Nervous System
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Atrial (Bainbridge) ReflexAtrial (Bainbridge) Reflex
Atrial (Bainbridge) reflex – a sympathetic Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atriareflex initiated by increased blood in the atria Causes stimulation of the SA nodeCauses stimulation of the SA node Stimulates baroreceptors (senses changes in Stimulates baroreceptors (senses changes in
pressure) in the atria, causing increased SNS pressure) in the atria, causing increased SNS stimulationstimulation
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Chemical Regulation of the Chemical Regulation of the HeartHeart
The hormones epinephrine and thyroxine The hormones epinephrine and thyroxine increase heart rateincrease heart rate
Intra- and extracellular ion concentrations Intra- and extracellular ion concentrations must be maintained for normal heart functionmust be maintained for normal heart function
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Congestive Heart Failure (CHF)Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is caused by:Congestive heart failure (CHF) is caused by: Coronary atherosclerosisCoronary atherosclerosis Persistent high blood pressurePersistent high blood pressure Multiple myocardial infarctsMultiple myocardial infarcts Dilated cardiomyopathy (DCM) Dilated cardiomyopathy (DCM)
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Developmental Aspects of the Developmental Aspects of the HeartHeart
Embryonic heart chambersEmbryonic heart chambers Sinus venousSinus venous AtriumAtrium VentricleVentricle Bulbus cordis (part of the primitive ventricle, Bulbus cordis (part of the primitive ventricle,
eventually forms ventricle)eventually forms ventricle)
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Developmental Aspects of the Developmental Aspects of the HeartHeart
Fetal heart structures that bypass pulmonary Fetal heart structures that bypass pulmonary circulationcirculation Foramen ovale connects the two atriaForamen ovale connects the two atria Ductus arteriosus connects pulmonary trunk and Ductus arteriosus connects pulmonary trunk and
the aortathe aorta
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Examples of Congenital Heart Examples of Congenital Heart DefectsDefects
Figure 18.25
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Age-Related Changes Affecting Age-Related Changes Affecting the Heartthe Heart
Sclerosis and thickening of valve flapsSclerosis and thickening of valve flaps Decline in cardiac reserveDecline in cardiac reserve Fibrosis of cardiac muscleFibrosis of cardiac muscle AtherosclerosisAtherosclerosis