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

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

Cardiac Membrane PotentialCardiac Membrane Potential

Figure 18.12

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)

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

Cardiac Intrinsic ConductionCardiac Intrinsic Conduction

Figure 18.14a

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

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

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

Heart SoundsHeart Sounds

Figure 18.19

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

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

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

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

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

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

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)

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

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

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

Preload and AfterloadPreload and Afterload

Figure 18.21

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

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

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

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

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

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

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)

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)

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

Examples of Congenital Heart Examples of Congenital Heart DefectsDefects

Figure 18.25

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