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Cardiac PhysiologyCardiac Physiology

Anatomy of the heartAnatomy of the heart

LocationLocation: :

Within mediastinun of medial cavity of thorax, Within mediastinun of medial cavity of thorax, anterior to vertebral column, posterior to sternum, anterior to vertebral column, posterior to sternum, superior to diaphragm (at rest), superior margin superior to diaphragm (at rest), superior margin (2nd rib), inferior margin (5th intercostal space), (2nd rib), inferior margin (5th intercostal space), 60% of mass to the left of midline, base (posterior 60% of mass to the left of midline, base (posterior surface) faces right shoulder, apex points inferiorly surface) faces right shoulder, apex points inferiorly toward left hip (contacts chest wall between 5th toward left hip (contacts chest wall between 5th and 6th ribs & PMI-point of maximum intensity)and 6th ribs & PMI-point of maximum intensity)

PericardiumPericardium

1. Fibrous pericardium: Tense connective tissue, 1. Fibrous pericardium: Tense connective tissue, protects heart, anchors heart to surrounding protects heart, anchors heart to surrounding tissues, prevents over fillingtissues, prevents over filling

2. Serous pericardium: Parietal layer (Internal 2. Serous pericardium: Parietal layer (Internal surface of fibrous pericardium), Visceral layer surface of fibrous pericardium), Visceral layer (epicardium: part of heart wall)(epicardium: part of heart wall)

3. Pericardial cavity: Between serous layers, fluid 3. Pericardial cavity: Between serous layers, fluid filled to reduces friction between serous membr.sfilled to reduces friction between serous membr.s

Layers of the heart Layers of the heart

1. Three layers1. Three layers

a. Epicardium a. Epicardium

b. Middle myocardiumb. Middle myocardium

c. Deep endocardiumc. Deep endocardium

Myocardium:Myocardium:

a. Cardiac muscle arranged in circular bundlesa. Cardiac muscle arranged in circular bundles

b. Fibrous skeleton: Holds cardiac muscle togetherb. Fibrous skeleton: Holds cardiac muscle together

Endocardium:Endocardium:

a. Inner myocardial surfacea. Inner myocardial surface

b. Lines heart & connective tissues of valvesb. Lines heart & connective tissues of valves

c. Squamous epitheliumc. Squamous epithelium

Chambers of the HeartChambers of the Heart

Four chambers: Two atria & two ventricles, heart Four chambers: Two atria & two ventricles, heart is divided longitudinally: Interatrial & interventr-is divided longitudinally: Interatrial & interventr-icular septa, atria receive returning blood (i.e., icular septa, atria receive returning blood (i.e., veins), auricles are appendages to increase atrial veins), auricles are appendages to increase atrial volume, fossa ovalis is residual impression of fetal volume, fossa ovalis is residual impression of fetal foramen ovaleforamen ovale

Veins of right atrium: Veins of right atrium:

a. Superior vena cava: Return flow from regions a. Superior vena cava: Return flow from regions superior to diaphragmsuperior to diaphragm

b. Inferior vena cava: Return flow from regions b. Inferior vena cava: Return flow from regions inferior to diaphragminferior to diaphragm

c. Coronary sinus: Drain blood from myocardiumc. Coronary sinus: Drain blood from myocardium

Veins of left atriumVeins of left atrium

Four pulmonary veins: Lungs back to heart, most Four pulmonary veins: Lungs back to heart, most of the posterior surface of the heartof the posterior surface of the heart

Ventricles: Ventricles: 1.1. Blood leaving the heart, Blood leaving the heart, 2.2. Most of Most of mass of heart, right: anterior surface, left: inferior mass of heart, right: anterior surface, left: inferior surface, surface, 3.3. Muscles: Trabeculae carneae (cross- Muscles: Trabeculae carneae (cross-bars), papillary muscles (valve function, project bars), papillary muscles (valve function, project into heart cavity), into heart cavity), 4.4. Pulmonary trunk: Right Pulmonary trunk: Right ventricle, routes blood to lungs, ventricle, routes blood to lungs, 5.5. Aorta: Left Aorta: Left ventricle, systemic circulationventricle, systemic circulation

Blood Flow Through the HeartBlood Flow Through the Heart

Two circuits: Two circuits: 1. Pulmonary: 1. Pulmonary: Right side of the heartRight side of the heart

a. Blood to lungs for gas exchangea. Blood to lungs for gas exchange

b. Right ventricle to left atrium of the heart b. Right ventricle to left atrium of the heart

c. Blood returns from body to right atrium, low O2 c. Blood returns from body to right atrium, low O2 concentration, relatively high CO2 concentrationconcentration, relatively high CO2 concentration

d. Rt. Atrium to right ventricled. Rt. Atrium to right ventricle

e. Rt. Ventricle to lungs: Take O2 & give CO2, e. Rt. Ventricle to lungs: Take O2 & give CO2, pulmonary arteries (away from heart, not CO2)pulmonary arteries (away from heart, not CO2)

f. Lungs to left atrium: Pulmonary veins, O2 rich f. Lungs to left atrium: Pulmonary veins, O2 rich

2. Systemic:2. Systemic: left side of the heart left side of the heart

a. Left atrium to left ventriclea. Left atrium to left ventricle

b. Left ventricle into aortab. Left ventricle into aorta

c. Aorta to body through systemic arteries: Gases c. Aorta to body through systemic arteries: Gases and nutrients are exchangedand nutrients are exchanged

d. Systemic veins to right atriumd. Systemic veins to right atrium

3. Work loads3. Work loads

a. Equal volumesa. Equal volumesb. Unequal work loadsb. Unequal work loads

c. Systemic: Five times as much resistance to blood c. Systemic: Five times as much resistance to blood flow, longer routeflow, longer route

d. Left ventricle is much larger & thicker to do d. Left ventricle is much larger & thicker to do more workmore work

Heart ValvesHeart Valves

A.A. Atrioventricular (AV) valves Atrioventricular (AV) valves11 . .Valves at atrium-ventricular junctionValves at atrium-ventricular junction

22 . .Prevent backflow into atriaPrevent backflow into atria33 . .Closed during ventricular contraction (systole)Closed during ventricular contraction (systole)

B.B. Right AV valve: tricuspid: Three cusps Right AV valve: tricuspid: Three cusps (reinforced endocardium)(reinforced endocardium)

C.C. Left AV valve:Bicuspid:Mitral valve:Two cusps Left AV valve:Bicuspid:Mitral valve:Two cuspsD.D. Chordae tendineae (heart strings): Collagen Chordae tendineae (heart strings): Collagen cords attached to cusps, anchor cusps to papillary cords attached to cusps, anchor cusps to papillary muscles during ventricular contraction, intraventr-muscles during ventricular contraction, intraventr-icular pressure rises forces blood against valve icular pressure rises forces blood against valve flaps, chordae tendinea anchor flaps in closed flaps, chordae tendinea anchor flaps in closed postionpostion

E.E. Semilunar (SL) valves: Two: Semilunar (SL) valves: Two: AorticAortic: Between : Between left ventricle & aorta & left ventricle & aorta & pulmonarypulmonary:Between right :Between right ventricle & pulmonary trunk. Open during ventr-ventricle & pulmonary trunk. Open during ventr-icular contraction (systole): Intraventricular press-icular contraction (systole): Intraventricular press-ure exceeds BP in aorta & pulmonary trunk. Three ure exceeds BP in aorta & pulmonary trunk. Three

crescent shaped cusps open against arterial wallscrescent shaped cusps open against arterial walls . .F.F. No valves between atria & venae cavae & pulm- No valves between atria & venae cavae & pulm-onary veins . Atrial contraction compresses venous onary veins . Atrial contraction compresses venous entry pointsentry points

Blood Flow to the HeartBlood Flow to the Heart

Heart requires its own circulatory system. Myocar-Heart requires its own circulatory system. Myocar-dium is too thick to permit diffusion. Coronary cir-dium is too thick to permit diffusion. Coronary cir-culation: Arterial supply: culation: Arterial supply: Right & left coronary Right & left coronary arteriesarteries (arise at base of aorta). (arise at base of aorta). LeftLeft: (supplies left : (supplies left side of heart by marginal branches: anterior inter-side of heart by marginal branches: anterior inter-ventricular & circumflex arteries). ventricular & circumflex arteries). Right:Right: (supplies (supplies right side of heart: Marginal & posterior interven-right side of heart: Marginal & posterior interven-tricular arteries). tricular arteries). Anastomoses: Collateral routes Anastomoses: Collateral routes of blood flow. of blood flow. Flow occurs only during diastole.Flow occurs only during diastole.

Cardiac veins: Cardiac veins: Follow course of coronary arteries, Follow course of coronary arteries, join to form coronary sinus to empty into right join to form coronary sinus to empty into right atrium. Tributaries: Great, middle & small cardiac atrium. Tributaries: Great, middle & small cardiac veins. veins. Anterior cardiac veins empty directly into Anterior cardiac veins empty directly into right atrium.right atrium.

PathologyPathology

Angina pectorisAngina pectoris: Temporary deficient blood flow to : Temporary deficient blood flow to myocardium, thoracic pain is symptommyocardium, thoracic pain is symptomMyocardial infarction (MI)Myocardial infarction (MI): Heart attack, Cardiac : Heart attack, Cardiac cells are amitotic, O2 deficiency causes necrosis cells are amitotic, O2 deficiency causes necrosis (cell death), dead cells are replaced by noncontra-(cell death), dead cells are replaced by noncontra-ctile scar tissue. ctile scar tissue.

Cardiac MuscleCardiac Muscle

CharacteristicsCharacteristics1. Branched, short, and interconnected fibers1. Branched, short, and interconnected fibers2. Striated2. Striated3. Cardiac muscle fibers are functionally connected3. Cardiac muscle fibers are functionally connected(intercalated discs, desmosomes, electrical coupling (intercalated discs, desmosomes, electrical coupling via gap junctions)via gap junctions)4. Functional syncytium: Entire myocardium acts 4. Functional syncytium: Entire myocardium acts as a single unit (result of gap junctions)as a single unit (result of gap junctions)

ContractionContraction1. All cardiac muscle cells contract as a single unit1. All cardiac muscle cells contract as a single unit2. Self-excitable (2. Self-excitable (i.e.,i.e., autorhytmic): Initiate APs, autorhytmic): Initiate APs, independent of nervous innervationindependent of nervous innervation3. Long refractory period: No tetanic contractions3. Long refractory period: No tetanic contractions

Autorhythmic fibers: Pace maker cells: 1% of Autorhythmic fibers: Pace maker cells: 1% of heart muscle, depolarize spontaneouslyheart muscle, depolarize spontaneouslyContractile muscle fibers: Depolarize in response Contractile muscle fibers: Depolarize in response to pacemaker cell activitiesto pacemaker cell activities

Heart PhysiologyHeart Physiology

Intrinsic conduction system: Noncontractile card-Intrinsic conduction system: Noncontractile card-iac cells that initiate & distribute impulses from iac cells that initiate & distribute impulses from atria to ventricles. Autorhythmic, unstable RMP: atria to ventricles. Autorhythmic, unstable RMP: Drift towards threshold. Pacemaker potentials: Drift towards threshold. Pacemaker potentials: Membrane potential changes spontaneouslyMembrane potential changes spontaneously

EventsEvents: Na+ influx (slow) offset by K: Na+ influx (slow) offset by K++ efflux (slow), efflux (slow), KK++ permeability gradually decreases, Influx of Na permeability gradually decreases, Influx of Na++ depolarizes cardiac cells, Depolarization opens fast depolarizes cardiac cells, Depolarization opens fast CaCa2+2+ channels, Ca channels, Ca2+2+ influx from ECS causes rising influx from ECS causes rising phase of AP, Repolarization increases Kphase of AP, Repolarization increases K++ permeab- permeab-ility (cardiac cells repolarize), Kility (cardiac cells repolarize), K++ channels channels inactivate, Cycle starts againinactivate, Cycle starts again

Location of autorhythmic cellsLocation of autorhythmic cells 1.1. Sinoatrial (SA) node: Pacemaker: Fastest rate of Sinoatrial (SA) node: Pacemaker: Fastest rate of depolarization, characteristic (sinus) rhythm. depolarization, characteristic (sinus) rhythm. Located in right atrial wall, after depolarization is Located in right atrial wall, after depolarization is initiated, depolarization wave sweeps via gap initiated, depolarization wave sweeps via gap junctions throughout atriajunctions throughout atria

2.2.Atrioventricular (AV) node: Depolarization wave Atrioventricular (AV) node: Depolarization wave initiated by SA node reaches AV node, AV node is initiated by SA node reaches AV node, AV node is located in interatrial septum near tricuspid valve, located in interatrial septum near tricuspid valve, dia. of fibers is smaller (slows impulse conduction dia. of fibers is smaller (slows impulse conduction ‘0.1 s’ & permits completion of atrial contraction), ‘0.1 s’ & permits completion of atrial contraction), impulse passes to bundle of Hisimpulse passes to bundle of His

3.3. Atrioventricular bundle (of His): Functional Atrioventricular bundle (of His): Functional passage of impulse from atria to ventricles (no gap passage of impulse from atria to ventricles (no gap junctions between cells in atria & ventricles), junctions between cells in atria & ventricles), Located in inferior interatrial septum, very short Located in inferior interatrial septum, very short (branches to form bundle branches)(branches to form bundle branches)4.4. Bundle branches: Course interventricular Bundle branches: Course interventricular septum toward apex of heartseptum toward apex of heart

5.5. Purkinje fibers: Reach apex then branch super- Purkinje fibers: Reach apex then branch super-iorly into ventricular walls, impulses in fibers iorly into ventricular walls, impulses in fibers moves faster than cell to cell contact (ensures moves faster than cell to cell contact (ensures greater pumping efficacy)greater pumping efficacy)

Pathology of Intrinsic Conductance SystemPathology of Intrinsic Conductance System

Arrhythmias: Uncoordinated contractions B. Arrhythmias: Uncoordinated contractions B. Fibrillation: Rapid, irregular contractionsFibrillation: Rapid, irregular contractionsEctopic focus: Excitable tissue other than SA node Ectopic focus: Excitable tissue other than SA node controls heart contractionscontrols heart contractionsHeart block: Damage to AV node: Impulse cannot Heart block: Damage to AV node: Impulse cannot reach ventriclesreach ventricles

Extrinsic Control of the HeartExtrinsic Control of the Heart

Brain-based control Brain-based control 1. Cardioaccelatory center in medulla, sympathetic 1. Cardioaccelatory center in medulla, sympathetic NS control, innervate SA and AV nodesNS control, innervate SA and AV nodes2.Cardioinhibitory center, X nerve, parasympathe-2.Cardioinhibitory center, X nerve, parasympathe-tic system, innervate SA & AV nodes, slows HR tic system, innervate SA & AV nodes, slows HR

ElectrocardiographyElectrocardiography

Electrical changes during heart activity (ECG): Electrical changes during heart activity (ECG): Deflection wavesDeflection waves1.1. P wave: Depolarization moving from SA node P wave: Depolarization moving from SA node through atriathrough atria2.2. QRS complex: Ventricular depolarization: QRS complex: Ventricular depolarization: Precedes contractionPrecedes contraction3.3. T wave: Ventr. repolarization, occurs slower T wave: Ventr. repolarization, occurs slower than depolarization: more spread out than QRSthan depolarization: more spread out than QRS

IntervalsIntervals1.1. P-R: Interval from beginning of atrial excitation P-R: Interval from beginning of atrial excitation &ventricular excitation, (includes: atrial depolariz-&ventricular excitation, (includes: atrial depolariz-ation & contraction, passage of impulse through ation & contraction, passage of impulse through intrinsic conduction system), lasts 0.16 sintrinsic conduction system), lasts 0.16 s2.2. Q-T: Ventricular depolarization through repola- Q-T: Ventricular depolarization through repola-rization, includes: time of ventricular contractionrization, includes: time of ventricular contraction

Mechanical Events during Heart ContractionMechanical Events during Heart Contraction

Cardiac cycleCardiac cycleSystole (contraction) & diastole (relaxation), Systole (contraction) & diastole (relaxation), Length: Total 0.8 s, atrial systole 0.1 s, ventricular Length: Total 0.8 s, atrial systole 0.1 s, ventricular systole 0.3 s & quiescent period 0.4 s systole 0.3 s & quiescent period 0.4 s

EventsEvents 1.1. Start point: Atria & ventricles are relaxed (mid- Start point: Atria & ventricles are relaxed (mid-to-late diastole)to-late diastole)2.2. Ventricular filling: Mid-to-late diastole, AV Ventricular filling: Mid-to-late diastole, AV valves are open, semilunar valves are closed, vent-valves are open, semilunar valves are closed, vent-ricles begin to fill (70% occurs prior to atrial cont-ricles begin to fill (70% occurs prior to atrial cont-raction), atrial systole (atria contract “preceded by raction), atrial systole (atria contract “preceded by P wave”, increased atrial pressure propels Bd from P wave”, increased atrial pressure propels Bd from atria into ventricles), atria relax & ventricles atria into ventricles), atria relax & ventricles depolarize (QRS wave)depolarize (QRS wave)

3.3. Ventricular systole: As contraction begins, intra- Ventricular systole: As contraction begins, intra-ventricular BP increase(AV valves close, semilunar ventricular BP increase(AV valves close, semilunar valves closed),isovolumetric contraction phase“vol-valves closed),isovolumetric contraction phase“vol-ume constant” (BP in aorta&pulm. trunk exceeds ume constant” (BP in aorta&pulm. trunk exceeds intraventricular pressure, pr. in ven. increases intraventricular pressure, pr. in ven. increases without volume changing), ven. ejection phase without volume changing), ven. ejection phase (intraventr. pressure exceeds pressure in large (intraventr. pressure exceeds pressure in large vessels, semilunar valves open, Bd is propelled out vessels, semilunar valves open, Bd is propelled out of ventricles) & atria begin to fill with bloodof ventricles) & atria begin to fill with blood

4.4. Isovolumetric relaxation: Occurs during early Isovolumetric relaxation: Occurs during early diastole, T wave, ventricles relax, intraventricular diastole, T wave, ventricles relax, intraventricular pressure drops, Bd in vessels outside heart begins pressure drops, Bd in vessels outside heart begins to flow back into ventricles (semilunar valves close, to flow back into ventricles (semilunar valves close, aortic pr. Increases “dicrotic notch”), AV valves aortic pr. Increases “dicrotic notch”), AV valves still closed (isovolumetric relaxation)still closed (isovolumetric relaxation)5.5. AV valves open when pr. in atria exceeds pr. AV valves open when pr. in atria exceeds pr. against AV valves exerted by Bd in ventricles: Start against AV valves exerted by Bd in ventricles: Start of cycle, quiescent periodof cycle, quiescent period

Cardiac PhysiologyCardiac Physiology

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Heart SoundsHeart Sounds

Associated with closing of heart valves: Lub-dupp- Associated with closing of heart valves: Lub-dupp- pause lub-dupp-pause, …Sound 1 (AV valves close, pause lub-dupp-pause, …Sound 1 (AV valves close, onset of systole, louder & longer than sound 2), onset of systole, louder & longer than sound 2), sound 2 (semilunar valves close, beginning of vent-sound 2 (semilunar valves close, beginning of vent-ricular diastole, short, sharp sound), pause ricular diastole, short, sharp sound), pause (quiescent period). Sounds of separate valves can (quiescent period). Sounds of separate valves can be differentiated: Timing (Mitral-Tricuspid-Aortic be differentiated: Timing (Mitral-Tricuspid-Aortic -Pulmonary) & location (four corners)-Pulmonary) & location (four corners)

Cardiac Output (CO)Cardiac Output (CO)

Amount of Bd pumped by each ventricle per min.= Amount of Bd pumped by each ventricle per min.= Stroke volume X HR (SV= volume of Bd pumped Stroke volume X HR (SV= volume of Bd pumped out of each ventricle per beat). CO increase or out of each ventricle per beat). CO increase or decrease with SV or HR, .. SV= EDV- ESVdecrease with SV or HR, .. SV= EDV- ESVEDV (end diastolic volume) is determined by EDV (end diastolic volume) is determined by length of ven. diastole & venous pr. (120 ml)length of ven. diastole & venous pr. (120 ml)ESV (end systolic volume) is determined by arterial ESV (end systolic volume) is determined by arterial pr. & Force of ven. contraction (50 ml)pr. & Force of ven. contraction (50 ml)

Factors that affect stroke volumeFactors that affect stroke volume1.1. Preload-degree of stretch prior to contraction Preload-degree of stretch prior to contraction (most important +ve factor affecting EDV), factors (most important +ve factor affecting EDV), factors increasing stretch: vol., speed of venous return & increasing stretch: vol., speed of venous return & HR (time for filling) HR (time for filling) 2.2. Contractility: Increase in contractile strength Contractility: Increase in contractile strength ( independent of muscle stretch), increase Ca( independent of muscle stretch), increase Ca2+2+ into into cardiac cells (increases contractility & vol. ejected cardiac cells (increases contractility & vol. ejected from heart), decreased ESV, molecular regulation from heart), decreased ESV, molecular regulation of contractile eventsof contractile events

3.3. Afterload-arterial BP: Pr. that ven. contraction Afterload-arterial BP: Pr. that ven. contraction must overcome (back pr. in aorta & pul. valves), must overcome (back pr. in aorta & pul. valves), normal: 80 mmHg (aorta) & 10 mmHg (pul. trunk)normal: 80 mmHg (aorta) & 10 mmHg (pul. trunk), not normally a factor in healthy individuals (may , not normally a factor in healthy individuals (may have an adverse effect in hypertensive subjects)have an adverse effect in hypertensive subjects)

Heart Rate regulationHeart Rate regulation

CO is homeostatically regulated: Extrinsic factors CO is homeostatically regulated: Extrinsic factors induce change to cardiac function through:induce change to cardiac function through:a. Neural mechanismsa. Neural mechanismsb. Chemical mechanismsb. Chemical mechanismsc. Physical mechanismsc. Physical mechanisms

Autonomic nervous systemAutonomic nervous system1.1. Sympathetic nervous system: Responds to real or Sympathetic nervous system: Responds to real or perceived threats: Flight, fright, fight and sexperceived threats: Flight, fright, fight and sex2.2. Sympathetic postganglionic neurons release NE Sympathetic postganglionic neurons release NE at cardiac targets (mediated by ß1 adr. receptors: at cardiac targets (mediated by ß1 adr. receptors: pacemaker cell RMP is brought closer to threshold pacemaker cell RMP is brought closer to threshold ‘depolarized’ & increased HR) & increases Ca‘depolarized’ & increased HR) & increases Ca2+2+ influx into contractile cells (increases ESV)influx into contractile cells (increases ESV)

3.3. Parasympathetic division: Opposes sym. NS Parasympathetic division: Opposes sym. NS ( decreases HR), mediated by acetycholine ( decreases HR), mediated by acetycholine (hyperpo-larizes ‘inhibits’ SA node)(hyperpo-larizes ‘inhibits’ SA node)4.4. Vagal tone: Sym. & parasym. divisions are Vagal tone: Sym. & parasym. divisions are continuously active (effect of parasym. division continuously active (effect of parasym. division predominates) & dominant effect = reduce activity predominates) & dominant effect = reduce activity of AV node (25 beats/min reduction in HR)of AV node (25 beats/min reduction in HR)

Chemical regulation: Chemical regulation: 1. Hormones: Adrenal medulla (Epinephrine ‘sym. 1. Hormones: Adrenal medulla (Epinephrine ‘sym. NS’ increases HR and contractility ‘like NE’)NS’ increases HR and contractility ‘like NE’)2. Ions: Ca2. Ions: Ca2+2+ conc. (decrease causes depressed ht conc. (decrease causes depressed ht function & increase causes ht irritabilityfunction & increase causes ht irritability

Physical factorsPhysical factors1. Age: Inverse relation1. Age: Inverse relation2. Gender: Female faster2. Gender: Female faster3. Exercise: Increased HR during exercise, resting 3. Exercise: Increased HR during exercise, resting rate is lower (bradycardia, SV & muscle mass rate is lower (bradycardia, SV & muscle mass increased in athlete)increased in athlete)4. Body temperature: HR lowered when cold4. Body temperature: HR lowered when cold