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Copyright © 2010 Pearson Education, Inc. The cells of the heart Two types of cardiac muscle cells that are involved in a normal heartbeat: Specialized muscle cells of the conducting system Contractile cells The heart is an autonomic system that can work without neural stimuli – an intrinsic conduction system. The autonomic function of the heart results from: The pacemaker function – Autorhythmic cells The conductive system that transfer those impulses throughout the heart
Copyright © 2010 Pearson Education, Inc. Properties of Cardiac Muscle Aerobic muscle No cell division after infancy - growth by hypertrophy 99% contractile cells (for pumping) 1% autorhythmic cells (set pace)
Copyright © 2010 Pearson Education, Inc. Electrical Conduction in Myocardial Cells Figure Membrane potential of autorhythmic cel Membrane potential of contractile cell Contractile cell Cells of SA node Depolarizations of autorhythmic cells rapidly spread to adjacent contractile cells through gap junctions. Intercalated disk with gap junctions
Copyright © 2010 Pearson Education, Inc. Intrinsic cardiac conduction system – autorhythmic cells Have unstable resting potentials/ pacemaker potentials constantly depolarized slowly towards AP At threshold, Ca 2+ channels open Ca 2+ influx produces the rising phase of the action potential Repolarization results from inactivation of Ca 2+ channels and opening of voltage-gated K + channels
Copyright © 2010 Pearson Education, Inc. Figure Pacemaker potential This slow depolarization is due to both opening of Na + channels and closing of K + channels. Notice that the membrane potential is never a flat line. Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca 2+ influx through Ca 2+ channels. Repolarization is due to Ca 2+ channels inactivating and K + channels opening. This allows K + efflux, which brings the membrane potential back to its most negative voltage. Action potential Threshold Pacemaker potential
Copyright © 2010 Pearson Education, Inc. Conduction System of Heart
Copyright © 2010 Pearson Education, Inc. Autorhythmic Cells LocationFiring Rate at Rest SA node70–80 APs/min* AV node40–60 APs/min Bundle of His20–40 APs/min Purkinje fibers20–40 APs/min Cardiac cells are linked by gap junctions Fastest depolarizing cells control other cells Fastest cells = pacemaker = set rate for rest of heart * action potentials per minute
Copyright © 2010 Pearson Education, Inc. Cardiac Electrical Connections
Copyright © 2010 Pearson Education, Inc. Cardiac contractile cells Depolarization opens voltage-gated fast Na + channels in the sarcolemma Depolarization wave causes release Ca 2+ that causes the cell contraction Depolarization wave also opens slow Ca 2+ channels in the sarcolemma Ca 2+ surge prolongs the depolarization phase (plateau)
Copyright © 2010 Pearson Education, Inc. Figure Electrical Activity: Contractile Cell
Copyright © 2010 Pearson Education, Inc. Figure Absolute refractory period Tension development (contraction) Plateau Action potential Time (ms) Depolarization is due to Na + influx through fast voltage-gated Na + channels. A positive feedback cycle rapidly opens many Na + channels, reversing the membrane potential. Channel inactivation ends this phase. Plateau phase is due to Ca 2+ influx through slow Ca 2+ channels. This keeps the cell depolarized because few K + channels are open. Repolarization is due to Ca 2+ channels inactivating and K + channels opening. This allows K + efflux, which brings the membrane potential back to its resting voltage Tension (g) Membrane potential (mV)
Copyright © 2010 Pearson Education, Inc. Action Potentials Table 14-3
Copyright © 2010 Pearson Education, Inc. Conduction System of Heart
Copyright © 2010 Pearson Education, Inc. Electrical Conduction in the Heart Figure 14-18, steps 1– THE CONDUCTING SYSTEM OF THE HEART SA node AV node Purkinje fibers Bundle branches AV bundle AV node Internodal pathways SA node SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. Depolarization spreads more slowly across atria. Conduction slows through AV node. Depolarization moves rapidly through ventricular conducting system to the apex of the heart. Depolarization wave spreads upward from the apex.
Copyright © 2010 Pearson Education, Inc. Cardiac Cycle Cardiac cycle - The period between the start of one heartbeat and the beginning of the next. refers to all events associated with blood flow through the heart During the cycle, each of the four chambers goes through Systole – contraction of heart muscle Diastole – relaxation of heart muscle An average heart beat (HR)/cardiac cycle is 75 bpm. That means that a cardiac cycle length is about 0.8 second. Of that 0.1 second is the atrial contraction, 0.3 is the atrial relaxation and ventricular contraction. The remaining 0.4 seconds are called the quiescent period which represent the ventricular relaxation
Copyright © 2010 Pearson Education, Inc. RelaxationAtria contract Ventricles contract Relaxation The sequence of events during a single heartbeat Figure 18 Section 2 2
Copyright © 2010 Pearson Education, Inc. Phases of the Cardiac Cycle 1.Ventricular filling — takes place in mid-to-late diastole AV valves are open 80% of blood passively flows into ventricles Atrial systole occurs, delivering the remaining 20% End diastolic volume (EDV): volume of blood in each ventricle at the end of ventricular diastole
Copyright © 2010 Pearson Education, Inc. Phases of the Cardiac Cycle 2.Ventricular systole Atria relax and ventricles begin to contract Rising ventricular pressure results in closing of AV valves Isovolumetric contraction phase (all valves are closed) In ejection phase, ventricular pressure exceeds pressure in the large arteries, forcing the SL valves open End systolic volume (ESV): volume of blood remaining in each ventricle
Copyright © 2010 Pearson Education, Inc. Phases of the Cardiac Cycle 3.Isovolumetric relaxation occurs in early diastole Ventricles relax Backflow of blood in aorta and pulmonary trunk closes SL valves and causes dicrotic notch (brief rise in aortic pressure)
Copyright © 2010 Pearson Education, Inc. Phases of the Cardiac Cycle Figure 20.16
Copyright © 2010 Pearson Education, Inc. Cardiodynamics Movements and forces generated during cardiac contractions End-diastolic volume (EDV) – the amount of blood in each ventricle at the end of ventricular diastole (before contraction begins) End-systolic volume (ESV) - the amount of blood remains in each ventricle at the end of ventricular systole
Copyright © 2010 Pearson Education, Inc. Cardiodynamics Stroke volume (SV) – The amount of blood that leaves the heart with each beat or ventricular contraction; EDV- ESV=SV Not all blood ejected Normal Adult 70 ml / beat Ejection fraction – The percentage of end-diastole blood actually ejected with each beat or ventricular contraction. Normal adult 55-70% (healthy heart)
Copyright © 2010 Pearson Education, Inc. Cardiac output (CO) – the amount of blood pumped by each ventricle in one minute. Physiologically, CO is an indication of blood flow through peripheral tissues Cardiac output equals heart rate times stroke volume; Normal CO: Approximately 4-8 liters/minute Stroke Volume and Cardiac Output CO Cardiac output (ml/min) = HR Heart rate (beats/min) X SV Stroke volume (ml/beat)
Copyright © 2010 Pearson Education, Inc. Figure Time (msec) Left AV valve closes. Aortic valve opens. Aortic valve closes. Left AV valve opens. Dicrotic notch Pressure (mm Hg) The correspondence of the heart sounds with events during the cardiac cycle Heart sounds S4S4 S1S1 S2S2 S3S3 S4S4 “Dubb” “Lubb” KEY Atrial contraction begins. Atria eject blood into ventricles. Atrial systole ends; AV valves close. Isovolumetric contraction. Ventricular ejection occurs. Semilunar valves close. Isovolumetric relaxation occurs. AV valves open; passive ventricular filling occurs. Left ventricle Left atrium The pressure changes within the aorta, left atrium, and left ventricle during the cardiac cycle ATRIAL DIASTOLE ATRIAL SYSTOLE ATRIAL DIASTOLE VENTRICULAR DIASTOLE VENTRICULAR SYSTOLE VENTRICULAR DIASTOLE ATRIAL SYSTOLE Aorta
Copyright © 2010 Pearson Education, Inc. Figure a2b3 Atrioventricular valves Aortic and pulmonary valves Open Closed Open Phase ESV Left atrium Right atrium Left ventricle Right ventricle Ventricular filling Atrial contraction Ventricular filling (mid-to-late diastole) Ventricular systole (atria in diastole) Isovolumetric contraction phase Ventricular ejection phase Early diastole Isovolumetric relaxation Ventricular filling 112a2b3 Electrocardiogram Left heart P 1st2nd QRS P Heart sounds Atrial systole Dicrotic notch Left ventricle Left atrium EDV SV Aorta T Ventricular volume (ml) Pressure (mm Hg)
Copyright © 2010 Pearson Education, Inc. Factors Affecting Cardiac Output Figure 20.20
Copyright © 2010 Pearson Education, Inc. Extrinsic Innervation of the Heart Heartbeat is modified by the ANS Cardiac centers are located in the medulla oblongata Cardioacceleratory center innervates SA and AV nodes, heart muscle, and coronary arteries through sympathetic neurons Cardioinhibitory center inhibits SA and AV nodes through parasympathetic fibers in the vagus nerves
Copyright © 2010 Pearson Education, Inc. Autonomic Inputs to Heart
Copyright © 2010 Pearson Education, Inc. Effect inotropy – (from Greek, meaning fiber) effect on contractility of the heart Effect chronotropy – effect on HR Effect dromotropy – Derives from the Greek word "Dromos", meaning running. A dromotropic agent is one which affects the conduction speed in the AV node Sympathetic stimuli has a positive effect (increase) all Parasympathetic stimuli has a negative effect (decrease) all
Copyright © 2010 Pearson Education, Inc. Autonomic Nervous System Regulation In healthy conditions, parasympathetic effects dominate and slows the rate of the pacemaker from bpm to a bpm. The binding of Ach to muscarinic receptors (M2) inhibit NE release (mechanism by which vagal stimulation override sympathetic stimulation) Sympathetic nervous system is activated by emotional or physical stressors Norepinephrine causes the pacemaker to fire more rapidly (and at the same time increases contractility) Parasympathetic nervous system opposes sympathetic effects Acetylcholine hyperpolarizes pacemaker cells by opening K + channels The heart at rest exhibits vagal tone (parasympathetic)
Copyright © 2010 Pearson Education, Inc. Na + and Ca 2+ influx Sympathetic neurons (NE) Rate of depolarization Heart rate Muscarinic receptors of autorhythmic cells K + efflux; Ca 2+ influx Parasympathetic neurons (Ach) Hyperpolarizes cell and rate of depolarization Heart rate 1 -receptors of autorhythmic cells Integrating center Efferent path Effector Tissue response Cardiovascular control center in medulla oblongata KEY Autonomic Neurotransmitters Alter Heart Rate Figure 14-27
Copyright © 2010 Pearson Education, Inc. Figure Heart rate under three conditions: at rest, under parasympathetic stimulation, and under sympathetic stimulation A prepotential or pacemaker potential in a heart at rest –30 –60 Threshold Heart rate: 75 bpm Membrane potential (mV) Normal (resting) Prepotential (spontaneous depolarization) Time (sec)
Copyright © 2010 Pearson Education, Inc. Figure Increased heart rate resulting when ACh released by parasympathetic neurons opens chemically gated K + channels, thereby slowing the rate of spontaneous depolarization Threshold +20 –30 0 –60 Heart rate: 40 bpm Membrane potential (mV) Slower depolarization Hyperpolarization Parasympathetic stimulation Heart rate under three conditions: at rest, under parasympathetic stimulation, and under sympathetic stimulation A prepotential or pacemaker potential in a heart at rest Time (sec)
Copyright © 2010 Pearson Education, Inc. Figure Decreased heart rate resulting when NE released by sympathetic neurons leads to the opening of ion channels, increases the rate of depolarization and shortens the period of repolarization More rapid depolarization Time (sec) Heart rate: 120 bpm Reduced repolarization Threshold – Membrane potential (mV) Sympathetic stimulation Heart rate under three conditions: at rest, under parasympathetic stimulation, and under sympathetic stimulation –60
Copyright © 2010 Pearson Education, Inc. Chemical Regulation of Heart Rate 1.Hormones Epinephrine from adrenal medulla enhances heart rate and contractility Thyroxine increases heart rate and enhances the effects of norepinephrine and epinephrine 2.Intra- and extracellular ion concentrations (e.g., Ca 2+ and K + ) must be maintained for normal heart function
Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalances Tachycardia: abnormally fast heart rate (>100 bpm) If persistent, may lead to fibrillation Bradycardia: heart rate slower than 60 bpm May result in grossly inadequate blood circulation May be desirable result of endurance training
Copyright © 2010 Pearson Education, Inc. Factors Affecting Stroke Volume Figure 20.23
Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume SV = EDV – ESV Three main factors affect SV Preload Contractility Afterload
Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume Preload The amount of tension on a muscle before it begins to contract. The preload of the heart is determined by the EDV. In general, the greater the EDV the larger is the stroke volume : EDV-ESV=SV These relationships is known as the Frank- Starling principle/Sterling’s law of the heart : The force of cardiac muscle contraction is proportional to its initial length The greater the EDV the larger the preload
Copyright © 2010 Pearson Education, Inc. Preload and Stroke Volume Frank-Starling law states Stroke volume increase as EDV increases EDV is affected by venous return Venous return is affected by Skeletal muscle pump Respiratory pump Sympathetic innervation
Copyright © 2010 Pearson Education, Inc. Stroke volume is the difference between the EDV and ESV. Changes in either one can change the stroke volume and cardiac output: The EDV volume is affected by 2 factors: The filling time – duration of ventricular diastole; depends on HR – the faster the HR the shorter is the available filing time The venous return – changes in response to several changes: cardiac output, blood volume, peripheral circulation. Factors Affecting stroke volume - Preload/EDV
Copyright © 2010 Pearson Education, Inc. Reminder - Length-tension relationship The force of muscle contraction depends on the length of the sarcomeres before the contraction begins On the molecular level, the length reflects the overlapping between thin and thick filaments The tension a muscle fiber can generate is directly proportional to the number of crossbridges formed between the filament
Copyright © 2010 Pearson Education, Inc. Preload = Contractility (to a point)
Copyright © 2010 Pearson Education, Inc. Stroke Volume Length-force relationships in intact heart: a Starling curve Figure 14-28
Copyright © 2010 Pearson Education, Inc. Diastolic filling increased EDV increase (preload increased) Cardiac muscle stretch increased Force of contraction increased Ejection volume increased
Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume - Afterload The amount of resistance the ventricular wall must overcome to eject blood during systole (influenced by arterial pressure). The greater is the afterload, the longer is the period of isovolumetric contraction (ventricles are contracting but there is no blood flow), the shorter the duration of ventricular ejection and the larger the ESV – afterload increase – stroke volume decrease Hypertension increases afterload, resulting in increased ESV and reduced SV
Copyright © 2010 Pearson Education, Inc. Regulation of Stroke Volume - Contractility Force of ventricular contraction (systole) regardless of EDV Positive inotropic agents increase contractility Increased Ca 2+ influx due to sympathetic stimulation Hormones (thyroxine and epinephrine) Negative inotropic agents decrease contractility Increased extracellular K + (hyperpolarization) Calcium channel blockers (decrease calcium influx)
Copyright © 2010 Pearson Education, Inc. Congestive Heart Failure (CHF) Progressive condition where the CO is so low that blood circulation is inadequate to meet tissue needs Caused by Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts (decreased blood supply and myocardial cell death) Dilated cardiomyopathy (DCM) – heart wall weakens and can not contract efficiently. Causes are unknown but sometimes associated with toxins (ex. Chemotherapy), viral infections, tachycardia and more
Copyright © 2010 Pearson Education, Inc. Electrocardiography (ECG or EKG) Body fluids are good conductors which allows the record of the myocardial action potential extracellularly EKG pairs of electrodes (leads) one serve as positive side of the lead and one as the negative Potentials (voltage) are being measured between the 2 electrodes EKG is the summed electrical potentials generated by all cells of the heart and gives electrical “view” of 3D object (different from one action potential) EKG shows depolarization and repolarization
Copyright © 2010 Pearson Education, Inc. Einthoven’s Triangle Figure Electrodes are attached to the skin surface. A lead consists of two electrodes, one positive and one negative. Right armLeft arm Left leg I IIIII
Copyright © 2010 Pearson Education, Inc. The Electrocardiogram Three major waves: P wave, QRS complex, and T wave Figure 14-20
Copyright © 2010 Pearson Education, Inc. Electrical Activity of Heart P wave: atrial depolarization QRS complex: ventricular depolarization and atrial repolarization T wave: ventricular repolarization PQ segment: AV nodal delay QT segment: ventricular systole QT interval: ventricular diastole
Copyright © 2010 Pearson Education, Inc. Figure Electrical Activity of Heart – normal values
Copyright © 2010 Pearson Education, Inc. Correlation between an ECG and electrical events in the heart
Copyright © 2010 Pearson Education, Inc. Electrical Activity Figure (1 of 9) P wave: atrial depolarization ELECTRICAL EVENTS OF THE CARDIAC CYCLE START P
Copyright © 2010 Pearson Education, Inc. Electrical Activity Figure (9 of 9) P Q R T S P T wave: ventricular repolarization PQ or PR segment: conduction through AV node and AV bundle P wave: atrial depolarization ELECTRICAL EVENTS OF THE CARDIAC CYCLE Repolarization START P Q P Q R P Q R T S R wave P Q R S S wave Q R P Q wave Ventricles contract ST segment The end P Atria contract S
Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalances Defects in the intrinsic conduction system may result in 1.Arrhythmias: irregular heart rhythms 2.Uncoordinated atrial and ventricular contractions (heart block) 3.Fibrillation: rapid, irregular contractions; useless for pumping blood
Copyright © 2010 Pearson Education, Inc. Figure Atrial Fibrillation (AF) Paroxysmal Atrial Tachycardia (PAT) Premature Atrial Contractions (PACs) Important examples of cardiac arrhythmias Premature atrial contractions (PACs) often occur in healthy individuals. In a PAC, the normal atrial rhythm is momentarily interrupted by a “surprise” atrial contraction. Stress, caffeine, and various drugs may increase the incidence of PACs, presumably by increasing the permeabilities of the SA pacemakers. The impulse spreads along the conduction pathway, and a normal ventricular contraction follows the atrial beat. In paroxysmal (par-ok-SIZ-mal) atrial tachycardia, or PAT, a premature atrial contraction triggers a flurry of atrial activity. The ventricles are still able to keep pace, and the heart rate jumps to about 180 beats per minute. During atrial fibrillation (fib-ri-LĀ-shun), the impulses move over the atrial surface at rates of perhaps 500 beats per minute. The atrial wall quivers instead of producing an organized contraction. The ventricular rate cannot follow the atrial rate and may remain within normal limits. Even though the atria are now nonfunctional, their contribution to ventricular end-diastolic volume is so small that the condition may go unnoticed in older individuals. P P P P P P P PP
Copyright © 2010 Pearson Education, Inc. Figure Ventricular Fibrillation (VF) Ventricular Tachycardia (VT) Premature Ventricular Contractions (PVCs) Premature ventricular contractions (PVCs) occur when a Purkinje cell or ventricular myocardial cell depolarizes to threshold and triggers a premature contraction. Single PVCs are common and not dangerous. The cell responsible is called an ectopic pacemaker. The frequency of PVCs can be increased by exposure to epinephrine, to other stimulatory drugs, or to ionic changes that depolarize cardiac muscle cell membranes. Ventricular tachycardia is defined as four or more PVCs without intervening normal beats. It is also known as VT or V-tach. Multiple PVCs and VT may indicate that serious cardiac problems exist. Ventricular fibrillation (VF) is responsible for the condition known as cardiac arrest. VF is rapidly fatal, because the ventricles quiver and stop pumping blood. P P PPT T T Important examples of cardiac arrhythmias
Copyright © 2010 Pearson Education, Inc. Figure (4 of 4) ECG Arrhythmias: Fibrillation Ventricular Fibrillation Loss of coordination of electrical activity of heart Death can ensue within minutes unless corrected
Copyright © 2010 Pearson Education, Inc. Homeostatic Imbalances Defective SA node may result in Ectopic focus: abnormal pacemaker takes over If AV node takes over, there will be a junctional rhythm (40–60 bpm) Defective AV node may result in Partial or total heart block Few or no impulses from SA node reach the ventricles
Copyright © 2010 Pearson Education, Inc. First and second degree Heart Block Slowed/diminished conduction through AV node occurs in varying degrees First degree block Increases duration PQ segment Increases delay between atrial and ventricular contraction Second degree block Lose 1-to-1 relationship between P wave and QRS complex Lose 1-to-1 relationship between atrial and ventricular contraction
Copyright © 2010 Pearson Education, Inc. Third Degree Heart Block Third degree block Loss of conduction through the AV node P wave becomes independent of QRS Atrial and ventricular contractions are independent
Copyright © 2010 Pearson Education, Inc. Cardiovascular system – the heart.
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