1 / 29

Chapter 14b

Chapter 14b. Cardiovascular Physiology. Action Potentials in Cardiac Autorhythmic Cells. Pacemaker potential - no resting -60mV drifts to -40 to action potential Spread through connections to contractile fibers I f channels are permeable to both K + and Na +. 20.

woods
Télécharger la présentation

Chapter 14b

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Chapter 14b Cardiovascular Physiology

  2. Action Potentials in Cardiac Autorhythmic Cells • Pacemaker potential - no resting • -60mV drifts to -40 to action potential • Spread through connections to contractile fibers • If channels are permeable to both K+ and Na+ 20 Ca2+ channels close,K+ channels open 0 Ca2+ in K+ out Lots of Ca2+channelsopen –20 Membrane potential (mV) Threshold –40 Some Ca2+channels open,If channels close Ca2+ in If channelsopen –60 Net Na+ in If channelsopen Pacemakerpotential Actionpotential K+ channels close Time Time Time (a) The pacemaker potentialgradually becomes less negativeuntil it reaches threshold,triggering an action potential. (b) Ion movements during an actionand pacemaker potential (c) State of various ion channels Figure 14-15

  3. Action Potentials in Cardiac Autorhythmic Cells PLAY Interactive Physiology® Animation:Cardiovascular System: Cardiac Action Potential

  4. Modulation of Heart Rate by the Autonomic Nervous System Sympathetic stimulation Normal Normal Parasympathetic stimulation 20 20 0 0 Membrane potential (mV) Membrane potential (mV) –20 –40 –60 –60 Depolarized More rapid depolarization Hyperpolarized Slower depolarization 0.8 1.6 2.4 0.8 1.6 2.4 Time (sec) Time (sec) (a) (b) Figure 14-16

  5. Action Potentials Table 14-3

  6. Electrical Conduction in Myocardial Cells Membrane potentialof autorhythmic cell Membrane potentialof contractile cell Cells ofSA node Contractile cell Intercalated diskwith gap junctions Depolarizations of autorhythmic cellsrapidly spread to adjacent contractilecells through gap junctions. Figure 14-17

  7. Electrical Conduction in the Heart 1 SA node depolarizes. 1 SA node AV node Electrical activity goesrapidly to AV node viainternodal pathways. 2 2 Depolarization spreadsmore slowly acrossatria. Conduction slowsthrough AV node. 3 THE CONDUCTING SYSTEMOF THE HEART Depolarization movesrapidly through ventricularconducting system to theapex of the heart. 4 SA node 3 Internodalpathways Depolarization wavespreads upward fromthe apex. 5 AV node AV bundle 4 Bundlebranches Purkinjefibers 5 Figure 14-18

  8. Electrical Conduction • SA node • Sets the pace of the heartbeat at 70 bpm • AV node (50 bpm) and Purkinje fibers (25-40 bpm) can act as pacemakers under some conditions • AV node • Routes the direction of electrical signals • Delays the transmission of action potentials

  9. Einthoven’s Triangle Right arm Left arm I Electrodes areattached to theskin surface. II III A lead consists of twoelectrodes, one positiveand one negative. Left leg Figure 14-19

  10. The Electrocardiogram • Three major waves: P wave, QRS complex, and T wave Figure 14-20

  11. Electrical Activity • Correlation between an ECG and electrical events in the heart P wave: atrialdepolarization START P The end R PQ or PR segment:conduction throughAV node and AVbundle P T P Q S Atria contract T wave:ventricularrepolarization Repolarization ELECTRICAL EVENTSOF THECARDIAC CYCLE R T P Q S Q wave P ST segment Q R P R wave R Q S R Ventricles contract P Q P S wave S Q Figure 14-21

  12. Electrical Activity P wave: atrialdepolarization START P The end R PQ or PR segment:conduction throughAV node and AVbundle P T P Q S Atria contract T wave:ventricularrepolarization Repolarization ELECTRICAL EVENTSOF THECARDIAC CYCLE R T P Q S Q wave P ST segment Q R P R wave R Q S R Ventricles contract P Q P S wave Q S Figure 14-21 (9 of 9)

  13. Electrical Activity • Comparison of an ECG and a myocardial action potential 1 mV 1 sec (a) The electrocardiogram represents the summedelectrical activity of all cells recorded from thesurface of the body. 110mV 1 sec (b) The ventricular action potential is recorded froma single cell using an intracellular electrode.Notice that the voltage change is much greaterwhen recorded intracellularly. Figure 14-22

  14. Electrical Activity • Normal and abnormal electrocardiograms Figure 14-23

  15. Mechanical Events • Mechanical events of the cardiac cycle Late diastole—both sets ofchambers are relaxed andventricles fill passively. 1 START Isovolumic ventricularrelaxation—as ventriclesrelax, pressure in ventriclesfalls, blood flows back intocusps of semilunar valvesand snaps them closed. 5 Atrial systole—atrial contractionforces a small amount ofadditional blood into ventricles. 2 S1 S2 Isovolumic ventricularcontraction—first phase ofventricular contraction pushes AVvalves closed but does not createenough pressure to open semilunarvalves. 3 Ventricular ejection—as ventricular pressurerises and exceeds pressurein the arteries, the semilunarvalves open and blood isejected. 4 Figure 14-24

  16. Cardiac Cycle PLAY Interactive Physiology® Animation: Cardiovascular System: Cardiac Cycle

  17. Cardiac Cycle • Left ventricular pressure-volume changes during one cardiac cycle KEY EDV = End-diastolicvolume Stroke volume 120 D ESV = End-systolicvolume ESV 80 C Onecardiaccycle Left ventricular pressure (mmHg) 40 EDV B A 0 65 100 135 Left ventricular volume (mL) Figure 14-25

  18. Wiggers Diagram Time (msec) 0 100 200 300 400 500 600 700 800 QRScomplex QRScomplex Electro-cardiogram(ECG) P T P 120 B 90 Aorta Dicrotic notch A Pressure(mm Hg) Leftventicularpressure 60 Left atrialpressure 30 D C 0 S1 S2 Heart sounds 135 E Leftventricularvolume (mL) F 65 Atrialsystole Ventricularsystole Ventriculardiastole Atrialsystole Isovolumicventricularcontraction Ventricularsystole Atrialsystole Earlyventriculardiastole Lateventriculardiastole Atrialsystole Figure 14-26

  19. Wiggers Diagram Time (msec) 0 100 200 300 400 500 600 700 800 QRScomplex QRScomplex Electro-cardiogram(ECG) P T P 120 B 90 Aorta Dicrotic notch A Pressure(mm Hg) Leftventicularpressure 60 Left atrialpressure 30 D C 0 S1 S2 Heart sounds 135 E Leftventricularvolume (mL) F 65 Atrialsystole Ventricularsystole Ventriculardiastole Atrialsystole Isovolumicventricularcontraction Ventricularsystole Atrialsystole Earlyventriculardiastole Lateventriculardiastole Atrialsystole Figure 14-26 (13 of 13)

  20. Stroke Volume and Cardiac Output • Stroke volume • Amount of blood pumped by one ventricle during a contraction • EDV – ESV = stroke volume • Cardiac output • Volume of blood pumped by one ventricle in a given period of time • CO = HR  SV • Average = 5 L/min

  21. Autonomic Neurotransmitters Alter Heart Rate KEY Integrating center Cardiovascularcontrolcenter in medullaoblongata Efferent path Effector Tissue response Parasympatheticneurons (Ach) Sympathetic neurons(NE) 1-receptors ofautorhythmic cells Muscarinic receptorsof autorhythmic cells K+ efflux; Ca2+ influx Na+ and Ca2+ influx Hyperpolarizes cell and rate of depolarization Rate of depolarization Heart rate Heart rate Figure 14-27

  22. Stroke Volume • Frank-Starling law states • Stroke volume increase as EDV (ending diastolic volume) increases – stretch -> more force • EDV is affected by venous return • Venous return is affected by • Skeletal muscle pump • Respiratory pump • Sympathetic innervation of vessels • Force of contraction is affected by • Stroke volume • Length of muscle fiber and contractility of heart

  23. Stroke Volume • Length-force relationships in intact heart: a Starling curve Figure 14-28

  24. Inotropic Effect • The effect of norepinepherine on contractility of the heart Figure 14-29

  25. Cardiac Output PLAY Interactive Physiology® Animation:Cardiovascular System: Cardiac Output

  26. Catecholamines Modulate Cardiac Contraction Epinephrineandnorepinephrine bind to 1-receptors that activate cAMP secondmessenger system resulting in phosphorylation of Voltage-gated Ca2+ channels Phospholamban Open time increases Ca2+-ATPase on SR Ca2+ removed from cytosol faster Ca2+ stores in SR Ca2+ entry from ECF Shortens Ca-troponinbinding time Ca2+ released KEY SR = Sarcoplasmicreticulum Shorterdurationof contraction ECF = Extracelllularfluid More forcefulcontraction Figure 14-30

  27. Stroke Volume and Heart Rate Determine Cardiac Output CARDIAC OUTPUT is a function of Heart rate Stroke volume determined by determined by Rate of depolarizationin autorhythmic cells Force of contraction inventricular myocardium is influenced by Decreases Increases increases End-diastolicvolume Contractility Sympatheticinnervation andepinephrine Due toparasympatheticinnervation which varies with increases Venous constriction Venous return aided by Skeletal musclepump Respiratorypump Figure 14-31

  28. Summary • Cardiovascular system—anatomy review • Pressure, volume, flow, and resistance • Pressure gradient, driving pressure, resistance, viscosity, flow rate, and velocity of flow • Cardiac muscle and the heart • Myocardium, autorhythmic cells, intercalated disks, pacemaker potential, and If channels • The heart as a pump • SA node, AV node, AV bundle, bundle branches, and Purkinje fibers

  29. Summary • The heart as a pump (continued) • ECG, P wave, QRS complex, and T wave • The cardiac cycle • Systole, diastole, AV valves, first heart sound, isovolumic ventricular contraction, semilunar valves, second heart sound, and stroke volume • Cardiac output • Frank-Starling law, EDV, preload, contractility, inotropic effect, afterload, and ejection fraction

More Related