Cardiovascular Physiology 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 If channels are permeable to both K+ and Na+ 20 Ca2+ channels close, K+ channels open Ca2+ in K+ out Lots of Ca2+ channels open –20 Membrane potential (mV) Threshold –40 Ca2+ in Some Ca2+ channels open, If channels close –60 If channels open Net Na+ in If channels open Pacemaker potential Action potential K+ channels close Time Time Time (a) The pacemaker potential gradually becomes less negative until it reaches threshold, triggering an action potential. (b) Ion movements during an action and pacemaker potential (c) State of various ion channels Figure 14-15

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

Modulation of Heart Rate by the Autonomic Nervous System Normal Sympathetic stimulation Normal Parasympathetic stimulation 20 20 Membrane potential (mV) –20 Membrane potential (mV) –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

Action Potentials Table 14-3

Electrical Conduction in Myocardial Cells Membrane potential of autorhythmic cell Membrane potential of contractile cell Cells of SA node Contractile cell Intercalated disk with gap junctions Depolarizations of autorhythmic cells rapidly spread to adjacent contractile cells through gap junctions. Figure 14-17

Electrical Conduction in the Heart 1 1 SA node depolarizes. SA node AV node 2 2 Electrical activity goes rapidly to AV node via internodal pathways. 3 Depolarization spreads more slowly across atria. Conduction slows through AV node. THE CONDUCTING SYSTEM OF THE HEART 4 Depolarization moves rapidly through ventricular conducting system to the apex of the heart. SA node 3 Internodal pathways 5 Depolarization wave spreads upward from the apex. AV node AV bundle 4 Bundle branches Purkinje fibers 5 Figure 14-18

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

Einthoven’s Triangle Right arm Left arm I Electrodes are attached to the skin surface. II III A lead consists of two electrodes, one positive and one negative. Left leg Figure 14-19

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

Correlation between an ECG and electrical events in the heart Electrical Activity Correlation between an ECG and electrical events in the heart START P wave: atrial depolarization P The end R PQ or PR segment: conduction through AV node and AV bundle P T Q S P Atria contract T wave: ventricular repolarization Repolarization ELECTRICAL EVENTS OF THE CARDIAC CYCLE R P T Q S P Q wave ST segment Q R P R wave R Q S Ventricles contract R P Q P S wave Q S Figure 14-21

Electrical Activity Figure 14-21 (9 of 9) P wave: atrial depolarization START P The end R PQ or PR segment: conduction through AV node and AV bundle P T Q S P Atria contract T wave: ventricular repolarization Repolarization ELECTRICAL EVENTS OF THE CARDIAC CYCLE R P T Q S Q wave P ST segment Q R P R wave R Q S Ventricles contract R P Q P S wave Q S Figure 14-21 (9 of 9)

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

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

Mechanical events of the cardiac cycle 1 Late diastole—both sets of chambers are relaxed and ventricles fill passively. START 5 Isovolumic ventricular relaxation—as ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed. 2 Atrial systole—atrial contraction forces a small amount of additional blood into ventricles. S1 S2 3 Isovolumic ventricular contraction—first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. 4 Ventricular ejection— as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected. Figure 14-24

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

Left ventricular pressure-volume changes during one cardiac cycle KEY EDV = End-diastolic volume Stroke volume 120 D ESV = End-systolic volume ESV 80 C One cardiac cycle Left ventricular pressure (mmHg) 40 EDV B A 65 100 135 Left ventricular volume (mL) Figure 14-25

Wiggers Diagram Figure 14-26 Time (msec) 100 200 300 400 500 600 700 100 200 300 400 500 600 700 800 QRS complex Electro- cardiogram (ECG) QRS complex P T P 120 B 90 Aorta Dicrotic notch Pressure (mm Hg) A Left venticular pressure 60 30 Left atrial pressure D C S1 S2 Heart sounds 135 E Left ventricular volume (mL) 65 F Atrial systole Ventricular systole Ventricular diastole Atrial systole Atrial systole Isovolumic ventricular contraction Ventricular systole Early ventricular diastole Late ventricular diastole Atrial systole Figure 14-26

Wiggers Diagram Figure 14-26 (13 of 13) Time (msec) 100 200 300 400 100 200 300 400 500 600 700 800 QRS complex Electro- cardiogram (ECG) QRS complex P T P 120 B 90 Aorta Dicrotic notch Pressure (mm Hg) A Left venticular pressure 60 30 Left atrial pressure D C S1 S2 Heart sounds 135 E Left ventricular volume (mL) 65 F Atrial systole Ventricular systole Ventricular diastole Atrial systole Atrial systole Isovolumic ventricular contraction Ventricular systole Early ventricular diastole Late ventricular diastole Atrial systole Figure 14-26 (13 of 13)

Stroke Volume and Cardiac Output 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

Autonomic Neurotransmitters Alter Heart Rate KEY Integrating center Cardiovascular control center in medulla oblongata Efferent path Effector Tissue response Sympathetic neurons (NE) Parasympathetic neurons (Ach) 1-receptors of autorhythmic cells Muscarinic receptors of autorhythmic cells Na+ and Ca2+ influx K+ efflux; Ca2+ influx Hyperpolarizes cell and rate of depolarization Rate of depolarization Heart rate Heart rate Figure 14-27

Frank-Starling law states 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

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

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

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

Catecholamines Modulate Cardiac Contraction Epinephrine and norepinephrine bind to 1-receptors that activate cAMP second messenger system resulting in phosphorylation of Voltage-gated Ca2+ channels Phospholamban Open time increases Ca2+-ATPase on SR Ca2+ entry from ECF Ca2+ stores in SR Ca2+ removed from cytosol faster Shortens Ca-troponin binding time Ca2+ released KEY SR = Sarcoplasmic reticulum Shorter duration of contraction ECF = Extracelllular fluid More forceful contraction Figure 14-30

Stroke Volume and Heart Rate Determine Cardiac Output is a function of Heart rate Stroke volume determined by determined by Rate of depolarization in autorhythmic cells Force of contraction in ventricular myocardium is influenced by Decreases Increases increases Contractility End-diastolic volume Sympathetic innervation and epinephrine Due to parasympathetic innervation which varies with increases Venous constriction Venous return aided by Skeletal muscle pump Respiratory pump Figure 14-31

Cardiovascular system—anatomy review 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

The heart as a pump (continued) The cardiac cycle 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