[PHYSIO]LEC_203_CARDIOVASCULAR-PHYSIOLOGY-ELECTRICAL-PROPERTIES-RHYTHMICAL-EXCITATION-OF-THE-HEART.pdf

(003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart)...

(003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 Mitral valve - separates left atrium from left ventricle OUTLINE Pulmonary artery - rises from the right ventricle going to I. PURPOSE OF THE CARDIOVASCULAR SYSTEM the pulmonary circulation connected to the lungs for gas A. Pumps/Circulation exchange B. Structures II. CARDIAC CONDUCTING SYSTEM A. Sequence of Cardiac Excitation B. Types of Cardiac Cells III. TYPES OF ACTION POTENTIAL A. Fast Type Cardiac Action Potential 1. Ionic basis for fast response type of action potential 2. Fast Na Channels C. Slow Response Action Potential (Pacemaker Cell) 1. Slow Response of Pacemaker IV. SELF-EXCITATION OF SINUS NODAL FIBERS A. Automaticity Figure 1. The Heart B. Conditions that alter automaticity 1. Decreased Automaticity Aorta - rises from the left ventricle; serves as a conduit 2. Increased Automaticity that distributes oxygenated blood going to the systemic V. INTERNODAL AND INTERNAL PATHWAYS circulation and distributes to all other tissues of the body VI. THE ATRIOVENTRICULAR NODE The heart is endowed with a special system for : A. Cause of the slow conduction 1. generating rhythmical electrical impulses to cause VII. RAPID TRANSMISSION IN THE VENTRICULAR rhythmical contraction of the heart muscle and PURKINJE SYSTEM 2. conducting these impulses rapidly through the heart A. Purkinje Fibers B. One-way conduction through the AV bundle Cardiac rhythmicity- a special mechanism in the heart C. Distribution of the Purkinje Fibers in the causes a continuing succession of heart contractions, Ventricles transmitting action potentials throughout the cardiac D. Transmission of the Cardiac Impulse in the muscle to cause the heart’s rhythmical beat. Ventricular Muscle VIII. CONTROL OF EXCITATION AND CONDUCTION IN A. PUMPS/CIRCULATION THE HEART Pulmonary circulation A. The Sinus Node is the Normal Pacemaker of - propels blood → lungs the Heart - for exchange of oxygen and carbon dioxide B. Abnormal Pacemakers – “Ectopic” Pacemaker Systemic circulation 1. Stokes-Adams Syndrome - blood → tissues IX. ROLE OF THE PURKINJE SYSTEM IN CAUSING Unidirectional flow of blood in heart SYNCHRONOUS CONTRACTION OF THE VENTRICULAR MUSCLE B. STRUCTURES X. SYMPATHETIC AND PARASYMPATHETIC NERVE Atrium – weak primer pump for ventricle RHYTHMICITY AND IMPULSE CONDUCTION Ventricle – main pumping force through A. Parasympathetic (Vagal) Stimulation B. Sympathetic Stimulation o Pulmonary circulation via Right Ventricle o Systemic Circulation via Left Ventricle Left chambers larger > right I. PURPOSE OF THE CARDIOVASCULAR SYSTEM Transport and distributes essential substances to II. CARDIAC CONDUCTING SYSTEM tissues and removes metabolic by products Generates rhythmical electrical impulses to initiate Participates in homeostatic mechanisms rhythmical contraction of the heart muscle o Regulation of body temperature Conducts these impulses rapidly through all parts of o Maintenance of fluid balance the myocardium Adjustment of O2 and nutrient supply under various Sinus node (also called sinoatrial or SA node)- in physiological states which the normal rhythmical impulses are generated; Heart - serves as a pump Internodal pathways- conduct impulses from the 4 Chambers of the Heart: sinus node to the atrioventricular (AV) node. o Right and Left Atrium (2) AV node- which impulses from the atria are delayed o Right and Left Ventricle (2) before passing into the ventricles; Tricuspid valve - separates right atrium from right AV bundle- which conducts impulses from the atria ventricle into the ventricles; and the left and right bundle Page 1 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 branches of Purkinje fibers, which conduct the cardiac Located in the right posterior portion of the interatrial impulses to all parts of the ventricles. septum Heart - rhythmic self-excitation with repetitive If SA node fails to generate impulse, the AV node takes over contraction approximately about 100,000x per day or but at a slower rate around 3 billion times in an average lifetime Electrical impulse = action potential A. SEQUENCE OF CARDIAC EXCITATION 1. SA node - normal pacemaker of heart; determines the rate to which the heart beats; initiates action potential 2. Internodal pathways 3. AV node 4. Common bundle of His 5. Left and right his bundles 6. Purkinje system - or Purkinje fibers; peripheral/ smaller areas 7. Ventricular muscle Sinoatrial (SA) node → Atrioventricular (AV) node via Internodal atrial pathways → Common bundle of His →Left & Right bundle branches → Purkinje fibers or system →Ventricular muscle Figure 3. Frontal Section of the Heart 3 BRANCHES OF INTERNODAL ATRIAL PATHWAYS TYPE Function Location Type of 1. Anterior (Bachman’s bundle) action 2. Middle (Wenckebach’s bundle) potential 3. Posterior (Thorel’s tract) Free wall Contractile Contracts and of atrium of working Fast pumps blood and Left bundle branch: anterior and posterior fascia cell ventricles Transmits Purkinje Conducting action conduction Fast potential system Generates an SA & AV Pacemaker action Slow node potential Table 1. Types of Cardiac Cells SA node: 60-80 beats/minute AV node 40-60 beats/minute (slower) III. TYPES OF ACTION POTENTIAL Fast – atrial, ventricle and Purkinje Figure 2. Pathway of Electrical Conduction Slow – SA and AV node SA NODE – NATURAL PACEMAKER Small, flattened, ellipsoid strip of specialized cardiac A. FAST TYPE CARDIAC ACTION POTENTIAL muscle about 3 millimeters wide, 15 millimeters long, Along concentration gradient - higher to lower concentration and 1 millimeter thick (diameter: 2-7 micrometer) Location: superior posterolateral wall of the right atrium 1. Ionic Basis for Fast Response Type of Action Potential immediately below and slightly lateral to the opening of Ions moves across membrane (via channels) along its the superior vena cava concentration and electrical gradient. have the capability of self-excitation, a process that can Opening of the fast sodium channels for a few cause automatic rhythmical discharge and contraction 10,000ths of a second is responsible for the rapid Generates spontaneous action potential → atrial upstroke spike of the action potential observed in muscle → contraction ventricular muscle because of rapid influx of positive Sinus nodal fibers connect directly with the atrial sodium ions to the interior of the fiber muscle fibers so that any action potential that begins in Na and Ca → mostly outside cell the sinus node spreads immediately into the atrial the “plateau” of the ventricular action potential is muscle wall. caused primarily by slower opening of the slow sodium- calcium channels, which lasts for about 0.3 second. AV NODE K → mostly inside cell Page 2 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 Ion channels open up o Na and Ca move into cell (NA and Ca influx) ▪ Positive generating events inside Higher Movement Type of cell concentration when its ion electrical o K moves out of cell (K efflux) channels event ▪ Negative generating events inside open generated cell inside the cell Sodium (Na+) concentration - higher outside the cell Na+ Outside the cell Influx Positive compared to the inside Potassium (K+) concentration - higher inside the cell Ca++ Outside the cell Influx Positive compared to the outside opening of potassium channels allows diffusion of K+ Inside the cell Efflux Negative large amounts of positive potassium ions in the Table 2. Ionic basis for fast response type of action potential outward direction through the fiber membrane and returns the membrane potential to its resting level. Efflux - going out of the cell (potassium) Influx - going inside the cell (sodium and calcium) Figure 4. Movement of ions across membrane in resting and depolarized stage. Figure 6. Conduction of fast action potential. State 1 2 3 M gates Close Open Open (Activation) H gates Open Open Close (inactivation) Excitability Yes No No Table 3. Excitability, Closing and Opening of Gates. Changes in cell membrane permeability - alter the rate of ion movement across the membrane and thereby change the membrane voltage -90 millivolts - Resting Membrane Potential; muscle is not stimulated Phase 0 = rapid influx of Na RMP for cardiac muscles & ventricles = -90 mV Threshold = -65 mV, it becomes less negative. If you say it’s reaching the threshold of -65 therefore the environment of the inner cell is becoming less negative and more positive. This diagram (figure 6) still depicts the conduction of fast action potential. When the resting membrane potential (which is -90 mV) is suddenly depolarized from -90mv to the Figure 5. Action Potential of cardiac muscle threshold potential of about -65 mV, the cell membrane Page 3 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 properties change dramatically. From this, the sodium enters the Period Correspond Responsiven Na myocyte through specific fast voltage-gated sodium channels ing phases ess to Channels that exist in the membrane. The channels open very rapidly or Stimulus Configurati become activated. on We have the M gate or the activation gate and the H Absolute Phase 0 till Unresponsive All of the Na gate or the inactivation gate (pointing at the Na channel). At the Refractory part of phase to any type of channels are resting stage, the M gate is closed and the H gate is open. Upon 3 that is stimulus open and stimulation by an action potential, the M gate opens and the above therefore threshold unexcitable channels become active. So, the sodium channels become potential active allowing the sodium ions to travel into the cell. This (TP) opening of the channel (the fast sodium ion channel), however, Relative Phase 3 that Responsive to Some of the is limited by time which lasts for about 1-2 milliseconds and the Refractory is below TP suprathreshold Na channels sodium concentration gradient rapidly decreases. After a till the start stimulus (with higher fraction of a second, the H gate closes spontaneously rendering of phase 4 threshold) the channels inactive. The sodium channels enter a refractory are now open and period during which they cannot be activated no matter how may be strong the stimulus is. This is referred to as the effective excitable refractory period (in some cases- absolute refractory period). with a higher During this time, the Na channels remain inactivated until the than membrane begins to repolarize or until it again reaches the threshold resting membrane potential. With repolarization, the channel intensity of transitions to the close state from which it can be reopened by the stimulus. Non- Phase 4 Responsive to All of the Na another depolarization of the membrane voltage to the threshold Refractory a threshold channels are potential. The properties of the sodium channel underlie the stimulus close and basis of the action potential refractory period. excitable When the sodium channels are in the inactivated state, Table 4. Three periods of the action potential (based on they cannot be reopened and another action potential cannot be response to a stimulus) generated. This prevents sustained tetanic contraction because if you’re going to think of it, there is continuous generation of 2. Fast Na Channels impulse without the absolute refractory period, then you expect When RMP → depolarized to threshold potential, ALL that there would be tetanic contractions of the cardiac muscle. If Na channels open (activate 0.1 msec) then rapidly there is tetanic contraction of the cardiac muscle, it would cause inactivate (1-2 msec) o Na+ channel in inactivated state failure of a ventricular relaxation and if there is failure of a ▪ Cannot be reopened and generate ventricular relaxation, therefore, it interferes with the function of AP the cardiovascular system of the heart per se which is to ▪ ERP normally intermittently pump blood from the heart going to your ▪ No available excitable closed Na systemic circulation. channels that can be stimulated As the cell repolarizes (phase 3) or as the cell tries to go back Phase 3 repolarization, Na channels that close first to its resting membrane potential, the inactivated channels (become excitable) are those with higher threshold begin to transition to the closed state (in which you can reopen followed later by channels with lower threshold o Relative refractory period or reactivate it) sodium channels. During this period, it is called o Other action potential can be generated but it the relative refractory period in which another action potential requires a larger than normal depolarization can be generated however, requiring a larger than normal of the intensity of stimulus depolarization of your membrane voltage. That is how the fast Greater than threshold intensity of the stimulus is needed action potential exhibited by the ventricles conducting system because it is the only intensity of the stimulus that can open the of the Purkinje and atria go about. Only when the membrane Na channels with high threshold for opening voltage has returned to its resting membrane potential of -90 These channels are voltage gate channels which exist mV are all sodium channels close thus able to reactivate the in 3 states (kindly see illustration) normal depolarization or normal generation of electrical The change in membrane potential which triggers its impulse. opening is not uniform. Based on the membrane potential that will trigger its opening, the fast Na channel can be classified as: Page 4 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 1. Slow Response of Pacemaker Type of fast Na Membrane potential that triggers channel the channels opening Low threshold -89 to -80 Moderate -79 to -70 threshold High threshold -69 to -65 Table 5. Types of Fast Na channels Phase Other Primary ion Main Negative names channels ion of involved flow membrane Potential 0 Depolarizat - Opening of Na Decreasing Figure 7. Action potential in a pacemaker cell. ion / Initial Na Channels Influx Depolarizat ion 1 Rapid - Closing of K Increasing Repolarizat Na channels efflux ion and maximum opening of K channels 2 Plateau - Opening of K No calcium Efflux significant channels and change while the K Ca channels are influx Figure 8. Action potential in a pacemaker cell open 3 Gradual - Closing of K Increasing Compared to a fast response, a slow response type of action repolarizati calcium efflux potential has the following features: on channels o Less steep phase 0 slope while the K o Lower overshoot channels are o No phase 1 open o Less sustained plateau phase 4 Resting -Nonper- o More gradual phase 3 membrane meability of o Less negative phase 4 potential protein anion o Phase 4 which shows gradual or diastolic (RMP) depolarization - Na-K pump o Longer refractory period which extends to the phase 4 (3 na efflux and 2 K These unique features are due to the difference in influx or 1 composition of the cell’s ion channels proton efflux) o Pacemaker cells lack the fast Na channel and therefore the slow Ca channels generates phase 0 (less steep -Permeability phase 0 slope &b lower overshoot) of the K leak o Pacemaker cells have less leaky K channels and channels therefore less K efflux during phase 4 (less negative Table 6. Phases of Action Potential RMP) Slow response action potential is exhibited by the IV. SELF-EXCITATION OF SINUS NODAL FIBERS pacemaker cells, the SA and AV nodes. Because of the high sodium ion concentration in the extracellular fluid outside the nodal fiber, as well as a B. SLOW RESPONSE ACTION POTENTIAL moderate number of already open sodium channels, positive sodium ions from outside the fibers normally (PACEMAKER CELL) tend to leak to the inside between heartbeats, influx of positively charged sodium ions causes a slow rise in the resting membrane potential in the positive direction Page 5 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 “resting” potential gradually rises and becomes less o Cardiac dilatation negative between each two heartbeats. When the o Hyperthermia potential reaches a threshold voltage of about −40 o Hypercalcemia millivolts, the L-type calcium channels become o Hypercapnia “activated,” thus causing the action potential the inherent leakiness of the sinus nodal fibers to V. INTERNODAL AND INTERATRIAL sodium and calcium ions causes their self-excitation PATHWAYS TRANSMIT CARDIAC IMPULSES High Na concentration in ECF with moderate number of THROUGH THE ATRIA open Na channels → Na ions leak from outside going inside the cell → influx of positively charged sodium ions causes a slow rise in the RMP → when the potential reaches a threshold voltage at about -40 mv, the L type calcium channels become “activated” → action potential RMP for pacemaker cells = -55 - -60 mV Threshold = -40 mV A. AUTOMATICITY The self-excitation of sinus nodal fibers is otherwise known as automaticity ability of the cardiac cells to generate a spontaneous action potential on its own. Although all cardiac cells have this property, it is particularly well developed among the pacemaker cells of the SA and AV node. the ionic events responsible for the pacemaker potential (phase 4 diastolic depolarization) are: o Leaky Na channels o Leaky Ca channels Figure 9. Internodal and Interatrial Pathways o Tight K channels Ends of the sinus nodal fibers connect directly with Why does this leakiness to sodium and calcium ions not surrounding atrial muscle fibers cause the sinus nodal fibers to remain depolarized all the The action potential spreads through the entire atrial time? muscle mass and eventually, to the AV node 2 events to prevent constant state of depolarization” There is a delay of.03 seconds on the generation of o L-type calcium channels become inactivated (i.e., they impulse on the sinoatrial nodes to the AV internodal close within about 100-150 milliseconds after opening atrial pathways gate going to your A-V node. o Increased numbers of potassium channels open → Velocity of conduction in most atrial muscle is about 0.3 Influx of Ca and Na through L type Ca channel ceases m/sec while at the same time large quantities of K ions dilute out → reduce the intracellular potential back to its negative resting level and therefore terminate the action VI. THE ATRIOVENTRICULAR NODE DELAYS potential IMPULSE CONDUCTION FROM THE ATRIA TO Why is this new state of hyperpolarization not maintained THE VENTRICLES forever? AV node delay: 0.09 second before the impulse enters After action potential is over → More Potassium channel as the penetrating portion of the A-V bundle. close progressively → inward leaking Na and Ca overbalance Before the impulse is conducted to the ventricles, there the outward fluid of K → slow rise in RMP until finally reaching is a delay of conduction of impulse of around.09 the threshold potential of -40 millivolts → discharge of action seconds in the AV node. potential This delay allows time for the atria to empty their blood into the ventricle before ventricular contraction begins B. CONDITIONS THAT ALTER AUTOMATICITY AV node to ventricular muscles 0.04 secs ( main delay VIA ALTERATION IN PHASE 4 SLOPE in penetrating bundle) 1. Decrease automaticity (decreases phase 4 slope) Total Delay in AV nodal (0.09 secs) and AV bundle Increased parasympathetic activity – vagal stimulation system (0.04 secs) = 0.13 second (the vagus nerve innervation of heart) Total time taken from SA node to ventricular muscle = Hyperoxemia 0.03 + 0.09+ 0/04 = 0.16 secs (before excitatory signal 2. Increase automaticity (increased phase 4 slope) reaches ventricular muscle from SA node - Increases rate of discharge of action potential brought about by: o Increased sympathetic activity Page 6 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 A. CAUSE OF THE SLOW CONDUCTION VIII. CONTROL OF EXCITATION AND Caused mainly by diminished numbers of gap junction CONDUCTION IN THE HEART between successive cells in the conducting pathways, so there is great resistance of conduction of excitatory ions from one conducting fiber to the next A. THE SINUS NODE IS THE NORMAL PACEMAKER OF THE HEART VII. RAPID TRANSMISSION IN THE Impulse normally arises in the sinus node VENTRICULAR PURKINJE SYSTEM The discharge rate of the sinus node is considerably faster From SA → AV via internodal atrial pathway → common bundle than the natural self-excitatory discharge rate of either the A-V of his → eventually branching out to left & right bundle branch node or the Purkinje fibers making the sinus node the primary → Purkinje fibers → eventually stimulating all parts of the heart veins of the heart. A. PURKINJE FIBERS Site Rate Are very large fibers, even larger than the normal SA Node 70-80/min ventricular muscle fibers, and they transmit action AV Node 40-60/min potentials at a velocity of 1.5 to 1.4 m/sec Purkinje 15-40/min Rapid transmission of action potentials by Purkinje fibers is believe to be caused by a very high level of Table 7. Rate of SA node, AV node and Purkinje permeability of the gap junctions at the intercalated discs between the successive cells that make up the AV nodes also have the capacity to generate electrical Purkinje fibers impulse however, compared to SA node, the AV node can generate electrical impulse at a slower rate. B. ONE-WAY CONDUCTION THROUGH THE In any event that the SA nodes become damaged, the AV nodes will take charge of generating electrical impulses or action A-V BUNDLE potential that will stimulate the contraction of the heart. With that, AV bundle characteristic: inability of the action you expect that with the AV node takes over, you expect that the potentials to travel backward from ventricles to the atria heart rate would only fall around 40-60/min but in the event that Everywhere, except at the A-V bundle, the atrial the AV node is also damaged, the Purkinje will take charge but muscle is separated from the ventricular muscle by a it will generate action potential at a much slower rate (15- continuous fibrous barrier, which normally acts as an 40/min), which is not compatible with life. 15/min is good as dead insulator to prevent passage of the cardiac impulse and cannot sustain life. between atrial and ventricular muscle through any other route besides forward conduction through the A- Why is SA node the normal pacemaker of the heart? V bundle SA node generates the highest rate of spontaneously generated action potential (SGAP) because it has C. DISTRIBUTION OF THE PURKINJE FIBERS IN o The steepest phase 4 slope THE VENTRICLES – THE LEFT AND RIGHT o A RMP that is nearest its TP SA node subdues the other potential pacemaker BUNDLE BRANCHES Overdrive suppression. After penetrating the fibrous tissue between the atrial o Hyperpolarization of the other cells due to and ventricular muscle, the distal portion of the A-V repeated stimulation of the NA-K pump. bundle passes downward in the ventricular septum for 5-15 millimeters toward the apex of the heart Rationale for potential automaticity of the other cells. o serves as a backup pacemaker when the SA Total elapsed time: only 0.03 second from the time the node fails to generate a SGAP cardiac impulse enters the bundle branches in the ventricular septum until it reaches terminations of the Purkinje fibers B. ABNORMAL PACEMAKERS – “ECTOPIC” rapid conduction of the Purkinje system normally PACEMAKERS permits the cardiac impulse to arrive at almost all a pacemaker elsewhere than the sinus node is called portions of the ventricles within a narrow span of time, an “Ectopic” Pacemaker exciting the first ventricular muscle fiber only 0.03 to o An ectopic pacemaker causes an abnormal 0.06 second ahead of excitation of the last ventricular sequence of contraction of the different parts of muscle fiber. the heart and can cause significant debility of heart D. TRANSMISSION OF THE CARDIAC IMPULSE pumping or it can eventually lead to arrhythmia - the irregular rhythm of the cardiac activity. IN THE VENTRICULAR MUSCLE CAUSES: Once the impulse reaches the ends of the Purkinje A place in the atrial or ventricular muscle develops fibers, it is transmitted through the ventricular muscle excessive excitability and becomes the pacemaker mass by the ventricular muscle fibers Blockage of transmission of the cardiac impulse from Velocity of transmission is 0.3 to 0.5 m/sec the sinus node to the other parts of the heart Page 7 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 Atria continue to beat at the normal rate of rhythm of the sinus node Figure 10. Cardiac Sympathetic and Parasympathetic Nerves. 1. STOKES – ADAMS SYNDROME After sudden AV bundle block, the Purkinje system does not begin to emit its intrinsic rhythmical impulses until 5 to 20 A. PARASYMPATHETIC (VAGAL) STIMULATION seconds, in which the ventricle fails to pump leading to fainting SLOWS THE CARDIAC RHYTHM AND after the first 4-5 secs due to lack of blood flow to the brain. CONDUCTION Stimulation of parasympathetic nerves in the heart → In the Stokes - Adams syndrome there is a delayed pick acetylcholine release at the vagal endings → effects: Decrease up of the heartbeat. If the delay is prolonged, it can lead to the rate of rhythm of the sinus node, decrease excitability of A- death. V junctional fibers → slowed rate of heart pumping strong stimulation of the vagi can stop completely the IX. ROLE OF THE PURKINJE SYSTEM IN rhythmical excitation by the sinus node or block CAUSING SYNCHRONOUS CONTRACTION OF completely transmission of the cardiac impulse from the THE VENTRICULAR MUSCLE atria into the ventricles through the AV node. In either case, rhythmical excitatory signals are no longer Rapid conduction of the Purkinje system normally transmitted into the ventricles. The ventricles may stop permits the cardiac impulse to arrive at almost all beating for 5 to 20 seconds, but then some small area in portions of the ventricles within a narrow span of the Purkinje fibers, usually in the ventricular septal time, exciting the first ventricular muscle fiber only portion of the AV bundle 0.03 to 0.06 second ahead of excitation of the last ventricular escape - a rhythm of its own and causes ventricular muscle fiber ventricular contraction at a rate of 15 to 40 beats per o Effective pumping by the two ventricular minute chambers requires this synchronous type of contraction o If the cardiac impulse should travel B. SYMPATHETIC STIMULATION INCREASES THE through the ventricles slowly, much of the CARDIAC RHYTHM AND CONDUCTION ventricular mass would contract before Stimulation of sympathetic nerves → norepinephrine release at contraction of the remainder, in which sympathetic nerve endings → stimulation of beta-1 adrenergic case the overall pumping effect would be receptors → increase in heart rate; increase force of contraction; greatly depressed. increase conduction velocity Sympathetic stimulation increases the overall activity X. SYMPATHETIC AND PARASYMPATHETIC of the heart. Maximal stimulation can almost triple the NERVE RHYTHMICITY AND IMPULSE heartbeat frequency and can increase the strength of heart contraction as much as twofold. CONDUCTION Increase in heart rate - Chronotropic The parasympathetic nerves (vagus nerve) is mainly Increase force of contraction- Inotropic distributed to SA and AV nodes to a lesser extent to the Increase in conduction velocity - Dromotropic muscle of atria and very little directly to the ventricular muscle. The sympathetic nerves conversely are distributed all over the heart with a strong TEST YOUR KNOWLEDGE representation to the ventricular muscle. 1. Small, flattened, ellipsoid strip of specialized cardiac muscle located at the superior posterolateral wall of the right atrium immediately below and slightly lateral to the opening of the superior vena cava. A. AV NODE B. SA NODE C. PURKINJE 2. Phase 2 is characterized by: A. Na influx B. K efflux C. K efflux and Ca influx 3. The negative of membrane potential of gradual repolarization is A. Decreasing B. No significant change C. Increasing 4. It is responsive to a threshold stimulus and all of the Na channels are close and excitable. A. Absolute Refractory Period Page 8 of 9 CMED 1C  (003) CARDIOVASCULAR PHYSIOLOGY (Electrical Properties of the Heart: Rhythmical Excitation of the Heart) Dr. Maeflor Ofilas | 12/14/2020 B. Relative Refractory Period C. Non-refractory Period 5. It has -89 to -80 membrane potential that triggers the fast Na channels opening. A. Low threshold B. Moderate threshold C. High threshold 6. The following are ionic events responsible for the pacemaker potential except: A. Leaky Na channels B. Leaky K channels C. Leaky Ca channels 7. The following increases automaticity except, A. Increased sympathetic activity B. Hyperoxemia C. Cardiac dilatation 8. Are very large fibers that transmit action potentials at a velocity of 1.5 to 1.4 m/sec. A. Bundle of his B. AV node C. Purkinje fibers 9. The following are features of a slow response type of action potential except A. Less steep phase 0 slope B. Lower overshoot C. More gradual phase 4 10. Effective pumping by the two ventricular chambers requires this A. Parasympathetic Stimulation B. Synchronous contraction C. Sympathetic Stimulation Answers: B, C, C, C, A, B, B, C, C, B REFERENCES 1. Guyton, A.C., Hall, J.E. Guyton and Hall textbook of Medical Physiology. 13th ed., W. B. Saunders, 2015. 2. Doc Ofilas’ PPT and lecture Page 9 of 9 CMED 1C