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Cardiovascular Physiology.docx

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Physiology 3120
Tom Stavraky

Cardiovascular Physiology General Function & Organization Role As Transportation System • Transport system: circulatory system o Transports oxygen & nutrients to various tissues o Transports carbon dioxide & waste products of metabolism from tissues to environment o Regulates body temperature (transporting excess heat out of the body) o Transports hormones & other substances (clotting factors, antibodies, hormones) • Components o Central pump: heart o Closed system of blood vessels o Fluid medium: blood – through which various substances are transported • Facts o Heart beats 2.5 billion times in an average life (66 years) o Begins on the 23 of fetal development o At rest – pumps 5 L/min o During exercise – pumps 20-40 L/min o 160, 000 km of blood vessels o Everyday 2,000 people die of heart disease General Organization of Cardiovascular System • Pulmonary system & lungs o Blood vessels that carry blood to & form the lungs o Provide exchange of gases o Contraction of right ventricle (EV) ejects venous blood into pulmonary artery – blood is low 2n O & high in CO2 o Pulmonary artery branches into smaller & smaller vessels until they become pulmonary capillaries o Blood picks up 2 from air & removes some of the C2 from the blood o Capillaries drain into venules & into pulmonary vein which carries oxygenated blood back to the left atrium (LA) of the heart o When atria contract, this blood is pumped into left ventricle (LV) • Systemic system o All the vessels that carry blood to & from the rest of the body o Contraction of LV ejects the blood into aorta o Aorta splits into numerous & smaller arteries for distribution of blood into the tissues o Arteries branch to form smaller arterioles & arterioles branch into smaller capillaries o Capillaries are exchange vessels where 2 & nutrients pass into tissues 2 CO & waste products are taken up into the blood o Capillaries reunite to form venules & veins – return the venous blood to right atrium (RA), from the RA blood flows into the RV – cycle repeats o Presence of valves in the heart & veins ensures the forward movement of blood • Heart is excluded – circulatory means blood vessels Series & Parallel Circuit • Various vascular beds (capillaries) are arranged in parallel – whereas the pulmonary circulation is connected in series to the heart • Parallel arrangement of vessels for the distribution of blood to various organs in system – advantages • Amount of blood flow to individual vascular beds can be controlled separately by dilating or constricting artery supplying a vascular bed • Such regulation is important – enables shifting of blood flow in accordance with physiological demands • Ex. to deliver more O2& nutrients to exercising muscles, blood to muscles can be increased temporarily decreasing flow to other organs such as kidneys, liver & GI tract • Parallel arrangement of vessels also contributes to relatively low resistance to blood flow; this in turn lowers the pressure requirement for blood flow & decreases work load on the heart Blood Volume Distribution • Roughly a total of 5 L blood in the human body • Heart & pulmonary circulation (blood to & from the lungs) contains 15% of total blood volume • Arteries of the system circulation contains about 10% of total blood volume • Systemic circulation contain about 5% • Very low value for capillaries is significant • Capillaries have the largest cross sectional area in circulatory system • When a small amount of blood, which is moving very slowly in the capillaries – exposed to large area • Facilitates very efficient diffusional exchange of substances between blood & tissues • Largest part of blood volume (70%) is contained in venous system Cardiac Function Function at Macroscopic Level General Anatomy of Heart • Contraction of ventricular myocardium (muscle) serves to drive up intraventricular pressure & thereby cause ejection of blood into aorta (in the case of the left ventricle) or pulmonary artery (in case of RV) • Valves associated with these chambers are passively opened or closed by pressure gradients & thereby serve to ensure unidirectional blood flow Location & Function of Heart Valves • Right Heart o Right atrioventricular (AV) valve (tricuspid) located between right atrium (RA) & right ventricle (RV) o Pulmonic valve (pulmonary valve) valve between pulmonary artery & RV o When RV contracts (systole), pressure in RV rises causing closure of right AV valve & opening of pulmonic valve o Right AV valve (& left AV valve) prevents backflow of blood from RV to RA during systole o When RV relaxes (diastole), pressure falls in RV, consequent momentary backflow of blood in pulmonary artery results in closure of pulmonic valve • Left Heart o Left atrioventricular (AV) valve (mitral) located between left atrium (LA) & left ventricle (LV) o Aortic valve located between aorta and LV o When LV contracts (systole), pressure in LV increases causing closure of left AV valve & opening of aortic valve o Left AV valve prevents back flow of blood from LV to LA during systole o When the LV relaxes (diastole), pressure falls in LV falls & momentary backflow of blood in aorta causes the closure of aortic valve o Aortic valve functions to prevent backflow of blood from aorta to LV during diastole Myocardial Cells Types of Myocardial Cells & Structural Organization • Two types of myocardial cells in the heart o Contractile cells – found in atria & ventricle muscle o Specialized excitatory (nodal) & conductive cells • Atrial & ventricular contractile muscle cells/fibres have many similar features & contract in a very similar fashion as skeletal muscle fibres but they are structurally different • Cardiac muscle o Similarities  Striated in the same manner as skeletal muscle  Typical myofibrils that contain actin & myosin filaments – almost identical to those found in skeletal muscle (isoforms)  Filaments interdigitate & slide along each other during process of contraction in the 2+ same manner as occurs in skeletal muscle (involves Ca ) o Differences  Fibres branch and recombine – yet each fibre is a complete unit surrounded by a cell membrane – sarcolemma  1/3 of their volume is occupied by mitochondria for production of ATP • Cardiac contractile cells can extract 80% of oxygen out of blood as it passes cells (60% at skeletal muscles) • Shorter • Made up of many cardiac muscle cells arranged in series with each other • Where 2 ends of cardiac cells meet – cell membranes form extensive folds: intercalated discs  • Electrical resistance through intercalated disc is only one four- hundredth the resistance through membrane of cardiac muscle fiber • Cell membranes fuse with each other & contain very permeable (gap) junctions that allow relatively free diffusion of ions • From a functional point of view – ions move with ease along the axes of cardiac muscle fibres so that AP travel from one cardiac muscle cell to another, past the intercalated discs with only slight hindrance • Cardiac muscle is said to be in a functional syncytium, in which cardiac muscle cells are so tightly bound that when one of these cells become excited, the AP spreads to all of them – form cell to cell through interconnections (skeletal muscle cells do not propagate APs from one cell to another – limited recruitment of motor unit only) • Heart is composed of two separate functional syncytia: o Atrial syncytium o Ventricular syncytium • Two syncytia are separated from each other by fibrous tissue called atrioventricular ring o Surrounds valvular openings between atria & ventricles • AP can be conducted from atrial syncytium to the ventricular syncytium by way of a special conductive system (AV node & Bundle of His) • Division of muscle mass of the heart to 2 separate functional syncytia allows atria to contract a short time ahead of ventricular contraction, which is important for proper heart pumping Specialized Excitatory/Conductive Cells • Contract very weakly because they contain very few contractile elements (myofibrils) • Have special properties of self-excitability (able to spontaneously generate an action potential) • Able to rapidly conduct these impulses to atrial and ventricular muscles • Specialized excitatory cells consist of: o Sinoatrial (SA) node o Atrioventricular (AV) node • Specialized conductive cells consist of: o Bundle of His o Purkinje fibres Excitation & Electrical Activity of the Cells • Origin of self-excitability – adult human heart normally contracts at rhythmic rate of 72 beats/min in vivo • Self-excitatory impulse originates in small crescent shaped structure: sinoatrial (SA) node – located in posterior wall of right atrium • Most cardiac cells have capability of self-excitation – process that can cause automatic rhythmic contractions • Capability of self-excitation is greatest in SA node • SA node ordinarily controls heart rate – called the pacemaker • SA node action potential (sometimes called a slow response AP) • Ventricular muscle AP (fast response AP) • Reason for differences is due to different cells utilizing special ion channels to produce different currents which in turn produce distinctive action potentials • Table shows ion channels & resulting currents that are responsible for the action potentials found in the heart – along with their functional role • Some channels are V.G and some are ligand (chemically) gated & some are both • Relative distribution of ions  Origin of Self-Excitability • Two major characteristics of the SA node, largely responsible for its self-excitability + 2+ o Cells of SA node have a relatively greater Na and Ca permeability (creating a +ve inward current), compared to other cells of the heart o K permeability of SA node cells declines during diastole • Because of the above properties, the SA nodal cells do not have a stable “resting” membrane potential • Maximum negativity of the “resting” potential of the SA node fiber is only about -60 mV in comparison with -90 mV for the ventricular fibre • Spontaneous generation of action potentials in the SA node is believed to occur as follows: SA Nodal Action Potential • Slow depolarization o During diastole, membrane potential slowly drifts toward a less negative value (diastolic depolarization due to higher permeability of the + SA 2+dal cells for Na (funn2+channels) and Ca (transient or t-type Ca channels) & steady decreases in K permeability during diastole o Slow drift of the membrane potential is called pre-potential (or pacemaker potential) • Depolarization o When the membrane potential reaches the threshold voltage of -40 mV, this rising voltage suddenly opens the slow L-Type Ca 2+ cha2+els o Ca flows into the cell causing total depolarization of the membrane followed by an overshoot of the membrane potential to about +20 mV o Slow response AP • Repolarization o At the peak of action potential, when the slow L-Type Ca channels close, greatly increased numbers of K channels become open + o Consequently, a large amount of K diffuses out of the cells o Repolarization carries membrane potential to about -60 mV • Cycle repeats o Repolarized state does not last long o Reason is that during the next few tenths of a second after AP is over – progressively more and more K channels begin to close o Inward-leaking Na & Ca ions once again overpower outward flux of K ions – causes membrane potential to depolarize, finally reaching threshold & firing another AP + • Figure shows that the V.G. K channels contribute to both the pre-potential & repolarization phase of SA nodal action potential + + 2+ • Inward Na current c2+ated by the funny channels (Na conductance) along with transient (T-type) Ca channels & the Ca V.G. (slow L-type) channel are all responsible for pre-potential • Slow L-type channels are responsible for depolarizing phase of SA node action potential • Rhythmic generation of action potential in the SA node determines the heart rate • Rate of discharge of action potentials by the SA node (& therefore heart rate) can be altered by: o Changing the slope of the prepotential (diastolic depolarization) – increase slope = increase HR o Changing the membrane potential from -60 mV i.e. ° of diastolic hyperpolarization – decrease in membrane potential = decrease in heart rate Conductive System of the Heart • Pathways for the conduction of impulses are shown in the figure below • SA nodal fibres fuse with surrounding atrial muscle fibres • Impulses generated in SA node spreads throughout atria • There is a special bundle of fibres – anterior interatrial myocardial band – conducts impulses from SA node directly to the left atrium • Anterior, middle & posterior intermodal pathway – conducts impulses form SA node to AV node • Band consists of ordinary myocardial cells & specialized conducting fibres • From the AV node - impulse is transmitted to the Bundle of His and then to right & left bundle branches • From the bundle branches the impulses are conducted through purkinje fibres which transmit the impulses to the ventricular muscle fibres • Within ventricular muscle mass, impulses are transmitted by muscle fibres themselves through gap junctions • Velocity of impulse conduction varies in different parts of the conductive system • Average velocities are given in table below • Differences in the speed of the conduction are importance in determining the proper sequence of events in the cardiac cycle & in the rhythmic performance of the heart Note that: • After a moderate velocity of conduction in the atria, the velocity slows in the AV node • Therefore at AV node, there is a delay in transmitting impulse from atria to the ventricle • Allows time for atria to contract & to empty blood into the ventricles before ventricular contraction begins • In contrast to AV node, in purkinje system conduction velocity is very high • Allows almost immediate transmission of the impulse throughout the entire ventricular system • On ce the impulse enters the Bundle of His from AV node, it takes only about 0.06 second to excite the entire ventricular muscle • Ventricular muscle remains contracted for 0.3 second • Rapid spread of excitation throughout the entire ventricular mass causes all portions of the ventricular muscle in both ventricles to contract almost at the same time • Effective simultaneous pumping of the 2 ventricles requires this synchronous type of contraction • Under abnormal conditions, other parts of the heart can initiate rhythmic contractions in the same way that fibres of the SA node can – particularly true of AV nodal & purkinje fibres • AV fibres discharge at an intrinsic rhythmic rate of 40-60 times per minute • Purkinje fibres discharge at a rate somewhere between 15-40 times per minute • Rates are in contrast to normal rate of SA node of 90 times per minute Electrocardiogram (ECG) • Body fluids are good conductors of electricity and heart sits in the middle of conducting fluid • When a cardiac impulse generated at SA node passes through various parts of the heart, electrical currents spread to surrounding tissues, & a small proportion spreads all the way to surface of the body • If electrodes are placed on the skin on opposite sides of the heart – electrical potentials generated by the heart can be recorded • Is the sum of all electrical events in the heart – both depolarizing and repolarizing • Different waves of the normal ECG, their sequence and timing of occurrence, and their relationship to events during cardiac cycle are summarized in Figure 15 and the accompanying Table • Because the movement of charge has both a 3 dimensional direction and magnitude, the signal measured on an ECG is a vector • P-wave: depolarization of atria muscle • QRS-Complex: rapid depolarization of right & left ventricles (large muscle mass compared to atria = larger amplitude) • T-wave: repolarization (or recovery) of the ventricles • U-wave: repolarization of papillary muscles in ventricles (not often seen on ECG) ECG Intervals Interval Average Range Events in Heart During Interval PR interval 0.18 0.12-0.20 Atrial depolarization & conduction (Tests AV node) through AV node (changes as HR SA node  AV node  Ventricles changes) QRS interval 0.08 To 0.10 Ventricular depolarization QT interval 0.40 To 0.43 Ventricular depolarization & Ventricular repolarization ST interval (QT-QRS) 0.32 ---- Ventricular repolarization PR interval decreases as heart rate increases • At a heart rate of 70 beats/min the PR interval is roughly 0.18 sec • At a heart rate of 130 beats/min the PR interval is roughly 0.14 sec Action Potentials in Other Parts of the Heart • Different cardiac tissues uniquely combine ionic currents to produce distinctively different APs • This can be seen in figure below – which shows action potentials recorded from single fibres of SA node, atrial muscle, AV node, bundle of His, Purkinje fibres & ventricular muscle • Many tissues use the same channels but in a different sequence – result is completely different AP • Note: slow & fast response APs: rate of depolarizing phase in SA node vs. atrium where SA node is not as steep (slower conduction velocities) • Greater amplitude of AP = greater rate of change of potential during depolarization = more rapid is the conduction down the fibre Action potential in ventricular contractile cells • Various phases of AP of ventricular muscle fiber and associated ion fluxes are summarized below • Also shown are the absolute refractory period (during which the muscle fibre cannot be excited by another AP) and relative refractory period (during which the muscle fibre may be excited by strong AP) A = absolute (effective) refractory period B = relative refractory period 1. Depolarization  Current flowing from a neighbouring cell (gap junctions) causes partial depolarization and opens + fast V.G. Na channels  Increases permeability for Na +  Sudden influx of this ion (fast inward current) causes the inferior of the cell to become positive with respect to extracellular fluid (up to 20 to 30 mV) 2. Rapid repolarization  At the positive membrane potentials the permeability of the cell membrane for Na decreases + - (fast Na channels close), but that for Cl increases  Inward movement of the negative ion combines with the leakage of K to create an outward current & cell begins to repolarize 3. Plateau Phase  AP opens slow (L-type) Ca channels & causes a slow inward movement of Ca which results2+ in a slow inward current +  Latter neutralizes the outward movement of K , and as a result the membrane potential is relatively steady 4. Restoration of resting potential 2+  Slow (L-type) Ca channels begin closing  Inward movement of Ca decreases while K continues to move outwards and restores membrane potential 5. Resting potential  -90 mV Excitation-Contraction Coupling • Refers to the process where an action potential on the cardiac contractile cell leads to release of Ca from the sarcoplasmic reticulum, which then causes muscle contraction • Process is similar to skeletal muscle but there are also some important differences • Similarities o AP on cardiac cell membrane (sarcolemma or SR) spreads to transverse (T) tubules 2+ o Depolarization of T-tubules causes release of Ca from sarcoplasmic reticulum (SR) into sarcoplasm (intracellular fluid) • Differences 2+ o Extracellular Ca enters sarcoplasmic during depolarization of sarcolemma o Ca interacts with SR to cause further release of Ca from SR o Process called Ca -induced Ca release (CICR) Switches during AP + 3 Na out  • During contraction, the concentration of free intracellular Ca in the sarcoplasm is increased by: o Depolarization-induced Ca 2+ influx from ECF through slow, L- 2+ type Ca channels (also called DHPR/Ca receptor) in the SL 2+  This Ca directly interacts with myofibrils to 2+ bring about contraction o Ca can also enter through Na /Ca exchanger since pump + is bidirectional & depends upon concentration gradients (Na and membrane potential) o Extracellular Ca induced Ca release+ 2+ 2+  Extracellular Ca that has entered via (a) can also open ryanodine/Ca channel on SR  Ca can also cause muscle contraction 2+  Some evidence that the depolarization of the SL can directly open ryanodine/Ca channels on SR but this is still controversial 2+ 2+ o Intracellular Ca -induced-Ca release from SR  Physical interaction of intracellular Ca with other ryanodine/Ca release channels (on 2+ SR) opens these channels causing Ca release • During excitation contraction coupling intracellular Ca levels increase 1000 times (from 0.1 μM to 100 μM) • Amount that enters through DHPR channels is very small compared with that released by SR • Extracellular Ca is not only essential for triggering Ca release from SR but also 2+ for maintaining adequate levels of Ca intracellular stores over the long run • Extracellular Ca is essential for cardiac muscle contraction Cardiac Muscle Contraction • Increased free [Ca ] in sarcoplasm causes activation of myofibrils to contract muscle 2+ • Mechanism of activation of myofibrils by Ca is similar skeletal muscle • Ca binds to troponin rolling tropomyosin of myosin binding sites on actin • Promotes actin-myosin interaction & stimulation of myosin ATPase • Sliding of actin filaments over myosin filaments produces contraction Cardiac Muscle Relaxation 2+ • Lowering Ca concentration in sarcoplasm brings about muscle relaxation – accomplished by: o Ca is actively pumped back into lumen of SR by Ca pump (Ca ATPase), which is on SR mem2+ane (80%) 2+ 2+ o Ca pump (similar to SR Ca pump) on SL - pumps Ca out into ECF (5%) o Na /Ca exchanger protein on SL moves Ca into the ECF in exchange for Na (3 Na for 1 + 2+ Ca )  Thought to function bidirectionally – capable of promoting 2+ + Ca influx coupled to efflux of Na Relaxation Relaxation  Activity of exchanger is dependent on transmembrane gradients for Na & Ca 2+ Temporal Relationship of Electrical Activity (Action Potential) & Mechanical Response in Cardiac Muscle Fibre • Contractile response of muscle begins just after the start of depolarization and lasts for about 300 ms • Contractile response of muscle fibre occurs during most of the absolutely refractory of the AP • When refractory period ends, more than 75% of the contractile response is over; the muscle has already relaxed considerably • Therefore, summation of twitches & a resulting tetanic type of contraction seen in skeletal muscle cannot occur in cardiac muscle Cardiac Cycle • Consists of a period of ventricular diastole (prolonged – 0.53 seconds of relaxation) & a period of ventricular systole (0.27 seconds of contraction) • Initiated by spontaneous generation of AP in the pacemaker: SA node • Impulse spreads rapidly throughout atria & is conducted into atrioventricular (AV-node) & then into ventricles • Propagation of this AP must be well coordinated in order for the heart to function efficiently as a pump • AP leads to contraction of cardiac muscle which causes precisely timed pressure changes in various parts of the heart • Pressure changes which then lead to opening & closing of valves as the blood moves through the heart • Cardiac cycle diagram o Shows all pressure & volume changes o Electrical events during a single contraction  Pressure changes in aorta, left atria & left ventricle  Volume changes in left ventricle  ECG  Phonocardiogram (heart sounds) • 7 phases in one cardiac cycle o Atrial systole o Isometric (ventricular) contraction o (Rapid) ejection period o protodiastole o Isometric (ventricular) relaxation o Rapid inflow o Diastasis • On cardiac cycle diagram – look for: o Points where lines of pressure cross (in most cases – except one – this indicates that valves are opening or closing o Blood pressure gradients (from regions of high pressure to low pressure) – if a valve is open, then blood flowing either from the left atria to the left ventricles or ventricle into the aorta o When blood is flowing – ventricular volume changes Pressure changes in aorta, left aria & left ventricle Volume changes in left ventricle 1. Atrial Systole  P wave represents atrial depolarization leading to atrial contraction  Atrial pressure is greater than ventricular pressure (AV valves are already open)  Ventricles fill (last 30%) – End Diastolic Volume (EDV) 2. Isovolumetric (Ventricular) Contraction – no volume change  QRS complex represents the depolarization of the ventricles and ventricles begin contracting  Causes pressure to build up in ventricles  Ventricular pressure exceeds atrial pressure – AV valves close  With all valves closed there is no change in volume (ventricular pressure is still less than aortic pressure) 3. Ejection Period  Ventricles continue to contract  Eventually ventricular pressure exceeds aortic pressure  Aortic valve opens and blood leaves ventricles  Ventricular volume decreases  T-wave (end of ejection period) 4. Protodiastole  Ventricles begin to relax  Ventricular pressure falls slightly (nothing to push against)  Aortic pressure is higher than ventricular pressure since blood is still moving into aorta due to considerable inertia (pressure change does not effect direction of blood flow)  Very little blood leaves the ventricle during this period  Not all the blood leaves the ventricle during phases 3 and 4 – End Systolic Volume (ESV) 5. Isovolumetric (Ventricular) Relaxation – no volume change  Ventricles continue to relax causing ventricular pressure to continue dropping  Blood in aorta reverses direction & causes aortic valve to close (2 heart sound)  Ventricular pressure is still greater than atrial pressure so AV valves are closed (in fact all valves are closed) – with all valves closed there is no change in ventricular volume 6. Rapid Inflow  Occupies the first 1/3 of ventricular diastole  Ventricles continue to relax  Ventricular pressure eventually drops below atrial pressure – causes AV valves to open  Blood rapidly enters ventricles (ventricular volume increases) Heart Sounds • First heart sound “lub” o First heart sound is caused by the sudden block of reverse blood flow due to closure of the AV valves, at the beginning of ventricular contraction o Results from reverberation within blood associated with sudden block of flow reversal by valves • Second heart sound “dub” o Second heart tone is caused by sudden block of reversing blood flow due to closure of aortic and pulmonary valves at the end of ventricular systole o Results from reverberation within the blood associated with the sudden block of flow reversal • Third heart sound o Not of valvular origin o Occurs at the beginning of diastole o Occurs when left ventricle is not very compliant, & at the beginning of diastole - rush of blood into left ventricle suddenly is halted, resulting in a vibration of ventricle & surrounding structures o Normal in children & young adults o Disappears before middle age as walls become more compliant Mechanical Performance of the Heart Cardiac Output & Blood Flow Distribution • Cardiac Output (CO) o Referred to as Q o Amount of blood pumped by left ventricle per minute 7. Diastasis  Occupies the middle 1/3 of ventricular diastole  Ventricles relaxed  Ventricular pressure is still lower than atrial pressure so AV valves are still open  Blood continues to enter ventricles but much more slowly  3 heart sound o Matched to cellular demand for oxygen – increases when the demand for oxygen increases Cardiac Output = Heart Rate (bpm) x Stroke Volume (ml) • Stroke volume o Amount of blood ejected form ventricle when it contracts • Normal resting values of CO in a normal healthy adult is ~ 5L/min (HR of 72 beats/min & SV of 70 ml) • Total blood volume of an average individual (5 L) is circulated roughly every minute at rest • Since systemic venous blood returns to right side of heart – output of right ventricle is almost exactly the same as that of the left ventricle • If resting output of the heart is 5 L/min – the distribution of these 5 litres or blood flow – matched to the demand for oxygen from various vascular beds • Blood flow at rest is very high in the brain, liver & kidneys despite their small body mass o Liver – to support high level of metabolic activity o Brain – provide nutrition & to prevent C2 & H concentrations from becoming too high in fluids o Kidneys – for adequate excretion so as to maintain a safe body fluid composition • Skeletal muscle represents 35-40% of body mass – in inactive state blood flow is ~15% of CO • As muscles become active – metabolic activity increases ~50-fold & blood flow ~20-fold Factors Controlling Cardiac Output • Depending on level of fitness CO can increase during exercise to 20L/min in untrained athletes & to 40 L/min in highly trained athletes • Increase in CO matches demand for oxygen • When CO increases in a healthy abut untrained individual, most of increase can be attributed to increase in heart rate (HR) • In trained individuals both HR & stroke volume (SV) increases • In untrained individuals o HR can vary by a factor of approximately 3 - between 60 & 180 beats per min o Stroke volume (SV) can vary by a factor of 1.7 - between 70 – 120 mL Control of cardiac output through changes in HR • Heart rate is set by spontaneous generation of AP in SA node • Self-excitability comes about because of the slow depolarization to firing threshold of the SA nodal cells – pre-potential (pacemaker potential) • Any change in rate of depolarization to threshold to threshold will ultimately change heart rate • Rate can be altered by: o Changing the slope of the pacemaker potential (slope =  heart rate) o Hyperpolarizing the membrane potential ( hyperpolarization =  in HR) • Heart rate is controlled primarily by input from autonomic nervous system – 2 divisions o Sympathetic  Stimulation causes increase in HR & therefore CO o Parasympathetic  Stimulation causes a decrease in HR and therefore CO • Parasympathetic nerves are distributed mainly to SA & AV nodes – indirect effect on atrial & ventricular muscle • Sympathetic nerves are distributed to SA & AV nodes but have a stronger representation to ventricular muscle Autonomic Neurotransmitters: • Preganglionic neurons of SNS & PNS secrete acetylcholine (Ach) – all cholinergic • Postganglionic neurons of PNS secrete acetylcholine (Ach) – PNS is completely cholinergic • Most postganglionic neurons of SN secrete norepinephrine (NE) – most are noradrenergic • Exception: some postganglionic neurons of SNS secrete acetylcholine (Ach) o Fibres to sweat glands & piloerector muscles o Vasodilator nerves to blood vessels of skeletal muscles o Fibres to adrenal medulla - Ach binds to nicotinic (N2) receptors to release epinephrine (80%) & norepinephrine (20%) Effects of Parasympathetic Vagal Stimulation: • Parasympathetic stimulation to the heart causes a decrease in heart rate (negative chronotropic response) owing to decrease in SA node rhythm and velocity of AP conduction through the AV node • PNS also causes a slight decrease in force of contraction (negative inotropic effect) Ach binds to muscarinic receptors Increase K permeability 2+ Dec+ease in Ca permeability (& possible Na ) Hyperpolarization Decrease slope Mechanisms of Parasympathetic Effects • Ach, released by cholinergic nerves, binds with muscarinic receptors + + o Open special K channels causing a2+increase in K permeability 2+ o Slow opening of slow L-type Ca channels causing a small decrease in Ca permeability o Effect on Na conductance is controversial but may decrease by closing “funny” Na channels • Overall result is a hyperpolarization of the membrane & a decrease in the slope of the pre-potential • Would take a longer time to reach threshold, which would cause a decrease in heart rate • Effect on AV node is similar causing slowing of AP conduction through AV node • Powerful PNS activation form a strong electrical stimulation of vagus nerve can completely stop impulse generation at SA node &/or completely block transmission of impulse through AV node • In either case impulses are no longer transmitted into ventricles; ventricles will stop beating for 4 to
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