PDF (004) Cardiovascular Physiology: Heart as a Pump (University of Northern Philippines)

(004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21...

(004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 OUTLINE I. CARDIAC MUSCLE PHYSIOLOGY A. Cardiac Muscle Contraction B. Action Potentials in Cardiac Muscle II. THE ATRIA FUNCTION AS PRIMER PUMPS FOR THE VENTRICLES A. Function of the Ventricles as pumps B. The Heart Valves C. Papillary Muscle III. HEART SOUNDS IV. MYOCARDIAL CONTRACTILE MACHINERY AND CONTRACTILITY V. REGULATION OF HEART PUMPING VI. INTRINSIC REGULATION OF HEART PUMPING – THE FRANK-STARLING MECHANISM VII. CONTROL OF THE HEART BY THE SYMPATHETIC AND PARASYMPATHETIC NERVES A. Parasympathetic (Vagal) Stimulation Slows the Cardiac Rhythm and Conduction B. Sympathetic Stimulation Increases the Figure 1. Structure of the heart and course of blood flow through the heart chambers and heart valves. Cardiac Rhythm and Conduction C. Effect of Sympathetic or A. CARDIAC MUSCLE CONTRACTION Parasympathetic Stimulation on the CARDIAC MUSCLE – striated with myofibrils containing Cardiac Function Curve actin and myosin filaments VIII. EFFECTS ON HEART FUNCTION INTERCALATED DISCS – dark areas crossing cardiac muscle fibers I. CARDIAC MUSCLE PHYSIOLOGY o Cell membranes of individual cells that The heart consists of 2 pumps working in series. separate individual cardiac muscle cells from o The right heart that pumps blood through the one another lungs o Gap junctions are present in the intercalated o The left heart that pumps blood through the discs which forms permeable communicating systemic circulation junctions and allow rapid diffusion of ions. PUMPS/CIRCULATION ▪ Enables action potentials in adjacent o PULMONARY CIRCULATION – propels blood myocytes to depolarize target cells – lungs (heart to lungs via Right ventricle) ▪ Allow rapid diffusion of ions o SYSTEMIC CIRCULATION – blood – tissues o Functional point of view: Ions movement is in (propels blood from the heart going to different the intracellular fluid or on the longitudinal axis tissues of the body) of the cardiac muscle fibers so that action o Unidirectional flow of blood in heart (a forward potential travel easily from one cardiac muscle motion only; no regurgitation under normal cell to the next circumstances) STRUCTURES o ATRIUM – weak primer pump for ventricle o VENTRICLE – main pumping force through ▪ Pulmonary circulation via RV ▪ Systemic circulation via LV Left chambers > right Cardiac Rhythmicity is the continuing succession of the heart contraction that aids in the transmitting of the action potential throughout the cardiac muscle Figure 2. Syncytial, interconnecting nature of cardiac muscle fibers. Gap functions Page 1 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 Ventricular muscle fibers averages about 105 millivolts Diagram shows the AP recorded in a ventricular muscle (blue) involves the intracellular potential rises from a very negative value of more of less -85 mV (RMP of ventricular muscle -85 to -90 mV) between beats to a slightly positive value of about 20 mV during each beat. After the usual spike the membrane remains depolarize for about 0.2 second exhibiting a plateau then followed at the end of plateau by abrupt repolarization. WHAT CAUSES THE LONG ACTION POTENTIAL AND THE PLATEAU? Figure. 3 Microscopic image of cardiac muscle and its diagram In the cardiac muscle the action potential is caused by (pointed at the intercalated discs). the opening of 2 types of channels: 1. VOLTAGE GATED FAST SODIUM Cardiac muscle as syncytium of many heart muscle cells CHANNELS in which the cardiac cells are so interconnected that when o facilitates rapid influx of sodium and is one cell becomes excited, the action potential rapidly inactivated rapidly spreads to all of them (if one cell is stimulated, it spreads 2. (CA-NA CHANNEL) L TYPE SLOW CALCIUM all throughout) CHANNEL 2 SYNCYTIA o slower to open and they remain open o ATRIAL SYNCYTIUM – walls of the 2 atria for a several tenths of a second. o VENTRICULAR SYNCYTIUM – constitutes the o large quantity of both Ca and Na ions walls of 2 ventricles flows through these channels to the ATRIA interior of cardiac muscle fibers - separated from the ventricles by fibrous tissue o this activity maintains a prolonged that surrounds the atrioventricular valvular period of DEPOLARIZATION causing openings between the atria and ventricles the plateau in the action potential. - prevents action potential conduction directly o the calcium influx during the plateau from atria syncytium to ventricular syncytium. phase activates the muscle contractile DIVISION OF THE MUSCLE OF THE HEART IN 2 process making the inside of the cell SYNCYTIA: more positive - allows the atria to contract a short time a head o presence of delayed potassium of ventricular contraction for effective heart channels which are open pumping. counterbalances the influx of calcium that results in PLATEAU PHASE. B. ACTION POTENTIALS (AP) IN CARDIAC DEPOLARIZATION (PHASE 0) – RAPID REPOLARIZATION (PHASE 1) – PLATEAU (PHASE 2) MUSCLE - GRADUAL REPOLARIZATION (PHASE 3) – RESTING MEMBRANE POTENTIAL (PHASE 4) Immediately after the onset of the action potential: o The permeability of the cardiac muscle membrane for K+ ions decrease about 5 folds, due to the excess Ca2+ influx through the Ca2+ channels, an effect that does not occur in skeletal muscle. Presence of Plateau in cardiac muscle is caused by: o Increased Ca Ion Permeability o Decreased K Ion Permeability Figure 4. Rhythmical action potentials (in millivolts) from a Purkinje fiber and from a ventricular muscle fiber, recorded by means of microelectrodes. Page 2 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 cannot re-excite an already excited area of cardiac muscle. o Normal refractory period of Ventricle: 0.25 to 0.30 seconds (approximately the duration of the prolonged plateau phase of the action potential) o Normal refractory period of Atria: 0.15 second EXCITATION-CONTRACTION COUPLING o refers to the mechanism by which the action potential causes the myofibrils of muscle to contract (action potential of the cardiac myocytes leads to contraction) o in skeletal muscles, when an action potential passes over the cardiac muscle membrane, the action potential spreads to the interior of the cardiac muscle fiber along the membranes of the transverse (T) tubules Figure 5. Action potential of cardiac muscles o in cardiac muscles, calcium ions also diffuse into the sarcoplasm from the T tubules themselves at the time of the action potential, which opens voltage-dependent calcium channels in the membrane of the T tubule o cardiac muscle excitation – wave of excitation spreads along sarcolemma (cell to cell) via gap junctions o excitation spread into interior of the cells via T tubules (invaginate at z lines) ▪ Ca++ enter via L type Ca++ channel but not enough to induce contraction but act as trigger to release Ca from SR ▪ Ca++ leaves SR through Ca release channel (Ryanodine Receptors). The movement of Ca++ ions in the SR going to the cytosol, increases the amount of calcium ions present intracellularly. ▪ Ca++ binds to troponin C, forming the Calcium-troponin Complex. This complex eventually interacts with tropomyosin which unblocks the active Figure 6. Phases of action potential. site between actin and myosin. This unblocking initiate cross bridge VELOCITY OF SIGNAL CONDUCTION IN CARDIAC cycling which subsequently leads to MUSCLE contraction of myocyte. o Excitatory action potential signal along both o Generation of Action Potential is made atrial and ventricular muscle fibers – 0.3 to 0.5 possible by the constant ionic movement m/sec (calcium ion influx) o Purkinje fibers – velocity of conduction: 4 o Cardiac muscle cells cannot be in the state of m/sec. This allows rapid conduction of the constant contraction, otherwise, it can lead to excitatory signal to the different parts of the death. heart. o T tubules of cardiac muscle have a diameter 5 o Made possible by presence of gap junctions times as great as that of the skeletal muscle tubules, which means a volume 25 times as REFRACTORY PERIOD OF CARDIAC MUSCLE great. o Cardiac muscle, like all excitable tissue, is o In contrast, the strength of skeletal muscle refractory to re-stimulation during the action contraction is hardly affected by moderate potential changes in extracellular fluid calcium o Refractory period of the heart is the interval of concentration. time which a normal cardiac muscle impulse Page 3 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 o Cardiac action potential, the influx of calcium ions to the interior of the muscle fiber is Refer to Figure 8. At the end systole, the influx of calcium suddenly cut off, and calcium ions in the stops, and the SR is no longer stimulated to release sarcoplasm are pumped back out of the muscle calcium. The SR then reuptake the calcium by means of fibers via calcium–adenosine triphosphatase Sarcoplasmic Reticulum ATPase. Sarcoplasmic (ATPase) pump. Reticulum ATPase pumps cytosolic calcium going to the SR. If there will be reuptake, there will be a decrease level of calcium in the cytosol or cytoplasm. Cytosolic calcium is also reduced during diastole through the action of the Sodium-Calcium exchanger: 3 Na and 1 Ca antiporter. This antiporter facilitates the entrance of 3 Na ion inside the cell in exchange in extrusion of 1 Ca ion going outside the cell. This mechanism result in relaxation of cardiac muscle. Decrease in cytosolic calcium will lead to release of calcium from the calcium-troponin complex and the cross-bridge cycling stops and eventually myofibrils relax. Figure 7. Excitation Contraction Coupling. Ca ions that move from the extracellular to intracellular triggers the release of Ca from SR where the Ca stores are located intracellularly. During the AP, the Ca channels open therefore facilitating the entry of Ca ions inside the cell. The Ca ion that has entered the cell are not enough to induce contraction. Higher Ca ion level is needed to stimulate contraction. RELAXATION OF CARDIAC MUSCLE o SR Ca++ - ATPase – reuptake Ca o Sarcolemma Ca++ - ATPase Figure 9a. Key concepts of cardiac muscle contraction. o Sarcolemma 3Na+-1 Ca++ antiporter Refer to Figure 9a. Auto rhythmicity (neural input is not required though both neural and hormonal factors can affect the rate of depolarization.). EC Coupling (skeletal muscle EC coupling requires only sarcoplasmic reticulum calcium release.). Contractility can be increased or decreased by various factors including availability of calcium. (e.g. (1) Cardiac glycosides are prescribed for heart failure. (2) Calcium channel blockers-blocks the L- type calcium channels and prohibit calcium influx and therefore reduced contractility as a treatment for hypertension, angina and some arrhythmias) Figure 8. Mechanisms of excitation-contraction coupling and relaxation in cardiac muscle. ATP, adenosine triphosphate. Page 4 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 binding and crossbridge cycling to shorten the sarcomeres. Contraction via the sliding filament mechanism occurs as in skeletal muscle. HOW EXCITATION CONTRACTION COUPLING LINKS THE ACTION POTENTIAL TO SARCOMERE SHORTENING AND THEREFORE CARDIAC MUSCLE CONTRACTION. o The excitation contraction coupling, and cardiac muscle cells relies on calcium induces calcium release. STEPS OF EC COUPLING o Action potentials generated typically by pacemaker cells in a SA node and is then transferred from cell to cell via gap junction. o As the action Potential travels along the sarcolemma triggers the opening of the voltage- gated-l-type calcium channels. This allows the calcium to move down its electrochemical gradient into the cell. o Calcium influx opens the ryanodine receptors on the sarcoplasmic reticulum and large quantities of calcium ions move into the intracellular fluid. o Calcium induced calcium release creates a calcium spark which amplifies the calcium signal o Calcium binds troponin and ultimately allows cross bridge cycling and sarcomere shortening contract the myocardial cells. Figure 9b. Excitation-Contraction Coupling. o Muscle cells cannot be in a state constant contraction; calcium influx ends when the Refer to Figure 9b. Z disc anchor the thin filaments. In the channels closed but we also need to remove the spaces between thin filaments, the thick filaments extend calcium already present in the intracellular fluid. from the perpendicular M line. I band (light band) of the o This is achieved by the continuous action of myofibril comprises the area where there is no overlap Sodium calcium exchange which moves between the thick and thin filaments. The area where the calcium into the sarcoplasmic reticulum in thick and thin filaments do overlap is referred to as A extracellular space, respectively. band (dark band). The sarcomeres span from Z disc to Z o 3 Na ions exchange for 1 Calcium ion. Sodium disc. The sarcomere is the functional contractile unit of is then pumped outside the cell via Na-K myofibril. As in skeletal muscle, cardiac muscle ATPase. contraction requires binding of thick and thin filaments o As a result of reduces intracellular stores and and cross bridge cycling to shorten the sarcomere create troponin release of calcium crossbridge cycling muscle tension. stops and the sarcomere relaxes. THICK FILAMENTS feature the protein myosin and actin. During contraction, the myosin heads bind with actin to form cross bridges. 3 KEY PROTEINS OF THIN FILAMENTS o primary proteins actin which comprises multiple polypeptide subunits called globular actin arranged in a double helix with myosin binding Figure 10. Any mechanism that raises cytosolic calcium increase site and 2 regulatory proteins associated with the force developed, those that lower the cytosolic calcium actin. decrease the force developed with the force of contractions. o Tropomyosin strands wrapped around the actin molecules and in a relaxed state covers their Mechanisms: myosin binding site. o Catecholamines o Troponin is a three-polypeptide complex. One of o Increased extracellular Calcium gradient the polypeptides serves as a calcium binding o Reduced Na+ gradient across the sarcolemma site. Troponin binds intracellular calcium causing tropomyosin movement and exposure of myosin binding sites allowing myosin actin Page 5 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 Decrease in Sodium gradient likewise increase in force via the 3 Na+-1Ca++ antiporter. So, if there is low Na+ concentration gradient outside, no Na+ that can be transported inside, hence there will be no or reduced Ca++ extrusion leading to an increase Ca++ in the cytosolic area, thereby facilitating contraction and increasing force. Cardiac glycoside inhibit Na+,K+-ATPase (responsible for the efflux of Na++), so if Na+,K+-ATPase is blocked, the Na++ is not transported out from the intracellular space, thus accumulating intracellularly causing increased Na++ ion level in the cell, which in turns reverses the 3Na+-1Ca++ exchanger pump, whereby causing a lesser Ca++ extruded and increasing the cytosolic Ca++ PKA o Phosphalamban → inhibitor of SR Ca ATPase o If SR Ca ATPase (Serca 2a/Sarcoendoplasmic reticulum Ca2+ ATPase 2a) inhibited → ↑Ca o PKA phosphorylates phospholamban → inhibitory function ↓ → uptake of Ca into SR ↑ → Figure 11. Diagram that shows the mechanism in calcium ↓Ca → relaxation concentration changes. o PKA phosphorylates trop I → inhibit binding of Ca by trop C tropomyosin return to blocking Refer to figure 11. Catecholamines bind to their position of myosin to actin → relaxation receptors, Adenylyl cyclase activated, thereby increasing o the level of intracellular level of cAMP, leads to the II. THE ATRIA FUNCTION AS PRIMER PUMPS FOR activation of cAMP-PK. THE VENTRICLES Catecholamines - phosphorylation of sarcolemmal Ca channel via cAMP dependent protein kinase A Blood flows continually from the great veins into the atria phosphorylates sarcolemmal Ca ↑ Ca entry to the cell 80% of blood flows directly through atria into ventricles stimulates release of CA from SR ↑ force even before the atria contracts ↓ Na gradient → ↑force Atrial contraction causes additional 20% filling of the Less Na enter → via 3 Na+ -1Ca++ antiporter (extrude ventricles. Therefore, the atria functions as a primer Ca) pumps that increase the ventricular pumping effectiveness as much as 20%. Cardiac glycoside inhibits Na+, K+ -ATPase → ↑[Na+] in cells → reverse 3Na+ -1Ca++ → less Ca extruded ↓Ca→↓force Ca channel antagonist prevent Ca from entering cell CAMP-PK HAS MULTIPLE EFFECTS IN THE CELL: 1. Phosphorylates the calcium channel in the sarcolemma, causes increase entry of calcium into the cell thus increasing the force of contraction 2. Phosphorylates the Troponin I which in turns inhibits the binding of Calcium with troponin C, as a result tropomyosin returns to its position of blocking the myosin binding site on the active filaments thus promoting relaxation. 3. Phosphorylates the Phospholamban normally inhibits the sarcoplasmic calcium ATPase. When phospholamban is phosphorylated the inhibitory action is reduced, and the uptake of calcium into the sarcoplasmic reticulum is therefore enhanced. There is enhanced reuptake of cytosolic calcium, leading to a decrease cytosolic calcium level causing Figure 12. Parts of the Heart relaxation. Page 6 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 Pressure Changes in the Atria- a, c, and v Waves Table 2. Differences of right and left ventricles o a wave is caused by atrial contraction (right atrial pressure increases 4 to 6 mm during atrial B. THE HEART VALVES contraction, and the left atrial pressure increases about 7 to 8 mm Hg) o c wave occurs when the ventricles begin to contract o v wave occurs toward the end of ventricular contraction ATRIA VENTRICLE Thin-walled, low-pressure Muscular chambers Ejects blood into lungs/ Smaller systemic circulation Reservoir Apex contracts before base Primer ↑ ventricular pumping by 20% Table 1. Differences of heart chambers Figure 13. Mitral and aortic valves (the left ventricular valves). A. FUNCTION OF THE VENTRICLES AS PUMPS ATRIO-VENTRICULAR VALVE SEMIILUNAR VALVES The Ventricles Fill with Blood During Diastole TRICUSPID & MITRAL VALVES AORTIC & PULMONIC o during ventricular systole, large amounts of blood These are regarded as an VALVES accumulate in the right and left atria. Inlet which controls blood Outlet o as soon as systole is over and the ventricular flow from the atria going to High pressure in pressures fall again to their low diastolic values, the ventricle. arteries valves o the moderately increased pressures that have Atrial Ventricle close developed in the atria during ventricular systole Unidirectional ↑ velocity of immediately push the A-V valves open - prevent backflow to blood o allow blood to flow rapidly into the ventricles (period atria during systole ↑ mechanical of rapid filling of the ventricles which lasts for about - placement of atrio- abrasion ventricular valve *The high pressure in the the first third of diastole. makes it possible that arteries facilitates the o during the middle third of diastole, only a small the blood flow through closure of these valves. amount of blood normally flows into the ventricles the atria going to the Because of the smaller o during the last third of diastole, the atria contract and ventricle is opening the velocity of give an additional thrust to the inflow of blood into the unidirectional or blood ejection through the ventricles forward motion. aortic and pulmonary Outflow of Blood from the Ventricles During Systole supported by chordae valves is far greater than Period of Isovolumic (Isometric) Contraction tendinae that through the much o after ventricular contraction begins, the ventricular TRICUSPID VALVE larger AV valve. So, there pressure rises abruptly - 3 flaps is increase velocity of blood o contraction is occurring in the ventricles, but no - it regulates or controls ejection and because of the emptying occurs (period of isovolumic or isometric blood flow from right rapid closure and rapid contraction, meaning that cardiac muscle tension is atrium to right ejection the edges of the increasing but little or no shortening of the muscle fibers ventricle aortic and pulmonary is occurring) MITRAL VALVE valves are subjected too - 2 flaps much greater mechanical RIGHT VENTRICLE LEFT VENTRICLE abrasion than that of AV - controls blood flow 3 motions Dual motion valves. from left atrium to left Longitudinal Circular muscle ventricle shortening with contraction traction of the tricuspid - More powerful Table 3. Differences between AV valve and semilunar valve annulus towards apex - High pressure Radial motion of free Spiral muscle wall- “bellows effect” contraction C. PAPILLARY MUSCLE Anteroposterior - Squeezing Pull the vanes of the valves inward toward the ventricles to shortening of toothpaste prevent valves from bulging too far backward toward the atria chamber by stretching - Smaller Papillary muscles contract when the ventricular walls free wall over the surface-to- contract septum. volume ratio A ruptured chordae tendinea or if one of the papillary Eject large vol. w/ low Generate higher pressure muscles becomes paralyzed, the valve bulges far backward intraventricular pressure during ventricular contraction, sometimes so far that it leaks Page 7 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 severely and results in severe or even lethal cardiac o Pressure in the aorta that must be overcome by incapacity. the contracting left ventricle to open the aortic valve and eject blood III. HEART SOUNDS V. REGULATION OF HEART PUMPING AT REST - heart pumps only 4-6 L of blood per minute First heart sound (S1) DURING STRENOUS EXERCISE After closure of MV & TV - heart may be required to pump 4-7x Stronger, prolonged and lower frequency FACTORS THAT REGULATE THE VOLUME PUMPED S1 Initiated at the onset of ventricular systole or ventricular BY THE HEART: contractions. o Intrinsic cardiac regulation of pumping in Heard best at the apical region of the heart. response to changes in volume of blood flowing into the heart o Control of heart rate and strength of heart Second heart sound pumping by the autonomic nervous system AV & PV closure Shorter, high pitched VI. INTRINSIC REGULATION OF HEART PUMPING S2 Occurs with the abrupt closure semilunar valves the AV & PV – THE FRANK-STARLING MECHANISM Composed of higher frequency vibrations, higher pitch, shorter duration and lower intensity than the 1st heart sound Intrinsic ability of the heart to adapt to increasing volumes of inflowing blood Venous return o rate of blood flow into the heart from the veins. Third heart sound o Each peripheral tissue of the body controls its Coincides w/ rapid ventricular filling own local blood flow, and all the local tissue Vibration due to sudden inrush of blood flows combine and return by way of the veins to Diastolic filling gallop/ protodiastolic gallop the right atrium. S3 Physiologic in children o The heart automatically pumps this incoming Pathologic in adults (low compliance) blood into the arteries so that it can flow around Sometimes heard among patients who have congestion or heart failure. (Normal Heart Sound – Lub dub: 3rd Heart Sound the circuit again – Lub dudub) Frank-Starling mechanism o means that the greater the heart muscle is stretched during filing, the greater is the force of Fourth heart sound contraction & the greater the quantity of blood Coincides w/ atrial contraction pumped into the aorta. Due to ↑ atrial pressure or still LV S4 Always pathologic when an extra amount of blood flows into Presystolic gallop the ventricles, the cardiac muscle is Occurs before S1 stretched to a greater length. this stretching in turn causes the muscle IV. MYOCARDIAL CONTRACTILE MACHINERY & to contract with increased force because the actin and myosin filaments are CONTRACTILITY brought to a more nearly optimal degree The contraction of cardiac muscle is influenced by both of overlap for force generation preload and afterload. PRELOAD o Force that stretches the relaxed muscle fibers ventricle automatically pumps extra blood o The blood filling & thus stretching the wall during into the arteries diastole represents the preload o the amount of blood in the ventricles during diastole. Can be increased by greater filling during diastole VII. CONTROL OF THE HEART BY THE AFTERLOAD SYMPATHETIC & PARASYMPATHETIC NERVES o The force against which the contracting muscle VAGUS NERVE must act o Distributed mainly to SA & AV nodes o Pressure in the aorta w/c the contracting muscle must act Page 8 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 The pumping effectiveness of the heart is also controlled B. SYMPATHETIC (VAGAL) STIMULATION by the sympathetic (increases the amount of cardiac output often by more than 100%) and parasympathetic INCREASES THE CARDIAC RHYTHM AND (vagus) (decreases it to almost zero) nerves. CONDUCTION Stimulation of sympathetic nerves Norepinephrine release at the sympathetic nerve endings Stimulation of beta-1 adrenergic receptors Increase in heart rate; increase force of contraction; increase conduction velocity C. EFFECT OF THE SYMPATHETIC OR PARASYMPATHETIC STIMULATION ON THE CARDIAC FUNCTION CURVE Figure 14. Cardiac sympathetic and parasympathetic nerves. At any given right atrial pressure, the cardiac output (The Vagus nerves to the heart are parasympathetic nerves.) A- increases during increased sympathetic stimulation and V, atrioventricular; S-A, sinoatrial. decreases during increased parasympathetic stimulation. A. PARASYMPATHETIC (VAGAL) STIMULATION SLOWS THE CARDIAC RHYTHM AND CONDUCTION Stimulation of parasympathetic nerves in the heart Acetylcholine release at the vagal endings Effects: Figure 15. 4 cardiac function curves of the entire heart. Relation 1. Decreases the rate of rhythm of the between right atrial pressure at the input of the right heart and sinus node cardiac output from the left ventricle into the aorta. 2. Decreases excitability of AV junctional fibers VIII. EFFECTS ON HEART FUNCTION Effects of ↑ Body temperature, ↑ HR Slowed rate of heart pumping o heat presumably increases the permeability of the cardiac muscle membrane to ions that control heart rate, resulting in acceleration of the self- excitation process. o Contractile strength is enhanced temporarily by a moderate increase in temperature, but prolonged elevation exhausts the metabolic systems of the heart causing weakness Effects of ↓ Body temperature, ↓ HR Effects of Potassium o ↑K+ in ECF (hyperkalemia) causes the heart to become dilated and flaccid and also slows the heart rate Page 9 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 o ↑K+ concentration in the extracellular fluids D. pulse rate decreases the resting membrane potential in the cardiac muscle fibers. 7. The second heart sound is caused by o As the membrane potential decreases, the intensity A. closure of the aortic and pulmonary valves of the action potential also decreases contraction of B. vibrations in the ventricular wall during systole the heart progressively weaker. C. ventricular filling o can block conduction of the cardiac impulse from the D. closure of the mitral and tricuspid valve atria to the ventricles through AV bundle E. retrograde flow in the vena cava o cardiac weakness (effect of high potassium) Effects of Calcium 8. This is caused by spread of depolarization through the o ↑Ca2+ = spastic contraction, tetanic contractions atria. A. P wave TEST YOUR KNOWLEDGE B. T wave 1. What is the normal refractory period of an atria muscle? C. a wave A. 0.22 sec D. c wave B. 0.18 sec C. 0.16 sec 9. During the middle third of diastole, D. 0.13 sec A. small amount of blood normally flows into the E. 0.15 sec ventricles 2. In which phase of the ventricular muscle action potential B. atria give an additional thrust to the inflow of blood is the potassium permeability the highest? into the ventricles A. 0 C. large amounts of blood accumulate in the right and B. 1 left atria C. 2 D. Large amount of blood abnormally flows into the D. 3 ventricles E. 4 10. The work performed by the left ventricle is substantially 3. Which of the following events occurs at the phase 3 greater than that performed by the right ventricle, (Rapid repolarization) of the cardiac muscle membrane because in the left ventricle potential? A. the contraction is slower A. Closing of the Fast sodium channel B. the wall is thicker B. Opening of the Fast potassium channels C. the stroke volume is greater C. Opening of the L type slow Calcium channels D. the preload is greater D. Opening of the slow potassium channels E. the afterload is greater E. Closing of the all the Potassium channels 11. Which of the following statements are CORRECT about 4. Prevents action potential conduction directly from atria the heart valves? syncytium to ventricular syncytium A. AV valve prevent backflow of blood from the A. Atrioventricular valve ventricles to the atria during diastole while Semilunar B. Atrioventricular bundle valve prevent backflow from the aorta and C. Deep connective tissue pulmonary arteries into the ventricles during systole. D. Fibrous tissue B. Semilunar valve has lesser blood velocity than AV E. Subendocardial layer valve. C. AV valve and Semilunar valve are both supported by 5. All are the characteristics of a cardiac muscle except: chordae tendinae A. Presence of cross Striations D. Semilunar valve is subjected to much greater B. Pumps blood via rhythmic contraction mechanical abrasion than AV valve. C. Pumps blood via Voluntary movement D. Cardiac cells are interconnected 12. Which of the following statements are TRUE about E. Has a negative resting membrane potential papillary muscles? A. Pull the vanes of the valves inward toward the 6. If the ejection fraction increases, there will be a ventricles to prevent their bulging too far forward decreased in toward the atria A. cardiac output B. Pull the vanes of the valves outward toward the B. end-systolic volume ventricles to prevent their bulging too far backward C. heart rate toward the atria Page 10 of 11 CMED 1C  (004) CARDIOVASCULAR PHYSIOLOGY: HEART AS A PUMP DR. MAEFLOR OFILAS | 01/04/21 C. Papillary muscles contract when ventricular walls A. sinoatrial (SA) node contract B. atrioventricular (AV) node D. Papillary muscles contract when ventricular walls C. bundle of His relax D. Purkinje system E. ventricular muscle 13. A heart sound which involves the closure of the aortic and pulmonary valve at the end of systole that vibrate for 19. Blood flow to which organ is controlled primarily by the a shorter period of time. sympathetic nervous system rather than by local A. First Heart Sound metabolites? B. Second Heart Sound A. Skin C. Third Heart Sound B. Heart D. Fourth Heart Sound C. Brain D. Skeletal muscle during exercise 14. At what phase of the Volume Pressure Diagram does the systolic pressure rises even higher and the volume of the 20. Which of the following parameters is decreased during ventricle decreases? moderate exercise? A. Phase I A. Arteriovenous 0 2 difference B. Phase II B. Heart rate C. Phase III C. Cardiac output D. Phase IV D. Pulse pressure E. Total peripheral resistance (TPR) 15. Which of the following statements is CORRECT? ANSWERS: E, D, D, D, C, C, A, A, A, E, D, C, B, C, D, E, E, B, A, E A. Preload is the force against which contracting muscle must act. B. Afterload is the force that stretches the relaxed REFERENCES muscle fibers. 1. Berne, R. M., Koeppen, B. M., & Stanton, B. A. C. Preload is the blood filling and stretching the wall (2010). Berne & Levy Physiology. Philadelphia, PA: during systole. Mosby/Elsevier. D. Afterload is the pressure in the aorta that must be 2. Costanzo, L. S. (2014). Physiology (Fifth edition.). overcome by contracting left ventricle to open the Philadelphia, PA: Saunders/Elsevier. aortic valve and eject blood. 3. Guyton, A.C., Hall, J. E. Guyton and Hall Textbook 16. A 24-year-old woman presents to the emergency of Medical Physiology. 13th ed., W B Saunders, 2015. ddepartment with severe diarrhea. When she is supine (lying down), her blood pressure is 90/60 mm Hg (decreased) and her heart rate is 100 beats/min (increased). When she is moved to a standing position, her heart rate further increases to 120 beats/min. Which of the following accounts for the further increase in heart rate upon standing? A. Decreased total peripheral resistance B. Increased venoconstriction C. Increased contractility D. Increased afterload E. Decreased venous return 17. At which site is systolic blood pressure the highest? A. Aorta B. Central vein C. Pulmonary artery D. Right atrium E. Renal artery F. Renal vein 18. A person's electrocardiogram (ECG) has no P wave but has a normal QRS complex and a normal T wave. Therefore, his pacemaker is located in the: Page 11 of 11 CMED 1C