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Anatomy & physiology for the EP professional part II 8.4.14
- 1. Anatomy & PhysiologyAnatomy & Physiology for the EP professionalfor the EP professional Part II
- 2. ObjectivesObjectives • Identify the venous system of the heart • Identify the electrophysiology properties of the heart • Describe the flow of conduction through the heart • List the properties of cardiac cells • Identify the internal structures of the heart • Describe cardiac innervation and the effects on heart rate. • Identify the components of cardiac output • Describe preload and afterload
- 3. Cardiac Venous SystemCardiac Venous System • Cardiac veins lie next to the arteries. • Coronary sinus (CS) is the largest vein – Traverses posterior in the AV sulcus and lies next to the LCX. • The CS receives blood from the Great, middle and small cardiac veins, the oblique vein of the LA and posterior vein of the LV. • Anterior cardiac venules drain directly into the RA. • Ostium of the CS is located in the RA posterior and slightly inferior to the MV structure.
- 5. Coronary Sinus AnatomyCoronary Sinus Anatomy
- 6. Coronary Sinus Anatomy:Coronary Sinus Anatomy: AP viewAP view CS Os Middle Posterior Postero-lateral Great Lateral Antero- lateral Anterior
- 7. Coronary Sinus Anatomy:Coronary Sinus Anatomy: LAO viewLAO view Anterior Cardiac Vein Lateral Cardiac Vein Postero-Lateral Cardiac Vein Posterior Vein
- 8. Coronary Sinus Anatomy:Coronary Sinus Anatomy: RAO viewRAO view Anterior Cardiac Vein Middle Cardiac Vein Posterior Cardiac Vein
- 9. Anatomy of specialized conduction system Specialized conduction system • Sinoatrial (SA), or Sinus Node • Atrioventricular (AV) Node • His Bundle • Left Bundle Branch • Right Bundle Branch
- 10. Conduction SystemConduction System • Electrophysiology properties – SA Node – AV Node – His Bundle – Right and left bundle branches to include the Purkinje fibers
- 11. Normal sinus rhythm Intracardiac tracings show the normal intervals between •initiation of atrial depolarization A •His bundle activation H •ventricular depolarization V • AH + HV = PR interval
- 12. Right Atrium conductionRight Atrium conduction • Right Atrium –SA node (SAN) –Internodal pathways –Interatrial pathways –Bachmann’s Bundle –AV node • Triangle of Koch
- 13. Right Atrium – SA nodeRight Atrium – SA node conductionconduction • Located in the RA at the junction of the anterior RA and the SVC • 2 cm long and .05 cm wide • Thought to extend inferiorly in to the Christa trerminalis • SA node has the fastest automaticity generating impulses at 100-110 bpm – vagal tone suppresses this… 60-100bpm – Conduction speed w/i SAN: 0.05m/sec • Calcium dependent action potential • Transitional cells at the border of the node.
- 14. SA Node CellsSA Node Cells • P cells (pole cells) – main characteristic: automaticity – the fastest depolarizing conduction system cells – aka. pacemaker cells • Transitional cells – form a network of fibers – mainly found on the SA node periphery (border) – attached to the P cells on one side and to the atrial myocardium on the other side – transmits activation from the SA node to the atrium
- 15. SA Node - stained cross-SA Node - stained cross- sectionsection atrial myocytes Cross section RA wall epicardium endocardium adipose SAN artery SA node
- 16. 3 Internodal Tracks3 Internodal Tracks • There is evidence for preferential spread of atrial activation between SA & AV nodes by way of intranodal pathways but whether these are distinct “true” tracts or simply areas of preferential conduction is unclear • Text have described 3 Internodal tracks: – Anterior – Bachman’s Bundle –Travels concurrently from the SA node to the left atrium and AV node. (white arrows) – Middle -Travels from the SA node posteriorly around the SVC, down the inter-atrial septum to the AV node, (red arrows) – Posterior -Travels from the SA node posteriorly through the Crista Terminalis, to the posterior interatrial septum to the AV node. (yellow arrow)
- 17. SA Node & Internodal tracksSA Node & Internodal tracks
- 18. AV NodeAV Node • Impulse reaches the AV Node. – AV node is located at the base of the RA at the apex of the Triangle of Koch. • Triangle of Koch comprised of the Tendon of Todaro, septal leaflet of the Tricuspid valve and the Os of the CS – AV node is comprised of specialized conducting tissue allowing the impulse to travel through the fibrous septum. – The AV node is slower to conduct (calcium dependent). – Acts as the “gate Keeper”
- 19. AV nodeAV node • Specialized collection of conducting cells provide the only link between the A & V passage of a wave of depolarization • Oval-shaped, 60 x 30mm in size • Located subendocardially on the interatrial septum – RA side: within the triangle of Koch. – LA side: next to the base of the mitral valve annulus • Anteriorly and inferiorly, continuous with the His bundle • Rich blood supply from AV nodal artery branch of RCA in 90% • 2 types of cells – rod-shaped: contains Na channels – ovoid-shaped: responsible for spontaneous activity
- 20. AV nodeAV node • AVN conduction speed is approximately 0.1msec • AVN conduction speed is inversely proportional to prematurity of the impulse received • The cells of the AV node are responsible for the slowing of conduction between atria and ventricles • This functions to permit sequential atrial then ventricular contraction • AVN node is richly innervated… – sympathetic fibers: increase the speed of conduction – parasympathetic fibers: have the opposite effect
- 21. Cells of the AV JunctionCells of the AV Junction •AN (atrio-nodal) cells •in the transitional region •activated shortly after the atrial cells •Action potential (AP) visual appearance is between the fast & brief atrial AP and the slower nodal APs •N (nodal) cells •"most typical" of the nodal cells •have slow rising and longer AP duration •the site of Wenckebach •NH (nodal-His) cells •typically distal to the site of Wenckebach block •AP’s closer in visual appearance to the fast rising and long AP of the His bundle.
- 22. AV nodeAV node
- 23. The His BundleThe His Bundle • The impulse reaches the His bundle. – The His bundle is the most proximal portion of the His Purkinje System – Rapidly conducting – Branches to form the right bundle branch, and left anterior and posterior bundle branches, located within the AV septum – Further branches to Purkinje fibers within the ventricular myocardium
- 24. Bundle BranchesBundle Branches • His purkinje trifurcates • Right bundle within the membranous septum • Exits septum via the moderator band • Moderator band attaches to the RV free wall
- 25. Bundle branchesBundle branches • At trifurcation of the His... • Left bundle further bifurcates • Anterior bundle traverses the interventricular septum to the apex • Posterior bundle traverses posteriorly, in a fan like fashion, innervating the basilar portion of the LV
- 26. His Purkinje systemHis Purkinje system • specialized heart muscle cells for electrical conduction • Diameter: 3 mm • Length: 12 to 40 mm – (penetrating 8-10 mm) • begins at the AV node and passes through the right annulus fibrosis to the membranous part of the interventricular septum • starts to branch at the lower part of the membranous septum • named after the Swiss cardiologist Wilhelm His, Jr., who discovered them in 1893
- 27. His Purkinje SystemHis Purkinje System
- 28. Purkinje fibersPurkinje fibers peripheral branching of the bundle branches made up of individual myofibrils divided by collagen fibers that prevent the lateral spread of activation form a subendocardial network that spreads among the ventricular muscle fibers directly innervate the myocardial cells and initiate the ventricular depolarization cycle Purkinje conduction speed subendocardial: 2-10m/sec ventricular muscle proper: 0.3m/sec
- 29. Four Properties of CardiacFour Properties of Cardiac CellsCells • Rhythmicity (Automaticity) • Excitability • Conductivity • Contractility
- 30. Rhythmicity:Rhythmicity: (Automaticity)(Automaticity) • Pacemaker cells can discharge an electrical current without an external stimulus. • Once the cells are stimulated, the flow is passed from one to another in the conduction system until the muscle contracts.
- 31. ExcitabilityExcitability The ability of the cardiac cell to respond to an electrical stimulus with an abrupt change in its electrical potential. (All or none phenomenon)
- 32. ConductivityConductivity The ability of the cardiac cells to rapidly pass on the electrical stimulus to neighboring cells.
- 33. ContractilityContractility The ability of the fibers to shorten when stimulated.
- 34. Right Atrium internal -Right Atrium internal - StructuresStructures • Endocardium divided into • Anterior trebeculated portion • Posterior smooth portion • Christa Terminalis • Separation of the smooth & trebeculated atrium • External landmark – Phrenic Nerve • Internal: • Christa Terminalis laterally • Eustachian Ridge inferiorly
- 35. Right Atrium internal -Right Atrium internal - StructuresStructures • Tendon of Todaro- – Fibrous strand from the union of the Eustachian and Thebesian valves which inserts into the AO root passing thru the atrial wall myocardium. • Triangle of Koch- – Comprised of the membranous septum, the Os of the CS and the tricuspid annulus – Location of the AV Node • Eustachian Ridge – – fold of tissue at the anterior of the IVC • Thebesian Valve – – Fold of tissue that guards the Coronary Sinus
- 36. Right Atrium internalRight Atrium internal structuresstructures Triangle of KochTriangle of Koch
- 37. Right Ventricle internalRight Ventricle internal structuresstructures • Divided into the postero-inferior portion and the antero-superior outflow portion. • Demarcated by prominent muscle bands • Parietal band, septal band and the moderator band. • Inflow wall is heavily trebeculated • Outflow portion few trebeculae • Sub-Pulmonic area smooth muscled • Papillary muscles anchor to ventricular myocardium • Chordae tendonae anchor papillary muscles to the valve leaflets.
- 38. Right Ventricle internal structures
- 39. Left Atrium internalLeft Atrium internal StructuresStructures • Mainly smooth walled structure – Atrial septal surface smooth – Left appendage offers small pectinate muscle • Posterior wall may be .05 – 4.0 mm thick • On the right – two, sometimes, three pulmonary veins enter • On the left – two, sometimes one, pulmonary veins enter.
- 40. Structures that are external toStructures that are external to the Left Atriumthe Left Atrium • External structures to the LA – Right superior PV – Aorta – Right & Left Superior PV – Pulmonary Artery – Posterior medial to lateral atrial wall – Esophagus
- 41. Left Atrium internalLeft Atrium internal StructuresStructures
- 42. Left Ventricle internalLeft Ventricle internal StructuresStructures • Thickness 3 times greater than RV • Majority of LV trebeculated • Basilar third is smooth walled • Two papillary muscles anchor the Mitral Valve • Ventricular septum muscular.
- 43. Left ventricle internalLeft ventricle internal structuresstructures
- 44. Autonomic InnervationAutonomic Innervation Autonomic nervous system (ANS) influences: Heart rate Conductivity Contractility
- 45. ParasympatheticParasympathetic StimulationStimulation • Right and left vagus nerves • Innervate heart at SA and AV nodes –Primary postganglionic neurotransmitter is acetylcholine Slows heart rate Slows AVN conduction
- 46. Sympathetic StimulationSympathetic Stimulation Sympathetic fibers arise in accelerator center in medulla oblangata Primary postganglionic neurotransmitter is norepinephrine
- 47. Receptor SitesReceptor Sites • Alpha – Vascular smooth muscle • Beta-1 – Heart • Beta-2 – Bronchial smooth muscle – Skeletal blood vessels • Dopaminergic – Coronary arteries, renal, mesenteric, and visceral blood vessels
- 48. Effect of NorepinephrineEffect of Norepinephrine • Alpha –No cardiac effect –Peripheral vasoconstriction • Beta-1 –Increased heart rate –Increased conductivity –Increased contractility
- 49. Chronotropic EffectChronotropic Effect • Refers to change in rate –Positive chronotropic effect results in increased heart rate –Negative chronotropic effect results in decreased heart rate
- 50. Inotropic EffectInotropic Effect • Refers change in myocardial contractility –Positive inotropic effect results in increased contractility –Negative inotropic effect results in decreased contractility
- 51. BaroreceptorsBaroreceptors Specialized nerve tissue Found in internal carotid arteries and aortic arch Detect and respond to changes in blood pressure
- 52. ChemoreceptorsChemoreceptors – Located in internal carotid arteries and aortic arch • Detect and respond to changes in: –Oxygen content of the blood –pH –Carbon dioxide tension
- 53. Cardiac OutputCardiac Output • Volume of blood ejected from the heart over 1 minute • RV and LV output usually equal • CO = HR X SV
- 54. SSx of Decreased COSSx of Decreased CO • Cold, clammy skin • Color changes in skin/mucous membranes • Dyspnea • Orthopnea • Crackles (rales) • Changes in mental status • Changes in blood pressure • Arrhythmias • JVD • Fatigue • Restlessness
- 55. Stroke VolumeStroke Volume • Amount of blood ejected during one contraction • Dependent on: –Preload –Afterload –Myocardial contractility
- 56. PreloadPreload • Force exerted by the walls of the ventricles at the end of diastole • Influenced by venous return –Hypovolemia decreases preload –Heart failure increases preload
- 57. Frank-Starling Law of theFrank-Starling Law of the HeartHeart • Up to a limit, the more a myocardial muscle is stretched, the greater the force of contraction (and thus stroke volume) –Influenced by both preload and afterload
- 58. Frank-Starling Law of theFrank-Starling Law of the HeartHeart
- 59. AfterloadAfterload • Afterload is the pressure or resistance against which the ventricles must pump to eject blood –Results in • Increased myocardial workload • Increased myocardial O2 demand
- 60. AfterloadAfterload • Vasoconstriction results in increased afterload and increased myocardial work and O2 demand • Vasodilation results in decreased afterload decreased myocardial work and O2 demand
- 61. Blood PressureBlood Pressure • Force exerted by circulating blood volume on arterial walls • Influenced by peripheral vascular resistance (PVR) –Resistance to blood –Determined by vessel diameter and muscle tone • BP = CO X PVR
- 62. Normal Heart PressuresNormal Heart Pressures Pressure Measurement Normal RA Mean 2-8 mm Hg RV Systolic 25-35mm Hg End Diastolic 2 -8 mm Hg PA Systolic 25-35mm Hg End Diastolic 8-12mm Hg
- 63. Normal Heart PressuresNormal Heart Pressures Pressure Measurement Normal PCW Mean 8-12mm Hg Aorta Systolic 90-140mm Hg Diastolic 60-90mm Hg LV Systolic 90-140mm Hg End Diastolic 8-12mm Hg
- 64. ReferencesReferences • Netter, F H (1987) The CIBA collection of medical Illustrations. Volume 5 The heart. Colorpress, New York NY • Mazgalev, T.N., Tchou, P.J. (2000) Atrial AV Nodal Electrophysiology; A view from the millennium. Futura, Armonk, NY • Podrid, P.J., Kowey, P.R. (2001) Cardiac Arrhythmia, Mechanisms, Diagnosis & Management, 2nd Ed. Lippincott, Williams & Wilkins. Philadelphia PA • Anderson, R.H. (2000) Electrical Anatomy of the Atrial Chambers. Medtronic USA • Anderson R.H., Ho, S.W. ( n.d.) The Anatomy of the Atrioventricular Node. Article review by Sechler, D.A., RN
Hinweis der Redaktion
- Normal Anatomy We begin with a frontal view of the heart, from a superior aspect, to bring the left atrium more into view. Removing the anterior portions of the right and left ventricles reveals the interior of the 4 chambers and the mitral and tricuspid valves. Use the Step control under the heart to add and remove layers of the illustration. The specialized conduction system consists of the •Sinoatrial (SA), or Sinus Node, which is located below the anterior Superior Vena Cava, the •Atrioventricular (AV) Node, which is in the atrial septum just superior to the coronary sinus, the •His Bundle, which transverses the membranous septum before branching into the •Left Bundle Branch, and the •Right Bundle Branch [©2003 Blaufuss Multimedia. All rights reserved.]
- Normal Sinus Rhythm The cardiac impulse originates in the Sinus Node and begins the process of atrial depolarization. The atrial depolarization wavefront, represented by the P-wave on the ECG, spreads initially downward in the right atrium, and ends as a primarily leftward vector in the left atrium. Conduction through the AV Node is normally slow. Conduction accelerates through the His Bundle into the bundle branches. The septal fascicles of the Left Bundle Branch cause the first wave of ventricular depolarization, in a left-to-right direction across the septum, creating a Q-wave in leads I and II, and an R-wave in lead III. This is followed by apical depolarization, creating R-waves in leads I, II, and III, and finally left ventricular depolarization, creating an S-wave in lead III and increasing the R-waves in leads I and II. [©2003 Blaufuss Multimedia. All rights reserved.]
- Triangle of Koch comprised of the Tendon of Todaro, septal leaflet of the Tricuspid valve and the Os of the CS
- The heart is innervated by both the sympathetic and parasympathetic divisions of the autonomic nervous system. The sympathetic division mobilizes the body, allowing the body to function under stress (“fight or flight” response). The parasympathetic division is responsible for the conservation and restoration of body resources (“feed and breed” response). Autonomic regulation of the cardiovascular system requires sensors, afferent pathways, an integration center, efferent pathways, and receptors. Sympathetic (accelerator) nerve fibers supply the sinoatrial (SA) node, the atrioventricular (AV) node, the atrial muscle, and the ventricular myocardium. Stimulation of sympathetic nerve fibers results in the release of norepinephrine, a neurotransmitter, which increases the force of ventricular contraction, heart rate, blood pressure, and cardiac output. Parasympathetic (inhibitory) nerve fibers supply the SA node, the atrial muscle, and the AV junction of the heart by means of the vagus nerves. Acetylcholine, a neurotransmitter, is released when parasympathetic (cholinergic) nerve fibers are stimulated. Acetylcholine binds to parasympathetic receptors. Parasympathetic stimulation slows the rate of discharge of the SA node, slows conduction through the AV node, decreases the strength of atrial contraction, and can cause a small decrease in the force of ventricular contraction. (There is little effect on the strength of ventricular contraction because of the minimal parasympathetic innervation of these chambers). The net effect of parasympathetic stimulation is a slowing of the heart rate.
- Parasympathetic (inhibitory) nerve fibers supply the SA node, atrial muscle, and the AV junction of the heart by means of the vagus nerves. Acetylcholine, a neurotransmitter, is released when parasympathetic (cholinergic) nerve fibers are stimulated. Acetylcholine binds to parasympathetic receptors. The two main types of cholinergic receptors are nicotinic and muscarinic receptors. Nicotinic receptors are located in skeletal muscle, and muscarinic receptors are located in smooth muscle.
- Sympathetic (accelerator) nerve fibers supply the SA node, the AV node, the atrial muscle, and the ventricular myocardium. Stimulation of sympathetic nerve fibers results in the release of norepinephrine, a neurotransmitter that increases the force of ventricular contraction, heart rate, blood pressure, and cardiac output.
- Sympathetic (adrenergic) receptor sites are divided into alpha-, beta-, and dopaminergic receptors. Dopaminergic receptor sites are located in the coronary arteries, renal, mesenteric, and visceral blood vessels. Stimulation of dopaminergic receptor sites results in dilation. Different body tissues have different proportions of alpha- and beta-receptors. In general, alpha-receptors are more sensitive to norepinephrine and beta-receptors are more sensitive to epinephrine. Stimulation of alpha-receptor sites results in the constriction of blood vessels in the skin, cerebral, and splanchnic circulation. Beta-receptor sites are divided into beta-1 and beta-2 categories. Beta-1–receptors are found in the heart. Stimulation of beta-1–receptors results in an increased heart rate, contractility, and, ultimately, irritability of cardiac cells. Beta-2–receptor sites are found in the lungs and skeletal muscle blood vessels. Stimulation of these receptor sites results in dilation of the smooth muscle of the bronchi and blood vessel dilation. Increases in heart rate shorten all phases of the cardiac cycle, but the most important is a decrease in the length of time spent in diastole. If the length of diastole is shortened, there is less time for adequate ventricular filling. In some cases of a rapid heart rate, vagal maneuvers (e.g., carotid sinus pressure) may be performed to attempt to slow the rate. When vagal maneuvers are performed, baroreceptors in the carotid arteries are stimulated to slow AV conduction, resulting in slowing of the heart rate.
- Baroreceptors (pressoreceptors) are specialized nerve tissue (sensors) located in the internal carotid arteries and the aortic arch. These sensory receptors detect changes in blood pressure and cause a reflex response in either the sympathetic or parasympathetic divisions of the autonomic nervous system. If the systolic blood pressure decreases, the body’s normal compensatory response to increase blood pressure is peripheral vasoconstriction, increased heart rate (chronotropy), and increased myocardial contractility (inotropy). In this example, the compensatory responses occur because of a reflex sympathetic response (also called adrenergic response). If the systolic blood pressure increases, the baroreceptor reflex response decreases sympathetic stimulation and increases parasympathetic stimulation (cholinergic response).
- Chemoreceptors in the internal carotid arteries and aortic arch detect changes in the concentration of hydrogen ions (pH), oxygen, and carbon dioxide in the blood. The response to these changes by the autonomic nervous system can be sympathetic or parasympathetic. Decreased pH or oxygen levels or increases in carbon dioxide levels in the blood cause a sympathetic response, resulting in increased heart rate, contractility, and vasoconstriction.[i] Increased pH or decreased carbon dioxide levels in the blood causes a decrease in vasoconstrictor effects, leading to a general vasodilatory effect. Nerve impulses are carried from the sensory receptors to the brain by means of the vagus and glossopharyngeal nerves (afferent pathways). The medulla of the brain serves as the integration center and interprets the sensory information received. The medulla determines what body parameters need adjustment (if any) and transmits that information to the heart and blood vessels by means of motor nerves (efferent pathways). [i] Thibodeau GA, Patton KT: Anatomy & Physiology, ed 2, St. Louis, 1993, Mosby.
- Cardiac output is the amount of blood pumped into the aorta each minute by the heart. It is defined as the stroke volume (amount of blood ejected from a ventricle with each heartbeat) multiplied by the heart rate. In the average adult, normal cardiac output is between 4 and 8 liters/min. The cardiac output at rest is approximately 5 liters/min (stroke volume of 70 mL times a heart rate of 70 beats/min). Because the cardiovascular system is a closed system, the volume of blood leaving one part of the system must equal that entering another part. For example, if the left ventricle normally pumps 5 liters/min, the volume flowing through the arteries, capillaries, and veins must equal 5 liters/min. Thus, the cardiac output of the right ventricle (pulmonary blood flow) is normally equal to that of the left ventricle on a minute-to-minute basis.
- Cardiac output varies depending on hormone balance, an individual’s activity level and body size, and the body’s metabolic needs. Factors that increase cardiac output include increased body metabolism, exercise, and the age and size of the body. Factors that may decrease cardiac output include shock, hypovolemia, and heart failure. Signs and symptoms of decreased cardiac output include cold, clammy skin; color changes in the skin and mucous membranes; dyspnea, orthopnea, and crackles (rales); changes in mental status; changes in blood pressure; dysrhythmias; jugular venous distention; fatigue; and restlessness.
- Cardiac output may be increased by an rise in heart rate or stroke volume. An increase in myocardial contractility (and subsequently, stroke volume) may occur because of norepinephrine and epinephrine released from the adrenal medulla; thyroxin, insulin, and glucagon released from the pancreas; or medications such as calcium and digitalis. A decrease in contractility may result from severe hypoxia, decreased pH, hypercapnea (elevated carbon dioxide levels), and medications such as propranolol (Inderal).
- Stroke volume is determined by the degree of ventricular filling during diastole (preload), the pressure against which the ventricle must pump (afterload), and the myocardium’s contractile state.
- Preload is the force exerted on the walls of the ventricles at the end of diastole. The volume of blood returning to the heart influences preload. More blood returning to the right atrium increases preload; less blood returning decreases preload.
- According to the Frank-Starling law of the heart, to a point, the greater the volume of blood in the heart during diastole, the more forceful the cardiac contraction, and the more blood the ventricle will pump (stroke volume). This is important so that the heart can adjust its pumping capacity in response to changes in venous return, such as during exercise. If, however, the ventricle is stretched beyond its physiological limit, cardiac output may fall due to volume overload and overstretching of the muscle fibers.
- Afterload is the pressure or resistance against which the ventricles must pump to eject blood. Afterload is influenced by arterial blood pressure, arterial distensibility (ability to become stretched), and arterial resistance. The less resistance there is (lower afterload), the more easily blood can be ejected. Increased afterload (increased resistance) results in increased cardiac workload. Conditions that contribute to increased afterload include increased blood viscosity, hypertension, and aortic stenosis.
- The mechanical activity of the heart is reflected by the pulse and blood pressure. Blood pressure is the force exerted by the circulating blood volume on the walls of the arteries. Peripheral resistance is the resistance to the flow of blood determined by blood vessel diameter and the tone of the vascular musculature. Blood pressure is equal to cardiac output times peripheral resistance. Blood pressure is affected by any condition that increases peripheral resistance or cardiac output. Thus, an increase in either cardiac output or peripheral resistance will result in an increase in blood pressure. Conversely, a decrease in either will result in a decrease in blood pressure. Tone is a term that may be used when referring to the normal state of balanced tension in body tissues.
- The heart functions as a pump to propel blood through the systemic and pulmonary circulations. As the heart chambers fill with blood, the heart muscle is stretched. The most important factor determining the amount of blood pumped by the heart is the amount of blood flowing into it from the systemic circulation (venous return).