Functions of the Heart

Transcription

1 Cardiovascular System The Heart What is the Cardiovascular System? Blood circulated in Arteries, veins, and capillaries by the Pumping action of the heart Functions of the Heart Generating blood pressure sufficient to efficiently cause blood to flow from heart to veins Keeping oxygenated and low-oxygen blood separate Adjusting blood pressure as conditions change (maintain homeostasis) Changes in contraction rate and force match blood delivery to changing metabolic needs Heart Anatomy The and Systemic Circuits Heart is a transport system consisting of two side-by-side pumps side receives low-oxygen blood from tissues Moves blood to lungs to get rid of CO 2, pick up O 2, and return via pulmonary circuit Left side receives oxygenated blood from lungs Moves blood to body tissues via systemic circuit 1

2 To the lungs and back reoxygenate the blood, transport Venae cavae atrium Circuit arteries ventricle Heart Left atrium Systemic Circuit Left ventricle Capillary beds of lungs where gas exchange occurs veins Aorta and branches Out to body tissues and back oxygenate the tissues, collect and transport Oxygen-rich, CO 2-poor blood Oxygen-poor, CO 2-rich blood Capillary beds of all body tissues where gas exchange occurs Location of the heart in the mediastinum. Midsternal line 2nd rib Diaphragm Sternum Base (posterior surface) leans toward right shoulder Apex points toward left hip More of mass on left lack of bilateral symmetry Fist-sized, g Mediastinum = medial cavity of thorax Chambers and Associated Great Vessels Internal features Four chambers Two superior atria (singular atrium) Two inferior ventricles Interatrial septum: separates atria Fossa ovalis: remnant of foramen ovale of fetal heart Interventricular septum: separates ventricles Walls consist of cardiac muscle, fibrous connective tissue, others in lesser amounts 2

3 Brachiocephalic trunk Superior vena cava pulmonary artery Ascending aorta trunk Left common carotid artery Left subclavian artery Aortic arch Ligamentum arteriosum Left pulmonary artery Left pulmonary veins pulmonary veins atrium coronary artery (in coronary sulcus) Anterior cardiac vein ventricle marginal artery Small cardiac vein Inferior vena cava Anterior view Auricle of left atrium Circumflex artery Left coronary artery (in coronary sulcus) Left ventricle Great cardiac vein Anterior interventricular artery (in anterior interventricular sulcus) Apex Aorta Left pulmonary artery Left pulmonary veins Auricle of left atrium Left atrium Great cardiac vein Posterior vein of left ventricle Left ventricle Superior vena cava pulmonary artery pulmonary veins atrium Inferior vena cava Coronary sinus coronary artery (in coronary sulcus) Posterior interventricular artery (in posterior interventricular sulcus) Middle cardiac vein Apex ventricle Posterior surface view Aorta Superior vena cava pulmonary artery trunk atrium pulmonary veins Fossa ovalis Pectinate muscles Tricuspid ventricle Chordae tendineae Trabeculae carneae Inferior vena cava Left pulmonary artery Left atrium Left pulmonary veins Mitral (bicuspid) Aortic Left ventricle Papillary muscle Interventricular septum Epicardium Myocardium Endocardium Frontal section 3

4 Chambers and Associated Great Vessels (cont.) Atria Small, thin-walled Receive blood from veins Convey blood to ventricles below Auricle vs atrium atrium: receives deoxygenated (aka lowoxygen) blood from body Superior & inferior vena cava, coronary sinus Left atrium: receives oxygenated blood from lungs Four pulmonary veins Chambers and Associated Great Vessels (cont.) Ventricles Contain most of the volume of heart Primary pump Thickness of ventricular myocardium reflects workload ventricle Pumps blood into pulmonary trunk and pulmonary circulation Left ventricle Pumps blood into aorta (largest artery in body) and begins systemic circulation Trabeculae carneae Prevent suction, aid papillary muscles Papillary muscles Anchor chordae tendineae that are attached to heart s The layers of the pericardium and of the heart wall. Pericardium Myocardium trunk Fibrous pericardium Parietal layer of serous pericardium Pericardial cavity Epicardium (visceral layer of serous pericardium) Myocardium Heart wall Endocardium Heart chamber 1. Superficial fibrous pericardium: functions to protect, anchor heart to surrounding structures, and prevent overfilling 2. Deep two-layered serous pericardium Parietal layer lines internal surface of fibrous pericardium Visceral layer (epicardium) on external surface of heart Two layers separated by fluid-filled pericardial cavity (decreases friction) 4

5 Three Layers Of Heart Wall 1. Epicardium: visceral layer of serous pericardium 2. Myocardium: circular or spiral bundles of contractile cardiac muscle cells Cardiac skeleton: crisscrossing, interlacing layer of connective tissue Anchors cardiac muscle fibers Supports great vessels and s Limits spread of action potentials to specific paths 3. Endocardium: innermost layer; is continuous with endothelial lining of blood vessels Lines heart chambers and covers cardiac skeleton of s Heart s Aortic Area of cutaway Mitral Tricuspid Myocardium Cardiac skeleton Anterior Mitral (left atrioventricular) Tricuspid (right atrioventricular) Aortic The function of the atrioventricular (AV) s 1 Blood returning to the heart fills atria, pressing against the AV s. The increased pressure forces AV s open. 2 As ventricles fill, AV flaps hang limply into ventricles. 3 Atria contract, forcing additional blood into ventricles. Ventricle Direction of blood flow Atrium Cusp of atrioventricular (open) Chordae tendineae Papillary muscle AV s open; atrial pressure greater than ventricular pressure 5

6 The function of the semilunar (SL) s Aorta trunk As ventricles contract and intraventricular pressure rises, blood is pushed up against semilunar s, forcing them open. Semilunar s open As ventricles relax and intraventricular pressure falls, blood flows back from arteries, filling the cusps of semilunar s and forcing them to close. Semilunar s closed Pathway of Blood Through Heart and Connected Vessels Equal volumes of blood are pumped to pulmonary and systemic circuits circuit is short, low-pressure circulation reoxygenation of blood returned to heart from body Systemic circuit is long, high-friction circulation distribution of oxygen-saturated pulmonary blood Anatomy of ventricles reflects differences Left ventricle walls are much thicker than right Pumps with greater pressure 6

7 Pathway of Blood Through Heart and Connected Vessels Superior vena cava (SVC) Inferior vena cava (IVC) Coronary sinus atrium Tricuspid ventricle semilunar trunk Oxygen-poor blood Oxygen-rich blood SVC Coronary sinus arteries trunk IVC atrium Tricuspid ventricle semilunar To heart Oxygen-poor blood returns from the body tissues back to the heart. Oxygen-poor blood is carried in two pulmonary arteries to the lungs (pulmonary circuit) to be oxygenated. To lungs Systemic capillaries capillaries To body Oxygen-rich blood is delivered to the body tissues (systemic circuit). Oxygen-rich blood returns to the heart via the four pulmonary veins. To heart Aorta veins Aortic semilunar Mitral Left ventricle Left atrium Aorta Aortic semilunar Left ventricle Mitral Left atrium Four pulmonary veins Coronary Circulation Coronary arteries and veins Functional blood supply to heart muscle itself Living muscle tissue with limited anaerobic capabilities Delivered when heart is relaxed, too much pressure in cardiac arteries for blood to flow while myocardium contracted Shortest circulation in body Left ventricle receives most of coronary blood supply; Heart receives 1/20th of body s blood supply Arteries contain many anastomoses (junctions) Provide additional routes for blood delivery Cannot compensate for coronary artery occlusion Narrowing, closing, plugging leads to ischemia and/or infarction Branching of coronary arteries varies among individuals Both left and right coronary arteries arise from base of aorta and supply arterial blood to heart Superior vena cava Anastomosis (junction of vessels) atrium coronary artery ventricle marginal artery Aorta Posterior interventricular artery trunk Left atrium Left coronary artery Circumflex artery Left ventricle Anterior interventricular artery 7

8 Superior vena cava Anterior cardiac veins Great cardiac vein Coronary sinus Small cardiac vein Middle cardiac vein 2016 Pearson Education, Inc. Microscopic anatomy of cardiac muscle fibers Cardiac muscle cell Intercalated disc Mitochondrion Nucleus Mitochondrion T tubule Sarcoplasmic reticulum Z disc Nucleus Sarcolemma I band A band I band Similarities with skeletal muscle Muscle contraction is preceded by depolarizing action potential Depolarization wave travels down T tubules; causes sarcoplasmic reticulum (SR) to release Ca 2+ Excitation-contraction coupling occurs Ca binds to troponin causing filaments to slide Microscopic anatomy of cardiac muscle. Cardiac muscle cell Nucleus Intercalated discs Gap junctions (electrically connect myocytes) Desmosomes (keep myocytes from pulling apart) 8

9 Pacemaker myocytes Long absolute refraction Differences in the Physiology of Skeletal and Cardiac Muscle Heart contracts as a unit All cardiomyocytes contract as unit (functional syncytium) for effective pumping action, or none contract Skeletal muscle fibers contract independently Influx of Ca 2+ from extracellular fluid triggers Ca 2+ release from SR Depolarization opens slow Ca 2+ channels in sarcolemma, allowing Ca 2+ to enter cell Extracellular Ca 2+ then causes SR to release its intracellular Ca 2+ Skeletal muscles do not use extracellular Ca 2+ Differences in the Physiology of Skeletal and Cardiac Muscle The heart relies almost exclusively on aerobic respiration Cardiac muscle has more mitochondria than skeletal muscle so has greater dependence on oxygen Skeletal muscle (depending on type) can go through fermentation when oxygen not present Both types of tissues can use other fuel sources Cardiac is more adaptable to other fuels, including lactic acid, but must have oxygen 9

10 Membrane potential (mv) Setting the Basic Rhythm: The Intrinsic Conduction System Coordinated heartbeat is a function of: 1. Presence of gap junctions 2. Intrinsic cardiac conduction system Network of noncontractile (autorhythmic) cells Cardiac pacemaker cells have unstable resting membrane potentials called pacemaker potentials or prepotentials Initiate and distribute impulses to coordinate depolarization and contraction of heart What is extrinsic control? The Intrinsic Conduction System Action potential initiation by pacemaker cells 1. Pacemaker potential: K + channels are closed, but slow Na + channels are open, causing interior to become more positive 2. Depolarization: Ca 2+ channels open (around 40 mv), allowing huge influx of Ca 2+, leading to rising phase of action potential 3. Repolarization: K + channels open, allowing efflux of K +, and cell becomes more negative Pacemaker and action potentials of typical cardiac pacemaker cells Action potential Threshold 1 Pacemaker potential This slow depolarization is due to both opening of Na + channels and closing of K + channels. Notice that the membrane potential is never a flat line Depolarization The action potential begins when the pacemaker potential reaches threshold. Depolarization is due to Ca 2+ influx through Ca 2+ channels Time (ms) Pacemaker potential 1 3 Repolarization is due to Ca 2+ channels inactivating and K + channels opening. This allows K + efflux, which brings the membrane potential back to its most negative voltage. 10

11 Superior vena cava atrium Pacemaker potential 1 The sinoatrial (SA) node (pacemaker) generates impulses. SA node Internodal pathway 2 The impulses pause (0.1 s) at the atrioventricular (AV) node. Left atrium Atrial muscle 3 The atrioventricular (AV) bundle connects the atria to the ventricles. 4 The bundle branches conduct the impulses through the interventricular septum. Subendocardial conducting network (Purkinje fibers) Interventricular septum Pacemaker potential AV node Ventricular muscle Plateau 5 The subendocardial conducting network depolarizes the contractile cells of both ventricles. Anatomy of the intrinsic conduction system showing the sequence of electrical excitation Milliseconds Comparison of action potential shape at various locations The Intrinsic Conduction System 1. Sinoatrial (SA) node Primary pacemaker of heart in right atrial wall Spontaneously depolarizes faster than rest of myocardium Generates impulses about 75 /minute sinus rhythm Inherent rate of 100 /minute tempered by extrinsic factors including parasympathetic inhibition Impulse spreads across atria cell to cell, reaching AV node The Intrinsic Conduction System 2. Atrioventricular (AV) node In inferior interatrial septum Delays impulses approximately 0.1 second Cause: fibers are smaller in diameter, have fewer gap junctions Allows atrial contraction prior to initiation of ventricular contraction Inherent rate of 50 /minute in absence of SA node input ectopic focus if it becomes primary pacesetter 11

12 The Intrinsic Conduction System 3. Atrioventricular (AV) bundle (bundle of His) In superior interventricular septum Only electrical connection between atria and ventricles Atria and ventricles not connected via gap junctions Carries AP through electrically-neutral cardiac skeleton 4. and left bundle branches Two pathways in interventricular septum Carry impulses toward apex of heart The Intrinsic Conduction System 5. Subendocardial conducting network Also referred to as Purkinje fibers Complete pathway through interventricular septum into apex and ventricular walls, then cell to cell AV bundle and subendocardial conducting network depolarize 30 /minute in absence of AV node input ectopic focus Ventricular contraction initiates at apex toward atria Process from initiation at SA node to complete contraction takes ~0.22 seconds Autonomic (extrinsic) innervation of the heart The vagus nerve (parasympathetic) decreases heart rate. Cardioacceleratory center Sympathetic trunk ganglion Sympathetic cardiac nerves increase heart rate and force of contraction. SA node AV node Dorsal motor nucleus of vagus Cardioinhibitory center Medulla oblongata Thoracic spinal cord Sympathetic trunk Parasympathetic neurons Sympathetic neurons Interneurons Heartbeat modified by ANS via cardiac centers in medulla oblongata Cardioacceleratory center: sends signals through sympathetic trunk to increase both rate and force Stimulates SA and AV nodes, heart muscle, and coronary arteries Cardioinhibitory center: parasympathetic signals via vagus nerve to decrease rate Inhibits SA and AV nodes via vagus nerve Remember: nervous stimulation is dependent on AP frequency, type of neurotransmitter, type of receptor 12

13 Action Potentials of Contractile Cardiac Muscle Cells Contractile muscle fibers make up bulk of heart and are responsible for pumping action Different from skeletal muscle contraction; cardiac muscle action potentials have plateau Steps involved in AP: 1. Depolarization opens fast voltage-gated Na + channels; Na + enters cell Action Potentials of Contractile Cardiac Muscle Cells (cont.) 2. Depolarization by Na + also opens slow Ca 2+ channels At +30 mv, Na + channels close, but slow Ca 2+ channels remain open, prolonging depolarization Seen as a plateau 3. After about 200 ms, slow Ca 2+ channels close, and voltage-gated K + channels open Rapid efflux of K + repolarizes cell to RMP Ca 2+ is pumped both back into SR and out of cell into extracellular space Action Potentials of Contractile Cardiac Muscle Cells (cont.) More differences between contractile muscle fiber and skeletal muscle fiber contractions AP in skeletal muscle lasts 1 2 ms; in cardiac muscle it lasts 200 ms Contraction in skeletal muscle lasts ms; in cardiac contraction lasts over 200 ms Benefit of longer AP and contraction: Sustained contraction ensures efficient ejection of blood Longer refractory period prevents tetanic contractions 13

14 Membrane potential (mv) Tension (g) The action potential of contractile cardiac muscle cells. 20 Plateau Action potential Tension development (contraction) 1 Depolarization is due to Na + influx through fast voltage-gated Na + channels. A positive feedback cycle rapidly opens many Na + channels, reversing the membrane potential. Channel inactivation ends this phase. 2 Plateau phase is due to Ca 2+ influx through slow Ca 2+ channels. This keeps the cell depolarized because most K + channels are closed Absolute refractory period 3 Repolarization is due to Ca 2+ channels inactivating and K + channels opening. This allows K + efflux, which brings the membrane potential back to its resting voltage Time (ms) Mechanical Events Systole: period of heart contraction Diastole: period of heart relaxation Cardiac cycle: Atrial systole and diastole and ventricular systole and diastole Cycle represents series of pressure and blood volume changes leading to movement of blood in vessels Mechanical events follow electrical events seen on ECG Blood flows from area of high pressure to area of low pressure unless impeded (by things like s) Mechanical Events of Heart and Phases of the Cardiac Cycle Ventricular filling 1. Passive filling phase = atrial and ventricular diastole, all chambers filling 2. Active filling phase = atrial systole but ventricles relaxed forced filling of ventricles End diastolic volume (EDV): volume of blood in each ventricle at end of ventricular diastole Ventricular systole 3. Isovolumetric contraction phase: all s are closed 4. Ejection phase: ventricular pressure exceeds pressure in large arteries, forcing SL s open Pressure in aorta around 120 mm Hg End systolic volume (ESV): volume of blood remaining in each ventricle after systole 5. Isovolumetric relaxation phase: early ventricular diastole, atria already in diastole and accepting venous blood 14

15 Heart Sounds Two sounds (lub-dup) Associated with closing of heart s First sound is closing of AV s at beginning of ventricular systole Second sound is closing of SL s at beginning of ventricular diastole Pause between lub-dups indicates heart relaxation Electrocardiography Electrocardiograph can detect electrical currents generated by heart Electrocardiogram (ECG or EKG) is a graphic recording of electrical activity Composite of all action potentials at given time; not a tracing of a single AP Electrodes are placed at various points on body to measure voltage differences A diagnostic tool An electrocardiogram (ECG) tracing. QRS complex R Ventricular depolarization Sinoatrial node Atrial depolarization P Ventricular repolarization T Atrioventricular node P-R Interval Q S S-T Segment Q-T Interval Time (s) 15

16 Ventricular volume (ml) Pressure (mm Hg) Q S Q S Q S Q S Q S SA node R P T 1 Atrial depolarization, initiated by the SA node, causes the P wave. AV node R P T 2 With atrial depolarization complete, the impulse is delayed at the AV node. R P T 3 Ventricular depolarization begins at apex, causing the QRS complex. Atrial repolarization occurs. R P T 4 Ventricular depolarization is complete. R P T 5 Ventricular repolarization begins at apex, causing the T wave. R P T Q S 6 Ventricular repolarization is complete. Depolarization Repolarization Left heart Electrocardiogram Heart sounds P QRS 1st T 2nd P 120 Dicrotic notch Putting it all together! Atrial systole Left atrium Left v entricle Aorta 120 EDV SV 50 ESV Atrioventricular s Open Closed Open Aortic and pulmonary s Phase Closed Open Closed 1 2a 2b 3 1 Left atrium atrium Left ventricle ventricle Ventricular Atrial Isovolumetric Ventricular Isovolumetric filling contraction contraction phase ejection phase relaxation 1 2a 2b 3 Ventricular filling Ventricular filling (mid-to-late diastole) Ventricular systole (atria in diastole) Early diastole Cardiac Output (CO) Volume of blood pumped by each ventricle in 1 minute Highly variable CO changes (increases/decreases) if either or both SV or HR is changed CO = heart rate (HR) stroke volume (SV) HR = number of beats per minute SV = volume of blood pumped out by one ventricle (left) with each beat Average Values At rest: CO (ml/min) = HR (75 beats/min) SV (70 ml/beat) = 5.25 L/min 16

17 Cardiac Reserve Difference between resting and maximal CO Maximal CO is 4 5 times resting CO in nonathletic people (20 25 L/min) Maximal CO may reach 35 L/min in trained athletes Regulation of Cardiac Output Stroke Volume Mathematically: SV = EDV ESV EDV is affected by length of ventricular diastole and venous pressure ( 120 ml/beat) ESV is affected by arterial BP and force of ventricular contraction ( 50 ml/beat) Normal SV = 120 ml 50 ml = 70 ml/beat Three main factors that affect SV: Preload Contractility Afterload Regulation of Stroke Volume Preload: degree of stretch of heart muscle Just before systole Cardiac muscle exhibits a length-tension relationship At rest, cardiac muscle cells are shorter than optimal length When stretched by increases in EDV a big increase in contractile force results Most important factor in preload stretching of cardiac muscle is venous return amount of blood returning to heart 17

18 Regulation of Stroke Volume (cont.) Preload (cont.) Slowed heart rate or exercise increase venous return Increased venous return distends (stretches) ventricles and increases contraction force Frank-Starling law of the heart ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return Venous EDV SV CO Return Frank-Starling Law Regulation of Stroke Volume (cont.) Contractility Contractile strength at given muscle length Independent of muscle stretch and EDV Increased contractility lowers ESV; caused by: Sympathetic epinephrine release stimulates increased Ca 2+ influx, leading to more cross bridge formations Positive inotropic agents increase contractility Thyroxine, glucagon, epinephrine, digitalis, high extracellular Ca 2+ Decreased by negative inotropic agents Acidosis (excess H + ), increased extracellular K +, calcium channel blockers Norepinephrine Receptor ( 1-adrenergic) G protein (Gs) Adenylate cyclase ATP is converted to camp Extracellular fluid GT P GDP GTP ATP camp Inactive protein kinase Active protein kinase Phosphorylates Ca 2+ Ca 2+ channels in the SR Ca 2+ channels in the plasma membrane Sarcoplasmic reticulum (SR) Cardiac muscle cytoplasm Ca 2+ release Ca 2+ entry from from SR extracellular fluid Ca 2+ binding to troponin; Cross bridge binding for contraction Force of contraction 18

19 Regulation of Stroke Volume (cont.) Afterload: back pressure exerted by arterial blood on semilunar s ventricles must overcome afterload to eject blood Back pressure from arterial blood pushing on SL s is major pressure Aortic pressure is around 80 mm Hg trunk pressure is around 10 mm Hg Hypertension increases afterload, resulting in increased ESV and reduced SV Factors involved in determining cardiac output. Exercise (by sympathetic activity, skeletal muscle and respiratory pumps; see Chapter 19) Ventricular filling time (due to heart rate) Bloodborne epinephrine, thyroxine, excess Ca 2+ CNS output in response to exercise, fright, anxiety, or blood pressure Venous return Contractility Sympathetic activity Parasympathetic activity EDV (preload) ESV Stroke volume (SV) Heart rate (HR) Initial stimulus Physiological response Result Cardiac output (CO = SV HR) 19