Heart Anatomy PDF

Heart Anatomy Figure 17.1  Anatomy: Coverings of the Heart Pericardium – a double-walled sac around the heart composed of: – Outer layer of dense white fibrous connective tissue – Inner double layer serous membrane Composed of simple squamous epithelium The p...

Heart Anatomy Figure 17.1  Anatomy: Coverings of the Heart Pericardium – a double-walled sac around the heart composed of: – Outer layer of dense white fibrous connective tissue – Inner double layer serous membrane Composed of simple squamous epithelium The parietal layer lines the internal surface of the fibrous pericardium The visceral layer or epicardium lines the surface of the heart They are separated by the fluid-filled pericardial cavity Serous fluid secreted to decrease friction  Anatomy: Heart Wall Epicardium – visceral layer of the serous pericardium Myocardium – cardiac muscle layer forming the bulk of the heart – Fibrous skeleton of the heart: layer of connective tissue around the muscle Endocardium – endothelial layer of the inner myocardial surface – Continuous throughout the entire cardiovascular system Pericardial Layers of the Heart Figure 17.2  Atria of the Heart Atria are the receiving chambers of the heart Each atrium has a protruding auricle Pectinate muscles mark right atrial wall Atrioventricular septum separates the atria and the ventricles; atrioventricular sulcus (coronary) Interatrial septum separates the left & right atria Blood enters right atria from superior and inferior venae cavae and coronary sinus Blood enters left atria from pulmonary veins  Ventricles of the Heart Ventricles are the discharging chambers of the heart Papillary muscles and trabeculae carneae muscles mark ventricular walls Interventricular septum separates the left & right ventricles; anterior & posterior interventricular sulci Right ventricle pumps blood into the pulmonary trunk Left ventricle pumps blood into the aorta Gross Anatomy of Heart: Frontal Section Figure 17.4e  Heart Valves Heart valves ensure unidirectional blood flow through the heart Atrioventricular (AV) valves lie between the atria and the ventricles – Right AV valve (tricuspid) has 3 flaps of tissue – Left AV valve (bicuspid) has 2 flaps of tissue Chordae tendineae anchor AV valves to papillary muscles Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk Aortic semilunar valve lies between the left ventricle and the aorta Heart Valves Figure 17.8a, b Atrioventricular Valve Function Figure 17.9 Semilunar Valve Function Figure 17.10  Major External Vessels of the Heart Vessels returning blood to the heart include: – Superior and inferior venae cavae – Coronary sinus – Right and left pulmonary veins Vessels carrying blood away from the heart include: – Pulmonary trunk, which splits into right and left pulmonary arteries – Ascending aorta (three branches) – brachiocephalic, left common carotid, and subclavian arteries External Heart: Anterior View Figure 17.4b External Heart: Posterior View Figure 17.4d Pulmonary Circuit: Oxygenation of Blood Pathway – Deoxygenated blood through the vena cava to the right atrium – Deoxygenated blood through the right atrioventricular valve to the right ventricle – Deoxygenated blood through the pulmonary semilunar valve to the pulmonary trunk and the lungs – Oxygenated blood through the pulmonary veins to the left atrium – Oxygenated blood through the left atrioventricular valve to the left ventricle Systemic Circuit: Delivery of Oxygenated Blood to Tissues and Return of Blood to the Heart Pathway – Oxygenated blood from the left ventricle through the aortic semilunar valve to the aorta – Oxygenated blood through branching arteries and arterioles to the tissues – Gas exchange at the level of the tissues – Deoxygenated blood from capillaries into veins – Ultimately to the vena cava and into the right atrium  Pathway of Blood Through the Heart and Lungs Right atrium  tricuspid valve  right ventricle Right ventricle  pulmonary semilunar valve  pulmonary trunk pulmonary arteries  lungs Lungs  pulmonary veins  left atrium Left atrium  bicuspid valve  left ventricle Left ventricle  aortic semilunar valve  aorta Aorta  systemic circulation right atrium Blood Pathway Through the Heart & Lungs Figure 17.5  Coronary Circulation Coronary circulation is the functional blood supply to the heart muscle itself Left coronary artery- circumflex & anterior interventricular artery Right coronary artery- marginal & the posterior interventricular artery Cardiac Veins – small cardiac, middle cardiac and great cardiac veins empty into the coronary sinus; anterior cardiac veins empty directly into the right atrium Coronary Circulation: Arterial Supply Figure 17.7a Coronary Circulation: Venous Supply Figure 17.7b  Microscopic Anatomy of Heart Muscle Cardiac muscle is striated, branched, and interconnected; uni- or binucleate Intercalated discs anchor cardiac cells together and allow free passage of ions Heart muscle behaves as a functional syncytium due to intercalated discs, desmosomes, and gap junctions Microscopic Anatomy of Heart Muscle Figure 17.11  Cardiac Muscle Contraction Heart muscle: – Is stimulated by nerves and is self-excitable (autorhythmicity) – Contracts as a unit using sliding filament mechanism – Respires aerobically only – Tetanic contractions do not occur Cardiac muscle contraction is similar to skeletal muscle contraction  Heart Physiology: Intrinsic Conduction System Autorhythmic cells: – Initiate action potentials – Have unstable resting potentials called pacemaker potentials – Sodium channels leak ions into the cells in the absence of any nerve impulse; at depolarization calcium channels open up – Use calcium influx (rather than sodium) for rising phase of the action potential – Has a long (250 ms) absolute refractory period Pacemaker & Action Potentials of the Heart Figure 17.13  Cardiac Muscle Contraction Depolarization opens voltage-gated fast Na + channels in the sarcolemma that will lead to Ca2+ influx just like skeletal muscle Then Ca2+ channels (slow) open up allowing influx from the extracellular space; triggers Ca2+ release from SR Even though Na + channels have inactivated, the Ca2+ surge prolongs depolarization; plateau of action potential tracing Duration of the action potential and the contractile phase is much greater in cardiac muscle than in skeletal muscle Repolarization results from inactivation of Ca 2+ channels and opening of voltage-gated K+ channels  Action 1 Depolarization is potential due to Na+ influx through Plateau fast voltage-gated Na+ channels. A positive feedback cycle rapidly 2 opens many Na+ Membrane potential (mV) Tension channels, reversing the development membrane potential. (contraction) Channel inactivation ends Tension (g) this phase. 1 3 2 Plateau phase is due to Ca2+ influx through slow Ca2+ channels. This keeps the cell depolarized because few K+ channels Absolute are open. refractory period 3 Repolarization is due to Ca2+ channels inactivating and K+ channels opening. This allows K+ efflux, which Time (ms) brings the membrane potential back to its resting voltage. Figure 18.12  Heart Physiology: Sequence of Excitation Sinoatrial (SA) node in right atrium generates impulses about 75 times/minute; dominant autorythmic cells; nervous system may regulate Atrioventricular (AV) node delays the impulse approximately 0.1 second Impulse passes from atria to ventricles via the atrioventricular bundle (AV bundle) AV bundle splits into two pathways in the interventricular septum (bundle branches) – Bundle branches carry the impulse toward the apex of the heart – Purkinje fibers carry the impulse to the heart apex and ventricular walls Sequence of Excitation Figure 17.14a  Electrocardiography Electrical activity is recorded by electrocardiogram (ECG) P wave corresponds to depolarization of SA node and atria QRS complex corresponds to ventricular depolarization T wave corresponds to ventricular repolarization Atrial repolarization record is masked by the larger QRS complex Electrocardiography Figure 17.16 Heart Excitation Related to ECG Figure 17.17  Cardiac Cycle Cardiac cycle refers to all events associated with blood flow through the heart; electrical events, valve activity, heart sounds, chamber contractions and changes in blood pressure – Systole – contraction of heart muscle – Diastole – relaxation of heart muscle Cardiac Cycle Figure 8.12  Phases of the Cardiac Cycle Ventricular filling – mid-to-late diastole – Heart blood pressure is low as blood enters atria and flows into ventricles – AV valves are open, then atrial systole occurs – SA node depolarizes, remaining blood forced into ventricles Ventricular systole – Atria relax and repolarize – Rising ventricular pressure due to contraction results in closing of AV valves – Isovolumetric contraction phase; both valves closed – Ventricular ejection phase opens semilunar valves  Phases of the Cardiac Cycle Isovolumetric relaxation – early diastole – Ventricles relax and repolarize – Backflow of blood in aorta and pulmonary trunk closes semilunar valves Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves  Heart Sounds Heart sounds (lub-dup) are associated with closing of heart valves – First sound occurs as AV valves close and signifies beginning of systole – Second sound occurs when SL valves close at the beginning of ventricular diastole Heart murmurs-obstruction in the flow of blood, valve irregularity Phases of the Cardiac Cycle Figure 17.20  Cardiac Output (CO) and Reserve CO is the amount of blood pumped by each ventricle in one minute CO is the product of heart rate (HR) and stroke volume (SV); directly correlated HR is the number of heart beats per minute SV is the amount of blood pumped out by a single ventricle with each beat Cardiac reserve is the difference between resting and maximal CO  Stroke Volume SV = end diastolic volume (EDV) minus end systolic volume (ESV) EDV = amount of blood collected in a ventricle during diastole ESV = amount of blood remaining in a ventricle after contraction Factors Affecting Stroke Volume Preload – amount ventricles are stretched by contained blood Contractility – cardiac cell contractile force due to factors other than EDV Afterload – back pressure exerted by blood in the large arteries leaving the heart; must be overcome by ventricles in order to eject blood  Frank-Starling Law of the Heart Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume Main variable is venous return flow- slow heartbeat and exercise increase venous return to the heart, increasing SV Blood loss and extremely rapid heartbeat decrease SV Afterload is influenced by preload- the more the heart stretches the stronger the recoil contraction.  Extrinsic Factors Influencing Stroke Volume Contractility is the increase in contractile strength, independent of muscle stretch and EDV Increase in contractility comes from: – Increased sympathetic stimuli – Certain hormones – Ca2+ and some drugs Agents/factors that decrease contractility include: – Acidosis (excess H+) – Increased extracellular K+ – Calcium channel blockers  Regulation of Heart Rate: Autonomic Nervous System Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise; releases norepinephrine Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone  Extrinsic Innervation of the Heart Heart is stimulated by the sympathetic cardioacceleratory center (CAC) Heart is inhibited by the parasympathetic cardioinhibitory center (CIC) Figure 17.15  Figure 18.22 Factors involved in determining cardiac output. Exercise (by Heart rate Bloodborne Exercise, sympathetic activity, (allows more epinephrine, fright, anxiety skeletal muscle and time for thyroxine, respiratory pumps; ventricular excess Ca2+ see Chapter 19) filling) Venous Sympathetic Parasympathetic return Contractility activity activity EDV ESV (preload) Initial stimulus Stroke Heart volume rate Physiological response Result Cardiac output © 2013 Pearson Education, Inc.  Atrial (Bainbridge) Reflex Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria – Causes stimulation of the SA node – Stimulates baroreceptors in the atria, causing increased SNS stimulation – Results in increased rate and force of contraction causing increased cardiac output  Carotid Sinus Reflex & Aortic Reflex Carotid sinus reflex- Prevents major changes in blood supply to the brain; rapid response to short term changes Mediated by baroreceptors in carotid sinus Regulates the activity of the CIC and the CAC Aortic sinus reflex- regulates blood flow to the systemic blood vessels Action similar to the carotid sinus reflex Chemical Regulation of the Heart The hormones epinephrine and thyroxine increase heart rate Intra- and extracellular ion concentrations must be maintained for normal heart function Regulation of Heart Rate Other factors that influence heart rate – Age Fetus has fastest HR; declines with age – Gender Females have faster HR than males – Exercise Increases HR Trained atheles can have slow HR – Body temperature HR increases with increased body temperature Homeostatic Imbalance Tachycardia: abnormally fast heart rate (>100 beats/min) – If persistent, may lead to fibrillation Bradycardia: heart rate slower than 60 beats/min – May result in grossly inadequate blood circulation in nonathletes – May be desirable result of endurance training Congestive Heart Failure (CHF) Congestive heart failure (CHF) is caused by: – Coronary atherosclerosis – Persistent high blood pressure – Multiple myocardial infarcts – Dilated cardiomyopathy (DCM)  Cardiac Conditioning Exercise will increase cardiac muscle mass Increased cardiac muscle mass increases the strength of contraction Heart beats less and rests more