Chapter 18 - The Heart PDF

Chapter 18 --The Heart Location and size of heart Located in the thoracic cavity in the mediastinum About same size as a closed fist the base is the wider superior portion the apex is the point Pericardium Fibrous Pericardium Muncle that helps you Rests on an...

Chapter 18 --The Heart Location and size of heart Located in the thoracic cavity in the mediastinum About same size as a closed fist the base is the wider superior portion the apex is the point Pericardium Fibrous Pericardium Muncle that helps you Rests on and is attached to diaphragm > Breath - A tough, inelastic sac of fibrous connective tissue > Made of - Anchored to the blood vessels entering and leaving the base of the heart > go in and out of the hert - Protects and anchors the heart; prevents overfilling of the chambers of the heart Presents the heart from with gettery to full blood  Parietal (Outer) Serous Pericardium Simple squamous epithelium > Made of - Forms outer parietal layer bound to fibrous pericardium ProduceSecretes a serous (watery) lubricating fluid Reduces friction as the heart contracts and twistsHilp = Visceral (Inner) Serous Pericardium Made of Simplesquamous epithelium that forms the epicardium > Also known - of Forms visceral layer bound to the myocardium of the heart Produc Secretes serous fluid Reduces friction as the heart pumps, contracts and twists  attached to the heart · It is meety muscle called myocecum Fluid th heart · helps relue frection as pump , confronts and twists Homeostatic Imbalances Pericarditis Inflammation of pericardium Painful; damage to the lining tissues Can damage myocardium Cardiac tamponade A buildup of pericardial fluid, or Bleeding into the pericardial cavity May result in cardiac failure Heart wall - Three layers Epicardium (outer) visceral layer of pericardium thin, transparent smooth, slippery Myocardium (middle) mass of cardiac muscle Endocardium (inner) endothelium over thin connective tissue smooth lining for the chambers and valves continuous with blood vessel endothelium Cardiac Muscle Myocardium (Cardiac Muscle) Fibers are connected to the others by intercalated discs Gap junctions allow action potentials to pass from fiber to fiber Desmosomes (“spot welds”) prevent cardiac fibers from separating during contractions Surface of the Heart External landmarks Atrioventricular grooves separate atria from ventricles Grover Anterior/posterior interventricular sulcus separates right and left ventricles Coronary vessels run in these grooves Blood vessels that run along the grooves Chambers of the heart 4 compartments R/L atria with auricles R/L ventricles Interatrial septum separates atria Interventricular septum separates ventricles Left ventricular wall is much thicker because it must pump blood throughout the body and against gravity RA-LA = Awucles - RV - LV Ventricles Blood Flow through the Heart Right atrium (RA) - receives deoxygenated blood from three sources ❿ Superior vena cava (SVC) ❿ Inferior vena cava (IVC) ❿ Coronary sinus (CS) SVC = Blood from upper boy IVC = Blood from lower body Cs = Blood from the hunt itsly  16 O g To The RA sends blood to RV Most blood drains to the right ventricle RV Right ventricle (RV) pumps blood to pulmonary trunk (PT) Pulmonary trunk (PT) – conducts blood to pulmonary arteries (PA) T PA (Pulmuncy Artey) = Senes Blood the lunge , where picks up ozgen Pulmonary Circulation + 05 - Pulmonary arteries Carry deoxygenated blood from the heart to the lungs for gas exchange Right and left branches for each lung Blood gives up CO and picks up O in the lungs 2 2 Pulmonary veins (PV) a D Carry oxygenated blood from the lungs to the heart to the left atria PV"Bring rich oxygen blood to the heart to the by ↑ Blood flow through the heart atree LA sends orgen to the LV Left atria pumps to left ventricle (LV) Left ventricle pumps oxygenated blood to the body via the ascending aorta Aortic arch curls over heart three branches off of it feed superior portion of body Thoracic aorta Abdominal aorta Body -> Right Akrium RA Right Ventricle RV - Leys (to get oxy) Lungs Lest Akriu LA Let Ventril LV - Body Myocardial Blood Supply Myocardium has its own blood supply Coronary vessels branch off the aorta comes from Simple diffusion of nutrients and O into the myocardium is 2 impossible due to its thickness  Blood moves more easily into the myocardium when it is relaxed between beats à during diastole > allel - Heart can survive on 10-15% of normal arterial blood flow Myocardial Blood Supply Arteries conduct blood to coronary capillary beds Collateral circulation = duplication of supply routes and anastomoses (crosslinked connections) Coronary veins conduct Deoxygenated blood from cardiac muscle to the coronary sinus Coronary sinus returns blood to the right atrium Coronary Circulation Pathologies Compromised coronary circulation due to: Problems with the Blood Emboli: blood clots, air, amniotic fluid, tumor fragments flow Fatty atherosclerotic plaques Smooth muscle spasms in coronary arteries Problems Ischemia (decreased blood supply)  Hypoxia (low supply of O ) 2 Angina pectoris - classic chest pain Pain is due to temporary myocardial ischemia – oxygen starvation of the tissues tight/squeezing sensation in chest labored breathing, weakness, dizziness, perspiration, foreboding Often during exertion - climbing stairs, etc. Pain may be referred to arms, back, abdomen, even neck or teeth Silent myocardial ischemia can exist Pathologies (cont.) Myocardial infarction (MI) - heart attack Thrombus/embolus in coronary artery Some or all tissue distal to the blockage dies If pt. survives, muscle is replaced by scar tissue Long term results Size of infarct, position Pumping efficiency? Conduction efficiency, heart rhythm Pathologies (cont.) Treatments Clot-dissolving agents Angioplasty (bypass surgery) Reperfusion damage Re-establishing blood flow may damage tissue oxygen free radicals - electrically charged oxygen  atoms with an unpaired electron radicals indiscriminately attack molecules: proteins (enzymes), neurotransmitters, nucleic acids, plasma membrane molecules Further damage to previously undamaged tissue or to the already damaged tissue Valve Structure & Function Dense connective tissue covered by endocardium Prevent backflow of blood Opening and closing a passive process The valves open when pressure is lower in the second chamber than in the first chamber. Blood can then flow Brub ↑ With contraction, pressure increases in the second chamber. This causes the valve to close Atrioventricular (AV) valves Separate the atria from the ventricles  Bicuspid (mitral) valve – left side Tricuspid valve – right side Note the feathery edges to the cusps Atrioventricular (AV) valves AV valves Chordae tendineae - thin fibrous cords Connect valves to papillary muscles Papillary muscles contract and prevent valves from opening as pressure increases suret Yo musehe & I-chodae tendineue Papilling muscle = When muscles as contracts Prevent values pressure from incre opening in Semilunar valves the muscle In the arteries that exit the heart to prevent back flow of blood to the ventricles  Aortic semilunar valves Pulmonary semilunar valves Pathologies Incompetent – does not close correctly Stenosis – hardened, even calcified, and does not open correctly Aortic Pulmancog Pacemakers and the Conduction System Autorhythmic cardiac pacemaker cells repeatedly fire spontaneous action potentials to make the heart bet SA node = Sends signals origin of cardiac excitation fires 60-100/min AV node Conduction system AV bundle (Bundle of His) R and L bundle branches  Purkinje fibers Pacemaker Potentials - Leaky membranes Spontaneously depolarize Creates autorhythmicity The fact that the membrane is more permeable to K and Ca + 2+ ions helps explain why concentration changes in those ions affect cardiac rhythm Cardiac Muscle Action Potential In contractile cells the heart and blood Help squege pomp - Quick depolarization is necessary for efficient pumping change queekly Long absolute refractory period allows adequate time for contraction and relaxation helps the heart to pump blood = Prevents summation or tetany smochly Conduction System and Pacemakers Arrhythmias Irregular rhythms: slow (brady-) & fast (tachycardia) Abnormal atrial and ventricular contractions  Pare maker Potential · alls that crut ebetrical synul on their own , with her the went to real regulary sealed ebetrievedcompletly · The cells have walls that we not this mens is and out kin amount of ions can more · There don't need wls a synal from somewhere be to Start their ebetrial aturf they start , their own on the heart keeps without The wls makes sure else to kell it when seating to but Neely someone · alls let k- and cast ioms These these our help control the herds through When more carey rhythm how -. the it can have slow of these ins mark change , beaks affed fast or your Fibrillation Rapid, fluttering, out of phase contractions – no pumping Heart resembles a squirming bag of worms Ectopic pacemakers (ectopic focus) Abnormal pacemaker controlling the heart SA node damage, caffeine, nicotine, electrolyte imbalances, hypoxia, toxic reactions to drugs, etc. Heart block AV node damage - severity determines outcome May slow conduction or block it Conduction System and Pacemakers SA node damage (e.g., from an MI) AV node can run things (40-50 beats/min) If the AV node is out, the AV bundle, bundle branch and conduction fibers fire at 20-40 beats/min Conduction System and Pacemakers Artificial pacemakers Can stimulate single, or dual chambers (ventricle or ventricle & atrium) Can also stimulate both ventricles Can be activity dependent Atrial,Ventricular Excitation Timing It takes about 0.05 sec from SA to AV 0.1 sec to get through AV node – conduction slows Allows atria time to finish contraction and to better fill the ventricles Once action potentials reach the AV bundle, conduction is rapid to rest of ventricles Extrinsic Control of Heart Rate Basic rhythm of the heart is set by the internal pacemaker system Central control from the medulla is routed via the ANS to the pacemakers and myocardium sympathetic input - norepinephrine parasympathetic input – acetylcholine Electrocardiogram Measures the sum of all electro-chemical activity in the myocardium at any moment P wave  QRS complex T wave Electrocardiogram Cardiac Cycle: Electrical & Mechanical Events Systole Heat muscle = squeyes to push blood out of Body Diastole = Heart rulaxes Heart squeyes Isovolumetric - to hard , are contraction but blood no haves yet Ventricular After squezig = ejection hav the heart Pushes blood inte , the back Isovolumetric the heart reluxe - Relaxation but blood comes no in get Cardiac Output Amount of blood pumped by each ventricle in 1 minute Cardiac Output (CO) = Heart Rate x Stroke Volume  HR = 70 beats/min SV = 70 ml/beat CO = 4.9 L/min * Cardiac Reserve Cardiac Output is variable Cardiac Reserve = maximal output (CO) – resting output (CO) Average individuals have a cardiac reserve of 4X or 5X CO Trained athletes may have a cardiac reserve of 7X CO Heart rate does not increase to the same degree Regulation of Stroke Volume SV = EDV – ESV EDV End Diastolic Volume Volume of blood in the heart after it fills 120 ml ESV End Systolic Volume Volume of blood in the heart after contraction 50 ml Each beat ejects about 60% of the blood in the ventricle Regulation of Stroke Volume The 3 most important factors in regulating SV: Preload – the degree of stretching of cardiac muscle cells  = Mou struck means more before contraction blood gels pumped our Contractility – increase in contractile strength separate from the head stretch and EDV How strong equezes to pump flood out, even if its not strech mucht Afterload – pressure that must be overcome for ventricles to eject blood from heart Pressure the hea his to work agains to pump blood our Preload: Frank-Starling Law of the Heart The length tension relationship of heart, where Length = EDV and Tension = SV Normally, muscle fibers are shorter than the optimal increasing/decreasing fiber length increases/decreases force generation Fiber length is determined by filling of heart – EDV Anything that effects venous return to the heart) increases/decreases filling increases/decreases SV Contractility The contractile strength at a given muscle length Sympathetic nervous stimulation (NE) opens Ca channels, 2+ allowing it to enter the cell Ca increases 2+ the number of cross bridges between actin and mysin This increases SV by lowering ESV Contractility: Inotropic Effects Positive Increase contractility Glucagon Thyroxin Epinephrine Digitalis Negative Reduce contractility Acidosis (too much H ) + High extracellular K + Calcium channel blockers Afterload If blood pressure is high, it is difficult for the heart to eject blood More blood remains in the chambers after each beat Heart has to work harder to eject blood, because of the increase in the length/tension of the cardiac muscle cells Regulation of Heart Rate Normally, SV is constant The control of CO is exerted through changes in heart rate These are chronotropic effects Intrinsic controls Bainbridge effect Increase in EDV increases HR Filling the atria stretches the SA node increasing  depolarization and HR Regulation of Heart Rate Extrinsic controls Autonomic Nervous System Sympathetic – norepinephrine (β receptor) 1 Parasympathetic – acetylcholine Normally, this vagal tone keeps the brakes on HR Hormones – epinephrine, thyroxine Ions (especially K and Ca ) + 2+ Body temperature Age/gender Body mass/blood volume Exercise Stress/illness An Overview of Heart Rate Regulation End Chapter 18