Cardiac Guided Notes PDF

Cardiac Background information: Functions: ● Generating blood pressure ● Routing blood ○ ● Heart separates pulmonary and systemic circulations; Ensures one-way blood flow Regulating blood supply ○ Changes in contraction rate and force match blood delivery to changing metabolic needs Definit...

Cardiac Background information: Functions: ● Generating blood pressure ● Routing blood ○ ● Heart separates pulmonary and systemic circulations; Ensures one-way blood flow Regulating blood supply ○ Changes in contraction rate and force match blood delivery to changing metabolic needs Definitions: Autorhythmicity -- generating action potentials by itself, generating its own rhythm Cardiac output -- amount of blood pumped by each ventricle in one minute Electrocardiogram (ECG) -- record of overall spread of electrical activity through heart Etymology Fun: Peri-- “around” or “enclosing” Epi--”above” Myo-- “muscle” Endo-- “within” Key Players: ● Heart -- largest organ of mediastinum, located between lungs; apex lies to the left of the midline, base is the broad posterior surface ● Atria -- thin, upper chambers that receive blood (capped by auricles that serve as blood reservoirs) ● Ventricles -- thick, lower chambers that pump blood ● Interventricular septum -- wall separating left and right sides of the heart How It Works: 1) Conduction Pathway Cardiac impulse originates at SA node Action potential spreads throughout right and left atria Impulse passes from atria into ventricles via AV node (only point of electrical contact between chambers) Action potential delayed at AV node to ensure atrial contraction precedes ventricular contraction for complete ventricular filling Impulse travels rapidly down interventricular septum by means of bundle of His Impulse rapidly disperses throughout myocardium by means of Purkinje fibers Rest of ventricular cell activated by cell-cell spread of impulse via gap junctions 2) Cardiac Histology Intercalated discs allow branching of the myocardium Gap junctions (instead of synapses) create fast cell-cell signals Many mitochondria Large T tubes 3) Pacemaker Potential Autorhythmic cells have “drifting” resting potentials called pacemaker potentials Membrane slowly depolarizes “drifts” to threshold, initiates action potential, membrane repolarizes to -60mV Use calcium influx (rather than sodium) for rising phase of the action potential 4) Purpose of Longer AP in Cardiac Contractile Fibers A long refractory period + prolonged plateau phase prevents summation and tetanus in myocardium Plateau ensures alternate periods of contraction and relaxation essential for pumping blood 5) Excitation-Contraction Coupling in Cardiac Contractile Cells Action potential from autorhythmic cells is passed to contractile cells, propagating down T-tubules AP in T-tubules cause a small influx of Ca2+ via Ca2+ L-channels, triggering larger release of Ca2+ from sarcoplasmic reticulum Ca2+ induced Ca2+ release leads to cross-bridge cycling and contraction 6) Electrocardiogram (ECG) Not direct recording of actual electrical activity of heart or a single action potential in a single cell at a point in time Comparisons in voltage detected by electrodes at two different points on body surface, not the actual potential Does not record potential at all when ventricular muscle is either completely depolarized or completely repolarized 7) Cardiac Cycle -- Filling of Heart chambers Heart = right and left pumps working together Repetitive contraction (systole) and relaxation (diastole) of heart chambers Ventricle contraction produces pressure Blood moves from areas of higher to lower pressure 12) Medulla Oblongata Centers Affect Autonomic Innervation Receives input from higher centers, monitoring blood pressure (baroreceptors) and dissolved gas concentrations (chemoreceptors) Cardio-acceleratory center activates sympathetic neurons while cardio-inhibitory center controls parasympathetic neurons Difference Between: Layers of the Heart Wall Pericardium Epicardium Myocardium Endocardium Fibrous -- strong, dense CT Serous -- parietal and visceral (a.k.a. epicardium) Visceral layer of the serous pericardium Consists of cardiac muscle Arranged in circular and spiral patterns Endothelium resting on layer of CT Lines the internal walls of the heart Action Potentials of Cardiac Cells Autorhythmic Contractile Cause Effect K+ channels closed Decreased efflux of K+ Constant influx of Na+ No voltage-gated Na+ channels Drifting depolarization K+ builds up and NA+ flows inward Voltage-gated Ca2+ T-channels open at -55 mV Small influx of Ca2+ further depolarizes to threshold (-40 mV) via transient channels Voltage-gated Ca2+ channels open at threshold Sharp depolarization due to activation of Ca2+ due to activation of Ca2+ L channels allow large influx of Ca2+ via long lasting channels Peak at +20 mV Ca2+ L channels close, voltage-gated K channels open, repolarization due to normal K+ efflux K+ channels close -60 mV 1) Rapid Na+ influx causes depolarization 2) Rapid Partial early repolarization followed by prolonged period of slow repolarization --Exhibit plateau (prolonged positive phase) accompanied by prolonged period of contraction to ensure adequate ejection time; plateau primarily due to activation of slow L-type Ca2+ channels 3) Rapid Final repolarization phase Cardiac Muscle Tissue Fibers Forms a thick layer of myocardium Striated, like skeletal muscle Contractions pump blood through the heart and into blood vessels via sliding filament mechanism Short, branching, with one or two nuclei Cells join at intercalated discs to connect and support synchronized contraction of cardiac tissue Cells are separated by delicate endomysium --binds adjacent cardiac fibers --contains blood vessels and nerves Chambers of the Heart Right Atrium Gross Anatomy Function Additional Information Receives oxygen poor blood from superior and inferior vena cava Pumps blood to right ventricle through tricuspid valve Fossa ovalis -- a depression in interatrial septum; a remnant of foramen ovale (fetal heart) Pumps blood into pulmonary circuit via pulmonary trunk Pulmonary semilunar valve -located at opening of right ventricle and pulmonary trunk Opens into left ventricle through mitral valve (bicuspid valve) Makes up heart’s posterior surface Pumps blood into systemic circuit via aortic semilunar valve (aortic valve) Forms apex of the heart Three times thicker than right ventricle Right Ventricle Left Atrium Receives oxygen-rich blood from lungs through pulmonary veins Left Ventricle Internal Structures of the Heart Internal Walls of Ventricles Heart Valves Atrioventricular (AV) Valves Aortic and pulmonary valves Papillary muscles -- attach to mitral and tricuspid valves’ chordae tendineae; contract to prevent inversion of valves beyond point of closure Valves within the heart Regulate blood flow based on blood pressure Composed of endocardium with CT core Between atria and ventricles Mitral (bicuspid) and tricuspid Cusps (flaps) are semilunar in shape At junction of ventricles and great arteries (pulmonary and aortic) Chordae tendineae -- cord-like tendons that connect the papillary muscles to the mitral and tricuspid valves Coronary Arteries Cardiac Veins Left and right coronary arteries branch into smaller coronary arteries Originate from left side of heart, at root of the aorta Deliver oxygen-rich blood to cardiac muscle Drain blood into the coronary sinus which delivers deoxygenated blood to the right atrium Specialized Cardiac Muscle Cells and Electrical Activity of the Heart Heart beats rhythmically as a result of autorhythmicity Contractile cells Autorhythmic Cells Do mechanical work of pumping Normally do not initiate own action potentials 99% of cardiac muscle cells Do not contract Specialized for initiating and conducting action potentials responsible for contraction of working cells Intrinsic Conduction System SA Node AV Node Purkinje Fibers Function Sets the pace of the heartbeat Delays the transmission of action potentials Can act as pacemaker under some conditions Beats per minute (bpm) 70-80 40-60 20-30 Heart Sounds First: Lubb Second: Dupp AV valves close and surrounding fluid vibrations at systole Closure of aortic and pulmonary semilunar valves at diastole, lasts longer Abnormalities of the Heart Extrasystole V-Fib Complete Heart Block Myocardial Infarction Congestive Heart Failure (CHF) Effect Extra beats Disordered electrical activity No conduction through AV node Heart doesn’t pump blood as well as it should Caus e Autorhythmic cells other than SA node fires out of sequence Ventricles contract in unsynchronized way No blood is pumped Cardiac arrest Atria and ventricles contract out of sync Death of myocardial tissue Blockage of coronary artery Phases of Ventricular Systole Coronary atherosclerosis Persistent high blood pressure Multiple myocardial infarcts Dilated cardiomyopathy First: Isovolumic Contraction Second: Ventricular Ejection Cause Ventricles begin to contract, pushing AV valves close, SL valves still closed, pressure in ventricles rises Ventricular pressure rises and exceeds pressure in the arteries, Effect Pressure in ventricles is not enough to open semilunar valves All valves are closed Semilunar valves open and blood is ejected Cardiac Output and Reserve Definition Equation Average Range Additional Info Cardiac Output (CO) amount of blood pumped by each ventricle in one minute CO = HR x SV 5 L/min Maximal CO can be 4-5x greater than resting CO in non-athletes Cardiac Reserve difference between resting and maximal CO Max CO Resting CO Stroke Volume the volume of blood pumped from one ventricle of the heart with each beat SV = EDV ESV 20-25 L during intense exercise 20-25 L/min 5 L/min = 15-20 L/min 70 mL End Diastolic Volume (EDV) End Systolic Volume (ESV) Blood volume in heart before ventricular ejection Blood volume remaining in heart after ventricular ejection 135 mL 65 mL Factors Affecting Cardiac Output Heart Rate Stroke Volume Autonomous innervation Hormones -- epi, NE, and thyroid hormone (T3) Cardiac reflexes Starling’s Law Venous Return Cardiac Reflexes Intrinsic Extrinsic Normal functional characteristics of heart Contractility, HR, preload stretch Neural and hormonal control (ANS) Factors Affecting Stroke Volume The individual’s heart can pump 15-20 L/min more than is required for normal circumstances, 300-400%! A trained athlete’s heart has a greater SV, which equates to decreased need to pump less frequently both at rest and during exercise and a substantially lower HR than the average person Determined by Extent of Venous Return and Sympathetic Activity Increased Stroke Volume = Increased Strength of Contraction Sympathetic stimulation releases norepinephrine and initiates a cAMP second-messenger system Intrinsic Extrinsic Preload – amount ventricles are stretched by contained blood EDV Venous return - skeletal, respiratory pumping Afterload – back pressure exerted by blood in the large arteries leaving the heart Contractility – cardiac cell contractile force from other factors independent of EDV and stretch Increase in contractility comes from: Increased sympathetic stimuli Hormones -- Epinephrine and Thyroxine Increased Ca2+ and some drugs Intra- and extracellular ion concentrations must be maintained for normal heart function Frank-Starling Law Cause Increased Preload* Slow heartbeat and exercise Blood loss and extremely rapid heartbeat Effect Increased force of contraction Increased venous return Decreased venous return Stroke Volume Increased Increased Decreased *critical for controlling Establishing Normal Heart Rate *SA node establishes baseline and modified by ANS Stemming from Hormones Released Effect on HR and Force of Contraction Sympathetic Sympathetic trunk Epinephrine and norepi Increase Parasympatheti c Vagus nerve Acetylcholine Decrease