Physiology Exam 3 Electrical & Mechanical Properties of Cardiac Muscle Blood Flow Deoxygenated Blood o Superior & inferior

r vena cava o Right Atrium o Tricuspid (Right AV) Valve o Right Ventricle o Pulmonary valve o Right & left pulmonary arteries o Lungs Oxygenated Blood o Lungs o Right & Left Pulmonary Veins o Left Atrium o Mitral (Left AV) Valve o Left Ventricle o Aortic Valve o Aorta o Systemic Circulation Valves o Most blood flows passively into ventricle occurs when atrial pressure > ventricular pressure Tricuspid valve is open & ventricles relaxed o When ventricular pressure > atrial pressure - AV valve will close o Opening & closing of valves depends on the pressure gradient across the valve o There are no valves between the veins & atria Pulmonary Circulation low pressure, low resistance Systemic Circulation high pressure, high resistance o Left ventricle wall is much thicker & stronger organ systems are arranged in parallel o allows body to shut off flow to one area & divert blood to another area o this would not be possible if organ systems blood flow was in series

Cardiac Muscle Characteristics o Striated o Many mitochondria more than skeletal muscle o Intercalated discs adjacent cardiac cells are joined end-to-end Contain gap junctions allows each chamber to function as a single unit (functional syncytium) by allowing the spread of AP And desmosomes holds cells together, can withstand mechanical stress Cardiac cells exhibit autorhythmicity can generate AP on their own allows some cells to become pacemakers Cardiac muscle RMP is closer to -90 mV less Na+ leakage & greater [K+] Properties of Cardiac Muscle Excitability Ability to generate & respond to an action potential

Physiology Exam 3 3 types of cardiac tissues all 3 exhibit excitability to some degree o nodal tissue SA node is primary pacemaker o Purkinje fibers (bundle fibers) o Muscle only exhibits autorythmicity if other tissues arent working properly

Stages of AP o Most of AP myocardial fiber in absolute refractory cannot generate/respond to AP o Relative refractory period o Superexcitatory All-or-None o Applies to a single myocardial fiber either contract or not at all o Can be extended to the entire heart Functional syncytium intercalated discs allow transmission of AP When one fiber generates an AP, depolarization spreads rapidly over entire heart All-or-none refers to ability of all cardiac muscle to contract to a stimulus @ one point or not at all Mechanical behavior of fiber is determined prior to contraction o Resting length o Inotropic state o Each fiber does not always contract maximally when stimulated Rhythmicity autoexcitability cardiac muscle can initiate its own contraction Pacemaker potential o Cardiac muscle undergoes gradual depolarization until threshold is reached AP initiated repolarization gradual depolarization o Due to gradual reduction in K+ conductance (less movement outward) OR a gradual increase in Ca2+ conductance (inward current) o Nodal RMP ~ 60 mV (oscillating RMP) Due to Ca2+ voltage-gated channels ([Ca2+]out > [Ca2+]in) L-type channels long lasting; depolarization phase T-type channels transient; open only a short time; gradual depolarizations (oscillations) Na+ does not play a role Frequencies of Autorhythmicity o SA Node = 70-80 beats/min o AV Node = 40-60 beats/min o Purkinje Fibers = 15-40 beats/min Primary Pacemaker o Normally atrial & ventricular muscle does not exhibit autorhymicity o Overall rhythmicity of heart established by the SA Node (it has the highest rhythmic rate) o Whatever node has the highest frequency will become primary pacemaker (if not SA Node called ectopic focus) Chronotropy o Change in heart rate o Positive chronotropy increase heart rate Higher temperature Atropine epinepherine Sympathetic stimulation o Negative Chronotropy decreased heart rate Hypothermia Parasympathetic stimulation

Physiology Exam 3 ACh Beta-adrenergic block

Conductivity ability to conduct an AP & how fast conduction occurs Varying degrees on conductivity o Fastest Purkinje fibers (2-4 m/sec) o Slowest Junctional tissue (.02-.05 m/sec) b/t Atria & Ventricles; allows for AV Nodal Delay (ventricular filling) Separates atrial & ventricular systole Dhromotrophy o Speed of conduction o Positive dhromotropy increased rate of conductivity Sympathetic stimulation o Negative dhromotropy decreased rate of conductivity Parasympathetic (vagal) stimulation quinidine Compliance describes elasticity change in dimension w/ respect to a change in stress (force/unit area) applies to both heart & lungs Extensibility ability of a body to extend o x/F = change in distance change in force o 2-deminsional o applies to muscle strips Distensibility ability of a hollow object to distend due to an increase in internal pressure fractional change in volume per unit change in pressure o % V/P o 3-deminsional measurement accounts for original size o applies to cardiac chambers non-compliant large change in pressure causes a small change in volume compliant small change in pressure causes large change in volume Contractibility increasing the strength of contraction ability to shorten/develop tension Cardiac muscle can increase force in 2 ways: (cannot occur simultaneously) o Heterometric Autoregulation Frank-Starling Law More stretch = stronger strength of contraction Resting length of cardiac muscle is NOT optimal length (unlike skeletal muscle) End diastolic volume determines amount of stretch Venous return determines EDV Stroke volume = volume of blood ejected w/ each contraction Starlings Law = venous return = EDV = stretch & contraction = stroke volume Never due to contractility

Physiology Exam 3 o Homeometric Autoregulation Inotropic State Do not vary the length of muscle Inotropic agents cause change in myocardial contractility Positive inotropic agent increase in force of contraction from the same or small EDV or fiber length o Increase [Ca2+]in o NE, digitalis, increased extracellular Ca2+ Negative inotropic agent o Decrease [Ca2+]in o Increased extracellular Na+, quinidine, Ca2+ channel blockers Contractility increase in contractile force independent of fiber length Contractility = [Ca2+]out / [Na+]3out Receptors Adrenergic 1 increase HR & contractility Muscarinic decrease HR Steps Catecholamine binds to 1 receptor Adenylyl cyclase increase cAMP Activates cAMP protein kinase (PK) Phosporylates L-type Ca2+ channel in sarcolemma (prolongs opening) Trigger Ca-Induced Ca release from SR Must have extracellular Ca2+ for heart muscle to contract Na-Ca exchanger Antiport (secondary active transport) 1 Ca out for every 3 Na in (down concentration gradient) Ex: increase extracellular [Na+] o Activates Na-Ca exchanger more Na into cell o ( - ) inotropic effect o smaller contraction Ex: glycosides inhibit Na-K pump o Increase in intracellular [Na+] o Less active Na-Ca exchanger o Increase in intracellular [Ca2+] o (+) inotropic effect o stronger contraction