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Circulatory System Class Notes Clear and concise notes taken during lecture for the circulatory system. (Finished with an A)

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York University
Kinesiology & Health Science
KINE 3012
Tara Haas

Circulatory System  Pulmonary circulation takes the blood to the lungs via the pulmonary arteries and back to the heart via the pulmonary veins  Systemic circulation takes the blood throughout the body through arteries and returns back to the heart through the veins  Hematocrit is the concentration of RBC found in a sample of blood o Anemia is an insufficient hematocrit o Polycythemia is an elevated hematocrit  Primary polycythemia is a tumour-like condition of the bone marrow which causes unregulated erythropoiesis  Secondary polycythemia is an adaptive response to improve 2 delivery to the tissues, typically occurring to people living in high altitudes o Dehydration contains the same amount of RBC but the volume of plasma is lower so the hematocrit is increased (relative polycythemia) Cardiac Muscle  The spiralling pattern of cardiac muscle allow the ventricles to contract upwards and physically push the blood out of the heart o Only contain one nucleus for cells  Has intercalated discs which are composed of desmosomes (tight junctions) and gap junctions which allow for easy transmission of electrical impulses  All cardiac cells are excitable and must be excited in the correct order o Some cells are more excitable than others (pacemaker cells which can spontaneously depolarize) Conducting System of the Heart  Initiated by the sinoatrial node  Interatrial pathway causes simultaneous contraction of the atria  Internodal pathway carries the impulse to the atrioventricular node o The AV node takes 100 ms to pass on the signal (delay required for the atria to fully contract)  The left and right bundle of His branch off the AV node which travel to the Purkinje fibres, contracting the ventricles o This allows the ventricles to contract at the apex first  ECG tracks changes in electrical activity of the ENTIRE heart—not single cells  Consist of SA node action potentials and myocyte action potentials SA Node (pacemaker) Action Potential  Resting potential of -60 mV but does not stay there (pacemaker potential “drifts”)  Naming convention of phase 4-0-3  Phase 4: There is a slow depolarization to -40 mV (threshold) known as the pacemaker potential that allows these cell+ to self-stimulate 2+ o Initiated by Na entry, with some Ca entry at -50 mV  Phase 0: An influx of Ca causes the depolarization to 0 mV +  Phase 3: An efflux of K afterwards causes repolarization back to resting potential Ion Channels in Pacemaker Cells  Ifchannels o Specific type of Na+ channel (funny, “leaky”) o Unique to pacemaker cells o Voltage gated: open at -60 mV o Small gradual depolarization because it is “leaky” and start to close around -40 mV 2+ 2+  Ca Tand Ca L channels o T (transient) helps cell reach threshold, open around -50 mV o + L (long lasting) open at -40 mV which cause full depolarization  Slow K channels o Same as in skeletal muscle o Open at the peak of depolarization and close at repolarization (-60 mV) Ventricular Myocytes Action Potential  Resting membrane potential at -90 mV  Threshold is at -70 mV +  Depolarization is extremely rapid due to opening of fast Na ion channels  The plateau phase is caused by the slow Ca channels remaining open and the fast K channels closing o This results in an elongated depolarization  Naming convention: phase 4-0-1-2-3-4 2+ 2+  Ca -induced Ca release is when Ca2+ entering the cytosol from the ECF induces a much larger release of Ca from the sarcoplasmic reticulum which is responsible for the prolonged muscular contraction during systole Ion Channels in Ventricular Myocytes +  Fast Na channels open at -70 mV to -65 mV and close at +20 mV o Has 3 states: Closed, Open, Inactive  Must go from inactive to closed before it can open again, this occurs during repolarization o The inactive state prevents another action potential from occurring (refractory period)  Slow Ca channels open at -40 mV but only see an effect during the plateau phase +  Fast K channels open at +20 mV but close very quickly so there is no observable effect o Help to prolong the depolarization because K cannot leave the cells +  Slow K channels open at +20 mV but only see effect after the plateau phase in repolarizing the cells Differences between SA Node and Ventricular Myocyte Action Potentials  The resting membrane potential is lower in the ventricular (-90 mV) than in the SA node (-60 mV)  There is a lower threshold for depolarization in ventricular (-65 mV) than the SA node (-40 mV)  “Funny” Na channels are only present pacemaker cells  The rapid depolarization only occur in myocytes with fast Na+ channels Action Potential and Contraction  Contraction is developed during the plateau phase of the action potential o As the calcium ions are moving in, they are responsible for contraction o Initiated briefly after the initiation of the action potential Cardiac Cycle  Blood passively fills the atria and ventricles  Movement due to differences in pressure Regulation of Cardiac Output  The heart intrinsically beats at 100 bpm but in our bodies it is roughly 70 bpm due to various chemicals and hormones (parasympathetic nervous system)  Cardiac output is the product of heart rate and stroke volume Heart Rate  Intrinsic heart rate (100 BPM) is determined by the rate of SA depolarization  Heart rate is modified through the autonomic nervous system o Sympathetic nervous system increases the heart rate through norepinephrine (and epinephrine) by increasing intake of Na+ o Parasympathetic nervous system decreases th+ heart rate through acetylcholine by hyperpolarizing the cells through keeping K channels open Stroke Volume  Regulated intrinsically (end-diastolic volume) and extrinsically (sympathetic nervous system)  “Preload” refers to the end volume of the ventricle at the end of diastole o This is the intrinsic regulation of stroke volume—the more the ventricle is filled, the more the myocytes stretch and as a result contract harder (Frank-Starling Mechanism)  Contractility is modified by the sympathetic nervous system o This is the extrinsic regulation of stroke volume 2+ o Norepinephrine binds to beta-1 adrenergic receptors which cause more Ca to enter the cell via plasmalemmal Ca channels  More crossbridges are formed more troponin is unwound to allow actin to bind to myosin 2+ 2+ o Increases the SR Ca pump’s action to allow faster relaxation as more Ca is made available o Increases both the rate of contraction and the rate of relaxation  The ejection fraction is (typically 0.5-0.75) o Stroke volume is end systolic volume – end diastolic volume Compensated Heart Failure  Improper contracting of myocytes—not generating enough force  Initially there is a significant decrease in stroke volume, but is compensated through stimulation by the sympathetic nervous system to increase stroke volume to normal levels Blocking Blood Delivery to the Heart  Atherosclerosis: development of plaques that narrow arteries, decreasing arter
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