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Systemic Physiology

by: Mrs. Sierra Bailey

Systemic Physiology NPB 101

Mrs. Sierra Bailey
GPA 3.85

Jack Goldberg

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Jack Goldberg
Class Notes
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This 25 page Class Notes was uploaded by Mrs. Sierra Bailey on Tuesday September 8, 2015. The Class Notes belongs to NPB 101 at University of California - Davis taught by Jack Goldberg in Fall. Since its upload, it has received 12 views. For similar materials see /class/191817/npb-101-university-of-california-davis in Neurobiology,Physio & Behavior at University of California - Davis.

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Date Created: 09/08/15
CV 1 Topical Organization of the Cardiovascular Lectures 1 Function amp Anatomy Heart amp Vascular System Chapter 9 2 Cardiac Electrophysiology Chapter 9 3 Hemodynamics Static amp Dynamic Hemodynamic Properties Chapter 10 4 Cardiac Mechanics Chapter 9 5 Cardiac Output Chapter 9 6 Peripheral Vascular System Chapter 10 7 Regulation of Blood Pressure Chapter 10 June 28 2010 CV 2 Topic 1 Functions amp Anatomy of the CV System Chapter 9 Functions 1 Delivery System for oxygen carbon dioxide nutrients products of metabolism amp hormones 2 Temperature Regulation 3 HydraulicSkeleton 4 Motor Function jump movement for Jumping Spiders June 28 2010 Anatomy ofthe Cardiovascular System amp Flow of Blood synmu clrwllllun ni MI W 5 sum in lcmm my cmulnlnn Kev l ofncn blood I exp mm l Fig 91 June 28 2010 Right Heart and Left Heart Flow of Blood through Heart Components of Vascular System Arteries Aorta Large Arteries Small Arteries Distributing network Arterioles Resistance Vessels Capillaries Exchange Vessels Venules amp Small Veins some exchange capacitance vessels Large Veins and Inferior and Superior Vena Cava Collecting Vessels returning blood to the heart CV 4 Specialized Cells and Structures within the Heart Specialized Cells cells with differing properties and functions Muscle Cells Contractile Proteins amp Generate Pressure Atria amp Ventricles Pacemaker Cells Self Depolarize and Initiate Activation Hean Purkinje Fibers Cells Specialized for Rapid Conduction Cells in AV Node Slow Rate of Rise and Low Amplitude 9 slow cell to cell spread of activation Specialized Structures within the Heart SA Node Activation normally originates from Pacemaker Cells Localized here Internodal and Interatrial Preferential Conduction Pathways AV Node Site conduction delay in atrioventricular activation Filter atrial arrythymias from ventricles Contains some Pacemaker Cells His Bundle amp Bundle Branch System Composed of Purkinje Fibers Specialized Ventricular Conducting System Purkinje Fibers can develop pacemaker activity June 28 2010 Interatrial pathway Atrioventricular AV node Sinoatrial SA node Left Flight atrium atrium Internodal Left Pathway branch of bundle Right of His branch of bundle Left f 395 ventricle Purkinje ventricle fibers 9 2mm Thumson Hem Education Figu re 98 9 CV 5 Topic 2 Cardiac Electrophysiology Chapter 9 Outline Myogenicity of Vertebrate Heart Action Potentials from Regions ofthe Heart Ion Channel Activation amp Generation of the Cardiac Action Potential Purkinje Fiber amp SA Nodal Pacemaker Cell Sequence of Activation ofthe Heart timing function of capacity of one group of cells to generate action potentials in the adjacent cells Concept ofthe Absolute and Relative Refractory Periods for Cardiac Cells Concept of Effective and Relative Refractory Periods for Cardiac Tissue Concept Heart Muscle Cannot be Tetanized Electrocardiogram Recording Sequential Activation of the Cells of the Heart from the Surface ofthe Body ANS Control of Heart Rate and Conduction within the Heart 10 Changes in Heart Rate and Conduction Reflected in the Electrocardiogram June 28 2010 5 CV 6 Activation of the Vertebrate Heart Vertebrate Heart Myogenic cf Skeletal Muscle Neurogenic Initiation activation occurs in muscle cells Cell to Cell spread of Activation Neural input can change heart rate change activation and change force of muscle contraction but neural input not reguired Electrical Coupling among Cardiac Muscle Cells occurs through Connexons within the lntercalated Disks lntercalated Disk with Gap Junction amp Connexons lntercalatedDiskSp07tc3 June 28 2010 CV 7 Parameters that Determine Spread of Activation throuqh Cardiac Tissue 1 Rate of Rise and Amplitude of the Action Potential of Cells within a Tissue 2 Electrical Coupling among Cells Presence and of Low Resistance Junctions 3 Geometric Relationship among Cells with the Tissue 4 Refractory Properties of the Inward Depolarizing Current Channels June 28 2010 CV 8 Action Potentials from Cells within the Heart Specialized Cells in Heart Cardiac Muscle Cell 30 MV Pacemaker 0 70 MV Potential or Diastolic Depolarization SA Nodal Pacemaker Cell 90 MV 0 KL Ventricular Muscle Cell 3960 MV AV Nodal Cell 200 msec 30 MV D Differences in Shape and Duration of APs determined by differences in sequential activation of ion specific channels APRegionsH n8p08tc3 v90 MV Purkinie Fiber Question Based on properties of action potentials predict cell to cell spread of activation within the SA node AV node and Purkinje fibers to that through cardiac muscle ssue June 28 2010 CV 9 Basic Principles in Understanding Ionic Generation of Cardiac Action Potentials 1 Affect of inward and outward ionic current flow on the membrane potential referenced to the resting membrane potential inside the cell negative 2 For our purposes current flow represents movement of charge Inward ionic Current Flow Depolarizes the Cell makes the inside ofthe cell less negative or more positive Outward ionic Current Flow Repolarizes the Cell makes the inside of the cell less positive or more negative 3 Depolarization occurs when there is net movement charge into cell 4 Repolarization occurs when there is net movement charge out of cell June 28 2010 9 CV 10 Ionic Currents and Channels in Cardiac Action Potential Ionic Current Carried by 3 ions and their ion Channels 1 K ionic current through a number of K channels 2 Na ionic current through a few types of Na channels 3 Ca ionic current through a few types Ca channels Depolarization 9 Activation of Na and Ca Channels and Current Flow Repolarization 9 Activation of K Channels and Current Flow June 28 2010 10 CV 11 Ionic Current Flow and the Purkinje Fiber Action Potential Ion Channel Activation amp Cardiac Action Potential Depolarization Net Movement charge into cell Repolarization Net Movement charge out of cell Three Ions and their Associated Channels Generate Cardiac Action Potentials 1 K ions and multiple K channels 2 Na ions and couple of Na channels 3 Ca ions and couple of Ca channels Inactivation Fast Na Channels Full Activation Latent Ca Channels Open K Channels Inactivation ofall Ca Channels Activation ofadditional K Channels 0 Activation ofTransient Ca Channels Initiation Activation Latent Ca Channels Open KChanneIs Activation Fast Na Channels 4 Closure T most K Channels K Channels responsible RMP Open 4 Na leak Channels Purkinje Fiber lonChanActampApSpO9 Questions for you to consider 1 2 3 4 During both Phases 0 amp 2 is there more inward amp outward current current channels open than during Phase 4 If there is more outward current than during Phase 4 why is the slope of Phase 0 so steep amp why is it not rounded Is inward or outward current flow dominating the membrane potential during Phase 0 During Phase 2 is Ca or K current dominating the membrane potential Eq Ca 30 to 50 mv Eq K 95 mv June 28 2010 11 CV 12 Ion Channel Activation and Generation of SA Nodal Pacemaker Cell AP Ca channels inactivated O mv Activation of repolarizing K Channels amp Current Activation of lNaf lCa Very slowly activated 50 mv Threshold Gradual Closure K Channels lNaf 70 mv Repolarizing K channels MDP Difference Closed Pacemaker Potential or Diastolic Depolarization MDP Maximal Diastolic Potential Difference lNaf funny Na Channel and Current activated with repolarization June 28 2010 12 CV 13 Sequence of Activation of the Heart SA NOde 7 7777 W Very Slow Conduction V Atrial Muscle 77 v RapidConduction AV Node W Very Slow Conduction V His Bundle Bundle Branch System B Very Rapid Conduction V Ventricular Muscle 7 77 Tl M E LadderActivSpuBJca June 282010 13 CV 14 Concept of ARPamp RRP in Cardiac Cells Example of Purkinje Fiber or Muscle Cell CARDIAC CELLS APS NOT ALL OR NONE AP AMPLITUDE amp RATE OF RISE INCREASES FROM BEGINNING TO THE END OF THE RRP June 28 2010 14 CV 15 Concepts of Effective and Relative Refractory Periods for Cardiac Tissues Refractory Properties of Cardiac Tissue amp Conduction through Tissue ERP for Tissue Tissue behaves as if its cells are inexcitable No Spread of Activation throuqh tissue Therefore conduction block RRP for Tissue Tissue is excitable Spread of Activation throuoh tissue However conduction velocity slowed amp conduction time prolonged because time course for cell to cell spread of activation is prolonged During ERP of a tissue an AP may or may not be generated in cells within the tissue but the APs are incapable of generating an AP in the adjacent tissue Therefore the tissue behaves as if it is inexcitable refractory Question If a tissue segment is Effectiver Refractory can you conclude that all the cells in the tissue are in their ARP June 28 2010 15 CV 16 Concept Cardiac Muscle Cannot be Tetanized Relationship ARP of a muscle cell and Contraction of Cardiac Muscle Tissue RRP Contraction Ventricular Muscle ARP encompasses majority about 23 of cardiac muscle contraction Heart muscle cannot be tetanized Question Considering how the heart functions as a pump would tetany enhance or impede the function ofthe heart June 28 2010 16 CV 17 Electrocardiogram SA Node P I F I Atrial Muscle m AV Node EA 1 p N l quotl A V A 7 interval Time i which venlncles are relax d idling His Bundle BB Syst m Vent MUSCIG m I amen seamen I PR 59 men AV nodal delay F eZde Wienllal TIME Note The TP interval identi ed in Fig 914 has no electrophysiological significance OHS complex 2 Ventricular depolarization atria repolanzlng Simultaneously Intervals in the Electrocardioq ram M9 Atrial Ventricular Conduction time Fig 914 PP or RR nterva9 Heart Period Interval between successive activations of the head June 28 2010 17 CV 18 Electrophysiological Information Derived from the Electrocardiogram ECG Note ECG does not provide information on the mechanical properties of the heart 1 Heart Rate Tachycardia Heart Beating too Fast Bradycardia Heart Beating too Slow 2 Rhythm of the Heart Irregular Activation ofthe Atria or Ventricles Atrial or Ventricular Flutter or Fibrillation Bag of writhing snakes 3 Conduction Slower than Normal Conduction Through the AV Node Conduction Block within the AV Node Abnormal Conduction through the His Bundle amp Bundle Branch Systems June 28 2010 CV 19 ANS Affects on SA Nodal Pacemaker Cells amp Heart Rate Sympathetic Stimulation 9 Increase Heart Rate Parasympathetic Vagal Stimulation 9 Decreases Heart Rate Threshold H H n Maximum U Diastolic Potential f Increase Slope Sympathetic Pacemaker Stimulation Potentlal ecrease Slope f Pacemaker Threshold Maximum Diastolic Potential Potential Increase Maximum Parasympathetic Diastolic Potential June 28 2010 Stimulation 19 CV 20 ANS Affects on Conduction through the AV Node Sympathetic Stimulation 9 enhanced conduction through the AV Node 9 Shortening of AV Conduction time amp Shortening ofthe PR interval in ECG Parasympathetic Vagal Stimulation 9 Delayed or cessation of conduction through the AV Node 9 Prolongation in AV Conduction time amp Lengthening of the PR interval in ECG No QRS if there is conduction block Changes in the ECG Observed with Sympathetic Activity to both SA and AV Nodes P R P control M R sympath MW Question What would you observe in the ECG in response to increases in parasymapthetic activity to SA Node orAV Node or both June 28 2010 20 PFJON Topic 3 Hemodynamics CV 21 Chapter 10 Hemodynamics Parameters that determine Pressure within and Flow through the Cardiovascular System Some questions for vou to consider as we develop hemodynamics within the cardiovascular system What determines Systolic Blood Pressure What determines Diastolic Blood Pressure Why is Systolic Blood Pressure higher than Diastolic Blood Pressure If there is less volume of blood on the arterial side than on the venous side of the circulatory system why is arterial pressure higher than venous pressure Why are the arterioles considered the resistance elements within the circulatory system and not the capacitance elements Why are the venules and small veins considered the capacitance elements within the circulatory system and not the resistance elements If the capillaries are the smallest diameter blood vessels why are they not the principle site of resistance to flow through the circulatory system The outputs of the right and left hearts are equal over time Why is the pressure in the pulmonary vascular system about 15 to 14 that ofthe systemic vascular system June 28 2010 21 CV 22 Topic Hemodynamics Static and Dynamic Hemodynamic Properties Static Hemodynamic Properties Parameters that determine Pressure Pressure Function of 1 Capacitance or Compliance of the vessels or chamber 2 amp Volume contained within the capacitance or compliance Specifically Pressure VolumeCapacitance I D namic Hemod namic Pro erties Parameters that determine Flow Volmin Flow Function of 1 Pressure Gradient P1 P2 2 amp Resistance Function of Length Viscosity amp Radius Specifically Flow Pressure Gradient Resistance June 28 2010 22 Blood120 Pressure Rn Distribution Blood Volume CV 23 also Fig 109 textbook PRESSURE CHANGE THROUGH THE VASCULAR SYSTEM DISTRIBUTION OF BLOOD VOLUME WITHIN VASCULAR SYSTEM Systolic BP Pulse Pressure Diastolic BP 50 Blood Volume in Venules amp Small Veins SMALL ARTER CAPIL AORTA LARGE ART ART 10 Volume 5 Pulmonary System 12 Heart 3 June 28 2010 IOLES LARIES I ENULESI SMALL VEINS LARGE ICENTRALI VEINS VEINS 70 Volume 62107 23 CV 24 Arterial Pressure Pulse Mean Arterial Pressure resting Systolic BP Dicrotic Notch Closure of the Aortic Valve 120 mm Hg 80 mm Hg 39 39 Diastolic BP Systole Diastole 13 23 cycle cycle Mean Arterial Blood Pressure 1l3systole 23 diastole 93 mm Hg 62707 June 28 2010 24


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