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CARDIOVASCULAR PHYSIOLOGY STUDENT MANUAL Dr. Guido E. Santacana CARDIOVASCULAR PHYSIOLOGY LECTURES STUDENT LECTURE NOTEBOOK Guido E. Santacana Ph.D. DEPT. of PHYSIOLOGY INTRODUCTION TO CARDIOVASCULAR PHYSIOLOGY GENERAL ASPECTS OF THE CARDIOVASCULAR SYSTEM MAIN FUNCTIONS OF THE CIRCULATORY SYSTEM Transport and distribute essential substances to the tissues. Remove metabolic byproducts. Adjustment of oxygen and nutrient supply in different physiologic states. Regulation of body temperature. Humoral communication. THE MAIN CIRCUIT COLLECTING PUMP TUBULES DISTRIBUTING THIN VESSELS TUBULES Pressure Profile of the Circulatory System ELASTIC TISSUE MUSCLE Distribution of Blood in the Circulatory System Organization in the Circulatory System SERIES AND PARALLEL CIRCUITS CARDIAC ELECTROPHYSIOLOGY LECTURE NOTEBOOK Guido E. Santacana Ph.D. GENESIS OF THE MEMBRANE POTENTIAL AND EQUATIONS TO REMEMBER!! EK = -60 LOG ([Ki]/[Ko]) = -94mv ENa = -60 LOG ([Nai]/[Nao]) = +70mv Em = RT/F ln PK (K+)o + PNa(Na+)o + PCl(Cl-)i PK (K+)I + PNa(Na+)i + PCl(Cl-)o THE RESTING MEMBRANE POTENTIAL OF THE CARDIAC CELL If membrane permeable only to K+ If membrane permeable To both Na+ and K+ If membrane permeable To Na+, K+ plus with A Na+/K+ Pump WHY NOT Na+ 0R Ca++ FOR THE CARDIAC CELL MEMBRANE POTENTIAL ? EXTRA CELL. INTRACELL. Em Na+ 145Mm 15Mm 70mv Ca++ 3Mm 10-7 M 132mv K+ 5Mm 145Mm -100mv ACTION POTENTIALS FROM DIFFERENT AREAS OF THE HEART ATRIUM VENTRICLE 0 mv mv 0 -80mv -80mv SA NODE mv 0 -80mv time ELECTROPHYSIOLOGY OF THE FAST RESPONSE FIBER PHASE 0 OF THE FAST FIBER ACTION POTENTIAL Na+ Na+ m A -90mv B h -65mv m m h Na+ Na+ m C 0mv Chemical Gradient Electrical Gradient m D h +20mv Na+ m E +30mv h h K+ CURRENTS AND REPOLARIZATION PHASE 1-TRANSIENT OUTWARD CURRENT (TOC) Ito PHASE 1-3-DELAYED RECTIFIER CURRENT IK PHASE 1-4-INWARDLY RECTIFIED CURRENT IKl THE PLATEAU PHASE AND CALCIUM IONS OPEN CLINICAL VALUE L Ca++ CHANNELS +10MV Ca++ BLOCKERS T Ca++ CHANNELS -20MV NO (physiological) EFFECTS OF Ca++ CHANNEL BLOCKERS AND THE CARDIAC CELL ACTION POTENTIAL CONTROL FORCE 30 10 10 CONTROL 30 TIME DILTIAZEM 10 uMol/L 30 uMol/L Clinical Correlation Early After-Depolarizations Torsades de Pointes 0mV -60mV -90mV Early After-Depolarization OVERVIEW OF SPECIFIC EVENTS IN THE VENTRICULAR CELL ACTION POTENTIAL Overview of Important Channels in Cardiac Electrophysiology Sodium Channels Fast Na+ Phase 0 depolarization of non-pacemaker cardiac action potentials Slow Na+ "Funny" pacemaker current (If) in cardiac nodal tissue Potassium Channels Inward rectifier (Iir or IK1) Maintains phase 4 negative potential in cardiac cells Transient outward (Ito) Contributes to phase 1 of non-pacemaker cardiac action potentials Delayed rectifier (IKr) Phase 3 repolarization of cardiac action potentials More Channels! Calcium Channels L-type (ICa-L) Slow inward, long-lasting current; phase 2 non-pacemaker cardiac action potentials and phases 4 and 0 of SA and AV nodal cells; important in vascular smooth muscle contraction T-type (ICa-T) Transient current that contributes to phase 4 pacemaker currents in SA and AV nodal cells ELECTROPHYSIOLOGY OF THE SLOW RESPONSE FIBER 0 2 0 mvs -40 3 4 -80 ERP RRP time (msec) RECALL: INWARD Ca++ CURRENT CAUSES DEPOLARIZATION CONDUCTION OF THE ACTION POTENTIAL IN CARDIAC FIBERS LOCAL CURRENTS - ------++++++++ +++++++ -------- FIBER A FIBER B DEPOLARIZED ZONE POLARIZED ZONE CONDUCTION OF THE ACTION POTENTIAL FAST RESPONSE: Depends on Amplitude,Rate of Change,level of Em. SLOW RESPONSE: Slower conduction.More apt to conduction blocks. WHAT ABOUT MYOCARDIAL INFARCTS AND CONDUCTION? AP-AMP EFFECTS OF HIGH K+ ON CONDUCTION AND AP OF FAST FIBERS Em 0MV K+=3mM K+=7mM K+=14mM 0MV K+=16mM K+=3mM WHAT HAS VARIED? LOOK AT: Em,AP SLOPE-AMPLITUDE HIGH K+ AND m/h Na+ GATES HIGH K+ LOWER Em CLOSED h GATES (SOME) LOWER AP AMPLITUDE LOWER Na+ ENTRY EXCITABILITY OF FAST AND SLOW FIBERS FAST m/h GATES COMPLETE RESET AFTER PHASE 3 CONSTANT AND COMPLETE RESPONSE IN PHASE 4 SLOW LONG RELATIVE REFRACTORY PERIOD. POST-REPOLARIZATION REFRACTORINESS AFTER THE EFFECTIVE OR ABSOLUTE REFRACTORY PERIOD (FAST FIBER) 0 MV ARP -80 RRP TIME POST-REPOLARIZATION REFRACTORINESS (SLOW FIBER) 200 MSEC 0 MV B A -60 POSTREPO TIME C RHYTMICITY AUTOMATICITY SA NODE AV NODE IDIOVENTRICULARPACEMAKERS ectopic foci THE SA NODE PACEMAKER POTENTIAL CHARACTERISTICS OF THE PACEMAKER POTENTIAL RECALL: PHASE 4-PACEMAKER POTENTIAL(PP) OBSERVED HERE. FREQUENCY DEPENDS ON: THRESHOLD,RESTING POTENTIALS AND SLOPE OF THE PP CAUSES OF THE PACEMAKER POTENTIAL if iCa K+ iK Na+ Ca++ OUT IN THE PACEMAKER POTENTIAL CURRENTS AFTER DEPOLARIZATION if iCa iK WHICH CURRENT WILL BE MORE AFFECTED BY ADRENERGIC STIMULATION? WHICH BY CHOLINERGIC STIMULATION? LOOKING AT THE PACEMAKER CURRENTS voltage iK if ionic currents iCa EFFECTS OF Ca++ CHANNEL BLOCKERS ON THE PACEMAKER POTENTIAL NIFEDIPINE CONTROL (5.6 X 10-7 M) 0 MV -60 TIME OVERDRIVE SUPRESSION AND AUTOMATICITY OF PACEMAKER CELLS Na+/K+ ATPase ENHANCEMENT BY HIGH FREQUENCY. CONSEQUENT HYPERPOLARIZATION. SUPRESSION OF AUTOMATICITY. RECOVERY TIME REQUIRED. ECTOPIC FOCI/SICK SINUS SYNDROME. THE CONDUCTION SYSTEM OF THE HEART ATRIAL AND ATRIOVENTRICULAR CONDUCTION RA BACHMANS PATH SAN LA AN REGION INTERNODAL PATHS AV NODE N REGION NH REGION BH RV RIGHT BUNDLE BRANCH LV LEFT BUNDLE BRANCH NODAL DELAY AV NODE REGION OF DELAY NA REGION FAST CONDUCTION N REGION SLOW CONDUCTION LONGER PATH SHORTER PATH NH REGION FAST CONDUCTION REFLECTED IN THE P-QRS INTERVAL OF THE ECG UNI AND BIDIRECTIONAL BLOCK CLINICAL IMPLICATIONS A NORMAL C BI B ANTEGRADE BLOCK REENTRY UNIDIRECTIONAL BLOCK D Clinical Correlation Re-entry Tachycardias Paroxysmal Supraventricular Tachycardia Ischemic Tissue Slow Pathway Fast Pathway Normal Conduction Slow Pathway Fast Pathway Re-Entry Circuit AV NODE AND AV BLOCKS FOCUS ON N REGION NORMA L 1ST DEGREE PROLONGUED AV CONDUCTION TIME 2ND DEGREE 1/2 ATRIAL IMPULSES CONDUCTED TO VENTRICLES 3RD DEGREE VAGAL MEDIATION IN N REGION/COMPLETE BLOCK ECG CONDUCTION IN THE VENTRICLES PURKINJE FIBERS WITH LONG REFRACTORY PERIODS. PROTECTION AGAINST PREMATURE ATRIAL DEPOLARIZATIONS AT SLOW HEART RATES. AV NODE PROTECS AT HIGH HEART RATES. QUICK QUIZ Which of the following is not true about the effect of acetylcholine (Ach) in the electrophysiology of the cardiac pacemaker cell: A. Ach lowers the magnitude of the minimum repolarization potential. B. Ach lowers the slope of the pacemaker potential. C. Ach decreases the SA node frequency. D.Ach increases the ik current of the pacemaker cell. E. Ach decreases the iCa++ current of the pacemaker cell. The main reason why the AV node filters out high stimulation frequencies from the SA node is: A. The long pathway that the stimulus must traverse in the AV node. B. Post Repolarization Refractoriness of AV nodal cells. C. The AV nodal cell is always hyperpolarized D. Ca++ is the main ion in Phase 0 of the AV nodal cell. E. I need to review this section very fast. CARDIAC MECHANICS MAIN THEMES THE HEART AS A PUMP THE CARDIAC CYCLE CHAPTER 3 B&L CARDIAC OUTPUT LEFT VENTRICULAR PRESSURE LENGHT/ TENSION AND THE FRANKSTARLING RELATION INITIAL MYOCARDIAL FIBER LENGHT LEFT VENTRICULAR END-DIASTOLIC VOLUME PRELOAD AND AFTERLOAD IN THE HEART INCREASE IN FILLING PRESSURE=INCREASED PRELOAD PRELOAD REFERS TO END DIASTOLIC VOLUME. AFTERLOAD IS THE AORTIC PRESSURE DURING THE EJECTION PERIOD/AORTIC VALVE OPENING. LAPLACES’S LAW & WALL STRESS, WS = P X R / 2(wall thickness) LEFT VENTRICULAR PRESSURE LEFT VENTRICULAR PRESSURE AND AFTERLOAD AT CONSTANT PRELOADS EFFECT OF INCREASED PRELOAD PEAK ISOMETRIC FORCE AFTERLOAD (aortic pressure) NOTE: WHAT HAPPENS IN THE NORMAL HEART VS ONE IN THE LAST PHASES OF CARDIAC FAILURE? CONTRACTILITY:THE VENTRICULAR FUNCTION CURVE EFFECT? CHANGES IN CONTRACTILITY LEFT VENTRICULAR PRESSURE (mmHg) dP/dt AS A VALUABLE INDEX OF CONTRACTILITY MAX dP/dt B 120 A C 40 .2 TIME (s) .6 CARDIAC CYCLE Atrial Systole Mitral Closes S1 S2 Atrial Systole Reduced Ventricular Filling Rapid Ventricular Filling Isovolumic Relax. Reduced Ejection Rapid Ejection Isovolumic contract. Aortic opens Aortic closes Mitral opens QUICK QUIZ How to find out that you know the Cardiac Cycle. 150 Atrial Mitral systolecloses Aortic opens Aortic Mitral closes opens 50 TIME (SEC) Clinical Correlation Diagnosis of Aortic Stenosis by Pressure Graphs Aortic Stenosis Normal Aorta Aorta Ventricle Ventricle LEFT VENTRICULAR PRESSURE (mmHg) LEFT VENTRICULAR PRESSURE/VOLUME P/V LOOP END OF SYSTOLE 120 F E D 80 40 A 0 50 B C 100 END OF DIASTOLE 150 LEFT VENTRICULAR VOLUME (ml) LEFT VENTRICULAR PRESSURE (mmHg) EFFECT OF PRELOAD ON THE VENTRICULAR P/V LOOP ESV 1 2 3 EDVs VOLUME (ml) EFFECT OF AFTERLOAD IN THE LEFT VENTRICULAR P/V LOOP ESV LEFT VENTRICULAR PRESSURE (mmHg) ESV 3 ESV 2 1 EDV VOLUME (ml) LEFT VENTRICULAR PRESSURE (mmHg) EFFECT OF CONTRACTILITY ON THE LV P/V LOOP 2 1 VOLUME (ml) QUICK QUIZ PRELOAD AFTERLOAD CONTRACTILITY CARDIAC OUTPUT AND THE FICK PRINCIPLE BODY O2 CONSUMPTION Lungs 250mlO2/min PULMONARY ARTERY PULMONARY VEIN PaO2 0.15mlO2/ml blood PvO2 0.20mlO2/ml blood Pulmonary capillaries O2 CONSUMPTION (ml/min) CARDIAC OUTPUT= PvO2 - PaO2 HEMODYNAMICS VELOCITY,FLOW,PRESSURE LAMINAR FLOW POISEUILLE’S LAW RESISTANCE(SERIES-PARALLEL) TURBULENT FLOW AND REYNOLD’S NUMBER CHAPTER 5 B&L REQUIRED CONCEPTS VELOCITY = DISTANCE / TIME V = D / T FLOW = VOLUME / TIME Q = VL / T VELOCITY -FLOW- AREA V = Q / A CROSS SECTIONAL AREA AND VELOCITY A= 2cm2 Q=10ml/s a V= 5cm/s 10cm2 b 1cm/s V=Q/A 1cm2 c 10cm/s HYDROSTATIC PRESSURE 136cm 0 100 200 0 100 200 P=pxgxh 0 100mmHg P = Pressure mmHg p = density g = gravity h = height 136cm 0 100 200 0 0 100 200 ENERGY OF A STATIC VS A DYNAMIC FLUID TOTAL ENERGY= POTENTIAL E. + KINETIC E. TE = PE + KE FLUID AT REST (HYDROSTATIC ) FLUID IN MOTION (HYDROSTATIC + HYDRODYNAMIC) VELOCITY AND PRESSURE 0 0 100 200 POISEUILLE’S LAW GOVERNING FLUID FLOW(Q) THROUGH CYLINDRIC TUBES (FLOW)Q = DIFFERENCE IN PRESSURE (Pi - Po) r 8nL VISCOSITY 4 LENGHT RADIUS RESISTANCE TO FLOW IN THE CARDIOVASCULAR SYSTEM BASIC CONCEPTS Rt = R1 + R2 + R3…. SERIES RESISTANCE 1/Rt = 1/R1 + 1/R2 + 1/R3… PARALLEL RES. PARALLEL SERIES R1 R2 R3 R1 R2 R3 WHAT REALLY HAPPENS IN THE CVS? LOWER R HIGHER R LOWER R CAPILLARIES ARTERY ARTERIOLES LAMINAR VS TURBULENT FLOW THE REYNOLD’S NUMBER LAMINAR FLOW TURBULENT FLOW Nr = pDv / n laminar = 2000 or less p = density D = diameter v = velocity n = viscosity QUICK QUIZZ 1. Which of the following vessels will produce a dramatic decrease in blood flow through the tissues by a change in radius? A. Aorta B. Venules C. Arterioles D. Capillaries 3. After a bout with hemorrhagic Dengue you would expect to find a heart murmur at a lower level than before the disease. A. True B. False PV Loop Refresher B A B A What happens from A to B? ARTERIAL SYSTEM COMPLIANCE MEAN ARTERIAL PRESSURE PULSE PRESSURE PRESSURE MEASUREMENT CHAPTER 26 B&L THE CONCEPT OF THE HYDRAULIC FILTER SYSTOLE DIASTOLE COMPLIANT RIGID O2 CONSUMPTION (mlO2/100g/beat) EFFECTS OF PUMPING THROUGH A RIGID VS A COMPLIANT DUCT 0.1 PLASTIC TUBING NATIVE AORTA 0 5 STROKE VOLUME (ml) 15 % INCREASE IN VOLUME STATIC P-V RELATIONSHIP IN THE AORTA PRESSURE (mmHg) ELASTIC MODULUS OR ELASTANCE Ep = P / Da/Db ELASTANCE P V Ep= ELASTIC MODULUS Da= MAX. CHANGE IN AORTIC DIAMETER. Db= MEAN AORTIC DIAM. COMPLIANCE V P EP IS INVERSELY PROPORTIONAL TO C MEAN ARTERIAL PRESSURE (MAP) REMEMBER OHMS LAW? CARDIAC OUTPUT PERIPHERAL RESISTANCE INSTANTANEOUS INCREASE STEADY STATE INCREASE ARTERIAL PRESSURE (mmHg) EFFECT OF COMPLIANCE ON MAP Pa = Qh - Qr / Ca SMALL Ca LARGE Ca INCREASE CARDIAC OUTPUT TIME Qh- inflow (CO) Qr- outflow Ca- Compliance Pa- MAP PULSE PRESSURE STROKE VOLUME COMPLIANCE V4 VB VOLUME V3 V2 VA V1 P1 PA P2 P3 PB P4 PRESSURE PULSE PRESSURE EFFECTS OF: COMPLIANCE TOTAL PERIPHERAL RESISTANCE TPR A B CHAPTER 9 B&L COUPLING OF THE HEART AND BLOOD VESSELS VASCULAR FUNCTION CURVE HOW CARDIAC OUTPUT REGULATES CENTRAL VENOUS PRESSURE CARDIAC FUNCTION CURVE HOW CENTRAL VENOUS PRESSURE (PRELOAD) REGULATES CARDIAC OUTPUT VASCULAR FUNCTION CURVE CENTRAL VENOUR PRESSURE (mmHg) HOW CHANGES IN CARDIAC OUTPUT INDUCE CHANGES IN CENTRAL VENOUS PRESSURE? 8 Pmc B VASCULAR FUNCTION CURVE A -1 0 8 CARDIAC OUTPUT (L/min) CENTRAL VENOUR PRESSURE (mmHg) HOW BLOOD VOLUME AND VENOMOTOR TONE CHANGE THE VASCULAR FUNCTION CURVE? VASCULAR FUNCTION CURVE 8 -1 0 8 CARDIAC OUTPUT (L/min) CENTRAL VENOUR PRESSURE (mmHg) TOTAL PERIPHERAL RESISTANCE AND THE VASCULAR FUNCTION CURVE. 8 VASCULAR FUNCTION CURVE -1 0 8 CARDIAC OUTPUT (L/min) CARDIAC OUTPUT (L/min) THE CARDIAC FUNCTION CURVE CENTRAL VENOUS PRESSURE (mmHg) CARDIAC OUTPUT (L/min) EFFECTS OF SYMPATHETIC STIMULATION ON THE CARDIAC FUNCTION CURVE CENTRAL VENOUS PRESSURE (mmHg) HOW BLOOD VOLUME AND PERIPHERAL RESISTANCE CHANGE THE CARDIAC FUNCTION CURVE? CARDIAC OUTPUT (L/min) VOLUME CENTRAL VENOUS PRESSURE (mmHg) RESISTANCE CARDIAC OUTPUT (L/min) THE CARDIAC FUNCTION CURVE IN HEART FAILURE CENTRAL VENOUS PRESSURE (mmHg) HEART - BLOOD VESSELS COUPLING MORMAL FUNCTION PUMP VEINS ARTERIES Qh 5L/min Pa CPV=2mmHg=Pv 5L/min COMPLIANCES Cv = 19Ca Cv>>>>Ca Qr PERIPHERAL R= Pa - Pv / Qr R = 20mmHg/L/min MPA=102mmHg CARDIAC ARREST! INMEDIATE EFFECT FLOW STOPS HERE PUMP VEINS ARTERIES Qh 0L/min Pa CPV=2mmHg=Pv 5L/min FLOW CONTINUES HRE TRANSFER ART-->VEINS Qr R = 20mmHg/L/min Qr= Pa - Pv/20 Qr CONTINUES AS LONG AS A PRESSURE GRADIENT IS SUSTAINED CARDIAC ARREST STEADY STATE FLOW STOPPED PUMP VEINS ARTERIES Qh 0L/min Pa = 7mmHg Pv = 7mmHg = MEAN CIRCULATORY PRESSURE OR Pmc 95mmHg 5mmHg FLOW STOPPED 0L/min Qr Qr = 0 ( NO Pa - Pv DIFFERENCE) WE START PUMPING! INMEDIATE EFFECT FLOW STARTS SOME VENOUS BLOOD PUMP VEINS ARTERIES Qh 1L/min Pa = 7mmHg Pv = 7mmHg NO FLOW HERE YET 0L/min Qr FLOW RETURNS AT Qr AT THE NEW Qh PUMP VEINS ARTERIES Qh 1L/min Pa = 26mmHg Pv = 6mmHg FLOW STARTS 1L/min Qr R = 20mmHg Qr = Pa - Pv / 20 = 1L/min THE END