Chapter 14 Heart, Part 2

Chapter 14 Heart, Part 2 - Ch 14: Cardiovascular...

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Unformatted text preview: Ch 14: Cardiovascular Physiology, Part 2 Ch concepts: Fluid flow APs in contractile & autorhythmic cells Cardiac cycle (elec. & mech. events) Cardiac (elec. HR regulation Stroke volume & cardiac output Running Problem: Heart Attack Modulation of Heart Rate by ANS Modulation ANS can alter permeability of autorhythmic cells ANS to different ions to NE/E (i.e. sympathetic stimulation): ↑ flow through 2+ If and Ca2+ channels – Rate AND force of contraction go up Rate AND Ach (parasympathetic): ↑ flow through K+ Ach 2+ channels ↓ flow through Ca2+ channels channels – Membranes become hyperpolarized Fig 14-16 The Heart as a Pump (p477) (p477) Communication starts in autorhythmic cells in the Communication SA node (the Pacemaker) Pacemaker Move from events in single cell to events in whole Move heart heart Cardiac cycle 1. 2. electrical events mechanical events Electrical conduction in heart coordinates Electrical contraction contraction Fig 14-18 Fig Pacemaker sets HR Pacemaker SA node firing rates set HR SA Why? Why? If SA node defective? AV node: 50 bpm ventricular cells: 35 bpm ⇒ ventricular Implant mechanical pacemaker! Electrocardiogram ECG (EKG) Electrocardiogram Fig 14 -20 Electrocardiogram ECG (EKG) Electrocardiogram • Surface electrodes record electrical activity deep Surface within body - How possible? How • Reflects electrical activity of whole heart not of Reflects single cell! single EC fluid = “salt solution” (NaCl) ⇒ good conductor EC of electricity to skin surface of Signal very weak by time it gets to skin • • – ventricular AP = ? mV – ECG signal amplitude = 1mV EKG tracing = Σ of all electrical potentials generated by all cells of heart at any given moment by Fig 14-22 Since: Depolarization = signal for contraction Depolarization Segments of EKG reflect mechanical heart events Components of EKG Components Waves (P, QRS, T) (P, Segments (PR, ST) Intervals (wave- segment combos: PR, QT) Fig 14-20 Mechanical events lag slightly behind electrical events. Einthoven’s Triangle and the 3 Limb Leads: I RA – RA – + LA – Fig 14-19 II III + + LL Why neg. tracing for depolarization ?? Net electrical current Net in heart moves towards in + electrode EKG tracing goes up from baseline Net electrical current in Net heart moves towards - electrode electrode EKG tracing goes Down from baseline Down from Info provided by EKG: Info 1. 2. 3. HR Rhythm Relationships of EKG components j each P wave followed by QRS complex? j PR segment constant in length? etc. etc. For the Expert: For Find subtle changes in shape or Find duration of various waves or segments. segments. Indicates for example: Change in conduction velocity Enlargement of heart Tissue damage due to ischemia Tissue (infarct!) (infarct!) Prolonged QRS complex Injury to AV bundle can increase duration of QRS Injury complex (takes longer for impulse to spread throughout ventricular walls). throughout Fig 14-23 Heart Sounds (HS) 1st HS: during early ventricular contraction ⇒ AV valves close 1st 2nd HS: during early ventricular relaxation ⇒ semilunar valves close close Fig 14-26 Gallops, Clicks and Murmurs (clinical focus, p 486) Turbulent blood flow produces Turbulent heart murmurs upon auscultation upon Cardiac Cycle: some definitions Cardiac Systole (time during which cardiac muscle contracts) – atrial – ventricular Diastole (time during which cardiac muscle relaxes) – atrial – ventricular\ • EDV = End diastolic volume • ESV = End systolic volume • SV = Stroke Volume—that which is pumped in one stroke stroke Heart at rest: atrial & ventricular diastole Heart atrial SV = EDV - ESV 70mL = 135 mL - 65 mL Cardiac Output (CO) – a Measure Cardiac of Cardiac Performance of CO = HR x SV calculate for average person! HR controlled by ANS (p 475) (p – – – parasympathetic influence ? sympathetic influence ? without ANS, SA node fires 90-100x/min What happens with ANS when resting HR goes What up (e.g. during exercise)? up CO = HR x SV SV Force of contraction Force Fig 14-28 Length of muscle fibers (Starling curve/law) due to venous return, venous influenced by skeletal muscle pump and influenced respiratory pump respiratory Sympathetic activity (and adrenaline) venous constriction by sympathetic NS and Increased Ca2+ availability Frank-Starling Law (p 490) (p SV α EDV SV – ii.e., the heart pumps all the blood sent to it via venous .e., return return Therefore, Venous Return = SV Preload = the amount of load, or stretch of the myocardium before diastole myocardium Afterload = Arterial resistance and EDV combined Ejection Fraction = % of EDV that is actually ejected; e.g., 70 ml/135ml x 100 = 52% at rest ejected; Myocardial Infarction ...
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This note was uploaded on 12/24/2011 for the course STEP 1 taught by Professor Dr.aslam during the Fall '11 term at Montgomery College.

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