Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Heart failure wikipedia , lookup
Management of acute coronary syndrome wikipedia , lookup
Coronary artery disease wikipedia , lookup
Hypertrophic cardiomyopathy wikipedia , lookup
Cardiac contractility modulation wikipedia , lookup
Cardiac surgery wikipedia , lookup
Myocardial infarction wikipedia , lookup
Arrhythmogenic right ventricular dysplasia wikipedia , lookup
Dextro-Transposition of the great arteries wikipedia , lookup
Electrocardiography wikipedia , lookup
Ch 14: Cardiovascular Physiology concepts: Fluid flow APs in contractile & autorhythmic cells Cardiac cycle (electr. & mech. events) HR regulation Stroke volume & cardiac output Overview of Cardiovascular System 3 basic components: ? The heart is a dual pump! Blood Flow Why does blood flow through cardiovascular system? (teleological vs. mechanistic answers) Mechanistic approach: Blood Flow Rate P/ R Pressure gradient (P) is main driving force for flow through the vessels Fig 14-4 Pressure of fluid in motion decreases over distance because of energy loss due to friction Fig 14-2 Resistance Opposes Flow 3 parameters determine resistance (R): 1. Tube length (L) 2. Tube radius (r) 3. Fluid viscosity () Poiseuille’s law 8L R= r4 Constant in human body R 1 / r4 Fig 14-5 Velocity of Flow Depends on Flow Rate and Cross-Sectional Area: Flow rate = volume of blood passing one point in the system per unit of time – If flow rate velocity Cross-Sectional area (or tube diameter) – If cross sectional area velocity Velocity = flow rate / cross section area Cardiac Muscle & Heart Review heart and circulatory system anatomy One way flow in heart is ensured by ? Heart muscle cells: – 99% contractile – 1% autorhythmic Fig 14-1 Follow Path of Blood through Heart Compare to Fig 14-7 Microanatomy of Contractile Cardiac Muscle Cells Intercalated discs sSR smaller than in skeletal muscle, indicates ? Abundant mitochondria extract about 80% of O2 Cardiac Muscle Cell Contraction is Graded Skeletal muscle cell: all-or-none contraction in any single fiber for a given fiber length. Graded contraction in skeletal muscle occurs through? Cardiac muscle: – force to sarcomere length (up to a maximum) Fig 12-16 – force to # of activated crossbridges (Function of intracellular Ca2+: if [Ca2+]in low not all crossbridges activated) Foxglove for a Failing Heart See cardiac glycosides p. 492 Cardiac glycosides from Digitalis purpurea digitoxin Highly toxic in large dosage: destroys all Na+/K+ pumps In low dosage: partial block of Na+ removal from myocardial cells Explain mechanism of action ! APs in Contractile Myocardial Cells Similar to skeletal muscle Stable resting pot. ~ -90 mV Rapid depolarization due to voltage gated Na+ channels (Na+ movement?) Repolarization due to voltage gated K+ channels (K+ movement?) What is unique? Fig 14-13 Flattening of AP into plateau phase due to K+ perm. and Ca2+ perm. Flattening of AP into plateau phase due to K+ perm. and Ca2+ perm. Much longer AP Refractory period and contraction end simultaneously - Why important? Fig 14-14 AP in skeletal muscle : 1-5 msec AP in cardiac muscle :200 msec Refractory Period of Skeletal Muscle Fig 14-14 Summation and Tetanus Fig 14-14 Refractory Period of Cardiac Muscle guarantees chamber filling! No summation and tetanus possible Fig 14-14 APs Autorhythmic Cells Anatomically distinct from contractile cells – Also called pacemaker cells Spontaneous AP generation (Do not need ___________) Unstable resting membrane potential (= pacemaker potential) Pacemaker potential starts at ~ -60mV, slowly drifts to threshold AP Fig 14-15 Heart Rate = Myogenic Skeletal Muscle contraction = ? If-channel Causes Mem. Pot. Instability Autorhythmic cells have different membrane channel: If - channel allow current (= I ) to flow f = “funny” researchers didn’t understand initially If channels let K+ & Na+ through at -60mV Na+ influx > K+ efflux (why??) slow depolarization to threshold Channels involved in APs of Cardiac Autorhythmic Cells Slow depolarization due to If channels As cell slowly depolarizes: If -channels close & Ca2+ channels start opening At threshold: lots of Ca2+ channels open AP to + 20mV Repolarization due to? Modulation of Heart Rate by NS NS can alter permeability of autorhythmic cells to different ions NE/E: flow through If and Ca2+ channels – Rate AND force of contraction go up Ach: flow through K+ channels flow through Ca2+ channels Fig 14-16 – Consequence? Sympathetic Heart Rate Modulation Parasympathetic Heart Rate Modulation The Heart as a Pump Move from events in single cell to events in whole heart Cardiac cycle 1. electrical events 2. mechanical events Electrical conduction in heart coordinates contraction Electrical Conduction in Heart Fig 14-18 Leads to Pacemaker sets HR SA node firing rates set HR Why? If SA node defective? AV node: 50 bpm Implant ventricular cells: 35 bpm mechanical pacemaker! Electrocardiogram ECG (EKG) Reflects electrical activity of whole heart not of single cell! Surface electrodes record electrical activity deep within body - How possible? Fig 14 20 EC fluid = “salt solution” (NaCl) good conductor of electricity to skin surface Signal very weak by time it gets to skin – ventricular AP = ? mV – ECG signal amplitude = 1mV Fig 14-22 EKG tracing = of all electrical potentials generated by all cells of heart at any given moment Since: Depolarization = signal for contraction Segments of EKG reflect mechanical heart events Components of EKG Waves (P, QRS, T) Segments (PR, ST) Intervals (wave- segment combos: PR, QT) Fig 14-20 Mechanical events lag slightly behind electrical events. Why neg. tracing for depolarization ?? Net electrical current in heart moves towards + electrode Net electrical current in heart moves towards - electrode EKG tracing goes up from baseline EKG tracing goes Down from baseline Einthoven’s Triangle and the 3 Limb Leads: + I RA – – Fig 14-19 II III + + LL LA – Info provided by EKG: 1. 2. 3. HR Rhythm Relationships of EKG components each P wave followed by QRS complex? PR segment constant in length? etc. etc. For the Expert: Find subtle changes in shape or duration of various waves or segments. Indicates for example: Change in conduction velocity Enlargement of heart Tissue damage due to ischemia (infarct!) Prolonged QRS complex Injury to AV bundle can increase duration of QRS complex (takes longer for impulse to spread throughout ventricular walls). Fig 14-23 Mechanical Events of Cardiac Cycle Systole (time during which cardiac muscle contracts) – atrial – ventricular Diastole (time during which cardiac muscle relaxes) – atrial – ventricular Compare to Fig 14-24 Summary Heart at rest: atrial & ventricular diastole Completion of ventricular filling: atrial systole Ejection: ventricular systole Heart Sounds (HS) 1st HS: during early ventricular contraction AV valves close 2nd HS: during early ventricular relaxation semilunar valves close Fig 14-26 Gallops, Clicks and Murmurs (clinical focus) Turbulent blood flow produces heart murmurs upon auscultation Cardiac Output (CO) – a Measure of Cardiac Performance CO = HR x SV calculate for average person! HR controlled by ANS – parasympathetic influence ? – sympathetic influence ? – without ANS, SA node fires 90-100x/min What happens with ANS when resting HR goes up (e.g. during exercise)? Stroke Volume (SV) = Ventricular blood volume pumped in one contraction = mL / beat = EDV - ESV For average person: SV = EDV - ESV 70mL = 135 mL - 65 mL CO = HR x SV Force of contraction Fig 14-28 Length of muscle fibers (Starling curve/law) due to venous return, influenced by skeletal muscle pump and respiratory pump Sympathetic activity (and adrenaline) venous constriction by sympathetic NS and Increased Ca2+ availability Myocardial Infarction