Cardiovascular Physiology: Heart and Cardiac Function - PDF

Cardiovascular Physiology The Heart- Part 1 (Week 4) Blood Vessels and Circulation- Part 2 (Week5) Lab 5 Chapter 19 &20 Overview Electricity of the heart Action potential, conduction, etc. Including some info on ECG (also studied in Lab 5) Cardiac cycle,...

Cardiovascular Physiology The Heart- Part 1 (Week 4) Blood Vessels and Circulation- Part 2 (Week5) Lab 5 Chapter 19 &20 Overview Electricity of the heart Action potential, conduction, etc. Including some info on ECG (also studied in Lab 5) Cardiac cycle, stroke volume, cardiac output, basic functioning of the heart Blood pressure, blood flow, and capillary exchange Regulation of cardiovascular function NS and hormones Path of blood flow through the heart (Anatomy review) Inferior vena cava and superior vena cava deliver blood from body to right atrium 🡪 right ventricle, then out to lungs via pulmonary arteries From the lung to pulmonary veins 🡪 left atrium 🡪 left Saladin, 2007 ventricle See also Fig. 20-5  The Heart is Electric! Electrical activity coordinates and causes the contraction of the heart muscle… Conducting cells (create AP, Including SA and AV) Contractile cells (Myochardium) This activity can be measured (ECG), as  Action Potential Review: Action potential in a typical neuron on 30mV zati repo i olar l ariza dep ti threshold on -50mV -70mV resting potential Action Potential Review: Action potential in a typical neuron Action Potentials in Cardiac Muscle: (contractile cells) Overview: Resting potential Depolarization Early repolarization Plateau Final repolarization (Refractory period) 1 = depolarization Return to resting 2 = early repolarization and plateau 3 = final repolarization potential Fig 19.19 APs in cardiac muscle (more detail…) Depolarization: Voltage-gated Na+ channels open (fast) Voltage-gated Ca2+ channels start to open (slow) (Voltage-gated K+ channels are closed) Early repolarization and Plateau: Voltage-gated Na+ channels close Voltage-gated Ca2+ channels are open (Ca2+ moves in) while some voltage-gated K+ channels are also open (K+ moves out…) Final repolarization: Voltage-gated Ca2+ channels close Lots of voltage-gated K+ channels open Describe the movement of ions through these channels, in and out of the cell - how does this cardiac vs neuron AP Cardiac - no hyperpolarization - depolarization starts with voltage gated sodium channels opening - more polar at resting - takes longer - calcium channels (slow, takes a long time to close) - repolarization happens in phases - dependant on potassium channels to open Neuron - faster (1ms) - depolarization starts with voltage gated sodium channels opening - dependant on potassium channels to open  Action Potentials in Cardiac Muscle: other views Sherwood (2013)  Cardiac Conducting System (review of anatomy) Initiates and distributes stimulus to contract (“automaticity”, or “autorhythmicity”) Consists of: Sinoatrial (SA) node Atrioventricular (AV) node Conducting cells: internodal pathways (between SA and AV Heartbeat is Series of Contractions and Relaxations Thanks to the unique qualities of cardiac muscle, the heart has a coordinated contraction (systole) and relaxation (diastole) of the atria and ventricles The sinoatrial (SA) node (1) in the right atrium sets the pace of the muscular contractions ( o The muscle cells here have the fastest pace 12 SA node and AV node Separate Atrial and Ventricular Contractions Sinoatrial (SA) node (1) sends signal to left atrium so both atria contract together in unison Signal is also sent to atrioventricular (AV) node (2), which delays this signal before sending it to ventricles (120-200ms) Ventricles thus contract together AFTER atria 13 14  Cardiac Conducting System Nodal cells: Cannot hold stable resting potential Gradually “drift” toward threshold (depolarize) = prepotential: WHY? SA Node - PACEMAKER (able to spontaneously depolarize and get action potential more than the AV node) In wall of right atrium Fig 19.18 80-100 action potentials / min (with no other input) AV Node Between atria and ventricles  ECG: electrocardiogram (+ more detail in Lab 5…) Used to measure the activity of specific nodal, conducting, and contractile cells in the heart Damage to the heart will reveal an abnormal ECG pattern… P wave = depolarization of the atria Note: QRS wave = this is NOT an depolarization of the action potential ventricles (and graph! repolarization the of atria) How ECG relates to conduction through heart & muscle activity (Also Fig 19.24) How ECG relates to muscle activity (Saladin, 2007) Saladin (2007) Abnormal ECGs  Treat abnormal heart rhythms. Defibrill Stops the heart to allow the SA node ator to reestablish a normal rhythm.  Cardiac Cycle: Overview Period between start of one heart beat and start of next… Systole + diastole Changes in pressure in chambers result in flow of blood From high pressure 🡪 low pressure described on the next two slides…  Cardiac Cycle (cont’d) Atrial systole Atria contract Higher pressure, to push (a little more) blood into ventricles Atrial systole ends, atrial diastole begins Ventricular systole Ventricles contract Pressures in ventricles rise, closing the AV valves, no blood flow out yet (isovolumetric contraction) Pressure in ventricle eventually exceeds that of aorta/arteries, semilunar valves open, blood 🡪 out Cardiac Cycle (cont’d) Ventricles have reached the peak of their contraction then begin to relax (end of ventricular systole, start of ventricular diastole) Ventricular diastole Pressure drops to end ventricular systole, enter isovolumetric relaxation (no blood flow in or out of ventricles – all valves are still closed) Cells continue to relax, pressure drops more, blood flows from atria to ventricles (passively) as AV valve can now open Heart Sounds / Cardiac Cycle Auscultation: listening to heart sounds 4 heart sounds: S1 – S4 S1 = “lupp” Recoil of blood due to AV valves closing (start of ventricular systole) S2 = “dupp” Recoil of blood due to Semilunar valves closing (start of ventricular diastole) S3 and S4: very faint, seldom audible… S3 = blood flowing into ventricles S4 = atrial contraction https://www.youtube.com/watch?v=zNHI-l_c-ls Pressure and Resistance: Two of the forces that affect blood flow (and airflow) Flow is directly proportional to pressure and inversely proportional to resistance Increased pressure = increased flow Increased resistance = decreased flow Significance to physiology? Pressure gradients determine direction of flow (of blood through the heart and through blood vessels, of air through the lungs, and also for exchange of materials across capillaries…) Pressure and resistance can be changed, and will affect blood flow (and airflow, etc.) … Stroke Volume (SV) The volume of blood pumped out of each ventricle for each beat (contraction) SV = EDV - ESV (EDV = end-diastolic volume) (ESV = end-systolic volume) Normal ~70-80 ml Volume ejected by EACH ventricle per “beat” Model of Stroke Volume (Fig. 20-20) Factors affecting stroke volume (slide 1 of 3) EDV: amount of blood in ventricle just before contraction Volume affected by filling time and venous return How can these factors affect EDV? How would a change in EDV affect SV? ESV: amount of blood in ventricle after systole Influenced by preload, contractility, and afterload How would a change in ESV affect SV?  Factors affecting stroke volume (slide 2 of 3) Preload: degree of stretching by ventricular muscle cells, during diastole Directly proportional to EDV More full = more stretch = more preload = more efficient, forceful contraction (similar to skeletal muscle) The Frank-Starling principle (“more in = more out”) How will this affect ESV (and SV)? Contractility: amount of force produced during a contraction (at a given preload) Affected (increased or decreased) by autonomic nervous system and hormones (and medications) Often related to calcium levels How will this affect ESV (and SV)? Factors affecting stroke volume (slide 3 of 3) Afterload: amount of tension needed to force open the semilunar valves and eject blood Increased by any factor that restricts blood flow through arteries (thereby raising pressure in the arteries)...such as? How would this affect ESV and SV? Cardiac Output (CO) Amount of blood pumped by each ventricle in one minute CO = HR x SV Example: If HR = 75 beats/min and SV = 80 ml/beat CO = 75 beats/min x 80 ml/beat = 6000 ml/min (or 6 L/min) An indication of blood flow through peripheral tissues and efficiency of the ventricles Can be altered by changes in HR or SV Factors that affect heart rate: overview (details to come Delicatesoon…) adjustments to the natural rhythm of the heart using: Autonomic nervous system Sympathetic (↑ HR) and parasympathetic(↓ HR) Controlled by cardiac centers in medulla oblongata Hormones Epinephrine, norepinephrine, thyroid hormone (affect the SA node, more on this later) Summary of factors affecting cardiac output