* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download The Heart, Day 4 (Professor Powerpoint)
Stimulus (physiology) wikipedia , lookup
Exercise physiology wikipedia , lookup
Homeostasis wikipedia , lookup
Hemodynamics wikipedia , lookup
Common raven physiology wikipedia , lookup
Biofluid dynamics wikipedia , lookup
Electrocardiography wikipedia , lookup
Defibrillation wikipedia , lookup
Haemodynamic response wikipedia , lookup
Cardiac action potential wikipedia , lookup
The Heart Chapter 18 – Day 4 2/13/08 Wrap up Physiology Muscle contraction in cardiac tissue Pacemaker cells (aka cells of the SA node) ♦ Rhythmic depolarization and repolarization ♦ Triggers depolarization through internodal cells (aka – start of action potential) Cardiac tissue ♦ Ca2+ enters muscle cells via “slow calcium channels” ♦ This results in plateau (Fig. 18-15) ♦ Arrival of extracellular Ca2+ triggers the release of additional Ca2+ from reserves in SR ♦ Sarcomeres shorten = muscle contraction ♦ Period of active muscle contraction continues until the plateau ends 2/13/08 Heart – Anatomy: Cardiac muscle 2/13/08 Fig. 18.5 Order of Rhythm in Heart 2/13/08 Fig. 18.13 2/13/08 Fig. 18.15 Journal of Action Potential in Heart 2/13/08 Fig. 18.12 Wrap up Physiology Stimulates intercalated discs ♦ Moves action potential nearly instantaneously cell-to-cell ♦ Action potential simultaneously affects all tissue in the area All muscle cells in ATRIA contract together Action potential is transferred to AV node (100msec delay from SA node = Ventricles contract after atria) All muscle cells in VENTRICLES contract together We’ve covered EKG/ECG, make sure you are comfortable with it for lecture AND lab exam 2/13/08 Heart 2/13/08 Fig. 18.11 2/13/08 Fig. 18.14 Cardiac Cycle Cardiac cycle = 1 heart beat Figure 18-16 2 important events ♦ Systole = contraction ♦ Diastole = relaxation Each chamber has it’s own systole and diastole 2/13/08 Cardiac Cycle ATRIAL SYSTOLE ♦ Pushes blood into relaxed ventricles Ventricles build up pressure VENTRICULAR SYSTOLE ♦ Early – there is enough pressure to close AV valves, but not enough to exceed pressure in blood vessels ♦ Pressure exceeds that in blood vessels = 2nd phase of v. systole… ♦ Ejects blood out of heart into circulation ♦ Meanwhile….ATRIAL DIASTOLE is in progress At the beginning of VENTRICULAR DIASTOLE ♦ Atria fill up with blood (returning = venous return) In late ventricular diastole all chambers are relaxed 2/13/08 2/13/08 Fig. 18.16 2/13/08 Fig. 18.17 2/13/08 Fig. 18.18 Heart Health Resting heart rate is efficient Cardiac cycle can give information about heart efficiency As the heart rate increases, less time is spent in each phase, thus… …blood is ejected at a different volume Heart efficiency can be measured as CARDIAC OUTPUT 2/13/08 Cardiac Output = volume of blood ejected every minute P. 523 and on board Example Cardiac Output = a major factor in determining blood pressure How hard does the heart have to work for proper circulation 2/13/08 Cardiac Output Depends on ♦ ♦ ♦ ♦ Venous return Stretching of heart muscles Heart rate End diastolic volume (EDV) • Volume remaining in ventricle after contraction b/c not all blood is ejected out Figure 18-23 Amount of muscle stretching affects the force of contractions (e.g. pulling a rubber band) Starlings Law of the Heart “Stretch” builds up resistance against the blood ♦ More blood is pushed out Why is C.O. important? ♦ Maintains proper BP levels to provide efficient blood supply 2/13/08 Factors Affecting Stroke Volume 2/13/08 Fig. 18.23 Cardiac Output Blood Pressure ♦ Pressure of blood within blood vessels ♦ Pressure exerted on ARTERY walls ♦ How would C.O. relate?? • Higher cardiac output ◦ More blood = ↑ BP ◦ Less blood = ↓ BP ♦ Resistance of blood vessel walls • Small diameter = ↑ BP • Blood flow is proportional to the radius of the “pipe” ♦ Polycythemia (↑ in RBCs) • Thicker blood viscocity = ↑ BP (↑ RBCs or loss of water) ♦ Length of blood vessel – longer length = ↑ BP 2/13/08 Cardiac Output Cardiac output can be influenced by many factors One of these is HEART RATE ♦ Heart conduction system ♦ Autonomic nervous system Exercise can increase C.O. ♦ Heart muscles are working out ♦ Skeletal muscle cells need a fast blood supply ♦ The heart has to meet that demand – when exercising, it meets increased demands ♦ The force of contraction increases ♦ Blood moves faster, so venous return is faster ♦ More blood volume is pushed out ♦ Does not increase indefinitely, the Heart Rate can outcompete C.O. 2/13/08 Factors Affecting Heart Rate Hormones, ions, nervous system… ANS ♦ Fibers connect to the SA node and the AV node Sympathetic Control ♦ Medulla – remember the cardiovascular center ♦ Norepinephrine, epinephrine • Affects the SA node, AV node & myocardium Cardiac Nerve ♦ Dilates coronary vessels Parasympathetic control ♦ Medulla – cardio-inhibitory center Vagus Nerve (at S.A. node & A.V. node) ♦ Secretes ACh ♦ ACh changes ion distribution = decrease in heart rate 2/13/08 Factors Affecting Heart Rate Ions affect heart rate ♦ Ca2+ , Na+ - needed for depolarization ♦ K+ - needed for repolarization Ion concentration in blood affects the action potential in the heart Increase K+ outside ♦ Less K+ will leave the cell ♦ Partial repolarization – slower action potential HR Increase Ca2+ outside cell ♦ force of contraction – can lead to spasms 2/13/08 Factors Affecting Cardiac Output 2/13/08 Fig. 18.24 Heart Problems The normal rhythm of the heart can be disrupted in many ways – be ready to discuss on Friday those in book & those in handouts – you’ll also form your groups for the case study… 2/13/08