Cardiovascular Physiology: The Adventure of a Lifetime! PDF

Cardiovascular Physiology: The adventure of a lifetime! Dr. K. Thaxter Nesbeth Department of Basic Medical Sciences Physiology Section [email protected] Welcome to Wakanda! Ask questions! Request do-overs! Let’s learn together! I l...

Cardiovascular Physiology: The adventure of a lifetime! Dr. K. Thaxter Nesbeth Department of Basic Medical Sciences Physiology Section [email protected] Welcome to Wakanda! Ask questions! Request do-overs! Let’s learn together! I like this book https://www.youtube.com/watch?v=wq7edb qi9n0 Keep your head up 2027!! Electrical Activity of the Heart: Ionic Basis  We will Remember the cardiac cell types, structure and function Discover the roles of ions responsible for passage of electricity from cell to cell in the heart Cardiac cells Two important types of cardiac cells  2 types of cardiac muscle cells Contractile cells = working myocardium – 99% of heart muscle – Activated by change in the membrane potential (just like skeletal muscle) – Produce contractions, generate force Auto-rhythmic cells (Conducting system) – Initiate and distribute electrical activity – Control and coordinate the heart beat but do not contribute to contractile force of the heart – Smaller, few contractile fibers Myocardial Contractile Cells  Cardiac muscle cells Striated, short, branched Single, central nucleus Connected by Gap junctions & Intercalated discs Sarcolemma: specialized ion channels (not in skeletal muscle) – voltage-gated Ca2+ channels Fibers are not anchored at ends; allows for greater sarcomere shortening and lengthening.  The Action Potential in Skeletal vs Cardiac Muscle contractile cells AP passes through sarcolemma Contractile elements within the cell become excited Actin and myosin cross-bridge, contraction of cell Cardiac muscle cell – action potential wider Contraction phase longer Cardiac muscle action potential and myocardial contraction Cardiac muscle cell action potential Current spreads from autorhythmic cell to contractile cell through GAP JUNCTIONS Action potential spreads along plasma membrane to T-tubules Ca2+ channels open in plasma membrane and sarcoplasmic reticulum  Ca2+ induces Ca2+ release from SR (must use Ca2+ stores for enough Ca2+ to be present to cause contraction) Ca2+ binds to troponin, causing tropomyosin to shift, exposing myosin binding sites Cross bridge cycling takes place: muscle contraction occurs  Once contraction has taken place Ca2+ is pumped back into the SR and out of the cell ATP dependent pumps and Na + /Ca2+ exchanger  The refractory period is short in skeletal muscle, but very long in cardiac muscle. This means that skeletal muscle can undergo summation and tetanus, via repeated stimulation Cardiac muscle CANNOT sum action potentials or contractions and cannot be tetanized Autorhythmic Cardiac Cells  Autorhythmic cells: Intrinsic Conduction System of the heart Autorhythmic cells: – Initiate action potentials – Found throughout the conducting system: – Sinoatrial node – Atroventricular node – Bundle of His – Purkinje fibers Action potential in a pacemaker cell Pacemaker and Action Potentials  Videos Inspiration for the wonderfully made: We all matter https://www.youtube.com/watch?v=U1RRfnJpZKg https://www.youtube.com/watch?v=DSDf_db Wy_I ionic basis of cardiac electrical activity http://www.interactivephysiology.com/demo/ systems/buildframes.html?cardio/actnpot/01  http://highered.mheducation.com/sites/007249 5855/student_view0/chapter22/animation__co nducting_system_of_the_heart.html https://www.youtube.com/watch?v=RYZ4daFw Ma8 Conduction sys and ECG Internal Factors affecting electrical activity in the heart  Pathways for flow of Electrical Signals in the Heart S-A node pacemaker cells generate the signal (fastest recovery from refractory period). Signal travels through internodal pathways and atrial muscle A-V node and bundle (slowest conduction in the system) convey the signal to the ventricles.  Flow of electricity in the heart Purkinje fibres rapidly carry the signal throughout the ventricles, where it then spreads, causing contraction. Bundle branch delays AP from reaching the ventricles, allowing the atria to empty blood into ventricles before the ventricles contract.  How is electrical activity precisely controlled? Making sure the atria empty into the ventricles before ventricular contraction Preventing simultaneous contraction of atria and ventricles Ensuring ventricles are relaxed while atria contract Facilitating order 1: Fibrous skeleton Fibrous ‘cardiac skeleton’ electrically separates atria from ventricles Pierced only by fibers extending from AV node to Purkinje Prevents electrical activity from spreading from atrial muscle to ventricular muscle  Facilitating order (2): Timing of electrical events The (sinoatrial) SA node has the shortest cycle of repolarization and depolarisation of all Its sodium channels become ready for the next depolarization most quickly, so it fires most frequently and creates the heart rate Once it fires the impulse travels through the rest of the conducting system rendering the others unable to initiate impulses This makes it the pacemaker of the heart S i A A V n j n n o e o d f e i d b e e r s  Facilitating order 3: Delay in conduction between atria and ventricles at the AV node Allows complete atrial depolarization, contraction Complete emptying of atrial blood into ventricles before ventricular depolarization Limits frequency of impulses passing through the AV node Prevents excessively fast atrial contraction rates from leading to fast ventricular rates  Delay in conduction between atria and ventricles at the AV node Diameter of cells at the AV node is small Few gap junctions =slow conduction  Refractory periods of the myocyte ▪ Absolute refractory period: the myocyte is unexcitable to stimulation as all sodium channels are inactivated following the open (depolarized) state. This prolonged plateau and prevents tetany of the myocardium. ▪ Relative refractory period: stimulation produces a weak action potential that propagates, because some of the Na channels have moved from inactivated to closed, making them able to reopen in response to electrical stimulus. External factors affecting electrical activity in the heart  Central control of cardiac function  Influence of Autonomic Nervous System (ANS) on the Heart ANS does not generate the heart rate, but modulates (adjusts) the cardiac activities Specific connections to important areas of heart enable precise cardiac changes for coping with external stimuli  Influence of Autonomic Nervous System (ANS) on the Heart At rest, VAGAL influences dominate over sympathetic influences = Vagal tone Increase in HR = positive chronotropic effect - via decreased vagal and increased SS activity on SA node Negative chronotropic effect = increased vagal tone  Autonomic nervous system modulates the frequency of depolarization of pacemaker Sympathetic stimulation (neurotransmitter = Noradrenaline); binds to β1 receptors on the SA nodal membranes Parasympathetic stimulation (neurotransmitter =Acetylcholine); binds to muscarinic receptors on nodal membranes; increases conductivity of K+ and decreases conductivity of Ca2+  Influence of Autonomic Nervous System (ANS) on the Heart ▪ Force of contraction: inotropic effect via sympathetic action on ventricles. ▪ Rate of impulse conduction through AV Node: dromotropy ▪ Rate of attainment of threshold/automatism – AV node and ventricles: bathmotropic effect.