CBIO 2210 Week 5 Notes
CBIO 2210 Week 5 Notes CBIO2210
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This 10 page Class Notes was uploaded by Elise Weidner on Thursday February 11, 2016. The Class Notes belongs to CBIO2210 at University of Georgia taught by Rob Nichols in Spring 2016. Since its upload, it has received 37 views. For similar materials see Anatomy and Physiology II in Anatomy at University of Georgia.
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Date Created: 02/11/16
CBIO 2210 Class Notes 2/11/16 Top Hat Questions 1. Unlike skeletal muscle fibers, cardiomyocytes (pick 2) : a. Are branched b. Have gap junctions that allow ion flow to adjacent cells 2. The pacemaker potential of autorhythmic cells is due to: a. Sodium flowing through “slow” sodium channels (never get a resting period) 3. Parasympathetic(slows heartrate back down) impulses from the vagus nerve releases_____, causing a ______ of the pacemaker cells a. Acetylcholine; hyperpolarization(makes them slightly more negative which makes them slightly less likely to respond to a stimulus) ARP in Skeletal Muscle Due to this short ARP, skeletal muscle can respond to a new stimulus before it has relaxed fully. This may lead to tetany, a sustained contraction of the muscle ﬁber. o Important in skeletal muscle, deadly in cardiac muscle. ARP in Cardiac Muscle The ARP of cardiac muscle spans almost the entire time that it is contracted, preventing tetany. Repolarization is delayed- caused by calcium flowing into cytoplasm (both from outside the cell and from the SR inside the cell) which causes the cell to remain positive a little longer than in skeletal muscle (diagram on PowerPoint) Red line indicates change in membrane potential Blue line shows muscle response Cardiac Muscle Physiology: Cardiomyocytes Plateau phase caused by calcium from o Effect: delays repolarization which allows the cardiac muscle to reach full potential Role of Calcium in Myocardial Contraction -only takes about 3/10 of a second to contract, rests between beats 5/10ths of second) Ca2+ that is needed for contraction enters cytoplasm from both the ECF and the SR. o In fact, it’s the Ca2+ inﬂux from the ECF triggers release of Ca2+ from SR The [Ca2+] in the cytoplasm determines the force of contraction (FOC) of the cardiocytes. o Calcium concentration is proportional to FOC o Later we’ll see how increased FOC ⇒ increased blood pressure o Ca2+ channel blockers Electrocardiogram (ECG or EKG) (measures electrical activity of heart) A composite of all the action potentials generated by nodal (SA or AV) cells or contractile cells at any given time Resulting tracing on the ECG is known as a PQRST wave P = atrial depolarization o What does that mean is happening/where? Ions are moving, so Na+ ions moving into cells of atria QRS complex = ventricular depolarization (and technically atrial repolarization) o What’s happening/where? Na+ ions moving into AD nodes and ventricles T = ventricular repolarization o What’s happening? K+ is going out of ventricle cells o What’s event is missing? Atrial repolarization is missing, it is during the QRS complex Heart Sounds (caused by heart valves closing) “Lubb-dupp” (two of four heart sounds) Lubb = 1st heart sound (S1) = closing of AV valves Dupp = 2nd heart sound (S2) = closing of SL valves Know locations of auscultation “APe To Man” Top Hat Questions 1. Where can you listen to the tricuspid valve on heart a. In the fifth intercostal space, to the right (or left) of the sternum 2. The P wave of a normal EKG corresponds to a. Atrial depolarization The Cardiac Cycle Cardiac cycle: all events associated with blood ﬂow through the heart during one complete heartbeat o diastole (cardiac muscle relaxing) o systole (cardiac muscle contracting) o the whole cycle lasts about 0.8 s during resting heart rate (about 75 bpm) 4 major phases: o 1. Ventricular ﬁlling (to fill the ventricles must relax) diastole Requires a change in shape of ventricle to change volume which changes pressure (like syringe) As volume goes up pressure goes down and vice versa Ventricles suck the blood in, it is not pushed into ventricles o 2. Isovolumetric contraction systole ventricles begin to contract but the volume remains the same o 3. Ventricular ejection systole ventricles eject blood out which does change their volume o 4. Isovolumetric relaxation Diastole 1.Ventricular Filling AV valves open; SL valves closed rapid ﬁlling begins when atrial pressure > ventricular pressure passive ﬁlling i. due to lower ventricular pressure, which is… ii. due to increased ventricular volume as ventricles relax diastasis = ﬁlling slows ventricles ﬁll to 70-80% of capacity 1c. Atrial Systole AV valves still open; SL valves still closed signaled by P wave o SA node ﬁres Atrial pressure increases, blood pushed into ventricles “atrial kick” adds 20-30% more to ventricle’s ﬁnal volume (EDV) (their one big job) EDV = 120-140 mL o Reaches End Diastolic Volume (around 120 or 140) 2. Isovolumetric Contraction (first sound) AV valves slam shut causing S1 sound o SL valves don’t open yet Signaled by QRS complex Ventricles contract until their pressure exceeds pressure in aorta (or pulmonary artery) 3. Ventricular Ejection AV valves still closed; SL valves burst open Rapid initial ejection which slows down as pressures equalize T wave signals ventricular diastole ESV = 60 mL (End Systolic Volume) Stoke volume (60-80 mL)- amount pumped out for one contraction 4. Isovolumetric Relaxation AV valves still closed; SL valves slam shut causing S2 SL valves shut because pressure in ventricles < aortic (and pulmonary) pressure because… T wave causes ventricles to relax and rebound, expanding, increasing volume/decreasing pressure (…and back to ventricular ﬁlling) (between S1 and S2 the ventricles empty) Timing the Cardiac Cycle Cardiac cycle: the whole cycle lasts about 0.8 s during resting heart rate (about 75 bpm) If your heart beats 75 X per minute for your whole life, when does it rest? atrial systole = 0.1 s ventricular systole = 0.3 s quiescence = 0.4 s (neither atria or ventricles are contracting, the mitochondria are recharging ATP) Top Hat Question 1. Which of the following is happening between S1 and S2 heart sounds? (2 answers) a. Ventricles emptying b. SL valves are open CBIO2210 Notes 2/9/16 Cardiac Conduction System (electrical activity of heart-heart is able to create its own rhythm) Two populations of cells o Cardiomyocytes (or cardiocytes) Cardio muscle cells 99% of population of cells of wall of heart Contract when activated o Autorhythmic pacemaker cells 1% of population of cells of wall of heart Non-contractile Own internal rhythm Spontaneously depolarize themselves and activate cells they are attached to with gap junctions Wilhelm His and Jan Evangelista Purkinje examined hearts and found these authorhythmic cells. Found that the sinoatrial node (SA) depolarizes 75 times per minute when taken out of the heart SA node activates the atria and the AV node AV node don’t depolarize as quickly (50 times a minute) as SA but it should be depolarized by SA node, so SA node sets the pace If SA node does not work then atria wont contract and AV node will depolarize slower (not great but better than nothing) AV node depolarizes the ventricles Purkinje fibers (subendocardial conducting network) depolarize even slower than AV but can depolarize their own rhythm (30 times a minute) *look at sequence of excitation image* Extrinsic Control of Heart Rate o Central nervous system can extrinsically control the responsiveness o Although the heart is autorhythmic, the nervous system will assist in regulating the heart rate. o The ANS alters HR by altering the responsiveness of the conduction system of the heart. hyperpolarizing pacemaker cells (makes them more negative which makes beginning point lower so threshold is harder to reach) = less likely to depolarize slightly depolarizing PM cells (makes less negative) = more likely to depolarize o every cell more positive outside and more negative inside because of sodium (+1 charge) potassium(+1 charge) pump becomes more positive as sodium enters, (more negative if potassium goes out) when it reaches the threshold calcium floods in (+2 charge) Extrinsic Innervation of Heart o need balance or sympathetic and parasympathetic controls for negative feedback of controlling blood pressure o In addition to the heart’s own auto-rhythmicity, heart rhythm may be affected by ANS input o Neurotransmitters from autonomic post-ganglionic neurons alter the cardiac cell’s permeability to Na+ hyperpolarization: less irritable cells depolarization: more irritable cells o Sympathetic (increases heart rate) Comes from Cardioacceleratory center Using Cardiac nerve 230 bpm Neurotransmitters alter the PM cell’s permeability to Na+ and Ca2+ allowing some Na+ and Ca2+ to leak in causes slight depolarization = more irritable cells Uses norepinephrine (NE) neurotransmitter o Parasympathetic (decreasing heart rate) Comes from cardioinhibitory center Uses CN X and cardiac nerve Vagal tone (vagus nerve sends impulses to maintain the normal heartrate at rest-slow it down) Neurotransmitters alter PM cell’s permeability to K+ Allowing some K+ to leak out causes hyperpolarization=less irritable cells o Resting membrane potential for cell (-70mv polarized) in cytoplasm in cell When stimulate the cell (bring positive sodium inside) it becomes depolarized and gets closer to zero Sodium keeps coming in until hits threshold at +30 where it stops coming (if this were all that happened would level off) but the cell instead repolarizes and potassium begins to leave the cell making it negative again Undershoot sometimes happens where it is hyperpolarized (goes under starting negative point) and then goes back to normal Process of Pacemaker cells: (they never rest, no resting potential) o “slow” Na+ channels allow Na+ to leak back into cardiac muscle cells (they never really close) o these cells never really have a stable “resting” potential (get to around -60 and immediately begins to depolarize again) o rather, they exhibit what are known as pacemaker potentials (because not resting potential) o at threshold, Ca2+ channels open depolarization is due to both Na+ and Ca2+ influx Cardiac v. Skeletal Muscle Cellular Anatomy o Similarities to skeletal muscle striated (actin-myosin overlapping) T tubules, sarcoplasmic reticulum regulates Ca2+ sliding filaments (troponin-tropomyosin activated by Ca2+) o Differences from skeletal muscle cardiac muscle fibers are shorter, thicker, branched, and interconnected one (maybe 2) centrally located nuclei spaces between cells filled with connective fibers acting as insertions for cardiac muscle fibers intercalated discs: desmosomes and gap junctions (means cells are electrically coupled: the contraction of one activates the contraction of adjacent cell) –when one cell depolarizes, it depolarizes next cell large mitochondria (25-35% of cell volume)-give muscle cells fatigue resistance, so can more rapidly resupply with ATP and not likely wear out(skeletal muscles wear out when you exercise, heart does not) Cardiac v. Skeletal Muscle Physiology o Means of stimulation: skeletal muscle fibers are stimulated by nerve endings some cardiac cells are auto-rhythmic (can depolarize themselves and the rest of the heart) o Organ v. motor unit contraction skeletal muscle motor unit contraction does not stimulate neighboring motor units the heart either contracts as a coordinated unit, or it doesn’t “functional syncytium” (organ contracts as a single unit) due to gap junctions between adjacent cells o Length of absolute refractory period skeletal muscle: 1 - 2 ms, resulting in a twitch of 15 - 100 ms. (does not force relax, needs to be able to retain contraction) cardiac muscle: 250 ms,(long refractory period-not as much variation) resulting in a 300 ms contraction –forces heart to rest/relax between beats prevents tetany(the retaining of contraction/not relaxing)
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