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Physio Note

The document provides an overview of cardiovascular system physiology, detailing the concentrations of sodium and potassium ions, resting membrane potential, and the mechanisms of cardiac muscle contraction. It explains the roles of the heart and blood vessels, the conduction system including the SA and AV nodes, and factors influencing heart rate and autorhythmicity. Additionally, it discusses action potentials in cardiac and skeletal muscle, highlighting differences in contraction duration and the structure of myocardial muscle types.

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0% found this document useful (0 votes)
8 views13 pages

Physio Note

The document provides an overview of cardiovascular system physiology, detailing the concentrations of sodium and potassium ions, resting membrane potential, and the mechanisms of cardiac muscle contraction. It explains the roles of the heart and blood vessels, the conduction system including the SA and AV nodes, and factors influencing heart rate and autorhythmicity. Additionally, it discusses action potentials in cardiac and skeletal muscle, highlighting differences in contraction duration and the structure of myocardial muscle types.

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mechafikadu5
Copyright
© All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF or read online on Scribd
Cardiovascular System Physiology (D-1, Page-1) aie ere lle a el Lally Sodium (Na*) Concentration: Around 140 mEq inside (ICF), while outside (ECF) is 142 mEq. Potassium (K*) Concentration: 10-14 mEq inside, 4 mEq outside. Resting Membrane Potential (RMP): Measured when muscles are not working. Membrane Potential: It is an electric potential because of the distribution of electrons (negative and positive charges) inside and outside the cell. During resting membrane potential, the negative charge is accumulated inside more than outside. Excitability: The ability to change the resting state to an active potential when stimulated by the threshold frequency. + Threshold frequency: Minimum frequency required. Secu ame eM Le eer) (cre RTM el oo Function of CVS BIC leat) Endocrine role: e.g., produce ANP (Atrial Natriuretic Hormone), which causes excretion of Na. Distribution of substances based on body demand. pS Regulation Cedi eoe 1m ec) 1. Heart: « Naturally, our heart beats between 80-120/min, but actually, it beats between 60-90 times/min. ¢ 3 Layers: Endocardium, Myocardium, and Epicardium (Visceral pericardium). 2. Blood Vessels: (Arteries, Capillaries, Veins) CMD ital lice Cad) led se ole ol (ele]° « Exchange (Capillaries) * Collection (Veins): 64% of blood. 3. Blood Distribution Summary: ee Ome Lo Caer Na Ci Hla (ob Ca te o + Pulmonary Circulation: 9% Note: The lateral part of the Hypothalamus controls glucose CNS RATAN CRC ee a BU wala ¢ Formed at 21 days (at the end of the 3rd week). + Central pumping organ located at the mediastinum area. + For each individual, it is equivalent to its own clenched fist (about 12x9x6 cm). + Itweighs between 280-340 mg. (Note: Likely intended as grams, g). # Myocardium ¢ Made up of many muscle fibers; each muscle fiber is covered with intercalated disks. ¢ Anintercalated disk is a cell membrane of cardiac muscle fiber that connects muscle fibers together. Cardiac and Skeletal Muscle Physiology Notes Cardiac Muscle and Action Potentials (AP) en ¢ Between Intercalated disks, there is a "Gap junction" that aids to move impulse from one cardiac muscle to another. « AP measured at the Ventricles is 105 mv. RMP (Resting Membrane Potential) of Ventricular muscle is (-85 mv to Ee hoe * During AP, the Ventricular muscle produces a voltage up to CAB he * Threshold stimulation opens Voltage-gated Na* channels. * Positive feedback mechanism opens more and more Voltage-gated Nat channels. * So, Opening of Na* gated channel is because of positive feedback mechanism and threshold stimulation. Mechanism of Contraction of Cardiac Muscle (Excitation-Contraction Coupling) ¢ Is the process in which an AP causes muscle contraction. * Somatic muscle Neurons: Is the only stimulation of skeletal muscle. « Action potential has properties of all or none rule (either all heart parts stimulated or none at all). Neuromuscular and Chemical Factors The impulse that is brought from nerve to skeletal muscle is always Excitatory. Epinephrine binds with £, > vasodilation. (Question in notes: What about with a, ?) Impulse from: [Incomplete in notes] Graded potential cannot transmit information so far; it is usually local. ATT sre MNCL RST TUT La produces AP > Spacial [Spatial Summation]. Muscle Cell Structure and Proteins Ea Smooth EPR [Endoplasmic Reticulum] is called Sarcoplasmic Reticulum. Actin and Myosin are contractile proteins. Troponin has more affinity for Ca?*. In case of Skeletal muscle, T-tubule is less developed unlike smooth muscle. Dilated portion of sarcoplasmic reticulum is called Terminal et een aR Oka ¢ Incase of cardiac muscle Nerve impulse not only cause opening of ligand gated Nat channel but also Ligand gated K* channel. * Cardiac muscle has very large T-tubule. * The strong contraction of cardiac muscle depends on the Pere liter Tal rele Mo LM Or came-Liccteuit-le ROM Eat] elt] 0 ¢ The T-tubule contains mucopolysaccharide which is used for attaching of Ca’* to T-tubule. + Why it used for attaching Ca?* to T-tubules > B/c Mucopolysaccharide has negative charge. ¢ This calcium is found on Extracellularly, not intracellularly. Myocardial Muscle Ap (Action Potential) Ee (Graph depicts Phases 0 through 4) ¢ RMP (Resting Membrane Potential) * Threshold * Voltage gated Na* channel opens * Some plateau Banos + Phase-O: rapid depolarization b/c of VG Na* channel. Here, muscle generates/transmits an impulse. + Phase-t1: early brief repolarization b/c of VG Ci- channel. * Phase-2: prolonged depolarization b/c of opening of Na* Be eaaelaT CMe Teel TMT te aC ol A Mee eam CUNT R L skeletal muscle. * This is slow to open & slow to close; it takes 0.2sec - [Ve R78 Oi tec Eee CMC MeV ae ea * Phase-4: --- Skeletal Muscle Ap (Graph depicts a sharp peak without a plateau) + Depolarization, Contraction, Excitation: They are the Tut + Voltage levels indicated: +20, 0, —65, —85. Key Takeaway + Duration of contraction of cardiac muscle is more greater than skeletal muscle. Note on Phase-3: Your notes cut off slightly on the reasons for Phase-3 repolarization. Usually, this is primarily due to the closure of those slow Ca”*+ channels and a big increase in Kt permeability. a The SA Node (Sinoatrial Node) * Why is the SA node called the pacemaker? Because of its generation of a high rate of impulse discharge. * Impulse Transmission: The impulse generated at the SA node can be transmitted to the atrial muscle (directly) and to the AV node by the internodal pathway (indirectly). * Internodal Pathway: * Connects SA node to AV node. + Maximum conductive velocity is 1 m/s. * Do not produce impulse discharge. * Conduction delay from SA node to AV node is 0.03 sec. * Heart Rates: At the SA node, the beat is 80-120 beats/ min, while the beat at the AV node is 40-60 beats/min. The AV Node (Atrioventricular Node) Goa * Transmits impulses from atria to ventricle. * Generates an inherent impulse of 40-60 beats/min. ¢ The site of delay is known as AV Nodal delay. ¢ Functions of the delay: ¢ Makes the atria contract 1/6 sec prior to ventricular contraction. ¢ Promotes ventricular filling before it contracts. TO * The delay is a “useful delay” caused by a small amount of gap junctions. * Total Delay Calculation (0.16 sec): * 0.03 sec delay from SA to AV node. a * 0,09 sec delay at AV node itself. * 0,04 sec delay for penetrating portion of AV bundle. © Total = 0.16 sec (This means time delay from atrium to ventricle impulse transmission). AV Bundle (Bundle of His) * It branches into left and right bundles and is distributed to irre 10am le aT Nae MU) 0m + Prevents re-entry of impulse (prevents backflow of impulse from ventricle to atrial). Simm (vel MCR Ke RU ROM nl ROL al + Generates an impulse of 20-40 beats/min in addition to what it takes from the SA node. Purkinje Fibers * Maximum conduction is here. + It takes 0.06 sec totally to depolarize the ventricle. This is fast because there is a maximum amount of gap junctions. + The impulse timeline: The impulse generated at the SA node is transmitted to the AV node in 0.03 sec. To be transmitted to all parts, an additional 0.03 sec is added. Purkinje fibers are the fastest. Clinical Note: Ventricular Escape + lf the atria are separated from the ventricle, the ventricle stops beating for 5-20 seconds. ¢ After 20 seconds, it starts to beat by its own beat. * During those 5-20 seconds, the person gets fainting (Ventricular escape / Over-driven suppression). + Also known as Stokes-Adams Syndrome. Factors Controlling Autorhythmicity pee 1. ANS (Autonomic Nervous System) ¢ Parasympathetic NS: Synapsed with SA & AV; to some extent, atrial muscle. « Vagus Nerve strongly affects the SA node. * Mechanism: Release of ACh (Acetylcholine). ACh binds with 4, receptors, resulting in the opening of Lee Omi MUM RUM iene eae which decreases the heart rate to 60-90 from 80-120. * The ventricle is hardly (negatively) affected (almost not affected). « Sympathetic NS: Stimulates all parts of the heart, totally unlike PSNS. Sympathetic is excitatory. 2. lon Levels & Temperature ¢ K* (Potassium): ¢ High level in ECF (Hyperkalemia): Decreases heart activity. « Low level in ECF (Hypokalemia): Increases the activity elma M ola * Ca** (Calcium): ¢ High level (Hypercalcemia): Increases heart activity. ¢ Body Temperature: ¢ Anincrease in temperature by 1°C results in an increase of 15-20 beats/min. FETs (wcll * Triggered by Right atrial distention. OMe e-M yi alee ite 1. Directly increases excitability of SA node. 2. Impulse goes to Hypothalamus — then goes to SA node. Cardiac Muscle Physiology + Immediately after the opening of Nat-Ca*+ channels, the membrane permeability for K* decreases by 5x in the case of cardiac muscle contraction. Phases of Action Potential eae * Phase 3: Repolarization — The process of returning back of Action Potential (AP) to Resting Membrane Potential (RMP) due to Voltage-Gated K* channels (VG-K* channels). * Phase 4: Hyperpolarization > Excessive efflux (removal) of K+ ions because the VG-Kt channel is slow to close. * This means being more negative > slow close of VG-K* channel — outflow of K+ ions (positive ions) > inside becomes more negative + means: Hyperpolarization. ¢ Atlast + The hyperpolarization returns back to RMP by the Na*-K* ATPase. Types of Myocardial Muscle The myocardium has three types of muscle: 1. Atrial Muscle: High contractibility, less excitatory. Pritt la Ye 3. Specialized Excitatory & Conductive Cells: High excitatory, less contractible. PT ela Catala 2) Autoretemicity is the ability of our heart to produce its own beat, unlike all skeletal muscles (most but not all smooth muscle). Specialized Conductive Cells pee These include: 1. SA Node (Sinoatrial node): The pacemaker because of the maximum frequency of impulse. * Located at the posterolateral aspect of the Right rN * RMP of SAnodeis —55 to -65 mV. * Generates a heart beat of 80-120 beats/min. Internodal fiber AV Node AV Bundle a ed Purkinje fiber Diagram Note The diagram at the bottom illustrates an Action Potential curve: « The descending limb is labeled: Repolarization (b/c of VG-K* Channel). * The graph shows voltage points at 0, —40, and —-60. ¢ Caption: Fig. Skeletal muscle (Note: Your notes use this for comparison to the cardiac phases mentioned above).

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