CVS 201 Physiology of Cardiovascular System PDF

. CVS 201 MUST University Physiology of Cardiovascular System Dr. Amr Shams  Dr. Amr Shams Physiological anatomy of the heart The cardiovascular system is composed of: ▪The Heart ▪Blood vessels A-The Heart (Central Pump): a mus...

. CVS 201 MUST University Physiology of Cardiovascular System Dr. Amr Shams  Dr. Amr Shams Physiological anatomy of the heart The cardiovascular system is composed of: ▪The Heart ▪Blood vessels A-The Heart (Central Pump): a muscular organ (300 gm) formed of: ▪2 Separate Pumps Right side (low pressure volume pump): pumps blood through lungs against low resistance. Left side (high pressure pump): pumps blood through all body organs against high resistance. ▪Each Pump is composed of Atria: act as reservoir, contract weakly to pump 30% of blood to the ventricles Ventricles (thicker muscular wall): pumps blood through arteries MCQs: Left ventricle wall is 3 times thicker than right ventricle wall because it pumps blood against Higher pressure. Cardiac valves: allow the blood to flow in one direction only -From atria → ventricles -From Lt. ventricle → aorta -From Rt. ventricle → pulmonary artery ▪Cardiac valves open and close passively, according to pressure gradient Types of cardiac Valves ▪Atrioventricular (AV) valves: between Atria & Ventricles Mitral (Bicuspid) valve: between LEFT atrium & LEFT ventricle Tricuspid valve: between RIGHT atrium & RIGHT ventricle MCQs: AV Valves: Prevent regurgitation of blood from Ventricle to Atrium ▪Semilunar (SL) valves (3 cusps): Aortic valve: Between LEFT ventricle & aorta Pulmonary valve: Between RIGHT ventricle & pulmonary artery MCQs: Semilunar Valves: Prevent backflow of blood from the arterial trunks to the ventricles MCQs: Papillary muscles contraction leading to closure of AV valves. MCQs: If papillary muscles fail to contract, AV vale will not close properly 1  Dr. Amr Shams B-Closed system of blood vessels ▪1-Arteries (ELASTIC arteries). As Aorta and big arteries Expands during systole (To receive blood ejected to them) -Prevents excessive rise in systolic blood pressure Recoils during diastole (To push blood to tissues) -Prevents excessive drop in diastolic blood pressure ▪2-Arterioles (Resistance vessels): Can constrict or dilate to regulate local blood flow Maintain peripheral resistance essential for regulating ABP ▪3-Capillaries (Exchange Vessels): Have very thin wall to allow exchange. Have the greatest cross-sectional area ▪4-Venules and Veins (Reservoir or Capacitance vessels): can change their capacity by contraction or relaxation of their muscular walls. MCQs: The largest part of the blood volume is found in Veins The circulation can be divided into: General or Systemic circulation: ▪The left ventricle (pressure pump) ejects oxygenated blood into aorta at high pressure, then blood distributes through all arteries, arterioles, & capillaries. ▪Exchange of gasses and nutrients and waste products will occur at capillaries. ▪Then deoxygenated blood collects into the venules and veins, to the SVC and IVC which open in the RA, which contract to eject blood to right ventricle. Pulmonary circulation: ▪The right ventricle (volume pump) pumps deoxygenated blood to pulmonary artery to reach lungs, to be oxygenated and give out excess CO2. ▪The oxygenated blood will return through pulmonary veins to LA which pumps the blood to the left ventricle. 2  Dr. Amr Shams Functional histology of cardiac muscle 1-Fibrous skeleton of the heart: dense connective tissue ▪Causes electrical separation between atria and ventricles. ▪Contains four rings forming the opening of AV valves, pulmonary & aortic valves. ▪Acts as skeleton by giving the attachment of the cardiac muscle 2-Ordinary cardiac muscle fibers: Responsible for contraction. Branched striated involuntary fibers Shorter & smaller than skeletal muscle fibers Contains: Typical myofibrils (Actin & myosin & Troponin & tropomyosin) -Titin: Very large protein (extend from Z-disk to M-line). Keeps myosin centered in sarcomere. -Dystrophin: provides structural support connects actin to ECM. Its congenital deficiency leads to dystrophy & weakness. ▪The cardiac muscle is a functional syncytium → Act as one unit ▪There are 2 functional syncytia: atrial & ventricular ▪Intercalated discs (on the cell membrane) provide mechanical cohesion between separated cells. ▪Gap junctions provide low electrical resistance that allow spread of cardiac excitation wave (Action Potential) from one cell to the others. 3-Nodal tissue (autorhythmic pacemaker excitatory) specialized modified cells ▪Initiate & propagate cardiac excitation wave (AP) all over the heart. A-Nodal tissue: ▪Sinoatrial (SA) node (Sinus Rhythm) Present in the RA near SVC opening It is the Normal pacemaker of the heart Has the FASTEST rate of auto rhythmicity (rate of 90-105 ⁄min) Supplied by right vagus and sympathetic fibers. ▪Atrioventricular (AV) node at the junction of the atrium and ventricle. Has lower rhythm than SA Node (60/min) The ONLY electrical connection between A & V. Has the SLOWEST conduction velocity Prevent abnormal high rhythms originating in atria from reaching the ventricles. Prevent atria and ventricles from contracting simultaneously Supplied by left vagus and sympathetic fibers. 3  Dr. Amr Shams B-Conducting system: ▪Carries the cardiac excitation wave ▪1-Internodal pathways: ▪2-Atrio-ventricular bundle: or bundle of His. ONLY electrical connection that transmits the impulses from atria to the ventricles. ▪3-Right and left bundle branches ▪4-Purkinje fibers: Discharge at a rate of 30/min (Have the FASTEST conduction velocity to allow ventricles to contract as one unit) Scan to Test yourself 4  Dr. Amr Shams Cardiac properties 1-Excitability 2-Rhythmicity 3-Contractility 4-Conductivity 1-Excitability Ability of cardiac muscle to respond to an adequate stimulus with action potential. This action potential will be conducted along the membrane followed by contraction RMP (phase 4) in cardiac muscles varies between -80 to -100 mv, due to: -Selective permeability. -Sodium-potassium pump. Ordinary cardiac muscle action potential (fast response) & its Ionic Basis Phase (0) Rapid DP & reversal of polarity (from -90mv to +20mv) ▪Due to rapid Na+ inflow caused by opening of fast voltage Na+ channels ▪Fast-voltage Na+ channel could be blocked by tetradotoxins. Q: Phases 1,2 and 3 represent repolarization which is slow and triphasic Phase 1 (SMALL Repolarization): (from +20mv to +10mv) due to: ▪Closure of Na+ channels ▪Opening of K+ channels causing K+ outflow ▪Opening of Cl- channels causing Cl- inflow Phase 2 (Plateau): RP slows down (around 0 mV) Due to balance between: ▪K+ outflow. ▪Slow Ca++ INFLOW through slow calcium Long lasting (L-channels) ▪Ventricular AP shows a prolonged plateau and lasts for 300 msec While that of atrial fibers have less prominent plateau and lasts for 150 msec N.B: Plateau prolongs Absolute refractory period Phase 3 (Rapid Repolarization): till reaching RMP (-90mv) Caused by: ▪K+ outflow ▪Closure of Ca++ channels (no more calcium influx) Phase 4 (Resting membrane potential): (-90mv) ▪Then Na+-K+ pump drive out excess Na+ and bring in K+ 5  Dr. Amr Shams Absolute Refractory Relative Refractory Supernormal Phase Period (ARP) Period (RRP) (vulnerable period) Period during which any Period during which Period during which stimulus reaches the heart strong stimulus (supra- weak (sub-threshold) Definition during this period, there threshold) is needed to stimulus can will be no response. produce a weak response produce response Membrane till -50 mv till -75 mv till full RP (-90mv) potential Coincides Phases 0,1,2, part of 3 Rest of phase 3 late part of phase 3 with (All period of systole) Is lost (Returns gradually) more than normal Excitability (Zero%) above 0% & below 100% (100%) Extrasystole: It is a weak stimulation of the -LONGER (due to plateau) contraction, resulting, heart during this than ARP in skeletal from an impulse reaching period may produce Significance muscles. the heart during RRP. a fatal condition -Prevents Tetanus followed by called ventricular -Prevents Fatigue. compensatory pause fibrillation.. Q: Refractory period of ventricles is LONGER than that of atrial muscles. N.B: Altering systole will affect ARP duration (Since ARP coincides with systole) For example : Increased HR (by sympathetic) shortens ARP. Relation between mechanical response and Action Potential: ▪Mechanical response lasts 1.5 times as AP. ▪Contraction (systole) Starts just after DP Ends at end of the plateau. ▪Relaxation (diastole) Starts with rapid RP. ▪Repolarization Ends by the end of first half of diastole 6  Dr. Amr Shams 2-Rhythmicity Ability of cardiac muscle to beat regularly and initiate its own regular impulses Present in (Self-excitable or autorhythmic or pacemaker cells) ▪Sino-atrial (SA) node: 90-105 / Minute. MCQs: SA node is the NORMAL ▪Atrio-ventricular (AV) node: 60 / Minute. pacemaker because it has the ▪Purkinje fibers: 30-40 / Minute FASTEST rate of discharge These fibers differ from ordinary cardiac muscle fibers in: ▪1-Its membrane potential is less negative (-60 mv). ▪2-UNSTABLE potential during rest to discharge impulses spontaneously (do not require external stimulus). ▪3-There is no plateau in their action potential. ▪4-Repolarization is one phase Pacemaker potential of autorhythmic cells (slow response fibers) Phase 4 (Slow spontaneous DP, diastolic DP, prepotential) Due to: ▪Decreased K+ outflow ▪Increased Na+ inflow (funny current) ▪Increased Ca++ inflow (through T-Channels) Prepotential DP reaching the firing level (-40 mV) Phase 0 (Depolarization) (peak above 0mv) ▪Influx of Ca++ through Long lasting L-Channels Phase 3 (Repolarization) (to -60mv) ▪Efflux of K+ 7  Dr. Amr Shams MCQs: SLOPE of diastolic DP (prepotential) determines the HEART RATE Factors affecting Autorhythmic Positive chronotropic factors Negative chronotropic factors (Increasing Heart Rate) (Decreasing Heart Rate) By decreasing the slope (more gradual) By increasing the slope (more steep) by increasing K+ permeability of SAN. by increasing NA+ permeability of SAN Causing K+ EFFLUX → more negative Causing NA+ INFFLUX → more positive (about -75 mv) and takes longer time to Reaching firing level faster reach the firing level. 1-Sympathetic stimulation secretes 1-Parasympathetic (vagal) stimulation Noradrenaline secretes Acetylcholine 2-Catecholamines, Thyroxine 2-Cholinergic drugs (as methacholine) 3-Fever 3-Hypothermia The Pacemaker of the heart: ▪It is the part of the heart that has the highest rhythm, and all the heart obeys it. ▪Normally, it is SA node. If it stops functioning, AV node will be the pacemaker. ▪90 / minute is the discharging rate of SA node ▪70 / minute is the Normal HR (due to Vagal Tone) ▪120 / minute is the rate If the vagus is cut or blocked (due to sympathetic tone) ▪90 / minute is the rate if the vagus & Sympathetic get cut (denervated heart) This means that during rest, there are both parasympathetic and sympathetic tones to the heart, but the vagal tone is much more powerful 8  Dr. Amr Shams 3-Conductivity Ability of the cardiac muscle to transmit or conduct the cardiac excitation wave. The rate of conduction of cardiac impulse over the different parts of the heart differs Atrial Muscle: 0.5 Meter / sec Inter nodal pathways: 1 meter / sec. AV node: 0.05 meter/sec. AV bundle (bundle of his): 2 meter/sec Purkinje fibers: 5 meter / sec Ventricular muscle: 0.5 meter / sec. AV Node has the SLOWEST conductivity (AV nodal delay): ▪Due to: few gap junction in AV node tissue ▪Significance 1-To let the cardiac impulse to cover both atria before it reaches the ventricles. To delay ventricular contraction till the end of atrial contraction The atria will pump blood into the ventricles, then the ventricles contract. (Prevent the atria and ventricles from contracting simultaneously) 2-Allow time for filling of the ventricles 3-Prevent abnormal high rhythms originating in the atria from reaching the ventricles. (Maximal rate of conduction is 230/min) AV. bundle and Purkinje fibers has the FASTEST conductivity: ▪Due to: presence of many gap junctions ▪Significance The ventricular muscles are thick; the action potential (excitation wave) must spread rapidly to cover all parts of the ventricle in very short time so that they can contract as one unit (simultaneously) to pump the blood. Abnormalities in cardiac rhythm are called arrhythmias. 1-Extrasystole (premature beat): ▪When an abnormal impulse arises from an area in the heart other than the SAN. ▪An ectopic focus sends impulse that reaches the heart during RRP causing an extrasystole, which has excitability changes as the normal (ARP) & (RRP). ▪Followed by a compensatory pause (CP) because the impulse coming normally from the pacemaker (S.A.N.) will reach the heart during ARP of the extrasystole, so it will be ineffective, and a dropped beat will be felt ▪The normal beat that follows the extrasystole is stronger (post-extrasystole potentiation) due to release of more Ca2+ from the sarcoplasmic reticulum. 9  Dr. Amr Shams 2-Ectopic pacemaker: ▪When the AV node or Purkinje fibers discharge at faster rate than SA node. 3-Paroxysmal atrial or ventricular tachycardia: ▪Occurs when an ectopic focus discharges at rate of 150-200 /minute. ▪Occurs in attacks that may last for seconds, minutes, or hours then they terminate suddenly. 4-Atrial or ventricular flutter: ▪Occurs when the ectopic focus rate is 200-350/min 5- Atrial fibrillation: ▪Multiple ectopic foci in atria causing contractions at a rate of 300-500/minute. 6- Ventricular fibrillation: ▪Multiple ectopic foci in ventricles causing contraction at a rate of 300-500/min. ▪Decrease ventricle pumping leading to death if it is not immediately corrected 7- Heart block: ▪The excitation wave passing from atria to ventricles is either delayed or blocked due to damage of the AVN, AV bundle or bundle branch. ▪First degree heart block: impulses arising from the atria are conducted to the ventricles but with delay. ▪Second degree (or partial) heart block: occurs with more severe damage 2:1 rhythm: One atrial impulse will reach the ventricles, but the next atrial impulse will not be conducted 3:1 rhythm: One of each 3 atrial impulses will be conducted to ventricles ▪Third degree heart is called “ventricular escape” (complete heart block). Atria contracts according to the rhythm of SA node Ventricles contract at a rate of 30-40 beats / minutes (because Purkinjie fibers become the pacemaker of the ventricles) (idioventricular rhythm) Leads to marked decrease in cardiac output that causes fainting and even loss of consciousness (Stokes-Adams syndrome). N.B: If one of the bundle branches (right or left) is damaged: BBB Impulse will pass through the healthy branch at a faster rate and then it will transmitted through ventricular muscles to the diseased ventricle (slower rate) So, the 2 ventricles will not contract at the same time. 10