Test 2 Outline - cardiovascular system and cardiac function PDF

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cardiovascular system and cardiac function...

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Ch. 13: Cardiovascular System / Cardiac Fx (Green book) 13.1: Overview of Cardiovascular System 3 main components of cardiovascular system: 1. Heart: muscular pump that drives the flow of blood thru blood vessels 2. Blood vessels: conduits thru which blood flows 3. Blood: fluid that circulates around body, carrying materials to & from cells Fx of cardiovascular system: supply O2 to the body; remove waste & CO2  Performs sensory & endocrine Fx that help regulate cardiovascular variables (blood volume & pressure)  Blood vessels are sensory & effector organs that regulate BP & distribution of blood to body parts  Blood carries nutrients, wastes, hormones & acts like a communication link w/ nervous system The heart  4 chambers  Atria: 2 upper chambers o Receive blood that comes back to the heart from vasculature  Ventricles: 2 lower chambers o Receive blood from atria & generate force that pushes blood away from heart & thru blood vessels  Left & right heart separated by wall: septum that prevents blood in left heart from mixing w/ blood in right heart o Interatrial septum: separates left & right atria o Interventricular septum: separates left & right ventricle  Base: wider upper pole of heart  Apex: narrower lower pole of heart Blood vessels  As the blood travels thru different blood vessels, it goes in a series  Vasculature, a closed system: system of blood vessels throughout body heart → arteries → arterioles → capillaries →venules →veins  Blood flowing from heart: blood vessels branch, become numerous, smaller in diameter  After passing through capillaries, blood flows back to heart, vessels converge, become less numerous, larger in diameter  Capillaries: smallest blood vessels, serve as a site of exchange b/t blood & interstitial fluid  Arteries: large, branching vessels taking blood AWAY from heart; MORE ELASTIC, can take lots of distention; transported to body’s organs & tissues (largest artery = AORTA)  Arterioles: small branching vessels w/ high resistance  Venules: small converging vessels  Veins: relatively large converging vessels that conduct blood to heart

Blood  Blood = fluid & cells  Erythrocytes: red blood cells; contain hemoglobin (protein carries oxygen)  Leukocytes: white blood cells; help body defend itself against invading microorganisms  Platelets: cell fragments, blood clotting  Plasma: water containing dissolved proteins, electrolytes, other solutes 13.2: Path of Blood Flow  Path of blood flow is in series  Pulmonary circuit: pulmonary arteries, pulmonary trunk; begins at pulmonary trunk, goes to pulmonary arteries, then arterioles, then capillaries, then back thru pulmonary veins into left atrium o Site of gas exchange = at the alveoli / alveolar sacs o Oxygen is coming in & CO2 is exchanged  Systemic circuit: leaving aorta, circulate thru body, exchange gases & other waste products & nutrients in tissues; returning thru vena cava  Circulatory system: 2 divisions pulmonary circuit (all blood vessels within lungs & connecting lungs to heart) & systemic circuit (the rest of blood vessels in body) Systemic circuit → heart → pulmonary circuit → heart  Right heart supplies blood to pulmonary circuit o Right poor !  Left heart supplies blood to system circuit o Left rich !  Capillary beds: exchange of nutrients & gases  Oxygenated blood leaving pulmonary capillaries o OXYGENATED BLOOD = BRIGHT RED / red  Deoxygenated blood leaving systemic capillaries o DEOXYGENATED BLOOD = DARK RED / blue Path of blood flow thru cardiovascular system 1. Left ventricle pumps oxygenated blood thru aortic valve into aorta 2. Aorta carries blood to capillary beds of organs & tissues in systemic circuit 3. Blood becomes deoxygenated in systemic capillaries, travels back to heart in venae cavae - Superior vena cava carries blood from parts above diaphragm - Inferior vena cava carries blood from parts below diaphragm 4. From right atrium, blood passes thru tricuspid valve into right ventricle 5. Right ventricle pumps blood thru pulmonary semilunar valve into pulmonary trunk, which branches into pulmonary arteries 6. Pulmonary arteries carry deoxygenated blood to lungs *pulmonary arteries = only arteries carrying deoxygenated blood*

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7. Blood becomes oxygenated in lungs, then travels to left atrium in pulmonary veins *pulmonary veins = only veins carrying oxygenated blood* 8. From left atrium, blood passes thru bicuspid valve into left ventricle Parallel flow: right heart is pumping blood to lungs & left heart is pumping blood to systemic organs simultaneously o ALLOWS INDEPENDENT REGULATION OF BLOOD FLOW TO ORGANS  Why is this important to have? Every organ will get their share of blood. Sometimes we need blood in other places (in digestion, exercise, fight/flight)

CORONARY CIRCULATION  Coronary arteries: supply heart muscle w/ nourishment; branch from aorta & run thru heart muscle  How is cardiac tissue supplied w/ oxygenated blood? Coronary circulation  How is deoxygenated blood removed? Coronary veins          

3 pockets at base of aorta, which is where source of blood for cardiac tissue is “Afterload”: back pressure forces blood into left & right coronary after closure of semilunar valves (after contraction) Cardiac muscle fibers get its oxygenated blood from ventricular contraction; as it is going into aorta & contraction makes semilunar valve closed Arterial Anastomoses = artery connecting to another artery, which ensures full coverage of the tissue, so every bit gets the right amount of blood that it needs Marginal artery = first branch from right artery Circumflex artery branches into another marginal artery Great cardiac vein = runs together w/ interventricular artery Small cardiac vein Middle cardiac vein Coronary blockage o Blockage on circumflex coronary o Blockage of common trunk of left coronary artery: LESS BLOOD FLOW TO EVERYWHERE

13.3: Anatomy of Heart  Heart is located in thoracic cavity, above diaphragm  Pericardium: membranous sac around heart, contains pericardial fluid that lubricates heart o Serous membrane that protects the heart o 2 layers: attached to fascia w/ rest of body & the other is in contact w/ heart

o Pericarditis: inflammation of pericardium; pain due to friction as heart beats  Tissues are inflamed  B/t serous membranes: pericardial cavity, which has pericardial fluid, helps w/ contracting & relaxing o What is Pericardial Effusion? When you contract & there is lots of fluid around, which puts pressure on the heart; when you can’t relax muscle fibers, not an optimal length to contract; lots of pressure wanting to fill pericardial cavity  Muscle around ventricles, allows for greater force of contraction Myocardium & heart wall  Epicardium: outer layer of CT  Myocardium: middle layer of cardiac muscle o Wall moves inward & squeezes blood in chamber, which forces blood out; when muscle relaxes, chamber expands & fills w/ blood  Endothelium: inner layer of epithelial cells o Extends throughout entire cardiovascular system  VENTRICULAR MUSCLE IS THICKER THAN ATRIAL MUSCLE o Ventricles pump blood over long distances thru vasculature, so they work harder to pump a given volume of blood o LEFT SIDE OF VENTRICULAR MUSCLE IS THICKER = enables left ventricle to develop greater pressure than right ventricle b/c left ventricle pumps blood to all organs except lungs Valves & unidirectional blood flow  Atrioventricular (AV) valves: o Right AV valve: tricuspid valve o Left AV valve: bicuspid valve o Both are supported by papillary muscles & chordae tendinae  Papillary muscles & Chordae tendinae: holds AV valve in place; prevents PROLAPSE; prevents blood from flipping back o Atrioventricular valve OPEN = ventricle relaxed o Atrioventricular valve CLOSED = ventricle contracted  Semilunar valves: leave thru this to get to lungs or systemic circulation o Aortic semilunar valve OPEN = ventricle contracted o Pulmonary semilunar valve CLOSED = ventricle relaxed  Cardiac cycle: atria contract first, then ventricles  Blood flows thru heart in 1 direction  Atrioventricular valves (AV valves): separate atrium & ventricle; allow blood to flow from atrium to ventricle but NOT in opposite direction o Open & close passively in response to cyclic changes in pressure w/ every heartbeat o Inhibit prolapse = potential danger that 1 or more valve cusps could be pushed into atria, preventing the valve to seal completely

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Bicuspid valve / mitral valve: LEFT, 2 cusps of CT Tricuspid valve: RIGHT, 3 cusps Chordae tendineae: strands of CT holding valve cusps in place, which prevents prolapse of AV valves Semilunar valve: b/t ventricles & arteries Aortic valve: b/t left ventricle & aorta o Open when ventricular pressure is greater than arterial pressure (contraction) Pulmonary valve: b/t right ventricle & pulmonary trunk o Open when ventricular pressure is greater than arterial pressure (contraction)

13.4: Electrical Activity of Heart Conduction system of heart  Conduction system: spreads electrical activity throughout the heart muscle; tells heart how fast & strongly to contract o Based on ionic differences in excitable cells, which are able to fire action potentials o Electrocardiogram records the electrical activity of the heart  Cardiac muscle contractions are triggered by signals from muscle itself  Cardiac muscle = “myogenic”  Autorhythmicity: heart generates signals that trigger its contraction; the ability to generate independent rhythm o Authorhythmic cells: provide a pathway for spreading excitation thru the heart; muscle cells that coordinate & provide rhythm to heartbeat / 2 types (make up conduction system of heart) 1. Pacemaker cells: initiate action potential & establish heart rhythm 2. Conduction fibers: transmit action potentials thru heart in coordinated manner Pacemaker cells of myocardium  Pacemaker cells (excitable cells) spontaneously generate action potentials for contractions o Spontaneously depolarizing membrane potentials generate action potentials o Activity is coordinated (rhythmicity) o Fastest depolarizing cells control other cells, which sets rate for rest of cells, thus pacemakers  Pacemaker cells determine rate / “pace” of heartbeat by firing action potentials  Found in 2 Locations: o Sinoatrial node (SA node): primary pacemaker  First place of excitation  Right atrium where it joins w/ superior vena cava

Drives depolarization of cells in AV & throughout heart, establishing the heartrate o Atrioventricular node (AV node):  Near tricuspid valve Conduction fibers of myocardium  Conduction fibers connect SA node & AV node  Conduction fibers conduct action potential generated by pacemaker cells, triggering heart muscle contraction  Conduction fibers = larger in diameter, conduct action potentials faster Spread of excitation b/t cells  Action potential initiated in pacemaker cells, action potential moves rapidly thru conduction fibers to coordinate spread of excitation  First, wave of excitation moves thru atria, causing atria to depolarize then contract  Next, wave of excitation moves thru ventricles, causing ventricles to depolarize then contract  Gap junctions b/t pacemaker cells, conduction fibers, contractile cells to allow electrical current to pass in form of ions o Cardiac cells are linked by gap junctions  Why are gap junctions vital to cardiac conduction system? Gap junctions allow fast conduction thru muscle fibers  In heart = gap junctions are “intercalated discs” = form junctions b/t adjacent muscle fibers o Intercalated discs have desmosomes, which form physical bond b/t disks that resist mechanical stress (allows myocardium to resist stretching) Initiation & conduction of impulse during heartbeat 1. Action potential initiated in SA node - Sinoatrial (SA) node: (Sinus is a hole); sits as hole from vena cava in right atrium, sends electrical signals throughout rest of cardiac tissue to contract 2. From SA node, 2 electrical pathways: action potentials travel to AV node by internodal pathway & to rest of atrial muscle by interatrial pathways 3. Impulse is conducted to cells of AV node, which transmit action potentials less rapidly than other cells of conduction system [Why is firing slower at AV node? To give time for the atria to fully contract 4. From AV node, impulse travels thru bundle of His in interventricular septum *AV node & bundle of His = only electrical connection b/t atria & ventricle* 5. Signal splits into left & right bundle branches, which conduct impulses to left & right ventricles 6. Action potential travel rapidly to apex of heart [Why do ventricles contract from Apex first? To get all of the blood from the heart 

out, so squeeze from bottom & you get more blood out of heart] 7. Purkinje fibers begin at Apex & spread action potential to rest of myocardium 8. Eventually, heart returns to resting state, remaining there until another action potential is generated in SA node  Why are cardiac conduction fibers so much faster? To allow for rhythmicity & coordination of ventricles; if fast enough, it can get signal to ventricles first; they’re larger in diameter, causing faster conduction Control of heartbeat by pacemakers  Heartbeat is triggered by impulses in SA node  If SA node fails to fire action potential or slows down dramatically, AV node will initiate action potential  AV node = emergency backup that keeps ventricles beating  Purkinje fibers = backup when AV node unable to drive ventricular contraction Spread of excitation thru heart muscle  AV node = bottleneck effect to allow for efficient cardiac Fx o Allows wave of excitation to spread completely thru atria before it reaches ventricles, ensuring that atrial contraction is complete before ventricular contraction starts Electrical activity in pacemaker cells  Pacemaker cell can fire action potential spontaneously b/c it does not have a steady resting potential  PACEMAKER CELLS IN SA & AV NODES  Electrical signals are caused by changes in plasma membrane ion permeability  Increased sodium / calcium permeability makes membrane potential more positive  Increased potassium permeability makes membrane potential more negative  Closing of potassium channels & opening IF channels [K+ OUT OF CELL, NA & CA INTO CELL] causes slow depolarization of pacemaker potential  Initial depolarization triggers opening of voltage-gated calcium channels: T-type channels, which raises calcium permeability & depolarizes cell more  Before T-type channels inactivate, they trigger opening of 2nd voltagegated calcium channels: L-type channel (LONG LASTING)  L-type channels increase in calcium permeability & allow Na into cell, which trigger K permeability [repolarization] & terminating action potential, channels close Ionic basis of electrical activity  Pacemaker cells produce pacemaker potentials

1. Spontaneous depolarizations caused by closing K+ channels & opening Na+/K+ (Funny) channels & T-type (transient: little time) Ca2+ channels (leaky membrane) 2. Fast depolarization to threshold (fire action potential) thru Na+ channels 3. Further depolarization due to extended channel open time of L-type (longer lasting) Ca2+ channels 4. Repolarization mediated by K+ channels to allow positive charge to leave thru potassium ions Pacemaker cells: action potential  Because IF channels are constantly leaky, membrane potential is -70 mV (resting)  Threshold = -50 mV, opening of Na+ channels into pacemaker cell Electrical activity in cardiac contractile cells  Gap junctions connect pacemaker & conducting cells to contractile cells, which allow the spread of action potential b/t cells  Contractile cells from different regions of heart vary in shape & speed of propagation  Role of ion channels in contractile cell action potential: **NO LEAKY CHANNELS o Phase 0: rapid depolarization  Depolarization of membrane triggers opening of voltage-gated sodium channels, rising sodium permeability & increase of sodium into cell  Membrane potential becomes more positive, triggering more sodium channels, more depolarization o Phase 1: small repolarization  Sodium channels from phase 0 start to inactivate, reducing sodium permeability  Membrane potential becomes more negative  Voltage-gated potassium channels close & reduces potassium flow out of cell  L-type channels open, rising calcium permeability & increase of calcium into cell o Phase 2: plateau  Potassium channels remain closed  Calcium channels remain open o Phase 3: repolarization  Potassium permeability increases, potassium flow out cell increases  Membrane potential becomes more negative  Calcium channels close, reduces flow of calcium in cell, allowing for repolarization, thereby terminating action potential o Phase 4: resting potential

Calcium / sodium / potassium permeability = at resting potential  Why is calcium making such a giant plateau? Why do we have so much calcium? We need calcium to come into cell & allow it to bind to cardiac contractile cells: bind to troponin on actin  What is the purpose for refractory periods? This extended period is critical since the heart muscle must contract to pump blood effectively and the contraction must follow electrical events. Without extended refractory periods, premature contractions would occur in the heart & would not be compatible w/ life Excitation-contraction coupling in cardiac contractile cells  Cardiac contractility occurs thru excitation-contraction coupling 1. Depolarization of cardiac contractile cells to threshold via gap junctions 2. Opening of Ca2+ channels in sarcolemma 3. Action potential spreads thru plasma membrane, down T-tubules 4. Calcium channels on sarcoplasmic reticulum to open & release calcium into cytosol 5. Action potential triggers opening of voltage-gated calcium channels on plasma membrane, more calcium enter cell 6. Calcium-induced calcium release occurs 7. Cytosolic calcium triggers contraction of cardiac muscle… 8. Calcium binds to troponin, shifting tropomyosin off of the myosinbinding site on actin, crossbridge cycling occurs 9. Relaxation of cardiac muscle requires removal of calcium from cytosol by: Ca2+-ATPase a. CA2+-ATPase unit in sarcoplasmic reticulum actively transports calcium from cytosol to sarcoplasmic reticulum b. CA2+-ATPase in plasma membrane actively transports calcium from cytosol into interstitial fluid c. Na+-Ca2+ exchanger in plasma membrane actively transports calcium out of cell by countertransport w/ sodium 10. Without calcium bound to troponin, tropomyosin shifts over myosin-binding sites on actin & muscle fiber relaxes  Similarities to skeletal muscle o T-tubules o Sarcoplasm reticulum (source of Ca2+) o Troponin-tropomyosin regulation  Similarities to smooth muscle o Gap junctions o Lots of extracellular Ca2+ Recording electrical activity of heart w/ electrocardiogram  Electrocardiogram / ECG: monitoring the electrical activity of the heart; non-invasive test for clinical abnormalities related to conduction system o Distance & amplitude of signals depends on:  Size of potentials  Synchronicity of potentials from other cells 

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P wave: upward deflection that is due to atrial depolarization QRS complex: series of sharp upward & downward deflections due to ventricular depolarization T wave: upward deflection caused by ventricular repolarization R-R interval: time b/t peaks of 2 successive QRS complexes; the time b/t heartbeats; when muscle fibers are fully depolarized (positive cations in), crossbridge cycle of excitation-contraction coupling P-wave: atrial depolarization QRS: ventricular depolarization; atrial repolarization T-wave: ventricular repolarization PQ interval: AV nodal activity o AV node: where things slow down; conduction from atria to AV node QT interval: ventricular systole TQ segment: ventricular diastole Ventricular systole: onset of QRS complex to end of T wave; time the ventricles are contracting o AV closed = b/c finished filling, now build pressure to eject blood thru semilunar valves o Semilunar open [aortic & pulmonary valves] Ventricular diastole: end of T wave to beginning of QRS complex; time the ventricles are relaxing o AV open [bicuspid & tricuspid...