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52 Cards in this Set
- Front
- Back
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Cardiac Muscle Cells |
cardiomyocytes - involuntary - striated - lines the heart walls |
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3 Tissue layers of Heart |
Endocardium: Myocardium: cardiac muscle Epicardium: membrane coat |
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Cardiac Hypertrophy |
Beneficial Cardiac Hypertrophy: from endurance training - heart bigger, stronger = less ATP for same amount of cardiac output Pathological Cardiac Hypertrophy: aka cardiomegaly - enlarged heart does not pump blood effectively = work extra hard (after load) b/c they have to work against pressure - chronic hypertension |
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Right vs Left Chambers of Heart |
Right: pumps deO2 blood to lung - blood-gas exchange Left: pumps O2 blood to body tissue - remove waste metabolites for renal filtration - removes CO2 |
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4 Functions of the Heart |
1. Generates blood pressure 2. Delivers Blood to Cells 3. Ensures 1 way Blood Flow 4. Matches Blood Flow to Changing Metabolic Needs |
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Key Features of Cardiomyocytes |
High concentration of mitochondria b/c need lots of ATP from Oxidative Phosphorylation - lots of ATP for its Na+/K+ pumps - consumes 70% of O2 from blood, Rhythmically contract & relax Are Myogenic & Autorhythmic |
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Myogenic Vs Autorhythmic |
Myogenic: spontaneously contracts w/o external stimulation from CNS - automatically pumps based on how much blood gets to the blood vessels - done w/o the control of brain Autorhythmic: spontaneously depolarizes w/o external stimulation from CNS - myocytes establish the cardiac conduction system - depolarization spreads rapidly via gap junctions This allows for an intrinsic heart rate independent of the CNS |
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Common Cytoplasm |
Cardiomyocytes can fuse together to form a continuous branching network --> common cytoplasm - facilitates rapid flow of electrical impulses and ions throughout the myocardium - rapid propagation of action potentials among cardiomyocytes -coordinated contraction and relaxation of atria and ventricles - allowing for instantaneous/simultaneous contraction |
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Gap junctions |
intercellular connection that modulates the flow of electrical impulses through the common cytoplasm |
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Intercalated Discs |
ends of cardiac muscle fibers - support the synchronized contraction of cardiomyocytes (like structural support wall) - essential for autorhythmicity |
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Laminar Flow Rate |
faster it goes in the center of the blood vessel, the slower blood travels on the side - facilitates absorption of O2 and transport of waste metabolites - if its not smooth (like for folks with atherosclerosis) there will be turbulence which screws up the laminar flow rate |
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Atherosclerosis and Chronic Hypoxia |
Plaque build up causes the narrowing of arteries - creates turbulent flow = reduces diffusion rate of gas, ions and metabolites - insufficent blood glucose delivery - restrics flow to distal tissue - increases cardiac hypertrophy, increases peripheral resistance |
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Atherosclerosis and Acute Ischemia |
Completely occlude artery locally or detach and block arteries and/or capillaries downstream -creates embolysms - complete cessation of blood glucose transport |
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Oxygen deprivation in Heart |
heart cells cannot live w/o oxygen for more than 3 min - oxygen deprivation can be acute (ischemic) or chronic (hypoxia) |
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Ischemic Heart Attack |
complete deprivation but acute - fermentation provides ATP for Na/K pumps, but renders insufficient - heart stops beating & cells undergo necrosis - area of necrosis = myocardial infarct |
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Hypoxia (Heart Failure) |
intermittent deprivation but chronic - recovery from fermentation and requires more oxygen than normal to restore phosphagen system - heart muscle atrophies and thus fatigues more easily b/c of impaired vasculature |
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Atrioventricular Valves |
tricuspid before bicuspid - 1-way valves prevent backflow of blood - referred to as S1 heart sounds (they close at the same time) - Tricuspid: Separates the right atrium from right ventricle - Bicuspid: Separates the left atrium from left ventricle |
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AV Valves Open or Closed |
chamber pressure determines whether AV valves are open or closed - closure is mechanically helped by special tendons [chordae tendinae] pulled by papillary muscles |
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AV Valves Open |
during passive filling of ventricles [preload] and during atrial systole [atrial kick] -inflow of blood opens the AV valves - Preload: pressure from the venous system - preload and atrial kick opens AV valves |
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AV Valves Close |
During ventricular systole, ventricles contract = rising ventricular pressure = AV Valves close - close makes S1 sound - closure augmented by chordae tendinae and papillary muscles - ensures blood flows 1 way to lungs and systemic circuit |
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Ventricular Filling |
Ventricles fill with blood - pressure from venous return (aka Preload) and atrial kick opens AV valves - Tendons and papillary muscles relaxed |
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Ventricular Contraction |
Pressure from ventricular contraction close AV valves - tendons tightened by papillary muscle contraction to augment AV valve closure during high ventricular pressure - prevent backflow of blood into atria during ventricular systole (ejection) |
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Semilunar Valves |
1 Way valves prevent backflow of blood - open during ventricular systole (depolarization) - closed during ventricular diastole (repolarization) - aortic and pulmonary arterial pressure greater than ventricular pressure - closure produces S2 heart sound |
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blood flow |
inferior vena cava --> R atrium --> R ventricle --> pulmonary artery --> lung --> pulmonary veins --> L atrium --> L ventrical --> aorta --> systemic circuit |
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Cardiac Action Potential Why is it different from a Skeletal Muscle A/P? |
200-500 ms duration (so longer than skeletal ap) - conducted cell to cell - have a sustained depolarization phase = plateau phase - Ca2+ depolarizes the membrane along with Na+ |
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Steps of a Cardiac Action Potential |
1. Rapid Depolarization: from voltage gated Na+ channels. Na enters cytoplasm 2. Sustained Depolarization: plateau phase. Voltage gated Ca+ channels open slowly and enters the cytoplasm = opposing the repolarizing effects of effluxed K+ 3. Repolarization: Ca2+ channels close but potassium channels remain open. * No hyperpolarization |
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What are the benefits of having a long refractory period and plateau phase? |
~Cardiac muscle relaxes almost completely before another action potential can be produced ~ Prevents cardiac tetany b/c with the refractory period and plateau phase, there's always going to be a brief period where everything is relaxed for blood to flow through - If tetany occurs, full contraction, no passive filling = fatal * These ensure a rhythm of contraction and relaxation |
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SA Node |
The Heart's Pace Maker - myogenic component occurs, spontaneous depolarization - originator of the intrinsic action potential - where Ca2+ blockers can work to manipulate depolarization |
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AV Node |
knocks heart rate down a bit and gets all cells the signal at the same time - lower wall of right atrium - slows rate of action potential generated by SA node, which allows atria to complete their contraction before another action potential is delivered to ventricles - becomes the pacemaker if the SA node is damaged |
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Conduction System of Action Potentials |
1. Action Potentials originates from SA node and travel across atrial wall to AV node 2. Action Potentials pass through the AV node and along the bundle of His to the interventricular septum 3. Bundle of His bifurcates into R and L branches (apex) 4. Purkinje fibers transmit Action potential to outermost portion of ventricular walls and atria |
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What is an ECG? |
record of cardiac electrical activity P: atria depolarizes (systole) QRS: ventricular depolarization = spike (systole), atrial depolarization = relax (diastole) T: ventricular repolarization (diastole) |
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Atria |
Primer Pumps reservoirs of venous blood 1. passive filling of ventricles (~70%) 2. then atrial contraction forcibly ejects remaining blood into ventricles -Passive priming + Atrial contraction (atrial kick) = maximal ventricular filling and stretching ~ more stretch = more forceful contraction = maximum compressive force from preload |
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Ventricles |
Power Pumps - pumps blood into lungs and systemic circulation via arterial flow - establish arterial blood pressure - have denser musculature than atria because they pump against higher pressure |
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Systole |
contraction of chambers - depolarization of cardiac muscle sarcolemma |
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Diastole |
relaxation of chambers - repolarization of cardiac muscle sarcolemma |
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Preload |
The pressure of blood in the ventricles before they contract - Preload is driven by venous return to the heart - Preload augmented by abdominal/ leg muscles & inspiring/expiring (toracoabdominal pump) -Preload determines how much ventricles will passively stretch before ventricular contraction & ensures ventricular stretching - More stretch = more forceful contraction = higher stroke volume |
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Thoracoabdominal pump |
respiration increases venous return to the heart (preload) -important in intrinsic regulation of heart - Inhalation: pleural cavity pressure decreases = pulls blood into the inf. vena cava and R atrium from smaller veins of abs and legs - Exhalation: pleural cavity pressure increases = increases venous return into R atrium |
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How are leg muscles auxillary pumps? |
Leg muscles function as secondary pumps to help in the process of venous return from lower extremities - muscle contraction forces blood up through the veins of calf toward heart - Leg muscle contraction (esp in calves) and venous valves counteract gravity = ensure venous return to heart |
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Afterload |
The pressure that ventricles must overcome to eject blood Increases with: - atherosclerosis, systemic hypertension, increased blood volume, aortic stenosis, mitral regurgitation Chronic afterload makes the left ventricle work harder to pump blood to systemic circuit = cardiomegaly |
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Cardiac Cycle |
1. Preload passively fill atria and ventricles - atria and ventricles in diastole - blood enters atria = AV valves open = flows to ventricle w/ 70% capacity 2. Atria contract maximally filling ventricles - atria contract (systole) = atrial kick = forces ejection of ~30% blood into ventricles - AV valves open, semilunar valves closed 3. Increased Ventricular Pressure - Atria relax = diastole - ventricles contract = increase chamber pressure = AV valves close (S1 sound) 4. Increased Ventricular Pressure opens Semilunar Valves -Ventricles completely contract = chamber pressure reaches apex & greater than aortic/pulmonary artery pressure - maximal ventricular pressure forces semilunar valves to open simultaneously 5. Ventricles relax, Semilunar valves close - Ventricle diastole - aortic/ pulmonary artery pressure greater than ventricular pressure = close semilunar valves = S2 heart sound - relaxation period to allow preload to occur and prevent tetany |
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S1 vs S2 |
S1: first heart sound - closure of AV valves (tricuspid, bicuspid) - lower pitched than S2 (lubb) - beginning of ventricular systole S2: second heart sound - caused by closure of semilunar valves - occurs at beginning of ventricular diastole - higher pitched than S1 (dubb) |
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Pathological murmers |
Valve Stenosis: incomplete valve opening - forward blood flow turbulent - shhh sound before heart sound Valve regurgitation: incomplete valve closure - backflow of blood creates turbulence - shhh sound after heart sound - most common murmur (ex. chordae tendinae doesnt work well/atherosclerosis) -Bicuspid valve regurgitation = most common - Aortic valve stenosis = systolic ejection murmur= 2nd most common |
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If mitral valve is stenosed, when do you expect a murmur? |
stenotic: incomplete opening, S1 lub precede sound - shhh lub dub |
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If a mitral valve has a regurgitation, when would you expect to hear its murmur? |
leaky valves make shhh after heart sound in S1 - lubshhhh- dub |
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Frank Starling Law |
CO = SV x HR Cardiac Output: volume of blood ejected by L ventricle during cardiac cycle - measure of tissue perfusion Stroke Volume: volume of blood ejected by L ventricle per heart beat - determined by compressive force/contractibility - increases w/ cardiomyocyte stretching from preload and atrial kick Heart Rate: frequency of atrial and ventricular contraction/ relaxation |
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How does the Frank Starling Law explain Intrinsic Regulation of the Heart? |
explains how the heart adapts automatically to changes in blood volume entering ventricles during diastole - more ventricular filling = more cardiac output - force of cardiomyocyte contraction increases as these cells become stretched Cardiac output increases naturally from increased preload created by rhythmic breathing and skeletal muscle contraction |
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What does intrinsic cardiac regulation rely on? |
- PRELOAD - Cardiomyocyte stretching as ventricles fill with blood - Atrial kick |
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How is stroke volume modulated? |
Modulated by venous return to heart (preload) and atrial kick. The stretching of ventricles increases their compressive force. - influenced by thoracoabdominal pump (breathing) |
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Orthostatic Hypotension |
Sudden drop in blood pressure when standing from seated/supine position - gravity pulls blood away from brain - delayed baroreceptor response Common in elderly, low bp folks, drug sedation, heart problems, prolonged bedrest Can result in fainting & is most common cause of falls |
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Extrinsic Cardiac Regulation |
1. Receptor senses change in bp via plasma volumes 2. Control center signals release of E or Ach 3. Epinephrine increases heart rate Acetylcholine decreases heart rate (heart is effector) |
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Baroreceptors |
stretch sensitive receptors - located in carotids and aortic arch - senses changes in bp from plasma volumes - low bp = baroreceptor under stretched = less action potentials fire - high bp = baroreceptors over stretched = more action potentials fire |
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Extrinsic Cardiac Regulation and Autonomic System |
Sympathetic Response - Epinephrine - Efferent signaling via cardiac nerves - increase heart rate Parasympathetic Response - Acetylcholine - Efferent signaling via vagus nerve - decrease heart rate |
