Don's Lecture 10-13
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| 3 major types of cardiac muscle | atrial, ventricular, and specialized exciatory and conducting muscle fibers
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| atrial and ventricular muscle fibers contract the same as skeletal but | the duration of contraction is much longer
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| excitatory and conductive fibers exhibit | automaticity rhythmical electricl discharges in the form of an AP, or conduct AP through the heart provicing and exciatory system that controls the rhythmic beating of heart
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| cardiac muscles are | striated
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| cardiac muscle fibers are arranged in | latticework
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| cardiac muscle contains | actin & myosin filaments like skeletal muscle
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| intercalated discs (DEFINE) | cell membraines that seperate individual cardiac muscls from one another and form permeable gap junctions
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| Purpouse of intercalated discs and gap junctions formed | gap junctions allow rapid diffusion of ions along the longitudinal axis of uscle fibers so the AP easily travles from one cardiac muscle cell to the next via latticework
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| Intercalated discs form a synctium which is | where cardiac cells are so interconnected, that when one cell becomes excited, the AP then spread throughout the lattice work.
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| What are the two synctiums in the heart | atrial (2 walls of atria) and ventricular (2 walls of ventricle)
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| atria are separated from ventricles by | fibrous tissue and surrounds AV valves
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| Normally action potentials are conducted from the? | atrial synctium to the ventricle synctium via the A-V bundle.
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| A-V bundle | allows for the conduction from atria to ventricles
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| division of the syntiums (atrial and ventricular) allows for atria | to contract a short time before ventricles
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| AP in cardiac muscle are _____ than skeletal | longer (15X)
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| resting potential is | higher more negative -70 to -90.
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| cardiac muscle depolarization has a _____ that is unquie | plateau
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| Plateau is the _____ of the chambers | squeeze
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| Cardiac Muscle action potential is caused by 2 channels | fast Na+ channels & slow Ca++ channels (skeletal has only fast Na+)
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| Calcium channels are | slower to open and slower to close
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| The large amount of calcium and sodium influx maintains a prolonged period of | depolarization or plateau
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| In addition the calcium that is entering the cell from these slow Ca+ channels also | stimulates the contraction
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| Immediately after the onset of AP, the K permeability decreases causing | a decrease of outflux of + charge K+ prevening early return of AP voltage to resting potential
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| Once calcium-sodium channels close | there is a rapid outflux of K+ and cell reaches resting potential.
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| Velocity of atrial and ventricle conduction | 0.3 - 0.5 m/second
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| Velocity of perkinje fibers | 4 m/s (fast) compared to arial and ventricular depolariation)
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| Refactory period | 0.25-0.3 seconds. Period where no new impulse can excite
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| Relative refractory period | 0.05 sec. Period where the muscle is more difficult to excite than normal, but can be exccited by a very strong premature excitatory signal resulting in a PVC or PAC
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| Excitation coupling mechanism of cardiac muscle (mechanism by which AP causes contraction) | 1.) T-tubles acct on longitudal SR to relase CA++ into sarcoplasm 2.) Ca++ diffuse from the ECF in the T-tubules into the muscle cell 3.) Ca++ entering the cell activate ryanodine receptors in SR membrane releasing more Ca++
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| Ryanodine receptors located in & function | in the SR membrane, activated by influx of Ca++ and triggers a further release of Ca++ into the cell.
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| Cardiac muscle needs to have all 3 sources of Ca++ because | The SR in cardiac muscle is less developed than in skeletal, and not enough Ca++ would be provided for adequate contraction
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| T-tubles size in cardiac vs skeletal | T-tubles are larger in diameter, allowing for more Ca++ to diffuse in.
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| Strength of cardiac contraction is determined by? | concentraction of Ca++ in ECF
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| skeletal muscle concentraction is not affected by extracellular Ca++ concentration b/c | Ca++ in skeletal muscle is release from SR inside the cell.
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| At end of plateau of the AP, influx of Ca++ is | cut off, and Ca++ is rapidly pumped back out to the ECF with use of atp-ase pumps and calc/sodium exchange.
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| 2 types of cardiac action potential | 1. pacemaker i.e. SA node. 2. non-pacemaker, i.e. Ca++ influx prolongs duration of AP plateau.
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| SA node is located | in R atrium near opening of the superior vena cava.
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| Spontaneous generation of AP for each cardia cycle is generated here in a healthy individaul | SA node
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| SA node rate is determined by spontaneous changes in | K+, Na+ and Ca+
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| SA spontaneous firing rate is | 100-115. This intrinsic rate is lower due to Parasympathetic control of vagus nerve.
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| SA node is primarily innervated by the | RIGHT vagus nerve
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| spontaneous SA rate can also be changed by | circulating thyroxin (increases), febrile (increase) increased catecholamines norepinephrine (increase, beta 1 effects)
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| AV node is primarly innervated by | LEFT vagus nerve
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| NTS or nucleus tractus solitarius of the medulla | recieves sensory input sending out PSNS (vagus) and SNS stimulation to heart to release catecholamines.
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| the slight delay of the impluse from atria to the ventrile in the AV bundle allows for | the atria to contract first before the ventricles
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| diasole | relation or filling
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| systole | contraction
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| isometric ventricular relaxation | no change in volume, ventricles are relaxed and the AV and semilunar valves remain closed
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| Ventricular filling or diastole | Increased pressure of the full atria, pushes open the AV valves. Rapid filling for first 1/3. Second 1/3 is diastasis or slower filling with smaller amount. Last 1/3 is provided by the atrial kick. Reach EDV.
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| End Diastolic Volume (EDV) | 110-120 mL in a normal heart
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| Isovolumetric Contraction in ventricular systole | no change in volume at this point. ventricles are full, contraction starts, ventricular pressure begins to increase causing AV valves to close (S1 or "lub"), all along semilunar valves are still closed.
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| S1 or "lub" | is heard as AV valves close in isvolumetric contraction in ventricle systole
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| Ventricular ejection | ventricular pressure continues to increase and overcomes aortic pressure opening the semiluar valves. Blood pours out of ventricles, reach end systolic volume here.
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| Ventricular relaxation | b/c all the blood ejected into larger distended arteries from the contraction, blood immediately flows backward from aorta into ventricles (higher pressure to lower pressure) causing a snap shut of the semilunar valves "dub"
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| Snap of the semilunar aortic valve is also called | dicrotic notch
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| AV (mitral & tricuspid) valves prevent backflow of blood from ventricles to atria during | during ventricular systole
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| Semilunar valves (aortic & pulmonic) valves prevent backflow from aorta and pulm areries into the ventricle during | ventricular diastole
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| Valves close when | when backward pressure gradient pushes blood backwards (Higher pressure to low, think blood from full arteries after ventricular ejection tries to go back into the ventricle (low presure) causing the close
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| Valves open when | forward pressure gradient forces blood forward. (atrial pressure builds so much, it forces AV valve open to get into the ventrile (low pressure)
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| AV valves are specialized b/c | they have chordae tendineae
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| purpose of the chordae tendinea | attaches the papiillary muscles to the AV valves. preventing bulging too far back into the atria when the ventricles contract. Keeps blood from leaking back into the atria.
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| Semilunar Valves are specialized b/c | they have rapid closure (snap shut) due to a smaller opening in comparison to AV valves. Much more wear and tear on these valves.
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| CO = | SV x HR
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| Stroke volume (SV) | volume of blood ejected per beat - if normal heart around 70.
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| Aortic stenosis patients are complicated to tx because | They have fixed stroke volumes. Changing HR is the only way to change cardiac output, which can be detrimental in other ways.
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| Stroke volumes 3 factors | 1. Preload 2. Contractility 3. afterload
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| Preload | volume or stretch, EDV (filling volume). Frank Starling Law
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| Frank Starling Law | Greater the stretch, greater the contraction (withing reason, overstretch and will have problems)
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| Atrial kick will affect what of stroke volumes 3 factors | preload
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| contractility | inotropic fx or chemical factors. Na+, K+, CALCIUM (biggest fx), epiniephrine, thyroxine
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| afterload | resistance, SVR, think BP. What ever is impeding your flow
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| Profound hypertension affects which factor of SV | Afterload
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| Dehydrated, increased H&H, hypovolemic | affect preload
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| Conditions that alter CO | HR, BP, Fluid volume statis, HCT, ionotropic factors, status of cardiac muscle, conduction
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| Heart effects from excess K+ in ECF | causes heart to dialate and becomes flaccid. Slows HR, can block conduciton throug AV bundles, making contraction very weak
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| Heart effects from increased Ca++ | spacicity of heart muscle, because Ca+ causes contraction
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| Heart effects from decreased Ca++ | heart becomes flaccid
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| S1 | closure of AV valves, isovolumetric conctraction (ventricles just starting to contract)
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| S2 | closure of semilunar valves in ventricular relaxation after blood has been ejected into arteries.
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| Split S2 | caused by closure of the aortic and pulmonic valve respectively. can be called gallop or S3. CAn hear this even better with deep inspiration because create neg intrathoracic pressure increasing blood return to the R side of heart
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| LCA | supplies anterior and L lateral portion of the L ventricle
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| RCA | supplies most of the R ventricle AND posterior part of L ventricle
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| Coronary circulation dependant on | Stroke volume, HR (fills during diasole), condition of arteriers (plaque or no plaque), collateral circulation
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| Coronary filling occurs with | diastole
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| How to improve collateral circulation | exercise
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| worse case scenario for your patient is | tachycardia and hypotension, (supply/demand)
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| Coronary circulation most important factor is a good | SRV (not too high, not too low) because the back pressure which is the driving pressure in the heart. Forces blood back to the coronary cirulation.
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| Cardiac center regulates | Cardiac output
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| Vasomotor center regulates | B/P, and vessel diameter
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| Cardiovascular center gets information from | baroreceptors & chemoreceptors
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| Baroreceptorss are located | carotid sinus, aortic arch, and R atrium
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| Chemoreceptors | monitor levels of CO2,O2, H+ (pH)
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| Renin-Angiotensine-Aldost-system | 1.) juxtaglomerular cells secrete renin in kidneys. 2.) changes angiotensinogen to angiotensin I 3.) angiotensin I is converted to angiotensin II in lungs which constricts vessels & stim secretion of aldosterone from adrenal cortex
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| aldosteron function | to hold onto Na+, H2O follows salt increasing blood volume.
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| ADH | secreted by hypothalamus, increases volume
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| Aterial natriuretic (ANP) | secreted by atria of heart, vasodilation and increased urine output (decreases BP)
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| Nitric oxide (NO) | secreted by endothelial cells, causes vasodilation. Sets tone in blood vessels. Most potent vasodilator in the body.
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| Electrical current | rate of charge flow past a given point
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| Ampere | measures electrical current, = coulombs/second
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| EKG measures | change in electrical potentials
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| Phase I Action Potenial ions are | K+ and Cl- move out
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| Phase II of AP ions are | Ca+ in (plateau) K+ delayed to release but starts its move
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| Phase III of AP | K+ out reapid repolarization
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| Phase IV of AP | Resting membrane potential
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