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40 Cards in this Set
- Front
- Back
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What are some nurse characteristics
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Clinical Judgment, Advocacy, caring practices, collaboration, systems thinking, response to diversity, clincial inquirey facilitator of learning
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Layers of the cardiac wall
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Pericardium, Epicardium, Myocardium, Endocardium,
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Cardiac skeleton
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Located at base of the heart and interventricular septum
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Atria
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Act as reservoirs and booster pumps,
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Atria filling of ventrical %
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75% passive, 30% active filling of ventricals,
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Myocardium receives what % of cardiac output
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Recevies 5% of CO and extracts ~70% of O2
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Effect of aortic pressure
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The pressure of aorta outside aortic valvied is significant in coronary arter filling
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How is Coronary arter perfusion pressure is calculated how? What is the standard Range
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Diastolic BP minus the Pulmonary artery occlusive pressure AKA (Pulmonary wedge pressure)……. the normal CAPP is 60-80mm Hg
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What are some determinants of myocardial oxygen demand, and supply
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Demand-HR, Preload, afterload, Contractility, ……….Supply- Patent arteries, Diastolic pressure diastolic time, oxygen extraction-- note (imbalances between supply and demand cause ischemia)
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Coronary ateries anatomy
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.
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Left main coronary divides into… and the divided Coronaries provide what with blood
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LAD, and left circumflex, LAD=Anterior LV, Apex of LV, bundle of His and bundle branches, The left Circumflex supplies the left atrium, sinoatrial node, atrioventicular node,
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The Right coronary artery supplies the
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Right atrium, SA node, AV node,
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What is collateral circulation, and what cause the heart to do it
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Interaterial vessles that connect or anastomose with each other, factors that foster this include, anemia, hypoxemia, and arteriosclerosis,
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Action Potential of myocardial cells……………… Application- What kind of medications work on phase 0, Phase 2, Phase 3 of myocardial depolrization?
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Phase 4 resting, between T and QRS,… Phase 0- rapid depolarization, QRS Na+ into cell, reaches threashold cell depolarizes, Class I antidysrhythmic agets (lidocaine) block this influx of sodium thus preventing depolarization…
Phase 1- Breif repolrization, sodium channels close, K efflux continues…. Phase 2 slowing of repole causing plateau, Calcium influx, K+ eflux, is the ST segment, Class IV antidysrhythmic (Calcium channel blockers, Cardizem, Verappamil- block the movement of calcium and prolong repolarization….. Phase 3 sudden accelaration of repolarization, K+ efflux exceeds the influx of calcium and K+ influx occurs at end of phase 3, repolariztion compled, Class III antidysrhythmics block the movement of K+ and prolong refractoriness (amiodarone)…. Phase 4 resting membrane potential |
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Phase 0,1,2,3,4 What medications effect the phases, what occurs during these phases?
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4 resting, between T and QRS,… Phase 0- rapid depolarization, QRS Na+ into cell, reaches threashold cell depolarizes, Class I antidysrhythmic agets (lidocaine) block this influx of sodium thus preventing depolarization… Phase 1- Breif repolrization, sodium channels close, K efflux continues…. Phase 2 slowing of repole causing plateau, Calcium influx, K+ eflux, is the ST segment, Class IV antidysrhythmic (Calcium channel blockers, Cardizem, Verappamil- block the movement of calcium and prolong repolarization….. Phase 3 sudden accelaration of repolarization, K+ efflux exceeds the influx of calcium and K+ influx occurs at end of phase 3, repolariztion compled, Class III antidysrhythmics block the movement of K+ and prolong refractoriness (amiodarone)…. Phase 4 resting membrane potential, SEE chart for more accurate description.
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What is the rate of pacemaker cells in the various areas of the heart
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SA node-60-100, AV node, 40-60, Purkinje fibers 20-40,
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As related to Action potentials of the Heart what the 3 refractory periods and what do the mean?
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Absolute refractory period- No matter how strong cannot depolarize- phase0-3…Relative refractory period, may respond but will be abnormal (R on T phenomon), may cause Vtach or V-fib correlates with at Late Phase 3 and the dscending limb of the T wave,…. Effective refractory period..
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Determinants of Cardiac output
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HR, Preload, Afterload, Contractility,
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What is Preload as it pertains to Cardiac output… what are treatments to increase or decrease preload
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The stretch on the myofibrils at the end of diastole.. It is measured as the pressure in the ventrical at the end of diastole or-Pulmonary artery occlusive pressure (pulmonary wedge pressure), Things that increase Preload-HF, Hypervolemia… Things that decrease- Hypovolemia, cardiac tamponade, a-fib… Treatment to increase-Vasodilator, Colloids-albumin, plasma, Blood products… Treatment to decrease- Diuretics, Venous vasodialtors, ACE inhibitors (catopril)
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How do you evaluate Preload as it relates to Cardiac output?
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Invasive eval and noninvasive eval… Invasive-RV correlates to Central Venous pressure, Lt Ventricular correlates to Wedge pressure… Non invasive Rt venttfical JVD, Hepatomegaly, Peripheral edema, Lt ventricular, Crackels dyspnea,
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Starlings’s Law
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The greater the stretch on myofibrils the greater the force of subsequent contration.
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Effect of preload on myocardial O2 consumption
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As preload increases myocardial O2 consumption increases.
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What is the definition of Afterload
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The pressure against which the ventricle must pump to open the semilunar valve… This is effected by vascular resistance, ventricular diameter, and mass and viscosity of blood.
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How do you evaluate Afterload, both invasive and noninvasive
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Invasive- Rt Vent After Load correlates to Pulmonary vascular resistance index. Lev ventricular afterload correlates to systemic vascular resitance index…. Non invasive = heart sounds loud P2 and A2,
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Effect of afterload on Stroke Volume and CO
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A high afterload =less stroke volume
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Effect of afterload on myocardial O2 consumption
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As Afterload increases myocardial consiumption increases,
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Afterload as it pertains to Treatment, What do use to increase AL and decrease AL
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To increse- Vaospressors (phenyleprine, norepi, dopamine, and vosopressin) to Decrease – DDilators (Nitro, nitro prusside, hydralazine, CCB, ACE (Captopril) ARB, Intraortic ballon pump,
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Contractility as it pertains to Cardiac output, and treatment methods to increase and decrease contractility
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Increase- SNS stimulation, Sympathomemetic (epinephrine, Decrease- Myocardial ischemia, cardiomyopathy, hyposemia… Treatments. Increase-Digoixin, dobutamine, Glucagon, …Treatments to Decrease. Beta Blockers (metoprolol, CCB-diltiazem and verapamil)
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Contractility as it pertains to Cardiac out put, def… evaluation, invasive, noninvasive,
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Def. Contractile fore of the heart, Is effected by endogenous catecholamines(epi) Evaluation… NonInvasive- Hypoperfusion, Diminshed Heart sounds, EF
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Effect of contractility on myocardial O2 consumption
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As contractility increases, myocardial oxygen consumption increases
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Terms used to describe cardiac effects
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Chronotropic- effect on heart rate…. Inotropic- effect on contractility… Dromotropic- effect on conductivity
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Sympathetic Nervous system. What is it referred to as, what does it cause, think terms that describe cardiac effect, How do drugs relate?
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Fight or flight, innervated by physiological or psycholocial stress, Causes postive chronotropic, inotropic and dromotropic effects… Sympathomimetic drugs augment effects due to receptro stimuation when the pt’s has been depleted.
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Sympathetic nervous system AKA ? what kind receptors and what effects happen?
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Adrenergic receptors, Alpha-vessels-vasoconstriction… Beta1-Heart- Increase HR(chronotropic)Contractility(inotropic effect) Conductivity(dromotropic effect)…. Beta2- Bronchial and vascual smooth muscel- Brochodilation, vasodilation
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Sympothomimetic Agents and Receptor Stimulation. Phenylephrine, nore, epi, dopa, dobuta, isoproterenol (HUGE)(KNOW THIS)
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Phenylephrine-Alpha-++++, Norepinephrine-alpha++++ and Beta1-++…. Epi-Alpha++++, Beta1-++++, Beta2-++…. Dopamine Alpha++, Beta1-++++, Beta2-+… dobutamine, Alpha+, Beta1++++, Beta2++, Isoproterenol, Beta1++++, Beta2++++
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Parasympathetic (vagal) Nerve system
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Maintains steady state… Negative chronotropic, inotropic, dromotropic… Typically not desired in ICU but can decrease O2 consumption,
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Chemoreceptors, Baroreceptor,
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Chemoreceptor-located in carotid and aortic bodies-Sensitive to pH, Paco2 and Pao2, hypoxia, hypercapnia, acidosis cause changes in HR and vetilatory rate…….. Baroreceptor-Locate in carotid sinus and aortic arch- sensitive to arterial pressure-Increased blood pressure causes vagal stimuation, resulting in decrease in HR and contractility.
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BNP, what does it stand for? What does it do?
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Brain natriuretic peptide (first discovered in animal brain), Produced by Ventricular muscle tissue, Triggers for BNP release-increased intravascular volume… Measurement of BNP-used as diagnostics study for HR.
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Action Potential of myocardial cells,Movement of K+, Na and effect of EKG,Phase 0,1,2,3,4 What medications effect the phases, what occurs during these phases?
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4 resting, between T and QRS,… Phase 0- rapid depolarization, QRS Na+ into cell, reaches threashold cell depolarizes, Class I antidysrhythmic agets (lidocaine) block this influx of sodium thus preventing depolarization… Phase 1- Breif repolrization, sodium channels close, K efflux continues…. Phase 2 slowing of repole causing plateau, Calcium influx, K+ eflux, is the ST segment, Class IV antidysrhythmic (Calcium channel blockers, Cardizem, Verappamil- block the movement of calcium and prolong repolarization….. Phase 3 sudden accelaration of repolarization, K+ efflux exceeds the influx of calcium and K+ influx occurs at end of phase 3, repolariztion compled, Class III antidysrhythmics block the movement of K+ and prolong refractoriness (amiodarone)…. Phase 4 resting membrane potential, SEE chart for more accurate description.
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This is sthe question I'm thinking of.
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Oxy hemaglobin dissasocation curve
A) This is one B) This is two C) This is three D) Testing |
