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60 Cards in this Set
- Front
- Back
Heart Rate
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Normal range: 60-100 beats.min
Avg range: 70-72 beats.min |
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EDV
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End Diastolic Volume: amount of blood in each ventricle at the end of ventricular diastole
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ESV
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End Systolic Volume: Amount of blood left in the centricles at the end of ventricular systole
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SV
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Stroke Volume: EDV-ESV
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Cardiac Output (CO)
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Stroke volume * Heart Rate
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Avg. Stroke volume
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70-80 ml/beat
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Avg Heart Rate
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70-72 beats/min
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Resting Co levels
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5-6 liters/min
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To change CO, one can...
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*Change HR by 250 percent
*Change SV by doubling |
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Preload
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*Amount of ventricular stretching that occurs BEFORE ventricular systole
*Greater the EDV, greater the preload *Larger teh EDV, larger the storke volume, ventricles will stretch and fill with blood |
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"starlings law of heart"
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*The greater the preload "stretch", the greater the force of contraction and therefore, stroke volume
*As the myocardium is stretched the muscle approaches the optimal length for contraction strength |
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Myocardium is normally below...
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optimal length...provides safty margin, allows heart to expand without failure to completely contract
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Inotropic Factors
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Factors that change contractility, and effect stroke volume
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Positive Inotropic factors
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*Sympathetic Stimulation
*Cause increase in contractility *Activates Beta-1 receptors *Decrese ESV, rise in SV |
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Hormones that increase contractility
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Glucagon: used to stimulated cardiac function in cardiac emergencies
Thyroid Hormones: general increase in cell metabolism |
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Negative iontropic factors
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*Parasympathetic activation
*release of Ach, activation of mAchR *ventricles contract less forecefully *increases ESV, decreasing SV *Beta-1 blockers |
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Afterload
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*Amount of tension needed to eject blood by ventricles
*increase ESV, reduces SV *Problem with damaged, deseased myocardium that cannot generate normal levels of force |
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Infraction
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Death of tissue caused by lack of Oxygen
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Both pathways are active
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Resting heart rate reflects a balance between the two systems.
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What happens when Vagus nerve is cut
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Heart rate increases
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What happens when we block sympathetic receptors
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Heart Rate Decreses
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Negative Chronotopic
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Slows heart rate
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Positive Chronotopic
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Accelerates Heart Rate
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What agents Mediate Chronotropic Changes?
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Ach-Epi-Norrpinephrine
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Negative Chronotropic agents
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*Acetlycholine
*Acetylcholine agonists (pilocarpine) *Beata-1 blockers |
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Positive chronotropic Agents
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*Norepinephrine (Beta 1- Adrenergic Receptors)
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Where are the CNS centers which cause release of Chronotropic agents?
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*In medulla oblangata
*Cardiaacceleratory center: ACTIVATED sympathetic pathways *Cardioinhibitory Cener: ACTIVATEs parasympathetic (vagus nerve) pathways **These centers receieve sensory input from atrial stretch receptors, aortic baroreceptors, and chemoreceptors. |
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Mechanisms which regulate Cardiac Output
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*Bainbridge Reflex
*Baroreceptor Relfex |
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Bainbridge Reflex (Atrial Stretch Relex)
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*Stretch receptors in atria, central center activated
*Effector: SA modal Vells *Increase in heart rate, due to release of norepinephrine *Increase borth heart rate and stroke volume |
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Baroreceptor Reflex
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*reponds to circulatory pressure changes
*Sensory component: Baroceptors, carotid sinus, aortic sinuses, tonically active receptors that fire A.P at normal Circulatory system pressures *Central cardiovascular control venter *Effector: AV node and myocardium |
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Baro. Reflex: if pressure in teh aorta or acrotid sinus increases...
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*Baroreceptors fire more A.P
*Cardiovascular control central integration causes....parasympathetic pathway stimulation, sympathetic pathways decreased activity These activites result in : Decrease heart rate, decreased stroke volume, and decreased cardiac output |
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Baro. Reflex: If pressure in teh aorta or carotid sinus is lowered...
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*baroreceptore fire less A.P
*Cardiovascular control central intergration causes: parasumpathetic inhibition, sympathetic pathway activation *causes...increased heart rate, stroke volume, and cadiac output |
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Hydrostatic Pressure
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Pressure exerted by a liquid in response to an applied force
*an applied forece is heart pumping blood |
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Circulatory Pressure
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Pressure differece between the base of the aorta and teh right atrium. 100 mmHg
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3 components of circulatory pressure
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*Arterial Blood Pressure
*Capillary Hydrostatic pressure (CHP) *Venous Pressure |
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Arterial Blood Pressure
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Pressure pushing blood to capillary bed
*100 to 35 mmHg |
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Capillary hydrostatic Pressure (CHP)
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Pressure within the capillary beds
*35 to 18 mmHg |
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Venous Pressure
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Pressure within the venous system
*18 to 2 mmHg |
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Total Peripheral Resistance (TPR)
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*resistance of the arterial system primarily
*ignore venous resistance- very low |
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Vascular resistance
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*length- resistance increases with increasing length
*diameter- resistance increases with decreasing radius |
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Poiseullies law
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increase the radius by a factor of 2 decreases the resistance 16 times
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Increase vascular resistance
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*Vasoconstriction
*Reduce radial diameter of vessels *increase sympathetic stimulation |
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Decrease vascular resistance
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*Vasodilation
*increased radial diameter of vessels *decrease sympathetic stimulation |
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Arterial Blood Pressure
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*Systolic Pressure (120 mmHg)
*Diastolic Pressure (80 mmHg) |
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Sphygmomanometer
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*Compression of brachial artery measured
*systolic pressure: blood begins to blow through artery, sounds of korotkoff *Diastolic pressure: point at which blood turulence stops, no sounds |
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Pulse Pressure
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Systolic-diastolic
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Mean Arterial Pressure (MAP)
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Diastolic pressure + 1/3 of pulse pressure
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Pressure
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Flow * Resistance
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M.A.P
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Cardiac output * TPR
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CO
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M.A.P/TPR
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TPR
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MAP/CO
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Capillary exchange
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Movement of materials across capillary walls.
forces water and solutes out of plasma (3.6 liters enter a day) |
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Lymphatic System
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*Ensures mixing of plasma and interstital fluid
*accelerates distribution of molecules through tissue *carries bacteria to lymph nodes |
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Capillary exchange (what causes it to occur)
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*Diffusion- concentration gradient
*Filtration- CHP, greatest at aterial side of capillary *Reabsorption- osmosis, blood collois osmotic pressure, greatest at venous side of capillary bed |
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Filtartion Pressure
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Capillary hydropstatic pressure- blood colloidal osmotic pressure
*If positive, water moves out *if negative, water moves in |
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If CHP rises, or BCOP declines...
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fluid moves out of blood, causes edema
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Venous Pressure...resistance to flow caused by gravity over come in 2 ways:
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1. Muscle conpression
2. Repiratory pump |
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Cardiovascular Regulation
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Ensures that tissue perfusion meets demand for oxygen and nutrients
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Vasomotor Tone
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* Adrenergic cells have basal level of activty which cause some contraction of arteriole smooth muscle, allows in crease or decrease in sumpathertic activity.
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Light exercise
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lowers TPR, Increases bloodflow, Increases venous flow
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