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60 Cards in this Set

  • Front
  • Back
Heart Rate
Normal range: 60-100 beats.min
Avg range: 70-72 beats.min
EDV
End Diastolic Volume: amount of blood in each ventricle at the end of ventricular diastole
ESV
End Systolic Volume: Amount of blood left in the centricles at the end of ventricular systole
SV
Stroke Volume: EDV-ESV
Cardiac Output (CO)
Stroke volume * Heart Rate
Avg. Stroke volume
70-80 ml/beat
Avg Heart Rate
70-72 beats/min
Resting Co levels
5-6 liters/min
To change CO, one can...
*Change HR by 250 percent
*Change SV by doubling
Preload
*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
"starlings law of heart"
*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
Myocardium is normally below...
optimal length...provides safty margin, allows heart to expand without failure to completely contract
Inotropic Factors
Factors that change contractility, and effect stroke volume
Positive Inotropic factors
*Sympathetic Stimulation
*Cause increase in contractility
*Activates Beta-1 receptors
*Decrese ESV, rise in SV
Hormones that increase contractility
Glucagon: used to stimulated cardiac function in cardiac emergencies
Thyroid Hormones: general increase in cell metabolism
Negative iontropic factors
*Parasympathetic activation
*release of Ach, activation of mAchR
*ventricles contract less forecefully
*increases ESV, decreasing SV
*Beta-1 blockers
Afterload
*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
Infraction
Death of tissue caused by lack of Oxygen
Both pathways are active
Resting heart rate reflects a balance between the two systems.
What happens when Vagus nerve is cut
Heart rate increases
What happens when we block sympathetic receptors
Heart Rate Decreses
Negative Chronotopic
Slows heart rate
Positive Chronotopic
Accelerates Heart Rate
What agents Mediate Chronotropic Changes?
Ach-Epi-Norrpinephrine
Negative Chronotropic agents
*Acetlycholine
*Acetylcholine agonists (pilocarpine)
*Beata-1 blockers
Positive chronotropic Agents
*Norepinephrine (Beta 1- Adrenergic Receptors)
Where are the CNS centers which cause release of Chronotropic agents?
*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.
Mechanisms which regulate Cardiac Output
*Bainbridge Reflex
*Baroreceptor Relfex
Bainbridge Reflex (Atrial Stretch Relex)
*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
Baroreceptor Reflex
*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
Baro. Reflex: if pressure in teh aorta or acrotid sinus increases...
*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
Baro. Reflex: If pressure in teh aorta or carotid sinus is lowered...
*baroreceptore fire less A.P
*Cardiovascular control central intergration causes: parasumpathetic inhibition, sympathetic pathway activation
*causes...increased heart rate, stroke volume, and cadiac output
Hydrostatic Pressure
Pressure exerted by a liquid in response to an applied force
*an applied forece is heart pumping blood
Circulatory Pressure
Pressure differece between the base of the aorta and teh right atrium. 100 mmHg
3 components of circulatory pressure
*Arterial Blood Pressure
*Capillary Hydrostatic pressure (CHP)
*Venous Pressure
Arterial Blood Pressure
Pressure pushing blood to capillary bed
*100 to 35 mmHg
Capillary hydrostatic Pressure (CHP)
Pressure within the capillary beds
*35 to 18 mmHg
Venous Pressure
Pressure within the venous system
*18 to 2 mmHg
Total Peripheral Resistance (TPR)
*resistance of the arterial system primarily
*ignore venous resistance- very low
Vascular resistance
*length- resistance increases with increasing length
*diameter- resistance increases with decreasing radius
Poiseullies law
increase the radius by a factor of 2 decreases the resistance 16 times
Increase vascular resistance
*Vasoconstriction
*Reduce radial diameter of vessels
*increase sympathetic stimulation
Decrease vascular resistance
*Vasodilation
*increased radial diameter of vessels
*decrease sympathetic stimulation
Arterial Blood Pressure
*Systolic Pressure (120 mmHg)
*Diastolic Pressure (80 mmHg)
Sphygmomanometer
*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
Pulse Pressure
Systolic-diastolic
Mean Arterial Pressure (MAP)
Diastolic pressure + 1/3 of pulse pressure
Pressure
Flow * Resistance
M.A.P
Cardiac output * TPR
CO
M.A.P/TPR
TPR
MAP/CO
Capillary exchange
Movement of materials across capillary walls.
forces water and solutes out of plasma (3.6 liters enter a day)
Lymphatic System
*Ensures mixing of plasma and interstital fluid
*accelerates distribution of molecules through tissue
*carries bacteria to lymph nodes
Capillary exchange (what causes it to occur)
*Diffusion- concentration gradient
*Filtration- CHP, greatest at aterial side of capillary
*Reabsorption- osmosis, blood collois osmotic pressure, greatest at venous side of capillary bed
Filtartion Pressure
Capillary hydropstatic pressure- blood colloidal osmotic pressure

*If positive, water moves out
*if negative, water moves in
If CHP rises, or BCOP declines...
fluid moves out of blood, causes edema
Venous Pressure...resistance to flow caused by gravity over come in 2 ways:
1. Muscle conpression
2. Repiratory pump
Cardiovascular Regulation
Ensures that tissue perfusion meets demand for oxygen and nutrients
Vasomotor Tone
* Adrenergic cells have basal level of activty which cause some contraction of arteriole smooth muscle, allows in crease or decrease in sumpathertic activity.
Light exercise
lowers TPR, Increases bloodflow, Increases venous flow