Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
42 Cards in this Set
- Front
- Back
what are the three types of capillaries
|
continuous, sinusoidal, fenestrated
|
|
describe continuous capillaries
|
most common, in muscles and skin, structural basis of blood-brain-barrier, endothelial cells=uninterrupted lining
|
|
describe sinusoidal capillaries
|
leaky/ in liver, bone marrow, spleen, adrenal medula/fenestrated w/ irregular lumens/passage of large molecules and blood cells
|
|
describe fenestrated capillaries
|
eliptical pores or fenestrations/more permeable to fluids and small solutes/ located where active cappillary absorbtion occurs (small intestines, endorine organs, kidneys)
|
|
what do veins and arteries/arterioles serve as (blood aspect)
|
veins-capacitance vessels
arteries/arterioles-resistance vessels |
|
what is/are anastomoses
|
interconnection of vascular channels
arterial-around joints, organs, brian arteriovenous-metarterioles-shunts venous-common and abundant |
|
how does pressure and resistance affect bloodflow
|
R is more important in influencing BF, P results when flow is apposed by R, Flow indirectly proportional to resistance
|
|
What is the relationship between resistance and vessel radius
|
the bigger the vessel the less resistance because less friction against walls
|
|
how do you find the MAP
|
Map=Dp+(PP/3)
|
|
How do you find PP
|
Systolic Pressure-Diastolic Pressure
|
|
What does cardiac output and resistance both influence
|
vascular pressure
|
|
describe short term mechanisms of bp
|
mediated by nervous system and bloodborne chem.//Maintains MAP by altering vessel diameter and CO, alters blood dist. for spec. demands of organs
|
|
Describe long term mechanisms of bp
|
mediated by renal mech./counter fluxuations by altering blood volume/Baroreceptors adapt to prolonged ^ or v in pressure/kidneys restore+maintain it
|
|
What does the vasomotor center do
|
changes diameter of blood vessels, located in medulla, innervates smooth muscles in vessels, actively modifies by baroreceptors, chemoreceptors and higher brain centers
|
|
how do the kidneys directly effect blood volume
|
alters independently of hormones, rate at which fluid filters from bloodstream into kidney tubules is sped up
|
|
how do the kidneys indirectly affect blood volume
|
renin-angiotensin mechanism, bp v so kidneys release renin, renin catalyzes making angiotension II, Angiotension-vasoconstritor that stimulates aldosterone secretion, promotes ADH
|
|
What is autoregulation
|
automatic adjustment of flow to tissue in proportion to its requirements
|
|
describe the metabolic controls and what some are
|
stimuli for auto regulation
NO-vasodilator acts via cGMP 2nd messenger system Endothelins-potent vasoconstrictors |
|
what is myogenic control/response
|
smooth muscle responds to passive stretch arising via ^ intravascular pressure w/ increased tone
|
|
what is hydrostatic pressure
|
force exerted by fluid pressing against a wall, it forces fluids through capillary walls and apposed by HP of the interstitial fluid
|
|
What is osmotic pressure
|
force opposing HP and pulls fluid into capillary, created by presence of large nondiffusable molecules
|
|
Explain Hydrostatic pressure and osmotic pressure interactions
|
determine Net filtration pressure by, NFP=(HPc-HPif)-(OPc-OPif), at any point along capillary fluid leaves if net Hp>net OP, enters capillary if net OP> net HP
|
|
What is systole
|
ventricular contraction
|
|
what is diastole
|
ventricular relaxation
|
|
what is autorhymicity and what does the SA node have to do with it
|
automaticity- ability to initiate its own beat
rhythmicity- regularity of such pace-making activity SA node generates impulses at greatest frequency |
|
How do the different branches of the heart affect the heart rate
|
SNS-increase rate and force
PNS-decrease rate |
|
what information does an ECG provide
|
anatomical orientation of heart, relative size of chambers, various disturbances of rhythm and conduction, ischemic damage to myocardium, influence of drugs, effects of electrolyte concentrations
|
|
how long does the cardiac cycle last
|
.8s in total, .1 for atrial systole, .3 for ventricular systole, .4 for total heart relaxation
|
|
What are the steps in the cardiac cycle
|
ventricular filling(atrial systole), ventricular systole, early diastole
|
|
describe ventricular filling
|
atrial systole/mid to late diastole, sl valves are closed, 80% of vent. filling is passive, P-wave creates slight atrial pressure that empties atria of residual blood
|
|
describe ventricular systole
|
atria relax, ventricles contract, pressure rises rapidly closing AVs opening sl valves, flows through pulmanary circuit
|
|
describe isovolumetric relaxation
|
early diastole, follows t-wave, ventricles relax, ventricular pressure decreases closing SL valves
|
|
How do you find cardiac output
|
CO=HRxSV
|
|
How do you find stroke volume
|
SV=EDV-ESV
|
|
what is stroke volume
|
volume of blood pumped out by one ventricle w/ each beat
|
|
how does norepinephrine contribute to increasing contractility
|
Ne bind B1 adrenergic receptors, and cause threshold to be reached more quickly and SA fires more rapidly
|
|
what are the ionic basis of the fast response (phases)
|
phase 0-genesis of the upstroke
phase 1-genesis of early repolarization phase 2-genesis of the plateau phase 3-genesis of final repolarization phase 4- restoration of ionic concentration |
|
what is/happens during phase 0 during fast response
|
Na+ enters myocyte via fast Na+ channels, goes from -90 to 0, continues in and Na+ gate starts to close at 20, completely closes at 30
|
|
what is/happens in phase 1 of fast activation
|
genesis of early repolarization, brief period of limited repolarization due to transient outward current (K+), activation of K+ channels cause brief efflux
|
|
what is/happens in phase 2 of fast activation
|
genesis of Plateau,Ca++ enters myocardial cell but slower, membrane potential plateau's as eflux of K+ is balanced by influx of Ca++
|
|
what is/happens in phase 3 of fast activation
|
genesis of final repolarization, when eflux of K+ is great than influx of Ca++
|
|
what is/happens during phase 4 of fast activation
|
restoration of ionic concentrations, by 3Na+ out for 1K+ in/ Ca++ eliminated by 3Na+ for 1Ca++/ Ca++ is eliminated via ATP driven Ca++ pump
|