ch 19- the cardiovascular system, blood vessels 2-5 Flashcards
what r the 3 BP regulation factors
cardiac output, peripheral resistance, blood volume
what happens if wanna increase BP
must increase blood volume, CO, SV, and HR
factors affecting peripheral resistance (R)
Blood viscosity, blood vessel length, blood vessel diameter
neural regulation
short term regulation, cardiovascular center of medulla oblongata, makes 2 centers cardiac and vasomotor
cardiac center of cardiovascular center in neural control
cardioaccelatory center is sympathetic, cardioinhibitory is parasympathetic, controls HR and CO. parasympathetic will slow HR and CO and BP sympathetic does opposite q
vasomotor center of cardiovascular center in neural control
controls vessel diameter, arteriole diameter, causes vasoconstriction in sympathetic, increases BP.
what are the 3 receptors that modify cardiovascular center
baroreceptor, chemoreceptor, higher brain center
baroreceptor
stretch walls of large arteries in neck and top thorax, activated when pulled or stretched, more pressure means more stretch. this INHIBITS cardioacceeratory system- so BP slows bc sympathetic makes HR slow
chemoreceptor
changes CO2 levels, blood pH, O2 content. if CO2 increases, pH decreases, and O2 decrease stimulates cardioaccelatory center SO BP increases bc CA center is fast
higher brain center
activates sympathetic division, an emotional state will raise BP and we cannot control it
hormonal long term control of BP
EPI and NEPI increases BP, angiotensin II makes BP increase, atrial natriuretic peptide (ANP) slows BP, Antidiuretic hormone (ADH) increases BP.
angiotensin II
kidney produces it, stimulates intense vasoconstriction, blood vessel diameter decreases so BP UPPP
atrial natriuretic peptide (ANP)
produced by atria of heart, increases excretion of solute/water. more solute in urine, so water follows and therefore blood volume decrease as well as BP . vasodilation here will decrease R
antidiuretic hormone (ADH)
anti urine formation, produced by hypothalamus, increases water reabsorption by blood to kidneys, BP up bc BV up
long term BP regulation renal mechanism
alters blood volume in kidneys, kidneys filter blood to form urine! constantly adjust to maintain 5 L. when BV up, kidneys filter more blood so more urine is made, and BV and BP will decrease
indirect mechanism of renal mechanism
renin-angiotensin-aldosterone mechanism increases BP, renin catalyzes angiotensin I, which goes to angiotensin II, so aldosterone releases and Na+ absorbed more in kidneys, so BV up and BP top bc water follows solute, also ADH comes in and thirst center of brain and stimulates vasoconstriction.
hypertension
consistent high BP, crisis is over 180/120
chronic hypertension can lead to heart failure, vascular disease, and renal failure
primary or essential hypertension
high BP that has multiple influences, can be heredity, diet, obesity, age, stress, smoking. cannot cure- can treat with weight loss and lifestyle changes, diuretics, ACE inhibitors
diuretics and ACE inhibitors
diuretic- increase urine and so decrease BV and BP
ACE is angiotensin converter, I to II, if no more angio II, BP must lower
secondary hypertension
caused by diff underlying condition, such as obstructed arteries, kidney disease, hyperthyroidism. can be treated or cured by underlying condition
pduomeyom
pudo
hypotension
consistent low BP, 90/60 or lower, not as serous as hypertension, issue when circulation is bad and tissues don’t get what is needed
orthostatic hypotensiuon
dizzy feeling from fast head change position, blood drops bc of gravity, sympathetic NS can correct this fast
chronic hypotension
low BP caused by some underlying condition, like hypothyroidism, malnutrition, inadequate renal function
shock
inadequate circulation of blood to body tissues, the O2 needs and disposal needs r not met. can cause cell death and tissue death
hypovolemic shock
shock resulting from severe hemorrhage or 3rd degree burns or too much vomit/diarrhea. BP dangerously low, weak pulse and intense vasoconstriction
vascular shock 3 types n what is it
poor circulation due to extreme vasodilation, the BV is normal the vessels are the issue
anaphylactic shock- allergic reaction way too much histamine so vasodilation
neurogenic shock- Autonomic NS incorrectly regulated, para won’t oppose sympathetic usually spinal cord issues
septic- severe blood infection caused by bacteria
cardiogenic shock
heart is insufficient to provide blood to tissues, causes myocardial damage. heart cannot propel enough.
why do we need blood to flow through tissues
gas exchange in lungs, kidney filter, deliver O2 and nutrients to cells, absorbs digestive tract, removes waste
why do all tissues not receive same amount of blood at same time
if they did, Bp would decrease so much that circulation would be awful or stop. instead, it is controlled intrinsically and extrensically
autoregulation of blood flow
automatic adjustment of blood flow to organs, independent of hormones or neural mechanisms
changes arteriole resistance, can occur due to chemical changes or physical. (metabolic vs myogenic)
metabolic control of blood flow
auto regulation due to inadequate blood supply, leads to waste buildup in tissues and tissue hypoxia
causes nitric oxide (NO)release. that is a very strong vasodilator. it goes to arterioles and increases blood to capillary beds, which is temporary and localized to tissues that need it
myogenic control
physical control of the stretch of smooth muscle in arteries and arterioles
increase pressure- increase stretch in walls of vessel, blood supply to capillaries decrease when organ has tooooo much
decrease pressure- decrease in smooth muslce of vessel walls, blood supply to capillary bed increases when organ does not have what it needs
where will blood flow the absolute slowest
capillaries, they r the exchange vessels, we have billions, and their combined cross sectional area is the greatest.
diffusion in capillary exchange
moves high to low, gases nutrients and waste passes from blood to tissues through tiny capillary walls.
O2 FLOWS FROM BLOOD INTI TISSUES, CO2 FLOWS FROM TISSUES TO BLOOD FOR DISPOSAL
can also move in intracellular clefts, fenestrations, vesicle
how is movement of fluid in and out of capillary beds done
pressure! hydrostatic and colloid osmotic.
20 L of fluid is filtered out arteriolar end of capillary bed, 17L is returned to capillary bed at venous end.
important determinant of fluid volume in bloodstream and interstitial fluid
bulk flow, pressure
hydrostatic pressure (this is really hard)
pressure exerted by blood pressure against vessel wall, the PUSH out the capillary.
capillary hydrostatic pressure (HPc)- pressure forces fluids out of capillary to interstitial space, higher at arterial end of capillary bed
interstitial fluid hydrostatic pressure (HPif)- opposing pressure that forces fluid from interstitial to capillary. pressure negligible
colloid osmotic pressure (also hard)
draws water into a PULL direction, back into capillary at venous end, plasma proteins act as solutes, pulls water from interstitial to capillary.
small opposing force,
interstitial fluid osmotic pressure (OPif)- pulls water out of capillary. negligible force
net filtration pressure
pressure created by hydrostatic and osmotic
NFP= (HPc+OPif) - (HPif+OPc) USUALLY 10 MMHG. as long as that NFP is a positive value, means net loss of fluids
do fluids really get lost from NFP?
well, more fluid is pumped out than is returned, lost fluid goes into lymphatics, which is returned (the 3L from 20-17) eventually
