Lecture/Lab 11 Blood Pressure / Cardiovascular Flashcards
elasticity vs compliance
- elasticity = how much recoil
- compliance = amount of expansion
elasticity and compliance - passive/active dilation/constriction and intrinisic/extrinsic property
- passive dilation and constriction
- intrinsic property
3 layers of arteries and veins
- tunica externa = connective tissue
- tunica media = smooth muscle
- tunica interna = endothelial cells, sqamous, elastin, subendothelial collagen layer
layers of capillaries
trick question - there are only endothelial cells
large arteries, main properties and why
- muscular and elastic
- during systole/diastole expand and contract to accomodate changes in blood volume
- ^helps blood pressure from fluctuating too much
small arteries and arterioles - many properties and why
- muscular
- heavily innervated by sympathetic system –> smooth muscle innervation –> vasoconstriction and increase bp
arteriovenous anastomoses
- arterioles bypass capillaries and go straight to venules
venous return meaning
return of deoxygenated blood to heart
skeletal muscle pump
contraction and movement of muscles in lower extremetieis squeezes blood up veins towards the heart. 1 way valves prevent blood from flowing back
respiratory pump
- inhalation –> negative pressure –> blood pulled up the chest
veins - main characteristics
- high compliance, thin, holds majority of blood, low blood pressure
TPR and main cause
- total pressure that heart has to pump against
- mainly caused by small arteries and arterioles
3 alternate name for vessels and why
- resistance vessels = small arteries and arterioles because they contribute most to TPR
- capacitance vessels = veins because they hold 2/3 of blood
- exchange vessels = capillaries because exchange occurs here
preload and afterload
- preload = EDV, work before contraction
- afterload = TPR, work downstream from the heart
hypertension effects on heart
hypertension = increased TPR –> left ventricle works harder and hypertrophies –> smaller lumen and decreased cardiac output –> congestive heart failure
precapillary sphincters
- sphincters before capillaries
- constriction = less blood in capillaries and higher bp upstream
3 types of capillaries (just list them)
- continuous, fenestrated, and discontinuous
continuous capillaries - characteristics and where
- sown together by gap junctions which have intercellular channels for small molecule transfer
- muscle, lung, adipose tissue
fenestrated capillaries - characteristics and where
- very permeable and wide intercellular pores for filtration
- kidneys, intestines, and glands
discontinuous capillaries - characteristics and where
- large gaps between cells
- liver, spleen, and bone marrow so produced RBC can escape
stroke volume and 3 factors
- contractility
- EDV aka preload
- TPR aka afterload
ejection fraction
stroke volume / end diastolic volume
frank starling law of the heart
increased EDV –> increased stretch of heart muscle –> increased contracility –> increased stroke volume and cardiac output
cardiac output formula
cardiac output (volume / minute) = heart rate (beat / minute) * stroke volume (volume / beat)
chronotropic effect meaning
- effects heart rate
parasympathetic chronotropic effect and mechanism
Ach –> M2 muscarinic receptor –> K+ enters –> hyperpolarization –> harder to reach threshold and decreased heart rate
sympathetic chronotropic effect and mechanism
epi/norepi –> beta 1 adrenergic receptor –> cAMP increases –> HCN opens faster and steeper pacemaker potential –> increased heart rate
inotropic effect meaning
- effects contractility
parasympathetic inotropic effect and mechanism
NONE
sympathetic inotropic effect and mechanism
- increases contractility by direct innervation of myocardial cells
sympathetic effect on venous return
- increases venous return
sympathetic –> mass activation –> venoconstriction –> increased blood pressure and venous return
blood volume effect on venous return
increased volume increases venous return
2 pressures exerted by fluids
hydrostatic (away) and oncotic (towards)
BHP, BOP, IOP, IHP
- BHP = blood hydrostatic pressure, pushes against walls of vessels
- BOP = blood oncotic pressure aka blood colloid pressure, pulls liquid into blood vessels
- IOP = interstitial fluid oncotic pressure pulls iiquid out of blood vessels
- IHP = interstitial fluid hydrostatic pressure pushes fluid into vessels
forces affecting reabsorption vs filtration
- reabsorption = BOP and IHP
- filtration = BHP and IOP
arterial side vs venule side filtration vs reabsorption
- arterial = filtration higher
- venule = reabsorption higher
what accounts for filtration force being higher than reabsorption force
- some interstitial fluid filtered out through lymphatic system
edema
build up of fluid in interstitial space causing swelling
elephantiasis
parasitic infection blocks lymph nodes and drainage causing swelling due to build up of fluids in interstitial space
hypoalbuminemia - flow
liver disease –> less albumin production –> decrease in BOP –> less reabsorption and edema
albuminuria flow
kidney disease –> albumin in urine –> BOP decrease and less reabsorption –> edema
myxedema flow
- hypothyroidism
- higher IOP –> more filtration and edema
right congestive heart failure flow
- pitting edema, fluid back up in veins
left congestive heart failure and flow
- pulmonary congestion
3 triggers for RAA system
hypovolemia, hypotension, and hyponatremia
RAA flow
baroreceptor in aortic arch or carotid artery –> renin enzyme activated –> angiotensinogen in liver –> angiotensin 1 –> converted by ACE enzyme in lungs to angiotensin 2 –> many effects
3 main affects of angiotensin 2
- direct vasconstriction to increase bp
- stimulates aldosterone release from adrenal cortex so that Na+ and water are reabsorbed by kidneys
- thirst center in hypothalamus stimulated –> increased blood volume and pressure
ACE inhibitors
- prevents conversion of angiotensin 1 to angiotensin 2
- very powerful drug for hypertension
angiotensin 2 receptor blockers
- blocks receptors for angiotensin 2, also very powerful hypertension drug
ANP effects
atria natriuretic hormone
- endogenous hormone that increases urine production and decrease blood volume to decrease bp
- inhibits aldosterone
- also causes vasodilation to decrease bp
2 main factors effecting BHP and blood flow - how do radius and stroke volume/contractility relate
- volume and pressure from opposite directions
- smaller radius = increased pressure and increased BHP
- increased stroke volume and contractility = increased volume and increased bp
Poiseuilles Law - numerator vs denominator, what are the 4 variables, which remain constant, effect of radius
- law for blood flow
- numerator = directly proportional, radius and change in blood pressure DP
- denominator = inversely proportional, length of blood vessel and viscosity
- only radius changes
- radius effect = r^4
baroreceptor reflex flow and reflex tachycardia
baroreceptor in arotic arch / c arotid artery detect drop in bp –> information coded as frequency of AP sent to MO –> sympathetic system activated –> increased heart rate and reflex tachycardia
orthostatic hypotension
- going from lying to standing cause dangerous drop in bp
- no compensatory mechanism or baroreceptor reflex
laminar vs turbulent flow
- laminar = quiet and layered, highest velocity in the center
- turbulent = noisy, caused by obstruction
taking blood pressure steps
inflate cuff greater then systolic pressure so blood vessel collapsed and no sounds heard –> decrease pressure until just lower then systolic, blood squirts out and sounds are heard –> decrease pressure until just under diastolic where all sounds stop
pulse pressure
systolic bp - diastolic bp
mean arterial pressure and why
diastolic bp + 1/3 pulse pressure
- diastolic is longer then systolic
- MAP = average pressure of blood flow through system
systolic and diastolic BP range
systolic = 100-120 mmHg diastolic = 60-80mmHg
prehypertension
120-140/80-90
hypertension stage 1
140-160/90-100
hypertension stage 2
160-180/100-110
hypertension urgency and possible effect
> 180/>110
- can cause hemorrhagic stroke
