physiology Flashcards

Question

how does the body measure blood flow?

Answer 1

infers it from pressure

Answer 2

neural = baroreflex

baroreceptors (arterial) = stretch receptors
↑stretch = ↑firing

receptors: carotid sinus, aortic arch

response is quick - within 1 cardiac cycle, but will reset to a new threshold within 1-2 days if there is a persistent change in pressure

Answer 3

baroreceptors measure pressure (↑stretch = ↑firing = ↑pressure; ↓pressure = ↓stretch = ↓firing)

change in blood pressure is conveyed to the medulla

medulla acts through parasympathetics and sympathetics to alter bp

to ↑P -> sympathetics
- ↑CO by ↑HR, ↓AV conduction time, ↑cardiac contractility
- ↑TPR (alpha receptors - vasoconstriction)
↓venous tone (push blood to arterial side)

to ↓P -> parasympathetics
- ↓CO by ↓HR, ↓AV conduction time
- parasympathetics do not innervate small arterioles/arteries - have no effect on TPR

Answer 4

very low bp - baroreflex is silenced

chemoreceptors respond to very low MAP by sensing very low O2, high CO2, low pH

location: carotid bodies, aortic bodies (outside arteries)

Answer 5

sex
- m >f

age
- systolic ↓
- diastolic ↑until 60yo then get ↑pulse pressure with widening gap

body size
- ↑bp

diurnal variation
- low bp at night (low sympathetic activity)

seasonal variation
- summer < winter - vasodilation (heat), sweating, weight tends to be lower

Answer 6

see positive skew

population paradox - more people die with middle bp than high - simply because there are more people at that range (even though bp - higher risk of cardiovascular event)

Answer 7

input = preload = venous return heart rate contractility (strength of pump) resistance = afterload

Answer 8

works on a cellular level muscle fibre has length-tension relationship - increase sarcomere length (stretch) - increases number of cross-bridges - increased force of contraction

Answer 9

EDV determines CO (stretch -> contractility -> ↑SV) important to allow autoregulation (is an intrinsic function of the heart) - increased filling -> increased pumping you want to match CO to venous return, and LH output to RH output

Answer 10

RVEDP = preload = RA pressure = JVP - can also use catheter, insert across tricuspid valve - directly measure

Answer 11

LVEDP = LA pressure = pulmonary vein pressure = pulmonary wedge pressure to measure - can insert catheter across aortic avlve - or measure LA pressure - or pulmonary wedge - through swan ganz catheter (fem vein -> RH -> pulmonary artery => balloon is inflated, occludes artery and just read pulm vein pressure)

Answer 12

CO < body needs usually systolic failure (decrease contractility) diastolic failure - if reduced LV compliance (scar from infact, stiff from hypertrophy) -> need higher pressure to fill LV -> increased pulmonary pressure)

Answer 13

loss of contractillity - loss of cardiac muscle (most common) - ischaemic heart disease - cardiomyopathy pressure overload - valve stenosis - aortic stenosis - hypertension volume overload - valve regurgitation - shunts (septal defects)

Answer 14

baroreceptor senses low BP -> sympathetic outflow increase contractility increase preload: kidney: = b-receptors - ↑renin -> ↑angII - ↑aldosterone to ↑Na+ renetion -> ↑preload (is also done through ↓GFR) increase TPR to raise BP = alpha-receptors -> vasoconstriction fails because this all increases afterload - apha receptors (SNS) and angII - vasoconstriction afterload ↑O2 demand by the heart - worsen the function - need myocardial remodelling

Answer 15

hypertrophy of cardiac myocytes - due to increased mechanical load - cells grow to increase CO Na+ and water retention - to increase venous return - lose K+ - increase afterload (vasoconstriction from angII) - pulmonary congestion - SOB Activation of nervous system - ↑NA - in the short run is good - increases contractility - in LR - deleterious (vasoconstriction increases afterload, can get vent arrhythmias, direct toxic effect on myocardium)

Answer 16

- treat underlying cause (eg coronary artery bypass, valve replacement, hypertension) - transplant - drugs

Answer 17

mortality: - beta blockers (afterload) - ACE inhibitors (afterload) - aldosterone antagonists (preload) symptoms - diuretics (preload) - venodilators (preload) - ionotropes to remove fluid - diuretics - aldosterone antagonists - ACEI - angiotensin receptor antagonists contractility - digoxin

Answer 18

fluid moves in/out of capillaries according to the balance of hydrostatic + oncotic forces hydrostatic forces = pressure exerted by fluid oncotic = pressure exerted by proteins net force determines where the fluid moves along a vessel: - arterial end - high hydrostatic pressure - fluid tends to flow out - venous end - tends to flow in, lower hydrostatic pressure and relatively higher oncotic pressure

Answer 19

excess venous pressure (eg heart failure) decrease oncotic pressure (plasma protein loss - renal/liver failure) blocked lymphatics (cancer) increased capillary permeability (infection, inflammation)

Answer 20

decreased contractility -> Frank-starling graph shifts down = need higher EDP to get same CO the body will increase its EDP to maintain the CO. up to a certain point, the kidneys can take care of the extra fluid - but >20-30mmHg, get venous congestion => ↑EDP at the expense of oedema pulmonary congestion may occur because at severe cardiac failure, the heart may not be able to ↑EDP enough to compensate for to CO

Answer 21

venous high arterial pressure puts a strain on the ventricle, which may eventually lead to ventricular failure, and thus oedema

Answer 22

decrease cardiac work and improve cardiac function (improve preload, afterload, contractility) reduce signs/symtpoms (oedema, fatigue, ventricular remodelling, arrhythmias) increase survival

Answer 23

ionotrops - increase contractility symptomatic relief for cardiac failure - but they increase work required of the heart