physiology Flashcards
what does pressure in the ventricle depend on (2)`
compliance in teh wall<br></br>
- ability of chamber to accept an increased bolume
<br></br><br></br>
active tension in the wall when it contracts<br></br>
- muscle contraction will stiffen the wall and apply force to the blood inside
when is compliance of the wall important in determining pressure in a ventricle?
diastole/systole
during diastole
when is active tension of the wall important in determining pressure in a ventricle?
diastole/systole
during systole
how do right and left ventricles differ in their ability to generate force
left ventricle = thicker walls
- generates more force<br></br>
<br></br>
is less compliant
what is the afterload on the heart?
what imposes it
load encountered by the ventricle as it commences contraction<br> <br> = pressure load<br> <br> imposed by:<br> - arterial hypertension<br> - LV outflow tract obstruction<br>
what is the preload on the heart?
what imposes it
the stretch on the myocyte fibres before they commence contraction<br> <br> = volume load <br><br> imposed by ↑venous return
what is the Frank-Starling relationship?
more stretch (EDV -> more tension ->↑stroke volume
how can you increase stroke volume?
- ↑EDV (move along frank-starling curve)<br></br>
- ↓HR - more time for filling -> ↑EDV <br></br>
- ↑ventricular contractility (shift F-S curve up) <br></br>
what is contractility?
how can you increase it
contractility: degree to which muscle shortens - eg through ↑Ca2+ with each action potential <br> <br> occurs through<br> - SNS activation <br> - caffeine <br> - adrenaline
what is isovolumetric contraction?
whe LV pressure is greater than LA pressure but smaller than aortic pressure<br></br>
<br></br>
= the flat points of the LV volume curve<br></br>
what does a systolic murmur indicate
turbulent flow over valve during systole <br><br> likely:<br> - mitral regurgitation/incompetence - aortic stenosis
what does a diastolic murmur indicate
turbulent flow across vale during diastole<br></br><br></br>
- mitral valve stenosis<br></br>
- aortic incompetence
when do the frank-starline gna pressure-volume loops coincide1
at the end of systole<br></br><br></br>
here is the maximum pressure that you can get for the volume
why does pressure generated in the isovolumetric contraction phase fall short of where it theoreticaly could be in the ventricle/
it overcomes aortic pressure and the aortic valve opens
<br></br><br></br>
allows for reserve (If valve doesnt open for some reason)
what parameters change to decrease venous tone
co,tpr
↓CO<br></br>
↓TPR
%of blood that is in:<br></br>
- systemic veins<br></br>
- systemic arteries<br></br>
- systemic capillaries<br></br>
- lungs <br></br>
- heart <br></br>
veins - 65%<br> arteries - 13%<br> caps - 5%<br> lungs - 10%<br> heart - 7%
what is the mean circulatory filling pressure (definition, and value)
what factors does it depend on
= how much pressure there is if the heart stops and blood settles<br></br><br></br> 7mmHg <br></br><br></br>depends on <br></br>- volume of blood<br></br>- compliance of vessels
what is the filling pressure of the heart? what is it important for
= cetral venous pressure (pressure in great veins) <br></br><br></br> needed to maintain cardiac output<br></br><br></br> = 1-5mmHg
how is the JVP used as a clinical measure
if heart fails - blood banks up - raised JVP<br></br><br></br>JVP will fall if venous return is poor
what vasoactive substances do WBC release?
NO, histamine, cytokines
nitric oxide - what is its action, what is it mediated by>
vasodilator<br></br><br></br> modulated by<br></br> - hypoxia<br></br>- physical stimuli<br></br> - circulating/paracrine vasoactive factors (adj cells, blood)
sympathetic nervous system and heart rate<br></br><br></br> what tissue in the heart is the target for the SNS<br></br> what is the chemical transmitter<br></br>which receptors
target: SA node, conducting tissue, myocardial tissue<br></br><br></br>transmitter: NA, adrenalin<br></br><br></br>b1-adrenoceptors<br></br><br></br>response:<br></br>- ↑rate (SA node) <br></br>- ↑force (myocardium) = positive ionotropic effect <br></br>- ↑conduction velocity (AV node) <br></br>- ↑automaticity at ventricles, AV node
parasympathetic nervous system and heart rate <br></br><br></br>what tissue in the heart is the target for the PS<br></br> what is the chemical transmitter<br></br>which receptors
target: SA node, AV node <br></br><br></br> transmitter: Ach<br></br><br></br>receptor: muscR<br></br><br></br>response:<br></br>- ↓rate (SA node)<br></br>- ↓coduction velocity (AV node)
how do NA and Ach work to modulate heart rate
NA binds b1-adrenoceptor; <br></br> this activates adenylate cyclase<br></br><br></br> adenylate cyclase converts ATP -> cAMP<br></br><br></br>cAMP activates protein kinase A<br></br><br></br>protein kinase A phosphorylates calcium channels -> influx of calcium increases contraction of the heart<br></br><br></br>ACh binds MuscR<br></br>
=> this inhibits adenylate cyclase, thus decreasing calcium influx
how does the body measure blood flow?
infers it from pressure
what is short term control of blood pressure mediated by?
where are the receptors found
how quick is this response?
neural = baroreflex<br></br><br></br>baroreceptors (arterial) = stretch receptors<br></br>↑stretch = ↑firing<br></br><br></br>
receptors: carotid sinus, aortic arch
<br></br><br></br>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
describe short term blood pressure control
baroreceptors measure pressure (↑stretch = ↑firing = ↑pressure; ↓pressure = ↓stretch = ↓firing)<br></br><br></br>
change in blood pressure is conveyed to the medulla<br></br><br></br>medulla acts through parasympathetics and sympathetics to alter bp<br></br><br></br>
to ↑P -> sympathetics<br></br>- ↑CO by ↑HR, ↓AV conduction time, ↑cardiac contractility<br></br>- ↑TPR (alpha receptors - vasoconstriction)<br></br>↓venous tone (push blood to arterial side)<br></br><br></br>
to ↓P -> parasympathetics<br></br>- ↓CO by ↓HR, ↓AV conduction time<br></br>
- parasympathetics do not innervate small arterioles/arteries - have no effect on TPR
what happens to the baroreflex at very low bp? what controls bp then
very low bp - baroreflex is silenced<br></br><br></br> chemoreceptors respond to very low MAP by sensing very low O2, high CO2, low pH<br></br><br></br>location: carotid bodies, aortic bodies (outside arteries)
how do the following factors affect bp?<br></br>- sex<br></br>-age<br></br>-body size<br></br>- time of day<br></br>- season
sex<br></br>- m >f<br></br><br></br>age <br></br>- systolic ↓<br></br>- diastolic ↑until 60yo then get ↑pulse pressure with widening gap<br></br><br></br>body size<br></br>- ↑bp<br></br><br></br>diurnal variation<br></br>- low bp at night (low sympathetic activity)<br></br><br></br>seasonal variation<br></br>- summer < winter - vasodilation (heat), sweating, weight tends to be lower
what kind of blood pressure skew is seen in the population?<br></br> what is the population paradox
see positive skew<br></br><br></br>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)
which 4 broad categories of factors affect cardiac output
input = preload = venous return
heart rate
contractility (strength of pump)
resistance = afterload
cardiac contracility - explain
works on a cellular level
muscle fibre has length-tension relationship
- increase sarcomere length (stretch) - increases number of cross-bridges
- increased force of contraction
what is starling’s law?
why is it important
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
how can you measure RV end diastolic pressure?
RVEDP = preload = RA pressure = JVP
- can also use catheter, insert across tricuspid valve - directly measure
how can you measure LV end diastolic pressure?
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)
what is cardiac failure?
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)
by which mechanisms can heart failure occur (3)
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)
what are some ways that the body attempts to compensate for ↓CO in heart failure
why do these fail over time?
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
what are some of the body’s inappropriate adaptations to heart failure?
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)
Treatment for heart failure
- treat underlying cause (eg coronary artery bypass, valve replacement, hypertension)
- transplant
- drugs
drugs in heart failure - categories
- those that improve mortality
- those that improve symptoms
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
Describe Starling’s forces
how do they change along a vessel
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
Causes of oedema (4)
excess venous pressure (eg heart failure)
decrease oncotic pressure (plasma protein loss - renal/liver failure)
blocked lymphatics (cancer)
increased capillary permeability (infection, inflammation)
why does cardiac failure lead to oedema?
when may pulmonary congestion occur?
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
oedema - is it due to venous or arterial pressure?
venous
high arterial pressure puts a strain on the ventricle, which may eventually lead to ventricular failure, and thus oedema
what is the aim of treatment in heart failure?
decrease cardiac work and improve cardiac function (improve preload, afterload, contractility)
reduce signs/symtpoms (oedema, fatigue, ventricular remodelling, arrhythmias)
increase survival
what are ionotropes
what are they used for
ionotrops - increase contractility
symptomatic relief for cardiac failure - but they increase work required of the heart
