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Cardio block > physiology > Flashcards

physiology Flashcards

1
Q

what does pressure in the ventricle depend on (2)`

A

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

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2
Q

when is compliance of the wall important in determining pressure in a ventricle?

diastole/systole

A

during diastole

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3
Q

when is active tension of the wall important in determining pressure in a ventricle?

diastole/systole

A

during systole

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4
Q

how do right and left ventricles differ in their ability to generate force

A

left ventricle = thicker walls
- generates more force<br></br>
<br></br>
is less compliant

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5
Q

what is the afterload on the heart?

what imposes it

A 
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>
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6
Q

what is the preload on the heart?

what imposes it

A 
the stretch on the myocyte fibres before they commence contraction<br>
<br>
= volume load
<br><br>
imposed by ↑venous return
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7
Q

what is the Frank-Starling relationship?

A

more stretch (EDV -> more tension ->↑stroke volume

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8
Q

how can you increase stroke volume?

A
  • ↑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>
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9
Q

what is contractility?

how can you increase it

A 
contractility: degree to which muscle shortens - eg through ↑Ca2+ with each action potential <br>
<br>
occurs through<br>
- SNS activation <br>
- caffeine <br>
- adrenaline
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10
Q

what is isovolumetric contraction?

A

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>

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11
Q

what does a systolic murmur indicate

A 
turbulent flow over valve during systole
<br><br>
likely:<br>
- mitral regurgitation/incompetence
- aortic stenosis
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12
Q

what does a diastolic murmur indicate

A

turbulent flow across vale during diastole<br></br><br></br>

  • mitral valve stenosis<br></br>
  • aortic incompetence
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13
Q

when do the frank-starline gna pressure-volume loops coincide1

A

at the end of systole<br></br><br></br>

here is the maximum pressure that you can get for the volume

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14
Q

why does pressure generated in the isovolumetric contraction phase fall short of where it theoreticaly could be in the ventricle/

A

it overcomes aortic pressure and the aortic valve opens
<br></br><br></br>
allows for reserve (If valve doesnt open for some reason)

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15
Q

what parameters change to decrease venous tone

co,tpr

A

↓CO<br></br>

↓TPR

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16
Q

%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>
A 
veins - 65%<br>
arteries - 13%<br>
caps - 5%<br>
lungs - 10%<br>
heart - 7%
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17
Q

what is the mean circulatory filling pressure (definition, and value)

what factors does it depend on

A

= 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

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18
Q

what is the filling pressure of the heart? what is it important for

A

= cetral venous pressure (pressure in great veins) <br></br><br></br> needed to maintain cardiac output<br></br><br></br> = 1-5mmHg

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19
Q

how is the JVP used as a clinical measure

A

if heart fails - blood banks up - raised JVP<br></br><br></br>JVP will fall if venous return is poor

20
Q

what vasoactive substances do WBC release?

A

NO, histamine, cytokines

21
Q

nitric oxide - what is its action, what is it mediated by>

A

vasodilator<br></br><br></br> modulated by<br></br> - hypoxia<br></br>- physical stimuli<br></br> - circulating/paracrine vasoactive factors (adj cells, blood)

22
Q

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

A

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

23
Q

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

A

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)

24
Q

how do NA and Ach work to modulate heart rate

A

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

25
Q

how does the body measure blood flow?

A

infers it from pressure

26
Q

what is short term control of blood pressure mediated by?
where are the receptors found

how quick is this response?

A

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

27
Q

describe short term blood pressure control

A

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

28
Q

what happens to the baroreflex at very low bp? what controls bp then

A

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)

29
Q

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

A

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

30
Q

what kind of blood pressure skew is seen in the population?<br></br> what is the population paradox

A

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)

31
Q

which 4 broad categories of factors affect cardiac output

A

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

32
Q

cardiac contracility - explain

A

works on a cellular level

muscle fibre has length-tension relationship

  • increase sarcomere length (stretch) - increases number of cross-bridges
  • increased force of contraction
33
Q

what is starling’s law?

why is it important

A

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

34
Q

how can you measure RV end diastolic pressure?

A

RVEDP = preload = RA pressure = JVP

  • can also use catheter, insert across tricuspid valve - directly measure
35
Q

how can you measure LV end diastolic pressure?

A

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)
36
Q

what is cardiac failure?

A

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)

37
Q

by which mechanisms can heart failure occur (3)

A

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)
38
Q

what are some ways that the body attempts to compensate for ↓CO in heart failure

why do these fail over time?

A

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
39
Q

what are some of the body’s inappropriate adaptations to heart failure?

A

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)
40
Q

Treatment for heart failure

A
  • treat underlying cause (eg coronary artery bypass, valve replacement, hypertension)
  • transplant
  • drugs
41
Q

drugs in heart failure - categories

  • those that improve mortality
  • those that improve symptoms
A

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

42
Q

Describe Starling’s forces

how do they change along a vessel

A

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
43
Q

Causes of oedema (4)

A

excess venous pressure (eg heart failure)

decrease oncotic pressure (plasma protein loss - renal/liver failure)

blocked lymphatics (cancer)

increased capillary permeability (infection, inflammation)

44
Q

why does cardiac failure lead to oedema?

when may pulmonary congestion occur?

A

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

45
Q

oedema - is it due to venous or arterial pressure?

A

venous

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

46
Q

what is the aim of treatment in heart failure?

A

decrease cardiac work and improve cardiac function (improve preload, afterload, contractility)

reduce signs/symtpoms (oedema, fatigue, ventricular remodelling, arrhythmias)

increase survival

47
Q

what are ionotropes

what are they used for

A

ionotrops - increase contractility

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

Cardio block (6 decks)

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