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HDT 2.2 > functioning of the heart > Flashcards

functioning of the heart Flashcards

1
Q

what is the composition of blood vessels?

A
  1. elastin; can stretch and recoil
  2. collagen; tough and flexible
  3. endothelium - single cell layer + mainly in capillaries
  4. smooth muscle; contracts/reflexes and is in all blood vessels except capillaries; surrounds lumen circularly
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2
Q

what do the endothelium release in response to shear stress?

A

they will release NO or PGs to act on smooth muscle and cause tonic dilation
and they will cause inhibition of RBC, platelet and neutrophil adherence so atherosclerosis can occur

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3
Q

what is endothelium dysfunction?

A
  • it is when impaired dilation can occur
  • vasoconstrictor PGs, endothelin and adhesion molecules which attracts platelets and neutrophils to artery walls
  • so inflammation, atherosclerosis and CV risk
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4
Q

what is the structure of the elastic arteries?

A

you have the intima, media and the adventitia
intima is endothelium, media is smooth muscle and elastin and adventitia is collagen

  • the elastic arteries converts intermittent flow from heart to continuous for the rest of circulation
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5
Q

how do elastic arteries act in systole and diastole?

A

systole; elastin stretches and the systolic pressure rises in the elastic artery. valves are open
diastole; elastin recoils giving energy to blood, pressure kept high by elastic recoil and valves are closed

-collagen limits stretch of artery in systole

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6
Q

what is the arteriole pressure wave?

A

graph where at systole pressure increase until it hits a peak
then small decrease as aortic valve closes and then increases for small peak and then decrease during diastole
when it decreases to 80mmHg this is when aortic valve opens

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7
Q

how to calculate pulse pressure and mean ABP from SP and DP?

A

PP = SP- DP

mean ABP = DP + 1/3(PP)

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8
Q

what factors influence ABP?

A
  • inflow into aorta during systole (CO)
  • the TPR of blood leaving aorta during diastole
  • composition of aorta
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9
Q

what happens as patients age?

A

they have stiffer aorta so less stretch and recoil; lose elastin

  • high TPR so high DP
  • higher SV so increase ventricular contractility
  • high SP but lower DP
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10
Q

what muscles determine the TPR?

A

the arterioles- most pressure is lost here

muscular arteries contribute to a small extent

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11
Q

what are arterioles surrounded by and what do they supply?

A

they are surrounded by interstitial fluid and tissue cells

supply capillaries

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12
Q

what do arterioles regulate?

A

TPR, tissue blood flow and capillary pressure

  • can have arteriole constriction in different tissues; increases ABP - more constriction so more resistance so can lose more pressure and tissue flow so decreased pressure in capillaries
  • can have constriction and dilation of arterioles in different tissues; ABP doesn’t change much
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13
Q

how can you regulate arteriolar resistance?

A

use sympathetic noradrenergic nerve fibres
- form a network around vessels
sympathetic activity- release of Nor from nerve fibres so more intracellular Ca2+ so more vasoconstriction

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14
Q

when are sympathetic nerve fibres used?

A
  1. maintains TPR and ABP
    - used in reflex response to correct any ABP changes
    when ABP falls more sympathetic activity for vasoconstriction to increase ABP and TPR
  2. reflex response to body temp change
    - when hot less sympathetic activity so more dilation and this redistributes more blood flow to skin to cause heat loss
    vice versa for cold
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15
Q

what is the local metabolic influence on arterioles when you have functional hyperaemia?

A
  • arteriolar dilation occur
  • substances released into interstitial space when tissue cell activity increases ; K+, adenosine, tissue specific substances
  • dilation means more blood flow; increased shear stress and more release of NO and PG so more dilation
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16
Q

when and where does functional hyperaemia occur?

A
  1. skeletal muscle ; exercise
  2. cardiac muscle ; exercise and condition
  3. sweat glands ; body temp change
  4. salivary glands ; chewing
  5. smooth muscle and gut wall glands ; digestion
  6. brain ; activated neurones
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17
Q

how do cerebral arterioles respond when ABP rises or falls?

A

when ABP rises, there’s a stretch so smooth responds to this by increasing pressure ; this is auto regulation
- blood flow will remain constant
- as pressure increases you have myogenic constriction so increase resistance
too high pressure can lead to stroke and too low too much myogenic dilation so feels faint

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18
Q

what’s the process of cardiac conduction?

A 
impulse generated at SA node
atrai contracts 
impulse to AV node
brief delay 
sweeps to bundle of his 
goes to left and right bundle branches 
conduction to purkinje fibres
ventricles contract
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19
Q

what is sinus bradycardia?

A

<60/min
due to depressed SA node function
can have a vagal tone

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20
Q

what is sinus tachycardia?

A

> 100/min
accelerated SA node firing
due to exercise, stress or HF

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21
Q

what is first degree heart block?

A

greater PR interval delay
>0.2s or one big ECG block!
slow conduction in AV node so heart block

22
Q

what is second degree heart block?

A

intermittently skipped ventricular beat
intermittent non-conducted P waves so a QRS complex absent
when fraction of impulses from atria are conducted

23
Q

what is third degree heart block?

A

atria and ventricles depolarise independently
no association
alchemic damage in nodal tissue

24
Q

what is cardiac cycle made up of?

A

systole and diastole
systole- ventricles contract so blood -> aorta and P arteries
diastole- relaxed ventricles

25
Q

what are the phases of a cardiac cycle?

A 
Phase 1= atrial contraction
Phase 2= isovolumetric contraction 
Phase 3 = rapid ejection
Phase 4 = reduced ejection 
Phase 5 = isovolumetric reflex 
Phase 6 = rapid filling 
Phase 7 = reduced filling
26
Q

how does para/sympathetic activity affect HR?

A 
parasympathetic = decrease HR 
sympathetic = increased HR
27
Q

what does the autonomic nervous system do?

A

it modifies HR
contains parasympathetic centre; SA node firing is less so lower HR
sympathetic centre; more depolarisation occurs so HR increases as more pacing of SA node

28
Q

what are chronotropic agents?

A

they influence the currents and alter slope of pacemaker and so the heart rate
e.g. noradrenaline

29
Q

what is positive inotropic agents related and what is negative inotropic agents related to?

A

+ve agents are related to sympathetic; release Nor and activate the adrenergic receptors which increase myocyte contraction and so heart rate
-ve agents release Ach and binds on to muscarinic receptors which attenuates contract so less binding of calcium to myofilament so decreased HR

30
Q

what does contraction of myocyte happen because of?

A

calcium binding to myofilament

31
Q

how is cAMP produced?

A

hormones cause beta receptors to make adenylcyclase change ATP to form cAMP
cAMP allows phosphorylation to occur and troponin to be produced
so contractions can occur

32
Q

how to calculate SV?

A

SV = EDV - ESV
EDV should usually be 120ml
ESV should usually be 50ml

33
Q

what is the usual atrial and ventricular pressure and aortic pressure?

A 
atrial = 0-10mmHg 
ventricular = 0-120 mmHg 
aortic = 80-120 mmHg
34
Q

how does preload and afterload influence SV?

A

preload - filling of ventricles
- pressure increases
- initial stretching of myocytes before contraction
afterload - resistance of blood leaving ventricles into arteries
- aortic pressure must be overcome to eject blood
- higher AP so higher afterload

35
Q

when does afterload and preload increase?

A

pre load increases in hypovolemia- high venous pressure and low heart rate
after load increases in hypertension

36
Q

what is the Frank Starling mechanisms?

A
  • muscle stretching increases calcium sensitivity
  • due to ATP energy heart muscles contract more forcefully when muscle fibres stretch
    a higher EDV means more muscle fibre length so more cross bridges can be formed between actin and myosin -> more ventricular contractility
37
Q

how does heart failure affect EDV?

A

heart failure increases EDV and so decreases SV as less contractility

38
Q

what does having a myocardial injury lead to?

A
  • reduced CO
  • less renal perfusion
  • activates RAAS and SNS
  • increase HR and myocardial toxicity
  • vasoconstriction occurs so more afterload
  • this worsens LV function when inhibited by BB, ace inhibitors, aldosterone antagonists
  • can all lead to HF symptoms
39
Q

how does exercise effect CO?

A

central command -> medulla -> more sympathetic outflow and more vagal tone -> higher HR and more contractility -> more venoconstriction and more blood supply and oxygen to working muscles -> release of vasodilation metabolites so vasodilation -> increase in CVP -> more cardiac work and more CO

40
Q

what exchange occurs in the capillaries?

A
  1. solutes such as oxygen, glucose and amino acids enter interstitial space via diffusion and waste products pass to plasma by diffusion
  2. fluid - plasma without proteins will go across endothelial cells to IF and back in opposite direction by filtration
41
Q

what are the characteristics of capillaries?

A
  1. endothelium
  2. 3-6mm
  3. intermittent blood flow; can become continuous so allows easier exchange
  4. has large SA
  5. low speed of blood flow to allow exchange to occur
42
Q

how does arteriolar constriction affect capillaries?

A

pressure at capillary opening decreases
no flow
RBC block flow
so capillary SA for exchange is reduced

43
Q

when does diffusion rate increase?

A

arterioles dilate and tissue blood flow increases
- functional hyperaemia
and vice versa for diffusion rate decreasing

44
Q

what is filtration?

A

when fluid moves across capillary endothelium
depends on:
balance between hydrostatic and osmotic forces across wall of capillary
- measured in mmHg

45
Q

what does oncotic and hydrostatic pressure do?

A

oncotic pulls water into arteriolar and hydrostatic pressure pushes water out down a gradient

46
Q

how is oedema caused?

A

when there is net fluid out > net fluid in
increase in vascular permeability and lymphatics are blocked
protein leaks out - so tissue OP increases
POP and TOP gradient reduced
outwards filtration > lymph drainage
so oedema

47
Q

where do right lymphatic duct and thoracic duct enter?

A

right lymphatic duct enters into right subclavian vein

thoracic duct enters into left subclavian vein

48
Q

what kind of shape are venules/veins and how do they change?

A

they are supine usually but can become circular as they fill with blood more
determine EDV in diastole

49
Q

when you stand how does this affect ur pressure?

A

when you stand gravity will increase pressure in all vessels below heart
arteries can withstand stretch due to strong muscle
but venous vessels will have venous pooling -> leg vein pressure increases so venous distension; decrease CVP so redistribution of blood vol.

50
Q

how can heart failure affect CVP?

A

impaired ventricular contraction
- distended ventricles and central veins
so high increase of CVP

51
Q

how does skeletal muscle pump and respiratory pump increase CVP?

A

skeletal muscle pump- contraction of leg muscles pushes blood in veins toward heart
respiratory pump - inspirations pulls blood in veins towards heart so high CVP

HDT 2.2 (10 decks)

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