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CVS > CVS Physiology > Flashcards

CVS Physiology Flashcards

1
Q

What is the CVS system made up of

A

Heart
Vessels
Blood

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2
Q

What is the function of the CVS system

A

Transport 02 and C02
Transport nutrients and metabolites
Hormones
Heat

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3
Q

What is the cardiac output of the heart

A

5l / minute

CO = SV x HR

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4
Q

What is 02 consumption compared to cardiac output

A

Organs use similar %02 to cardiac output
Kidney’s get more cardiac output
Heart gets 4% CO but uses 10% of the 02 so more prone to disease

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5
Q

What is flow through vessels determined by

A

Pressure difference (MAP - central venous pressure)
High in artery to low in venous system
Resistance of vessels

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6
Q

How is the heart and vascular system wired

A

R+L in series so both outputs equal
Vascular beds parallel so flow at same time
Hypothalamus + pituitary, gut + liver = series as need blood flow after each other

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7
Q

How should flow through CVS system be

A

At any point should be the same

Vary throughout day / clinical situation as arteries constrict and alter resistance

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8
Q

What is the aorta

A

Elastic artery
Very low resistance
High pressure blood to pump through higher pressure of arterioles
Dampens pressure variation in between systole + diastole as energy stored in wells so blood keeps coming out

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9
Q

What are arteries made up like

A

Muscular and non elastic
Wide lumen
Low resistance

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10
Q

What are arterioles made up like

A

Muscular wall with narrow lumen
Constrict to control total peripheral resistance and blood flow to organs
Pressure falls as goes through vascular tree
Small drop through artery but large drop through arterioles as high resistance

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11
Q

What are capillaries made up like

A

Exchange vessels
Very narrow lumen and thin wall
BP very low

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12
Q

What are veins made up like

A

Low resistance so blood can get back to the heart
Wide lumen
2/3 of blood stored in veins = capacitance vessels

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13
Q

What is MAP determined by

A

Cardiac output and total peripheral resistance

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14
Q

How is arteriolar resistance controlled

A

Extrinsic neural control
Extrinsic hormonal control
Intrinsic control - individual tissue

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15
Q

What is extrinsic control

A

Sympathetic release noradrenaline which binds to A1 receptors on smooth muscle
Cause contraction
Para has no effect

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16
Q

What is arteriolar resistance at rest

A

Largely high as tissue don’t require as much 02

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17
Q

What is hormonal control of resistance

A

Epinephrine binds to A1 receptor = constriction
Can also bind to B2 receptor = dilation if tissue needs 02
Angiotensin II = constriction
Vasopressin = constriction
ANP + BNP = dilatation

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18
Q

What is intrinsic control measures of controlling resistance

A

Active hyperaemia
Pressure auto regulation
Reactive hyperaemia
Injury response

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19
Q

What is active hyperaemia

A

When activity increase metabolites released from tissue - H, Co2, K, lactate etc.
EDRF released causing dilatation to match needs
When metabolites decrease tone goes back to normal

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20
Q

What is pressure autoregulation

A

If pressure goes down flow will decrease and metabolites will increase
Cause dilatation to maintain blood supply despite changes in MAP
Body can do to certain extent but if drops too low will fail

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21
Q

What is reactive hyperaemia

A

Occlusion of blood = metabolites increase

Extreme form of auto regulation

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22
Q

What is the injury response

A

C fibres release action potential stimulates substance P

Acts on mast cells = histamine + dilatation

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23
Q

What are special circulations

A

Coronary
Cerebral
Pulmonary
Renal

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24
Q

What happens in coronary

A

Blood is interrupted by systole

Has excellent active hyperaemia with B2 receptors

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25
Q

What is special about cerebral

A

Excellent pressure auto regulation so perfusion maintained if pressure drops

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26
Q

What is special about pulmonary

A

If 02 decreased = constriction so blood will go to well ventilated area

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27
Q

What happens win renal circulation

A

Filtration is dependent on MAP

Arterioles constrict and dilate depending on how much absorption is needed

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28
Q

What is Raynaud’s an example of

A

Reactive hyperaemia
Blood flow decreased so increase in metabolites
Dilate to wash out metabolites
When blood flow returns resistance is very low

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29
Q

Cardiac output

A

SV X HR

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30
Q

How is HR controlled and what achieves tonic control

A

The Autonomic Nervous System

Parasympathetic - sit at 60bpm

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31
Q

How do you increase your HR

A

Decrease para and increase sympathetic
Sympathetic - noradrenaline on B1 on SA node + AVN
Spreads up depolarisation
Also increase contractility (inotropic affect)

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32
Q

How do you decrease HR

A

Increase parasympathetic input
Vagus nerve release Act acts on muscarinic 2 receptor on SA + AVN
Hyperpolaries cell

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33
Q

What causes a tachycardia

A 
Anxiety
Infection
Hypoglycaemia
Hypovolaemia
Hyperthyroidism
Problems with conductance in the heart
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34
Q

What type of conductance issues can you get

A

Wide Complex Tachy - broad QRS

  • Ventricular tachy
  • Wolff parkinson white

Narrow complex tachy

  • Sinus tachy
  • AF and flutter
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35
Q

How do you treat wide complex and narrow complex

A

Wide

  • Amiodarone
  • DC conversion if unstable

Narrow

  • Vagal manouvere
  • IV adenosine
  • DC conversion if unstable
  • AF = BB to control rate + anti-coagulant
36
Q

What is the stroke volume

A

The amount of blood expelled by the heart in a cardiac cycle
Determined by filling of heart in diastole and how easy it is to be expelled in systole
EDV + ESV
Contractility and inotropy
In HF these compensatory mechanism fail so can’t maintain CO

37
Q

What affects stroke volume

A

Central venous pressure - if increases then increases filling of ventricles in diastole
Total peripheral resistance - decreases so easier for blood to be expelled

ESV
Contractility
Afterload

38
Q

What affects contractility of heart

A

Para little effect

Sympathetic - Na on B1 of mycoytes

39
Q

What does sympathetic do to calcium

A

More calcium from ECF = more forceful contraction
Also increases Ca-ATPase on sarcoplasmic retinaculum
Ca removed faster so shorter contraction

40
Q

What else affects contractility

A

Inotropes - epinephrine,
Hypercalcaemia
Thyoid hormones
Glucagon

41
Q

What decreases contractility

A 
Ach by vagus nerve on m2 
Hypocalcaemia
Ischaemia - hypoxia
Hyperkalaemia 
Barbituarates
42
Q

What is Starling’s Law

A

The more the heart fills e.g. EDV, the harder it will contract and the larger the SV
Therefore a rise in central venous pressure will increase SV
This only occurs up to a certain point

43
Q

What is pre-load

A

The degree of myocardial stretch (due to venous filling) before contraction

44
Q

What determines preload

A

The end diastolic volume - the volume of blood in the heart at the end of diastole
Venous return and filling time

45
Q

Sum this up

A 
Increased venous return 
Increased EDV
Increases Preload 
Increased SV
Increased CO 
Self regulating mechanism summing up Starling's law
46
Q

What factors affect venous return

A

Skeletal muscle pump - exercise
Respiratory pump - inspiration decrease pressure so more blood drawn in
Sympathetic - contract veins and increase return (venomotor tone)
Systemic filling pressure from ventricle
Gravity - orthostatic hypotension as decreased EDV when lying flat

47
Q

What decreases preload

A 
Decreased thyroid
Decreased calcium
High or low K / Na
Low body temp
Hypoxia
Abnormal pH
Drugs - CCB
48
Q

What is after load

A

The load against which myocardial cells have to contract
If TPR increases then aorta at higher pressure so ventricle needs to work harder
SV decreases

49
Q

SO

A

Resistance vessels affect after load

Capacitance veins affect pre-load

50
Q

What happens in exercise

A

CO increases 4-6x
HR and contractility increases due to sympa
Venous return increases to maintain preload by sympa causing contraction
TPR falls due to dilatation so decreased after load

51
Q

How does the heart compensate for reduced pumping ability

A

Works with increases EDV

Results in lower ejection fraction and reduced exercise capacity

52
Q

What is the ejection fraction

A

Stroke volume / EDV

53
Q

How do capillaries work

A

Allow gas exchange
One cell thick so quick diffusion
Individual high resistance but in parallel so reduces

54
Q

What are the types of capillaries

A

Continuous - no clefts or channels e.g. in brain so anything polar is stuck inside

Fenetrated - contains cleft and channels e.g. intestine

Discontinous - cleft and massive channels e.g. in liver

02 nd C02 able to freely diffuse across

55
Q

What affects diffusion rate

A

Concentration gradient
Distance
SA of area receiving

56
Q

What forces control movement across capillaries

A

Blood hydrostatic - forces fluid out

Blood osmotic - pressure exerted by proteins which can’t get out so pulls fluid in

Interstitial hydrostatic - forces fluid back into capillary

Interstitial osmotic - pulls fluid out of capillary

57
Q

Whats bulk flow mechanism

A

Hydrostatic pushes fluid out of capillary
Oncotic pressure builds up as protein conc increases
Draws fluid back in
Capillary hydrostatic vs ISF hydrostatic
Capillary oncotic vs ISG oncotic

58
Q

What volumes of blood move in and out of the capillaries

A

20l
17l regained
3l picked up by lymphatics

59
Q

What do lymph capillaries do

A

Same structure but no return valves so fluid goes to the heart

60
Q

What causes oedema

A

Excess fluid caused by lymph obstruction, raised CVP, huypopoteinaemia (no oncotic to pull water in), increased capillary permeability

61
Q

What is shock

A

Inadequate blood flow

62
Q

What can cause shock

A

Cardiogenic - pump failure reduces CO so decreased MAP, CVP may be normal or raised,
Mechanical - pump doesn’t fill, e.g. cardiac tamponade, high CVP and low MAP
Hypovolaemic - loss of blood volume
Distibutive - uncontrollable fall in TPR
Toxic shock - endotoxins released in infection = vasodilation and drop in TPR

63
Q

What are typical symptoms of shock

A

Tachycardia
Rapid and shallow breathing
Reduced BP
Fluid resus and treat cause

64
Q

What is systolic blood pressure

A

The pressure during ventricular systole / heart contraction

65
Q

What is diastolic BP

A

The pressure during ventricular diastole / after contraction but before the next

66
Q

What is the mean arterial pressure MAP

A

CO x TPR
The driving force of blood through the circulation
Pulse pressure + 1/3 of your diastolic

67
Q

What controls short term regulation of BP

A

Autonomic nervous system

68
Q

What detects change in BP

A

Baroreceptor in aortic arch + carotid sinus

69
Q

What happens when there is an increase in BP

A

Increased MAP = greater stretch which baroreceptor detect
Send AP to medullary CVS control centre
Parasympathetic acts to reduce BP

70
Q

What does aortic arch baroreceptor stimulate and carotid sinus

A

Aortic arch = vagus

Carotid sinus = glossopharyngeal

71
Q

What are other inputs to short term control

A

Cardiopulmonary - in low pressure areas of heart and lung which fire if high volume
Central chemoreceptors - if low O2
Muscle chemoreceptors - increased metabolites
Joint receptors - movement

72
Q

What is the valsalva manouvre

A

Forced expiration against a closed glottis

73
Q

What happens in the valsalva manoeuvre

A

Increase in thoracic pressure transported to vessel
Decreased venous return
Decreased EDV, SV, CO + MAP
Common when you strain and go to toilet
Decreased MAP detected by baroreceptors which work to increase BP

74
Q

What is the reflex

A

Deceased vagal = increased HR + CO
Increased sympa = Increased HR, CO, contractility, venoconstriction so increased VR, arteriolar constriction so increased TPR

75
Q

What is the long term control of BP

A

Renin-angiotensin system (RAAS)

76
Q

Where is renin produced

A

JG of kidney

77
Q

What triggers renin production

A

Activation of sympathetic ( reduced MAP post JG)
Decreased distention of afferent / blood flow
Decreased delivery of NACL detected by macula densa

78
Q

What does renin do

A

Converts angiotensinogen to ANG 1

ANG1 - ANG2 by ACE

79
Q

What does ANG2 do

A

Release of aldosterone from adrenal cortex
Na reabsorption in proximal tubule
Increased release of ADH from PP
Potent vasoconstrictor so increases TPR

80
Q

What does aldosterone do

A

Increase NA reabsorption in distal tubule so increased volume

81
Q

What does ADH do (Vasopressin)

A

Increased water permeability of collecting duct

Increased thirst

82
Q

What else triggers ADH

A

Decrease in blood volume - cardiopulmonary

Increased osmolarity

83
Q

What does ANP do

A

Released from myocardial cells when increased distension
Inhibits renin
Dilates afferent arterioles so increased GFR
Increases NA excretion
Decreases MAP

84
Q

What is the link between respiratory system + CVS

A

If hypoxia / hypercapnia = often pulmonary hypertension (constrict) + R heart failure (due to hypertension as increased after load)
Initially compensate but won’t get enough 02 in vessels
Leads to L HF and further pulmonary hypertension
Increased hydrostatic pressure so fluid out = pulmonary oedema
Decreased gas exchange as increased distance
CO2 decreases respiratory drive

85
Q

What do prostaglandins do

A

Local vasoconstrictor to increase GFR and reduce Na reabsorption

CVS (30 decks)

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