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Year 1 Systems (JBR) > Cardio Physiology > Flashcards

Cardio Physiology Flashcards

1
Q

What does auto-rhythmicity mean?

A

That the heart can generate it’s own heart beat

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2
Q

What is meant by a heart that is in sinus rhythm?

A

Electrical signals coming from the SA node are controlling the rhythm

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3
Q

Parasympathetic stimulation acts via _____ on which receptors on the heart?

A

acetylcholine

M2 muscarinic receptors

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4
Q

What is the effect of parasympathetic stimulation of the heart?

A

Increase potassium efflux, decrease Na and Ca influx, increase AV node delay

Decrease slope of pacemaker potential
Decrease HR

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5
Q

Vagal tone lower to HR from _____ to ______

A

100 to 70

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6
Q

Sympathetic stimulation acts via ______ on beta-1-adrenoreceptors

A

noradrenaline

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7
Q

What is the normal MAP range?

A

75-105

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8
Q

What is defined as hypertension?

A

BP above 140/90

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9
Q

How is MAP calculated?

A

((2 x diastolic) + Systolic) / 3

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10
Q

The pressure gradient (MAP-CVP) pushes blood around the body. What is the main resistance vessel to this?

A

Arterioles

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11
Q

What are the (5) Korotkoff sounds?

A
  1. Peak systolic
    2-3. Intermittent sounds due to turbulent flow
  2. Minimum diastolic pressure (last sound)
  3. No sound due to laminar flow
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12
Q

Short-term BP changes are controlled by?

A

The Baroreceptor Reflex

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13
Q

Outline the baroreceptor reflex?

A

Pressure sensor in aortic arch (CNX), central in carotid sinus (CNIX)
Firing reduced when BP low
Causes decreased vagal and increased sympathetic tone
HR increases
Baroreceptor reflex increases TPR

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14
Q

What can occur as a consequence of the baroreceptor reflex in elderly patients with a worn out baroreceptor reflex?

A

Postural hypotension

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15
Q

Which hormones/systems are involved in longterm control of BP?

A

RAAS
APN
ADH

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16
Q

Explain how RAAS influences BP

A

Renin released from kidneys
ACE converts angiotensin I to 2 stimulating aldosterone from adrenal cortex
Vasoconstriction, increased TPR and ADH
Conserves water

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17
Q

What stimulates RAAS?

A

Renal hypotension
Renal sympathetic nerve stimualtion
Decreased sodium concentration in tubular fluid

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18
Q

Which sensor detects decreased sodium concentration in tubular fluid?

A

Macula densa

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19
Q

Where is APN synthesised and stored?

A

Atrial myocytes

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20
Q

When is APN released?

A

In Hypervolaemia

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21
Q

What does APN result in?

A

Excretion of salt (and therefore water) by the kidneys + decreased renin release

Acts as a vasodilator (counteracts RAAS)

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22
Q

What is the main condition where ADH (vasopressin) is significant?

A

Hypovolaemic Shock

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23
Q

Where is ADH synthesised?

A

Hypothalamus

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24
Q

Where is ADH stored and released?

A

Pituitary gland

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25
Q

When is ADH secreted?

A

If ECFV is decreased or ECF osmolarity is increased

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26
Q

What is the effect of ADH?

A

Acts on kidney tubule to increase tubular reabsorption (antidiuresis - more concentrated uric)
Increased ECF and plasma volume
Increased CO and BP

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27
Q

Which cell junctions allow for low resistance conductance and tension spread in striated muscles?

A

Conductance = Gap junctions

Tension spread - Desmosomes

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28
Q

Contraction and relaxation of myocytes requires?

A

ATP

Calcium

29
Q

What is Stroke Volume?

A

The volume of blood ejected by each ventricle per heart beat = EDV - ESV

30
Q

What are intrinsic regulators of SV? (5)

A 
Length of myofibrils
EDV
Stretch 
Venous return 
Afterload
31
Q

What are extrinsic regulators of SV? (2)

A

Sympathetic - calcium influx - via noradrenaline (inotropic + chronotropic)

Parasympathetic (affects rate not force) via acetylcholine

32
Q

What is the Frank-Starling Law?

A

The greater the EDV the greater the SV until maximal force by optimal fibre length is reached

33
Q

What is after load?

A

Resistance into which the heart is pumping

34
Q

Persistent increase in after load can lead to?

A

LVH

35
Q

How is the AP in the SA node generated (3)

A

Decrease in K efflux, increase in Na Influx (funny current)
Once @threshold, Ca influx raises to AP
K efflux results in fall of membrane potential

36
Q

The Bundle of His and Purkinje fibres spread excitation to the _____?

A

Ventricles

37
Q

The AV node ___ the pulse slightly

A

delays

38
Q

Outline the AP in Ventricular Myocytes

A 
0 - Fast Na influx 
1 - close Na, transient K efflux 
2 - Ca influx - plateau
3 - K efflux 
4 - resting membrane potential (-90)
39
Q

What are the approximate duration times of diastole and systole?

A

Diastole - 0.5

Systole - 0.3

40
Q

What are the 5 stages of the cardiac cycle?

A 
Passive filling 
Atrial contraction
Isovolumetric contraction
Ventricular ejection
Isovolumetric relaxation
41
Q

What happens during passive filling?

A

No pressure
All valves open
80% of filling

42
Q

What happens during atrial contraction?

A

Remaining blood enters ventricles

43
Q

What happens during isovolumetric contraction

A

AV valves shut, S1
Pressure in ventricles > atria
Tension rises around ventricles

44
Q

What happens during ventricular ejection?

A

Pressure in ventricles > aorta/pulmonary
A/P valves open
SV ejected (ESV remains)

45
Q

What happens during isovolumetric relaxation?

A

Ventricles repolarise and pressure falls - A/P shut, S2

Tension falls and ventricular pressure < atrial pressure

46
Q

JVP occurs right after and mimics the ____________

A

atrial pressure wave

47
Q

What is Shock?

A

Abnormality in the circulatory system resulting in inadequate tissue perfusion and oxygenation leading to cellular failure

48
Q

The body can compensate BP until more than __% of blood volume is lost

A

30

49
Q

Hypovolaemia is classified into which 4 severity categories?

A

I - <15
II - <30
III - <40
IV - >40

50
Q

Hypovolaemic shock refers to?

A

Lowered volume due to haemorrhage / non-haemmorhage

51
Q

How is hypovolaemic shock treated?

A

Ideally blood transfusion; can maintain for a wee while with fluids

52
Q

How does the body compensate for hypovolaemic shock?

A

Decreased SV - Tachycardia

Decreased CO - increased sympathetic vascular resistance

53
Q

What is the cause of carcinogenic shock?

A

Heart can’t contract

54
Q

What is the cause of obstructive shocK?

A

Tension on the heart (e.g. tamponade) means it can’t pump

55
Q

What is the cause of distributive shock?

A

Neurogenic - loss of sympathetic tone

Vasoactive

56
Q

How is shock treated?

A

ABCDE

Then treat the cause

57
Q

When do the coronary arteries get blood from the base of the aorta?

A

During diastole

58
Q

Coronary arteries are drained by…?

A

The coronary sinus

59
Q

What are intrinsic adaptations of the coronary circulation?

A

high oxygen extraction
Adenosine and decreased PO2 dilate vessels
Adrenaline dilates by beta 1

60
Q

What are extrinsic adaptations of the coronary circulation?

A

Metabolic hyperaemia matches flow to demand

61
Q

What are adaptations of the cerebral circulation?

A

Circle of Willis (anastomoses btw. basilar and carotid arteries)
Raised MABP - constriction vs. reduced - dilation
Regulators: PCO2 (increase = vasodilation), regional hyperaemia, changes in ICP (increase = decreased perfusion)

62
Q

What are adaptations of the pulmonary circulation?

A

Low resistance/pressure protects against oedema

Hypoxia - vasoconstriction

63
Q

What are adaptations of the skeletal circulation?

A

Low resting blood flow because of sympathetic vasoconstrictor tone
Exercise: local metabolic hyperaemia > sympathetic tone + circulating adrenaline (via beta-2) = vasodilation
Skeletal muscle pump increases venous return

64
Q

Blow flow through capillaries depends on __________ in terminal arterioles

A

pre capillary sphincters

65
Q

Forces favouring filtration

A

Capillary hydrostatic pressure

Interstitial fluid osmotic pressure

66
Q

Forces opposing filtration

A

Interstitial fluid hydrostatic pressure

Capillaryy osmotic pressure

67
Q

What prevents oedema under normal conditions?

A

Lymphatic drainage

68
Q

Oedema forms under which conditions?

A

Raised capillary pressure
Reduced plasma pressure
Lymphatic insufficiency
Permeability

–> Reabsorption is bad

Year 1 Systems (JBR) (21 decks)

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