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Year 1 MBChB Cardiology > Physiology > Flashcards

Physiology Flashcards

1
Q

Intercalated discs contain what 2 things + function?

A

Desmosomes (tension) and gap junctions (electrical spread of signal)

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2
Q

AVN has …. cells, is …. conducting and is the only point …..?

A

Smaller, slow and of electrical activity between atria and ventricles

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3
Q

What does sympathetic vs parasympathetic innervation do to HR and AVN delay?

A

Speeds up and decreases vs slows down and increases

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4
Q

What dominates the HR under resting conditions?

A

Vagal tone

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5
Q

What area of the heart does the vagus nerve not supply that the sympathetic does?

A

Myocardium

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6
Q

Which neurotransmitter acts on which receptor in parasympathetic vs sympathetic control of the heart?

A

ACh on M2 receptors vs NA on beta 1 receptor

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7
Q

Name a competitive inhibitor (muscarinic antagonist) of ACh that is used in bradycardia?

A

Atropine

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8
Q

Effect of sympathetic and parasympathetic innervation on the pacemaker potential slope?

A

Parsympathetic decreases and sympathetic increases

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9
Q

Which blood vessel supplies the SAN?

A

Right coronary artery

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10
Q

What creates the striated appearance of cardiac muscle?

A

Myofibrils of actin and myosin in sarcomeres

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11
Q

Shape and colour of actin + myosin filaments?

A

Actin (thin and pale) + myosin (thick and dark)

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12
Q

Which way does actin and myosin slide?

A

Actin slides over myosin

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13
Q

What 2 things is required to allow cross bridge formation?

A

ATP

Calcium

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14
Q

What is the role of calcium in sliding of filaments?

A

Forms cross bridge by binding to troponin and shifting tropomyosin out of the actin cleft

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15
Q

What is meant by the refractory period?

A

Period following action potential where it is not possible to generate another action potential

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16
Q

What are the 2 phases where a new action potential cannot be generated?

A

Phase 2 and 3

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17
Q

What is the clinical benefit of the refractory period?

A

Prevents tetanic contractions of the heart

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18
Q

Define stroke volume + normal value + how to calculate?

A

Volume of blood ejected by each ventricle per heart beat + 70 ml + EDV-ESV

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19
Q

EDV/pre-load is determined by ….. which is determined by which 3 things?

A

Venous return + skeletal, respiratory pump and venoconstriction

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20
Q

Describe the Frank-Starling Law of the Heart + sympathetic effect?

A

Greater EDV the greater the SV + shift curve left

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21
Q

Other effect of stretching the heart fibers to increase SV?

A

Stretch increases affinity of troponin C for Ca

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22
Q

ESV/afterload is determined by?

A

The resistance against which the heart has to pump into

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23
Q

How does the Frank-Starling law compensate partially for decreased stroke volume?

A

EDV increases (due to failure to pump full SV) so force of contraction increases

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24
Q

What does chronotropic mean + can this be affected by sympathetic or parasympathetic innervation?

A

Speed of the heart + both

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25
Q

What does ionotropic mean + can this be affected by sympathetic or parasympathetic innervation?

A

Force of contraction + only sympathetic (para does not supply myocardium)

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26
Q

What is meant by cardiac output + how to calculate?

A

Volume of blood pumped out by each ventricle per minute + SV x HR

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27
Q

How much blood fills the ventricles in passive filling?

A

80%

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28
Q

Pressure in the atria and ventricles + aorta is normally?

A

Close to zero + 80 mm Hg

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29
Q

Duration of diastole and systole?

A

0.5 seconds and 0.3 seconds

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30
Q

Are the ventricles filled in isovolumetic contraction and relaxation + explain the state of the ventricles?

A

Filled in contraction and empty in relaxation + in a closed box (all valves shut)

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31
Q

What produces the dicrotic notch in the aortic pressure curve?

A

Aortic valve closing

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32
Q

Cause of S1, S2, S3 and S4?

A

Systole, diastole, pathologic in younger people but CHF in older, stiff ventricles e.g. LVH

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33
Q

Splitting of S2 is heard on … and is caused by + why?

A

Inspiration and pulmonary valve closing later than aortic + intrapulmonary pressure decreases so venous return increases

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34
Q

Cp needs to be around …. to stop blood flow and below …. to allow blood flow?

A

120 and 80 mm Hg

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35
Q

Which sort of blood flow can be heard through a stethoscope?

A

Turbulent

36
Q

What is the 1st Korotkoff sound?

A

Peak systolic pressure

37
Q

What are the 2nd and 3rd Korotkoff sounds?

A

Intermittent sounds of turbulent flow

38
Q

What is the 4th Korotkoff sound?

A

Muffled sound

39
Q

What is the 5th Korotkoff sound?

A

No sound (minimum diastolic)

40
Q

What are the 4 formula for calculating MAP?

A

2 x diastolic + systolic]/3
1/3 pp + diastolic
CO x SVR
SV x HR x SVR

41
Q

What is the normal range for MAP?

A

70-100 mm Hg

42
Q

What MAP is needed to perfuse organs?

A

At least 60 mm Hg is needed

43
Q

How to calculate pulse pressure?

A

Systolic - diastolic pressure

44
Q

What regulates long term vs short term control of MAP?

A

Blood volume vs baroreceptors

45
Q

Increased MAP causes baroreceptors to …. firing?

A

Increase

46
Q

Which nerves innervate the carotid vs aortic baroreceptors fire through?

A

CN IX (glossopharyngeal) + CN X (vagus)

47
Q

Decreased MAP baroreceptor summary?

A

Decreased firing, decreased vagal tone, increased sympathetic tone (increases HR) and increased veno/vasoconstrictor tone

48
Q

What causes postural hypertension + drug that can cause it (+ example) + key value for postural hypertension

A

Failure of baroreceptors + alpha 1 antagonist (doxazosin) drop of 20 mm Hg

49
Q

How much of the body fluid is extracellular vs intracellular fluid + what 2 things make up the ECFV?

A

1/3 vs 2/3rds + PV and IFV

50
Q

What is the function of renin in the RAAS + where is it released from + 2 stimuli?

A

Stimulates conversion of angiotensinogen to angiotensin I + kidneys + low plasma volume and low Na

51
Q

What is the function of ACE + where is it released from?

A

Converts angiotensin I to angiotensin II + pulmonary vascular endothelium

52
Q

4 effects of angiotensin II?

A

Aldosterone release, vasoconstriction, increased ADH and thirst

53
Q

What is the function of aldosterone in the RAAS + where is it released from?

A

Na+ and water retention + adrenal cortex (above the kidneys)

54
Q

Where is ANP + BNP stored + what stimulates release?

A

Atria + ventricle + distension of the heart

55
Q

Molecule that opposes the RAAS + 3 effects?

A

ANP + increases Na and water retention and decreases renin release

56
Q

What does osmolality mean?

A

The amount of solute in a liquid

57
Q

What 2 things trigger ADH release + where is it normally produced and stored?

A

Low plasma volume and increased osmolality + produced in hypothalamus and stored in pituitary

58
Q

ADH causes which 2 things?

A

Na and water retention and vasoconstriction

59
Q

ADH effect is most important in?

A

Hypovolaemic shock

60
Q

Blood flow is proportional to …. and …. and inversely proportional to the …?

A

Blood viscosity and length of blood vessel and radius of blood vessel

61
Q

What is SVR determined by?

A

Radius of the arterioles

62
Q

What is meant by vasomotor tone + what causes it?

A

Vascular smooth muscle being partially constricted + tonic discharge of the sympathetic system

63
Q

Only place of parasympathetic innervation of vascular smooth muscle?

A

Penis and clitoris

64
Q

Alpha receptors are predominant in?

A

Skin, gut and kidney

65
Q

What is the effect of angiotensin II on vascular smooth muscle?

A

Vasoconstriction

66
Q

How does metabolic hyperaemia override vasomotor tone?

A

Metabolic waste products cause local vasodilation

67
Q

Explain the effect of sheer stress on endothelium?

A

Causes calcium release which activates NOS to synthesise NO from L-arginine
L-arginine causes cGMP which facilitates relaxation

68
Q

Describe myogenic response to stretch?

A

Increased MAP causes vasodilation and decreased MAP causes vasoconstriction

69
Q

Blood flow to the kidney and gut is …. during exercise and …. to the heart and muscles?

A

Decreased and increased

70
Q

How does shock cause cell death?

A

Decreased tissue perfusion causes anaerobic metabolism and cell death

71
Q

How does hypovolaemic shock arise?

A

Loss of blood volume leads to decreased SV

72
Q

How does cardiogenic shock arise + Frank-Starling curve shape?

A

Decreased myocardial contractility leads to decreased SV + rainbow shape

73
Q

How does tension pneumothorax lead to obstructive shock?

A

Increased intrathoracic pressure leads to decreased venous return

74
Q

How does neurogenic shock arise?

A

Loss of sympathetic innervation causes vasodilation and decreased HR

75
Q

How does vasoactive shock arise?

A

Release of vasoactive mediators leads to increased vasodilation

76
Q

Compensatory blood volume loss mechanisms compensate until?

A

30% volume is lost

77
Q

General treatment of shock + exception?

A

ABCDE and fluids (except cardiogenic)

78
Q

Which organ has the greatest oxygen demand?

A

The heart

79
Q

How does the heart increase oxygen supply + 2 ways?

A

Increases coronary blood flow + metabolic hyperaemia or NA on beta 2 receptors

80
Q

Beta 2 receptors are mainly found where in the heart?

A

The small coronary arteries

81
Q

When does peak coronary flow occur?

A

Diastole

82
Q

Which brain matter - grey or white - is very sensitive to hypoxia?

A

Grey matter

83
Q

If MAP rises, cerebral vessels ….?

A

Constrict

84
Q

When does autoregulation of cerebral blood flow fail + cause fainting?

A

MAP less than 60 or greater than 160 mm Hg + below 50

85
Q

Decreased PCO2 results in cerebral vasodilation or vasoconstriction + clinical relevance?

A

Vasoconstriction + hyperventilation causes fainting

86
Q

Normal intracranial pressure?

A

5-15 mm Hg

87
Q

Increasing intracranial pressure does what to cerebral blood flow?

A

Decreases it

Year 1 MBChB Cardiology (15 decks)

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