Physiology Flashcards

1
Q

Why does pulse pressure increase during acute exercise?

A

increased CO - increased systolic BP, vasodilation - decreased systemic vascular resistance - decreases diastolic BP

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2
Q

Cerebral perfusion pressure = ?

A

MAP - intracranial pressure

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3
Q

What is the role of atrial contraction?

A

complete end diastolic volume

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4
Q

What is a negative chronotropic effect?

A

decreases HR

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5
Q

What decreases resistance to blood flow?

A

increased radius of blood vessel

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6
Q

Why is a long refractory period important in cardiac muscle?

A

prevents tetanic contraction (sustained muscle contraction) - would cause cardiac arrest

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7
Q

How is the brain protected from fluctuating ion levels in the blood?

A

blood brain barrier impermeable to ions

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8
Q

Where is ADH/vasopressin stored?

A

posterior pituitary gland

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9
Q

What forces favour transcapillary filtration?

A

capillary hydrostatic pressure and interstitial fluid osmotic pressure

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10
Q

How do baroreceptors prevent postural hypotension?

A

decreased MAP - reduces rate of firing in baroreceptors - sympathetic tone to the heart increases - increases HR and SV - sympathetic constrictor tone increases - increases systemic vascular resistance - increases venous return - increases SV

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11
Q

What happens when systolic press > cuff pressure > diastolic pressure?

A

blood flow becomes turbulent - recorded systolic BP = 1st Korotkoff sound - recorded diastolic BP = 5th Korotkoff sound

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12
Q

What is the treatment for shock?

A

ABCDE, high flow oxygen - 15L/min in a non-rebreather mask, volume replacement -bloods or fluid, inotropes for cardiogenic shock - increase force of contraction, immediate chest drain for a tension pneumothorax, adrenaline for anaphylactic shock, vasopressors for septic shock

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13
Q

What is obstructive shock?

A

increased intra-thoracic pressure - decreased venous return - decreased EDV - decreased SV - decreased CO - decreased BP

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14
Q

What causes vasomotor tone?

A

tonic discharge of sympathetic nerves

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15
Q

What happens during isovolumetric ventricular relaxation?

A

ventricles relax around a certain volume of blood (ESV) atrial pressure > ventricular pressure - AV valves open

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16
Q

What stimulates secretion of ADH?

A

reduced extracellular fluid volume, increased extracellular fluid osmolarity (monitored by osmoreceptors)

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17
Q

What is the role of aldosterone?

A

acts on the kidneys - increase sodium and water retention - increases plasma volume - increases BP

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18
Q

What covers the actin binding site on the myosin head

A

troponin-tropomyosin

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19
Q

What causes vasodilation of skeletal and cardiac arterioles during acute exercise?

A

adrenaline released, decreased local PO2 and increased local PCO2 which overrides sympathetic stimulation - to match supply to demand

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20
Q

How is the cerebral blood flow autoregulated?

A

MAP rises = vasoconstriction to limit blood flow

MAP falls = vasodilation to maintain blood flow

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21
Q

What triggers the power stroke?

A

cross bridge formation pulls actin filaments over myosin filaments

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22
Q

What causes the dicrotic notch in the aortic pressure curve?

A

valve vibration as aortic and pulmonary valves close

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23
Q

What are the effects of endothelial produced vasoconstrictors?

A

pro-thrombotic, pro-inflammatory, pro-oxidants

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24
Q

What is a positive chronotropic effect?

A

increases HR

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25
Q

How does adrenaline causes vasoconstriction?

A

acts on alpha adrenoceptors

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26
Q

What occurs during isovolumetric contraction?

A

ventricular pressure > atrial pressure - AV valves shut - first heart sound - lub - beginning of systole. aortic and pulmonary valves still shut - ventricles contracting around a certain volume of blood (EDV) - ventricular pressure rises steeply

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27
Q

What is the function of renin?

A

stimulates the formation of angiotensin I in the blood from angiotensinogen which is released from the liver

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28
Q

What arterioles have beta 2 adrenoceptors?

A

cardiac and skeletal muscle

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29
Q

What is neurogenic shock?

A

loss of sympathetic tone - massive venous and arterial dilation - decreased venous return and total peripheral resistance - decreased CO - decreased BP

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30
Q

What forces oppose transcapillary filtration?

A

capillary osmotic pressure and interstitial fluid hydrostatic pressure

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31
Q

What are the endothelial produced vasodilators?

A

histamine, bradykinin, nitric oxide

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32
Q

How does the sympathetic system increase HR?

A

increases rate of firing of SA node - slope of pacemaker potential increases - pacemaker potential reaches threshold quicker - frequency of APs increases – positive chronotropic effect (also decreases AV nodal delay)

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33
Q

What happens during passive filling?

A

atrial pressure > ventricular pressure - AV valves open - blood flows into ventricles

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34
Q

What is the aldosterone?

A

steroid hormone

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35
Q

What is hypovolemic shock?

A

loos of blood volume - decreased venous return - decreased EDV - decreased CO - decreased BP

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36
Q

What is tachycardia?

A

resting HR > 110

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37
Q

What is the result of increased sympathetic discharge on vascular smooth muscle?

A

vasoconstriction

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38
Q

What causes increased CO during acute exercise?

A

sympathetic nerve active increases - HR and SV increases

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39
Q

What causes adrenaline release?

A

sympathetic stimulation

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40
Q

What causes an increased resistance to blood flow?

A

increased blood vessel length, increased blood viscosity

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41
Q

What are the endothelial produced vasoconstrictors?

A

serotonin, thromboxane A2, leukotrienes and endothelin

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42
Q

What happens if cardiac myocytes are stretched too much?

A

stroke volume falls, doesn’t happen in a normal heart

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43
Q

What is cardiogenic shock?

A

sustained hypotension caused by decreased cardiac contractility - decreased SV - decreased CO - decreased BP

44
Q

What is the role of the nitric oxide?

A

vasodilator - diffuses into smooth muscle cells - cGMP acts as a second messenger for signalling smooth muscle relaxation

45
Q

Which arterioles have alpha adrenoceptors?

A

skin, gut and kidney

46
Q

What is Starling’s Law of the Heart/Frank-Starling mechanism?

A

greater venous return = greater end diastolic volume = greater stretch in myocytes = greater stroke volume

47
Q

What is a positive inotropic effect?

A

increases force of contraction

48
Q

What is the function of ADH?

A

acts in kidney tubules to increase reabsorption of water - increases extracellular plasma volume - increases CO - increases BP causes vasoconstriction - increased SVR - increased BP - small effect in normal people - important in hypovolemic shock/haemorrhage

49
Q

What is stroke volume?

A

volume of blood ejected by each ventricle per heart beat

50
Q

What is the result of increase intracranial pressure?

A

decreases cerebral perfusion pressure - decreases cerebral blood flow

51
Q

What causes vasoconstriction in kidneys, gut and skin during acute exercise?

A

sympathetic stimulation and adrenaline released

52
Q

What is the role of the AV node?

A

slows conduction velocity to delay impulse slightly to allow atrial systole to precede ventricular systole

53
Q

What is the effect on increased local PCO2 on vascular smooth muscle?

A

vasodilation

54
Q

What is the effect of sympathetic stimulation on ventricular muscle?

A

positive inotropic effect - activation of calcium channels - greater calcium influx, reduces duration of systole, increases duration of diastole

55
Q

What is cardiac output?

A

volume of blood pumped by each ventricle per minute

56
Q

What is vasoactive shock?

A

release of vasoactive mediators - massive venous and arterial dilation and increased capillary permeability - decreased venous return and total peripheral resistance - decreased CO - decreased BP

57
Q

What are the special adaptations of the coronary circulation?

A

oxygen demand of the cardiac muscle is high, high capillary density, high basal blood flow, high oxygen extraction at rest

58
Q

How does adrenaline cause vasodilation?

A

acts on beta 2 adrenoceptors

59
Q

What is the jugular venous pulse?

A

occurs after right atrial pressure waves - no valves from inferior jugular vein to right atrium

60
Q

What is the role of the Renin-Angiotensin-Aldosterone system?

A

regulation of plasma volume and SVR and hence MAP

61
Q

What is shock?

A

inadequate tissue perfusion and oxygenation - anaerobic metabolism and accumulation of metabolic waste products - cellular failure

62
Q

What areas of the heart are supplied by the parasympathetic nervous system?

A

SA node and AV node

63
Q

How does parasympathetic stimulation decrease HR?

A

cell hyperpolarises and the slope of the pacemaker potential decreases - longer to reach threshold - AP frequency decreases - negative chronotropic effect

64
Q

Where is the SA node located?

A

upper right atrium close to where the superior vena cava enters

65
Q

What type of shock is caused by a tension pneumothorax?

A

obstructive shock

66
Q

Where is ACE (angiotensin converting enzyme) produced?

A

vascular endothelium

67
Q

What is the result of decreased local PO2 on vascular smooth muscle?

A

vasodilation

68
Q

What is the role of angiotensin II?

A

causes systemic vasoconstriction - increases SVR - increases BP stimulates thirst and ADH release - increases plasma volume - increases BP stimulates aldosterone release from the kidneys

69
Q

How is renin released?

A

from the kidneys, stimulated by renal artery hypotension, stimulation of renal sympathetic nerves, decreased sodium concentration in renal fluid

70
Q

What tone dominates in the heart under resting conditions?

A

vagal/parasympathetic

71
Q

What is the effect of sympathetic stimulation on the heart?

A

increases heart rate, decreases AV nodal delay, increases force of contraction

72
Q

What is bradycardia?

A

resting HR < 60

73
Q

What happens when cuff pressure is greater than systolic pressure?

A

flow blocked - no sound

74
Q

What areas of the heart are supplied by the sympathetic nervous system?

A

SA node, AV node and myocardium

75
Q

What are the chronic CVS responses to exercise?

A

reduces BP, reduces sympathetic tone, increased parasympathetic tone to the heart, cardiac remodelling, reduction in plasma renin levels, improved endothelial functions - increased vasodilators and decreased vasoconstrictors, decreased arterial stiffening

76
Q

What are the compensatory mechanisms to maintain BP in response to haemorrhage?

A

tachycardia via baroreceptor reflex - small volume pulse due to decreased SV - cool peripheries due to increased SVR via baroreceptor reflex

77
Q

How can vomiting, diarrhoea and excessive sweating cause hypovolemic shock?

A

decreased extracellular fluid - decreased plasma volume

78
Q

Where is the AV node located?

A

at the base of the right atrium

79
Q

What is the Circle of Willis?

A

basilar (formed by two vertebral arteries) and carotid arteries anastomose together to form the circle of Willis, major cerebral arteries arise from the circle of Willis

80
Q

What are the effect of endothelial produced vasodilators?

A

anti-thrombotic, anti-inflammatory, anti-oxidants

81
Q

What is afterload?

A

resistance into which the heart is pumping

82
Q

What provides mechanical adhesion between cardiac myocytes?

A

desmosomes within intercalated discs

83
Q

What happens after acute exercise?

A

post exercise hypotensive response

84
Q

CO = ?

A

SV x HR

85
Q

What is the function of ACE (angiotensin converting enzyme)?

A

converts angiotensin I to angiotensin II

86
Q

What is the result of decreased sympathetic discharge on vascular smooth muscle?

A

vasodilation

87
Q

What could a raised jugular venous pulse indicate?

A

heart failure

88
Q

How does the electrical impulse spread between cardiac myocytes?

A

via gap junctions at intercalated discs through low resistance protein channels

89
Q

What is the result of sheer stress on blood vessels?

A

dilatation of arterioles - sheer stress in arteries upstream due to increased flow - sheer stress on vascular endothelium activates nitric oxide synthase - produces nitric oxide from L-arginine - vasodilation upstream

90
Q

What is the effect of myogenic response to stretch on vascular smooth muscle?

A

MAP rises = vasoconstriction to decrease blood flow

MAP falls = vasodilation to maintain blood flow

91
Q

What happens if the afterload increases?

A

fall in stroke volume initially until end diastolic volume increases

92
Q

What is metabolic hyperaemia?

A

increased local H+ concentration/decreased pH, increased extracellular fluid K+ concentration, increased osmolality of ECF , increased adenosine released from ATP

93
Q

What happens during ventricular ejection?

A

ventricular pressure > arterial pressure - aortic and pulmonary valves open arterial pressure > ventricular pressure - aortic and pulmonary valves shut - second heart sound - dub - beginning of diastole

94
Q

Why is arterial pressure not zero during diastole?

A

walls of major arteries have elastic fibres - recoil when heart relaxes - keeps blood moving forward

95
Q

What neurotransmitter is released by the parasympathetic system and what does it act on?

A

acetylcholine acting on muscarinic 2 receptors

96
Q

What is the result of chronic increased afterload?

A

ventricular hypertrophy

97
Q

How does blood flow increase to active regions of the brain?

A

rise in K+ concentration - efflux from neurones

98
Q

What is the effect of temperature on vascular smooth muscle

A
cold = vasoconstriction 
warm = vasodilation
99
Q

What is the effect of metabolic hyperaemia on vascular smooth muscle?

A

vasodilation

100
Q

How is the actin binding site on the myosin head exposed?

A

calcium influx occurs during the plateau phase of AP during systole - calcium is released from sarcoplasmic reticulum in presence of extracellular calcium - calcium binding causes a conformational change - binding site exposed

101
Q

Where is antidiuretic hormone (ADH)/vasopressin produce?

A

hypothalamus

102
Q

What is the function of natriuretic peptides?

A

cause excretion of salt and water from the kidneys - reduces blood volume - reduces BP decreases renin release act as vasodilators - decreased SVR - decreased BP

103
Q

What causes release of natriuretic peptides?

A

cardiac distension or neurohormonal stimuli

104
Q

stoke volume = ?

A

end diastolic volume - end systolic volume

105
Q

What neurotransmitter is released by the sympathetic system and what does it act on?

A

noradrenaline acting on beta 1 adrenoceptors

106
Q

What is the role of calcium ATPase?

A

return calcium to sarcoplasmic reticulum during diastole

107
Q

What are the 5 stages of the cardiac cycle?

A
  1. passive filling 2. atrial contraction 3. isovolumetric contraction 4. ventricular ejection 5. isovolumetric ventricular relaxation