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brs stuff > cardio > Flashcards

cardio Flashcards

1
Q

where is the SAN

A

junction of crista terminalis

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2
Q

where is the AVN

A

triangle of Koch at base of right atrium

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3
Q

length-tension relation

A

active force production increases with muscle length: as the stretch increases, force increases => force decreases with over exertion

passive force increases with muscle length: as the stretch increases, elasticity of the muscle also increases

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4
Q

why is passive force much grater in cardiac muscle

A

cardiac muscle is more resistant to stretch + less compliant due to properties of the extracellular matrix and cytoskeleton

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5
Q

why is the ascending limb of length-tension relation graph important for cardiac muscle

A

can’t overstretch as its contained in pericardium

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6
Q

total force =

A

active force + passive

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7
Q

preload

A

initial stretchon heart muscle as chambers fill indiastole

before stimulated to contract

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8
Q

afterload

A

pressure againstwhich the heart must eject blood duringsystole

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9
Q

isometric contraction

A

muscle fibres do not change length but pressures increase in both ventricles

e.g when ventricles fill with blood

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10
Q

isotonic contraction

A

shortening of fibres and blood is ejected from ventricles

e.g blood expelled through arteries

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11
Q

measures of preload

A

end-diastolic volume
end-diastolic pressure
right atrial pressure

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12
Q

measures of afterload

A

diastolic blood pressure

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13
Q

Frank-Starling Relationship

A

increased diastolic fibre length increases ventricular contraction - venous return = cardiac output

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14
Q

2 theories for FS relationship

A

shorter than optimal filaments = overlap on themselves = less am cross bridges = less force

stretch = conformational change in TnC on actin => increased affinity to calcium => less Ca required for same force

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15
Q

stroke work

A

work done by heart to eject blood under pressure into aorta and pulmonary artery

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16
Q

stroke work calc

A

stroke volume x pressure of ejection

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17
Q

law of laplace

A

when the pressure within a cylinder is held constant, the tension on its walls increases with increasing radius

T = P x R / h

h= wall thickness

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18
Q

when is end diastolic + systolic volume measured

A

diastolic: isovolumetric contraction
systolic: slow ejection

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19
Q

stroke volume =

A

end diastolic volume - end systolic

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20
Q

ejection fraction =

A

stroke volume / end diastolic

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21
Q

pressures in 2 circuits (systemic + pulmonary)

A

systemic = much greater pressure than pulmonary but pressure changes and volume are the same

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22
Q

end systolic PV line

A

represents maximum pressure that can be developed by ventricle at a given volume

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23
Q

increased preload on PV loop

A

increased preload = increased diastolic volume

increased stretch of ventricular walls = increased force of contraction = increased stroke volume

fatter PV loop

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24
Q

increased afterload on PV loop

A

increased aortic pressure = increased ventricular pressure to overcome

more pressure = less shortening of fibres = less SV

long + thin loop

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25
Q

cardiac output =

A

heart rate x stroke volume

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26
Q

contractility

A

contractile capability (strength of contraction) of the heart

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27
Q

ESPVR lines and contractility

A

increased contractility = steeper = more force produced with less volume (less stretch)

decreased contractility = less steep = less force produced with same volume

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28
Q

how increasing contractility causes greater force

A

increased = sympathetic stimulation activating extrinsic mechanism

increased Ca2+ delivery to myofilaments = more force made by less stretch

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29
Q

what happens to PV loop during exercise

A

gets fatter

increased venous return of blood from muscles = increased preload = increased end diastolic volume

increased sympathetic activation = increased contractility = more blood ejected = decreased end systolic volume

SV = EDV - ESV = greater SV = expands

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30
Q

cell types in airways

A

type 1 = thin = exchange

type 2 = replace 1 & make surfactant/role in xenobiotic metabolism

fibroblasts

capilary endothelium

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31
Q

mucins

A

glycosylated proteins in mucus

made by goblet cells in compact granules => expand in water when released = mucus

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32
Q

2 things that make mucous

A

goblet cells

submucosal glands (mucous acini inside + serous acini secreting anti-bac enzymes outside)

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33
Q

cilia arrangement

A

9 pairs outside connected by nexin links w/inner + outer arms (dyenins)

2 unpaired in middle connected to 9 via rsdial spokes

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34
Q

what regulatory + inflammatory mediators are released by epithelia of airway

A

NO
CO
arachidonic acid e.g prostaglandins
chemokines
cytokines
proteases

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35
Q

NO function

A

made by NOS (made by epithelia) which stains brown

speed up cilia movement

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36
Q

importance of airway vasculature

A

gas exchange
warming air
humidification

clearing inflammatory mediators
clearing inhaled drugs
supply lumen tissue with inflammatory cells

supply tissue with proteinaceous plasma

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37
Q

whats so special about airway nerves

A

no nerve endings => nts released from bulbous sections into ciliated cells

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38
Q

airway control

A

protases
nerves
reactive gases
inflammatory + regulatory mediators

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39
Q

contraction and relaxation control

A

contraction => parasympathetic cholinergic motor pathway => ACh => constriction

relaxation => adrenaline + NO species

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40
Q

labels of volume time graph

A

inspiratory reserve volume
tidal volume
expiratory reserve volume
residual volume

inspiratory capacity
functional residual capacity
total lung capacity

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41
Q

minute ventilation (L/min)

A

tidal volume (L) x breathing frequency (breaths/min)

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42
Q

alveolar ventilation (L/min)

A

[tidal volume (L) - dead space (L)] x breathing frequency

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43
Q

what is measured by minute vs alveolar ventilation

A

minute = gas entering/exiting lungs

alveolar = gas entering/exiting alveoli

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44
Q

2 zones of alveoli

A

conducting => no exchange - first 16 gens - anatomical dead space

respiratory => exchange - alveolar ventilation - 7 gens

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45
Q

dead spaces (2 kinds)

A

anatomical = normal - in conduction zone - no alveoli

alveolar = non perfused parenchyma (malfunction where alveoli dont get blood supply)

anatomical + alveolar = physiological dead space

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46
Q

what happens when you increase the length of the breathing tube e.g diving

A

increased dead space = reduced tidal volume

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47
Q

chest wall relationship (+ what happens in breathing)

A

chest has tendency to spring out, lung has tendency to recoil in
at end of tidal resp (neutral position of chest) => forces in eqbm

inspiratory muscle effort + chest recoil > lung recoil => breathe in

chest recoil < lung recoil + expiratory muscle effort => breathe out

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48
Q

what is negative pressure breathing

A

air forced in due to vacuum created by alveolar pressure dropping below atmospheric (0) (changing Palv)

how we normally breathe

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49
Q

what is positive pressure breathing

A

air forced into lungs by pushing - making atmospheric pressure increase about alveolar (changing Patm)

CPR, pilots, ventilation aids

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50
Q

daltons gas law

A

pressure in gas mixture = sum of individual pressures of gases

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51
Q

ficks gas law

A

diffusion rate of gases = (surface area [A]/thickness of membrane [T]) x diffusion capacity [D] x concentration gradient [P1 - P2]

52
Q

henrys gas law

A

at constant temperature: C = a x P

conc of dissolved gas is proportional to partial pressure of gas - a = henrys gas law constamt

53
Q

boyles gas law

A

pressure is indirectly proportional to volume at constant temperature

54
Q

charles gas law

A

volume is directly proportional to temperature

55
Q

gases at high altitudes

A

same proportions just less of each

56
Q

mmHg to kPa

A

mmHg/7.5 = kPa

57
Q

how is air changed as it moves into lungs

A

at start: high PO2, low PCO2 + H2O

nose: humidified (increased PH2O) + warmed

respiratory zone: gas exchange => PCO2 increased + PO2 decreased

58
Q

loading + unloading in Hb

A

4 O2 bind with positive co-operativity
when 4 bind => opens space for 2,3-DPG

59
Q

why is finding O2 saturation not useful alone

A

if less blood, even if fully saturated, body is still receiving less oxygen

60
Q

what causes left shift of oxygen dissociation curve

A

increased affinity to O2 => increased loading

decreased temperature, alkalosis, hypocapnia (low CO2), low 2,3-DPG

carbon monoxide (oxygen cant unload), foetal Hb (get O2 from mother), myoglobin (extract O2 from blood for storage)

61
Q

down vs up shift of oxygen dissociation curve

A

down: anaemia
up: polycythaemia

62
Q

CO2 transport out of tissues

A

direct diffusion into plasma:
CO2 + H2O2 => H2CO3 => H+ + HCO3-
non enzymatic

into blood cell:
CO2 + H2O2 => H2CO3 => H+ + HCO3-
carbonic anhydrase

H+ used to form globins
HCO3- exchanged at AE1 antiporter with Cl-

63
Q

what are the sounds heard during BP measurement called

A

korotkoff sounds

64
Q

vessels in microcirculation

A

1st order arteriole
terminal arteriole
capillaries
pericytic venule
venule

65
Q

darcys law

A

flow rate = pressure gradient (A-B) / resistance

66
Q

pressure gradient in arteriole vs tissue vs whole CVS

A

arteriole => 1st order arteriole - capillary

tissue => mean arterial pressure

CVS => MAP

67
Q

flow rate equation for whole CVS

A

cardiac output = flow rate = MAP / total peripheral resistance

68
Q

resistance in a vessel (calculation + what has an effect)

A

8 x vessel length [L] x viscosity / pi x radius^4

only radius is variable so has an effect

69
Q

how arteriole matches blood flow to metabolic needs of specific tissues chemically

A

active hyperaemia

blood drawn towards organs by vasodilation induced by O2 + metabolite usage (chemical changes) = lower resistance

70
Q

how arteriole matches blood flow to metabolic needs of specific tissues physically

A

myogenic auto-regulation

blood taken away from tissues by vasoconstriction when stretch increased = greater resistance

e.g when organs don’t need much blood at that moment => high BP of body = stretching = autoreg triggered

71
Q

ultimate function of CVS

A

deliver metabolic substances to cells of organism

72
Q

3 types of capillaries

A

continuous (h20 filled gap junctions)

fenestrated

discontinuous (v.large gaps e.g BM for WBCs to escape)

blood brain barrier = continuous with tight junctions

73
Q

2 functions of arterioles

A

local => match blood flow to the metabolic needs of specific tissues

general => constricted/dilated to help regulate systemic arterial blood pressure
(neural via baroceptors, hormonal via adh etc)

74
Q

metabolic activity and capillary relation

A

increased ma = increased capillaries

exceptions: lung (not ma but need caps fro exchange), skm (ma but too many caps would make them too bulky)

75
Q

what is bulk flow

A

volume of protein-free plasma filters out of capillary, mixes with surrounding interstitial fluid (IF) + reabsorbed

76
Q

starling’s hypothesis

A

there must be a balance between hydrostatic pressure of blood in capillaries + osmotic attraction of blood for the surrounding fluids

77
Q

hydrostatic vs oncotic pressure

A

hydrostatic = pushing force - fluid driven out => high at start of capillary

oncotic = pulling force - fluid drawn in by osmosis => high at end of capillary

78
Q

ultrafiltration vs reabsorption in capillaries

A

U: Pa inside > IF

R: IF > inside

79
Q

importance of lymphatic capillaries

A

ensures blood volume does not fall too much by draining back into major lymphatic vessels → blood

80
Q

where does the throacic duct of lymphatic system empty into

A

junction of the left subclavian and internal jugular veins

81
Q

oedema

A

rate of production of fluid + release into IF > rate of drainage

82
Q

elephantitis

A

type of oedema caused by parasitic blockage of lymph nodes → enlargement of affected lower limb

83
Q

what 3 things does airway resistance depend on

A

fluid viscosity
tube length
radius

84
Q

why does pressure generally fall across circulation

A

viscous (frictional pressure losses)

(as vessels get smaller artery => capillary - resistance increases)

85
Q

laminar vs turbulent blood flow

A

laminar => normal - flows in layers with the centre of the lumen being the fastest due to low friction

turbulent => pathological - erratic flow + formation of eddys (vortex) - prone to pooling

86
Q

total, pulse + mean arterial pressure

A

total pressure = cardiac output x resistance

pulse pressure = systolic - diastolic

MAP = diastolic pressure + 1/3(pulse pressure)

87
Q

what is compliance

A

tendency of vessel to distort under pressure

= change in volume/change in pressure

88
Q

what is elastance

A

tendency to recoil to original pressure after pressure is applied

= change in pressure/volume

89
Q

why ventricular pressure falls rapidly but aortic pressure falls slowly

A

explained by high elasticity of aorta + large arteries which act to “buffer” the change in pulse pressure

90
Q

how does diastolic flow still occur after aortic valve is closed

A

recoil force of artery - arterial compliance

91
Q

what are varicose veins (varicosity)

A

dilated superficial veins caused by incompetent valves

prolonged elevation of venous pressure leads to oedema

92
Q

aneurysm

A

bulging, weakened area in wall of a blood vessel => abnormal widening or ballooning

weakened vessel walls => weak muscle fibre => cant generate enough energy to generate pressure to pump blood through => continues expanding

93
Q

venous vs arterial compliance

A

venous compliance is much greater than arterial compliance at low pressures

94
Q

venoconstriction

A

neurogenically induced contraction of the smooth muscle in the walls of veins

increase venous return by pushing excess blood in veins back to heart

95
Q

ventilation and perfusion in lungs

A

ventilation and perfusion are greater at the base of the lung (due to gravity)

ventilation varies more than perfusion between base and apex

96
Q

ap in nodal cells

A

pre potential = Na+ influx through funny channel - no RMP

upstroke = calcium influx

repolarisation = k+ efflux

97
Q

ap in cardiac muscle

A

phase 0 - upstroke due to Na+ influx
phase 1 - early repolarisation due to K+ efflux
phase 2 - plateu - maintains cell at a level of depolarisation due to Ca+ influx
phase 3 - repolarisation due to k+ efflux
phase 4 - RMP

98
Q

absolute refractory period

A

time during which no AP can be initiated regardless of stimulus intensity

limits max HR

99
Q

PNS effect on heart

A

medulla to heart via vagus nerve

through cranial + sacral spinal cord => ACh

decreases slope of pre-potential in nodal cells = longer pre potential = AP formed slower => decreased HR

ACh → M2 muscarinic receptors on SAN cell membrane → Gi protein → inhibits adenyl cyclase → ATP not converted to PKA

100
Q

SNS effect on heart

A

through thoracic + lumbar spinal cord => ACh + NA

increases pre-potential slope => less time for AP to be generated => faster

NA → beta-1 receptors on SAN cell membrane → stimulate adenyl cyclase → ATP converted to PKA

101
Q

effect of brainstem on HR

A

vasomotor centre => impulses to all blood vessels

pressor area = constriction
depressor area = dilation
cardioregulatory inhibitory area

102
Q

control of heart by kidneys

A

SNS + aldosterone = decrease glomerular filtration = less Na+ excretion = increased blood volume - affects cardiac function

SNS also causes jxgm cells => renin = ang 2 => vasoconstriction => increased BP => detected by arterial baroreceptors

103
Q

control of heart in cardiopulmonary circuit

A

volume sensors in pulmonary vessels = signals through glossopharyngeal & vagus nerves

less filling => less baroreceptor firing => increased SNS => increased HR

104
Q

control of heart in arterial circuit

A

pressure sensors: send signals through glossopharyngeal & vagus nerves

decreased pressure = decreased br firing = increased SNS activity

in aortic arch, carotid sinus + afferent arterioles of kidneys

105
Q

what is central venous pressure equivalent to

A

mean pressure in right atrium

106
Q

endothelium-derived mediators regulating blood flow (intrinsic to smooth muscle)

A

nitric oxide - vasodilator
prostacyclin - vasodilator + antiplatlet/anticoagulant

thromoxane A2 - vasoconstrictor also made in platlets
endothelins - vasoconstrictors made in endo nuclei

107
Q

non-endothelium-derived mediators regulating blood flow (extrinsic to smooth muscle)

A

kinins - bind endo + cause NO release = vasodilator
atrial atriuretic peptide - vasodilator by atria

vasopressin - vasoconstriction
NA/A - vasoconstriction
Ang 2 - vasoconstriction

108
Q

control of lung function - medulla oblongata

A

DIVE

apneustic centre => switched on dorsal respiratory group (inhibited by VRG)

pneumotaxic centre => inspiratory off switch

109
Q

chemo-sensitivity in controlling lung function

A

H+ stimulates DRG
cant cross blood brain barrier

CO2 => CSF from blood
H2O + CO2 => H+ + HCO3-
H+ to medulla

110
Q

3 lung receptors

A

irritant (trachea)
stretch (bronchi)
j-receptors (bronchiole ends)

111
Q

irritant receptors

A

detect foreign objects
induce cough => forceful expiration against closed glottis

112
Q

stretch receptors

A

exxcessive inflation
send afferent signals to inhibit DRG + apneustic centre & trun on VRG + pneumotaxic

113
Q

j-receptors

A

detect oedema + capillary enlargement
increase breathing frequency

114
Q

what happens during volitional apnoea

A

1 - CO2 crosses threshold for breathing = increased urgency to breathe

2 - if urge is resisted => O2 crosses threshold for blackout

115
Q

acid/alkaemia vs acid/alkalosis

A

aemia = low/high pH

osis = circumstance that increases/decreases pH

116
Q

how is acid-base homeostasis maintained

A

pH buffered by proteins - proton acceptors

detected by peripheral chemoreceptors in aortic arch (aortic body), carotid bifurcation (carotid body)

117
Q

what happens in stress

A

limbic system increases breathing frequency

118
Q

what happens in exercise

A

proprioceptive afferents from muscle spindle + golgi tendons stimulate medulla to increase breathing

119
Q

what is the cold shock response

A

many cold receptors activated all over the body => stimulates increased breathing

120
Q

pH and [H+]

A

pH = -log10[H+]

[H+] = 10^-pH

121
Q

HR from ecg

A

1500/no: small squares between 2 Rs

122
Q

ecg for: myocardial infarct, atrial flutter, 1st degree & second degree heart block

A

MI: elevated ST
AF: sawtooth pattern
Ist: long PV interval + slow conduction through AVN
2nd: slow HR, no QRS, no conduction through AVN

123
Q

how to carry out volume-time PFT

A

nose clip + inhale to total capacity
lip around mouthpiece => exhale hard + fast

124
Q

FEV1/FVC ratio

A

FEV1: forced expiratory volume in 1 second
FVC: forced vital capacity

FEV1/FVC ratio

125
Q

FEV1/FVC ratio for obstructive vs restrictive

A

obs => <70%
res => >80%

126
Q

how to carry out flow volume loop PFT

A

nose clip + lips around mouth piece
1 tidal breath + inhale slowly to TLC
exhale until RV + inhale again to TLC

(width = FVC)

brs stuff (8 decks)

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