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phase 2 cardiovascular and respiratory block > week 3 > Flashcards

week 3 Flashcards

1
Q

factors that modulate breathing

A 
physiological challenges - exercise, sleep
emotional events - crying
vocalisation - singing
volitional control - breath hold
reflexes - cough
temperature, cardiovascular
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2
Q

function of mechanoreceptors

A

sensory receptors that detects changes in pressure, movement, touch
in respiratory system - provide feedback to brain on mechanical status of lungs, chest wall and airways (detects movement of lung and chest wall)
different types with different reflexes

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3
Q

function of chemoreceptors

A

detect chemical changes in surrounding environment
in respiratory system - provide feedback to brain on blood Po2, Pco2 and pH after detecting changes to these in blood
hypercapnia and hypoxia would trigger

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4
Q

where does the brain send signals to in order to control breathing

A

respiratory muscles - to produce rhythmic breathing movements
upper airway muscles eg tongue
produces reflexes to keep airways patent eg cough

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5
Q

two types of chemoreceptors

A

peripheral and central

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6
Q

function of peripheral chemoreceptors

A

responds to decreases in Po2 (hypoxia)

information sent via glossopharyngeal and vagus nerves to the nucleus in brainstem called NTS

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7
Q

NTS

A

nucleus tractus solitarus

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8
Q

structure and location of peripheral chemoreceptors

A

small highly vascularised bodies in region of aortic arch and carotid sinus

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9
Q

how chemoreceptors respond to hypoxia

A

reduction in arterial Po2
peripheral chemoreceptors stimulated
neural signals sent from carotid and aortic bodies to NTS
ventilation increases to restore Po2 levels

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10
Q

when does hyperventilation take place in terms of Po2

A

progressive reductions in inspired O2 have little effect until about 60mmHg
below 60 there is hyperventilation

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11
Q

location of central chemoreceptors

A

these are clusters of neurons located in the brainstem

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12
Q

when are central chemoreceptors activated

A

when Pco2 is increased (hypercapnia) or pH is decreased

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13
Q

mechanism of central chemoreceptors

A

increase in arterial Pco2
central chemoreceptors stimulated
signals processed and info passed to neuronal clusters in brainstem involved in generating breathing
signals sent to respiratory muscles
ventilation increases to restore Pco2 levels

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14
Q

how does hypercapnia effect ventilation

A

small changes in Pco2 have very large effects on ventilation unlike O2

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15
Q

mechanism of mechanoreceptors

A

inflation of lungs activates mechanoreceptors
neural signals sent via vagus nerve to NTS in brainstem
ventilation adjusted
mechanoreceptors located throughout respiratory tree

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16
Q

role of brainstem in breathing control

A

NTS receives info from mechanoreceptors and peripheral chemoreceptors - processed by respiratory neurones
cluster of respiratory neurones in brainstem generate rhythm of breathing - rhythmic signal sent to respiratory muscles

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17
Q

respiratory rhythm generating neurones

A

bilateral cluster of neurones with rhythm generating properties
continues to produce a respiratory-like rhythmic output when isolated

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18
Q

output from brainstem to respiratory muscles

A

brainstem neurones produce rhythmic output
rhythmic neural signals sent to spinal cord
phrenic nerve innervates diaphragm
nerves exiting thoracic spinal cord innervate intercostal muscles

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19
Q

pathway of respiratory rhythm generated in brainstem

A

pontine respiratory group ->
ventral respiratory group (pattern and rhythmic generating neurones) or dorsal respiratory group (NTS)
neural output to muscles

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20
Q

how does volitional control of breathing work

A

upper motor neurones originate in the primary motor cortex
descend as corticospinal tract
synapse with lower motor neurones, either directly or indirectly via interneurones located in the anterior horn of C3-5
motor neurones projects as phrenic nerve to the diaphragm

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21
Q

properties that the respiratory and circulatory systems have to facilitate gas diffusion

A

large surface area for gas exchange
large partial pressure for gradients
gases with advantageous diffusion properties
specialised mechanisms for transporting O2 and CO2 between lungs and tissues

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22
Q

what is partial pressure

A

sum of the partial pressures or tensions of a gas must be equal to total pressure
barometric pressure = 760mmHg

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23
Q

gas concentration gradients in pulmonary and systemic capillaries

A

O2 and CO2 move down their pressure gradients from high to low concs
similar volumes of both gases move each movement
CO2 is more diffusible

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24
Q

what is between alveoli and a RBC

A

type 1 alveolar epithelial cell, capillary endothelial cell and basement membrane

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25
Q

how is O2 carried in blood

A

dissolved and bound to haemoglobin

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26
Q

how is dissolved O2 measured clinically

A

in an arterial blood sample Po2

amount of dissolved O2 is proportional to its partial pressure

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27
Q

describe levels of dissolved O2

A

only a small percentage of O2 in blood is in the dissolved form
not adequate for body’s requirements even at rest

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28
Q

structure of haemogloblin

A

four heme groups joined to globin protein
two alpha chains and two beta chains
each heme group contains iron in the reduced ferrous form (Fe+++) which is the site of O2 binding

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29
Q

how oxyhemoglobin dissociation curve can be altered

A

increase in temp shifts curve to the right
decrease in pH shifts curve to the right
high percent of saturation at low Po2 with low temp and high pH
drop in Po2 from 100 to 60 mmHg has little effect

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30
Q

describe the oxyhemoglobin dissociation curve

A

O2 to Hb is reversible
flat portion - drop in Po2 from 100 to 60 mmHg has little effect
steep portion - O2 released from Hb with a small change in PO2

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31
Q

O2 saturation

A

refers to the amount of O2 bound to Hb relative to maximal amount that can bind
100% sat = all heme groups of Hb fully saturated with O2
1g Hb combines with 1.39ml O2

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32
Q

how O2 saturation is measured

A

pulse oximeters used in clinic

measures ratio of absorption of red and infrared light by oxyHb and deoxyHb

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33
Q

normal respiratory exchange ratio is 0.8

A

80 CO2 to 100 O2

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34
Q

how is CO2 transported in blood

A

7% dissolved
23% bound to haemoglobin
70% converted to bicarbonate

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35
Q

bicarbonate production equation

A

H2O + CO2 -> H2CO3 -> H+ + HCO-3
reversible
rightwards in systemic capillaries when CO2 produced b tissues and expelled into blood
leftwards in pulmonary capillaries when CO2 is expelled into alveoli

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36
Q

how is acidity regulated

A

using ventilation to adjust PCO2 or by using kidneys to regulate the bicarbonate concentration

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37
Q

V/Q ratio

A

ratio of ventilation to blood flow

can be defined for a single alveolus, a group or an entire lung

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38
Q

V/Q ratio for a single alveolus or lung

A

alveolar ventilation divided by capillary flow

total alveolar ventilation divided by CO

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39
Q

healthy V/Q ratio

A

for lung - 0.8-1.2
varies greatly for individual units
>1 when ventilation exceeds perfusion

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40
Q

possible triggers of asthma

A 
cold air and scents
inflammation:
allergy
viral/bacterial infection 
exercise
drugs:
beta-blockers 
non steroidal anti-inflammatory drugs
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41
Q

presentation of asthma symptoms

A

bronchospasm - tightening of the smooth muscle mesh surrounding the airway - wheeze, dyspnoea, exercise intolerance
inflammation - cough

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42
Q

consequence of having a shared entrance and exit in airways

A

limits maximum ventilation as must utilise airways for both phases

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43
Q

normal adult peak flow rate

A

Normal adult peak flow scores range between around 400 and 700 litres per minute
higher in taller, younger people and men

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44
Q

function of airway resistance

A

maintains flow of air - in absence of airway wall tesnion, air would simply compress due to low viscosity
slows airway flow by r4 - small changed to airway calibre with result in a large drop in airflow

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45
Q

ways of narrowing an airway in asthma

A

dynamic (acute) - rapid muscle contraction and secretions

fixed (chronic asthma) - smooth muscle bulk and thickened BM cause a stiff airway wall

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46
Q

pathology of asthma

A

weakened and denuded airway epithelium
thickened BM
increased SM
mast cells in smooth muscle

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47
Q

consequence of increased SM in asthma

A

increased force of contraction

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48
Q

consequence of mast cells in SM in asthma

A

twitchy SM variable airway calibre

mast cells have bags of histamine

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49
Q

consequence of increased BM in asthma

A

loss of relaxation after contraction

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50
Q

symptoms from increased contraction in asthma

A

triggered breathlessness/wheeze eg. histamine
daily variation
cough

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51
Q

symptoms of variable airway calibre in asthma

A

bronchial hyper-reactivity - exaggerated response to usually constricting stimuli eg metacholine or histamine

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52
Q

clinical measurement for variable airway calibre in asthma

A

peak flow variability would show this

keeping a peak flow diary and seeing day to day variability of FEV1 value - also diurnal variability (lower in morning)

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53
Q

clinical measurement for inflammatory secretions in asthma

A

exhaled nitric oxide
increased in eosinophilic inflammation
normal value is 30ppb

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54
Q

clinical measurement for reversible airflow contraction

A

spirometry

narrowed constricted airway relaxes and dilates in response to salbutamol - narrowing would be irreversible in COPD

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55
Q

3 phases that contribute to asthma

A

smooth muscle only - triggered by direct mediator release eg histamine - rare wheezy episodes
chronic inflammation - irritates SM and causes regular wheezy episodes
acute inflammation - viral infection - clinical exacerbations

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56
Q

molecules associated with type 2 inflammation (asthma)

A

cells - lymphocytes (Th2), eosinophils and mast cells
cytokines - IL-4,5
prostanoids - PGE2, leukotriene D4
immunoglobulins - specific IgE

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57
Q

problem with immunity to infection in asthma

A

immunity drives inflammation
memory in IgE on mast cell surface - way it is remembered and retained is dependent on cytokine environment in which it happens
on second exposure - antigen binds to IgE on MCs and cross links MC receptors for IgE - activates signalling cascade and mast cell mediator release which promotes inflammation

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58
Q

mast cell mediators and their effect on airway

A

histamine - smooth muscle contraction - immediate
leukotrieneD4 - smooth muscle contraction and airway wall oedema - slightly longer response than histamine
prostaglandin - airway wall oedema and inflammation and increased secretions - slightly longer response than histamine
VEGF - blood vessel formation - reduces airway wall space by expanding bulk of airway wall - chronic change

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59
Q

result of SM contraction in asthma

A

bronchospasm and wheeze

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60
Q

result of alveolar wall oedema in asthma

A

airway narrowing

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61
Q

result of BV hypertrophy in asthma

A

airway wall thickening and lumen narrowing - chronic

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62
Q

chemical ways of triggering mast cells in asthma

A

IgE - allergen exposure
salicylates - aspirin
scents

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63
Q

how exercise triggers mast cells in asthma

A

exercise increases ventilation
exceeds humidifying capacity of upper airway
drying air causes osmotic rupture of mast cells
this can be mimicked by mannitol bronchial challenge testing

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64
Q

cells different infections use to stimulate inflammation

A

viral - neutrophils/lymphocytes
parasitic - eosinophils
bacterial - neutrophilic

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65
Q

asthma treatment

A

B2 agonists
corticosteroids
anti-leukotriene receptor drugs

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66
Q

corticosteroid action in asthma

A

mainstay of treatment prevents and treats inflammation non-selectively
reduces airway twitchiness and reduces exhaled NO
these are inhaled straight to lung

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67
Q

anti-leukotriene receptor drug action in asthma

A

add on treatment for resistant inflammation
targets only leukotriene D4 in the airway
direct effect on mast cells and smooth muscle
good in exercise asthma

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68
Q

emerging asthma treatment

A

anti-IgE biological therapy - blocks IgE peripherally and results in down regulation of IgE in MCs - leads to down regulation of twitchiness of asthma

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69
Q

bronchial thermoplasty

A

still unproven
reduces bulk of airway SM
reduction in twitchiness

70
Q

upper respiratory tract

A

nasal cavity
pharynx
larynx

71
Q

lower respiratory tract

A

trachea
bronchi
bronchioles
alveoli

72
Q

distribution of SM in airway

A

SM becomes increasingly responsible for calibre of airways as you get into the smaller airways

73
Q

activation of muscarinic receptors

A

activated by vagus parasympathetic nerve
ACh and methacholine used
causes smooth muscle to contract
bronchoconstriction - want to block this in asthma
PSNS also controls airway secretions

74
Q

activation of adrenergic receptors in lung

A

circulating adrenaline stimulates not nerves

B2 agonist for asthma - smooth muscle relaxation

75
Q

mechanism of steroids

A

take hours to work
not acting on SM to relax
bind to an intracellular receptor and influence transcription
acting to produce proteins that will interact with interleukins

76
Q

some of the side effects of steroids

A 
easy bruising
poor wound healing
increased abdominal fat
thinning of skin
osteoporosis 
increased appetite
obesity
77
Q

describe asthma

A

recurrent reversible airflow obstruction
wheezing, cough, dyspnoea, hyperinflation
largely reversible airflow obstruction

inflammatory changes in airways
bronchospasm
bronchial hyper-reactivity

78
Q

pathology of asthma

A

epithelial shedding exposes nerves
increased number of eosinophils
exposed nerves are sensitive to kinins (hyperstimulation)
mucous gland hypersecretion
smooth muscle constriction leads to hypertrophy
leaking blood vessels

79
Q

drugs for asthma

A

bronchodilators

anti-inflammatory drugs - corticosteroids and other agents

80
Q

types of bronchodilators

A

B2 adrenoreceptor agonists
anticholinergic agents
leukotriene antagonists
xanthines

81
Q

types and examples of B2 adrenoreceptor agonists

A

short acting - salbutamol, terbutaline
long acting (LABA) - salmeterol, formoterol - these are short acting molecules held by chemical arms so they repeatedly act on the receptor
main action - dilate bronchi
also stabilise mast cells, monocytes, cilia

82
Q

problems with B2 adrenoreceptor agonists

A

tremor is a principle side effect
tolerance may occur
some concerns regarding excess mortality

83
Q

types and examples of anticholinergic agents

A

short acting - ipratropium
long acting - tiotropium
they bronchodilate and are antisecretory

84
Q

function and examples of leukotriene antagonists

A

montelukast, zafirlukast
mild bronchodilators by acting on interleukins
possibly weak anti-inflammatory agents

85
Q

describe xanthines

A 
oral or IV
bronchodilators
have weak anti-inflammatory action
throphylline, aminophlyline
many side effects
narrow therapeutic window
86
Q

anti-inflammatory agents

A

glucocorticoids
cromoglycate/nedocromil
anti IgE antibodies

87
Q

describe glucocorticoids

A

inhaled, tablet, IV
intracellular receptor and then intranuclear action
decreases Th2 cytokines

88
Q

asthma therapy

A

regular inhaled corticosteroid with or without a LABA in the same inhaler
B2 agonist in blue inhaler - rescue treatment or used before exercise

89
Q

bronchial thermoplasty

A

all visible airways are treated excepted RML
3 treatment sessions to treat all accessible airways
max 30 minutes, approx 45 activations per session

90
Q

COPD

A

largely irreversible airflow obstruction

often includes emphysema

91
Q

differences between asthma and COPD

A

cause of COPD is cigarette smoke, cause of asthma is unknown
epithelial cells and mast cells involved in asthma, alveolar macrophages and epithelial cells involved in COPD
CD4+ cells and eosinophils increased in asthma, CD8+ cells and neutrophils involved in COPD
result is bronchoconstriction in asthma, small airway narrowing and alveolar destruction in COPD

92
Q

treatment of COPD

A 
smoking cessation 
LABA/ICS combination 
LAMA
LAMA/LABA
LAMA/LABA/ICS
93
Q

where does the right lymphatic duct empty

A

at junction of right internal jugular and right subclavian veins

94
Q

function of lymphatic ducts

A

carry lymph from abdomen to circulatory system

95
Q

cisterna chyli

A

most inferior part of the thoracic duct

96
Q

where does the thoracic duct empty

A

into junction of left internal jugular and left subclavian veins

97
Q

chylothorax

A

lymphatic fluid in the pleural space

98
Q

effect of ANS on SA node

A

rate increase with sympathetic system and decreases with parasympathetic

99
Q

effect of ANS on AV node

A

conduction velocity is faster with SNS and slower with PSNS

100
Q

effect of ANS on ventricles

A

contract harder and relax faster with SNS

101
Q

autonomic innervation of the heart

A

vagus nerve is the PS innervation

sympathetic ganglia from lower cervical and T1-4

102
Q

how can the firing rate of the SA node be altered

A

changes in autonomic activity - sympathetic or vagal
circulating hormones - hyperthyroidism and hypothyroidism
serum ion concentration - hyperkalemia and hypokalemia (K ions)
cellular hypoxia - usually from ischemia
drugs

103
Q

fainting caused by standing for a long period of time

A

blood pools in legs
less blood is being pumped
brain is insufficiently perfused

104
Q

sick carotid sinus syndrome

A

overactive problem with carotid vagus nerve
with little trigger, vagus nerve is stimulated
pass out, heart doesnt beat properly

105
Q

ductus venosus

A

allows blood to bypass the liver

106
Q

ductus arteriosus

A

allows blood to bypass lungs

connects arch of the aorta and pulmonary trunk

107
Q

patent ductus arteriosus

A

medical condition in which the ductus arteriosus fails to close after birth
allows a portion of oxygenated blood from the left heart to flow back to the lungs

108
Q

barium swallow

A

a test that shows the inside of your oesophagus
helps diagnose oesophageal cancer
white barium liquid is drunk, which shows up on x-rays
x-rays taken while liquid is swallowed

109
Q

where does the pleural cavity extend to superiorly

A

2-3cm above medial clavicle

110
Q

pneumothorax

A

air in pleural cavity

111
Q

haemothorax

A

blood in pleural cavity

112
Q

empysema

A

pus in pleural cavity

113
Q

atelectasis

A

the collapse or closure of a lung resulting in reduced or absent gas exchange
can occur with obstruction of a bronchus

114
Q

which bronchi is an inhaled object more likely to block

A

right as it is shorter, wider and more vertical

115
Q

left vagus nerve and phrenic nerve in relation to the hilum of the lung

A

LVN passes posteriorly whereas the phrenic nerve passes anteriorly

116
Q

pericardial effusion

A

excess fluid in pericardial cavity

117
Q

pericardial tamponade

A

compression of heart due to excess fluid and fibrous pericardium

118
Q

impressions on the left lung

A

arch of the aorta and descending thoracic aorta

119
Q

impressions on the right lung

A

SVC and azygous azygos vein

120
Q

effect of aortic stenosis on the heart

A

left ventricular hypertrophy

121
Q

ligamentum arteriosum

A

remnant of ductus arteriosus

122
Q

what forms the superior vena cava

A

left and right brachiocephalic vein

123
Q

what vein drains into the SVC

A

azygous vein

124
Q

blood in coronary sinus

A

deoxygenated blood from heart walls

125
Q

crista terminalis

A

a boundary
smooth wall - sinus venarum posteriorly
rough wall - pectinate muscles anteriorly

126
Q

fossa ovalis

A

remnant of opening between L and R atria

allows blood to bypass lungs in embryonic development

127
Q

explain foetal circulation

A

oxygenated blood enters through umbilical vein
some blood enters the liver and the rest enters the ductus venosus to bypass liver and enter IVC
IVC enters the RA and most of the blood passes through foramen ovale to LA, LV and aorta
blood entering RA from SVC is poorly oxygenated as is blood returning from the lungs
this passes through the ductus arteriosus and reduces the oxygenation of the blood in the aorta

128
Q

where are the SA and AV nodes located

A

RA

129
Q

function of tricuspid valve

A

prevents backflow of blood into RA during systole

130
Q

cordae tendineae

A

attaches cusps to papillary muscles

131
Q

papillary muscles function

A

contract to prevent cusps reverting into atria during systole

132
Q

function of pulmonary valve

A

prevents backflow of blood into right ventricle during diastole

133
Q

what are trabeculae carnea

A

muscular ridges in wall of ventricle

134
Q

function of mitral valve

A

prevents backflow of blood into LA during systole

135
Q

function of aortic valve

A

prevents backflow of blood into LV during diastole

136
Q

components of the posterior mediastinum

A

oesophagus
descending thoracic aorta
azygos vein and hemi-azygous
thoracic duct

137
Q

what are conchae/turbinates

A

shelves of bone in nasal cavity
surface of these are lined with collated respiratory epithelium - secrete mucous and fluid, warm, filter and humidify air and increase turbulence of inspired air to ensure greater contact with RE

138
Q

turbulent air

A

airflow is turbulent higher in tract
this flow produces numerous collisions between molecules so the air quickly loses speed and a higher pressure gradient is require to maintain rate
more work required to move same volume of air
mixes better with surroundings

139
Q

laminar flow

A

layers of air moving in same direction
resistance is lower
from bronchi downwards

140
Q

role of diaphragm in breathing

A

contraction causes it to flatten - increases volume of the thoracic cavity lowering the pressure within it and allowing lungs to fill with air
relaxation of the muscle causes it to become dome shaped which decreases volume of thoracic cavity and raises pressure within the cavity - helps push air out of lungs
primary muscle involved in breathing

141
Q

role of external intercostal muscles in breathing

A

fibres run downwards and forwards between ribs
contraction raises and rotates the ribs to increase thoracic cavity volume
involved in quiet and forced breathing
innervated by intercostal nerves

142
Q

role of internal intercostal muscles in breathing

A

fibres run downwards and backwards between ribs
contraction pulls ribs down and in - decreases volume of thoracic cavity and assists forced expiration
intercostal nerves innervate

143
Q

role of abdominal muscles in breathing

A

relax during inspiration

contract during forced expiration and help decrease volume of thoracic cavity by pushing diaphragm up

144
Q

role of accessory muscles in breathing

A

become active if respiration is more vigorous or in disease when breathing is difficult

145
Q

interactions of gas particles depends on the following

A

dimensions of the airway
density of gas - high water vapour in humid air increases air density
flow type

146
Q

inspiratory capacity (IC)

A

all air breathed in during a maximal inspiration at the end of a normal expiration
IRV +Vt

147
Q

expiratory capacity (EC)

A

Vt + ERV

all air breathed out during a maximal expiration at the end of a normal inspiration

148
Q

functional residual capacity (FRC)

A

volume of air remaining in the lungs at the end of the normal expiration ERV + RV

149
Q

vital capacity (VC)

A

all the air that can be expired from a maximal inspiration

IRV + Vt + ERV

150
Q

total lung capacity (TLC)

A

all the air that is possible for lungs to contain

IRV + Vt + ERV + RV

151
Q

inspiratory reserve volume (IRV)

A

maximum volume above tidal volume that we can inspire into our lungs (approx 3L)

152
Q

tidal volume (Vt)

A

volume we inspire and expire during restful breathing

approx 0.5L in restful breathing

153
Q

expiratory reserve volume (ERV)

A

max volume below the tidal volume that we can expire

approx 1.5L

154
Q

residual volume (RV)

A

volume of air remaining in the lungs after a full expiration
can never empty lungs completely
approx 1.2L

155
Q

causes of heart failure

A 
common:
MI
dilated cardiomyopathy
excess alcohol
high BP
less common:
chemotherapy
genetics
nutritional
156
Q

symptoms of heart failure

A

breathlessness
ankle swelling
fatigue

157
Q

signs of heart failure

A 
sinus tachycardia
raised JVP
murmurs
ankle/sacral oedema 
pulmonary crackles
pleural effusion
etc
158
Q

waves on a JVP graph

A

a wave - atrium contracting; tricuspid valve open
x descent - atrium filling; tricuspid closed
v wave - atria tense, full; tricuspid closed
y decent - atrium emptying; tricuspid open

159
Q

diagnosis of heart failure

A 
CXR - can be normal
blood tests
ECG
angiography
history
CMRI - dead/scarred heart is white
CMR
VO2
ECHO
examination 
not in order
160
Q

signs of heart failure on an ECHO

A

regional wall motion abnormality (eg post MI)
dilated chambers
valvular dysfunction

161
Q

treatment of heart failure

A

beta blockers
ACE inhibitors
aldosterone antagonists
diuretics

162
Q

SGLT2 inhibitors

A

inhibit proximal tubular glucose reabsorption
cause diuresis, natriuresis
lower BP
reduces weight

163
Q

drugs which may precipitate/aggravate heart failure

A 
NSAIDs
Ca2+ antagonists 
anti-arrhythmics
tricyclic antidepressants 
corticosteroids
164
Q

implantable cardioverter defibrillator

A 
if heart goes chaotic it will fire - returns heart to sinus rhythm
problems:
does not improve symptoms
expensive
inappropriate shocks
psychological burden
driving implications
165
Q

intra-aortic balloon pump

A 
1st line for cardiogenic shock
diastolic augmentation of aortic pressure
increased coronary perfusion 
reduces afterload
improves cardiac output
166
Q

heart transplantation for heart failure

A 
last resort
mean survival of ~10 years
increased risk of:
opportunistic infection 
malignancy 
renal failure
hypertension 
coronary artery disease
167
Q

function of the azygous vein

A

drains posterior thoracic wall
back up if vena cava is blocked
hemiazygous vein is similar but on the left and is smaller

168
Q

where does gas exchange take place in a foetus

A

placenta not lungs

169
Q

what carries oxygenated blood in fetal circulation

A

IVC

170
Q

function of autorhythmic cells

A

have the capacity to get excited
tell heart to contract and relax
grouped at SA and AV nodes
the AR cells at SA node are dominant - set pacing for rest of the heart - start electrical impulse causing RA to contract

phase 2 cardiovascular and respiratory block (5 decks)

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