RESPIRATORY Flashcards

Question

what is meant by the term closing capacity?

Answer 1

closing capacity is the volume of lung in which the small airways begin to close of during expiration. it is made up of the closing volume + residual capacity. in health this is well below the FRC so in normal tidal breathing, small airways don't close if FRC is reduced, CC can encroach on normal breathing and airways can collapse leading to gas trapping and atelectasis.

Answer 2

reduction in FRC - anaesthesia, lithotomy, pneumoperitoneum, pregnancy etc age - increase in closing volume due to less ability to hold open airways with connective tissue. other causes of increased closing volume = asthma, COPD, smoking. can add PEEP to splint open the airways at end of expiration.

Answer 3

phenomena whereby the state of a system depends on its history i.e. if the measured value is rising or falling. in respiratory physiology, hysteresis describes the change in pressure-vol curve of the lung in expiration and inspiration this is because in expiration, there is no need to overcome elastic forces and surface tension. hence the pressure required to inflate the lungs is more than to exhale.

Answer 4

rearrange equations work = area in curve = P x V not pressure and volume arent at 0. due to residual volume and PEEP. could draw the pressure at 0 and then demonstate adding PEEP moves the curve towards more compliant region. the curve is exactly the same in spontaneous however - the values on x are negative i.e. more negative towards right.

Answer 5

elastic work - work needed to overcome elastic forces of chest wall, lungs and surface tension resistive work - work against friction to air flow e.g. asthma/ bronchoconstriction

Answer 6

volume of inspired air that does not take part in gas exchange i.e. ventilated areas of lung that are not perfused. in a typical healthy individual TV = 500 Alveolar ventilated volume = 350 deadspace 150ml (around 2ml/kg)

Answer 7

physiological DS = anatomical DS + alveolar DS anatomical = volume of conducting airways e.g. nose, pharynx,larynx, up to terminal bronchi alveolar DS = poorly perfused alveoli that do not take part in gas exchange. in anaesthesia DS is increased by apparatus e.g. HMEF, tubing, facemask, bronchodilators , neck extension/jaw thrust.

Answer 8

anatomical dead space = fowler method (nitrogen washout) physiological = bohr equation

Answer 9

all expired CO2 comes from alveolar gas FACO2 x VA = FECO2 x TV alveolar vent volume = TV - VD FACO2 x (TV-VD) = FECO2 x TV the FACO2 can be approximated to PaCO2 and FECO2 to PECO2 (pp of expired CO2) PaCO2 (TV-VD) = PECO2 x TV Rearrange VD/VT = PaCO2- PeCO2 / PaCO2 usually the ratio is around 0.2-0.4

Answer 10

Spirometry is a test that measures lung function by assessing the volume and flow of air that a person can inhale and exhale. It is commonly used to diagnose and monitor respiratory conditions like asthma, COPD, and other lung disorders. 2 types - water sealed spirometry and dry spirometry in water sealed spirometry - patient breaths into a closed chamber that is partially submerged in water. breathing in and out causes it to be displaced up and down causing a pen to move on a piece of paper (diagram) dry - air moves bellows which move a pen to draw.

Answer 11

method used to measure FRC , RV , TLC relies on boyles law. it can also measure airway resistance - can be used for asthma etc person sits in air tight box and breathes in and out through a mouth piece connected to outside world. there is a pressure sensor within the cabin that measures cabin pressure pressure sensor in mouth piece that measures pressure inside lungs as patient breaths in, the thorax increases in volume, the cabin reduces in volume and hence increases in pressure. after some normal breathing, a valve in mouth piece closes before inspiration. now patient inspires and pressure reduces in lung but no airflow. this negative pressure generated is measured at a pressure transducer in the mouth. can use the pressure through various calculations and application of boyles law, FRC and TLC can be measured.

Answer 12

measurement of total lung capacity.. patient breaths in O2 and helium helium is not very soluble - goes in and comes out. (not absorbed) CO2 is absorbed by soda time. conc of helium inspired is known conc of helium at end of expiration is measured. volume in is known hence CxV = CxV. can work out unknown volume.

Answer 13

air has 79% N2 FRC should have 79% N2 as N2 is not absorbed. patient breaths in and out into closed system of 100% O2. The N2 in lungs will equibrillate into the bag of O2. after equilibration, the conc of N2 is measured in the bag. N2 conc in bag x vol = FRC x 0.79 as the amount of N2 should be the same as it is not being added / removed.

Answer 14

under estimation as poorly ventilated areas of lung are not measured. body plethysmography has the advantage here.

Answer 15

measures dead space via a single nitrogen wash out test after normal breathing of 79% N2, the subject takes one vital capacity breath of O2 the expired gases after this are measured over time. N2 concentration is plotted on y axis and volume/time on x axis. phase 1 = anatomical dead space filled of 100% O2 phase 2 = rise in N2 as deadspace is mixed with alveolar N2 Phase 3 = alveolar gases containing N2 so plateus. no dead space phase 4 = steep rise as poorly ventilated alveoli empty - these had minimal O2 entering them as poorly ventilated. also determines the closing volume. just before this is the closing capacity. deadspace is calculated by measuring midpoint of phase 2 and it is the volume before that point (including phase 1)

Answer 16

note volume decreasing on x axis max flow in expiration = 8-10L/sec max in inspiration = 4-6L/sec during expiration - more forceful and the flow rates peak more due to elastic recoil of the lungs less explosive in inspiration so less of a peak.

Answer 17

body plethosmyography nitrogen wash out helium dilution

Answer 18

pregnancy = progesterone causes airway dilation age - loss of elastic tissue, number of alveoli diminish so relatively deadspace is increased

Answer 19

changing minute vent by increasing RR and reducing TV will increase proportion of deadspace

Answer 20

physiological - pregnancy - age - standing - shallow faster breathing > slow deep breathing for same MV - cardiac output - reducing cardiac output pharmacological - bronchodilators equiptment and anaesthesia - more tubing/ face mask/ HMEF - jaw thrust

Answer 21

decrease transporting airways e.g. tracheostomy, bronchoconstriction increase perfusion of alvolei - increase CO

Answer 22

increase in dead space and RV decrease in TLC and VC

Answer 23

almost 0 before birth then increases gradually from birth to 5yrs then static for rest of life. no change with elderly

Answer 24

the taller you are the larger the lung volume all slightly lower in female than males for a given height

Answer 25

chest wall - always trying to expand so in the negative values. lung is always trying to collapse - in the more positive region. note both start at RV combined curve in dark blue - this is combined values for each e.g. at bottom -20 vs 0 means it starts at -20. at the top +5 and +20 = +25. at the point where both are equal e.g -10 and +10 = 0 this is equivalent to FRC as this is the resting state where outward recoil balances inward recoil of lungs. the compliance of chest wall and lung separately is similar - can be demonstrated by similar shape. however compliance of them together is slightly flatter so reduced compliance

Answer 26

T = PR (no division by 2)

Answer 27

reduced inward pressure of alveoli - hence less drawing effect on fluid into lungs

Answer 28

obstructive disease - top image blue line. - can see during expiration peak expiratory flow not as high due to resistance, scalloped appearance due to airway collapse so early decline in flow - also increased RV and increased TLC due to gas trapping or loss of elastic tissue in emphysema restrictive disease - bottom smaller volumes - shifted to right (remember values are decreasing on x axis). max flow rates are reduced. thinner curve - reduced VC - smaller stiff lungs

Answer 29

e.g. tracheal stenosis , external compression - goitre volumes are unchanged but peak flow rates are less due to resistance to flow in both inspiration and expiration.

Answer 30

intra thoracic - effects expiratory flow extra thoracic - effect inspiratory flow for upper airway both effected intrathoracic e.g. bronchial tumour, tracheomalacia, bronchoconstriction. extrathoracic e.g. goitre, oesophageal tumour.

Answer 31

subject takes deep breath in and then exhales as quickly as possible until forced expiratory reserve exhaled. FVC = forced vital capacity = volume at end of expiration FEV1 = volume exhaled in 1 second of max expiration. FEV1/FVC normally 0.75 to 0.8 in obstructive - eventually get to FVC but slower, hence lower FEV1. thus ratio <0.7. in restrictive - lower lung volumes due to small fibrotic lungs so reduced FVC. FEV1 same or slightly reduced. may get an increased ratio.

Answer 32

measure of diffusion capacity defined by the volume of carbon monoxide transferred across alveolar membrane into the blood per minute per unit partial pressure of CO. = TLCO patient inhales single VC breath of 0.3% CO and hold breath for 10seconds. inspired and expired CO is then measured. the difference between them is how much eas taken up by lungs. normal value = 17-25ml/min/mmHg

Answer 33

increase = pulmonary haemorrhage, polycytheaemia, exercise, obesity decrease = fibrosis, emphysema, pulmonayry oedema, P.E , lobectomy , anaemia

Answer 34

capacity is the sum of 2 or more lung volumes. e.g. FRC = RV + ERV

Answer 35

FEV1 = GOLD criteria FEV1 >/= 80% = class 1 50-79% - class 2 30-49 - class 3 <30 - class 4

Answer 36

ventilation is the process of moving air into and out of the lungs for gas exchange inspiration: - diaphragm & external intercostals contracts - causes chest wall expansion - increases intrathroacic volume and hence reduces pressure - transmits to negative pressure in alveoli - flow of gas down pressure gradient expiration - relaxation of muscles - recoil of lungs and chest wall to resting state - reduced volume, increased pressure - gas flows out. under normal ventilation inspiration is active = work needed to overcome elasticity of lung and surface tension and chest wall. expiration is passive as recoil to resting state. forced expiration involved internal intercostals and abdominal muscles to help force further air out.

Answer 37

gradient of volume time curve during forced expiration more commonly using mini wrights peak flow meter.

Answer 38

intrapleural pressure = pressure between parietal and visceral pleura (negative pressure) intrapulmonary pressure = pressure inside alveoli and resp tract transpulmonary = difference of the above (intrapulmonary - intrapleural) = always positive because intrapleural is negative.

Answer 39

flow in the airways can be laminar or turbulent describe laminar and turbulent flow at this stage. laminar = flow in parrallel lines, obeys hagen poiselle equation. turbulent = flow disorganised, eddie currents, swirls. does not obey hagen poiseulle. reynolds number can determine which type of flow Re = V p d / n p = density, V = velocity, d = diameter, n = viscoity. >2000 turbulent, <2000 laminar hence laminar flow more likely at low velocity, small diameter airways. also smooth surfaces. hence large airways = turbulent - beneficial as helps filter particles as currents colide with walls and particles are trapped by mucus. smaller airways = laminar - less work of breathing, more efficient

Answer 40

FLOW = ΔP πr4 / 8nl

Answer 41

reynolds number dimensionless number that can determine which type of flow is more likely. Re = V p d / n p = density, V = velocity, d = diameter, n = viscoity. >2000 turbulent, <2000 laminar

Answer 42

increased resp rate = increases velocity increased diameter = more likely in large areas obstructions in airway / at bifurcations increasing density of gas - e.g. diving

Answer 43

Heliox = 21% O2, 79% helium helium is less dense than N2 so reduces reynolds number more likely to promote laminar flow less work of breathing - laminar breathing is proportional to ΔP. whereas turbulent is proportional to root ΔP so more negative pressure needs to be created in turbulent to have same effect on flow. i.e. more work.

Answer 44

the opposition to flow in the airways. change in pressure for a given charge in flow cmH20 / L/ second

Answer 45

different lung units take different times to fill and empty the time constant defines the time taken for a lung to fill by 63% of its total volume. it is a product of the compliance and resistance of that lung unit. time constant = resistance x compliance this means different parts of lungs empty/ fill at different rates. (the more compliant, the more volume for a pressure change hence takes longer to fill)

Answer 46

high = asthma = slow filling and emptying low = ARDS = lower volume

Answer 47

apex = lung is pulled down by gravity - high resting volume - at top of compliance curve where it flattens out. hence poor compliance base = less distended, on steeper part of the curve - more compliant

Answer 48

west zones describe the relationship between alveolar pressure, venous pressure and arterial pressure to determine whether alveoli are perfused or not. west zone 1 = PA> Pa >Pv - top of lung West zone 2 = Pa>PA>Pv - middle of lung west zone 3 = Pa>Pv >PA - base of lung in Z1 lung is stretched out by gravity and PA is high. blood pressure reduced due to gravity. pulmonary arteries are compressed by alveoli = dead space. In health not seen. In Z2 - artery pressure is more than alveolar due to less gravity effects/ better systolic. perfusion occurs and is determined by Pa-PA difference. blood flow only in systole In Z3 - pulmonary and venous pressure both higher. perfusion dependant on PA-Pv difference. some alveoli may be compressed in this zone - shunt.

Answer 49

top = -8cm H20 bottom = -1.5cm H20 hence apex the alveoli are more distended

Answer 50

in health unlikely to occur because Pa is adequate. however in IPPV the PA can increase > Pa or if high intrinsic PEEP e.g. asthma OR hypovolaemia - reduces Pa on the other hand - exercise increases blood flow and reduces likelihood of Z1

Answer 51

represents ratio of ventilation to perfusion in the lungs. normally around 0.8 in an ideal lung they would be perfectly matched at 1.

Answer 52

high V:Q >1 = deadspace more common at top of lungs low V:Q <1 = shunting more common at base of lungs

Answer 53

both ventilation and perfusion reduced at apex but perfusion more so. so high V:Q both ventilation and perfusion increased at base (ventilation due to better compliance, perfusion due to gravity) but perfusion more so increased. so low V:Q

Answer 54

high V:Q - causes of deadspace - respiratory - bronchodilation , emphysema - circulatory - hypovolaemia/ P.E low V:Q - causes of shunt - physiological - atelectasis from obesity, age, pregnancy - pathological - pneumonia, atelectasis behind obstruction e.g. tumour, pneumothorax/ collapsed lung.

Answer 55

falls as less perfusion more ventilation to dilute CO2

Answer 56

from the picture QTCaO2 = Qs(CvO2) + (QT-Qs)(CcO2) expand and rearrange.. QTCaO2 = Qs(CvO2) + QTCcO2 - Qs(CcO2) Qs(CcO2)- Qs(CvO2) = QTCcO2 - QTCaO2) Qs (CcO2-CvO2) = QT (CcO2-CaO2) Qs/QT = (CcO2 -CaO2)/ (CcO2-CvO2) Qs/QT normally around 0.2 QT = cardiac output CcO2 can be calculated from PAO2 - alveolar gas equation and then using O2 dissociation curve. (cant be measured directly) CvO2 - from mixed venous gas e.g. central venous catheter (pulmonary artery) CaO2 - arterial O2 gas

Answer 57

reduced PaO2 no change in PaCO2

Answer 58

An area of lung that is perfused but not ventilated. blood that passes through the lung without participating in gas exchange. this blood will then mix with oxygenated blood and enters systemic circulation. can be categorised into phsyiological - bronchial circulation = bronchial veins drain into pulmonary vein and LA - Thebesian veins = coronary venous blood draining into LV - normal pulmonary shunting - some areas of lung will be collapsed e.g. bases when lying down. pathological - extrapulmonary = congenital heart disease (R to L shunts), pulmonary AV fistula. - pulmonary = atelectasis, pneumonia

Answer 59

CO2 diffusion is fast, other areas that are ventilated can compensate. if PaCO2 rises, increase resp rate to compensate.

Answer 60

the blood mixed from shunted blood and oxygenated blood from capillaries involved in gas exchange describes the amount of shunting.

Answer 61

minimal effect because those areas that are not ventilated are still adding deoxygenated blood to the arterial blood. the more shunting , the less of an effect increasing FiO2 has.

Answer 62

respiratory failure describes the failure of the functions of the respiratory system either in oxygenation or removal of CO2 can be divided into type 1 or 2 type 1 = hypoxia, normal CO2 type 2 = hypoxia, hypercapnia normal values PaO2 >8kpa, PaCO2<6kpa

Answer 63

pathological reduction in alveolar ventilation below levels required to maintain normal gas tensions. respiratory failure may result from ventilatory failure (normally type 2)

Answer 64

type 1 - V:Q mismatch / shunting - pneumonia , P.E, pulmonary oedema - hyperventilation will keep CO2 normal or lower it. it will also reduce PaO2 via alveolar gas equation but not enough to account for V:Q/shunts. type 2 - hypoventilation - now CO2 effected - failure of respiratory centre - opioids, anaesthesia, COPD - chest wall issues - flail chest, neuropathic (guillian bare), muscular dystrophies/ relaxation, fatigue (asthma attack)

Answer 65

describe as the pathway of ventilatory control higher centres - damage by tumours etc, changed sensitivity by opioids, anaesthesia upper motor neurons - distruption of UMN to spinal cord connection. lesions above C3/4/5 e.g. brainstem stroke/ trauma anterior horn cells - affects connection between UMN and LMN polio lower motor neuron - e.g. GBS, phrenic nerve palsy (interscalene block), MND NMJ - myasthenia gravis, lambert eaton, organophosphate poisoning, muscles - affects ability to contract e.g, muscular dystrophies, splinted diaphragm from increased abdominal pressure lung and chest wall - disrupted mechanics e.g. kyphoscoliosis, flail chest. increased resistance of airways - COPD/ asthma upper airway obstruction - foreign body, tumour

Answer 66

inversely proportional as MV increases, PaCO2 decreases rectangular hyperbolic relationship

Answer 67

This can be described by Ficks law of diffusion and grahams law of diffusion diffusion rate = (Conc difference x area x solubility) / (thickness x root molecular weight) conc gradient - maintained through ventilation and blood flow area = high surface area from many alveoli thickness = minimal epithelial, BM, endothelial. high cap density solubilty = higher for CO2 than O2

Answer 68

CO2 much quicker due to higher solubility factor in blood. hence diffusion defects effect PaO2 first.

Answer 69

PaO2 = FiO2 (Atm - SVP) - PaCO2/R SVP = 6.3 kpa R = 0.8 this is used to estimate the PaO2 in alveolus. describes the relationship between O2 delivery to alveoli and removal. The O2 removal is deduced from the PaCO2 and respiratory quotient. PaCO2 is a better predictor of ventilation and not affected by shunting like PaO2 is and hence used instead of PaO2

Answer 70

the ratio of CO2 produced to O2 consumed depends on respiratory substrate carbs = 1 protein = 0.8 fats = 0.7 european diet around 0.8 PECO2 / PiO2 - PeO2 = RQ

Answer 71

assumes full saturation with H20 at alveoli assumes no CO2 in inspired air assumes CO2 and O2 are ideal gases assumes RQ PAO2 and PaO2 assumed to be in equilibrium

Answer 72

use alveolar gas equation to explain e.g. FiO2, Patm, alveolar ventilation (PACO2 is inversely proportional to alveolar ventilation so used as a surrogate)

Answer 73

PAO2 - PaO2 describes the difference between alveolar O2 and arterial O2 always >0 due to shunting in normal health around 1.5Kpa increases with increased FiO2 because PAO2 increases much more than PaO2 (FiO2 doesnt really improve shunt) can also be increased if there is impairment in diffusion and equilibrium not reached.

Answer 74

mostly bound to Hb small amount dissolved in blood Total O2 content = (Hb x sats x 1.34) + (0.0225 x PaO2) (if in mmHg use 0.003 instead of 0.0225) hb in g/100ml answer is in ml O2 /100ml plasma

Answer 75

describes the mls of O2 carried per g of Hb theortical value in vitro = 1.39 in vivo = 1.34ml/g due to presence of other forms of Hb e.g. methamoglobin and carboxyHb

Answer 76

RBC - 6-8 um - biconcave - no nucleus / mitochondria - glycolysis only - extensive cytoskeleton - flexible Hb - 4 chains polypeptide = 2a and 2b - globular protein with quarternary structure - each has heme group with Fe2+

Answer 77

physiological: - HbA = 2a,2b = adult, most abundant - HbA2 = 2%, 2a,2d, not as efficient - HbF = 2a2g , increased affinity for 02, <1% by 6month pathological - HbS = sickle cell, abnormal B -MetHb = methamoglobin (Fe3+ cant bind 02) COHb = usuallty <2%, higher in smokers

Answer 78

labelled x = O2 in kpa labelled y = % saturation important points p50 = 3.5 - 50% venous = 5.3 - 75% arterial around 100% = 13

Answer 79

due to cooperative binding whereby before any O2 are bound Hb is said to be in tense state whereby binding sites are less accessible hence binding is harder after first binds, conformational change, increases affinity for next O2 moves to relaxed state. hence shallow gradient to start with then increase then at the end shallow gradient as less binding sites available. so rate of saturation reduced.

Answer 80

25% extracted hence venous saturations around 75%

Answer 81

To the right - hyperthermia, hypercapnia, acidosis, 23DPG , sickle cell, pregnancy, exercise to the left - opposite of above, fetal Hb, COHb

Answer 82

rightward shift due to increase H+ hence acidosis promotes unloading. this occurs due to changes in Hb affinity for O2 in presence of H+. this couples metabolism to oxygen delivery.

Answer 83

hyperbolic relationship much higher affinity myoglobin acts as a temp store for O2 in muscles.

Answer 84

organophosphate molecule produced during glycolysis in RBC binds Hb residues and reduces affinity for O2 hence promotes unloading of O2 at tissues - right shift. links metabolism to O2 delivery. increase in metabolism, chronic hypoxia (altitude, anaemia), pregnancy, exercise

Answer 85

at lungs - low CO2, higher pH - left shift, increases affinity at tissues - metabolism - right shift - increases unloading.

Answer 86

Erythropoeisis is the production of RBC which occurs in the bone marrow of axial skeleton in adults. in the fetus this occurs in liver and spleen in neonates this occurs in all bones. RBC are produced from pleuripotent haemopoietic stem cells which are driven by the hormone Erythropoietin (EPO) reticulocytes are released into the plasma where they mature into RBC this is controlled by EPO which is produced by renal parenchyma and liver in response to hypoxia. stimulates haemopoeitic stem cells to differentiate to proerythroblasts which undergo series of transformations to reticulocytes

Answer 87

autosomal recessive genetic condition resulting from a point mutation (A to T) that causes an abnormality of B chain of Hb (glutamate to valine) leading to sickling of Hb and RBCs results in sickle crisis and anaemia more prevelent in africa, asia and southern europe.

Answer 88

HbSS = homozygous = sickle cell disease HbAS = heterozygous = sickle trait. the presence of other Hb varients can promote/ inhibit sickling of HbS

Answer 89

A--> T glutamate --> valine hydrophobic pocket - promotes polymerisation of Hb RBC less flexible and resistant to changes in shape. result in haemolysis and anaemia and various crisis ... 1. haemolytic crisis 2. vaso-occlusive crisis - inflammation of vascular endothelium +/- sickling of Hb blocking vessels - thrombosis and vascular stasis. ischaemia (acute chest syndrome, stroke, bony pain) 3. visceral sequestration crisis = massive pooling in spleen, splenomegaly, anaemia, hypotension, abdo pain 4. aplastic crisis - parvovirus triggers this. drop in Hb and reticulocytes.

Answer 90

acidosis dehydration hypoxia infection

Answer 91

avoid sickling - avoid hypoxia = preoxygenate etc - avoid dehydration - pre op IV fluids - avoid infection - micro discussion r.e. additional prophylaxis - avoid acidosis - good MV to maintain normal CO2 - avoid hypothermia - bear hugger

Answer 92

autosomal recessive genetic disease involving imbalance in alpha and beta chains of Hb. 2 forms alpha thalessemia - deletion of alpha gene beta thallesemia - deletion of beta gene various degrees of severity depending on how many chains absent/ mutated. e.g. B thal minor = 1 chain mutated, may have microcytic anaemia, but relatively assymptomatic. e.g. B thal major = severe anaemia and tranfusion dependant. becomes apparent from 6 months when gamma is replaced by beta. similarly alpha thalaessmia can be trait where 1 mutated gene to 4 mutated genes is incompatible with life and results in hydrops fetalis and death in utero. found more in mediterranean and south asian populations.

Answer 93

CO binds Hb x300 more affintiy hence fewer binding sites for O2 conformational change increases the affintiy for O2 of the remaining binding sites hence reduced ability to off load O2

Answer 94

RBC are removed by reticuloendothelial system macrophages in liver spleen and blood. globin chains are broken down to aa and reused. iron also reused. porphyrin ring is converted to bilirubin and then undergoes conjugation by liver converted to bile which is excreted in small bowel.

Answer 95

describes a stepwise reduction in pp of O2 between atmosphere and mitochondria 21% O2 inspired = hence 101x 0.21=21kpa humidification in trachea and airways (101 - 6.3) x 0.21 = 19 kpa alveoli - this air mixes with PaCO2 and O2 is taken up. hence less O2. can be calculared by alveolar gas equation = 13.3 capillary blood - small drop to maintain diffusion gradient however equilibrium basically reached so 13kpa arterial blood = mixing of shunted blood A-a gradient. in health usually 1- 1.5kpa. now drops to 12kpa at mitochondria - steady drop as it diffuses throughout tissue. by time it reaches mitochondria 1.5-4kpa depends on capillary density, how deep mitochondria is etc

Answer 96

the minimum partial pressure of O2 at which oxidative phosphorylation occurs in mitochondria. 0.13Kpa usually O2 reaches mito at 1.5 kpa so large safety margin

Answer 97

term used to describe flow and consumption of O2 throughout the body. i.e how much is delivered. O2 flux (DO2) = CO x O2 content of blood

Answer 98

critical DO2 is the minimum O2 delivery needed to meet the oxygen consumption of the tissue. this can be explained using VO2 max VO2 = consumption of O2 by tissues DO2 = delivery of O2 to tissues. initially VO2 is limited by delivery of O2 to tissues and by increasing delivery, VO2 can increase. At VO2 max, DO2 is no longer the limiting factor

Answer 99

VO2 = oxygen consumption = CO x (CaO2 - CvO2)

Answer 100

VO2 / DO2 consumed / delivered normally around 0.25 i.e. 4 x more delivered than needed. cardiac muscle is highest at around 0.6 OER increases if VO2 increases (sepsis) or DO2 decreases (low CO/ hypoxia)

Answer 101

high lactate = anaerobic respiration venous sats <75% bigger difference in arterial venous sats - i.e. higher extraction of O2

Answer 102

defined by the inadequate delivery of O2 to tissues or by the inability of tissues to use O2 that is required to meet metabolic demands of the tissue. may be systemic or regional.

Answer 103

hypoxaemia = low PaO2. may be the cause of hypoxia hypoxia may occur without hypoxaemia e.g. cyanide poisoning (unable to use) or anaemia cyanosi s = clinical signs associated with hypoxaemia e.g. deoxy Hb visible in capillaries of skin/ mucus membranes.

Answer 104

hypoxic hypoxia - PaO2 <12. also reduced saturations of Hb due to dissociation curve. e.g. high altitude, pneumonia, oedema/ fibrosis. anaemic hypoxia - low Hb or CO poisoning ischaemic / stagnant hypoxia - regional embolism/thrombus, systemic - low CO , microcirculatory failure (sepsis) histotoxic hypoxia - unable to use O2 e.g. cyanide poisoning uncouples oxidative phosphorylation (high PaO2 and high PvO2)

Answer 105

draw a normal curve - O2 sats at 13.3 100%. venous sats at 5.3 75%. p50 at 3.5 hypoxic hypoxia = both O2 sats and venous lower histocytic - both high stagnant bigg A-v difference. anaemia = normal sats but scale for content is lower.

Answer 106

can be categorised into the effects of - lack of aerobic respiration - by products of anaerobic respiration lack of aerobic respiration - cells have creatine phosphate stores that last about 90 seconds. glycolysis can produce 2ATP from then on. normally aerobic respiration produces 38ATP. without aerobic respiration a lot les ATP for cellular processes to occur e.g. cardiac muscle cant contract and will fatigue, neurons can't maintain membrane potential and hence fire AP. Cells become stressed and can apoptose. anaerobic resp - lactic acid - lowers pH - effects on enzymes and membrane potential cell death - release of K+ - hyperkalaemia inflammation

Answer 107

This can be divided into short term and long term measures immediate term/ local: - local tissue hypoxia - anerobic respiration - metabolites cause reactive hyperaemia. - bohr effect - release of more O2 short term - peripheral chemoreceptors found in carotid bodies and aorta - detect low PaO2 and low O2 content. When PaO2 <13 they discharge and send impulses (via glossopharyngeal and vagus) to the medulla (nucleus tractus solitarius) - increase in minute ventilation (however mostly sensitive below 8Kpa) - sympathetic activation - increase HR and CO. overall vasoconstriction to divert O2 to important places. later - kidneys detect hypoxia and release EPO - EPO acts on bone marrow to stimulate erythropoiesis

Answer 108

local effects of hypoxia in cardiac tissue and heart is to cause vasodilation to improve blood flow in response to hypoxia. this would increase cerebral blood flow, although this is only significant below 6.7kpa similarly in the heart. lungs however have opposite effect - hypoxic vasoconstriction. this is to improve V:Q

Answer 109

O2 content = (Hb x 1.34 x sats ) + (Kpax0.0225) O2 is carried via Hb - majority and dissolved in blood - v small amount huffner constant = amount of O2 in ml per g of Hb

Answer 110

VO2 = CO x (CaO2 - CvO2)

Answer 111

CO2 has a number of modes of transport in the blood. Mostly as Bicarbonate (HCO3) - in RBC, carbonic anhydrase catalyses H20+CO2 --> H2CO3 --> HCO3 + H+ - H+ buffered by haemaglobin - HCO3 exchanged for chloride and travels in plasma. Also some as Carbamino compounds - carbaminohaemaglobin formed when CO2 binds Hb amino acid residues. - deoxy Hb is x3.5 more affinity for CO2 than oxy (haldane) and a small amount dissolved in the blood - CO2 more soluble in blood than O2 - henrys law states amount dissolved is proportional to partial pressure - PaCO2 x 0.223 at 37 degrees (or 0.03 mmHg)

Answer 112

enzyme that catalyses CO2 +H20 to H2CO3 (carbonic acid) which can further dissociate to HCO3. This is found in RBC, kidneys, lungs, aqueous humour of the eye and GIT. major role in CO2 transport

Answer 113

This decribes the ability for deoxyHb to bind to CO2 with higher affinity and thus have better carrying capacity than oxygenated Hb. This couples O2 release and CO2 removal. It means Hb binds to CO2 at the tissues where Hb is deoxygenated and then releases it at the lungs where Hb is more likely to be oxygenated.

Answer 114

pink line = dissolved in plasma purple = dissolved + bicarb blue = dissolved + bicarb + carbamino biggest jump between pink and puple, hence mostly as bicarbonate. could point out some typical values - venous blood 50ml/100ml blood at 6.1kpa - arterial blood 40ml/100ml blood at 5.3kpa drawing O2 curve on top of this - sigmoid shape. plus total content is half so the top of sigmoid curve should end half way of emax of CO2.

Answer 115

ventilation is controlled by tight neuronal homeostatic mechanisms in order to maintain PaCO2, PaO2 and pH of the blood. As with all homeostatic mechanisms, it involves sensors, control centre and effectors. Sensors - peripheral and central chemoreceptors, pulmonary stretch receptors, irritant receptors, joint receptors control centre = all feed in and are integrated at the medulla and pons. effectors = muscles of inspiration (diaphragm, intercostals ) and muscles of expiration. The control centres have 4 main nuclei - dorsal respiratory group (DRG) - medulla - ventral respiratory group (VRG) - medulla - pneumotaxic centre - in pons - apneustic centre - pons

Answer 116

stimulates peripheral chemoreceptors to stimulate ventilation

Answer 117

carotid and aortic bodies contain chemoreceptors. (arch of aorta, carotid bifucation) mostly responsible to detecting and responding to low PaO2 (rather than PaCO2). carotid bodies: very high blood flow of 2L/100g of tissue / min. hence have a small AV difference, hence small changes to arterial PaO2 can be detected through reduced ATP production which results in dopamine NT release. The response is augmented with pH changes. hence carotid bodies increase in firing when PaO2 low or pH low. Aortic arch - less sensitive than carotid bodies because blood flow not as high. but also can to some extent respond to content of O2 (i.e anaemias) as well as PaO2

Answer 118

located on ventral surface of the medulla respond to changes in PaCO2 which results from changes to pH of CSF CO2 crosses BBB. in CSF reacts with H20 to form carbonic acid. lowers pH of CSF. the increased H+ conc is detected by the chemoreceptors. leads to increased firing to respiratory centre to increase MV less protein and HCO3 in CSF, hence less buffering capacity so sensitive to small changes However slightly slower response time as it relies on this reaction.

Answer 119

after 48 hrs of persistently high CO2 HCO3 is transported into CSF to correct for pH changes. now pH of CSF is normalised for that level of CO2 hence now the set point for CO2 is higher. the central chemorecpetors will respond to further CHANGES in PaCO2 peripheral chemoreceptors are now more significant hence CO2 retainers may rely more of hypoxic drive to stimulate ventilation.

Answer 120

chronically high CO2 Opioids / anaesthetic agents/ barbiturates other factors - age, genetics, exercise

Answer 121

located in the brainstem nuclei that lie in medulla and pons 4 main anatomical areas medulla: - dorsal respiratory group - - ventral respiratory group these are collectively called central pattern generator and responsible for main control pons: - pneumotaxic group - apneustic area collectively called the pontine respiratory group and fine tune the resp patterns. dorsal resp group - found on floor of 4th ventricle and most neurons within nucleus tractus solitarus where the sensory afferents of CN IX and X end. - responsible for sending outputs to inspiratory afferents involved in normal breathing - intercostals nerves and phrenic nerve ventral resp group - located in ventral medulla and more responsible for active expiration and forced inspiration pneumotaxic centre = modulates outputs of DRG to reduce depth of inspiration hence involved in fine tubing. stimulation causes a terminaiton in inspiration apneustic centre = modifies activity of DRG to prolong inhalation time. again fine tunes

Answer 122

inputs from the cortex can overide the respiratory centre basal output and modulate ventilation e.g. hyperventilate, breath hold etc however eventually brainstem control overides i.e. cant hold breath until death.

Answer 123

cortex - voluntary control limbic system - emotions / anxiety pain pathways pulmonary stretch receptors - protect lungs from over inflation - when there is an increase in transpulmonary pressure they will inhibit inspiration = Hering Breuer reflex irritant receptors = respond to chemical and cold. involved in coughing and bronchoconstiction but also modulate vent J receptors = stimulated by oedema in alveoli and chemicals in pulmoanry circulation. joint and muscle proprioceptors - exercise increases MV before PaCO2 builds up muscle spinal in diaphragm and intercostal - negative feedback

Answer 124

MV on y axis - L/min Kpa on x axis - KpA Increase in PaCO2 increase in MV - linear reponse from about 5 to 10Kpa at 10Kpa - falls - CO2 narcosis. in opioid use. this is shifted to the right

Answer 125

in response to hypoxia - increased response to PaCO2 - towards the left and more exponential similarly low pH also shifts to the left.

Answer 126

not much affect until <8kpa then exponential rise before 8kpa, MV much more sensitive to PaCO2 than PaO2 if PaCO2 is low, then hypoxic curve shifted to the left - doesnt rise until below 5kpa

Answer 127

muscle and joint proprioceptors - at start of exercise before CO2 builds up increase inputs to DRG to prepare for rise in PaCO2 metabolism - increase PaCO2 - increases ventilation via central chemoreceptors. due to tight control, PaCO2 wont change in exercise. may even decrease (over compensation)

Answer 128

These can be considered as local effects and systemic effects locally - pCO2 causes vasodilation in most organs due to reactive hyperaemia. allows blood flow to the tissue to match metabolism - including the brain - increases CBF and ICP if v high. - lungs have opposite effect - vasoconstriction and increase in PVR - cardiac - myocardial depressive effects and arrhythmias. systemically - chemoreceptors detect - increase in MV, increase in sympathetic response - HR and CO. helps in removal. - O2 dissociation curve - shifted to right clinical signs - tachycardia, bounding pulse, raised BP, tachypnoea, confusion, tremor, narcosis and coma.

Answer 129

hypocapnia - reduced production e.g. hypothermia, hypothyroid reduces BMR - increased elimination - hyperventilation from anxiety, hypoxia, pain. hypercapnia - increased uptake - more inspirated (exhausted soda lime), pneumoperitoneum - increased production - sepsis, MH, hyperhyroid

Answer 130

general anaesthesia can affect the respiratory system in many ways. can be divided into the effects of airway devices, drugs, PPV , positioning, and anaesthetic drugs... airway devices: - manipulation of airway can cause laryngospams and bronchospasm. - bypass humidification process - irritation of mucosa, increased risk of infections and crusting. (HME can help prevent) - loss of physiological PEEP e.g. endotracheal tube. 3-5cmH20 normally created by larynx to help splint open alveoli. without can lead to atelectasis - increased work of breathing - narrow ET tube , increased resistance (r^4) - deadspace increased by tubing/eqiptment positioning: - usually supine and pneumoperitoneum or trendelenburg - reduces FRC - can result in closing capacity > FRC --> atelectasis and V:Q mismatch --> hypoxaemia - lower on compliance curve - reduced compliance - increased work of breathing/ airway pressures. - less O2 reservoir, increased risk of hypoxia PPV: - increased airway pressures - risk of pneumothorax - also reduces blood flow by reducing preload/venous return hence increases deadspace - increase in west zone 1 (due to drop in CO / pulmonary BP and increase in alveolar pressures) hence V:Q mismatch drug effects: - muscle relaxants including volatiles - reduced FRC - volatiles inhibit hypoxic vasocontriction - worsening of V:Q mismatch - opioids and benzos - depression of MV response to CO2 - volatiles - dose dependant reduction in TV (also increase RR) - propofol - apnoea and drop in VT, supresion of airway reflexes - ketamine - preserves airway reflexes and spontaneous ventilation. - certain ones cause histamine release and bronchospasm - atracurium, morphine , NSAIDs

Answer 131

atelectasis --> pneumonia bronchospasm --> hypoxia pulmonary oedema (negative pressure e.g. from laryngospasm risk of aspiration

Answer 132

pre - op - assess and make good aanesthetic plan e.g. asthma avoid using atracurium, could you use regional anaesthesia if bad COPD intra op - PEEP, spinal, pressure control ventilation? post op - promote deep breathing after (pain releif, adequate reversal of NMBA)

Answer 133

prolonged operation / positioning that reduces FRC - leads to atelectasis and risk of pneumonia. can reduce by using PEEP pre-existing lung disease e.g. asthma and copd - more reactive airways - bronchospasm inadequate analgesia /addo surgery - reduces depth of breathing after - atelectasis etc.

Answer 134

endothelium of pulmonary vasculature is metabolically active ACE = conversion of angiotensin 1 to 2. breakdown of certain hormones - NA, 5HT3, progesterone. COMT enzyme present Production of arachidonic acid metabolites - leukotrienes, thromboxane (bronchoconstriction), prostaglandins (bronchodilation)

Answer 135

ventilation and gas exchange- uptake of O2, removal CO2 pH homeostasis - compensation via excretion of CO2 metabolism - breakdown of NA and 5HT3 endocrine functions -ACE filtration and protection - cilia and goblet cells, macrophages, vocalisation temp regulation - evapouration, latent heat of vapourisation

Answer 136

where a particle settles depends on its size and speed of inhalation. 30um - sediment in larger airways and are filtered / prevented from reaching alveoli 3-15um - smaller airways 1-3um - alveoli <1um - inhaled and exhaled out, too small to settle so just diffuse in and out. breath holding can promote sedimentation.

Answer 137

refers to the situation across the placenta CO2 travels down conc gradient into maternal blood... increased CO2 in maternal circulation - promotes unloading of O2 decreased CO2 in fetal - promotes O2 uptake (plus fetal Hb has higher affinity than mum)

Answer 138

In spontaneous ventilation - dependant lung (lower down lung) - both ventilation and perfusion are higher here due to gravity (perfusion) and sitting further down on compliance curve (ventilation). However Q>V hence, low V:Q - independant lung (higher lung) - both V:Q are lower here but perfusion more affected than ventilation due to gravity. hence V>Q so high V:Q in these areas. overall the V and Q follow same pattern so V:Q is more matched than in IPPV... Whereby dependant lung - better perfused but less well ventilated V:Q still low but even more so than in SV independant lung - worse perfusion, better ventilation. again bigger mismatch in V:Q - higher. overall more V:Q mismatch in IPPV - mostly due to ventilation favouring independant lung in IPPV vs dependant lung in SV. this is because compliance is low in independant lung and hence takes more force of SV to open it, whereas postive pressure can fill this more easily.

Answer 139

age, BMI functional history smoking respiratory disease - how severe, inhalers, hospital admissions etc may need CXR, spirometry , transfer factor testing.

Answer 140

non invasive, objective measure of evaluating both cardiac and pulmonary function. slowly increase intensity of exercise whilst monitoring breath to breath analysis of CO2, O2 hence can work out CO2 production, O2 consumption VO2 max can be deduced and anaerobic threshold.

Answer 141

emphysema= breakdown of elastin in alveolar walls. results in larger less numerous alveoli. less capacity for gas exchange (reduced S.A) elastin is also present to hold terminal bronchi open via radial traction. this is lost so they collapse - gas trapping.

Answer 142

picture of brain stem very top, not labelled = midbrain next = pons last = medulla top arrow points to pneumotaxic centre next = apneustic centre in medulla = at the back = dorsal respiratory group in front = ventral respiratory group (ventral group made up of 4 other nuclei) nucleus tractus solitarus lies at top of dorsal respiratory group within medulla

Answer 143

shows the CO2 dissociation curve bottom line shows dissolved content can see how increasing PaCO2 increases CO2 dissolved in blood - minimal amount compared to total next line = dissolved + Bicarbonate = can see this is the biggest increase hence bicarb is the biggest contributor to CO2 carriage next 2 are as carbamino compounds in arterial vs venous blood. top one is venous which we can see carries more than arterial. this is because of the haldane effect