Applied respiratory physiology - inc humidification

Question 1

Define saturated vapour pressure

Answer 1

the maximum pressur exerted by the evaporated molecules above the liquid at equilibrium

Question 2

Define humidity

Answer 2

The amount ofwater vapour present in the air

Absolute humidity - the mass of water molecules present per unit of volume g/cm^3

Relative humidity - the percentage of actual humidity relative to maximal humidity possible (saturation point) at a given temperature

Question 3

What effect does temperature have on humidity

Answer 3

The saturated vapour pressure or maximum pressure exerted by evaporated molecules above a liquid at equilibrium is higher at higher temperatures i.e. when water is hot it has a higher saturated vapour pressure and increased potential humidity. Note it is not the air temperature but the water temperature in the air that matters - this is because when the water molecules have more energy they evaporate more readily –> but when they cool they clump together and liquid forms (dew point)

Question 4

Explain how a cloud is formed

Answer 4

he greater the partial pressure of water in the air, the less dense it is and so the more humid air will rise. As air rises the effect of the earth’s gravitational field becomes lower, spreading the molecules further apart and decreasing the atmospheric pressure. This process of expansion requires energy and so the air cools. As the saturated air cools down its constituent water molecules now contain less energy and condensation occurs. The water condenses out (onto dust and other hygroscopic particles present in the air) and becomes visible as cloud. The humidity of the air decreases as the water condenses out and the air becomes denser. It therefore stops rising and an evaporation/condensation equilibrium is reached between the surrounding air and the floating body of water in the form of a cloud.

Question 5

How is air humidified in the respiratory tract

Answer 5

Nose - inferior turbinates. As cold air passes over the inferior turbinates it si warmed to 36 degrees. Additional water vapour is added fro the moist lining of the mucosa. By the time it reaches large bronchi it is fuly saturated 44mg/L giving partial pressure of 6 kPA

Question 6

Why is humidity a probem when considering medical gasses

Answer 6

1. Gasses are manufactured as dry as possible to eliminate ice and water damage to valves and regulators
2. Artificial airways bypass normal humidification

Question 7

Why is moisture important to the respiratory tract

Answer 7

1. Ciliary function and mucous transport - prolonged dry gas causes tenacious secretions –> mucous plugging and susbsequent hypoventilation
2. Dry gas will increase humidification by the lower respiratory tract causing heat loss - this also has a detrimental effect on cilia function

Question 8

Heat loss from respiration - how would you calculate it?

Answer 8

Heat loss from warming inspired air = ventilation x specific heat capacity x temperature rise

Humidifying air = ventilation x water required x specific latent heat of vapourisation

Aggreagted is 10% fo total heat loss for adults

Question 9

Advantages of a HME filter?

Answer 9

Inexpensive
Disposable
passive
Efficient enough to work for 24 hours

Question 10

What makes up a HME filter and how does it work?

Answer 10

Seal unit, hygroscopic material e.g. calcium chloride or silica gel whcih condenses the gas meating the surface simultaneously heating it via the latent heat of condensation and with the next inspiration this is reversed

A 0.2 micrometer filter renders the itnerface impermeable to bacteria and viruses avoiding contamination of circuits

Question 11

What is the efficiency with HME filters

Answer 11

80%

Question 12

Disadvantages of a HME filter?

Answer 12

Passive - therefore not 100% efficient and loss of heat ad moisture does occur over time
Filter adds dead space and resistance
Dead space can range from 8mL in paediatrics to 100mL in adult. Resistance 2cmH20 - also add a dam to secretions increasing work of braething

Question 13

What is the principle of water bath humidifers?

Answer 13

Dry gas is bubbled through a water bath causing humidification as energy is conveyed to water molecules which are then evaporurated

Question 14

What is is the problem with a passive water bath

Answer 14

Inspired gas is bubbled through a unheated water bath therefore humidification is limited by SVP at a lower temperature. Humidification will therefore not be 100% when raised to 37 degrees. Effect exacerbated by cooling of water bath seconddary to latent heat of vapoourations after water vapourised

Question 15

Explain why a active humidification with a water bath may be ideal?

Answer 15

Temperature of water bath raised to allow for increased humdification as SVP will be higher, less cool air causing tenacious secretions and cilia paralysis

Question 16

Draw different configurations of water baths
- No fluid warming configuration
- Fluid warmed to 35 degrees
- Fluid warmed to 45 degrees
- Effect of warming coil in the elephant trunk to the patient

Answer 16

Question 17

What is a water trap in the context of humidification equipment

Answer 17

Water baths in active heating produce very humdified gas that subsequently cools as it leaves the chamber and enters the circuit limb going to the patient and can cause a reduntant pool of water in the tubing

Question 18

What are the different approaches to how much to heat a water bath

Answer 18

Unheated - incomplete humidification, and energy still lost and secretions still affected by cool air

Heated to 40 degrees - minimises the risk of scalding the patietn airways but ideal for microbial growth

Heated to 60 bacterial contamination risk low but gas must now be carefully monitored to prevent airway scalding

Question 19

What are aerosols

Answer 19

Small particles of liquids or solids suspended in carrying gas including dusts, bacteria, yeast, water drolets

Question 20

For liquid medications to enter the alveoli as an aerosol what conditions are required

Answer 20

Stability of the aerosol - to remain in suyspension
Penetration is dependent on particle size - <3 micrometres and less than 1 micrometre the most ideal. Smaller than this the particles will be exhaled without effect

Question 21

Particles or droplets 5-10micromtres deposit where when inhaled

Answer 21

upper airways

Question 22

Particles 1-3 micrometres deposit where when inhaled

Answer 22

Alveoli

Question 23

What is an atomiser

Answer 23

Jet or gas driven nebiuliser - high flow gas over a capillary tube immersed in fluid being nebilised

Question 24

How is a gas different ot a vapour?

Question 25

How does a vapouriser basically work?

Answer 25

Question 26

Draw a vapouriser

Answer 26

Question 27

What is the SvO2 of each of these locations Jugular vein Renal vein Hepatic vein IVC SVC Muscles

Answer 27

ugular vein (55%) ◦ Renal vein (81%) ◦ Hepatic vein (66%) ◦ IVC (71%) ◦ SVC (79%) ◦ Muscles (72%)

Question 28

PO2 of mixed venous blood

Answer 28

40mmHg

Question 29

How does PO2 related to SVO2

Answer 29

* The PO2 describes the proportion of dissolved oxygen (PO2 × 0.03) * The PO2 also determines the SvO2 (usually 70-75%) according to the shape of the oxygen-haemoglobin dissociation curve in mixed venous blood ◦ This curve is slightly right-shifted (compared to arterial blood) because of the Bohr effect

Question 30

How do you calculate blood oxygen content?

Answer 30

* Total blood oxygen content = (SvO2 × ceHb × BO2) + (PvO2 × 0.03) ◦ ceHb = the effective haemoglobin concentration ◦ PvO2 = the partial pressure of oxygen in mixed venous blood ◦ 0.03 = the content, in ml/L/mmHg, of dissolved oxygen in blood ◦ BO2 = the maximum amount of Hb-bound O2 per unit volume of blood (normally 1.39) ◦ SvO2 = oxygen saturation of mixed venous blood

Question 31

Mixed venous blood oxygen is determined by what factors according to the Fick principle?

Answer 31

(CO = VO2 / CaO2 - CvO2): ◦ Arterial oxygen content: decreased arterial oxygenation will produce a decreased SvO2 ◦ VO2, the oxygen consumption rate: decreased VO2 will produce an increased SvO2 ◦ Cardiac output: a decreased cardiac output will produce a reduced SvO2

Question 32

What is the normal PaCO2

Answer 32

40mmHg

Question 33

What are the factors affecting partial pressure of CO2 in mixed venous blood

Answer 33

VCO2 = cardiac output x (CvCO2 - CaCO2) As CaCO2 and CvCO2 are directly proportional/linearly related to their partial pressures this can be used PCO2 = VCO2 / MV Therefore PvCO2 will be dependent on CO, VCO2 and PaCO2

Question 34

What factors increase rate of CO2 production? or decrease it?

Answer 34

* ↑production: hypermetabolic state (MH); ◦ exercise, fever, pregnancy * ↓production: ↓T°C; anaesthesia

Question 35

How is minute ventilation ralted to PCO2

Answer 35

* pCO2 = Vco2/MV

Question 36

What is PEEP

Answer 36

* The maintenance of positive pressure at the end of expiration

Question 37

WHat is baseline PEEP

Answer 37

3mmHg when breathign through your nose

Question 38

Physiological consequences of PEEP in the heart - RV

Answer 38

‣ Reduced preload - due to increased intrathroacic pressure ‣ Increased afterload reducing stroke volume - increased pulmonary vascular resistance due to increased intrathoracic pressure occurring in West zone 1 and 2 where increased alveolar pressure exceeeds venous pressure.Leads to preferential blood flow to diseased lung in heterogenous disease ‣ IV septum displacement can reduce LV compliance - can be significant in an already pressure overloaded RV ‣ Can exacerbate a R->L shunt intracranial

Question 39

Physiological consequences of PEEP on LV heart

Answer 39

◦ LV - decreased preload and decreased afterload (reduced LV transmural pressure reducing myocardial work) with generally decreased cardiac output especially if hypovolaemia ‣ Decreased preload from bulging of the septum from dilated RV ‣ Decreased afterload - LV transmural pressure and wall stress, pressure gradient from thoracic to abdominal aorta improving flow

Question 40

What 4 major factors does PEEP change in the lung

Answer 40

1. Lung recruitment 2. Compliance 3. Increased mean alveolar pressure 4. Dead space

Question 41

How is lung recruitment affected by PEEP 2

Answer 41

‣ Prevents cyclic de-recruitment/atelectasis on expiration - raising FRC above closing volume * Trauma ◦ Decreased atelectrauma and VILI ◦ Decreases bio trauma from alveolar collapse and release of inflammatory mediators ◦ Minimised denitrogenation atelectasis with high FiO2 * Improved FRC ◦ It increases the FRC above the closing volume which becomes more important with age, meaning that in expiration gas exchange can continue to occur as there is no collapse (i.e.increased total gas exchange surface) ◦ Creating an oxygen resevoir ◦ Improved V/Q matching - reduced shunt potentially

Question 42

How is mean airway/alveolar pressure changed by PEEP 2 positive, 2 negative

Answer 42

‣ Displaces interstitial fluid improving gas exchange ‣ Improved partial pressure of gasses —> increased oxygenation via increased capillary-alveoli interface (recruitment and fluid displacement) and partial pressure ‣ Risk of overdistension and barotrauma increases —> cytokine leak and neutrophil retention * Overinflation of non dependent alveoli or focal areas of unaffected lung ‣ Can impair lymphatic drainage - pulmonary oedema and pneumonia resolution * Neutrophil retention in pulmonary capillaries

Question 43

How does PEEP affect static compliance

Answer 43

‣ Depending on the portion of the static pressure volume relationship curve increasing the PEEP may either improve recruitment and improve lung compliance or over-distend and worse. For most who do not already have auto-PEEP and PEEP is being newly applied it will move inspiration at the start of tidal volume breathing towards the steeper portion of the volume pressure curve ‣ If improved compliance —> improved WOB. Less effort to trigger if improved compliance

Question 44

How does PEEP affected dynamic compliance

Answer 44

‣ Dynamic compliance effect - Decreased turbulent flow on inspiration through increased airway diamtre creating less resistance on inspiration (more on expiration though depending if stenting open and obstruction), and improved lung compliance at moderate volumes

Question 45

How does PEEP change dead space

Answer 45

◦ The change in dead space via the chosen device to deliver PEEP will also have an increase or a decrease in minute ventilation ‣ Additionally increased dead space due to decreased flow in West’s zones 1 (PA > Pa > Pv)

Question 46

How does PEEP affect the brain

Answer 46

◦ Raised ICP if high PEEP - only with impaired cerebral autoregulation, PEEP above 15 appears to be where this is signifciant

Question 47

How does PEEP affect the kidney 4

Answer 47

◦ Water retention - ADH release/vasopressin related to atrial stretch ◦ Aldosterone secondary to dropped systemic BP ◦ Sodium retnetion - ANF release drops due to reduced preload —>water and salt retention ◦ Decreased renal perfusion and GFR - cardiac output drop, increased renal vein pressure

Question 48

How does PEEP affect the gut 3

Answer 48

◦ Decreased hepatic perfusion and decreased metabolic clearance of drugs ‣ Due to increased intrathoracic pressure —> decreased hepatic artery and portal venous flow and subsequent liver congestion and LFT changes ◦ Decreased splanchnic perfusion - reduced mortality and poor gastric emptying ◦ Decreased gastric perfusion - stress ulcers

Question 49

What effect does 100% FiO2 have on a pneumothorax

Answer 49

Relative composition of air in a pneumothorax - partial pressures will depend on the pressure within the pneumothorax - 78% nitrogen - 21% oxygen - 1% Argon/Co2 Diffusion out of a pneumothorax depends on Ficks laws of diffusion and will be equivalent to partial pressure If we first calculate the effect of breathing air for diffusion gradient to alveoli vs 100% FiO2 Then compare this to blood as this will be the additional source of reabsorption The solubility coefficient of N2 is poor, requiring 2x the partial pressure of O2 to dissolve

Question 50

Why does gas flow into the pleural space if there is a hole

Answer 50

* Pleura separated by thin layer of pleural fluid --> surface tension keeping membranes apposed, balanced between elastic recoil (natural tendancy to collapse) and elastic recoil of the chest leaves normal intrapleural pressure -2.5 -6 cmH20

Question 51

Once air enters the pleural space what happens to lung mechanics?

Answer 51

◦ Air enters pleural space ‣ Simple pneumothorax - air enters until pressure intrapleural is 0 OR until hole is closed ‣ Tension --> via a one way valve in the lung --> intrapleural pressure rises ◦ Air entry into intrapleural space --> lost surface tension and negative pressure causing dissociation between chest wall resting state and lung resting state ‣ Chest cavity expands outwards ‣ Lung collapses --> towards resting state, if intrapleural pressure rises above atmospheric pressure (1 way valve) compressive resistance to alveoli exacerbates collapse

Question 52

If air enters into the pleural space causing a pneumothorax how does this impact volumes, compliance, work of breathing, gas exchange adn perfusion?

Answer 52

◦ Lung collapse causes ‣ Reduced lung volumes, reduced vital capacity ‣ This may be below closing capacity ◦ Increased work of breathing ‣ Lung compliance is poor at postitive intrapleural pressure --> increased work of breathing ‣ Falling PO2 and rising PCO2 --> stimulation of central and peripheral chemoreceptors increasing work of breathing without much increase in TV ◦ Gas exchange ‣ Reduced partial pressure of oxygen - due to V/Q mismatch in atelectatic segments, anatomical shunts (if pneumothorax is >25% of hemithorax) and alveolar hypoventilation ‣ Reduced ventilation causes rise in PCO2 ◦ Perfusion ‣ Lung perfusion stops when alveolar pressure rises and lung volume drops

Question 53

How is perfusion affected by a simple pneumothorax

Answer 53

◦ Lung collapse causes ‣ Reduced lung volumes, reduced vital capacity ‣ This may be below closing capacity ◦ Increased work of breathing ‣ Lung compliance is poor at postitive intrapleural pressure --> increased work of breathing ‣ Falling PO2 and rising PCO2 --> stimulation of central and peripheral chemoreceptors increasing work of breathing without much increase in TV ◦ Gas exchange ‣ Reduced partial pressure of oxygen - due to V/Q mismatch in atelectatic segments, anatomical shunts (if pneumothorax is >25% of hemithorax) and alveolar hypoventilation ‣ Reduced ventilation causes rise in PCO2 ◦ Perfusion ‣ Lung perfusion stops when alveolar pressure rises and lung volume drops

Question 54

How is gas exchange affected by a simple pneumothorax

Answer 54

◦ Lung collapse causes ‣ Reduced lung volumes, reduced vital capacity ‣ This may be below closing capacity ◦ Increased work of breathing ‣ Lung compliance is poor at postitive intrapleural pressure --> increased work of breathing ‣ Falling PO2 and rising PCO2 --> stimulation of central and peripheral chemoreceptors increasing work of breathing without much increase in TV ◦ Gas exchange ‣ Reduced partial pressure of oxygen - due to V/Q mismatch in atelectatic segments, anatomical shunts (if pneumothorax is >25% of hemithorax) and alveolar hypoventilation ‣ Reduced ventilation causes rise in PCO2 ◦ Perfusion ‣ Lung perfusion stops when alveolar pressure rises and lung volume drops

Question 55

How is work of breathing affected by a simple pneumothorax

Answer 55

◦ Lung collapse causes ‣ Reduced lung volumes, reduced vital capacity ‣ This may be below closing capacity ◦ Increased work of breathing ‣ Lung compliance is poor at postitive intrapleural pressure --> increased work of breathing ‣ Falling PO2 and rising PCO2 --> stimulation of central and peripheral chemoreceptors increasing work of breathing without much increase in TV ◦ Gas exchange ‣ Reduced partial pressure of oxygen - due to V/Q mismatch in atelectatic segments, anatomical shunts (if pneumothorax is >25% of hemithorax) and alveolar hypoventilation ‣ Reduced ventilation causes rise in PCO2 ◦ Perfusion ‣ Lung perfusion stops when alveolar pressure rises and lung volume drops

Question 56

With tension pneumothorax what happens from a respiratory perspective

Answer 56

◦ With tensioning pneumothorax the icnreasing pressure causes ipsilateral lung collapse --> shunting, V/Q mismatch adn worsening hypoxia --> contralateral lung compression compromises gass exchange further Worsening collapse Worsening work of breathing due to having to overcome positive pressure in the chest at baseline to move air Worsening V/Q mismatch Increasing shunt With increasing pressure West Zone 2 increases and eventually West zone 1 with rising intrapulmonary pressure Reduction in pulmonary blood flow

Question 57

Cardiovascular consequences of a pnuemothorax transforming into a tension pneumothorax

Answer 57

◦ Compression of vena cava and right atrium --> reduced preload and decreased SV ◦ Compression of aorta --> increased afterload and reduced stroke volume ◦ Cardiac arrest due to hypoxia and above ◦ Compression of ventricles increased transmural pressure gradient and increased contracility

Question 58

How is pneumothorax physiology different to a pleural effusion?

Answer 58

When a pneumothorax is present, the pleural pressure increases as it does with the presence of a pleural effusion. However, with a pneumothorax the pressure is the same throughout the entire pleural space if it is not loculated. In contrast, with a pleural effusion there is a gradient in the pleural pressure due to the hydrostatic column of fluid. Accordingly, the pleural pressure with a pleural effusion in the dependent part of the hemithorax is much greater than it is in the superior part of the hemi thorax. IN a pneumothorax the upper lobes are affected mroe than than lower lobes as suually the pressure int he apices is more negative than the bases, therefore when all symmetrical atmospheric pressure the increase in pressure is greater in the apex. Diaphragmatic work is greater with pleural effusions

Question 59

What are the cardiovascular consequences of hypoxia

Answer 59

* Pulmonary circulation vasoconstriction - increased afterload (normal value 100-200 dynes/sec/cm and doubles with severe hypoxia over 5 minutes) * Systemic circulation vasodilation - in arteriolar beds (in response to local hypoxia) which is combatted by the more powerful systemic symapthetic response * Coronary and cerebral vasodialtion remain marked * Sympathetic driven response ◦ Hypertension - mild - slighty temporised by systemic vasodilation ◦ Increased cardiac output ◦ Tachycardia ◦ (Vagal tone also increases but to a lesser degree) * Eventually the brain becomes hypoxaemic and respiratory drive is depressed, thereby removing respiratory compensation and resulting in increasing acidosis, failure of the Na.K.ATPase pumps in most cells, cell lysis and death.

Question 60

What acid base changes occur with hypoxia

Answer 60

* Mild hypoxaemia results in a respiratory alkalosis (respiratory stimulant) * Hypoxia results in both fixed and volatile acid-base disturbances in severe cases ◦ Anaerobic metabolism results in lactate production ◦ Production of fixed acid results in a base deficit, and a low bicarbonate ◦ Drop in pH further stimulates the respiratory centre * Hypoxia and metabolic acidosis stimulate ventilation and hypocarbia

Question 61

How are other organ systems affected by hypoxia - other than heart, lungs

Answer 61

Brain - cerebral vasodilation, ischaemic reflex if severe Renal release of EPO, decrease in diuresis and natriuresis Liver decreases O2 consumption Reduced blood flow as part of symathetic response to gut. kdineys. skin Release of hypxoia inducible factors stimulates immune cells to produce inflammatory cytokines

Question 62

What are the 4 causes of hypoxia to cells

Answer 62

Hypoxaemic hypoxia Anaemic hypoxia Ischaemic hypoxia Histotoxic hypoxia - failure to utilise oxygen

Question 63

In hypoxaemic hypoxia what are the 4 causes

Answer 63

1. Reduced oxygen delivery to alveoli - Hypoventilation a) Airway obstruction b) Depressed respiratory drive - central, medications c) depressed respiratory strength - Reduced FIO2 - high altitude 2. Decreased diffusion capacity - Decreased surface area - Emphysema, ARDS, pneumonia - reduced permeability - fluid, fibrosis 3. Decreased V/Q - Pneumonia - Shunt - Dead space 4. Decreased mixed venous oxygen content - Increased o2 consumption or decreased cardiac output

Question 64

What does the barometric pressure vary by with altitude

Answer 64

Barometric pressure 200mmHg at 10 000 m (paO2 42) Barometric pressure is 580mHg and PaO2 of 60 at 2700m

Question 65

What happens to saturated vapour pressure with altitude

Answer 65

Stable as the upper respiratory tract continues humidification and therefore remains at 47mmHg reducing the space for O2

Question 66

What happens to respiratory status with altitude

Answer 66

MV increases (hypoxic respiratory drive) moderated in part by response to hypocapnoea Decreased PCO2

Question 67

Cardiovascular consequences of altitude

Answer 67

Tachycardia and increased cardiac output -- sympathetic drive over the first few days Mild BP increase as PVR decreases

Question 68

Neurological effects of increased altitude

Answer 68

Decreased cognitive funtion Delirium

Question 69

Renal and electrolyte consequences of altitude

Answer 69

Diuresis Decreased serum bicarbonate

Question 70

Chronic respiratory adaption to Altitude

Answer 70

* Minute volume remains the same * Tidal volume may gradually increase due to thoracic remodelling * Decreased PaCO2 * Increased pulmonary artery pressure and vascular density - allows for improved pulmonary perfusion * Total pulmonary diffusing capacity increases - increased alveolar surface area, increased pulmonary blood volume * Oxygen carrying capacity - increased 2,3 DPG in erythrocytes shifting O2 curve to the right facilitating release of O2 to the tissues

Question 71

Cardiovascular chronic changes to altitude

Answer 71

HR remains elevates Increased BP from SVR Increased blood viscocity SV return to normal

Question 72

Acid base in chronic altitude

Answer 72

Bicarbonate decreases due to chronic hypocapnoea

Question 73

Haematological changes in chronic altitude exposure

Answer 73

* Haematocrit increases over days/weeks, largely due to haemopoiesis and haemoconcentration * Plasma volume reduces - high altitude diuresis due to BNP, renin, aldosterone and decreased vasopressin

Question 74

Stimulus for cough comes from 2 potential sources

Answer 74

Chemical and biological stimuli Mechanical stimuli

Question 75

What chemical and biological stimuli can trigger cough?

Answer 75

Acids Biological pathogens Mediators associated with inflammation

Question 76

What mechanical stimuli can trigger cough?

Answer 76

Aspiration of liquids Solids - secretions

Question 77

What is the purpose of cough 3

Answer 77

◦ Protective function ‣ Defense against foreign material in the airway ◦ Pathological consequences ‣ Damage to the mucosa with persistent or unproductve cough ◦ Diagnostic purpose ‣ Evidence of intact medullary function

Question 78

What 3 types of receptors are implicated in cough

Answer 78

Rapidly adapting receptors - Responding to dynamic lung inflation - bronchospasm, lung collapse and sporadically active during the respiratory cycle Slowly adapting stretch receptors - Responsive to mechanical forces - Particiapte in the Hering Breuer reflex (increased HR to lung stretch) C fibres - nociceptors

Question 79

Afferent nerve supply for the cough reflex

Answer 79

Bronchial mucosa - vagus - the pulmonary, pharyngeal, superior larungeeal branches Diaphragm 0 cardiac and oeosphageal branches of the vagus

Question 80

Where is the central integrated control of the cough reflex

Answer 80

Caudal 2/3 of the NTS

Question 81

Efferent pathway of the cough reflex?

Answer 81

◦ To the diaphragm: via the phrenic nerve ◦ To the abdominal muscles: via the spinal motor nerves ◦ To the larynx: via the laryngeal branches of the vagus, from the nucleus ambiguus

Question 82

4 Phases of the cough

Answer 82

◦ Sensory phase: afferent fibres conduct mechanoreceptor and chemoeceptor stimuli to the central interator in the medulla, and a cough reflex is triggered ◦ Inspiratory phase: glottis opens and a deep breath is inhaled ◦ Compressive phase: glottis closes and expiratory muscles forcibly contract; the intrathoracic pressure may transiently rise to over 100 cm H2O. ◦ Expulsive phase: the glottis opens and rapid airflow begins; the bronchial tissues oscillate due to the rapid turbulent flow, which loosens the secretions.

Question 83

What is viscocity?

Answer 83

Used to indicate a fluid’s internal resistance to flow. Also thought of as a measure of the friction of a fluid.

Question 84

What is density

Answer 84

(ρ): relates the mass of a substance to its volume such that ρ = kg/m3

Question 85

What is Reynolds number?

Answer 85

preidcts the likelihood of turbulent flow Re = 2rvp / n i.e. radius x velocity x density/viscicity

Question 86

How is density related to laminar flow

Answer 86

Density is related to Reynolds number, not resistance precisely Increasing density increases the Reynolds number and favours turbulent flow

Question 87

How is viscocity related to flow

Answer 87

It is both related directly to the resistance of laminar flow And it decreases the Reynolds number increasing the likelihood of laminar flow

Question 88

What is the equation for resistance in turubulent flow?

Answer 88

= pl/pi x r^5 i.e. density x length / pi x radius ^5 Therefore radius becomes even more important, and viscocity is not a factor

Question 89

Non respiratory functions of the lung

Answer 89

Filtering - Particle filtering - Filtering clots in the circulation Blood - reservoir - modulates the clotting cascade Immunological Metabolism - Surfactant - Protein - Removal of proteases e.g. alpha 1 antitrypsin - Carbohydrate metabolism - Metabolism of NA and vasoactive substances Organ of speech Acid base balance Heat regulation in upper respiratory tract Route of administration for drugs

Question 90

How does particle filtering work in the airways

Answer 90

◦ Particle filtering ‣ 5-10 micrometre deposited in upper airway (impaction) - hit the walls ‣ 2-6 micromtres - lower respiratory tract ‣ 0.5-2 micrometres in alveoli - deposition ‣ 0.2-0.5 micromtres wash in and out of alveoli without interacting with walls ‣ <0.2 micrometres deposit into the walls

Question 91

What immunological role does the lung have?

Answer 91

Physical defence systems - Sneezing, coughing - Mucociliary elevator Cellular defence systems ‣ Alveolar macrophages ‣ Lung neutrophils ‣ Mast cells in the lung and bronchi ◦ Immunologic defence mechanisms ‣ Lymphatic system of the lung and antigen presentation site with lymphoid tissue in the lung ‣ Immunoglobulin in mucus and cell surfaces - IgA ‣ Direct antibacterial action of surfactant (Wu et al, 2003)

Question 92

What role does the lung have in medications

Answer 92

◦ Route of drug administration (eg. nebulised steroids and bronchodilators) ‣ Droplets <5micromtres if absorption required and ideally - high lipid solubility, small size, and inhalation technique matters dependent on site desired. ◦ Route of drug elimination (eg. volatile anaesthetics, paraldehyde) ‣ Ammonia, alcohol, acetone

Question 93

How does the lung function with respect to blood (3)

Answer 93

◦ Modulator of the clotting cascade: the lungs contain thromboplastin (procoagulant converting prothrombin to thrombin), heparin (from lung mast cells) and tissue plasminogen activator (fibrinolytic product) ◦ Filter for the bloodstream: particles larger than an RBC are trapped (~8 μm size barrier), which includes clots, tumour cells and other emboli - fat and amniotic fluid can pass through to systemic circulation ◦ Reservoir of blood: the lungs contain about 10% of the circulating blood volume ‣ 200-300ml/metre squared ‣ 20-25% in pulmonary capirllaries, and this may increase to 50% (250mls) with heavy exercise

Question 94

What is the lung involved in from a metabolism perspective

Answer 94

◦ Modulation of body temperature: heat loss can occur by respiration ◦ Metabolism (eg. conversion of of angiotensin-I, and degradation of neutrophil elastase by α1-antitrypsin) ‣ Inactivation of neutrophil proteases ‣ Activation of deadly toxins - chlorine gsa to HCl ‣ Activation of circulating hormones e.g. angiotensin activation by ACE ‣ Noradrenaline, serotonin, PGE 1 and 2, adenosine and bradykinin metabolism ◦ Metabolised and released - arachadonic acid metabolites ---> leukotrienees and prostaglandins ◦ Secreted - Ig, especially IgA in bronchial mucous

Question 95

Describe the characteristics of CO2 as a drug pharmaceutically

Answer 95

◦ Colourless gas, pungent smell in high concentration ◦ Non flammable ◦ Specific gravity 1.98 ◦ Critical temperature 31 degrees and critical pressure 73 atmospheres ◦ Melting point -55.6 degrees ◦ boiling point -78 degrees - sublimates ◦ In aqueous solution acts as a Lewis acid - slowly spontaneously hydrating to produce carbonic acid ◦ More soluble with reducing temperatures ◦ Base concentration 0.03% in room air

Question 96

Effects on respiratory function of CO2

Answer 96

1. Depressed airway reflexes 2. Respiratory drive with mild hypercapnoea 3. Respiratory function - bronchodilation, right shift of oxyhaemoglobin dissocaition curve

Question 97

How does CO2 affect the cardiac system

Answer 97

◦ Sympathetic overactivity, thus: ‣ Hypertension ‣ Tachycardia ‣ Serum catecholamine excess - however catecholamine sensitivity is reduced by the acidosis ‣ Increase in cardiac output despite direct CO2 cardiodepressant effect ‣ Coronary artery vasodilator ◦ Prolonged QT interval and arrhtyhmias ◦ Vasodilation generally ◦ Myocardial depressant - although balanced with sympathetic effects often warm, flushed, sweaty, tachycardic with bounding pulse * Vasoactive effects: ◦ Systemic arterial vasodilation - relaxes smooth muscle - however net effect of CO2 is still increase in BP ◦ Pulmonary arterial vasoconstriction - hypocapnoea reverses the positive effects of pulmonary hypoxic vasoconstriction

Question 98

CNS effects of high CO2

Answer 98

◦ Progressively increasing sedation - disorientation, confusion --> obtunded ◦ Increased intracranial pressure - due to increases in cerebral blood flow doubles with CO2 of 8-11kPa PaCo2 - periarteriolar pH leads to a change in nitric oxide synthase activity --> intracellular cGMP production --> change in IC calcium ‣ 1-2ml/100g/min increase in blood flow for every 1mmHg change in PCO2 * 4% increase in cerebral blood flow per 1mmHg rise ‣ This mechanism becomes lost in damaged brain - which results in areas of undamaged brain vasodilating and stealing the blood supply fromt eh damaged area (which is what the damaged area usually does anyway); in hypocapnoea the reverse happens and undamaged vessels contrsict diverting blood into vasoplegic vessels

Question 99

How does increasing CO2 affect cerebral blood flow

Answer 99

‣ 1-2ml/100g/min increase in blood flow for every 1mmHg change in PCO2 * 4% increase in cerebral blood flow per 1mmHg rise ‣ This mechanism becomes lost in damaged brain - which results in areas of undamaged brain vasodilating and stealing the blood supply fromt eh damaged area (which is what the damaged area usually does anyway); in hypocapnoea the reverse happens and undamaged vessels contrsict diverting blood into vasoplegic vessels

Question 100

Pharmacokinetics of CO2

Answer 100

* Freely absorbed through normal alveolar tissue * CO2 transported in solution in bloodstream as bicarbonate or in combination with plasma protiens inc Hb * Excretion by exhalation and in urine as bicarbonate

Question 101

CO2 storage in the body

Answer 101

1.8L/kg of CO2 stored * Bone stores: ◦ Part of the matrix of bone - dissolved in cytosol ◦ As bicarbonate (30%) ◦ As carbonate (70%) ◦ Vast stores (1.6L/kg of body weight; 120L in 70kg adult) - very slow to mobilise * Of the bone stores: ◦ about 9% are accessible to assist with buffering ◦ ~ 200ml/kg, or 14L ◦ 15% of daily CO2 production * Dissolved carbon dioxide ◦ 3L are available for immediate use in buffering ‣ 80-90% is stored in the form of bicarbonate anions (HCO3-) - 2.7L ‣ 5-10% is present as unchanged gas, dissolved in the water of extracellular fluid (predominantly in the blood). - 0.2L ◦ 5-10% or so is stored as carbamino compounds inside erythrocytes ◦ 2-5% is available as a free gas in the alveolar gas mixture. ◦ Miniscule amount available as carbonic acid

Question 102

Oxygen storage in the human body

Answer 102

61-64% oxygen by weihgt, 88% of body water weight is oxygen, some in fat, protein and carbon hydroxyappatatie Bound oxygen to Hb, myoglobin, other molecuels Gas in cavities - FRC the most clinically important O2 stores on room air - 270mls as FRC - 820ml bound to HB - 200ml bound to myoglobin - 45ml dissolved in tissues O2 storage after preoxygenation 1825ml FRC 910ml bound to Hb 200ml bound to myoglobin 50ml in tissue fluids

Question 103

How does preoxygenation affect oxygen storage

Answer 103

O2 stores on room air - 270mls as FRC - 820ml bound to HB - 200ml bound to myoglobin - 45ml dissolved in tissues O2 storage after preoxygenation 1825ml FRC 910ml bound to Hb 200ml bound to myoglobin 50ml in tissue fluids

Question 104

Gravity dependent processes affecting pulmonary blood flow

Answer 104

Vertical gradient of pulmonary pressure affecting alveolar volume Vertical gradient of arterial hydrostatic pressure Gravity related changes in lung volume

Question 105

How does the vertical gradient of pulmonary pressure affect ventilation

Answer 105

◦ In the upright subject, pleural pressure is more negative in the apices, and less negative in the bases ◦ Apical alveoli are more distended than basal alveoli ◦ Bases of the lungs are therefore more compliant

Question 106

How does the vertical gradient of pulmonary hydrostatic pressure affect pulmonary blood flow

Answer 106

◦ Lungs of an adult may be 30cm in height ◦ Blood in pulmonary vessels therefore represents a column of blood which exerts a hydrostatic pressure (i.e. at the bottom of it, the pressure would be 30 cm H2O, or 22 mmHg) ◦ This increase in hydrostatic pressure tends to recruit capillaries and increase blood flow to the basal regions of the lung.

Question 107

How does gravity change lung volumes

Answer 107

◦ Pulmonary vascular resistance is lowest at FRC ◦ At low lung volumes, it increases due to the compression of larger vessels ◦ Gravity-induced collapse of lung bases can reduce pulmonary blood flow by: ‣ increased intestitial pressure compressing extraalveolar vessels ‣ hypoxic pulmonary vasoconstriction

Question 108

What changes result from an increase in pulmonary artery pressure

Answer 108

* Increased pressure in the pulmonary arteries leads to compensatory changes that buffer the pressure increase by decreasing pulmonary vascular resistance: * Dilatation of pulmonary arterioles * Distension and recruitment of pulmonary capillaries * Thus, decreased pulmonary vascular resistance and increased pulmonary blood flow * Also increased pulmonary arterial volume (acting as capacitance vessels) * These mechanisms can compensate for acute changes in pulmonary arterial pressure until capillary recruitment is exhausted

Question 109

Advantages of Aa gradient as an indice of oxygenation

Answer 109

◦ Simple ◦ Minimally invasive ◦ Distinguish hypoventilation from other causes

Question 110

Disadvantages of AA gradient

Answer 110

non specific Age dependent Magnitude dependent on FiO2 especially if shunt

Question 111

PaO2 advantages as an indice of oxygenation

Answer 111

◦ Accurate impression of oxygenation ◦ Not confounded by dyshaemoglobinaemias ◦ Allows accurate calculation of haemoglobin saturation

Question 112

Disadvantages fo PaO2 as an indice of oxygenation

Answer 112

Invasive Requries ABG machine Confounded by measurement error and delay

Question 113

Disadvantages of saturations as a measure of oxygenation

Answer 113

◦ Confused by dyshaemoglobins ◦ Does not reflect level of oxygenation if hyperoxic ◦ Not direct measurement of haemoglobin saturation - instead uses signal intensity and compares with look up table ◦ No absolute method for calibration ◦ Unreliable if ‣ severely hypoxic ‣ Poorly perfused ‣ Arrhythmias ‣ Motion artefact ◦ Positional

Question 114

Daltons law

Answer 114

◦ The total pressure of a mixture of gases is equal to the sum of the partial pressures of all of the constituent gases

Question 115

Partial pressure

Answer 115

n a mixture of gases, partial pressure is the pressure that a gas would have exerted if it had occupied that volume alone.

Question 116

Henry's law

Answer 116

◦ The amount of a given gas dissolved in a given liquid is directly proportional to the partial pressure of the gas in contact with the liquid. ‣ P = molar concentration of the gas x Henry's proportionality constant ◦ For each gas and each liquid, the proportionality constant (Henry;s constant) is different. ◦ For any given partial pressure of a gas, the solubility will be inversely proportional to temperature.

Question 117

Boyles lw

Answer 117

◦ For a fixed mass of gas at constant temperature, the pressure (P) and volume (V) are inversely proportional, such that P ×V = k, where k is a constant.

Question 118

Charles law

Answer 118

◦ The volume occupied by a fixed mass of gas at constant pressure is directly proportional to its absolute temperature (V/T = k).

Question 119

Gay Lussacs law

Answer 119

◦ The pressure of a fixed mass of gas at constant volume is directly proportional to its absolute temperature (P/T = k).

Question 120

Avogadros law

Answer 120

◦ Equal volumes of gases at the same temperature and pressure contain the same number of molecules (6.023 × 1023, Avogadro’s number).

Question 121

Universal gas law

Answer 121

◦ The state of a fixed mass of gas is determined by its pressure, volume and temperature (PV = nRT)

Question 122

Work of breathing equation

Answer 122

* Work of breathing = pressure × volume

Question 123

Complaince equation

Answer 123

* Compliance = volume / change in pressure

Question 124

Resistance

Answer 124

* Resistance = change in pressure / flow

Question 125

Pressure =

Answer 125

flow x resisatnce

Question 126

Volume =

Answer 126

flow/time

Question 127

flow =

Answer 127

volume /time

Question 128

Bohr equation for dead sapce

Answer 128

* VD/VT = (FACO2 - FECO2) / FACO2 * Where: ◦ VD = dead space volume ◦ VT = tidal volume ◦ FECO2 = fraction of expired CO2 ◦ FACO2 = fraction of alveolar CO2 ◦ Diffusing capacity = Net rate of gas transfer / Partial pressure gradient

Question 129

The shunt equation

Answer 129

The shunt equation * Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2 * where * Qs/Qt = shunt fraction (shunt flow divided by total cardiac output) * CcO2 = pulmonary end-capillary O2 content, same as alveolar O2 content * CaO2 = arterial O2 content * CvO2 = mixed venous O2 content

Question 130

What is a colligative property?

Answer 130

Properties dependent on the number of molecules in a solution

Question 131

What are examples of colligative properties

Answer 131

Vapour pressure Boiling point Freezing point Osmotic pressure

Question 132

What is vapour pressure

Answer 132

Pressure exerted by a vapour above the surface of a liquid

Question 133

Saturated vapour pressure

Answer 133

Pressure exerted by a vapour at equilibrium with a liquid of the same substance i.e. rate of evaporation = rate of condensation voltaile gas has a high vapour pressure i.e. tendancy to be a gas In general saturated vapour pressure is influenced by temperature and pressure

Question 134

Boiling point

Answer 134

* The boiling point temperature is the temperature at which vapour pressure equals atmospheric pressure. A lower atmospheric pressure will result in a lower boiling point temperature ◦ Above this temperature bubbles of vapour form within the liquid, below this temperature evaporation only occurs at the surface (i.e. the vapour pressure is high enough to overcome atmospheric pressure and pressure from the column of liquid at depth)

Question 135

Critical temperature

Answer 135

* Critical temperature is the temperature above which it is not possible to liquefy a given gas by increasing its pressure ◦ A substance is a gas when it is above its criticial temperature, and a vapour when it remains in gaseous phase below its critical temperrature If a graph was drawn with nitrous oxide at 40 degrees it is above its critical temperature and therefore no additional pressure would force it to become a liquid. (36.5)

Question 136

Critical pressure

Answer 136

* Critical pressure is the minimum pressure which would suffice to liquefy a substance at its critical temperature - above the critical pressure increasing temperature will not cause a fluid to vapourise If a graph was drawn with nitrous oxide at 40 degrees it is above its critical temperature and therefore no additional pressure would force it to become a liquid. (36.5)

Question 137

Critical point

Answer 137

* Critical point is the point of minimum pressure and maximum temperature at which both a gaseous and a liquid phase of a given compound can coexist.

Question 138

Latent heat of vapourisation

Answer 138

* Latent heat of vapourisation is the heat required to convert a substance from liquid to vapour at a given temperature. Latent heat of vapourisation decreases as ambient temperrature increases, and is reduced to zero at the critical temperrature of that substance.

Question 139

Absolute humidiy

Answer 139

Mass of water vapour present in a given volume of air

Question 140

Relative humidity

Answer 140

* Relative humidity is the percentage ratio of the mass of water vapour in a given volume of air to the mass required to saturate that given volume of air at the same temperature.

Question 141

When does latent heat of vapourisation reach zero

Answer 141

* The amount of energy required for evaporation to occur * Specific latent heat is the ehat required to convert 1kg of a substance from one phase to another at a given temperature * As temperature increases latent heat capacity reduces - it reaches zero at the critical temperature

Question 142

What is the standard units of latent heat of vapourisation

Answer 142

* The amount of energy required for evaporation to occur * Specific latent heat is the ehat required to convert 1kg of a substance from one phase to another at a given temperature * As temperature increases latent heat capacity reduces - it reaches zero at the critical temperature

Question 143

Why is the nose such an effective site for heat exchange and humidification

Answer 143

Inspired gas passes through convuluted air passages --> turbulence * This turbulence increases evaporative heat exchange between the air and the mucosa; such that at the posterior nasal cavity the relative humidity is already 85% * In the lower pharynx, the temperature is about 33° C and relative humidity approaches 100%

Question 144

Alveolar gas has what water content

Answer 144

* Alveolar gas has a water content of around 47g/kg (100% humidity, 37° C)

Question 145

What is the humidity in the nasal mucosa

Answer 145

85%

Question 146

What happens to the heat from the nasal mucosa

Answer 146

◦ Mucosa as it releases water vapour donates heat to the process of evaporation and is cooled ◦ Heat trapped as latent heat of vapourisation which does not change the temperature of the air ◦ It is released again by condensation which occurs when expired air flows over the cooled mucosa

Question 147

What happens to expired gas as it passes back through the upper airway?

Answer 147

* Expired gas passes over the cooler upper airway mucosa, and returns some of its heat to it * Expired air at the nares is usually 32° C and close to 100% humidified * Some of the water is also reclaimed by the process of condensation * This process is less efficient - expired air is generally cooler at 32 degrees and this is due to cool mucosal surfaces being warmed --> the saturated vapour pressure drops and 32 degree gas has a water content aof 34g/metre cubed --> 13g/ metre cubed condensation along route * This process is highly dependent on the temperature of the ambient air; the cooler the ambient air the more moisture is reclaimed.

Question 148

How is reclamation of moisture during respiration temperature dependent?

Answer 148

* Expired gas passes over the cooler upper airway mucosa, and returns some of its heat to it * Expired air at the nares is usually 32° C and close to 100% humidified * Some of the water is also reclaimed by the process of condensation * This process is less efficient - expired air is generally cooler at 32 degrees and this is due to cool mucosal surfaces being warmed --> the saturated vapour pressure drops and 32 degree gas has a water content aof 34g/metre cubed --> 13g/ metre cubed condensation along route * This process is highly dependent on the temperature of the ambient air; the cooler the ambient air the more moisture is reclaimed.

Question 149

What happens during expiration in hot environements to water vapour

Answer 149

* In hot environments, humidity cannot be reclaimed and the net water loss increases ◦ This is because body cools the inhaled gas on inhalation, and therefore on expiration mucosa is warmer preventing condensation on expiration ◦ The water reclamation halves between 15 degrees and 30 degrees

Question 150

How much heat is lost per day under normal conditions

Answer 150

350kcal per day

Question 151

How much water is lost during respiration under normal conditions

Answer 151

250ml water

Question 152

Exercise has what effect on water loss due to respiration

Answer 152

◦ humidifcation maintained even with tachypnoea however the isothermic saturation boundary moves deeper into the lung ‣ Once minute volume >50L/min it has moves from first generation bronchi to 1mm diamtre airways ◦ Increasing moisture loss - as moisture loss proportional to minute volume and cardiac output

Question 153

What is moisture loss proportional to as a function of respiration

Answer 153

Temperature - hot = more looss Cardiac output Minute volume Inspired gas humidiity

Question 154

How can the fraction of water reclaimed during respiration be reduced

Answer 154

Hotter outside temperatures Lower ambient humidity Tachypnoea Increased cardiac output Bypassing reclamation structures e.g. tracheostomy, ETT

Question 155

Why is humidification important (2)

Answer 155

impaired bronchial innate immunity ◦ Cilial paralysis ◦ Reduced mucous flow rates (reduced humidiity)

Question 156

What is a better tool for airway humidification?

Answer 156

Passive and active measures the same efficacy

Question 157

What are benefits of passive humidification

Answer 157

Less cost Transportable

Question 158

What are cons of passive humidification

Answer 158

Less effective Higher resistance to flow - problem in spontaneous modes Increases dead space volume which is problematic in low tidal volume ventilation

Question 159

What factors determine the gas temperature and humidity reaching the patient in tubing along the way

Answer 159

Ambient temperature and pressure Ambient humidifity of supplied gas Temperature of moisture source Surface area available for evaporations Length of tubing INsulating properties of tubing

Question 160

What types of active humidifiers are there

Answer 160

◦ Bubble humidifers - rely on bubble water interface to enrich inspired gas. Used less. Require slower flow, have a flow resistance and can be noisy. More subject to bacterial contamintaion ◦ Passover humidifers - quiet, flow dependent, a wick can increase surface area to assist with efficency in water evaporation. ◦ Counterflow humidifers - increased efficency of evaporation, more expensive and cumbersome ◦ Inline vapourisers

Question 161

What are pros a cons of a bubble humidifer

Answer 161

◦ Bubble humidifers - rely on bubble water interface to enrich inspired gas. Used less. Require slower flow, have a flow resistance and can be noisy. More subject to bacterial contamintaion ◦ Passover humidifers - quiet, flow dependent, a wick can increase surface area to assist with efficency in water evaporation. ◦ Counterflow humidifers - increased efficency of evaporation, more expensive and cumbersome ◦ Inline vapourisers

Question 162

What are pros and cons of a passover humidifier

Answer 162

◦ Bubble humidifers - rely on bubble water interface to enrich inspired gas. Used less. Require slower flow, have a flow resistance and can be noisy. More subject to bacterial contamintaion ◦ Passover humidifers - quiet, flow dependent, a wick can increase surface area to assist with efficency in water evaporation. ◦ Counterflow humidifers - increased efficency of evaporation, more expensive and cumbersome ◦ Inline vapourisers

Question 163

What is pros and cons of counterflow humidifer

Answer 163

◦ Bubble humidifers - rely on bubble water interface to enrich inspired gas. Used less. Require slower flow, have a flow resistance and can be noisy. More subject to bacterial contamintaion ◦ Passover humidifers - quiet, flow dependent, a wick can increase surface area to assist with efficency in water evaporation. ◦ Counterflow humidifers - increased efficency of evaporation, more expensive and cumbersome ◦ Inline vapourisers

Question 164

Active heated circuit tubing has what problems potentially associated

Answer 164

◦ Flow limited - heating efficiency drops with increasing flow >60L/min ◦ Volume limited - minute volume drop in efficiency once >20L/min ◦ Can cause burns ◦ Do not prevent precipitation in the expiratory limb ◦ Cannot be extended ◦ May not be MRI compatible

Question 165

How does cold humidification work

Answer 165

* Bubbles gas through cold water, delivering relative humidity of 50% at ambient temperatures, if high inspiratory flow of oxygen with tenacious secretions will be inadequate * Condensation from heated or cold humidification should be considered infectious waste and disposed of as such , never allow it to drain into a reservoir

Question 166

What is the structure of a HME

Answer 166

* Rolls of metal gauze or condenser element (corrugated paper, fibre sheet, propylene sponge) placed onto the end of the tracheostomy tube or breathing circuit ◦ Hygroscopic in line air filter * Conserve heat and moisture on expiration and allow this to be returned on inspiration * Need to ensure they are checked regularly to make sure they are not becoming occluded, change at least 24 hourly

Question 167

What are problems with HMEs

Answer 167

Single use Low efficiency - 50% of required humidiity achieved Increased dead sapce Increased resistance to gas flow Potential source of ifnection

Question 168

Heat is

Answer 168

Temperature is average kinetic energy of molecules within a material, and is measured in degrees. It is distinct from heat, which describes the transfer of thermal energy from one body to another body, and is measured Joules. The two are related by the specific heat capacity, which describes how much energy (J) must be applied to a body to raise its temperature by 1°K, without a change in state.

Question 169

Temperature is

Answer 169

Temperature is average kinetic energy of molecules within a material, and is measured in degrees. It is distinct from heat, which describes the transfer of thermal energy from one body to another body, and is measured Joules. The two are related by the specific heat capacity, which describes how much energy (J) must be applied to a body to raise its temperature by 1°K, without a change in state.

Question 170

Specific heat capacity is

Answer 170

Temperature is average kinetic energy of molecules within a material, and is measured in degrees. It is distinct from heat, which describes the transfer of thermal energy from one body to another body, and is measured Joules. The two are related by the specific heat capacity, which describes how much energy (J) must be applied to a body to raise its temperature by 1°K, without a change in state.

Question 171

Absolute humidiity

Answer 171

Question 172

Relative humidiity

Answer 172

Question 173

How do you divide the effects of positive pressure ventilation on pulmonary system?

Answer 173

1. Effect on dead space 2. Effect on FRC 3. Effect on lung compliance and work of breathing 4. Effects on pressure

Question 174

What effect does positive pressure ventilation have on dead space?

Answer 174

• Intubation + tracheostomy decrease anatomical dead space by up to 50% • NIV increases anatomical dead space by the volume of the mask ~50ml ◦ 10-20ml with nasal masks ◦ 50ml small face masks ◦ Over a litre with full head helmets ◦ 150-200ml with the most common form of face mask

Question 175

How does positive pressure ventilation effect FRC? At what PEEP does this occur?

Answer 175

• Increased FRC through PEEP - this is evident only after PEEP is raised to 7.5 in normal healthy people as it actually drops prior to that. Increasing FRC increases an oxygen storage reservoir. The more diseased the lung the more this is the case, as if its a normal lung you are already in the best part of the curve from a compliance POV at baseline

Question 176

How does positive pressure ventilation effect alveolar recruitment? (2)

Answer 176

1 ‣ Improved V/Q matching - by ventilating areas that previously were collapsed • Re-opens alveoli collapsed due to compression, which are also the areas getting the most blood flow (reducing shunt) • Notably this works in physiological circumstances but once lung pathology is introduced e.g. pneumonia increasing PEEP can just open up more of the normal lung rather than reducing shunting in the bad lung 2 ‣ Increased total gas exchange surface • Recruitment of collapsed alveoli • Increase in total alveolar surface area - the already open alveoli are stretched as are the blood vessels that surround them improving the diffusing surface area (this area only has animal research and probably doesn’t occur under normal physiological conditions)

Question 177

How is V/Q matching effected by positive pressure ventilation

Answer 177

‣ Improved V/Q matching - by ventilating areas that previously were collapsed • Re-opens alveoli collapsed due to compression, which are also the areas getting the most blood flow (reducing shunt) • Notably this works in physiological circumstances but once lung pathology is introduced e.g. pneumonia increasing PEEP can just open up more of the normal lung rather than reducing shunting in the bad lung ‣ Increased total gas exchange surface • Recruitment of collapsed alveoli • Increase in total alveolar surface area - the already open alveoli are stretched as are the blood vessels that surround them improving the diffusing surface area (this area only has animal research and probably doesn’t occur under normal physiological conditions)

Question 178

How is gas exchange surface area affected by increased PEEP

Answer 178

‣ Improved V/Q matching - by ventilating areas that previously were collapsed • Re-opens alveoli collapsed due to compression, which are also the areas getting the most blood flow (reducing shunt) • Notably this works in physiological circumstances but once lung pathology is introduced e.g. pneumonia increasing PEEP can just open up more of the normal lung rather than reducing shunting in the bad lung ‣ Increased total gas exchange surface • Recruitment of collapsed alveoli • Increase in total alveolar surface area - the already open alveoli are stretched as are the blood vessels that surround them improving the diffusing surface area (this area only has animal research and probably doesn’t occur under normal physiological conditions)

Question 179

How is compliance effected by increased positive airway pressure

Answer 179

◦ Increases lung compliance ‣ The point at which alveoli close at end expiration is generally below the FRC in healthy people, but as people age or when they are sick the volume at which these close will become higher than their FRC, and they will only be ventilated during part of tidal breathing with increased energy expenditure to open them during each respiratory cycle (reduced compliance) ‣ It is easier to increase the volume of already inflated alveoli than it is is to recruit collapsed alveoli

Question 180

How is work of breathing effected by positive pressure ventilation What components of work of breathing are effected

Answer 180

◦ Decreases work of breathing - done by improving compliance ‣ WOB due to airway resistance • Decreases WOB on inspiration by increasing airway diameter - reduced turbulent flow, and decreasing resistance • However increases WOB on expiration as it is against airway pressure ‣ WOB due to tissue resistance • Decreased WOB because fo improved lung compliance at moderate volumes • increased WOB because of decreased compliance at high and low lung volumes

Question 181

How does positive pressure effect pressure within the airways - what consequences does this have (4)

Answer 181

• Redistribute lung water out of the intersititum ◦ Has been proven - movement of fluid out fo the alveolus • Increases the gradient for gas transfer ◦ Partial pressure is augmented by the added pressure aiding O2 diffusion ◦ Minimal effect clinically • Excessive pressure ◦ Overdistension and lung injury ◦ Worsening V/Q mismatch ◦ Bio trauma - cytokine leak and extra-pulmonary dysfunction ◦ Impaired lymphatic drainage of the lungs - net effect is decreased lymph flow with increased lymph production • Neutrophil retention in pulmonary capillaries due to poor transit through pulmonary circulation compressed by increased pressure (no known clinical effects)

Question 182

How does positive pressure effect the RV

Answer 182

• RV and pulmonary circulation ◦ Reduced preload ‣ Increased intrathoracic pressure transmitted to central veins and right atrium —> decreases RV preload ‣ PEEP > CVP will collapse the vessels (in reality the PEEP is not directly transmitted and instead in a lung with normal compliance no more than 25% is transmitted; however in a patient relatively under filled this can be disastrous) ◦ Increased afterload ‣ Increased intrathoracic pressure transmitted directly to arteries + transmitted alveolar pressure —> increased PVR (as the RV needs to overcome PEEP + pulmonary artery pressure) ‣ Increased PVR increases RV ventricular afterload ◦ Increasing after load and decreased preload —> reduces RV stroke volume

Question 183

How does positive pressure effect LV preload

Answer 183

◦ Decreased preload ‣ PEEP increases RV pressures so EDP in the RV is higher than in the LV leading to bulging of the septum contralaterally reducing LV preload

Question 184

How does positive pressure ventilation effect afterload?

Answer 184

◦ Decreased afterload ‣ LV transmural pressure/wall stress • In order to actually produce an adequate LV pressure when someone breathes in at normal tidal volumes (generating negative intrapleural pressures of negative 1-2) you have to overcome the negative pressure; however in a spontaneous breathing patient you increase LV preload on inspiration leading to an increase in RV stroke volume • However when effort increases substantially e.g. pulmonary oedema; decreased lung compliance demands increased negative pressure which increases LV transmural pressure - intra-LV pressure vs intrapleural pressure difference increases transmural pressure increasing afterload • Positive pressure ventilation reverses this problem decreases LV transmural pressure - improved wall stress and oxygen consumption • Additionally positive pressure on intrathoracic aorta causes a pressure gradient between he thoracic and extra-thoracic aorta improving systemic BF • PEEP decreases LV afterload ‣ Increased pressure gradient between intra-thoracic aorta and extra-thoracic system Decreased LV stroke volume

Question 185

How does positive pressure ventilation affect the brain?

Answer 185

• Raised ICP if high PEEP ◦ Cerebral perfusion pressure is MAP - ICP (or CVP whichever is highest). ◦ Only appears to have an effect multiple days into the illness where cerebral auto regulation is impaired and when PEEP is increased ICP also increased resulting in a drop in CPP ◦ As long as noradrenaline kept their CPP at adequate levels as long as auto regulation is still in place it had no effect ◦ PEEP above 15 seems to be where it starts coming in to play; and it seems to result in fairly trivial rises in ICP until PEEP is at >20 ◦ Does not appear to effect non brain injured patients

Question 186

How does positive pressure effect the kidney?

Answer 186

• Water retention ◦ ADH release/vasopressin - also likely related to atrial stretch receptors, secretion fron the posterior pituitary increases during positive pressure ventilation ◦ Aldosterone - RAAS response secondary to drop in systemic BP • Sodium retention ◦ ANF release - drops by 2/3 in response to reduced preload with increasing PEEP, and returned to normal with volume administration (atrial stretch being the trigger for release) ◦ Aldosterone • Decreased renal perfusion and GFR ◦ Due to reduced cardiac output - reduced renal blood flow ◦ Increased renal venous pressure The above also explains post extubation diuresis

Question 187

How does positive pressure effect the GIT?

Answer 187

• Decreased hepatic perfusion and decreased metabolic clearance of drugs • Decreased splanchnic perfusion - reduced motility and poor gastric emptying ◦ Not only due to poor cardiac output but the subsequent redistribution of BF • Decreased gastric perfusion - stress ulcers ◦ Intubation and positive pressure ventilation appears to the most important predictor of stress ulceration

Question 188

Define venous admixture? What is the normal level?

Answer 188

Definition • Venous admixture is that amount of mixed venous blood which would have to be added to ideal pulmonary end-capillary blood to explain the observed difference between pulmonary end-capillary PO2 and arterial PO2 • Normal venous admixture is usually about 3% of the cardiac output. • Shunt - is the blood which enters the systemic arterial circulation without participating in gas exchange

Question 189

How is venous admixture different to shunt?

Answer 189

Definition • Venous admixture is that amount of mixed venous blood which would have to be added to ideal pulmonary end-capillary blood to explain the observed difference between pulmonary end-capillary PO2 and arterial PO2 • Normal venous admixture is usually about 3% of the cardiac output. • Shunt - is the blood which enters the systemic arterial circulation without participating in gas exchange

Question 190

What is the normal % of venous admixture?

Answer 190

Definition • Venous admixture is that amount of mixed venous blood which would have to be added to ideal pulmonary end-capillary blood to explain the observed difference between pulmonary end-capillary PO2 and arterial PO2 • Normal venous admixture is usually about 3% of the cardiac output. • Shunt - is the blood which enters the systemic arterial circulation without participating in gas exchange

Question 191

What are the main causes of venous admixture?

Answer 191

1. Anatomical - Physiological - bronchial and thebesian veins - True shunt - V/Q = 0 lung regions - Intracardiac 2. V/Q scatter where V/Q <1 3. Pathological - Intrapulmonary AV connections, intrapulmonary sources of poorly oxygenated blood e.g. portopulmonary shunts and lung tumours

Question 192

Explain the physiological anatomical causes of veinous admixture

Answer 192

◦ Physiological shunt ‣ Bronchial veins - which drain the bronchial walls (<1% of cardiac output) - drains into pulmonary veins and in bronchiectasis or COPD contribution can be 10% of cardiac output ‣ Thebesian veins - which contribute myocardial venous blood with low oxygen content (contributer 0.1 - 0.4% of cardiac output)

Question 193

What equation determines venous admixture?

Answer 193

• The ratio of venous admixture to cardiac output is defined by the Berggren equation which calculates the shunt fraction • Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2) • where ◦ Qs/Qt = shunt fraction (shunt flow divided by total cardiac output) ◦ CcO2 = pulmonary end-capillary O2 content, same as alveolar O2 content • CtO2 (A) is the alveolar oxygen content • CcO2 - CvO2 is the difference between mixed venous and perfect end capillary blood ◦ CaO2 = arterial O2 content - lower than the CcO2 ◦ CvO2 = mixed venous O2 content - returning to the lungs at a flow rate equal to cardiac output (Qt) ◦ O2 content can be calculated by removing the dissolved oxygen from the equation for oxygen content and calculating based on Sats x 1.39 x Hb

Question 194

WHat is the Berggren equation?

Answer 194

• The ratio of venous admixture to cardiac output is defined by the Berggren equation which calculates the shunt fraction • Qs/Qt = (CcO2 - CaO2) / (CcO2 - CvO2) • where ◦ Qs/Qt = shunt fraction (shunt flow divided by total cardiac output) ◦ CcO2 = pulmonary end-capillary O2 content, same as alveolar O2 content • CtO2 (A) is the alveolar oxygen content • CcO2 - CvO2 is the difference between mixed venous and perfect end capillary blood ◦ CaO2 = arterial O2 content - lower than the CcO2 ◦ CvO2 = mixed venous O2 content - returning to the lungs at a flow rate equal to cardiac output (Qt) ◦ O2 content can be calculated by removing the dissolved oxygen from the equation for oxygen content and calculating based on Sats x 1.39 x Hb

Question 195

Draw a diagram demonstrating V/Q ratio to height of the lung

Answer 195

Question 196

Why does V/Q mismatch occur at baseline?

Answer 196

• V/Q mismatch occurs at baseline in the erect lung due to gravity and its effect on blood flow through the low pressure pulmonary circulation - both ventilation and perfusion increase as you pass from apex to the base of the lung

Question 197

Lung spices V/Q ratio

Answer 197

◦ Lung apices - V/Q ratio >1 generally~3

Question 198

Where in the upright lung does V/Q = 1

Answer 198

3rd rib (midzones)

Question 199

V/Q at bases of upright lung

Answer 199

0.6

Question 200

Define dead space and shunt using V/Q

Answer 200

◦ Dead space is V/Q of infinity; and shunt occurs when V/Q = 0

Question 201

Explain the effect of V/Q < 1

Answer 201

• V/Q < 1 ◦ A low V/Q ratio is seen at baseline in the lung in the areas below the 3rd rib where blood flow > ventilation. The lower the V/Q ratio the closer the efflunet blood composition is to mixed venous blood (PaCO2 = 46; PaO2 40) as there is diminished oxygen delivery to the alveoli (reduced ventilation) but an excess of blood. ◦ Therefore V/Q < 1 results in hypoxia - and when V/Q is 0.1 - 1 there is capacity for FiO2 increases to compensate for reduced ventilation; however in true shunt increased FiO2 does not increase PaO2

Question 202

Explain the concept of V/Q >1 and the effect it has on oxygenation

Answer 202

◦ A V/Q ratio >1 is seen in the apices of the lung and there is excellent gas exchange but as at room air at V/Q =1 the oxyhaemoglobin dissociation curve operates on the plateau there is limited capacity for increased oxygen extraction and these units provide minimal compensation for poor gas exchange elsewhere ◦ The higher the V/q ratio the closer the effluent blood gets to alveolar gas (PaO2 150, PACO2 0)

Question 203

How is V/Q related to PaO2 and PaCO2 - depict graphically

Answer 203

Question 204

What effect does V/Q have on PaCO2

Answer 204

◦ This change has minimal effect on CO2 because the relationship of CO2 clearance to V/Q ratio is more flat and linear. Ventilatory responses to increasing CO2 are able to compensate for reduced V/Q in part due to the increased diffusion capacity of CO2 (24x oxygen)

Question 205

Explain the concept of west’s zones and the determinants of flow in each zone

Answer 205

West zones (upright lung) - describe regional blood flow through the lungs accounting for the starling resistory moel where the resistive force is alveolar pressure • Definition ◦ PA = alveolar ◦ Pa = arterioles ◦ Pv veinous • Zone 1: PA > Pa > Pv ◦ Practically no blood flow in these regions as BV collapse producing V/Q >1 and dead space (V/Q = infinity). Does not occur in healthy lung • Zone 2: Pa > PA > Pv ◦ Rate of blood flow determined by difference between Pa and PA - BF increases linearly from the upper parts of the zone to the lower parts of the zone as hydrostatic pressure increases Pa ◦ V/Q ~3 in the upper lung falling to 0.6 in the lower parts of the lung • Zone 3: Pa > Pv > PA ◦ Blood flow determined by arteriovenous driving pressure, blood flow highest and V/Q <1 • Zone 4: the interstitial pressure is higher than alveolar and pulmonary venous pressure (but not pulmonary arterial pressure)1st

Question 206

What are the physiological effects/changes the body is subject to at high altitude? 4

Answer 206

Reduce atmospheric pressure Reduced temperature Reduced relative humidity Increased solar radiation

Question 207

What are some key pressures relating to altitude? - PaO2 60 at what level? - What height is consciousness lost in? - At what height does 100% O2 only give PAO2 of 100? - When is consciousness lost despite 100% FiO2 - What is the Armstrong Limit?

Answer 207

Reduced air pressure results in a proportional decrease in PO2: At 3,000m, alveolar PO2 is 60mmHg At 5,400m, consciousness is lost in unacclimatised individuals At 10,400m, air pressure is 187mmHg With 47mmHg of water vapour and an alveolar PCO2 of 40, breathing 100% O2 gives an alveolar PO2 of 100mmHg. At 14,000m, consciousness is lost despite 100% O2 At 19,200m, the ambient pressure is so low that the boiling point of water is 37°C This is the Armstrong limit.

Question 208

What is the body response to altitude?

Answer 208

Fall in PaO2 is compensated by increasing minute ventilation, which decreases PACO2 and therefore increases PAO2 Limits of compensation are reached on 100% oxygen at 13,700m Effective compensation is limited by the respiratory alkalosis, this is known as the braking effect: Peripheral chemoreceptors detect hypocapnea Central chemoreceptors detect alkalosis

Question 209

What is the breaking effect in the context of high altitude exposure?

Answer 209

Effective compensation is limited by the respiratory alkalosis, this is known as the braking effect: Peripheral chemoreceptors detect hypocapnea Central chemoreceptors detect alkalosis It takes time for bicaronate to centrally equilibrate and restore ECG H+ to normal removing inhibition on ventilation

Question 210

What occurs with acclimatisation in altitude exposure?

Answer 210

1. Ventilation increased Effective compensation is limited by the respiratory alkalosis, this is known as the braking effect: Peripheral chemoreceptors detect hypocapnea Central chemoreceptors detect alkalosis The subsequent respiratory alkalosis generates a compensatory metabolic acidosis This acidosis relaxes the braking effect and allows further hyperventilation, and is therefore am important part of acclimatisation. 2. Increased O2 transport and delivery - Increased Hb concentration (EPO) by up to 20 points - increased capillaries in muscles to improve perfusion 3. Oxyhaemoglobin dissocation curve - left shifted due to hypocapnoea, right shfited by icnreased 2,3 DPG Polycythaemia increases blood viscocity and decreases flow rates, hypoxic pulmonary vasoconstriction increases pulmonary arterial pressures. Cardiac output increased by 20-50% on ascent, and returns to normal with acclimitasation

Question 211

What happens to oxygen delivery with high altitude? Acutely Chronically

Answer 211

Fall in PaO2 is compensated by increasing minute ventilation, which decreases PACO2 and therefore increases PAO2 Limits of compensation are reached on 100% oxygen at 13,700m There is an initial left-shift of the oxygen-haemoglobin dissociation curve due to alkalosis This stimulates a compensatory increase in 2,3-DPG to right-shift the curve and improve oxygen offloading at the tissues Chronically - increased Hb, decreased blood volume due to diuresis

Question 212

How does altitude affect the heart

Answer 212

1. PVR increases due to HPV 2. Heart rate increases due to increased SNS outflow 3. Stroke volume falls (cardiac output remains the same) due to decreased preload: pressure diuresis, insensible losses due to reduced humidity --> on initial ascent CO increased by 20-50% due to SNS tone but returns to normla 4/ Increased myocardial work - increased HR, viscocity, RV afterload (especially of the RV)

Question 213

What is the mechanism of pulmonary oedema in the context of altitude?

Answer 213

Increased RV afterload from high PVR --> heterogenous hypoxia-induced pulmonary vasoconstriction Increased pulmonary capillary hydrostatic pressures lead to fluid transudation and pulmonary oedema in less constricted areas Diminished reabsorption of alveolar fluid is also likely to be important, with hypoxia inhibiting Na+ transport across the alveolar membrane.

Question 214

What is the mechanism of acute mountain sickness and cerebral oedema?

Answer 214

A vasogenic mechanism is thought to be responsible for the cerebral oedema. 1. Hypoxia-induced cerebral vasodilation 2. BBB permeability alteration of the permeability of cerebral capillaries are likely causes. 3. Impaired autoregulation of cerebral blood flow 4. Higher ratio of brain mass to CSF volume so reduced buffering Cytotoxic oedema may also play a role, with failure of the Na+-K+ ATPase due to oxygen radicals.

Question 215

Acetazolamide helps in altitude sickness how?

Answer 215

Acetazolamide is the most effective prophylaxis. It is a carbonic anhydrase inhibitor that causes a bicarbonate diuresis (maximum inhibition is 45% of bicarbonate) and metabolic acidosis. It increases the hypoxic ventilatory response, decreases CSF production and may also have effects on the perripheral chemoreceptors. It is usually well tolerated. Side effects include paraesthesia and metallic taste.

Question 216

What drugs other than acetazolamide can help with altitude sickness?

Answer 216

Dexamethasone - for acute mountain sickness, sort exposures only Pulmonary artery pressure can be reduced by nifedipine or the phosphodiesterase inhibitors sildenafil and tadalafil. Both have been shown to decrease the incidence of HAPE when taken as prophylaxis. Salmeterol decreases the risk of HAPE by increasing alveolar fluid clearance through its action on Na+ transport. avoiding over-exertion avoidance of alcohol and smoking eating a high carbohydrate diet ensuring adequate hydration. Best thing is slow ascent, sleep low and climb high

Question 217

What body systems does high altitude effect?

Answer 217

Resp - increased minute volume Cardiovascular - Tachycardia and increased CO due to increased sympathetic drive - Mild BP increase Neuro 0 Decreased function, delirium possible Renal - Diuresis and decreased serum bicarbonate

Question 218

How does the body adapt to chronic altitude exposure

Answer 218

Minute volume the same Tidal volume increases due to thoracic remodelling HR and SV return to normal values as haematocrit adapts Haematocirt increases and haemoconcentration

Question 219

What determines respiratory rate

Answer 219

PaCO2 pH Hypoxia Centrally prior to exercise

Question 220

Explain how a HME filter works

Answer 220

Sealed unit Hygroscopic material on patient side - cardboard/paper coated with calcium chloride or silica gel During expiration warm humidified gas expired condenses on the hygroscopic surface heating and wetting the surface Dry cool gas fromt he breathing system then pases over the surface on inspiration and is warmed and humidified as it enters the aptient

Question 221

Humidity

Answer 221

Refers to thew water content of a gas volume

Question 222

Absolute humidity

Answer 222

The mass of water molecules preent per unit of volume Grams per cubic metreR

Question 223

Relative humidity

Answer 223

Ratio of water vapour present compared to maximum amount of water vapour the air could hold at that temprature Actual vapour pressure/saturation vapour density x 100%

Question 224

Describe the normal process of humidifying air entering the body

Answer 224

Inspired air has a water content of 10g/metre cubed if it is 50% humidity and 22 degrees Mucosa of upper airway structures warm and humidify as it passes through nasopharynx and pharynx creating turbulence. Turbulence increases evaporative heat exchange between air and mycosa Posterior nasal pharynx relativive humidity is 85% and lower pharynx at 33 degrees is 100% humidity but as insoured air is body temperature fully warming and humidification does not cocur until 5cm above the carina Alveolar gas has a water content of 47g/cubic metre

Question 225

Colligative properties

Answer 225

Properties depending on the number of moelcuels in a solution Boiling point Freezing point Vapour pressure Osmotic pressure

Question 226

Describe the improvement found in oxygen present in the lung following preoxygenation

Answer 226

13% x 30ml/kg (roughly 2100mls) --> 270mls of O2 PO2 660 at 100% O2 via alveolar gas equation (87%) --> 1825mls

Question 227

Hyperventilation effect on preoxygenation

Answer 227

1/ Rate of washout improved 2. Decrease in alveolar CO2 means FRC can contain a small amount more of O2

Question 228

Total body oxygen when supine adn breathing room air

Answer 228

1330mls 270mls lungs 820mls blood 45mls tissue 200ml myglobin

Question 229

Total body oxygen preoxygenated

Answer 229

3000mls (vs 1330 room air supine) 1825mls lungs 910mls blood 50mls dissolve in tissues 200mls myoglobin

Question 230

What would you expect mixed venous saturations to be with 100% O2 preoxygenatino for 3 minutes

Answer 230

84% PvO2 50

Question 231

What catalyses the final step of oxidative phosphorylation

Answer 231

Cytochrome oxidase

Question 232

What is the highest PO2 you can get to without positive pressure

Answer 232

660 without hyperventilation

Question 233

What effect does breathing 100% oxygen have on PCO2

Answer 233

Increases it Reverse Haldane --> PCO2 increases to 50-55mmHg in arterial circulation In veinous circulation CO2 comes back to 46mmHg and the Haldane effect persists unless in a hyperbaric environment where mixed veinous O2 remains high >100mmHg

Question 234

How much O2 is dissolved at PO2 of 100

Answer 234

0.3mls

Question 235

How much O2 is dissolved at a PaO2 of 600mmHg

Answer 235

1.8mls

Question 236

What would an expected arterial PaO2 be for a patient on 100% O2 even if their lungs aren't great

Answer 236

>500mmHg They are shunting if its any lower

Question 237

What are the key features of pneumothorax resolution

Answer 237

1. Gasses move down concentration gradients - partial pressure gradient 2. Total pressure of the pneumothoax does not vary despite reabsirption of agsses because the VOLUME changes - total pressure remains close to atmospheric 3. Because of volume reduction at constant rpessure absorption of gasses down their concentration gradients has a concentrating effect on all remaining gasses

Question 238

What is the one gas within a pneumothorax that is always present and whose partial pressure remains constant throughout reabsorption?

Answer 238

Water vapour 47mmHg at its saturated vapour pressure No gradient for reabsorption

Question 239

Where is a pneumothorax reabsorbed into?

Answer 239

Into blood in adjacent pleural capillaries

Question 240

Describe the movement of oxygen out of pneumothoraxes

Answer 240

PO2 of pneumothorax higher than capillary blood in mot circumstances This decreases pneumothroax size but total pressure the same This concentrates remaining gasses favouring reabsorption

Question 241

How does the sum of partial pressures in capillary blood compare to atmospheric pressure?

Answer 241

Reduced due to PO2 drop This is initiallly the largest gradient present favouring absiorption of O2

Question 242

What gas formulation might increase a pneumothorax size

Answer 242

Nitrous oxide as it will diffuse down its concentration gradient into the pneumothorax

Question 243

What is the gas compoisition of a pneumothorax

Answer 243

Depends on its origin If room air the origin then resmebles this with low pCO2 causing entry of CO2 from capillaries

Question 244

How might a pneumothorax reabsorption be improved?

Answer 244

Oxygen Eliminates nitrgoen from capillary blood favouring nitrogen reabsorption Mixed venous O2 lrgely unchanged so gradient for O2 reabsorption not dramatically affected

Question 245

When is cyanosis detectable?

Answer 245

5g/dL or more of de-oxyhaemoglobin or 1.5g/dL of methaemoglobin

Question 246

What is haemoglobin autooxidation

Answer 246

Where the oxygen takes the lectrons of the iron becoming a superoxide leaving the iron in ferric form

Question 247

What metabolised methaemoglobin

Answer 247

Methaemoglobin reductase - Requiring NADH and cytochrome B5 as cofactors. Minimal also done by NADPH methaemoglobin reductase but in presence of methyelene blue increases markedly