1.1 Respiratory Mechanics Flashcards

1
Q

What is the FRC

Elastic recoil?

Sum of what volumes?
How much is it

How can it be measured

A

Functional residual capacity (FRC) is the volume of air present in the lungs, specifically the parenchyma tissues, at the end of passive expiration.

At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and there is no exertion by the diaphragm or other respiratory muscles.

FRC is the sum of expiratory reserve volume (ERV) and residual volume (RV) and measures approximately 2400 ml in a 70 kg, average-sized male.

It cannot be estimated through spirometry, since it includes the residual volume.

In order to measure RV precisely, one would need to perform a test such as nitrogen washout, helium dilution or body plethysmography.

The helium dilution technique is a common way of measuring the functional residual capacity of the lungs.

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2
Q

Functions of lungs

x 6

A
  1. The main function of the lungs is gas exchange, but they have many other functions including:
  2. The synthesis of surfactant, prostaglandins and histamine
  3. Activation and deactivation of angiotensin, bradykinin, 5-hydroxytryptamine and the handling of amide local anaesthetics..
  4. They act as a blood reservoir, in that the pulmonary circulation contains up to 900 ml of blood and this volume increases by up to 400 ml when in the supine position.
  5. Substances are filtered from the pulmonary circulation, for example, thrombus and air;
  6. the mucous lining the air passages also traps particles.

Humidification is a function of the nose and the upper airway rather than of the lungs themselves.

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3
Q

Compliance is defined as

Decreased with -

Explain complaince at different position of volumes

Normal lung compliance
Chest wall compliance -

A

Compliance is the volume change per unit change in pressure (mL per cmH2O).

Compliance is decreased with

  1. pulmonary oedema,
  2. Increased venous pressure
  3. pulmonary fibrosis.

Compliance describes the ability of the lung to stretch. It is the volume change per unit change in pressure. At resting lung volumes the compliance curve is steep, meaning that for a small change in pressure there is a large volume change.

At higher lung volumes the curve is flatter meaning there is a smaller change in volume for the same pressure change. Compliance is hence smaller at higher lung volumes.

Normal lung compliance is 200 ml/cmH2O and combined lung and chest wall compliance is normally about 70-80 ml/cmH2O

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4
Q

Blood gas changes in asthma attack varying severtiy

Arterial Pco2

FRC

Serum Bic

FEV1
Po2

A

In mild to moderate asthma attacks the arterial pCO2 may decrease. With increasing severity the pCO2 returns to normal and in severe asthma attacks it may be increased.

With airways obstruction the functional residual capacity increases (not decreases).

The serum bicarbonate concentration would not be raised in moderately severe asthma but it could be in a life-threatening attack for the same reasons as the arterial PCO2 increases.

The forced expiratory volume in 1 sec (FEV1) is a good indication of airway obstruction.

Do not be confused with chronic obstructive pulmonary disease (COPD) where reduced FEV1 is normally mentioned. It measures airways obstruction and is reduced in acute asthma.

The arterial pO2 is usually normal in a moderate attack but may decrease during a severe asthma attack.

If a pneumothorax occurs then the fall in arterial PO2 may be greater.

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5
Q

ODC
What is the signinficance of the shape

Steep part =

Right shift

Decreased Hb =

A

The curved shape of the oxygen dissociation curve (ODC) means that the loading of oxygen to the tissues is little affected by significant drops in alveolar pO2.

The steep lower part of the dissociation curve means that peripheral tissues can take off large amounts of oxygen for only a small drop in capillary pO2, assisting the diffusion of oxygen into the tissues.

The oxygen dissociation curve is shifted to the right by

Acidosis
Hypercapnia, raising the temperature and
Increasing the amount of 2,3-DPG (2,3- diphosphoglycerate)
which is an end product of red cell metabolism, the concentration of which increases in chronic hypoxia, at altitude, or in chronic lung disease.

A decreased haemoglobin reduces the total oxygen carrying capacity of the blood, but does not change the shape of the curve.

In chronic anaemia there is a compensatory increase in 2,3-DPG that does cause a rightward shift in the ODC, but this effect does not occur immediately.

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6
Q

Hct

Is what

Normally what

Is it higher in venous or arterial blood - why

What does a fall in Hct do to consitution of blood

A

The haematocrit or packed cell volume (PVC) is the total red blood cell volume as a proportion of blood volume. It is the volume percentage (%) of the red blood cells in blood. It is sometimes expressed as a fraction.

Normal values are 40-54% (0.4-0.54) in males and 37-47% (0.37-0.47) in females.

Venous blood has a higher haematocrit than arterial blood because of the entry of chloride ions into red cells (chloride shift) which is followed by water entry by osmosis.

A fall in haematocrit decreases the viscosity and thus increases the flow. Therefore, a haematocrit of about 30% (0.3) after acute blood loss is thought to be optimal.

In addition to reducing the viscosity and improving tissue blood flow the hazards of blood transfusion and deep vein thrombosis are reduced. However, a value below 30% is undesirable because of reduced oxygen carrying capacity.

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7
Q

Smoking & FEV1

What happens to Fev1 through childhood
when does it decline

What is the deceline compared to smokers

What age do smoker need to stop

A

The forced expiratory volume in 1-second (FEV1) increases through childhood and peaks between the ages of 18 and 25 years. There is then a slow decline. This decline of 50-70 mls per year in 15-20% of smokers compares with a decline of 30 mls per year in non-smokers. Cessation of smoking returns the decline in FEV1 to that of non-smokers thus preserving lung function.

Smokers who abstain before the age of 40 years eventually have an FEV1 similar to those who have never smoked. The FEV1 is lower by 7 % in smokers who gave up between the ages of 40 and 60 years of age. However, If a lifelong smoker gives up after the age of 60 the FEV1 will at best be 14% less than that of a non-smoker of the same age. Lung function is related inversely to pack-years of cigarette use.

Therefore the FEV1 will not return to normal in this gentleman in five years, let alone six months.

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8
Q

PHTN recog compication of

x5

A

ulmonary hypertension is a recognised complication of:

Thromboembolic disease
Life at high altitude
Chronic alveolar hypoventilation, and
Patent ductus arteriosus.
Polycythaemia rubra vera is usually associated with systemic hypertension but pulmonary hypertension1 can also be a feature
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9
Q

Change if PFTs and obesity

FRC

Airway closure
how much is frc decrease

Resp complaince reduced du to

A

In morbid obesity, even in the upright position, the fall in FRC can be so marked that it approaches residual volume (RV).

The patient is at risk of premature airway closure and significant ventilation perfusion mismatch resulting in hypoxia. The FRC decreases by 40% when supine as the diaphragm is pushed upward into the thorax by the abdominal contents. Further falls in FRC occur following induction of anaesthesia.

Total respiratory compliance is reduced by up to two-thirds of normal:

Chest wall; due to fat deposition around diaphragm, ribs and abdomen, and
Lung; due to increased pulmonary blood.
This can further deteriorate in the recumbent position volume as the chest wall become less compliant and increase in respiratory resistance.

Whilst morbid obesity results in an increase in inspiratory reserve volume and reduced FEV1, PEFR and ERV, the reduction of FRC (an oxygen reservoir) is very important.

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10
Q

Chemoreceptors

Central located where
Sensitive to what

CSF sensitive because

What receieves high blood flow per 100g tissue

Dopaine contained in what type cell

A

The central chemoreceptors are on the ventral surface of the medulla (not dorsal) and are sensitive to hydrogen ion concentration [H+].

The cerebrospinal fluid (CSF) is very sensitive to changes in [H+] because it lacks proteins and other buffers (it does not have a good buffering system). The pH of CSF is 7.32 and for a given change in PCO2 the change in CSF pH is greater than in the blood.

Each carotid body receives 0.04 ml of blood per min, which is the equivalent of 2 litres per100g of tissue per min, and is the highest blood flow to any body tissue.

Dopamine is contained within glomus type 1 cells (not type 2 cells).

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11
Q

What is staic lung compliance

when is measured
what is the formaula

How man it be measured

Normal compliance is what

A

Static lung compliance is the change in volume for any given change in pressure. Static compliance is measured at a period when there is no gas flow, for example during an inspiratory or expiratory pause.

Compliance = ΔV/ΔP

The units are ml/cmH2O or L/cmH2O.

Intrapleural pressure can be measured indirectly using an oesophageal manometer. Respiratory volumes can be measured at the mouth using a pneumotachograph or spirometer.

The normal compliance (Cl) of a normal lung is 200 ml/cmH2O.

For example, if a patient inhales 600 mL of air from a spirometer with an intrapleural pressure before inspiration of -6 cm H2O and -12 cm H2O at the end of inspiration.

Cl = 600mL/-6 -(-12)cmH2O = 600/6 = 100ml/cmH2O.

In this example with a ventilated patient the static compliance represents pulmonary compliance during periods without gas flow, such as during an inspiratory pause.

It can be calculated with the formula:

Cstat = Vt/Pplateau-PEEP

where:

Vt = tidal volume
Pplateau = plateau pressure
PEEP = peak end-expiratory pressure.
So:

Cstat = 800/50-10 = 20 ml/cmH2O.

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12
Q

Ficks lawWhat is the formula

A

The rate of gas transfer of gas across a semi-permeable membrane is directly proportional to its area, the gas partial pressure differential and the diffusion permeability coefficient.

Fick’s law relates to the rate of transfer of a gas across a sheet of tissue.

The rate of gas transfer is directly proportional to the area of tissue (A), the difference in gas partial pressure between the two sides (P1 − P2) and the diffusion permeability coefficient (D). The rate transfer of gas across a sheet of tissue is inversely proportional to the thickness of the membrane (T).

dV/dt = A/T × D × (P1 − P2)

V = mL/minute
A = area
T = tissue thickness
D = diffusion constant
P1 − P2 = partial pressure gradient
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13
Q

PVR - lung volumes

increased by

Lowered by

Anaemia

A

Pulmonary vascular resistance varies with lung volume in a U shaped curve, such that PVR is at its lowest when lung volumes approximate to the functional residual capacity.

PVR is increased by:

Vasoconstrictor drugs
5-HT, and
Histamine.
Hypoxia, hypercapnia and acidosis

It is lowered by:

Vasodilator drugs
Prostacycline, and
Acetylcholine.

Hypoxia, hypercapnia and acidosis increase PVR whilst their opposites decrease PVR.

Anaemia reduces blood viscosity which decreases PVR and SVR.

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14
Q

Compliance is defined

Which is related to airways resitance

what is specific compliance

Which is greater - static or dynamic
why x3

What is normal

A

Compliance is defined as the volume change per unit pressure change.

Dynamic (not static) compliance is related to airways resistance.

Specific compliance allows comparison to be made between patients with varying body sizes.

Dynamic compliance is less than static compliance (not greater) for the following reasons.

Airway resistance affects airflow.
Incomplete filling of alveoli in the available time
True pressure equilibrium between applied and alveolar pressure is not obtained, and lung appears stiffer than it really is
Static compliance in the normal lung during spontaneous ventilation is 200 ml per cm of water.

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15
Q

What has the leftest ODC

What is the p50 for that odc

A

The myoglobin ODC is a rectangular hyperbola with a very low P50 0.37 kPa (2.75 mmHg). It needs a lower P50 to enable offloading of oxygen from haemoglobin and it is low enough to be able to offload oxygen onto myoglobin where it is stored. The myoglobin, however, does release its oxygen at the very low PO2 values found inside the mitochondria.

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16
Q

what is the p50 decribing

What is it for adult hb

A

The term P50 is used to describe the affinity of haemoglobin for oxygen. The P50 is the PO2 at which the haemoglobin becomes 50% saturated with oxygen. The P50 of adult haemoglobin under normal conditions is 3.47 kPa(26 mmHg).

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17
Q

Whats foetal hb

Whats it ODC

A

Foetal haemoglobin has 2 α and 2 γchains. The ODC is left shifted (P50 lies between 2.34-2.67 kPa [18-20 mmHg]) compared with the adult curve it has a higher affinity for oxygen. Because foetal haemoglobin has no β chains there is less binding of 2.3 diphosphoglycerate (2.3 DPG).

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18
Q

What does CO do to Hb

Whats the p50 in SCD

A

Carbon monoxide binds to haemoglobin with an affinity more than 200-fold higher than that of oxygen, and thus decreases the amount of haemoglobin available for oxygen transport. Carbon monoxide binding also increases the affinity of haemoglobin for oxygen, thus shifting the oxygen-haemoglobin dissociation curve to the left and impeding oxygen unloading in the tissues.

In sickle cell disease (HbSS) has a P50 of 4.53 kPa(34 mmHg).

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19
Q

HPV

Response to
what
where

Dependent on innervation to vessel walls?

What does it result in

what level of nitric will inhibit HPV

is it affected by volatiles?

A

Hypoxic pulmonary vasoconstriction (HPV) is the reflex constriction of pulmonary arterioles in response to low a PO2 (below 80 - 100 mmHg; 11 - 13 kPa) in adjacent alveoli.

It is independent of the innervation to the vessel walls and can occur when blood with a high PO2 is perfused through lung which has a low alveolar PO2.

Thus a low PO2 in the alveoli has been shown to influence hypoxic pulmonary vasoconstriction (HPV) more than a low PO2 in the blood.

HPV results in the blood flow being directed away from poorly ventilated areas of the lung and helps to reduce the ventilation/perfusion mismatch (not increase).

Volatile anaesthetic agents reduce HPV in animals, but in adults the evidence is less convincing, although it certainly does not increase the effect.

20 parts per million (ppm) of nitric oxide will inhibit the HPV response.

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20
Q

PVR

Where does the PVR reside

A

The pulmonary vascular resistance (PVR) is analogous to the systemic vascular resistance (SVR) but the resistance is distributed more evenly.

Approximately:

50% of the PVR resides in the arteries and arterioles
30% in the alveolar capillaries (not 50-60%) and
20% in the veins.

21
Q

How do you calculate the PVR - what law

A

The PVR can be calculated using the principle of Ohm’s law. PVR equals the mean pulmonary arterial pressure (MPAP) minus the mean left atrial pressure (MLAP) and divided by the cardiac output (CO) or cardiac index (CI) this is then multiplied by a correction factor (80)

PVR = MPAP − MLAP × 80
CO
The correction factor does not have units:

80 = Correction factor for mmHg to dyne/cm2 and L/m to cm3/sec yielding the most often quoted unit of vascular resistance dyne·sec·cm−5

The normal PVR is 20-120 dyne·sec·cm−5

22
Q

According to the Hagen-Poiseuille formula:

A

R = 8 η l/π r4

Where:

R is resistance
η is viscosity
l is length
π is a constant of 3.142
r is radius.

Halving the radius of the pulmonary vessels will increase the pulmonary vascular resistance by a factor of 16 (not 4). However, the pulmonary arteries are thin walled and distensible and in fact are more dependent on the effect of gravity and posture than on vascular tone.

23
Q

Extra alveolar vessels -

A

Extra-alveolar vessels (so-called corner vessels) , found at the junction of the alveolar septa are compressed at lung volumes below functional residual capacity (FRC). High lung volumes result in a stretching/elongation of the alveolar vessels resulting in an increased PVR whereas the extra-alveolar vessels are subject to radial traction and negative pleural pressure resulting in a decreased PVR.

At high lung volumes the hyperexpansion and high airway pressures may compress alveolar vessels which will similarly increase PVR. Therefore, PVR is at its lowest at lung volumes around FRC.

24
Q

Surfactant
mix of what
produced by

what is its purpose

A

Surfactant is a complex mixture of phsopholipids and proteins and is produced by the type 2 alveolar cells.

Surfactant reduces surface tension throughout the lung, thereby contributing to its general compliance.

Surfactant differentially reduces surface tension, more at lower volumes and less at higher volumes, leading to alveolar stability and reducing the likelihood of alveolar collapse.

25
Q

What explains a higher PaO2 in apical units v basal

Which area is better ventialted

What

A

The ventilation/perfusion (V/Q) ratio is greater in the apex compared with the basal units

The basal units are better ventilated than the apical units.
The mechanical advantage of diaphragmatic contraction at the lung bases enhances compliance.

Ventilation at the base is approximately three times more than at the apices.

The regional differences in perfusion in the upright lung are more profound, with a 10-fold difference (bases best perfused) due to the effects of gravity. The ventilation perfusion ratio is high at the apex (3.3 compared with 0.63). Therefore the alveolar partial pressure of oxygen (PAO2) is high (= 130 mmHg) at the apex. The apical units contribute less to gas exchange of O2 because of relatively poor perfusion. The converse is the case at the lung bases where the V/Q is lower than “ideal” (PAO2 is lower = 90 mmHg).

Apical alveoli have more volume than the basal units because the weight of the lung stretches them to nearly their maximal size. For the same reason the weight of the lung tends to pull it away from the thoracic wall resulting in a more negative intrapleural pressure compared with that at the bases. These factors do not directly affect PAO2.

26
Q

FRC is what

can it be measured
what is it

how much in a man & woman

How is affected by GA
by how much

how is it affected by body positon

how is it affected by aging
why

What about obesity

A

The functional residual capacity (FRC) is the volume remaining in the lungs at the end of a passive expiration. It cannot be measured directly and is the sum of the expiratory reserve volume (ERV) and the residual volume (RV). The FRC in a 70 kg man is approximately 3000 mL and in a woman 2500 mL (approximately 17% difference).

General anaesthesia results in the loss of muscle tone and change in respiratory mechanics. There is an alteration in the balance between outward forces (i.e., respiratory muscles) and inward recoil forces (i.e., elastic tissue in the lung) leading to a fall in FRC, typically 400-500 mL in an adult. This is also accompanied by an increase in the elastic behavior of the lung (reduced compliance) and an increase in respiratory resistance.

Changing the body position from supine to upright results in an increase of FRC by 800-1000 mL.

As one ages there is a gradual change in lung volumes and capacities. The FRC slightly increases secondary to the loss of elastic recoil of the lung tissue (and increased compliance).

Obesity will often negate this and decrease FRC. The most significant change in lung volume with age is the closing capacity (CC) and its relation to FRC. CC approaches the FRC in a 45-year-old in the supine position and exceeds FRC in a 60-year-old in the erect position, leading to small airway closure.

27
Q

Body pleth

What can it measure

How can it measure a certain capacity

How do we directly measure TV

How does the body pleth work

A

The body plethysmograph is a large box that is used to measure lung volumes and pressures.

The functional residual capacity (FRC) can be measured using a body plethysmograph and can be measured using Boyle’s Law.

Spirometry is used to directly measure tidal volume

The subject sits in the air-tight box breathing through a mouthpiece. Before respiratory effort is made the volume (V1) and presssure (P1) inside the box are known. At the end of a normal expiration a shutter closes in the mouthpiece (obstructing respiration). Whilst taking inspiratory efforts the lung expands by an unknown volume (∆V). The pressure in the box, according to Boyle’s Law, must increase because the chest expansion (P2)

P1 x V1 = P2 x (V1 x ∆V)

The ∆V can be calculated by rearranging the equation

The values then have to be calculated for the patient

P3 is the mouth pressure (unobstucted) at the end of a normal respiration at the FRC. The patient takes inspiratory effort against an obstructed airway as before with a increase in lung volume ∆V but a decrease in mouth pressure (P4).

P3 x FRC = P4 x (FRC +∆V). The FRC can be calculated by rearranging the equation as all the other values are known

The application of Boyle’s law to measure FRC is particularly useful in patients with respiratory disease where air trapping occurs. This is missed using the helium dilution technique as these areas do not communicate with the mouth thus underestimating the true volume. In young healthy subjects, both methods achieve similar lung volume values.

The body plethysmograph can also be used to measure airways resistance and the pulmonary blood flow.

28
Q

FRC is how ml kg

What is a capacity
what is the TLC made up of

RV measured how

CC is what
Increase when
when is it relevant

at what age does frc = cc supine & standing

A

Functional residual capacity (FRC) is 30 ml per kg (not litres).

In lung volume measurement, a capacity is the sum of two or more volumes. Total lung capacity (TLC) equals the vital capacity (VC) and the residual volume (not FRC).

The residual volume (RV) can be measured using a body plethysmograph and using the helium dilution technique.

Closing capacity (CC) is the lung capacity at which small airways begin to close during expiration.

CC = Closing volume (CV) + Residual volume (RV).

The CC increases with age and becomes relevant when CC becomes larger then FRC, leading to alterations in ventilation/perfusion mismatch and hypoxia.

In a patient with a normal body mass index and without lung-associated pathology, the closing capacity (CC) equals the FRC even in the supine position at the age of 40-years of age. Whilst at 65-years of age the CC is likely to equal the FRC when standing, it will be greater in the supine position leading to hypoxia.

29
Q

TLC is sum of

VC = diff between what and what or sum what

RV is what
FRC

A

The total lung capacity (TLC) is the sum of

The inspiratory reserve volume (IRV)
Tidal volume (TV)
Expiratory reserve volume (ERV) and the
Residual volume (RV).

Alternatively it is the sum of the inspiratory capacity (IC) and the functional residual capacity (FRC).

The vital capacity (VC) is equal to the difference between the TLC and the RV. It is also the sum of the ERV, TV and the IRV.

The IC is the sum of the TV and the IRV.

The RV is the volume of gas remaining in the lungs at the end of forced maximal expiration, whereas the FRC is the volume of gas remaining in the lungs at passive end-expiration.

30
Q

What is the closing capacity

What is fowlers method used to anaylse

what are the 4 phases

A

Closing capacity
Lung volume at which small airways in the dependent parts of the lung begin to close.
It equals the closing volume (CV) plus the residual volume (RV).
In young adults the closing capacity (CC) is less than the functional residual capacity (FRC), but it equals and then exceeds it with increasing age (from middle age onwards).

Fowler’s method is used to measure the closing volume (CV). A vital capacity breath of 100% oxygen is taken by the patient and then asked to exhale to residual volume. Expired nitrogen concentration is measured using a rapid response analyser. The nitrogen concentration is plotted against lung volume. There are four phases:

In phase I only oxygen is exhaled from the system and airway deadspace
In phase II there is a linear rise in N2 concentration representing a mixture of large airway and alveolar gas
In phase III the nitrogen concentration plateaus and its slope depends the uniform distribution of gas in the alveoli
In phase IV as airway closure begins (in the basal lung units) the expired nitrogen concentration rises abruptly because an increasing volume of expired gas is coming from the alveoli in the apical regions of the lungs. These apical alveoli have the highest nitrogen concentration.
The RV will then have to be measured using a plethysmograph to enable the CC to be determined.

At 40 years the CC equals the FRC in the supine position and at 65 years the CC equals the FRC when standing. When CC exceeds the FRC, airway closure and a ventilation/perfusion mismatch occurs during normal tidal ventilation, and is an important cause of hypoxaemia. Thus, CC increases with age (not decreases); CC decreases with the onset of anaesthesia; but it is unaffected by changes in body position.

However, factors that reduce FRC may result in the CC encroaching upon the FRC which will cause airway closure.

31
Q

FRC is made up of what
how much ml kg
what % of VC is it

Affect position

how is it measured

A

The functional residual capacity (FRC) is the residual volume plus the expiratory reserve volume, is approximately 30mL/kg representing less than 50% of vital capacity.

It is decreased when supine, increases on standing and varies in relation to height and body habitus.

Expiratory reserve can be measured directly and residual volume calculated by helium.

32
Q

What determines regional dsitribtuion of ventilation

does fio2

A

At normal lung volumes the intra-pleural pressure is greater (less negative) in the dependent part of the lung (this greater pressure provides support to the weight of lung suspended above it). This greater pressure results in the lung being at a lower volume (residual volume) at the lung bases . The alveolar volume increases progressively towards the apex. At the apex of the lungs the ventilation is greater as it sits on the steep part of the compliance curve.

The distribution of ventilation is not primarily dependent on oxygen concentration. Other factors which influence regional ventilation are airway diameter and intra-thoracic pressure.

33
Q

Pressures in west zones

Alveolar (PA), arterial (Pa), and venous (Pv) pressures in different West zones of the lung

A

Zone 1: PA>Pa>Pv

Zone 2: Pa>PA>Pv

Zone 3: Pa>Pv>PA

google image diagr

34
Q

What is the benefit of peep

what is the problem

which physiological effect of peep contributes greatest to this problem

A

Positive end-expiratory pressure (PEEP) of 5-20 cmH2O can be applied during positive pressure ventilation to improve ventilation perfusion mismatch. Improvement of oxygenation results from an increase in functional residual capacity. The application of PEEP is a ‘double-edged sword’ - on the one hand it may improve oxygenation, while on the other a concomitant reduction in cardiac output has the potential to impair oxygen delivery and flux.

While all of the options are associated with the reduction in cardiac output associated with the use of PEEP, the option that is most responsible is the progressive decrease in venous return of blood to the right atrium. The heart rate usually does not change with PEEP so the entire fall in cardiac output is a consequence of a reduction in left ventricular (LV) stroke volume (SV).

The interventricular septum does shift toward the left and there is increased pulmonary vascular resistance (PVR) from overdistention of alveolar air sacs that contribute to the reduction in cardiac output. Any increase in PVR will be associated with reduced pulmonary vascular capacitance.

35
Q

acute respiratory acidosis

What is the single most likely direct central influence on his respiratory rate?

where are they located

what do they respond to changes of

what about periph what they respond

A

The central chemoreceptors are located in the ventral surface of the medulla and are particularly sensitive to changes in blood PCO2 tension. They respond primarily to changes in CSF pH and indirectly to changes in PaCO2.

CO2 readily diffuses across the blood brain barrier and combines with water to produce carbonic acid (H2CO3). This reaction is catalysed by the ezyme carbonic anhydrase. The carbonic acid subsequently dissociates to to H+ and HCO3- ions. The CSF has less buffering capacity than plasma and a fall in CSF pH will then cause reflex respiratory stimulation.

The central chemoreceptors are not stimulated by a fall in PaO2.

The peripheral chemoreceptors are the carotid bodies located at the bifurcation of the common carotid artery and the aortic bodies lie in the arch of aorta. The carotid bodies are sensitive to changes in arterial PaCO2, PaO2 and pH whereas the aortic bodies are principally sensitive to changes in arterial PaO2 and PaCO2 only.

36
Q

Static lung compliance is what

what is the calculation total static compliance

A

Static lung compliance is the change in volume for any given change in pressure.

Static compliance is measured at a period when there is no gas flow, for example during an inspiratory or expiratory pause.

Compliance = ΔV/ΔP

The units are ml/cmH2O or L/cmH2O

Intrapleural pressure can be measured indirectly using an oesophageal manometer.

Respiratory volumes can be measured at the mouth using a pneumotachograph.

The normal compliance (Cl) of a normal lung is 200 ml/cmH2O.

Total static compliance (Ct) includes the compliance of the chest wall (Ccw) that is also 200 ml/cmH2O.

Summation of elastance = 1/compliance.

Ct = Cl + Ccw

1/Ct = 1/200 + 1/200 =

1/Ct = 0.005 + 0.005 = 0.01

1/Ct = 0.01 by rearranging equation Ct = 1/0.01 = 100ml/cmH2O.

37
Q

Surfactant is what

prod what

how much does it reduce surface tension

how does the variation in respiration affect reduction surf tension

what are its function

what type of molecular layer occurs

A

Surfactant is a complex mixture of phospholipids and proteins and is produced by the type 2 alveolar cells.

Surfactant reduces surface tension throughout the lung by about 15 times, thereby contributing to its general compliance.

Surfactant differentially reduces surface tension, more at lower volumes and less at higher volumes, leading to alveolar stability and reducing the likelihood of alveolar collapse.

Surfactant has the following functions:

Prevents alveolar collapse during respiration
Supports lung expansion during inspiration
Prevents pulmonary oedema by balancing hydrostatic force
Stabilizes and maintains small airways structure
Improves mucociliary function, and
It also has an immunomodulatory role.

The layer of surfactant may vary in thickness but a monomolecular layer occurs.

38
Q

What can spirometer measure

how is anatomic dead space measure

how is rv
frc
measured

A

A spirometer is a device used for measuring lung volumes either directly or indirectly using dilution techniques, for example, helium. It can also be used to calculate flow rates and the basal metabolic rate.

Spirometry provides timed measurements of expired volumes from the lung and is the foundation of pulmonary function testing. Wet and dry spirometers exist and with automated equipment it is possible to interpret more than 15 different measurements from spirometry alone.

Forced vital capacity (FVC)
Forced expiratory volume in one second (FEV1)
FEV1/FVC ratio, and
The flow between 25% and 75% of the FVC
are the most clinically helpful indices obtained from spirometry.

The anatomical dead space is measured by Fowler’s method (single breath nitrogen washout)
Residual volume and total lung capacity can be measured using the body plethysmograph or helium dilution
The functional residual capacity can be measured by nitrogen washout or the helium dilution technique.
It should be noted that the helium dilution technique is performed by the patient breathing air with a known concentration of helium, starting from the end of normal expiration from a spirometer.

The question asks which can be measured directly, thus the only correct option is vital capacity.

39
Q

What volumes make up frc
how much is it

how can it be measured

what are the effect of peep and cpap on frc

how is it reduced

how is it related to total pulomary compliance

what is the effect during exercise

A

The functional residual capacity (FRC) is the sum of the expiratory reserve volume (ERV) and the residual volume (RV), and in a healthy male it is 2-3 litres.

Measurement of the FRC can be achieved using the body plethysmograph, nitrogen washout and helium dilution techniques.

Positive end-expiratory pressure (PEEP) and continuous positive airway pressure (CPAP) increases the FRC by raising the intra-alveolar pressure above the ambient pressure.

FRC is reduced in the supine position, pregnancy and in obesity, as the abdominal contents displace the diaphragm into the thorax.

The FRC and the total pulmonary compliance (TPC) are related in that if the FRC rises or falls, then the change in TPC is dictated by the shape of the compliance curve.

The FRC increases during exercise due to the fall in airway resistance and the sustained tone in the inspiratory muscles.

40
Q

Diaphragm

innerv - motor and sesns

how much of tv does it control

A

all motor innerv c3-c5
pass ant to scal ant

periph part = sens from lower thoracic nerves

75% tv

openings

41
Q

Airway physiology

how does gas move beyond term bonch

how does nasal breathing affect resistance

A

Beyond terminal bronchioles - gas movement is dependent upon diffusion not bulk flow
large airways - movement second to bulk flow

Nasal breathing increases resistance 50% compared to mouth breathing

42
Q

Airway resistance

how calc

where is a/way resistance most

turb flow what

o2 cost norma breathin

A

Pressure diff between alveoli + mouth divide by flow rate

most a/way resisnace =- occurs at terminal bronchi - <20% resistance beyond airway <2mm

turbulent flow = flow proportional sq root pressure

He - decrease density
turb flow - decreasy density
laminar - decrease viscosity

5-10~%
increase 30% during exertion

43
Q

Measure of airway resistance

A

body plethymosgraph

44
Q

Herring breuer reflex

A

increase in expiratory time - large inspiratory vol

det pulmonary stretch

45
Q

J receptors stm cause

A

juxtacapillary found alveolar wall

respod cap enrogrg and interstit oedema - shallow rapid breathing

via non myelinated vagal

46
Q

is hypoxaemia detected in brain

A

no - resp centred depressed without peripheral

47
Q

Old people
affect lung mech

poor response to execise

A
decreased tlc fvc vc fev1
rv increase - 
frc unchanged 
inc CV = red alveol surf area
alveolar wall thcik v/q mm
reducton gas exchange

downreg of beta receptors

impair baro fxn + perip vcon - postural hypo
more marked in htn ting diuretic

less complaint chest wall w/ decreased chostochonral mobilty seen
tissue lacks elasticity + changes sim to emphesema

48
Q

TLCO

?hb affect

combo what

meausre with what fio2

phtn
asthma

A

Hb conc affect TLCO
1g reduction 4% reduction

Combo Aveolar volume x efficiency spec gas tfter
va x kco

.18

decrease kco - normal Va (also pe)

eleavated in asthma
marked elvated hamerhage - elecated hb bind co

49
Q

Airway resistance

A

Driving pressure/ gas flow rate

Driving pressure = Diff alveolar + mouth pressure
- measured body pleth

gas flow - measure pneuto

measured cmH2O or Kpa/ L/ s

High flow rates - turbuelent increased

Increase durin inhalation
drop frc/lung vol/ tubes/ connex

PEEP - reduces resitnace - inverse relastionship vol /+ resistance