Resp Physiology Flashcards

1
Q

Surfactant

A

Phosopholipid-rich detergant

Produced by type II alveolar cells

Coats luminal surface of alveoli

reduces surface tension which is apposing expansion

Water molecules are attracted more to each other than they are to gas molecules.
When any liquid surrounds a gas, i.e. in the alveolus, this produces an inward pressure.

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2
Q

Functions of surfactant

A

Lowers surface tension
–> increases compliance of lungs
–> reduces work of breathing

Prevents fluid accumulating in the alveoli

Reduces the tendency of alveoli to collapse (alveolar instability).

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3
Q

Conditions that decrease lung compliance

A

Fibrosis

Pulmonary oedema

Deficiency of surfactant e.g. premature babies

Decreased lung expansion e.g. respiratory muscle paralysis

Supine position

Breathing 100 O2

Mechanical ventilation due to reduced pulmonary blood flow

Age

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4
Q

Conditions that increase compliance

A

COPD - due to destruction of elastic parenchyma
Emphysema

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5
Q

Components of work of breathing

A

Two major compenents:
Work required to over-come elastic recoil of lungs

Non-elastic forces:
-Air resistance (most significant)
-Frictional forces
-Inertia of air and tissues

One-third of airway resistance occurs in the upper
airways – nose, pharynx and larynx. This can be
greatly reduced by breathing through the mouth

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6
Q

Ventilation of upper vs lower zones

A

Lower zones better ventilated because:

-the weight of the lungs
-the compliance curve is sigmoid, and the upper
and lower parts of the lung lie on different parts
of this curve.

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7
Q

Definition of tidal volume

A

Volume of air inspired and expired during quiet breathing

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8
Q

Definition of functional residual capacity

A

Functional residual capacity is the volume of air in the the lungs at the end of passive expiration

FRC = Residual volume + expiratory reserve volume

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

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9
Q

Measuring functional residual capacity

A

As it consists partly of residual volume, it cannot be measured by spirometry

Nitrogen wash-out test, helium dilution or body plethysmography

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10
Q

Definition of vital capacity

A

Volume of air that is expelled from maximal inspiration to maximal expiration

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11
Q

Fowler’s method

A

Measures anatomical deadspace using single breath of 100% O2 and a nitrogen analyser

As subject starts to expire, the nitrogen content of
alveolar air is measured.

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12
Q

Increasing anatomical deadspace

A

Increasing size of person

Standing position

Increased lung volume

Bronchodilatation

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13
Q

Increasing physiological deadspace

A

Hypotension

Hypoventilation

Emphysema

PE

Positive pressure ventilation

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14
Q

Nitrogen expiration curve

A

Phase 1
-Pure O2 = dead space

Phase 2
-Mixture of dead space and alveolar gas
-Increasing nitrogen / volume
-Mid-point here represents calcuation of anatomical deadspace

Phase 3
-Plateu of nitrogen as pure alveolar has is expired

Phase 4
-Abrupt increase in nitrogen concentration as airways at the base of the lung close
-Expired air at this point is from the apex, which has received less O2, and thus the nitrogen is less dilute.

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15
Q

Factors affecting the closing capacity

A

Closing capacity is volume at which airways begin to close
–> phase 4 of single breath nitrogen test

Factors:
Age: increases with age

Posture: in a supine position in a 40-year-old
subject, the closing capacity is equal to the FRC

Anaesthesia: decrease in lung volumes results in closing capacity exceeding FRC, even in the youngest patients.

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16
Q

Diffusion capacity

A

Measured by inhaling carbon monoxide and measuring it in the blood

Diffusion capcity is decreased by:
Pulmonary oedema
Emphysema

17
Q

Hypoxic pulmonary vasoconstriction (HPV)

A

In order to match perfusion to ventilation areas of the lung that are poorly ventilated recieve less blood which is mediated by the HPV

Hypoxia –> vasoconstiction
Hypercapnoea —> Vasoconstriction

NOTE this is the opposite to the normal physiological response in other tissues which is vasodilatation

18
Q

3 zones of blood supply

A

Zone 1: Apex
Alveolar pressure is greater than that of the pulmonary artery and hence poor blood flow

Zone 3: Base
Pulmonary artery pressure greatly exceeds the alveolarpressure and thus vessels are fully open.
Blood flow is very good.

The variations in regional blood flow are abolished
on lying down.

19
Q

V/Q of 3 zones

A

At the apex V/Q = 3, thus indicating that the alveoli
are ventilated better than they are perfused

Ay the base V/Q = 0.6, thus indicating that the alveoli are perfused better than they are ventilated

Ideal V/Q = 1 and is found approximately two-thirds of the way up the chest

20
Q

Pathophysiological effects of pulmonary oedema

A

Reduces diffusion capacity

Decreased lung compliance due to the reduction
in surface tension and alveolar shrinkage

Increased airway resistance: this can occur due
to the reduction in lung volume and fluid filling
the airways.

Resistance is also due to reflex bronchoconstriction

Alveolar oedema leads to a ventilation–perfusion
mismatch as alveoli filled with fluid are still perfused
but not ventilated.

Pulmonary vascular resistance increases due to
hypoxic vasoconstriction and external compression
from interstitial oedema.

21
Q

Lymphangitis carcinomatosa

A

Pulmonary oedema due to obstruction of lymphatics in lung from cancer

22
Q

Causes of pulmonary oedema

A

Neurogenic: head injuries due to increased sympathetic output

Obstruction to lymphatics: lymphangitis carcinomatosa

Increased capillary permeability: ARDS, endotoxic shock, irritant gases

High altitude: likely to be due to hypoxic vasoconstriction leading to elevated pulmonary artery pressure

Raised pulmonary hydrostatic pressure, the
commonest cause, occurs with left ventricular
failure – left atrial pressure rises and this is
transmitted into the pulmonary circulation,
resulting in increased pulmonary capillary
pressure, and thus capillary hydrostatic pressure

23
Q

Criteria for diagnosing ARDS

A

Known cause

Refractory hypoxia

New fluffy changes on CXR

Not cardiac: Pulmonary artery wedge pressure <18mmHg

24
Q

Right-shift of haemoglobin

A

A shift of the curve to the right will result in:
-Decreased oxygen affinity
-Release of oxygen from Hb at higher PaO2

Factors causing right-shift
-Increased Temperature
-Increased 2,3 DPG
-Increased H, i.e. lower pH / acidosis

These are the factors present in metabolically active tissues so it causes off-loading of O2

Right shift –> Rid of O2

25
Q

Mocules with far left-curve

A

Fetal haemoglobin is left-shifted
Allows for it to take up PaO2 from maternal circulation and not release it until it reachesthe tissues

Myoglobin
-Acts as oxygen store in muscles and released in profound anaerobic conditions

26
Q

Haldane effect

A

As PO2 falls

Haemoglobin uptake of CO2 increases

Hence in hypoxic tissues red cells off-load O2 and uptake more PCO2

27
Q

Medulla control of respiration

A

Inspiratory neurons
-Ryhthmic firing

Expiratory nuerons
-Inactive during normal respiration

28
Q

Pons control of respiration

A

Pons modulates the medulla inspiratory neurons

Two centres

Apneustic centre:
-Lower pons
-Prolong inspiratory phase
-Shorten expiratory phase

Pneumotaxic centre
-Upper pons
-Inhibits inspiratory neurons and shortens inspiration

29
Q

Chemoreceptors for respiration

A

Modulate the output from medulla

Central and Peripheral

Central
-Sensitive to changes in PCO2
-Situated in medulla close to respiration centre
-CO2 diffuses from the blood into the brain and reacts with water to produce H+ and causes the pH to fall, thus directly stimulating the chemoreceptors
–> increase in ventilation

Peripheral
-Carotid bodies close to bifurcation of the common carotid
-AND in aortic bodies that lie in aortic arch
-Respond to changes in arterial pH and to low
levels of PO2;

30
Q

Hering-Breuer reflex

A

Inhibits ventilation due to excessive stretch of the lungs

Stretch receptors pass signal via the vagus nerve

31
Q

J receptors

A

Lie adjacent to capillaries in alveoli

Stimulaton in response to low O2 causes increased ventilation

32
Q

Vasomotor centre and respiration

A

vasomotor centre: low blood pressure detected
by baroreceptors results in an increase in the ventillation