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POEM > Breathing Part 1 > Flashcards

Breathing Part 1 Flashcards

1
Q

What is FiO2?

A

FiO2 = fraction of inspired oxygen
This describes the fraction of oxygen being inspired and can be explained by thinking about the composition of room air
Room air = 21% O2
Therefore when we breathe, FiO2 of O2 = 0.21

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2
Q

What is a hudson face mask?

A

A clear plastic face mask that sits over the nose and mouth. Delivers a variable FiO2 of oxygen depending on the rate of flow/patient’s respiratory pattern.

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3
Q

What is the maximum flow rate of oxygen through a hudson face mask? What FiO2 of O2 can this achieve?

A

15 L/min.

Up to 0.6/60% FiO2.

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4
Q

What are the disadvantages of a hudson face mask?

A
  • Can be claustrophobic for patients
  • Patient compliance can be low
  • Variable performance oxygen device (unsure of FiO2 patient receiving - anywhere between 0.35-0.60)
  • Cannot eat/drink
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5
Q

What are the advantages of nasal cannulae?

A
  • Claustrophobic patients more compliant
  • Can eat/drink
  • More comfortable for long-term oxygen therapy
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6
Q

How do nasal cannulae work?

A

Utilise the dead space of the nasopharynx as an oxygen reservoir. This means that when a patient inspires, the entrained air will mix with the reservoir of oxygen and and the inspired air is therefore enriched

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7
Q

What FiO2 is achieved with nasal cannulae?

A

Between 0.24-0.36 (O2 flow rate dependent)

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8
Q

What O2 flow rates are used with nasal cannulae?

A

2-4 L/min (high flow rates result in turbulence in tubing without increase in FiO2/uncomfortable for patient and cause nosebleeds)

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9
Q

Which oxygen therapy device should always be used in a deteriorating/critically ill patient?

A

Reservoir/non-rebreather/trauma mask.
ALWAYS reach for a non-rebreather mask in these cirumstance - 15 L/min high flow 100% O2
Can titrate down depending on patient’s condition

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10
Q

What flow rates can be achieved by non-rebreather masks?

A

10-15 L/min

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11
Q

What FiO2 can be achieved by non-rebreather masks?

A

FiO2 = 0.6-0.85

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12
Q

How does a nebuliser mask work?

A

Simply: convert liquids to aerosols

Complicated: utilise the Venturi effect - the pressure drop and increased velocity of gas flow through a narrowing is utilised to entrain the nebuliser fluid into the jet stream causing it to be sheared and split into droplets. The baffle, which is placed within the jet stream further decreases the size of the droplets and returns bigger droplets back to the reservoir of fluid to be aersolised.

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13
Q

What are nebuliser masks commonly used for?

A

Commonly used in a hospital setting for inhaled bronchodilators

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14
Q

What is the optimal flow rate for nebuliser masks?

A

4-6 L/min

Any lower and the droplets will not aerosolise.

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15
Q

What is a self-inflating/bag-valve mask/ambu bag?

A

This is a device used for the ventilation of patients who are not breathing/are critically ill
Consists of an oxygen reservoir, one-way valve and a mask
System can deliver ambient air but is most often attached to a supplemental oxygen supply

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16
Q

What is the flow-rate of O2 through an ambu bag?

A

12-15 L/min

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17
Q

What FiO2 may be achieved through an ambu bag?

A

FiO2 - 0.8 (depending on quality of seal of mask/depth of ventilations)

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18
Q

What is the main disadvantage of ambu bag use?

A

Overzealous bagging can result in gastric distension - increasing intra-abdominal pressure and thereby increasing risk of aspiration. Additionally this will go on to increase intrathoracic pressure and making ventilation more difficult. Aim for 10 ventilations a minute when bagging with an ambu bag.

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19
Q

What is the difference between variable and fixed performance O2 delivery devices?

A

Variable performance oxygen devices vary in their delivery of known FiO2 whereas fixed performance devices reliably deliver known FiO2.

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20
Q

Define variable performance oxygen delivery devices.

A

Low flow systems referring to the fact that they cannot meet the patients inspiratory flow demands (normal flow 25-30L/min) and therefore additional flow is provided by surrounding room air
• The room air Fi02 alongside the Oxygen enriched gas and dilutes the mixture
• The true FiO2 depends on the patients’ respiratory demand; governed by their respiratory rate, the inspiratory flow rate and also the length of expiratory pause, i.e. a patient in respiratory distress, their respiratory demand will far exceed that of normal healthy individuals

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21
Q

Give examples of variable performance oxygen delivery devices.

A

Examples: nasal cannulae, the Hudson mask, non-rebreather facemask, and ambu bag.

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22
Q

Define fixed performance oxygen delivery devices?

A

Oxygen delivery devices which deliver predictable and reliable FiO2

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23
Q

Give examples of fixed performance oxygen delivery devices (2)

A

Venturi masks and anaesthetic breathing circuits

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24
Q

What are the characteristics of a venturi mask?

A
  • Increasing flow will not increase FiO2
  • The size of entrainment port determines the FiO2
  • The larger the entrainment port, the more room air entrained, and the lower the FiO2
25
Q

What FiO2 ranges are possible with venturi masks?

A

0.24, 0.28, 0.31, 0.4, 0.6 (the coloured apertures will tell you what O2 flow rate to set to achieve this FiO2)

26
Q

Explain the haemoglobin-oxygen dissociation curve (right and left shift).

A

Rightward shift (inc. temp/2,3-DPG/[H+]: Hb has decreased affinity for O2. Makes it more difficult for Hb to bind O2. Requires higher PO2 to achieve same O2 saturation and makes it easier for Hb to release O2. The effect of a rightward shift is to increase PO2 in tissues where it is most needed e.g. in exercise/haemorrhagic shock.

Leftward shift (dec. temp/2,3-DPG/[H+]: Hb has increased affinity for O2. Hb binds O2 more easily. Unloaded O2 more reluctantly. Physiological example is at the lungs.

27
Q

Explain the Bohr effect.

A

We blow off CO2 when we breathe, shifting blood pH toward the alkaline side of the equation. Hb therefore has a greater affinity for O2 in these conditions for when air is inhaled. Then at the tissue level, where CO2 is produced via metabolism, the CO2 diffuses into the blood, shifting the pH to the acidic side of the equation weakening the affinity of Hb for O2, leading to its release into tissues.

28
Q

What is respiratory failure?

A

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic or hypercapnic.

29
Q

What is type 1 respiratory failure?

A

PO2 < 8 kPa
with a normal or low PaO2
This is the most common form of respiratory failure, and it can be associated with virtually all acute diseases of the lung, which generally involve fluid filling or collapse of alveolar units.
E.g. of type I respiratory failure are cardiogenic or non-cardiogenic pulmonary edema, pneumonia, and pulmonary hemorrhage.

30
Q

What is type 2 respiratory failure?

A

PaCO2 > 6.5 kPa
and PaO2 < 8 kPa
Hypoxemia is common in patients with hypercapnic respiratory failure who are breathing room air. The pH depends on the level of bicarbonate, which, in turn, is dependent on the duration of hypercapnia. Common aetiologies include drug overdose, neuromuscular disease, chest wall abnormalities, and severe airway disorders (eg, asthma and COPD).

31
Q

Explain relative hypoxia.

A

PaO2 should be -10 in relation to the FiO2. E.g. if you are supplying 60% O2 - PaO2 should be 50 kPa. If in the case of a deteriorating patient be CAREFUL if you have what appears to be a normal PaO2 (11-13 kPa) if they are receiving high flow O2.

32
Q

What is Allen’s test (in relation to ABGs)?

A

A test for ulnar insufficiency. Instruct patient to clench their wrist and then occlude both arteries (radial and ulnar). Allow the patient to unclench their wrist. Release the ulnar artery, if colour returns to the hand within 10 seconds this indicates adequate circulation.

33
Q

What is restrictive respiratory disease?

A

A decrease in the volume of air the lungs are able to hold, often due to a decrease in the elasticity of the lungs, or due to a problem of chest wall movements during inhalation. Both FEV1 and FVC are reduced, however, the decline in FVC is greater than in FEV1 and therefore results in a normal or higher than normal FEV1/FVC ratio. (Full exhalation achieved in 2-3 seconds).

34
Q

What is obstructive respiratory disease?

A

Disease where patients have difficulties exhaling the air in their lungs. Often due to damage to the lung or narrowing of the airways. FEV1 is reduced while FVC remains within normal limits. Leads to a reduced FEV1/FVC ratio. (Exhalation prolonged - normal volume, exhaled more slowly).

35
Q

Give examples of restrictive respiratory disease.

A
  • Interstitial lung disease e.g. idiopathic pulmonary fibrosis
  • Sarcoidosis
  • Obesity
  • Neuromuscular disease e.g. ALS
36
Q

Give examples of obstructive respiratory disease.

A
  • Asthma
  • Bronchiectasis
  • COPD (emphysema + bronchitis)
  • Cystic fibrosis
37
Q

Explain minute volume.

A

Volume of gas inhaled or exhaled in 1 minute i.e. minute volume (Vm) = respiratory rate x tidal volume

38
Q

Explain ventilation perfusion (V/Q) ratio.

A

A measurement used to assess the efficiency and adequacy of the matching of two variables:

  • V - ventilation - the volume of air that reaches the alveoli
  • Q - perfusion - the volume of blood that reaches the alveoli

1 L of blood = 200 mL O2. In these conditions the ideal VQ ratio would be about 0.95. True values depend on the location in the lung. Apex ratio is higher than base ratio, with an average of 0.8.

39
Q

Why does the V/Q ratio lower at the base of the lungs?

A

This is because BOTH ventilation and perfusion increase towards the bases of both lungs BUT Q does so more strongly thus lowering the V/Q ratio.

40
Q

How much O2 is dissolved in 1 L of blood?

A

200 mL

41
Q

What is dead space?

A

An area with ventilation but no perfusion. V/Q therefore undefined (infinity). May be anatomical or pathological.

42
Q

Distinguish between anatomical and pathological dead space.

A

Anatomical: air spaces with no gas exchange e.g. mouth, nose, trachea, mainstem bronchi, secondary and tertiary bronchi.
Pathological: pulmonary embolism/shock.

43
Q

What is a shunt?

A

An area with perfusion but no ventilation (V/Q of 0). Most often happens when alveoli fill with fluid - meaning there is no ventilation but still perfusion.

44
Q

Explain continuous positive airway pressure (CPAP).

A

CPAP is a form of positive airway pressure ventilator, which applies mild air pressure on a continuous basis to keep the airways continuously open in a
person who is able to breathe spontaneously on their own. It stents the lungs’ alveoli open and thus recruit more of the lung’s surface area for ventilation. It is used in those with sleep aponea (mild pressure from CPAP prevents the airway from collapsing or becoming blocked) and pre=term infants (those within sufficient
surfactant)

45
Q

Explain invasive positive pressure ventilation (IPPV).

A

IPPV is a method of mechanical ventilation. Positive-
pressure ventilators work by increasing the patient’s airway pressure through an endotracheal or
tracheostomy tube. The positive pressure allows air to flow into the airway until the ventilator breath is
terminated. Then, the airway pressure drops to zero, and the elastic recoil of the chest wall and lungs
push the tidal volume — the breath-out through passive exhalation. Positive end-expiratory pressure
(PEEP) can be used to prevent conditions that can lead to shunting (e.g. atelectasis, alveolar collection of
material other than gas such as from pneumonia or ARDS).

46
Q

Explain the risks of invasive positive pressure ventilation (IPPV).

A

Barotrauma including pneumothorax, subcutaneous emphysema, pneumomediastinum, and
pneumoperitoneum
Ventilator-associated lung injury clinically indistinguishable from acute lung injury or acute
respiratory distress syndrome
Diaphragmatic atrophy can develop within the first day of mechanical ventilation
Impaired motility of mucocilia in the airway leading to retention of secretions and pneumonia

47
Q

Distinguish between oxygenation and ventilation.

A

Oxygenation is the amount of oxygen in the blood, as measured by SaO2 (although there may be up
to 5 min lag in pre-oxygenated patients before changes are seen in pulse oximetry) reflects PaO2.
• Ventilation is the rate at which we ventilate, as measured by capnography (EtCO2 measures exhaled
CO2 and reflects changes in ventilation within 10 seconds) and reflects blood PaCO2

48
Q

Review D for details in interpreting a chest X-ray.

A 
Patient name, age / DOB, sex, HSC number
•  Type of film – PA or AP, erect 
or supine, correct L/R marker, 
inspiratory/expiratory series 
•  Date and time of study
49
Q

Review R for RIPE in interpreting a chest X-ray.

A

Rotation – medial clavicle ends equidistant from
spinous process
• Inspiration – 5-6 anterior ribs
in MCL or 8-10 posterior ribs
above diaphragm, poor inspiration?, hyperexpanded?
• Picture – straight vs oblique, entire lung fields, scapulae outside lung fields, angulation (i.e. ’tilt’ in vertical plane)
• Exposure (Penetration) – IV disc spaces, spinous processes to ~T4, L) hemidiaphragm visible through cardiac shadow.

50
Q

Review A for airway in interpreting a chest X-ray.

A

Trachea – central or slightly to right lung as crosses aortic arch
• Paratracheal/mediastinal masses or adenopathy
• Carina (division of trachea) & RMB/LMB
• Mediastinal width <8cm on PA film (wider may indicate aortic dissection)
• Aortic knob
• Hilum – T6-7 IV disc level, left hilum is usually higher (2cm) and squarer than the V-
shaped right hilum, lymphadenopathy?
Check vessels/calcification

51
Q

Review B for breathing in interpreting a chest X-ray.

A

Lung fields
• Vascularity – to ~2cm of pleural surface (~3cm in
apices), vessels in bases > apices
• Pneumothorax – don’t forget apices
• Lung field outlines – abnormal opacity/lucency,
atelectasis, collapse, consolidation, bullae
• Horizontal fissure on Right Lung
• Pulmonary infiltrates – interstitial (linear, reticular,
nodular, reticulonodular) vs alveolar pattern
(fluffly, cotton wool)
• Coin lesions (cancer, TB, abscess)
• Cavitary lesions
• Pleura: reflections or thickening

52
Q

Review C for circulation in interpreting a chest X-ray.

A
  • Heart position –⅔ to left, ⅓ to right
  • Heart size – measure cardiothoracic ratio on PA film (normal <0.5)
  • Heart borders – R) border is R) atrium, L) border is L) ventricle & atrium
  • Heart shape
  • Aortic stripe
53
Q

Review D for diaphragm in interpreting a chest X-ray.

A

• Hemidiaphragm levels – Right Lung higher than Left Lung (~2.5cm / 1 intercostal
space)
• Diaphragm shape/contour (may be flat in asthma or COPD)
• Cardiophrenic and costophrenic angles – clear and sharp
• Gastric bubble / colonic air
• Subdiaphragmatic air (pneumoperitoneum)

54
Q

Review E for extras and everything else in interpreting a chest X-ray.

A

ETT, CVP line, NG tube, PA catheters, ECG electrodes, PICC line, chest tube, PPM, AIDC,
metalwork?
• Ribs, sternum, spine, clavicles – symmetry, fractures, dislocations, lytic lesions, density
• Soft tissues – looking for symmetry, swelling, loss of tissue planes, subcutaneous air,
masses
• Breast shadows
• Calcification – great vessels, carotids

55
Q

List the 5 step approach to interpreting ABGs.

A
  1. Is the patient hypoxic? (>10kPa on RA)
  2. Is the pH <7.35 or >7.45?
  3. What is the respiratory component? (PaCO2 – normal: 4.5-6.0kPa)
  4. What is the metabolic component? (HCO3 – 22-26mmol/L, Base excess -2 to 2)
  5. Interpret data
56
Q

What is the anion gap and how is it interpreted?

A

Difference in the measured cations and anions in serum, plasma or urine; often calculated to
identify the cause of an acidosis
• If the gap is greater than normal a high anion gap acidosis is diagnosed
• Potassium can be ignored as it has little impact on the result
• Normally there are more cations (positively charged ions) than anions resulting in a positive integer
for the gap
• Given that plasma is electro-neutral, we can say that the anion gap valve represents the
unmeasured ions
([Na+] + [K+]) – ([Cl-] + [HCO3-]) = 3-11mEq/L

57
Q

What are the causes of a high anion gap metabolic acidosis?

A 
o  Ketones 
o  Uraemia  
o  Lactate  
o  Toxins (Methanol, ethylene glycol, lactic acid, aspirin, ureamia 
phenformin, iron, isoniazid, cyanide)  
o  Renal failure
58
Q

What are the causes of a normal anion gap metabolic acidosis/hyperchloraemic acidosis?

A

Normal anion gap metabolic acidosis is also known as hyperchlorarmic acidosis as Cl- is the only
other major anion that can compensate for the loss of HCO3; caused by (usually diarrhoea or renal
tubular acidosis) FUSED CARS:
o Pancreatic Fistula (loss of bicarbonate rich pancreatic fluid)
o Uretero-enterostomy (Large amounts of Cl- are exchanged for HCO3 in stool, so HCO3 is lost)
o Saline administration (NaCl provides a chloride load)
o Endocrine (Hyperparathyroidism)
o Diarrhoea (Loss of HCO3)
o Carbonic anhydrase inhibitors (Diuretic by reduces NaCl and HCO3 reabsorption in the
proximal tubule but distal segment partially compensates for the sodium loss but not HCO3)
o Ammonium chloride
o Renal tubular acidosis (failure of HCO3− resorption)
o Spirolactone

59
Q

What are the causes of a reduced anion gap metabolic acidosis? (Very rare).

A 
Loss of albumin  
•  Nephrotic syndrome  
•  Haemorrhage 
•  Liver cirrhosis 
•  Intestinal obstruction  
•  Multiple Myeloma (albumin level decreases as disease progresses)

POEM (11 decks)

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