Week 2 Respiratory Failure Flashcards

1
Q

Define the Two types of respiratory failure

A
  1. Type 1- Hypoxaemic:
    • Respiratory failure whereby the lungs fail to obtain sufficient oxygen to meet metabolic demands of the body.
    • Severe hypoxaemia- PaO2 under 8kPa
  2. Type 2- Hypercapnic:
    • Respiratory failure whereby the lungs fail to obtain enough oxygen to meet metabolic demands of the body and to excrete sufficient carbon dioxide.
    • Hypoxaemia accompanied by hypercapnia
    • Hypercapnia- PaCO2 above 6.7 kPa.
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2
Q

Explain the Oxygen cascade

A
  • Oxygen cascade describes the declining oxygen tension from the atmosphere down to the mitochondria.
  • Starting in the atmosphere where the partial pressure of oxygen is 21kPa, the fraction of inspired oxygen is 0.21.
  • Drop in oxygen tension with the humidification of air as air enters the tracheobronchial tree.
  • Drop again to end tidal gas. End tidal gas is the gas left in the mouth after exhalation and contains both alveolar gas and dead space gas (which does not take part in gas exchange)- therefore oxygen tension of end tidal gas slightly above that of alveolar gas.
  • Drop in oxygen tension to alveolar gas as gas exchange is occuring here- addition of CO2, O2 removal.
  • Slight drop in O2 tension from alveolar gas to arterial blood. This can be explained by normal physiological V/Q mismatch or shunting (normally shunting minimal, perfuse only well ventilated alveoli) and diffusion.
  • Drop in oxygen tension as arterial blood supplies tissue undergoing active metabolism. Oxygen diffuses out of arterial blood and into cell cytoplasm- mitochondria down its concentration gradient.
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3
Q

What is the alveolar gas equation used for?

What is the equation?

What can be calculated once a value for this equation has been calculated?

A
  • Alveolar gas equation is used to calculate the partial pressure of oxygen in the alveoli= PAO2
  • PAO2= Fraction of inspired oxygen (FiO2)- PaCO2/R
  • Where PaCO2= partial pressure of CO2 in arterial blood
  • R= Respiratory quotient- a constant, is a ratio that expressed the amount of Oxygen needed to produce a certain amount of CO2.
  • Once a value for PACO2 is found, it can be used to determine the alveolar- arterial Oxygen difference. This can be used to determine a patients level of hypoxaemia.
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4
Q

What is the alveolar- arterial oxygen difference?

What is its clinical relevance?

How is it calculated?

What are normal values and how do they change with age?

A
  • The alveolar arterial oxygen difference is the difference in the partial pressure of oxygen in the alveoli compared to the arterial blood. It is clinically relevant as it can show a patients severity of hypoxaemia and source of hypoxaemia.
  • E.g. increased alveolar arterial gradient could suggest diffusion abnormality, R-L shunting, ventilation/perfusion mismatch
  • Hypoventilation would present with hypoxia but A-a gradient normal.
  • Calculated by 1) using the alveolar gas equation to calculate PAO2 (alveolar oxygen) 2) take arterial blood gases to get PaO2 3) PAO2- PaO2 (Alveolar- arterial).
  • Normal value for healthy 18 year old- 1.1 kPa
  • Normal value for healthy 8- year old- 3.1 kPa- larger difference due to lung damage with age and loss of muscle function.
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5
Q

What law governs the alveolar pressure?

A
  • Dalton’s Law: states the the total pressure of a mixture of gases is equal to the sum of all the partial pressures of those gases.
  • Alveolar pressure= PAO2 + PACO2 + PAH2O+ PAN2 (oxgyen/carbondioxide/watervapour/nitrogen)
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6
Q

What is the arterial partial pressure of oxygen influenced by?

What can affect it?

What is the saturation of haemoglobin dependent on?

A
  • PaO2 is influenced by PAO2 (partial pressure oxygen in alveolus).
  • PaO2 can be affected by:
    • Diffusion capacity/ barrier - ability to get oxygen across to blood
    • Perfusion - decreased perfusion lowers PaO2
    • Ventilation/ perfusion mismatch - perfused blood reaching well ventilated areas, affects gas exchange
  • The saturation of haemoglobin is dependent on the PaO2.
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7
Q

What is ventilation perfusion matching?

A
  • Normally average ventilation rate is 5/L/min (V).
  • Ventilation- air that reaches the alveoli.
  • Average perfusion rate is 5/L/min (Q)
  • Perfusion- blood reaching alveoli via capillaries
  • Ventilation perfusion matching describes the ideal ratio of 1, where ventilation with oxygen perfectly matches perfusion of alveoli with venous blood carrying CO2.
  • In this case all O2 is inhaled, saturates haemoglobin and is carried to the metabolising tissues, and all CO2 from metabolising tissues is removed at the lung.
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8
Q

Describe the spectrum of ventilation perfusion ratio

A
  • Ideal value of 1 where ventilation and perfusion match
  • Dead space:
    • V/Q = ∞
    • ventilated areas without any perfusion
    • Essentially dead space, alveolar oxygen matches the fraction of inspired air, no CO2
  • Shunting:
    • V/Q= 0
      • Pathophysiological condition where alveoli are well perfused but not ventilated
      • Partial pressure of oxygen in alveoli matches that of venous blood, blood remains poorly oxygenated.
      • Desaturation of haemoglobin in blood leaving lungs
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9
Q

Describe the shape of the oxygen saturation curve and explain its shape

A
  • The oxygen saturation curve is sigmoid in shape, the saturation of oxyhaemoglobin increases with increasing partial pressure of oxygen in arterial blood.
  • This is due to the positivie cooperativity of oxygen binding with haemoglobin
  • At first it is difficult to bind the first oxygen molecule as haemoglobin is in its tensed state
  • After the binding of the next oxygen molecule, oxyhaemoglobin is in its relaxed form, increased affinity for binding next oxygen molecule.
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10
Q

What is the oxygen saturation of oxyhaeoglobin in the pulmonary veins/ arterial blood?

What is the O2 sat of blood in the venous blood/ pulmonary artery?

A
  1. arterial/ pulmonary vein- 99%
  2. venous/ pulmonary artery- 75%
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11
Q

At a constant metabolic rate what is the paCO2 reliant on?

A
  • At a constant metabolic rate the paCO2 is dependent on alveolar ventilation.
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12
Q

What is the equation for alveolar ventilation rate?

What two types of dead space are there?

A

Alveolar ventilation rate= Resp Rate (RR) x (Tidal volume- Dead space)

  1. Anatomical dead space provided by non respiratory conducting airways- trachea and non respiratory bronchioles
  2. Physiological dead space- formed by diseases alveoli and ventilation/ perfusion mismatch
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13
Q

What can cause hypoxaemia?

A
  1. Low inspired O2 concentration/High altitude- low barometric pressure leading to lower partial pressure of oxygen in inspired air (dalton’s law- total pressure decreased therefore partial pressure of oxygen also decreased despite it still making up 21% of atmospheric air).
  2. Hypoventilation- e.g. respiratory depression due to opiate use/ brainstem injury/ COPD
  3. Ventilation/ perfusion mismatch:
    • Shunting: perfusion of poorly ventilated alveoli, V/Q ratio of below 1
    • Diffusion barrier abnormality/pathology- fibrosis/scarring/inflammation of alveolar walls e.g. pneumonia and pulmonary oedema
  4. Low cardiac output:
    • ​Less O2 delivery per unit time
    • Tissue have to extract higher percentage of oxygen to meet demands
    • Blood returning to the heart is more desaturated than normal
    • Lower CO means blood moves through pulmonary circulation slower, has more time to reach full saturation.
  5. Anaemia
  6. R to L shunt
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14
Q

Define hypoventilation

A

State where decreased air enters the alveolus resulting in decreased partial pressure of oxygen and increase partial pressure of carbon dioxide in the blood.

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15
Q

List some common causes of hypoventilation

A
  • Central hypoventilation: Brainstem and spinal cord
    • secondary to underlying neurological disease
    • Drugs that depress CNS
    • Stroke
    • Trauma
    • Neoplasms
  • COPD: Bronchitis and emphysema
    • Airway narrowing and destruction
    • Loss of elastic tissue and recoil- hyperinflation leading to hypoventilation
  • NMJ disorders and muscular atrophy/inflammation of respiratory muscles
  • Pleural disease- scarring/fibrosis restricting inflation
  • Chest wall deformities
  • Obesity hypoventilation syndrome
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16
Q

Define pathological shunting in the lungs

In general, what is a shunt?

A

Pulmonary shunt is a pathological condition that results when the alveoli are perfused with blood as normal but ventilation fails to supply the perfused region leading to a V/Q ratio of 0.

Generally, a shunt is a condition whereby blood from the right side of the heart enters the left side without taking part in any gas exchange.

17
Q

Explain the overall effect of shunting in the lungs.

Why does oxygen therapy not help in the treatment of hypoxia when shunting is present?

A
  • When a pathological shunt is present, this leads to certain alveoli being supplied with blood in the absence of ventilation. The venous blood arriving at the alveolus can deliver CO2 but will not pick up any oxygen.
  • Blood leaving the pulmonary capillary surrounding that alveolus will have an oxygen saturation the same as that of venous blood- 75%.
  • In normal alveoli with a normal ventilation/perfusion ratio, blood leaving the pulmonary capillary bed will have an oxygen saturation of 100%.
  • The blood carried by these capillary beds eventually joins together in pulmonary veins and carried towards the LA of the heart.
  • The overall saturation of blood with oxygen will be a combined value of the well perfused/ventilated alveoli and the pathologically shunted alveoli- overall O2 sat% of 87.5.
  • Oxygen therapy will not help in this situation as the ventilated alveoli will already be at 100% saturated with oxygen and the non-ventilated alveoli will still not be able to allow air movement.
18
Q

What is the physiological mechanism by which alveoli in the lung may improve the overall ventilation (V) : perfusion (Q) ratio?

Name the mechanism

Explain how this may occur.

When clinically might this mechanism be important?

A
  • The name of the mechanism is hypoxaemic pulmonary vasoconstriction and it refers to a reflex mechanism in which blood flow in the lungs can be redirected to well ventilated alveoli.
  • Local reflex contraction of vascular smooth muscle in pulmonary capillaries in response to hypoxia (detects Partial pressure of oxygen in pulmonary arteriole and alveolus) to restrict blood flow to poorly ventilated alveoli
  • Increase in resistance to blood flow, directing blood flow to alveoli with dilated pulmonary capillaries and lower pulmonary vascular resistance
  • Helps match alveolar ventilation and perfusion
  • Proportion of shunted blood is reduced in abnormally ventilated areas
  • Hypoxaemic pulmonary vasoconstriction is significant in chronic respiratory disease such as COPD. Maintaining normal gas exchange is dependent on optimizing V/Q matching and involves this mechanism. However increased pulmonary vascular resistance can lead to pulmonary hypertension, right ventricular hypertrophy and cor pulmonale.
  • HPV also has a role in acute respiratory diseases e.g. acute asthma and pneumonia, pulmonary embolism. -HPV redirects blood to better ventilated regions improves V/Q matching.
19
Q

Pathphysiology of hypoxaemia:

1) Low inspired O2 and altitude

2) Hypoventilation

3) Ventilation perfusion mismatch:

  • Shunting: Can be either no ventilation and V/Q ratio= 0 (O2 therapy does not improve) or low ventilation and high perfusion V/Q ratio low- some improvement with O2 therapy.
  • Qu: What two types of shunting exist in the body?
  • What can be the cause of shunting in these areas of the body?
A
  • Shunting can be intrapulmonary or intracardiac
  • Intrapulmonary shunting causes:
    • ​pneumonia
    • pulmonary oedema
    • alveolar collapse/ atelectasis (partial collapse or incomplete inflation of the lung)
    • Pulmonary haemorrhage or lung contusion (bruising)
  • ​Intracardiac shunt can be cause by congenital heart disease e.g. patent foramen ovale or ductus arteriosus/ atrial septal defect/ ventricular septal defect allows R - L shunt of blood.
20
Q

Causes of hypoxaemia include:

1) Low inspired O2 and altitude
2) Hypoventilation
3) Ventilation perfusion mismatch:

  • Shunting
  • Diffusion abnormality: ​
    • ​​What is a diffusion abnormality?

A
  • Diffusion abnormality refers to deficiency in oxygen pulmonary gas exchange that yeilds abnormally low partial pressures of oxygen.
  • Diffusion of oxygen from alveolar space into pulmonary capillaries is normally perfusion limited.
  • In defective diffusion the rate of oxygen diffusion from alveolar space to blood is slowed such that full saturation of haemoglobin does not occur.
  • Oxygen diffusion becomes diffusion limited with diffusion abnormalities.
21
Q

Causes of hypoxaemia include:

1) Low inspired O2 and altitude
2) Hypoventilation
3) Ventilation perfusion mismatch:

  • Shunting
  • Diffusion abnormality: ​
    • What causes a diffusion abnormality physiologically?
    • what clinical conditions are indicated with diffusion abnormality?
    • What is the hallmark feature of diffusion abnormality?
A
  • Caused either by abnormality in the alveolar/ capillary membrane or reduced number of pulmonary capillaries surrounding the alveolus.
  • Results in reduced surface area for gas exchange.
  • Clincial conditions associated are:
    • Acute respiratory distress syndrome- life threatening syndrome characterised by fluid infiltration into lung alveoli without obvious cause (eg heart failure) leading to severe hypoxaemia.
    • Alveolitis - inflammation of alveoli
  • Hallmark feature: Desaturation of haemoglobin on exercise:
    • Under normal circumstances haemoG is fully saturated 25% of the way through the pulm. capillaries
    • With a diffusion abnormality, time for full saturation is longer, requires whole length of capillary bed
    • In severe cases full saturation may not occur as blood leaves the capillary bed
    • During exercise there is an increased CO and blood moves faster through pulm. circulation, leaving less time to saturate haemoglobin.
    • Under normal conditions there is no problem, there is reserve to be able to fully saturate blood through the capillary
    • With diffusion abnormality there is no reserve, meaning blood is not fully saturated with exercise.
22
Q

Causes of hypoxaemia include:

1) Low inspired O2 and altitude
2) Hypoventilation
3) Ventilation perfusion mismatch:

  • Shunting
  • Diffusion abnormality

4) Low cardiac output - how can this lead to hypoxaemia?

A
  • Low CO means there is less delivery of oxygen to tissues per unit time
  • Tissue extract a higher percentage of oxygen from the blood as required for their metabolism
  • Blood returning to the heart is less saturated with oxygen
  • However low cardiac output means there is more time for blood to fully saturate in the pulmonary circulation.
23
Q

What are the clinical features of respiratory failure?

A
  • Abnormal arterial blood gas result: Hypoxia (below 8 kPa) and in type 2 hypercapnia (above 6.7kPa).
  • Respiratory compensation- activation of peripheral chemoreceptors that respond to hypoxia. If type 2 resp. failure activation of peripheral and central chemoreceptors (responding to hypercapnia). Increase respiratory rate.
  • Hypercapnia related signs:
    • ​CO2 retention flap/ tremor
    • Confusion and coma
    • Respiratory acidosis
    • SNS stimulation
  • Sympathetic stimulation:
    • ​Increased HR
    • Sweating
    • Increased BP
  • Haemoglobin desaturation and evidence of tissue hypoxia:
    • Cyanosis
    • Low pulse oximetry result (below 92 is very worrying).
    • Lactic acidosis from anaerobic metabolism
    • Altered mental status/ coma
24
Q

What are the respiratory compensatory mechanisms in respiratory failure?

A
  • Increased respiration rate (Tachypnoea)
  • Use of accessory muscles
  • Nasal flaring
  • Intercostal recession in children
25
Q

Why is a reading of PaO2 under 8kpa worrying in relation to the oxygen saturation curve?

A
  • PaO2 under 8 kPa relates to around 90 % saturation on the O2 curve.
  • This is worrying as anything under this value and haemoglobin starts to desaturate quickly (becomes its tensed form).
26
Q

What are common sources of error in pulse oximetry?

A
  • Poor peripheral perfusion
  • Poorly positioned probe
  • Nail varnish/ false nails
  • Excessive motion
  • Bright ambient light
  • Carboxyhaemoglobin or methaemoglobin
  • Lipaemia
  • Oxygen saturation below 85% inaccurate
27
Q

What are signs of severe respiratory failure?

A
  • RR above 30
  • Deterioration despite therapy
  • Pulse oximetry value below 90 (SpO2 < 90)
  • Cyanosis
  • Difficulty completing sentences/ confusion and coma
  • Remember normal SpO2 value does not mean there arent severe ventilatory issues present e.g. hypercapnia.