Respiratory Pathophysiology 1 and 2 (Kolbe) Flashcards Preview

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Flashcards in Respiratory Pathophysiology 1 and 2 (Kolbe) Deck (37):
1

What is respiratory failure?

When the lungs fail to adequately oxygenate the arterial blood and/or fail to prevent undue CO2 retention

 

Practical terms:

  • When PaO2 < 8kPa (60mmHg) - hypoxic type I
  • When PaCo2 > 6.6kPa (50mmHg) - hypercapnic type II

 

2

What is the partial pressure of oxygen?

partial pressure of oxygen in arterial blood (PaO2) the portion of total blood gaspressure exerted by oxygen.

3

Define hypercapnia

Alveolar hypoventilation (not minute ventillation)

V(dot)/ Q(dot) mismatch

 

A condition of abnormally elevated carbon dioxide (CO2) levels in the blood. 

4

Describe the relationship between partial pressure of carbon dioxide and alveolar ventilation

Inverse relationship

 

 

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5

Is minute ventillation same as alveolar ventillation?

No.

VE = V(Alveolar) + V(Dead space)

 

In  pathology, it is possible to have increased minute ventillation but decreased alveolar ventillation because of increased deadspace

6

______ in association with ______ may cause hypercapnia

Hypoventilation in association with metabolic alkalosis may cause hypercapnia

7

What are the 5 causes of hypoxaemmia?

  1. Reduced PiO2 (inspired O2) – occurs at altitude
  2. Hypoventilation
  3. V/Q Mismatch
  4. R-L Shunt
  5. Diffusion

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8

Why the is the PO2 of arterial blood greater than in the tissues

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9

HWat is the difference between Partial pressure of oxygen, oxygen content and oxygen saturation?

  • Partial Pressure of Oxygen (Pa02) = pressure that is exerted by oxygen when you have a mixture of gases  
  • Oxygen content (CaO2) = Amount of O2 bound to Hb + amount of O2 dissolved in blood (mL/dL)
  • Oxygen saturation = Fraction of oxygen saturated Hb relative to total Hb (saturated & unsaturated)

10

What are the 3 causes of hypoventilation?

Hypoventilation in association with metabolic alkalosis may cause hypercapnia

 

1) Decreased respiratory drive

2) Neuromuscular competence

  • Decreased drive
  • Decreased neuromuscular transmission
  • Muscle weakness/fatigue (reversible)
    • Electrolytic disturbances
    • Malnutrition
    • Abnormal length tension relationship

3) Abnormal load

  • Increased resistive load
  • Increased lung elastic load
    • Chest wall elastic load
    • Minute ventillation load

11

Mr Smith is now 75

At age of 20 years, he contracted poliomyelitis and spent many months in an "iron lung".He subsequently developed markey kypho-scolosis.

 

He has put on 25 kg.He now presents iwth worsening shortness of breath, reduced exrcise tolerance and morning headache.

His ABG shows PaCO2 = 7.5kPa (NA 4.5-6.0)

 

Why is he hypercapnic?

1) Respiratory drive

2) Neuromuscular transmission

3) Load

 

Hypercapnic because of

1- impairment of Neuromscular transmimssion

  • (less anterior horn cells - polio) and

2- increased load/work (kypho-scolosis and 25kg)

  • reduced chest wall compliance b/c of distortion of kypho-scoliosis& obesbity)

3- reduced drive

  • (may be associated with obesity or congenital?)

 

 

12

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Hypoventilation.

 

Respiratory drive reduced due to generalised cerebral depression secondary to drug narcotics e.g. heroin

13

  • If the lungs were perfect ______ = _____
  • This measures the adequacy of gas exchange
  • In clinical practise _____ is measured, _____is estimated

  • If the lungs were perfect PAO2 = PaO2
  • This measures the adequacy of gas exchange
  • In clinical practise – PaO2 is measured, PAO2 is estimated

14

How do you calculate the PAO2?

  • Things that influence PAO2 (alveolar partial pressure)
    • Patm - Atmospheric pressure
    • Fi02 - Fraction of inspired O2
    • PH2O - Water vapour pressure
    • PACO2 - Alveolar CO2
    • RQ?Pb = Patm

 

  • PACO2 = can measure with PaCO2 (good at diffusion)

  • R = Respiratory quotient/exchange ratio = 0.8

  • k=?

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15

What are the 2 consequences of working in a mine?

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1) Pulmonary fibrosis

2) Malignant mesothelioma 

16

Why is he Short of Breath and Hypoxaemic?

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Interstitial lung disease.

  • X-ray 
    • shadowing around periphery of lungs, worse on R
  • CT
    • characteristic fibrosis, distortion of lungs, scarring.

 

Fibrous tissue laid down in alveolar walls, can progress to distort and damage lungs.

  • Interstitial lung disease ( affects loose CT, not airway, air space or blood vessel).
  • Collagen thickened in airway wall (space between alveoli and capiillary) & around small BVs.
    • ​Alveolar- capillary block

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17

Why does the hypoxemia worsenw hen he walks across the room?

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O2 stat 92% at rest, fall to 86% walking across room.

 

  • Muscles use more O2
  • Transit time of RBC in the capillaries is reduced
    • Collagen / fibrous tissue is laid down around small airways but also laid down in space between alveolus and capillary = alveolar-capillary block.
    • ** With exercise, cardiac output increases to allow for increased oxygen intake and delivery to tissue.
    • With increased CO, the transit time of RBC in the pulmonary capillary goes down.
      • ​The small reduction in transit time will not affect healthy individuals, however in a diseased individual (thickening of alveolar wall) it excerbates this issue. 
    • So even if hypoxemia is OK and rest, it is unmasked on exercise.
    • Thickened wall + Less time = Worsening of hypoxemia
  • Diffusion is impaired.

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18

Decribe DLCO

Diffusing capacity of CO

 

Lung Function Lab – DLCO

Use of CO

  • Diffusion (and not perfusion limited)
  • Soluble
  • Avidly binds to Hb, therefore zero back pressure

Diffusion Depends on

  • gas
  • diffusion distance/thickness
  • surface area
  • (Hb)
  • Capillary volume

19

What are 3 processes that give you Abnormal Diffusion?

  1. Alveolar capillary block  -
    • Interstitial/diffuse lung disease
  2. Loss of diffusing surface area (alveolar surface area) –
    • Emphysema
      • primarily causes shortness of breath due to over-inflation of the alveoli (air sacs in the lung).
  3. Capillary volume/Haemoglobin
    • Group of diseases that affect pulmonary vasculature (pulmonary hypertension, anemia, pulmonary embolism)

 

Diffusion Depends on

  • gas
  • diffusion distance/thickness
  • surface area
  • (Hb)
  • Capillary volume

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20

What is the normal A-a gradient

A – a Gradient

= 20 – PaCO2/0.8 – PaO2

= 1-2kPa

 

. Young healthy person A-a grad <1 kPa. Gets wider, more V/Q mismatch as get older.

21

How do you make the distinction between pure hypoventillation (or hyperventillation) and intrinsic lung disease?

A-a gradient

 

. Young healthy person A-a grad <1 kPa. Gets wider, more V/Q mismatch as get older.

 

A – a Gradient = 20 – PaCO2/0.8 – PaO2 = 1-2kPa

22

What are 3 other features of this "classical" pattern of abnormality?

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1) Restricted lung volumes

2) Hypocapnic/resp alkalosis

3) Pattern of resp/work of breathing. 

23

Define COPD

  • Definition:
    • A disease state characterised by airflow limitation that is not fully reversible (differs from asthma which is reversible).
    • The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases

 

  • Cause: Cigarette smoking is the primary cause of COPD in “developed” countries

24

What are 3 symptoms/consequences of COPD?

  1. Chronic mucus hyper- secretion
  2. Emphysema (destruction of alveolar walls with major agent being proteases from neutrophils)
  3. Small airway inflammation (and obstruction)

25

Describe the pattern of pulmonary decline over time of cigarette smoking

  • Fall in FEV1 over time
  • All on the decline after 25years
  • Some are more susceptible to cigarette smoking than others
  • Some are relatively more resistant
  • If you stop smoking, although you don't get an increase in LF, your rate goes back to the same as a non smoker

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26

Describe the why a person with COPD may show compensatory hyperventillation

 

What are the consequences of this compensatory hyperventillation?

In a normal patient, you have mostly compartment 2 (V/Q=1). As you smoke, you get more of compartment 1 and 3, but compartment 1 is just dead space and does not contribute to the arterial blood gases. We are only interested in compartments with V/Q between 1 and 0.

 

Compartment 2 (I): Normal content of O2 and CO2. Compartment 3 (II): mixed venous blood you have decreased content of O2 and increased content of CO2. If you mix them together you get an increased content CO2 and decreased O2.

 

Hypercapnic vs Hypoxic drive

  • In response to hypercapnia (high CO2), the patient will increase ventilation rate and alveolar ventilation (deeper and faster).

The respiratory centre is also very sensitive to H+ ions in the CSF as a result from the acidosis from hypercapnia.

  • Patients will only respond to a low O2 (hypoxemia) when you are significantly hypoxic (<80% saturation).

 

  • Hyperventilation will normalise CO2.
  • Oxygen content will not be normalized because you can only effectively hyperventilate the "normal" compartment 2 but still you cannot get more oxygen through the abnormal compartment 3.

27

When someone undergoes compensatory hyperventillation, ___ content becomes normalised but ____ remains reduced.

 

Explain why this occurs.

CO2 content becomes normalised, but O2 remains reduced.

 

O2: In the normal compartment you are already on the flat part of the oxygen dissociation curve. Hyperventilation will increase PA02 but that will lead to little/no change in oxygen

 

CO2: Hyperventilation reduces PACO2 and content of CO2 significantly (different shape of the curve

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28

Describe the difference between Hypercapnic vs Hypoxic drive

Hypercapnic drive

  • In response to hypercapnia (high CO2), the patient will increase ventilation rate and alveolar ventilation (deeper and faster).
  • The respiratory centre is also very sensitive to H+ ions in the CSF as a result from the acidosis from hypercapnia. Patients will only respond to a low O2 (hypoxemia) when you are significantly hypoxic (<80% saturation).
  • Hyperventilation will normalise CO2. Oxygen content will not be normalized because you can only effectively hyperventilate the "normal" compartment 2 but still you cannot get more oxygen through the abnormal compartment 3.

 

  • PaO2 is reduced, PaCO2 is normal, normal pH but this is through hyperventilation and metabolic compensation. 
  • H2O + CO2  à ß H+ + HCO3-
  • Patient continues to smoke and her V/Q gets worse. She becomes hypercapnic and hypoxic. She hyperventilates to reduce CO2 but her O2 remains low. She continues to do this until she can no longer maintain this level of hyperventilation.
  • She will then let her CO2 climb and reset chemoreceptors to a higher level of CO2. BUT body does not like acidosis so H+ is excreted by the kidneys.
  • Chronic hypercapnia seen in a raised blood bicarbonate (compensated chronic respiratory acidosis)

 

Hypoxic drive

  • Now you have an elevated CO2 so respiratory centre is no longer particularly responsive to CO2.
  • Now dependent on hypoxic drive to keep her ventilated
  • If you give her supplementary oxygen you turn off her drive and stop ventilation

29

What will the arterial blood gases show?

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pH: low

PaCo2: high

PaO2: high (patient must be on gas)

HCO3: High

 

CHRONIC RESPIRATORY ACIDOSIS WITH RENAL COMPENSATION - BUT NORMOXIA?

NORMOXIA -Patient must be on gas!

  • A-a gradient of someone breathing room air and sea level = 20 - PaCO2/0.8 - PaO2
  • A-a gradient has to be greater than zero (otherwise oxygen moving from blood to alveolus) Therefore, PaCO2/0.8 - PaO2 < 20.
  • If it is greater than 20 then they are not acting at sea level. Patient value is over 20 so you can see that she is breathing oxygen.

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30

PaCo2/0.8 - PaO2 is above 20.

 

What does this indicate?

NORMOXIA -Patient must be on gas!

A-a gradient of someone breathing room air and sea level = 20 - PaCO2/0.8 - PaO2

A-a gradient has to be greater than zero (otherwise oxygen moving from blood to alveolus) Therefore, PaCO2/0.8 - PaO2 < 20.

If it is greater than 20 then they are not acting at sea level. Patient value is over 20 so you can see that she is breathing oxygen.

31

What are the dangers of administering high amounts of O2?

 

What are the dangers of increased PaCo2 (although pH is normalised by renal and other mechanisms?)????

Danger of administered high (as opposed to low) inspired O2 (hypoxic drive abolished, depression of ventilation increase in PaCO2 and development of acidosis (respiratory and metabolic - hypoxic lactic acidosis) with depressant effects.

  • Even if O2 is discontinued, may get profoundly hypoxic and take time to unload large accumulation of CO2 in tissues due to large body stores of this gas.
  • Role of worsened V/Q mismatch.

 

Danger of monitoring only O2 saturation

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32

33

Describe the 2 types of shunts

Shunt in the lung bypass alveoli due to either

  1. Arterio-venous malformations (abnormal BVs in the lung that does not go near the alveoli) or
  2.  Shunt at cardiac level (from right side of heart to left side). R--> L shunt in some congenital heart disease  (note that VSD still would have L--> R shunt)

34

What does the "high colour" suggest?

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Blue = cyanosed

Red = red complexion due to erythropoietin (hypoxemia causes a lot of epo production from kidney) ->  excessive Hb/RBC à polycythaemia

35

What does the pan systolic murmur suggest?

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Cardiac lesion

36

How do you differentiate between shunts and VS mismatch?

  • Administer 100% oxygen (>700mmHg) and measure PaO2
  • In V/Q mismatch, the PaO2 rises to >600mmHg with 100% O2 despite the mismatch due to
    • Absorption atelectasis
    • Relaxation of hypoxic vasoconstriction
  • A shunt will not reach >600mmHg. You must measure the blood gas not just 02 saturation
    • Shunt will show 100% saturation still but it is a low PaO2. Saturation does not tell you about PaO2, PaCO2 or the pH.

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37

____kPa = ___mmHg

1kPa = 7.5mmHg