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RESPIRATORY > RESPIRATORY FAILURE AND ABG > Flashcards

RESPIRATORY FAILURE AND ABG Flashcards

1
Q

What is V/Q?

A

Ventilation-to-perfusion ratio - the ratio of alveolar ventilation to avoleolar perfusion
In the average adult… alveoli are ventilated by 4L of air and perfused by 5L of blood each minute = V/Q ratio of 0.8

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2
Q

How does V/Q ratio very within different parts of the lung?

A

whilst standing, perfusion is better to the bases due to gravitational and hydrostatic forces
Ventilation is also higher at the bases but to a far lesser degree

V/Q ratio is around 3.3 at apices and 0.6 at bases

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3
Q

What does a low V/Q mean? What is this caused by?

A

Alveoli have poor ventilation compared with perfusion = hypoxaemia
Airway disease or interstitial lung disease (i.e. ventilation is reduced)

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4
Q

What happens in response to low V/Q?

A

Areas with low V/Q have hypoxia-induced pulmonary vasoconstriction and blood is diverted to better ventilated areas of the lung

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5
Q

What does high V/Q mean?

A

Albvolar units have poor perfusion compared to ventilation e.g. in a PE

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6
Q

What happens in response to high V/Q?

A

Blood is diverted to other areas and low V/Q regions are created to compensate.

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7
Q

Why is perfusion lower at the apices of the lungs?

A

As its higher than the heart and gravity takes the blood down to bases of the lungs
Therefore we have wasted ventilation here

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8
Q

Why are lung alveoli larger at the apex compared to the bases?

A

More negative intrapleiural pressure so alveoli are larger
At the bases the weight of fluid in the pleural cavity increases the intrapleural pressure so alveoli are less expanded - large increase in volume on inspiration for increased ventilation

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9
Q

Which zone of the lungs is alveolar pressure highest?

A

Zone 1 (apex)

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10
Q

Which zone of the lung has the highest pulmonary arterial pressure?

A

Zone 3 (bases)

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11
Q

What is type 1 respiratory failure?

A

Hypoxaemia and normal or low CO2

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12
Q

What causes T1RF?

A

Most commonly caused by V/Q mismatch (volume of air passing in/out of lungs is comparatively smaller than volume of blood perf using lungs)

E.g. things that cause low V/Q pneumonia, COPD< asthma, pulmonary oedema, obesity, pneumothorax
E.g. things that cause high V/Q e.g. PE

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13
Q

What are signs of chronic hypoxaemia in T1RF?

A

Polycythemia and development of cor pulmonale

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14
Q

what is T2RF?

A

Hypoxaemia and hypercapnia
Aka hypercapnic respiratory failure

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15
Q

How do we identify an acute T2RF?

A

Acute insult with a new respiratory acidosis and no evidence of chronic compensation (i.e. normal bicarbonate)

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16
Q

What can cause acute T2RF?

A

Alveolar hypoventilation (i.e. lungs fail to effectively oxygenate and blow off CO2)
Exacerbations of COPD, severe asthma, CF or bronchiectasis, IPF, rib fractures or neuromuscular diseases
Respiratory depression e.g. opiate overdosr

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17
Q

How do we identify chronic T2RF?

A

Evidenc eof compensatory mechanisms on ABGs - increase in bicarbonate

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18
Q

What can cause chronic T2RF?

A

COPD
Asthma
Chronic neurological disorders (e.g. motor neuron disease)
Chronic neuromuscular disorders (e.g. myopathies)
Chest wall diseases
Obesity hypoventilation syndrome

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19
Q

Outline the pathophysiology of type 1 respiratory failure?

A

Damage to lung tissue -> prevents adequate oxygenation of blood (hypoxaemia) -> but rest of normal lung is sufficient to excrete CO2

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20
Q

Outline the pathophysiology of type 2 respiratory failure?

A

Inadequate ventilation of whole lung -> Alveolar ventilation is insufficient to excrete the carbon dioxide being produced -> hypercapnia

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21
Q

Outline the cause of oxygen-induced hypercapnia in COPD?

A

Increased V/Q mismatch - increased oxygen administration impairs hypoxia pulmonary vasoconstriction and results in physiological dead specs ena increased V/Q mismatch
Haldane effect - The presence of oxygen causes Hb to have a reduced affinity for CO2 which results CO2 being displaced from Hb
Decreased minute ventilation

This is why COPD patients have target sats 88-92%

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22
Q

Outline the steps of reading an ABG>

A
  1. How is the patient?
  2. Look at PaO2
  3. Is patient acidaemic or alkalaemic?
  4. Check PaCO2
  5. Check bicarbonate
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23
Q

Once you identify an acidosis or alkalosis from an ABG, how do you determine if its respiratory or metabolic?

A

Acidosis with raised PaCO2 - resp acidosis
Alkalosis with low PaCO2 - resp alkalosis
Acidosis with low HCO3- - metabolic acidosis
Alkalosis with raised HCO3- - metabolic alkalosis

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24
Q

What causes the acidosis?

A

CO2 is broken down into H2CO3

25
Q

Why does raised bicarbonate indicate a pt chronically retaining CO2?

A

Bicarbonate is a buffer to neutralise the acid and maintain a normal pH. It takes a while for kidneys to produce bicarbonate
Kidneys respond to chronic retaining acidic CO2 by producing additional bicarbonate e.g. in COPD

In an acute exacerbation of COPD, the kidneys cannot keep up with the rising level of CO2, so the patient becomes acidotic despite having higher bicarbonate than someone without COPD.

26
Q

What can cause respiratory acidosis?

A

decompensation in respiratory conditions e.g. COPD, life-threatening asthma / pulmonary oedema
neuromuscular disease
Obstructive sleep apnoea
sedative drugs: benzodiazepines, opiate overdose

27
Q

What can cause respiratory alkalosis?

A

anxiety leading to hyperventilation
pulmonary embolism
salicylate poisoning*
CNS disorders: stroke, subarachnoid haemorrhage, encephalitis
altitude
pregnancy

28
Q

What can cause metabolic acidosis?

A

Raised lactate – lactate is released during anaerobic respiration (indicating tissue hypoxia)
Raised ketones – typically in diabetic ketoacidosis
Increased hydrogen ions – due to renal failure, type 1 renal tubular acidosis or rhabdomyolysis
Reduced bicarbonate – due to diarrhoea, renal failure or type 2 renal tubular acidosis

29
Q

What can cause metabolic alkalosis?

A

Loss of H+ e,g. Vomiting, increased activity of aldosterone (conns, liver cirrhosis, HF, loop diuretics, thiazide diuretics)

30
Q

Whats the moa of metabolic alkalosis?

A

Loss of H+ or gain of HCO3-

31
Q

How does kidney disease cause metabolic alkalosis?

A

Activation of RAAS -> aldosterone causes reabsorption of Na+ in exchange for H+ in distal convoluted tubule

32
Q

How does vomiting and diuretic use cause metabolic alkalosis?

A

Na+ and Cl- loss -> activation of RAAS -> raised aldosterone levels -> reabsorption of Na+ in exchange for H+ in the distal convoluted tubule

33
Q

How does hypokalaemia cause metabolic alkalosis?

A

K+ shifts out from cells and H+ shifts into cells to maintain neutrality

34
Q

Whats the normal anion gap?

A

10-18mmol/L

35
Q

How do you calculate anion gap?

A

(Na+ + K+) - (Cl- + HCO-3)

36
Q

How is metabolic acidosis classified?

A

Normal anion gap
Raised anion gap

37
Q

What can cause metabolic acidosis with a normal anion gap?

A

gastrointestinal HCO3- loss e.g. prolonged diarrhoea
renal tubular acidosis

Others : less common!
drugs: e.g. acetazolamide
ammonium chloride injection
Addison’s disease

38
Q

What can cause metabolic acidosis with a raised anion gap?

A

lactate: shock, sepsis, hypoxia
ketones:.DKA, alcohol
urate: AKI or CKD
Toxic ingestions: salicylates, methanol. Ethylene glycol

39
Q

What ABG findings will you get in metabolic acidosis?

A

Ph<7.35
HCO3- <22
PCO2 may be raised due to the respiratory centre being stimulated as a compensatory measurement

40
Q

How do you check if a respiratory compensation is appropriate for a metabolic acidosis?

A

Using winters formula - compare pCO2 from ABG to calculate value

41
Q

What is Winter’s formula?

A

PCO2 = (1.5 x HCO3- +8) +/- 2

This gives you a range and if your measured pCO2 is within this ranges then its an appropriate respiratory compensation. If its below the range then there’s an associated respiratory alkalosis and if its above the range then there is an associated respiratory acidosis

42
Q

How do you calculate serum anions gap? Whats the normal range?

A

Cations - anions
Na+ - (Cl- + HCO3-)

7-13mEq/L

43
Q

Why is the normal anion gap not 0?

A

Because there are some unmeasured cations and anions
e.g. albumin - when albumin, which is negatively charged, is lost then HCO3- and Cl- are retained so levels increase causing a decrease in the calculated serum anion gap

44
Q

What is hyperchloraemic metabolic acidosis?

A

Normal anion gap acidosis

45
Q

What should you do if you have a high anion gap metabolic acidosis?

A

Delta delta ratio

46
Q

How do you do the delta delta ratio?

A

Delta anion gap/delta HCO3-

Delta anion gap is the calculated anion gap - 12mEq/L
Delta HCO3- is 24mEq/L - measured serum HCO3-

47
Q

What does the delta delta ratio tell you?

A

If its <1 then there is a coexisting Normal anion gap acidosis alongside the high anion gap metabolic acidosis
E.g. severe diarrhoea

If its 1 then there’s a high anion gap acidosis

If its >1 then there is either a coexisting metabolic alkalosis or a chronic respiratory acisosis

48
Q

Why does severe diarrhoea cause a high anion gap metabolic acidosis with coexisting normal anion gap acidosis?

A

Because the loss of HCO3- in the diarrhoea = normal anion gap acisosis
Hypovolaemia = haemoconcentration = increased albumin = high anion gap acidosis

49
Q

How do you differentiate between normal anion gap metabolic acidosis caused by renal causes from other causes?

A

Measure urine anion gap

50
Q

How do you calculate urine anion gap?

A

(Urine Na+ + urine K+) - urine Cl-

51
Q

Whats the most prominent cation unmeasured in the urine?

A

NH4+ (ammonium)

52
Q

How do you interpret urine anion gap results?

A

If >0 then it suggests urinary ammonium is low so the cause is likely renal
If <0 then it suggests urinary NH4+ is high so cause is likely diarrhoea

53
Q

What can cause ketoacidosis?

A

DKA
Alcoholic ketoacidosis

Rare: fasting

54
Q

What can cause lactic acidosis?

A
55
Q

What can cause lactic acisosi?

A

Tissue hypoperfusion e.g. sepsis, shock, HF
Biguanides therapy
Malignancy
Alcoholism
HIV infection

56
Q

Why does Cushing’s cause hypokalaemia?

A

Excess cortisol which has mineralocorticoid activity = increases activity of renal tubular Na+/K+ pump = K+ excreted into urine

57
Q

Why does Cushings cause metabolic alkalosis?

A

Cortisol has mineralocorticoid activity i.e. it can act like aldosterone
= increases reabsorption of Na+ and excretion of K+ = hypokalaemia
K+ plays a crucial role in maintaining acid base balance so when its low it impairs the ability of kidneys to secrete H+ and reabsorb HCO3-

58
Q

What VBG findings would you get after salicylate overdose? Why

A

Respiratory alkalosis followed by metabolic acidosis

This is because salicylates initially stimulates the CNS respiratory centre = tachypnoea = fall in PaCO2 = resp alkalosis
Lactic and ketoacidosis build up, as well as metabolites of aspirin which are weak acids = anion gap metabolic acisosi

RESPIRATORY (22 decks)

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