assessment of acid-based balance part 3 W3

Question 1

case: male, 24, acute asthma, treated with O2 and nebulised salbutamol. feels worse. good air entry and no wheeze.
low H+
low pCO2
slightly high pO2
normal bicarbonate

Answer 1

not hypoxic
alkalaemic
respiratory alkalosis - primary disorder
no metabolic change - no compensation from body (acute so no time for response from kidneys)

Question 2

resp alkalosis - acute causes (acute more common)

Answer 2

-asthma, COPD exacerbation, PE
-pain, panic attack
-iatrogenic (overventilation)
-altitude sickness (raised RR)
-inappropriate stimulation of resp centre in brainstem (head injury, raised ICP, local tumour)

Question 3

resp alkalosis - chronic causes (rarer)

Answer 3

pregnancy (but physiological) - mild resp alkalosis which is fully compensated by very minor metabolic acidosis (renal)

Question 4

clinical affects of resp alkalosis?

Answer 4

acute hypocapnia causing:
-cerebral vasoconstriction (light-headedness, confusion, syncope, fits)
-fall in ionised calcium - perioral, peripheral paraesthesia

cardiovascular:
-increased heart rate, vasoconstriction (possibly chest tightness/angina in those with coronary artery disease)

Question 5

case: after acute asthma attack, patient is tired and resumes O2. O/E less wheeze and quiet. blood gas: pO2 just below reference range, everything else normal

Answer 5

O2 should be higher given he is being given O2
concerning there is no longer significant respiratory effort to get rid of CO2
requires HDU/ITU urgently, on verge of decompensation

Question 6

case 4: female, 36, 2 days of vomiting, semi-conscious
acute pancreatitis on background of EtOH cirrhosis
O/E: ascites, splenomegaly
BP: 96/54 S, 74/44 E
low H+
high pCO2
very high HCO3
hypokalaemia

Answer 6

alkalaemic
respiratory acidosis (raised CO2) (compensation)
metabolic acidosis (raised HCO3) (primary disorder)

not vice versa as nothing to suggest resp disease. underlying cause is vomiting - hydrogen ion rich gastric fluid is being lost, therefore metabolic

Question 7

why does case 4 have hypokalaemia? how does this worsen the patients alkalaemia?

Answer 7

vomiting
hyperaldosteronism secondary to cirrhosis leads to urinary loss
shift of K+ from plasma/ECF into cells due to alkalaemia
(K+ deficiency will lead to further renal H+ loss, worsening alkalaemia. in absence of K+, Na+ may be exchanged by kidney for excretion of H+.)

Question 8

metabolic alkalosis: causes - loss of hydrogen ions?

Answer 8

vomiting
renal:
-hypokalaemia resulting in H+ excreted for Na+ reabsorption. can be caused by loop and thiazide diuretics. also primary hyperaldosteronism

Question 9

metabolic alkalosis causes - gain of bicarbonate?

Answer 9

iatrogenic - sodium bicarbonate infusion

Question 10

clinical effects of metabolic alkalosis?

Answer 10

not usually significant - may cause shift of K+ into cells
beware effect of IV sodium bicarb in CKD. acute fall in acidity may reduce solubility of calcium salts and increase risk of systemic calcification

Question 11

how to consider each ABG result in turn?

Answer 11

pO2? - resp problem or prob delivering to tissues?
pH/H+? - normal/acidaemia/alkalaemia
how did this happen - pCO2/HCO3- which is driving H+ change:
pCO2 disturbance = respiratory
HCO3- disturbance = metabolic
use clinical context to find out primary disorder
figure out compensation - does it make sense? (eg only renal compensation if chronic, eg alkalosis compensation is limited)

Question 12

what to think about if nothing makes sense in ABG?

Answer 12

error in sampling/transport/measurement? repeat ABG?
several pathologies?

Question 13

categories of acid-base disorder causes?

Answer 13

abnormal acid production
resp/renal pathologies
fluid loss