acid base disorders

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Acid Base Disorders


Acid Base Controversy

Traditional approach Peter Stewart (‘80s) Bronsted & Lowry

definitions of acids & bases

[H+] related to PaCO2/ HCO3.

‘acids as ions that shift equilibrium of water to higher or lower [H+]’

Mathematical equations (6)

Strong ions (SID) Plasma weak acids

(buffers) phosphate / albumin (Atot)

PaCO2

Follow this approach –Does not utilise albumin levels but can be taken into accountNot sure really helps management.


DefinitionsBase : proton or H+ acceptor.

Acid : proton or H+ donator.

H-H equation relates arterial pH to PaCO2 and bicarbonate.pH = 6.1 + log [HCO3]/0.23(paCO2)

pH = -log [H+].

[H+] – 45nmol/L to 35nmol/L ( pH 7.35-7.45).Nanomol (1 x106 in 1mmol)


Acid Base Haemostasis Mean Body pH 7.4 range 7.35-7.45 ICF pH 7.0-7.2 exceptions urine 4.5-5.0, gastric

Metabolism – food makes ‘acid’.15000mmols CO2 – lungs

60mmol/day [H+] Buffered & metabolized


Regulation of pHExcretion of H+ & reabsorption of bicarbonate*. Bicarbonate filtration & reabsorption Ammonium secretion / Deamination glutamine – NH3

excrete H H+ loss with phosphate Na absorbed for H+ excretion.

Excretion of CO2 *.

Buffer H+ - inorganic phosphates, proteins, Hb & bone.


Basic Definitions Acidaemia /alkalemia – pH lower or higher than

normal.

Acidosis/alkalosis – process if unopposed will lead to a change in pH.

Compensation may mean pH ~ normal.

Aim identify primary disturbance of AB disorder.


Compensatory Mechanisms

Metabolic acidosis – respiratory compensation 1.2mmHg fall pCO2 for every 1mmol/L drop in HCO3.

hours Metabolic alkalosis – respiratory compensation raise

0.7mmHg for every 1mmol/L rise in HCO3. less likely to be seen due to hypoxia.

Respiratory acidosis – acute 1mmol/L rise per 10mmHg rise in pCO2. goes upto 3.5mmol/L in Chronic respiratory acidosis. Days

Respiratory alkalosis : acute 2mmol/L drop HCO3 for every 10mmHg . Chronic 4mmol/L.

pH depend [HCO3] : [CO2] 20:1


Consequences of Acid/Base Disturbance


Effects of Body of DisturbanceACIDOSIS

CVSReduced inotropyConduction defectsArterial vasodilationVenous constrictionDO2Reduces HbO2 bindingReduces 2,3,DPG (late)NMJResp depressionRed awarenessMetabolismProtein wastingBone demineraliztionCatecholamine releaseInsulin resistanceFree radicals

GIEmesisImmune dysfuctionElectrolytesHigh K,Ca,Uric acid

ALKALOSISCVSReduced inotropyAltered coronary flowDig toxicityMetabolismLow K,Ca,PO,enzymesDO2Increase HbO2 affinityIncrease 2,3,DPG

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Acid Base Disturbance

Primarily METABOLIC or RESPIRATORY


61 year old man, rescued from caravan fire. Brought to A&E –agitated, confused. Oxygen saturation reasonable. ABG on high flow 100% oxygen.

pH 7.162 pCO2 5.38 pO2 54.6 COHb 37.4 % Lactate 10.5 BE -13.1

Case Scenario 1


pH Is this an acidaemia or alkalaemia?

pCO2 is this normal, low or high?Shound this give us a acidosis or alkalosis?

BE (or bicarbonate) – is this normal or low ? Should this give us a acidosis or alkalosis?

Are there clues to which is predominant? Can use equations.

Remember respiratory changes occur quickly to compensate

Metabolic take days

History can help

Normal rangesph 7.35 – 7.45pO2 11.5 – 13 kPApCO2 – 4.1 – 6 kPaBic 22.5 to 26BE -2.5 to +2.5



pCO2 is this normal, low or high?Should this give us a acidosis or alkalosis?



pH = 7.162 acidaemia

pCO2 = 5.38Essentially normal – neutral.NB chronic smoker ? Possibly expect to be higher

BE -13.1, lactate 10.5

Loss of base i.e significant metabolic acidosis.

COHb should < 2% (sometimes up to 10% in smokers

Carbon monoxide poisoning +/-CN

Metabolic lactic acidosis (unsuccesful

respiratory compensation )


Metabolic Acidosis1. Rate of acid production in excess of kidney’s ability to

excrete and regenerate bicarbonate.

2. Decreased kidney ability to excrete acid and regenerate bicarbonate

3. Loss of bicarbonate from ECF (kidneys or GI tract)


Lactic Acid (Lactate) Metabolism (1) Traditional type A (hypoxia) and type B no evidence

poor perfusion. Arterial [2mmol/l]. Make @ 1500mmol/day. Muscles 25%, skin 25% brain 20%, RBC 20%,

intestine 10%. Metabolized kidney & liver. Fuel for glucose. L –lactate : levels exercise 20mmol/L D-lactate


Lactic Acid Metabolism (2)

Krebs

Glucose

pyruvate lactate

aerobic

anaerobic

mitochondria

Anaerobic conditions increases


CausesK KETOACIDOSIS {DIABETIC,ALCOHOL,STARVATION}

U URAEMIAS SALICYLATESM METHANOL FORMIC ACID

A ALDEHYDE (paraldehyde)L LACTIC ACIDOSIS {L & D}E ETHYLENE GLYCOL OXALIC ACID


23 year old female, presents short of breath. No associated chest pain, no haemoptysis, respiratory rate >35bpm.

pH 7.6 pCO2 2.2 pO2 15.0 HCO3 18.0 Lactate 1 BE -3.0

Case Scenario 2



pCO2 is this normal, low or high?Shound this give us a acidosis or alkalosis?



pH 7.6 alkalaemic

pCO2 2.2 low so should give you alkalosis

Fits with pH ? Respiratory alkalosis

BE / Bicarbonate – little low – tend towards mild acidosis

Why not compensated ? Remember takes days for metabolic compensation

HYPERVENTILATION


Respiratory Alkalosis Reflex hyperventilation Respiratory centre stimulation – chemoreceptors Altitude Right to left shunt CO poisoning Aspirin Liver failure Local brain lesion iatrogenic


76 year old man previous operations presents with lethargy, tiredness and increased breathlessness for the past few months. Previous surgery – cystectomy and ureteric diversion surgery (ileal conduits).

pH 7.23 pCO2 3.5 pO2 13.0 HCO3 16.0 Lactate 1 BE -6.0

Case scenario 3

Metabolic acidosis

Anion gap – 140 + 4 – ( 114 + 16) = 14normal

Hyperchloraemic Loss bicarbonate –ileal output.

Na 140

K 4.0

Cl 114


Gamblegram

Cl

HCO3

AG

Na K

Unmeasured anions

Unmeasured cations

ANION GAP = UA-UC

‘AG’= [Na +K} – {Cl + HCO3}

10-18mmol/L

UC = Ca & Mg UA = organic acids, phosphate, sulphate and protein


Metabolic Acidosis / High AG

Generation of acid metabolite not normally present e.g. salicylate

Overproduction of endogenous acid (lactic, keto-acids)

{Na + K} - { Cl- + HCO3-} > 18.


Metabolic Acidosis/ Normal AG

Diarrhoea or intestinal losses - pancreatic fistulae RTA II Toluene ingestion Carbonic anhydrase inhibitors -acetozolamide, topiramate Ureteric diversion RTA I, IV Some causes renal failure

LOSS BICARBONATE

DECREASED ACID LOSS

‘HYPERCHLORAEMIC’ACIDOSIS


A Respiratory acidosis B Lactic Acidosis C Metabolic Acidosis compensating for respiratory alkalosis D Metabolic acidosis.

What is the correct explanation of these blood gases? (on 2l O2 nc)

pH 7.30 PCO2 3.8 kPaPO2 11.0 kPaBE -4.0Lactate 1.8

Case scenario 4


83 year old lady confused, vomiting, agitated and blurred vision.

pH 7.49 pO2 12.4 pCO2 3.0 HCO3 20 BE -3

Na 144 K 3.2 ur 17 Cr 190 Lactate 5, chloride 110

pH 7.3 pO2 11.8 pCO2 3.8 HCO3 15 BE -7

ABG 1 shows Respiratory Alkalosis

ABG 2 shows Metabolic Acidosis

Anion Gap = 144 + 3.2 – (15 + 110) = 22.2 (ANION GAP)SALICYLATE POISONING

Case scenario 5


Case Scenario 6 40 year old with history of persistent vomiting. Previous

peptic ulcer disease. pH 7.5, PO2 13.3kPa, PCO2 5.5, HCO3 36 Cl- 75 BE +18

pH alkalotic

CO2 normal

High Bicarbonate

Metabolic Alkalosis – diagnosis of pyloric stenosis


Metabolic Alkalosis Milk alkali syndrome Alkaline overshoot in Rx AG acidosis Forced alkaline diuresis Loss acid – pyloric stenosis, H depletion other RTA, Cl

loss, hyperaldosteronism Contractional alkalosis Hepatic failure


Alcoholic / Starvation Ketoacidosis Chronic Prolonged period of heavy alcohol no food Vomiting stop alcohol Ketoacid production for fuel. Make lactate Liver damage means can’t metabolize. Accumulate NH4 cause alkalosis.


Summary

A/B disturbance – look for primary change Metabolic or respiratory Method of interpretation of ABG Awareness of importance of acid base balance.


End


Renal Tubular Acidosis


RTA

TYPE I distal

TYPE II proximal

TYPE IV hyporeninic hypoaldosteronism

•TYPE III – does not exist. Has been used AR syndrome Carbonic anhydrase deficiency

Normal AG hyperchloraemic acidosis


Type II Proximal RTA Inability to absorb all bicarbonate in the proximal

tubule. Increase amount to distal tubule Lose bicarbonate in urine Bicarbonate drops level : can reabsorb HCO3 : 12-20mmol/L Urinary pH >5.3 K will often be low normal. Rx : none. Bicarbonate – lower K


Causes of Type II RTA PrimaryIdiopathicFanconi syndrome{light chains, acetozolamide,

ifosfamide]Cystinosis, tyrosaemia,

glycogen storage disorder I/ Wilson/

SecondaryAmyloidHeavy metal {Cu, Cad, Hg}Vitamin D deficiencyTransplant PNH


Distal Type I RTA RTA type I predominately [H] secretion

problem. Progressive [H+] accumulation, HCO3 falls

<10mmol/L Bone – buffer acid load. Ca salts excreted. Urine pH > 5.3 during acidosis. Ca precipitate – nephrocalcinosis Hypokalaemic (retention Na loss K) Rx treat K; base buffer for daily acid –

potassium citrate 1mmol/day


Causes Distal Primary

IdiopathicFamilial

Secondary‘Autoimmune’Sjogrens, SLE, RA,

Hypergammaglobulinaemiaamphotericin, cirrhosis, Li,Tx, sickle cell


Type IV RTA Hyporeninemic hypoaldosteronism Aldosterone deficiency or resistance at receptor. Acidify urine ph<5.3. High K out of proportion to renal impairment

DM,CRF, chronic transplant rejection,congenital adrenal hyperplasia, chronic tubulointerstitial disease,obstructive uropathy, sickle cell.

HCO3 @ 17. Rx fludrocortisone & diuretics.


Bicarbonate Recyclinga. 100%

filtered

b. H+ excreted

c. Lumen with CA makes CO2 & water

d. CO2 into cell

e. Intrac CA-HCO3-

f. Out into peritubular capillaries


AMMONIUM Secretion

NH4 not secreted liver urea + H+ (loss HCO3)


D-Lactate Not made mammals Do not metabolise Bacteria Short bowel syndrome – bacterial overgrowth high cbh diet

accumulate d lactate slowly Progressive increased AG acidosis. Lactate normal

(measure L lactate)


Blood Gas Analyzers Measure pH, pCO2 calculate bicarbonate Standard bicarbonate – represents plasma bicarbonate if

pCO2 corrected 5.33 kPa (40mmHg) Base excess / deficit – amount alkali needed to change

1L blood to normal pH at pCO2 5.33. titration curves not same in vivo.


The End!

acid base disorders

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