Acid Base Disorders

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org
Acid Base Disorders
Cardiff MRCS OSCE Course www.doctorsacademy.org
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 account
Not sure really helps management.
Definitions
Base : proton or H
+
acceptor.
Acid : proton or H
+
donator.
H-H equation relates arterial pH to PaCO
2
and bicarbonate.
pH = 6.1 + log [HCO
3
]/0.23(paCO
2
)
pH = -log [H
+
].
[H+] 45nmol/L to 35nmol/L ( pH 7.35-7.45).
Nanomol (1 x10
6
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 pH
Excretion 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 CO
2
*.
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 HCO
3
.
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 Disturbance
ACIDOSIS
CVS
Reduced inotropy
Conduction defects
Arterial vasodilation
Venous constriction
DO2
Reduces HbO2 binding
Reduces 2,3,DPG (late)
NMJ
Resp depression
Red awareness
Metabolism
Protein wasting
Bone demineraliztion
Catecholamine release
Insulin resistance
Free radicals
GI
Emesis
Immune dysfuction
Electrolytes
High K,Ca,Uric acid
ALKALOSIS
CVS
Reduced inotropy
Altered coronary flow
Dig toxicity
Metabolism
Low K,Ca,PO,enzymes
DO2
Increase HbO2 affinity
Increase 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
pCO25.38
pO254.6
COHb37.4%
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
Are there clues to which
is predominant? Can use
equations.
Remember respiratory
changes occur quickly
to compensate
Metabolic take days
History can help
Normal ranges
ph 7.35 7.45
pO2 11.5 13 kPA
pCO2 4.1 6 kPa
Bic 22.5 to 26
BE -2.5 to +2.5
or alkalaemia?
or high?
Are there clues to which is
predominant? Can use
equations.
pH =7.162 acidaemia
pCO2 =5.38
Essentially 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 Acidosis
1. Rate of acid production in excess of kidneys 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
Causes
K KETOACIDOSIS {DIABETIC,ALCOHOL,STARVATION}
U URAEMIA
S SALICYLATES
MMETHANOL 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
pCO22.2
pO215.0
HCO318.0
Lactate 1
BE -3.0
Case Scenario 2
or alkalaemia?
or high?
Shound this give us a
Are there clues to which
is predominant? Can use
equations.
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
pO213.0
HCO3 16.0
Lactate 1
BE -6.0
Case scenario 3
Metabolic acidosis
Anion gap 140 +4 ( 114 +16) =
14
normal
Hyperchloraemic
Loss bicarbonate
ileal output.
Na 140
K 4.0
Cl 114
Gamblegram
Cl
HCO
3
AG
Na K
Unmeasured anions
Unmeasured
cations
ANION GAP = UA-UC
AG= [Na +K} {Cl + HCO
3
}
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
DMetabolic acidosis.
What is the correct explanation of these blood gases?
(on 2l O
2
nc)
pH 7.30
PCO
2
3.8 kPa
PO
2
11.0 kPa
BE -4.0
Lactate 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 cant 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
Primary
Idiopathic
Fanconi syndrome
{light chains, acetozolamide,
ifosfamide]
Cystinosis, tyrosaemia,
glycogen storage disorder
I/ Wilson/
Secondary
Amyloid
Heavy metal {Cu, Cad, Hg}
Vitamin D deficiency
Transplant
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
Idiopathic
Familial
Secondary
Autoimmune
Sjogrens, SLE, RA,
Hypergammaglobulinaemia
amphotericin, 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 Recycling
a. 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, pCO
2
calculate bicarbonate
Standard bicarbonate represents plasma bicarbonate if
pCO
2
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!

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