See book: [Own the Arterial Blood Gas - Lawton](x-devonthink-item://645DC5F2-F669-4F46-AF3E-9E5F4A066001)
**Acidosis** - a condition that if left untreated would lead to acidemia
**Acidemia** - the presence of elevated \[H+] in the blood
# Standard approach
## 1. Acid/base disturbance
1. Decide ph acidemia/ alkalemia
2. Decide CO2 and HCO3 resp and metabolic acidosis/alkalosis
3. Decide on major disturbance (eg resp acidosis, metabolic acidosis)
4. Correct the dependent variable for major disturbance (ie **check for appropriate compensation**)
1. ==If primary disturbance is metabolic, [[#CO2 compensation met acidosis?|correct CO2 for HCO3]]==
2. if primary disturbance is respiritory, correct HCO3 for CO2 [[#HCO3 correction resp acidosis| correct HCO3 for CO2]]
3. if both disturbances occur in same direction (eg resp acidosis and metabolic acidosis), correct for each other
5. If there is a metabolic acidosis, calculate [[#anion gap]] and [[#delta ratio]]
## 2. oxygenation (A-a gradient)
See [[Oxygen dissociation curve]], [[Oxygen delivery devices FiO2]]
> [!info] Definition
> The difference between alveolar O2 (PAO2) and arterial O2 (PaO2)
>
> **A-a gradient** = PAO2 - PaO2
>
> = (\[760 - vapour pressure] x FiO2) - 1.25xPaCO2 - PaO2
>
> = (700 x FiO2) - 1.25 x PaCO2 - PaO2
> pAO2 =pinspired - palveCO2/R
> PAO2 = FiO2 * (Patm - 50 for H2O vapor) - 1.25xPaCO2
- if FiO2 =21%, then equation for PAO2 is 150 - 1.25xPaCO2
- IF fiO2 is 40%, then 300 - 1.25xPaCO2
Normally 5-10 mmHg. A-a gradiant is measure of difference between alveolar and arterial concentration of O2.
**Normal A-a gradient:** < \[age in years/4] + 4.
| Altitude | Insp pO2 |
| :------------------- | :------: |
| Sea level | 150 |
| Canberra (580m) | 141 |
| Mt buller (1500m) | 125 |
| Mt kosciusko (2225m) | 112 |
**Evaluate hypoxemia:**
| Normal A-a | Raised A-a |
| :------------------------ | :------------------------------------------------------------------------------------------------------------------ |
| Hypoventilation, low PiO2 | 1. [[VQ mismatch and its discontents\|V/Q mismatch]]<br>2. Right-left shunt<br>3. Increased O2 extraction<br>4. Diffusion defect (rare) |
**Main concerns in ED of elevated A-a gradient hypoxemia:**
- APO
- ARDS
- PE
- LRTI
- even though alveolar pressure O2 at apex of 40 mmHg above base, most of the blood flow comes from base where p alveoloar O2 is low --> decrease in p arterial O2
- shunt - bronchial blood and coronary blood
### respiratory quotient
Ratio of CO2 production and O2 consumption at steady state
200 mL/min / 250mL/min
= 0.8
Factors affecting it:
- tissue thpe
- Time
### limitations of A-a gradient
- Gradient varies with age and FiO2:
- FiO2 0.21 – 7 mmHg in young, 14 mmHg in elderly
- FiO2 1.0 – 31 mmHg in young, 56 mmHg in elderly
- For every decade a person has lived, their A–a gradient is expected to increase by 1 mmHg – a conservative estimate of normal A–a gradient is < *\[age in years/4] + 4*.
- an exaggerated FiO2 dependence in intrapulmonary shunt (PAO2 vs PAO2/PaO2 difference diagram with regard to increasing percentage of shunt) and even more so in V/Q mismatch.
## 3. electrolytes
### correct Na for glucose
see also: [[hypernatremia#Free water deficit / fluid deficit|Free Water deficit for ↑ Na]], [[hyponatremia#pseudohyponatremia|Pseudohyponatremia]]
> = 1/3 (glucose-5) + Na
### calculate expected k for ph
>[!info] Definition
>**For each pH fall 0.1 below 7.4, K should rise by 0.5 mmol/L above 5.0**
- therefore, expected K for pH 7.2 = 5.0 + 2x0.5 = 6mmol/L
* therefore, if K measures =4, patient would be relatively hypokalemic, and need k replaced as pH corrected.
### urea:Cr ratio
urea x 1000/Cr (to convert units mcgmol to mmol)
| | U:Cr |
| :-------- | :----: |
| Pre-renal | ~100 |
| Intrinsic | <50 |
### osmolality and osmolar gap
see: [[Osmolality and Osmolarity]]
> [!info] Definition
> **Calculated osmolality** = 2xNa + urea + glucose *+ 1.25 x EtOH*
> [!info] Definition
> **Osmolar gap** = measured osmolality - calculated osmolality
> - indicates the quantity of osmotically active substances in the serum **not measured by standard electrolyte tests**
> - ==>10 suggests an abnormal solute== , eg [[toxic alcohols]]
Non measured osmotically active substances:
- other ions
- potassium
- lactate
- calcium
- sulfate
- phosphate
- magnesium
- ammonia
- [[Lithium Toxicity|lithium]]
* proteins -- amino acids - in end organ failure
* glycerin
* alcohols
- toxic alcohols
- IV mannitol
- sorbitol
* other low-molecular-weight substances
* acetone
* fructose
* formaldehyde
* paraldehyde
* diethyl ether
**Conditions that may increase the osmolar gap:**
* [[toxic alcohols|toxic alcohol]] poisoning
* alcoholic ketoacidosis
* chronic renal failure
* diabetic ketoacidosis
* hyperlipidaemia
* hyperproteinaemia
* massive hypermagnesaemia
* severe lactic acidosis
* trauma and burns
> [!pearl] Tip
> calculate these if the stem gives us a measured osmolality
Rationale:
**total osmolality** : the concentration of all solutes in a given weight of water (mOsm/kg), regardless of whether or not the osmoles can move across biological membranes
**effective osmolality** (tonicity) : the **number of osmoles that contribute water movement** between the intracellular and extracellular compartment. is a function of the relative solute permeability properties of the membranes separating the intracellular and extracellular fluid compartments. urea is an ineffective osmotic substance (as it crosses membranes freely) so does not contribute to effective osmolality (tonicity)
### glucose
Eg if paeds hypoglycemia, then need 5ml/kg 10% dextrose per APLS
## 4. Interpret
Eg give full summary, assessment, and plan
## pH
Knowing the ph is valuable for the management of
- [[hyperkalemia]]
- [[Coagulopathy]]
- Hypocalcemia
- [[toxic alcohols]] ingestion
### effects of acidosis
- increase serum K -- each decrease in pH of 0.1 increases K+ 0.5mmol/L
- Increases off loading of oxygen from Hb in tissues
- Decrease activity of clotting factors
- may Decrease Ca2+ by direct binding (opposite to effect expected by acidosis alone)
- Decrease myocardial contractility for pH < 7.1
- Arterial vasodilation
- Pulmonary artery and peripheral vein vasoconstriction
- Increase toxicity of [[Sodium channel blocker|Na-channel blocker]]
# ABG vs VBG
- only advantage of arterial over venous is exact pCO2 and pO2
| Value | VBG difference |
| :------ | :------------------------------ |
| pH | Venous 0.05 lower |
| HCO3 | Approx 1.7 higher than arterial |
| Hb | 2g/dL lower than arterial |
| Lactate | 0.4mmol higher than arterial |
# arterial vs capillary sampling
- capillary pretty good, inacurate to determine pO2 and in shocked patient
# Metabolic acidosis
* either increased acid production or decreased elimination
* Calculated HCO3 is [mostly accurate](https://derangedphysiology.com/main/cicm-primary-exam/required-reading/acid-base-physiology/Chapter%20601/actual-bicarbonate-value)
## anion gap
- set AG of 12 for calculating without potassium, set at 16 if using potassium
- Because all solutions must be electrically neutral, the normal AG represents **unmeasured anions and cations**
- For example, lactate is the conjugate base of lactic acid
> [!info] Definition
> **ANION GAP** = [Na+] - ([Cl-] + [HCO3-])
> \>12 [[#HAGMA]] -- perform delta ratio as well
> \<12 [[#NAGMA]]
Nb **use measured, not corrected, sodium** for anion gap
### albumin correction
because albumin most abundant anion and major contributor to the gap, in ==low albumin== states, ==may cause anion gap to appear falsely low.== (see also [[Lactic acidosis#What happens when you have a NAGMA but ↑ lactate??|↑ lactate but NAGMA]])
> Albumin corrected AG = AG + (40 - albumin)/4
Example: albumin = 30, observed AG = 12
AGcorr = 12 + (40-30)/4 = 14.5
### elevated AG without acidosis
- Penicillin - elevated due to k+/h+ excretion, usually has hypokalemic alkalosis
- gamma-globulinaemia
- ↑ serum paraprotein in myeloma
- high serum phosphate or sulfate
### low anion gap <5
- hypoalbumin
- Increase chloride
- Increase in other cations (calcium, manesium, [[Lithium Toxicity|lithium]])
- Myeloma (increase protein)
- Nitrites
- Sedatives
***negative anion gap***
- ↑ unmeasured cations
- lithium
- magnesium
- calcium
- interference with measurement of chloride
- iodine
- bromide
- halides
- artifact of calculation
- extreme hyperlipidaemia or hyperprotinaemia (by decreasing reported sodium level from [[hyponatremia#pseudohyponatremia|pseudohyponatremia]]
- extreme hypoalbuminaemia (hence the [[#albumin correction]] above)
## delta ratio
"of little, if any, clinical usefulness but unfortunately common in postgraduate exams" - Dunns
examples from Lawton Own the Arterial Blood Gas: [problem 19 - smoker w/metabolic acidosis](x-devonthink-item://645DC5F2-F669-4F46-AF3E-9E5F4A066001?page=92), [Problem 17 - kid with iron ingestion + vomiting](x-devonthink-item://645DC5F2-F669-4F46-AF3E-9E5F4A066001?page=84)
Evaluate if there is a concurrent NAGMA:
$\frac {AG-12}{24-HCO3} $
> - **\< 0.4** (large drop in HCO3 without change in AG) = [[#NAGMA]]
> - **0.4 - 0.8** (intermittent drop in AG compared to HCO3) = *combined* HAGMA and NAGMA, eg consider renal impairment
> - **1.0** (equal drop in HCO3 and AG) = [[#HAGMA]]
> - **\>2** (less drop in HCO3 than would be expected for magnitude of AG, usually because chloride is disproportionately low) = previously existing or *concurrent metabolic alkalosis* (or chronic [[#respiratory acidosis]]. This occurs because the resting HCO3 for the patient is greater than 24 mmol/L).
> - cause of concurrent metabolic alkalosis may be HCl loss from vomiting. other ddx would be something like frusemide co-ingestion in tox. I’ve seen a practice question on [[Aspirin overdose]] with a delta ratio of 2.4 due to concurrent metabolic alkalosis. rare would be primary hyperaldosteronism
### delta gap
= delta anion gap - delta HCO3
= Na - (Cl + HCO3) - 12 - (24-HCO3)
= Na - Cl - 36
\> +6 indicate presence of metabolic alkalosis
\< -6 i dicate a hyperchlorawmic acidosis
## CO2 compensation met acidosis?
Expected CO2 will be **low** for appropriate compensation
> [!info] Definition - Winter's formula
> **Expected CO2 = 1.5 x(HCO3) +8 (+/-2)**
==Shortcut==: last 2 digits of the pH between pH 7.4 - 7.1
- a pCO2 **higher** than expected suggests an incomplete respiratory response (i.e. relative respiratory acidosis)
- a pCO2 **lower** than expected suggests an excessive respiratory response (i.e. relative respiratory alkalosis)
## HAGMA
- results from an accumulation of organic acids or impaired H+ excretion
### KULT
* ketoacidosis
* Diabetes
* Starvation
* profound dehydration
* [[Lactic acidosis]]
* Shock
* Anaemia
* Haemorrhage
* Liver failure
* Sepsis
* Mudpiles drugs
* Metformin
* Uraemic renal failure
* Toxins
* [[Aspirin overdose|Salicylates]]
* [[Cyanide]]
* [[toxic alcohols#Methanol]]
* [[toxic alcohols#Ethylene Glycol]]
* [[Iron overdose]]
* Others… [[Lactic acidosis#toxic causes]]
### CATMUDPULES
- CO, CN
- Alcoholic and starvation ketosis
- Toluene
- Metformin, methanol
- Uremia
- DKA
- Pyroglutamic acidosis, paradetamol, phenformin, propylene glycol, paraldehyde
- Iron, isoniazid
- [[Lactic acidosis]]
- Ethylene glycol
![[Pasted image 20230330160406.png]]
## NAGMA
See also: [[Lactic acidosis#What happens when you have a NAGMA but ↑ lactate??]]
In patients with a normal anion gap the drop in HCO3 is the primary pathology. Since there is only one other major buffering anion, it must be compensated for almost completely by an increase in Cl−. This is therefore also known as hyperchloremic metabolic acidosis.
The HCO3- lost is replaced by a chloride anion, and thus there is a normal anion gap.
**Causes**
Large volumes of IV NaCl
Renal losses
Carbonic anhydrase inhibitors
Lower GIT fluid losses (high HCO3-)
CHOLESTYRAMINE (BINDS HCO3 IN GIT)
### CAGES
- chloride (excessive NaCl)
- [[Adrenal insufficiency|Addison's disease]]/acetazolamide
- GI loss (diarrhoea)
- Extra ([[Renal tubular acidosis]], ingestion of oral salts, pancreatoduodenal fistulas)
- Spironolactone
![[Pasted image 20230814142216.png]]
### assess NAGMA
**URINARY ANION GAP**
> Na + K - Cl
> - \> 20 abnormal
**urinary osmolar gap**
= (2 xNa + 2K +Urine urean nitrogen + urine glucose
<4 indicates impaired urinary ammonium excretion
![[Pasted image 20230330165752.png]]
# Metabolic alkalosis
[example problem metabolic alkalaosis](x-devonthink-item://645DC5F2-F669-4F46-AF3E-9E5F4A066001?page=38)
> the pH will be high (alkalemia) and CO2 will be high from resp acidosis compensation
> - compare to resp acidosis and acidemia with high CO2 but low pH
## CO2 correction met alkalosis?
Expect CO2 higher to compensate for met alkalosis
> [!info] Definition
> Expected CO2 = 0.7x(HCO3) + 21
Very variable, above formula fairly inaccurate
pCO2 does not exceed 60 mmHg in compensation
==Shortcut==: pCO2 = last 2 digits of the pH between pH 7.4 - 7.6
**causes**
Acute:
- exogenous (eg NaHCO3 infusion, citrate from blood transfusion)
- *diuretics* (frusemide and thiazide interfeere with reabsorption of chloride and sodium) usually volume depleted as well and aldosteroine is high; hypoklamie common in these patients (due to excess mineralocorticoid)
- vomiting, NG suction (loss of H+)
- chloride depletion (eg vomiting due to pyloric stenosis or obstruction)
primary [[Hyperaldosteronism]] (increase Na reabsorption and K and H+ losses): met alkalosis with hypochloraema and hypokalemia with expanded EF vol
# Respiritory Acidosis
## HCO3 correction resp acidosis
Expect HCO3 to compensate up in resp acidosis
| | Each 10 mmHg increase in pCO2 increases HCO3 |
| :--------------- | :------------------------------------------- |
| Acute | 1 mmol/L |
| Chronic (4 days) | 4 mmol/L |
each 10 mmHg increase in pCO2 decreases the pH by
- 0.05 acutely
- 0.03 chronically
HCO3- usually only increases in chronic respiratory acidosis to a maximum of 45 mmol/L
- a HCO3- higher than expected suggests the presence of a relative metabolic alkalosis
- a HCO3- lower than expected suggests the presence of a relative metabolic acidosis
## causes
- acute/chronic [[COPD]] exacerbation
- [[Asthma]]
- Airway obstruction
- Central resp depression
- [[Opiate overdose]], etc
- [[traumatic brain injury|TBI]]
- trauma (pulm contusion, [[Trauma/pneumothorax]], haemothorax)
- LRTI, aspiration, [[ARDS]], APO
- inadequate resp effort
- Toxins ([[organophosphates]], envenomation)
- Myopathies
- guillian-barre syndrome
# Respiratory alkalosis
## correct HCO3 for acute and chronic resp alkalosis
Expect HCO3 to go down
> - acute: HCO3 decrease by 2 per dime change CO2 below 40
> - Chromic: HCO3 decreases by 5 per 10 mmolhcg below 40
## causes
- central stimulation of resp drive
- [[intracerebral haemorrhage|ICH]]/ [[traumatic brain injury|TBI]]
- Anxiety or pain
- [[Aspirin overdose|Salicylates]]
- MDMA, other sympathetic agents
- Hypoxia causing resp stimulation
- PE
- pneumonia
- [[Pulmonary oedema]]
- Acute asthma
- ARDS
- Note, these can also causw resp acidosis
#investigations/vbg
#core