A male patient aged 65 years of COPD and cor pulmonale admitted with the complain of increase in Breathlessness. ABG was done before giving oxygen therapy on 12/02/2015 at 6.13 PM.
ABG Analysis 1. Gas Analysis :- Step: 1
PaO2 = 47.1 mm of Hg – Moderate Hypoxenia. Step: 2
PAO2 = 72.5 – decrease Alveolar oxygen content. Step: 3
P(A-a)O2 = 72.5-47.1
Nearly Normal = age/4+4
= 65/4+4 = 16+4 = 20
Supposed to be no paregnel lup disease. Step: 4
PaCo2 = 66.5 Increased more than 49.
So, Hypoxemia with Hypercapnia
= Type 2 Respiratory failure. Step: 5
Since PaCo2 is increased and P(A-a)O2 not increased so, hypo ventilation alone and important cause of it is decrease respiratory drive and neuromuscular disease. Step: 6
P/F = 224.3 – there are features of heart failure so is not an indication of ALI. Step: 7
PaO2 of (40 – 60) mm of Hg Correspond to SPO2 of (75 – 91)%. Here, SPO2 69.7% & PaO2 47.1 mm of Hg. So, SPO2 a bit low. Step: 8
Cao2 = 17.1 X 10 X 1.34 X 69.7/100 + 0.003 X 47 ml/L
= 159.71 + 0.1413
= 159.85 ml/L
2. Electrolyte Analysis :-
Ca++ -> 0.561 – low – Cause, Pancreatis, hypoalbuminemia, Renal failure, Vit deficiency and alkalosis to be searched.
K+ -> 4.90 – normal Anion Gap :-
AG = 12.5 – near normal Delta Gap :-
Delta gap = 12.5 – 12 = 0.5 Gap – Gap ratio :-
Delta gap / HCo3 gap = 0.5/(30.6-24) = 0.5/6.6 = 0.08 <1 (to be taken in consideration if there is metabolic cause.) Base Excess :-
BE = 1.5 mm/L –> if metabolic cause it suggest metabolic alkalosis.
3. Acid Base Analysis :- Step: 1
HCo3 = 30.6 mmol/L (> 24 mmol/L) metabolic alkalosis . Step: 3
PaCo2 = 66.5 mm of Hg (> 40 mm of Hg) so, respiratory acidosis. Step: 4
H+ & HCo3– move in same direction. so, respiratory cause. Step: 5 So, PaCo2 & HCo3– move in same direction.so, simple cause.So, respiratory acidosis with compensatory metabolic alkalosis.
Compensation in chronic cause of respiratory acidosis
HCo3 rise = (2.62 X 66.5)/7.50 = 23.23
So, expected HCo3 = 40 + 23.23 = 63.23 , so fully compensatory.
So, chronic respiratory acidosis with fully compensatory metabolic acidosis with Type 2 respiratory failure due to decrease respiratory drive in a patient of COPD.
A young adult of 30 Years suffering from Type 1 Diabetes mellitus from last 5 years, not taking insulin, admitted in emergency department of DMCH with the complain of vomiting, loose motion drowsiness and found tachycardia, hypotension, dehydration , increased rate of respiration (34/m). ABG was done on 12/02/15 at 4.36 PM.
(i) Gas Analysis Step:1
PaO2 – 139.0 mm of Hg –> High due to use of High Fio2 Step:2
PAO2 – 139.0 mm of Hg –> Above normal alveolar oxygen content due to high Fio2 . Step:3 P(A-a)O2 = (139.0-139.0) mm of Hg
= 0 mm of Hg –> No Parenchymal
lung disease. Step:4 PaCo2 -> 11.3 mm of Hg –> Hyperventilation Step:5 No Hypoxemia/No respiratory failure. Step:6 P/F = 661.8 –> No ALI/ARDS –> gas exchange is very good. Step:7 SPO2– = 96.5 –> Probably due to increase H+ there is Rt shift of the Hb dissociation curve. So, PaO2 increase and SpO2 relatively Low. Step:8 CaO2 = 15.9X10X1.34X96.5/100+0.003X139.0
= 205.60 + 0.417
= 206.01 ml/L
Normal value for this 40 Mg adult man should be approximate 111 ml/L. So oxygen to be avoided to protect from oxygen toxicity.
(ii) Electrolyte Analysis
Upper limit – due to loss of body water content & Cl- is a bit high due to metabolic acidosis.
Ca++ -> 1.172 – High
K+ -> 4.18 – normal , but its value should be high due to decrease blood pH.
For 0.10 decrease of pH.
Increase of K+ should approximate 0.6 mmol/L.
So for 7.029 of pH –> K+ should have increased value upto (N+2.226)mmol/L.
Low level is due to GIT and / or Renal loss.
AG = 144.9-(116.7+2.9)
=144.9-119.6 = 25.3/29.5 (derived by machine)
Perhaps K+ is also taken in consideration by the machine.
Delta gap+ measured HCo3 = 17.5 +2.9=20.4 –> low (normal 22-26 mmol/L)
i.e. non anion gap metabolic acidosis.
Gap – Gap Ratio
Gap -gap ratio = (29.5-12) / (24-2.9) = 17.5 / 21.1 = 0.83 <1
i.e. normal AG metabolic acidosis and treatment with N/S (Hyperchloronic).
In this case patient had been gives 3L of N/S before the ABG was done.
BE = 2.9-24 = -21.1 (Derived value by machine -25.8)
Negative value suggestion metabolic acidosis. (So non respiratory cause of Acidosis).
(iii) Acid – Base Analysis
Step:1 pH = 7.029
H+ = 93.6 nmol/L So acidemia. Step:2 HCo3 = 2.9 mmol/L (< 24 mmol/L) so, metabolic acidosis. Step:3 PaCo2 = 11.3 mm of Hg (< 40 mm of Hg) so, respiratory alkalosis. Step:4
H+ & HCo3– moves in opposite direction.
so, metabolic cause. Step:5
So, PaCo2 & HCo3– moves in same direction.
so, simple cause.
So, the patient have metabolic acidosis (primary cause) with compensatory respiratory alkalosis. Step:6
Compensation –Expected PaCo2 fall = 1.2 X (24-2.9)
= 1.2 X 21.6
So, expected PaCo2 = 40-25.32
High and normal AG metabolic acidosis with fully compensatory respiratory alkalosis with hyperventilation with low value of K+ is this condition.
Causes of high AG metabolic acidosis
M – Methanol – No history in this patient
U – Uraemia – Blood urea/ s.creatinine/spot urinary ACR / Input- output chart.
D – Diabetes mellitus – This is the cause
P – Paraldehyde – No history
I – Infection,Ischaemia,Isoniazide – CBC,ECG required
L – S.lactate – to be estimated
E – Ethanol – No history
S – Starvation, – Present for 2 days
Salicylat – No history.
Causes of Normal AG metabolic acidosis
Gastrointestinal loss of HCO3 in diarrhoea (which was presenting problem).
Renal Tubular Acidosis -> to be excluded by normal AG with no evidence of gastrointestinal disturbance and urinary pH is inappropriately high >5.5 .
A patient of constrictive pericarditis, who had breathlessness on slight movement from one month admitted in stuporosed condition in emergency department of DMCH on 15/01/15.
ABG was done on 15/01/15 at 9.39 PM.
(i) Gas Analysis
PaO2 – 49.8 mm of Hg–Moderate hypoxemia
SPo2 – 70.5 % – Severe hypoxemia
There is slight left shift of the oxygen dissociation curve, most probably due to decrease in temperature.
PAO2 – 49.8 mm Hg – low
So, either Fio2 low or PaCo2 high.
P(A-a)O2 = (49.8 – 49.8) mm Hg.
= 0 mm of Hg – normal
PaCo2 – 122.5 – Hypercapnea – hypoventilation
So, the patient has hypoxemia with Hypercapnea
i.e. Type 2 Respiratory failure.
Due to advanced stage of LVF.
Here PaCo2 is increased, and P(A-a)O2 is not increased , so the cause is hypoventilation alone and since the patient had no neuromuscular disease , so it is due to decreased respiratory drive due to critical illness.
P/F index or hypoxemia index = 237.3
x-ray finding does not suggest progressive diffuse pulmonary infiltration , feature of pneumonia . So it can be due to heart failure or arterial hypoxemia.
There is slight mismatch in the relation between SPo2 and PaO2.
Cause of mismatch is left shift of the oxygen dissociation curve most probably due to low temperature.
Hemoglobin and HCT value are high indicating polycythaemia mosr probably due to hypercapnea . we calculate arterial oxygen content
CaO2= 16.4X10(gm/L) X 1.34 X 70.5 / 100 + 0.003 X 49.8
= 154.93 + 0.149
= 155.08 ml/L
Expected CaO2 in a 70 Kg person is 194.44 ml/L.
(ii) Electrolyte Analysis
S.Na+ – 130.7 mmol/L – low
S.Cl– – 86.5 mmol/l – low
S.iCa – 0.915 mmol/L – normal
S.K+ – 5.31 mmol/L – high
Decrease level of s.Na+ and Cl-is due to fluid retention.high level of K+ matches with the change in pH due to acidosis.
Anion Gap :-
AG = [130.7]-[86.5+43.4]
= 0.8 mmol/l
Derived AG is 6.1 mmol/L
This increased level of AG is due to increased in unmeasured anion.
Delta Gap :-
Delta gap + HCo3 = -5.9+43.4
= 37.5 – metabolic alkalosis.
Expected cause of Acid-Base change in simple.
So, respiratory acidosis with compensated metabolic alkalosis.
Compensation of Hco3 In chronic condition
= 2.62 X 122.5/7.50 kpa=42.79
So, expected value of Hco3 = 24+42.79=66.70
Compensation of Hco3 In acute condition
= 0.75X 122.5/7.5 = 12.25
So, expected value of Hco3 = 24+12.25=36.25
So,respiratory acidosis with chronic compensated metabolic alkalosis.
PaCo2=30.2 mm of Hg -> low
So, Type 1 respiratory failure.
O2 therapy (6 L/m through C-PAP) for 2 hrs
Improved to some extent. So the causes may be Ventilation / perfusion mismatch i.e.
Airway disease .
Interstitial lung disease.
Pulmary vascular disease.
P/F=36.9/21 X 100
= 175.7 mm Hg.
ALI/ARDS to be decided by excluding, pneumonia or heart failure. There should be (progressive diffuse pulmonary infiltration in x-ray) and arterial hypoxemia.
Relation of PaO2 and SPO2 is normal.
CaO2 = 10X5.6(gm/L)X1.34X52.4/100+0.003X36.9 ml/L
= 39.43 ml/L
Wt. Of the patient is 58 kg.
So,expected CaO2 = 161.11 ml/L
Available CaO2 = 39.43 ml/L
So, Blood transfusion is also indicated.
S.Na – Normal
S.Cl – raised -> may be due to metabolic acidosis.
S.Ca++ – low -> may be due to hypoalbuminemia.
S.K+ – high -> may be due to acidosis/Renal Dysfunction Anion Gap :-
AG = 140.5-[110.7+11.4]
= 18.4 but it is 25.6 as derived by machine. It may be due to hypoalbuminemia.
AG > 20 so, primary metabolic acidosis.
Delta Gap :-
Delta Gap = 25.6-12
Delta Gap + HCo3– = 13.6+11.4
= 25 -> Normal range
Gap-Gap Ratio :-
Gap/Gap ratio = 13.6/12.6 >1
But delta gap + HCo3 is normal.
So their is less chance of associated metabolic alkalosis.
BE = 11.4-24
= -12.6 -> Base deficit
So, Metabolic acidosis.
PaCo2 = 30.2 mm of Hg
(< 40 mm of Hg) so, respiratory alkalosis.
Expected, PaCo2 fall = 1.2 X (24-11.4 )
= 1.2 X 12.6
So, expected PaCo2 = 40-15.12
So, metabolic acidosis with incomplete compensatory respiratory alkalosis.
AG = 25.6
High anion gap metabolic acidosis.
Delta gap + HCo3 -> normal.
So, no normal anion gap metabolic acidosis and no metabolic alkalosis.
Final diagnosis – High anion gap metabolic acidosis with incomplete compensatory respiratory alkalosis with type 1 respiratory failure with Hyperkalaemia with Hypocalcaemia.
Causes of High Anion Gap Metabolic Acidosis
M – Methanol – No history in this patient
U – Uraemia – Present
D – Diabetes mellitus – Not present
P – Paraldehyde – No history
I – Infection, Ischaemia, Isoniazide – Infection present, No Ischaemia , No H/O Isoniazide
L – S.lactate – Not done
E – Ethanol – No history
S – Starvation, Salicylate – Starvation present, No H/O Salicylate intoxication
So, Acidosis is most probably due to Infection, Uraemia.
Cause of Type 1 RF
X – Ray chest suggest pneumonia.
Since hypoxemia is severe and there is associated Anaemia, hyperkalaemia, pneumonia and uraemia, so prognosis is not good even with haemodialysis, blood transfusion and close monitoring of the patient.
Arterial Blood Gas (ABG) is now widely done in hospitals. So direct measurement of pH, PaO2, PaCo2 are most precise in medicine .The value of such data depends upon the ability of the doctors to interpret the results properly and if the analysis is made systematically, it becomes interesting for the doctors and fruitful for the patient.
Analysed report of ABG helps the clinician in diagnosis, sometimes it has prognostic value and is important monitor in ventilated patients.
Before analysis patient’s history and clinical condition should be carefully reviewed.
ABG Analysis is done in three headings :-
1. Gas Analysis:- Gas Analysis is done to decide the
Type of respiratory failure
Severity of hypoxemia
Cause of hypoxemia i.e. FiO2, ventilatory defect, ventilation-perfusion mismatch, shunt, diffusion defect and finally decide arterial oxygen content.
For gas analysis we proceed in the following manner
Step: 1 We look for PaO2 (partial pressure of oxygen) and SpO2 (oxygen saturation) and compare
< 75% – severe hypoxemia (Clinical symptom of serious arrhythmia, brain damage and death may ensue in elderly)
PAo2 (Alveolar oxygen content)
PAo2 is derived value and is calculated as
Normal value is 96-108mm/Hg.
P (A-a)O2 (Alveolar-arterial oxygen difference)
Normally <15 mm of Hg, may be as high as 30mm of Hg in elderly. Other simple way to decide the normal value is Age/4+4, If this value is increased, Indicates parenchymal lung disease.
PaCo2 (Partial pressure of Co2)
Normal value is 36-45 mm of Hg and for the purpose of ABG analysis it is taken as 40 mm of Hg. More than 49 mm of Hg is considered as hypoventilation.
Now the type of respiratory failure is decided which is defined as type 1 when there is hypoxemia without carbon diaoxide retention and type 2 when there is hypercapnia. The calculation of the gradient between the alveolar and arterial oxygen tensions (A-a gradient) in type 2 respiratory failure will help to determine whether the patient has associated lung disease or just reduced respiratory effort. Examples of type 1 respiratory failure are consolidation, collapse, fibrosis, pulmonary oedema, pulmonary embolism, aspiration, atelectesis. Example of type 2 respiratory failure are COPD, Guillenbare syndrome, Myasthenia gravis, disease anywhere from brain to neuromuscular junction of respiratory muscle, drug toxicity, exhausted patient, critically ill patient may change from type 1 to type 2 respiratory failure.
Decision of the cause of hypoxemia from the value of PaCo2, P(A-a)O2 and the knowledge of response to O2 inhalation is done by the flow chart given below.
We calculate P/F i.e. PaO2/FiO2. It is known as hypoxemia index which is a measure of gas exchange. In the absence of pneumonia or heart failure, progressive diffuse pulmonary infiltration and arterial hypoxemia (P/F<300) indicates the development of Acute Lung Injury (ALI). More severe hypoxemia(P/F<200) denotes the acute respiratory distress syndrome (ARDS).
The relation between SpO2 and PaO2. It is decided by sigmoid saturation curve for haemoglobin which is also written in step1. If mismatch we search the cause of shift.
Calculate the arterial oxygen content(CaO2).
CaO2=Hb(gm/L)X1.34XSpO2/100+0.003XPaO2. In a adult of 72Kg the normal value of CaO2 is 200ml O2/L of blood.
O2 dissolved in plasma=3ml/L. When the cardiac output is low, we should calculate oxygen delivery=CoXCaO2 and then evaluate tissue diffusion. ************************************************************************************************************************************
2. Electrolyte Analysis: –
ABG gives us the status of Na+,K+,Ca++, and Cl–. The normal values of them are serum Na+ 136-145mmol/L,serum K+ 3.5-5.1 mmol/L,ionized (serum,plasma) Ca++ 1.15-1.33 mmol/L, Serum Cl– 98-107 mmol/L. Then we search the cause of hypo and hyper condition of different electrolytes.
In general sodium largely reflects reciprocal change in body water content. Chloride (Cl–) generally change in parallel with plasma Na+. It is low in metabolic alkalosis and high in metabolic acidosis. Potassium may reflect potassium shift in and out of cells-related to H+ ion. For each decrease in blood pH of 0.10, the plasma potassium should rise by 0.6 mmol/L. This relation is not invariable. Generally low level means excessive losses (gastrointestinal or renal). High level usually means renal dysfunction.
From the value of electrolytes and HCo3 we derive Anion gap, delta gap, gap-gap ratio and base excess/deficit.
Anion Gap (AG) :- Anion gap is calculated as AG=[Na+]-[(Cl–)+(HCo3–)] and is usually 12 mmol/L. AG increases most often due to increase of unmeasured anion and less commonly due to decrease in unmeasured cation (K+,Ca++,Mg++). Unmeasured anion are protein, phosphate, sulfate and organic anion. Albumin is the principal unmeasured anion and principal determinant of the anion gap. Since hypoalbuminaemia is present in as many as 90% of the ICU Patients. The following formula for the “Corrected AG” (AGc) has been proposed to include the contribution of albumin.
AGc=AG+2.5[4.5-(albumin in gm/dl)]
Example of a patient with a AG of 12 mmol/L and Plasma albumin 2gm/dl.
So, normal anion gap becomes high anion gap.
AG is useful to decide the cause of metabolic acidosis. AG should always be calculated for two reasons.
Abnormal AG even if Na+,Cl–,HCo3– are normal.
A large AG>20mmol/L supports a primary metabolic acid-base disturbance, regardless of the pH or Serum HCo3. A markedly rise of AG is never a compensatory response to a respiratory disorder.
So the cause of metabolic acidosis has been grouped as High, Normal and Low anion gap metabolic acidosis. In a patient all three can be present simultaneously and there can be simultaneous presence of metabolic alkalosis. To segregate these four, we take the help of delta gap, gap-gap ratio, BE and serum Albumin of the patient.
Delta Gap :-
Delta gap = pt’s AG-Normal value of AG.
= Pt’s AG-12.
When delta gap is added with measured HCo3, the sum value should satisfy the normal range of HCo3– i.e. 22-26 mmol/L. If this value is greater than 26mmol/L, indicates the additional presence of metabolic alkalosis and reduction less than 22 indicates non-anion gap metabolic acidosis.
Gap-Gap Ratio :-
Gap-gap ratio is calculated by comparing the anion gap excess(difference of measured and normal AG) to the HCo3 deficit(difference between the measured and normal HCo3 in plasma). Keeping in mind the normal
AG=12mmol/L & normal HCo3–=24 mmol/L.
AG excess/HCo3 deficit=(AG-12)/(24-HCo3).This ratio is sometimes called as gap-gap ratio because it involves two gaps (AG excess and HCo3 deficit).
Application of Gap-Gap Ratio :-
It gap-gap ratio is 1 – indicates high AG metabolic acidosis
It gap-gap ratio is <1 – indicates normal AG metabolic acidosis or treatment with N/S (hyperchloremic).
It gap-gap ratio is >1 – indicates associated metabolic alkalosis or when NHCo3 is added.
Base Excess(BE) :-
Base excess is defined as the fully ionised acid which could be required to return the patient blood pH 7.4 when Co2 has been adjusted to 40mm of Hg. It is calculated as
BE=HCO3(Measured)-24(Normal value of HCO3).
Positive value indicates metabolic alkalosis and negative value indicates metabolic acidosis. BE is true reflection of non-respriratory component of A-B balance. It is measure of metabolic acid level and normally is zero. A metabolic acidosis with base deficit>5 mmol/L requires explanation.
From the value of BE,NaHCo3 needed for neutralization can be calculated.
NaHCo3(mmol)=BE(mmol/L) X BW(Kg)/3
8.4% NaHCo3 solution contains 1 mmol NaHCo3 per ml.
Half of the amount is given and the ABG is done. Then calculate the amount required for final correction and administration.
In lactic acidosis,NaHCo3 decrease cardiac output and lowers blood pressure, so it should be used with caution.
The sole purpose of the A-B-analysis is to decide the primary disorder, compensatory effect (incomplete or complete in metabolic cause and acute or chronic in respiratory cause), disorder is simple or complex. If complex decide respiratory acidosis or alkalosis with metabolic alkalosis and/or metabolic acidosis. If metabolic acidosis decide high anion gap, normal anion gap, low anion gap. Lastly to conclude the aetiology of the defect. To conclude we proceed systematically in steps.
We look for pH and H+ simultaneously and decide acidemia/ alkalemia (net change present in blood). H+ is a derived value. It is calculated by simplified formula as H+ = 24XPaCo2/HCo3 .
Normal value of pH 7.4 and H+ 40 nmol/L for all calculation of ABG.
A normal pH can be normal, mixed defect or compensated defect.
Severe acidemia (pH<7.25) reduce the efficacy of endogenous & exogenous administered catecholemine.
See for HCo3– . Its normal value for ABG analysis is 24mmol/L. It is increased >24 mmol/L in metabolic alkalosis. If it is decreased <24mmol/L in metabolic acidosis.
See for PaCo2. Its normal value for ABG analysis is 40 mm of Hg. If it is increased >40 mm of Hg – respiratory acidosis, if it is decreased <40 mm of Hg –respiratory alkalosis
We see the direction of movement of H+ and HCo3– . If H+ and HCo3– moves in opposite direction – metabolic cause, if H+ and HCo3 – moves in same direction – respiratory cause. If one is normal and another moves – moving factor decides the cause.
We see the direction of movement of PaCo2 and HCo3–. If the movement of PaCo2 and HCo3– is in the same direction – simple cause. If movement of PaCo2 and HCo3– is in opposite direction – mixed disorder. If one value is normal – simple cause. Other way to know about mixed disorder is to know the expected value of PaCo2 from last two digit of pH. If expected value and the actual value match – mixed disorder unlikely. If expected value and actual value differ – mixed disorder likely.
Compensatory change of Acid – Base disorder is decided by Rule of thumb for compensatory changes
Rule of Thumb
PaCo2 falls = 1.2XHCo3– fall in mmol/L
PaCo2 rise = 0.6XHCo3 rise is mmol/L
Acute-HCo3 rise in mmol/L =0.75XPaCo2 rise in KPa.=0.1XPaCo2 in mm of HgChronic-HCo3 rise in mmol/L=2.62 X PaCo2 in KPa. =0.35 PaCo2 in mm of Hg.
Acute-HCo3 fall in mmol/L =1.50XPaCo2 fall in KPa=0.2 X PaCo2 in mm of HgChronic-HCo3 fall in mmol/L=3.75 XPaCo2 fall in KPa =0.5 X PaCo2 in mm of Hg
Where 1 KPa=7.50 mm of Hg.
If Metabolic acidosis or mixed disorder, to conclude we take help of AG/Delta Gap / Gap-Gap ratio and BE. In mixed disorder respiratory acidosis and respiratory alkalosis do not Co-exist.
Then we look for the etiology of the A-B disturbances.
Pattern A – Normal anion gap i.e. hyperchloremic acidosis
Pattern B – Increased anion gap metabolic acidosis.
Pattern A i.e. normal anion gap metabolic acidosis may be due to (a) Inorganic acid (NH4Cl,HCl), (b) gastrointestinal base loss (loss of HCo3 in diarrhoea, small intestinal fistula) and (c) renal tubular acidosis (RTA) –urinary loss of HCo3 in proximal RTA and tubular acid secretion in distal RTA. So the diagnosis of RTA can be made if normal AG with no evidence of gastrointestinal disturbance and urinary pH is inappropriately high>5.5 in the presence of systemic acidosis.
Pattern B is high anion gap metabolic acidosis, causes of which are Methanol poisoning presented with blindness, Uraemia with obevious finding, diabetes mellitus as calculated by plasma glucose, Infection (CBC), Ischaemia(ECG), isoniazide toxicity(history), Lactic acidosis(s.lactate), ethanol toxicity, starvation and salicylate poisoning. Best pneumonic of it is (MUDPILES). Lactic acidosis is of two types. Type1 due to tissue hypoxia and the causes are peripheral generation of lactate as in patient with circulatory failure and shock. Type2 is due to impaired metabolism of Lactate as in liver disease, drugs (Metformin) and toxins.
Sometimes we get the low anion gap metabolic acidosis. The causes are hypoalbuminaemia and multiple myeloma. This condition is read by evaluating the corrected AG (AGc).
Cause of Metabolic Alkalosis
Abnormality that generate HCo3– are called “initiation factor” and abnormality that promote renal conservation of HCo3 are called “maintenance factor” . Metabolic alkalosis remain even after initiation factor have resolved.
Causes of metabolic alkalosis have been classified into two groups based on “saline responsiveness”. One group is saline responsive i.e. sign of extracellular volume contraction – most common pattern. They are vomiting , nasogastric suction , gastric fistula and diuretic therapy.
Another group is saline unresponsive metabolic alkalosis which implies excessive total body HCo3 i.e. HCo3 retention which can be associated with either euvolemia or hypervolemia and the causes are corticosteroid excess status eg . Primary hyperaldosteronism (conn’s syndrome), corticosteroid therapy, cushing’s syndrome and overuse of antacid salt for treatment of dyspepsia. Treat underlying cause. Response to metabolic alkalosis is decrease in minute volume by decreasing the respiratory rate. It starts 30-120 minute after and can take 12-24 hrs to complete.
It seems important to mention that in metabolic alkalosis compensatory increase in PaCo2 rarely exceeds 55 mm of Hg Higher PaCo2 values imply a superimposed primary respiratory acidosis. It is the most common abnormality found in critical care unit. Metabolically alkalotic patients may be sufficiently sick from their underlying disease, so the respiratory compensation is absent and hyperventilation may occur instead. Mortality with metabolic alkalosis in substantial. The mortality rate is 45% in patient with an arterial pH>7.55 and 80% when pH>7.66 . So, severe alkalosis should be viewed with concern.
Causes of Respiratory Acidosis
Common causes of respiratory acidosis are COPD (Type-II RF), ventilatory failure eg. Acute severe asthma, severe pneumonia, respiratory muscle weakness due to neuromuscular disorder, thoracic and skeletal deformaties , other causes are obesity which can make breathing difficult, sedative misuse including overuse of alcohol.
Causes of Respiratory Alkalosis
Common causes of respiratory alkalosis are L-Liver disease, E- embolism, D-drugs(eg. Salicylate, nicotine, xanthine derivatives and progesterone), A-Anxiety, V- patient on ventilator, P- pregnancy, H- heart failure other than this pleurisy, stroke, SAH, high fever, hyperventilation and those living at high altitude.
Response to metabolic acid – base disorder
The response to a metabolic acid-base disorder involves a change in minute ventilation that is mediated by peripheral chemoreceptor located in the carotid body at the carotid bifurcation in the neck.
Response starts within 30-120 m and take 12-24 hrs to complete.
Minute volume = Tidal volume X respiratory rate.
Response of Respiratory acid- base disorder
Secondary response to changes in PaCo2 occurs in the kidney. The renal response is relatively slow and can take 2 or 3 days to reach completion Because of the delay in the secondary response, respiratory acid-base disorder are separated into Acute and chronic disorder.
Mixed disorder means complex disease.
Independently co-existing disorders
Not merely a compensatory response
Dangerous extreme of pH
There can be combination of
Metabolic Acidosis + Alkalosis + Respiratory Acidosis/Alkalosis (Normal AG + High Anion gap + low AG)
Metabolic Acidosis + Respiratory Acidosis -> Leads to severe Acidamia – Poor outcome
Metabolic Acidosis + Metabolic Alkalosis (patient may be normal or near normal pH, AG increased) -> Metabolic Acidosis
Diabetic ketoacidosis + CRF -> Metabolic Acidosis
Sedation + salicylates -> Mixed disorder
Triple acid-base defect -> Alcoholic ketoacidosis may develop metabolic alkalosis due to vomiting and superimpose of Respiratory Alkalosis.