Download ACID*BASE DISORDERS

Normal Acid-Base Homeostasis
Systemic arterial pH is maintained between 7.35 and 7.45
by extracellular and intracellular chemical buffering
together with respiratory and renal regulatory
mechanisms.
The control of arterial CO2 tension (Paco2) by the central
nervous system (CNS) and respiratory systems and the
control of the plasma bicarbonate by the kidneys stabilize
the arterial pH by excretion or retention of acid or alkali.
Normal Values
Arterial
Venous
7.40
<7.35
HCO3
24
24
pCO2
40
>40
>70
<60
pH
pO2
Effects of Metabolic acidosis
Cardiovascular
Impaired cardiac contractility
Arteriolar dilation
Venoconstriction
Centralization of blood volume
Increased pulmonary vascular resistance
Decreased cardiac output
Decreased systemic BP
Decreased hepatorenal blood flow
Decreased threshold for cardiac arrhythmias
Attenuation of responsiveness to catecholamines
METABOLIC ACIDOSIS
METABOLIC EFFECTS
 Insulin resistance
 Inhibition of anaerobic glycolysis
 Reduction in ATP synthesis
 Hyperkalemia
 Protein degradation
 Bone demineralization (chronic)
METABOLIC ACIDOSIS
Neurologic
Respiratory
 Inhibition of metabolism and
 Compensatory
cell-volume regulation
 Obtundation and coma
hyperventilation with
possible respiratory muscle
fatigue
METABOLIC ALKALOSIS
CARDIOVASCULAR
 Arteriolar constriction
METABOLIC
 Stimulation of anaerobic
glycolysis
Reduced coronary blood flow
 Formation of organic acids
Reduced anginal threshold
 Decreased oxyhemoglobin
Decreased threshold for
dissociation
cardiac arrhythmias
 Decreased ionized calcium
 Hypokalemia
 Hypomagnesemia
 Hypophosphatemia
METABOLIC ALKALOSIS
NEUROLOGIC
RESPIRATORY
 Tetany
 Compensatory
Seizures
Lethargy
Delirium
Stupor
hypoventilation with
hypercapnia and hypoxemia
Acid–Base Balance Disturbances
Disorders:
1.



Circulating buffers
Respiratory performance
Renal function
Cardiovascular conditions:
2.


Heart failure
Hypotension
Conditions affecting the CNS:
3.

Neural damage or disease that affects respiratory and
cardiovascular reflexes
Overview of Acid-Base Physiology
 Intracellular acid and base production
 Intravascular transport of acids or bases
 Elimination of acids and bases by kidneys and CO2 by
the lungs
Normal Serum Values
 Normal serum pH:
7.36 – 7.44
 Normal serum [H+] :
40 mEq/L
 Normal serum [HCO3]: 24 mEq/L
 Normal serum pCO2 :
40 mmHg
Acid–Base Balance
Sources of Hydrogen Ions
 Most hydrogen ions originate from cellular
metabolism
 Breakdown of phosphorus-containing proteins releases
phosphoric acid into the ECF
 Anaerobic respiration of glucose produces lactic acid
 Fat metabolism yields organic acids and ketone bodies
 Transporting carbon dioxide as bicarbonate releases
hydrogen ions
Acid–Base Balance
 Hydrogen Ions (H+)
 Are gained
 At digestive tract
 Through cellular metabolic activities
 Are eliminated
 At kidneys and in urine
 At lungs
 Must be neutralized to avoid tissue damage
 Acids produced in normal metabolic activity
 Are temporarily neutralized by buffers in body
fluids
Acid–Base Balance
Figure 27.7
Acid–Base Balance
 Major Buffers in Urine
 Glomerular filtration provides components of
Carbonic acid–bicarbonate buffer system
 Phosphate buffer system
 Tubule cells of PCT
 Generate ammonia

Carbonic acid–
bicarbonate buffer
system
Phosphate buffer system
Ammonium
Ion
Excretion
Figure 26.14
Primary and Compensatory Changes in Acid-Base
Disorders
Disorder
Metabolic
acidosis
Metabolic
alkalosis
Respiratory
acidosis
Respiratory
alkalosis
Primary
Process
HCO3
Compensation
pCO2
HCO3
pCO2
pCO2
HCO3
pCO2
HCO3
MANAGEMENT
General Guidelines in Treatment of Metabolic Acidosis
1. Identifying and correcting the specific underlying cause of the metabolic
acidosis.
2. some types of metabolic acidosis will require HCO3- therapy and some will
not.
3. The decision to use HC03- replacement should be weighed carefully,
depending upon the severity of the acidemia (blood pH) and the type of acidosis.
4. If the pH falls below 7.10, emergency HC03- administration should be
considered, regardless of the cause of the acidosis.
This is especially important if there appears to be respiratory fatigue or developing
hemodynamic instability
5. Never give HC03- without a determination of blood Ph
6. When the decision to give IV bicarbonate is made in the acute setting, calculate the
amount of HCO3- required to increase the HC03- concentration to a specified value,
often several mEq/L above the measured value.
In general, assume that HC03- distributes in about 50% of Body weight (kg).
HC03- deficit = 0.5 X Body weight (kg) X ([HCO3-(desired)]- [HC03(measured)])
7. In severe acidosis (pH in the 7.10 range, HC03- <10mEq/L), the amount of HCO3required to increase the HCO3- concentration to the range 10-12mEq/L is initially
calculated.
For example, in a 70 kg patient, if the HC03- is 6 mEq/L, and it is desired to bring the
HC03- to 10mEq/L:
HC03- deficit = .5 X 70 X (10 mEq/L - 6 mEq/L) = 140mEqn
Give this calculated amount slowly and remeasure pH, HC03- and PCO~after the
HCO3- is given to assess the effect of therapy on the acid-base status.
8. The relationship between amount of HCO3- given and the increase in HCO3- is
not linear: At mild levels of acidemia, 2 mEq/kg will increase the HC03- by roughly 4
mEqL. At severe levels of acidemia, 2 mEq/kg will only raise the HC03- by roughly 2
mEq/L.
9. In the case of an ongoing acidosis, repeated doses of HCO3- may be required until
the underlying cause of the acidosis can be corrected.
Treatment of L Lactic Acidosis
Consider alkali therapy in cases of severe lactic acidosis when the pH falls below 7.10.
When the underlying condition is corrected, however, lactate is converted to HC03-,
and there may be an "overshoot alkalosis" during recovery.
Treatment of Diabetic Ketoacidosis
Diabetic ketoacidosis generally responds well to therapy with insulin,
saline, and potassium.
Because the circulating ketoanions will be converted to HC03- by the liver once
insulin and fluids reverse ketosis, they represent "potential" HC03-.
The majority of patients should not receive HC03- replacement for this reason.
TreatmentofD-Lactic Acidosis
Intravenous fluids and HC03-, but also requires oral antibiotics to eliminate the
offending flora.
Treatment of Alcoholic Acidosis
Treatment consists of the administrationof dextrose-containing saline to
reverse ketogenesis and correct any ECFV depletion.
D5 0.9% saline with supplemental KC1 is usually appropriate for this purpose.
HCO3- is not usually required because the ketones are converted to HC03-, once the
ketosis is reversed and the ECFV normalized.
In the case of alcoholic ketoacidosis with severe hypokalemia, the administration of
Glucose should be postponed until potassium replacement is well underway
Treatment of Distal (Type I) RTA
Determine and correct the cause, if possible, and replace HC03and potassium.
Distal RTA may require an amount of HC03- replacement that roughly equals the
daily production of hydrogen ion (50-100 mEq/ day).
Some of the HC03- should be given as KHC03 to correct potassium
losses as long as there is no renal failure.
Treatment of Type II (Proximal)RTA
HC03- can be given as KHC03 (often as K-citrate) as long as there is no
significant degree of renal failure.
Mild to moderate hypokalemia is common in PRTA and is worsened by
alkali therapy.
Causes of Metabolic Alkalosis
ECFV depletion--chloride depletion syndrome (saline-responsive)
Vomiting/nasogastric suction
Diuretic therapy
Post hypercapnea
Chronic diarrheal laxative abuse
Severe potassium depletion from any cause (saline-resistant)
Mineralocorticoid excess syndromes (saline-resistant)
Primary hyperaldosteronism
Cushing's syndrome
Ectopic ACTH
Secondary hyperaldosteronism
Renovascular disease
Malignant hypertension
Congestive heart failure (with diuretic therapy)
Cirrhosis (with diuretic therapy)
Gitelman's syndrome (saline-resistant)
Bartter's syndrome (saline-resistant)
Metabolic alkalosis maintained by renal failure (saline generally
contraindicated)
Interpreting ABG - Check pH
 Step 1 – evaluate pH, narrow to 2 processes
 If the pH is < 7.36
 Either metabolic acidosis or respiratory acidosis or both
are present
 If the pH is >7.44
 Either metabolic alkalosis or respiratory alkalosis or
both are present
Check pCO2
 Step 2: evaluate pCO2 , narrow to 1 process
 For a pH < 7.36





If pCO2 < 40 - metabolic acidosis
If pCO2 > 40 - respiratory acidosis
For a pH > 7.44
If pCO2 < 40 - respiratory alkalosis
If pCO2 > 40 - metabolic alkalosis
Use proper compensation formula
 For metabolic acidosis:

pCO2 = 1.5 [HCO3] + 8 (WINTER’S)
 For metabolic alkalosis:

pCO2 = 0.9 [HCO3] + 16
Use proper compensation formula
 For respiratory acidosis:





For every increase of 10 in pCO2:
pH decreases by :
0.08 (acute) / 0.03 (chronic)
HCO3 increases by:
1 meq/l (acute) / 3meq/l (chronic)
Use proper compensation formula
 For respiratory alkalosis:





For every decrease of 10 in pCO2:
pH increases by :
0.08 (acute) / 0.03 (chronic)
HCO3 decreases by:
2 meq/l (acute) / 4meq/l (chronic)
Use proper compensation formula
 Simply choose the formula for the one disorder
identified from step 1 and step 2.
 The purpose of using the appropriate formula is to
discover if any other acid-base process is present ( to a
lesser / greater degree )
Identify other disorders
 After applying chosen formula, compare the calculated
(expected) value with the actual value
 If the measured pH, pCO2 , HCO3 doesn’t coincide
with calculated value, then another acid-base
disturbance is present
Identify
other
disorders
 Step 4:
 For a metabolic acidosis: if actual pCO2 is
 higher than calculated – respiratory acidosis
 lower than calculated – respiratory alkalosis
 For a metabolic alkolosis: if actual pCO2 is


higher by (>5mmHg) – respiratory acidosis
lower by (>5mmHg) – respiratory alkolosis
Identify other disorders
 Step 4:
 For a respiratory acidosis/ alkalosis:
 if pH or [HCO3] is higher – metabolic alkalosis
 if pH or [HCO3] is lower – metabolic acidosis
 What if pH is normal? [pCO2 & HCO3] abnormal
 An acidosis and alkalosis / to same degree
Identify other disorders
 Possibilities:
 Metabolic alkalosis and respiratory acidosis
 Metabolic acidosis and respiratory alkalosis
 Metabolic acidosis and metabolic alkalosis
Identify other disorders
pH in normal range ( 7.36 – 7.44)
pCO2 < 36 mmHg
[HCO3 ] < 21 meq/l
pCO2 >44 mmHg
[HCO3 ] > 27 meq/l
Mixed respiratory alkalosis and
Metabolic acidosis
Mixed respiratory acidosis and
Metabolic alkalosis
Anion gap
 Step 5:
 Evaluate anion gap [ Na – (Cl + HCO3)]
 If Elevated – indicate elevated gap -
metabolic acidosis
Check urine pH
 Step 6:
 Urine is normally acidic unless the serum is alkalemic.
 If urine is alkalotic (pH > 6.0) in face of an acidosis, a
RTA or a UTI may be present
Generate differential diagnosis
 Step 7:
 Identifying the primary pathology from analyzing
differential diagnosis of various acid-base
disturbances.
Metabolic acidosis
Metabolic
acidosis
HIGH ANION GAP
(KUSSMALE)
K – Ketosis (Diabetic, Alcoholic,)
U – Uremia
S – Salicylate poisoning
S – Sepsis
M – Methanol poisoning
A – Alcohol (Ethanol Poisoning)
L – Lactic acidosis
E – Ethylene glycol
NORMAL ANION-GAP
RENAL
RTA TYPE I
RTA TYPE II
RTA TYPE IV
EARLY RENAL
FAILURE
NORMAL ANIONGAP
EXTRARENAL
DIARRHOEA
GI-URETHRAL
CONNECTIONS
LOSS OF
PANCREATIC AND
BILIARY
SECRETIONS
CORRECTION
PHASE OF DKA
Metabolic alkalosis
Metabolic alkalosis
Saline (chloride) responsive
Saline (chloride) unresponsive
Diuretics
Adenoma of colon
Misc. (Bartter’s, penicillin
K+ defi., bulimia)
Posthypercapnia
Emesis
Nasogastric tube
Alkali ingestion with decreased GFR
11 β hydroxylase deficiency
Exogenous steroids
Licorice ingestion
Cushing’s syndrome
Hyperaldosteronism
Respiratory acidosis
Respiratory acidosis
Respiratory center depression:
Sedative medications
Brain stem lesions
Central sleep apnoea, myxedema
Neuromuscular failure:
Myopathic and motor end plate dysfunction –
polymyositis, hypokalemia, OPC
Neuropathic – GBS, ALS, status epilepticus
Decreased compliance
Parenchymal – pulmonary
fibrosis, ARDS
Extra parenchymal – abdominal
distension,
severe kyphoscoliosis
Increased airway resistance
COPD, emphysema, severe asthma
Obstructive sleep apnoea
Increased dead space:
Large pulmonary embolus
Emphysema
Respiratory alkalosis
 Hypoxia – pneumonia, pulmonary embolism,
pulmonary edema, interstitial fibrosis
 Hyperdynamic states – pain, fever, sepsis, pregnancy,
hyperthyroidism, hepatic failure, anxiety, mechanical
hyprventilation
 CNS – CVA, tumor, infection, ICH, SAH
 Drugs – salicylates, catecholamines, progestrone,
nicotine
Pneumonics for pnuemonic lovers
Metabolic
Acidosis Anion
Gap
Metabolic
Acidosis NonGap
Acute Resp.
Acidosis
Metabolic
Alkalosis
Respiratory
Alkalosis
“CLEVERPD”
“CHAMPS”
“HARDUPS”
“anything
causing
hypoventilation”
“MUDPILERS”
•Methanol
•Hyperalimentation
•CNS
•Uremia
•Acetazolamide
•DKA/Alcoholic
•Renal
ketoacidosis
•Paraldehyde
•Isoniazid
•Lactic acidosis
•Ethanol
•Renal
failure/Rhabdo
•Salicylates
Tubular
Acidosis
•Diarrhea
•Uretero-Pelvic
shunt
•Post-hypocapnia
•Spironolactone
depression •Contraction
•Airway
•Licorice
obstruction
•Endocrine
•Pulmonary
(Conn/Cushing
edema
/Bartters)
•Pneumonia
•Vomiting
•Hemo/Pneumo •Excess alkali
thorax
•Refeeding
•Neuromuscular
•Posthypercapnia
•Diuretics
•CNS
disease
•Hypocapnia
•Anxiety
•Mech. Ventilation
•Progesterone
•Salicylates
•Sepsis
Interpretation – case 1
 1) A surgeon refers a 22-year old man with a hernia to

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
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

you, with history of renal stones.
pH - 7.29
pCO2 – 32 mmHg
[HCO3] – 15 meq/l
Na+ - 138 meq/l
K+ - 3.0 meq/l
Cl- - 110 meq/l
Urine pH – 6.0
Interpretation – case 1
 Step 1 – pH < 7.36 So,
 pH - 7.29
 Met. / resp. acidosis exist
 pCO2 – 32
 Step 2 – pCO2 < 40 mmHg So,
mmHg
 [HCO3] – 15
meq/l
 At least a Metabolic acidosis exists
 Step 3 – formula
 Expected pCO2 = 1.5[HCO3] + 8;
i.e., = 30
 Actual pCO2 = 32 mmHg
Interpretation – case 1
 Step 4 - any other process involved?
 Actual and expected pCO2 values match closely
 So, a metabolic acidosis, fully compensated exists
 Step 5 – evaluate anion gap
 Anion gap = 138 – (110 +15) = 13
 A normal gap METABOLIC ACIDOSIS exists
Case 2
 A 40 year old lady with obesity and newly detected

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
hypertension
pH - 7.49
pCO2 – 45 mmHg
[HCO3] – 33 meq/l
Na+ - 142 meq/l
K+ - 4.1 meq/l
Cl- - 98 meq/l
Urine pH – 6.5
Case
2
 Step 1 – pH > 7.44 So,
 pH - 7.49
 Met. / resp. alkalosis exist
 pCO2 – 45
 Step 2 – pCO2 > 40 mmHg So,
mmHg
 [HCO3] – 33
meq/l
 At least a Metabolic alkalosis exists
 Step 3 – formula
 Expected pCO2 = 0.9[HCO3] + 16;
 i.e., = 46
 Actual pCO2 = 45 mmHg
Case 2
 Step 4 - any other process involved?
 pH - 7.49
 Actual and expected pCO2 values appr.
 pCO2 – 45






match closely
So, a metabolic alkalosis, fully
compensated exists
Step 5 – evaluate anion gap
Anion gap = 142 – (98 +34) = 10 (normal)
Step 6 – check urine pH = 6.5 ( in
alkalemia)
DD – cushings / hyperaldosteronism
So, a simple Metabolic alkalosis exists
mmHg
 [HCO3] – 33
meq/l
Case 3
 A 25 year old patient with fever, chest pain and

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

breathlessness, was toxic and had a patch in his right
middle lobe was treated for 3 days but respiratory rate
was still high.
pH - 7.47
pCO2 – 21 mmHg
[HCO3] – 15 meq/l
Na+ - 136 meq/l
Cl- - 110 meq/l
Urine pH – 6.5
Case 3

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

Step 1 – pH > 7.44 So,
Met. / resp. alkalosis exist
Step 2 – pCO2 < 40 mmHg. So,
At least a respiratory alkalosis is
present
Step 3 – apply formula for chronic
resp.alk.
If we use pH :
Expected pH – 7.40 + (2x0.03) =
7.46
Actual pH – 7.47
 pH - 7.47
 pCO2 – 21
mmHg
 [HCO3] – 15
meq/l
Case 3
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If we use [HCO3]:
Expected [HCO3] – 24 - (2x4) = 16meq/l
Actual [HCO3] – 15meq/l
Step 4 - any other process involved?
Actual and expected pH &[HCO3] values
appr. match closely
So, a chronic respiratory alkalosis, fully
compensated exists.
Step 5 – evaluate anion gap
Anion gap = 136 – (110 +15) = 11
Step 6 – check urinepH =6.5(alkalemia)
A simple chronic (fully compensated)
resp. alk. exists
 pH - 7.47
 pCO2 – 21
mmHg
 [HCO3] –
15 meq/l
Case 4







If in the same patient – history is not known:
pH - 7.47
pCO2 – 21 mmHg
[HCO3] – 15 meq/l
Na+ - 136 meq/l
Cl- - 110 meq/l
Urine pH – 6.5
 With pH and pCO2 – respiratory alkalosis exists
Case 4

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

Step 3 – apply formula for acute resp.alk.
If we use pH :
Expected pH – 7.40 + (2x0.08) = 7.56
Actual pH – 7.47
If we use [HCO3]:
Expected [HCO3] – 24 - (2x2) = 20meq/l
Actual [HCO3] – 15meq/l
Step 4 - any other process involved?
Actual pH &[HCO3] values are both LOWER
than the expected values. So, which could lower
both?
 Only a metabolic acidosis could lower both
values
 So, a mixed resp. alkalosis and metabolic
acidosis exists.
 pH - 7.47
 pCO2 – 21
mmHg
 [HCO3] – 15
meq/l
Case 5
 A 20 year old man is brought to the emergency room

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
by his sister, who tells you he took a bottle of pills
pH - 7.35
pCO2 – 15 mmHg
[HCO3] – 8 meq/l
Na+ - 140 meq/l
K+ - 3.5meq/l
Cl- - 104meq/l
Urine pH – 5.0
Case 5
 Step 1 – pH < 7.36 So,
 pH - 7.35
 Met. / resp. acidosis exist
 pCO2 – 15
 Step 2 – pCO2 < 40 mmHg So,
mmHg
 [HCO3] – 8
meq/l
 At least a Metabolic acidosis exists
 Step 3 – formula
 Expected pCO2 = 1.5[HCO3] + 8; i.e.,
= 20
 Actual pCO2 = 15 mmHg
Case 5
 Step 4 - any other process involved?
 Actual pCO2 value is less than expected
 Only process that could decrease the pCO2 value
beyond predicted is RESPIRATORY ALKALOSIS
 So, a mixed metabolic acidosis & resp. alk. exists
 Step 5 – evaluate anion gap
 Anion gap = 140 - (104 + 8) = 28 (elevated)
 Urine pH = 5.0 (fits to acidemia)
 A mixed elevated gap Metabolic acidosis and
Respiratory alkalosis exists
 DD – only sepsis/salicylate overdose cause both
 So, given the history salicyalate overdose is possibile
Case 6
 A 57 year old patient with long history of smoking

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
presents without distress and with h/o BOE, ABG
shows:
pH - 7.35
pCO2 – 50 mmHg
[HCO3] – 27 meq/l
Na+ - 143 meq/l
Cl- - 105 meq/l
Urine pH – 5.0
Case 6





Step 1 – pH < 7.36 So,
Met. / resp. acidosis present
Step 2 – pCO2 > 40 mmHg So,
At least a respiratory acidosis is present
Step 3 – apply formula for respiratory
acidosis
 If we use pH : use chronic formula
 Expected pH – 7.40 - (1x0.03) = 7.37
 Actual pH – 7.35
 pH - 7.35
 pCO2 – 50
mmHg
 [HCO3] – 27
meq/l
Case 6
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If we use [HCO3]:

Expected [HCO3] – 24 + (1x3) = 27 meq/l
Actual [HCO3] – 27meq/l

Step 4 - any other process involved?
Actual and expected pH &[HCO3] values appr.
match closely
So, a pure chronic respiratory acidosis, fully
compensated exists.
Step 5 – evaluate anion gap
Anion gap = 143 – (105 +28) = 10(normal)
Step 6 – check urine pH = 5.0 ( fit for acidemia)
A simple chronic fully compensated resp. acid.
exists
pH - 7.35
pCO2 – 50
mmHg
[HCO3] – 27
meq/l
Case 6
 The same patient presents to emergency room 1 month

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later in respiratory distress. He has wheezing and his
RR – 33 B/min
pH - 7.29
pCO2 – 61 mmHg
[HCO3] – 28 meq/l
Na+ - 142 meq/l
Cl- - 100 meq/l
Urine pH – 5.0
Case 6


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

Step 1 – pH < 7.36 So,
Met. / resp. acidosis present
Step 2 – pCO2 > 40 mmHg So,
At least a respiratory acidosis is present
Step 3 – apply formula for respiratory
acidosis, both acute and chronic
 If we use pH : chronic
 Expected pH – 7.40 - (2x0.03) = 7.34
 Actual pH – 7.29
 pH - 7.29
 pCO2 – 61
mmHg
 [HCO3] – 28
meq/l
Case 6

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If we use [HCO3]: chronic
 pH - 7.29
Expected [HCO3] – 24 + (2x3) = 30 meq/l
 pCO2 – 61
Actual [HCO3] – 28 meq/l
mmHg
Actual pH &[HCO3] values are lower than
 [HCO3] – 28
expected:
meq/l
Possibilities:
1) Mixed resp. acid. / small met. acid.
2) Resp. acid. – partially compensated
(acute – on –chronic / mixed acute & chronic
resp. acid.)
Case 6

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If we use pH : acute
Expected pH – 7.40 - (2x0.08) = 7.24
Actual pH – 7.29
If we use [HCO3]: acute
Expected [HCO3] – 24 + (2x1) = 26 meq/l
Actual [HCO3] – 28meq/l
Actual pH &[HCO3] values are higher than
expected:
 Possibilities:
 1) a mixed acute resp.acid./small met. Alk.
 2) a resp. acid. that is partially compensated.
 pH - 7.29
 pCO2 – 61
mmHg
 [HCO3] – 28
meq/l
Case 6
 Step 4 – identify other processes
 Summarising step 3 :
 1)A mixed chonic resp.acid./small met. Acid.
 2)An acute resp. acid./ small met. Alk.
 3) A resp.acid. Not fully compensated
 In our patient we consider the third possibility
since patient is having acute exacerbation of COPD
 So, a mixed acute and chronic resp. acidosis.
Case 7
 A 45 year old diabetic patient presents with
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obtundation
pH - 7.01
pCO2 – 80 mmHg
[HCO3] – 20 meq/l
Na+ - 140 meq/l
K+ - 5.5 meq/l
Cl- - 97 meq/l
Urine pH – 5.0
Case 7
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Step 1 – pH < 7.36 So,
Met. / resp. acidosis exist
Step 2 – pCO2 > 40 mmHg So,
At least a respiratory acidosis exists
Step 3 – formula – acute resp. acid.
If we use pH : acute
Expected pH – 7.40 - (4x0.08) = 7.08
Actual pH – 7.01
 pH - 7.01
 pCO2 – 80
mmHg
 [HCO3] – 20
meq/l
Case 7
 If we use [HCO3]: acute
 pH - 7.01
 Expected [HCO3] – 24 + (4x1) = 28
 pCO2 – 80
meq/l
 Actual [HCO3] – 20 meq/l
 Actual and expected pH & [HCO3]
values are lower than expected:
 Since [HCO3] value is lower as against
an increase a metabolic acidosis coexists
mmHg
 [HCO3] – 20
meq/l
Case 7
 Step 5 – evaluate anion gap
 Anion gap = 140 – (97 +20) = 23(elevated)
 Step 6 – check urine pH = 5.0 ( fit for acidemia)
 DD – predominant respiratory acidosis and an
elevated gap metabolic acidosis (DKA)
Case 8
 A 78 year old patient has been vomiting for several
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days, developed fever and breathlessnessover few
hours. Her RR – 35b/min and has consolidation over
Rt. Base.
pH - 7.69
pCO2 – 20 mmHg
[HCO3] – 25 meq/l
Na+ - 138 meq/l
Cl- - 97 meq/l
Urine pH – 8.0
Case 8
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Step 1 – pH > 7.44 So,
Met. / resp. alkalosis exist
Step 2 – pCO2 < 40 mmHg So,
At least a respiratory alkalosis exists
Step 3 – formula – acute resp. alkalosis
If we use pH :
Expected pH – 7.40 + (2x0.08) = 7.56
Actual pH – 7.69
 pH - 7.69
 pCO2 – 20
mmHg
 [HCO3] – 25
meq/l
Case 8
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If we use [HCO3]:
Expected [HCO3] – 24 - (2x2) = 20meq/l
Actual [HCO3] – 25meq/l
Step 4 - any other process involved?
Actual pH &[HCO3] values are both higher
than the expected values. So, which could
increase both?
Only a metabolic alkalosis could elevate both
values
Step 5 – evaluate anion gap
Anion gap = 138 – (97 +28) = 13(normal)
Step 6 – check urine pH = 8.0 ( fit for
alkalemia)
A mixed acute resp. alk. & met. Alk.
 pH - 7.69
 pCO2 – 20
mmHg
 [HCO3] – 25
meq/l
Case 9
 A 27 year old diabetic patient with 1hr of shortness of
breath. He was nauseated and has had increased
urination over the past 2 days. So, he didn’t take
insulin and was bedridden for past 2 days. He has
family history of hypercoagulable disorder.
Case 9
 pH - 7.40
 pCO2 – 20 mmHg
 [HCO3] – 12 meq/l
 Na+ - 136 meq/l
 Cl- - 102 meq/l
 Urine pH – 5.0, ketones +
 Glucose – 650 mg/dl
For pH in normal range
pH in normal range ( 7.36 – 7.44)
pCO2 < 36 mmHg
[HCO3 ] < 21 meq/l
pCO2 >44 mmHg
[HCO3 ] > 27 meq/l
Mixed respiratory alkalosis and
Metabolic acidosis
Mixed respiratory acidosis and
Metabolic alkalosis
Case 9
 Step 1 – pH is 7.40 (normal)
 pH - 7.40
 pCO2 and [HCO3] are abnormal, So
 pCO2 – 20
 A mixed acid-base disturbance is present
mmHg
 [HCO3] – 12
meq/l
 At least one acidosis and one alkalosis
present
 Alkalosis is exactly balancing acidosis
Case 9
 Step 2
 pH - 7.40
 pCO2 < 40 mmHg and [HCO3] < 25 meq/l  pCO – 20
2
 Respiratory alkalosis & metabolic acidosis
mmHg
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is the process that can cause this
 [HCO3] – 12
Step 3 – check with formula for both
meq/l
Metabolic acidosis:
Expected pCO2 = 1.5[HCO3] + 8; i.e., = 26
Actual pCO2 = 20 mmHg
Actual is lower than expected value, So a
respiratory alkalosis is lowering pCO2
Case 9
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For respiratory alkalosis:
If we use pH :
Expected pH – 7.40 + (2x0.08) = 7.56
Actual pH – 7.40
If we use [HCO3]:
Expected [HCO3] – 24 - (2x2) = 20 meq/l
Actual [HCO3] – 12 meq/l
Step 4 - any other process involved?
Actual pH & [HCO3] values are lower than
expected. So, a metabolic acidosis exists.
 pH - 7.40
 pCO2 – 20
mmHg
 [HCO3] – 12
meq/l
Case 9
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Step 5: evaluate anion gap
Anion gap = 136 – (102+12) = 24
An elevated gap metabolic acidosis is present
Step 6 : check the urine pH
Urine pH = 5.0 (fit for acidemia)
DD – 1) DKA – elevated gap metabolic acidosis
2) an acute respiratory alkalosis - ?PE
So, both equally balances to maintain pH.
Thank you