acid base imbalance and electrolyte disturbance in critical ill patients

1. University of Gondar
College of medicine and health science
department of anesthesia
Prepared by Misganaw M
1
Acid- Base disorder and
Electrolyte Imbalance In ICU

2. INTRODUCTION
 Disorders in acid-base balance are commonly
found in critically ill patients.
 Clinicians responsible for these patients need a clear
understanding of acid-base pathophysiology in order to
provide effective treatment for these disorders
2

3. INTRODUCTION
Definition:
 pH is defined as potential of H+ Ion concentration in
body fluid and acid- base balance is:
 Balance of H conc. In extracellular fluid (ECF) .
 To Achieve Homeostasis .
 Balance Between:
 H+ is produced as a by-product of metabolism
3

4. INTRODUCTION
The body maintains a narrow pH range by 3 mechanisms:
1. Chemical buffers (extracellular and intracellular)
react instantly to compensate for the addition or
subtraction of H+ ions.
2. CO2 elimination is controlled by the lungs
(respiratory system). Decreases (increases) in pH result
in decreases (increases) in PCO2 within minutes.
4

5. 3. HCO3- elimination is controlled by the kidneys.
 Decreases (increases) in pH result in increases
(decreases) in HCO3-.
 It takes hours to days for the renal system to compensate
for changes in pH
5

6. INTRODUCTION
 The three different buffering systems are:
1) Respiratory buffering system
• Uses co2
2) Blood buffering system
• Uses bicarbonate, phosphate, and protein
3) Renal buffering system
• Uses bicarbonate, phosphate, and ammonia
6

7. INTRODUCTION
 A normal [H+] of 40 nEq/L corresponds to a pH of
7.40.
 Because the pH is a negative logarithm of the [H+],
changes in pH are inversely related to changes in [H+]
(e.g., a decrease in pH is associated with an increase
in [H+])
7

8. ACID-BASE DISORDERS
 Types of Acid-Base Disorders
 . A respiratory acid-base disorder is a change in [H+] that is a
direct result of a change in PCO2, an increase in PCO2 will
increase the [H+] and produce a respiratory acidosis, while a
decrease in PCO2 will decrease the [H+] and produce a
respiratory alkalosis.
 . A metabolic acid-base disorder is a change in [H+] that is a
direct result of a change in HCO3.
 an increase in HCO3 will decrease the [H+] and produce a
metabolic alkalosis, while a decrease in HCO3 will
increase the [H+] and produce a metabolic acidosis.
8

9.  Metabolic acid-base disorders elicit prompt ventilatory
responses that are mediated by peripheral
chemoreceptors located in the carotid body at the carotid
bifurcation in the neck.
 A metabolic acidosis stimulates these chemoreceptors
and initiates an increase in ventilation and subsequent
decrease in arterial PCO2(PaCO2).
9

10. NORMAL BLOOD GAS ANALAYIS

10
Variables Arterial Blood Mixed Venous Blood
pH 7.35–7.45 7.31–7.41
Pco2 35–45 41–51
Po2 80–100 35–40
HCO3 22–26 22–26
Base
excess
-2 to +2 -2 to +2
O2
saturation
> 95% 70%–75%

11. INTERPRETING ABGS
 a. Acidemia (pH less than 7.35) versus alkalemia (pH
greater than 7.45)
 b. Acidemia and alkalemia refer to an abnormal pH being
either low or high, respectively.
 Acidosis and alkalosis refer to the metabolic or
respiratory processes that led to the abnormal pH.
11

12. ADVERSE EFFECTS OF SEVERE
ACIDOSIS (PH OF 7.25 OR LESS
Impaired cardiac output Increased metabolic demands
Peripheral ischemia
(centralization of blood)
Insulin resistance
Increased pulmonary vascular
resistance
Decreased ATP synthesis
Hypotension Increased protein breakdown
Increased risk of arrhythmias Hyperkalemia
Decreased catecholamine
responsiveness
Diaphragmatic fatigue/dyspnea
Obtundation/coma Hyperventilation
12
Adverse
Effects
of
Severe
Acidemia
(pH
7.25
or
less)

13. ADVERSE EFFECTS OF SEVERE ALKALEMIA (PH OF 7.55
OR GREATER
Arteriolar constriction Hypokalemia
Hypotension Hypophosphatemia
Increased risk of arrhythmias Hypocalcemia/tetany
Decreased coronary blood
flow/decreased angina
threshold
Organic acid production
Seizures
Hypoventilation/hypercapnia/h
ypoxemia
Lethargy, delirium, stupor 13

14. INTERPRETING ABG
 Use of base excess
a. Reflects the amount of base needed in vitro to return the
plasma pH to 7.40 at standard conditions
(Pco2 40 mm Hg, 37°C)
b. Base excess reflects the metabolic component to
interpreting the ABG.
 A pH change of 0.15 is equivalent to a base change of 10
mEq/L
 A decrease in base (i.e, [HCO3-]) is termed a base deficit,
and an increase in base is termed a base excess.
14

15.  Despite its simplicity, it has limitations (J Trauma Acute
CareSurg 2012;73:27-32).
 Crystalloid resuscitation (leading to hyperchloremic
acidosis), exogenous bicarbonate administration, ethanol
ingestion, and acetate/bicarbonate buffer in hemodialysis
or CRRT solutions can lead to erroneous base excess
calculations and errors in interpretation
(J Trauma Acute Care Surg 2012;73:27-32).
15

16. Compensatory response to acid-base disorders
primary Disorder
Serum HCO3
(mEq/L)
Anticipated Pco2 (mm Hg)
Metabolic acidosis ≤ 22 (1.5 x HCO3) + 8 (± 2)
Metabolic alkalosis ≥ 28 (0.7 x HCO3) + 21
Primary disorder Pco2 (mm Hg) Anticipated serum HCO3 (mEq/L)
Respiratory acidosis (acute)a
Respiratory acidosis
(chronic)a
> 45
> 45
[(Pco2 - 40)/10] + 24
[(Pco2 - 40)/3] + 24
Or
HCO3 should increase by ~4 mEq/L per 10-
mm Hg
Respiratory alkalosis (acute)a
Respiratory alkalosis
(chronic)a
< 35
< 35
24 - [(40 - Pco2)/5]
24 - [(40 - Pco2)/2]
Or
For each 10-mm Hg decrease in Pco2, HCO3
should
decrease by ~5 mEq/L
16

17. ACUTE RESPIRATORY ACID-BASE DISORDERS
 Prior to the onset of renal compensation, a change in
PaCO2 of 1 mm Hg will produce a change in pH of 0.008
pH units. ∆pH = 0.008 × ∆PaCO2.
This equation then defines the expected pH for an
acute respiratory acidosis.
Expected pH = 7.40 – [0.008 × (PaCO2 – 40)]
The expected arterial pH for an acute respiratory
alkalosis can be described in the same manner using
following Equation .Expected pH = 7.40 + [0.008 × (40 -
PaCO2)]
17

18. CHRONIC RESPIRATORY ACID-BASE DISORDERS
 When the compensatory response in the kidneys is
fully developed, the arterial pH changes only 0.003 pH
units for every 1 mm Hg change in PaCO2.
 ∆pH = 0.003 × ∆PaCO2
 This equation then defines the expected pH for a
chronic(compensated) respiratory acidosis.
 Expected pH = 7.40 – [0.003 × (PaCO2 – 40)]
 The expected arterial pH for a chronic(compensated)
can be described in the same manner using following
Equation .
 Expected pH = 7.40 + [0.003 × (40 - PaCO2)]
18

19. SIMPLE ACID-BASE DISORDERS
 The first step in acid-base analysis is to identify all abnormalities
in pH, Pco2, and HCO3-.
 The next is to decide which abnormalities are primary and which
are compensatory.
 three rules of thumb to help in making this determination.
 The first rule directs us to look at the pH.
 Whichever side of 7.40 the pH is on, the process or processes
that caused it to shift to that side are the primary abnormalities.
19

20. RULES OF THUMB FOR RECOGNIZING PRIMARY ACID-BASE
DISORDERS
 Rule I
 Look at the pH. Whichever side of 7.40 the pH is on, the
process that caused it to shift to that side is the primary
abnormality
 Principle: The body does not fully compensate for primary
acid-base disorders
 Rule 2
 Calculate the anion gap. If the anion gap is 20 mmol per liter,
there is a primary metabolic acidosis regardless of pH or
serum bicarbonate concentration
 Principle: The body does not generate a large anion gap to
compensate for a primary disorder 20

21.  Rule 3
 Calculate the excess anion gap (the total anion gap minus the
normal anion gap [12 mmol per liter) and add This value to the
measured HCO3-; if the sum is greater than a normal HCO3-
(>30 mmol per liter,). there is an underlying metabolic alkalosis;
if the sum is less than a normal bicarbonate(<23 mmol per liter),
there is an underlying nonanion gap metabolic acidosis
 Princple: 1 mmol of unmeasured acid titrates 1 mmol of
bicarbonate (+ A anion gap = - A IHC03-1)
21

22.  If the pH is lower than 7.40, then an elevated Pco2 (respiratory
acidosis) or a lowered HCO3-(metabolic acidosis) would be
primary abnormalities.
 If the pH is higher than 7.40, then a lowered Pco2 (respiratory
alkalosis) or a raised HCO3-
(metabolic alkalosis) would be primary.
 The pathophysiologic principle behind this rule is that the body
does not fully compensate even for chronic acid-base disorders.
 .
22

23. EVALUATE COMPENSATORY
RESPONSES
 If the compensatory responses are adequate and if there are
additional acid base derangements.
 If there is a primary metabolic acidosis or alkalosis, use the
measured serum HCO3- concentration in Equation to identify
the expected PaCO2
 If the measured and expected PaCO2 are equivalent, the
condition is fully compensated. If the measured PaCO2 is
higher than the expected PaCO2 there is a superimposed
respiratory acidosis. 23

24.  If there is a respiratory acidosis or alkalosis, use the PaCO2
to calculate the expected pH using Equations (for respiratory
acidosis & respiratory alkalosis).
 Compare the measured pH to the expected pH to
determine if the condition is acute, partially compensated, or
fully compensated.
 For respiratory acidosis, if the measured pH is lower than
the expected pH for the acute, uncompensated condition,
there is a superimposed metabolic acidosis. 24

25.  If the measured pH is higher than the expected pH for
the chronic, compensated condition, there is a
superimposed metabolic alkalosis.
 For respiratory alkalosis, if the measured pH is higher
than the expected pH for the acute, uncompensated
condition, there is a superimposed metabolic alkalosis,
 and if the measured pH is below the expected pH for the
chronic, compensated condition, there is a
superimposed metabolic acidosis
25

26.  Consider a patient with a
 PaCO2 23 mm Hg
 a pH o7.54.
 The PaCO2 and pH change in opposite directions so the
primary problem is respiratory and, since the pH is alkalemic,
this is a primary respiratory alkalosis.
 The expected pH for an acute respiratory alkalosis is
described in Equation and is 7.40 + [0.008 × (40 - 23)] =
7.54. 26

27.  This is the same as the measured pH, so this is an
acute, uncompensated respiratory alkalosis.
If the measured pH was higher than 7.55, this would be
evidence of a superimposed metabolic alkalosis
 Over time the pH approaches but does not completely
return to normal.
 This observation allows us to use the direction of pH
change to identify the primary disorder.
27

28. RESPIRATORY ALKALOSIS
 Consider a patient with
 a pH of 7.50,
 a Pco2 of 29 , and HCO3 22 mmol per-liter.
 Because the patient is alkalemic, the low Pco2 is a
primary disturbance and a respiratory alkalosis is present.
The lack of metabolic compensation-that is, the normal
bicarbonate-indicates that the disorder is acute.
28

29. ACUTE RESPIRATOR ALKALOSIS
 Arterial Gas Value Interpretation
Ph. 7.50 Alkalemia
 Pco2*. 29 mm of mercury Respiratory alkalosis
HCO3-. 22 mmol/liter Normal HC03-
Causes
Anxiety, Hypoxia
Lung disease with or without hypoxia
Central nervous system disease
Drug use-salicylates, catecholamines, progesterone
Pregnancy, Sepsis
Hepatic encephalopathy
29

30. RESPIRATORY ACIDOSIS
 What about a patient with
 a pH of 7.25,
 a Pco2 of 60 mmhg, and a HCO3 of 26 mmol per liter?
 This person is acidemic with an increased Pco2 and a normal
bicarbonate: a respiratory acidosis with no evidence of metabolic
compensation.
 What if the next patient presented with a pH of 7.34, aPco2 of 60
mm of mercury, and a bicarbonate of 31 mmol per
liter ? In this person, both the Pco2 and the bicarbonate levels are
elevated, two abnormalities with opposite effects on pH. Which one
30

31.  Because the pH is lower than 7.40, the primary disorder is
still a respiratory acidosis. The elevated bicarbonate (and
near-normal pH) indicates that metabolic compensation has
occurred and that the acidosis is chronic.
Differentiating acute from chronic respiratory acidosis
has important clinical implications. Acute respiratory acidosis is a
medical emergency that may require emergent intubation and
mechanical ventilation, whereas chronic respiratory
acidosis is often a clinically stable condition. Attention to the
pH and bicarbonate values will differentiate acute from
chronic hypoventilation.
31

32. RESPIRATORY ACIDOSIS
 Causes
 Central nervous system (CNS) depression-drugs, CNS event
 Neuromuscular disorders-myopathies, neuropathies
 Acute airway obstruction-upper airway, laryngospasm,
bronchospasm
 Severe pneumonia or pulmonary edema
 Impaired lung motion-hemothorax, pneumothorax
 Thoracic cage injury-flail chest
 Ventilator dysfunction 32

33. METABOLIC ALKALOSIS
 Assess the following blood gas combination:
 pH 7.50,
Pco2 48 mm of mercury, and HCO3 level 36 mmol per
liter.
 Because the patient is alkalemic, the elevated bicarbonate level is
the primary abnormality and the patient has a metabolic alkalosis
with respiratory compensation.
A Pco2 in excess of 55 mm of mercury is
unlikely to be solely compensatory, however, and an additional
primary respiratory abnormality should be sought.
33

34. METABOLIC ACIDOSIS
• Next consider a patient with
• a pH of 7.20, a Pco2 of 21mm hg and a HCO3 level of 8
mmol per liter.
• The patient is acidemic; therefore, the lowHCO3 is the
primary abnormality and a metabolic acidosis with
respiratory compensation is present.
• To help in distinguishing the cause, metabolic acidosis
are commonly divided into those
with and those without an anion gap. 34

35. • Because the serum potassium contributes little to the total
extracellular electrolyte pool, the anion gap is traditionally
calculated by excluding the potassium value and
subtracting the sum of the chloride and bicarbonate (total
carbon dioxide) levels from the sodium concentration.
• In the literature, the normal anion gap is reported as 12 +
2 (mean + SD) mmol per liter
• Anion Gap is Na - (CL + HCO3) = UA – UC
35

36. Metabolic Acidosis With Respiratory
Compensation
 Arteriol Gas value Interpretation
pH .. 7.20 Acidemia
Pco2.. 21 Respiratory compensation
HCO3-- 8 mmol/liter Metabolic acidosis
Causes
Nonanion Gap Anion Gap
GI bicarbonate loss Ketoacidosis
Diarrhea Diabetic
Ureteral diversions Alcoholic
Renal bicarbonate loss Renal failure
Renal tubular acidosis Lactic acidosis
Early renal failure
Carbonic anhydrase inhibitors Rhabdomyolysis
Aldosterone inhibitors Toxins
Hydrochloric acid administration Ethlyene gylcol
Posthypocapnia Paraldehyde
Salicylates
36

37. MIXED ACID-BASE DISORDERS
 In each of the previous examples, we have assumed that
only one primary abnormality is present. In real life,
however, patients often have more than one disorder.
 Mixed acid-base disorders can be identified by determining
the expected compensatory response to a given change in
the primary abnormality and assuming that any value that
falls outside this range represents an additional primary
disorder.
37

38. CONT…..
 Consider a patient with a PaCO2 of 23 mm Hg, a pH of 7.32,
and a serum HCO3 of 15 mEq/L. The pH is acidemic and the pH
and PCO2 change in the same direction, so there is a primary
metabolic acidosis
 Equation should be used to calculate the expected PCO2
 : (1.5 × 15) + (8 ±2) =30.5 ± 2 mm Hg.
 The measured PaCO2 (23 mm Hg) is lower than the expected
PaCO2, so there is an additional respiratory alkalosis. Therefore, this
condition can be described as a primary metabolic acidosis with a
superimposed respiratory alkalosis.
38

39. CONT….
 We have already discussed the first rule of thumb that
directs us to look at the pH to determine which abnormality is
primary if more than one abnormality is present.
 The second rule instructs us to determine the serum
electrolyte values sodium, chloride, and total carbon dioxide-
and to calculate the anion gap. If the anion gap is 20 mmol per
liter or greater, then a metabolic acidosis is present regardless
of the pH or serum bicarbonate concentration.
39

40.  The physiologic principle behind this assertion is that the
body does not generate a large anion gap to compensate even
for a chronic alkalosis. Therefore, a substantial increase in
unmeasured anions indicates a primary disorder, a metabolic
acidosis, regardless of the pH or the bicarbonate concentration
 The greater the anion gap, the more likely it is that a specific
metabolic acidosis will be found. 40

41.  If the anion gap is increased, then the third rule instructs
us to calculate the excess anion gap-the total anion gap
minus the normal anion gap (12 mmol per liter)-and add
this value to the measured bicarbonate concentration (total
venous carbon dioxide content).
 If the sum of the excess anion gap and the measured
bicarbonate is greater than a normal serum bicarbonate
concentration (normal range, 23 to 30 mmol per liter), then
an underlying metabolic alkalosis 41

42.  is present regardless of the pH or measured bicarbonate
value. If the sum is less than a normal bicarbonate
concentration, then an underlying nongap metabolic acidosis
is present.
 The physiologic basis for this statement is that for each
millimole of acid titrated by the carbonic acid buffer system, 1
mmol of bicarbonate is lost through conversion to carbon
dioxide and water and 1 mmol of the sodium salt of the
unmeasured acid is formed. 42

43.  Because each millimolar decrease in bicarbonate is
accompanied by a millimolar increase in the anion
gap, the sum ofthe new (excess) anion gap
and the remaining (measured) bicarbonate value
should be equal to a normal bicarbonate
concentration
43

44. Respiratory Alkalosis and Metabolic Acidosis
 Consider a patient with
 a pH of 7.50, a Pco2 of 20 mmhg, a of HCO3 15 mmol per liter,
a sodium concentration of 140 mmol per liter,
 a chloride level of 103 mmol per liter.
This person is alkalemic with a low Pco2 and a low HCO3
concentration.
 Because the pH is high, the low Pco2 represents a primary
disorder, and a respiratory alkalosis is present. At first
inspection, the low bicarbonate level appears to be in
metabolic compensation for a chronic alkalosis.
44

45.  Follow the second rule, however, and calculate the anion gap: 140
- (103 + 15) = 22 mmol per liter.
 A gap of 22 mmol per liter is greater than would be
expected solely in compensation for a chronic alkalosis and
suggests that a second primary disorder, an anion gap metabolic
acidosis, is also present. If the anion gap had not been calculated,
the underlying metabolic acidosis would have been missed.
 Now, proceed to the third rule and calculate the
excess anion gap: 22 - 12 = 10 mmol per liter, and add it to
the measured bicarbonate level: 45

46. CONT…
 15 mmol per liter. The sum,25 mmol per liter, is normal,
indicating that no further primary disorder
 This patient had ingested a large quantity of aspirin and
displayed the centrally mediated respiratory alkalosis and
the anion gap metabolic acidosis associated with
salicylate overdose.
 Respiratory alkalosis and metabolic acidosis, however,
can occur together in a
variety of related and unrelated clinical conditions
46

47. METABOLIC ACIDOSIS AND METABOLIC ALKALOSIS
 pH 7.40,
 Pco2 40 mmhg, HCO3 24 mmol per liter,
 sodium 145 mmol per liter, and chloride 100 mmol per liter.
This is a seemingly normal set of values until the anion gap
is calculated: 145 - (100 + 24) =21 mmol per liter. The
increased gap defines a metabolic acidosis even though
the pH is normal. Now calculate the excess anion gap: 21 -
12 = 9 mmol per liter, and add it to the measured
bicarbonate: 24 mmol per liter.
47

48.  The sum, 33 mmol per liter, is higher than a normal HCO3
concentration, indicating a metabolic alkalosis is also present.
 These laboratory values are from a patient with chronic renal failure
(causing the metabolic acidosis) who began vomiting (hence the
metabolic alkalosis) as his uremia worsened.
 The acute alkalosis of vomiting offset the chronic acidosis of renal
failure, resulting in .* normal pH. Without a systematic approach to
acid-base disorders, including calculation of the anion gap and of
the excess anion gap, these mixed acid-base disorders could easily
have been overlooked.
48

49. RESPIRATORY ALKALOSIS, METABOLIC ACIDOSIS, AND
METABOLIC ALKALOSIS
 Analyze the following blood gas and electrolyte values:
pH 7.50, Pco2 20 mmhg, HCO3 15 mmol per liter, sodium
145 mmol per liter, and chloride 100 mmol per liter.
 The pH is high, the Pco2 and HCO3 values are low, and
there is an increased anion gap.
 Because the pH is above 7.40, the low Pco2 is a primary
abnormality, and the patient has a respiratory alkalosis
 Because the anion gap is elevated(30 mmol per liter), a
metabolic acidosis is also present.)
49

50. CONT…
 Because the sum of the excess anion gap (18 mmol per
liter and the measured HCO3 (15 mmol per liter) is greater
than a normal c HCO3 concentration, the patient also has
a metabolic alkalosis.
 The near-normal pH reflects the competing effects of these
three primary disorders. This person had a history of
vomiting (the metabolic alkalosis), evidence
of alcoholic ketoacidosis (causing metabolic acidosis), and
findings compatible with a bacterial pneumonia (hence the
respiratory alkalosis).
50

51. CONT…
 These three independent disorders can occur
concurrently in other clinical settings
 Four primary acid-base disorders cannot coexist, as a
patient cannot hypoventilate and hyperventilate at the
same time
51

52. Respiratory Acidosis, Metabolic Acidosis, and
Metabolic Alkalosis
 What if a patient presents with
 a pH of 7.10, a Pco2 of 50 mmhg, a HCO3 level of 15 mmol per
liter, a sodium level of 145 mmol per liter, and a chloride level of
100 mmol per liter?
 The person is acidemic with an elevated Pco2, a lowered
HCO3 , and an increased anion gap (30 mmol per liter).
 Because the pH is low, the increased Pco2
(respiratory acidosis) and decreased bicarbonate
(metabolic acidosis) are both primary disorders.
52

53.  Because the sum of the excess anion gap (18 mmol per
liter) and the measured bicarbonate (15 mmol per liter)
is greater than the normal bicarbonate concentration, a
metabolic alkalosis is also present: three primary
disorders.
 This patient presented in an obtunded state (respiratory
acidosis), with a history of vomiting (metabolic alkalosis)
and laboratory findings consistent with diabetic
ketoacidosis (metabolic acidosis). 53

54. ANION GAP
 The is an estimate of the relative abundance of
unmeasured anions, and is used to determine if a
metabolic acidosis is due to an accumulation of non-volatile
acids (e.g., lactic acid) or a net loss of bicarbonate (e.g.,
diarrhea).
54

55.  To achieve electrochemical balance, the concentration of
negatively-charged anions must equal the concentration of
positively-charged cations.
 All ions participate in this balance, including those that are
routinely measured, such as sodium (Na), chloride (CL),
and bicarbonate (HCO3), and those that are not measured.
 The unmeasured cations (UC) and unmeasured anions
(UA) are included in the electrochemical balance equation
shown below: 55

56. AN ANION GAP
 Na + UC = (CL + HCO3) + UA
 Rearranging the terms in this equation yields Anion Gap
Na - (CL + HCO3) = UA – UC
 The difference (UA - UC) is a measure of the relative
abundance of unmeasured anions and is called the anion
gap (AG).
 The difference between the two groups reveals an anion
excess (anion gap) of 12 mEq/L, and much of this
difference is due to the albumin concentration.
56

57. INFLUENCE OF ALBUMIN
 Another source of error in the interpretation of the AG occurs
when the contribution of albumin is overlooked
 albumin is major source of unmeasured anions, and a 50%
reduction in the albumin concentration will result in a 75%
reduction in the anion gap.
 Since hypoalbuminemia is common in ICU patients, the
influence of albumin on the AG must be considered in all
ICU patients.
57

58.  The anion gap is increased; therefore, the metabolic acidosis is
of the anion gap variety.
 Two methods have been proposed to correct the AG for
the influence of albumin in patients with a low serum
albumin.
 One method is to calculate the expected AG using just the
albumin and phosphate concentrations, since these
variables are responsible for a majority of the normal anion
gap.
The calculated AG using the traditional method [Na - (CL
+HCO3)] is then compared to the expected AG
58

59.  If the calculated AG is greater than the expected AG, the
difference is attributed to unmeasured anions from
nonvolatile acids. Expected
AG(mEq/L)=[2×Albumin(g/dL)]+[0.5×PO4(mg/dL)
 The second method of adjusting the AG in
hypoalbuminemic patients involves the following equation
(where the factor 4.5 is the normal albumin concentration in
g/dL)
 Adjusted AG = Obserbed AG + 2.5 × [4.5 - Measured
Albumin(g/dL)]
59

60.  Data:
 [Na+] = 137 mEq/L;
 [Cl−] = 102 mEq/L;
 [HCO−3] = 24 mEq/L;
 [Normal Albumin] = 4.4 g/dL;
 [Observed Albumin] = 0.6 g/dL.
 Calculations:
 Anion Gap = [Na+] - ([Cl−] + [HCO−
 3]) = 137 - (102 + 24) = 11 mEq/L.
 Albumin-Corrected Anion Gap = Anion Gap + 2.5 x ([Normal Albumin] -
[Observed Albumin]) = 11 + 2.5 x (4.4 - 0.6) = 20.5 mEq/L.
 In this example, the albumin-corrected anion gap reveals the presence of
a significant quantity of unmeasured anions
60

61. ANION GAP AND NONANION GAP
METABOLIC ACIDOSES
 Consider a patient with the following values: pH 7.15, Pco2 15 mm
of mercury, bicarbonate level 5 mmol per liter, sodium level 140
mmol per liter, and chloride value 110 mmol per liter.
 The patient is acidemic with a low Pco2, a low bicarbonate, and an
increased anion gap (25 mmol per liter).
At first glance, this patient has a simple anion gap metabolic
acidosis with respiratory compensation.
 The sum, however, of the excess anion gap (13 mmol per liter),
and the measured bicarbonate (5 mmol per liter) is lower than the
normal bicarbonate concentration, metabolic acidosis are present.
61

62.  suggesting that additional gastrointestinal or renal loss of
bicarbonate has occurred and that both an anion gap and a
nonanion gap
 Diabetic ketoacidosis was responsible for the anion
gap acidosis in this patient. The nonanion gap (hyperchloremic)
acidosis is that phenomenon observed in the recovery phase of
diabetic ketoacidosis due to failure to regenerate bicarbonate
from ketoacids lost in the urine.If the sum of the excess anion gap
and the measured bicarbonate had not been calculated, the
underlying nongap acidosis would not have been appreciated. 62

63. 63

64. ELECTROLYTE IMBALANCE IN ICU
 Electrolyte disturbances are common clinical problems
encountered in the intensive care unit (ICU)
 Associated with increased morbidity and mortality
 Early recognition and prompt correction of these
abnormalities are necessary to avoid catastrophes
64

65. SODIUM PHYSIOLOGY
 Major cation in ECF
 Crucial in determining IC & EC osmolarity
 Serum osmolarity is tightly regulated b/n 275 –
290mOsm/kg
 By the action ADH
 What is the action of ADH?
65

66.  Serum osmolarity = (2 X Na) + (glucose/18 ) +
(urea/2.8)
 Osmoreceptors in the hypothalamus can detect
changes of 1% osmolarity
 The ratio of sodium b/n plasma and interstitial fluid is 5:1
at equilibrium
66

67.  Extracellular sodium balance is determined by
sodium intake relative to Na excretion – critically ill
pts –can’t
 We consume far more salt than we need
 The kidneys main function in Na balance is
excretion of excess Na
 Sodium requirements vary with age
67

68.  AgeAge Daily Na requirement
{meq/kg/day}
 Preterm infants {<32weeks GA} 3 mEq/kg/day
 Term infants 2 – 3 mEq/kg/day
 Adult 1.5meq/kg/day
68
Urinary excretion of sodium represents most of Na
loss
Extra renal Na loss – profuse sweating, burns,
severe vomiting or diarrhea

69. HYPONATREMIA
 Hyponatremia may be present on ICU admission or can
develop later.
 In either case it is associated with poor prognosis.
 A recent study of 151,486 adult patients from 77 intensive
care units over a period of 10 years demonstrated that
severity of dysnatremia is associated with poor outcome in
a graded fashion.
 Another study reported that both ICU-acquired
hyponatremia and hypernatremia were associated with
increased mortality
69

70.  Hyponatremia-induced cerebral edema occurs with
sudden fall in the serum sodium concentration, usually
within 24 hours.
 Clinically, hyponatremia manifests with primarily
neurologic symptoms.
 Their severity depends on rapidity of the change in the
serum sodium concentration in addition to level of
sodium. 70

71.  When serum sodium falls acutely below 120 meq/L,
patients become symptomatic with lethargy, apathy,
confusion, seizures and coma.
 When determining the cause of hyponatremia, serum
osmolality must be obtained to determine whether the
hyponatremia reflects true hypotonicity
 Hyponatremia can occur in patients who are
hypotonic, normotonic, or hypertonic 71

72.  Plasma Na < 135 mmol/L
 Mild Na+ 125 – 134 mmol/L
 Moderate Na+ 120 – 124 mmol/L
 Severe Na+ < 120 mmol/L
72

73. CAUSES OF HYPONATREMIA AS RELATED TO
INTRAVASCULAR VOLUME STATUS
73

74.  Normal osmolarity – pseudohyponatraemia
 Due to a measurement error which can result when
the solid phase of plasma (that due to lipid and
protein) is increased.
• Typically caused by hypertriglyceridemia or
paraproteinaemia.
 High osmolarity - translocational hyponatraemia
• Occurs when an osmotically active solute that
cannot cross the cell membrane is present in the
plasma.
74

75.  Most solutes such as urea or ethanol can enter the
cells, and cause hypertonicity without cell dehydration.
• However, in the case of the insulinopenic diabetic
patient, glucose cannot enter cells and hence water is
displaced across the
cell membrane, dehydrating the cells and ‘diluting’ the
sodium in the serum.
• This is also the cause of hyponatraemia seen in the
TURP
syndrome, in which glycine is inadvertently infused to
75

76. MAJOR CAUSES OF NATRIURESIS AND
ANTINATRIURESIS
76

77. HYPOVOLAEMIC HYPONATREMIA
 Loss of both sodium and water, but proportionately more
sodium.
• Caused by solute and water losses from either a renal
or gastrointestinal source.
• Usually these patients are consuming water or
hypotonic fluid, although not in quantities sufficient to
restore normovolaemia.
• An estimation of the urinary sodium level can be
helpful: a level
below 30mmol.l-1 suggests an extrarenal cause, while a
level
77

78. EUVOLAEMIC HYPONATRAEMIA
 The most common form seen in hospitalized patients.
 May have a slight increase or decrease in volume, but it is
not clinically evident, and they do not have oedema.
 The most common cause is the inappropriate
administration of hypotonic fluid.
 The syndrome of inappropriate ADH secretion (SIADH)
also causes euvolaemic hyponatraemia; in order to make
this diagnosis one must first exclude renal, pituitary,
adrenal or thyroid dysfunction, and the patient must not be
taking diuretics.
78

79. HYPERVOLAEMIC HYPONATRAEMIA
 Characterized by both sodium and water retention, with
proportionately more water.
• Therefore have an increased amount of total body
sodium.
• Causes are all characterised by disordered water
excretion, and are usually easy to diagnose.
79

80. CLINICAL MANIFESTATIONS OF
HYPONATREMIA
 Speed of onset is much more important for
manifestation of symptoms than the absolute Na+
concentration however, levels between 125mmol.l-1
and 150mmol.l-1 are often asymptomatic.
 Outside this range there is an increasing frequency of
nausea, lethargy, weakness and confusion, and levels
above 160mmol.l-1 or below 110mmol.l-1 are strongly
associated with seizures, coma and death. 80

81. MANAGEMENT OF SYMPTOMATIC
HYPONATRAEMIA
 The dose of sodium required to correct a deficit may be
calculated using the following formula:
 Na deficit = TBW X {desired Na – present Na}
 The optimal rate of correction seems to be 0.6 to 1
mmol/L/hr until the sodium concentration is 125 mEq/L;
correction then proceeds at a slower rate. 81

82. MANAGEMENT OF SYMPTOMATIC
HYPONATRAEMIA
 Speed of onset determines speed of correction
 Acute hyponatraemia < 48hr
 Maximum increase 2 mmol/L/hour until symptoms
resolve.
 Hypertonic saline 3% 1.2-2.4 mL/kg/hour through a large
vein
 If fluid excess give frusemide
82

83.  Rapid correction can cause central pontine
myelinosis, subdural haemorrhage and cardiac
failure
 Treat the cause
 Consult an endocrinologist
 Monitor Na+ levels and re-evaluate clinically
83

84.  Speed of onset determines speed of correction
 Chronic hyponatraemia > 48hr
 Maximum increase 0.5 mmol/L/hour (10 mmol day)
 Use 0.9% normal saline
 If fluid excess give frusemide
 If SIADH fluid restrict
84

85. HYPERNATREMIA
85

86. MAJOR CAUSES OF HYPERNATREMIA
 Inadequate intake of water
 Lack of ADH, or
 Excessive intake of sodium (e.g., with solutions
containing a high sodium concentration, such as
sodium bicarbonate or hypertonic saline)
86

87. MAJOR CAUSES OF HYPERNATREMIA
87

88. CAUSE OF HYPERNATREMIA
88

89. Diabetes insipidus
 A deficiency of ADH (vasopressin) or inability of the
kidney to produce a hypertonic medullary interstitial
 Diabetes insipidus is characterized by production of a
large volume of dilute urine
 Deficiency of vasopressin is known as central diabetes
insipidus and is an endocrine disorder 89

90.  Vasopressin deficiency is seen after pituitary surgery, basal
skull fracture, and severe head injury
 Nephrogenic diabetes insipidus is defined as renal tubule
cell insensitivity to the effects of vasopressin
 Nephrogenic diabetes insipidus can result from any systemic
or kidney disease that impairs tubular function.
 Various insults to the collecting system, such as after
ureteral obstruction or medullary cystic disease, lead
to decreased sensitivity to vasopressin 90

91.  Patients with continued urine output of more than
100 mL/hr who develop hypernatremia
should be evaluated for diabetes insipidus by
determining the osmolalities of urine and
serum
If the urine osmolality is less than 300
mOsm/L, and serum sodium exceeds 150
mEq/L, the diagnosis of diabetes insipidus is
likely
91

92. Management of Hypernatremia
during Diabetes insipidus
 In patients with central diabetes insipidus, a vasopressin
analog called desmopressin acetate, may be administered
to correct the deficiency in vasopressin
 The underlying cause of nephrogenic diabetes insipidus
should be sought and treated if possible.
 A slight increase in serum sodium concentration (e.g., 3 to
4 mmol/L) above baseline values elicits intense thirst
 The lack of thirst in the presence of hypernatremia in a
mentally alert patient indicates a defect in the
Osmoreceptors or in the cortical thirst center
92

93. Signs and symptoms of hypernatremia
 The most common - lethargy or mental status changes,
which can proceed to coma and convulsions.
 Additional include thirst, shock, peripheral edema,
myoclonus, ascites, muscular tremor, muscular rigidity,
hyperactive reflexes, pleural effusion, and expanded
intravascular fluid volume
93

94.  With acute and severe hypernatremia, the osmotic shift
of water from the cells can lead to
shrinkage of the brain with tearing of the meningeal
vessels and intracranial hemorrhage
 Slowly developing hypernatremia is usually well
tolerated because of the brain's ability to regulate its
volume
94

95.  The speed of correction depends on the rate of
development of hypernatremia and associated
symptoms
 Restore normal osmolality and volume and includes
removal of excess sodium by the administration of
diuretics and hypotonic crystalloid solutions
 Rapid correction offers no advantage and may be
extremely harmful or lethal because it may result in brain
edema
 A maximum of 10% of the serum sodium concentration,
or about 0.7 mmol/L/hr, should be the goal rate of
correction
95

96. Management of hypernatremia and
intravascular volume ass’t
 Correct slowly over at least 48 hours to prevent cerebral
oedema, convulsions and central pontine myelinolysis
 If hypovolaemic – (total body Na deficient) 0.9% saline
until hypovolaemia corrected
 If euvolaemic – (TBW depletion) treat with 5% dextrose
 If hypervolaemic – (Na excess) diuretics or 5% dextrose*
 * Caution with 5% dextrose may correct Na too rapidly,
monitor serum Na 1-2 x per day 96

97. Hypokalemia
 Hypokalemia (<3.5 mEq/L) may occur because of an absolute
deficiency or redistribution into the intracellular space
 A reduction in serum K of 1 mEq/L indicates a net loss of 100 to
200 mEq of K in a normal adult
 Hypokalemia in the range of 2 to 2.5 mEq/L is likely to cause CM
 Clinical manifestations are muscular weakness, arrhythmias, and
electrocardiographic abnormalities
Sagging of the ST segment, depression of the T wave, U wave
elevation, atrial fibrillation and premature ventricular systoles
97

98. Major causes of Hypokalemia
98

99.  Surgical stress may reduce the serum potassium concentration
by 0.5 mEq/L
Counter balanced in SUX induced increment 0.5 mEq/L
 The administration of exogenous catecholamines, such as
terbutaline and epinephrine also decreases potassium levels
 If perioperative therapy is indicated, intravenous potassium
chloride should be used
 The rate of potassium administration is typically limited to
approximately 0.5 mEq/kg/hr
99

100.  The typical replacement rate is 10 to 20 mEq/hr for a normal
adult with constant monitoring of the electrocardiogram
 Safe administration of potassium is enhanced by
the use of continuous electrocardiogram monitoring,
bedside potassium measurement, and
delivery with an infusion pump 100

101. Hyperkalemia
 Hyperkalemia (>5.5 mEq/L) can occur in various disease states
In response to drugs that diminish renal potassium excretion
or
After sudden transcellular shifts of potassium from the
intracellular fluid to the ECF
 Potentially lethal hyperkalemia during anesthesia may occur
with reperfusion of a large vascular bed after a period of
ischemia (usually >4 hours)
 Ischemia results in significant acidosis in the affected area,
which causes an outflow of intracellular potassium
101

102.  Any condition or drug resulting in adrenal inhibition
or decreasing aldosterone levels can cause potassium
retention
 Hyperkalemia also should be considered in the
conditions with lysis of the cellular components of
blood.
•Drugs Causing
Hyperkalemia
 Spironolactone
 Angiotensin II antagonist
Angiotensin-converting enzyme inhibitors
Succinylcholine
102

103. Major Causes of
Hyperkalemia
103

104.  Acute hyperkalemia is more poorly tolerated than
chronic hyperkalemia
 The most common cause of chronic hyperkalemia
occurring with anesthesia is renal failure
 A patient undergoing anesthesia with even moderately
elevated potassium concentration (>5.5 mEq/L) should
have continuous ECG monitoring
104

105.  Hyperkalemia can cause muscle weakness and
paralysis
 Alterations in cardiac conduction increase automaticity
and enhance repolarization
 Mild elevations in K levels (6 to 7 mEq/L) may
manifest with peaked T waves; as levels approach 10 to
12 mEq/L, a prolonged P–R interval, widening of the
QRS complex, ventricular fibrillation, or asystole can
occur
105

106. Treatments
 Physiologic antagonists (calcium)
 Agents to shift potassium into cells (glucose, insulin,
hyperventilation, bicarbonate, and β-adrenergic agonists)
 Drugs and treatments to eliminate potassium from the body
(diuretics, aldosterone agonists, dialysis
 Stabilization of the heart with IV calcium (500 mg of calcium
chloride or 1 g of calcium gluconate in an adult)
 Redistribution of potassium from the plasma into cells
 Intravenous glucose, insulin, and bicarbonate (1 mEq/kg) and
hyperventilation are the major therapies
106

107.  Intravenous regular insulin, 5 to 10 U, administered with
dextrose at a dose of 25 to 50 g (i.e., one to two 50-mL
ampoules of 50% dextrose solution),
reduces serum potassium levels within 10 to 20 minutes,
and the effects last 4 to 6 hours
 Resin exchange, dialysis, diuretics (e.g., furosemide, 20-40
mg IV), aldosterone agonists (e.g., fludrocortisones), and
inhaled or intravenous β-adrenergic agonists are
established additional therapies
107

108. Hypomagnesaemia
Causes of hypomagnesaemia
• Decreased Intake
• Inappropriate IV fluid/ Nutritional replacement
therapy
• Malabsorption
• Dietary deficiency
• Increased Loss
• Diuretics
108

109. • Nephrotoxic drugs (aminoglycosides)
• Alcohol abuse
• Diarrhoea, small bowel fistulas
• Excessive nasogastric drainage
• Genetic renal disorders i.e. Gitelman’s syndrome
• Redistribution
• Massive transfusion of citrated blood
• Insulin administration
• Hyperparathyroidism
109

110. Manifestations
• Anorexia, nausea, muscular weakness, cramps,
• lethargy and weight loss are early symptoms.
• Later, hyperirritability, hyperexcitability,
• muscle spasms, stridor and tetany can ensue, and
ultimately convulsions.
• Hypertension is common and pulmonary oedema
can occur. 110

111.  The ECG may show prolonged PR and QT
intervals, ST depression and flattening of T
waves.
 Supraventricular and ventricular
tachyarrhythmias may also occur
111

112. • Management???
112

113. Hypermagnesemia
• 10-12.5mmol/L - CARDIAC ARREST
• 5-7.5mmol/L - RESPIRATORY PARALYSIS
• 4-5mmol/L - MUSCLE WEAKNESS
• Initial clinical presentation includes headache, nausea, vomiting
and diarrhoea, hypotonia and muscle weakness.
113

114. • IV calcium gluconate (2.5-5mmol) can antagonise the
actions of magnesium and therefore is useful in the
immediate management of patients with severe
hypermagnesaemia, followed by inducing a diuresis
or dialysis.
114

115. Chloride
• An abundant an ion in ECF.
• Moves in and out of cells with Na+
• Found mainly CSF, bile, gastric and pancreatic
fluids.
• Helps transport carbon dioxide to RBC
115

116. • Hyper or hypochloremia?
116

117. Reading Assignment
• Calcium?
• Phosphate?
117

118. 118