This document provides an overview of acid-base disorders. It discusses normal acid-base physiology and the key factors involved in maintaining balance. It then examines different types of acid-base disorders including metabolic and respiratory acidosis and alkalosis. For each disorder it covers etiology, pathology, clinical features, diagnostic studies, and management. The document also addresses mixed disorders and provides steps for calculating and analyzing acid-base measurements from arterial blood gases.

1. Acid-Bases Simplified
Eric Cucchi MS,PA-C

2. Acid-Base Disorders

3. Acid Base Disorders
H+ + HCO3 <-->H2CO3 <-->CO2 + H2O
Henderson-Hasselbalch equation: pH=pK + log[HCO3-]/ 0.03 × PCO2
non-specific Brønsted acid-base reaction

4. Acid-Base Disorders
 Nml serum pH is 7.35-7.45
 Lower pH is called acidemia and Higher pH is called
alkalemia
 pH < 7.2 is severe acidemia
 pH > 7.55 severe alkalemia
 The body tolerates acidemia much better than alkalemia.

5. Acid-Base Disorders
 Acidemia
 Reduced CO
 Increased Pulm resistance
 Increased arrythmias
 Reduced Cardiovascular response to catecholamines
 Insulin resistence
 Hyperkalemia
 Coma
 Hyperventilation/dyspnea
 Decreased Resp muscle strength and respiratory fatigue.

6. Acid-Base Disorders
 Two organ systems balance the system
 Pulmonary
 Acute
 Chronic
 Renal

7. Normal Physiology
 Etiology
 Acid–base balance is dependent on maintenance of the
hydrogen (H+) ion concentration in body fluids, especially
in the extracellular space, where it is more easily
measured.
 H+ ions at cellular levels have a low concentration
compared with that of other ions.
 Normal pH is 7.35 to 7.45, even minor deviations can affect
physiologic responses.

8. Normal Physiology
 Acidosis is when pH is <7.35, resulting from exposure to an
acid load. Acidemia is the term when the arterial pH has
been measured and reflects this change.
 Alkalosis is when pH is >7.45, resulting from an alkaline
load; alkalemia is when this is reflected by the measured
pH.
 Total venous CO2 is a better measurement of bicarbonate
because it is almost all in the bicarbonate form within in
the serum.Therefore, the CO2 level is  3 mEq/L of the
actual serum bicarbonate level.

9. Normal Physiology
 Pathology
 Normal physiologic processes cause increased amounts of
carbonic acid and noncarbonic acids.The body has
processes that correct these under normal circumstances.

10. Acid-Base homeostatis is
maintained by:
 Buffer: internal, rapid changes that work within a fraction
of a second to change strong acids and bases (alkalines)
into weak ones.
 Respirations: because CO2 and H+ are closely connected,
altering rate and depth of respiration can compensate for
pH shifts.Takes approximately 1 to 3 minutes for an
adjustment to occur.
 (CO2– + H2O2)  H2CO3 (carbonic acid)  H+ and HCO3–
(bicarbonate).

11. Acid-Base homeostatis is
maintained by:
 H+ can then be secreted into the tubules and HCO3– into
blood at the level of the proximal tubules.These changes
in secretion also can be reversed. Can take hours or days to
see changes.
 The body’s attempts at normalization are called
compensation.
 Chronic disease states are rarely compensated fully.
 Full compensation of acute changes is rare, despite
metabolic (renal) and respiratory changes.

12. Metabolic Acidosis
 Etiology
 Characterized by decreased bicarbonate and decreased pH.
 Separated into two categories: with increased anion gap or without
increased anion gap.
 Caused by one of two things: increased acid other than carbonic acid,
or loss of bicarbonate.
 Anion gap is measurement of the difference between anions, which
are negatively charged, and cations, which are positively charged
[(Na+) – (HCO3– + Cl–)], normal equals <12 mEq/L.
 Cations are usually slightly greater in concentration.

13. Metabolic Acidosis
 Anion Gap Metabolic Acidosis
 Need to determine if there is an Anion Gap
 Na – (HCO3 + Chloride)
 Depends of lab > 12 usually there is anion
gap, meaning there is some other
unmeasured anion or cation in the serum.

14. Metabolic Acidosis
 Metabolic acidosis with an increased or widened anion gap
includes:
 Lactic acidosis
 Ketoacidosis—DM, alcohol (ETOH) abuse, starvation.
 Intoxication overdose (salicylates, methanol, ethylene
glycol).
 Uremia

15. Metabolic Acidosis
 Causes (may still have AGMA but cannot find below causes)
 “MUDPILES”
 Methanol
 Uremia
 Diabetic Ketoacidosis (any type of ketoacidosis)
 Paraldehyde
 Iron, isoniazid (INH)
 Lactic Acidosis
 Ethanol, Ethylene Glycol
 Salicylate

16. Metabolic Acidosis
 Metabolic acidosis with normal anion gap includes:
 Diarrhea.
 Mild renal insufficiency.
 Diuretic treatment.
 Renal tubular acidosis types I (classic distal), II (proximal),
and IV (hyporeninemic-hypoaldosteronemic).

17. Metabolic Acidosis
 Pathology
 Pathology of metabolic acidosis is due to underlying
causes.
 Patients may hyperventilate to cause a respiratory
alkalsosis as a compensation mechanism

18. Metabolic Acidosis
 Clinical Features
 If pH is >7.2, usually will be well tolerated.
 Symptoms depend on underlying cause.
 Diagnostic Studies
 ABGs show: ↓ HCO3– and ↓ pH.
 May see a ↓PCO2 if there is a compensatory respiratory
response.
 Calculation of anion gap.
 Other studies as needed for underlying cause.

19. Metabolic Acidosis
 Management
 Treat underlying cause.
 Varying practices on administration of bicarbonate to
correct acidemia. If patient is given too much, can lead to
overcompensation, resulting in respiratory acidosis, and
hypokalemia. Usually correction of initial cause is enough
to resolve the acidemia.
 Alkali administration forType I and II RTA.Type IV RTA
may need potassium restriction.

20. Metabolic Alkalosis
 Etiology
 Characterized by increased bicarbonate and increased pH.
 Happens in two ways: by adding bicarbonate or by the loss
of H+ ions.
 If lost H+ through stomach, will always be associated with
the accompanying loss of chloride.

21. Metabolic Alkalosis
 Mechansims causing a primary metabolic alkalosis:
 Vomiting/too aggressive suctioning of gastric contents.
 Diuretics (depletion of K+ leads to stimulation of proximal tube
secretion and H+causing the so-called contraction alkalosis).
 Overcorrection of bicarbonate in cardiac arrest or respiratory acidosis.
 Volume depletion (especially as the kidney tries to compensate for
other problems; ie, diuretics, chloride depletion).
 Adrenal cortical overactivity

22. Metabolic Alkalosis
 Pathology
 Pathology of the metabolic alkalosis is due to the underlying
cause
 Patients hypoventilate to increase PCO2, as a
compensation mechanism
 Clinical Features
 Weakness, irritability, hyporeflexia and tetany.
 Hypoventilation.
 Orthostatic hypotension
 Rarely symptoms other than those of underlying illness

23. Metabolic Alkalosis
 Diagnostic Studies
 ABGs with showing of: ↑ HCO3–. and ↑ pH.
 May see a ↑ CO2 if there is a compensatory respiratory
response.
 May see a hypokalemia.
 Check for urine chloride levels.
 Other studies as needed for underlying cause.

24. Metabolic Alkalosis
 Management
 Mild alkalosis is well tolerated
 Severe alkalosis (pH > 7.6) needs immediate treatment.
 Treat underlying cause.
 Acetazolamide will increase renal bicarbonate excretion.
 Fluids with sodium chloride (NaCl) as determined by
underlying causes
 Administration of potassium chloride (KCl) as determined
by underlying causes

25. Respiratory Acidosis
 Etiology
 Hypoventilation leading to increased PCO2.
 Disorders that result in hypoventiation may cause
respiratory acidosis
 COPD.
 Paralysis of chest/respiratory muscles (ie, trauma,
neuromuscular disorders).
 Narcotic or sedative-hypnotic overdose.

26. Respiratory Acidosis
 Pathology
 May have an acute or chronic respiratory acidosis.
 Renal compensation occurs with increased H+ excretion and increased
reabsorption of HCO3– at proximal renal tubules.
 Clinical Features
 Symptoms depend on underlying cause.
 CNS depression: as PCO2 regulates blood flow to brain and increases
cerebrospinal fluid (CSF) pressure, leads to generalizedCNS
depression.
 Cardiac output decreases, leading to decreased blood flow to organs.
 Asterixis and myoclonus

27. Respiratory Acidosis
 Diagnostic Studies
 ABGs show: ↑ PCO2 and ↓ pH.
 May see a ↑ HCO3– if there is a compensatory metabolic
response
 Studies determined by underlying cause.
 Management
 Treat underlying cause.
 Hyperventilate to “blow-off” excess CO2 if an acute
respiratory acidosis

28. Respiratory Alkalosis
 Etiology
 Hyperventilation leading to decreased PCO2.
 Disorders that result in hyperventiation may cause respiratory
alkalosis
 Psychiatric disorders, anxiety—most common.
 Fever.
 Head injury.
 CVA.
 Pulmonary disorders: asthma, pneumonia, fibrosis.
 Acetylsalicylic acid (ASA)—in extremely high doses, it increases
respirations by directly affecting the respiratory center

29. Respiratory Alkalosis
 Pathology
 Renal compensation occurs with decreased H+ excretion and
decreased HCO3– reabsorption in proximal renal tubules.
 Clinical Features
 Carpal/pedal spasm.
 Tetnay, paresthesias and perioral numbness
 Lightheadedness.
 Anxiety
 Cardiac output increases due to alkalemia, but can then decrease if
the pH is >7.7.
 Symptoms also depend on underlying cause.

30. Respiratory Alkalosis
 Diagnostic Studies
 Arterial blood gases (ABGs) show: ↓ PCO2 and ↑ pH.
 May see a ↓ HCO3– if there is a compensatory metabolic
response
 Studies determined by need, depending on underlying
cause.

31. Respiratory Alkalosis
 Management
 Treat underlying cause.
 Evaluate underlying cause, then may need to control
ventilation to increase CO2, although usually only in
severe cases.

32. Mixed Acid-Base Disturbances
 Etiology/Pathology
 Many patients present with two to three concomitant acid–base
disturbances.
 Most common combination is respiratory acidosis with a
compensatory metabolic alkalosis; COPD with new onset CHF (sodium
restriction and diuresis leading to metabolic alkalosis).
 pH from any combination can be high, normal, or low, depending on
which is more acute or severe, whether they add to each other or
cancel each other out.
 The only combination that cannot coexist is respiratory alkalosis and
respiratory acidosis, because one is secondary to hypoventilation and
the other to hyperventilation.

33. Mixed Acid-Base Disturbances
 How do we clinically compensate?
 Lungs- this process happens of minutes
 Normal PaCO2 is 45-55 mmHg
 For the CO2 to rise
 RR goes down (Bradypnea)
 Tidal volume (Vt) goes down (Shallow Breathing)
 For the CO2 to decrease (to blow off CO2)
 RR increases (Tachypnea)
 Vt will increase (Deep Breathing)

34. Mixed Acid-Base Disturbances
 Kidneys- this process occurs usually over hours to days.
 Normal Bicarb is 24-32 mmol/L
 For the Bicarb to rise
 Holds on to HCO3 in the proximal tubules
 For the Bicarb to decrease
 Excretes HCO3

35. Some acids can change the osmolality of
the serum (nml factors in nml serum is
sodium, glucose and BUN)
 Osmolar gap = Measured Osms- Calculated Osms
 Calculated Osms = 2 (Na) + Glucose/18 + BUN/2.8
 Can also add ETOH/4.6; Isopropanol/6; Methanol/3.2;
Ethylene glycol/6.2
 Nml Serum Osms 275-290 mOsm/kg
 Nml Osm gap is < 10 mOsm/kg > 20 is very high and
concerning.

36. Calculating ABGs Stepwise
 1) Look at the pH is is high, low, or normal?
 High means alkalosis
 Low means acidosis
 Normal does not mean there is no abnormality

37. Calculating ABGs Stepwise
 2) Look at the CO2 and the HCO3 for the primary acid-base
disorder (or the reason the pH is high or low)
 High PaCO2 (nml 35-45) means Respiratory Acidosis
 Low PaCO2 (nml 35-45) means RespiratoryAlkalosis
 High HCO3 (nml 24-32) means Metabolic Alkalosis
 Low HCO3 (nml 24-32) means Metabolic Acidosis

38. Calculating ABGs Stepwise
 3) Is there appropriate compensation?
 Need to calculate the compensation
 The point of the compensation equations is to determine a
second, if any, acid-base disorder. OR if there is appropriate
compensation by the opposite molecule (HCO3 or CO2)
 When determining the change, example
 If the range is 35-45 (as in PaCO2)
 If the PaCO2 is 20 than the change would be 35-20=15
 If the PaCO2 is 55 than the change would be 55-45=10

39. Calculating ABGs Stepwise
Disorder pH PCO2 HCO3
Respiratory
Acidosis
Low High High
(To compensate)
Respiratory
Alkalosis
High Low Low
(To compensate)
Metabolic Acidosis Low Low
(To compensate)
Low
Metabolic Alkalosis High High
(To compensate)
High

40. Advanced Acid-Base Disorders

41. Calculating ABGs Stepwise
 For a Primary Acute Respiratory Acidosis
 Use the following equations to determine
compensation.
 ΔpH=0.008x ΔPaCO2
 OR
 Δ[HCO3]=0.1 x ΔPaCo2(±3)

42. Calculating ABGs Stepwise
 For Primary Acute Respiratory Alkalosis
Use the following equations to determine
compensation.
ΔpH=0.008x ΔPaCO2
OR
Δ[HCO3]=0.2 x ΔPaCo2

43. Calculating ABGs Stepwise
 For a primary Chronic Respiratory Acidosis
 Use the following equations to determine
compensation.
 PaCO2=2.4 x [HCO3]-22
 OR
 Δ[HCO3]=0.35 x ΔPaCo2(±4)

44. Calculating ABGs Stepwise
 For a primary Chronic Respiratory Alkalosis
 Use the following equation to determine compensation.
 Δ[HCO3]=0.4 x ΔPaCo2

45. Calculating ABGs Stepwise
 For a Primary Metabolic Acidosis
 Use the following equations to determine compensation.
 PaCO2= 1.5 x [HCO3] +8 (±2) (Winter’s Formula)
 OR
 PaCO2≅last two digits of pH
 OR
 ΔPaCO2 =1.2 x Δ[HCO3]

46. Calculating ABGs Stepwise
 For a Primary Metabolic Alkalosis
 Use the following equations to determine compensation
 PaCO2= 0.9 [HCO3]+9 (±2)
 OR
 ΔPaCO2= 0.6 x Δ[HCO3]

47. Calculating ABGs Stepwise
 May use the follow Nomogram to determine the type of
primary acid base disorder. Does not tell you what the
second, if any, acid-base disorder is.

48. Advanced Acid-Base Disorders

49. Calculating ABG Stepwise
 4) Is there and anion gap?
 Only needed to perform if you find a
metabolic acidosis
 Sodium level – (HCO3+Chloride)
 > 12 equals and anion gap

50. Calculating ABGs Stepwise
 5) Is there a third disorder?
 If there is an anion gap acidosis check a Delta-Delta
 H+ + HCO3 <-->H2CO3 <-->CO2 + H2O
 If there is another acid causing the anion gap that is NOT
HCO3 (see “mudpiles”) then you want to see what the
HCO3 is doing in the equation above is it higher than it
should be (alkalosis) or is it lower than it should be
(acidosis)
 Therefore a separate acid is (one in the “mudpiles”
acronym) causing the pH to change.You still need to know
what the bicarb is doing.The Delta-Delta is how you
determine this.

51. Advanced Acid Base
 Delta-Delta
 ΔAG/ΔHCO3 < 1
 Means there is a Non- anion gap acidosis superimposed on top
of an anion gap metabolic acidosis
 ΔAG/ΔHCO3 > 1.5
 Means there is a metabolic alkalosis superimposed on top of an
anion gap metabolic acidosis

52. Case Study #1
 27 yom whom just ingested aspirin in a suicide attempt
presents with the following labs
 Sodium is 145
 Chloride is 97
 HCO3 is 20
 pH is 7.21
 PCO2 is 33

53. Case Study # 1
 What is the pH?
 What is causing it?
 Is there an AG?
 Is there appropriate compensation?
 Is there a third abnormality?
 What is the Diagnosis?

54. Case Study #1
 What is the pH?
 Acidemic
 Sodium is 145
 Chloride is 97
 HCO3 is 20
 pH is 7.21 is lower than 7.35
 PCO2 is 33

55. Case Study # 1
 What is causing it?
 Low Bicarb (metabolic)
 Sodium is 145
 Chloride is 97
 HCO3 is 20 is lower than 24 therefore acidemic
 pH is 7.21
 PCO2 is 33

56. Case Study #1
 Is there an AG?
 Yes
 145 –(97+20)= 28
 Therefore the primary cause is anion gap metabolic acidosis
 Sodium is 145
 Chloride is 97
 HCO3 is 20
 pH is 7.21
 PCO2 is 33

57. Case Study # 1
 Is there appropriate compensation?
 No
 PaCO2= 1.5 x [HCO3] +8 (±2)
 20 x 1.5 +8 (±2) =36-40
 Therefore there is a Respiratory alkalosis (PCO2 is too low (33 is
lower than 36) for a bicarb of 20, Lungs are not compensating
Remember that a PaCO2 that is lower than is should be is alkalotic
and a PaCO2 that is higher than it should be is acidemic)
 Sodium is 145 Chloride is 97 HCO3 is 20 pH is 7.21 PCO2 is 33

58. Case Study # 1
 Is there a third abnormality?
 Need a Delta/Delta as there is a anion-gap metabolic acidosis
 Yes
 ΔAG/ΔHCO3
 28-12/24-20 = 4 (which is > 1.5 which suggest a metabolic
alkalosis due to the bicarbonate)
 A metabolic alkalosis in addition to AGMA
 Remember that a nml AG is < 12 and that the nml range of
Bicarb is 24-32

59. Case Study # 1
 Diagnosis
 Anion gap metabolic acidosis with an acute respiratory
alkalosis and a metabolic alkalosis
 There is a low pH due to an unknown acid (“mudpiles”) there
is “overcompensation” of the lungs and causing the PaCO2
to be too low and therefore, alkalosis. AND the bicarbonate
is too high causing an metabolic alkalosis.

60. Case Study #2
 45 yof presents postop from a ORIF of her LLE and is
complaining of severe pain, below are her labs.
 Sodium is 133
 Chloride is 101
 HCO3 is 22
 pH is 7.50
 PCO2 is 35

61. Case Study # 2
 What is the pH?
 What is causing it?
 Is there an AG?
 Is there appropriate compensation?
 Is there a third abnormality?
 What is the Diagnosis?

62. Case Study #2
 What is the pH?
 Alkalotic
 Sodium is 133
 Chloride is 101
 HCO3 is 22
 pH is 7.50 (pH is greater than 7.45 therefore alkalosis)
 PCO2 is 35

63. Case Study #2
 What is causing it?
 Low CO2 (respiratory)
 Sodium is 133
 Chloride is 101
 HCO3 is 22Yes it is lower than normal but when bicarb is low it is
acidosis and in this case the pH is high suggesting that the primary is
alkalosis.
 pH is 7.50
 PCO2 is 35 is lower than normal, which means ALKALOSIS

64. Case Study #2
 Is there an AG?
 NO
 133 –(101+ 22)= 10
 Normal gap is < 12.Therefore there is no gap here suggesting
there is no “other uknown” acid causing the issue. Also since
this is an alkalosis you do not even need to do this step as
there will not be a gap
 Sodium is 133 Chloride is 101 HCO3 is 22 pH is 7.50 PCO2 is
35

65. Case Study # 2
 Is there appropriate compensation?
 Yes
 Δ[HCO3]=0.2 x ΔPaCo2
 (45-35) x 0.2=2 should be the change in Bicarb
 24 -2 = 22
 Nml Bicarb is 24-32, therefore the bicarb (22) should be
between 22-26 to compensate appropriately and it is
therefore the pt has appropriately compensated
 Sodium is 133 Chloride is 101 HCO3 is 22 pH is 7.50 PCO2 is
35

66. Case Study # 2
 Is there a third abnormality?
 No
 Only can be a third when there is an anion gap metabolic
acidosis

67. Case Study # 2
 Diagnosis
 Acute Respiratory Alkalosis with appropriate Compensation

68. Case Study #3
 65 yom with a PMHx of COPD presents with SOB, his labs
are below.
 Sodium is 150
 Chloride is 100
 HCO3 is 48
 pH is 7.37
 PCO2 is 90

69. Case Study # 3
 What is the pH?
 What is causing it?
 Is there an AG?
 Is there appropriate compensation?
 Is there a third abnormality?
 What is the Diagnosis?

70. Case Study # 3
 What is the pH?
 Normal
 Sodium is 150
 Chloride is 100
 HCO3 is 48
 pH is 7.37, As I mentioned before a normal pH does not mean no
acid base issues.
 PCO2 is 90

71. Case Study # 3
 What is abnormal?
 High CO2 and a High Bicarbonate

72. Case Study # 3
 Is there an AG?
 NO
 150 –(100+48)= 2
 Normal gap is < 12.Therefore there is no gap here suggesting
there is no “other uknown” acid causing the issue. Also since
this is an alkalosis you do not even need to do this step as
there will not be a gap
 Sodium is 150 Chloride is 100 HCO3 is 48 pH is 7.37 PCO2 is
90

73. Case Study # 3
 Is there appropriate compensation?
 Yes-ish
 PaCO2=2.4 x [HCO3]-22
 (2.4x 48)-22=93.2, close to 90
 Sodium is 150
 Chloride is 100
 HCO3 is 48
 pH is 7.37
 PCO2 is 90

74. Case Study # 3
 Is there a third abnormality?
 No
 Only can be a third when there is an anion gap metabolic
acidosis

75. Case Study # 3
 Diagnosis
• Chronic Respiratory Acidosis with compensation

76. Case Study # 4
 This is an advanced question and is only used as an
example of complex clinical scenario that you may come
across at some point in your career. At this point you
should be able to at least diagnosis the acid base disorders

77. Case Study # 4
 48 yom with PMHx of CHF (EF of 25% in 2010) secondary
to hypertension, CAD, ETOH abuse and IDDM presents
comatose. He is immediately intubated and labs are sent.
The labs are as follows.

78. Case Study # 4
 Sodium is 122 (is this high or low?)
 K 4.1
 Chloride is 88
 HCO3 is 12
 BUN 78
 Cr 3.4
 Glucose is 700

79. Case Study # 4
 Calcium of 7.8
 Magnesium of 1.8
 Phosphorus of 1.8
 pH is 6.9
 PCO2 is 30
 Lactate 4.8
 ETOH 267
 Serum Osm 340

80. Case Study # 4
 What is the pH?
 What is causing it?
 Is there an AG?
 Is there appropriate compensation?
 Is there a third abnormality?
 What is the Diagnosis?
 How do you treat this?

81. Case Study # 4
 What is the pH?
 acidemic
 What is causing it?
 Low Bicarb
 Is there an AG?
 Yes
 122 –(88+12)= 22
 Primary cause is a anion gap metabolic acidosis

82. Case Study # 4
 Is there appropriate compensation?
 No there is a respiratory acidosis
 PaCO2= 1.5 x [HCO3] +8 (±2)
 12 x 1.5 + 8 (±2)=24-28
 CO2 is > 28 (30) and therefore there is a respiratory acidosis
 Is there a third abnormality?
 No
 ΔAG/ΔHCO3
 28-12/24-12 = 1.333
 No delta/delta gap

83. Case Study # 4
 Diagnosis
• Acute Anion Gap Metabolic acidosis with a respiratory acidosis
 What else is going on? Well lets find out
 CalculatedOsms = 2 (Na) + Glucose/18 + BUN/2.8 + ETOH/4.6
 CalculatedOsms =2(122) + 700/18 + 78/2.8 + 267/4.6 = 368.78
 Osmolar gap =368.89-340=28.9 (suggesting that the pt has
something other than sodium, glucose and BUN causing an
elevated serum osm in this case it is ETOH)
 Corrected Sodium = Measured sodium + (((Serum glucose -
100)/100) x 1.6) =131.60 mEq/L (Don’t forget to correct serum
sodium for hyperglycemia)

84. Case Study # 4
 Treatment
 NS at 100 ml/hr (need an isotonic solution for rehydration)
 D5NS with 60 meq of KCl with 3 amps of Bicarb at 100 ml/hr
IV (need to replete K and bicarb as pH is dangerously low)
 NS with 30 mmol of KPhos at 50 ml/hr (to replete phosphate)
 Magnesium sulfate 2 gm IV (to replete magnesium)
 Calcium Gluconate 2 gms IV x 1 (to replete calcium)
 Insulin at 10 units/hr IV (to correct glucose, pt may have DKA)

85. FIN