Acid Base Discorders MIU BCPS 2015

Taher Hegab, PharmD, PhD, BCPS
Identify acid/base disorders

Discuss etiologies for primary acid/base
disorders
Interpret acid/based disorders by interpreting
arterial blood gas & serum chemistry values
Develop optimal pharmacotherapy plans for
acid/base disorders
Acid Base Disorders Taher Hegab
What is acid?
Acids are H+ donors.
What is base
Bases are H+ acceptors
What is pH?
pH = - log [H+]
Range is from 0 14
A change of 1 pH unit corresponds to a 10-fold
change in hydrogen ion concentration
If [H+] is high, the solution is acidic; pH < 7

If [H+] is low, the solution is basic or alkaline ;
pH > 7
What is the normal pH of the blood and ECF?
Blood and Extracellular fluid has a pH of

7.35 7.45
(average 7.4)
Blood is:
A. Acidic
B. Basic
Physiological sources of acids in blood and ECF:

CO2 (volatile acid, from carbohydrate and fat
metabolism)
Metabolism of proteins (sulfur and phosphorus
containing amino acids).
Incomplete oxidation of carbohydrates and fats (lactic
and keto-acid generation)
Acid excretion:
Lung (CO2)
Kidney (non volatile acids, as ammonium and phosphate)
Physiological sources of bases in blood and

ECF:
HCO3- from kidneys (production and reclamation)
Buffers are solutions which can resist changes in pH when

acid or base is added.
Physiological buffers:
Bicarbonate: most important Extracellular buffer
H+ + HCO3- H2CO3 CO2 + H2O
Proteins: important intracellular and plasma buffers

H+ + Hb- HHb
Phosphate: important intracellular and renal tubular buffer

H+ + HPO42- H2PO4-
Ammonia: important renal tubular buffer

H+ + NH3 NH4+
Acidemia is pH < 7.35

Alkalemia is pH > 7.45
Acidosis: process of causing acidemia
Alkalosis: process of causing alkalemia
10
Compensation:
pH is returned toward normal by altering the
component NOT primarily affected
Correction:
pH is returned toward normal by altering the
component PRIMARILY affected
11
Maintaining near constant hydrogen ion

concentration is essential for life
The lung and kidney work to maintain pH
around 7.4
The compensation for pH alteration is
described as respiratory if it was
accomplished through the lung.
Metabolic compensation is done through the
kidney
12
PCO2 is pressure of
CO2 gas in the blood
13
14
15
blood test that is performed using blood from

an artery and is used to measure blood pH
The most common puncture site is the radial
artery at the wrist
Alternate sites include femoral artery
16
Measure pH, CO2, and O2 in arterial blood

Arterial blood is used as is best reflect the
ability of the lung to perform the gas
exchange as O2 and CO2 level are measured
before blood enter tissues
17
Respiratory disease that carries a risk of

inadequate lung ventilation and inadequate
tissue oxygenation (Pulse oximetry indicates an
O2 saturation < 95%)
COPD
Severe asthma
Metabolic disease that carries a risk of acid-base

abnormalities
Acute renal failure
Sepsis
DKA
18
Arterial blood gas sampling is used for:

A. only in patients with pulmonary disease
B. only in patients with renal disease
C. to assess lung ventilation, tissue oxygenation, and
acid base status
19
Arterial
Mixed Venous
pH
7.4 (7.35-7.45)
7.38 (7.33-7.43)
PO2
80-100 mmHg
35-40 mmHg
SaO2
95%
70 75%
PCO2
35-45 mmHg
45-51 mmHg
HCO3
22-26 mEq/L
24-28 mEq/L
20
Primary
Disorder
Primary
problem
Effect
on pH
Compensatory
mechanism
Respiratory
acidosis
PCO2
HCO3
Respiratory
alkalosis
PCO2
HCO3
Metabolic
acidosis
HCO3
PCO2
Metabolic
alkalosis
HCO3
PCO2
21
Disorder
Rate of Compensation
Metabolic acidosis
For 1mEq/L HCO3

PCO2 1 1.5 mmHg
Metabolic alkalosis
For 1mEq/L HCO3

PCO2 0.5 2 mmHg
Respiratory Acidosis
(acute)
For 10 mmHg PCO2 ,

HCO3 1 mEq/L
Respiratory Acidosis
(chronic)
For 10 mmHg PCO2 ,

HCO3 4 mEq/L
Respiratory
Alkalosis (acute)
For 10 mmHg PCO2 ,

HCO3 1-3 mEq/L
Respiratory
Alkalosis (chronic)
For 10 mmHg PCO2 ,

HCO3 2-5 mEq/L
22
23
Normal value:
Check you lab!!!

Classical value: 12 2 mEq/L
Newer instrumentation 9-11 mEq/L
Again check your lab
24
Anion gap is expected to increase with

accumulation of acids that consume
bicarbonate in serum
Example of acid are:
Lactic acid
Ketoacids
Phosphoric acid
Sulfuric acid
25
Steps to perform Acid/Base Analysis

1
Determine if the ABG is acidemic, alkalemic, or normal (assess pH)
Determine if the disturbance is respiratory or metabolic (Assess PCO2

and HCO3)
If the disturbance is respiratory, determine if it is acute or chronic

(Compare measured HCO3 with expected HCO3)
If the disturbance is metabolic acidosis, determine if it is an anion gap

or non-anion gap
If metabolic, determine if the respiratory system is adequately

compensating
If an anion gap exists, are other metabolic disturbances present?

26
27
A 22 year old student is admitted to the ED

after taking an overdose of morphine. He is
unconscious and breathing at a rate of 6-7
breaths per minute.
His ABG values on room air are pH 7.25, PCO2
60, PO2 74, HCO3 26.
What is wrong with him?
28
Primary change is an increase in PCO2

(hypercapnea) due to decreased CO2
excretion
CO2
29
Causes
Central nervous system depression

Drugs, CNS events
Acute airway obstruction

Upper airway, laryngospasm, bronchospasm
Severe pneumonia or pulmonary edema

Impaired lung motion
Hemothorax, pneumothorax
Thoracic cage injury

Flail chest
Neuromuscular disorders
Myopathies, neuropathies
Ventilator dysfunction
30
Signs and symptoms

Acute
Marked restlessness, dyspnea and tachypnea
May progress to stupor and coma
Chronic
SOB and fatigue with or without right-sided heart
failure (cor pulmonale)
31
Acute
Increased PCO2, moderately elevated HCO3 (25-30
mEq/L) and a dramatic decrease in pH
Also see decreased PO2 on room air
Normal plasma Na, K and Cl with an increased total

CO2 content
Compensatory increase in HCO3
For each 10 mmHg increase in PCO2, HCO3 increases1
mEq/L
32
Chronic
Moderately decreased arterial pH (7.25-7.4),
elevated HCO3 and PCO2
In a patient with chronic bronchitis:
PCO2 50-60, PO2 45-60
Normal plasma Na and K

Compensatory increase in HCO3
For each 10 mmHg increase in PCO2, HCO3 increases 4

mEq/L
33
Acute
Goal of therapy: normalize arterial blood pH within
8-24 hours
Administer oxygen; intubate and mechanically
ventilate if needed
34
Chronic
Goal of therapy: make patient comfortable and able
to continue with daily activities
Supportive care
Lung transplantation
35
A 22 yo student is admitted to the ED after

taking an overdose of morphine. He is
unconscious and breathing at a rate of 6-7
breaths per minute.
His ABG values on room air are pH 7.25, PCO2
60, PO2 74, HCO3 26.
What is wrong with him?
36
ABG interpretation:
Step 1: assess pH
pH 7.25 (acidemia)
Step 2:Assess PCO2 and HCO3
PCO2 60 (), HCO3 26 () = respiratory acidosis

Primary disorder = respiratory acidosis
Step 3: Compare measured HCO3 with expected

HCO3
PCO2 by 20, HCO3 by 2 10/1 Appropriate

metabolic compensations for acute respiratory acidosis
37
Assessment:
Acute respiratory acidosis secondary to narcotic
overdose resulting in hypoventilation
Initial management
Oxygen therapy
Naloxone
Intubate and mechanically ventilate, if necessary
38
A 67 yo man presents with complaints of

increased cough and shortness of breath for
the past 12 hrs. PMH includes severe COPD.
Current labs are:
ABG: pH 7.2, PCO2 80, PO2 47
Electrolytes: Na 135, K 4.0, Cl 90, HCO3 34
3 months ago her serum HCO3 was 34
What is your acid/base assessment?
39
Step 1: assess pH
pH 7.2 (acidemia)
PCO2 80 (), HCO3 34 () = respiratory acidosis

Primary disorder = respiratory acidosis

HCO3
PCO2 by 40, HCO3 by 10 10/2.5 Closer to
expected compensation for chronic respiratory
acidosis
40
Assessment:
Chronic respiratory acidosis secondary to severe
COPD
Initial management
Oxygen therapy
Optimize COPD medications
Lung transplant
41
42
A 55 yo woman is admitted to the hospital for

a breast biopsy. While the resident is
explaining the procedure to her she becomes
noticeably anxious and says she feels dizzy.
You note that her respirations have increased
to 45 bpm. The resident orders ABGs and the
results are as follows:
pH 7.5, PCO2 29, PO2 80, HCO3 22.
Interpret this ABG and discuss initial
management for this patient
43
Primary change is a decrease in PCO2 due to

increase in elimination of CO2
CO2
44
Causes:
Anxiety
Hypoxia
Central nervous system disease
Drug-induced: Salicylates, catecholamines,
progesterone
Pregnancy
Sepsis
Mechanical ventilation
45
Signs and symptoms

Neuromuscular irritability
Periorbital and extremity parathesias, muscle cramps,
tinnitus, hyperreflexia, seizures
Cerebral thrombosis or ischemic events in patients

with sickle cell disease
Ischemic changes in ECG or arrhythmias
46
Acute:
pH > 7.45, PCO2 < 35 and a small compensatory
decrease in HCO3
For each 10 mm Hg decrease in PCO2, HCO3
decreases1-3 mEq/L
47
Chronic:
Normal-high pH with hypocapnea, mild
hypokalemia, hyperchloremia and metabolic
acidosis
Compensatory decrease in HCO3
For each 10 mm Hg decrease in PCO2, HCO3 decreases

2-5 mEq/L
48
No specific treatment
Treat cause or underlying condition
Stop hyperventilation, manage pain/anxiety
Use of acidifying agents is generally NOT

recommended
49
A 55 yo woman is admitted to the hospital for

a breast biopsy. While the resident is
explaining the procedure to her she becomes
noticeably anxious and says she feels dizzy.
You note that her respirations have increased
to 45 bpm. The resident orders ABGs and the
results are as follows:
pH 7.5, PCO2 29, PO2 80, HCO3 22.
Interpret this ABG and discuss initial
50
Step 1: assess pH
pH 7.5 (alkalemia)
PCO2 29 (), HCO3 22 () = respiratory alkalosis

Primary disorder = respiratory alkalosis

HCO3
PCO2 by 11, HCO3 by 2 10/2 Closer to

expected compensation for acute respiratory alkalosis
51
Assessment:
Acute respiratory alkalosis secondary to
hyperventilation related to pre-procedure anxiety
Initial management
Calm and reassure the patient
Encourage slow, deep breathing
Have patient breathe into a paper bag or place an
oxygen mask with a CO2 reservoir on the patient
52
53
EW is a 19 yo diabetic female who recently

became engaged. Over the past week she has
been staying up late each night planning her
wedding after working full time during the day.
She has not been watching her diet closely and
developed flu-like symptoms 3 days ago. Today
she called her MD who referred her to the ED. On
assessment in the ED you note rapid breathing
and a fruity odor to EWs breath.
Her ABGs and glucose values are:
pH 7.2, PCO2 21, PO2 94, HCO3 8, glucose 460.
Interpret this ABG and describe initial

54
Primary change is a decrease in plasma HCO3

with a decrease in arterial pH below 7.35
Causes of metabolic acidosis:
Buffering of added strong acids by HCO3
Loss of HCO3 through the GI tract or kidneys
Rapid dilution of extracellular fluid by HCO3-free
solutions
55
56
Increased anion gap acidosis (more acids

added to plasma, increase in unmeasurable
anions)
Renal failure
Ketoacidosis
Diabetic, alcoholic
Lactic acidosis
Rhabdomyolysis
Toxins
Methanol, ethylene glycol, paraldehyde, salicylates
57
Causes of normal anion gap acidosis (loss of HCO3, no

increase in unmeasurable anions)
Renal bicarbonate loss
Renal tubular acidosis

Early renal failure
Carbonic anhydrase inhibitors
Aldosterone inhibitors
GI bicarbonate loss
Hyperalimentation (TPN)
Diarrhea
Ureteral diversion
Small bowel, biliary, pancreatic or fistula drainage
58
Signs and symptoms:

Severe
Kussmaul hyperventilation:
Rapid, deep, irregular respirations
Atrial tachycardia
Ventricular fibrillation
Arterial vasodilation and hypotension
Hyperkalemia
CNS depression
59
Arterial pH, plasma HCO3, PCO2
Compensatory decrease in PCO2:
Increased AG is diagnostic
For each 1 mEq/L in HCO3, PCO2 decreases 1-1.5 mmHg

An indication of the etiology can be made by evaluating the AG
and the plasma K+
Hyperchloremic, hypokalemic metabolic acidosis >> GI

losses of HCO3 and GI or ureteral diversions
Hyperchloremic, hyperkalemic metabolic acidosis >>
decreased ability of kidney to excrete H+ and K+ >>
Hypoaldosteronism or mineralocorticoid deficiencies
60
Goal: restore hemodynamic stability by pH
Correct electrolyte abnormalities
Treat underlying causes
61
NaHCO3
Mainstay of therapy
Initial doses range from 100-150 mEq
Monitor ABG 30 minutes after each dose
Bolus then continuous NaHCO3 infusion
150 mEq NaHCO3 in 1 L D5W
62
NaHCO3
HCO3 deficit:
NaHCO3 dose = (25 [HCO3] observed) X 50% TBW (kg) If the

arterial blood pH < 7.1, use 80% TBW
Administer 30-50% of the calculate dose initially
Increase pH over 3-6 hours, but not > 7.25
Monitor serum K+ closely
ADRs
THAM
Left shift in the oxyhemoglobin curve, increased serum

osmolality, hypernatremia, volume overload, worsening
of intracellular acidosis
63
EW is a 19 yo diabetic female who recently

became engaged. Over the past week she has
been staying up late each night planning her
wedding after working full time during the day.
She has not been watching her diet closely and
developed flu-like symptoms 3 days ago. Today
she called her MD who referred her to the ED. On
assessment in the ED you note rapid breathing
and a fruity odor to EWs breath.
Her ABGs and glucose values are:
pH 7.2, PCO2 21, PO2 94, HCO3 8, glucose 460.
Interpret this ABG and describe initial

64
Step 1: assess pH
pH 7.2 (acidemia)
PCO2 21 (), HCO3 8 () = metabolic acidosis

Primary disorder = metabolic acidosis likely due to
DKA
Initial management
Treat DKA
Insulin, volume resuscitation, correct electrolyte
abnormalities (e.g., hypokalemia)
65
66
A 59 yo male is admitted to the hospital with cc

of increased SOB and acute pulmonary edema.
PHM includes 2 MIs and chronic CHF. Current
medications include metoprolol, ASA, enalapril,
digoxin and furosemide. On day 3, his ABG are as
follows:
pH 7.5, PCO2 48, PO2 85, HCO3 36. His K is 2.5.
Interpret this ABG and discuss interventions for

this patient
67
Primary change is an increase in HCO3 with an

increase in pH
Caused by a loss of H+ from the body or a net
gain in HCO3
68
69
Signs and symptoms:

Mild to moderate:
Usually asymptomatic
Severe:
Compromised cerebral and myocardial perfusion
Neurologic abnormalities
Headache, tetany, seizures, lethargy, delirium, stupor
Hypoventilation
SVT and ventricular arrhythmias
Hypokalemia (muscle weakness)
70
Diagnosis
Characterized by elevated arterial blood HCO3
and pH and hypokalemia
Compensatory increase in PCO2
For each 1 mEq/L increase in HCO3, PCO2 increases
0.5-2 mm Hg
71
Goal: normalize blood pressure, heart rate,

urine output and laboratory parameters
within 24-48 hours
Therapy based on diagnosis of the underlying
disorder
Address precipitating causes
Administration of alkali, mineralocorticoid, potent
diuretics, excessive NG suction, etc.
72
Chloride-responsive metabolic alkalosis:

NS volume replacement
Acetazolamide
HCl infusion
Dose (mEq)=[(0.5L/kg)(Wt kg)][desired current
HCO3]
Ammonium chloride limited value
73
Chloride unresponsive metabolic alkalosis:

Treat underlying cause of mineralocorticoid excess
Diuretics (spironolactone, amiloride, triamterene)
Potassium repletion
74
A 59 y/o male is admitted to the hospital with

c/o increased SOB and acute pulmonary edema.
PHM includes 2 MIs and chronic CHF. Current
medications include metoprolol, ASA, enalapril,
digoxin and furosemide. On day 3, his ABG are as
follows:
pH 7.5, PCO2 48, PO2 85, HCO3 36. His K is 2.5.
Interpret this ABG and discuss interventions for

this patient
75
Step 1: assess pH
pH 7.5 (alkalemia)
PCO2 48 (), HCO3 36 () = metabolic alkalosis

Primary disorder = metabolic alkalosis
Step 3: respiratory compensation
Appropriate respiratory compensation

HCO3 by 12; PCO2 by 8 (between 0.5 - 1)
Acute metabolic alkalosis secondary to diuresis

Hypokalemia secondary to diuresis and metabolic alkalosis
Initial management
NaCl and K replacement
76
77
Two or three acid-base disturbances occur

simultaneously
Determine the expected compensatory response to a
primary acid-base disorder, any value that falls
outside that range represents an additional primary
disorder
Diagnosis
Treatment
Based on history, concurrent medical conditions,

medication history and laboratory abnormalities
Similar to the management for simple acid-base disorders
78
When to suspect a mixed acid base disorder:

1. The expected compensatory response does not
occur
2.
3.
Compensatory response occurs, but level of

compensation is inadequate or too extreme
Whenever the PCO2 and HCO3 becomes
abnormal in the opposite direction. (i.e. one is
elevated while the other is reduced). In simple
acid base disorders, the direction of the
compensatory response is always the same as
the direction of the initial abnormal change.
79
4.
4.
5.
pH is normal but PCO2 or HCO3 is abnormal

In anion gap metabolic acidosis, if the
change in bicarbonate level is not
proportional to the change of the anion gap.
In simple acid base disorders, the
compensatory response should never return
the pH to normal. If that happens, suspect a
mixed disorder.
80
Calculate corrected HCO3:
Corrected HCO3= HCO3 + AG

Corrected HCO3 > 28Alkalosis
Corrected HCO3 < 20Acidosis
Calculate delta ratio

Delta ratio = AG / HCO3
81
AG / HCO3 =1-2 uncomplicated high anion gap

metabolic acidosis
AG / HCO3 <1 Combined high AG metabolic
acidosis and non-AG metabolic acidosis
AG / HCO3 >2 Combined high AG metabolic

acidosis and concurrent metabolic alkalosis
82
A diabetic patient with viral gastroenteritis

presents to your service with the following
laboratory parameters:
Na 130, K 2.5, Cl 80, HCO3 10, pH 7.2, PCO2
25
Interpret this ABG and discuss interventions
for this patient
83
84
Step 5: Is respiratory compensation adequate

PCO2 by 15 for HCO3 by 14 1/1 (expected PCO2
by14-21) Adequate respiratory compensation
No added respiratory disorder
Step 6: Are other metabolic disturbance present?

Corrected HCO3= 10 + (40-12)= 38
Corrected HCO3> 28Alkalosis
85
Assessment:
Anion gap metabolic acidosis (from DKA?) + metabolic
alkalosis (vomiting?)
Initial management:
Treat DKA and volume resuscitate
86
EMTs bring a patient to your ED who was

found down on the street. The patient is
presumed homeless and no PMH is available.
The following labs are obtained on
admission:
Na 125, K 2.5, Cl 100, HCO3 8, pH 7.07, PCO2
28
for this patient
87
88
Step 5: Is respiratory compensation adequate

PCO2 by 12 for HCO3 by 16 < 1/1 (expected
PCO2 by 16-24) Not adequate respiratory
compensation, higher PCO2
Respiratory acidosis

Corrected HCO3= 8 + (17-12)= 13
Corrected HCO3< 20acidosis
89
Assessment:
Anion gap metabolic acidosis + respiratory acidosis +
non anion gap metabolic acidosis
Initial management:
Protect air (intubate) and determine underlying cause
of metabolic acidosis and treat accordingly
90
A patient just arrived to the emergency

department following ingestions of a large
quantity of aspirin. His initial laboratory panel
is as follows:
pH 7.5, PCO2 20, HCO3 15, Na 140, Cl 103
for this patient
91
92

Corrected HCO3= 15 + (22-12)= 25
Corrected HCO3 is between 20-28, no additional
metabolic disorder
93
Assessment:
Respiratory alkalosis + metabolic acidosis
Initial management:
Treat salicylate toxicity
94
Pharmacotherapy: Principles and Practice,

2013.
PNA Taher Hegab 2015
95

Acid Base Discorders MIU BCPS 2015

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Taher Hegab, PharmD, PhD, BCPS

Identify acid/base disorders

Acid Base Disorders Taher Hegab

Acids are H+ donors.

Bases are H+ acceptors

Acid Base Disorders Taher Hegab

If [H+] is high, the solution is acidic; pH < 7

Acid Base Disorders Taher Hegab

What is the normal pH of the blood and ECF?

Blood and Extracellular fluid has a pH of

Acid Base Disorders Taher Hegab

Physiological sources of acids in blood and ECF:

Acid Base Disorders Taher Hegab

Physiological sources of bases in blood and

Acid Base Disorders Taher Hegab

Buffers are solutions which can resist changes in pH when

Proteins: important intracellular and plasma buffers

Phosphate: important intracellular and renal tubular buffer

Ammonia: important renal tubular buffer

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

Acidemia is pH < 7.35

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

Maintaining near constant hydrogen ion

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

blood test that is performed using blood from

Acid Base Disorders Taher Hegab

Measure pH, CO2, and O2 in arterial blood

Acid Base Disorders Taher Hegab

Respiratory disease that carries a risk of

Metabolic disease that carries a risk of acid-base

Acid Base Disorders Taher Hegab

Arterial blood gas sampling is used for:

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

For 1mEq/L HCO3

For 1mEq/L HCO3

For 10 mmHg PCO2 ,

For 10 mmHg PCO2 ,

For 10 mmHg PCO2 ,

For 10 mmHg PCO2 ,

Acid Base Disorders Taher Hegab

Acid Base Disorders Taher Hegab

Check you lab!!!

Acid Base Disorders Taher Hegab

Anion gap is expected to increase with

Acid Base Disorders Taher Hegab

Steps to perform Acid/Base Analysis

Determine if the ABG is acidemic, alkalemic, or normal (assess pH)

Determine if the disturbance is respiratory or metabolic (Assess PCO2

If the disturbance is respiratory, determine if it is acute or chronic

If the disturbance is metabolic acidosis, determine if it is an anion gap

If metabolic, determine if the respiratory system is adequately

If an anion gap exists, are other metabolic disturbances present?

Acid Base Disorders Taher Hegab

A 22 year old student is admitted to the ED

Acid Base Disorders Taher Hegab

Primary change is an increase in PCO2

Acid Base Disorders Taher Hegab