Acid–Base Imbalance_A Case-based Overview

Acid–Base Imbalance
A Case-based Overview
Prepared and presented by:
Marc Imhotep Cray, M.D.

Capsular Overview
1. Arterial pH ([H+] ) must be maintained in a close range (7.35-7.45)
for individual to be alive
2. Arterial pH is based on relationship of plasma bicarbonate (HCO−
3)
to carbon dioxide tension (Pco2 )
3. Simplify Henderson–Hasselbach equation to: pH = HCO−
3 / Pco2
4. Metabolic disorder = ∆ HCO−
3 = kidney = slow response
5. Respiratory disorder = ∆ Pco2 = lung = fast response
6. A disorder that is primarily associated w ventilation, e.g.,
pneumonia, drug overdose, causes a respiratory acid-base disorder
with a compensatory metabolic response
7. A disorder that is primarily assoc. w. renal disease, an
endocrinopathy, or GI disease causes a metabolic acid-base disorder
w a compensatory respiratory response Examples include severe
vomiting or diarrhea; uncontrolled diabetes; and uremia
2

Definition
Acid–base imbalance is an abnormality
of human body's normal balance of acids
and bases that causes plasma pH to deviate
out of normal range (7.35 to 7.45)
3

Background Definitions
4
 Acidemia versus Acidosis
 Acidemia describes an increased concentration of H+ in
plasma
 Acidosis is a process in which there is an addition of H+ to the
body this may or may not cause acidemia
 Acids and Bases
 Acids are compounds that are capable of donating H+
 Bases are compounds that are capable of accepting H+
 When an acid (HA) dissociates, it yields H+ and its conjugate
base or anions (A−)
HA ⇌ H+ + A−

Arterial pH or H+ Conc.
5
[H+] (pH) in body fluids must be maintained in a
very narrow range
 If this concentration rises H+ will bind to important
compounds (proteins) this changes their charge, shape,
and possibly function with potentially dire consequences
 Accordingly, there is a H+ removal process (the bicarbonate
buffer system)
 The strategy that permits this H+ removal system to function is
that a low PCO2 obliges H+ to react with HCO−
3
HCO−
3 + H+ ↔ CO2 (venous)+ H2O
 Therefore, a high [H+] stimulates breathing (lungs) & thereby
ensures that there is a lower [CO2] in each liter of alveolar air 
and hence in arterial blood

H+ Concentration (2)
6
As shown in eq. above this safe way to remove H+
leads to a deficit of HCO3
−
 Accordingly, one must have another system that adds new
HCO3
− to body as long as acidemia persists this is task of
kidney
Most important component is excretion of ammonium
ions (NH4
+) b/c kidney makes NH4
+ + HCO3
− in same
metabolic process:
Glutamine →2NH4
+ + 2HCO3
−
NB: Maintaining a urine pH of 6 will permit a high rate of excretion of NH4
+
diminishes risk of precipitation or uric acid

Classification
 An excess of acid is called acidosis or acidemia
 An excess in bases is called alkalosis or
alkalemia
 Process that causes imbalance is classified based
on etiology of disturbance (respiratory or
metabolic) and direction of change in pH
(acidosis or alkalosis)
7

Classification (2)
simple acid–base disorders
process pH carbon dioxide compensation
metabolic
acidosis
down down respiratory
respiratory
acidosis
down up renal
metabolic
alkalosis
up up respiratory
respiratory
alkalosis
up down renal
Presence of only one of above derangements is called
a simple acid–base disorder
8

Mixed disorders
In a mixed disorder more than one derangements is
occurring at same time
Mixed disorders may feature an acidosis and alkalosis
at same time that partially counteract each other, or
there can be two different conditions affecting pH in
same direction
 Phrase "mixed acidosis", for example, refers to metabolic
acidosis in conjunction with respiratory acidosis
 Any combination is possible, except concurrent
respiratory acidosis and respiratory alkalosis since a
person cannot breathe too fast and too slow at the same time...
9

Causes
There are numerous reasons that each of four
processes can occur (detailed to follow)
Sources of acid gain include:
1.Retention of carbon dioxide
2.Production of nonvolatile acids from
metabolism of proteins and other organic
molecules
3.Loss of bicarbonate in feces or urine
4.Intake of acids or acid precursors
10

Causes (2)
Sources of acid loss include:
1.Use of hydrogen ions in the metabolism of
various organic anions
2.Loss of acid in the vomitus or urine
3.Gastric aspiration in hospital
4.Severe diarrhea
5.Carbon dioxide loss through hyperventilation
11

Compensation
Body's acid–base balance is tightly regulated
Several buffering agents exist which reversibly bind
hydrogen ions and impede any change in pH
 Extracellular buffers include bicarbonate and ammonia
 Proteins and phosphate act as intracellular buffers
o Bicarbonate buffering system is especially key as
carbon dioxide (CO2) can be shifted through carbonic
acid (H2CO3) to hydrogen ions and bicarbonate (HCO−
3 )
HCO−
3 + H+ ↔H2CO3↔ CO2+ H2O
12

Compensation (2)
 Expected degree of compensation can be
calculated from “renal rules”
 These rules predict appropriate compensatory
responses for simple acid–base disorders (see Table
that follows)
 For example, in simple metabolic acidosis,
renal rules can determine whether lungs are
hyperventilating to extent expected for a given
decrease in HCO−
3 concentration
13

Compensation (3)
 If HCO3 concentration is ↓ to 8 mEq/L (nml, 24
mEq/L) rules can be used to predict expected
decrease in Pco2 for this decrease in HCO−
3
 If actual Pco2 is same as predicted Pco2
respiratory compensation is considered appropriate,
and no other acid–base abnormality is present
 If actual Pco2 is different from Predicted value
then another acid–base disorder is present (in
addition to metabolic acidosis)
14

Compensation (4)
 Renal rules (slide 17) tell us that in simple metabolic acidosis,
expected change in Pco2 (from normal value of 40 mm Hg) is 1.3
times change in HCO−
3 concentration (from normal value of 24
mEq/L)
Doing the Math
Thus, in example case:
Decrease in HCO−
3 (from nml) = 24 mEq/L - 8 mEq/L= 16 mEq/L
Predicted decrease in Pco2 (from nml) = 1.3 × 16 mEq/L= 20.8 mm Hg
Predicted Pco2 = 40 mm Hg − 20.8 mm Hg = 19.2 mm Hg
15

Compensation (5)
 Predicted Pco2 is 19.2 mm Hg
 Actual in example Pco2 was 20 mm Hg
 Thus, degree of respiratory compensation was
both appropriate and expected for a person w
an HCO−
3 concentration of 8 mEq/L no
additional acid–base disorders is present
16

Calculating Compensatory Responses
to Simple Acid–Base Disorders
Costanzo LS. BRS Physiology. 5th ed. Baltimore: Lippincott Williams & Wilkins; 2011:176.
“renal rules”
17

Understanding Acid-Base
Disorders via Linkage
18
The linkage is laboratory value to body organ
to physiologic response
 HCO3 is linked to metabolic that links to kidney
with a final linkage to “slow”
 Remember: The term metabolic relates to plasma
bicarbonate
 A low pH is acidosis low pH assoc. w a low
bicarbonate conc. is metabolic acidosis
 A high pH is alkalosis a high pH assoc. w a high
bicarbonate conc. is metabolic alkalosis

Acid-Base Disorders via
Linkage cont’d.
19
 Pco2 is linked to respiratory that links to ventilation
that links to lung with a final linkage to “fast”
 Remember: Pco2 relates only to alveolar ventilation
 A low pH is acidosis a low pH due to elevated Pco2
is hypoventilation-induced respiratory acidosis
 A high pH is alkalosis a high pH due to a reduced
Pco2 is hyperventilation-induced respiratory alkalosis

Acid-Base Disorders via
Linkage cont’d.
20
 Fast and slow refer to compensatory efforts of lungs
or kidney in response to acidosis or alkalosis
 If primary illness is in ventilation causing respiratory
acidosis (high Pco2) or respiratory alkalosis (low Pco2),
kidney is slow meaning it takes 3 to 5 days for kidney to
retain or secrete bicarb. in an effort to keep pH close to
normal
contrastly,
 Lung can start its compensation in seconds to a minute
when there is a primary metabolic acid–base abnormality
For more detail and examples see:
Acid–Base Balance Linkage_pdf notes

Two other clinical points
21
1. Acid–base compensation is never complete or perfect
 In other words, compensation brings pH back toward
normal, but body does not reach a normal pH value
o If pH reaches nml or beyond mixed disorder
2. In case of metabolic acidosis a compensatory
increase in ventilation never causes dyspnea
 Thus, patient who has Kussmaul breathing in diabetic
ketoacidosis is never short of breath

Acid-Base Disorders
Assessment
 Assessment of a patient’s acid–base status requires
measurement of arterial pH, PCO2, and plasma
bicarbonate (HCO−
3 )
 Blood gas analyzers directly measure pH and PCO2
HCO−
3 value is calculated from the Henderson–
Hasselbalch equation (or in clinical setting using
bicarbonate on chemistry panel)
pH = pK + log (HCO−
3 ) / (H2CO3)
 H–H eq. can be simplified to pH = HCO−
3 / PCO2
22

FLOW CHART
Initial Dx of acid-base disorders
23
Kamel KS, Halperin ML. Fluid, Electrolyte, and Acid-Base Physiology: A Problem-Based Approach, 5th Ed.
Philadelphia: Elsevier, 2017.

Case 1
A 35-year-old man with T1DM has not been taking his
daily insulin injections for 1 week. He presents to the
emergency room with deep, regular, sighing respirations,
abdominal pain, vomiting, and signs of severe dehydration.
You conduct ABG and chemistry studies, which are
significant for a low blood pH, low HCO-
3, decreased
PCO2, extreme hyperglycemia, and increased blood
ketones. You immediately treat the patient with fluids and
insulin to try and reverse this metabolic disturbance.
What is the Diagnosis?
24

Metabolic Acidosis
 Etiology
 Anion gap metabolic acidosis: Causes include renal failure
(azotemia), lactic acidosis, diabetic ketoacidosis, certain
toxins (methanol, paraldehyde, phenformin, iron, carbon
monoxide, ethanol, ethylene glycol, salicylate), and INH
o (One way to remember all of causes of anion gap acidosis is mnemonic MUD PILES=
Methanol, Uremia, Diabetic ketoacidosis, Paraldehyde or Phenformin, Iron tablets or
Isoniazid, Lactic acidosis, Ethylene glycol, Salicylates)
 Normal anion gap metabolic acidosis: Causes include traveler’s
diarrhea, acetazolamide overdose, renal tubular acidosis , and
glue sniffing hyperchloremic metabolic acidosis
 If primary cause of acidosis is a loss of HCO-
3 there will be an ↑ in Cl-
 Anion gap will be nml as seen in severe diarrhea
25

 Pathophysiology
 Primary disturbance: Decrease in HCO-
3
concentration
 Compensatory response: Decrease in
PCO2  results in vascular bed
dilatation and ↓ cardiac contractility
(resistant to catecholamines)  can lead
to shock
26

 Clinical Manifestations
 Hyperventilation or Kussmaul breathing (deep, sighing
respirations); other specific signs and symptoms depend on
cause of metabolic acidosis
Lab findings: Decreased pH, decreased PCO2, decreased HCO-
3
 Treatment Treat with bicarbonate if pH < 7.1 and treat underlying
condition
 Note:
 Anion gap calculation: Anion gap = Na+– (Cl-+ HCO-
3)
Anion gap is normally 10–15 mEq/L and is increased if
unmeasured anion replaces HCO-
3
 Compensation calculation: (Winter’s formula): Decrease in
PCO2 = 1.5 (HCO-
3) + 8  2
27

Case 2
A 45-year-old man presents to the emergency department with
increased dizziness and weakness. After taking a history, you learn
that he has been accidentally taking twice the amount of a prescribed
diuretic. On physical examination, you notice that he has sunken
eyes, poor skin turgor, hyporeflexia in all reflexes, and orthostatic
hypotension. Laboratory studies show an arterial pH of 7.56 and an
arterial PCO2 of 45. Serum potassium and chloride are decreased.
No other abnormalities are noted. You immediately begin to
administer IV fluids and you suspect that this will reverse his
metabolic abnormality.
28

Metabolic Alkalosis
Etiology
 Saline-responsive metabolic alkalosis: Caused by
extracellular volume contraction caused by vomiting,
diuretics
 Saline-resistant metabolic alkalosis: Caused by
mineralocorticoid excess (Conn syndrome,
renovascular disease, Cushing disease) or alkali
administration with decreased GFR (eg, antacid
admin.) or severe hypokalemia
29

Pathophysiology
Primary disturbance: Increase in HCO-
3 concentration
Compensatory response: Increase in PCO2
hypoventilation causes PCO2 to increase in order to
increase bicarbonate concentration
Metabolic alkalosis is generally associated w
hypokalemia that acts to worsen the metabolic
alkalosis by increasing bicarbonate absorption in the
proximal tubule and hydrogen ion secretion in the distal
tubule
30

May present w signs of dehydration (sunken eyes, poor skin turgor,
lethargy, and hypotension) and muscle weakness (b/c of hypokalemia);
can also cause ↓ cerebral blood flow and cardiac arrhythmias
Lab findings: Increased pH, increased PCO2, increased HCO-
3,
hypokalemia
 Treatment
Saline-responsive: Fluid replacement
Saline-resistant: Treat underlying cause of mineralocorticoid excess;
replete potassium
 Notes
Compensation: PCO2 increases 0.7 mm Hg for every 1 mEq/L HCO-
3
increase
31

Case 3
A 28-year-old male heroin addict presents to the emergency
room with shallow, deep breathing as well as nausea,
vomiting, and constipation. On physical examination, the
patient is confused and somnolent. Myoclonus with
asterixis is apparent, as are pinpoint pupils. Track marks are
found on both arms. Laboratory studies indicate an arterial
pH of 7.30 and an arterial PCO2 of 55. To reverse the drug
overdose and thereby relieve the metabolic disturbance, you
decide to administer 0.4 mg of naloxone IV.
What is the diagnosis?
32

Respiratory Acidosis
 Etiology
Caused by acute lung disease (ARDS, airway obstruction), chronic
lung disease (COPD), CNS depression (opioids, sedatives, narcotics),
or weak respiratory muscles (ALS, kyphoscoliosis, MS, polio)
 Pathophysiology
Primary disturbance: Increase in PCO2 (hypercapnia) owing to
decreased alveolar ventilation
Compensatory response: Increase in HCO-
3 caused by increased
renal HCO-
3 reabsorption as stimulated by low pH and high PCO2
33

Hypoventilation; somnolence; confusion; myoclonus with asterixis;
signs of ↑intracranial pressure (eg, papilledema, pseudotumor
cerebri= Idiopathic intracranial hypertension [IIH])
Lab findings: Decreased pH, increased PCO2, increased HCO-
3
 Treatment
Treat underlying condition of acute respiratory acidosis
No treatment necessary for chronic respiratory acidosis
 Notes
Acute compensation: 1 mEq/L HCO-
3 increase for every 10 mm Hg
PCO2 increase
Chronic compensation: 3.5 mEq/L HCO-
3 increase for every 10 mm
Hg PCO2 increase
34

Case 4
A 30-year-old woman just learns that her brother was in a
serious car accident, but is currently in stable condition.
She begins to hyperventilate and starts complaining of
feeling light-headed and having tingling in her hands and
feet. Realizing that she is in danger of experiencing a
metabolic disturbance, you hand her a paper bag and ask
her to breathe into it.
35

Respiratory Alkalosis
 Etiology
Acute respiratory alkalosis: Caused by hyperventilation, early
phase of salicylate overdose, pneumonia, sepsis, pregnancy,
pulmonary edema, pulmonary embolism, or cirrhosis
Chronic respiratory alkalosis: Caused by high altitude or
pregnancy
 Pathophysiology Primary disturbance: Decrease in PCO2
Compensatory response: Decrease in HCO-
3 because of increased
renal HCO-3 secretion
36

 Clinical Manifestations Sx in acute respiratory alkalosis are related
to ↓ cerebral blood flow (light-headedness, anxiety, paresthesias,
numbness about mouth, tingling in distal extremities,
hyperventilation); may also cause cardiac arrhythmias
Lab findings: Increased pH, decreased PCO2, decreased HCO-
3
 Treatment Acute hyperventilation syndrome from anxiety can be
treated by breathing into paper bag to increase PCO2; otherwise, treat
underlying cause (ie, sepsis or pneumonia)
 Notes
 Acute compensation: 2 mEq/L HCO-
3 decrease for every 1 mm
Hg PCO2 decrease
 Chronic compensation: 5 mEq/L HCO-
3 decrease for every 10
mm Hg PCO2 decrease
37

Step-By-Step Analysis of
Acid-Base Status
1. Is the patient acidemic or alkalemic?
2. Is the primary disturbance respiratory or metabolic?
3. For a respiratory disturbance, is it acute or chronic?
4. For metabolic acidosis, is an anion gap present?
5. If an anion gap is present, are there still other
coexistent metabolic disturbances?
6. What is the degree of compensation by respiratory
system for a metabolic disturbance?
38

Key Points to Remember
1. Arterial pH must be maintained in a close range (7.35-7.45) for
individual to be alive
2. Arterial pH is based on relationship of plasma bicarbonate (HCO−
3)
to carbon dioxide tension (Pco2 )
3. Simplify Henderson–Hasselbach equation to: pH = HCO−
3 / Pco2
4. Metabolic disorder = ∆ HCO−
3 = kidney = slow response
5. Respiratory disorder = ∆ Pco2 = lung = fast response
6. A disorder that is primarily associated w ventilation, e.g.,
pneumonia, drug overdose, causes a respiratory acid-base disorder
with a compensatory metabolic response
7. A disorder that is primarily assoc. w. renal disease, an
endocrinopathy, or GI disease causes a metabolic acid-base disorder
w a compensatory respiratory response Examples include severe
vomiting or diarrhea; uncontrolled diabetes; and uremia
39

Le T, Bhushan, et al. First Aid for the USMLE Step 1 2017. McGraw-Hill Education, 2017. 40

Sources and further study:
Companions:
 Acid-Base Balance and Disorders_ SDL Tutorial.pdf
 Acid–Base Balance Linkage_SDL Note.pdf
Sources and further study:
 Baron SJ, Lee CI. Lange Pathology Flash Cards, 2nd Ed. New York: McGraw-Hill, 2009.
 Cho, CH. Electrolyte & Acid-Base Disorders, Ch. 21, In: Current Medical Diagnosis and
Treatment 2017, 56th Ed. Papadakis MA, McPhee SJ, (Eds). New York: McGraw-Hill,
2017.
 Costanzo LS. BRS Physiology. 5th ed. Baltimore: Lippincott Williams & Wilkins. 2011.
 Diamond MA. Medical Insights: From Classroom to Patient. Sudbury, MA: Jones and
Bartlett Publishers, LLC, 2010.
 Le T, Bhushan, et al. First Aid for the USMLE Step 1 2017. New York: McGraw-Hill, 2017
 Kamel KS, Halperin ML. Fluid, Electrolyte, and Acid-Base Physiology: A Problem-Based
Approach, 5th Ed. Philadelphia: Elsevier, 2017.
 Jameson LJ, Loscalzo J. Harrison’s Nephrology and Acid-Base Disorders, 2nd Ed. New
York: McGraw-Hill, 2013.
41

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