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NCPXXX10.1177/0884533614562842Nutrition in Clinical PracticeAyers et al
Invited Review
Nutrition in Clinical Practice
Volume XX Number X
Month 201X 1­–7
© 2014 American Society
for Parenteral and Enteral Nutrition
DOI: 10.1177/0884533614562842
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Acid-Base Disorders: Learning the Basics
Phil Ayers, PharmD, BCNSP, FASHP1; Carman Dixon, PharmD1;
and Andrew Mays, PharmD1
Abstract
Nutrition support practitioners should be confident in their ability to recognize and treat various metabolic and respiratory disorders
encountered in daily practice. A clinician’s comprehension of the underlying physiologic processes and/or exogenous causes that
occur during acid-base disorders is essential when making therapeutic decisions regarding fluids, parenteral nutrition, and electrolyte
management. This invited review will discuss basic metabolic and respiratory disorders while briefly addressing mixed acid-base
disorders. (Nutr Clin Pract. XXXX;xx:xx-xx)
Keywords
acid-base imbalance; acid-base equilibrium; acidosis; alkalosis; nutritional support; parenteral nutrition
Introduction
Acid-base disorders are often present in patients requiring
nutrition support. The body maintains acid-base homeostasis
through a complex system that involves the lungs, the kidneys,
and endogenous buffers. Therefore, the interpretation of acidbase disorders should be done with a patient’s overall clinical
condition in mind. Clinician uncertainty can be caused from a
lack of experience, a misunderstanding of the significance of
arterial blood gas results, or a lack of understanding the physiologic and pathophysiologic issues that accompany acid-base
disorders. The purpose of this tutorial is to enhance the nutrition support clinician’s ability to recognize these disorders,
identify precipitating causes, and provide specialized nutrition
support to these patients.
Definition of an Acid and a Base
An acid is a substance that can donate a proton (H+).
HCl ( hydrochloric acid ) → H + + Cl−
A base is a substance that can accept a proton (H+).
NH3 + H + → NH + 4 ( base )
Some common acid-base pairs include carbonic acid/bicarbonate, monobasic/dibasic phosphate, and lactic acid/lactate.1-3
The acidity of body fluids is expressed in terms of the
hydrogen ion concentration. The degree of acidity is expressed
as pH. The pH varies inversely with the H+ concentration; thus,
an increase in H+ reduces the pH and a decrease elevates the
pH. The normal pH of the body is maintained within a range of
7.35-7.45. Hydrogen regulation involves 3 steps: (1) extracellular and intracellular chemical buffering mechanisms, (2) partial pressure of carbon dioxide control by alterations in the rate
of ventilation, and (3) plasma bicarbonate concentration control by renal H+ excretion. A pH of < 6.7 or > 7.7 is considered
incompatible with life.
Buffers
Buffering is defined as the ability of a weak acid and its corresponding base to resist change in the pH upon the addition of
a strong acid or base.1,3,4 The principal buffer in the body is the
carbonic acid/bicarbonate system. Carbonic acid (H2CO3−), a
weak acid, and its conjugate base (HCO3−) exist in equilibrium
with H+.
HCO3− + H + ↔ H 2CO3−
Essentially all carbonic acid in the body exists as carbon dioxide gas; thus, carbon dioxide is the acid form of the carbonic
acid/bicarbonate buffer system. When hydrogen ions are
released, the concentration of bicarbonate will fall and the concentration of carbon dioxide gas will rise as the acid is
buffered.
From 1Mississippi Baptist Medical Center, Jackson, Mississippi.
Financial disclosure: None declared.
Corresponding Author:
Phil Ayers, PharmD, BCNSP, FASHP, Mississippi Baptist Medical
Center, 1225 N. State Street, Jackson, MS 39202, USA.
Email: [email protected]
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Nutrition in Clinical Practice XX(X)
The Henderson-Hasselbalch equation for the carbonic acid/
bicarbonate buffer system describes the mathematical relationship of pH, bicarbonate concentration in milliequivalents per
liter, and partial pressure of carbon dioxide (pCO2) in millimeters of mercury.
(
pH = 6.1 + log HCO3− / 0.03 x pCO 2
)
The Henderson-Hasselbalch equation demonstrates that the
ratio alone and not the absolute values of bicarbonate and carbon dioxide determines pH.
The normal range for the anion gap is 3-11 mEq/L. Unmeasured
serum anions such as proteins, phosphate, sulfate, and organic
ions make the normal range for the anion gap a positive
number.
Serum albumin levels account for a significant portion of
the unmeasured serum anions. A 1 g/dl drop in albumin will
lower the anion gap by 2.5 mEq/L. Application of the anion
gap allows the clinician to differentiate between
Normal anion gap acidosis (hyperchloremic acidosis)
Elevated anion gap acidosis
Common causes of normal and elevated anion gap metabolic
acidosis are listed in Tables 1 and 2.
Role of the Kidneys in Acid-Base
Regulating the concentration of bicarbonate is the principal
role of the kidneys in acid-base balance.3-5 Approximately
90% of bicarbonate reabsorption occurs in the proximal
tubule. This process is catalyzed by carbonic anhydrase.
Filtered bicarbonate combines with hydrogen ions to form
carbonic acid. Carbonic anhydrase, located in the brush border of the tubule, catalyzes carbonic acid to carbon dioxide
(CO2). The unchanged CO2 crosses the cell membrane and
passively diffuses into the renal tubule. Inside the cell, bicarbonate and carbonic acid are reformed. This process is also
catalyzed by carbonic anhydrase. Bicarbonate is then reabsorbed into the capillary blood. Sodium and bicarbonate reabsorption are the net result of this process. Carbonic anhydrase
inhibitors (eg, acetazolamide) cause excessive amounts of
bicarbonate to be lost in the urine, which may lead to a metabolic acidosis.
The kidneys also excrete 50-100 mEq/day of nonvolatile
acids produced by the body. This process requires carbonic
anhydrase. The distal tubule is the primary site of occurrence.
The hydrogen ions secreted into the tubule lumen are buffered
by phosphates and ammonia. The urine is normally acidic but
usually not < 4.5.
Case #1
A 21-year-old female presented to the emergency department
(ED) with complaints of nausea, vomiting, and confusion.4,7,8
She is a type 1 diabetic with a continuous subcutaneous insulin
infusion (CSII). Her last fingerstick blood glucose read “High”
on her glucometer, and she realized that her insulin pump was
disconnected from her body right before coming to the ED.
Labs and ABGs are shown in Table 3.
Disorder: Elevated Anion Gap Metabolic
Acidosis
Anion gap is elevated at 25 mEq/L. Hypovolemia should be
addressed with expansion of the extracellular volume.
Intravenous insulin infusion should be initiated to stop production of ketoacids. Potassium should be replaced once volume is
replenished and insulin is administered. The patient should be
transitioned off of insulin infusion back to CSII when deemed
appropriate.
Metabolic Alkalosis
Metabolic Acidosis
A metabolic acidosis is defined as an arterial pH < 7.35 (acidemia) and/or a low serum bicarbonate concentration.1-4,6 The
bicarbonate concentration can be determined by the arterial
blood gases (ABGs) (calculated) or as the total carbon dioxide
concentration on the serum chemistry panel (measured). In
most circumstances, the body compensates by hyperventilating
to increase carbon dioxide excretion. This is seen by a low
PaCO2 on arterial blood gas measurement.
Once a metabolic acidosis is diagnosed, the next step is calculation of the anion gap.
The most commonly used equation for the anion gap is
noted below:
(
Anion Gap = Na + - Cl− + HCO3 _
)
An elevated pH on ABGs and an elevated serum bicarbonate
concentration are hallmark signs of a metabolic alkalosis.1,2,4,6,9
Respiratory compensation is minor in patients presenting with a
metabolic alkalosis. The most common causes are loss of gastric acid secondary to vomiting or nasogastric suctioning and/or
loss of intravascular volume and chloride as a result of diuretic
use. Patients receiving parenteral nutrition may develop a metabolic alkalosis from excessive acetate and inadequate chloride
in the formulation. Acetate is metabolized to bicarbonate, which
leads to the alkalosis. A metabolic alkalosis can be classified
into volume mediated (saline responsive) and volume independent (saline resistant). Obtaining a urine chloride concentration
is useful in the diagnosis of patients who may respond to volume replacement. Table 4 lists the most common causes of
saline responsive and saline resistant metabolic alkalosis.
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Table 1. Causes of Normal Anion Gap Metabolic Acidosis.1-4,6
Gastrointestinal
Bicarbonate Loss
••
••
••
••
••
••
••
Diarrhea
Pancreatic fistula
Small bowel fistula
Obstructed ileal conduit
Ureterosigmoidostomy
Calcium
Magnesium
Drug-Induced Hyperkalemia with
Renal Insufficiency
Renal Acidosis
Hypokalemic
RTA type II (proximal)
Drug induced:
•• Acetazolamide
•• Topiramate
RTA type I (distal)
Drug induced:
•• Amphotericin B
•• Ifosfamide
Hyperkalemic
•• RTA type IV (distal nephron
dysfunction)
•• Mineralocorticoid deficiency
•• Hypoaldosteronism
•• Tubulointerstitial disease
•• Potassium sparing diuretics
•• Angiotensin converting
enzyme inhibitors
•• Angiotensin receptor blockers
•• Nonsteroidal antiinflammatory drugs
•• Trimethoprim
•• Pentamidine
Other
••
••
••
••
••
Acid loads
Ammonium chloride
Parenteral nutrition
Rapid saline administration
Cation exchange resins
RTA, renal tubular acidosis.
Table 2. Causes of Elevated Anion Gap Metabolic Acidosis.1-4,6
Renal Failure
Failure to excrete acid
Ketoacidosis
Lactic Acidosis
•• Diabetes
•• Starvation
•• Ethanol ingestion
•• Shock (septic,
cardiogenic,
hypovolemic)
•• Carbon monoxide
poisoning
•• Tonic-clonic seizures
•• Hepatic disease
Drugs
Intoxications
Linezolid
Lorazepam (intravenous)
Metformin
Nitroprusside (cyanide
accumulation)
•• Nucleoside reverse
transcriptase inhibitors
•• Methanol
•• Ethylene glycol
••
••
••
••
Table 3. Case #1.
Laboratory
Laboratory Value (normal range)
Laboratory
Sodium
Potassium
Chloride
CO2
BUN
Creatinine
Phosphorus
Glucose
136 (135–145 mEq/L)
4.8 (3.5–5 mEq/L)
101 (98–107 mEq/L)
10 (22–31 mEq/L)
23 (7–20 mg/dL)
1.4 (0.7–1.5 mg/dL)
2.7 (2.5–4.5 mg/dL)
540 (70–110 mg/dL)
pH
pCO2
pO2
HCO3−
WBC
Hgb
Hct
UA
Laboratory Value (normal range)
7.25 (7.35–7.45)
20 (35–45 mmHg)
130 (80–100 mmHg)
8.5 (24–30 mEq/L)
16 × 103/mm3 (4.8–10.8 × 103/mm3)
14.1 (13.5–17.5 g/dL)
52% (41%–53%)
(+) ketones, glucose
BUN, blood urea nitrogen; Hct, hematocrit; Hgb, hemoglobin; UA, urinalysis; WBC, white blood cell count.
Case #2
A 60-year-old male postoperative day 4 of exploratory laparoscopy with lysis of adhesions had a positive kidney ureter
bladder (KUB) for postoperative ileus.4,8 He currently has a
nasogastric tube to suction with > 1000 mL output per 24
hours. He is receiving lactated ringers at 60 mL/hour and
parenteral nutrition at 60 mL/hour with maximized acetate
load. He also has furosemide 40 mg intravenous push (IVP)
scheduled every 12 hours. Labs and ABGs are shown in
Table 5.
Disorder: Metabolic Alkalosis
The patient has metabolic alkalosis secondary to maximized
acetate load in PN, lactate from lactated ringers, nasogastric
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Nutrition in Clinical Practice XX(X)
Table 4. Causes of Metabolic Alkalosis.1,2,4,6,9
Saline Responsive (Urine Chloride < 10 mEq/L)
••
••
••
••
••
••
Saline Resistant (Urine Chloride > 10 mEq/L)
••
••
••
••
Vomiting
Nasogastric suction
Diuretic therapy
Excessive bicarbonate administration
Acetate salt in parenteral nutrition
Rapid correction of hypocapnia
Excessive mineralocorticoids
Cushing’s syndrome
Hyperaldosteronism
Profound potassium and magnesium
depletion
•• Excessive licorice ingestion
Sodium
Potassium
Chloride
CO2
Creatinine
Laboratory Value
(normal range)
••
••
••
••
Bartter syndrome
Gitelman syndrome
Renin secreting tumor
Renal artery stenosis
Table 6. Causes of Respiratory Acidosis.1,4,6,10
Table 5. Case #2.
Laboratory
Other
Laboratory
145 (135–145 mEq/L)
pH
3 (3.5–5 mEq/L)
pCO2
96 (98–107 mEq/L)
pO2
40 (22–31 mEq/L)
HCO3−
1.2 (0.7–1.5 mg/dL) Base excess
Laboratory Value
(normal range)
7.52 (7.35–7.45)
48 (35–45 mmHg)
70 (80–100 mmHg)
39 (24–30 mEq/L)
14 (± 2)
tube to suction, and furosemide diuresis. PN acetate load
should be changed to maximize chloride load. Base intravenous fluids (IVF) should be changed to a non-lactate containing fluid and to maintain fluid balance. The PN and base
IVF are exogenous sources of bicarbonate as acetate and lactate are both metabolized to bicarbonate. The nasogastric
tube to suction is causing a loss of gastric acid. Thiazide or
loop diuretics can cause a contraction metabolic alkalosis
secondary to extracellular volume loss and stimulation of
aldosterone secretion.
Respiratory Acidosis
Respiratory acidosis can be a chronic or acute condition that is
due to hypoventilation secondary to a disruption in the respiratory system.1,2,4,6,10 Common causes of acute respiratory acidosis include central nervous system depression, acute
exacerbations of chronic pulmonary diseases, and neuromuscular disorders. Chronic respiratory acidosis is commonly
associated with chronic obstructive pulmonary disease,
Pickwickian syndrome (obesity hypoventilation syndrome),
and interstitial pulmonary disease. Patients have complications
of altered mental status, motor disturbances, and dyspnea.
Both chronic and acute respiratory acidosis will present in
patients with a decreased pH and elevated PaCO2 on ABGs.
However, patients who are in a state of chronic respiratory
acidosis will have adequate time for renal compensation and
have a smaller alteration of pH compared to those with acute
respiratory acidosis.
Patients with severely impaired CO2 excretion and/or
life-threatening hypoxemia should have adequate oxygenation
Acute
CNS depression
•• Opiates, benzodiazepines,
propofol
•• Head trauma
Muscle weakness
•• Guillain-Barre syndrome
•• Myasthenia gravis crisis
•• Severe hypokalemia or
hypophosphatemia
Diseases affecting gas exchange
in pulmonary capillary
•• Status asthmaticus
•• COPD exacerbation
•• Pneumothorax
Chronic
Extreme obesity
Pickwickian syndrome
Amyotropic lateral sclerosis
Multiple sclerosis
Poliomyelitis
Muscular dystrophy
Myasthenia gravis
Kyphoscoliosis
COPD
Chronic ILD
CNS, central nervous system; COPD, chronic obstructive pulmonary
disease; ILD, interstitial lung disease.
provided. This may require mechanical ventilation. The underlying cause of the acidosis should be treated accordingly (eg,
reversal of narcotics or benzodiazepines with naloxone and
flumazenil, bronchodilators and steroids for bronchospasm,
adjustment of mechanical ventilation). Sodium bicarbonate
(NaHCO3) should be reserved for the severely acidotic patient
(pH < 7.15) to assist with ventilation and possibly restore
responsiveness to bronchodilators. NaHCO3 should be used
with caution because of the following potential complications:
increased pulmonary congestion, no central nervous system
protection, increased CO2 generation, and metabolic alkalosis.
Table 6 lists some of the most common causes of respiratory
acidosis.
Case #3
A 28-year-old male was brought to the ED with unknown medical history.4,8 Medication bottles of alprazolam and hydrocodone were found empty. He arrived at the ED with laboratory
and ABGs as shown in Table 7.
After questioning of girlfriend, it was found that the patient
recently returned from deployment in Afghanistan, and he has
been dealing with chronic pain and anxiety.
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Table 8. Causes of Respiratory Alkalosis.1,4,6,11
Table 7. Case #3.
Laboratory
Sodium
Potassium
Chloride
CO2
Creatinine
Laboratory Value
(normal range)
Laboratory
Laboratory Value
(normal range)
137 (135–145 mEq/L)
pH
7.25 (7.35–7.45)
60 (35–45 mmHg)
4.5 (3.5–5 mEq/L)
pCO2
55 (80–100 mmHg)
100 (98–107 mEq/L)
pO2
25 (22–31 mEq/L)
HCO3− 26 (24–30 mEq/L)
0.7 (0.7–1.5 mg/dL) Glucose 89 (70–110 mg/dL)
Disorder: Respiratory Acidosis Secondary to
Opiate and Benzodiazepine Overdose
The patient’s airway should be protected and adequate oxygen
delivered. Naloxone and flumazenil should be administered for
reversal of causative agents.
Hypoxemia
•• Pneumonia
•• Pulmonary emboli
•• Pulmonary edema
•• Diffuse interstitial fibrosis
•• Congestive heart failure
Medications
•• Salicylates
•• Nicotine
•• Xanthine
CNS disorders
•• CVA
•• Pontine tumors
•• Meningitis, encephalitis
•• Head trauma
•• Anxiety
CNS, central nervous system; CVA, cerebral vascular accident.
Respiratory Alkalosis
Respiratory alkalosis is characterized by a decrease in PaCO2 and
elevation in pH secondary to hyperventilation, as the lungs are
excreting more CO2 than is being produced metabolically.1,4-6,11
Common causes of respiratory alkalosis are increased central
stimulation of respiration, hypoxemia, and pulmonary disease.
Patients can present with light-headedness, confusion, muscle
cramps, and tetany. Respiratory alkalosis is found in many pulmonary diseases such as pneumonia, interstitial lung disease, and
pulmonary emboli. This hyperventilation can be caused from
hypoxemia, anemia, pain, or anxiety. Chemoreceptors in the
brainstem and in the carotid and aortic bodies regulate ventilation, and these receptors sense increases in PaCO2 or decreases in
serum bicarbonate, triggering hyperventilation. The correction of
respiratory alkalosis should be geared toward correcting the
underlying disorder. Respiratory depressants or the administration of acid has no place in the treatment of respiratory alkalosis.
Many cases can be corrected by breathing into a paper bag to
increase inspired CO2 and relieve symptoms. Table 8 shows
causes of respiratory alkalosis.
Case #4
A 65-year-old obese male s/p total knee arthroplasty 2 weeks
ago presented to the ED after developing chest pain, shortness
of breath, and tachypnea.4,8 Oxygen administered via nasal
cannula at 2 L/minute did not increase oxygen saturation. After
questioning, it was determined that he had not taken his enoxaparin as directed. He arrived to the ED with laboratory and
ABGs as shown in Table 9.
Disorder: Respiratory Alkalosis
Computed tomography angiogram of the chest confirms pulmonary embolus. Appropriate treatment dose anticoagulation
should be initiated after oxygenation and hemodynamic
Table 9. Case #4.
Laboratory
Laboratory Value
(normal range)
Sodium
135 (135–145 mEq/L)
Potassium
4 (3.5–5 mEq/L)
Chloride 100 (98–107 mEq/L)
25 (22–31 mEq/L)
CO2
Creatinine 0.8 (0.7–1.5 mg/dL)
Laboratory
Laboratory Value
(normal range)
pH
pCO2
pO2
HCO3−
O2 Sat
7.5 (7.35–7.45)
25 (35–45 mmHg)
52 (80–100 mmHg)
24 (24–30 mEq/L)
92% (97%–99%)
O2 Sat, oxygen saturation.
Table 10. Reference Blood Gas Values.1,4,6
Laboratory
pH
PaCO2, mmHg
PaO2, mmHg
HCO3−, mEq/L
Base excess, mEq/L
Arterial Blood Value
7.40 (7.35–7.45)
35–45
> 70
24–30
–2.4 to +2.3
support is addressed. Venous dopplers and further cardiac
workup may be indicated.
Arterial Blood Gases
A key in the assessment of acid-base disorders is the interpretation of arterial blood gases to determine a patient’s oxygenation and acid-base status.1,4,6,12 The results from the ABGs
will consist of the following: pH, partial pressure of carbon
dioxide (PaCO2), partial pressure of oxygen (PaO2), calculated
bicarbonate (HCO3−), and base excess. The reference values
for ABGs are listed in Table 10.
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Nutrition in Clinical Practice XX(X)
The pH should be the first value assessed when diagnosing acid-base disorders. A pH < 7.35 represents an acidemia,
and a pH > 7.45 represents an alkalemia. However, the pH
can be within the normal range (7.35–7.45) when mixed
acid-base disorders are present. Once it is determined
whether the patient is acidemic or alkalemic based on pH,
the PaCO2, commonly reported as pCO2 on ABG reports,
should be evaluated to determine the lungs’ ability to excrete
carbon dioxide (CO2). An elevated PaCO2 shows that the
body is abnormally retaining CO2, and a decreased PaCO2
shows that the body is increasing the excretion of CO2. Once
the pH and PaCO2 are measured, the bicarbonate concentration is then calculated using the Henderson-Hasselbalch
equation. The calculated bicarbonate and serum bicarbonate
can then be used to determine a patient’s metabolic component of acid-base disorder. Base excess/deficit is a calculated
value that estimates the metabolic component of a patient’s
acid-base status. This is calculated by determining the
amount of H+ ions required to return the blood to a pH of 7.4
if the PaCO2 were adjusted to normal. Base excess could represent a patient with metabolic alkalosis, and base deficit
could represent a patient with metabolic acidosis.
tubule, leading to an increase of serum HCO3−. After 3–5 days,
a new steady state is obtained solely due to the increase in renal
H+ secretion. The opposite occurs during periods of respiratory
alkalosis. A decrease in hydrogen ion secretion causes a loss of
bicarbonate secondary to a rise in renal tubular cell pH.
Therefore, the increased renal loss of bicarbonate produces a
drop in serum HCO3−. This compensatory mechanism begins
in about 2 hours but is not complete for 2–3 days. This compensatory mechanism typically occurs in 2 phases. The change
in HCO3− is approximately equal to 0.1 times the variation in
PaCO2 in acute respiratory acidosis and equal to 0.2 times the
variation in PaCO2 in acute respiratory alkalosis. A more dramatic change in HCO3− is seen with respiratory conditions that
persist for several hours. The increase or decrease in HCO3− is
approximately equal to 0.4 times the variation in PaCO2 in
respiratory acidosis or alkalosis, respectively. These calculations are estimates of normal compensation and are dependent
on multiple factors. A > 10% variation in the predicted correction of PaCO2 or HCO3− in response to an alkalosis or acidosis
could indicate a mixed acid-base disorder.
Compensation
Most of the discussion to this point has focused on singular
acid-base disturbances and subsequent compensatory mechanisms. In practice, however, patients often experience a combination of more than 1 of these 4 primary disorders. Both
metabolic acidosis and alkalosis can occur in tandem or in
combination with respiratory acidosis or alkalosis as a double
acid-base disorder. A triple acid-base disorder can occur if metabolic acidosis, metabolic alkalosis, and either respiratory acidosis or alkalosis are present. Respiratory acidosis and alkalosis
are not seen in combination, though patients on a respirator can
quickly change between hyperventilation and hypoventilation.
Compensation via renal and respiratory systems will move the
pH toward normal, but they will rarely correct pH to normal.
Therefore, patients who present with a normal pH and alterations in PaCO2 and plasma HCO3− should be expected to have
a mixed acid-base disorder.1-3,6,9-11,13
The body naturally corrects for simple acid-base disturbances
via respiratory and renal mechanisms.1,3,9-12 The compensatory response to each of the previously listed disorders is predictable and occurs over varying lengths of time. Respiratory
compensation begins within minutes and continues over a
period of hours. However, it may take several days for renal
mechanisms to fully compensate for acid-base abnormalities.
The degree to which the body responds to a simple variance
in pH may also be affected by the acute or chronic nature
of the causative disorder, lung capacity, and normal renal
function.
In metabolic acidosis, the normal physiologic mechanism
to compensate is to expel available carbon dioxide through
hyperventilation. This action will decrease PaCO2 by approximately 1.2 times the decrease in HCO3−. If the change in PaCO2
is greater than this calculated value, a respiratory alkalosis
could be present, and if the calculated change is less than
expected, respiratory acidosis may be suspected.
Hypoventilation and subsequent increase in PaCO2 is the
body’s respiratory response to metabolic alkalosis. The
expected increase in PaCO2 is equal to 0.6 times the measured
increase in HCO3−. A minimal increase in PaCO2 could indicate the presence of respiratory alkalosis, a common disorder
in critically ill patients. A higher than expected compensation
would suggest an underlying respiratory acidosis.
Compensatory mechanisms in the kidney are primarily
responsible for the correction of respiratory acid-base disorders. In respiratory acidosis, the kidneys increase secretion of
hydrogen ions and reabsorption of bicarbonate in the proximal
Mixed Acid-Base Disorders
Summary
Interpreting acid-base disorders begins by understanding normal physiologic function. The body uses buffering processes,
rate of ventilation, and renal mechanisms to maintain acid-base
status. The relationship of carbonic acid and bicarbonate as
described by the Henderson-Hasselbalch equation in addition
to the partial pressure of gases, calculated bicarbonate, and
base excess are used to help identify a potential variation in
acid-base homeostasis. Each of these values is assessed by
evaluating the patient’s arterial blood gases and aids in the
identification of metabolic and respiratory acidosis or alkalosis. Metabolic acidosis may be further classified as having a
normal or elevated anion gap. Knowledge of the typical causes
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of these disorders in combination with a thorough history and
physical can aid the clinical practitioner to accurately assess
the patient’s condition.
Several tutorials and tools are available to further enhance a
clinician’s understanding of acid-base disturbances. Nomograms
using pH, pCO2, and HCO3 as coordinates can facilitate the recognition of compensation and mixed acid-base disorders. With
the appropriate practice and understanding, they may be useful
in the differentiation of acid-base conditions. These tools can be
complex and are not necessary to diagnosis the patient’s status.
An understanding of the principles outlined in this article will
give the nutrition support clinician confidence in his or her ability to recognize metabolic and respiratory acid-base disorders
in daily practice.
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