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Indian
DAS J. Anaesth.DISORDERS
: ACID-BASE 2003; 47 (5) : 373-379 373

ACID-BASE DISORDERS
Dr. Bibhukalyani Das

Hydrogen bonding is a key force that maintains
the structural integrity of biologic molecules. The
structure of all proteins, enzymes that are critical
determinant of function is extremely sensitive to local H+
concentration. So, H+ concentration must be maintained
within tight limits not to disrupt cellular function. Failure
to do this will cripple enzyme mediated reactions in the
cell, leading to cell death. pH represents a convenient
scale of expressing H+ concentration (pH=log[H+]). Limits
of pH compatible with life generally are in range of
7.0 to 7.8, which represents a change in H+ concentration
of 86 nEq/L.
Fortunately, in terms of compatibility with life, the
body is 100,000 and 1,000,000 times more sensitive to
changes in extracellular H + than to K + and Na +
respectively.
The most significant contribution to H+ comes from
the cellular oxidation of substrates that produce CO2 (mainly
TCA cycle). Total daily production of CO2 ranges from
13000 to 15000 mmol, obviously a vast amount. But as
CO2 is a soluble gas and quickly diffuses through biological
membranes, the body utilizes CO2 as a buffer rather than
allowing as a burden.
CO2 + H2O Õ H2CO3 Õ H+ + HCO-3
CO2 rapidly leaves the oxidizing cell and enters
the interstitial fluid. While diffusing comes in contact
of carbonic anhydrase (RBC) and the above reversible
reaction results in conversion of excess bicarbonate to
CO2 which is excreted through lung – “Open System
buffer”.
Increase or decrease in PaCO2 represent derangements
of (1) Neural – respiratory control (2) Compensatory
changes in response to alternation in plasma HCO-3.
Under most circumstances, CO2 production and
excretion are matched and PaCO2 is maintained at a steady
state at 40 mmHg. Primary CO2 regulation is by neural
and respiratory factors i.e. elimination rather than
production. Hypercapnia is usually due to hypoventilation,
CO2 retention and hypocapnea is by hyperventilation and
excessive CO2 washout.
Primary changes in PaCO2 can cause Acidosis
(PaCO2 > 40 mmHg) or Alkalosis (PaCO2 < 40 mmHg).
This primary change evokes cellular buffering (fast system)
and renal adaption (slow process).
Any change in plasma HCO-3 due to metabolic or
renal factor results in compensatory changes in ventilation
and thereby blunts the change in blood pH.
The kidneys regulate plasma HCO-3 by 3 processes:
reabsorption of filtered HCO-3, formation of titratable acid
and excretion of NH+4 in urine.
PROXIMAL TUBULE

Normal Acid-Base homeostasis

System arterial pH is maintained between 7.35
and 7.45 by extracellular and intracellular buffering
together with respiratory and renal regulatory mechanisms.
Control of PaCO2 by CNS and respiratory system and
control of plasma HCO-3 by kidneys stabilize the arterial
pH. The components are described by Henderson –
Hasselbalch equations – pH = 6.1 + log (HCO-3 / PaCO2
X 0.0301)

Prof. and HOD of Anaesthesiology

Fig. 1 - Bicarbonate reclamation in the proximal renal tubule.
Bangur Institute of Neurology, Kolkata.
E-mail : bibhukalyani@hotmail.com
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374
Kidneys filter 4000 mmol of HCo-3 per day and
renal tubules secrete equal amount of H+ to absorb this
HCO-3. 80-90% if biocarbonate is reabsorbed in the
proximal tubule. The magnitude of this process is modulated
by the state of ECF volume, Serum K and pCO2.
The distal nephron secretes protons (NH+4 and
titratable acid) generated by metabolism amounting
40-60 mmol dl-1. Major means of net H+ excretion is renal
ammoniagenesis. Net H+ excretion take place in the distal
tubule where it is used to titrate NH3 and HPO-24. At a
urine pH of 4.5, only 0.00006 mEq of H+ is excreted in
1500 ml of urine without buffer. Fortunately, the urine
contains several buffers that permit the excretion of large
amounts of H+ without requiring urinary pH to fall lower
than 4.5. H+ excretion by these buffers results in what is
termed titratable acidity. The major member of this buffer
group is HPO-42 which is available for buffering to about
10 meq of H+ / 24 hours (i.e. 1000 fold of without buffer).
Other urinary buffers include creatinine, uricacid and B-
hydroxybutyice acid. Metabolic acidosis in face of normal
excretion. NH+4 production and excretion are impaired in
chronic renal failure, hyperkalaemia and renal tubular
acidosis.
Fig. 2 – Distal tubular mechanism of net H+ excretion.
Renal pH regulation occurs in the distal tubule,
where active transport of H+ derived from cytosolic
generation of H2CO3 and net reabsorption of HCO-3 occur.
This mechanism is distinct from that of the proximal tubule
because of the H+ transport does not need Na+/H+ exchange
another important feature of this region is the presence of
“nonleaky” tight functions, which facilitate maintenance
of the large gradients thus established. Finally, the gradient
INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003
is largely dissipated through combination of the eliminated
H+ with the urinary buffers, chiefly NH3 and disodium
phosphate. Reabsorption of a HCO-3 molecule results in
elimination of a Cl- and a K+ that offsets the sodium
simultaneously reabsorbed.
Hepatic ureagenesis
consumes HCO-3
and NH-4
Glucose 2HCO3-
Blood
Glutamine a-ketoglutarate +2NH 4 +
Lumen of URINE
proximal tubule
Fig.3 : Renal ammoniagencies.
Disturbances of the acid-base equilibrium occur in
a wide variety of critical illnessess and are among the
most commonly encountered disorders in the ICU. In
addition to reflecting the seriousness of the underlying
disease, these disorders have their own morbidity and
mortality.
A blood pH less than normal (normal range 7.35-
7.45) is called acidemia; the underlying process causing
acidemia is called acidosis. Similarly, alkalemia and
alkalosis refer to the pH and the underlying process,
respectively. While an acidosis and an alkalosis may
coexist, there can be only one resulting pH. Therefore,
acidemia and alkalemia are mutually exclusive conditions.
The approach to acid-base derangements should
emphasize a search for the cause, rather than an immediate
attempt to normalize the pH. Many disorders are mild and
do not require treatment. Further, treatment may more
detrimental than the acid-base disorder itself. More
important is a full consideration of the possible underlying
pathologic states, which may facilitate a directed
intervention that will benefit the patient more than
normalization of the pH would.
Types of Acid-Base disorders:
(A) Simple acid-base disorders: are common clinical
disturbances where compensation is incomplete and pH is
abnormal. Examples are -
• Metabolic acidosis • Metabolic alkalosis
• Respiratory acidosis and • Respiratory alkalosis
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DAS : ACID-BASE DISORDERS
(B) Mixed acid-base disturbances : are not merely
compensatory disturbances but independently coexisting
disorders seen in critically ill patients with extreme changes
in pH.
Primary respiratory disturbances (primary changes
in PaCO2) invoke compensatory metabolic response –
secondary changes in HCO-3. Similarly primary metabolic
disturbances cause compensatory respiratory responses.
The degree of respiratory compensation in metabolic
disturbances can be predicated by the equation : PaCO2 =
(1.5 x HCO-3) + 8 i.e. the PaCo2 is expected to decrease
1.25 mmHg for each mmol per liter decrease in HCO-3.
Physiologic Effects of Acidosis and Alkalosis
ON CVS:
Acidemia can cause a decrease in cardiac
contractility that is directly proportional to the degree of
fall in pH. Both metabolic and respiratory acidemia cause
a similar degree of myocardial depression, but the effect
of the later occurs more promptly, presumably because of
the rapid entry of CO2 into the cardiac cell. Although
metabolic acidemia decreases the threshold for ventricular
fibrillation is established acidemia has no effect on the
success of defibrillation. Acidemia also causes stimulation
of the sympathetic-adrenal axis, and in severe acidemia
this effect is countered by a depressed responsiveness of
adrenergic receptors to circulating catecholamines.
Alkalemia appears to increase myocardial contractility, at
least to a pH of 7.7. There is little effect on the threshold
for ventricular fibrillation. Also hyperventilation can cause
a decrease in systemic vascular resistance, although
alkalemia can also cause coronary artery spasm with ECG
evidence of ischemia (in fact respiratory alkalosis can be
used as a provocative stimulus in the diagnosis of
vasospastic angina).
ON CNS:
Acute respiratory acidemia causes marked increases
in cerebral blood flow. Acute elevations of PCO2 to more
than 60 mmHg causes confusion and headache, and when
it exceeds 70 mmHg loss of consciousness and seizures
can occur. However, chronic elevations in CO2 are typically
well tolerated, even when it is as high as 150 mmHg.
Also, acute hypercapnia causes depression of diaphragmatic
contractility and a decrease in endurance time. The effect
of metabolic acidemia on the respiratory muscles is less
clear, but probably also consists of depression of
contractility. Acute respiratory alkalemia causes a decrease
in cerebral blood flow, an effect that last only about 6
hours. It produces confusion, myoclonus, asterixis, loss of
consciousness and seizures.
375
On Electrolytes:
The effects of acidemia on electrolyte levels are
quite complex. Acute infusions of HCI causes an increase
in serum potassium. However, administration of organic
acids, such as lactic acid and ketoacids, does not raise
potassium levels, and may even lower it. The hyperkalemia
commonly observed in both lactic acidosis and ketoacidosis
is due to factors other than the pH change. Acute respiratory
academia causes no change, or a slight increment, in serum
potassium. Both respiratory and metabolic academia cause
increased extracellular phosphate concentrations. Clinically,
lactic acidosis and ketoacidosis are associated with
hyperphosphatemia. Acute hypocapnea causes a slight
reduction in the serum levels of sodium, potassium and
phosphorus. Alkalemia also causes an increase in
hemoglobin’s affinity for oxygen. However, there are also
an increase in the concentration of 2, 3 DPG in red blood
cells and a change in its morphology, which oppose this
effect. The clinical effect of alkalemia-induced changes in
oxygen delivery are minimal, and only in patients with
tissue hypoxia are the small, acute changes potentially
relevant.
Diagnosis of acid-base disorders
• History and Clinical findings
Most common causes of acid-base disorders should
be kept in mind. Such as :
i) Chronic renal failure expected to cause metabolic
acidosis
ii) Intestinal obstruction and chronic vomiting likely to
cause metabolic alkalosis
iii) COPD patients or patients with overdose of sedatives
usually exhibit respiratory acidosis and
iv) Patients with pneumonia, sepsis or cardiac failure
frequently have respiratory alkalosis
• Investigations
a) Arterial blood Gases estimation shows both pH
and PaCO2.
[HCO-3] is calculated from Henderson-Hasselbalch
equation. Calculated value has to be compared with
measured [HCO-3] or total CO2 on electrolyte panel. The
two values should agree within 2 mmolL-1.
Blood for electrolytes and ABG should be drawn
simultaneously prior to therapy as increase in [HCO-3]
occurs both in metabolic alkalosis and respiratory acidosis
conversely decrease in [HCO-3] seen both in metabolic
acidosis and respiratory Alkalosis.
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376 INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003

b) Serum electrolytes: Metabolic acidosis leads to
hyperkalaemia. For each 0.1 decrease in blood pH, the
plasa K+ rises by 0.6 mmolL-1.
Diabetic ketoacidosis, Lactic acidosis, diarrhoea,
renal tubular acidosis (RTA) are often associated with
potassium depletion due to urinary K+ wasting.
7.4, HCO-3 to 25 mmolL-1 and PaCO2 to 40 mmHg i.e.
ABG is almost normal but AG shows elevation at
30 mmolL-1 indicating a mixed metabolic alkalosis and
metabolic acidosis.
Responses on Simple Acid-Base Disturbances

Disorder Prediction of Compensation

Anion Gap:
Anion gap represents unmeasured anions in plasma Metabolic acidosis Paco2 = (1.5 x HCO-3) + 8
Or
(normal value – 10 to 12 mmolL-1) AG=Na+-(Cl-+ HCO-3). Paco2 will 1.25 mmHg per mmolL-1 in [HCO-3]
The unmeasured anions include–Anionic proteins, Or
Phosphate, Sulphate and organic anions. Paco2 = [HCO-3] + 15

An increase in AG is due to increase in unmeasured Metabolic alkalosis Paco2 will - 0.75 mmHg per mmolL-1 - in [HCO-3]
Or
anions and less commonly due to decrease in unmeasured Paco2 will - 6 mmHg per 10-mmolL-1 - in [HCO-3]
cations (Ca++, Mg++, K+). The AG may increase with an Or
increase in anionic albumin, either due to increased albumin Paco2 = [HCO-3] + 15

concentration or alkalosis which alters albumin charge. Respiratory alkalosis

Acute [HCO-3] will 2 mmolL-1 per 10-mmHg in Paco2
AG is decreased due to – (1) an increase in unmeasured Chronic [HCO-3] will 4 mmolL-1 per 10-mmHg in Paco2
cations, (2) addition of abnormal cations (Lithium or
Cationic immunoglobulins), (3) a reduction in major plasma Respiratory acidosis
Acute [HCO-3] will - 1 mmolL-1 per 10-mmHg - in Paco2
anion i.e. albumin (nephrotic syndrome), (4) Decrease in Chronic [HCO-3] will 4 mmolL-1 per 10-mmHg - in Paco2
anionic charge on albumin (acidosis) or (5) Hyper viscosity
and severe hyperlipidemia (which lead to an under Metabolic acidosis
estimation of Na+ and Cl- concentration). So simple
calculation of the Anion gap evaluates the acid-base disorder. Causes :
1) Increased endogenous acid production (eg. Lactate
Normal values for HCO-3, PaCO2 and pH do not
and Ketoacids)
ensure the absence of an acid-base disturbance. For
example, an alcoholic who has been vomiting may 2) Loss of HCO-3 (Diarrhoea)
develop a metabolic alkalosis with a pH of 7.55, PaCO2
3) Accumulation of endogenous acid (eg. Renal facture)
of 48 mmHg HCO-3 of 40 mmolL-1, Na+ - 135, Cl- - 80
and K+-2.8. If he develops superimposed alcoholic Clinical metabolic acidosis are of 2 types –
ketoacidosis with a b-hydroxybutyrate 15 mm, pH falls to
(1) High A.G. acidosis, (2) Normal AG or
Hyperchloremic acidosis.
Arterial blood [H+] (nmol/L)
High Anion Gap metabolic acidosis
Causes are – (1) Lactic acidosis, (2) Ketoacidosis
(diabetic, alcoholic ,starvation) (3) Ingested toxins (ethylene
glycol, methanol,salicylates ) and (4) Renal failure (acute
and chronic)

Normal Anion-Gap metabolic acidosis

(1) Gastrointestinal loss of bicarbonate(Diarrhea , Urinary
diversion)
(2) Small bowel, pancreatic, or bile drainage (fistulas,
surgical drains)
(3) Renal loss of bicarbonate (or bicarbonate equivalent)
Renal tubular acidosis, Recovery phase of
Ketoacidosis , Renal Insufficiency
Fig. 4 -Acid-base nomogram.
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DAS : ACID-BASE DISORDERS
(4) Acidifying Substances
HCl, NH4Cl, Arginine HCl, Lysine HCl, Sulfur.
Lactic acidosis is the most common and most
important acidosis encountered in the ICU. The acidaemia
has physiologic significance and, perhaps most important,
serve as a marker for a diverse group of serious underlying
conditions. Its definition is somewhat arbitrary, but it is
commonly defined as an arterial lactate level greater than
5 mmolL-1, with an arterial pH less than 7.35. Increased
lactate levels correlate well with increasing mortality in
patients with cardiogenic shock. In other types of shock
the correlation is not as good, and there is considerable
overlap between survivors and non-survivors, which is
due, in part, to the influence on lactate levels of such
factors as nutritional status and liver disease. However,
the trend in lactate levels in a given patient can be helpful
in judging the effect of therapy and assessing prognosis.
Etiologies of lactic acidosis
1. Increase Oxygen Consumption:
Strenuous exercise, Grand mal seizures, Neuroleptic
malignant syndrome, Severe asthma, Pheochromocytoma
2. Decreased Oxygen Delivery:
Decreased Cardiac Output , Hypovolemia ,
Cardiogenic shock
3. Decreased Arterial Oxygen Content:
Profound anemia , Severe hypoxemia
4. Regional Ischemia:
Microcirculatory Disturbances , Sepsis
5. Alterations in Cellular Metabolism:
Diabetes, Thiamine deficiency, Severe
alkalemia, Hypoglycemia, Malignancy
6. Toxins and Drugs
7. Congenital
8. Decreased Lactate Clearance
Fulminant hepatic failure
Treatment of metabolic acidosis :
Underlying condition must be treated.
Lactic acidosis mostly occur secondarily to a handful
of processes as shock (the most common), hypoxia,
seizures, regional ischemia (mesenteric or in an extremity),
and toxin exposure accounts for the majority of remaining
causes. So in lactic acidosis circulatory insufficiency must
be corrected, tissue perfusion restored. Vasoconstrictors
377
must be avoided. The treatment of lactic acidosis is
primarily the treatment of the disease causing the metabolic
derangement. Therapies aimed at ameliorating the acidosis
itself are attempts to prevent further deterioration until the
primary process can be controlled.
HCO3 has long been the standard therapy, but its
use is suffering a dramatic change in the recent years.
There is often a near stiochiometric relationship between
HCO 3 administered and lactate production. Its
administration causes an increase in CO2 production,
because of its metabolism to H2O and CO2. Ventilation
must be increased if a rise in PaCO2 is to be avoided. In
patients on controlled mechanical ventilation, an increase
in the minute ventilation can be used to lower the PaCO2
and raise the pH without the administration of HCO3.
Also, increased CO2 translates into decreased intracellular
pH (pHi), since CO2 equilibrates across cell membranes
more rapidly than HCO3.
Carbicarb is a buffer that has been developed as an
alkalinizing agent and to cause a smaller increase in PaCO2
than HCO3. It effectively increases arterial pH, equal to
that produced by HCO3, but with a lower sodium load and
lower osmolality. Its use is undergoing clinical trials.
Dichloroacetate increases the activity of the pyruvate-
dehydrogenase complex, thereby enhancing the conversion
of pyruvate into acetyl-CoA and its entry into the Krebs
cycle. The results to date are promising, but results of
randomized trials are still waiting.
Both hemodialysis and peritoneal dialysis have been
used to treat lactic acidosis. It uses either HCO3 or Acetate
as a buffer and does not correct the acidemia by removing
hydrogen ions; its utility lies in its ability to prevent volume
overload during the administration of large amounts of
HCO3, so having the same potential adverse effects as
intravenous HCO3. It has the advantage of removing lactate,
which may have negative effects on the myocardium and
cellular metabolism.
So, the decision of whether to use HCO3 is a difficult
one. Due to lack of supporting data, some authors, do not
recommend its use in lactic acidosis regardless of the
pH. Others use it when the pH approaches 7.0 . If it is
used, it should be administered slowly and preferably in
an isotonic mixture.
Diabetic Ketoacidosis (plasma glucose >300 mgdl-1)
must be treated with Insulin. Insulin also prevents
production of ketones.
In Alcoholic ketoacidosis ECF deficits should be
replaced by 5% dextrose in 0.9% Nacl. In drug induced
metabolic acidosis due to salicylates, vigorous gastric lavage
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378 INDIAN JOURNAL OF ANAESTHESIA, OCTOBER 2003

with isotonic saline followed by administration of activated when rapid correction (pH > 7.6) is needed. In
charcoal should be done. mineralocorticoid excess, removal of the source is the best
In case of ingestion of ethylene glycol , prompt therapy, combination of sodium restriction, potassium
institution of a saline osmotic diuresis, followed by thiamine replacement, and spironolactone or amiloride being
and pyridoxine supplement, fomepizole or ethanol and alternatives.
haemodialysis has to be done. Fomepizole 7 mgkg-1 loading
dose has the advantage of a predictable decline in ethylene Respiratory Acid-Base Disorders
glycol level without any adverse effects.
I. Alkalosis I I . Acidosis
Both uraemic acidosis and hyperchloremic acidosis A. Central nervous system stimulatio A. Central
require oral alkali replacement to maintain HCO-3 between 1. Pain 1. Drugs (anesthetics,
20 and 24 mmolL-1. This can be accomplished with alkali morphine, sedatives)
of 1.0 to 1.5 mmolkg-1 per day. Alkali replacement prevents 2. Anxiety, psychosis 2. Stroke
muscle catabolism and harmful effect of H+ on bone. 3. Fever 3. Infection
Sodium citrate (Shohl’s solution) or NaHCO3 tablets are
4. Cerebrovascular accident B. Airway
equally effective. Associated hyperkalemia should be treated
5. Meningitis, encephalitis 1. Obstruction
with frusemide (60-80 mgday-1).
6. Tumor 2. Asthma
Metabolic alkalosis 7. Trauma C. Parenchyma
Metabolic alkalosis is characterized by a primary B. Hypoxemia or Tissue hypoxia 1. Emphysema
increase in HCO-3 concentration and a compensatory 1. High attitude, Paco2 2. Pneumoconiosis
increase in PaCO2. As the normal kidney can excrete
2. Pneumonia, pulmonary edema 3. Bronchitis
HCO-3 loads of up to 10 meqkg-1day-1, for metabolic
3. Aspiration 4. Adult respiratory distress
alkalosis to persist there must be both a process that elevates
syndrome
its serum levels and a stimulus for renal reabsoption. The
4. Severe anemia 5. Barotrauma
former is usually acid loss from the stomach or from the
kidney, and the last due to hypovolemia with a Cl- deficit C. Drugs or hormones D. Neuromuscular

(renal tubules with a strong sodium avidity), hypokalemia 1. Pregnancy, progesterone 1. Poliomyelitis
or an increase in mineralocorticoid activity. When Cl- 2. Salicylates 2. Kyphoscoliosis
deficit is present, HCO-3 is reabsorbed with sodium and 3. Nikethamide 3. Myasthenia
metabolic alkalosis will persist until the Cl- deficit is D. Stimulation of chest receptors 4. Muscular dystrophies
replaced. Hypokalemia increases tubular HCO-3 reabsorption
1. Hemothorax E. Miscellaneous
and mineralocorticoid excess increases HCO-3 by increased
2. Flail chest 1. Obesity
secretion of H+ ions in the cortical collecting tubule.
3. Cardiac failure 2. Hypoventilation
The major causes in the ICU are vomiting,
4. Pulmonary embolism 3. Permissive hypercapnia.
nasogastric suction, diuretics, corticosteroids, overventilation
E. Miscellaneous
of patients with chronically increased HCO-3 levels, and
acetate used in total parenteral nutrition. If the etiology is 1. Septicemia

not clear, a trial of volume and Cl- replacement, correction 2. Hepatic failure
of hypokalemia, can be attempted. If it fails, a search for 3. Mechanical hyperventilation
increased mineralocorticoids may be warranted. 4. Heat exposure
Most cases are predictable and preventable by 5. Recovery from metabolic
replacing diuretic induced potassium losses, minimizing acidosis

nasogastric suction, use of H2+ blockers, and avoidance

PaCO2 in patients with chronic obstructive pulmonary
disease. Once it is established, removal of precipitating
factors and correction of electrolyte deficits generally
suffice to restore acid-base balance. Rarely, acetazolamide,
continuous hemodialysis and hydrochloric acid are used
Respiratory acidosis
Respiratory acidosis is characterized by a primary
increase in PaCO2 and a compensatory increase in
HCO-3. Respiratory acidosis represents ventilatory failure.
Decreased alveolar ventilation arises from a decrease in
minute ventilation or from an increase in dead space without
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DAS : ACID-BASE DISORDERS
a compensatory rise in minute ventilation. A rise in CO2
production will produce hypercapnea unless ventilation does
not increase appropriately. The etiologies can be classified
according to which part of the respiratory system is
affected. Thus hypercapnea can result from abnormalities
in the neural control of ventilation, in the chest wall and
respiratory muscles, or in the lungs and upper airways.
Pulmonary diseases are the most common in the ICU.
Drugs that depress respiratory drive should always be
sought in a patient presenting with ventilatory failure,
particularly if no pulmonary disease is present.
Treatment includes reversing causal disorders,
increasing minute ventilation, decreasing dead space, and
decreasing CO2 production. This often requires intubation
and mechanical ventilation.
Respiratory alkalosis
Respiratory alkalosis is characterized by a primary
reduction in the arterial PCO2, followed by a secondary
two-phase reduction in HCO-3, a small acute decrease due
to tissue buffers and a larger chronic decrement due to a
decrease in renal titratable acid excretion and an increase
in renal HCO-3 excretion. It occurs when alveolar ventilation
is increased relative to CO2 production.
Hyperventilation is a nonspecific response to a
variety of stimuli. The challenge is to distinguish those
that are manifestations of serious diseases. Virtually any
pulmonary disorder can cause stimulation of pulmonary
parenchymal receptors and hyperventilation. Hypoxia,
toxins and inadequate mechanical ventilation can stimulate
the respiratory center.
Treatment is that of the underlying cause. In cases
where a severe alkalemia is present, generally with
superimposed metabolic alkalosis, sedation may be
necessary. In sepsis, where a significant portion of cardiac
output can go to respiratory muscles, intubation and muscle
relaxation are often required to control hyperventilation
and redirect blood flow.
Mixed acid-base disorders
Mixed acid-base disorders are defined as
independently coexisting disorders, not merely
compensatory responses are often seen in patients in critical
care units and can lead to dangerous extremes of pH. A
patient with diabetic ketoacidosis (metabolic acidosis) may
develop an independent respiratory problem leading to
respiratory acidosis or alkalosis. Patients with underlying
pulmonary disease may not respond to metabolic acidosis
with appropriate ventilatory response because of insufficient
respiratory reserve. Such imposition of respiratory acidosis
379
on metabolic acidosis can lead to severe acidemia and a
poor outcome. When metabolic acidosis and metabolic
alkalosis coexist in the same patient the pH may be normal
or near normal. When the pH is normal, an elevated anion
gap denotes the presence of a metabolic acidosis. A diabetic
patient with ketoacidosis may have renal dysfunction
resulting in simultaneous metabolic acidosis. Patients who
have ingested an overdose of drug combinations such as
sedatives and salicylates may have mixed disturbances as
a result of the acid-base response to the individual drugs
(metabolic acidosis mixed with respiratory acidosis or
respiratory alkalosis, respectively). Even more complex
are triple acid-base disturbances. For example, patients
with metabolic acidosis due to alcoholic ketoacidosis may
develop metabolic alkalosis due to vomiting and
superimposed respiratory alkalosis due to the
hyperventilation of hepatic dysfunction or alcohol
withdrawal.
To be comprehensive, when dealing with an acid
base disorder, one should check for appropriate
compensations of the primary disturbance, as to be able to
distinguish simple from combined acid-base disorders,
which are very frequent in ICU patients. The following
formulas summarize this knowledge :
Metabolic Acidosis :
PCO2 = ( 1.5 x HCO3 ) + 8
Metabolic Alkalosis :
PCO2= ( 0.7 x HCO3 ) + 21
Respiratory Acidosis :
Acute - HCO3 = [ ( PCO2 - 40 ) / 10 ] + 24
Chronic - HCO3 = [ ( PCO2 - 40 ) / 3 ] + 24
Respiratory Alkalosis :
Acute - HCO3 = [ ( 40 - PCO2 / 5 ) ] + 24
Chronic - HCO3 = [ ( 40 - PCO2 ) / 2 ] + 24
For further reading :
1) “Acid Base Disorders” – in Principles of Critical
Care Medicine, Mc Graw Hill 1992.
2) “Critical Care Medicine” – in Cecil Textbook of
Medicine, Saunders 1996.
3) “Intensive Care” – in Oxford Textbook of
Medicine, Oxford Medical Publications 1996.
4) “Harrison’s Principles of Internal Medicine” –15th
Edition, Volume I.
5) “Biochemistry and Disease” – Bridging Basic
Science and Clinical Practice:
Robert M. Cohn, Kark S. Roth 1996.