These complex disorders must then be characterized by 60 56 52 48 44 40 36 32 28 24 20 16 12 8 4 0 CHRONIC RESPIRATORY ACIDOSIS METABOLIC ALKALOSIS ACUTE RESPIRATORY ACIDOSIS NORMAL ACUT
Trang 1quantitative assessment of the expected compensatory changes (Table 5.1 )
A systematic approach to an acid – base abnormality
Several different approaches for blood gas interpretation have been devised [53 – 55] A six - step approach modifi ed from Narins and Emmitt provides a simple and reliable method to analyze a blood gas, particularly when a complicated mixed disorder is present [33,56,57] This method, adjusted for pregnancy, is as follows (Figure 5.3 )
1 Is the patient acidemic or alkalemic? If the arterial blood pH
is < 7.36, the patient is acidemic, while a pH > 7.44 defi nes alkalemia
2 Is the primary disturbance respiratory or metabolic? The primary
alteration associated with each of the four primary disorders is shown in Table 5.1
3 If a respiratory disturbance is present, is it acute or chronic? The
equations listed in Table 5.1 are used to determine the acuteness
of the disturbance The expected change in the pH is calculated and the measured pH is compared to the pH that would be expected based on the patient ’ s PCO 2
4 If a metabolic acidosis is present, is the anion gap increased?
Metabolic acidosis is classifi ed according to the presence or absence of an anion gap
methods of acid – base interpretation have been devised, including
graphic nomograms and step - by - step analysis Each method is
detailed in this section to aid in rapid and correct diagnosis of
disturbances in acid – base balance
Blood gas results are not a substitute for clinical evaluation of
a patient, and laboratory values do not necessarily correlate with
the degree of clinical compromise A typical example is the patient
with an acute exacerbation of asthma who experiences severe
dyspnea and respiratory compromise before developing
hyper-capnea and hypoxemia Thus, a blood gas is an adjunct to clinical
judgment, and decision - making should not be based on a single
test
Graphic nomogram
Nomograms are a graphic display of an equation and have been
designed to facilitate identifi cation of simple acid – base
distur-bances [49 – 52] Figure 5.2 is an example of a nomogram with
arterial blood pH represented on the x - axis, HCO3 − concentration
on the y - axis, and arterial PCO 2 on the regression lines
Nomograms are accurate for simple acid – base disturbances,
and a single disorder can be identifi ed by plotting measured
blood gas values When blood gas values fall between labelled
areas, a mixed disorder is present and the nomogram does not
apply These complex disorders must then be characterized by
60 56 52 48 44 40 36 32 28 24 20 16 12 8 4 0
CHRONIC RESPIRATORY ACIDOSIS
METABOLIC ALKALOSIS
ACUTE RESPIRATORY ACIDOSIS NORMAL
ACUTE RESPIRATORY ALKALOSIS CHRONIC
RESP.
ALKALOSIS METABOLIC
10 15 20 25
30 35
40 50 60 70 80 90 100 120 110
Arterial blood pH
Figure 5.2 Nomogram for interpretation of simple
acid – base disorders (Reproduced by permission
from Cogan MJ In: Brenner BM, Rector FC Jr, eds
The Kidney Philadelphia: WB Saunders, 1986: 473.)
Trang 2by a change in maternal position [3] Abnormal gas exchange, inadequate ventilation or both can lead to a fall in P a O 2 Hypoxemia is defi ned as a P a O 2 below 60 mmHg or a saturation less than 90% At this level, the oxygen content of blood is near its maximum for a given hemoglobin concentration and any additional increase in arterial oxygen tension will increase oxygen content only a small amount
The amount of oxygen combined with hemoglobin is related
to the P a O 2 by the oxyhemoglobin dissociation curve and infl u-enced by a variety of factors (Figure 5.4 ) The shape of the oxy-hemoglobin dissociation curve allows P a O 2 to decrease faster than oxygen saturation until the P a O 2 is approximately 60 mmHg A left shift of the curve increases hemoglobin ’ s affi nity for oxygen and oxygen content, but decreases release of O 2 in peripheral tissues The fetal or neonatal oxyhemoglobin dissociation curve
is shifted to the left as a result of fetal hemoglobin and lower levels of 2,3 - DPG (Figure 5.4 ) The increased affi nity of hemo-globin for oxygen allows the fetus to extract maximal oxygen from maternal blood A shift to the right has the opposite effect, with decreased oxygen affi nity and content but increased release
in the periphery
5 If a metabolic disturbance is present, is the respiratory
compensation adequate? The expected PCO 2 for a given degree
of metabolic acidosis can be predicted by Winter ’ s formula
(Table 5.1 ), since the relationship between PCO 2 and HCO3 −
is linear Predicting respiratory compensation for metabolic
alkalosis, however, is not nearly as consistent as with
acidosis
6 If the patient has an anion gap metabolic acidosis, are additional
metabolic disturbances present? The excess anion gap represents
bicarbonate concentration before the anion gap acidosis
developed By calculating the excess gap, an otherwise undetected non
anion gap acidosis or metabolic alkalosis may be detected
Respiratory components of the arterial blood gas
The P a O 2 refl ects the lung ’ s ability to provide adequate arterial
oxygen Normal arterial oxygen tension during pregnancy ranges
from 87 to 106 mmHg, depending upon the altitude at which a
patient lives Although P a O 2 has been reported to decrease by 25%
when samples are obtained from gravidas in the supine position
[11] , arterial blood gas values have been shown to be unaffected
pH
Metabolic acidosis (HCO3 < 20)
Metabolic alkalosis (HCO3 > 20)
Respiratory acidosis
(PCO2 > 30)
Respiratory alkalosis
(PCO2 < 30)
Measure:
Determine:
Calculate:
Calculate:
Serum Na + ,Cl-,CO2
Anion gap =
Na+ – (Cl- + HCO3-) Is respiratorycompensation
adequate?
Is it acute or chronic?
Expected pH See Table 5.1
< 20
< 24
> 20
> 24
Excess anion gap = Measured bicarb + (anion gap –12)
Coexisting primary
metabolic acidosis Coexisting nongapmetabolic acidosis Figure 5.3 A systematic approach to the interpretation of an arterial blood gas during
pregnancy
Trang 3ratio is 500 – 600 and correlates with a shunt of 3 – 5% while a shunt of 20% or more is present when the ratio is less than 200 Calculation of the alveolar – arterial oxygen gradient is also an oxygen tension calculation The A – a gradient is most reliable when breathing room air and is normally less than 20 An increased gradient indicates pulmonary dysfunction A – a gradi-ent values, however, can change unpredictably with changes in
F i O 2 and vary with alterations in oxygen saturation and con-sumption Thus, the utility of this measurement in critically ill patients has been questioned since these patients often require
a high F i O 2 and have unstable oxygenation [61] Additionally, the A – a gradient appears to be unreliable in the assessment of lung impairment during pregnancy [11]
Oxygen content - based indices include the shunt equation and estimated shunt as derived from the shunt equation (Table 5.3 ) The estimated shunt has been shown to be superior to the oxygen tension - based indices described above [58] The patient is given 100% oxygen for at least 20 minutes before determining arterial and venous blood gases and hemoglobin Since the estimated shunt equation does not require a pulmonary artery blood sample, the C (a – v) O 2 difference is assumed to be 3.5 mL/dL A normal shunt in non - pregnant patients is less than 10%, while a
20 – 29% shunt may be life - threatening in a patient with compro-mised cardiovascular or neurologic function, and a shunt of 30% and greater usually requires signifi cant cardiopulmonary support Intrapulmonary shunt values during normal pregnancy, however, have been reported to be nearly three times above the mean for non - pregnant individuals [12] The mean Qs/Qt in normotensive primiparous women at 36 – 38 weeks gestation ranges from 10% in the knee – chest position to 13% in the stand-ing position and 15% in the lateral position The increased Qs/
Qt can be explained by the physiologic changes of pregnancy as follows Lung volumes decrease during gestation and the amount
of shunt increases In addition, pulmonary blood fl ow increases secondary to increased cardiac output The combined effect of decreased lung volumes and increased pulmonary fl ow results in
a higher intrapulmonary shunt during pregnancy
Oxygenation of peripheral tissues
An adequate P a O 2 is only the initial step in oxygen transport, however, and it does not guarantee well - oxygenated tissues The degree of intrapulmonary shunt, oxygen delivery, and oxygen consumption all contribute to adequate tissue oxygenation Accurate assessment of peripheral oxygenation requires measure-ment of arterial and venous partial pressures of oxygen, arterial and venous oxygen saturation, hemoglobin, and cardiac output (Table 5.3 )
The amount of O 2 (mL) contained in 100 mL of blood defi nes oxygen content Oxygen delivery (DO 2) is the volume of O 2 brought to peripheral tissues in 1 minute and consumption (VO 2 ) is the volume used by the tissues in 1 minute Under normal conditions, delivery of oxygen is 3 – 4 times greater than consumption Oxygen extraction measures the amount of O 2 transferred to tissues from 100 mL of blood and can be thought
Assessment of lung function
Impairment of lung function can be estimated using an oxygen
tension - or oxygen content - based index Oxygen tension - based
indices include: (i) expected P a O 2 for a given fraction of inspired
oxygen (F i O 2); (ii) P a O 2 /F i O 2 ratio; and (iii) alveolar – arterial
oxygen gradient (P (A – a) O 2 ) These methods are quick and easy to
use but have limitations in the critically ill patient [58] The shunt
calculation (Qsp/Qt) is an oxygen content - based index and is the
most reliable method of determining the extent to which
pulmo-nary disease is contributing to arterial hypoxemia The need for
a pulmonary artery blood sample is a disadvantage, however, as
not all patients require invasive monitoring The estimated shunt
calculation (est Qsp/Qt) is derived from the shunt equation and
is the optimal method to estimate lung compromise when a
pul-monary artery catheter is not in place
The expected P a O 2 is an oxygen tension - based calculation and
can be quickly estimated by multiplying the actual percentage of
inspired oxygen by 6 [59] Thus, a patient receiving 50% oxygen
has an expected PO 2 of (50 × 6) or 300 mmHg Alternatively, the
F i O 2 (e.g 0.50 in a patient receiving 50% oxygen) may be
multi-plied by 500 to estimate the minimum PO 2 [60] The P a O 2 /F i O 2
ratio has been used to estimate the amount of shunt The normal
100
90
80
70
60
50
40
30
20
10
0
0
Left shift
Alkalosis
2,3-DPG
PCO2
Hypothermia
Carbon monoxide
Fetal hemoglobin
Right shift
Acidosis 2,3-DPG
PCO2
Hyperthermia 10
Adult
20
30 40 50 60 70 80 90 100
PO2 mmHg (pH 7.40)
Neonatal
(a–v)O2
Figure 5.4 Maternal and fetal oxyhemoglobin dissociation curves 2,3 - DPG,
2,3 - diphosphoglycerate (Reproduced by permission from Semin Perinatol WB
Saunders, 1984; 8:168.)
Trang 4can no longer provide adequate excretion of CO 2 Clinically, this
is recognized as tachypnea, tachycardia, intercostal muscle retraction, accessory muscle use, diaphoresis and paradoxical breathing
The metabolic component of the arterial blood gas: bicarbonate
Measurement of bicarbonate refl ects a patient ’ s acid – base status The bicarbonate concentration reported with a blood gas is cal-culated using the Henderson – Hasselbalch equation and repre-sents a single ionic species Total serum CO 2 (tCO 2 ) content is measured with serum electrolytes and is the sum of the various forms of CO 2 in serum Bicarbonate is the major contributor to tCO 2 , and additional forms include dissolved CO 2 , carbamates, carbonate, and carbonic acid The calculated bicarbonate con-centration does not include carbonic acid, carbonate, and carbamates
Frequently, arterial and venous blood samples are obtained simultaneously, making arterial blood gas bicarbonate and venous serum tCO 2 measurements available Venous serum tCO 2 content is 2.5 – 3 mEq/L higher than arterial blood gas bicarbon-ate, since CO 2 content is higher in venous than arterial blood and all species of carbon dioxide are included in the determination of tCO 2 If the blood sample is arterial, the tCO 2 content reported
on the electrolyte panel should be 1.5 – 2 mEq/L higher than the calculated bicarbonate The tCO 2 measured directly with serum electrolytes will be higher because it includes the different forms
of CO 2 Since both blood gas bicarbonate and electrolyte tCO 2 determinations are usually available, there is a split of opinion as
to the relative clinical utility of each [63] A recent review, however, concludes that calculated and measured bicarbonate values are close enough in most cases that either is acceptable for clinical use [64]
Disorders of acid – base balance
Metabolic acidosis
Metabolic acidosis is diagnosed on the basis of a decreased serum bicarbonate and arterial pH The baseline bicarbonate concentra-tion during pregnancy should, of course, be kept in mind when interpreting bicarbonate concentration Metabolic acidosis develops when fi xed acids accumulate or bicarbonate is lost Accumulation of fi xed acid occurs with overproduction as in diabetic ketoacidosis or lactic acidosis, or with decreased acid excretion as in renal failure Diarrhea, a small bowel fi stula, and renal tubular acidosis can all result in loss of extracellular bicarbonate
Although the clinical signs associated with metabolic acidosis are not specifi c, multiple organ systems may be affected Tachycardia develops with the initial fall in pH, but bradycardia usually predominates as the pH drops below 7.10 Acidosis causes venous constriction and impairs cardiac contractility, increasing venous return while cardiac output decreases Arteriolar dilation
of as CaO 2 – CvO 2 Thus, an O 2 extraction of 3 – 4 mL/dL suggests
adequate cardiac reserve to supply additional oxygen if demand
increases Inadequate cardiac reserve is indicated by an O 2
extrac-tion of 5 mL/dL or greater, and tissue extracextrac-tion must be increased
to meet changing metabolic needs [62]
Mixed venous oxygen tension (P v O 2 ) and saturation (S v O 2 ) are
measured from pulmonary artery blood These measurements are
better indicators of tissue oxygenation than arterial values since
venous blood refl ects peripheral tissue extraction Normal arterial
oxygen saturation is 100% and venous saturation is 75%, yielding
a normal arteriovenous difference (S a O 2 – S v O 2) of 25% An
increased S v O 2 ( > 80%) can occur when oxygen delivery increases,
oxygen consumption decreases, (or some combination of the
two), cardiac output increases, or the pulmonary artery catheter
tip is in a pulmonary capillary instead of the artery A decrease in
S v O 2 ( < 50 – 60%) may be due to increased oxygen consumption,
decreased cardiac output or compromised pulmonary function
The venous oxygen saturation may not change at all, however,
even with signifi cant cardiovascular changes
The metabolic rate determines the amount of carbon dioxide that
enters the blood Carbon dioxide is then transported to the lung
as dissolved CO 2 , bicarbonate, and carbamates It diffuses from
blood into alveoli and is removed from the body by ventilation,
or the movement of gas into and out of the pulmonary system
Measurement of the arterial partial pressure of carbon dioxide
allows assessment of alveolar ventilation in relation to the
meta-bolic rate
Ventilation (V E ) is the amount of gas exhaled in 1 minute and
is the sum of alveolar and dead space ventilation (V E = V A + V DS )
Alveolar ventilation (V A ) is that portion of the lung that removes
CO 2 and transfers O 2 to the blood, while dead space (V DS ) has no
respiratory function As dead space increases, ventilation must
increase to maintain adequate alveolar ventilation Dead space
increases with a high ventilation – perfusion ratio (V/Q) (i.e an
acute decrease in cardiac output, acute pulmonary embolism,
acute pulmonary hypertension, or ARDS) and positive - pressure
ventilation
Since P a CO 2 refl ects the balance between production and
alve-olar excretion of carbon dioxide, accumulation of CO 2 indicates
failure of the respiratory system to excrete the products of
metab-olism The primary disease process may be respiratory or a
process outside the lungs Extrapulmonary processes that increase
metabolism and CO 2 production include fever, shivering,
sei-zures, sepsis, and physiologic stress Parenteral nutrition with
glucose providing more than 50% of non - protein calories can
also contribute to high CO 2 production
Recognizing respiratory acid – base imbalance is important
because of the need to assist in CO 2 elimination As V E increases,
the work of breathing can cause fatigue and respiratory failure It
is important to recognize that the P a CO 2 may initially be normal,
but rises as the work of breathing exceeds a patient ’ s functional
reserve Ventilatory failure occurs when the pulmonary system
Trang 5sured ions Na + and K + account for 95% of cations while HCO3− and Cl − represent 85% of anions [66] Thus, unmeasured anions are greater than unmeasured cations The anion gap is the differ-ence between measured plasma cations (Na + ) minus measured anions (Cl − , HCO3 −) and is derived:
Total anions Total cations unmeasured
anions
=
Measured anions
m measured cations
+
unmeasured cations unmeasured
aanions
unmeasured cations Unmeasured
anions
unme
⎛
−
Na ++
aasured cations =[ ]−( [ ]+[ ] )
=[ ]− [ ]
++
Anion gap Na (Cl + ttCO[ 2] )
A normal anion gap is 8 – 16 mEq/L Potassium may be included
as a measured cation, although it contributes little to the accuracy
or utility of the gap If K + is included in the calculation, however, the normal range becomes 12 – 20 mEq/L [67]
A change in the gap involves a change in unmeasured cations
or anions An elevated gap is most commonly due to an accumu-lation of unmeasured anions that include organic acids (i.e keto-acids or lactic acid), or inorganic keto-acids (i.e sulfate and phosphate) [68] A decrease in cations (i.e magnesium and calcium) will also increase the gap, but the serum level is usually life - threatening
occurs at pH < 7.20 Respiratory rate and tidal volume increase in
an attempt to compensate for the acidosis Maternal acidosis can
result in fetal acidosis as H + ions equilibrate across the placenta,
and fetal pH is generally 0.1 pH units less than the maternal pH
The compensatory response to metabolic acidosis is an
increase in ventilation that is stimulated by the fall in the pH
Hyperventilation lowers PCO 2 as the body attempts to return the
HCO3 − PCO2
[ ] ratio toward normal The respiratory response is
proportional to the degree of acidosis and allows calculation of
the expected PCO 2 for a given bicarbonate level (Table 5.1 )
When the measured PCO 2 is higher or lower than expected for
the measured serum bicarbonate, a mixed acid – base disorder
must be present This formula is ideally applied once the patient
has reached a steady state, when PCO 2 nadirs 12 – 24 hours after
the onset of acidosis [56]
The classifi cation of metabolic acidosis as non - anion gap or
anion gap acidosis helps determine the pathologic process Once
a metabolic acidosis is detected, serum electrolytes should be
obtained to calculate the anion gap Frequently the clinical history
and a few additional diagnostic studies can identify the
underly-ing abnormality (Figure 5.5 ) [65]
Electroneutrality in the body is maintained because the sum of
all anions equals the sum of all cations Na + , K + , Cl − , and HCO3−
are the routinely measured serum ions while Mg + , Ca 2+ , proteins
(particularly albumin), lactate, HPO4− and SO4− are the
unmea-pH, HCO 3 2–
Calculate anion gap
Elevated anion gap
Measure:
Serum glucose Serum ketones Serum creatinine Lactate
Serum osmolality Toxin screen Salicylate level
Ethylene glycol ingestion Lactic acidosis
Methanol ingestion Paraldehyde ingestion Propylene glycol ingestion Salicylate toxicity Renal failure (late acute or early chronic) Ketoacidosis
Diabetic Alcoholic Starvation
Normal anion gap
Gastrointestinal bicarbonate loss Diarrhea
Small bowel fistula Renal tubular acidosis Medication
Carbonic anhydrase inhibitors (e.g., acetozolamide)
Amphotericin B Cyclosporine Cholestyramine Acid ingestion Hypoaldosteronism Renal failure (early acute or mild chronic)
Figure 5.5 Etiology and evaluation of metabolic
acidosis
Trang 6The following example demonstrates use of the anion gap in a
patient who had been experiencing dysuria, polyuria, and
polydypsia of several days duration Initial evaluation of this 19 year
old gravida at 24 weeks gestation was notable for a serum glucose
level of 460 mg/dL and 4+ urinary ketones Further investigation
revealed: arterial pH of 7.30, HCO3 − of 14 mEq/L, serum Na + of
133 mEq/L, K + of 4.1 mEq/L, tCO 2 of 15 mEq/L, and Cl − of
95 mEq/L The anion gap was determined:
=[ ]−( [ ]+[ ] )
=
2
23
Anion gap mEq L
−
The elevated anion gap is the result of unmeasured organic
anions or ketoacids that have accumulated and decreased serum
bicarbonate As this patient with type I diabetes mellitus receives
insulin therapy, the anion gap will normalize, refl ecting
disap-pearance of the ketoacids from the serum
The limitations of the anion gap, however, should be
recog-nized Various factors can lower the anion gap, but its importance
is not so much in the etiology of the decrease as in its ability to
mask an elevated gap Since albumin accounts for the majority of
unmeasured anions, the gap decreases as albumin levels fall For
each 1 g decrease in albumin, the gap may be lowered by 2.5 –
3 mEq/L The most common cause of a lowered gap is decreased
serum albumin Other less common causes include markedly
elevated levels of unmeasured cations (K + , Mg + , and Ca 2+ ),
hyper-lipidemia, lithium carbonate intoxication, multiple myeloma,
and bromide or iodide intoxication
Although an elevated anion gap is traditionally associated with
metabolic acidosis, it may also occur in the presence of severe
metabolic alkalosis The ionic activity of albumin changes with
increasing pH and protons are released The net negative charge
on each molecule increases, thereby increasing unmeasured
anions Volume contraction leads to hyperproteinemia and
aug-ments the anion gap
If an anion gap acidosis is present, the ratio of the change in
the anion gap (the delta gap) to the change in HCO3 − can be
helpful in determining the type of disturbances present:
∆
∆
gap
HCO
Anion gap
HCO
12 24
−[ ]
In simple anion gap metabolic acidosis, the ratio approximates
1.0, since the decrease in bicarbonate equals the increase in
anions The delta gap for the patient with diabetes and
ketoaci-dosis previously described is calculated as follows:
∆
∆
gap
HCO
Anion gap
HCO
12 24
23 12
24 14
11
10 1 1
−
The delta gap is 0 when the acidosis is a pure non - anion gap acidosis A delta gap of 0.3 – 0.7 is associated with one of two mixed metabolic disorders: (i) a high anion gap acidosis and respiratory alkalosis and (ii) high anion gap with a pre - existing normal or low anion gap A ratio greater than 1.2 implies a meta-bolic alkalosis superimposed on a high anion gap acidosis or a mixed high anion gap acidosis and chronic respiratory acidosis The use of the delta gap is, however, limited by the wide range of normal values for the anion gap and bicarbonate, and its accuracy has been questioned [69]
When a normal anion gap metabolic acidosis is present, the urinary anion gap may be helpful in distinguishing the cause of the acidosis:
urinary anion gap=[urine Na+]+[urine K+]−[urine Cl−] The urinary anion gap is a clinically useful method to estimate urinary ammonium ( NH4 +) excretion Since the amount of NH4 + excreted in the urine cannot be directly measured, the urinary anion gap helps determine whether the kidney is responding appropriately to a metabolic acidosis [70] Normally, the urine anion gap is positive or close to zero A negative gap (Cl − > Na + and K + ) occurs with gastrointestinal bicarbonate loss and NH4 + excretion by the kidney increases appropriately In contrast, a positive gap (Cl − < Na + and K + ) in a patient with acidosis suggests impaired distal urinary acidifi cation with inappropriately low
NH4 + excretion
A variety of processes can lead to metabolic acidosis and therapy will depend on the underlying condition Adequate oxy-genation should be ensured and mechanical ventilation instituted for impending respiratory failure The use of bicarbonate solu-tions to correct acidosis has been suggested when arterial pH is less than 7.10 or bicarbonate is lower than 5 mEq/L Bicarbonate solutions must be administered with caution since an “ over-shoot ” alkalosis can lower seizure threshold, impair oxygen avail-ability to peripheral tissues, and stimulate additional lactate production
Metabolic alkalosis
Metabolic alkalosis is characterized by a rise in serum bicarbonate concentration and an elevated arterial pH The most impressive clinical effects of metabolic alkalosis are neurologic and include confusion, obtundation, and tetany Cardiac arrhythmias, hypo-tension, hypoventilation and various metabolic aberrations may accompany these neurologic changes
Metabolic alkalosis results from a loss of acid or the addition
of alkali The development of metabolic alkalosis occurs in two phases, with the initial addition or generation of HCO3 − followed
by the inability of the kidney to excrete the excess HCO3 − The two most common causes of metabolic alkalosis are excessive loss of gastric secretions and diuretic administration Once established, volume contraction, hypercapnea, hypokalemia, glucose loading, and acute hypercalcemia promote HCO3 − reabsorption by the kidney and sustain the alkalosis
Trang 7a responsive disorder, infusion of sodium chloride will correct the abnormality Conversely, saline administration will not correct a chloride resistant disorder and can be harmful Treatment of the primary disease will concurrently correct the alkalosis Although mild alkalemia is generally well tolerated, critically ill surgical patients with a pH ≥ 7.55 have increased mortality [72,73]
Respiratory acidosis
Respiratory acidosis is characterized by hypercapnea (a rise in PCO 2 ) and a decreased arterial pH The development of respira-tory acidosis indicates the failure of carbon dioxide excretion to match CO 2 production A variety of disorders can contribute to this acid – base abnormality (Table 5.4 ) It is important to remem-ber that the normal PCO 2 in pregnancy is 30 mmHg, and norma-tive data for non - pregnant patients do not apply to the gravida The clinical manifestations of acute respiratory acidosis are particularly evident in the central nervous system Since carbon dioxide readily penetrates the blood – brain barrier and cerebro-spinal fl uid buffering capacity is not as great as blood, PCO 2 elevations quickly decrease the pH of the brain Thus, neurologic compromise may be more signifi cant with respiratory acidosis than metabolic acidosis [59] Acute hypercapnia also decreases
The degree of respiratory compensation for metabolic alkalosis
is more variable than with metabolic acidosis, and formulas to
estimate the expected P a CO 2 have not proven useful [56] Alkalosis
tends to cause hypoventilation but P a CO 2 rarely exceeds 55 mmHg
[56,71] Tissue and red blood cells attempt to lower HCO3 − by
exchanging intracellular H + ions for extracellular Na + and K +
Once metabolic alkalosis is diagnosed, determination of
urinary chloride concentration can be helpful in determining the
etiology (Figure 5.6 ) Urinary chloride is a more reliable indicator
of volume status than urinary sodium concentration in this group
of patients Sodium is excreted in the urine with bicarbonate to
maintain electroneutrality and occurs independently of volume
status Therefore, low urinary chloride in patients with volume
contraction accurately refl ects sodium chloride retention by the
kidney
A urinary chloride concentration < 10 mEq/L that improves
with sodium chloride administration is a chloride - responsive
metabolic alkalosis In contrast, a urine chloride > 20 mEq/L
indi-cates that the alkalosis will not improve with saline
administra-tion and is a chloride - resistant alkalosis Urine chloride levels
must be interpreted with caution since levels are falsely elevated
when obtained within several hours of diuretic administration
Treatment of metabolic alkalosis is aimed at eliminating
excess bicarbonate and reversing factors responsible for
main-taining the alkalosis If the urinary chloride level indicates
pH, HCO 3 Measure urinary chloride
Chloride resistant
(Urine Cl– > 20 mEq/L)
Hypertensive:
Mineralocorticoid excess Hyperaldosteronism
Normotensive:
Magnesium depletion Diuretic use (current) Profound hypokalemia Alkali ingestion Bicarbonate therapy Antacids
Lactate Acetate Citrate Massive blood transfusion Hypercalcemia
Medications Carbenicillin Penicillin Sulfates Parathyroid disease Refeeding alkalosis
Chloride responsive
(Urine Cl– < 10 mEq/L)
Gastrointestinal
Vomiting
Nasogastric suction
Diuretic use (discontinued)
Contraction alkalosis
Posthypercapnea
Figure 5.6 Etiology and evaluation of metabolic alkalosis
Table 5.4 Causes of respiratory acidosis
Airway obstruction Aspiration Laryngospasm Severe bronchospasm
Impaired ventilation Pneumothorax Hemothorax Severe pneumonia Pulmonary edema Adult respiratory distress syndrome
Circulatory collapse Massive pulmonary embolism Cardiac arrest
CNS depression Medication Sedatives Narcotics Cerebral infarct, trauma or encephalopathy Obesity – hypoventilation syndrome
Neuromuscular disease Myasthenic crisis Severe hypokalemia Guillain – Barr é Medication
Trang 8acid – base disorder in which the compensatory response can return the pH to normal
Respiratory alkalosis may be diagnostic of an underlying con-dition and is usually corrected with treatment of the primary problem Hypocapnea itself is not life - threatening but the disease causing the alkalosis may be The presence of respiratory alkalosis should always raise suspicion for hypoxemia, pulmonary embo-lism, or sepsis These conditions, however, can be overlooked if the only concern is correction of the alkalosis Mechanical venti-lation may lead to iatrogenic respiratory alkalosis and the PCO 2 can usually be corrected by lowering the machine - set respiratory rate [75]
References
1 Kruse JA Acid – base interpretations Crit Care 1993 ; 14 : 275
2 MacRae DJ , Palavradji Maternal acid – base changes in pregnancy J
Obstet Gynaecol Br Cwlth 1967 ; 74 : 11
3 Hankins GDV , Harvey CJ , Clark SL , Uckan EM The effects of mater-nal position and cardiac output on intrapulmonary shunt in normal
third - trimester pregnancy Obstet Gynecol 1996 ; 88 : 327
4 Cruikshank DP , Hays PM Maternal physiology in pregnancy In:
Gabbe S , Niebyl J , Simpson JL , eds Obstetrics: Normal and Problem
Pregnancies , 2nd edn New York : Churchill Livingstone , 1991 : 129
cerebral vascular resistance, leading to increased cerebral blood
fl ow and intracranial pressure
The compensatory response depends on the duration of the
respiratory acidosis In acute respiratory acidosis, the respiratory
center is stimulated to increase ventilation Carbon dioxide is
neutralized in erythrocytes by hemoglobin and other buffers, and
bicarbonate is generated An acute disturbance implies that renal
compensation is not yet complete Sustained respiratory acidosis
(longer than 6 – 12 hours) stimulates the kidney to increase acid
excretion, but this mechanism usually requires 3 – 5 days for full
compensation [74]
The primary goal in the management of respiratory acidosis is
to improve alveolar ventilation and decrease arterial PCO 2
Assessment and support of pulmonary function are paramount
when a patient has respiratory acidosis Carbon dioxide
accumu-lates rapidly, and PCO 2 rises 2 – 3 mmHg/min in a patient with
apnea The underlying condition should be rapidly corrected and
may include relief of an airway obstruction or pneumothorax,
administration of bronchodilator therapy, narcotic reversal, or a
diuretic
Adequate oxygenation is crucial because hypoxemia is more
life - threatening than hypercapnia In the pregnant patient,
hypoxemia also compromises the fetus Uterine perfusion should
be optimized and maternal oxygenation ensured since the
com-bination of maternal hypoxemia and uterine artery
hypoperfu-sion profoundly affects the fetus When a patient cannot maintain
adequate ventilation despite aggressive support, endotracheal
intubation and mechanical ventilation should be performed
without delay
Respiratory alkalosis
Respiratory alkalosis is characterized by hypocapnea (decreased
PCO 2 ) and an increased arterial pH Acute hypocapnea frequently
is accompanied by striking clinical symptoms, including
pares-thesias, circumoral numbness, and confusion Tachycardia, chest
tightness, and decreased cerebral blood fl ow are some of the
prominent cardiovascular effects Chronic respiratory alkalosis,
however, is usually asymptomatic
Respiratory alkalosis is the result of increased alveolar
ventila-tion (Table 5.5 ) Hyperventilaventila-tion can develop from stimulaventila-tion
of brainstem or peripheral chemoreceptors and nociceptive lung
receptors Higher brain centers can override chemoreceptors and
occurs with involuntary hyperventilation Respiratory alkalosis is
commonly encountered in critically ill patients in response to
hypoxemia or acidosis, or secondary to central nervous system
dysfunction
The compensatory response is divided into acute and chronic
phases In acute alkalosis, there is an instantaneous decrease in
H + ion concentration due to tissue and red blood cell buffer
release of H + ions If the duration of hypocapnea is greater than
a few hours, renal excretion of bicarbonate is increased and acid
excretion is decreased This response requires at least several days
to reach a steady state Chronic respiratory alkalosis is the only
Table 5.5 Causes of respiratory alkalosis
Pulmonary disease Pneumonia Pulmonary embolism Pulmonary congestion Asthma
Drugs Salicylates Xanthines Nicotine CNS disorders Voluntary hyperventilation Anxiety
Neurologic disease Infection Trauma Cerebrovascular accident Tumor
Other causes Pregnancy Pain Sepsis Hepatic failure Iatrogenic mechanical hyperventilation
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