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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
Interpretation of Blood Gas Measurements
Determine the primary problem:
Step 1: Assess the pH to determine whether it is within the normal
rage (7.35–7.45), low (acidemia) or high (alkalemia).
Step 2. If the pH is abnormal, assess the pCO
2
level to determine
whether it is primarily a respiratory or metabolic problem. If the pH
and pCO
2
are moving in opposite directions (e.g. pH rises while pCO
2
falls), the problem is primarily respiratory in nature.
Step 3. Just to confirm, now assess the serum HCO
3
. If the pH and
HCO
3
are moving in the same direction, the problem is primarily
metabolic in nature.
Step 4. Check the compensatory response. If the observed compensation is not the expected compensation, it is likely than more than one
acid-base disorder is present.
In general, a normal pH accompanied by an abnormal pCO
2
or HCO
3
indicates a mixed metabolic-respiratory disorder. Over- or undercompensation does not occur and is only indicative of another primary acid-base
disorder. Any combination of acid-base disorder can occur, except for respiratory acidosis and respiratory alkalosis. For example, patients with a
metabolic acidosis (acidemia plus a low plasma HCO
3
), whose calculated
pCO
2
is less than the measured value, have, in addition, an underlying respiratory alkalosis. Conversely, patients with a calculated value greater
than the measured value have a primary respiratory acidosis in addition to
the metabolic acidosis (provided the disorder has been present for more
than a few hours).
In another example, a patient with metabolic alkalosis and a meas-
ured pCO
2
greater than 60 mmHg, or significantly greater than the value
calculated from the compensation equation, is considered to have an
additional underlying primary respiratory acidosis, whereas the patient
with a pCO
2
less than the calculated value (provided the condition has
been present for more than a few hours) has an additional respiratory
434
J. Uribarri
alkalosis. In mixed acid-base disorders, therapeutic decisions should be
based on the pH level.
References
1. Mitchell L, Halperin, Marc B, et al. Fluid, Electrolyte & Acid-base
Physiology. A Problem-based Approach, 4th ed. Saunders, Elsevier.
2. Rose B. Clinical Physiology of Acid-Base and Electrolyte Disorders,
5th ed. McGraw-Hill.
3. Robert W. Schrier. Renal and Electrolyte Disorders, 7th ed. Kluwer/
Lippincot, Williams and Wilkins.
435
A Practical Approach to Acid-Base Disturbances
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Hyponatremia and Hypernatremia
Zygimantas C. Alsauskas†and Michael J. Ross*
Key Pearls
• Hyponatremia and hypernatremia are usually caused by abnormal
water balance.
• Neurologic symptoms of hyponatremia and hypernatremia are caused
by changes in effective plasma osmolality.
• Assessment of volume status is key in evaluation of both hypona-
tremia and hypernatremia.
• Overly rapid correction of chronic hyponatremia and hypernatremia can
cause central pontine myelinolysis and cerebral edema, respectively.
• Prediction equations should only be a rough guide for estimating the
fluid administration rates. Frequent plasma sodium monitoring is
essential in order to prevent overcorrection.
General Concepts
In most disorders of serum sodium concentration (SNa+), the primary disturbance is abnormal handling of water.
1,2
SNa+reflects the ratio of
sodium to water and has no relationship to the total body sodium content.
Changes in SNa
+
can alter effective plasma osmolarity, leading to trans-
cellular water shifts and potentially serious neurologic sequelae.
437
37
Chapter
*Mount Sinai School of Medicine, New York, NY, USA.
†
University of Louisville, Louisville, KY, USA.
The normal plasma osmolarity (Posm) is 275–290 mOsm/L. Urea is
an ineffective osmole, i.e. it does not contribute to transcellular water
shifts. Therefore, if BUN is elevated, effective Posm must be used when
dealing with sodium disorders (effective Posm = Posm — BUN/2.8).
Rising effective Posm stimulates hypothalamic osmoreceptors, causing
increased ADH production in the hypothalamus (supraoptic and paraventricular nuclei) and secretion in the posterior pituitary. ADH, acting via V2
receptors, promotes insertion of water channels (aquaporin 2) into luminal membranes of collecting tubule principal cells. As a result, water is
passively absorbed into hypertonic renal interstitium, promoting excretion
of concentrated urine. Hypertonicity also stimulates thirst (hypothalamic
receptors), leading to increased free water intake. Conversely, as effective
Posm decreases, ADH secretion ceases, collecting tubules become impermeable to water, and free water is excreted in dilute urine. Hypovolemia
is a powerful stimulus for ADH secretion, regardless of Posm.
Hyponatremia
Hyponatremia is defined as SNa+<135 mEq/L. A practical way to classify
it is based on the effective Posm and volume status (see Fig. 1).
Hypertonic hyponatremia occurs due to translocation of water out of cells
caused by increased concentration of extracellular osmoles (e.g. hyperglycemia, hypertonic mannitol infusion). SNa
+
decreases by about
2.4 mEq/L for each 100 mg/dL rise in glucose above normal.
Isotonic hyponatremia occurs due to absorption of large volumes of (near)
isotonic solutions of glycine, sorbitol, or mannitol solutions used in
transurethral prostate procedures.
Pseudohyponatremia is a lab artifact caused by severe hyperproteinemia
(e.g. multiple myeloma) or severe hyperlipidemia.
3
Since Na+is present
only in the aqueous portion of plasma, increasing the nonaqueous plasma
components (protein or lipid, which normally constitutes 7% of plasma
438
Z. C. Alsauskas and M. J Ross
439
Hyponatremia and Hypernatremia
Fig. 1. Approach to hyponatremia.
Hyponatremia
Check effective Posm
Hypotonic
hyponatremia
(effective Posm <275)
Hypotonic hypovolemic
hyponatremia
Renal losses (UNa+ >40)
Diuretics
(thiazide > loop; UNa
high only while
diuretic is active)
Hypoaldosteronism
Extrarenal losses
+
(UNa
<25)
Gastrointestinal
losses
Vomiting (UNa
may be high due to
bicarbonaturia,
check UCl-)
Diarrhea
Tube drainage
Skin losses
Sweating
Burns
+
Isotonic hyponatremia
(effective Posm = 275–290)
Pseudohyponatremia
Severe hyperproteinemia
Severe
hyperlipidemia
Absorption of glycine,
sorbitol, or mannitol
solutions in transurethral
or endouterine
procedures
Check volume status
Hypotonic euvolemic
hyponatremia
+
>40mEq/L, may
(UNa
be diluted in
psychogenic polydipsia)
Uosm <100
Psychogenic polydipsia
Low solute intake
Beer potomania
“Tea-and-toast” diet
Reset osmostat
with Posm below
setpoint
Pregnancy
Malnutrition
Quadriplegia
Psychosis
Uosm >100
Hypothyroidism
Adrenal insufficiency
(cortisol deficiency)
SIADH
Reset osmostat
with Posm above
set point
Hypertonic
hyponatremia
(effective Posm >290)
Hyperglycemia
Hypertonic mannitol
Hypotonic hypervolemic
hyponatremia
Advanced cirrhosis
Advanced CHF
Nephrotic syndrome with severe
hypoalbuminemia
Advanced chronic kidney
disease
volume) can factitiously lower the measured SNa+. The use of ionselective electrodes and direct potentiometry can control for this artifact.
Hypotonic hypovolemic hyponatremia occurs when volume-depleted persons replace fluid losses with electrolyte-free water. In this setting,
decreased Posm cannot suppress ADH secretion due to the overriding
effect of hypovolemia. Hyponatremia ensues due to impaired free water
excretion by the kidneys.
Hypotonic euvolemic hyponatremia can occur in hypothyroidism or adrenal
insufficiency, and these conditions must be excluded before diagnosing
SIADH.
4
Excessive pituitary or ectopic ADH in the absence of physiologic
stimuli for its secretion (hypovolemia or hyperosmolarity) causes SIADH
(see Table 1). In a reset osmostat, osmotic regulation of ADH secretion occurs
at a lower Posm, causing mild stable hyponatremia (125–135 mEq/L).
When ADH is suppressed, persons with normal renal function and
diet can excrete large volumes of free water in the urine. For example, a
person with a typical solute intake (900 mOsm/day) who dilutes urine to
the minimum attainable value (50 mOsm/L) can excrete <
18 L/day [(900
mOsm/day)/(50 mOsm/L)] of free water. Ingestion of massive quantities
of fluid (e.g. psychogenic polydipsia) can overwhelm the kidneys’ capacity to excrete water. When solute intake is low, e.g. 250 mOsm/day (beer
potomania, tea-and-toast diet), hyponatremia may develop after drinking
only ≥5 L/day [(250 mOsm/day)/(50 mOsm/L)] of fluid.
Hypotonic hypervolemic hyponatremia can occur in disease states characterized by signs of volume overload, but decreased effective arterial blood
volume (EABV), including nephrotic syndrome with severe hypoalbuminemia, advanced cirrhosis, and congestive heart failure. Low EAVB activates
baroreceptors and causes nonosmotic secretion of ADH. Hyponatremia is a
poor prognostic factor, underscoring the severity of heart or liver disease.
Free water excretion is also impaired in late stages of CKD.
In hypotonic hyponatremia, water enters brain cells, thereby increasing brain volume. When acute, it can cause neurologic symptoms, such as
headache, seizures, coma, and even fatal brainstem herniation in the most
440
Z. C. Alsauskas and M. J Ross
extreme cases. Acute hyponatremia may become symptomatic when SNa
+
decreases to <125 mEq/L. Chronic hyponatremia, unless severe, is usually
asymptomatic due to osmotic adaptation (efflux of osmolytes from brain
cells, decreasing brain volume to normal).
Workup (also see Fig. 1)
History
• Symptoms of hyponatremia: malaise, nausea/vomiting, headache,
lethargy, seizures, and coma.
• Clues to etiology in history: hypovolemia (weakness, postural dizzi-
ness, muscle cramps, diarrhea, vomiting, diuretics), volume overload
(CHF, cirrhosis, nephrotic syndrome, ascites, edema, dyspnea),
underlying causes of SIADH, etc.
441
Hyponatremia and Hypernatremia
Table 1. Common Causes of SIADH
CNS or Psychiatric Lung Diseases
• Meningitis • Pneumonia
• Encephalitis • Acute respiratory failure
• Stroke • Asthma
• Intracranial hemorrhage • Pneumothorax
• Brain neoplasms
• Trauma
• Psychosis
Medications Miscellaneous
• Carbamazepine • Ectopic production by carcinomas
• Cyclophosphamide (IV high-dose therapy) (e.g. small cell lung cancer, duodenal
• Selective serotonin reuptake inhibitors cancer, or pancreatic cancer)
(fluoxetine, sertraline) • Postoperative state
• Phenothiazines (thioridazine, thiothixene) • Severe nausea
• Haloperidol
• Amitriptyline
• Vasopressin, dDAVP
• Oxytocin
Physical exam
• Assessment of volume status: weight changes, blood pressure,
orthostatic hypotension, decreased skin turgor, dry mucous mem-
branes, jugulovenous distension, respiratory rales, dependent edema,
and ascites.
Labs
• Posm (effective Posm = Posm − BUN/2.8)
• Serum sodium, potassium, bicarbonate, BUN, creatinine, and glucose
• Uosm (indicates ADH action in the kidney)
• UNa
+
Treatment
Treatment of hypotonic hyponatremia should be aimed at correcting the
underlying condition and normalizing SNa
+
. The increase in SNa+must be
limited to <10 mEq/L/24 hr. More rapid correction, especially in the case
of chronic hyponatremia (>2 days), may cause central pontine myelinolysis, an often devastating and irreversible syndrome, manifesting as paraparesis or quadriparesis, dysphagia, dysarthria, lethargy, or coma.
5
When
hyponatremia is severely symptomatic (e.g. seizures), a more rapid initial
correction is appropriate, e.g. 1–2 mEq/L/hr for 2–3hr, or until symptoms
abate.
In hypotonic hypovolemic hyponatremia, SNa
+
normalizes with
volume repletion (IV 0.9% saline, oral NaCl solutions). Once the hypovolemic stimulus for ADH secretion is reversed, rapid excretion of free
water ensues. Care must be taken to avoid an overly rapid rise in SNa
+
,
especially if the hyponatremia is chronic.
Hypotonic hypervolemic hyponatremia is treated with free water
restriction in addition to optimizing therapy for underlying disease (CHF,
cirrhosis). Vasopressin receptor antagonists (tolvaptan) may have a limited role in cirrhosis and CHF.
6–9
442
Z. C. Alsauskas and M. J Ross
SIADH is treated with free water restriction to less than 1–1.2 L/day.
If hyponatremia is symptomatic or severe, more rapid correction with
hypertonic (3%) saline may be required. A formula can be used to estimate the initial rate of infusion of hypertonic saline (see Fig. 2). However,
it does not take into account ongoing renal and extrarenal losses water and
solutes. Close monitoring of SNa
+
is key to preventing undesirable
overcorrection.
443
Hyponatremia and Hypernatremia
Fig. 2. Estimating the initial rate of infusion of intravenous fluids to treat hyponatremia
or hypernatremia.
Adrogué-Madias formula can be used to estimate the initial rate for the infusion
of intravenous fluids to treat hyponatremia or hypernatremia:
∆SNa+ with1 L infusion =
Hyponatremia
A 40 year-old man (weight = 70 kg)
with small cell lung cancer develops
headache and somnolence, and is
found to have acute hyponatremia
(SNa+=120 mEq/L). A diagnosis of
SIADH is made. Estimate the initial
rate of 3% saline infusion to raise
SNa+ to 130 mEq/L over 24 hr.
Infusate Na+ + InfusateK+ − SNa
TBW + 1
Hypernatremia
A 77-year-old female nursing home
patient (weight = 70 kg) has had
diarrhea and decreased PO intake for
one week. After volume repletion with
normal saline, SNa+=165 mEq/L.
Estimate the rate of D5 W infusion to
lower SNa+ to 155 mEq/L over 24hr.
+
TBW = 0.6 x 70 = 42 kg.
3% NaCl [Na+] = 512 mEq/L.
∆SNa+ with 1 L infusion=[512-
120]/(42 + 1) = 9 mEq/L
If the goal is to raise SNa+ from 120
to 130 mEq/L, i.e. by 10 mEq/L over
24 hr, 10/9=1.11L 3% saline would
have to be infused, which amounts to
1111/24 = 46.3 mL/hr.
Alternatively, free water deficit can be calculated in hypernatremia, and used to
estimate the rate of free water administration:
Free water deficit = TBW
77 year-old female, weight = 70 kg, SNa+ = 165 mEq/L.
Free water deficit = 0.5 x 70 x (165-140)/140 = 6.25 L.
SNa
+
140
− 140
TBW = 0.5 x 70 = 35 kg.
∆SNa+ with 1L infusion = [0-
165]/(35+1)=-4.6mEq/L (sodium will
decrease, hence the negative value).
If the goal is to decrease her SNa
from 165 to 155mEq/L, i.e. by
10 mEq/L over 24 hr, 10/4.6 = 2.2 L D5W
would have to be infused, which
amounts to 2200/24 = 92 mL/h. In
addition, insensible losses and any
ongoing losses (e.g. diarrhea) must
also be replaced.
+