Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5537_Библиотеки_им_академика_М_И_Перельмана.pdf
and atheroembolism — A critical review. Am J Kidney Dis 24:
713–727.
6. Merten G, Burgess W, Gray L, et al. (2004) Prevention of contrastinduced nephropathy with sodium bicarbonate: Arandomized controlled
trial. JAMA 291(19): 2329–2334.
7. Sankar D, Navaneethan, Singh S, Appasamy S, et al. (2009) Sodium
bicarbonate therapy for prevention of contrast-induced nephropathy:
A systematic review and meta-analysis. Am J Kid Dis 54: 617–627.
8. Barnett J, Parfrey P. (2006) Preventing nephropathy induced by
contrast medium. New Engl J Med 354: 379–386.
9. Zeidel M, Pirtskhalaishvili G. (2004) Urinary tract obstruction. In:
Brenner B (ed.), Brenner and Rector’s The Kidney Saunders,
Philadelphia, pp. 1880–1885.
10. Lim W, Dentali F, Eikelboom J, Crowther M. (2006) Meta-analysis:
Low-molecular-weight heparin and bleeding in patients with severe
renal insufficiency. Ann Intern Med 144: 673–684.
11. Markowitz G, Perazella M. (2009) Acute phosphate nephropathy.
Kidney Int 76: 1027–1034.
12. Davies G, Kingswood C, Street M. (1996) Pharmocokinetics of
opioids in renal dysfunction. Clin Pharmacokinet 31: 410–412.
13. Murphy E. (2005) Acute pain management pharmacology for the
patient with concurrent renal or hepatic disease. Anaesth Intensive
Care 33: 311–325.
14. DeFronzo R. (1999) Pharmacologic therapy for type 2 diabetes
mellitus. Ann Intern Med 131: 281–303.
15. Kuo P, Kanal E, Abu-Alfa A, Cowper S. (2007) Gadolinium-based MR
contrast agents and nephrogenic systemic fibrosis. Radiology 242: 647.
424
T.K. Kim
A Practical Approach to Acid-Base
Disturbances
Jaime Uribarri*
Key Pearls
• At least two of three components in the Henderson-Hasselbalch equation (pH, pCO
2
and HCO3) need to be known to make an accurate
diagnosis of a primary acid-base disorder. A low HCO
3
in the serum
chemistry profile alone does not allow making the diagnosis of primary metabolic acidosis.
• A set of blood-gas and electrolyte results cannot be interpreted
independent of the clinical details and knowledge of the condition being
diagnosed — a normal blood gas may represent perfectly compensated
metabolic alkalosis and acidosis in a renal failure patient who is vomiting.
• The urinary anion gap is useful to differentiate between gastrointestinal (GI) and renal causes of a hyperchloremic metabolic acidosis. A
negative urinary anion gap suggests GI loss of bicarbonate (e.g. diarrhea), while a positive urinary anion gap suggests impaired renal distal acidification (e.g. distal renal tubular acidosis).
• Serum osmolal gap of ≥ 25 mOsm/kg, in the absence of obvious
causes, such as alcohol intake, strongly suggests methanol or ethylene
glycol intoxication.
• The most common cause of an increased anion gap is errors in measurements of sodium, chloride or total CO
2
.
425
36
Chapter
*Mount Sinai School of Medicine, New York, NY, USA.
Initial Considerations
Arterial blood gas is not a routine blood test and can be replaced by
venous blood gas when only assessing acid-base balance. The arterial
blood gas machine usually has electrodes for direct measurement of pH,
PCO
2
and PO2and the HCO3is estimated from the first two using the
Henderson-Hasselbalch equation.
The HCO
3
from serum chemistries is actually total CO2and is there-
fore slightly higher than true HCO
3
by about 1 mEq/l. Because of this rea-
son and the fact that actual HCO
3
is slightly higher in venous than arterial
blood, the total CO
2
obtained from venous blood (serum chemistry pro-
file) is expected to be about 2 mEq/l higher than the actual HCO
3
estimated from arterial blood.
A common misconception is that total CO
2,
because it is measured
directly, is more reliable than HCO
3
estimated from arterial blood gas.
There is no a priori reason to justify this statement. If pH and pCO
2
are measured correctly, the estimated HCO3should be very reliable.
Moreover, there are many potential mistakes in measuring venous total
CO
2
including: difficulty obtaining blood requiring use of tourniquet
and local increase of CO
2
, small amount of blood in the vacuum tube
which may be left uncovered with gas CO
2
escaping before actual
measurement, etc.
Metabolic Acidosis
Definition: Blood pH < 7.35 with serum HCO3< 22 mEq/L
Causes
1. Extrarenal:
• Endogenous generation of acids: DKA, lactic acidosis
• GI HCO
3
loss (diarrhea, enteric fistula, etc.)
• Administration of acid (NH
4
Cl, cholestyramineHCL, sevelamerHCL,
hyperalimentation solutions containing arginine HCl or lysine HCl)
426
J. Uribarri
2. Renal:
• Renal HCO
3
loss (proximal RTA)
• Failure to regenerate HCO
3
(uremia or type I and type IV RTA).
Classification of metabolic acidosis by anion gap:
AG = Na–(Cl + HCO
3
) and is normally about 12 mEq/L
High AG acidosis (normochloremic):
• DKA
• Beta-hydroxybutyric acidosis
• Lactic acidosis
• D-lactic acidosis (suspect in short bowel syndrome with metabolic
encephalopathy)
• Pyroglutamic acidosis (use of acetaminophen in critically ill patient)
• Uremic acidosis (serum creatinine ≥ 5 mg/dL)
• Ingestion of toxins: (a) ethylene glycol with antifreeze (urinary oxalate
crystals); (b) methanol with bootlegged alcohol (ophthalmic neuritis);
(c) salicylates (both metabolic acidosis and respiratory alkalosis)
Normal AG acidosis (hyperchloremic):
• Renal tubular acidosis (RTA)
• GI HCO
3
loss
• Use of carbonic anhydrase inhibitors such as acetazolamide (Diamox)
• Early uremic acidosis
• Urinary diversion procedures: ureterosigmoidostomy, ileal conduit
• Dilutional acidosis
• Acidosis following respiratory alkalosis
• Administration of chloride-containing acids: NH
4
Cl, sevelamer-HCl
Clinical Manifestations
They are variable depending on the severity and chronicity of the acidosis. Acute severe acidosis can lead to cardiovascular collapse with
hypotension and shock. Chronically, acidosis induces protein breakdown,
osteomalacia and in children, failure to grow.
427
A Practical Approach to Acid-Base Disturbances
Compensatory Mechanisms
Compensation is achieved by hyperventilation that reduces pCO2according to the following formula: ∆pCO
2
=∆HCO3× 1.2 ± 2
Diagnosis
The diagnosis is suggested by a low total CO2in the blood chemistry profile together with the clinical picture, but has to be confirmed with blood
gas measurement (low HCO
3
and low pH). Next, the AG is calculated and
the patient is assessed for the conditions listed above.
Treatment
In extrarenal acidosis the emphasis is on therapy of the underlying cause
of acidosis, such as lactic acidosis. In renal acidosis, therapy with NaHCO
3
650 mg po tid should be initiated and titrated upwards. In acute severe
acidosis (in general, pH <
7.2), intravenous alkali administration is indi-
cated, starting with 2 ampoules of NaHCO
3
(44.6 mEq/ampoule) and
repeating pH measurement; the goal should be to raise the blood pH to
just above 7.20 while the underlying problem is corrected.
Metabolic Alkalosis
Definition: Blood pH > 7.45, with serum HCO3> 26 mEq/L
Causes:
Metabolic alkalosis requires simultaneously a mechanism to raise serum
HCO
3
concentration as well as a mechanism to maintain the high serum
HCO
3
concentration.
Causes of high serum HCO
3
concentration:
• Excessive endogenous production of HCO
3
: GI H+loss (vomiting,
nasogastric suction), renal H
+
loss (K depletion), intracellular H+shift
428
J. Uribarri
(K depletion), conversion of organic anions (ketones, lactate) to
HCO
3
(recovery phase of organic acidosis).
• Ingestion of HCO
3
or its precursors (citrate, etc.)
• Contraction alkalosis (sudden decrease in extracellular fluid volume
caused by loop diuretics).
Mechanisms maintaining high serum HCO
3
concentration:
• Low effective arterial volume
• K
+
depletion
• Hypercalcemia
• Hypoparathyroidism
• Severe renal failure
Clinical Manifestations
Clinical manifestations commonly include tetany and increased neuromuscular irritability, but metabolic alkalosis may also lead to metabolic
encephalopathy with confusion or even coma.
Compensatory Mechanisms
Compensation is achieved by hypoventilation that results in high pCO
2
according to the formula: ∆pCO2=∆HCO3× 0.7 + 5.
Partly because of the hypoxemia that follows hypoventilation, com-
pensation in metabolic alkalosis is very ineffective and incomplete.
Diagnosis
The diagnosis is suggested by a high total CO2in the blood chemistry
profile together with the clinical picture, but it has to be confirmed with
blood gas measurement (high HCO
3
and high pH). The next step should
be assessing the patient for a cause of increased serum HCO
3
and what
keeps it high.
429
A Practical Approach to Acid-Base Disturbances
Treatment
• Clinically, the most common factors sustaining metabolic alkalosis
are K depletion and low effective arterial volume. Thus, administration of K and fluids is usually very effective in correcting metabolic
alkalosis.
• Acetazolamide. Increased urinary excretion of HCO
3
can be obtained
by using carbonic anhydrase inhibitors such as acetazolamide (250
mg po or intravenously bid), with close follow up of serum K levels.
• Administration of acid. In cases of severe alkalosis (pH > 7.55 and
serum HCO
3
> 40), especially in conditions such as cardiac arrythmias, hepatic encephalopathy, IV administration of an acid could
effectively reduce serum HCO
3
(arginine-HCl, lysine-HCl or dilute
HCl acid [0.1N HCl] at a rate of about 0.2 mEq/kg/hr with frequent
titration of arterial blood gases).
Respiratory Acidosis
Definition: Blood pH < 7.35 (can be normal with good compensation) and
pCO
2
> 40 mmHg.
Causes — any factor causing inadequate ventilation leading to CO
2
retention:
1. Pharmacological CNS suppression: Drugs
2. Neuromuscular problem affecting breathing
3. Trauma or disease of the thoracic cage
4. Primary alveolar hypoventilation
5. Airway obstruction
6. Acute or chronic lung diseases.
Clinical Manifestations
Respiratory acidosis may be asymptomatic, if well compensated. There
may be symptoms due to hypoxemia. Acute pCO
2
elevation produces a
metabolic encephalopathy with confusion, asterixis and even coma.
430
J. Uribarri
Compensatory Mechanisms
Normal compensation raises HCO3by tissue buffering (very fast, within
seconds by the formula: ∆HCO
3
=∆pCO2× 0.07 + 1.5), and then by
increased renal excretion of acid (in many hours or days; formula: ∆HCO
3
=
∆pCO
2
× 0.4 + 3).
Diagnosis
The diagnosis is usually suspected based on a clinical presentation, but
should be confirmed by blood gas measurement (low pH and high pCO
2
).
Treatment
Treatment of the underlying process causing CO2retention will correct
respiratory acidosis. Acutely, the patient may require intubation and
mechanical ventilation, regardless of the cause.
Respiratory Alkalosis
Definition: Blood pH > 7.45 (but it could be normal with good compensation) and pCO
2
< 40 mmHg.
Causes (anything that produces hyperventilation leading to low
pCO
2
):
• Hypoxia: High altitude, ventilation/perfusion abnormalities, alveolar
capillary block
• CNS disorders such as stroke, infection
• Drugs that stimulate the respiratory center: Salicylates, progesterone
• Psychogenic hyperventilation
• Reflex stimulation of the respiratory center by any process causing
lung stiffness such as pneumonia or congestion
• Hepatic failure
• Early gram-negative sepsis.
431
A Practical Approach to Acid-Base Disturbances
Clinical Manifestations
Chronic respiratory alkalosis tends to be asymptomatic, but acute alkalosis produces symptoms of dizziness, nervousness, paresthesias, tetany and
altered level of consciousness.
Compensatory Mechanisms
Normal compensation lowers HCO3by tissue buffering (very fast, within
seconds by the formula: ∆HCO
3
=∆pCO2× 0.2 + 2.5), and then by decreased
renal excretion of acid (in many hours or days; formula: ∆HCO
3
= ∆pCO2×
0.2 +
2.5).
Diagnosis
The diagnosis is usually suspected based on clinical presentation, but
should be confirmed by blood gas measurement (high or normal pH, low
pCO
2
and low serum HCO3). Once the diagnosis of respiratory alkalosis
is confirmed, the patient should be assessed taking into consideration the
conditions listed above in relation to the clinical picture.
Treatment
• Correction of underlying disorder whenever possible
• Rebreathing bag. Breathing into a paper bag may be used for sup-
pression of symptoms in acute alkalosis
• Sedation. This is particularly effective in psychogenic hyperventilation
• Pharmacological paralysis of respiratory muscles and mechanical
ventilation. This may be necessary in cases of severe alkalosis when
its cause cannot be rapidly eliminated.
Mixed Acid-Base Disorders
This is a clinical condition in which two or more primary acid-base
disorders coexist. For example, the following acid-base disorders may
432
J. Uribarri
present together: respiratory alkalosis with metabolic acidosis; respiratory
alkalosis with metabolic alkalosis; metabolic acidosis with respiratory acidosis; metabolic alkalosis with respiratory acidosis or metabolic acidosis
with metabolic alkalosis.
A mixed acid-base disorder should be suspected in the following
situations:
• Clinical background that suggests a combined mechanism; for exam-
ple, a known CO
2
retainer who now develops severe diarrhea with
expected GI HCO
3
loss;
• Whenever blood pH approaches normal despite abnormal PCO
2
and
HCO
3
;
• When the blood gas shows ∆PCO or ∆HCO
3
outside the predicted
range using the formulas above.
433
A Practical Approach to Acid-Base Disturbances
Table 1. Common Causes of Mixed Acid-Base Disorders
Mixed Acid-Base Disorder Examples
1) Metabolic acidosis and respiratory a) Respiratory failure with anoxia
acidosis
2) Metabolic alkalosis and respiratory a) Congestive heart failure and
alkalosis vomiting
b) Diuretic therapy and hepatic failure
c) Diuretic therapy and pneumonia
3) Metabolic alkalosis and respiratory a) Diuretic therapy and chronic obstructive
acidosis airway disease
b) Vomiting and chronic obstructive airway
disease
4) Metabolic acidosis and respiratory a) Salicylate overdose
alkalosis b) Septic shock
c) Sepsis and renal failure
d) Congestive heart failure and renal
disease failure
5) Metabolic alkalosis and metabolic a) Diuretic therapy and ketoacidosis
acidosis b) Vomiting and renal failure
c) Vomiting and lactic acidosis or
ketoacidosis