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Table 17.6.15 Compensatory changes in Paco2 and HCO3 in response to acidosis and alkalosis
Primary disorder Compensatory change Expected compensation
Metabolic acidosis Fall in PaCO2 PaCO2 = 1.2 x HCO3
Fall in HCO3
Metabolic alkalosis Rise in PaCO2 PaCO2 = 0.7 x HCO3
Rise in HCO3
Respiratory acidosis Rise in HCO3 Acute : HCO3 = 0.1 x PaCO2
Rise in PaCO2 Chronic : HCO3 = 0.3 x PaCO2
Respiratory alkalosis Fall in HCO3 Acute : HCO3 = 0.2 x PaCO2
Fall in PaCO2 Chronic : HCO3 = 0.5 x PaCO2
vip.persianss.ir
Clinical Features Chloride resistant metabolic alkalosis: Treat the
Manifestations of acidosis are related to the degree of underlying cause and give potassium supplementation
acidosis. Worsening acidosis may produce hypotension, or potassium sparing diuretic.
lethargy, stupor and progresses to coma. pH <7.2 is Respiratory Acidosis
associated with increased risk of cardiac arrhythmias.
Increased work of breathing (kussmauls breathing) may In respiratory acidosis there is decreased elimination of
predispose to superimposed respiratory acidosis. Chronic carbon dioxide from the body due to poor ventilation, which
acidemia results in osteopenia, muscle wasting, and growth leads to accumulation of carbon dioxide. Acute respiratory
retardation. acidosis is characterized by a primary rise in paCO2 above
45 mm Hg that remains at this high value up to 612 hours.
Management Sustained elevation of paCO2 beyond 12 hours is defined as
Emergency measures: Prevent further production of chronic respiratory acidosis.
H+ by ensuring a proper airway, adequate peripheral
Clinical Features
perfusion, oxygen delivery
Treat underlying disorder if possible Signs and symptoms are related to the degree of
Bicarbonate therapy: Intravenous bicarbonate should hypercapnia. Child develops headache with either
be used very judiciously if the pH is <7.2 and/or HCO3 irritability or depression due to increase in intracranial
5 mEq/L aiming to raise pH to 7.2. NaHCO3 needs to pressure (ICP). There is impairment of consciousness
be diluted at 1:1 concentration for IV infusion and the varying from drowsiness to deep coma. Muscular tremors
amount of bicarbonate to be given = 0.3 x body weight can occur. Tachycardia, flushing of skin or perspiration may
x base deficit. be present. Blood pressure may be low with signs of shock.
Ventricular fibrillations may occur.
Disadvantages of NaHCO3 therapy are hyperosmolality,
hypernatremia, hypokalemia, decrease in ionized calcium, Management
intracerebral acidosis, shift of oxygen dissociation curve Treatment is directed at the underlying cause and
resulting in worsening of tissue hypoxia and worsening of improvement of alveolar gas exchange by assisted
intracellular acidosis. ventilation. Oxygen administration with high flow rates
Hemodialysis or peritoneal dialysis can be done to treat may help to wash out carbon dioxide. If hyperkalemia
metabolic acidosis if severe or if associated with renal or ventricular fibrillation develops in a child with acute
failure (uremic acidosis), or in poisonings. respiratory acidosis, sodium bicarbonate may be life saving.
It should be administered after establishing ventilation.
Metabolic Alkalosis
Metabolic alkalosis is defined as HCO3 >2830 mEq/L, Respiratory Alkalosis
usually with a rise in pH >7.45. It usually occurs due to hyperventilation; psychogenic or
Clinical Features neurogenic. It may be one of the earliest signs of sepsis.
Acute respiratory alkalosis last no longer than 612
Symptoms are due to hypokalemia and decreased ionized
hours. The compensatory response to this phase involves
calcium levels.
consumption of HCO3 by body buffers. In the chronic phase
Mild metabolic alkalosis (HCO3 < 36) is asymptomatic.
renal suppression of H+ ion excretion and chloride retention
Moderate metabolic alkalosis: (HCO3 3642 mEq/L) can
occurs.
cause paresthesia, weakness, orthostatic hypotension,
fatigue, muscle cramps, lethargy, hyporeflexia, muscular clinical feature
irritability. Usually there is hyperventilation with features of tetany as
Severe metabolic alkalosis: (HCO3 > 4550 mEq/L) alkalosis decreases blood levels of ionized calcium.
arrhythmias, tetany, seizures, delirium, stupor. Child may
Treatment
develop hypoventilation which could result in hypoxemia,
difficulty in weaning from ventilator, increased digoxin Breathing in a closed circuit would cause accumulation
toxicity, worsening of hepatic encephalopathy. of carbon dioxide. The underlying condition should be
treated. Sodium bicarbonate therapy is not indicated.
Management
Chloride responsive: Treating the underlying cause is Mixed Acid-base Disorders
the primary therapy. Correct the hydration status with Mixed acidbase disturbances are conditions where
intravenous 0.9% saline infusion at 10 mL/kg over 10 more than one primary acid disturbance occurs. The four
30 minutes and if there is coexisting hypokalemia, that commonly encountered mixed acidbase disorders are: (1)
needs to be corrected with KCl supplementation. In case respiratory acidosis + metabolic acidosis, (2) respiratory
of diuretic-induced metabolic alkalosis, stop the loop acidosis + metabolic alkalosis, (3) respiratory alkalosis +
diuretic and it can be replaced by K sparing diuretics. metabolic acidosis and (4) respiratory alkalosis + metabolic
alkalosis (Table 17.6.16). The most serious acidbase
disorders are of mixed type when respiratory and metabolic
disturbances result in a pH change in the same direction.
4 Acid-Base Balance and
Disturbance
Monitoring
Ensure the airway breathing circulation (ABC). Then, the
form and type of monitoring will be dictated by the patients
condition. Start with continuous pulse oximetry and ECG
monitoring, and intermittent BP monitoring. Follow hourly
output.
Therapy
Correction of Dehydration
If the patient is dehydrated then this problem should be treated
with oral or IV replacement. This alone may improve serum
HCO3. Other interventions if required are follows:
Fig. 1: Clinical features of metabolic acidosis Inotropes in persistent hypotension after fluid resuscitation
Identify the underlying cause and treat accordingly
CNS: Altered sensorium in sepsis, poisoning and metabolic (antibiotic in sepsis)
disorder associated with metabolic acidosis The use of buffers is common but lacks consensus on
Abdomen indications and possible benefits
Growth: Usually retarded in renal failure, untreated Sodium bicarbonate (NaHCO3) may worsen intracellular
diabetes mellitus acidosis, hypokalemia and hypocalcemia. It may increase
1. Confirm diagnosis (blood gas analysis): the risk of cerebral edema in diabetic ketoacidosis.
Arterial pH less than 7.34 However, HCO 3/alkali therapy may be used for specific
Base excess less than 3 mmol/L
metabolic disorders.
PaCO2 appropriate for acidosis, i.e. it is usually low
when hyperventilatory compensation occurs but
Metabolic Acidosis with Increased AG
is often high if there is also a respiratory acidosis
component or normal in ventilated paralyzed patients. Identify the cause and treatment; IV NaHCO 3 is only
2. Check blood and urine: given as last resort (child must be able to excrete the CO2
Measure serum Na, K, Cl, urea, creatinine, lactate, generated)
glucose and albumin Sodium bicarbonate 8.4% (1 mmol/mL) is commonly used
Check urine for pH, ketones and may be indicated in:
Imaging: Renal ultrasound scan looking for nephro Severe acidosis (pH <7.1) and hypotension when
calcinosis (type I RTA) inotropes appear to be ineffective due to receptor
Once diagnosis of metabolic acidosis is confirmed, dysfunction
attempt to identify the underlying cause by calculation of Sodium bicarbonate should not be given as rapid bolus
corrected AG.
but as slow infusion (i.e. 12 mL/kg/hr of 8.4% NaHCO3 =
3. AG more than 16consider clinical context and treat cause:
12 mmol/kg/hr) and titrate to effect, i.e. target pH more
Lactic acidosis: Does this fit with clinical context, e.g.
than 7.2
hypotension, fluid/blood loss, myocardial dysfunction,
septic shock, seizures, etc. Estimate the deficit = (20 [HCO3]) weight (kg) 0.5 mmol
Ketoacidosis ( blood sugar) Replace over 2448 hours with oral supplements
Renal failure ( urea, creatinine) Tham (tromethamine) is a sodium-free buffer that does
If none of these, consider underlying metabolic disease not generate CO2. Despite its attractive qualities, it has
or poisoning. not yet been shown to have clinical advantages over
4. AC less than 16 consider clinical context and treat cause: NaHCO3. It has also been linked with the adverse effects
HCO3 loss from gastroenteritis (GIT). of hyperkalemia, hypoglycemia and apnea.
HCO3 loss from kidneys (RTA).
Check chloride, whether it is raised. Metabolic Acidosis with Normal Anion Gap
Excess chloride from drugs, infusions. This indicates HCO3 loss. Diarrhea is the most common cause;
acidosis is corrected by fluid and electrolyte correction by oral
Treatment rehydration salt or in severe rehydration by IV polyelectrolyte
Most metabolic acidoses seen in PICU are lactic acidosis solution. Usually do not require extra IV NaHCO3.
with normal plasma lactate. This only rises in more severe Other causes of metabolic acidosis with normal AG are:
cases, secondary to shock (reduced oxygen delivery) Distal or proximal RTA: Treatment includes HCO 3
or seizures (oxygen consumption) and improves with supplementation
attention to fluid resuscitation and oxygen. Hyperkalemic RTA: Correct serum HCO3 and increased
Aim for target pH more than 7.25, if possible. Consider fluids to improve sodium delivery to the distal tubule (this
ventilatory support if pH less than 7.2. will enhance potassium secretion).
165
Severe and very severe pneumonia (pneumonia usually respiratory distress syndrome, etc. In both acute severe
causes respiratory alkalosis due to hyperventilation) bronchiolitis and acute severe bronchial asthma, initially there
Severe pulmonary edema is decreased pO2 and decreased pCO2 due to hyperventilation
Tension pneumothorax and respiratory alkalosis follows. As bronchial obstruction
Respiratory muscle disorders like Guillain-Barr syndrome and hypoventilation finally occur due to exhaustion, pCO 2
(GBS), poliomyelitis, myopathies, spinal muscular atrophy increased. If increased pCO 2 and decreased pO 2 are not
Restrictive disease of thorax (scoliosis, pectus excavatum). corrected timely by assisted ventilation, respiratory acidosis
takes place. If respiratory acidosis and hypoxemia continue
Acute versus Chronic Respiratory Acidosis then anaerobic glycolysis and lactic acidosis take place causing
metabolic acidosis. Serum HCO3 then falls inappropriately
Most of the acute respiratory acidoses are short-lived with short
to increased pCO2 and decreased pH. Here increased pCO2 is
lived increased PaCO2. There is a small secondary increment of
associated with decreased HCO3. Such clinical setting sets in
HCO3 (23 mEq/L), and pH still remains low (acidic).
mixed respiratory and metabolic acidosis.
In chronic respiratory acidosis (most often the consequence
of chronic obstructive lung disease), secondary renal responses
Example
result in more marked increase in plasma HCO3 concentration.
The mean increment in HCO3 concentration in an individual A 1-year-old child with acute severe bronchiolitis, developed
fully adapted to chronic hypercapnia is approximately 0.4 type II respiratory failure with pO2 of 50 mm Hg and pCO2 60
mEq/L for each mm Hg increment in PaCO2. The coexistence mm Hg, serum HCO3 of 12 mEq/L and pH of 6.9. A rise of pCO2
of metabolic acid-base disturbance in patients with primary of 20 (6040 mm Hg) is supposed to increase serum HCO3 to
respiratory acidosis can be assessed by determining whether 20 0.4 = 8 mEq/L, that is serum HCO3 is expected to be (24 +
the level of plasma HCO3 concentration corresponds to the 8) = 32 mm Hg. However, serum HCO3 (base deficit) was found
level anticipated for the observed degree and duration of to be 12 mEq/L. This indicates another primary process (here
hypercapnia. lactic acidosis due to hypoxia) working in opposite direction
to make acidemia worse.
Example
A child with long-standing chronic lung disease (cystic Practice
fibrosis) has a PaCO 2 of 55 mm Hg, pH 7.34 and plasma
A 4-day-old preterm newborn baby presented with respiratory
HCO 3 concentration of 30 mEq/L. The increment above
distress, since birth with pO2 of 55 mm Hg and pCO2 60 mm
normal PaCO2 is approximately 15 mm Hg (5540 mm Hg).
Hg. His HCO3 level is 8 mEq/L and pH is 6.9. X-ray shows air
Thus one might anticipate an increment in plasma HCO3
bronchogram.
concentration of approximately 6 mEq/L just on the basis of
1. What is his respiratory status?
chronic hypercapnia (15 0.4 mEq/L). The increment in HCO3
2. What is the most likely clinical diagnosis?
concentration will make serum HCO3 (considering mean
3. What is the acid-base status?
serum HCO3 as 24 mEq/L) level to be (24 + 6) 30 mEq/L, which
is called partially or completely compensated (if pH becomes Answers:
normal) respiratory acidosis. This sort of compensated 1. The baby has developed type II respiratory failure (pO2
respiratory acidosis may also be found in chronic obstructive and pCO2)
airway disease in adult and sometimes in persistent (moderate 2. Most likely, diagnosis is respiratory distress syndrome
to severe) asthma in children. Compensatory respiratory (RDS) as evidenced by air bronchogram on chest X-ray
acidosis is unusual in acute respiratory conditions. If HCO3 3. Mixed respiratory acidosis and metabolic acidosis.
level increases more than 30 mEq/L, than independent
Explanation:
process also works, which is an evidence of mixed acid-base
pH: Less than 7.4 (Acidemic).
disturbance in which an element of metabolic alkalosis is
pCO2: More than 40 mm Hg respiratory acidosis as primary
present (the respiratory acidosis + metabolic alkalosis). clinical setting is respiratory problem (RDS)
Plasma HCO3: Decreased instead of physiological response
Mixed Respiratory Acidosis with of increased HCO3.
Metabolic Acidosis
pCO2 is 20 mm Hg (6040 mm Hg) more than normal. In
This is not an uncommon mixed acid-base disturbance, where simple respiratory acidosis, there will be increase of 23 mEq/L
two primary mechanisms work. Important steps are: of serum HCO 3 in acute hypercapnia (within few hours)
Clinical settings and 0.4 mEq/L for each mm Hg increase of pCO2 in chronic
+ hypercapnia. If condition continues further (chronic), 8 mEq/L
Step 1: Confirm the pH (<7.5) (20 0.4) increase in serum HCO3 above normal is expected. If
Step 2: Confirm the PaCO2 (>5.3 kPa or >40 mm Hg) normal mean serum HCO3 is considered to the 24 mEq/L than
Step 3: High negative BE (base deficit) and decreased HCO3 is expected to be 32 mEq/L (24 + 8). However, the baby
HCO3 instead of usual increased BE and increased had serum HCO3 of 8 mEq/L which indicates another primary
HCO3 found in chronic respiratory acidosis with its process, which has inappropriately decreased serum HCO3.
appropriate physiological response. Here, prolonged hypoxia has caused tissue hypoperfusion
and lactic acidosis. Therefore mixed respiratory acidosis with steady state is maintained, the average reduction in plasma 167
metabolic acidosis occurred instead of respiratory acidosis HCO3 is approximately 0.5 mEq/L for each mm Hg reduction
with usual physiological compensated (partially or completely) of PaCO2.
metabolic alkalosis. For example, if PaCO2 is 20, than fall in HCO3 will be 4020
excess removal of CO 2 (respiratory alkalosis), and those Try to find the source of anxiety and take steps accordingly
resulting from loss of nonvolatile acids or accumulation of If occurs in patients on ventilators due to excessive minute
buffer (metabolic alkalosis). Respiratory alkalosis can occur volume then measures to be taken include reducing minute
due to: volume and/or introducing dead space into the ventilator
Hyperventilation from different causes leading to circuit.
respiratory alkalosis (pneumonia, bronchiolitis, bronchial
asthma) KEY POINTS OF ACID-BASE DISTURBANCE AS A WHOLE
Other causes include anxiety, hysterical hyperventilation Regulation of normal extracellular pH (7.4) and intracellular
and central hyperventilation from brain injury, encephalo pH (7.0) is vital for organ function in the long-term
Apart from primary metabolic disorders, most acid-base
pathy, encephalitis, salicylate toxicity, hypoxia
disorders in PICU should be viewed as a complex physiological
Also commonly occurs in ventilatory support from excessive response to an underlying pathological abnormality
minute volume when a patient is initially intubated and Despite some controversy in mechanisms, it is best to
ventilated. It can be minimized from monitoring early approach acid-base disorders via the principles of:
pH
arterial gases or from use of EtCO2 monitoring-severe
PaCO2 relationship (Henderson-Hasselbalch equation) to pH
hypocapnia. Respiratory alkalosis from overventilation can Calculation of the base excess (BE)
significantly reduce brain perfusion and aggravate cerebral Anion gap (AG)
ischemic injury.
Bibliography
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characteristics and treatment. Am J Kidney Dis. 2005;45:978-93.
In addition to hyperventilation symptomatic respiratory 2. Rodriguez Soriano J. Renal tubular acidosis. The clinical entity. J Am
alkalosis appear only in acute severe respiratory alkalosis Soc Nephrol. 2002;13: 2160-70.
which are one or more of the followings: 3. Rose BD. Clinical physiology of acid base and electrolyte disorders,
Tingling around mouth and fingers 2nd edition. New York: McGraw-Hill, New York; 1984.
4. Scchwaderer AL, Schwartz GJ. Back to basics. Acidosis and alkalosis.
Parasthesias, numbness Pediatr Rev. 2004;25:350-7.
Tetany and convulsion due to decrease in ionic calcium 5. Shaw, Patricia, (Ed). Fluids & Electrolytes Made Incredibly Easy!
commonly found in hysteric hyperventilation. Springhouse, PA: Springhouse Publishing Co.; 1997.