Acid-base balance

Acid-Base Balance

Acid-Base Homeostasis
Important buffers include intracellular proteins and phosphates and the extracellular bicarbonate–carbonic acid system

Compensation for acid-base derangements can be by respiratory mechanisms (for metabolic derangements) or metabolic mechanisms (for respiratory derangements)

Acidosis stimulates the chemoreceptors to increase ventilation, whereas alkalosis decreases the activity of the chemoreceptors and thus decreases ventilation

The kidneys provide compensation for respiratory abnormalities by either increasing or decreasing bicarbonate reabsorption in response to respiratory acidosis or alkalosis

The compensatory response in the kidneys to respiratory abnormalities is delayed. Significant compensation may not begin for 6 hours and then may continue for several days. Because of this delayed compensatory response, respiratory acid-base derangements before renal compensation are classified as acute, whereas those persisting after renal compensation are categorized as chronic

Metabolic Derangements

Metabolic Acidosis results from ether from:
Increased intake of acids,
Increased generation of acids,
Increased loss of bicarbonate


The body responds by several mechanisms, including producing buffers (extracellular bicarbonate and intracellular buffers from bone and muscle), increasing ventilation (Kussmaul’s respirations), and increasing renal reabsorption and generation of bicarbonate. The kidney also will increase secretion of hydrogen and thus increase urinary excretion of NH4 + (H+ + NH3 + = NH4+)

The anion gap (AG), an index of unmeasured anions

AG = (Na) – (Cl + HCO3)

The normal AG is <12 mmol/L

The estimated AG must be adjusted for albumin (hypoalbuminemia reduces the AG)
Corrected AG = actual AG – [2.5(4.5 – albumin)]

Metabolic Derangements

Etiology of metabolic acidosis
Increased Anion Gap Metabolic Acidosis
Exogenous acid ingestion
Ethylene glycol
Salicylate
Methanol
Endogenous acid production
Ketoacidosis
Lactic acidosis
Renal insufficiency
Normal Anion Gap
Acid administration (HCl)
Loss of bicarbonate
GI losses (diarrhea, fistulas)
Ureterosigmoidostomy
Renal tubular acidosis
Carbonic anhydrase inhibitor


Metabolic Derangements
A common cause of severe metabolic acidosis in surgical patients is lactic acidosis. In circulatory shock, lactate is produced in the presence of hypoxia from inadequate tissue perfusion

The treatment is to restore perfusion with volume resuscitation

The overzealous administration of bicarbonate can lead to metabolic alkalosis, which shifts the oxyhemoglobin dissociation curve to the left; this interferes with oxygen unloading at the tissue level and can be associated with arrhythmias that are difficult to treat. An additional disadvantage is that sodium bicarbonate actually can exacerbate intracellular acidosis

Metabolic acidosis with a normal AG ,in these settings, the bicarbonate loss is accompanied by a gain of chloride; thus, the AG remains unchanged.

To determine whether the loss of bicarbonate has a renal cause, the urinary [NH4+] can be measured. A low urinary [NH4+] in the face of hyperchloremic acidosis would indicate that the kidney is the site of loss, and evaluation for renal tubular acidosis should be undertaken.

Metabolic Derangements

Metabolic alkalosis
Etiology
Increased bicarbonate generation
1. Chloride losing (urinary chloride >20 mEq/L)
Mineralocorticoid excess
Profound potassium depletion
2. Chloride sparing (urinary chloride <20 mEq/L)
Loss from gastric secretions (emesis or nasogastric suction)
Diuretics
3. Excess administration of alkali
Acetate in parenteral nutrition
Citrate in blood transfusions
Antacids
Bicarbonate
Milk-alkali syndrome
Impaired bicarbonate excretion
1. Decreased glomerular filtration
2. Increased bicarbonate reabsorption (hypercarbia orpotassium depletion)


The majority of patients also will have hypokalemia, because extracellular potassium ions exchange with intracellular hydrogen ions and allow the hydrogen ions to buffer excess HCO3–

Respiratory Derangements

Respiratory Acidosis
Etiology of respiratory acidosis: hypoventilation
Narcotics
Central nervous system injury
Pulmonary: significant
Secretions
Atelectasis
Mucus plug
Pneumonia
Pleural effusion
Pain from abdominal or thoracic injuries or incisions
Limited diaphragmatic excursion from intra-abdominal
pathology
Abdominal distention
Abdominal compartment syndrome
Ascites

Respiratory Derangements

Respiratory acidosis is associated with the retention of CO2 secondary to decreased alveolar ventilation.


Because compensation is primarily a renal mechanism, it is a delayed response.

Treatment of acute respiratory acidosis is directed at the underlying cause. Measures to ensure adequate ventilation are also initiated.

This may entail patient-initiated volume expansion using non-invasive bilevel positive airway pressure or may require endotracheal intubation to increase minute ventilation.

In the chronic form of respiratory acidosis, the partial pressure of arterial CO2 remains elevated and the bicarbonate concentration rises slowly as renal compensation occurs.

Respiratory Derangements

Respiratory Alkalosis In the surgical patient, most cases of respiratory alkalosis are acute and secondary to alveolar hyperventilation.

Causes

pain, anxiety, and neurologic disorders, including central nervous system injury and assisted ventilation.
Drugs such as salicylates, fever, gram-negative bacteremia,and ,thyrotoxicosis.

Acute hypocapnia can cause an uptake of potassium and phosphate into cells and increased binding of calcium to albumin, leading to symptomatic hypokalemia, hypophosphatemia, and hypocalcemia with subsequent arrhythmias, paresthesias,muscle cramps, and seizures.

Treatment should be directed at the underlying cause, but direct treatment of the hyperventilation using controlled ventilation may also be required.

Arterial blood gas profile

Acidosis (pH<7.35)


If pCO2 high =respiratory acidosis
if HCO3 high = renal compensation

B. If pCO2 normal or low = ? Metabolic acidosis

If HCO3 low= metabolic acidosis
if pCo2 low=respiratory compensation
Alkalosis (pH>7.45)

A.If pCO2 low =Resp alkalosis

if HCO3 is low= renal compensation

B. If pCo2 normal or high=? Metabolic alkalosis

If HCO3 is high =metabolic alkalosis
if PCO2 is high = respiratory compensation