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ACID-BASE HOMEOSTASIS
ACID-BASE HOMEOSTASIS
Acid-base homeostasis is responsible for maintaining blood hydrogen ion concentration [H+] near normal despite the daily acidic and/or alkaline loads derived from the intake and metabolism of foods.
ACID-BASE HOMEOSTASIS Acid-base status is traditionally represented in terms of pH, the negative logarithm of [H+].
ACID-BASE HOMEOSTASIS
The best way to assess a patients acid-base status is to review the results of an arterial blood gas (ABG) specimen. Blood gas analyzers directly measure the pH and PaCO2 while the HCO3 value is measured from serum HCO3 and obtained by measuring the total venous carbon dioxide (tCO2). The pH and PaCO2 values come from an arterial blood gas while HCO3 values should be considered to be measured serum concentrations.
ACID-BASE HOMEOSTASIS
BASIC PATHOPHYSIOLOGY
BASIC PATHOPHYSIOLOGY
A respiratory acid-base disorder is a pH disturbance caused by pathologic alterations of the respiratory system or its central nervous system control.
A metabolic acid-base disorder is a pH disturbance caused by derangement of the pathways responsible for maintaining a normal HCO3 level.
In contrast to the lungs rapid effects on CO2, the kidneys change the HCO3 very slowly (hours to days).
Acid-base disorders
Simple (uncomplicated) Disorder
The most common clinical disturbances are simple acid-base disorders.
Chronic disorder
If acid-base disturbance is present for days or longer. All metabolic disorders are chronic.
Acid-base disorders
This means that there are six simple acid-base disorders:-
Acid-base disorders
Chronic respiratory acid-base disorders are typically accompanied by attempts at metabolic compensation
BUT
Acute respiratory acid-base disorders there is insufficient time for the metabolic pathways to compensate significantly. The amount of compensation (metabolic or respiratory) can be reliably predicted by measuring the difference between calculated and measured values.
Acid-base disorders
Anion gap
o The measured cations are higher than the measured anions by 10 to 12 mEq/L (mmol/L).
Anion gap
o The anion gap may be artificially lowered by decreased serum albumin, multiple myeloma, lithium intoxication, or a profound increase in the serum potassium, calcium, or magnesium. o Calculation of the anion gap also facilitates determination of the excess gap or the degree to which the calculated anion gap exceeds the normal anion gap. Excess gap = [sodium (chloride + bicarbonate)] 12
Assessment
the approach to assessment of acid-base status involves four key steps:
(1) Initial inspection of the pH, PaCO2, and HCO3. (2) Assessment of the adequacy of compensation. (3) Calculation of the anion gap. (4) Calculation of the excess gap.
Assessment
the approach to assessment of acid-base status involves four key steps:
(1) Initial inspection of the pH, PaCO2, and HCO3. (2) Assessment of the adequacy of compensation. (3) Calculation of the anion gap. (4) Calculation of the excess gap.
Assessment
the approach to assessment of acid-base status involves four key steps:
(1) Initial inspection of the pH, PaCO2, and HCO3. (2) Assessment of the adequacy of compensation. (3) Calculation of the anion gap. (4) Calculation of the excess gap.
Assessment
the approach to assessment of acid-base status involves four key steps:
(1) Initial inspection of the pH, PaCO2, and HCO3. (2) Assessment of the adequacy of compensation. (3) Calculation of the anion gap. (4) Calculation of the excess gap.
Metabolic Acidosis
Metabolic acidosis is characterized by a reduced arterial pH, a primary decrease in the HCO3 concentration, and a compensatory reduction in the PaCO2.
Metabolic Acidosis Causes: High anion gap metabolic acidosis is most frequently caused by lactic acidosis, ketoacidosis, and/or renal failure.
Metabolic Acidosis Symptoms: Changes in the cardiovascular (ventricular arrhythmias and reduces cardiac contractility). Musculoskeleta (impaired growth, rickets, osteomalacia, or osteopenia)l. Neurologic (range from lethargy to coma and are usually proportional to the severity of the pH changes). Pulmonary function (pulmonary edema, systemic hypotension).
Metabolic Acidosis
Tromethamine (THAM).
Tromethamine (THAM)
THAM augments the buffering capacity of the blood without generating excess CO2. The usual empiric dosage for tromethamine is 1 to 5 mmol/kg administered IV over 1 hour . THAM is less effective in patients with renal failure and toxicities may include hyperkalemia, hypoglycemia, and possible respiratory depression.
Metabolic Alkalosis
It is an increased arterial pH, a primary increase in the HCO3 concentration, and a compensatory increase in the PaCO2.
muscle cramps, positional dizziness, and weakness. muscle weakness, polyuria, and polydipsia.
Metabolic Acidosis
Metabolic Alkalosis
treatment: Identify the causative process and treat it. D/C diuretics, nasogastric suction, and corticosteroids if patient have one. Any fluid deficits should be treated with IV normal saline.
Metabolic Alkalosis
treatment: In patients with mild or moderate alkalosis who require ongoing diuresis but have rising HCO3 levels,the carbonic anhydrase inhibitor acetazolamide can be used to reduce the HCO3 concentration. Acetazolamide is typically dosed at 250 mg every 6 to 12 hours as needed
Sever alkalosis may be life-threatening (due to seizures or ventricular tachyarrhythmias) can be given to hemodialysis or transient HCl infusion. H+ deficit = 0.4 weight (HCO3curr HCO3post)
Metabolic Alkalosis
is infused at 20 to 50 mEq/hour (mmol/hour) into a central vein. Ammonium chloride and arginine hydrochloride, agents that result in the formation of HCl, should not be given.
Respiratory Alkalosis
It is an increased arterial pH, a primary decrease in the arterial PaCO2 and, when present for sufficient time, a compensatory fall in the HCO3 concentration.
Respiratory Alkalosis Symptoms:Light-headedness. Altered consciousness. Distal extremity paresthesias. Circumoral paresthesia. Cramps. Carpopedal spasms. Syncope. Various supraventricular and ventricular cardiac arrhythmias may occur in extreme cases. Chronic respiratory alkalosis is generally asymptomatic.
Respiratory Alkalosis
treatment: Identify the cause and treat it. Respiratory alkalosis is typically only mild or moderate in severity and no specific therapy is indicated. A rebreathing device (e.g., paper bag) can help control hyperventilation. Patients receiving mechanical ventilation are treated with reduced minute ventilation achieved by decreasing the respiratory rate and/or depth. If the alkalosis persists in the ventilated patient, high-level sedation or paralysis is effective.
Respiratory Acidosis
It is a reduced arterial pH, a primary increase in the arterial PaCO2 and, when present for sufficient time, a compensatory rise in the HCO3 concentration.
Respiratory Acidosis
Symptoms
Chronic respiratory acidosis: Cor pulmonale and peripheral edema. Severe, acute respiratory acidosis: headache, blurred vision, restlessness, and anxiety, if untreated may progress to tremors, asterixis, somnolence, and/or delirium, terminal manifestations include peripheral vasodilation leading to hypotension and cardiac arrhythmias.
Respiratory Acidosis
Respiratory Acidosis