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Acid Base Imbalances
Acid-Base Regulation
Body produces significant amounts of carbon dioxide & nonvolatile acids daily
Regulated by: Renal excretion of acid (H+ combines with
phosphate or ammonia, which are excreted) Respiratory excretion of CO2 Buffer systems (hemoglobin, phosphate,
bicarbonate, proteins)
Measurement
Arterial: Normal pH 7.36-7.44; normal HCO3 25;
normal pCO2 40 Peripheral venous:
pH is 0.02-0.04 lower than arterial HCO3 is 1-2 mEq/L higher than arterial pCO2 is 3-8 mmHg higher, depending on
peripheral extraction and use of O2
Respiratory Acidosis
Definition
Decreased pH due to pulmonary CO2 retention (hypoventilation causes hypercapnea)
CO2 retention causes increased H2CO3 production – causes acidemia
Serum HCO3 is normal acutely, and increases as compensation occurs
Causes
Increase in PaCO2 Anything which causes a decrease in
minute ventilation has the potential to cause respiratory acidosis Airway CNS depression Pulmonary disease Hypoventilation of neuromuscular conditions
Symptoms
CO2 narcosis: Headache, blurred vision Asterixis, tremors, weakness Confusion, somnolence
If prolonged: Signs of increased ICP Papilledema
Compensation
Acutely: intracellular proteins buffer HCO3 is formed by the intracellular buffers Compensation is insignificant
Chronically Renal retention of HCO3 is the primary
buffering system Onset: 6-12 hrs, takes days to complete
Compensation
Acute: HCO3 increases 1 mEq/L for every 10 mmHg
rise in PCO2 Insignificant effect on pH
Chronic: HCO3 increases 3.5-5 mEq/L for every
10mmHg rise in PCO2 Can almost normalize pH Usually results in hypochloremia
Management
Must increase minute ventilation Must also improve ventilation
Bronchodilators, postural drainage, antibiotics (i.e. treat underlying cause)
Role of hypoxic drive???
Respiratory Alkalosis
Causes
Increased minute ventilation Leads to low pCO2, high pH If acute, HCO3 is normal If chronic, HCO3 will drop due to renal comp.
Causes: CNS diseases, hypoxemia, anxiety,
hypermetabolic states, toxic states, hepatic insufficiency, assisted ventilation
Symptoms
Mimic hypocalcemia Depend on degree, acuity & cause Due to irritability of CNS & PNS, and
increased cerebral vascular resistance Paresthesias of lips, extremities;
lightheadedness, dizziness, muscle cramps, carpopedal spasms
Management
Treat underlying cause i.e. remove stimulus
Treat symptoms E.g. benzos, pain medication, rebreathing
mask (allows CO2 retention)
Metabolic Alkalosis
Definition
Low pH due to increased HCO3 or decreased H+
Requires loss of H+ or retention of HCO3 Must know PCO2… elevation of HCO3
could be due to renal compensation for chronic respiratory acidosis
Causes
Increased HCO3 reabsorption due to volume, K+ or Cl- loss
Loss of H+ and Cl- from vomiting and NG suctioning can lead to HCO3 retention
Renal impairment of HCO3 excretion
Causes
Hypovolemic Vomiting/suction, diuretics, adenomas
Euvolemic/Hypervolemic Exogenous mineralocorticoids, ectopic ACTH,
Cushing’s, severe hypoK, adenoCA Unclassified
Milk-alkali syndrome, IV PCN rx, metabolism of organic acid anions, massive transfusion, nonparathyroid hypercalcemia
Treatment
Treat underlying causes Replace losses May be saline-responsive or saline
resistant
Metabolic Acidosis
Mechanism
Increased production of acids Decreased renal excretion of acids Loss of alkali
Alcoholic Ketoacidosis
Normal glucose High ketones Drinking binge; starvation
Lactic Acidosis
2 different forms; l- and d- Increased production vs. decreased
elimination Systemic
Sepsis, hypovolemia, hypoxia Localized
E.g. bowel ischemia, metformin, HIV meds
Treatment
Correct underlying cause Reduce O2 demand Ensure adequate O2 delivery to tissues
HCO3 Given to improve hemodynamic
consequences of acidosis
Summary
Look at pH Look at pCO2 and HCO3 Look at patient!!
Treat the patient, not the numbers