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