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



 If


narcosis:
Headache, blurred vision
Asterixis, tremors, weakness
Confusion, somnolence
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

i.e. remove stimulus
 Treat

underlying cause
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