Electrolytes and Arterial Blood Gases

James H. Harrison, Jr., M.D., Ph.D.

Center for Oncology and Pathology Informatics
Department of Pathology
Cancer Pavilion 310
University of Pittsburgh Medical Center
Pittsburgh, PA
jhrsn@pitt.edu

12/2/2003
Agenda

Quick review of renal tubular function

Quick review of pulmonary function
Pulmonary-renal cooperation in maintaining pH
Respiratory acid-base imbalances
Metabolic acid-base imbalances
Sodium, potassium, chloride and bicarbonate balance
Measurement of blood gases and electrolytes
Case studies
Nephron Function

Maintenance of internal fluid volumes

Maintenance of appropriate plasma concentrations of
dissolved ions
> Excitable membrane function and osmotic balance
Internal pH balance
Metabolic conversion of a variety of substrates
Hormone production
Waste product excretion

Nephron Animation

The systems managing water balance, ion concentration, and pH are inter-related.
Problems may appear as overlapping pH, electrolyte and water balance disorders.
Pulmonary Function: Oxygenation

The lungs absorb oxygen from inspired air

> Expected PaO2 = 95 5 mm Hg
> Expected O2 saturation = 97 2 %
> Age-related: PaO2 = 104.2 - (0.27 * age)
Or about 100 - 1/3 of the patients age
> PaO2 < 55 is hypoxemic (O2 sat < 90%)

Alveolar:arterial oxygen gradient (A - a gradient)

> PAO2 = 150 - 1.25(PaCO2)
> Normal A-a gradient is 10-20 mm Hg
> If on O2: PAO2 = FIO2(760-47) - 1.25(PaCO2)
Pulmonary Function: CO2 Removal

Expected value: PaCO2 = 40 2 mm Hg

CO2 diffuses easily through tissue
> CO2 retention based on gas exchange problems only in
severe (end-stage) pulmonary fibrosis or COPD
CO2 elimination can be increased by increased
respiration and decreased by decreased respiration

Internal pH strongly influenced by PaCO2

Internal pH Depends on Renal-Pulmonary
Cooperation

Normal metabolism continually produces acid

Carbonic acid/bicarbonate is the bodys main buffer (pKa = 6.1)

The lungs eliminate acid as carbon dioxide, maintaining a normal

PCO2 of about 40 mm Hg
The kidneys remove H+ (DT) and conserve bicarbonate (PT),
maintaining a normal bicarbonate of about 24 meq/l
This cooperative relationship maintains an internal pH very close
to 7.4 (< 6.8 or > 7.8 is incompatible with life)
Normal Lung and Kidney pH Balance
Respiratory Acidosis: Impaired Lung Function

Retention of carbon dioxide (PaCO2 > 40)

CNS depression (trauma, anesthesia, drugs):
hypoventilation
Neuromuscular disorders/paralysis: hypoventilation
Severe COPD: chronic bronchitis/emphysema (V/Q
mismatch)
Severe restrictive lung disease (pulmonary fibrosis)
Respiratory Acidosis
with Metabolic Compensation

Respiratory acidosis Metabolic compensation

when chronic
Respiratory Alkalosis: Hyperventilation

Excess respiratory loss of carbon dioxide (pCO2 < 40)

Chronic hypoxia in COPD
Excitement, anxiety
Moderate or early salicylate toxicity
Respiratory Alkalosis
with Renal Compensation

Respiratory alkalosis Metabolic compensation

when chronic
Metabolic Acidosis (bicarbonate depletion)

Retention of protons or loss of bicarbonate (bicarb < 24)

> Urine more alkaline than expected

Pulmonary compensation (rapid and robust)

Metabolic Acidosis
with Respiratory Compensation

Metabolic acidosis Respiratory compensation

(rarely seen uncompensated) (rapid)
The Anion Gap in Metabolic Acidosis

Increased "anion gap" in metabolic acidosis (expected,

6 - 18 meq/l)

Anion Gap
> Renal failure
> Ketosis
> Lactic acidosis
> Poisoning

Non-Anion Gap
> Renal tubular dysfunction (Fanconi's syndrome, carb. anh.)
> Diarrhea (bicarbonate loss)
Metabolic Alkalosis (bicarbonate retention)

Loss of acid or retention of bicarbonate

Pulmonary compensation (rapid but limited)

Vomiting (loss of gastric acid)

Diuretics (renal loss of potassium and acid in the distal tubule)
Elevated corticosteroids (Cushing's syndrome and
hyperaldosteronism; distal tubule)
Severe potassium depletion
Acute alkali ingestion
Metabolic Alkalosis
with Respiratory Compensation

Metabolic alkalosis Respiratory compensation

(rapid but limited)
Practice Case

A patient presents with the following results from a blood gas study:
pH = 7.43
pCO2 = 21 mm Hg
Bicarb = 14 meq/l

Questions:
1. What is the patient's acid-base status?
2. Is the lung retaining or removing acid?
3. Is the kidney retaining or removing bicarbonate?
4. Which organ is the primary culprit in this problem?
Method 1: Eyeball

A patient presents with the following results from a blood gas study:
pH = 7.43
pCO2 = 21 mm Hg
Bicarb = 14 meq/l

Questions:
1. What is the patient's acid-base status? >> Look at pH
2. Is the lung retaining or removing acid? >> Compare pCO2 to 40
3. Is the kidney retaining or removing bicarbonate? >> Compare bicarb to 28
4. Which organ is the primary culprit in this problem?
>> The organ producing the effect seen in the pH is the primary problem
Method 2: Math

A patient presents with the following results from a blood gas study:
pH = 7.43
pCO2 = 21 mm Hg
Bicarb = 14 meq/l
Serum Electrolytes: Sodium

The major extracellular cation

In general, sodium balance defines water balance
Sodium is the most important contributor to plasma osmotic
pressure: POsm = 2(NaP) + Gluc/18 + BUN/2.8
> Expected = 280 - 296 mOsm/kg
Renal sodium management is dependent on distal tubule
function
Reference range about 136-145 meq/l (mmol/l)
< 120 produces muscular weakness
< 100 causes neurological symptoms
Sodium deficit/excess must be corrected carefully
Hyponatremia

Assess plasma osmolality first, then clinical volume status and urine osmolality
Low plasma osmolality with elevated urine osmolality
> Hypovolemia: GI, dermal, renal fluid loss; salt wasting states; potassium depletion;
ketoacidosis
> Effective volume depletion (dilution): heart failure, cirrhosis, nephrotic syndrome
> Diuretics, chronic renal disease, SIADH, hypocortisolism, hypoaldosteronism
Low plasma osmolality with low urine osmolality
> Replacement of lost fluid (vomiting, burns, etc.) with hypotonic solutions
> Primary polydipsia
Increased plasma osmolality
> Elevated glucose, mannitol (not clinically significant from a sodium standpoint)
Clinical hyponatremia is associated with decreased plasma osmolality
Pseudohyponatremia with flame photometry in hyperproteinemia and
hyperlipidemia; plasma osm is normal (not a problem with ISE)
Hypernatremia

Poor fluid intake or excess loss from skin (diaphoresis, burns)

Water loss from the kidney (diabetes insipidus, osmotic diuresis)
GI loss (vomiting, diarrhea)
Increased mineralocorticoids (hyperaldosteronism)
Cushing's syndrome

Evaluate volume status, serum/urine osmolality and sodium

> Low urine osmolality: osmotic diuresis or diabetes insipidus
> Elevated urine osmolality
Hypervolemic: renal water/sodium retention (mineralocorticoid excess)
Hypovolemic: extrarenal water loss (diaphoresis, diarrhea)
Potassium Balance

The major intracellular cation (ca. 150 meq/l, gradient

maintained by Na-K ATPase)
Serum concentration of about 3.5 - 5 meq/l, plasma values 0.1 -
0.7 lower
Potassium concentration dramatically affects excitable
membrane function (muscle and nerve)
Symptoms: muscle weakness, nausea, lethargy, arrhythmias,
characteristic EKG changes, cardiac arrest
Levels < 3 produce marked neuromuscular symptoms, levels >
7.5 produce symptoms and levels > 10 are lethal
Renal potassium management is dependent on distal tubule
function
Hypokalemia

Inadequate intake
Treatment of normokalemic dehydration without
potassium supplementation
Mineralocorticoid excess (Cushing's syndrome
and hyperaldosteronism)
Renal loss (diuretics and corticosteroids)
Insulin treatment (K enters cells with glucose)
Alkalosis (H+ exits cells in exchange for K)
GI loss (protracted vomiting or diarrhea)
Hyperkalemia

Dehydration
Shock, severe hemolysis, tumor lysis, burns (cellular
release)
Renal failure (decreased excretion)
Endocrine diseases with mineralocorticoid deficiency
"Potassium sparing" diuretics
Acidosis (K exits cells in exchange for H)
Artifactual hemolysis of blood specimens; K leak in
chilled or unprocessed specimens
Chloride Balance

The major extracellular anion (expected, 118 - 132 meq/l in serum)

Important in water distribution, osmotic pressure, and anion-cation balance
Hypochloremia
> Fluid volume expansion (dilution)
> Renal diseases (reabsorption failure)
> Metabolic acidosis with increased "unmeasured anions" (e.g. DKA)
> SIADH
> GI loss (protracted vomiting)
Hyperchloremia
> Dehydration
> Renal tubular acidosis, acute renal failure
> Bicarbonate loss (diarrhea)
> Mineralocorticoid excess (Cushing's syndrome and hyperaldosteronism)
> Diabetes insipidus
Process specimens promptly; changes in bicarbonate with air equilibration
cause shifts in chloride between the extra- and intracellular compartments
Bicarbonate Balance

The primary acid-base buffer in the body

Serum/plasma concentration of about 23 - 29 meq/l
Provides a rough assessment of acid-base balance,
but is subject to error
Equilibration vs. pCO2 of 0.25 in air; decline of 6
meq/l per hr
Chemical assay rather than ISE, susceptible to
volume effects
Bicarbonate < 10 is a critical value (reflects low pH)
Blood Gas Testing

Blood gas analysis may be carried out in a main laboratory, in an ER or OR

lab or using POC devices
Provides accurate measurement of PO2, PCO2, pH, hemoglobin saturation,
bicarbonate and hematocrit (some analyzers also offer electrolytes, lactate,
glucose, Hgb, CO-Hgb, met- and sulfHgb)
Arterial blood, drawn in appropriate equipment and transported quickly (10-
15 min) on ice to the lab
Check ulnar artery patency before radial artery draws
"Arterialized capillary blood" (warmed heel or earlobe) may be acceptable in
some cases
Specimen is accompanied by history with FIO2 and clinical status of patient,
and patient temperature (all are important for interpretation and are included
in the returned report)
Erroneous results from room temp specimens and specimens with air bubbles
or improper capping
Blood Gas Instrumentation

Radiometer 625
Pulse Oximetry
Electrolyte Measurement

Standard serum or heparinized venous plasma specimen (Li or NH4 heparin)

Chem 7: sodium, potassium, chloride, CO2 content (bicarb), BUN, creatinine, glucose

Vitros 250/Slide technology

Issues of frequency and utility for this test

panel
Hemolysis, refrigeration, waiting, high
leukocytes or platelets increase K
CO2 content not particularly accurate
(equilibration vs. pCO2 of 0.25 in air; decline
of 6 meq/l per hr)
Na, K, Cl measured by ion-selective electrodes
Bicarbonate measured using a carboxylation
reaction followed by NADH oxidation