Arterial Blood Gas Analysis

Electrolyte Disturbances
• ABG analysis is typically performed on whole blood.
• The partial pressure of oxygen (PaO2), partial pressure of carbon
dioxide (PaCO2), and pH are directly measured with standard
electrodes and digital analyzers;
• oxygen saturation is calculated from standard O2 dissociation curves
or may be directly measured with a cooximeter.
• The bicarbonate (HCO3) concentration is calculated using the
Henderson-Hasselbalch equation
 Base excess

• The base excess is defined as the quantity of strong acid required to

titrate blood to pH 7.40 with a PaCO2 of 40 mmHg at 37 °C.
An ABG provides a rapid and accurate assessment
of oxygenation, ventilation, and
acid-base status.

• Blood sampling must be done during steady state following the

initiation or change in oxygen therapy or changes in ventilatory
parameters in patients on mechanical ventilation. In most ICU
patients a steady state is reached between 3 and 10 min and in about
20–30 min in patients with chronic airways obstruction.
• Excess of heparin may affect the pH. Only 0.05 mL is required to
anticoagulate 1 mL of blood.
 Alveolar Ventilation
• The arterial CO2 content as reflected by arterial CO2 tension (PaCO2)
at any given moment depends on the quantity of CO2 produced and
its excretion through alveolar ventilation (VA).
• The alveolar ventilation is that portion of total ventilation that
participates in gas exchange with pulmonary blood.
• PaCO2 becomes very usefulfor the assessment of alveolar ventilation.
High PaCO2 (>45 mmHg) indicates alveolar hypoventilation and low
PaCO2 (<35 mmHg) implies alveolar hyperventilation.
 Oxygenation
• PaO2 is a measure of the oxygen tension in plasma; while the
dissolved fraction makes a negligible contribution to oxygen delivery
(<2 %) it is a major factor affecting hemoglobin saturation.
• PaO2 is dependent on the concentration of oxygen in the inspired air
(FiO2), oxygen exchange in the lung (V/Q mismatching) and the
venous oxygen saturation (SmvO2).
• The PaO2 must always be interpreted in conjunction with the FiO2

• Hypoxemia is defined as a PaO2 of less than 80 mmHg.

 Hypoxia and hypoxemia
• The degree of hypoxia in patients with hypoxemia depends on the
severity of the hypoxemia and the ability of the cardiovascular system
to compensate.
• Hypoxia is unlikely in mild hypoxemia (PaO2 = 60–79 mmHg).
Moderate hypoxemia (PaO2 = 45–59 mmHg) may be associated with
hypoxia in patients with anemia or cardiovascular dysfunction.
• Hypoxia is almost always (but with a few exceptions) associated with
severe hypoxemia (PaO2 <45 mmHg)
• The PaO2 is determined largely by the FiO2 and the degree of intra-
pulmonary shunting.
• The PaO2 to FiO2 ratio (PaO2/FiO2) is commonly used to quantitate
the degree of ventilation/perfusion mismatching (V/Q).
• The normal PaO2 in an adult breathing room air with a FiO2 of 0.21 is
80–100 mmHg, the normal value for PaO2/FiO2 is between 400 and
500 mmHg.
 Respiratory Failure

• Hypoxemic respiratory failure (type 1)– PaO2 ≤60 mmHg when

breathing room air (sea level)

• Hypercapnic respiratory failure (type 2)– PaCO2 >= 45 mmHg

 Acid-Base Balance
• The normal diet generates volatile acid (CO2), primarily from carbohydrate
metabolism, and nonvolatile acid (hydrogen ion, H+) from protein
metabolism.
• pH homeostasis is accomplished through the interaction of the lungs,
kidneys and blood buffers
• Alveolar ventilation allows for excretion of CO2. The kidneys must reclaim
filtered bicarbonate (HCO3), because any urinary loss leads to gain of H+.
• The kidney must excrete the daily acid load generated from dietary protein
intake. Less than half of this acid load is excreted as titratable acids (i.e.,
phosphoric and sulfuric acids); the remaining acid load is excreted as
ammonium.
 The Anion Gap
• AnionGap = Na-(Cl+ HCO3)
• Normal= 12+/- 4meq/L
• Following the principle of electrochemical neutrality, total [cations]
must equal total [anions], and so in considering the commonly
measured cations and anions and subtracting them, a fixed number
should be derived.
• Mathematically this ‘gap’ is filled with unmeasured anions ensuring
electrochemical neutrality. There is never a ‘real’ anion gap, in line
with the law of electrochemical neutrality; it is rather an index of non-
routinely measured anions.
Normal Values
Identify if the patient is acidemic (pH < 7.35) or alkalemic (pH >
7.45) and whether the primary process is metabolic (initiated
by change in HCO3) or respiratory (initiated by a change in
PaCO2)
 Expected compensation
• Any alteration in acid-base equilibrium sets into motion a
compensatory response by either the lungs or the kidneys. The
compensatory response attempts to return the ratio between PaCO2
and HCO3 to normal and thereby normalize the pH.
• Determine whether the compensatory response is of the magnitude
expected i.e. is there a secondary (uncompensated) acid-base
disturbance.
 Calculate the Anion Gap
• In high anion gap metabolic acidosis, acid dissociates into H+ and an
unmeasured anion. H+ is buffered by HCO3 and the unmeasured
anion accumulates in the serum, resulting in an increase in the anion
gap.

• In non-anion gap metabolic acidosis, H+ is accompanied by Cl− (a

measured anion); therefore, there is no change in the anion gap.
 Metabolic Acidosis
• The clinical manifestations of a metabolic acidosis are largely
dependent on the underlying cause and the rapidity with which the
condition develops
• Acute severe metabolic acidosis results in myocardial depression with
a reduction in cardiac output, decreased blood pressure and
decreased hepatic and renal blood flow.
• Reentrant arrhythmias and a reduction in the ventricular fibrillation
threshold can occur.
• Brain metabolism becomes impaired with progressive obtundation
and coma
• Metabolic acidosis in the critically ill patient is an ominous sign and
warrants an aggressive approach to the diagnosis and management of
the cause
• The causes of the metabolic acidosis are usually clinically obvious,
with hypoperfusion, ketoacidosis and renal failure being the
commonest causes.
• The treatment of a metabolic acidosis involves the treatment of the
underlying disorder.
 Metabolic Alkalosis
• Metabolic alkalosis is a common acid-base disturbance in ICU
patients, characterized by an elevated serum pH (>7.45) secondary to
plasma bicarbonate (HCO3)retention
• Nasogastric drainage, diuretic induced intravascular volume
depletion, hypokalemia and the use of corticosteroids are common
causes of a metabolic alkalosis in these patients.
• The citrate in transfused blood is metabolized to bicarbonate which
may compound the metabolic alkalosis.
• Over-ventilation in patients with type 2 respiratory failure may result
in a posthypercapnic metabolic alkalosis.
 Part II
Electrolyte Disturbances
 Hyponatremia
• Hyponatremia defined as a serum sodium <135 mEq/L
• The traditional diagnostic approach and management of
hyponatremia is based on an assessment of the patient’s volume
status; i.e. fluid overloaded, euvolemia or dehydration
• Most patients with hyponatremia are “asymptomatic” and have a
plasma sodium concentration above 120 mEq/L. In these patients
there is no urgency in correcting the serum sodium concentration and
treatment should occur over a number of days.
 Hyponatremia
• The treatment of hyponatremia requires either the addition of
sodium or removal of water.
• Hypertonic saline can be given initially to raise the plasma sodium
concentration (to ~120 mEq/L), although the rate at which this occurs
must be carefully monitored to minimize the risk of central
demyelinating lesions
• Acute symptomatic hyponatremia (less than 48 h) results in cerebral
edema to due water movement into the brain.
Hyponatremia

• The amount of Na+ required to raise the plasma Na+ concentration to

a safe level (120 mEq/L) can be calculated from the following formula:

• Na deficit =0.6*lean bodyweight(kg) * ( 120-plasma Na)

 Hypernatremia
• Hypernatremia is not uncommon in ICU patients primarily due to
excessive resuscitation with 0.9 NaCl ([Na+] 154 mEq/L). The
treatment of the former is free water
• Hypernatremia may also occur in dehydrated patients in whom thirst
is impaired (e.g. bed ridden or altered mental status). In hypertonic
dehydration volume status should be corrected first (Ringers Lactate)
followed by correction of tonicity (0.45 % saline and/or free water)
 Hypernatremia

• Rapid correction of hypernatremia can induce cerebral edema,

seizures,permanent neurological damage and death.
• The maximum rate at which the plasma Na+ should be corrected is
0.5 mEq/L/h or 12 mEq/L per day
• Water deficit Na =Body weight*0.5 * [(Na-140)/140]
 Hypokalemia
• Only a small fraction of the total body K+ is extracellular. Therefore
serum K+ levels do not accurately reflect the total body K+
• In patients with chronic hypokalemia 1 mEq fall in serum K+ is
approximately equal to a 200 mEq total body deficit
• In critically ill ICU patients it is generally recommended to keep the
serum [K+] ≥4.0 mEq/L.
• Normal K levels 3.5-4.5 mmol/l
 Hyperkalemia
• Acute hyperkalemia is usually the result of renal failure
• K+ >6.5 mEq/L or hyperkalemia associated with ECG changes should
be regarded as life-threatening requiring immediate treatment
 Hyperkalemia
• ECG changes include:
• peaked T waves
• flattened P
• prolonged PR interval
• widening of the QRS complex
• sine wave leading to V. fibrillation or asystole
 Hyperkalemia
• Patients should be treated when the K+ is greater than 5.5 mEq/L
• urgent treatmentis required when the K+ >6.5 mEq/L
• protect the heart from the effects of K+ by antagonizing the effect on
cardiac
• conduction (calcium)
• to shift the K+ from the extracellular to intracellular compartment
(glucose/insulin infusion)
• reduce the total body potassium (dialysis)
 Hypophosphatemia
• Causes of severe hypophosphatemia
• alcohol abuse and withdrawal
• refeeding after starvation
• Hypophosphatemia becomes life threatening when the serum levels are
less than 1 mg/dL
• Manifestations include:
• myocardial depression
• weakness, rhabdomyolysis and respiratory failure
• confusion, stupor, coma, seizures
• hemolysis, platelet dysfunction, leukocyte dysfunction
 Part III
Acute Kidney Injury
• Acute kidney injury (formally known as acute renal failure) is a
common problem in the ICU.
• AKI is a syndrome characterized by the rapid loss of the kidney’s
excretory function and is typically diagnosed by the accumulation of
the end products ofnitrogen metabolism (urea and creatinine) or
decreased urine output or both.
• Although serum creatinine (Scr) is not a perfect marker of GFR, it is
frequently used as a surrogate to estimate GFR.
• The therapeutic intervention of choice in patients with intravascular
volume depletion and oliguria is fl uid resuscitation and not
furosemide.
• Excessive volume resuscitation with a high central venous pressure
will impair renal function
• A rational evidence-based approach to fl uid resuscitation is therefore
essential to reduce the risk of renal dysfunction in critically ill
patients.
• In patients who remain oliguric/anuric after adequate fl uid
resuscitation it is important to exclude urinary tract obstruction (and
urinary catheter obstruction), as this as an immediately reversible
cause of acute renal failure.
• In patients with compromised renal function nephrotoxic drugs
(particularly aminoglycosides and contract agents) should be avoided
When to Initiate Renal Replacement Therapy
(RRT)

• hyperkalemia (K > 6.5 mmol/L)

• progressive acidosis with pH < 7.20
• fluid overload with pulmonary edema
• uremic symptoms, i.e. nausea, vomiting, altered mental status,
asterixis
• Continuous renal replacement therapies were developed with the
aim of providing a more physiological method of renal replacement
therapy; i.e., to function more like a normal kidney