Download Respiratory Failure

Arterial blood gases and oximetry
 The measurement of hydrogen ion
concentration (pH), PaO2 and PaCO2, and
bicarbonate concentration in an arterial
blood sample is essential in assessing the
degree and type of respiratory failure and for
measuring acid–base status
 The pH of the arterial plasma is normally
7.40
 Corresponds to a H+ concentration of 40
nmol/L
 An increase in H+ concentration
corresponds to a decrease in pH
 pH is under tight homeostatic regulation, so
that the it does not vary outside the range of
7.44–7.36 under normal circumstances
 To preserve function of many pH-sensitive
enzymes
 A variety of physiological mechanisms
maintain the pH of the ECF
 The first is the action of blood and tissue
buffers, of which the most important
involves reaction of H+ ions with
bicarbonate to form carbonic acid, which,
under the influence of the enzyme
carbonic anhydrase dissociates to form
CO2 and water
 CO2+ H2O --H2CO3 --H+ HCO3−
 This buffer system is important because
bicarbonate is present in relatively high
concentration in the ECF (21–28 mmol/L)
 Two of its key components are under
physiological control: the CO2 by the lungs,
and the bicarbonate by the kidneys
 Respiratory compensation for acid–base
disturbances occurs quickly
 In response to acid accumulation, pH
changes in the brain stem stimulate
ventilatory drive, serving to reduce the
PCO2 and hence drive up the pH
 Systemic alkalosis leads to inhibition of
ventilation
 The kidney also provides of defence against
disturbances of arterial pH
 When acid accumulates due to chronic
respiratory or metabolic (non-renal) causes,
the kidney has the long-term capacity to
enhance urinary excretion of acid, &
increase the plasma bicarbonate
Respiratory acidosis
 Respiratory acidosis can be due to severe
pulmonary disease, respiratory muscle
fatigue, or abnormalities in ventilatory
control and is recognized by an increase in
Paco2 and decrease in pH
 In acute respiratory acidosis, there is an
immediate compensatory elevation (due to
cellular buffering mechanisms) in HCO3–,
which increases 1 mmol/L for every 10mmHg increase in Paco2
 In chronic respiratory acidosis (>24 h),
renal adaptation increases the [HCO3–] by 4
mmol/L for every 10-mmHg increase in
Paco2.
Clinical features
 Vary according to the severity and duration
of the respiratory acidosis, the underlying
disease, and whether there is accompanying
hypoxemia
 A rapid increase in Paco2 may cause anxiety,
dyspnea, confusion, psychosis, and
hallucinations and may progress to coma
 Acute hypercapnia follows sudden occlusion
of the upper airway or generalized
bronchospasm as in severe asthma,
anaphylaxis, inhalational burn, or toxin
injury
 Chronic hypercapnia and respiratory
acidosis occur in end-stage obstructive lung
disease
 Restrictive disorders involving both the
chest wall and the lungs can cause
respiratory acidosis because the high
metabolic cost of respiration causes
ventilatory muscle fatigue
Treatment
 The management of respiratory acidosis
depends on its severity and rate of onset
 Acute respiratory acidosis can be lifethreatening, and measures to reverse the
underlying cause should be undertaken
simultaneously with restoration of adequate
alveolar ventilation
 This may include tracheal intubation and
assisted mechanical ventilation
 Oxygen administration should be titrated
carefully in patients with severe obstructive
pulmonary disease and chronic CO2
retention who are breathing spontaneously
 The Paco2 should be lowered gradually in
chronic respiratory acidosis, aiming to
restore the Paco2 to baseline levels
 To provide sufficient Cl– and K+ to enhance
the renal excretion of HCO3–
 Chronic respiratory acidosis is frequently
difficult to correct
RESPIRATORY ALKALOSIS
 Characterized by a primary decrease in Pco2
an increased arterial pH and decreased
plasma bicarbonate concentration
 It is most commonly the result of alveolar
hyperventilation rather than
underproduction of CO2
Causes
 Hypoxemia, due to pulmonary disease,
congestive heart failure, and high-altitude
living, or anemia
 Mechanical ventilation
Primary stimulation of the central
chemoreceptor as seen in
 Endotoxemia
 Hepatic cirrhosis
 Salicylate intoxication
 Correction of metabolic acidosis
 Hyperthermia
 Pregnancy
 Cortical hyperventilation from anxiety and
pain
Clinical Manifestations
 Symptoms of acute hypocapnia are largely
attributable to the alkalemia and include
dizziness, perioral or extremity paresthesias,
confusion, asterixis, hypotension, seizures,
and coma
 Symptoms are due to decreased cerebral
blood flow or reduced free calcium (because
alkalosis increases calcium's protein-bound
fraction)
Treatment
 Address the underlying cause of the
disturbance
 Patients who exhibit symptoms, such as
tetany and syncope, and do not have more
serious causes of hyperventilation can be
treated with a rebreathing mask
Respiratory failure
 The term respiratory failure is used when pulmonary
gas exchange fails to maintain normal arterial oxygen
and carbon dioxide levels
 Its classification into types I and II relates to the
absence or presence of hypercapnia (raised PaCO2)
Pathophysiology
 When disease impairs ventilation of part of a lung
(pneumonia), perfusion of that underventilated region
results in hypoxic and CO2-laden blood entering the
pulmonary veins
 Increased ventilation of neighbouring regions of
normal lung can increase their CO2
excretion, correcting arterial CO2 to normal,
but cannot augment their oxygen uptake because the
haemoglobin flowing through these normal regions is
already fully saturated
Causes of Hypoxic ARF(type I)
 Acute lung injury/ARDS
 Pneumonia
 Pulmonary thromboembolism
 Acute lobar atelectasis
 Cardiogenic pulmonary edema
Causes of Hypercapnic-Hypoxic ARF
(type II )
Pulmonary disease
 COPD
 Asthma: advanced acute severe asthma
 Drugs causing respiratory depression
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Neuromuscular
Guillain-Barré syndrome
Acute myasthenia gravis
Spinal cord tumors
Musculoskeletal
Kyphoscoliosis