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Lecture

BIOC33H3 Lecture Notes - Asthma, Ranitidine, Orciprenaline


Department
Biological Sciences
Course Code
BIOC33H3
Professor
Stephen Reid

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Chapter 68: Respiratory Failure and Acute Respiratory Distress Syndrome
ACUTE RESPIRATORY FAILURE
Respiratory failure results when gas exchange, which involves the transfer of oxygen
(O2) and carbon dioxide (CO2) between the atmosphere and the blood, is inadequate.
Respiratory failure is not a disease; it is a condition that occurs as a result of one or more
diseases involving the lungs or other body systems.
Respiratory failure can be classified as hypoxemic or hypercapnic.
o Hypoxemic respiratory failure:
Commonly defined as a PaO2 <60 mm Hg when the patient is receiving an
inspired O2 concentration >60%.
Disorders that interfere with O2 transfer into the blood include pneumonia,
pulmonary edema, pulmonary emboli, heart failure, shock, and alveolar
injury related to inhalation of toxic gases and lung damage related to
alveolar stress/ventilator-induced lung injury.
Four physiologic mechanisms may cause hypoxemia and subsequent
hypoxemic respiratory failure: (1) mismatch between ventilation and
perfusion, commonly referred to as V/Q mismatch; (2) shunt; (3) diffusion
limitation; and (4) hypoventilation.
Hypoxemic respiratory failure frequently is caused by a combination of
two or more of these mechanisms.
o Hypercapnic respiratory failure:
Also referred to as ventilatory failure since the primary problem is
insufficient CO2 removal.
Commonly defined as a PaCO2 >45 mm Hg in combination with acidemia
(arterial pH <7.35).
Disorders that compromise CO2 removal include drug overdoses with
central nervous system (CNS) depressants, neuromuscular diseases, acute
asthma, and trauma or diseases involving the spinal cord and its role in
lung ventilation.
Hypercapnic respiratory failure results from an imbalance between
ventilatory supply and ventilatory demand. Ventilatory supply is the
maximum ventilation that the patient can sustain without developing
respiratory muscle fatigue, and ventilatory demand is the amount of
ventilation needed to keep the PaCO2 within normal limits.
Though PaO2 and PaCO2 determine the definition of respiratory failure, the major threat
of respiratory failure is the inability of the lungs to meet the oxygen demands of the
tissues. This may occur as a result of inadequate tissue O2 delivery or because the tissues
are unable to use the O2 delivered to them.
Manifestations of respiratory failure:
o Are related to the extent of change in PaO2 or PaCO2, the rapidity of change
(acute versus chronic), and the ability to compensate to overcome this change.

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o Clinical manifestations are variable and it is important to monitor trends in ABGs
and/or pulse oximetry to evaluate the extent of change.
o A change in mental status is frequently the initial indication of respiratory failure.
o Tachycardia and mild hypertension can also be early signs of respiratory failure.
o A severe morning headache may suggest that hypercapnia may have occurred
during the night, increasing cerebral blood flow by vasodilation and causing a
morning headache.
o Cyanosis is an unreliable indicator of hypoxemia and is a late sign of respiratory
failure because it does not occur until hypoxemia is severe (PaO2 ≤45 mm Hg).
o Hypoxemia occurs when the amount of O2 in arterial blood is less than the
normal value, and hypoxia occurs when the PaO2 falls sufficiently to cause signs
and symptoms of inadequate oxygenation.
o Hypoxemia can lead to hypoxia if not corrected, and if hypoxia or hypoxemia is
severe, the cells shift from aerobic to anaerobic metabolism.
Clinical Manifestations
Clinical findings include a rapid, shallow breathing pattern or a respiratory rate that is
slower than normal. A change from a rapid rate to a slower rate in a patient in acute
respiratory distress such as that seen with acute asthma suggests extreme progression of
respiratory muscle fatigue and increased probability of respiratory arrest.
The position that the patient assumes is an indication of the effort associated with
breathing.
o The patient may be able to lie down (mild distress), be able to lie down but prefer
to sit (moderate distress), or be unable to breathe unless sitting upright (severe
distress). The patient may require pillows to breathe when attempting to lie flat
and this is termed orthopnea.
o A common position is to sit with the arms propped on the overbed table.
Pursed-lip breathing may be used.
The patient may speak in sentences (mild or no distress), phrases (moderate distress), or
words (severe distress).
There may be a change in the inspiratory (I) to expiratory (E) ratio. Normally, the I:E
ratio is 1:2, but in patients in respiratory distress, the ratio may increase to 1:3 or 1:4.
There may be retractions of the intercostal spaces or the supraclavicular area and use of
the accessory muscles during inspiration or expiration. Use of the accessory muscles
signifies moderate distress.
Paradoxic breathing indicates severe distress and results from maximal use of the
accessory muscles of respiration.
Breath sounds:
o Crackles and rhonchi may indicate pulmonary edema and COPD.

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o Absent or diminished breath sounds may indicate atelectasis or pleural effusion.
o The presence of bronchial breath sounds over the lung periphery often results
from lung consolidation that is seen with pneumonia.
o A pleural friction rub may also be heard in the presence of pneumonia that has
involved the pleura.
Diagnostic Studies
ABGs are done to obtain oxygenation (PaO2) and ventilation (PaCO2) status, as well as
information related to acid-base balance.
A chest x-ray is done to help identify possible causes of respiratory failure.
Other diagnostic studies include a complete blood cell count, serum electrolytes,
urinalysis, and electrocardiogram.
o Cultures of the sputum and blood are obtained as necessary to determine sources
of possible infection.
o For the patient in severe respiratory failure requiring endotracheal intubation, end-
tidal CO2 (EtCO2) may be used to assess tube placement within the trachea
immediately following intubation.
o In severe respiratory failure, a pulmonary artery catheter may be inserted to
measure heart pressures and cardiac output, as well as mixed venous oxygen
saturation (SvO2).
Nursing and Collaborative Management: Acute Respiratory Failure
The overall goals for the patient in acute respiratory failure include: (1) ABG values
within the patient’s baseline, (2) breath sounds within the patient’s baseline, (3) no
dyspnea or breathing patterns within the patient’s baseline, and (4) effective cough and
ability to clear secretions.
Prevention involves a thorough physical assessment and history to identify the patient at
risk for respiratory failure and, then, the initiation of appropriate nursing interventions
(coughing, deep breathing, incentive spirometry, and ambulation as appropriate).
The major goals of care for acute respiratory failure include maintaining adequate
oxygenation and ventilation.
o The primary goal of O2 therapy is to correct hypoxemia.
o The type of O2 delivery system chosen for the patient in acute respiratory failure
should (1) be tolerated by the patient, and (2) maintain PaO2 at 55 to 60 mm Hg or
more and SaO2 at 90% or more at the lowest O2 concentration possible.
o Additional risks of O2 therapy are specific to the patient with chronic hypercapnia
as this may blunt the response of chemoreceptors in the medulla, a condition
termed CO2 narcosis.
o Retained pulmonary secretions may cause or exacerbate acute respiratory failure
and can be mobilized through effective coughing, adequate hydration and
humidification, chest physical therapy (chest physiotherapy), and tracheal
suctioning.
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