Air way Management

• Maintaining an open and patent airway is an important aspect of

critical care management.
• Patency can be ensured through conservative techniques such as
coughing, head and neck positioning, and alignment.
• If conservative techniques fail, insertion of an oral or nasal airway or
ET may be required
Oropharyngeal Airway
• The oropharyngeal airway, or oral bite block, is used to relieve upper
airway obstruction caused by tongue relaxation (e.g., postanesthesia
or during unconsciousness), secretions, seizures, or biting down on
oral
• Oral airways are made of rigid plastic or rubber material, semi-circular
in shape, and available in sizes ranging from infants to adults.
• oral airways are not recommended for use in alert patients be-cause
they may trigger the gag reflex and cause vomiting.
• Oropharyngeal airways are temporary devices for achieving airway
patency.
• The airway is removed at least every 12 hours to check for pressure
areas and to provide oral hygiene.
Nasopharyngeal Airway (nasal trumpet)
• is another device to maintain airway patency, especially in the semi-
conscious patient, also used to facilitate nasotracheal suctioning
• Complications of these airways include bleeding, sinusitis, and erosion
of the mucous membranes..
• Care of the patient with a nasal airway includes frequent assessment
for pressure areas and occlusion of the air-way with dried secretions.
Sinusitis has been documented as a complication.
• The continued need for the nasal airway is assessed daily and rotation
of the airway from nostril to nostril is done on a daily basis
Laryngeal Mask Airway
• The laryngeal mask airway (LMA) is an ET with a small mask on one
end that can be passed orally over the larynx to provide ventilatory
assistance and prevent aspiration.
• Placement of the LMA is easier than intubation using a standard ET.
• It should, however, only be considered a tempo-rary airway for
patients who require prolonged ventilatory support.
Combi-tube
• The Combitube is an esophageal/tracheal double-lumen airway that
allows for rapid airway establishment through either esophageal or
tracheal placement.
• It is used primarily for difficult or emergency intubation and its design
permits blind placement without the need for a laryngoscope.
• The Combitube design permits positive-pressure ventilation, but an
ET or tracheostomy is eventually needed.
• COMBITUBE is contraindicated in responsive patients with intact gag
reflexes, patients with known esophageal pathology, patients who
have ingested caustic substances, and patients under 5 feet in height.
Artificial Airways
• Artificial airways (oral and nasal endotracheal tubes, tracheostomy
tubes) are used when a patent airway cannot be maintained with an
adjunct airway device for mechanical ventilation or to manage severe
airway obstruction.
• The artificial airway also protects the lower airway from aspiration of
oral or gastric secretions and allows for easier secretion removal.
Endotracheal tube ETT
• ET tubes are inserted into the patient's trachea either through the
mouth or nose.
• Orally inserted endotracheal tubes are more common than the nasal
route because nasal intubation is associated with sinus infections and
are considered an independent risk factor for developing ventilator-
associated pneumonia (VAP)
• A radiopaque line is also located on all tubes so as to aid in
determining proper position radiographically
• ET tubes can be safely left in place for up to several weeks, but
tracheostomy is often considered following 10 to 14 days of intubation.
• If the need for an artificial airway is anticipated for an extended period of
time, a tracheostomy tube may be indicated earlier, but the decision is
always individualized.
• Complications of ET intubation are numerous and include laryngeal and
tracheal damage, laryngospasm, aspiration, infection, discomfort, sinusitis,
and subglottic injury.
• Tracheostomy tubes may be inserted as an elective procedure using a
standard open surgical technique in the operating room or at the bedside
via a percutaneous insertion.
• Complications of tracheostomies include hemorrhage from erosion of the
innominate artery; tracheal stenosis, malacia, or perforation; laryngeal nerve
injury; aspiration; infection; air leak; and mechanical problems.
• Most complications rarely occur with proper management.

Cuff Inflation
Following insertion of an endotracheal or tracheostomy tube, the cuff of the tube
is inflated with just enough air to create an effective seal.
The cuff is typically inflated with the lowest possible pressure that prevents air
leak during mechanical ventilation and decreases the risk of pulmonary aspiration.
Cuff pressure is maintained under 25 mm Hg
Endotracheal Suctioning
• Pulmonary secretion removal is normally accomplished by coughing. An
effective cough requires a closed epiglottis so intrathoracic pressure can be
increased prior to sudden opening of the epiglottis and secretion expulsion.
• The presence of an artificial airway such as an ET prevents glottic closure
and effective coughing, necessitating the use of periodic endo-tracheal
suctioning to remove secretions.
• The number of suction passes are limited to only those necessary to clear
the airway of se-cretions-usually two or three. The mechanical act of in-
serting the suction catheter into the trachea can stimulate the vagus nerve
and result in bradycardia or asystole. Each pass of the suction catheter
should be 10 seconds or less
Complications
• A variety of complications are associated with ET suctioning. Decreases in Pao2
have been well documented when no hyperoxygenation therapy is provided with
suctioning.
• Serious cardiac arrhythmias occur occasionally with suctioning, and include
bradycardia, a systole, ventricular tachycardia, and heart block. Less severe
arrhythmias frequently
• Other complications associated with suctioning include increases in arterial
pressure and intracranial pressure, bronchospasm, tracheal wall damage, and
nosocomial pneumonia.
• Many of these complications can be minimized by using sterile technique, vigilant
monitoring during and after suctioning, and hyperoxygenation before and after
each suction pass.
Extubation
• Removal of an artificial airway usually occurs following weaning from
mechanical ventilatory support
• The reversal or significant improvement of the underlying condition(s)
that led to the use of artificial airways usually signals the readiness for
removal of the airway.
• Common indicators of readiness for artificial airway removal include the
ability to
• maintain spontaneous breathing and adequate ABO values with minimal to
moderate amounts of 02 ad-ministration (Fio2 <0.50);
• protect the airway; and
• clear pulmonary secretions
• Hyperoxygenation with 100% 02 is provided for 30 to 60 seconds prior to
extubation in case respiratory distress occurs immediately after extubation and
reintubation is necessary.
• Monitor the patient's response to the extubation. Sig-nificant changes in heart
rate, respiratory rate, and/or blood pressure of more than 10% of baseline
values may indicate respiratory compromise, necessitating more extensive
assessment and possible reintubation.
• Pulmonary auscultation is also performed.
• Complications associated with extubation include as-piration, bronchospasm,
and tracheal damage.
• Coughing and deep breathing are encouraged while monitoring vital signs and
the upper airway for stridor. Inspiratory stridor occurs from glottic and
subglottic edema and may develop imme-diately or take several hours.
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OXYGEN THERAPY
• Oxygen is used for any number of clinical problems. The overall goals
for oxygen use include increasing alveolar 02 tension (Pao2) to treat
hypoxemia, decreasing the work of breathing, and maximizing
myocardial and tissue oxygen supply.
• As with any drug, oxygen should be used cautiously. The hazards of
oxygen misuse can be as dangerous as the lack of appropriate use.
Alveolar hypoventilation, absorption atelectasis, and oxygen toxicity
can be life threatening.

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Indication of oxygen
• Decreased cardiac performance
• Increased metabolic need for 02 (fever,
burns)
• Acute changes in level of
consciousness (restlessness, confusion)
• Acute shortness of breath
• Decreased 02 saturation
• Pao2 <60 mm Hg or Sao2 <90%
• Normal Pao2 or Sao2 with signs and
symptoms of significant hypoxia
• Myocardial infarction
• Carbon monoxide (CO) poisoning
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• Acute anemia
• Cardiopulmonary arrest
• Reduced cardiac output
• Consider in the presence of
hypotension, tachycardia, cyanosis,
chest pain, dyspnea, and acute
neurologic dysfunction
• During stressful procedures and
situations, especially in high-risk
patients (e.g., endotracheal
suctioning, bronchoscopy,
thoracentesis, PA catheterization,
travel at high altitudes)
 Acid-Base Analysis
• Optimal cellular functioning occurs when the pH of the blood is between
7.35 and 7.45.
• Decreases in pH below 7.35 are termed acidemia, and increases in pH
above 7.45 are termed alkalemia.
• When the amount of acids or bases in the body increases or decreases.
• there are strong systems in place to maintain the balance between acids
and bases, even if one of those components is functioning abnormally.
• Although a variety of regulatory systems are involved in acid-base balance,
the bicarbonate (HC03 and carbon dioxide (C02) levels are the primary
regulators.

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• Metabolic component: HC03 levels are controlled primarily by the kidneys
and have been termed the metabolic component of the acid-base system. By
in-creasing or decreasing the amount of HC03- excreted in the kidneys, the pH
of the blood can be increased or decreased.
• Changes in HC03- excretion may take up to 24 hours or longer to accomplish,
but can be maintained for prolonged periods.
• Respiratory component: C02 levels are controlled primarily by the lungs and
are termed the respiratory component of the acid-base system.
By increasing or decreasing the amount of C02 excreted by the lungs, the pH of
the blood can be increased or decreased.
• Changes in C02 excretion can occur rapidly, within a minute, by increasing or
decreasing respiration (minute ventilation). Compensation by the respiratory
system is difficult to maintain over long periods of time (>24 hours).

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Metabolic alkalemia

• Ph > 7.45
• Hco3 > 28
• Primary increase in hydrogen ion (H+) loss or HC03- gain.
• Causes:
A. loss of body acids (nasogastric suction of HCl, vomiting, ex-cessive diuretic
therapy, steroids, hypokalemia)
B. ingestion of exogenous bicarbonate or citrate substances.
• Management:
treating the underlying cause, decreasing or stopping the acid loss (e.g.,
use of antiemetic therapy for vomiting), and replacing electrolytes.
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 Metabolic acidemia
• pH is below 7.35 and the HC03- is below 22 mEq/L.
• excessive loss of HC03- from the body by the kidneys or the accumulation of acid.
Causes:
• metabolic formation of acids (diabetic ketoacidosis, uremic acidosis, lactic acidosis),
• loss of bicarbonate (diarrhea, renal tubular acidosis),
• hyperkalemia,
• toxins (salicylates overdose, ethylene and propylene glycol, methanol, paraldehyde)
Management of metabolic acidosis is
• directed at treating the underlying cause, decreasing acid formation (e.g., decreasing lactic acid
production by improving cardiac output [CO] in shock),
• decreasing bicarbonate losses (e.g., treatment of diarrhea),
• removal of toxins through dialysis or cathartics, or administering sodium bicarbonate (NaHC03)
in extreme metabolic acidemia states
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Respiratory alkalemia

• pH above 7.45 and the Paco2 below 35 mm Hg.

• an excessive amount of ventilation (alveolar hyperventilation) and removal
of C02 from the body.
Causes:
• neurogenic hyperventilation, inter-stitial lung diseases, pulmonary
embolism, asthma,
• acute anxiety/stress/fear, hyperventilation syndromes, excessive
mechanical ventilation, and severe hypoxemia.
Management
• treating the underlying cause and decreasing excessive ventilation if
possible
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Respiratory acidemia
• pH is below 7.35 and the Paco2 is above 45 mm Hg.
• an inadequate amount of ventilation (alveolar hypoventilation) and removal of
C02 from the body.
Causes:
• overall hypoventilation associated with respiratory failure (e.g., acute
respiratory distress syndrome [ARDS], severe asthma, pneumonia, chronic
obstructive pulmonary diseases, sleep apnea), pulmonary embolism,
pulmonary edema, pneumothorax, respiratory center depression, and
neuromuscular disturbances in the presence of normal lungs, and inadequate
mechanical ventilation.
Management of respiratory acidosis is directed at treating the underlying cause
and improving ventilation.
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Hypoxemia
Low inspired oxygen:
• Usually, the fraction of in-spired oxygen concentration (Fio2) is reduced at high
altitudes or when toxic gases are inhaled.
• Inadequate or inappropriately low Fio2 administration may con-tribute to
hypoxic respiratory failure in patients with other cardiopulmonary diseases.
Overall hypoventilation:
• Decreases in tidal volume (Vt), respiratory rate, or both reduce minute
ventilation and cause hypoventilation.
• Causes include respiratory center depres-sion from drug overdose, anesthesia,
excessive anal-gesic administration, neuromuscular disturbances, and fatigue

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Ventilation-perfusion mismatch:
• When the balance between adequately ventilated and perfused
alveoli is altered, hypoxemia develops.
• Perfusion of blood past, underventilated alveoli decreases the
availability of oxygen for gas exchange, leading to poorly oxy-genated
blood in the pulmonary vasculature.
• Examples of this include bronchospasm, atelectasis, secretion
retention, pneumonia, pulmonary embolism, and pulmonary edema.

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Diffusion defect:
• Thickening of the alveolar-capillary membrane decreases oxygen diffusion and leads to
hypoxemia. Causes of diffusion defects are chronic disease states such as pulmonary
fibrosis and sarcoidosis.
• Hypoxemia usually responds to supplemental oxygen in conditions of diffusion
impairment (e.g., interstitial lung disease)
Shunt:
• When blood bypasses or shunts past the alveoli, gas exchange cannot occur and blood
returns to the left side without being oxygenated. Shunts caused in congenital cardiac
anomalies of the heart and great vessels, such as tetralogy of Fallot.
• Physiologic shunts are caused by a variety of conditions that result in closed, non
ventilated alveoli such as seen in ARDS.
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• Low mixed venous oxygenation: Under normal conditions, the lungs
fully oxygenate the pulmonary arterial blood and mixed venous
oxygen tension (Pvo2) does not affect Pao2 significantly.
• However, a reduced Pvo2 can lower the Pao2 significantly when either
ventilation-perfusion mismatch or intrapulmonary shunting is present.
• Conditions that can contribute to low mixed venous oxygenation
include low CO, anemia, hypoxemia, and increased oxygen
consumption.
• Improving tissue oxygen delivery by increasing CO or hemoglobin
usually improves mixed venous oxygen saturation (Svo2)
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Complications of oxygenation
• Alveolar Hypoventilation
• Absorption Atelectasis : results when high concentrations of 02
(>90%) are given for long periods of time and nitrogen is washed out
of the lungs..
• Oxygen Toxicity: nausea, vomiting, numbness, visual disturbances,
muscular twitching, and grand mal seizures..

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Oxygen Delivery
Noninvasive Devices
• Face masks and nasal cannulas are standard oxygen delivery devices for the
spontaneously breathing patient ..
• Venturi mask 24, 28, 35, 40, 50 %
Invasive devices
• Manual Resuscitation Bags : 40% to 100% 02 at adult Vt and respiratory
rates to an ET or tracheostomy tube
• Mechanical ventilator
most common method for delivering oxygen invasively
is with a mechanical ventilator. Oxygen delivery can be accurately delivered from 21% to
100% 02

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BASIC VENTILATORY MANAGEMENT
• Mechanical ventilation is indicated when noninvasive management modalities
fail to adequately support oxygenation and/or ventilation. The decision to
initiate mechanical ventilation is based on the ability of the patient to support
their oxygenation and/or ventilation needs. The inability of the patient to
maintain clinically acceptable C02 levels and acid-base status is referred to as
respiratory failure and is a common indicator for mechanical ventilation.
Inadequate alveolar ventilation (acute ventilatory failure)
Hypoxemia (acute oxygenation failure)
lnadequate lung expansion
Inadequate respiratory muscle strength
Excessive work of breathing
Unstable ventilatory drive

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