Transcript RESPIRATORY FAILURE

RESPIRATORY FAILURE
and ARDS
BY
NANCY JENKINS
Respiratory Failure
the inability of the cardiac and
pulmonary systems to maintain
an adequate exchange of
oxygen and CO2 in the lungs
Acute Respiratory Failure
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Hypoxemia- inadequate O2 transfer
• PaO2 of 60mmHg or less when pt.
Receiving 60% or greater O2
Hypercapnia- insufficient CO2 removal
Increases PaCO2
Classification of Respiratory
Failure
Inhaling
Exhaling
Affects
PaO2
Affects
PCO2
Fig. 68-2
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Hypoxemic Respiratory Failure(Affects the pO2)
V/Q Mismatch
 Shunt
 Diffusion Limitation
 Alveolar Hypoventilation- inc. CO2 and
dec. PO2
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VentilationPerfusion Mismatch
(V/Q)
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Normal V/Q =1 (1ml air/ 1ml of blood)
Ventilation=lungs
Perfusion or Q=perfusion
Pulmonary Embolus- (VQ scan)
Shunt
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2 Types
• 1. Anatomic- passes through an anatomic channel
of the heart and does not pass through the lungs
ex: ventricular septal defect
• 2. Intrapulmonary shunt- blood flows through
pulmonary capillaries without participating in gas
exchange ex: alveoli filled with fluid
• * Patients with shunts are more hypoxemic than
those with VQ mismatch and they may require
mechanical ventilators
Diffusion Limitations
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Gas exchange is compromised by a
process that thickens or destroys the
membrane
• 1. Pulmonary fibrosis
• 2. ARDS
* A classic sign of diffusion limitation is
hypoxemia during exercise but not at rest
Alveolar Hypoventilation
Mainly due to hypercapnic respiratory
failure but can cause hypoxemia
 Increased pCO2 with decreased PO2
 Restrictive lung disease
 CNS diseases
 Neuromuscular diseases
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Hypercapnic Respiratory Failure
Ventilatory Failure- affects CO2
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1. Abnormalities of the airways and alveoliair flow obstruction and air trapping
• Asthma, COPD, and cystic fibrosis
2. Abnormalities of the CNS- suppresses drive to
breathe
drug OD, narcotics, head injury, spinal cord injury
Hypercapnic Respiratory Failure
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3. Abnormalities of the chest wall
• Flail chest, morbid obesity, kyphoscoliosis
4. Neuromuscular Conditions- respiratory
muscles are weakened:
Guillain-Barre, muscular dystrophy,
myasthenia gravis and multiple sclerosis
Tissue Oxygen needs
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Tissue O2 delivery is determined by:
• Amount of O2 in hemoglobin
• Cardiac output
• *Respiratory failure places patient at more
risk if cardiac problems or anemia
O2 delivery devices and amounts of O2
delivered- FYI
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1. Room air- 21%
2. NC- 24-40% at 1-6 L
3. Face mask- 24-60% at 6-10L
4.Venturi mask- 24-60% at 4-15L
5. Partial rebreather mask- 60-90% at 8-10L
6. Non-rebreather mask-90-100% at 10-15L
7. Bag mask- up to100%
8. ET tube- up to 100%
Signs and Symptoms of
Respiratory Failure- ABG’s
hypoxemia pO2<50-60
 May be hypercapnia pCO2>50
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• only one cause- hypoventilation
*In patients with COPD watch for acute drop
in pO2 and O2 sats along with inc. C02
and KNOW BASELINE!!!
Hypoxemia
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Compensatory Mechanisms- early
• Tachycardia- more O2 to tissues
• Hypertension- fight or flight
• Tachypnea –take in more O2
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Restlessness and apprehension
Dyspnea
Cyanosis
Confusion and impaired judgment
**Later dysrhythmias and metabolic acidosis,
dec. B/P and Dec. CO.
Hypercapnia
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Dyspnea to respiratory depressionif too high CO2 narcosis
Headache-vasodilation- Increases
ICP
Papilledema
Tachycardia and inc. B/P
Drowsiness and coma
Respiratory acidosis
• **Administering O2 may eliminate
drive to breathe especially with COPD
patients
- WHY??
Specific Clinical Manifestations
Respirations- depth and rate
 Patient position- tripod position
 Pursed lip breathing
 Orthopnea
 Inspiratory to expiratory ratio (normal
1:2)
 Retractions and use of accessory
muscles
 Breath sounds
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Diagnosis
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Physical Assessment
Pulse oximetry (90% is PaO2 of 60)
ABG
CXR
CBC
Electrolytes
EKG
Sputum and blood cultures, UA
V/Q scan if ?pulmonary embolus
Pulmonary function tests (PFT’s)
Treatment Goals
O2 therapy
 Mobilization of secretions
 Positive pressure ventilation(PPV)
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O2 Therapy
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If secondary to V/Q mismatch- 1-3Ln/c or
24%-32% by mask
If secondary to intrapulmonary shunt- positive
pressure ventilation-PPV
• May be via ET tube
• Tight fitting mask
• **Goal is PaO2 of 55-60 with SaO2 at 90% or
more at lowest O2 concentration possible
• **O2 at high concentrations for longer than 48
hours causes O2 toxicity
Mobilization of secretions
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Effective coughing- quad cough, huff cough,
staged cough
Positioning- HOB 45 degrees or recliner chair
or bed
• “Good lung down”
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Hydration - fluid intake 2-3 L/day
Humidification- aerosol treatments- mucolytic
agents
Chest PT- postural drainage, percussion and
vibration (30mls sputum)
Airway suctioning
Positive Pressure Ventilation
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Invasively through oro or nasotracheal
intubation
Noninvasively( NIPPV) through mask
• Used for acute and chronic resp failure
• BiPAP- different levels of pressure for inspiration
and expiration- (IPAP) higher for
inspiration,(EPAP) lower for expiration
• CPAP- for sleep apnea
• **Used best in chronic resp failure in patients with
chest wall and neuromuscular disease, also with
HF and COPD.
Should hear equal breath
sounds if in correct place.
Always get a CXR to check
placement also
Drug Therapy
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Relief of bronchospasm- bronchodilators
• alupent and albuterol-(Watch for what side effect?)
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Reduction of airway inflammationCorticosteroids by inhalation or IV or po
Reduction of pulmonary congestion-diuretics
and nitroglycerine with heart failure• why HF with pulmonary problems?
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Treatment of pulmonary infections- IV
antibiotics, vancomycin and rocephin
Reduction of anxiety, pain and agitationdiprivan, ativan, versed, propofol, opioids
May need sedation or neuromuscular
blocking agent if on ventilator.(Norcuron,
nimbex) assess with peripheral nerve stim.
Medical Supportive Treatment
Treat underlying cause
 Maintain adequate cardiac outputmonitor B/P and MAP.
 Maintain adequate Hemoglobin
concentration- need 9g/dl or greater
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• **Need B/P of 90 systolic and MAP of 60 to
maintain perfusion to the vital organs
Nutrition
During acute phase- enteral or
parenteral nutrition
 In a hypermetabolic state- need more
calories
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• If retain CO2- avoid high carb diet
Acute Respiratory Failure
Gerontologic Considerations
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Physiologic aging results in
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↓ Ventilatory capacity
Alveolar dilation
Larger air spaces
Loss of surface area
Diminished elastic recoil
Decreased respiratory muscle strength
↓ Chest wall compliance
• **Dec. PO2 and inc. CO2
ARDS
Also known as DAD
(diffuse alveolar disease)
or ALI (acute lung injury)
a variety of acute and diffuse
infiltrative lesions which cause
severe refractory arterial
hypoxemia and life-threatening
arrhythmias
150,000 adults dev. ARDS
About 50% survive
**Patients with gram negative septic shock and
ARDS have mortality rate of 70-90%
ALI versus ARDS- continuum
Acute Lung injury
 PaO2/ FiO2 ratio is 200-300
 Example 86/.40=215
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ARDS
 PaO2/ FiO2 ratio is less than 200
 Example 80/.80=100
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Direct Causes (Inflammatory
process is involved in all)
Pneumonia*
 Aspiration of gastric contents*
 Pulmonary contusion
 Near drowning
 Inhalation injury
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Indirect Causes (Inflammatory
process is involved)
Sepsis* (most common) gm  Severe trauma with shock state
that requires multiple blood
transfusions*
 Drug overdose
 Acute pancreatitis
↓CO
Metabolic acidosis
↑CO
Interstitial & alveolar
edema
Severe & refractory
hypoxemia
*Causes (see
notes)
DIFFUSE
lung injury
(SIRS or
MODS)
Damage to alveolar
capillary membrane
Pulmonary capillary
leak
SHUNTING
Stiff lungs
Inactivation of
surfactant
Alveolar atalectasis
Hyperventilation
Hypocapnea
Respiratory Alkalosis
Hypoventilation
Hypercapnea
Respiratory Acidosis
Pathophysiology of ARDS
Damage to alveolar-capillary membrane
 Increased capillary hydrostatic pressure
 Decreased colloidal osmotic pressure
 Interstitial edema
 Alveolar edema or pulmonary edema
 Loss of surfactant
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Pathophysiologic Stages in ARDS
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Injury or Exudative- 1-7 days
• Interstitial and alveolar edema and atelectasis
• Refractory hypoxemia and stiff lungs
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Reparative or Proliferative-1-2 weeks after
• Dense fibrous tissue, increased PVR and
pulmonary hypertension occurs
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Fibrotic-2-3 week after
• Diffuse scarring and fibrosis, decreased surface
area, decreased compliance and pulmonary
hypertension
The essential disturbances of
ARDS
**interstitial and alveolar edema
and atelectasis
**Progressive arterial
hypoxemia in spite of inc. O2 is
hallmark of ARDS
Clinical Manifestations: Early
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Dyspnea-(almost always present),
tachypnea, cough, restlessness
Chest auscultation may be normal or
reveal fine, scattered crackles
ABGs
• **Mild hypoxemia and respiratory
alkalosis caused by hyperventilation
Clinical Manifestations: Early
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Chest x-ray may be normal or show
minimal scattered interstitial infiltrates
• Edema may not show until 30% increase
in lung fluid content
Clinical Manifestations: Late
Symptoms worsen with progression of fluid
accumulation and decreased lung
compliance
 Pulmonary function tests reveal decreased
compliance and lung volume
 Evident discomfort and increased WOB
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Clinical Manifestations: Late
Suprasternal retractions
 Tachycardia, diaphoresis, changes in
sensorium with decreased mentation,
cyanosis, and pallor
 Hypoxemia and a PaO2/FIO2 ratio <200
despite increased FIO2 ( ex: 80/.8=100)
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Clinical Manifestations
As ARDS progresses, profound
respiratory distress requires
endotracheal intubation and
positive pressure ventilation
 Chest x-ray termed whiteout or
white lung because of
consolidation and widespread
infiltrates throughout lungs
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Clinical Manifestations
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If prompt therapy not initiated, severe
hypoxemia, hypercapnia, and metabolic
acidosis may ensue
Nursing Diagnoses
Ineffective airway clearance
 Ineffective breathing pattern
 Risk for fluid volume imbalance
 Anxiety
 Impaired gas exchange
 Imbalanced nutrition: Less than body
requirements
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Planning
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Following recovery
• PaO2 within normal limits or at
baseline
• SaO2 > 90%
• Patent airway
• Clear lungs or auscultation
Nursing Assessment
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Lung sounds
ABG’s
CXR
Capillary refill
Neuro assessment
Vital signs
O2 sats
Hemodynamic monitoring values
Diagnostic Tests
ABG-review
 CXR
 Pulmonary Function Tests- dec.
compliance and dec vital capacity- (max
exhaled after max inhale)
 Hemodynamic Monitoring- (Pulmonary
artery pressures) to rule out pulmonary
edema
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ABG Review and Practice
ABG review
RealNurseEd (Education for Real
Nurses by a Real Nurse)
*Goal of Treatment for ARDS
Maintain adequate ventilation and
respirations.
Prevent injury
Manage anxiety
Treatment
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Mechanical Ventilation-goal PO2>60 and 02
sat 90% with FIO2 < 50
PEEP- can cause dec. CO, B/P and
barotrauma
Positioning- prone, continuous lateral rotation
therapy and kinetic therapy
ECMO
Hemodynamic Monitoring- fluid replacement
or diuretics
Enteral or Parenteral Feeding- high calorie,
high fat. Research shows that formulas
enriched with omega -3 fatty acids may
improve the outcomes of those with ARDS
Cont.
Crystalloids versus colloids
 Mild fluid restriction and diuretics
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PEEP
pt. can not expire completely. Causes
alveoli to remain inflated
(Complications can include decreased cardiac
output, pneumothorax, and increased
intracranial pressure).
Vent settings to improve <oxygenation>
PEEP and FiO2 are adjusted in tandem
• PEEP
• Increases FRC
• Prevents progressive atelectasis and
intrapulmonary shunting
• Prevents repetitive opening/closing (injury)
• Recruits collapsed alveoli and improves
V/Q matching
• Resolves intrapulmonary shunting
• Improves compliance
• Enables maintenance of adequate PaO2
at a safe FiO2 level
• Disadvantages
• Increases intrathoracic pressure (may
require pulmonary a. catheter)
• May lead to ARDS
• Rupture: PTX, pulmonary edema
Oxygen delivery (DO2), not PaO2, should be
used to assess optimal PEEP.
Proning
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Proning typically reserved for
refractory hypoxemia not
responding to other therapies
• Plan for immediate repositioning
for cardiopulmonary resuscitation
Proning-Principles
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Positioning strategies
• Mediastinal and heart contents place more
pressure on lungs when in supine position
than when in prone
– Predisposes to atelectasis
• Turn from supine to prone position
– May be sufficient to reduce inspired O2 or PEEP
• Fluid pools in dependent regions of lung
Prone Device
•Prone positioning
With position change to prone,
previously nondependent air-filled
alveoli become dependent, perfusion
becomes greater to air-filled alveoli
opposed to previously fluid-filled
dependent alveoli, thereby improving
ventilation-perfusion matching.
No benefit in mortality
Benefits to Proning
Before proning ABG on
100%O2 7.28/70/70
After proning ABG on
100% 7.37/56/227
Positioning
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Other positioning strategies
• Kinetic therapy
• Continuous lateral rotation therapy
ECMO- Blood drains by gravity from the patient
through a tube (catheter) placed in a large neck
vein. This blood passes through a plastic
pouch, or bladder, and then in pumped through
the membrane oxygenator that serves as an
artificial lung, putting oxygen into the blood and
removing carbon dioxide. The blood then
passes through a heat exchanger that
maintains the blood at normal body
temperature. Finally, the blood reenters the
body through a large catheter placed in an
artery in the neck.
Medications
Inhaled Nitric Oxide
 Surfactant therapy
 NSAIDS and
 corticosteroids
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Nitric Oxide
Dilates pulmonary blood
vessels and helps
reduce shunting
Assessment Data and Priority
Respiratory rate of 10
 Absent breath sounds on the left
 O2 sat 82%
 High pressure alarm on vent going off
 Bilateral wheezing
 Respiratory rate of 30
 ABG respiratory acidosis
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Ventilator
VentWorld What is a
Ventilator?
a machine that moves air
in and out of the lungs
Mechanical Ventilation
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Indications
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Apnea or impending inability to breathe
Acute respiratory failure
Severe hypoxia
Respiratory muscle fatigue
Mechanical Vent Objective
support circulation and maintain
pt. respirations until can breathe
on own
Goal of Mechanical Ventilation
adequate controlled ventilation
 relief of hypoxia without hypercapnia
 relief of work of breathing
 access to airways
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Criteria to put on vent
Apnea or impending inability to breathe
 Acute respiratory failure
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• pH<7.25
• pCO2>50
Severe hypoxia - pO2<50
 Respiratory muscle fatigue
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Mechanical Ventilation
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Types of mechanical
ventilation
• Negative pressure ventilation
– Uses chambers that encase chest
or body and surround it with
intermittent subatmospheric or
negative pressure
– Noninvasive ventilation that does
not require an artificial airway
– Not used extensively for acutely ill
patients
– Mostly used for neuromuscular
diseases, CNS and injuries of the
spinal cord
Mechanical Ventilation
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Types of mechanical ventilation (cont’d)
• Positive pressure ventilation (PPV)
– Used primarily in acutely ill patients
– Pushes air into lungs under positive pressure
during inspiration
– Expiration occurs passively
Mechanical Ventilator
Settings to Monitor
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FIO2 -% of O2
TV-<5ml/kg for ARDS (normal 8-10)
Rate 12-15
• Control mode
• Assist control
• SIMV
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inspiratory pressure and flow
Pressure support- only in spontaneous
breathes (gets the balloon started) Pt.
controls all but pressure limit
Ventilator Modes- depends on WOB
Mode refers to how the machine
will ventilate the patient in
relation to the patient’s own
respiratory efforts. There is a
mode for nearly every patient
situation, plus many can be used
in conjunction with each other.
Mechanical Ventilation
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Modes of volume ventilation
• Based on how much work of breathing
(WOB) patient should or can perform
• Determined by patient’s ventilatory status,
respiratory drive, and ABGs
Control Mode or CMV
1. TV and RR are fixed.
2. Used for patients who are unable to
initiate a breath (anesthetized or
paralyzed). CMV delivers the preset
volume or pressure at pre-set rate
regardless of the patient’s own inspiratory
effort
3. Spontaneously breathing patients must be
sedated and/or pharmacologically
paralyzed so they don’t breathe out of
synchrony with the ventilator.
3. *Ventilator does all the work
Assist Contol
1. A/C delivers the preset volume or pressure in
response to the patient’s own inspiratory effort,
but will initiate the breath if the patient does not
do so within the set amount of time.
2. Patient Assists or triggers the vent –can breathe
faster but not slower
3. Vent has back-up rate
4. May need to be sedated to limit the number of
spontaneous breaths since hyperventilation can
occur.
5. This mode is used for patients who can initiate a
breath but who have weakened respiratory
Synchronous Intermittent
Mandatory Ventilation-SIMV
1. SIMV delivers the preset volume or pressure and rate while
allowing the patient to breathe spontaneously in between
ventilator breaths.
2. Each ventilator breath is delivered in synchrony with the patient’s
breaths, yet the patient is allowed to completely control the
spontaneous breaths at own TV.
3. SIMV is used as a primary mode of ventilation, as well as a
weaning mode.
4. During weaning, the preset rate is gradually reduced, allowing
the patient to slowly regain breathing on their own.
5. The disadvantage of this mode is that it may increase the work of
breathing and respiratory muscle fatigue
Pressure Support Ventilation
1. PSV is preset pressure that augments the
patient’s spontaneous inspiratory effort and
decreases the work of breathing.
2. The patient completely controls the respiratory
rate and tidal volume.
3. PSV is used for patients with a stable respiratory
status and is often used with SIMV to overcome
the resistance of breathing through ventilator
circuits and tubing.
High Frequency Ventilation
1. HFV delivers a small amount of gas at a rapid
rate (as much as 60-100 breaths per minute.)
2. This is used when conventional mechanical
ventilation would compromise hemodynamic
stability, during short-term procedures, or for
patients who are at high risk for
pneumothorax.
3. Sedation and pharmacological paralysis are
required.
Pressure Control
Inverse Ratio Ventilation
1. The normal inspiratory:expiratory ratio is 1:2 but this is reversed
during IRV to 2:1 or greater (the maximum is 4:1).
2. This mode is used for patients who are still hypoxic even with the
use of PEEP. The longer inspiratory time increases the amount of
air in the lungs at the end of expiration (the functional residual
capacity) and improves oxygenation by re-expanding collapsed
alveoli- acts like PEEP.
3. The shorter expiratory time prevents the alveoli from collapsing
again.
4. Sedation and pharmacological paralysis are required since it’s
very uncomfortable for the patient.
5. For patients with ARDS continuing refractory hypoxemia
despite high levels of PEEP
Case Study
Mr. Hill has been on the ventilator for 24 hours. You
volunteered to care for him today, since you know
him from the intubation yesterday. The settings
ordered by the pulmonologist after intubation were
as follows: A/C, rate 14, VT 700, FIO2 60%. Since
0700, Mr. Hill has been assisting the ventilator with
a respiratory rate of 24 (It’s now 1100).
1.
1. Describe the ventilator settings.
Case Study
You notice that Mr. Hill’s pulse oximetry has been
consistently documented as 100% since intubation.
You also notice that his respiratory rate is quite high
and that he’s fidgety, doesn’t follow commands, and
doesn’t maintain eye contact when you talk to him.
He hasn’t had any sedation since he was intubated.
2.
2. Which lab test should you check to find out
what his true ventilatory status is?
Case Study
3. Which two parameters on the ABG will give you a
quick overview of Mr. Hill’s status?
Case Study
4. What are some possible causes of Mr.
Hill’s increased respiratory rate? (Give the
corresponding nursing interventions as
well.)
Case Study
Mr. Hill didn’t have an ABG done this morning, so
you get an order from the pulmonologist to get one
now (1130). When it comes back, the PaCO2 is 28,
the pH is 7.48, and the PaO2 is 120 (normals:
PaCO2 35-45 mm Hg, pH 7.35-7.45 mm Hg, PaO2
80-100 mm Hg).
5.
Based on the ABG, the pulmonologist
changes the vent settings to SIMV, rate 10, PS 10,
FIO2 40%. The VT remains 700. How will these
new settings help Mr. Hill?
Low Pressure Alarms
•Circuit leaks
•Airway leaks
•Chest tube leaks
•Patient disconnection
High Pressure Alarms
•Patient coughing
•Secretions or mucus in
the airway
•Patient biting tube
•Airway problems
•Reduced lung
compliance (eg.
pneumothorax)
•Patient fighting the
ventilator
•Accumulation of water
in the circuit
•Kinking in the circuit
Mechanical Ventilation
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Complications of PPV (cont’d)
• Cardiovascular system (cont’d)
– ↑ Intrathoracic pressure compresses thoracic
vessels
• ↓ Venous return to heart, ↓ left ventricular enddiastolic volume (preload), ↓ cardiac output
• Hypotension
• Mean airway pressure is further ↑ if PEEP
>5 cm H2O
Mechanical Ventilation
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Complications of PPV (cont’d)
• Pulmonary system
– Barotrauma
• Air can escape into pleural space from alveoli or
interstitium, accumulate, and become trapped
pneumothorax , subcutaneous emphysema
• Patients with compliant lungs are at ↑ risk
• Chest tubes may be placed prophylactically
Mechanical Ventilation
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Complications of PPV (cont’d)
• Ventilator-associated pneumonia (VAP)
– Pneumonia that occurs 48 hours or more after
ET intubation
– Clinical evidence
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Fever and/or elevated white blood cell count
Purulent or odorous sputum
Crackles or rhonchi on auscultation
Pulmonary infiltrates on chest x-ray
Mechanical Ventilation
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Complications of PPV (cont’d)
• Guidelines to prevent VAP
– HOB elevation at least 30 to 45 degrees unless medically
contraindicated
– No routine changes of ventilator circuit tubing
– Use of an ET that allows continuous suctioning of
secretions in subglottic area
– Drain condensation that collects in ventilator tubing
Mechanical Ventilation
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Complications of PPV (cont’d)
• Fluid retention
– Occurs after 48 to 72 hours of PPV, especially
PPV with PEEP
– May be due to ↓ cardiac output
– Results
• Diminished renal perfusion
• Release of renin-angiotensin-aldosterone
– Leads to sodium and water retention
Mechanical Ventilation
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Complications of PPV (cont’d)
• Gastrointestinal system
– Risk for stress ulcers and GI bleeding
– ↑ Risk of translocation of GI bacteria
• ↓ Cardiac output may contribute to gut ischemia
– Peptic ulcer prophylaxis
• Histamine (H2)-receptor blockers, proton pump
inhibitors, tube feedings
– ↓ Gastric acidity, ↓ risk of stress
ulcer/hemorrhage
Mechanical Ventilation
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Complications of PPV (cont’d)
• Musculoskeletal system
– Maintain muscle strength and prevent problems
associated with immobility
– Progressive ambulation of patients receiving
long-term PPV can be attained without
interruption of mechanical ventilation
Mechanical Ventilation
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Psychosocial needs
• Physical and emotional stress due to
inability to speak, eat, move, or breathe
normally
• Pain, fear, and anxiety related to tubes/
machines
• Ordinary ADLs are complicated or
impossible
Mechanical Ventilation
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Psychosocial needs (cont’d)
• Involve patients in decision making
• Encourage hope and build trusting relationships
with patient and family
• Provide sedation and/or analgesia to facilitate
optimal ventilation
• If necessary, provide paralysis to achieve more
effective synchrony with ventilator and increase
oxygenation
• Paralyzed patient can hear, see, think, feel
– Sedation and analgesia must always be administered
concurrently
Ventilator Bundle Components
1. Elevate HOB 30-45 degrees
 2. Daily sedation vacations and
assessment of readiness to extubate
 3. Peptic ulcer disease prophylaxis
 4. Venous thromboembolism
prophylaxis
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Respiratory Therapy
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Alternative modes of mechanical
ventilation if hypoxemia persists
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Pressure support ventilation
Pressure release ventilation
Pressure control ventilation
Inverse ratio ventilation
High-frequency ventilation
Permissive hypercapnia
Independent Lung Ventilation
Research
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LiquiVent is an oxygen-carrying liquid
drug (perflubron) used for respiratory
distress syndrome.
The goal of "liquid ventilation" therapy is to
open up collapsed alveoli (air sacs) and
facilitate the exchange of respiratory gases
while protecting the lungs from the harmful
effects of conventional mechanical ventilation.