Transcript respiratory failure - Austin Community College

RESPIRATORY FAILURE
and ARDS
BY
NANCY JENKINS
Respiration


Exchange of O2 and
CO2
gas exchange


Respiratory Failure
the inability of the
cardiac and
pulmonary systems to
maintain an adequate
exchange of oxygen
and CO2 in the lungs
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 Failuremost common type (Affects the pO2)
Physiologic mechanisms:
V/Q Mismatch
 Shunt
 Diffusion Limitation

Hypoxemia-VentilationPerfusion
Mismatch(V/Q)
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Normal V/Q =1 (1ml air/ 1ml of blood)
Ventilation=lungs (breathing in and out)
Perfusion or Q=perfusion- heart (delivery of blood to
a capillary bed to tissues)
Q greater than V , V greater than Q
Ex-Pulmonary Embolus- (VQ scan)
Range of V/Q Relationships
Fig. 68-4
Pulmonary Embolus- V greater
than Q
Hypoxemia
Shunt
Anatomic
• blood passes through an
anatomic channel of the heart
and does not pass through the
lungs ex: ventricular septal
defect
Intrapulmonary
• 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
Hypoxemia
Diffusion Limitation
Gas exchange is
compromised by a
process that
thickens or destroys
the membrane
1.
2.
Pulmonary
fibrosis
2. ARDS
* A classic sign of
diffusion limitation is
hypoxemia during
exercise but not at
rest- Why??
Hypercapnic Respiratory Failure
Ventilatory Failure- affects CO2
1. Abnormalities of the airways and alveoli- air 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

3. Abnormalities of the chest wall- (dec tidal volume)
• Flail chest, morbid obesity, kyphoscoliosis
4. Neuromuscular Conditions- respiratory muscles are
weakened:- Guillain-Barre, muscular dystrophy,myasthenia
gravis and multiple sclerosis
Keeps air in, can’t exhale the CO2- inc. CO2 acidemia,
pH < 7.35
In which of the following patients would you expect
to see hypercapneic respiratory failure? Review of
patients with potential respiratory failure.
1.
2.
3.
4.
A patient with an
anxiety attack
A patient on a PCA
of dilaudid
A patient with
COPD
A patient with a RR
of 30
Hypoxemia causes dec. O2 to
tissues (can cause death of cells)
Tissue O2 delivery is determined by:
• Amount of O2 in hemoglobin- Keep at 9
• Cardiac output-4-8L/min
• *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
hypoxemia pO2<50-60
 May be hypercapnia pCO2>50

• 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- Signs & Symptoms

Compensatory Mechanisms- early
• Tachycardia- more O2 to tissues
• Hypertension- fight or flight (cause?)
• 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.(MODS)
Hypercapnia- signs and symptoms
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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 ManifestationsAssessment- Respiratory
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Respirations- depth and rate
O2 sat -oximeter, CO2- capnometer
Patient position- tripod position,
Pursed lip breathing
Orthopnea, PND
Inspiratory to expiratory ratio (normal 1:2)
Retractions and use of accessory muscles
Breath sounds- crackles, rhonchi, wheezes
Exhaled C02 (ETC02) normal 35-45-
called capnography- lots
of uses now
Used when trying to wean
patient from a ventilator
TSB- trial of spontaneous
breathing
Diagnosis
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Physical Assessment
Pulse oximetry (90% is PaO2 of 60)
ABG
CXR
CBC
Electrolytes-BMP
EKG
Sputum and blood cultures, UA
V/Q scan if ?pulmonary embolus
Pulmonary function tests (PFT’s) TV, FRC
Treatment Goals
O2 therapy
 Mobilization of secretions
 Positive pressure ventilation(PPV)

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


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
What is the correct placement of the
ET tube?
1.
2.
3.
4.
In the right main
stem bronchus
In the left main
stem bronchus
Above the carina
Just below the
vocal cords
Surgical Intervention-Tracheostomy
Tracheotomy
Surgical
procedure
performed
when need for
an artificial
airway is
expected to be
long term
If tube in greater than
4-5 days, perform a
trach-research shows
benefit to early trach
Drug Therapy

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 (SE)
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)
Medical Supportive Treatment

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Treat underlying cause
Maintain adequate cardiac output- monitor B/P and
MAP.
• **Need B/P of 90 systolic and MAP of 60 to maintain
perfusion to the vital organs

Maintain adequate Hemoglobin concentration- need
9g/dl or greater
Nutrition- During acute phase- enteral or parenteral nutrition

(research enteral better)
In a hypermetabolic state- need more calories

• If retain CO2- avoid high carb diet-WHY
Acute Respiratory Failure
Gerontologic Considerations

Physiologic aging results in
• ↓ Ventilatory capacity
• Alveolar dilation
• Larger air spaces
• Loss of surface area
• Diminished elastic recoil
• Decreased respiratory muscle strength
• ↓ Chest wall compliance
Causing Dec pO2 and Inc. pCO2
ARDS- intro
Also known as DAD
(diffuse alveolar disease)
a variety of acute and diffuse
infiltrative lesions which cause
severe refractory arterial
hypoxemia and life-threatening
arrhythmias
Memory Jogger
 Assault to the pulmonary system
 Respiratory distress
 Decreased lung compliance
 Severe respiratory failure
150,000 adults dev. ARDS
About 50% survive
**Patients with gram negative septic shock and
ARDS have mortality rate of 70-90%
Now distinguish between:
ALI versus ARDS- continuum
Same Signs and Symptoms
except:
 Acute Lung injury
 PaO2/ FiO2 ratio is 200-300
 Example 86/.40=215

ARDS
 PaO2/ FiO2 ratio is less than 200
 Example 80/.80=100

Direct Causes (Inflammatory
process is involved in all)
Pneumonia* (community acquired)
 Aspiration of gastric contents*
 Pulmonary contusion
 Near drowning
 Inhalation injury

Indirect Causes (Inflammatory
process is involved)
Sepsis* (most common) gm  Severe trauma with shock state
that requires multiple blood
transfusions*
 Drug overdose
 Acute pancreatitis
Stages of Edema Formation in
ARDS
A, Normal alveolus and
pulmonary capillary
B, Interstitial edema
occurs with increased
flow of fluid into the
interstitial space
C, Alveolar edema
occurs when the fluid
crosses the blood-gas
barrier
Fig. 68-8
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
↓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
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Damage to alveolarcapillary membrane
Increased capillary
hydrostatic pressure
Decreased colloidal
osmotic pressure
Interstitial edema
Alveolar edema or
pulmonary edema
Loss of surfactant
What does surfactant do?
stiff lungs
Pathophysiologic Stages in ARDS

Injury or Exudative- 1-7 days
• Interstitial and alveolar edema and atelectasis
• Refractory hypoxemia and stiff lungs

Reparative or Proliferative-1-2 weeks after
• Dense fibrous tissue, increased PVR and
pulmonary hypertension occurs

Fibrotic-2-3 week after
• Diffuse scarring and fibrosis, decreased surface
area, decreased compliance and pulmonary
hypertension
The essential disturbances of
ARDS are
**interstitial and alveolar edema
and atelectasis causing
**Progressive arterial
hypoxemia in spite of inc. O2
which is hallmark of ARDS
(refractory hypoxemia)
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
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
• PFTs show decreased compliance and lung
volumes
• Evident discomfort and increased WOB
– 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)
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
Clinical Manifestations

If prompt therapy not
initiated, severe
hypoxemia,
hypercapnia, and
metabolic acidosis
may ensue
Nursing Diagnoses
Potential Safety Issues?? Nursing Care
Ineffective airway clearance
 Ineffective breathing pattern
 Risk for fluid volume imbalance
 Anxiety
 Impaired gas exchange
 Imbalanced nutrition: Less than body
requirements

Planning
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Following recovery
• PaO2 within normal limits or at
baseline ( may not be possible)
• SaO2 > 90%
• Patent airway
• Clear lungs or auscultation
Nursing Assessment
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Lung sounds-The Auscultation
Assistant - Breath Sounds
ABG’s
CXR
Capillary refill
Neuro assessment
Vital signs
O2 sats
Hemodynamic monitoring values
Diagnostic Tests- Most important
ABG reviewRealNurseEd (Education for Real Nurses
by a Real Nurse)
 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. **If ARDS, PAW normal

Severe ARDS
ARDS Autopsy
*Goal of Treatment for ARDS
Maintain adequate ventilation and
respirations.
Prevent injury
Manage anxiety
Treatment
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. Monitor
cardiac outputs and daily weights
Hemodynamics- (distiguish between pulmonary edema from
heart versus from ARDS) wedge PAWP increases with Heart Failure
,PAWP does not increase with ARDS.
 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
 Crystalloids versus colloids
 Mild fluid restriction and diuretics- watch for pulmonary edema, strict I
and O
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Mechanical Ventilation
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Patients will commonly need intubation with
mechanical ventilation because PaO2 cannot be
maintained at acceptable level
High flow systems used to maximize O2 delivery
SaO2 continuously monitored
Give lowest concentration that results in PaO2
60 mm Hg or greater
Risk for O2 toxicity increases when FIO2 exceeds
60% for more than 48 hours
PEEPPositive End Expiratory Pressure
pt. can not expire completely. Causes alveoli to
remain inflated- so can dec the FIO2
(Complications can include decreased cardiac
output, pneumothorax, and inc. ICP.
FRC- air in after normal exhalation
PEEP- Positive end-expiratory 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

Proning typically
reserved for
refractory
hypoxemia not
responding to
other therapies
• Plan for immediate
repositioning for
cardiopulmonary
resuscitation
Proning- Rotoprone
• Mediastinal and heart contents place more
pressure on lungs when in supine position
than when in prone
• Fluid pools in dependent regions of lung
• Predisposes to atelectasis
– With prone position
• nondependent air-filled alveoli become dependent
• perfusion becomes greater to air-filled alveoli
• thereby improving ventilation-perfusion matching.
Benefits to ProningNone to mortality
Before proning ABG on
100%O2 7.28/70/70
After proning ABG on
100% 7.37/56/227
Other positioning strategies
Kinetic
therapy
Continuous
lateral rotation
therapy
Ecmo story
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.
ECMO

Extracorporeal membrane oxygenation
• Alternative form of pulmonary support for
patient with severe respiratory failure
• Modification of cardiopulmonary bypass
• Involves partially removing blood through
use of large-bore catheters, infusing
oxygen, removing CO2, and returning blood
back to patient
Medications
Inhaled Nitric Oxide
 Surfactant therapy
 NSAIDS and
 corticosteroids

Nitric Oxide
Dilates pulmonary blood
vessels and helps
reduce shunting
Ventilator
song Ventilate me
a machine that moves air
in and out of the lungs
Mechanical Ventilation

Indications
• Apnea or impending inability to breathe
• Acute respiratory failure
– pH<7.25
– pCO2>50
• Severe hypoxia
– pO2<50
• Respiratory muscle fatigue
– RR<12
Mechanical Ventilation

Purpose
• Support circulation and
• Maintain pt. respirations until can breathe
on own

Goal
• Adequate controlled ventilation
• Relief of hypoxia without hypercapnia
• Relief of work of breathing
Types of Mechanical Ventilation
Negative PressureVentilation
– Chambers encase chest or
–
–
–
–
–
body
Surround with intermittent
subatmospheric or negative
pressure
Noninvasive ventilation
Does not require an artificial
airway
Not used extensively for
acutely ill patients
Used for neuromuscular
diseases, CNS and injuries of
the spinal cord
Types of Mechanical Ventilation
Positive pressure
ventilation (PPV)
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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
Mode-WOB
•
•
•
•
Control mode
Assist control
SIMV
Pressure support- only in spontaneous breathes
(gets the balloon started) Pt. controls all but
pressure limit
inspiratory pressure and flow
SETTING
FUNCTION
USUAL PARAMETERS
Respiratory Rate (RR)
Number of breaths delivered by the
Usually 4-20 breaths per minute
ventilator per minute
Tidal Volume (VT)
Volume of gas delivered during each
Usually 5-15 cc/kg
ventilator breath
Fractional Inspired Oxygen (FIO2)
Inspiratory:Expiratory (I:E) Ratio
Pressure Limit
Amount of oxygen delivered by ventilator
21% to 100%; usually set to keep PaO2 > 60
to patient
mmHg or SaO2 > 90%
Length of inspiration compared to length of
Usually 1:2 or 1:1.5 unless inverse ratio
expiration
ventilation is required
Maximum amount of pressure the ventilator
10-20 cm H2O above peak inspiratory
can use to deliver breath
pressure; maximum is 35 cm H2O
Ventilator Modes

Mode
• 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
• Can be used in conjunction with each other

Two types
• Volume
• Pressure
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


Types
• CMV- Control Mode
• AC- Assist Control- Most used mode
• SIMV- Synchronous Intermittent Mandatory
Ventilation
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 Ventilationonly with spontaneous breaths
1.Preset pressure that
augments patients own
inspiratory effort- (gets
balloon started)
2.Decreases WOB
3.Patient completely
controls rate and volume
4.Used for stable patients
often with SIMV to
overcome resistance of
breathing through
ventilator tubing
High Frequency Ventilation
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Small amounts of gas delivered at a rapid
rate
• As much as 60-100 breaths /minute
Used when conventional mechanical
ventilation would compromise hemodynamic
stability
For short term procedures
For patients at high risk for pneumothorax
Sedation and pharmacological paralysis
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
Alarms
high pressure
 low pressure

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
NEVER TURN ALARMS
OFF!
Assess your patient not the
alarms
Complications of Postive
Pressure Ventilaton
• Cardiovascular system
• ↑ Intrathoracic pressure compresses thoracic
vessels
• ↓ Venous return to heart
• ↓ left ventricular end- diastolic volume
(preload)
• ↓ cardiac output
• Hypotension
• Mean airway pressure is further ↑ if PEEP >5
cm H2O
Complications of PPV
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
What could happen?
Mechanical Ventilation

Complications of PPV (cont’d)
• Ventilator-associated pneumonia (VAP)
– Definition-Pneumonia that occurs 48 hours or
more after ET intubation
– Clinical evidence- Detection
•
•
•
•
Fever and/or elevated white blood cell count
Purulent or odorous sputum
Crackles or rhonchi on auscultation
Pulmonary infiltrates on chest x-ray
VAP Prevention

• 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 – oral care
Drain condensation that collects in ventilator tubing
http://www.youtube.co
m/watch?v=ska5mS_T
oA4
Mechanical Ventilation

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

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

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

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

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
Evidence Based Practice
Ventilator Bundle Components
What is a Bundle?
 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

Respiratory Therapy

Alternative modes of mechanical
ventilation if hypoxemia persists
•
•
•
•
Pressure release ventilation
Pressure control ventilation
Permissive hypercapnia- from low TV
Independent Lung
Ventilation
Research


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.
Liquid Ventilation

Partial liquid ventilation with
perflubron
• Perflubron is an inert, biocompatible,
clear, odorless liquid that has affinity
for O2 and CO2 and surfactant-like
qualities
• Trickled down ET tube into lungs
Research and New

video
YouTube - Superman breather - USA