Transcript RESPIRATORY FAILURE

RESPIRATORY FAILURE
and ARDS
By Laurie Dickson
with thanks to Nancy Jenkins
Exchange of O2 and CO2
gas exchange
www.le.ac.uk/pathology/teach/va/
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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

Hypoxemia
• Inadequate O2 transfer
• PaO2 of 60 mmHg or less when patient
receiving 60% or greater O2

Hypercapnia
• Insufficient CO2 removal
• Increases PaCO2
Classification of Respiratory
Failure
Fig. 68-2
Hypoxemic Respiratory Failure(Affects the pO2)
V/Q Mismatch
 Shunt
 Diffusion Limitation
 Alveolar Hypoventilation- inc. CO2 and
dec. PO2

VentilationPerfusion Mismatch
(V/Q)
Normal V/Q =1 (1ml air/ 1ml of blood)
 Ventilation=lungs
 Perfusion or Q=perfusion
 Pulmonary Embolus- (VQ scan)

Range of V/Q Relationships
Fig. 68-4
Pulmonary Embolus
Shunt

2 Types
1. Anatomic- blood passes through an anatomic
channel of the heart and does not pass through
the lungs ex: ventricular septal defect
Shunt
2. 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
Diffusion Limitations

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
Diffusion Limitation
Fig. 68-5
Alveolar Hypoventilation
Mainly due to hypercapnic respiratory
failure but can cause hypoxemia
 Increased pCO2 with decreased PO2

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Restrictive lung disease
CNS diseases
Chest wall dysfunction
Neuromuscular diseases
Hypercapnic Respiratory Failure
Failure of Ventilation

PaCO2>45 mmHg in combination with
acidemia (arterial pH< 7.35)
Hypercapnic Respiratory Failure
Ventilatory Failure- affects CO2


1. Abnormalities of the airways and alveoliair flow obstruction and air trapping
• Asthma, COPD, and cystic fibrosis
2. Abnormalities of the CNSsuppresses drive to breathe
drug OD, narcotics, head injury, spinal cord injury
Hypercapnic Respiratory Failure

3. Abnormalities of the chest wall

Restrict chest movement
• Flail chest, morbid obesity, kyphoscoliosis
4. Neuromuscular Conditionsrespiratory muscles are weakened:
Guillain-Barre, muscular dystrophy,
myasthenia gravis and multiple sclerosis
Tissue Oxygen needs

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
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
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

Hypoxemia
Tachycardia and Hypertension to comp.
 Dyspnea and tachypnea to comp.
 Cyanosis
 Restlessness and apprehension
 Confusion and impaired judgment
 Later dysrhythmias and metabolic
acidosis, decreased B/P and CO.

Hypercapnia

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Dyspnea to respiratory depression- if too high
CO2 narcosis
Headache-vasodilation
Papilledema
Tachycardia and inc. B/P
Drowsiness and coma
Respiratory acidosis
• **Administering O2 may eliminate drive to breathe
especially with COPD patients
Diagnosis
Physical Assessment
 Pulse oximetry
 ABG
 CXR
 CBC
 Electrolytes
 EKG
 Sputum and blood cultures, UA
 V/Q scan if ?pulmonary embolus
 Pulmonary function tests

Treatment Goals
O2 therapy
 Mobilization of secretions
 Positive pressure ventilation(PPV)

O2 Therapy


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, prercussion and
vibration
Airway suctioning
Positive Pressure Ventilation


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.
NPPV
NPPV

endotrachael intubation
Endotracheal Tube
Fig. 66-17
Tracheostomy
Tracheotomy
Surgical
procedure
performed
when need for
an artificial
airway is
expected to be
long term
Exhaled C02 (ETC02) normal 35-45
Used when trying to wean
patient from a ventilator
Drug Therapy

Relief of bronchospasm• Bronchodilators
• metaproterenol (Alupent) and albuterol-(Ventolin,
Proventil, Proventil-HFA, AccuNeb, Vospire,
ProAir )
• Watch for what side effect?

Reduction of airway inflammation
• corticosteroids by inhalation or IV or po

Reduction of pulmonary congestion• diuretics and nitroglycerine with heart failure
Drug Therapy

Treatment of pulmonary infections• IV antibiotics- vancomycin and ceftriaxone (Rocephin)

Reduction of anxiety, pain and agitation
• propofol (Diprivan), lorazepam (Ativan), midazolam (Versed),
opioids

May need sedation or neuromuscular
blocking agent if on ventilator
• vecuronium (Norcuron), cisatracurium besylate (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


**Need B/P of 90 systolic and MAP of
60 to maintain perfusion to the vital
organs
Nutrition
During acute phase- enteral or
parenteral nurtition
 In a hypermetabolic state- need more
calories


If retain CO2- avoid high carb diet
Acute Respiratory Failure
Gerontologic Considerations

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
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
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%
Direct Causes (Inflammatory
process is involved)
Pneumonia*
 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
*Causes
(see notes)
DIFFUSE
lung injury
(SIRS or
MODS)
Damage to alveolar
capillary membrane
Pulmonary
capillary leak
Severe &
refractory
hypoxemia
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

What does surfactant do?
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
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

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
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)
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
Ineffective airway clearance
 Ineffective breathing pattern
 Risk for fluid volume imbalance
 Anxiety
 Impaired gas exchange
 Imbalanced nutrition: Less than body
requirements

Planning

Following recovery
• PaO2 within normal limits or at
baseline
• SaO2 > 90%
• Patent airway
• Clear lungs or auscultation
ARDS Diagnosis
Progressive hypoxemia due to shunting

Decreased lung compliance

Bilateral diffuse lung infiltrate
Chest X-Ray of ARDS
Fig. 68-10
The Auscultation Assistant Breath Sounds
Dyspnea and Tachypnea
Cyanosis
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- decreased
compliance and vital capacity
 Hemodynamic Monitoring- to rule out
pulmonary edema

ABG REVIEW
.
ABG review
ABG Review and Practice
RealNurseEd (Education for Real
Nurses by a Real Nurse)
ARDS X-Ray
Severe ARDS
ARDS Lungs on 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

Hemodynamic Monitoring• fluid replacement or diuretics
Treatment

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

PEEP
pt. can not expire completely. Causes
alveoli to remain inflated
Complications can include decreased
cardiac output, pneumothorax, and
increased intracranial pressure
PEEP ( Positive end-expiratory pressure)
Proning

Proning typically reserved for
refractory hypoxemia not
responding to other therapies

Plan for immediate repositioning
for cardiopulmonary
resuscitation ***
Proning

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
clinical trial
Benefits to Proning
Before proning ABG on
100%O2 7.28/70/70
After proning ABG on
100% 7.37/56/227
Positioning

Other positioning strategies
• Kinetic therapy
• Continuous lateral rotation therapy
Continuous Lateral Rotation
Fig. 68-12
Oxygen Therapy

High flow systems used to
maximize O2 delivery

SaO2 continuously monitored

Give lowest concentration that
results in PaO2 60 mm Hg or
greater
Respiratory Therapy

Risk for O2 toxicity increases
when FIO2 exceeds 60% for
more than 48 hours

Patients will commonly need
intubation with mechanical
ventilation because PaO2
cannot be maintained at
acceptable levels
Oxygen Therapy

Mechanical ventilation

PEEP at 5 cm H2O compensates for
loss of glottic formation

Opens collapsed alveoli
Mechanical ventilation

Higher levels of PEEP are often needed
to maintain PaO2 at 60 mm Hg or
greater

High levels of PEEP can compromise
venous return
–↓ Preload, CO, and BP
Medical Supportive Therapy

Maintenance of cardiac output
and tissue perfusion
• Continuous hemodynamic
monitoring
• Continuous BP measurement via
arterial catheter
Medical Supportive Therapy

Pulmonary artery catheter to
monitor pulmonary artery
pressure, pulmonary artery
wedge pressures, and CO
• Administration of crystalloid fluids or
colloid fluids, or lower PEEP if CO
falls
Medical Supportive Therapy
Use of inotropic drugs may be
necessary
 Hemoglobin usually kept at levels
greater than 9 or 10 with
SaO2 ≥90%
 Packed RBCs
 Maintenance of fluid balance

Medical Supportive Therapy
May be volume depleted and
prone to hypotension and
decreased CO from mechanical
ventilation and PEEP
 Monitor PAWP, daily weights,
and I and Os to assess fluid
status

Medications
Inhaled Nitric Oxide
 Surfactant therapy
 NSAIDS and
 corticosteroids

Nitric Oxide
Dilates pulmonary blood
vessels and helps
reduce shunting
ARDS Prioritization and Critical
Thinking Questions #28
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When assessing a 22 Y/o client admitted 3 days ago with
pulmonary contusions after an MVA, the nurse finds shallow
respirations at a rate of 38. The client states he feels dizzy and
scared. O2 sat is 80% on 6 Ln/c. which action is most
appropriate?
A.Inc. flow rate of O2 to 10 L/min and reassess in 10 min.
B.Assist client to use IS and splint chest using a pillow as he
coughs.
C.Adminster ordered MSO4 to client to dec. anxiety and reduce
hyperventilation.
D.Place client on non-rebreather mask at 95-100% FiO2 and
call the Dr.
#25.The nursing assistant is taking VS
for an intubated client after being
suctioned by RT. Which VS should be
immediately reported to the RN?
 A. HR 98
 B.RR 24
 C.B/P 168/90
 D.Temp 101.4

#15. After change of shift report, you are assigned to
care of the following clients.
Which should be assessed first?
68 y/o on ventilator who needs a sterile sputum
specimen sent to the lab.
59y/o with COPD and has a pulse ox on previous shift
of 90%.
72y/o with pneumonia who needs to be started on IV
antibiotics.
51y/o with asthma c/o shortness of breath after using
his bronchodilator inhaler.

Ventilators
song Ventilate me
Ventilator
a machine that moves air in and
out of the lungs
Mechanical Ventilation

Indications
•
•
•
•
Apnea or impending inability to breathe
Acute respiratory failure
Severe hypoxia
Respiratory muscle fatigue
Mechanical Ventilator
What is a ventilator tutorial
VentWorld - What is a Ventilator?
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

Criteria to put on vent
Apnea or impending inability to breathe
 Acute respiratory failure

• pH<7.25
• pCO2>50
Severe hypoxia - pO2<50
 Respiratory muscle fatigue

Mechanical Ventilation

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
Negative Pressure Ventilator
Fig. 66-21
Mechanical Ventilation

Types of mechanical ventilation
• Positive pressure ventilation (PPV)
– Used primarily in acutely ill patients
– Pushes air into lungs under positive pressure
during inspiration
– Expiration occurs passively
Patient Receiving PPV
Fig. 66-22
Mechanical Ventilator
Settings to Monitor

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FIO2 -% of O2
Vt-<5ml/kg for ARDS (normal 10-12)
rate
•
•
•
•
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
Control (CMV) Continuous Mandatory Ventilation
assist control
IMV
SIMV
inspiratory pressure
Pressure support- only in spontaneous
breaths (gets the balloon started) Pt. controls
all but pressure limit
SETTING
FUNCTION
USUAL PARAMETERS
RespiratoryRate (RR)
Number of breaths delivered bythe
Usually4-20 breaths per minute
ventilator per minute
Tidal Volume (VT)
Volume of gas delivered duringeach
Usually5-15 cc/kg
ventilator breath
Fractional Inspired Oxygen(FIO2)
Inspiratory:Expiratory (I:E) Ratio
Pressure Limit
Amount of oxygendelivered by ventilator
21%to100%; usually set tokeepPaO2 >60
topatient
mmHgor SaO2 >90%
Lengthof inspirationcompared tolengthof
Usually1:2 or 1:1.5unless inverse ratio
expiration
ventilationis required
Maximumamount of pressure the ventilator
10-20 cmH2Oabove peak inspiratory
canuse todeliver breath
pressure; maximumis 35 cmH2O
Ventilator Modes
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

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. Vt 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
Spontaneously breathing patients must be sedated
and/or pharmacologically paralyzed so they don’t
breathe out of synchrony with the ventilator.
*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.
Patient Assists or triggers the vent –can breathe faster but not
slower
Vent has back-up rate
May need to be sedated to limit the number of spontaneous
breaths since hyperventilation can occur.
This mode is used for patients who can initiate a
breath but who have weakened respiratory
muscles.
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.
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
Vt.

SIMV is used as a primary mode of
ventilation, as well as a weaning mode.
• During weaning, the preset rate is
gradually reduced, allowing the patient to
slowly regain breathing on their own.
• 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.
Pressure support
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.
Inverse Ratio Ventilation
The normal inspiratory:expiratory ratio is 1:2 but this is
reversed during IRV to 2:1 or greater (the maximum is
4:1).
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 reexpanding collapsed alveoli- acts like PEEP.
Inverse Ratio Ventilation
The shorter expiratory time prevents the
alveoli from collapsing again.
Sedation and pharmacological paralysis
are required since it’s very
uncomfortable for the patient.
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).
Describe the ventilator settings.
Answer
The ventilator delivers 14 breaths per minute, each
with a tidal volume of 700 ml. The A/C mode delivers
the breaths in response to Mr. Hill’s own respiratory
effort, but will initiate the breath if he doesn’t within
the set amount of time. (He’s currently breathing
above the vent setting.) The oxygen concentration is
60%.
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.
Which lab test should you check to find out what
his true ventilatory status is?
Answer
Arterial blood gas (ABG) - which he should have
had done with his morning labs. If not, check with
the pulmonologist about getting one.
Case Study
Which two parameters on the ABG will give you a quick
overview of Mr. Hill’s status?
Answer
PaCO2 (which affects the pH) and PaO2. With
his high respiratory rate, Mr. Hill is at risk for
hypocapnia from “blowing off CO2.” If the PaO2
is adequate, the FIO2 could be decreased, since
his oxygen saturation has been consistently
100%.
Case Study
What are some possible causes of Mr. Hill’s
increased respiratory rate? (Give the
corresponding nursing interventions as
well.)
Answer
1. Secretions - suction through the ETT, as well
as his mouth.
2. Anxiety or pain - Mr. Hill hasn’t received any
sedation since he was intubated. At this point,
he should at least have a prn order for sedation,
if not a continuous IV infusion.
3. The vent settings may not be appropriate –
check the ABG’s and notify the pulmonologist
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).
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?
Answer
SIMV will deliver 10 breaths with the full tidal volume
each minute, but in synchrony with Mr. Hill’s
spontaneous breaths. This mode is not triggered to
deliver a breath each time Mr. Hill inhales, and the tidal
volume of his spontaneous breaths is under his control.
Pressure support decreases the work of breathing that
results from breathing through the ventilator circuits
and tubing. The PaO2 was higher than desired,
indicating that the FIO2 could be decreased. We need
to be careful to prevent oxygen toxicity.
The pulmonologist also orders midazolam (Versed) 1-2
mg every hour prn for sedation.
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
Mechanical Ventilation

Complications of PPV
• Cardiovascular system
– ↑ 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

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
Subcutaneous Emphysema
Mechanical Ventilation

Complications of PPV
• Ventilator-associated pneumonia (VAP)
– Pneumonia that occurs 48 hours or more after
ET intubation
– Clinical evidence
•
•
•
•
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

Complications of PPV
• Guidelines to prevent VAP
– HOB elevation at least 30 to 45 degrees unless
medically contraindicated
– No routine changes of ventilator circuit tubing
Mechanical Ventilation

Complications of PPV
• Guidelines to prevent VAP
– Use of an ET that allows continuous suctioning
of secretions in subglottic area
– Drain condensation that collects in ventilator
tubing
Continuous Subglottal Suctioning
Fig. 66-20
Mechanical Ventilation

Complications of PPV
• 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
• Fluid retention
– Pressure changes within thorax are associated
with ↓ release of atrial natriuretic peptide, also
causing sodium retention
– As part of the stress response, antidiuretic
hormone and cortisol may be ↑
• Contributes to sodium and water retention
Mechanical Ventilation

Complications of PPV
• 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
• 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
• Involve patients in decision making
• Encourage hope and build trusting
relationships with patient and family
• Provide sedation and/or analgesia to
facilitate optimal ventilation
Mechanical Ventilation

Psychosocial needs
• 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
Respiratory Therapy

Alternative modes of mechanical
ventilation if hypoxemia persists
•
•
•
•
•
•
•
Pressure support ventilation
Pressure release ventilation
Pressure control ventilation
Inverse ratio ventilation
High-frequency ventilation
Permissive hypercapnia
Independent Lung Ventilation
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.
Mechanical 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
Mechanical Ventilation

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
Research and New
YouTube - Superman breather - USA
Prioritization and Delegation
Questions on Vent





The nurse is assigned to provide nursing care for a
client receiving mechanical ventilation. Which action
should be delegated to the experienced nursing
assistant?
A. Assess respiratory status q 4 hours.
B. Take VS and pulse ox reading q4 hours.
C. Check ventilator settings to make sure they are as
prescribed.
D.Observe client’s need for suctioning q 2 hours.





#27 The high pressure alarm on the vent goes off
and when you enter the room to assess a client with
ARDS, her O2 sat is 87% and she is struggling to sit
up. What action should be taken next?
A. Reassure client that the vent will do the work of
breathing for her.
B. Manually ventilate the client while assessing
possible reasons for the alarm.
C. Inc. the FiO2 to 100% in preparation for
endotracheal suction.
D. Insert an oral airway to prevent client from biting
the endotracheal tube.