RESPIRATORY

FAILURE
and
ARDS

GARY PRADHANA
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 60mmHg or less when pt. Receiving
60% or greater O2

▪ Hypercapnia- insufficient CO2 removal

▪ Increases PaCO2 > 45 mmHg, pH <7.35
 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
Range of V/Q Relationships

Fig. 68-4
VentilationPerfusion Mismatch
(V/Q)

▪ Normal V/Q =1 (1ml air/ 1ml of blood)

▪ Ventilation=lungs
▪ Perfusion or Q=perfusion
▪ Pulmonary Embolus- (VQ scan)

pulmonary embo
lism
Pulmonary Embolus
Shunt

▪ 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

▪ 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
▪ Restrictive lung disease
▪ CNS diseases
▪ Neuromuscular diseases
 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
Hypercapnic Respiratory Failure

▪ 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

▪ 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-
ABG’s

▪ 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

▪ Compensatory Mechanisms- early

▪ Tachycardia- more O2 to tissues
▪ Hypertension- fight or flight
▪ Tachypnea –take in more O2
▪ Restlessness and apprehension
▪ Dyspnea
▪ Cyanosis
▪ Confusion and impaired judgment
▪ **Later dysrhythmias and metabolic
acidosis, dec. B/P and Dec. CO.
Hypercapnia

▪ Dyspnea to respiratory depression- if 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
 Diagnosis

▪ 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)
 Exhaled C02 (ETC02) normal 35-45

Used when trying to wean

patient from a ventilator
 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”
▪ Hydration - fluid intake 2-3 L/day
▪ Humidification- aerosol treatments- mucolytic
agents
▪ Chest PT- postural drainage, percussion 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
Endotracheal tube

Should hear equal breath

sounds if in correct place.
Always get a CXR to check
placement also
Endotracheal Tube

Fig. 66-17
 Surgical Intervention-Tracheostomy

If tube in greater than 4-5

Tracheotomy days, perform a trach

Surgical
procedure
performed
when need for
an artificial
airway is
expected to be
long term
Drug Therapy

▪ Relief of bronchospasm- bronchodilators

▪ alupent and albuterol-(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-
▪ why HF with pulmonary problems?
▪ Treatment of pulmonary infections- IV antibiotics,
vancomycin and rocephin
▪ Reduction of anxiety, pain and agitation- diprivan, 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 output- monitor 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

nutrition
▪ In a hypermetabolic state- need more calories

▪ If retain CO2- avoid high carb diet

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

▪ **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
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
in all)

▪ 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

Severe & refractory

hypoxemia
*Causes (see DIFFUSE Damage to alveolar Pulmonary capillary
notes) lung injury capillary membrane leak
(SIRS or
MODS) SHUNTING
Stiff lungs
Inactivation of
surfactant

Hyperventilation
Hypocapnea
Respiratory Alkalosis
Alveolar atalectasis

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

▪ 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
Chest X-Ray of ARDS

Fig. 68-10
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
Dyspnea and Tachypnea

The Auscultation Assistant - Breath Sounds

Cyanosis
Nursing Assessment

▪ 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
ARDS X-Ray
Severe ARDS
X-RAY 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
▪ 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
PEEP

▪ pt. can not expire completely.

Causes alveoli to remain inflated

▪ (Complications can include

decreased cardiac output,
pneumothorax, and increased
intracranial pressure).

YouTube - Peep
FRC- air in after normal exhalation
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-Principles

▪ 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 No benefit in mortality
alveoli become dependent, perfusion
becomes greater to air-filled alveoli
opposed to previously fluid-filled
dependent alveoli, thereby improving
ventilation-perfusion matching.
Benefits to Proning

Before proning ABG on After proning ABG on

100%O2 7.28/70/70 100% 7.37/56/227
Positioning

▪ Other positioning strategies

▪ Kinetic therapy
▪ Continuous lateral rotation therapy
Continuous Lateral Rotation

Fig. 68-12
Oxygen Therapy

▪ Oxygen
▪ High flow systems used to maximize O2 delivery
▪ SaO2 continuously monitored, Usually have arterial line for
frequent ABG’s
▪ 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
Mechanical ventilation

▪ PEEP
▪ 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 O’s to assess fluid
status
Medications

▪ Inhaled Nitric Oxide

▪ Surfactant therapy
▪ NSAIDS and
▪ corticosteroids
Nitric Oxide

Dilates pulmonary blood

vessels and helps
reduce shunting
Case Study Case Study:

Case Study Assignments

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
ARDS Prioritization and Critical Thinking
Questions #28

▪ 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

VentWorld - W
hat is a Vent
ilator?

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 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
Mechanical Ventilation

▪ 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
Patient Receiving PPV

Fig. 66-22
Mechanical Ventilator
Settings to Monitor

▪ FIO2 -% of O2
▪ TV-<5ml/kg for ARDS (normal 8-10)
▪ Rate 12-15
▪ Control (CMV) Continuous Mandatory Ventilation
▪ assist control
▪ SIMV
▪ 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
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. 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.
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
 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.
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

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
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.
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.
2.        2. 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

3. 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

4. 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).
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?
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
Alarms

▪ high pressure
▪ low pressure
Low Pressure Alarms High Pressure Alarms

•Patient coughing
•Circuit leaks •Secretions or mucus in
•Airway leaks the airway
•Chest tube leaks •Patient biting tube
•Patient disconnection •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 (cont’d)

▪ Cardiovascular system (cont’d)
▪ ↑ 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
Mechanical Ventilation

▪ 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
Subcutaneous Emphysema
Mechanical Ventilation

▪ Complications of PPV (cont’d)

▪ 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 (cont’d)

▪ 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 (cont’d)

▪ Guidelines to prevent VAP (cont’d)
▪ Use of an ET that allows continuous suctioning of
secretions in subglottic area
▪ Drain condensation that collects in ventilator tubing
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)

▪ Fluid retention (cont’d)
▪ 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 (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
Mechanical Ventilation

▪ Psychosocial needs (cont’d)

▪ 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.
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
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.
Research and New

▪ video

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.