Transcript RESPIRATORY FAILURE

By Laurie Dickson
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
Fig. 68-2
Hypoxemic Respiratory Failure(Affects the pO2)
 Causes- 4 Physiologic Mechanisms
 1. V/Q Mismatch
 2. Shunt
 3. Diffusion Limitation
 4. Alveolar Hypoventilation-
CO2 and
PO2
VentilationPerfusion Mismatch (V/Q)
 Normal V/Q =1 (1ml air/
1ml of blood)
 Ventilation=lungs
 Perfusion or
Q=perfusion
Pulmonary
Embolus
 Pulmonary Embolus (VQ scan)
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
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
Alveolar Hypoventilation
 Mainly due to hypercapnic respiratory failure but can
cause hypoxemia
 Increased pCO2 with decreased PO2
 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)
 Caused by conditions that keep the air in
Hypercapnic Respiratory Failure
 Abnormalities of the:
 Airways and Alveoli-air flow obstruction and air trapping
 Asthma, COPD, and cystic fibrosis
 CNS-suppresses drive to breathe
 drug OD, narcotics, head injury, spinal cord injury
 Chest wall-Restrict chest movement
 Flail chest, morbid obesity, kyphoscoliosis
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>45-50
 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
 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
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Physical Assessment
Pulse oximetry
ABG
CXR
CBC
Electrolytes
EKG
Sputum and blood cultures, UA
V/Q scan if ?pulmonary embolus
Pulmonary function tests
Treatment
 Goal- to correct Hypoxia
 O2 therapy
 Mobilization of secretions
 Positive pressure ventilation(PPV)
 Noninvasively( NIPPV) through mask
 Invasively through oro or nasotracheal intubation
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
 Noninvasive ( 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
NPPV
 Used best in chronic resp failure in
patients with chest wall and
neuromuscular disease, also with HF and
COPD.
Endotracheal Tube
Endotracheal intubation
Fig. 66-17
Tracheostomy
 Surgical procedure
 Used when need for
artificial airway is
expected to be long term
 Research shows benefit
to early trach
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 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 nurtition
 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
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 develop 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
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,
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restlessness
Lung sounds-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 volume
 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
 Ineffective airway clearance
 Ineffective breathing pattern
 Risk for fluid volume imbalance
 Anxiety
 Impaired gas exchange
 Imbalanced nutrition
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
Nursing Assessment
 Lung sounds
 ABG’s
 CXR
 Capillary refill
 Neuro assessment
 Vital signs
 O2 sats
 Hemodynamic monitoring values
 The Auscultation Assistant - Breath Sounds
Diagnostic Tests
 ABG
 CXR
 Pulmonary Function Tests
 Hemodynamic Monitoring
 ABG review
 RealNurseEd (Education for Real Nurses by a Real Nurse)
ARDS
Severe ARDS
Goal of Treatment for ARDS
 Maintain adequate ventilation and respirations.
 Prevent injury
 Manage anxiety
Treatment
 Mechanical Ventilation goal PO2>60 and O2 sat 90% with FIO2 < 50
 PEEP can cause
CO + B/P and barotrauma
 Positioning prone, continuous lateral rotation therapy and kinetic
therapy
 Hemodynamic Monitoring fluid replacement or diuretics
 Crystalloids vs Colloids
 Enteral or Parenteral Feeding high calorie, high fat.
PEEP
 Cannot expire completely. Causes alveoli to remain
inflated Peep
 Complications can include decreased cardiac
output, pneumothorax, and increased intracranial
pressure
Proning
 typically reserved for
refractory hypoxemia not
responding to other
therapies
 Plan for immediate
repositioning for
cardiopulmonary
resuscitation ***
Proning
 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.
 May be sufficient to reduce inspired O2 or PEEP
Benefits to Proning
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
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
 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 at 5 cm H2O compensates for loss of glottic
function
 Opens collapsed alveoli
 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 cath
 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
 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
Medical Supportive Therapy
 Pulmonary Artery Wedge Pressure
 Pressure in pulmonary artery
 Indirect estimate of L Arterial
pressure
 Keep as low as possible without
imparing cardiac output
(normal 6-12)
 Prevent pulmonary edema
 PAWP increases with Heart Failure
 PAWP does not increase with ARDS
Other Treatments
 Inhaled Nitric Oxide
 Surfactant therapy
 NSAIDS and
 Corticosteroids
ARDS Prioritization and Critical
Thinking Questions #28
 When assessing a 22 Y/o client admitted 3 days ago with pulmonary
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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 100% O2 and call the Dr.
 #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.
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
 Access to airways
Types of Mechanical Ventilation
Negative Pressure
Ventilation
 Chambers encase chest or body
 Surround with intermittent
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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)
 Used primarily in acutely ill
patients
 Pushes air into lungs under
positive pressure during
inspiration
 Expiration occurs passively
Mechanical Ventilator
Settings to Monitor
 FIO2 -% of O2
 Vt-<5ml/kg for ARDS (normal 10-12)
 rate
 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
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
 SIMV- Synchronous Intermittent Mandatory Ventilation
Control Mode- CMV
 Volume and RR are fixed
 Used for patients who are unable to initiate a breath
 Anesthetized or paralyzed
 CMV delivers the preset volume or pressure at a
preset rate regardless of 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 Control
 Preset Volume or pressure in response to the
patient’s own inspiratory effort
 Will initiate the breath if the patient does not do so with
in the set amount of time
 Patient Assists of triggers the vent
 Can breathe faster but not slower
 Vent has back up rate
 May need sedation to limit the number of spontaneous
breaths- can hyperventilate
 For patients who can initiate a breath but have
weakened respiratory muscles
Synchronous Intermittent
Mandatory Ventilation- SIMV
 Preset volume or pressure and rate while allowing the
patient to breathe spontaneously in between breaths.
 Each ventilator breath is delivered in synchrony with the
patients breaths
 The patient is allowed to completely control the
spontaneous breaths at own tidal volume (Vt)
 Used as primary mode and for weaning
 Weaning- preset rate gradually reduced
 Risk- may increase work of breathing and cause
respiratory muscle fatigue
Pressure Support Ventilation
 Preset pressure that
augments patients own
inspiratory effort
 Decreases WOB
 Patient completely controls
rate and volume
 Used for stable patients
often with SIMV to
overcome resistance of
breathing through
ventilator tubing
High Frequency Ventilation
 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
Inverse Ration Ventilation
 Inspiratory/expiratory ratio set at 2:1 or greater max 4:1
 Normal inspiratory/expiratory ratio is 1:2
 Longer inspiratory time
 Increases the amount of air in the lungs at the end of
expiration (FRC)
 Improves oxygenation by re-expanding collapsed alveolI
 Acts like PEEP
 Shorter expiratory time
 prevents alveoli from collapsing again
 Very uncomfortable, sedation required
 For patients with continuing refractory hypoxemia
despite high levels of PEEP- (ARDS)
Ventilator Alarms
Low Pressure
High Pressure
 Circuit Leaks
 Coughing
 Airway leaks
 Patient biting tube
 Chest tube leaks
 Fighting Ventilator
 Patient disconnection
 Secretions or mucus in the
 NEVER TURN OFF
ALARMS!!
 Assess the patient NOT the
Alarm!!
airway
 Airway problems
 Reduced lung compliance
 Water in the circuit
 Kink
Complications of PPV
 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
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
Complications of PPV
Guidelines to prevent VAP
 HOB at least 45 degrees
 No routine changing of
ventilator circuit tubing
 Use ET that allows
continuous suctioning of
secretions
 Drain condensation that
collects in ventilator tubing
Complicationof 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
Complications of PPV
 Fluid retention
 Pressure changes within thorax
 ↓ release of atrial natriuretic peptide (ANP)
 Causing sodium retention
 Stress response
 Antidiuretic hormone and cortisol may be ↑
 Contributes to sodium and water retention
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
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
 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
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
 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
Alternative modes
 If hypoxemia persists
 Pressure support ventilation
 Pressure release ventilation
 Pressure control ventilation
 Inverse ratio ventilation
 High-frequency ventilation
 Permissive hypercapnia
 Independent Lung Ventilation
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 largebore catheters, infusing oxygen, removing CO2, and
returning blood back to patient
 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.