Nursing Management: Respiratory

Failure, Acute Respiratory Distress

Syndrome and Status Asthmaticus

ARIF SETYO UPOYO

CAPAIAN PEMBELAJARAN

Peserta didik mampu menjelaskan

manajemen keperawatan pada pasien dengan
gagal nafas, ARDS dan status asmatikus

ICU
bedside monitor

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

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.

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

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 emboli
sm

Pulmonary Embolus

Shunt
2

Types

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
1.

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.

2.

Abnormalities of the airways and alveoliair flow obstruction and air trapping. Ex:
Asthma, COPD, and cystic fibrosis
Abnormalities of the CNS- suppresses drive to
breathe. Ex. 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

Signs and Symptoms of

Respiratory Failure- ABGs
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
Dyspnea

Cyanosis

Confusion

and apprehension

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

Acute Respiratory Failure

Nursing and Collaborative Management
Primary

survey
A : Obstructive?
B : Tachipne, Dyspnea to respiratory depression
C : Tachicardia, hipertension, cyanosis
Nursing

Assessment in critical care

Health
Health

information

history
Medications
Surgery

Acute Respiratory Failure

Nursing and Collaborative Management
Nursing

Assessment

Functional
Health

health patterns

perceptionhealth management
Nutritional-metabolic
Activity-exercise
Sleep-rest
Cognitive-perceptual
Copingstress tolerance

Acute Respiratory Failure

Nursing and Collaborative Management
Nursing

Assessment

Physical

assessment

General
Integumentary
Respiratory
Cardiovascular
Gastrointestinal
Neurologic

Laboratory

findings

Acute Respiratory Failure

Nursing and Collaborative Management
Nursing

Diagnoses

Impaired gas exchange

Ineffective airway clearance
Ineffective breathing pattern
Risk for fluid volume imbalance
Anxiety
Imbalanced nutrition: Less than body
requirements

Acute Respiratory Failure

Nursing and Collaborative Management
Planning:

ABG

Overall goals

values within patients

baseline
Breath sounds within patients
baseline
No dyspnea or breathing
patterns within patients
baseline
Effective cough and ability to
clear secretions

Acute Respiratory Failure

Nursing and Collaborative Management
Prevention

Thorough history and physical assessment to

identify at-risk patients
Early recognition of respiratory distress

Acute Respiratory Failure

Nursing and Collaborative Management
Respiratory

therapy

Oxygen therapy: Delivery system should

Be

tolerated by the patient

Maintain PaO2 at 55 to 60 mm
Hg or more and SaO2 at 90% or
more at the lowest O2
concentration possible

Acute Respiratory Failure

Nursing and Collaborative Management
Respiratory

therapy

Mobilization of secretions

Hydration

and
humidification
Chest physical therapy
Airway suctioning
Effective coughing and
positioning

Acute Respiratory Failure

Nursing and Collaborative Management
Respiratory

therapy

Positive pressure ventilation (PPV)

Noninvasive PPV

BiPAP

(bilevel positive airway

pressure)
CPAP (continous positive
airway pressure)

NPPV

NPPV

Endotracheal tube

Should hear equal breath sounds if

in correct place. Always get a CXR
to check placement also

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

Acute Respiratory Failure

Nursing and Collaborative Management
Drug

Therapy

Relief of bronchospasm
Bronchodilators

Reduction of airway inflammation

Corticosteroids

Reduction of pulmonary congestion

Diuretics,

nitrates if heart failure present

Acute Respiratory Failure

Nursing and Collaborative Management

Drug

Therapy

Treatment of pulmonary infections

IV

antibiotics

Reduction of severe anxiety, pain, and

agitation

Benzodiazepines
Narcotics

Acute Respiratory Failure

Nursing and Collaborative Management
Nutritional

Therapy

Maintain protein and energy stores

Enteral or parenteral nutrition
Nutritional supplements
In a hypermetabolic state- need more calories
If retain CO2- avoid high carb diet

Acute Respiratory Failure

Nursing and Collaborative Management
Medical

Supportive Therapy

Treat the underlying cause

Maintain adequate cardiac output and
hemoglobin concentration
monitor B/P and MAP.
Maintain adequate Hemoglobin concentrationneed 9g/dl or greater
**Need B/P of 90 systolic and MAP of 60 to
maintain perfusion to the vital organs

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

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)
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
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
Diffuse

week after

scarring and fibrosis, decreased surface

area, decreased compliance and pulmonary
hypertension

The essential disturbances of

ARDS
**interstitial and alveolar edema and
atelectasis

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

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

Dyspnea and Tachypnea

The Auscultation Assistant - Breath Sounds

Cyanosis

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

Chest X-Ray of ARDS

Fig. 68-10

Nursing Assessment
Lung

sounds
ABGs
CXR
Capillary refill
Neuro assessment
Vital signs
O2 sats
Hemodynamic monitoring values

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

*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

Status Asthmaticus

Pathophysiology
Primary

Airway inflammation & hyper-reactivity

Smooth muscle spasm
Mucosal edema & plugging

Status

pathophysiology

asthmaticus

Reversible
Recurrent
Diffuse
Obstructive

Pathophysiology
changes in the airway airflow
obstruction premature airway closure on
expiration dynamic hyperinflation
hypercarbia

Pathologic

Dynamic

hyperinflation or air-trapping also

leads to ventilation / perfusion (V/Q)
mismatching causing hypoxemia

PaO2

= FiO2(Patm PH2o) paCO2/0.8

Interstium

Epithelium

Pathophysiology

Hypersecretio
Hypersecretio
n
n
Epithelial
Epithelial damage
damage
with
with exposed
exposed nerve
nerve
endings
endings

Hypertrophy
Hypertrophy of
of
goblet
goblet cells
cells and
and
mucus
mucus glands
glands
Equals airway
obstruction and
resultant air
trapping

Primary survey
A : obtructive , whezing
B : Dyspnea, I : E
C : Bradicardia

Management
The

use of mechanical ventilation during

an asthma exacerbation is associated
with significant morbidity and increased
risk of death.
The decision to intubate a patient
should not be delayed until respiratory
failure is imminent. If progressing
toward respiratory muscle fatigue, NPPV
may avoid intubation

Intubation
The

two primary indications to intubate an SA patient are:

Severe hypoxia & Depressed level of consciousness

Other potential indications for mechanical ventilation include:
Obvious

life-threatening respiratory distress not responding to

bronchodilator therapy
Impending respiratory failure
Hemodynamic compromise, including bradycardia, severe pulsus
paradoxus
Lactic acidosis associated with increased work of breathing
Apnea or near-apnea
Peak flows <40% of predicted

Intubation

General guidelines for mechanical ventilation management:

Start with low tidal volume, permissive hypercapnia strategy.

Tidal

volume 4-7 ml/kg (prevents barotrauma / volutrauma,

minimize lung distension)
Goal pH>7.25 (may require HCO3)

Low ventilatory rate 10-14 breaths per minute

I:E ratio 1:4 to 1:6 (avoid air trapping by allowing for complete
exhalation)
PEEP match intrinsic
Peak pressures <30-35 (prevent barotrauma)
Keep well sedated consider ketamine and versed infusions.
As the patient is on steroids, limit use of paralytics (to avoid
myopathy)

Pharmacologic Targets
Relaxation

of bronchial smooth muscles

B2 receptors
M1 receptors

Improving

oxygen delivery
Attenuating underlying inflammation
Instituting vigorous pulmonary toilet

Pharmacologic Therapies
Albuterol
Atrovent
Methylprednisone/Decadron
Magnesium Sulfate
Terbutaline
Aminophylline
Heliox
Ketamine
Oxygen
Epineprhine

SELAMAT BELAJAR..........