Problem 6 Emergency

Medicine
Faza Ghani Y.
405140214
Definition & etiology ARDS
(COPD exacerbation, Tracheal aspiration, Pneumothorax, Pulmonary TB,
Status Asthmaticus, Avian Influenza, SARS, Massive pleural effusion,
Pulmonary edema, Aspiration pneumonia)
CHRONIC OBSTRUCTIVE PULMONARY
DISEASE (COPD)
• Chronic obstructive pulmonary disease (COPD)  as an illness characterized by
irreversible, progressive airway obstruction that is associated with inflammatory
pulmonary changes
• COPD exacerbation  characterized by a worsening of the patient's respiratory
symptoms beyond the normal day-to-day variation.
• Typically, involves : worsening dyspnea, ↑sputum + change in the character of sputum, & ↑
frequency & severity of cough.

Clinical emergency medicine, Lange. p. 95-9

COPD :
Staging the Severity of Disease

Rosen’s emergency
medicine, 8th ed. p. 956-
64
COPD :
Clinical Presentation
• History
• Assess the severity of exacerbation, determine a cause
• Physical Examination
• Tachypnea, tachycardia, and hypoxia
• Prolonged COPD  evidence of right heart failure
• PEFR <200 L/min  of airflow obstruction.

Clinical emergency medicine, Lange. p. 95-9

COPD :
Diagnostic Studies
• Laboratory
• CBC, electrolytes, and an assessment of renal function
• Arterial blood gases (ABG)  primary respiratory acidosis, with ↑C02 levels
(>40 mmHg) ↓ pH ( <7.30)
• B-type natriuretic peptide (BNP)  >500 pg/mL (decompensated heart
failure), & levels 100 pg/mL (absence of CHF)
• Imaging
• CXR  hyperinflation & bullous changes
• ECG

Clinical emergency medicine, Lange. p. 95-9

COPD :
Diagnostic Alogarithm

Clinical emergency medicine,

Lange. p. 95-9
Rosen’s emergency
medicine, 8th ed. p. 956-
64
COPD :
Treatments
• IV line, monitor, and oxygen
• Noninvasive ventilatory support (NIVS)
• beta-adrenergic agonists (albuterol 2.5 mg in 3 mL of saline) +
anticholinergic agents (ipratropium bromide 0.5 mg in 3 mL saline) via a
nebulizer.
• Corticosteroid
• ED  methylprednisolone (Solu-Medrol 125 mg IV)
• Mild  prednisone 80 mg oral.
• prednisone 40-60 mg  taken daily for at least 1 week after discharge
• Antibiotics  ceftriaxone, fluoroquinolone (levofloxacin)
Clinical emergency medicine, Lange. p. 95-9
Rosen’s emergency medicine, 8th ed. p. 956-64
COPD

Rosen’s emergency medicine, 8th ed. p. 956-64

Pneumothorax
• Pneumothorax is usually secondary to an accumulation of air in the pleural
• spaces from alveolar rupture or from infection with gas-producing
microorganisms.

Diagnosis
■ Signs and symptoms may vary according to the extent of lung collapse,
degree of intrapleural pressure, and rapidity of onset.
■ On examination: chest bulging on the affected side if one side is involved,
shift of cardiac impulse away from the site of the pneumothorax, decreased
breath sounds on the affected side, grunting, severe respiratory distress and
cyanosis may occur late in the progression of the complication.
■ Differential diagnosis include lung cyst, lobar emphysema, bullae,
diaphragmatic hernia
■ Chest X-ray is crucial in the confi rmation of diagnosis.
SPONTANEOUS
PNEUMOTHORAX
• Under normal conditions, the visceral and parietal
pleurae lie in close apposition, with only a potential
space between them.
• Pneumothorax is defined as the presence of free air in
the intrapleural space.
• A spontaneous pneumothorax occurs in the absence of
any external precipitating factor, either traumatic or
iatrogenic.
• Primary spontaneous pneumothorax occurs in
individuals without clinically apparent lung disease.
Secondary spontaneous pneumothorax arises in the
context of an underlying pulmonary disease process.
Sign and symptoms SPONTANEOUS
PNEUMOTHORAX
• Tachycardia
• Decreased or absent breath sounds with hyper-sonorous to percusion
• Unilateral enlargement of the hemithorax
• Decreased excursion with respirations
• Absent tactile fremitus
• Tension pneumothorax => asphyxia and decreased cardiac output
• Hypotension
• Distention of the jugular veins
Treatment
• Insert needle for urgent decompression, before insertion of an intercostal
• chest drain.
Tuberculosis
Definitions of estimates used to evaluate the algorithms
• Positive predictive value (PPV): the likelihood that a person diagnosed with TB
has true culture-positive TB (also the proportion of all detected cases that are
true culture-positive TB cases)
• Negative predictive value (NPV): the likelihood that a person who is not
diagnosed with TB does not have culture-positive TB (1 – NPV = the probability
that a person not diagnosed with TB actually has culture-positive TB)
• Pretest probability (PTP): the prevalence of culture-positive TB among persons
eligible for a test (for a second test in an algorithm this equals the PPV of the
previous test); the pretest probability increases with each screening step

http://www.who.int/tb/publications/Final_TB_Screening_guidelines
Clinical Manifestation
• Post-primary TB
• Also referred to as reactive or secondary TB
• X-ray images are limited to the apical or posterior segments of the upper lobe
(due generally to high oxygen pressures in this region)
• The superior segment of the lower lobes is also frequently affected
• The extent of parenchymal involvement varies, from the formation of small
infiltrate to extensive cavity formation
• Lung lesions that experience healing experience fibrosis and then calcification
but the cavity image remains persistent
• Most patients who respond to treatment are characterized by decreased
fever, reduced cough, weight gain and general improvement in weeks
Clinical Manifestation
Early symptoms are usually asymptomatic and non-specific :
• Diurnal fever
• Nocturnal diaphoretic caused by fever
• Weight loss
• Anorexia
• Malaise
• Physical weakness
• Non-productive cough (limited in the morning)  progresses to purulent sputum
production and becomes hemoptysis
• Pleuritic chest pain
• Dyspnea
• Sometimes formed a mace (Clubbing finger)
• Hematologic findings: mild anemia, leukocytosis, thrombocytosis, elevated ESR and CRP
Investigation
• Acid-resistant bacterial Microscopy
• Bacterial Culture
• Nucleic acid amplification
• AB resistant test
• CXR
• Serology test
http://www.aafp.org/afp/2000/0501/p2667.html
 Treatment of Adults and Children with Active
Tuberculosis: First-Line Medications
DRUG DAILY DOSING TWICE-WEEKLY THRICE-WEEKLY
DOSING* DOSING*
Isoniazid (INH) Children: 10 mg/kgBb Children: 20 to 40 Children: 20 to 40
orally or IM mg/kgBb orally or IM mg/kgBb orally or IM
Adults: 300 mg orally or Adults: 15 mg/kgBb Adults: 15 mg/kgBb
IM orally or IM orally or IM
Maximum: 300 mg
Rifampin (Rifadin) Children: 10 to 20 mg/kgBb orally or IV
Adults: 10 mg/kgBb orally or IV
Maximum: 600 mg
Pyrazinamide Children: 20 to 30 Children: 50 to 70 mg/kgBb orally
mg/kgBb orally
Adults: 25 mg/kgBb orally Adults: 50 to 70 mg/kgBb orally
Maximum: 2 g Maximum: 4 g Maximum: 3 g
Ethambutol Children and adults: 15 to Children and adults: Children and adults:
(Myambutol) 25 mg/kgBb orally 50 mg/kgBb orally 25-30 mg/kgBb orally

http://www.aafp.org/afp/2000/0501/p2667.html
Acute Severe Asthma

Status Asthmaticus
• Exacerbations of asthma  feared by patients  life-
threatening
• Controller therapy : prevent exacerbations
 ICS* and combination inhalers (very effective)

Harrison’s Principle of Medicine, 18th ed

 Clinical Features
• Chest tightness
• Wheezing
• Dyspnea : not or poorly relieved by usual reliever inhaler
• So breathless - unable to complete sentences  may become
cyanotic

Harrison’s Principle of Medicine, 18th ed

 Examination
• ↑ ventilation
• Hyperinflation*
• Tachycardia
• Pulsus paradoxus : rare
• Marked fall in spirometric values and PEF (Peak Expiratory Flow)
• ABG :
– Hypoxia
– PaCO2 low (hyperventilation)
– A normal or rising PaCO2 : impending respiratory failure  requires immediate monitoring and
therapy.
• Chest roentgenogram : not usually informative, but may show pneumonia or
pneumothorax.

Harrison’s Principle of Medicine, 18th ed

Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/
Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/
 Treatment*
• High concentration of oxygen (by face mask)  achieve oxygen saturation of >90%
• High doses of short-acting inhaled β2-agonists (nebulizer or via a metered dose inhaler with a spacer)
• Not satisfactory response β2-agonists  add : inhaled anti-cholinergic
• Refractory to inhaled therapies  slow infusion of aminophylline
– MONITOR BLOOD LEVELS! Especially in oral theophylline
• IV or nebulizer Magnesium sulfate + inhaled β2-agonists : effective, well tolerated, but not routinely
recommended

• Severely ill patients w/ impending respiratory failure : IV β2-agonists + prophylactic intubation

• Patients with respiratory failure :
– Intubate + institute ventilation
– Conventional bronchodilator
– Not respond  Anesthetic : halothane
– NO Sedatives : may depress ventilation
– Antibiotics : not routinely unless there are signs of pneumonia.

Harrison’s Principle of Medicine, 18th ed

 ASTHMA :
Diagnostic Algorithm

Clinical emergency medicine, Lange.

p. 89-94
 ASTHMA :
Management Of Acute Exacerbations
• Home & First-Responder Strategies
– Home management  ↑ use of inhaled beta2agonists, systemic
corticosteroids, & specific instructions regarding emergency care.
– Emergency medical service providers  provide albuterol inhalation
therapy by protocol
• Management in the Emergency Department
– Oxygen Administration  Maintain Sao2 ≥90%
– Beta agonists  Albuterol
– Corticosteroids  Prednisone 60 mg orally or methylprednisolone
(Solu -Medrol) 125 mg IV
– Anticholinergic agents  Ipratropium bromide 0.5 mg via nebulizer
– Other  Magnesium sulfate (MgSO) 2 g IV over 20 minutes ;
Noninvasive positive pressure ventilation (NPPV) ; Intubation with
Rosen’s emergency medicine, 8th ed. p. 941-55
mechanical ventilation Clinical emergency medicine, Lange. p. 89-94
Rosen’s emergency medicine, 8th ed. p. 941-55
Clinical review: Severe asthma, http://www.ncbi.nlm.nih.gov/pmc/articles/PMC137395/
 Severe, Near-Fatal, and Fatal Asthma
• Severe & refractory asthma 
unresponsive to conventional
therapies (Fig. 73-6)
• Status asthmaticus  severe
bronchospasm that does not
respond to aggressive therapies
within 30 to 60 minutes.
• Near fatal asthma  identified
by respiratory arrest or
evidence of respiratoryfailure
(Paco2 >50 mm Hg).

Rosen’s emergency medicine, 8th ed. p. 941-55

Saharan S, Lodha R, Kabra SK. Management of Status Asthmaticus in Children.
Saharan S, Lodha R, Kabra SK. Management
of Status Asthmaticus in Children.
Saharan S, Lodha R, Kabra SK. Management
of Status Asthmaticus in Children.
 Avian Influenza
an infectious viral disease of birds (especially wild water fowl such as ducks and
geese), often causing no apparent signs of illness.
Etiology:
– virus influenza tipe A
– Reservoir : unggas
– Hidup dalam saluran pencernaan unggas
– Highly Pathogenic Avian Influenza (HPAI)  H5N1
• Direct contact of mucous membranes with infectious secretions or excreta from
infected poultry.
• Pathway: respiratory tract and conjunctiva
• The incubation period: ≤ 7 days
World Health Organization, Pedoman pelayanan kesehatan anak di rumah sakit rujukan tingkat pertama di kabupaten/ WHO ; alihbahasa, Tim
Adaptasi Indonesia. – Jakarta : WHO Indonesia, 2008
 Diagnosis

World Health Organization, Pedoman pelayanan kesehatan anak di rumah sakit rujukan tingkat pertama di kabupaten/ WHO ; alihbahasa, Tim
Adaptasi Indonesia. – Jakarta : WHO Indonesia, 2008
 Supporting investigation Treatment
• Laboratory WHO:
– Limfopeni and thrombocytopenia – Oseltamivir (Tamiflu®) : 1st
– Increased liver enzymes (SGOT line
and SGPT) • mechanism: Inhibitor
– Increase in urea-N and creatinine neuraminidase (NA)
• Microbiology • 36-48 hours after symptoms
– RT-PCR • Dose: 2 mg/kg ( dosis maks.
– nasopharyngeal culture 75 mg)  2 dd 1 for 5 days
– throat swab • Alternatif doses (WHO):
– ≤ 15 kg : 30 mg 2x sehari
• Chest X-ray > 15-23 kg :45mg 2x sehari
– Infiltrates diffuse multifocal > 23-40 kg : 60mg 2x sehari
– interstitial infiltrates > 40 kg : 75mg 2x sehari
Anak usia ≥ 13 th dan
– Consolidated segmental / lobar
dewasa: 75 mg 2 x sehari

World Health Organization, Pedoman pelayanan kesehatan anak di rumah sakit rujukan tingkat pertama di kabupaten/ WHO ; alihbahasa, Tim
Adaptasi Indonesia. – Jakarta : WHO Indonesia, 2008
https://www.ammi.ca/Content/Guidelines/h7n9_algorithm_fi
https://www.ammi.ca/Content/Guidelines/h7n9_algorithm_fi
 Pleura Effusion
• Pleural effusion implies the presence of an abnormally large
amount of fluid in the pleural space.
• Etiology :
– Tuberculosis
– Viral infections of the lung parenchyma or pleura, uremia, myxedema,
cirrhosis, nephrotic syndrome, ovarian hyperstimulation syndrome,
SLE, RA, acute pancreatitis, subphrenic abscess, ascites.

Rosen 8th Edition Pg.992

Rosen 8th Edition Pg.992
 Pleura Effusion
• Parapneumonic effusion  a pleural effusion associated with
bacterial pneumonia, bronchiectasis, or lung abscess
• Loculated effusion  fluid anatomically confined and not
freely flowing in the pleural space

Rosen 8th Edition Pg.992

 Pleura Effusion

Rosen 8th Edition Pg.992

 Pleura Effusion
Pathophysiology :
• Under normal circumstances, the direction of pleural fluid flow is
largely governed by the difference in hydrostatic pressure between
the systemic and the pulmonary circulations
• Influx = efflux  1 L of fluid traversing the pleural space in 24 hours
• Normal conditionsfluid that remains in the pleural space  0.1-
0.2 mL/kgBB
• Pleural effusion develops influx > efflux (fluid into the pleural
space)

Rosen 8th Edition Pg.992

 Pleura Effusion
Pathophysiology :
• Pleural effusions classically are divided into two groups :
transudates (small amounts of protein) and exudates (high)
• Massive effusions >1.5-2 L  associated with malignancy,
congestive heart failure, cirrhosis, and other conditions.
• Massive effusions restrict respiratory movement, compress
the lungs, and result in intrapulmonary shunting.
• In extremely rare cases, tension hydrothorax can develop,
with mediastinal shift and circulatory embarrassment

Rosen 8th Edition Pg.992

 Pleura Effusion
Clinical Features :
• Symptoms associated with pleural effusion are most often caused by
the underlying disease process
• Small pleural effusions often asymptomatic
• A new or enlarging pleural effusion localized pain or pain referred
to the shoulder
• Viral pleuritis and pulmonary infarction chest pain
• Volume of pleural fluid reaches 500 mL  dyspnea on exertion or at
rest

Rosen 8th Edition Pg.992

 Pleura Effusion
Physical examination :
• Classic physical signs of pleural effusion
include diminished breath sounds, dullness to
percussion, decreased tactile fremitus
• Auscultation  Egophony and enhanced
breath sounds can often be appreciated at the
superior border of the effusion because of
underlying atelectatic lung tissue

Rosen 8th Edition Pg.992

 Pleura Effusion
PP :
• Classic radiographicblunting of the costophrenic angle on the upright
chest radiograph, massive pleural effusion can appear as a totally opacified
hemithorax
• USG  pleural effusions are typically visualized as hypoechoic fluid located
above the diaphragm
• USG  more sensitive than plain radiograph  thoracentesis
• Pleural fluid analysis  to distinguish between transudate and exudate
• A predominance of monocytes or lymphocytes suggest malignancy or
established tuberculosis

Rosen 8th Edition Pg.992

 Pleura Effusion
PP :
• In exudative effusion :
– A pleural fluid pH < 7.3 associated with parapneumonic effusions,
malignancies, rheumatoid effusions, tuberculosis, and systemic
acidosis.
– pH <7.0 suggests empyema (or esophageal rupture).
– pH < 7.0 and glucose < 50 mg/dL  indications for tube
thoracostomy
– exudative pleural fluid may contain >10,000 white blood cells/mm .
3

Rosen 8th Edition Pg.992

Rosen 8th Edition Pg.992
 Pleura Effusion

Rosen 8th Edition Pg.992

 Pleura Effusion
Management :
• In patients with large effusions, urgent therapeutic
thoracentesis  stabilize respiratory or circulatory status.
• Empyema needs insertion of a chest tube
• Pleura effusion associated with hemothorax tube
thoracostomy  If bleeding exceeds 200 mL/hr  thoracotomy
• NSAID treating pleural pain
• After thoracocentesis  CXR find complication

Rosen 8th Edition Pg.992

Pulmonary Edema
http://www.racgp.org.au/afp/2010/december/acu
te-pulmonary-oedema/
http://www.racgp.org.au/afp/2010/december/acute-
pulmonary-oedema/
http://www.racgp.org.au/afp/2010/december/acute-
pulmonary-oedema/
http://www.racgp.org.au/afp/2010/december/acute-
pulmonary-oedema/
Acute Pulmonary Edema
Figure 3 - Proposed Diagnostic Algorithm For Patients With Suspected
High-risk PE, i.e. Presenting With Shock Or Hypotension.

http://eurheartj.oxfordjour
nals.org/content/early/20
14/08/28/eurheartj.ehu28
3
Figure 4 - Proposed diagnostic algorithm for patients with suspected not
high-risk pulmonary embolism.

http://eurheartj.oxfordjour
nals.org/content/early/20
14/08/28/eurheartj.ehu28
3
 Figure 5 - Risk-adjusted
Management Strategies
In Acute PE

http://eurheartj.oxfordjournals.org/content/early/
2014/08/28/eurheartj.ehu283
http://www.jointemsprotocols.
com/pulmonary-edema
Type of Respiratory Failure
 RESPIRATORY FAILURE
• Clinically = Respiratory failure is defined as PaO2 <60 mmHg while
breathing air, or a PaCO2 >50 mmHg.

• Respiratory failure may be acute or chronic:

– Acute hypercapnic respiratory failure develops over minutes to hours. The pH is usually therefore
less than 7.3.
– Chronic respiratory failure develops over several days or longer. There is sufficient time for renal
compensation and an increase in bicarbonate so the pH is usually only slightly decreased.
– Clinical markers of long-standing hypoxaemia include polycythaemia and cor pulmonale.
Range of V/Q Relationships
Respiratory failure is Classifieds into type I or type II relates to the absence or
presence of hypercapnia respectively.
Type 1  hypoxemia without hypercapnia, and indeed the
PaCO2 may be normal or low.
• It is typically caused by a ventilation/perfusion (V/Q) mismatch; the
volume of air flowing in and out of the lungs is not matched with
the flow of blood to the lungs.
• The basic defect in Type 1 respiratory failure is failure of
oxygenation characterized by:
PaO2 decreased (< 60 mmHg (8.0 kPa))
PaCO2 normal or decreased (<50 mmHg (6.7 kPa))
PA-aO2 increased
 Common causes of type I respiratory failure
• Chronic obstructive pulmonary disease • Pulmonary hypertension.
(COPD). • Cyanotic congenital heart disease.
• Pneumonia. • Bronchiectasis.
• Pulmonary oedema. • Acute respiratory distress syndrome.
• Pulmonary fibrosis. • Kyphoscoliosis.
• Asthma. • Obesity.
• Pneumothorax.
• Pulmonary embolism.
Type 2  Hypoxemia (PaO2 <8kPa) with hypercapnia (PaCO2 >6.0kPa).

The basic defect in type 2 respiratory failure is characterized by:

PaO2 decreased (< 60 mmHg (8.0 kPa))

PaCO2 increased (> 50 mmHg (6.7 kPa))
PA-aO2 normal
pH decreased

Type 2 respiratory failure is caused by:

• Inadequate alveolar ventilation; both oxygen and carbon
dioxide are affected.
• Defined as the build up of carbon dioxide levels (PaCO2)
that has been generated by the body but cannot be
eliminated.
Type II respiratory failure caused by:
1. Increase airway resistance (Chronic obstructive pulmonary
disease, asthma, suffocation)

2. Reduced breathing effort (drug effects, brain stem lesion, extreme

obesity).
3. A decrease in the area of the lung available for gas exchange (such as
in chronic bronchitis).

4. Neuromuscular problems (Guillain-Barré syndrome, myasthenia gravis,

motor neurone disease).

5. Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.

 Common causes of type II respiratory failure
• COPD. • Head injuries and neck injuries.
• Severe asthma. • Obesity.
• Drug overdose poisoning. • Pulmonary oedema.
• Myasthenia gravis. • Adult respiratory distress
• Polyneuropathy. syndrome.
• Poliomyelitis. • Hypothyroidism.
• Muscle disorders
 Signs & Symptoms:
Symptoms
• The history may indicate the underlying cause,
e.g. paroxysmal nocturnal dyspnoea, and
orthopnoea in pulmonary oedema.
• Both confusion and reduced consciousness
may occur.
Signs
• Localised pulmonary findings are determined
by the underlying cause.
• Neurological features may include
restlessness, anxiety, confusion, seizures, or
coma.
• Tachycardia and cardiac arrhythmia may result
from hypoxaemia and acidosis.
• Cyanosis.
• Polycythaemia is a complication of long-
standing hypoxaemia.
• Cor pulmonale: pulmonary hypertension is
frequently present and may induce right
ventricular failure, leading to hepatomegaly
and peripheral oedema.
 Respiratory Failure
Clinical Manifestations
• Sudden or gradual onset
• Severe morning headache
– Rapid, shallow breathing pattern
– Tripod position
• Cyanosis
– Late sign
• Tachycardia and mild hypertension
– Early signs
 A sudden decrease in PaO2 or rapid increase in PaCO2 indicates a
serious condition
Diagnostic considerations
 Respiratory failure is a common and
a life-threatening condition that
demands prompt diagnosis and
assessment and appropriate
management.
 Failure to visualize an obvious
abnormality on chest radiographs
in hypoxemic respiratory failure
suggests the possibility of right-to-
left shunting.
 The vast majority of patients in
acute respiratory failure due to
cardiogenic pulmonary edema
respond to measures to reduce
preload and afterload.
 Those with acute respiratory distress
syndrome (ARDS) require early
elective intubation because the
duration of respiratory failure is
longer.
 Hypercapnic respiratory failure occurs
secondary to a variety of causes:
 Increased respiratory muscle load.
 Impaired neuromuscular
function.
 Decreased respiratory drive
caused by central nervous system
(CNS) depression.
 Differential Diagnoses
• Acute Respiratory Distress Syndrome
• Sleep Apnea
• Asthma
• Atelectasis
• Cardiogenic Shock
• Cardiomyopathy, Dilated
• Cardiomyopathy, Hypertrophic
• Cor Pulmonale
• Diaphragmatic Paralysis
• Emphysema
• Myocardial Infarction
• Pneumonia, Aspiration
• Pneumonia, Bacterial
• Pneumonia, Community-Acquired
• Pneumonia, Viral
• Pneumothorax
• Pulmonary Edema
• Cardiogenic Shock
• Pulmonary Edema, Neurogenic
• Pulmonary Embolism
• Pulmonary Fibrosis, Idiopathic
• Pulmonary Fibrosis, Interstitial
• Primary Pulmonary Hypertension
• Secondary Pulmonary Hypertension
• Respiratory Acidosis
• Restrictive Lung Disease
• Shock, Distributive
• Ventilation, Mechanical
• Ventilation, Noninvasive
 Investigations
• Arterial blood gas analysis: Confirmation of diagnosis
• CXR: often identifies the cause of respiratory failure.
• FBC: anemia can contribute to tissue hypoxia;
polycythaemia may indicate chronic hypoxaemic
respiratory failure.
• Renal function tests and LFTs: may provide clues to the
aetiology or identify complications associated with
respiratory failure.
• Right heart catheterization: if there is uncertainty about
cardiac function, adequacy of volume replacement, and
systemic oxygen delivery.
• Pulmonary capillary wedge pressure may be helpful in
distinguishing cardiogenic from noncardiogenic oedema.
• Serum creatine kinase and troponin I: to help
exclude recent myocardial infarction.
• Elevated creatine kinase may also indicate
myositis.
• TFTs (hypothyroidism may cause chronic
hypercapnic respiratory failure).
• Spirometry: useful in the evaluation of
chronic respiratory failure.
• Echocardiography: if a cardiac cause is
suspected for ARF.
• Pulmonary function tests in the evaluation
of CRF.
• ECG: to evaluate a cardiovascular cause.
 Management
• A patient with acute respiratory failure
generally needs prompt hospital admission in
an intensive care unit.
• Many patients with chronic respiratory failure
can be treated at home, depending on the
severity of respiratory failure, underlying
cause, comorbidities and social circumstances.
• Immediate resuscitation may be required.
• Appropriate management of the underlying
cause.
Hypoxemia
• Ensure adequate oxygen delivery to tissues,
generally achieved with a PaO2 of 60 mm Hg or
an arterial oxygen saturation (SaO2) of greater
than 90%.
• Beware the prolonged use of high-
concentration oxygen in chronic sufferers who
have become reliant on their hypoxic drive to
maintain an adequate ventilation rate.
• Elevating the PaO2 too much may reduce the
respiratory rate so that the PaCO2 may rise to
dangerously high levels.
Assisted ventilation:
• Mechanical ventilation is used to increase PaO2
and to lower PaCO2.
• Mechanical ventilation also rests the
respiratory muscles and is an appropriate
therapy for respiratory muscle fatigue.
• Weaning patients with chronic respiratory
failure off of mechanical ventilation may be
very difficult.
• Non-invasive ventilation (NIV) has been increasingly
used as an alternative to intubation.
• NIV improves survival and reduces complications for
selected patients with acute respiratory failure.
• The main indications are exacerbation of COPD,
cardiogenic pulmonary oedema, pulmonary
infiltrates in immunocompromised patients, and
weaning of previously intubated stable patients
with COPD.
 Complications
• Pulmonary: PE, pulmonary fibrosis, and
complications secondary to the use of
mechanical ventilation.
• CVS: Cor pulmonale, hypotension,
reduced cardiac output, arrhythmias,
pericarditis, and acute MI.
• Gastrointestinal: Gastric distension,
haemorrhage, ileus,
pneumoperitoneum. diarrhoea, and
duodenal ulceration caused by stress is
common in patients with acute
respiratory failure.
• Polycythaemia.
• Hospital-acquired infection: pneumonia, UTI,
and catheter-related sepsis, are frequent
• Renal: acute kidney injury (ARF) and
abnormalities of electrolytes and acid-base
balance are common.
• Nutritional: Malnutrition and complications
related to administration of enteral or
parenteral nutrition.
• Complications associated with nasogastric
tubes, e.g. abdominal distention and
diarrhea.
Acute respiratory failure

Adult Respiratory Distress Pulmonary Edema

Syndrome
Aspiration Pneumonia
COPD