Jakarta, 30 Oct 2017

“Sixth Problem.Gasping for

Air”
Emergency Medicine Block
FAKULTAS KEDOKTERAN
UNIVERSITAS TARUMANAGARA
JAKARTA 2017
 GROUP 17
• Tutor : dr. Octa
• Ketua : Nadya Arini P 405140225
• Sekretaris : Aldi Firdaus 405140098
• Penulis : Natasya Yustika P 405140101
• Anggota:
– Arianto Salim 405140012
– Indry Agatha 405140028
– Putu Devara Karunia Esa 405140111
– Daniel Yohanes P 405140157
– Riyanti Devi W N 405140159
– Ni Luh Putu Citramas L. D 405140218
– Nadya Arini P 405140225
– Feras Zaki A 405140248
– Yulianto Haryono 405140253
 Gasping for Air
• A 65-year old male is brought to an ED by ambulance for being
unresponsive. He was being cared for in a nursing facility from previous
stroke incident. His breathing is shallow and rapid when he was brought to
ED. In the past 3 to 4 days, he had been coughing and there were wet
sounds heard in cough. Paramedic report that his saturationis 67% when
he was found. He has a history of bronchial asthma and was diagnosed
with pulmonary tuberculosis 10 years ago but have not completed his
medication. He was also a heavy smoker in his young age.
• In the emergency depertment, his vital signs are as follow, temperature is
38,7 ⁰C, blood pressure is 100/78 mmHg, heart rate is 118 beats per
minute, respiratory rate is 30 breaths per minute and his oxygen
saturation is 84% on a non-rebreather face mask. On his physical thorax
examination, his breathing is labored with intercostal muscle retractions
visible on inspection. There is an asymmetrical chest wall expansion when
he breathes. On percussion, his thorax sounds sonorous on some part of
his chest, and on auscultation, there are crackles and wheezing. His initial
blood gas analysis shows that his pH is 7.26, PCO₂ is 60 mmHg, PO₂ is 55
mmHg and his HCO₃⁻ is 26 mEq/L
• Discuss the case, assess the patient’s condition, plan proper diagnostic
procedures and treatment while considering all posibilities !
 Unfamilar Terms
• Crackles : suara dari paru, pendek, terputus2,
kasar. Saat inspirasi krn cairan di alveolus.
ARDS
 Rumusan Masalah
1. Apakah hub riwayat stroke dgn keluhan batuk & hasil PF ?
2. Napas dangkal & cepat dgn riwayat bronkial asma & TBC ?
3. PP apa yg diperlukan ?
4. Management th/ di ED ?
5. Interpretasi PF & PP ?
6. Apakah hub riwayat 3-4 hari lalu batuk dgn penurunan
sdaturasi O₂ ?
7. Mengapa dinding asimetris saat bernapas ?
8. Apakah hub rokok berat di usia muda dgn kelainan skrg ?
9. Perkusi suara sonor didada, retraksi dada asimetris,
crackles & wheezing kenapa ?
10. Efek di OS krn abnormalitas AGD ?
11. Apa yg menyebabkan OS alami penurunan kesadaran ?
 Curah Pendapat
1. Tdk ada hub dgn riwayat stroke. Berbaring lama krn stroke 
risiko pneumonia  batuk lendir, sesak
2. Riwayat asma , lendir  napas cepat & dangkal  DD : ARDS,
edema paru akut, PPOK, asma, TBC
3. Foto thorax, CT-Scan/MRI u/ melihat hambatan, bronkoskopi,
darah lengkap  infeksi, albumin & LDH  edema paru, cek
sputum, FiO₂  ARDS, kadar antitripsin  COPD, kultur resistensi
AB
4. Th/ O₂  intubasi, suction cairan sputum
AB empirik kalau suspect infeksi
Kontrol TTV, saturasi O₂  pulse oxymetri
Kontrol gas darah
5. PF : T : Febris, TD : Hipotensi, HR : Takikardi, RR : Takipneu,
saturasi O₂ menurun, inspeksi retraksi interkostal, asimetris (ada
sumbatan), perkusi : sonor di beberapa tempat, auskultasi :
crackles & wheezing  lendir
5,9,10. PP : AGD : asidosis respiratorik,
hiperventilasi  napas cepat & dangkal
Perkusi : hipersonor (pneumotorax), redup (efusi
pleura)
6. Batuk  produksi sputum  hambat jalan
napas  ggg perfusi (saturasi O₂ menurun)
7. Dinding asimetris  adanya cairan di rongga
pleura  efusi pleura  riwayat TB
Adanya udara di rongga pleura  pneumotorax
8. Faktor risiko PPOK
11. Saturasi O₂ menurun  penurunan kesadaran
 tanda gagal napas
 Mind Map
Laki-Laki Riwayat
65 tahun penyakit :
•TBC
•Asma
•Stroke  Crackles &
rawat lama Wheezing

•Saturasi O₂ menurun
Pneumonia
•Saturasi CO₂ Meningkat
FR: Rokok
Infeksi
Asidosis
respiratorik
Demam
Penurunan
Risiko u/ kesadaran
ARDS/COPD

Obstruksi berat Gagal Napas

 Learning Issues
1. Menjelaskan tentang ARDS & Gagal Napas
 ARDS
• Acute respiratory distress syndrome (ARDS) occurs when fluid
builds up in alveoli. More fluid in your alveoli means less oxygen can
reach your bloodstream. This deprives your organs of the oxygen
they need to function.

• The signs and symptoms of ARDS can vary in intensity, depending

on its cause and severity, as well as the presence of underlying
heart or lung disease. They include:

1. Severe shortness of breath

2. Labored and unusually rapid breathing
3. Low blood pressure
4. Confusion and extreme tiredness
 ARDS (Precipitating Causes)
• Direct
– aspiration of gastric contents
– viral pneumonia
• Indirect
– sepsis, ingested toxins, hypotension
– ischemia reperfusion injury

Elias JA, Fishman JA, Grippi MA, Kaiser LR, Senior RM (eds). Fishman’s Manual of
Pulmonary Disease and Disorder 5th Edition. New York. Mc GrawHIll, 2015
Elias JA, Fishman JA, Grippi MA, Kaiser LR, Senior RM
(eds). Fishman’s Manual of Pulmonary Disease and
Disorder 5th Edition. New York. Mc GrawHIll, 2015
 Diagnosa
• Imaging:
1. Chest X-ray(reveal either ARDS cause by cardiogenic or non-
cardiogenic, reveal how much fluid in your lung)
2. CT-scan.

• Lab tests
1. Arterial Blood Gas(ABG) -> reveal oxygen saturation to Hb
2. Sputum culture -> if suspect of infection

• Heart test
1. Electrocardiogram. -> diagnostic right side-heart hypertrophy
2. Echocardiogram -> reveal heart structure abnormalities
 Management
• Supplemental oxygen -> milder symptoms or as a
temporary measure. Delivered through non-rebreathing
mask.

• Mechanical ventilation -> last choice if supplemental

oxygen not adequate

• Fluid -> preventing shock. Carefully managing the amount,

too much -> lung edema.

• Antibiotic -> if ARDS cause by infection.

• Analgesic or sedation -> for pain reliever
Fishman's Pulmonary Diseases and Disorders, 5e
 Oxygen exchange inhibited due to excess serum fluid in
alveoli hypoxia  death.

 More common in men than in women and has mortality rate of

over 65%.

 Complications include respiratory failure, cardiac

dysarrythmias, disseminated intravascular coagulation,
barotrauma, congestive heart failure and renal failure.
ACUTE EXACERBATION OF COPD
 • Characterized by: worsening of respiratory
symptoms beyond normal day-to-day
variations
– usually triggered by an infection or respiratory
irritant.
– Other common trigger: hypoxia, cold weather, β-
blockers, narcotics, or sedative hypnotic agents.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Clinical features
• Most life-threatening feature  hypoxemia
(arterial saturation <90%)
– Sx: tachypnea, tachycardia, systemic hypertension,
cyanosis, and a change in mental status
• The patient tries to overcome severe dyspnea
and orthopnea by sitting in an up-and-forward
position, using pursed-lip exhalation, and
engaging accessory muscles to breathe.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 • Pneumonia, pneumothorax, pulmonary
embolism, or an acute abdomen  may
exacerbate COPD.
• Other acute triggers  asthma, congestive
heart failure, pneumonia, pulmonary
embolism, tuberculosis, and metabolic
disturbances

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Dx
• History:
– Seek causes for exacerbation & triggers + sputum changes
– Assess oxygenation & acid-base status
– Perform a physical examination
• Pulse oxumetry  identify hypoxemia
• Capnography  identify hypercarbia
• Respiratory failure characterized by arterial PaO2 of <60
mm Hg or an arterial SaO2 <90% in room air
• Respiratory acidosis present if the partial pressure of
carbon dioxide (PCO2) is >44 mm Hg.
• Assessment of sputum includes questions about changes in
volume and color, especially an increase in purulence.
– Increase in sputum volume & change color  bacterial
infection  need antibiotik th/
Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
 DD

Tintinalli’s Emergency Medicine a

Comprehensive Study Guide 8th ed.
 Treatment
• Goals: correct tissue oxygenation, alleviate reversible
bronchospasm, and treat the underlying cause

Tintinalli’s
Emergency Medicine
a Comprehensive
Study Guide 8th ed.
 Treatment
• Oxygen : Administer oxygen to raise the Pao2
above 60 mm Hg or the Sao2 above 90%
• β2-Adrenergic Agonists
– Short-acting β2-agonists and anticholinergic agents
are first-line therapies in the management of acute,
severe COPD
– β2-Agonists are best given every 30 to 60 minutes if
tolerated
– Nebulized aerosols every 20 minutes may result in
more rapid improvement of FEV1, but more frequent
side effects (tremor, anxiety, and palpitations)

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Treatment
• Anticholinergics
– Some guidelines favor β2-agonists as a first-line
therapy, whereas others favor anticholinergic agents
• Ipratropium bromide given as a single dose by metered-dose
inhaler with a spacer or as an inhalant solution by
nebulization (0.5 milligram or 2.5 mL of the 0.02% inhalant
solution) is the usual agent of choice
• aerosolized glycopyrrolate (2 milligrams in 10 mL of saline)
is also effective.
– Side effects are minimal and appear to be limited to
dry mouth and an occasional metallic taste.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

• Corticosteroids
Treatment Tintinalli’s Emergency Medicine a
Comprehensive Study Guide 8th ed.

– The use of a short course (5 to 7 days) of systemic steroids improves lung

function and hypoxemia and shortens recovery time in acute COPD
exacerbations
– There appears to be no clear benefit from a dose >40 to 60 milligrams of oral
prednisone daily.
– Hyperglycemia is the most common adverse effect.
• Antibiotics
– Prescribe antibiotics if there is evidence of infection, such as change in volume
of sputum and increased purulence of sputum
– Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis
– Initial antibiotics include macrolides (azithromycin), tetracyclines (doxycycline),
or amoxicillin with or without clavulanic acid.
– Duration of treatment: 3 to 14 days.
• Methylxanthines  theophylline (oral) and aminophylline (parenteral)
– may induce nausea and vomiting
– Methylxanthines (aminophylline 3 to 5 milligrams/kg IV over 20 minutes) are
third-line options after inhaled therapies and steroids and when first-line
therapies fail
 Treatment
• Noninvasive ventilation
– Can be delivered by nasal mask, full facemask, or
mouthpiece
– Contraindications:
• An uncooperative or obtunded patient,
• inability of the patient to clear airway secretions,
• hemodynamic instability,
• respiratory arrest,
• recent facial or gastroesophageal surgery,
• burns,
• poor mask fit, or
Tintinalli’s Emergency Medicine a Comprehensive
• extreme obesity Study Guide 8th ed.
Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
 Treatment
• Assisted ventilation
– Indicated if there is evidence of respiratory muscle
fatigue, worsening respiratory acidosis, deteriorating
mental status, or refractory hypoxemia
– Goal: to rest ventilatory muscles and to restore
adequate gas exchange.
– Adverse events associated with invasive ventilation
include pneumonia, barotrauma, and inability to wean
the COPD patient from the ventilator.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
 Acute Severe Asthma (Status
Asthmaticus)
• Is an acute severe asthma attack that does not
improve w/ usual doses of inhaled
bronchodilators & steroids
• s/s hypoxemia, tachypnea, tachycardia,
accessory muscle use, wheezing
• Rapid treatment to preventing
cardiopulmonary arrest

Tintinalli’s Emergency Medicine: A Comprehensive

Study Guide, 8e
Tintinalli’s Emergency Medicine: A Comprehensive
Study Guide, 8e
2017 GINA Report, Global Strategy for Asthma
Management and Prevention
• Magnesium
– IV mg sulfate for acute, very severe asthma (FEV1<25% predicted)
– 1-2 gr IV over 30 mnts
– Nebulized Mg effective, imprve pulmonary fx in severe asthma when it follows aggressive b-agonist
& steroid th/
• Noninvasive positive-pressure ventilation
• Ketamine
– Inhibits reuptake of noradrenaline & increase circulating catecholamines, aiding some severe asthma
– IV bolus dose of 0.2 mg/kg followed by an infusion 0.5mg/kg/h
• Epinephrine
– SC/IM, 0.5mg in adults (standard adult EpiPen® dose), in refractory situations
• Mechanical ventilation
– If the patient manifest progressive hypercarbia/ acidosis/ becomes exhausted/ confused intubation
& mechanical intubation
– Mechanical ventilation does not relieve the airflow obstruction—it merely eliminates the work of
breathing and enables the patient to rest while the airflow obstruction is resolved
– Complications: extremely high peak airway pressure w/ subsequent barotrauma & hemodynamic
impairment
– Mucus plugging increased airway resistance, atelectasis, pulmonary infx
– Using rapid inspiratory flow rates at a reduced respiratory frequency (12-14 breaths/min) & allowing
adequate time for the expiratory phase can mitigate these effect
– Target adequate arterial o2 saturation (≥90%) without concern for “normalizing” the hypercarbic
acidosis is called controlled mechanical hypoventilation/permissive hypoventilation.
– Require sedation

Tintinalli’s Emergency Medicine: A Comprehensive

Study Guide, 8e
 Agents of uncertain/ no benefit in
status asthmaticus
• Heliox
• Methyxanthies
• Other agents
– Mast cell modifiers
– Leukotriens

Tintinalli’s Emergency Medicine: A Comprehensive

Study Guide, 8e
Tintinalli’s Emergency Medicine: A Comprehensive
Study Guide, 8e
2017 GINA Report, Global Strategy for Asthma
Management and Prevention
2017 GINA Report, Global Strategy for Asthma
Management and Prevention
2017 GINA Report, Global Strategy for Asthma
Management and Prevention
http://www.samj.org.za
/index.php/samj/article
/view/6658/4940
TB
 • Slow growing aerobic rod
• Settles in areas of high oxygen content and
blood flow
• Transmission: droplet inhalation to the lung
• Active tuberculosis + excrete mycobacteria in
saliva / sputum  most infectious

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

• Primary TB
Clinical features Tintinalli’s Emergency Medicine a
Comprehensive Study Guide 8th ed.

– Asymptomatic
– Detected only by a + screening TB skin test / by abnormalities on chest
radiograph
– Infeksi primer dan aktif : fever, malaise, weight loss, and chest pain
• Reactivation TB
– Latent  reactivation : symptoms bisa sistemik / pulmonary
• Most common: similar to those of primary tuberculosis and include fever,
night sweats, malaise, fatigue, and weight loss
– Productive cough, hemoptysis, dyspnea, and pleuritic chest pain  muncul pas
infeksinya ud nybar di dlm paru
– PF: unremarkable; rales may be noted in areas of pulmonary infection
– extrapulmonary site of TB: lymphatic system—painless lymphadenopathy (i.e.,
scrofula, cervical lymphadenitis).
• Include abdominal pain due to hepatosplenomegaly, peritoneal tubercles,
prostatitis, epididymitis, or orchitis; adrenal insufficiency; bone pain with
arthritis, osteomyelitis, or Pott’s disease (bony destruction, often in the spine);
hematuria and sterile puree; and meningitis.
• also cause pericarditis  lead to tamponade and constrictive symptoms
 Dx & DD
• DD: community acquired pneumonia
– Clue that suggest TB : hemoptysis, night sweats,
and weight loss.
– Chest radiograph: look carefully for upper lung
field involvement, fibrocalcific changes, pleural
capping, or a calcified Ghon complex.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Dx & DD
• MANTOUX OR TUBERCULIN SKIN TEST
– Most common method
– Uses intracutaneous injection of 0.1 mL of purified protein
derivative into the forearm
– Result: 48 and 72 hours after administration
– All persons with a new positive skin test or recent
conversion should be referred for treatment of latent
tuberculosis.
– Bacillus Calmette-Guérin (BCG) immunization for
tuberculosis prevention  a positive skin test response in
absence of infection.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

Tintinalli’s Emergency Medicine a
Comprehensive Study Guide 8th ed.
• BLOOD TESTS
– Interferon-gamma release assays (IGRA)
– Seeks the response to peptides present in all M.
tuberculosis proteins  trigger the release of interferon-
gamma by the infected host.
– These proteins are absent in the BCG vaccine and in
most nontuberculous mycobacteria  more specific
than skin testing
– Result: 16 to 24 hours

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

• Chest radiograph
– Identify disease in those with pulmonary symptoms or after
a positive skin test
– Primary infection: parenchymal infiltrates in any area of the
lung may be found (67.2)
• Isolated ipsilateral hilar or mediastinal adenopathy is sometimes the
only finding
• Pleural effusions  unilateral and occur alone or in association with
parenchymal disease
• The enlarged lymph nodes  commonly encountered in children 
external compression  bronchial obstruction, atelectasis, and
postobstructive hyperinflation.
– Latent TB
• Nonspecific findings include upper lobe or hilar nodules and fibrotic
lesions, which may be calcified
• Bronchiectasis, volume loss, and pleural scarring.
• Healed primary areas of infection  Ghon foci (67.1), areas of
scarring, and calcification
Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
• Chest radiograph
– Reactivations infections
• Classic findings: cavitary or noncavitary lesions in the upper
lobe or superior segment of the lower lobe of the lungs (67.3 –
67.4)
• Microscopy/cultures
– Sputum; gastric aspirates, pleural and other body fluids,
or tissue samples
– Ziehl-Neelsen stain / fluorochrome; followed by
exposure to an acidic agent.
– the best method of confirming diagnosis.
– also can aid detecting resistance to treatment regimens.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

Tintinalli’s Emergency
Medicine a Comprehensive
Study Guide 8th ed.
Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
Respiratory Failure
 Respiratory Failure
• A syndrome that respiratory fail either in gas exchange function or
ventilation function

• Classification:

1. Hypoxemic(Type I – Pulmonary fail) : most common. Mostly because of

collapse or filling in alveolar units. In this type, both PO2 and PCO2
decrease.
2. Hypercapnic(Type II – Ventilatory fail) : Mostly because of drug
overdose, chest wall abnormalities(barrel chest), or severe airway
disorders(asthma, COPD). In this type, PCO2 elevated >50mmHg.
3. Acute : develops over minutes – hours. Life-threatening because
derangement in arterial blood gases and acid-base status. Usually pH
<7.3
4. Chronic: develops over several days or longer. Usually pH is normal
Respiratory Failure
 Hypoxemic Respiratory Fail
• CNS manifestations : agitation, headache,
somnolence, coma, and seizures.
• Tachypnea
• Cyanosis
• polycythemia
 Diagnosis and Treatment
• arterial blood gas analysis.
• Pulse oximetry is useful for screening purposes and
decreased Sao2 readings accurately predict significant
hypoxemia

initial approach remains the same:

1. ensuring a patent airway and providing supplemental
oxygenation with a goal of maintaining a Pao2 >60
mmHg.
2. in patients with right-to-left shunts, arterial
oxygenation responds to supplemental oxygen.
 HYPERCAPNIA
• Hypercapnia is exclusively caused by alveolar
hypoventilation and is defined as a Paco2 >45 mm Hg.
Alveolar hypoventilation has many causes, including rapid
shallow breathing, small tidal volumes, underventilation of
the lung, or reduced respiratory drive.
 Clinical Features
• Headache
• Confusion
• Lethargy
• Severe hypercapnia can produce seizures and
coma.
• Extreme hypercapnia can result in
cardiovascular collapse, but this is usually
seen only with acute elevations of Paco2 >100
mmHg.
 Diagnosis
• arterial blood gas analysis
• Pulse oximetry assessment can be normal.
• Acute hypercapnia, the serum bicarbonate
level increases slightly
• Patients with chronic hypercapnia have an
elevated serum HCO3
Aspiration Pneumonia
 Aspiration pneumonia is an inflammation of lungs and bronchial
tubes. Happens after you inhale foreign matter.

 Also known as anaerobic pneumonia. This condition is caused

by inhaling materials such as vomit, food, or liquid.

 Risk factors
 Coma
 Drinking large amounts of alcohol
 General anesthesia
 Poor Gag reflex
 Old age

 Symptoms are cyanosis, shortness of breath, chest pain, fever,

coughing up foul sputum. Bronchoscopy is helpful in diagnosing
the condition.
Treatment

1) Immediate Hospitalization

2) Oxygen supplementation, cardiac monitoring & pulse oximetry.

3) Oropharyngeal / tracheal suctioning may be indicated to

further remove aspirate.

4) Reassess the need for intubation on frequent basis depending

on patient’s oxygenation, mental status, signs of increased
work of breathing, or impending respiratory failure. IV fluids &
electrolyte replacement.

5) Bronchoscopy helpful when aspiration of foreign body or food

material suspected, also helpful in guiding antibiotic therapy.
6) Thoracentesis (pleural fluid aspiration) is a
diagnostic therapeutic procedure in which fluid (or
air) is removed from between the pleura and chest
wall.

7) Antibiotics to treat respiratory infections &

Mechanical ventilation if needed.
 Pleural Effusion
• Result from fluid
accumulating in the
potential space between
the visceral and parietal
pleurae
• Can result from many
causes, most common
causes: CHF, pneumonia,
and cancer

Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th Ed. 2014.
 Pathophysiology
• Normal: small amount of fluid is secreted from the parietal
pleura  pleural space  absorbed by visceral pleural
microcirculation
• Any process that increases fluid production or decreased
fluid removal by the lymphatics  accumulation in the
pleural space
• Pleural effusions are traditionally divided based on
mechanism:
– Exudative effusions: influenced by local factors; pleural disease
(usually inflammation or neoplasia) that results in active fluid
secretion or leakage with high protein content
– Transudative effusions: influenced by systemic factors; an
imbalance between hydrostatic (e.g., CHF) and oncotic (e.g.,
nephrotic syndrome) pressures, this imbalance results in the
production of an ultrafiltrate with low protein content across
the pleural membrane Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7 th Ed. 20
Harrison’s Principles of Internal Medicine. 18th Ed. Volume II. Chapter 263.
 Clinical Features
• May be clinically silent or come to detection from:
– Symptoms of an underlying disease
– Volume of pleural fluid reaches 500 ml  dyspnea on
exertion/at rest
– New/enlarging pleural effusion, viral pleuritis, pulmonary
infarction  Development of inflammation and associated
pain with respiration
• Physical findings: percussion dullness and decreased
breath sounds, localized pleural friction rub

Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Ed. 2011.
Harrison’s Principles of Internal Medicine. 18th Ed. Volume II. Chapter 263.
 Diagnosis
• Thoracocentesis
• Chest radiography
• Ultrasound  bedside thoracic ultrasound to guide
thoracocentesis
• CT scan

Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 8th Ed. 2014.
Harrison’s Principles of Internal Medicine. 18th Ed. Volume II. Chapter 263.
Harrison’s Principles of Internal Medicine. 18th Ed. Volume II. Chapter 263.
 Treatment
• In patients with large effusions  urgent therapeutic
thoracentesis may stabilize respiratory or circulatory status
– Thoracocentesis under ultrasound guidance
– Drainage of 1.0 -1.5 ml in one session, if >1500 ml: reexpansion
pulmonary edema
– Contraindications for thoracocentesis: coagulopathy, other bleeding
disorders, pleural adhesions
• Patients with pleural empyema (gross pus or organisms on
Gram stain) require insertion of a chest tube to drain the
pleural space adequately & prevent the development of
loculations
• Pain relief for patients with significant pleuritic pain: NSAIDs,
opioid analgesia

Tintinalli JE. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide. 7th Ed. 2011.
Harrison’s Principles of Internal Medicine. 18th Ed. Volume II. Chapter 263.
 Acute Pulmonary Edema
• Acute development of alveolar lung edema due to
one or more of the following :
– Elevation of hydrostatic pressure in the pulmonary
capillaries (left heart failure, mitral stenosis)
– Specific precipitants, resulting in cardiogenic pulmonary
edema in patients with previously compensated heart
failure or without previous cardiac history
– Increased permeability of pulmonary alveolar-capillary
membrane (non-cardiogenic pulmonary edema)
• Pulmonary edema occurs when fluid is filtered into
the lungs faster than it can be removed
• Accumulation of fluid may have major consequences
on lung function because efficient gas exchange
cannot occur in fluid-filled alveoli
 • Non-cardiogenic pulmonary edema
Acute Pulmonary Direct injury to Lung
– Chest trauma, pulmonary contusion
– Aspiration
Edema – Smoke inhalation
– Pneumonia
• Cardiogenic pulmonary edema
– Left heart failure – Oxygen toxicity
– Mitral stenosis – Pulmonary embolism, reperfusion
– ACS with left heart failure Hematogenous Injury to Lung
– Arrhythmia – Sepsis
– Myocarditis – Pancreatitis
– Endocarditis – Nonthoracic trauma
– Cardiomyopathy – Multiple transfusion
– Pericardial Effusion – IV drug use, e.g heroin
– Crisis Hypertension – Cardiopulmonary bypass
– CKD Possible Lung Injury Plus Elevated
Hydrostatic Pressures
– High –altitude pulmonary edema
– Neurogenic pulmonary edema
– Reexpansion pulmonary edema
 Acute Pulmonary Edema
Physical Finding
• Pt appears severely ill, often diaphoretic, sitting bolt
upright, tachypnea, and cyanosis
• Bilateral pulmonary rales (crackles), S3 gallop
• Frothy, blood-tinged sputum
Laboratory
• ABG  reductions of both PaO2 and PaCO2 with
progression respiratory failure, hypercapnia develops with
academia
• CXR  pulmonary vascular redistribution, diffuse haziness
in lung field with perihillar “butterfly” appearance
 Acute Pulmonary Edema
Therapy
• Administer 100% O2 by mask to achieve PaO2 >60 mmHg; if
inadequate, use positive pressure ventilation by face or nasal
mask, and if necessary proceed to ETI
• Reduced preload :
– Seat upright to reduced venous return, if not hypotension
– IV loop diuretic (furosemide, initially 0.5-1 mg/kg); use lower dose
if does not take diuretic chronically)
– Nitroglycerin (sublingual 0.4 mg x 3 q5min) followed by 5-20
microgram/min IV if needed
– Morphine 2-4 mg IV; asses frequently for hypotension or
respiratory depression; naloxone should be available to reverse
effect of morphine if necessary
– Consider ACE-I if hypertension, or insetting of acute MI with HF
– Consider Nesiritide (2 microgram/kg bolus IV followed by 0.01
microgram/kg per min)for refractory symptoms – don’t use in
acute MI or cardiogenic shock
 Acute Pulmonary Edema
Therapy
• Inotropic agent are indicated in cardiogenic
pulmonary edema and severe LV dysfunction
(dopamine, dobutamine, milrinone)
• The precipitating cause of non-cardiogenic or
cardiogenic pulmonary edema should be treated,
particularly acute arrhythmia or infection
• For refractory pulmonary edema associated with
persistent cardiac ischemia  early coronary
revascularization
Acute Pulmonary Edema
Pneumothorax
 Pneumothorax
• Occurs when free air enters the potential
space between the visceral and parietal
pleura.
• Classification:
1. Primary pneumothorax : occur without
clinically apparent lung disease
2. Secondary pneumothorax : occur in patients
with underlying lung disease.

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Pneumothorax
• Classic symptoms: sudden onset of dyspnea
and ipsilateral, pleuritic chest pain.
– Peluritic component: resolve within 24 hours
– Sinus tachycardia  the most common physical
finding
– Clinical hallmarks of tension pneumothorax:
tracheal deviation away from the involved side,
hyper-resonance of the affected side,
hypotension, and significant dyspnea

Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.

 Pneumothorax
• Imaging:
– Chest X-ray: demonstrates loss of lung markings in
the periphery and a pleural line that runs parallel
to the chest wall.
Critically ill patients (cannot be moved to an erect
position) look for the deep sulcus sign, a deep
lateral costophrenic angle, on the affected side.
– US  detects traumatic pneumothorax
– Chest CT  can detect other pathology such as
pulmonary blebs.
Tintinalli’s Emergency Medicine a Comprehensive Study Guide 8th ed.
 Conclusion
Laki-Laki Riwayat
65 tahun penyakit :
•TBC
•Asma
•Stroke  Crackles &
rawat lama Wheezing

•Saturasi O₂ menurun
Pneumonia
•Saturasi CO₂ Meningkat
FR: Rokok
Infeksi
Asidosis
respiratorik
Demam
Penurunan
Risiko u/ kesadaran
ARDS/COPD

Obstruksi berat Gagal Napas

 Daftar Pustaka
• Tintinalli’s Emergency Medicine a Comprehensive Study Guide
8th ed.
• 2017 GINA Report, Global Strategy for Asthma Management
and Prevention
• http://www.samj.org.za/index.php/samj/article/view/6658/4
940
• Marx JA, Hockberger RS, Walls RM. Rosen’s Emergency
Medicine: Concepts and Clinical Practice. 8th Ed. 2014.
• Harrison’s Principles of Internal Medicine. 18th Ed. Volume II.
Chapter 263.
• Elias JA, Fishman JA, Grippi MA, Kaiser LR, Senior RM (eds). Fishman’s Manual of Pulmonary
Disease and Disorder 5th Edition. New York. Mc GrawHIll, 2015