Respiratory

Emergency
Bambang Heru
2011

Respiratory System

Lung parenchyma
Respiratory tract
Neromuscular system
Rib cage
Respiratory muscle
Pulmonary circulation

Emergency
Respiratory Failure

Pneumothorax
Massive Hemoptysis
Pulmonary Embolism
Pulmonary Edema
Pleural Effusion Massive
Aspiration: Near Drowning, Corpus
Alienum
ARDS Severe Acute Lung Injury

Respiratory
Failure

Definition
Clinical condition of a significant
impairment in the capacity of the
respiratory system to perform gas
exchange and is recognized by
the presence of arterial
hypoxemia and/or hypercapnea

RESPIRATION
Respiration is gas exchange between the
organism and its environment. Function of
respiratory system is to transfer O2 from
atmosphere to blood and remove CO2 from
blood.
Clinically respiratory failure is defined as PaO2
<60 mmHg while breathing air, or a PaCO2
>50 mmHg.

Respiratory failure
Respiratory failure and the diseases responsible for it are a
major cause of death throughout the world
Many patients are healthy and feel well before they develop acute
respiratory failure.
In contrast, most patients with chronic respiratory failure
experience progressively more severe symptoms as their
pulmonary function declines
Their downhill course often is punctuated by acute exacerbations
(acute-on-chronic respiratory failure) caused either by
worsening of their primary disorder or by superimposed secondary
illnesses such as pneumonia

Types of respiratory failure

Respiratory failure may be classified as
hypoxemic or hypercapnic and may be either
acute or chronic
Type 1 respiratory failure :
Hypoxemia with normal or low Pa CO2

Type 2 respiratory failure :

PaCO2 is elevated

Hypoxemic respiratory failure (type I)

Characterized by a PaO2 of less than 60 mm Hg

with a normal or low PaCO2.
The most common form of respiratory failure, and
it can be associated with virtually all acute
diseases of the lung, which generally involve fluid
filling or collapse of alveolar units.
E.g: cardiogenic or noncardiogenic pulmonary
edema, pneumonia, and pulmonary hemorrhage.

Type I
Conditions that affect oxygenation such
as:
Parenchymal disease (V/Q mismatch)
Diseases of vasculature and shunts: rightto left shunt, pulmonary embolism
interstitial lung diseases: ARDS,
pneumonia, emphysema.

What are the causes of acute respiratory failure?

Structure

Examples of Possible Diagnoses

Air spaces (alveoli)

Pulmonary edema (cardiogenic)

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS)
Pulmonary hemorrhage
Pneumonia

Interstitium
Heart/pulmonary
vasculature

Pulmonary fibrosis (e.g., Hamman-Rich syndrome)

Extrinsic allergic alveolitis
Viral or "atypical" pneumonia
Pulmonary embolism
Intracardiac or intrapulmonary shunt
Congestive heart failure

Airway

Asthma
Chronic obstructive pulmonary disease
(acute on chronic respiratory failure)
Mucous plugging
Right main-stem bronchus intubation

Pleura

Pneumothorax
Pleural effusion
Mason: Murray & Nadel's Textbook of Respiratory Medicine, 4th ed.

Hypercapnic respiratory failure (type II)

Characterized by a PaCO2 of more than 50 mm Hg.
Hypoxemia is common in patients with hypercapnic
respiratory failure who are breathing room air.
The pH depends on the level of bicarbonate, which, in
turn, is dependent on the duration of hypercapnia.
Common etiologies include drug overdose,
neuromuscular disease, chest wall abnormalities, and
severe airway disorders (eg, asthma, chronic obstructive
pulmonary disease [COPD])

Type II
increased airway resistance; both oxygen and
carbon dioxide are affected.. The underlying
causes include:
Reduced breathing effort (in the fatigued patient)
A decrease in the area of the lung available for
gas exchange (such as in emphysema).
Neuromuscular problems like, GB syndrome.
Flail chest.

Treatment
Respiratory Failure should be treated
with Mechanical Ventilation in the ICU
Non Invasive Ventilation can be applied
for
Supportif Treatment: Nutrition,
Physiotherapi, Cardiovascular,
Oxygenation, Underlying Diseases or
comorbid problem

Pneumothorax
:

Definition
Gas or air in pleural cavity
Classification of pneumothorax
Primary Spontaneous Pneumothorax
Secondary Spontaneous Pneumothorax
Traumatic Pneumothorax
Iatrogenik Pneumothorax
Artificial Pneumothorax
Sahn SA. Spontaneous pneumothorax. N Engl J Med 2000; 342: 868-74.

 Primary spontaneous pneumothorax occurs

in persons without clinically apparent lung
disease
Secondary spontaneous pneumothorax is a
complication of preexisting lung disease

Sahn SA. Spontaneous pneumothorax. N Engl J Med 2000; 342: 868-74.

 Iatrogenic pneumothorax results from a

complication of a diagnostic or therapeutic
intervention
Traumatic pneumothorax is caused by
penetrating or blunt trauma, with air entering
the pleural space directly through the chest
wall; visceral pleural penetration; or alveolar
rupture due to sudden compression of the chest
Sahn SA. Spontaneous pneumothorax. N Engl J Med 2000; 342: 868-74.

PHYSICAL EXAMINATION
Inspection: - static : concave on affected side
- dynamic: decrease movement
of chest wall
Palpation:
- widened intercostal space
- diminished fremitus
Percussion: - hyperresonant
Auscultation: - decrease / absent breath sounds
on affected side
Sahn SA. Spontaneous pneumothorax. N Engl J Med 2000; 342: 868-74.

GENERAL MANAGEMENT

o Evacuating air from pleural space

o Preventing Recurrences

Sahn SA. Spontaneous pneumothorax. N Engl J Med 2000; 342: 868-74.

RADIOLOGICAL EXAMINATION
Chest X-Ray:

Identification of a thin, visceral pleural line (<1 mm

in width) that is found to be displaced from the chest
wall
Radioluscent Image - avasculair
Collapse of Lung
Mediastinal Shift

CT Scan: should be performed to

differentiate between these two
conditions (bullae-PnTh)
Sahn SA. Spontaneous pneumothorax. N Engl J Med 2000; 342: 868-74.

Management pneumothorax
1.
2.
3.
4.
5.
6.
7.
8.

Observation - Oxygenation
Simple Aspiration with a catheter
Chest tube insertion
Pleurodesis
Thoracoscopy
VATS
Thoracotomy
Physiotherapy Incentive Spirometri
Sahn SA. Spontaneous pneumothorax. N Engl J Med 2000; 342: 868-74.

TENSION PNEUMOTHORAX
Progressive Dyspnea
Decrease Conciousness
Emergency treatment
decompression pressure

TENSION PNEUMOTHORAX
Intrapleural pressure exceeds from atmosphere
pressure at inspiration or expiration
Valve Mechanism
Inspired Air can not escape as expiration
Mediastinum compression decrease cardiac
output, as well as venous return

Tension Pneumothorax

ICS 2
Mid clavicular line (MCL)

Hemoptysis
-massive-

DEFINITION
the expectoration of blood or of
blood-stained sputum from the
bronchi, larynx, trachea or lungs
Some abnormal condition and with
fatality result
Volume: stained to massive
In this session: from distal of glottis

Etiologi
Penyebab tersering
Hadiarto M (rawat inap RSUP
Persahabatan): Tb paru (50%), Ka. paru
(32%), Bronkitis (8%), BE (5%),lainlain(5%)
Retno W (UGD RSUP Persahabatan): Tb
paru (64,5%), BE (16,7 %), Ka. paru (3,5
%)

 Batuk darah yang mengancam jiwa

Suatu keadaan gawat darurat
Harus ditanggulangi segera,untuk
mencegah komplikasi berat/kematian (75%)
.-------------- asfiksia,perdarahan,hipotensi
Rawat ICU

BATUK DARAH MASIF,

KRITERIA ?
600 ml/24 jam atau lebih, belum terhenti
250 ml/24 jam atau lebih tapi kurang dari 600
ml/24 jam, Hb kurang 10 g%, masih berlangsung
250 ml/24 jam atau lebih tapi kurang dari 600%
ml/24 jam, Hb lebih 10 g%, dalam 48 jam terakhir
masing berlangsung
(RSUP Persahabatan, 1970)

PERBEDAAN HEMOPTISIS
DENGAN HEMATEMESIS
Keadaan
Prodromal

Hemoptisis
Hematemesis
Rasa tidak enak di Mual, gangguan
tenggorok, batuk
lambung, muntah

Onset

Darah dibatukkan, Darah

dpt disertai muntah dimuntahkan, dpt
disertai batuk

Penampilan

Berbuih

Tidak berbuih

Warna
Isi

Merah segar
Tanpa sisa
makanan

Merah tua
Sisa makanan

PEMERIKSAAN
LABORATORIUM
Darah rutin : Hb, lekosit, Ht, Tr
Uji faal pembekuan darah
Kuman BTA, MO lain, jamur
Sitologi sputum

BATUK DARAH
TATALAKSANA (Maria CHW, 2000)
Tahap I.
Pembebasan saluran napas dan stabilisasi penderita
Tahap II.
Lokalisasi sumber dan mencari penyebab
perdarahan :
rontgen, bronkoskopi
Tahap III. Terapi
- Dengan bronkoskop : bilas NaCl dingin,
vasokonstriktor, tamponade, koagulasi
- Tanpa bronkoskop : obat-obat, embolisasi, bedah

Tahap I : Pembebasan jalan

napas dan stabilisasi penderita
Menenangkan dan mengistirahatkan
penderita dan diberitahu agar tidak takut
membatukkan darahnya.
Menjaga agar jalan napas tetap terbuka,
bila perlu dilakukan pengisapan (dengan
bronkoskop akan lebih baik)
Resusitasi cairan / darah

Tahap I: Pembebasan jalan

napas dan stabilisasi penderita
Bila perlu pemberian
- Obat hemostatik
- Obat penekan refleks batuk
- Obat sedasi
Pemeriksaan faal hemostasis

Skema sirkulasi bronkial dan anastomosis sirkulasi bronkial dengan sirkulasi

pulmonar
Am Rev Respir Dis 1987;135:463-81

ETIOLOGI
Etiologi beragam
Terbanyak akibat tuberkulosis, keganasan
(bronchogenic carcinoma), bronkiektasis,
pneumonia dan bronkitis
Penyebab lain : kelainan jantung,
hematologis, pembuluh darah, kelainan
sistemik, akibat obat, trauma/iatrogenik,
benda asing, endometriosis, infeksi
lainnya

Sumber
perdarahan

Etiolog
i

Sirkulasi bronkial
95% radang paru,
kanker paru
Sirkulasi pulmonal
5% infark paru, emboli
paru, aneurisma
Rassmusen

6 kelompok
utama :

1. Trauma atau benda asing

2. Infeksi / radang (TB, bakteri, jamur,
virus)
3. Neoplasma (Ca paru, metastase paru
4. Kelainan kardiopulmo-vaskuler (MS,
emboli / infark paru)
5. Perdarahan alveoler (sindr.
GoodPasture)

Common causes of massive

hemoptysis

DIAGNOSIS
Hemoptisis, epistaksis atau
hematemesis
Definisi hemoptisis masif berbeda di
berbagai institusi yaitu antara 200-1000
mL/24 jam
Kebanyakan : laju perdarahan 600
ml/24 jam.

TATALAKSANA
Prinsip penatalaksanaan hemoptisis :
Menjaga jalan napas dan stabilisasi penderita
Menentukan lokasi perdarahan
Memberikan terapi

Prioritas tindakan awal penderita lebih stabil, kemudian

mencari sumber dan penyebab perdarahan.
Mencegah risiko berulangnya hemoptisis
Penderita dengan hemoptisis masif harus dimonitor dengan
ketat di instalasi perawatan intensif

LANGKAH I : MENJAGA JALAN NAPAS

DAN STABILISASI PENDERITA

Menenangkan dan mengistirahatkan penderita

Menjaga jalan napas tetap terbuka
Resusitasi cairan dan bila perlu transfusi
Laksan (stool softener)
Obat sedasi ringan
suplementasi oksigen
Instruksi cara membatukkan darah dengan benar

PROGNOSIS
Dengan tatalaksana tepat kebanyakan
penderita memiliki prognosis yang baik
Akibat keganasan dan gangguan
pembekuan darah memiliki prognosis yang
lebih buruk

Pulmonary
Embolism

Pulmonary Embolism
Pulmonary embolism is a blockage of the main
artery of the lung or one of its branches by a
substance that has travelled from elsewhere in
the body through the bloodstream
Usually this is due to embolism of a thrombus
(blood clot) from the deep veins in legs (venous
thromboembolism) some fat, air
The obstruction of the blood flow through the
lungs and the resultant pressure on the right
ventricle of the heart leads to the symptoms and
signs of PE

Sign and Symptoms

Difficulty breathing
Chest pain on inspiration
Palpitation
Clinical signs:

low blood O2 saturation

Cyanosis
Rapid breathing
Increased JVP

Severe PE: sudden death

The Wells score

clinically suspected DVT - 3.0 points
alternative diagnosis is less likely than PE - 3.0
points
Tachycardia - 1.5 points
immobilization/surgery in previous four weeks 1.5 points
history of DVT or PE - 1.5 points
Hemoptysis - 1.0 points
malignancy (treatment for within 6 months,
palliative) - 1.0 points

Traditional interpretation
Score >6.0 - High (probability 59% based on
pooled data)
Score 2.0 to 6.0 - Moderate (probability 29%)
Score <2.0 - Low (probability 15%)
Alternate interpretation
Score > 4 - PE likely. Consider diagnostic
imaging.
Score 4 or less - PE unlikely. Consider Ddimer to rule out PE.

Obstructive
Disesase

PENCEGAHAN dan
PENGOBATAN ASMA

Pelega - Reliever
Bronkodilator
SABA short acting beta agonis
Golongan Xantin: teofilin, aminofilin
Golongan beta2 agonis: salbutamol, terbutalin,
procaterol, formoterol dll.
Anticholinergik: ipratropium bromide,
tioproprium

Pencegah - Controller
Korticosteroid inhalasi (ICS) (kombinasi) LABA inhalasi
ICS: fluticason, budesonide, mometason,
LABA long acting beta2 agonis
LABA: formoterol, salmeterol, bambuterol, clenbuterol
Antileukotriene: zafirlukast, montelukast
Teofilin Slow Release
Anti-IgE: omalizumab (10-30K$ /year)
Glukokortikoid Oral

Penyebab dan faktor pencetus asma

Iritan : asap, bau-bauan, polutan
Alergen seperti debu rumah, spora jamur, tepung
sari rerumputan,dll
Perubahan cuaca
Kegiatan jasmani yang berlebihan
Infeksi saluran napas
Stress, emosi, kecapaian
Obat-obatan
Genetik
Lain-lain : kehamilan, refluks gastro esofagus,
menstruasi,dll

Penatalaksanaan Asma Akut

Oksigen untuk mengatasi hipoksia

Bronkodilator: Inhalasi / Nebulizer dengan salbutamol /
terbutalin dan dapat dikombinasikan dengan ipratropium.
Antiinflamasi: Inhalasi (bude, flutic, mome) - Sistemik, oral
atau intravena (metilpred, deksamet, pred, hidrokort) jangka
pendek 5-10 hari tanpa harus tappering dosis
Bronkodilator lain kadang efektif bila obat standard gagal
memberikan hasil seperti:

Intravena salbutamol, terbutalin subkutan; Nonspesifik beta-agonists, injeksi/ inhalasi

(epineprin, isoproterenol, metaproterenol); Anticholinergics, IV or nebulizer, dg efek
sistemik (atropin, ipratropium, glikopirolat); Metilxantin (aminofilin, teofilin); Obat
anastesi inhalsi dengan efek bronkodilator (isofluran, halotan, enfluran) dan kadang
ketamin; Magnesium sulfat pada kasus status asmatikus

Pada pasien dengan gagal napas perlu dilakukan intubasi dan

ventilasi mekanik.
Campuran gas Heliox (helium-oksigen) dapat diberikan pada
rumah sakit yang lengkap.

 Indikasi pasien asma dirawat :

Dalam penatalaksanaan 2-3 jam di UGD masih
terdapat mengi yang nyata
Menggunakan otot-otot pernapasan
Memerlukan oksigen
Fungsi paru belum membaik

Indikasi memasukan pasien asma ke ICU :

Obstruksi saluran napas menjadi berat
Distress pernapasan
Gangguan status mental

 Komplikasi :

Pneumotoraks,
Pneumomediastinum dan emfisema subcutis
Atelektasis
Bronkopulmonar alergik
Gagal napas
Fraktur iga
Bronkitis Bakterialis

ARDS

ARDS
ARDS is a severe acute lung injury
Characterized by inflammation of lung
parenchyma leading to impaired gas exchange
with systemic release of inflammatory mediators
Causing inflammation, hypoxemia and usually
resulting in multi organ failure.
This condition is often fatal, needs mechanical
ventilation and admission to an ICU..

Characterized - ARDS
Acute onset
Bilateral infiltrates on CXR
Pulmonary artery Wedge Pressure < 18 mmHg (by
pulmonary artery catheterization if available); if
unavailable, then lack of clinical evidence of left
ventricular failure suffices
if PaO2/FiO2 < 300 acute lung injury (ALI) is
considered to be present
if PaO2/FiO2 < 200 acute respiratory distress
syndrome (ARDS) is considered

Signs and symptoms

SOB, tachypnea and occasionally with
decrease conciousness from low O2 levels.
ARDS can occur within 24-48 hours of an
injury (trauma, burns, aspiration, massive
transfusion, drug/alcohol abuse) or an acute
illness (infectious pneumonia, sepsis).
Criteria for ARDS: 1) Hypoxia 2) CXR:
Bilateral diffuse infiltrates of the lungs 3) No
cardiovascular lesion 4) PaO2/FiO2< than 200

Diagnosis
An arterial blood gas analysis
Chest X-Ray
Any cardiogenic cause of pulmonary
edema should be excluded - this can be
done by placing a
pulmonary artery catheter
As Scoring in Acute Lung Injury in MV

Treatment
ARDS is usually treated with Mechanical
Ventilation in the ICU
NIV in early periode
Antibiotic therapy as Microbial data available.
Empirical therapy may be appropriate for VAP
(nosocomial)
Supportif: Nutrition, Physiotherapy, Steroid,
Airway management (mucous, bronchodilator)
Plus: + + +