KEGAWATAN RESPIRASI

Sumardi
Pulmonology Division of Internal Medicine Departement
Faculty of Medicine GMU/ Pulmonology Departement
Sardjito General Hospital
 INTRODUCTION DYSPNEA
(SESAK NAFAS)
DEFINITION
DYSPNEA IS SENSATION NOT ENOUGH TO BREATH

The American Thoracic Society defines dyspnea as a "subjective

experience of breathing discomfort that consists of qualitatively
distinct sensations that vary in intensity. The experience derives
from interactions among multiple physiological, psychological,
social, and environmental factors, and may induce secondary
physiological and behavioral responses.

" Dyspnea”, a symptom, must be distinguished from the signs of

increased work of breathing

Harrison’s Principle of Internal Medicine 16 Ed. 2005

 SEPULUH BESAR PENYAKIT
DENGAN SIMPTOM DISPNEA

• PULMONARY
– COPD
– Infection
– Pleural effusion
– Cancer  primary or metastasis
– Asthma
• NON PULMONARY
– Chronic heart failure (CHF)
– Myocardial infarction (MCI)
– Chronic kidney disease
– Hepatic cirrhosis
– OBGYN cancer
 DYSPNEA, caused by
• Pulmonary system
• Non pulmonary system:
– Cardiovascular system
– Neuromuscular system
– Metabolic system
– Psychiatric origin
• Mixed
• Acute or chronic
 Dyspnea in Pulmonary system
• Acute:
– Infection: Pneumonia  bacterial,viral, other
– Acute Lung Injury (ALI)
– Acute Respiratory Distress Syndrome (ARDS)
– Pneumothorax
– Foreign body
– Embolism
• Chronic:
– TBC Paru milier
– COPD: Chronic Bronchitis, Emphysema
– Asthma
– Pleural Effusion  infection or non infection
– Infected bronchiectasis
– Cancer: primary or metastasis
– Interstitial Lung Disease
 DYSPNEA, non pulmonary
• CARDIOVASCULAR:
– Myocardial Infarction (MCI)
– Acute lung edema
• NEUROMUSCULAR
– Stroke
– CNS infection
• METABOLIC
– Thyroid crisis
– Hyperurecemia
• PSYCHIATRIC:
– Psychoneurosis
– Panic disorder, etc
 DYSPNEA: differential diagnosis

• ACUTE or CHRONIC  first anamnesis

• YOUNG MEN or OLDER>50 years old
• ACUTE ONSET THINK FIRST :
CARDIAL or NON CARDIAL (pulmonary)
• Old man + acute  think first: CARDIAL
– Pulse irregular  aware  ASAP  ICCU
– Trial nitrate sub lingual  better  cardial
 DYSPNEA: differential diagnosis

• Usually: chronic mean pulmonary, except

embolism and foreign body
• Febrile or Non febrile  infection?
• Acute + febrile  mean lung infection
• Acute + febrile + old man  mean worse
– Refer to hospital
– Oxygen first
– Think  comorbid factor  complication
 DYSPNEA:comorbid factor
• Old man
• Cardial
• Diabetic
• Renal impairement
• Cancer
• Chronic disease
• Immobilization:
– Arthritis
– Stroke
– Malnutrition
– Debility
• COMORBID FACTOR  REFER TO HOSPITAL
 PNEUMONIA
• ACUTE DYSPNEA,FEBRILE,RALES (+)
• YOUNG MAN < 40 YO
• OXYGEN 3-5 L/MINUTE CANULE
• BROADSPECTRUM ANTIBIOTICS
• MUCOLYTIC
• BEDREST
• PLUS COMORBID
(elderly,DM,stroke,CHF)  REFER TO
HOSPITAL
 ASTHMA
• ACUTE ONSET IN CHRONIC DISEASE
• History: treatment by more 1 doctor
• Many medication
• TREAT :
1. Anti Inflamation : steroid methylprednisolon
2. Bronchodilator : beta agonist + anticholinergic inhalation
3. Continuous steroid inhalation
4. Bronchodilator inhalation as needed
5. Antibiotics only for infection (febrile+leukocytosis)
DO NOT TREAT MUCOLYTIC
Plus comorbid factor  refer to hospital → ER
 DEFINISI ASMA
 Inflamasi kronik saluran napas
 berbagai sel memainkan peranannya:
• sel mast
• Eosinofil
• limfosit T
• Pada individu yang susceptible, inflamasi ini menyebabkan episode klinis:
• bising mengi
• sesak napas
• dada terasa tegang
• batuk khususnya diwaktu malam/dini hari
• Gejala klinis berhubungan dengan :
• penyempitan saluran napas yang sangat luas dan bervariasi
• reversible sebagian baik secara spontan maupun dengan pengobatan
• Proses inflamasi meningkat dipacu oleh faktor pencetus
• udara dingin
• Infeksi
• Makanan
• bau bahan kimia
• bulu binatang
• gangguan psikhis, dan lain-lain.
ASTHMA
ASTHMA pathology
PROSES INFLAMASI BRONKHUS
 STATUS ASTHMATICUS
• INFLAMASI KRONIK BRONKHUS
• BRONKHOKONTRIKSI YANG TIDAK DAPAT
DIATASI DENGAN OBAT YANG LAZIM DIGUNAKAN
• Manifestasi Berat:
• FEV1 < 1 liter; PEF < 80 liter/menit.
• PaCO2 > 45 & PaO2 < 55 mmHg
• KLASIFIKASI GINA 2015 DISEBUT SEVERE
PERSISTENT, EPISODE EXACERBATION
 Classification of Asthma Severity by
Clinical Features Before Treatment
(GINA 2015)
Intermittent Moderate Persistent
 Symptoms less than once a week
 Brief exacerbations Symptoms daily
 Nocturnal symptoms not more than
twice a month Exacerbations may affect activity and
sleep
 • FEV1 or PEF < 80% predicted
 • PEF or FEV1 variability < 20% Nocturnal symptoms more than once a
Mild Persistent week

 Symptoms more than once a week Daily use of inhaled short-acting 2-

but less than once a day agonist
 Exacerbations may affect activity
and sleep • FEV1 or PEF 60-80% predicted
 Nocturnal symptoms more than • PEF or FEV1 variability > 30%
twice a month
 • FEV1 or PEF ] 80% predicted Severe Persistent
 • PEF or FEV1 variability < 20 –
30% Symptoms daily

Frequent exacerbations

Frequent nocturnal asthma symptoms

 STATUS ASTHMATICUS,
tujuan pengobatan

• Perbaikan perlambatan aliran udara secepat mungkin

 meningkatkan PEF
• Perbaikan hipoksemia
• Kembalikan fungsi paru senormal mungkin
• Rencanakan pencegahan eksaserbasi
 STATUS ASTHMATICUS,
faktor risiko
• Sering menggunakan kortikosteroid sistemik
(oral/injeksi)
• Riwayat perawatan di IGD karena serangan asma
• Punya masalah psikiatri/psikososial
• Tidak patuh pada rencana pengobatan asma jangka
panjang
 STATUS ASTHMATICUS,
klinis
• Sesak nafas >25x/menit
• Sukar menjawab anamnesis  bingung  somnolen
(bahaya)
• Mengi  silent chest (bahaya)
• Sianosis  saturasi Oksigen<90%
• Bradikardi
• Aritmia
• Respirasi paradoksal
 STATUS ASTHMATICUS,
manajemen
SEGERA TERAPI
1) OKSIGEN 3-4 L/MENIT
2) NEBULIZER:
A) BETA AGONIST: salbutamol 1-2 mg,terbutalin 1 mg
B) ANTIKOLINERGIK: ipatriumbromid 0,25-0,5 mg
C) KORTIKOSTEROID:budesonid 0,5-1 mg,atau flutikason 0,5-1 mg
3) SISTEMIK KORTIKOSTEROID: metilprednisolon oral 64 mg / injeksi iv 125
mg/6jam  500 mg/12 jam (pulse dose)
4) DIBERIKAN SIMULTAN 1,2,3
5) EVALUASI SETELAH 30 menit-60 menit
6) DAPAT DIULANG 2-3 KALI
7) BILA TAK ADA PERBAIKAN, SEGERA RAWAT ICU
8) TARGET: saturasi >90%

GINA 2007; Fundamental Critical Care and Support 2005

 MAGNESIUM
 Magnesium. Intravenous magnesium sulphate
(usually given as a single 2 g infusion over 20
minutes)
 Reduces hospital admission rates in adults and older
children with severe bronchospasm who fail to
improve promptly to bronchodilators (Evidence A).
 Nebulized salbutamol administered in isotonic
magnesium sulfate provides greater benefit than if it
is delivered in normal saline (Evidence A).

GINA 2007
 KAPAN RAWAT JALAN?
• KLINIS:
•
sesak nafas berkurang
• Dapat tidur terlentang
• Dapat menggunakan inhaler
• Infeksi teratasi (demam↓)
• OBYEKTIF:
• PEF: 50-70% prediksi normal
• Saturasi oksigen >90%
• GINA 2007; Fundamental Critical Care and Support 2005
 TARGET RAWATAN
• PENURUNAN PEMAKAIAN INHALER BETA
AGONIS (reliever/pelega)
• DOSIS INHALER STEROID (controller)
MENURUN  100 MCGR/HARI (target –
berapa lama?-individual)
• KEKAMBUHAN BERKURANG
• PEF > 80% PREDIKSI NORMAL

GINA 2015; Fundamental Critical Care and Support 2005

 OBAT ASMA YANG
TERSEDIA (Indonesia)
KORTIKOSTEROID INHALASI:
• Budesonide
• Flutikason
• Beclomethason
KORTIKOSTEROID SISTEMIK:
• Metilprednisolon tablet/injeksi
• Deksametason tablet/injeksi
• Triamsinolon tablet/injeksi
• Prednison tablet
• Betametason tablet
BETA AGONIST INHALASI:
• Formoterol(LABA)
• Salmeterol(LABA)
• Procaterol
• Salbutamol
• Terbutalin
 OBAT ASMA YANG
TERSEDIA (Indonesia)
 BETA AGONIST SISTEMIK
• Epinefrin injeksi
• Salbutamol tablet/injeksi
• Terbutalin tablet/injeksi
 ANTIKOLINERGIK INHALASI
• Ipatrium bromid
• Tiotropium bromid
 BRONKODILATOR LAIN.
• Aminofilin tablet/injeksi
• Aminofilin lepas lambat (controlled release) tablet
 ANTI INFLAMASI LAIN (Non steroid-Antileukotrien).
• Zafirlucast tablet
• Montelucast tablet
 COPD(PPOK)
• SMOKER
• > 40 years old
• Acute on chronic disease
• Febrile+leukocytosis  acute exacerbation
• Treat :
antibiotics+steroid+bronchodilator
• Plus comorbid factor  refer to hospital
 PLEURAL EFFUSION
• SILENT AUSCULTATION
• TRIAL PROOF PLEURAL PUNCTION
• DISCHARGE 500-700 CC ONLY
• IF BLOODY EFFUSION  REFER TO
HOSPITAL
• OXYGEN 3-5 L/MINUTE CANULE
• FAWLER POSITION
 TBC PARU MILIER
 SESAK NAFAS
 TAMPAK KURUS
 SIANOSIS
 DEMAM TANPA LEKOSITOSIS
 PENURUNAN KESADARAN SOMNOLEN
 RADIOLOGIK TAMPAK BINTIK MILIER
MERATA SELURUH LAPANGAN PARU
 SERING BATUK TANPA DAHAK—BTA (-)
 TERAPI OBAT ANTI TBC (OAT)+Steroid
 GAGAL NAFAS
Gagal nafas terjadi bila kebutuhan proses
metabolik tubuh tidak dapat dicukupi
oleh sistem pernafasan. Kebutuhan
metabolik ini berupa eliminasi CO2 dan
oksigenasi hemoglobin
 GAGAL NAFAS
• HYPOKSEMIA : kandungan O2 arteri
<50 torr  inflamasi parenkhim,
edema paru
• HIPERKAPNEA : kandungan CO2
>50 torr  obstruksi sal.nafas,
neuromuskuler
 GAGAL NAFAS
 AKUT
 KRONIK
 ACUTE on CHRONIC
 PENYEBAB GAGAL NAFAS
AKUT
Gagal nafas akut timbul dari bermacam kondisi klinis
 Primer paru:
 Infeksi: pneumonia berat, Acute Lung Injury (ALI), Acute
Respiratory Distress Syndrome (ARDS)
 Pulmonary embolism, Aspiration, Status Asmatikus
 Cancer: Primary Lung Cancer, Metastatic
 Kelainan sistemik nonpulmoner:
 Infeksi: Septicemia, Acute Lung Injury (ALI), Acute
Respiratory Distress Syndrome (ARDS)
 Metabolic: Uremia
 Kardial: lung edema disebabkan gagal jantung
 Penyebab gagal nafas akut pada dewasa  multifaktor.
 Mixed
 Hypoxemia
 Penyebab hipoksemia lain yang jarang
ditemukan:
 Penurunan diffusi oksigen melalui
alveolocapillary membrane complex
akibat dari edema interstitial, inflamasi,
fibrosis interstitial
 Alveolar hypoventilation
 High altitude (outside negative
pressure)
 PATOFISIOLOGI
GAGAL NAFAS AKUT

• HIPOKSEMIA: gangguan ventilasi alveolar dan perfusi

pulmoner  pneumonia, Acute Lung Injury (ALI),Acute
Respiratory Distress Syndrome (ARDS),aspirasi, lung
edema, Asma,atelektasis
• HIPERKAPNEA: sering terjadi krn volume tidal
menurun  COPD, obat, neuromuskular (miastenia
gravis,dll), distrofi otot, malnutrisi,kelelahan
• KOMBINASI HIPOKSEMIA & HIPERKAPNEA
 MANIFESTASI KLINIS
GAGAL NAFAS AKUT
1. Gangguan Kasus flu burung: gejala flu 2-3 hari,
kesadaran: gelisah, diikuti sesak nafas akut
somnolen, koma
2. Sesak nafas&
meningkatnya
penggunaan otot
pernafasan: retraksi
interkostal, nafas
paradoksal
3. Sianosis: bibir, lidah,
mulut
4. Takhikardi, hipertensi
 ACUTE RESPIRATORY DISTRESS
SYNDROME (ARDS)

 ARDS is another type of acute respiratory

failure (non-cardial lung edema)
 Increased alveolar capillary permeability in
ARDS have centered upon
 the neutrophil,
 the macrophage,
 the pulmonary vascular endothelium and
 The cytokine imbalance
 PATHOPHYSIOLOGY ARDS
 Neutrophil sequestration and migration
within the lung remain histologic
hallmarks of ARDS
 Chemotactic stimuli released within the
lung and the activation of neutrophils by
circulating mediators :
– TNFa ,
– IL-1, and
– IL-8
CLINICAL MANIFESTATIONS OF
ACUTE RESPIRATORY FAILURE
 mental status : GELISAH ---- SOMNOLEN
 Evidence of increased work of breathing:
– nasal pharing
– use of accessory respiratory muscles
– intercostal/suprasternal/supraclavicular retraction
– Tachypnea
– Hyperpnea
– paradoxical or dysynchronous breathing pattern
 Cyanosis of mucosal membranes (tongue, mouth) or nail beds
CLINICAL MANIFESTATIONS
ARF
 MANAGEMENT
CONSIDERATIONS
 Oxygen Supplementation
 Nasal Cannula

 Air-Entrainment Face Masks ("Venturi

Masks")
 Aerosol Face Mask

 Reservoir Face Masks

 High Flow Nasal Canule (60 L/minute)

 Noninvasive Positive-Pressure Ventilation

MANAGEMENT
 Noninvasive Positive-Pressure
Ventilation (NIPPV)

 Do not use NPPV for rapidly

deteriorating patients at risk for sudden
respiratory arrest.
 Do not use NPPV unless the physician
or respiratory care practitioner is familiar
with its technical operation.
 Consider NPPV primarily in alert,
oriented, hemodynamically stable, and
cooperative patients.
 Pharmacologic Adjuncts

1.Beta2-Agonists
2.Anticholinergic Agents
3.Corticosteroids
4.Theophylline preparations
MANAJEMEN GAGAL NAFAS
1. 1.Oksigenasi:
* kanul nasal,
* masker venturi,
* masker dng aerosol
* masker reservoir
* high flow nasal canule (HFNC)
2. VENTILASI TEKANAN POSITIP NONINVASIF (NIPPV)
3. INTUBASI TRAKHEA
4. FARMAKOLOGIK: beta-agonis, antikolinergik, kortikosteroid,
aminofilin, epinefrin
5. ANTIBIOTIK : pada infeksi paru, sistemik (sepsis)
6. MUKOLITIK
 GAGAL NAFAS AKUT

KESIMPULAN:
- Sebab pulmoner atau non-pulmoner (sistemik)
- atau hiperkapnea, campuran
- Patofisiologi: gagal ventilasi/perfusi atau defek
alveolar, volume tidal ↓
- Klinis: gagal perfusi pada organ,Multi Organ
Dysfunction Syndrome (MODS)
- Manajemen: oksigenasi, non-invasif, invasif,
farmakologik
 EMBOLI PARU
SESAK NAFAS AKUT
TANPA SIMPTOM PARU SEBELUMNYA
ADA FAKTOR RISIKO:
Trauma
Non Trauma (medical)
 Medical Risk factor
 Hypercoagulable state predisposing to the
thromboembolic complications
 Sepsis
 Cancer & Radio-Chemotherapy
 Autoimmune disease
 Deep Vein Thrombosis
 Cardiac Arrythmia
 Congestive Heart Failure
 Elderly debillity
 Prolonged inactivity/bedrest
 Pulmonary Embolism
Three major clinical presentations:

1. dyspnea with or without pleuritic chest pain

and hemoptysis
2. hemodynamic instability and syncope
(usually associated with massive pulmonary
embolism)
3. mimicking indolent pneumonia or heart
failure, especially in the elderly
 Clinical
 Abrupt onset dyspnea
 Chest pain → non cardial
 Cyanosis
 Pulmonary hypertension → ECG → Right
Axis
 Elevation Jugular vein tension
 Common symptoms of
Acute PE
• PIOPED study found
– Dyspnea
– Pleuritic chest pain
– Tachypnea (resp rate  20 / min)
in 97% of patients with angiographic proven
PE
• The absence of this triad reduces the clinical
probability of PE
 Estimating Clinical Probability of
Pulmonary Embolism
High Risk factor present (80-100% probable)
Otherwise unexplained dyspnea, tachypnea, or
pleuritic chest pain
Otherwise unexplained radiographic or gas
exchange abnormality
Intermediate Neither high nor low clinical probability (20-79%
probable)
Low Risk factor not present (1-19% probable)
Dyspnea, tachypnea, or pleuritic pain possibly
Present but unexplained by another condition
Radiographic or gas exchange abnormality
Possibly present but explainable by another
condition

Am J Respir Crit Care Med. Vol 159: 1-14; 1999

 Labotarory&Radiology
 High D-dimer >1500
 Hypercoagulable state: haematocrite, fibrin
 Lower PO2 in BGA
 Deep infiltrate unilateral in CXR or Thorax
USG (Pneumonia like appearance)
 Thorax CT Scan: lung consolidated
unilateral
 Scintigraphy: segmental lung necrosis
 Diagnostic Test
• Ventilation-perfusion lung scan
  2 moderate-to-large perfusion defects (>25% of a lung
segment) with intact ventilation in a clear chest x-ray in the
involved area
• Widened (A-a) O2 gradient
– low PO2, low PCO2
• Chest x-ray
– central pulmonary artery engorgement, paucity of
peripheral vessels (Westermark sign)
• Electrocardiogram
– nonspecific ST-T changes, right-axis, S1-Q3-T3, P-
pulmonale
 Suspect Pulmonary Embolism ?
Give heparin IV and order V/Q scan

Low V/Q probability, Intermediate V/Q probability, High V/Q probability +

low clinical probability Low or high V/Q prob with high clinical probability
discordant clinical probability

_
+
No treatment Leg Ultrasound Treat

+
Pulmonary
Probability Angiography
Probability V/Q Clinical
V/Q Clinical 3. Low High
1. Low Mid 4. Mid Mid / High
2. Mid Low 5. High Low / Mid

Am J Respir Crit Care Med. Vol 159: 1-14; 1999

 PNEUMOTORAK
 RONGGA PLEURA TERISI UDARA
 PENYEBAB:
 TRAUMA
 NONTRAUMA:
 PRIMER : KONGENITAL
 SEKUNDER :
 PPOK
 BEKAS TBC
 ASMA
 KLINIS
• BATUK
• MENDADAK SESAK NAFAS
• ADA PENYAKIT PARU YG MENDASARI
• BISA FATAL PADA PNEUMOTORAK VENTIL
• KETINGGALAN GERAK DADA
• AUSKULTASI DADA: VESIKULER NEGATIP
• RONTGEN:
– UDARA DALAM PLEURA
– MEDIASTINUM TERDESAK KEARAH PARU
SEHAT
 TERAPI
• TUSUKKAN JARUM SUNTIK PADA
DADA
• PASANG DRAIN TORAK
• PASANG MINI WSD DI SIC 1 ATAU 2
• POSISI FAWLER (½ DUDUK)
• OKSIGEN 3-4 L/MENIT
• EVALUASI RONTGEN SETELAH
KLINIS MEMBAIK
 Bronchiectasis

Kelainan anatomis bronkus dengan

diameter < 3 mm (kebanyakan), berupa
kerusakan jaringan elastik sehingga
terbentuk kantung2 (saccus)  ektasis
Disebabkan:
– infeksi kronik paru pada masa muda
– tbc yang mengenai bronkus
– Merokok
 BRONCHIECTASIS
KLINIS :
 Hemoptisis/hemoptoe/batuk darah
kambuhan
 Riwayat penyakit paru kronis :
 tbc paru,
 COPD/merokok
 Anemia
 Risiko kematian o.k. asfiksia
MANAJEMEN BRONKIEKTASIS
 Posisi tidur miring pada sisi sakit
 Antitusif
 Koagulansia
 Antibiotika
 Transfusi bila Hb < 8,0 gr%
 Oksigenasi
 Lobektomi/pneumektomi emergency bila
hemoptysis>500 cc/24 jam
ALHAMDULILLAH

TERIMA KASIH