DYSPNEA

Allen Widysanto

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MAJOR SYMPTOMS OF PULMONARY
DISEASE
 DEFINITION

Difficult, laboured, uncomfortable

breathing. Subjective feeling which may
DYSPNEA be associated with mild anxiety or
extreme fear

HYPERVENTILATION Rapid-deep breathing

TACHYPNEA Rapid-shallow breathing

Sensation of not being able to get

BREATHLESSNESS enough air
 ETIOLOGY

LUNG HEART MUSCULOSCELETAL

DYSPNEA

METABOLIC KIDNEY BRAIN

 PROBLEM

?????
Pulmonary Cardiac
dyspnea dyspnea

EVALUATION OF A PATIENT WITH DYSPNEA ARE ITS DURATION, CONSTANCY

OR INTERMITTENCY
Edema paru kardiogenik vs nonkardiogenik
• Riwayat: didahului oleh
penyakit jantung
• Pemeriksaan fisis;
kardiomegali, gallop, efusi
pleural bilateral.
• Foto toraks: kardiomegali,
efusi pleura bilateral, Kerley B
line
• EKG: LVH, infark
• Tekanan baji paru > 12
• Respons terhadap diuretik baik
• Riwayat etiologi antara lain
trauma, infeksi, inhalasi gas
toxic, sepsis.
• Pemeriksaan fisis: ukuran
jantung normal, gallop –
• Kardiomegali dan efusi pleura
sering negatif, Kerley B line
sering negatif
• Perubahan akibat iskemik
sering dijumpai
• Tekanan baji < 12
• Respons terhadap diuretik
tidak baik
• Kerley B lines
 PULMONARY DYSPNEA

OBSTRUCTION

RESTRICTION
VENTILATION
IMPAIRMENT
IMPAIRMENT OF
OXYGEN TRANSFER
DIFFUSION
SHUNTING
PERFUSION ANEMIA
INADEQUATE
CARDIAC OUTPUT
 3 MAJOR CATEGORIES

DYSPNEA

CHRONIC RECURRENT
ACUTE DYSPNEA PROGRESSIVE PAROXYSMAL
DYSPNEA DYSPNEA
 Acute dyspnea
LOWER UPPER
RESPIRATORY RESPIRATORY
TRACT TRACT

ACUTE PULMONARY ACUTE LARYNGEAL

EDEMA EDEMA

PULMONARY INHALED FOREIGN

THROMBOEMBOLISM BODY

NEOPLASMA
PNEUMONIA

TRACHEA
SPONTANEOUS OBSTRUCTION/COMPRESSION
PNEUMOTHORAX
INFECTIOUS CROUP
ATELECTASIS
 SIGNS AND SYMPTOMS

• Depend on the causa

UPPER AIRWAY OBSTRUCTIONS ARE CHARACTERIZED BY
STRIKING INSPIRATORY STRIDOR, INSPIRATORY WHEEZING

LARYNGEAL OR
TRACHEAL
OBSTRUCTION
 Chronic progressive dyspnea
CONGESTIVE
INTERSTITIAL DISEASE
HEART (Occupational Lung Diseases)
FAILURE

CHRONIC OBSTRUCTIVE
PULMONARY
DISEASE

ASTHMA

HYPERSENSITIVITY
PNEUMONIAS SARCOIDOSIS
COLLAGEN DISEASES
(scleroderma, SLE,
GRANULOMATOUS Polyarteritis nodosa,
DISEASE Wagener’s
granulomatosis,
rhematoid lung )
RECURRENT PAROXYSMAL DYSPNEA

ASTHMA

Allergen LVH
Viral MS

Bacterial
Parasit

Fungi
 ONSET of BREATHLESSNESS

SUDDEN
ONSET

Pulmonary embolus A few hour

Pneumotoraks
Inhalation of a foreign body
Asthma
Over days or
Pulmonary edema weeks

Accumulation of PE GRADUAL
Partial/complete airway occlusion ONSET OVER
due to growth of lung cancer MONTHS OR YEARS

COPD
Lung fibrosis
Non-respiratory causes
(anemia, hyperthyroidism)
 RISK FACTORS FOR RESPIRATORY DISEASE

• Childhood respiratory illness

• Tobacco smoking (pack year smoking)
• Family history ( asthma and atopy, emphysema, thromboembolic disease)
• Occupational and home environment
• Exposure to animals and birds
• Infectious contacts
• Immunosupression (HIV, immunosuppresant drugs, DM)
 DIAGNOSIS
Presenting complaint-breathlessness
Consider

Respiratory Cardiovascular Other

causes causes causes

Differentiate between main groups of causes

Exacerbating and relieving factors
Associated features
Risk factors

Identify likely organ system involved

Consider specific differential diagnosis

eg. respiratory

COPD Asthma Pulmonary embolus Pulmonary fibrosis Pleural effusion

Further history + examination

Differentiate between specific causes
 MANAGEMENT STRATEGIES FOR ACUTE DYSPNEA

• Several validated and more sensitive one-dimensional

instruments can be used to measure the patient’s level of
dyspnea such as : The modified Borg Scale
The most important : Elicit underlying diseases

• Using Medical Research Council (MRC) dyspnea score

1. Gets breathless with strenuous exercise
2. Gets short of breath when hurrying on the level or walking up a slight hill
3. Walks slower than people of the same age on the level because of
breathlessness, or has to stop for breath when walking at own pace on the
level
4. Stops for breath after walking about 100 yards or after a few minutes on
the level
5. Too breathless to leave the house or breathless when dressing or
undressing
 FOUR KEY QUESTIONS HAVE
BEEN SUGGESTED TO ELICIT
UNDERLYING DISEASE

• Are you short of breath?

• Do you have any chest pain?
• What were you doing before and at the onset of breathlessness?
• Do you have any major medical or surgical conditions?
 THE BORG SCALE

• The Borg Scale is used to measure your sensation

of breathlessness during various activities.
Monitoring your breathlessness can help you
safely adjust your activity by speeding up or
slowing down your movements. It can also
provide important information to your health care
provider.
0 No breathlessness at all
0.5 Very very slight ( just noticable)
1 Very slight
2 Slight breathlessness
3 Moderate
4 Somewhat severe
5 Severe breathlessness
6
7 Very severe breathlessness
8
9 Very very severe (almost maximum)
10 Maximum
 MANAGEMENT STRATEGIES

Decreasing the central drive to breathe

Reducing the sense of effort or improve respiratory muscle function

Altering the central perception of dyspnea

 Decreasing central drive to breathe

• Oxygen
• Opiates
• Anxiolytics
 Reduce the sense of effort and improve
respiratory muscle function

• Hyperinflation as a primary mechanism of dyspnea :

breathing techniques and changing breathing paterns
for reducing dyspnea.
• The patient should be allowed to get the most
convenient position until she/he experiences the least
shortness of breath
• NISV
• Pursed lip breathing
Help the patient to maintain a slow, rhythmic and deep pattern of breathing
 Alter the central perception of dyspnea

• When acute dyspnea persists despite optimal

treatment, care focuses on the symptom rather than
the disease.
• Breathing-relaxation training
• Counseling and support
• Distraction with music
• Acupunture /acupressure
• Chest wall vibration
• Neuro-electrical muscle stimulation
 COMPLICATION

RESPIRATORY
FAILURE

Inability of the respiratory system to maintain a normal state of gas exchange

from the atmosphere to the cells as required by the body = To maintain
normal arterial blood PO2, PCO2 and pH
• Respiratory failure is present if:
1. PaO2 is < 60 mmHg or
2. PaCO2 is > 45 mmHg, except when elevation in PCO2
is compensation for metabolic alkalosis

PaO2 < 60 mmHg : Hypoxemic respiratory failure

PaCO2 > 45 mm Hg: Hypercapnic respiratory failure

 TREATMENT
• Supplemental oxygen
• Bronchodilators
• Diuretics
• Antibiotics
• Mechanical ventilation

THE UNDERLYING DISEASE LEADING TO

RESPIRATORY FAILURE MUST BE ADDRESSED
 DEVICE

Nasal Flow rate 2-6 L/min

cannula
Low flow delivery
device
Simple Flow rate 4-8 L/min
mask

Venturi Flow rate 2-12 L/min

mask
High flow delivery
device

NRM Flow rate 6-15 L/min

 OTHER DRUGS

• Corticosteroids
• Leucotriene antagonists and inhibitors
• Expectorant
• Sedative ( Lorazepam )and muscle relaxant ( Propofol)
particularly for the patients who are receiving
mechanical ventilator.
In patients not receiving MV, sedative drugs (
barbiturates, benzodiapines, opioids) are
contraindicated.
• Chest physiotherapy
 MECHANICAL VENTILATION
• Indications for intubation and MV:
Physiologic Clinical

Hypoxemia persists after O2 Altered mental status with

administration impaired airway protection

Respiratory distress with

PCO2 > 55 mmHg with pH < 7.25 hemodynamic instability

Vital capacity < 15 mL/kg with

Upper airway obstruction
neuromuscular disease

High volume of secretions not

cleared by patient, requiring
suctioning
 4 take home messages

• Dyspnea = Shortness of breath is one of the major

symptoms of pulmonary disease which is giving
sensation such as uncomfortable breathing .
• There are many etiologies of shortness of breath
either from the lung or the other organs.
• Management of dyspnea is depend on the
underlying disease, however supplemental
oxygen is a must.
• Respiratory failure ( type 1 or type 2 ) is the
complication of unmanaged shortness of breath.
• PENATALAKSANAAN SERANGAN AKUT

ASMA
OBSTRUCTION

REVERSIBILITY

VARIABILITY
• Obstruction
Ratio
FEV 1
 75% atau FEV 1  80% pred
FVC
 Reversibility
At least 12 percent improvement in FEV1 or 15 %
improvement either spontaneously, after inhalation of
a bronchodilator or in response to a trial of glucocorticoid
Variability
PFR night – PFR morning
X 100 %
½ ( PFR night + PFR morning)
 Penatalaksanaan Eksaserbasi di Rumah Sakit (1)
Penilaian awal (sesuai derajat berat/ringannya serangan asma)
Riw. penyakit, pemeriksaan fisik, penggunaan otot bantu napas, frek. nadi, frek. napas,
APE atau VEP1, saturasi O2, AGD pada pasien berat & pemeriksaan lain jika ada indikasi.

Terapi awal
• Inhalasi agonis  2 aksi singkat, dg nebulisasi, TERUS MENERUS selama 1 jam
• Oksigen untuk mencapai saturasi O2  90% (95% pada anak-anak)
• Kortikosteroid sistemik jika tidak ada respons segera/jika akhir-akhir ini mendapat steroid
peroral atau jika serangan asmanya berat
• Sedasi merupakan kontraindikasi pada penanganan serangan akut/eksaserbasi

Penilaian ulang : tanda-tanda fisik, APE, saturasi O2, & pemeriksaan lain yang diperlukan

Tingkat Sedang Tingkat Berat

• APE 60-80% dari nilai prediksi/terbaik • APE < 60% dari nilai prediksi/terbaik
• Pem.fisik : gejala asma sedang, penggunaan • PF: Gej. asma berat, istirahat ada retraksi dada
otot bantu napas • Riw. risiko tinggi, tak ada perbaikan stl t/ awal
• Inhalasi agonis  2 dan antikolinergik setiap 60 • Inhalasi agonis  2 tiap 60 menit atau kontinyu
menit  inhalasi antikolinergik
• Pertimbangkan kortikosteroid • Oksigen, Kortikosteroid sistemik, IV magnesium
• Lanjutkan pengobatan 1-3 jam, sepanjang ada • Pertimbangkan agonis  2 SK, IM, atau IV
perbaikan Allen W, RS Jati Husada, 121106
 Penatalaksanaan Eksaserbasi di Rumah Sakit (2)
Respons baik 1-2 jam
• Respons menetap 60 menit
sesudah t/ terakhir
• Pem. fisik normal
• APE > 70%
• Tidak ada distres
• Saturasi O2 >90% (anak 95%)
Rawat jalan :
• Agonis  2 inhalasi
• Pertimbangkan kortikosteroid
oral (pada kebanyakan pasien)
• Pendidikan pasien
• Minum obat secara benar
• Tinjau rencana kerja
• Tindak lanjut pengobatan
secara tepat
Dipulangkan jika APE >70% &
menetap dalam pengobatan
peroral/inhalasi
Respons tidak lengkap
1-2 jam
• Riw. risiko tinggi
• Pem. fisik gejala asma
ringan/sedang
• APE < 60%
• Saturasi O2 tidak membaik
Rawat inap (bangsal):
• Oksigen
• Inhalasi agonis  2  inhalasi
antikolinergik
• Kortikosteroid sistemik
• IV magnesium
• Pertimbangkan aminofilin IV
• Pantau APE, saturasi O2, nadi.
Perbaikan Tidak ada perbaikan
Allen W, RS Jati Husada, 121106
Respons buruk dalam 1-2
jam
• Riw. risiko tinggi
• Pem. fisik gejala asma berat,
mengantuk, & bingung
• APE <30%
• PCO2 >45 mmHg
• PO2 <60 mmHg
Rawat ICU :
• Oksigen
• Inhalasi agonis  2  inhalasi
antikolinergik
• Kortikosteroid IV
• Pertimbangkan agonis  2 IV
• Pertimbangkan teofilin IV
• Mungkin perlu intubasi &
ventilasi mekanis
Masuk ICU jika tidak ada
perbaikan dalam 6-12 jam
• PENATALAKSANAAN SERANGAN

ARDS
 TERAPI

Terapi pada ARDS dapat dibagi dalam tiga bagian, yaitu :

• Memperbaiki kelainan yang mencetuskannya.
Meliputi pemberian antibiotik, penggantian volume cairan dan
atau darah pada syok hipovolemik. Antidot / eliminasi /
neutralisasi pada kelebihan dosis obat dan kemoterapi pada
limfoma.
• Mencegah atau memulihkan mekanisme cedera kapiler alveol.
Pemberian metilprednisolon dosis tinggi dimaksudkan untuk
usaha tersebut, tetapi peran steroid tersebut masih kontroversi.
• Mengurangi konsekuensi patofisiologis melalui terapi suportif
 TERAPI

Cedera ARDS akan minimal karena :

a. Berkurangnya jumlah edema paru melalui penurunan rasio
pembentukan cairan atau peningkatan rasio pengeluarannya.
Untuk itu dapat diberikan :
Diuretik atau dialisis
Obat kardiotonik
Koloid, albumin atau koloid artifisial (Heta strach)
peranannya kecil.
b. Meminimalkan efek pada pertukaran gas
Terapi O2 dengan ventilasi mekanis dan atau PEEP adalah pilar
utama terapi suportif pada ARDS.
 TERAPI

Tujuan PEEP dan ARDS akan menyebabkan :

• Peningkatan PaO2 sehingga menurunkan pirau intra
pulmoner sebagai akibat menurunnya curah jantung.
• Penurunan preload
• Redistribusi cairan edema dari alveol ke ruang
interstitial.
• Teratasinya kebocoran kapiler.
• Penggunaan kembali unit-unit paru yang kolaps.
• Kekakuan miokardial yang terjadi sekunder akibat
iskemia dan stimulasi katekolamin.
 TERAPI
Untuk mengurangi efek pada pertukaran gas dapat dilakukan hal-
hal berikut :
• Suplemen O2, peningkatan FiO2 akan memperbaiki PaO2.
• Ventilasi mekanis, Intermittent positive – pressure ventilation
(IPPV) dapat digunakan untuk menyingkirkan kerja pernapasan
yang berat.
• Positive end-expiratory pressure (PEEP/CPAP) dapat
memeperbaiki tekanan O2 arteri, dapat meningkatkan kapasiti
residu fungsional, memperbaiki compliance dan menurunkan
meluasnya pirau kanan ke kiri parenkim paru.
• Extracorporeal membrane Oxygenation (ECMO). Dari
pengalaman klinis tidak menunjukkan perbaikan survival yang
berarti dibandingkan dengan cara konvensional (IPPV dan
PEEP).
Lung protective ventilation dengan volume tidal
kecil
Ventilasi dengan volume tidal kecil dan tekanan jalan
napas yang terkendali dapat mengurangi cedera paru
akibat ventilator karena overdistensi. Volume tidal paru
dianjurkan berkisar 4-6 ml/kg berat badan.
 THE MEDULLARY RESPIRATORY CNTRE

Dorsal respiratory Nucleus of the tractus solitarius

centre Consists mainly inspiratory neurons

Retrofacial nucleus, nucleus ambiguus and

Ventral respiratory
nucleus retroambiguus
centre
Consists of Inspiratory and Expiratory cells
REFLEX MECHANISMS OF RESPIRATORY
CONTROL

HERING-BREUER INFLATION REFLEX

HERING-BREUER DEFLATION REFLEX

PARADOXICAL REFLEX OF HEAD

 HERING-BREUER INFLATION REFLEX

• Stimulus : Lung inflation

• Receptor : Stretch receptor within smooth muscle
of large and small airways
• Afferent pathway : Vagus
• Effect :
• Respiratory : Cessation of inspiratory effort,
apnea, or decreased breathing frequency,
bronchodilation
• Cardiovascular : increased heart rate, slight
vasoconstriction
 HERING-BREUER DEFLATION REFLEX

• Stimulus : Lung deflation

• Receptor : possibly J receptors, irritant receptors
in lungs or stretch receptors in airways
• Afferent : Vagus
• Effect : Hyperpnea
 PARADOXICAL REFLEX OF HEAD

• Stimulus : Lung inflation

• Receptor : Stretch receptors in lungs
• Afferent : Vagus
• Effects: inspiration