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Meidy 4
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RESPIRATORY FAILURE Ketidakmampuan paru-paru untuk memenuhi
tuntutan metabolisme tubuh. Ini dapat dari
kegagalan oksigenasi jaringan dan / ataukegagalan homeostasis CO2
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RESPIRATORY FAILURE
Definisi Respirasi adalah pertukaran gas antara
organisme dan lingkungannya. Fungsi sistem
pernapasan adalah untuk mentransfer O2 dari
atmosfer ke darah dan menghilangkan CO2 daridarah.
Kegagalan klinis pernapasan didefinisikan sebagai
PaO2 50 mmHg.
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Respiratory system includes:
CNS (medulla)Peripheral nervous system (phrenic nerve)Respiratory muscles
Chest wallLungUpper airwayBronchial tree
AlveoliPulmonary vasculature
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Clinical Manifestation
Hypercapnia
somnolence
lethargy
coma
asterikscan not be quiet
tremor
garbled speech
headache
papil edema
Hypoxemia
anxiety
tachycardia
tachypnea
diaphoresisarrhythmias
change in mental status
confused
cyanosis
hypertension
hypotension
convulsions
lactic acidosis
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Cause of respiratory failure
A. Extrinsic lung disorders
1. The emphasis of the respiratory center
- An overdose of the drug (narcotic
sedative)
- Trauma cerebral or myocardial
- Poliomyelitis bulbar
- Encephalitis
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2. Neuromuscular disorders
- Cervical spinal injury
- Guillan barre syndrome
- Amiotrofik lateral sclerosis
- Miatenia gravis
- Muscular dystrophy3. Pleura and chest wall disorders
-Chest Injury
-pneumothorax- Pleural effusion
-Kifoskoliosis
-Obesity: pickwickan Syndrome
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B. Intrinsic Pulmonary Disorder
1. Diffuse obstructive disorders
a. Emphysema, COPD
b.Asma, status asthmaticus
c. cystic fibrosis
2. Restrictive lung disorders
a. Interstitial fibrosis due to various reasons
b. sarcoidosis
c. scleroderma
d. pulmonary edema
e. Ateletaksis
f. pneumonia consolidation3. Pulmonary vascular disorders
a. pulmonary embolism
b. severe emphysema
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RESPIRATORY FAILURE
HYPERCAPNIC HYPOXEMIC
ACUTE CHRONIC ACUTE CHRONIC
CLASSIFICATION
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Hypoxemia (Type 1)
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PATHOPHYSIOLOGY
Hipoksia adalah pengiriman oksigen yang
tidak memadai ke jaringan dan disebabkan
oleh salah satu dari lima mekanisme yang
berbeda. Hipoksia secara sewenang-wenang
didefinisikan sebagai PaO2 60 mmHg.
Hipoventilasi: Meningkatnya PaCO2
menggantikan oksigen dari alveolus,menurunkan PaO2 dan mengurangi gradien
difusi O2 melintasi membran paru
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Right-to-left shunting: Unoxygenated blood
enters the systemic circulation. This may occur
secondary to perfusion of underventilated
lung or with congenital heart anomalies.
Ventilation/perfusion mismatch: Results from
regional alterations of ventilation or
perfusion.
Diffusion impairment: Caused by impairment
of the alveolar blood barrier.
Low FiO2: The cause of high-altitude hypoxia
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PATHOPHYSIOLOGY
HYPOXEMIA
Decreased PIO2or fraction
Hypoventilation
Impaired diffusion
Shunt
V/Q mismatch
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CLINICAL FEATURES
Signs and symptoms are nonspecific, rangingfrom tachycardia and tachypnea to centralnervous system (CNS) manifestations such as
agitation, seizures, and coma. At PaO2 20 mmHg, there is a paradoxical
depression of the respiratory drive.
Dyspnea mungkin saja atau mungkin tidakhadir, dan sianosis merupakan indikatorsensitif dari PaO2 status.
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DIAGNOSIS AND DIFFERENTIAL
Pulse oximetry is a useful screening test, but
arterial blood gas analysis defines the
diagnosis.
pemeriksaan tambahan serupa digunakan
untuk menentukan penyebab dyspnea
mungkin menjelaskan kelainan yang
menyebabkan hipoksia.
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EMERGENCY DEPARTMENT CARE AND
DISPOSITION
Hipoksia diperlakukan sama seperti dyspnea,
dukungan, mengidentifikasi, dan agresif
mengobati gangguan yang mendasari,
berusaha mempertahankan PaO2 60 mmHg.
Semua pasien dengan hipoksia persisten
memerlukan rawat inap sampai kelainan
memadai dan stabil. Sampel darah arterisering mungkin memerlukan garis arteri.
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Hypercapnia (Type 2)
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PATHOPHYSIOLOGY
didefinisikan sebagai 45 mmHg PaCO2 dandisebabkan oleh hipoventilasi. Hal ini hampirtidak pernah disebabkan oleh penyakit paru-paru
intrinsik atau peningkatan produksi CO2. Menit ventilasi tergantung pada laju pernapasan
dan volume tidal; menurun aku baik akanmenyebabkan hipoventilasi.
Gangguan yang menyebabkan hipoventilasi danhiperkapnia bervariasi, tetapi efeknya selaludapat ditelusuri hubungan menit ventila
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Alveolar ventilation is less than minute
ventilation; although this term is moreappropriately used in describing ventilation,
alveolar ventilation is impractical to measure. Ventilasi alveolar kurang dari satu menit
ventilasi, meskipun istilah ini lebih tepatdigunakan dalam menggambarkan ventilasi,ventilasi alveolar tidak praktis untukmengukur.
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Kedua parameter di menit ventilasi
dikendalikan melalui keluaran saraf eferen dari
kemoreseptor di medula.
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CLINICAL FEATURES
Signs and symptoms of hypercapnia aredependent on the rate and degree of elevation.Acute rises are associated with an increase in
intracranial pressure, confusion, lethargy,seizures, and coma. On physical exam, asterixismay also be found.
Acute changes to PaCO2 100 mmHg may lead to
cardiovascular collapse. In acute retention, foreach 10-mmHg ncrease of PaCO2 , the pH willdecrease 0.1 U.
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Chronic changes in PaCO2 may be well
tolerated. To maintain a neutral milieu, the
kidneys retain [HCO3]. In the chronic setting,
for every 10 mmHg of PaCO2 over 40 mmHg,[HCO3 ] increases 3.5 meq/L.
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DIAGNOSIS AND DIFFERENTIAL
Given clinical suspicion, the diagnosis will be
confirmed
on arterial blood gas analysis. See Table
32-2 for further differential diagnosis.
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EMERGENCY DEPARTMENT CARE
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EMERGENCY DEPARTMENT CARE
AND DISPOSITION
Hiperkapnia diperlakukan dengan cara yang samasebagai hipoksia: mengidentifikasi ancamanterhadap kehidupan, mengevaluasi dan agresifmengobati kekurangan dalam ABC.
Identifikasi etiologi yang mendasari akanmemungkinkan pengobatan terfokus.
Sebagai contoh, dosis narkotika menyebabkandepresi pernafasan akan menanggapi nalokson,
sementara ventilasi tidak efektif sekunder untukkelemahan otot pernafasan akan meresponhanya untuk ventilasi dibantu atau mekanis.
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Oksigen tambahan harus diberikan untuk
mempertahankan tingkat yang dianggap
normal untuk pasien. Oksigen tidak harus
ditahan berdasarkan khawatir'' penurunanritme pernafasan.'' Hipoksia akan membunuh
pasien, sementara hanya hiperkapnia ekstrim
akan melakukan hal yang sama.
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BiPAP or CPAP may be used as a bridge until a
definitive diagnosis of hypercapnia and a
treatment plan can be made, but it is never a
longterm option. If all else fails, mechanicalventilation is indicated.
Disposition depends on the underlying cause
and frequently requires admission to amonitored bed.
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Respiratory Failure : Medication
Farmakoterapi adalah untuk edema paru
kardiogenik dan eksaserbasi akut PPOK
Tujuan terapi edema paru kardiogenik:
mencapai tekanan kapiler paru irisan 15-18
mm Hg dan indeks jantung lebih besar dari 2,2
L/min/m2while mempertahankan tekanan
darah adekuat dan perfusi organ
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Respiratory Failure : Medication
Furosemide : IV
Metolazone: sebagai terapi tambahan padapasien awalnya refrakter terhadap
furosemide dan digunakan dalam kombinasi
dengan furosemide untuk diuresis lebihagresif
Diuretics : 1stline
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Respiratory Failure : Medication
Mengurangi kebutuhan oksigen miokard
dengan menurunkan preload dan afterload Nitrogliserin sublingual: berguna dalam
pasien yang datang dengan edema paru akut
dengan tekanan darah sistolik paling sedikit100 mm Hg
Nitrates
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Respiratory Failure : Medication
Topical: wajar pada pasien menyajikan
dengan kelas I-II CHF IV: Tanda-tanda parah edema paru atau HF
Nitroprusside natrium: menghasilkan
vasodilatasi vena dan sirkulasi arteri, Padadosis yang lebih tinggi, hal itu mungkin
memperburuk iskemia miokard dengan HR
Nitrates
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Respiratory Failure : Medication
Morphine IV is an excellent adjunct in the
management of acute pulmonary edema Venodilation : reduces preload
Arterial dilatation : reduces systemic vascular
resistance and may increase cardiac output
Opioid Analgesics
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Respiratory Failure : Medication
Dopamine : Lower doses : stimulate mainly dopaminergic
receptors that produce renal and mesentericvasodilation
Higher doses : produce cardiac stimulation and renalvasodilation
Doses of 2-10 g/kg/min
tachycardia, ischemia,dysrhythmias
Doses > 10 g/kg/min vasoconstrictionafterload
Inotropic Agents
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Respiratory Failure : Medication
Norepinephrine :
used in protracted hypotension after adequatefluid replacement
It stimulates beta1- and alpha-adrenergic
receptors cardiac muscle contractility & HR
SBP & CO
Adjust and maintain infusion to stabilize BP
Inotropic Agents
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Respiratory Failure : Medication
Dobutamine :
produces vasodilation and increases the inotropicstate
At higher dosages heart rates
exacerbating myocardial ischemia
Inotropic Agents
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Respiratory Failure : Medication
Terbutaline : relax bronchial smooth muscle,
relieving bronchospasm and reducing airwayresistance
Albuterol : relaxation of bronchial smooth
muscle
relieves bronchospasm and reducesairway resistance
Beta2 Agonists
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Respiratory Failure : Medication
Effective in accelerating recovery from acute
COPD exacerbations and are an importantanti-inflammatory therapy in asthma
Corticosteroids
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Pneumothorax
Pneumotoraks - udaraberada di antara paru-parudan dinding dada dan paru-paru runtuh.
Biasanya, dua lapisan tipisdari jaringan (pleura)memisahkan paru-paru dandinding dada.
Setiap udara yang bocor kedalam ruang ini (ruangpleura) akan menyebabkanparu-paru colaap
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Normal Physiology
Chest Wall
Pleura
Pleural Space
Diaphragm
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Pneumothorax
Signs and symptoms
of a pneumothorax
include:
Tiba-tiba, nyeri dada
yang tajam
Sesak napas
dada sesak nadi cepat
Cepat, napas pendek
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Clasification
Pneumothorax
Etiology
SpontaneousPneumothorax
Primary
Secondary
Traumatic
Non-Iatrogenic
Iatrogenic
Type of Fistula
SimplePneumothorax
OpenPneumothorax
TensionPneumothorax
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Spontaneous Pneumothorax
Primary Spontaneous Pneumothorax (PSP)
Pneumothorax occurs without a history of
underlying lung disease before Attack : the healthy person, young adult, heavy
physical activity, but at rest
Secondary Spontaneous Pneumothorax (SSP)
Peumothorax due to underlying lung disease (TB,COPD, bronchial asthma, pneumonia, lung tumors)
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Traumatic Pneumothorax
Penetrating trauma or notruptur of thepleura, chest wall, lung
Non-Iatrogenic Traumatic Pneumothorax Injury due to accident (injury of chest wall
open-close, barotrauma)
Iatrogenic Traumatic Pneumothorax
Accidental
Artificial/deliberate
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Iatrogenic Traumatic Pneumothorax
Accidental
Due to medical treatmenterrors /
complications the action (paresthesias chest,pleural biopsy, etc)
Artificial
Deliberatefilling air into the pleural cavitythrough a needle with a Maxwell Box (TBtherapy before AB)
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Pathology
Pneumothorax
Closed
pneumothorax
Open
pneumothorax
Tension
pneumothorax
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Closed
pneumothorax
Open
pneumothorax
Tension
pneumothorax
The pleural tear
Is sealed
The pleural tear
is open
The pleural tear
act as a ball &
valve mechanism
The pleural
cavity pressure
is < theatmospheric
pressure
The pleural
cavity pressure
is = theatmospheric
pressure
The pleural cavity
pressure is > the
atmosphericpressure
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Physical Examination
pasien dengan pneumotoraks dapat berkisar darisepenuhnya bergejala hingga gangguan pernapasanyang mengancam jiwa.
Gejala mungkin termasuk diaforesis, splinting dinding
dada untuk meredakan nyeri pleuritik, dan sianosis(dalam kasus tension pneumothorax).
Temuan pada auskultasi paru juga bervariasitergantung pada luasnya pneumotoraks.
Pasien yang terkena juga dapat mengungkapkandiubah perubahan status mental, termasuk penurunankewaspadaan dan / atau kesadaran (sebuah temuanlangka)
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Physical Examination
Respiratory findings may include the following: Respiratory distress (considered a universal finding) or respiratory arrest
Tachypnea (or bradypnea as a preterminal event)
Asymmetric lung expansion: A mediastinal and tracheal shift to thecontralateral side can occur with a large tension pneumothorax.
Distant or absent breath sounds: Unilaterally decreased or absent lungsounds is a common finding, but decreased air entry may be absent evenin an advanced state of the disease.
Lung sounds transmitted from the unaffected hemithorax are minimalwith auscultation at the midaxillary line
Hyperresonance on percussion: This is a rare finding and may be absent
even in an advanced state of the disease. Decreased tactile fremitus
Adventitious lung sounds (crackles, wheeze; an ipsilateral finding)
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Physical Examination
Cardiovascular findings may include the following: Tachycardia: This is the most common finding. If the heart rate is
faster than 135 beats per minute (bpm), tension pneumothorax islikely.
Pulsus paradoxus
Hypotension: This should be considered as an inconsistentlypresent finding; although hypotension is typically considered a keysign of a tension pneumothorax, studies suggest that hypotensioncan be delayed until its appearance immediately precedescardiovascular collapse.
Jugular venous distention: This is generally seen in tension
pneumothorax, although it may be absent if hypotension is severe. Cardiac apical displacement: This is a rare finding.
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Work up
Arterial Blood Gas Analysis
Chest Radiography
Other Radiographs and Translumination
Contrast-Enhanced Esophagography
Chest CT Scanning
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Medication summary
Local Anesthetics Lidocaine hydrochloride (Xylocaine, LidaMantle, Anestacon)
Opiate Fentanyl citrate (Sublimaze)
Morphine (Astramorph, Infumorph 200, MS Contin, Oramorph SR)
Analgesics Benzodiazepines
Midazolam
Lorazepam (Ativan)
Antibiotics
Doxycycline (Vibramycin, Vibra-Tabs, Doryx) Cefazolin (Kefzol)
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Complications
Hypoxemic respiratory failure Respiratory or cardiac arrest
Hemopneumothorax
Bronchopulmonary fistula
Pulmonary edema (following lung reexpansion)
Empyema
Pneumomediastinum
Pneumopericardium
Pneumoperitoneum
Pyopneumothorax
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Differential Diagnoses
Acute Coronary Syndrome Acute Respiratory Distress Syndrome
Aortic Dissection
Congestive Heart Failure and Pulmonary Edema Esophageal Rupture and Tears
Myocardial Infarction
Pericarditis and Cardiac Tamponade
Pulmonary Embolism Rib Fracture
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Parah dan persisten asma yang tidak
menanggapi terapi konvensional
Suatu bentuk parah asma di mana obstruksi
jalan napas tidak responsif terhadap terapi
obat biasa.
* Status Asthmaticus
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Faktor-faktor pencetus berikut mungkin bertanggung
jawab atas kerusakan akut dalamnegara status dan
harus dievaluasi dan ditangani untuk terapi untuk
menjadi sukses:1. Infection :Viruses, bacteria, fungi (bronchitis,
pneumonia)
2. Allergic Factors :
Pollens, animal danders, dusts, foods,
drugs
Precipitating Factors
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3. Irritative Factors :
Dusts, fumes, smoke (air pollutants)
4. Trigger Mech.Sinobronchitic disease, nasal
polypi, otitis media 5. Emotional :
Stress, fatigue
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genetic predisposition
environmental factors
Patients often have a history of atopy Gastroesophageal reflux disease is another
risk factor for asthma
Risk factors
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Risk factors for asthma also include the following:
Viral infections
Air pollutants - Eg, dust, cigarette smoke, and
industrial pollutants Medications - Including beta-blockers, aspirin,
and nonsteroidal anti-inflammatory drugs(NSAIDs)
Cold temperature
Exercise
M h i f St t A th ti
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Mechanisms of Status Asthmaticus
Mucous
Hypersecretion
Bronchospasm
Mucosal edema
Increased resistance to air flow
Atelectasis Uneven
ventilation
AbnormalV/Q
Hyperinflation
deadspace compliance
alveolar
hypoventilation WOB
pCO2pO2
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Asthma
Lower airway obstruction
Bronchospasm
Edema
Mucus
Caused by
Irritants
Respiratory infection
Emotional distress
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Asthma
Underlying Problem: VENTILATION ANDINFLAMMATION
Assessment/Associated Symptoms
Non productive cough Wheezing
Speech dyspneaone word sentences
Use of accessory muscles
Status Asthmaticusnot responding to treatment
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Classification asthma disease
Intermitten
Mild persistent
Moderate persistent
Hard persistent
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Episodic of Asthma
Mild
Moderate
Hard
Apnoe, emergency
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REFERENCES
Longo D, Fauci AS, Kasper D, Hauser S, Jameson Jl,
Loscalzo J, editors. Harrisons principles of internal
medicine. 18thed. New York: McGraw-Hill, 2011.
Sjaifoellah Noer, Sarwono Waspadji, Muin RachmanA, Lesmana LA, Djoko Widodo, dkk, editor. Ilmu
Penyakit Dalam. Jilid I edisi III. Jakarta: FKUI, 1996.
John, Md. Marx, Robert, Md. Hockberger, editors.
Rosen's Emergency Medicine: Concepts and ClinicalPractice. 7thed. Philadelphia: Mosby Elsevier, 2007.