Sixth Problem

“Gasping for Air “

Emergency Medicine
Group 10
Monday,30th October 2017
 Tutor: dr. Agus & dr.Haming
• Ketua : Renald Patria Dharmasyah
• Sekretaris : Cindy Claudia
• Penulis :Nikolaus Ronald Karnadi

• Anggota :
– Wenny Agustin Biang
– Farrel Uttu
– Vamelda Agustin
– Melani Nugraha
– Wenny Damayanti
– Nailah Rahmah
– Chyntia Winata
– Yoko Septian Jaya
– Sinta Gotama
 6th problem
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 & rapid when he was
brought to the ED .In the past 3 to 4 days ,he had been coughing & there were wet sounds heard in
his cough.Paramedics report that his saturation is 67% when he was found.He has a history of
bronchial asthma & was diagnosed with pulmonary tuberculosis 10 years ago but have not
completed this medication.He was also a heavy smoker in his young age.

• In the ED ,his vital sign are as follow ,temperature is 38.7 C ,BP 100/78 mmHg,heart rate is
118beats/min,RR : 30 breaths /min,& his oxygen saturation is 84% on a non-rebreather face
mask.On his physical throax examination,his breathing is labored with intercostal muscle retraction
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 & wheezing .His initial blood gas analysis shows that his pH is 7.26 ,PCO2 is 60 mmHg
,PO2 is 55 mmHg ,his HCO3 is 26 mEq/L
• Discuss the case,assess the patient condition ,plan proper diagnostic procedure & treatment while
considering all possibilities
• References for some supplementary diagnostic examination:
– pH : 7.35-7.45
– pCO2 : 35-45 mmHg
– P02 : 90-100mmHg
– HCO3: 22-26mmHg
 LANGKAH 2
1. Apakah ada hubungan keluhan dengan stroke ?
2. Apakah ada hubungan keluhan riwayat asma dan
TB yg tidak dirawat?
3. Hubungan perokok dengan keluhan sekarang ?
4. Bagaimana intepretasi Pf & PP
5. Apa penyebab wet sound coughing?
6. Mengapa HCO3 ada dibatas atas ?
7. SaO2 84% walaupun ttp diberikan NRM ,apa
yang harus dilakukan?
 Langkah 3
1.Kemungkinan,faktor resiko pneumonia
2.Ada
3.Bisa COPD ( bronikitis kronik & emfisema)
4.Demam( 38.7 c) ,SaO2 : 84% ( N: > 95%)
-PP : asidosis respiratorik ( AGD)
-TD: normal
-RR: takipneu
-retraksi interkostal
-tidak simetris pengembangan kedua
parupneumothorax ( perkusi : hipersonor) /efusi pleura
(perkusi : redup ( hemothorax/pneumonia)
-Crackles : COPD
-wheezing : Asthma
5.Akibat infeksi/TB,pneumonia,COPD
6.Komplikasi asidosis respiratorik sdh mulai terjdi
7.Ditambahkan dengan ventilasi mekanik
 Mind Map
Anamnesa PF
Pulmonary Emergency

1) ARDS Respiratory failure

2) Avian influenza - Type 1 & Type 2
3) Pulmonary tuberculosis
4) COPD exacerbation
5) Status Asthmaticus
6) SARS
7) Aspiration pneumonia
8) Pneumothorax
9) Tracheal aspiration
10) Massive pleural effusion
11) Pulmonary edema
12) Hemothorax

Tatalaksana awal farmako & non farmakoprognosis & komplikasi

 LEARNING ISSUES
1. Explain the definition,etiologies,sign &
symptom,diagnosis,physical
examination,laboratory,imaging
,radiology,invasive diagnostic
procedure),initial management ,complication
& prognosis of respiratory failure & ARDS
2. Differentiate type of respiratory failure
 Acute Respiratory Distress Syndrome
• A clinical syndrome of
severe dyspnea of rapid
onset, hypoxemia, and
diffuse pulmonary
infiltrates leading to
respiratory failure
• ARDS is caused by diffuse
lung injury (direct/indirect)
from many underlying
medical and surgical
disorders

Harrison’s Principles of Internal Medicine. 18th Ed.

 ARDS
• Etiology
– Severe sepsis syndrome and/or bacterial pneumonia
(~40–50%)
– Trauma
– Multiple transfusions
– Aspiration of gastric contents
– Drug overdose
– Pulmonary contusion
– Multiple bone fractures
– Chest wall trauma/flail chest

http://clinicalgate.com/acute-respiratory-distress-syndrome-2/
ARDS

http://clinicalgate.com/acute-respiratory-distress-syndrome-2/
 ARDS
• Physical examination
– Tachypnea, tachycardia and the need for a high
fraction of inspired oxygen (FiO2) to maintain
oxygen saturation
– Febrile or hypothermic
– Cyanosis of the lips and nail beds
– Sepsis  hypotension and peripheral
vasoconstriction with cold extremities
– Examination of the lungs  bilateral rales
– Manifestations of the underlying cause

http://emedicine.medscape.com/article/165139-clinical#b2
 ARDS
• Differential diagnosis
– Aspiration Pneumonitis and Pneumonia
– Bacterial Pneumonia
– Bacterial Sepsis
– Hypersensitivity Pneumonitis
– Multiple Organ Dysfunction Syndrome in Sepsis
– Hospital-Acquired Pneumonia (Nosocomial
Pneumonia) and Ventilator-Associated Pneumonia
– Perioperative Pulmonary Managemen
– Respiratory Failure
– Transfusion Reactions
– Ventilator-Associated Pneumonia
– Viral Pneumonia

http://emedicine.medscape.com/article/165139-differential
 ARDS
• Test & diagnosis
– Arterial blood gas
– Hematologic
– Renal
– Cytokines
– To exclude cardiogenic pulmonary edema 
obtain a plasma B-type natriuretic peptide
(BNP) value and echocardiogram
– Chest X-ray  bilateral pulmonary infiltrates
– CT-scan
– Bronchoscopy

http://emedicine.medscape.com/article/165139-differential
 ARDS
• Management
– Positive end-expiratory pressure (PEEP) is
empirically set to minimize FIO2 (inspired O2
percentage) and maximize PaO2 (arterial partial
pressure of O2)
– Fluid management
– Neuromuscular blockade
– Glucocorticoids

http://clinicalgate.com/acute-respiratory-distress-syndrome-2/
 COPD: an umbrella term

• Umbrella term used to describe

progressive lung diseases which
include:

– Emphysema
– Chronic bronchitis
– Refractory (irreversible) asthma
– Severe bronchiectasis
 COPD
• Chronic obstructive pulmonary disease
(COPD) is a lung ailment that is characterized
by a persistent blockage of airflow from the
lungs.

• It is an under-diagnosed, life-threatening lung

disease that interferes with normal breathing
and is not fully reversible.
 Understanding COPD
• Critical to first understand normal
lung function

Image courtesy of The National Institute

of health
Lungs with COPD

Image courtesy of The National Institute

of health
 Causes
• Most cases of COPD occur
as a result of long-term
exposure to lung irritants
that damage the lungs and
the airways
• The most common irritant
that causes COPD is
cigarette smoke
• In rare cases, a genetic
condition called alpha-1
antitrypsin deficiency may
play a role in causing COPD
Symptoms
• breathlessness
• abnormal sputum (a
mix of saliva and
mucus in the
airway)
• a chronic cough
• daily activities can
become very
difficult as the
condition gradually
worsens
 Tripod Hoover sign  inward
position movement of lower ribcage
on inspiration
Purse lips breathing

n
 Diagnosis
• A simple diagnostic test
called "spirometry“
measures how much air
a person can inhale and
exhale, and how fast air
can move into and out
of the lungs

• Spirometry can detect

COPD long before its
Symptoms appear.
 Treatment
• COPD has no cure

• Quitting smoking is the most important step an

individual can take to treat COPD

• Other treatments for COPD may include

medicines, vaccines, pulmonary rehabilitation
(rehab), oxygen therapy, and surgery
 Managing COPD
• COPD symptoms usually • Avoid lung irritants
slowly worsen over time
• Get ongoing care
• A cold, the flu, or a lung
infection may cause • Manage the disease and its
symptoms to intensify symptoms
• Prescription antibiotics may • Prepare for emergencies
treat infections and other
medicines, such as
bronchodilators and inhaled
steroids, can help facilitate
breathing
Noninvasive ventilation
Status Asthmaticus
• extreme form of an
asthma exacerbation
that can result in
hypoxemia,
hypercarbia, and
secondary respiratory
failure
Status asthmaticus: severe
bronchospasm, doesn’t respond to
aggressive therapies within 30-60
mins.
Background
• Acute Exacerbation
• Unresponsive
• Mild to Severe form
• Trend is towards less number
of admissions in intensive
care
Treatment goals
• Reverse airway obstruction
• Correct Hypoxemia
• Prevent or treat complications like
pneumothorax and respiratory arrest
 Risk factors
• Genetic
• GERD
• Viral infections
• Air pollutants
• Medications
• Cold exposure
• Exercise
 Etiology
• Acute Bronchospastic component marked by smooth
muscle bronchoconstriction.
• Later inflammatory airway swelling and edema

Early bronchospastic response

• Exposure to allergen
• Mast cell degranulation
• Release of histamine, PGD2, LT-C4
• airway smooth muscle contraction, increased
capillary permeability, mucus secretion, and
activation of neuronal reflexes
• Bronchoconstriction typically responds to
bronchodilator therapy like beta 2 agonist adrenergic
 Later inflammatory response
• Inflammatory mediators prime endothelium and
epithelium of
bronchial mucosa.
• Inflammatory cells like eosinophils, neutrophils and
basophils attach to primed endothelium and
epithelium and later enter into the tissues
• Eosinophils release ECP and MBP which induce
desquamation of
airway epithelium and expose nerve endings
• It leads to further hyper responsiveness.
 Later inflammatory response
• Airway resistance and obstruction
• caused by Bronchospasm, mucus plugging,
and edema in the peripheral
• Air trapping
• results in lung hyperinflation,
ventilation/perfusion (V/Q)
mismatch, and increased dead space
ventilation.

• Increase in pleural and intra alveolar pressure and

distended alveoli leads to hypoxemia and increase
in minute ventilation.
 Complications Prognosis
• Slow compartments vs fast
compartments
• Generally good except
• Respiratory alkalosis vs when combined with
hypercarbia heart failure or COPD
• Cardiac arrest • Poor prognostic factors
• Respiratory failure or arrest include delay in starting
• Hypoxemia with hypoxic treatment especially
ischemic central nervous system steroids
(CNS) injury
• Pneumothorax or
pneumomediastinum
• Toxicity from medications
 Risk factors for developing status
asthmaticus
• Increased use of home
bronchodilators without
improvement or
effect
• Previous intensive
care unit (ICU)
admissions, with or
without intubation
• Asthma exacerbation despite
recent or current use of
corticosteroids
• Frequent emergency department
visits and/or hospitalization
• Less than 10% improvement in
peak expiratory flow rate
(PEFR)
• History of syncope or seizures
during acute exacerbation
• Oxygen saturation below 92%
despite supplemental oxygen
History
• Severe dyspnea or hours or days.
• Previous intubation and ventilation

Asthma with No Wheezing

• Silent chest
• Severe obstruction
• fatigue
Physical Examination
• Tachypnea
• Wheezing in early stages
• Initially expiratory
• Later in both phases, may have absent breath sound in
advance stage
• Use of accessory muscles
• Inability to speak more than 1 to 2 words
• Decreased oxygen saturation
• Tachycardia and Hypertension
• Signs of complication, tension pneumothorax,
pneumomediastinum
• Peak expiratory flow meter measurement
Assessment of severity of asthma
exacerbation
• Moderate asthma exacerbation:
• Increasing symptoms.
• PEFR >50-75% best or predicted.
• No features of acute severe asthma.
• Acute severe asthma - any one of:
• PEFR 33-50% best or predicted.
• Respiratory rate ≥25 breaths/minute.
• Heart rate ≥110 beats/minute.
• Inability to complete sentences in one breath.
• Life-threatening asthma - any one of the
following in a patient with severe asthma:
• Clinical signs: altered conscious level, exhaustion, arrhythmia,
hypotension, cyanosis, silent chest, poor respiratory effort.
• Measurements: PEFR <33% best or predicted, SpO2 <92%, PaO2 <8 6.0
kPa, 'normal' PaCO2 (4.6- kPa).
Differential diagnosis
• In children
• Viral infections, bronchiolitis
• Foreign body
• Congestive heart failure
• Extrinsic compression, lymph node,
tumor, blood vessel
• Tracheomalacia, primary or secondary
• Inhalational injury
• Other diagnosis, like cystic fibrosis,
bronchiectasis etc
Workup
• Blood test
• CBC, ABG, Electrolytes, RBS, Theophillne level
• Chest X-ray
• To rule out pneumothorax, pneumomediastinum, heart
failure, pneumonia

4 stages of blood gas progression with

status asthmaticus
PaCO2 PaO2
Stage 1 Decrease Normal
Stage 2 Decrease Decreased
Stage 3 NORMAL Decreased
Stage 4 High Decreased
 Treatment
• Mainstay of treatment of status asthmaticus are beta
2 agonist, systemic steroids and theophyllines.
• Pregnant and non pregnant are treated in the same
manner
• Fluid replacement, hypokalemia and
hypophosphatemia are important to treat.
• Routine use of antibiotics is discouraged
• Oxygen monitoring and therapy
• Maintain SatO2 above 92% except in pregnant and cardiac
patients where maintain above 95%.
• Endotracheal intubation, ventilation and chest tube
placement as needed.
• ECMO when needed.
 Need for hospitalization
• If after treatment PEF and FEV1 is between 50%
to 70%
• If less than 50% then intensive care admission is
indicated

National Heart, Lung, and Blood Institute. Managing exacerbations

of asthma. In: National Asthma Education and Prevention Program
(NAEPP). Expert panel report 3: guidelines for the diagnosis and
management of asthma. National Guideline Clearinghouse
 Extracorporeal life support
• high risk of developing refractory status
asthmaticus.
• Patients with a history of multiple incubations
• Respiratory failure requiring intubation within 6 hours of
admission
• Hemodynamic instability
• Neurologic impairment at the time of admission
• Duration of respiratory failure greater than 12 hours
despite maximal medical
therapy.
• Practiced in limited centers of the world
Sunil Saharan & Rakesh Lodha
& Sushil K. Kabra.
Management of Status
Asthmaticus in Children. Indian
J Pediatr (2010) 77:1417–1423
DOI 10.1007/s12098-010-
0189-8.
Avian Influenza
 Suspected

Probable
•  antibody (min 4x) against H5
with HI test or ELISA
Observation • H5 specific antibody detected (single serum)
Temperature >38oC (neutralization test)
• Severe Pneumonia/ respiratory failure
with one or more: / dead with no other cause
-cough
-sore throat
-cold (pilek )
-shortness of breath
(pneumonia) Confirmed
- Virus culture (+)
- PCR (+)
- IFA test (+)
- H5 specific antibody detected
(paired serum) (neutralization
test)   antibody (min 4x)
 Hospital care
• Suspected
+ shortness of breath with RR ≥ 30x/minutes
+ HR ≥ 100x/minutes with consciousness disorder
• Suspected with leucopenia
• Suspected with pneumonia ( radiology imaging)
• Probable and Confirmed

Treatment

• M2 Inhibitor : Amantadin and Rimantadin (100 mg 2x/day or 5 mg/kgBB for

3-5 days)
• Neuramidase Inhibitor : Zanamivir and Oseltamivir ( 2 x 75mg for a week)

Suspected case  Oseltamivir 2 x 75 mg for 5 days, symptomatic and antibiotic

if indicated
Probable  Oseltamivir 2 x 75 mg for 5 days, large spectrum AB and steroid if
indicated(severe pneumonia, ARDS)
Prophylactic  Oseltamivir 75 mg 1x/day for > 7 days (until 6 weeks)
 Pulmonary Edema
• Mechanism of Fluid favors movement of fluid into
accumulation the vessel ( level of albumin
,the primary protein in the
– Fluid accumulates in the plasma ,may be low in
interstisium of the lung condition ( such as cirrhosis
depends on the balance of & nephrotic syndrome )
hydrostatic & oncotic forces
within the pulmonary
capillaries & in the • Hypoalbumin favors
surrounding tissue. movement of fluid into the
– Hydrostatic pressure :favours tissue for any hydrostatic
movement of fluid from the pressure in the capillary
capillary into the interstisium.
– Oncotic pressure which is
determined by the protein
concentration in the blood

Harrison Princples Internal Medicine 19th

 Cardiogenic Pulmonary Edema
• Cardiac abnormalities lead to an increase in pulmonary venous pressure
shift the balance of forces between capillary & the interstisium.

• Hydrostatic is increased  fluid exits the capillary at an increased rate

resulting in interstitial ( more severe cases : alveolar edema )
– Development of pleural effusion may further compromise
respiratory system function & contribute to breathing discomfort.

• Early sign of pulmonary edema :

– Exertional dyspnea
– Orthopnea
– Chest radiograph peribronchial thickening ,prominent vascular
marking in the upper lung zones & kerley B lines

Harrison Princples Internal Medicine 19th

Non cardiogenic pulmonary edema
• Non cardiogenic pulmonary edema characterized by
intrapulmonary shunt + hypoxemia & decreased
pulmonary compliancelower functional residual
capacity

• Pathologic examination hyaline membranes are

evident in the alveoli & inflammation leading to
pulmonary fibrosis may be seen
• Clinically : mild dypnea to respiratory failure
• Auscultation : may be realtively normal despite chest
radiograph that show diffuse alveolar infiltrate
Harrison Princples Internal Medicine 19th
http:/ambulance.qld.gov.au/clinical.html
Goldman Cecil 24th edition
 Pulmonary Edema
• Non Cardiogenic
• Cardiogenic Edema Edema

Cardiogenic edema  with severe, Noncardiogenic edema, with

symmetric, basilar-predominant airspace severe,symmetric, more diffuse
opacities,associated with cardiomegaly airspace opacities; however, the cardiac size
and likely small effusions. is normal and no pleural effusions are
present
https://www.ncbi.nlm.nih.gov/pmc/
articles/PMC5408000/figure/f1/
https://www.ncbi.nlm.nih.gov/pmc/articles/PM
C5408000/
 Aspiration Pneumonia

• The development of a radiographic infiltrate and

clinical features consistent with pneumonia in a patient
with risk factors for increased oropharyngeal aspiration
• Any condition that increases the volume and/or
bacterial burden of oropharyngeal secretions in the
setting of impaired host defense mechanism may lead
to aspiration pneumonia
 Risk Factor
• Dysphagia (major)
• Volume of the aspirate
• Colonization of the oropharynx :
especially in elderly that increased
colonization of Staphylococcus
aureus and aerobic gramnegative
bacilli (e.g., Klebsiella pneumoniae
and Escherichia coli)
• lack of oral hygiene care as well as
conditions of peridental and/or
dental disease
• Marked depression of the cough
reflex
 Diagnosis

• There is no “gold standard” test to diagnose

aspiration pneumonia
• The diagnosis is therefore inferred when a
patient with known risk factors for aspiration
develops clinical features compatible with
pneumonia (fever, shortness of breath,
purulent sputum) with an infiltrate in a
characteristic bronchopulmonary segment
 Management
• Antimicrobial therapy
 Streptococcus pneumoniae, S. aureus, and Haemophilus
influenza : narrow spectrum antibiotics
 third generation cephalosporins, fluoroquinolones, piperacillin,
or carbapenems : for aerobic gram (-)
 vancomycin or linezolid should be considered in patients at risk
of infection with methicillin-resistant S. aureus (MRSA)
• ACE-Inhibitor
• Nicergoline & an ergot alkaloid derivative
• Oral hygiene
 Massive pleural effusion
• Result from fluid accumulating in the potential
space between the visceral & parietal pleurae

Rosen's Emergency Medicine 9th Edition

 Differential
Clinical features Diagnosis
• May be silent/ come to detection
from other symptom(mild pleural
effusion)
• Increase in volume of the effusion
w/ the production of dyspnea/
development of inflammation &
associated pain w/ respiration
• Percusion dullness & decreased
breath sounds
• Small/ moderate-size effusion
percusion dullness & decreased
breath sounds at the lung base with
relative normal lung findings above
the level of fluid
• Large/ massive effusions
imposibble to distinguish a fluid
level on clinical examination

Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e

 Diagnosis
• Adult: 150-200 mL of pleural fluid in the hemithorax
• Supine chest radiographs hazy appearance of pleural
fluid in the posterior pleural space
• CT scan chest clarify findings on chest radiograph
• Diagnostic thoracocentesis obtain pleural fluid for
analysis
• Light developed the most widely used criteria to
differentiate transudates from exudates using serum
and pleural fluid protein and lactate dehydrogenase
levels

Tintinalli’s Emergency Medicine: A Comprehensive

Tintinalli’s Emergency Medicine: A Comprehensive
• Small free-flowing pleural effusions better visualized on decubitus
radiographic views
USG
• A significant pleural effusion is large enough to produce a pleural fluid
strip >10mm wide on lateral decubitus radiographic views/ by USG

Tintinalli’s Emergency
Medicine: A
Tintinalli’s Emergency Medicine: A Comprehensive
 Treatment
• Therapeutic thoracentesis w/ drainage of 1.0-1.5 L of
fluid if the patient has dyspnea at rest
• Diuretic therapy resolves >75% of effusions due to HF
within 2-3 days
• Patients w/ pleural empyema (gross pus/ organism on Gram
stain) drainage w/ large bore thoracostomy tubes
• Massive effusions (>1.5-2L) urgent thoracentesis may
stabilize respiratory/ circulatory status
• Empyema chest tube drainage/ operating room to prevent
complications
• Relative contraindications to thoracocentesis
coagulopathy & other bleeding disorders

Tintinalli’s Emergency Medicine: A Comprehensive

Rosen's
Study Guide, 8e Emergency Medicine 9th Edition
Harrison's Principles of
Internal Medicine
 Pneumothorax
Pneumothorax is defined as the presence of air in the pleural
space.

If air is present in the pleural space, one of three events must

have occurred: (1) communication between alveolar spaces and
pleura, (2) direct or indirect communication between the
atmosphere and the pleural space, or (3) presence of gas-
producing organisms in the pleural space.
Respiratory Failure
• Respiratory Failure: condition in which the
respiratory system fails in one or both of its gas-
exhanging function; that is, oxygenation of and
carbon dioxide elimination from, mixed venous
(pulmonary arterial) blood.

Fishman Jay A et al. Fishman’s Pulmonary Diseases and Disorders. 5th edition.
 Classification of Respiratory
Failure

Fishman Jay A et al. Fishman’s Pulmonary Diseases and Disorders. 5th edition.
2008. New York: Mc Graw Hill
• Hypercapnic respiratory failure  arterial Pco2
(Paco2) > 45 mmHg.
• Hypoxemic respiratory failure  arterial Po2 (PaO2)
< 55 mmHg when
the fraction of oxygen in inspired air (FIO2) >= 0,60

Fishman Jay A et al. Fishman’s Pulmonary Diseases and Disorders. 5th edition.
 Pathophysiology
• Respiratory failure can arise from an
abnormality in any of the ”effector”
components of the respiratory system

A defect in any
of this, which
constitute the
“respiratory
pump”, may
cause
coexistent
hypercapnia
and hypoxemia
• Hypoxemic respiratory failure
• It can be caused by alveolar hypoventilation, ventilation-
perfusion mismatch, shunt, and diffusion limitation
• Alveolar hypoventilation  occurs in neuromuscular
disorders that affect the respiratory system.
• Diffusion limitation  disease that increase the diffusion
pathway for oxygen from the alveolar space to
pulmonary capillary impair oxygen transport across the
alveolar capillary membrane.
• Hypercapnic respiratory failure
• Constant rate of CO2 production is determined
by the level of alveolar ventilation.

Fishman Jay A et al. Fishman’s Pulmonary Diseases and Disorders. 5th edition.
 • Ventilatory supply versus demand
• Ventilatory supply  maximal spontaneous ventilation
that can be maintained without development of
respiratory muscle fatigue
• Normally: Ventilatory supply exceeds ventilatory
demand.
• When ventilatory demand > ventilatory supply 
result: PaCO2
>>

Fishman Jay A et al. Fishman’s

Pulmonary Diseases and Disorders. 5th
edition. 2008. New York: Mc Graw Hill
• Factor that
reduce
ventilatory
supply or
increase
ventilatory
demand
Categories of Respiratory Failure
• Abnormalities of the central nervous system
• A variety of pharmacologic, structural and metabolic
disorders of the CNS are characterized by suppression of the
neural drive to breathe  hypoventilation and
hypercapnia
• Pharmacologic: narcotic overdose or sedative drug
• Structural CNS abnormalities : meningoencephalitis,
localized tumors or vascular abnormalities of the
medulla, stroke
• metabolic  depression of respiratory control centers 
hypercapnia;
example: severe myxedema, hepatic failure and advanced
uremia.
• Abnormalities of the alveoli
• Example: cardiogenic and noncardiogenic pulmonary
edema, diffuse pneumonia, extensive pulmonary
hemorrhage.
• Abnormalities of the peripheral nervous system or chest
wall
• Inability to maintain a level of minute ventilation appropriate
for the rate of CO2 production
• Many of the disorders are complicated by impaired
expiratory muscle strength, atelectasis and aspiration.
• Neuromuscular causes of hypecapnic respiratory failure are
GBS, myastenia gravis
• Obesity, massive abdominal distention due to ascites
• Etc
• Abnormalities of the airways
• Obstructive disease of the airways, either upper or lower 
causes acute and chronic hypercapnia
• Upper airways: acute epiglotitis, aspirated foreign body,
tracheal tumor
• Lower airway: COPD, asthma
 Principles of Management
• Airway management
• Emergency intubation is required depends on the
clinical circumstances
• When progressive hypoxemia or hypercapnia is
observed over the first few minutes or hours of care
 intubation and mechanical ventilation are
warranted.
• For the therapy  search for the cause of
the problem and its management must be
undertaken.
• Arterial blood gas
Fishman Jay A et al. Fishman’s Pulmonary Diseases and Disorders. 5th edition.
Fishman Jay A et al. Fishman’s Pulmonary Diseases and Disorders. 5th edition.
 Tuberculosis
• TB is a disease caused by a bacterium called
Mycobacterium tuberculosis.
• Infection with M tuberculosis  exposure of the
lungs or mucous membranes to infected
aerosols.
• Person with active pulmonary TB, a single
cough can generate 3000 infective droplets, with
as few as 10 bacilli needed to initiate infection.
 Clinical features
• Cough
• Weight loss/anorexia
• Fever
• Night sweats
• Hemoptysis
• Chest pain
• Fatigue
• Abnormal breath sounds, especially over the
upper lobes or involved areas.
 Diagnosis: Screening method
• Mantoux tuberculin skin test with purified
protein derivative (PPD)  active and latent
TB
• An in vitro blood test based on interferon-
gamma release assay (IGRA) with antigens
specific for Mycobacterium tuberculosis 
latent TB
 Laboratory test
• Acid-fast bacilli (AFB) smear and culture -
Using sputum obtained from the patient
• HIV serology in all patients with TB and
unknown HIV status
 Work up
• Chest radiograph to evaluate for possible
associated pulmonary findings. If chest
radiography findings suggest TB and a sputum
smear is positive for AFB, initiate treatment
for TB.
• A computed tomography (CT) scan of the
chest may help to better define abnormalities
in patients with vague findings on chest
radiography.
 Treatment

Latent TB
• Recommended regimens  isoniazid and rifampin
• An alternative regimen  isoniazid plus rifapentine as
directly observed therapy (DOT) once-weekly for 12 weeks
http://www.aafp.org/afp/2000/0501/p2667.html
http://www.aafp.org/afp/2000/0501/p2667.html
 SARS
Definition
• a rapidly progressive illness caused by a coronavirus /
the severe acute respiratory syndrome coronavirus.

• Isolation procedures for suspected SARS patients:

airborne, droplet, and contact isolation.
• Healthcare providers should wear a higher respiratory
facemask when caring for patients with SARS, in
addition to glove, gown, and eye protection.

• RF for death in coronavirus infection include:

– age >60 years, diabetes mellitus, and hepatitis B
infection.
 Clinical Features
• The clinical features of coronavirus infection:
– fever (99% frequency)
– nonproductive cough
– Dyspnea
– myalgias
– headache
– diarrhea
• Many cases progress to a moderate-severe condition
characterized by hypoxia and dyspnea at rest.
• Respiratory failure requiring mechanical ventilation
occurs in 10% to 20% of hospitalized patients with
SARS
http://payload.cargocollective.com/1/3/102448/1513469/SARS_spread02.jpg
https://www.cdc.gov/sars/
clinical/images/clinicalgu
idance1.gif
 Conclusion & Suggestion
• According to patient history,sign & symptom
,physical examination ,we concluded that the
patient maybe has :
– aspiration pneumonia (being cared in nursing facility
for a long time ) ,acute COPD excacerbation ( because
of heavy smoker in his young age) ,pneumothorax (
asymmetrical chest wall expansion when he breathes)/
pleural effusion
• Based on his initial blood gas analysis ,we
concluded that he has hypercapnic respiratory
failure (because his PCO2 > 60 mmHg)
 References
• Fishman Jay A et al. Fishman’s Pulmonary
Diseases and Disorders. 5th edition. 2008. New
York: Mc Graw Hill
• Tintinalli’s Emergency Medicine: A
Comprehensive Study Guide, 8th ed
• Harrison’s Principles of Internal Medicine. 18th
Ed. Volume II.
• Goldman’s Cecil Medicine 24th edition
• https://www.cdc.gov/sars/clinical/images/clinicalg
uidance1.gif