Pemicu 6

Jovian Lutfi Daniko

405140116
RESPIRATORY FAILURE
 Respiratory Failure
• Is a condition in which the respiratory system fails in one or
both of its gas-exchanging functions; that is, oxygenation of,
and carbon dioxide elimination from, mixed venous
(pulmonary arterial) blood.
 Hypoxemic respiratory failure
• V/Q mismatch:
– V/Q mismatch is the most common cause of hypoxemia.
– The low-V/Q units contribute to hypoxemia and hypercapnia.
– The high-V/Q units waste ventilation but do not affect gas exchange unless the
abnormality is quite severe.
• Alveolar hypoventilation:
– Alveolar hypoventilation occurs in neuromuscular disorders that affect the respiratory
system.
• Shunt
– Shunt is defined as the persistence of hypoxemia despite 100% oxygen inhalation. The
deoxygenated blood (mixed venous blood) bypasses the ventilated alveoli and mixes
with oxygenated blood that has flowed through the ventilated alveoli, consequently
leading to a reduction in arterial blood content.
 Hypercapnic respiratory failure
PaCO2 = VCO2 × K/VA
• The relation between PaCO2 and alveolar ventilation is
hyperbolic.
• As ventilation decreases below 4-6 L/min, PaCO2 rises
precipitously. A decrease in alveolar ventilation can result from
a reduction in overall (minute) ventilation or an increase in the
proportion of dead space ventilation.
• A reduction in minute ventilation is observed primarily in the
setting of neuromuscular disorders and CNS depression
 Etiology
• Hypoxemia respiratory • Hypercapnia respiratory
failure failure
– ARDS – Drug Overdoses
– Pulmonary edema – Pulmonary edema
– Pneumothorax – Asthma severe
– Pneumonia – COPD
– Asthma – Neuromuscular disease
– COPD – ARDS
– Pulmonary arterial
hypertension
 Management
• Adequate oxygen delivery to tissues, generally achieved with a
PaO2 of about 60 mm Hg.
• Airway
– When progressive hypoxemia or hypercapnia is observed over the
first few minutes or hours of care, intubation and mechanical
ventilation are warranted
 Prognosis
• For patients with COPD and acute respiratory failure, the
overall mortality has declined from approximately 26% to 10%.
Acute exacerbation of COPD carries a mortality of
approximately 30%. The mortality rates for other causative
disease processes have not been well described.
• Younger patients (<60 y) have better survival rates than older
patients
ACUTE COPD EXACERBATION
• Acute exacerbations of COPD are characterized by worsening of respiratory symptoms
beyond normal day-to-day variations and are usually triggered by an infection or
respiratory irritant.
• More than 75% of patients with acute exacerbations have evidence of viral or bacterial
infection, with up to half specifically due to bacteria. Other important triggers for
exacerbations are hypoxia, cold weather, β-blockers, narcotics, or sedativehypnotic
agents.
• The final common pathway for an exacerbation is the release of inflammatory
mediators that result in bronchoconstriction, pulmonary vasoconstriction, and mucus
hypersecretion.
• The work of breathing increases due to higher airway resistance and lung hyperinflation.
• The oxygen demand of respiratory muscles increases  generating additional carbon
dioxide and causing hypercapnia, resulting in further physiologic stress.
• Acute exacerbations of COPD are primarily due to ventilation–perfusion mismatch
rather than the expiratory airflow limitation seen with asthma exacerbations.

• Supplemental oxygen increases blood oxygen concentrations and can help reverse
pulmonary vasoconstriction.
 Pathophysiology
• Tobacco smoke and air pollutants  trigger an increase in inflammatory cells in the
airways, lung interstitium, and alveoli.
• Proteases break down lung parenchyma and stimulate mucus secretion  Mucus-
secreting cells replace cells that normally secrete surfactant and protease inhibitors 
loss of elastic recoil, narrowing, and collapse of the smaller airways  Mucous stasis
and bacterial colonization develop in the bronchi.
• Airflow obstruction results from a combination of airway secretions, mucosal edema,
bronchospasm, and bronchoconstriction. Exaggerated airway resistance reduces total
minute ventilation and increases respiratory work.
• In emphysema, alveolar and capillary surfaces are distorted or destroyed, resulting in
alveolar hypoventilation and ventilation–perfusion mismatch  The result is hypoxemia
and hypercarbia.
• Sleep may blunt the ventilatory response to hypercarbia.
• The right ventricle hypertrophies and dilates, resulting in pulmonary hypertension and
right ventricular failure.
• Right ventricular pressure overload is associated with atrial and ventricular arrhythmias.
 Clinical Features
- Hypoxemia (arterial saturation <90%). Signs of hypoxemia include tachypnea, tachycardia,
systemic hypertension, cyanosis, and a change in mental status.
- With increased work of breathing, carbon dioxide production ncreases; alveolar
hypoventilation creates arterial carbon dioxide retention and respiratory acidosis.
- The patient tries to overcome severe dyspnea and orthopnea by sitting in an up-and-forward
position, using pursed-lip exhalation, and engaging accessory muscles to breathe.
- Pulsus paradoxus (a drop of >10 mmHg in systolic blood pressure during respiratory cycles)
may be noted
- Complications, such as pneumonia, pneumothorax, pulmonary embolism, or an acute
abdomen, may exacerbate COPD.
- Other acute triggers include asthma, congestive heart failure, tuberculosis, and metabolic
disturbances.
 Diagnosis
- With the history, seek causes for exacerbation and triggers plus sputum changes (Assessment of
sputum includes questions about changes in volume and color, especially an increase in
purulence. An increase in sputum volume and change in sputum color suggest a bacterial
infection and the need for antibiotic therapy. Sputum cultures usually contain mixed flora and do
not help guide ED antibiotic selection)  then assess oxygenation and acid-base status, and
perform a physical examination.
- Pulse oximetry may identify hypoxemia, and capnography may identify hypercarbia.
- Arterial blood gas analysis is the best tool in acute evaluation for assessing oxygenation,
ventilation, and acid-base disturbances. Arterial blood gases clarify the severity of exacerbation
and the probable clinical course.
- Respiratory failure is characterized by an arterial Pao of <60 mmHg or an arterial Sao <90% in
2 2

room air.
- Respiratory acidosis is present if the partial pressure of carbon dioxide (Pco ) is >44 mm Hg. If the
2

pH is <7.35, there is an acute and uncompensated component of respiratory or metabolic

acidosis present. (In acute respiratory acidosis, the serum bicarbonate rises by 1 mEq/L for each
10-mmHg increase in Pco and the pH will change by 0.008 × (40 – Pco ). In chronic respiratory
2 2

acidosis, the bicarbonate rises by 3.5 mEq/L for each 10-mm Hg increase in Pco , and the pH will
2

change by 0.03 × (40 – Pco ) Changes outside of these ranges suggest an accompanying
2

metabolic disorder too dyspneic to perform bedside pulmonary function tests

 Diagnosis
• Radiographic abnormalities are common in COPD exacerbation and
may identify the underlying cause of the exacerbation, such as
pneumonia, or may identify an alternative diagnosis such as acute
heart failure.
• The ECG can identify ischemia, acute myocardial infarction, cor
pulmonale, and dysrhythmias.
• Measure levels in patients who take theophylline.
• Other tests, such as CBC, electrolytes, B-type natriuretic peptide, d-
dimers, and CT angiography of the chest, are chosen based on
clinical findings.
ASPIRATION PNEUMONIA
• Aspiration Pneumonia results from the swallowing of colonized
oropharyngeal contents into the lower respiratory tract with subsequent
inflammation and infection.
• The incidence of aspiration pneumonia in those who aspirate with acute
stroke / chronic degenerative neurologic conditions is higher than in
patients without those conditions.
• Risks for aspiration pneumonia include conditions that promote
oropharyngeal colonization with pathogenic bacteria / conditions that
impair the swallowing / gag mechanism.
• Typical bacterial species involved in aspiration pneumonia include S.
pneumoniae, S. aureus, H. influenzae, and Enterobacteriaceae in
community-acquired aspiration pneumonia.
• Common bacterial species in hospital-acquired aspiration pneumonia
include P. aeruginosa and gram-negative organisms.
• Aspiration pneumonitis is from exposure of sterile gastric contents
into the lower respiratory tract  results in a rapid chemical
pneumonitis due to irritation of the pulmonary tissues from the
acidic material. Aspiration pneumonia—infection occurring from
the exposure—is often unwitnessed, especially in the elderly. Other
aspiration syndromes include drowning, solid foreign body
aspiration with or without asphyxia, and lipoid pneumonia.
• Sterile pneumonitis and aspiration pneumonia are difficult to
distinguish from one another, even with bronchial lavage.
• Placement of nasogastric or gastric feeding tubes and the use of
sedative and neuroleptic drugs also increase the risk of
aspiration. Aspiration pneumonia is the most common cause of
death in gastric tube–fed patients.
• Small bowel obstruction, gastroesophageal reflux, esophageal
dysmotility, esophageal obstruction, and tracheoesophageal
fistula are GI risk factors for aspiration.
• Chronic degenerative neurologic conditions such as Parkinson’s
disease, myasthenia gravis, amyotrophic lateral sclerosis, acute
stroke, encephalopathy, seizures, and alteration of
consciousness increase the risk of aspiration.
 Pathophysiology
• The development of pneumonitis depends on the volume and pH
of the aspirate, with consensus that gastric contents with pH <2.5
and an aspirated volume of 0.3 to 0.4 mL/kg (20 to 30 mL in adults)
are required to develop aspiration pneumonitis. The injury
produced by acid aspiration is initially a direct caustic effect
followed by an inflammatory response that peaks in 4 to 6 hours.
Proinflammatory cytokines increase capillary permeability and
cause fluid and inflammatory cells to enter the area of irritation.
These reactions may manifest clinically as cough, pleuritic chest
pain, fever, and radiographic findings. Aspiration of solid or viscous
material blocking the airway may result in precipitous asphyxiation.
 Diagnosis
• Chest radiographs in aspiration pneumonia usually show unilateral
focal or patchy consolidations in the dependent lung segments
(Figure 65-4).
• Occasionally, a bilateral or interstitial pattern can be seen. The right
lower lobe is the most common area of consolidation if the
aspiration occurs when the patient is upright.
• Early in the course, the white blood cell count may not be elevated.
• Arterial blood gases to identify hypoxemia or hypoventilation aid
care and are best compared to previous values if chronic lung
disease exists.
 Clinical Features
• The clinical symptoms of aspiration pneumonia include fever, dyspnea,
and productive cough. Other symptoms of systemic infection in the
elderly and debilitated may be present, including a change in mental
status, lethargy, and nausea / vomiting. The physical examination may
reveal signs classic for pneumonia, including tachycardia, tachypnea, fever,
rales, or decreased breath sounds in an ill-appearing patient.
• “Silent aspirators” are typically older and have a chronic neurologic
disorder and will present with a cough / fever / general malaise. Silent
aspirators are more likely to be from a chronic care facility and have a
history of prior pneumonia episodes. Historical features that suggest silent
aspiration include general debility, recurrent cough, hoarseness, or
dysphagia.
PULMONARY TUBERCULOSIS
• Tuberculosis (TB) is a severe and contagious disease caused by
infection with members of the Mycobacteria tuberculosis.
• It is the second leading cause of death among infectious
diseases and a major cause of death among those with HIV.
 Primary Infection
• Once the organisms reach the lungs, host defenses are
activated. Some organisms survive and are transported to the
regional lymph nodes, where the host cell-mediated immunity is
activated to contain the infection.
• Granulomas, known as tubercles, form as a result of this
process, which involves activated macrophages and T
lymphocytes in addition to active bacteria in most cases.
Tubercles are a sign of primary infection and may progress to
caseation necrosis and calcification. In the lung, the Ghon
complex (Figure 67-1) is a manifestation, appearing as calcified
hilar lymph nodes.
 Latent Infection
• If the tubercle fails to contain the infection, the mycobacteria may
spread by hematogenous, lymphatic, or direct mechanical routes.
The tendency is for survival in areas of high oxygen content or
blood flow, such as the apical and posterior segments of the upper
lobe and the superior segment of the lower lobe of the lung, the
renal cortex, the meninges, the epiphyses of long bones, and the
vertebrae. In these areas, the mycobacteria can remain dormant
for years. During dormancy (or latent infection), the disease is
detected by a positive tuberculin skin test. The skin test generally
becomes positive 1 to 2 months after initial exposure.
 Reactivation Disease from latent infection
• For the individuals who successfully contain the initial infection and avoid
primary disease, mycobacteria lie latent within healed, fibrotic and/or calcific
granulomata. At this stage, mycobacteria cannot be cultured from host sputum
or tissue specimens and symptoms are not present. It is believed that latent
tuberculous infection (LTBI), with the potential for future reactivation, persists
for life of the host. In a small minority, granulomas break down, mycobacteria
replication increases, and symptomatic disease develops. Such reactivation can
occur with age-related immune senescence or in those with acquired risk factors
for active TB.
• Reactivation most commonly occurs in the apical-posterior segments of the
lungs, where higher oxygen tension favors bacillary replication, but disease can
occur at any previously seeded site. Once reactivated, bacilli can usually be
cultured from sputum and/or tissue samples.
 Caseation and Cavitation
• Differences in quality of host adaptive immune response determine clinical
presentation. Some individuals develop a particularly robust, caseating
granulomatous inflammatory response with resultant tissue destruction and
lung cavitation—they discharge large amounts of bacilli into airways and are
highly contagious. At the other end of the spectrum, a severely weak or
immature granulomatous response allows hematogenous dissemination of
bacilli, accompanied by widespread inflammatory foci of poorly formed
granulomas. Each focus typically enlarges to about 3 mm in size, or about the
size of millet seed. This severe form of TB (miliary TB) has a high case-fatality
rate
 Clinical Features
• Fevers (may be absent in eldery)
• Night sweats
• Anorexia
• Weight loss
• Cough may be dry but after several months becomes
productive
 Diagnosis
• Mantoux or tuberculin skin test
Uses intracutaneous injection of 0.1 mL
of purified protein derivative into the
forearm. The test relies on a delayed-
type hypersensitivity reaction that’s
triggered in those with past infection
or those w/ a significant recent
exposure to tuberculosis.
The test is read between 48 and 72
hours by measuring the extent of skin
induration at the test site.
• Blood Test
Interferon-gamma release assays (IGRA)
 give results in 16 to 24 hours
• Cultures
For the diagnosis of pulmonary TB at
least 3 sputum samples, each 5 to 10 mL,
should be collected at least 1-hour apart.
For those patients unable to expectorate
spontaneously, sputum induction (with
nebulized hypertonic saline) or
bronchoalveolar lavage (BAL) is an
alternate established method.
• Direct Microscopy
Two methods are commonly used for
acid-fast staining of mycobacteria:
carbolfuchsin (e.g., Ziehl–Neelsen [ZN])
and fluorochrome-based procedures
(e.g., auramine–rhodamine dye)
• NAAT (Nucleic Acid Amplification Test)
Culture methods can detect as few 10 viable bacilli per millimeter of
sample, can yield results within 1 day.
• Chest Radiograph
In primary infection, parenchymal infiltrates in any area of the lung may
be found. Younger patients are more likely to have enlarged hilar lymph
nodes, whereas adults more frequently have parenchymal abnormalities
and effusions.
In latent tuberculosis, nonspecific findings include upper lobe or hilar
nodules and fibrotic lesions, which may be calcified. Other findings are
bronchiectasis, volume loss, and pleural scarring. Healed primary areas of
infection appear as Ghon foci, areas of scarring, and calcification
Reactivation infections often have the classic findings of tuberculosis:
cavitary or noncavitary lesions in the upper lobe or superior segment of
the lower lobe of the lungs
STATUS ASTMATICUS/ ACUTE SEVERE ASTHMA
• A heterogeneous disease, usually characterized by chronic
airway inflammation.
• Characteristics:
– History of respiratory symptoms such as wheeze,
– Shortness of breath,
– Chest tightness and cough that vary over time and in intensity,
– Together with variable expiratory airflow limitation.
 Symptomps
• More than one symptom (wheeze, shortness of breath, cough,
chest tightness), especially in adults
• Symptoms often worse at night or in the early morning
• Symptoms vary over time and in intensity
• Symptoms are triggered by viral infections (colds), exercise,
allergen exposure, changes in weather, laughter, or
• irritants such as car exhaust fumes, smoke or strong smells.
 Symptomps of severe asthma
• Frequent or persistent asthma symptoms,
• Frequent exacerbations,
• Persistent loss of lung function,
• Substantial impairment of quality of life,
• And troublesome comorbidities (anxiety and depression)
Diagnostic
MASSIVE PLEURAL EFFUSION
 Massive Pleural Effusion
• Massive pleural fluid collection is commonly caused by
malignancy.
• A malignant pleural effusion is diagnosed by detecting
exfoliated malignant cells in pleural fluid or demonstrating
these cells in pleural tissue obtained by percutaneous pleural
biopsy, thoracoscopy, thoracotomy, or at autopsy.
 Clinical presentation
• Large pleural effusion – dyspnea on exertion and cough
• Weight loss when malignant involves of the pleura
• Chest pain because of involvement of the parietal pleura, ribs,
or chest wall
• Cachexia and lymphadenopathy are present in about one –
third of patient on initial presentation
 Severe acute respiratory syndrome
• Is a rapidly progressive illness caused by a coronavirus.
• Isolation procedures for suspected severe acute respiratory
syndrome patients include airborne, droplet, and contact
isolation
 Sign & symptoms
Risk factors
• Fever >38°C
• Age: >60 year
• Fatique
• Headache • Diabetes melitus
• Myalgia • Hepatitis B infectiom
• Nonproductive cough
• Dyspnea
• Mylagias
• Diarrhea
• anorexia
 Diagnosis
• Initial test: • Laboratory findings:
– Pulse oximetry – Lymphopenia, leukopenia,
– Blood culture thrombocythopenia
– Sputum gram stain & culture – Hyponatremia, hypokalemia
– Viral respiratory pathogen test – Elevated of lactate
dehydrogenase, alanine
aminotransferase, hepatic
transaminase
– Elevated of creatinin kinase
 Diagnosis Management
• Chest X-ray • Mechanical ventilation
– Infiltrat peripheral • Ribavirin &
– Frank corticosteroid standard
consodilation therapy
– Ground – glass
opacification
PULMONARY EDEMA
http://www.racgp.org.au/afp/2010/december/acu
te-pulmonary-oedema/
http://www.racgp.org.au/afp/2010/december/acute-
pulmonary-oedema/
http://www.racgp.org.au/afp/2010/december/acute-
pulmonary-oedema/
http://www.racgp.org.au/afp/2010/december/acute-
pulmonary-oedema/
Figure 3 - Proposed Diagnostic Algorithm For Patients With Suspected
High-risk PE, i.e. Presenting With Shock Or Hypotension.

http://eurheartj.oxfordjou
rnals.org/content/early/20
14/08/28/eurheartj.ehu28
3
Figure 4 - Proposed diagnostic algorithm for patients with suspected not
high-risk pulmonary embolism.

http://eurheartj.oxfordjou
rnals.org/content/early/20
14/08/28/eurheartj.ehu28
3
ARDS
• Acute respiratory distress syndrome (ARDS) is 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 from many
underlying medical and surgical disorders.
• The lung injury may be direct, as occurs in toxic
inhalation, or indirect, as occurs in sepsis

• While many medical and surgical illnesses have been

associated with the development of ARDS, most cases
(>80%) are caused by a relatively small number of clinical
disorders: severe sepsis syndrome and/or bacterial
pneumonia (~40–50%), trauma, multiple transfusions,
aspiration of gastric contents, and drug overdose.
• Among patients with trauma, the most frequently
reported surgical conditions in ARDS are pulmonary
contusion, multiple bone fractures, and chest wall
trauma/flail chest, whereas head trauma, near-drowning,
toxic inhalation, and burns are rare causes.
• The risks of developing ARDS are increased in patients
with more than one predisposing medical or surgical
condition.
Disease Inspection Palpation Percussion Auscultation

Tracheal
aspiration
Aspiration • Fever • Rales
pneumonia • Dyspnea/tacyhypnea • Decreased breath
• Productive cough sounds in an ill-
appearing patient
Acute COPD • Chronic and • Hyperressonance • Expiratory wheezing
exacerbation progressive dyspnea, during maximum forced
cough, and sputum exhalation, and
production prolongation of the
• Emphysema -> expiratory time
expansion of the • Chronic bronchitis ->
thorax (barrel chest) coarse crackles
• Tachypnea,
tachycardia, cyanosis
• Sitting in an up and
forward position
using pursed lip
exhalation and
engaging accessory
muscles to breathe
Disease Inspection Palpation Percussion Auscultation

SARS

Status asthmaticus & • Rapid breathing • Hyperressonance • Loud wheezing

acute severe asthma • Accessory muscle use (maybe audible
may ensue without a
• Expiration becomes stethoscope)
prolonged • Decreased intensity
• Paradoxical respiration of breath sounds
• Prolongation of the
expirations phase

Massive pleural
effusion
Pulmonary edema • Dyspnea • Wheezing
• Cough • Moist, bilateral
• Diaphoresis, perioral, pulmonary rales
and peripheral cyanosis • Increased
• Pink, frothy sputum pulmonary second
• Bulging neck veins with sound, S3 gallop
elevated jugular venous
pressure
Disease Inspection Palpation Percussion Auscultation

Pneumothorax • Sudden onset of • Decreased tactile • Hyperresonance • Decreased breath

dyspnea and ipsilateral fremitus sounds
• Pleuritic chest pain
SARS
 SARS
• Severe acute respiratory syndrome (SARS ) : rapidly progressive
illness caused by a coronavirus.
• Isolation procedures for suspected severe acute respiratory
syndrome patients include airborne, droplet, and contact
isolation.
• The clinical features of coronavirus infection include fever (99%
frequency), nonproductive cough, dyspnea, myalgias,
headache, and diarrhea (many cases) progress to a moderate-
severe condition characterized by hypoxia and dyspnea at rest.
Diagnosis Treatment
• Chest radiographs  subtle • Treatment for severe acute
peripheral pulmonary infiltrates. respiratory syndrome is largely
• Chest CT demonstrates ground- supportive
glass consolidation during early • lopinavir-ritonavir  standard
phases of illness. therapy (ribavirin and
• Lymphopenia, thrombocytopenia, corticosteroids)
elevated lactic dehydrogenase, liver
enzymes, and creatine
phosphokinase levels
• Polymerase chain reaction testing
and obtain serum for serologic
testing (detecting corona virus)