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Exudative
Diagnostic Criteria
KRENOVIANTZ 17
JEVAI M.D.
KRENOVIANTZ 17
JEVAI M.D.
Proliferative
Progressive lung injury
Early pulmonary fibrosis
Lasts from day 7 21 days of illness
Shift to a lymphocyte-predominant pulmonary
infiltrate
Proliferation of Type II pneumocyte along alveolar
basement membranes
Alveolar type III procollagen peptide marker of
pulmonary fibrosis with a protracted clinical
course and increased mortality
Fibrotic
Initiation of ductal and interstitial fibrosis leading
to emphysema-like changes
Intimal proliferation pulmonary hypertension
Increased mortality
Clinical Characteristics
tachypnea - earliest sign
dyspnea
low pO 2, low PCO2
fine rales
CXR clear or few scattered infiltrates
cyanosis, dyspneic
prominent rales
extensive infiltrates
intractable hypoxemia
Treatment
General Principles
Treat underlying medical and surgical disorder
Minimize procedures and their complications
Deep venous thrombosis prophylaxis, stress gastritis, CVP
catheter infections
Treat nosocomial infection
Provide adequate nutrition
Management of Mechanical Ventilation
Ventilator induced lung injury
Alveolar overdistention
Recommend low tidal vol 5 ml/kg
Alveolar collapse
reduced lung compliance (stiff lungs)
optimal PEEP (12 15 ) to minimize
FiO2 and maximize PaO2
inverse ration ventilation (I:E >1:1)
prone position
Low VT in ARDS
KRENOVIANTZ 17
JEVAI M.D.
KRENOVIANTZ 17
JEVAI M.D.
DIC
Functional recovery within 6 months from ARDS
ECMO in ARDS
Table 258-1
Major
Etiologies of
Bronchiectasis
and Proposed
Workup
Pattern of
Etiology by Categories (with Workup
Lung
Specific Examples)
Involvement by
Bronchiectasis
Focal
Diffuse
Gram's stain/culture;
stains/cultures for
acid-fast bacilli and
fungi. If no pathogen
is identified, consider
bronchoscopy with
bronchoalveolar
lavage (B AL)
Immunodeficiency (e.g.,
hypogammaglobulinemia,
HIV infection, bronchiolitis
obliterans after lung
transplantation)
Measurement of
chloride levels in
sweat (for cystic
fibrosis), 1 antitrypsin
levels; nasal or
respiratory tract
brush/biopsy (for
dyskinetic/immotile
cilia syndrome);
genetic testing
Autoimmune or
rheumatologic causes (e.g.,
rheumatoid arthritis,
Sjgren's syndrome,
inflammatory bowel
disease); immune-mediated
disease (e.g., allergic
bronchopulmonary
aspergillosis)
Clinical examination
with careful joint
exam, serologic testing
(e.g., for rheumatoid
factor). Consider
workup for allergic
bronchopulmonary
aspergillosis,
especially in patients
with refractory
asthma a
Recurrent aspiration
Test of swallowing
function and general
neuromuscular
strength
Guided by clinical
condition
Idiopathic
Exclusion of other
causes
KRENOVIANTZ 17
JEVAI M.D.
Aspiration-Prone Host
Immunocompromised Host
Lemierre's disease.
Often in a young patien t with influenza.
RESPIRATORY FAILURE
Types of respiratory failure
Type I, Acute Hypoxemic Respiratory Failure
alveolar flooding and subsequent intrapulmonary
shunt physiology occur.
KRENOVIANTZ 17
JEVAI M.D.
Diagnosis
rapid onset of dyspnea at rest, tachypnea, tachycardia, and
severe hypoxemia.
Rales and wheezing due to airway compression from
peribronchial cuffing may be audible.
Hypertension is usually present due to release of endogenous
catecholamines.
difficult to distinguish between cardiogenic and
noncardiogenic
KRENOVIANTZ 17
JEVAI M.D.
medulla
the dorsal respiratory group (DRG)
ventral respiratory column (VRC).
These neurons have widespread
projections, including the descending
projections into the contralateral spinal
cord, where they perform many
functions.
Hypoventilation
Diseases that reduce minute ventilation or increase dead space
Four major categories:
parenchymal lung and chest wall disease
sleep disordered breathing
neuromuscular disease
respiratory drive disorders
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JEVAI M.D.
Treatment:
Nocturnal noninvasive positive-pressure ventilation (NIPPV)
improve daytime hypercapnia, prolong survival, and improve
health-related quality of life when daytime hypercapnia is
documented.
ALS guidelines recommend nocturnal NIPPV
Paco2 45 mmHg
nocturnal oximetry demonstrates oxygen saturation
88% for 5 consecutive minutes
maximal inspiratory pressure <60 cm H2O; and
FVC <50% predicted. nocturnal, but not daytime,
hypercapnia
Treat the underlying disorder.
medroxyprogesterone and acetazolamide
supplemental oxygen is effective in attenuating hypoxemia,
polycythemia, and pulmonary hypertension.
Phrenic nerve or diaphragm pacing for high cervical spinal
cord lesions or respiratory drive disorders.
Clinical course
An asymptomatic stage where daytime PaO2 and
PaCO2 are normal,
nocturnal hypoventilation, initially during rapid
eye movement (R EM) sleep and later in non-REM
sleep.
If vital capacity drops further, daytime hypercapnia
develops.
the hallmark of all alveolar hypoventilation
syndrom es is an increase in alveolar PCO2
(PACO2) and, therefore, in PaCO2.
respiratory acidosis --- compensatory increase in
plasma bicarbonate concentration.
erythrocytosis.
induce pulmonary vasoconstriction, pulmonary
hypertension, right-ventricular hypertrophy, and
right heart failure.
Diagnosis
ABG - elevated PaCO2 with a normal pH, elevated plasma
bicarbonate
Physical examination, imaging studies (chest x-ray and/or
CT scan), and pulmonary function tests are sufficient to
Hypoventilation Syndromes
Obesity Hypoventilation Syndrome
body mass index (B MI) 30 kg/m2
sleep-disordered breathing and chronic
daytime alveolar hypoventilation,
defined as PaCO2 45 mmHg, and PaO2 <
70 mmHg in the absence of other known
causes of hypercapnia.
obstructive sleep apnea syndrome,
defined by an apnea hypopnea index 5
AND daytime sleepiness, is
approximately 34% in middle-aged men
and 2% in middle-aged women.
KRENOVIANTZ 17
JEVAI M.D.
Treatment:
weight reduction
continuous positive airway pressure (C PAP) therapy during
sleep
Hyperventilation
ventilation in excess of metabolic requirements (CO2
production) leading to a reduction in PaCO2
Treatment:
few well-controlled treatment studies.
reassurance and frank discussion
Identifying and eliminating habits that perpetuate hypocapnia
(yawning or sigh breathing)
breathing exercises and diaphragmatic retraining may be
beneficial for some patients.
Beta-blockers (sym pathetically mediated symptoms)
Once neural input has been delivered to the respiratory pump muscles,
normal gas exchange requires an adequate amount of respiratory
muscle strength to overcome the elastic and resistive loads of the
respiratory system (F ig. 264-1A, Chap. 252). In health, the strength of
the respiratory muscles readily accomplishes this, and normal
respiration continues indefinitely.
KRENOVIANTZ 17
JEVAI M.D.
medulla
the dorsal respiratory group (DRG)
ventral respiratory column (VRC). These
neurons have widespread projections,
including the descending projections into
the contralateral spinal cord, where they
perform many functions.
Hypoventilation
shortness of breath and diminished exercise tolerance.
Episodes of increased dyspnea and sputum production are
hallmarks of obstructive lung diseases, such as chronic
obstructive pulmonary disease (C OPD)
whereas progressive dyspnea and cough are common in
interstitial lung diseases. Excessive daytime somnolence,
poor quality sleep, and snoring are common among patients
with sleep-disordered breathing. Sleep disturbance and
orthopnea are also described in neuromuscular disorders.
Mallampati Grading
KRENOVIANTZ 17
JEVAI M.D.
KRENOVIANTZ 17
JEVAI M.D.
BRONCHIECTASIS
Focal
diffuse
Pathology:
Pseudomonas, Haemophilus
Staph, Klbesiella, TB
Non-infectious causes
Pathogenesis
Clubbing
CTscan
Bronchography
Reid s Classification
Bronchograp hy
KRENOVIANTZ 17
JEVAI M.D.
Table 258-1
Major
Etiologies of
Bronchiectasis
and Proposed
Workup
Pattern of
Etiology by Categories (with Workup
Lung
Specific Examples)
Involvement by
Bronchiectasis
Focal
Diffuse
Gram's stain/culture;
stains/cultures for
acid-fast bacilli and
fungi. If no pathogen
is identified, consider
bronchoscopy with
bronchoalveolar
lavage (B AL)
Immunodeficiency (e.g.,
hypogammaglobulinemia,
HIV infection, bronchiolitis
obliterans after lung
transplantation)
Measurement of
chloride levels in
sweat (for cystic
fibrosis), 1 antitrypsin
levels; nasal or
respiratory tract
brush/biopsy (for
dyskinetic/immotile
cilia syndrome);
genetic testing
Autoimmune or
rheumatologic causes (e.g.,
rheumatoid arthritis,
Sjgren's syndrome,
inflammatory bowel
disease); immune-mediated
disease (e.g., allergic
bronchopulmonary
aspergillosis)
Clinical examination
with careful joint
exam, serologic testing
(e.g., for rheumatoid
factor). Consider
workup for allergic
bronchopulmonary
aspergillosis,
especially in patients
with refractory
asthma a
Recurrent aspiration
Test of swallowing
function and general
neuromuscular
strength
Guided by clinical
condition
Idiopathic
Exclusion of other
causes
KRENOVIANTZ 17
JEVAI M.D.
Aspiration-Prone Host
Immunocompromised Host
Lemierre's disease.
Often in a young patien t with influenza.
Treatment
Eliminate identifiable problem
Bronchial hygiene - chest PT
Control infection -antibiotics
reverse airflow obstruction - bronchodilators
Bronchial artery embolization, resection, transplant
Comp lications:
Recurrent infection
hemoptysis
Prognosis:
KRENOVIANTZ 17
JEVAI M.D.