Pulsus paradoxus (a decrease in the systolic blood pressure during inspiration) results from 

a decrease in
cardiac stroke volume with inspiration due to greatly increased left-ventricular afterload.
Arus puncak ekspirasi  (APE) or Peak Expiratory Flow (PEF) menggambarkan keadaan saluran napas dan
besarnya aliran udara maksimum yang dicapai saat ekspirasi dengan usaha paksa secara maksimal dari
kapasitas paru total (Dermawan et al., 2013)
Sc: kapita selekta
COPD
Early stages  usually have an entirely normal physical examination.
Perokok  tanda2 perokok aktif bisa dari baunya atau dari nicotine staining di jarinya. Kek warna kuning
kecoklatan gitu.

Methylxanthines and Short-Acting β-Adrenergic Receptor Agonists

Both methylxanthines and short-acting β-adrenergic receptor agonists (SABAs)

promote mucus clearance by several mechanisms:

 Increase airway luminal diameter;

  Increase ciliary beat frequency via an increase in intracellular cyclic adenosine
monophosphate levels; and
 Increase mucus hydration by stimulating airway Cl− secretion via activation of the
cystic fibrosis transmembrane regulator.

This decreases mucus viscosity, allowing for easier transport by airway cilia.

Long-Acting β-Adrenergic Receptor Agonists

LABAs also reduce hyperinflation and increase peak expiratory flow, which are
essential components of effective cough. In vitro evidence has shown that salmeterol
can stimulate ciliary beat frequency (81). Similarly, formoterol significantly improves
mucociliary clearance compared with placebo in patients with bronchitis.

Anticholinergics
Anticholinergics, by their action on the muscarinic receptor, are believed to help mucus
clearance by increasing luminal diameter and by decreasing surface and submucosal
gland mucin secretion.

Glucocorticoids
decrease goblet cell hyperplasia. Dexamethasone has also been shown to decrease
epithelial mucin gene MUC5AC gene expression in human bronchial epithelial cells.
They may also hasten mucociliary clearance. Inhaled corticosteroids reduce
exacerbation frequency and improve quality-of-life scores in COPD.

Phosphodiesterase-4 Inhibitors
Phosphodiesterase-4 (PDE-4) inhibition decreases inflammation and promotes airway
smooth-muscle relaxation by preventing the hydrolysis of cyclic adenosine
monophosphate to its inactive metabolite. Contoh Cilomilast, roflumilast.

Antioxidants
 The two most extensively studied antioxidant medications for COPD are N-
acetylcysteine and carbocysteine. N-Acetylcysteine is a precursor of L-cysteine and
reduced glutathione, which reduces cellular levels of oxidative stress and production of
reactive oxygen species, also reduces disulfide bonds and sulfhydryl bonds that link
together mucin polymers, thereby reducing sputum viscosity.

Antibiotics
is not indicated in the treatment of chronic bronchitis however macrolide therapy has
been shown to have anti-inflammatory property and hence may have a role in the
treatment of chronic bronchitis. They have been shown to inhibit proinflammatory
cytokines, decrease neutrophil burst, inhibit migration and increase apoptosis,
decrease eosinophilic inflammation, increase mucociliary transport, reduce goblet cell
secretion, and decrease bronchoconstriction.
Phosphodiesterase-4 inhibitors
decrease inflammation and promote airway smooth muscle relaxation by preventing
the hydrolysis of cyclic adenosine monophosphate a substance when degraded leads to
the release of inflammatory mediators.
Sc: American thoracic society. Chronic Bronchitis and COPD. Dan NCBI statpearls.

EMFISEMA

Pathophysiology
The clinical manifestations of emphysema are the consequences of damage to airways
distal to terminal bronchiole, which include respiratory bronchiole, alveolar sacs,
alveolar ducts, and alveoli, collectively known as the acinus. There is abnormal
permanent dilatation of the airspaces and destruction of their walls due to the action of
the proteinases. This results in a decrease in the alveolar and the capillary surface area,
which decreases the gas exchange. The part of the acinus affected determines the
subtype.
It can be subdivided pathologically into the following:
 Centrilobular (proximal acinar) is the most common type and is commonly
associated with smoking. It can also be seen in coal workers' pneumoconiosis.
 Panacinar is most commonly seen with alpha one antitrypsin deficiency.
 Paraseptal (distal acinar) may occur alone or in association with the above two.
When it occurs alone, the usual association is a spontaneous pneumothorax in a
young adult.
After long-term exposure to noxious smoke, inflammatory cells such as macrophages,
neutrophils, and T lymphocytes are recruited, which play an important role in the
development of emphysema. First, macrophages are activated, which release
neutrophil chemotactic factors like leukotriene B4 and interleukin-8. Once the
neutrophils are recruited, these, along with macrophages, release multiple proteinases
and lead to mucus hypersecretion.
Elastin is an important component of the extracellular matrix that is required to
maintain the integrity of lung parenchyma and small airways. Elastase/anti-elastase
imbalance increases the susceptibility to lung destruction leading to airspace
enlargement. Cathepsins and neutrophil-derived proteases (i.e., elastase and
proteinase) act against elastin and destroy the connective tissue of the parenchyma of
the lung. Cytotoxic T cells release TNF-a and perforins, which destroy the epithelial
cells of the alveolar wall.
Cigarette smoking not only causes mucus hypersecretion and release of neutrophilic
proteolytic enzymes, but it also inhibits anti-proteolytic enzymes and alveolar
macrophages. Genetic polymorphisms have a role in inadequate antiproteases
production in smokers. All of these contribute to the development of emphysema.
Lung parenchyma produces alpha one antitrypsin (AAT), which inhibits trypsinize and
neutrophil elastase in the lung. AAT deficiency can lead to panacinar emphysema.
PNEUMONIA

Diagnosis
Evaluation
Evaluation of CAP and HAP involves:
Clinical Evaluation
Involves performing a thorough history and physical examination as summarized in the
section above.
Radiological Evaluation
According to the Infectious Diseases Society of America (IDSA) and American Thoracic
Society (ATS) guidelines, a demonstratable infiltrate by chest x-ray is necessary and is
considered the best method (with supportive clinical findings) for the diagnosis of
pneumonia.[2] Findings may vary from lobar to interstitial infiltrate, to
occasionally cavitary lesions with air-fluid levels suggestive of a more severe disease
process.
Laboratory Evaluation
These include a series of tests like blood culture, sputum culture and microscopy,
routine blood counts, and lymphocyte count. Special tests such as urinary antigen
testing, bronchial aspirate, or induced sputum may be used for certain pathogens. Two
tests, procalcitonin and C-reactive protein help differentiate viral from bacterial causes
when clinical and radiological findings may not be obvious. It is also noteworthy that
empiric antibiotic treatment may be initiated in all typical cases of pneumonia, and the
entire battery of tests is seldom needed.[2]
Evaluation of VAP, on the other hand, is a bit different from that of CAP. It requires
radiological and microbiological evidence prior to initiation of antimicrobial therapy.
VAP should be suspected in ventilated patients who have new onset dyspnea, fall in
oxygen saturation on the same ventilator settings, fevers with chills or new onset lung
infiltrates. All suspected patients require a chest x-ray (or a CT scan if x-ray findings are
inconclusive). This must be followed by invasive sampling techniques like mini
broncho-alveolar lavage (BAL) or bronchoscopic BAL or even protected specimen
brush (PSB) to identify causal organisms. Once the diagnosis is confirmed, the
appropriate antimicrobial therapy can be initiated
TERAPI

Treatment / Management
Management of CAP involves initial risk stratification of the patient and to decide whether to manage
the patient on an outpatient basis, in a general medicine ward, or in an intensive care unit (ICU)
setting. The "CURB-65" scale has been used extensively for this purpose. The components of this scale
include confusion, uremia (BUN greater than 20 mg/dl), a respiratory rate greater than 30 per minute,
blood pressure less than 90 mm Hg systolic or less than 60 mm Hg diastolic, and age greater than 65.
One point is awarded for every positive criterion that the patient meets. Patient disposition is decided
as follows.
 A score of 0 to 1: Outpatient management. These patients are treated empirically using
Fluoroquinolones or Beta-lactams+ Macrolides if adverse comorbidities are present and with
Macrolides or Doxycycline if no comorbidities are present. 
 A score of 2 to 3 indicates admission and management in a general medicine ward. The first
line of treatment is a choice between fluoroquinolones or macrolides plus beta-lactams.
 A score of 4 or more warrants management in an ICU. The empiric regimen, in this case, is a
choice between a combination of a beta-lactam plus fluoroquinolones or beta-lactams plus
macrolides.[17][2]
Management of VAP and HaP is in accordance with the ATS/IDSA guidelines. It is much more
prolonged, complicated, and involves the use of broad-spectrum antibiotics as compared to the
management of CAP. It involves early identification of signs of pneumonia and thorough evaluation as
discussed above, before starting empiric therapy. Empiric therapy is guided by resistance patterns
prevalent in that region as well as patient risk factors for multi-drug resistant organisms. Generally,
regimes coving S. aureus, Pseudomonas, and gram-negative bacilli are designed for patients of HAP and
VAP. For patients without MDR risk factors, the regimen generally followed is piperacillin/tazobactam
plus cefepime plus levofloxacin. For patients with MDR risk factors, the preferred regime involves a
combination of an Aminoglycoside along with one of imipenem, meropenem, aztreonam,
piperacillin/tazobactam, ceftazidime, or cefepime