Patologi Kardiopulmonal

Abdurrasyid, SSt.Ft, M. Fis

 Patologi
Kardiopulmonal

Penyakit Penyakit
Obstruktif
paru Jantung
Paru
Restriktif Koroner
• manifestasi dari
• menurunnya kecepatan
beberapa geajala seperti
ekspirasi  adanya
• Paru tidak dapat aterosklerosis pada kedua
resitensi jalan napas
mengembang/ekspansi sisi arteri koroner
•Adanya pembatasan
• paru mampu • performa jantung
inspirasi kurang dari
mengembang namun menurun
normal
dinding dada tidak •Berpengaruh thdp
•Terjadi overlap/tumpang
bergerak ekspansi volume darah yg
tindih antara kedua
dipompakan dan denyut
problem diatas
Penyakit Paru Obstruktif
Batuk dgn sputum sampai 3 bulan- 2 tahun
Apa Penyebabnya?
 Hipersekresi
Sputum

Penebalan
Dinding
Mukosa

Kerusakan
Cilia
Bronchitis
Bronchiectasis
Kronis

Obstruktif
Paru

Emfisema Asma
 Chronic Bronchitis
• Chronic bronchitis is a disease characterized
by a cough producing sputum for at least 3
months and for 2 consecutive years (American
Thoracic Society, 1962)
• Pathologically, there is an increase in the size ofthe
tracheobronchial mucous glands (increased Reid
index) and goblet cell hyperplasia (Mitchell, 1968;
Reid, 1960; Stoller and Wiedemann, 1990). Mucous cell
metaplasia of bronchial epithelium results in a
decreased number of cilia. Ciliary dysfunction and
disruption of the continuity of the mucous blanket are
common. In the peripheral airways, bronchiolitis,
bronchiolar narrowing, and increased amounts of
mucus are observed (Cosio, 1978; Wright, 1992).
• Individuals with bronchitis often expectorate mucoid brownish-
colored sputum. In an exacerbation, usually from infection, they
have an even greater amount of purulent sputum. Ventilation-
perfusion abnormalities are common, which increase hypoxemia
and Paco2 retention (Rochester and Brown, 1976). The respiratory
rate increases, as does the use of accessory muscles. The resultant
increased work of breathing requires greater oxygen consumption
by these muscles, with a greater production of carbon dioxide
(C02) than the respiratory system can adequately meet. This
contributes to a further drop in the arterial partial pressure of
oxygen (Pao2) and a rise in Paco2. The hypoxemia and acidemia
increase pulmonary vessel constriction, which raises pulmonary
artery pressure and ultimately leads to right heart failure
(corpulmonale).
Emphysema
• The expiratory phase of breathing is
prolonged with audible wheezing and rhonchi.
However, when severe obstruction is present,
the chest becomes silent (Gold, 1976). The
patient may cough often, though
unproductively, and may complain of tightness
in his chest.
• Early in the attack, arterial blood gases reflect
slight hypoxemia and a low Paco2 (from
hyperventilation). If the attack progresses, the
Pao2 continues to fall as the Paco2 climbs
above the normal range.
• Characteristic of asthma, the basement
membrane is thickened. The mucous glands are
enlarged, and there is an increase in the number
of goblet cells. Evidence of bronchospasm is seen
by the hypertrophied and thickened smooth
muscle. The lumens of most bronchioles, down to
the terminal bronchioles, are filled with viscous,
sticky mucus
 Bronchiectasis
• Bronchiectasis is defined as an abnormal
dilation of medium-size bronchi and
bronchioles (about the fourth to ninth
generations), generally associated with a
previous, chronic necrotizing infection within
these passages. Ordinarily, there is sufficient
cartilage within the walls of the larger bronchi
to protect them from dilation.
• Pathologically, the mucosa appears edematous and
ulcerated. Destruction of the elastic and muscular
structures of the airway walls is evident with
resultantdilation and fibrosis. The walls are lined with
hyperplastic, nonciliated, mucus-secreting cells that
have replaced the normal ciliated epithelium. This
change is significant, because it interrupts the
mucociliary blanket and causes pooling of infected
secretions, which further damage and irritate the
bronchial wall
• Some 60% of the cases of bronchiectasis are
preceded by an acute respiratory infection.
The infection involves the bronchial walls.
Portions of the mucosa are destroyed and are
replaced by fibrous tissue.
• Pulmonary function tests of patients with
localized bronchiectasis show few or no
abnormalities. However, in more widespread
disease, there is a reduction in the FEV I,
maximum midexpiratory flow rate, maximal
voluntary ventilation (MVV), diffusing apacity,
and an increase in the residual volume
 Prognosis of bronchiectasis
• Before the antibiotic era, the prognosis for
individuals with bronchiectasis was poor. As
might be expected, infection was usually the
precipitating cause of death. However, at the
present time, the prognosis of patients with
proper medical management is much
improved
Restrictive Lung Desease
 INTRODUCTION
Restrictive lung diseases adalah:
Kumpulan penyakit paru yang penyebabnya berbeda-beda,
gangguan pada umumnya kesulitan pengembangan
paru dan terjadi penurunan volume paru.
Penyakit restrictive dapat disebabkan karena penyakit
parenchyma alveolar atau pleurae, fibrotic alveolar,
interstitial parenchyma, dapat juga karena gangguan
dinding dada atau neuromuskular apparatus (Julie
AS,1991)
 Restrictive lung diseases
1. Intrinsic : Perubahan
parenchyma paru .
2. Extrinsic :
a. Penyakit pleura,
b. Penyakit dinding
thorac,
c. Penyakit
neuromuscular yg
ada gangguan
fungsi pernafasan.
 Etiology of restrictive lung disease
• This group of disorder has veriety of causes:
(Kelompok penyakit ini macam-macam kasus)
1. Radiation therapy.
2. Inorganic dust
3. Inhalation of noxious gases
4. Oxygen toxicity
5. Tuberculosis
6. Pleuritis.
 Pathophysiology

Diseases of the Lung

Parenchyma
 Intrinsic parenchyma
1. Parenchymal changer often Inflammation or fibrotic of the
lung tissue (interstitial lung disease) to making more
resistant to expansion ( less distensible). (Perubahan
parenchym setelah imflamasi atau fibrotik dari jaringan paru.
interstitial lung disease menyebabkan pengembangan paru
terhambat).
2. Consequently lung volume ate reduced.
3. Reduced pulmonary vasculer  Hypoxemia and cor
pulmonal.
4. In pleural desease thickened (mengentalkan) plaques of
collagen fibers cause fibrosis.
5. These changes may be due to injury.
A Vicious Cycle (linkaran kejam)
 PATHOPHYSIOLOGY
1. Elastic recoil paru  outward recoil forces dari dinding
thorac (chest wall)  lung volumes ↓
2. Udara yg dikeluarkan saat ekspirasi tidak sebanding
dng volume paru yg masuk.
3. Arterial hypoxemia: V/Q mismatching (intrapulmonary
shunt)
4. Exercise - induced desaturation: impaired diffusion of
oxygen
5. Hyperventilation : maintain VE ∵VT and forced↓
 CAUSES
1. Collagen vascular diseases
1. Scleroderma
2. Polymyositis/dermatomyositis
3. Systemic lupus erythematosus
4. Rheumatoid arthritis
5. Ankylosing spondylitis.
 CAUSES
2. Drugs induced
1. Nitrofurantoin
2. Amiodarone
3. Dilantin
4. Bleomycin
5. Cyclophosphamide
6. Methotrexate
7. Radiation.
 CAUSES
3. Primary or unclassified diseases
1. Sarcoidosis
2. Pulmonary histiocytosis X
3. Lymphangioleiomyomatosis (LAM)
4. Pulmonary vasculitis
5. Alveolar proteinosis
6. Eosinophilic pneumonia
7. Bronchiolitis obliterans organizing pneumonia
(BOOP)
 CAUSES
4. Idiopathic fibrotic disorders
1. Acute interstitial pneumonia
2. Idiopathic pulmonary fibrosis (usual intersttial
pneumonitis)
3. Lymphocytic interstitial pneumonitis
4. Desquamative interstitial pneumonitis
5. Non-specific interstitial pneumonitis
 CAUSES
1. Inhaled inorganic dust
1. Silica: silicosis
2. Asbestos: asbestosis
3. Beryllium: berylliosis
4. Cobalt: hard metal fibrosis
5. Coal workers pneumoconiosis
2. Inhaled organic dust
1. Hypersensitivity pneumonitis: farmer’s lung Bird
fanciers lung….
 SKEMA VENTILASI PPOk
PPOk
NORMAL RESTRICTIVE
I RV
I RV TV I RV
ERV
TV TV
ERV
ERV RV
RV
RV