IX.

PATHOPHYSIOLOGY OF PNEUMONIA

Legend:

Clinical manifestations: C.M.

Medical interventions:

Result:

Precipitating Factors

Bacteria: normal flora Predisposing factor

Fatigue Age: 77 years old
Overexposure to air pollutants

Staphylococcus
pneumoniae

Organisms enter the respiratory tract

through inspiration/aspiration

Activation of defense
mechanism

Lose effectiveness of
defense mechanism

Penetrate the sterile lower

respiratory tract (lungs)
 alveoli

multiplies Irritation of airway

Invasion of the Increase goblet cell

alveolar epithelium

Pneumococci spread from

alveolus to alveolus through
spores of Khon

Colonization

Release of damaging toxins

AA BB CC
C
infection Occluded Increase mucus
the airway production

Exudates come inflammation

from bacteria cough crackles
erode the lung
vasodilation

Dead space hyperventilation Airway constriction

Increase blood flow
happened

Plasma and CHON

rich fluid leakage
increased difficulty of
respiratory rate breathing

Accumulation of
edematous fluid
Combivent 1/2neb +
1/2PNSS
Inflamed and fluid filled
alveolar sacs
Impaired O2 Increased
and CO2 ventilatory
exchange demands
Alveolar air sacs
become engorged
admission

Decrease CO2
Hypotension Altered
mentation

Lung consolidation
Betaloc 5mg
1 tab BID
hypoxia

Peripheral
vasoconstriction Hypertension

Increased peripheral
Blood pressure
resistance
 IX. PATHOPHYSIOLOGY OF PNEUMONIA (Continuation)

The invading organism causes symptoms, in part, by provoking an overly exuberant

immune response in the lungs. The small blood vessels in the lungs (capillaries)
become leaky, and protein-rich fluid seeps into the alveoli. This results in a less
functional area for oxygen-carbon dioxide exchange. The patient becomes relatively
oxygen deprived, while retaining potentially damaging carbon dioxide. The patient
breathes faster and faster, in an effort to bring in more oxygen and blow off more carbon
dioxide.

Mucus production is increased. Mucus plugs actually further decrease the efficiency of
gas exchange in the lung since it obstructs the airways causing bronchoconstriction.
The alveoli fill further with fluid and debris from the large number of white blood cells
being produced to fight the infection.

Consolidation, a feature of bacterial pneumonias, occurs when the alveoli, which are
normally hollow air spaces within the lung, instead become solid, due to quantities of
fluid and debris.

Viral pneumonias, and mycoplasma pneumonias, do not result in consolidation. These

types of pneumonia primarily infect the walls of the alveoli and the parenchyma of the
lung.