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fModifiable Risk

Lifestyle (Smoking)
Environment

Non Modifiable Risk


Age
Gender

Compromised cough/gag reflex,


mucocilary system, or immune
system

Tuberculosis

Bacteria and other pneumoniacausing agents enter the normally


sterile lung fields via inhalation or
the bloodstream

Lymphocytes and
macrophages are attracted
to these bacteria
Immune cells begin producing
antibodies and walling off the
infection by forming a type of
granuloma called a tubercule

Caseous necrosis (cheesy


appearance from a tubercule)

Tubercules change by
fibrosing and calcifying

Immune system walls off


bacteria (disease may be
arrested or rendered inactive
for long period of time)

Antibodies produced will


circulate in the blood for the
remainder of the infected
individuals life in readiness to
attack future TB bacteria
(+ TB Skin test)

Pneumonia
Signs and Symptoms:
Fever
Chills
Aching chest
Malaise
Dyspnea
Watery phlegm
Inc. WBC
Fine crackles
Hempotysis

Diagnostic Tests:
Culture and
Sensitivity
CBC:
Hct- 0.35
RBC- 3.41
Hgb- 107
Wbc- 12.2
Lymph- 0.11
Polys- 0.82
ABG:
PCO2- 40.4
PO2-36
02 sat-71

Vascular engorgement of the


capillary bed

Serous fluid leaks into the alveoli

RBC and fibrin enter the alveoli

Fibrin and disintegrating RBC/WBC


accumulate in the affected area

Enzymes digest and remove the


products of inflammation

Exudate is either coughed up or


removed by WBC

Necrosis of the lung

Respiratory Failure

Impaired gas exchange (movement


of gases into and out of the alveolar
capillary membrane)

Ventilation (movement of gases into


and out of the alveoli due to the
action of the respiratory muscles

Hypoxemic Respiratory Failure

Hypercapnic/hypoxemc
respiratory failure (unable to

Mismatching of
ventilation and
perfusion
Gas exchange cannot
take place

Carbon Dioxide
Retention

Impaired Diffusion

maintain a level of alveolar


ventilation sufficient to eliminate
carbon dioxide and keep arterial
oxygen levels within Normal range

Trauma or depression of lungs


Gas exchange between the
alveolar air and pulmonary
blood s impeded because of an
increase in the dstance for
diffusion or a decrease in the
permeability or surface area of
the repiratory membranes to
the movement of gases

Volume of fresh air moving into


and out of the lungs is
significantly reduced
Hypoventilation

Severe Hypoxemia
Increase partial carbon dioxide

Hypercapnia

Increase cerebral Blood Flow

Pulmonary vasculature
constricts in response to low
alveolar PO2

Hypoxemia
Increased respiratory drive and
sympathetic tone

Acute Right Ventricular failure

Signs and symptoms:

Dilatation of the cerebral


vessels

Signs and Symptoms


Headache
Warm flushed skin
Mild to moderate BP increase

Signs and Symptoms


Jugular Vein distension
Edema

Cyanosis
Restlessness
Confusion
Anxiety
Delirium
Fatigue
Tachypnea
Hypertension
Cardiac arrhythmias
Tremor