Download as docx, pdf, or txt
Download as docx, pdf, or txt
You are on page 1of 4

Disease: Community Acquired Pneumonia

Introduction

Pneumonia is the result of inhalation of bacteria, viruses, parasites, or irritating agents or


aspiration of liquids or foods. It leads to infection and inflammation, resulting in increased
mucus production, thickening alveolar fluid, and decreased gas exchange. Moreover,
community acquired pneumonia is a common infectious disease, occurs either in the
community setting or within the first 48 hours after hospitalization or institutionalization. The
need for hospitalization for CAP depends on the severity of the pneumonia.

Signs and Symptoms


 Dyspnea.  Pain on respiration.
 Crackles.  Tachypnea.
 Rhonchi.  Tachycardia.
 Discolored blood tinged, sputum.  Muscle pain (myalgia)
 Cough.  Hypoxemia.
 Fever.  Sweating (diaphoresis).
 Chills.  Wheezing.

Anatomy and Physiology

Normally, as you breathe, air moves freely through your trachea, or windpipe, then through
large tubes, called bronchi, through smaller tubes, called bronchioles, and finally into tiny sacs,
called alveoli. Your airways and alveoli are flexible and springy.
When you breathe in, each air sac inflates like a small balloon. And when you exhale, the sacs
deflate.

Oxygen from the air you breathe passes into your capillaries, then carbon dioxide from your
body passes out of your capillaries into your alveoli soli so that your lungs can get rid of it when
you exhale.

Ventilation

Air is moved in and out of the lungs by a combination of mechanics and atmospheric pressure
called ventilation. Inspiration draws air in from outside the body when contraction of the
diaphragm and intercostal muscles result in the lungs expanding, dropping the intra-alveolar
pressure to 2mmHg less than atmospheric pressure (i.e. negative pressure) (Waugh and Grant,
2010). Expiration is the passive process of relaxation of the diaphragm and intercostal muscles
resulting in the intra-alveolar pressure increasing to more than atmospheric pressure and,
consequently, air moving out of the lungs.
The inspiration cycle of ventilation requires effort. Part of this effort is required to overcome
the cohesive effect of the moist membranes that line the respiratory tract and the alveoli. This
moisture is important to facilitate diffusion of gases but, because water molecules are more
attracted to each other than to air surface tension, it could cause the tiny alveoli to collapse and
make it difficult for them to expand on inspiration. The surfactant that is produced by the septal
cells in the alveoli helps to reduce the cohesive force of the water molecules, therefore
stabilizing the alveoli and reducing the effort required to expand them during inspiration.

Respiration
External respiration is the process of gas exchange between the air in the alveoli and the blood
in the capillaries that surround them. The diffusion of gases across the respiratory membrane
relies on their partial pressure and solubility in water. Gases will diffuse from a mixture with
greater partial pressure to one with lesser partial pressure. The partial pressure of oxygen in the
alveoli is higher than that in the blood in the capillaries, while the partial pressure of carbon
dioxide in the capillaries is higher than that in the alveoli. The result is oxygen diffusing into, and
carbon dioxide diffusing out of, the capillary blood.

Internal respiration is the exchange of gases by the same mechanism between the blood in the
systemic capillaries and the tissue cells.

Cellular respiration is the utilization of the oxygen and the production of carbon dioxide by the
cells (Waugh and Grant, 2010).

Upper respiratory tract and pleura


The upper respiratory tract, which consists of the nasal cavity, pharynx, larynx and trachea,
warms and moistens inspired air and protects the lower respiratory tract from potential
pathogens. Ciliated mucus membranes line the upper airways and help to intercept pathogens
and propel them up the tract rather than down. The cough reflex also protects by closing the
epiglottis and stimulating contraction of respiratory and abdominal muscles, which forces air up
expelling any foreign material out of the airways.

The pleura covers each lung and are essentially sacs with one layer adherent to the lung and
the other to the wall of the thoracic cavity. The pleural cavity separates the two layers and it
contains a thin film of serous fluid, which allows the two surfaces to slide over each other,
avoiding friction during inspiration and expiration. The surface tension created by the serous
fluid prevents the two layers from becoming separated.

If you have pneumonia, your airways or lungs have an infection caused by germs such as
bacteria, viruses, fungi or parasites. Your airways catch most germs in the mucus that lines your
trachea, bronchi, and bronchioles. Hair-like cilia lining the tubes constantly push the mucus and
germs out of your airways, where you may expel them by coughing. Sometimes germs make it
past your mucus and cilia, and enter your alveoli. Normally, cells of your immune system attack
these germs, which keep them from making you sick. However, if your immune system is
weakened due to age, illness, or fatigue, pneumonia-causing germs can overwhelm your
immune cells and begin to multiply. Your bronchioles and alveoli become inflamed as your
immune system attacks the multiplying germs. The inflammation causes your alveoli fill with
fluid, making it difficult for your body to get the oxygen it needs.

Bacterial pneumonia is commonly caused by organisms that are normal commensals of the
upper respiratory tract, and which are then transmitted to susceptible individuals via airborne
droplets followed by migration of the pathogen to the lower respiratory tract. Defective cough
reflex or damage to the microcilia, which line the airways, facilitate aspiration of infectious
organisms to the lower airways

Viral pneumonia may be caused by organisms that originate in the upper respiratory tract and
migrate to the terminal bronchioles (e.g. influenza or respiratory syncytial virus) or the
organisms may enter the upper airways but disseminate systemically until reaching the lower
respiratory tract, as happens in measles infection. Some infections may originate elsewhere but
find their way systemically to the lower respiratory tract, e.g. cytomegalovirus (Figueiredo,
2009).

Sometimes pneumonia is classified as either ‘typical’ or ‘atypical’. Typical pneumonia generally


has an acute onset with fever, chills and a productive cough, whereas atypical pneumonia may
present with a dry cough, fever, sore throat and headache (Eddy,2005).The term atypical may
also refer to the causative organism when it is not one of the more common pathogens, such as
legionella, chlamydophila or mycoplasma pneumonia (Murdoch and Chambers, 2009).

If you have lobar pneumonia, one lobe of your lungs is affected.


If you have bronchopneumonia, many areas of both lungs are affected.

In order to reach the alveoli, microorganisms have had to evade many of the host’s respiratory
defense mechanisms so are, by nature, likely to present a challenge to the alveolar
macrophages, which would normally be able to kill low numbers of less virulent pathogens. If
they are overwhelmed, however, an inflammatory response ensues, which results in production
of a fibrin-rich exudate that fills the infected and neighboring alveolar spaces causing them to
stick together and so rendering them airless. The inflammatory response also results in a
proliferation of neutrophils, which can damage lung tissue, leading to fibrosis and pulmonary
oedema, which also impairs lung expansion. The inflammatory response can also lead to the
development of a pleural effusion, which is thought to complicate up to 40% of cases of
pneumonia (Koegelenberg et al, 2008).

These changes result in reduced gas exchange, the consequences of which will depend on the
extent of lung tissue involved and the underlying health of the individual’s lungs. Not only is
there a lack of oxygen reaching the vital organs but the respiratory effort required with each
breath will be increased as a result of the disturbance in normal physiology. Respiratory and
heart rate will increase in response to falling oxygen and rising carbon dioxide levels.

Medical management
Medical tests
• Pulse oximeter shows decreased oxygen saturation.
• Chest x-ray shows infiltration.
• White blood cell count (WBC) elevated.
• ABGs show respiratory acidosis.
• Culture and sensitivity of the sputum.

Pharmacological
•Antibiotics for bacteria
•Antiviral medication for flu virus
• Antifungal medication for fungal cause
• Rest and fluids
• OTC anti-fever and pain medications
•Intravenous antibiotics and oxygen
Reference:

Alcon, A, Valencia M, Fabregas N, torres A. Pathophysiology of Pneumonia in Ed Rello J,


Nosocomial pneumonia: Strategies for Management. 2007 John Wiley & Sons Ltd

British Thoracic Society (2009) Guidelines for the Management of Commu- nity Acquired
Pneumonia in Adults. Update 2009. www.brit-thoracic. org.uk/clinical-
information/pneumonia/pneumonia-guidelines (ac- cessed 3 February 2014)

Eddy O (2005) Community-acquired pneumonia: from common pathogens to emerging


resistance. http://bit.ly/1j6Ybwu (accessed 3 February 2014)

Ellis H (2011) The respiratory system. Anaesthesia and Intensive Care Medi- cine 12(12): 533–
8

Figueiredo LT (2009) Viral pnuemonia: epidemiological, clinical, patho- physiological and


therapeutic aspects. J Bras Pneumol 35(9): 899–906 Janssens JP, Krause KH (2004)
Pneumonia in the very old. Lancet Infect Dis

4: 112–24
Koegelenberg CF, Diacon AH, Bolliger CT (2008) Parapneumonic pleural

effusion and empyema. Respiration 75(3): 241–50


Levy ML, Le Jeune I, Woodhead MA et al (2010) Primary care summary

of the British Thoracic Society Guidelines for the management of com- munity acquired
pneumonia in adults: 2009 update. Prim Care Respir J 19(1): 21–7

Lim WS, Woodhead M; British Thoracic Society (2011) British Thoracic Society adult community
acquired pneumonia audit 2009/10. Thorax 66(6): 548–9

Murdoch DR, Chambers ST (2009) Atypical pneumonia-time to breath new life into a useful
term? Lancet Infectious Diseases 9: 512–9

Nair GB, Niederman MS (2011) Community-acquired pneumonia: an un- finished battle. Med
Clin North Am 95(6): 1143–61

Ruuskanen O, Lahti E, Jennings LC, Murdoch DR (2011) Viral pneumonia. Lancet 377(9773):
1264–75

Waugh A, Grant A (2010) The respiratory system. In: Waugh A, Grant A, eds. Ross and Wilson
Anatomy and Physiology in Health and Illness, 11th edition. Churchill Livingstone Elsevier.

World Health Organization (2011) Pneumonia fact sheet. www.who.int/


mediacentre/factsheets/fs331/en/ (accessed 3 February 2014)

You might also like