Respiratory

Respiratory Physiology

Lung Embryology

LRT (lower respiratory tract) arises from laryngotracheal diverticulum.
Wk 24 – resp bronchi form, respiration is possible
Wk 29 – type II secrete surfactant (reaches adequate levels 2 wks before birth)
Trachea – C-shaped cartilage
Left bronchus longer, narrower, greater angle; bronchi have circum rings of crtlg; pseudostrat colum epi, Goblet, neuosecr, basal, brush cells
Epi à lamina propria à submuc à cartilage
Bronchioles – no cartilage, submucosal glands

1) membranous – smooth muscle wall; ciliated columnar cells + Clara cells

2) respiratory – alveolar ducts, alveoli budding from wals; no musc. wall; cuboidal cells +/- cilia

Lung Anatomy & Histology

Alveolar histology

Alveolar Histology

Cells that make up the aveoli.

1) Type I Pneumocytes – flat sqm cells (alveolar epithelial cells)

2) Type II – cuboidal cells that do alveolar repair and make surfactant

3) Macrophage – phagocytic fxn; filled w/golden-brown “smoker’s pigment” in smokers

4) Pores of Kohn – connect adjacent alveoli, does collateral ventilation

5) Lambert’s canals – comm. b/w airway and adj alveoli, collateral ventilation

6) Capillary endothelial cells

7) Reticular elastic fibers and myofibroblasts

Alveolar Epithelial Cells

Alveolar epithelial cells refers to Type I and Type II pneumocytes which make up an alveoli. Type I cells compose more than 95% and are involved in gas exchange. Type II cells make surfactant.

Type I Pneumocytes

Type I pneumocytes are flat squamous cells of alveoli that are used for gas exchange. They cover most (more than 95%) of the surface area of an aveoli.

Lung Anatomy

· 3 right lobes; 2 left lobes + lingula; 10 bronchopulm segments bilat w/i lobes

· lobule – smallest gross anatomic compartment of lung (3-5 terminal bronchioles, 30 pulm acini)

· bronchial arteries arise from intercostals and aorta; bronchial veins return to azygos and intercostals veins

· superficial lymphatics along pleural surface; deep (intrapulm) lymph adj to bronchovasc bundle and along interlob septa; connected

Lung Volumes Definitions

Meanings of Lung Volumes and Capacities

Tidal Volume: during each normal breath, this the volume of air that is inspired and expired.
Expiratory Reserve Voume: after expiration of normal amount of air (in Tidal volume), this is the amount of air that can still be expired with more effort.
Inspiratory Reserve Volume: similar to the expiratory reserve volume, this is the amount of air that can still be inspired with more effort (after taking in a normal breath of air during a tidal volume). Think of it as the extra amount of air that you can still breathe in after a normal breath.
Residual Volume: when we breath (inspire/expire), this is the volume of air that never actually leaves the lungs (this is because the alveoli still have some air in them even after we breathe out which keeps structural integrity of the lungs).
Dead space: there are 2 types of dead spaces: anatomic and physiologic. Both refer to air that is not involved in gas exchange.

Lung Volumes

Calculating Ventilation Rate

Ventilation Rate

There are different ways to express the rate a person is breathing. In respiratory physiology, these include Minute Ventilation and Alveolar Ventilation.

Minute Ventilation

Minute ventilation is equal to the Tidal Volume times the Breaths per minute.

MV = tidal volume x Breaths/minute

Alveolar Ventilation

Alveolar Ventilation is equal to Tidal Volume minus Dead Space times the breaths per minute.

AV = (tidal volume – dead space) x Breaths/minute

Dead Space

To get the Dead Space (for using in the alveolar ventilation equation), you can use the following formula:

Dead space = Tidal Volume x (PCO2 arterial – PCO2 expired air) / PCO2 arterial

This formula measures the physiological dead space.

Respiratory Diseases

Chronic Obstructive Pulmonary Disease

Causes of Chronic Obstructive Lung Disease

Chronic obstructive lung disease or chronic obstructive pulmonary disease (COPD) is a very common problem that consists of chronic bronchitis and emphysema. It is common knowledge that COPD may be caused by cigarette smoking. In fact up to 90% or more of the COPD cases may be caused by smoking and it is the most common cause. However, there are many other etiologies for this disease that need to be considered. These include occupational exposure, air pollution, genetics, or autoimmune processes.

Occupation exposure is a known cause for COPD. People that work in coal mines, gold mines, textile factories, welding jobs, or jobs that involve working with cadmium or silicone are examples occupations that often lead to COPD. As an example of how real this is, you can see commercials by lawyers that promise big rewards for suing companies that exposed their workers to these chemicals without proper protection. This also leads to the point that certain occupation exposures can lead to other health problems as well (such as cancers or silicosis). However, keep in mind that this is still not as major a risk factor as cigarette smoking.

Air pollution is another cause of COPD. This is more of an issue in larger cities where there are a lot more automobile traffic producing the harmful gasses that can cause COPD. Besides outdoor air pollution, indoor air pollution can also occur (for example from not have having ventilated living areas and being exposed to chemicals or toxins from burning fuel inside a home).

Genetics (what you get from your parents) is another possible cause for COPD. Some people are more prone to get COPD than others. This explains why some people can smoke all their life and still not get lung cancer or COPD (because they have genes that allow them to repair damage caused by cigarette smoke).

An autoimmune process is another etiology to consider when thinking about causes of chronic obstructive lung disease. It has been observed that there are inflammatory processes (caused by the body’s own immune cells) going on in the lungs of COPD patients. This is a process that is independent of smoking but may be triggered by smoking and then continue on its own (even after the person stops to smoke).

In conclusion, we must realize that smoking is the most common cause of COPD or chronic obstructive lung disease but we should also be aware of other causes of this debilitating disorder.

Cryptogenic Organizing Pneumonia

Cryptogenic Organizing pneumonia (COP) is also known as Bronchiolitis obliterans organizing pneumonia. Using COP is preferred to avoid mixing up with brochiolitis obliterans. Cryptogenic organizing pneumonia is essentially inflammation of the bronchioles and also the surrounding tissue of the lungs. It is suspected that prior inflammatory conditions and certain drugs may cause COP. Although COP presents similar to pneumonia (such as the pneumonia caused by streptococcus pneumonia bacteria), a diagnosis of COP is often indicated when treatment with antibiotics fails and sputum cultures turn up negative for any organisms.

Why is it called organizing?

This term organizing refers to the presence of exudates and fibrosis tissue in and around alveolar tissue. This is from the unresolved pneumonia. In normal (bacterial) pneumonia, the exudates would have resolved with anti-bacterial treatment.

What type of symptoms to patients with COP have?

Most common symptoms include those similar to a bacterial pneumonia. These include cough, shortness of breath, flu like symptoms, crackles on lung exam, and fevers. Weight loss is also common

What is the incidence of COP?

Most patients are between the ages of 40 and 60. COP effects about .01% of people. Males are just as likely as females to get this disease. It can be deadly – often killing 7% of people effected.

Tratment of COP:

Treatment involves giving the patient corticosteroids. This is dosed by the weight of the patient at about .75 mg/Kg (which typically leads to starting dose of about 50 mg per day). Corticosteroids can have side-effects and the patient has to be slowly taken off the medication. Most patients will recover and other medications may be provided to counter the side-effects of corticosteroids.

Pneumonia

Definition of Pneumonia
Symptoms of Pneumonia
Causes of Pneumonia
Treatment of Pneumonia

Definition of Pneumonia:
Pneumonia itself is described as an inflammation of the lungs (specifically the lung tissue and alveoli). Besides inflammation (consolidation), there is also involved exudate (or filling of the lungs with fluid).

Symptoms of Pneumonia:
Typical symptoms of pneumonia include production of sputum, chills, shortness of breath, and chest pain.

Causes of Pneumonia:
Pneumonia can be caused by bacteria (Bacterial Pneumonia), viruses (Viral Pneumonia), fungi (Fungal Pneumonia), or parasites (Parasitic Pneumonia). In some cases the cause may be unknown (idiopathic).

Treatment of Pneumonia:

The treatment will depend on the cause of the pneumonias. In bacterial pneumonia, antibiotics will be used depending on the causative organisms. Antibiotics can also be used in preventing bacterial pneumonia from developing in a patient that already has a viral pneumonia. Antiviral can help in the treatment of viral pneumonias.

Pulmonary Hypertension

Pulmonary hypertension refers to the abnormal elevation fo pulmonary artery pressure.

There are 2 types of Pulmonary HTN:
1) Primary Pulmonary HTN (idiopathic)
2) Secondary pulmonary HTN (associated with an underlying disease/process)

Primary Pulmonary Hypertension

Primary Pulmonary Hypertension refers to an abnormally elevated blood pressure of the pulmonary artery for which the cause is unknown.

There is an increase in pulmonary vascular resistance, an increased pulmonary artery pressure, and certain changes in the pathology.

Pathological changes in Primary Pulmonary HTN:
-Hypertrophy and fibrosis of the vascular bed
-In situ thrombosis

pulmonary hypertension artery with fibrosis and hypertrophy

Respiratory H&P (history and physical)

Respiratory H&P

Reaspiratory Symptoms

1) Cough:

a) dry --> asthma, interstitial fibrosis

b) productive – voluminous, thin sputum (bronchorrea) seen in bronch-alv carc

c) early morning – bronchitis, bronchiectasis

2) dyspnea – SOB is usually b/c ©-pulm dysfxn; correlates best w/work of breathing

3) chest pain

a) rad to neck/left hand - © pain

b) worse with inspire – pleuritic (infxn) pain

4) hemoptysis (massive = 500 ml in 24 h)

5) FHx Tb, Occ Hx, Exp to dusts, Smoke Hx

Respiratory Inspection

1) Color – Pallor = anemia

3) Nails – look for cyanosis, clubbing (obliteration of nail bed angl); b/c lung CA, chron pulm infxn.

4) Breath – ketone = DKA; putrid = bad dental hygiene OR anaerobic pulm infxn

5) Resp Distress – nl = 10-12/min, 5-6 sighns/hour; tachypnea à impending resp failure

6) Acc musc retract – inward movement of supraclav notch, intercostals during insp à UAO

7) Respiratory alternans – intercostals, diaphragm alternate being dom musc of insp; imp resp fail

8) Paradoxical motion – opp mvmt of intercostals and diaphragm (one cntrct, other pass) --> IRF

9) Wheezing – severe asthma; stridor – UAO

10) Ant-post diameter increased w/hyperinfl of lung (COPD)

11) Use of acc musc of resp (scalene, SCM) à severe pulm dysfxn; good index of dz severity

Respiratory Palpation –

ID tender areas, diff ref’d pain from underlying lung vs. pain orig in chest wall; helps assess parenchymal status

1) Fremitus – palpable vibr transm thru bronch-pulm system to chest wall when pt speaks

2) ß/absent fremitus = pleural effusion, pneumothorax, fibrothorax

Respiratory Percussion

–
assess density of tissue under area; assess liver span, diaphragmatic mtn.

Flatness – fluid

Dullness – parenchymal consolidation

Resonance – nl lung

Hyperresonance- free air/hyperinfl lung

Tympany – large pneumothorax

Respiratory Auscultation

Vesicular – most of lungs; I > E

Bronchovesicular – b/w scapulae; I = E

Bronchial – over manubrium; I < E

Tracheal- over trachea in neck; I = E

Crackles

1) late inspiratory – fine, profuse, repeat breath-to-breath; first at base of lungs, spread upward as condition worsens; caused by ILD, early CHF

2) early inspiratory – coarse, few, at mouth and chest wall; chronic bronchitis and asthma

3) midinspiratory, expiratory – bronchiectasis?

Wheezes/rhonchi – air flows rapidly thru bronchi that

are narrowed nearly to closure; bronchial asthma, chronic bronchitis, CHF

Persistent local wheeze – partial bronch obstruct

Stridor – insp wheeze; larynx/trachea obstruct

Pleural rub – creaking/grating sounds due to inflamm

mediastinal emphysema