Chapter 26: Alterations of Pulmonary Function

wake up at night gasping for air

have to either sit up or stand up to relieve dyspnea

form of hyperventilation - breathing pattern reduces CO2 in the blood due to increased rate or depth of respiration

labored breathing, no expiratory pause (extreme exercise, metabolic acidosis

abnormal breathing pattern

abnormal breathing pattern

characterized by alternating periods of shallow and deep breathing and apnea of 15-60 seconds (supratentorial brain injury)

seen especially in comatose patients

CO2 removal doesn't keep up with CO2 production (build up of CO2 in blood)

level of CO2 in the arterial blood increases (hypercapnia)

results in respiratory acidosis

lungs remove CO2 faster than it's produced by cellular metabolism (hypocapnia)

results in respiratory alkalosis (low levels of CO2 in blood)

resolves within 2-3 weeks

most commonly the result of upper respiratory infection, allergic rhinitis, acute bronchitis, pneumonia, congestive heart failure

persisted for more than 3 weeks

most commonly the result of postnasal drainage, asthma or with smokers chronic bronchitis or cancer

coughing up blood (never a good sign)

indicates localized abnormality - usually infection or inflammation, cancer or pulmonary infarction

bluish discoloration of the skin and mucous membranes

s&s of pulmonary disease

caused by: decreased cardiac output; cold environment (vasoconstriction); severe anemia, CO poisoning)

s&s of pulmonary disease

infection and inflammation of the parietal pleura (outer layer) causes sharp or stabbing pain when pleura stretches during inspriation

s&s of pulmonary disease

bulbous enlargement of the end of digit (painless)

most commonly associated with lung cancer, cystic fibrosis, pulmonary fibrosis, lung abscess, and congenital heart disease

s&s of pulmonary disease

changes in amount and consistency of sputum (color may indicate infection, ex. yellow, green, rust)

inadequate gas exchange caused by pulmonary disease/injury

PO2: <50; PCO2: >50; pH: <7.25

excess water in lungs (caused by pulmonary disease/injury)

passage of fluid and solid particles into the lungs (caused by pulmonary disease/injury)

FALSE.

the RIGHT lung is more susceptible than the LEFT

(right lung has a more direct route than left)

collapsed lung caused by pulmonary disease/injury

clinical manifestations include:

-dyspnea, cough, fever, and leukocytosis

collapsed lung caused by proximal obstruction

most common

ex. aspiration blocking passage of air to lungs

persistent abnormal dilation of bronchi caused by pulmonary disease/injury

occurs in conjuction with other respiratory condition

can be caused by obstruction of airway with mucus plugs, aspiration of foreign body, infection, cystic fibrosis, tuberculosis

inflammatory obstruction of the small airways (bronchioles) caused by pulmonary disease/infection

occurs in adults with chronic bronchitis, in association with viral infection, or with inhalation of toxic gases

most common is children with upper/lower respiratory infection

late-stage fibrotic disease of the airways causing permanent scarring of lungs

can occur with all causes of bronchiolitis (permanent scarring of lungs)

presence of air/gas in pleural space caused by rupture in visceral pleura or parietal pleura and the chest wall

increased pressure in pleural space

s&s: decrease breath sounds; hyperresonance/typanitic to percussion; hypotensio

air pressure in pleural space = barometric pressure

air drawn in on inspiration is forced back out on expiration (lungs cannot pull air in = collapse)

open to outside atmopshere

air is permitted in on inspiration BUT prevents escape on expiration (air cant get out = increased press)

pressure in pneumothorax > barometric pressure

s&s = tracheal deviation

pressure pushes importants structures left/right

*life threatening

sponteneous rupture of bleb on visceral pleura at the apex of lungs

bleb = blister-like tissue forms on lung tissue

occurs without trauma

caused by chest trauma, COPD

**primary condition has caused it to occur

presence of fluid in the pleural space

water fluid in pleural space (cardiovascular disease)

low content of cells

high concentration of WBC's and plasma proteins in plueral space

infection, inflammation. or palignancy of pleura

presence of blood in pleural space

traumatic injury, surgery, rupture

infected pleural effusion

presence of pus

pleural space containing lymph and fat droplets

trauma or infection

pleural inflammation

can be viral, bacterial, or allergic

excessive amount of fibrous or connective tissue in lungs (scar tissue = decrease in expansion)

most common form as no known cause (called idiopathic pulmonary fibrosis)

can be caused by formation of scar tissue after active pulmonary disease or by inhalation of harmful substances

compromised chest wall (decreases ability to breathe)

deformation, immobilization, and/or obesity, neuromuscular disease (impairs respiratory muscle function)

*degree of ventialtory impairment depends on severity of chest wall abnormality

instability of a portion of the chest wall

results from fracture of several ribs in more than one place or fracture of the sternum and ribs

impaired movement of gas in and out of lungs

inhalation disorder (smoke, ammonia, NO2, Cl, O2, toxicity)

inhalation results in severe inflammation of airways, alveolar and capillary damage, and pulmonary edema

inhalation of inorganic dust particles (ususally in workplace)

ex. silica, asbestos, coal

**individuals history of exposure is important in making diagnosis

lead to chronic inflammation with scarring leading to fibrosis

acute lung inflammation injures alveolocapilary membrane

causes severe pulmonary edema, shunting and hypoexima

injury to pulmonary capillary endothelium stimulates platelet activation and intravascular thrombus formation

surfactant inactivation

atelectasis

development of hyaline membrane at alveolocappilary interface (inpairs gas exchange)

hyperventilation

respiratory alkalosis

dyspnea and hypoxemia

metabolic acidosis

hypoventilation

respiratory acidosis

futher hypoxemia

hypothension, decreased cardiac output, death

physical examination, blood gases, and radiologic examination

supportive therapy with oxygenation and ventilation and prevention of infection

surfactant to improve compliance

airway obstruction that is worse with expiration

dyspnea and wheezing = common s&s

obstructive pulmonary disorder

chronic inflammatory disorder of the airways (IgE mediated)

familial disorder (over 20 genes may play a role)

inflammation results from hyperresponsiveness of the airways

-inflammatory process produces: vronchial smooth muscle spasm, vascular congestion, edema, production of thick mucus, impaired mucocillary function, thickening of airway walls

allergen exposure

urban residence

exposure to air pollution and cigarette smoke

recurrent respiratory viral infection

TRUE.

severe bronchospasms where hypoxicworsens, acidosis develops, and if not reversed becomes life threatening

expiratory wheezing

dyspnea

tachypnea (rapid breathing)

peak flow meters

oral corticosteroids (as anti-inflammatories)

inhaled beta-agonists (bronchodilators)

hypersecretion of mucus and chronic productive cough lasting for at least 3 months of the year and for at least 2 consecutive year

*caused primarily from smoking

irritation/inflammation > metaplasia > dysplasia

thick mucus is produced but cannot be cleared because of impaired ciliary function

cigarette smoking

exposure to air pollution

*best treatment = prevention

irreversible (only stop further progression/damage)

by the time individual seeks medical care for symptoms, considerable airway damage is present

bronchodilators (beta agonists, anticholinergics), expectorants (decrease mucus), chest physical therapy

abnormal permanent enlargement of gas-exchange airways

destruction of alveolar walls without obvious fibrosis

loss of elastic recoil within aveoli (major mechanism of airflow limitation)

aveoli begin clumping together = decreased surface area

destruction occurs in the respiratory bronchioles and alveolar ducts causing inflammation

occurs in smokers and those with chronic bronchitis

involves lower lobes of lungs

occurs in elderly and those with alpha1-antitrypain deficiency (also affects liver early on - put on transplant list just in case)

genetic (recessive trait)

develop emphysema later on - missing enzyme causing body to break down elastic

**avoid alcohol and smoke

infection of lower respiratory tract

caused by bacteria, virus, fungi, and parasites

s&s: dullness to percussion; inspiratory crackles, whisper pectorilogy (sounds louder than normal) (auscultation)

different organisms than community-acquired pneumona

-pseudomonas aeruginosa

-staphylococcus aureus

-klebsiella

usually mild and self-limiting (can be severe)

can set stage for 2nd bacterial infection (because of decreased immune function) < if viral infection isnt getting better may need antibiotics (treat 2nd bacterial infection)

can be primary infection or complication of another viral illness

destroys ciliated epithelial cells and also invades goblet cells and bronchial mucous glands (preventing mucociliary clearance)

infection caused by Mycobacterium tuberculosis (can remain dormant for life)

airborne transmission (respiratory droplets) - microorganisms lodge in lung periphery, usually upper lobe (multiply and cause inflammation)

tubercle formation (immune response) - neutrophils and macrophages seal off colonies

caseous necrosis - infected tissue within tubercle die, forming cheeselike material; scar tissue grows around tubercle

diagnosed by positive tuberculin skin test (PPD); sputum culture; chest x-ray

*not considered clear of infection until suptum test comes back negative (put on treatment until then)

long treatment (3-9 months) - people do not stay of meds (non compliance)

acute infection or inflammation of airways or bronchi

commonly follows viral illness (may cause secondary bacterial infection)

usually self-limiting

causes similar symptoms to pneumonia but no pulmonary consolidation and chest infiltrates (x-ray shows no white areas)

occlusion of portion of pulmonary vascular bed by thromubs, embolus, tissue fragment, lipids, or air bubble

commonly arise from deep veins in thigh

pregnancy increases clotting factors by 6-10% (hypercoagulability) (preparing for birth to decrease hemorrhages)

increased venous stasis from uterus sitting on femoral vein (delivers most blood back up)

3 causes of DVTs

venous stasis (blood pooling in area from decreased blood flow)

hypercoagulability

injuries to endothelial cells that line vessels

mean pulmonary artery pressure 5-10 mm Hg above normal (above 20 mm Hg)

*normal pulmonary artery pressure = 25/10

idiopathic (usually hereditary component)

-pulmonary arterial hypertension

-pulmonary venous hypertension (due to CHF)

-pulmonary hypertension due to respiratory disease/hypoxemia (causes vasoconstriction)

-pulmonary hypertension due ot thrombotic/embolic disease

-pulmonary hypertension due to diseases of pulmonary vasculature

FALSE.

respiratory system disease and hypoxemia are MORE common causes of pulmonary hypertension

pulmonary heart disease - right ventricular enlargement

secondary to pulmonary hypertension - creates chronic pressure overload in right ventricle with eventual right ventricular failure (called cor pulmonale)

most common form of lower lip cancer: exophytic (sun exposure, smoking) - develop in outer part of lip; lip becomes thickened with ulcerated center and raised borders

squamous cell carcinoma

increased with amount of tobacco smoked and smoking + alcohol

HPV also implicated (subtype)

*most common form = carcinoma of true vocal cords

uncommon/rare form = supraglottic-epiglottis, false vocal cords, subglottic

cigarette smoking

heavy smokers have 20 times greater chance of developing lung cancer than nonsmokers

smoking is related to cancers of larynx, oral cavity, esophagus, and urinary bladder

most common cause of cancer deaths (30% of all deaths in US)

non-small cell lung cancer (30% in hilum)

slow growing

s&s = cough, hemoptysis (coughing up blood), sputum, airway obstruction (dyspnea)

non-small cell lung cancer (40% in periphery)

moderate growth

not assocaited with smoking

more common in women

pleural effusion (something located in pleural space (exodate (WBCs, plasma proteins; or endoate)

rapid growth (usually diagnosed and dead within months)

s&s = chest wall pain, pleural effusion, cough, sputum production, hemophysis

rapid growth rate

metastasize early and widely (spreads all over body -brain, stomach, bone, liver) <more than 85% of tumors will metastasize by time of diagnosis* (usually already stage 3)

**s&s usually start as those of bronchitis but don't go away

worst prognosis (survival = 6-12 months)

TNM classification for non-small cell cancer (tumor - size; nodual involvement -biopsy; metastasis?)

surgery, chemotherapy, radiation

*can remove portion of lung and still function normally (depends on location of tumor)