- An obstructive disorder
- Features chronic inflammation of the airways and is characterized by recurrent episodes of:

wheezing

breathlessness

coughing and

chest tightness

Chronic Obstructive Pulmonary Disorder--

Pathologic lung changes characteristic with Emphysema or Chronic Bronchitis

coughing up of blood or bloody secretions;

(usually indicates local infecction or inflammation that damages bronchi or lung parenchima w/ rupture of pulmonary blood vessels)

Most common causes:

Bronchiectasis

Lung Cancer

Bronchitis

Pneumonia

Bluish discoloration of the skin and mucous membranes caused by increaing amounts of desaturated hemoglobin in the blood

Causes:

Low PaO2

Pulmonary/Cardiac right-to-left shunts

Decreased Cardiac Output

Cold Environments

Bulbous enlargement of the end of a finger that is commonly associated with diseases that interfere with oxygenation

Conditions that manifest with clubbing:

lung cancer

bronchiectasis

cystic and pulmonary fibrosis

lung abscess

congenital heart disease

increased CO2 in the arterial blood; PaCO2 > 45 mmHg

caused by hypoventilation-- usually result of decreased drive to breath or inadequate ability to respond to ventilatory stimulation.

Arterial Blood Gas--

Measures:

PaO2

PaCO2

HCO3

pH

oxygen content & saturation

reduced oxygenation in the arterial blood;

PaO2 < 80 mmHg at sea level

is caused by respiratory alterations

↓ed PIO2

Hypoventilation

Alveolocapillary diffusion abnormality

V/Q mismatch ** (most important)

Acute Respiratory Failure

inadequate gas exchange where PaO2 is less than or equal to 60 mmHg / PaCO2 is greater than or equal to 50 mmHg

Type I- (most common type) is called hypoxemic resp. failure and is characterized by a PaO2 <60 w/ a normal or low PaCO2; is the result of inadequate O2 exchange b/t alveoli and pulmonary capillaries

Type II- hypercapnic respiratory failure = PaCO2 > 50

Is the result of inadequate alveolar ventilation

Shows: ↓ PaO2 and pH

excess water in the lung

3 main causes:

Heart disease (most common cause)

Capillary injury

Obstruction of lymphatic system

(I feel like it would be a good idea to look over Dolan's flowchart for the pathogenesis of pulmonary edema)

Clinical Manifestations of pulmonary edema

dyspnea

orthopnea (dyspnea when lying down)

hypoxemia

increased work of breathing

passage of fluid and solid particles into the lung;

clinical manifestations:

sudden onset of choking

cough w/ or w/o vomiting

dyspnea

wheezing

collapse of lung tissue

2 types:

compression- external pressure collapses alveoli

absorption- caused by removal of air from obstructed or hypoventilated alveoli or inhalation of concentrated oxygen or anesthetic agents

clinical manifestations=

dyspnea, cough, fever, leukocytosis

persistant abnormal dilation of the bronchi

is often assoc. with recurrent lower resp. tract infections (bronchitis) and has similar symptoms; coughing up of large amounts of sputum

inflammatory obstruction of the bronchioles; more common in children; usually accompanies chronic bronchitis in adults

clinical manifestations

wheezing d/t bronchospasm

tachypnea

use of assessory muscles

low-grade fever

nonproductive cough

hyperinflation

Pneumothorax

presence of air/gas in the pleural space caused by a rupture of the visceral pleura or a rupture of the parietal pleura/chest wall; it removes fluid surface tension b/t the lungs and chest wall

types=

Traumatic; Tension; Spontaneous: primary or secondary

presence of fluid in the pleural space; can cause compression atelectasis

Types:

Transudative- watery fluid that diffuses out of capillaries beneath pleura

Exudative- fluid rich in proteins that migrates from capillaries

Hemothorax- hemorrhage into pleural space

infected pleural effusion (pus in pleural space)

pulmonary lymph vessels become blocked --> infection with debris accumulating in pleural space

inflammation of the pleura;

clinical manifestations: chills, fever, pain on inspiration

a pleural friction rub may be heard over affected area

pleurisy is usually preceded by an upper resp. infection

results from the fracture of several consecutive ribs in more than one place

causes paradox movement of the chest wall w/ inspiration and expiration

are the result of exposure to toxic gases

Examples:

Pneumoconiosis

Allergic alveolitis

disease of the lungs caused by habitual inhalation of inorganic dust particles

Deposition of particles --> chronic inflammation with scarring of the resp. membrane --> pulmonary fibrosis

disease frequently seen in miners or stonecutters (is an occupational disorder)

allergic inflammatory response to inhalation of organic dust particles (grains, bird poop, silage)

can be acute or chronic-- with continued exposure, the disease becomes chronic --> pulmonary fibrosis

Restrictive Diseases resulting from alterations in the

lung parenchyma

ARDS

IRDS

Pneumonia

Restrictive diseases caused by changes in the:

a. pleura

b. chest wall

c. neuromuscular apparatus

a- pneumothorax

b- flail chest

c- myasthenia gravis

characterized by:

reduced lung volumes

reduced compliance

(reduced compliance representa and increase in overall stiffness of the lungs)

suddenly occuring, severe form of respiratory failure characterized by inflammation and diffuse alveolar-capillary injury

hallmark= hypoxemia that doesn't respond to supplemental oxygen therapy

Noncardiogenic pulmonary edema

atelectasis

fibrosis

pulmonary hypertension

PFTs- ↓ VC, ↓ FRC, ↓compliance, ↓tidal volume

Manifestations:

Tachypnea-- restrictive pattern

respiratory alkalosis

marked dyspnea

↓d lung compliance

refractory hypoxemia -- hypoxemia is unresponsive to Tx

diffuse alveolar infiltrates that are seen on X-ray

it reduces the work of breathing by ↓ing surface tension-- less pressure is needed to inflate an alveolus to a given radius

it prevents the collapse of smaller alveoli-- allows surface tenstion to become reduces as lung volume decreases

caused by inadequate pulmonary surfactant- an L/S ratio <2.1 is assoc. with a higher risk of IRDS

In premature infant, lack of pulmonary surfactant causes:

atelectasis and increased work of breathing

end results of increased work of breathing and ↓d ventilation are:

progressive atelectasis

increased pulmonary vascular resistance

profound hypoxemia

acidosis

excessive amount of fibrous/connective tissue in the lung

is marked by a ↓d lung compliance

classified based on site of obstruction--

w/in luminal wall = asthma; chronic bronchitis

increased pressure around the outside of lumen= emphysema secondary to loss of lung tissue&elasticity

obstruction in airway lumen-= cystic fibrosis

one of the most common obstructive diseases; characterized by:

reversible obstruction

airway inflammaation

airway hyperresponsiveness

common triad that cause an episode: bronchoconstriction, excessive mucus prod., swelling of bronchial mucosa

common features of an episode: wheezing, breathlessness, chest tightness, coughing

Intrinsic

Extrinsic

Exercised-induced

Occupational

Drug-induced

Asthma spirometry

Asthma blood gases

↓d: Expiratory flow rate, FEV1, FVC, FEV1/FVC

Increased: FRC and TLC

blood gases show hypoxemia with early resp. alkalosis or late respiratory acidosis

lung changes consistent with empysema or chronic bronchitis; 4th leading cause of death in US (prevalence and mortality have been increasing over past 30 yrs)

risk factors: primarily caused by cig. smoke, genetics, air pollution, occupational exposures

inflammatory disorder of the airways; most commonly results from long-term smoking; damage is irreversible

is a chronic productive cough that lasts at least 3 months of the year for at least 2 consecutive years

assoc. with persistent narrowing of the airways d/t chronic inflammation, scarring, and excessive mucus production-- is not d/t bronchospasm like asthma

↓d exercise tolerance

wheezing

SOB

productive cough

airway obstruction (seen by ↓d FEV1)

results from destruction of alveoli and small airways (no obvious fibrosis); risk factor= smoking; marked by a loss in elastic recoil

Obstruction is d/t changes in the lung tissue, not changes d/t mucus production (like asthma/chronic bronchitis)

Autosomal recessive disorder of exocrine glands & mucus cells;

most common genetic lung disease in US

 in the disease, thick mucus secretions cause:

airway obstruction

atelectasis

air trapping

Typical features= mucus plugging, chronic inflam., and infection; progressive ↓ in functional lung tissue

inflammation of the lung; lower resp. tract infection;

may be bacterial or viral (coughing is nonproductive in viral pneumonia)

8th leading cause of death in US; most common cause of death d/t infectious disease;

advanced age

immune deficiency

underlying lung disease

alcoholism, smoking

altered consciousness

malnutrition

endotracheal intubation

immobilization

Community Acquired-- Streptococcus pneumonia is the most common pneumonia-causing bacteria; Mycoplasma is common in young people; Haemophilus influenzae is most common viral form in adults

Nosocomial

Immuno - compromised individuals

upper resp. infection --> productive cough, dyspnea, fever

may have chills, malaise, and pleuritic chest pain

4 stages: congestion; red hepatization (from RBC in alveoli); gray hepatization (from WBC in alveoli); resolution

(hepatization = conversion of loose tissue into a firm mass)

lung infection caused by Myobacterium tuberculosis

leading cause of death from a curable infectious disease in the world

self limiting, acute infection/inflammation of the airways; most cases are caused by viruses

clinical manifestations:

fever, cough, chills, malaise

obstruct BF through part of the pulmonary system; can cause right ventricular HF;

emboli may be compased of fat, air, amniotic fluid, or thrombi (thrombi are th emost common cause)

is suspected with sudden dyspnea and chest pain

dyspnea is the most common symptom

predisposing factors (Virchow triad):

venous stasis/slow BF (immobility, HF)

hypercoagulability (pregnancy, cancer, estrogen use)

damage to venous intima (trauma)

a sustained increase in pulmonary arterial pressure

(>30 mmHg)

Primary: rare; no known cause; usually occurs in women aged 20-40

Secondary: caused by any respiratory/cardiovascular disorder that: increases the V or P entering pulm. arteries or narrows/obstructs the pulm. arteries

1. elevated L ventricular filling pressures (CHF)

2. Increased BF through pulmonary circulation (right-to-left shunt)

3. obstruction of pulmonary vascular bed by embolus or by chronic destruction of alveolar wall (emphysema)

4. vasoconstriction of vascular bed (occurs w/ acidosis, hypoxemia, or a combo of the 2)

most common cause= hypoxic vasoconstriction seen in COPD

right ventricular hypertrophy and dilation d/t pulmonary HTN-- caused by primary disorders of the lung parenchyma or vasculature

usually leads to R sided HF when pulmonary artery pressure =s sytemic BP

Large cell carcinoma

small cell carcinoma

squamous cell carinoma

adenocarcinoma

smoking is #1 cause

manifestations:

cough, hemoptysis, hoarseness,

chest pain, pleural effusion

Hypoxemia caused by decreased F1O2

high altitude

low O2 content of gas mixture

enclosed breathing spaces (suffocation)

lack of neuro stim. of the respiratory center

(oversedation; drug overdose; brain damage)

Diseases that restrict chest expansion

COPD

common clinical causes:

Emphysema

Fibrosis

Edema

Asthma; chronic bronchitis

Pulmonary edema

Pulmonary embolism

Pneumonia

ARDS/IRDS

Atelectasis

Restrictive-- marked by a loss of lung compliance

ARDS/IRDS, pulmonary fibrosis, pneumonia, TB, pleural effusions, SARS, pneumothorax

Obstructive- marked by increase in resistance to airflow (Raw); airway obstruction that is worse with expiration; Asthma, chronic bronchitis, emphysema

Infectious- pneumonia, tuberculosis, acute bronchitis

Vascular- pulmonary HTN, pulmonary embolism, cor pulmonale

Obstructive Disease

with this type of disease more force is required to expire a given volume of air, or emptying of the lungs is slowed, or both.

unifying sign of Obstructive disease= wheezing

unifying symptom= dyspnea

(most common cause)

1. L ventricular HF causes increased filling pressures on L side of heart --> increased pulmonary hydrostatic pressure

2. Fluid moves out of the pulm. capillaries into pulm. interstitium when pulm. hydrostatic pressure > oncotic pressure

3. fluid volume entering interstitium > lymph system's ability to remove it, causing Pulm. Edema

1. injury increases capillary permeability

2. Plasma proteins leak out and increase the interstitial osmotic pressure

examples that involve capillary injury:

ARDS; inhalation of toxic gases

increased pH

decreased temperature and PCO2

carboxyHb

abnormal Hb

lower levels of 2,3 DPG

Decreased pH

Increased temp and PCO2

High levels of 2,3 DPG

Abnormal Hb