Patho Respiratory 2

54問 • 2年前

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Association with bacterial infections (H flu). Rapid edema of glottis - severe and life-threatening obstruction. Inspiratory stridor, tripoding, drooling. Try to keep the kid calm!

Acute Epiglottis

Autosomal recessive, defective chloride transport, thick secretions of respiratory and/or digestive and/or respiratory tract leads to mucus plug, chronic inflammation and prone to infections

Cystic Fibrosis

Structural lung restrictions leads to decreased Tv, Dyspnea, Tachypnea, difficulty clearing secretions. Shows Decreased Compliance Curve.

Scolisis, Morbid Obesity, Muscular Dystrophy

Bronchial damage with inflammation—> loss of cilia function—> Bronchospam. Alveolar-capillary membrane damage—> hemorrhagic pneumonitis—> stiff non-compliant alveoli

Aspiration

Blockage of airway from outside pressure inhibits lung expansion and not enough surfactant available. Increased pulmonary shunt —> hypoxemia. Decreased compliance curve. Caused my tumors, PNE, and mucous buildup.

Atelectasis

Excessive fibrosis—> fibrosis of alveolar epithelium—> myofibroblast proliferation—> stiff alveoli—> decreased compliance—> V/Q mismatch—> hypoxemia

Pulmonary Fibrosis

Excessive fibrosis and connective tissue in lungs. Etiology: ARDS, TB, RA, Sarcoidosis, Coal Dust, Asbestos, Idiopathic

Pulmonary Fibrosis

Inadequate gas exchange (hypoxic or hypercarbic) assessed by clinical exam and labs (AA gradient)

Respiratory Failure

PaO2 < 50 mmHg, can occur with or without hypoxia. Etiology: hypoventilation (CNS depression), V/Q mismatch, increased alveolocapillary membrane thickness, HF. Clinical s/s: Tachycardia, Cyanosis, Confusion

Hypoxemic Respiratory Failure

PaCO2 >/= 50 and pH </= 7.25. Etiology: hypoventilation-decreased respiratory drive, neuromuscular disease, airway obstruction, physiological dead space (V/Q mismatch), chest wall deformities. Clinical s/s: confusion, VERY lethargic

Hypercarbic/Hypercapnic Respiratory Failure

AA Gradient = Alveolar O2 (PAO2) - Arterial O2 (PaO2)–> normal 5-15 mmHg.

If elevated think though pulmonary causes

PaO2/FiO2: Severity of Hypoxemic Respiratory Failure

P/F Ratio = PaO2/FiO2

Inflammatory process in lungs that lead to alveolar epithelial band vascular endothelial injury with infective and non-infective etiology

ALI/ARDS

3 criteria: acute onset < 7 days, bilateral infiltrates, respiratory failure not explained by cardiac cause or FO

ALI/ARDS

P/F ratio </= 300

ALI

P/F ratio </= 200

ARDS

3 phases: Exudative, Proliferate, Fibrotic

ALI/ARDS

Movement of air in and out of the lungs

Ventilation

Diffusion of O2 and CO2 between alveoli in lungs and the blood

Gas Exchange

Movement of blood into and out of the capillary beds

Perfusion

Movement of O2 and CO2 via blood and circulatory system?

Transport

Purpose is to allow passage of air into and out of gas exchange areas of lung, but no gas exchange occurs in these areas

Conducting Zone

Respiratory Passages are lined with:

Goblet Cells and Cilia

Structure that blocks airway when eating except in infants

Epiglottis

Respiratory Cells that secrete mucous

Goblet Cells

Clear debris from airways and keep airways moist

Cilia

Relies on pressure to maintain patency

Intra-Thoracic

More solid structures that doesn’t require pressure to maintain patency

Extra-Thoracic

Originate from the glottis and are stretched by muscles, ligaments, and cartilage. Open during breathing and Closed during phonation.

Vocal Cords

Have Cartilage Rings

Trachea

Have Cartilage Plates

Bronchi

Have No Cartilage and Depend on Transpulmonary Pressue to Remain Open (where there is no cartilage there is smooth muscle)

Bronchioles

For a very small change in airway radius there is a 4-fold increaed in:

Airway Resistance

More significantly impacted by changes in diameter of airway

Neonate/Children

Takes much greater pressure with less volume on inhalation, and greater pressure to get air out on exhalation

Increased Resistance Curve

Harder to get alveoli to cooperate and allow the air in. Don’t get as much air in and with higher pressures and less volume.

Decreased Compliance

Volume of air that remains after either inspiratory and/or expiratory reserve volume

Residual Volume

Gives us a measure of how compliant and healthy lungs are (e.g. in asthma)

FEV

Extend through connective tissue and hilum that contribute to pulmonary circulation

Lymphatics

When O2 concentration falls <70% causing vasoconstriction, results in increased pulmonary vascular resistance in the lung unit that is not well perfused shunting blood to areas that are adequately perfused

Hypoxic Pulmonary Vasconstriction Response

Sending blood to areas of the lung that are not ventilating

V/Q Mismatch

Most common cause of hypoxia and found in asthma, chronic bronchitis, PNE, PE, and atelectasis

V/Q Mismatch

Blood Flow in Apices

Zone 2

Blood Flow in Areas Below Apices

Zone 3

Gases move from areas of high to low concentration

Concentration Gradient

Movement of Gases Between Air and Blood

Net Diffusion

Percent of O2 consumption the body uses from O2 transport via Hgb

Approximately 25%

Decreased: pCO2, H+, 2,3-DPG, Temp, HbF

Left Shift (increased affinity for O2)

Increased: pCO2, H+, 2,3-DPG, Temp

Right Shift (decreased affinity for O2)

Etiology of PAH

Chronic Hypoxia, LHF, Valve Disease

More common in girls than boys as they age

Asthma

Inflammatory Stage where there is edema and fluid that builds up and damages alveoli produces exudate from inflammatory response that creates a barrier that prevents gas exchange

Exudative Phase

Signs of early healing, improvement of pulmonary edema and begins to drain-reabsorption of fluid (increased lymphatic drainage and increased pleural fluid—> pleural effusions), recovery of capillary alveolar barrier (improved gas exchange), proliferation of squamous cells start the healing process

Proliferative Phase

Stage where fibroblasts move in and proliferate causing fibrosis in alveoli. Can also have interstitial and capillary fibrosis. Risk for developing PAH and chronic pulmonary changes.

Fibrotic Phase

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