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Pulmonary Disorders, smoking is a primary risk factor in some forms of…
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- smoking is a primary risk factor in some forms of lung disease
- secondhand smoke also plays role
- occupational and environmental exposures to harmful substances
- Smooth muscle in bronchi and bronchioles
- control diameter of airway and air flow
- Innervated by autonomic nervous system
- Sympathetic: bronchiole dilation
-- Beta-2 adrenergic receptors
- parasympathetic: bronchiole constriction
- Chemical mediator of bronchoconstriction
- Leukotrienes: secreted by WBCs
- Histamines: released by mast cells
- lines chest cavity and envelops lungs
- thin film of fluid lubricates membrane layers
- Pleural space:
- area between membrane linings
- negative intrathoracic pressure enables lungs to inflate easily
- if air/fluid enter pleural space, lung expansion more difficult
- pleural effusion: fluid in pleural space
- Hypoxia: lack of oxygen
- hypoxemia
-- lack of O2 in bloodstream
- Hypercapnia: elevated carbon dioxide levels
- Hypoxia and hypercapnia may occur together
- lungs cannot exchange adequate oxygen or carbon dioxide
- PaCO2 greater than 45mmHg (normal 35-45mmHg)
- Normal response
-- Elevated CO2 stimulates medulla and incr. ventilation
- chronic hypercapnia
-- headache, drowsiness, intellectual impairment
- if hypercapnia prolonged, central chemoreceptors become insensitive to CO2 levels
- chronic hypercapnia
-- elevated CO2 no longer serves as primary stimulus for ventilation
-- Stimulus for breathing shifts to the chemoreceptors in carotids and aorta
-- low O2 drives ventilation (hypoxic drive)
- ideal PaO2: 90 to 100mmHg
- mild hypoxemia causes few symptoms
-- PO2 levels as low as 70mmHg have hemoglobin saturation of almost 90%
- dramatic drop in hemoglobin saturation at PO2 of 60mmHg or less
-- inadequate oxygen delivery
- restlessness, uncoordinated movement, impaired judgement
- stimulates incr. ventilation
- stimulated incr. erythropoietin (EPO)
-- EPO secreted by kidneys
-- stimulates the bone marrow to synthesize RBCs
- stimulates pulmonary vasoconstriction
-- vasoconstriction in areas of lungs with low O2
-- may lead to pulmonary hypertension, which may cause right-side heart failure (cor pulmonale)
- current/past smoking habits
- smoking history in pack-years
-- number of years smoked multiplied by number of packs per day
-- Eg: 76 year old patient smoked two packs per day since age 16
-- therefore 120 packs/year smoking history (2 packs per day x 60 years)
- occupational exposure to toxic agents
- drug use (marijuana, cocaine)
- nonpreparatory disorders
-- cardiac disease, HIV, immunosuppression, lupus, sarcoidosis
- genetics
-- alpha-1 antitrypsin (AAT) deficiency (incr. risk for lung disorders)
- auscultation (listening to heart)
- rate, rhythm, depth of breathing
- accessory muscle use
- cyanosis
-- bluish discoloration
- thoracic cage
-- normal (width 2x size of depth of chest)
-- Long term COPD (width and depth equal)
- adventitious breath sounds
- percussion
-- dull/hyperresonant
- clubbing of fingers
-- occurs with chronic hypoxia
- chest xrays
- CT scan, MRI
- V-Q scan
- ABGs
- bronchoscopy
- PFTs (pulmonary function tests)
- total lung capacity (TLC)
-- amount of air in lungs after maximal inhalation
- Functional residual capacity (FRC)
-- amount of air remaining in lungs after normal exhalation
- Residual volume (RV)
-- amount of air in lungs after a complete exhalation
- Tidal volume (TV)
-- normal breathing volumes in inhalation and exhalation
- forced vital capacity (FVC)
-- maximal amount of air exhaled after maximal inhalation
- forced expiratory volume (FEV)
-- amount of air exhaled usually within a time interval
-- FEV1.0 amount of air exhaled first second
-- Ratio: FEV1/FVC
- forced expiratory flow (FEV25%-75%)
-- airflow halfway through an exhale
- peak expiratory flow (PEF)
-- how quickly an individual can exhale
- hypersecretion of mucus in airways
-- patient can not get air into lungs
-- cough present for 3 months of year for consecutive years
- Hypoxia and cyanosis results
- overdistension of alveoli
-- loss of elastic recoil
-- patient cant get air out of lungs
- air trapping
-- high residual volume (RV)
-- high CO2 in lungs
- Chronic bronchitis (AKA blue bloater)
- mucus and edema
- cannot get air IN
cyanosis
- cough
- chronic hypoxia
pulmonary arterial vasoconstriction
- Emphysema (AKA pink puffer)
- air trapping
- cannot get air out
- chromic hypercapnia
- prolonged exhalation
- barrel shaped chest
- normal breathing stimulus: incr. CO2
- severe COPD causes CO2 levels to chronically elevate
- chemoreceptors and respiratory center become insensitive to high CO2
-- respiratory drive then comes from peripheral chemoreceptors and O2 levels (hypoxic drive)
-- O2 titration to keep hypoxic drive
-- use caution with agents that depress respiratory drive
- stepwise approach with medications
-- SABAs, LABAs, long-acting anticholinergic (anti-muscarinic) agents (LAMAs)
-- ICs
-- Leukotriene antagonists
- smoking cessation, pulmonary rehabilitation, vaccinations
- O2 therapy: continuous O2 when PaO2 less than 55mmHG or SaO2 less than 88%
- obstructive sleep apnea (OSA), central sleep apnea (CSA), or combination
-- apnea: reduction of airflow by 90% for at least 10 seconds
- OSA
-- intermittent collapse of upper airway tissues
- CSA
-- Loss of respiratory drive from brainstem
- results in sleep disturbance, daytime sleepiness, hypoxemia
- Diagnosis
-- sleep study (polysomnography)
- treatment
-- behavioral changes
-- CPAP (continuous positive airway pressure)
-- oral appliance that pulls tongue forward may help
- surgery to open upper airway structures
- collapsed lung
- air in pleural cavity causes collapse of a large section or whole lobe of lung tissue
- forms:
-- primary spontaneous pneumothorax (PSP)
-- secondary spontaneous pneumothorax (SSP)
-- traumatic
-- tension
-- iatrogenic
- air in intrapleural space, no preceding trauma or underlying lung disease
- most common in tall, young men between the ages of 10 and 30 years old
- unclear etiology, but ruptured alveoli are theorized to be the cause
- occurs in a wide variety of lung diseases
- underlying pathological process in the lung
- air enters the pleural space via ruptured blebs (overly distended and damaged alveoli)
- patients with long term emphysema most at risk
- Tension
- escalating buildup of air within lung compresses the lung, bronchioles, cardiac structures, vena cava
- closed, penetrating wound allows air into pleural cavity, BUT not out
- life threatening as cardiac structures compressed
- iatrogenic
- complication of medical procedures
- often: transthoracic needle aspiration
- Symptoms
- chest pain, dyspnea, and incr. respiratory rate
- Diagnosis
- chest xray or CT scan
- chest xray
-- linear shadow of visceral pleura with lack of lung markings peripheral to the shadows
-- mediastinal shift toward the contralateral undamaged lung
- pulse oximetry and ABGs may reveal hypoxemia
- Treatment
- chest tube with suction
-- pulls the air out of the pleural cavity and allows the lung to re-expand
- tension pneumothorax
-- large bore needle inserted into affected side to pull out air
- O2 administration
- pleurodesis
-- prevents recurrence
-- intentional irritation of pleural membrane causes membrane to adhere together
-- closes off pleural space
- abnormal collection of fluid in pleural cavity
-- compresses lung tissue
- fluid accumulates due to heart failure, severe pulmonary infection, or neoplasm
-- fluid may be exudate or transudate, purulent, lymph, or sanguineous (bloody)
- thoracentesis
-- relieve pressure on the lungs and provide fluid for analysis
- signs
- dyspnea, tachypnea
- sharp pleuritic chest pain
- dullness to percussion
- diminished breath sounds on the affected side
- lack of breath sounds over area of effusion
- kyphoscoliosis
-- kyphosis: curve of cervical spine
-- scoliosis: twisting of thoracic vertebral column
- noticeable deformity
-- 1 shoulder or hop higher than the other
- orthopedic brace or surgical intervention
- injury of lung tissue by an unidentified agent
-- repeated alveoli inflammation causes fibrotic changes (lung tissue stiffens)
- dyspnea, tachypnea, crackles, and eventual cyanosis
- chest xray
-- "ground glass" appearance
- treatment
-- decrease inflamm. and fibrotic changes
- immunologically mediated due to prolonged intense exposure to inhaled organic dusts
- bacterial spores, fungi, or animal proteins
- abnormally heightened sensitivity to the antigen causes alveolar inflamm.
- prolonged exposure can lead to pulmonary fibrosis
- most common cause: LV failure (LVF)
- LVF
-- LV can not eject blood forward
-- blood accumulation in LA and pulmonary circulation
-- incr. hydrostatic pressure in pulmonary capillaries results in pulmonary edema
- severe respiratory distress
- chest x-ray for diagnosis
- clot that has traveled and lodged in pulmonary arterial circulation
-- DVT from lower extremity
-- atrial thrombus
- obstruction of blood flow to lung
- presentation is vague, without warning
- can lead to death
- primary
-- genetic disorder
-- abnormal structure of pulmonary vessels
- secondary
-- increased pulmonary artery pressure as a result of other factors (ie., hypoxemia)
- Diagnosis
-- xray, ECG
- treatment
-- vasodilators
- diffuse alveolar injury, pulmonary capillary damage, bilateral pulmonary infiltrates, severe hypoxemia
- seen in critically ill patients
- sequel to trauma, sepsis, drug overdose, massive transfusion, aspiration
- sepsis is most common risk factor
- major cause of death
- sudden, progressive pulmonary edema
- arterial hypoxemia that does not improve with administration of O2
- ABGs
-- PO2 of 50mmHg or LESS
-- PCO2 of 50 mmHg or MORE
- berlin criteria
-- diagnostic conditions of ARDS
- treatment
-- mechanical ventilation