Pulmonary Flashcards
Pulmonary Characteristics
o Air going OUT goes faster than air going in because tubes are narrower during expiration
o Amount of air breathed in = amount of breathed out
o Alveoli have the fastest flow rate when lungs are most full and decrease as the lungs deflate
o It takes some effort to breath in because the alveoli must be inflated, but the elastic recoil of the alveoli assists us in process of exhalation
o Once the alveoli are opened, its easier to keep open; rather than for us to exhale all the air in our lungs and have the alveoli collapse/close between breaths
Law of Laplace
Tension = (Alveolar Pressure x Radius) / Wall thickness OR T = P x R
o If pressure inside alveoli increase, then the radius increases and wall thickness decreases overall tension increases
o Emphysema – elastic recoil of the wall is destroyed resulting in decreased tension and increased radius patient will have decreased pressure in alveoli leading to lower capacity to exhale fully
o ARDS – washing away of surfactant that normally help reduce surface tension of water in lungs
Results in increased tension and tendency to collapse, leading to decreased radius collectively act to increase alveolar pressure eventually causing alveolar collapse
Obstructive Pulmonary Disease
– emphysema, asthma, or chronic bronchitis
o Airway obstruction is worse with expiration and is progressive; may be accompanied by airway hyper-reactivity and may be partially reversible
o Increase in compliance tends to cause an obstructive disease
o Limited by their recoil
o Symptoms: dyspnea (painful breathing) and wheezing
o Diagnosis: Lung volume measurements – larger TLC, RV and FRC; smaller TV air trapping result of breathing more air in than breath out lungs get progressively larger & non-beneficial
Change in inspiration/expiration ratio reduction in FEV1/FVC ratio
• Normally 2 seconds inspiration, 4 seconds expiration 1:2
• Obstructive Disease 1:3 decreased inspiratory/expiratory flow
o Risk Factors: smoking, air pollution, hyperresponsive airways, occupational factors
alpha1-antitrypsin deficiency – only KNOWN genetic abnormality that leads to COPD
• accounts for < 1% of cases
• regulates elastase – results in breakdown of elastin causing a loss in recoil and increase in compliance
Mechanisms of Air Trapping in COPD
o Physiological insults destroy bronchial elastin protein fibers
o Mucous plugs and narrowed airways cause air trapping
o During inspiration the airways are pulled open allowing gast to flow past the obstruction
o During experiation, decreased elastic recoil of the bronchial walls result in collapse of the airways and prevents normal expiratory airflow
Flow Volume Loops (Obstructive, Restrictive, Tracheal Stenosis)
o Obstructive lung disease – concave and shallow curve; larger lung volume
o Treacheal stenosis – narrowing of trachea – max inhalation is smaller; max exhalation is smaller
o Restrictive – small lung volume; narrow and steep curve
Asthma
– NOT COPD but is obstructive disorder
o Chronic inflammation disorder causes recurrent episodes of wheezing, breathlessness, chest tightness and cough particularly at night and early morning (airways get smaller at rest), hyper-responsive to stimuli
o Atopy – genetic predisposition for the development of an IgE-mediated response to common aeroallergens, cold, or exercise; results in cascade of inflammatory events leading to acute/chronic airway dysfunction
Strongest identifiable predisposing factor for developing asthma
o Associated with widespread but variable airflow obstruction that is often reversible (spontaneous or with treatment
Beta-agonists (Norepinephrine-adrenaline) and anti-cholinergics reduce parasympathetic innervation and are good good short-term rescue (~15 minutes)
Asthmatic Response/Mechanism
o Early: inhale antigen binds to IgE on mast cells causing degranulation inflammatory response local edema and release mediators antigen activates submucosal mast cells
Secreted vasoactive mediators – cause increased vasodilation & capillary permeability cause bronchospasm, vascular congestion, mucus secretion, impaired mucociliary function, thickening of airway walls, increased contraction of bronchial smooth muscle
Secreted chemotactic mediators – induce cellular infiltration of immune cells through new permeable capillaries release of toxic neuropeptides from eosinophils that will lead to irreversible epithelail membrane destruction
o Desquamation of epithelial cells causes abnormal permeability and further exposure to irritants
o Elastin destruction leads to air trapping & enhanced contraction of bronchial smooth muscles
o Fibrosis increases epithelium thickness through scar tissue that impedes gas exchange
Chronic Bronchitis
o Bronchial infection causing hypersecretion of mucus and chronic productive cough that lasts for >3 months of year and for atleast 2 consecutive years
o Inspired irritants increase mucus production and the size and number of mucous glands
o Mucus is thicker than normal due to constant exposure to irritants; cough is to get rid of mucus
o Some fibrosis is noted
Emphysema
o Abnormal permanent enlargement of the gas-exchange airways (acinar cells) accompanied by destruction of alveolar walls with NO fibrosis
o Loss of elastic recoil because of enlargement of a alveoli difficulty exhaling
Remove air by increasing thoracic pressure which increases chance of airway collapse
o Centriacinar emphysema OR panacinar emphysema treatment is the same for both
o Pathogenesis: tobacco increases reactive oxygen species inactivation of antiproteases increase neutrophil elastase tissue damage
Alveolar macrophage increases macrophage elastase and metallo-proteinases increase tissue damage
COPD Eventual Causes
– Cor Pulmonale (right-sided heart failure)
o Difficult to treat due to lack of extensive innervation
o Best treatment: pulmonary vasodilators to decrease RV afterload
Absorption Atelectasis
o Collapsed lung combined with fluid exudation
o Alveoli become isolated by a mucous plug and closed pore of Kohn
o Alveoli in West Zone 3 most susceptible – lower ventilation/perfusion ratio
Lower ventilation increases the probability of obstruction
Higher perfusion increase the chances of fluid exudation and infection
o Prevention/Treatment – opening pores of Kohn via deep breaths or positive pressure breathing which bypasses the mucous plug and restores ventilation
Bronchiectasis
– bronchial smooth muscle infection
o Seen in immune-compromised and cystic fibrosis patients
o Treatment: antibiotics
Restrictive Lung Diseases
o Restrictions to both inflow and outflow
Inspiration limited due to reduced compliance of the lung or chest wall = “stiff lungs”
Reduction in lung compliance = increased work of breathing and dyspnea
o Rapid, shallow breathing pattern is observed = increased dead space ventilation
o No loss of elasticity
o Normal gas exchange until advanced stage of disase
increased PaCO2, decreased PaO2 with pulmonary hypertension and cor pulmonale – right sided heart failure as a result of some lung problem
o Decreased TLC, FRC, RV, VC, FEV1, FVC, total volume exhaled
o Normal expiratory flow rates, FEV1/FVC ratio
Classification of Restrictive Lung Diseases
o Acute intrinsic – all cause pulmonary edema
o Chronic Intrinsic (disease lung parenchyma)
o Chronic Extrinsic (chest wall, intra-abdominal, & neuromuscular diseases) – lungs are okay
o Disorders of the Pleura and Mediastinum
Pulmonary Edema
o Fluid leakage from the intravascular space into the lung interstitium or alveoli caused by:
Increased capillary/hydrostatic pressure (cardiogenic) – left side of heart is failing - transudate
Increased capillary permeability (underlying inflammatory process) - exudate
o Decrease in oxygen diffusion
o Chest X-ray will show bilateral symmetrical opacities
o Treatment: supportive care (positive pressure ventilation and increased FiO2)
Acute Respiratory Distress Syndrome
o Diffuse pulmonary endothelial injury from exposure to environmental pollutants
o H20, solutes, and macromolecules diffuse from intravascular space/capillaries into lung parenchyma and alveoli
Do not want water lining alveoli because surface tension is increased and decreases compliance, increases recoil
Water also washes away surfactant, further increasing recoil
o Sepsis often co-exists producing further lung injury via inflammatory mediators
o Often ARDS signals the beginning of multiple organ system failure
Aspiration Pneumonitis
o Result of swallowing acidic gastric secretions (vomit) that destroys surfactant-producing cells; damages pulmonary capillary endothelium
o Similar to ARDS – increased permeability pulmonary edema with atelectasis
o Symptoms: hypoxia, tachypnea, bronchospasm (vomit contains some irritant), pulmonary vascular constriction can develop into pulmonary hypertension, chest X-ray shows abnormalities 6-12 hours later; usually right lower lobe
o Treatment: increase FiO2, PEEP (to prevent alveoli from collapsing), B-2 agonists for bronchospasm, +/- lavage to wash out gastric agents, fiberoptic bronchoscopy if suspected solid material aspirated, antibiotics, steroids
Cardiogenic Pulmonary Edema
o Result of LV failure which causes increased pulmonary vascular hydrostatic pressures
o SNS activation usually causes pulmonary vasoconstriction and further contributes to edema
o Transudate
o Symptoms: extreme dyspnea, tachypnea, hypertension, tachycardia, diaphoresis (sweating)
Neurogenic Pulmonary Edema
o Occurs minutes to hours following an acute brain injury (especially medulla)
o Edema is secondary to massive SNS discharge in response to CNS insult
o Generalized vasoconstriction will shift large blood volume into pulmonary vessels = vessel injury and transudation of fluid into lung parenchyma/alveoli
o Similar to cardiogenic form
o Treatment is supportive
Control intracranial pressure elevations, increased FiO2, positive pressure ventilation, PEEP, NO diuretics (edema is secondary to SNS so once SNS innervation is reduced, edema will disappear)
Drug-Induced Pulmonary Edema
o Heroin – directly impacts capillaries; causes increased capillary permeability pulm. edema
o Cocaine – mimics SNS causing massive vasoconstriction; causes increased pulmonary vascular hydrostatic pressure result in pulmonary edema
o Treatment is supportive
High Altitude Pulmonary Edema
o Mechanism: intense hypoxic pulmonary vasoconstriction after 48-96 hours at high altitude
Shunt blood away from poorly ventilated portions of lung
Entire lung poorly ventilated try to shunt blood away from entire lung increased pulmonary vasoconstriction
o Increased pulmonary vascular pressures result in high permeability pulmonary edema
o Treatment: bottled O2, prompt descent from altitude, and inhaled nitric oxide
Give diuretic that induces acidosis and hypoventilation
Re-expansion Pulmonary Edema
o Re-expanding lung after a pneumothorax or thoracentesis results in fluid being pulled in; enhanced capillary membrane permeability
o Increased risk with longer collapses or greater volumes of fluid/air removed
o Supportive treatment: NO diuretics
Negative-Pressure Pulmonary Edema
o Difficulty inhaling; inhaling against a closed glottis or obstruction; results in drawing of blood into chest because of highly negative intrapleural pressure
o Occurs minutes/hours after acute upper airway obstruction in spontaneously breathing patients
o Symptoms: tachypnea, cough, failure to maintain SaO2 > 95%
o Usually self limited – 12-24 hour duration
o Causes: post-extubation laryngospasm, obstructive sleep apnea, epiglottitis, tumors, obesity, hiccups
o Treatment: supplemental O2, maintenance of airway, mechanical ventilation if necessary
Chronic Intrinsic Restrictive Lung Disease - Pulmonary Fibrosis
– results in pulmonary hypertension
o Will result in cor pulmonale (R. heart failure) due to increased workload due to lung resistance
o Smoking and development of pulmonary fibrosis are main causes of pulmonary HTN
Fibrotic areas = irreversible damage = do not participate in gas exchange, results in regional vasoconstriction and increased pulmonary resistance
o Symptoms: dyspnea (rapid and shallow), predisposition for spontaneous pneumothorax
o Mechanism: activated macrophages recruit neutrophils neutrophils release oxidative proteases injury to Type 1 pneumocytes
Macrophage activation cytokine and chemokine recruitment of fibroblasts hypertrophy and hyperplasia of Type 2 pneumocytes
o Treatment: if prior to fibrosis, the disease can be reversed
Chronic Intrinsic Restrictive Lung Disease: Sarcoidosis
o Systemic granulomatous (micro tumors) disorder; often in thoracic lymph nodes & lungs
o Granulomas elicit immune response that leads to fibrosis, pulmonary HTN, and cor pulmonale
o Decreased alveolar diffusion capacity
o Laryngeal sarcoid 1-5% of patients – can interfere with passage of endotracheal tube
o Myocardial sarcoid rare (heart block, dysrhythmias, restrictive cardiomyopathy)
o Liver, spleen, optic, and facial nerve often involved
o Patients often present for mediastinoscopy for diagnosis
o Watch for hypocalcemia
Chronic Intrinsic Restrictive Lung Disease: Other Etiologies (Hypersensitivity Pneumonitis, Eosinophilic Granuloma, Pulmonary Alveolar Proteinosis, Lymphagiolyomyomatosis)
o Hypersensitivity Pneumonitis – diffuse interstitial granulomatous reactions in the lungs after inhalation of dust containing fungi, spores, or anima/vegetable material
o Eosinophilic granuloma – pulmonary fibrosis is common
o Pulmonary alveolar proteinosis – unknown cause
Deposition of lipid-rich proteinaceous material in the alveoli
o Lymphangiolyomyomatosis – proliferation of smooth muscle in the abdominal and thoracic lymphatics, veins, and bronchioles
Chronic Extrinsic Restrictive Lung Disease - thoracic cage abnormalities & insufficient muscular system
o Compressed lungs result in increased work of breathing (like weight on chest)
Decreased lung volumes with corresponding increase in airway resistance
Abnormal chest wall mechanics
o With thoracic deformity, right ventricular dysfunction common with chronic compression of pulmonary vasculature due to lack of oxygenation of blood and vasoconstriction to shunt blood away from lung
o Impaired cough = chronic infection; development of obstructive component
Chronic Extrinsic Restrictive Lung Disease: Obesity
o Diaphragm and chest wall movement restricted by excessive weight that compresses abdomen
o Dyspnea - increased resistance to breathing and increased work to move excess weight
o Decreased FRC can rapidly progress to V/Q mismatch – difficulty keeping alveoli open
Will need super high PEEP with mechanical ventilation
Chronic Extrinsic Restrictive Lung Disease: Skeletal Structure Deformities – Costovertebral
o Scoliosis – lateral curvature with rotation of the vertebral column; most common in teenage girls
o Kyphosis – anterior flexion of (thoracic) vertebral column; hunched over appearance
o Lordosis – extra curvature of lumbar spine
o CNS depressants – increased risk of hypoventilation and pneumonia
Chronic Extrinsic Restrictive Lung Disease: Skeletal Structure Deformities – Sternum
o Pectus excavatum – inward concavity of the sternum
o Pectus carinatum – outward protuberance of sternum
o Some patients are asymptomatic; others require surgical correction to reduce pulmonary restriction and resultant cardiovascular dysfunction
Chronic Extrinsic Restrictive Lung Disease: Flail Chest
o Secondary to rib fractures/sternotomy dehiscence – paradoxical inward movement of the unstable portion of the thoracic cage during inspiration
o Lung increases volume during exhalation and decreases volume during inhalation
o Decreased PaO2 & increase PaCO2 secondary to alveolar hypoventilation
o Treatment: positive pressure ventilation required until thoracic cage stabilization occurs
Chronic Extrinsic Restrictive Lung Disease: Neuromuscular Disorders
– diaphragmatic paralysis, spinal cord transection C4, Guillian-Barre syndrome, myasthenia gravis, myasthenic syndrome, muscular dystrophy
o Spinal cord, peripheral nerve, neuromuscular junction, or skeletal muscle pathology that prevents the generation of normal respiratory pressures
o Life threatening when it affects the diaphragm can’t breathe without the diaphragm
o Impairment of effective cough generation, retained secretions, pneumonia, respiratory failure may result
o Very sensitive to CNS depressants
o Vital capacity useful to measure extent of impact of disease on ventilation
Disorders of the Pleura and Mediastinum
– mechanical changes interfere with effective lung expansion
o Pneumothorax – open, tension, spontaneous, or secondary – air in the pleural space causes the lung to collapse around the hilus and may push mediastinal contents toward the other lung
o Pleural effusion – fluid in lung
o Empyema – infected pus in pleural effusion
o Pleural fibrosis – scars form between the pleura and chest wall
Pneumothorax Types, Symptoms, & Treatments
o Idiopathic – gas in the pleural space secondary to a defect in the parietal or visceral pleura
Treatment: evacuation of air via catheter aspiration or chest tube
o Tension – MEDICAL EMERGENCY – when air enters pleural space during inspiration and is not allowed to exit on expiration; opening during inhalation but closes during expiration
Common after rib fracture or barotrauma – symptoms more sudden and severe
Treatment: small bore plastic catheter into second anterior intercostal space
o Open – there is an opening to outside (ex: from stab wound)
o Symptoms: acute dyspnea, ipsilateral chest pain, decreased PaO2, increased PaCO2, hypotension, tachycardia, decreased chest wall movement, decreased/absent breath sounds, hyperresonant percussion (tap on rib and it will sound hollow)
o Treatment: evacuate the air; increase FiO2 improves the rate of air Resorption by pleura 4x
Pleural Effusion Types
o Transudative effusion – interstitial fluid (blood without proteins); due to systemic factors like HTN or heart failure
o Exudative effusion – blood with plasma proteins as a result of inflammation; due to local factors such as infection or sepsis
o Pleurisy – inflammation of pleura as result of infection in pleural effusion liquid
o Hemothorax – blood in pleural effusion
Obstructive vs. Restrictive Lung Disease (FVC, FEV, FEV/FVC%)
o Obstructive (asthma, emphysema, bronchitis)-normal FVC, decrease FEV1, decreas FEV1/FVC% o Restrictive (pneumonia, pulmonary edema, fibrosis) – decreased FVC, normal/decreased FEV1, normal FEV1/FVC%
Pulmonary Embolism
Occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or an air bubble
Causes: Virchow Triad – venous stasis, hypercoagulability, and injuries to the endothelial cells that line the vessels
• Commonly arise from the deep veins in the thigh lungs act as filter
Symptoms: tachypnea, dyspnea, chest pain, increased dead space, V/Q imbalance, decreased PaO2, pulmonary hypertension, decreased cardiac output, systemic hypotension, shock
Pulmonary Hypertension
Normal = 0-10mmHg
Mean pulmonary artery pressure 5-10 mmHg above normal or above 20mmHg
Many different ways to get pulmonary hypertension: respiratory disease/hypoxemia, thrombus/embolism, disease of pulmonary vasculature
Endothelial dysfunction
• Overproduction of vasoconstrictors – thromboxane, endothelin
• Under production of vasodilators – prostacyclin, nitric oxide
Usually idiopathic – environmental or genetic
Lung Cancer Causes
Most common cause is cigarette smoking
• Heavy smokers have 20x greater chance
• Smoking related to cancers of larynx, oral cavity, esophagus, & urinary bladder
Environmental or occupational risk factors
Lung Cancer Types - non-small cell lung cancer
Squamous (epidermal) cell carcinoma – slow; near hilus; obstructive with cough and hemoptysis (coughing up blood)
Adenocarcinoma – moderate; usually on periphery; least correlated with smoking
Lung Cancer Types - large/small cell carcinoma
o Large cell carcinoma (undifferentiated) - rapid o Small (oat) cell carcinoma – very rapid; most correlated with smoking; very high mortality; ectopic hormone production
Staging of Lung Cancer
o Number 0,1,2 given to each Tumor size, advancement to nodes, metastasis
Stage 1 – T1 tumors confined/starting to spread; No lymph nodes; no metastasis
• Also, tumors classified as T2 but having no nodal or distant metastases
Stage 2 – T2 tumors that begin to invade other cells; lymph node involvement; metastasis only to ipsilateral hilar lymph nodes
Stage 3 – Any tumor past T2; high number of lymph nodes involved; metastasis to distant lymph nodes
