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
