Pulmonary Flashcards

1
Q

Pulmonary Characteristics

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Law of Laplace

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Obstructive Pulmonary Disease

A

– 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Mechanisms of Air Trapping in COPD

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Flow Volume Loops (Obstructive, Restrictive, Tracheal Stenosis)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Asthma

A

– 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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Asthmatic Response/Mechanism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Chronic Bronchitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Emphysema

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

COPD Eventual Causes

A

– 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Absorption Atelectasis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bronchiectasis

A

– bronchial smooth muscle infection
o Seen in immune-compromised and cystic fibrosis patients
o Treatment: antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Restrictive Lung Diseases

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Classification of Restrictive Lung Diseases

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pulmonary Edema

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Acute Respiratory Distress Syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Aspiration Pneumonitis

A

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

18
Q

Cardiogenic Pulmonary Edema

A

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)

19
Q

Neurogenic Pulmonary Edema

A

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)

20
Q

Drug-Induced Pulmonary Edema

A

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

21
Q

High Altitude Pulmonary Edema

A

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

22
Q

Re-expansion Pulmonary Edema

A

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

23
Q

Negative-Pressure Pulmonary Edema

A

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

24
Q

Chronic Intrinsic Restrictive Lung Disease - Pulmonary Fibrosis

A

– 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

25
Q

Chronic Intrinsic Restrictive Lung Disease: Sarcoidosis

A

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

26
Q

Chronic Intrinsic Restrictive Lung Disease: Other Etiologies (Hypersensitivity Pneumonitis, Eosinophilic Granuloma, Pulmonary Alveolar Proteinosis, Lymphagiolyomyomatosis)

A

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

27
Q

Chronic Extrinsic Restrictive Lung Disease - thoracic cage abnormalities & insufficient muscular system

A

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

28
Q

Chronic Extrinsic Restrictive Lung Disease: Obesity

A

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

29
Q

Chronic Extrinsic Restrictive Lung Disease: Skeletal Structure Deformities – Costovertebral

A

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

30
Q

Chronic Extrinsic Restrictive Lung Disease: Skeletal Structure Deformities – Sternum

A

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

31
Q

Chronic Extrinsic Restrictive Lung Disease: Flail Chest

A

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

32
Q

Chronic Extrinsic Restrictive Lung Disease: Neuromuscular Disorders

A

– 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

33
Q

Disorders of the Pleura and Mediastinum

A

– 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

34
Q

Pneumothorax Types, Symptoms, & Treatments

A

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

35
Q

Pleural Effusion Types

A

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

36
Q

Obstructive vs. Restrictive Lung Disease (FVC, FEV, FEV/FVC%)

A
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%
37
Q

Pulmonary Embolism

A

 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

38
Q

Pulmonary Hypertension

A

 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

39
Q

Lung Cancer Causes

A

 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

40
Q

Lung Cancer Types - non-small cell lung cancer

A

 Squamous (epidermal) cell carcinoma – slow; near hilus; obstructive with cough and hemoptysis (coughing up blood)
 Adenocarcinoma – moderate; usually on periphery; least correlated with smoking

41
Q

Lung Cancer Types - large/small cell carcinoma

A
o	Large cell carcinoma (undifferentiated) - rapid
o	Small (oat) cell carcinoma – very rapid; most correlated with smoking; very high mortality; ectopic hormone production
42
Q

Staging of Lung Cancer

A

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