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Pathophysiology Ch.33 Pulmonary Function Study Guide
Alterations of Pulmonary Function
Terms in this set (126)
What two clinical manifestations are most common in pulmonary disease?
Cough & Dyspnea
Explosive expiration to clear the lower airways
An important reflex that helps clear airways of inhaled material, excessive secretions or abnormal substances
What does the cough reflex result from?
Sensory receptors in the airways (less receptors in distal bronchi permits secretions to accumulate without stimulating cough)
Cough receptors also located in auditory canal, diaphragm, pericardium, pleura, and stomach
Acute Cough vs Chronic Cough
Acute: Underlying condition, resolved in 2-3wks
Chronic: Persists >3months
What medication commonly causes chronic cough?
Angiotensin-converting enzyme inhibitors
The most common cause of chronic cough in smokers is _____
What are the four causes of chronic cough in non smokers?
1. Postnasal Drainage
2. Nonasthmatic Eosinophil Asthma
4. Reflux Disease
"What is dyspnea?
SUBJECTIVE sensation of uncomfortable breathing
(breathlessness, air hunger, SOB, labored breathing)
Commonly seen in respiratory & heart disease
T/F Increased dyspnea=increased severity of disease
FALSE. Severity of dyspnea may not directly correlate with severity of underlying disease
List three common SIGNS of dyspnea
1. Flaring Nostrils
2. Use of Accessory Muscles
What is Orthopnea?
Dyspnea when an individual lies flat (common in heart failure)
What is paroxysmal nocturnal dyspnea?
Severe attacks of SOB waking an individual up at night gasping for air
Paroxysmal nocturnal dyspnea is a symptom of _____________ & ____________
Heart failure & Lung Disease
List three characteristics of blood that is coughed up (hemoptysis).
1. Bright Red
2. Alkaline pH
3. Mixed with frothy sputum
List the 5 most common causes of Hemopytsis
2. Lung Cancer
List signs that will be observed if large airways are obstructed
SLOW ventilatory rate, increased effort, prolonged inspiration or expiration, and stridor (audible wheezing)
Are small or large airways most commonly obstructed in asthma & COPD?
List signs that will be observed if small airways are obstructed
RAPID ventilatory rate, small tidal volume, increased effort, prolonged expirations, wheezing
Define Cyanosis and list both types
Bluish coloration of skin and mucous membranes caused by desaturated or reduced Hgb
1. Pheripheral Cyanosis (poor circulation, ie Raynauds, cold, best seen in nails)
2. Central Cyanosis (pulmonary disease or cardiac shunting, best seen in mucus membranes)
Regardless of Hgb concentration, when will Cyanosis develop?
When 5g of HgB on desaturated (it doesn't matter if you have Hgb of 8 or 20, therefore cyanosis doesn't always indicate oxygenation)
Bulbous enlargement of the end of a finger or toe. Graded from 1-5 based on hypertrophy of nail
T/F Clubbing is extremely painful and irreversible
FALSE. Clubbing is usually PAINLESS and REVERSIBLE with treatment of underlying pulmonary condition
Inceased CO2 in arterial blood (PaCO2)
Reduced O2 of arterial BLOOD (PaO2)
Caused by respiratory alterations
Reduced O2 of cells in TISSUE
Can be caused by alterations of many systems
What is the most common cause of hypoxemia?
An abnormal ventilation-perfusion ratio (V/Q)
What conditions cause low V/Q ratio?
Low V/Q=inadequate ventilation of well-perfused area
This is shunting (right-to left shunting) and is seen in Atelectasis, Asthma, Pulmonary Edema, and Pneumonia
What is the most common cause of high V/Q ratio?
High V/Q=Poor perfusion of well-ventilated areas (embolus impairs blood flow)
What is Alveolar Dead Space?
An area where alveoli are ventilated but not perfused
Chest wall disorders primarily affect _________ __________ & result in _______ Chest wall disorders affect TIDAL VOLUME and result in HYPERCAPNIA
Pleural disease affect __________ & _________
Ventilation and Oxygenation
Chest wall disorders primarily affect _________ __________ & result in _______
Chest wall disorders affect TIDAL VOLUME and result in HYPERCAPNIA
What are the three components of pulmonary function tests used to diagnose lung restriction?
1. Reduction in forced vital capacity (FVC)
2. Arterial blood gas measurements (hypercapnia)
Explain Fail Chest
Results from fracture of several ribs causing instability in a portion of the chest wall. Pardoxical movement of chest (inspiration-unstable portion moves inward, expiration-unstable portion moves outward)
Pulmonary Structure Review
Visceral pleura lines lungs
Parietal pleura lines chest
visceral+ parietal=Pleural Space
What is a Pneumothorax
The presence of AIR or GAS in the pleural space. Causes collapse of a lung.
What happens when gas separates the visceral & parietal pleura?
It destroys the negative pressure of the pleural space-->Pneumothorax
List two types of Pneumothorax
1. Primary (spontaneous)
Etiology of Pneumothorax (list for both primary & secondary)
1. Primary: Unknown cause of bleb formation (blister-like) on the visceral pleural--> Bleb rupture (usually in apexes)
2. Secondary: Chest truama, rupture of bleb/bulla as occurs in COPD, mechanical ventilation (especially PEEP)
Define open & closed pneumothorax
1. Open Pneumothorax (air pressure is pleural space=barometric pressure; air moves in & OUT of damaged pleura)
2. Closed Pneumothorax (air pressure in pleural space>barometric pressure, this causes tension pneumo)
Pathophysiology of tension pneumothorax
Pleural rupture acts as one-way valce--> air moves into pleural space (can't get out)--> build up of air in pleural space--> Increase pressure against already collapsed lung & mediastinum--> compression atelectasis & displacement of heart/great vessels=life threatening emergency
Risk Factors for Pneumothorax (for both primary & secondary)
Primary: Men, 20-40y.o., unexplained emphysema-like changes in lung, genetics?(folliculin mutations)
Secondary: Surgery, People prone to injury, Lung disease (COPD), mechanical ventilation
T/F Spontaneous pneumothorax usually occurs in healthy individuals unexpectedly
TRUE. They can occur during rest, sleep, or exercise
Clincal Manifestations of Pneumothorax
1. Sudden Pleural Pain
3. Mild dyspnea
4. Absent/decreased lung sounds
6. Tracheal deviation away from affected lung (tension pneumo)
7. Severe hypoxemia (tension pneumo)
8. Hypotension (tension pneumo)
What is Pleural Effusion?
The presenence of fluid in the pleural space
What are some of the main differences between pneumothorax and pleural effusion?
Pneumo: Gas filled, cause lung collapse, hyperresonance
Effusion: Fluid fluid, does NOT cause lung collapse, hyporessonance
*Both can cause compression atelectasis and displacement of mediastinal contents
List and define the five types of fluid associated with pleural effusion
1. Transudate: watery fluid that diffused out of capillaries
2. Exudate: (less watery) Fluid rich in WBC & plasma proteins that migrated out of capillaries
3. Empyema: Pus, detritus of infection dumped into pleural space
4. Hemothorax: Blood, hemorrhage into pleural spave
5. Chylothorax: Chyle (milky fluid containing lymp & fat)
What does FVC stand for & what does it measure?
Force Vital Capacity=Maximum amount of gas that can be displaced from the lung during forced expiration
What is restrictive lung disease?
A category of respiratory diseases that are chracterized by decreased compliance of lung tissue on INSPIRATION(restircted lung expansion)
Pathophysiology of restrictive lung disease
Respiratory disease cause V/Q mismatch-->alveolocapillary membrance changes--> decreased diffusion of O2 from alveoli to blood-->hypoxemia
Sy/Sy of restrictive lung disease
Dyspnea, increased effot of breathing, increased respiratory rate
How do restrictive lung diseases change pulmonary function testing
Tidal volume (amount inspired): DECREASED
List the most common restrictive lung diseases in adults (multiple diseases)
Aspiration, Atelectasis, Bronchiectasis, Bronchiolitis, Pulmonary Fibrosis, Inhalation disorders, Pneumoconiosis, Allergic alveolitis, Pulmonary edema, Acute respiraltory distress syndrome
Passage of fluid & solid particles into the lung
Is the right or left lung more susceptible to aspiration?
Branching angle of the right bronchus is straighter than the left (easier to go down)
The collapse of lung tissue
List the three types of atelectasis
1. Compression: Caused by external pressure (tumors, fluid/air in pleural space)
2. Absorption: Gradual absorption of air (hypovent. alveoli, inhalation of anesthetic)
3. Surfactant Impairment: Decreased production or impairment (Prematurity, ARDS, anesthesia, mechanical vent)
Persistent abnormal dilationof the bonchi
Cylindrical Bronchiectasis (bronchial dilatation that is cylindrical) is seen in what disease?
Cylindrical bronchiectasis is irreversible or reversible dilation
Inflammation of the small airways or bronchioles
Is bronchiolitis more common in children or adults?
Define Pulmonary Fibrosis
Excessive amount of fibrous or connective tissue in the lung
Scarring has many causes (inhalation of toxic gases or dust particles, hypersensitivity, pneumonitis, RA, SLE, medications)
Causes marked decrease in lung compliance
1. Idiopathic: Poor prognosis (men, older than 60)
2. Exposure to harmful substance: Most respond quickly to treatment
List two conditions that usually incorporate pulmonary fibrosis
2. Allergic Alveolitis (organic dust particles, IgG, granuloma formation)
Any change in the lung caused by inhalation of inorganic dust particles
Silica, asbestos, coal most common
Define Pulmonary Edema
Excess water in lung
What is the most common cause of pulmonary edema?
Clinical manifestations of pulmonary edema
Despnea, orthopnea, hypoxemia, increased effort to breath
Rales, dullness to percussion, S3 gallop, cardiomegaly, pink-frothy sputum (severe cases)
Process of absecess emptying (into a bonchus) & cavity formation
Define Acute Respiratory Distress Syndrome (ARDS)
Capillaries or alveoli of the lungs are damaged as a result of infection, injury, blood loss causing fluid to leak from capillaries into the alveoli causing pulmonary edeam and some of alveoli to collapse
In ARDS the pulmonary edema is not caused by heart failure, this is why ARDS is often referred to as_________
Noncardiogenic pulmonary edema
Etiology of ARDs
Most common: Sepsis & Multiple Trauma
(other causes: pneumonia, burns, aspiration, cardiopulmonary bypass surgery, pancreatitis, drug overdose, smoke inhalation, O2 toxicity, radiation, DIC)
Pathophysiology of ARDS
Injury to lung causes:
1. Endothelial Damage--> complement & platelet-->neutrophils-->inflammatory cytokines-->Extensive alveolocapillary membrane damage & pulmonary vasocontriction--> Increased permeability-->Pulmonary edema & hemorrhage-->Severe reduction in compliance & ventilation-->Resp failure
2. Alveolar Epithelial Damage--> Decreased surfactant production--> Atelectasis & Impaired compliance-->Resp failure
What WBC has a central role in the development of ARDS?
It releases a ton of inflammatory mediators (Oxygen radicals, proteolytic enzymes, arachidonic acid metabolites, platelet-activating factor)
What is a hallmark of ARDS
Increased capillary permeability allows fluids, proteins, and blood cells to leak from capillary bed into the pulmonary interstitium & alveoli
When will hyaline membranes form in ARDS?
Within 24-48hrs after the hemorrhagic phase
When will fibrosis occur in ARDS
7 days after hyaline membrane formation. Fibrosis obliterates alveoli, bronchioles, and interstitium
What is a lethal progression that can occur following or as a result of ARDS
The chemical mediators that cause ARDS can cause widespread inflammation-->Systemic Inflammtory Response Syndrome (SIRS)-->Multiple Organ Dysfunction Syndrom (MODS)
What are some changes in pulmonary function testing associated with ARDS?
1. V/Q mismatch, eventually progressing to severe right-to-left shunting
2. Decreased minute ventilation (hypercapnia)
3. Decreased Functional residual capacity (FRC)
4. Decreased Tidal Volume
Clinical manifestations of ARDS
1. Progressive Dyspnea
2. Initially tachypnea (will progress to hypoventilation with worsening of disease)
3. XRay shows alveolar infiltrates
7. Respiratory Alkalosis
8. Metablic Acidosis
Obstructive Pulmonary Disease
It is characterized by airway obstruction that is worse with EXPIRATION
More force (accessory muscles) or/and more time is needed to expire air
List the effects of pulmonary function tests of obstructive pulmonary disease
1. Increased work of breathing
2. V/Q mismatching
3. Decreased force expiratory volume in 1 sec (FEV1)
List the most common obstructive pulmonary disease
2. Chronic Bronchitis
What is the name of the disease when bronchitis and emphysema occur together?
What is the unifying symptom and unifying sign of obstructive pulmonary disease?
1. Symptoms: Dyspnea
2. Sign: Wheezing
A chronic inflammatory disorder of the airways involving bronchial hyperresponsiveness and airway obstruction marked by periodic attacks of wheezing, SOB, tight feeling in the chest, and a cough that produces mucus to an allergic reaction triggered by drugs, irritants, viral infection, exercise, or emotional stress
What is a major pathological feature of asthma?
Inflammation resulting in hyperresponsiveness of the airways
Although most episodes of asthma causing airflow obstruction are reversible, what can occur if asthma remains untreated?
Untreated inflammation can lead to long term airway damage that is irreversible (airway remodeling)
Etiology of Asthma
"Familial/Genetic (more than 100 genes may play a role in susceptibility)
Specific interactions of susceptible gens and environment that trigger inflammation and hyperresponsiveness
List the risk factors for Asthma
1. Family history
2. Allergen exposure
3. Air Pollution
4. Exposure to cigarette smoke
5. Urban residence
6. Recurrent respiratory infections
Pathophysiology for Asthma
Genetic predisposition + allergen/irritant exposure--> Immune activation (IgE) & Mast cell degranulation--> Vasodilation(increased permeability) & Cellular infiltration (neuts, lymphs, eosinophils)--> Bronchospasm, vascular congestion, mucus secretion, thickening of airway walls, increased contractile response of bronchial smooth muscle & Epithelial desquamation/fibrosis--> Bronchial hyperresponsiveness & airway obstruction
What happens to the inspired air during an asthmatic episode?
Due to the airway obstruction it is difficult to EXPIRE the air in asthms, so the air gets trapped. Air trapping increases intrapleural and alveolar gas pressures and decreases perfusion of aveoli
In Asthma, what dose respiratory acidosis signal?
What are the sx/sy at the beginning of an asthma attack?
Chest constriction, expiratory wheezing, dsypnea, nonproductive cough, prolonged expiration, tachycardia, tachypnea, hypoxemia, resp. alkalosis
What are the sx/sy present if an asthma attack persists?
Use of accessory muscles, wheezing heard during both inspiration & expiration, pulsus paradoxus (decreased in SBP during inspiration >10mmHg), hypercapnia, respiratory acidosis
Hypoxemia--> expiratory flow decreases further--> decreased effective ventilation-->Hypercapnia--> Acidosis
What is it called if severe bronchospasms do not reverse by unual measures?
Explain Late Asthma Response
In cases of significant allergen exposure, asthma symptoms can recur 4-12hrs after initial attack due to persistent eosinophil & lymphocyte activation
T/F Late Asthma response can be even more severe than the initial attack
What can help determine whether an asthmatic individual is responding to treatment?
Repeated peak flow rates
Define Chronic Obstructive Pulmonary Disease (COPD)
Any of a group of irreversible respiratory disease (chronic bronchitis, empysema, alpha-1-antitripsin deficiency) that are characterized by airflow obstruction
Pathological lung changes, not fully reversible
What is the primary cause of COPD?
Cigarette smoking (active and second hand smoke)
Other causes: Genetic susceptibility, occupational exposures, childhood resp. infections
Define Chronic Bronchitis
IInflammation of Bronchi: Bonchial edema, hypersecretion of mucus,, bacterial colonization of airways
List the criteria to determine chronic bronchitis
Hypersecretion of mucus and chronic productive cough lasting at least 3 months of a year for at least 2 years
Risk factors for chronic bronchitis
Smokers, exposure to air pollution
Pathophysicology of Chronic Bronchitis
Tobacco smoke/Air pollution--> Epithelium inflammation--> Infiltation of inflammatory cells & release of cytokines--> increase in size and of mucus glands & goblet cells--> increased mucus & thicker mucus--> further inflammation & irritation--> Decreased ciliary function--> Chronic Bronchitis--> Airway obstruction, Air Trapping, Frequest infections, Bronchospasms
Why is an individual with chronic bronchitis at risk for infection?
The abnormal sticky mucus accumulates (due to decreased clearance), microorganisms become embedded in secretions & proliferate rapidly (H.influenzae & Streptococcus pneumoniae)
List the clinical manifestations of chronic bronchitis
Productive cough (classic symptom), prolonged expiration, decrased exercise tolerance, wheezing, SOB, cyanosis, chronic hypoventilation, frequent pulmonary infections, polycythemia, cor pulmonale
List how the pulmonary function tests are affected by chronic bronchitis
FRC (functional residual capacity): Increase (air trapping)
Residual Volume: increase ( air trapping)
arterial blood: Hypoxemia & Hypercapnia (causes polycythemia)
Abnormal permanent enlargement of gas-exchange airways (acini) accompanied by destrution of alveolar walls without obvious fibrosis
What is the major mechanism of airflow limitations in emphysema?
Destruction of alveolar septa & loss of elastic recoil of bronchial walls
Etiology of Emphysema
1. Smokers/Air Pollution (most common)
2. Inherited deficiency of enzyme alpha-antitrypsin (autosomal recessive)
Pathophysiology of Emphysema (explain for both primary and secondary emphysema)
1. Primary (inherited deficiency of alpha-antitrypsin)-->proteolysis in lung tissue is not inhibited-->Increased breakdown of elastin in connective tissue of lungs-->Emphysema
2. Secondary: Tobacco/Air Pollution--> Inflammation--> Infiltration of inflammatory cells & cytokines--> inhibits antiproteases--> Increased breakdown of elastin in connective tissue of lungs--> Emphysema
Emphysema--> Airway obstruction, Air Trapping, Loss of surgafe area for gas exchange, frequent infections, bronchospasms
What does the hyperinflation of alveoli seen in emphyseam cause?
It causes large air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleura (blebs) to develop
List the clinical manifestations of emphysema
Dyspnea on exertion (that progresses to occur even at rest during later stages), Barrel chest, Prolonged expiration, tachypnea, use of accessory muscles, hyperresonant sound w/ percussion, leans forward with arms extended when sitting, purse lips w/ exhale, usually has little coughing with very little sputum production
Describe the typical changes in pulmonary function tests associated with emphysema
FRC, RV, TLC: Increased
Radiograph: Diaphrahm appears flattened & lung fields overdistended
Infection of lower respiratory tract caused by bacteria, viruses, fungi, protozoa, & parasites
List the risk factors of Pneumonia
1. Advance age
5. Altered LOC (impaired swallow)
6. ET intubation
9. Cardiac or Liver disease
10. Residence in nursing home
T/F Nosocomial infections and those affecting immunocompromised individuals have a higher mortality rate than community acquired pneumonias
What is the most common cause of community acquired pneumonia?
What is the most common VIRAL cause of community aquired pneumonia?
Etiology of Pneumonia (what starts it all)
Infection agent proliferates in lower airways
What is the most common route of lower respiratory tract infection?
Aspiration of oropharyngeal secretions
Other routes: inhalation of microorganisms that have been released into the air (TB)
What is the most important guardian cell of the lower respiratory tract?
Pathogenesis for bacterial pneumonia
Infectious agent (s.pneumoniae) enters lower respiratory tract--> Innate and Adaptive immune response initiated--> Complement activation & antibody production--> Rapid lysis of bacteria--> Release of bacterial proteins (pneumolysin toxic to cells)--> Consolidation of lobe (tissue filling with exudate)-->Stage of red hepatization (alveoli fills with blood, fibrin, fluid, and bacteria)--> Stage of gray hepatization (fibrin deposition over pleural surgaces & presence of fibrin and leukocytes)--> Macrophages appear--> degeneration of neutrophils & digestion of fibrin and remain bacteria aided by macrophage
T/F If an individual with pneumonia is being treated with the correct antibiotic, the immediate response of the patient is always an improvement of clinical symptoms
FALSE. The lysis of bacteria causes a release of intracellular bacterial proteins (pneumolysin) that can be toxic to the human cell. The is partially responsible for the WORSENING in clinical symptoms sometimes seen in individuals immediately after they begin antibiotic treatment
T/F Viral pneumonia is usually mild and self-limiting
TRUE. However it often sets the stage for a secondary bacterial infection
What are the clinical manifestations of pneumonia?
Most cases preceded by an upper respiratory tract infection, that is followed by the following:
6. Pleuritic chest pain
7. Crackles (sx of pulmonary consolidation/alveolar edema)
8. Tactile fremitus
9. Egophony (increased resonance of voice sounds hear wtih ausc.)
10. Whispered pectoriloquy (increase in loudness of whispher with ausc.)
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