Chapter 36: Alterations of Pulmonary Function Flashcards
s/sx of pulm dz
Dyspnea and cough
Altered breathing patterns
Hyperventilation -> resp alk. CO2 lost.
Hypoventilation -> resp acidosis. CO accumulates
Hemoptysis -> coughing up blood
Abnormal sputum
Cyanosis
Chest pain
Clubbing
dyspnea
Subjective sensation of uncomfortable breathing
severe dyspnea
Flaring of the nostrils
Use of accessory muscles of respiration
Retraction of the intercostal spaces
dyspnea on exertion
SOB with activity
orthopnea
Dyspnea when lying down
Often related to left side heart failure
paroxysmal nocturnal dyspnea
Awaking at night and gasping for air; must sit up or stand up
cough and sputum
Cough: Protective reflex that helps clear the airways by an explosive expiration. Acute coughm-> Resolves within 2 to 3 weeks. Chronic cough -> Lasts longer than 3 weeks.
Abnormal sputum: Changes in amount, consistency, color, and odor provide information about the progression of disease and the effectiveness of therapy.
Hemoptysis: Coughing up blood or bloody secretions
abnormal breathing patterns
Adjustments made by the body to minimize the work of the respiratory muscles
kussmaul respirations (hyperpnea)
Slightly increased ventilatory rate, very large tidal volume, and no expiratory pause
Trying to blow off acid -> metabolic acidosis.
labored breathing
increased work of breathing
restricted breathing
Disorders that stiffen the lungs or chest wall and decrease compliance
Ex. Obesity. Weight compresses breathing
Cheyne-stokes respirations
Alternating periods of deep and shallow breathing; apnea lasting 15 to 60 seconds, followed by ventilations that increase in volume until a peak is reached, after which ventilation decreases again to apnea
hypoventilation
Alveolar ventilation is inadequate in relationship to the metabolic demands.
Leads to respiratory acidosis from hypercapnia.
Low RR and Low vT
Result is -Increased CO2 (>40mm Hg) and Decreased pH (Resp Acidosis)
Is caused: Over sedation #1, airway obstruction, chest wall restriction, altered neurologic control of breathing.
Causes:
- Central
Drugs (narcotics), Head injury/Spinal Cord injury - Chest wall disorder: Neuromuscular Diseases, Obesity, Kyphosis/scoliosis
- Damaged Lung Structure: asthma, COPD
hyperventilation
Alveolar ventilation exceeds the metabolic demands.
Leads to respiratory alkalosis from hypocapnia.
Is caused: anxiety, Pain, fever
cyanosis
Bluish discoloration of the skin and mucous membranes
Develops with five grams of desaturated hemoglobin, regardless of concentration
peripheral cyanosis
Most often caused by poor circulation
Best observed in the nail beds
central cyanosis
Caused by decreased arterial oxygenation (low partial pressure of oxygen [Pao2])
Best observed in buccal mucous membranes and lips
clubbing
Bulbous enlargement of the distal segment of a finger or toe.
Graded 1-5 based on nailbed changes
Associated with diseases causing hypoxemia
chest pain
pleural and chest wall
pleural pain
Is the most common pain caused by pulmonary diseases.
Is usually sharp or stabbing in character.
Infection and inflammation of the parietal pleura (pleuritis or pleurisy) can cause pain when the pleura stretch during inspiration and are accompanied by a pleural friction rub.
chest wall pain
may be from the airways
may be from muscle or rib pain
conditions caused by pulm dz or injury
Hypercapnia: Increased carbon dioxide (CO2) in the arterial blood, Occurs from hypoventilation
Hypoxemia: Hypoxemia (blood) versus hypoxia (tissue), Reduced oxygenation of arterial blood
caises of hypoxemia
in order of most to least common
1. V:Q Mismatch** Ventilation and perfusion are different than what it should be
- Hypoventilation
- Shunt
- Thickened diffusion barrier
- Low inspired O2 (Altitude)
most common cause of hypoxemia in pt with pneumonia, atelectasis, PE
V:Q mismatch
* does improve with O2
alveolar shunt
Alveoli blocked from ventilation
Entry of blood into the systemic arterial system without going through ventilated areas of lung
causes: Severe pneumonia, Pulmonary Edema, Atelectasis, ARDS* -> diseased alveoli and inflamed caps, need put on a ventilator
Does not improve with oxygen
thicken diffusion barrier
Diffusion Capacity is reduced by diseases in which the thickness is increased.
Causes: pulmonary fibrosis, asbestosis, sarcoidosis, ILD
low V/Q
ventilation problem. Perfusion is fine.
shunt (very low) V/Q
blocked vent -> collapse alveolus –any cap passing will not get any O2
high V/Q
no problem with ventilation, problem with perfusion. Ex. PE. Dead space: any O2 that gets into alveoli and not used for perfusion
low inspired ppO2
Low PaO2. Pressure pushes O2 in from high level to low level
Normal or Decreased PaCO2 (hyperventilation)
Causes:
1. FiO2 decreases at higher altitude. hyperventilate. May have normal or deceased PaCO2. People who live high alt accumulates and they have normal PaCO2. Alt sickness is from hyperventilation an low CO2 -> get medicine
2. Decrease in FiO2 (accidental ex.) COPD pt who needs 3L O2 at all time has NC fall off and now they have decrease Fi02
pulmonary vascular resistance
Amount of right ventricular force required to pump blood into lungs depends on resistance to flow present in the pulmonary vascular system
This resistance to flow is PVR
Hypoxemic -> vasoconstriction
Emphasema is common cause for pulm HTN
COPD. -> right vent. Hypertrophy -> death
cor pulmonale
Right ventricular hypertrophy secondary to pulmonary disease
Can cause right sided heart failure
Major cause of death in COPD patients
Increased PVR makes it harder for right side of the heart to pump blood into pulmonary circulation
acute resp. failure
Hypoxia (Gas exchange is inadequate)
Pao2 is ≤50 mm Hg.
Hypercapnia (ventilation is inadequate)
Paco2 is ≥50 mm Hg with a pH of ≤7.25.
Requires ventilatory support, oxygen, or both.
emergency condition, can affect all ages, major cause of death, successful outcome depends on prompt recognition and immediate initiation of supportive rx
chest wall restriction
Chest wall is deformed, traumatized, immobilized, or made heavy by fat; work of breathing is increased, and ventilation may be compromised because of a decrease in tidal volume.
Impaired respiratory muscle function is caused by neuromuscular disease.
can be caused by amiodarone and nitrofurantoin
restrictive lung diseases: parenchymal
interstitial pulm fibrosis: 1ry (idiopathic) occupational, collagenic, granulomatous, irradiation, resection, drug-induced (bleomycin, methotrexate, cyclophosphamide)
restrictive lung diseases: extra parenchymal pleura
pleural effusion, pneumothorax, pleural fibrosis, pleural tumors, pleural thickening.
restrictive lung diseases: extra parenchymal abdomen
severe distension
restrictive lung diseases: chest wall
trauma, kyphoscoliosis, ankylosing spondylitis, NM dz (MG, GB), morbid obesity, scleroderma
flail chest
Is the instability of a portion of the chest wall from rib or sternal fractures.
Causes paradoxical movement of the chest with breathing.
pneumothorax
Pneumothorax refers to air in the intrapleural space
hemothorax
hemothorax refers to blood in the intrapleural space around the lung.
s/sx of pneumotorax
Signs of chest trauma
Tachypnea, tachycardia
Shortness of breath
Unequal Lung Excursion
Diminished or absent breath sounds on one side or one area of lung
ABG: decreased PaO2 and SaO2, respiratory alkalosis
Patient might complain of sharp chest pain on one side of chest
Positive chest x-ray for pneumothorax
spontaneous pneumothorax patho
rupture of a bleb on the lung surface allows air to enter pleural space from airways.
primary affects prev. healthy people. common for a young, tall, thin man. secondary affects people with preexisting lung dz (COPD)
spontaneous pneumothorax s/sx
abrupt onset, pleuritic chest pain, dyspnea, SOB, tachypnea, tachycardia, unequal lung excursion, decreased breath sound and hyperresonant percussion tone on affected side.
traumatic pneumo patho
trauma to the chest wall or pleura disrupts the pleural membrane. open occurs with penetrating chest trauma that allows air from the environment to enter the pleural space. closed occurs with blunt trauma that allows air from the lung to enter the pleural space. iatrogenic involves laceration of visceral pleura during a procedure such as thoracentesis or central line insertion.
traumatic pneumo s/sx
pain, dyspnea, tachypnea, tachycardia, decreased resp. excursion, absent breath sounds in affected area, air movement thru an open wound
tension pneumo patho
air enters pleural space thru chest wall or from airways but is unable to escape, resulting in rapid accumulation. lung on affected side collapses. as intrapleural pressure increases, heart, great vessels, trachea, and eso shift toward unaffected side.
tension pneumo s/sx
hypotension, shock, distended neck veins, severe dyspnea, tachypnea, tachycardia, decreased resp. excursion, absent breath sounds on affected side, tracheal deviation toward unaffected side.
dx of tension pneumo
CXR
ex. left side tension pneumo. sides of push to right, trachea and mediastinum are pushes to right side, not the density bw 2 sides, right side is normal, left side hyperlucent
signs of push:
1. collapse left lung
2. air under tension in left pleural cavity. no bronchovascular markings
3. tracheal shift to right side
4. mediastinal shift to right side
tension pneumo left side
tension penumo tx
needle decompression: 2nd rib space in the mid-clavicular line, immediate rush of air, concerts a tension pneumo to a simple pneumo, asso with complications
penumo tx: chest drainage management
Removal of air or fluids from intrapleural space of the lungs or from the mediastinal compartment.
May be short term or long term
Used to treat large pleural effusions and pneumothorax
plural effusions
Build up of excess fluid between the layers of the pleura
causes of pleural effusions
Transudative (watery and diffuses out of the caps). HF and Pulmonary edema
Exudative (protein rich and high concentrations of WBC, less watery). Pneumonia (para pneumonic) and Cancer
tx pf pleural effusoins
Diuretic
Thoracentesis
Chest Tube
- take sample of fluid to dx
empyema
Infected pleural effusion
Pus in the pleural space
causes of empyema
chest trauma, pneumonia, or tb
s/sx of empyema
Cyanosis, fever, tachycardia, cough, and pleural pain
tx of empyema
Administration of antimicrobial medications
Drainage of the pleural space with a chest tube
Severe cases: Ultrasound-guided pleural drainage, instillation of fibrinolytic agents TPA, or deoxyribonuclease (DNase) injected into the pleural space
aspiration
Passage of fluid and solid particles into the lungs
Right lower lobe: Is the most frequent site.
notice after eat or drink
aspiration s/sx
Both choking and intractable cough have a sudden onset.
aspiration tx
Supplemental oxygen; may require mechanical ventilation with positive end-expiratory pressure (PEEP).
May need steroids and antibiotics
atelectasis
Collapse of lung tissue. loss of lung vol caused by inadequate expansion of the airspaces
types of atelectasis
Compression atelectasis: External compression on the lung
Absorption atelectasis: Gradual absorption of air from obstructed or hypoventilated alveoli. closed pore of Kohn
Surfactant impairment: Decreased production or inactivation of surfactant
atelectasis s/sx
Dyspnea, cough, fever, and leukocytosis
tx of atelectasis
prevention and deep breathing
bronchiectasis
Persistent abnormal dilation of the bronchi
Dilated with filled with mucous. Can’t cough mucous out -> frequent infections. Pseudomonas. Sx doesn’t work well
Cylindrical, saccular, and varicose
bronchiectasis s/sx
Chronic productive cough
bronchiectasis tx
Sputum culture antibiotics
Bronchodilators, antiinflammatory drugs
Chest physiotherapy
Supplemental oxygen
Surgery
pulmonary fibrosis
Excessive amount of fibrous or connective tissue in the lung
scarred tissue impairs gas exchange
Idiopathic pulmonary fibrosis: No specific cause
pulmonary fibrosis s/sx
Increasing dyspnea on exertion
pulmonary firosis tx
Corticosteroids
antifibrotic drugs
lung transplantation
O2 toxicity
Prolonged exposure to high concentrations of supplemental oxygen
Severe inflammatory response mediated primarily by oxygen radicals
Causes damage to alveolocapillary membranes, disruption of surfactant production, interstitial and alveolar edema, and decrease in compliance
O2 toxicity tx
Ventilatory support and reduction of inspired oxygen concentration to less than 60% as soon as tolerated
factors on which O2 toxicity depends
pressure: normobaric hypoxia and hyperbaric hypoxia
time of exposure and O2 concentration: FiO2 > 60% longer than 36 hr. FiO2 >80% longer than 24 hr and FiO2 >100 % longer than 12 hr
pneumoconiosis
any change in lung caused by the inhalation of inorganic dust particles, usually from the workplace
pneumoconiosis
Silica (concrete workers), asbestos (steel workers), and coal: Most common causes
pneumoconiosis s/sx
Cough, sputum production, dyspnea, decreased lung volumes, and hypoxemia, large nodules on lungs, stiff lungs -cant fully expand, progressive masive fibrosis
pneumoconiosis tx
Palliative and prevention of further exposure
Improved working conditions
Pulmonary rehabilitation and management of associated hypoxemia and bronchospasm
pulmonary edema
Excess water in the lung from disturbances of capillary hydrostatic pressure, capillary oncotic pressure, or capillary permeability
Most common cause of pulmonary edema: Left-sided heart disease
s/sx of pulm edema
Dyspnea, orthopnea, hypoxemia, and increased work of breathing
pulm edema tx
Increased hydrostatic pressure caused by heart failure:
Improve cardiac output and volume status with diuretics, vasodilators, and drugs that improve the contraction of the heart muscle.
Increased capillary permeability resulting from injury (ARDS) :
Remove offending agent and supportive therapy to maintain adequate oxygenation, ventilation, and circulation.
Any type of pulmonary edema:
Provide supplemental oxygen and/or mechanical ventilation.
ARDS
Most severe expression of Acute lung injury
ARDS is a devastating often fatal, inflammatory disease of the lung characterized by the sudden onset of pulmonary edema and respiratory failure.
Involves both capillary and alveoli
causes of direct ARDS
pneumonia, gastric aspiration, near drowning, inhalation injury, direct chest injury
causes of indirect ARDS
sepsis, trauma, pancreatitis, drug overdose
s/sx of ARDS
Refractory Hypoxemia is a HALLMARK SX**
Etiologic Factors:
Worsening respiratory symptoms
Bilateral opacities on CXRay
Hypoxic Respiratory failure
pul. edema
tx of ARDS
Treat the Cause!
Mechanical Ventilation -> Increased PEEP
Patient positioning strategies -> Include prone positioning
Prognosis/mortality rate of ARDS
Varies widely: 30% to more than 85%
Quality of life key for survivors -survivors may not have good quality of life
Predictors associated with high mortality:
Severity of illness
Non pulmonary organ dysfunction
Comorbidities
Sepsis
Increased Age
Phases of ARDS
Inflammatory/exudative, proliferative, fibrotic
Inflammatory phase of ARDS
Within 72 hr
Alveolocapilary membrane damage, increased cap membrane permeability, pulmonary edema, surfactant inactivated
Proliferative phase of ARDS
4-21 days
Resolution of pulm edema and proliferation of type II pnemocytes, fibroblasts, myofibroblasts
hyaline membranes
hypoxia
Fibrotic phase of ARDs
14-21 days
Remodeling and fibrous
Alveoli destruction
Severe right to left shunting
Acute resp. Failure
Obstructive pulm dz
Asthma
COPD -> chronic bronchitis and emphysema
Asthma
Chronic inflam disorder of bronchial mucosa
Causes bronchial hyperresponsiveness, constriction of the airways and variable airflow obstruction that is reversible.
One half of all cases develop during childhood.
Episodic attacks of bronchospasm, bronchial inflammation, mucosal edema, and increased mucous production
Asthma s/sx
Asymptomatic between attacks
Chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, tachypnea, sleep prob, fatigue, allergies, common cold, chest pain
Pulsus paradoxus -> drop in BP on inspiration
Status asthematicus
Bronchospasm not reversed by usual measures
Life threatening
Ominous signs of impending death in asthma
Silent chest (no audible air movement) and a Paco2greater than 70 mm Hg
Causes of triggers of asthma
Pollution, smoking, household chemicals, genetics, fat foods, dust, pets, bacteria, viruses
Asthma tx
Administration of oxygen and inhaled beta-agonist bronchodilators, HFA or nebulizers
Oral corticosteroids administration early in the course of management
Antibiotics are not indicated for acute asthma unless a bacterial infection is documented
Education over allergens and irritants
COPD
Airflow limitation that is not fully reversible
Inadequate exhalation
Usually progressive
Third leading cause of death in the United States and the sixth leading cause of death worldwide
COPD: Chronic bronchitis plus emphysema
RF of COPD
obacco smoke
Environmental -> ETS, indoor and outdoor air pollution, occupational dust and chemicals
Aging
Infections
Socio-economic status
Genetic susceptibilities
Inherited mutation in the alpha-1 antitrypsin gene results in the development of emphysema even in nonsmokers.
Chronic bronchitis
Hypersecretion of mucus and chronic productive cough that lasts at least 3 months of the year and for at least 2 consecutive years
-Inspired irritants increase mucous production, size and number of mucous glands, and bronchial edema; mucus is thicker than normal
-Hypoxemia and hypercapnia
-Airways collapse early in expiration, trapping gas in the lung
-hyperinflation of alveoli
Chronic bronchitis s/sx
Decreased exercise tolerance
Wheezing and shortness of breath
Productive cough (“smoker’s cough”) becomes copious
Polycythemia
Barrel Chest
Emphysema
Abnormal permanent enlargement and destruction of the alveolar walls
Loss of elastic recoil
Alveolar destruction also produces large air spaces within the lung parenchyma (bullae) and air spaces adjacent to pleurae (blebs).
S/sx of emphysema
Later progresses to marked dyspnea, even at rest
Little coughing and very little sputum
Thin
Tachypnea with prolonged expiration; use of accessory muscles for ventilation; pursed lips
Increased anteroposterior diameter of the chest (barrel chest)
To increase lung capacity: Leans forward with arms extended and braced on knees when sitting
COPD tx
Oxygen; may require noninvasive positive pressure ventilation or mechanical ventilation
Inhaled bronchodilators by either an inhaler or a nebulizer
Immediate administration of oral corticosteroids and antibiotics
Inhaled anticholinergic agents and beta agonists -> bronchodilators
Inhaled corticosteroids can be added
Smoking cessation
Pulmonary rehabilitation
Improved nutrition
Breathing techniques
Pneumonia
Infection of the lower respiratory tract
Responsible for more disease and death than any other infection
Community-acquired pneumonia
Streptococcus pneumoniae
Health care-associated pneumonia
More virulent bacteria
Hospital-acquired (nosocomial) pneumonia
More virulent bacteria
Ventilator-associated pneumonia
Routes of infection for pneumonia
Aspiration
Inhalation
Endotracheal tubes and suctioning
Respiratory defenses cannot destroy the microorganism
Viral pneumonia
Is seasonal; usually mild and self-limiting.
Can set the stage for a secondary bacterial infection.
Provides an ideal environment for bacterial growth and by damaging ciliated epithelial cells, which normally prevent pathogens from reaching the lower airways.
Most common form: Influenza
Viral pneumonia s/sx
Preceded by an upper respiratory infection
Cough, dyspnea, and mild fever
Chills, malaise, and pleuritic chest pain
Prevention of viral pneumonia
Vaccination for appropriate populations
Pneumonia tx
Establishment of adequate ventilation and oxygenation
May require mechanical ventilation
Adequate hydration
Good pulmonary hygiene (e.g., deep breathing, coughing, chest physical therapy)
Bacterial pneumonia: Antibiotics
Viral pneumonia: Supportive therapy alone, unless secondary bacterial infection is present. Severe cases: Antiviral medications and/or antifungal, multiple drugs
TB
Infection caused by Mycobacterium tuberculosis, an acid-fast bacillus
Leading cause of death from a curable infectious disease throughout the world
TB patho
Airborne droplet transmission
Tubercle formation: Granulomatous lesion
Caseous necrosis: Cheeselike material
May remain dormant for life or cause active disease
Isolation of bacilli by enclosing them in tubercles and surrounding the tubercles with scar tissue
TB s/sx
Latent: Asymptomatic
Active: Fatigue, weight loss, lethargy, anorexia , a low-grade fever, and night sweats; purulent cough
Dx of TB
Positive tuberculin skin test: a purified protein derivative (PPD): Does not differentiate past, latent, or active disease
Sputum culture
Chest radiographs
Tx of TB
Rifampin, Isoniazid, pyrazinamide, and ethambutol
Drug-resistant bacilli: Combination of at least four drugs to which the microorganism is susceptible, administering for 6-9 months.
Latent TB get over length of tx just rifampin for ~4month
Acute bronchitis
Is an acute infection or inflammation of airways or bronchi; commonly follows a viral illness.
Acute bronchitis s/sx
Causes symptoms similar to pneumonia but does not demonstrate pulmonary consolidation and chest infiltrates.
Nonproductive cough occurs in paroxysms and is aggravated by cold, dry, or dusty air.
Acute bronchitis s/sx
Rest, aspirin, humidity, and cough suppressant (codeine).
PE
Is the occlusion of a portion of the pulmonary vascular bed by a thrombus, embolus, tissue fragment, lipids, or air bubble.
Pulmonary emboli commonly arise from the deep veins in the calf.
Virchow triad:
Venous stasis,
hypercoagulability,
endothelial damage
PE s/sx
Dyspnea*
Tachypnea*
Pleuritic pain*
(often sudden onset)
Cough
Unilateral leg pain and swelling
Wheezing
Crackles (rales)
PE Dx
Clinical probability assessment
D-dimer (< 200)
95% negative predictability
Ventilation-perfusion scan
CT angiogram
Compression ultrasound
PE Tx
Anticoagulant therapy!!
Heparin IV, Enoxaparin SQ, Oral Warfarin, oral Factor Xa inhibitors -> Xarelto (rivaroxaban) & Eliquis (apixiban)
Vena cava filter
Embolectomy
PE prevention
DVT prophylaxis
Early ambulation
Compression Stockings
Elevation of injured leg
Assess for DVT
Asymptomatic OR Swelling, pain, redness, tenderness, cramping
