Acute respiratory conditions Flashcards
Pneumonia Definition
inflammation of alveoli caused by viral or bacterial infection
Pneumonia patho
○ Inhalation of a foreign pathogen
§ Normally a natural defense mechanism prevents infection
§ If defense mechanism compromised (from smoking, immune system compromise) foreign pathogen enter lungs
Body’s defense mechanism triggered –> inflammation of lung parenchyma –> exudate congestion and pneunomia
Lobar pneumonia & the 4 stages
○ Lobar pneumonia
§ Diffuse consolidation involving the whole lobe (consolidation = normal air filled space in lungs is filled with fluid)
§ 4 stages
□ Congestion: vascular engorgement and accumulation of alveolar fluid with infectious organism
□ Red hepatization: infiltration of RBC, neutrophils and fibrin into alveolar fluid. Lung appear red and firm
□ Grey hepatization: RBC break down and produce exudate that causes red to grey transition
Resolution: clearing of exudate by macrophage
Bronchopneumonia
§ Inflammation localized in patches around bronchi, can impact one or multiple lobes
§ May cause lung abscess or an empyema
□ Lung abcess: tissue breakdown and formation of pus filled pocket in lung
Empyema: infection spreads to. Pleural space forming an exudate
Pneumonia etiology (Community, vs hospital vs ventilation)
○ Community
§ Most common
§ Risk factors:
□ Age <2 or >65
□ Comorbidities
□ Smoking, substance use
□ Weakened immune system
□ Cognitive impairement
○ Hospital
§ Risk factors:
□ Hospitalized >5 days
□ ICU admission
□ Co-morbidities
○ Ventilator
§ Risk factors
□ Mechanical ventilation >48hrs
□ Older age
Pneumonia clinical features
○ Increased RR
○ Fever with or without chills
○ Dullness on percussion
○ Tactile fremitus
Decreased or bronchial breath sounds pr crackles on auscultation
Pneumonia treatment and diagnosis
Diagnosis
○ Clinical history and exam
○ Chest Xray looking for infiltrates
○ Blood culture
Treatment
○ Infection prevention: vaccination, hand hygiene
○ Medication: antibiotic/antiviral/antifungal
○ At hospital: IV fluid, oxygen, respiratory support
Physio: airway clearance, breathing exercises for SOB
Acute bronchitis definition and patho
lower respiratory tract infection involving bronchi without COPD or pneumonia
Patho: acute inflammation of bronchi secondary to various triggers (virus, allergen or pollutant)
Acute bronchitis clinical features
○ Coughing 1-3 weeks, with or without sputum
○ Wheeze or mild dyspnea
Chest wall or subtle MSK pain from prolonged coughing
Acute bronchitis diagnosis and treatment
Diagnosis
○ History of acute onset of persistent cough in absence of pneumonia or COPD
○ Chest Xray to rule out pneumonia
Treatment
○ Self limiting in 1-3 weeks
OTC management of symptoms
Influenza
viral infection affecting upper and lower respiratory tract
3 main groups that mutate constantly and make it difficult to mount a immune defense
Influenza features and treatment
Clinical features: sudden, acute onset with fever, marked fatigue and aching pains
Treatment: antiviral drugs for first 2 days. Prevention via vaccination
Tuberculosis patho
○ Transmitted via aerosol droplets containing TB bacteria from coughing, sneezing or talking
○ New host inhales TB bacteria and travels to alveoli (primary infection) which triggers host response –> Macrophage ingestion
○ Immune system forms a barrier around it called granuloma
○ TB inactive in granuloma = latent TB
If immune response becomes weakened, TB bacteria can break free, multiple and can damage to lung = active TB
Tuberculosis clinical features
○ Primary infection: low fever, fatigue, cough
○ Active TB
§ Cough, may have sputum
§ Chest pain
§ Pain breathing or coughing
§ Fever, chills, night sweats
§ Weight. Loos
§ Fatigue and General malaise
Tuberculosis diagnosis and treatment
Diagnosis
○ Tuberculin tests
Treatment
○ Medication for 4,6 or 9 months
Prevention with vacine common
Atelectasis patho
on-aeration or collapse of lung tissue affecting part of lobe, whole lobe or lung
○ Alvoili become airless –> collapse due to natural elasticity of the tissue
○ This changes both ventilation and perfusion and impacts oxygen diffusion
CO2 can still difuse as its amaller
Atelectasis etiology
Can be result of
○ Obstruction: air cannot enter due to sputum or tumor
○ Non obstruction: compression on part of the lung which prevents air from entering
§ Increased surface tension in alveoli with pulmonary edema or respiratory distress syndrome prevents expansion of lung
§ Fibrotic tissue cam prevent expansion –> collapse
Postop can occur due to restricted ventilation from pain or abdominal distension, shallow respiration or increased secretions and decreased cough
Atelectasis risk factors
○ Immobolization
○ Obesity
○ Smoking
○ Lung and heart comborbidities
General aneasthetic
Atelectasis clinical features
small areas asymptomic
○ Large areas can cause
§ Dyspnea
§ Imapired gas exchange
§ Reduced chest expansion
Decreased breath sounds
Atelectasis diagnosis and treatment
Diagnosis:
○ Auscultation, percussion
○ Xray: Contents shift to the collapses side to fill empty space
Treatment
○ Oxygen therapy
○ Treat underlying pathology
○ Strategies to increase lung volume
§ Positioning, mobility
§ Breathing exercises
Positive pressure devices
Pneumothorax patho
air in pleural cavity causing collapse of some or all of the lung
Patho: pulmonary alveoli or airway become connected to the pleural cavity and air migrates from alveoli to pleural cavity until the pressures of both are equal
Spontanous pneumothorax
○ Spontaneous/closed: air enters the pleural cavity through an opening directly from internal airways
§ Tear in visceral pleura leads to air entering pleural space from lung –> atelectasis
□ This makes the kung seal itself and no more air enters
§ Primary spontaneous - pneumothorax which presents without a precipitating external event
□ Risk factors: smoking, male, tall & thin, genetics, drop in atmospheric pressure
§ Secondary: presents as a complication of underlying lung disease
Risk factor: COPD, CF, lung infection
Open pneumothorax
atmospheric air enters pleural cavity through opening in chest wall
§ Causes immediate atelectasis on affected side
§ Inspiration: mediastinum pushed to unaffected side
§ Expiration: moves back
§ This can compromise venous return
Risk factors: male, violence
Tension pneumothorax
can be the result of open or closer
§ Can be open or closed but has 1 way valve only allowing air in during inspiration
§ Causes atelectasis on affected lung and compression on mediastinum and unaffected lung–> heart failure
Severe hypoxia and respiratory distress.
CLinical features pneumothorax
○ Pleuritic pain
○ Trachea deviation (to unaffected side)
○ Hyper resonanance
○ Sudden onset
○ Reduced breath sounds
○ Absent fremitus
X ray shows collapse
Pneumothorax diagnosis and treatment
Diagnosis
○ Clinical presentation, presence of risk factors
○ Mechanism of injury
○ CXRAY
Treatment
○ Medical
§ Chest tube or needle decompression
§ Supplemental O2
§ Treatment of underlying issue
○ Physio: Augment lung volume to reinflate lungs
§ Positioning, mobilizing, breathing exercises
Avoid positive pressure therapies
Pleural effusion patho
presence of fluid in pleural cavity
Patho
○ Large amount of fluid accumulate and increase pressure in pleural cavity–> pleural membranes separate and prevent cohesion during inspiration
○ Prevents expansion of the lungs –> atelectasis and, if large enough, a shift of trachea and mediastinum to unaffected side
Venous return and cardiac filling may also be impaired
Pleural effusion etiology
○ Exudate effusion: in response to inflammation –> increase capillary permeability –> fluid leaks into pleural cavity
○ Transudate effusion: water effusion that results from increased hypostatic pressure or decreased somotic pressure
○ Hemothorax: blood from trauma, cancer or surgery
Empyema - purulent fluid related to infection (E.g. pneumonia)
Pleural effusion clinical features
○ Dyspnea, chest pain, increased HR and RR
○ Dull percussion, absent breath sounds
○ Pleuristy (inflammation of pleura), pleuritic pain
Tracheal deviation and hypotension
Pleural effusion diagnosis and treatment
Diagnosis
○ Auscultation
○ CXRay, US
Treatment
○ Medical
§ Treat cause, O2
§ Needle aspiration
§ Chest drain
○ Physio: techniques to increase lung volume
§ CBreathing exercises, mobility, positioning
Pulmonary edema patho
Fluid collecting in alveoli and interstitial area
Patho:
○ Hydrostatic pressure in pulmonary capillaries becomes high –> shift in fluid out of capillaries into alveoli
Collection of fluid in alveoli and interstitial space reduces ability of oxygen to diffuse from alveoli into blood and reduces lung expansion
Pulmonary edema etiology
○ Cardiogenic: congestive heart failure: back up of blood causing high pressure in pulmonary circulation and pushes fluid out of capillaries into alveoili
○ Non-cardiogenic: inflammation of lungs can increase capillary permeability
§ Low plasma protein levels can decrease plasma osmotic pressure
Pulmonary hyper tension
Pulmonary edema clinical features
§ Mild
□ Cough
□ Decreased breath sounds
□ Lower SpO2
□ Orthopnea
□ Crackles on auscultation
□ Fatigue
§ Sever
□ Frothy pink sputum
□ Feel like they’re drowning
□ Hypoxia, cyanosis
Cardiac changes
Pulmonary edema treatment
○ Medical
§ Treat cause
§ Medication - diuretics
§ O2 or positive pressure mechanical ventilation
Physio: not indicated
