Respiratory Diseases Flashcards
Dyspnea
- Subjective feeling of discomfort that occurs when a person is unable to inhale enough air
- Severe: accompanied with nasal flaring, accessory muscle use
- Orthopnea: SOB that occurs when the person is lying down, results as blood pools in the lungs with gravity
- PND- common with LVF
- Cyanosis: bluish discoloring of the skin resulting from large amounts of deoxygenated hemoglobin in the blood
Breathing Patterns
- May be altered with respiratory disease
- Normal rate is 10-18/min, regular and effortless
- Changes:
- Kussmaul Respirations- deep, rapid, “air hunger”, typical with acidosis or following strenuous exercise
- Laboured with prolonged inspiration/expiration- often associated with airway - obstructions
- Wheezing- obstructions of the small airways
- Stridor- Upper airway obstruction
General Manifestations
Sneezing- reflex response to irritation in the URT and acts to remove the irritant
Coughing- may result from irritation due to nasal discharge dripping into the oropharynx, or inflammation/irritation in the LRT (eg. smoke inhalation)
Sputum- mucoid discharge from the respiratory tract
Yellow-green, cloudy, thick- indicates a bacterial infection
Rusty/dark sputum is usually associated with pneumonia
Blood tinged sputum- associated with pulmonary edema
Upper Respiratory Tract Infections
- Common cold is caused by a viral infection of the URT
- Over 100 possible causative organisms can cause this
- Spread through respiratory droplets, either directly inhaled or spread through touch
- Highly contagious as virus can survive for several days outside of the body
- Signs and Symptoms:
Red mucous membranes of the nose and pharynx
Copious watery discharge
Mouth breathing, change in voice tone
Cough may develop from irritation of discharge
URTI TX
- Acetaminophen for fever and headache
- Decongestants to reduce congestion
- Humidifiers- keep secretions liquid to aid in removal
- Antibiotics DO NOT cure viral infections
Sinusitis
- Bacterial infection secondary to a cold or an allergy that has obstructed drainage of one or more of the paranasal sinuses
- Causes build up of the exudate which leads to severe pain in the face
- Decongestants and analgesics are recommended until the sinuses are draining well
- Antibiotics are often required to eradicate the infection
Croup
- AKA Layngotracheobronchitis
- Common viral infection most commonly in children between 1 and 2
- Begins as an upper respiratory condition with nasal congestion and cough
- The larynx and subglottic area become inflamed with swelling and exudate- leads to the characteristic “Barking Cough”, hoarse voice and inspiratory stridor
- Often more severe at night
- Treatment- cool, moisturized air from a humidifier or shower
- Full recovery usually in several days
Epiglottis
- Acute infection from a bacterial organism
- Most common in children aged 3-7
- Infection causes swelling of the larynx, supraglottic area and epiglottis
- Onset is rapid, fever and sore throat develop, and the child refuses to swallow
- Excessive drooling is present
- Child will appear anxious, mouth open, struggling to breathe
- Use caution when examining the throat- ensure you don’t cause complete obstruction of the airway
- Treatment involves O2/airway and management
Pneumonia
- May develop as a primary acute infection in the lungs or secondary to another respiratory or systemic condition
- Always a risk following aspiration or inflammation in the lung, when fluids pool or cilia are reduced
- Most cases the organisms enter the lungs directly via inhalation or aspiration
- Can be classified as viral, bacterial or fungal
Types of pneumonia
- Lobar Pneumonia- infection localized to one or more lobes
- Bronchopneumonia- diffuse pattern of infection in both lungs, more often in the lower lobes
- Legionnaires Disease- gram negative bacteria that thrives in warm moist environments such as A/C’s and spas
- Viral Pneumonia- caused by influenza and respiratory viruses
- Begins with inflammation of the mucosa of the URT and then moves into the lungs
- Primary Atypical Pneumonia (PAP)- viral and involves interstitial inflammation around the alveoli
Tuberculosis
- Infection that affects the lungs primarily, but may also invade other organs
- Transmitted by oral droplets released from a person with active infection inhaled into the lungs
- Primary Infection- occurs when the microorganisms enter the lungs- fought off by your body’s immune system
- Creates a small area of necrotic tissue on the lungs visible on x-ray
- Stays dormant for years
- As long as the individuals resistance and immune system are strong, they will remain asymptomatic
- Secondary Infection- Stage of active Infection
- Often arises years after primary infection when resistance is down
Creates large areas of necrosis in the lung tissue that form open areas and erosion into the bronchi and blood vessels
S+S Tuberculosis
- Primary- Asymptomatic
- Initially- vague manifestations such as malaise, fatigue and weight loss
- Low grade fevers and nigh sweats
- Cough is prolonged and gets increasingly
severe, often contains blood
Cystic Fibrosis
- Genetic disorder (affecting the 7th chromosome) that results in a thick, sticky mucus secretion in the lungs
- Mucus obstructs airflow in the bronchioles causing air trapping and permanent damage to alveoli
- The stagnant mucus also creates a breeding ground for bacteria
- Infections are common
S+S of Cystic Fibrosis
- Chronic cough and frequent respiratory infections
- As lung damage proceeds, hypoxia, fatigue and exercise intolerance develop
- Chest may appear overinflated due to air trapping
- Audible rhonchi
- Failure to meet the normal growth milestones due to chronic respiratory problems
- Dyspnea, tachypnea, accessory muscle use, cyanosis, diminished breath sounds
Tx Cystic Fibrosis
In Hospital:
- Therapy to minimize bronchial plugging and inhibit bacterial growth
- Treatment of infections with antibiotics
- Chest physiotherapy including coughing techniques to facilitate mucous removal
Pre-Hospital:
- Airway management
- Supplemental O2
- Bronchodilators to promote drainage
Aspiration
- Passage of food or fluid, vomit or drugs, or any other foreign material into the trachea or lungs
- Right lower lungs is most commonly affected
- Why?
Normally, a cough removes such material from
the URT and the epiglottis and vocal cords from
the LRT - Solids:
Complete airway obstruction
Collapse of the area of lung distal to the obstacle - Ball valve effect- air goes in but gets trapped (pneumo)
- Sharp objects- traumatizes the tissues and mucosa causing inflammation and bronchoconstriction
- Liquids:
Materials cause severe inflammation leading to narrowing of airways and increased secretions making the lungs difficult to expand
Gas diffusion is impaired if alveoli are affected
May be dissolved into the blood causing systemic effects
S+S of Aspiration
- Most at risk are young children, children with congenital abnormalities, stroke patients or any where the gag reflux is depressed, bed bound patients
- S&S:
Coughing with dyspnea
Stridor and hoarseness
Wheezes with aspiration of liquids into the lungs
Tachycardia and tachypnea as a response to SOB
Complete obstruction- no sound will be produced
Tx Aspiration
- Full Obstruction: Abdominal thrusts on adults and back blows on infants
If progresses to unconscious- CPR ensuring visualization of A/W - Partial: encourage coughing
Oxygen and supportive therapy
Monitor for potential signs of pneumonia or infection
COPD
- Chronic Obstructive Pulmonary Disease
- Group of chronic respiratory disorders that are characterized by progressive tissue degeneration and obstruction of the airways
- Causes irreversible damage to the lungs
- Debilitating conditions
- Examples are emphysema, bronchitis and asthma
Asthma
- Disease that involves periodic episodes of severe but reversible bronchial obstruction in persons with hypersensitive/hyper responsive airways
- May be acute (single episode) or chronic (long term condition)
- Can be triggered by an inhaled antigen (extrinsic) or respiratory infections, exposure to cold, exercise, drugs, stress (intrinsic)
- Extrinsic is more commonly in children and symptoms disappear by adulthood
Intrinsic is more commonly developed during adulthood
Patho of Asthma
- Bronchi and bronchioles respond to the stimuli in 3 ways:
1) Inflammation of the mucosa with edema
2) Constriction of smooth muscle (bronchoconstriction)
3) Increased secretions of thick mucous in the passages - Partial obstruction of the bronchioles results in air trapping and hyperinflation of the lungs
- Air passes into the areas distal to the obstruction and is only partially expired
- Air builds up and the pt. tries to force the expiration which leads to collapse of the bronchial walls
- Residual volume increases- becomes more difficult to breathe fresh air and cough to remove the mucus
- Hyperinflation analogy
- Total Obstruction of the bronchioles results when mucus plugs completely block flow of the already narrowed passages
- This leads to non aeration of the tissue distal
- Air in the distal area diffuses out and is not replaced resulting in collapse of that section of lung
- O2 demands increase as the body senses the
stress response to hypoxia as the pt. fights for
air
Status Asthmaticus/Asthma Exacerbation
- Status: persistent, severe asthma attack that does not respond to therapy
- Fatal secondary to hypoxia and cardiac arrhythmias
- Exacerbation: severe narrowing of the airways in an asthma attack to the point that no air is able to pass through
- Results in no RR and no breath sounds- “silent chest”
S+S Asthma
- Cough, dyspnea, tightness in the chest
- Agitation as obstruction increases
- Wheezes as air passes through narrowed bronchioles
- Rapid, laboured breathing with accessory muscle use
- Thick, tenacious mucus coughed up
- Tachycardia
- Respiratory failure- decreased LOC, cyanosis
Tx Asthma
- Minimize the exposure to known irritants
- Good ventilation
Acute Attacks: - Controlling breathing
- Bronchodilators- acts on Beta 2 receptors to relax smooth bronchial muscle
- Epi 1:1,000- decreases airway edema and is a beta 2 agonist
- Dexamethasone PO
- O2
- Airway Management
Emphysema
- Destruction of the alveolar walls which leads to large, permanently inflated alveolar air spaces
- Often called “Pink Puffers”
- Several factors can contribute to this destruction:
1) Genetic deficiency of the protein present to inhibit breakdown of elastase during an inflammatory response
2) Cigarette smoking stimulates the release of elastase
Patho of emphysema
- Breakdown of alveolar walls results in:
- Loss of surface for gas exchange
- Loss of elastic fibers affecting lung recoil
- Altered V/Q ratios
- Decreased support for bronchial structures leading to obstruction of airflow in expiration
- Thickening of bronchial walls leads to narrowed airways
- Difficult expiration leads to air trapping and increased Residual volumes and over-inflation
- Fixation of ribs in inspiratory position (barrel chest)
- Hypercapnia
- Hypoxic drive as pt’s respiratory center adapts to high CO2 levels and fails to be the respiratory centers regulatory mechanism
- The large air spaces (blebs) can create the tissues and pleural membranes around the bleb to rupture, causing a pneumothorax
- Frequent infections as secretions are difficult to remove
- Pulmonary HTN and cor pulmonale develop as pulmonary blood vessels are destroyed causing increases pressure in the pulmonary circulation
- This can lead to RV failure
S+S Emphysema
- Dyspnea initially on exertion, then even at rest
- Hyperventilation with prolonged expiratory phases and accessory muscle use
- Barrel chest from hyperinflation
- Tripod positioning to facilitate breathing
- Fatigue contributes to weight loss- often these
patients are extremely thin - Clubbed fingers
- Polycythemia
Tx Emphysema
- Avoidance of respiratory irritants
- Cessation of smoking
- Respiratory rehab- purse lipped breathing
- Maintenance of nutrition
Pre Hospital: - Bronchodilators
- Airway management and O2- 2 lpm or 2 lpm above home levels unless severe SOB (see BLS Standards)
- CPAP
Chronic Bronchitis
- Significant changes to the bronchi resulting from constant irritation from smoking or exposure to pollutants
- Effects are irreversible and progressive
- Results in inflammation and obstruction to the bronchi, repeated infections and chronic coughing
Pathophysiology of Bronchitis
- Mucosa is inflamed and swollen
- Hypertrophy of mucous glands and increased secretions are produced
- Chronic irritation and inflammation lead to thickening of bronchial walls and further obstruction
- Secretions pool and are difficult to remove
- Low O2 levels- cyanosis will be evident.
- “Blue Bloaters”- edema, cyanosis and low O2 levels
- Severe dyspnea and fatigue interfere with nutrition
- Pulmonary HTN results
S+S Bronchitis
- Constant, productive cough
- Tachypnea
- SOB
- Frequent secretions that are thick
- Rhonchi- usually more prevalent in the morning as secretions have pooled
- Cyanosis and hypoxia
TX Bronchitis
- Reducing exposure to irritants
- Prompt treatment of infections to slow the progress of the disease
- Use of expectorants and bronchodilators
- Chest therapy
- Ensuring adequate nutrition
- Pre Hospital:
- Airway management- O2/BVM
- Bronchodilators
- CPAP
Pulmonary Embolism
- Blood clot or mass of other material that obstructs the pulmonary artery or branch of it, blocking blood flow through the lung tissue
- Effects depend largely on the size and location of the clot
- Small are often asymptomatic
- Large emboli often affect the respiratory system but also the cardiovascular system causing right sided failure and decreased cardiac output
S+S PE
- Transient chest pain that often increases with coughing or deep breathing
- Cough
- SOB
- Tachypnea
- Hypoxia stimulates sympathetic response- anxiety, restlessness, tachycardia
Massive emboli can cause: - Crushing chest pain
- Low BP
- Rapid, weak pulse
- Loss of consciousness
Atelectasis
- Non aeration or collapse of a lung or part of a lung leading to decreased gas exchange or hypoxia
- When the alveoli become airless, they shrivel up
- This interferes with blood flow through the lungs and alters both ventilation and perfusion
If the lungs are not re inflated quickly, the lung tissue can become necrotic and permanently damaged
S+S Atelectasis
- Small areas are asymptomatic
- Large areas:
- Dyspnea
- Tachycardia
- Tachypnea
- Chest expansion may appear abnormal or asymmetrical
- Treatment:
- Pre Hospital primarily focused again on airway management and support
Pleural Effusion
- Presence of excessive fluid in the pleural cavity
- Normally small amounts are present for lubrication
- Both lungs may be involved but often just 1 is as each lung has its own pleural sac
- Pleurisy may follow- inflammation/swelling of the pleural membranes
- The fluids create higher pressures which prevents normal lung expansion, leading to atelectasis
S+S Plueral Effusion
- Dyspnea
- Chest pain
- Tachypnea
- Tachycardia
- Absence of breath sounds over affected area
- Tracheal deviation
- Hypotension
ARDS - Adult Respiratory Distress Syndrome
- Restrictive disorder
- Secondary to an injury- sepsis, shock, burns, aspiration, smoke inhalation
- Usually occurs 1-2 days after an injury
- Often associated with multiple organ dysfunction
ARDS Patho
- Changes to the lungs result from injury to the alveolar wall and capillary membranes
- This leads to increased alveolar permeability increased fluid in the alveolar and interstitial areas of the lungs
- This results in :
- Decreased diffusion of O2
- Reduced blood flow to the lungs
- Difficulty in expanding the lungs
- Reductions in tidal volumes
- Excess fluids predispose the pt. to pneumonia or CHF
S+S ARDS
- Dyspnea
- Restlessness
- Rapid, shallow respirations
- Tachycardia
- Accessory muscle use as lung congestion increases
- Crackles
- Productive cough with frothy sputum
ARS - Acute Respiratory Failure
- End result of many pulmonary disorders
- Happens when there are inadequate O2 and - CO2 levels for the body’s needs at rest
CNS including the respiratory control center is affected - Ends in respiratory Arrest- cessation of respiratory activity
TX Acute Respiratory Failure
- Treat as per BLS Standards “Respiratory Failure” and “O2 Therapy” Standards
- BVM ventilations
- OPA/NPA
- SGA
- ETT (ACP Only)