Resp Emergencies Flashcards
Restrictive vs Obstructive
Restrictive
* Harder to get air in due to a
reduced lung expansion, and, in
turn, reduced lung volumes,
particularly with reduced total
lung capacity
* Interstitial lung disease
* Obesity
* Scoliosis
* Reduced Forced Lung Capacity
(FLC)
Obstructive
* Harder to get air out due to
narrowing or destruction of the
airways or inflammation
* COPD
* Asthma
* Cystic Fibrosis
* Bronchiectasis
Intrinsic vs extrinsic restrictive
Intrinsic disorders come from a problem within the lungs themselves.
* Interstitial lung disease
* Pulmonary Fibrosis
Extrinsic restrictive lung disorders cause lung problems to occur from
disorders outside of the lungs.
* This means that the restriction and lung problems originate from outside of the lungs.
* Sometimes, restriction is caused by weak muscles, stiffness in the chest wall or damaged
nerves.
* Obesity
* Pleural Effusion
* Myasthenia gravis
* Scoliosis
* Neuromuscular disease
What is asthma
chronic inflammatory disorder characterized by increased responsiveness of the small airways to multiple stimuli.
three main processes in asthma
bronchoconstriction,
* mucus hyper-secretion
* airway inflammation
Pathophys of asthma
- Individual previous exposed and sensitized to specific antigen and hence formed antibodies
- allergen reaches the bronchial epithelium, they activate the dendritic cells on cell membrane to take up the allergen and start phagocytosis
- immune response by activating the T-cells (T2)
- Interleuken 4+5 lead to release of histamine and Leukotrienes Causing:
- Bronchoconstriction due to contraction of
smooth muscle
➢ Mucus hyper-secretion due to excess
goblet cell activation
➢ Airway inflammation
➢ Increase in vascular permeability
mechanics of airflow obstruction
Bronchoconstriction, mucus production and airway inflammation causes a decrease in airway diameter
no issue inspiring as there is still negative intrathoracic pres.
Inspired air cant escape during expiration due to the inflammation and excessive mucus
Consequences of Airflow
Obstruction
Increased airway resistance
* Decreased maximum expiratory flow rates
* Air trapping
* Increased airway pressure
* Barotrauma
* Adverse hemodynamic effects
* Ventilation–perfusion imbalance
* Hypoxemia
* Hypercarbia
* Increased work of breathing
* Pulsus paradoxus
* Respiratory muscle fatigue with ventilatory failure
Signs and Symptoms of asthma
Cough
* Dyspnea
* Chest tightness
* Shortness of Breath
* Wheezing – may be absent
* Tachypnea
* Prolonged expiration time
* Tachycardia
* Retractions
* Use of accessory respiratory muscles
* Speaking in short sentences
* Anxious
* Diaphoretic
* Pulsus Paradoxis
Treatment of Asthma
Treatment
B2 nebulizer
* Binds to B2 receptors on bronchial wall, causing bronchial smooth muscle relaxation and dilation
Anticholinergic nebulizer
* Blocks parasympathetic nervous system to airways, causing bronchial smooth muscle relaxation
Corticosteroids IV
* Stabilization of mast cell membranes, so decrease inflammation and mucus production by Histamine
* Suppression of antibody production
b2 stims
Salbutemal 5mg
Fenoterol 1.25mg
Hydrocort
5mg/kg IV
precautions
Diabetes
Petic ulcer
Anticholernergic Nebulizer
Ipratropium bromide
0.5 mg
Status Asthmaticus treatment
IM adrenaline binds to b2 recepters
0.3mg (1:1000). Can be repeated every 20 mins to a
maximum of 3 doses
Mg sulph 2g over 20 mins via syringe drive
decreases uptake of Ca by bromchial smooth muscles causing dilation
Chronic Obstructive Pulmonary Disease
persistent respiratory symptoms and airflow
limitation that is due to airway and/or alveolar abnormalities
emphysema and chronic bronchitis
Emphysema
abnormal permanent enlargement of air
spaces distal to the terminal bronchioles
Chronic bronchitis
chronic productive cough for 3 months during each of 2 consecutive years
Risk factors for COPD
- Smoking
- Dust
- Chemicals
- Air pollution
Pathophys of chronic bronchitis
Inflammatory response
* Mucus-secreting cells replace cells that normally secrete surfactant and protease inhibitors
* Proteases break down lung parenchyma
Mucus production
* The number and size of Goblet cells as well as bronchial submucosal glands of the airways also increase and secrete more mucus
Destruction of the cilia
* Ciliary dysfunction and motility leads to a decrease in mucus clearance
Air entrapment
* Small airways collapse on expiration, leading to less air being exhaled and air
entrapment
VQ mismatch
* Due to narrowing of the airways and excessive mucus plugs, there is decreased Oxygen reaching the alveoli and less CO2 being expired
- Leads to Type II respiratory failure & Acidosis
Infection - Excessive mucus leads to recurring bacterial infections
Patho phys emphysema
Destruction of alveoli
* The Protease also leads to the destruction of the alveolar wall and capillary
beds
* Leading to a decrease in perfusion
Air trapping
* Loss of alveolar wall elasticity leads small airways collapse on expiration,
leading to less air being exhaled and air entrapment
* Increase in end expiratory volume
* Barrel chest
VQ mismatch
* Due to the collapsing of the airways, there is decreased Oxygen reaching the
alveoli and less CO2 being expired
* Decrease in perfusion due to destruction of alveolar capillary bed
* Lead to Type II respiratory failure & Acidosis
Treatment of COPD
Same as Asthma then CPAP
Presentation of COPD exacerbation
Tachypnea and respiratory distress with simple activities
– Use of accessory respiratory muscles and paradoxical indrawing of
lower intercostal spaces (Hoover sign)
– Diaphragm is flat due to increased lung volume, so can’t contract properly
– Cyanosis
– Elevated jugular venous pressure (JVP) & Peripheral edema
Hyperinflation (barrel chest)
* Wheezing – Frequently heard on forced and unforced expiration
* Diffusely decreased breath sounds
* Hyperresonance on percussion
* Prolonged expiration
* Coarse crackles beginning with inspiration in some cases
Risk factors for COPD
Suspect COPD in:
* >35 years
* Chronic smoker
* Exertional breathlessness
* Chronic cough
* Regular sputum production
* Frequent winter bronchitis with wheezing
* Infection history
* Trigger history
* Gastric reflux
* Beta blocker use
* Cold weather
* Opioid and sedative hypnotic use
Presentation of bronchiectasis
Chronic Symptoms:
Persistent, productive cough with large volumes of purulent sputum.
Hemoptysis in severe cases.
Recurrent Respiratory Infections:
Frequent exacerbations marked by increased sputum production, dyspnea, and systemic symptoms like fever.
Dyspnea and Wheezing:
Resulting from airway obstruction and reduced gas exchange.
Systemic Features:
Fatigue, weight loss, or digital clubbing in advanced disease.
Pathophys of Bronchiectasis
Bronchiectasis is a chronic condition characterized by abnormal and permanent dilation of the bronchi and bronchioles due to the destruction of their walls. The underlying mechanisms include:
Cycle of Infection and Inflammation:
Recurrent or chronic infections damage the airway epithelium, leading to impaired mucociliary clearance.
This promotes microbial colonization and persistent inflammation, causing further structural damage.
Structural Changes:
Loss of elastic tissue and smooth muscle in the bronchial walls leads to weakened and dilated airways.
Inflammatory mediators and enzymes (e.g., proteases) contribute to tissue destruction.
Airway Obstruction:
Mucus stasis and thick secretions obstruct airflow, further exacerbating infection and inflammation.
Patho phys of bronchiolitis
Common in children inflamation of bronchioles
Viral Infection: Commonly caused by respiratory syncytial virus (RSV), leading to infection of the lower respiratory tract.
Airway Inflammation: Edema, mucus production, and sloughing of epithelial cells narrow the small airways (bronchioles).
Air Trapping: Partial airway obstruction causes hyperinflation, atelectasis, and impaired gas exchange.
Presentation of bronchiolitis
Nasal congestion, rhinorrhea, mild cough, and low-grade fever.
Progression: Tachypnea, wheezing, crackles, and increased work of breathing (e.g., nasal flaring, retractions).
Severe Cases: Cyanosis, hypoxemia, and apnea (especially in young infants).
Presentation of Bronchopneumonia
Respiratory Symptoms: Cough with purulent sputum, dyspnea, and pleuritic chest pain.
Systemic Symptoms: Fever, chills, and fatigue.
Physical Signs: Crackles, bronchial breath sounds, and dullness to percussion over affected areas.
Pathophysiology of Bronchopneumonia
Inflamation of bronchi
Infection: Typically bacterial (e.g., Streptococcus pneumoniae, Staphylococcus aureus), spreading through the airways.
Patchy Inflammation: Affects multiple lobules, causing alveolar congestion and consolidation.
Impaired Gas Exchange: Inflammation and exudate in alveoli reduce oxygenation.
Presentation of Pleural Effusion
Symptoms:
Dyspnea (most common).
Pleuritic chest pain (if inflammation is present).
Cough, typically non-productive.
Physical Signs:
Diminished breath sounds.
Dullness to percussion.
Reduced chest expansion on the affected side.
Pathophysiology of Pleural Effusion
Excess Fluid Accumulation: Occurs in the pleural space due to:
Increased hydrostatic pressure (e.g., heart failure).
Decreased oncotic pressure (e.g., hypoalbuminemia).
Increased vascular permeability (e.g., infections, malignancy).
Impaired lymphatic drainage (e.g., cancer, trauma).
Presentation of Pulmonary TB
Pulmonary Symptoms: Persistent cough (often productive), hemoptysis, and chest pain.
Systemic Symptoms: Fever, night sweats, weight loss, and fatigue.
Physical Signs: May include crackles or bronchial breath sounds over affected areas.
Pathophysiology of Pulmonary Tuberculosis (TB)
Infection
: Caused by Mycobacterium tuberculosis, spread via inhaled respiratory droplets.
Primary Infection:
Bacilli are phagocytosed by alveolar macrophages but may survive and replicate.
Formation of granulomas (tubercles) to contain the infection.
Latent TB: Bacteria remain dormant within granulomas, potentially reactivating later.
Active TB: Granuloma breakdown leads to caseating necrosis, cavitation, and spread within the lungs and systemically.
