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Unit 5 - Respiratory Disorders (Pneumonia Inflammation of alveoli and…
Unit 5 - Respiratory Disorders
Lung Compliance
Ability of lungs to stretch and expand
Low
= More work needed to inflate
High
= Hard to expel air out
Factors Influencing Ventilation (SNS & PNS)
Low O2 demands
PNS when demand is low
Vagus nerve secretes Ach --> stimulates bronchial smooth muscle --> decreases airway radies (bronchconstriction)
High O2 demands
SNS when demand is increased
Norepinephrine & epinephrine from adrenal medulla --> stimulates beta 2 receptors on bronchial smooth muscles --> increase airway radii (bronchodilation)
Geriatric Considerations
Reduced elastin and increased collagen
Decreased elastic recoil d/t rib & cartilage calcification
Less strength of diaphragm, intercostal muscles, and accessory muscles
Cilia loss with reduced cough power
Reduced pulmonary blood flow
All increase work of breathing
Alterations in Pulmonary Function
Hypoxemia
Hypoxia
Hypercapnia
Hypocapnia
Hypercapnia
Aka hypercarbia
Increased blood CO2
Inversely related to ventilation
Severe hypoventilation has hypoxemia and hypercapnia
Causes
Hypoventilation
Lung disease
Decrease LOC
Rebreathing CO2
Clinical Manifestations
Increased PO2 --> Increased H+ --> Decreased pH blood = Respiratory Acidosis
Kidneys compensate by increasing H+ excretion and HCO3- retention
Chronic hypercapnia doesn't show S&S until PCO2 is greatly elevated or PO2 is greatly reduced
Hypocapnia
Low PCO2
From hyperventilation
Causes:
Pain, fever, anxiety, sepsis
High altitude
Brainstem injury
Hypoxemia
Reduced blood oxygen levels (PO2), leading to
hypoxia
Causes
:
Hypoventilation
Obstruction
Inadequate amount of O2 in air
Altered circulatory function
Neurological dysfunction
Decreased LOC/euphoria
Obesity
Obstructive sleep apnea (OSA)
Clinical Manifestations
SNS compensation of shunting
CNS effects:
Slight impairment of mental performance/euphoria
Agitation, confusion, impaired judgment
Pulmonary vasoconstriction
Increased pulmonary arterial pressure to increase perfusion
Increased production of erythrocytes
Cyanosis
Ventilation Perfusion Ratio (V/Q Ratio)
Volume of air (V) in alveoli matches blood flow (Q) for adequate diffusion
Normal:
4ml/5ml = 0.8
Under-perfusion V/Q
Under-perfused
Adequate ventilation but inadequate perfusion
Abnormal pulmonary blood flow
Pulmonary embolus, heart failure, hypotension
High V/Q Ratio
4ml/ <5ml = >0.8
Physiological Dead Space
Under-ventilated V/Q
Under-ventilated
Adequate perfusion but inadequate ventilation
Alveolar collapse/consolidation, obstruction
Low V/Q Ratio
4ml/ >5ml = <0.8
Shunt
Deep Vein Thrombosis (DVT)
3 Factors (Virchow's Triad)
Venous stasis/slow blood
From immobility, trauma, pregnancy, obstetric surgery, cancer, and estrogen use
50% idiopathic
Hypercoagulability
Damage to the venous wall
Clinical Manifestations
Warm, painful, swollen, edematous, red
Pulmonary Embolus
Traveled DVT blood clot that obstructs pulmonary blood flow
Causes
:
90% from deep veins in pelvis or legs
Air from IV infusion
Fat from broken bone marrow
Amniotic fluid entering maternal circulation at delivery
Mortality rate = >30% with big PE
Under-perfusion V/Q mismatch
Clinical Manifestations
Obstruction --> reflexive bronchoconstriction --> Poor ventilation & diffusion --> Loss of surfactant
Depends on size of thrombus
Restlessness, anxiety
Increased HR & RR, dyspnea
Chest pain
Hemoptysis
Hypoxemia
Usually undetected unless it's a massive PE
Treatment & Prevention
Mobilize patients and teach lower leg movements (q1h, per hour)
Anti-coagulants, active ROM, compression hose w/pneumatic compression
If confirmed DVT/PE, anticoagulants, thrombolytics, oxygen, bed rest
DON'T RUB IT
Obstructive Airway Disorders
Asthma
Chronic inflammation disorder of the airways
Bronchial hyper-responsiveness to stimuli with airway inflammation and obstruction
1. Extrinsic (Atopic)
Type 1 hypersensitivity reaction from extrinsic allergen
Allergy disorder (childhood onset with genetic link)
2. Intrinsic (Nonatopic)
Respiratory infection
Emotional factors
Cold air
Exercise
GERD/strong odours
Drugs/chemicals
Smoke/air pollution
Pathophysiology (Atopic Asthma)
Acute Phase (10-20 min after contact with allergen)
Antigens bind to presensitized mast cells on mucosal surface of airways
Chemical mediators released resulting in mucous production and bronchospasm from stimulation from PNS receptors on airway surface
Late Phase (4-8 hours)
Release of inflammatory mediators from mast cells, macrophages, and epithelial cells, leading to migration of other inflammatory cells
Changes in mucociliary function and epithelial edema and injury
Respiratory tract clearance of secretions decreases
Airway responsiveness increases to hypersensitivity
Chronic inflammation --> Airway remodeling & airflow limitations
Pathopyshiology (Exercise-Induced)
Common in children and adolescents
Bronchospasm occurs within minutes of exercise
Resolves in an hour
Heat & water loss activates inflammatory mechanisms
Mediator release from basophils & tissue mast cells
Leads to bronchoconstrction
Clinical Manifestations of Asthma
Acute episode
Dyspnea, orthopnea (flat dyspnea) with dry/productive cough
Hypoxemia
Decreased ventilation with wheezing, chest tightness, accessory muscle use
Increased O2 demands = Increased WOB (work of breathing)
Under-ventilation V/Q
May be symptom free between attacks
Nocturnal asthma
Status asthmaticus
Treatment & Prevention
Avoid triggers
Annual influenza vaccine
Fast-acting medications to alleviate acute attacks
Early treatment for respiratory infections
Longer-acting inhaled corticosteroids inhaled daily
Chronic Obstructive Pulmonary Disease (COPD)
Consists of Crhonic Bronchitis + Emphysema
1. Chronic Obstructive Bronchitis
Obstruction of small airways d/t inflammation
Irritation by smoking and recurrent infections
Hypertrophy of mucous gland
2. Emphysema
Enlargement of air spaces, destruction of lung tissue and loss of lung elasticity
1, Chronic Bronchitis
Diagnosed by:
Hypersecretion of bronchiol mucous
Hypertrophy of submucosal glands in trachea and bronchi
Chronic or recurrent productive cough >3 months duration for >2 successive years
Persistent, irreversible
Male:Female = 1:2
Etiology
Smoking (90%)
Repeated airway infections & genetics
Physical/chemical irritants
Pathophysiology
Irritants activate neutrophils
Chronic airway inflammation and obstruction of major & small airways
Leads to swelling of bronchial mucosa & alveoli, resulting in scarring, fibrosis, increased wall thickness, mucous, and mucous plugs
Airway narrowed & proper oxygenation prevented
Chronic hypoxia & hypercapnia, leading to pulmonary vessel vasoconstriction
Under-ventilation V/Q mismatch
Impaired or absent cilia
Colonized with H.influenza (bacterial, not flu) and S.pneumoniae
Clinical Manifestations
Peripheral edema
Digital clubbing
Polycythemia (increased RBC abnormally)
Recurrent cough/sputum
Cyanosis
2. Emphysema
Damaged distal alveoli
Progressive over long time
Etiology
Smoking
Air pollution
Certain occupations
Alpha1-Antitrypsin deficiency (if patients <50 years old)
Pathophysiology
Irritants stimulate inflammatory cells into the lungs
Increase in proteases release, which destroy elastin
DIstal alveoli enlarged & damaged
Loss of elastic tissue in lung
Loss of radial traction (normally holds airway open)
Alveolar collapse with air trapping
Loss of elastic alveolar wall and air trapping leads to
bullae
(large thin-walled cysts in the lung) forming
Clinical Manifestations
Thin, pink
Airways collapse during exhalation
Forced exhalation
Pursed-lips and accessory muscles
Minimal or absent cough
Barrel chest with CO2 retention
Clinical Manifestations for COPD
History of smoking
Laboured breathing (air hunger)
Accessory muscle use
Hypoxemia/hypercapnia
Right sided heart failure (cor pulmonale)
Increased thoracic pressures --> RV afterload increases --> R heart failure
Frequent pulmonary infections
Gradual, progressive, with frequent exacerbations
Ultimately develop respiratory failure
COPD Treatment & Prevention
Prevention
Adequate rest & hydration
Physical reconditioning
Influenza and pneumococcal vaccines
Smoking cessation
Treatment
Low dose O2 therapy
SaO2 86-90%
-Medications
Inhaled Beta2 agonists & anticholinergic agents
Cough suppressants
Antimicrobial agents (infections)
Atelectasis
Incomplete expansion of lung
Primary in premature neonates
Lung lacks surfactant or hasn't been inflated
Secondary in adults
Airway obstruction
Mucous plug, increased secretions, collapsing airway
Increases after surgery
Pain, anaesthesia, immobility promotes retention of bronchial secretions
Crompression from tumour, fluid, blood
Clinical Manifestations & Prevention (Secondary)
Decreased or no breath sounds
Increased RR, dyspnea, cyanosis, hypoxemia, intercostal retractions
Pneumonia risk
Reduce airway obstruction and re-inflate akveoli
Prevention
Ambulation
Deep breathing and coughing
Positiioning
Incentive spirometer q1h
Pneumonia
Inflammation of alveoli and bronchioles from infectious/non-infectious agents
High-risk:
Less than 2 years & >65 years of age
Diminished gag reflex
Seriously ill patients
Hypoxic patients and immunocompromised patients
Etiology
Aspiration of oro-pharyngeal secretions with normal flora/gastric contents (25-35%)
Inhalation of contaminants
Contamination from circulatory system
Pathophysiology
Organisms enter lung, grow, trigger inflammation
Invades alveolar septa
Alveolar spaces fill with exudative fluid
Consolidates and difficult to expectorate
No exudative fluids with viral pneumonia
Community Acquired
Bacterial/Viral
Commonly S.pneumoniae
Could be admitted to hospital
Hospital Acquired
Mostly bacterial (P.aeruginosa, S,aureus, E.coli)
2nd most common hospital acquired infection
60% mortality rate
Clinical Manifestations
Productive cough with pus and phlegm (sputum)
Fever and chills
General discomfort, unease, ill feelings (malaise)
Loss of appetite with N&A
Sharp chest pains that get worse with breathing/coughing
SOB
Hypotension & tachycardia
Prevention
Infection control
HOB 30-45 degrees
Feed upright
Oral care
Promote adequate nutrition
Limit visitors
Pneumothorax
Accumulation of air in pleural space
1. Spontaneous
Rupture of bleb or lesion on lung surface
Primary: Occurs in healthy, tall, thin men w/o risk factors
Secondary: In people with COPD and other lung diseases
Alveolar pressure > pleural pressure = aur flows from alveoli to pleural space --> collapse of lung
2. Traumatic
From penetrating or blunt chest injuries
Commonly dislocated ribs or central line insertion
3. Tension
Trauma where intrapleural pressure > atmospheric pressure
Air enters pleural space during inspiration but can't leave (trapdoor)
Air builds up in pleural space --> lung on ipsilateral (same) side collapses
Forces mediastinum toward contralateral (opposite) side
Compresses vena cava
Decrease venous return and cardiac output
Hemothorax
Collection of blood
Rupture of big vessel, like an aortic aneurysm
Chest surgery
Clinical Manifestations
Chest pain & tachypnea
Dyspnea with cough
Hypotension with tachycardia
Hypoxemia with O2 desaturation
On examination:
Midline shift (mediastinal shift)
Absent breath sounds on side of collapse
Treatment
Chest tube drainage with suction to let air escape without re-entry
Supplemental O2
Pleural Effusion
Normal: Fluid enters from capillaries in parietal pleura or small holes from diaphragm which is removed by lymphatics in parietal pleura
Abnormal collection of fluid in pleural cavity d/t:
Rate of fluid formation > rate of removal
Etiology
Heart/renal/liver failure
Malignancy
Empyema
Contains pus, glucose, proteins, leukocytes
Infections/abscess in pleural cavity that ruptures
Transudative effusion (CHF, hypoproteinemia)
Exudative effusion
Protein rich with inflammation
In TB, malignancies, immune disorders, infections
Needs thoracentesis