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Respiratory
Pathophysiology
NUR5703
Advanced Pathophysiology &
Health Assessment 1
Md. Nadim Rahman
2015
Mechanics of breathing
Pressure gradients
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Surface Tension
Lungs have a tendency to recoil or collapse
due to 2 factors
Elastic fibers
Surface Tension
Clinical alterations
Surfactant
Alveoli collapse
lung expansion
WOB
Creates severe gas exchange abnormalities
Surfactant
A lipoprotein secreted by Type II cells in
alveoli
Reduces the surface tension of the fluid lining
alveoli
Advantages:
compliance
reduces WOB
stabilizes alveoli
keeps alveoli dry
Airway Resistance
The opposition to force within the airways
Volume of airflow is directly proportional to the
pressure gradient
Flow of air in and out is inversely proportional to
airway resistance
RESISTANCE = PRESSURE
FLOW
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Clinical alterations
Asthma
Oedema
Length of airway
Obstruction
Airway radius
Compliance
Compliance
C = V
P
Clinical Alterations
Compliance
Age
COAD
Compliance
Pulmonary fibrosis,
oedema
Pneumonia
ARDS, NRDS, Trauma
Kyphosis, Scoliosis,
Muscular dystrophy
Obesity, Post-op
surgical splinting
Oxygen toxicity
500ml
6000ml
3000ml
1100ml
1200ml
3500ml
2300ml
4600ml
6000ml
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Clinical applications
Ventilatory failure
Caused by:
Metabolic acidosis
PCO2
[H+] / pH
Temperature
2,3 DPG
Fever
Septic Shock
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Clinical applications
Hypothermia
HYPOXIA
An inadequate supply of oxygen to the
tissues.
Metabolic alkalosis
Respiratory alkalosis
CELLULAR CONSEQUENCES
Intracellular dysfunction
CELL DEATH
HYPERCAPNIA
An accumulation of carbon dioxide in
the blood
Decreased tissue and cellular function
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CLINICAL MANIFESTATIONS
Depression of the CNS
headache
papilloedema
flapping tremor of hands and arms
narcosis
Coma
ASTHMA
Results in:
cerebral vasodilation, increased cerebral blood
flow, raised ICP
BRONCHIAL ASTHMA
Chronic disorder of the airways causing
episodes of airway obstruction, bronchial
hyper-responsiveness and airway
inflammation (reversible).
Inflammation
Increased mucus production
bronchoconstriction
Pathophysiology
T1H cells differentiate in response to microbes
and stimulates the differentiation of B cells
into IgM and IgG-producing plasma cells.
T2H cells on the other hand respond to
allergens and helminths by stimulating B cells
to differentiate into IgE-producing plasma
cells, produce growth factors for mast cells
and activate eosinophils.
Cytokines, TNF , IL-4 & IL-5 play roles in the
pathogenesis.
ASTHMA DEFINITION
TYPES OF ASTHMA
Extrinsic asthma
Initiated by an extrinsic trigger
Intrinsic asthma
Diverse non-immune mechanisms
Respiratory tract infections
Exercise
Ingestion of aspirin
Emotional upset
Exposure to bronchial irritants (eg. smoking)
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PATHOGENESIS
An exaggerated hypersensitivity response to a
variety of stimuli.
Airway inflammation (manifested by presence
of inflammatory cells eosinophils,
lymphocytes, mast cells)
TNF increases migration and activation of eosinophils and neutrophils
MECHANISM OF RESPONSE
Late Phase
Develops 4-8 hours after exposure
Triggers include;
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CLINICALLY
Diagnosis
Based on clinical and physical examination
Respiratory function testing/ spirometry
Inhalation testing
Peak expiratory flow monitoring over a period of time
TREATMENT
Control of trigger factors
Exposure prevention
Relaxation and controlled breathing techniques
Desensitisation measures
Pharmacological management
Quick relief medications (Acute)
B2 Bronchodilators [MDI/Nebs]
Relax bronchial smooth muscle
Anticholinergic medications (ipratropium)
Block vasoconstriction via efferent Vagal pathways
Corticosteroids to management of inflammation
CHRONIC OBSTRUCTIVE
LUNG DISORDERS
COAD/ COPD
COPD or COAD
A group of respiratory disorders characterised by
chronic and recurrent obstruction of airflow in the
pulmonary airways.
The airway obstruction is progressive, may be
accompanied by hyper-responsiveness, and may be
partially reversible.
Most common cause is smoking (10-15% of
smokers will develop the disease)
Condition is well advanced before it becomes
symptomatic
COPD
Mechanisms
Inflammation and fibrosis of bronchial
wall
Hypertrophy of submucosal glands and
hyper-secretion of mucus
Loss of alveolar tissue and elastic lung
fibres
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COPD
EMPHYSEMA
COAD/COPD
COPD
Emphysema
Chronic
Bronchitis
Pathophysiology
EMPHYSEMA
Characterised by;
loss of lung elasticity
abnormal enlargement of the air spaces distal
to the terminal bronchioles, with
destruction of the alveolar walls and capillary
beds.
Enlargement of the alveolar air spaces leads to
hyperinflation of the lungs and Total Lung
Capacity (TLC)
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Causes:
smoking-incites lung injury
inherited deficiency of 1-antitrypsin (protects
the lung from injury) (1% of all COPD cases,
more common in young people with
emphysema)
CHRONIC BRONCHITIS
Airway obstruction of the major and small airways
Seen most commonly in middle-aged men
Emphysema
lung tissue
CHRONIC BRONCHITIS
Hypersecretion of mucus in the large airways,
associated with hypertrophy of the submucosal
glands in the trachea and bronchi.
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PNEUMONIA
PNEUMONIA
Inflammation of parenchymal structures of the
lungs (alveoli, bronchioles).
May be due to infection or inhalation (irritating
fumes, aspiration of gastric contents)
Classified according to:
Type of agent causing infection (typical/atypical)
Distribution of the infection (lobar pneumonia,
bronchopneumonia)
Setting ( community/hospital)
PNEUMONIA
Typical pneumonias results from infection by
bacteria that multiply extracellularly in the alveoli
and cause inflammation and exudation of fluid
into the alveoli
Atypical pneumonias are caused by viral and
mycoplasma infections that involve the alveolar
septum and interstitium of the lung. They
produce less striking symptoms and physical
findings that typical pneumonia produce.
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Pathophysiology
Pneumococcus remains the most common
cause possessing a capsule of polysaccharide.
The polysaccharide is an antigen that primarily
elicits a B cell response with antibody
production.
In the absence of antibody, clearance of
pneumococci from body relies on the
reticuloendothelial system.
Macrophages in the spleen play a major role
in antibody production.
COMMUNITY-ACQUIRED
PNEUMONIA
Infections from organisms found in the community rather
than in hospitals or nursing homes.
An infection that begins outside the hospital or is
diagnosed within 48 hours of admission in a person who
has not resided in a long-term facility for 14 days or more
before admission.
Most common cause S. pneumoniae
Others include H. Influenzae, S. Aureus, influenza virus, respiratory
syncytial virus, adenovirus
OTHER FACTORS
Antibiotic therapy that alters the normal
bacterial flora
Diabetes
Smoking
Chronic bronchitis
Viral infection
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SYMPTOMS
Vary widely depending on the age and health
of the infected person
Previously healthy:
Sudden onset
Characterised by malaise, severe shaking chill, fever
Temperature as high as 41C
Initial stage coughing of watery sputum, limited
breath sounds
Progresses to-blood tinged/purulent sputum
Pleuritic pain
THE ELDERLY
In the aged the only sign of
pneumonia may be a loss of
appetite and deterioration in
mental status
ARDS
Mechanisms involved
Barotrauma
Volutrauma
Atelectotrauma
Biotrauma
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Aspiration
Drugs, Toxins, therapeutic agents
Infections
Trauma & Shock
Disseminated Intravascular Coagulation
Multiple blood transfusions
PATHOGENESIS
Pathological lung changes in ARDS are similar
regardless of the precipitating condition.
Diffuse epithelial injury
Increase capillary permeability of alveolar-capillary
membrane.
Formation of a hyaline membrane (prevents gas exchange)
Surfactant inactivation
Increase in the intrapulmonary shunt
CLINICALLY
TREATMENT
Supportive
Ventilation; High PEEP
Improve Oxygenation; Positioning
Aim to improve gas exchange without further
lung injury.
Pneumothorax
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Primary Pneumothorax
Secondary Pneumothorax
RESPIRATORY
FAILURE
RESPIRATORY FAILURE
Respiratory failure exists as a
consequence of acutely impaired
respiratory function,
Because the;
Lungs fail to oxygenate arterial blood
DIAGNOSTIC PICTURE
Hypoxaemia
Arterial PO2 < 60 mmHg
Hypercapnia
Arterial CO2 >60
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Causative Mechanisms
THREE MECHANISMS
Pulmonary failure
OTHER FACTORS
Increased oxygen demands
Thyroid disease
Extreme exercise
Extreme stress
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