-
Disablement Model
-Pathology/pathophysiology (disease, disorder,or condition) in the following systems ( cardiovascular, multiple systems)
-Impairments in the following categories ( circulation, ventilation and respiration/gas exchange)
-Functional limitations in the ability to perform actions,tasks, and activities in the following categories (self care, home management)
-Disability – the inability or the restricted ability toperform actions, tasks, or activities within theindividual’s sociocultural context – in the following categories ( self-care, home management)
-
Lobes of lungs
3 right ( upper, middle, lower)
2 left (upper, lower)- lingual
lower lobe is most of posterior view
-
nose
air enters and filters
warms it, humidify it
-
pharynx
musculomembraneous tube
- 3 parts:
- -nasopharynx
- -oropharynx
- -laryngopharynx
-
larynx
cartilaginous framework
composed of the thyroid, cricoid,and the epiglottis cartilages
Extends anteriorly from thelaryngopharynx between thegreat vessels of the neckdownward to the trachea
-
trachea
Tube about 4 inches long and aninch in diameter consisting ofcartilaginous rings
-
carina
Point of bifurcation into right andleft mainstem bronchi
"Y-shaped" split
-
Bronchi
the right mainstembronchi is most direct–
Right is wider andshorter than the leftmainstem bronchi.
-
alveoli
where the actualexchange of gases (O2and CO2) occurs
-
Ribs
– True Ribs (1-8)
– False Ribs (9-10)
– Floating Ribs (11-12)
-
2 main categories of pulmonary pathophysiology
obstructive dysfunction
restrictive dysfunction
number of diseases can be both
-
Obstructive dysfunction
If the flow of air is impeded, the defect is obstructive
bronchi, tracheae,bronchus, etc.cold, bronchitis
-
Restrictive dysfunction
If the volume of air or gas is reduced, the defect is restrictive
gas exchange
-
Restrictive Lung Disease
Restriction of the lung parenchyma (lung tissue) characterized by stiffness or reducedcompliance
Reduced lung volume
abnormal pulmonary ventilation
- dec. chest wall compliance
- dec. lung volumes
- incr. respiratory rate
-
Classic Clinical Manifestationsof RLD
- Hallmark symptoms include:
- – Dyspnea – shortness of breath
- – Wasted, emaciated appearance
- Pulmonary fibrosis is most commonly associated with RLD
V/Q ratio is low
- Cough, usually dry-sounding and nonproductive
- Tachypnea – fast rate of breathing
Hypoxemia
Corpulmonale- right sided heart failure
-
Abnormalities in Fetal LungDevelopment
- Respiratory Distress Syndrome (RDS) orhyaline membrane disease (HMD)
- – a disorder of prematurity or lack of complete lung maturity.
- Infants of less than 36 weeks gestation often exhibit ( surfactant - developed at 36 weeks- keeps alvelois open- not from collapsing)
Ventilatory dependent infants can alsodevelop RLD. ( higher risk for developing fibrotic lungs if on ventilators too long)
-
Pleural effusions
accumulation of fluidwithin the pleural space
in lung lining
-
Pulmonary edema
an increase in theamount of fluid within the lung. First the fluidis in the interstitium, then the alveoli
in lung tissue
-
Pulmonary emboli
severe back/upper thoracic pain
-
PT Treatment of RLD
- Bronchial hygiene techniques
- – Breathing exercises
- – Coughing techniques
- – Respiratory muscle training
- – Chest mobility,
- posture exercises
- – Exercise training
-
Chronic obstructive lung diseases
obstruction to airflow
This affects both the mechanical function and gas exchangingcapability of the lungs.- poor difussion
-
Physical symptoms characteristic of COPD include
- Chronic, productive cough–
- Wheezing (expiratory sound)
- – Dyspnea on exertion (DOE)
cilia are dying
-
Important markers for COPD
expiratory flow rates ( FEV1)- increase
residual volume (RV)- increase
-
Pathological changes seen in most COPD
- Increased mucus production (or impairment of mucusclearance)
- – Inflammation of the mucosal lining of the bronchi andbronchioles
- – Changes decrease the size of bronchial lumen and increaseresistance to airflow.
- – Loss of normal elastic recoil of lung tissue
- – Tendency of bronchial walls to collapse and trap air
- – Over time, entire lung becomes hyper-inflated.
-
Chronic Bronchitis
- Long-term irritation of lining of the tracheobronchial tree
- -Inflammation of the lining
- – Hypersecretion of mucous and destruction of cilia
- Chronic productive cough.
- – Smoke irritation of airways produces bronchoconstriction.
- – Hypoxia _ pulmonary vasoconstriction _ increased pulmonarypressures _ increased workload of RV _RV hypertrophy (RVH)
-
Emphysema
- • Repeated inflammation ofthe bronchial tubes or airpassages
- • edema, inflammation, andbronchial dilation
- • destruction of respiratorybronchioles and alveolarwalls
- • bronchiolar collapse duringexpiration.
increased airway resistance and decreased lung elastic recoil
decreased elastic recoil of lungs
-
Clinical manifestations of emphysema
- Dyspnea
- • Cough
- • Diminished nutritionalstatus,
- weight loss
- • Possible spontaneouspursed-lip breathing
- • Distant breath sounds, especially at bases
- • Prolonged expiration
- • Possible end expiratory wheeze, especially on forcedexpiration.
- • Later: signs and symptoms of cor pulmonale
- • “pink puffers” due to increased work of breathing tomaintain relatively normal ABGs.
-
Asthma
- Increased airwayresistance
- • increased WOB
- • increased V/Qmismatching
- • Possibility of respiratorymuscle fatigue
- • respiratory failure
-
Cystic fibrosis (CF)
The most common lethal genetic disease in children
- Characterized by exocrine gland dysfunction
- – involving almost every body system
- – thick, excessive secretions
- – abnormal ciliary function
- – GI (pancreatic enzyme deficiency)
- – integumentary (increased secretion of highly ionized sweat) systems
- – poor growth and weight gain
develop chronic obstructive lung disease
-
Bronchopulmonary Dysplasia
A chronic lung disease of infancy- destroy lung tissue b/c air being forced into lungs on ventilator is too fast and too strong
oxygen dependency lasting beyond 1 month of age
-
pneumonia
- Obstructive-Restrictive disorder
- • Inflammation of the lungparenchyma
- • Caused by– Bacteria– Viruses– Damage to the lungs (rare)
- • Creates an immune response
-
Bronchiectasis
- Bronchial obstruction
- • bronchial dilationwith inflammation
- • increasedintrathoracicpressure required to
- over come increased resistance
- • dilation of airway
- • eventual atelectasis ( alveolar collapse)
- increased hypoxia
- prolonged bronchial obstruction
-
with moderate to severe COPD
x-ray will show
- – widening intercostal spaces
- – flattening of the diaphragm,
- – squared off costophrenic angles
- – rib angles that approach 90 degree angles
-
MRI
Indications:– individuals with abnormal chest x-rays shownodule or mass
May show: an enhanced picture of the massprior to surgical resection or biopsy.
May help to distinguish between a fibrosisand nodule.
-
Bronchography
study of abnormal variationsin anatomy, or grosspathological changes in thebronchial wall and lumen
indications:evaluation of congenitalanomalies, bronchiectasis
-
Bronchoscopy
inspectionof the interior of thetracheobronchial treethrough a bronchoscope
-
ABG
Inverse relationship between PaCO2 and pH
PaC02 decreases- Respiratory Alkalosis
PaC02 increases- Respiratory Acidosis
-
ABG
direct relationship between HCO3 and pH
metabolic involvement
-
Tracheal Deviation
- Tracheas shifts away from affected side
- Pneumothorax (fluid/air in part of lung)• Tumor• Pleural Effusion
- Toward the affected side:
- • Atelectasis (collapse lung)
-
Pharmacokinetics
- Absorption
- – Distribution
- – Metabolism
- – Elimination
-
Pharmacodynamics
- mechanism of action
- drug concentraion
drug effect- cellular, systemic
-
Median effective dose
50% of the populationresponds in the expectedway
-
Median Toxic dose
dose where 50% of thepopulation exhibit toxiceffects
-
Dose response curves
Range of effectiveness– Potency
-
Bronchoconstriction process
Within the (ANS), there aretwo nucleotides associatedwith smooth muscle tone - cAMP, cGMP
-
cAMP
– responsible for smooth musclerelaxation or bronchodilation
– as well as inhibition of mastcell
-
cGMP
– increase in cGMP causes smooth muscle contraction or bronchoconstriction
– the release of histamines andother mediators may also beenhanced by increasing cGMPbronchoconstriction
-
Adganergic receptors
- Beta 1- heart
- Beta 2- lungs, if stimulated increase cAMP- increase bronchodilation
- Alpha- if stimulated- decrease cAMP and inc cGMP- increase brochoconstricion
-
Stimulation of alpha receptors
causes contraction of bronchial smooth muscle and the myocardium
-
Stimulation of beta 1
receptors stimulatecardiac tissue
-
Stimulation beta 2 receptors
cause relaxation of bronchial smooth muscle
-
Bronchodilator Therapy Drugs
- – have no alpha-receptor activity
- – more specific beta 2 receptor activity
both are sympathomymemtic- mimic sympatheticnervous system
-
Beta 2-specific agents
- – produce bronchiolardilation by relaxing bronchial smooth muscle
- – dilating effects of increased cAMP levels.
both are sympathomymemtic- mimic sympatheticnervous system
-
Bronchodilators
- Medication is inhaled
- increases the diameter of the lumen of a bronchus
- side effects are less severe
- Positive effects on exercise:
- -Bronchodilation, increased strength of diaphragm, decreased dyspnea, improved exercise tolerance, improved ventilation
- Negative effects on exercise:
- -Tachycardia, chest pain, palpitations
improves quality of life not survival rate
-
Anticholinergics
- Bronchodilator
- Competitive inhibition of muscarinic cholinergic receptors
- Blocks acetylcholine at parasympathetic sites in bronchial smooth muscle
- May block reflex bronchoconstriction
- Side Effects: headache, nervousness, nausea, dry mouth, cough, nasal dryness
-
Sympathomimetics
Drugs that stimulate the sympathetic receptors
- Response varies depending on
- -the intensity of the receptor reaction, the route of administration, the dosage
Epinephrine and ephedrine- stimulates alpha, beta 1 and beta 2 receptors
-
Beta 2 agonists
Mediate bronchodilation & vasodilation
Bronchodilation of smooth muscle of the airways
Increases cAMP- results in smooth muscle relaxation, mast cell stabilization
-
Alpha sympatholytics
Reduce vasoconstriction and bronchoconstriction
Inhibit the decrease of cAMP
-
parasympatholytics
work to inhibit parasympathetic stimulation-preventing an increase in cGMP, thus producing an increase in cAMP
Bronchodilation
-
Bronchodilators- LABD
act by suppressing the immune system
More for preventive measures
No effect for immediate relief of asthma attack
-
Methylzanthines
- LABD
- Intracellular level of cAMP enhanced by inhibiting its degradation process
- Blocks inactivation of cAMP
- Inhibits prostaglandins, adenosine receptor blockade
- Enhances of endogenous catecholamine levels
- Inhibit cGMP and enhancement
- Improved diaphragmatic contractility & ↓ diaphragmatic fatigue
-
Glucocorticoids (corticosteroids)
- SABD
- Mechanism of Action (Hypothesized)-Suppresses the process of IgE-mediated bronchoconstriction- Blocks or inhibit many mediator substances.
Considered the drug of choice during an acute attack
methyprednisolone-usually administered intravenously-severe episodes
Oral (prednisone) or inhaled route- prolonged used, fewer side effects
-
Leukotriene Inhibitors - LABD
Leukotriene: strong inflammatory mediators
- induce bronchoconstriction
- increase airway hyper-responsiveness
- cause smooth muscle hypertrophy
- mucus hypersecretion
- influx of eosinophils into airway tissues
inhibition of the action of leukotrienes
- taken orally and are combined with other drugs
- Side effects: hepatic impairment, headaches, fatigue, nausea, and vomiting
-
Decongestants
- Reduce edema and discharge in upper respiratory tract
- Stimulate vasoconstriction
- Positive effects on exercise
- Allow for increased respiratory ability
- Negative effects on exercise
- Hypertension, palpitations
-
Antihistamines
- Treat allergic responses caused by seasonal allergies
- Decrease mucosal congestion, irritation and discharge
- Positive effects on exercise
- Improved air flow to and from the lungs
- Negative effects on exercise
- Fatigue, loss of coordination
-
Antitussives
- Decrease ineffective, hacking cough
- -blocks receptors in the brain that control cough
- Positive effects on exercise
- -Allow for breathing with decreased irritation, therefore and increased ability to exercise
- Negative effects on exercise
- -Decreased motivation for physical activity
-
Mucoactive
Increase movement and removal of lung secretions
- Positive effects on exercise
- -Less mucus in lungs-therefore increased surface area
- Negative effects on exercise
- -Bronchospasms▪decrease the flow of air to and from the lungs
- -Coughing▪limiting a person’s activity level
-
Respiratory Stimulants
Increase output of central respiratory centers
Analeptics
Positive effects on exercise- Increase available oxygen to body
Negative effects on exercise-May cause hyperventilation-decreased respiratory capacity-convulsions
|
|