week 5 respiratory Flashcards
pleura
Thin, transparent, double-layered serous membrane lining thoracic cavity & encasing lungs
Parietal layer: lines pulmonary cavities & adheres to thoracic wall, mediastinum & diaphragm
Visceral layer: covers lung & adheres to all its surfaces
conducting airway
Nasal passages, mouth & pharynx, larynx, trachea, bronchi & bronchioles
mucociliary blanket
- Cilia are in constant motion to remove foreign materials
- Cilia are in constant motion to remove foreign materials
Gas exchange within lungs depends on
Open airways
Expansion of lungs
Adequate surface area for gas diffusion
Blood flow through the pulmonary capillary bed.
Acute Respiratory Failure - Hypoxemic
lack of O2 or insufficient amount
Acute Respiratory Failure - Hypoxemic- Ventilation-Perfusion Mismatch
Ventilation-Perfusion Mismatch: areas of lung are ventilated but not perfused, or vice versa
Portion of lung is either being inadequately ventilated, or perfused
Results in carbon dioxide retention
CO2 is a stimulus for respiration, so respiratory rate (RR) increases to prevent hypercapnia (excessive carbon dioxide levels
Increased RR & work of breathing extremely tired patient
Acute Respiratory Failure - Hypoxemic- Impaired Diffusion
gas exchange between alveolar air & pulmonary blood impeded
Due to increased distance for diffusion OR decreased permeability of respiratory membranes
Gas exchange affected, often due to surface area issue (E.g. ARDS pulmonary oedema, pneumonia – all involve fluid within lung)
Acute Respiratory Failure – Hypercapnic/Hypoxemic
-Ventilating insufficiently to clear CO2 & maintain normal O2 levels (hypoventilation)
-Causes increased PCO2 &, typically, hypoxemia
-results from Respiratory centre (CNS) depression (drug overdose, brain injury)
Diseases of nerves supplying respiratory centre (Guillain-Barre syndrome, spinal cord injury)
Disorders of respiratory muscles (muscular dystrophy)
Chronic lung disease (COPD)
Thoracic cage disorders (crushed chest)
acid-base balance
If acidosis/alkalosis occur, respiratory system regulates respiratory rate to return normal pH
Chemoreceptors detect changes in pH & respond:
Acidaemia: increased respiratory rate & depth to eliminate CO2
Alkalaemia: decreased respiratory rate & depth to retain CO2
solubility of CO2
CO2 is 20x more soluble in plasma than O2
respiratory acidosis
Pulmonary ventilation decreases so CO2 rises
Retained CO2 combines with H2O carbonic acid
Dissociates to release free hydrogen & bicarbonate ions
Stimulate increased respiratory drive to expel CO2
respiratory alkosis
Pulmonary ventilation increases leading to excessive CO2 exhalation
-↓CO2 causes cerebral vessel constriction
Dizzy, light headed, tingling & numbness of fingers & toes
-Short periods of apnoea may occur as CO2 level short-term stimulus for respiration
CORD – Emphysema
- caused by smoking and Inherited deficiency of α1-antitrypsin
- results from elastin & other alveolar component breakdown by protease enzymes this breakdown leads to increased airspace size, & loss of elasticity, alveolar wall, and cappilary bed destruction, impairing gas exchange
- leads to hyperinflation of lungs- barrel chest
- pink puffers
AAT
-Protease enzymes damage healthy lung tissue while removing bacteria in acute respiratory dysfunction
-α1-antitrypsin (AAT): protease-inhibitor, protects lung
-Some individuals born without AAT; smokers have inadequate production & release of AAT
Cigarette smoke & other irritants stimulate inflammatory cells in lungs to increase protease enzymes, as part of an inflammatory response
-not enough anti-protease can be produced
-Elastic tissue destruction occurs, & cellular resources cannot counter this
CORD – Bronchitis
- Major & small airway obstruction
- Chronic irritation from smoking & recurrent infections
- History of chronic productive cough for ≥3 consecutive months in ≥2 consecutive years
- Large airways: mucus hypersecretion, associated with hypertrophy of submucosal glands in trachea and bronchi
- Small airways: obstructed,Increased goblet cell numbers Mucus plugging of lumen,Inflammation, Fibrosis of bronchial wall
COPD
both emphesema and bhronchitis
main factors contibuting to CORD
Inflammation
Fibrosis of the bronchial wall
Excess mucus secretion
Obstruct airflow leading to VQ mismatch
PE pulmonary embolism
Blood-borne substance lodges in a pulmonary artery branch, mechanically obstructing flow (obstructive shock)
- thrombus (blood clot), air, fat (occurring from fracture), or amniotic fluid (maternal waters break
- leads to bronchoconstriction in affected area, Wasted ventilation,Impaired gas exchange,Loss of alveolar surfactant
- right heart failure may develop due to massive vasoconstriction if embolism big enough
pneumonia
Inflammation of parenchymal structures of the lung
Four stages of development:
Oedema: alveoli filled with fluid containing multiple organisms causing capillary congestion.
Red hepatisation: massive outpour of leukocytes and red blood cells.
Grey hepatisation: (2+++ days) arrival of macrophages, phagocytose fragmented bacterial cells, red blood cells, cellular debris.
Congestion diminished but lung still firm
Resolution: alveolar exudate removed, lung slowly returns to normal
2 types
-bacterial
-viral
plerisy
Inflammation of pleura
Common in infectious processes, especially pneumonia
pleural effusion
Abnormal collection of fluid in pleural cavity
either excess rate of formation or decreased lymphatic clearance.
-fluid can be pus, blood, intravascular oe extravascular.
-Fluid enters pleural space from capillaries in parietal pleura, & removed by lymphatics
pleural effusion-hydrothorax
accumulation of serous transudate; unilateral or bilateral
Typically caused by congestive heart failure; also renal failure, nephrosis, liver failure or malignancy
pleural effusion= Chylothorax
lymph effusion from GI tract
Trauma, inflammation, or malignant infiltration obstructing chyle transport
pnemothorax
Presence of air in pleural space, causing partial or complete collapse of affected lung
May be spontaneous or traumatic.
