Respiratory Flashcards
Describe the causes of upper airway obstruction
Tongue.
- if a pt has altered level of consciousness, the jaw relaxes and the tongue can fall back against the posterior wall of the pharynx, closing off the airway.
- partial obstruction will cause snoring respirations.
- complete obstruction will cause no respirations.
Foreign Body.
- signs include:
- choking
- gagging
- stridor
- dyspnoea
- aphonia(inability to speak)
- dysphonia(difficulty speaking)
- typical victim of foreign body airway obstruction is middle-aged or older, wears dentures, and has been drinking alcohol which depresses protective reflexes, adversely affecting their judgement regarding how large a piece of food can sensibly be place in the mouth.
- pt’s with conditions that decrease the airway reflexes(eg, stroke) are also at increased risk.
- a foreign body may cause a mild or sever airway obstruction, depending on the size of the object and its location in the airway.
Layngeal Spasm(Laryngospasm) and Oedema.
- laryngospasms results in spasmodic closure of the vocal cords, completely occluding the airway.
- often caused by trauma during overly aggressive intubation or immediately upon extubation, especially if pt has altered level of consciousness.
- laryngeal oedema causes the glottis opening to narrow or close completely.
- commonly caused by:
- epiglottitis
- anaphylaxis
- inhalation injury(eg, burns to upper airway)
Fractured Larynx.
- airway patency relies on good muscle tone to keep the trachea open.
- fracture of the larynx increases airway resistance by decreasing airway size secondary to decreased muscle tone, laryngeal oedema, and ventilatory effort
- advanced airways may be required to maintain open airway.
Aspiration.
- in addition to obstructing an airway, aspiration destroys delicate bronchiolar tissue, introduces pathogens into the lungs, and decreases a pt’s ability to ventilate(or be ventilated).
- suction should be readily available for any pt who is unable to maintain their own airway, and the assumption should be made that their stomach is full.
- aspiration of blood or other fluid significantly increases mortality.
Describe the causes of common upper respiratory tract infections; pharyngitis, otitis media, sinusitis
Upper Respiratory Infections(URI’s) are contagious.
The causative agent is transmitted by aerosolised droplets, eg. sneezing/coughing
Pharyngitis.
- Pharyngitis is inflammation of the back of the throat, known as the pharynx
- symptoms include:
- sore throat
- fever
- runny nose
- cough
- headache
- hoarse voice
- most cases are caused by a viral infection
- acute pharyngitis may be catarrhal, purulent or ulcerative, depending on the causative agent and the immune capacity of the affected individual
- chronic pharyngitis may be catarrhal, hypertrophic or atrophic
Otitis Media.
- inflammation of the middle ear
- most common in infants and young children as consequence of URI’s
- rare in adults as, during growth of the head and neck the Eustachian tube straightens, enabling gravity to facilitate drainage of the middle ear
- pharyngeal oedema causes obstruction of the Eustachian tube, with reluctant loss of air in the middle space, development of negative pressure, and seepage of fluid into the middle ear from the surrounding membranes
- virus’s causing URI’s can infect the lining of the Eustachian tube and middle ear, causing both swelling and subsequent blocking of the tube, and increased secretions
- the accumulated fluid in the middle ear causes severe pain, and provides a fertile culture medium for bacteria to grow, if present
- child may be irritable and inconsolable, and often is feverish
- with suppurative otitis media the ear drum can rupture, resulting in drainage of pus from the external ear
- This infection may spread into the skull bone, in particular the mastoid process(thick bony peg behind the ear), and can lead to permanent hearing loss or spread of infection into the brain
- repeated episodes of otitis media can lead to hearing impairment
- chronic low grade otitis media can lead to formation of a mass of keratinised tissue within the middle ear, called a cholesteatoma, which in turn can become infected or erode the structure of the middle ear, resulting in hearing loss
Sinusitis.
- inflammation of the respiratory mucosa lining the sinus cavities, and obstruction of the openings that drain them result in accumulation of fluid within the sinuses.
- obstruction to drainage can be anatomical, such as:
- deviated nasal septum
- oedematous thickening of the respiratory mucosa during inflammation
- inflammation can be result of an infectious agent, usually viral and accompanying a URI, or it my be allergic
- although inflammation and fluid accumulation are enough to trigger the symptoms of sinusitis, the fluid or mucus can also become infected by bacteria/fungi
- symptoms include:
- nasal congestion
- headaches
- facial pain(particularly over affected sinus)
- thick/discoloured mucoid discharge from the nose
- postnasal drainage
- fungal sinusitis is more common in diabetic /immunocompromised pt’s
Differentiate between croup and epiglottitis
Croup.
- viral infection of the upper airway
- the virus has an affinity for the SUBglottic space(the narrowest part of a paediatric airway)
- causes oedema and progressive airway obstruction
- turbulent airflow through the narrowed subglottic airway causes stridor and barking cough
- most common in children between 6mths and 6yrs
- usually occurs at night in spring/autumn/cool air
Epiglottitis.
- inflammation of the SUPRAglottic structures, usually due to bacterial infection
- any age
- any time
- typical signs are:
- drooling
- fever
- hoarse voice
- hyperextension of the neck
Describe the pathophysiology of Asthma
Results from spasm of the bronchi.
Episodic: certain triggers cause bronchospasm. and removal of the trigger usually resolves the bronchial obstruction.
Signs/symptoms:
- chest tightness
- S.O.B
- wheeze on inhalation/exhalation
- cough
- anxious/frightened
- excessive mucus formation during attack, which is coughed up during recovery
Chronic cases cause histologic changes:
- bronchial muscle hypertrophy
- hyperplasia of mucus glands
Diagnosis:
- clinical demonstration of airway obstruction by spirometry and its reversibility by administration of bronchodilators
Bronchospasm:
- caused by constriction of the smooth muscle that surrounds the larger bronchi.
- When air is forced through the constricted tubes, the airflow speeds up and becomes turbulent, causing the tube to vibrate, this creates the sound of wheezing.
- Bronchospasm and turbulent airflow will reduce the peak expiratory flow.
Bronchial oedema:
- swelling of the bronchioles, also creates turbulent airflow, wheezing, and air trapping
Increased Mucous Production:
- thick secretions may plug the distal airways and contribute to air trapping
- asthmatics may be significantly dehydrated due to increased fluid loss from tachypnoea and often poor fluid intake
- dehydration makes secretions thicker, worsening symptoms
Describe the pathophysiology of Emphysema
Chronic weakening and destruction of the walls of the terminal bronchioles and alveoli.
Most cases caused by smoking
Some caused by congenital enzyme deficiency(Alpha-antitrypsin deficiency).
In pure emphysema, breakdown of the connective tissue structure of the terminal airways results in groups of alveoli merging into large ‘blebs’ or ‘bullae’, which are far less efficient and collapse far more easily(causing obstruction) than does normal lung tissue.
Many pt’s with emphysema have a barrel chest caused by chronic lung hyperinflation, and are often tachypnoeic, as they attempt to maintain normal CO2 levels despite their dysfunctional lungs.
Pt’s often use extreme amounts of energy attempting to breathe, cannabalising their own muscle mass in the process.
Pink Puffers.
Describe the pathophysiology of Bronchitis
Chronic bronchitis defined as:
- sputum production on most days of the month
- for 3 months of more, of the year
- for more than 2 years
Hall mark of the disease is excessive mucous production in the bronchial tree, which is nearly always accompanied by a chronic or recurrent productive cough.
Typical pt:
- heavy cigarette smoker
- obese
- congested
- bluish complexion
- abnormal blood gases:
- elevated pCO2(hypercapnia)
- decreased pO2(hypoxaemia)
- often associated heart disease/R-heart failure
Blue Bloaters.
Describe the pathophysiology of pulmonary infections, including pneumonia
Bacteria, viruses, fungi, mycoplasmas and other agents cause infections.
Respiratory tract is vulnerable to airborne agents, as well as those normally found in the nose and throat that migrate into the bronchi and lungs.
Generally infectious disease cause:
- swelling of the respiratory tissues
- increase in mucus production
- production of pus
Swelling in well-perfused Respiratory tissue can be dramatic, particularly in the upper airway.
This is problematic because the resistance to airflow goes up exponentially when tube diameter is narrowed(Poiseuille’s Law).
Alveoli can become non-functional when filled with pus, eg. pneumonia.
Similar to collapsed or fluid-filled alveoli, pus filled alveoli do not participate in gas exchange, instead contributing to a ‘shunt’ where blood passes through the lungs without being oxygenated, sometimes causing hypoxaemia.
Problems with ventilation, perfusion, or both prevent oxygen reaching the bloodstream.
Briefly describe the pathophysiology of lung cancer
Most lung cancers(bronchogenic carcinoma’s) arise from stem cells in the bronchial epithelium.
classification involves determining the type of cell the malignant ones resemble.
Most commonly:
- squamous cell carcinoma
- adenocarcinoma
For purpose of treatment and prognostication cancers classified as:
- small cell carcinoma(more common, initial response to chemotherapy, not curable surgically, rapidly fatal)
- non-small cell carcinoma(curable surgically)
Numerous variants of non-small cell carcinoma, of which, some have predilection for certain areas of the lungs, eg. squamous cell is more often central(hilar), while adenocarcinoma often arises in scar tissue in the periphery of the lung.
These carcinomas invade adjacent tissues, such as pleura, chest wall and mediastinal structures.
Some symptoms of cancer can be related to direct extension of the tumour, such as hoarseness, from involvement of the recurrent laryngeal nerve.
Others are related to obstructive symptoms, as the cancer grows into and occludes the bronchi, such as:
- dyspnea
- pneumonia
- haemoptysis
Spread to lymph nodes of the hilar region is common, as is haematogenous spread to many organs.
Metastasis to the brain/bone Is notorious for producing clinical problems. Liver metastasis is fairly universal in terminal stages.
Briefly describe pulmonary oedema
Fluid from the blood plasma has migrated into lung parenchyma(tissue making up the walls of the capillaries and alveoli), compromising gas exchange, long before signs of wetness become noticeable.
Causes of Pulmonary oedema:
- heart failure resulting from L-side acute M.I
- inhaled toxins, causing direct damage to alveolar tissue, resulting in fluid seepage into the lungs
- drugs in the blood stream, eg. heroin
- irritants, eg. inhaled water after drowning event
- high altitude pulmonary oedema, can occur in people who climb above 2,000m
- systemic inflammatory response syndrome, eg. trauma, large burns, pancreatitis, infections can result in pulmonary oedema and potentially acute respiratory distress syndrome
Describe the pathophysiology of pulmonary emboli
potentially fatal condition resulting when a thrombus from the leg or pelvic veins is carried to the right heart and pumped into the pulmonary arteries.
diagnosis difficult but usually involves some degree of dyspnoea of sudden onset, and sometimes accompanying pleuritic chest pain.
if they are small and carried to the periphery of the lung, emboli often resolve without significant injury.
various conditions can cause P.E:
- prolonged immobility/bed rest
- recent surgery
- leg/pelvic fractures
- pregnancy
- obesity
- underlying malignancy
- airplane rides
- underlying coagulopathy
when a large embolus occludes the pulmonary arteries at their bifurcation(saddle embolus), P.E. can cause sudden death.
Describe the pathophysiology of the chest injury - Tension pneumothorax
life threatening condition that results from continued accumulation of air under pressure within the intrapleural space.
Air enters the pleural space via an open thoracic injury, an injury to the lung parenchyma due to blunt trauma, barotrauma due to positive-pressure ventilation, or tracheobronchial injuries due to shearing forces.
the associated injury causes a one-way valve to develop, allowing air to enter the pleural space, nut not to exit from it.
as it continues to accumulate, the air exerts increasing pressure against the surrounding tissues.
this pressure compresses the involved lung, diminishing its ability to oxygenate blood or eliminate CO2 from the blood.
left untreated the affected lung begins to exert pressure on the mediastinum, pushing/displacing it away from the injured side.
the pressure may exceed that within the major venous structures, decreasing venous return to the heart, diminishing preload, and eventually resulting in shock.
as venous return decreases, compensation increases the heart rate in an attempt to maintain cardiac output.
Describe the pathophysiology of the chest injury - Open pneumothorax
occurs when a defect in the chest wall allows air to enter the pleural space.
results from penetrating trauma, eg. gunshot/knife wounds.
penetrating injury creates a link between the external environment and the pleural space.
with each inspiration, the negative pressure created within the thoracic cavity draws more air into the pleural space.
as the pneumothorax increases in size, the lung on the involved side loses its ability to expand.
if the defect in the chest wall is more than 2/3 the diameter of the glottic opening, air is more likely to enter the chest wall rather than entering via the trachea.
as a consequence, expansion of the chest wall may draw air through the chest wound, potentially creating a ‘sucking chest wound’.
collapse of the affected lung creates a mismatch between ventilation and perfusion.
assuming that the pulmonary vasculature on the injured side is intact, the heart will continue to perfuse the lung, whilst the pneumothorax prevents ventilation.
the result is an inability to deliver oxygen to the affected lung, therefore reduced oxygenation and an inability to eliminate CO2.
Describe the pathophysiology of the chest injury - Massive haemothorax
occurs when blood accumulates between the parietal and visceral pleura.
most commonly caused by tears of the lung parenchyma or rib fractures, but may also result from penetrating wounds that puncture the heart or major vessels within the mediastinum, or from blunt trauma with deceleration shearing of major vessels.
the collection of blood within the pleural space compresses and displaces the surrounding lung, limiting capacity for adequate oxygenation and ventilation.
unlike pneumothorax, this injury has potential to cause hypovolaemia.
massive haemothorax is defined as accumulation of more than 1,500ml of blood within the pleural space(25-30% blood volume loss in the average adult), with the potential for a pt to progress into decompensated shock.
as each lung can hold up to 3,000ml, it is possible for a pt to completely bleed out into the thoracic cavity.
Describe the pathophysiology of the chest injury - Flail chest
a major injury to the chest wall, that may result from a variety of blunt force mechanisms such as:
- falls
- RTC
- assault
- birth trauma
flail segment defined as 2 or more adjacent ribs that are fractured in 2 or more places.
the segment between those 2 fracture sites becomes separated from the surrounding chest wall.
the location and the size of the segment, affect the degree to which the flail segment will impair chest wall motion and subsequent air movement.
in flail sternum, the sternum is is completely detached from the ribs because of fractures or ruptured costal cartilage, resulting in mechanical dysfunction of both sides of the chest and more severe respiratory impairment.
when a flail segment occurs, the underlying physiological pressures begin to cause paradoxical movement of the segment when compared to the rest of the chest wall:
- expansion of the chest wall on inspiration results in negative pressure within the thoracic cavity, which in turn draws the segment in towards the central of the chest
- as chest muscles relax, the resulting positive pressure forces air out of the lungs, and the segment is pushed outwards, and away from the thoracic cavity
because of these movements, the lung tissue beneath the flail segment is not adequately ventilated.
during early stages of the injury, muscular spasm may contribute to splinting the chest wall, and the condition may not become apparent until a pt becomes exhausted and the paradoxical movement ensues.
