Week 5: Resp Flashcards
Which structures compose the large airways?
The trachea and two segmental bronchi
Describe the 3 layers of the large airways
The trachea and bronchi have the following 3 layers:
inner layer - epithelial lining that has ciliated cells and goblet cells. The goblet cells secrete mucous to catch bacteria and protect that airway. The ciliated cells then work to move that mucous out of the airway to either be expectorated or swallowed.
middle layer - smooth muscle. The muscle is innervated by the autonomic nervous system.
The outer layer is a connective tissue layer of cartilage that supports the structure
What is the significance of beta 2 adrenergic receptors in the airways?
The middle muscle layer is innervated by the autonomic nervous system.
The SNS if activated stimulates beta 2 adrenergic receptors which result in bronchodilation.
The PNS if activated stimulates the muscarinic receptors which result in bronchoconstriction.
Which structures compose the small airways?
Bronchioles and alveoli
What are the two major differences between the makeup of the small airways and large airways?
The small airways lack cartilage
The small airways contain club cells (secrete gylcosaminogylcans to protect airways)
Define Tidal Volume
The volume exhaled in a normal breath (normally about 500mls of air)
Define Expiratory Reserve Volume
The amount of extra air, (above normal tidal volume) exhaled during a forceful breath out. (normally an extra 1000mls of air can be expired)
Define Inspiratory Reserve Volume
The volume that can be inhaled above tidal volume is the inspiratory reserve volume (normally an extra 3300mls of air can be inspired)
Define Vital Capacity
The largest volume of air that can be moved in and out during ventilation
Define FEV1
Forced expiratory volume in 1 second
Define Residual Volume
Air that remains in the respiratory tract after maximal expiratory effort (The residual volume is the amount of air that is left after expiratory reserve volume is exhaled)
What is lung compliance?
the measure of lung and chest wall distensibility and is defined as volume change per unit of pressure change
Which 2 factors influence lung compliance
Determined by the alveolar surface tension (surfactant lowers surface tension) and elastic recoil of lung and chest wall.
Provide 2 examples of conditions that result in decreased lunch compliance
Pulmonary Fibrosis:
Excessive amount of fibrous or connective tissues, lungs become stiff and difficult to ventilate–>hypoxemia
Caused by pulmonary diseases (ARDS, TB), autoimmune disorders (rheumatoid arthritis), or inhalation of harmful substances (coal dust, asbestos). (chronic inflammation)
Pulmonary Edema
excess fluid in the lung
most common cause is left sided heart disease. Left ventricle fails = increase in capillary hydrostatic pressure = fluid moves from the capillary to interstitial space. When the flow of fluid out of the capillaries exceeds the lymphatics systems ability to remove it pulmonary edema develops
Capillary injury can result in water and plasma proteins leaking out of capillary and into interstitials pace
What is a V/Q mismatch?
an imbalance between alveolar ventilation and perfusion
Name the two types of V/Q mismatches?
Shunting
Alveolar dead space
Describe shunting and provide a clinical example of when this may occur
Inadequate ventilation of well-perfused areas of the lung
Airway obstruction – blood flow is normal (normal Q), ventilation is decreased (low V) = results in low V/Q
When blood passes through parts of the capillary bed that receive no ventilation, pulmonary capillaries in the area constrict, causing right-to-left shunt = decreased systemic PaO2 and hypoxemia
Examples: atelectasis, asthma, result of bronchoconstriction and in pulmonary edema and pneumonia when alveoli are filled with fluid
Describe alveolar dead space and provide a clinical example of when this may occur
Alveoli are ventilated but not perfused
blood flow is decreased (low Q), ventilation is normal (normal V) = high V/Q
Poor perfusion of well-ventilated areas of the lungs impairs or prevents gas exchange and is wasted ventilation
Most common example: Pulmonary Embolism
What are the 4 types of neurons in the respiratory center
- Dorsal respiratory group (DRG)
- Ventral respiratory group (VRG)
- Pneumotaxic centre
- Apneustic centre
What are the 3 types of lung receptors?
Irritant receptors (C fibres)
Stretch Receptors
J-Receptors (Juxtapulmonary capillary receptors)
Describe sympathetic innervation to the lungs
Fibres in the lung branch to upper thoracic and cervical ganglia of the spinal cord
Cause smooth muscle to relax - control airway calibre (interior diameter of the airway lumen) by stimulating bronchial smooth muscle relaxation
Describe parasympathetic innervation to the lungs
Travel in the Vagus nerve of the lung
Cause smooth muscle to contract - control airway calibre (interior diameter of the airway lumen) by stimulating bronchial smooth muscle to contraction
Main controller of airway calibre under normal conditions
What are the two types of chemoreceptors that contribute to the regulation of ventilation and where are they located?
Central chemoreceptors – located near respiratory center in the brain stem
Peripheral chemoreceptors – located in the carotid and aortic bodies
Which type of chemoreceptor responds to changes in pH(PaCO2) and which type responds to changes in Pa02?
Central chemoreceptors are sensitive to pH or PaCO2 changes, while peripheral chemoreceptors are sensitive to changes in Pa02
Note that Pa02 must drop well below normal (to approx. 60 mmHg) before peripheral chemoreceptors have an influence on ventilation.
What would you expect to see in terms of CO2 level in an acidosis? What would the respiratory system do to compensate for this?
Acidosis would have a high PaC02, the body would increase respiratory rate (to “blow off” extra CO2)
What would you expect to see in terms of CO2 level in an alkalosis? What would the respiratory system do to compensate for this?
Alkalosis would have a lowPaC02, the body would decrease respiratory rate
Explain the changes that occur with chemoreceptors in conditions with chronic hypoventilation, such as COPD or CHF
In cases of chronic hypoventilation (i.e., COPD, CHF) central chemoreceptors become “reset” and are less sensitive & become dysregulated - leads to poor ventilation
The peripheral chemoreceptors become the major stimulus to ventilation when the central chemoreceptors are reset by chronic hypoventilation
What is the mechanism of hypoventilation? Does it lead to respiratory acidosis or alkalosis?
inadequate alveolar ventilation in relation to metabolic demands
Decreased ventilation (frequency (RR), breath depth (tidal volume) = lungs blow off too little CO2
CO2 gain = decreased blood pH (<7.35) = respiratory acidosis
What is the mechanism of hyperventilation? Does it lead to respiratory acidosis or alkalosis?
alveolar ventilation exceeds metabolic demands
Increased ventilation (frequency, breath depth) = lungs blow off too much CO2
CO2 loss = increased blood pH (>7.45) = respiratory alkalosis
Provide examples of causes of hypoventilation
Respiratory-center abnormality in brainstem (stroke/medication overdose, etc)
Respiratory muscle-contraction failure (obesity, trauma, neuromuscular disorders such myasthenia gravis)
Airway obstruction
Impaired gas exchange between alveoli/capillary (COPD, pneumonia, pulmonary edema)
Provide examples of causes of hyperventilation
Resp-centre abnormality in brainstem
Low O2 levels (hypoxia): pneumonia, PE, etc.
Anxiety, panic attacks, sepsis, salicacylates
Asthma is an inflammatory disorder of the airways characterized by paroxysmal or persistent symptoms, such as:
Dyspnea
Chest tightness
Wheezing
Sputum production and cough
-From Mark RRT presentation
Discuss the patho of COPD
Inhaled irritant (cig smoke, other noxious particles) cause lung inflammation
Persistent inflammation of small and large airways, lung parenchyma and its vasculature
Chronic inflammation results in tissue destruction
-Air trapping
-Progressive airflow limitation
The inflammatory process in COPD is different than in asthma
-From Mark RRT presentation
What does spirometry do?
-Measures volumes and airflow
-Provides objective assessment of severity of airflow limitation: Reversibility and variability
-Uses predicted values based on age, height, sex, ethnic background
-From Mark RRT presentation
In spirometry, what measurement is this referring to:
“Maximal volume of air exhaled in the first second of forced expiration.”
Forced Expiratory Volume in first second (FEV1)
-From Mark RRT presentation
In spirometry, what measurement is this referring to:
“Volume of air exhaled during a maximal rapid complete exhalation.”
Forced Vital Capacity (FVC)
-From Mark RRT presentation
In spirometry, what does this measure:
“FEV1/FVC
Proportion (%) of total volume of air which can be exhaled in first second.
-From Mark RRT presentation
What is a normal or expected FEV1 percentage?
80% and above. Meaning 80% of lung expiratory volume (or Forced Vital Capacity FVC) is forcefully exhaled in the first second.
-From Mark RRT presentation
What FEV1/FVC value would indicate COPD?
Anything below 0.7, or 70%
-From Mark RRT presentation
What are the ranges (in %) of FEV1 that indicate the severity of COPD?
Normal = 80%+
Moderate = 50-79%
Severe = 30-49%
Very severe = less than 30%
-From Mark RRT presentation
What measurable changes are you looking for in post-bronchodilator spirometry that would be considered clinically significant indicator or reversibility in an obstructive airway disease such as COPD or asthma?
At least a 12% improvement and an increased FVC of at least 200 mls
-From Mark RRT presentation
In patients with COPD, what is a useful breathing technique to help them with activities that require some exertion?
Pursed-lipped breathing. It helps them to force additional air out of their lungs before they begin movement, and decreases the amount of air trapped in lungs before they get going.
-From Mark RRT presentation
What is the recommended criteria for referring a patient for spirometry?
Currently smoking/have ever smoked and >40 yrs of age with ONE of:
-persistent cough & sputum production; or
-frequent respiratory tract infections; or
-progressive SOBOE
Consider workplace history if patient is not/has never been a smoker. -noxious inhalants
-From Mark RRT presentation
What is Benign Paroxysmal Positional Vertigo (BPPV)?
Dizziness caused from crystals moving into semicircular canals that obstruct the normal flow of endolymph
T/F Meniere’s disease is the most common cause of peripheral vertigo?
False - BPPV is more common
Risk factors for BPPV
Older age
History of head trauma or whiplash
Inflammation of the vestibular nerve
Ear surgery
Residual effect of Meniere’s Disease
Herpes zoster oticus and inner ear ischemia
Patho of BPPV
Calcium carbonate crystals normally found in the utricle and saccule, detach and land in the semicircular canals
Crystals in the semicircular canals obstructs the normal flow of endolymph when the head moves in a specific direction
Without normal endolymphatic flow, the semicircular canal cannot properly detect angular acceleration causing vertigo or a sensation of spinning when the head shifts
Does BPPV have sudden or slow onset?
Sudden
How long does BPPV last (each episode) and how long does it take to resolve?
Sudden onset
Sensation of vertigo lasts one minute or less
Usually resolves spontaneously over days to weeks. If treated with repositioning maneuvers, 85% find single maneuver effective
2% require more than 3 treatments
Recurrence fairly common
Does BPPV commonly affect men or women? Young or old?
In one study, one-year prevalence increased with age and was 7 times higher in those older than 60 years compared with those 18-39
Rarely occurs in people younger than 35 unless there is a history of head trauma
More common in women than men in all age groups
S&S of BPPV
Vertigo or a feeling that you are spinning or tilting when you are not which can worsen with certain head movement – like rolling over in bed. Sensation lasts one minute or less
Can be associated with nausea and vomiting
Approximately half of patients complain of imbalance between attacks
Nystagmus during a provoking maneuver
Does BPPV or Menieres present with hearing loss?
Meniere’s
What are the two diagnostic/provoking maneuvers for BPPV?
1) Dix-Hallpike (for posterior canal BPPV)
2) Supine-roll maneuver (horizontal canal BPPV)
What two maneuvers are used as treatment for BPPV?
1) Epley maneuver
2) Semont maneuver
Describe the Epley maneuver
Pt is seated upright facing examiner. Examiner places hands on either side of head and patient holds onto examiners forearms for stability
Examiner turns patient’s head to 45° to affected side and quickly lowers patient to supine position with head extending just beyond examining table with outside ear downward
Examiner moves to head of table and repositions hands. Then head is rotated rapidly to the other side with opposite ear now facing down. This position is held for 30 seconds
Patient then rolls onto L side while examiner rapidly rotates head until nose is angled toward floor. Position is held for 30 seconds
Patient is then rapidly lifted into sitting position.
Repeat entire sequency until no nystagmus can be elicited
Describe the Semont maneuver
Examiner turns patient head 45° to unaffected side and patient is quickly lowered to the affected side. Position is held for 30 seconds or until any provoked vertigo subsides
Patient is quickly sat up and is rapidly lowered down to other side with head will turned at 45° to unaffected side – face is now partly down into the bed. Position is held for 30 seconds or until vertigo subsides
Patient returns to upright position.
Maneuver is repeated until patient is asymptomatic
Patient teaching for acute episodes of BPPV
Bedrest with head of bed up and reassurance that most recover spontaneously over a period of several weeks to months
Encourage compliance of bedrest and exercises
Patient can perform repositioning maneuvers on their own tid until vertigo free for 24 hours
What causes Meniere’s disease?
Dizziness caused by build up of fluid – endolymph in inner ear
Onset of Menieres
Symptoms typically begin between the ages of 20 and 40 years.
Incidence ranges from 10 to 150 per 100,000 persons
Among those who have Meniere’s disease, bilateral disease occurs in 10 to 50% of patients
Risk factors for Meniere’s disease
Family history
Autoimmune disease (diabetes, lupus or rheumatoid arthritis
Head injury, especially if it involved the ear
Viral infection of inner ear
Allergies
Patho of Meniere’s. Is there a physical exam that we can do to confirm excess endolymph?
Also known as Endolymphatic hydrops – pathologic lesion of Meniere’s disease, which can only be diagnosed by post-mortem histopathologic analysis of the temporal bone
Causes distortion and distension of the membranous, endolymph-containing portions of the labyrinth that disrupts vestibular and hearing functions
Unknown etiology
Menieres: How long does an attack last? Are they recurrent? How do you feel between attacks?
Comes on quickly and can last from 20 minutes to 24 hours
Most people have repeated attacks over a period of years
Can have disequilibrium between attacks
10% of patients can have disabling symptoms despite treatment and lifestyle changes
What is the triad of symptoms in Menieres disease?
1) Vertigo – feeling that you or your surroundings are spinning that can minutes to hours often accompanied by severe nausea and vomiting
2) Tinnitus – can be constant or fluctuate. Pitch and intensity vary
3) Hearing loss – can be temporary or permanent.
- Usually fluctuates and often initially affects only the lower frequencies
- Typically progresses and often results in permanent hearing loss at all frequencies
Diagnostic criteria for Menieres?
2 or more spontaneous episodes of vertigo, each lasting 20 min to 12 hours
Low-mid frequency sensorineural hearing loss in affected ear – measured with audiometry
Fluctuating symptoms of reduced or distorted hearing, tinnitus or fullness in affected ear
Ruled out other vestibular diagnoses
To meet diagnostic criteria, patients typically have auditory and/or vestibular symptoms for 3-5 days
Tx of Menieres
Goals of treatment are symptom relief. Treatment cannot fix underlying abnormal pathophysiology
Diet and lifestyle adjustments to limit sodium, caffeine, alcohol and nicotine
Vestibular rehabilitation therapy for residual disequilibrium between attacks
Pharmacotherapy to reduce intensity and severity of attacks include daily vasodilators and diuretic therapy and PRN vestibular suppressants and antiemetics
For chronic management: vasodilators (betahistine), duretics, antiemetics…
What is labrynthitis?
Viral or post-viral inflammatory disorder affecting the inner ear. Inflammation causes vertigo
AKA Vestibular Neuritis
Risk factor for labrynthitis?
Recent cold or flu
Patho of labrynthitis?
Inflammation of the membranous labyrinth caused by virus, bacteria or systemic disease
Inflammation affects the vestibular portion of cranial nerve VIII – the vestibular nerve which causes the nerve to send incorrect signals to the brain that the body is moving
Other senses such as vision, do not detect same movement
Confusion of signals causes feeling of vertigo
Time course of labrynthitis?
Severe symptoms for 1-2 days followed by gradual diminution of symptoms and a return of equilibrium
Residual imbalance and non-specific dizziness can last for months
Often starts 1-2 weeks after flu or cold
Usually not recurrent
S&S of labrynthitis?
Vertigo that begins without warning
Nausea & vomiting
Gait instability
When you do the Dix-Hallpike maneuvers for diagnosis of posterior canal BPPV, what do you see for nystagmus?
Nystagmus and vertigo usually appear with a latency of a few seconds and lasts less than 30 seconds
Nystagmus has typical trajectory, beating upward and turning to affected side
After nystagmus stops and the patient sits up, the nystagmus will recur but in the opposite direction
If nystagmus is provoked, maneuver should be repeated to the same side, with each repetition, the intensity and duration of nystagmus will diminish
If nystagmus not provoked, maneuver should be repeated with the head turned to the other side
How do nystagmus present in labrynthitis?
Physical exam finds:
Spontaneous vestibular nystagmus that is unidirectional and horizontal
Nystagmus is suppressed with visual fixation and does not change direction with gaze
Fast phase of nystagmus beats away from affected side
With rapid turning of the head, patient is unable to maintain visual fixation
Diagnosis is largely based on clinical presentation of an acute sustained vestibular syndrome with features consistent with the nystagmus described above
