Week 5: Resp

Question 1

Which structures compose the large airways?

Answer 1

The trachea and two segmental bronchi

Question 2

Describe the 3 layers of the large airways

Answer 2

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

Question 3

What is the significance of beta 2 adrenergic receptors in the airways?

Answer 3

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.

Question 4

Which structures compose the small airways?

Answer 4

Bronchioles and alveoli

Question 5

What are the two major differences between the makeup of the small airways and large airways?

Answer 5

The small airways lack cartilage

The small airways contain club cells (secrete gylcosaminogylcans to protect airways)

Question 6

Define Tidal Volume

Answer 6

The volume exhaled in a normal breath (normally about 500mls of air)

Question 7

Define Expiratory Reserve Volume

Answer 7

The amount of extra air, (above normal tidal volume) exhaled during a forceful breath out. (normally an extra 1000mls of air can be expired)

Question 8

Define Inspiratory Reserve Volume

Answer 8

The volume that can be inhaled above tidal volume is the inspiratory reserve volume (normally an extra 3300mls of air can be inspired)

Question 9

Define Vital Capacity

Answer 9

The largest volume of air that can be moved in and out during ventilation

Question 10

Define FEV1

Answer 10

Forced expiratory volume in 1 second

Question 11

Define Residual Volume

Answer 11

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)

Question 12

What is lung compliance?

Answer 12

the measure of lung and chest wall distensibility and is defined as volume change per unit of pressure change

Question 13

Which 2 factors influence lung compliance

Answer 13

Determined by the alveolar surface tension (surfactant lowers surface tension) and elastic recoil of lung and chest wall.

Question 14

Provide 2 examples of conditions that result in decreased lunch compliance

Answer 14

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

Question 15

What is a V/Q mismatch?

Answer 15

an imbalance between alveolar ventilation and perfusion

Question 16

Name the two types of V/Q mismatches?

Answer 16

Shunting

Alveolar dead space

Question 17

Describe shunting and provide a clinical example of when this may occur

Answer 17

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

Question 18

Describe alveolar dead space and provide a clinical example of when this may occur

Answer 18

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

Question 19

What are the 4 types of neurons in the respiratory center

Answer 19

1. Dorsal respiratory group (DRG)
2. Ventral respiratory group (VRG)
3. Pneumotaxic centre
4. Apneustic centre

Question 20

What are the 3 types of lung receptors?

Answer 20

Irritant receptors (C fibres)

Stretch Receptors

J-Receptors (Juxtapulmonary capillary receptors)

Question 21

Describe sympathetic innervation to the lungs

Answer 21

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

Question 22

Describe parasympathetic innervation to the lungs

Answer 22

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

Question 23

What are the two types of chemoreceptors that contribute to the regulation of ventilation and where are they located?

Answer 23

Central chemoreceptors – located near respiratory center in the brain stem

Peripheral chemoreceptors – located in the carotid and aortic bodies

Question 24

Which type of chemoreceptor responds to changes in pH(PaCO2) and which type responds to changes in Pa02?

Answer 24

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.

Question 25

What would you expect to see in terms of CO2 level in an acidosis? What would the respiratory system do to compensate for this?

Answer 25

Acidosis would have a high PaC02, the body would increase respiratory rate (to “blow off” extra CO2)

Question 26

What would you expect to see in terms of CO2 level in an alkalosis? What would the respiratory system do to compensate for this?

Answer 26

Alkalosis would have a lowPaC02, the body would decrease respiratory rate

Question 27

Explain the changes that occur with chemoreceptors in conditions with chronic hypoventilation, such as COPD or CHF

Answer 27

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

Question 28

What is the mechanism of hypoventilation? Does it lead to respiratory acidosis or alkalosis?

Answer 28

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

Question 29

What is the mechanism of hyperventilation? Does it lead to respiratory acidosis or alkalosis?

Answer 29

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

Question 30

Provide examples of causes of hypoventilation

Answer 30

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)

Question 31

Provide examples of causes of hyperventilation

Answer 31

Resp-centre abnormality in brainstem Low O2 levels (hypoxia): pneumonia, PE, etc. Anxiety, panic attacks, sepsis, salicacylates

Question 32

Asthma is an inflammatory disorder of the airways characterized by paroxysmal or persistent symptoms, such as:

Answer 32

Dyspnea Chest tightness Wheezing Sputum production and cough -From Mark RRT presentation

Question 33

Discuss the patho of COPD

Answer 33

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

Question 34

What does spirometry do?

Answer 34

-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

Question 35

In spirometry, what measurement is this referring to: "Maximal volume of air exhaled in the first second of forced expiration."

Answer 35

Forced Expiratory Volume in first second (FEV1) -From Mark RRT presentation

Question 36

In spirometry, what measurement is this referring to: "Volume of air exhaled during a maximal rapid complete exhalation."

Answer 36

Forced Vital Capacity (FVC) -From Mark RRT presentation

Question 37

In spirometry, what does this measure: "FEV1/FVC

Answer 37

Proportion (%) of total volume of air which can be exhaled in first second. -From Mark RRT presentation

Question 38

What is a normal or expected FEV1 percentage?

Answer 38

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

Question 39

What FEV1/FVC value would indicate COPD?

Answer 39

Anything below 0.7, or 70% -From Mark RRT presentation

Question 40

What are the ranges (in %) of FEV1 that indicate the severity of COPD?

Answer 40

Normal = 80%+ Moderate = 50-79% Severe = 30-49% Very severe = less than 30% -From Mark RRT presentation

Question 41

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?

Answer 41

At least a 12% improvement and an increased FVC of at least 200 mls -From Mark RRT presentation

Question 42

In patients with COPD, what is a useful breathing technique to help them with activities that require some exertion?

Answer 42

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

Question 43

What is the recommended criteria for referring a patient for spirometry?

Answer 43

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

Question 44

What is Benign Paroxysmal Positional Vertigo (BPPV)?

Answer 44

Dizziness caused from crystals moving into semicircular canals that obstruct the normal flow of endolymph

Question 45

T/F Meniere's disease is the most common cause of peripheral vertigo?

Answer 45

False - BPPV is more common

Question 46

Risk factors for BPPV

Answer 46

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

Question 47

Patho of BPPV

Answer 47

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

Question 48

Does BPPV have sudden or slow onset?

Answer 48

Sudden

Question 49

How long does BPPV last (each episode) and how long does it take to resolve?

Answer 49

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

Question 50

Does BPPV commonly affect men or women? Young or old?

Answer 50

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

Question 51

S&S of BPPV

Answer 51

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​

Question 52

Does BPPV or Menieres present with hearing loss?

Answer 52

Meniere's

Question 53

What are the two diagnostic/provoking maneuvers for BPPV?

Answer 53

1) Dix-Hallpike (for posterior canal BPPV) 2) Supine-roll maneuver (horizontal canal BPPV)

Question 54

What two maneuvers are used as treatment for BPPV?

Answer 54

1) Epley maneuver 2) Semont maneuver

Question 55

Describe the Epley maneuver

Answer 55

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

Question 56

Describe the Semont maneuver

Answer 56

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

Question 57

Patient teaching for acute episodes of BPPV

Answer 57

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

Question 58

What causes Meniere's disease?

Answer 58

Dizziness caused by build up of fluid – endolymph in inner ear

Question 59

Onset of Menieres

Answer 59

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

Question 60

Risk factors for Meniere's disease

Answer 60

Family history Autoimmune disease (diabetes, lupus or rheumatoid arthritis Head injury, especially if it involved the ear Viral infection of inner ear Allergies

Question 61

Patho of Meniere's. Is there a physical exam that we can do to confirm excess endolymph?

Answer 61

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

Question 62

Menieres: How long does an attack last? Are they recurrent? How do you feel between attacks?

Answer 62

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​

Question 63

What is the triad of symptoms in Menieres disease?

Answer 63

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​

Question 64

Diagnostic criteria for Menieres?

Answer 64

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​

Question 65

Tx of Menieres

Answer 65

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...

Question 66

What is labrynthitis?

Answer 66

Viral or post-viral inflammatory disorder affecting the inner ear. Inflammation causes vertigo AKA Vestibular Neuritis

Question 67

Risk factor for labrynthitis?

Answer 67

Recent cold or flu

Question 68

Patho of labrynthitis?

Answer 68

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

Question 69

Time course of labrynthitis?

Answer 69

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

Question 70

S&S of labrynthitis?

Answer 70

Vertigo that begins without warning Nausea & vomiting Gait instability

Question 71

When you do the Dix-Hallpike maneuvers for diagnosis of posterior canal BPPV, what do you see for nystagmus?

Answer 71

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

Question 72

How do nystagmus present in labrynthitis?

Answer 72

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