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NUNP531 Applied Pathophysiology > Week 5: Resp > Flashcards

Week 5: Resp Flashcards

1
Q

Which structures compose the large airways?

A

The trachea and two segmental bronchi

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2
Q

Describe the 3 layers of the large airways

A

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

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3
Q

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

A

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.

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4
Q

Which structures compose the small airways?

A

Bronchioles and alveoli

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5
Q

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

A

The small airways lack cartilage

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

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6
Q

Define Tidal Volume

A

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

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7
Q

Define Expiratory Reserve Volume

A

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

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8
Q

Define Inspiratory Reserve Volume

A

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

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9
Q

Define Vital Capacity

A

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

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10
Q

Define FEV1

A

Forced expiratory volume in 1 second

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11
Q

Define Residual Volume

A

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)

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12
Q

What is lung compliance?

A

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

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13
Q

Which 2 factors influence lung compliance

A

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

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14
Q

Provide 2 examples of conditions that result in decreased lunch compliance

A

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

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15
Q

What is a V/Q mismatch?

A

an imbalance between alveolar ventilation and perfusion

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16
Q

Name the two types of V/Q mismatches?

A

Shunting

Alveolar dead space

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17
Q

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

A

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

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18
Q

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

A

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

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19
Q

What are the 4 types of neurons in the respiratory center

A
  1. Dorsal respiratory group (DRG)
  2. Ventral respiratory group (VRG)
  3. Pneumotaxic centre
  4. Apneustic centre
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20
Q

What are the 3 types of lung receptors?

A

Irritant receptors (C fibres)

Stretch Receptors

J-Receptors (Juxtapulmonary capillary receptors)

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21
Q

Describe sympathetic innervation to the lungs

A

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

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22
Q

Describe parasympathetic innervation to the lungs

A

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

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23
Q

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

A

Central chemoreceptors – located near respiratory center in the brain stem

Peripheral chemoreceptors – located in the carotid and aortic bodies

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24
Q

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

A

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.

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25
Q

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

A

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

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26
Q

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

A

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

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27
Q

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

A

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

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28
Q

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

A

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

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29
Q

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

A

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

30
Q

Provide examples of causes of hypoventilation

A

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)

31
Q

Provide examples of causes of hyperventilation

A

Resp-centre abnormality in brainstem

Low O2 levels (hypoxia): pneumonia, PE, etc.

Anxiety, panic attacks, sepsis, salicacylates

32
Q

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

A

Dyspnea
Chest tightness
Wheezing
Sputum production and cough

-From Mark RRT presentation

33
Q

Discuss the patho of COPD

A

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

34
Q

What does spirometry do?

A

-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

35
Q

In spirometry, what measurement is this referring to:

“Maximal volume of air exhaled in the first second of forced expiration.”

A

Forced Expiratory Volume in first second (FEV1)

-From Mark RRT presentation

36
Q

In spirometry, what measurement is this referring to:

“Volume of air exhaled during a maximal rapid complete exhalation.”

A

Forced Vital Capacity (FVC)

-From Mark RRT presentation

37
Q

In spirometry, what does this measure:

“FEV1/FVC

A

Proportion (%) of total volume of air which can be exhaled in first second.

-From Mark RRT presentation

38
Q

What is a normal or expected FEV1 percentage?

A

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

39
Q

What FEV1/FVC value would indicate COPD?

A

Anything below 0.7, or 70%

-From Mark RRT presentation

40
Q

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

A

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

-From Mark RRT presentation

41
Q

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?

A

At least a 12% improvement and an increased FVC of at least 200 mls

-From Mark RRT presentation

42
Q

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

A

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

43
Q

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

A

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

44
Q

What is Benign Paroxysmal Positional Vertigo (BPPV)?

A

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

45
Q

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

A

False - BPPV is more common

46
Q

Risk factors for BPPV

A

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

47
Q

Patho of BPPV

A

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

48
Q

Does BPPV have sudden or slow onset?

A

Sudden

49
Q

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

A

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

50
Q

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

A

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

51
Q

S&S of BPPV

A

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​

52
Q

Does BPPV or Menieres present with hearing loss?

A

Meniere’s

53
Q

What are the two diagnostic/provoking maneuvers for BPPV?

A

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

54
Q

What two maneuvers are used as treatment for BPPV?

A

1) Epley maneuver
2) Semont maneuver

55
Q

Describe the Epley maneuver

A

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

56
Q

Describe the Semont maneuver

A

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

57
Q

Patient teaching for acute episodes of BPPV

A

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

58
Q

What causes Meniere’s disease?

A

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

59
Q

Onset of Menieres

A

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

60
Q

Risk factors for Meniere’s disease

A

Family history

Autoimmune disease (diabetes, lupus or rheumatoid arthritis

Head injury, especially if it involved the ear

Viral infection of inner ear

Allergies

61
Q

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

A

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

62
Q

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

A

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​

63
Q

What is the triad of symptoms in Menieres disease?

A

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​

64
Q

Diagnostic criteria for Menieres?

A

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​

65
Q

Tx of Menieres

A

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…

66
Q

What is labrynthitis?

A

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

AKA Vestibular Neuritis

67
Q

Risk factor for labrynthitis?

A

Recent cold or flu

68
Q

Patho of labrynthitis?

A

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

69
Q

Time course of labrynthitis?

A

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

70
Q

S&S of labrynthitis?

A

Vertigo that begins without warning

Nausea & vomiting

Gait instability

71
Q

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

A

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

72
Q

How do nystagmus present in labrynthitis?

A

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

NUNP531 Applied Pathophysiology (24 decks)

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