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BIOL 2200 > module 6: respiratory disorders > Flashcards

module 6: respiratory disorders Flashcards

1
Q

what is dyspnea and signs of it?

A

discomfort in breathing (SOB)

  • signs:
    • flaring of the nostrils
    • use of accessory muscles for respiration
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2
Q

what is orthopnea dyspnea?

A

dyspnea upon lying down

  • causes abdominal contents to put pressure on the diaphragm
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3
Q

what is paroxysmal nocturnal dyspnea (PND)

A

awakening at night with dyspnea

  • doesn’t last too long.. catch breath and all good
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4
Q

what are 7 other symptoms/signs of respiratory disease

A
  1. cough
  2. abnormal sputum
  3. hemoptysis
  4. abnormal breathing pattern
  5. cyanosis
  6. clubbing
  7. pain
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5
Q

why would a cough be a sign/symptom of respiratory disease?

A

can build up mucous because irritant receptors are lower down the “respiratory tree”, so the body doesn’t recognize it right away = secretion build up

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6
Q

what is abnormal sputum?

A

mix of saliva and mucous… changes in the amount, colour, and consistency depending on infection

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7
Q

what is hemoptysis?

A

expectoration (coughing) of blood

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8
Q

what is cyanosis?

A

bluish discoloration of the skin and mucous membranes

  • caused by deoxygenated hemoglobin in the blood
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9
Q

what is clubbing?

A

selective bulbous enlargement of the end of a digit and irregularity of nail bed

  • often seen with cystic fibrosis
  • chronic lack of O2
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10
Q

Define hypercapnia (hypercarbia)

A

increased carbon dioxide in the arterial blood

  • too much CO2
    • CO2 normally diffuses way easier… problem is not CO2 diffusion to alveoli, the problem is ventilation into the lungs
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11
Q

what is the immediate cause of hypercapnia?

A
  • hypoventilation of the alveoli
    • CO2 passes very easily from the blood to the alceolar space = NOT the problem
    • problem is with the echange in the alveolar gasses that occurs with ventilation
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12
Q

what are 3 occurances that can bring the immediate cause to happen with hypercapnia?

A
  1. drugs
  2. diseases of the medulla (because responsible for breathing pattern/functions that keep us alive)
  3. physiologic dead space (areas where we are not able to have normal gas exchange)
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13
Q

Define hypoxemia and explain the difference from hypoxia

A
  • hypoxemia = reduced oxygenation of arterial blood (lack of o2 in blood stream)
  • hypoxia = reduced oxygenation of cells
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14
Q

what are the 3 mechanisms of hypoxemia?

A
  1. oxygen delivery to the alveoli
  2. diffusion of oxygen from the alveoli into the blood
  3. anatomical right to left shunting
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15
Q

explain how oxygen delivery to the alveoli can reduce oxygenation of the blood

A
  • not enough o2 in the atmosphere
  • not vetilating O2 properly to hold air in (not able to draw air fully)
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16
Q

By what two means can oxygen delivery to the alveoli be decreased? Be familiar with examples of conditions/diseases that can cause this

A
  1. balance between alveolar ventilation (V) and perfusion (Q):
  • perfusion = the amount of blood passing through the alveolar capillaries
  • V/Q imbalance/mismatch causes hypoxemia
    • inadequate perfusion of well-ventailated area (high V/Q), producing alveolar dead space (blod not going anywhere)
    • low ventilation, but high perfusion (low V/Q) = physiologic right to left shunt (figure 1) = blood flow is fine, but at lungs, there is a disruption, so not picking up o2
  1. decreased diffusion across the alveolocapillary membrane
  • due to thickened membrane brought about through edema or fibrosis
  • alveolocapillary = area that is diffusing there to disrupt o2 movement
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17
Q

what is the difference between the physiologic right to left shunt and an atomic right to left shunt?

A
  • physiologic right to left shunt = blood flow is fine, but at lungs, there is a disruption = not picking up o2 (look at figure)
    • problem with drawing air in
  • anatomic right to left shunt = hole in heart septum = instead of blood pushing to lungs fully, some goes to the left side of the heart = problem with blood flow
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18
Q

What does V/Q refer to?

A
  • alveolar ventilation (V) = bringing air to lungs/alveoli
  • perfusion (Q) = ability of blood to get to capillaries and out
  • high V/Q = inadequate perfusion of well-ventilated area, producing alveolar deadspace
  • low V/Q = inadequate ventilation of well-perfusion area of lung (AKA physiologic right to left shunt)
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19
Q

What is the most common cause of hypoxemia?

A

V/Q mismatch

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20
Q

what are examples of diseases that cause low and high V/Q

A
  • high V/Q = pumonary embolism
  • low V/Q = atelectasis, asthma, pulmonary edema
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21
Q

What conditions can decrease diffusion across the alveolocapillary membrane?

A
  • thickened membrane brought on through edema or fibrosis
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22
Q

how can an uncorrected left-to-right shunt progress to a right-to-left shunt?

A
  • muscle through LV is a lot thicker because it is pumping blood to the whole body, whereas RV pump blood to lungs only
  • since left-to-right shunt = blood pushing to right side of heart (more preload to RV), the right side will start to pump harder to compensate for the increased blood flow = increase of RV muscle size
  • increase of RV muscle size eventually shifts the left-to-right shunt to a right-to-left-shunt
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23
Q

What causes, and is the result of, chest wall restriction?

A
  • cause - when the chest wall is:
    • deformed
    • traumatized
    • immobilized
    • heavy from the accumulation of fat
  • results - a decrease in tidal volume
    • amount of air taken in and released during normal breathing in reduced
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24
Q

Describe flail chest

A
  • multiple consecutive ribs that are broken (example of trauma to the chest)
  • if you break ribs, it disrupts the attachment onto ribs = no attachment of muscle = can’t move well = loses structure
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25
Q

Define pneumothorax and its effect on the lung

A
  • air in the pleural space caused by a rupture in the visceral or parietal pleura
  • effect on lung:
    • air pushes on the outside of the lung and makes it collapse
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26
Q

what is open pneumothorax?

A
  • air comes in through pleura on the side
  • when we inhale, diaphragm pulls down, but air coming from the side pushes collapsed lung and shfits everything over
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27
Q

explain tension pneumothorax

A
  • when inhaling, air comes in and shifts everythign over
  • air is not able to leave during expiration (due to flap/opening closing) = huge amount of air iin lung, causing major compression on both lungs
  • the tissue folds over and blocks opening as. we exhale and opens as we inhale
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28
Q

Define pleural effusion and how it usually occurs

A
  • excess fluid in pleural space from pressure of membranes in pleura
  • occurs through migration of fluid through walls of capillaries bordering the pleura
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29
Q

Define empyema and how it can occur

A
  • infection of pleural space/effusion = a collection of pus in pleural space
  • can occur through complications of pneumonia, surgery, etc.
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30
Q

what is atelectasis?

A
  • collapsed lung by external compression, obstructed airways (alveoli colllapses), inhalation of concentrated oxgen, or decreased production of surfactant (lungs stick is there is lack of surfactant)
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31
Q

what are the causes of atelectasis?

A
  • post-surgery
    • patients in pain
    • breathe shallowly
    • produce viscous secretions
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32
Q

what are the manifestations of atelectasis?

A
  • dyspnea
  • cough
  • fever
  • leukocytosis
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33
Q

What medical procedure often results in atelectasis and what measures can be taken to improve patients’ condition?

A
  • surgery
  • measures taken:
    • breathe deeply
    • become ambulatory (up and moving) asap
    • change positions frequently when lying down to avoid obstruction of airway
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34
Q

Describe bronchiectasis and identify some causes

A
  • permanent dilaion of the bronchi
    • con’t move air through trees well and damage epithelial lining = lack of circulation = can’t kill pathogens as well
  • causes: chronic inflammation = destruction of elastic and muscular components on bronchi walls = permanent dilation
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35
Q

Describe the pathophysiology behind cystic fibrosis and its treatment

A
  • autosomal (chromosomes that aren’t sex chromosomes) recessive disorder
  • Pathophysiology:
    • mutation of chromosome (2 bad genes) produces inability of cell membranes to transport chloride ion = series of events happen = increased absorbance of sodium and water from respiratory secretions
    • increased sodium and water = production of thick mucous that cilia has trouble moving
    • mucous accumulaes and increases risk of infections

***CAN HAVE 1 BAD GENE AND NOT NOTICE A DIFFERENCE.. If parents both have shitty chromosome, can have 25% chance of having child with cystic fibrosis***

  • treatment:
    • antibiotics to control infection
    • possible replacement of pancreatic enzymes
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36
Q

What is a pulmonary embolism and of what is the most common embolus comprised?

A
  • occlusion of a portion of the pulmonary vascular bed by an embolus
    • embolus went from deep vein thrombosis to the heart
  • most common embolus comprised = a clot from deep venous thrombosis involving the lower leg
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37
Q

What does obstruction of blood flow cause in the lung and what is the result if the clot is not dissolved soon enough?

A
  • obstruction causes pulmonary vessels to constrict = impaired gas exchange (V/Q mismatch- high V/Q problem)
  • right heart failure can happen if clot is not dissolved soon enough
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38
Q

What are the clinical manifestations of a pulmonary embolism?

A

depends upon size and location of obstruction

  • small emboli may go unnoticed unless patient’s health is otherwise compromised
  • moderate emboli: sudden onset chest pain, dyspnea, tachypnea, tachycardia
  • massive emboli: sudden collapse, crushing chest pain, shock - often fatal
39
Q

Define pulmonary hypertension, and explain how hypoxemia and certain heart conditions can lead to this condition

A
  • increase in pulmonary artery pressure, normally due to something else causing high blood pressure
  • how hypoxemia & certain conditions lead to this:
    • normally, blood vessel dilates when low on o2 in order to draw more blood to tissues to get o2 there
    • the opposite happens though because as blood goes to the lungs, it causes constriction due to better contact with alveoli to diffuse o2 from RBC
    • other conditions raise left atrial pressure
40
Q

What is cor pulmonale, its primary cause, and its effects?

A
  • right heart failure without left heart failure
  • primary cause: right ventricular enlargement caused by chronic pulmonary hypertension
  • effects: increased systemic venous circulation = peripheral edema, etc.
41
Q

What is pulmonary edema? How is it commonly caused? how does it result in hypoxemia?

A
  • excess “water” in the lungs
  • cause: left-sided heart failure
    • failure of left ventricle = increased filling pressure = back-up of blood in lungs = increased pressure in lung capillaries
    • too much pressure on the lung capillaries leads to leakage into the interstitial space
    • leaking in interstitial space eventually causes the fluid to leak into the alveoli = less o2 diffusion rates = hypoxemia
42
Q

Describe clinical manifestations of pulmonary edema.

A
  • dyspnea
  • cyanosis
  • increased physical effort in breathing
  • blood-tinged frothy sputum
43
Q

To what are obstructive lung diseases due?

A

airway obstruction that is worse with an expiration - emptying of the lungs is slowed

44
Q

What two diseases are grouped together under the title “chronic obstructive pulmonary disease”?

A
  • chronic bronchitis
  • emphysema
45
Q

What are the unifying symptom and signs of obstructive lung diseases?

A
  • unifying symptom = dyspnea
  • unifying sign = wheezing (obstruction worse w/exhalation)
46
Q

Define bronchial asthma

A
  • a chronic inflammatory disorder to the bronchial mucosa that causes hypersensitivity and constriction of the airways
  • interplay of genetic and environmental factors
  • exposure to an allergen results in cascade of inflammatory events
47
Q

Describe the early response stage of an asthma attack, including clinical manifestations

A
  • type 1 hypersensitivity response
    • allergen exposure activates B cells to produce IgE to bind to mast cells
  • another exposure to the allergen binds to IgE, causing mast cells to release a host of chemicals = vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction, and mucous secretion
  • clinical manifestations:
    • chest constriction
    • expiratory wheezing
    • dyspnea
    • tachycardia
    • coughing
48
Q

Describe the steps in the late response stage of an asthma attack

A
  • release of inflammatory chemicals
    • chemokines call other inflammatory cells: neutrophils, eosinophils, and lymphocytes = release of inflammatory chemicals = further bronchospasm, edema, and mucous secretion
  • cell damage & mucous accumulation
    • ciliated epithelial cells damaged due to mucous accumulation = impede ventilation
  • air trapping → hypoxemia → respiratory alkalosis
  • impairment of respiratory muscles → respiratory acidosis
49
Q

describe how respiratory alkalosis can arise in the late stage of an asthma attack

A

air trapping → hypoxemia → respiratory alkalosis

  • difficulty breathing out traps the air in lungs (air trapping) = increase gas pressure in alveoli = decrease in perfusion of blood
  • alveoli pressure is expanding alveoli and compressing capillaries = no blood flow/passage = decrease o2 (hypoxemia)
  • is hypoxemia gets serious, as a compensatory mechanism, it stimulates the respiratory center in medulla oblongata to trigger hyperventilation to compensate for the lack of o2
  • the body thinks by compensating, it is doing what is best, but during hyperventilation, we lose a lot of co2 = decrease blood hydrogen ions
  • decrease blood hydrogen ions = respiratory alkalosis (increase pH = basic air)
50
Q

explain how respiratory alkalosis can lead to respiratory acidosis

A

impairment of respiratory muscles → respiratory acidosis

  • still having difficulty breathing from respiratory alkalosis
  • not able to exhale all of our air = hyperexpanding lungs and thorax, even more, = not able to compress and re-expand like normal = decrease in tidal volume
  • decrease in tidal volume (unable to inhale/exhale all of that air to bring sufficient levels of o2 to blood) = harder to breathe
  • harder to breathe = even more hypoxemia
  • eventually, co2 levels will rise and we are unable to blow it out/get rid of co2
  • increase of co2 and hydrogen ions = acidosis in the respiratory system
51
Q

What are the mainstays of treatment for asthmatics?

A
  • avoidance of allergens
  • inhalation of anti-inflammatories
  • bronchodilators
  • adrenaline in acute attack
52
Q

What is chronic obstructive pulmonary disease characterized by?

A

airway obstruction that causes difficult exhalation

  • both emphysema and chronic bronchitis
53
Q

Define chronic bronchitis. What is it very commonly caused by?

A
  • hypersecretion of mucous and chronic productive cough for at least 3 months of the year, for at least 2 consecutive years
  • commonly caused by smoking
54
Q

escribe the development of chronic bronchitis

A
  • the airway becomes inflamed with the inspiration of irritants = edema and mucous production
  • continuous inflammation = increase in size and number of mucous glands and goblet cells in airway epithelium, and brings in macrophages and neutrophils to release proteases
  • proteases harm ciliated epithelial cells = mucous cannot be cleared
  • airways become constricted by thickened bronchial and mucous = difficult expiration
  • difficult expiration leads to hypoxemia
  • eventually, airways collapse early in expiration = air trapping = decrease tidal volume, hypoventilation, and hypercapnia

**not reversible after pathologic changes occur

55
Q

Why is the term “blue bloaters” used?

A
  • hypoxemia and edema, caused by eventual right heart failure
  • someone who is bloated/swollen and blue because they are not getting enough air
56
Q

Describe the treatment of chronic bronchitis

A
  • bronchodilators and expectorants as needed to control cough and reduce dyspnea
  • stop smoking
  • chest physical therapy
  • eventually antibiotics, steroids (last resort), home oxygen therapy
57
Q

What is emphysema characterized by?

A

loss of lung elasticity and abnormal enlargement of the airspaces distal to the terminal bronchioles, with destruction of the alveolar walls and capillaries

58
Q

What is the difference between the physiological/anatomical causes of the obstruction of emphysema and chronic bronchitis?

A
  • obstruction of emphysema results from changes in the lung tissue (primary loss of elastic recoil)
  • chronic bronchitis is from mucous production and inflammation
59
Q

What are two causes of emphysema?

A
  • inherited condition: insufficiency of alpha 1-antitrypsin that combats proteases
  • through inhalation of cigarette smoke, air pollution, etc. that increases number of inflammatory cells
60
Q

Describe the development of emphysema

A
  • inflammation occurs and inflammatory cells release proteases = destruction of alveolar septae and increase the volume of acini (alveoli cluster distal to terminal bronchioles)
  • increase volume of acini produces large air spaces within the lungs (bullae) and on the surface of the lugs, next to the pleura (blebs) = increases hypoxemia
  • damage from inflammation includes a loss in the elastic lung tissue = difficult expiration = trapping air in lungs
  • trapping in air lungs hyperextends the thorax, making it hard to breathe = hypoventilation and hypercapnia
61
Q

Define blebs and bullae.

A

blebs = large air spaces next to the pleura

bullae = large air spaces within the lungs

62
Q

Why is the term “pink puffer” used?

A
  • initially, little hypoxemia/ increased breathing can keep up with oxygen demand until the late stages of the disease
  • classic tripod breathing position and lips pursed to increase lung pressure during exhalation
63
Q

Describe the treatment of emphysema

A
  • cessation of smoking
  • inhalation of corticosteroids
  • bronchodilating drugs
64
Q

Describe Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS) including their causes

A
  • ARDS = more severe aspect of ALI
  • both involve acute lung inflammation and injury to the alveolocapillary (wall between alveoli and bloodstream) membrane = severe pulmonary edema and hypoxemia
  • causes:
    • sepsis
    • trauma
    • pneumonia
    • drug overdose
    • smoke inhalation
    • aspiration of gastric contents
65
Q

What is the difference between these ALI and ARDS?

A

ARDS is more severe than ALI

  • difficult to diagnose and can prove fatal if not properly treated within 48 hours
  • mortality = 50-70%
66
Q

describe the development of ALI/ARDS

A
  • neutrophils and platelets release inflammatory chemicals (histamine/inflammatory mediators) that damage the alveolocapillary membrane and increase capillary membrane permeability
  • damage to membrane allows for blood to leak into interstitial spaces and alveoli = edema
  • there is surfactant (biofilm to prevent alveoli from collapsing) inactivation, causing the collapse of alveoli = further decrease in gas exchange
  • hyaline membrane (composed of dead cells, fluids, and residual surfactant & proteins) forms (second image) = impaired gas exchange
  • may cause fibrosis
67
Q

Describe clinical manifestations of ALI/ARDS and the treatment

A
  • rapid onset of respiratory distress, usually within 12-18 hours of injury
  • marked hypoxemia occurs that can’t be successfully treated with supplemental oxygen therapy
  • may be a systemic response as the inflammatory compound spread through the body
  • treatment: supplying oxygen until lungs heal
68
Q

Define Acute Respiratory Failure (there are three parts to the definition).

A
  • inadequate gas exchange, leading to lower partial pressure of carbon dioxide (PcCO2) and pH < 7.30
69
Q

Identify the two types of acute respiratory failure (ARF) and their general causes

A
  1. hypoxemic = due to failure of gas exchange within the lungs
  2. hypercapnic/hypoxemic = due to failure of ventilation
  • the two types can overlap
70
Q

What medical procedure can often cause acute respiratory failure? Be familiar with the problems that this procedure can cause that may result in acute respiratory failure.

A

complication of surgery

  • atelectasis
  • pneumonia
  • pulmonary edema
  • pulmonary embolism
71
Q

Describe how hypoxemic respiratory failure can be brought about and how it is usually treated.

A

2 ways:

  • ventilation/perfusion mismatch = not enough o2 brought in (either problem of ventilation or perfusion)
    • often seen in people with COPD
  • impaired diffusion = leads to low o2 levels
    • often seen in interstitial lung disease, ARDS, pulmonary edema, and pneumonia

treatment: administrating high concentrations of oxygen to produce ATP

72
Q

Describe how hypercapnic/hypoxemic respiratory failure can be brought about and how it is usually treated

A
  • the increase in arterial co2 is due to a failure in ventilation, which also causes hypoxemia
    • reducing ventilation by half causes a doubling of PCO2
  • anything interfering with the ventilation mechanism can bring this about
    • ex: diseases of the nervous system, respiratory muscles, COPD, etc.
  • treatment: mechanical ventilation
73
Q

What is croup characterized by?

A
  • inspiratory stridor (wheezing tone produced during inspiration, indicating obstruction of upper respiratory pathway)
  • hoarseness
  • barking cough
74
Q

Define stridor

A

wheezing tone produced during inspiration, indicating obstruction of upper respiratory pathway

75
Q

What is the most common cause of croup?

A

laryngotracheobronchitis (LTB) caused by viruses, mainly in children 6 months- 5 y/o

  • inflammation to respiratory tree
76
Q

What is a retraction?

A

indentations of skin around ribs and sternum, showing use of accessory muscles of respiration

77
Q

Define bronchiolitis and give its cause.

A
  • inflammation of small airways (bronchioles), caused by virus
78
Q

Define epiglottitis and give its cause.

A
  • swelling of larynx and epiglottis
  • caused by bacterial infection
79
Q

To what is respiratory distress syndrome in infants due?

A

surfactant deficiency

80
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

Based on her recent history and the signs and symptoms that arose in the hospital waiting room, what condition was Julie likely initially experiencing in the hospital waiting room? On what signs/symptoms do you base this choice?

A

Pulmonary embolism

Faint, short of breath, sudden and sharp chest pain, coughing up blood, blue skin around mouth and tongue.

81
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

The listed signs suggest that another condition was subsequently developing in Julie. Name and describe this condition - be as specific as possible.

A

obstructve shock

82
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

Give an explanation for each of the listed signs

A
  • Blue skin – cyanosis due to decreased oxygenated hemoglobin in blood.
  • Increased pulse – heart beat has increased to compensate for decrease in blood pressure
  • Decreased blood pressure – due to blood having to flow around blockage in artery within lung
  • Increased respiratory rate – due to compensation for decreased oxygenation of blood
83
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

Would her blood pH likely be above or below normal level? Explain your choice

A

Wouldn’t be lower than normal, as she must be “blowing off” CO2 with increased breathing rate. Must be higher than normal

84
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

What type of heart failure is Julie in danger of developing? Explain your choice

A

With obstruction in lung, she could end up with right sided heart failure. As this would be due to problem in lung, it would be classified as “cor pulmonale”

85
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

Based on her breathing rate, would Julie’s respiratory disorder be classified as hypoxemic or hypercapnic? Explain your choice.

A

It would be hypoxemic, because it couldn’t be hypercapnic due to increased breathing rate. Also, see next question

86
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

Would a V/Q mismatch be present? If present, would it be high or low? Explain your choice

A

A V/Q mismatch would be present, as perfusion in a portion of her lungs is less than normal, while ventilation isn’t decreased. The decrease in Q would result in a high V/Q. These mismatches result in hypoxemia.

87
Q

Julie is a 65 year old grandmother recently returned home to Victoria, BC, after visiting her daughter and four grandchildren who live in Australia. She tried to get through the long flights by watching several movies and then sleeping for as long as possible. She does not like to drink too much during the flight because of those annoying line-ups for the washroom. A day after returning home, Julie noticed that her left leg was painful and swollen. The next morning the pain in her left leg was worse and her leg was so swollen that she couldn’t even fit her left foot into her slipper. She decided to visit the emergency room of the local hospital. While waiting for the doctor Julie began to feel faint and short of breath and experienced sudden, sharp chest pain, mostly on the right side. Her shortness of breath became worse, as did the chest pain. Julie coughed and produced sputum mixed with bright red blood. The nurse with Julie subsequently noted the following: • The skin around the patient’s mouth and her tongue had a blue tinge • Pulse: 120 per minute • Blood pressure: 85/50 mmHg • Respiratory rate: 30 per minute

What previously occurring condition had Julie developed that most likely caused her sudden collapse in the emergency department? What factors increased the likelihood of this occurring?

A

Deep vein thrombosis. Risk factors are her age, the long period of inactivity and the likely dehydration on the plane. This increased the possibility of a clot developing in a vein of her legs

88
Q

Mr. Tims, a 58-year old retired ferry controller with a 30 year history of smoking two packages of cigarettes per day, presents himself at the emergency department, saying he is presently having great difficulty breathing. He admits that he has become more short of breath during the past decade. At first it was only when he was doing some form of physical activity, but lately breathlessness can occur even during a slow walk. The last few years have also seen extended periods of heavy productive coughing in the morning. The nurse observes that at the present moment, he is visibly anxious and dyspnoeic, but his colour is nevertheless still relatively good with a pink complexion. However, he is leaning on the overbed table to facilitate breathing and is using accessory muscles. His expiration time is prolonged and he is breathing through pursed lips. He has a loose productive cough with thick greenish-yellow sputum. He is slow to respond to questions, with frequent pauses to “catch his breath” and cough. His vital signs are: T - 39ºC, Pulse - 110, BP-160/96, respiration -36 bpm.

What general chronic respiratory condition is Mr. Tims likely suffering from? What are the risk factor(s) in his case?

A
  • COPD
  • Smoking and age
89
Q

Mr. Tims, a 58-year old retired ferry controller with a 30 year history of smoking two packages of cigarettes per day, presents himself at the emergency department, saying he is presently having great difficulty breathing. He admits that he has become more short of breath during the past decade. At first it was only when he was doing some form of physical activity, but lately breathlessness can occur even during a slow walk. The last few years have also seen extended periods of heavy productive coughing in the morning. The nurse observes that at the present moment, he is visibly anxious and dyspnoeic, but his colour is nevertheless still relatively good with a pink complexion. However, he is leaning on the overbed table to facilitate breathing and is using accessory muscles. His expiration time is prolonged and he is breathing through pursed lips. He has a loose productive cough with thick greenish-yellow sputum. He is slow to respond to questions, with frequent pauses to “catch his breath” and cough. His vital signs are: T - 39ºC, Pulse - 110, BP-160/96, respiration -36 bpm.

Does he have both aspects of this chronic condition? Support your conclusion with facts from the case.

A

Yes. Both

  • breathlessness
  • prolonged expiration time
  • Emphysema
  • pink complexion
  • breathing in tripod position with pursed lips
  • Chronic Bronchitis
  • yellow sputum
  • heavy productive coughing during last few years
  • fever
90
Q

Mr. Tims, a 58-year old retired ferry controller with a 30 year history of smoking two packages of cigarettes per day, presents himself at the emergency department, saying he is presently having great difficulty breathing. He admits that he has become more short of breath during the past decade. At first it was only when he was doing some form of physical activity, but lately breathlessness can occur even during a slow walk. The last few years have also seen extended periods of heavy productive coughing in the morning. The nurse observes that at the present moment, he is visibly anxious and dyspnoeic, but his colour is nevertheless still relatively good with a pink complexion. However, he is leaning on the overbed table to facilitate breathing and is using accessory muscles. His expiration time is prolonged and he is breathing through pursed lips. He has a loose productive cough with thick greenish-yellow sputum. He is slow to respond to questions, with frequent pauses to “catch his breath” and cough. His vital signs are: T - 39ºC, Pulse - 110, BP-160/96, respiration -36 bpm

explain his vital signs

A
  • Increased temperature – inflammation / infection
  • Increased heart rate – makes up for hypoxemia
  • Increased blood pressure – due to increased heart rate
  • Increased respiration – makes up for hypoxemia
91
Q

Mr. Tims, a 58-year old retired ferry controller with a 30 year history of smoking two packages of cigarettes per day, presents himself at the emergency department, saying he is presently having great difficulty breathing. He admits that he has become more short of breath during the past decade. At first it was only when he was doing some form of physical activity, but lately breathlessness can occur even during a slow walk. The last few years have also seen extended periods of heavy productive coughing in the morning. The nurse observes that at the present moment, he is visibly anxious and dyspnoeic, but his colour is nevertheless still relatively good with a pink complexion. However, he is leaning on the overbed table to facilitate breathing and is using accessory muscles. His expiration time is prolonged and he is breathing through pursed lips. He has a loose productive cough with thick greenish-yellow sputum. He is slow to respond to questions, with frequent pauses to “catch his breath” and cough. His vital signs are: T - 39ºC, Pulse - 110, BP-160/96, respiration -36 bpm

s he more of a “pink puffer” or a “blue bloater”? Explain your choice by describing the basis behind each description.

A
  • More of a pink puffer
    • He’s still pink (due to increased respiratory rate)
    • breathing through pursed lips to keep airways open
  • Blue bloater
    • blue due to cyanosis due to hypoxemia
    • bloater due to peripheral edema due to right heart failure
92
Q

Mr. Tims, a 58-year old retired ferry controller with a 30 year history of smoking two packages of cigarettes per day, presents himself at the emergency department, saying he is presently having great difficulty breathing. He admits that he has become more short of breath during the past decade. At first it was only when he was doing some form of physical activity, but lately breathlessness can occur even during a slow walk. The last few years have also seen extended periods of heavy productive coughing in the morning. The nurse observes that at the present moment, he is visibly anxious and dyspnoeic, but his colour is nevertheless still relatively good with a pink complexion. However, he is leaning on the overbed table to facilitate breathing and is using accessory muscles. His expiration time is prolonged and he is breathing through pursed lips. He has a loose productive cough with thick greenish-yellow sputum. He is slow to respond to questions, with frequent pauses to “catch his breath” and cough. His vital signs are: T - 39ºC, Pulse - 110, BP-160/96, respiration -36 bpm

Describe the pathophysiological development of both aspects of Mr. Tims’ chronic condition. What are “blebs” and “bullae” and where do they fit in?

A
  • Emphysema
    • smoke causes inflammation.
    • Inflammatory cells release proteases that destroy respiratory membrane and elastic tissue.
    • There’s a loss of exchange surface and loss of ability to open airway during exhalation
    • air trapping leads to hypoventilation which leads to hypercapnia and hypoxemia (at end of disease when can’t breathe fast enough to compensate).
    • blebs = air space on the surface of lung
    • bullae = airspace within the lung
  • Chronic bronchitis
    • inflamed airway
    • Edema and mucous
    • Increased size of mucous glands and goblet cells
    • Loss of cilia due to proteases
    • Constriction of airway due to mucous and thicker walls.
    • Hypoxemia (V/Q mismatch)
    • Air trapping leads to hypoventilation, which leads to hypoxemia and hypercapnia
93
Q

Mr. Tims, a 58-year old retired ferry controller with a 30 year history of smoking two packages of cigarettes per day, presents himself at the emergency department, saying he is presently having great difficulty breathing. He admits that he has become more short of breath during the past decade. At first it was only when he was doing some form of physical activity, but lately breathlessness can occur even during a slow walk. The last few years have also seen extended periods of heavy productive coughing in the morning. The nurse observes that at the present moment, he is visibly anxious and dyspnoeic, but his colour is nevertheless still relatively good with a pink complexion. However, he is leaning on the overbed table to facilitate breathing and is using accessory muscles. His expiration time is prolonged and he is breathing through pursed lips. He has a loose productive cough with thick greenish-yellow sputum. He is slow to respond to questions, with frequent pauses to “catch his breath” and cough. His vital signs are: T - 39ºC, Pulse - 110, BP-160/96, respiration -36 bpm

What would be a likely cardiovascular explanation should Mr. Tims develop signs including neck vein extension, swelling of the lower extremities and hepatomegaly over subsequent years? Support your conclusion by explaining the appearance of these signs.

A

Right heart failure (cor pulmonale)

  • Peripheral edema, vein extension and swelling of liver due to back-up of blood into veins of the body.
94
Q

Mr. Tims, a 58-year old retired ferry controller with a 30 year history of smoking two packages of cigarettes per day, presents himself at the emergency department, saying he is presently having great difficulty breathing. He admits that he has become more short of breath during the past decade. At first it was only when he was doing some form of physical activity, but lately breathlessness can occur even during a slow walk. The last few years have also seen extended periods of heavy productive coughing in the morning. The nurse observes that at the present moment, he is visibly anxious and dyspnoeic, but his colour is nevertheless still relatively good with a pink complexion. However, he is leaning on the overbed table to facilitate breathing and is using accessory muscles. His expiration time is prolonged and he is breathing through pursed lips. He has a loose productive cough with thick greenish-yellow sputum. He is slow to respond to questions, with frequent pauses to “catch his breath” and cough. His vital signs are: T - 39ºC, Pulse - 110, BP-160/96, respiration -36 bpm.

Mr. Tims encounters a fellow patient who suffers only from emphysema. “How many years did you smoke?” he asks. The other patient declares: “I never touched a cigarette in my life!” Explain how this may be possible.

A

Genetic condition causing lack of alpha-1-antitrypsin, a naturally produced compound that neutralizes proteases released by neutrophils / macrophages.

BIOL 2200 (12 decks)

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