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Acute care > Week 4 > Flashcards

Week 4 Flashcards

1
Q

What are the forces that affect the work of breathing?

A
  • Elastic recoil of the lungs and chest wall

* Airway resistance

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2
Q

What are the components of the elastic recoil of the lungs and chest wall that affects the work of breathing?

A

Static lung compliance is the change in volume for any given applied pressure
• Compliance = change in volume/change in pressure
• Increases with age and COPD
• Decreases with RLD

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3
Q

What are the components of the airway resistance that affects the work of breathing?

A
  • Bronchoconstriction
  • Mucous plugs
  • Airway Thickening
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4
Q

How do we assess lung function?

A 
• Lung Volume/Capacity
  - PFT
• Gas Exchange
  - DLCO
  - ABG
• Imaging
  - CXR,
  - CT Scan,
  - Perfusion Scan
• Function
  - 6MWT
  - ETT
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5
Q

What does Diffusion capacity of the lung for carbon dioxide (DLCO) do?

A

It infuses a known volume of carbon monoxide, and assess the amount of inspired and expired gases

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6
Q

What are the normal conditions of a DLCO?

A

80-100% of predicted uptake occurs

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7
Q

What is considered pulmonary pathology in a DLCO?

A

< 80% of predicted uptake occurs

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8
Q

What are the factors that DLCO is dependent upon?

A
  • Volume inspired (ventilation)
  • Pulmonary blood flow (perfusion)
  • Alveolar capillary surface area
  • Hemoglobin
  • Thickness of alveolar capillary membrane
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9
Q

What are the factors that cause a general reduce of DLCO?

A

Emphysema, and restriction, normal in asthmatics

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10
Q

What is the common sequelae of Chronic Lung Disease?

A
  • Pulmonary Hypertension
  • Right Heart failure (cor pulmonale)
  • Atrial Fibrillation (Especially COPD)
  • Obstructive Sleep Apnea (Especially COPD)
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11
Q

_____ is the most common cause of clubbing

A

Lung cancer is the most common cause of clubbing

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12
Q

When does clubbing occur?

A

In heart and lung diseases that reduce the amount of oxygen in the blood, however may not always be present.

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13
Q

What is pulmonary hypertension due to?

A

If there are issues with the oxygenation of the lungs, the removal of CO2 can change the vasculature/vascular tone in the lungs.

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14
Q

What is the role of CO2 in the periphery?

A

It is a vasodilator

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15
Q

What is the role of CO2 in the pulmonary arteries?

A

It is a vasoconstrictor

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16
Q

What is the primary issue of obstructive pulmonary disease?

A

Problems with getting “air out”

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17
Q

What is our normal FEV1(maximal amount of air you can forcefully exhale in one second)?

A

80%

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18
Q

What is the FEV1/FVC ( the total amount of air exhaled during the FEV test) ratio seen in patients with obstructive pulmonary disease?

A

FEV1/FVC ratio

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19
Q

What is obstructive pulmonary disease?

A

A common preventable and treatable disease, characterized by persistent
progressive airflow limitation and is associated with an enhanced chronic inflammatory response to noxious particles or gases

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20
Q

What is the most common risk factor for COPD worldwide?

A

Tobacco smoking

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21
Q

What are the types of Chronic Obstructive Pulmonary

Disease (COPD)?

A
  • Chronic Bronchitis
  • Emphysema
  • Alpha 1 antitrypsin deficiency
  • Asthma
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22
Q

What are the other types of obstructive pulmonary diseases?

A
  • Bronchiectasis

* Cystic Fibrosis (in later stages)

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23
Q

What is chronic bronchitis?

A

Cough and sputum production, especially during the winter, not due to specific or localized disease, present on most days for at least 3 months per year for 2 consecutive years

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24
Q

What is emphysema?

A

Loss of alveolar walls associated with increase in the size of the acinar airways of the upper lobe segments in a Centrilobular “centriacinar” pattern

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25
Q

What is alpha-antitrypsin 1 deficiency?

A

Genetic deficiency, where people develop pancinar emphysema: lower
regions of the lungs are typically first affected.

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26
Q

What is asthma?

A

A disorder characterized by reversible bronchospasm with wheezing, the symptoms occurring in short lived episodes, manifests early in life

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27
Q

What is alpha-antitrypsin 1?

A

A chemical in the body that allow our lungs to repair when they are exposed to a noxious stimulus

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28
Q

What is the pathophysiology of COPD?

A

You inhale some sort of noxious gas/particles, which leads to overtaxing of the macrophages, which may rupture protolytic enzymes, breakdown the alveolar walls, which will signal mucus production, and some of the antibodies released from the macrophages and WBC facilitate mucus hypersecretion, often leading to hypertrophy of the mucosal glands, may also see fibrosis(flimsy, prone to collapsing). We see weakening of the cartilage that supports the airways and destruction of the alveolar walls

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29
Q

What is a feature of the pathophysiolgy of COPD?

A

They can usually take in air, but when they start to try to exhale, they have trouble and the airway can collapse, and the presence of the air in the lungs, leads to vasodilation

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30
Q

What are the classic signs of COPD?

A

Air trapping. Issues removing air, because the walls are so flimsy they collapse

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31
Q

What are the muscle pathophysiological changes we see in patients with COPD?

A

• Metabolic inefficiency
- Fiber type shift in some skeletal muscle from type I to type II
• Reduced Fat Free Mass FFM (especially in quadriceps)
• Increased resting energy expenditure (REE), 15–20% above predicted values
due to the increased work of breathing.
• Impaired Mitochondrial function and decreased density
• Multiple suspected causes

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32
Q

What are some of the suspected causes of the muscle pathophysiological changes we see in patients with COPD?

A
  • Disuse atrophy

* Mitophagy: mitochondrial autophagy (pre-programmed cell death), which leads to skeletal muscle dysfunction

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33
Q

Why does the resting energy expenditure in patients with COPD increase?

A

Their diaphragm is over-worked due to some adaptation, which makes it work harder

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34
Q

What are the diaphragmatic adaptations we see in patients with COPD?

A

• Patients with severe COPD generate 60% of normal max trans-diaphragmatic pressure
• Changes at the cellular and molecular level in the muscle can fully account for the reduced diaphragm strength.
• Similowski et al suggested that weakness of the diaphragm could also be explained by
hyperinflation-induced diaphragm shortening.

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35
Q

What are the changes at the cellular and molecular level in the muscle that can fully account for the reduced diaphragm strength?

A
  • Fiber type “switch” to type 1 to compensate for increased diaphragmatic loading
  • Reduction of max force generated by COPD diaphragm fibers was associated with an approximate 30% loss of heavy chain myosin content.
  • These physiological changes are present in both mild and moderate cases
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36
Q

What does hyperinflation-induced diaphragm shortening do?

A

Places the diaphragm on a suboptimal position on its pressure–length relationship.

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37
Q

What are the signs and symptoms of COPD found upon physical exam?

A
  • Chronic Cough
  • Sputum production
  • Exertional dyspnea
  • Barrel Chest
  • Paradoxical Chest wall movements
  • Decreased breath sounds
  • Crackles (atelectasis)
  • Early satiety and difficulty eating
  • Balance and strength deficits
  • Body weight changes*
  • Cyanosis (severe cases)
  • Get full fast
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38
Q

What are the signs and symptoms of COPD found upon diagnostic testing?

A

• Impaired FEV1/FVC Ratio (

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39
Q

What are the common impairments of COPD?

A 
• Reduced Functional capacity
  - 6MWD
  - Or other ETT
• Decreased strength
• Impaired balance (LE muscles lose a lot)
  - Increased Fall risk and mortality/morbidity
• Dyspnea with minimal activity
• Reduced Gait speed
• Altered cardiorespiratory response
to exercise
• Back pain and chronic pain
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40
Q

What do we see in patients with COPD during pulmonary function testing?

A

Expiratory scooping. When inspiration is pretty normal, but during the 1st sec of expiration where we are supposed to be getting most of our volume out, patient with COPD get compression and flow reduction happens much sooner than it is supposed to

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41
Q

What is the cause of dyspnea in patients with COPD?

A

Due to air trapping and flimsy airways, as they begin to work harder and breathe faster, they hold more and more air in, because the respiratory rate is increasing to maintain oxygenation. Their issue is not having enough time

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42
Q

What are the skeletal muscle changes we see in patients with COPD?

A
  • Barrel chasting

- Hyper kyphosis

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43
Q

What are the diffusion and blood gas changes seen in COPD?

A

• Hypoxemia develops with mild to moderate COPD
• Hypoxemia and hypercapnea
develops in more severe cases when FEV1 <1L or 50%
- CO2 retainers (becomes more reliant on oxygen)
- May down-regulate chemoreceptor response to [CO2]

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44
Q

What does DLCO do?

A

Measures the diffusing capacity of CO through the alveolar membrane to hemoglobin

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45
Q

Why do we see reductions in DLCO in patients with COPD?

A 
• Damage to alveolar capillary membrane
or vasculature will reduce it.
• Often adjusted by the alveolar volume (VA) for severe COPD
• Generally reduced in reduced with most
obstructive and restrictive diseases,
  - Normal in patients with asthma
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46
Q

What is considered mild COPD according to the COPD- Gold classification?

A

FEV1 >/= 80%

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47
Q

What is considered moderate COPD according to the COPD- Gold classification?

A

FEV1: 50-80%

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48
Q

What is considered severe COPD according to the COPD- Gold classification?

A

FEV1: 30-50%

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49
Q

What is considered very severe COPD according to the COPD- Gold classification?

A

FEV1 < 30%

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50
Q

According to the Bode index, what are the domains taken into consideration in the assessment of 4 year survival of COPD?

A
  • Disease severity on FEV1
  • Distance on 6MWT
  • Score on MMRC dyspnea scale
  • BMI
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51
Q

What is the general minimum distance covered on the 6MWT that patients with COPD must achieve?

A

Minimum of 200 meters

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52
Q

What is the FEV1 predicted scale used in the Bode index?

A
  • > 65% (0 points)
  • 50-64% (1 point)
  • 36%-49% (2 points)
  • < 35% (3 points)
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53
Q

What is the 6 MWT scale used in the Bode index?

A
  • > 1150 feet (0 points)
  • 820-1150 feet (1 point)
  • 490- 820 feet (2 points)
  • < 490 feet (3 points)
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54
Q

What is the MMRC dyspnea scale used in the Bode index?

A
  • 0: dyspnea with strenuous exercise (0 points)
  • 1: dyspnea with walking on a slight hill (0 points)
  • 2: dyspnea with walking on level ground, must stop d/t SOB (1 point)
  • 3: must stop d/t SOB after 100 yards (2 points)
  • 4: dyspnea with dressing ADL (3 points)
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55
Q

What is the BMI scale used in the Bode index?

A
  • > 21 (0 points)

- < 21 (1 point)

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56
Q

What is the score and 4 year survival scale used by the Bode index?

A
  • Score: 0-2, 4yr survival: 80%
  • Score: 3-4, 4yr survival: 67%
  • Score: 5-6, 4yr survival: 57%
  • Score: 7-10, 4yr survival: 18%
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57
Q

What are the highlights of emphysema?

A 
• Increased airway compliance.
   - Air trapping/Hyperinflation
• Decreased surface area of alveoli for gaseous exchange.
  - (V/Q) mismatch.
• Reduced expiratory flow
  - Reduced elastic recoil pressure
  - Narrow &amp; poorly supported airways
  - Increased airflow resistance
• “Pink Puffer
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58
Q

What are the presentations of emphysema?

A
  • Barrel chesting
  • Potential compression of the abdominal contents
  • Impairments of the diaphragm, because it is flattened out
  • Pursing of lips to help slow the respiration cycle
  • Arms resting on chairs o help ribcage take in more air
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59
Q

How is chronic bronchitis primarily identified?

A

By submucosal gland hypertrophy in bronchioles producing increased thickness resulting from exposure to smoking or other irritants.

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60
Q

What are the presentations of chronic bronchitis?

A
  • Always producing mucus

- Arms resting on chairs o help ribcage take in more air

61
Q

What are the characteristics of asthma?

A 
• Reversible bronchoconstriction
• Hyper-reactive airways
  - Multiple triggers
• Manifests earlier in life
• Associated with chronic inflammation.
• Several varieties.
• If severe, may be cyanotic
• Status Asthmaticus
62
Q

Patients with Alpha-Antitrypsin 1 deficiency will eventually develop ____

A

Emphysematic COPD

  • Accelerated by smoking
  • Develops usually ages 30-40
63
Q

What are the characteristics of COPD: Alpha-Antitrypsin 1 Deficiency?

A
  • Patients may develop cirrhosis from abnormal build up of AAT in the liver
  • No cure for Alpha-1, there are treatments available for the symptoms, as well as augmentation therapy, which may slow down the destruction
64
Q

What is Bronchiectasis?

A

Irreversible airway dilation

65
Q

What are the types of focal (localized area of the lung) Bronchiectasis?

A
  • Extrinsic

- Intrinsic

66
Q

What is extrinsic focal Bronchiectasis?

A

Compression by adjacent

lymphadenopathy or parenchymal tumor mass

67
Q

What is intrinsic focal Bronchiectasis?

A

Airway tumor or aspiration, a

scarred/stenotic airway, bronchial atresia

68
Q

What is diffuse bronchiectasis?

A

Widespread, often arises from an underlying systemic or infectious disease process.

69
Q

What are the signs and symptoms of bronchiectasis?

A

Persistent productive cough with thick, tenacious sputum, crackles and wheezing on
lung auscultation, obstructive pattern on PFT

70
Q

What is Cystic Fibrosis (CF)?

A

A monogenic disorder that results in a multisystem disease

  • Lungs, sinuses, pancreas (DM1), liver, sweat ducts, GI tract, reproductive pathways
  • Children with CF often are physically underdeveloped due to malabsorption
71
Q

What does Cystic Fibrosis (CF) result from?

A

A genetic defect in the Na+ and Cl- channels resulting excessive in salty mucous formation

72
Q

What are the components of Cystic Fibrosis (CF) diagnosis?

A
  • Assessed at birth using a sweat Chloride test, >60 mmol/L, cystic fibrosis is present
  • Most patients are diagnosed in before 2y/o, 5% diagnosed as adults, multiple types
73
Q

What is the life expectancy and mortality of Cystic Fibrosis (CF)?

A

Life expectancy is improved, currently 37y/o
• >95% of patients die of complications from lung infection (high risk for developing)
• Consistent airway clearance, exercise and nutritional supplementation critical.
• Lung transplantation(only cure)

74
Q

What should come in mind when we think of restrictive lung disease (RLD)?

A

Problems with getting “air in”

75
Q

What are the main features of restrictive lung disease (RLD)?

A
  • Both FEV1 and FVC reduced, FEV1/FVC ratio normal or increased, total lung capacity (TLC) reduced
  • Reduced DLCO (extrinsic normal DLCO)
  • Lungs prevented from fully expanding
  • Reduced Minute Ventilation
76
Q

What is intrinsic restrictive lung disease (RLD)?

A

Reduced airway compliance, due to thickening and scarring of lung interstitial tissue and pleura

77
Q

What is extrinsic restrictive lung disease (RLD)?

A

Reduced chest wall compliance, Obesity, Chest wall deformities, diaphragm, neuromuscular diseases, chest wall trauma, burns

78
Q

What are the drug related causes of intrinsic restrictive lung disease (RLD)?

A

Bleomycin, methotrexate, amiodarone, chronic oxygen therapy

79
Q

What are the occupational causes of intrinsic restrictive lung disease (RLD)?

A

Asbestosis, silicosis, coal workers’ pneumoconiosis.

80
Q

What are the environmental causes of intrinsic restrictive lung disease (RLD)?

A

Hypersensitivity pneumonitis (Bird watcher’s lung)

81
Q

What are the autoimmune causes of intrinsic restrictive lung disease (RLD)?

A

Systemic lupus erythematosus (SLE), Wegener granulomatosis, rheumatoid arthritis

82
Q

What are the idiopathic causes of intrinsic restrictive lung disease (RLD)?

A

Idiopathic pulmonary fibrosis, sarcoidosis.

83
Q

What is honeycomb lung as seen in intrinsic restrictive lung disease (RLD)?

A

The resultant appearance of the fibrotic lung parenchyma, caused by exposure to the inciting agent causes alveolitis that leads to the release of cellular mediators, causing injury and eventually fibrosis of the alveolar septae

84
Q

What are the symptoms of intrinsic restrictive lung disease (RLD)?

A

Insidious onset of dyspnea on
exertion, frequent dry nonproductive cough;
tachypnea, air hunger, difficulty eating

85
Q

What are the signs of intrinsic restrictive lung disease (RLD)?

A

Fine bibasilar end-inspiratory crackles; clubbing of fingers. Signs and symptoms of rightsided heart failure may be present.

86
Q

What is seen upon chest radiograph in patients with intrinsic restrictive lung disease (RLD)?

A

Reticular or reticulonodular

pattern with diminished lung volumes.

87
Q

How is intrinsic restrictive lung disease (RLD) diagnosed?

A

Lung biopsy

88
Q

What are some of the main differences between a person with COPD and RLD?

A

People with COPD will have problems getting air out, especially within the 1st couple of seconds, but given enough time they will get there(their FVC will increase over time), however in people with RLD, their FVC stays constant

89
Q

What is the minimum ratio of FEV1/FVC for COPD?

A

< 0.7

90
Q

What is the disease staging prognosis for intrinsic restrictive lung disease (RLD)?

A
  • FVC 60-80%: Mild
  • FVC 50-60%: Moderate
  • FVC < 50%: Severe
91
Q

What are the characteristics of the use of 6MWT for the prognosis of intrinsic restrictive lung disease (RLD)?

A
  • Distance <212m

* Associated with poor 2-3 year survival rate

92
Q

What are the characteristics of Intrinsic RLD: Idiopathic Pulmonary Fibrosis (IPF)?

A

• Chronic restrictive lung disease occurring with no identifiable etiology,
- Ie, exposure to asbestos or drugs
• Destruction of alveoli and surrounding capillary network
• Progressive scar tissue formation which reduces lung compliance
• Loss of alveolar capillary density, impaired gas exchange, hypoxemia

93
Q

What are the characteristics of Intrinsic RLD: Sarcodosis?

A
  • Multisystem disease of uncertain (possibly autoimmune)
  • 90% of cases; can lead to diffuse interstitial fibrosis and PAH.
  • Younger than 40 years of age; African Americans have a 10 to 15 times higher incidence
94
Q

What are the characteristics of Intrinsic RLD: Asbestosis?

A
  • Chronic restrictive lung disease occurring with evidence of exposure to asbestos.
  • Increased risk for development of bronchogenic carcinoma
95
Q

What are the characteristics of Intrinsic RLD: Silicosis?

A
  • Chronic restrictive lung disease occurring with evidence of exposure to crystalline silica.
  • Acute and Chronic types
  • Involvement of upper lobe with nodules and “eggshell-like” calcification of hilar nodes.
  • Silicosis predisposes to infection with mycobacteria
96
Q

What are the characteristics of Intrinsic RLD: Hypersensitivity Pneumonitis (HNP)?

A
  • Hypersensitivity to certain allergens. Unlike asthma, which affects the larger airways (HNP) affects the alveolar septae.
  • Extremely aggressive progression
97
Q

What are the extrinsic causes of restrictive lung disease?

A
  • SCI

- Burns

98
Q

What are the characteristics of SCI causing extrinsic restrictive lung disease?

A
  • Above C3: require mechanical ventilation
  • C3- C5: variable impairment in diaphragm and accessory respiratory muscle strength; impaired cough
  • C6-8: Intact diaphragm and neck accessory muscles; impaired cough
  • Thoracic level: typically close to normal respiratory function
99
Q

What are the characteristics of burns causing extrinsic restrictive lung disease?

A

Inhalation damage

100
Q

What are the characteristics of acute inhalation damage that causes extrinsic restrictive lung disease?

A
  • Upper airway edema within first 24 hours
  • Bronchospasm 12-36 hours
  • Gas exchange impairment: pulmonary edema; carbon dioxide poisoning

Long term: increased risk for development of interstitial fibrosis

101
Q

What are the neuromusc dysfunction: abnormal breathing patterns seen in patients with extrinsic restrictive lung disease?

A 
• Brainstem: Abnormal breathing (Apnea)
• Quad and paraplegics
  - Abdomen rises
  - Upper thorax sucks in
• Post polio
  - Upper throrax rises
  - Abdomen sinks
102
Q

What are the pulmonary implications of obesity?

A

Obesity-hypoventilation syndrome (Pickwickian syndrome)
• Fat deposits over chest wall decrease chest wall excursion/mobility
- Mechanical loading of respiratory system
• Chest wall compliance is lower, work of breathing higher
• Combines obesity and arterial hypercapnea (high CO2)
• Chronic hypoxia blunts responsiveness of chemoreceptors that increase respiration
• Early signs/symptoms include headache, fatigue, hyper-somnolence (as with OSA)
• Can eventually lead to pulmonary HTN and right ventricular failure
• Change in lung volumes
• Respiratory muscle weakness
• Impaired aerobic capacity
• Obstructive sleep apnea (OSA)

103
Q

What is the diagnostic criteria for obesity hypoventilation syndrome?

A
  • Body mass index >/= 30 kg/kg^2
  • Daytime PaCO2 > 45 mmHg
  • Associated with sleep related breathing disorder (obstructive sleep apnea- hypopnea syndrome or sleep hypoventilation or both)
  • Absence of other known causes of hypoventilation
104
Q

What are the components of the change in lung volume that is a pulmonary implication of obesity?

A

• Decreased expiratory reserve and functional residual capacity (further enhanced in supine)
• Total Lung Capacity (TLC) and Vital capacity (VC) reduced.
• Residual Volume Spared
• Reduction in Forced expiration in 1 second (FEV1) but FEV1/FVC ratio is usually
spared (Restrictive Lung Disease Pattern)

105
Q

What are the components of respiratory muscle weakness that is a pulmonary implication of obesity?

A

Muscle inefficiency

106
Q

What are the components of obstructive sleep apnea (OSA) that is a pulmonary implication of obesity?

A
  • Intermittent upper airway obstruction
  • Pharyngeal musculature does not maintain upper airway patency
  • Fall in SaO2, increased CO2 levels (hypercapnea)
  • Sleep disturbance, hypersomnolence
107
Q

What are the treatments/ ways to improve obstructive sleep apnea (OSA)?

A
  • Treated with CPAP (continuous positive airway pressure)

* Weight reduction has been shown to improve OSA

108
Q

What are the characteristics of asthma as a pulmonary implication of obesity?

A

• Narrowed peripheral airways due to fatty deposits in neck muscles
• Narrow airways = increased responsiveness
• Rapid shallow breathing pattern in morbidly obese
• GERD, low antioxidants, and enzymes related to adipose tissue increase airway
inflammation

109
Q

What are the characteristics of exacerbation of inactivity as a pulmonary implication of obesity?

A

• Chronic respiratory disease is associated with inactivity
• Dyspnea on exertion (DOE) makes prolonged aerobic activity difficult for obese
individuals

110
Q

What is pulmonary hypertension (PH)?

A

A spectrum of diseases involving the pulmonary
vasculature
• Defined as an elevation in Pulmonary arterial pressures
• Diagnosed with a right heart catheritization
• >25 mmHg at rest or >30mmHg during exercise

111
Q

What are the types/groups of pulmonary hypertension (PH)?

A
  1. Pulmonary arterial hypertension (PAH)
  2. PH due to left ventricular dysfunction
  3. PH due to lung disease
  4. PH due to chronic blood clots
  5. PH due to other miscellaneous diseases
112
Q

What are the signs and symptoms of pulmonary hypertension (PH)?

A

• In its early stages, symptoms are due primarily to the underlying disease
• Progressive dyspnea, particularly with exertion and later, at rest
• Dull retrosternal chest pain
• Fatigue, lightheadedness, Malaise, fatigue and
• Exertional syncope
• Normal Spirometry, reduced DLCO
• Non-productive cough, hemoptysis (rare)
• Narrow splitting of second heart sound (S2) with loud accentuated pulmonary
component (P2)
• May progress to R heart failure (cor pumonale)
- Right sided S3, elevated JVP, abdominal distention, hepatomegaly, ascites, lower extremity edema (in advanced disease)

113
Q

What are the characteristics of pulmonary arterial hypertension (PAH)?

A

• Relatively rare
• Can have idiopathic causes or due to drugs, toxins, genetic
• Symptoms of dyspnea, chest pain, and syncope
• Leads to R heart failure,
• High mortality rate
• Primary reported symptom is dyspnea on exertion are
- Frequently misdiagnosed with more common diseases such as asthma or chronic
obstructive pulmonary disease (COPD)
• No cure

114
Q

What are the characteristics for current pharmacologic therapies for pulmonary arterial hypertension (PAH)?

A

Improve morbidity and, in some
cases, mortality.
• Consistently fatal condition with no effective medical treatment options before 1996
• Prostacyclin and prostacyclin
analogues, phosphodiesterase-5 inhibitors(viagra), a soluble guanylyl cyclase stimulator, and endothelin receptor antagonists

115
Q

What is atelectasis?

A

Small airway collapse

116
Q

What are the causes of atelectasis?

A

• Common post surgery, obese individuals at a greater risk
• May be caused by prolonged dependency (especially lower lobes), secretions resulting
from chronic obstructive pulmonary disease, intubation, or anesthetic agents

117
Q

What are the signs and symptoms of atelectasis?

A

Fever, tachypnea, tachycardia, scattered rales, and decreased breath sounds

118
Q

What is likely to happen if a segment remains atelectatic >72 hours?

A

Likely to develop pneumonia.
• Easily preventable by taking full breaths (at least 10 and hour), early mobilization, frequent changes in position, encouragement to cough, and use of an incentive spirometer

119
Q

What are the histological phases of bacterial pneumonia?

A
  • Congestion
  • Red Hepatization
  • Grey Hepatization
  • Resolution
120
Q

What is congestion as a histological phases of bacterial pneumonia?

A

Presence of a proteinaceous exudate, forms consolidation

121
Q

What is red hepatization as a histological phases of bacterial pneumonia?

A

Congested vessels pour out exudate with fibrin and RBCs
which fill the alveolar spaces and give the consolidation a reddish appearance, neutrophil influx. Body is trying to trap the infection

122
Q

What is grey hepatization as a histological phases of bacterial pneumonia?

A

No new RBCs are extravasating and most have been degraded, gives the consolidation a greyish look

123
Q

What is resolution as a histological phases of bacterial pneumonia?

A

The debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory response, some exudate may remain in alveolus

124
Q

What is pneumonia?

A

An infection of the pulmonary parenchyma

125
Q

What are the bacterial causes of pneumonia?

A
  • CCAP: Streptococcus pneumonia, Staphylococcus aureus,

* HCAP: methicillin-resistant S. aureus (MRSA), Pseudomonas aeruginosa

126
Q

What are the viral causes of pneumonia?

A

Haemophilus influenza, Adenoviridae

127
Q

What are the other causes of pneumonia?

A
  • Community-acquired (CAP)

* Health care–associated pneumonia (HCAP)

128
Q

What are the characteristics of bacterial pneumonia?

A
  • Onset: Abrupt
  • Symptoms: fever, nausea, vomiting, malaise, pain (referred)
  • Signs: apprehension, flaring, grunting, tachypnea, decreased breath sounds
  • CXR: lobar, segmental consolidations, pleural fluid
  • Diagnosis: Sputum Culture
  • Treatment: Antibiotics
129
Q

What are the characteristics of viral pneumonia?

A

• Onset: Insidious (gradual)
• Symptoms: coughing with scant production, malaise, runny nose, low grade fever,
(think flu-like or URI)
• Signs: wheezing, rales, nasal flaring, tachypnea, overdistened chest
• CXR: diffuse airway changes, increased interstitial markings, area of atelectasis
• Diagnosis: clinical exam, cultures (to r/o bacterial), serology
• Treatment: Supportive, oxygen if needed, if indicated antivirals, no antibiotics, steroids not likely.

130
Q

What is acute respiratory failure?

A

Inadequate gas exchange by the respiratory system

131
Q

What are the characteristics of Type 1 acute respiratory failure?

A

Hypoxia without hypercapnia

  • Low PaO2 (< 55mmHg)
  • Normal PCO2 (35-45 mmHg)
132
Q

What are the characteristics of Type 2 acute respiratory failure?

A

Hypoxia with hypercapnia

  • Low PaO2 (< 55mmHg)
  • High PCO2 (> 45 mmHg)
  • Low PH (<7.3)
133
Q

____ is contraindicated during acute respiratory failure

A

Inspiratory muscle training is contraindicated during acute respiratory failure

134
Q

What are the causes of acute respiratory failure?

A
  • Pulmonary embolism
  • Pneumonia
  • Restrictive lung disease
  • Obstructive lung disease
  • Neuromuscular disease
  • Congestive heart failure
  • Unstable arrhythmia
  • Pulmonary edema
  • CVA
  • Overdose
135
Q

What are the goals of acute respiratory failure treatment: respiratory support?

A
  • Correct hypoxia and hypercapnia

- Rest respiratory muscles

136
Q

What are the methods of treatment of acute respiratory failure?

A
  • Non- invasive pressure ventilation
    - CPAP: continuous positive airway pressure
    • BiPAP: Bi-level positive airway pressure
  • Invasive: mechanical ventilation
137
Q

What are the characteristics of rib fractures?

A
  • Most common bony injuries in chest trauma and are diagnosed in approximately 50% of patients admitted to the hospital
  • Painful and closely associated with mortality and morbidity.
  • Fractures of ribs 1-3 indicate high-energy trauma
  • Lower rib fractures high risk of a possible intra-abdominal injury.
138
Q

What is flail chest?

A

Segmental fractures (in two or more locations on the same rib) of three or more adjacent ribs anteriorly or laterally that often result in an unstable chest

139
Q

What do we see upon inspiration in patients with flail chest?

A

Chest wall falls in

140
Q

What do we see upon expiration in patients with flail chest?

A

Chest wall falls out

141
Q

What are the characteristics of unequal chest expansion as seen in patients with flail chest?

A
  • V:Q mismatch
  • Atelectasis
  • Impaired pulmonary drainage
142
Q

What are the other presentations of flail chest?

A

• Lacerated organs
• Pain, dyspnea, hypoventilation, hypoxemia
(due to lung contusion)
- Possible respiratory failure

143
Q

What is Pneumothorax?

A

Air in the pleural space which can occur as a result of a breach in either the parietal (trauma,, surgery, etc) or visceral pleura (bulla, fine needle aspirations, etc).

144
Q

What are the characteristics of pneumothorax?

A

• Open chest wound may be termed an open PNX or
sometimes a “sucking chest wound.”
• Tension and open pneumothoraces are surgical
emergencies because both ventilation and venous return of blood to the heart are compromised.
• Ipsilateral lung collapses and causes hypoxia. Continued
pressure increases causes the mediastinum shift toward the
contralateral side and compresses both, the contralateral lung and the vasculature, worsening the hypoxia

145
Q

What are the signs and symptoms of pneumothorax?

A

Dyspnea, Sudden sharp

pain, fall in BP, Tachycardia, Cessation of normal respiration patterns, Hypoxemia, JVD, Tracheal Shif

146
Q

What are the characteristics of pulmonary embolism?

A

• Third most common cause of death in hospitalized patients
• Usually occurs in patients wither with previous venous thrombosis or at risk for
thrombosis
- Thrombus usually starts in the lower extremities and embolizes
• Can lead to cor pulmonale and eventually death

147
Q

What are the most common symptoms of pulmonary embolism?

A
  • Dyspnea, Sharp chest pain, pain with breathing, tachypnea, tachycardia hemoptysis
  • Muddled appearance when progressed
148
Q

What are the components of the Wells Score for pulmonary embolism?

A
  • Clinically suspected DVT — 3.0 points
  • Alternative diagnosis is less likely than PE — 3.0ptss
  • Tachycardia (heart rate > 100) — 1.5 pts
  • Immobilization (≥ 3d)/surgery in previous four weeks — 1.5 pts
  • History of DVT or PE — 1.5 pts
  • Hemoptysis — 1.0 pts
  • Malignancy (with treatment within 6 months) or palliative — 1.0 pts
149
Q

What is the interpretation of the Wells Score for pulmonary embolism?

A

• Score >6.0 — High (probability 59%])
• Score 2.0 to 6.0 — Moderate (probability 29%)
• Score <2.0 — Low (probability 15%)
• Score > 4 — PE likely. Consider diagnostic
imaging.
• Score 4 or less — PE unlikely. Consider D-dimer to rule out PE.

Acute care (9 decks)

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