CCP 215 - Respiratory Emergencies Flashcards

1
Q

What is expected of a patient’s HCO3 on ABG if they are chronically hypercapniec?

A

Use the “10-4” rule to determine appropriate HCO3 compensation. For example: A chronic PaCO2 of 60 (20 above normal) should have an expected bicarbonate of 32 (8 above normal).

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2
Q

What is the gold standard in assessing for PE?

A

CT-PE.

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3
Q

What are the three highest yield factors for differentiating shock?

A
  1. Skin temperature (distributive vs all)
  2. JVP (cardiogenic/obstructive vs distributive/hypovolemic)
  3. U/S (cardiogenic vs obstructive)
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4
Q

pH below ‘x’ requires resuscitation.

A

7.2

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5
Q

PaO2 and PaCO2 general limits:

A
PaO2 = No less than 60.
PaCO2 = No greater than 60.
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6
Q

PE CXR presents with:

A

No abnormalities. Though may later present with small areas of infarcted lung.

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7
Q

What is another scan that can be performed to assess for PE, other than CT-PA?

A

VQ scan.

Performed by sensing the gradient of diffusion of a test gas across the alveolar membrane.

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8
Q

List three populations that are at higher risk of PE (consider Virchow’s triad).

A
  1. Coagulopathy (ie. hormone replacement therapy).
  2. Endothelial dysfunction (ie. obesity).
  3. Stasis.
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9
Q

Why are trauma patients at a higher risk of PE?

A

Trauma patients have an impaired coagulation cascade.

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10
Q

What is Virchow’s triad?

A

Virchow’s triad describes the factors that lead to an increased risk of thrombosis.

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11
Q

What type of DVT indicates a high risk of PE?

A

Popliteal and upwards (ie. above the knee).

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12
Q

How can the presence of DVT be assessed?

A

An incompressible femoral vein may indicate the presence of a DVT.

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13
Q

What labs are expected to be elevated in PE?

A
  1. D-dimer, as a non-specific marker of clot degredation.

2. Troponin, from dilation of the RV and stretching of the myocardium.

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14
Q

Explain the treatment options of massive PE:

A
  1. Systemic thrombolysis for acute PE in any centre.
  2. Catheter directed thrombolysis (CDT) for patients who have had a cardiac arrest.
  3. Thrombectomy for pregnant patients or those in large centres.
  4. Anticoagulation to support the clot breakdown and no-further growth over a period of days.
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15
Q

Explain the treatment of sub-massive PE:

A

Anticoagulation.

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16
Q

Where do the lungs receive blood from?

A

The RV (though deoxygenated), as well as from the aorta.

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17
Q

Explain the RV spiral of death:

A
  1. Bulging of the interventricular septum into the LV.
  2. Impaired LV function from LV compression.
  3. Impaired right heart filling from high RV pressure.
  4. LVOT obstruction from the interventricular septum.
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18
Q

When should a pneumothorax be drained?

A

When there is hemodynamic compromise, or when deterioration is expected.

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19
Q

Explain obstructive atelectasis:

A

Obstructive atelectasis is the closure of alveoli from obstruction of the bronchiole (ie. from mucous plug). This is the cause of atelectatic lung in ARDS.

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20
Q

How does obstructive atelectasis cause mediastinal shift?

A

The mediastinum may be “pulled” towards the atelectatic lung from reduction in space-occupying lung in that particular region the thorax. There is a negative pressure exerted in the pleura during inspiration, which “pulls” the mediastinum towards the lowest area of pressure.

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21
Q

Explain the pathogenesis of negative pressure pulmonary edema:

A

Occurs in patients who are extubated and experience laryngospasm. Also occurs in chokings. Negative pleural pressure during inspiration “pulls” on the alveoli, but is unable to expand them with air due to obstruction. Instead, fluid is pulled from the adjacent capillaries.

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22
Q

What happens to the empty thoracic space when a lobectomy is performed?

A

The empty space gradually fills with transudate.

23
Q

Explain exudate vs transudate:

A

Exudate is caused by damage to the barrier (ie. membrane). Transudate is fluid shift across the barrier.

24
Q

Pleural effusions should always be drained, why?

A
  1. Obtains a diagnosis by culture.
  2. Relieves pressure.
  3. Reduces bacterial load and medium.
25
Q

Provide a brief explanation of Light’s criteria:

A

A traditional method of differentiating transudates and exudates using serum/pleural protein and LDH measurements.

26
Q

Uncomplicated vs complicated pleural effusion:

A
Uncomplicated = No bacteria.
Complicated = Cells present in effusion, suggesting either current or impending infection.
27
Q

What is an empyema, and what is the management of empyema?

A

A purulent infection within the pleural space. It requires chest tube or vacuum-assisted closure (VAC) thoracotomy.

28
Q

When is a pig tail appropriate for effusion drainage?

A

When draining air or thin fluid. Use a chest tube for blood.

29
Q

If a continuous bubbling occurs in the pleura-vac, what may be the cause?

A

Continuous communication with leaking air, indicating either bronchopleural fistula or air leak in the system.

30
Q

Improving pneumothorax may present as _______ on the pleura-vac

A

Decreasing drainage.

31
Q

Hemothorax that is draining excessive blood should be managed how?

A

Clamping of the pleura-vac. Consider auto-transfusion in large centres.

32
Q

What may worsen bronchopleural fistula?

A

PPV and over-suction by pleura-vac.

33
Q

What are the treatment goals of flail segment?

A
  1. PPV or CPAP to fixate the segment.

2. Pain control to promote appropriate breathing mechanics.

34
Q

How is contusional lung injury managed?

A
  1. Conservative fluid resuscitation to prevent further capillary leakage.
  2. Consider diuresis to reduce hydrostatic pressure.

Antibiotics not usually required for pneumonitis associated with traumatic ALI.

35
Q

How should severe hemoptysis & lung hemorrhage be managed?

A

Position “bad lung down” to contain hemorrhage. Consider right main-stem bronchus ventilation if the left lung is hemorrhaging.

36
Q

Diagnosis of capillary bleeding in the alveoli is diagnosed using ____.

A

Bronchial alveolar lavage.

In BAL, the alveoli are washed using a bronchoscope; if bleeding increases with lavage, it indicates alveolar hemorrhage with clot disruption.

37
Q

What is pulmonary-renal syndrome?

A

PRS is diffuse alveolar hemorrhage with subsequent glomerulonephritis. It is almost always caused auto-immune disease (ie. Goodpasture’s).

38
Q

What is the treatment of pulmonary-renal syndrome?

A

Immunosuppression with corticosteroids and cytotoxic medication.

39
Q

Describe the approach to bronchopleural fistula ventilation:

A

ACV with low tidal volume, low PEEP, low flow, and low suction. The goal is to keep the fistula closed as much as possible.

40
Q

What is the pathogenesis of cystic fibrosis?

A

CF manifests as autoimmune destruction of the bronchi, which prevents expulsion of mucous and results in severe mucous collections in the alveoli.

They are prone to pneumonia, pulmonary cysts, and blebs.

41
Q

Should blebs be drained?

A

NO! A bleb is a collection of air/fluid encapsulated by a thin layer of lung tissue.

If drained, it may result in pneumothorax, with possibility of a large bronchopleural fistula.

42
Q

What is idiopathic pulmonary fibrosis?

A

It is end-stage PF, thought to be caused by chronic gastric aspiration that gradually causes breakdown of lung tissue.

43
Q

What lobe is most commonly affected during aspiration?

A

Right middle lobe, due to ease of aspiration into this lobe.

44
Q

List two factors that increase the risk of pneumonia from aspiration:

A
  1. Poor oral hygiene.
  2. PPI therapy.

PPI therapy alkalinizes the gastric acid, creating an ideal environment for bacteria that thrive in alkalotic environments.

45
Q

What is the onset of aspiration pneumonitis, and are they usually sick?

A

Usually 1-2 from the event.

Yes, aspiration pneumonitis patients are some of the sickest we will see, but they often improve drastically with therapy.

46
Q

Why do asthmatics use inhaled steroids vs systemic?

A

Inhaled steroids exert local effects.

47
Q

Why are COPD/asthmatics at risk of chronic infections?

A

They are unable to clear mucous well, which is a medium for bacterial growth.

48
Q

Describe the approach to mechanical ventilation of asthmatics:

A
  1. Low PEEP (often autoPEEP is present, we want to avoid DHI).
  2. RR low (to allow for exhalation; don’t worry about matching RR once intubated).
  3. High flow (in order to allow prolonged expiratory phase)
49
Q

What is happening when a ventilated asthmatic patient begins having higher autoPEEP, but Pplat is reduced?

A

This is a good sign.

Decreasing Pplat correlates to an increase in compliance. Increase in autoPEEP correlates with additional air trapping, but the autoPEEP increases from additional alveoli being recruited.

50
Q

List three characteristics of COPD exacerbation:

A
  1. Hypercapnia.
  2. Hypoxemia.
  3. Change in sputum.
51
Q

In acute respiratory acidosis, what would the expected HCO3 compensation be?

A

PCO2 increase of 10 should correlate to an HCO3 increase of 1.

52
Q

At what measurement does PaCO2 begin producing drowsiness?

A

120 mmHg.

53
Q

What is the treatment of choice for steroids in asthma/COPD?

A

Methylprednisone. Prednisone is also an acceptable choice.