SOB Flashcards

1
Q

In the emergent SOB pt, while you are assessing your patient’s ABCs, you should request the following to occur simultaneously:

A
  • Vital signs
  • O2 via nasal cannula, non-rebreather mask, or bag-valve mask
  • IV access
  • Cardiac and pulse oximetry monitoring
  • /+ EKG

May need to consider non-invasive positive pressure ventilation (NIPPV)

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2
Q

What are some indications for non-invasive positive pressure ventilation?

A
  • Moderate to severe dyspnea
  • Accessory muscle use
  • Paradoxical abdominal movement
  • Fatigue
  • RR > 25 bpm
  • pH < 7.35, pCO2 >45
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3
Q

*What are some CONTRAindications for non-invasive positive pressure ventilation?

A
  • Respiratory arrest/absent respiratory drive
  • Hemodynamic instability
  • Aspiration Risk
  • Airway obstruction
  • Unable to tolerate mask
  • Mask does not fit
  • AMS
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4
Q

Orthopnea is typically thought of as a symptom of CHF but can also occur in these conditions.

A
  • COPD
  • Neuromuscular disorders
  • Pleural/pericardial effusions
  • Ascites
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5
Q

Rales in the setting of JVD and peripheral edema can be suspicious for __________.

A

CHF

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6
Q

List some conditions that rales can be seen in.

A

PNA, PE, pleural effusions, CHF

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7
Q

Signs of chest trauma, including crepitus, bruising, and tenderness can be suggestive of: (3)

A

PTX, hemothorax, pulmonary contusion.

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8
Q

Explain some reasons why US can be useful in SOB pts.

A
  • Can ID pneumothorax, pleural effusion, or consolidation. - Cardiac views can identify left ventricular dysfunction, right heart strain, pericardial effusions, and tamponade.
  • LE DVTs
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9
Q

An non-rebreather mask requires that the patient can breathe unassisted, but unlike low flow nasal cannula, the NRB offers what advantage?

A

Delivery of higher concentrations of oxygen.

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10
Q

____________________ is the leading diagnosis of patients older than 65 who are admitted to the hospital annually.

A

Acute decompensated CHF

- 75-80% of these pts are admitted from the ED

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11
Q

Describe the difference b/w systolic and diastolic heart failure.

A
  • Systolic failure is the hearts inability to pump the blood forward in the circulatory system. It is essentially has lost the “squeeze.”
  • Diastolic heart failure occurs due the fact that the muscles of the heart are unable to relax adequately (loss of elasticity) and allow the heart to fill appropriately.
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12
Q

In what type of heart failure is EF preserved?

A

Diastolic

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13
Q

List some causes of systolic HF.

A
  • Ischemic Heart Disease s/p MI
  • Coronary artery Disease
  • Hypertension
  • Fluid overload (and fluid retention)
  • Cardiac Dysrhythmias
  • Renal Disease
  • Valvular Disease (i.e. regurgitation, chordae tendonae rupture)
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14
Q

List some causes of diastolic HF.

A
  • Hypertension
  • Infiltrative Cardiomyopathy
  • Coronary Artery Disease
  • Diabetes Mellitus
  • Left ventricular hypertrophy
  • Chronic heart valve stenosis
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15
Q

*Recall what an s3 and s4 indicate in suspected CHF pts.

A

An S3 on exam can be indicative of fluid overload, while a S4 heart sound is associated with diastolic heart failure with stiff, non-pliable ventricles.

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16
Q

List the most common sx of CHF (4).

A
  • DOE
  • Orthopnea
  • PND
  • Hemoptysis
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17
Q

List the common PE signs of CHF (8).

A
  • Rales/wheezing
  • JVD
  • BLE edema
  • LE venous stasis
  • S3/S4
  • Hepatomegaly/hepatojugular reflex
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18
Q

What labs and tests should you order in the CHF pt?

A
  • EKG, cardiac enzymes (r/o cardiac ischemia)
  • BMP (*r/o renal involvement, lyte disturbance)
  • CBC (r/o contribution of anemia/thrombocytopenia)
  • CXR
  • BNP
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19
Q

BNP is released as a response to ___________________.

A

increased ventricular wall stress

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20
Q

Patients whose respiratory distress is secondary to HF will have elevated level of BNP greater than ____ pg/mL.

A

500 pg/mL

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21
Q

In CHF patients with moderate or severe respiratory distress, the application of _____________________ has been the only therapy used in management of HF that has consistently demonstrated decreased morbidity and mortality.

A

non-invasive ventilation (CPAP or BiPAP)

  • Reduces need for endotracheal intubation and mechanical ventilation
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22
Q

In the past, what was the main tx of acute CHF exacerbation?

A

Diuretic monotherapy

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23
Q

When is diuretic therapy indicated for the CHF pt?

A

If there is clinical evidence of FLUID OVERLOAD with increased jugular venous distention and other clinical findings

  • *It is imperative to note, that many patients presenting with heart failure are, in fact, euvolemic and will become hypotensive with diuretic therapy.
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24
Q

What is now the first-line tx for CHF exacerbation, and how does it work?

A

Focus on the use of nitrates to decrease pre-load, myocardial O2 consumption and systemic vascular resistance.
- The net result increases cardiac output and allows the heart to pump blood more efficiently through the vasculature.

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25
Q

Using nitroglycerin and occasionally nitroprusside (for CHF), healthcare providers must continually reassess for evidence of expected side effects including these 2 sx.

A

headaches and hypotension

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26
Q

There is a small sub-segment of the HF population who present not only with signs and sx of decompensated heart failure, but are also noted be hypotensive with cardiogenic shock. It is imperative that these patients be treated aggressively and efficiently. What medications do they require to support their BPs?

A

Inotropic medications including Levophed, dopamine and other peripheral vasoconstrictors (i.e. neosynephrine)

  • While on these medications, vital signs and evidence of end organ perfusion must be monitored carefully.
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27
Q

If, despite inotropic medications for CHF pts w/decompensated HF, there is continued evidence of progressive hemodynamic collapse, what should you consider doing next? (tough question)

A

Mechanical circulatory support including intra-aortic balloon pumps (IABP) and ventricular assist devices (VAD) may be utilized as temporary therapy.

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28
Q

On average, once diagnosed CHF, most patients succumb to their illness within ___ years.

A

5 years

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29
Q

Recall the 3 categories of ACS.

A

unstable angina, NSTEMI, STEMI

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30
Q

*What’s the difference b/w stable angina and unstable angina?

A
  • Stable angina: unchanged exertional pain lasting 5-15 minutes and relieved by rest or nitroglycerin
  • Unstable angina: increasing in frequency, at lower exertional levels or occurs at rest. This is a dynamic process which may lead to MI or death.
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31
Q

*How is acute MI diagnosed?

A

Requires 2 of 3:

  • A consistent clinical history
  • EKG changes
  • Changes in cardiac enzymes

(Later in article: “The diagnosis of ACS is ultimately made using cardiac catheterization”)

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32
Q

Which artery is typically affected in the following types of MIs?

  • Anterior
  • Septal
  • Inferior
  • Lateral
  • Posterior
  • Right ventricular
A
  • Anterior: LAD
  • Septal: LAD
  • Inferior: RCA (80%) or L circumflex (20%)
  • Lateral: L circumflex
  • Posterior: RCA or L circumflex
  • Right ventricular: RCA
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33
Q

For posterior MI, what ST changes would you expect?

A

Reciprocal ST depression in V1, V2, V3

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34
Q

For inferior MI, what ST changes would you expect?

A

Reciprocal ST depression in I, aVL

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35
Q

Describe what leads will show ST elevation in the following types of MIs.

  • Anterior
  • Septal
  • Inferior
  • Lateral
  • Posterior
  • Right ventricular
A
  • Anterior: V1, V2, V3, V4, V5, V6
  • Septal: V2, V3, V4
  • Inferior: II, aVF, III
  • Lateral: I, aVL, V5, V6
  • Posterior: V7, V8, V9
  • Right ventricular: V1, 4VR
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36
Q
Troponin I
Following cardiac ischemia, what is the time to:
- Initial elevation
- Peak elevation
- Return to baseline
A
  • Initial elevation: 3-12 hrs
  • Peak elevation: 10-12 hrs
  • Return to baseline: 3-10 days
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37
Q
Troponin T
Following cardiac ischemia, what is the time to:
- Initial elevation
- Peak elevation
- Return to baseline
A
  • Initial elevation: 3-12 hrs
  • Peak elevation: 12-48 hrs
  • Return to baseline: 5-14 days
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38
Q
CK-MB
Following cardiac ischemia, what is the time to:
- Initial elevation
- Peak elevation
- *Return to baseline
A
  • Initial elevation: 4-12 hrs
  • Peak elevation: 10-24 hrs
  • *Return to baseline: 48-72 hrs
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39
Q
Myoglobin
Following cardiac ischemia, what is the time to:
- Initial elevation
- Peak elevation
- Return to baseline
A
  • Initial elevation: 1-4 hrs
  • Peak elevation: 6-7 hrs
  • Return to baseline: 18-24 hrs
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40
Q

What is the most sensitive cardiac marker?

A

Troponin I

- Detectable in serum 3-6 hours after an MI, and its level remains elevated for 14 days.

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41
Q

Besides cardiac enzymes, what other tests should you consider ordering for MI w/u?

A
  • CBC (anemia may be a cause),
  • CXR (may show pulmonary edema or other causes of chest pain),
  • electrolyes, BUN and creatinine (may effect treatment regimens),
  • echocardiogram (usually after admission to look for regional wall motion abnormality),
  • stress testing (either exercise or chemically-induced exertion to look for EKG changes and/or decreased radionuclide uptake in the ischemic region).
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42
Q

*For a ST-elevation MI (STEMI), what criteria is needed to actually say there is ST elevation in the lumb leads? In the precordial leads?

A
  • Limb leads: ST-elevations of 1 mm or more in two contiguous limb leads (high lateral: I, aVL; inferior: II, III, aVF)
  • Precordial leads: 2 mm elevations (anterior: V1, V2, V3; lateral: V4, V5, V6).
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43
Q

If you’re strongly considering dx of MI in a pt w/o quite enough troponin and EKG evidence, how do you make the diagnosis?

A

TIMI Risk Score for Unstable Angina and Non-ST-Elevation MI’s (UA/NSTEMI)

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44
Q

Describe the criteria of the TIMI Risk Score for UA/NSTEMI.

A
65 or older?
3+ CAD risk factors?
Known CAD?
Aspirin use in past week?
Severe angina?
ST segment changes?
Positive cardiac markers?
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45
Q

*What is the initial tx for MI?

A

IV O2 monitor!

MONA greets all patients at the door.

  • IV access
  • Cardiac monitor
  • Morphine (no longer given)
  • O2
  • Nitroglycerin
  • Anti-thrombin therapy (e.g. heparin)
  • Anti-platelet therapy (e.g. ASA)
  • Beta-blockers
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46
Q

Besides pharmacological tx, what is the next step for STEMI and NSTEMI pts?

A
  • Those with persistent ST-elevations will need some sort of revascularization procedure – either pharmacological (thrombolytic) or an angioplasty in the cardiac catheterization lab.
  • Those without ST-elevations should get an angiogram when appropriately as determined by the interventional cardiologist.
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47
Q

In ACS pts, get an EKG within ___ minutes of presentation to the ED.

A

10 min

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48
Q

True or false: One set of negative enzymes and a normal EKG does not rule-out an MI.

A

False

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49
Q

True or false: Cardiac enzyme testing will be negative in patients with angina, functional testing is needed to discover any partially occluded coronary arteries.

A

True

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50
Q

The most common trigger of acute asthma is ________________.

A

URI

- Others: allergens, exercise, and psychosocial stress

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51
Q

*What are the indications for definitive airway management in acute asthma exacerbation (rapid sequence induction and intubation)?

A

Severe respiratory distress AND one of the following:

  • β2-adrenergic agonists (albuterol) or other medical therapies do not reverse symptoms
  • Significant hypoxia even with supplemental oxygen
  • Too tired to continue breathing on their own
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52
Q

What % of asthma pts in the ED will require airway mgmt (rapid sequence induction + intubation)?

A

< 1%

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53
Q

What tx’s/interventions are required in the ED asthma pt?

A
  • O2 (6-8L, nasal canula or non-rebreather)
  • Aerosolized B2 agonist (handheld or nebulizer)
  • Cardiac monitor
  • Pulse ox.
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54
Q

In asthma exacerbation tx, the goal of oxygen therapy should be to maintain SpO2 more than ___%

A

92%

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55
Q

*In a patient with a severe acute asthma exacerbation that is not improving with aerosolized albuterol, ____________ or ____________ should be administered.

A

SQ or IM epinephrine (0.2 mg, q20 min, up to 3 doses) or terbutaline (0.25 mg)

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56
Q

For asthma exacerbation patients who do not respond initially to albuterol, or who have a moderate to severe exacerbation, PO or IV ______________ should be administered early in the presentation.

A

Corticosteroids

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57
Q

What is the time to onset of action of corticosteroids (asthma exacerbation)?

A

4-6 hrs

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58
Q

What labs are required in EVERY asthma dx?

A

None, truely, unless you suspect infection as source

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59
Q

When is abg a good lab to order in asthmatic pts?

A

Only required when the pt remains hypoxic after the initiation of supplemental O2

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60
Q

When are PFTs helpful in asthma exacerbation?

A
  • Confirm that the patient’s symptoms are due to obstructive lung disease
  • Assess the severity of the exacerbation
  • Monitor the response to treatment.
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61
Q

In PFTs, peak expiratory flow rate is based on which of the following: sex, age, weight, height.

A

sex, age, height.

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62
Q

The first line therapy for acute asthma in the ED is _______________ in all age groups.

A

inhaled β2-adrenergic agonists (available as albuterol)

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63
Q

Besides aerosol, how else can albuterol be given? (1)

A

MDI

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64
Q

Albuterol has an onset of action of ________ and duration of action of _________.

A

5 min

6 hrs

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65
Q

What dose of albuterol is typically given in an MDI (used for mild-mod asthma exacerbation).

How often can you repeat the dose?

A

two 90 mcg puffs

q 4-6 hrs

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66
Q

In asthma exacerbation, nebulized albuterol is usually administered every ___ minutes for up to ___ doses.

A

20 min

3 doses

  • Each dose is 0.5-1.0 mL (2.5-5 mg) of solution in 3 mL of saline.
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67
Q

What’s an anticholinergic asthma agent?

When are these indicated?

A

Ipratropium

severe asthma or Beta-blocker induced asthma

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68
Q

Are anticholinergic agents ever given alone in asthma exacerbations?

A

No

- It can be combined with albuterol in a nebulized treatment (Duoneb) or in MDI form (Combivent)

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69
Q

High-risk patients who benefit from steroids in asthma exacerbation are those with frequent ED visits for:

A
  • exacerbations,
  • a history of intubation,
  • currently taking steroids, or
  • having a prolonged exacerbation.
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70
Q

For corticosteroids (asthma exacerbation tx), onset of action is ______, but it may take up to ______ to exert a significant clinical effect.

A

4-6 hrs

24 hrs

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71
Q

Besides tiotroprium, epinephrine, corticosteroids, what are some agents that may also be useful in acute, severe asthma exacerbation?

A
  • Mg2+
  • Abx (if infectious cause)
  • Heliox (80:20 or &0:30 He:O2 ratio)
  • Intubation (if all other measures fail)
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72
Q

What are some of the risks of resorting to intubation in acute asthma pts?

A

May result in barotrauma, PTX or hypotension from decreased venous return

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73
Q

What asthma tx agent is not recommended in acute asthma exacerbation?

A

Theophylline

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74
Q

Is the decision to admit an asthma pt based on their severity of initial clinical presentation or their response to tx?

A

Response to tx

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75
Q

In asthma exacerbation, the goal for discharge from the ED is to obtain more than ___% predicted or personal best FEV1 or PEFR.

A

70%

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76
Q

If you d/c an asthma pt from the ED, what should you make sure they go home with?

A
  • Action plan

- β2-adrenergic agonists and corticosteroids

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77
Q

*What necessitates ICU admission from the ED in asthma pts?

A

Any FEV1 or PEFR <25% of predicted that improves by <10% after treatment

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78
Q

*What typically necessitates hospital admission from the ED in asthma pts?

A

Pts with poor response to treatment, persistent severe sx, persistent hypoxia (< 90% SpO2) despite supplemental O2, and those with a PEFR or FEV1 <40% predicted require additional therapies and should be admitted to the hospital (still typically the ICU)

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79
Q

What are some secondary causes of copd?

A

air pollution, use of indoor cooking fires, and alpha-1 antitrypsin deficiency

(smoking #1 cause)

80
Q

The classic presentation of a patient with a COPD exacerbation includes these sx:

A
Cough
Wheezing
Chest congestion
Fatigue
Sputum change in color or quantity
Fever/chills
DOE
81
Q

List Causes of an Acute Decompensation of a COPD Patient.

A
Superimposed infection
Continued smoking
Non-compliance
Lack of usual medications or oxygen therapy
Spontaneous pneumothorax
82
Q

List Typical Signs of a Patient with a COPD Exacerbation.

A
Pursed lip breathing
Cyanosis/clubbing
Use of accessory muscles
Intercostal retractions
Barrel chest
Hyper-resonant chest
Wheezing
Prolonged expiratory phase
Tachycardia
Rhonchi, maybe rales

: jugular venous distention, leg edema, and hepatomegaly.

83
Q

In addition to typical COPD sx, those patients affected with cor pulmonale (ie, pulmonary hypertension) will present with:

A

R heart CHF sx: JVD, leg edema, and hepatomegaly.

84
Q

In COPD exacerbation, what type of O2 delivery device should be avoided?

*Why?

A

non-rebreather mask with 15 L/min of oxygen (unless not responding to lower flow rates)

  • In some patients with chronic CO2 retention, high flow O2 may cause RESPIRATORY DEPRESSION with the rapid rise in oxygen depressing the central ventilatory drive.
85
Q

Avoid this bias in COPD pts, since they are older and a broad ddx is required.

A

anchoring bias

86
Q

List some COPD exacerbation mimics to keep on the COPD ddx.

A

CHF, ACS, PE, PTX, pericardial effusion, and PNA

87
Q

What tests should be ordered to help narrow your DDX in COPD exacerbation?

A

CXR, EKG, BNP, ABG, and cardiac markers may be necessary.

88
Q

Recall some CXR findings in COPD exacerbation.

A
  • Increased AP diameter,
  • flattening of the diaphragm,
  • decreased lung markings and
  • the absence of another acute abnormality, such as pneumothorax, pulmonary edema or infiltrate.
89
Q

A rare, but specific heart rhythm finding in COPD patients is:

A

multifocal atrial tachycardia

90
Q

List some common EKG findings in COPD.

A

Low voltage, right axis deviation
P pulmonale- peaked P waves in II, III, aVF
Right atrial hypertrophy
Tachycardia
Multifocal atrial tachycardia (rare, but specific to COPD)

91
Q

Describe how these would change on ABG in acute decompensated CHF:

  • pH
  • pCO2
  • pO2
  • O2 sat
A
  • pH: < 7.35
  • pCO2: rising
  • pO2: falling
  • O2 sat: < 92%
92
Q

Describe how these values would be on ABG in acute compensated CHF:

  • pH
  • pCO2
  • pO2
  • O2 sat
A
  • pH: low nl
  • pCO2: high
  • pO2: nl
  • O2 sat: > 92%
93
Q

Why might you order a bedside US in COPD pts?

A

R/o pericardial effusion or to look for a PTX

94
Q

*In general, besides O2, treatment of COPD exacerbation revolves around use of these 3 medications:

A
  • bronchodilators,
  • corticosteroids, and
  • antibiotics to treat superimposed infection
95
Q

True or false: after albuterol, you can go on to uses a LABA for COPD exacerbation.

A

False–salmeterol not indicated

96
Q

True or false: ipatropium can be used as an alternative to albuterol in COPD exacerbation.

A

True (q 4 hrs)

- Can combine albuterol and ipratropium as well (duoneb)

97
Q

For COPD exacerbations, the optimum steroid regimen is not established, but typical regimens are __-__ days with tapering doses in contrast to the 5 day pulse therapy employed with asthma.

A

10-14 days

98
Q

What are some hx findings that would indicate use of abx in COPD exacerbation?

A

Fever, color change of sputum, and increased volume of sputum

99
Q

What are some common abx used in COPD exacerbation?

A
  • macrolides,
  • fluoroquinolones,
  • tetracyclines
  • cephalosporins

Complications of antibiotics include: allergic reaction, gastritis, and C dificile colitis.

100
Q

*Continuing respiratory decompensation with worsening CO2 retention and hypoxia despite standard treatment are indications for: (2)

A

Adjunctive therapy with non-invasive positive pressure ventilation (NIPPV) or endotracheal intubation

101
Q

*While there are no absolute indications for starting positive pressure ventilation or intubating in COPD exacerbation, these are some good reasons to start them: (2)

A
  • worsening acidosis

- unresponsive hypoxia

102
Q

Which should you resort to first in COPD exacerbation, NPPV or intubation?

A

NIPPV (not invasive)

  • it should be started early before acute neurologic deterioration or respiratory depression occurs
103
Q

In COPD exacerbation, rapid sequence intubation (RSI) may be necessary for airway control, correction of hypoxia, and correction of CO2 retention. After intubation and sedation, the ventilator is set with a tidal volume of __-__mL per kg of ideal body weight (best calculated by length measurement of the patient).

A

4-5 mL per kg

104
Q

What mode should you set the ventilator to, once you intubate a COPD pt?

A

Assist control

105
Q

What’s a good method in figuring out if a COPD exacerbation pt can be d/c’d?

A

One simple test is a structured walk around the ED with continuous pulse oximetry. Patients who de-saturate significantly or become too dyspneic to complete ambulation cannot be discharged home.

106
Q

Which COPD exacerbation pts are admitted to the ICU?

A

Those who require non-invasive ventilation or intubation.

107
Q

Where are those with moderate COPD exacerbations dispo’d?

A

Wards

- Typically, for O2, steroid, and bronchodilator therapy.

108
Q

Recall:

In general, where are mild, mod, and severe ED COPD exacerbations dispo’d?

A
  • Mild: home usually
  • Mod: Floor (further medical mgmt)
  • Severe: ICU (they’re on NIPPV or intubated)
109
Q

Review the veins of the LE deep venous system.

A
  • calf veins (anterior tibial, posterior tibial, and peroneal veins)
  • popliteal vein
  • femoral veins
  • external iliac veins
  • Superficial femoral vein (is actually part of the deep system)
110
Q

What are some typical sx of DVT?

A

Complaints include general leg pain or a cramping sensation, fullness in the calf, swelling, edema or tenderness on palpation.

111
Q

What’s a good ddx for DVT?

A
  • Musculoskeletal strain or tear
  • Cellulitis
  • Superficial thrombophlebitis
  • Venous insufficiency
  • Lymphedema
  • Popliteal (Baker’s) cyst
112
Q

Discuss classic PE signs of DVT.

A
  • Unilateral swelling or edema of the extremity
  • Tenderness to palpation
  • Palpable venous “cord”

Homan’s sign is the classic sign of pain in the calf on passive dorsiflexion of the foot with the knee in extension; neither specific nor sensitive for DVT.

113
Q

What criteria are used to evaluate for pre-test probability DVT?

What are the cutoffs for low, mod, and high probability of DVT?

A

Well’s score

Score: 0=low probability, 1-2=moderate, >3=high

114
Q

Review/read the Well’s criteria for DVT

A
  • Active cancer-treated within previous 6 months (1 point)
  • Parlaysis, paresis, or recent immobilization (1 point)
  • Recent bedridden >3 days or major surgery within 12 weeks requiring general anesthesia (1 point)
  • Localized tenderness along the distribution of the deep venous system (1 point)
  • Entire leg swollen (1 point)
  • Calf swelling at least 3 cm greater than other side (1 point)
  • Pitting edema confined to symptomatic leg (1 point)
  • Collateral superficial veins (non-varicose) (1 point)
  • Previously documented DVT (1 point)
  • Alternative diagnosis at least as likely as DVT (-2 points)
115
Q

What criteria are used to evaluate for pre-test probability PE?

What are the cutoffs for low, mod, and high probability of PE?

A

Modified Well’s Criteria

Clinical Probability: Low probability < 2, Moderate 2-6, High > 6

116
Q

Review/read the Modified Well’s criteria for PE.

A
  • Clinical symptoms of DVT (3 points)
  • Other diagnosis less likely than PE (3 points)
  • Heart rate >100 (1.5 points)
  • Immobilization (3 days) or surgery in the past 4 weeks (1.5 points)
  • Previous DVT/PE (1.5 points)
  • Hemoptysis (1 point)
  • Malignancy (1 point)
117
Q

*What are some history / sx you should suspect in PE?

A
  • SOB or CP (classically)
  • Syncope
  • General malaise or functional deterioration
  • Pleuritic component to the chest pain (hurts worse with deep breaths)
  • Unilateral leg symptoms
  • Signs of R sided heart failure (JVD, peripheral edema)
  • Tachycardia in the setting of normal pulse oxygenation
118
Q

*Before modified Well’s criteria for PE risk stratification, what criteria can you use prior to help make a diagnostic decision?

A

PERC
(PE r/o criteria)
- A patient who is not judged as lowest risk, or who does not pass PERC, may be evaluated using Well’s Criteria

119
Q

Low risk PE patients have a low enough pretest probability, a negative __________ test will essentially rule out PE, while moderate and high risk patients need further workup.

A

d-dimer

120
Q

Why order a CXR in PE?

*What findings might you see?

A
  • Useful to rule out other diagnoses such as PTX, CHF, PNA.
  • Sometimes one can see unilateral ATX (as suggestive of PE)
  • May see Hampton’s hump (pulmonary infarct leading to pleural based wedge shaped area of infiltrate) or Westermark’s sign (unilateral lung oligemia; *dilation of pulm vessels proximal to the clot).
121
Q

What could you see on EKGs of PE pts?

A
  • Usually nonspecific.
  • Most common is sinus tachycardia
  • May see RBBB or evidence of R heart strain (S1Q3T3)
122
Q

Biologically, what is d-dimer?

A

A protein derived enzymatic breakdown of cross-linked fibrin.

123
Q

Besides PE, review some causes of elevated d-dimer.

A

malignancy, infection, inflammation, MI, strokes, advanced age, and pregnancy
- Therefore, only order if there is pre-test probability of PE/DVT.

124
Q

Is d-dimer better to rule out or rule in PE/DVT?

A

Rule out (good sensitivity and NPV, bad specificity and PPV)

125
Q

What is the current diagnostic test of choice for DVT?

A

LE doppler US

- Can also r/o Baker’s cyst

126
Q

Patients with a moderate or high pre-test probability for PE should have a imaging study with either _________ or __________.

A

CT Pulmonary Aniography (CTPA) or V/Q scan.

127
Q

When is V/Q scan useless?

A

Those with other airway dz

128
Q

_________ is now the accepted study to diagnosis PE in most emergency departments

A

CT PA

- Also rules out pneumonia, masses, effusions, aortic dissection or pneumothorax

129
Q

True or false: a negative VQ scan or CTA rules out PE in a pt with high pre-test probability of PE.

A

False (do further testing to empiric tx)

130
Q

Tx of PE?

A

Anticoagulant (heparin or NOAC)

131
Q

If anticoagulant contra’d for PE pt, what can you do?

A

IVC filter

132
Q

If anticoagulation is successfully started in a PE pt, do they still need to be admitted?

A

Yes (further monitoring and INR checking if warfarin)

133
Q

*When is tPA indicated for PE?

A

Thrombolytic therapy in the setting of PE is controversial and indicated in the setting of a massive PE with significant cardiopulmonary compromise or submassive PE with evidence of right heart strain (most commonly echocardiographic diagnosis.)
- 50mg bolus (unlike stroke, which is 0.9mg/kg, 10% push with 90% over 60 min)

134
Q

While all PE pts require admission, which require ICU admission?

A

If the PE is large enough to case cardiopulmonary compromise (large A-a gradient, low BP or pulse ox)

135
Q

List the 3 most common bugs seen in typical CA-PNA.

A

Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis

(seen on gram stain)

136
Q

What type of abx is usually adequate to stop the most common types of typical CA-PNA?

A

PCNs

137
Q

List the 4 most common bugs seen in atypical CA-PNA

A

Mycoplasma pneumonia
Chlamydophila pneumonia
Legionella species
Respiratory viruses

(can’t be seen on gram stain, require special cx)

138
Q

_____________ is the single most common pathogen causing CAP and is responsible for 20-50% of infections.

A

S. pneumoniae

139
Q

What are eg’s of pts at risk for Health-care associated PNA (HCAP)?

A
  • patients residing in nursing homes,
  • patients that have been recently hospitalized,
  • those that receive dialysis, IV medications, or home wound care.
140
Q

What is the criteria required to dx HCAP?

A

1 of 3:

  1. hospitalization for ≥2 days in the preceding 90 days
  2. residence in a nursing home/facility
  3. in the past 30 days:
    - attendance at a hospital or hemodialysis clinic
    - home or clinic IV therapy (abx and chemotherapy)
    - home wound care
141
Q

What are some common bugs to cause HCAP?

A
  • Pseudomonas aerugunosa
  • Escherichia coli
  • Klebsiella pneumonia
  • Acinetobacter
  • Staphylococcus aureus
142
Q

Hospital-acquired pneumonia (HAP) develops in patients ≥ ___ hours after hospitalization and (is / is not) incubating at the time of admission.

A

48

is not

143
Q

A subtype of HAP, ventilator-associated pneumonia (VAP) develops > ___-___ hours after intubation

A

48-72

144
Q

Why was the category of HCAP derived from HAP?

A

W/ the goal of identifying patients at increased risk for multi-drug resistant pathogens coming from community settings.

145
Q

List some PNA sx.

A

fever, chills, productive cough, pleuritic pain, chest pain, and shortness of breath or malaise.

146
Q

List a quick ddx of PNA.

A

Bronchitis, viral URIs, influenza, PE, TB, pleural effusion, and other cardiac-pulmonary pathologies.

147
Q

List some PE signs of respiratory distress in PNA pts.

A
  • nasal flaring,
  • retractions,
  • tripoding
148
Q

Describe the classic presentation of atypical CAP.

A

May have a more protracted course beginning with upper respiratory sx, slowly worsening cough, malaise and fatigue.

149
Q

What does rust-colored sputum typically indicate?

A

Strep pneumo PNA

150
Q

What bug would you suspect in a PNA pt with fever, myalgias, and fatigue?

A

Haemophilus influenzae

151
Q

Describe the presentation of chlamydiophila pneumonia.

A
  • pharyngitis, laryngitis and sinusitis

- outbreaks in close-contact settings (dorms, prisons)

152
Q

What type of atypical PNA often has GI sx?

A

Legionella

153
Q

*What are some r/f’s for S aureus HCAP? (5)

A
  • vent-dependence
  • IV drug use
  • immunocompromised
  • recent influenza infection
  • aspiration
154
Q

*What are some r/f’s for pseudomonas HCAP? (3)

A
  • high-dose steroid use
  • prolonged hospitalization or nursing home residence
  • preexisting lung disease
155
Q

What is aspiration pneumoNITIS?

A

A chemical injury from inhalation of gastric contents due to regurgitation that can occur with drug OD, seizures, stroke, or use of anesthesia.

156
Q

What GI tract pathogens may be seen in aspiration PNA?

A
  • Enterobacteriaceae
  • Pseudomonas aerguinosa
  • Staphylococcus aureus
157
Q

What types of abx are recommended for tx of aspiration PNA?

A

Antibiotics with activity against gram-negative organisms such as third-generation cephalosporins, FQs, and piperacillin

158
Q

What do the following types of pts have in common: solid organ transplants, cystic fibrosis, HIV/AIDS, hematopoietic cell transplants, pregnant women, and patients with immune defects.

A

Immunocomprimised

159
Q

Besides PCP, what is another important consideration for immunocompromised PNA pts?

A

TB (night sweats, weight loss, or exposure from shelters, prisons, or recent travel to endemic areas)

160
Q

The main diagnostic modality for both community and hospital acquired pneumonia is:

A

CXR

161
Q

How might atypical PNA appear on CXR?

A

patchy infiltrates

162
Q

*Fill in the organism:
On PNA CXR, lobar consolidation is typical of ________________ or ________________ while multi-lobar infiltrates are more consistent with _________________ or ________________.

A

Streptococcus pneumoniae or Klebsiella pneumoniae

Staphylococcus aureus or Pseudomonas aeruginosa

163
Q

True or false: bedside US is useful in ID’ing PNA.

A

True: sensitivity of 86% and specificity of 89%

164
Q

The gold standard for the identification of pneumonia is:

A

CT chest (but often just CXR is enough)

165
Q

Why should you order an EKG even if you are 101% sure it’s PNA?

A

Patients with CHF, cardiothoracic disease, and severe sepsis/septic shock may develop cardiac ischemia and infarction secondary to a severe pneumonia.

166
Q

Review some r/f’s for CAP.

A
cavitary lesions
leukopenia
severe liver disease
asplenia
pleural effusion
alcohol abuse
severe CAP
167
Q

True or false: In PNA pts, sputum induction for gram stain and culture should not be routinely performed in the emergency department.

A

False, as it poses an infection risk to both providers and other patients and is unlikely to change ED management.

168
Q

List some abx for CAP. (you know this, think)

A

Macrolides
Fluoroquinolones
Doxycycline

169
Q

List some abx for HCAP. (*what 2 major bugs do you need to target?)

A
*Antipseudomonal B-Lactam (Piperacillin) + tazobactum
Imipenem
Meropenem
Cefepime
Ceftazidime
Anti-MRSA agent
*Vancomycin
Linezolid
170
Q

List some abx for aspiration PNA. (think about what broad category you need to target).

A

Ampicillin / sulbactam
Piperacillin / tazobactum
or
Clindamycin plus an aminoglycoside

171
Q

What antibiotic is indicated for PCP?

*What antibiotic should you avoid in TB, and why?

A

Bactrim for PCP

*Suspected TB avoid use of fluoroquinolones as can increase resistance

172
Q

HCAP was created in 2004 because these pts were at increased risk for multi-drug resistance (MDI) infections, but why is this sometimes a problem?

A

Not all HCAP patients are actually at increased risk for MDR infections (overkill)

  • exposes patients to risks such as medication toxicities,
  • increases in morbidity associated with broader medications,
  • longer duration of antibiotic treatment,
  • longer lengths of stay.
173
Q

*List reasons why a PNA pt will require admission (4).

A
  • inability to tolerate oral antibiotic treatment,
  • hypoxia,
  • sepsis,
  • respiratory distress
174
Q

When will PNA pts need to be admitted to the ICU instead of the floor? (2)

A
  • septic shock

- severe sepsis

175
Q

*Why was the Pneumonia Severity Index (PSI) Scale developed?

A

Because it may help the provider identify lower risk patients for outpatient treatment with oral antibiotics.
- 5 risk classes

176
Q

What is the CURB-65 scale?

A

PNA risk stratification scale

177
Q

Review the CURB-65 criteria (for PNA risk stratification).

When does a pt require admission?

A
1 point for each:
C	Confusion
U	Urea nitrogen > or = 20 mg/dL
R	Respiratory rate > or = 30
B	Systolic BP <90 mm Hg or Diastolic BP < or =60 mmHg
65	Age > or = 65
  • Admit if score is 3 or higher.
178
Q

What specific layer part of the thorax fills w/ air during PTX?

A

Occurs when the potential space between the parietal and visceral pleura of the lung fills with air and collapses the lung

179
Q

A primary pneumothorax occurs in what group of pts?

A

patients that have no underlying pulmonary disease

180
Q

A secondary pneumothorax occurs in patients with an underlying medical disease, such as:

A
  • COPD
  • CF
  • Lung cancer
  • Marfan
181
Q

Occasionally, PTX pain is more severe in these 2 regions instead of the chest:

A

back and shoulder

182
Q

List some procedures that more commonly cause PTX.

A
  • central line,
  • thoracentesis,
  • pacemaker,
  • tracheostomy
  • biopsy
  • CPR
  • CPAP
183
Q

Classic presentation of tension PTX?

A

A patient in distress with tachycardia, tachypnea, hypotension and hypoxia

184
Q

Do PTX occur gradually or quickly?

A

Can be either

185
Q

*What are the classic exam signs of PTX (4-7)? (may need to treat before taking long hx)

A
  • Hypotension,
  • tracheal deviation away from the side of the injury,
  • distended neck veins,
  • respiratory distress/arrest.
    Others:
  • unequal breath sounds,
  • hyperresonance with percussion over the chest wall,
  • decreased wall movement on the affected side
186
Q

What’s a great question to ask pts whom you suspect of PTX?

A

Any procedures lately?

- Also ask about lung dz’s that could predispose

187
Q

True or false: CXR should be done for all PTX pts before tx.

A

False, if HDUS and suspicion high.

188
Q

An ___________ is the optimal study for demonstrating a collapsed lung.

A

upright CXR

189
Q

Recall some CXR signs of PTX.

A
  • Shifting mediastinum (if tension)
  • Subcutaneous air
  • Deep sulcus sign
190
Q

*When might US be useful in PTX pts?

A

When an upright chest x-ray cannot be obtained (eg, intubated patients and those in spinal precautions), ie when the pt must remain *supine.

191
Q

Recall some US signs of PTX.

A

Place probe in the 3-4th intercostal space on the anterior chest, look for:

  • lack of sliding movement of the pleura on the ribs
  • absence of the comet tail artifact
  • a “lung point” can also be seen at the location of the PTX, where the lung sliding (or lack thereof) are seen within the same view
192
Q

How is the dx of PTX made?

What about tension PTX?

A

The diagnosis of PTX is made by the combination of hx, PE, and radiography.

Tension PTX should be diagnosed and treated based on your H and P, without waiting for radiographic imaging.

193
Q

*Tx of tension PTX?

A

1a. O2 + cardiac monitor
1b. Needle decompression: Place a 14-gauge angiocatheter into the 2nd intercostal space at the midclavicular line (converts it to regular PTX)
2. Chest tube should be placed immediately thereafter as needle decompression is only temporizing

194
Q

*Tx of large PTX?

A

O2 + cardiac monitor

A large pneumothorax is usually defined as greater than 20%. In this situation, a chest tube is usually indicated.

195
Q

*Tx of small PTX? (3 options)

A
  • Needle aspiration
  • Small pigtail catheter
  • Simple observation with repeat CXR to assess for spontaneous resolution
196
Q

Dispo of majority of PTX pts?

A

Admission

197
Q

Consider a _______________________ in the post-CPR patient on positive pressure ventilation that again begins to decompensate.

A

tension pneumothorax