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EM > Chest Pain > Flashcards

Chest Pain Flashcards

1
Q
  • In almost every case of undifferentiated chest pain the experienced clinicians will at least initially consider the top 3 common causes of morbidity and mortality: (3)
  • In many cases, the experienced clinician will also consider and prepare for potential several other less common life-threatening conditions: (3)
A

ACS, pulmonary embolism, and aortic dissection.

Tension PTX, esophageal rupture, and pericarditis with potential cardiac tamponade.

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2
Q

What’s a good start for IVF in a pt with chest pain?

A

20-30 ml/kg of normal saline

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3
Q

*Describe the typical progression of EKG waveform changes during STEMI.

A
  1. T waves become wide/tall
  2. ST elevation
  3. T wave inversion, Q waves
  4. ST elevation improves
  5. Q wave remains, T wave normalizes
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4
Q

Describe the lung auscultation findings on a typical PE.

A

CTAB

May see unilateral leg swelling!

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5
Q

Besides sudden onset severe ripping pain to back, what other sx might be seen in aortic dissection?

A

paresthesia or paralysis

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6
Q

What is Hamman’s crunch, and what condition is it a/w?

A

crackle sound heard or felt in time w/ heart beat, a/w esophageal rupture

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7
Q

Describe the pain a/w pericarditis/tamponade.

A

Pleuritic chest pain and dyspnea

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8
Q

Review some less acute causes of chest pain.

A

Costochondritis, pleurisy, gastroesophageal reflux or an anxiety attack.

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9
Q

Genetic syndromes that place patients at increased risk of thoracic aortic dissection include: (4)

A
  • Marfan syndrome,
  • Loeys-Dietz syndrome,
  • Turner syndrome, and
  • Ehlers-Danlos syndrome (vascular type).
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10
Q

*Besides genetic syndromes, what else are r/f’s for thoracic aortic dissection?

A
  • Family history of aortic dissection or aneurysm
  • Personal history of aortic aneurysm or coarctation
  • Chronic or acute hypertension (as in stimulant abuse)
  • Polycystic kidney disease
  • Inflammatory vasculitis (e.g., giant cell arteritis)
  • Pre-existing aortic valvular disease (e.g., bicuspid aortic valve)
  • Recent surgical aortic manipulation
  • Pregnancy in women with chronic connective tissue disorders
  • Long-term exposure to corticosteroids or other immunosuppressive drugs
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11
Q

What are the Stanford classifications of aortic dissection? (used more often than DeBakey)

A

Type A: involves the ascending aorta

Type B: doesn’t involve ascending aorta

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12
Q

What are the DeBakey classifications of aortic dissection?

A

Type I: involves both ascending and descending aorta
Type II: involves only ascending aorta
Type III: involves only descending aorta

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13
Q

Aortic dissection is considered acute if less than ___ days have elapsed since the dissection occurred.

A

14

otherwise, considered chronic

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14
Q

Describe the vascular pathophysiology of aortic dissection. (i.e., which layer does blood enter into?)

A
  1. Entry of blood into the media through intimal tear.
  2. Pulsatile flow into the rent created by the tear propagates proximally and/or distally along the length of the aorta.
    - This may disrupt flow at the origin of any of the branch vessels, or the dissection may continue along the branch vessels to disrupt flow more distally. This includes any branches off the aorta, from the coronaries all the way down to the iliacs.
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15
Q

Consider the DDX of someone w/ suspected thoracic aortic dssection.

A
  • ACS
  • Aortic aneurysm
  • Cardiac tamponade (from another cause)
  • Esophageal rupture (Boerhaave syndrome)
  • PNA
  • PTX
  • PE
  • Stroke / transient ischemic attack.
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16
Q

Although vague and rare, what is the typical presentation of aortic dissection? (sex, age, PMH, type of pain)

A

Male in his 60s with a history of chronic hypertension who presents with “sharp/ripping/tearing,” sudden-onset, severe chest pain that radiates to the back.

  • may radiate to the interscapular area of the back (i.e., “between the shoulder blades”) or to the abdomen and low back
  • Neuro sx not uncommon
  • Syncope
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17
Q

What initial labs/studies/procedures should you do for suspected aortic dissection?

A
  • ABCs
  • 2 large-bore IVs
  • Uncrossmatched blood to the bedside
  • Cardiorespiratory monitoring
  • 12-lead ECG
  • Portable CXR
  • Bedside cardiac ultrasound for pericardial effusion & systolic function
  • Labs: CBC, CMP, PT/PTT, type & cross, troponin, lactate
  • Page cardiothoracic surgeon
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18
Q

What PE signs would make you suspect aortic dissection?

A

(Variable, nothing pathognomonic)

  • HTN (esp. in Type B)
  • Tachycardia (2/2 pain, anxiety vs compensatory). May see bradycardia if concomittent MI -> AV block.
  • Tachypnea (anxiety vs. lactic acidosis vs hemorrhagic pleural effusions)
  • systolic BP differential of greater than 20 mmHg between arms is obtained.
  • aortic insufficiency (diastolic) murmur
  • / + peripheral pulse deficit
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19
Q

Does CXR rule in, rule out, both, or neither, for aortic dissection?

A

Neither

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20
Q

What CXR findings lean toward thoracic aortic dissection?

A
  • Widened mediastinum
  • Abnormal aortic or cardiac contour
  • Displaced intimal calcification
  • Widened right paratracheal stripe (≥5 mm)
  • Tracheal deviation (usually rightward)
  • Opacified aortopulmonary window
  • Pleural effusion (usually left)
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21
Q

Should you always delay tPA for MI until you’ve r/o’d a thoracic aortic dissection?

A

Although 5% of thoracic aortic dissections may present with MI, can’t always r/o dissection first because it is so rare, and delayed tx of MI may increase overall population mortality.

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22
Q

In thoracic dissection, is Stanford type A or B more likely to present with HTN? Hypotension?

A

HTN: type B
Hypotension: type A

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23
Q

*For aortic dissection, a variety of imaging modalities are available in the emergency department, though _______________ is the most widely used definitive study.

A

CT angiography

sn/sp approaching 100%!

24
Q

In suspected thoracic dissection, for unstable pts who can’t leave the ED for CTA, what is the next best imaging option?

A

TEE

- Also allows you to assess valves

25
Q

Is TTE useful in thoracic aortic dissection?

A

Not as good as TEE, but can detect presence or absence of a pericardial effusion or wall motion abnormalities.
- Poorly sensitive for type B dissections

26
Q

The only lab test that has been reasonably studied and shows any promise as a screening tool for thoracic aortic dissection is __________. But…

A

D-dimer

  • however, lack of specificity -> may result in an increase imaging studies
  • many false negatives
  • Not recommended for screening
27
Q

What labs should you consider in thoracic aortic dissection?

A

> Hemoglobin acute or minor hemorrhage may not be reflected in the hgb immediately after the hemorrhage)
WBC count: elevated from stress response
Lactic acid: elevated from intestinal malperfusion
Creatinine: elevated from renal malperfusion
Troponin: elevated if myocardial necrosis
D-dimer may be useful

28
Q

In general, what is the major difference b/w Stanford A and B thoracic dissection management?

A
  • Type A dissections require emergent surgical repair
  • Type B dissections are largely managed medically in the acute phase.
    “Complicated” type B dissections may be managed medically or by open surgical or endovascular techniques, depending on features
29
Q

What are the general HR/BP goals in aortic dissection pts?

*What med class is recommended?

A

Keeping both the heart rate and blood pressure as low as possible while still ensuring end-organ perfusion is the objective.

  • BBs (eg esmolol)
  • Also nicardipine
30
Q

*When giving thrombolytics for STEMI, what should you make sure to document so that you show you’ve consider thoracic aortic dissection?

A

E.g., normal mediastinum on CXR, no upper extremity BP differential, equal pulses in all extremities, no neurologic findings, no murmur, gradual onset of pain, absence of back pain

31
Q

*When treating aortic dissection, _____________ should not be initiated prior to rate-controlling agents, as they may result in reflex tachycardia that serves to propagate the dissection.

A

vasodilators

32
Q

Do you need surgical consultations for pts with presumed chronic, stable stanford B aortic dissections?

A

Yes

33
Q

Review some precipitating events to CHF.

A

cardiac ischemia or dysrhythmias, infection, PE, physical or emotional stress, noncompliance in medication or diet, volume overload

34
Q

*Explain the NYHA CHF Classification system.

A

Class I – Ordinary activity not limited by symptoms
Class II – Ordinary activity leads to dyspnea, fatigue, etc
Class III – Marked limitation of ordinary activity
Class IV – Symptoms at rest or with any physical activity

35
Q

What has a better prognosis, systolic or diastolic HF?

A

Diastolic

36
Q

Whats the difference b/w low and high-output CHF?

A
  • In low output failure, there is decreased CO secondary to myocardial damage
  • In high output failure, the cardiac output is high or normal, but remains insufficient to supply oxygen demands
37
Q

What are some causes of low-output CHF?

A

ischemia, dilated cardiomyopathy, valvular disease or chronic hypertension

38
Q

What are some causes of high-output CHF?

A

hyperthyroidism, pregnancy, anemia, AV fistulas, beriberi or paget’s disease.

39
Q

*Come up with a basic ddx for CHF.

A 
COPD
PE
PTX
Anaphylaxis
Asthma
PNA
FB obstruction
ACS
40
Q

What are the initial actions to take/order for CHF exacerbation?

A
  • ABCs
  • Cardiac monitor, pulse oximetry, IV access with 2 large bore IVs
  • If hypoxic, give oxygen via 100% NRB facemask and consider CPAP, BiPAP or intubation.
  • *Elevate the head of the bed.
  • If chest pain, obtain an EKG and consider nitroglycerin.
  • CXR.
  • Labs for CBC with diff, CMP, Troponin, PT/PTT, BNP. May want to include lactate and blood cultures x2 if febrile.
41
Q

In CHF exacerbation, *you may need to have the patient dangle their legs over the side of the stretcher. Why?

A

To reduce venous return and decrease preload

42
Q

Describe the classic signs/sx of CHF presentation.

- Also, describe the sputum color/texture

A
  • Dyspnea
  • DOE
  • Orthopnea
  • PND
  • If sputum: pink and frothy.
  • Swelling, often lower extremities.
43
Q

*Is DOE more sensitive or specific for CHF?

A

Sensitivity of 100% and specificity 17%.

- The absence of DOE decreases the likelihood of CHF

44
Q

Is PND more sensitive or specific for CHF?

A

sensitivity 39%, specificity 80%

- The presence of paroxysmal nocturnal dyspnea increases the likelihood of CHF

45
Q

What major PE findings may be seen in CHF?

A 
HTN, diaphoresis, tachycardia
RHF
- JVD
- S3
- LE Edema

LHF

  • Rales (2/2 alveolar edema)
  • Wheezing (peribronchial edema)
46
Q

List different CXR findings in the CHF pt.

A
  • CM (common)
  • Effusions (common)
  • Peribronchial cuffing (thickened bronchial walls 2/2 edema)
  • Perihilar congestion
  • Cephalization (blood flow to upper lobes)
  • Pleural effusions
  • Kerley B lines (dilated lymphatics)
47
Q

What lab test is highly sensitive for CHF?

- At what level is CHF most likely?

A

BNP

<100 Unlikely CHF
100-500 Potentially CHF, although could also be PE,
Pulmonary HTN, ESRD, cirrhosis, or hormone replacement therapy
>500 Most likely CHF

48
Q

Normal ejection fraction is ___-___%. Patients with severe CHF may have EF less than ___%

A

55-75%

20%

49
Q

*Besides CXR, what’s a second radiographic study that may be useful in CHF, and *why?

A

Echocardiogram

- Determining EF
Visualize:
- ventricular size
- wall abnormalities 
- valvular pathology
- pericardial thickening
- tamponade
- constrictive pericarditis 
...as additional contributors to CHF
50
Q

What medication tx for CHF is indicated for normotensive pts?

A
  • Nitrates (SL, IV, TD)
  • IV Morphine for pain + vasodilates
  • IV diuretics if indicated
51
Q

*What medications can be added for severe, persistent HTN in CHF tx?

A

IV Nitroprusside

52
Q

*What medications should be avoided in hypotensive CHF pts?

What should you give instead?

A
  • Avoid nitrates and morphine! (drops BP)

- Instead: dopamine, dobutamine, norepinephrine, amrinone or milrinone.

53
Q

*What medication class is indicated for severe or low-output CHF?

A

ACEI (increases hemodyanmic stability and exercise capability)

54
Q

What medication may help in the tx of DIASTOLIC CHF?

A
  • CCB may help (don’t use if concurrent depressed LV function -> ^ mortality)
55
Q

As pts’ CHF worsens, what surgeries may become an option? (3)

A
  • Automatic Internal Cardiac Defibrillator (AICD)
  • Left Ventricular Assistance Device (LVAD)
  • Heart transplant
56
Q

What is the only long-term definitive tx for heart failure?

A

Heart transplant (10 year survival is 50%)

57
Q

In CHF, CXR may lag by ___ hours.

A

12 hours (therefore, treat clinical sx)

EM (13 decks)

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