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43yo M w/no sig pHx presents to the ED for left-sided chest pain x3 days.

Atypical Chest Pain

Express

7-8/10 pleuritic chest pain onset during flight to Albuquerque 3 days prior. At the time, had not been exerting himself. Was seen at a hospital in New Mexico, treated with pain medications and had a negative cardiac work up. Patient went to urgent care today with persistent similar chest pain radiating to the neck. ECG was obtained and the patient was transferred here with concern for STEMI. Never had pain like this prior to onset. Notes some congestion and increased temperature up to 100 overnight at home, but no cough, orthopnea. Currently having chest pain associated with deep breaths.

ACS

"Typical" Angina

Substernal Chest Pressure

Brought on by exertional or emotional stress

Relieved with rest or nitroglycerin

Can be anything!

ACS

"Atypical" Chest Pain

Systematic reviews have tried to explore common non-ACS descriptions of chest pain and (with limited reliability) identified the following characteristics:

  • Pleuritic pain, sharp or knife-like pain related to respiratory movements or cough.
  • ●Primary or sole location in the mid or lower abdominal region.
  • ●Any discomfort localized with one finger.
  • ●Any discomfort reproduced by movement or palpation.
  • ●Constant pain lasting for days.
  • ●Fleeting pains lasting for a few seconds or less.
  • ●Pain radiating into the lower extremities or above the mandible.

Unstable Angina

Key features:

  • Angina at rest
  • ●New onset, severe, activity limiting angina
  • ●Increasing angina that is more frequent, longer in duration, or occurs with less exertion than previous angina

These patients present with:

  • NO elevation in troponins
  • MAY have EKG changes indicative of ischemia, but this isn't required!

This is a herald of myocardial infarction to come

TIMI

  • ●Age ≥65 years
  • ●Presence of at least three risk factors for coronary heart disease (CHD)
  • ●Prior coronary stenosis of ≥50 percent
  • ●Presence of ST segment deviation on admission ECG
  • ●At least two anginal episodes in prior 24 hours
  • ●Elevated serum cardiac biomarkers
  • ●Use of aspirin in prior seven days

TIMI Score

A higher TIMI risk score correlated significantly with increased numbers of events (all-cause mortality, new or recurrent MI, or severe recurrent ischemia requiring revascularization) at 14 days:

●Score of 0/1 – 4.7 percent

●Score of 2 – 8.3 percent

●Score of 3 – 13.2 percent

●Score of 4 – 19.9 percent

●Score of 5 – 26.2 percent

●Score of 6/7 – 40.9 percent

**This also applies to NSTEMI's as UA-NSTEMI are part of the same clinical spectrum!!**

Determine a patient's risk

When to be concerned ACS is real

If cardiac enzymes or EKG changes are consistent with ACS, it should be treated as real unless there is an overwhelming confounding explanation for this.

Even then, intervention may be necessary.

Beyond this, patients with intermediate risk and good stories consistent with ACS chest pain may need further workup or even cardiac catheterization, once other potential causes have been excluded.

Thombus and Embolus sure... but what else?

Coronary thrombosis with rapid clot lysis

Small vessel disease

Vasospasm (Prinzmetal angina)

Macro- and microemboli

Vasculitis

Coronary microvascular dysfunction

Myocarditis

Cocaine

Myocardial infarction after cocaine use involves several mechanisms.

It is related to the block of the re-uptake of norepinephrine that leads to and adrenergic effects.

  • Increased heart rate and blood pressure
  • Coronary vasospasm
  • Reduced oxygen delivery leads to myocardial ischemia.

Some evidence cocaine also:

  • Activates platelets
  • Increases platelets aggregation
  • Potentiates thromboxane production

UTOX

Treat this the same as ACS!

What do we do though?

In addition to this, benzos are indicated to decrease the stimulatory effects of the drug.

But DON'T give BBlockers alone, that would lead to unopposed alpha activity!!

Some of the big things you should make sure you don't miss!!

Non-ACS Chest Pain Emergencies

Pulmonary Embolism

Clots!

Invisible Lines

Pneumothorax

Letting things RIP

Aortic Dissection

Coughing up a storm

Pneumonia

Ba-dump Ba-dump

Arrhythmias

Swinging Hearts

Pericardial Effusions and Tamponade

Everything else

Pericarditis

Bronchitis

Volume overload in Heart Failure

Reflux

Esophageal spasm (may be relieved with nitroglycerin!)

Panic attacks

Musculoskeletal pain

Non-emergent Chest Pain

What other stuff do you want to ask this patient?

I'll ask the questions here

First things first

Temp: 98.3

BP: 125/74

HR: 76

RR: 16

pO2: 97% on RA

Eyeball 'em

General: NAD, WDWN, comfortable appearing

HEENT: NC/AT, PERRL/EOMI, anicteric sclera, MMM, OP clear

NECK: Supple, no JVD

Heart: Clear S1/S2, RR, HR 70s, no murmurs/rubs/gallops, no chest wall tenderness

Chest: Decreased breath sounds R base, otherwise CTAB, nlb, symmetrical expansion

Abd: Soft, nontender/nondistended, normal bowel sounds, no organomegaly

Ext: +2 peripheral pulses, no LE edema or other edema

Neuro: A&Ox4, cognitively intact, no focal defects, CN2-12 intact, sensation intact throughout, 5/5 BUE/BLE strength

Phlebotomize him, sheriff

"Stuck" in the waiting phase

The usual suspects

WBC: 10.5, Segs: 57%

Hgb: 12.1

PLT: 119

Na+: 141

K+: 4.3

Cl-: 104

CO2: 29

BUN: 11

Cr: 0.83

Glu: 104

Ca2+: 8.7

ALT: 44

AST: 29

Alk Phos: 36

TBili: 0.69

Albumin: 4.0

Total Protein: 6.3

INR: 1.2

PT: 12.6

aPTT: 29

Troponin T5: 36

CKMB: 1.0

CKMB Index: 1.0

CPK: 104

Heartbreakers

4 Hours Later

Troponin T5: 38

CKMB: 1.0

CKMB Index: 1.1

CPK: 95

Sure

Never got a BNPP

For arguments sake let's say it's 80

His heart grew 3 sizes that day

When is it elevated?

- Pulmonary embolism

- DVT

- Aortic dissection

- Trauma

- Other normal reasons

His D-Dimer: 1052

What the heck is a 'D-Dimer'?

Age-adjusted?

Study in BMJ (2013) showed baseline levels of D-Dimer increase with age; recalculation of ULN based on this is:

[patient's age in years × 10 mcg/L]

- for those >50

- 500 = ULN ≤age 50 or less≤≤

Case-crackers

Other labs

ABG: 7.38/43/208

ESR: 7

CRP: 5.40

In a fantasy world where EMRs are connected...

Cardiac Criminal Records

Clinic and in ED:

EKG

Nada: but here's an abdominal ultrasound report?

4 months prior:

"Ectasia of the bilateral iliac arteries without aneurysm.

No abdominal aortic aneurysm."

ECHO

Nothin'

Stress Testing

Super nada.

Left Heart Catheterization

Mugshots

Pics or it didn't happen

CXR

Radiology read:

"Small to moderate volume right pleural effusion. Right base opacity compatible with passive atelectasis with the without superimposed infection."

Read as:

Bedside

Good squeeze

No wall motion abnormalities identified

Trace pericardial effusion

ECHO

Formal ECHO later

Formal ECHO later on

Stress Testing

None available, but what could you get?

Adenosine MIBI

Exercise Stress Test

Dobutamine Stress Test

Stress ECHO

Options

CTA Coronary

None available, but when would you use this?

Unhelpful when:

The patient has stents!!

The artifact from the stents makes it near-impossible to identify coronary lesions occuring within the stent.

Having many stents can make it challenging to assess patency at all due to artifact.

Well what now?

CTA Chest or CTPE

Where do we go now?

This circle exists solely in case I accidentally click on it and almost ruin the mystery

Lock him up, deputy

Aortic Dissection

Our diagnosis

Stanford (Daily) classifications

Classified

Risks

- HTN (particularly severe/sudden)

- Syndromic genetic disease (Marfan, Ehlers-Danlos, Turner syndrome, Osteoarthritis syndrome)

- Nonsyndromic genetic disease (Familial aortic aneurysm/dissection, bicuspid AV, coarctation)

- Personal aortic aneurysm history

- Inflammatory conditions

- Aortic instrumentation, trauma, surgery

Risk Factors

Classic Signs/Symptoms

Presentation

1) Pain

- typically 'radiating' to the back

- sharp, knife-like

- occurs in over 90 percent of patients, with 85 percent noting the onset to be abrupt

2) Pulse deficit

- from intimal flap or compression by hematoma

- can be greater that 20mmHg systolic

3) Aortic Regurgitation murmur

4) Hypotension

5) Syncope

6) Ischemia in sites distally (Stroke, Horner's syndrome, Paraplegia, Mesenteric ischemia)

Preferred Modalities

Diagnosis

EKG - RCA STEMI (Interior leads)

CXR - Widened mediastinum

D-Dimer - Not commonly used!! Some studies have shown up to 18% of patients with acute dissection have levels <400!!

Stable: CT Angiography (lucky we had aortic phase and it was so obvious!)

Unstable patients: TEE

- Post intubation and in OR

Presence of all 3 of the following is 96% sensitive and 83% specific for aortic dissection

Clinical Triad

  • ●Abrupt onset of thoracic or abdominal pain with a sharp, tearing, and/or ripping character

  • ●A variation in pulse (absence of a proximal extremity or carotid pulse) and/or blood pressure (>20 mmHg difference between the right and left arm)

  • ●Mediastinal and/or aortic widening on chest radiograph

Why the RCA?

Type A

-Life-threatening risks: Aortic regurgitation, Tamponade, Stroke, Frank rupture, MI

- Mortality rates 1-2%/hr after symptom onset w/o surgical intervention.

- Overall mortality: w/surgery: 7-36% at experienced centers; >50% with medical therapy alone

Type B: ONLY Descending involvement

- Typically managed medically; surgery reserved for those who develop complications (dextension/malperfusion)

- Endovascular repair is rising in interest

- Mortality (in-hospital) 10% per the IRAD (384 managed 73% medically)

The risks to the patient

Not a moment to lose!

IRAD review (547 patients w/A dissection; in-hosp mort 27 vs 56% for surgery vs medical alone. not perfect as medically treated patients were sicker/more comorbidities). another study of 487 patients showed similar survival rates.

Reasons surgery might be avoided: Limited prognosis for other reasons (age/frailty/surgical op risk/dementia/advanced malignancy/wishes).

Hemorrhagic stroke is a relative contraindication (surgery requires intra-op heparinization).

MI 2/2 dissection is NOT a relative contraindication to surgical intervention, and coronary angiography is typically NOT performed prior to intervention. (studies have shown no mortality difference between those that do or don't undergo coronary angiography prior to surgery)

What happened?

CT surgery was notified immediately after images were uploaded and screened through.

Patient went to OR within an hour, underwent an ascending and aortic arch replacement, antegrade TEVAR, resuspension of aortic valve.

His course and future care

Extubated on POD#1.

PT/OT on POD#2.

AFib w/RVR on POD#5, converted back with Amiodarone gtt.

Chest tubes were removed POD#6.

Small PE noted on POD#8, warfarin started after heparin bridge.

PT was discharged home on POD#10.

Still has some post-op pain and mild SOB, but otherwise patient appears to be doing well at home.

Post-Op

What to take from this:

Grand takeaways

1) When to be concerned for ACS

- Good stories

- Cardiac enzyme changes

- EKG signs of ischemia

2) Other causes of chest pain that shouldn't be missed, but are less common or more obscure

3) Typical presentation and workup for aortic dissection

4) Don't just dismiss atypical pain in young patients, make sure you do your due diligence!

References

Panju et al. "The rational clinical examination. Is this patient having a myocardial infarction?" JAMA. 1998;280(14):1256.

Morrow et al. "An integrated clinical approach to predicting the benefit of tirofiban in non-ST elevation acute coronary syndromes. Application of the TIMI Risk Score for UA/NSTEMI in PRISM-PLUS." Eur Heart J. 2002;23(3):223.

Schouten et al. "Diagnostic accuracy of conventional or age adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis." BMJ. 2013;346:f2492.

von Kodolitsch et al. "Clinical prediction of acute aortic dissection." Arch Intern Med. 2000;160(19):2977.

Paparella et al. "D-dimers are not always elevated in patients with acute aortic dissection." J Cardiovasc Med (Hagerstown). 2009;10(2):212.

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