You are on page 1of 52

Approach to Patient with

Acute Chest Pain


Prof. Bryan Yan
Head, Division of Cardiology
Objectives
1. To be able to rapidly & accurately assess a patient
complaining of acute chest pain

2. To formulate a list of likely differential diagnosis

3. To confirm or exclude differential diagnosis with


investigations

4. Not to miss life threatening causes


Wide Differential Diagnosis
§ Cardiac § Aorta
§ MI § Dissection
§ Pericarditis § Perforated ulcer
§ Myocarditis
§ Aortic Stenosis § Chest wall
§ Costocondiritis/musculoskeletal
§ Pulmonary
§ PE § Esophagus
§ Pneumonia § Esophageal Spasm
§ Asthma/COPD § Eosinophilic Esophagitis
§ Acute Chest Syndrome § Esophageal Rupture/Perforation
§ GERD
§ Pleura
§ Pleuritis § Mediastinitis
§ Pneumothorax § RUQ pathology
§ Panic attack
What are the 5 causes of chest
pain that can kill?
Chest Pain That Can Kill

1. Acute Coronary Syndromes


2. Pulmonary Embolism
3. Aortic Dissection
4. Esophageal Rupture
5. Pneumothorax

• Others: Myocarditis, Tamponade


Common “Benign” Causes of
Chest Pain?
Benign Chest Pain

• Musculoskeletal
• Esophagitis
• Bronchitis (secondary to cough)
• “Non-specific chest pain”
= we don’t know but it is not going to kill you
What are the key parts of the
history in chest pain patients?

• What can you get out of the patient in 5 minutes?


Good history will narrow your DDx in
most cases …… textbook approach
• HOPC
– Location: Central, left, or right
– Associated symptoms: SOB, sweating, nausea
– Timing: Gradual or sudden onset
– Provocation: What makes worse or better?
– Quality: Visceral vs somatic
– Radiation: Back, neck, arm
– Severity: Scale of 1-10
• PMH – CV risk factors (DM, HTN, Lipid)
• Meds
• Allergies
• Social
• Family
My unorthodox approach to acute
chest pain Patient Background
• PMH
– CV risk factors (Age, DM, HTN, Lipid, smoking)
– Known Dx, Ix, Rx (e.g. stress test, CTCA, PCI, CABG, PE & when?)
• Meds - Cardiac meds? (esp. when patient does not know his history)
• Family – Sudden Death? Early MI? DVT/PE?
• HOPC (line of questions directed by patient background)
– Location (point to it) & radiation
– Focal & reproducible by palpation vs. diffuse discomfort vs. sharp/tearing?
– If 1st time: what were you doing at the time?
– If recurrent: when was 1st episode? Pattern & changes over time
(frequency, duration, intensity, exertional, what makes worse or better?)
– Associated SOB, sweating, nausea, syncope, calf tenderness, cough etc
– Recent events? (surgery? Infection? investigations for same problem? etc)
Relief of pain by GTN ≠ ischemic
chest pain
• Value of pain relief by GTN is overrated at best
– Relieve both ischemic chest pain & esophageal spasm

• Need to ask about timing of pain improvement


after GTN
– GTN effect should begin within minutes
– Pain that starts to go away 30 minutes after a
sublingual GTN is probably not “relieved by GTN” but
it may be inappropriately reported as such in the
medical record
What are the key parts of the
physical examination?

• What can you exam in only 2 minutes?


Key Physical Signs
• General appearance
• Vital signs (BP, PR, O2Sat)
– BP both arms if suspicious of aortic dissection
– Atrial fibrillation?
• Heart sounds (Muffled? Murmur? Rub?)
• Lungs (Equal? Tympanic? APO?)
• Chest wall (localize palpable tenderness?)
• Neck (JVP?)
• Abdomen (Distension?)
• Lower Limb (Edema? Calf tenderness?)
Typical vs. Atypical Chest Pain
Typical Atypical

• Characterized as • Pain that can be localized with


discomfort/pressure rather one finger
than pain • Constant pain lasting for days
• Time duration >2 mins • Fleeting pains lasting for a few
• Provoked by activity/exercise seconds
• Radiation (i.e. arms, jaw) • Pain reproduced by
• Does not change with movement/palpation
respiration/position
• Associated with • BEWARE elderly & female
diaphoresis/nausea often present with atypical
• Relieved by rest/nitroglycerin symptoms!!!
Typical vs. Atypical Chest Pain
What are 3 bedside tests to
consider next?
Bedside Tests to Consider
• ECG (always ask for old ECG to compare)
• Portable erect CXR
• Bloods for hs-TnT (point-of-care testing available)

• Optional (Future): Hand-held echo


Case 1
• You are called by the nurse because Ms. Z has developed
chest pain in the ward.
• Ms. Z is a 65F with PMHx of CAD s/p remote MI & PCI,
COPD and right hip surgery 3 weeks ago who was
admitted for a COPD exacerbation.

• What would you do next?


Evaluation of Chest Pain in Ward

• Determine if patient is stable or unstable


• Perform focused history* & physical exam
• Interpret (& compare old) ECG
• Call for help if patient looks unstable or has concerning
ECG findings
• Documentation

• Review chart & CMS in real life but


BEWARE info error & subjective bias
Case 1
• Patient feeling better with paracetamol but suddenly
developed left-sided chest pain again, 8/10 and worse
with breathing. This pain is not like her prior MI.
• Vital signs: Afebrile, HR 120, BP 110/70, RR 28, O2 sat
89% on 2L (was 95% on RA this morning)
• Physical exam others: nasal flaring, intercostal/subcostal recession,
cyanosis, restless
– Gen – in distress, using accessory muscles of respiration
– Lungs – equal air-entry, no rales/wheezes
– Heart – H1H2 nil else
– Lower Ext – no edema or calf tenderness
• Labs:
– Hs-TnT 23.4 (normal <0.014)
Case 1 ECG: What do you see?
Case 1 CXR
What is your DDx?
§ Cardiac § Aorta
§ MI § Dissection
§ Pericarditis § Perforated ulcer
§ Myocarditis
§ Aortic Stenosis § Chest wall
§ Costocondiritis/musculoskeletal
§ Pulmonary
§ PE § Esophagus
§ Pneumonia § Esophageal Spasm
§ Asthma/COPD § Eosinophilic Esophagitis
§ Acute Chest Syndrome § Esophageal Rupture/Perforation
§ GERD
§ Pleura
§ Pleuritis § Mediastinitis
§ Pneumothorax § RUQ pathology
§ Panic attack
What is your next move?
Further investigations to rule out PE
• D-DIMER: 95% sensitive, VERY nonspecific
• ABG – Elevated A-a gradient fairly sensitive, highly
nonspecific
• ECG – most commonly nonspecific changes (tachycardia,
ST/T wave changes, S1Q3T3, etc)
• V/Q scan – helpful in patients with HIGH or LOW pretest
probabilities in whom a CTPE cannot be obtained (e.g. CKD)
• Lower limb Ultrasound: not sensitive (esp. proximal DVT)
• CTPA
– Sensitivity 83% (not exclude small PE): Specificity 96%
– Moderate-high clinical probability & positive CTPA: 92-96%
chance of PE
Case 1: Bilateral PE
Diagnostic approach is simple
if you suspect PE…
• Probability low: obtain D-DIMER
– If positive: obtain CTPA
– If negative: PE excluded

• Probability moderate-high: obtain CTPA


– If positive: treat
– If negative: PE excluded
Acute Pulmonary Embolism
Management
• Stabliize patient
– Oxygen
– Fluids if hypotensive
– Admit CCU/ICU for monitoring
• Anticoagulants
– Preferred: LMWH (vs. UFH)
– Switch to warfarin/NOAC on same day
• IVC filter an alternative in patients with mod-high bleeding risk
• PE with shock (i.e. massive PE)
– IV Thrombolysis
– Catheter-directed thrombolysis/thrombectomy
– Surgical thrombectomy
• PE with right heart dysfunction on echo/CT (i.e. submassive PE)
– Catheter-directed thrombolysis/thrombectomy
Case 2
• You have a new patient in the A&E. Mr. C is a 67M with PMHx
of HTN, T2DM, dyslipidemia and CAD s/p PCI in 2017. He
presents with new onset chest pain x 2 hours that is
retrosternal, 7/10, associated with nausea and diaphoresis. He
says he is having a heart attack.

• HR 108 BP 105/60 RR 20 O2 sat 93% on RA

• Physical exam:
– Gen – actively having chest pain, diaphoretic
– Lungs – crackles at bilateral bases
– Heart – H1H2 nil else
– Rest of the exam benign

• What’s your next move?


Case 2: Next Steps

• Review ECG
• Review CXR
• Troponin
• Stablize patient:
– Oxygen
– TNG/morphine
– Fluids
Case 2 Diagnosis: UA/NSTEMI
• ECG changes in Acute Coronary Syndromes:
– ST elevations
– ST depressions
– T wave inversions
• “pseudonormalization” – inversion of previously inverted T
waves when compared with old EKG
– New conduction block
– Q waves

• Importance of serial ECG monitoring: sensitivity of single


ECG is only 50% sensitive for acute MI
Current Guideline: 3 hour rule-out
Beware Non ACS Causes of TnT
Rise
Algorithm for risk stratification of
patients with ACS
UA/NSTEMI: Initial Management
• “Stabilize” plaque
– Dual antiplatelet therapy
• P2Y12 inhibitor: clopidogrel / ticagrelor
• ASA 320mg chewable, then 80-150 daily
– Anticoagulant
• LMWH
– High dose statin

• Optimize Myocardial O2 supply/demand


– Control HR to ~60 bpm if BP allows. Be wary of beta-blockers in
patients with heart failure!
– Supplemental O2 if hypoxemic
– Nitroglycerin infusion if ongoing pain
– Morphine if still having active chest pain
ECG QUIZ
NSTEMI or STEMI?

Wellen’s Syndrome
(Biphasic or deep TWI V1-4)
= Tight Proximal LAD stenosis
= high risk ACS
Out-of-hospital cardiac arrest &
cardiogenic shock.
NSTEMI or STEMI?

• Left Main Coronary Artery Occlusion


– ST elevation in AVR
– Widespread ST depression
NSTEMI or STEMI?

Posterior STEMI
NSTEMI vs. STEMI vs. Other

• Pericarditis
– Diffuse concave upward ST segment elevation in most leads,
– PR depression in most leads
What typical ACS meds should you
NOT give this patient?
Avoid

• Nitroglycerine
– Inferior MI = RV infarct -> RV failure -> preload
dependence
– Give fluids++ if hypotensive

• Beta-blocker
– PR 60bpm
– Risk of heart block
Case 3
• You are called to admit a 65 M for ACS rule out.
• Mr L has a history of T2DM, remote ACS and HTN
presenting with severe retrosternal chest pain.
• Pain is different than prior MI & radiates to neck.
• Began 3 hours ago; has subsided slightly but is still 8/10
• Right arm weakness
• HR110, BP145/80 in R arm, RR16, Pox 98%RA
• GEN: in discomfort but mentating well
• JVPNE. Left carotid bruit
• H1H2, soft EDM
• Lung clear
• ECG: TWI similar to before
What do you suspect & what are
you going to do next?
• Widened aortic knob
• Mediastinal widening
56% (type B) & 63%
(type A);
• Pleural effusion 19%
• Normal 11% (type A)
& 16% (type B)
Thoracic Aortic Dissection
Diagnosis
• CT angiography – first line
– 83-100% sensitive, specificity 87-100%
• TEE – second line; good for proximal, cannot visualize
descending aorta well
• MRI – useful for surveillance
Thoracic aortic dissection
Risk Factors
§ Hypertension
§ Atherosclerosis
§ Preexisting aneurysm (known history in 13% of patients)
§ Inflammatory conditions affecting aorta (Takayasu, Giant Cell
Arteritis, RA, syphilis)
§ Collagen disorders (Marfan, Ehlers-Danlos)
§ Bicuspid aortic valve
§ Aortic coarctation
§ Turner syndrome
§ History of CABG, AVR, Cardiac Cath
§ High intensity weight lifting
§ Cocaine use
§ Trauma
Aortic Dissection Presentation
(Difficult clinical diagnosis)
• 85% have chest or back
pain
• “Ripping” or “tearing” in
50%
• Neurologic symptoms in
20%
• Hematuria
• Asymmetric pulses
• Inferior STEMI
• Tamponade
• Aortic regurgitation
Thoracic aortic dissection
Management
Type A Type B
• Beta blockers, titrate to HR
• Surgery! 50-60 (labetalol, esmolol)
• Beta blockers, titrate to HR • BP control to SBP goal 100-
50-60 (labetalol, esmolol) 120mmHg
• BP control (nitroprusside) • Surgery for those with end
• Watch for hypotension – organ damage (renal,
give fluids if needed, mesenteric, lower-limb or
consider tamponade, MI, or those who do not respond
to medical therapy
rupture as complications
Thank You

You might also like