10.11 Non-Cardiac Chest Pain: Differential and Triage

The Discipline of Not Anchoring on ACS

Only a minority of patients who present with chest pain are having an acute coronary syndrome. On a cardiac unit the base rate is higher, and that is precisely the danger: anchoring bias means the aortic dissection gets aspirin and heparin, the esophageal rupture gets a troponin, and the tension pneumothorax gets a nitroglycerin drip. The 2021 AHA/ACC chest pain guideline made two framing changes worth knowing — it discourages the word "atypical" in favor of "cardiac," "possible cardiac," or "noncardiac" because "atypical" was being heard as "benign," and it foregrounds structured risk stratification and high-sensitivity troponin over gestalt.

The Immediate Life Threats and What Gives Each One Away

The Common and Benign Causes

• Gastroesophageal reflux and esophageal spasm. Burning, postprandial or recumbent pain; spasm can be squeezing and substernal and is genuinely indistinguishable from angina at the bedside. The critical trap: response to a "GI cocktail" (antacid plus viscous lidocaine) does NOT rule out ischemia — studies show no discriminative value, and the same is true of relief with nitroglycerin, which relaxes esophageal smooth muscle just as it does coronary smooth muscle.
• Peptic ulcer disease — epigastric, food-related, with a bleeding risk that matters enormously when dual antiplatelet therapy is being considered.
• Biliary colic and cholecystitis — right upper quadrant or epigastric pain radiating to the right scapula, Murphy sign; can present as inferior-sounding pain.
• Pancreatitis — epigastric pain boring to the back, elevated lipase; can produce ST changes and a raised troponin.
• Musculoskeletal and costochondritis — reproducible by palpation or movement, often after coughing, lifting or a recent procedure; Tietze syndrome adds visible swelling.
• Herpes zoster — burning, dermatomal, unilateral pain that precedes the rash by 2–5 days, so early cases have no rash to find.
• Panic disorder and anxiety — a diagnosis of exclusion in anyone with cardiac risk factors, never a first-pass explanation.

Cardiac but Not ACS

• Acute pericarditis — sharp, pleuritic, positional pain relieved by sitting forward, a friction rub, and the classic ECG of diffuse concave ST elevation with PR-segment depression (and PR elevation in aVR) that does not respect a coronary territory.
• Myocarditis — a young patient with a viral prodrome, a raised troponin, heart failure or arrhythmia, and non-obstructive coronaries.
• Hypertrophic cardiomyopathy — exertional chest pain, dyspnea and syncope; a murmur that increases with Valsalva or standing; nitrates and diuretics worsen the obstruction.
• Severe aortic stenosis — the triad of angina, syncope and heart failure with a crescendo-decrescendo murmur radiating to the carotids and a delayed, low-amplitude pulse.
• Stress (Takotsubo) cardiomyopathy — typically a postmenopausal woman after an intense emotional or physical stressor (bereavement, critical illness, an intracranial event, surgery), presenting with ST elevation or deep T-wave inversions and a troponin rise that is modest relative to the extent of wall motion abnormality, with apical ballooning and a hypercontractile base on ventriculography or echocardiography and normal coronary arteries. A marked QTc prolongation on day 2–3 puts these patients at risk for torsades. Most recover ventricular function within weeks, but the acute phase can include cardiogenic shock and LV outflow obstruction — in which case inotropes make things worse.

Diagnostic Reasoning: What the Findings Are Actually Worth

No single symptom rules ACS in or out, but likelihood ratios (LR) tell you which findings shift probability.

Reproducible chest wall tenderness is the most misused of these. It lowers probability substantially, but roughly 7% of patients with confirmed acute coronary syndrome have chest wall tenderness on palpation, so it is a modifier, never a rule-out — especially in a patient with a high pre-test probability or a rising troponin. In the same vein, a completely normal ECG does not exclude ACS; up to a fifth of patients with NSTEMI have a normal or non-diagnostic initial tracing.

High-Sensitivity Troponin Pathways

High-sensitivity cardiac troponin (hs-cTn) assays detect concentrations at the limit of detection in most healthy people, which enables rapid rule-out and rule-in.

• 0/1-hour and 0/2-hour algorithms use an initial value plus the absolute change (delta) across the interval. Rule-out requires a very low baseline value (below the assay's limit of detection with symptom onset more than 3 hours earlier) or a low baseline with a small delta. Rule-in requires a markedly elevated baseline or a large delta.
• The delta matters more than the absolute value. A static mildly elevated troponin in a dialysis patient is chronic myocardial injury; a rising and falling pattern is acute.
• Sex-specific 99th-percentile upper reference limits are used, because using a single male-derived cutoff systematically under-diagnoses women.
• Assay results are not interchangeable between hs-cTnT and hs-cTnI or between manufacturers — never compare a value drawn at another facility with a local one.

Non-ACS causes of a raised troponin — this list is heavily tested:

The HEART Score

Each component scores 0, 1 or 2 for a total of 0–10:

Disposition: 0–3 is low risk with under about 2% 30-day major adverse cardiac events and supports early discharge with follow-up; 4–6 is moderate risk and warrants observation, serial troponin and usually further testing; 7–10 is high risk and prompts an early invasive strategy. The score assumes a non-diagnostic ECG and hemodynamic stability — a STEMI or an unstable patient bypasses risk scoring entirely.

Sex, Age and Equity in Chest Pain Triage

Chest pain remains the most common presenting symptom of myocardial infarction in women, which corrects a widespread misconception. What differs is that women more often also report dyspnea, fatigue, nausea, indigestion, palpitations, and jaw, neck, back or interscapular pain, and are more likely to have a longer prodrome. Labeling those additional symptoms "atypical" has measurably contributed to under-triage.

The documented disparities are the exam-relevant point: women, Black and Hispanic patients, and patients with limited English proficiency experience longer door-to-ECG and door-to-balloon times, are less likely to be admitted to a monitored bed, less likely to receive guideline-directed medications, and less likely to be referred for revascularization or cardiac rehabilitation. Older adults and patients with diabetes present with dyspnea, confusion, syncope, weakness or falls instead of pain because of autonomic neuropathy and blunted perception. Patients with prior MINOCA, SCAD (spontaneous coronary artery dissection, which disproportionately affects younger women and peripartum patients) or microvascular disease are frequently dismissed as anxious.

The nursing countermeasure is protocol-driven rather than intuition-driven care: apply the same ECG timing standard and the same risk score to everyone, and escalate on objective criteria.

Nursing Triage Priorities

1. A 12-lead ECG obtained and shown to a qualified interpreter within 10 minutes of presentation with chest pain — the single most reproducible standard in this section.
2. Serial ECGs every 15–30 minutes when symptoms persist and the first tracing is non-diagnostic; changes are dynamic. Add posterior leads V7–V9 for suspected posterior infarction (tall R waves and ST depression in V1–V3) and right-sided V4R for inferior infarction to detect RV involvement, where nitroglycerin can cause profound hypotension.
3. Bilateral blood pressures on any severe or tearing chest pain before antithrombotics are given.
4. Continuous cardiac and oxygen saturation monitoring, IV access, and a full set of vital signs including respiratory rate — which is the vital sign that flags pulmonary embolism and pneumothorax.
5. Document pain characteristics precisely — onset (sudden versus gradual), quality, radiation, provocation, palliation, intensity and duration — before and after every intervention, and note whether the pain changed with palpation, position or respiration.
6. Do not use response to therapy as a diagnostic test. Neither nitroglycerin nor an antacid rules out ischemia.
7. Escalate on objective triggers: new ST deviation, a rising troponin, hemodynamic instability, hypoxemia, or a blood pressure or pulse differential.
8. Hand off structurally. Use SBAR and state the time of symptom onset, the ECG times and findings, the troponin values with their draw times, the risk score, the differential still open, and what has and has not been ruled out — the next nurse or provider inherits your anchoring unless you name the alternatives you are still considering.