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Step 2 CK · Internal Medicine · Cardiology

Syncope & Cardiac Risk Assessment

Fainting from the benign to the deadly — plus who is fit for the OR

Cardiology·Cardiac Evaluation & Diagnostics·4 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy
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Syncope: three mechanisms

Definition. Syncope is a transient loss of consciousness from global cerebral hypoperfusion, with spontaneous, complete recovery. Every case falls into one of three buckets: reflex (neurocardiogenic), orthostatic, or cardiac. Cardiac syncope is the one that kills.

Types of syncope
FeatureReflex (vasovagal)OrthostaticCardiac
SettingPain, fear, sight of blood, prolonged standing, heatOn standing upExertion, while supine, or with no trigger at all
WarningProdrome: nausea, warmth, diaphoresis, tunnel visionLightheadedness on risingSudden, no prodrome; palpitations just before
CausesVagal surge with vasodilation and bradycardiaVolume depletion; diuretics, α-blockers, vasodilators; autonomic failure (diabetes, Parkinson disease)Arrhythmic: brady- or tachyarrhythmia, long QT, WPW, Brugada. Structural: aortic stenosis, HCM, PE, tamponade
PrognosisBenign; most common typeDepends on cause; falls in the elderlyMost dangerous; risk of sudden death

Reflex syncope. Vasovagal syncope is the most common cause overall and recovers quickly once the patient is supine. Situational syncope (cough, micturition, defecation) and carotid sinus hypersensitivity (shaving, a tight collar, turning the head) belong to the same reflex family. Management is reassurance, hydration, avoiding triggers, and physical counterpressure maneuvers at the first symptoms; tilt-table testing is reserved for recurrent or unclear cases.

Orthostatic hypotension is a fall in systolic BP of ≥20 mmHg or diastolic BP of ≥10 mmHg within 3 minutes of standing, confirmed with orthostatic vital signs. Polypharmacy in older adults is a frequent culprit. Stop offending drugs and restore volume; compression stockings, fludrocortisone, or midodrine help neurogenic cases.

Exertional syncope signals a fixed outflow obstruction, aortic stenosis or hypertrophic cardiomyopathy, until proven otherwise, so get an echocardiogram. A murmur that grows louder with Valsalva points to HCM.

Red flags and workup

Red flags for cardiac syncope. Any of these mandates a cardiac workup and often admission:

  • Onset during exertion or while supine
  • No prodrome, or palpitations just before the event
  • Known structural heart disease
  • An abnormal ECG
  • Family history of sudden death
  1. ECG for everyoneLook for long QT, delta wave (WPW), Brugada pattern, AV block, and LVH.
  2. Orthostatic vital signsA drop of ≥20 systolic or ≥10 diastolic within 3 minutes of standing.
  3. EchocardiogramFor suspected structural disease: murmur, exertional syncope, heart failure.
  4. Ambulatory monitoringHolter for frequent symptoms; event monitor or implantable loop recorder for infrequent ones.
  5. Tilt-table testFor recurrent, unexplained reflex syncope.

What not to order. Neuroimaging and EEG are low-yield without focal neurologic signs or features of seizure. A seizure is suggested by lateral tongue-biting, prolonged postictal confusion, and sustained tonic-clonic activity, whereas brief jerks with rapid recovery are common in plain syncope.

Long QT syndrome

>450 msprolonged QTc in men
>470 msprolonged QTc in women
>500 mshigh risk of torsades

Why it matters. A prolonged QT interval predisposes to torsades de pointes, a polymorphic VT that causes syncope and sudden death.

Congenital vs acquired long QT
FormFeaturesManagement
Romano-WardAutosomal dominant; normal hearingβ-blocker, avoid triggers and QT-prolonging drugs; ICD if high risk
Jervell-Lange-NielsenAutosomal recessive; sensorineural deafnessSame approach; typically higher risk
AcquiredDrugs; hypokalemia, hypomagnesemia, hypocalcemiaStop the drug and correct electrolytes

Drugs that stretch the QT. Antiarrhythmics (sotalol, class IA agents), macrolides, fluoroquinolones, antipsychotics (haloperidol), ondansetron, and methadone. Risk multiplies when several are combined or when potassium, magnesium, or calcium is low.

Acute torsades: give IV magnesium, stop the offending drugs, and correct electrolytes. Defibrillate if the patient is unstable.

Preoperative cardiac risk assessment

  1. Emergency surgery?Proceed without delay.
  2. Active cardiac condition?Unstable angina, recent MI, decompensated heart failure, severe valvular disease (especially severe aortic stenosis), or significant arrhythmia: delay elective surgery and optimize first.
  3. Estimate riskRevised Cardiac Risk Index plus the type of surgery.
  4. Functional capacity ≥4 METs?Climbing a flight of stairs or walking uphill without symptoms: proceed with no further cardiac testing.
  5. Under 4 METs or unknown, with risk factorsStress testing only if the result would change management.

Revised Cardiac Risk Index (RCRI). One point each for high-risk surgery (intraperitoneal, intrathoracic, or suprainguinal vascular), ischemic heart disease, heart failure, cerebrovascular disease, insulin-treated diabetes, and creatinine >2 mg/dL. Zero or one predictor means low risk; more predictors mean progressively higher risk of major cardiac events. Combine the score with functional capacity.

Perioperative medications. Continue β-blockers and statins in patients already taking them. Do not start a high-dose β-blocker on the day of surgery: in the POISE trial, perioperative metoprolol reduced MIs but increased strokes, hypotension, and total deaths. Coronary revascularization before noncardiac surgery is done only when it would be indicated anyway.