Cardiology — Heart Failure
101. Heart Failure
acute decompensated HF (HFrEF / HFpEF / volume overload / cardiogenic pulmonary edema) + the new-HF workup · decongest, identify the trigger, characterize the substrate · separate dosed plans per subtype · Super Compact
Approach — decongest the wet patient, then ask three questions: warm-or-cold, reduced-or-preserved EF, and what triggered this. Acute decompensated heart failure (ADHF) is mostly a congestion (volume) problem — relieve it with IV loop diuretics and NIPPV for flash edema — but the perfusion axis (warm/cold) flags the low-output patient who needs inotropes, not just diuresis. In parallel, characterize the substrate: HFrEF vs HFpEF, and in new presentations sort ischemic vs nonischemic cardiomyopathy. Always hunt the trigger (ischemia, arrhythmia/new AF, nonadherence/dietary, infection, uncontrolled HTN, PE, anemia, thyroid).
Key discriminators: orthopnea/PND/edema/JVD/S3 + congestion → wet (diurese) · cool extremities/narrow pulse pressure/hypotension/rising lactate/worsening renal function → cold/low-output (consider inotropes) · reduced EF (≤40%) → HFrEF (GDMT) · preserved EF (≥50%) with diastolic dysfunction/HTN/AF → HFpEF · regional wall-motion abnormality/known CAD → ischemic CM · global hypokinesis without CAD → nonischemic CM · flash pulmonary edema with severe HTN → afterload-driven (vasodilators)
Initial Sx/Data (all comers): dyspnea, orthopnea/PND, edema, fatigue, weight gain; exam — JVD, crackles, S3, edema, perfusion (extremity temp, pulse pressure) · BNP/NT-proBNP, troponin, ECG, CXR, BMP, CBC, LFTs, TSH; bedside US (B-lines, IVC); echo (EF, valves, wall motion, diastology) · daily weights + strict I/O · (don't anchor — HFpEF, HFrEF, and high-output states all present "wet," and an MI or new AF is often the hidden trigger)
Neg (don't-miss): denies missed ACS (ECG + troponin) · denies missed PE · denies missed tamponade/severe valve lesion (echo) · denies cardiogenic shock (cold + hypotensive + end-organ hypoperfusion → ICU, not just more diuretic) · denies anchoring on "CHF" when sepsis/anemia/thyroid drive it
DDx: ADHF — HFrEF vs HFpEF · cardiogenic pulmonary edema · volume overload (cardiorenal, ESRD, iatrogenic) · ischemic vs nonischemic cardiomyopathy · (also: PE, pneumonia, COPD, ARDS, high-output failure, constrictive/restrictive disease, valvular emergency)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (new/decompensated HF, shock, GDMT, advanced therapies) · CICU (shock, inotropes, mechanical support) · Nephrology (cardiorenal, ultrafiltration) · EP (device/CRT)
ADHF — HFrEF exacerbation
– Confirm: known/new EF ≤40%, congestion, ↑BNP, CXR congestion; echo confirms EF
– Decongest: furosemide ~1–2.5× total home daily PO dose IV (loop-naïve: 40 mg IV) BID, or continuous infusion 5–10 mg/h after a 40–80 mg bolus; add metolazone 2.5–5 mg PO daily for resistance; O2, NIPPV for distress
– GDMT (start/continue once euvolemic, as BP/renal allow): ARNI sacubitril-valsartan 24/26 mg PO BID → target 97/103 mg BID (or ACEi lisinopril 2.5–5 mg PO daily if ARNI not feasible; 36 h washout between) · BB carvedilol 3.125 mg PO BID or metoprolol succinate 12.5–25 mg PO daily (NOT during active decompensation) · MRA spironolactone 25 mg PO daily (if K <5.0, eGFR >30) · SGLT2i dapagliflozin 10 mg PO daily
– Monitor / daily labs: daily BMP (K, Cr, Mg), daily weights, strict I/O, telemetry; watch over-diuresis (AKI, hypokalemia)
– Dispo: PT/OT for deconditioning + ADLs, cardiac rehab referral, dietitian (≤2 g Na, fluid restriction); HF teaching (daily weights, when to call); cardiology/HF-clinic follow-up ≤7 days; med reconciliation
– Diuresis is the lever; the four pillars (ARNI/BB/MRA/SGLT2i) change mortality — start/uptitrate before discharge. Never push a beta-blocker in a decompensated, congested, or low-output patient.
ADHF — HFpEF exacerbation
– Confirm: EF ≥50% with congestion, diastolic dysfunction, typical substrate (HTN, AF, obesity, age); ↑BNP (may be lower in obesity)
– Decongest: IV loop diuretic to euvolemia (furosemide as above), avoiding over-diuresis (preload-dependent)
– Targeted Rx: aggressive BP control (afterload-sensitive); rate + rhythm control of AF (atrial kick matters); SGLT2i dapagliflozin or empagliflozin 10 mg PO daily (reduces HF hospitalization in HFpEF); treat OSA, obesity, CKD
– Monitor / daily labs: daily BMP, weights, I/O, telemetry; BP trend
– Dispo: PT/OT, dietitian (Na/fluid, weight management), BP self-monitoring teaching; cardiology follow-up ≤7–14 days; med rec
– HFpEF is a stiff ventricle — control the BP and rhythm, decongest carefully, add an SGLT2i. Over-diuresis tanks the output (preload-dependent).
Cardiogenic pulmonary edema (incl. flash)
– Confirm: acute severe dyspnea/hypoxemia, diffuse B-lines, often markedly ↑BP or an acute precipitant
– Rx: sit upright, high-flow O2, early NIPPV (CPAP/BiPAP); IV nitroglycerin start 10–20 mcg/min, titrate up q3–5 min (dominant lever in hypertensive flash edema); IV loop diuretic (furosemide 40–80 mg IV); intubate if failing NIPPV
– Treat precipitant: ischemia → ACS pathway; acute MR/AS → urgent cardiology/surgery; arrhythmia → rate/rhythm control
– Monitor: continuous SpO2/telemetry, BP q15 min on nitro drip, serial ABG, daily BMP/weights
– Dispo: step-down/ICU until stable; PT/OT once off NIPPV; HF teaching; cardiology follow-up
– Hypertensive flash edema is an afterload problem first — IV nitroglycerin + NIPPV do more than diuretics (fluid is redistributed, not always overloaded).
Volume overload (cardiorenal / mixed)
– Confirm: congestion + worsening renal function (cardiorenal), or ESRD/iatrogenic overload; assess true volume (IVC, JVD, weights)
– Rx: aggressive IV loop diuretics to net negative (venous congestion drives most cardiorenal AKI — adequate decongestion improves renal function); add metolazone 2.5–5 mg PO for resistance; ultrafiltration/urgent dialysis if diuretic-refractory or ESRD; hold ACEi/ARB/ARNI + nephrotoxins during significant AKI
– Monitor / daily labs: daily BMP (K, Cr), Mg, daily weights, strict I/O; tolerate modest creatinine rise during effective decongestion
– Dispo: nephrology if refractory; PT/OT; dietitian; resume GDMT when renal-stable; close follow-up
– In cardiorenal syndrome congestion is usually the culprit — under-diuresing for fear of the creatinine is the classic mistake; effective decongestion typically improves the kidneys (see the volume-overload card).
HF Workup — new HFrEF / new cardiomyopathy
– Confirm: new reduced EF on echo without prior history; characterize + find etiology
– Workup: echo (EF, wall motion, valves, diastology); ECG, troponin; coronary evaluation (cath or CT coronary angiography) — ischemic vs nonischemic; labs (TSH, iron studies, HIV as indicated, SPEP/free light chains + cardiac MRI if amyloid/infiltrative suspected); history (alcohol, anthracyclines, peripartum, family)
– Rx: initiate GDMT (as in HFrEF block); treat the specific cause
– Monitor: daily BMP, telemetry; repeat echo to track EF recovery
– Dispo: PT/OT, cardiac rehab; HF education; cardiology + heart-failure clinic follow-up; arrange outpatient device re-evaluation ~90 days post-optimization
– The first fork in new cardiomyopathy is ischemic vs nonischemic — that's why coronary evaluation is part of the workup. Then hunt reversible causes before calling it idiopathic.
HF Workup — ischemic vs nonischemic CM
– Confirm — ischemic: regional wall-motion abnormalities matching coronary territories, obstructive CAD, prior MI · nonischemic: global hypokinesis without CAD + a specific etiology (alcoholic, peripartum, tachycardia-mediated, myocarditis, infiltrative, familial, chemo, Takotsubo)
– Rx — ischemic: aspirin 81 mg PO daily, high-intensity statin (atorvastatin 80 mg PO daily), BB, ACEi/ARB; revascularization (PCI/CABG) for ischemia/viable myocardium; full HFrEF GDMT · nonischemic: treat the cause (abstinence; rate/rhythm control for tachycardia-mediated; immunosuppression for selected myocarditis per cardiology; disease-specific for amyloid); full GDMT
– Monitor: daily BMP, telemetry; serial echo for EF recovery
– Dispo: ICD/CRT evaluation per EF and QRS AFTER ~90 days optimized therapy; PT/OT, cardiac rehab; cardiology follow-up
– Some nonischemic cardiomyopathies recover with targeted therapy + GDMT (alcohol, tachyarrhythmia, thyroid, peripartum) — don't lock in an ICD before giving optimized therapy ~90 days to remodel the EF.
101. Heart Failure
complete reference · acute decompensated HF and the new-HF workup · congestion and perfusion axes · HFrEF, HFpEF, cardiogenic pulmonary edema, ischemic vs nonischemic · a dosed, bulleted plan per subtype · Full Card
Approach — Differentiate, Then Treat the Subtype
Acute decompensated heart failure is mostly a congestion problem — relieve it with IV loop diuretics and NIPPV for flash edema — but the perfusion axis (warm versus cold) flags the low-output patient who needs inotropes rather than just diuresis.
In parallel, characterize the substrate: reduced versus preserved ejection fraction, and in new presentations ischemic versus nonischemic cardiomyopathy, because that determines long-term therapy.
Always hunt the trigger — ischemia, a new arrhythmia such as atrial fibrillation, nonadherence or dietary indiscretion, infection, uncontrolled hypertension, pulmonary embolism, anemia, or thyroid disease.
Key discriminators: congestion (orthopnea, PND, edema, JVD, an S3) marks the wet patient; cool extremities, a narrow pulse pressure, hypotension, a rising lactate, or worsening renal function mark the cold low-output patient; a reduced EF (40% or less) is HFrEF, a preserved EF (50% or more) with diastolic dysfunction is HFpEF; regional wall-motion abnormalities with known CAD suggest ischemic cardiomyopathy, global hypokinesis without CAD suggests a nonischemic cause; and flash pulmonary edema with severe hypertension is afterload-driven.
Initial Symptoms / Data (all comers)
Dyspnea, orthopnea and PND, edema, fatigue, and weight gain, with an exam for JVD, crackles, an S3, edema, and perfusion (extremity temperature, pulse pressure).
BNP or NT-proBNP, troponin, ECG, CXR, BMP for renal function and electrolytes, CBC, LFTs, and TSH; bedside ultrasound (B-lines, IVC); and an echocardiogram for EF, valves, wall motion, and diastolic function.
Daily weights and strict intake and output.
Neg (don't-miss)
Pt denies a missed ACS (obtain the ECG and troponin, since ischemia is a top trigger and a separate emergency) and a missed PE (especially with a right-heart-failure picture).
Pt denies a missed tamponade or severe valve lesion (echo) and denies cardiogenic shock (a cold, hypotensive patient with end-organ hypoperfusion belongs in the ICU, not on more diuretic alone).
Pt denies anchoring on "CHF" when sepsis, anemia, or thyroid disease is the true driver.
DDx
Acute decompensated heart failure — HFrEF versus HFpEF · cardiogenic pulmonary edema · volume overload (cardiorenal, ESRD, iatrogenic) · ischemic versus nonischemic cardiomyopathy · (also pulmonary embolism, pneumonia, COPD, ARDS, high-output failure, constrictive or restrictive disease, and valvular emergencies)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (new or decompensated HF, cardiogenic shock, GDMT optimization, advanced therapies) · Cardiac ICU (shock, inotropes, mechanical support) · Nephrology (cardiorenal disease, refractory congestion, ultrafiltration) · Electrophysiology (device or CRT candidacy) · PT/OT and cardiac rehab · Dietitian (sodium and fluid)
ADHF — HFrEF exacerbation
Confirm: a known or new reduced EF (40% or less) with congestion (orthopnea, PND, JVD, edema, B-lines), an elevated BNP, and CXR congestion; echo confirms the EF.
Decongestion: an IV loop diuretic — furosemide at about 1–2.5 times the total home daily oral dose given IV (40 mg IV if loop-naïve) twice daily, or a continuous infusion of 5–10 mg/h after a 40–80 mg bolus; bumetanide 1 mg IV or torsemide are alternatives; add metolazone 2.5–5 mg PO daily (given 30 minutes before the loop) for diuretic resistance; O2 to keep SpO2 at least 90%, with NIPPV for respiratory distress.
GDMT — the four pillars (initiate or continue once euvolemic, as blood pressure and renal function allow): an ARNI, sacubitril-valsartan 24/26 mg PO twice daily uptitrated every 2–4 weeks toward 97/103 mg twice daily (or an ACEi such as lisinopril 2.5–5 mg PO daily, or an ARB, if an ARNI is not feasible — allow a 36-hour washout between an ACEi and an ARNI); an evidence-based beta-blocker, carvedilol 3.125 mg PO twice daily or metoprolol succinate 12.5–25 mg PO daily or bisoprolol 1.25 mg PO daily, uptitrated when stable (do not start or push it during active decompensation); a mineralocorticoid receptor antagonist, spironolactone 25 mg PO daily or eplerenone 25 mg PO daily (only if potassium is under 5.0 and eGFR over 30); and an SGLT2 inhibitor, dapagliflozin 10 mg PO daily or empagliflozin 10 mg PO daily.
Monitoring / daily labs: a daily BMP (potassium, creatinine) with magnesium, daily weights, strict intake and output, and continuous telemetry; watch for over-diuresis (a rising creatinine, hypokalemia) and adjust.
Mobility / consults: PT and OT for deconditioning and a functional and ADL assessment; a cardiac rehab referral; and a dietitian for sodium (2 g or less) and fluid-restriction education.
Discharge: the patient should be euvolemic and transitioned to an oral diuretic regimen with GDMT initiated and uptitrated; provide a daily-weight log, sodium and fluid-restriction instructions, medication reconciliation, structured HF education with teach-back (daily weights, symptoms prompting a call), and an early cardiology or HF-clinic follow-up within 7 days.
ADHF — HFpEF exacerbation
Confirm: a preserved EF (50% or more) with congestion, diastolic dysfunction on echo, and the typical substrate (hypertension, AF, obesity, age); the BNP may be lower than in HFrEF for the same congestion, especially in obesity.
Decongestion: IV loop diuretics to euvolemia (furosemide dosed as above), avoiding over-diuresis since these preload-dependent patients drop their output and pressure.
Targeted therapy: aggressive blood pressure control, since HFpEF is exquisitely afterload-sensitive; rate and rhythm control of AF, since the loss of atrial kick is poorly tolerated; an SGLT2 inhibitor, dapagliflozin 10 mg PO daily or empagliflozin 10 mg PO daily, which reduces HF hospitalizations in HFpEF; and treatment of comorbidities (obesity, OSA, CKD).
Monitoring / daily labs: a daily BMP, daily weights, strict I/O, telemetry, and a blood-pressure trend.
Mobility / consults: PT and OT; a dietitian for sodium, fluid, and weight management.
Discharge: euvolemic on an oral regimen with optimized blood pressure control; blood-pressure self-monitoring teaching, sodium and fluid instructions, medication reconciliation, and cardiology follow-up within 7–14 days.
Cardiogenic pulmonary edema (including flash edema)
Confirm: acute severe dyspnea and hypoxemia with diffuse B-lines, often a markedly elevated blood pressure (afterload-driven flash edema) or an acute precipitant.
Immediate therapy: sit the patient upright with high-flow O2 and early NIPPV (CPAP or BiPAP), which reduces work of breathing and preload and afterload and often averts intubation; IV nitroglycerin starting at 10–20 mcg/min and titrated up every 3–5 minutes for afterload and preload reduction in the hypertensive patient (the dominant lever in flash edema); an IV loop diuretic (furosemide 40–80 mg IV); and intubation if NIPPV fails.
Treat the precipitant: ischemia via the ACS pathway, an acute valve lesion (MR or AS) via urgent cardiology and surgery, or an arrhythmia via rate or rhythm control.
Monitoring / daily labs: continuous SpO2 and telemetry, blood pressure every 15 minutes while on a nitroglycerin drip, serial ABG, and a daily BMP and weights.
Mobility / consults: PT and OT once off NIPPV; a dietitian.
Discharge: manage in a step-down or ICU setting until stable, then transition to the HFrEF or HFpEF pathway as appropriate with HF education and cardiology follow-up.
Volume overload (cardiorenal or mixed)
Confirm: congestion with worsening renal function (cardiorenal), or overload from ESRD or iatrogenic fluids, with a careful assessment of true volume status (IVC, JVD, weights).
Decongestion: aggressive IV loop diuretics titrated to net negative, since venous congestion rather than low output drives most cardiorenal AKI and adequate decongestion usually improves renal function; add metolazone 2.5–5 mg PO daily for resistance; use ultrafiltration or urgent dialysis for diuretic-refractory overload or ESRD; and hold ACEi/ARB/ARNI and nephrotoxins during significant AKI, resuming when stable.
Monitoring / daily labs: a daily BMP (potassium, creatinine) with magnesium, daily weights, and strict I/O; tolerate a modest creatinine rise during effective decongestion.
Mobility / consults: nephrology if refractory; PT and OT; a dietitian.
Discharge: euvolemic on an oral diuretic regimen with GDMT resumed once renal-stable, medication reconciliation, daily-weight monitoring, and close cardiology and (if applicable) nephrology follow-up.
Heart Failure Workup — new HFrEF or new cardiomyopathy
Confirm: a new reduced EF on echo without a prior history, to be characterized with an etiologic search.
Workup: an echocardiogram (EF, chamber size, wall motion, valves, diastolic function), ECG, and troponin; an ischemia assessment with coronary evaluation (cardiac catheterization or CT coronary angiography) to distinguish ischemic from nonischemic disease; labs for reversible and secondary causes (TSH, iron studies, HIV as indicated, SPEP and free light chains with cardiac MRI if amyloid or infiltration is suspected); and a history for alcohol, chemotherapy (anthracyclines), the peripartum state, and family history.
Therapy: initiate GDMT (the four pillars dosed as in the HFrEF block) and treat the specific cause.
Monitoring / daily labs: a daily BMP and telemetry, with a repeat echo to track EF recovery over time.
Mobility / consults: PT and OT, cardiac rehab, and a dietitian.
Discharge: HF education, medication reconciliation, cardiology and HF-clinic follow-up, and a planned outpatient device re-evaluation at about 90 days after therapy optimization.
Heart Failure Workup — ischemic versus nonischemic cardiomyopathy
Confirm: ischemic disease shows regional wall-motion abnormalities matching coronary territories with obstructive CAD or a prior MI, while nonischemic disease shows global hypokinesis without obstructive CAD plus a specific etiology (alcoholic, peripartum, tachycardia-mediated, myocarditis, infiltrative or amyloid, familial, chemotherapy-related, or stress cardiomyopathy).
Ischemic therapy: guideline-directed CAD management — aspirin 81 mg PO daily, a high-intensity statin (atorvastatin 80 mg PO daily or rosuvastatin 20–40 mg PO daily), a beta-blocker, and an ACEi or ARB — with revascularization (PCI or CABG) for appropriate ischemia and viable myocardium, plus full HFrEF GDMT.
Nonischemic therapy: treatment of the specific cause (abstinence for alcoholic disease, rate or rhythm control for tachycardia-mediated disease, immunosuppression for selected myocarditis per cardiology, disease-specific therapy for amyloid) plus full GDMT.
Monitoring / daily labs: a daily BMP and telemetry, with serial echo for EF recovery.
Mobility / consults / disposition: PT and OT and cardiac rehab; an ICD or CRT evaluation per EF and QRS after about 90 days of optimized therapy (the EF may recover and remove the indication); and cardiology follow-up.
Red Flags
A cold, hypotensive patient with end-organ hypoperfusion → cardiogenic shock; ICU, inotropes, and mechanical support, not more diuretic alone
Flash pulmonary edema with severe hypertension → an afterload emergency; NIPPV and IV nitroglycerin take priority over diuresis
A rising troponin or ischemic ECG → an ACS trigger that is its own emergency
Refractory congestion with worsening renal function → diuretic resistance needing escalation or ultrafiltration
A new murmur with decompensation → an acute valvular emergency (acute MR, critical AS) requiring urgent echo and cardiology
Senior IM Resident Pearls
Congestion is the lever; perfusion is the alarm. Most ADHF is wet and warm and needs diuresis, but the cold low-output patient needs inotropes and the ICU, not just a bigger furosemide dose.
Flash edema is an afterload problem. The hypertensive patient with diffuse B-lines responds to NIPPV and nitroglycerin more than to diuretics, because the fluid is redistributed, not always overloaded.
The four pillars change mortality. ARNI/ACEi-ARB, beta-blocker, MRA, and SGLT2 inhibitor — start and uptitrate them in HFrEF before discharge, but never push a beta-blocker in a decompensated patient.
In cardiorenal syndrome, congestion is usually the culprit. Under-diuresing for fear of the creatinine is the classic mistake — effective decongestion typically improves the kidneys.
HFpEF is a stiff ventricle. Control the blood pressure and rhythm, decongest gently, and add an SGLT2 inhibitor; over-diuresis drops the output.
Always find the trigger. Ischemia and new AF are the usual hidden culprits behind a decompensation.
Common mistake: treating every "CHF" the same — missing the ischemia, the new AF, or the afterload that actually drove the decompensation, and discharging without optimizing the mortality-changing GDMT.
Cardiology — Ischemic Heart Disease
102. Acute Coronary Syndrome (ACS)
STEMI (occlusion → reperfuse now) · NSTEMI (type 1 plaque vs type 2 supply-demand) · unstable angina · the chest-pain rule-out · separate dosed plans per subtype · Super Compact
Approach — ECG first within 10 minutes, then troponin, then decide: reperfuse, risk-stratify, or rule out. The branch point is the ECG: ST-elevation (STEMI) = acute coronary occlusion → immediate reperfusion (primary PCI, or lytics if PCI unavailable) — minutes matter. Without ST-elevation, the troponin sorts it: a rise/fall = NSTEMI (then ask type 1 plaque rupture vs type 2 supply-demand mismatch), a normal serial troponin with unstable symptoms = unstable angina, and a reassuring evaluation = a chest-pain rule-out. Give the shared anti-ischemic + antithrombotic backbone, but tailor the plan — type 2 MI is treated by fixing the stressor, not by emergent cath.
Key discriminators: ST-elevation (or new LBBB/posterior MI) → STEMI — reperfuse now · ischemic symptoms + troponin rise/fall, no ST-elevation → NSTEMI · rise/fall with a primary plaque event → type 1 · rise/fall driven by another illness (sepsis, tachyarrhythmia, anemia, hypoxia, hypertensive crisis) → type 2 / demand · unstable symptoms + normal serial troponin → unstable angina · reassuring story, normal ECG/troponin, low HEART → non-cardiac / rule-out
Initial Sx/Data (all comers): chest pressure ± radiation to arm/jaw, exertional, diaphoresis, dyspnea, nausea (atypical/silent in diabetic/elderly/female) · ECG within 10 min (repeat if evolving) + serial high-sensitivity troponin · CXR, telemetry, IV access, vitals/SpO2; BMP, CBC, lipids, HbA1c; risk score (HEART/TIMI/GRACE) · (don't anchor — don't miss the can't-miss mimics: aortic dissection, PE, tension pneumothorax, tamponade, esophageal rupture)
Neg (don't-miss): denies missed aortic dissection (tearing pain to back, pulse/BP differential — antithrombotics here are catastrophic) · denies missed PE · denies a STEMI-equivalent on ECG (posterior MI, de Winter, Wellens, new LBBB) · denies right-ventricular infarct (inferior STEMI — preload-dependent, nitrates can crash them) · denies treating a type 2/demand troponin as a type 1 plaque event
DDx: STEMI · NSTEMI (type 1 vs type 2) · unstable angina · demand ischemia · non-cardiac chest pain (musculoskeletal, GERD, anxiety, costochondritis) · emergencies — aortic dissection, PE, pneumothorax, pericarditis/tamponade, esophageal rupture, myocarditis, Takotsubo
Plan — by Diagnosis
CONSULT (as relevant): Cardiology / Interventional cardiology (STEMI — activate cath lab; NSTEMI risk-stratification + angiography) · CICU (shock, arrhythmia, mechanical complications) · Cardiac surgery (mechanical complications, left main/multivessel for CABG)
STEMI — acute coronary occlusion
– Confirm: ischemic symptoms + ST-elevation ≥2 contiguous leads (or new LBBB, posterior MI, de Winter); don't wait for troponin to reperfuse
– Reperfuse: ACTIVATE cath lab — primary PCI (door-to-balloon ≤90 min); if PCI not available ≤120 min, fibrinolysis (tenecteplase weight-based IV bolus) then transfer
– Antithrombotic load: aspirin 325 mg chewed; P2Y12 — ticagrelor 180 mg PO (or prasugrel 60 mg PO, or clopidogrel 600 mg PO per cath plan); anticoagulation — unfractionated heparin 60 U/kg bolus (max 4000 U) + infusion, or bivalirudin per protocol
– Adjuncts: high-intensity statin (atorvastatin 80 mg PO daily); beta-blocker once stable — metoprolol tartrate 25 mg PO q6h (AVOID if low-output/bradycardia/RV infarct); nitroglycerin for pain/HTN (AVOID in RV infarct/hypotension/recent PDE5i); O2 only if hypoxic
– Monitor / daily labs: CICU, continuous telemetry, serial ECG + troponin, daily BMP/CBC/Mg; watch mechanical complications + arrhythmia
– Dispo: DAPT 12 months, high-intensity statin; cardiac rehab referral; PT/OT; smoking cessation, risk-factor counseling; cardiology follow-up 1–2 weeks; med rec
– STEMI is a clock — reperfuse in minutes. Inferior STEMI with hypotension = RV infarct until proven otherwise: preload-dependent, give fluids, avoid nitrates/morphine that drop preload.
NSTEMI — type 1 (plaque rupture)
– Confirm: ischemic symptoms + troponin rise/fall, no persistent ST-elevation; ST-depression/T-inversion possible; primary atherothrombotic event
– Antithrombotic: aspirin 325 mg load → 81 mg PO daily; P2Y12 (ticagrelor 90 mg PO BID, or clopidogrel/prasugrel per cath plan); anticoagulation — enoxaparin 1 mg/kg SC q12h or heparin infusion or fondaparinux
– Anti-ischemic + adjuncts: high-intensity statin (atorvastatin 80 mg PO daily); beta-blocker (metoprolol tartrate 25 mg PO q6h); nitrates for symptoms
– Strategy: risk-stratify (GRACE/TIMI) → early invasive angiography ≤24 h for high-risk; immediate if refractory ischemia/instability/dynamic changes; revascularize (PCI/CABG) per anatomy
– Monitor / daily labs: telemetry, serial ECG + troponin, daily BMP/CBC
– Dispo: DAPT 12 months, statin; cardiac rehab; PT/OT; risk-factor modification; cardiology follow-up 1–2 weeks; med rec
– Type 1 NSTEMI is a thrombus problem — antiplatelet + anticoagulant + timely angiography. High-risk features push the cath earlier.
NSTEMI — type 2 / demand ischemia
– Confirm: troponin rise/fall from a supply-demand mismatch (sepsis, sustained tachyarrhythmia, severe anemia, hypoxemia, hypertensive crisis, hypotension) WITHOUT acute plaque rupture
– Primary Rx: treat the underlying stressor — control the arrhythmia, transfuse/treat anemia (transfuse if Hb <7–8 g/dL per context), treat sepsis/hypoxia, control BP
– Adjuncts: aspirin 81 mg PO daily + statin reasonable in most; emergent cath usually NOT indicated unless true type 1 features
– Monitor / daily labs: telemetry, serial troponin (trend toward resolution as stressor treated), daily BMP/CBC
– Dispo: risk-factor modification, outpatient ischemic evaluation as appropriate; PT/OT; follow-up; med rec
– Type 2 MI is the heart caught in the crossfire of another illness — fixing the stressor, not rushing the cath lab, is the treatment. Over-anticoagulating a septic type-2 troponin causes harm.
Unstable angina
– Confirm: unstable ischemic symptoms (rest/new/crescendo/post-MI) with NORMAL serial troponin, no infarction
– Rx: aspirin 325 mg load → 81 mg PO daily ± P2Y12 per risk; anticoagulation (enoxaparin/heparin); anti-ischemics (beta-blocker, nitrates); high-intensity statin (atorvastatin 80 mg PO daily)
– Strategy: risk-stratify; ischemic evaluation/angiography per risk (high-risk → invasive)
– Monitor / daily labs: admit/observe, serial ECG + troponin, telemetry, daily BMP
– Dispo: DAPT per stenting; cardiac rehab; PT/OT; risk-factor modification; cardiology follow-up; med rec
– Unstable angina is ACS without the troponin bump — symptoms and risk drive urgency. With high-sensitivity troponin, much true UA is reclassified as NSTEMI.
Chest Pain Workup — ACS rule-out
– Confirm: chest pain under evaluation; serial ECGs + serial high-sensitivity troponin + structured score (HEART/EDACS)
– Workup: serial ECG + hs-troponin (0/1-h or 0/3-h algorithm) + HEART score; low-risk + negative serial troponin/ECG → discharge + outpatient follow-up ± stress test/coronary CTA; intermediate/high → admit, further testing; always exclude dissection/PE/pneumothorax/tamponade
– Monitor / daily labs: telemetry during rule-out, repeat ECG with symptoms
– Dispo: if ruled out → discharge with return precautions + outpatient stress/CTA + PCP/cardiology follow-up; aspirin/statin per risk; risk-factor counseling
– The rule-out is a structured serial process — a single normal troponin doesn't clear ACS. HEART + serial hs-troponin identifies who can go home, but the dangerous non-ACS mimics must be actively excluded.
Chest Pain Workup — non-cardiac chest pain
– Confirm: reassuring story (reproducible/positional/pleuritic/burning), normal ECG + serial troponin, low score, plausible alternative — after dangerous causes excluded
– Rx: treat the cause — NSAIDs (ibuprofen 400–600 mg PO TID)/reassurance for musculoskeletal/costochondritis; PPI trial (omeprazole 20–40 mg PO daily) for GERD; address anxiety
– Monitor: ensure dangerous mimics excluded before labeling non-cardiac
– Dispo: follow-up + return precautions; lifestyle/risk-factor counseling; PCP follow-up
– "Non-cardiac" is a diagnosis you earn by excluding the dangerous causes first — only after the ECG, serial troponin, and risk assessment are reassuring and the emergencies are off the table.
102. Acute Coronary Syndrome (ACS)
complete reference · ECG-first triage · STEMI reperfusion, NSTEMI type 1 vs type 2, unstable angina, and the structured chest-pain rule-out · a dosed, bulleted plan per subtype · Full Card
Approach — ECG First, Then Troponin, Then Decide
Obtain an ECG within 10 minutes. The branch point is the ECG: ST-elevation (STEMI) is an acute coronary occlusion requiring immediate reperfusion (primary PCI, or lytics if PCI is unavailable) — minutes matter.
Without ST-elevation, the troponin sorts it: a rise-and-fall pattern is an NSTEMI (then ask whether it is type 1, from plaque rupture and thrombus, or type 2, from a supply-demand mismatch caused by another illness); a normal serial troponin with unstable symptoms is unstable angina; and a reassuring full evaluation is a chest-pain rule-out.
Give the shared anti-ischemic and antithrombotic backbone, but tailor the plan — a type 2 MI is treated by fixing the underlying stressor, not by emergent catheterization.
Key discriminators: ST-elevation (or a new LBBB or posterior MI) means STEMI; ischemic symptoms with a troponin rise and no ST-elevation mean NSTEMI; a primary plaque event marks type 1, while a troponin driven by sepsis, tachyarrhythmia, anemia, hypoxia, or hypertensive crisis marks type 2; unstable symptoms with a normal serial troponin mean unstable angina; and a reassuring story with a low HEART score means a non-cardiac or rule-out pathway.
Initial Symptoms / Data (all comers)
Chest pressure or tightness with possible radiation to the arm or jaw, exertional symptoms, diaphoresis, dyspnea, and nausea, which may be atypical or silent in diabetic, elderly, or female patients.
An ECG within 10 minutes (repeated if symptoms are ongoing or evolving) and serial high-sensitivity troponin.
CXR, continuous telemetry, IV access, and vitals with SpO2; BMP, CBC, lipids, and HbA1c; and a risk score (HEART, TIMI, or GRACE).
Neg (don't-miss)
Pt denies a missed aortic dissection (tearing pain to the back, a pulse or blood-pressure differential — giving antithrombotics here is catastrophic) and a missed PE (pleuritic pain, hypoxia, VTE risk).
Pt denies a STEMI-equivalent missed on the ECG (posterior MI, de Winter or Wellens patterns, a new LBBB) and a right-ventricular infarct (an inferior STEMI is preload-dependent, and nitrates can crash these patients).
Pt denies treating a type 2 or demand troponin as a type 1 plaque event.
DDx
STEMI · NSTEMI (type 1 versus type 2) · unstable angina · demand ischemia · non-cardiac chest pain (musculoskeletal, GERD, anxiety, costochondritis) · and the emergencies — aortic dissection, pulmonary embolism, pneumothorax, pericarditis or tamponade, esophageal rupture, myocarditis, and stress (Takotsubo) cardiomyopathy
Plan — by Diagnosis
CONSULT (as relevant): Cardiology and Interventional cardiology (STEMI — activate the cath lab immediately; NSTEMI risk stratification and angiography) · CICU (shock, arrhythmia, mechanical complications) · Cardiac surgery (mechanical complications, left main or multivessel disease for CABG) · Cardiac rehab and PT/OT
STEMI — acute coronary occlusion
Confirm: ischemic symptoms with ST-elevation in two or more contiguous leads (or a new LBBB, true posterior MI, or de Winter or hyperacute T-waves); the troponin will rise but do not wait for it to reperfuse.
Reperfusion: activate the cath lab immediately for primary PCI (door-to-balloon 90 minutes or less); if PCI is not available within about 120 minutes, give fibrinolytics (weight-based tenecteplase IV bolus) unless contraindicated and then transfer.
Antithrombotic loading: aspirin 325 mg chewed; a P2Y12 inhibitor — ticagrelor 180 mg PO, prasugrel 60 mg PO, or clopidogrel 600 mg PO per the cath plan; and anticoagulation — unfractionated heparin 60 U/kg IV bolus (maximum 4000 U) with an infusion, or bivalirudin per protocol.
Adjuncts: a high-intensity statin (atorvastatin 80 mg PO daily); a beta-blocker once stable (metoprolol tartrate 25 mg PO every 6 hours, transitioning to a long-acting agent), avoided in low-output, bradycardia, or RV infarct; nitroglycerin for pain or hypertension but avoided in RV infarct, hypotension, or recent PDE5-inhibitor use; and O2 only if hypoxic.
Monitoring / daily labs: CICU care with continuous telemetry, serial ECG and troponin, and a daily BMP, CBC, and magnesium; watch for mechanical complications (new murmur, shock) and arrhythmia.
Mobility / consults: cardiac rehab referral and PT/OT for early mobilization and a functional assessment; a dietitian.
Discharge: dual antiplatelet therapy for 12 months (aspirin 81 mg PO daily plus the P2Y12 inhibitor), a high-intensity statin, a beta-blocker, and an ACEi or ARB if reduced EF or hypertension; smoking cessation and risk-factor counseling; medication reconciliation; and a cardiology follow-up within 1–2 weeks.
NSTEMI — type 1 (plaque rupture)
Confirm: ischemic symptoms with a troponin rise and fall, no persistent ST-elevation, possible ST-depression or T-inversion, and a primary atherothrombotic event.
Antithrombotic: aspirin 325 mg load then 81 mg PO daily; a P2Y12 inhibitor (ticagrelor 90 mg PO twice daily, or clopidogrel or prasugrel per the cath plan); and anticoagulation (enoxaparin 1 mg/kg SC every 12 hours, a heparin infusion, or fondaparinux).
Anti-ischemic and adjuncts: a high-intensity statin (atorvastatin 80 mg PO daily), a beta-blocker (metoprolol tartrate 25 mg PO every 6 hours), and nitrates for symptoms.
Strategy: risk stratification (GRACE or TIMI) leading to early invasive angiography within about 24 hours for high-risk patients (immediately for refractory ischemia, instability, or dynamic changes), with revascularization (PCI or CABG) per anatomy.
Monitoring / daily labs: telemetry, serial ECG and troponin, and a daily BMP and CBC.
Mobility / consults: cardiac rehab and PT/OT; a dietitian.
Discharge: dual antiplatelet therapy for 12 months, a high-intensity statin, a beta-blocker, and an ACEi or ARB if indicated; risk-factor modification and counseling; medication reconciliation; and a cardiology follow-up within 1–2 weeks.
NSTEMI — type 2 or demand ischemia
Confirm: a troponin rise and fall driven by a supply-demand mismatch from another acute illness (sepsis, sustained tachyarrhythmia, severe anemia, hypoxemia, hypertensive crisis, hypotension) without evidence of acute plaque rupture.
Primary therapy: treat the underlying stressor as the primary therapy — control the arrhythmia, transfuse or treat anemia (transfusion if hemoglobin is below about 7–8 g/dL per context), treat sepsis or hypoxia, and control the blood pressure.
Adjuncts: aspirin 81 mg PO daily and a statin are reasonable in most; emergent catheterization is usually not indicated unless there are features of a true type 1 event.
Monitoring / daily labs: telemetry, serial troponin (which should trend down as the stressor is treated), and a daily BMP and CBC.
Mobility / consults: PT and OT; a dietitian as appropriate.
Discharge: risk-factor modification and an outpatient ischemic evaluation as appropriate, medication reconciliation, and follow-up directed at both the cardiac risk and the precipitating illness.
Unstable angina
Confirm: unstable ischemic symptoms (rest, new, crescendo, or post-MI angina) with a normal serial troponin and no infarction, possibly with high-risk features.
Therapy: aspirin 325 mg load then 81 mg PO daily with a P2Y12 inhibitor per risk; anticoagulation (enoxaparin 1 mg/kg SC every 12 hours or a heparin infusion); anti-ischemics (a beta-blocker such as metoprolol tartrate 25 mg PO every 6 hours, and nitrates); and a high-intensity statin (atorvastatin 80 mg PO daily).
Strategy: risk stratification with an ischemic evaluation or angiography per risk (high-risk features warrant an invasive approach).
Monitoring / daily labs: admission or observation with serial ECG and troponin, telemetry, and a daily BMP.
Mobility / consults: cardiac rehab and PT/OT; a dietitian.
Discharge: dual antiplatelet therapy per stenting, a high-intensity statin, a beta-blocker, risk-factor modification, medication reconciliation, and cardiology follow-up.
Chest Pain Workup — ACS rule-out
Confirm: chest pain under evaluation, assessed with serial ECGs, serial high-sensitivity troponin, and a structured risk score (HEART or EDACS).
Workup: serial ECG and high-sensitivity troponin (a 0/1-hour or 0/3-hour algorithm) with a HEART score; for low-risk patients with negative serial troponin and ECG, discharge with outpatient follow-up and possible stress testing or coronary CT angiography; for intermediate or high-risk patients, admission with further cardiac testing; and always exclude the can't-miss mimics (dissection, PE, pneumothorax, tamponade).
Monitoring / daily labs: telemetry during the rule-out and a repeat ECG with any recurrent symptoms.
Mobility / consults: PT and OT as needed; cardiology if testing is positive.
Discharge: if ruled out, discharge with return precautions, an outpatient stress test or coronary CTA, aspirin and a statin per risk, risk-factor counseling, and PCP or cardiology follow-up.
Chest Pain Workup — non-cardiac chest pain
Confirm: a reassuring story (reproducible, positional, pleuritic, or burning pain), a normal ECG and serial troponin, a low risk score, and a plausible alternative (musculoskeletal, GERD, anxiety, costochondritis) after dangerous causes are excluded.
Therapy: treat the identified cause — NSAIDs (ibuprofen 400–600 mg PO three times daily) and reassurance for musculoskeletal or costochondritis pain, a PPI trial (omeprazole 20–40 mg PO daily) for GERD, and addressing anxiety.
Monitoring: confirm the dangerous mimics are excluded before applying the non-cardiac label.
Discharge: follow-up and return precautions, lifestyle and risk-factor counseling, and PCP follow-up.
Red Flags
ST-elevation, a new LBBB, or a STEMI-equivalent → an acute occlusion; activate the cath lab and reperfuse without waiting for troponin
An inferior STEMI with hypotension → a right-ventricular infarct; it is preload-dependent, so give fluids and avoid nitrates and morphine
Tearing pain to the back with a pulse or blood-pressure differential → aortic dissection; antithrombotics are catastrophic
A new murmur, hypotension, or pulmonary edema after MI → a mechanical complication (papillary muscle rupture, VSD, free-wall rupture); urgent echo and surgery
Refractory ischemia, hemodynamic or electrical instability → an immediate invasive strategy
Senior IM Resident Pearls
The ECG is the branch point, and STEMI is a clock. Get it within 10 minutes and reperfuse occlusions in minutes — don't wait for the troponin.
Type 1 versus type 2 changes everything. A plaque event needs antithrombotics and the cath lab; a demand troponin needs the underlying illness fixed, and over-anticoagulating it causes harm.
Inferior STEMI plus hypotension is an RV infarct. Give fluids and avoid the nitrates and morphine that drop preload and crash them.
Know the STEMI-equivalents. Posterior MI, de Winter T-waves, Wellens, and a new LBBB are occlusions that don't show classic ST-elevation.
A single troponin doesn't clear ACS. The rule-out is a structured, serial process with a risk score — and the dangerous mimics must be actively excluded.
"Non-cardiac" is earned, not assumed. Only after the ECG, serial troponin, risk assessment, and emergency exclusion are reassuring.
Common mistake: treating a septic patient's demand troponin like a plaque rupture — loading antithrombotics and rushing the cath lab instead of treating the sepsis.
Cardiology — Arrhythmias
103. Arrhythmias
unstable → cardiovert/pace now · AF (RVR / new-onset / with HF) · flutter · SVT · VT · symptomatic bradycardia · heart block (Mobitz II / complete) · palpitations workup · separate dosed plans per rhythm · Super Compact
Approach — first ask "stable or unstable," then name the rhythm. Any arrhythmia with hypotension, ischemic chest pain, acute heart failure, or altered mental status (the instability criteria) gets immediate electricity — synchronized cardioversion for unstable tachyarrhythmias, transcutaneous pacing (and atropine) for unstable bradyarrhythmias. If stable, get a 12-lead and classify: narrow vs wide, regular vs irregular. Narrow-irregular = AF; narrow-regular = SVT/flutter; wide-regular = VT until proven otherwise; bradycardia → find the level of block. Then treat the specific rhythm and always hunt the reversible trigger (ischemia, electrolytes, thyroid, sepsis, drugs, hypoxia, PE).
Key discriminators: irregularly irregular, no P-waves → AF · regular ~150 with sawtooth waves → flutter · regular narrow ~150–250, abrupt onset/offset → SVT · wide regular, AV dissociation/fusion/capture beats → VT (assume VT in any WCT, esp with structural disease/prior MI) · HR <50 with symptoms → symptomatic bradycardia · dropped QRS, constant PR → Mobitz I (benign) · dropped QRS without PR prolongation / 2:1 wide QRS → Mobitz II (dangerous — pace) · complete AV dissociation → complete heart block
Initial Sx/Data (all comers): palpitations, lightheadedness, syncope/presyncope, dyspnea, chest pain, fatigue; assess perfusion + instability criteria · 12-lead ECG (diagnostic) + telemetry; BMP/Mg/Ca, TSH, CBC, troponin if ischemia; med/drug review; echo for structural disease · IV access, defibrillator/pads at bedside for unstable/wide-complex · (don't anchor — treat a regular wide-complex tachycardia as VT, always look for the electrolyte/ischemic/thyroid trigger)
Neg (don't-miss): denies instability needing immediate cardioversion/pacing · denies a WCT misread as SVT with aberrancy (treating VT with a nodal blocker can be lethal) · denies Mobitz II / complete heart block treated as benign · denies the reversible trigger (ischemia, hyperkalemia, drug toxicity) · denies WPW with AF given AV-nodal blockers (can precipitate VF)
DDx: AF (RVR / new-onset / with HF) · atrial flutter · SVT · VT · symptomatic bradycardia · Mobitz II / complete heart block · (also: MAT, junctional rhythm, sinus tach from a secondary cause, Mobitz I, WPW)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (rhythm management, structural disease) · Electrophysiology (ablation, VT, device/pacing, WPW) · CICU (unstable arrhythmia, VT storm, refractory shock)
Unstable tachy- or bradyarrhythmia (any rhythm)
– Confirm: the arrhythmia + hypotension, ischemic chest pain, acute HF, or altered mental status
– Rx: unstable tachy → immediate synchronized cardioversion (sedate if able; energy per rhythm); unstable brady → atropine 1 mg IV (repeat q3–5 min to 3 mg) + transcutaneous pacing; dopamine 5–20 mcg/kg/min or epinephrine 2–10 mcg/min infusion as bridge; pulseless VT/VF → defibrillate + ACLS; treat reversible causes
– Monitor: continuous telemetry, defibrillator at bedside, serial BMP/Mg, troponin
– Dispo: CICU/monitored bed; address the cause; EP/cardiology as relevant
– The instability criteria override the differential — if they're crashing from the rhythm, the answer is electricity now, not a drug you have to wait on.
Atrial fibrillation — RVR
– Confirm: irregularly irregular, no discrete P-waves, rapid ventricular rate; assess trigger + onset time
– Rate control: if stable — metoprolol tartrate 5 mg IV q5min ×3 then 25–50 mg PO q6h, OR diltiazem 0.25 mg/kg IV bolus then 5–15 mg/h infusion → PO; target HR <110 at rest. AVOID CCB/BB in decompensated HFrEF (use digoxin or amiodarone); AVOID AV-nodal blockers in WPW/pre-excited AF
– Anticoagulation: per CHA₂DS₂-VASc (apixaban 5 mg PO BID, or 2.5 mg BID if 2 of age≥80/weight≤60kg/Cr≥1.5; or warfarin/other DOAC), balanced against bleeding risk
– Treat trigger: sepsis, PE, ischemia, thyroid, alcohol
– Monitor / daily labs: telemetry, HR/BP trend, daily BMP/Mg, TSH
– Dispo: PT/OT as needed; anticoagulation education; cardiology follow-up; med rec
– Rate control first for most; reserve CCB/BB in a failing heart and never give AV-nodal blockers in pre-excited (WPW) AF. CHA₂DS₂-VASc, not the heart rate, decides anticoagulation.
Atrial fibrillation — new-onset
– Confirm: first documented AF; establish onset (<48 h vs ≥48 h/unknown)
– Strategy: rate vs rhythm control (rhythm control favored for symptomatic/younger/HF/recent-onset per cardiology)
– Cardioversion timing: if <48 h, cardiovert with periprocedural anticoagulation; if ≥48 h/unknown, anticoagulate ≥3 weeks OR TEE to exclude LA thrombus first, then anticoagulate ≥4 weeks after
– Anticoagulation: start per CHA₂DS₂-VASc (apixaban 5 mg PO BID etc.); treat reversible triggers
– Monitor / daily labs: telemetry, daily BMP/Mg, TSH
– Dispo: EP referral for rhythm-control/ablation; anticoagulation education; cardiology follow-up; med rec
– The 48-hour rule governs cardioversion safety: beyond 48 h (or unknown), you need 3 weeks of anticoagulation or a TEE before shocking, then anticoagulation afterward — cardioverting an unanticoagulated chronic AF can throw a stroke.
Atrial fibrillation — with heart failure
– Confirm: AF with HF (esp HFrEF/decompensation); AF both cause and consequence
– Rate control: beta-blocker preferred when tolerated; AVOID diltiazem/verapamil in HFrEF (negative inotropes); alternatives — digoxin 0.125–0.25 mg IV/PO (load then daily, renally adjusted) or amiodarone 150 mg IV then infusion for decompensated HFrEF
– Rhythm control: often favored in HF — cardioversion/ablation (AF ablation improves outcomes in selected HFrEF)
– Concurrent: decongest the HF; anticoagulate per CHA₂DS₂-VASc
– Monitor / daily labs: telemetry, daily BMP/Mg, digoxin level if used, TSH/LFTs if amiodarone
– Dispo: EP referral; HF + anticoagulation education; cardiology/HF follow-up; med rec
– In HFrEF, diltiazem and verapamil are off the table (negative inotropes). Lean on beta-blockers, digoxin, or amiodarone for rate, and consider rhythm control — restoring sinus rhythm (and atrial kick) often helps the failing heart.
Atrial flutter
– Confirm: regular narrow ~150 (2:1) with sawtooth waves (inferior leads)
– Rx: unstable → synchronized cardioversion (low energy); stable → rate control (metoprolol or diltiazem as in AF — often harder to control than AF); anticoagulation per CHA₂DS₂-VASc (same risk as AF)
– Definitive: EP referral — cavotricuspid isthmus ablation, highly effective/often curative for typical flutter
– Monitor / daily labs: telemetry, HR/BP trend, daily BMP
– Dispo: EP follow-up for ablation; anticoagulation education; med rec
– Typical flutter is the arrhythmia ablation cures — often refractory to rate control, so refer to EP early. Anticoagulation rules mirror AF.
Supraventricular tachycardia (SVT)
– Confirm: regular narrow ~150–250, abrupt onset/offset (AVNRT/AVRT)
– Rx: unstable → synchronized cardioversion; stable → vagal maneuvers (modified Valsalva) first, then adenosine 6 mg rapid IV push (then 12 mg) — diagnostic + therapeutic; if recurrent/refractory → IV beta-blocker or diltiazem; CAUTION: adenosine/AV-nodal blockers dangerous in pre-excited AF/WPW
– Monitor: telemetry, rhythm strip during adenosine, BMP
– Dispo: EP referral for ablation (curative for recurrent SVT); cardiology follow-up
– Vagal maneuvers then adenosine break most SVT and reveal the rhythm if they don't — but if irregular or you suspect WPW, hold the AV-nodal agents. Ablation is definitive.
Ventricular tachycardia (VT)
– Confirm: wide regular tachycardia — assume VT (AV dissociation, fusion/capture beats, structural disease/prior MI favor VT)
– Rx: pulseless VT → defibrillate + ACLS; unstable VT with pulse → synchronized cardioversion; stable monomorphic VT → amiodarone 150 mg IV over 10 min (then 1 mg/min ×6 h, 0.5 mg/min ×18 h) or procainamide, cardiovert if fails; polymorphic VT/torsades → magnesium 2 g IV, correct QT/electrolytes, defibrillate if unstable
– Treat substrate: ischemia, electrolytes (K/Mg); EP + ICD evaluation; VT storm → beta-blockade + sedation + EP
– Monitor / daily labs: CICU/telemetry, serial BMP/Mg, troponin, QT
– Dispo: EP/ICD evaluation; reassess HF/GDMT; cardiology follow-up; med rec
– Treat every regular wide-complex tachycardia as VT until proven otherwise — a nodal blocker for a misdiagnosed "SVT with aberrancy" can be lethal. Magnesium is the move for torsades; fix the ischemic/electrolyte trigger.
Symptomatic bradycardia
– Confirm: HR <50 with symptoms (hypotension, syncope/presyncope, altered mentation, ischemia, HF) from the bradycardia
– Rx: atropine 1 mg IV (repeat q3–5 min to 3 mg) for unstable; if refractory → transcutaneous pacing and/or dopamine 5–20 mcg/kg/min or epinephrine 2–10 mcg/min infusion; prepare transvenous pacing
– Reversibles: stop/reverse offending drugs (BB/CCB/digoxin), correct hyperkalemia, treat ischemia/hypothyroidism
– Monitor / daily labs: telemetry, daily BMP, drug levels, TSH
– Dispo: permanent pacemaker for irreversible symptomatic bradycardia/SND (EP); cardiology follow-up; med rec
– Atropine, then pacing — but always look for the reversible cause: a beta-blocker overdose, hyperkalemia, hypothyroidism, or an inferior MI can all present this way with specific antidotes.
Heart block — Mobitz II
– Confirm: intermittently dropped QRS WITHOUT progressive PR prolongation (or 2:1 with wide QRS) — infranodal/His-Purkinje; high risk of progression to complete block
– Rx: dangerous — admit, telemetry, transcutaneous pacing pads ready; transvenous pacing for symptoms/instability; atropine often ineffective (infranodal) and can worsen it; stop AV-nodal blocking drugs
– Reversibles: ischemia, Lyme, infiltrative disease
– Monitor / daily labs: continuous telemetry, daily BMP, drug review
– Dispo: permanent pacemaker indicated (cardiology/EP); cardiology follow-up; med rec
– Mobitz II is not benign — it sits in the His-Purkinje system and can drop into complete heart block without warning, so it earns pacing pads and a pacemaker, not observation. Atropine can paradoxically worsen infranodal block.
Heart block — complete (third-degree)
– Confirm: complete AV dissociation — independent P-waves and QRS, slow escape; symptoms of hypoperfusion
– Rx: transcutaneous pacing immediately for instability (atropine while preparing, often ineffective if infranodal); transvenous pacing as bridge; dopamine/epinephrine infusion if needed
– Reversibles: ischemia (esp inferior MI), drug toxicity, hyperkalemia, Lyme, infiltrative disease
– Monitor / daily labs: continuous telemetry, serial BMP, troponin
– Dispo: permanent pacemaker definitive (cardiology/EP); cardiology follow-up; med rec
– Complete heart block is a pacing emergency — get the pads on and a transvenous wire in while treating reversible causes. An inferior MI can cause transient, often atropine-responsive block, but most needs a permanent pacemaker.
Palpitations Workup
– Confirm: sensation of irregular/rapid/forceful heartbeat; capture the rhythm during symptoms
– Workup: 12-lead ECG; if not captured, ambulatory monitoring (Holter for frequent, event/patch monitor or implantable loop recorder for infrequent) to correlate symptoms with rhythm; labs (TSH, electrolytes, CBC for anemia); echo if structural disease suspected; reduce stimulants/caffeine/alcohol
– Monitor: telemetry if high-risk; correlate symptom diary with rhythm
– Dispo: red flags (syncope, exertional palpitations, family Hx of sudden death, structural disease) → expedited cardiology/EP; routine → outpatient monitor + follow-up
– The whole game in palpitations is catching the rhythm during a symptomatic episode — match the monitor to the symptom frequency. Exertional palpitations, syncope, or a family history of sudden death move the workup to the front of the line.
103. Arrhythmias
complete reference · stable-versus-unstable triage · AF, flutter, SVT, VT, bradycardia, heart block, and the palpitations workup · a dosed, bulleted plan per rhythm · Full Card
Approach — Stable or Unstable First, Then Name the Rhythm
Any arrhythmia with hypotension, ischemic chest pain, acute heart failure, or altered mental status (the instability criteria) gets immediate electricity — synchronized cardioversion for unstable tachyarrhythmias and transcutaneous pacing with atropine for unstable bradyarrhythmias — regardless of the precise diagnosis.
If stable, obtain a 12-lead and classify by narrow versus wide and regular versus irregular: irregular and narrow is AF; regular and narrow is SVT or flutter; wide and regular is VT until proven otherwise; and bradycardia prompts a search for the level of block.
Then treat the specific rhythm and always hunt the reversible trigger — ischemia, electrolytes, thyroid, sepsis, drugs, hypoxia, or PE.
Key discriminators: an irregularly irregular rhythm with no P-waves is AF; a regular rate near 150 with sawtooth waves is flutter; a regular narrow tachycardia with abrupt onset and offset is SVT; a wide regular tachycardia with AV dissociation is VT; a rate under 50 with symptoms is symptomatic bradycardia; dropped beats with a constant PR are Mobitz I; a dropped QRS without PR prolongation is Mobitz II; and complete AV dissociation is complete heart block.
Initial Symptoms / Data (all comers)
Palpitations, lightheadedness, syncope or presyncope, dyspnea, chest pain, and fatigue, with an assessment of perfusion and the instability criteria.
A 12-lead ECG (the diagnostic test) and continuous telemetry; BMP with magnesium and calcium, TSH, CBC, and troponin if ischemia is suspected; a medication and drug review; and an echocardiogram for structural disease.
IV access and a defibrillator with pads at the bedside for unstable or wide-complex rhythms.
Neg (don't-miss)
Pt denies instability requiring immediate cardioversion or pacing (don't dawdle on chemical therapy in an unstable patient) and denies a wide-complex tachycardia misread as SVT with aberrancy (treating VT as SVT with a nodal blocker can be lethal).
Pt denies Mobitz II or complete heart block treated as benign (these need pacing, not observation) and denies a missed reversible trigger (ischemia, hyperkalemia, drug toxicity).
Pt denies WPW with AF given AV-nodal blockers, which can precipitate ventricular fibrillation.
DDx
AF (RVR, new-onset, or with HF) · atrial flutter · SVT · VT · symptomatic bradycardia · Mobitz II or complete heart block · (also multifocal atrial tachycardia, junctional rhythm, sinus tachycardia from a secondary cause, Mobitz I, and WPW)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (rhythm management, structural disease) · Electrophysiology (ablation candidacy, VT, device and pacing decisions, WPW) · CICU (unstable arrhythmia, VT storm, refractory shock)
Unstable tachy- or bradyarrhythmia (any rhythm)
Confirm: the arrhythmia with hypotension, ischemic chest pain, acute heart failure, or altered mental status.
Therapy: for an unstable tachyarrhythmia, immediate synchronized cardioversion (with sedation if able, energy per rhythm); for an unstable bradyarrhythmia, atropine 1 mg IV (repeated every 3–5 minutes to 3 mg total) and transcutaneous pacing with a dopamine 5–20 mcg/kg/min or epinephrine 2–10 mcg/min infusion as a bridge and preparation for transvenous pacing; for pulseless VT or VF, defibrillation and ACLS; and treatment of reversible causes throughout.
Monitoring / daily labs: continuous telemetry with a defibrillator at the bedside, serial BMP and magnesium, and troponin.
Mobility / consults / disposition: CICU or a monitored bed; address the underlying cause; involve EP and cardiology as relevant.
Atrial fibrillation — RVR
Confirm: an irregularly irregular rhythm with no discrete P-waves and a rapid ventricular rate; assess the trigger and onset.
Rate control: if stable, metoprolol tartrate 5 mg IV every 5 minutes up to 3 doses then 25–50 mg PO every 6 hours, or diltiazem 0.25 mg/kg IV bolus then a 5–15 mg/h infusion transitioned to oral, targeting a resting heart rate under 110; avoid calcium channel blockers and beta-blockers in decompensated HFrEF (use digoxin or amiodarone) and avoid AV-nodal blockers in WPW or pre-excited AF.
Anticoagulation: per the CHA₂DS₂-VASc score — apixaban 5 mg PO twice daily (or 2.5 mg twice daily if two of age 80 or older, weight 60 kg or less, or creatinine 1.5 or higher), or another DOAC or warfarin — balanced against bleeding risk.
Treat the trigger: sepsis, PE, ischemia, thyroid disease, or alcohol.
Monitoring / daily labs: telemetry, a heart-rate and blood-pressure trend, a daily BMP with magnesium, and TSH.
Mobility / consults / disposition: PT and OT as needed; anticoagulation education; cardiology follow-up; and medication reconciliation.
Atrial fibrillation — new-onset
Confirm: first documented AF, establishing the onset (under 48 hours versus 48 hours or more or unknown, which affects the cardioversion and anticoagulation strategy).
Strategy: rate versus rhythm control (rhythm control favored for symptomatic, younger, HF, or recent-onset patients per cardiology).
Cardioversion timing: if onset is under 48 hours, cardiovert with periprocedural anticoagulation; if onset is 48 hours or more or unknown, anticoagulate for at least 3 weeks first or perform a TEE to exclude a left atrial thrombus before cardioversion, then anticoagulate for at least 4 weeks after.
Anticoagulation: start per CHA₂DS₂-VASc (apixaban 5 mg PO twice daily and similar); identify and treat reversible triggers.
Monitoring / daily labs: telemetry, a daily BMP with magnesium, and TSH.
Mobility / consults / disposition: EP referral for a rhythm-control strategy or ablation; anticoagulation education; cardiology follow-up; medication reconciliation.
Atrial fibrillation — with heart failure
Confirm: AF in the setting of HF (especially HFrEF or decompensation), where AF may be both cause and consequence.
Rate control: a beta-blocker when tolerated, avoiding non-dihydropyridine calcium channel blockers (diltiazem, verapamil) in HFrEF because they are negative inotropes, with alternatives of digoxin 0.125–0.25 mg IV or PO (a load then a renally adjusted daily dose) or amiodarone 150 mg IV then an infusion in decompensated HFrEF.
Rhythm control: often favored in HF — cardioversion or ablation, since AF ablation improves outcomes in selected HFrEF.
Concurrent: decongest the HF; anticoagulate per CHA₂DS₂-VASc.
Monitoring / daily labs: telemetry, a daily BMP with magnesium, a digoxin level if used, and TSH and LFTs if amiodarone is used.
Mobility / consults / disposition: EP referral; HF and anticoagulation education; cardiology and HF follow-up; medication reconciliation.
Atrial flutter
Confirm: a regular narrow tachycardia near 150 (2:1 conduction) with sawtooth flutter waves, best seen in the inferior leads.
Therapy: synchronized cardioversion if unstable (flutter cardioverts at low energy); if stable, rate control with metoprolol or diltiazem as in AF (often harder to rate-control than AF); and anticoagulation per CHA₂DS₂-VASc (the same thromboembolic risk as AF).
Definitive: EP referral, since cavotricuspid isthmus ablation is highly effective and often curative for typical flutter.
Monitoring / daily labs: telemetry, a heart-rate and blood-pressure trend, and a daily BMP.
Mobility / consults / disposition: EP follow-up for ablation; anticoagulation education; medication reconciliation.
Supraventricular tachycardia (SVT)
Confirm: a regular narrow-complex tachycardia near 150–250 with abrupt onset and offset (AVNRT or AVRT).
Therapy: synchronized cardioversion if unstable; if stable, vagal maneuvers (a modified Valsalva) first, then adenosine 6 mg rapid IV push (then 12 mg), which is both diagnostic and therapeutic; an IV beta-blocker or diltiazem for recurrent or refractory cases; with caution that adenosine and AV-nodal blockers are dangerous in pre-excited AF or WPW.
Monitoring / daily labs: telemetry, a rhythm strip during adenosine, and a BMP.
Mobility / consults / disposition: EP referral for ablation (curative for recurrent SVT); cardiology follow-up.
Ventricular tachycardia (VT)
Confirm: a wide-complex regular tachycardia, assumed to be VT, with AV dissociation, fusion or capture beats, or structural heart disease or prior MI strongly favoring VT.
Therapy: for pulseless VT, defibrillation and ACLS; for unstable VT with a pulse, synchronized cardioversion; for stable monomorphic VT, amiodarone (150 mg IV over 10 minutes, then 1 mg/min for 6 hours and 0.5 mg/min for 18 hours) or procainamide, with cardioversion if it fails; for polymorphic VT or torsades, magnesium 2 g IV with correction of QT-prolonging causes and electrolytes and defibrillation if unstable.
Substrate: treat ischemia and electrolytes (potassium, magnesium); pursue EP and ICD evaluation; and manage VT storm with beta-blockade, sedation, and EP.
Monitoring / daily labs: CICU or telemetry, serial BMP and magnesium, troponin, and the QT interval.
Mobility / consults / disposition: EP and ICD evaluation; reassess HF and GDMT; cardiology follow-up; medication reconciliation.
Symptomatic bradycardia
Confirm: a heart rate under 50 with symptoms (hypotension, syncope, altered mentation, ischemia, HF) attributable to the bradycardia.
Therapy: atropine 1 mg IV (repeated every 3–5 minutes to 3 mg total) for unstable bradycardia, and if refractory, transcutaneous pacing with a dopamine 5–20 mcg/kg/min or epinephrine 2–10 mcg/min infusion and preparation for transvenous pacing.
Reversibles: stop or reverse offending drugs (beta-blockers, calcium channel blockers, digoxin), correct hyperkalemia, and treat ischemia or hypothyroidism.
Monitoring / daily labs: telemetry, a daily BMP, drug levels, and TSH.
Mobility / consults / disposition: a permanent pacemaker for irreversible symptomatic bradycardia or sinus node dysfunction (EP); cardiology follow-up; medication reconciliation.
Heart block — Mobitz II
Confirm: an intermittently dropped QRS without progressive PR prolongation (or 2:1 block with a wide QRS), localizing to the His-Purkinje system with a high risk of progression to complete block.
Therapy: recognize this as dangerous — admit with telemetry and prepare transcutaneous pacing pads, use transvenous pacing for symptoms or instability, recognize that atropine is often ineffective (infranodal) and can worsen it, and stop AV-nodal blocking drugs.
Reversibles: ischemia, Lyme disease, and infiltrative disease.
Monitoring / daily labs: continuous telemetry, a daily BMP, and a drug review.
Mobility / consults / disposition: a permanent pacemaker is indicated (cardiology and EP); cardiology follow-up; medication reconciliation.
Heart block — complete (third-degree)
Confirm: complete AV dissociation with independent P-waves and QRS complexes, a slow escape rhythm, and symptoms of hypoperfusion.
Therapy: transcutaneous pacing immediately for instability (with atropine while preparing, though often ineffective if infranodal), transvenous pacing as a bridge, and a dopamine or epinephrine infusion if needed.
Reversibles: ischemia (especially inferior MI), drug toxicity, hyperkalemia, Lyme disease, and infiltrative disease.
Monitoring / daily labs: continuous telemetry, serial BMP, and troponin.
Mobility / consults / disposition: a permanent pacemaker is the definitive therapy (cardiology and EP); cardiology follow-up; medication reconciliation.
Palpitations Workup
Confirm: a sensation of an irregular, rapid, or forceful heartbeat, with the goal of capturing the rhythm during symptoms.
Workup: a 12-lead ECG, and if not captured, ambulatory monitoring (a Holter for frequent symptoms, an event or patch monitor or implantable loop recorder for infrequent symptoms) to correlate symptoms with rhythm; labs (TSH, electrolytes, a CBC for anemia); an echocardiogram if structural disease is suspected; and reduction of stimulants, caffeine, and alcohol.
Monitoring: telemetry if high-risk, correlating a symptom diary with the rhythm.
Mobility / consults / disposition: expedited cardiology or EP evaluation for red flags (syncope, exertional palpitations, a family history of sudden death, structural heart disease); routine cases get an outpatient monitor and follow-up.
Red Flags
Hypotension, ischemic chest pain, acute HF, or altered mental status with an arrhythmia → instability; immediate cardioversion or pacing
A regular wide-complex tachycardia → VT until proven otherwise; a nodal blocker can be lethal
Mobitz II or complete heart block → high risk of asystole; pacing pads and a pacemaker, not observation
A pre-excited (WPW) AF → never give AV-nodal blockers; they can precipitate VF
Polymorphic VT or torsades → magnesium and correction of the QT and electrolytes; defibrillate if unstable
Senior IM Resident Pearls
Instability overrides the differential. If the rhythm is crashing the patient, the answer is electricity now — cardioversion or pacing — not a drug you have to wait on.
Every regular wide-complex tachycardia is VT. Treating a misdiagnosed "SVT with aberrancy" with a nodal blocker can be fatal, especially with prior MI.
The 48-hour rule protects against stroke. Beyond 48 hours or unknown onset, anticoagulate for 3 weeks or get a TEE before cardioverting AF.
Mobitz II is not Mobitz I. Infranodal block drops into complete heart block without warning — pace it; atropine can make it worse.
Avoid diltiazem and verapamil in HFrEF. They're negative inotropes — use beta-blockers, digoxin, or amiodarone for rate in a failing heart.
Never give AV-nodal blockers in pre-excited AF. Blocking the node sends everything down the accessory pathway and can precipitate VF.
Common mistake: treating a wide-complex tachycardia as SVT, or observing a Mobitz II, or anticoagulating-then-shocking a chronic AF without the TEE or the 3 weeks.
Cardiology — Syncope
104. Syncope Workup
separate the dangerous cardiac syncope (arrhythmia / structural) from the benign reflex/orthostatic causes · risk-stratify · ECG + targeted workup · separate dosed plans per cause · Super Compact
Approach — the whole task is separating cardiac syncope (potentially lethal) from reflex and orthostatic syncope (usually benign). Syncope is transient loss of consciousness from global cerebral hypoperfusion with spontaneous, complete recovery. The history, exam, and a 12-lead ECG do most of the work. Red flags for cardiac syncope: exertional syncope, syncope while supine, no prodrome (sudden), palpitations preceding it, structural heart disease or low EF, an abnormal ECG, or a family history of sudden cardiac death. A reassuring picture (clear vasovagal/orthostatic trigger, typical prodrome, normal ECG, no cardiac disease) is low-risk. Admit and work up the cardiac/high-risk ones; the benign ones often need only reassurance and counseling.
Key discriminators: exertional/supine/sudden-no-prodrome/palpitations-first/structural disease/abnormal ECG/family Hx of SCD → cardiac syncope (arrhythmic or structural) · positional (standing), volume depletion/autonomic/medications, orthostatic vitals drop → orthostatic syncope · clear trigger (pain, emotion, prolonged standing, micturition), prodrome (nausea, warmth, diaphoresis, tunnel vision) → vasovagal/reflex · presyncope without complete LOC → near-syncope (same risk stratification)
Initial Sx/Data (all comers): the event (trigger, prodrome, position, exertion, witness account, recovery), injury, cardiac/family history, medications · 12-lead ECG (essential — every syncope), orthostatic vitals, BMP, CBC, glucose; troponin/BNP if cardiac concern; telemetry for high-risk; echo if structural disease suspected; targeted testing (ambulatory monitor, stress test, EP study) per risk · (don't anchor — syncope can be the first warning of a lethal arrhythmia, PE, or aortic stenosis; exertional syncope is dangerous until proven otherwise)
Neg (don't-miss): denies exertional syncope (aortic stenosis, HCM, arrhythmia, ischemia — high-risk) · denies syncope from a lethal arrhythmia (long QT, Brugada, WPW, high-grade AV block, VT) · denies PE/aortic dissection/ruptured AAA/subarachnoid as the cause · denies it was actually a seizure (tongue-biting, postictal confusion, prolonged) · denies anchoring on "vasovagal" without excluding cardiac causes in an older/high-risk patient
DDx: cardiac syncope — arrhythmic vs structural · orthostatic syncope · vasovagal/reflex syncope · near-syncope · (also: PE, aortic dissection, GI bleed, seizure, hypoglycemia, situational syncope, carotid sinus hypersensitivity, medication effect)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (cardiac syncope, structural disease, device/ablation) · Electrophysiology (arrhythmic syncope, channelopathy, EP study/ICD) · Neurology (if seizure/neurologic cause suspected)
Cardiac syncope — arrhythmic
– Confirm: sudden syncope without prodrome, palpitations preceding it, structural/conduction disease, abnormal ECG (high-grade AV block, long/short QT, Brugada, pre-excitation, prior MI), or documented arrhythmia
– Rx: admit with continuous telemetry; identify the arrhythmia (telemetry, ambulatory/extended monitoring, implantable loop recorder if infrequent; EP study in selected cases); treat the specific rhythm (see the arrhythmias card); stop QT-prolonging/proarrhythmic drugs; correct electrolytes; treat ischemia
– Monitor / daily labs: continuous telemetry, daily BMP/Mg, troponin, QT trend
– Dispo: pacemaker for high-grade AV block/symptomatic bradycardia, ICD for life-threatening ventricular arrhythmia/high-risk substrate, ablation for SVT/VT (EP); cardiology follow-up; med rec
– Arrhythmic syncope is the one that kills on the next episode — sudden, no-warning syncope with an abnormal ECG or structural disease earns admission, monitoring, and often a device. Don't discharge it home on a "probably vasovagal."
Cardiac syncope — structural
– Confirm: exertional syncope, a murmur, or known structural disease; echo reveals the lesion — severe AS, HCM (with outflow obstruction), severe PH, or critical CAD/ischemia
– Rx: echocardiogram to define the lesion; treat the structural problem — AVR (TAVR/SAVR) for severe symptomatic AS; HCM management (beta-blockers, septal reduction, ICD if high-risk); revascularization for ischemia; PH-directed therapy; AVOID preload/afterload reducers (nitrates, aggressive diuresis, vasodilators) in fixed-obstruction lesions (AS/HCM)
– Monitor / daily labs: telemetry, daily BMP; echo-guided management
– Dispo: structural/EP referral; cardiology follow-up; activity counseling; med rec
– Exertional syncope is a structural red flag — severe AS and HCM present this way, and the dangerous reflex is to give a vasodilator or diurese, which drops the preload across a fixed obstruction and can crash them. Get the echo.
Orthostatic syncope
– Confirm: syncope on standing with a documented orthostatic drop (≥20 mmHg systolic or ≥10 mmHg diastolic within 3 min of standing); volume depletion, autonomic dysfunction, or offending medications
– Rx: treat the cause — volume repletion (IV/oral fluids) for dehydration/blood loss; review/reduce offending meds (antihypertensives, alpha-blockers, diuretics, vasodilators); EXCLUDE occult GI bleed; non-pharmacologic (slow position changes, compression stockings, increased salt/fluid if appropriate); pharmacologic for refractory autonomic orthostasis — midodrine 2.5–10 mg PO TID or fludrocortisone 0.1 mg PO daily
– Monitor / daily labs: orthostatic vitals, BMP, CBC (Hgb if bleed suspected), telemetry if cardiac concern
– Dispo: treat underlying autonomic disease; PT/OT for fall risk/conditioning; PCP/cardiology follow-up; med rec
– Orthostatic syncope is usually about volume or medications — replete fluids, prune the offending drugs, and crucially exclude a GI bleed, which can present as orthostatic syncope before the hemoglobin or melena shows up.
Vasovagal / reflex syncope
– Confirm: a clear trigger (pain, emotional stress, prolonged standing, heat, micturition/defecation/cough) with a typical prodrome (nausea, warmth, diaphoresis, tunnel vision), normal ECG, no structural disease, quick recovery
– Rx: reassurance + education (benign once cardiac causes excluded); counsel on trigger avoidance and prodrome recognition (lie down, counterpressure maneuvers at onset); adequate hydration + salt; review medications; generally NO admission or extensive cardiac workup if classic with normal ECG/exam; tilt-table testing only in unclear recurrent cases
– Monitor: single ECG + orthostatics; no telemetry needed if classic
– Dispo: discharge with reassurance + return precautions; PCP follow-up
– Classic vasovagal syncope — a trigger, a prodrome, a normal ECG, and a healthy heart — needs reassurance and counseling, not a hospital admission or a million-dollar cardiac workup. The skill is being confident it's vasovagal, which means having excluded the dangerous causes first.
Near-syncope (presyncope)
– Confirm: presyncopal symptoms (lightheadedness, graying/tunnel vision, impending faint) without complete LOC
– Rx: apply the SAME risk stratification as true syncope (similar prognostic significance — don't dismiss); ECG, orthostatic vitals, targeted workup by red flags (cardiac history/exertional/abnormal ECG → cardiac workup; positional → orthostatic; trigger+prodrome → reflex)
– Monitor / daily labs: telemetry + serial workup for high-risk; ECG/orthostatics for low-risk
– Dispo: admit/monitor the high-risk; reassure + discharge the low-risk; follow-up per risk
– Near-syncope is not automatically more benign than syncope — it gets the same risk stratification. A patient who "almost passed out" while exercising deserves the same concern as one who did.
104. Syncope Workup
complete reference · separating cardiac from reflex and orthostatic syncope · red-flag risk stratification · ECG and targeted testing · a dosed, bulleted plan per cause · Full Card
Approach — Separate Cardiac From Reflex and Orthostatic Syncope
Syncope is a transient loss of consciousness from global cerebral hypoperfusion with spontaneous, complete recovery; the entire task is separating cardiac syncope (potentially lethal) from reflex and orthostatic syncope (usually benign).
The history, exam, and a 12-lead ECG do most of the work. Red flags pointing to cardiac syncope include exertional syncope, syncope while supine, no prodrome (sudden onset), palpitations preceding the event, structural heart disease or a low EF, an abnormal ECG, and a family history of sudden cardiac death.
A reassuring picture (a clear vasovagal or orthostatic trigger, a typical prodrome, a normal ECG, and no cardiac disease) is low-risk.
Admit and work up the cardiac and high-risk cases; the benign cases often need only reassurance and counseling.
Initial Symptoms / Data (all comers)
A detailed event description (trigger, prodrome, position, exertion, witness account, recovery), any injury, the cardiac and family history, and medications.
A 12-lead ECG (essential for every syncope), orthostatic vitals, BMP, CBC, and glucose; troponin and BNP if there is cardiac concern; telemetry for high-risk patients; an echocardiogram if structural disease is suspected.
Targeted testing (ambulatory monitor, stress test, EP study) per risk.
Neg (don't-miss)
Pt denies exertional syncope (aortic stenosis, HCM, arrhythmia, ischemia — high-risk) and syncope from a lethal arrhythmia (long QT, Brugada, WPW, high-grade AV block, VT).
Pt denies PE, aortic dissection, a ruptured AAA, or a subarachnoid hemorrhage as the cause (these masquerade as syncope) and denies that the event was actually a seizure (tongue-biting, postictal confusion, prolonged duration).
Pt denies anchoring on "vasovagal" without excluding cardiac causes in an older or high-risk patient.
DDx
Cardiac syncope — arrhythmic versus structural · orthostatic syncope · vasovagal or reflex syncope · near-syncope · (also pulmonary embolism, aortic dissection, GI bleed, seizure, hypoglycemia, situational syncope, carotid sinus hypersensitivity, and medication effect)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (cardiac syncope, structural disease, device or ablation) · Electrophysiology (suspected arrhythmic syncope, channelopathy, EP study or ICD) · Neurology (if a seizure or neurologic cause is suspected)
Cardiac syncope — arrhythmic
Confirm: sudden syncope without prodrome, palpitations preceding it, structural or conduction disease, an abnormal ECG (high-grade AV block, long or short QT, Brugada, pre-excitation, prior MI), or a documented arrhythmia.
Therapy: admit with continuous telemetry; identify the arrhythmia (telemetry, ambulatory or extended monitoring, an implantable loop recorder for infrequent symptoms, an EP study in selected cases); treat the specific rhythm (see the arrhythmias card); stop QT-prolonging and proarrhythmic drugs; correct electrolytes; and treat ischemia.
Monitoring / daily labs: continuous telemetry, a daily BMP with magnesium, troponin, and a QT trend.
Mobility / consults / disposition: a pacemaker for high-grade AV block or symptomatic bradycardia, an ICD for life-threatening ventricular arrhythmia or a high-risk substrate, and ablation for SVT or VT (EP); cardiology follow-up; medication reconciliation.
Cardiac syncope — structural
Confirm: exertional syncope, a murmur, or known structural disease, with an echo revealing the lesion — severe aortic stenosis, hypertrophic cardiomyopathy with outflow obstruction, severe pulmonary hypertension, or critical CAD.
Therapy: an echocardiogram to define the lesion and treatment of the structural problem — aortic valve replacement (TAVR or SAVR) for severe symptomatic AS, HCM management (beta-blockers, septal reduction, an ICD if high-risk), revascularization for ischemia, and PH-directed therapy; and avoidance of preload and afterload reducers (nitrates, aggressive diuresis, vasodilators) in fixed-obstruction lesions (AS, HCM).
Monitoring / daily labs: telemetry, a daily BMP, and echo-guided management.
Mobility / consults / disposition: structural or EP referral; cardiology follow-up; activity counseling; medication reconciliation.
Orthostatic syncope
Confirm: syncope on standing with a documented orthostatic blood pressure drop (20 mmHg systolic or 10 mmHg diastolic within 3 minutes of standing) and volume depletion, autonomic dysfunction, or offending medications.
Therapy: treat the cause — volume repletion (IV or oral fluids) for dehydration or blood loss and review and reduction of offending medications (antihypertensives, alpha-blockers, diuretics, vasodilators); exclude occult bleeding (a GI bleed); non-pharmacologic measures (slow position changes, compression stockings, increased salt and fluid if appropriate); and pharmacologic therapy for refractory autonomic orthostasis — midodrine 2.5–10 mg PO three times daily or fludrocortisone 0.1 mg PO daily.
Monitoring / daily labs: orthostatic vitals, a BMP, a CBC (hemoglobin if bleeding is suspected), and telemetry if there is cardiac concern.
Mobility / consults / disposition: treat the underlying autonomic disease; PT and OT for fall risk and conditioning; PCP or cardiology follow-up; medication reconciliation.
Vasovagal or reflex syncope
Confirm: a clear trigger (pain, emotional stress, prolonged standing, heat, or a situational trigger such as micturition, defecation, or cough) with a typical prodrome (nausea, warmth, diaphoresis, tunnel vision), a normal ECG, no structural disease, and quick recovery.
Therapy: reassurance and education, since this is benign once cardiac causes are excluded; counseling on trigger avoidance and prodrome recognition (lying down and using counterpressure maneuvers at onset); adequate hydration and salt; medication review; generally no admission or extensive cardiac workup when the picture is classic and the ECG and exam are normal; and tilt-table testing only in unclear recurrent cases.
Monitoring: a single ECG and orthostatics, with no telemetry needed if the picture is classic.
Mobility / consults / disposition: discharge with reassurance and return precautions; PCP follow-up.
Near-syncope (presyncope)
Confirm: presyncopal symptoms (lightheadedness, graying or tunnel vision, an impending faint) without complete loss of consciousness.
Therapy: apply the same risk stratification as true syncope, since near-syncope carries similar prognostic significance and should not be dismissed — an ECG, orthostatic vitals, and a targeted workup based on red flags (a cardiac history, exertional symptoms, or an abnormal ECG prompt a cardiac workup; a positional pattern prompts an orthostatic evaluation; a trigger with a prodrome suggests reflex syncope).
Monitoring / daily labs: telemetry and a serial workup for high-risk patients; an ECG and orthostatics for low-risk patients.
Mobility / consults / disposition: admit and monitor the high-risk; reassure and discharge the low-risk; follow-up per risk.
Red Flags
Exertional syncope → severe aortic stenosis, HCM, or arrhythmia; high-risk and requiring an echo and admission
Sudden syncope with no prodrome or preceding palpitations → an arrhythmic cause; admit and monitor
An abnormal ECG or a family history of sudden cardiac death → a channelopathy or structural disease; expedited cardiology and EP
Syncope with chest pain, dyspnea, or hypoxia → PE, aortic dissection, or ACS masquerading as syncope
Giving a vasodilator or diuretic in suspected severe AS or HCM → can precipitate collapse across a fixed obstruction
Senior IM Resident Pearls
The job is separating cardiac from benign syncope. The ECG, the exertional/supine/no-prodrome red flags, and the family history do most of the sorting.
Exertional syncope is dangerous until proven otherwise. Severe AS and HCM present this way — get the echo and don't reach for a vasodilator.
Arrhythmic syncope kills on the next episode. Sudden, no-warning syncope with an abnormal ECG or structural disease earns admission, monitoring, and often a device.
Exclude a GI bleed in orthostatic syncope. It can present as orthostasis before the melena or the hemoglobin drop announces itself.
Near-syncope is not automatically benign. It gets the same risk stratification as a completed faint.
"Vasovagal" is a confident diagnosis, not a default. Earn it by excluding the dangerous causes, especially in older patients.
Common mistake: discharging an exertional or sudden no-prodrome syncope as "vasovagal" and missing the aortic stenosis or the arrhythmia that returns fatally.
Cardiology — Volume / Congestion
105. Volume Overload
decongest, but characterize the physiology · cardiorenal syndrome · CHF exacerbation · right heart failure · separate dosed plans per driver · Super Compact
Approach — confirm the patient is truly overloaded, decongest, and define which physiology is driving it. Volume overload is a final common pathway — the work is figuring out whether it's left-heart congestion (CHF exacerbation), the heart-kidney interaction (cardiorenal syndrome), or right-heart failure backing up into the systemic veins — because each has a different lever. The mainstay is IV loop diuretics titrated to net negative, but the right-heart and cardiorenal patients need nuance: don't over-diurese a preload-dependent failing RV, and don't under-diurese a cardiorenal patient out of fear of the creatinine. Always assess true volume status (JVD, IVC, weights) and hunt the trigger.
Key discriminators: orthopnea/PND/B-lines/pulmonary congestion/↑BNP → left-sided CHF exacerbation · congestion + rising creatinine, venous congestion driving the AKI → cardiorenal syndrome · elevated JVP/hepatomegaly/ascites/peripheral edema with clear lungs, RV dysfunction on echo → right heart failure · global overload from ESRD/iatrogenic fluids → non-cardiac source
Initial Sx/Data (all comers): dyspnea, orthopnea, edema, weight gain, abdominal fullness/early satiety (right-sided); exam — JVD, crackles, edema, hepatomegaly, ascites, perfusion · BNP/NT-proBNP, BMP (renal/electrolytes), CBC, LFTs; CXR; bedside US (B-lines, IVC, effusions); echo (LV/RV function, valves, filling pressures, PA pressure); daily weights + strict I/O · (don't anchor — distinguish true overload from redistribution, and right- from left-sided failure, because management diverges)
Neg (don't-miss): denies cardiogenic shock / low-output state (cold + hypotensive → inotropes/ICU, not just diuresis) · denies tamponade or constrictive physiology (a "right heart failure" that's actually pericardial — echo) · denies PE as the cause of acute RV failure · denies hepatic/renal/nutritional causes of edema (cirrhosis, nephrotic syndrome, hypoalbuminemia) · denies over-diuresing a preload-dependent RV into hypotension
DDx: cardiorenal syndrome · CHF exacerbation (left-sided) · right heart failure · (also: ESRD/dialysis overload, cirrhosis with ascites, nephrotic syndrome, tamponade/constriction, high-output failure, iatrogenic fluid overload)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (HF, RV failure, advanced therapies) · Nephrology (cardiorenal, ultrafiltration/dialysis) · CICU (low-output/shock, RV failure with instability) · Pulmonology/PH (RV failure from PH)
CHF exacerbation (left-sided congestion)
– Confirm: orthopnea/PND, pulmonary congestion/B-lines, ↑BNP, CXR congestion; known/new HF (see the heart failure card for HFrEF vs HFpEF specifics)
– Decongest: furosemide ~1–2.5× home daily PO dose IV BID (loop-naïve: 40 mg IV), or continuous infusion 5–10 mg/h; add metolazone 2.5–5 mg PO daily for resistance; O2, NIPPV for distress; nitroglycerin for hypertensive presentations
– Then: daily weights, strict I/O, Na/fluid restriction; treat trigger (ischemia, arrhythmia, nonadherence, infection); optimize/resume GDMT when decongested + stable
– Monitor / daily labs: daily BMP (K, Cr, Mg), daily weights, strict I/O, telemetry
– Dispo: PT/OT, cardiac rehab, dietitian; HF education (daily weights, when to call); cardiology/HF-clinic follow-up ≤7 days; med rec
– Diuresis to true euvolemia is the goal — incomplete decongestion at discharge is the main driver of HF readmission. Always find what triggered the exacerbation.
Cardiorenal syndrome
– Confirm: HF with worsening renal function; venous congestion (high CVP/right-sided pressures), not low output, drives the AKI in most type-1 cardiorenal; assess true volume status
– Decongest: aggressive IV loop diuretics to net negative — effective decongestion usually IMPROVES renal function, so tolerate a modest creatinine rise; add metolazone 2.5–5 mg PO daily for resistance; ultrafiltration/urgent dialysis if diuretic-refractory or true cardiorenal failure
– Caveats: distinguish the low-output subset (cold/hypotensive → inotropes, NOT more diuresis); hold ACEi/ARB/ARNI + nephrotoxins during significant AKI, resume when stable
– Monitor / daily labs: daily BMP (K, Cr) + Mg closely, daily weights, strict I/O
– Dispo: nephrology if refractory; PT/OT; dietitian; resume GDMT when renal-stable; close cardiology + nephrology follow-up; med rec
– The central teaching point: in congestive cardiorenal syndrome the kidneys are strangled by venous congestion, so the treatment is MORE effective decongestion, not less — but first make sure it isn't the low-output subset, which needs the opposite (inotropes).
Right heart failure
– Confirm: systemic venous congestion — elevated JVP, hepatomegaly/pulsatile liver, ascites, peripheral edema — often with clear lungs; RV dilation/dysfunction on echo; identify cause (left HF → group 2 PH, PAH, PE, RV infarct, chronic lung disease/cor pulmonale, valvular)
– Treat the cause (essential): left HF → treat the left heart; PAH → PH-specific therapy; PE → anticoagulation/reperfusion; RV infarct → preload + revascularization
– Volume + support: diurese congestion (furosemide IV) but AVOID over-diuresis of the preload-dependent failing RV AND avoid over-filling it; maintain systemic perfusion — norepinephrine 0.05–0.5 mcg/kg/min if hypotensive (keep systemic > pulmonary pressure); inotropy (dobutamine 2.5–10 mcg/kg/min or milrinone) for low output; avoid hypoxia/hypercarbia/acidosis (raise PVR)
– Monitor / daily labs: daily BMP, lactate, daily weights/I-O; CICU if unstable
– Dispo: PH/cardiology/pulmonary follow-up; treat the driver; PT/OT; med rec
– Right heart failure is a "treat the cause + don't break the RV" problem: decongest carefully without over-diuresing the preload-dependent RV, keep the systemic pressure up, and fix what's driving it. The failing RV punishes both over- and under-filling.
105. Volume Overload
complete reference · decongestion with attention to physiology · cardiorenal syndrome, left-sided CHF exacerbation, and right heart failure · a dosed, bulleted plan per driver · Full Card
Approach — Decongest, but Characterize the Physiology
Volume overload is a final common pathway; the work is determining whether it is left-heart congestion (a CHF exacerbation), the heart-kidney interaction (cardiorenal syndrome), or right-heart failure backing up into the systemic veins, because each has a different lever.
The mainstay is IV loop diuretics titrated to net negative, but the right-heart and cardiorenal patients need nuance: don't over-diurese a preload-dependent failing RV, and don't under-diurese a cardiorenal patient out of fear of the creatinine.
Always assess true volume status (JVD, IVC, weights) and hunt the trigger.
Key discriminators: orthopnea, PND, B-lines, and an elevated BNP mark a left-sided CHF exacerbation; congestion with a rising creatinine marks cardiorenal syndrome; an elevated JVP, hepatomegaly, ascites, and edema with clear lungs mark right heart failure; and global overload from ESRD or iatrogenic fluids marks a non-cardiac source.
Initial Symptoms / Data (all comers)
Dyspnea, orthopnea, edema, weight gain, and abdominal fullness or early satiety (right-sided), with an exam for JVD, crackles, edema, hepatomegaly, ascites, and perfusion.
BNP or NT-proBNP, BMP for renal function and electrolytes, CBC, and LFTs; CXR; bedside ultrasound (B-lines, IVC, effusions); and an echocardiogram (LV and RV function, valves, filling pressures, PA pressure).
Daily weights and strict intake and output.
Neg (don't-miss)
Pt denies cardiogenic shock or a low-output state (a cold, hypotensive patient needs inotropes and the ICU, not just diuresis) and denies tamponade or constrictive physiology (a "right heart failure" that is actually pericardial — get the echo).
Pt denies PE as the cause of acute RV failure and denies hepatic, renal, or nutritional causes of edema (cirrhosis, nephrotic syndrome, hypoalbuminemia) masquerading as cardiac.
Pt denies over-diuresing a preload-dependent RV into hypotension.
DDx
Cardiorenal syndrome · left-sided CHF exacerbation · right heart failure · (also ESRD or dialysis-related overload, cirrhosis with ascites, nephrotic syndrome, tamponade or constriction, high-output failure, and iatrogenic fluid overload)
Plan — by Diagnosis
CONSULT (as relevant): Cardiology (HF management, RV failure, advanced therapies) · Nephrology (cardiorenal disease, refractory congestion, ultrafiltration or dialysis) · CICU (low-output or shock, RV failure with instability) · Pulmonology and PH services (RV failure from pulmonary hypertension)
CHF exacerbation (left-sided congestion)
Confirm: orthopnea and PND, pulmonary congestion and B-lines, an elevated BNP, and CXR congestion, in known or new HF (see the heart failure card for HFrEF versus HFpEF specifics).
Decongestion: furosemide at about 1–2.5 times the home daily oral dose given IV twice daily (40 mg IV if loop-naïve), or a continuous infusion of 5–10 mg/h, with metolazone 2.5–5 mg PO daily added for resistance; O2 with NIPPV for distress; and nitroglycerin for hypertensive presentations.
Then: daily weights, strict I/O, and sodium and fluid restriction; treat the trigger (ischemia, arrhythmia, nonadherence, infection); and optimize or resume GDMT once decongested and stable.
Monitoring / daily labs: a daily BMP (potassium, creatinine, magnesium), daily weights, strict I/O, and telemetry.
Mobility / consults / disposition: PT and OT, cardiac rehab, and a dietitian; HF education (daily weights, when to call); cardiology or HF-clinic follow-up within 7 days; medication reconciliation.
Cardiorenal syndrome
Confirm: heart failure with worsening renal function, in which venous congestion (a high CVP and right-sided pressures) rather than low forward output drives the AKI in most type-1 cardiorenal cases, with a careful assessment of true volume status.
Decongestion: aggressive IV loop diuretics titrated to net negative, since effective decongestion usually improves renal function, so tolerate a modest creatinine rise; add metolazone 2.5–5 mg PO daily for resistance; and use ultrafiltration or urgent dialysis for diuretic-refractory overload or true cardiorenal failure.
Caveats: distinguish the low-output subset (cold, hypotensive), which needs inotropes rather than more diuresis; and hold ACEi/ARB/ARNI and nephrotoxins during significant AKI, resuming when stable.
Monitoring / daily labs: a daily BMP (potassium, creatinine) with magnesium followed closely, daily weights, and strict I/O.
Mobility / consults / disposition: nephrology if refractory; PT and OT; a dietitian; resume GDMT when renal-stable; close cardiology and nephrology follow-up; medication reconciliation.
Right heart failure
Confirm: systemic venous congestion (an elevated JVP, hepatomegaly or a pulsatile liver, ascites, and peripheral edema), often with relatively clear lungs, and RV dilation or dysfunction on echo, identifying the cause (left heart failure causing group 2 PH, pulmonary hypertension or PAH, PE, RV infarct, chronic lung disease or cor pulmonale, or a valvular cause).
Treat the cause (essential): left heart failure → treat the left heart; PAH → PH-specific therapy; PE → anticoagulation or reperfusion; RV infarct → preload and revascularization.
Volume and support: diurese congestion (furosemide IV) but avoid over-diuresing the preload-dependent failing RV and avoid over-filling it; maintain systemic perfusion with norepinephrine 0.05–0.5 mcg/kg/min if hypotensive (keeping systemic pressure above pulmonary pressure); add inotropy (dobutamine 2.5–10 mcg/kg/min or milrinone) for low output; and avoid hypoxia, hypercarbia, and acidosis, which raise pulmonary vascular resistance.
Monitoring / daily labs: a daily BMP, lactate, and daily weights and I/O; CICU care if unstable.
Mobility / consults / disposition: PH, cardiology, and pulmonary follow-up; ongoing treatment of the driver; PT and OT; medication reconciliation.
Red Flags
A cold, hypotensive patient with end-organ hypoperfusion → cardiogenic shock or low-output cardiorenal disease; inotropes and the ICU, not more diuretic
Diuretic-refractory congestion → escalation to a continuous infusion, a thiazide, or ultrafiltration
Right heart failure with hypotension → don't over-diurese the preload-dependent RV; support the systemic pressure
Acute RV failure → exclude PE and RV infarct as the precipitant
A "right heart failure" with equalized pressures → tamponade or constriction on echo, not primary RV disease
Senior IM Resident Pearls
Decongest to true euvolemia. Incomplete decongestion at discharge is the main driver of HF readmission — the residual congestion brings them back.
In congestive cardiorenal syndrome, more decongestion helps the kidneys. Venous congestion is strangling them; under-diuresing for fear of the creatinine is the harmful mistake.
But check it isn't the low-output subset. A cold, hypotensive cardiorenal patient needs inotropes, the opposite of more diuresis.
Right heart failure is "treat the cause and don't break the RV." The failing RV punishes both over- and under-filling — decongest carefully and keep the systemic pressure up.
Clear lungs with massive edema and JVD points right-sided. Look for PH, PE, RV infarct, or left heart disease driving it.
Always find the trigger. Treating congestion without the precipitant guarantees a bounce-back.
Common mistake: under-diuresing a congestive cardiorenal patient because the creatinine ticked up, or over-diuresing a preload-dependent RV into hypotension.