Cardiology
Showing 49 of 49 topics
A
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Tearing chest/back pain with pulse/BP differential warrants immediate anti‑impulse therapy and CTA. Type A → emergent surgery; Type B complicated → TEVAR/branch-first strategies; all receive strict BP/HR control, analgesia, and intensive monitoring.
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Tearing chest/back pain with pulse deficits or mediastinal widening suggests dissection. Rapidly control HR (<60) and SBP (100–120) with beta-blockade and vasodilators; obtain CTA chest/abdomen/pelvis. Type A requires emergent surgery; Type B usually medical unless complications warrant TEVAR.
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Risk-stratify using ECG and troponin trends plus TIMI/GRACE; initiate DAPT, anticoagulation, anti-ischemic therapy; early invasive strategy for high-risk; tailor P2Y12 and anticoagulant to bleeding risk and PCI plans.
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Acute dyspnea with rales and frothy sputum indicates pulmonary edema. Provide high-flow oxygen and early noninvasive ventilation, give IV nitrates to reduce preload/afterload (especially in hypertensive ADHF), and administer loop diuretics; investigate triggers (ischemia, arrhythmia, dietary/medication nonadherence).
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Identify perfusion/congestion profile (wet/dry; warm/cold). Use IV loop diuretics (1–2× home dose), consider vasodilators in hypertensive pulmonary edema, and escalate to inotropes/ultrafiltration for diuretic resistance and hypoperfusion.
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Volume overload or flash pulmonary edema requires loop diuretics, vasodilators when blood pressure allows, and noninvasive ventilation to improve oxygenation. Identify precipitating factors (ischemia, arrhythmia, nonadherence) and tailor therapy by hemodynamic profile (warm/wet vs cold/wet).
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Treat pulmonary edema with nitrates and diuretics, oxygen/ventilation support, and afterload reduction; identify precipitants; use ultrasound to guide volume.
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Rapid dyspnea relief with noninvasive ventilation and nitrates when hypertensive; add diuretics and treat triggers such as ischemia or arrhythmia.
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Sharp pleuritic chest pain relieved by sitting forward with pericardial friction rub; diffuse ST elevation and PR depression on ECG; treat with NSAID and colchicine after excluding high risk causes and tamponade.
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Adults with congenital heart disease require lifelong surveillance. Primary care priorities: immunizations, dental care, endocarditis guidance, pregnancy counseling, exercise advice, and coordination with ACHD specialists.
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Suspect with sudden tearing chest or back pain and pulse or BP differentials; confirm with CTA; control pain and shear stress; surgery for Stanford type A; medical therapy for uncomplicated type B.
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Acute chest/back pain with imaging showing intramural hematoma (IMH) or penetrating atherosclerotic ulcer (PAU)—entities within acute aortic syndrome.
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Unstable patients need immediate synchronized cardioversion; otherwise control rate with beta blocker or diltiazem, consider rhythm control in select cases, and address anticoagulation.
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Rapid AF can cause hypotension, ischemia, or heart failure. Stabilize ABCs; if unstable, perform synchronized cardioversion. If stable, choose rate control (β‑blocker or nondihydropyridine CCB; amiodarone if LV dysfunction/hypotension) versus rhythm control based on duration and comorbidities, and address anticoagulation using CHA₂DS₂‑VASc and bleeding risk.
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Use CHA₂DS₂‑VASc to guide anticoagulation; DOACs preferred. Choose rate vs rhythm strategy based on symptoms and HF; consider early ablation for symptomatic paroxysmal AF. Manage risk factors (BP, OSA, obesity).
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Stabilize if unstable; rate control first for most; rhythm control for persistent symptoms or HF; anticoagulate per CHA₂DS₂-VASc; DOACs preferred unless mechanical valve or moderate–severe mitral stenosis.
B
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Inherited sodium‑channelopathy with coved ST elevation (type 1) in V1–V3 and risk of polymorphic VT/VF. Avoid fever and offending drugs; treat electrical storms with isoproterenol and consider quinidine. ICD is indicated for survivors of VT/VF and often for syncope with spontaneous type‑1 ECG plus inducible arrhythmias; counsel family screening.
C
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Infiltrative cardiomyopathy; suspect with HFpEF, thick walls, low‑voltage ECG, apical sparing strain. Screen for monoclonal proteins; use bone scintigraphy for ATTR; treat with disease‑specific therapy and cautious diuresis.
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Beck’s triad and pulsus paradoxus with effusion on ultrasound suggests tamponade. Provide IV fluids as a bridge, avoid positive-pressure ventilation if possible, and perform urgent pericardiocentesis with echo guidance; reverse anticoagulation and treat underlying cause.
D
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Use Wells score and D dimer to guide ultrasound; start anticoagulation when DVT is confirmed or highly suspected without major contraindications.
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Bradyarrhythmias, gastrointestinal symptoms, and hyperkalemia suggest toxicity; treat unstable rhythms, give digoxin immune Fab for standard indications, and correct electrolytes.
H
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Initiate and up-titrate quadruple therapy (ARNI/ACEi/ARB, β-blocker, MRA, SGLT2 inhibitor); manage diuretics for congestion; add hydralazine–isosorbide dinitrate in selected patients; evaluate for devices.
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Quadruple therapy (ARNI/ACEi/ARB, beta‑blocker, MRA, SGLT2i) for all HFrEF as tolerated; up‑titrate to target doses with close monitoring of BP, K+, and creatinine; diuretics for congestion; consider ICD/CRT.
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Acute severe BP elevation with target-organ damage; admit, place arterial line when indicated, and lower MAP ~10–20% in first hour using titratable IV agents tailored to condition.
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Acutely elevated blood pressure with target organ damage requires controlled reduction using IV agents tailored to the condition.
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Acute severe hypertension with target-organ damage (e.g., encephalopathy, pulmonary edema, ACS, AKI) requires rapid but controlled BP lowering with IV agents; general goal is ≤25% MAP reduction in the first hour, then to 160/100–110 mmHg over the next 2–6 hours, except in special conditions.
K
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Chest pain and ST‑changes during anaphylaxis or hypersensitivity reaction suggests Kounis syndrome (allergic ACS).
L
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Measure Lp(a) once in adulthood (earlier if strong family history). Values ≥50 mg/dL (≥125 nmol/L) are risk‑enhancing; intensify LDL‑C lowering and risk factor control; consider PCSK9 inhibitors; anticipate Lp(a)‑specific agents.
M
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MINOCA is MI with non‑obstructive coronaries (≤50% stenosis). Systematically evaluate for plaque disruption, spasm, SCAD, embolism, microvascular dysfunction, and myocarditis/Takotsubo mimics; tailor secondary prevention.
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Suspect in chest pain, troponin rise, and non‑obstructive coronaries. Use CMR (Lake Louise) and consider EMB in fulminant cases. Treat HF/arrhythmias; restrict exercise for 3–6 months with normalization before return.
N
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Confirm with high-sensitivity troponin and ECG changes; start aspirin, P2Y12, and anticoagulation; use risk scores to guide early invasive strategy and admitted level of care.
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Chest pain with troponin rise and non-ST elevation ECG changes. Start aspirin, P2Y12 inhibitor, and anticoagulation; apply high-intensity statins and anti-ischemic therapy. Use risk scores (TIMI/GRACE) to guide timing of angiography and revascularization.
P
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Life-threatening shock from pericardial effusion; diagnose with bedside ultrasound; give fluids as a bridge and perform urgent pericardiocentesis while preparing for definitive management.
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Beck triad is uncommon; rely on echocardiography showing chamber collapse and IVC plethora. Resuscitate, avoid positive-pressure ventilation if possible, and perform pericardiocentesis (ultrasound-guided) for hemodynamic compromise.
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Pericarditis: pleuritic chest pain, pericardial rub, and diffuse ST elevation; treat with NSAIDs plus colchicine. Tamponade: shock physiology with echo evidence; urgent pericardiocentesis.
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HF with reduced EF developing in late pregnancy or ≤5 months postpartum without other cause. Manage with pregnancy‑safe HF therapy; anticoagulate if LV thrombus/EF ≤35%; consider bromocriptine selectively; counsel on future pregnancy risk.
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Post‑MI care: DAPT after PCI, high‑intensity statin, beta‑blocker, ACEi/ARB (± MRA if EF ≤40%), smoking cessation, BP/DM control, and enrollment in cardiac rehab; consider ezetimibe/PCSK9i if LDL‑C ≥70.
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Use pretest probability and D dimer to guide imaging; stratify risk for disposition; anticoagulate when diagnosis is likely or confirmed unless contraindicated.
S
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Younger women with ACS symptoms, often without classic risk factors; angiography shows coronary dissection not due to atherosclerosis.
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Activate reperfusion on first medical contact: primary PCI within guideline time targets; fibrinolysis if PCI delay; give antiplatelets and anticoagulation; manage complications and initiate secondary prevention.
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Obtain ECG within 10 minutes; activate cath lab for primary PCI; if PCI cannot be achieved in time, give fibrinolysis when not contraindicated; start antiplatelet and anticoagulation promptly.
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Activate the cath lab for PCI‑capable patients with goal first‑medical‑contact‑to‑device ≤90 min (≤120 min for transfers). If PCI unavailable in time, give fibrinolysis within 30 min of arrival if no contraindications and plan pharmaco‑invasive strategy. Load antiplatelets and anticoagulate; control pain and blood pressure; initiate secondary prevention.
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Stable regular narrow-complex SVT responds to vagal maneuvers and adenosine; unstable requires synchronized cardioversion; choose calcium channel blocker or beta blocker if adenosine contraindicated.
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Stable narrow complex tachycardia responds to vagal maneuvers and adenosine; unstable rhythms need synchronized cardioversion.
T
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Stress‑induced cardiomyopathy mimicking ACS; transient LV dysfunction with typical apical ballooning. Diagnose with angiography excluding obstructive CAD and CMR; manage supportively; avoid inotropes if LVOTO; anticoagulate if LV thrombus.
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Polymorphic ventricular tachycardia with prolonged QT; give IV magnesium, correct electrolytes, defibrillate if unstable, and use overdrive pacing or isoproterenol for pause dependent episodes.
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Polymorphic VT with prolonged QT requires IV magnesium sulfate regardless of serum level, aggressive potassium repletion, and cessation of QT-prolonging drugs. Unstable patients need immediate defibrillation; recurrent cases benefit from overdrive pacing or isoproterenol if pause-dependent.
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Polymorphic VT with prolonged QT; correct precipitants (electrolytes, QT-prolonging meds), give magnesium, increase heart rate via overdrive pacing or isoproterenol if bradycardic, and treat hemodynamic instability per ACLS.
V
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Differentiate stable from unstable VT; provide immediate synchronized cardioversion for instability and consider procainamide or amiodarone for stable monomorphic VT.
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