Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodeling, stasis, and stroke riskExplains how long-term irregular heartbeat in the upper heart chambers changes their structure and function, causes blood to pool, and raises clot and stroke risk, combining biology with stroke prediction tools, scans, and blood thinner plans.
Electrical and structural atrial remodelingLoss of atrial kick and hemodynamic impactLeft atrial appendage stasis and clotCHA₂DS₂-VASc and bleeding risk scoresImaging of atrial thrombus and flowPathophysiology of cardioembolic strokeLesson 2Ischemia pathophysiology in ST-elevation myocardial infarction (STEMI): plaque rupture, thrombosis, transmural infarction and inferior wall-specific anatomyCovers the process from artery plaque breaking to full blockage and deep heart muscle damage in STEMI, focusing on artery layout, lower heart wall risks, right heart involvement, and effects on symptoms, heart tracing, and urgent treatments.
Plaque rupture and thrombosis cascadeComplete occlusion and wavefront necrosisTransmural injury and ST-elevation patternsInferior wall blood supply and variantsRight ventricular infarction physiologyReperfusion injury and salvageable myocardiumLesson 3Interaction of common comorbidities (hypertension, diabetes, CKD, prior stroke, smoking, hyperlipidemia) with cardiac pathophysiologyShows how high blood pressure, sugar diabetes, kidney disease, past stroke, tobacco use, and high blood fats worsen heart structure, vessels, clotting, speeding up artery hardening, heart reshaping, irregular beats, and heart weakness.
Hypertension and pressure overload LVHDiabetes, microvascular disease, and HFCKD, uremic toxins, and volume overloadHyperlipidemia and atherosclerotic burdenSmoking, endothelial injury, and thrombosisPrior stroke and cardio-cerebral interplayLesson 4Limitations of pathophysiologic models and translation to patients with multimorbidity and advanced ageDiscusses why standard disease models don't always fit elderly patients with multiple illnesses, due to reduced body reserves, many medicines, weakness, and other risks complicating diagnosis, predictions, and choices in resource-limited settings.
Physiologic aging and reduced reserveAtypical presentations in older patientsMultimorbidity and competing mechanismsPolypharmacy and altered drug responseRisk scores in heterogeneous populationsIndividualizing goals and shared decisionsLesson 5Pharmacologic mechanisms: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet and anticoagulant agents, reperfusion therapies and their physiologic effectsReviews how key heart medicines work, from receptor actions to effects on blood flow, hormones, and clotting, and how they ease symptoms and improve survival in patients we manage daily.
RAAS blockade with ACEi, ARB, and ARNIBeta-blockers and sympathetic modulationMRAs and aldosterone-driven remodelingSGLT2 inhibitors and cardiorenal effectsAntiplatelet pathways and platelet inhibitionAnticoagulants and coagulation cascade targetsLesson 6Hemodynamic consequences of reduced LVEF: preload, afterload, contractility, and congestion explaining dyspnea, orthopnea, JVP, crackles, edemaDetails how weak left heart pumping affects filling pressure, resistance, squeezing power, causing fluid buildup and poor output, linking to signs like breathlessness, lying-flat discomfort, neck vein swelling, lung crackles, and leg swelling.
Frank–Starling curve in systolic failureAfterload, arterial tone, and LV performanceNeurohormonal responses to low outputPulmonary venous hypertension and dyspneaSystemic venous congestion and edemaJVP, hepatojugular reflux, and exam cluesLesson 7Physiologic basis for diagnostic test findings: ECG changes (LVH, inferior ST-elevations, AF), echo findings in HFrEF and wall-motion abnormalities, biomarkers (troponin, BNP/NT-proBNP)Shows how heart changes produce typical heart tracing, ultrasound, and blood test patterns, helping interpret thickened heart walls, blocked arteries, irregular beats, weak pump, and failure markers practically.
Voltage criteria and repolarization in LVHInferior ST-elevation and coronary anatomyAF mechanisms and ECG irregularityEcho features of HFrEF and wall motionTroponin kinetics and myocardial necrosisBNP/NT-proBNP and wall stress physiologyLesson 8Cardiac remodeling and systolic dysfunction mechanisms leading to heart failure with reduced ejection fraction (HFrEF)Describes cell and tissue changes causing heart reshaping and weak squeezing in HFrEF, from hormone surges, cell damage, scarring, chamber stretch, worsening overall pump function over time.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodelingMitral regurgitation from LV dilationReverse remodeling with guideline therapy
