Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodeling, stasis, and stroke riskExplains how long-term atrial fibrillation changes the heart's upper chambers, causes blood to pool, and raises clot and stroke risks, combining biology of changes with clinical tools for predicting strokes, imaging, and blood-thinning treatments.
Electrical and structural atrial changesLoss of atrial push and blood flow effectsLeft atrial pouch pooling and clotsCHA₂DS₂-VASc and bleeding risk toolsImaging clots and blood flowBiology of heart-related strokesLesson 2Ischemia pathophysiology in ST-elevation myocardial infarction (STEMI): plaque rupture, thrombosis, transmural infarction and inferior wall-specific anatomyDescribes the process from plaque breaking to blood clot blockage and full-thickness heart damage in STEMI, focusing on heart vessel layout, lower wall weaknesses, right heart involvement, and effects on symptoms, heart tracing, and treatments.
Plaque break and clot formation chainFull blockage and wave of cell deathFull wall damage and ST lift patternsLower wall blood supply and variationsRight heart attack biologyReopening damage and savable heart tissueLesson 3Interaction of common comorbidities (hypertension, diabetes, CKD, prior stroke, smoking, hyperlipidemia) with cardiac pathophysiologyShows how high blood pressure, diabetes, kidney disease, past strokes, smoking, and high fats interact with heart structure, vessels, and clotting, speeding up artery hardening, heart changes, irregular beats, and heart failure worsening.
High blood pressure and heart strain thickeningDiabetes, small vessel issues, and heart failureKidney disease, waste toxins, and fluid overloadHigh fats and artery clogging loadSmoking, vessel lining harm, and clotsPast stroke and heart-brain linksLesson 4Limitations of pathophysiologic models and translation to patients with multimorbidity and advanced ageDiscusses why standard disease models may not work well for elderly patients with many conditions, pointing out reduced body reserves, multiple medicines, weakness, and competing dangers that make diagnosis, risk guessing, and treatment harder.
Body aging and lowered reservesUnusual signs in older folksMultiple conditions and overlapping causesMany drugs and changed medicine responsesRisk tools in mixed groupsPersonalizing aims and joint choicesLesson 5Pharmacologic mechanisms: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet and anticoagulant agents, reperfusion therapies and their physiologic effectsReviews how major heart medicines work, connecting targets and pathways to blood flow, hormone, and anti-clot effects, and how these lead to symptom easing and better results in patients.
Hormone block with ACEi, ARB, and ARNIBeta-blockers and nerve system calmingMRAs and hormone-driven heart changesSGLT2 blockers and heart-kidney benefitsAnti-clot paths and platelet stoppingBlood thinners and clot chain targetsLesson 6Hemodynamic consequences of reduced LVEF: preload, afterload, contractility, and congestion explaining dyspnea, orthopnea, JVP, crackles, edemaExplains how weak left heart pumping affects filling, resistance, squeezing, causing fluid buildup and low flow, linking to signs like breathlessness, lying-down breathing trouble, neck vein rise, lung crackles, and swelling.
Frank–Starling curve in weak squeezing failureResistance, vessel tone, and left heart workHormone responses to low flowLung vein high pressure and breathlessnessBody vein fluid buildup and swellingNeck vein, liver push, and exam hintsLesson 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)Looks at how heart body workings create typical heart tracing, heart scan, and blood marker patterns, helping interpret thickening, lack of blood, irregular beats, and failure signs in a practical way.
Voltage signs and recovery in thickeningLower ST-lift and vessel layoutIrregular beats mechanisms and tracing wobbleScan features of weak failure and wall movesTroponin timing and heart cell deathBNP/NT-proBNP and wall strain biologyLesson 8Cardiac remodeling and systolic dysfunction mechanisms leading to heart failure with reduced ejection fraction (HFrEF)Describes tiny, cell, and structure processes causing heart reshaping and weak squeezing in HFrEF, including hormone activation, cell harm, scarring, chamber widening, and how these weaken pumping.
Heart cell loss, planned death, and damageThickening, widening, and shape shiftsScarring, stiffness, and beat delayHormone causes of reshapingValve leak from left chamber wideningReversing changes with standard treatments
