Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodeling, stasis, and stroke riskWe go detail how long-term atrial fibrillation change di heart structure and function, cause blood to stay still, and raise di risk of blood clots, mixing biology of changes wid clinical prediction of stroke, imaging, 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 anatomyWe cover di steps from plaque break to blood clot block and full wall heart attack in STEMI, stressing heart blood vessel layout, weakness in di lower wall, right heart side involvement, and effects on symptoms, ECG, and treatment.
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 pathophysiologyWe mix how high blood pressure, sugar sickness, kidney problem, past stroke, smoking, and high fat in blood work wid heart structure, vessels, and blood clotting, speeding up hardening of arteries, changes, irregular beats, and heart failure worsening.
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 ageWe talk why old-style problem models may not work for older people and dem wid many sicknesses, pointing out reduced strength, many medicines, weakness, and other risks dat make diagnosis, risk guess, and treatment hard.
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 effectsWe review how main heart medicine groups work, linking targets and paths to blood flow, hormone, and anti-clot effects, and explain how dem bring relief from symptoms and better results.
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, edemaWe explain how low left heart pump fraction change preload, afterload, and squeezing power, causing buildup and low flow, and link dem to bed signs like shortness of breath, lying down breath trouble, neck vein rise, lung crackles, and 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)We look at how heart body workings make special ECG, echo, and marker patterns, helping learners read left heart thick, lack of blood, atrial fib, and heart failure signs in a way dat explain and help in clinic.
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)We describe small, cell, and structure processes driving heart changes and weak squeezing in HFrEF, including hormone start, cell damage, scar, and chamber widen, and how dem make pump worse.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodelingMitral regurgitation from LV dilationReverse remodeling with guideline therapy
