Lesson 1Atrial Arrhythmogenesis and Thromboembolism in Chronic Atrial Fibrillation: Atrial Remodelling, Stasis, and Stroke RiskExplains how long-term atrial fibrillation changes the heart's atrial structure and function, causes blood to pool, and raises clot and stroke risks, combining biology of changes with clinical prediction of strokes, imaging, and blood-thinning treatments.
Electrical and structural atrial remodellingLoss of atrial kick and blood flow impactLeft atrial appendage stasis and clot formationCHA₂DS₂-VASc and bleeding risk scoresImaging of atrial thrombus and blood flowPathophysiology of heart-related strokesLesson 2Ischaemia Pathophysiology in ST-Elevation Myocardial Infarction (STEMI): Plaque Rupture, Thrombosis, Transmural Infarction and Inferior Wall-Specific AnatomyCovers the process from plaque breaking to blood clot blockage and full-thickness heart muscle death in STEMI, focusing on heart vessel layout, lower wall weaknesses, right ventricle involvement, and effects on symptoms, ECG readings, and treatments.
Plaque rupture and thrombosis processComplete blockage and wave of cell deathFull-thickness damage and ST-elevation patternsInferior wall blood supply and variationsRight ventricular infarction physiologyReperfusion injury and savable heart muscleLesson 3Interaction of Common Comorbidities (Hypertension, Diabetes, CKD, Prior Stroke, Smoking, Hyperlipidaemia) with Cardiac PathophysiologyShows how high blood pressure, diabetes, chronic kidney disease, past strokes, smoking, and high fats in blood affect heart structure, vessels, and clotting, speeding up artery hardening, heart changes, irregular beats, and heart failure worsening.
Hypertension and pressure overload left ventricle hypertrophyDiabetes, small vessel disease, and heart failureCKD, waste toxins, and fluid overloadHyperlipidaemia and artery plaque buildupSmoking, vessel lining damage, and clottingPrior stroke and heart-brain connectionsLesson 4Limitations of Pathophysiologic Models and Translation to Patients with Multimorbidity and Advanced AgeDiscusses why standard body function models may not work well for elderly and patients with many illnesses, pointing out reduced body reserves, multiple drugs, weakness, and competing dangers that make diagnosis, risk guessing, and treatment harder.
Body ageing and reduced reservesUnusual symptoms in older patientsMultiple illnesses and competing causesMany drugs and changed drug responsesRisk scores in mixed patient groupsPersonalising goals and joint decisionsLesson 5Pharmacologic Mechanisms: ACEi/ARB/ARNI, Beta Blockers, MRAs, SGLT2 Inhibitors, Antiplatelet and Anticoagulant Agents, Reperfusion Therapies and Their Physiologic EffectsReviews how major heart drugs work, linking their targets and pathways to blood flow, hormone, and anti-clot effects, and how these lead to better symptoms and long-term results in patients.
RAAS blockage with ACEi, ARB, and ARNIBeta-blockers and nerve system controlMRAs and hormone-driven heart changesSGLT2 inhibitors and heart-kidney effectsAntiplatelet paths and clot preventionAnticoagulants and clotting targetsLesson 6Haemodynamic Consequences of Reduced LVEF: Preload, Afterload, Contractility, and Congestion Explaining Dyspnoea, Orthopnoea, JVP, Crackles, OedemaExplains how low left ventricle pumping fraction affects preload, afterload, and squeezing power, causing fluid buildup and low output, linking these to signs like shortness of breath, lying flat breathing trouble, neck vein swelling, lung sounds, and swelling.
Frank–Starling curve in systolic failureAfterload, artery tone, and left ventricle workHormone responses to low outputLung vein high pressure and breathlessnessBody vein congestion and swellingNeck vein, liver push, and exam signsLesson 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 functions create typical ECG, heart scan, and blood marker patterns, helping learners read left ventricle thickening, lack of blood, irregular beats, and heart failure signs in a practical, cause-based way.
Voltage signs and recovery in left ventricle hypertrophyInferior ST-elevation and vessel layoutAF causes and ECG unevennessEcho signs of HFrEF and wall movementTroponin timing and muscle deathBNP/NT-proBNP and wall strain body functionLesson 8Cardiac Remodelling and Systolic Dysfunction Mechanisms Leading to Heart Failure with Reduced Ejection Fraction (HFrEF)Describes cell, tissue, and structure processes causing heart remodelling and weak squeezing in HFrEF, including hormone activation, cell damage, scarring, chamber widening, and how these reduce pumping power.
Heart cell loss, death, and necrosisThickening, widening, and shape changeScarring, stiffness, and signal delayHormone drivers of remodellingValve leak from left ventricle wideningReverse remodelling with standard treatments
