Lesson 1Atrial Arrhythmogenesis and Thromboembolism in Chronic Atrial Fibrillation: Atrial Remodelling, Stasis, and Stroke RiskExplains how long-term atrial fibrillation changes the heart's upper chambers, causes blood to pool, and raises clot risks, combining biology of changes with predicting strokes, scans, and blood-thinning treatments in Ghanaian patients.
Electrical and structural atrial remodellingLoss of atrial kick and blood flow impactLeft atrial appendage pooling and clotsCHA₂DS₂-VASc and bleeding risk scoresImaging of atrial clots and flowPathophysiology of heart-related strokesLesson 2Ischaemia Pathophysiology in ST-Elevation Myocardial Infarction (STEMI): Plaque Rupture, Thrombosis, Transmural Infarction and Inferior Wall-Specific AnatomyDiscusses the process from plaque breaking to full blockage and deep heart muscle damage in STEMI, focusing on heart vessel layout, lower wall weaknesses, right ventricle effects, and links to symptoms, ECG readings, and treatments.
Plaque rupture and clotting processFull blockage and wave of cell deathDeep tissue damage and ST-elevation on ECGLower wall blood supply and variationsRight ventricle infarction effectsReopening injury and savable heart tissueLesson 3Interaction of Common Comorbidities (Hypertension, Diabetes, CKD, Prior Stroke, Smoking, Hyperlipidaemia) with Cardiac PathophysiologyShows how high blood pressure, sugar disease, kidney problems, past strokes, tobacco use, and high fats work with heart structure, vessels, and clotting, speeding up artery hardening, changes, irregular beats, and heart failure in local contexts.
Hypertension and pressure overload on left heart thickeningDiabetes, small vessel disease, and heart failureCKD, waste toxins, and fluid overloadHyperlipidaemia and artery plaque loadSmoking, vessel lining damage, and clottingPast stroke and heart-brain connectionsLesson 4Limitations of Pathophysiologic Models and Translation to Patients with Multimorbidity and Advanced AgeExplores why standard body process models may not fit elderly or multi-ill patients, noting reduced body reserves, many medicines, weakness, and other risks that make diagnosis, prediction, and treatment harder in Ghanaian clinics.
Body ageing and lowered reservesUnusual signs in older folksMultiple illnesses and overlapping causesMany drugs and changed medicine responsesRisk scores in mixed groupsPersonalising aims and joint choicesLesson 5Pharmacologic Mechanisms: ACEi/ARB/ARNI, Beta Blockers, MRAs, SGLT2 Inhibitors, Antiplatelet and Anticoagulant Agents, Reperfusion Therapies and Their Physiologic EffectsLooks at how main heart medicines work, connecting targets and pathways to blood flow, hormone, and anti-clot effects, and how they bring symptom ease and better results in everyday patient care.
RAAS blocking with ACEi, ARB, and ARNIBeta-blockers and nerve system controlMRAs and hormone-driven changesSGLT2 inhibitors and heart-kidney benefitsAntiplatelet paths and clot preventionAnticoagulants and clotting targetsLesson 6Haemodynamic Consequences of Reduced LVEF: Preload, Afterload, Contractility, and Congestion Explaining Dyspnoea, Orthopnoea, JVP, Crackles, OedemaDescribes how low left heart pumping changes fluid load, resistance, and squeezing power, causing fluid buildup and low flow, linking to signs like breathlessness, lying-flat trouble, neck vein rise, lung sounds, and swelling.
Frank–Starling curve in squeezing failureAfterload, 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 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)Shows how heart body processes create typical ECG, heart scan, and blood marker patterns, helping interpret left thickening, lack of blood, irregular beats, and failure signs in a practical way for clinicians.
Voltage signs and recovery in left thickeningLower ST-elevation and vessel layoutAF causes and ECG unevennessEcho signs of HFrEF and wall movementTroponin timing and muscle deathBNP/NT-proBNP and wall strain processesLesson 8Cardiac Remodelling and Systolic Dysfunction Mechanisms Leading to Heart Failure with Reduced Ejection Fraction (HFrEF)Outlines cell, tissue, and structure shifts driving heart changes and weak squeezing in HFrEF, including hormone triggers, cell damage, scarring, chamber widening, and how they weaken pumping in affected patients.
Heart cell loss, death, and damageThickening, widening, and shape shiftsScarring, stiffness, and beat delaysHormone drivers of changesValve leak from left wideningReversing changes with standard treatments
