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 and stroke risks, combining biology of changes with tools for predicting strokes, scans, and blood-thinning treatments used in Botswana clinics.
Electrical and structural atrial remodellingLoss of atrial kick and blood flow impactLeft atrial appendage pooling and clotsCHA₂DS₂-VASc and bleeding risk scoresScanning for clots and blood flowBiology of heart-related strokesLesson 2Ischaemia Pathophysiology in ST-Elevation Myocardial Infarction (STEMI): Plaque Rupture, Thrombosis, Transmural Infarction and Inferior Wall-Specific AnatomyDetails 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 how this affects signs, heart tracings, and urgent care in Botswana settings.
Plaque rupture and clotting processFull blockage and wave of cell deathDeep tissue damage and ST-elevation signsLower wall blood supply and variationsRight ventricle infarction biologyReopening injury and savable heart tissueLesson 3Interaction of Common Comorbidities (Hypertension, Diabetes, CKD, Prior Stroke, Smoking, Hyperlipidaemia) 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 in Botswana patients.
High blood pressure and pressure overload left ventricle thickeningDiabetes, small vessel disease, and heart failureKidney disease, toxins, and fluid overloadHigh fats 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 AgeDiscusses why standard disease models may not fit older or multi-ill patients in Botswana, noting reduced body reserves, multiple medicines, weakness, and other risks that make diagnosis, risk assessment, and treatment more challenging.
Body ageing and lowered reservesUnusual signs in older patientsMultiple illnesses and competing causesMany medicines and changed drug effectsRisk 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 EffectsReviews how key heart medicines work, from targets in the body to effects on blood flow, hormones, and clotting prevention, and how these lead to better symptoms and results in Botswana clinical practice.
RAAS blocking with ACEi, ARB, and ARNIBeta-blockers and nerve system controlMRAs and hormone-driven heart changesSGLT2 inhibitors and heart-kidney benefitsAntiplatelet paths and clot preventionAnticoagulants and clotting chain targetsLesson 6Haemodynamic Consequences of Reduced LVEF: Preload, Afterload, Contractility, and Congestion Explaining Dyspnoea, Orthopnoea, JVP, Crackles, OedemaDescribes how weak left ventricle pumping affects blood volume, resistance, and squeezing power, causing fluid buildup and low flow, linking to signs like breathlessness, lying-flat discomfort, neck vein rise, lung sounds, and swelling seen in Botswana wards.
Frank–Starling curve in weak pumping failureAfterload, vessel tone, and left ventricle workHormone responses to low outputLung 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)Shows how heart body processes create typical heart tracing, ultrasound, and blood marker patterns, helping interpret thickened ventricle, blocked flow, irregular beats, and failure signs in a practical way for Botswana doctors.
Voltage signs and recovery in thickened ventricleLower ST-elevation and vessel layoutIrregular beat mechanisms and tracing unevennessUltrasound signs of weak failure and wall movementTroponin timing and heart cell deathBNP/NT-proBNP and wall strain biologyLesson 8Cardiac Remodelling and Systolic Dysfunction Mechanisms Leading to Heart Failure with Reduced Ejection Fraction (HFrEF)Outlines cell, tissue, and structure shifts causing heart reshaping and weak squeezing in HFrEF, including hormone triggers, cell damage, scarring, and chamber widening, worsening overall pump function in Botswana contexts.
Heart cell loss, programmed death, and necrosisThickening, widening, and shape shiftsScarring, stiffness, and beat delayHormone triggers of reshapingValve leak from ventricle wideningReversing changes with standard treatments
