Lesson 1Atrial arrhythmogenesis and thromboembolism in chronic atrial fibrillation: atrial remodelling, stasis, and stroke riskExplains how chronic atrial fibrillation changes atrial structure and function, causes blood stasis, and raises thromboembolic risk, combining remodelling biology with clinical stroke prediction, imaging, and anticoagulation strategies suitable for local practice.
Electrical and structural atrial remodellingLoss of atrial kick and haemodynamic impactLeft atrial appendage stasis and clotCHA₂DS₂-VASc and bleeding risk scoresImaging of atrial thrombus and flowPathophysiology of cardioembolic strokeLesson 2Ischaemia pathophysiology in ST-elevation myocardial infarction (STEMI): plaque rupture, thrombosis, transmural infarction and inferior wall-specific anatomyCovers the process from plaque rupture to thrombotic blockage and full-thickness infarction in STEMI, focusing on coronary anatomy, inferior wall risks, right ventricular involvement, and effects on symptoms, ECG, and treatment in resource-limited settings.
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, hyperlipidaemia) with cardiac pathophysiologyShows how hypertension, diabetes, CKD, prior stroke, smoking, and hyperlipidaemia affect cardiac structure, vessels, and clotting, speeding up atherosclerosis, remodelling, arrhythmias, and heart failure in multimorbid patients common in Zimbabwe.
Hypertension and pressure overload LVHDiabetes, microvascular disease, and HFCKD, uraemic toxins, and volume overloadHyperlipidaemia and atherosclerotic burdenSmoking, endothelial injury, and thrombosisPrior stroke and cardio-cerebral interplayLesson 4Limitations of pathophysiologic models and translation to patients with multimorbidity and advanced ageDiscusses why standard pathophysiologic models may not work well for older adults and those with multiple conditions, noting reduced reserves, multiple medications, frailty, and competing risks that complicate diagnosis, risk prediction, and treatment in elderly Zimbabwean patients.
Physiologic ageing and reduced reserveAtypical presentations in older patientsMultimorbidity and competing mechanismsPolypharmacy and altered drug responseRisk scores in heterogeneous populationsIndividualising goals and shared decisionsLesson 5Pharmacologic mechanisms: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet and anticoagulant agents, reperfusion therapies and their physiologic effectsReviews how major cardiovascular drug classes work, linking receptor targets and pathways to haemodynamic, neurohormonal, and anti-clotting effects, and how these lead to symptom relief and better outcomes in local clinical scenarios.
RAAS blockade with ACEi, ARB, and ARNIBeta-blockers and sympathetic modulationMRAs and aldosterone-driven remodellingSGLT2 inhibitors and cardiorenal effectsAntiplatelet pathways and platelet inhibitionAnticoagulants and coagulation cascade targetsLesson 6Haemodynamic consequences of reduced LVEF: preload, afterload, contractility, and congestion explaining dyspnoea, orthopnoea, JVP, crackles, oedemaExplains how low left ventricular ejection fraction affects preload, afterload, and contractility, causing congestion and low output, and links these to clinical signs like shortness of breath, lying flat discomfort, neck vein elevation, lung crackles, and swelling in heart failure patients.
Frank–Starling curve in systolic failureAfterload, arterial tone, and LV performanceNeurohormonal responses to low outputPulmonary venous hypertension and dyspnoeaSystemic venous congestion and oedemaJVP, 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)Explores how heart physiology creates typical ECG, echo, and biomarker patterns, helping interpret left ventricular hypertrophy, ischaemia, atrial fibrillation, and heart failure in a practical, mechanistic way for Zimbabwean clinicians.
Voltage criteria and repolarisation 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 remodelling and systolic dysfunction mechanisms leading to heart failure with reduced ejection fraction (HFrEF)Describes molecular, cellular, and structural changes driving cardiac remodelling and systolic dysfunction in HFrEF, including hormone activation, cell injury, scarring, and chamber widening, worsening heart pump function in chronic cases.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodellingMitral regurgitation from LV dilationReverse remodelling with guideline therapy
