Aralin 1Atrial arrhythmogenesis at thromboembolism sa kronikong atrial fibrillation: atrial remodeling, stasis, at stroke riskNagdedetalye kung paano ang kronikong atrial fibrillation ay nagbabago ng istraktura at function ng atrial, nagpo-promote ng blood stasis, at nagpapataas ng thromboembolic risk, na pinagsasama ang remodeling biology sa klinikal na stroke prediction, imaging, at anticoagulation strategies.
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 strokeAralin 2Ischemia pathophysiology sa ST-elevation myocardial infarction (STEMI): plaque rupture, thrombosis, transmural infarction at inferior wall-specific anatomyTinutustos ang sequence mula plaque rupture hanggang thrombotic occlusion at transmural infarction sa STEMI, na binibigyang-diin ang coronary anatomy, inferior wall vulnerability, right ventricular involvement, at implikasyon para sa symptoms, ECG, at therapy.
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 myocardiumAralin 3Interaction ng common comorbidities (hypertension, diabetes, CKD, prior stroke, smoking, hyperlipidemia) sa cardiac pathophysiologyNag-iintegrate kung paano ang hypertension, diabetes, CKD, prior stroke, smoking, at hyperlipidemia ay nakikipag-ugnayan sa cardiac structure, vessels, at hemostasis, na nagpapabilis ng atherosclerosis, remodeling, arrhythmias, at heart failure progression.
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 interplayAralin 4Limitations ng pathophysiologic models at translation sa patients na may multimorbidity at advanced ageNagdidiskus ng bakit maaaring mabigo ang classic pathophysiologic models sa matatanda at multimorbid patients, na binibigyang-diin ang altered reserves, polypharmacy, frailty, at competing risks na nagpapalala ng diagnosis, risk prediction, at treatment choices.
Physiologic aging and reduced reserveAtypical presentations in older patientsMultimorbidity and competing mechanismsPolypharmacy and altered drug responseRisk scores in heterogeneous populationsIndividualizing goals and shared decisionsAralin 5Pharmacologic mechanisms: ACEi/ARB/ARNI, beta blockers, MRAs, SGLT2 inhibitors, antiplatelet at anticoagulant agents, reperfusion therapies at kanilang physiologic effectsNagre-review ng mechanisms ng major cardiovascular drug classes, na nag-uugnay ng receptor targets at signaling pathways sa hemodynamic, neurohormonal, at antithrombotic effects, at nagpapaliwanag kung paano ito nai-translate sa symptom relief at outcome benefits.
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 targetsAralin 6Hemodynamic consequences ng reduced LVEF: preload, afterload, contractility, at congestion na nagpapaliwanag ng dyspnea, orthopnea, JVP, crackles, edemaNagpapaliwanag kung paano ang reduced left ventricular ejection fraction ay nagbabago ng preload, afterload, at contractility, na lumilikha ng congestion at low output, at nag-uugnay ng mga pagbabageng ito sa bedside signs tulad ng dyspnea, orthopnea, JVP elevation, crackles, at edema.
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 cluesAralin 7Physiologic basis para sa diagnostic test findings: ECG changes (LVH, inferior ST-elevations, AF), echo findings sa HFrEF at wall-motion abnormalities, biomarkers (troponin, BNP/NT-proBNP)Nag-e-explore kung paano ang underlying cardiac physiology ay lumilikha ng characteristic ECG, echocardiographic, at biomarker patterns, na nagbibigay-daan sa mga mag-aaral na i-interpret ang LVH, ischemia, atrial fibrillation, at heart failure findings sa mekanistikong, klinikal na kapaki-pakinabang na paraan.
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 physiologyAralin 8Cardiac remodeling at systolic dysfunction mechanisms na humuhantong sa heart failure with reduced ejection fraction (HFrEF)Naglalarawan ng molecular, cellular, at structural processes na nagmamaneho ng cardiac remodeling at systolic dysfunction sa HFrEF, kabilang ang neurohormonal activation, myocyte injury, fibrosis, at chamber dilation, at kung paano ang mga pagbabageng ito ay lumalala ng pump performance.
Myocyte loss, apoptosis, and necrosisHypertrophy, dilation, and geometry changeFibrosis, stiffness, and conduction delayNeurohormonal drivers of remodelingMitral regurgitation from LV dilationReverse remodeling with guideline therapy
