Frank-Starling Mechanism🫀Preload & Afterload Explained | USMLE Step 1 CVS Physiology Made Easy скачать в хорошем качестве

Frank-Starling Mechanism🫀Preload & Afterload Explained | USMLE Step 1 CVS Physiology Made Easy

📌𝗝𝗼𝗶𝗻 𝗢𝘂𝗿 𝗧𝗲𝗹𝗲𝗴𝗿𝗮𝗺 𝗖𝗵𝗮𝗻𝗻𝗲𝗹 𝗛𝗲𝗿𝗲:- https://t.me/bhanuprakashdr 📌 𝐅𝐨𝐥𝐥𝐨𝐰 𝐨𝐧 𝐈𝐧𝐬𝐭𝐚𝐠𝐫𝐚𝐦:-   / drgbhanuprakash   📌𝗦𝘂𝗯𝘀𝗰𝗿𝗶𝗯𝗲 𝗧𝗼 𝗠𝘆 𝗠𝗮𝗶𝗹𝗶𝗻𝗴 𝗟𝗶𝘀𝘁:- https://linktr.ee/DrGBhanuprakash Frank-Starling Mechanism, Preload & Afterload🫀Cardiovascular Physiology - USMLE Step 1 The Frank-Starling mechanism is a foundational concept in cardiovascular physiology, describing how the heart intrinsically regulates its stroke volume in response to changes in venous return (preload). It is high-yield for USMLE Step 1, especially when interpreting cardiac output curves, heart failure dynamics, and hemodynamic responses to volume changes or afterload alterations. The core principle is: The more the ventricular muscle is stretched during diastole (increased preload), the stronger the subsequent contraction, up to an optimal point. This occurs because sarcomere length increases, improving actin-myosin overlap and enhancing contractile force—leading to increased stroke volume and cardiac output. This mechanism allows the heart to match its output to venous return without external neural input. Preload refers to the ventricular end-diastolic volume (or pressure)—essentially the stretch on myocardial fibers before contraction. It is increased by fluid resuscitation, venoconstriction, or slower heart rate, and decreased by hemorrhage, dehydration, or nitroglycerin (venodilator). Afterload is the resistance the heart must pump against, primarily influenced by systemic vascular resistance (SVR) and aortic pressure. Increased afterload (e.g., in hypertension or aortic stenosis) makes it harder for the ventricle to eject blood, potentially decreasing stroke volume if not compensated by contractility. Graphically, the Frank-Starling curve plots stroke volume or cardiac output on the Y-axis against ventricular end-diastolic volume (preload) on the X-axis. The curve shifts: Upward with increased contractility (e.g., from sympathetic stimulation or inotropic drugs like dobutamine) Downward in systolic heart failure (weakened myocardium fails to respond to preload) Clinically, this explains why patients in heart failure benefit from diuretics (reducing preload) or vasodilators (reducing afterload), and how inotropes help increase output when contractility is poor. On USMLE Step 1, expect questions that test your ability to interpret pressure-volume loops, cardiac output graphs, or predict outcomes of preload/afterload changes due to pharmacologic agents or disease states like heart failure or valve disorders. #FrankStarlingLaw #Preload #Afterload #CardiovascularPhysiology #USMLEStep1 #StrokeVolume #HeartFailure #CVSPhysiology #Inotropes #PressureVolumeLoop #MedicalEducation #Step1Buzzwords #WhiteboardMedicine #MCQPrep #USMLEBuzzwords #DrGBhanuPrakash #VenousReturn #SympatheticStimulation #HeartFunctionCurve #USMLE2025 #Hemodynamics #Contractility #medicalanimations #fmge #fmgevideos #rapidrevisionfmge #fmge2024 #mbbslectures #nationalexitexam #nationalexittest #neetpg #usmlepreparation #usmlestep1 #fmge #usmle #drgbhanuprakash #medicalstudents #medicalstudent #medicalcollege #neetpg2025 #usmleprep #usmlevideos #usmlestep1videos #medicalstudents #neetpgvideos #usmlestep2videos