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📌 𝐅𝐨𝐥𝐥𝐨𝐰 𝐨𝐧 𝐈𝐧𝐬𝐭𝐚𝐠𝐫𝐚𝐦:- / drgbhanuprakash 📌𝗝𝗼𝗶𝗻 𝗢𝘂𝗿 𝗧𝗲𝗹𝗲𝗴𝗿𝗮𝗺 𝗖𝗵𝗮𝗻𝗻𝗲𝗹 𝗛𝗲𝗿𝗲:- https://t.me/bhanuprakashdr 📌𝗦𝘂𝗯𝘀𝗰𝗿𝗶𝗯𝗲 𝗧𝗼 𝗠𝘆 𝗠𝗮𝗶𝗹𝗶𝗻𝗴 𝗟𝗶𝘀𝘁:- https://linktr.ee/DrGBhanuprakash Cardiac Muscle Physiology | USMLE Step 1 Quick Review | AP Phases, Ca2+ Handling, PV Loops & Exam Pearls This rapid, high-yield review distills cardiac muscle physiology into the exact concepts you need for USMLE Step 1 and bedside reasoning. We start with the cellular architecture—cardiomyocytes connected by intercalated discs (desmosomes for mechanical strength and gap junctions for low-resistance electrical coupling) that create a functional syncytium. Then we map the fast-response ventricular action potential (Phases 0–4): Phase 0 rapid Na⁺ influx (INa), Phase 1 transient K⁺ out (Ito), Phase 2 plateau via L-type Ca²⁺ influx (ICaL) balanced by K⁺ efflux, Phase 3 repolarization (IKr/IKs), and Phase 4 resting potential (IK1). We contrast this with slow-response nodal tissue (SA/AV) driven by funny current (If via HCN), T- then L-type Ca²⁺ for upstroke, and a less negative resting potential—key to automaticity, chronotropy, and dromotropy. Refractory period physiology (effective vs relative) explains why the heart avoids tetany and why Class III antiarrhythmics prolong repolarization. Next, we tie excitation–contraction coupling to performance: Ca²⁺-induced Ca²⁺ release from the sarcoplasmic reticulum via ryanodine receptors, cross-bridge cycling regulated by troponin C, and SERCA/phospholamban control of lusitropy (relaxation). Inotropy increases with β₁-stimulation (cAMP/PKA enhances ICaL and SERCA), drops with Ca²⁺-channel blockers, and rises with digoxin (↑ intracellular Ca²⁺ via Na⁺/K⁺-ATPase inhibition). We integrate mechanics with the Frank–Starling law (↑ preload → ↑ stroke volume), afterload effects (↑ afterload shifts the pressure–volume loop up/right, ↓ stroke volume), and force–velocity relations. Quick clinical anchors include long-QT torsades risk (congenital or drugs), ischemia reducing ATP and Ca²⁺ handling, heart failure with ↓ contractility and compensatory neurohormonal changes, and how β-blockers slow rate to improve diastolic filling. Finally, we connect physiology to the cardiac cycle (Wiggers) and EKG: isovolumic phases, ejection, filling; S1/S2 timing, effects of preload/afterload/inotropy on PV loops, and why AV node decremental conduction protects ventricles in atrial tachyarrhythmias. Memorize the high-yield contrasts: skeletal vs cardiac (source of Ca²⁺, refractory period), ventricular vs nodal AP, and preload vs afterload vs contractility on stroke volume. With crisp mnemonics and image-ready mental models, this quick review locks in the physiology you’ll see in Step 1 vignettes and Western clinical practice. #CardiacPhysiology #USMLEStep1 #ActionPotential #CalciumHandling #FrankStarling #PressureVolumeLoop #Inotropy #Chronotropy #Lusitropy #CardiacCycle #EKG #BetaBlockers #CalciumChannelBlockers #Digoxin #Arrhythmias #LongQT #Neurophysiology #MedicalStudentsUSA #USMLEPreparation #MedicalEducationUSA #Step1Prep #USMLEVideos