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  • Overview
  • Anatomy and conduction
  • Cardiac cycle and sounds
  • ECG basics
  • Hemodynamics
  • Regulation
  • Blood components
  • Worked micro‑examples
  • Pitfalls
  • Practice prompts
  • References

Anatomy and Physiology - Cardiovascular System

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Type: Study
Divisions: B, C
Participants: Up to 2
Approx. Time: 50 minutes
Allowed Resources: Binders/notes allowed per rules; non‑programmable calculator as permitted.

Overview

The cardiovascular system delivers oxygen and nutrients, removes wastes, and maintains pressure/flow homeostasis. Mastery requires linking anatomy and electrophysiology to hemodynamics and regulation.

Anatomy and conduction

  • Chambers/valves: RA (tricuspid) → RV (pulmonic) → LA (mitral) → LV (aortic). Valve function prevents backflow; papillary muscles/chordae stabilize AV valves.
  • Conduction: SA node → atrial pathways → AV node (delay) → His bundle → bundle branches → Purkinje fibers; automaticity gradients.

Cardiac cycle and sounds

  • Phases: isovolumic contraction → ejection → isovolumic relaxation → rapid/diastasis filling → atrial systole.
  • Heart sounds: S1 (AV closure), S2 (semilunar closure); physiologic splitting of S2 with inspiration; extra sounds (S3/S4) context (qualitative recognition).

ECG basics

  • P: atrial depolarization; PR interval reflects AV conduction. QRS: ventricular depolarization; width suggests conduction velocity. T: repolarization. Axis and intervals (PR 120–200 ms; QRS < 120 ms).

Hemodynamics

  • Ohm analog: ΔP = Q·R. Mean arterial pressure (MAP) ≈ (SBP + 2·DBP)/3; pulse pressure ≈ SBP − DBP; arterial compliance influences PP.
  • Starling law: increased venous return → increased stroke volume (within limits) via sarcomere length‑tension relation.
  • Microcirculation: Starling forces govern filtration/reabsorption; lymphatics return interstitial fluid; edema mechanisms (↑Pc, ↓πc, ↑Kf/↓σ, lymph obstruction).

Regulation

  • Baroreflex: carotid sinus/aortic arch stretch → autonomic adjustments in HR/contractility/vascular tone. Rapid buffering of BP.
  • Chemoreflex and local control: CO₂/H⁺/O₂ influence ventilation and peripheral resistance; metabolic hyperemia matches flow to demand.
  • RAAS (qualitative): renin → Ang II (vasoconstriction, aldosterone) → volume/pressure effects.

Blood components

  • Plasma vs formed elements; RBCs (hemoglobin), WBC differentials (qualitative), platelets and hemostasis overview.
  • ABO/Rh basics: transfusion compatibility and hemolytic disease of the newborn (qualitative scope).

Worked micro‑examples

  1. Pressure–volume loop shift
  • Increased afterload (hypertension) raises end‑systolic pressure/volume; stroke volume falls; discuss compensations (hypertrophy long‑term, Frank–Starling acutely).
  1. Starling forces and edema
  • Reduced plasma proteins (low πc) in liver disease favors filtration → edema; contrast with venous hypertension (↑Pc) in heart failure.
  1. Baroreflex scenario
  • Standing quickly: transient ↓venous return → ↓SV/MAP; baroreflex increases HR and vasoconstriction to restore MAP; failure leads to orthostatic hypotension.

Pitfalls

  • Confusing valve names/locations; misattributing S1/S2 to wrong valves.
  • Ignoring compliance effects on pulse pressure with aging (stiffer arteries → higher PP).
  • Mixing osmotic (πc) vs hydrostatic (Pc) roles in edema.

Practice prompts

  • Label a PV loop and identify effects of preload/afterload/inotropy changes.
  • Trace conduction and annotate corresponding ECG segments/waves.
  • Explain how arteriolar dilation in exercising muscle affects systemic vascular resistance and MAP.

References

  • SciOly Wiki – Anatomy & Physiology (Cardiovascular)
  • OpenStax Anatomy & Physiology (Cardiovascular physiology)