Page 28 - YORAM RUDY BOOK FINAL

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pacing at CL< 230 ms caused 2 to 1 block (failed AP every other beat) because APD began to

encroach upon the pacing CL, leading to enhanced refractoriness of I due to incomplete
Na
repolarization.

Figure 2.13. Schematic diagram of human ventricular myocyte model. Formulations for all
currents and fluxes were based either directly (gray) or indirectly (white) on undiseased or non-
failing human experimental data. The model includes four compartments: 1) bulk myoplasm
(MYO), 2) junctional sarcoplasmic reticulum (JSR), 3) network sarcoplasmic reticulum (NSR), and
4) subspace (SS) representing the space near T-tubules. Currents into the myoplasm: Na current
+
(I ; representing both fast and late components), transient outward K current (I ), rapid delayed
+
Na
to
rectifier K current (I ), slow delayed rectifier K current (I ), inward rectifier K current (I ), 80% of
+
+
+
Kr
K1
Ks
Na /Ca exchange current (I NaCa ), Na /K pump current (I NaK ), background currents (I Nab , I Cab , I ) and
+
+
2+
+
Kb
sarcolemmal Ca pump current (I pCa ). Currents into subspace: L-type Ca current (I CaL , with Na
2+
2+
+
and K components I CaNa , I CaK ) and 20% of of Na /Ca exchange current (I NaCa,ss ). Ionic fluxes:
+
+
2+
Ca through ryanodine receptor (J ), NSR to JSR Ca translocation (J ), Ca uptake into NSR
2+
2+
2+
tr
rel
via SERCA2a/PLB (J ; PLB – phospholamban), diffusion fluxes from subspace to myoplasm
up
(J diff,Na , J diff,Ca , and J diff,k ) Ca buffers: calmodulin (CMDN), troponin (TRPN), calsequestrin (CSQN),
2+
anionic SR binding sites for Ca (BSR), anionic sarcolemmal binding sites for Ca (BSL).
2+
2+
Ca /calmodulin-dependent protein kinase II (CaMKII) and its targets are labeled. From O’Hara et.
2+
al. [18]. Reproduced under PLOS ONE Creative Commons Attribution (CC BY) license.