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The cellular and ionic mechanisms by which ranolazine reduces ACh-mediated AF are likely multifold: (i) depression of I Na-dependent parameters, which reduces action potential upstroke, and increases in diastolic threshold of excitation and post-repolarization refractoriness; (ii) I Kr inhibition, which counteracts ACh-induced shortening of action potential duration; (iii) late I Na inhibition, which suppresses late phase 3 early after-depolarizations and reduces I Ti, thereby suppressing delayed after-depolarizations and triggered activity.

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Some weaknesses that could be found during evaluation are vague or inaccurate statement of the problem because of poor assessment or faulty analysis and interpretation of data, unrealistic goal-setting due to overestimating capabilities of the patient or available resources, and well-intentioned but inappropriate nursing interventions that do not effectively meet the hoped-for outcome criteria.

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