A 35 y/o male is seen by his physician complaining of shortness of breath, dizzi

Question

A 35 y/o male is seen by his physician complaining of shortness of breath, dizziness, intermittent palpitations and chest pain. The Px has a history of paroxysmal atrial dysrhythmia and has been taking 400 mg/3x/day quinidine over the past year. He has not had an episode since going on the medication. The Px lives alone and is the CEO of a local software company. He states that he recently suffered a serious bout of the flu where he experienced diarrhea and vomiting for five days. However, he has been feeling better, started taking his medication again and returned to work the previous day. The physical test shows that he is alert, but is experiencing dizziness. His respiration is 28 breaths/min but lung sounds are clear in all lobes. He has normal bowel sounds, yet is complaining of nausea. His pulse is 150 and irregular with a BP of 102/56. His nailbeds are pink and his O2 stats are 96.    

His blood work shows:

Na+          = 135 mEq/L

            K+            = 2.9 mEq/L

            Cl-            = 96 mEq/L

            BUN         = 29 mg/dL

            Creatinine = 1.3 mg/dL

            Glucose     = 100 mg/dL (fasting)

The physician ran an ECG and during recording, the Px had another arrhythmic episode shown below:

How would the conductance of the action potential during systole be affected? Explain in detail

Explanation / Answer

The patient in the above question has tachycardia alongwith low blood pressure with a history of paroxysmal vantricular tachycardia . on antiarrythmic quinnidine

So the patient had an episode of atrial fibrillation and the changes in the conduction of action potential during systole in atrial fibrillation can be explained as

Changes in atrial electrophysiology that are induced by AF and promote its perpetuation may occur through alteration in ion channel activities with partial depolarization and shortened atrial refractory period (electrical remodeling), which favors the initiation and perpetuation of AF, and modification of cellular calcium handling, which causes contractile dysfunction (contractile remodeling), as well as atrial dilation, with associated structural changes (structural remodeling).

Electrical remodeling results from the high rate of electrical activation. The EP changes typical of atrial myocytes during AF are a decrease in atrial refractory period, decrease in action potential duration, reduction in the amplitude of the action potential plateau, and loss of response of action potential duration to changes in rate (abnormal restitution).3 Whereas the normal atrial action potential duration shortens in response to pacing at shorter CLs, AF results in loss of this rate dependence of atrial action potential duration, and the atrial refractory period fails to lengthen appropriately at slow rates (e.g., with return to NSR).

Shortening of the atrial refractory period and the atrial action potential may be caused by a net decrease of inward ionic currents (Na+ or Ca2+), a net increase of outward currents (K+), or a combination of both. The decrease of L-type Ca2+ current seems to be responsible for shortening of the atrial action potential, whereas the decrease of transient outward K+ current (Ito) is considered to result in loss of physiological rate adaptation of the action potential.

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