arrythmia Flashcards

explain everything about arrythmia

1
Q

What is the most efficient rhythm for the heart, and how do arrhythmias affect cardiac function?

A

The heart functions most efficiently in sinus rhythm. Any arrhythmia compromises cardiac function by disrupting the normal sequence of heart muscle contractions.

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2
Q

Why is an understanding of the ionic basis of the cardiac action potential important in arrhythmia treatment?

A

Antiarrhythmic drugs work predominantly by altering the function of transmembrane ion channels, affecting the movement of ions across heart cell membranes and thus the cardiac action potential.

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3
Q

What is the principle of the Vaughan–Williams classification?

A

The Vaughan–Williams classification groups antiarrhythmic drugs based on their action on specific transmembrane ion channels involved in cardiac action potentials.

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4
Q

What are the risks associated with antiarrhythmic drugs?

A

Antiarrhythmic drugs may be proarrhythmic in certain circumstances, potentially causing or worsening arrhythmias.

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5
Q

What non-pharmacological treatments are increasing in use for arrhythmias?

A

Catheter ablation and device therapy (e.g., pacemakers, ICDs) are becoming more common for arrhythmia treatment, offering alternatives when drugs have limited efficacy or cause significant toxicity.

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6
Q

Why is atrial fibrillation (AF) significant, and what should all AF patients undergo?

A

AF is the most common arrhythmia and increases the risk of thromboembolic stroke. All AF patients should undergo an assessment of their stroke risk.

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7
Q

Describe the resting membrane potential in cardiac myocytes.

A

The resting membrane potential of −60 to −90 mV in cardiac myocytes is due to high intracellular potassium (K+) concentration, maintained by the Na+-K+-ATPase pump and K+ efflux through selective channels.

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8
Q

What triggers the pacemaker potential in certain heart cells?

A

The pacemaker potential is triggered by a gradual depolarisation during diastole, influenced by a reduction in K+ current, a reduction in acetylcholine-activated K+ current, and an increase in inward Na+ and K+ current (I f).

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9
Q

How does the autonomic nervous system influence heart rate?

A

The sympathetic nervous system increases heart rate by increasing I f current via β1-adrenoreceptors and cAMP. The parasympathetic nervous system decreases heart rate by reducing I f current and increasing outward K+ current (I KAch).

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10
Q

What initiates Phase 0 of the cardiac action potential?

A

The rapid influx of sodium (Na+) ions into the heart cell through “fast” Na+ channels.

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11
Q

What marks the beginning of Phase 1 (Initial Repolarisation) of the cardiac action potential?

A

Closure of the fast Na+ channels and the efflux of potassium (K+) ions through Ito channels.

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12
Q

What characterizes the Plateau Phase (Phase 2) of the cardiac action potential?

A

The balanced influx of calcium (Ca2+) ions and efflux of K+ ions, maintaining the membrane potential near 0 mV.

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13
Q

What occurs during Phase 3 (Repolarisation) of the cardiac action potential?

A

Decreased calcium influx and predominance of potassium efflux, returning the cell to its resting membrane potential.

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14
Q

What maintains the cell’s resting state in Phase 4 of the cardiac action potential?

A

The cell remains at a stable, negative resting potential, ready for the next action potential.

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15
Q

Where does the heartbeat initiation occur in the heart?

A

In the sinoatrial (SA) node, where pacemaker cells generate an electrical impulse.

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16
Q

What is the role of the annulus fibrosus in cardiac conduction?

A

It electrically insulates the atria from the ventricles, ensuring orderly contraction.

17
Q

What does the QRS complex on an ECG represent?

A

Ventricular depolarisation (contraction), reflecting rapid conduction through the His-Purkinje system.

18
Q

What does the P wave on an ECG represent?

A

Atrial depolarisation (contraction).

19
Q

What is indicated by the PR interval on an ECG?

A

The conduction time through the AV node, from atrial to ventricular depolarisation.

20
Q

What does the T wave on an ECG represent?

A

Ventricular repolarisation (relaxation).

21
Q

What is the significance of the QT interval on an ECG?

A

It represents the total time for ventricular depolarisation and repolarisation.

22
Q

What is abnormal automaticity in the context of cardiac arrhythmias?

A

Abnormal automaticity refers to the inappropriate generation of electrical impulses by cardiac cells outside the specialized conduction system or by an accelerated pace within it, disrupting normal heart rhythm.

23
Q

What factors determine the rate of firing of a pacemaker cell?

A

The rate of firing is determined by the maximum diastolic potential, the slope of diastolic depolarization, and the threshold potential required to generate a new action potential.

24
Q

What are early afterdepolarizations (EADs) and their association with cardiac arrhythmias?

A

EADs are unexpected electrical changes during or immediately after the repolarization phase of the cardiac action potential, associated with long QT syndromes and can lead to arrhythmias like Torsade de pointes.

25
Q

What causes delayed afterdepolarizations (DADs) and their potential effect on heart rhythm?

A

DADs are caused by spontaneous calcium release from the sarcoplasmic reticulum, leading to potential ectopic beats or tachycardia, especially under conditions like heart failure or digitalis toxicity.

26
Q

What is re-entry and its significance in arrhythmogenesis?

A

Re-entry is a mechanism where an electrical impulse circulates within a heart pathway, continuously reactivating it, leading to sustained arrhythmias due to specific conditions like unidirectional block and slow conduction.

27
Q

What electrophysiological conditions must be met for re-entry to occur?

A

Conditions include a non-conducting central obstacle, a unidirectional conduction block, slow enough conduction in the alternate pathway, and excitable tissue along the circuit.

28
Q

How do Class I antiarrhythmic drugs affect re-entry circuits?

A

Class I drugs block sodium channels, reducing the speed of the activation wavefront, which can prevent the continuation of a re-entry circuit by inhibiting conduction in diseased myocardium.

29
Q

What is the mechanism by which Class III antiarrhythmic drugs prevent re-entrant arrhythmias?

A

Class III drugs prolong the cardiac action potential duration and refractory period, preventing previously activated cells from reactivating when the re-entrant wavefront returns, thereby terminating the arrhythmia.

30
Q

What does a sudden onset of palpitations suggest compared to a gradual onset?

A

Sudden onset palpitations are indicative of an arrhythmia, whereas gradual onset palpitations may be due to heightened awareness of sinus tachycardia.