Ventricular depolarization

The mechanical activity of the heart (contraction of the atria and ventricles) occurs as a result of the electrical activity of the heart. The heart possesses an intrinsic electrical conduction system (Fig. 6-1). Normal myocardial contraction cannot occur without proper and normal function of the heart s electrical conduction system. Electrical depolarization of the atria results in atrial contraction, and ventricular depolarization is... 

Several intervals and durations are routinely measured on the ECG. The PR interval represents the time of conduction of impulses from the atria to the ventricles through the AV node the normal PR interval in adults is 0.12 to 0.2 seconds. The QRS duration represents the time required for ventricular depolarization, which is normally 0.08 to 0.12 seconds in adults. The QT interval represents the time required for ventricular repolarization. The QT interval varies with heart rate—the faster the heart rate, the shorter the QT interval, and vice versa. Therefore, the QT interval is corrected for heart rate using Bazett s equation3, which is ... 

Ventricular fibrillation is irregular, disorganized, chaotic electrical activity in the ventricles resulting in absence of ventricular depolarizations, and, consequently, lack of pulse, cardiac output, and blood pressure. 

Ventricular depolarization Change in the membrane potential of a ventricular myocyte, resulting in loss of polarization. Under... 

Figure 13.4 Electrocardiogram. The electrocardiogram (ECG) is a measure of the overall electrical activity of the heart. The P wave is caused by atrial depolarization, the QRS complex is caused by ventricular depolarization, and the T wave is caused by ventricular repolarization.

Finally, no recording occurs during the ST segment — the period between ventricular depolarization and ventricular repolarization. In other words, the ventricles are completely depolarized and the muscle cells are in... 

Figure 4.2 Cartoon representation of an ECC trace and ventricular cardiac action potential, (a) A representation of an ECC trace with its five typical deflections (PQRST) arising from the spread of electrical activitythrough the heart. The QRS wave denotes the ventricular depolarization, while the T wave represents ventricular repolarization. The QT interval therefore estimates the duration of a ventricular action potential, (b) Schematic of the five phases of a ventricular action potential. Phase 0 is the rapid depolarization phase due to a large influx of Na+ ions (Ina). Phase 1 occurs with the inactivation of Na+ channels and the onset of transient outward (repolarizing) currents (/to)...

The most frequent cardiovascular effects of an acute overdose are tachycardia and hypotension. The hypotension is partially related to a relative volume depletion, but correction does not bring complete resolution. Even though radionuclide and catheterization studies have shown that TCAs do not impair LVF, either at therapeutic plasma levels or with overdose, data are not available for victims who died. One study describes two cases of fatal overdose in which ventricular pacing produced regular ventricular depolarization but minimal cardiac output, suggesting that at very high concentrations, TCAs might directly impair the myocardium (as demonstrated in animal studies) (429). 

Cardiac arrhythmias are a common problem in clinical practice, occurring in up to 25% of patients treated with digitalis, 50% of anesthetized patients, and over 80% of patients with acute myocardial infarction. Arrhythmias may require treatment because rhythms that are too rapid, too slow, or asynchronous can reduce cardiac output. Some arrhythmias can precipitate more serious or even lethal rhythm disturbances for example, early premature ventricular depolarizations can precipitate ventricular fibrillation. In such patients, antiarrhythmic drugs may be lifesaving. On the other hand, the hazards of antiarrhythmic drugs—and in particular the fact that they can precipitate lethal arrhythmias in some patients—has led to a reevaluation of their relative risks and benefits. In general, treatment of asymptomatic or minimally symptomatic arrhythmias should be avoided for this reason. 

The most common cardiac manifestations of digitalis toxicity include atrioventricular junctional rhythm, premature ventricular depolarizations, bigeminal rhythm, and second-degree atrioventricular blockade. However, it is claimed that digitalis can cause virtually any arrhythmia. 

There are two forms of arrhythmia in acute myocardial ischemia. Type-la arrhythmias occur 2-10 min after the onset of ischemia with a peak at 5-6 min. These arrhythmias are often of the reentrant type and are caused by diastolic bridging (details see chapter 1). It is also possible that premature ventricular depolarizations occur in this phase and initiate reentry. 

ICH S7B Step 4. Non-chnical Evaluation of the Potential for Delayed Ventricular Depolarization (QT Interval Prolongation) by Human Pharmaceuticals, 2005. 

Atrial depolarization results in the P wave of the ECG, the QRS complex denotes ventricular depolarization and the T wave represents ventricular repolarization. 

The side-effects are associated with vagal effects on the gastrointestinal tract (anorexia, abdominal discomfort/pain, vomiting and diarrhoea), while cardiotoxic effects include premature ventricular depolarizations, nodal rhythms and AV dissociation, Toxicity is enhanced by hypokalaemia, and this may predispose to more complex arrhythmias. 

Nora MO, Chandrasekaran K, Hammill SC, Reeder GS. Prolongation of ventricular depolarization. ECG manifestation of mexiletine toxicity. Chest 1989 95(4) 925-8. 

Premature ventricular depolarizations, bigeminy, trigeminy, ventricular tachycardia, ventricular fibrillation Atrioventricular (AV) block... 

Jouven X, Zuerik M, Desnos M, et al. Long-term outcome in asymptomatic men with exercise-induced premature ventricular depolarizations. N Engl J Med 2000 343(12) 826—33. 

A typical ECG is shown in Figure 4.4, where the P wave corresponds to atrial depolarization and contraction the QRST complex corresponds to atrial repolarization and relaxation and the onset of ventricular depolarization and contraction and the T wave represents ventricular repolarization and relaxation. Analysis of the size and shape of the waves can indicate abnormalities of the heart. 

Quinidine (e.g., Cin-Quin) Depresses automaticity of ectopic foci. Siows conduction veiocity in atria His-Purkinje ceils. Prolongs refractory period throughout heart (except nodes) and accessory pathways. Has anticholinergic effects which may actuaiiy enhance A-V conduction in patients with rapid atrial depolarization. Multifocal atrial tachycardia, premature atrial depolarization, premature ventricular depolarization, atrial fibrillation (these result from increased automaticity of ectopic foci), and ventricular tachycardia. Torsades de pointes (recurrent, temporary arrhythmia), increases ventricle response to atrial tachyarrhythmia, nausea, vomiting, diarrhea, hypersensitivity, cinchonism, thrombocytopenic purpura. 

Procainamide (e.g., Pronestyl) II If Premature atnal depolarization, atrial fibrillation, Wolff-Parkinson-White, ventricular tachycardia, atrial flutter, premature ventricular depolarization. Fewer Gl effects and weaker anticholinergic effects than quinidine, but similar cardiac toxicity. Lupus-like syndrome and other hypersensitivity reactions. 

C. Cardiotoxicity with impaired ventricular depolarization (as evidenced by a prolonged QRS interval) caused by tricyclic antidepressants, type la or type Ic antiarrhythmics, and other membrane-depressant dmgs (see Table 11-7, p 88). Note Not effective for dysrhythmias associated with abnormal repolarization (prolonged QT interval and torsade de pointes). 

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