Fibrillation waves

When the innervation of muscles is severed by accident or disease, spontaneous action events known as fibrillation waves appear several weeks after the trauma. These waves result from weak random contraction and relaxation of individual motor units and produce no muscle tension. Fibrillation potentials persist as long as denervation persists and as long as the muscles are present. The... 

Furthermore, under certain conditions (e.g. local unidirectional block) it is possible that the activation wavefront is delayed and encounters areas already repolarized. This may result in a circulating wave-front (= reentrant circuit reentrant arrhythmia), from which centrifugal activation waves originate and elicit life-threatening ventricular fibrillation. 

Systemic anaphylaxis in man is frequently accompanied by electrocardiographic alterations ischemic ST waves, arrhythmias and atrial fibrillation [6-11]. Anaphylactic reactions after insect stings can lead to coronary spasm or acute myocardial infarction [12, 13]. Myocardial infarction can also occur as a consequence of idiopathic... 

Electrocardiogram (ECG) May be normal or could show numerous abnormalities including acute ST-T-wave changes from myocardial ischemia, atrial fibrillation, bradycardia, and LV hypertrophy. 

There is no glycemic response to glucagon or epinephrine (Fig. 42-1), whereas a galactose load causes a normal glycemic response. Forearm ischemic exercise produces a blunted venous lactate rise or no response. Serum CK activity is variably, often markedly, increased. The ECG shows left ventricular or biventricular hypertrophy in most patients, and the EMG may show myopathic features alone or associated with fibrillations, positive sharp waves and myotonic discharges. This mixed EMG pattern in patients with weakness and distal wasting often reinforces... 

Cardiovascular manifestations include hypertension and cardiac arrhythmias (e.g., heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation, and digitalis-induced arrhythmias). In severe hypokalemia (serum concentration <2.5 mEq/L), ECG effects include ST-segment depression or flattening, T-wave inversion, and U-wave elevation. 

The a wave This is caused by atrial contraction and is, therefore, seen before the carotid pulsation. It is absent in atrial fibrillation and abnormally large if the atrium is hypertrophied, for example with tricuspid stenosis. Cannon waves caused by atrial contraction against a closed tricuspid valve would also occur at this point. If such waves are regular they reflect a nodal rhythm, and if irregular they are caused by complete heart block. 

Cardiovascular - Ang na pectoris aggravated, arrhythmia, arrhythmia atrial, atrial fibrillation, bradycardia, bundle branch block, cardiac failure, extrasystole, heart murmur, heart sound abnormal, hypertension, hypotension. Ml, palpitation, Q-wave abnormality, tachycardia, ventricular tachycardia (5% or less). 

Atrial fibrillation (AF) is one of the most common rhythm disturbances, and is characterized by the absence of discrete P wave and an irregular ventricular rhythm. Fibrillatory waves are either fine or... 

Severe hyperkalemia may produce arrhythmias, bradycardia, and ECG changes (tented T waves, widening QRS complex, and ST segment depression). These may proceed to cardiac standstill or ventricular fibrillation. 

Between 30 days and six months postprocedure, 32 MACE were reported (18%), one patient experienced cardiac death (ventricular fibrillation), two patients had non-Q-wave Ml, and one experienced CABG, and 28 patients underwent TLR. (Table 5). 

Figure 11.17 The four snapshots show the evolution and breakup of a spiral wave pattern in 2-dimensional simulated cardiac tissue (300 x 300 cells). The chaotic regime shown in the final snapshot corresponds to fibrillation. Reprinted from [587] with permission from Lippincott, Williams and Wilkins.

Undoubtedly, the most promising modehng of the cardiac dynamics is associated with the study of the spatial evolution of the cardiac electrical activity. The cardiac tissue is considered to be an excitable medium whose the electrical activity is described both in time and space by reaction-diffusion partial differential equations [519]. This kind of system is able to produce spiral waves, which are the precursors of chaotic behavior. This consideration explains the transition from normal heart rate to tachycardia, which corresponds to the appearance of spiral waves, and the fohowing transition to fibrillation, which corresponds to the chaotic regime after the breaking up of the spiral waves, Figure 11.17. The transition from the spiral waves to chaos is often characterized as electrical turbulence due to its resemblance to the equivalent hydrodynamic phenomenon. 

Q8 Depolarization of the atria normally gives rise to one P wave which precedes the QRS complex and a coordinated atrial contraction. In fibrillation the cardiac impulses arise abnormally and discharge at a very high rate (>350 min-1), producing a fast series of small, irregular waves before the QRS complex of the ECG. When this happens, the atria are unable to contract in a coordinated manner. Only occasional impulses can move through to the AV node to excite the ventricle, and ventricular rhythm becomes irregular. Patients become aware of the abnormal ventricular rhythm and usually describe the sensation as palpitations . 

OPs cause QT prolongation on the ECG that subsequently can degenerate into TdP. In one reported OP case, 79.7% had QT prolongations with ST segment and T wave abnormalities (Karki et al, 2004 Rubinshtein et al, 2002 Saadeh, 2001 Saadeh et al, 1997). Changes are ultimately expressed in arrhythmia, ventricular fibrillation and TdP, and severe disturbance of the energy homeostasis of the heart. 

A breakdown of actual cardiac symptoms for OP poisoning in hospital admissions is given by Karki et al. (2004) and also by Saadeh et al. (1997). Sixty-seven percent of the acute OP cases had QT prolongation, 24% experienced ST-segment elevation, and 17% had inverted T-waves. Nine percent had atrial tachycardia, 9% ventricular tachycardia, and 4% had ventricular fibrillation. Sinus tachycardia was observed in 35% of admissions while sinus bradycardia was noted in 28%. Noting that acidosis and electrolyte derangement play a major role in the development of cardiac events, they recommend atropine in adequate doses very early in the course of the illness as the strategy to be implemented. 

The ECG of an individual executed by inhalation of cyanic acid revealed that initially, between the first and third minutes, a heart rate slowing was discernible with the disappearance of the P-wave. Later the heart rate increased shghtly. T-waves showed an increase in amphtude and a marked shortening of the ST-segment. One subject, unhke some others in this cohort, showed normal AV conduction until ventricular tachycardia and ventricular fibrillation developed. 

Abnormal Elevated, shortened T-wave beginning high on QRS 0.3-0.6 sodium nitrite as antidote with sodium thiosulfate, atrial fibrillation DeBusk et al. (1969) (man)... 

Unit vectors in the directions of the incident and scattered waves Area per fibril... 

These are common after myocardial infarction. Their particular significance is that the R-wave (ECG) of an ectopic beat, developing during the early or peak phases of the T-wave of a normal beat, may precipitate ventricular tachycardia or fibrillation (the R-on-T phenomenon). About 80% of patients with myocardial infarction who proceed to ventricular fibrillation have preceding ventricular premature beats. Lignocaine (lidocaine) is effective in suppression of ectopic ventricular beats but is not often used as its addition increases overall risk. 

Fig. 19.8 Torsade de pointes The QT interval represents the phase of myocardial spread of stimulus and repolarization. Excessive QT lengthening may be caused by certain drugs or electrolyte imbalance. In addition, a U wave can occur, whereby its amplitude exceeds the T wave in V4-Vg. Subsequently, a potential life-threatening arrhythmia of type torsade de pointes may develop. Clinical symptoms include vertigo and syncopes. This arrhythmia can spontaneously disappear, but also pass into ventricular fibrillation and thus end fatally...

A 65-year-old man with atrial fibrillation was given intravenous amiodarone 450 mg over 30 minutes followed by 900 mg over 24 hours (54). He reverted to sinus rhjdhm, but the electrocardiogram showed giant T wave alternans with a variable QT interval (0.52-0.84 seconds). He had a short bout of torsade de pointes and was given magnesium. Two days later the electrocardiogram was normal. 

Cardiac dysrhjdhmias have been reported after amsacrine therapy in association with hypokalemia. Pre-existing supraventricular dysrhjdhmias or ventricular extra beats are not absolute contraindications to its use (49). Of 5430 patients treated with amsacrine, 65 developed cardiotoxicity, including prolongation of the QT interval, non-specific ST-T wave changes, ventricular tachycardia, and ventricular fibrillation (50). There were serious ventricular dysrhythmias resulting in cardiopulmonary arrest in 31 patients 14 died as a result. The dysrhjdhmias occurred within minutes to several hours after drug administration. The cardiotoxicity was not related to total cumulative dose, and hypokalemia was possibly a risk factor for dysrhythmias. 

A 74-year-old man was to receive a combined sciatic nerve and psoas compartment block for a total hip arthroplasty the classic Labat s approach was used and 30 ml of 0.75% ropivacaine was injected over 1.5 minutes, after which he suddenly became unresponsive and developed tonic-clonic movements. Propofol was administered and the seizure resolved, but he developed sinus bradycardia with progressive lengthening of the QRS interval, which converted to nodal bradycardia. A ventricular escape rhythm at 20/minute with T wave inversion was treated with ephedrine 10 mg and adrenahne 0.1 mg, resulting in supraventricular tachycardia with transient atrial fibrillation. 

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