A malignant form of polymorphic ventricular tachycardia that is characterized by HEART RATE between 200 and 250 beats per minute, and QRS complexes with changing amplitude and twisting of the points. The term also describes the syndrome of tachycardia with prolonged ventricular repolarization, long QT intervals exceeding 500 milliseconds or BRADYCARDIA. Torsades de pointes may be self-limited or may progress to VENTRICULAR FIBRILLATION.
A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.
Agents used for the treatment or prevention of cardiac arrhythmias. They may affect the polarization-repolarization phase of the action potential, its excitability or refractoriness, or impulse conduction or membrane responsiveness within cardiac fibers. Anti-arrhythmia agents are often classed into four main groups according to their mechanism of action: sodium channel blockade, beta-adrenergic blockade, repolarization prolongation, or calcium channel blockade.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.
A group of compounds that are derivatives of beta- aminoethylbenzene which is structurally and pharmacologically related to amphetamine. (From Merck Index, 11th ed)
A family of voltage-gated potassium channels that are characterized by long N-terminal and C-terminal intracellular tails. They are named from the Drosophila protein whose mutation causes abnormal leg shaking under ether anesthesia. Their activation kinetics are dependent on extracellular MAGNESIUM and PROTON concentration.
Antihistamine drug now withdrawn from the market in many countries because of rare but potentially fatal side effects.
A selective histamine H1-receptor antagonist devoid of central nervous system depressant activity. The drug was used for ALLERGY but withdrawn due to causing LONG QT SYNDROME.
A substituted benzamide used for its prokinetic properties. It is used in the management of gastroesophageal reflux disease, functional dyspepsia, and other disorders associated with impaired gastrointestinal motility. (Martindale The Extra Pharmacopoeia, 31st ed)
Impaired impulse conduction from HEART ATRIA to HEART VENTRICLES. AV block can mean delayed or completely blocked impulse conduction.
Cardiac arrhythmias that are characterized by excessively slow HEART RATE, usually below 50 beats per minute in human adults. They can be classified broadly into SINOATRIAL NODE dysfunction and ATRIOVENTRICULAR BLOCK.
Impaired conduction of cardiac impulse that can occur anywhere along the conduction pathway, such as between the SINOATRIAL NODE and the right atrium (SA block) or between atria and ventricles (AV block). Heart blocks can be classified by the duration, frequency, or completeness of conduction block. Reversibility depends on the degree of structural or functional defects.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
A long-acting calcium-blocking agent with significant anti-anginal activity. The drug produces significant coronary vasodilation and modest peripheral effects. It has antihypertensive and selective anti-arrhythmia activities and acts as a calmodulin antagonist.
An impulse-conducting system composed of modified cardiac muscle, having the power of spontaneous rhythmicity and conduction more highly developed than the rest of the heart.
An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.
A small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of contractions. (From AMA Drug Evaluations Annual, 1992, p1083)
An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.
A transient left ventricular apical dysfunction or ballooning accompanied by electrocardiographic (ECG) T wave inversions. This abnormality is associated with high levels of CATECHOLAMINES, either administered or endogenously secreted from a tumor or during extreme stress.
Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.
Antiarrhythmic agent pharmacologically similar to LIDOCAINE. It may have some anticonvulsant properties.
A group of cardiac arrhythmias in which the cardiac contractions are not initiated at the SINOATRIAL NODE. They include both atrial and ventricular premature beats, and are also known as extra or ectopic heartbeats. Their frequency is increased in heart diseases.
A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.
Potassium channel whose permeability to ions is extremely sensitive to the transmembrane potential difference. The opening of these channels is induced by the membrane depolarization of the ACTION POTENTIAL.
Compounds based on N-phenylacetamide, that are similar in structure to 2-PHENYLACETAMIDES. They are precursors of many other compounds. They were formerly used as ANALGESICS and ANTIPYRETICS, but often caused lethal METHEMOGLOBINEMIA.
A group of compounds that contain the structure SO2NH2.
A transient loss of consciousness and postural tone caused by diminished blood flow to the brain (i.e., BRAIN ISCHEMIA). Presyncope refers to the sensation of lightheadedness and loss of strength that precedes a syncopal event or accompanies an incomplete syncope. (From Adams et al., Principles of Neurology, 6th ed, pp367-9)
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
A group of slow opening and closing voltage-gated potassium channels. Because of their delayed activation kinetics they play an important role in controlling ACTION POTENTIAL duration.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
Abnormally low potassium concentration in the blood. It may result from potassium loss by renal secretion or by the gastrointestinal route, as by vomiting or diarrhea. It may be manifested clinically by neuromuscular disorders ranging from weakness to paralysis, by electrocardiographic abnormalities (depression of the T wave and elevation of the U wave), by renal disease, and by gastrointestinal disorders. (Dorland, 27th ed)
Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.
A voltage-gated potassium channel that is expressed primarily in the HEART.
A type of cardiac arrhythmia with premature contractions of the HEART VENTRICLES. It is characterized by the premature QRS complex on ECG that is of abnormal shape and great duration (generally >129 msec). It is the most common form of all cardiac arrhythmias. Premature ventricular complexes have no clinical significance except in concurrence with heart diseases.
A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties.
Venoms from jellyfish; CORALS; SEA ANEMONES; etc. They contain hemo-, cardio-, dermo- , and neuro-toxic substances and probably ENZYMES. They include palytoxin, sarcophine, and anthopleurine.
Methods to induce and measure electrical activities at specific sites in the heart to diagnose and treat problems with the heart's electrical system.
The hollow, muscular organ that maintains the circulation of the blood.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Drugs which have received FDA approval for human testing but have yet to be approved for commercial marketing. This includes drugs used for treatment while they still are undergoing clinical trials (Treatment IND). The main heading includes drugs under investigation in foreign countries.
Preclinical testing of drugs in experimental animals or in vitro for their biological and toxic effects and potential clinical applications.
A drug formerly used in the treatment of angina pectoris but superseded by less hazardous drugs. Prenylamine depletes myocardial catecholamine stores and has some calcium channel blocking activity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1406)
'Azā compounds' are a class of organic molecules containing at least one nitrogen atom in a five-membered ring, often found in naturally occurring substances and pharmaceuticals, with the name derived from the Arabic word "azZa" meaning 'strong' referring to the ring's aromatic stability.
A family of delayed rectifier voltage-gated potassium channels that share homology with their founding member, KCNQ1 PROTEIN. KCNQ potassium channels have been implicated in a variety of diseases including LONG QT SYNDROME; DEAFNESS; and EPILEPSY.
Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.
A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.
The lower right and left chambers of the heart. The right ventricle pumps venous BLOOD into the LUNGS and the left ventricle pumps oxygenated blood into the systemic arterial circulation.
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
Cell membrane glycoproteins that are selectively permeable to potassium ions. At least eight major groups of K channels exist and they are made up of dozens of different subunits.
A voltage-gated sodium channel subtype that mediates the sodium ion PERMEABILITY of CARDIOMYOCYTES. Defects in the SCN5A gene, which codes for the alpha subunit of this sodium channel, are associated with a variety of CARDIAC DISEASES that result from loss of sodium channel function.
An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.
Regulation of the rate of contraction of the heart muscles by an artificial pacemaker.
Modified cardiac muscle fibers composing the terminal portion of the heart conduction system.
An abnormally rapid ventricular rhythm usually in excess of 150 beats per minute. It is generated within the ventricle below the BUNDLE OF HIS, either as autonomic impulse formation or reentrant impulse conduction. Depending on the etiology, onset of ventricular tachycardia can be paroxysmal (sudden) or nonparoxysmal, its wide QRS complexes can be uniform or polymorphic, and the ventricular beating may be independent of the atrial beating (AV dissociation).
The study of the generation and behavior of electrical charges in living organisms particularly the nervous system and the effects of electricity on living organisms.
Benzopyrans saturated in the 2 and 3 positions.
Method in which prolonged electrocardiographic recordings are made on a portable tape recorder (Holter-type system) or solid-state device ("real-time" system), while the patient undergoes normal daily activities. It is useful in the diagnosis and management of intermittent cardiac arrhythmias and transient myocardial ischemia.
Compounds based on reduced IMIDAZOLINES which contain no double bonds in the ring.
A potentially lethal cardiac arrhythmia that is characterized by uncoordinated extremely rapid firing of electrical impulses (400-600/min) in HEART VENTRICLES. Such asynchronous ventricular quivering or fibrillation prevents any effective cardiac output and results in unconsciousness (SYNCOPE). It is one of the major electrocardiographic patterns seen with CARDIAC ARREST.
A class of drugs that act by inhibition of sodium influx through cell membranes. Blockade of sodium channels slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, and reduces conduction velocity.
Membrane proteins whose primary function is to facilitate the transport of positively charged molecules (cations) across a biological membrane.
A family of hexahydropyridines.
A device designed to stimulate, by electric impulses, contraction of the heart muscles. It may be temporary (external) or permanent (internal or internal-external).
Ion channels that specifically allow the passage of SODIUM ions. A variety of specific sodium channel subtypes are involved in serving specialized functions such as neuronal signaling, CARDIAC MUSCLE contraction, and KIDNEY function.
Accidental or deliberate use of a medication or street drug in excess of normal dosage.

C-terminal HERG mutations: the role of hypokalemia and a KCNQ1-associated mutation in cardiac event occurrence. (1/333)

BACKGROUND: The long-QT syndrome (LQTS) is a genetically heterogeneous disease in which 4 genes encoding ion-channel subunits have been identified. Most of the mutations have been determined in the transmembrane domains of the cardiac potassium channel genes KCNQ1 and HERG. In this study, we investigated the 3' part of HERG for mutations. METHODS AND RESULTS: New specific primers allowed the amplification of the 3' part of HERG, the identification of 2 missense mutations, S818L and V822 M, in the putative cyclic nucleotide binding domain, and a 1-bp insertion, 3108+1G. Hypokalemia was a triggering factor for torsade de pointes in 2 of the probands of these families. Lastly, in a large family, a maternally inherited G to A transition was found in the splicing donor consensus site of HERG, 2592+1G-A, and a paternally inherited mutation, A341E, was identified in KCNQ1. The 2 more severely affected sisters bore both mutations. CONCLUSIONS: The discovery of mutations in the C-terminal part of HERG emphasizes that this region plays a significant role in cardiac repolarization. Clinical data suggests that these mutations may be less malignant than mutations occurring in the pore region, but they can become clinically significant in cases of hypokalemia. The first description of 2 patients with double heterozygosity associated with a dramatic malignant phenotype implies that genetic analysis of severely affected young patients should include an investigation for >1 mutation in the LQT genes.  (+info)

Cellular and ionic basis for T-wave alternans under long-QT conditions. (2/333)

BACKGROUND: T-wave alternans (TWA), an ECG phenomenon characterized by beat-to-beat alternation of the morphology, amplitude, and/or polarity of the T wave, is commonly observed in the acquired and congenital long-QT syndromes (LQTS). This study examines the cellular and ionic basis for TWA induced by rapid pacing under conditions mimicking the LQT3 form of the congenital LQTS in an arterially perfused canine left ventricular wedge preparation. METHODS AND RESULTS: Transmembrane action potentials from epicardial, M, and endocardial cells and 6 to 8 intramural unipolar electrograms were simultaneously recorded together with a transmural ECG and isometric tension development. In the presence of sea anemone toxin (ATX-II; 20 nmol/L), an increase in pacing rate (from a cycle length [CL] of 500 to 400 to 250 ms) produced a wide spectrum of T-wave and mechanical alternans. Acceleration to CLs of 400 to 300 ms produced mild to moderate TWA principally due to beat-to-beat alternation of repolarization of cells in the M region. Transmural dispersion of repolarization during alternans was exaggerated during alternate beats. Acceleration to CLs of 300 to 250 ms caused more pronounced beat-to-beat alternation of action potential duration (APD) of the M cell, resulting in a reversal of repolarization sequence across the ventricular wall, leading to alternation in the polarity of the T wave. The peak of the negative T waves coincided with repolarization of the M region, whereas the end of the negative T wave coincided with the repolarization of epicardium. In almost all cases, electrical alternans was concordant with mechanical alternans. Torsade de pointes occurred after an abrupt acceleration of CL, which was associated with marked TWA. Both ryanodine and low [Ca2+]o completely suppressed alternans of the T wave, APD, and contraction, suggesting a critical role for intracellular Ca2+ cycling in the maintenance of TWA. CONCLUSIONS: Our results suggest that TWA observed at rapid rates under long-QT conditions is largely the result of alternation of the M-cell APD, leading to exaggeration of transmural dispersion of repolarization during alternate beats, and thus the potential for development of torsade de pointes. Our data also suggest that unlike transient forms of TWA that damp out quickly and depend on electrical restitution factors, the steady-state electrical and mechanical alternans demonstrated in this study appears to be largely the result of beat-to-beat alternans of [Ca2+]i.  (+info)

Torsades de pointes in a case of hypertrophic cardiomyopathy with special reference to the pathologic findings of the heart including the conduction system. (3/333)

A clinicopathologic study was performed in a 77-year-old female with hypertrophic cardiomyopathy who had experienced recurrent syncopal attacks due to Torsades de Pointes (TdP) following QT prolongation and atrioventricular block. She died suddenly two years later while eating dinner. Pathologic findings of the heart showed a dilated and hypertrophied left ventricle. The heart weighed 550 g. There were two foci of localized endocardial fibroelastosis (EFE) beneath the aortic valve, one with a size of 3.5 x 3.5 cm, and the other (2 x 1 cm) located on the upper ventricular septum. Histologic findings showed hypertrophy and disarray in the left ventricular myocardium. The conduction system using serial sectioning revealed remarkable bilateral bundle branch fibrosis and hypertrophied Purkinje fibers in the left bundle branch adjacent to the EFE on the ventricular septum. These findings were thought to be related to the occurrence of TdP.  (+info)

Factors affecting epicardial dispersion of repolarization: a mapping study in the isolated porcine heart. (4/333)

OBJECTIVE: Non-uniform drug-induced prolongation of repolarization predominating in the midmyocardial (M) cell layers has been shown to be responsible for perpetuation of reentry, giving rise to torsade de pointes. However, the absence of M cells in immature animals, especially the pig, suggests other possible underlying mechanisms. We sought to examine, in this species, the effects of predisposing factors to torsade de pointes on the dispersion of epicardial repolarization and their contribution to arrhythmogenesis. METHODS: Computerized mapping of repolarization and activation was conducted on the epicardial surface in 29 Langendorff-perfused hearts of eight-week-old pigs. Activation-recovery intervals were measured simultaneously from 128 unipolar electrograms. RESULTS: Baseline iso-interval maps were dipolar (41%) or multipolar (59%). Dispersion of repolarization was reverse frequency-dependent but was unaffected by lowering [K+]o. DL-Sotalol (0.1 mmol/l) reinforced local gradients and thus increased epicardial dispersion, whereas intramural recordings did not demonstrate any predominant effect in midmyocardial layers. Phenylephrine (1 mumol/l) notably augmented DL-sotalol effects. After [Mg++]o lowering, although dispersion was not significantly increased, DL-sotalol was associated with the spontaneous occurrence of polymorphic ventricular tachycardia in seven out of nine experiments. When maps of repolarization of escape beats were compared with activation maps of first arrhythmic beats, an arc of functional dissociation was observed in the vicinity of a steep gradient of repolarization in two out of nine tachycardias. CONCLUSION: Epicardial dispersion of repolarization is increased by slow rates, DL-sotalol and phenylephrine but is not the only requirement for initiation of polymorphic ventricular tachycardia. In combination with other factors, it helps continuation of the arrhythmia in this model.  (+info)

Dofetilide in patients with congestive heart failure and left ventricular dysfunction. Danish Investigations of Arrhythmia and Mortality on Dofetilide Study Group. (5/333)

BACKGROUND: Atrial fibrillation occurs frequently in patients with congestive heart failure and commonly results in clinical deterioration and hospitalization. Sinus rhythm may be maintained with antiarrhythmic drugs, but some of these drugs increase the risk of death. METHODS: We studied 1518 patients with symptomatic congestive heart failure and severe left ventricular dysfunction at 34 Danish hospitals. We randomly assigned 762 patients to receive dofetilide, a novel class III antiarrhythmic agent, and 756 to receive placebo in a double-blind study. Treatment was initiated in the hospital and included three days of cardiac monitoring and dose adjustment. The primary end point was death from any cause. RESULTS: During a median follow-up of 18 months, 311 patients in the dofetilide group (41 percent) and 317 patients in the placebo group (42 percent) died (hazard ratio, 0.95; 95 percent confidence interval, 0.81 to 1.11). Treatment with dofetilide significantly reduced the risk of hospitalization for worsening congestive heart failure (risk ratio, 0.75; 95 percent confidence interval, 0.63 to 0.89). Dofetilide was effective in converting atrial fibrillation to sinus rhythm. After one month, 22 of 190 patients with atrial fibrillation at base line (12 percent) had sinus rhythm restored with dofetilide, as compared with only 3 of 201 patients (1 percent) given placebo. Once sinus rhythm was restored, dofetilide was significantly more effective than placebo in maintaining sinus rhythm (hazard ratio for the recurrence of atrial fibrillation, 0.35; 95 percent confidence interval, 0.22 to 0.57; P<0.001). There were 25 cases of torsade de pointes in the dofetilide group (3.3 percent) as compared with none in the placebo group. CONCLUSIONS: In patients with congestive heart failure and reduced left ventricular function, dofetilide was effective in converting atrial fibrillation, preventing its recurrence, and reducing the risk of hospitalization for worsening heart failure. Dofetilide had no effect on mortality.  (+info)

Systemic administration of calmodulin antagonist W-7 or protein kinase A inhibitor H-8 prevents torsade de pointes in rabbits. (6/333)

BACKGROUND: The ventricular arrhythmia torsade de pointes (TdP) occurs after QT interval prolongation and is associated with sudden cardiac death. The afterdepolarizations that initiate TdP are facilitated by protein kinase A and the multifunctional Ca(2+)/calmodulin-dependent protein kinase II (CaM kinase). METHODS AND RESULTS: In this study, we evaluated the feasibility of suppression of TdP through systemic therapy with kinase inhibitory agents in an established animal model. Under control conditions, TdP was inducible in 6 of 8 rabbits. CaM kinase blockade with the calmodulin antagonist W-7 reduced TdP in a dose-dependent fashion (4 of 7 inducible at 25 micromol/kg and 1 of 7 inducible at 50 micromol/kg). Increased intracellular Ca(2+) has been implicated in the genesis of afterdepolarizations, but pretreatment with high-dose W-7 did not prevent TdP in response to the L-type Ca(2+) channel agonist BAY K 8644 (300 nmol/kg), suggesting that CaM kinase-independent activation of L-type Ca(2+) current was not affected by W-7. Compared with control animals, W-7 reduced TdP inducibility without shortening the QT interval, increasing heart rate, or reducing the blood pressure. The protein kinase A antagonist H-8 also caused a dose-dependent reduction in TdP inducibility (5 of 6 at 1 micromol/kg, 4 of 6 at 5 micromol/kg, and 0 of 6 at 10 micromol/kg), but unlike W-7, H-8 did so by shortening the QT interval. CONCLUSIONS: These findings show that the acute systemic application of W-7 and H-8 is hemodynamically tolerated and indicate that kinase inhibition may be a viable antiarrhythmic strategy.  (+info)

Downregulation of delayed rectifier K(+) currents in dogs with chronic complete atrioventricular block and acquired torsades de pointes. (7/333)

BACKGROUND: Acquired QT prolongation enhances the susceptibility to torsades de pointes (TdP). Clinical and experimental studies indicate ventricular action potential prolongation, increased regional dispersion of repolarization, and early afterdepolarizations as underlying factors. We examined whether K(+)-current alterations contribute to these proarrhythmic responses in an animal model of TdP: the dog with chronic complete atrioventricular block (AVB) and biventricular hypertrophy. METHODS AND RESULTS: The whole-cell K(+) currents I(TO1), I(K1), I(Kr), and I(Ks) were recorded in left (LV) and right (RV) ventricular midmyocardial cells from dogs with 9+/-1 weeks of AVB and controls with sinus rhythm. I(TO1) density and kinetics and I(K1) outward current were not different between chronic AVB and control cells. I(Kr) had a similar voltage dependence of activation and time course of deactivation in chronic AVB and control. I(Kr) density was similar in LV myocytes but smaller in RV myocytes (-45%) of chronic AVB versus control. For I(Ks), voltage-dependence of activation and time course of deactivation were similar in chronic AVB and control. However, I(Ks) densities of LV (-50%) and RV (-55%) cells were significantly lower in chronic AVB than control. CONCLUSIONS: Significant downregulation of delayed rectifier K(+) current occurs in both ventricles of the dog with chronic AVB. Acquired TdP in this animal model with biventricular hypertrophy is thus related to intrinsic repolarization defects.  (+info)

QT dispersion. Is it an independent risk factor for in-hospital mortality in patients with intracerebral hemorrhage? (8/333)

Electrocardiographic repolarization changes, comprising QT prolongation, are most commonly seen after intracerebral hemorrhage. In this study in patients with intracerebral hemorrhage (ICH), QT dispersion and its daily changes were examined and the relation between QT dispersion and in-hospital mortality assessed. In 28 patients with intracerebral hemorrhage, diagnosed by computerized tomographic scanning, an ECG was obtained on the day of admission to hospital and then serial ECGs were recorded on the following four consecutive days. Blood electrolytes (K, Ca, Mg) were also analysed. The patients with intracerebral hemorrhage were followed until discharge or death (mean 14 +/- 4 days). QT, QT peak, and QT-QT peak dispersion were measured on simultaneous twelve lead electrocardiograms. Also, in 29 healthy subjects as a control group, five consecutive day serial electrocardiograms were recorded. There were no statistically significant differences between the study and control groups in terms of gender and age. During the five days, QT, QT peak, and QT-QTpeak dispersion values were significantly higher in patients with intracerebral hemorrhage than in the control subjects (p < 0.001). There were no statistically significant differences in two patient groups with intracerebral hemorrhage who died and who were discharged in terms of mean QT, QTpeak, and QT-QTpeak dispersion values. In conclusion, QT, QT peak, and QT-QTpeak dispersion values were significantly greater in patients with intracerebral hemorrhage than in the control subjects, but QT, QT peak, and QT-QT peak dispersions were not independent risk factors for in-hospital mortality in patients with intracerebral hemorrhage.  (+info)

Torsades de Pointes is a type of polymorphic ventricular tachycardia, characterized by a distinct pattern on the electrocardiogram (ECG) where the QRS complexes appear to twist around the isoelectric line. This condition is often associated with a prolonged QT interval, which can be congenital or acquired due to various factors such as medications, electrolyte imbalances, or heart diseases. Torsades de Pointes can degenerate into ventricular fibrillation, leading to sudden cardiac death if not promptly treated.

Long QT syndrome (LQTS) is a cardiac electrical disorder characterized by a prolonged QT interval on the electrocardiogram (ECG), which can potentially trigger rapid, chaotic heartbeats known as ventricular tachyarrhythmias, such as torsades de pointes. These arrhythmias can be life-threatening and lead to syncope (fainting) or sudden cardiac death. LQTS is often congenital but may also be acquired due to certain medications, medical conditions, or electrolyte imbalances. It's essential to identify and manage LQTS promptly to reduce the risk of severe complications.

Anti-arrhythmia agents are a class of medications used to treat abnormal heart rhythms or arrhythmias. These drugs work by modifying the electrical activity of the heart to restore and maintain a normal heart rhythm. There are several types of anti-arrhythmia agents, including:

1. Sodium channel blockers: These drugs slow down the conduction of electrical signals in the heart, which helps to reduce rapid or irregular heartbeats. Examples include flecainide, propafenone, and quinidine.
2. Beta-blockers: These medications work by blocking the effects of adrenaline on the heart, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include metoprolol, atenolol, and esmolol.
3. Calcium channel blockers: These drugs block the entry of calcium into heart muscle cells, which helps to slow down the heart rate and reduce the force of heart contractions. Examples include verapamil and diltiazem.
4. Potassium channel blockers: These medications work by prolonging the duration of the heart's electrical cycle, which helps to prevent abnormal rhythms. Examples include amiodarone and sotalol.
5. Digoxin: This drug increases the force of heart contractions and slows down the heart rate, which can help to restore a normal rhythm in certain types of arrhythmias.

It's important to note that anti-arrhythmia agents can have significant side effects and should only be prescribed by a healthcare professional who has experience in managing arrhythmias. Close monitoring is necessary to ensure the medication is working effectively and not causing any adverse effects.

Electrocardiography (ECG or EKG) is a medical procedure that records the electrical activity of the heart. It provides a graphic representation of the electrical changes that occur during each heartbeat. The resulting tracing, called an electrocardiogram, can reveal information about the heart's rate and rhythm, as well as any damage to its cells or abnormalities in its conduction system.

During an ECG, small electrodes are placed on the skin of the chest, arms, and legs. These electrodes detect the electrical signals produced by the heart and transmit them to a machine that amplifies and records them. The procedure is non-invasive, painless, and quick, usually taking only a few minutes.

ECGs are commonly used to diagnose and monitor various heart conditions, including arrhythmias, coronary artery disease, heart attacks, and electrolyte imbalances. They can also be used to evaluate the effectiveness of certain medications or treatments.

Sotalol is a non-selective beta blocker and class III antiarrhythmic drug. It works by blocking the action of certain natural substances in your body, such as adrenaline, on the heart. This helps to decrease the heart's workload, slow the heart rate, and regulate certain types of irregular heartbeats (such as atrial fibrillation).

Sotalol is used to treat various types of irregular heartbeats (atrial fibrillation/flutter, ventricular tachycardia) and may also be used to help maintain a normal heart rhythm after a heart attack. It is important to note that Sotalol should only be prescribed by a healthcare professional who has experience in treating heart rhythm disorders.

This medical definition is based on the information provided by the National Library of Medicine (NLM).

Phenethylamines are a class of organic compounds that share a common structural feature, which is a phenethyl group (a phenyl ring bonded to an ethylamine chain). In the context of pharmacology and neuroscience, "phenethylamines" often refers to a specific group of psychoactive drugs, including stimulants like amphetamine and mescaline, a classic psychedelic. These compounds exert their effects by modulating the activity of neurotransmitters in the brain, such as dopamine, norepinephrine, and serotonin. It is important to note that many phenethylamines have potential for abuse and are controlled substances.

Ether-à-go-go (EAG) potassium channels are a type of voltage-gated potassium channel that are widely expressed in the heart, brain, and other tissues. They are named after the ethereal dance movements observed in fruit flies with mutations in these channels.

EAG potassium channels play important roles in regulating electrical excitability and signaling in excitable cells. In the heart, they help to control the duration of the action potential and the refractory period, which is critical for maintaining normal heart rhythm. In the brain, they are involved in regulating neuronal excitability and neurotransmitter release.

Mutations in EAG potassium channels have been associated with various human diseases, including cardiac arrhythmias, epilepsy, and bipolar disorder. The medical definition of "Ether-A-Go-Go Potassium Channels" refers to the genetic components that make up these channels and their role in physiological processes and disease states.

Astemizole is a second-generation antihistamine that was previously used to treat symptoms associated with allergies, such as hay fever, hives, and other allergic skin reactions. It works by blocking the action of histamine, a substance in the body that causes allergic symptoms. However, astemizole has been withdrawn from the market in many countries due to rare but serious side effects on the heart.

Terfenadine is an antihistamine medication that has been used to treat symptoms of allergies such as hay fever, hives, and other allergic reactions. It works by blocking the action of histamine, a substance in the body that causes allergic symptoms. Terfenadine was first approved for use in the United States in 1985, but it is no longer available in many countries due to concerns about rare but serious side effects related to heart rhythm disturbances. It has been replaced by other antihistamines that are considered safer and more effective.

Cisapride is a medication that was used to treat gastrointestinal motility disorders, such as gastroparesis and constipation. It belongs to a class of drugs called "prokinetic agents" which work by increasing the contractions or movements of the muscles in the digestive tract, thereby helping to move food and waste through the system more efficiently.

Cisapride was first approved for use in the United States in 1993, but its use was later restricted due to concerns about serious side effects, including cardiac arrhythmias (irregular heartbeats) and interactions with other medications. In 2000, the U.S. Food and Drug Administration (FDA) requested that cisapride be withdrawn from the market due to these safety concerns.

While cisapride is no longer available for use in many countries, it may still be used in some cases under strict guidelines and monitoring conditions. It is important to note that the use of cisapride should only be initiated and monitored by a healthcare professional, and patients should inform their doctor about all other medications they are taking to avoid potential interactions.

Atrioventricular (AV) block is a disorder of the electrical conduction system of the heart that causes a delay or interruption in the transmission of electrical signals from the atria (the upper chambers of the heart) to the ventricles (the lower chambers of the heart). This results in an abnormal heart rhythm, also known as an arrhythmia.

There are three degrees of AV block:

1. First-degree AV block: In this type of AV block, there is a delay in the conduction of electrical signals from the atria to the ventricles, but all signals are eventually conducted. This condition may not cause any symptoms and is often discovered during a routine electrocardiogram (ECG).
2. Second-degree AV block: In this type of AV block, some electrical signals from the atria are not conducted to the ventricles. There are two types of second-degree AV block: Mobitz type I and Mobitz type II. Mobitz type I is characterized by a progressive prolongation of the PR interval (the time between the electrical activation of the atria and ventricles) until a QRS complex (which represents the electrical activation of the ventricles) is dropped. Mobitz type II is characterized by a constant PR interval with occasional non-conducted P waves.
3. Third-degree AV block: In this type of AV block, no electrical signals are conducted from the atria to the ventricles. The atria and ventricles beat independently of each other, resulting in a slow heart rate (bradycardia) and an irregular rhythm. This condition can be life-threatening if not treated promptly.

The causes of AV block include aging, heart disease, medications, and certain medical conditions such as hypothyroidism and Lyme disease. Treatment depends on the severity of the condition and may include medication, a pacemaker, or surgery.

Bradycardia is a medical term that refers to an abnormally slow heart rate, typically defined as a resting heart rate of less than 60 beats per minute in adults. While some people, particularly well-trained athletes, may have a naturally low resting heart rate, bradycardia can also be a sign of an underlying health problem.

There are several potential causes of bradycardia, including:

* Damage to the heart's electrical conduction system, such as from heart disease or aging
* Certain medications, including beta blockers, calcium channel blockers, and digoxin
* Hypothyroidism (underactive thyroid gland)
* Sleep apnea
* Infection of the heart (endocarditis or myocarditis)
* Infiltrative diseases such as amyloidosis or sarcoidosis

Symptoms of bradycardia can vary depending on the severity and underlying cause. Some people with bradycardia may not experience any symptoms, while others may feel weak, fatigued, dizzy, or short of breath. In severe cases, bradycardia can lead to fainting, confusion, or even cardiac arrest.

Treatment for bradycardia depends on the underlying cause. If a medication is causing the slow heart rate, adjusting the dosage or switching to a different medication may help. In other cases, a pacemaker may be necessary to regulate the heart's rhythm. It is important to seek medical attention if you experience symptoms of bradycardia, as it can be a sign of a serious underlying condition.

Heart block is a cardiac condition characterized by the interruption of electrical impulse transmission from the atria (the upper chambers of the heart) to the ventricles (the lower chambers of the heart). This disruption can lead to abnormal heart rhythms, including bradycardia (a slower-than-normal heart rate), and in severe cases, can cause the heart to stop beating altogether. Heart block is typically caused by damage to the heart's electrical conduction system due to various factors such as aging, heart disease, or certain medications.

There are three types of heart block: first-degree, second-degree, and third-degree (also known as complete heart block). Each type has distinct electrocardiogram (ECG) findings and symptoms. Treatment for heart block depends on the severity of the condition and may include monitoring, medication, or implantation of a pacemaker to regulate the heart's electrical activity.

Cardiac arrhythmias are abnormal heart rhythms that result from disturbances in the electrical conduction system of the heart. The heart's normal rhythm is controlled by an electrical signal that originates in the sinoatrial (SA) node, located in the right atrium. This signal travels through the atrioventricular (AV) node and into the ventricles, causing them to contract and pump blood throughout the body.

An arrhythmia occurs when there is a disruption in this electrical pathway or when the heart's natural pacemaker produces an abnormal rhythm. This can cause the heart to beat too fast (tachycardia), too slow (bradycardia), or irregularly.

There are several types of cardiac arrhythmias, including:

1. Atrial fibrillation: A rapid and irregular heartbeat that starts in the atria (the upper chambers of the heart).
2. Atrial flutter: A rapid but regular heartbeat that starts in the atria.
3. Supraventricular tachycardia (SVT): A rapid heartbeat that starts above the ventricles, usually in the atria or AV node.
4. Ventricular tachycardia: A rapid and potentially life-threatening heart rhythm that originates in the ventricles.
5. Ventricular fibrillation: A chaotic and disorganized electrical activity in the ventricles, which can be fatal if not treated immediately.
6. Heart block: A delay or interruption in the conduction of electrical signals from the atria to the ventricles.

Cardiac arrhythmias can cause various symptoms, such as palpitations, dizziness, shortness of breath, chest pain, and fatigue. In some cases, they may not cause any symptoms and go unnoticed. However, if left untreated, certain types of arrhythmias can lead to serious complications, including stroke, heart failure, or even sudden cardiac death.

Treatment for cardiac arrhythmias depends on the type, severity, and underlying causes. Options may include lifestyle changes, medications, cardioversion (electrical shock therapy), catheter ablation, implantable devices such as pacemakers or defibrillators, and surgery. It is essential to consult a healthcare professional for proper evaluation and management of cardiac arrhythmias.

Bepridil is a calcium channel blocker medication that is used to treat angina (chest pain) and certain types of irregular heart rhythms. It works by relaxing the blood vessels and increasing the supply of oxygen and blood to the heart.

Here is the medical definition of Bepridil:

Bepridil is a non-dihydropyridine calcium channel blocker that selectively inhibits the L-type calcium channels in cardiac and smooth muscle cells, resulting in vasodilation, negative inotropic and chronotropic effects on the heart. It is used in the management of chronic stable angina pectoris and certain types of arrhythmias. The most common side effects include dizziness, headache, nausea, and constipation. Bepridil has a negative inotropic effect and should be used with caution in patients with heart failure or reduced left ventricular function. It is also metabolized by the cytochrome P450 system and can interact with other medications that are metabolized by this pathway.

The heart conduction system is a group of specialized cardiac muscle cells that generate and conduct electrical impulses to coordinate the contraction of the heart chambers. The main components of the heart conduction system include:

1. Sinoatrial (SA) node: Also known as the sinus node, it is located in the right atrium near the entrance of the superior vena cava and functions as the primary pacemaker of the heart. It sets the heart rate by generating electrical impulses at regular intervals.
2. Atrioventricular (AV) node: Located in the interatrial septum, near the opening of the coronary sinus, it serves as a relay station for electrical signals between the atria and ventricles. The AV node delays the transmission of impulses to allow the atria to contract before the ventricles.
3. Bundle of His: A bundle of specialized cardiac muscle fibers that conducts electrical impulses from the AV node to the ventricles. It divides into two main branches, the right and left bundle branches, which further divide into smaller Purkinje fibers.
4. Right and left bundle branches: These are extensions of the Bundle of His that transmit electrical impulses to the respective right and left ventricular myocardium. They consist of specialized conducting tissue with large diameters and minimal resistance, allowing for rapid conduction of electrical signals.
5. Purkinje fibers: Fine, branching fibers that arise from the bundle branches and spread throughout the ventricular myocardium. They are responsible for transmitting electrical impulses to the working cardiac muscle cells, triggering coordinated ventricular contraction.

In summary, the heart conduction system is a complex network of specialized muscle cells responsible for generating and conducting electrical signals that coordinate the contraction of the atria and ventricles, ensuring efficient blood flow throughout the body.

Amiodarone is a Class III antiarrhythmic medication used to treat and prevent various types of irregular heart rhythms (arrhythmias). It works by stabilizing the electrical activity of the heart and slowing down the nerve impulses in the heart tissue. Amiodarone is available in oral tablet and injection forms.

The medical definition of 'Amiodarone' is:

A benzofuran derivative with Class III antiarrhythmic properties, used for the treatment of ventricular arrhythmias. It has a relatively slow onset of action and is therefore not useful in acute situations. Additionally, it has negative inotropic effects and may exacerbate heart failure. The most serious adverse effect is pulmonary fibrosis, which occurs in approximately 1-2% of patients. Other important side effects include corneal microdeposits, hepatotoxicity, thyroid dysfunction, and photosensitivity. Amiodarone has a very long half-life (approximately 50 days) due to its extensive tissue distribution. It is metabolized by the liver and excreted in bile and urine.

Sources:

1. UpToDate - Amiodarone use in adults: Indications, dosing, and adverse effects.
2. Micromedex - Amiodarone.
3. Drugs.com - Amiodarone.

Magnesium Sulfate is an inorganic salt with the chemical formula MgSO4. It is often encountered as the heptahydrate sulfate mineral epsomite (MgSO4·7H2O), commonly called Epsom salts. Magnesium sulfate is used medically as a vasodilator, to treat constipation, and as an antidote for magnesium overdose or poisoning. It is also used in the preparation of skin for esthetic procedures and in the treatment of eclampsia, a serious complication of pregnancy characterized by seizures.

Quinidine is a Class IA antiarrhythmic medication that is primarily used to treat and prevent various types of cardiac arrhythmias (abnormal heart rhythms). It works by blocking the rapid sodium channels in the heart, which helps to slow down the conduction of electrical signals within the heart and stabilize its rhythm.

Quinidine is derived from the bark of the Cinchona tree and has been used for centuries as a treatment for malaria. However, its antiarrhythmic properties were discovered later, and it became an important medication in cardiology.

In addition to its use in treating arrhythmias, quinidine may also be used off-label for other indications such as the treatment of nocturnal leg cramps or myasthenia gravis. It is available in various forms, including tablets and injectable solutions.

It's important to note that quinidine has a narrow therapeutic index, meaning that there is only a small difference between an effective dose and a toxic one. Therefore, it must be carefully monitored to ensure that the patient is receiving a safe and effective dose. Common side effects of quinidine include gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as visual disturbances, headache, and dizziness. More serious side effects can include QT prolongation, which can lead to dangerous arrhythmias, and hypersensitivity reactions.

Takotsubo cardiomyopathy, also known as Takotsubo syndrome or stress-induced cardiomyopathy, is a temporary heart condition usually triggered by emotional or physical stress. It's named after the Japanese word for "octopus pot" because of the shape of the left ventricle during the contraction phase, which resembles this pot.

In Takotsubo cardiomyopathy, a part of the heart muscle becomes weakened and doesn't pump well, often following a surge of stress hormones. The condition can be misdiagnosed as a heart attack because it has similar symptoms and test results. However, unlike a heart attack, there's no evidence of blocked heart arteries in Takotsubo cardiomyopathy.

The symptoms of Takotsubo cardiomyopathy include chest pain, shortness of breath, irregular heartbeat, and sometimes fluid retention. Treatment typically includes medication to manage symptoms and support the heart while it recovers. Most people with Takotsubo cardiomyopathy make a full recovery within a few weeks. However, in rare cases, complications such as heart failure or arrhythmias can occur.

Drug-related side effects and adverse reactions refer to any unintended or harmful outcome that occurs during the use of a medication. These reactions can be mild or severe and may include predictable, known responses (side effects) as well as unexpected, idiosyncratic reactions (adverse effects). Side effects are typically related to the pharmacologic properties of the drug and occur at therapeutic doses, while adverse reactions may result from allergic or hypersensitivity reactions, overdoses, or interactions with other medications or substances.

Side effects are often dose-dependent and can be managed by adjusting the dose, frequency, or route of administration. Adverse reactions, on the other hand, may require discontinuation of the medication or treatment with antidotes or supportive care. It is important for healthcare providers to monitor patients closely for any signs of drug-related side effects and adverse reactions and to take appropriate action when necessary.

Mexiletine is defined as an antiarrhythmic agent, classified as a Class IB medication. It works by blocking sodium channels in the heart, which helps to stabilize cardiac membranes and reduces the rate of firing of cardiac cells. This makes it useful for treating certain types of irregular heart rhythms (ventricular arrhythmias).

Mexiletine is also known to have analgesic properties and is sometimes used off-label for the treatment of neuropathic pain. It is available in oral form, and its use should be under the close supervision of a healthcare provider due to its potential side effects, which can include gastrointestinal symptoms, dizziness, tremors, and cardiac arrhythmias.

Premature cardiac complexes, also known as premature heartbeats or premature ventricular contractions (PVCs), refer to extra or early heartbeats that originate in the lower chambers of the heart (the ventricles). These extra beats disrupt the normal rhythm and sequence of heartbeats, causing the heart to beat earlier than expected.

Premature cardiac complexes can occur in healthy individuals as well as those with heart disease. They are usually harmless and do not cause any symptoms, but in some cases, they may cause palpitations, skipped beats, or a fluttering sensation in the chest. In rare cases, frequent premature cardiac complexes can lead to more serious heart rhythm disorders or decreased heart function.

The diagnosis of premature cardiac complexes is usually made through an electrocardiogram (ECG) or Holter monitoring, which records the electrical activity of the heart over a period of time. Treatment is typically not necessary unless the premature complexes are frequent, symptomatic, or associated with underlying heart disease. In such cases, medications, cardioversion, or catheter ablation may be recommended.

Potassium channel blockers are a class of medications that work by blocking potassium channels, which are proteins in the cell membrane that control the movement of potassium ions into and out of cells. By blocking these channels, potassium channel blockers can help to regulate electrical activity in the heart, making them useful for treating certain types of cardiac arrhythmias (irregular heart rhythms).

There are several different types of potassium channel blockers, including:

1. Class III antiarrhythmic drugs: These medications, such as amiodarone and sotalol, are used to treat and prevent serious ventricular arrhythmias (irregular heart rhythms that originate in the lower chambers of the heart).
2. Calcium channel blockers: While not strictly potassium channel blockers, some calcium channel blockers also have effects on potassium channels. These medications, such as diltiazem and verapamil, are used to treat hypertension (high blood pressure), angina (chest pain), and certain types of arrhythmias.
3. Non-selective potassium channel blockers: These medications, such as 4-aminopyridine and tetraethylammonium, have a broader effect on potassium channels and are used primarily in research settings to study the electrical properties of cells.

It's important to note that potassium channel blockers can have serious side effects, particularly when used in high doses or in combination with other medications that affect heart rhythms. They should only be prescribed by a healthcare provider who is familiar with their use and potential risks.

Voltage-gated potassium channels are a type of ion channel found in the membrane of excitable cells such as nerve and muscle cells. They are called "voltage-gated" because their opening and closing is regulated by the voltage, or electrical potential, across the cell membrane. Specifically, these channels are activated when the membrane potential becomes more positive, a condition that occurs during the action potential of a neuron or muscle fiber.

When voltage-gated potassium channels open, they allow potassium ions (K+) to flow out of the cell down their electrochemical gradient. This outward flow of K+ ions helps to repolarize the membrane, bringing it back to its resting potential after an action potential has occurred. The precise timing and duration of the opening and closing of voltage-gated potassium channels is critical for the normal functioning of excitable cells, and abnormalities in these channels have been linked to a variety of diseases, including cardiac arrhythmias, epilepsy, and neurological disorders.

Acetanilides are a group of chemical compounds that consist of an acetic acid molecule (CH3COO-) linked to aniline (C6H5NH2) through an amide bond (-CONH-). The most well-known member of this class is acetanilide itself (N-phenylacetamide, C8H9NO), which has been used historically as a pain reliever and fever reducer. However, its use in medicine has largely been abandoned due to the discovery of serious side effects, including the potential for causing methemoglobinemia, a condition that can lead to tissue hypoxia and even death.

Acetanilides have also been used as intermediates in the synthesis of other chemical compounds, such as dyes and pharmaceuticals. Some derivatives of acetanilide continue to be used in medicine today, including certain antipyretic and analgesic agents. However, these drugs are carefully designed and tested to minimize the risk of adverse effects associated with acetanilide itself.

Sulfonamides are a group of synthetic antibacterial drugs that contain the sulfonamide group (SO2NH2) in their chemical structure. They are bacteriostatic agents, meaning they inhibit bacterial growth rather than killing them outright. Sulfonamides work by preventing the bacteria from synthesizing folic acid, which is essential for their survival.

The first sulfonamide drug was introduced in the 1930s and since then, many different sulfonamides have been developed with varying chemical structures and pharmacological properties. They are used to treat a wide range of bacterial infections, including urinary tract infections, respiratory tract infections, skin and soft tissue infections, and ear infections.

Some common sulfonamide drugs include sulfisoxazole, sulfamethoxazole, and trimethoprim-sulfamethoxazole (a combination of a sulfonamide and another antibiotic called trimethoprim). While sulfonamides are generally safe and effective when used as directed, they can cause side effects such as rash, nausea, and allergic reactions. It is important to follow the prescribing physician's instructions carefully and to report any unusual symptoms or side effects promptly.

Syncope is a medical term defined as a transient, temporary loss of consciousness and postural tone due to reduced blood flow to the brain. It's often caused by a drop in blood pressure, which can be brought on by various factors such as dehydration, emotional stress, prolonged standing, or certain medical conditions like heart diseases, arrhythmias, or neurological disorders.

During a syncope episode, an individual may experience warning signs such as lightheadedness, dizziness, blurred vision, or nausea before losing consciousness. These episodes usually last only a few minutes and are followed by a rapid, full recovery. However, if left untreated or undiagnosed, recurrent syncope can lead to severe injuries from falls or even life-threatening conditions related to the underlying cause.

I believe there might be a misunderstanding in your question. "Dogs" is not a medical term or condition. It is the common name for a domesticated carnivore of the family Canidae, specifically the genus Canis, which includes wolves, foxes, and other extant and extinct species of mammals. Dogs are often kept as pets and companions, and they have been bred in a wide variety of forms and sizes for different purposes, such as hunting, herding, guarding, assisting police and military forces, and providing companionship and emotional support.

If you meant to ask about a specific medical condition or term related to dogs, please provide more context so I can give you an accurate answer.

Delayed rectifier potassium channels are a type of ion channel found in the membrane of excitable cells, such as nerve and muscle cells. They are called "delayed rectifiers" because they activate and allow the flow of potassium ions (K+) out of the cell after a short delay following an action potential, or electrical signal.

These channels play a crucial role in regulating the duration and frequency of action potentials, helping to restore the resting membrane potential of the cell after it has fired. By allowing K+ to flow out of the cell, delayed rectifier potassium channels help to repolarize the membrane and bring it back to its resting state.

There are several different types of delayed rectifier potassium channels, which are classified based on their biophysical and pharmacological properties. These channels are important targets for drugs used to treat a variety of conditions, including cardiac arrhythmias, epilepsy, and psychiatric disorders.

An action potential is a brief electrical signal that travels along the membrane of a nerve cell (neuron) or muscle cell. It is initiated by a rapid, localized change in the permeability of the cell membrane to specific ions, such as sodium and potassium, resulting in a rapid influx of sodium ions and a subsequent efflux of potassium ions. This ion movement causes a brief reversal of the electrical potential across the membrane, which is known as depolarization. The action potential then propagates along the cell membrane as a wave, allowing the electrical signal to be transmitted over long distances within the body. Action potentials play a crucial role in the communication and functioning of the nervous system and muscle tissue.

Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.

Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.

Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.

Tachycardia is a medical term that refers to an abnormally rapid heart rate, often defined as a heart rate greater than 100 beats per minute in adults. It can occur in either the atria (upper chambers) or ventricles (lower chambers) of the heart. Different types of tachycardia include supraventricular tachycardia (SVT), atrial fibrillation, atrial flutter, and ventricular tachycardia.

Tachycardia can cause various symptoms such as palpitations, shortness of breath, dizziness, lightheadedness, chest discomfort, or syncope (fainting). In some cases, tachycardia may not cause any symptoms and may only be detected during a routine physical examination or medical test.

The underlying causes of tachycardia can vary widely, including heart disease, electrolyte imbalances, medications, illicit drug use, alcohol abuse, smoking, stress, anxiety, and other medical conditions. In some cases, the cause may be unknown. Treatment for tachycardia depends on the underlying cause, type, severity, and duration of the arrhythmia.

The KCNQ1 potassium channel, also known as the Kv7.1 channel, is a voltage-gated potassium ion channel that plays a crucial role in the regulation of electrical excitability in cardiac myocytes and inner ear epithelial cells. In the heart, it helps to control the duration and frequency of action potentials, thereby contributing to the maintenance of normal cardiac rhythm. Mutations in the KCNQ1 gene can lead to various cardiac disorders, such as long QT syndrome type 1 and familial atrial fibrillation. In the inner ear, it helps regulate potassium homeostasis and is essential for hearing and balance functions. Dysfunction of this channel has been linked to deafness and balance disorders.

Ventricular Premature Complexes (VPCs), also known as Ventricular Extrasystoles or Premature Ventricular Contractions (PVCs), are extra heartbeats that originate in the ventricles, the lower chambers of the heart. These premature beats disrupt the normal sequence of electrical impulses in the heart and cause the ventricles to contract earlier than they should.

VPCs can result in a noticeable "skipped" or "extra" beat sensation, often followed by a stronger beat as the heart returns to its regular rhythm. They may occur occasionally in healthy individuals with no underlying heart condition, but frequent VPCs could indicate an underlying issue such as heart disease, electrolyte imbalance, or digitalis toxicity. In some cases, VPCs can be harmless and require no treatment; however, if they are frequent or associated with structural heart problems, further evaluation and management may be necessary to prevent potential complications like reduced cardiac output or heart failure.

Disopyramide is an antiarrhythmic medication that is primarily used to treat certain types of irregular heart rhythms (arrhythmias), such as ventricular tachycardia and atrial fibrillation. It works by blocking the activity of sodium channels in the heart, which helps to slow down and regulate the heart rate.

Disopyramide is available in immediate-release and extended-release forms, and it may be taken orally as a tablet or capsule. Common side effects of this medication include dry mouth, blurred vision, constipation, and difficulty urinating. More serious side effects can include dizziness, fainting, irregular heartbeat, and allergic reactions.

It is important to take disopyramide exactly as directed by a healthcare provider, as improper use or dosing can lead to serious complications. Additionally, individuals with certain medical conditions, such as heart failure, kidney disease, or myasthenia gravis, may not be able to safely take this medication.

Cnidarian venoms are toxic substances produced by members of the phylum Cnidaria, which includes jellyfish, sea anemones, corals, and hydroids. These venoms are primarily contained in specialized cells called cnidocytes or nematocysts, which are found in the tentacles of these animals. When a cnidarian comes into contact with prey or a potential threat, the cnidocytes discharge, injecting the venom into the target through a hollow tubule.

Cnidarian venoms are complex mixtures of bioactive molecules, including proteins, peptides, and small organic compounds. The composition of these venoms can vary significantly between different cnidarian species, as well as between different life stages or sexes of the same species. Some cnidarian venoms primarily serve a defensive function, causing pain or other unpleasant symptoms in potential predators, while others have a more offensive role, helping to immobilize prey before consumption.

The effects of cnidarian venoms on humans can range from mild irritation and stinging sensations to severe pain, swelling, and allergic reactions. In some cases, cnidarian envenomations can lead to more serious complications, such as respiratory distress, cardiac arrhythmias, or even death, particularly in individuals with underlying health conditions or allergies to the venom.

Research on cnidarian venoms has led to important insights into the biochemistry and molecular mechanisms of pain, inflammation, and neurotoxicity, as well as the development of new therapeutic strategies for treating various medical conditions. Additionally, understanding the structure and function of cnidarian venom components has inspired the design of novel bioactive molecules with potential applications in drug discovery, pest control, and other areas of biotechnology.

Electrophysiologic techniques, cardiac, refer to medical procedures used to study the electrical activities and conduction systems of the heart. These techniques involve the insertion of electrode catheters into the heart through blood vessels under fluoroscopic guidance to record and stimulate electrical signals. The information obtained from these studies can help diagnose and evaluate various cardiac arrhythmias, determine the optimal treatment strategy, and assess the effectiveness of therapies such as ablation or implantable devices.

The electrophysiologic study (EPS) is a type of cardiac electrophysiologic technique that involves the measurement of electrical signals from different regions of the heart to evaluate its conduction system's function. The procedure can help identify the location of abnormal electrical pathways responsible for arrhythmias and determine the optimal treatment strategy, such as catheter ablation or medication therapy.

Cardiac electrophysiologic techniques are also used in device implantation procedures, such as pacemaker or defibrillator implantation, to ensure proper placement and function of the devices. These techniques can help program and test the devices to optimize their settings for each patient's needs.

In summary, cardiac electrophysiologic techniques are medical procedures used to study and manipulate the electrical activities of the heart, helping diagnose and treat various arrhythmias and other cardiac conditions.

In medical terms, the heart is a muscular organ located in the thoracic cavity that functions as a pump to circulate blood throughout the body. It's responsible for delivering oxygen and nutrients to the tissues and removing carbon dioxide and other wastes. The human heart is divided into four chambers: two atria on the top and two ventricles on the bottom. The right side of the heart receives deoxygenated blood from the body and pumps it to the lungs, while the left side receives oxygenated blood from the lungs and pumps it out to the rest of the body. The heart's rhythmic contractions and relaxations are regulated by a complex electrical conduction system.

Heart rate is the number of heartbeats per unit of time, often expressed as beats per minute (bpm). It can vary significantly depending on factors such as age, physical fitness, emotions, and overall health status. A resting heart rate between 60-100 bpm is generally considered normal for adults, but athletes and individuals with high levels of physical fitness may have a resting heart rate below 60 bpm due to their enhanced cardiovascular efficiency. Monitoring heart rate can provide valuable insights into an individual's health status, exercise intensity, and response to various treatments or interventions.

Investigational drugs, also known as experimental or trial drugs, refer to medications that are currently being tested in clinical trials to evaluate their safety and efficacy for the treatment of various medical conditions. These drugs have not yet been approved by regulatory agencies such as the US Food and Drug Administration (FDA) for general use.

Before entering clinical trials, investigational drugs must undergo extensive preclinical testing in the lab and on animals to assess their safety and potential therapeutic benefits. Clinical trials are conducted in phases, starting with small groups of healthy volunteers to assess safety, followed by larger groups of patients to evaluate efficacy and side effects.

Participation in clinical trials is voluntary, and participants must meet certain eligibility criteria to ensure their safety and the validity of the trial results. Investigational drugs may ultimately be approved for general use if they are found to be safe and effective in clinical trials.

Preclinical drug evaluation refers to a series of laboratory tests and studies conducted to determine the safety and effectiveness of a new drug before it is tested in humans. These studies typically involve experiments on cells and animals to evaluate the pharmacological properties, toxicity, and potential interactions with other substances. The goal of preclinical evaluation is to establish a reasonable level of safety and understanding of how the drug works, which helps inform the design and conduct of subsequent clinical trials in humans. It's important to note that while preclinical studies provide valuable information, they may not always predict how a drug will behave in human subjects.

Prenylamine is not a medical term in and of itself, but it is the chemical name for a medication that is sometimes used in the medical field. The drug is known as Phenelzine sulfate in its brand name form, with trade names including Nardil.

Phenelzine sulfate (Prenylamine) is a type of medication called a monoamine oxidase inhibitor (MAOI). It works by blocking the action of an enzyme called monoamine oxidase, which helps break down certain chemicals in the brain called neurotransmitters. By blocking this enzyme's action, phenelzine sulfate increases the levels of these neurotransmitters in the brain, which can help to improve mood and alleviate symptoms of depression.

Phenelzine sulfate is used primarily to treat depression that has not responded to other treatments. It may also be used off-label for other conditions, such as anxiety disorders or panic attacks. However, it is important to note that phenelzine sulfate can have serious side effects and interactions with certain foods and medications, so it should only be taken under the close supervision of a healthcare provider.

'Aza compounds' is a general term used in chemistry to describe organic compounds containing a nitrogen atom (denoted by the symbol 'N' or 'aza') that has replaced a carbon atom in a hydrocarbon structure. The term 'aza' comes from the Greek word for nitrogen, 'azote.'

In medicinal chemistry and pharmacology, aza compounds are of particular interest because the presence of the nitrogen atom can significantly affect the chemical and biological properties of the compound. For example, aza compounds may exhibit enhanced bioavailability, metabolic stability, or receptor binding affinity compared to their non-aza counterparts.

Some common examples of aza compounds in medicine include:

1. Aza-aromatic compounds: These are aromatic compounds that contain one or more nitrogen atoms in the ring structure. Examples include pyridine, quinoline, and isoquinoline derivatives, which have been used as anti-malarial, anti-inflammatory, and anti-cancer agents.
2. Aza-heterocyclic compounds: These are non-aromatic compounds that contain one or more nitrogen atoms in a cyclic structure. Examples include azepine, diazepine, and triazole derivatives, which have been used as anxiolytic, anti-viral, and anti-fungal agents.
3. Aza-peptides: These are peptide compounds that contain one or more nitrogen atoms in the backbone structure. Examples include azapeptides and azabicyclopeptides, which have been used as enzyme inhibitors and neuroprotective agents.
4. Aza-sugars: These are sugar derivatives that contain one or more nitrogen atoms in the ring structure. Examples include azasugars and iminosugars, which have been used as glycosidase inhibitors and anti-viral agents.

Overall, aza compounds represent an important class of medicinal agents with diverse chemical structures and biological activities.

KCNQ potassium channels, also known as Kv7 channels, are a type of voltage-gated potassium channel that play important roles in regulating electrical excitability in various tissues, including the heart and nervous system. These channels are composed of several subunits, typically formed by combinations of KCNQ1 to KCNQ5 proteins, which form a pore through which potassium ions can flow in response to changes in membrane voltage.

KCNQ channels are characterized by their slow activation and deactivation kinetics, which contribute to their role in setting the resting membrane potential and modulating the frequency of action potentials in neurons. In the heart, KCNQ channels help to regulate the duration of the cardiac action potential and are therefore important for maintaining normal heart rhythm.

Mutations in KCNQ channel genes have been associated with a variety of inherited disorders, including long QT syndrome, a condition characterized by abnormalities in the electrical repolarization of the heart that can lead to life-threatening arrhythmias. Other diseases associated with KCNQ channel dysfunction include epilepsy, migraine, and various forms of hearing loss.

Histamine H1 antagonists, also known as H1 blockers or antihistamines, are a class of medications that work by blocking the action of histamine at the H1 receptor. Histamine is a chemical mediator released by mast cells and basophils in response to an allergic reaction or injury. It causes various symptoms such as itching, sneezing, runny nose, and wheal and flare reactions (hives).

H1 antagonists prevent the binding of histamine to its receptor, thereby alleviating these symptoms. They are commonly used to treat allergic conditions such as hay fever, hives, and eczema, as well as motion sickness and insomnia. Examples of H1 antagonists include diphenhydramine (Benadryl), loratadine (Claritin), cetirizine (Zyrtec), and doxylamine (Unisom).

Procainamide is an antiarrhythmic medication used to treat various types of irregular heart rhythms (arrhythmias), such as atrial fibrillation, atrial flutter, and ventricular tachycardia. It works by prolonging the duration of the cardiac action potential and decreasing the slope of the phase 0 depolarization, which helps to stabilize the heart's electrical activity and restore a normal rhythm.

Procainamide is classified as a Class Ia antiarrhythmic drug, according to the Vaughan Williams classification system. It primarily affects the fast sodium channels in the heart muscle cells, reducing their availability during depolarization. This results in a decreased rate of impulse generation and conduction velocity, which can help to suppress abnormal rhythms.

The medication is available as an oral formulation (procainamide hydrochloride) and as an injectable solution for intravenous use. Common side effects of procainamide include nausea, vomiting, diarrhea, headache, and dizziness. Procainamide can also cause a lupus-like syndrome, characterized by joint pain, skin rashes, and other autoimmune symptoms, in some patients who take the medication for an extended period.

It is essential to monitor procainamide levels in the blood during treatment to ensure that the drug is within the therapeutic range and to minimize the risk of adverse effects. Healthcare providers should also regularly assess patients' renal function, as procainamide and its active metabolite, N-acetylprocainamide (NAPA), are primarily excreted by the kidneys.

The heart ventricles are the two lower chambers of the heart that receive blood from the atria and pump it to the lungs or the rest of the body. The right ventricle pumps deoxygenated blood to the lungs, while the left ventricle pumps oxygenated blood to the rest of the body. Both ventricles have thick, muscular walls to generate the pressure necessary to pump blood through the circulatory system.

I believe there may be some confusion in your question. "Rabbits" is a common name used to refer to the Lagomorpha species, particularly members of the family Leporidae. They are small mammals known for their long ears, strong legs, and quick reproduction.

However, if you're referring to "rabbits" in a medical context, there is a term called "rabbit syndrome," which is a rare movement disorder characterized by repetitive, involuntary movements of the fingers, resembling those of a rabbit chewing. It is also known as "finger-chewing chorea." This condition is usually associated with certain medications, particularly antipsychotics, and typically resolves when the medication is stopped or adjusted.

Potassium channels are membrane proteins that play a crucial role in regulating the electrical excitability of cells, including cardiac, neuronal, and muscle cells. These channels facilitate the selective passage of potassium ions (K+) across the cell membrane, maintaining the resting membrane potential and shaping action potentials. They are composed of four or six subunits that assemble to form a central pore through which potassium ions move down their electrochemical gradient. Potassium channels can be modulated by various factors such as voltage, ligands, mechanical stimuli, or temperature, allowing cells to fine-tune their electrical properties and respond to different physiological demands. Dysfunction of potassium channels has been implicated in several diseases, including cardiac arrhythmias, epilepsy, and neurodegenerative disorders.

NAV1.5, also known as SCN5A, is a specific type of voltage-gated sodium channel found in the heart muscle cells (cardiomyocytes). These channels play a crucial role in the generation and transmission of electrical signals that coordinate the contraction of the heart.

More specifically, NAV1.5 channels are responsible for the rapid influx of sodium ions into cardiomyocytes during the initial phase of the action potential, which is the electrical excitation of the cell. This rapid influx of sodium ions helps to initiate and propagate the action potential throughout the heart muscle, allowing for coordinated contraction and proper heart function.

Mutations in the SCN5A gene, which encodes the NAV1.5 channel, have been associated with various cardiac arrhythmias, including long QT syndrome, Brugada syndrome, and familial atrial fibrillation, among others. These genetic disorders can lead to abnormal heart rhythms, syncope, and in some cases, sudden cardiac death.

Methoxamine is a synthetic, selective α1-adrenergic receptor agonist used in scientific research and for therapeutic purposes. It has the ability to stimulate the α1 adrenergic receptors, leading to vasoconstriction (constriction of blood vessels), increased blood pressure, and reduced blood flow to the skin and extremities.

In a medical context, methoxamine is primarily used as an experimental drug or in research settings due to its specific pharmacological properties. It may be employed to investigate the role of α1-adrenergic receptors in various physiological processes or to temporarily counteract the hypotensive (low blood pressure) effects of certain medications, such as vasodilators or anesthetics.

It is important to note that methoxamine is not commonly used in routine clinical practice due to its strong vasoconstrictive properties and potential adverse effects on organ function if misused or improperly dosed.

Artificial cardiac pacing is a medical procedure that involves the use of an artificial device to regulate and stimulate the contraction of the heart muscle. This is often necessary when the heart's natural pacemaker, the sinoatrial node, is not functioning properly and the heart is beating too slowly or irregularly.

The artificial pacemaker consists of a small generator that produces electrical impulses and leads that are positioned in the heart to transmit the impulses. The generator is typically implanted just under the skin in the chest, while the leads are inserted into the heart through a vein.

There are different types of artificial cardiac pacing systems, including single-chamber pacemakers, which stimulate either the right atrium or right ventricle, and dual-chamber pacemakers, which stimulate both chambers of the heart. Some pacemakers also have additional features that allow them to respond to changes in the body's needs, such as during exercise or sleep.

Artificial cardiac pacing is a safe and effective treatment for many people with abnormal heart rhythms, and it can significantly improve their quality of life and longevity.

Purkinje fibers are specialized cardiac muscle fibers that are located in the subendocardial region of the inner ventricular walls of the heart. They play a crucial role in the electrical conduction system of the heart, transmitting electrical impulses from the bundle branches to the ventricular myocardium, which enables the coordinated contraction of the ventricles during each heartbeat.

These fibers have a unique structure that allows for rapid and efficient conduction of electrical signals. They are larger in diameter than regular cardiac muscle fibers, have fewer branching points, and possess more numerous mitochondria and a richer blood supply. These features enable Purkinje fibers to conduct electrical impulses at faster speeds, ensuring that the ventricles contract simultaneously and forcefully, promoting efficient pumping of blood throughout the body.

Ventricular Tachycardia (VT) is a rapid heart rhythm that originates from the ventricles, the lower chambers of the heart. It is defined as three or more consecutive ventricular beats at a rate of 120 beats per minute or greater in a resting adult. This abnormal heart rhythm can cause the heart to pump less effectively, leading to inadequate blood flow to the body and potentially life-threatening conditions such as hypotension, shock, or cardiac arrest.

VT can be classified into three types based on its duration, hemodynamic stability, and response to treatment:

1. Non-sustained VT (NSVT): It lasts for less than 30 seconds and is usually well tolerated without causing significant symptoms or hemodynamic instability.
2. Sustained VT (SVT): It lasts for more than 30 seconds, causes symptoms such as palpitations, dizziness, shortness of breath, or chest pain, and may lead to hemodynamic instability.
3. Pulseless VT: It is a type of sustained VT that does not produce a pulse, blood pressure, or adequate cardiac output, requiring immediate electrical cardioversion or defibrillation to restore a normal heart rhythm.

VT can occur in people with various underlying heart conditions such as coronary artery disease, cardiomyopathy, valvular heart disease, congenital heart defects, and electrolyte imbalances. It can also be triggered by certain medications, substance abuse, or electrical abnormalities in the heart. Prompt diagnosis and treatment of VT are crucial to prevent complications and improve outcomes.

Electrophysiology is a branch of medicine that deals with the electrical activities of the body, particularly the heart. In a medical context, electrophysiology studies (EPS) are performed to assess abnormal heart rhythms (arrhythmias) and to evaluate the effectiveness of certain treatments, such as medication or pacemakers.

During an EPS, electrode catheters are inserted into the heart through blood vessels in the groin or neck. These catheters can record the electrical activity of the heart and stimulate it to help identify the source of the arrhythmia. The information gathered during the study can help doctors determine the best course of treatment for each patient.

In addition to cardiac electrophysiology, there are also other subspecialties within electrophysiology, such as neuromuscular electrophysiology, which deals with the electrical activity of the nervous system and muscles.

"Chromans" are a class of organic compounds that contain a benzene fused to a five-membered saturated carbon ring containing one oxygen atom. This particular ring structure is also known as a chromane. Chromans have various applications in the field of medicinal chemistry and pharmacology, with some derivatives exhibiting biological activities such as antioxidant, anti-inflammatory, and cardiovascular protective effects. Some well-known chroman derivatives include vitamin E (tocopherols and tocotrienols) and several synthetic drugs like chromanol, a calcium channel blocker used in the treatment of hypertension and angina pectoris.

Ambulatory electrocardiography, also known as ambulatory ECG or Holter monitoring, is a non-invasive method of recording the electrical activity of the heart over an extended period of time (typically 24 hours or more) while the patient goes about their daily activities. The device used to record the ECG is called a Holter monitor, which consists of a small, portable recorder that is attached to the patient's chest with electrodes.

The recorded data provides information on any abnormalities in the heart's rhythm or electrical activity during different stages of activity and rest, allowing healthcare providers to diagnose and evaluate various cardiac conditions such as arrhythmias, ischemia, and infarction. The ability to monitor the heart's activity over an extended period while the patient performs their normal activities provides valuable information that may not be captured during a standard ECG, which only records the heart's electrical activity for a few seconds.

In summary, ambulatory electrocardiography is a diagnostic tool used to evaluate the electrical activity of the heart over an extended period, allowing healthcare providers to diagnose and manage various cardiac conditions.

Imidazolidines are a class of heterocyclic organic compounds that contain a four-membered ring with two nitrogen atoms and two carbon atoms. The nitrogen atoms are adjacent to each other in the ring structure. These compounds have various applications, including as building blocks for pharmaceuticals and other organic materials. However, I couldn't find a specific medical definition related to disease or pathology for "imidazolidines." If you have any further questions or need information about a specific imidazolidine derivative with medicinal properties, please let me know!

Ventricular Fibrillation (VF) is a type of cardiac arrhythmia, which is an abnormal heart rhythm. In VF, the ventricles, which are the lower chambers of the heart, beat in a rapid and unorganized manner. This results in the heart being unable to pump blood effectively to the rest of the body, leading to immediate circulatory collapse and cardiac arrest if not treated promptly. It is often caused by underlying heart conditions such as coronary artery disease, structural heart problems, or electrolyte imbalances. VF is a medical emergency that requires immediate defibrillation to restore a normal heart rhythm.

Sodium channel blockers are a class of medications that work by blocking sodium channels in the heart, which prevents the rapid influx of sodium ions into the cells during depolarization. This action slows down the rate of impulse generation and propagation in the heart, which in turn decreases the heart rate and prolongs the refractory period.

Sodium channel blockers are primarily used to treat cardiac arrhythmias, including atrial fibrillation, atrial flutter, and ventricular tachycardia. They may also be used to treat certain types of neuropathic pain. Examples of sodium channel blockers include Class I antiarrhythmics such as flecainide, propafenone, lidocaine, and mexiletine.

It's important to note that sodium channel blockers can have potential side effects, including proarrhythmia (i.e., the development of new arrhythmias or worsening of existing ones), negative inotropy (decreased contractility of the heart muscle), and cardiac conduction abnormalities. Therefore, these medications should be used with caution and under the close supervision of a healthcare provider.

Cation transport proteins are a type of membrane protein that facilitate the movement of cations (positively charged ions) across biological membranes. These proteins play a crucial role in maintaining ion balance and electrical excitability within cells, as well as in various physiological processes such as nutrient uptake, waste elimination, and signal transduction.

There are several types of cation transport proteins, including:

1. Ion channels: These are specialized protein structures that form a pore or channel through the membrane, allowing ions to pass through rapidly and selectively. They can be either voltage-gated or ligand-gated, meaning they open in response to changes in electrical potential or binding of specific molecules, respectively.

2. Ion pumps: These are active transport proteins that use energy from ATP hydrolysis to move ions against their electrochemical gradient, effectively pumping them from one side of the membrane to the other. Examples include the sodium-potassium pump (Na+/K+-ATPase) and calcium pumps (Ca2+ ATPase).

3. Ion exchangers: These are antiporter proteins that facilitate the exchange of one ion for another across the membrane, maintaining electroneutrality. For example, the sodium-proton exchanger (NHE) moves a proton into the cell in exchange for a sodium ion being moved out.

4. Symporters: These are cotransporter proteins that move two or more ions together in the same direction, often coupled with the transport of a solute molecule. An example is the sodium-glucose cotransporter (SGLT), which facilitates glucose uptake into cells by coupling its movement with that of sodium ions.

Collectively, cation transport proteins help maintain ion homeostasis and contribute to various cellular functions, including electrical signaling, enzyme regulation, and metabolic processes. Dysfunction in these proteins can lead to a range of diseases, such as neurological disorders, cardiovascular disease, and kidney dysfunction.

Piperidines are not a medical term per se, but they are a class of organic compounds that have important applications in the pharmaceutical industry. Medically relevant piperidines include various drugs such as some antihistamines, antidepressants, and muscle relaxants.

A piperidine is a heterocyclic amine with a six-membered ring containing five carbon atoms and one nitrogen atom. The structure can be described as a cyclic secondary amine. Piperidines are found in some natural alkaloids, such as those derived from the pepper plant (Piper nigrum), which gives piperidines their name.

In a medical context, it is more common to encounter specific drugs that belong to the class of piperidines rather than the term itself.

An artificial pacemaker is a medical device that uses electrical impulses to regulate the beating of the heart. It is typically used when the heart's natural pacemaker, the sinoatrial node, is not functioning properly and the heart rate is too slow or irregular. The pacemaker consists of a small generator that contains a battery and electronic circuits, which are connected to one or more electrodes that are placed in the heart.

The generator sends electrical signals through the electrodes to stimulate the heart muscle and cause it to contract, thereby maintaining a regular heart rhythm. Artificial pacemakers can be programmed to deliver electrical impulses at a specific rate or in response to the body's needs. They are typically implanted in the chest during a surgical procedure and can last for many years before needing to be replaced.

Artificial pacemakers are an effective treatment for various types of bradycardia, which is a heart rhythm disorder characterized by a slow heart rate. Pacemakers can significantly improve symptoms associated with bradycardia, such as fatigue, dizziness, shortness of breath, and fainting spells.

Sodium channels are specialized protein structures that are embedded in the membranes of excitable cells, such as nerve and muscle cells. They play a crucial role in the generation and transmission of electrical signals in these cells. Sodium channels are responsible for the rapid influx of sodium ions into the cell during the initial phase of an action potential, which is the electrical signal that travels along the membrane of a neuron or muscle fiber. This sudden influx of sodium ions causes the membrane potential to rapidly reverse, leading to the depolarization of the cell. After the action potential, the sodium channels close and become inactivated, preventing further entry of sodium ions and helping to restore the resting membrane potential.

Sodium channels are composed of a large alpha subunit and one or two smaller beta subunits. The alpha subunit forms the ion-conducting pore, while the beta subunits play a role in modulating the function and stability of the channel. Mutations in sodium channel genes have been associated with various inherited diseases, including certain forms of epilepsy, cardiac arrhythmias, and muscle disorders.

A drug overdose occurs when a person ingests, inhales, or absorbs through the skin a toxic amount of a drug or combination of drugs. This can result in a variety of symptoms, depending on the type of drug involved. In some cases, an overdose can be fatal.

An overdose can occur accidentally, for example if a person mistakenly takes too much of a medication or if a child accidentally ingests a medication that was left within their reach. An overdose can also occur intentionally, such as when a person takes too much of a drug to attempt suicide or to achieve a desired high.

The symptoms of a drug overdose can vary widely depending on the type of drug involved. Some common symptoms of a drug overdose may include:

* Nausea and vomiting
* Abdominal pain
* Dizziness or confusion
* Difficulty breathing
* Seizures
* Unconsciousness
* Rapid heart rate or low blood pressure

If you suspect that someone has overdosed on a drug, it is important to seek medical help immediately. Call your local poison control center or emergency number (such as 911 in the United States) for assistance. If possible, try to provide the medical personnel with as much information as you can about the person and the drug(s) involved. This can help them to provide appropriate treatment more quickly.

... , torsade de pointes or torsades des pointes (TdP) (/tɔːˌsɑːd də ˈpwæ̃t/, French: [tɔʁsad də pwɛ̃t̪], ... The singular and plural forms (torsade de pointes, torsades de pointes and torsades des pointes) have all often been used. The ... The treatment of torsades de pointes aims to restore a normal rhythm and to prevent the arrhythmia recurring. While torsades ... Etiology of Torsade". 2021-04-03. {{cite journal}}: Cite journal requires ,journal= (help) "TORSADE DE POINTES , Meaning & ...
A medically significant subvariant of ventricular tachycardia is called torsades de pointes (literally meaning "twisting of the ... Philadelphia, PA: Lippinocott, Wilkins & Williams 2003 ISBN 0-7817-3486-X Mitchell LB (January 2023). "Torsades de Pointes ... Zaffalon Júnior JR, Viana AO, de Melo GE, De Angelis K (September 2018). "The impact of sedentarism on heart rate variability ( ...
The term "torsades de pointes" is translated from French as "twisting of the peaks" because the complexes appear to undulate, ... Long QT syndrome Torsades de pointes Roden DM, Woosley RL, Primm RK (1986). "Incidence and clinical features of the quinidine- ... El-Sherif N, Turitto G, Boutjdir M (2018). "Acquired long QT syndrome and torsade de pointes". Pacing and Clinical ... Yap YG, Camm AJ (November 2003). "Drug induced QT prolongation and torsades de pointes". Heart. 89 (11): 1363-72. doi:10.1136/ ...
Torsades de Pointes in patients with long QT refractory to magnesium and to treat patients with intermittent Torsades de ... Cohagan B, Brandis D (August 2022). "Torsade de Pointes". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID ... Procaccini DE, Sawyer JE, Watt KM (2019). "Pharmacology of Cardiovascular Drugs". Critical Heart Disease in Infants and ... Pointes refractory to treatment with magnesium. Historically, it was used to treat asthma via metered aerosol or nebulizing ...
An important differential diagnosis is torsades de pointes. Treatment is with cardiopulmonary resuscitation (CPR) and ... Robles de Medina, EO; Bernard, R; Coumel, P (1978). et al. "Definition of terms related to cardiac rhythm. WHO/ISFC Task Force ... 1922 De Boer S 1923 Katz LN 1928 Wiggers, CJ et al. 1940 Interactive models and information on ventricular fibrillation and ... Neumar, RW; Shuster, M; Callaway, CW; Gent, LM; Atkins, DL; Bhanji, F; Brooks, SC; de Caen, AR; Donnino, MW; Ferrer, JM; ...
El-Sherif N, Turitto G, Boutjdir M (April 2018). "Acquired long QT syndrome and torsade de pointes". Pacing and Clinical ... Other risk factors for developing torsades de pointes among those with LQTS include female sex, increasing age, pre-existing ... While there is strong evidence that the trigger for Torsades de Pointes comes from afterdepolarisations, it is less certain ... El-Sherif N, Turitto G, Boutjdir M (May 2019). "Acquired Long QT Syndrome and Electrophysiology of Torsade de Pointes". ...
Medication-induced QT-interval prolongation and torsades de pointes. US Pharm. 2011;36(2):HS-2-HS-8. Krantz MJ, Martin J, ... AZCERT focuses on drugs and drug-drug interactions, especially those that cause QT prolongation and Torsades de Pointes (TdP) ... Drug induced QT prolongation and torsades de pointes. Heart. 2003;89(11):1363-1372. doi:10.1136/heart.89.11.1363 Miranda DG, ... Predicting the Unpredictable: Drug-Induced QT Prolongation and Torsades de Pointes. Journal of the American College of ...
Beach, Scott (2013). "QTc prolongation, torsades de pointes, and psychotropic medications". The Academy of Psychosomatic ... Tonini M, Cipollina L, Poluzzi E, Crema F, Corazza GR, De Ponti F (February 2004). "Review article: clinical implications of ...
Torsades de Pointes can occur in a heart block setting. Initial treatment can be medical, involving the use of drugs like ... Asystole and torsade de pointes". Chart 63: Faintness and Fainting, page 161, ISBN 0-86318-864-8 (Articles with short ...
QT interval prolongation and torsades de pointes have been reported. Thrombotic microangiopathy has been reported. Thrombotic ...
It has been implicated in causing ventricular arrhythmia (torsades de pointes). In June 2015 a research paper was published ...
"Drug-Induced Prolongation of the QT Interval and Torsades de Pointes". Lexicomp. 29 April 2023. Retrieved 2 May 2023. Curry SC ...
Vernakalant Wiesfeld AC, Crijns HJ, Bergstrand RH, Almgren O, Hillege HL, Lie KI (October 1993). "Torsades de pointes with ...
"Torsades de pointes complicating atrioventricular block: evidence for a genetic predisposition". Heart Rhythm. 4 (2): 170-4. ... Long QT syndrome predisposes to potentially lethal ventricular cardiac arrhythmias including torsades de pointe, which can ... Roepke TK, Kontogeorgis A, Ovanez C, Xu X, Young JB, Purtell K, Goldstein PA, Christini DJ, Peters NS, Akar FG, Gutstein DE, ... de Vries B, Verschuren WM, Brand J, Freilinger T, Pfaffenrath V, Straube A, Ballinger DG, Zhan Y, Daly MJ, Cox DR, Dichgans M, ...
... can cause cardiac toxicity that effects in torsades de pointes. Also acecainide can decrease renal function when it ...
Early afterdepolarizations can result in torsades de pointes, tachycardia, and other arrhythmias. EADs can be triggered by ...
Torsades de pointes is the most serious side effect of dofetilide therapy. The incidence of torsades de pointes is 0.3-10.5% ... The majority of episodes of torsades de pointes have occurred within the first three days of initial dosing. Patients should be ... The risk of inducing torsades de pointes can be decreased by taking precautions when initiating therapy, such as hospitalizing ... Lenz TL; Hilleman DE (November 2000). "Dofetilide: A new antiarrhythmic agent approved for conversion and/or maintenance of ...
Mukarram O, Hindi Y, Catalasan G, Ward J (2016). "Loperamide Induced Torsades de Pointes: A Case Report and Review of the ... Baker DE (2007). "Loperamide: a pharmacological review". Reviews in Gastroenterological Disorders. 7 (Suppl 3): S11-8. PMID ... aktuelles.uni-frankfurt.de. Archived from the original on 23 December 2020. Mullen F (3 November 1982). "FR Doc. 82-30264" (PDF ... Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial" [Collegiate Board Resolution No ...
QT prolongation (which can lead to torsades de pointes arrhythmia) reported with spiramycin. Same precursor as for Quifenadine ... Ramírez Chanona N, del Rio Navarro BE, Pérez Martín J (November-December 2005). "[Efficacy of mequitazine (Primalan) on the ...
It is listed as having a "conditional risk" of causing torsades de pointes. Chloral hydrate is produced from chlorine and ...
QT prolongation or ventricular cardiac arrhythmias, including torsade de pointes. The most common side effects are ... Sekar VJ, Spinosa-Guzman S, De Paepe E, De Pauw M, Vangeneugden T, Lefebvre E, Hoetelmans RM (January 2008). "Darunavir/ ...
Hoshino K, Ogawa K, Hishitani T, Isobe T, Etoh Y (April 2006). "Successful uses of magnesium sulfate for torsades de pointes in ... Magnesium sulfate is an antiarrhythmic drug, but only used against very specific arrhythmias such as torsades de pointes. The ... "Optimal administration dosage of magnesium sulfate for torsades de pointes in children with long QT syndrome". J Am Coll Nutr. ... ISBN 978-0-07-139930-2. Lenz, TL; Hilleman, DE (2000). "Dofetilide, a New Class III Antiarrhythmic Agent". Pharmacotherapy. 20 ...
January 2001). "Torsades de pointes ventricular tachycardia induced by mosapride and flecainide in the presence of hypokalemia ... physicians should be alert for signs of toxicity before life-threatening arrhythmias occur like torsades de pointes. While the ... Gill JS, Mehta D, Ward DE, Camm AJ (October 1992). "Efficacy of flecainide, sotalol, and verapamil in the treatment of right ...
Torsades de pointes - A polymorphic arrhythmia that can be symptomatic and tends to resolve to a normal sinus rhythm. However, ... Specifically, it can lead to torsades de pointes than can then lead to ventricular fibrillation. It can be an inherited ... torsade de pointes). To classify a ventricular rhythm as vtach, at least 3 beats in a row must originate from the ventricles ...
... may increase the chance of QTC prolongation, specifically Torsades de Pointes which can be fatal. More serious ...
... 's most important adverse effect is torsades de pointes, which is a form of ventricular tachycardia. The drug is ...
Complications may include seizures or cardiac arrest such as from torsade de pointes. Those with low magnesium often have low ... Viering DH, de Baaij JH, Walsh SB, Kleta R, Bockenhauer D (July 2017). "Genetic causes of hypomagnesemia, a clinical overview ... de Baaij JH, Hoenderop JG, Bindels RJ (January 2015). "Magnesium in man: implications for health and disease". Physiological ... Gommers LM, Hoenderop JG, Bindels RJ, de Baaij JH (January 2016). "Hypomagnesemia in Type 2 Diabetes: A Vicious Circle?". ...
Cardiac abnormalities such as prolongation of the QT interval and torsades de pointes have also been observed. Dosages above ... Listas de Substâncias Entorpecentes, Psicotrópicas, Precursoras e Outras sob Controle Especial" [Collegiate Board Resolution No ...
There are concerns of higher rates of QT prolongation and torsades de pointes compared with other SSRIs. The US Food and Drug ...
Azimilide Bretylium Clofilium E-4031 Nifekalant Tedisamil Sematilide These agents include a risk of torsades de pointes. ... a very potent inhibitor of the rat Kv1.3 voltage-gated potassium channel Lenz TL, Hilleman DE (July 2000). "Dofetilide, a new ...

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