Ventricular Premature Complexes
Atrial Premature Complexes
Electrocardiography, Ambulatory
Arrhythmias, Cardiac
Electrocardiography
Purkinje Fibers
Heart Failure
Encyclopedias as Topic
Heart Valve Diseases
Cardiomyopathy, Dilated
Heart Valves
Cardiomyopathy, Hypertrophic
Detection of abnormal high-frequency components in the QRS complex by the wavelet transform in patients with idiopathic dilated cardiomyopathy. (1/286)
In order to investigate whether increased fine, fractionated signals within the QRS complex can detect arrhythmogenic substrates and how these fine signals link with ventricular mechanical dysfunction, wavelet analysis was performed on averaged QRS complexes obtained from the left precordial lead in 26 patients with idiopatic dilated cardiomyopathy (IDCM) and in 12 normal subjects. The number of local maxima and the duration of the wavelet transform were significantly greater in patients with IDCM than in normal subjects; the number at 100 Hz was 8.8+/-3.1 vs 6.0+/-1.1 (p<0.01), and the duration at 100Hz was 93+/-15 vs 75+/-7ms (p<0.01). Both of these indices were greater in the patients with than in those without late potentials, repetitive ventricular premature beats or cardiac death. In addition, significant inverse curvilinear relationships were observed between the left ventricular ejection fraction and both the number of local maxima and the duration of the wavelet transform. In conclusion, fine fragmented signals in the QRS complex detected by wavelet analysis would be an important marker for potentially arrhythmogenic substrates and seemed to progress in parallel with left ventricular mechanical dysfunction in IDCM. (+info)Correlation of ventricular mechanosensory neurite activity with myocardial sensory field deformation. (2/286)
The mechanosensory activity generated by ventricular epicardial sensory neurites associated with afferent axons in thoracic sympathetic nerves was correlated with sensory field deformation (long axis, short axis, and transmural dimension changes), regional intramyocardial pressure, and ventricular chamber pressure in anesthetized dogs. Ventricular mechanosensory neurites generated activity that correlated best with strain developed along either the long or short axis of their epicardial sensory fields in most instances. Activity did not correlate normally to local wall thickness or to regional wall or chamber pressure development in most cases. During premature ventricular contractions, the activity generated by these sensory neurites correlated best with maximum strain developed along at least one sensory field epicardial vector. Identified sensory neurites were also activated by local application of the chemical bradykinin (10 microM) or by local ischemia. These data indicate that the activity generated by most ischemia-sensitive ventricular epicardial sensory neurites associated with afferent axons in sympathetic nerves is dependent on not only their local chemical milieu but on local mechanical deformation along at least one epicardial vector of their sensory fields. (+info)Possible theophylline toxicity during anesthesia. (3/286)
Asthmatic patients who undergo outpatient anesthesia are typically prescribed one or more drugs for treatment. Some of these agents have narrow therapeutic ranges and are associated with potentially serious adverse reactions, toxic effects, or drug interactions. Various clinical signs of toxicity may be first uncovered during routine monitoring of an office anesthetic. The case reported here demonstrates the need for proper understanding of the asthmatic patient's medical history and an appreciation for the medications used to control the disease. A sudden cardiovascular event possibly related to drug toxicity is witnessed and treated in an asthmatic patient during intravenous sedation. A possible drug interaction with a non-asthmatic medication taken concomitantly by the patient is implicated and discussed. In addition to the case report, the broad classification of drugs employed for bronchial asthma and their effects is reviewed. (+info)Dental anesthetic management of a patient with ventricular arrhythmias. (4/286)
During routine deep sedation for endodontic therapy, a dentist-anesthesiologist observed premature ventricular contractions (PVCs) on a 62-yr-old woman's electrocardiogram (EKG) tracing. The dentist was able to complete the root canal procedure under intravenous (i.v.) sedation without any problems. The dentist-anesthesiologist referred the patient for medical evaluation. She was found to be free from ischemic cardiac disease with normal ventricular function. The patient was cleared to continue her dental treatment with deep sedation. She subsequently continued to undergo dental treatment with deep intravenous sedation without incident, although her EKG exhibited frequent PVCs, up to 20 per minute, including couplets and episodes of trigeminy. This article will review indications for medical intervention, antiarrhythmic medications, and anesthetic interventions for perioperative PVCs. (+info)Unsuitability of corrected QT dispersion as a marker for ventricular arrhythmias and cardiac sudden death after acute myocardial infarction. (5/286)
The present study investigated whether corrected QT (QTc) dispersion could play a role as a marker of ventricular arrhythmias and sudden cardiac death after acute myocardial infarction (MI). The study included 76 males and 24 females with a mean age of 60+/-11 years. Standard 12-lead ECGs were recorded during the recovery phase (15+/-9 days) after the onset of MI. The QTc was calculated according to Bazett's formula and QTc dispersion was calculated as the difference between the maximum and minimum QTc intervals. Patients were divided into 2 groups: 21 patients (group A) had a QTc dispersion of > or =80ms, and the other 79 patients (group B) had a QTc dispersion of <80ms in the recovery stage (15+/-9 days). Clinical, angiographical, and Holter monitoring data, and prognosis (mean follow-up period 29+/-18 months) were compared between these 2 groups. The frequencies of early coronary reperfusion and recanalization of infarct-related vessels during the recovery phase were significantly higher in group B than group A. The left ventricular ejection fraction was also higher in group B than group A (51+/-12 vs 43+/-12%, p=0.0029). There were no significant differences in the number of premature ventricular contractions, the percentage of patients with repetitive ventricular arrhythmias, or in the frequency of sudden cardiac death during the follow-up period between the 2 groups. In summary, QTc dispersion in the recovery stage is not a useful marker for ventricular arrhythmias or sudden cardiac death after acute MI, although increased QTc dispersion may correlate with an ineffective early coronary reperfusion and with the degree of depressed left ventricular function. (+info)Cyclic bursts of ventricular premature contractions of more than one minute intervals. (6/286)
Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts (n = 48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n = 30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 +/- 40 seconds and regular, whereas it was 210 +/- 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 +/- 31 seconds in the dome type and 98 +/- 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs. (+info)Pacing-induced delayed protection against arrhythmias is attenuated by aminoguanidine, an inhibitor of nitric oxide synthase. (7/286)
1. Cardiac pacing, in anaesthetized dogs, protects against ischaemia and reperfusion-induced ventricular arrhythmias when this is initiated 24 h after the pacing stimulus. Now we have examined whether this delayed cardioprotection afforded by cardiac pacing is mediated through nitric oxide. 2. Twenty-two dogs were paced (4 x 5 min periods at 220 beats min(-1)) by way of the right ventricle, 24 h prior to a 25 min period of coronary artery occlusion. Nine of these dogs were given the inhibitor of induced nitric oxide synthase, aminoguanidine (50 mg kg(-1) i.v.), 0.5 h prior to coronary artery occlusion. Sham-operated non-paced dogs with and without aminoguanidine treatment served as controls. 3. Pacing markedly (P<0. 05) reduced arrhythmia severity (ventricular fibrillation, VF, during occlusion 15%; survival from the combined ischaemia-reperfusion insult 62%) compared to control, sham-operated, unpaced dogs (VF during occlusion 58%; survival 17%). This protection was attenuated by the administration of aminoguanidine prior to coronary artery occlusion (survival from the combined ischaemia-reperfusion insult 11%, which was significantly (P<0.05) less than in the paced dogs not given aminoguanidine and similar to the controls). Aminoguanidine had no significant effects on coronary artery occlusion when given to dogs that had not been paced. In the dose used aminoguanadine transiently elevated systemic arterial pressure by a mean of 20 mmHg and reduced heart rate by a mean of 22 beats min(-1). 4. These results suggest that nitric oxide, probably derived from induced nitric oxide synthase, contributes significantly to the delayed cardioprotection afforded by cardiac pacing. (+info)Heart rate variability analysis of patients with idiopathic left ventricular outflow tract tachycardia: role of triggered activity. (8/286)
There have been several reports with respect to idiopathic ventricular tachycardias (VTs) originating from the left ventricular outflow tract (LVOT). A previous report suggested that triggered activity plays a partial role in idiopathic LVOT tachycardia from the electrophysiological as well as the electropharmacological viewpoint. However, the exact role of triggered activity in this type of VT remains unknown. In the present study the relationship of the frequency of premature ventricular contractions (PVCs) and heart rate was examined and heart rate variability (HRV) was analyzed in 2 cases of LVOT tachycardia using 24-h Holter electrocardiographic (ECG) monitoring. The relation between the PVCs frequency and heart rate showed a persistently positive correlation, indicating frequent PVCs as heart rate increased. In HRV analysis, NN50(%), a time-domain variable of parasympathetic activity, showed no change prior to ventricular arrhythmias. In frequency-domain analysis of HRV, the high frequency (HF) component tended to fall prior to repetitive PVCs and VTs. The ratio of the low frequency to high frequency (LF/HF) components increased prior to single PVCs, repetitive PVCs and VTs. Sympathetic predominance predisposes the genesis of these kinds of arrhythmias originating from the LVOT and it is suggested that triggered activity plays an important role in LVOT tachycardia, at least in its initiation. (+info)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.
Atrial premature complexes (APCs or APCTs) are extra heartbeats that originate in the atria, which are the upper chambers of the heart. These early beats disrupt the normal rhythm and cause a premature contraction before the next scheduled beat. APCs can sometimes be felt as a "skipped" beat or palpitation. They are usually benign and do not require treatment unless they occur frequently or are associated with underlying heart disease.
Moricizine is an antiarrhythmic medication that belongs to the class IC. It works by stabilizing the heart's electrical activity and correcting irregular heart rhythms (arrhythmias). Moricizine is used to treat certain types of serious, life-threatening ventricular arrhythmias.
It's important to note that moricizine has been discontinued in many countries due to the availability of safer and more effective antiarrhythmic medications. The use of moricizine should be under the close supervision of a healthcare professional, and it is usually reserved for situations where other treatments have not been effective.
The medical definition of 'Moricizine' is:
A class IC antiarrhythmic drug that prolongs the refractory period of the ventricles by selectively blocking sodium channels during phase 0 of the action potential, thereby stabilizing cardiac membranes and suppressing ectopic pacemaker activity. Moricizine is used in the treatment of certain types of serious, life-threatening ventricular arrhythmias.
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.
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.
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.
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.
Heart failure is a pathophysiological state in which the heart is unable to pump sufficient blood to meet the metabolic demands of the body or do so only at the expense of elevated filling pressures. It can be caused by various cardiac disorders, including coronary artery disease, hypertension, valvular heart disease, cardiomyopathy, and arrhythmias. Symptoms may include shortness of breath, fatigue, and fluid retention. Heart failure is often classified based on the ejection fraction (EF), which is the percentage of blood that is pumped out of the left ventricle during each contraction. A reduced EF (less than 40%) is indicative of heart failure with reduced ejection fraction (HFrEF), while a preserved EF (greater than or equal to 50%) is indicative of heart failure with preserved ejection fraction (HFpEF). There is also a category of heart failure with mid-range ejection fraction (HFmrEF) for those with an EF between 40-49%.
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.
Heart valve diseases are a group of conditions that affect the function of one or more of the heart's four valves (tricuspid, pulmonic, mitral, and aortic). These valves are responsible for controlling the direction and flow of blood through the heart. Heart valve diseases can cause the valves to become narrowed (stenosis), leaky (regurgitation or insufficiency), or improperly closed (prolapse), leading to disrupted blood flow within the heart and potentially causing symptoms such as shortness of breath, fatigue, chest pain, and irregular heart rhythms. The causes of heart valve diseases can include congenital defects, age-related degenerative changes, infections, rheumatic heart disease, and high blood pressure. Treatment options may include medications, surgical repair or replacement of the affected valve(s), or transcatheter procedures.
Dilated cardiomyopathy (DCM) is a type of cardiomyopathy characterized by the enlargement and weakened contraction of the heart's main pumping chamber (the left ventricle). This enlargement and weakness can lead to symptoms such as shortness of breath, fatigue, and fluid retention. DCM can be caused by various factors including genetics, viral infections, alcohol and drug abuse, and other medical conditions like high blood pressure and diabetes. It is important to note that this condition can lead to heart failure if left untreated.
Heart valves are specialized structures in the heart that ensure unidirectional flow of blood through its chambers during the cardiac cycle. There are four heart valves: the tricuspid valve and the mitral (bicuspid) valve, located between the atria and ventricles, and the pulmonic (pulmonary) valve and aortic valve, located between the ventricles and the major blood vessels leaving the heart.
The heart valves are composed of thin flaps of tissue called leaflets or cusps, which are supported by a fibrous ring. The aortic and pulmonic valves have three cusps each, while the tricuspid and mitral valves have three and two cusps, respectively.
The heart valves open and close in response to pressure differences across them, allowing blood to flow forward into the ventricles during diastole (filling phase) and preventing backflow of blood into the atria during systole (contraction phase). A properly functioning heart valve ensures efficient pumping of blood by the heart and maintains normal blood circulation throughout the body.
Hypertrophic cardiomyopathy (HCM) is a genetic disorder characterized by the thickening of the heart muscle, specifically the ventricles (the lower chambers of the heart that pump blood out to the body). This thickening can make it harder for the heart to pump blood effectively, which can lead to symptoms such as shortness of breath, chest pain, and fatigue. In some cases, HCM can also cause abnormal heart rhythms (arrhythmias) and may increase the risk of sudden cardiac death.
The thickening of the heart muscle in HCM is caused by an overgrowth of the cells that make up the heart muscle, known as cardiomyocytes. This overgrowth can be caused by mutations in any one of several genes that encode proteins involved in the structure and function of the heart muscle. These genetic mutations are usually inherited from a parent, but they can also occur spontaneously in an individual with no family history of the disorder.
HCM is typically diagnosed using echocardiography (a type of ultrasound that uses sound waves to create images of the heart) and other diagnostic tests such as electrocardiogram (ECG) and cardiac magnetic resonance imaging (MRI). Treatment for HCM may include medications to help manage symptoms, lifestyle modifications, and in some cases, surgical procedures or implantable devices to help prevent or treat arrhythmias.
Blood pressure is the force exerted by circulating blood on the walls of the blood vessels. It is measured in millimeters of mercury (mmHg) and is given as two figures:
1. Systolic pressure: This is the pressure when the heart pushes blood out into the arteries.
2. Diastolic pressure: This is the pressure when the heart rests between beats, allowing it to fill with blood.
Normal blood pressure for adults is typically around 120/80 mmHg, although this can vary slightly depending on age, sex, and other factors. High blood pressure (hypertension) is generally considered to be a reading of 130/80 mmHg or higher, while low blood pressure (hypotension) is usually defined as a reading below 90/60 mmHg. It's important to note that blood pressure can fluctuate throughout the day and may be affected by factors such as stress, physical activity, and medication use.