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Saturday, November 1, 2008
Maternal Deaths From Childbirth Still High
Read more and share your opinion.
Heart Attacks Dip Day After Daylight Savings Time Ends
Monday, August 18, 2008
Interventional cardiology
A large number of procedures can be performed on the heart by catheterization. This most commonly involves the insertion of a sheath into the femoral artery (but, in practice, any large peripheral artery or vein) and cannulating the heart under X-ray visualization (most commonly
fluoroscopy, a real-time x-ray).
Procedures performed by specialists in interventional cardiology:
Angioplasty (PTCA, Percutaneous Transluminal Coronary Angioplasty) - for coronary atherosclerosis
Valvuloplasty - dilation of narrowed cardiac valves (usually mitral, aortic or pulmonary)
Procedures for congenital heart disease - insertion of occluders for ventricular or atrial septal defects, occlusion of patent ductus arteriosus, angioplasty of great vessels
Emergency angioplasty and stenting of occluded coronary vessels in the setting of acute myocardial infarction
Coronary Thrombectomy - a procedure performed to remove thrombus (blood clot) from blood vessels.[1]
Invasive procedures of the heart to treat arrhythmias are performed by specialists in clinical cardiac electrophysiology
Surgery of the heart is done by the specialty of cardiothoracic surgery. Some interventional cardiology procedures are only performed when there is cardiothoracic surgery expertise in the hospital, in case of complications.
Circadian Rhythm-Metabolism Link Discovered
Common Vaginal Infection May Increase Likeliness of HIV Infection
Toxic Chemicals Found In Detergents, Air Fresheners
Trans Fat Labeling May Mislead
Tobacco Plants Make Cancer Vaccine
Saturday, June 28, 2008
West Nile Virus Expected For Summer 2008
High Fructose Corn Syrup Plans Resurgence
AMA Says Clinics And Tobacco Don't Mix
The Big Breakfast Diet
Rare Tuberculosis Strain Returning
Choosing Where To Live Based On Insurance Costs
Cigarette Sales Drop May Not Mean Less Tobacco Use
Diabetic Ulcer Gel Increases Cancer Mortality Risk
Marijuana Potency Highest In 30 Years
Silver Teeth Fillings Toxic To Fetuses and Children?
St. John's Wort No Better Than Placebo For ADHD
Full story.
Incentives Increase For Healthy Employees Amid Rising Health Care Costs
Wednesday, June 11, 2008
The Echocardiogram
The echocardiogram is an extremely useful test for studying the heart’s anatomy. It is non-invasive and entirely safe, and when interpreted by well-trained cardiologists, is very accurate.
How is the echocardiogram performed?
The patient lies on a bed or examination table, and the echo technician places a transducer (a device that resembles a computer mouse) over the chest wall. The transducer is moved back and forth across the chest wall, collecting several “views” of the heart. A Vaseline-like gel is applied to the chest wall to aid in sliding the transducer back and forth. The test takes 30 – 60 minutes to complete.
How does the echocardiogram work?
The transducer placed on the chest sends sound waves toward the heart. Like the sonar on a submarine, the sound waves bounce off the cardiac structures (that is, they “echo” off the heart).The sound wave "echos" are collected by by the transducer.
These returning sound waves are computer-processed, and a two-dimensional image of the beating heart is produced on a television screen. By “aiming” the transducer, most of the important cardiac structures can be imaged by the echocardiogram.
A Doppler microphone can be used during echocardiography to measure the velocity of blood flow in the heart. This information can be useful in assessing heart valve function.
Tuesday, June 10, 2008
What are the risks of having a catheterization or angiography?
What kinds of heart disease can catheterization and angiography help to evaluate?
How is a catheterization performed?
Heart caths - what you should know
Saturday, June 7, 2008
The Common Heart Tests:
Echocardiography (echo)
Electrocardiogram (ECG or EKG)
Electrophysiology study (EP study)
Holter monitor and event recorder
MUGA scan
Stress testing
Thallium and sestamibi (Cardiolite) scans
Tilt Table Testing
Transesophageal echocardiography (TEE)
Ultrafast CT scan
Cardiac MRI
Heart
The heart is the pump station of the body and is responsible for circulating blood throughout the body. It is about the size of your clenched fist and sits in the chest cavity between two lungs. Its walls are made up of muscle that can squeeze or pump blood out every time that the organ "beats" or contracts. Fresh, oxygen-rich air is brought to the lungs through the trachea (pronounced tray-kee-ya) or windpipe every time that you take a breath. The lungs are responsible for delivering oxygen to the blood, and the heart circulates the blood to the lungs and different parts of the body.
The heart is divided into FOUR chambers or "rooms". You can compare it to a Duplex apartment that is made up of a right and a left unit, separated from each other by a partition wall known as a SEPTUM (pronounced sep-tum).
Each "duplex" is subdivided into an upper and a lower chamber. The upper chamber is known as an ATRIUM (pronounced ay-tree-yum) while the lower chamber is referred to as a VENTRICLE (pronounced ven-trickle). The right atrium (RA) sits on top of the right ventricle (RV) on the right side of the heart while the left atrium (LA) sits atop the left ventricle (LV) on the left.
The right side of the heart is responsible for sending blood to the lungs, where the red blood cells pick up fresh oxygen. This OXYGENATED blood is then returned to the left side of the heart. From here the oxygenated blood is transported to the whole body supplying the fuel that the body cells need to function. The blood cells of the body extract or removes oxygen from the blood. The oxygen-poor blood is returned to the right atrium, where the journey began. This round trip is known as the CIRCULATION of blood.
The figure shown above is a section of the heart, as viewed from the front. It demonstrates the four chambers. You will also notice that there is an opening between the right atrium (RA) and the right ventricle (RV). This is actually a valve known as the TRICUSPID (pronounced try-cus-pid) valve. It has three flexible thin parts, known as leaflets, that open and shut. The figure below shows the mitral and tricuspid valves, as seen from above, in the open and shut position.
When shut, the edge of the three leaflets touch each other to close the opening and prevent blood from leaving the RV and going back into the RA. Thus, the tricuspid valve serves as a trapdoor valve that allows blood to move only in one direction - from RA to RV. Similarly, the MITRAL valve (pronounced my-trull) allows blood to flow only from the left atrium to the left ventricle. Unlike the tricuspid valve, the mitral valve has only two leaflets.
In the top diagram, you will also notice thin thread like structures attached to the edges of the mitral and tricuspid valves. These chords or strings are known as chordae tendineae (do not even try to pronounce it. However, if you really must, it is chord-ee tend-in-ee). They connect the edges of the tricuspid and mitral valves to muscle bands or papillary (pronounced pap-pill-lurry) muscles. The papillary muscles shorten and lengthen during different phases of the cardiac cycle and keep the valve leaflets from flopping back into the atrium.
The chords are designed to control the movement of the valve leaflets similar to ropes attached to the sail of a boat. Like ropes, they allow the sail to bulge outwards in the direction of a wind but prevents them from helplessly flapping in the breeze. In other words, they provide the capability of a door jamb that allows a door to open and shut in a given direction and NOT beyond a certain point.
When the three leaflets of the tricuspid bulge upwards during contraction or emptying of the ventricles, their edges touch each other and close off backward flow to the right atrium. This important feature allows blood to flow through the heart in only ONE direction, and prevents it from leaking backwards when the valve is shut. The two leaflets of the mitral valve functions in a similar manner and allows flow of blood from the left atrium to the left ventricle, but closes and cuts off backward leakage into the left atrium when the left ventricle contracts and starts to empty.
Thursday, June 5, 2008
Use of intraaortic balloon counter pulsation in a patient with tortuous aorta
Monday, May 26, 2008
Home blood pressure monitor can be great monitoring tool
The statement is issued in Hypertension: Journal of the American Heart Association and published in the June issue of the Journal of Cardiovascular Nursing.
The American Heart Association said monitoring blood pressure at home can be an effective way of tracking and treating hypertension.
It says that blood pressure checks at doctor's offices are vulnerable to normal fluctuations, caused by such things as anxiety. According to the association, previous research has shown that between 10 per cent and 20 per cent of people fall prey to the "white coat effect" in which their blood pressure, which is normal, suddenly spikes.
"It is also believed that some people with normal blood pressures in their doctors' offices have pressures that spike to potentially dangerous levels in other situations," said Thomas Pickering, director of the Center for Behavioral Cardiovascular Health at Columbia Presbyterian Medical Center in New York, in a statement.
Measuring blood pressure with an at-home monitor can provide a more accurate snapshot of a person's blood pressure — particularly among the elderly, diabetics, kidney patients and pregnant women, say the authors. And they believe the frequent readings can help doctors work with patients to treat their condition.
"Home blood pressure monitoring also gives patients the physiologic feedback they need to see regarding blood pressure," says Nancy Houston Miller, co-author and former president of the Preventive Cardiovascular Nurses Association.
"Rather than three to four office blood pressure checks per year, if they measure blood pressure at home in addition to following up with their health-care provider, patients are likely to achieve goals more quickly and be confident that medicines are working for them."
The authors point out that many monitors have a price point of $100, which they say is affordable.
The association recommends:
- People buy oscillometric monitors with cuffs that fit the upper arm — wrist monitors are not recommended.
- People take their blood pressure readings at the same time each day to maintain consistency.
- The optimal blood pressure with a home monitor is less than 135/85 millimetres of mercury or less than 130/80 in those patients who are high-risk.
The Heart and Stroke Foundation of Canada advises patients to talk to their health-care providers about which types of equipment are best and how to use them.
It recommends people select a unit that has been tested to meet the validation requirements of either the Association for the Advancement of Medical Instrumentation (AAMI), the British Hypertension Society (BHS) or the European Society of Hypertension (ESH).
It says that patients should still see their doctors concerning their blood pressure and that a home unit is not a substitute for regular testing.
For most adults, high blood pressure, or hypertension, is defined as a blood pressure greater than or equal to 140 mm/Hg over 90 mm/Hg systolic pressure, according to the Heart and Stroke Foundation of Canada.
Saturday, May 17, 2008
Cardiology – 5th Edition
By R. H. Swanton
Published 2003
Blakwell Publishing
Cardiology/ Handbooks, manuals, etc
464 pages
ISBN:1405101970
Cardiology is a rapidly changing and expanding field. Management protocols change regularly, new categories of treatment options are being discovered, and there is a new focus on the prevention of cardiovascular diseases.Pocket Consultant: Cardiology is a highly practical, user-friendly guide to this expanding field. Now in its fifth edition, this book has been highly praised for its readability, conciseness and clear illustrations, and is an indispensable guide for those dealing with common cardiological problems. The author, the current president of the British Cardiac Society, is internationally known in the field of clinical cardiology. This is an ideal book for the junior doctor who wants a quick, easily understandable guide to cardiology.
Friday, May 16, 2008
First Ever Triple Heart Valve Replacement Surgery
“It’s great. It turned out so well.” says Sandra Matthews, the triple valve replacement surgery recipient. Sandra Matthews is a young 65-year-old woman from Pocatello and Tuesday she under-went a very risky surgery.
One that is usually performed on a university level but for the first time in the history of the Portneuf Medical Center, a triple heart valve replacement surgery was successfully completed. Doctors expected a double valve replacement, but when they got inside, they found 3 valves had to be replaced. “These are such high risk operations to be able to be done and we can do these operations here in Pocatello.” Says Dr. Jacob DeLaRose, Chief of Cardiac Surgery at Portneuf Medical Center.
Doctors at PMC say triple heart valve replacement surgery is one of high risk but one thing helped Sandra get through the extraordinary surgery.
“I’m a firm believer that to have a positive attitude and positive outlook is what gets you through the operation. We’re the technicians but you have to have it inside and in here and you’ll be able to do great.” Says Dr. DeLaRosa. As for Sandra, she already has a game plan after she leaves the hospital. “To get home and see my little dogs that are going crazy because I’m not there.” Says Matthews.
Portneuf Medical Center says future operations of this stature depend on an individual case-by-case basis. Doctors say they hope to perform more in the future.
Thursday, May 15, 2008
Ventricular Premature Complexes
Ventricular premature complexes (VPCs) are ectopic impulses originating from an area distal to the His Purkinje system. VPCs are the most common ventricular arrhythmia. Assessment and treatment of VPCs is challenging and complex. The significance of VPCs is interpreted in the context of the underlying cardiac condition.
The approach to the evaluation and management of VPCs has undergone dramatic changes in the last decade. Ventricular ectopy leading to ventricular tachycardia (VT), which, in turn, can degenerate into ventricular fibrillation, is one of the common mechanisms for sudden cardiac death. The treatment paradigm in the 1970s and 1980s was to eliminate VPCs in patients after myocardial infarction (MI). Recent arrhythmia suppression studies have demonstrated that eliminating VPCs with available antiarrhythmic drugs increases the risk of death to patients without providing any measurable benefit.
Pathophysiology
Very few studies have evaluated the pathophysiology of VPCs in human subjects. Most of the information is derived from animal studies. Three common mechanisms exist for VPCs, (1) automaticity, (2) reentry, and (3) triggered activity, as follows:
Automaticity: This is the development of a new site of depolarization in nonnodal ventricular tissue, which can lead to a VPC. In animal models, focal mechanisms without evidence of macro-reentry play a major role in the origin of ventricular arrhythmia associated with ischemic cardiomyopathy. Increased automaticity could be due to electrolyte abnormalities or ischemic myocardium.
Reentry circuit: Reentry typically occurs when slow-conducting tissue (eg, infarcted myocardium) is present adjacent to normal tissue. The slow-conducting tissue could be due to damaged myocardium, as in the case of a healed MI.
Triggered activity: Afterdepolarizations triggered by a preceding impulse can lead to premature activation if the threshold is reached, and this can cause a VPC. Afterdepolarization can occur either during (early) or after (late) completion of repolarization. Early afterdepolarizations commonly are responsible for bradycardia associated VPCs, but they also can be present with ischemia and electrolyte abnormalities.
Frequency
United States
The reported prevalence of VPCs varies between studies, depending on the population studied, duration of observation, and method of detection. In asymptomatic patients, VPCs are infrequent when only a single 12-lead ECG is used for screening. The Framingham heart study (with 1-h ambulatory ECG) suggested that the prevalence rate of 1 or more VPCs per hour was 33% in men without coronary artery disease (CAD) and 32% in women without CAD. Among patients with CAD, the prevalence rate of 1 or more VPCs was 58% in men and 49% in women. Other studies using 24-hour ambulatory monitoring showed a VPC prevalence rate of 41% in healthy teenage boys aged 14-16 years, 50-60% in healthy young adults, and 84% in healthy elderly persons aged 73-82 years. VPCs also are common in patients with hypertension, ventricular hypertrophy, cardiomyopathy, and mitral valve prolapse.
International
Data from the Gruppo Italiano per lo Studio della Sopravvivenza dell'Infarto Miocardico 2 study demonstrated that 64% of patients who had MI then had ventricular arrhythmia and 20% of patients had more than 10 VPCs per hour when 24-h Holter monitoring was used.
Mortality/Morbidity
Prognosis depends on the frequency and characteristics of VPCs and on the type and severity of associated structural heart disease. VPCs are associated with an increased risk of death, especially when CAD is diagnosed, but the relationship between VPC frequency and mortality, even in this group, is not robust and no benefit results in suppressing VPCs to improve survival in any population.
In asymptomatic patients, frequent ventricular ectopy (defined as a run of 2 or more consecutive premature ventricular depolarizations or with premature ventricular depolarizations constituting >10% of all ventricular depolarizations on any of the ECG recordings with the subject at rest, during exercise, or during recovery) recorded during exercise testing was associated with 2.5-fold increased risk of cardiovascular death. Less frequent VPCs did not increase the risk.
In general, multimorphic VPCs connote a poorer prognosis than uniform morphologic VPCs. In patients post-MI, frequent VPCs (>10/h) are associated with increased mortality in the prethrombolytic era, but the association in patients receiving thrombolysis is weak.
In a recent study, a frequent VPC (defined as the presence of 7 or more ventricular premature beats per minute during any given stage, ventricular bigeminy, ventricular trigeminy, ventricular couplets, ventricular triplets, sustained or nonsustained ventricular tachycardia, ventricular flutter, torsade de pointes, or ventricular fibrillation) during recovery from exercise was an independent predictor of death. However, frequent VPCs only during exercise did not independently predict an increased risk.
Frequent VPCs, especially when they occur in a bigeminal pattern, can precipitate tachycardia-induced cardiomyopathy that can be reversed by elimination of the PVCs through catheter ablation.
Sex
The Framingham heart study demonstrated increased prevalence of VPCs in men compared with women. The difference was especially higher in men with CAD than in women with CAD.
Age
VPCs are uncommon in children (suggested prevalence rate of 0.8-2.2% from the Vanderbilt Medical Center; exact prevalence not known). Prevalence increases with age.
History
Various symptoms are associated with VPCs, but the exact prevalence of symptoms is not known. Typical symptoms include palpitations, light-headedness, syncope, atypical chest pain, or fatigue. Palpitations are due to an augmented post-VPC beat and may be sensed as a pause rather than an extra beat.
Physical
VPCs frequently are associated with variable or decreased intensity of heart sounds. The augmented beat following a dropped beat is heard frequently. Bounding jugular pulse (cannon A wave) from a loss of atrioventricular (AV) synchrony may be present. The follow-up beat after a VPC is stronger due to the postextrasystolic compensatory pause, allowing greater left ventricular (LV) filling, which usually causes greater intensity of that beat. This is known as extrasystolic potentiation.
Lab Studies
Look for correctable causes of VPCs, such as medications, electrolyte disturbances, infection, and myocardial ischemia or MI.
Obtain serum electrolyte and magnesium levels.
Imaging Studies
Look for underlying structural heart abnormalities that can predispose to VPCs.
·
Assess the degree of LV dysfunction by noninvasive techniques such as echocardiography or radionuclide imaging.
Echocardiography may be preferable because it also provides structural information about the heart.
Other Tests
In high-risk patients, ie, those with reduced ejection fraction (EF) and VPCs, a 24-hour Holter monitor may help establish the degree of electrical instability.
·
The severity of LV dysfunction, along with the complexity and frequency of the VPC, determines the aggressiveness of management.
Suppressing the VPCs themselves is not the focus of treatment unless patients are extremely symptomatic; rather, treatment may be implemented if the patient is felt to be at high risk of sudden cardiac death.
Treatment of the underlying structural heart disease also is extremely important. This includes acute syndromes, such as ischemia and infarction, the treatment of which involves reperfusion.
ECG should be performed to look for structural cardiac abnormalities. Diagnostic criteria include the following:
·
Wide (duration exceeding the dominant QRS complexes) and bizarre QRS complexes are present.
No preceding premature P waves occur, and, rarely, a sinus P wave is conducted.
The T wave usually is in the opposite direction from the R wave.
Full compensatory pause is common.
VPCs originating from the left ventricle typically produce a right bundle-branch block (BBB) pattern on QRS.
VPCs originating from right ventricle typically produce left BBB-like pattern on QRS.
Idiopathic VPCs often originate from the right ventricular outflow tract and have a left bundle rightward axis morphology.
Electrophysiologic study
·
Electrophysiologic study (EPS) may be indicated for 2 types of patients with VPCs, (1) those with a structurally normal heart with symptomatic VPCs, for whom pharmacological treatment or catheter ablation is indicated and (2) those with VPCs and structural heart disease, for whom risk stratification for sudden cardiac death is indicated.
According to current American College of Cardiology/American Heart Association guidelines, class I indications for EPS are patients with CAD, low EF (<0.36), and nonsustained VT on ambulatory ECG. Class II indications for catheter ablation apply to patients with a highly symptomatic uniform morphology of VPC, couplets, and nonsustained VT.
Exercise stress testing should be performed to look for coronary ischemia, exercise-induced arrhythmia, or both.
Tuesday, May 13, 2008
Influence of right ventricular pressure overload on left and right ventricular filling in cor pulmonale assessed with Doppler echocardiography.
Interventricular mechanical asynchrony in pulmonary arterial hypertension
OBJECTIVES: The purpose of this study was to explore in pulmonary arterial hypertension (PAH) whether the cause of interventricular asynchrony lies in onset of shortening or duration of shortening.
BACKGROUND: In PAH, leftward ventricular septal bowing (LVSB) is probably caused by a left-to-right (L-R) delay in myocardial shortening.
METHODS: In 21 PAH patients (mean pulmonary arterial pressure 55 +/- 13 mm Hg and electrocardiogram-QRS width 100 +/- 16 ms), magnetic resonance imaging myocardial tagging (14 ms temporal resolution) was applied. For the left ventricular (LV) free wall, septum, and right ventricular (RV) free wall, the onset time (T(onset)) and peak time (T(peak)) of circumferential shortening were calculated. The RV wall tension was estimated by the Laplace law.
RESULTS: The T(onset) was 51 +/- 23 ms, 65 +/- 4 ms, and 52 +/- 22 ms for LV, septum, and RV, respectively. The T(peak) was 293 +/- 58 ms, 267 +/- 22 ms, and 387 +/- 50 ms for LV, septum, and RV, respectively. Maximum LVSB was at 395 +/- 45 ms, coinciding with septal overstretch and RV T(peak). The L-R delay in T(onset) was -1 +/- 16 ms (p = 0.84), and the L-R delay in T(peak) was 94 +/- 41 ms (p < 0.001). The L-R delay in T(peak) was not related to the QRS width but was associated with RV wall tension (p < 0.05). The L-R delay in T(peak) correlated with leftward septal curvature (p < 0.05) and correlated negatively with LV end-diastolic volume (p < 0.05) and stroke volume (p < 0.05).
CONCLUSIONS: In PAH, the L-R delay in myocardial peak shortening is caused by lengthening of the duration of RV shortening. This L-R delay is related to LVSB, decreased LV filling, and decreased stroke volume.
Mechanical right ventricular dyssynchrony in patients after atrial switch operation for transposition of the great arteries.
Contraction pattern of the systemic right ventricle shift from longitudinal to circumferential shortening and absent global ventricular torsion.
METHODS: Fourteen Senning-operated patients age 18.4 +/- 0.9 years (mean +/- SD) with transposition of the great arteries were studied. We compared the contraction pattern of the systemic RV with findings in the RV and left ventricle (LV) of normal subjects (n = 14) using tissue Doppler imaging and magnetic resonance imaging.
RESULTS: In the systemic RV free wall, circumferential strain exceeded longitudinal strain (-23.3 +/- 3.4% vs. -15.0 +/- 3.0%, p < 0.001) as was also the case in the normal LV (-25.7 +/- 3.1% vs. -16.5 +/- 1.7%, p < 0.001), opposite from the findings in the normal RV (-15.8 +/- 1.3% vs. -30.7 +/- 3.3%, p < 0.001). Strain in the interventricular septum did not differ from normal. Ventricular torsion was essentially absent in the systemic RV (0.3 +/- 1.8 degrees ), in contrast to a torsion of 16.7 +/- 4.8 degrees in the normal LV (p < 0.001).
CONCLUSIONS: In the systemic RV as in the normal LV, there was predominant circumferential over longitudinal free wall shortening, opposite from findings in the normal RV. This may represent an adaptive response to the systemic load. Noticeably, however, the systemic RV did not display torsion as found in the normal LV.
Left ventricular function in patients with transposition of the great arteries operated with atrial switch.
Subpulmonary strain and strain rate values were intermediate between those in the normal LV and RV. Ventricular free-wall torsion was reduced in the subpulmonary LV compared with both the normal LV (5.7 +/- 3.2 degrees vs. 16.7 +/- 5.6 degrees , p < 0.001) and RV (5.7 +/- 3.2 degrees vs. 11.4 +/- 2.6 degrees , p < 0.05). Furthermore, early diastolic filling of the subpulmonary LV differed from that of the normal LV. The subpulmonary LV displayed predominantly longitudinal shortening, as did its functional counterpart, the normal RV. However, the degree and rate of both longitudinal and circumferential shortening were intermediate between those of the normal LV and RV. This could represent a partial adaptation to the reduced pressure load. Decreased ventricular torsion and diastolic abnormalities might indicate subclinical ventricular dysfunction.
Monday, May 12, 2008
Heart Disease on rise among Indian Youth
So what are the reasons or factors which have resulted in an increase in the number of heart patients in India? “Modern life style has proven to be the stimulus for the growth of heart diseases among the youth” says Dr Ashok Seth , Chief Invasive and Interventional Cardiology, Escorts Heart Institute. "Improper food habits, lack of physical activity and this coupled with high level of stress and increase in smoking and alcohol consumption are all classic risk factors which can put one high on the risk zone of coronary heart diseases. Sadly all these have become a part of the Indian youth’s life style.”
Not only college and school going students, but even working professionals have adopted the ways of this modern life style, and this has proved to be the instigator of heart diseases.
Cardiovascular disease
Saturday, May 10, 2008
Heart Rhythm Disorders
The electrical system regulating heartbeat consists of 2 main areas of control and a series of conducting pathways, similar to the electrical wiring in a house (See Multimedia File 1).
The sinoatrial, or SA, node is located in the right atrium. It provides the main control and is the source of each beat. The SA node also keeps up with the body's overall need for blood and increases the heart rate when necessary, such as during exercise, emotional excitement, or illness such as fever. The SA node is sometimes called the "natural pacemaker" of the heart.
Electrical impulses leave the SA node and travel through special conducting pathways in the heart to the other controller, the atrioventricular, or AV, node. The purpose of the AV node is to provide a pathway for impulses from the atria to the ventricles. It also creates a delay in conduction from the atria to the ventricle. This causes the atria to contract first and allow the ventricles to fill with blood before they contract themselves.
The delay ensures proper timing so that the lower chambers have time to fill completely before they contract.
Normally, the heart beats 60-100 times a minute. This state is called "normal sinus rhythm" or "normal rhythm." Depending upon the needs of the body, it may beat faster (sinus tachycardia) due to stress or slower (sinus bradycardia) such as during sleep.
Arrhythmias
Arrhythmias are abnormalities of the heartbeat. There are many types of arrhythmias, and they are classified by where they begin, (the atria, AV node, or the ventricles). Generally speaking, those that do not originate from the ventricles are called supraventricular arrhythmias while those that come from the ventricles are called ventricular arrhythmias.
The following are some of the more commonly encountered arrhythmias, starting with the supraventricular arrhythmias.
Premature atrial contractions, sometimes called PAC or APC, or premature supraventricular contractions: Another part of the atria sends an electrical impulse soon after the previous beat, causing the heart to contract earlier than expected. This is a very common occurrence in all ages and usually is not serious.
Supraventricular tachycardia, or paroxysmal SVT: Occurs when any structure above the ventricle (usually the atria or the AV node) produces a regular, rapid discharge.
Sick sinus syndrome: Irregular firing by the SA node causes a slower-than-normal heart rate (sometimes alternating with rapid heart rates).
Atrial fibrillation: A common condition caused by electrical impulses discharged at a rapid rate from many different areas of the atria. It usually causes a fast and irregular heartbeat.
Atrial flutter: A condition caused by a rapid discharge from a single place in the right atrium. Typically, the right atrium fires at a rate of 300 beats per minute, but only every other beat is conducted through the AV node, meaning that the ventricular rate is classically 150 beats per minute.
Arrhythmias arising in the ventricle are more likely to be found in people with more serious heart disease but may also be found in healthy individuals.
Premature ventricular complex, or PVC: This electrical impulse starts in the ventricle causing the heart to beat earlier than expected. Usually, the heart returns to its normal rhythm right away.
Ventricular tachycardia: Fast and usually regular impulses come from the ventricles and cause a very rapid heart rate. This is usually a life-threatening tachycardia and needs immediate medical attention, possibly electrical shock or defibrillation.
Ventricular fibrillation: Electrical impulses arise from the ventricles in a fast and disordered sequence. The resulting uncoordinated contractions cause the heart to quiver (appearing like a bag of worms) and lose the ability to beat and pump blood, leading to immediate cardiac arrest.
Arrhythmias can be frightening, but in many cases, especially in younger patients with normal underlying hearts, they are not life threatening and can be effectively treated with medications.
Supraventricular arrhythmias are very common in middle-aged and elderly adults. The older you get, the more likely you are to experience an arrhythmia, especially atrial fibrillation.
Many supraventricular arrhythmias are temporary and not serious, especially if no underlying heart disease is present. These arrhythmias are a response to normal activities or emotions.
Even if an arrhythmia has a serious underlying cause, the arrhythmia itself may not be dangerous. The underlying problem can often be treated effectively.
Thursday, May 8, 2008
Accelerated Idioventricular Rhythm
AIVR may also be defined as an ectopic rhythm with 3 or more consecutive premature ventricular beats and a rate faster than the normal ventricular intrinsic escape rate of 30-40 bpm but slower than VT.
AIVR is an electrocardiographic diagnosis and does not generally produce any particular symptoms. Making a correct diagnosis remains one of the most important concerns because the usual treatments for patients with the more common form of ventricular arrhythmia, such as VT, may not apply.
Pathophysiology
Enhanced automaticity appears to be the likely electrophysiologic mechanism behind the genesis of AIVR. Enhanced automaticity generally is ascribed to phase-4 depolarization of the action potential of the myocardial cell. AIVR can occur in the His-Purkinje fibers or myocardium under certain abnormal metabolic conditions.
AIVR arises from subordinate or second-order pacemakers and manifests itself when the patient's prevailing sinus rate becomes lower than the accelerated rate (AIVR) of the otherwise suppressed focus. Sinus bradycardia combined with enhanced automaticity of the subordinate site is the common pathophysiology.
Several conditions, including myocardial ischemia (especially inferior wall ischemia or infarction), digoxin toxicity, electrolyte imbalance (eg, hypokalemia), and hypoxemia may accentuate the phase-4 depolarization in the subordinate pacemaker tissues of the atrioventricular (AV) junction or His-Purkinje system, thus increasing the rate of impulse generation. Frequently, when inferior wall ischemia is present, the subordinate pacemaker acceleration coexists with sinus node depression. The latter permits escape and domination of the pacemaker function, which may occur with AV junctional or ventricular rates of only 60-70 bpm. The ectopic mechanism also can begin after a premature ventricular complex or, as described above, when the ectopic ventricular focus simply can accelerate sufficiently enough to overtake the intrinsic rhythm.
The onset of AIVR is gradual (nonparoxysmal). The ventricular rhythm can be regular or irregular and, occasionally, can show sudden doubling, suggesting the presence of exit block. The ventricular rate, commonly 60-110 bpm, usually stays within 10-15 beats of the sinus rate; therefore, the control of the cardiac rhythm occasionally passes back and forth between these 2 competing pacemaker sites.
Fusion beats often develop at the onset and termination of arrhythmia, which occurs when the pacemakers are competing for control of ventricular depolarization. Because of the slow rate, capture beats also are common. Due to the slow rate and nonparoxysmal onset, precipitation of more rapid ventricular arrhythmias rarely is observed. Rhythm termination generally occurs gradually, while the underlying sinus rhythm accelerates or the AIVR slows down.
Accelerated idioventricular rhythm in the reperfusion era
Ever since the beginning of the thrombolytic era, the occurrence of AIVR in patients with acute MI has been considered a specific marker of successful reperfusion following the infusion of the lytic agents.
Whether such association exists with reperfusion through direct percutaneous coronary intervention was investigated in a recent study of 125 consecutive patients undergoing direct percutaneous coronary intervention for a first acute MI. 24-hour Holter monitoring revealed that AIVR appeared in 15.2% of the patients. The incidence of AIVR was not different between patients with TIMI grade 2 flow and those with TIMI grade 3 flow (13% vs 16%). No differences were reported in the incidence of major cardiac events within 12-month follow-up in patients with and without AIVR. However, AIVR was associated with higher vagal tone and lower sympathetic activity, the occurrence of AIVR had no prognostic impact on the clinical course and was not able to discriminate between complete and incomplete reperfusion following percutaneous coronary intervention.