Ventricular: 09/2011

9/06/2011

Cardiac Arrhythmias 1/3 - Heart Physiology - USMLE Step 1

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Orignal From: Cardiac Arrhythmias 1/3 - Heart Physiology - USMLE Step 1

Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction Reviews

Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction

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ventricular system

This book presents new aspects on electrophysiological mechanisms and catecholaminergic contributions in the setting of acute and chronic myocardial ischemia. Special emphasis is placed on the full scope from basic molecular and cellular mechanisms to experimental models of close clinical proximity. A number of internationally distinguished scientists present their latest findings in this significant research area within the perimeter of cardiovascular disease which continues to lead mortality s

Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction

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Ventricular Fibrillation

Article by Michael A. Morales

Ventricular Fibrillation (also called v-fib or vf) is a lethal arrhythmia that originates in the ventricles. It commonly occurs in cardiac arrest patients and is the primary rhythm that AED's (automated external defibrillators) are looking for to initiate a shock to the victim of cardiac arrest

In v-fib there is no organized depolarization of the ventricles. The heart muscle simply quivers with no contraction to pump the blood. As a result, there is no pulse. There are a number of reasons that ventricular fibrillation can occur:

Electrolyte ImbalanceAcute Coronary SyndromesHeart failure DysrhythmiasHypertrophyIncreased sympathetic Nervous System Activity

The list really only provides a snap shot and is not all inclusive. The only known effective treatment for ventricular fibrillation is defibrillation. When defibrillation occurs, the heart is stopped for an instant and aloud to reset. You can think of it as kind of like rebooting your computer. Once reset, the heart may go back to an organized rhythm and blood flow can resume to the heart and vital organs.

Generally, CPR is performed while and AED is being accessed. CPR does not change ventricular fibrillation to a normal heart rhythm. CPR pumps the heart so that oxygen rich blood can continue to flow to the heart and vital organs until defibrillation is available. CPR buys the victims some time and may keep brain damage from occurring. Together early CPR and defibrillation saves lives if provided immediately and is currently the best defense against ventricular fibrillation for the victim of cardiac arrest.

Although the heart can go into a number of different rhythms in a cardiac arrest, ventricular fibrillation is one of the most common, and is treatable if address quickly. Without early defibrillation the hearts electrical system will cease to function. No electrical activity in the heart is a condition known as asystole or flat line. Defibrillation will correct asystole.

The 2005 American Heart Association guidelines recommend defibrillation within the first 3-5 minutes of a cardiac arrest. It is during this time period that the victim is more likely to be in v-fib and benefit from defibrillation.

Michael Morales

About the Author

Michael Morales is an EMT paramedic and director of education for Vital Ethics Inc., providing basic and advanced life support training and certification programs.

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Orignal From: Adrenergic System and Ventricular Arrhythmias in Myocardial Infarction Reviews

Can food trigger Atrial Fibrillation?

Can food trigger Atrial Fibrillation?
Yes. I experience all your symptoms. I have atrial fibrillation with episodes lasting from 3 - 10 hours and am taking warfarin and beta blockers. I also have a hiatus hernia (without relux, just gas). Many of my fibrillations start immediately after a heavy meal or eating too quickly. Also if I lean forward and press on the diaphragm immediately after eating. I can't get the doctor to agree the connection - in fact he thinks I am up the creek, but I am convinced that they are connected. The hospital heart doctor also said that he had never heard of a connection. However my osteopath/acupuncturist actually took the connection for granted and says it is because the vagus (or vagal) nerve goes past the diaphragm and close to the heart and when the hernia is bad it triggers off the fibrillations. I asked my doctor to treat the hernia just to see what happens. He has put me on very strong digestive tablets and the hernia has subsided. I am waiting to see what happens if it flares up again. I hope no more fibs.
I would suggest that you check out the possibilty that you have a hiatus hernia remembering that you don't necessarily have to have reflux to prove you have one, just bad indigestion. Eat slowly and don't bend over after meals or even do very much for about half an hour and try not to squash the diaphragm.
I have now had acupuncture and can't believe how much more comfortable I am now after meals and no fibrillations for the last 2 1/2 weks . It is difficult to tell because I have recently been in hospital for a few days because the fibrillations got very frequent so the fibs may have stopped because of the tablets I was given and the injections of warfarin and because I had to drink potassium which controls the electrical activity in the heart. My reading was 2 instead of 5 and this was causing the fibs every other day. They gave me potassium tablets to take until I reach level 5 and I hope that my test on Wednesday reaches normal and I can stop taking them.

No real answers but would suggest that you check out the possibilty that you have a hiatus hernia remembering that you don't necessarily have to have reflux to prove you have one. Eat slowly, have small meals frequently instead of one big one and don't bend over after meals or even do very much for about half an hour and try not to squash the diaphragm. I too was frightened to eat and got quite paranoid but that feeling has now gone although I am very careful in what I eat now. No fried, spicy or fatty foods.
Do have your potassium levels checked (through a simple blood test) if you have not already done so because the level is very important. Mine was depleted through diuretics but many things can deplete it and it definitely triggers of electrical activity in the heart.The hospital coudn't wait to get the potassium into me and my warfarin levels up.

Good luck. Let me know how you get on and I will post anything I find through my search for the link that I firmly believe is there.
Patsy72Can food trigger A-fib? Certain food groups can increase the odds of creating a-fib in those with a history of preexisting a-fib or those with existing heart disease. Not to get too detailed Xanthines (found in chocolate) and caffeine (found in coffee and tea) are two common sources that have been implicated-- but what t you describe is not food induced a-fib but rather the food induced retching that triggered the a-fib . For the most part a-fib can be stabilized and treated medically -- What is really of concern in this whole matter is your protracted history of nausea and,bloating after eating or drinking anything- your Doctor should be actively searching for reasons why you have these symptoms ie hiatal hernia,gall bladder, ulcer,pancreas etc...Very good advice here about getting your "hiatal hernia" risk assessed. Often GI reflux can irritate your heart as well. I would recommend a consult to a gastroenterologist. Also keep in mind that whenever food or drink enters the stomach, blood flow is diverted to that area to assist with digestion. That means blood flow is diverted away from your heart (not alot). Have you had complete cardiac workup to determine if you have any coronary blockages. Even small diversions of blood away from the coronaries in the presence of coronary occlusions can trigger cardiac arrythmias and/or chest pain. Some people are very sensitive to this. My experience with recovering heart attack patients is to insist on rest for at least 30-45 minutes after meals to avoid any additional stress to the heart while food is being digested. Sitting upright for 30 minutes after meals also helps if you have hiatal hernia and/or reflux disease. Just some tips, hope it helps.

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when reading the EKG of someone with right ventricular hypertrophy and right bundle branch block on the V1?

when reading the EKG of someone with right ventricular hypertrophy and right bundle branch block on the V1?
T wave inversion in V1 to V3 could be due to right bundle branch block or previous anterior wall myocardial infarction. T-wave inversion (what shows up in the three "abnormal" leads) can be caused by anything from hyperventilation to potassium depletion to positioning of the leads. It can, of course, also signify some non-specific heart disease, but in the absence of symptoms this is extremely difficult to know. I would move forward with a stress echo...t inversion in v1 alone is a normal phenomenon, if it extends to v2 and v3 it indicates ischemia.

Orignal From: when reading the EKG of someone with right ventricular hypertrophy and right bundle branch block on the V1?

Are Common Heart Skip Palpitations Dangerous?: Premature Ventricular and Atrial Contractions (PVCs and PACs)

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pvc ventricular

INTRODUCTION: Skipped heartbeats occur in most, if not 100% of the general population, at some point during their lives. Some medical sources state that about half of us experience them on a relatively frequent basis. For some people however, these heart palpitations called "Premature Ventricular Contractions" and "Premature Atrial Contractions" (PVCs and PACs), occur at a frequency or forcefulness, that can be concerning to them and that can result in chronic anxiety and/or panic att

Are Common Heart Skip Palpitations Dangerous?: Premature Ventricular and Atrial Contractions (PVCs and PACs)

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Photoplethysmograph

Article by jekky

(721, 'Sites for measuring PPG br While pulse oximeters are a commonly used medical device the PPG derived from them is rarely displayed and is nominally only processed to determine heart rate PPGs can be obtained from transmissive absorption as at the finger tip or reflective as on the forehead br In outpatient setting pulse oximeters are commonly worn on the finger and ear However in cases of shock hypothermia etc blood flow to the periphery can be reduced resulting in a PPG without a discernible cardiac pulse In this case a PPG can be obtained from a pulse oximeter on the head with the most common sites being the ear nasal septum and forehead br PPGs can also be obtained from the vagina and esophagus br Uses br Premature Ventricular Contraction PVC can be seen in the PPG just as in the EKG and the Blood Pressure BP br Venous pulsations can be clearly seen in this PPG br Monitoring Heart Rate and Cardiac Cycle br Because the skin is so richly perfused it is relatively easy to detect the pulsatile component of the cardiac cycle The DC component of the signal is attributable to the bulk absorption of the skin tissue while the AC component is directly attributable to variation in blood volume in the skin caused by the pressure pulse of the cardiac cycle br The height of AC component of the photoplethysmogram is proportional to the pulse pressure the difference between the systolic and diastolic pressure in the arteries As seen in the figure showing Premature Ventricular Contractions PVCs the PPG pulse for the cardiac cycle with the PVC results in lower amplitude blood pressure and a PPG Ventricular Tachycardia and Ventricular Fibrillation can also be detected br Monitoring Respiration br The effects of Sodium Nitroprusside Nipride a peripheral vasodilator on the finger PPG of a sedated subject As expected the PPG amplitude increases after infusion and additionally the Respiratory Induced Variation RIV becomes enhanced br Respiration affects the cardiac cycle by varying the intrapleural pressure the pressure between the thoracic wall and the lungs Since the heart resides in the thoracic cavity between the lungs the partial pressure of inhaling and exhaling greatly influence the pressure on the vena cava and the filling of the right atrium This effect is often referred to as normal sinus arrhythmia br During inspiration intrapleural pressure decreases by up to 4 mm Hg which distends the right atrium allowing for faster filling from the vena cava increasing ventricular preload and increasing the stroke volume Conversely during expiration the heart is compressed decreasing cardiac efficiency and reducing stroke volume However the overall net effect of respiration is to act as pump for the cardiovascular system When the frequency and depth of respiration increases the venous return increases leading to increased cardiac output Shelley et al 2006 br Monitoring Depth of Anesthesia br Effects of an incision on a subject under general anesthesia on the photoplethysmograph PPG and blood pressure BP br Anesthesiologist must often judge subjectively whether a patient is sufficiently anesthetized for surgery As seen in the figure if a patient is not sufficiently anesthetized the sympathetic nervous system response to an incision can generate an immediate response in the amplitude of the PPG br Monitoring Hypo and Hyper volemia br Shamir Eidelman et al studied the interaction between inspiration and removal of 10 of a patient blood volume for blood banking before surgery Shamir Eidelman et al 1999 They found that blood loss could be detected both from the photoplethysmogram from a pulse oximeter and an arterial catheter Patients showed a decrease in the cardiac pulse amplitude caused by reduced cardiac preload during exhalation when the heart is being compressed br References br M Shamir L A Eidelman Y Floman L Kaplan and R Pi zov Pulse Oximetry Plethysmographic Waveform During Changes in Blood Volume Br J Anaesth vol 82 pp 178 181 1999 br K Shelley and S Shelley Pulse Oximeter Waveform Photoelectric Plethysmography in Clinical Monitoring Carol Lake R Hines and C Blitt Eds W B Saunders Company 2001 pp 420 428 br K H Shelley D H Jablonka A A Awad R G Stout H Rezkanna and D G Silverman What Is the Best Site for Measuring the Effect of Ventilation on the Pulse Oximeter Waveform Anesth Analg vol 103 pp 372 377 2006 br A T Reisner P A Shaltis D McCombie and H H Asada Utility of the Photoplethysmogram in Circulatory Monitoring Anesthesiology vol 108 pp 950 958 2008 br External links br A student project building a device for collecting PPGs br See also br Hemodynamics br Categories Cardiology Medical tests')

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Orignal From: Are Common Heart Skip Palpitations Dangerous?: Premature Ventricular and Atrial Contractions (PVCs and PACs)

9/01/2011

left ventricular systolic pressure and aoritic systolic pressure?

left ventricular systolic pressure and aoritic systolic pressure?
Aortic valve stenosis.

Coarctation proximal to the aortic measurement site.

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Cardiac Resynchronization Therapy and Implantable Cardiac Defibrillators in Left Ventricular Systolic Dysfunction (Evidence Report/Technology Assessment)

ventricular defibrillator - click on the image below for more information.

ventricular defibrillator

Cardiac Resynchronization Therapy and Implantable Cardiac Defibrillators in Left Ventricular Systolic Dysfunction (Evidence Report/Technology Assessment)

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Orignal From: Cardiac Resynchronization Therapy and Implantable Cardiac Defibrillators in Left Ventricular Systolic Dysfunction (Evidence Report/Technology Assessment)