Cardiac Arrhythmias 1/3 - Heart Physiology - USMLE Step 1
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Orignal From: Cardiac Arrhythmias 1/3 - Heart Physiology - USMLE Step 1
9/06/2011
Cardiac Arrhythmias 1/3 - Heart Physiology - USMLE Step 1
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
ventricular system - click on the image below for more information.
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.
http://www.aclsclass.info/certification1.html
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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)
Are Common Heart Skip Palpitations Dangerous?: Premature Ventricular and Atrial Contractions (PVCs and PACs)
pvc ventricular - click on the image below for more information.
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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Rocket Speed Training On A Budget 2.
A Speed & Agility Training Resource Guide on how to create your own speed & agility training aids, primarily out of Pvc pipe, which helps you save money & can give you more training options than traditional speed/agility tools.
Rocket Speed Training On A Budget 2.
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')
About the Author
I am China Crafts Suppliers writer, reports some information about bostitch air, cordless framing nailer.
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)
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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8/31/2011
BES FIB-EZXL3000 -inchThe Extreme Light-inch Rechargable LED Work Light
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V-Ecommerce
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How To Use An Automated External Defibrillator (AED)
Article by Marcus Pierre
An automated external defibrillator (AED) is a device the size of a laptop that is used for medical emergencies, specifically cardiac arrest or when the heart stops beating. Sometimes, when a victim is in cardiac arrest, their heart start experiencing an irregular quivering caused by chaotic electrical activity in the heart cells.
This quivering is called ventricular fibrillation or V Fib for short. V Fib is treated by shocking the heart with controlled electric shock. This works because the heart muscle contains electrical cells. The AED is used to shock the heart that is in V Fib to a normal heart rhythm.
Studies show that if an AED is used within 3-5 minutes of cardiac arrest, the victim's chance of survival increases by approximately 70%. So you want to use the AED as soon as it becomes available.
Using the AED:
Once you get the AED at the vicitm's side -
1: Turn on the AED. Do this by wither pressing the on/off button or lifting the lid of the unit.
2: Follow the prompts exactly as directed. The device will instruct you to place the electrode pads on the bare skin of the victim. One of the pads are to be placed on the right upper chest of the victim, while the second pad is to be placed just under the left chest.
3: Once the pads are placed on the bare chese of the victim, you may be required to insert the pad connector to the AED. Some AEDs already have the pads preconnected to them.
4: Next you must make sure that no one (including yourself) is touching the victim. The machine will prompt that it is "analyzing." During the analysis, all CPR efforts must be paused in order for the AED to evaluate if the victim's heart is experiencing V Fib and can therefore be treated with a shock. This is one of the 2 time you must "clear" the victim of all bystander contact.
5: If the AED prompts that a shock is indicated, then you must "clear" the victim a second time ensuring that you or no bystanders are not in contact with the victim. If someone is touching the victim while the AED is delivering the shock, the bystander can experience a shock as well which can even render them unconscious. Once you see that victim is "clear," you must then press the "shock" button to deliver a shock. Fully automated AEDs will deliver the shock automatically.
6: Immediately after administering the shock, the defibrillator will instruct you to resume CPR. You must not remove the pads or turn off the unit at this time. Simply leave the pads on the victim's chest, leave the AED on and resume CPR beginning with chest compressions.Some of the new AED models have the CPR coaching feature which guides the rescuer in the CPR process.
AEDs are very simple to use as long as the instructions are followed completely. The information in this article does not substitute a CPR/AED course in which training is performed in its entirety. This information is provided solely as a reference to supplement CPR/AED training.
For more information or questions on AEDs please visit http://www.lifesaversny.com
About the Author
Marcus Pierre is a respiratory therapist, CPR instructor and AED consultant. He has worked at several hospitals in the New York area and has also trained many participants in CPR/AED & First Aid. He has serviced Regal Cinemas, the Governor's office, the Attorney General's office, DMV offices and many more NY state and personal clients. He is also the president of Lifesavers, Inc - a CPR & First Aid training company and an AED distributor. He can be contacted at http://www.lifesaversny.com
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What is 2nd degree AV block Mobitz type 1 Wenckebach?
What is 2nd degree AV block Mobitz type 1 Wenckebach?
AV block can be manifested as several different types. All of them being a conduction abnormality in your AV node. Try searching for just "Wenckebach" or "Mobitz type 1."
Ventricular bigeminy means that you have premature beats originating in the ventricles. The bigeminy part indicates that it was every other beat.
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What is the difference between the thickness of the aorta and ventricular walls?
What is the difference between the thickness of the aorta and ventricular walls?
Ventricular walls are much thicker as they have to pump blood in the arterial system, so muscle part (myocardium) is very thick..This Patient Guide is written for the loved ones of heart patients who are dealing with the short-term stress that comes with a test, procedure or recent diagnosis of heart disease. It explains why support is so important to a loved one with heart disease. It also offers practical strategies on how to support a loved one while also taking care of yourself.
Ventricular wall motion: International symposium, Lausanne, 1982
ventricular walls - click on the image below for more information.
ventricular walls
Ventricular wall motion: International symposium, Lausanne, 1982
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8/26/2011
Could this patient have survived?
Could this patient have survived?
I don't think the person would've
survived , and ididn'tt no any of the words you just mentionedd there lol x :L:LxxxxxxDepends. How long was the person in cardiac arrest before CPR was started? Was this a hypothermia situation? Or a drowning? Drowning, probably not. Hypothermia, slightly higher chances, but still probably not. Chances of surviving cardiac arrest are very slim. And when you say no reaction to defib, I'm assuming they remained in V fib? If they did, what about amio/lido?
If you can add extra details, I could give you a better idea, but I'd still ultimately say they probably would not have survived due to the fact that so few people survive.
I'm assuming finresus is "fin" meaning end and resus being short for resusciation. But I've never heard that before.It sounds like they did everything they could.
Orignal From: Could this patient have survived?
frequent premature ventricular contractions in a bigeminy pattern?
frequent premature ventricular contractions in a bigeminy pattern?
id ask your doctorHow did you have an ECG (EKG) and not get a doctor to tell you what it means? If you have had any chest pains, tell your doctor. You are not too young. Look at the news about athletes with heart trouble.
Premature Ventricular Contractions (PVC) like bigeminy are common, and not harmful alone if they are not long lasting or frequent.
I can get one or two strong heart thump-a-thumps when I turn my head after sitting still a long time, and they go away when I start moving and get my heart pumping. I do not have chest pain though, so ask your doctor your questions.
Somebody else had a PVC question answered here, check it out:
http://answers.yahoo.com/question/index?qid=20060703180529AAhA9SU
Ventricular bigeminy Anterior St elevation MI
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Heart Physiology (Ventricular filling: part 1/6)
Heart Physiology (Ventricular filling: part 1/6)
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Ventricular Relaxation Blood Filling Stretched Canvas Poster Print, 18x24
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Orignal From: Heart Physiology (Ventricular filling: part 1/6)
Help on overcoming Premature Ventricular Contractions?
Help on overcoming Premature Ventricular Contractions?
I also get skipped beats several times a day for years now. It used to really bother me, but now I've kind of gotten used to it. I don't know about the exercise part of your question, but would be curious to know as I'm thinking of joining the gym. I also take antidepressants called Efexor XR and am pretty sure this has only been happening since I've been taking them. What type do you take? and I wonder if there could be a link therea sideeffect of many antideppressants is that your heart skips a beat thatswhy i stopped taking them.I dont know if you had the symptom already before taking the medication......did you hear of arrhythmia, an abnormal heart rhythm.AF Atrial fibrillation is an irregular irregular heartbeat it must be thoroughly evaluated to determine the treatment,insist on it.an overactive thyroid gland can be the cause of it.important is the longer the arrhythmia is allowed to continue,the less likely it is to be succesfuly converted to regular rhythm.
WHAT to insist on if you have Atrial fibration
It is a common disturbance of cardiac rhythm in which yhe upper chambers of the heart, the atria,beat rapidly and irregular.The ventricles,the main pumps of the heart,receive too many of these impulses and beat too quickly.This may weaken the heart and cause it to fail.Blood within these quivering atria may stagnate and form clots which if expelle
from the heart , can result in a stroke. get an echocardiogram.Do you see a cardiologist specialized in rhythm disorders?When Atrial fib becomes chronic , the blood must be thinned to prevent clots.It is possible to lead a virtualy normal life as long as the rate at which the ventricles respond to the rapidly beating atria is controlled.SO exclude this disease by seeing a specialist .anything that causes a release of adrenaline into the blood can increase the likelihood of PVCs so exercise would do this. so would anxiety and it sounds like you are obsessing about this a little. although pretty harmless, PVCs can feel pretty scary so i can see why you are worried. speak to the Dr about this because often a small dose of beta blocker helps. alcohol even in small amounts can also increase PVCs and make them feel scarier than usual.pvc are not the same as atrial fibrillation or flutter
in pvc, the stimulus is coming from the ventricles and not the atria
pvcs are associated with low pottasium-eat more oranges bananas avocados but with hctz-you should have potassium supplements because you are peeing it out
reduce stress, reduce caffeine and if you feel anything worse go see your doctor because it can progress into something worse
list of potassium rich foods
whfoods.org/genpage.php?tname=nutrient&dbid=90
Determination of Premature Ventricular Contraction Beat in ECG signal: of heart with automated methods using the Empirical Mode Decomposition (EMD), ... transform and correlation coefficient
ventricular premature beat - click on the image below for more information.
ventricular premature beat
The electrocardiographic (ECG) signal represents the electrical activity of the heart. Any cardiac dysfunction associated with excitation from ectopic centers anywhere in the myocardium leads to premature contractions (with supraventricular (atrial) or ventricular origin), which alter the RR interval duration and/or the QRS waveform. My research has been conducted to seek a solution to this problem. In this book, I have researched on PVC beat characteristics and proposed two detection algorithm
Determination of Premature Ventricular Contraction Beat in ECG signal: of heart with automated methods using the Empirical Mode Decomposition (EMD), ... transform and correlation coefficient
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236_Team_HeartBit
236_Team_HeartBit
Problem Patients, who have survived cardiac arrest, ventricular tachycardia or cardiac syncope, have an increased risk of sudden cardiac death. Many of those patients are normally living at home without any kind of arrhythmia monitoring system or cardiac alarm solutions. In the United States alone, over 1.1 million individuals experience a heart attack each year. Approximately 540000 are fatal, and about half of these deaths occur within acute care settings. Even in the acute care environment up to half of fatal cardiac events are unwitnessed. Solution 'Non-Stop' is an integrated real-time monitoring system with an emphasis on early detection and treatment of life threatening events. It is a measurement and evaluation system of vital parameters focusing on the ongoing measurement of direct and indirect parameters of the cardiovascular system. The system is intended for high risk patients. With a wireless and wearable ECG (Electrocardiograph), the system continually logging heart rate data and providing detection of life threatening events and pass along these data to a respondent who is capable of treatment of such events. On the detection of arrhythmia situations, the system is possible to provide quick alarms to a central safety alarm system and thereby take necessary action for an emergency rescue.
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8/24/2011
Critical Care Ultrasonography (with DVD)
Critical Care Ultrasonography (with DVD)
left ventricular preload - click on the image below for more information.
left ventricular preload
A complete, hands-on guide to successful image acquisition and interpretation at the bedside "The real strength of this textbook is its clinical focus. The editors are to be complimented on keeping a consistent structure within each chapter, beginning with basic physical principles, practical "knobology," scanning tips, key findings, pitfalls and limitations, and how the key findings relate to bedside patho-physiology and decision-making. Thus, the authors have succeeded in providing
Critical Care Ultrasonography (with DVD)
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Slide2Call - Stop Accidental Dialing
Slide2Call is a mobile application that prevents you from making unwanted accidental calls. Each attempt to make a call is interrupted by a ready-to-confirm slider. To proceed with the call, simply move the slider from left to right. For Windows Mobile!
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Angiotensin
Article by jekky
Precursor, and types of angiotensin AngiotensinogenAngiotensinogen is an -2-globulin that is produced constitutively and released into the circulation mainly by the liver. It is a member of the serpin family, although it is not known to inhibit other enzymes, unlike most serpins. Plasma angiotensinogen levels are increased by plasma corticosteroid, estrogen, thyroid hormone, and angiotensin II levels.Angiotensinogen is also known as renin substrate.Human angiotensinogen is 452 amino acids long, but other species have angiotensinogen of varying sizes. The first 12 amino acids are the most important for activity.Asp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-Leu-Val-Ile Angiotensin IAsp-Arg-Val-Tyr-Ile-His-Pro-Phe-His-LeuRenin-angiotensin-aldosterone systemAngiotensin I (CAS# 11128-99-7) is formed by the action of renin on angiotensinogen. Renin is produced in the kidneys in response to both decreased intra-renal blood pressure at the juxtaglomerular cells, or decreased delivery of Na+ and Cl- to the macula densa. If more Na+ is sensed, renin release is decreased.Renin cleaves the peptide bond between the leucine (Leu) and valine (Val) residues on angiotensinogen, creating the ten amino acid peptide (des-Asp) angiotensin I (CAS# 9041-90-1).Angiotensin I appears to have no biological activity and exists solely as a precursor to angiotensin 2. Angiotensin IIAsp-Arg-Val-Tyr-Ile-His-Pro-PheAngiotensin I is converted to angiotensin II through removal of two C-terminal residues by the enzyme angiotensin-converting enzyme (ACE, or kinase), which is found predominantly in the capillaries of the lung. ACE is actually found all over the body, but has its highest density in the lung due to the high density of capillary beds there. Angiotensin II acts as an endocrine, autocrine/paracrine, and intracrine hormone.ACE is a target for inactivation by ACE inhibitor drugs, which decrease the rate of angiotensin II production. Angiotensin II increases blood pressure by stimulating the Gq protein in vascular smooth muscle cells (which in turn activates contraction by an IP3-dependent mechanism). ACE inhibitor drugs are major drugs against hypertension.Other cleavage products of ACE, 7 or 9 amino acids long, are also known; they have differential affinity for angiotensin receptors, although their exact role is still unclear. The action of angiotensin II itself is targeted by angiotensin II receptor antagonists, which directly block angiotensin II AT1 receptors.Angiotensin II is degraded to angiotensin III by angiotensinases that are located in red blood cells and the vascular beds of most tissues. It has a half-life in circulation of around 30 seconds, whereas, in tissue, it may be as long as 1530 minutes. Angiotensin IIIAsp | Arg-Val-Tyr-Ile-His-Pro-PheAngiotensin III has 40% of the pressor activity of Angiotensin II, but 100% of the aldosterone-producing activity. Angiotensin IVArg | Val-Tyr-Ile-His-Pro-PheAngiotensin IV is a hexapeptide that, like angiotensin III, has some lesser activity. EffectsSee also Renin-angiotensin_system#EffectsAngiotensins II, III & IV have a number of effects throughout the body: Cardiovascular effectsThey are potent direct vasoconstrictors, constricting arteries and veins and increasing blood pressure.Angiotensin II has prothrombotic potential through adhesion and aggregation of platelets and production of PAI-1 and PAI-2.When cardiac cell growth is stimulated, a local (autocrine-paracrine) renin-angiotensin system is activated in the cardiac myocyte, which stimulates cardiac cell growth through Protein Kinase C. The same system can be activated in smooth muscle cells in conditions of hypertension, atherosclerosis, or endothelial damage. Angiotensin II is the most important Gq stimulator of the heart during hypertrophy, compared to endothelin-1 and A1 adrenoreceptors. Neural effectsAngiotensin III increases thirst sensation (dipsogen) through the subfornical organ (SFO) of the brain, decreases the response of the baroreceptor reflex, and increases the desire for salt. It increases secretion of ADH in the posterior pituitary and secretion of ACTH in the anterior pituitary. It also potentiates the release of norepinephrine by direct action on postganglionic sympathetic fibers. Adrenal effectsAngiotensin II acts on the adrenal cortex, causing it to release aldosterone, a hormone that causes the kidneys to retain sodium and lose potassium. Elevated plasma angiotensin II levels are responsible for the elevated aldosterone levels present during the luteal phase of the menstrual cycle. Renal effectsAngiotensin II has a direct effect on the proximal tubules to increase Na+ reabsorption. It has a complex and variable effect on glomerular filtration and renal blood flow depending on the setting. Increases in systemic blood pressure will maintain renal perfusion pressure, however constriction of the afferent and efferent glomerular arterioles will tend to restrict renal blood flow. The effect on the efferent arteriolar resistance is, however, markedly greater, in part due to its smaller basal diameter; this tends to increase glomerular capillary hydrostatic pressure and maintain glomerular filtration rate. A number of other mechanisms can affect renal blood flow and GFR. High concentrations of Angiotensin II can constrict the glomerular mesangium reducing the area for glomerular filtration. Angiotensin II as a sensitizer to tubuloglomerular feedback preventing an excessive rise in GFR. Angiotensin II causes the local release of prostaglandins, which, in turn, antagonize renal vasoconstriction. The net effect of these competing mechanisms on glomerular filtration will vary with the physiological and pharmacological environment.Renal effects of Angiotensin IITargetActionMechanismRenal artery &afferent arteriolesvasoconstrictionVDCCs Ca2+ influxefferent arteriolevasoconstriction(probably) activate Angiotensin receptor 1 Activation of Gq LC activity P3 and DAG activation of IP3 receptor in SR ntracellular Ca2+mesangial cellscontraction iltration areaactivation of Gq LC activity P3 and DAG activation of IP3 receptor in SR ntracellular Ca2+VDCCs Ca2+ influxTubuloglomerular feedbackIncreased sensitivityIncrease in afferent arteriole responsiveness to signals from macula densamedullary blood flowReduction See alsoACE inhibitorAngiotensin receptorAngiotensin II receptor antagonist References^ Basso N, Terragno NA (December 2001). "History about the discovery of the renin-angiotensin system". Hypertension 38 (6): 12469. doi:10.1161/hy1201.101214. PMID 11751697. http://hyper.ahajournals.org/cgi/pmidlookup?view=long&pmid=11751697. ^ NCBI HomePage^ Physiology at MCG 7/7ch09/7ch09p16^ Skurk T, Lee YM, Hauner H (May 2001). "Angiotensin II and its metabolites stimulate PAI-1 protein release from human adipocytes in primary culture". Hypertension 37 (5): 133640. PMID 11358950. http://hyper.ahajournals.org/cgi/pmidlookup?view=long&pmid=11358950. ^ Gesualdo L, Ranieri E, Monno R, et al. (August 1999). "Angiotensin IV stimulates plasminogen activator inhibitor-1 expression in proximal tubular epithelial cells". Kidney Int. 56 (2): 46170. doi:10.1046/j.1523-1755.1999.00578.x. PMID 10432384. ^ Unless else specified in table, then ref is: Walter F., PhD. Boron (2005). Medical Physiology: A Cellular And Molecular Approaoch. Elsevier/Saunders. ISBN 1-4160-2328-3. Page 771 Further readingde Gasparo M, Catt KJ, Inagami T, "et al." (2000). "International union of pharmacology. XXIII. The angiotensin II receptors". Parmacol Rev. 52: 415472. PMID 10977869. Brenner & Rector's The Kidney, 7th ed., Saunders, 2004.Mosby's Medical Dictionary, 3rd Ed., CV Mosby Company, 1990.Review of Medical Physiology, 20th Ed., William F. Ganong, McGraw-Hill, 2001.Clinical Physiology of Acid-Base and Electrolyte Disorders, 5th ed., Burton David Rose & Theodore W. Post McGraw-Hill, 2001Lees KR, MacFadyen RJ, Doig JK, Reid JL (1993). "Role of angiotensin in the extravascular system". Journal of human hypertension 7 Suppl 2: S712. PMID 8230088. Weir MR, Dzau VJ (2000). "The renin-angiotensin-aldosterone system: a specific target for hypertension management". Am. J. Hypertens. 12 (12 Pt 3): 205S213S. doi:10.1016/S0895-7061(99)00103-X. PMID 10619573. Berry C, Touyz R, Dominiczak AF, et al. (2002). "Angiotensin receptors: signaling, vascular pathophysiology, and interactions with ceramide". Am. J. Physiol. Heart Circ. Physiol. 281 (6): H233765. PMID 11709400. Sernia C (2002). "A critical appraisal of the intrinsic pancreatic angiotensin-generating system". JOP 2 (1): 505. PMID 11862023. Varagic J, Frohlich ED (2003). "Local cardiac renin-angiotensin system: hypertension and cardiac failure". J. Mol. Cell. Cardiol. 34 (11): 143542. doi:10.1006/jmcc.2002.2075. PMID 12431442. Wolf G (2006). "Role of reactive oxygen species in angiotensin II-mediated renal growth, differentiation, and apoptosis". Antioxid. Redox Signal. 7 (9-10): 133745. doi:10.1089/ars.2005.7.1337. PMID 16115039. Cazaubon S, Deshayes F, Couraud PO, Nahmias C (2006). "[Endothelin-1, angiotensin II and cancer]". Med Sci (Paris) 22 (4): 41622. PMID 16597412. Ariza AC, Bobadilla NA, Halhali A (2007). "[Endothelin 1 and angiotensin II in preeeclampsia]". Rev. Invest. Clin. 59 (1): 4856. PMID 17569300. ... External linksMeSH Angiotensinsv d eCardiovascular system, physiology: cardiovascular physiologyHeartVolumesStroke volume = End-diastolic volume End-systolic volumeCardiac output = Heart rate Stroke volumeAfterload PreloadFrank-Starling law of the heart Cardiac function curve Venous return curveAortic valve area calculation Ejection fraction Cardiac indexInteraction diagramsCardiac cycle Wiggers diagram Pressure volume diagramTropismChronotropic (Heart rate) Dromotropic (Conduction velocity) Inotropic (Contractility) Batmotropic (Excitability) Lusitropic (Relaxation)Conduction system /Cardiac electrophysiologyCardiac action potential (Atrial action potential, Ventricular action potential) Effective refractory period Pacemaker potential EKG (P wave, PR interval, QRS complex, QT interval, ST segment, T wave, U wave) Hexaxial reference systemChamber pressureCentral venous pressure/right atrial pressure Right ventricular pressure Pulmonary artery pressure Pulmonary wedge pressure/left atrial pressure Left ventricular pressure Aortic pressureOtherVentricular remodelingVascular system/HemodynamicsBlood flowCompliance Vascular resistance (Total peripheral resistance) Pulse PerfusionBlood pressurePulse pressure (Systolic - Diastolic) Mean arterial pressureJugular venous pressurePortal venous pressureRegulation of BPBaroreflex Kinin-kallikrein system Renin-angiotensin system Vasoconstrictors/Vasodilators Autoregulation (Myogenic mechanism, Tubuloglomerular feedback) Paraganglia (Aortic body, Carotid body, Glomus cell)heart navs: anat/physio/dev, noncongen/congen/neoplasia, symptoms+signs/eponymous, procvascular navs: anat/physio/dev, noncongen/systemic vasculitis/congen/neoplasia, symptoms+signs/eponymous, procv d ePeptides: neuropeptidesHypothalamicSomatostatin CRH GnRH GHRH Orexins TRH POMC (ACTH MSH Lipotropin)Gastrointestinal hormonesCholecystokinin Gastric inhibitory polypeptide Gastrin Motilin Secretin Vasoactive intestinal peptideOther hormonesCalcitonin Oxytocin VasopressinOther neuropeptidesAngiotensin Bombesin Calcitonin gene-related peptide Carnosine Cocaine and amphetamine regulated transcript Delta sleep-inducing peptide FMRFamide Galanin Galanin-like peptide Gastrin releasing peptide Kinins (Bradykinin Tachykinins) Neuropeptide S Neuropeptide Y Neurophysins Neurotensin Pancreatic polypeptide Pituitary adenylate cyclase activating peptide VGFNeuromedinsB N S UOpioid peptidesDynorphin Endomorphin Endorphin Enkephalin Nociceptin Opiorphinv d eAutacoidsKininsKininogen (HMWK, LMWK) Bradykinin Kallidin Tachykinins Urotensin-IIOthersAngiotensin Eicosanoid Histamine Platelet-activating factor Serotonin Categories: Human proteins | Peptide hormones | Cardiovascular system | Endocrinology | Physiology
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I am an expert from Components Electronic suppliers, usually analyzes all kind of industries situation, such as airsoft thompson, skin care private label.
Orignal From: Critical Care Ultrasonography (with DVD)
During isovolumetric ventricular contraction which do the following do: increase, decrease, or do not change?
During isovolumetric ventricular contraction which do the following do: increase, decrease, or do not change?
There are 3 phases in the cardiac cycle:
the cardiac cycle: 1) Ventricular filling: mid-to-late diastole; 2) Ventricular systole; and 3) Isovolumetric relaxation: early diastole. In phase two, ventricular systole, the atria relax and the ventricles begin contracting. Their walls close in on the blood in their chambers, and ventricular pressure rises closing the atriaventricular (AV) valve. Because, for a split second, the ventricles are completely closed chambers and blood volume in the chambers remain constant, it is called the isovolumetric contraction phase.
Good luck.Have a good one always........
Orignal From: During isovolumetric ventricular contraction which do the following do: increase, decrease, or do not change?
8/23/2011
CPAP reversed left ventricular, atrial remodeling.(CARDIOVASCULAR MEDICINE)(continuous positive airway pressure)(Clinical report): An article from: Family Practice News
CPAP reversed left ventricular, atrial remodeling.(CARDIOVASCULAR MEDICINE)(continuous positive airway pressure)(Clinical report): An article from: Family Practice News
left ventricular pressure - click on the image below for more information.
left ventricular pressure
This digital document is an article from Family Practice News, published by International Medical News Group on July 1, 2010. The length of the article is 492 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available immediately after purchase. You can view it with any web browser.
Citation Details
Title: CPAP reversed left ventricular, atrial remodeling.(CARDIOVASCULAR MEDICINE)(continuous positive airway pressure)
CPAP reversed left ventricular, atrial remodeling.(CARDIOVASCULAR MEDICINE)(continuous positive airway pressure)(Clinical report): An article from: Family Practice News
Click on the button for more left ventricular pressure information and reviews.
What Is High Blood Pressure?
Article by Clive Harman
Orignal From: CPAP reversed left ventricular, atrial remodeling.(CARDIOVASCULAR MEDICINE)(continuous positive airway pressure)(Clinical report): An article from: Family Practice News
My Normal Heartbeat
My Normal Heartbeat
I have cardiac arrhythmia, this is a recording of my heartbeat when I am well-controlled on medication. I forgot to add in the slide, it is best heard with headphones. The rate in this one is 70-80 which is my normal resting rate. I think there may be one or two PVC's, but I am not sure, it could be my microphone.
Video Rating: 5 / 5
Sudden Cardiac Arrest - Precautionary measures and alternative treatment
Video Rating: 5 / 5
Orignal From: My Normal Heartbeat
A rare case of tako-tsubo cardiomyopathy complicated by a left ventricular thrombus.(Case Report): An article from: Southern Medical Journal
A rare case of tako-tsubo cardiomyopathy complicated by a left ventricular thrombus.(Case Report): An article from: Southern Medical Journal
left ventricular thrombus - click on the image below for more information.
left ventricular thrombus
This digital document is an article from Southern Medical Journal, published by Thomson Gale on January 1, 2006. The length of the article is 1943 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available in your Amazon.com Digital Locker immediately after purchase. You can view it with any web browser.
Citation Details
Title: A rare case of tako-tsubo cardiomyopathy complicated by a left ventricular thrombus.(Case
A rare case of tako-tsubo cardiomyopathy complicated by a left ventricular thrombus.(Case Report): An article from: Southern Medical Journal
Click on the button for more left ventricular thrombus information and reviews.
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Who Should Have An Echocardiography
Article by Armughan Riaz
An Echocardiography is actually the Ultrasound of Heart, this ultrasound produces sound waves and one can have moving picture of heart. This procedure does not involve any radiations and it gives more detail than X-ray. It is a good diagnostic tool for Valvular heart diseases, evaluating pumping function of heart, i.e ejection fraction, in heart attack patients. It is also a good screening test for certain heart disease. However, there are some situations or diseases that one should have an echocardiography test.
Following diseased patients must have an echocardiography. These are the situations in which an echo may influence the clinical management of a patient.
Assessment of valve function, e.g systolic or diastolic murmursAssessment of left ventricular function, systolic diastolic and regional wall motions, e.g suspected heart failure in a patient with breathlessness, or preoperative assessment.Suspected EndocarditisSuspected MyocarditisCardiac TemponadePericardial Disease (e.g Pericarditis) or pericardial effusion, especially if clinical evidence of temponadeComplications of myocardial Infarction, eg MR VSD or pericardial effusion.Suspicion of intracardiac masses- tumour or thrombusCardiac chamber size e.g Left atrial size in atrial fibrillation (AF), Cardiomegaly in chest X-ray.Assessment of artificial valve function.Arrhythmias, e.g Atrial fibrillation, ventricular techycardia (VT)Assessment of right ventricle and right heart Estimation of intracardiac and vascular pressures, e.g pulmonary artery systolic pressures in lung disease and suspected pulmonary hypertensionTo find out cardiac source of embolism in stroke and transient ischaemic attack patients.Exclusion of left ventricular hypertrophy in hypertentionAssessment of congenital heart diseases.These abnormalities are just few and most common that an echo can reveal. For details you may contact your doctor.
What can I expect during an echocardiogram?Often when you visit a Cardiologist, your doctor suggests you for echocardiography of your heart. It is basically the ultrasound of Heart to diagnose various diseases of heart. With the help of sound waves moving picture of heart can be taken.
Echo is a painless and simple procedure without involvement of any radiations. There are no known hazards or risks associated with echocardiography. When you are going to echo room, you will be asked to lie down on a bed and disrobe from the waist up. Doctor or echocardiographer will place electrode on your chest to record ECG during echocardiography. Small amount of gel is applied on your chest and then a small transducer will be placed near the sternum on your chest. Transducer produces sound waves towards the heart.
Echocardiographer may apply some pressure during echo on your chest with transducer. You may be asked to turn your side to left or right depending upon your technician position. You may be asked to hold your breath to take high quality pictures. Then technician will move transducer to different parts of chest to take picture of heart from different angles. Sometimes a dye may be injected before taking echo, as occasionally lungs ribs body tissue prevents sound waves to reach heart muscles. If your heart beat is too fast, then echo may give false result, so echo is avoided in fast tachycardia. A typical echo is performed in about 30-45 minutes. If you have a lung disease, obesity, restlessness or breathlessness, may result in longer test duration. During test, printed pictures are taken by technician from echo machine and later examined by a cardiologist.
Who should have an Echocardiography? Article written by Dr. Armughan Riaz M.B.B.S Dip Card. To Know more about High Blood Pressureand cardiovascular diseases please visit our site.
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Dr.Armughan maintaining site High Blood Pressure Symptoms Treatment
Orignal From: A rare case of tako-tsubo cardiomyopathy complicated by a left ventricular thrombus.(Case Report): An article from: Southern Medical Journal
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