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Vascular Surgery/ abdmonal aortic blockage


Expert: Lauri Ordway - 9/19/2000

Question I am scheduled next week for this surgery. My Doctor seems hopeful it can be balooned rather than open surgery. I can only find info on abdmonal anyorism. My legs are affected very bad. Extremely hard to walk. Please set me straight. I have just underwent right caritod, which was very blocked and will after the abdmonal have the left carotid done. Yee gads what a mess......very much in my family history. Thank You Get the answer below

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Answer There are two main reasons that the abdominal aorta requires surgery. The first is for an abdominal aortic aneurysm (AAA), which is an abnormal ballooning of the aorta that left untreated can rupture causing one to bleed to death. The second reason for surgery is aortic occlusive disease (blockage) that left untreated can sometimes lead to gangrene of the legs and amputation. Severe foot pain, non-healing wounds on the feet, and severe leg pain with walking are symptoms of occlusive disease. When the blockage is severe, intervention is needed to prevent the need for amputation. Angiography provides a road map of your arteries and tells us where to bypass. WHY are they doing the carotid AFTER the belly? this is just the opposite of what w would do...did they say why? Pre-operatively, other tests may be required to see if your heart, lung, and kidneys are strong enough to withstand the stress of surgery. When the final decision is made for surgery, you must take a bowel prep to clean out your intestines. You will be admitted the morning of surgery and stay in the hospital for 7-10 days afterwards in order to recover.

A large midline incision is made and the abdominal aorta is either replaced or bypassed with plastic tubing. Sometimes, incisions in the upper thigh (groin) are required. You will be monitored in the ICU immediately post-op and then transferred to the floor when stable. Risks of the procedure are rare but include; bleeding, infection, anesthesia, damage to internal organs, amputation, stroke, heart attack, and death. After surgery, YOU can reduce your risk of further problems by taking your medications and eating a low fat, low sodium diet. Don't forget, the most important thing that you can do is to STOP SMOKING! About the balloons, I am not sure if you mean an angioplasty- this the surgeon should know once he sees the angiogram (whether it can be plasties) or if you mean the newer endoluminal technique for aortic repair. this is still very new and the long term data is not out. traditional aortic bypass will last 20 years...we do not know how long the stent grafts will last, initial symptom resolution is good and this is confirmed with comparison of pre- and post-procedural ABI's. The long term patency rates and symptom control will need to be subjected to ongoing scrutiny.

Angina pectoris, commonly known as angina, is severe chest pain[1] due to ischemia (a lack of blood, hence a lack of oxygen supply) of the heart muscle, generally due to obstruction or spasm of the coronary arteries (the heart's blood vessels). Coronary artery disease, the main cause of angina, is due to atherosclerosis of the cardiac arteries. The term derives from the Latin angina ("infection of the ankhone ("strangling"), and the Latin pectus ("chest"), and can therefore be translated as "a strangling throat") from the Greek feeling in the chest". There is a weak relationship between severity of pain and degree of oxygen deprivation in the heart muscle (i.e., there can be severe pain with little or no risk of a heart attack, and a heart attack can occur without pain). Worsening ("crescendo") angina attacks, sudden-onset angina at rest, and angina lasting more than 15 minutes are symptoms of unstable angina (usually grouped with similar conditions as the acute coronary syndrome). As these may herald myocardial infarction (a heart attack), they require urgent medical attention and are generally treated as a presumed heart attack.



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1 Classification o 1.1 Stable angina o 1.2 Unstable angina o 1.3 Microvascular angina 2 Signs and symptoms 3 Cause o 3.1 Major risk factors o 3.2 Smoking o 3.3 Other medical problems o 3.4 Other cardiac problems 4 Pathophysiology 5 Diagnosis 6 Treatment o 6.1 Suspected angina 7 Epidemiology 8 History 9 See also 10 References 11 Major studies 12 External links

[edit] Classification
[edit] Stable angina
Also known as effort angina, this refers to the more common understanding of angina related to myocardial ischemia. Typical presentations of stable angina is that of chest discomfort and associated symptoms precipitated by some activity (running, walking, etc.) with minimal or non-existent symptoms at rest. Symptoms typically abate several minutes following cessation of precipitating activities and resume when activity resumes. In this way, stable angina may be thought of as being similar to claudication symptoms.

[edit] Unstable angina

Unstable angina (UA) (also "crescendo angina;" this is a form of acute coronary syndrome) is defined as angina pectoris that changes or worsens.[1] It has at least one of these three features:
1. it occurs at rest (or with minimal exertion), usually lasting >10 min; 2. it is severe and of new onset (i.e., within the prior 4 6 weeks); and/or 3. it occurs with a crescendo pattern (i.e., distinctly more severe, prolonged, or frequent than previously).

UA may occur unpredictably at rest which may be a serious indicator of an impending heart attack. What differentiates stable angina from unstable angina (other than symptoms) is the pathophysiology of the atherosclerosis. The pathophysiology of unstable angina is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms or coronary thrombosis.[2][3] The process starts with atherosclerosis, and when inflamed leads to an active plaque, which undergoes thrombosis and results in acute ischemia, which finally results in cell necrosis after calcium entry.[4] Studies show that 64% of all unstable anginas occur between 10 PM and 8 AM when patients are at rest.[5][6] In stable angina, the developing atheroma is protected with a fibrous cap. This cap (atherosclerotic plaque) may rupture in unstable angina, allowing blood clots to precipitate and further decrease the lumen of the coronary vessel. This explains why an unstable angina appears to be independent of activity.

[edit] Microvascular angina

Microvascular Angina or Angina Syndrome X is characterized by angina-like chest pain, but have different causes.The cause of Microvascular Angina is unknown, but it appears to be the result of poor function in the tiny blood vessels of the heart, arms and legs[7]. Since microvascular angina isn't characterized by arterial blockages, it's harder to recognize and diagnose, but its prognosis is excellent. [8] [9] [10]

[edit] Signs and symptoms

Most patients with angina complain of chest discomfort rather than actual pain: the discomfort is usually described as a pressure, heaviness, tightness, squeezing, burning, or choking sensation. Apart from chest discomfort, anginal pains may also be experienced in

the epigastrium (upper central abdomen), back, neck area, jaw, or shoulders. This is explained by the concept of referred pain, and is due to the spinal level that receives visceral sensation from the heart simultaneously receiving cutaneous sensation from parts of the skin specified by that spinal nerve's dermatome, without an ability to discriminate the two. Typical locations for referred pain are arms (often inner left arm), shoulders, and neck into the jaw. Angina is typically precipitated by exertion or emotional stress. It is exacerbated by having a full stomach and by cold temperatures. Pain may be accompanied by breathlessness, sweating and nausea in some cases. In this case, the pulse rate and the blood pressure increases. The pain usually lasts for about 3 to 5 minutes but the symptoms actually starts 15 to 20 minutes before the cardiac arrest and the pain is relieved by rest or specific anti-angina medication. Chest pain lasting only a few seconds is normally not angina. Myocardial ischemia comes about when the myocardia (the heart muscles) receive insufficient blood and oxygen to function normally either because of increased oxygen demand by the myocardia or by decreased supply to the myocardia. This inadequate perfusion of blood and the resulting reduced delivery of oxygen and nutrients is directly correlated to blocked or narrowed blood vessels. Some experience "autonomic symptoms" (related to increased activity of the autonomic nervous system) such as nausea, vomiting and pallor. Major risk factors for angina include cigarette smoking, diabetes, high cholesterol, high blood pressure, sedentary lifestyle and family history of premature heart disease. A variant form of angina (Prinzmetal's angina) occurs in patients with normal coronary arteries or insignificant atherosclerosis. It is thought to be caused by spasms of the artery. It occurs more in younger women.

[edit] Cause
[edit] Major risk factors

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Age ( 55 yo for men, 65 for women) Cigarette smoking Diabetes mellitus (DM) Dyslipidemia Family History of premature Cardiovascular Disease(men <55 yo, female <65)

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Hypertension (HTN) Kidney disease (microalbuminuria or GFR<60 mL/min) Obesity (BMI 30 kg/m2) Physical inactivity

Conditions that exacerbate or provoke angina


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Medications vasodilators excessive thyroid replacement vasoconstrictors polycythemia which thickens the blood causing it to slow its flow through the heart muscle

[edit] Smoking
One study found that smokers with coronary artery disease had a significantly increased level of sympathetic nerve activity when compared to those without. This is in addition to increases in blood pressure, heart rate and peripheral vascular resistance associated with nicotine which may lead to recurrent angina attacks. Additionally, CDC reports that the risk of CHD, stroke, and PVD is reduced within 12 years of smoking cessation. In another study, it was found that after one year, the prevalence of angina in smoking men under 60 after an initial attack was 40% less in those who had quit smoking compared to those who continued. Studies have found that there are short term and long term benefits to smoking cessation.[13] [14] [15] [16]

[edit] Other medical problems

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profound anemia uncontrolled HTN hyperthyroidism hypoxemia

[edit] Other cardiac problems



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bradyarrhythmia valvular heart disease hypertrophic cardiomyopathy [17][18]

Myocardial ischemia can result from:

1. a reduction of blood flow to the heart that can be caused by stenosis, spasm, or acute occlusion (by an embolus) of the heart's arteries. 2. resistance of the blood vessels. This can be caused by narrowing of the blood vessels; a decrease in radius,[19]. Blood flow is inversely proportional to the radius of the artery to the fourth power [20] 3. reduced oxygen-carrying capacity of the blood, due to several factors such as a decrease in oxygen tension and hemoglobin concentration [21]. This decreases the ability to of hemoglobin to carry oxygen to myocardial tissue [22].

Atherosclerosis is the most common cause of stenosis (narrowing of the blood vessels) of the heart's arteries and, hence, angina pectoris. Some people with chest pain have normal or minimal narrowing of heart arteries; in these patients, vasospasm is a more likely cause for the pain, sometimes in the context of Prinzmetal's angina and syndrome X. Myocardial ischemia also can be the result of factors affecting blood composition, such as reduced oxygen-carrying capacity of blood, as seen with severe anemia (low number of red blood cells), or long-term smoking.

[edit] Pathophysiology
Angina results when there is an imbalance between the heart's oxygen demand and supply. This imbalance can result from an increase in demand (e.g. during exercise) without a proportional increase in supply (e.g. due to obstruction or atherosclerosis of the coronary arteries).

[edit] Diagnosis
Suspect angina in people presenting with tight, dull, or heavy chest discomfort which is [23]: 1. Retrosternal or left-sided, radiating to the left arm, neck, jaw, or back. 2. Associated with exertion or emotional stress and relieved within several minutes by rest. 3. Precipitated by cold weather or a meal.

Some people present with atypical symptoms, including breathlessness, nausea, or epigastric discomfort or burping. These atypical symptoms are particularly likely in older people, women, and those with diabetes.[23] Angina pain is not usually sharp or stabbing or influenced by respiration. Antacids and simple analgesia do not usually relieve the pain. If chest discomfort (of whatever site) is precipitated by exertion, relieved by rest, and relieved by glyceryl trinitrate, the likelihood of angina is increased.[23] In angina patients who are momentarily not feeling any one chest pain, an electrocardiogram (ECG) is typically normal, unless there have been other cardiac problems in the past. During periods of pain, depression or elevation of the ST segment may be observed. To elicit these changes, an exercise ECG test ("treadmill test") may be performed, during which the patient exercises to their maximum ability before fatigue, breathlessness or, importantly, pain intervenes; if characteristic ECG changes are documented (typically more than 1 mm of flat or downsloping ST depression), the test is considered diagnostic for angina. Even constant monitoring of the blood pressure and the pulse rate can lead us to some conclusion regarding the angina. The exercise test is also useful in looking for other markers of myocardial ischaemia: blood pressure response (or lack thereof, particularly a drop in systolic pressure), dysrhythmia and chronotropic response. Other alternatives to a standard exercise test include a thallium scintigram (in patients who cannot exercise enough for the purposes of the treadmill tests, e.g., due to asthma or arthritis or in whom the ECG is too abnormal at rest) or Stress Echocardiography. In patients in whom such noninvasive testing is diagnostic, a coronary angiogram is typically performed to identify the nature of the coronary lesion, and whether this would be a candidate for angioplasty, coronary artery bypass graft (CABG), treatment only with medication, or other treatments. There has been researches which concludes that a freqency is attained when there is increase in the blood pressure and the pulse rate. This frequency varies normally but the range is 4550 kHz for the cardiac arrest or for the heart failure. In patients who are in hospital with unstable angina (or the newer term of "high risk acute coronary syndromes"), those with resting ischaemic ECG changes or those with raised cardiac enzymes such as troponin may undergo coronary angiography directly.

[edit] Treatment
The most specific medicine to treat angina is nitroglycerin. It is a potent vasodilator that makes more oxygen available to the heart muscle. Beta-blockers and calcium channel blockers act to decrease the heart's workload, and thus its requirement for oxygen. Nitroglycerin should not be given if certain inhibitors such as Viagra, Cialis, or Levitra have been taken by the casualty within the previous 12 hours as the combination of the two could cause a serious drop in blood pressure. Treatments are balloon angioplasty, in which the balloon is inserted at the end of a catheter and inflated to widen the arterial lumen. Stents to maintain the arterial widening

are often used at the same time. Coronary bypass surgery involves bypassing constricted arteries with venous grafts. This is much more invasive than angioplasty. The main goals of treatment in angina pectoris are relief of symptoms, slowing progression of the disease, and reduction of future events, especially heart attacks and, of course, death. Beta blockers (e.g., carvedilol, propranolol, atenolol) have a large body of evidence in morbidity and mortality benefits (fewer symptoms, less disability and longer life) and short-acting nitroglycerin medications have been used since 1879 for symptomatic relief of angina [24]. Calcium channel blockers (such as nifedipine (Adalat) and amlodipine), isosorbide mononitrate and nicorandil are vasodilators commonly used in chronic stable angina[citation needed]. A new therapeutic class, called If inhibitor, has recently been made available: ivabradine provides pure heart rate reduction[25] leading to major anti-ischemic and antianginal efficacy. ACE inhibitors are also vasodilators with both symptomatic and prognostic benefit and, lastly, statins are the most frequently used lipid/cholesterol modifiers which probably also stabilize existing atheromatous plaque[citation needed] . Low-dose aspirin decreases the risk of heart attack in patients with chronic stable angina, and was previously part of standard treatment, however it has since been discovered that the increase in haemorrhagic stroke and gastrointestinal bleeding offsets this gain so they are no longer advised unless the risk of myocardial infarction is very high.[26] Exercise is also a very good long term treatment for the angina (but only particular regimens - gentle and sustained exercise rather than intense short bursts),[27] probably working by complex mechanisms such as improving blood pressure and promoting coronary artery collateralisation. Identifying and treating risk factors for further coronary heart disease is a priority in patients with angina. This means testing for elevated cholesterol and other fats in the blood, diabetes and hypertension (high blood pressure), encouraging stopping smoking and weight optimisation. The calcium channel blocker nifedipine prolongs cardiovascular event- and procedure-free survival in patients with coronary artery disease. New overt heart failures were reduced by 29% compared to placebo; however, the mortality rate difference between the two groups was statistically insignificant.[28]

[edit] Suspected angina

Hospital admission for people with the following symptoms, as they may have unstable angina: Pain at rest (which may occur at night), pain on minimal exertion, angina that seems to be progressing rapidly despite increasing medical treatment. Refer urgently all people with suspected angina to a chest pain evaluation service, for confirmation of the diagnosis and assessment of the severity of coronary heart disease.[29]

[edit] Epidemiology
Roughly 6.3 million Americans are estimated to experience angina. Angina is more often the presenting symptom of coronary artery disease in women than in men. The prevalence of angina rises with increasing age, with a mean age of onset of 62.3 years.[30] After five years post-onset, 4.8% of individuals with angina subsequently died from coronary heart disease. Men with angina were found to have an increased risk of subsequent acute myocardial infarction and coronary heart disease related death than women. Similar figures apply in the remainder of the Western world. All forms of coronary heart disease are much less-common in the Third World, as its risk factors are much more common in Western and Westernized countries; it could therefore be termed a disease of affluence. The adoption of a rich, Westernized diet and subsequent increase of smoking, obesity and other risk factors, as chronicled in The China Study, has already led to an increase in angina and related diseases in countries such as China. Recently, angina was tied to exposure of Bisphenol-A[31] among adults in the US.

Cardiac arrest
From Wikipedia, the free encyclopedia Jump to: navigation, search For other uses, see Cardiac arrest (disambiguation).

Cardiac Arrest
Classification and external resources

CPR being administered during a simulation of cardiac arrest.







Cardiac arrest, (also known as cardiopulmonary arrest or circulatory arrest) is the cessation of normal circulation of the blood due to failure of the heart to contract effectively.[1] Medical personnel can refer to an unexpected cardiac arrest as a sudden cardiac arrest or SCA. A cardiac arrest is different from (but may be caused by) a heart attack, where blood flow to the muscle of the heart is impaired.[2] Arrested blood circulation prevents delivery of oxygen to the body. Lack of oxygen to the brain causes loss of consciousness, which then results in abnormal or absent breathing. Brain injury is likely if cardiac arrest goes untreated for more than five minutes.[3][4][5] For the best chance of survival and neurological recovery, immediate and decisive treatment is imperative.[6] Cardiac arrest is a medical emergency that, in certain situations, is potentially reversible if treated early. When unexpected cardiac arrest leads to death this is called sudden cardiac death (SCD).[1] The treatment for cardiac arrest is cardiopulmonary resuscitation (CPR) to provide circulatory support, followed by defibrillation if a shockable rhythm is present. If a shockable rhythm is not present after CPR and other interventions, clinical death is inevitable.


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1 Classification 2 Signs and symptoms 3 Causes o 3.1 Coronary heart disease o 3.2 Non ischemic heart disease o 3.3 Non cardiac o 3.4 Risk factors o 3.5 Hs and Ts 4 Diagnosis 5 Prevention o 5.1 Code teams o 5.2 Implantable cardioverter defibrillators 6 Management o 6.1 Cardiopulmonary resuscitation o 6.2 Defibrillation o 6.3 Medications o 6.4 Therapeutic hypothermia o 6.5 ECMO o 6.6 Chain of survival 7 Prognosis 8 Epidemiology 9 Ethical issues 10 See also 11 References 12 External links

[edit] Classification

Cardiac arrest is classified into "shockable" versus "nonshockable", based upon the ECG rhythm. The two shockable rhythms are ventricular fibrillation and pulseless ventricular tachycardia while the two nonshockable rhythms are asystole and pulseless electrical activity. This refers to whether a particular class of disrhythmia is treatable using defibrillation.[7]

[edit] Signs and symptoms

Cardiac arrest is an abrupt cessation of pump function in the heart (as evidenced by the absence of a palpable pulse). Prompt intervention can usually reverse a cardiac arrest, but without such intervention it will almost always lead to death.[1] In certain cases, it is an expected outcome to a serious illness.[8] However, due to inadequate cerebral perfusion, the patient will be unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest, (as opposed to respiratory arrest which shares many of the same features), is lack of circulation, however there are a number of ways of determining this.

[edit] Causes
Coronary heart disease is the leading cause of sudden cardiac arrest. Many other cardiac and noncardiac conditions also increase ones risk.

[edit] Coronary heart disease

Approximately 6070% of SCD is related to coronary heart disease.[9][10] Among adults, ischemic heart disease is the predominant cause of arrest[11] with 30% of people at autopsy showing signs of recent myocardial infarction[citation needed].

[edit] Non ischemic heart disease

A number of other cardiac abnormalities can increase the risk of SCD including: cardiomyopathy, cardiac rhythm disturbances, hypertensive heart disease,[9] congestive heart failure.[12] In a group of military recruits aged 1835, cardiac anomalies accounted for 51% of cases of SCD, while in 35% of cases the cause remained unknown. Underlying pathology included: coronary artery abnormalities (61%), myocarditis (20%), and hypertrophic cardiomyopathy (13%).[13] Congestive heart failure increases the risk of SCD by 5 fold.[12]

[edit] Noncardiac
SCDs is unrelated to heart problems in 35% of cases. The most common noncardiac causes were: trauma, non-trauma related bleeding (such as gastrointestinal bleeding, aortic rupture, and intracranial hemorrhage), overdose, drowning and pulmonary embolism.[14]

[edit] Risk factors

The risk factors for SCD are similar to those seen with coronary heart disease including: smoking, lack of physical exercise, obesity, diabetes, and family history.[15]

[edit] Hs and Ts
Main article: Hs and Ts

The Hs and Ts is a mnemonic used to aid in remembering the possible causes of cardiac arrest.[7][16]
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Hypovolemia - A lack of blood volume Hypoxia - A lack of oxygen Hydrogen ions (Acidosis) - An abnormal pH in the body Hyperkalemia or Hypokalemia - Both excess and inadequate potassium can be life-threatening. Hypothermia - A low core body temperature Hypoglycemia or Hyperglycemia - Low or high blood glucose

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Tablets or Toxins Cardiac Tamponade - Fluid building around the heart Tension pneumothorax - A collapsed lung Thrombosis (Myocardial infarction) - Heart attack Thromboembolism (Pulmonary embolism) - A blood clot in the lung


[edit] Diagnosis

Checking for respiration.

Checking carotid pulse.

Cardiac arrest is synonymous with clinical death. A cardiac arrest is usually diagnosed clinically by the absence of a pulse. In many cases lack of carotid pulse is the gold standard for diagnosing cardiac arrest, but lack of a pulse (particularly in the peripheral pulses) may be a result of other conditions (e.g. shock), or simply an error on the part of the rescuer. Studies have shown that rescuers often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals[17] or lay persons.[18] Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have deemphasised its importance. The Resuscitation Council (UK), in line with the ERC's recommendations and those of the American Heart Association,[16] have suggested that the technique should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.[7] Various other methods for detecting circulation have been proposed. Guidelines following the 2000 International Liaison Committee on Resuscitation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse.[16] These signs included coughing, gasping, colour, twitching and movement.[19] However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally.[16]

[edit] Prevention
With positive outcomes following cardiac arrest unlikely, an effort has been spent in finding effective strategies to prevent cardiac arrest. With the prime causes of cardiac arrest being ischemic heart disease, efforts to promote a healthy diet, exercise, and smoking cessation are important. For people at risk of heart disease, measures such as blood pressure control, cholesterol lowering, and other medico-therapeutic interventions are used.[1]

[edit] Code teams

In medical parlance, cardiac arrest is referred to as a "code" or a "crash". This typically refers to "code blue" on the hospital emergency codes. A dramatic drop in vital sign measurements is referred to as "coding" or "crashing", though coding is usually used when it results in cardiac arrest, while crashing might not. Treatment for cardiac arrest is sometimes referred to as "calling a code".

Extensive research has shown that patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs.[7][20] This has been attributed to a lack of knowledge and skill amongst ward based staff, in particular a failure to carry out measurement of the respiratory rate, which is often the major predictor of a deterioration[7] and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward based staff. A number of "early warning" systems also exist which aim to quantify the risk which patients are at of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being utilised more effectively in order to augment the work already being done at ward level. These include:

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Crash teams (or code teams) - These are designated staff members who have particular expertise in resuscitation, who are called to the scene of all arrests within the hospital. This usually involves a specialized cart of equipment (including defibrillator) and drugs called a "crash cart". Medical emergency teams - These teams respond to all emergencies, with the aim of treating the patient in the acute phase of their illness in order to prevent a cardiac arrest. Critical care outreach - As well as providing the services of the other two types of team, these teams are also responsible for educating non-specialist staff. In addition, they help to facilitate transfers between intensive care/high dependency units and the general hospital wards. This is particularly important, as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted - the outreach team offers support to ward staff to prevent this from happening.

[edit] Implantable cardioverter defibrillators

A technologically based intervention to prevent further cardiac arrest episodes is the use of an implantable cardioverter-defibrillator (ICD). This device is implanted in the patient and acts as an instant defibrillator in the event of arrhythmia. Note that standalone ICDs do not have any pacemaker functions, but they can be combined with a pacemaker, and modern versions also have advanced features such as anti-tachycardic pacing as well as synchronized cardioversion. A recent study by Birnie et al. at the University of Ottawa Heart Institute has demonstrated that ICDs are underused in both the United States and Canada.[21] An accompanying editorial by Simpson explores some of the economic, geographic, social and political reasons for this.[22] Patients who are most likely to benefit from the placement of an ICD are those with severe ischemic cardiomyopathy (with systolic ejection fractions less than 30%) as demonstrated by the MADIT-II trial.[23]

[edit] Management
Sudden cardiac arrest is treated via attempts at resuscitation. This is usually carried out based upon basic life support (BLS) / advanced cardiac life support (ACLS),[16] pediatric advanced life support (PALS)[24] or neonatal resuscitation program (NRP) guidelines.

[edit] Cardiopulmonary resuscitation

Main article: Cardiopulmonary resuscitation

CPR is a critical part of the management of cardiac arrest. It should be started as soon as possible and interrupted as little as possible. The component of CPR which seems to make the greatest difference is the chest compressions.

Tracheal intubation has not been found to improve survival rates in cardiac arrest cases.[25] A 2009 study has found that assisted ventilation may worsen outcomes over placement of an oral airway with passive oxygen delivery.[26] Intubation in the prehospital environment has been found to decrease survival.[27]
Bystander CPR

Correctly performed bystander CPR has been shown to increase survival; it is performed in less than 30% of out of hospital arrests.[25]

[edit] Defibrillation
Clinicians distinguish shockable and nonshockable causes of cardiac arrest - based on the presence or absence of ventricular fibrillation or pulseless ventricular tachycardia. The shockable rhythms are treated with CPR and defibrillation. Most out-of-hospital cardiac arrests occur following a myocardial infarction (heart attack), and present initially with a heart rhythm of ventricular fibrillation.[citation needed] The patient is therefore likely to respond to defibrillation, and this has become the focus of interventions. In addition, there is increasing use of public access defibrillation. This involves placing automated external defibrillators in public places, and training staff in these areas how to use them. This allows defibrillation to take place prior to the arrival of emergency services, and has been shown to lead to increased chances of survival. Some defibrillators even provide feedback on the quality of CPR compressions, encouraging the lay rescuer to press the patient's chest hard enough to circulate blood.[28] In addition, it has been shown that those who suffer arrests in remote locations have worse outcomes following cardiac arrest:[29] these areas often have first responders, whereby members of the community receive training in resuscitation and are given a defibrillator, and called by the emergency medical services in the case of a collapse in their local area.

[edit] Medications
Medications, while included in guidelines, have been shown not to improve survival to hospital discharge post cardiac arrest. This includes the use of epinephrine, atropine, and amiodarone. The study, however, only refers to the ineffectiveness of these drugs in reference to out-of-hospital cardiac arrests.[30] Though in their 2010 guidelines, the American Heart Association has singled out atropine, indicating that "Available evidence suggests that the routine use of atropine during PEA or asystole is unlikely to have a therapeutic benefit."[31]

[edit] Therapeutic hypothermia

Main article: Therapeutic hypothermia

Cooling a person after cardiac arrest with return of spontaneous circulation (ROSC) but without return of consciousness improves outcomes. This procedure is called therapeutic hypothermia. The first study conducted in Europe focused on people who were resuscitated 515 minutes after collapse. Patients participating in this study experienced spontaneous return of circulation (ROSC) after an average of 105 minutes. Subjects were then cooled over a 24 hour period, with a target temperature of 3234 C (9093 F). 55% of the 137 patients in the hypothermia group experienced favorable outcomes, compared with only 39% in the group that received standard care following resuscitation.[32] Death rates in the hypothermia group were 14% lower, meaning that for every 7 patients treated one life was saved.[32] Notably, complications between the two groups did not differ substantially. This data was supported by another similarly run study that took place simultaneously in Australia. In this study 49% of the patients treated with hypothermia following cardiac arrest experienced good outcomes, compared to only 26% of those who received standard care.[33]

[edit] ECMO
Sporadic reports of resuscitation with extracorporeal membrane oxygenation devices have appeared in recent years. [34]

[edit] Chain of survival

Several organisations promote the idea of a "chain of survival" The links are:

Early recognition - If possible, recognition of illness before the patient develops a cardiac arrest will allow the rescuer to prevent its occurrence. Early recognition that a cardiac arrest has occurred is key to survival - for every minute a patient is in cardiac arrest, their chances of survival drop by roughly 10%.[7]

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Early CPR - improves blood and oxygen flow to vital organs and an essential component of treating a cardiac arrest. In particular, by keeping the brain supplied with oxygenated blood, chances of neurological damage are decreased. Early defibrillation - is effective for the management of ventricular fibrillation and pulseless ventricular tachycardia[7] If defibrillation is delayed the rhythm is likely to degenerate into asystole for which outcomes are worse. Early advanced care - Early Advanced Cardiac Life Support is the final link in the chain of survival.

If one or more links in the chain are missing or delayed, then the chances of survival drop significantly. These protocols are often initiated by a Code Blue, which usually denotes impending or acute onset of cardiac arrest or respiratory failure, although in practice, Code Blue is often called in less life-threatening situations that require immediate attention from a physician.[citation needed]

[edit] Prognosis
Out-of-hospital cardiac arrest (OHCA) has a worse survival rate (2-8% for discharge and 8-22% for admission), than an in-hospital cardiac arrest (15% for discharge). The principal determining factor is the initially documented rhythm. People with ventricular fibrillation or pulseless ventricular tachycardia have 10-15 times greater chance of surviving than those suffering from pulseless electrical activity or asystole.[citation needed] Since mortality in case of OHCA is high, programs were developed to improve survival rate. Although mortality in case of ventricular fibrillation is high, rapid intervention with a defibrillator increases survival rate.[11][35] Survival is mostly related to the cause of the arrest (see above). In particular, patients who have suffered hypothermia have an increased survival rate, possibly because the cold protects the vital organs from the effects of tissue hypoxia. Survival rates following an arrest induced by toxins is very much dependent on identifying the toxin and administering an appropriate antidote. A patient who has suffered a myocardial infarction due to a blood clot in the left coronary artery has a lower chance of survival.[citation needed] A study of survival rates from out of hospital cardiac arrest found that 14.6% of those who had received resuscitation by ambulance staff survived as far as admission to hospital. Of these, 59% died during admission, half of these within the first 24 hours, while 46% survived until discharge from hospital. This gives us an overall survival following cardiac arrest of 6.8%. Of these 89% had normal brain function or mild neurological disability, 8.5% had moderate impairment, and 2% suffered major neurological disability. Of those who were discharged from hospital, 70% were still alive 4 years later.[36]

A review into prognosis following in-hospital cardiac arrest found a survival to discharge of 14% although the range between different studies was 0-28%.[37]

Prothrombin time
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Blood plasma after the addition of Tissue Factor (Quick-Test). The gel-like structure is strong enough to hold a steel ball.

The prothrombin time (PT) and its derived measures of prothrombin ratio (PR) and international normalised ratio (INR) are measures of the extrinsic pathway of coagulation. They are used to determine the clotting tendency of blood, in the measure of

warfarin dosage, liver damage, and vitamin K status. PT measures factors I, II, V, VII, and X. It is used in conjunction with the activated partial thromboplastin time (aPTT) which measures the intrinsic pathway.


y y y y

1 Laboratory measurement o 1.1 Normal range o 1.2 Methodology o 1.3 International normalised ratio o 1.4 Interpretation o 1.5 Factors determining accuracy 2 Statistics 3 Near-patient testing o 3.1 Guidelines 4 History 5 References

[edit] Laboratory measurement

[edit] Normal range
The reference range for prothrombin time is usually around 11-16 seconds; the normal range for the INR is 0.81.2. Clinicians desiring therapeutic anticoagulation may aim for a higher INR - in many cases 2.5 - using anticoagulants such as warfarin.

[edit] Methodology
The prothrombin time is most commonly measured using blood plasma. Blood is drawn into a test tube containing liquid citrate, which acts as an anticoagulant by binding the calcium in a sample. The blood is mixed, then centrifuged to separate blood cells from plasma. In newborns, a capillary whole blood specimen is used.[1]

The plasma is analyzed by a biomedical scientist on an automated instrument at 37C, which takes a sample of the plasma. An excess of calcium is added (thereby reversing the effects of citrate), which enables the blood to clot again. For an accurate measurement the proportion of blood to citrate needs to be fixed; many laboratories will not perform the assay if the tube is underfilled and contains a relatively high concentration of citrate. If the tube is underfilled or overfilled with blood, the standardized dilution of 1 part anticoagulant to 9 parts whole blood is no longer valid. For the prothrombin time test the appropriate sample is the blue top tube, or sodium citrate tube, which is a liquid anticoagulant. Tissue factor (also known as factor III) is added, and the time the sample takes to clot is measured optically. Some laboratories use a mechanical measurement, which eliminates interferences from lipemic and icteric samples. The prothrombin ratio is the prothrombin time for a patient, divided by the result for control plasma.

[edit] International normalised ratio

The result (in seconds) for a prothrombin time performed on a normal individual will vary depending on what type of analytical system it is performed. This is due to the differences between different batches of manufacturer's tissue factor used in the reagent to perform the test. The INR was devised to standardize the results. Each manufacturer assigns an ISI value (International Sensitivity Index) for any tissue factor they manufacture. The ISI value indicates how a particular batch of tissue factor compares to an internationally standardized sample. The ISI is usually between 1.0 and 2.0. The INR is the ratio of a patient's prothrombin time to a normal (control) sample, raised to the power of the ISI value for the analytical system used.

[edit] Interpretation
The prothrombin time is the time it takes plasma to clot after addition of tissue factor (obtained from animals). This measures the quality of the extrinsic pathway (as well as the common pathway) of coagulation. The speed of the extrinsic pathway is greatly affected by levels of factor VII in the body. Factor VII has a short half-life and its synthesis requires vitamin K. The prothrombin time can be prolonged as a result of deficiencies in vitamin K, which can be caused by warfarin, malabsorption, or lack of intestinal colonization by bacteria (such as in newborns). In addition, poor factor VII synthesis (due to liver disease) or increased consumption (in disseminated intravascular coagulation) may prolong the PT.

A high INR level such as INR=5 indicates that there is a high chance of bleeding, whereas if the INR=0.5 then there is a high chance of having a clot. Normal range for a healthy person is 0.91.3, and for people on warfarin therapy, 2.03.0, although the target INR may be higher in particular situations, such as for those with a mechanical heart valve, or bridging warfarin with a low-molecular weight heparin (such as enoxaparin) perioperatively.
Condition Vitamin K deficiency or warfarin Disseminated intravascular coagulation Von Willebrand disease Haemophilia Aspirin Thrombocytopenia Early Liver failure End-stage Liver failure Uremia Congenital afibrinogenemia Factor V deficiency Prothrombin time prolonged prolonged unaffected unaffected unaffected unaffected prolonged prolonged unaffected prolonged prolonged Partial thromboplastin time prolonged prolonged prolonged prolonged unaffected unaffected unaffected prolonged unaffected prolonged prolonged prolonged Bleeding time unaffected prolonged prolonged unaffected prolonged prolonged unaffected prolonged prolonged prolonged unaffected unaffected Platelet count unaffected decreased unaffected unaffected unaffected decreased unaffected decreased unaffected unaffected unaffected unaffected

Factor X deficiency as seen in amyloid purpura prolonged

Glanzmann's thrombasthenia Bernard-Soulier syndrome

unaffected unaffected

unaffected unaffected

prolonged prolonged

unaffected decreased

[edit] Factors determining accuracy

Lupus anticoagulant, a circulating inhibitor predisposing for thrombosis, may skew PT results, depending on the assay used.[2] Variations between various thromboplastin preparations have in the past led to decreased accuracy of INR readings, and a 2005 study suggested that despite international calibration efforts (by INR) there were still statistically significant differences between various kits,[3] casting doubt on the long-term tenability of PT/INR as a measure for anticoagulant therapy.[4]

[edit] Statistics
An estimated 800 million PT/INR assays are performed annually worldwide.[4]

[edit] Near-patient testing

In addition to the laboratory method outlined above, near-patient testing (NPT) or home INR monitoring is becoming increasingly common in some countries. In the United Kingdom, for example, near-patient testing is used both by patients at home, and by some anticoagulation clinics (often hospital-based) as a fast and convenient alternative to the lab method. After a period of doubt about the accuracy of NPT results, a new generation of machines and reagents seems to be gaining acceptance for its ability to deliver results close in accuracy to those of the lab.[5]

A Roche CoaguChek XS.

In a typical NPT setup a small table-top device is used; for example the Roche Coaguchek S, the International Technidyne Corporation Hemochron Signature, or the more recently (2005) introduced HemoSense INRatio. A drop of capillary blood is obtained with an automated finger-prick, which is almost painless. This drop is placed on a disposable test strip with which the machine has been prepared. The resulting INR comes up on the display a few seconds later. Similar testing methods are used by diabetics on insulin, and are easily taught and practiced. Local policy determines whether the patient or a coagulation specialist (nurse, general practitioner or hospital doctor) interprets the result and determines the dose of medication. In Germany, patients may adjust the medication dose themselves,[citation needed] while in the UK and the USA this remains in the hands of a health care professional. For example, patients using services such as Philips INR@Home [1] will phone in their INR results on a weekly basis and this information is transmitted to their doctor, who is also alerted if out-of-range levels should require an immediate intervention or adjustment to medications. A significant advantage of home testing is the evidence that patient self-testing with medical support and patient self-management (where patients adjust their own anticoagulant dose) improves anticoagulant control. A meta analysis which reviewed 14 trials showed that home testing led to a reduced incidence of complications (bleeding and thrombosis) and improved the time in the therapeutic range, which is an indirect measure of anticoagulant control.[6] Other advantages of the NPT approach are that it is fast and convenient, usually less painful, and offers, in home use, the ability for patients to measure their own INRs when required. Among its problems are that quite a steady hand is needed to deliver the blood to the exact spot, that some patients find the finger-pricking difficult, and that the cost of the test strips must also be taken into account. In the UK these are available on prescription so that elderly and unwaged people will not pay for them and others will pay only a standard prescription charge, which at the moment represents only about 20% of the retail price of the strips. In the USA, NPT in the home is currently reimbursed by Medicare for patients with mechanical heart valves, while private insurers may cover for other indications.Medicare is now covering home testing for patients with chronic atrial fibrillation. Home testing requires a doctor's prescription. There is some evidence to suggest that NPT may be less accurate for certain patients, for example those who have the lupus anticoagulant.[7]

[edit] Guidelines

International guidelines were published in 2005 to govern home monitoring of oral anticoagulation by the International SelfMonitoring Association for Oral Anticoagulation.[8] The international guidelines study stated, The consensus agrees that patient selftesting and patient self-management are effective methods of monitoring oral anticoagulation therapy, providing outcomes at least as good as, and possibly better than, those achieved with an anticoagulation clinic. All patients must be appropriately selected and trained. Currently available self-testing/self-management devices give INR results which are comparable with those obtained in laboratory testing. Medicare coverage for home testing of INR has been expanded in order to allow more people access to home testing of INR in the USA. The release on the 19th March 2008 said, [t]he Centers for Medicare & Medicaid Services (CMS) expanded Medicare coverage for home blood testing of prothrombin time (PT) International Normalized Ratio (INR) to include beneficiaries who are using the drug warfarin, an anticoagulant (blood thinner) medication, for chronic atrial fibrillation or venous thromboembolism. In addition, [t]hose Medicare beneficiaries and their physicians managing conditions related to chronic atrial fibrillation or venous thromboembolism will benefit greatly through the use of the home test.[9]

[edit] History
The prothrombin time was discovered by Dr Armand Quick and colleagues in 1935[10], and a second method was published by Dr Paul Owren[11], also called the "p and p" or "prothrombin and proconvertin" method. It aided in the identification of the anticoagulants dicumarol and warfarin,[12] and was used subsequently as a measure of activity for warfarin when used therapeutically. The INR was introduced in the early 1980s when it turned out that there was a large degree of variation between the various prothrombin time assays, a discrepancy mainly due to problems with the purity of the thromboplastin (tissue factor) concentrate.[13] The INR became widely accepted worldwide, especially after endorsement by the World Health Organisation.[14]

[edit] References

From Wikipedia, the free encyclopedia Jump to: navigation, search

Classification and external resources

Opened left ventricle of heart shows a thickened, dilated left ventricle with subendocardial fibrosis manifested as increased whiteness of endocardium.











Cardiomyopathy, which literally means "heart muscle disease," is the deterioration of the function of the myocardium (i.e., the actual heart muscle) for any reason. People with cardiomyopathy are often at risk of arrhythmia or sudden cardiac death or both.[1] Although in theory the term "cardiomyopathy" could apply to almost any disease affecting the heart, in practice it is usually reserved for "severe myocardial disease leading to heart failure".[2]

y y y y y y

1 Classification 2 Types 3 Signs and symptoms 4 Treatment 5 References 6 External links

[edit] Classification
Cardiomyopathies can be categorized as extrinsic or intrinsic.[3]

An extrinsic cardiomyopathy is a cardiomyopathy where the primary pathology is outside the myocardium itself. Most cardiomyopathies are extrinsic, because by far the most common cause of a cardiomyopathy is ischemia. The World Health Organization calls these specific cardiomyopathies:[3] An intrinsic cardiomyopathy is defined as weakness in the muscle of the heart that is not due to an identifiable external cause. This definition was used to categorize previously idiopathic cardiomyopathies although specific external causes have since been identified for

many. For example, alcoholism has been identified as a cause for some forms of dilated cardiomyopathy. To make a diagnosis of an intrinsic cardiomyopathy, significant coronary artery disease should be ruled out (amongst other things). The term intrinsic cardiomyopathy does not describe the specific etiology of weakened heart muscle. The intrinsic cardiomyopathies consist of a variety of disease states, each with their own causes. Many intrinsic cardiomyopathies now have identifiable external causes including drug and alcohol toxicity, certain infections (including Hepatitis C), and various genetic and idiopathic (i.e., unknown) causes.

It is also possible to classify cardiomyopathies functionally, as involving dilation, hypertrophy, or restriction.[4]

[edit] Types

Primary/intrinsic cardiomyopathies o Genetic  Hypertrophic cardiomyopathy (HCM or HOCM)  Arrhythmogenic right ventricular cardiomyopathy (ARVC)  Isolated ventricular non-compaction  Mitochondrial myopathy o Mixed  Dilated cardiomyopathy (DCM)  Restrictive cardiomyopathy (RCM) o Acquired  Takotsubo cardiomyopathy  Loeffler endocarditis Secondary/extrinsic cardiomyopathies o Metabolic/storage  amyloidosis  hemochromatosis o Inflammatory  Chagas disease[5][6] o Endocrine  diabetic cardiomyopathy  hyperthyroidism o Toxicity  chemotherapy

o o o

 Alcoholic cardiomyopathy Neuromuscular  muscular dystrophy Nutritional diseases Other  "Ischemic cardiomyopathy" is a weakness in the muscle of the heart due to inadequate oxygen delivery to the myocardium with coronary artery disease being the most common cause. Not supported by current cardiomyopathies classification schemes.[7][8]

[edit] Signs and symptoms

Symptoms and signs may mimic those of almost any form of heart disease. Chest pain is common. Mild myocarditis or cardiomyopathy is frequently asymptomatic; severe cases are associated with heart failure, arrhythmias, and systemic embolization. Manifestations of the underlying disease (e.g., Chagas' disease) may be prominent. Most patients with biopsy-proven myocarditis report a recent viral prodrome preceding cardiovascular symptoms. ECG abnormalities are often present, although the changes are frequently nonspecific. A pattern characteristic of left ventricular hypertrophy may be present. Flat or inverted T waves are most common, often with low-voltage QRS complexes. Intraventricular conduction defects and bundle branch block, especially left bundle branch block, are also common. An echocardiogram is useful to detect wall motion abnormalities or a pericardial effusion. Chest radiographs can be normal or can show evidence of congestive heart failure with pulmonary edema or cardiomegaly.

[edit] Treatment
Treatment depends on the type of cardiomyopathy, but may include medication, implanted pacemakers, defibrillators, or ventricular assist devices (LVADs), or ablation. The goal of treatment is often symptom relief, and some patients may eventually require a heart transplant. Treatment of cardiomyopathy (and other heart diseases) using alternative methods such as stem cell therapy is commercially available but is not supported by convincing evidence.

Carotid endarterectomy
From Wikipedia, the free encyclopedia

Jump to: navigation, search

The carotid artery is the large vertical artery in red. The blood supply to the common carotid artery starts at the arch of the aorta (left) or the subclavian artery (right). The common carotid artery divides into the internal carotid artery and the external carotid artery. Plaque often builds up at that division, and a carotid endarterectomy cuts open the artery and removes the plaque.

Section of carotid artery with plaque. Blood flows from the common carotid artery (bottom), and divides into the internal carotid artery (left) and external carotid artery (right). The atherosclerotic plaque is the dark mass on the left, which would be removed in an endarterectomy.

Carotid endarterectomy (CEA) is a surgical procedure used to prevent stroke, by correcting stenosis (narrowing) in the common carotid artery. Endarterectomy is the removal of material on the inside (end-) of an artery.

Atherosclerosis causes plaque to form in the carotid arteries, usually at the fork where the common carotid artery divides into the internal and external carotid artery. The plaque can build up in the inner surface of the artery (lumen), and narrow or constrict the artery. Pieces of the plaque, called emboli, can break off (i.e. embolize) and travel up the internal carotid artery to the brain, where it blocks circulation, and can cause death of the brain tissue. Sometimes the plaque causes symptoms first. The symptoms are temporary or transitory strokes, known as transient ischemic attacks (TIAs). By definition, TIAs last less than 24 hours; after 24 hours they are called strokes. Symptomatic stenosis has a high risk of stroke within the next 2 days. National Institute for Health and Clinical Excellence (NICE) guidelines recommend that patients with moderate to severe (50-99% blockage) stenosis, and symptoms, should have "urgent" endarterectomy within 2 weeks.[1] When the plaque doesn't cause symptoms, patients are still at higher risk of stroke than the general population, but not as high as patients with symptomatic stenosis. The incidence of stroke, including fatal stroke, is 1-2% per year. The surgical mortality of endarterectomy ranges from 1-2% to as much as 10%. Two large randomized clinical trials have demonstrated that carotid surgery done with a 30 day stroke and death risk of 3% or less will benefit asymptomatic patients with 60% stenosis who are expected to live at least 5 years after surgery.[2][3] Surgeons are divided over whether asymptomatic patients should be treated with medication alone or should have surgery.[4][5] In endarterectomy, the surgeon opens the artery and removes the plaque. A newer procedure, endovascular angioplasty and stenting, threads a catheter up from the groin, around the aortic arch, and up the carotid artery. The catheter uses a balloon to expand the artery, and inserts a stent to hold the artery open. In several clinical trials,the 30-day incidence of heart attack, stroke, or death was significantly higher with stenting than with endarterectomy (9.6% vs. 3.9%) [6][7] The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST)[8] funded by the National Institutes of Health (NIH) reported that the results of stents and endarterectomy were comparable. However, the European International Carotid Stenting Study (ICSS)[9] found that stents had almost double the rate of complications.[10]

y y

1 Procedure 2 History

y y y y y

3 Indications 4 Contra-indications 5 Complications 6 References 7 External links

[edit] Procedure
The internal, common and external carotid arteries are clamped, the lumen of the internal carotid artery is opened, and the atheromatous plaque substance removed. The artery is closed, hemostasis achieved, and the overlying layers closed. Many surgeons lay a temporary shunt to ensure blood supply to the brain during the procedure. The procedure may be performed under general or local anaesthesia. The latter allows for direct monitoring of neurological status by intra-operative verbal contact and testing of grip strength. With general anaesthesia indirect methods of assessing cerebral perfusion must be used, such as electroencephalography (EEG), transcranial doppler analysis and carotid artery stump pressure monitoring. At present there is no good evidence to show any major difference in outcome between local and general anaesthesia. Minimally-invasive procedures have been developed, by threading catheters through the femoral artery, up through the aorta, then inflating a balloon to dilate the carotid artery, with a wire-mesh stent and a device to protect the brain from embolization of plaque material. The FDA has approved 5 carotid stent systems as safe and effective in patients at increased risk of complications for neck surgery. In the SAPPHIRE study, Yadav concluded that this procedure, known as carotid stenting, was non-inferior to carotid endarterectomy in total adverse events, and lowered event rates for major stroke, cranial nerve palsy, and myocardial infarction, in patients at high risk for surgery.[11] It is the consensus of experts in the field that carotid artery stenting should be considered an option for patients who require carotid artery revascularization to prevent stroke and who are at increased risk of having surgical complications.[12]

[edit] History
Surgical intervention to relieve atherosclerotic obstruction of the carotid arteries was first successfully performed by Dr. Michael DeBakey in 1953 at the Methodist Hospital in Houston, TX.[13] The first case to be recorded in the medical literature was in The Lancet in 1954 [14] and the surgeon was Felix Eastcott, a consultant surgeon and deputy director of the surgical unit at St Mary's Hospital, London UK. Eastcott died, aged 92, on October 25, 2009.[15] A reprint of his article together with a modern commentary can

be found on-line [1].Since then, evidence for its effectiveness in different patient groups has accumulated. In 2003 nearly 140,000 carotid endarterectomies were performed in the USA (Halm).

[edit] Indications
The aim of CEA is to prevent the adverse sequelae of carotid artery stenosis secondary to atherosclerotic disease, i.e. stroke. As with any prophylactic operation, careful evaluation of the relative benefits and risks of the procedure is required on an individual patient basis. Peri-operative combined mortality and major stroke risk is 2 5%. Carotid stenosis is diagnosed with ultrasound doppler studies of the neck arteries, magnetic resonance angiography (MRA) or computed tomography angiography (CTA). The circle of Willis typically provides a collateral blood supply. Surgical management of symptomatic stenoses has a much higher therapeutic index with regard to asymptomatic lesions. The North American Symptomatic Carotid Endarterectomy Trial (NASCET) and the European Carotid Surgery Trial (ECST) are both large randomized class 1 studies which have helped define current indications for carotid endarterectomy. The NASCET found that for every six patients treated, one major stroke would be prevented at two years (i.e. a number needed to treat (NNT) of six) for symptomatic patients with a 70 99% stenosis, where percent stenosis was defined as:[16]
percent stenosis = ( 1 - ( minimal diameter ) / ( poststenotic diameter ) ) x 100%.

Symptomatic patients with less severe carotid occlusion (50 69%) had a smaller benefit, with a NNT of 22 at five years (Barclay). In addition, co-morbidity adversely affects the outcome; patients with multiple medical problems have a higher post-operative mortality rate and hence benefit less from the procedure. For asymptomatic patients (those without TIA or strokes) the European asymptomatic carotid surgery trial (ACST) found that asymptomatic patients may also benefit from the procedure, but only the group with a high grade stenosis (60% or more). For maximum benefit patients should be operated on soon after a TIA or stroke, preferably within the first month.

[edit] Contra-indications
The procedure cannot be performed in case of:

Complete internal carotid artery obstruction (because there is no benefit to treating chronic occlusion).

y y

Previous stroke on the ipsilateral side with heavy sequelae, because there is no benefit in preventing what has already happened, or risking making it worse. Patient deemed unfit for the operation by the anaesthesiologist.

[edit] Complications
About 3% of asymptomatic and 6% of symptomatic patients are expected to suffer stroke or death as a result of either the surgery or carotid stenting. Other surgical complications include Hemorrhage of the wound bed which is potentially life-threatening, as swelling of the neck due to hematoma could compress the trachea. Rarely, the hypoglossal nerve can be damaged during surgery. This is likely to result in fasciculations developing on the tongue and paralysis of the affected side: on sticking it out, the patients tongue will deviate toward the affected side. Another rare but potentially serious complication is hyperperfusion syndrome because of the sudden increase in perfusion of the vasculature distal to stenosis.[17]
What are femoral popliteal bypass surgery and percutaneous transluminal angioplasty of the femoral arteries?
Femoral popliteal (also called femoropopliteal) bypass surgery is a surgical procedure that may be used to treat severe blockage due to plaque in the femoral artery. A newer, minimally-invasive procedure is percutaneous transluminal angioplasty (PTA) of the femoral arteries. The femoral and popliteal arteries are located in the legs. Their function is to supply oxygen-rich blood and nutrients to the legs. Femoral and popliteal arteries are called peripheral arteries because of their location away from the center of the body. Disease of the arteries of the limbs (particularly the legs and feet) is referred to as peripheral arterial disease (PAD).

Click Image to Enlarge

What is peripheral arterial disease?

Peripheral arterial disease (PAD) is generally associated with blocked arteries of the legs. The blockage most often is the result of a chronic buildup of hard fatty material (atherosclerosis) into the inside lining of the arterial wall of the legs. This ultimately narrows and blocks the flow of blood which carries oxygen and nutrients to the limb. The femoral and popliteal arteries are the major arterial blood supply to the lower extremities and are a common location for atherosclerotic disease to develop. The presence of atherosclerosis in the leg arteries is a strong indicator that there is also atherosclerosis in the arteries of the heart and brain, because atherosclerosis is a widespread disease of the arteries. Atherosclerosis of the leg arteries may cause a blockage, obstructing blood flow, and potentially result in pain in the leg(s), ulcers or wounds that do not heal, and/or the need for amputation (surgical removal) of a foot or leg. Therefore, PAD has two major complications associated with its presence: limb complications (nonhealing wounds, ulcers, gangrene, loss of a limb) and risk for stroke and/or heart attack. Peripheral arterial disease caused by atherosclerosis may be present with symptoms or without symptoms. The presence of symptoms may depend on the degree to which blood flow to the leg muscles has been decreased. Symptoms may range from mild to moderate to severe.

Click Image to Enlarge

The most common symptom of peripheral arterial disease is called intermittent claudication. Claudication refers to limping because of pain in the thigh, calf, and/or buttocks that occurs when walking. The pain or discomfort of claudication starts with walking or exercise and stops with rest. Walking or exercise increases the demand for oxygen and nutrients needed for the leg muscles to do work. Decreased blood flow through the affected artery of the leg(s) due to narrowing or occlusion (blockage) decreases the amount of oxygen and nutrients to the muscles and may result in pain. This symptom is reproducible (the same exercise, at the same pace, and the same distance, will reproduce the same symptom), which is helpful in diagnosing the condition.

Just as chest pain or angina of the heart can signal a heart attack, intermittent claudication may be considered as "angina of the legs" and may indicate lack of blood flow to the legs. Other symptoms of peripheral arterial disease may include, but are not limited to, the following:

y y y y y y y y y y y

cool/cold feet to touch pain in the legs while lying flat and relieved by a sitting position loss of pulses in legs or feet pale color when legs are raised up dependent rubor (redness when legs are in a dependent [hanging down] position) shiny skin loss of hair on feet thickened toenail (may have fungal infections) nonhealing wound or ulcer gangrene loss of muscle or fatty tissue

The most severe symptom of peripheral arterial disease caused by atherosclerosis is called critical limb ischemia (lack of oxygen to the limb/leg at rest). Critical limb ischemia (CLI) is defined as pain in the leg(s) while at rest, or "rest pain." CLI is also associated with the breakdown of tissues (muscle/skin) in the form of ulcers or gangrene in the limb, which may occur because blood flow to the limb is so decreased that the basic needs of the limb for oxygen and nutrients are not being met. Critical limb ischemia may include some or all of the symptoms of peripheral arterial disease as well. Because peripheral arterial disease is associated with the two other major atherosclerotic conditions, coronary artery disease (heart disease) and cerebrovascular disease (stroke), treatment may range from management of risk factors to surgical procedures. The same risk factors that may contribute to a heart attack or stroke are the same for peripheral arterial disease. These include, but are not limited to, the following:

y y y y y

smoking (tobacco) diabetes hypertension (high blood pressure) hyperlipidemia (high blood cholesterol) family history of atherosclerosis

Surgical treatment of peripheral arterial disease of the femoral arteries:

There are two procedures used to treat PAD of the femoral arteries. The standard surgical procedure is femoral popliteal bypass surgery (fem-pop bypass), while a newer minimally invasive endovascular intervention is called percutaneous transluminal angioplasty (PTA) of the femoral artery.

femoral popliteal bypass Femoral popliteal bypass is the surgical opening of the upper leg to directly visualize the femoral artery. It is performed to bypass the blocked portion of the artery using a piece of another blood vessel. Blood vessels, or vein grafts, used for the bypass procedure may be pieces of a vein taken from the legs. One end of the vein graft is attached above the blockage and the other end is attached below the blockage, rerouting blood flow around the blockage

through the new graft to reach the muscle. In some situations, a prosthetic (made of artificial material) graft may be used for the bypass graft, rather than a vein graft. percutaneous transluminal angioplasty (PTA) of the femoral arteries Percutaneous transluminal angioplasty is a minimally invasive (without a large incision) procedure used to open the blocked or narrowed femoral artery and to restore arterial blood flow to the lower leg without open vascular surgery. A special catheter (long hollow tube) is inserted into the femoral artery. The catheter has a tiny balloon at its tip. The balloon is inflated once the catheter has been placed into the narrowed area of the artery. The inflation of the balloon compresses the fatty tissue in the artery and makes a larger opening inside the artery for improved blood flow. A stent (a tiny, expandable metal coil) may be inserted into the newly-opened area of the artery to help keep the artery from narrowing or closing again.

Reasons for the Procedure

Reasons a femoral popliteal bypass surgery or PTA of the femoral artery may be performed include, but are not limited to, the following:

y y y y y y

medical management that has not improved symptoms, or worsening of symptoms despite medical management severe disability (intermittent claudication that causes interference with lifestyle and/or ability to work) nonhealing wounds infection or gangrene ischemic rest pain (lack of oxygen and nutrients to the leg resulting in pain at rest) danger of losing the limb due to decreased blood flow

Not all peripheral arterial disease can be treated with PTA. Your physician will decide the best treatment of your PAD based on your individual circumstances. There may be other reasons for your physician to recommend femoral popliteal bypass surgery or PTA.

Risks of the Procedure

As with any surgical procedure, complications can occur. Some possible complications may include, but are not limited to, the following:

y y y y y y y y y y y

myocardial infarction (heart attack) cardiac arrhythmias (irregular heart beats) hemorrhage (bleeding) wound infection leg edema (swelling of the leg) thrombosis (clot in the leg) pulmonary edema (fluid in the lungs) bleeding at the catheter insertion site (usually the groin) after PTA procedure blood clot or damage to the blood vessel at the insertion site (PTA) restenosis (blockage in the blood vessels after PTA procedure) nerve injury

graft occlusion (blockage in the graft used in bypass surgery)

Patients who are allergic to or sensitive to medications, contrast dyes, iodine, shellfish, or latex should notify their physician. There may be other risks depending upon your specific medical condition. Be sure to discuss any concerns with your physician prior to the procedure.

Before the Procedure

y y y y y y y y y y y y y y
Your physician will explain the procedure to you and offer you the opportunity to ask any questions that you might have about the procedure. You will be asked to sign a consent form that gives permission to do the procedure. Read the form carefully and ask questions if something is not clear. In addition to a complete medical history, your physician may perform a physical examination to ensure you are in good health before you undergo the procedure. You may also undergo blood tests and other diagnostic tests. Your physician may recommend taking an aspirin prior to the procedure. You will be asked to fast for eight hours before the procedure, generally after midnight. If you are pregnant or suspect that you are pregnant, you should notify your physician. Notify your physician if you are sensitive to or are allergic to any medications, latex, iodine, tape, contrast dyes, and anesthetic agents (local or general). Notify your physician of all medications (prescribed and over-the-counter) and herbal supplements that you are taking. Notify your physician if you have a history of bleeding disorders or if you are taking any anticoagulant (blood-thinning) medications, aspirin, or other medications that affect blood clotting. It may be necessary for you to stop these medications prior to the procedure. If you smoke, you should stop smoking as soon as possible prior to the procedure, in order to improve your chances for a successful recovery from surgery and to improve your overall health status. You may receive a sedative prior to the procedure to help you relax. The areas around the surgical site may be shaved. Notify your physician if you have a pacemaker. Based upon your medical condition, your physician may request other specific preparation.

During the Procedure

Femoral popliteal bypass surgery and percutaneous transluminal angioplasty of the femoral artery require a stay in the hospital. Procedures may vary depending on your condition and your physician's practices.

Click Image to Enlarge

Femoral popliteal bypass surgery:

Generally, femoral popliteal bypass surgery follows this process: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. You will be asked to remove any jewelry or other objects that may interfere with the procedure. You will be asked to remove your clothing and will be given a gown to wear. An intravenous (IV) line will be started in your arm or hand. Additional catheters may be inserted in your neck and wrist to monitor the status of your heart and blood pressure, as well as for obtaining blood samples. An alternate site for the additional catheters includes the subclavian (under the collarbone) area. You will be positioned on the operating table, lying on your back. The anesthesiologist will continuously monitor your heart rate, blood pressure, breathing, and blood oxygen level during the surgery. You will be connected to an ECG monitor that records the electrical activity of the heart and monitors the heart during the procedure using small, adhesive electrodes. A femoral popliteal bypass may be performed under local anesthesia. You will not feel the area to be operated on. You will receive a sedative medication in your IV before the procedure to help you relax. However, you will likely remain awake, but sleepy, during the procedure. Under local anesthesia, you will receive oxygen through a nasal cannula, a tube that fits in your nose. Femoral popliteal bypass may also be performed under general anesthesia (you will be asleep). Once you are sedated, a breathing tube will be inserted through your throat into your lungs and you will be connected to a ventilator, which will breathe for you during the surgery. A catheter will be inserted into your bladder to drain urine. You will be given a dose of antibiotics through your IV to help prevent infection. The skin over the surgical site will be cleansed with an antiseptic solution. The physician will make an incision (cut) in the leg. The site of the incision will depend on the section of the arteries to be bypassed. The physician will determine whether to use a prosthetic graft or a vein from the leg to bypass the diseased artery. Once the physician has attached the graft onto the diseased artery, an arteriogram may be performed to confirm that blood flow has been restored to the leg through the new bypass graft. You may receive blood pressure medication through your IV during and after the procedure to keep your blood pressure within a certain range.

15. The incision will be sutured together. A sterile bandage/dressing will be applied.

Click Image to Enlarge

Percutaneous transluminal angioplasty (PTA) of the femoral artery:

Generally, a PTA of the femoral artery procedure follows this process: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. You will be asked to remove any jewelry or other objects that may interfere with the procedure. You will be asked to remove clothing and will be given a gown to wear. You will be asked to empty your bladder prior to the procedure. An intravenous (IV) line will be started in your hand or arm prior to the procedure for injection of medication and to administer IV fluids, if needed. You will be placed in a supine (on your back) position on the procedure table. You will be connected to an ECG monitor that records the electrical activity of the heart and monitors the heart during the procedure using small, adhesive electrodes. Your vital signs (heart rate, blood pressure, breathing rate, and oxygenation level) will be monitored during the procedure. You will receive a sedative medication in your IV before the procedure to help you relax. However, you will likely remain awake, but sleepy, during the procedure. Your pulses below the insertion site will be checked and marked so that the circulation to the limb below the site can be checked after the procedure. A local anesthetic will be injected into the skin at the insertion site. You may feel some stinging at the site for a few seconds after the local anesthetic is injected. Once the local anesthetic has taken effect, a sheath, or introducer, will be inserted into the blood vessel. This is a plastic tube through which the catheter will be inserted into the femoral artery. A special catheter/guidewire will be inserted into the femoral artery and advanced to the site of the blockage. The proper position of the catheter may be confirmed by injecting a small amount of contrast dye into the artery, which may then be seen on a TV-like monitor. The physician will insert an angioplasty catheter and advance it to the location of the blockage. A balloon at the tip of the catheter will be inflated to open the artery.

14. The physician may inflate and deflate the balloon several times to open the artery. In some situations, a stent (a tiny, expandable metal coil) may be inserted into the newly-opened area of the artery to help keep the artery from narrowing or closing again. 15. Once it has been determined that the artery is opened sufficiently, the angioplasty catheter will be removed. 16. The insertion site may be closed with a closure device that uses collagen to seal the opening in the artery or with sutures. Your physician will determine which method is appropriate for your condition. 17. A sterile dressing/bandage will be applied.

After the procedure

In the hospital - femoral popliteal bypass:
After the procedure you will be taken to the recovery room for observation. Once your blood pressure, pulse, and breathing are stable and you are alert, you may be taken to the intensive care unit (ICU) or your hospital room. Your pulses below the surgical site will be checked frequently to assist in monitoring blood flow to the limb. Your leg will also be monitored for color (pale or pink), warmth (coolness), sensations of pain, and movement. The surgical incision may be tender or sore for several days after the procedure. Take a pain reliever for soreness as recommended by your physician. You may be on special IV medications to help your blood pressure and your heart, and to control any problems with bleeding. As your condition stabilizes, these medications will be gradually decreased and discontinued as your condition allows. Your diet will be advanced to solid foods as tolerated. When your physician determines that you are ready, you will be moved from the ICU to a post-surgical nursing unit. Your recovery will continue to progress. Your activity will be gradually increased as you get out of bed and walk around for longer periods of time. Arrangements will be made for a follow-up visit with your physician.

In the hospital - PTA of the femoral artery:

After the procedure you will be taken to the recovery room for observation. Once your blood pressure, pulse, and breathing are stable and you are alert, you may be taken to the intensive care unit (ICU) or your hospital room. You should immediately inform your nurse if you feel any chest pain or tightness, or any other pain, as well as any feelings of warmth, bleeding, or pain at the insertion site in your leg or arm. The nurse will assist you the first time you get up. You should move slowly when getting up from the bed to avoid any dizziness from the long period of bed rest.

You may be given pain medication for pain or discomfort related to the insertion site or having to lie flat and still for a prolonged period. Your diet will be advanced to solid foods as tolerated. Your hospital stay will depend on your condition and the results of your procedure. You will receive detailed instructions for your discharge and recovery period. Arrangements will be made for a follow-up visit with your physician.

At home - femoral popliteal bypass:

Once you are home, it will be important to keep the surgical area clean and dry. Your physician will give you specific bathing instructions. You may be advised not to participate in any strenuous activities. Your physician will instruct you about when you can return to work and resume normal activities. Your physician may want you to continue on specific medications, such as aspirin or clopidogrel (Plavix), after the procedure. Your physician may perform ultrasound examination(s) on your leg after surgery to monitor the new graft. Notify your physician to report any of the following:

y y y y

fever and/or chills increased pain, redness, swelling, or bleeding or other drainage from the leg incision coolness, numbness and/or tingling, or other changes in the affected extremity chest pain/pressure, nausea and/or vomiting, profuse sweating, dizziness, and/or fainting

Your physician may give you additional or alternate instructions after the procedure, depending on your particular situation.

At home - PTA of the femoral artery:

Once at home, you should monitor the insertion site for bleeding, unusual pain, swelling, and abnormal discoloration or temperature change at or near the insertion site. A small bruise is normal. If you notice a constant or large amount of blood at the site that cannot be contained with a small dressing, notify your physician. If your physician used a closure device for your insertion site, you will be given specific information regarding the type of closure device that was used and how to take care of the insertion site. There will be a small knot, or lump, under the skin, where the insertion site was. This is normal. The knot should gradually disappear over a few weeks. It will be important to keep the insertion site clean and dry. Your physician will give you specific bathing instructions.

You may be advised not to participate in any strenuous activities. Your physician will instruct you about when you can return to work and resume normal activities. Notify your physician to report any of the following:

y y y y

fever and/or chills increased pain, redness, swelling, or bleeding or other drainage from the insertion site coolness, numbness and/or tingling, or other changes in the affected extremity chest pain/pressure, nausea and/or vomiting, profuse sweating, dizziness, and/or fainting

Your physician may give you additional or alternate instructions after the procedure, depending on your particular situation.

From Wikipedia, the free encyclopedia Jump to: navigation, search

Classification and external resources

Histopathological image of myocarditis at autopsy in a patient with acute onset of congestive heart failure.


I09.0, I51.4


391.2, 422, 429.0






med/1569 emerg/326



In medicine (cardiology), myocarditis is inflammation of heart muscle (myocardium). It resembles a heart attack but coronary arteries are not blocked. Myocarditis is most often due to infection by common viruses, such as parvovirus B19, less commonly non-viral pathogens such as Borrelia burgdorferi (Lyme disease) or Trypanosoma cruzi, or as a hypersensitivity response to drugs.[1] The definition of myocarditis varies, but the central feature is an infection of the heart, with an inflammatory infiltrate, and damage to the heart muscle, without the blockage of coronary arteries that define a heart attack (myocardial infarction) or other common noninfectious causes.[2] Myocarditis may or may not include death (necrosis) of heart tissue. It may include dilated cardiomyopathy.[1] Myocarditis is often an autoimmune reaction. Streptococcal M protein and coxsackievirus B have regions (epitopes) that are immunologically similar to cardiac myosin. After the virus is gone, the immune system may attack cardiac myosin.[1]

Because a definitive diagnosis requires a heart biopsy, which doctors are reluctant to do because they are invasive, statistics on the incidence of myocarditis vary widely.[1] The consequences of myocarditis thus also vary widely. It can cause a mild disease without any symptoms that resolves itself, or it may cause chest pain, heart failure, or sudden death. An acute myocardial infarction-like syndrome with normal coronary arteries has a good prognosis. Heart failure, even with dilated left ventricle, may have a good prognosis. Ventricular arrhythmias and high-degree heart block have a poor prognosis. Loss of right ventricular function is a strong predictor of death.[1]

y y

y y y y y

1 Signs and symptoms 2 Causes o 2.1 Infections o 2.2 Toxins o 2.3 Immunologic o 2.4 Physical agents 3 Diagnosis 4 Treatment 5 Epidemiology 6 References 7 External links

[edit] Signs and symptoms

The signs and symptoms associated with myocarditis are varied, and relate either to the actual inflammation of the myocardium, or the weakness of the heart muscle that is secondary to the inflammation. Signs and symptoms of myocarditis include:[3]
y y

Chest pain (often described as "stabbing" in character) Congestive heart failure (leading to edema, breathlessness and hepatic congestion)

y y y y

Palpitations (due to arrhythmias) Sudden death (in young adults, myocarditis causes up to 20% of all cases of sudden death)[4] Fever (especially when infectious, e.g. in rheumatic fever) Symptoms in infants and toddlers tend to be more non-specific with generalized malaise, poor appetite, abdominal pain, chronic cough. Later stages of the illness will present with respiratory symptoms with increased work of breathing and is often mistaken for asthma.

Since myocarditis is often due to a viral illness, many patients give a history of symptoms consistent with a recent viral infection, including fever, rash, diarrhea, joint pains, and easy fatigueability. Myocarditis is often associated with pericarditis, and many patients present with signs and symptoms that suggest concurrent myocarditis and pericarditis.

[edit] Causes
A large number of causes of myocarditis have been identified, but often a cause cannot be found. In Europe and North America, viruses are common culprits. Worldwide, however, the most common cause is Chagas' disease, an illness endemic to Central and South America that is due to infection by the protozoan Trypanosoma cruzi.[3]

[edit] Infections
y y y y y

Viral (Parvovirus B19, Coxsackie virus, HIV, enterovirus, rubella virus, polio virus, cytomegalovirus, human herpesvirus 6 and possibly hepatitis C) Protozoan (Trypanosoma cruzi causing Chagas disease and Toxoplasma gondii) Bacterial (brucella, Corynebacterium diphtheriae, gonococcus, Haemophilus influenzae, Actinomyces, Tropheryma whipplei, Vibrio cholerae, Borrelia burgdorferi, leptospirosis, Rickettsia) Fungal (aspergillus) Parasitic (ascaris, Echinococcus granulosus, Paragonimus westermani, schistosoma, Taenia solium, Trichinella spiralis, visceral larva migrans, and Wuchereria bancrofti)

Bacterial myocarditis is rare in patients without immunodeficiency.

[edit] Toxins

Drugs (ethanol, anthracyclines and some other forms of chemotherapy, and antipsychotics, e.g. clozapine)

[edit] Immunologic
y y y y y

Allergic (acetazolamide, amitriptyline) Rejection after a heart transplant Autoantigens (scleroderma, systemic lupus erythematosis, sarcoidosis, systemic vasculitis such as Churg-Strauss syndrome, Wegener's granulomatosis) Toxins (arsenic, toxic shock syndrome toxin, carbon monoxide, snake venom) Heavy metals (copper, iron)

[edit] Physical agents


electric shock, hyperpyrexia, and radiation

[edit] Diagnosis

Endomyocardial biopsy specimen. Extensive eosinophilic infiltrate involving the endocardium and myocardium (hematoxylin and eosin stain).

Myocarditis refers to an underlying process that causes inflammation and injury of the heart. It does not refer to inflammation of the heart as a consequence of some other insult. Many secondary causes, such as a heart attack, can lead to inflammation of the myocardium and therefore the diagnosis of myocarditis can not be made by evidence of inflammation of the myocardium alone.[5] Myocardial inflammation can be suspected on the basis of electrocardiographic results (ECG), elevated C-reactive protein (CRP) and/or Erythrocyte sedimentation rate (ESR) and increased IgM (serology) against viruses known to affect the myocardium. Markers of myocardial damage (troponin or creatine kinase cardiac isoenzymes) are elevated.[3] The electrocardiogram (ECG) findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis).[3] The gold standard is still biopsy of the myocardium, generally done in the setting of angiography. A small tissue sample of the endocardium and myocardium is taken, and investigated by a pathologist by light microscopy andif necessaryimmunochemistry and special staining methods. Histopathological features are: myocardial interstitium with abundant edema and inflammatory infiltrate, rich in lymphocytes and macrophages. Focal destruction of myocytes explains the myocardial pump failure.[3] Cardiac magnetic resonance imaging (cMRI or CMR) has been shown to be very useful in diagnosing myocarditis by visualizing markers for inflammation of the myocardium.[6] Recently, consensus criteria for the diagnosis of myocarditis by CMR have been published [7]

[edit] Treatment
As most viral infections cannot be treated with directed therapy, symptomatic treatment is the only form of therapy for those forms of myocarditis. In the acute phase, supportive therapy including bed rest is indicated. For symptomatic patients, digoxin and diuretics provide clinical improvement. For patients with moderate to severe dysfunction, cardiac function can be supported by use of inotropes such as Milrinone in acute phase followed by oral therapy with ACE inhibitors (Captopril, Lisinopril) when tolerated. Patients who do not respond to conventional therapy are candidates for bridge therapy with left ventricular assist devices (LVADs). Heart transplantation is reserved for patients who fail to improve with conventional therapy.

From Wikipedia, the free encyclopedia

Jump to: navigation, search Not to be confused with Dioxin.


Systematic (IUPAC) name

4-[(3S,5R,8R,9S,10S,12R,13S,14S)-3[(2S,4S,5R,6R)-5-[(2S,4S,5R,6R)-5[(2S,4S,5R,6R)-4,5-dihydroxy-6-methyloxan-2-yl]oxy-4-hydroxy-6-methyl-oxan2-yl]oxy-4-hydroxy-6-methyl-oxan-2-yl] oxy-12,14-dihydroxy-10,13-dimethyl-1, 2,3,4,5,6,7,8,9,11,12,15,16,17-tetra decahydrocyclopenta[a]phenanthren17-yl]-5H-furan-2-one


CAS number


ATC code

C01AA02 C01AA05 C01AA08


CID 2724385









Chemical data



Mol. mass

780.938 g/mol


eMolecules & PubChem

Physical data

Melt. point

249.3 C (481 F)

Solubility in water

0.0648 mg/mL (20 C)

Pharmacokinetic data


60 to 80% (Oral)

Protein binding



Hepatic (16%)


36 to 48 hours
(patients with normal renal function)

3.5 to 5 days
(patients with impaired renal function)



Therapeutic considerations

Pregnancy cat.

A (Au), C (U.S.)

Legal status

S4 (Au), POM (UK), -only (U.S.)


Oral, Intravenous

(what is this?) (verify)

Digoxin (INN) (pronounced /d d ks n/[1]), also known as digitalis, is a purified cardiac glycoside extracted from the foxglove plant, Digitalis lanata.[2] Its corresponding aglycone is digoxigenin, and its acetyl derivative is acetyldigoxin. Digoxin is widely used in the treatment of various heart conditions, namely atrial fibrillation, atrial flutter and sometimes heart failure that cannot be controlled by other medication. Digoxin preparations are commonly marketed under the trade names Lanoxin, Digitek, and Lanoxicaps. It is also available as a 0.05 mg/mL oral solution and 0.25 mg/mL or 0.5 mg/mL injectable solution. It is marketed by GlaxoSmithKline.

y y y y y y y y

1 Actions 2 Mechanism of action 3 Clinical use 4 Adverse effects 5 In the news 6 References 7 Further reading 8 External links

[edit] Actions
The main pharmacological effects of digoxin are on the heart. Extracardiac effects are responsible for many of the adverse effects (see below). It has mechanical effects as it increases myocardial contractility, however, the duration of the contractile response is just slightly increased. Overall, the heart rate is decreased, while blood pressure increases as the stroke volume is increased, leading to

increased tissue perfusion. Myocardial efficiency improves due to improved hemodynamics, and the ventricular function curve is improved. Other, electrical effects are an initial brief increase in action potential, followed by a decrease as the K+ conductance increases due to an increased intracellular amounts of Ca2+ ions. The refractory period of the atria and ventricles is decreased, while it increases in the sinoatrial and AV nodes. A less negative resting membrane potential is made, leading to increased excitability. Other, more indirect effects are cholinomimetic because of vagal stimulation, giving rise to AV nodal delay. The conduction velocity increases in the atria, but decreases in the AV node. The effect upon Purkinje fibers and ventricles is negligible. Automaticity is also increased, in the atria, AV node, Purkinje fibers and ventricles. ECG changes are increased PR interval, due to decreased AV conduction, and a decreased QT interval because of the altered duration of decreased action potential. Also, the T wave is inverted, accompanied by ST depression. It may cause AV junctional rhythm and ectopic beats (bigeminy) resulting in ventricular tachycardia and fibrillation. Slight vasodilation is seen in heart failure. This effect is contrary to effects that should be seen as a result of increased intracellular calcium levels, but this occurs since digoxin improves hemodynamics, which leads to restored angiotensin levels and decreased sympathetic discharge, causing indirect vasodilation. Digoxin also affects the kidney by increased renal blood flow and increased GFR. A mild diuretic effect is seen only in heart failure.

[edit] Mechanism of action

The mechanism of action is not completely understood; however the current hypothesis is outlined below. Digoxin binds to a site on the extracellular aspect of the -subunit of the Na+/K+ ATPase pump in the membranes of heart cells (myocytes) and decreases its function. This causes an increase in the level of sodium ions in the myocytes, which leads to a rise in the level of intracellular calcium ions. This occurs because of a sodium/calcium exchanger on the plasma membrane, which depends on a constant inward sodium gradient to pump out calcium. Digoxin decreases sodium concentration gradient and the subsequent calcium outflow, thus raising the calcium concentration in myocardiocytes and pacemaker cells. Increased intracellular calcium lengthens Phase 4 and Phase 0 of the cardiac action potential, which leads to a decrease in heart rate.[citation needed] Increased amounts of Ca2+ also leads to increased storage of calcium in the sarcoplasmic reticulum, causing a

corresponding increase in the release of calcium during each action potential. This leads to increased contractility, the force of contraction, of the heart. There is also evidence that digoxin increases vagal activity, thereby decreasing heart rate by slowing depolarization of pacemaker cells in the AV node. .[3] This negative chronotropic effect would therefore be synergistic with the direct effect on cardiac pacemaker cells. Digoxin is used widely in the treatment of various arrhythmias (see below).

[edit] Clinical use

Today, the most common indications for digoxin are probably atrial fibrillation and atrial flutter with rapid ventricular response, but beta- or calcium channel- blockers should be the first choice.[4][5] High ventricular rate leads to insufficient diastolic filling time. By slowing down the conduction in the AV node and increasing its refractory period, digoxin can reduce the ventricular rate. The arrhythmia itself is not affected, but the pumping function of the heart improves owing to improved filling. The use of digoxin in heart problems during sinus rhythm was once standard, but is now controversial. In theory the increased force of contraction should lead to improved pumping function of the heart, but its effect on prognosis is disputable and other effective treatments are now available. Digoxin is no longer the first choice for congestive heart failure, but can still be useful in patients who remain symptomatic despite proper diuretic and ACE inhibitor treatment. It has fallen out of favor because it was proven to be ineffective at decreasing morbidity and mortality in congestive heart failure. It is shown to increase quality of life, however. Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours, digoxin is given once daily, usually in 125 g or 250 g dosing. In patients with decreased kidney function the half life is considerably longer, calling for a reduction in dosing or a switch to a different glycoside (such as digitoxin which although having a much longer elimination half-life of around 7 days, is mainly eliminated from the body via the liver, and thus not affected by changes in renal function). Effective plasma levels are fairly well defined, 1-2.6 nmol/l. In suspected toxicity or ineffectiveness, digoxin levels should be monitored. Plasma potassium levels also need to be closely controlled (see side effects below). Quinidine, verapamil, and amiodarone increases plasma levels of digoxin (by displacing tissue binding sites and depressing renal digoxin clearance) so plasma digoxin must be monitored carefully.

Researchers at Yale University looked at data from an earlier study to see if digoxin affected men and women differently. That study determined that digoxin, which has been used for centuries and makes the heart contract more forcefully, did not reduce deaths overall but did result in less hospitalization. Researcher Dr. Harlan Krumholz said they were surprised to find that women in the study who took digoxin died more frequently (33%) than women who took a placebo pill (29%). They calculated that digoxin increased the risk of death in women by 23%. There was no difference in the death rate for men in the study. Digoxin is also used as a standard control substance to test for p-glycoprotein inhibition.

[edit] Adverse effects

Main article: Digoxin toxicity

The occurrence of adverse drug reactions is common, owing to its narrow therapeutic index (the margin between effectiveness and toxicity). Adverse effects are concentration-dependent, and are rare when plasma digoxin concentration is <0.8 g/L.[6] They are also more common in patients with low potassium levels (hypokalemia), since digoxin normally competes with K+ ions for the same binding site on the Na+/K+ ATPase pump. Common adverse effects (1% of patients) include: loss of appetite, nausea, vomiting and diarrhea as the gastrointestinal motility increase. Other common effects are blurred vision, visual disturbances (yellow-green halos and problems with color perception), confusion, drowsiness, dizziness, insomnia, nightmares, agitation, and depression, as well as a higher acute sense of sensual activities.[7][unreliable source?] Less frequent adverse effects (0.1%1%) include: acute psychosis, delirium, amnesia, convulsions, shortened QRS complex, atrial or ventricular extrasystoles, paroxysmal atrial tachycardia with AV block, ventricular tachycardia or fibrillation, and heart block[6] Rarely, digoxin has been shown to cause thrombocytopenia. Gynaecomastia (enlargement of breast tissue) is mentioned in many textbooks as a side-effect thought to be due to the estrogen-like steroid moiety of the digoxin molecule[8] but when systematically sought, the evidence for this is equivocal.[9] The pharmacological actions of digoxin usually results in electrocardiogram (ECG) changes, including ST depression or T wave inversion, which do not indicate toxicity. PR interval prolongation, however, may be a sign of digoxin toxicity. Additionally, increased intracellular Ca2+ may cause a type of arrhythmia called bigeminy (coupled beats), eventually ventricular tachycardia or fibrillation. The combination of increased (atrial) arrhythmogenesis and inhibited atrio-ventricular conduction (for example paroxysmal atrial tachycardia with A-V block - so-called "PAT with block") is said to be pathognomonic (i.e. diagnostic) of digoxin toxicity.[10] An often described but rarely seen adverse effect of digoxin is a disturbance of colour vision (mostly yellow and green colour) called xanthopsia. It has been proposed that the painter Vincent van Gogh's "Yellow Period" may have somehow been influenced by

concurrent digitalis therapy. Other oculotoxic effects of digoxin include generalized blurry vision as well as seeing a "halo" around each point of light.[11] The latter effect can also be seen in van Gogh's Starry Night. Evidence of van Gogh's digoxin use is supported by multiple self portraits that include the foxglove plant, from which digoxin is obtained. Digoxin plasma concentrations may increase while on antimalarial medication hydroxychloroquine (based on two case reports from 1982).[12] In overdose, the usual supportive measures are needed. If arrhythmias prove troublesome, or malignant hyperkalaemia occurs (inexorably rising potassium level due to paralysis of the cell membrane bound ATPase-dependent Na/K pumps), the specific antidote is antidigoxin (antibody fragments against digoxin, trade names of Digibind and Digifab).[13] Toxicity can also be treated with higher than normal doses of potassium. Digoxin is not removed by hemo or peritoneal dialysis with enough effectiveness to treat toxicity. Digoxin has potentially dangerous interactions with verapamil,[14] amiodarone, erythromycin, and epinephrine (as would be injected with a local anesthetic).

From Wikipedia, the free encyclopedia Jump to: navigation, search

This illustration shows where some types of diuretics act, and what they do.

A diuretic is any drug that elevates the rate of urination and thus provides a means of forced diuresis. There are several categories of diuretics. All diuretics increase the excretion of water from bodies, although each class does so in a distinct way.


1 Types
o o o o o o o o

1.1 High ceiling loop diuretics 1.2 Thiazides 1.3 Carbonic Anhydrase Inhibitors 1.4 Digitalis 1.5 Potassium-sparing diuretics 1.6 Calcium-sparing diuretics 1.7 Osmotic diuretics 1.8 Low ceiling diuretics

y y y y y y

2 Uses 3 Mechanism of action 4 Adverse effects 5 See also 6 References 7 External links

[edit] Types
[edit] High ceiling loop diuretics
High ceiling diuretics are diuretics that may cause a substantial diuresis up to 20%[1] of the filtered load of NaCl and water. This is huge when compared to normal renal sodium reabsorption which leaves only ~0.4% of filtered sodium in the urine.

Loop diuretics have this ability, and are therefore often synonymous with high ceiling diuretics. Loop diuretics, such as furosemide, inhibit the body's ability to reabsorb sodium at the ascending loop in the nephron which leads to a retention of water in the urine as water normally follows sodium back into the extracellular fluid (ECF). Other examples of high ceiling loop diuretics include ethacrynic acid, torsemide and bumetanide.

[edit] Thiazides
Thiazide-type diuretics such as hydrochlorothiazide act on the distal convoluted tubule and inhibit the sodium-chloride symporter leading to a retention of water in the urine, as water normally follows penetrating solutes. Frequent urination is due to the increased loss of water that has not been retained from the body as a result of a concomitant relationship with sodium loss from the convoluted tubule. The short-term anti-hypertensive action is based on the fact that thiazides decrease preload, decreasing blood pressure. On the other hand the long-term effect is due to an unknown vasodilator effect that decreases blood pressure by decreasing resistance.

[edit] Carbonic Anhydrase Inhibitors

Carbonic anhydrase inhibitors inhibit the enzyme carbonic anhydrase which is found in the proximal convoluted tubule. This results in several effects including bicarbonate retention in the urine, potassium retention in urine and decreased sodium absorption. Drugs in this class include acetazolamide and methazolamide.

[edit] Digitalis
Digitalis increase output of urine by increasing cardiac output and increased circulation through kidney. Digitalis has a diuretic effect on heart failure patients due to cardiac edema

[edit] Potassium-sparing diuretics

These are diuretics which do not promote the secretion of potassium into the urine; thus, potassium is spared and not lost as much as in other diuretics. The term "potassium-sparing" refers to an effect rather than a mechanism or location; nonetheless, the term almost always refers to two specific classes that have their effect at similar locations:

Aldosterone antagonists: spironolactone, which is a competitive antagonist of aldosterone. Aldosterone normally adds sodium channels in the principal cells of the collecting duct and late distal tubule of the nephron. Spironolactone prevents aldosterone from entering the principal cells, preventing sodium reabsorption. A similar agent is potassium canreonate.

Epithelial sodium channel blockers: amiloride and triamterene.

[edit] Calcium-sparing diuretics

The term "calcium-sparing diuretic" is sometimes used to identify agents that result in a relatively low rate of excretion of calcium.[2] The reduced concentration of calcium in the urine can lead to an increased rate of calcium in serum. The sparing effect on calcium can be beneficial in hypocalcemia, or unwanted in hypercalcemia. The thiazides and potassium-sparing diuretics are considered to be calcium-sparing diuretics.[3]
y y

The thiazides cause a net decrease in calcium lost in urine.[4] The potassium-sparing diuretics cause a net increase in calcium lost in urine, but the increase is much smaller than the increase associated with other diuretic classes.[4]

By contrast, loop diuretics promote a significant increase calcium excretion.[5] This can increase risk of reduced bone density.[6]

[edit] Osmotic diuretics

Compounds such as mannitol are filtered in the glomerulus, but cannot be reabsorbed. Their presence leads to an increase in the osmolarity of the filtrate. To maintain osmotic balance, water is retained in the urine. Glucose, like mannitol, is a sugar that can behave as an osmotic diuretic. Unlike mannitol, glucose is commonly found in the blood. However, in certain conditions such as diabetes mellitus, the concentration of glucose in the blood (hyperglycemia) exceeds the maximum reabsorption capacity of the kidney. When this happens, glucose remains in the filtrate, leading to the osmotic retention of water in the urine. Glucosuria causes a loss of hypotonic water and Na+ leading to a hypertonic state with signs of volume depletion such as: dry mucosa, hypotension, tachycardia, and decreased turgor of the skin. Use of some drugs, especially stimulants may also increase blood glucose and thus increase urination.

[edit] Low ceiling diuretics

The term "low ceiling diuretic" is used to indicate that a diuretic has a rapidly flattening dose effect curve (in contrast to "high ceiling", where the relationship is close to linear). It refers to a pharmacological profile, not a chemical structure. However, there are certain classes of diuretic which usually fall into this category, such as the thiazides.[7]

[edit] Uses
In medicine, diuretics are used to treat heart failure, liver cirrhosis, hypertension and certain kidney diseases. Some diuretics, such as acetazolamide, help to make the urine more alkaline and are helpful in increasing excretion of substances such as aspirin in cases of overdose or poisoning. Diuretics are often abused by sufferers of eating disorders, especially bulimics, in attempts at weight loss. The antihypertensive actions of some diuretics (thiazides and loop diuretics in particular) are independent of their diuretic effect. That is, the reduction in blood pressure is not due to decreased blood volume resulting from increased urine production, but occurs through other mechanisms and at lower doses than that required to produce diuresis. Indapamide was specifically designed with this in mind, and has a larger therapeutic window for hypertension (without pronounced diuresis) than most other diuretics.

[edit] Mechanism of action

Classification of common diuretics and their mechanisms of action:
Location (numbered in distance along nephron)



Acidifying salts Arginine vasopressin receptor 2 antagonists Aquaretics

Ethanol, Water CaCl2, NH4Cl amphotericin B, lithium citrate Goldenrod, Juniper

inhibits vasopressin secretion

1. 1.

inhibit vasopressin's action Increases blood flow in kidneys

5. collecting duct 1.

Na-H exchanger antagonists dopamine[8] Carbonic anhydrase inhibitors acetazolamide[8], dorzolamide bumetanide[8], ethacrynic acid[8], furosemide[8], torsemide

promote Na+ excretion

2. proximal tubule[8]

inhibit H+ secretion, resultant promotion of Na+ and 2: proximal tubule K+ excretion inhibit the Na-K-2Cl symporter 3. medullary thick ascending limb 2. proximal tubule, descending limb 5. cortical collecting ducts 4. distal convoluted tubules 1. tubules

Loop diuretics

Osmotic diuretics

glucose (especially in uncontrolled promote osmotic diuresis diabetes), mannitol amiloride, spironolactone, triamterene, potassium canrenoate. bendroflumethiazide, hydrochlorothiazide caffeine[citation needed], theophylline, theobromine inhibition of Na+/K+ exchanger: Spironolactone inhibits aldosterone action, Amiloride inhibits epithelial sodium channels[8] inhibit reabsorption by Na+/Cl- symporter inhibit reabsorption of Na+, increase glomerular filtration rate

Potassium-sparing diuretics



Chemically, diuretics are a diverse group of compounds that either stimulate or inhibit various hormones that naturally occur in the body to regulate urine production by the kidneys. Herbal medications are not inherently diuretics. They are more correctly called aquaretics.

[edit] Adverse effects

The main adverse effects of diuretics are hypovolemia, hypokalemia, hyperkalemia, hyponatremia, metabolic alkalosis, metabolic acidosis and hyperuricemia [8].

Adverse effect

y y y y y y y y y y y

Symptoms lassitude[8] thirst[8] muscle cramps[8] hypotension[8] muscle weakness[8] paralysis[8] arrhythmia[8] arrhythmia[8] muscle cramps[8] paralysis[8] CNS symptoms[8] [8] o coma arrhythmia[8] CNS symptoms[8] Kussmaul respirations[8] muscle weakness neurological symptoms[8] o lethargy o coma o seizures o stupor gout tissue calcification[8] fatigue


y y

loop diuretics thiazides[8]



y y y y y y y y y y

acetazolamides[8] loop diuretics[8] thiazides[8] amilorides[8] triamterenes[8] spironolactone[8] thiazides[8] furosemides[8] loop diuretics[8] thiazides[8]



metabolic alkalosis

y y y y y

metabolic acidosis

y y y

acetazolamides[8] amilorides[8] triamterene[8]



y y y

y y y y y y y y y y

depression confusion anorexia nausea vomiting constipation pancreatitis increased urination gou


thiazides[8] loop diuretics[8]

ACE inhibitor
From Wikipedia, the free encyclopedia Jump to: navigation, search

Captopril, the first ACE inhibitor

ACE inhibitors or angiotensin-converting enzyme inhibitors, are a group of pharmaceuticals that are used primarily in treatment of hypertension and congestive heart failure.

y y

y y y

y y y y y

1 Clinical use 2 Mechanism of action o 2.1 The renin-angiotensin-aldosterone system (RAAS) o 2.2 Effects 3 Adverse effects 4 Contraindications and precautions 5 Examples o 5.1 Sulfhydryl-containing agents o 5.2 Dicarboxylate-containing agents o 5.3 Phosphonate-containing agents o 5.4 Naturally occurring 6 Comparative information o 6.1 ACEI equivalents 7 Angiotensin II receptor antagonists o 7.1 Use in combination 8 History 9 See also 10 References

[edit] Clinical use

ACE inhibitors are used primarily in the treatment of hypertension, though they are also sometimes used in patients with cardiac failure, renal disease or systemic sclerosis ACEIs can also be used to treat diabetic nephropathy and left ventricular hypertrophy.

[edit] Mechanism of action

Angiotensin-converting enzyme inhibitors reduce the activity of the renin-angiotensin-aldosterone system.

[edit] The renin-angiotensin-aldosterone system (RAAS)

Main article: Renin-angiotensin system

Renin-angiotensin-aldosterone system

One mechanism for maintaining the blood pressure is the release of a protein called renin from cells in the kidney (to be specific, the juxtaglomerular apparatus). This produces another protein called angiotensin, which signals the adrenal gland to produce a hormone called aldosterone. This system is activated in response to a fall in blood pressure (hypotension) as well as markers of problems with the salt-water balance of the body, such as decreased sodium concentration in a part of the kidney known as the distal tubule, decreased blood volume and stimulation of the kidney by the sympathetic nervous system. In such a situation, the kidneys release renin, which acts as an enzyme and cuts off all but the first 10 amino-acid residues of angiotensinogen (a protein made in the liver, and

which circulates in the blood). These 10 residues are then known as angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE) which removes a further 2 residues and is found in the pulmonary circulation as well as in the endothelium of many blood vessels.[1] The system in general aims to increase blood pressure by increasing the amount of salt and water the body retains, although angiotensin is also very good at causing the blood vessels to tighten (a potent vasoconstrictor).

[edit] Effects
ACE inhibitors block the conversion of angiotensin I to angiotensin II.[2] They, therefore, lower arteriolar resistance and increase venous capacity; increase cardiac output, cardiac index, stroke work, and volume; lower renovascular resistance; and lead to increased natriuresis (excretion of sodium in the urine). Renin will increase in concentration in the blood due to negative feedback of conversion of AI to AII. Angiotenson I will increase for the same reason. AII will decrease. Aldosterone will decrease. Bradykinin will increase due to less inactivation that is done by ACE enzyme. Under normal conditions, angiotensin II will have the following effects:

vasoconstriction (narrowing of blood vessels), which may lead to increased blood pressure and hypertension constriction of the efferent arterioles of the kidney, leading to increased perfusion pressure in the glomeruli.

y y

y y

Contribute to ventricular remodeling and ventricular hypertrophy of the heart. stimulation of the adrenal cortex to release aldosterone, a hormone that acts on kidney tubules to retain sodium and chloride ions and excrete potassium. Sodium is a "water-holding" molecule, so water is also retained, which leads to increased blood volume, hence an increase in blood pressure. stimulation of the posterior pituitary to release vasopressin (also known as anti-diuretic hormone (ADH)), which also acts on the kidneys to increase water retention. decrease renal protein kinase C.

With ACE inhibitor use, the effects of angiotensin II are prevented, leading to decreased blood pressure. Epidemiological and clinical studies have shown that ACE inhibitors reduce the progress of diabetic nephropathy independently from their blood pressure-lowering effect.[3] This action of ACE inhibitors is utilised in the prevention of diabetic renal failure.

ACE inhibitors have been shown to be effective for indications other than hypertension even in patients with normal blood pressure. The use of a maximum-dose of ACE inhibitors in such patients (including for prevention of diabetic nephropathy, congestive heart failure, prophylaxis of cardiovascular events) is justified because it improves clinical outcomes, independent of the blood pressurelowering effect of ACE inhibitors. Such therapy, of course, requires careful and gradual titration of the dose to prevent the effects of rapidly decreasing blood pressure (dizziness, fainting, etc.). ACE inhibitors have also been shown to cause a central enhancement of parasympathetic activity in healthy volunteers and patients with heart failure.[4][5] This action may reduce the prevalence of malignant cardiac arrhythmias, and the reduction in sudden death reported in large clinical trials. The ACE inhibitor enalapril has also been shown to reduce cardiac cachexia in patients with chronic heart failure.[6] Cachexia is a poor prognostic sign in patients with chronic heart failure.[7] ACE-inhibitors are now used to reverse frailty and muscle wasting in elderly patients without heart failure.[citation needed]

[edit] Adverse effects

Common adverse drug reactions include: hypotension, cough, hyperkalemia, headache, dizziness, fatigue, nausea, and renal impairment.[8] There is also some evidence to suggest that ACE inhibitors might increase inflammation-related pain.[9] A persistent dry cough is a relatively common adverse effect believed to be associated with the increases in bradykinin levels produced by ACE inhibitors, although the role of bradykinin in producing these symptoms remains disputed by some authors.[10] Patients who experience this cough are often switched to angiotensin II receptor antagonists. Rash and taste disturbances, infrequent with most ACE inhibitors, are more prevalent in captopril and is attributed to its sulfhydryl moiety. This has led to decreased use of captopril in clinical setting, although it is still used in scintigraphy of the kidney. Renal impairment is a significant adverse effect of all ACE inhibitors. The reason for this is still unknown. Some suggest that it is associated with their effect on angiotensin II-mediated homeostatic functions such as renal blood flow. Renal blood flow may be affected by angiotensin II because it vasoconstricts the efferent arterioles of the glomeruli of the kidney, thereby increasing glomerular filtration rate (GFR). Hence, by reducing angiotensin II levels, ACE inhibitors may reduce GFR, a marker of renal function. To be specific, ACE inhibitors can induce or exacerbate renal impairment in patients with renal artery stenosis. This is especially a problem if the patient is concomitantly taking an NSAID and a diuretic. When the three drugs are taken together, there is a very high risk of developing renal failure.[11]

ACE inhibitors may cause hyperkalemia. Suppression of angiotensin II leads to a decrease in aldosterone levels. Since aldosterone is responsible for increasing the excretion of potassium, ACE inhibitors ultimately cause retention of potassium. A severe allergic reaction that rarely can affect the bowel wall and secondarily cause abdominal pain can occur. This "anaphylactic" reaction is very rare as well. Some patients develop angioedema due to increased bradykinin levels. There appears to be a genetic predisposition toward this adverse effect in patients that degrade bradykinin more slowly than average.[12] In pregnant women, ACE inhibitors taken during the first trimester have been reported to cause major congenital malformations, stillbirths, and neonatal deaths. Commonly reported fetal abnormalities include hypotension, renal dysplasia, anuria/oliguria, oligohydramnios, intrauterine growth retardation, pulmonary hypoplasia, patent ductus arteriosus, and incomplete ossification of the skull.[13]

[edit] Contraindications and precautions

The ACE inhibitors are contraindicated in patients with:
y y y

Previous angioedema associated with ACE inhibitor therapy Renal artery stenosis (bilateral, or unilateral with a solitary functioning kidney) Hypersensitivity to ACE inhibitors

ACE inhibitors should be used with caution in patients with:

y y y y

Impaired renal function Aortic valve stenosis or cardiac outflow obstruction Hypovolemia or dehydration Hemodialysis with high-flux polyacrylonitrile membranes

ACE inhibitors are ADEC Pregnancy category D, and should be avoided in women who are likely to become pregnant.[8] In the U.S., ACE inhibitors are required to be labeled with a "black box" warning concerning the risk of birth defects when taking during the second and third trimester. It has also been found that use of ACE inhibitors in the first trimester is also associated with a risk of major congenital malformations, particularly affecting the cardiovascular and central nervous systems.[14]

Potassium supplementation should be used with caution and under medical supervision owing to the hyperkalemic effect of ACE inhibitors.

[edit] Examples
ACE inhibitors can be divided into three groups based on their molecular structure:

[edit] Sulfhydryl-containing agents

y y

Captopril (trade name Capoten), the first ACE inhibitor Zofenopril

[edit] Dicarboxylate-containing agents

This is the largest group, including:
y y y y y y

Enalapril (Vasotec/Renitec) Ramipril (Altace/Tritace/Ramace/Ramiwin) Quinapril (Accupril) Perindopril (Coversyl/Aceon) Lisinopril (Listril/Lopril/Novatec/Prinivil/Zestril) Benazepril (Lotensin)

[edit] Phosphonate-containing agents


Fosinopril (Monopril) is the only member of this group

[edit] Naturally occurring

y y

Casokinins and lactokinins are breakdown products of casein and whey that occur naturally after ingestion of milk products, especially cultured milk. Their role in blood pressure control is uncertain.[15] The Lactotripeptides Val-Pro-Pro and Ile-Pro-Pro produced by the probiotic Lactobacillus helveticus or derived from casein have been shown to have ACE-inhibiting and antihypertensive functions.[16][17]

[edit] Comparative information

All ACE inhibitors have similar antihypertensive efficacy when equivalent doses are administered. The main point-of-difference lies with captopril, the first ACE inhibitor, which has a shorter duration of action and increased incidence of certain adverse effects. Certain agents in the ACE inhibitor class have been proven, in large clinical studies, to reduce mortality post-myocardial infarction, prevent development of heart failure, etc.. The ACE inhibitor most prominently recognized for these qualities is ramipril (Altace). Because ramipril has been shown to reduce mortality rates even among patient groups not suffering from hypertension, there are some (mostly drug-company representatives) who believe that ramipril's benefits may extend beyond those of the general abilities it holds in common with other members of the ACE inhibitor class.[citation needed]

[edit] ACEI equivalents

The ACE inhibitors have different strengths with different starting dosages. Dosage should be adjusted according to the clinical response. [18] [19] [20]
ACE inhibitors dosages for hypertension Dosage Note: bid = 2 times a day, tid = 3 times a day, d = daily Drug dosages from Drug Lookup, Epocrates Online. Name Equivalent daily dose 10 mg Start Usual 20 40 mg Maximum 80 mg

Benazepril 10 mg Captopril Enalapril 50 mg (25 mg bid) 5 mg

12.5 25 mg bid-tid 25 50 mg bid-tid 450 mg/d 5 mg 10 40 mg 40 mg

Fosinopril Lisinopril Moexipril

10 mg 10 mg 7.5 mg

10 mg 10 mg 7.5 mg 4 mg 10 mg 2.5 mg 1 mg Start

20 40 mg 10 40 mg 7.5 30 mg 4 8 mg 20 80 mg 2.5 20 mg 2 4 mg Usual

80 mg 80 mg 30 mg 16 mg 80 mg 20 mg 8 mg Maximum

Perindopril 4 mg Quinapril Ramipril 10 mg 2.5 mg

Trandolapril 2 mg Name Equivalent daily dose

Note: bid = 2 times a day, tid = 3 times a day, d = daily Drug dosages from Drug Lookup, Epocrates Online. ACE inhibitors dosages for hypertension

[edit] Angiotensin II receptor antagonists

ACE inhibitors possess many common characteristics with another class of cardiovascular drugs called angiotensin II receptor antagonists, which are often used when patients are intolerant of the adverse effects produced by ACE inhibitors. ACE inhibitors do not completely prevent the formation of angiotensin II, as there are other conversion pathways, and so angiotensin II receptor antagonists may be useful because they act to prevent the action of angiotensin II at the AT1 receptor, leaving AT2 receptor unblocked; the latter may have consequences needing further study.

[edit] Use in combination

The combination therapy of angiotensin II receptor antagonists with ACE inhibitors may be superior to either agent alone. This combination may increase levels of bradykinin while blocking the generation of angiotensin II and its activity at the AT1 receptor. This 'dual blockade' may be more effective than using an ACE inhibitor alone, because angiotensin II can be generated via non-ACEdependent pathways. Preliminary studies suggest that this combination of pharmacologic agents may be advantageous in the treatment of essential hypertension, chronic heart failure,[21] and nephropathy.[22][23] However, more studies are needed to confirm these highly preliminary results. While statistically significant results have been obtained for its role in treating hypertension, clinical significance may be lacking.[24] Patients with heart failure may benefit from the combination in terms of reducing morbidity and ventricular remodeling.[25][26] The most compelling evidence for the treatment of nephropathy has been found: This combination therapy partially reversed the proteinuria and also exhibited a renoprotective effect in patients afflicted with diabetic nephropathy,[22] and pediatric IgA nephropathy.[27]

[edit] History
Main article: ACE inhibitors drug design

The first step in the development of (ACE) inhibitors was the discovery of angiotensin-converting enzyme (ACE) in plasma by Leonard T. Skeggs and his colleagues in 1956. Brazilian scientist Sergio Ferreira reported in 1965 of a 'bradykinin-potentiating factor (BPFs) present in the venom of bothrops jararaca, a South American pit viper.[28] Dr SH Ferreira then proceeded to John Vanes laboratory as a Post-Doc with his already-isolated BPFs. The conversion of the inactive angiotensin I to the potent angiotensin II was thought to take place in the plasma. However, in 1967, Kevin K. F. Ng and John R. Vane showed that the plasma (ACE) is too slow to account for the conversion of angiotensin I to angiotensin II in vivo. Subsequent investigation showed that rapid conversion occurs during its passage through the pulmonary circulation.[29] Bradykinin is rapidly inactivated in the circulating blood and it disappears completely in a single passage through the pulmonary circulation. Angiotensin I also disappears in the pulmonary circulation due to its conversion to angiotensin II. Furthermore, angiotensin II passes through the lungs without any loss. The inactivation of bradykinin and the conversion of angiotensin I to angiotensin II in the lungs was thought to be caused by the same enzyme.[30] In 1970, Ng and Vane using bradykinin potentiating factor (BPF) provided by Srgio Henrique Ferreira showed that the conversion of angiotensin I to angiotensin II is inhibited during its passage through the pulmonary circulation.[31]

Bradykinin-potentiating factor (BPF) is derived from the venom of the pit viper (Bothrops jararaca). It is a family of peptides, whose potentiating action is linked to inhibition of bradykinin by ACE. Molecular analysis of BPF yielded a nonapeptide BPF teprotide (SQ 20,881), which showed the greatest (ACE) inhibition potency and hypotensive effect in vivo. Teprotide had limited clinical value, due to its peptide nature and lack of activity when given orally. In the early 1970s, knowledge of the structure-activity relationship required for inhibition of ACE was growing. David Cushman, Miguel Ondetti, and colleagues used peptide analogues to study the structure of ACE, using carboxypeptidase A as a model. Their discoveries led to the development of captopril, the first orally-active ACE inhibitor in 1975. Captopril was approved by the United States Food and Drug Administration in 1981. The first non-sulfhydryl-containing (ACE) inhibitor enalapril was marketed two years later. Since then, at least twelve other ACE inhibitors have been marketed. In 1991, Japanese scientists created the first ever milk-based ACE inhibitor in the form of a fermented milk drink, using specific cultures to liberate the IPP from the dairy protein. It is interesting to note that Val-Pro-Pro is also liberated in this processanother milk tripeptide with a very similar chemical structure to IPP. Together, these peptides are now often referred to as lactotripeptides. Shortly after this, in 1996, the first human study confirmed the blood pressure-lowering effect of IPP in fermented milk.[32] Although twice the amount of VPP is needed to achieve the same ACE inhibiting activity as the originally discovered IPP, it is assumed that VPP also adds to the total blood pressure lowering effect.[33][33] Since the first lactotripeptides discovery, more than 20 human clinical trials have been conducted in many different countries.[17]

From Wikipedia, the free encyclopedia Jump to: navigation, search Intervention: Angioplasty ICD-10 code:

ICD-9 code: MeSH Other codes:

00.6 36.0 39.50 D017130

Angioplasty is the technique of mechanically widening a narrowed or obstructed blood vessel, typically as a result of atherosclerosis. An empty and collapsed balloon on a guide wire, known as a balloon catheter, is passed into the narrowed locations and then inflated to a fixed size using water pressures some 75 to 500 times normal blood pressure (6 to 20 atmospheres). The balloon crushes the fatty deposits, so opening up the blood vessel to improved flow, and the balloon is then collapsed and withdrawn. The word is composed of the medical combining forms of the Greek words aggeos meaning "vessel" and plasts meaning "formed" or "moulded". Angioplasty has come to include all manner of vascular interventions typically performed in a minimally invasive or percutaneous method.

y y y y y y y y y y y

1 History 2 Causes of Coronary Artery Disease 3 Angioplasty risks 4 After the procedure 5 Peripheral angioplasty 6 Coronary angioplasty 7 Renal artery angioplasty 8 Carotid angioplasty 9 Cerebral arteries angioplasty 10 See also 11 References

12 External links

[edit] History

Diagram of a balloon catheter.

Angioplasty was initially described by interventional radiologist Charles Dotter in 1964. [1] Dr. Dotter pioneered modern medicine with the invention of angioplasty and the catheter-delivered stent, which were first used to treat peripheral arterial disease. On January 16, 1964, Dotter percutaneously dilated a tight, localized stenosis of the superficial femoral artery (SFA) in an 82-year-old woman with painful leg ischemia and gangrene who refused leg amputation. After successful dilation of the stenosis with a guide wire and coaxial Teflon catheters, the circulation returned to her leg. The dilated artery stayed open until her death from pneumonia two and a

half years later. [2] Charles Dotter is commonly known as the "Father of Interventional Radiology" and was nominated for the Nobel Prize in medicine in 1978. The first coronary angioplasty on an awake patient was performed by German cardiologist Andreas Gruentzig in September 1977. [3]

[edit] Causes of Coronary Artery Disease

Blockages in the arteries may be caused by hypertension, diabetes, sedentary lifestyle, smoking, high cholesterol levels, diets high in saturated fats, and cardiovascular disease. Removing blockages is done with angioplasty.[4]

[edit] Angioplasty risks

Angioplasties are safer than bypass surgery and according to statistics less than 1% of people die from complications after this procedure.[5] Complications that may occur after or during an angioplasty are the following:
y y y y y y y y y

Tearing of the artery resulting in total blockage and possible myocardial infarction - this can usually be repaired with a stent A dislodged clot may cause a stroke in some circumstances (in less than 1% of patients who undergo angioplasties); Bleeding or bruising where the catheters were inserted; Kidney problems, especially in people with underlying kidney disease and diabetes - this is caused by the iodine contrast dye used for the X-ray; intravenous fluids and medications can be given before and after the procedure to try to reduce this risk. Arrhythmia (irregular heartbeat);[6] Allergic reaction to the dye given during the angioplasty; Myocardial infarction happens in 3 to 5% of the cases; The need for emergency coronary artery bypass grafting during the procedure (2-4 percent of people). This may occur if an artery closes down instead of opening up; Restenosis is one of the most common complications of angioplasties and it consists in the gradual re-narrowing of the blood vessels within the next several weeks to months after the procedure. There are certain conditions that increase the risk of developing this complication and these are hypertension, diabetes, angina or kidney disease. Blood clots (in-stent thrombosis) can form within stents hours or months after angioplasty and they may cause myocardial infarction.[7]

The risks carried by angioplasty are greater in patients older than 75 years, patients who suffer from diabetes or kidney disease or who have extensive heart disease or blot clots in the heart arteries. Also, patients with poor pumping function in their hearts and women are considered to have an increased risk for complications.

Complications such as myocardial infarction, stroke or kidney problems are however among the rarest. The death rate among patients who have angioplasty is very small, about 0.1% (compared to 1% to 2% for routine bypass surgery). All in all, the risks are relatively low and acceptable in most cases when one balances the potential benefit against the expected risk (risk-benefit ratio).[8]

[edit] After the procedure

After angioplasty, most of the patients are monitored overnight in the hospital but if there are no complications, the next day, patients are sent home. The catheter site is checked for bleeding and swelling and the heart rate and blood pressure are monitored. Usually, patients receive medication that will relax them to protect the arteries against spasms. Patients are typically able to walk within two to six hours following the procedure and return to their normal routine by the following week.[9] Angioplasty recovery consists in avoiding physical activity for several days after the procedure. Patients are advised to avoid any type of lifting, babysitting grandchildren or other strenuous physical activity for a week.[10] Patients will need to avoid physical stress or prolonged sport activities for a maximum of two weeks after a delicate balloon angioplasty.[11] Patients with stents are usually prescribed a blood thinner medication, clopidogrel which is taken at the same time with acetylsalicylic acid. These medications are intended to prevent blood clots and they are usually taken for at least the first months after the procedure is performed. In most cases, patients are administrated this type of medication for 1 year. Also, patients who are doing dental work are advised to cancel it because there is a risk of endocarditis, an infection of the heart. Patients who experience swelling, bleeding or pain at the insertion site, develop fever, feel faint or weak, notice a change in temperature or color in the arm or leg that was used or have shortness of breath or chest pain should immediately seek medical advice.

[edit] Peripheral angioplasty

Peripheral angioplasty refers to the use of a balloon to open a blood vessels outside the coronary arteries. It is commonly done to treat atherosclerotic narrowings of the abdomen, leg and renal arteries. PA can also be done to treat narrowings in veins, etc. Often, peripheral angioplasty is used in conjunction with peripheral stenting and atherectomy.

[edit] Coronary angioplasty

A coronary angiogram (an X-ray with radio-opaque contrast in the coronary arteries) that shows the left coronary circulation. The distal left main coronary artery (LMCA) is in the left upper quadrant of the image. Its main branches (also visible) are the left circumflex artery (LCX), which courses top-to-bottom initially and then toward the centre-bottom, and the left anterior descending (LAD) artery, which courses from left-toright on the image and then courses down the middle of the image to project underneath the distal LCX. The LAD, as is usual, has two large diagonal branches, which arise at the centre-top of the image and course toward the centre-right of the image. Main article: Percutaneous coronary intervention

Percutaneous coronary intervention (PCI), commonly known as coronary angioplasty is a therapeutic procedure to treat the stenotic (narrowed) coronary arteries of the heart found in coronary heart disease. These stenotic segments are due to the build up of cholesterol-laden plaques that form due to atherosclerosis. PCI is usually performed by an interventional cardiologist. Treatment with PCI for patients with stable coronary artery disease reduces chest pain, but does not reduce the risk of death, myocardial infarction, or other major cardiovascular events when added to optimal medical therapy.[12]

[edit] Renal artery angioplasty

Atherosclerotic obstruction of the renal artery can be treated with angioplasty of the renal artery (percutaneous transluminal renal angioplasty, PTRA). Renal artery stenosis can lead to hypertension and loss of renal function.

[edit] Carotid angioplasty

Carotid artery stenosis is treated with angioplasty and stenting for high-risk patients in many hospitals.

After Angioplasty - Procedures, Angioplasty Complications

After Angioplasty - Procedures

Most angioplasty patients remain in the hospital overnightusually in the cardiac care unit (CCU)or a special unit for patients undergoing cardiac catheterization and angioplasty. They should arrange for someone to drive them home from the hospital.

After the procedure, the sheath or sheaths are removed and pressure is applied to the areausually for 5 to 15 minutesto close off holes in the arteries made by insertion of the sheaths. A gauze dressing is taped to the area and the patient must lie on their back for 4 to 6 hours, while normal blood clotting seals the holes in the arteries.

Alternatively, holes made in the femoral artery can be sealed immediately after catheterization by stitching them closed or plugging them with collagen. If either of these methods is used, the patient may be able to sit up within an hour of the procedure and begin walking within several hours.

During this time, patients are monitored for recurring chest pains, which could indicate the treated artery is re-closing; bleeding at the insertion site; and signs of dye-induced kidney damage. Certain medications may be given intravenously.

Before leaving the hospital, patients receive information about long-term therapy that may help prevent future coronary artery disease, and instructions regarding when and to what extent they can resume normal activity. Heavy lifting and vigorous activity should be avoided for several days to ensure that arteries heal properly. Other recommendations depend on the success of the procedure and whether there are other blockages.

Patients who have undergone angioplasty continue treatment with aspirin or another antiplatelet medication indefinitely after the procedure. The number of medications that the patient must take, particularly those previously taken to treat chest pains caused by the blockage, usually decreases.

Studies have shown that some patients are resistant to the effects of aspirin therapy. Regular blood tests may be performed to monitor the patient's response; the results of these tests can be used to adjust the aspirin dosage or change the medication.

If a stent has been implanted, clopedigrol (Plavix) is usually prescribed to be taken once a day for 2 to 4 weeks. Clopedigrol is a potent aspirin-like medicine that reduces the risk for development blood clots inside the stent during the first few weeks after implantation.

Because clopedigrol is critically important in preventing potentially life-threatening complications, patients should receive this medication when they leave the hospital and take it as prescribed.

In July 2009, the U.S. Food and Drug Administration (FDA) approved prasugrel (Effient tablets) to reduce the risk for blood clots in angioplasty patients. This medication can reduce the risk for heart attack or stroke during or following angioplasty. Prasugrel, which carries a black box warning indicating that the drug can cause serious, sometimes fatal, bleeding, should not be used in patients with a history of stroke, transient ischemic attack (TIA), or uncontrolled bleeding.

Cardiac catheterization
From Wikipedia, the free encyclopedia Jump to: navigation, search

From Wikipedia, the free encyclopedia

Jump to: navigation, search

Classification and external resources


I80., I82.1







Thrombophlebitis is phlebitis (vein inflammation) related to a thrombus (blood clot).[1] When it occurs repeatedly in different locations, it is known as "Thrombophlebitis migrans" or "migrating thrombophlebitis".

y y y y y y

1 Signs and symptoms 2 Causes 3 Diagnosis 4 Prevention 5 Treatment 6 Prognosis

y y y

7 Complications 8 References 9 See also

[edit] Signs and symptoms

The following symptoms are often (but not always) associated with thrombophlebitis:[2]
y y y

pain in the part of the body affected skin redness or inflammation (not always present) swelling (edema) of the extremities (ankle and foot)

[edit] Causes
Thrombophlebitis (another medical term is "White Leg") is related to a thrombus in the vein. Risk factors include prolonged sitting and disorders related to blood clotting. Specific disorders associated with thrombophlebitis include superficial thrombophlebitis (affects veins near the skin surface) and deep venous thrombosis (affects deeper, larger veins). Thrombophlebitis migrans can be a non-metastatic manifestation of malignancies such as pancreatic carcinoma (Trousseau sign of malignancy). .

[edit] Diagnosis
The health care provider makes the diagnosis primarily based on the appearance of the affected area. Frequent checks of the pulse, blood pressure, temperature, skin condition, and circulation may be required. If the cause is not readily identifiable, tests may be performed to determine the cause, including the following:
y y y

Doppler ultrasound Extremity arteriography Blood coagulation studies

[edit] Prevention
Routine changing of intravenous (IV) lines helps to prevent phlebitis related to IV lines. See the specific disorders associated with thrombophlebitis for other preventive measures.

[edit] Treatment
For more specific recommendations, see the particular condition. In general, treatment may include the following:

Medications o analgesics (pain medications) o anticoagulants e.g warfarin or heparin to prevent new clot formation o thrombolytics to dissolve an existing clot such as intravenous streptokinase. o nonsteroidal anti-inflammatory medications (NSAIDS) such as ibuprofen to reduce pain and inflammation o antibiotics (if infection is present) selection will usually depend with the causative agent. o Support stockings and wraps to reduce discomfort

The patient may be advised to do the following:

y y y y

Elevate the affected area to reduce swelling. Keep pressure off of the area to reduce pain and decrease the risk of further damage. Apply moist heat to reduce inflammation and pain. Surgical removal, stripping, or bypass of the vein is rarely needed but may be recommended in some situations.

[edit] Prognosis
Thrombophlebitis and other forms of phlebitis usually respond to prompt medical treatment.

[edit] Complications

Complications are rare, but when they occur they can be serious. The most serious complication occurs when the blood clot dislodges, traveling through the heart and occluding the dense capillary network of the lungs; this is a pulmonary embolism which can be potentially life threatening.

Coronary catheterization - Visualization of the coronary arteries (in this case, the left coronary artery which gives the circumflex branch of left coronary artery).

Catheterization of a cardiac chamber, in this case the left ventricle (a ventriculogram).

Cardiac catheterization (heart cath) is the insertion of a catheter into a chamber or vessel of the heart. This is done for both investigational and interventional purposes. Subsets of this technique are mainly coronary catheterization, involving the catheterization of the coronary arteries, and catheterization of cardiac chambers and valves.


y y y y

1 Coronary catheterization o 1.1 Procedure o 1.2 Indications for investigational use o 1.3 Investigative techniques used with coronary catheterization 2 Catheterization of chambers and valves 3 History 4 References 5 External links

[edit] Coronary catheterization

Main article: Coronary catheterization

[edit] Procedure
Local anaesthetic is injected into the skin to numb the area. A puncture is then made with a needle in either the femoral artery in the groin or the radial artery in the wrist, before a guidewire is inserted into the arterial puncture. A plastic sheath (with a stiffer plastic introducer inside it) is then threaded over the wire and pushed into the artery (Seldinger technique). The wire is then removed and the side-port of the sheath is aspirated to ensure arterial blood flows back. It is then flushed with saline. Catheters are inserted using a long guidewire and moved towards the heart. Once in position above the aortic valve the guidewire is then removed. The catheter is then engaged with the origin of the coronary artery (either left main stem or right coronary artery) and x-ray opaque iodine-based contrast is injected to make the coronary vessels show up on the x-ray fluoroscopy image.

When the necessary procedures are complete, the catheter is removed. Firm pressure is applied to the site to prevent bleeding. This may be done by hand or with a mechanical device. Other closure techniques include an internal suture and plug. If the femoral artery was used, the patient will probably be asked to lie flat for several hours to prevent bleeding or the development of a hematoma. Cardiac interventions such as the insertion of a stent prolong both the procedure itself as well as the post-catheterization time spent in allowing the wound to clot. A cardiac catheterization is a general term for a group of procedures that are performed using this method, such as coronary angiography, as well as left ventrical angiography. Once the catheter is in place, it can be used to perform a number of procedures including angioplasty, angiography, balloon septostomy, and an Electrophysiology study.

[edit] Indications for investigational use

This technique has several goals:
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confirm the presence of a suspected heart ailment quantify the severity of the disease and its effect on the heart seek out the cause of a symptom such as shortness of breath or signs of cardiac insufficiency make a patient assessment prior to heart surgery

[edit] Investigative techniques used with coronary catheterization

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to measure intracardiac and intravascular blood pressures to take tissue samples for biopsy to inject various agents for measuring blood flow in the heart; also to detect and quantify the presence of an intracardiac shunt to inject contrast agents in order to study the shape of the heart vessels and chambers and how they change as the heart beats

[edit] Catheterization of chambers and valves

Catheterization of cardiac chambers and valves may be performed in the same round as a coronary catheterization, and may also involve nearby major vessels, such as the aorta. It is the main method of cardiac ventriculography (another being radionuclide ventriculography, whose use has largely been replaced by echocardiography).

It has the ability to measure the pressure gradient across a valve and derive valve area from it. Thereby, it can assist in diagnosis of, for example, aortic stenosis.[1] This is also the procedure used in balloon septostomy, which is the widening of a foramen ovale, patent foramen ovale (PFO), or atrial septal defect (ASD) using a balloon catheter.

[edit] History
Further information: History of invasive and interventional cardiology

The history of cardiac catheterization dates back to Claude Bernard (1813-1878), who used it on animal models. Clinical application of cardiac catheterization begins with Werner Forssmann in the 1930s, who inserted a catheter into the vein of his own forearm, guided it fluoroscopically into his right atrium, and took an X-ray picture of it. Forssmann won the Nobel Prize in Physiology or Medicine for this achievement, though hospital administrators removed him from his position owing to his unorthodox methods. During World War II, Andr Frdric Cournand, a professor at Columbia University College of Physicians and Surgeons who also shared the Nobel Prize, and his colleagues developed techniques for left and right heart catheterization.

[edit] References
1. ^ Elizabeth D Agabegi; Agabegi, Steven S. (2008). Step-Up to Medicine (Step-Up Series). Hagerstwon, MD: Lippincott Williams & Wilkins. ISBN 0-7817-7153-6.

[edit] External links

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MedlinePlus Medical Encyclopedia: Cardiac catheterization eMedicine: Cardiac Catheterization (Left Heart) [hide]v d eHealth science

Medicine Surgery Cardiac procedures (ICD-9-CM V3 35-37)

Coronary heart disease

Angioplasty Bypass/Coronary artery bypass (MIDCAB Off-pump CAB TECAB)

Valve repair - Mitral valve repair, Valvuloplasty (aortic, mitral)

Heart valves Valve replacement - Aortic valve replacement (Ross procedure) Mitral valve replacement Great vessels Bentall procedure Pulmonary thromboendarterectomy Valve-sparing aortic root replacement Cardiomyoplasty Dor procedure Heart transplantation Septal myectomy Ventricular reduction Alcohol septal ablation Pericardiocentesis Pericardiectomy Pericardial window Atrial septostomy Blalock-Taussig shunt Fontan procedure Norwood procedure Rastelli procedure Kawashima procedure Jatene procedure Mustard procedure Glenn procedure Blalock-Hanlon procedure Balloon septostomy Maze procedure (Cox maze and minimaze) Pacemaker insertion Catheter ablation Bruce Protocol Cardiac stress test Echocardiography Cardiotocography Electrocardiography Electrophysiology study Myocardial perfusion imaging Cardiac catheterization/Coronary catheterization Ventriculography Impedance cardiography Ballistocardiography



Congenital heart disease

Conduction system

Cardiology diagnostic tests and procedures

Heart function tests


Heparin Drip
(800) 889-3898

Also referred to as a heparin lock IV, a heparin drip is a medication that is injected into IV or catheter lines to promote free flow of blood in the lines by preventing blood clots. This form of the heparin drug is not appropriate for direct injection into the body's veins. The heparin drug is commonly used in the treatment of:
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atrial fibrillation deep vein thrombosis (DVT) peripherial aterial embolism pulmonary embolism (PE)

Additionally, heparin drips may be administered following certain procedures, including:

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aterial or cardiac surgeries blood transfusions or extractions (for blood tests) dialysis major abdominal or thoracic surgeries

Heparin Drip Dose

The specific heparin drip dose and rate will vary according to the type and severity of a patient's individual conditions. Depending on the situation, doctors may opt to administer a(n):
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Continuous heparin drip, which requires a coagulation test every four hours Intermittent heparin drip, which requires a coagulation test before each new drip is administered

Regardless of the specific dosing and drip rate, regular blood tests and platelet counts will need to be performed to monitor any changes in patients' health during the entire course of heparin drip therapy.

Heparin Drip Side Effects

Although rare, heparin drip side effects have been known to develop primarily in patients over 60 or those with a history of:

bacterial endocarditis (an infection of the heart lining)

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bleeding disorders (such as hemophilia) hypertension (high blood pressure) liver disease menstruation disorders stomach or intestinal disorders

Possible heparin drip side effects may include:

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alopecia, hair loss excessive hemorrhage (bleeding) heparin induced thrombocytopenia (a condition in which the immune system destroys blood platelets. If left untreated, thrombocytopenia can result in stroke, heart attack and death.) hyperkalemia, high levels of potassium in the blood (If left untreated, this condition can result in life-threatening arrhythmias.) osteoporosis severe allergic reaction, marked by breathing problems, skin rash and, in the worst cases, anaphylactic shock

Compensation for Injured Heparin Drip Patients

Those who develop serious heparin drip side effects (or families of deceased heparin patients) can win compensation for their injuries by pursuing a heparin lawsuit. To find out if they have a case against Baxter Healthcare (the maker of heparin), prospective plaintiffs should meet with a heparin lawyer. For eligible heparin drip patients, attorneys will work on contingency to help affected individuals win compensation for:
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funeral and burial costs (if applicable) prior hospital bills ongoing treatment costs lost wages permanent disabilities future living expenses pain and suffering


Medication Uses | How To Use | Side Effects | Precautions | Drug Interactions | Overdose | Notes | Missed Dose | Storage | Medical Alert

USES: This medication relaxes blood vessels allowing more blood to flow through. This improves blood flow to the heart. Oral dose forms are used to prevent angina (chest pain). This medication is NOT for treating an attack of chest pain that is already happening. HOW TO USE: This medication is best taken on an empty stomach with a full glass of water. Take exactly as prescribed. To be effective in preventing chest pain, you must continue taking this drug even if you feel well. Sustained-release or long acting tablets and capsules must be swallowed whole. Crushing or chewing them destroys the long action and may increase side effects. Do not stop taking this drug suddenly without consulting your doctor. Some conditions may become worse when the drug is suddenly stopped. Your dose may need to be gradually decreased. Notify your doctor if the medication does not appear to be as effective. Do not increase your dose or take it more often than prescribed without consulting your doctor. SIDE EFFECTS: Headache, dizziness, flushing, rapid heartbeat or restlessness may occur as your body adjusts to the medication. If they persist or become bothersome, inform your doctor. To prevent dizziness and lightheadedness when rising from a seated or lying position, get up slowly. Notify your doctor if you experience: blurred vision, dry mouth, skin rash, nausea. Headache is often a sign the medication is working. Treat headaches with an aspirin or non-aspirin pain reliever as recommended by your doctor. If the headaches continue or become severe, notify your doctor. In the unlikely event you have an allergic reaction to this drug, seek medical attention immediately. Symptoms of an allergic reaction include: rash, itching, swelling, dizziness, trouble breathing. If you notice other effects not listed above, contact your doctor or pharmacist.

nitrates-oral (cont.)
PRECAUTIONS: Before using this medication tell your doctor your medical history especially of: heart problems, head injury or surgery, glaucoma, thyroid conditions, anemia, alcohol usage, drug allergies. Use caution engaging in activities that require alertness or in operating machinery if this medication makes you dizzy or drowsy. Alcoholic beverages may increase the risk of fainting or of experiencing dizziness. This medication should be used during pregnancy only if clearly needed. Discuss the risks and benefits with your doctor. It is not known if this drug is excreted into breast milk. Consult your doctor before breast-feeding. DRUG INTERACTIONS: This drug should not be used with the following medications because very serious (possibly fatal) interactions may occur: drugs to treat impotence (e.g., sildenafil, vardenafil, tadalafil). If you are currently using any of these medications, tell your doctor or pharmacist before starting nitrates. Tell your doctor of all medications you may use including prescription and nonprescription drugs, especially of: drugs for high blood pressure, certain migraine drugs (ergot alkaloids), high doses of aspirin. Do not start or stop any medicine without doctor or pharmacist approval. OVERDOSE: If overdose is suspected, contact your local poison control center or emergency room immediately. US residents can call the US national poison hotline at 1-800-222-1222. Canadian residents should call their local poison control center directly. Symptoms of overdose may include nausea, vomiting, dizziness, fainting, unconsciousness, slow or rapid heartbeat, confusion, fever, or persistent throbbing headache. NOTES: Some persons may develop a tolerance to the effects of this medication over time. Notify your doctor if the medication appears to be losing its effectiveness or if the chest pain continues while taking this drug. MISSED DOSE: If you miss a dose, take as soon as remembered; do not take if it is almost time for the next dose, instead, skip the missed dose and resume your usual dosing schedule. Do not "double-up" the dose to catch up. STORAGE: Store this medication away from heat or flame. Always keep this medication in its original container. Keep container closed tightly to avoid moisture. MEDICAL ALERT: Your condition can cause complications in a medical emergency. For enrollment information call MedicAlert at 1-800-854-1166 (USA), or 1-800-668-1507 (Canada).