throm·bus Pronunciation: Èthräm-bYs Function: noun Inflected Form(s): plural throm·bi -Ìb+, -Ìb : a clot of blood formed within a blood vessel and remaining attached to its place of origin—compare embolus isch·emia Variant(s): or chiefly British isch·ae·mia is-Èk-m-Y Function: noun : deficient supply of blood to a body part (as the heart or brain) that is due to obstruction of the inflow of arterial blood (as by the narrowing of arteries by spasm or disease)
: an·gi·na Pronunciation: an-Èj+-nY, Èan-jY- Function: noun : a disease marked by spasmodic attacks of intense suffocative pain: as a: a severe inflammatory or ulcerated condition of the mouth or throat —see ludwig's angina, vincent's angina b: angina pectoris Reperfusion therapy is medical treatment that restores blood flow through blocked arteries, typically after a heart attack (myocardial infarction). Categories of reperfusion therapy thus include clot-busting (thrombolytic) drugs and procedures to open arteries with stents, or to graft arteries around blockages.[1] These interventions have become so central to the modern treatment of acute myocardial infarction, that we are said to be in the reperfusion era.[2][3] Patients who present with suspected acute myocardial infarction and ST segment elevation (STEMI) or new bundle branch block on the 12 lead ECG are presumed to have an occlusive thrombosis in an epicardial coronary artery. They are therefore candidates for immediate reperfusion, either with thrombolytic therapy, percutaneous coronary intervention (PCI) or when these therapies are unsuccessful, bypass surgery. Individuals without a ST segment elevation are presumed to be experiencing either unstable angina (UA) or non-ST segment elevation myocardial infarction (NSTEMI). They receive many of the same initial therapies and are often stabilized with antiplatelet drugs and anticoagulated. If their condition remains (hemodynamically) stable, they can be offered either late coronary angiography with subsequent restoration of blood flow (revascularization), or non-invasive stress testing to determine if there is significant ischemia that would benefit from revascularization. If hemodynamic instability develops in individuals with NSTEMIs, they may undergo urgent coronary angiography and subsequent revascularization. The use of thrombolytic agents is contraindicated in this patient subset, however.[4] The basis for this distinction in treatment regimens is that ST segment elevations on an ECG are typically due to complete occlusion of a coronary artery. On the other hand, in NSTEMIs there is typically a sudden narrowing of a coronary artery with preserved (but diminished) flow to the distal myocardium. Anticoagulation and antiplatelet agents are given to prevent the narrowed artery from occluding. At least 10% of patients with STEMI don't develop myocardial necrosis (as evidenced by a rise in cardiac markers) and subsequent Q waves on EKG after reperfusion therapy. Such a successful restoration of flow to the infarct-related artery during an acute myocardial infarction is known as "aborting" the myocardial infarction. If treated within the hour, about 25% of STEMIs can be aborted.[5]
Thrombolytic therapy[edit] Main article: Thrombolysis Thrombolytic therapy is indicated for the treatment of STEMI if the drug can be administered within 12 hours of the onset of symptoms, the patient is eligible based on exclusion criteria, and primary PCI is not immediately available.[6] The effectiveness of thrombolytic therapy is highest in the first 2 hours. After 12 hours, the risk associated with thrombolytic therapy outweighs any benefit.[4][7] Because irreversible injury occurs within 2–4 hours of the infarction, there is a limited window of time available for reperfusion to work. Thrombolytic drugs are contraindicated for the treatment of unstable angina and NSTEMI[4][8] and for the treatment of individuals with evidence of cardiogenic shock.[9] Although no perfect thrombolytic agent exists, an ideal thrombolytic drug would lead to rapid reperfusion, have a high sustained patency rate, be specific for recent thrombi, be easily and rapidly administered, create a low risk for intra-cerebral and systemic bleeding, have no antigenicity, adverse hemodynamic effects, or clinically significant drug interactions, and be cost effective.[10] Currently available thrombolytic agents include streptokinase, urokinase, and alteplase (recombinant tissue plasminogen activator, rtPA). More recently, thrombolytic agents similar in structure to rtPA such as reteplase and tenecteplase have been used. These newer agents boast efficacy at least as well as rtPA with significantly easier administration. The thrombolytic agent used in a particular individual is based on institution preference and the age of the patient. Depending on the thrombolytic agent being used, adjuvant anticoagulation with heparin or low molecular weight heparin may be of benefit.[11][12] With TPa and related agents (reteplase and tenecteplase), heparin is needed to maintain coronary artery patency (openness.) Because of the anticoagulant effect of fibrinogen depletion with streptokinase[13] and urokinase[14][15][16] treatment, it is less necessary there.[11] Intracranial bleeding (ICB) and subsequent cerebrovascular accident (CVA) is a serious side effect of thrombolytic use. The risk of ICB is dependent on a number of factors, including a previous episode of intracranial bleed, age of the individual, and the thrombolytic regimen that is being used. In general, the risk of ICB due to thrombolytic use for the treatment of an acute myocardial infarction is between 0.5 and 1 percent.[11] Thrombolytic therapy to abort a myocardial infarction is not always effective. The degree of effectiveness of a thrombolytic agent is dependent on the time since the myocardial infarction began, with the best results occurring if the thrombolytic agent is used within two hours of the onset of symptoms.[17][18] If the individual presents more than 12 hours after symptoms commenced, the risk of intracranial bleed are considered higher than the benefits of the thrombolytic agent.[19] Failure rates of thrombolytics can be as high as 20% or higher.[20] In cases of failure of the thrombolytic agent to open the infarct-related coronary artery, the patient is then either treated conservatively with anticoagulants and allowed to "complete the infarction" or percutaneous coronary intervention (PCI, see below) is then performed. Percutaneous coronary intervention in this setting is known as "rescue PCI" or "salvage PCI". Complications, particularly bleeding, are significantly higher with rescue PCI than with primary PCI due to the action of the thrombolytic agent.
Percutaneous coronary intervention[edit] Main article: Percutaneous coronary intervention If these irregular, fast heart rhythms continue for a length of time, the body will not get enough oxygen-carrying blood. Without oxygen, the brain and body tissues cannot function normally and die.
Causes and Risk Factors What causes ventricular arrhythmia? Studies have shown that ventricular tachycardias (VT) often occur in patients who have had damage from a heart attack, cardiac surgery, or other conditions. Some people with inherited heart defects also experience VT. Sometimes VT affects individuals with no history of a heart condition. In cases of ventricular fibrillation (VF), patients usually lose consciousness very quickly. If a fast ventricular rhythm is not treated it can change into VF, can lead to sudden cardiac arrest and ultimately sudden cardiac death. Sudden cardiac arrest affects 350,000 people each year in the United States (meaning that every 38 seconds, someone dies from sudden cardiac arrest).1
Symptoms What are symptoms of ventricular arrhythmia? If you are in a fast ventricular arrhythmia, you may feel as though your heart is skipping beats or fluttering. If the rhythm is very fast, you may experience fainting spells, blackouts, temporary blind spots, or dizziness. Eventually, you may become unconscious and your heart might stop (cardiac arrest).
Diagnosis How is ventricular arrhythmia diagnosed? The diagnosis of ventricular arrhythmias, which are often unpredictable, can be challenging. To diagnose ventricular tachycardia (VT), your doctor may initially use an electrocardiogram (ECG) test. Some arrhythmias, however, are intermittent and may not always show up during an ECG test. Your doctor may suggest other monitoring tests that can identify when you are having an arrhythmia and what type of rhythm it is. There are two types of VTs that may be seen on ECG: Monomorphic VT looks the same from one beat to the next on the ECG Polymorphic VT has more than one shape on the ECG Ventricular tachycardias are often defined when three or more fast heart beat come from the same place in the ventricle. A VT is also described by how long it lasts: Nonsustained VT is a fast VT that stops within 30 seconds Sustained VT is a fast VT that stops after 30 seconds or with treatment In cases of ventricular fibrillation (VF), patients usually lose consciousness very quickly. Doctors typically consider a diagnosis of VF when a person suddenly collapses and experiences sudden cardiac arrest. An ECG at the time of collapse can confirm that the rhythm problem is VF. Further tests are usually necessary to determine the cause and possible treatments for VT or VF. An electrophysiology (EP) study test is a test used to evaluate heart rhythms from inside your heart.
Treatment How is ventricular arrhythmia treated? Both ventricular tachycardia (VT) and ventricular fibrillation (VF) are life-threatening heart rhythms. In emergencies, paramedics or medical personnel can treat these arrhythmias with external defibrillators, such as an AED. Long-term treatment options vary according to the type of arrhythmia and individual patient circumstances. Tachyarrhythmias can sometimes be stopped or treated with medicines or surgery. These treatments are used in an effort to control or destroy the portion of heart tissue that causes the abnormal rhythms. In other cases, an implanted electronic device may be used to treat the arrhythmia. An implantable cardioverter defibrillator (ICD) delivers electrical energy to the heart to slow it down to a more normal rhythm. This allows the S-A node to take control again. An ICD can use one or more types of energy to help your heart beat normally again. They include: Anti-tachycardia pacing (ATP) – If your rhythm is regular but fast, the ICD system can deliver a series of small, rapid electrical pacing pulses. These are used to interrupt the arrhythmia and return your heart to its normal rhythm. Cardioversion – If your arrhythmia is regular but very fast, the ICD can deliver a low-energy shock. This can stop the arrhythmia and return your heart to its normal rhythm. Defibrillation – For arrhythmias that are very fast and irregular, like VF, high-energy shocks can be used to stop the arrhythmia. Then your heart can return to its normal rhythm.
ICD Therapy - Watch the Video [00:19] Many people have arrhythmias that are dangerous and that can occur at any time. You might already have had an episode of VT or VF. This can happen even if you are taking medication to treat your abnormal heart rhythm. After studying test results, your doctor may decide that you might experience abnormal heart rhythms again, and perhaps, cardiac arrest. Your doctor may recommend an ICD for one or more of the following reasons: At least one experience of VT or VF Previous cardiac arrest or abnormal heart rhythm that caused you to pass out A fast heart rhythm that keeps returning and could cause death A fast heart rhythm that cannot be controlled with drugs Severe side effects from drug therapy A fast heart rhythm that cannot be cured by surgery Previous heart attack and a low ejection fraction
FPRIVATE "TYPE=PICT;ALT=Image of Patient Matt Noble" Matt Noble may be young—he’s in his 30s—but he has dealt with more heart problems than many people ever will. Born with a serious heart condition, he'd had three open-heart surgeries by age 5. When he received his first implantable cardioverter defibrillator at age 17, he'd already survived five sudden cardiac arrests. Matt knows about ICD therapy from his job and from his personal experience. “With my type of arrhythmia, I need to get full-energy shocks. So after the instant of pain from the shock, my chest is sore for a few seconds. But it's nothing compared to the pain I've had after CPR, before I had my defibrillator.” “I've probably had about 20 shocks in my life so far, but I still remember my first shock. For the first time, I realized that I actually felt safe after an arrhythmia instead of scared that I might die.” http://www.bostonscientific.com/lifebeat-online/heart-smart/ventricular-arrhythmias.html