i have pain in my lower right stomache and lower middle right back what is it???
IT STARTED TUESDAY MY STOMACHE ON THE RIGHT SIDE ABOUT 5 INCHES AWAY FROM MY BELLY BUTTON ONLY NOW AND THEN AFTER THAT I STARTED HAVING PAIN ON MY RIGHT SIDE ON MY BACK ABOVE MY BUTT ABOUT 8 INCHES THE PAIN SLOWLY STARTED THEN WED IT GOT WORSE NOW THURSDAY ITS REALLY PAINFUL IN MY BACK AND THESTOMACHE ISNT AS BAD AND NOW WHERE IT IS HURTING ON MY STOMACHE IT FEELS LIKE I RUBBED FIBERGLASS INSULATION ON THE ONE SPOT FEELS LIKE A MILLION NEEDLES AT ONCE WHEN I TOUCH IT PLEASE HELP THIS IS PAINFUL AND IBUPROFEN 800 MG DONT EVEN HELP
Differential diagnosis is 1. Kidney stones 2. Shingles if there is a rash 3. Appendicitis 4. Muscle strain 5. Disc problems 6. Gall stones 8. Kidney infection 9. Kidney infarction 10. Colitis 11. Abdominal hernias and so on …………………………..Need to go to ER if not getting better . Might need blood tests , urine tests and CT Scan of stomach.
It is a nerve tonic that also sharpens memory, while reducing both stress and elevated levels of the stress hormone cortisol, and it also helps to promote physical and emotional endurance. It is a pillar of the traditional Indian medicine holistic healing system and known as an adaptogen. An adaptogen is an agent that helps our bodies “adapt” to different forms of stressors (environmental, physical, mental and emotional). It also promotes a sense of well being, relieves stress, supports immunity, increases strength, and provides relief from cold, fever and flu symptoms. It is also amazing for soothing digestive issues, promoting a healthy metabolism and stimulating weight loss. Current research offers substantial evidence that Holy basil protects against and reduces stress; enhances stamina and endurance; increases the body’s efficient use of oxygen; boosts the immune system; reduces inflammation; protects against radiation damage; lessens aging factors; supports the heart, lungs and liver; has antibiotic, antiviral and antifungal properties; enhances the efficacy of many other therapeutic treatments; and provides a rich supply of antioxidants and other nutrients. Overall, Holy basil is a premier adaptogen, helping the body and mind to adapt and cope with a wide range of physical, emotional, chemical and infectious stresses, and restores disturbed physiological and psychological functions to a normal healthy state.
Gotu Kola
Gotu Kola is a rejuvenative nervine recommended for nervous disorders, epilepsy, senility and premature aging. As a brain tonic, it is said to aid intelligence and memory. It strengthens the adrenal glands and cleanses the blood to treat skin impurities. It is said to combat stress and depression, increase libido and improve reflexes. It energizes the central nervous system and rebuilds energy reserves.
In India, gotu kola is regarded as perhaps the most spiritual of all herbs. Growing in some areas of the Himalayas, gotu kola is used by yogis to improve meditation. It is said to develop the crown chakra, the energy center at the top of the head and to balance the right and left hemispheres of the brain, which the leaf is said to resemble. It is said to fortify the immune system, both cleansing and feeding it and to strengthen the adrenals. It has been used as a pure blood tonic and for skin health.
Gotu kola has been called ‘a pharmacy in one herb’, because of its offering of such impressive benefits.
Ashwagandha
Ashwagandha is a herb of the ages. It is the ‘ginseng’ of Indian medicine medicine, and is considered an ‘adaptogen’, a term used to describe herbs that improve physical energy and athletic ability, increase immunity to colds and infections and increase sexual capacity and fertility. In Indian medicine ashwaganda is considered a rasayana herb, a herb which works on a nonspecific basis to increase health and longevity. Ashwagandha is extremely nourishing for the nervous system. It helps strengthen the nerves and maintain nerve function. Ashwagandha is a also helps to enhance mental ability and performance–it helps support memory and problem-solving skills and enhances the coordinated functioning of all aspects of the brain.
One reason for ashwagandha’s reputation as a general energy-promoting, disease-preventing tonic may be its effect on the immune system. Ashwagandha may also have a mild sedative effect on the central nervous system and in animal studies it has been shown to be a muscle relaxant. It is commonly used to increase vitality, particularly when recovering from chronic illnesses and pain management for arthritic conditions. It may also help regulate blood sugar which aids in suppressing sugar cravings. Numerous modern studies have found that ashwagandha is very effective in reducing inflammation, treating tumors, decreasing stress, increasing mental activity, invigorating the body, and as an antioxidant.
Neem
Known in India as the “village pharmacy,” neem is a powerful balancing herb with numerous therapeutic uses. Neem leaf and its constituents have been demonstrated to exhibit immunomodulatory, anti-inflammatory, antihyperglycaemic, antiulcer, antimalarial, antifungal, antibacterial, antiviral, antioxidant, antimutagenic and anticarcinogenic properties.
Neem has a positive effect on many of the body’s internal systems–respiratory, circulatory, digestive and eliminative. Its universal healing ability merits its designation as a rasayana-a class of elite herbs known for their powerful positive influence on the physiology.
Neem is regarded as a powerful supporter of the body’s natural defense mechanisms. Thus it helps support natural immunity, and helps protect the body from free radical damage. Free radicals have been implicated in a number of diseases as well as premature aging. Neem leaves are regarded by Indian healers as an effective internal cleanser. Neem leaves have a powerful purifying effect on the blood and help cleanse the liver and skin of toxins.
Brandon Gilbert and Derrick A. Arnold, Jing Masters, Tonic Herbalists, Authors, Yogis, and Shamans, are the co-owners of Jing Masters, a superfood-tonic-herb elixir bar in Louisville, Ky. Jing Masters is the world’s number 1 source for the most elite herbs and superfoods.
These two wall charts access the “trigger point pain patterns” from Travell-Simons “Myofascial Pain and Dysfunction: the Trigger Point Manual”, volumes 1 and 2. The charts cover both upper and lower extremities….
Mouth ulcers-those small yellow or white eruption lined inside your mouth! They are simply painful and they can make your life miserable with their miniscule presence. These rashes as small as a few millimeters are caused inside your mouth by break in the mucous membrane and appear like a depression in them.
Although mouth ulcers may be of different types, the two most common types are
- Ulcers caused by minor injuries
- Aphthous ulcers
The first type of mouth ulcer occurs when a person has a sharp edge on a tooth, or poorly fitting dentures. In these cases, the mouth is continuously getting hit by the edgy tooth that ultimately results in ulcer. These ulcers are treated by removing the source of the injury.
Aphthous ulcers are very small, but painful ulcers that most people experience in their lives at least once, especially in adolescence or young adulthood. The aphthous ulcers occur mainly when the body’s own immune system attack the mucosal lining of the mouth. These ulcers often are the result of deficiency in vitamin B12, folic acid or iron. They can also appear at the time of stress or certain hormonal circulation. They commonly occur due to the eating of certain foods. This type of mouth ulcer also may appear as a result of certain types of viral infections.
The mouthwashes are the most effective way of healing both types of ulcers. The mouthwash may be of two types: home made or commercial. In certain ulcers, the simple salt and warm water solution come to great help. The compound thymol glycerin mouthwash is another simple solution for certain ulcers. For more advanced ulcers, antiseptic mouthwashes such as chlorhexidine povidone iodine mouthwashes are applied.
If the ulcers are too painful, the mouthwashes containing local anaesthetics are applied. Local anaesthetics like benzydamine hydrochloride, choline salicylate gel or lignocaine provide temporary numbness at the affected area. However, the mouthwashes containing local anesthetics are not recommended for young children suffering from mouth ulcers. Mouthwash containing Carbenoxolone can be used to relieve the irritations of certain types of ulcers.
So far as the aphthous ulcers are concerned, treatment is based on medical advice. To treat this ulcer, mouthwash containing corticosteroids is most commonly prescribed. However for more severe cases, in addition to mouthwash, oral medications or injections are also recommended. But before you start using corticosteroids containing mouthwash, it is important to make sure that the ulcers are not caused by a viral infection.
There is another type of mouthwash to treat aphthous mouth ulcer. These mouthwashes contain a type of antibiotic called tetracycline.
Most of the mouth ulcers can be easily treated by the application of the mouthwashes. If they persist long, it is recommended to seek medical help, as they may be the outcome of poor immunity or other medical conditions.
People who live with chronic pain often find themselves in a catch-22. The very medications that ease their pain can damage their stomachs and, in some cases, lead to life-threatening complications. The American College of Gastroenterology estimates that 14 million arthritis patients regularly use non-steroidal anti-inflammatory drugs or NSAIDS. This includes the popular pain relievers aspirin, ib…
TDP Mineral Lamp is a type of Far Infrared Therapy. It is often called the “Miracle Lamp”, as it helps with pain relief and treats back pain, arthritis, shoulder pain, joint pain, etc. as an alternative medicine treatment. The term TDP Lamp is an abbreviation for Teding Diancibo Pu which translates to “special electromagnetic spectrum” lamp. TDP lamps were invented by Chongqing Silicate Research I…
How long does it take to heal after getting back surgery for a herniated disk?
Im getting lower lumbar surgery for a herniated disk and want to know how long I’ll be on bed rest for. My neurosurgeon said I shouldnt work for 3-4 weeks but I dont think I’ll be able to take off for a month. Does it really take that long?
I had surgery on my L-5. I was up walking around the next day. I was told to stay out of work for 4 weeks but went back in two. It depends on the kind of work you do. You need to be careful. You can definitely re-injure it.
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Safe Techniques to Reduce Pain, Build Strength, and Speed RecoveryStudies suggest that proactive strengthening and flexibility-recovery exercises can speed healing after spine surgery. Whether you’re preparing for or recovering from spinal surgery, recuperating from a back injury, or just dealing with a back that has ‘issues,’ this book offers an effective program to help you manage pain and regai…
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The Prosepra Electronic Pulse Massager features Transcutaneous Electrical Nerve Stimulation (TENS) that can help back and neck pain caused by trauma or strain. TENS therapy can help break the pain cycle by loosening the muscles an relieving pain. Compact, portable, micro-computer-controlled device Can be used on your shoulders, legs, arms, neck, back, and feet May help to relieve pain and numbne…
Whether you’ve been injured or want to avoid injury, the American Physical Therapy Association Book of Body Repair and Maintenance can help you. Part 1 is the first place to go if you’ve been hurt. It presents nine common injury sites–back, neck, jaw, shoulder, elbow, wrist and hand, hip, knee, and ankle and foot–describing the anatomy and function of that area of the body, what can go wro…
“Practice guidelines have recently become prominent as a response to rising health care costs, reported regional practice variations, and reports of ‘inappropriate’ medical care. They are now expected to meet a number of agendas, including improvement of the quality of health care, protection of professional autonomy, reduction of litigation risk, minimization of practice variation, provision of s…
This digital document is an article from Family Practice News, published by International Medical News Group on September 15, 2009. The length of the article is 705 words. The page length shown above is based on a typical 300-word page. The article is delivered in HTML format and is available immediately after purchase. You can view it with any web browser.Citation DetailsTitle: Opioids in chronic…
The treatment of chronic low back pain – Guidelines for the treatment of back pain problems
There are many treatments that can be selected a number of different costs, and all give the same results. It is therefore important that the treatment of chronic low back pain have some guidelines ago.
American Pain Society and the American College of Physicians worked together and published a set of guidelines has been completed, and tells the doctor what to do for patients with chronic low back pain.
One thing is necessary to indicate the cause of pain back and put in the category that is accurate, such as back pain caused by a congenital disease such as scoliosis or pain caused by mechanical reasons, such as nerve roots, joints, discs, a process flow, or the spine of a vertebra.
Other types include tumors, infections and diseases are not caused by injury.
More than the new guidelines is that X-rays should have a clear statement of the criteria behind their use before they are performed in one patient. Under the guidelines, the type of back pain that the patient has to be specified, and the causes behind him.
In addition, chronic pain new treatment standards under the types of prescription drugs must be specified, along with the course of treatment chosen for each patient, depending on back pain.
Whatever the type of treatment is chosen, either massage, alternative therapy prescribing, physical or prescription, should be chosen on the basis of each of the causes of back pain and symptoms.
If doctors guidelines used to treat chronic low back pain, as they are intended, the chances of successful treatment in the early stages increases. Another side effect is good that people will pass by a small number of treatment until healed.
Moreover, it will cost much less cure a patient with back pain, if these guidelines are respected. As health care costs increasing every year, these guidelines provide a relief much needed authorities and patients.
This video shows you a unique multidisciplinary approach to the assessment, treatment, and rehabilitation of lower back pain, injuries to pelvis, quadriceps and hamstrings.
Learn how to address the balance of iliopsoas, quadratus lumborum, and the deep six hip rotators. Learn the relationship between quadriceps and hamstrings on pelvic imbalance and back pain. It also addresses patellar tendiniti…
QI GONG FOR BEGINNERS/ is the perfect way to explore and experience the numerous benefits of Qi Gong. Used for thousands of years in China to build energy, improve & maintain health and cultivate peace of mind, these easy to learn practices are designed to enhance you vitality and well being. This DVD contains 8 customized routines to increase your physical and mental energy, reduce stress, improv…
HELP!!! I need to be prepared for my next doc appointment…We’re trying to find the best treatment for FM
I have fibromyalgia and allready have tried numerous pain management avenues. So far, what has worked best is a strict percocet doseage, yoga, swimming, walking, hypnotism….but my doc and I haven’t found a muscle relaxant that works best….used flexeril up to soma and seemingly every NSAID…..what are the strongest muscle relaxants and NSAIDs? We FINALLY found a med combo so I can sleep, but I still wake up stiff and like my body is on fire head to toe – muscle spasms in back and neck, tender points in hips and knees and thighs; some days even if I or someone else touches my skin, it hurts. Headaches and pain in face and skin are helped by the percocet – although it doesn’t make me feel “high”, just relief, probably like a regular person with a normal headache feels after taking excederine. Anyway, I’d like to go into my next appointment with some good suggestions for the strongest muscle relaxants and NSAIDs. PLEASE help. I’m doing everything else right to manage pain.
I have been on the Fentanyl Patch for 3 years. I started out at 25mcg’s, then 50mcg’s & now I am being weaned off 100mcg’s to go on Morphine. I also take Percocet 7.5 for intermitten pain and I have Valium 10mg for #1-Stress & #2-for a muscle relaxant. I also took a muscle relaxant called Robaxin. I didn’t find that helpful but you might. My Fibro mainly hurts from my knees down. It hurts to sleep (I’m on Requip), it hurts to walk and that will be a problem because I am going to visit my daughter in Germany this summer and we are going sightseeing in Germany and Italy (which requires alot of walking) and I’m afraid the Morphine and Percocet won’t work together. I have been looking in my PDR under muscle relaxants and I think you have may have exhausted them all. There is another medicine called Parafon Forte DSC which is under Muscle relaxants. The PDR book says it is used for severe, painful muscle spasms. I hope I have offered you some kind of suggestions for your doctor and yourself. As far as people making comments about you being a junkie because of the Morphine-just tell them that they should be grateful that they don’t suffer from a debilatering desease, (as if they really care). Good Luck to you.
The Prosepra Electronic Pulse Massager features Transcutaneous Electrical Nerve Stimulation (TENS) that can help back and neck pain caused by trauma or strain. TENS therapy can help break the pain cycle by loosening the muscles an relieving pain. Compact, portable, micro-computer-controlled device Can be used on your shoulders, legs, arms, neck, back, and feet May help to relieve pain and numbne…
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Is Ultram the best medication for lower back pain? ?
It’s not real serious pain, but it mostly hurts when I wake up in the morning.
Ultram is a truly horrible drug in all aspects. you are better off taking real opiates. Type in Ultram sucks on Google and read my friend. and read some of my other answrs, not going through the horrors of this crappy drug again.
Our new lower back pain electrodes is getting incredible reviews. Works for approximately 20-30 uses. Perfect for lower back. Connected and powered to 2 leads in order to supply exceptional power and intensity for lower back pain control….
The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”
“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.
MYOCARDIAL INFARCTION
Myocardial infarction refers to a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood of subsequently, necrosis or death to the myocardial tissue occurs.
The onset of the myocardial infarction process may be sudden or gradual and the progression of the event to complete takes approximately 3 to 6 hours.
PREVALENCE
Myocardial infarction is the leading cause of death in the United States (US) as well as in most industrialized nations throughout the world. Approximately 800,000 people in the US are affected and in spite of a better awareness of presenting symptoms, 250,000 die prior to presentation to a hospital.4 The survival rate for US patients hospitalized with MI is approximately 90% to 95%. This represents a significant improvement in survival and is related to improvements in emergency medical response and treatment strategies.
In general, MI can occur at any age, but its incidence rises with age. The actual incidence is dependent upon predisposing risk factors for atherosclerosis, which are discussed below. Approximately 50% of all MI’s in the US occur in people younger than 65 years of age. However, in the future, as demographics shift and the mean age of the population increases, a larger percentage of patients presenting with MI will be older than 65 years.
Men are more susceptible than women, but the risk is more in female than in male after menopause.
CORONARY ARTERIES
The coronary arteries supply the capillaries of the myocardium with blood
The right coronary artery (RCA) supplies the right atrium and ventricle, the inferior portion of the left ventricle, the posterior septal wall and the SA and AV nodes
The left coronary artery (LCA) consists of two major branchiate left anterior descending (LAD) and the circumflex (LCX).
The LAD artery supplies below the anterior wall of the left ventricle, anterior ventricular septum and the apex of the left ventricle.
The LCX artery supplies blood to the lateral and posterior surfaces of the left ventricle.
CARDIAC ENZYMES
Levels of cardiac markers rise overtime. Hence, enzymes are drawn in a serial pattern usually on admission and over 6-24 hrs until 3 samples are obtained.
Enzymes commonly evaluated include CK, CKMB, LDH, TroponinT & I.
CK-MB ratio indicates the extent of damage of the cardiac muscle. The more the ratio, the more the damage of the cardiac muscle. Troponins are preferred markers of myocardial injury or they are very cardiac specific & are thought to rise before permanent injury develops.
Increased troponin concentrations should not be used by themselves to rule out a heart attack. Troponin will remain high for 1–2 weeks following MI allowing easy diagnosis if patient presents late with an old MI as other CE’s will not be raised unless reinfarction occurs.
Elevation of Cardiac Enzymes in Myocardial Infarction
Enzyme Rises in Peaks in Normalizes in Normal Value CKMB ratio
CK 12 hrs 16-30hrs 3-5 days 35-232IU/L
CKMB 4-8 hrs 24 hrs 72 hrs < 51IU/L <6%
Troponin I 3-6 hrs 20 hrs 14 days 0.0-0.4 ng/ml
Troponin T 2-4 hrs 8-12 hrs 14 days 0.0-0.1 ng/ml
LDH 12 hrs 12-24 hrs 10 days 100-190 IU/L
PATHOPHYSIOLOGY
The most common sites of MI are in the left ventricle, the chamber of heart which has the greatest work load. Tissue changes that occur in the myocardium are related to the extent to which the cells have been deprived of oxygen. Total deprivation results in an area of infarction in which the cells die and the tissue become necrotic.
Necrosis in this area is evident with in 5 to 6 hours after the occlusion. In response to this necrosis the body increases its products of leukocytes, which aid in the removal of dead cells. As collateral circulation enlarges, it brings fibroblasts, which form a connective tissue scar with in the area of infarction. Usually, the formation of fibrous scar tissue is complete with in 2 to 3 months.
Immediately surrounding the area of infarction is a less seriously damaged areaof injury. It may deteriorate and thus extend the area of infarction or with adequate collateral circulation; it may regain its function with in 2 weeks.
The outer most area of damage is the zone of ischemia which borders the area of injury. The cells in this area are weakened by decreased oxygen supply, but function can return usually with in 2 to 3 weeks after the onset of occlusion.
RISK FACTORS
There are two types of risk factors for heart attack, including
Inherited factors
Acquired factors
Inherited factors
These are risk factors you are born with that cannot be changed, but can be improved with medical management and life style changes. Following are most at risk-
persons with inherited hypertension
persons with inherited low levels of HDL or high levels of LDL
persons with a family history of heart disease aging men and women
persons with diabetes mellitus [ type 1 diabetes ]
women, after the onset of menopause- generally, men are at risk, at an earlier age than women, but after the onset women are equally at risk
Acquired factors
These are risk factors that are caused by activities that we choose to include in our lives that can be managed through life style changes and clinical care. Following are most at risk-
Persons with acquired hypertension
persons with acquired low level of HDL or high level of LDL
cigarette smokers
people who are under a lot of stress
individual who lives a sedentary life
persons overweight by 30 % or more
TYPE OF MYOCARDIAL INFARCTION
1. Different degrees of damage occurs to the heart muscle-
Zone of necrosis: death to the heart muscle caused by extensive and complete oxygen deprivation that is, irreversible damage
Zone of injury: region of heart muscle surrounding the area of necrosis; inflamed and injured, but still viable if adequate oxygen can be restored.
Zone of ischemia: region of the heart muscle surrounding the area of injury, which is ischemic and viable; not endangered unless extension of the infarction occurs.
2. According to the layers of the heart muscle involved, MI can be classified as-
Transmural or Q wave infarction; area of necrosis occurs throughout the thickness of the heart muscle. Subendocardial or non transmural infarction; area of necrosis is confined to the innermost layer of the heart muscle.
3. Location of the MI is identified as location of the damaged heart muscle within the left ventricle inferior, anterior, lateral and posterior-
Left ventricle is the most common and dangerous location for MI, as it is the main pumping chamber of the heart
Right ventricular infarction commonly occurs I junction with damage to the inferior and or posterior wall of the left ventricle
4. Region of the heart muscle that becomes damaged determine by the coronary artery that becomes obstructed
Left main coronary artery
Circumflex branch
Anterior ascending branch
Great cardiac vein
Middle cardiac vein
Right cardiac vein
CLINICAL MANIFESTATIONS
1) Chest pain
not relieved by the rest over sublingual vasodilator therapy
severe steady sub sternal chest pain of a crushing and squeezing nature
may radiate to the arms, neck, jaw and shoulders
continuous more than 15 minutes
may produce anxiety and fear
2) Diaphoresis
3) Hypertension or hypotension
4) Bradycardia or tachycardia
5) Palpitation, severe anxiety, dyspnea
6) Disorientation, confusion and restlessness
7) Fainting, marked weakness
8) Nausea, vomiting, hiccoughs
9) Atypical symptoms such as epigastric pain abdominal distress, dull aching or tingling sensation, shortness of breath, extensive fatigue
DIGNOSTIC EVALUATION
1. ECG changes
Generally occur within 2 – 12 hours, but may take 72 – 96 hours.
Necrotic, injured and ischemic tissue alter ventricular depolarization and repolarization
ST segment depression and T wave inversion indicate a pattern of ischemia
ST elevation indicates an injury pattern
Anterior small V3 – V4 leads
Anterior extensive V2 – V5 leads
Anteroseptal V1- V3 leads
Posterior V1 – V2 leads, progressive R wave and ST depression
Anterolateral V4 – V6, I, Avl leads
Apical V5 – V6 leads
Inferior lead ii, iii and avf [ reciprocal ]
2. Elevation of serum enzymes and isoenzymes:
Enzymes are drawn in a serial pattern usually on admission and every 6 – 24 hours until 3 samples are obtained. Enzyme activity then is correlated to the extent of heart muscle damage
Enzymes commonly evaluated include are CK, LDH, CK-MB, AST, Troponin I, Troponin T. [Fig.4 ]
LDH 2 is normally greater than LDH 1 except when the heart muscle is damaged a reversal occurs
3. Other findings:
White blood cell count and sedimentation rate elevates due to inflammatory process associated with damaged heart muscle.
Radionuclide imaging allows recognition of areas of decreased perfusion
Position emission tomography determines the presence of reversible heart muscle injury and irreversible or necrotic tissue, extends to which the injured heart muscle has responded to treatment also can be determined
MANAGEMENT
Therapy is aimed at the protection of ischemic and injured heart tissue to preserve muscle function, reduce the infarct size, and prevent death. Innovative modalities provide early restoration of coronary blood flow , and the use of pharmacologic agents improve oxygen supply and demand, reduce and/or prevent disarrhythmias, and inhibit the progression of coronary artery disease.
1. Opiate analgesic therapy: Morphine is used to relieve pain, improve cardiac hemodynamics by reducing preload and after load and to relieve anxiety.
Meperidine [Demerol] is useful for pain management in those patients contraindicated to morphine or sensitivity to respiratory depression.
2. Anxiolytic agents: Benzodiazepines are used with analgesics when anxiety complicates chest pain and its relief
3. Antiplatelet agents: Aspirin interfere with the function of the enzyme cyclooxygenase and inhibits the formation of thromboxane A2. Within minutes aspirin prevents additional platelet activation and interferes with platelet adhesion and cohesion
Other antiplatelet agents are, Clopidogrel, Ticlopidine, Dipyridamole, these agents, specifically Clopidogrel may be useful for patients who have a true allergy to aspirin and some times can be used with combination with Aspirin.
4. Supplemental oxygen: Supplemental oxygen should be administered. The rationale for use is the assurance that erythrocytes will be saturated to maximum carrying capacity. Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and by other tissue may be diminished.
5. Nitrates: Intravenous Nitrates should be administered in MI, persistent ischemia, hypertension or large anterior wall MI. Nitrates are metabolized to nitric oxide in the vascular endothelium. Nitric oxide relaxes vascular smooth muscle and dilates the blood vessel lumen. Vasodilatation reduces both cardiac preload and after load, and decreases the myocardial oxygen requirements. Vasodilatation of the coronary arteries improves the blood flow through the partially obstructed vessels as well as through collateral vessels. When administered sublingually or intravenously, Nitroglycerin has a rapid onset of action.
6. Beta adrenergic blocking agents: Beta blockers are recommended within 12 hours of MI symptoms and are continued indefinitely. Beta blockers decrease the rate and force of myocardial contraction and decreases overall myocardial oxygen demand. During the acute phase of MI beta blockers may be initiated intravenously
7. Heparin: Unfractionated Heparin: intravenous unfractionated Heparin is recommended who undergo percutaneous revascularization. It is alsorecommended in patients who receive fibrinolytic therapy and non selective fibrinolytic agents such as urokinase, streptokinase and anistreplace. Heparin inhibits the additional formation and propagation of thrombi, effective when administered intravenous or subcutaneously.
Low-molecular-weight-Heparin: can be administered to MI clients not treated with fibrinolytic therapy
8. Fibrinolytic or Thrombolytic agents: Fibrinolytic therapy is indicated with ST segment elevation. Plasminogen activators restore coronary vessels by dissolving obstructing thrombus. The plasminogen activators have been shown to restore coronary blood flow in 50% to 80% of MI patients. The successful use of fibrinolytic agents provides a definite survival benefit that is maintained for years. Reteplase has been shown to produce slightly higher 60- and 90-minute angiographic patency rates than accelerated alteplase, while adverse-event rates were equal.
However, the better early patency rate did not translate into any survival advantage at 30 days follow-up. The most critical variable in achieving successful fibrinolysis is time from symptom onset to drug administration. A fibrinolytic is most effective when the “door-to-needle” time is 30 minutes or less.
9. Angiotensin converting enzyme inhibitors: Oral ACEI are recommended within the first 24 hours of the onset of the MI symptoms, decreases myocardial after load through vasodilatation.
10. Anti dysarrhythmic agents: Lidocaine decreases ventricular irritability, which commonly occurs post MI.
11. Calcium channel blockers: Improves the balance between the oxygen supply and demand by decreasing heart rate, blood pressure and dilating coronary vessels.
Diltiazem has been shown to decrease the incidence of reinfarction in patients with non-Q-Wave MIs.
12. Percutaneous Coronary Intervention [Fig-15]: Mechanical opening of the coronary vessel can be performed during an evolving infarction. A balloon tipped catheter is introduced through a guide wire into a coronary vessel with a non calcified atheromatous lesion. The balloon of the catheter is the inflated, causing disruption of the intima and changes in the atheroma. The result is an increase in the diameter of the lumen of the coronary vessel and improvement of blood flow below the lesion.
Percutaneous coronary intervention is an alternative therapy to fibrinolysis Restoration of coronary blood flow in a MI can be accomplished mechanically by percutaneous coronary intervention (PCI). Mechanical revascularization by PCI is used as a primary therapy as an alternative to fibrinolysis when fibrinolysis is not clearly indicated or contraindicated. PCI can successfully restore coronary blood flow in 90% to 95% of MI patients.
13. Surgical Revascularization: Emergent or urgent coronary artery bypass graft surgery is warranted in the setting of failed percutaneous intervention in patients with hemodynamic instability and coronary anatomy amenable to surgical grafting. Surgical revascularization is also indicated in the setting of mechanical complications of MI such as ventricular septal defect, free wall rupture, or acute mitral regurgitation. Restoration of coronary blood flow with emergency Coronary Artery Bypass Grafting (CABG) can limit myocardial injury and cell death if it is performed within 2 or 3 hours of symptom onset. Emergency CABG carries a higher risk of perioperative morbidity (bleeding and MI extension) and mortality than elective CABG. The risk of operative mortality during emergency CABG is increased in patients, who are in cardiogenic shock, those with previous CABG surgery, and with multi-vessel disease. On the other hand, urgent CABG confers a survival benefit in patients with recurrent ischemia post-MI whose coronary anatomy is unsuitable for complete revascularization with PCI. Elective CABG improves survival in post-MI patients who have left main artery disease, three-vessel disease, or two-vessel disease that is not amenable to PCI. The timing of elective CABG post-MI is controversial, but retrospective studies indicate that when CABG is performed as early as 3 to 7 days post-MI, operative mortality is equivalent to CABG performed on non-MI patients.
14. Cardiac Stress Testing: Cardiac stress testing post-MI has established value in risk stratification and assessment of functional capacity. Stress testing is not recommended within several days post-MI. Only sub-maximal stress tests should be performed in stable patients 4 to 7 days after MI. Exercise testing identifies patients with residual ischemia for additional efforts at revascularization. Exercise testing also provides prognostic information and acts as a guide for post-MI exercise prescription and cardiac rehabilitation.
15. Lipid Management: All post-MI patients should be on an American Heart Association Step II diet (< 200 mg cholesterol/day, < 7% of total calories from saturated fats). Post-MI patients with LDL-cholesterol levels > 100 mg/dL on a Step II diet are recommended to be on drug therapy to lower LDL-cholesterol levels < 100 mg/dL. Post-MI patients with HDL-cholesterol levels < 35 mg/dL on a Step II diet are recommended to participate in a regular exercise program and on drug therapy designed to increase HDL-cholesterol levels.4 Recent data indicate the all MI patients should be on statin therapy, regardless of lipid levels or diet
16. Long-term Medications: Most oral medications instituted in the hospital at the time of MI will be continued long-term. Therapy with aspirin and beta-blockade is continued indefinitely in all patients. ACEI is continued indefinitely in patients with congestive heart failure, left ventricular dysfunction (ejection fraction < 0.40), hypertension, or diabetes. A lipid-lowering agent, specifically a statin, in addition to dietary modification is continued indefinitely
17. Cardiac Rehabilitation: Cardiac rehabilitation provides a venue for continued education, re-enforcement of lifestyle modification, and adherence to a comprehensive prescription of therapies for recovery from MI, which includes exercise training. Participation in cardiac rehabilitation programs post-MI is associated with a decrease in subsequent cardiac morbidity and mortality. Other benefits include improvement in quality of life, functional capacity and social support. A minority of post-MI patients actually participate in formal cardiac rehabilitation programs due to either lack of structured programs, physician referrals, low patient motivation, non-compliance, or financial constraints.
NEED FOR THE STUDY
Reperfusion therapy, within which we include thrombolytic therapy and percutaneous coronary intervention (PCI), which includes angioplasty and stent placement, is the greatest advance in the treatment of acute myocardial infarction
Studies have shown that many patients with AMI who are eligible for reperfusion therapy do not receive it. Moreover, of those who do receive it, the time to administration of thrombolytic therapy, or “door-to-needle time” is often delayed, jeopardizing myocardium and leading to greater morbidity and mortality.
Clinical criteria and simple ECG parameters have limited value for the non-invasive diagnosis of myocardial reperfusion. Other methods, such as ST segment monitoring and kinetic analysis of biochemical markers, may also be value of in early identification of IRA {Infarct Related Artery}, total CK activity, CK-MB isoenzymes appear to be the most promising biochemical markers.
In addition, the thresholds suggested for the diagnosis of reperfusion were generally derived from “time-to-peak” values. This rules out early diagnosis because peak CK plasma values are reached, on averages 9 -+ 6 hours after thrombolysis.
Determination of plasma total and MB CK concentration provides accuracy superior to any other currently available method for the diagnosis of acute MI.
In addition to providing precise diagnosis of acute MI, quantitative MB CK assays can also be used to obtain an accurate estimate of infarct size. In recent years, accuracy in the diagnosis of acute MI has assumed even greater importance, since the choice and timing of a variety of diagnostic and therapeutic options following coronary care unit admission hinge on whether infarction has occurred. Furthermore, the advent of thrombolytic therapy of acute MI has emphasized the need for more sensitive biochemical markers of necrosis in the first hours. The eventual realization that the reestablishment of blood flow was the dominant mechanism for the diminution of infarct size led to a therapeutic approach dominated by thrombolysis and more literally by the use of interventions to open vessels and maintain them open.
The key observation is that benefit by the use of a drug could be demonstrated if the drug was given prior to the period of ischemia.
Nevertheless, the greatest benefit in the management of patients with myocardial infarction ha unquestionably been the reestablishment of blood flow as early as possible after occlusion
The aim of this study is to determine the reperfusion of injury exacerbated by thrombolytic drugs in Myocardial Infarction through the process of elevation of cardiac enzymes which peaks and comes to normal levels within 24 hours, preventing prolonged injury and ischemia of myocardial tissue.
However, the aim was to evaluate prospectively biochemical markers for the diagnosis of coronary patency early after IV thrombolysis for Acute Myocardial Infarction.
STATEMENT OF THE PROBLEM
“The effect of thrombolytric drugs on cardiac enzymes, Creatine Phospho kinase and Creatine Kinase -MB, in myocardial Infarction”.
OBJECTIVES
To evaluate the effect of thrombolytic drugs on cardiac enzymes.
To compare the effect of thrombolytic drugs and non thrombolytic drugs on cardiac enzymes
To determine the importance of thrombolytics for a patient with myocardial infarction
To suggest teaching guidelines to public regarding early seeking of medical help at the onset of chest pain.
OPERATIONAL DEFIITIONS
Effect: Result or produce a result
Thrombolytic drugs: medications used to dissolve blood clots
CPK: A cardiac isoenzyme which releases into the blood in high levels when an injury occurs to the heart. It is also known as Creatine Kinase or Creatine Phophokinase.
CK-MB: It is also a cardiac isoenzyme releases into the blood from the heart muscle during an injury of the heart
Myocardial infarction: Necrosis of a region of the myocardium caused by an interruption in the supply of blood to the heart, usually as a result of occlusion of a coronary artery.
HYPOTHESIS
“Thrombolytic agents has effect on fall in peak levels on cardiac enzymes, CK and CK-MB”
LIMITATIONS
Coronary care unit: The data of this research is applicable in the settings of coronary care unit.
Age: Clients are selected only between 35 to 65 yrs of age.
Myocardial infarction: This is also applicable to the clients who were admitted in the hospital within 6 hours of the onset of the chest pain with myocardial infarction who received Inj. Metalyse.
Acute coronary syndrome: The clients who are admitted after 6 hours of the onset of the chest pain with acute coronary syndrome are included in the control group.
METHODOLOGY:
This study was done by an experimental method of research design in the settings of Coronary Care Unit in Dubai Hospital, U.A.E. A consecutive series of patients receiving IV Metalyse [ Tenecteplase ] for MI from May 2006 to November 2006 were included in this study.
RESEARCH DESIGN:
This study uses the comparative design.
THE SETTINGS:
This study was conducted in patients irrespective of age, sex and nationality, who were admitted in Coronary Care Unit through Emergency Department in Dubai Hospital, U.A.E.
SAMPLE SIZE:
This study included 60 clients, men and women, irrespective of nationalities, between 35 years to 65 years of age. Among 60 clients 30 were taken as experimental group and another 30 considered as control group.
SAMPLING TECHNIQUE:
The samples are selected as convenient sample, into two groups, the experimental and control groups. The clients who received thrombolytic agents within 6 hours of the onset of the chest pain are selected as an experimental group, and the clients who were presented late after 6 hours of the onset of the chest pain and not received thrombolytics, are selected as control group. All patients treated had the diagnosis of myocardial infarction confirmed by subsequent elevation of both Creatine Kinase [CK] and CK-MB isoenzymes levels. IV Metalyse is administered at a dose of 6000 units to 9000 units according to the weight of the patients. Patients with acute MI who were admitted to CCU more than 6 hours of onset of pain were also included.
DATA COLLECTION PROCEDURE:
Data for the study is collected by an instrument, which consists of 22 items including sample number, age, and sex. Religion, nationality, occupation, food habits, life style onset of chest pain, date and time of admission, signs and symptoms, vital signs, type of MI, protocol of thrombolytic therapy, levels of cardiac enzymes, post thrombolytic treatment, drugs received and date of discharge.
Study reveals that, majority of the clients who had MI was from the Indian subcontinents, constituting 63.3 % and the minority constituting just 1.6 %, from Great Briton and Turkey. 3.3 % of the clients were Egyptians and Syrians. Bangladeshis comprised, 6.6 % and Pakistanis were about 21.6 %. Only 9.9 % of the clients who had MI were Dubai Nationals. Among them 46.6% of the clients were aged between 46 – 55 years and 41.6 % of the clients were between 36 – 45 years and the remaining 11.6 % of the clients are between 56 – 65 years of age.
36.2 % of the clients had acute coronary syndrome and were not given thrombolytics. Remaining of the clients was with true MI and most of them were thrombolysed. However, all clients have undergone coronary angioplasty. Out of these clients only one client had normal coronary vessels, two were with mild coronary stenosis for conservative medical treatment and 4 clients with major triple vessel block were posted for CABG. Rest of the clients was treated with Percutaneous Coronary Angioplasty to LAD [50%], RCA [21.6%] and Circumflex [13.5%].
It is also evident from the study that most of the Indians are affected with MI and the major contributing factors are smoking, stress and lack of knowledge about the disease condition.
Based on Chi-Square deviation the association between normalization of cardiac enzymes levels in the study groups are as follows-
In Experimental group, 30 clients have received Inj. Metalyse . among them except 4 clients, remaining 26 clients reports seen that cardiac enzymes are normalized within 24 hours after the admission and administration of thrombolytic agent.
In control group, 30 clients blood reports for normalization of cardiac enzymes were anlysed, where we found 27 clients reports shown the higher levels of cardiac enzymes after 24 hours of the admission.
Critical Value 14.56, P value < 0.05 and Null hypothesis rejected
Inj. Metalyse has a good effect on the cardiac muscle provided with Critical Value- 14.56, Probability Value- < 0.05, as evidenced by fall in peak levels of cardiac enzymes CK and CK-MB within 24 hours after received thrombolytic agent.
DISCUSSION
Tenecteplase [ Metalyse] is a recombinant fibrin-specific plasminogen activator. It binds to the fibrin component of the thrombus and selectively converts thrombus-bound plasminogen to plasmin, which degrades the fibrin matrix of the thrombus. Tenecteplase is cleared from the circulation by binding to specific receptors in the liver followed by catabolism to small peptides.
After single intravenous bolus injection of tenecteplase in patients with acute myocardial infarction, tenecteplase antigen exhibits biphasic elimination from plasma. There is no dose dependence of tenecteplase clearance in the therapeutic dose range.
The initial dominant half-life is 24+_5.5 [mean=/-SD] min. the terminal half-life is 129+_87 minutes, and plasma clearance is 119+_49 ml/min
The main finding of this study is the early peaking of the total CPK level and CK-MB
isoenzymes have identified with successful reperfusion after Metalyse therapy. The peak CPK levels reached in 12 hours and CK-MB levels were shifted in 6 hours. The study reveals that the cardiac enzymes levels peaked and normalized within 24 hours time in the experimental group who received Thrombolytic agents within 6 hours of the onset of the chest pain. Where as it took 3- 5 days for the enzyme levels to peak for clients in the control group, who did not receive thrombolytic agents due to late arrival to the hospital, resulting in more damage to the myocardium.
Thus, it is evident that the extent of injury to the myocardium as well as the oxygen demand is less in the experimental group of the clients.
Finally, it may be used as a surrogate end point for angiographic demonstration of
patency in future clinical studies of reperfusion therapy. Diagnostic performance improved when the analysis was restricted to patients treated >6 hours after the onset of symptoms.
CONCLUSION
Clinical studies of fibrinolytic therapy in myocardial infarction show, that early thrombolytic treatment starting within 6 hours of the onset of the chest pain, significantly decreases the risk of further damage of the myocardium and oxygen demand, by the process of fall in peak levels of cardiac enzyme levels within 24 hours.
Inj. Metalyse has early peaking of cardiac enzymes in experimental group reflect the Infarction Related Artery opened, the clot has dissolved by Inj. Metalyse which means we have good thrombolytic effect, that is why we have early peaking levels.
Early identification of patients with persistent occlusion after thrombolyis during
Acute Myocardial Infarction also is important because it can pave the way for rescue interventions such as rescue Percutaneous Transluminal Coronary Angioplasty or repeated thrombolysis.
NURSING IMPLICATIONS:
SERVICE
Determine intensity of client’s angina
Observe for signs and symptoms
Place patient in a comfortable position
Administer oxygen if required
Obtain vital signs every 15 minutes for 2 hours, every half an hour for one hour and
every hour for two hours then as required
Obtain a 12 lead ECG
Monitor for relief of pain
Monitor patient’s response to drug therapy
Institute continuous cardiac monitoring and observe for- reperfusion, arrhythmias, rhythm changes, bradycardia and tachycardia
Interpret rhythm strips
Watch for complaints of headache with use of nitrates
Watch for recurrences of pain. Reinforce the importance of notifying nursing staff whenever pain is experienced.
Administer medications to relieve patient’s anxiety as directed such as sedatives and tranquilizers
Provide complete bed rest for 24 hours
Determine level of activity that precipitated anginal pain occurs.
Identify specific activities patient may engage in that are below the level at which anginal pain occurs
Prepare for the diagnostic and treatment procedures such as coronary angiogram and PTCA [ Percutaneous Transluminal Coronary Angioplasty]
EDUCATION
Counsel on risk factors and life style changes such as-
Methods of stress reduction such as biofeedback and relaxation techniques
Low fat and low cholesterol diet
Avoid excessive caffeine intake
Do not use diet pills, nasal decongestants
Follow up visits to control diabetes and hypertension
Educate patient and family members regarding-
Prevention of recurrence of pain
Regular use of medications
Hazards of smoking
Prevention of other contributing factors
Regular follow up
Importance of dietary modifications
Avoiding activities which cause anginal pain such as sudden exertion, walking against the wind, extremes of temperature, emotionally stressful situations, refraining from engaging in physical activity for 2 hours after meals, reduce weight etc.
Appropriate use of medications
Side effects of medications
ADMINISTARTION
Lead interdisciplinary intervention programs
Education of nursing students and staff
Provide in-service nursing education
Maintenance of records and reports
Maintenance of statistics
Making of policies and procedures
Supervision and evaluation of staff performance
Recommendations for further study
A majority of post MI patients actually not participating in formal cardiac rehabilitation programs due to either lack of structured programs, physician
referrals, low patient motivation, non compliance and financial constraints.
Cardiac rehabilitation provides a venue for continued education, reinforcement
of life style modification and adherence to comprehensive prescriptions of
therapies for recovery for MI, which includes exercise training.
Participation in cardiac rehabilitation programs, post MI with a decrease in
subsequent cardiac morbidity and mortality.
Adequate education in the hospitals and work places on causative and contributing factors, preventive measures of heart attacks and re heart attacks, is necessary.
All forms of reperfusion, depending on local facilities, need to be available to patients. Protocols must be written and agreed for the strategy of reperfusion to be applied within a network. Early diagnosis of ST Elevation Myocardial Infarction is essential and is best achieved by rapid ECG recording and interpretation at first medical contact, wherever this contact takes place.
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Taking the contraceptive pill to the other side of the world? What do I do?
It is a completely different time zone there.
I am from Australia and I take my pill at 5:15 PM Brisbane time.
I am going to San Diego, but at 5:15 PM in Brisbane it is 12:15 PM there? Obviously it would be a bit inconvienient for me to take it at that time… what should I do about this problem?
I am on the pill because I get really bad lower back pain during my period… so don’t say “don’t take it”. I will be over there for a month.
Has anyone ever been in this situation?
What time should I take it while I am over there?
I thought that I could gradually start taking it earlier and earlier in Brisbane time until it is equivalent to like 6PM in San Diego… Please Help?
After long days of exploring I doubt I will still be awake at 12:15 PM to take it… sorry…
When I say 12:15 PM.. I actually mean AM… at night. My Bad sorry.
Take it an hour earlier every night until you leave. It’s truly NOT that big of a deal unless you are planning on humping someone the day you get off the plane.
The “same time” thing is a guideline, and a tool to help you remember to take it.
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I suffer from a herniated L5-S1 disc and am wondering if i can apply for a card. I’m very curious because the pain i suffer from is there all day, and i can do little to take away the pain. Oxycodone and flexeril help slightly but i hate taking medication. I would rather deal with the horrible pain then to take those medicines,call me insane but I feel that if I take these meds then i will become dependent on them and become addicted to them.
I know marijuana isn’t addictive and its a more natural healing option then oxycodones and all other pain meds.
I’ll be 18 when the law takes effect and really want to try it.
I do smoke weed now but it is only to help my severe chronic back pain. Im worried if i mention this to my doctor that he will think that im so marijuana feign and taking advantage of the new law, im not.
Bottom line: Is/will chronic pain by added to the list of conditions that can be solved by medical marijuana.
Probably not. Right now it’s only for super harsh stuff. If they gave it for pain, even chronic pain, almost all of us would be in the line for something or other.
PS they’ll probably drug test you before hand anyway.
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