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Heart Attack (Myocardial Infarction)

Similar treatment also for: Congestive Heart Failure

1. QXCI Treatment Possibilities

1.1. Heart related treatment

Systemic Treatment

Click Programs (from menu bar on top of main test screen)


Click Spinal and Sarcodes (from drop down menu)
Show Sarcode System
Click Circulation (middle left of page)
Add an Additional therapy superimposed (by selecting or unselecting above and on left side)
Click Start Treatment

Sarcode Stimulation

Click Programs (from menu bar on top of main test screen)


Click Spinal and Sarcodes (from drop down menu)
Click Timed Therapies (from middle of page)
Select treatment time by moving bar

Optionally select or unselect any additional treatment


Click Circulation Stim (from first column)
To close click on OK in Therapy Over window and then
click Close
Click Heart Stabilaizer (from third column)
To close click on OK in Therapy Over window and then
click Close

Organ specific biofeedback

Click Programs (from menu bar on top of main test screen)


Click Biofeedback (from drop down menu)
Click Organ Systems (from menu bar on top of biofeedback screen)
Have patient look at screen and focus mind on area of concern
Click Cholesterol (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)

Additional specific biofeedback

Click Programs (from menu bar on top of main test screen)


Click Biofeedback (from drop down menu)
Click Additional (from menu bar on top of biofeedback screen)
Have patient look at screen and focus mind on area of concern
Click Heart (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)

Biofeedback

Click Programs (from menu bar on top of main test screen)


Click Biofeedback (from drop down menu)
Have patient look at screen and focus mind on area of concern
Click Heart Stabilization (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)

1.2. Pain related treatment

Additional specific biofeedback

Click Programs (from menu bar on top of main test screen)


Click Biofeedback (from drop down menu)
Click Additional (from menu bar on top of biofeedback screen)
Have patient look at screen and focus mind on area of concern
Click Pain (from drop down menu)
To stop click STOP PROGRAM (from upper right corner)

Timed Treatment

Click Programs (from menu bar on top of main test screen)


Click Timed Therapy Music Superlearning (from drop down menu)
For best results have patient focus mind on Area of Concern

Click Timed Treatments (from middle of page)


Click Start Auto Pain Treatment
To close click on OK in Therapy over window and then
click Close

2. General Information

2.1. Myocardial Infarction (Heart Attack)

Ischemic necrosis of the myocardium resulting from inadequate coronary artery blood flow. (See
also Coronary Artery Disease and Angina.)

Causes and Incidence More than 90% of all myocardial infarctions (MIs) are caused by
obstruction of a plaque-lined coronary artery by an acute thrombus. MI also may be caused by arterial
embolization from valvular stenosis or endocarditis and by arterial spasm after cocaine ingestion. Each
year more than 1 million people in the United States suffer an MI; one in four dies, and more than half of
the deaths occur within 1 hour of onset.
Disease Process Occlusion of a coronary artery causes a persistent cellular ischemia that interferes
with myocardial tissue metabolism, causing rapid, permanent cell damage and necrosis. The extent of
necrosis is dictated by the size of the infarct, the vessel occluded, and the length of time it remains
occluded. Damage initially occurs to the left ventricle but often extends to other cardiac chambers.
Infarcts may be classified by the thickness of the myocardial tissue involved. Transmural infarcts (Q
wave) involve the full thickness of the myocardium from the epicardium to endocardium and cause
abnormal Q waves on the ECG. Nontransmural infarcts (non--Q wave) do not extend through the
ventricular wall and cause ST segment or T wave ECG abnormalities.

Symptoms Most individuals have prodromal symptoms such as fatigue, shortness of breath, and
crescendo angina days or weeks before the acute attack. The first symptom of the attack is usually a deep,
substernal, visceral pain that may be described as aching, squeezing, or crushing, or as a heavy weight on
the chest. The pain may radiate to the back, neck, jaw, teeth, or left arm, and it is not relieved by rest,
nitroglycerin, or antacids. Other signs and symptoms include anxiety; restlessness; sweating; nausea;
vomiting; cold, clammy skin; low-grade fever; and dyspnea.

Potential Complications Complications include arrhythmia, cardiogenic shock, heart failure,


pulmonary edema, cerebral or pulmonary emboli, myocardial rupture, pericarditis, postmyocardial
infarction syndrome, and sudden death.

Diagnostic Tests The diagnosis is made using a clinical history; electrocardiography, which
illustrates an elevation in the ST segment, T wave inversion, and deep Q waves; laboratory tests of
cardiac enzymes (aspartate aminotransferase, creatine phosphokinase, lactate dehydrogenase), which are
elevated for days after the event; a complete blood count, which reveals an elevated white count and
erythrocyte sedimentation rate; a thallium perfusion scan, to determine the size and location of the infarct
and resulting ischemia; and an echocardiogram, to detect contraction abnormalities of ventricles.
Treatments

Surgery

Angioplasty post thrombolysis is contraindicated; recent clinical trials have shown no benefit and
possible harm from angioplasty performed within the first few days after an attack; angioplasty may have
a rescue role in cardiogenic shock that is unresponsive to other treatment

Drugs

Thrombolytic drugs are given within 6 hours of onset to interrupt MI evolution; aspirin and
anticoagulants for antiplatelet, anticoagulant effects; beta-adrenergic blockers to reduce reinfarction and
infarct size; vasodilators and narcotic analgesics for pain; stool softeners to avoid straining at stool;
sedatives and tranquilizers to increase rest

General

Cardiovascular monitoring; oxygen therapy; bed rest; decreased environmental stimuli; monitoring for
and treatment of depression, particularly about the third day; quitting smoking; restriction of caffeine and
cholesterol; antiembolism hose; rehabilitation with stepped exercise program; sexual counseling; regular
medical follow-up

2.2. Congestive Heart Failure

A complex clinical syndrome that results when the heart is unable to pump an adequate supply of
blood to meet the body's metabolic needs, leading to inadequate tissue perfusion; vascular, cardiac,
and pulmonary congestion; and diminished functional capacity.

Causes and Incidence Congestive heart failure (CHF) can have a number of causes, which can be
classified as either decreasing myocardial motility or increasing myocardial workload. Causes that
decrease motility include coronary artery disease, myocarditis, cardiomyopathy, tumors, lupus
erythematosus, and scleroderma, as well as drugs such as beta-blockers and calcium antagonists.
Workload is increased by hypertension, valvular heart disease, intracardiac shunting, anemia,
hyperthyroidism, and arteriovenous fistulas. Pericarditis, tamponade, and cardiac dysrhythmias interfere
with ventricular filling. The incidence of CHF is increasing as the population ages. It is estimated that 2.5
to 3 million Americans have CHF, and it is the most common hospital discharge diagnosis for individuals
over 65 years of age.

Disease Process When the heart is unable to pump a sufficient supply of blood to meet the body's
demands, three primary compensatory mechanisms attempt to maintain cardiac function: (1) the
sympathetic nervous system response increases, with increased catecholamine discharge, in an effort to
increase myocardial contractility, which in turn causes vasoconstriction that increases peripheral
resistance and cardiac workload; (2) cardiac fluid volume increases in an effort to stretch the fibers in the
ventricles and increase the force of the contraction; and (3) the myocardium hypertrophies in an attempt
to increase the amount of contractile tissue available and thus increase contractility.
When these compensatory mechanisms are insufficient or when they are active over extended periods,
they become ineffective and eventually contribute to failure of the pump. Pump failure usually begins
with the left ventricle and progresses to the right ventricle. It may be either acute or chronic, depending
on the cause.

Symptoms
Left ventricle failure
Tachycardia, fatigue and dyspnea on exertion, intolerance to cold, cough, bloodtinged sputum,
restlessness, paroxysmal nocturnal dyspnea, insomnia, crackles and wheezes in the lungs, ventricular and
atrial gallops
Right ventricle failure
Fatigue, fullness in the neck and abdomen, ankle swelling, distention of neck veins, weakness, anorexia,
nausea, liver enlargement, nocturia, ascites, tricuspid murmur

Potential Complications Acute pulmonary edema occurs with acute heart failure and is manifested
as extreme dyspnea, cyanosis, hyperpnea, and plunging oxygen saturation. Death occurs if the condition
is not treated immediately. Myocardial infarction and renal failure are other complications of CHF.
Diagnostic Tests
Blood chemistry
Elevated blood urea nitrogen, creatinine, glucose; decreased potassium, sodium; elevated aspartate
aminotransferase, bilirubin; prolonged partial thromboplastin time
Arterial blood gases
Decreased oxygen saturation
Complete blood count
Decreased hemoglobin and hematocrit with anemia

Chest x-ray
Cardiomegaly; engorged pulmonary vasculature
Echocardiography
To visualize increased or decreased chamber dimensions, decreased wall motion

Cardiac catheterization
Definitive diagnosis of cause and extent of damage
Treatments

Surgery

Heart transplantation for end-stage failure; intraaortic balloon pump to provide circulatory assistance; left
ventricular assistive device for those awaiting transplantation

Drugs

Diuretics to reduce edema and ventricular filling volume; vasodilators, antihypertensives, or alphaadrenergic blocking agents to dilate vessels and reduce venous filling pressure and peripheral resistance;
inotropics (digitalis) to increase contractility; angiotensinconverting enzyme inhibitors to reduce
angiotensin II in individuals with advanced CHF

General

Bed rest with head elevated; oxygenation; low-salt diet; fluid restriction; monitoring and support of vital
functions; prevention of thrombosis, pneumonia, and skin breakdown; stress reduction