Myocardial infarction

Definition.

Means the ischemia and necrosis of the myocardium of a district, that the damage that follows the failure of blood supply to a district rate, and then ultimately to glucose and oxygen through the bloodstream of the coronary arteries. The acute syndrome is linked, therefore, the loss of cardiac pump function and complications arising therefrom, first hyperkinetic arrhythmias (ventricular fibrillation, ventricular tachycardia, etc..) And hypokinetic (sinus arrest, bundle branch block, etc. emiblocchi ..)



Epidemiology.

In Italy ischemic heart disease (angina syndromes, stroke, congestive heart failure) affecting at least 5% of the population, with 2,000,000 new cases and 350,000 patients per year, due to the vascular maorte constitutes 45% of all deaths, and is socially important, so much so that patient care in full employment (managers, professionals, etc...)



Pathogenesis.

The attack depends on:

a) Acute coronary artery obstruction usually due to thrombosis in 80% of cases, almost always near an atheromatous plaque, which is a vascular lesion that starts from the deposition of a lipid gruel, a proliferation of tissue muscle, which then organizes and obstructs the lumen;

b) subintimal hemorrhage by rupture of newly formed capillaries within the atherosclerotic plaque itself;

c) a repeated spasm or spasms.

Necrosis begins 20-40 minutes after occlusion and the process, depending on the severity, can affect the subendocardial myocardium, ie the inner wall of the heart is subjected to a stress greater pressure (non-Q infarction), or in cases more severe, extend in direction transmural, full-thickness.

ECG findings.

Obviously from the point electrocardiogram, and depending on the vessel coronary heart attack may be interested:

Target vessel coronary anterior interventricular

extensive anterior infarction - ECG D1 and AVL and V1-V6 septal infarction - ECG D1 and aVL - V1-V3

myocardial tip - ECG aVL and D1 - V3-V5



Target vessel left circumflex

lateral myocardial ECG D1 and aVL - V5-V6



+ Right coronary vessels interventricular

deep septal infarction - ECG D2-D3 aVF V1-V3



Right coronary vessel

inferior myocardial ECG-D2-D3 aVF

Rear true - D2-D3 aVF ECG (with an increase of R in V1, V2)

Symptoms.

Intense chest pain, oppressive, burning, stabbing, stabbing as with feelings of imminent death; radiating to left arm or both arms, jaw, or radiate to the elbow and wrist, but can sometimes fail for diabetic neuropathy . It 'a pain that is accompanied by autonomic signs, such as cold sweat for system activation orthosympathetic, tachyarrhythmias, not subsiding with sublingual nitroglycerin in tablets.



Objective examination of the patient.

The patient is agitated, the blood pressure is mostly reduced and heart rate and tachycardia, low volume, small, often arrhythmic, in 20-30% of cases there are auscultation sounds of friction for the involvement of the pericardium ( post-myocardial infarction or pericarditis Dressler, and the appearance of a slight breeze pansistolico for infringement of a papillary muscle, or gallop, as a sign of seriousness.



Complications.

They are divided into early and late.

First are the early pace of the crowds that represent a major problem as they can aggravate the clinical picture already compromised due to increased metabolic demand and reduced cardiac output determining. Infarcts in the posterior wall we have the sinus bradycardia, meaning vagal hypertonia, it can generate repetitive ventricular arrhythmias. Sinus tachycardia is present in 30% of cases, the most common causes are anxiety, persistent pain, hypovolemia, atropine, atrial fibrillation occurs in 10-15%, and ventricular ectopic beats usually BEV are common and have a great meaning, but can degenerate into ventricular fibrillation and polymorphic if multifocal. Ventricular fibrillation cardiac arrest is pretty if nothing is done with resuscitation and heart massage to his will only introduce. This is a totally desynchronized tachyarrhythmia that accompany mechanical systole of the ventricles, then no cardiac output and thus collapse. Other arrhythmias or atrioventricular block are BAV first degree, as a simple extension of the PR, BAV Grade II with a period of Wenckebach, and BAV II and III level. Other disorders are emiblocchi front left and rear left and right bundle branch block.

. Among other complications, we ischemia who relapse early and late as angina or reinfarction. Also within 48 hours IMO there are signs of failure that occur with insufficient under the pump and with the framework of acute pulmonary edema. The left ventricular failure is marked by tachycardia, wet noises from the lung bases, by the appearance of gallop. The insufficiency of the right ventricle is given by the elevation of jugular venous pressure, hepatic congestion. But the failure of the contractile myocardium can reach the most dramatic paintings of cardiogenic shock, which is the main cause of IMA and includes cases in which blood pressure drops to below 90 mmHg, with polypnoea, cerebral hypoperfusion, decreased diuresis, hypoxia, acidosis. The systemic and pulmonary embolism can accompany myocardial infarction and depend on intramural thrombus of the atrium and ventricle. At IMA, we can be breaking one or more papillary muscle rupture of the left ventricular wall, with haemopericardium and sudden death. Otherwise can result in rupture of the interventricular septum with symptoms of shock, with a holosystolic murmur.





Diagnosis.

This leads to the diagnosis based on clinical signs, ECG and laboratory tests and instrumental.

ECG signs of injury that T-wave inversion, Q waves and ST segment soprasvlivellamenti, these changes are recorded in some outlets in relation to the seat of necrosis, depending on the viewing electrode searching, in the first stage which lasts 24 - 48 hours you can only have ST-segment elevation, following the track level but appears sull'isoelettrica the Q wave, in stage III negative T waves appear sharp and symmetrical expression of subendocardial ischemia .. The final stage, however, is always represented by the wave of necrosis + Q sottoslivellamento T wave in leads involved.

Laboratory. We are looking for the "cardiac enzymes", ie. creatinafosfochinasi MB, ie the enzyme that appears early in 6-8 hours and reaches a peak in 24 hours, negativity within 3 days; transaminases, the lactic dehydrogenase which is evident in the 24 th hour, the troponin that is released in 3 -6 hours.

Echocardiography. need to seek the myocardial function, the possible rupture of papillary muscles, the intramural thrombus, pericarditis, ventricular aneurysm and differentiate diagnosis with dissecting aortic aneurysm.!

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