notes by dr Claudio Italiano
This refers to ischemia and necrosis of a myocardial district, that is the damage that results from the lack of blood supply in a cardiac district, and therefore ultimately from glucose and oxygen, through the bloodstream of the coronary arteries.
The acute syndrome is linked, therefore, to the lack of cardiac pump function and to the complications that derive from it, in the first place the hyperkinetic arrhythmias (ventricular fibrillation, ventricular tachycardia etc.) and hypokinetic (sinus arrest, bundle branch block, hemiblocs etc. .).
In Italy, ischemic cardiopathies (angina syndromes, infarction, congestive heart failure) affect 5% of the population, with 2,000,000 patients and 350,000 new cases / year; the maesa for vascular cause constitutes 45% of all deaths, and is socially important, so much so that it affects the patient in full employment (managers, professionals, etc.).
The heart attack depends on:
a) the acute obstruction of a coronary artery generally due to thrombosis in 80%
of cases, almost always near an atherosclerotic plaque, that is a vasal lesion
that starts from the deposition of a lipid pappa, a proliferation of tissue
muscle, which is then organized and obstructs the vessel lumen;
b) by a subintimal hemorrhage due to the breakage of the newly formed
capillaries within the atheromatous plaque;
c) by a spasm or repeated spasms.
Necrosis begins 20-40 minutes after occlusion and the process, depending on the
severity, can affect the subendocardial myocardium, ie the innermost wall of the
heart that is subjected to a greater pressure stress (non-Q infarction), or in
cases more serious, extend in transmural sense, at full thickness.
Obviously from the electrocardiographic point, and depending on the coronary
vessel involved the infarct may be:
Anterior interventricular coronary vessel involved
extended front infarction - ECG D1 and AVL and from V1-V6 septal infarction -
ECG D1 and aVL - V1-V3
tip infarction - ECG D1 and aVL - V3-V5
Vessel interested in the left circumflex
lateral infarction ECG D1 and aVL - V5-V6
Interventricular vessels + right coronary
deep septal infarction - ECG D2-D3 aVF V1-V3
Right coronary vessel
lower infarction -ECG D2-D3 aVF
rear true - ECG D2-D3 aVF (with increase of R in V1, V2)
Thoracic pain intense, oppressive, burning, piercing, like stabbing, with a feeling of imminent death; irradiated to the left arm or both arms, also irradiated to the jaw or elbow and wrist; but in the diabetic sometimes it can be lacking for diabetic neuropathy. It is a pain that is accompanied by neurovegetative signs, such as cold sweat by activation of the orthosympathetic system, tachyarrhythmias; it does not subside with sublingual nitroglycerin to tablets.
Type 1 Spontaneous myocardial infarction related to ischemia due to a primary
coronary event, such as erosion and / or rupture, plaque fixation or dissection
Type 2 Myocardial infarction secondary to ischemia due to an imbalance between
oxygen demand and supply, as in the case of coronary spasm, coronary
embolization, anemia, arrhythmias, hypertension or hypotension
Type 3 Sudden and unexpected cardiac death, with cardiac arrest, often
accompanied by symptoms suggestive of myocardial ischemia, probably associated
with new ST-segment elevation, or new left bundle branch block or angiographic
and / or autoptic finding of recent coronary thrombosis. In any case, death
occurred before blood collection or when levels of cardiac biochemical markers
were not yet detectable
Type 4a Myocardial infarction related to percutaneous coronary intervention
Type 4b Myocardial infarction associated with angiographic or autoptic finding
of stent thrombosis
Type 5 Myocardial infarction related to coronary artery bypass surgery
The patient is agitated; the arterial pressure is mostly reduced and the pulse is tachycardic, of reduced volume, small, often arrhythmic; in 20-30% of cases there are auscultation rubbing noises due to the pericardial involvement (post-infarct pericarditis or Dressler, and the appearance of a mild pansystic murmur due to lesion of a papillary muscle, or as a gallop rhythm , as a sign of gravity.
They are divided into early and late. First of all, the rhythm disorders are a major problem since they can aggravate the already compromised clinical picture due to increased metabolic need and reduction of cardiac output that they determine. In the infarcts of the posterior wall we will have sinus bradycardia, understood as vagal hypertonicity; it can generate repetitive ventricular arrhythmias. Sinus tachycardia is present in 30% of cases, and the most common causes are anxiety, persistent pain, hypovolaemia, atropine; atrial fibrillation occurs in 10-15%; BEV ventricular ectopic beats are usually common and do not have much significance, but can degenerate into ventricular fibrillation if multifocal and polymorphic. Ventricular fibrillation is practically the cardiac arrest if no intervention is made with resuscitation maneuvers and cardiac massage at its presentari. It is a totally desynchronized tachyarrhythmia that does not accompany the mechanical systole of the ventricles, therefore without cardiac output and therefore to collapse.
Other arrhythmias are Atrioventricular blocks or BAVs of the I degree, as simple extension of PR, BAV of II degree with periodisms of Wenckebach, and BAV of II and III degree. Other disturbances are the left-hand emiblections of the left, and the posterior left, and the right bundle of bundles. Among other complications, we will have recurrent ischaemia such as early and late angina or reinfarction. Moreover, within 48 hours of the IME, signs of decompensation are manifested, manifested with a framework of pump failure and with a picture of acute pulmonary edema. Left ventricular failure is marked by tachycardia, wet noises at the pulmonary bases, by the appearance of cantering rhythm.
The insufficiency of the right ventricle is given by the elevation of the venous pressure of the jugular, by the hepatic congestion. But contractile insufficiency of the myocardium can reach the most dramatic pictures of cardiogenic shock, which is the main cause of IMA; it includes cases in which the arterial pressure falls below 90 mmHg, with polypnea, cerebral hypoperfusion, reduction of diuresis, hypoxia, acidosis. Pulmonary and systemic embolisms can be associated with myocardial infarction and depend on intramurous thrombi of the ventricle and atrium. In the course of IMA, one or more papillary muscles can rupture up to the rupture of the left ventricle wall, with hemopericardium and sudden death. Otherwise the interventricular septum may break with shock symptomatology, with holosystolic murmur.
The diagnosis is based on clinical signs, ECG and laboratory and instrumental
investigations.
- ECG with signs of injury, ie inversion of the T wave, Q waves and overlap of
the ST segment; these alterations are recorded in some derivations in relation
to the site of the necrosis, depending on the vision of the exploration
electrode; in the first stage, which lasts 24-48 hours, only the S-T section can
be overlapped; the trace is then leveled on the isoelectric, but the wave Q
appears; in the third stage appear sharp and symmetrical negative T-waves
expression of subendocardial ischemia. The final stage, however, is always
represented by the Q wave of necrosis + sub-division of the T wave in the
affected derivations.
- Laboratory. "Cardiac enzymes" are sought, e.g. creatine phosphokinase MB, ie
the iso-enzyme that appears early in 6-8 hours and reaches the peak in 24 hours,
to negativize in 3 days; the transaminases, the Lactic dehydrogenase which is
shown in 24th hour; the Troponina which is released in 3-6 hours.
- Echocardiography. it is used to search for myocardial function, the possible
rupture of papillary muscles, intramural thrombus, pericarditis, ventricular
aneurysm and to make a diagnosis differentiating with the dissecting aortic
aneurysm.
to deepen the infarct theme: vedi :
index cardiology