COMPLICATIONS OF MI:
A 'arrhythmia of any kind, occurs in > 90% of patients with myocardial infarction. In an early stage, one can observe bradycardia or ventricular ectopic beats (VEB). The conduction disorders may reflect damage to the sinus node, atrioventricular node conduction and tissue specific. The potentially lethal arrhythmia, which is the main cause of death in the first 72 h, include tachycardia of any origin, fast enough to reduce cardiac output and lower the PA, the second-degree AV block type Mobitz II or third degree ventricular tachycardia (VT) and ventricular fibrillation (VF). The complete heart block with wide QRS (atrial impulses fail to reach the ventricle, the ventricular rate is low) is rare and is usually indicative of a massive heart attack earlier. Complete atrioventricular block with narrow QRS usually indicates a heart attack or lower back. The asystole is uncommon, except for cases in which it appears as a terminal event of progressive left ventricular failure and shock.
VENTRICULAR TACHYCARDIA
VENTRICULAR FIBRILLATION
SECOND DEGREE HEART BLOCK
The disturbances of the function of the sinus node artery depends on the source of the vase that sprays (ie left or right coronary artery) and the possibility, especially in patients in older age, a previous illness. Sinus bradycardia usually does not have any meaning, unless the heart rate is less than 50 bpm. The persistent sinus tachycardia is usually an ominous sign, often an expression of failure of VS and low cardiac output. However, other causes must be sought (eg., Sepsis, hyperthyroidism).
Atrial arrhythmias, including atrial ectopic beats (BEA), atrial fibrillation and flutter (fibrillation less common) are found in approximately 10% of patients with AMI and may be an expression of left ventricular failure or right atrial infarction. Paroxysmal atrial tachycardia is rare and usually occurs in patients who have had previous episodes.
Atrial fibrillation that occurs within the first 24 hours is usually transient. Risk factors include age> 70 years, heart failure, a previous AMI, a large anterior infarction, a heart fibrillation, pericarditis, hypokalemia, hypomagnesemia, chronic respiratory disease and hypoxia. Thrombolytic therapy reduces the incidence. Paroxysmal atrial fibrillation applicant is a poor prognostic sign and increases the risk of systemic embolism.
In atrioventricular block, reversible changes in atrioventricular conduction, conduction disorders that Mobitz type I with PR prolongation or Wenckebach phenomenon, observed with relative frequency, particularly nell'infarto inferior-diaphragmatic, in which case, they are interested vessels that supply the posterior wall of the LV, which gives branches to the atrioventricular node. These disorders are usually self-limiting. The correct ECG diagnosis of the type of block is important. The progression to complete heart block is unusual, the real block Mobitz type II, with missing beats or atrioventricular block with wide QRS complex and slow, and usually represents an ominous complication of massive anterior infarction.
Ventricular arrhythmias are common. The primary VF occurs in the first hours after an AMI. The late PV may be associated with myocardial ischemia continues or delayed and, when associated with hemodynamic instability, is a poor prognostic sign. Ventricular arrhythmias may reflect hypoxia, electrolyte imbalance, or sympathetic hyperactivity.
The 'heart failure occurs in about 2 / 3 of patients hospitalized for AMI. It is usually the predominant LV dysfunction with dyspnea, inspiratory crackles at the lung bases and hypoxemia. The clinical signs depend on infarct size, increased LV filling pressure and extent of the reduction in cardiac output. -Indicated in the VS, the Pa O2 before and after administration of an effective fast-acting diuretic (eg., Furosemide 40 mg IV) may be helpful for diagnosis: reduced Pa O2 caused by failure of the VS should increase after diuresis. The mortality rate varies in direct proportion to the severity of left ventricular.
In 'RV infarction, the clinical signs include high pressure filling of the RV, jugular turgor, no significant pathology of the lung fields and hypotension. ST-segment elevation of 1 mm in the right precordial leads (V 4R) is highly indicative of myocardial VD. The RV myocardial infarction complicating a VS is associated with increased mortality.
The 'hypoxemia that commonly accompanies an AMI is usually secondary to increased left atrial pressure resulting in alteration of ventilation / perfusion ratio in the lung, pulmonary edema in the interstitial phase, collapse of alveoli and increasing the share of the physiological shunt. In patients aged between 50 and 70 years, normal values of Pa O2 at rest in bed is about 82 ± 5 mm Hg.
The 'hypotension in the course of AMI may be due to the reduction of ventricular filling or loss of contractile force secondary to a massive heart attack. A reduced LV filling is most often the consequence of a reduced venous return, in turn, secondary to hypovolemia, especially in patients receiving diuretic therapy intense, but it may also reflect a myocardial VD. To determine the cause of hypotension, it is sometimes necessary to measure intracardiac pressures by means of transcutaneous balloon floating catheter (Swan-Ganz). If (in the presence of systemic hypotension) the pressure in the left atrium is low, it should run a load test fluid (NaCl 0.9% or 0.45%) are administered 200-400 ml of NaCl in 30 min monitoring the systemic and left atrial PA. If the PA salt with only a modest increase in atrial pressure, the diagnosis of hypovolemia is likely. Alternatively (if you do not measure intracardiac pressures), a rise in BP with the clinical improvement and absence of pulmonary congestion suggests hypovolemia.
Cardiogenic shock characterized by hypotension, tachycardia, decreased urine output, confusion, profuse sweating and cold extremities, has a mortality rate of 65%. It is mainly associated with massive infarction in the anterior and the loss of a share> 50% of the left ventricular myocardium functioning.
A 'recurrent ischaemia may follow an IMA. Chest pain usually disappears within 12-24 hours of the EPI. Any chest pain or residual following may be a pericarditis, pulmonary embolism or other complications (eg., Pneumonia, gastric disorders or recurrent ischaemia). The recurrent ischaemia is usually accompanied by reversible changes of the T wave and ST segment ECG. The PA can be high. Up to 1 / 3 of patients without chest pain were more likely to have silent ischemia (ECG changes without pain). The evidence of continuous post-AMI ischemia suggests the presence of myocardium at risk.
A 'functional insufficiency of the papillary muscle occurs in about 35% of patients. Mitral insufficiency, some of which has permanent scarring caused by a lesion of the papillary muscle or free wall. Auscultation frequently during the first hours of infarction can often enjoy a transient apical systolic murmur, believed linked to ischemia of a papillary muscle that causes a complete failure coaptazione mitral valve leaflets.
There are 3 forms of myocardial rupture: that of the papillary muscle, rupture of the interventricular septum and the free wall.
The papillary muscle rupture is often associated with an inferior-posterior infarction, coronary artery occlusion had right. It produces an acute and severe mitral regurgitation is characterized by the sudden appearance of a systolic murmur with thrill intense spike in the presence of pulmonary edema.
Rupture of the interventricular septum, although rare, is 8-10 times more common than papillary muscle rupture. It is characterized by the sudden appearance of an intense systolic murmur with thrill, more medial than the apex along the left sternal border at the level of 3 or-4 or intercostal space, accompanied by hypotension with or without signs of left ventricular failure. The diagnosis can be confirmed by inserting a balloon catheter for the determination and comparison of O 2 saturation or Po 2 of blood samples taken from the right atrium from the RV and the pulmonary artery. A significant increase in the values of Po 2 in the VD is diagnostic. Doppler Echocardiography is often diagnostic.
The incidence of heart failure increases with age and is higher in women. It is characterized by the sudden collapse of the PA, with momentary persistence of sinus rhythm, and the frequent presence of signs of cardiac tamponade. It is almost always fatal.
The pseudoaneurysm is a form of rupture of the LV free wall, where a wall made from aneurysmal thrombus and pericardium prevents extravasation of blood.
The 'ventricular aneurysm is common, especially in the presence of a large transmural infarction (more commonly the front) and good function of the myocardium remaining. Aneurysms can form in a few days, weeks or months. Do not undergo rupture, but may be accompanied by recurrent ventricular arrhythmias and low cardiac output. Another risk from ventricular aneurysm is the formation of a mural thrombus and systemic embolization. The suspected diagnosis is derived from the relevant inspection or palpation of precordial movements paradoxes accompanied by persistent ST-segment elevation ECG or a characteristic protrusion of the shadow cardiac chest x-ray. Echocardiography helps to diagnose and detect the presence of a thrombus. The administration of ACE inhibitors during the acute phase of stroke affects the LV remodeling and may reduce the incidence of aneurysms.
A 'asinergia ventricle may occur because of the juxtaposition of normal and abnormal myocardium in the course of AMI. An akinetic segment does not contract and does not show the characteristic movement of retraction in systole. Hypokinetic segment has a reduced range of contraction and a partial impairment of systolic retraction. In the case of multiple infarcts, the myocardial hypokinesia has spread and, if dominated by low cardiac output and heart failure with pulmonary congestion, it is called ischemic cardiomyopathy. One segment shows dyskinetic systolic expansion or bulging (paradoxical movement). These alterations can be identified by two-dimensional echocardiography, ventriculography or radionuclide angiography and may contribute to the reduction of ventricular function and exercise tolerance in the long term.
The mural thrombosis occurs in approximately 20% of patients with AMI (60% of patients with large anterior infarction). Systemic embolism occurs in approximately 10% of patients with thrombosis of the VS (best diagnosed on echocardiography), the risk is higher in the first 10 days but persists for at least 3 months.
Pericarditis can cause a pericardial rub in about 1 / 3 of patients with transmural AMI. The rubbing usually appears 24-96 h after the onset of the EPI. An earlier onset is unusual and suggests the possibility of other diseases (eg., Acute pericarditis), although the hemorrhagic pericarditis may occasionally complicate the early stage of the EPI. Tamponade is rare.
Postinfarction syndrome (Dressler syndrome) develops in some patients several days or weeks or even months after the AMI, but in recent years its incidence appears to have decreased. It is characterized by fever, pericarditis with a rub, pericardial effusion, pleuritic pain, pleural effusion, pulmonary infiltrates, and joint pain. It can be difficult to differentiate this condition from a reinfarction or infarct extension, but the cardiac enzymes do not increase significantly. This syndrome may be recurrent.
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