Patients with cardiogenic shock have a significantly higher incidence of atrioventricular block, intraventricular conduction defects, congestive heart failure, cardiac arrest, cardiac arrhythmia, ventricular septal rupture, and significant mitral regurgitation. The inhospital mortality rate among these individuals is approximately 65%. In patients who have increased risk factors for cardiogenic shock, initiation of early aggressive therapy, including a specific invasive intervention, may be warranted to prevent further myocardial damage.
Do all patients who develop hypotension post-MI require inotropic support or/and a pulmonary artery catheter?
Hypotension that develops post-MI has many causes and is not necessarily secondary to left ventricular dysfunction. RV infarction is a common cause of hypotension post-MI. Hypovolemia (absolute or relative) is frequent in the setting of acute MI; patients may be fluid-depleted due to anorexia, vomiting, diaphoresis, or fever, as well as the common use of many drugs that have hypotensive effects. These drugs include narcotic analgesics or tranquilizers, nitrates, diuretics, and most antianginal and antiarrhythmic drugs that tend to be used in patients with acute MI. Recognition and treatment of these reversible causes of hypotension often improve the hemodynamic status of the patient without the need of inotropic drug support or invasive monitoring procedures.
Why do patients with complete heart block and acute MI have a higher mortality?
Acute heart block complicates MI in 5-8% of all cases. Most of the cases of complete heart block occur with inferior wall MI; however, mortality is higher with anterior wall MI. This increased mortality is due to the fact that heart block developing during MI signifies increased infarct size, which explains the higher incidence of congestive heart failure, cardiogenic shock, and cardiac arrest in this group of patients.
What is the clinical implication of left ventricular mural thrombus formation post-MI?
Left ventricular mural thrombi are common, occurring in 20-40% of patients with anterior infarcts, usually are well visualized by echocardiography, and are mainly seen in anteroseptal and apical MI. Unfortunately, embolism occurs in, these patients with a highly variable incidence of 0-25%, usually in the first 10 days post-MI, although thrombus formation may persist during the first 1-3 months. Infarct size is directly related to the thromboembolic risk. The clinical problem is how to prevent emboli rather than how to treat “left ventricular thrombus.” It is not entirely clear whether heparinization or combined thrombolytic-heparin therapy prevents emboli. Recommendations for anticoagulation vary, but a reasonable approach is to recommend anticoagulation for 3-6 months with warfarin in patients with demonstrable mural thrombi, particularly if the thrombus is mobile, and in patients in whom an embolic event has already occurred.
Differentiate the kinds of pericarditis that develop post MI.
Two kinds of pericarditis occur in the post-MI period. Early pericarditis usually develops 24—72 hours after the onset of MI and is seen in patients with transmural MI and congestive heart failure. Delayed pericarditis (Dressier syndrome) is characterized by fever, persistent and recurrent pericarditis, and pericardial and pleural effusions and usually appears days to weeks after MI.
Early pericarditis is a marker of extensive myocardial damage and frequently is seen in anterior infarction that may be complicated by the development of atrial and ventricular arrhythmias. Despite a frequently stormy hospital course, patients with early pericarditis usually do not have increased early mortality; however, their 12-month mortality is higher than that of patients who do not develop this complication (18% vs 12%).