In this case the troponin levels are not elevated and the condition is classified as unstable angina pectoris or aborted myocardial infarction. The ECG may be treacherous in some patients with acute transmural ischemia i. For example, some patients have underlying ECG abnormalities e. Other patients may have acute transmural ischemia located in areas not detected by any of the 12 standard leads. Thus, there are circumstances that all clinicians must be aware of.
Left bundle branch block LBBB occurs if the left bundle branch is dysfunctional and thus incapable of conducting the electrical impulse to the left ventricle. Activation of the left ventricle will depend on impulses spreading from the right ventricle.
This results in abnormal activation depolarization and recovery repolarization of the left ventricle. These ST-T changes are illustrated in Figure 6. There are three reasons why LBBB complicates the assessment of patients with suspected acute myocardial infarction:. Due to these circumstances, researchers decided to experiment with patients presenting with LBBB and a suspected acute myocardial infarction.
They did so by referring these patients for urgent angiography with the goal to perform PCI and noted that many of these patients had complete coronary artery occlusions and outcomes improved by managing them as acute STEMI i.
These recommendations were evaluated over almost a decade and several studies found that this management resulted in many unnecessary activations of the catheterization laboratory. In summary, guidelines still recommend that these patients should be referred immediately to the catheterization laboratory.
The most useful and validated criteria were developed by Elena Sgarbossa and associates. The Sgarbossa criteria are presented in Figure 7. There are situations in which acute transmural ischemia does not cause ST elevations on the lead ECG and these situations are as follows:. Note that Posterolateral posterior, inferobasal infarction and right ventricular infarction have also been discussed previously. Transmural myocardial ischemia may occasionally create sufficient ST elevation to meet the criteria in one lead but have slightly less than the required ST elevation in the neighboring contiguous lead.
The atherothrombotic process is dynamic during the course of STEMI, which implies that the size of the thrombus and thus the obstruction of blood flow may vary from one minute to the next. It is wise to perform several ECG recordings e. Large T-waves occur in several conditions such as hyperkalemia and early repolarization. However, transmural ischemia may cause hyperacute T-waves , which are very large, broad-based, symmetric T-waves. Hyperacute T-waves emerge within seconds after the occlusion of a coronary artery and usually resolve within minutes; they are then succeeded by ST elevations.
QRS changes are mostly permanent, particularly Q-waves. These models typically include information regarding medical history, ECG findings, presenting features notably hemodynamic status and cardiac troponins. These vary with respect to the type of risk estimated short-term, long-term, myocardial infarction, death.
Occlusion of a coronary artery immediately results in ischemia in the myocardium supplied by the artery and its branches. Myocardium can endure approximately 30 minutes of ischemia before the cells die i.
As discussed previously Classification of Acute Myocardial Infarction STEMI is the result of a complete artery occlusion which leads to extensive ischemia and a very high risk of life-threatening ventricular arrhythmias ventricular tachycardia, ventricular fibrillation.
The risk of death is highest in the first hour after symptom onset, which is due to the high risk of ventricular arrhythmias during that phase. Virtually all deaths in the acute phase are due to ventricular arrhythmias, which lead to asystole and ultimately cardiac arrest Figure 8.
Death due to pumping failure cardiogenic shock is uncommon in the acute phase. Due to the risk of ventricular arrhythmias and the progressive loss of myocardium, rapid assessment and initiation of treatments are crucial in patients with acute STEMI. Both older and recent studies indicate that the great majority of all fatal myocardial infarctions occur outside the hospital, typically within the first hour. Hence, American and European guidelines recommend that patients with chest pain should use the EMS Emergency Medical Service for transportation to the hospital.
The prehospital chain of care is initiated at the emergency dispatch center. The dispatcher typically uses standardized protocols to assess the risk of acute STEMI, triage the patient set a dispatch priority , give pre-arrival instructions and coordinate EMS to the scene. EMS can then immediately start a diagnostic workup, establish intravenous lines, assess vital functions, address hemodynamic and electrical instability.
Administration of aspirin, nitroglycerin, morphine and oxygen is generally safe in the prehospital setting. Importantly, the EMS can obtain a lead ECG, which can be transmitted electronically to the hospital for further evaluation.
In some instances, the EMS may even administer reperfusion therapy fibrinolysis en route to the hospital. Recognizing the prehospital potential can therefore reduce delay to interventions and subsequently reduce morbidity and mortality in patients with acute STEMI.
Without unnecessary delay, the patient should then be transported to a hospital with the facilities and expertise to perform percutaneous coronary intervention PCI , as it improves outcomes markedly. The first step in the management of patients with STEMI is obviously rapid recognition since the effects of interventions antithrombotic therapy, anti-ischemic therapy and reperfusion are greatest when performed early.
The diagnosis is confirmed with ECG supplementary leads may be necessary, as discussed above. The presence of significant ST elevations in patients with chest pain or other symptoms suggestive of myocardial ischemia is sufficient to diagnose STEMI. All interventions including reperfusion may be performed before biomarkers troponins are available.
Once the diagnosis is confirmed the patient must be continuously monitored heart rate and rhythm, blood pressure, respiration, consciousness, symptoms, general appearance. A defibrillator must be ready and venous access should be secured. It is always wise to make a rapid assessment of the probability of aortic dissection before administering drugs that increase bleeding risk. For clarity, STEMI is a clinical syndrome defined by symptoms and ECG and biomarkers are not necessary to initiate potentially life-saving interventions.
Therefore, anti-ischemic and antithrombotic medications should be administered immediately, provided that there are no contraindications. In some instances discussed below reperfusion may also be administered without any delay. The clinical examination must include vital parameters consciousness, heart rate and rhythm, oxygen saturation, blood pressure, respiratory rate , signs of heart failure and pulmonary edema, murmurs mitral regurgitation, ventricle septum defect.
Rapid assessment of bleeding risk should also be performed discussed below. Patients with symptoms of ischemia preceding cardiac arrest should be transported to the catheterization laboratory immediately if circulation returns.
There is no evidence that oxygen affects survival. Randomized controlled trials are currently underway. Randomized controlled trials comparing oxygen with room air are underway. Oxygen is also appropriate for patients with pulmonary edema, heart failure and mechanical complications free wall rupture, ventricular septum defect, mitral prolapse of acute STEMI.
Morphine sulfate is administered to all patients with acute STEMI 1 to 5 mg, may repeat in 5 to 30 min if necessary. Caution is required in patients with hypotension. Pain activates the sympathetic nervous system which results in 1 peripheral vasoconstriction, 2 positive inotropic effect and 3 positive chronotropic effect. Consequently, sympathetic activity will increase the workload on the heart and thus aggravate the ischemia.
This may be detrimental in patients with acute STEMI, which must therefore receive adequate doses of analgesics. Morphine sulfate is the drug of choice; it relieves pain and anxiety. Morphine also causes dilatation of the veins, which reduces cardiac preload. Reduction in preload results in reduced workload on the left ventricle and this may alleviate both ischemia and severity of pulmonary edema.
The required dose of morphine depends on age, BMI and circulatory status. Reduced doses are warranted in patients with hypotension because morphine may cause additional vasodilatation. An initial dose of 2 mg to 5 mg IV may be recommended. This may be repeated every 5 minutes until 30 mg have been administered. Naloxone 0. Morphine may cause bradycardia which can be countered with atropine 0. If large amounts of morphine is insufficient to relieve the pain, one should suspect aortic dissection and ask the patient to reiterate the characteristics of the symptoms.
Note that nitrates and beta blockers also exert analgesic effects explained below. It does not affect the prognosis but relieves symptoms. Sublingual nitroglycerin 0. Intravenous nitroglycerin is considered if ischemic discomfort is not relieved. Nitroglycerin is also considered in patients with congestive heart failure as well as patients with uncontrolled hypertension. Nitrates nitroglycerin induces vasodilatation by relaxing smooth muscle in arteries and veins.
The ensuing vasodilatation reduces the venous return to the heart which decreases cardiac preload. This reduces the workload on the myocardium and thus the oxygen demand. Nitrates, therefore, relieve both ischemic symptoms chest pain and pulmonary edema. The vast majority of patients should be offered nitrates. A dose of 0. Nitroglycerin infusion should be considered if the effect is inadequate severe angina or if there are signs of heart failure.
Nitrates should not be administered in 1 patients with hypotension, 2 if there is suspicion of right ventricular infarction, 3 severe aortic stenosis, 4 hypertrophic obstructive cardiomyopathy or 5 pulmonary embolism.
As with morphine, use of nitrates must not limit the use of beta blockers and ACE inhibitors these drugs affect blood pressure and heart rate. Oral beta-blockers should be initiated during the first 24 hours after admission.
Intravenous beta-blockers are only considered in patients with persistent hypertension. Beta-blockers are avoided if the patient has risk factors for cardiogenic shock. The message is clear. We need to specifically discover the ST-segment elevation of acute myocardial infarction. Consider Sejersten et al. Am J Cardiol Nov 1;90 9 :.
One reason for this may be that the paramedics were concerned about missing patients with this condition. In an additional 4 patients 3. In 13 of patients Their conclusion? This is in contrast to an experienced cardiologist whose true-positive rate was high and not affected by confounding factors.
Ann Emerg Med Jan;23 1 :. ST-segment elevation alone lacks the positive predictive value necessary for reliable prehospital myocardial infarction diagnosis. ST-segment elevation criteria that include reciprocal changes identify patients who stand to benefit most from early interventional strategies. Most interventional cardiologists I speak with believe that prehospital activation of the cardiac cath lab should be reserved for clear-cut STEMI.
Other patients, they argue, can and should receive further investigation in the Emergency Department. Some paramedics bristle at the idea of transmitting lead ECGs to the hospital for physician over-read. Sgarbossa criteria, Cabrera's sign and Chapman's sign can be used in the setting of an old left bundle branch block to diagnoses an acute myocardial infarction.
The typical pattern with LVH includes deviation of the ST segment in the opposite direction of the QRS complex discordance and a typical T wave inversion pattern is present. Enlarge 2.
Early repolarization:. Early repolarization is a common finding in young, healthy individuals. It appears as mild ST segment elevation that can be diffuse, however is more prominent in the precordial leads. Enlarge 3. Enlarge 4.
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