Which leads show stemi

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. With an anterior or apical aneurysm, the persistent ST elevation is in lead V1 and V2. 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.

With respect to long-term treatment, beta blockers should be given to all patients in maximal tolerated dosis and continued indefinitely. Beta blockers have negative inotropic and chronotropic effect, which reduces heart rate duration of diastole is therefore prolonged , cardiac output and blood pressure. The workload on the myocardium is reduced and the oxygen consumption and oxygen demand is reduced.

Prolongation of diastole will give extra time for the myocardium to be perfused the myocardium is perfused only during diastole. Beta blockers increase survival, reduce morbidity, improve left ventricular function and may also reduce or limit infarct size. Beta blockers presumably also protect against ventricular tachyarrhythmias ventricular tachycardia.

Treatment with beta blockers should start early within 24 hours , provided that the patient is hemodynamically stable. Beta blockers may be used in patients with hypertension on presentation.

Metoprolol 5 mg IV may be given three times with 5—10 minutes intervals in the acute setting. Heart rate and blood pressure should be monitored during administration of intravenous beta blockers. If tablets are preferred, metoprolol 25 mg may be given every sixth hour until the maximal tolerated dose or mg daily is reached. The dose is limited by bradycardia and hypotension. Patients with acute heart failure should not be give beta blockers during the acute phase.

However, beta blockers should be started early when heart failure has stabilized. Second-degree and third-degree AV block without pacemaker are contraindications. Patients with COPD chronic obstructive pulmonary disease should be given beta-1 selective agents e. A loading dose oral of aspirin mg to mg should be given immediately to all patients. Aspirin is given in the prehospital setting and before PCI. Aspirin is then continued indefinitely maintenance dose 80 mg daily.

In addition to aspirin, a loading dose of an oral P2Y 12 -receptor inhibitor should also be given immediately before PCI. The options include:. Clopidogrel is inferior to prasugrel and ticagrelol. Ticagrelol appears to cause fewer bleeding complications as compared with prasugrel. P2Y12receptor inhibitor is continued for 12 months in patients receiving a stent during PCI. Maintenance doses are clopidogrel 75 mg daily, prasugrel 10 mg daily, and ticagrelol 90 mg twice daily.

Note that the interventionist may add additional antiplatelet agents abciximab, tirofiban, eptifibatide during PCI. These drugs, however, are not administered outside of the catheterization laboratory. All patients should immediately be given aspirin loading dose of to mg and then continued indefinitely maintenance dose 80 mg daily.

Aspirin is combined with either clopidogrel, prasugrel or ticagrelol. Patients who are unable to swallow may be given mg as a suppository or 80 to mg IV. All patients should receive a maintenance dose of 80 mg daily which is continued indefinitely. Hypersensitivity to aspirin is uncommon and in that scenario, clopidogrel may be used instead. Note that aspirin is a highly effective drug in both the acute setting and in secondary prevention to prevent re-infarction and the drug must never be terminated without careful consideration.

As noted above, optimal antiplatelet effect requires the addition of either ticagrelol, prasugrel or clopidogrel. Combining aspirin with any of these is referred to as DAPT dual antiplatelet therapy. An individual assessment of bleeding risk is warranted and DAPT should be avoided if the risk is high. DAPT is continued for 12 months in all patients, and the indication is stronger in patients who undergo PCI with placement of stent both bare metal stents and drug eluting stents.

A loading dose of mg followed by maintenance dose of 80 mg daily is recommended. The additional increase in bleeding risk is smaller with clopidogrel, as compared with prasugrel and ticagrelol. Prasugrel is more potent than clopidogrel. However, cocaine use can also cause a STEMI due to coronary vasospasm, rather than occlusion with thrombosis.

Pericarditis: The hallmark features of pericarditis are diffuse global concave ST elevations with associated PR depressions. Patients with pericarditis will classically have chest pain that is worse with laying back and improved by sitting forward. LBBB is caused by blockage of the left segment of the Bundle of His and causes ventricular depolarization to occur in a right to left direction as opposed to the normal left to right.

Leads V will have deep S waves and V will have tall R waves. In general, one should look for concordant ST changes i. In the past, a new LBBB in a patient with ischemic chest pain was considered to be an indication for a patient to undergo cardiac catheterization. However, in recent years this has become more controversial with evidence suggesting these patients may be managed more conservatively.

This condition is important to recognize because it can lead to sudden cardiac death in patients. The one noticeable difference will be the presence of pacer spikes. In general, uou cannot read ischemia in a v-paced rhythm! Benign Early Repolarization BER : Benign early repolarization usually represents a normal variant most often seen in young, healthy patients.