Acute coronary syndrome: Clinical sciences

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Acute coronary syndrome or ACS is a critical diagnosis to consider in all individuals presenting with acute chest pain. It's caused by a sudden reduction in coronary blood flow, known as cardiac ischemia.
In most cases, this sudden reduction results from the rupture or erosion of an atherosclerotic plaque, which triggers thrombosis.
There are 3 types of ACS including ST elevation myocardial infarction or STEMI, non-ST elevation myocardial infarction or NSTEMI, and unstable angina.
Now, if your patient presents with a chief concern suggesting acute coronary syndrome, first perform an ABCDE assessment to determine if they're unstable or stable.
If unstable, stabilize their airway, breathing, and circulation, which might require endotracheal intubation and mechanical ventilation.
Next, obtain IV access and start continuous vital sign monitoring and cardiac telemetry. Finally, ensure that a defibrillator is available and the defibrillator pads are in place.
OK, now that we've covered the approach to unstable patients, let's return to the ABCDE assessment and focus on stable individuals.
If your patient is stable, obtain a focused history and physical examination. Patients often describe chest pain along with chest discomfort, pressure, or tightness, like something heavy is sitting on their chest.
Often, this feeling doesn't stay in one place, it can radiate down the left arm, up into the neck, or even to the jaw. When the pain is due to acute cardiac ischemia, it tends to get worse with exertion, doesn't go away with rest, and doesn't change with movement or position.
Along with chest pain, individuals might report non-specific symptoms such as shortness of breath, sweating, epigastric pain, or nausea.
When taking a history, be sure to look for risk factors for heart conditions, such as hypertension, diabetes mellitus, hyperlipidemia, obesity, tobacco use, and a family history of coronary artery disease.
Individuals with ACS might have a completely normal physical exam, but they can also present with dyspnea, tachycardia, and diaphoresis.
Findings can also vary based on the location and extent of heart damage. For example, the involvement of the papillary muscle can cause mitral regurgitation and a new systolic murmur.
On the flip side, extensive damage to the heart muscle can lead to heart failure and signs like jugular venous distention, hepatomegaly, lung crackles, and lower extremity edema.
At this point, you should suspect ACS, so act fast. Immediately order a 12 lead ECG and check cardiac troponin, which is a serum marker of myocardial injury.
Make sure to obtain the ECG within 10 minutes of the patient's arrival. Do not delay it for history taking or physical examination.
Time is critical. As you're doing this, begin initial management, since assessment and treatment should happen simultaneously.
Start by obtaining IV access and setting up continuous vital sign monitoring with cardiac telemetry. If needed, provide supplemental oxygen to maintain saturation above 90%.
Initial management also includes several key medications. Have the patient chew a high dose aspirin to inhibit platelet aggregation and give sublingual nitroglycerin to improve coronary blood flow and relieve chest pain.
To help stabilize the plaque impairing blood flow, administer a high intensity statin. Finally, if there are no contraindications such as acute heart failure or heart block, give a beta-blocker to reduce myocardial oxygen demand.
If the chest pain persists despite nitroglycerin, think of IV morphine for additional relief. As soon as you receive ECG results, you need to assess the type of ACS.
First, let's focus on STEMI. STEMI occurs due to complete acute blockage of a coronary artery, leading to infarction.
If there is elevation of the ST segment of 1 millimeter or greater in 2 or more contiguous leads, it confirms the diagnosis of STEMI.
However, a left bundle branch block can mask ST elevation, so the diagnosis can also be made if there's a new left bundle branch block, along with a presentation strongly suggestive of MI.
In this case, look for a wide QRS complex greater than 120 milliseconds, a dominant S wave in V1, and broad notched R waves with absent Q waves in the lateral leads like V5 and V6.
Cardiac troponin levels will be elevated in STEMI, but these results may not be available right away. The key point is not to wait for the troponin level before making the diagnosis.
ECG findings alone are enough to diagnose SEmi. Once you diagnose STEMI, the primary goal of treatment is to achieve rapid reperfusion and minimize myocardial damage.
However, while preparing for reperfusion, you should also initiate additional medical therapy. All individuals should receive dual antiplatelet therapy, known as DAPT, which means adding an oral P2Y12 inhibitor, such as clopidogrel or ticagrelor to aspirin.
Additionally, administer a parenteral anticoagulant to reduce the risk of further thrombosis. Administer these medications promptly, but never at the cost of delaying reperfusion therapy, which includes percutaneous coronary intervention, or PCI for short, and fibrinolytic therapy.
PCI is the preferred strategy over fibrinolytic therapy for reperfusion in patients with STEMI. However, PCI cannot be used in all patients.
Then assess the time of symptom onset to presentation, because it is a key factor that determines which treatment can be used safely and effectively.
If it has been less than 12 hours since symptom onset, the next step is to assess if PCI is available within 120 minutes of the patient's first medical contact, either at the patient's current location or by transfer to a PCI capable medical center.
If PCI is available within 120 minutes, proceed with emergent coronary angiography and PCI. During PCI, an interventional cardiologist inserts a catheter, usually through the radial or femoral artery.
Using imaging guidance, they thread it up to the coronary arteries. Once the blockage is identified, they advance a balloon-tipped catheter across it, inflate the balloon to open the artery, and place a stent to keep the vessel open and restore blood flow.
If PCI is not available within 120 minutes, administer fibrinolytic therapy within 30 minutes of arrival at the hospital.
Fibrinolytic therapy involves medications that dissolve blood clots, such as Altaplace and streptokinase. However, keep in mind that these medications are contraindicated in some individuals, such as those with active bleeding, recent stroke, or significant head trauma.
Finally, after giving fibrinolytic therapy, arrange immediate transfer to a PCI capable center. Now that we've covered what to do in a patient presenting within the 1st 12 hours of symptom onset, let's switch gears and look at what to do when more than 12 hours have passed.
Since fibrinolytic therapy is only effective in the 1st 12 hours after symptom onset, at this point it is no longer an option for reperfusion therapy.
Next, assess for evidence of ongoing ischemia or complications such as refractory chest pain, hemodynamic instability, dynamic ECG changes, arrhythmias, and heart failure.
If any of these are present, proceed with emergent coronary angiography and PCI. If they are absent, continue current medical therapy and arrange for follow-up coronary angiography and PCI.
OK, now switching gears from STEMI to non-ST elevation ACS or NSTACS for short. If the ECG does not reveal ST elevation or left bundle branch block, but instead shows other ischemic changes like ST segment depressions or T wave inversions, think NSTE ACS.
Next, assess the cardiac troponin level to determine the type of NSTE ACS. Elevated troponin levels suggest Nstemi, while normal levels point to unstable angina.
But when myocardial damage happens, it can take several hours for troponin levels to rise in the blood. This means Estey and unstable angina often look the same when a patient first presents.
Either way, begin medical therapy with an oral P2Y12 inhibitor for dual antiplatelet therapy, along with parenteral anticoagulation.
Next, assess for signs of ongoing ischemia or complications. If present, proceed with emergency coronary angiography.
Based on the findings, the patient might need either immediate PCI or coronary artery bypass graft surgery, also known as CABIG.
Some of the main indications for CAABB include 3 vessel involvement or left main coronary artery disease. This is because cabbage offers more complete revascularization and better outcomes than PCI in these situations.
On the flip side, if there are no signs of ongoing ischemia or complications, the next step is to assess the patient's risk of major adverse cardiac events.
Common clinical tools for this include the thrombosis and myocardial infarction score or TIMI score, and the global registry of acute coronary events score, or simply Grace score.
If the patient is at high risk, proceed with coronary angiography within 24 hours, followed by PCI or CABIG, depending on the findings.
Alternatively, if the patient is low risk. The next step is a non-invasive stress test or coronary CT angiography.
If the results are abnormal, move forward with coronary angiography with PCI or CABIG as indicated. If the results are normal, continue current medical therapy.
Finally, let's return to our initial ECG findings one more time and discuss individuals who present with high suspicion for ACS but have non-diagnostic ECG findings and normal troponin levels.
In this situation, repeat serial ECGs and troponin measurements to assess for any changes. If ECGs show ST elevation in two or more contiguous leads, or a new left bundle branch block with strong clinical suspicion for MI, diagnose STEMI.
Then begin medical management with an additional antiplatelet medication and anticoagulation therapy. Proceed to emergent reperfusion therapy with coronary angiography with PCI or fibrinolytic therapy.
Remember, troponin will be elevated in this case, but you don't need to wait for the results to diagnose Stemi. Next, if ECGs show ST depression or T wave inversion and troponin levels rise, diagnose NSTEMI.
On the other hand, if ECG findings show ST depression or T wave inversion, but troponin levels stay normal, diagnose unstable angina.
For either NSTEMy or unstable angina, begin medical management with an additional antiplatelet medication and anticoagulation therapy.
If indicated, schedule coronary angiography and based on the findings, proceed with revascularization, either with PCI or CABH.
But if the ECGs and troponin remain normal, the next step is non-invasive stress testing or coronary CT angiography. If the results are abnormal, diagnose coronary artery disease.
Next, encourage lifestyle modifications and start a low dose daily aspirin. In many cases, a patient will require elective coronary angiography, and if the findings reveal significant coronary disease, proceed with revascularization with PCI or CABH.
Alright, as a quick recap, if you suspect ACS, the first step is to order a 12 lead ECG and cardiac troponin levels as soon as possible.
Next, provide acute management, which involves aspirin, nitroglycerin, and a statin with beta blockers and morphine if indicated.
If the ECG reveals ST elevation in two or more contiguous leads or a new left bundle branch block with strong clinical suspicion for MI, diagnose STEMI and treat with additional antiplatelet therapy, anticoagulation, and reperfusion therapy.
If the ECG shows other ischemic changes, including ST depression or T wave inversion, diagnose NSTE ACS. Further, if cardiac troponin levels are elevated, diagnose NSTEMI.
However, if they are normal, think of unstable angina. For both NSTEMI and unstable angina, treat with additional antiplatelet therapy and anticoagulation.
Based on ongoing conditions and complications and risk stratification, reperfusion therapy or medical therapy is used. Finally, if the initial ECG is non-diagnostic.
Monitor with serial ECGs and troponins to identify stemi and STEMI, and unstable angina. If none are present, use non-invasive stress testing or coronary CT angiography to look for stable coronary artery disease.