A middle aged male with several CAD risks has had several months of exertional angina relieved by rest and nitro. He had the onset of chest discomfort at rest and presented by ambulance about 3 hours later with "severe crushing chest pain," with a blood pressure of 200/100 and pulse of 100. The prehospital ECG cannot be found. Here is his initial ED ECG:
Exam was otherwise normal, including clear lungs and the absence of any murmur.
The pain continued and a second ECG was recorded 20 min later, after 2 sublingual NTG. This second ECG was unchanged.
At t=102 min, after 2 more sublingual NTGs, another ECG was recorded. It is unclear to me whether the patient was still having chest pain.
The ST depression was not commented on, and the initial troponin was less than the 99% reference value. A 3 hour troponin I returned elevated (and it eventually peaked at 0.15 ng/mL). The patient was given an aspirin, 600 mg of clopidogrel, and heparin bolus and drip. A bedside ultrasound was done that was of imperfect quality but showed good left ventricular function.
What the patient was not given was a medication to definitively bring down his blood pressure. There are additional measures beyond antiplatelet and antithrombotic medications for the treatment of ACS. Ischemia is a problem of both oxygen supply and demand. Adjunctive anti-ischemic therapies such as intravenous nitroglycerin or beta blockade can be useful to minimize ischemia.
This is a perfect patient for beta blockade. He has ischemia and has hypertension and tachycardia. The tachycardia is not due to volume deficit (hemorrhage, dehydration, sepsis) nor is it due poor LV function nor valvular disease (at least no murmur). The patient has no contraindications such as prolonged PR interval, high grade AV block, bradycardia, hypotension, or heart failure. Metoprolol 5 mg IV every 5 minutes for 3 doses, then 25-50 mg orally every 6 hours, would be very useful to control BP and lower the pulse, diminishing the demand for coronary blood flow, which is in short supply due to ACS in this patient.
The controversy over beta blockade in the ED (early in ACS) is for patients at risk for cardiogenic shock, principally patients with acute STEMI, especially anterior STEMI. Formerly, beta blockade was recommended as an ED treatment for all MI, including STEMI. However, in 2005 the COMMIT trial was published: 45,000 Chinese STEMI patients (who were being reperfused with thrombolytics, not PCI) randomized to early intravenous then oral metoprolol vs. placebo. Mortality was equal in the two groups, but the mechanism of death differed between them: dysrhythmias were more common in the placebo group and cardiogenic shock was more common in the metoprolol group. After publication of this study, much more caution was used in treating STEMI patients with early (ED) beta blockade, especially in those at risk for cardiogenic shock: tachycardia, anterior STEMI, low stroke volume, any signs of heart failure.
A more recent small study (Circulation 2013;128:1495) of patients with anterior STEMI and Killip class II or less heart failure who were undergoing PCI resulted in significantly smaller infarct size, as measured by MRI, in patients who received IV metoprolol compared to placebo. Perhaps beta blockade will make a comeback for STEMI in this age of PCI, but a larger study is needed.
Until then, however, beta blockade is still indicated in NonSTEMI when the patient has hypertension and also if there is tachycardia (tachycardia that is not compensatory for low stroke volume, which may be due to poor LV function, valvular disease, low left ventricular end-diastolic volume, or low systemic vascular resistance). The 2007 ACC/AHA guideline is the most recent guideline that comments on beta-adrenergic blockade in Unstable Angina/NonSTEMI; the more detailed statement is in agreement with the above (see page e188-189).
If the BP is not significantly reduced with metoprolol, or metoprolol is contraindicated, then Intravenous Nitroglycerine is indicated. See the ACC/AHA guideline, page e186-187. In addition, if there is continued ischemic chest pain, IV NTG indicated. How much should BP be lowered? MAP should not be reduced more than 25-30% of the premorbid (baseline) blood pressure, if that is known. Steeper reductions risk ischemic stroke. Additionally, it should not be lowered below a systolic pressure of 100-110 mmHg.
If ischemia cannot be controlled with these measures, immediate angiography with PCI, if indicated by angiogram, should be undertaken.
Lesson:
Patients with cardiac ischemia (in particular with unstable angina or NonSTEMI) and hypertension in the ED must have their BP lowered. In the absence of contraindications, metoprolol is an excellent choice. If there are contraindications to metoprolol, especially evidence of low stroke volume, then nitroglycerin should be used. Both hypertension and tachycardia increase myocardial oxygen demand at a time when the oxygen supply is diminished by ACS.
Outcome:
The patient did get beta blockade as an inpatient and the pulse and BP were reduced. He went for angiogram and had an 80% left main culprit, 100% circumflex and 80% RCA. He will undergo CABG.
 | |||
| Sinus rhythm, nearly tachycardia. Left axis deviation with QRS of 90 ms, R-wave peak time in aVL perhaps reaches 45 ms, so possible left anterior fascicular block. There is minimal ST depression (but also a wandering baseline) in V3-V6. |
Exam was otherwise normal, including clear lungs and the absence of any murmur.
The pain continued and a second ECG was recorded 20 min later, after 2 sublingual NTG. This second ECG was unchanged.
At t=102 min, after 2 more sublingual NTGs, another ECG was recorded. It is unclear to me whether the patient was still having chest pain.
 |
| Now there is definite ST depression in V2 and V3, diagnostic of ischemia. There is very slight ST depression in I, II, and V4-V6, and minimal reciprocal ST elevation in aVR. So there appears to be subtle widespread subendocardial ischemia. |
The ST depression was not commented on, and the initial troponin was less than the 99% reference value. A 3 hour troponin I returned elevated (and it eventually peaked at 0.15 ng/mL). The patient was given an aspirin, 600 mg of clopidogrel, and heparin bolus and drip. A bedside ultrasound was done that was of imperfect quality but showed good left ventricular function.
What the patient was not given was a medication to definitively bring down his blood pressure. There are additional measures beyond antiplatelet and antithrombotic medications for the treatment of ACS. Ischemia is a problem of both oxygen supply and demand. Adjunctive anti-ischemic therapies such as intravenous nitroglycerin or beta blockade can be useful to minimize ischemia.
This is a perfect patient for beta blockade. He has ischemia and has hypertension and tachycardia. The tachycardia is not due to volume deficit (hemorrhage, dehydration, sepsis) nor is it due poor LV function nor valvular disease (at least no murmur). The patient has no contraindications such as prolonged PR interval, high grade AV block, bradycardia, hypotension, or heart failure. Metoprolol 5 mg IV every 5 minutes for 3 doses, then 25-50 mg orally every 6 hours, would be very useful to control BP and lower the pulse, diminishing the demand for coronary blood flow, which is in short supply due to ACS in this patient.
The controversy over beta blockade in the ED (early in ACS) is for patients at risk for cardiogenic shock, principally patients with acute STEMI, especially anterior STEMI. Formerly, beta blockade was recommended as an ED treatment for all MI, including STEMI. However, in 2005 the COMMIT trial was published: 45,000 Chinese STEMI patients (who were being reperfused with thrombolytics, not PCI) randomized to early intravenous then oral metoprolol vs. placebo. Mortality was equal in the two groups, but the mechanism of death differed between them: dysrhythmias were more common in the placebo group and cardiogenic shock was more common in the metoprolol group. After publication of this study, much more caution was used in treating STEMI patients with early (ED) beta blockade, especially in those at risk for cardiogenic shock: tachycardia, anterior STEMI, low stroke volume, any signs of heart failure.
A more recent small study (Circulation 2013;128:1495) of patients with anterior STEMI and Killip class II or less heart failure who were undergoing PCI resulted in significantly smaller infarct size, as measured by MRI, in patients who received IV metoprolol compared to placebo. Perhaps beta blockade will make a comeback for STEMI in this age of PCI, but a larger study is needed.
Until then, however, beta blockade is still indicated in NonSTEMI when the patient has hypertension and also if there is tachycardia (tachycardia that is not compensatory for low stroke volume, which may be due to poor LV function, valvular disease, low left ventricular end-diastolic volume, or low systemic vascular resistance). The 2007 ACC/AHA guideline is the most recent guideline that comments on beta-adrenergic blockade in Unstable Angina/NonSTEMI; the more detailed statement is in agreement with the above (see page e188-189).
If the BP is not significantly reduced with metoprolol, or metoprolol is contraindicated, then Intravenous Nitroglycerine is indicated. See the ACC/AHA guideline, page e186-187. In addition, if there is continued ischemic chest pain, IV NTG indicated. How much should BP be lowered? MAP should not be reduced more than 25-30% of the premorbid (baseline) blood pressure, if that is known. Steeper reductions risk ischemic stroke. Additionally, it should not be lowered below a systolic pressure of 100-110 mmHg.
If ischemia cannot be controlled with these measures, immediate angiography with PCI, if indicated by angiogram, should be undertaken.
Lesson:
Patients with cardiac ischemia (in particular with unstable angina or NonSTEMI) and hypertension in the ED must have their BP lowered. In the absence of contraindications, metoprolol is an excellent choice. If there are contraindications to metoprolol, especially evidence of low stroke volume, then nitroglycerin should be used. Both hypertension and tachycardia increase myocardial oxygen demand at a time when the oxygen supply is diminished by ACS.
Outcome:
The patient did get beta blockade as an inpatient and the pulse and BP were reduced. He went for angiogram and had an 80% left main culprit, 100% circumflex and 80% RCA. He will undergo CABG.
Thank you for this. There's so much discussion out there regarding sexier topics like which antiplatelet and antithrombotic agents to use that very often these other medications commonly indicated in ischemia get downplayed or ignored. And as always, we need a reminder that failure to resolve symptoms or ischemia is an indication for immediate angiography; I know at my shop that indication is commonly either ignored or ischemia is downplayed resulting in delayed treatment.
ReplyDeleteThanks Steve. Interesting and timely post for me. As you know, where I trained we seemed to err on the side of less beta blockade. Where I practice now there is a culture of aggressive beta blockade for NSTEMI which I think is misunderstood by the ED and cardiology residents, often leading to inappropriate treatments and bad patient outcomes. It is critical to think through the physiology (consider bedside lung and cardiac utz if you're skilled) to make sure you have a sense of cardiac function etc before using beta blockers.
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