Mrs. Smith, 70, is admitted to your unit for pre-op testing, due to her history of hypertension and diabetes, before her scheduled cholecystectomy. Upon arrival, her BP is 90/60 mm Hg and her heart rate is 110 beats/minute. When asked about pain, Mrs. Smith says her abdominal pain is intermittently a 7 on a 0-to-10 scale (with 0 being no pain and 10 being the worst pain imaginable), but she indicates that she's having a horrible “heartburn” sensation that she attributes to not taking her “reflux medicine.” After further examination, you find Mrs. Smith to be slightly diaphoretic and pale. Although she denies shortness of breath, her oxygen saturation level is only 93%. She has taken her usual medications, which include hydrochlorothiazide, 25 mg, and glyburide, 5 mg, and her morning blood glucose level was 166 mg/dL. You alert the healthcare provider, and he orders a 12-lead ECG.
Is Mrs. Smith experiencing a myocardial infarction (MI)?
According to the American Heart Association (AHA), coronary artery disease is the number one cause of death in the United States and a leading cause of disability. One of the manifestations of this disease is MI, which accounts for approximately 1.5 million hospitalizations in the United States each year, according to the American College of Cardiology (ACC).
A block in the road
There are two types of MI: non–ST-elevation MI (NSTEMI) and ST-elevation MI (STEMI). Both of these conditions fall under the umbrella term acute coronary syndrome, or ACS. An NSTEMI is an imbalance between myocardial oxygen supply and demand caused by decreased myocardial perfusion that results from coronary narrowing. This narrowing is caused by nonocclusive thrombus formation due to disruption of an atherosclerotic plaque. A STEMI develops as a result of an occlusive thrombus. Let's take a closer look.
Blockages in the heart occur in response to damage to the interior portion of the coronary vessel. Over time, the inner lining of the blood vessel becomes damaged due to multiple factors, such as hypertension, tobacco use, diabetes, and an elevated low-density lipoprotein cholesterol level. To help repair the damage, platelets attach to the endothelium and white blood cells move to the area. This congregation of platelets and blood cells develops into a fibrous plaque over time, and the plaque then creates a narrowing in the lumen of the coronary artery. This plaque may remain stable, but a rupture can occur due to the turbulent flow within the narrowed artery. When the rupture occurs, platelets continue to move to the area and then become exposed to activating factors, such as collagen and thrombin. After the platelets become activated, they produce glycoprotein IIb and IIIa receptors that bind fibrinogen. This platelet aggregation continues, creating a larger thrombus, eventually leading to complete blockage of the vessel (see How MI happens).
Give me a sign
Classically, patients suffering from an MI will describe a pain on the left side of their chest as a squeezing, crushing, heaviness, or pressure sensation. Patients may also describe the pain as burning or knife-like. The pain may radiate to other areas of the body, typically the left arm and jaw, and may be continuous or intermittent depending on activity. The patient may complain of nausea or vomiting and shortness of breath. Other symptoms may include weakness, dizziness, palpitations, or a feeling of impending doom.
Although many patients present with one or more of the above symptoms, some patients may have no symptoms at all or those that they don't attribute to the heart. For example, Mrs. Smith thought her pain was from indigestion related to her gallbladder. Did she have any of the symptoms listed above? No! Women, older patients, diabetics, and dialysis patients may have very different symptoms, such as feeling the pain on the right side of the chest and describing it as discomfort, indigestion, or tightness. For example, Mrs. Smith's history of diabetes may have masked some of the chest pain symptoms. The patient may not experience nausea, vomiting, or shortness of breath. It's especially important to take these factors into consideration when assessing a patient like Mrs. Smith.
So, why the pain? The pain felt when a patient is having an MI is related to the lack of blood flow to an area beyond the occlusion. Think about when you're asleep and you wake up to find your arm feels heavy and tingles. This is because you've put pressure on that arm, disrupting blood flow to the area and compressing nerves. Decreased blood flow to the arm deprives the tissue of much-needed oxygen, thus sending signals back to the brain, waking you up and prompting you to move your arm. The same is similar with the heart; once blood flow to a portion of the heart is blocked, the tissue goes without needed oxygen, sending out signals that something is wrong.
Getting the picture
The most common diagnostic study for MI is a 12-lead ECG. An ECG can be used to evaluate the patient's heart rate and rhythm and to look for ST-segment elevation or T-wave inversion, which may indicate myocardial ischemia. A 12-lead ECG is a quick and inexpensive way of evaluating the heart, but there are times when the result may be normal or indeterminate, even if the patient is experiencing an MI. In addition to an ECG, serial cardiac enzyme tests are done to evaluate the enzymes released from the myocardial tissue in response to damage.
Cardiac enzymes commonly used to evaluate for cardiac damage are creatine kinase (CK), creatine kinase–myocardial band isofraction (CK-MB), and troponin I. All three enzymes are useful in the diagnosis of an MI, but CK and CK-MB aren't as specific as troponin I. Troponin I levels are now the standard for defining and diagnosing MI, according to the ACC/AHA guidelines. A serial test is needed because each enzyme rises and peaks at different times. The CK level rises within 4 to 6 hours of onset of chest pain and peaks at 24 to 36 hours. CK-MB, which was previously the diagnostic standard, rises within 3 to 12 hours of onset of chest pain, peaks at 24 hours, and returns to baseline after 48 to 72 hours. Troponin I rises within 3 to 12 hours of onset of chest pain, peaks at 24 to 48 hours, and reaches baseline over 5 to 14 days.
Other diagnostic tests that can be used to detect MI include a cardiac stress test and cardiac catheterization. A cardiac stress test is usually done if cardiac enzyme testing comes back negative and the 12-lead ECG is normal. This can be done on an outpatient basis or may be performed before the patient is discharged. Cardiac catheterization is usually ordered if there's a high suspicion of MI, sometimes even before completion of serial cardiac enzyme testing. The earlier a definitive diagnosis is made, the quicker treatment can be started.
Mrs. Smith's 12-lead ECG shows ST-segment elevations in the V5 and V6 leads, indicating injury to the lateral wall of the heart (see Tissue destruction in MI). Her lab results are as follows: CK, 132; CK-MB, 46; and troponin I, 1.3.
Treatment coming right up
So what are we going to do for Mrs. Smith? Immediate treatment goals include restoring oxygen supply, pain relief, and preventing and treating complications. Mrs. Smith will be placed on a cardiac monitor for continuous heart monitoring. Oxygen via nasal cannula at 2 to 3 L/minute will be administered to maintain her oxygen saturation level above 95%. (If a patient is unstable, she may require more aggressive methods, such as 100% oxygen via non-rebreather mask or even intubation.) Aspirin, 324 mg (four chewable 81-mg tablets), should be given if not contraindicated, such as in the case of recent bleeding from the gastrointestinal tract, stroke, or surgery.
Sublingual nitroglycerin, 0.4 mg, may be given every 5 minutes for up to three doses to help relieve chest pain. If Mrs. Smith's pain isn't relieved with sublingual nitroglycerin, I.V. nitroglycerin may be ordered. It's important to document the patient's BP and heart rate before and after any administration of nitroglycerin, especially when it's given I.V., because many patients may have a significant drop in BP after administration.
I.V. morphine may be ordered to help relieve pain. Morphine can also be helpful because of its vasodilation properties; if there's an occlusion, the coronary artery may dilate enough to allow blood to flow past the blocked area. The patient may also be given beta-blockers to control heart rate and decrease myocardial oxygen demand.
Clearing the blockage
There are several treatments that can be performed to open up the blocked coronary vessel. Treatment depends on the determination of STEMI, NSTEMI, or unstable angina.
Patients with persistent ST-segment elevation will be considered for reperfusion with thrombolytics or primary percutaneous coronary intervention (PCI), also known as angioplasty, percutaneous transluminal coronary angioplasty (PTCA), or balloon angioplasty (see Understanding PTCA). An intravascular stent may be inserted in conjunction with the angioplasty to help prevent restenosis of the artery. Thrombolytics can be helpful in opening up the coronary artery, but they're associated with complications, the most serious being intracranial hemorrhage. Patients with no ST-segment elevation should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission. The ideal door-to-drug time is 30 minutes; door-to-balloon time, 90 minutes.
With a quickness
Thanks to your quick response to the subtle change in Mrs. Smith, she's sent to the catheterization lab for an emergent cardiac catheterization with stenting of her blocked artery. Upon returning from the cath lab, assess Mrs. Smith's vital signs, ECG, oxygen saturation, urinary output, and pulmonary and peripheral vascular status. Also evaluate her for complaints of chest pain and bleeding from the catheterization site. Mrs. Smith's cholecystectomy is put on hold for now until she recovers from her cardiac catheterization.
To remember the AHA's pre-hospital empiric protocol for suspected STEMI, think