B.C. is a 71-year-old sedentary, African-American woman who has been living with type 2 diabetes for 10 years. Her medical history includes stroke, valve prolapse, restless leg syndrome, and hip replacement. There is no family history of diabetes or symptoms at presentation. B.C.'s baseline weight is 160.8 lb, and her waist circumference is 99 cm. Resting blood pressure is 144/68 mm Hg. She is currently taking metformin, glyburide, simvastatin, and gabapentin. Baseline laboratory analyses reveal a fasting blood glucose of 303 mg/dl, A1C of 9.9%, C-reactive protein of 1.6 mg/dl, total cholesterol of 205 mg/dl, LDL cholesterol of 144 mg/dl, total cholesterol-to-HDL cholesterol ratio of 4.8, VO2max of 15.6 ml/kg/min, systolic blood pressure of 144 mm Hg, and percent body fat of 40. Her daily physical activity consists of low-intensity walking and housework for < 30 minutes per day.
B.C. enrolls in a 12-week supervised aerobic exercise program. After a preliminary screening consisting of height, weight, waist-to-hip ratio, systolic and diastolic blood pressures, and cardiovascular disease risk assessment, B.C. reports to the general clinical research center for pre- and posttraining 12-hour fasting blood draws, body composition assessment (dual-energy X-ray absorptiometry), and maximal exercise testing (treadmill with indirect calorimetry). B.C. receives clearance from her physician before beginning the exercise training.
What type of exercise program should be prescribed for B.C.?
What outcomes might be expected from the 12-week exercise program?
Can the risk factors for cardiovascular disease be lowered with a 12-week exercise program in a 71-year-old woman with type 2 diabetes?
Because B.C. was not currently meeting the U.S. Surgeon General's recommendations for physical activity,1 she was placed on a 12-week training program with a frequency of 3 days per week for a duration of 30 minutes/day. The mode was self-selected exercise, consisting of treadmill walking and recumbent stationary cycling. Training intensity was set at 50-85% VO2peak as recorded during maximal exercise testing. Warmup consisted of 5 minutes of light-intensity walking on a treadmill.
B.C. wore a heart rate monitor (Polar Electro, Finland) and her heart rate was recorded every 5 minutes. Rating of perceived exertion was recorded every 10 minutes. She was closely monitored and encouraged by an exercise physiologist during each training session, which took place at a fitness center on a medical school campus.
Blood glucose and blood pressure were measured before and after each exercise bout. She was instructed to consume a light snack 30-60 minutes before exercise. Preexercise blood glucose was checked to verify that it was between 100 and 250 mg/dl, in the absence of hypo- or hyperglycemic symptoms.1 On one occasion, B.C. arrived at the exercise facility with a blood glucose reading of 290 mg/dl and for safety reasons was not permitted to exercise that day. In addition, B.C. was monitored postexercise to verify that her blood glucose was > 70 mg/dl; lower readings are indicative of exercise-induced hypoglycemia. There were no occurrences of hypoglycemia.
Posttraining laboratory analyses revealed the following values: fasting blood glucose of 181 mg/dl, A1C of 9.2%, C-reactive protein of 1.1 mg/dl, total cholesterol of 178 mg/dl, LDL cholesterol of 114 mg/dl, total cholesterol-to-HDL cholesterol ratio of 4.1, systolic blood pressure of 114 mm Hg, VO2max of 16.8 ml/kg/min, and percent body fat of 37.6 (Table 1). Training compliance was 100%. She remained on metformin and glyburide.
After 12 weeks of moderate-intensity exercise, B.C. decreased five risk factors for cardiorespiratory disease: percent body fat, fasting glucose, LDL cholesterol, systolic blood pressure, and sedentary lifestyle. Additionally, her C-reactive protein and A1C were lowered, while her maximum aerobic capacity was increased. The improved lipid profile was especially crucial, considering that the combination of dyslipidemia and diabetes magnifies the risk for cardiovascular disease.2 The posttraining LDL cholesterol value of 114 mg/dl represented a substantial improvement in her targeted LDL value that was not possible with therapeutic agents alone.
Another major change for B.C. as a result of the exercise training was the 40% decrease in fasting blood glucose. Although still higher than the recommended preprandial blood glucose values of 70-130 mg/dl,2 B.C. was able to improve her glycemic control to a greater degree after including walking and stationary cycling to her diabetes treatment plan. The mechanism for her improved glycemic control may have been achieved through the changes in body composition, specifically reductions in percent body fat.3
B.C.'s 0.7% reduction in A1C is comparable to the 0.66% reported in a meta-analysis on exercise training and glycemic control in type 2 diabetic patients.4 Decreases in A1C have been shown to be related to exercise intensity: reductions of 2.3% have been reported after 8 weeks of cycling at 75% VO2max.5 The exercise intensity of the current study ranged from 50 to 85% VO2peak; however, given B.C.'s history with hyperglycemia, lowering her A1C to the recommended level of < 7.0%2 will probably require continued or additional medication. Also, the expected improvement in glycemic control may have been limited by the 12-week duration of the study, since A1C and fasting glucose levels may not have reached their lowest end points.
B.C. was aware that she needed to make lifestyle changes, especially after her hip replacement surgery. As a septuagenarian with diabetes, she faced an increased risk of functional disability, premature death, and cognitive impairment compared to older women without diabetes.2 Further, the majority of older women with type 2 diabetes also report comorbidities such as stroke, heart failure, myocardial infarction, and nephropathy.6
Injuries and subsequent disability related to falling are also more prevalent with increasing age and lack of physical activity.7 Older adults with diabetes also face an increased fall risk due to peripheral neuropathy and poor vision. Improving glycemic control has been shown to reduce fall risk.8
Exercise interventions involving septuagenarian women with type 2 diabetes are limited. In one study, patients with type 2 diabetes (aged 55-75 years) showed no differences in insulin sensitivity after a 12-week aerobic exercise training program, despite lower triglyceride and LDL cholesterol levels.9 It is important to note that patients in B.C.'s situation should obtain cardiac clearance before initiating a moderate-intensity exercise program.
Changes in Cardiovascular Disease Risk After 12 Weeks of Aerobic Exercise Training
Septuagenarian women with type 2 diabetes can improve their glycemic control through moderate aerobic exercise training.
Twelve weeks of aerobic exercise reduced the blood pressure, blood lipids, body fat, and C-reactive protein levels in a 71-year-old woman with type 2 diabetes.
A supervised aerobic exercise program can be prescribed safely for older women with type 2 diabetes.
This project was funded by the Faculty Development Fund of the University of San Francisco and through UCSF's Medical Center General Clinical Research Center. The original study (four subjects) was presented as “The Effects of an Exercise Intervention on Cardiovascular Risk Factors in Postmenopausal Type 2 Diabetics” and appears in the New Horizons in Coronary Artery Disease proceedings of the 7th International Congress on Coronary Artery Disease.
Julia C. Orri, PhD, is an assistant professor, and Christian J. Thompson, PhD, is an associate professor in the Department of Exercise and Sport Science at the University of San Francisco in California. Deborah E. Sellmeyer, MD, is associate professor of medicine at The Johns Hopkins Bayview Medical Center in Baltimore, Md.
- American Diabetes Association(R) Inc., 2009
Use this case study as an educational tool by answering the questions posed by the author, then reviewing the answers further down.
At 6:45 a.m., your unit is dispatched for a 50-year-old male with chest pain. You and your partner proceed to the scene, with a response time of approximately eight minutes. The closest hospital from the scene is 40 miles away.
You arrive at the scene, don appropriate BSI precautions and ensure that the area is safe, then knock on the door of the patient's residence. A middle-aged male answers the door and identifies himself as the patient. You note that he is diaphoretic and anxious, and is clenching his fist against the center of his chest.
1. What is the significance of the patients clenched fist in the center of his chest?
You sit the patient down and perform an initial assessment (Table I). Your partner attaches a pulse oximeter and prepares to administer oxygen to the patient.
Your partner administers 100% oxygen to the patient with a nonrebreathing mask while you perform a focused history and physical examination (Table II). The patient tells you that his doctor prescribed nitroglycerin for him; however, because he recently moved into the house, he thinks it's still packed in one of the boxes.
2. What are the physiologic effects of nitroglycerin?
After confirming no history of bleeding disorders or allergies, you administer 324 mg of aspirin to the patient. Your partner obtains baseline vital signs and a SAMPLE history (Table III). The patient remains conscious and alert, but is becoming increasingly restless. You attach the patient to a cardiac monitor and interpret his cardiac rhythm as sinus tachycardia at 110 beats per minute.
After administering 0.4 mg of nitroglycerin sublingually to the patient, you and your partner attach the remaining ECG leads and obtain a 12-lead tracing of the patient's cardiac rhythm. As your partner stands up to retrieve the stretcher from the ambulance, you tell him that it looks as though the patient may be having an anterior wall MI.
3. How could this patient's current blood pressure and heart rate affect his condition?
The patient's chest pressure is unrelieved following two more doses of sublingual nitroglycerin. You place him on the stretcher and load him into the ambulance. En route to the hospital, you continue oxygen therapy and successfully establish an IV of normal saline with an 18-gauge catheter. Reassessment of his blood pressure reveals a reading of 140/88 mmHg. Because three doses of nitroglycerin failed to relieve his pain, you administer 2 mg of morphine sulfate via IV push. Within 10 minutes, the patient tells you that the pressure in his chest has improved and is now a "3" on a 0--10 scale. With an estimated time of arrival at the ED of 20 minutes, you begin an IV infusion of nitroglycerin at 10 µg/min and perform an ongoing assessment (Table IV).
The patient's condition continues to improve en route to the hospital. You ask him if he has a history of ulcers, bleeding disorders, recent surgeries or stroke. He tells you that other than his high blood pressure and occasional chest pain, he has no other medical problems. You call your radio report to the receiving facility and continue to monitor the patient.
4. Why are you asking the patient these specific questions?
The patient tells you that he is still experiencing chest pressure; however, it is less severe. Since his blood pressure remains stable (130/84 mmHg), you administer another 2 mg dose of morphine via IV push. You continue to monitor the patient's vital signs and cardiac rhythm. Your estimated time of arrival at the hospital is 5--10 minutes.
5. Are there any special considerations for this patient?
Upon arriving at the emergency department, the patient states that he is pain-free. You give your verbal report and field-obtained 12-lead ECG to the attending physician. Following additional assessment in the emergency department, the patient is diagnosed with an acute anterior wall myocardial infarction. Following successful treatment with fibrinolytic therapy, he is admitted to the cardiac care unit and transferred to a cardiac rehabilitation facility 10 days later.
Cardiac Case Study: Answers and Summary
1. What is the clinical significance of the patient’s clenched fist in the center of his chest?
Ischemic cardiac chest pain is typically described as being crushing, tight, oppressive, pressuring or constricting in nature. Patients may describe their pain as though a vise were placed around their chest or the sensation that an elephant is sitting on their chest, while others may only report a vague or "strange" sensation in their chest. The pain associated with cardiac ischemia is usually substernal; however, it may be localized to the epigastrium and is commonly mistaken for indigestion.
A clenched fist in the center of the chest (the precordium) conveys the feeling of pressure or squeezing and is called Levine's sign (see the photo on page 50). The presence of Levine's sign is suggestive, but not conclusive, of cardiac-related chest pain and should increase your index of suspicion.
Chest pain or discomfort is the most common presenting symptom of an acute coronary syndrome (ACS), occurring in 70%--80% of patients. However, 20% or more of patients with acute myocardial infarction present with no pain or discomfort at all. Elderly patients and patients with diabetes may present without classic symptoms or with only vague, nonspecific symptoms, such as malaise, lightheadedness, syncope, changes in mentation or sudden diaphoresis.
Patients with cardiac ischemia may also present with referred pain to other areas of their body, such as the jaw, arm, shoulder or back. Less commonly, patients may present with atypical chest pain, which may be described as sharp or stabbing in nature.
During your general impression of the patient with chest pain or pressure, look for clues suggestive of cardiac compromise, such as diaphoresis, restlessness or apprehension. The absence of chest pain or the presence of atypical chest pain, however, does not rule out an ACS--especially if the patient has other signs and symptoms and a history of cardiac disease (e.g., prescribed nitroglycerin).
Acute coronary syndrome is a term used to describe many types of compromised circulation to the heart muscle, including unstable angina pectoris or acute myocardial infarction. Because the clinical presentations of the two are extremely similar, if not identical (i.e., unrelieved chest pain, ECG changes, diaphoresis), treatment should focus on the assumption that acute myocardial infarction is occurring.
2. What are the physiologic effects of nitroglycerin?
Before discussing the physiologic effects of nitroglycerin, a brief review of coronary atherosclerosis, myocardial ischemia and angina pectoris is in order.
Coronary atherosclerosis is a progressive disease characterized by the buildup of lipid-laden plaque within the lumen (channel) of the coronary artery. Atherosclerosis causes narrowing of the artery (decreasing coronary blood flow) and hardening of the artery (limiting the ability of the artery to dilate). These negative consequences of atherosclerosis reduce the ability of the heart to accommodate increases in myocardial oxygen demand, such as that caused by stress or exertion.
When the scale of myocardial oxygen supply and demand is unbalanced, the patient develops ischemic chest pain or pressure (angina pectoris). Ischemia, which is defined as a relative deprivation of oxygen, occurs when oxygen demand exceeds supply, and is a reversible condition with prompt treatment.
Angina is described as being stable or unstable. Stable angina is characterized by a relatively predictable sequence of events. Patients are often aware of the extent of exertion that precipitates their chest pain (e.g., walking one block); therefore, they limit their activities in order to avoid symptoms. Additionally, patients are also aware of what they need to do to resolve their symptoms (e.g., a specific period of rest, nitroglycerin). Following resolution of their chest discomfort, many patients with stable angina never call EMS.
Unstable angina occurs when the patient experiences a change in his typical anginal pattern, indicating advanced coronary atherosclerosis and an oxygen supply-demand mismatch that is not so easily balanced with rest and nitroglycerin. Relative to stable angina, the patient with unstable angina experiences "off-pattern" chest pain, such as when exertion is minimal or when myocardial oxygen demand is otherwise low (e.g., during sleep). Additionally, the usual treatment modalities of rest and/or nitroglycerin afford them minimal or no relief from their symptoms. This change may prompt a call to EMS.
Nitroglycerin (NTG) causes relaxation of vascular smooth muscle (vasodilation), promoting systemic pooling of venous blood. This decreases the volume of blood that is returned to the heart (preload), as well as the amount of resistance that the heart must pump against (afterload). The combined effects of decreased preload and afterload cause an overall decrease in myocardial oxygen demand and consumption.
Additionally, nitroglycerin may dilate the coronary arteries and promote collateral circulation, thus improving oxygen supply to the ischemic myocardium. Collateral circulation, also referred to as "arteriogenesis," is a process in which smaller arteries that are normally closed become patent (open up) and connect two larger arteries or different parts of the same artery. Over time, myocardial ischemia can promote collateral vessels to grow, forming a "detour" for blood flow around the blocked coronary artery.
Because nitroglycerin dilates the systemic blood vessels, it can result in hypotension. Therefore, its use is generally contraindicated in patients with a systolic BP of less than 90 mmHg, as well as in patients who have taken Viagra (sildenafil), Levitra (vardenafil) or Cialis (tadalafil) within the past 24--36 hours. These drugs, which are used to treat sexual dysfunction, also cause vasodilation and, when used concomitantly with nitroglycerin, can result in potentially life-threatening hypotension. EMS providers should follow local protocol or contact medical control as needed regarding the use of nitroglycerin.
3. How could this patient's current blood pressure and heart rate affect his condition?
This patient's history, physical examination and 12--lead ECG findings suggest acute myocardial infarction (AMI) involving the anterior (front) wall. The patient's hyperdynamic vital signs--hypertension and tachycardia--indicate a discharge of epinephrine and norepinephrine from the sympathetic nervous system, most likely caused by a combination of pain, anxiety/fear and myocardial ischemia and injury. Epinephrine increases the rate (chronotropy) and strength (inotropy) of cardiac contractions and norepinephrine increases systemic blood pressure by constricting the blood vessels.
This patient's vital signs represent a classic case of "more is not better!" In order for the heart to beat stronger and faster, it requires and uses more oxygen. Additionally, an elevated blood pressure increases afterload (ventricular resistance), further increasing myocardial oxygen demand.
Unfortunately, in this patient, an occluded coronary artery is blocking the flow of oxygenated blood to the area of the myocardium that needs it most--the injured area. This increase in myocardial oxygen demand and consumption and decrease in myocardial oxygen supply can enlarge the area of injury, resulting in greater myocardial damage.
The anterior wall is the largest part of the heart and tends to sustain significant damage as the result of an MI. As the area of injury increases, lethal cardiac dysrhythmias, such as ventricular fibrillation (v--fib) or ventricular tachycardia (v--tach), can occur. Additionally, if an extensive area of the anterior wall is damaged, the patient can develop acute CHF and, in more severe cases, cardiogenic shock. Cardiogenic shock, which has a very high mortality rate, occurs when the heart is severely damaged and is no longer able to adequately perfuse the body.
4. Why are you asking the patient these specific questions?
This patient is a potential candidate for fibrinolytic (clot-buster) therapy; therefore, you should conduct a field screening to determine if he is eligible for this treatment. Although fibrinolytic therapy is not commonly initiated in the prehospital setting, the information you obtain regarding the patient's eligibility or ineligibility, in addition to the 12-lead ECG obtained in the field, will be valuable to the physician and can decrease the "door-to-drug" time when the patient arrives in the emergency department.
Fibrinolytic agents (Table V) work by a chemical process that converts plasminogen to plasmin, the central enzyme of the physiologic plasminogen system. Plasmin in turn digests fibrin, the active component of the clot matrix, through a process called fibrinolysis. Fibrinolysis dissolves the clot that is occluding the coronary artery, thus reestablishing distal perfusion. The goal of fibrinolytic therapy is to halt the infarction process and salvage areas of ischemic and injured myocardium.
The indications or inclusion criteria for fibrinolytic therapy are summarized in Table VI. Although EMT-Basics and EMT-Intermediates are not usually trained to interpret ECG rhythms, they can, through index of suspicion based on the patient's signs and symptoms, suspect AMI and conduct a field screening, especially if the time of onset is less than 12 hours.
Because of the interaction of fibrinolytics with the body's hematologic system, strict criteria must be met before the patient can be eligible for fibrinolytic therapy. If given to the wrong patient, fibrinolytics can cause life-threatening hemorrhage. Table VII summarizes the absolute and relative contraindications or exclusion criteria for fibrinolytic therapy. Some patients with certain relative contraindications may still be eligible for fibrinolytic therapy, based on a careful evaluation by the physician.
5. Are there any special considerations for this patient?
There are several issues to consider when treating and monitoring this patient. As previously discussed, nitroglycerin (being administered to this patient via continuous IV infusion) can cause hypotension. Therefore, careful monitoring of the patient's blood pressure is essential. Hypotension in a patient with a sick heart can have disastrous consequences.
You have also administered a total of 4 mg of morphine to the patient. Morphine, a narcotic analgesic, can depress the central nervous system, resulting in a decreased level of consciousness, hypoventilation, bradycardia and hypotension. While most people will not experience significant CNS depression with low doses of morphine, you should have a BVM handy to assist ventilations, as well as naloxone (Narcan) to reverse the effects of the morphine. Narcan competitively binds with opiate receptor sites in the body and reverses the CNS depression associated with narcotic administration.
Continuous cardiac monitoring is an essential part of cardiac patient management, especially in this patient, whose 12-lead ECG indicates that an MI is in progress. You must be alert for the development of warning signs of a potentially lethal dysrhythmia, such as premature ventricular complexes (PVCs). You should also observe the patient for any sudden changes in his heart rate. Anterior wall MIs can result in significant tachycardia or bradycardia, both of which can further complicate the clinical picture.
When caring for a potentially unstable cardiac patient, especially when your transport time is lengthy, you must remain cognizant of the fact that because you are alone in the back with the patient, your capabilities are limited to defibrillation and one-person CPR if the patient develops cardiac arrest. Therefore, it would be prudent to request additional assistance or arrange to rendezvous with another EMT or paramedic while en route to the hospital.
This case study represented a patient with a relatively uncomplicated myocardial infarction that, after prompt prehospital care and transport, was successfully halted in the emergency department with fibrinolytic therapy.
This patient was provided excellent care in the prehospital setting because the paramedic and his EMT-B partner worked together effectively as a team. Although ECG monitoring, IV therapy and medication administration are beyond the usual scope of practice of an EMT-B, many EMS systems are training their EMT-Bs to assist with these important procedures and interventions. This involves preparing IV equipment and supplies, applying the cardiac monitor, and recognizing and handling the various paramedic medications. This enhanced role of the EMT-B allows the paramedic to perform a more focused and careful patient assessment.
A cohesive working relationship between BLS and ALS personnel is absolutely crucial to the outcome of the patient. Although each level of prehospital provider possesses a different knowledge of pathophysiology and patient management, it is the combined contributions and efforts of each provider that will afford patients the high quality of care they deserve.
- ACLS for EMT-Basics. Jones and Bartlett, Publishers/AAOS, 2003.
- Advanced Cardiac Life Support: Principles and Practice. American Heart Association, 2003.
- Emergency Care and Transportation of the Sick and Injured, 8th Edition. Jones and Bartlett, Publishers/AAOS, 2002.
- Prehospital Advanced Cardiac Life Support, 2nd Edition. Brady Publishing, 2004.