Patient A is white, 60 years of age, and works as a cab driver. While driving home after work, he develops an aching in his chest and slight, regular palpitations. The ache is still present when he goes to bed, when he wakes several times during the night, and when he gets up in the morning, seven hours after retiring. He drinks some soda water, but when the aching does not improve, he decides to go to the emergency department.

At the hospital, Patient A complains of chest pain accompanied by diaphoresis, slight shortness of breath, and nausea. Relief of pain is obtained with IV morphine sulfate. When the patient is admitted to the critical care unit (CCU), his symptoms are generally unremarkable except for recurrent pain.

Patient A experienced the usual childhood illnesses without rheumatic fever. As an adult, he has a history of hypertension (documented on discharge from the Army at 45 years of age and when hospitalized two years ago) that has not been treated. Past surgery includes tonsillectomy and adenoidectomy as a child. A cataract was removed from his right eye two years ago.

Patient A's father died of an MI at 55 years of age. His mother is alive and well, although the patient does not know her age. Two brothers, 65 and 58 years of age, are alive and well. The patient lives alone and works approximately 72 hours per week. He has been married and divorced twice; the last divorce was four years ago. He has no children.

Upon admittance to the CCU, a full physical exam is conducted (Table 4). An ECG is done and shows ST elevation. Several laboratory tests are ordered, with the following results:

Based on the results of the assessment, Patient A is diagnosed with:

Patient A's vital signs are stable for the remainder of the day, with a sinus bradycardia of 56 bpm. Early in the morning the next day, the patient awakes with nausea and diaphoresis. His blood pressure has decreased to 90/60 mm Hg with sinus bradycardia of 40 bpm. PVCs are present. The patient is treated with 0.5 mg IV atropine sulfate twice, after which his heart rate increases to 70 bpm and his blood pressure increases to 130/68 mm Hg. Unifocal PVCs are then treated with 150 mg of amiodarone IV over 10 minutes followed by an amiodarone drip at 1 mg/minute for 6 hours, then 0.5 mg/minute for 12 hours.

Later in the day, Patient A's vital signs are:

The patient has no further chest pain, but he reports that his nausea persists after meals.

Two days later, Patient A's LDH value rises to 310 IU/L; other enzyme levels remain essentially the same as the admission values. ECG shows ST elevation diminishing from previous levels. The amiodarone is discontinued without return of the PVCs. His vital signs remain stable, no further arrhythmias are noted, and his nausea is resolved. On day three, Patient A is moved out of the CCU and started on cardiac rehabilitation.

On day four, a treadmill test is done at 50% effort with negative results. Patient A is discharged on day seven. The medical plan is to continue treatment of his hypertension with propranolol. The patient plans to return to driving his cab, but for fewer hours per week.

Patient B is 42 years of age and works as a newspaper editor. He presents to the emergency department complaining of chest pain radiating into both arms, accompanied by diaphoresis and shortness of breath. He has been having episodes of transient substernal and shoulder pain over the past week. He is admitted to the CCU.

Patient B is being treated for hypertension and is currently taking 100 mg metoprolol twice per day. He does not exercise and has smoked a pack of cigarettes daily for 20 years. He reports being under considerable job stress. He is overweight, with a body mass index of 35.

Upon admittance to the CCU, a full physical exam is conducted (Table 5). An ECG shows ST segment depression and T wave inversion consistent with subendocardial ischemia in the inferior and anterior leads. An incomplete left bundle branch block is also noted. Laboratory studies (CBC, urinalysis, and cardiac isoenzyme levels) are all within normal limits, although cardiac isoenzymes are in the upper range.

Based on the results of the assessment, Patient B is diagnosed with:

Patient B stays in the CCU for three days. During that time, serum cardiac enzyme levels and repeat ECGs confirm a diagnosis of subendocardial ischemia rather than MI. Coronary artery angiography is done to clarify the coronary artery anatomy and finds a 35% to 45% occlusion of the left anterior descending artery. The possibility of coronary artery vasospasm is not excluded because no ergonovine trial is done. Repeat evaluation for coronary artery bypass surgery is planned for the future, with conservative medical treatment in the interim.

At discharge, Patient B is prescribed:

Patient C, 44 years of age, is brought to the emergency department by ambulance after collapsing at an airport prior to departing on a business trip. He had eaten a large lunch before going to the airport. During the assessment and initiation of treatment, the patient is anxious to return to work. After several short bursts of ventricular tachycardia cause him to become nauseated and short of breath, Patient C agrees to be admitted to the CCU until he feels better.

About three years ago, Patient C noted chest discomfort unrelated to exertion. He tried without success to relieve the chest discomfort with various over-the-counter antacids. Eventually, the pain subsided and he dismissed it with various rationalizations. Two years ago, an ECG done during a routine physical exam was interpreted as normal. This is his first hospital admission.

Family history is positive for early CHD among the men and type 2 diabetes among the women. There are no family members with renal disease, tuberculosis, or cancer.

Patient C is a vice president for a large advertising agency. His job involves frequent travel and entertainment of clients, and he reports frequently drinking alcohol as part of "doing business." This usually consists of a martini at lunch and two whiskey sours before dinner. He smokes occasionally, especially while working on important business deals. He engages in no regular exercise program but does play racquetball occasionally as part of his business-related social life. He owns a home in an affluent neighborhood with his wife; their lifestyle includes entertaining at home and at their country club. Their three teenaged children attend private schools.

Upon admittance to the CCU, a full physical exam is conducted (Table 6). ECG shows sinus tachycardia with frequent PVCs. The atrial and ventricular rate is 114 bpm, and ST segment elevation and depression are noted. Extensive laboratory studies find:

A second set of serum enzymes shows an LDH of 298 IU/L and a SGOT of 192 IU/L. Urinalysis reveals straw-colored urine with specific gravity of 1.009, pH of 6, and rare white blood cells per high power field. Patient C's ABGs are also assessed (Table 7).

Based on the results of the assessment, Patient C is diagnosed with acute anterior and inferior MI with early carcinogenic shock.

In the emergency department, oxygen is administered at 4 L/minute via a nasal cannula. Patient C is given lidocaine, 100 mg, as a bolus IV; a lidocaine infusion is started at 2 mg/minute. On arrival in the CCU, the patient is noted to have frequent PVCs as well as one period of five ectopic ventricular beats. A 0.5 mg/kg bolus of IV lidocaine is given, and the infusion rate is increased to 4 mg/minute. The nurse instructs Patient C to notify them if he develops numbness or tingling, chest pain, light-headedness, or other discomfort. A portable chest x-ray is done shortly after he arrives in the CCU and shows pulmonary vascular congestion. IV furosemide (Lasix), 20 mg, is administered, and an indwelling urinary catheter is inserted and connected to a urinometer.

One hour after his arrival in the CCU, Patient C's blood pressure is noted to be barely audible at 60/35 mm Hg. An arterial line is placed in the left radial artery, and a pulmonary artery thermodilution catheter is placed via the left subclavian artery.

An infusion of dopamine hydrochloride (400 mg in 500 mL D5W) is begun at 5 mg/kg/minute. Morphine sulfate is titrated intravenously to reduce the patient's pain, anxiety, and dyspnea. Patient C continues to have 10 to 15 PVCs per minute despite the lidocaine infusion continuing at 4 mg/minute. The oxygen is changed to 15 L/minute by mask. Sodium nitroprusside is cautiously administered as an IV infusion of 50 mg in 250 mL D5W at 0.5 mcg/kg/minute. The patient's blood pressure and cardiac output begin to improve.