15

15 CASE 15


A 66-year-old woman presents to the emergency department complaining of shortness of breath and chest pain that extends to her neck.


The patient has had difficulty sleeping for the past few nights and reports being more tired than usual. She is a retired office worker who smokes (1 pack/day) and drinks socially. Her body mass index (BMI) is 33, and she had been taking captopril, an angiotensin I converting enzyme (ACE) inhibitor to control her blood pressure. She ran out of captopril 2 weeks ago and has not refilled the prescription.



PHYSICAL EXAMINATION



VS: T 37°C, P 88/min, R 23/min, BP 150/105 mm Hg

PE: The patient is pale and diaphoretic. Neurologic examination is normal, but the patient is anxious.


LABORATORY STUDIES



ECG: Wide Q wave in leads I and aVL; ST segment elevation in leads I, aVL, and V2-5

Blood tests (CBC, chem panel, cardiac markers): Elevated troponin and CK-MB

Lipid panel: Cholesterol high, HDL low, LDL high


DIAGNOSIS


Coronary artery disease



COURSE


Electrocardiographic findings and patient symptoms are consistent with a recent anteroapical infarction. Cardiac catheterization showed atherosclerosis in all major vessels with a 99% occlusion of the left anterior descending coronary artery. A stent was successfully inserted, and the patient was transferred to the coronary care unit.



PATHOPHYSIOLOGY OF KEY SYMPTOMS


Myocardial infarction results from interruption of blood flow through the coronary blood vessels. About 95% of the oxygen contained in the arterial blood is extracted as blood flows through the coronary circulation. Therefore, any increase in myocardial metabolism must be balanced by an equivalent increase in coronary blood flow and oxygen delivery.


Ischemia results when oxygen delivery is no longer adequate to meet myocardial oxygen demand, and an infarction occurs when blood flow is reduced so that myocardial function is impaired. One common cause of myocardial infarction is the development of a clot or thrombus at the site of an atherosclerotic plaque. The atherosclerotic plaque extends into the lumen of the coronary arteries, causing a partial occlusion. A thrombus formed at the side of the plaque can abruptly occlude the blood vessel, creating an area of infarcted tissue downstream from the occlusion.


Myocardial infarction causes a referred pain that often presents as a crushing pain in the chest that radiates to the left arm. However, many patients, particularly women, experience a less prominent set of symptoms. Symptoms in women may include a burning sensation in the upper abdomen, lightheadedness, and upset stomach or a sudden weakness or unexplained tiredness. This patient also shows many risk factors for coronary artery disease, including smoking, elevated cholesterol, high BMI, and hypertension.


The pain and other symptoms cause a pronounced activation of the sympathetic nervous system. The presenting appearance of elevated blood pressure, elevated heart rate, elevated respiratory rate, and diaphoresis all reflect the actions of the sympathetic nerves.


The initial treatment of a suspected myocardial infarction is to help restore adequate oxygen delivery to the damaged area of the heart. This requires adequate oxygenation, adequate blood flow, and diminished metabolic need.


Supplemental oxygen ensures that the arterial blood is well oxygenated. Nitroglycerin acts to increase nitric oxide formation, and nitric oxide is a potent vasodilator in the circulation. Aspirin or some other cyclooxygenase inhibitor is used to diminish the formation of platelet plugs, which can occlude vascular segments. If a thrombus is suspected, a clot-dissolving compound such as tissue plasminogen activator (tPA) can also be administered. Early (within 1 hour) restoration of coronary blood flow greatly limits the damage and increases the chance of recovery.


Morphine is useful for pain relief and is particularly important because pain increases sympathetic nervous system (SNS) activity, exacerbating the progression of myocardial damage through multiple pathways. SNS activation increases arterial blood pressure and thus increases the workload on the left ventricle. The majority of blood flow to the left ventricle occurs during diastole, and the SNS-mediated increase in heart rate diminishes diastolic duration and impairs blood flow particularly to the left ventricle. SNS activation also increases ventricular contractility and, therefore, ventricular work load (Fig. 15-1).


image

FIGURE 15–1 Phasic flow of blood through the coronary capillaries of the human left ventricle during cardiac systole and diastole (as extrapolated from measured flows in dogs).

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Jul 4, 2016 | Posted by in PHYSIOLOGY | Comments Off on 15

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