Electrocardiographic and Arterial Blood Pressure Changes in Hypertensive Crisis After Using Sublingual Nifedipine

摘要

1% of all hypertensive patients suffer from hypertensive crisis (HC). Although not the treatment of choice, in some Latin American countries is still common the use of sublingual nifedipine in the emergency room. In this study we will compare the electrocardiographic (EKG) and arterial blood pressure changes after 30 minutes of using sublingual nifedipine. Results: We included 23 patients without cardiac disease, with urgency HC and treated with 10-mg nifedipine sublingually. Most of the patients had mild to moderate changes in the EKG, such as changes in heart rate and nonspecific ST segment deviations. One patient had symmetric inverted T waves in leads V5 and V6. PR and QT intervals with no changes. The BP after 30 minutes was not the ideal. Conclusion: Sublingual nifedipine does not absorb well and does produce changes in the EKG. Patients did not achieve an optimal BP after the administration of sublingual nifedipin. Work Done in Lic. Benito Juarez, IMSS General Hospital-6. Cd. Juarez, Chihuahua, Mexico. Introduction Hypertension (HTN) is a worldwide epidemic. It is a chronic disease that has a high morbidity, mortality and has a very high cost to society. Overall, 20% of the population in the world has HTN. In Mexico, approximately 15.2 millions of people suffer from HTN of a whole population of 97,483,412. 51% of the population (49.8 millions) is between 20 and 69 years old [1]. A hypertensive crisis (HC) occurs in about 1% of all HTN patients and they will suffer at least one event of HC in the course of the disease [2]. Before the emerging of antihypertensive drugs, the prevalence of HC was 7%. Males are affected twice than women [3]. Most of the patients that suffer from HC have been diagnosed previously with HTN. This may be caused because they do not have an adequate monitoring of BP and poor treatment compliance as well. From 1983 to 1990 the incidence of hypertensive crisis tripled from 23,000 cases per year to 73,000 cases per year in the United States. There have been some reports of few cases of post surgical hypertensive crisis with an incidence of 4-35%. Most of the patients that have suffered a HC had a past medical history of poorly controlled BP [4].The etiology has not been shown and it is not well understood but what is known is that is secondary to a variety of events. Some related causes are: an autonomous hyperactivity, preeclampsia, poor treatment compliance, drug cross reactivity and general anesthesia [5]. Physiopathology of Hypertensive crisisIt is believed that an uprising of BP secondary to a stimulus known or unknown trigger this event. During the initial uprising of BP the endothelium releases nitric oxide. When the arteries and arterioles detect this high BP, they respond with vasoconstriction and subsequently with hypertrophy to limit that the high blood pressure reaches cellular levels. The prolonged contraction of smooth muscle causes an endothelial dysfunction, a loss of nitric oxide release and an irreversible elevation of peripheral vascular resistance. Without the response of nitric oxide, there is a major endothelial damage. The endothelial dysfunction is triggered by inflammation induced by a distention mechanism that increases the expression of inflammatory markers such as cytokines, endothelial adhesion molecules and endothelin-1. These molecular events increase the endothelial permeability, inhibit fibrinolysis and as a result, they produce an activation of the coagulation cascade. This coagulation event, plus the adhesion and platelet aggregation cause the deposition of fibrinoid material, and also an increase in arterial inflammation and vasoconstriction. In addition of the whole event, there is an amplification of the renin-angiotensin system which contributes to vascular lesion and ischemia [67].Types of Hypertensive crisis Hypertensive emergency could be potentially threatening to life and is characterized by an elevated diastolic BP of 110 mm of Hg with end organ damage man