Single-Dose Sublingual Nifedipine as the Only Treatment in Hypertensive Urgencies and Emergencies Victor M. González-Carmona, M.D.* + Carlos Ibarra-Pérez, M.D. and Carlos
Jerjes-Sánchez,
M.D.*
MÉXICO CITY, MÉXICO
Abstract One hundred and eighteen patients with hypertensive urgencies and emergencies and diastolic blood pressure (DBP) at least 120 mm Hg by the cuff method were seen at the Emergency Care Department; none had received calcium channel blockers during the previous twelve hours. Patients with DBP of 120 to 139 mm Hg received 10 mg of sublingual nifedipine; patients with left ventricular hypertrophy or failure, renal disease, hypertensive encephalopathy, angina, papilledema, or a DBP over 140 mm Hg received 20 mg of the drug. The criterion for control was the achievement of a DBP of 100 mm Hg or less within sixty minutes of receiving sublingual nifedipine and maintenance of the effect until discharge. Control was achieved in all patients; a sixty-three-year-old man died of a brain hemorrhage after pulmonary edema and a DBP of 210 had been controlled; the other 117 were discharged to their attending physicians, either as outpatients or to a hospital ward. No patient developed hypotension, clinical or electrocardiographic signs of myocardial ischemia, or clinical signs of neurologic dysfunction. Practical, fast, safe, and dependable control of hypertensive urgencies and emergencies has made sublingual nifedipine the treatment of choice of such patients in the
Emergency
Care
Department.
From the *Emergency Care Department and the + Education and Research Division, Hospital de Cardiologia Luis Méndez, Centro, Médico Nacional, Instituto Mexicano del Seguro Social, México City, México.
908
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
909 Introduction Vital target organ damage due to hypertensive urgencies and emergencies should be prevented or lessened by adequate reduction of the blood pressure. This is achieved by oral, intramuscular, or intravenous medication that, unfortunately, is associated with considerable morbidity and mortality’’2; during recent years, calcium channel blockers have been added to the therapeutic arsenal against such hypertensive syndromes, with a good 2
outcome .
This report presents our results in the treatment of 118 patients admitted to the Emergency Care Department of our hospital with hypertensive urgencies and emergencies, over a one-year period; all received a single dose of sublingual nifedipine as the only form of
therapy. Patients and Methods
Patients were included when there was a sudden and sustained blood pressure elevation to 120 mm Hg or greater, regardless of the presence of papilledema, abnormalities in renal function, or neurologic dysfunction. Patients with coexisting valvular heart disease, acute myocardial infarction, pregnancy, or suspicion of pregnancy or those receiving calcium channel blockers within the previous twelve hours were not included. One hundred and eighteen patients fulfilling these criteria were included, 88 men and 30 women with ages ranging from forty-two to seventy-one years, mean 59 ± 9.8 years. All had clinical history, physical examination including blood pressure recordings with an adequately sized arm cuff and a mercurial manometer, fundoscopy, 12-lead resting electrocardiogram, and chest roentgenogram and venous blood samples for hemoglobin, hematocrit, sodium (Na) chloride (Cl), potassium (K), glucose blood urea nitrogen (BUN), and creatinine values. For safety reasons, a monitor for continuous electrocardiographic display and a short venous catheter were installed and D5W was infused by slow drip during the stay in the Emergency Care Department. According to their clinical, electrocardiographic, radiologic, and laboratory profile, patients were assembled into four groups. (Table I). In an open trial, patients arriving with a diastolic blood pressure (DBP) of 120 to 139 mm Hg received 10 mg of sublingual nifedipine by chewing a multipierced capsule; patients with left ventricular hypertrophy or failure, renal disease, hypertensive encephalopathy, angina, and/or a DBP of 140 mm Hg or more received 20 mg of sublingual nifedipine (two capsules) in the same manner. Heart rate and supine blood pressure were recorded every five minutes until the DBP was 100 mm Hg or less and every ten to twenty minutes after that, with phase V of the Korotkoff sounds as the DBP. The criterion for control was the achievement of a DBP of 100 mm Hg or less within sixty minutes of receiving nifedipine and continued effect of the drug until discharge. Statistical analysis was done by the chi square and Student’s t test; differences at the level were considered significant. DBP and time means were calculated and exp < 0.01
pressed
as
± one
standard deviation.
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
910 TABLE I Characteristics of 118 Patients with Hypertensive Urgencies and
Emergencies
DBP
=
diastolic blood pressure, pts =
patients.
Results All patients achieved control. No patient required additional medication for control. The mean values on initial and controlled DBP, in mm Hg, were from 132 ± 9.4 to 96 ± 6 for Group A, from 130 ± 8.1 to 93 ± 5.7 for Group B, from 138 ± 4.7 to 100 ± 8.1 for Group C, and from 136 ± 10.1 to 92 ± 6.5 for Group D (p < 0.01). The times elapsed between sublingual nifedipine and control, in minutes, were 26 ± 6.2 for Group A, 28 ± 5.5 for Group B, 41 ± 9.8 for Group C, and 38 ± 7.3 for Group D. Thirty patients in Group A, 53 in Group B, 6 in Group C, and 3 in Group D were controlled within thirty minutes of receiving the drug. After 180 to 240 minutes of continued observation and with the DBP still under control, 117 patients were discharged to their attending physician, either to one of the hospital wards or as outpatients; oral medications were initiated for long-term control before
discharge. No patient developed a DBP of 80 mm Hg or less, increased angina, electrocardiographic signs of myocardial ischemia, or neurologic dysfunction. A sixty-three-year-old man arrived comatose with a DBP of 210 mm Hg and pulmonary edema; these problems were satisfactorily controlled with the 20 mg dose of sublingual nifedipine, but he subsequently died of a brain hemorrhage. Three other patients had control of the elevated DBP and pulmonary edema with single doses of sublingual nifedipine as the only treatment. Discussion
is known to be a useful drug for the treatment of chronic systemic hypertension2-’ and of hypertensive crises and emergencies by the buccal route. Our series, the largest reported to date, shows that every patient achieved control of the elevated DBP and confirms the efficacy of the drug for the treatment of hypertensive urgencies and emergencies. A statistically significantly higher number of patients in Group A and B responded within thirty minutes to sublingual nifedipine (pO.01) than in the other two groups, who took more time to achieve control, despite a larger dose. Apparently, this had no clinical
Nifedipine
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
911
for there were no obvious untoward effects related to the delay in the onset of action of the drug. Nifedipine has a well-recognized potential to induce cerebral and myocardial ischemia ; however, not only was it not harmful in our patients, but those in Group D, probably the sickest, had improvement of the elevated DBP, angina and left ventricular failure, including pulmonary edema and encephalopathy2’8-&dquo; without dire consequences. These beneficial actions are due to a favorable effect on the vascular beds of the heart, lungs, kidneys, and brain2’’2’’3 and contribute to making nifedipine a drug of choice in various
significance,
hypertensive syndromes.’3-&dquo; Nevertheless, serious adverse effects have been reported, including excessive hypotension, myocardial ischemia, myocardial infarction, various arrhythmias, and renal dysfunction in patients with preexisting renal damage, plus myocardial ischemia and pulmonary edema in a patient with aortic stenosis and three-vessel coronary disease . 2,4,18-26 In this respect, the user of a vasodilator such as nifedipine should always bear in mind the degree of left ventricular dysfunction, since there is a higher risk of circulatory collapse when the drug is used in cases of severely compromised function of the left ventricle. Since we did not obtain a second blood sample, we were unable to determine whether there was any chemical deterioration of the renal function in such a short time; on the other hand, a mild diuretic effect was frequently seen. We do not know whether the brain hemorrhage of the only patient in our series to die was present at arrival in the Emergency Care Department or whether it developed at a later time, so we cannot rule out nifedipine, which controlled both his elevated DBP and pulmonary edema, as having a causal relationship to the hemorrhage , 27 which passed undiagnosed during the first hours; the drug has, however, been used in similar circum-
stances. 10,12,14,24,28 All the adverse effects, including ours, have occurred in people over fifty years of age, which emphasizes that nifedipine, and for that matter, any other drug 13 capable of inducing a rapid and &dquo;uncontrolled&dquo; blood pressure reduction should be used with great care in the management of hypertensive urgencies and emergencies of the elderly. The ideal drug for the treatment of hypertensive urgencies and emergencies should (1) be nontoxic, with a very low incidence of clinical and chemical side effects; (2) have a rapid onset and a relatively long duration of action; (3) be easy to administer and easy to reverse; (4) not require determinations in body fluids or invasive hemodynamic monitoring ; (5) be inexpensive; (6) be effective in all conditions; (7) have a favorable therapeutic index and a predictable dose-response curve; (8) lack any major depressant action on myocardial contractility, sinus or AV nodes, and mental status; and (9) counteract peripherally constricted vascular smooth muscle and selectively dilate vascular beds in the brain, myocardium, and kidneys and thus maintain or improve flow to vital organs without inducing &dquo;steal&dquo; syndromes. From the analysis of the pertinent literature and of our own results, we consider that such a drug is far from being available at the present time; however, nifedipine comes close to meeting many of the criteria. It has a rapid onset of action when it is removed from the capsule because it is more easily absorbed from the gastric mucosa; the sublin,
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
912
gual route can be used in comatose, stuporous, and alert patients; it does not require the establishment of an intravenous route, preparation of a solution, or the setting up of an expensive infusion pump; it does not require the moment-to-moment monitoring needed to control the effect of other drugs; it induces arteriolar dilatation that improves afterload and global left ventricular function; and it is reliable, moderately potent, and capable of controlling the urgency or emergency by itself, without additional therapy.29 Conclusions
study confirms that sublingual nifedipine provides fast, practical, safe, and dependable control of hypertensive urgencies and emergencies, and this makes it our preferred therapy in the Emergency Care Department; other physicians may consider the drug as another choice3~’3’ in the management of similar patients. Our
Carlos
Ibarra-Pérez,
M.D.
Head, Education and Research Division Hospital de Cardiología Luis Mendez Centro Médico Nacional, I.M.S.S. c/o Retorno De Los Leones 58 México City CP 01710, México
References 1. Conen LD, Bertel O, Dubach UC: An oral calcium antagonist for treatment of hypertensive emergencies. J Cardiovasc Pharmacol 4:S378-S382, 1982. 2. Houston MC: Pathophysiology, clinical aspects and treatment of hypertensive crises. Progr Cardiovasc Dis 32:99-148, 1989. 3. Frishman WH, Charlap S, Michelson EL: Calcium channel blockers in system hypertension. Am J Cardiol 58:157-160, 1986. 4. Frishman WH, Charlap S: Editorial: Nifedipine in the treatment of systemic hypertension. Arch Intern Med 144:2335-2336, 1984. 5. Robinson BF: Calcium-entry blocking agents in the treatment of systemic hypertension. Am J Cardiol 55:102B-105B, 1985. 6. Opie LH, Jennings AA: Role of calcium blockade in chronic hypertension following successful management of hypertensive emergency. Am J Med 81 (Suppl 6A):35-41, 1986. 7. González-Carmona VM, Torres-Zamora M, CuanPérez M, et al: Efecto de la nifedipina en el tratamiento de la hipertensión arterial esencial. Rev Med IMSS (Mex) 21:397-407, 1983. 8. Bertel O, Conen LD: Treatment of hypertensive emergencies with the calcium channel blocker nifedipine. Am J Med 79(Suppl 4A):31-35, 1985.
9. Polese A, Fiorentini C, Olivari MT, et al: Clinical use of a calcium antagonistic agent (nifedipine) in acute pulmonary edema. Am J Med 66:825-830, 1979. 10. Ellrodt AG, Ault MJ, Riedinger MS, et al: Efficacy and safety of sublingual nifedipine in hypertensive emergencies. Am J Med 79(Suppl 4A):19-25, 1985. 11. Jerjes-Sánchez C, Ibarra-Pérez C, Ramirez-Rivera A, et al: Intubación traqueal temprana y ventilación mecánica para el tratamiento de edema pulmonar secundario a cardiopatia isquémica. Arch Inst Cardiol Mex 59:161-167, 1989. 12. Bauer JH, Reams GP: The role of calcium entry blockers in hypertensive emergencies. Circulation 75(Suppl V):V174-V180, 1987. 13. Bertel O. Conen LD, Radü EW, et al: Nifedipine in hypertensive emergencies. Br Med J 286:19-21, 1983. 14. Frishman WH, Weinberg P, Peled HB, et al: Calcium entry blockers for the treatment of severe hypertension and hypertension and hypertensive crisis. Am J Med 77(Suppl 2B):35-45, 1984. 15. Opie LH, Jennings A: Sublingual captopril versus nifedipine in hypertensive crisis. Lancet 2:555, 1985. 16. White SR, Hall JB: Control of hypertension with nifedipine in the setting of aortic dissection. Chest 88:780-781, 1985
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
913 C, Nightingale S, Mandami B: A randomized comparison of nifedipine and sodium nitroprusside in severe hypertension. Chest 90:500-503, 1986. Guazzi MD, Olivari MT, Polese A, et al: Nifedipine, a new antihypertensive with rapid action. Clin Pharmacol Ther 22:528-532, 1977. Jariwalla AG, Anderson EG: Production of ischemic cardiac pain by nifedipine. Br Med J 1:1181-1182, 1978. Gillmer DJ, Kark P: Pulmonary edema precipitated by nifedipine. Br Med J 280:1420-1421, 1980. Diamond JR, Cheung JY, Fang LST: Nifedipineinduced renal dysfunction. Am J Med 77:905-909, 1984. Aromatoro GJ, Uretsky BF, Reddy PS: Hypotension and sinus arrest with nifedipine in pulmonary hypertension. Chest 87:265-267, 1985. Boden WE, Koee KS, Bough EW: Nifedipineinduced hypotension and myocardial ischemia in refractory angina pectoris. JAMA 253:1131-1135, 1985. Zangerle KF, Wolford R: Syncope and conduction disturbances following sublingual nifedipine for hypertension. Ann Emerg Med 14:1005-1006, 1985.
17. Franklin
18.
19.
20. 21.
22.
23.
24.
25. O’Mailia JJ, Sander GE, Giles TD: Nifedipineassociated myocardial ischemia or infarction in the treatment of hypertensive urgencies. Ann Intern Med 107:185-186, 1987. 26. Gonzalez DG, Ram CVS: New approaches for the treatment of hypertensive urgencies and emergencies. Chest 93:193-195, 1988. 27. Strangaard S, Paulson OB: Cerebral blood flow and its pathophysiology in hypertension. Am J Hyperten 2:486-492, 1989. 28. Guazzi MD, De Cesare N, Galli C, et al: La nifédipine en tant q’antihypertenseur vasodilateur d’effet rapid. Arch Mal Coeur 78 (Special No.):59-65, 1985. 29. Thompson WL: Hypertensive urgencies and emergencies. In: Textbook of Critical Care, ed. by Shoemaker WC, Ayres S, Grenvik A et al. Philadelphia: WB Saunders, 1989, pp 391-412. 30. Ferguson RK, Vlasses PH: Hypertensive urgencies and emergencies. JAMA 255: 1607-1613, 1986. 31. Rahn KH: How should we treat a hypertensive emergency ? Am J Med 63:48C-50C, 1989.
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
Jerjes-Sánchez,
M.D.*
MÉXICO CITY, MÉXICO
Abstract One hundred and eighteen patients with hypertensive urgencies and emergencies and diastolic blood pressure (DBP) at least 120 mm Hg by the cuff method were seen at the Emergency Care Department; none had received calcium channel blockers during the previous twelve hours. Patients with DBP of 120 to 139 mm Hg received 10 mg of sublingual nifedipine; patients with left ventricular hypertrophy or failure, renal disease, hypertensive encephalopathy, angina, papilledema, or a DBP over 140 mm Hg received 20 mg of the drug. The criterion for control was the achievement of a DBP of 100 mm Hg or less within sixty minutes of receiving sublingual nifedipine and maintenance of the effect until discharge. Control was achieved in all patients; a sixty-three-year-old man died of a brain hemorrhage after pulmonary edema and a DBP of 210 had been controlled; the other 117 were discharged to their attending physicians, either as outpatients or to a hospital ward. No patient developed hypotension, clinical or electrocardiographic signs of myocardial ischemia, or clinical signs of neurologic dysfunction. Practical, fast, safe, and dependable control of hypertensive urgencies and emergencies has made sublingual nifedipine the treatment of choice of such patients in the
Emergency
Care
Department.
From the *Emergency Care Department and the + Education and Research Division, Hospital de Cardiologia Luis Méndez, Centro, Médico Nacional, Instituto Mexicano del Seguro Social, México City, México.
908
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
909 Introduction Vital target organ damage due to hypertensive urgencies and emergencies should be prevented or lessened by adequate reduction of the blood pressure. This is achieved by oral, intramuscular, or intravenous medication that, unfortunately, is associated with considerable morbidity and mortality’’2; during recent years, calcium channel blockers have been added to the therapeutic arsenal against such hypertensive syndromes, with a good 2
outcome .
This report presents our results in the treatment of 118 patients admitted to the Emergency Care Department of our hospital with hypertensive urgencies and emergencies, over a one-year period; all received a single dose of sublingual nifedipine as the only form of
therapy. Patients and Methods
Patients were included when there was a sudden and sustained blood pressure elevation to 120 mm Hg or greater, regardless of the presence of papilledema, abnormalities in renal function, or neurologic dysfunction. Patients with coexisting valvular heart disease, acute myocardial infarction, pregnancy, or suspicion of pregnancy or those receiving calcium channel blockers within the previous twelve hours were not included. One hundred and eighteen patients fulfilling these criteria were included, 88 men and 30 women with ages ranging from forty-two to seventy-one years, mean 59 ± 9.8 years. All had clinical history, physical examination including blood pressure recordings with an adequately sized arm cuff and a mercurial manometer, fundoscopy, 12-lead resting electrocardiogram, and chest roentgenogram and venous blood samples for hemoglobin, hematocrit, sodium (Na) chloride (Cl), potassium (K), glucose blood urea nitrogen (BUN), and creatinine values. For safety reasons, a monitor for continuous electrocardiographic display and a short venous catheter were installed and D5W was infused by slow drip during the stay in the Emergency Care Department. According to their clinical, electrocardiographic, radiologic, and laboratory profile, patients were assembled into four groups. (Table I). In an open trial, patients arriving with a diastolic blood pressure (DBP) of 120 to 139 mm Hg received 10 mg of sublingual nifedipine by chewing a multipierced capsule; patients with left ventricular hypertrophy or failure, renal disease, hypertensive encephalopathy, angina, and/or a DBP of 140 mm Hg or more received 20 mg of sublingual nifedipine (two capsules) in the same manner. Heart rate and supine blood pressure were recorded every five minutes until the DBP was 100 mm Hg or less and every ten to twenty minutes after that, with phase V of the Korotkoff sounds as the DBP. The criterion for control was the achievement of a DBP of 100 mm Hg or less within sixty minutes of receiving nifedipine and continued effect of the drug until discharge. Statistical analysis was done by the chi square and Student’s t test; differences at the level were considered significant. DBP and time means were calculated and exp < 0.01
pressed
as
± one
standard deviation.
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
910 TABLE I Characteristics of 118 Patients with Hypertensive Urgencies and
Emergencies
DBP
=
diastolic blood pressure, pts =
patients.
Results All patients achieved control. No patient required additional medication for control. The mean values on initial and controlled DBP, in mm Hg, were from 132 ± 9.4 to 96 ± 6 for Group A, from 130 ± 8.1 to 93 ± 5.7 for Group B, from 138 ± 4.7 to 100 ± 8.1 for Group C, and from 136 ± 10.1 to 92 ± 6.5 for Group D (p < 0.01). The times elapsed between sublingual nifedipine and control, in minutes, were 26 ± 6.2 for Group A, 28 ± 5.5 for Group B, 41 ± 9.8 for Group C, and 38 ± 7.3 for Group D. Thirty patients in Group A, 53 in Group B, 6 in Group C, and 3 in Group D were controlled within thirty minutes of receiving the drug. After 180 to 240 minutes of continued observation and with the DBP still under control, 117 patients were discharged to their attending physician, either to one of the hospital wards or as outpatients; oral medications were initiated for long-term control before
discharge. No patient developed a DBP of 80 mm Hg or less, increased angina, electrocardiographic signs of myocardial ischemia, or neurologic dysfunction. A sixty-three-year-old man arrived comatose with a DBP of 210 mm Hg and pulmonary edema; these problems were satisfactorily controlled with the 20 mg dose of sublingual nifedipine, but he subsequently died of a brain hemorrhage. Three other patients had control of the elevated DBP and pulmonary edema with single doses of sublingual nifedipine as the only treatment. Discussion
is known to be a useful drug for the treatment of chronic systemic hypertension2-’ and of hypertensive crises and emergencies by the buccal route. Our series, the largest reported to date, shows that every patient achieved control of the elevated DBP and confirms the efficacy of the drug for the treatment of hypertensive urgencies and emergencies. A statistically significantly higher number of patients in Group A and B responded within thirty minutes to sublingual nifedipine (pO.01) than in the other two groups, who took more time to achieve control, despite a larger dose. Apparently, this had no clinical
Nifedipine
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
911
for there were no obvious untoward effects related to the delay in the onset of action of the drug. Nifedipine has a well-recognized potential to induce cerebral and myocardial ischemia ; however, not only was it not harmful in our patients, but those in Group D, probably the sickest, had improvement of the elevated DBP, angina and left ventricular failure, including pulmonary edema and encephalopathy2’8-&dquo; without dire consequences. These beneficial actions are due to a favorable effect on the vascular beds of the heart, lungs, kidneys, and brain2’’2’’3 and contribute to making nifedipine a drug of choice in various
significance,
hypertensive syndromes.’3-&dquo; Nevertheless, serious adverse effects have been reported, including excessive hypotension, myocardial ischemia, myocardial infarction, various arrhythmias, and renal dysfunction in patients with preexisting renal damage, plus myocardial ischemia and pulmonary edema in a patient with aortic stenosis and three-vessel coronary disease . 2,4,18-26 In this respect, the user of a vasodilator such as nifedipine should always bear in mind the degree of left ventricular dysfunction, since there is a higher risk of circulatory collapse when the drug is used in cases of severely compromised function of the left ventricle. Since we did not obtain a second blood sample, we were unable to determine whether there was any chemical deterioration of the renal function in such a short time; on the other hand, a mild diuretic effect was frequently seen. We do not know whether the brain hemorrhage of the only patient in our series to die was present at arrival in the Emergency Care Department or whether it developed at a later time, so we cannot rule out nifedipine, which controlled both his elevated DBP and pulmonary edema, as having a causal relationship to the hemorrhage , 27 which passed undiagnosed during the first hours; the drug has, however, been used in similar circum-
stances. 10,12,14,24,28 All the adverse effects, including ours, have occurred in people over fifty years of age, which emphasizes that nifedipine, and for that matter, any other drug 13 capable of inducing a rapid and &dquo;uncontrolled&dquo; blood pressure reduction should be used with great care in the management of hypertensive urgencies and emergencies of the elderly. The ideal drug for the treatment of hypertensive urgencies and emergencies should (1) be nontoxic, with a very low incidence of clinical and chemical side effects; (2) have a rapid onset and a relatively long duration of action; (3) be easy to administer and easy to reverse; (4) not require determinations in body fluids or invasive hemodynamic monitoring ; (5) be inexpensive; (6) be effective in all conditions; (7) have a favorable therapeutic index and a predictable dose-response curve; (8) lack any major depressant action on myocardial contractility, sinus or AV nodes, and mental status; and (9) counteract peripherally constricted vascular smooth muscle and selectively dilate vascular beds in the brain, myocardium, and kidneys and thus maintain or improve flow to vital organs without inducing &dquo;steal&dquo; syndromes. From the analysis of the pertinent literature and of our own results, we consider that such a drug is far from being available at the present time; however, nifedipine comes close to meeting many of the criteria. It has a rapid onset of action when it is removed from the capsule because it is more easily absorbed from the gastric mucosa; the sublin,
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
912
gual route can be used in comatose, stuporous, and alert patients; it does not require the establishment of an intravenous route, preparation of a solution, or the setting up of an expensive infusion pump; it does not require the moment-to-moment monitoring needed to control the effect of other drugs; it induces arteriolar dilatation that improves afterload and global left ventricular function; and it is reliable, moderately potent, and capable of controlling the urgency or emergency by itself, without additional therapy.29 Conclusions
study confirms that sublingual nifedipine provides fast, practical, safe, and dependable control of hypertensive urgencies and emergencies, and this makes it our preferred therapy in the Emergency Care Department; other physicians may consider the drug as another choice3~’3’ in the management of similar patients. Our
Carlos
Ibarra-Pérez,
M.D.
Head, Education and Research Division Hospital de Cardiología Luis Mendez Centro Médico Nacional, I.M.S.S. c/o Retorno De Los Leones 58 México City CP 01710, México
References 1. Conen LD, Bertel O, Dubach UC: An oral calcium antagonist for treatment of hypertensive emergencies. J Cardiovasc Pharmacol 4:S378-S382, 1982. 2. Houston MC: Pathophysiology, clinical aspects and treatment of hypertensive crises. Progr Cardiovasc Dis 32:99-148, 1989. 3. Frishman WH, Charlap S, Michelson EL: Calcium channel blockers in system hypertension. Am J Cardiol 58:157-160, 1986. 4. Frishman WH, Charlap S: Editorial: Nifedipine in the treatment of systemic hypertension. Arch Intern Med 144:2335-2336, 1984. 5. Robinson BF: Calcium-entry blocking agents in the treatment of systemic hypertension. Am J Cardiol 55:102B-105B, 1985. 6. Opie LH, Jennings AA: Role of calcium blockade in chronic hypertension following successful management of hypertensive emergency. Am J Med 81 (Suppl 6A):35-41, 1986. 7. González-Carmona VM, Torres-Zamora M, CuanPérez M, et al: Efecto de la nifedipina en el tratamiento de la hipertensión arterial esencial. Rev Med IMSS (Mex) 21:397-407, 1983. 8. Bertel O, Conen LD: Treatment of hypertensive emergencies with the calcium channel blocker nifedipine. Am J Med 79(Suppl 4A):31-35, 1985.
9. Polese A, Fiorentini C, Olivari MT, et al: Clinical use of a calcium antagonistic agent (nifedipine) in acute pulmonary edema. Am J Med 66:825-830, 1979. 10. Ellrodt AG, Ault MJ, Riedinger MS, et al: Efficacy and safety of sublingual nifedipine in hypertensive emergencies. Am J Med 79(Suppl 4A):19-25, 1985. 11. Jerjes-Sánchez C, Ibarra-Pérez C, Ramirez-Rivera A, et al: Intubación traqueal temprana y ventilación mecánica para el tratamiento de edema pulmonar secundario a cardiopatia isquémica. Arch Inst Cardiol Mex 59:161-167, 1989. 12. Bauer JH, Reams GP: The role of calcium entry blockers in hypertensive emergencies. Circulation 75(Suppl V):V174-V180, 1987. 13. Bertel O. Conen LD, Radü EW, et al: Nifedipine in hypertensive emergencies. Br Med J 286:19-21, 1983. 14. Frishman WH, Weinberg P, Peled HB, et al: Calcium entry blockers for the treatment of severe hypertension and hypertension and hypertensive crisis. Am J Med 77(Suppl 2B):35-45, 1984. 15. Opie LH, Jennings A: Sublingual captopril versus nifedipine in hypertensive crisis. Lancet 2:555, 1985. 16. White SR, Hall JB: Control of hypertension with nifedipine in the setting of aortic dissection. Chest 88:780-781, 1985
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
913 C, Nightingale S, Mandami B: A randomized comparison of nifedipine and sodium nitroprusside in severe hypertension. Chest 90:500-503, 1986. Guazzi MD, Olivari MT, Polese A, et al: Nifedipine, a new antihypertensive with rapid action. Clin Pharmacol Ther 22:528-532, 1977. Jariwalla AG, Anderson EG: Production of ischemic cardiac pain by nifedipine. Br Med J 1:1181-1182, 1978. Gillmer DJ, Kark P: Pulmonary edema precipitated by nifedipine. Br Med J 280:1420-1421, 1980. Diamond JR, Cheung JY, Fang LST: Nifedipineinduced renal dysfunction. Am J Med 77:905-909, 1984. Aromatoro GJ, Uretsky BF, Reddy PS: Hypotension and sinus arrest with nifedipine in pulmonary hypertension. Chest 87:265-267, 1985. Boden WE, Koee KS, Bough EW: Nifedipineinduced hypotension and myocardial ischemia in refractory angina pectoris. JAMA 253:1131-1135, 1985. Zangerle KF, Wolford R: Syncope and conduction disturbances following sublingual nifedipine for hypertension. Ann Emerg Med 14:1005-1006, 1985.
17. Franklin
18.
19.
20. 21.
22.
23.
24.
25. O’Mailia JJ, Sander GE, Giles TD: Nifedipineassociated myocardial ischemia or infarction in the treatment of hypertensive urgencies. Ann Intern Med 107:185-186, 1987. 26. Gonzalez DG, Ram CVS: New approaches for the treatment of hypertensive urgencies and emergencies. Chest 93:193-195, 1988. 27. Strangaard S, Paulson OB: Cerebral blood flow and its pathophysiology in hypertension. Am J Hyperten 2:486-492, 1989. 28. Guazzi MD, De Cesare N, Galli C, et al: La nifédipine en tant q’antihypertenseur vasodilateur d’effet rapid. Arch Mal Coeur 78 (Special No.):59-65, 1985. 29. Thompson WL: Hypertensive urgencies and emergencies. In: Textbook of Critical Care, ed. by Shoemaker WC, Ayres S, Grenvik A et al. Philadelphia: WB Saunders, 1989, pp 391-412. 30. Ferguson RK, Vlasses PH: Hypertensive urgencies and emergencies. JAMA 255: 1607-1613, 1986. 31. Rahn KH: How should we treat a hypertensive emergency ? Am J Med 63:48C-50C, 1989.
Downloaded from ang.sagepub.com at NANYANG TECH UNIV LIBRARY on June 21, 2015
