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Background: There is currently no consensus on the appropriate selection of inotropic therapy in ventricular dysfunction. The objective of the study was to detect the effects of different inotropes on the hemodynamics of patients who developed low cardiac output. Methods: PubMed, Embase, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched (all updated December 31, 2017). The inclusion criteria were as follows: low cardiac index (CI < 2.5 L/min/m2) or New York Heart Association class II–IV, and at least 1 group receiving an inotropic drug compared to another group receiving a different inotropic/placebo treatment. The exclusion criteria were studies published as an abstract only, crossover studies, and studies with a lack of data on the cardiac index. Results: A total of 1402 patients from 37 trials were included in the study. Inotropic drugs were shown to increase the cardiac index (0.32, 95%CI:0.25, 0.38), heart rate (7.68, 95%CI:6.36, 9.01), and mean arterial pressure (3.17, 95%CI:1.96, 4.38) than the placebo. Overall, the pooled estimates showed no difference in terms of cardiac index, heart rate, mean arterial pressure, systemic vascular resistance, and mean pulmonary arterial pressure among the groups receiving different inotropes. Conclusions: Our systematic review found that inotrope therapy is not associated with the amelioration of hemodynamics. An accurate evaluation of the benefits and risks, and selection of the correct inotropic agent is required in all clinical settings.
Background: There is currently no consensus on the appropriate selection of inotropic therapy in ventricular dysfunction. The objective of the study was to detect the effects of different inotropes on the hemodynamics of patients who developed low cardiac output. Methods: PubMed, Embase, and the Cochrane Central Register of Controlled Trials (CENTRAL) were searched (all updated December 31, 2017). The inclusion criteria were as follows: low cardiac index (CI < 2.5 L/min/m2) or New York Heart Association class II–IV, and at least 1 group receiving an inotropic drug compared to another group receiving a different inotropic/placebo treatment. The exclusion criteria were studies published as an abstract only, crossover studies, and studies with a lack of data on the cardiac index. Results: A total of 1402 patients from 37 trials were included in the study. Inotropic drugs were shown to increase the cardiac index (0.32, 95%CI:0.25, 0.38), heart rate (7.68, 95%CI:6.36, 9.01), and mean arterial pressure (3.17, 95%CI:1.96, 4.38) than the placebo. Overall, the pooled estimates showed no difference in terms of cardiac index, heart rate, mean arterial pressure, systemic vascular resistance, and mean pulmonary arterial pressure among the groups receiving different inotropes. Conclusions: Our systematic review found that inotrope therapy is not associated with the amelioration of hemodynamics. An accurate evaluation of the benefits and risks, and selection of the correct inotropic agent is required in all clinical settings.
Stimulating cardiac beta 1-adrenoceptors with oxyfedrine causes dilatation of coronary vessels and positive inotropic effects on the myocardium. beta 1-adrenergic agonists increase coronary blood flow in nonstenotic and stenotic vessels. The main indication for the use of the phosphodiesterase inhibitors pamrinone, mirinone, enoximone and piroximone is acute treatment of severe congestive heart failure. Theophylline is indicated for the treatment of asthma, chronic obstructive pulmonary disease, apnea in preterm infants ans sleep apnea syndrome. Severe arterial occlusive disease associated with atherosclerosis can be beneficially affected by elcosanoids. These drugs must be administered parenterally and have a half-life of only a few minutes. Sublingual or buccal preparations of nitrates are the only prompt method (within 1 or 2 min) of terminating anginal pain, except for biting nifedipine capsules. The short half-life (about 2.5 min) of nitroglycerin (glyceryl trinitrate) makes long term therapy impossible. Tolerance is a problem encountered with longer-acting nitric oxide donors. Knowledge of the pharmacokinetic properties of vasodilating drugs can prevent a too sudden and severe blood pressure decrease in patients with chronic hypertension. In considering the administration of a second dose, or another drug, the time necessary for the initially administered drug to reach maximal efficacy should be taken into account. In hypertensive emergencies urapidil, sodium nitroprusside, nitroglycerin, hydralazine and phentolamine are the drugs of choice, with the addition of beta-blockers during catecholamine crisis or dissecting aortic aneurysm. Childhood hypertension is most often treated with angiotensin-converting enzyme (ACE) inhibitors or calcium antagonists, primarily nifedipine. Because of the teratogenic risk involved with ACE inhibitors, extreme caution must be exercised when prescribing for adolescent females. The propagation of health benefits to breast-fed infants, combined with more women delaying pregnancy until their fourth decade, has entailed an increase in the need for hypertension management during lactation. Low dose hydrochlorothiazide, propranolol, nifedipine and enalapril or captopril do not pose enough of a risk of preclude breastfeeding in this group. The most frequently used antihypertensive agents during pregnancy are methyldopa, labetalol and calcium channel antagonists. Methyldopa and beta-blockers are the drugs of choice for treating mild to moderate hypertension. Prazosin and hydralazine are used to treat moderate to severe hypertension and hydralazine, urapidil or labetalol are used to treat hypertensive emergencies. The use of overly aggressive antihypertensive therapy during pregnancy should be avoided so that adequate uteroplacental blood flow is maintained. Methyldopa is the only drug accepted for use during the first trimester of pregnancy.
The digitalis drugs are plant-derived cardenolide compounds used medicinally for several hundred years. These drugs elicit inotropic and chronotropic effects on the heart, but they also affect many other tissues. The mechanism of action involves inhibition of the ion-transport activity of a membrane-associated protein called Na, K-ATPase (sodium pump). Present theory holds that the sodium pump is the principal molecular receptor for the digitalis drugs. Recent evidence indicates the presence of naturally occurring digitalis-like compounds in mammals. It is believed these compounds, collectively known as either digitalis-like (DLF) or ouabain-like (OLF) factors, may be endogenous hormones regulating the biological activity of the sodium pump and its isoforms. The presence of deglycosylated and other congeners of one specific DLF, the digoxin-like immunoreactive factor (DLIF), has very recently been described in humans. Digoxin as a drug is the most widely prescribed digitalis in the U.S., and its measurement in serum has established a model for present-day therapeutic drug monitoring (TDM). Historically, the accurate measurement of digoxin in blood has been difficult. This article focuses on the present understanding of the clinical use of digoxin, factors that affect the accuracy of measuring digoxin, the principle of measuring metabolically active species of digoxin, and the effects of DLIF and other interfering substances in digoxin immunoassay.
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