Hemodynamic Effects Of Epinephrine Research Articles

Utilization of epinephrine-soaked gauzes to address bleeding from osteotomy sites in non-tourniquet total knee arthroplasty: a retrospective cohort study

BackgroundReducing tourniquet inflation time is important because of the complications of tourniquet extensively used for the control of hemorrhage in total knee arthroplasty (TKA). Bleeding management is critical to acquire a relative bloodless arthrotomy interface for maximize cement fixation in non-tourniquet TKA. The purpose of this study was to investigate hemostatic and hemodynamic effects of epinephrine-soaked gauzes in cemented TKAs.MethodsA retrospective cohort study of 101 patients in two groups was performed. The first group (n = 51) underwent unilateral TKA with our procedures of epinephrine use, the second group (n = 50) had the same protocol with tourniquet and no epinephrine utilization. Surgical field visualization was assessed by grading scale for difficulty of intraoperative visualization due to blood and number of surgical field clearances. Perioperative blood loss was recorded. Hemodynamic parameters were observed in the epinephrine group.ResultsThere was statistically significant difference (p < 0.01) on surgeon-rated difficulty in visualization in the epinephrine group between before and after use of epinephrine, and no statistically significant difference (p = 0.96) between two groups before cementing. No statistically significant result on numbers of surgical field clearances between two groups (p = 0.25) was found. Epinephrine group showed significant difference in hidden blood loss compared with no epinephrine group (576.6 ± 229.3 vs 693.2 ± 302.9, respectively, p = 0.04). The hemodynamic effects of epinephrine may be under control.ConclusionThe procedure of epinephrine soaked gauzes, as a prudent adjunct, may be effective to reduce blood loss and obtain bloodless bone sections in non-tourniquet TKAs, regardless of hemodynamics.

Hemodynamic effects of epinephrine in rats: evaluation by impedance cardiography.

This study was aimed to examine how inotropic effects of intravenously injected epinephrine change thoracic impedance measurements and to reveal the possible effects of this change on other hemodynamic parameters by using the technique of impedance cardiography. 10 male Wistar Albino rats were divided into two equal groups: control and epinephrine. 0.2 mg/kg of epinephrine was administered to the rats in the epinephrine group via the tail vein. All hemodynamic parameters obtained by impedance cardiography [the base impedance (Z0), the maximum rate of change in impedance (dZmax/dt), the left ventricular ejection time (LVET), stroke volume (SV), cardiac output (CO), contractility index (IC), thoracic fluid content (TFC), heart rate (HR)] were recorded using the EBI 100C, DA 100 and ECG modules in the BIOPAC MP100 system. CO (p ≤ 0.05), HR (p ≤ 0.001), dZmax/dt (p ≤ 0.05) and IC (p ≤ 0.05) increased statistically significantly in the epinephrine group compared to the control group. However, LVET (p ≤ 0.001) decreased statistically significantly in the epinephrine group compared to the control group. Tachycardia was detected in the epinephrine group. There was an inverse correlation between LVET and dZmax/dt and IC. This is based on the fact that epinephrine increases inotropic effect (Tab. 2, Fig. 4, Ref. 30).

The Hemostatic and Hemodynamic Effects of Epinephrine During Endoscopic Sinus Surgery

To assess the hemodynamic and hemostatic effects of 2 different concentrations of epinephrine in local anesthetic used during functional endoscopic sinus surgery (FESS). Injection of local anesthetic containing epinephrine during endoscopic sinus surgery, while providing hemostasis, has been associated with cardiac adverse effects such as tachycardia, hypertension, as well as arrhythmias. Double-blind, randomized clinical trial. Tertiary referral center. A total of 140 patients undergoing FESS randomly divided into 2 groups, with group 1 receiving lidocaine hydrochloride, 2%, with 1:100 000 epinephrine and group 2, lidocaine, 2%, with 1:200 000 epinephrine. Baseline and postinjection hemodynamic parameters were recorded at 1-minute intervals for 5 minutes. Patient demographics, the extent of surgery, and the presence of polyps were recorded in both groups. Hemodynamic and hemostatic parameters and intraoperative blood loss were compared. Significant hemodynamic fluctuations were noted following injection of lidocaine, 2%, with 1:100 000 epinephrine (group 1). Increases in heart rate and systolic, diastolic, and mean arterial blood pressure were noted in group 1 patients. The increase was found to be significant (P < .001) in the first and second minutes after injection and decreased to baseline level by the fifth minute. This fluctuation was not noted in group 2 patients, who received lidocaine, 2%, with 1:200 000 epinephrine. Using a standardized scale to assess surgical bleeding, no statistical difference in the 2 groups was observed (P > .05). Submucosal injection of lidocaine, 2%, with 1:200 000 epinephrine during FESS does not lead to hemodynamic fluctuations or increased intraoperative bleeding compared with lidocaine, 2%, with 1:100 000 epinephrine. clinicaltrials.gov Identifier: NCT00852410.

EPINEPHRINE VERSUS DOPAMINE TO TREAT SHOCK IN HYPOXIC NEWBORN PIGS RESUSCITATED WITH 100% OXYGEN

Shock and tissue hypoperfusion are common after asphyxia. We compared systemic and regional hemodynamic effects of epinephrine and dopamine in the treatment of shock and hypotension in asphyxiated newborn piglets resuscitated with 100% oxygen. Twenty-four piglets (1-3 days old; weight, 1.4-2.6 kg) were acutely instrumented to measure cardiac index (CI), carotid, mesenteric and renal arterial blood flows, and mean systemic (SAPs) and pulmonary arterial pressures (PAPs). Piglets had normocapnic alveolar hypoxia (F(IO2)=0.08-0.10) for 50 min and reoxygenated with F(IO2)=1.0 for 1 h then F(IO2)=0.21 for 3.5 h. After 2 h reoxygenation, either dopamine (2 microg kg(-1) min(-1)) or epinephrine (0.2 microg kg(-1) min(-1)) was given for 30 min in a blinded randomized manner, which was then increased to maintain SAP (within 10% of baseline, pressure-driven dose) for 2 h. Hypoxia caused hypotension (SAP, 44%+/-3% of baseline), cardiogenic shock (CI, 41%+/-4%), and metabolic acidosis (mean pH, 7.04-7.09). Upon reoxygenation, hemodynamic parameters immediately recovered but gradually deteriorated during 2 h with SAP at 45+/-1 mmHg, CI at 74+/-9% of baseline, and pH 7.32+/-0.03. Low doses of either drug had no significant systemic and renal hemodynamic response. Epinephrine (0.3-1.5 microg kg(-1) min(-1)) for 2 h increased SAP and CI (with higher stroke volume) and decreased pulmonary vascular resistance (with reduced PAP-SAP ratio), whereas the responses with dopamine (10-25 microg kg(-1) min(-1)) were modest. Low-dose epinephrine improved mesenteric and carotid arterial flows, whereas the pressure-driven doses of epinephrine and dopamine increased carotid and mesenteric arterial flows, respectively. To treat shock in asphyxiated newborn piglets resuscitated with 100% oxygen, epinephrine exhibits an inotropic action compared with dopamine, whereas both catecholamines can increase carotid and mesenteric perfusion.

Hemodynamic Effects of Epinephrine, Bicarbonate and Calcium in the Early Postnatal Period in a Lamb Model of Single-Ventricle Physiology Created In Utero

A reproducible fetal animal model of single-ventricle physiology was created to examine the effects of pharmacologic agents commonly used in the perinatal and perioperative intensive care management of patients with a single ventricle. Single-ventricle physiology is characterized by parallel pulmonary and systemic circulations, with effective blood flow to each determined by the relative resistances in the pulmonary and systemic vascular beds. Perinatal and perioperative management of these patients is largely based on empiric observations and differs considerably between institutions and is further complicated by the transitional physiology of the newborn. The lack of animal models of single-ventricle physiology has hindered the understanding of this problem. A 10-mm, Damus-Kaye-Stansel-type aortopulmonary anastomosis was created in 10 fetal sheep at 140 +/- 1.2 days of gestation. The main pulmonary artery was ligated distally, and pulmonary blood flow (Qp) was provided through a 5-mm aortopulmonary shunt. Eight lambs were delivered at term and placed on cardiopulmonary bypass (30 min) 48 to 72 h after birth. Pharmacologic interventions (0.1 microgram/kg body weight per min of epinephrine, 2 mEq/kg of sodium bicarbonate and 10 mg/kg of calcium chloride) were performed before and after bypass, and hemodynamic responses were observed. The response to the epinephrine bolus was determined only in the postbypass study. Both before and after bypass, epinephrine infusion and calcium and bicarbonate administration increased Qp and systemic blood flow (Qs) (total cardiac output) but produced only small changes in the Qp/Qs ratio (-0.5% to -7.3% change). With the epinephrine bolus, Qp increased enormously, and the Qp/Qs ratio increased by 584% (p < 0.001). In neonatal lambs with single-ventricle physiology created in utero, epinephrine infusion and calcium and bicarbonate administration increased total cardiac output without significantly compromising the Qp/Qs ratio. However, epinephrine bolus seems to be hemodynamically detrimental in circumstances of single-ventricle physiology and should be used with caution and probably in relatively lower doses in the resuscitation of patients with single-ventricle physiology. Further investigation of the dose-dependent effects and the effects of prolonged administration of common pharmacologic agents will enable better management of patients with single-ventricle physiology.

Hemodynamic effects of epinephrine in combination with different alkaline buffers during experimental, open-chest, cardiopulmonary resuscitation

To evaluate the hemodynamic actions of epinephrine combined with different alkaline buffers during experimental, open-chest, cardiopulmonary resuscitation (CPR). Prospective, randomized, controlled trial. Experimental animal laboratory in a university hospital. A total of 28 anesthetized piglets. After catheterization and application of a pulmonary artery flow probe (transit-time ultrasound flowmetry), the animals were stabilized. Induction of ventricular fibrillation was followed by a 15-min period of CPR, including manual heart compressions and mechanical ventilation with pure oxygen. On commencement of CPR, a 4-min alkaline buffer infusion began, with 50 mmol of sodium bicarbonate (n = 7), tris buffer mixture (n = 7), or tris buffer (n = 7), or, as a control (n = 7), the same volume of normal saline. After 8 mins of CPR, 0.5 mg of epinephrine was given intravenously; after 15 mins, direct current shocks were used to revert the heart to sinus rhythm. Blood flow measured in the pulmonary artery during open-chest CPR was approximately 20% of normal cardiac output. Administration of epinephrine reduced pulmonary artery flow irrespective of buffer. Sodium bicarbonate alone resulted in higher systemic blood pressure than pure tris: tris buffer mixture and normal saline were intermediate. Sodium bicarbonate combined with epinephrine tended to produce lower systemic blood pressure than other combinations. Experimental open-chest CPR generates pulmonary artery blood flows (20% of normal cardiac output) that are at best at the lower level of those blood flow rates previously reported (25% to 40% of normal cardiac output) from studies of closed-chest CPR. Different alkaline buffers influence circulatory and acid-base parameters differently before and after administration of epinephrine.

Potential risks of high-dose epinephrine for resuscitation from ventricular fibrillation in a porcine model

The arterial plasma concentrations and hemodynamic effects of epinephrine, 10 μg/kg, IV (group A, N = 8) and 50 μg/kg, IV (group B, N = 8) were compared in a porcine resuscitation model after 3 minutes of circulatory arrest induced by ventricular fibrillation. All animals in group A were successfully resuscitated after 4.9 ± 2.8 minutes and 2.8 ± 1.6 defibrillations. In group B, only 6 of 8 animals were successfully resuscitated after 6.3 ± 1.1 minutes and 4.0 ± 2.7 defibrillations (mean ± SD). During CPR, cardiac output (CO), left ventricular systolic pressure (LVSP), and mean arterial pressure (MAP) were nearly identical in the groups. The hemodynamic situation during the first hour after restitution of spontaneous circulation in group B was characterized by a significantly higher heart rate, combined with significantly lower values for cardiac inotropy, CO, LVSP, and MAP compared to group A. Mean arterial peak epinephrine concentrations (group A 197 ± 133 ng/mL, group B 1173 ± 298 ng/mL) were approximately fivefold higher in group B. After resuscitation, plasma concentrations returned to baseline levels within 7 minutes in group A and 15 minutes in group B. Later hemodynamic differences between the groups are thereby attributed to a detrimental impact of high-dose epinephrine on the heart during resuscitation.

Hemodynamic Effects of Epinephrine, Dopamine, Nitroglycerin, and Nitroprusside in a Patient with a Total Artificial Heart (TAH)

Hemodynamic Effects of Epinephrine, Dopamine, Nitroglycerin, and Nitroprusside in a Patient with a Total Artificial Heart (TAH)

Hemodynamic effects of epinephrine: concentration-effect study in humans.

The hemodynamic effects of three different infusion rates of epinephrine (25, 50, or 100 ng X kg-1 X min-1 for 14 min) were examined in 10 normal human subjects. Ejection fraction and changes in cardiac volumes were assessed by radionuclide ventriculography. Plasma epinephrine was increased to levels that spanned the normal physiological range (178 +/- 15, 259 +/- 24, and 484 +/- 69 pg/ml, respectively). Epinephrine infusions resulted in dose-dependent increases in heart rate (8 +/- 3, 12 +/- 2, and 17 +/- 1 beats/min, mean +/- SE) and systolic pressure (8 +/- 1, 18 +/- 2, and 30 +/- 6 mmHg). Although epinephrine infusions had minimal effects on end-diastolic volume, there were significant increases in stroke volume (+26 +/- 2, 31 +/- 4, and 40 +/- 4%), ejection fraction (+0.10 +/- 0.01, 0.14 +/- 0.02 and 0.16 +/- 0.03 ejection fraction units), and cardiac output (+41 +/- 4, 58 +/- 5, and 74 +/- 1%). These increases in left ventricular performance were associated with a decreased systemic vascular resistance (-31 +/- 3, -42 +/- 2, and -48 +/- 8%). Supine bicycle exercise resulted in similar plasma epinephrine levels (417 +/- 109 pg/ml) and similar changes in stroke volume, ejection fraction, and systemic vascular resistance but greater increases in heart rate and systolic blood pressure. Since infusion-associated hemodynamic changes occurred at plasma epinephrine levels commonly achieved during many types of physical and emotional stress, epinephrine release may have an important role in regulating systemic vascular resistance, stroke volume, and ejection fraction responses to stress in man.

The isolated, perfused head of the marine teleost fish,Myoxocephalus octodecimspinosus: Hemodynamic effects of epinephrine

An isolated, perfused-head preparation utilizing the marine teleost (Myoxocephalus octodecimspinosus) was developed, and the hemodynamic effects of epinephrine on this preparation were studied.