Use Of Alpha-agonists Research Articles

Abstract 17166: Comparison Between Use of Vasoactive Medications in Patients Undergoing PVC and VT Ablation

Background: Societal guidelines have set prerequisites regarding procedures conducted in the EP lab. Despite metrics for management of EP cases, no clear guidelines exist for use of hemodynamic drugs to support complex ablations, particularly in setting of structural heart disease. Objectives: We sought to understand the variety and range of vasoactive medication use in patients undergoing PVC/VT ablation. Methods: Patients undergoing PVC or VT ablation, from January 2015 to December 2016, at our institution were analyzed. Demographics, echocardiography, and procedural details, including vasoactive medication use, were analyzed. Results: Sequential patients undergoing PVC or VT ablation (70 in each arm) were studied. Those undergoing PVC ablation (56 +/- 14 years, 30% female) had an average EF of 58% in comparison to 44% (p<0.01 for EF difference) in VT ablation patients (60 +/- 13 years, 20% female); more VT patients (62%) were under general anesthesia. Pressors were administered in 86% of cases with the significant majority (63%) consisting of alpha-agonists (phenylephrine, ephedrine, epinephrine). Importantly, 48% of cases required continuous drip initiation (Figure). Regardless of case type or abnormal EF, drip initiation with or administration of multiple bolus doses of alpha-agonists was much more frequent compared to inotropes (Figure). In a subset of patients with EF ≤ 35%, 96% received vasoactive medications with 73% receiving a continuous drip or multiple bolus doses of phenylephrine. Conclusions: Vasoactive medication use during ventricular EP cases is common. Regardless of baseline EF, a propensity for use of alpha-agonists exists that may affect the treatment of patients with abnormal LV function. More studies are needed to assess the impact of pressor use on patient safety and procedural endpoints in the EP lab. Figure:

EComment. Spinal cord protection during thoracoabdominal aneurysm repair

The study ‘Novel application of acetazolamide to reduce cerebrospinal fluid production in patients undergoing thoracoabdominal aortic surgery’ by Jafarzadeh and associates [1] comes to cover a large practice gap in the prolepsis of spinal cord ischaemia in patients undergoing thoracoabdominal aortic aneurysm (TAAA) repair. Our practice so far is to protect the spinal cord during TAAA repair with a spinal drain that is kept for 48-72 h in the postoperative period. Strict guidelines are applied for the management of the drain for optimal protection. In addition, permissive hypothermia and liberal use of alpha-agonists in order to increase the mean arterial pressure during the postoperative period is the standard routine. Finally, recent studies have stressed that adding intrathecal papaverine to the neuroprotective protocol for descending thoracic aneurysm and TAAA repairs may enhance spinal cord perfusion and provide additional spinal cord protection [2]. We agree with the authors that in cases of contra-indication to the use of a spinal drain or the inability to insert it, the use of other agents that increase spinal cord perfusion is promising. There is an imperative need of a randomized trial, which will determine the efficacy of acetazolamide in the spinal cord protection during TAAA repair.

Lessons from liver transplantation

Lessons from liver transplantation

Alpha‐agonists for the treatment of anaphylactic shock

We are writing following the two cases reported regarding the use of alpha-agonists for the management of anaphylaxis occurring under anaesthesia [1]. We would like to present another case of anaphylactic shock occurring under spinal anaesthesia, which required the use of alpha-agonists for successful management. An 83-year-old lady presented for a pelvic floor repair. She had no significant past medical history, and had had previous general anaesthetics, which had proved to be uneventful. She had no known drug allergies. Spinal anaesthesia was induced using hyperbaric 0.5% bupivacaine 2.5 ml and for the first 20 min of the procedure the patient remained stable. Co-amoxiclav 1.2 g was subsequently administered. Within minutes the patient became hypotensive and progressed to pulseless electrical activity (PEA). There were no other signs present that were consistent with anaphylaxis. Cardiopulmonary resuscitation was commenced in accordance with ALS guidelines. The patient's trachea was intubated and ventilated with oxygen 100%, and she received an initial crystalloid bolus of 1 litre. The patient received a total of 3 mg of epinephrine. The first two doses produced no cardiovascular change. The third dose, which was accompanied by a 10 mg bolus of metaraminol, led to a rhythm change to ventricular fibrillation, which reverted to sinus rhythm with one 200 J DC shock. After defibrillation, hypotension was treated with incremental boluses of metaraminol; a total of 30 mg was required to maintain a systolic blood pressure of 100 mmHg. The patient made a good recovery and was extubated within 24 h. We think that it is important to highlight this as a further case where the use of an alpha-agonist proved beneficial in the face of epinephrine-resistant anaphylactic shock. Adrenaline remains an empirical agent in the treatment of anaphylactic/anaphylactoid reactions, despite human studies that have not been totally supportive of its ability to reverse the haemodynamic changes associated with this condition. In-vitro studies have compared epinephrine with vasopressin, and inhibitors of nitric oxide and prostanoid pathways (for example methylene blue and indomethacin) on histamine-induced relaxation of the internal mammary artery. They found that epinephrine only partially reversed histamine-induced vasodilation whereas the other agents led to complete reversal of vascular relaxation [2]. There have also been a number of case reports describing the successful use of vasopressin to reverse anaphylaxis-associated vasodilation and haemodynamic collapse. Kill et al.[3] described successful resuscitation of two patients who had PEA. One patient received 10 units, followed by a 40-unit infusion, the other received 40 units of vasopressin. In both patients there was a rapid restoration of blood pressure [3]. Vasopressin has also been described in the treatment of aprotonin-induced anaphylaxis, where hypotension proved to be resistant to phenylephrine. The dose used in this case was 5 units [4]. Schummer et al. used 2 units of pitressin after epinephrine 1.5 mg and administration of norepinephrine to restore adequate blood pressure [5]. Due to the nature of the disease process, it seems unlikely that there will ever be any formal evidence to support a change to the current guidelines, other than work performed in animal models. As a result, it is important that further case reports advocating the use of alternate agents in the treatment of anaphylaxis are published in the literature, in order to create a body of evidence to facilitate changes to our current guidelines. It may be time to rewrite the guidelines and move away from the traditional belief that there is only one inotropic agent available for the treatment of anaphylaxis. We feel that early use of alpha-agonists, with the second dose of epinephrine, may reduce the morbidity and mortality associated with anaphylaxis and reduce the unwanted side-effects produced by high dose epinephrine. With time and improved availability of vasopressin, it may represent the third line agent for resistant anaphylactic shock.

Effects of ephedrine and phenylephrine on uterine and placental circulations and fetal outcome following fetal hypoxaemia and epidural-induced hypotension in a sheep model

Recent studies support the use of alpha-agonists during regional anaesthesia in uncomplicated term pregnancies. We hypothesized that ephedrine and phenylephrine, administered for maternal hypotension following fetal hypoxaemia, are equal in respect of fetal outcome. At 117-132 days gestation, chronically instrumented, anaesthetized and mechanically ventilated ewes were randomized to receive boluses of ephedrine (n=9) or phenylephrine (n=8) for maternal epidural-induced hypotension after a period of fetal hypoxaemia. Uterine (QUtA) and placental (QUA) volume blood flows were measured with perivascular transit-time ultrasonic flow probes, and uterine (RUtA) and placental (RUA) vascular resistances were computed from volume blood flows and maternal and fetal mean arterial pressures. Uterine (PIUtA) and umbilical artery (PIUA) pulsatility indices were obtained by Doppler ultrasonography. Ephedrine increased QUtA and decreased RUtA and PIUtA from a hypotensive to baseline level and had no significant effect on umbilical circulation. With phenylephrine, QUtA remained lower (P=0.011) and RUtA higher (P=0.043) than at baseline, although PIUtA decreased to baseline level. PIUA increased from baseline with phenylephrine (P=0.007), whereas QUA decreased (P=0.050). Maternal volume expansion with hydroxyethyl starch decreased RUtA significantly irrespective of the vasopressor used. There were no significant differences in fetal blood gas values or lactate concentrations between the ephedrine and phenylephrine groups. Despite the more favourable effects on uterine and placental circulations of ephedrine over phenylephrine, no significant differences in fetal acid-base status or lactate concentrations were observed.

PRIAPISM: From Priapus to the Present Time

Advances in the pharmacotherapeutic options available to treat erectile dysfunction over the past decade have transformed the field of impotence. The initial foray into this field with intracavernous injections of papaverine rapidly expanded the number of men seeking attention for priapism, a previously rare clinical condition. The recent widespread use and acceptance of oral agents for the treatment of erectile dysfunction, with a reduced incidence of priapism has decreased the number of men at risk for injection-related prolonged erections. The use of recreational drugs (cocaine) and perineal trauma leading to presentations of priapism seem to be rising in incidence. The urologist remains the consultant-specialist ultimately responsible for these men and should be cognizant of the array of treatments described for this condition. Early determination of the state of corporal oxygenation is essential and will define the optimal management approach. A wide range of medical conditions and risk factors may be etiologic and should be elicited from the patient at the initial interview. Low-flow ischemic priapism requires a rapid resolution, often achieved through use of alpha-agonists orally or by direct injection into the penile circulation, whereas nonischemic priapism can be treated more conservatively. Research into this condition has only recently been initiated. Through greater understanding of the pathophysiology of priapism, the clinician may become armed with etiology-specific medical alternatives providing timely detumescence for men with prolonged erections.

Determinants of postoperative hypothermia after normothermic cardiopulmonary bypass

Inadvertent postoperative hypothermia in the cardiac surgical patient can have various adverse physiologic effects. Previous studies have investigated the relationship of patient, surgical, and anesthetic factors with postoperative hypothermia in patients undergoing noncardiac surgery. This study was designed to assess the relationship between postoperative hypothermia after normothermic cardiopulmonary bypass (CPB) for cardiac surgery and a variety of perioperative and patient factors. Fifty-six patients undergoing daytime elective or urgent cardiac surgery with warm (37 degrees C) CPB were studied. The following patient variables were included: age, weight, height, sex, history of previous cardiac surgery, and prebypass temperature. The following treatment factors were recorded: type of surgery, type and dose of anesthetic, use of airway humidifier, use of an intravenous (i.v.) fluid warmer, total volume of i.v. fluid administered during surgery, net fluid volume administered via CPB, total time spent on CPB, use of nitroglycerin, use of alpha-agonists during surgery, and elapsed time from end of CPB to end of surgery. Core temperature readings, as measured by a pulmonary artery catheter thermistor, were noted as follows: (1) on insertion of the pulmonary artery catheter; (2) after the patient was weaned from CPB; (3) within 30 minutes of intensive care unit (ICU) arrival; (4) 3 to 5 hours after ICU arrival; (5) 7 to 9 hours after ICU arrival; and (6) 11 to 13 hours after ICU arrival. Multiple linear regression and logistic regression for categorical variables with backward elimination were employed to determine the impact of all variables on lowest postoperative temperature. The lowest mean temperature occurred during CPB.(ABSTRACT TRUNCATED AT 250 WORDS)