A comparative study of ketofol and fentafol for evacuation of retained products of conception (ERPC)

Objectives: Conventional evacuation of retained products of conception (RPOC) is a blind technique which may not remove focal RPOC and is associated with perforation and adhesion risks. Ultrasound (USS) guided evacuation of retained products of conception (ERPC) is a commonly used alternative but we hypothesised that for focal retained tissue following miscarriage, termination of pregnancy (TOP) or delivery hysteroscopic removal of tissue under direct visualisation was an effective and safe alternative which allows intraoperative confirmation of an empty uterus. Methods: For 15 months women with small well-defined intrauterine focal mixed hyperechogenic tissue, with or without vascularity, following miscarriage, TOP or delivery were selected for hysteroscopic management. Under general anaesthesia an 8 mm saline resectoscope without an active electrode was used. Operative findings, procedures, complications, repeat USS and histology are reported. Results: 15 patients were identified retrospectively. Initial presentation was miscarriage (6), TOP (3) and post delivery (6). In 4/15 findings followed blind ERPC. Mean AP diameter of tissue was 17.3 mm (range 4.3–29 mm). In 15/15 (100%) USS findings were confirmed by direct visualisation of frond-like pale tissue or an isolated nodule at hysteroscopy. 1/15 (7%) was complicated by uterine perforation. In 15/15 (100%) blood loss was minimal. Histology confirmed RPOC in 12/15 (80%), implantation site reaction in 2/15 (13%) and chronic endometritis in 1/15 (7%). 7/7 who returned for follow up at 8/52 had an empty uterine cavity confirmed. Conclusions: The ultrasound criteria perform well in identifying focal RPOC. The 7% negative histology may be due to false positive USS or sample collection problems. We propose prospective comparison of USS guided ERPC with hysteroscopy.

Objectives: The aim of our study is to observe the pain difference as experienced by the pediatric patient when administered different preparations of propofol utilizing the verbal rating scale. Study Design: Prospective double-blind randomized control trial. Setting: A large tertiary care hospital in Karachi, Pakistan. Period: 6 months from June 2016 to November 2016. Material & Methods: The final patient population included in the study was n= 180 and were divided into six groups. These patients received general anesthesia and underwent surgery. Patients in Group A received 2ml of normal saline and a mixture of propofol and normal saline after waiting for half a minute. Group B patients received 0.5mg/kg Lidocaine followed by normal saline after waiting for half a minute. Group C received 2ml of normal saline followed by a mixture of propofol and Lidocaine after half a minute. Group D received 0.2mg/kg of Ketamine followed by a mixture of normal saline and propofol. Group E patients received 2ml of normal saline followed by a mixture of propofol and Ketamine half a minute later. And finally, patients belonging to group F received 2ml of normal saline followed by a mixture of propofol M/LCT and normal saline half a minute later respectively. Results: The gender, age, body weight and ASA grade of all the pediatric patients were similar having a P value of >0.05. The incidence rate of propofol injection pain in the groups were found to be Group A= 76.66%, Group B= 66.66%, Group C= 50%, Group D= 60%, Group E= 63.33%, Group F= 60% respectively. The incidence rate for adverse events was significantly lower in all the groups as compared to Group A that is the normal saline and propofol group having a p-value of less than 0.01. And the incidence rate of adverse events was lower in Groups C, D, E, and F were significantly lower than Group B having a p-value of less than 0.05. All the experimental groups had significantly lower scores of the VRS scale as compared to the control group (Group A) and the intergroup differences were found to be statistically significant having a p-value of less than 0.01. Conclusion: In our study, we found that the injection pain of propofol administration in the pediatric population was significantly reduced when using M/LCT pre-injection, 0.5mg/kg lidocaine or 0.2mg/kg of Ketamine. Another good combination is mixing 180mg propofol with 40mg of lidocaine or mixing propofol with 16mg of Ketamine.

After completing this article, readers should be able to: 1. Delineate the short- and long-term adverse outcomes associated with low systemic blood flow. 2. Explain why it is not appropriate to use blood pressure and population criteria for hypotension to determine which infants who have low systemic blood flow need cardiovascular support. 3. Describe the various hemodynamic states in neonates and the assessment that is useful in allowing discrimination between these states. 4. Characterize the hemodynamic effects of dopamine and dobutamine in neonates. 5. Delineate the most common characteristics of infants who fail to maintain superior vena cava flows despite the use of inotropes. Low systemic blood flow (SBF) commonly occurs in preterm infants who have respiratory distress in the first postnatal day. Such low flows are strongly associated with neonatal morbidity, including peri/intraventricular hemorrhage (P/IVH), developmental impairments, and mortality. Diagnosing which infants have low SBF is problematic; use of blood pressure (BP) and signs of poor tissue perfusion, including capillary refill times (CRT), poor renal function, and acidosis, results in substantial delays in the initiation of cardiovascular support and a proportion of affected infants missing treatment. The traditional approach to cardiovascular support of the preterm infant has been to identify infants who have hypotension and to use agents, particularly dopamine, titrated to improve BP. However, this strategy may not be the best for improving SBF, and it is yet to be demonstrated that this approach improves neonatal outcomes. This review focuses on identifying which infants have low SBF or organ blood flow, discusses mechanisms for low flows, and examines potential therapies for treating or preventing low flow. Cardiovascular compromise occurs in a number of clinical scenarios in preterm infants, but it is most common on the first postnatal day. Not all infants who have low SBF will be suspected based on clinical signs, including …

A prospective comparative study was done on lignocaine versus lignocaine with pethidine to observe the effect on cardiovascular response to laryngoscopy and endotracheal intubation. One hundred such elective surgical patients of active age group (16 - 60 years) having American Society of Anaesthesiologist (ASA) physical status I & II irrespective of surgical procedure were randomly assigned to one of the two groups of 50 each. Group I received injection lignocaine 1 mg/kg intravenously 02 minutes before induction of general anaesthesia. Patients in group II received injection pethidine 1 mg/kg body weight and injection lignocaine 1 mg/kg body weight intravenously 02 minutes before induction of general anaesthesia. Haemodynamic parameter i.e. blood pressures (systolic blood pressure, diastolic blood pressure and mean blood pressure), heart rate, rate pressure product were monitored after 1st, 3rd, 5th minutes following intubation. There were statistically significant (p<0.001) increase in blood pressures, heart rate and rate pressure product in group I i.e. pretreatment with 1 mg/kg body weight intravenous lignocaine and remained so after 5 minutes. On the other hand there were no statistically significant (p>0.05) increase in heart rate, blood pressures and rate pressure product in group II, where pretreatment done with pethidine 1 mg/kg body weight with lignocaine 1 mg/kg body weight and the values returned control level before 5 minutes. The study showed that pethidine 1 mg/kg body weight with lignocaine 1 mg/kg body weight pretreatment suppresses the cardiovascular response due to laryngoscopy and intubation. Key words: Cardiovascular response; laryngoscopy; lignocaine with pethidine. DOI: 10.3329/jafmc.v6i2.7274JAFMC Bangladesh. Vol 6, No 2 (December) 2010 pp.40-43

AT our institution, thoracic epidural anesthesia (TEA) is being used with increasing frequency to provide surgical anesthesia for breast surgery. 1 Until recently, we have not seen any morbidity associated with this technique. Although profound bradycardia and asystole after spinal anesthesia have been described, 2-10 to our knowledge, there has been no clinical report describing such cardiovascular event after TEA. Therefore, we report a case of postoperative bradycardia and asystole complications TEA performed on a healthy woman for surgical removal of bilateral breast tissue expanders

Pharmacokinetics of propofol infusions, either alone or with ketamine, in sheep premedicated with acepromazine and papaveretum

Three strategies were employed to better define the afferent site(s) at which desflurane initiates its neurocirculatory activation. Young (aged 19-28 yr) healthy volunteers were employed in three separate studies. Monitoring included electrocardiography, radial artery blood pressure, and direct recordings of sympathetic outflow to skeletal muscle blood vessels by microneurography. In each study, anesthesia was established with 2.5 mg/kg propofol, and in studies 1 and 2 was maintained with 5.4% desflurane via a double-lumen tube. In study 1 (n = 7) a double-lumen tube was placed with the bronchial cuff just below the vocal cords to selectively give 14.5% desflurane or 2.4% isoflurane to the upper airway (via the tracheal lumen) or lower airway (via the bronchial lumen). Study 2 (n = 14) consisted of standard placement of a left side double-lumen tube to selectively increase the inspired desflurane concentration of either right or left lung to 11% while decreasing the inspired concentration in the opposite lung to 0%, thereby maintaining constant systemic concentrations of desflurane (gas chromatography). Study 3 consisted of lidocaine or placebo airway treatment before anesthetic induction and administration of 11% inspired desflurane by mask: group A-n = 9, topical and nebulized lidocaine, glossopharyngeal and superior laryngeal nerve blocks, and transtracheal administration of lidocaine; group B-n = 7, similar treatment as group A with placebo (saline); and group C-n = 8, systemic infusions of 2% lidocaine to match plasma concentrations of lidocaine in group A. In study 1, significant increases in heart rate, mean arterial pressure, and sympathetic neural activity (26%, 23%, and 62%, respectively) occurred when desflurane was directed to the upper airway. These responses were approximately twofold to sixfold larger when desflurane was given to the lower airway (lungs). There were no significant increases in these variables when isoflurane was administered to the upper airways, and a significant increase in heart rate occurred only when isoflurane was delivered to the lower airways. In study 2, separate right or left lung increases in desflurane did not change the blood concentration of desflurane or sympathetic neural activity but led to significant increases in heart rate (44%) and mean arterial pressure (32%). The simultaneous administration of desflurane to both lungs increased the millimolar (mM) concentration of desflurane in the blood from 1.17 to 2.39 mM and led to increases in sympathetic neural activity (750%), heart rate (90%), and mean arterial pressure (63%). In study 3, neither regional nor systemic administration of lidocaine reduced the significant neurocirculatory activation caused by the rapid increase in the inspired concentration of desflurane by mask. There are sites in the upper airway (larynx and above) that respond with sympathetic activation during rapid increases in desflurane concentration independent of systemic anesthetic changes. These responses, while lesser than those seen with rapid increases to the lung, may represent direct irritation of airway mucosa. Heart rate and mean arterial pressure responses to desflurane can be initiated by selectively increasing concentrations to either right or left lung without altering systemic levels of desflurane. From this it is inferred that there are sites within the lungs, separate from systemic sites, that mediate this response. Neither systemic lidocaine nor attempted blockade of upper airway sites with cranial nerve blocks combined with topical lidocaine was effective in attenuating the neurocirculatory activation associated with desflurane.

Background: Propofol is a commonly used induction agent. Propofol does not possess any strong analgesic effect, when used alone for induction of anaesthesia. In dose of more than 2 mg/kg bolus known to cause hypotension even requiring vasopressors. Nitrous oxide (N2O) has been in use for more than 150 years. Although N2O reduces the requirement of propofol for induction and maintenance, the effects of both the drugs on overall haemodynamic remain controversial. The aim of this study was to evaluate the efficacy and safety of induction dose of propofol when N2O was concurrently administered and haemodynamic alteration with addition of N2O to therapeutic dose of propofol. Materials and Methods: This was a prospective, randomized and double blinded comparison study that was conducted after obtaining institutional ethical approval. The study population consisted of eighty patients aged between 18 to 60 years from either sex and classified as American Society of Anaesthesiologists (ASA) physical status I or II which were scheduled for various elective surgical procedures under general anaesthesias. Participants were randomly allocated into two groups comprising 40 subjects each. Group PN received breathed 67% N2O (4 L/min) + 33% O2 (2L/min) and propofol. Group PO: breathed 100 % O2 (6L/min) and propofol. Changes in heart rate (HR), systolic blood pressure (SBP), mean arterial pressure (MAP) and Oxygen saturation (SpO2) were measured Preoperatively (baseline T0), After 3minutes of premedication (T1), After 1minute of inhalation of 100% O2 before induction of anesthesia (T2), After induction (T3), At 2, 5 and 10 minutes after induction (T4), (T5), and (T6). Results: Induction time and dose of propofol in PN group were significantly less. As 42.5% of the patients were induced in less than 100 sec, 57.5% in less than 200 sec and none of the patients required more than 200 sec for induction as compare to group PO where 77.5% required more than 200 sec, 22.5% in less than 200 sec and none of the patients were induced in less than 100 sec. The mean ± SD of induction time in groups PN and PO were 113.38±35.93 and 258.00±59.43 seconds respectively with p < 0.001. In group PN, 57.5% required 0.5-1.0mg/kg, 40% required less than 0.5mg/kg unlike group PO where 77.5% required 1-2mg/kg. The mean ± SD induction dose required for induction of anesthesia were 0.58±0.19 mg/kg and 1.43±0.40 mg/kg with and without 67% N2O in O2. Increase in HR in groups PN and PO 16.38% and 6.42% respectively. Conclusions: Co-administration of N2O during induction of anaesthesia achieves significant reduction in induction dose as well as induction time of propofol. It provides significant stability in SBP, and MAP, without affecting arterial oxygen saturation. N2O causes significant increase in HR.

General cardiovascular properties of ketamine: "In vitro", ketamine has moderate negative inotropic effects. "In vivo", a significant central sympathomimetic action with consecutive hemodynamic effects is dominant. The sympathomimetic potency of ketamine is one of the most significant pharmacological features of the substance with direct clinical implications. Monoanaesthesia with S-(+)-ketamine: After application of racemic ketamine or S(+)-ketamine as well, identic and significant increases in plasma catecholamines, arterial pressure and heart rate are observed. This outstanding sympathomimetic action is beneficial in induction of patients with shock or asthmatic state. TIVA and analgosedation with S-(+)-ketamine and midazolam: The sympathomimetic effect of S(+)-ketamine, and racemic ketamine as well, is mitigated by midazolam. Nevertheless, significant increases in heart rate and arteriel pressure might be observed. Clinical use of the combination is common in short procedures like reposition maneuvers. Of greater importance is the use for analgosedation in patients with cardiovascular instability, particularly in patients with exogenous catecholamine demand. TIVA and analgosedation with S-(+)-ketamine and propofol: When S(+)-ketamine is combined with propofol, the sympatholytic effects of propofol are counteracted by S(+)-ketamine, and stable hemodynamic conditions are presented. This combination seems useful for TIVA in patients with hypotonic dysregulation or endocrine deficits like hypothyreosis and adrenal insufficiency. Furthermore, analgosedation with S(+)-ketamine and propofol is advantageous, when rapid recovery is necessary and negative circulatory effects should be avoided. Sympathoadrenergic and hemodynamic effects of S(+)-ketamine and racemic ketamine are generally identical. The distinctest action is observed, when S(+)-ketamine is used as a monoanaesthetic. In combination with midazolam, a significant reduction is achieved. In combination with propofol, the sympatholytic effects of this hypnotic agent are compensated by S(+)-ketamine. With respect to sympathoadrenergic and hemodynamic reactions, the clinical position of S(+)-ketamine is unchanged. Nevertheless, a significant clinical progress can be expected due to improved recovery and reduced substance load, when racemic ketamine is replaced by S(+)-ketamine.

The purpose of the present study was to develop an experimental model of inappropriate sinus tachycardia (IST) by injecting a catecholamine into a fat pad containing autonomic ganglia (AG) innervating the sinus node (SN). Initial protocols in 3 groups of pentobarbital anesthetized dogs consisted of (1) slowing the heart rate (HR) by electrical stimulation of AG in the fat pad; (2) the effect of intravenous injection of epinephrine (0.1-0.3 mg) on the HR and systolic blood pressure (BP); (3) the response of SN rate to intravenously injected isoproterenol (1 microgm/kg). These studies established a reference for the response to epinephrine injection (mean dose 0.2 +/- 0.9 mg, n = 14) into the fat pad at the base of the right superior pulmonary vein (RSPV). ECG leads, right atrial and His bundle electrograms, BP and core body temperature were continuously monitored. Epinephrine, injected into the fat pad, caused a significant increase in heart rate (HR, average: 211 +/- 11/min, p < 0.05 compared to control) but little change in systolic BP, 149 +/- 10 mmHg, p = NS (Group I, N = 8). The tachycardia lasted >30 minutes. Ice mapping and P wave morphology showed the tachycardia origin in the SN in 6/8 and in the crista terminalis (CT) in 2. Injection of 0.4 cc of formaldehyde into the FP restored HR (159 +/- 16) toward baseline (154 +/- 18). In Group II (N = 6), the same regimen induced a significant increase in both HR and systolic BP (194 +/- 17/min and 230 +/- 24 mmHg, respectively) compared to control values (143 +/- 23/min, 162 +/- 24 mmHg) which lasted for > 30 minutes. Ice mapping and P wave morphology showed that the pacemaker was in the SN (1), overlying the CT (2), or atrioventricular junction (2). Formaldehyde (0.4 cc) injected into the FP restored both HR and systolic BP toward baseline values (148 +/- 29/min and 152 +/- 24 mmHg, p = NS) and prevented, slowing of the HR by electrical stimulation of the AG; moreover, the same dose of epinephrine injected intravenously increased HR and SBP but only for 2-5 minutes; Isoproterenol (1 microg/kg) injected intravenously induced essentially the same increase in sinus rate after AG ablation as in the control state (194 +/- 15/min vs 193 +/- 23/min, p = NS). Experimental IST is mainly localized in the SN or CT. Ablation of the AG terminates IST without impairing the SN response to an adrenergic challenge.

Comparison of the efficacy of esmolol and alfentanil to attenuate the hemodynamic responses to emergence and extubation

The time course of heart rate and body weight alterations during the natural period of dormancy were determined in active feeding and dormant juvenile specimens of Megalobulimus sanctipauli. In both groups, heart rate markedly decreased during the first 40 days of dormancy, tending to stabilize thereafter. This time period coincided with the decrease in environmental temperature during autumn-winter. At the end of the dormancy period, surviving active feeding and dormant snails showed a significant decrease in heart rate which, however, was significantly greater in the latter group. Total body weight decreased concomitantly with heart rate in dormant snails but remained constant in active feeding snails. Body hydration induced significant increases in weight and heart rate in surviving dormant snails. Feeding following hydration promoted a new significant increase in heart rate but not in weight. These results indicate that the decrease in heart rate observed in juvenile specimens of M. sanctipauli during dormancy may be due to at least three factors: 1) decrease in environmental temperature during autumn-winter, 2) starvation which leads to the depletion of endogenous fuel reserves and to a probable decrease in hemolymph nutrient levels, and 3) dehydration which leads to a probable decrease in hemolymph volume and venous return and/or to an increase in hemolymph osmolarity.

Running is a popular recreational activity and additional weight is often carried in backpacks on longer runs. Our aim was to examine running economy and other physiological parameters while running with a 1-kg and 3-kg backpack at different submaximal running velocities. Ten male recreational runners (age 25±4.2 years, VO2peak 60.5±3.1 mL/kg/min) performed runs on a motorized treadmill of 5 minutes durations at three different submaximal speeds of 70, 80 and 90% of anaerobic lactate threshold (LT) without additional weight, and carrying a 1-kg and 3-kg backpack. Oxygen consumption, heart rate, lactate and RPE were measured and analyzed. Oxygen consumption, energy cost of running and heart rate increased significantly while running with a backpack weighing 3 kg compared to running without additional weight at 80% of speed at lactate threshold (sLT) (P=0.026, P=0.009 and P=0.003) and at 90% sLT (P<0.001, P=0.001, and P=0.001). Running with a 1-kg backpack showed a significant increase in heart rate at 80% sLT (P=0.008) and a significant increase in oxygen consumption and heart rate at 90% sLT (P=0.045 and P=0.007) compared to running without additional weight. Also running at 70% sLT running economy and cardiovascular effort increased with weighted backpack running compared to running without additional weight, however these increases did not reach statistical significance. Running economy deteriorates and cardiovascular effort increases while running with additional backpack weight especially at higher submaximal running speeds. Backpack weight should therefore be kept to a minimum.

1. The effects of bilateral hindlimb ischaemia (BHLI), and of administration of the neuropeptide corticotrophin-releasing factor (CRF), were tested on cardiovascular variables in propofol-anaesthetized Sprague-Dawley rats. In addition, the effects of antagonizing endogenous CRF on the cardiovascular response to BHLI was investigated. 2. BHLI produced significant increases in mean arterial pressure and heart rate. Baroreflex sensitivity was reduced in all animals tested both 10 and 30 min after the induction of ischemia and this was accompanied by changes which are consistent with an underlying baroreflex resetting. 3. Intracerebroventricular (I.C.V.) administration of CRF (1.5 nmol) produced significant increases in heart rate but not mean arterial pressure. CRF also produced significant reductions in baroreflex sensitivity 10 and 30 min after administration, but there was no consistent evidence of baroreflex resetting. These effects of CRF could be prevented by pretreatment with the synthetic CRF antagonist, alpha-helical CRF(9-41) (alpha hCRF, 6.5 nmol, I.C.V.), which itself had no effect on these cardiovascular variables. 4. Pretreatment with alpha hCRF (6.5 nmol, I.C.V.) prevented the reduction in baroreflex sensitivity observed 10 min after the induction of BHLI, but had no consistent effect on the pressor or tachycardiac responses to BHLI and allowed a clear expression of BHLI-induced baroreflex resetting. alpha-Helical CRF(9-41) had no effect on the reduction in baroreflex sensitivity after 30 min of BHLI. 5. We conclude that corticotrophin-releasing factor mediates, at least in part, the early reduction in baroreflex sensitivity observed during hindlimb ischaemia in the rat.

The purpose of the present study was to determine the effects of left ventricular (LV) outflow obstruction on plasma renin activity (PRA) and the contribution from afferent receptors located in the LV myocardium. In chronically instrumented, conscious dogs (n = 12), changes in PRA during a 15- to 20-mmHg decrease in arterial blood pressure were assessed during 1) intravenous infusions of nitroprusside (NP) alone and 2) infusions of NP while peak systolic LV pressure was elevated by acute ascending aortic occlusion (AAO + NP). Infusions of NP alone elicited significant increases in heart rate (24.9 +/- 5.1 beats/min; P less than 0.01) and in PRA [3.31 +/- 0.53 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.01]. These were accompanied by decreases in both LV pressure (-13.8 +/- 3.6 mmHg; P less than 0.05) and left atrial pressure (-3.0 +/- 0.7 mmHg; P less than 0.05). During AAO + NP, LV pressure was elevated to an absolute level of 169.2 +/- 4.6 mmHg (+53.3 +/- 4.2 mmHg; P less than 0.001), whereas left atrial pressure was not changed. Both the hypotension-induced rise in PRA and tachycardia were significantly inhibited during AAO + NP (+0.59 +/- 0.29 ng ANG I.ml-1.h-1 and +6.3 +/- 4.6 beats/min, respectively; NS). The topical application of a local anesthetic in the region of the main coronary artery, sufficient to block the heart rate and arterial blood pressure responses to selective LV receptor stimulation by intracoronary veratridine (0.1-0.4 microgram/kg), resulted in significant increases in PRA and heart rate during AAO + NP.(ABSTRACT TRUNCATED AT 250 WORDS)