Degree Of Hypotension Research Articles

Bone cement implantation syndrome in cemented hemiarthroplasty for femoral neck fracture: incidence, risk factors, and effect on outcome

Bone cement implantation syndrome (BCIS) is characterized by hypoxia, hypotension, and loss of consciousness occurring around the time of bone cementation. Using a recently proposed severity classification of BCIS, we estimated the incidence of and risk factors for BCIS and its impact on mortality in cemented hemiarthroplasty for femoral neck fractures. In this retrospective study, 1016 patients undergoing cemented hemiarthroplasty were included. Medical history and medication were obtained from medical records. Anaesthesia charts for all patients were reviewed for mean arterial pressure, arterial oxygen saturation, and heart rate before, during, and after cementation. Each patient was classified as having no BCIS (grade 0) or BCIS grade 1, 2, or 3, depending on the degree of hypotension, arterial desaturation, or loss of consciousness around cementation. The incidence of BCIS grade 1, 2, and 3 were 21%, 5.1%, and 1.7%, respectively. Early mortality in BCIS grade 1 (9.3%) did not differ significantly from BCIS grade 0 (5.2%), while early mortality in BCIS grade 2 (35%) and grade 3 (88%) were significantly higher when compared with grades 0 and 1. Early mortality was also higher in BCIS grade 3 when compared with grade 2. Independent predictors for severe BCIS were: ASA grade III-IV, chronic obstructive pulmonary disease, and medication with diuretics or warfarin. Severe BCIS was associated with 16-fold increase in mortality. BCIS is a commonly occurring phenomenon in cemented hemiarthroplasty and severe BCIS has a huge impact on early and late mortality.

Perfusion Index Derived from a Pulse Oximeter Can Predict the Incidence of Hypotension During Spinal Anaesthesia for Caesarean Delivery

Toyama, S.; Kakumoto, M.; Morioka, M.; Matsuoka, K.; Omatsu, H.; Tagaito, Y.; Numai, T.; Shimoyama, M. Author Information

Adverse events in HEAAL: when to hold and when to fold

This editorial refers to ‘Predicting adverse events during angiotensin receptor blocker treatment in heart failure: results from the HEAAL trial’, by M.S. Kiernan et al., published in this issue on pages 1401–1409. In 2009, the HEAAL investigators 1 reported that losartan 150 mg/ day reduced the rate of death and admissions for heart failure with reduced ejection fraction (HFREF) compared with patients receiving losartan 50 mg/day, the dose previously recommended and evaluated in ELITE II 2 to compare losartan with captopril. This important contribution pointed out the necessity to determine the effective dose of a drug in patients with HFREF rather than relying upon the dose used to lower blood pressure in patients with essential hypertension. In this issue of the journal, the HEAAL investigators 3 report that investigator-reported adverse events (AEs), including kidney impairment, hyperkalaemia, and hypotension, were associated with an increased risk of death compared with those patients who did not experience them, and that these AEs were more frequent in the losartan 150 mg than the losartan 50 mg group. The median serum creatinine on the day of their investigator-reported AE was 1.8 mg/dL, potassium 5.8 mmol/L, and systolic and diastolic blood pressures were 86 and 60 mmHg, respectively. Independent of the dose of losartan, these AEs were more frequent in older patients, those receiving an aldosterone blocker, and in those who reported the incident AE as the reason for intolerance to angiotensin-converting enzyme inhibitor therapy, one of the criteria for treatment with losartan. Baseline levels of serum creatinine were predictive of subsequent renal impairment, while entry levels of serum potassium predicted the occurrence of hyperkalaemia, and baseline systolic blood pressure predicted subsequent hypotension. Diabetes mellitus, baseline haemoglobin, and diuretic use were also predictive of subsequent kidney impairment and hyperkalaemia. However, while these factors were predictive of subsequent AEs, the association between investigator-reported kidney impairment, hyperkalaemia, and hypotension and the excess risk of subsequent death and first hospitalization for HF was independent of these baseline factors. Also of note was the finding that the frequency of these AEs continued to increase over time and was not limited to the period surrounding initiation of therapy with losartan. On the basis of these findings, the HEAAL investigators 3 suggest close monitoring in patients with the baseline risk factors they identified and in patients treated with losartan 150 mg/day. The finding that these AEs were associated with an increase in mortality, while not surprising, is nevertheless of importance and raises the issue of how we can avoid these AEs and how we should respond once they occur. It is important to emphasize that while there were significantly more AEs associated with the use of losartan 150 than 50 mg/day the strategy of losartan 150 mg significantly reduced cardiovascular events in comparison with 50 mg 1 and that the same AEs were associated with an increase in mortality when they occurred in patients on losartan 50 mg. While avoiding these AEs that were associated with an increase in mortality is desirable, it should be pointed out that these AEs are often difficult to predict in an individual patient and may be the cost of some strategies shown to be effective in reducing total mortality in patients with HFREF. One might conclude given the dictum ‘primun non nocere’ that since losartan 150 mg/day is associated with an increase in the incidence of AEs that resulted in an increase in mortality, it is better to avoid this strategy, especially in individuals at high risk for the development of these AEs with losartan such as those with chronic kidney disease, diabetes mellitus, or low haemoglobin, the very old, and those on an aldosterone blocker. These are, however, the very individuals who are at greatest risk and most in need of effective therapy to reduce their cardiovascular risk. Many clinicians have used this reasoning and have, for example, avoided the use of indicated aldosterone blockers in patients with HFREF 4 due to the fear of inducing hyperkalaemia, despite the evidence that aldosterone blockers reduce cardiovascular events even in these high-risk individuals. 5 While close monitoring should be instituted when prescribing losartan or similar agents to patients with the baseline risk factors identified by the HEAAL investigators, 3 the failure to attempt initiation may place the patient at greater risk than that associated with the development of these AEs. A more difficult question is what should one do once these AEs occur in a patient with HFREF. Our initial impulse might be to withhold or reduce the dose of the drug thought to be responsible for

Blood Pressure and Adverse Perioperative Neurologic Outcomes

—Donald Rumsfeld, 2002 In the era of evidence-based medicine, case reports, presenting anecdotal experience of a practitioner, are a vanishing entity in medical journals. It is even more unusual to write an editorial on a case report. But 2 case reports in this issue of the Journal by Drummond et al. touch on the important issue of the role of intraoperative hypotension in the development of neurologic injury and, in doing so, raise a question about whether case reports can or should affect clinical practice. The common theme for the 2 cases reported is that systemic hypotension resulted in devastating central nervous system (CNS) injury (spinal cord and brain, respectively). Systemic hypotension, as a cause of CNS injury, is not a novel concept. What is unusual is the apparent lack of major preoperative risk factors in these patients, other than the operating position (Trendelenburg position in the first case, and beach chair position [BCP] in the second case). The authors propose that the presence of an anatomic variant in the vascular supply of the respective patient (no corroborative evidence of vascular anomaly in the spinal cord in the first case, but a common variant of the circle of Willis in the second case), in conjunction with the systemic hypotension, resulted in a devastating injury. Perhaps more importantly, the question is whether this represents a cause and effect or simple association. The first is a case report of a 19-year-old woman who developed a spinal cord infarction after an ileoanal pullthrough performed under combined general and epidural anesthesia. The epidural catheter was inserted at L3-4 and the infarction involved T9 to conus, which was discovered on day 4 postoperatively, and the actual time of onset of injury was uncertain. Other than the initial test dose, the epidural infusate contained no epinephrine. The hypothesis was that the patient developed spinal cord infarction secondary to induced mild systemic hypotension to control blood loss, with the mean arterial blood pressure (MAP) maintained between 50 to 55 mm Hg for 2.5 hours. (There was some discrepancy between the systolic/diastolic blood pressure and MAP, with the former values lower than the recorded corresponding MAP.) The degree of hypotension was mild, and the authors speculated that the lumbosacral segment of the spinal cord may experience a lower blood pressure than was indicated by the cuff because of the hydrostatic gradient due to the Trendelenburg position, that local pressure within the neuraxis was higher, and/or that the patient may have a “normal congenital” vascular anatomic variation that made her spinal cord vulnerable. The second case involved an otherwise healthy 50-year-old man who underwent a shoulder procedure under general anesthesia in the BCP and subsequently developed a stroke within the distribution of the left middle cerebral artery. Risk factors included hyperlipidemia and history of smoking. Systolic blood pressure, as measured from the arm, was maintained between 95 to 100 mm Hg with a 10minute period at 90 mm Hg. Total anesthesia duration was 137 minutes. Postoperatively, the patient remained unresponsive and a magnetic resonance angiography obtained 4.5 hours later showed ischemic changes in left anterior and middle cerebral artery distribution. Computed tomography angiogram did not reveal any stenosis or occlusion in any of the cerebral arteries. Subsequent magnetic resonance imaging confirmed infarctions in the left frontal, temporal, and parietal lobes. Time-of-flight magnetic resonance angiography demonstrated a predominantly fetal posterior cerebral artery in the right hemisphere with a small proximal segment, absent anterior communicating artery, and the left posterior communicating artery could not be visualized. The authors concluded that a combination of relative systemic hypotension due to the BCP and the anatomic variant of the circle of Willis caused the ischemic infarction. The problem is this: despite a time-honored, tantalizing association between hypotension and adverse neurologic outcome, evidence linking hypotension of this degree and duration to infarction of the CNS is weak and reports of single cases do not make it stronger. In the spinal injury case, there is no indication of “anatomic variation” and the patient underwent a similar surgical procedure (colectomy) 3 months before, with a similar degree of hypotension (by MAP) of uncertain duration, with no neurologic sequelae. Furthermore, a cardiac echo revealed the presence of a patent foramen ovale, and there was evidence of a clot in From the Physician Anesthesia Service, Swedish Neuroscience Institute, Swedish Medical Center, Seattle, Washington.

Limiting the dose of local anaesthetic for caesarean section under spinal anaesthesia - has the limbo bar been set too low?

Limiting the dose of local anaesthetic for caesarean section under spinal anaesthesia - has the limbo bar been set too low?

Rapid Ventricular Pacing for Flow Arrest During Cerebrovascular Surgery

Intraoperative rupture of a cerebral aneurysm can be a devastating event that increases operative morbidity and mortality. Rapid ventricular pacing (RVP) is a technique used in interventional cardiology to obtain flow arrest for short periods of time. To present our experience using RVP for flow arrest during cerebrovascular surgery. We used RVP to produce flow arrest for periods of 40 seconds in 12 patients who underwent craniotomy for a cerebrovascular disorder (11 aneurysms and 1 arteriovenous malformation). During RVP, there was an immediate and significant reduction of blood pressure in each patient. The maximum degree of hypotension was obtained 3.2 ± 0.7 seconds (mean ± SD) after the start of RVP. When RVP was terminated, normal sinus rhythm returned instantaneously, along with recovery of indexes of hemodynamic function. Subjectively, the decrease in blood pressures facilitated dissection, and during clipping, the aneurysm sac felt softer and was easier to manipulate. No complications related to RVP occurred. Rapid ventricular pacing during cerebrovascular surgery is an effective method for lowering the arterial blood pressure in a controlled and directly reversible manner. Advances in cardiology now make RVP a promising and safe technique that can facilitate complex cerebrovascular surgery.

Commentary to “Penile ischemic injury in the exstrophy/epispadias spectrum: New insights and possible mechanisms”

The authors should be commended for this paper, which emphasizes an important yet under-reported pediatric urological issue; namely, penile tissue loss following the surgical treatment of classic bladder exstrophy. They report data from 28 patients who suffered this complication after bladder exstrophy or epispadias repair, and were transferred to their institution, described in the literature or presented in scientific meetings. Understandably some details are missing since the report incorporates cases from other centers, presented at various meetings or collected from limited data provided in the literature. Noticeably, 19 of 20 patients with enough information (as presented in the table) underwent repair in the newborn period and three had the Kelly procedure, which mandates extensive softtissue mobilization. The majority of these children did not undergo concurrent pelvic osteotomies, leading the authors to conclude that this is one of the major factors associated with the development of penile tissue loss. Whereas we agree that osteotomies are an important adjuvant procedure to improve wound closure with less tension, other potential factors are equally or perhaps even more relevant. For instance, in cases with large pubic diastasis significant pelvic tension is produced during approximation, generating high pressures in the underlying structures, with or without osteotomies. Additionally, with primary bladder closure and epispadias simultaneous repair (CPRE), extensive penile and pelvic soft-tissue mobilization is carried out. This dissection is likely to induce reflex vasoconstriction and edema, factors that predispose to ischemia, especially when associated with some degree of hypotension. One can imagine the result of such manipulation when performed in the neonate, who is recognized to be more prone to hypothermia and hemodynamic instability. Therefore, it comes with no surprise that the vast majority of patients in this paper were newborns undergoing CPRE. However, there are unquestionable benefits associated with CPRE performed in the neonatal period. Improved bladder capacity and continence have been observed after CPRE and are likely related to the increased urethral resistance generated by the deep pelvic positioning of the proximal urethra during this repair. This has been considered a good reason to perform this extensive repair in the newborn period. However, it carries an increased risk of developing penile tissue loss, as demonstrated in this series. In order to maintain some of the advantages of CPRE we developed an alternative strategy for the primary closure of bladder exstrophy. Aiming to increase urethral resistance, but without concomitant epispadias repair, we have been performing bladder neck tailoring and concurrent bilateral ureteral reimplantations during the primary closure of exstrophy [1]. In this way, urethral resistance and early bladder cycling can be safely achieved, factors that ultimately may be relevant to improving bladder capacity and possibly urinary continence. Another aspect explored by the authors is the grade of expertise of the surgeons performing CPRE. Although this speculation is appealing, only 5 out of 28 surgeons did not have fellowship training, implying that the surgeon’s

Diversified cardiovascular actions of six homologous natriuretic peptides (ANP, BNP, VNP, CNP1, CNP3, and CNP4) in conscious eels

The natriuretic peptide (NP) family consists of seven paralogs [atrial NP (ANP), brain NP (BNP), ventricular NP (VNP), and C-type NP 1-4 (CNP1-4)] in teleosts, but relative biological activity of the seven NPs has not been comprehensively examined using homologous peptides. In this study, we newly identified CNP3 and CNP4 in eels to use homologous peptides, but the CNP2 gene may have been silenced in this species. The CNP4 gene was expressed exclusively in the brain as CNP1, but the CNP3 gene, from which cardiac ANP, BNP, and VNP were generated by tandem duplication, was most abundantly expressed in the pituitary, suggesting its local action. All NPs induced hypotension dose dependently after intra-arterial injection with a potency order of ANP > VNP > BNP > CNP4 > CNP1 = CNP3. The degree of hypotension was similar at the ventral and dorsal aorta, indicating similar actions on the branchial and systemic circulation. The hypotension induced by cardiac NPs was longer lasting than CNPs, probably because of the difference in preferential receptors. Among cardiac NPs, the hypotensive effect of VNP lasted much longer than those of ANP and BNP, even though VNP disappeared from the blood more quickly than ANP. To analyze the unique effect of VNP, we examined possible involvement of the autonomic nervous system using ANP, VNP, and CNP3. Beta-adrenergic blockade diminished hypotensive effects of all three NPs, but alpha-adrenergic and cholinergic blockade enhanced only the effect of VNP, suggesting a specific mechanism for the VNP action. The NP-induced tachycardia was diminished by all blockers examined. Furthermore, the cardiovascular action of VNP was not impaired by a blocker of NP receptor, HS-142-1. Taken together, the homologous NPs exhibit diverse cardiovascular actions in eels partially through the autonomic nervous system, and the unique VNP action may be mediated by a novel receptor that has not been identified in teleosts.

WHAT'S NEW IN SHOCK, OCTOBER 2009?

WHAT'S NEW IN SHOCK, OCTOBER 2009?

Hemorrhagic Fever with Renal Syndrome

Hemorrhagic fever with renal syndrome (HFRS) is an acute febrile illness caused by Eurasian hantaviruses and characterized by renal insufficiency, hemorrhage, thrombocytopenia, and shock. Each hantavirus is primarily associated with a single rodent host species or genus, and is transmitted to human via aerosols of rodent excreta. During the last decades, clinical features of HFRS in Korea have changed with mild degree of hypotension and very low prevalence of oliguria. Treatment of HFRS is mainly supportive. Recently, however, treatment of HFRS patients with ribavirin in China and Korea, within 7 days after the onset of fever, resulted in a reduced mortality as well as shortened course of illness. Although a commercial inactivated Hantaan virus vaccine has been on the market in Korea for more than 15 years, the effect of vaccination is not clear. Further efforts are necessary to develop safer and more effective hantavirus vaccines.

Insufficient Vasopressin Release From Adequate Pituitary Stores Contributes to Inappropriately Low Plasma Vasopressin Levels in the Acute Response to Septic Shock

Inadequate endogenous vasopressin (eVP) levels have been well described in catecholamine resistant hypotension in the setting of septic shock. In a piglet model of endotoxin (ETX) induced septic shock, we examined possible mechanisms for why eVP may not achieve adequate levels to reverse hypotension. eVP response to a 37% decrease in mean arterial pressure achieved levels of 150 ± 10 pg/mL (n=45) which were not sufficient to raise blood pressure. Plasma VP (pVP) levels achieved with pharmacologically administered vasopressin (VP) at 1, 10, and 100 ng/kg/min revealed that pVP levels of at least 400 pg/mL were needed to reverse hypotension (p<0.05). For piglets given ETX, pituitary levels of VP were measured and found to still contain adequate stores (735 ± 51 ng/pit) although decreased from non‐ETX controls (1297 ± 290 ng/pit) . Next we examined whether eVP could be further released by other stimuli in the face of endotoxic hypotension. Dopamine was infused in piglets who had the same degree of hypotension as untreated controls and was found to further increase pVP to 203.5 pg/mL ± 34.5, p<0.02. Given these results it appears that the pituitary has the stores and the capacity to release more eVP in septic shock. The mechanism responsible for low levels of pVP therefore seems to be due at least in part to the inability of the pituitary to adequately release the hormone in response to endotoxin‐induced hypotension.

Anthrax Toxins Induce Shock in Rats by Depressed Cardiac Ventricular Function

Anthrax infections are frequently associated with severe and often irreversible hypotensive shock. The isolated toxic proteins of Bacillus anthracis produce a non-cytokine-mediated hypotension in rats by unknown mechanisms. These observations suggest the anthrax toxins have direct cardiovascular effects. Here, we characterize these effects. As a first step, we administered systemically anthrax lethal toxin (LeTx) and edema toxin (EdTx) to cohorts of three to twelve rats at different doses and determined the time of onset, degree of hypotension and mortality. We measured serum concentrations of the protective antigen (PA) toxin component at various time points after infusion. Peak serum levels of PA were in the µg/mL range with half-lives of 10–20 minutes. With doses that produced hypotension with delayed lethality, we then gave bolus intravenous infusions of toxins to groups of four to six instrumented rats and continuously monitored blood pressure by telemetry. Finally, the same doses used in the telemetry experiments were given to additional groups of four rats, and echocardiography was performed pretreatment and one, two, three and twenty-four hours post-treatment. LeTx and EdTx each produced hypotension. We observed a doubling of the velocity of propagation and 20% increases in left ventricular diastolic and systolic areas in LeTx-treated rats, but not in EdTx-treated rats. EdTx-but not LeTx-treated rats showed a significant increase in heart rate. These results indicate that LeTx reduced left ventricular systolic function and EdTx reduced preload. Uptake of toxins occurs readily into tissues with biological effects occurring within minutes to hours of serum toxin concentrations in the µg/mL range. LeTx and EdTx yield an irreversible shock with subsequent death. These findings should provide a basis for the rational design of drug interventions to reduce the dismal prognosis of systemic anthrax infections.

Incidence and Types of Arrhythmias After Mediastinal Manipulation During Transhiatal Esophagectomy

Transhiatal esophagectomy (THE) is a common operative procedure for carcinoma esophagus. Complications of this procedure include arrhythmias and hypotension during blunt dissection of the esophagus from posterior mediastinum. In the literature, exact incidence and type of arrhythmias have not been reported. We employed Holter monitoring during mediastinal manipulation in patients undergoing THE, for this purpose. This prospective study was carried out in 20 consecutive American Society of Anesthesiologists grade I-II patients undergoing THE. Anesthetic technique included induction with thiopentone and maintenance with morphine, vecuronium, and isoflurane. In addition to routine parameters, Holter monitoring was undertaken to record the exact incidence and types of arrhythmias. "Premanipulation" or control period included duration of 30 minutes preceding mediastinal manipulation, while "during manipulation" or study period included the duration of mediastinal manipulation. The incidence of arrhythmias was studied for 48 hours in the postoperative period. The Fisher exact test was applied to analyze incidence of arrhythmias and hypotension. Out of 20 patients, only 2 had arrhythmias in the premanipulation period, while 13 had arrhythmias during the manipulation period (p < 0.01). During the manipulation period, arrhythmias included supraventricular ectopics and ventricular ectopics in 2 patients each and a combination of both in 9 patients. Arrhythmias were transient and had no correlation with either duration or degree of hypotension in all the patients. However, there was a linear relationship between hypotension and duration of mediastinal manipulation. Two patients (10%) had atrial arrhythmias in the postoperative period. In transhiatal esophagectomy, there is a significant incidence of both arrhythmias and hypotension during mediastinal manipulation. The incidence of arrhythmias can be minimized by limiting the duration of the manipulation. The incidence of postoperative arrhythmias was not significant.

Heart Rate Variability Predicts Severe Hypotension after Spinal Anesthesia

Hypotension due to vasodilatation after spinal anesthesia (SA) may be harmful. Heart rate variability, an indirect measure of autonomic control, may predict hypotension. One hundred patients were studied. Retrospectively, heart rate variability was analyzed in 30 patients, classified depending on the lowest systolic blood pressure (SBP) after SA. Seventy patients were studied prospectively, assigned to one of two groups by their low to high frequency ratio (LF/HF) before SA. Sensitivity and specificity of LF/HF for prediction of decrease of SBP greater 20% of baseline were tested. Retrospective analysis showed differences of LF/HF depending on the degree of hypotension after SA. Prospective analysis demonstrated significant differences of SBP after SA depending on baseline LF/HF (mean +/- SD): low LF/HF (1.3 +/- 0.7) = > SBP: 91 +/- 8% of baseline versus high LF/HF (5.5 +/- 2.4) = > SBP: 66 +/- 10% of baseline (P < 0.05). Baseline LF/HF as well as high frequency and proportional decrease of SBP after SA correlated significantly, in contrast to baseline hemodynamic parameters heart rate and SBP. A receiver operator curve characteristic analysis showed a sensitivity and specificity of LF/HF > 2.5 of 85% to predict SBP decrease of greater than 20% of baseline after SA. Heart rate variability analysis before SA may predict hypotension after SA with high sensitivity and specificity. LF/HF may be a tool to detect patients at high risk of hypotension due to SA. This indicates that the predictive value of LF/HF is superior to established predictors.

Complications and Carotid Stenting

Puncture site: Carotid stenting should be undertaken within an interventional (endovascular) program in which personnel are familiar with efficient and safe arterial sheath removal with minimal patient discomfort. Adequate hydration and pretreatment with atropine can prevent and treat hypotension associated with a vaso-vagal response to sheath removal. An unexplained decrease in blood pressure may be caused by retroperitoneal bleeding. Closure devices are recommended if used by trained personnel. Complications of closure devices could be disastrous (hematoma, infection, torn artery). The occurrence of spasm in the distal internal carotid artery is a common angiographic event caused by the mechanical irritation of the vessel. It usually resolves spontaneously after the catheter or guide wire has been removed. Usage of 0.014-inch softtipped wires minimizes the occurrence of spasm. Injections of 100 to 200 mg of nitroglycerine through the carotid access sheath will hasten the resolution of spasm. Spasm must be differentiated from kinking of the internal carotid artery. Bradycardia and episode of transient asystole are not uncommon during balloon inflations within the carotid bulbous. More prolonged hypotension and bradycardia were seen with balloon-expandable stents which place more sustained pressure on the baroreceptors. Both, bradycardia and asystole during balloon inflation are transient and respond promptly to balloon deflation. Prevention is pre-medication with atropine. Larger doses of atropine should be avoided in elderly patients. Hypotension is not uncommon after carotid stenting and may last from hours to days, depending on the sensitivity of the baroreceptors, the type of stent used, and whether CAS was performed bilaterally. The degree of hypotension appears to be more pronounced in heavily calcified lesions. Usually, there are no clinical sequelae and the modest decrease in blood pressure requires no specific intervention. Bed rest, sedation or narcotics exacerbate hypotension and mitigate against rapid ambulation and recovery. Patients, particularly the elderly, should be assisted with ambulation if Complications and Events Encountered During Carotid Stenting

Critical incidents: the cardiovascular system

Perioperative hypertension may precipitate myocardial ischaemia, haemorrhage at the operative site and elsewhere, and neurological complications. Whether it needs to be treated depends on its cause, severity and duration, and the condition of the patient. Treatment should be directed towards the underlying cause. If the cause cannot be found, an antihypertensive drug may be used. Mild to moderate hypotension is common during anaesthesia, but seldom results in any harm to the patient. It is unclear when the degree of hypotension is dangerous. Management is directed towards the underlying cause. Supportive treatment includes maintaining oxygenation, supine positioning, intravenous fluids and vasoactive drugs. Massive haemorrhage is a significant cause of mortality and morbidity because of the loss of blood volume and its constituents, and also the effects of the infusion of products aimed at compensating for the loss. It is essential to restore an adequate circulating blood volume rapidly and effectively. Initially, warm fluids (crystalloids and/or colloids) should be given intravenously. Red cell transfusions are given to increase the haemoglobin concentration and improve oxygen delivery to the tissues. About 80% of patients develop diffuse ooze from cut surfaces. The causes are multifactorial. Infusions of platelets, fresh frozen plasma and/or cryoprecipitate may be required. Perioperative arrhythmias are common. Treatment is required if there is a risk of developing ventricular tachycardia or fibrillation, a significant decrease in cardiac output or evidence of myocardial ischaemia. Fluid, electrolyte and acid-base disturbances should be corrected. Intervention can be with a specific antiarrhythmic agent or DC cardioversion.

Combination Spinal Analgesic Chemotherapy: A Systematic Review

Combination Spinal Analgesic Chemotherapy: A Systematic Review

Combination spinal analgesic chemotherapy: a systematic review.

Combination spinal analgesic chemotherapy: a systematic review.

Clonidine for treatment of postoperative pain: a dose-finding study

The aim of this double-blind randomized study was to evaluate the optimal intravenous dose of clonidine administrated during the peri-operative period, after lumbar hemilaminectomy for herniated disk repair. The ‘optimal intravenous dose’ was defined as that providing minimal analgesic request, stable haemodynamic profile and a minimal sedation score during 12h after extubation. Eighty adult patients, ASA physical status I–II, undergoing lumbar hemilaminectomy for herniated disk (L4–L5, L5–S1) were included in the study. All the patients were randomly assigned to one of four study groups (A, B, C, D), 20 patients each. The same standardized general anaesthesia was performed for each group. Thirty minutes before the end of surgery, group A, B and C patients received three different loading doses of intravenous clonidine (5μg/kg, 3μg/kg, 2μg/kg respectively), followed by the same infusion of intravenous clonidine (0.3μg/kg per hour). Group D patients received a bolus dose and a continuous infusion of NaCl 0.9%. In the recovery unit, postoperative pain was treated by a patient-controlled analgesia device, containing morphine. Pain relief was evaluated by the total morphine requirement during the postoperative period. Systolic blood pressure (SBP), heart rate and sedation were also noted during the first 12h postoperatively. Intravenous clonidine decreased morphine requirements in a dose-dependent manner. Group A, B, C and D patients requested 5±2, 11±3, 19±4 and 29±8 doses of morphine respectively. Clonidine also affected SBP in a dose-related manner. Group A, B and C patients had an SBP decrease respectively of 26±3%, 7±4% and 2±2% compared with basic values while, at the same time, in group D patients no SBP variation was registered. In conclusion, this study demonstrates that, when sedation and analgesic effect of clonidine is required, 3μg/kg bolus dose followed by a continuous infusion of 0.3μg/kg per hour has to be considered the optimal intravenous dose. The higher dose of intravenous clonidine (5μg/kg) produced better analgesia but the degree of hypotension and sedation was more severe and longer lasting; it required ephedrine administration and careful monitoring of the patient. On the other hand, the bolus of intravenous clonidine 2μg/kg (group C) was less effective in terms of pain relief but with similar side-effects to the 3μg/kg dosage (group B).

Effect of Calcium Chloride on Protamine Sulfate-Induced Systemic Hypotension in Adult Open-Heart Patients

Background: Protamine sulfate (PS), used to neutralize the anticoagulant effect of heparin, is often associated with systemic hypotension. The present study was aimed to investiate the protective effects of calcium chloride () on adverse hemodynamic reactions to PS in patients undergoing open heart surgery. Methods: After IRB approval, sixty-one patients undergoing open heart surgery were allocated randomly to receive either saline 10 ml (control group, n = 26), 5 mg/kg ( 5 group, n = 18) or 10 mg/kg ( 10 group, n = 18), added to PS 3 mg/kg given over 3 min through the right atrium to reverse heparinization. Hemodynamic measurements, including systolic (SAP), diastolic (DAP), and mean arterial pressure (MAP), heart rate, and central venous pressure (CVP) were continuously recorded in a baseline condition and up to 10 minutes after PS infusion. Plasma level and arterial blood gas tension were also measured. Results: PS caused immediate and significant decreases in SAP, DAP, and MAP in all three groups. However, the degree of hypotension was significantly less in the 10 group than in the 5 and control groups. Heart rate and CVP remained unchanged throughout the study in all groups. Intravenous 5 and 10 mg/kg IV caused an increase in plasma by 0.13 0.08 mM and 0.45 0.08 mM at 2 min after its injection, respectively. Arterial oxygen tension did not change significantly throughout the study in any group. Conclusions: These results suggest that simultaneous administration of 10 mg/kg attenuates the hypotensive effect of PS used to reverse heparin anticoagulation in patients undergoing open heart surgery. However, hypotensive reactions may still occur