HAEMODYNAMIC EFFECTS OF DOPAMINE AND DOPAMINE COMBINED WITH NITROGLYCERIN IN PATIENTS SUBJECTED TO CORONARY BYPASS SURGERY

The haemodynamic effects of dopamine and dopamine with nitroglycerinwere evaluated in eight patients with coronary heart diseasewho underwent aortocoronary bypass surgery. The study was performedunder anaesthesia and before surgery. Dopamine 8 µg kg^–1min^–1 alone produced a marked increase of the cardiacindex from 2.47 to 3.47 litre min^–1 m^–2 but onlysmall changes in heart rate (from 65 to 68 beat min^–1).This improvement in cardiac performance was accompanied by anincrease of the mean pulmonary artery pressure from 10.9 to21.3 mm Hg and in the left ventricular filling pressure from6.1 to 13.8 mm Hg with unchanged systemic and pulmonary vascularresistance. Mean arterial pressure increased from 72 to 103mm Hg. Simultaneous infusion of dopamine (8 µg kg^–1min^–1 and nitroglycerin (mean dose 0.5 µg kg^–1min^–1) resulted in a favourable reduction of mean pulmonaryartery pressure (from 21.3 to 14.4 mm Hg) and of left ventricularfilling pressure (from 13.8 to 7.9 mm Hg). Cardiac index (from3.47 to 3.34 litre min^–1 m^–2) and mean arterialpressure (from 103 to 95 mm Hg) were not reduced to the sameextent by the addition of nitroglycerin. The combined treatmentof dopamine with nitroglycerin seems to be of value in patientswith pre-existing high lseft ventricular filling pressure orwith pulmonary hypertension.     

THE EFFECTS OF DROPERIDOL AND FENTANYL ON INTRACRANIAL PRESSURE AND CEREBRAL PERFUSION PRESSURE IN NEUROSURGICAL PATIENTS

The effects of droperidol and fentanyl on the intracranial pressure(i.c.p.) and cerebral perfusion pressure (c.p.p.) were studiedin eight anaesthetized normocapnic patients with intracranialspace-occupying lesions. The injection of droperidol resultedin a small and not significant increase in i.c.p. from 24.0to 27.2 mm Hg, while c.p.p. decreased from 75.9 mm Hg to 57.8mm Hg, as a result of a decrease in systemic arterial pressure.The addition of fentanyl produced no change in i.c.p., but afurther decrease in arterial pressure decreased c.p.p. from60.4 mm Hg to 47.8 mm Hg. In four patients values of c.p.p.less than 40 mm Hg were obtained. C.p.p. was increased by hyperventilationin all but one of these patients. It is concluded that droperidoland fentanyl should be used in patients with intracranial hypertensiononly if hypocapnia has been established and when the arterialpressure is normal or increased. ^*Present address: Department of Anaesthesia, Bornholm, Centralsygehüs,3700 Rønne, Denmark.     

EFFECTS OF HALOTHANE AND SODIUM NITROPRUSSIDE ON RENAL FUNCTION AND AUTOREGULATION

The effects of sodium nitroprusside and halothane on renal autoregulationand kidney function were studied in 14 mongrel dogs at meanarterial pressures of 120, 100, 80, 60 and 40mm Hg. In group1, stepwise decreases in mean arterial pressure were achievedby increasing the halothane concentration In group II, meanarterial pressure was decreased by infusing sodium nitroprussideduring halothane anaesthesia. In group I, renal blood flow decreasedsignificantly at mean arterial pressures of 100, 80, 60 and40mmHg. In group II, renal blood flow was well maintained atmean arterial pressures of 100 and 80 mm Hg, but decreased significantlyat 60 and 40 mm Hg; at these low pressures flow was greaterin group II than in group I. There were no significant differencesbetween two groups in inulin clearance, inulin clearance/renalplasma flow, urine output, urine osmolanty and sodium excretionrate. Significantly larger fractions of cardiac output weredistributed to the kidneys in group I. ^*Present address: Department of Anaesthesia, Teikyo UniversitySchool of Medicine, Tokyo, Japan.     

THE CENTRAL AND PERIPHERAL CIRCULATION DURING AND AFTER SODIUM NITROPRUSSIDE INDUCED HYPOTENSION IN THE RAT

Central haemodynamics and regional blood flow were investigatedduring and after sodium nitroprusside (SNP) infusion in halothaneanaesthetized rats. The administration of SNP 40 (µg kg^–1min^–1, decreased mean arterial pressure (MAP) to 52 (mean)mm Hg. Cardiac output (CO) remained unchanged, while heart rate(HR) and systemic vascular resistance (SVR) decreased. The regionalblood flow in the splanchnic organs increased. When the SNPinfusion was discontinued, MAP returned rapidly to, but notabove, its initial vahie. Fifteen minutes later, CO was increased,while SVR and HR remained decreased. Cerebral, myocardial andrenal perfusion increased and the changes in the splanchnicarea persisted. It is obvious that, although MAP was reversedrapidly upon withdrawal of SNP, central and regional haemodynamiceffects were prolonged     

THE RESPONSE OF CANINE INTRACRANIAL PRESSURE TO SYSTEMIC HYPOTENSION INDUCED WITH NITROGLYCERINE

Changes in intracranial pressure were studied in 18 greyhoundsin relation to decreases in systemic arterial pressure producedby nitroglycerine At normal values of i.c.p. (< 12 mm Hg)GTN produced an increase in i.c.p. of 3.1 (±0 6) mmHg(mean±SEM). Under conditions of increased i.e.p. (12mm Hg) small decreases in mean arterial pressure (m a p.) (<25% control) were associated with an increase of 4.7 (±0.5)mm Hg, whereas larger decreases in m.a.p. (>25% control)were associated with a decrease of 3.2 (±0.9) mm Hg ini.c.p. In 11 of 19 observations in which a decrease in intracranialpressure had occurred in association with systemic hypotensionthere was a rebound increase in i.c.p. as m a.p. was restored.It is suggested that i.c.p be decreased before this drug isused to produce hypotension during neurosurgery. ^*Present addresses: University Hospital of South Manchester,Manchester. Present addresses: Department of Anaesthetics and IntensiveCare, University Hospital of the West Indies, Mona, Kingston7, Jamaica, West Indies.     

The effects of 10 degrees reverse trendelenburg position on ICP and CPP in prone positioned patients subjected to craniotomy for occipital or cerebellar tumours

Summary. Summary.   Background: Control of ICP-hypertension is of utmost importance during craniotomy. The effects of reverse Trendelenburg position (RTP) upon ICP and CPP have recently been studied in supine positioned patients.   Method: In this study we investigated changes in intracranial pressure (ICP), mean arterial blood pressure (MABP), CPP and jugular bulb pressure (JBP) before and one minute after 10^° RTP in 26 prone positioned patients with either occipital (n=12) or cerebellar tumours (n=14). ICP was measured by a subdural approach after removal of the bone flap. Tension of the dura was estimated by the surgeons by digital palpation before and after change in position.   Findings: In patients with occipital tumours ICP decreased from 21.0 to 15.6 mm Hg (p<0.05). MABP decreased from 87.9 to 83.3 mm Hg (p<0.05), JBP decreased from 14.3 to 7.7 mm Hg (P<0.05), while CPP was unchanged. In patients with cerebellar tumours ICP decreased from 18.3 to 14.2 mm Hg (p<0.05). MABP decreased from 93,8 to 90.5 mm Hg (p<0.05), JBP decreased from 12.1 to 5.0 mm Hg (P<0.05), while CPP was unchanged. There were no significant differences between the two groups with regard to changes in ICP, MABP, CPP and JBP. The change in ICP was accompanied by a significant decrease in dural tension (p<0.05).   Interpretation: In prone positioned patients 10^° RTP significantly reduces ICP, JPB and MABP within one minute, while CPP is unchanged. Published online July 18, 2002     

EFFECT OF PROPOFOL ON BRAIN RETRACTION PRESSURE AND CEREBRAL PERFUSION PRESSURE

We have studied the effect of propofol, at a rate of 30 mg kg^–1h^–1 for 5 min reducing to 6 mg kg^–1 h^–1 fora further 5 min, on brain retraction pressure (BRP) in 15 patientsundergoing craniotomy. The response of BRP showed two distinctpatterns. BRP was reduced by an average of 3.3 mm Hg (P = 0.005).Mean arterial pressure was reduced in all patients by an averagemaximum of 28.3 mm Hg (P < 0.001), which caused a significantreduction in cerebral perfusion pressure (CPP) by 22.9 mm Hg(P < 0.001). It is concluded that, by reducing BRP, propofolprovided suitable conditions for intracranial surgery, but careshould be taken to avoid excessive reduction in CPP.     

EFFECTS OF HYPOTENSION INDUCED BY HALOTHANE, ON THE CEREBRAL CIRCULATION IN BABOONS WITH EXPERIMENTAL RENOVASCULAR HYPERTENSION

The effect of graded, progressive hypotension on the autoregulationof cerebral blood flow was studied in anaesthetized baboonswith experimental renovascular hypertension. Graded hypotensionwas induced over a period of 5–6 h by the administrationof increasing concentrations of halothane. In these chronicallyhypertensive animals cerebral blood flow remained constant untilthe mean arterial pressure had decreased to approximately 90mm Hg. At mean arterial pressures of less than this value cerebralblood flow was pressure passive. At the completion of the investigationthe brains were fixed by perfusion and submitted to neuropathologicalexamination. Evidence of chronic hypertension and of ischaemicbrain damage was found in every animal. ^* Present address: Cardiac Department, The Radcliffe Infirmary,Oxford.     

Reverse Trendelenburg position reduces intracranial pressure during craniotomy.

Cerebral swelling and herniation pose serious surgical obstacles during craniotomy for space-occupying lesions. Positioning patients head-up has been shown previously to reduce intracranial pressure (ICP) in neurotraumatized patients, but has not been investigated during intracranial surgery. The current study examined the effects of 10-deg reverse Trendelenburg position (RTP) on ICP and cerebral perfusion pressure (CPP). Forty adult patients subjected to craniotomy for supratentorial tumors were given standardized propofol-fentanyl-cisatracurium general anesthesia and were moderately hyperventilated. In 26 of 40 patients with expected poor clinical outcome, an additional catheter was placed in the internal jugular bulb to determine internal jugular bulb pressure (JBP). ICP was determined by subdural measurement using a 22-gauge needle advanced through the dura after removal of the bone flap. ICP was referenced to the level of the dural incision. ICP, mean arterial blood pressure, and CPP were compared with repeat measurements 1 minute after RTP. The tension of the dura was graded qualitatively by the surgeon by digital palpation and was compared to post-RTP. ICP decreased from 9.5 mm Hg to 6.0 mm Hg ( P <.001; all values are median) within 1 minute after 10-deg RTP. Mean arterial blood pressure decreased from 82.0 mm Hg to 78.5 mm Hg ( P <.001). CPP was unchanged (70.5 mm Hg versus 71 mm Hg after RTP), whereas JBP decreased from 8 mm Hg to 4 mm Hg ( P <.001). High initial ICP was correlated to the greatest magnitude of decrease in ICP. No significant correlation was found between change in ICP and change in JBP. Intracranial pressure after RTP resulted in decreased tension of the dura. RTP appears to be an effective means of reducing ICP during craniotomy, thereby reducing the risk of cerebral herniation. CPP is not affected. Studies over longer periods of time are warranted, however.     

ATTENUATION OF THE PRESSOR RESPONSE TO TRACHEAL INTUBATION IN HYPERTENSIVE PROTEINURIC PREGNANT PATIENTS BY LIGNOCAINE, ALFENTANIL AND MAGNESIUM SULPHATE

The pressor response to intubation is known to be exaggeratedin patients with gestational proteinuric hypertension (GPH).The effect of pretreatment with lignocaine 1.5 mg kg^–1,magnesium sulphate 40 mg kg^–1 or alfentanil 10 µgkg^–1 on this pressor response was studied in 69 patientswith moderate to severe GPH. Systolic arterial pressure exceededbaseline values for the first 5 min after tracheal intubationin the lignocaine group, with a peak increase of 31.6 (SEM 3.6)mm Hg at 2 min after intubation, but no mean increase in pressureoccurred in the two other groups. Following intubation, sixof 24 mothers in the alfentanil group, six of 21 in the lignocainegroup and one of 24 in the magnesium group (P < 0.05) exhibiteda systolic arterial pressure (SAP) greater than 180 mm Hg sustainedfor 2 min or more. Alfentanil caused the least change in heartrate, but resulted in significant fetal depression.     

RAPID ADMINISTRATION OF CRYSTALLOID PRELOAD DOES NOT DECREASE THE INCIDENCE OF HYPOTENSION AFTER SPINAL ANAESTHESIA FOR ELECTIVE CAESAREAN SECTION

Twenty parturients undergoing elective Caesarean section wereallocated randomly to receive crystalloid preload 20 ml kg^–1over either 20 min or 10 min before spinal anaesthesia. Significanthypotension (systolic arterial pressure <100mm Hg and <80% of baseline value) occurred in six of the 10 patients inthe 20-min preload group and seven of 10 patients in the 10-minpreload group (ns). Both groups had a significant (P < 0.05)increase in central venous pressure during the preload period.The mean central venous pressure in the 10-min group was 11.9mm Hg (range 6–19 mm Hg), which was significantly greater(P < 0.05) than that in the 20-min group (mean 7.3 mm Hg,range 2–13 mm Hg). Three patients in the 10-min grouphad clinically unacceptable increases in central venous pressure.This study has demonstrated that rapid administration of crystalloidpreload before spinal anaesthesia did not decrease the incidenceor severity of hypotension, and questions the role of crystalloidpreload.     

Intraperitoneal carbon dioxide insufflation and cardiopulmonary functions. Laparoscopic cholecystectomy in pigs.

We studied the effects of laparoscopic cholecystectomy on respiratory and hemodynamic function in eight adult pigs. Minute ventilation was adjusted to normalize baseline arterial blood gases, then fixed throughout carbon dioxide insufflation. A metabolic measurement cart recorded total CO2 excretion, oxygen consumption, and minute ventilation. Carbon dioxide pneumoperitoneum was maintained at a constant pressure of 15 mm Hg as cholecystectomy was performed. After 1 hour of insufflation, CO2 excretion increased from 115 +/- 10 mL/min to 149 +/- 9 mL/min but O2 consumption remained unchanged. The PaCO2 increased from 35 +/- 2 mm Hg to 49 +/- 3 mm Hg and arterial pH fell from 7.47 +/- 0.02 to 7.35 +/- 0.03. Systemic and pulmonary hypertension occurred and stroke volume dropped from 35.5 +/- 3.5 mL to 28.6 +/- 2.2 mL with compensatory tachycardia. Right atrial pressure remained unchanged as inferior vena cava pressure increased to reflect the intraperitoneal pressure. We conclude that CO2 pneumoperitoneum resulted in significant transperitoneal CO2 absorption, with secondary hypercapnia and acidemia. The accumulation of CO2 was also associated with an increase in systemic and pulmonary arterial pressure. Heart rate increased to compensate for the decreased stroke volume to maintain cardiac output.     

HAEMODYNAMIC STUDIES DURING INDUCTION OF ANAESTHESIA FOR OPEN-HEART SURGERY USING DIAZEPAM AND KETAMINE

In 14 patients undergoing open-heart operations the haemodynamiceffects of diazepam 0.4 mg kg-¹ followed by ketamine 2 mg kg-¹were studied. In eight patients undergoing coronary bypass surgery,the mean arterial pressure decreased significantly after diazepamfrom 90.3±7.4 (SEM) to 78.0±5.0 mm Hg (P <0.05). However, no changes occurred in six patients undergoingvalve replacement. The subsequent administration of ketamineproduced no significant changes in mean arterial pressure. Nosignificant change in heart rate occurred in any patient atany time during the period of study. No patient reported unpleasantemergence reactions after operation. ^*Present address for correspondence: c/o University Departmentof Anaesthesia, Queen Elizabeth Hospital, Birmingham B15 2TH.     

CARDIOVASCULAR SUPPORT DURING COMBINED EXTRADURAL AND GENERAL ANAESTHESIA

We have examined the effect of prophylactic treatment with i.v.fluid 1000 ml, ephedrine 24mg or methoxamine 4 mg on cardiovascularresponses to both extradural and combined extradural and generalisoflurane anaesthesia in 45 adult patients undergoing kneearthroplasty. Heart rate (HR) and systemic arterial pressure(AP) were measured using automated oscillotonometry and cardiacoutput was measured using continuous wave suprasternal Dopplerultrasonography. After lumbar extradural anaesthesia (LEA) therewere no significant differences in arterial pressure betweentreatments, although cardiac index was significantly greaterafter fluid preloading (mean 4.3 (95% confidence interval 3.7–4.9)litre min^–1 m^–2 than after ephedrine (3.1 (2.6–3.6)litre min^–1 m^–2 or methoxamine (2.6 (2.0–3.2)litre min^–1 m^–2 During combined LEA and generalanaesthesia, systolic AP was significantly greater after ephedrine(114 (103–125) mm Hg) than after either preloading (98(88–107) mm Hg) or methoxamine (97 (89–105) mm Hg).The reduction in AP after induction of general anaesthesia wasassociated with a decrease in cardiac index after fluid preloadingand a decrease in vascular resistance after methoxarnine.     

Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

Profound arterial hypotension is a commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.     

Effects of nifedipine on intracranial pressure in neurosurgical patients with arterial hypertension

The effects of nifedipine, 20 mg administered via a nasogastric tube, on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were examined. Nifedipine was administered to treat arterial hypertension (greater than 180 mm Hg, systolic). Ten measurements were made in eight patients with cerebrovascular disease or head trauma. The mean arterial blood pressure (MABP) and ICP were measured before and for 30 minutes after the administration of nifedipine. The MABP gradually decreased and reached its lowest value at approximately 10 minutes after initiation of nifedipine administration, and thereafter remained unchanged. The MABP decreased significantly from 128 +/- 8 (mean +/- standard deviation) to 109 +/- 7 mm Hg, and the CPP decreased from 105 +/- 11 to 84 +/- 10 mm Hg. The ICP increased by 1 to 10 mm Hg in eight of 10 measurements, and the mean change of ICP from 19 +/- 7 to 22 +/- 6 mm Hg was statistically significant. These changes were not accompanied by alterations in neurological signs. The results suggest that enteral nifedipine produces a small but statistically significant increase in ICP. Accordingly, neurological signs must be closely observed to detect deterioration, which can be caused by an increase in ICP and/or a decrease in CPP.     

EFFECT OF BOLUS DOSES OF MIDAZOLAM ON INTRACRANIAL PRESSURE AND CEREBRAL PERFUSION PRESSURE IN PATIENTS WITH SEVERE HEAD INJURY

We have studied the effects of bolus doses of midazolam 0.15mg kg^–1 i.v. on intracranial pressure (ICP), mean arterialpressure (MAP) and cerebral perfusion pressure (CPP) in 12 patientswith severe head injury (Glasgow Coma Scale score 6). The studywas performed in patients aged 17–44 yr who were sedated(phenoperidine 20 µg kg^–1 h^–1) and paralysed(vecuronium 2 mg h^–1). Midazolam reduced MAP from 89.0mm Hg to 75.0 mm Hg (P<0.0001), while CPP decreased from71.0 mm Hg to 55.8 mm Hg (P<0.0001). During the study, CPPdecreased to less than 50 mm Hg in four patients. Midazolaminduced small, non-significant changes in ICP. However, whencontrol ICP was less than 18 mm Hg (n=7 patients), an increasein ICP was observed. The remaining five patients (control ICP18 mm Hg) exhibited a slight decrease in ICP. These findingssuggest that bolus administration of midazolam should be performedwith great caution in patients with severe head injury, especiallywhen ICP is less than 18 mm Hg.     

EFFECT OF PROSTAGLANDIN E1-INDUCED HYPOTENSION ON CARBON DIOXIDE REACTIVITY AND LOCAL CEREBRAL BLOOD FLOW AFTER SUBARACHNOID HAEMORRHAGE

The effect of prostaglandin E, (PGE,) on local cerebral bloodflow (LCBF) and carbon dioxide reactivity (CO₂R) was studiedduring cerebral aneurysm surgery for subarachnoid haemorrhagein 24 patients under neuroleptanaesthesia. Eleven patients hadgood neurological status (Hunt and Kosnik grade I: group A)and 13 patients poor status (grades II-IV: group B). Arterialhypotension was induced with PGE, 0.1 ng kg^–1 min^–1initially and adjusted to maintain mean arterial pressure atabout 70 mm Hg. PGE, was discontinued at the completion of aneurysmclipping. LCBF and CO2R were measured during and after administrationof PGE,. LCBF was unchanged and CO₂R preserved in both groups.The carbon dioxide response was better in group A than in groupB (P < 0.01). PGE, may be a suitable agent for hypotensiveanaesthesia in these patients     

CEREBRAL ELECTRICAL ACTIVITY INFLUENCES THE EFFECTS OF ETOMIDATE CEREBRAL PERFUSION PRESSURE IN TRAUMATIC COMA

The effects of 124 boluses of etomidate 0.2 mg kg^-1 i.v. onintracranial pressure (ICP), mean arterial pressure (MAP) andcerebral perfusion pressure (CPP) were studied in eight patientswith severe head injury (Glasgow coma score < 8). The datawere divided into two groups based on the minimum voltage ofthe cerebral function monitor (CFM) recording before the bolus.In group A this was less than 5 µV (representing profoundcortical electrical depression), while in group B the minimumvoltage was greater than 5µV. The mean decrease in ICPfollowing etomidate was significantly greater in group B (mean±SEM:–8.6 ±0.7 mm Hg) than in group A (–3.8±0.6mm Hg) (P < 0.0001). The decrease in arterial pressure wassimilar in both groups. Consequently, there was a small meanincrease in CPP in group B (2.2±0.9mm Hg), whereas ingroup A CPP decreased (–4.7±1.5mm Hg) (P < 0.001).There was a strong correlation between the decreases in ICPand MAP in group A (r = 0.70, P<0.01), but not in group B(r= 0.05). Thus, when cortical electrical activity was alreadymaximally suppressed, further administration of an i.v. anaestheticagent produced only relatively small decreases in ICP, largelyas a passive response to decreases in MAP. CPP was thereforeusually reduced. Conversely, in the absence of such depressionlarger decreases in ICP, unrelated to hypotension, occurredand these were usually associated with increases in CPP. However,even under these circumstances, potentially dangerous decreasesin CPP may be seen.     

CHANGES IN BRAIN SURFACE OXYGEN TENSION DURING PROFOUND HYPOTENSION INDUCED WITH SODIUM NITROPRUSSIDE OR ADENOSINE IN THE SHEEP

Brain suface oxygen tensions were measured, in sheep (n = 8),with a seven-barrelled mini-electrode polarized by sweep potentials.Mean arterial pressure was reduced to 30 mm Hg with either sodiumnitroprusside or adenosine. At this value of mean arterial pressure,oxygen supply to cerebral tissue was impaired. There was nosignificant difference between the two agents in the degreeto which the oxygen supply was reduced. ^*Presnet address for correspondence: Department of Anaesthetic,Royal Victoria Hospital,687 Pine Avenue West, Room H522, Montreal,Canada H3A 1A1