Maintain Heart Rate Research Articles

Thermal physiology of the fingered limpet Lottia digitalis under emersion and immersion

Marine animals living high in the rocky intertidal zone experience long durations of aerial emersion, sometimes enduring rapid increases in temperature. To date, much of our understanding of the thermal physiology of intertidal organisms comes from studies in which organisms are exposed to increasing temperatures when immersed, with the added effect of aerial emersion rarely considered. In this study, we examined the physiological response of the finger limpet, Lottia digitalis, to increases in temperature under both immersed and emersed conditions. We investigated the thermal sensitivity and upper temperature tolerance of limpets through assessment of cardiac performance, metabolic rate, glycogen depletion and maintenance of protein integrity. Cardiac performance in response to ecologically relevant increases in temperature was similar in emersed and immersed limpets from 15 to 35°C and showed multiple break patterns in heart rate as temperature was increased. Overall, emersed limpets had a greater upper thermal limit on cardiac performance, with the ability to maintain heart rate at a temperature 3-5°C higher than that for immersed limpets. Metabolism in limpets also differed significantly between emersion and immersion, where a significant depression in aerobic metabolic rate was observed under immersion with increasing temperature. Greater levels of ubiquitin-conjugated proteins were found under emersed conditions compared with immersed limpets. Maintaining cardiac performance and aerobic metabolism to higher temperatures under emersed conditions is likely reflective of physiological adaptations to live in an aerially exposed environment. Measured field temperatures where fingered limpets were collected demonstrated that limpets have a narrow thermal safety margin for aerobic performance, and currently experience multiple days where summer temperatures might exceed their threshold limits.

Arrhythmias After Heart Transplantation: Mechanisms and Management

Heart transplantation (HT) has significantly altered the treatment paradigm for end-stage heart disease. With current surgical techniques and postoperative immunosuppression, 1-year survival after HT is ≈90%, 5-year survival is ≈70%, and median survival exceeds 10 years.[1][1]–[3][2] These

Insulin, C‐peptide, Glucose, and Heart Rate Responses to Acute Intermittent Hypoxia in the Neonatal Rat: Body Temperature and Chemical Sympathectomy

Apnea due to immature respiratory control is a common cause of neonatal intermittent hypoxia (IH). We hypothesized that IH disrupts glucose homeostasis and is a metabolic stressor. Rats at postnatal days (PD) 2–3, 7–8, or 11–12 were exposed to 6 @ 30‐sec cycles of IH (3% O2) over 1 hr. An additional group of PD7‐8 pups underwent IH for 3 cycles over 0.5 hr, but were pretreated (on PD3, 5, and 6) with guanethidine (chemical sympathectomy). In PD2‐3 rats, plasma glucose, insulin, and C‐peptide were increased at the 6th cycle of IH. In PD7‐8 rats, plasma glucose, insulin, and C‐peptide increased by the 3rd cycle, but by the 6th cycle, glucose had returned to baseline. PD11‐12 pups experienced a similar increase in plasma glucose, but a much larger increase in insulin and C‐peptide compared to PD7‐8. IH caused bradycardia and a decrease in body temperature. Pretreatment with guanethidine in PD7‐8 rats augmented the increase in insulin and C‐peptide; heart rate at baseline, and heart rate and body temperature at their nadirs during IH were lower after guanethidine pretreatment. We conclude that IH alters glucose homeostasis and induces bradycardia in neonates. The sympathetic nervous system restrains the insulin response and maintains heart rate during IH in the neonate.

Isolated Dynamic Left Ventricular Outflow Tract Obstruction Can Cause Hypotension That Rapidly Responds to Intravenous Beta Blockade

Dynamic left ventricular outflow tract obstruction occurs in hypertrophic cardiomyopathy, stress cardiomyopathy, acute coronary syndromes, and with inotrope use. We describe three critical care patients who developed "isolated" left ventricular outflow tract obstruction with hypotension in the absence of these precipitants. Systolic anterior motion of anterior mitral valve leaflet with peak left ventricular outflow tract gradients of greater than 120 mmHg was noted in Cases 1 and 2. Under close supervision, intravenous (IV) β blocker was initiated with 5 mg metoprolol repeated every 5 minutes up to 15 mg and continued to maintain heart rate less than 70 beats/min. IV fluids were replaced aggressively. Bedside Doppler echocardiogram confirmed near normalization of left ventricular outflow tract gradient with improvement in systolic anterior motion and hypotension within minutes after IV β blocker confirming its specific therapeutic effect. Isolated left ventricular outflow tract obstruction can occur in the absence of recognized precipitants. Early recognition is crucial because this potentially fatal condition responds well to adequate β blocker and IV fluids with rapid relief of hypotension and symptoms.

Physiological importance of the coronary arterial blood supply to the rattlesnake heart

The reptilian heart consists of a thick inner spongy myocardium that derives its oxygen and nutrient supply directly from the blood within the ventricular cavity, which is surrounded by a thin outer compact layer supplied by coronary arteries. The functional importance of these coronary arteries remains unknown. In the present study we investigate the effects of permanent coronary artery occlusion in the South American rattlesnake (Crotalus durissus) on the ability to maintain heart rate and blood pressure at rest and during short term activity. We used colored silicone rubber (Microfil) to identify the coronary artery distribution and interarterial anastomoses. The coronary circulation was occluded and the snakes were then kept for 4 days at 30 degrees C. Microfil injections verified that virtually all coronary arteries had successfully been occluded, but also made visible an extensive coronary supply to the outer compact layer in untreated snakes. Electrocardiogram (ECG), blood pressure (Psys) and heart rate (fH) were measured at rest and during enforced activity at day 1 and 4. Four days after occlusion of the coronary circulation, the snakes could still maintain a Psys and fH of 5.2+/-0.2 kPa and 58.2+/-2.2 beats min(-1), respectively, during activity and the ECG was not affected. This was not different from sham-operated snakes. Thus, while the outer compact layer of the rattlesnake heart clearly has an extensive coronary supply, rattlesnakes sustain a high blood pressure and heart rate during activity without coronary artery blood supply.

Pretreatment with a stress-dose but not a high-dose infusion of hydrocortisone maintains heart rate variability during human endotoxemia

Results: A total of 410 patients (23%) developed VAP at median day 5.7. Heart rate multiscale entropy differed between groups at all scales (figure). Reduced HR-MSE (loss of complexity) was independently associated with increased risk of VAP (table). Intraquartile variation in HR-MSE reflects a 30% change in VAP risk. Conclusion: Heart rate multiscale entropy within hours of admission identifies risk of VAP occurring days later.

The Blue Baby Blues: A Rare Case of Cyanosis in the Newborn

HISTORY OF PRESENT ILLNESS J.S. was a full-term, large-f gestational-age boy born to a year-old gravida 2 para 1 mothe a referring hospital. His mother ceived appropriate prenatal car and the pregnancy was uncomp cated. Maternal laboratory tes were negative for rapid plasmin agin, hepatitis B surface antige and human immunodeficiency v rus and revealed that she was mune to Rubella; group B Streptococcus status was unknown. J. was delivered via spontaneo vaginal delivery 7 hours after r ture of membranes for clear am otic fluid. The delivery was complicated, with a reassurin fetal heart rate tracing througho At birth, the infant was found t cyanotic with poor respiratory fort. Bag and mask ventilation w administered but he did not prove and thus was intubated the delivery room. He did not quire chest compressions or medications because he maintained heart rate greater than 60 beats minute throughout the resuscit tion (Kattwinkel, 2006). Apgar scores were 5 and 6 at 1 a minutes of life. J.S. was transferred to the n natal intensive care unit (NIC immediately and placed on m chanical ventilation with 100% o ygen, and umbilical venous a arterial lines were inserted to propriate placement. Oxygen sat ration measurements (Sa O2) on admission were found to be in 50s, and his initial arterial blo gas (ABG) measurement was s nificant for a mixed respiratory metabolic acidosis (pH, 6.9 PaCO2,72 mmHg; Pa O2, 12 mmHg HCO3, 13 mEq/L; base defi 16). Over several hours, respi tory support was increased to m imal settings on conventional ve tilation and inhaled nitric oxi (iNO) was initiated at 20 parts million (ppm) without improv ment. Multiple normal saline (N solution boluses and doses of dium bicarbonate were admini tered with minimal improveme in blood pressure, Sa O2, or ABG measurements. Dopamine was in tiated and titrated up to 10 g/kg/

Delayed-onset encephalopathy and coma in acute organophosphate poisoning in humans

The objective of the study was to describe the clinical characteristics and course of delayed-onset organophosphate (OP) poisoning. In our clinical experience, we have noticed patients with onset of deep coma 4–7 days after hospital admission, clinical features that have not been previously described. We set up a prospective observational study over 1 year to formally characterize this observation. Thirty-five patients admitted to the intensive care unit (ICU) with severe OP poisoning and treated with atropine and supportive therapy were followed up. Oximes were not administered. Three patients developed delayed-onset coma after presenting with normal or near normal Glasgow coma score (GCS). They developed altered conscious state rapidly progressing to deep coma, 5.0 ± 1.0 (mean ± S.D.) days after OP ingestion. The GCS persisted at 2T for 4.3 ± 2.1 days despite the cessation of sedative drugs at the onset of coma. During this period, the patients had miosed non-reacting pupils and no clinically detectable cortical or brainstem activity. Computed tomography of the brain and cerebrospinal fluid analysis were normal. Electroencephalogram showed bihemispheric slow wave disturbances. Two patients required atropine during this period to maintain heart rate and reduce secretions. In all three patients, no metabolic, infective or non-infective cause of altered conscious state was identified. With supportive therapy the GCS improved to 10T in 8.0 ± 2.0 days. All patients survived to hospital discharge. Three other patients who developed a reduction in GCS (3T–7T) by 4.7 ± 1.2 days but not progressing to coma and recovering (GCS 10T) in 3.3 ± 0.6 days may have manifested delayed-onset encephalopathy. Delayed-onset coma appears to have a distinct clinical profile and course with complete resolution of symptoms with supportive therapy. Although persistent cholinesterase inhibition is likely to have contributed to the manifestations, the mechanism of coma and encephalopathy need to be explored in further trials. The good outcomes in these patients suggest that therapy should not be limited in OP-poisoned patients developing profound coma or encephalopathy during hospitalization.

Pharmacokinetics of dexmedetomidine in postsurgical pediatric intensive care unit patients: Preliminary study*

To characterize the pharmacokinetics of dexmedetomidine and monitor any dexmedetomidine-related adverse events in postoperative pediatric patients requiring short-term mechanical ventilation, analgesia, and sedation in the pediatric intensive care unit (PICU). Prospective, case series. Operating room and PICU in a large, urban children's hospital. Enrollment from February 14 to November 25, 2002. Ten children (4 months to 7.9 yrs of age) who received postoperative infusions of dexmedetomidine. Toward the end of the operation, patients received dexmedetomidine at 1 microg/kg per hr for 10 mins. The anesthesiologist then titrated the infusion, as clinically indicated, to a rate of 0.2-0.7 microg/kg per hr. In the PICU, the infusion was titrated by the nursing staff based on assessment with a modified Ramsey Sedation Scale, while maintaining heart rate and blood pressure within normal limits for age. Dexmedetomidine was continued until the intensivist felt the patient no longer benefited, but for no longer than 24 hrs. At specified times during the infusion and after discontinuation, dexmedetomidine plasma concentrations were determined. Pharmacokinetic parameters were calculated using a two-compartment model. Vital signs, sedation scores, adjunct sedative or analgesic medications, and adverse events were recorded. Average duration of infusion was 18.8 hrs (range, 8-24 hrs). Means (+/-sd) were calculated for the following: clearance, 0.57 (+/-0.14) L/hr per kg; volume of distribution at steady state, 1.53 (+/-0.37) L/kg; and terminal elimination half-life, 2.65 (+/-0.88 hrs)-all similar to published values in adults. There were no serious adverse events related to dexmedetomidine. Dexmedetomidine, administered as a continuous infusion, produces consistent, predictable concentrations in children and infants. Further evaluations of the safety, efficacy, and pharmacodynamics of dexmedetomidine are warranted.

Skeletal Muscle Metabolic Adaptations in Response to 6 Weeks of High-Intensity Interval Training

PURPOSE: There is sparse data in regards to skeletal muscle metabolic adaptations that occur in response to high intensity (80-100% VO2max) interval training (HIIT). Repeated short bouts of exercise at this intensity challenges both the aerobic and anaerobic ATP producing pathways and leads to an increased capacity of these pathways. We investigated the adaptive responses in the skeletal muscle's aerobic capacity and ability to distribute pyruvate to oxidative phosphorylation during high intensity exercise following 6 wks of HIIT, and hypothesized that there would be improved sensitivity in the regulation of PDH and reduced reliance on glycogenolysis and PCr. METHODS: 8 untrained but recreationally active subjects trained 3 d/wk for 6 wks on a cycle ergometer following a VO2max test and time trial to exhaustion (TTE) at 90% VO2max, which were repeated after training. Workouts consisted of ten 4 min bouts at 90% VO2max separated by 2 min of rest. This equated to 12 hours of training over 6 wks. Training power outputs (PO) were increased to maintain heart rate at ∼95 % of maximum. Muscle biopsies were taken during the TTE at rest, 5 min and exhaustion (EX). RESULTS: PO increased by 21% over 6 wk (209 ± 47 to 252 ± 51 W). Following training, VO2max increased by 9% (3.29 ± 0.24 to 3.58 ± 0.26 l/min) and TTE by 111% (7.1 ± 0.2 to 15.0 ± 1.1 min). The maximal activity of citrate synthase increased by 26% (18.4 ± 1.4 to 23.1 ± 1.2 mmol/min/kg wet muscle) and β-hydroxyacyl-CoA dehydrogenase increased by 29% (15.8 ± 1.1 to 20.3 ± 0.9 mmol/min/kg). PDH total increased by 23% (2.54 ± 0.21 to 3.09 ± 0.29 mmol/min/kg). Activation of PDH (PDHa) at 5 min in the TTE did not change with training (Pre, 2.32 ± 0.24; Post, 2.39 ± 0.18 mmol/min/kg) but was higher at EX (Pre, 1.94 ± 0.20; Post, 2.55 ± 0.27 mmol/min/kg wet muscle). The rate of glycogenolysis in the first 5 mins of TTE decreased (34.1 ± 4.8 to 23.3 ± 3.5 mmol/min/kg dry muscle) as did PCr utilization (12.5 ± 0.7 to 10.5 ± 1.1 mmol/min/kg dry muscle) and lactate accumulation (22.4 ± 1.1 to 17.9 ± 1.6 mmol/min/kg dry muscle) following training. Free ADP (ADPf) was reduced at 5 min after training (366.1 ± 42.5 to 265.4 ± 34.1 mmol/kg wet muscle). CONCLUSIONS: Only 12 hours of HIIT over 6 wks resulted in impressive increases in the aerobic capacity of the skeletal muscle. The reduced levels of ADPf but similar PDHa post-training suggest an improved sensitivity in the regulation of PDH. This, coupled with attenuated glycogenolysis, resulted in a greater proportion of pyruvate directed to oxidative phosphorylation. A decrease in PCr utilization supports these findings of HIIT-induced enhancements in aerobic ATP production and endurance performance during very intense exercise.

Transmural Gradients of Repolarization and Excitation–Contraction Coupling in Mouse Ventricle

See related article, pages 1306–1313 The effects of changes in action potential waveform on excitation–contraction coupling in mammalian ventricle were first identified almost 40 years ago.1 Many important details concerning the relationship between action potential duration and tension development have been elucidated.2 Recent work has demonstrated significant effects on the intracellular Ca transient and excitation–contraction coupling of early repolarization of the action potential, which is strongly regulated by a Ca2+-independent transient outward K+ current denoted I to.3–6 The molecular physiology and some aspects of the pharmacology of this current are now quite well understood, based, in part, on a series of comprehensive articles from the Nerbonne et al,7,8 Strauss and Campbell,9 and others.6 Interestingly, a somewhat similar transient outward K+ current is expressed in neurons10 and in selected regions near the intraventricular septum of mammalian hearts.11–13 One of the most striking features of the transient outward K+ current in mammalian ventricle is the difference in its transmural expression, with significantly higher expression levels in epi- than in endocardium14 (see also references 8, 9, 11). The basis for this transmural heterogeneity, and also for the higher levels of expression in the right ventricle compared with the left, continues to be a topic of intense investigation. Significant new information and plausible working hypotheses for the way in which this heterogeneity …

β1-Adrenergic Receptors Maintain Fetal Heart Rate and Survival

β-Adrenergic receptor (βAR) activation has been shown to maintain heart rate during hypoxia and to rescue the fetus from the fetal lethality that occurs in the absence of norepinephrine. This study examines whether the same subtype of βAR is responsible for survival and heart rate regulation. It also investigates which βARs are located on the early fetal heart and whether they can be directly activated during hypoxia. Cultured E12.5 mouse fetuses were treated with subtype-specific βAR antagonists to pharmacologically block βARs during a hypoxic insult. Hypoxia alone reduced heart rate by 35–40% compared to prehypoxic levels. During hypoxia, heart rate was further reduced by 31% in the presence of a β₁AR antagonist, CGP20712A, at 100 nM, but not with a β₂ (ICI118551)- or a β₃ (SR59230A)-specific antagonist at 100 nM. Survival in utero was also mediated by β₁ARs. A β₁ partial agonist, xamoterol, rescued 74% of catecholamine-deficient (tyrosine-hydroxylase-null) pups to birth, a survival rate equivalent to that with a nonspecific βAR agonist, isoproterenol (87%). Receptor autoradiography showed that β₁ARs were only found on the mouse heart at E12.5, while β₂ARs were localized to the liver and vasculature. To determine if the response to hypoxia was intrinsic to the heart, isolated fetal hearts were incubated under hypoxic conditions in the presence of a βAR agonist. Heart rate was reduced to 25–30% by hypoxia alone, but was restored to 63% of prehypoxic levels with 100 nM isoproterenol. Restoration was completely prevented if β₁ARs were blocked with CGP20712A at 300 nM, a concentration that blocks β₁ARs, but not β₂- or β₃ARs. Our results demonstrate that β₁ARs are located on the heart of early fetal mice and that β₁AR stimulation maintains fetal heart rate during hypoxia and mediates survival in vivo.

Comparing Exercise Echocardiography of Children in Upright and Recumbent Postures

0461 Exercise echocardiography in children is difficult due to movement artifacts. Cardiac physiologic measures may change with different postures. Because the recumbent cycle ergometer offers support to the upper torso, in contrast to the traditional upright cycle ergometer and treadmill, we hypothesized a reduction in movement artifacts during exercise in children. PURPOSE: To determine if exercise echocardiogram of children in a recumbent position is superior to an upright position with no difference in physiologic measurements. METHODS: Twenty healthy children, 8 to 10 years of age (10 males), completed two exercise tests on an upright and a recumbent cycle ergometer at a random order. The work rate was adjusted to maintain heart rate at 70% predicted peak heart rate (140–150 bpm). Echocardiograms were performed at rest and during exercise. Echocardiographic measurements were made offline and study quality was graded by a blinded reader. Echocardiographic measurements, acquisition time, work rate and child's preference were compared. RESULTS: There was no difference between upright and recumbent postures at rest or during exercise in the following echocardiographic measures: left ventricle end-systolic and end-diastolic dimensions, ejection fraction, stroke volume, cardiac output, mitral inflow E and A waves and left atrial dimension. The work rate required to maintain heart rate was similar between upright and recumbent ridings (38.5 ± 9.9 and 38.9 ± 12.1 watts, p = 0.90). More children (65%) preferred the recumbent cycle than the upright cycle (35%), but the difference was not significant (p = 0.14). Acquisition time was significantly shorter for recumbent studies (129 ± 26 sec) than upright studies (151 ± 30 sec, p = 0.02). The quality of resting echocardiograms was similar between the recumbent and upright studies (p = 0.16), however, the quality of exercise echocardiograms in recumbent studies was significantly better than upright studies (p = 0.03). CONCLUSIONS: Exercise echocardiograms in a recumbent position require less acquisition time and produce better study quality than an upright position. For pediatric patients, exercise echocardiography in a recumbent position is superior to an upright position with no difference in cardiac physiologic measures.

Comparing Exercise Echocardiography of Children in Upright and Recumbent Postures

0461 Exercise echocardiography in children is difficult due to movement artifacts. Cardiac physiologic measures may change with different postures. Because the recumbent cycle ergometer offers support to the upper torso, in contrast to the traditional upright cycle ergometer and treadmill, we hypothesized a reduction in movement artifacts during exercise in children. PURPOSE: To determine if exercise echocardiogram of children in a recumbent position is superior to an upright position with no difference in physiologic measurements. METHODS: Twenty healthy children, 8 to 10 years of age (10 males), completed two exercise tests on an upright and a recumbent cycle ergometer at a random order. The work rate was adjusted to maintain heart rate at 70% predicted peak heart rate (140–150 bpm). Echocardiograms were performed at rest and during exercise. Echocardiographic measurements were made offline and study quality was graded by a blinded reader. Echocardiographic measurements, acquisition time, work rate and child's preference were compared. RESULTS: There was no difference between upright and recumbent postures at rest or during exercise in the following echocardiographic measures: left ventricle end-systolic and end-diastolic dimensions, ejection fraction, stroke volume, cardiac output, mitral inflow E and A waves and left atrial dimension. The work rate required to maintain heart rate was similar between upright and recumbent ridings (38.5 ± 9.9 and 38.9 ± 12.1 watts, p = 0.90). More children (65%) preferred the recumbent cycle than the upright cycle (35%), but the difference was not significant (p = 0.14). Acquisition time was significantly shorter for recumbent studies (129 ± 26 sec) than upright studies (151 ± 30 sec, p = 0.02). The quality of resting echocardiograms was similar between the recumbent and upright studies (p = 0.16), however, the quality of exercise echocardiograms in recumbent studies was significantly better than upright studies (p = 0.03). CONCLUSIONS: Exercise echocardiograms in a recumbent position require less acquisition time and produce better study quality than an upright position. For pediatric patients, exercise echocardiography in a recumbent position is superior to an upright position with no difference in cardiac physiologic measures.

Haemodynamic changes during high spinal anaesthesia in children having open heart surgery

This prospective series examined the haemodynamic effects of high spinal anaesthesia in combination with light general anaesthesia in infants and children undergoing open heart surgery who were candidates for immediate or early postoperative extubation. After midazolam premedication and sevoflurane inhalation induction, 30 patients, aged 7 months to 13 years, who were undergoing open heart surgery, received spinal anaesthetics with 0.5% tetracaine D10 mixed with morphine. The spinal blocks were placed at the L2,3 or L3,4 interspace with cephalad spread being promoted by positioning the patient in 30 degrees of Trendelenburg for a minimum of 10 min. Maintenance of anaesthesia was with isoflurane 0.2-0.5% in 70% nitrous oxide to maintain heart rate and blood pressure within 20% of postinduction baseline values. Haemodynamic values were recorded at predetermined timed intervals and intraoperative events up to and including aortic cannulation. For analysis of the data, patients were divided into four age groups (< 1 years, 1-3 years, 4-6 years and > 7 years). Haemodynamic stability was demonstrated in all four age groups. Statistically significant slowing of the heart rate did occur in the groups older than 1 year at 25 min, although clinically significant bradycardia requiring treatment never occurred. Hypotension did occur during specific surgical manipulations but recovered spontaneously. Atropine, fluid boluses and vasopressors were never used. At the conclusion of surgery, all patients met extubation criteria and could move all four extremities. High spinal anaesthesia with hyperbaric tetracaine and morphine in combination with light general anaesthesia is well tolerated haemodynamically by the paediatric population studied.

Noninvasive cardiac output by partial CO2 rebreathing after severe chest trauma.

In multiple trauma patients, early continuous cardiac output (CCO) monitoring is frequently desired but is difficult to routinely employ in most emergency departments because it requires invasive procedures. Recently, a noninvasive cardiac output (NICO) technique based on the Fick principle and partial CO2 rebreathing has shown promise under a variety of conditions. Since this method has not been tested after lung damage, we evaluated its utility in a clinically relevant model. Anesthetized, ventilated swine (n = 11, 35-45 kg) received a unilateral blunt trauma via a captive bolt gun followed by a 25% hemorrhage. After 60 min of shock, crystalloid resuscitation was given as needed to maintain heart rate < 100 beats/min and mean arterial pressure > 70 mm Hg. Standard CCO by thermodilution (Baxter Vigilance, Irvine, CA) was compared with NICO (Novametrix Medical Systems Inc., Wallingford, CT) for 8 hr. The severity of the injury is reflected by seven deaths (average survival time = 4.25 hr). Trauma increased dead space ventilation (19%), airway resistance (30%), and lactate (3.2 mmol/L), and decreased dynamic compliance (48%) and Pao2/Fio2 (54%). In these extreme conditions, the time course and magnitude of change of CCO and NICO were superimposed. Bland-Altman analysis reveal a bias and precision of 0.01 +/- 0.69 liters/min. The linear relationship between individual CCO and NICO values was significant (p < 0.0001) and was described by the equation NICO = (0.74 +/- 0.1)CCO + (0.65 +/- 0.16 liters/min) but the correlation coefficient (r2 = 0.541) was relatively low. The cause for the low correlation could not be attributed to increased pulmonary shunt, venous desaturation, anemia, hypercapnia, increased dead space ventilation, or hyperlactacidemia. NICO correlated with thermodilution CCO, but underestimated this standard by 26% in extreme laboratory conditions of trauma-induced cardiopulmonary dysfunction; 95% of the NICO values fall within 1.38 liters/min of CCO; and with further improvements, NICO may be useful in multiple trauma patients requiring emergency intubation during initial assessment and workup.

Catecholamine release in heat-stressed Antarctic fish causes proton extrusion by the red cells

Two species of Antarctic fish were stressed by moving them from seawater at -1 degrees C to seawater at 10 degrees C and holding them for a period of 10 min. The active cryopelagic species Pagothenia borchgrevinki maintained heart rate while in the benthic species Trematomus bernacchii there was an increase in heart rate. Blood pressure did not change in either species. Both species released catecholamines into the circulation as a consequence of the stress. P. borchgrevinki released the greater amounts, having mean plasma concentrations of 177 +/- 54 nmol.l(-1) noradrenaline and 263 +/- 131 nmol.l(-1) adrenaline at 10 min. Pla.sma noradrenaline concentrations rose to 47 +/- 14 nmol.l(-1) and adrenaline to 73 +/- 28 nmol.l(-1) in T. bernacchii. Blood from P. borchgrevinki was tonometered in the presence of isoprenaline. A fall in extracellular pH suggests the presence of a Na+/H+ antiporter on the red cell membrane, the first demonstration of this in an Antarctic fish. Treatment with the beta-adrenergic antagonist drug sotalol inhibited swelling of red blood cells taken from temperature-stressed P. borchgrevinki, suggesting that the antiporter responds to endogenous catecholamines.

Emergency Management of Atrial Fibrillation and Flutter: Intravenous Diltiazem Versus Intravenous Digoxin

Study objective: To compare the effects of IV diltiazem and IV digoxin on ventricular rate control in the emergency treatment of acute atrial fibrillation and flutter (AFF). Methods: This prospective, randomized, open-label trial involved 30 consecutive patients who presented with acute AFF to the emergency department of an urban, 420-bed community teaching hospital from April 1993 through March 1994. Exclusion criteria included systolic blood pressure lower than 100 mm Hg, treatment with calcium-channel blockers other than diltiazem, lack of informed consent, and objection of the private physician. Patients were randomly assigned to receive either IV diltiazem alone, IV digoxin alone, or both. Heart rate control was defined as a ventricular rate of less than 100 beats/minute. IV digoxin, .25 mg, was given as a bolus at time 0 and at time 30 minutes. An initial dose of .25 mg/kg diltiazem was given intravenously over the first 2 minutes, followed by a dose of .35 mg/kg at time 15 minutes and then a titratable IV infusion at a rate of 10 to 20 mg/hour to maintain heart rate control. The dosing regimens were the same whether the drugs were given alone or in combination. Heart rhythm, heart rate, and blood pressure were measured at times 0, 5, 10, 15, 30, 60, 120, and 180 minutes. Statistical significance was assessed with the use of Student's t test and ANOVA methodology. Results: At time 0, the heart rate (mean±SD) was 150±19 beats/minute in the diltiazem group and 144±12 in the digoxin group (difference not significant, P=.432). The decrease in heart rate from time 0 reached statistical significance at time 5 minutes in the diltiazem group ( P=.0006); the mean rates at time 5 minutes were 111±26 beats/minute for diltiazem and 144±13 for digoxin. The decrease in heart rate achieved with digoxin did not reach statistical significance until time 180 minutes ( P=.0099), at which time the rates were 90±13 for diltiazem and 117±22 for digoxin. Conclusion: Treatment of acute AFF with IV diltiazem decreases ventricular heart rate significantly within 5 minutes, compared with 3 hours for treatment with IV digoxin. No advantage was noted within 3 hours for IV treatment with a combination of diltiazem and digoxin. IV diltiazem is superior to IV digoxin in the emergency control of ventricular rate in acute AFF and should be considered as a drug of choice for this condition. This study was not large enough to adequately assess adverse effects, and further studies may be warranted for clinical validation. [Schreck DM, Rivera AR, Tricarico VJ: Emergency management of atrial fibrillation and flutter: Intravenous diltiazem versus intravenous digoxin. Ann Emerg Med January 1997;29:135-140.]

Control of heart rate during transition from intravenous to oral diltiazem in atrial fibrillation or flutter

We tested whether patients presenting with atrial fibrillation (AF) or flutter (AFl) with a rapid ventricular response could maintain control of heart rate while transferring from a bolus and continuous infusion of intravenous diltiazem to oral diltiazem. Forty patients with AF or AFl and sustained ventricular rate ≥120 beats/min received intravenous diltiazem “bolus” (20 to 25 mg for 2 minutes) and “infusion” (5 to 15 mg/ hour for 6 to 20 hours). Oral long-acting diltiazem (diltiazem CD 180, 300, or 360 mg/24 hours) was administered in patients in whom stable heart rate control was attained during constant infusion. Intravenous diltiazem infusion was discontinued 4 hours after the first oral dose, and patients were monitored during 48 subsequent hours of “transition” to oral therapy. Response to diltiazem was defined as heart rate < 100 beats/min, ≥20% decrease in heart rate from baseline, or conversion to sinus rhythm. Other rate control or antiarrhythmic medications were not allowed during the study period. Thirty-seven of 40 patients maintained heart rate control during the bolus, and 35 of the remaining 37 maintained control during the infusion of intravenous diltiazem. Of the 35 patients achieving heart rate control with intravenous diltiazem who entered the transition to oral therapy, 27 maintained heart rate control (response rate of 77%, 95% confidence interval 63% to 91%). The median infusion rate of intravenous diltiazem was 10 mg/hour, and the median dose of oral diltiazem CD was 300 mg/ day. Oral long-acting diltiazem was 77% effective in controlling ventricular response over 48 hours in patients with AF or AFl in whom ventricular response was initially controlled with intravenous diltiazem.

Effect of oral clonidine premedication on anesthetic requirement, hormonal response, hemodynamics, and recovery in coronary artery bypass graft surgery patients

Study Objective: To examine how premedication with clonidine affects opioid use, hemodynamic effects, hormonal responses, and recovery effects. Design: Double-blind, placebo-controlled study. Setting: Operating room and surgical intensive care unit of a university medical center. Patients: 54 patients undergoing elective coronary artery bypass graft (CABG) surgery. Interventions: Patients received approximately 5 μg/kg of oral clonidine or a placebo together with 40 μg/kg lorazepam 90 minutes prior to titrated sufentanil induction of anesthesia. Thirty minutes prior to cardiopulmonary bypass, a second dose of either approximately 5 μg/kg clonidine or placebo was given as a slurry via a nasogastric tube. Measurements and Main Results: Opioid use, hemodynamic effects, hormonal responses, and recovery effects were recorded. Values for ten hemodynamic variables were compiled on the evening prior to surgery, prior to induction, and during seven additional events and compared. Catecholamines and β-endorphins were measured prior to induction, after intubation, and after sternotomy. The amount of sufentanil used for induction, maintenance, and total opioid were compared. The times to awakening and response to verbal commands were compared. The two groups exhibited similar patient demographics, cardiopulmonary bypass time, and duration of surgery. Patients receiving clonidine required significantly (p < 0.04) less sufentanil for induction (clonidine: 2.19 ± 0.95 μg/kg vs. placebo: 2.93 ± 1.07 μg/kg) and total amount of sufentanil (clonidine: 9.1 ± 3.9 μg/kg vs. placebo: 11. 7 ± 4.6 μg/kg). Patients receiving clonidine required significantly (p < 0.01) less isoflurane (9.7 ± 6.8 MAC min vs. 19.7 ± 9.9 MAC min) to maintain heart rate (HR) and mean arterial pressure (MAP) to within 15% of baseline without significant differences in other vasoactive drugs. Catecholamine concentrations were significantly (p < 0.02) lower in patients receiving domaine without any difference in β-endorphin concentrations. Patients receiving clonidine had significantly (p < 0.02) lower HR, systolic arterial pressure, MAP, and systemic vascular resistance prior to induction than patients receiving placebo without differences in other hemodynamic variables. Conclusion: Clonidine decreases opioid use and lowers hormonal response while maintaining stable hemodynamics in patients undergoing CABG with sufentanil anesthesia.