Venous Blood Temperature Research Articles

Temperature‐controlled Rate Responsive Pacing with the Aid of an Optimized Algorithm

On the basis of earlier studies of the behavior of the central venous blood temperature at rest and during exercise, we have developed an algorithm for the rate control of cardiac pacemakers. The central venous blood temperature serves as the control variable for the pacing rate. Control is effected via two different characteristic lines that relate pacing rate and temperature. A rest characteristic line relates absolute temperature values to heart rate and exercise lines relate relative changes in temperature to heart rate changes. The rest characteristic corresponds to conditions of slow temperature fluctations (e.g., fever and temperature changes due to circardian rhythm) and has a slope of 15 to 20 bpm per centigrade degree of temperature change. Starting at this rest characteristic, there are exercise characteristic lines that have a much greater slope and serve to regulate the pacing rate under exercise conditions. The two characteristics are distinguished via the temperature change per unit of time. In addition, a return characteristic connects the rest and exercise characteristics. This algorithm allows for optimized rate adaption of physiological cardiac pacemakers by central venous blood temperature. Clinical studies with the implanted device (Intermedics Nova MR) prove the correct function and beneficial effect of this algorithm in patients' everyday life.

Measurement of Right Ventricular Blood Temperature During Exercise as a Means of Rate Control in Physiological Pacemakers

Several biological parameters have been suggested for rate control in physiological pacemakers in the past. Up to now, measurements of central venous blood temperature have been mostly done on dogs. We studied central venous blood temperature and heart rate in 14 healthy volunteers under conditions of treadmill and bicycle exercise with different workloads. A custom-made 5F lead with a thermistor incorporated near the tip was placed at the right ventricle under fluoroscopic control. Temperature was recorded with an accuracy of 1/100 degrees C on a digital memory device at a sampling rate of 5-10 s. We found the increase in blood temperature to be not only a function of absolute workloads but also a function of the individual's maximum exercise tolerance. Independent of the absolute increase in heart rate and temperature at a given workload, the individual's relation of increase in temperature and heart rate was found to be highly correlating (r = 0.9095). At a load of 100 W, we found a mean increase in heart rate of 52 beats and of temperature of 0.57 degree C, at 150 W of 74 beats/min and 0.84 degree C. During, as well as after, the exercise, heart rate and temperature have a parallel course. According to our data, control of physiological pacemakers by means of central venous blood temperature is possible.

A Central Venous Temperature Sensing Lead

Pacemaker rate responsiveness derived from changing central venous blood temperature requires the development of sensor leads that are stable and reliable. The relevant characteristics of one such design are described. Temperature response time, data acquisition time, temperature sensitivity, and long-term sensor shunt impedance have been studied both in vitro and in vivo. These parameters are analyzed with respect to the intrinsic temperature signal and to pacemaker implementation problems.

Rate control of physiologic pacemakers by central venous blood temperature.

Heart rate and central venous blood temperature (CVT) were measured in 31 people with different exercise capacities by means of a thermistor integrated into a lead that was placed in the right ventricle. Bicycle ergometric and treadmill stress tests with increasing workloads were performed. The maximum increase in CVT with ergometric exercise was found to be 1.3 degrees C at 250 W in healthy young volunteers and 1.0 degrees C at 125 W in cardiac patients. Despite a relatively greater increase in CVT in the elderly patients compared with the volunteers, the correlation between the increase in CVT and that in heart rate at the end of each exercise stage was found to be very high (r = .9693 in volunteers and r = .9864 in cardiac patients), independent of physical fitness. Even with everyday activities such as walking there was a marked increase in CVT. Due to its close relationship to human metabolism, CVT represents a good parameter for physiologic control of pacing rate.

Mixed venous blood temperature response to exercise in heart failure patients treated with short-term vasodilators.

Deep-body or core temperature decreases during exercise in patients with heart failure, primarily due to the circulatory inadequacies associated with the pathophysiology of this condition. Vasodilators are commonly used to treat patients suffering from heart failure because these drugs improve total cardiac output and blood-flow to the regional circulations. In heart failure patients, the core temperature response to exercise should also be affected if the circulation is improved by vasodilators. Patients with severe heart failure were studied at rest and during upright bicycle exercise before, and after, short-term treatment with vasodilators (2-minoxidil, 3-hydralazine, 5-captopril). Their heart rate increased significantly (P less than 0.05) from rest to exercise before (87 +/- 15 109 +/- 14 beats/min), and after 89 +/- 13- 112 +/- 15 beats/min) vasodilators, but there was no drug-related affect on these changes. Mean arterial and pulmonary capillary wedge pressures were significantly (P less than 0.05) decreased at rest and after the administration of vasodilators (mean arterial pressure 88 +/- 7 mmHg before; 77 +/- 8 mmHg after; pulmonary capillary wedge pressure 25 +/- 8 mmHg before, 19 +/- 9 mmHg after). During exercise, the increases in mean arterial and pulmonary capillary wedge pressures were not significantly different from the before vasodilator values (mean arterial pressure 92 +/- 14 mmHg before, 87 +/- 14 mmHg after; pulmonary capillary wedge pressure 31 +/- 11 mmHg before, 29 +/- 11 mmHg after). Vasodilators increased cardiac output significantly (P less than 0.05) at rest (3.1 +/- 0.6 litre/min to 4.1 +/- 1.1 litre/m) and during exercise (4.8 +/- .2 litre/min-5.6 +/- 1.7 litre/min). The core temperature (mixed venous blood temperature) decreased significantly (P less than 0.05) during exercise from 37.04 +/- 0.62 degrees C to 36.65 +/- 0.65 degrees C, before treatment with vasodilators. After administration of vasodilators, resting core temperature was not significantly different (36.95 +/- 0.54 degrees C) and still decreased significantly (P less than 0.05) during exercise to 36.73 +/- 0.53 degrees C. This decrease was significantly (P less than 0.05) different from the core temperature response before the administration of vasodilators. We conclude that heart failure patients, treated with short-term vasodilators, have an attenuation of the core temperature response that typically occurs during exercise. This change in the core temperature response is the result of the vasodilator-induced improvement in circulation.

Increasing cardiac rate by measurement of right ventricular temperature.

A pacemaker that increases pacing rate in response to exercise enables the pacemaker patient to improve his state of well-being. Possible sensors include atrial rate, Q-T interval, pH, venous oxygen saturation, respiratory rate, cardiac output, body motion, and blood temperature. To determine the efficacy of right ventricular blood temperature as an indicator of exercise, an experimental temperature-controlled pacemaker was developed and was evaluated in dogs. A resulting algorithm was implemented in a microcomputer-based VVI pacemaker which reliably detected exercise and rest from blood temperature when totally implanted. The pacemaker generated two pacing rates to provide increased cardiac output. Data is being obtained to establish feasibility in humans.

The central venous blood temperature as a guide for rate control in pacemaker therapy.

True physiologic pacing is only feasible in patients with heart block and normal sinus rhythm using atrial synchronized pacing. In sick sinus syndrome (SSS) or atrial fibrillation no adequate sensing possibility is present. For these conditions something other than electrical signals must be found to guide rate control. In clinical experiments a thermistor integrated in a bipolar pacing lead was implanted in one of the authors as well as in a pacemaker patient. Treadmill tests at 3, 6, and 10 km per hour have shown no substantial increase of the central venous temperature (CVT) in the lower effort range; an increase of 0.6-0.75 degrees Celsius (degrees C) in the medium range; and an increase of 1.35 degrees C in the higher range, respectively. External pacing in the author, or rate variations by programming the VVI, M unit in the patient at rest do not influence CVT. CVT correlates well in the medium-range group, which mostly reflects the capabilities of the average pacemaker patient. In the higher effort range a delay between rate increase and increase of CVT is noticed. There is no increase in CVT beyond the physiologic variations in the lower effort range.

Skeletal muscle metabolism and insulin resistance during endotoxin shock in the dog

The effect of locally infused endotoxin on gracilis muscle glucose uptake was determined in anesthetized mongrel dogs. The effects of infusion of small amounts of Escherichia coli endotoxin into the arteries of isolated, innervated, constant flow perfused gracilis muscles on glucose uptake and other metabolic variables were determined. Locally infused endotoxin consistently caused a significant and substantial increase in skeletal muscle glucose uptake with no alterations in muscle arteriovenous difference of insulin, oxygen, carbon dioxode, or pH, or in venous blood hematocrit or temperature. These data demonstrate that endotoxin can act locally to increase glucose uptake by skeletal muscle, independent of the action of insulin or other metabolic factors. During natural (free flow) conditions, glucose uptake by the muscle increased markedly during six hours of shock. Increased glucose uptake occurred concomitantly with muscle ischemia and hypoxia. However, when muscle blood flow was held constant, thereby preventing local muscle ischemia and hypoxia, glucose uptake by the gracilis muscle did not change during shock. These results implicate local muscle ischemia and/or hypoxia as the mediator(s) of the increased muscle glucose uptake during shock. Further studies demonstrated that local muscle hypoxia was the stimulus for increased glucose uptake by skeletal muscle during endotoxin shock, and muscle ischemia per se did not after muscle glucose uptake. Since approximately 50% of body mass is composed of skeletal muscle, the contribution of this organ system to the hypoglycemia of endotoxin shock in the dog may be substantial. The ability of insulin to promote glucose diffusion into skeletal muscle before and during gram-negative endotoxin shock was studied in mongrel dogs anesthetized with sodium pentobarbital. The in vivo, isolated, innervated, constant flow perfused gracilis muscle preparation was used. Prior to shock induction, close intra-arterial insulin infusion resulted in a 320% increase in muscle glucose uptake. However, at one, two, and three hours of endotoxin shock, gracilis muscle glucose uptake was unaltered by insulin infusion. This loss of responsiveness to insulin occurred with no alteration in gracilis muscle oxygen uptake, muscle venous P O 2 , or muscle blood flow. During control experiments, however, the muscle response to intra-arterial infusion of insulin (increased glucose uptake) was unaltered during the three-hour control period. These data demonstrate that skeletal muscle insulin resistance develops early and is maintained during three hours of endotoxin shock in the dog.

Effects of hemodynamic changes induced by hyper- or hypothermia on intravenous lipid clearance rate and lipoprotein lipase activity in dogs.

Hyper- and hypothermia was induced in dogs by peritoneal perfusion with warm or cold Lactate-Ringer's solution, the objective being to alter cardiac output. Changes in cardiac index, intravenous lipid clearance rate (K-value), and lipoprotein lipase (LPL) activity, concomitantly with changes of the temperature of the mixed venous blood were investigated. The cardiac index increased significantly with the hyperthermia and there was a close correlation between the cardiac index and the K-value. The LPL activity did not change significantly with changes in blood temperature, and the correlation between the LPL activity and the K-value was not significant. The hemodynamics has to be considered when attempting to discuss the intravenous lipid clearance rate.

Cerebral temperature regulation in resting and running guinea-pigs (Cavia porcellus

1.1. Cerebral, pytegoid plexal venous blood (PP), nasal mucosal (nm) and deep-trunk temperatures (s.c. intrascapular or rectal temperature) were recorded in guinea-pigs during resting exposure to 40°C and during running at 15, 25 and 35°C.2.2. Thermal changes in blood returning from the nm to PP were followed by parallel shifts in brain temperatures which were independent of fluctuations in trunk temperature. In normothermia the brain was warmer than the trunk. In hyperthermia cranial temperatures became distinctly lower than trunk temperature. During exercise hypothalamic (Hyp) temperature increased to 40°C and then decreased due to cooling of PP blood. Trunk temperature, however, rose steeply until the end of the running. Consequently, the brain became 1.5—1.6°C cooler than trunk.3.3. It is proposed that there is a double mechanism of heat removal from the brain. In normothermia cerebral heat is dissipated through arterial blood leaving the heart, in hyperthermia, however, cool nasal blood is collected by the venous lakes adjoining the neurocranium to protect the brain against overheating.

Relationship between peripheral blood flow and blood temperatures in lambs during hypoxemia and hemorrhage.

The relationships between the peripheral blood flow and arterial and venous blood temperatures were examined in 5 lambs (mean weight 10.5 kg, 4-12 weeks old) during hypoxemia and hemorrhage. Blood flow to one hind limb was measured continuously with an electromagnetic flow transducer around the femoral artery. Aortic and venous blood temperatures were monitored by means of thermistor catheters in the descending aorta and iliac vein. The intravascular catheters and flow transducer were implanted chronically and all studies were performed in conscious lambs, resting quietly. Skin temperatures were recorded at the hip and at the foot. The total heat in the hind limb (Htot), the net heat transported by circulating blood (Hbl), and the metabolic heat produced in the hind limb were calculated. The arterial and venous blood temperature were related to peripheral blood flow. When the flow was constant over a control period, blood temperatures remained constant. Hypoxemia, produced by administering a low oxygen gas mixture to the lamb, did not alter femoral blood flow, nor did it affect vascular temperatures. During hemorrhage, femoral blood flow fell, arterial temperature rose by 0.46 degrees C and venous temperature by 0.85 degrees C; arteriovenous temperature difference decreased from 0.85 to 0.44 degrees C. There was an inverse relationship between femoral blood flow and venous temperature in each individual lamb subjected to hemorrhage, with a correlation of 0.91. For each 10-ml/min decrease in peripheral blood flow the venous temperature rose an average of 0.33 degrees C. Changes in peripheral blood flow were immediately reflected by changes in the venous temperature.

Metabolic assessment of exercise in chronic heart failure patients treated with short-term vasodilators.

Metabolic assessment of exercise in chronic heart failure patients treated with short-term vasodilators.

Effects of beta-adrenergic receptor blockade on metabolic rate and mixed venous blood temperature during dynamic exercise.

Mixed venous blood temperature and energy exchange were measured in sixteen healthy male volunteers at rest and during bicycle exercise of 12 min duration performed before and after intravenous administration of propranolol. The rise in blood temperature induced by exercise was about 30% greater following propranolol. This effect was probably due to a reduction of skin blood flow, which impaired the conditions for heat loss from the blood. The exercise induced rise in total energy exchange was reduced after propranolol by around 20 W. In consequence, the calculated mechanical efficiency increased significantly. Since the respiratory quotient showed no increase but rather the reverse, the observed effect could not be attributed to any transient changes in body oxygen stores. The results thus indicate that propranolol caused a true deceleration of the metabolic rate. This effect might be secondary to inhibition of catecholamine-dependent oxygen consuming metabolic processes in peripheral organs. A possible hypothalamic mechanism, triggered by the blood temperature level, is also discussed.

Temperature of Mixed Venous Blood during Exercise

The temperature of mixed venous blood (PA-temp) was measured in the pulmonary artery of healthy male volunteers at rest and during bicycle exercise in the supine position. Oxygen uptake, arteriovenous oxygen difference, and heart rate were determined simultaneously. The subjects were studied both in their basal normokinetic circulatory state and in a hypokinetic circulatory state induced by beta-receptor blockade with propranolol. The PA-temp increased linearly with rising oxygen uptake. During beta-receptor blockade the exercise-induced rise in PA-temp was considerably steeper in relation to work load and to oxygen uptake. Thus when the ordinary ability to increase cardiac output was suppressed by propranolol, an identical dynamic exercise induced a significantly higher PA-temp. A significant correlation (r = 0.92) was found between the rise in PA-temp during exercise and the increase in the arteriovenous oxygen difference. This correlation, which has not been described previously, was not altered by beta-receptor blockade. It is concluded that the close correlation between blood temperature and arteriovenous oxygen difference has a clinical potential for hemodynamic measurements. A simple method for the indirect estimation of arteriovenous oxygen difference by means of blood thermometry would be a considerable laboratory advantage.

Modification of the skin blood flow-body temperature relationship by upright exercise.

Modification of the skin blood flow-body temperature relationship by upright exercise.

The effects of exercise and changes in body temperature on the intrinsic heart rate in man

The intrisic heart rate (IHR) was measured after autonomic blockade by propranolol and atropine in normal human subjects during changes in central body temperature and at two levels of exercise. A direct linear relationship was found between the IHR and mixed venous blood temperature over the range from 35 to 40° C., with a mean slope of 7.1 beats per minute per degree Centigrade. The IHR increased during exercise, both at mild and near maximal levels, in each case by approximately one guarter of the rate increase during the same exercise before autonomic blockade. Neither rises in body temperature nor incomplete blockade of sympathetic stimuli appeared to account for these changes. By analogy with the effects of early hypoxia on cardiac function in dogs after autonomic blockade, it is suggested that increases in the IHR in exercise may represent a direct response of the myocardium to mild hypoxia. Although in 50-year-old normal subjects the IHR was lower than in young adults, and the maximum heart rate in exercise was correspondingly lower, the capacity to increase heart rate in exercise, above its intrinsic level was equal at different ages. Previous exercise increased the variability of serial measurements of the IHR in normal subjects. When exertion was avoided on the day of study, paired measurements one week apart showed a standard deviation of 1.6 beats per minute, or 1.7 per cent.

Effects of respiration and circulation on central blood temperature of the dog.

ARTICLESEffects of respiration and circulation on central blood temperature of the dogHU Wessel, GW James, and MH PaulHU Wessel, GW James, and MH PaulPublished Online:01 Dec 1966https://doi.org/10.1152/ajplegacy.1966.211.6.1403MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAvian Anatomy and Physiology25 July 2014Continuous versus intermittent thermodilution for cardiac output measurement during alveolar recruitment manoeuvres in sheepVeterinary Anaesthesia and Analgesia, Vol. 38, No. 5Cagebirds14 April 2008Pulmonary artery blood temperature and the measurement of cardiac output by thermodilution14 May 2002 | Anaesthesia, Vol. 57, No. 6Semicontinuous cardiac output monitoring using a neural networkCritical Care Medicine, Vol. 27, No. 8Continuous Cardiac Output Monitoring During Adult Liver 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during Cardiac OperationsThe Annals of Thoracic Surgery, Vol. 21, No. 1Clinical applications of thermodilution cardiac output determinationsThe American Journal of Surgery, Vol. 129, No. 4Measurement of Cardiac Output by ThermodilutionNew England Journal of Medicine, Vol. 292, No. 13Alveolar to arterial transmission of oxygen fluctuations due to respiration in anesthetized dogsPfl�gers Archiv European Journal of Physiology, Vol. 340, No. 4The effects of O2 and CO2 and of ambient temperature on ventilatory patterns of dogsRespiration Physiology, Vol. 16, No. 1Respiratory fluctuations of oxygen tension in central venous blood of anesthetized dogsRespiration Physiology, Vol. 15, No. 3Measurement of blood flow by thermodilutionThe American Journal of Cardiology, Vol. 29, No. 2Design of an optimized continuous mini-bolus thermodilution cardiac output monitor using artificial neural networks and genetic algorithms More from this issue > Volume 211Issue 6December 1966Pages 1403-1412 Copyright & PermissionsCopyright © 1966 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1966.211.6.1403PubMed5956557History Published online 1 December 1966 Published in print 1 December 1966 Metrics

COOLING GRADIENTS AND BRAIN DAMAGE WITH DEEP HYPOTHERMIA

M ental changes have been reported by several investigators following operations with the use of cardiopulmonary bypass. 1-6 The reasons for these changes have been numerous: emboli of calcium, muscle, air, 7 fat, 3,10 fibrin, silicon, 9,11 denatured protein, 8 and other factors, such as too rapid warming 5 or cooling. 4 Brain damage has been reported following cardiac operations utilizing surface cooling, 2 cardiopulmonary bypass with moderate cooling and deep cooling, with or without an oxygenator, by Drew, 4,5 Björk, 1 Ehrenhaft, 6 and Brierley. 2 Examination of the brain following death in our own patients who had been cooled rapidly with the use of profound hypothermia demonstrate brain damage. Björk reported brain damage as the cause of death in 5 children undergoing cardiac operations in which deep hypothermia was used with various types of perfusion. Drew 4,5 found mental changes in his first 3 patients who were operated upon after a change was made from a relatively inefficient heat exchanger to an efficient one. After first considering this as a problem of rewarming he found that the symptoms could be prevented by maintaining the cooling gradient (difference between the temperature of venous blood removed from the animal and arterial blood returned) between 10° and 15° C. This experiment is devised to determine whether the width of the cooling gradient during cardiopulmonary bypass has an effect upon brain damage in the dog.

Extremity venous blood temperature and blood clotting mechanisms

The effect of extremity venous blood temperature on the clotting mechanisms was studied. In 20 normal adults, under ordinary indoor conditions, the mean temperatures and standard errors, as measured with needle thermistors, were: greater saphenous vein (lower 3rd of leg), 30.2°C ± 0.29; antecubital vein, 34.6°C ± 0.21; deep gastrocnemius muscle, 36.1±C ± 0.18. In 20 afebrile bed-confined patients the findings were: greater saphenous vein, 29.1°C ±1.12; antecubital vein, 34.2°C ± 0.55, gastrocnemius muscle, 33.7°C ± 0.71. In the range from 22° to 37°C the following linear negative temperature coefficients were found: one-stage prothrombin time, 4%/°C; Lee-White clotting time, 7%/°C; whole blood viscosity, 0.15 centipoise/°C. In vitro clot cohesiveness, as indicated by resistance to compressive and longitudinal stresses, and in vivo clot adhesiveness, as indicated by resistance to dislodgment of clots formed in rabbit venae cavae, were significantly less for clots formed at 25°–30°C than for clots formed at core body temperature. Such effects of low temperature on blood viscosity and the clotting mechanisms have pertinence in regard to the problem of thromboembolism. Submitted on November 27, 1959

A note on the temperature of venous blood and its use in estimating rate of blood flow to the hand: Harris, Kenneth E. and Marvin, H. M.: Heart, 1927, xiv, 49

Convergent syntheses of branched tetraribonucleotide 39, nonaribonucleotide 40 and decaribonucleotide 41, modelling the lariat of pre-mRNA processing reaction, are reported. The first key step in the present strategy involves the condensation of the phosphodiester blocks 1, 5 or 15 with the 3′,5′-dihydroxy-6-N-benzoyl-2′-0-pixyl(9-phenylxanthen-9-yl) adenosine 29 to give 30a (65%), 31a (63%) or 32a (70%). Chemospecific phosphorylation at 3′-OH of these intermediates afforded the intermediates 30b (92%), 31b (83%) or 32b (80%) which were treated with mild acid to achieve a regiospecific removal of the 2′-0-pixyl group to give compounds 30c (74%), 31c (86%) or 32c (85%). The second key step involved the introduction of biscyanoethylphosphotriester moiety to the 2′-OH of the branch-point adenosine in 30c, 31c or 32c in one single step using (biscyanoethoxy)-(diisopropylamino)phosphine to give the crucial branch-point building blocks 30d (46%), 31d (64%) or 32d (62%) with two dissimilar vicinal phosphates at 2′- and 3′- of the branch-point. These blocks were then converted to the fully protected intermediates 33a (59%) [30d+28 → 33a], 34a (69%) [31d+19 → 34a] and 35a (56%) [32d+19 → 35a], and were subsequently treated with a bulky tertiary amine to give the branch-point 2′-cyanoethylphosphodiester blocks 33b (64%), 34b (67%) and 35b (68%). These were then condensed in the usual way with the appropriate 5′-hydroxy block (27 or 25) to give the fully protected branched oligomers 36 (69%) [33b+27 → 36], 37 (67%) [34b+25 → 37] and 38 (63%) [35b+25 → 38]. These oligomers were then deprotected in the usual manner to give the final branched oligoribonucleotides 39,40 and 41 in 62%, 21% and 21% yields respectively. Detailed 500 MHz 1H-NMR and 202.4 MHz 31P-NMR studies on 39,40 and 41 have unequivocally established their purities. Detailed spectroscopic studies such as COSY, HOHAHA & NOESY have also clearly established the structural integrity of the synthetic target compounds.