Measuring the level of agreement between directly measured blood pressure and pressure readings obtained with a veterinary-specific oscillometric unit in anesthetized dogs

2013 ◽  
Vol 23 (1) ◽  
pp. 37-40 ◽  
Author(s):  
Mark J. Acierno ◽  
Erika Fauth ◽  
Mark A. Mitchell ◽  
Anderson da Cunha
2020 ◽  
Vol 48 ◽  
Author(s):  
Bárbara Silva Correia ◽  
Eduardo Raposo Monteiro ◽  
João Victor Barbieri Ferronatto ◽  
Luciana Branquinho Queiroga ◽  
José Ricardo Herrera Becerra

Background: Arterial blood pressure is one of the most commonly variables monitored during anesthetic procedures in veterinary patients. The most reliable method for measuring arterial blood pressure in dogs and cats is the direct (invasive) method. However, the oscillometric method is less complex and more practical for clinical routine in small animals. Nevertheless, oscillometric monitors present great variability in accuracy. The present study aimed to determine the accuracy of the Delta Life DL 1000 oscillometric monitor for measurement of systolic, mean and diastolic blood pressures (SAP, MAP and DAP, respectively) in anesthetized dogs of different weight ranges.Materials, Methods & Results: This study was approved by the Institutional Ethics Committee of Animal Use. Fifteen female dogs of different breeds, weighing 11.6 ± 10.0 kg and with a mean age of 48 ± 51 months were used. All animals were scheduled for elective surgery under general anesthesia in the Institution Veterinary Hospital. Dogs were anesthetized with morphine, propofol and isoflurane and had one 20 or 22 gauge catheter introduced into the dorsal pedal artery for continuous, invasive monitoring of SAP, MAP and DAP. A blood pressure cuff was positioned over the middle third of the radius and connected to Delta Life DL 1000 monitor. Oscillometric readings of SAP, MAP and DAP were registered every 5 minutes, and invasive values were simultaneously recorded. Values obtained with both methods were compared (invasive versus oscillometric) by use of the Bland Altman method to determine the bias, standard deviation of bias and 95% limits of agreement. The percentages of errors between the methods within 10 mmHg and within 20 mmHg were calculated. The results obtained were compared with the criteria from the American College of Veterinary Internal Medicine (ACVIM) for validation of indirect methods of arterial blood pressure measurement. Data were stratified into two groups according to the weight: < 10 kg (Group 1; n = 9); and ≥ 10 kg (Group 2; n = 6). In Group 1, 119 paired measurements were obtained, four of which classified as hypotension (SAP < 90 mmHg), 98 as normotension (SAP from 90 to 140mmHg) and 17 as hypertension (SAP > 140 mmHg). Bias (± SD) values in Group 1 were as follows: SAP, 5.2 ± 18.1 mmHg; MAP, -3.4 ± 17.2 mmHg; and DAP, 12.0 ± 17.5 mmHg. The percentages of errors within 10 mmHg were 40.3% for SAP; 45.4% for MAP and 28.6% for DAP. The percentages of errors within 20 mmHg were 72.3% for SAP, 84.0% for MAP and 68.1% for DAP. In Group 2, 66 paired measurements were obtained, nine of which classified as hypotension, 56 as normotension and one as hypertension. Bias (± SD) in Group 2 were as follows: SAP, 13.6 ± 14.3 mmHg; MAP, -1.1 ± 13.5 mmHg; and DAP, 8.2 ± 16.0 mmHg. The percentages of errors within 10 mmHg were 33.3% for SAP, 77.3% for MAP and 33.3% for DAP. The percentages of errors within 20 mmHg were 65.1% for SAP, 92.4% for MAP and 83.4% for DAP.Discussion: Based on the results of this study and reference criteria from the ACVIM, the Delta Life DL 1000 monitor had a poor accuracy for SAP, MAP and DAP and did not meet the criteria from the ACVIM in anesthetized dogs under 10 kg. Measurements of MAP in dogs ≥ 10 kg met the ACVIM criteria, but measurements of SAP and DAP did not. Based on the findings in this study, the DL 1000 oscillometric monitor is not recommended for blood pressure measurement in anesthetized dogs < 10 kg. In dogs ≥ 10 kg, measurements of MAP yielded acceptable values, but SAP and DAP measurements did not.


1998 ◽  
Vol 34 (1) ◽  
pp. 84-91 ◽  
Author(s):  
A Bufalari ◽  
SM Miller ◽  
C Giannoni ◽  
CE Short

Cardiovascular, pulmonary, and quantitative electroencephalographic parameters were assessed in 12 anesthetized dogs to determine the compatibility of the injectable anesthetic propofol with halothane and isoflurane. No cases of apnea were observed during induction of anesthesia. An adequate level of anesthesia was established in each protocol as judged by both the lack of response to mechanical noxious stimuli (i.e., tail clamping) and evidence of reduction in total amplitude of brain wave activity. The initial propofol-mediated decrease in arterial blood pressure continued during either halothane (52.4%) or isoflurane (38%) anesthesia without a simultaneous increase in heart rate. The results of this study suggest that propofol, in combination with inhalant agents, can be used effectively and safely for canine anesthesia in veterinary practice.


1984 ◽  
Vol 247 (4) ◽  
pp. R655-R662
Author(s):  
S. Koyama

The time course of changes in mean blood pressure (MBP), heart rate (HR), and renal blood flow (RBF) in a control group of anesthetized dogs given only endotoxin (1 mg/kg iv) was compared with groups pretreated with alpha-antagonists either intravenously or intracisternally (ic). The decreases in MBP and RBF in the control group were abolished by intracisternal prazosin (0.1 mg/kg ic). MBP response to endotoxin after intravenous prazosin did not differ from that of the control group; however, the endotoxin-induced decrease in RBF after intravenous prazosin was significantly greater than that in the control group. HR responses to endotoxin were not altered by either intracisternal or intravenous prazosin. MBP and RBF responses to endotoxin after intravenous or intracisternal yohimbine (0.5 mg/kg iv or ic) did not differ from the control responses. However, significant differences occurred in the time course of changes in HR only when yohimbine was administered intracisternally. These observations suggest that the hypotensive effect and reduction of RBF due to endotoxin may be mediated by alpha 1-adrenoceptors at least in the central nervous system and that of HR response may be mediated alpha 2-adrenoceptors.


1993 ◽  
Vol 265 (1) ◽  
pp. H103-H107 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
T. Okamura

Basilar arterial diameters were angiographically measured in anesthetized dogs in which systemic blood pressure and heart rate were also monitored. Injections of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, into the cisterna magna produced a significant, persistent decrease in arterial diameter, the effect being reversed by intracisternal injections of L-arginine. The vasoconstrictor effect of L-NNA was diminished in dogs treated with hexamethonium. On the other hand, treatment with phentolamine in a dose sufficient to lower blood pressure to a level similar to that attained with hexamethonium did not inhibit, but rather potentiated, the effect of intracisternal L-NNA. Nicotine injected into the vertebral artery significantly dilated the basilar artery. The effect was abolished by treatment with L-NNA applied intracisternally, the inhibition being reversed by the addition of L-arginine. Systemic blood pressure and heart rate were not altered by intracisternally applied L-NNA and L-arginine. These findings support the hypothesis that basilar arterial constriction caused by intracisternal L-NNA is associated with a suppression of NO synthesis in nitroxidergic nerves innervating the cerebroarterial wall rather than an elimination of basal release of NO from the endothelium. Functional importance of nitroxidergic vasodilator innervation in cerebral arteries in vivo is thus clarified.


1965 ◽  
Vol 209 (4) ◽  
pp. 751-756 ◽  
Author(s):  
Vincent V. Glaviano ◽  
Mary Ann Klouda

Cardiac responses to electrical stimulation of the right or left stellate ganglion were recorded from 16 open-chest anesthetized dogs in hemorrhagic shock. Shock was induced by bleeding the animals to a mean blood pressure of 40 mm Hg. This level of pressure was maintained for 4 hr, during which time blood pressure, heart rate, force of myocardial contraction, and intraventricular pressures were recorded. Stimulation of the stellate ganglion for 15–40 sec every 30 min after hemorrhage showed a gradual decrease in these parameters to levels below control. The reinfusion of blood and the infusion of exogenous l-norepinephrine did not restore an increase in force of cardiac contraction to stellate stimulation. Myocardial epinephrine and norepinephrine levels in shock were found not to differ from those in 14 normal dog hearts. In contrast to almost complete myocardial refractoriness to stellate stimulation in hemorrhagic shock, stimulation of the vagus nerve elicited bradycardia and eventual cardiac arrest. The decrease observed in force of cardiac contraction to stimulation of the stellate ganglion in hemorrhagic shock may be due to depletion of norepinephrine stores in the heart.


1965 ◽  
Vol 209 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson

The possibility that mechanisms secondary to the increased ventilation may contribute significantly to the circulatory responses to systemic hypoxia was explored in anesthetized dogs. In 14 spontaneously breathing dogs systemic hypoxia induced by breathing 7.5% oxygen in nitrogen increased cardiac output, heart rate, mean arterial blood pressure, and femoral arterial flow, and decreased systemic and hindlimb vascular resistances. In 14 dogs whose ventilation was kept constant by means of a respirator pump and intravenous decamethonium, systemic hypoxia did not change cardiac output, femoral arterial flow, or limb vascular resistance; it significantly decreased heart rate and significantly increased systemic vascular resistance. In seven spontaneously breathing dogs arterial blood pCO2 was maintained at the resting level during systemic hypoxia. The increase in heart rate was significantly less pronounced but the other circulatory findings were not different from those found during hypocapnic hypoxia. Thus, mechanisms secondary to increased ventilation contribute significantly to the circulatory responses to systemic hypoxia. Hypocapnia accounts partly for the increased heart rate, but not for the other circulatory responses.


1957 ◽  
Vol 189 (3) ◽  
pp. 576-579 ◽  
Author(s):  
E. Allbaugh Farrand ◽  
R. Larsen ◽  
Steven M. Horvath

The changes in splanchnic blood flow and related metabolic functions which occurred as the result of the infusion of 0.1 µg/kg/min. of l-epinephrine and l-norepinephrine for 10 minutes were measured in anesthetized dogs. l-Epinephrine elicited a marked increase in estimated splanchnic blood flow and no change in mean arterial pressure. While a significantly increased mean arterial blood pressure was observed following the administration of l-norepinephrine, no change in estimated splanchnic blood flow occurred. Arterial oxygen content was increased significantly with both drugs. Utilization of oxygen by the splanchnic bed was not changed during the infusion of either drug but was increased during the postepinephrine infusion period.


1978 ◽  
Vol 234 (2) ◽  
pp. H152-H156
Author(s):  
G. S. Geis ◽  
G. Barratt ◽  
R. D. Wurster

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.


1990 ◽  
Vol 259 (4) ◽  
pp. F645-F652 ◽  
Author(s):  
S. Y. Chou ◽  
A. Dahhan ◽  
J. G. Porush

The renal actions of endothelin were examined by infusing it intrarenally in anesthetized dogs at 4 ng.min-1.kg-1 without affecting arterial blood pressure or cardiac output. Endothelin infusion caused a transient and significant increase in renal blood flow (RBF) by 13 +/- 2%, followed by large decreases in RBF and glomerular filtration rate (GFR; by 26 +/- 2 and 23 +/- 7%, respectively) but did not alter urine flow rate or absolute sodium excretion. After endothelin infusion, renal venous and arterial plasma 6-ketoprostaglandin F1 alpha increased from 250 +/- 58 and 117 +/- 31 to 1,044 +/- 249 and 617 +/- 211 pg/ml, respectively, and its renal output increased from 339 +/- 99 to 963 +/- 202 pg.min-1.g-1 (P less than 0.01 for all). The renal prostacyclin synthesis was augmented by endothelin without stimulating the renal renin release or norepinephrine output. Inhibition of prostaglandin synthesis with indomethacin partially prevented the early renal vasodilation induced by endothelin, which then caused a more pronounced decline in RBF and GFR (by 65 +/- 7 and 54 +/- 8%, respectively). With suppression of prostacyclin synthesis, inhibition of renin release by endothelin was observed. Thus the vasoconstrictive effects of endothelin on renal hemodynamics are significantly modified by its ability to enhance production of vasodilators, including prostacyclin.


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