Respiratory Rates Derived From Arterial Blood Pressure Waveforms in Telemetered Dogs

2020 ◽  
Vol 39 (6) ◽  
pp. 542-546
Author(s):  
Hai-Ming Tang ◽  
Carrie Laduke ◽  
Dave Reynolds ◽  
Cynthia Carey ◽  
Suzette Hahn ◽  
...  

The objective of this study was to extract low frequency respiratory “artifacts” from a standard arterial blood pressure (ABP) waveform to simultaneously derive reliable breathing rates (BR). Arterial blood pressure derived BR values were characterized against respiratory rates simultaneously obtained from the Respiratory Inductive Plethysmography (RIP) system (EMKA). Reference compounds were introduced to evaluate responsiveness of the derived measures to respiratory depressants and stimulants. Male beagle dogs (n = 3) were instrumented with minimally invasive telemetry devices for measurements of ABP and heart rate. The RIP system was utilized simultaneously to collect respiratory rate, tidal volume, and minute volume of each animal following pharmacological challenges. Early results revealed the derived BR’s from ABP waveforms did not correlate well with those measured from the RIP system. Post study X-ray visualization revealed suboptimal catheter positioning, causing poor concordance of BR tallied from the ABP waveforms. Follow-up evaluations were conducted using additional animals instrumented with the ABP catheter tip placement advanced proximal to the thoracic diaphragm. Preliminary data from this subset of animals significantly improved the correlation of BR derived from ABP and respiratory rates recorded by the RIP. This proof of concept investigation was intended to evaluate an algorithm designed to extract additional data from routine cardiac waveforms. We clearly demonstrated that with optimal blood pressure catheter placement and acquisition algorithm, a reliable breathing rate can also be extracted from safety studies without the need for additional studies/animals to capture those respiratory end points.

1964 ◽  
Vol 19 (1) ◽  
pp. 153-156
Author(s):  
W. G. Kubicek ◽  
R. P. Patterson

An electronic system was developed that: computes the oxygen consumption rate of a human subject while breathing room air; measures the flow rate of the expired air, expired air minute volume, tidal volume, arterial blood pressure, and pulse rate; and records the electrocardiogram. The flow rate of the expired air and the fraction concentrations of the CO2 and O2 in the expired air are measured with electronic gas analyzers and then electronically computed to give a continuous analog record of the oxygen consumption rate. All of the variables are continuously recorded in analog form. The average values of oxygen consumption rate, arterial blood pressure, or expired air minute volume and pulse rate are recorded in digital form with print out every minute. analog computer analysis of O2 consumption; continuous analog recording of expired airflow rate and minute volume, tidal volume, arterial blood pressure, and pulse rate; analog-to-digital conversion of O2 consumption, arterial blood pressure, pulse rate, and expired air minute volume; continuous recording of O2 consumption for subject breathing air; continuous electronic computation of O2 consumption Submitted on June 24, 1963


2002 ◽  
Vol 93 (4) ◽  
pp. 1466-1470 ◽  
Author(s):  
William H. Cooke ◽  
Rong Zhang ◽  
Julie H. Zuckerman ◽  
Jian Cui ◽  
Thad E. Wilson ◽  
...  

Animal studies suggest that nitric oxide (NO) plays an important role in buffering short-term arterial pressure variability, but data from humans addressing this hypothesis are scarce. We evaluated the effects of NO synthase (NOS) inhibition on arterial blood pressure (BP) variability in eight healthy subjects in the supine position and during 60° head-up tilt (HUT). Systemic NOS was blocked by intravenous infusion of N G-monomethyl-l-arginine (l-NMMA). Electrocardiogram and beat-by-beat BP in the finger (Finapres) were recorded continuously for 6 min, and brachial cuff BP was recorded before and after l-NMMA in each body position. BP and R-R variability and their transfer functions were quantified by power spectral analysis in the low-frequency (LF; 0.05–0.15 Hz) and high-frequency (HF; 0.15–0.35 Hz) ranges.l-NMMA infusion increased supine BP (systolic, 109 ± 4 vs. 122 ± 3 mmHg, P = 0.03; diastolic, 68 ± 2 vs. 78 ± 3 mmHg, P = 0.002), but it did not affect supine R-R interval or BP variability. Beforel-NMMA, HUT decreased HF R-R variability ( P= 0.03), decreased transfer function gain (LF, 12 ± 2 vs. 5 ± 1 ms/mmHg, P = 0.007; HF, 18 ± 3 vs. 3 ± 1 ms/mmHg, P = 0.002), and increased LF BP variability ( P < 0.0001). After l-NMMA, HUT resulted in similar changes in BP and R-R variability compared with tilt without l-NMMA. Increased supine BP afterl-NMMA with no effect on BP variability during HUT suggests that tonic release of NO is important for systemic vascular tone and thus steady-state arterial pressure, but NO does not buffer dynamic BP oscillations in humans.


2006 ◽  
Vol 291 (6) ◽  
pp. H2816-H2824 ◽  
Author(s):  
David R. Brown ◽  
Lisa A. Cassis ◽  
Dennis L. Silcox ◽  
Laura V. Brown ◽  
David C. Randall

The slope of the log of power versus the log of frequency in the arterial blood pressure (BP) power spectrum is classically considered constant over the low-frequency range (i.e., “fractal” behavior), and is quantified by β in the relationship “1/ fβ.” In practice, the fractal range cannot extend to indefinitely low frequencies, but factor(s) that terminate this behavior, and determine β, are unclear. We present 1) data in rats ( n = 8) that reveal an extremely low frequency spectral region (0.083–1 cycle/h), where β approaches 0 (i.e., the “shoulder”); and 2) a model that 1) predicts realistic values of β within that range of the spectrum that conforms to fractal dynamics (∼1–60 cycles/h), 2) offers an explanation for the shoulder, and 3) predicts that the “successive difference” in mean BP (mBP) is an important parameter of circulatory function. We recorded BP for up to 16 days. The absolute difference between successive mBP samples at 0.1 Hz (the successive difference, or Δ) was 1.87 ± 0.21 mmHg (means ± SD). We calculated β for three frequency ranges: 1) 0.083–1; 2) 1–6; and 3) 6–60 cycles/h. The β for all three regions differed ( P < 0.01). For the two higher frequency ranges, β indicated a fractal relationship (β6–60/h = 1.27 ± 0.01; β1–6/h = 1.80 ± 0.16). Conversely, the slope of the lowest frequency region (i.e., the shoulder) was nearly flat (β0.083–1 /h = 0.32 ± 0.28). We simulated the BP time series as a random walk about 100 mmHg with ranges above and below of 10, 30, and 50 mmHg and with Δ from 0.5 to 2.5. The spectrum for the conditions mimicking actual BP time series (i.e., range, 85–115 mmHg; Δ, 2.00) resembled the observed spectra, with β in the lowest frequency range = 0.207 and fractal-like behavior in the two higher frequency ranges (β = 1.707 and 2.057). We suggest that the combined actions of mechanisms limiting the excursion of arterial BP produce the shoulder in the spectrum and that Δ contributes to determining β.


2001 ◽  
Vol 281 (5) ◽  
pp. H1870-H1880 ◽  
Author(s):  
D. Walter Wray ◽  
Kevin J. Formes ◽  
Martin S. Weiss ◽  
Albert H. O-Yurvati ◽  
Peter B. Raven ◽  
...  

This study was designed to investigate the importance of vagal cardiac modulation in arterial blood pressure (ABP) stability before and after glycopyrrolate or atropine treatment. Changes in R-R interval (RRI) and ABP were assessed in 10 healthy young (age, 22 ± 1.8 yr) volunteers during graded lower body negative pressure (LBNP) before and after muscarinic cholinergic (MC) blockade. Transient hypertension was induced by phenylephrine (1 μg/kg body wt), whereas systemic hypotension was induced by bilateral thigh cuff deflation after a 3-min suprasystolic occlusion. Power spectral densities of systolic [systolic blood pressure (SBP)] and diastolic ABP variability were examined. Both antimuscarinic agents elicited tachycardia similarly without significantly affecting baseline ABP. The increase in SBP after phenylephrine injection (+14 ± 2 mmHg) was significantly augmented with atropine (+26 ± 2 mmHg) or glycopyrrolate (+27 ± 3 mmHg) and associated with a diminished reflex bradycardia. The decrease in SBP after cuff deflation (−9.2 ± 1.2 mmHg) was significantly greater after atropine (−15 ± 1 mmHg) or glycopyrrolate (−14 ± 1 mmHg), with abolished reflex tachycardia. LBNP significantly decreased both SBP and RRI. However, after antimuscarinic agents, the reduction in SBP was greater ( P < 0.05) and was associated with less tachycardia. Antimuscarinic agents reduced ( P < 0.05) the low-frequency (LF; 0.04–0.12 Hz) power of ABP variability at rest. The LF SBP oscillation was significantly augmented during LBNP, which was accentuated ( P < 0.05) after antimuscarinic agents and was correlated ( r = −0.79) with the decrease in SBP. We conclude that antimuscarinic agents compromised ABP stability by diminishing baroreflex sensitivity, reflecting the importance of vagal cardiac function in hemodynamic homeostasis. The difference between atropine and glycopyrrolate was not significant.


1997 ◽  
Vol 4 (1) ◽  
pp. 56-61 ◽  
Author(s):  
Petter Aadahl ◽  
Jan Lundbom ◽  
Staal Hatlinghus ◽  
Hans O. Myhre

Purpose: To investigate the feasibility of regional anesthesia for endovascular repair of abdominal aortic aneurysms (AAAs). Methods: Since February 1995, 21 patients (17 men and 4 women; median age 67 years, range 49 to 80) have been treated with endovascular technique for true infrarenal AAA using Mialhe Stentor bifurcated grafts. A single dose of spinal anesthesia combined with epidural anesthesia was used in all procedures. Electrocardiography and arterial blood pressure were monitored. Results: No cases of emboli, hematoma, or graft migration were seen, and there were no reoperations or conversions to open operation. Arterial blood pressure was stable at a satisfactory level from induction of anesthesia throughout the procedure, and there was no period of clinically significant hypotension during any implantation. One patient died on the second postoperative day from cardiac and renal insufficiency. Three endoleaks were observed during the procedure; one healed spontaneously within 5 weeks, and the other two were repaired by endovascular techniques after 1 and 4 months, respectively. During follow-up, one patient died at 6 months from pancreatic carcinoma. Conclusions: The application of regional anesthesia is feasible for endovascular treatment of AAA. The arterial blood pressure remained stable throughout the procedure, and all patients, with two exceptions, were mobilized on the first day and placed on a regular diet. Based on these early results, it appears that regional anesthesia is feasible, effective, and safe for endovascular AAA repair.


1997 ◽  
Vol 272 (6) ◽  
pp. R2034-R2039 ◽  
Author(s):  
C. D. Wagner ◽  
A. Just ◽  
B. Nafz ◽  
P. B. Persson

The aim of this study was to investigate spontaneous variability of arterial blood pressure in conscious foxhounds in the absence of direct sympathetic and parasympathetic influences. Autonomic blockade was achieved by administration of the ganglionic blocking agent hexamethonium (n = 7). In contrast to the control group (n = 7), marked oscillations with a cycle length of 100 s (0.01 Hz) were observed. The relationship of the power densities of the oscillation band (0.01 +/- 0.005 Hz) to the total power increased threefold (0.213 +/- 0.007 vs. 0.057 +/- 0.005; P < 0.01). The 0.01-Hz oscillations typically commenced after some delay. To test whether the absence of the mechanoreceptor afferents was responsible for these fluctuations, we investigated an additional group of foxhounds that were subjected to total baroreceptor and cardiopulmonary receptor denervation (n = 7). Neither in this protocol, nor in a group subjected to denervation and ganglionic blockade (n = 6), did we observe sustained oscillations in this frequency range. Since the oscillations were not seen after combined afferent (mechanoreceptor denervation) and efferent (ganglionic) blockade, central oscillators as a source of the oscillations can be ruled out. A simple model of a circulating pressoric factor may explain the fluctuations, provided that there is a time delay between the stimulus and the release or action of the factor. The findings suggest that a circulating factor accounts for the 0.01-Hz oscillations, which is dependent on intact pathways from the cardiac receptors or baroreceptors to the central nervous system. This hypothesis is put forward since cardiopulmonary and baroreceptor denervation blocked the oscillations seen after ganglionic blockade.


Author(s):  
G.F. Stegmann ◽  
L. Bester

Midazolam was administered intravenously to 8 bitches in a randomised, placebo-controlled clinical trial before propofol induction of surgical anaesthesia. Anaesthesia was maintained with isoflurane-in-oxygen during surgical endoscopic examination of the uterus and ovariohysterectomy. Clenbuterol was administered at the start of surgery to improve uterine muscle relaxation, and to facilitate endoscopic examination of the uterus. Ventilation was controlled. Induction of anaesthesia with propofol to obtain loss of the pedal reflex resulted in a statistically significant (P < 0.05) decrease in minute volume and arterial oxygen partial pressure in the midazolam group. Apnoea also occurred in 50 % of dogs in the midazolam group. The dose for propofol in the midazolam group was 7.4 mg/kg compared to 9.5 mg/kg in the control. Minute volume was significantly (P < 0.05) higher in both groups during isoflurane maintenance, compared to the value after incremental propofol to obtain loss of the pedal reflex. Propofol induction resulted in a 25-26 % reduction in the mean arterial blood pressure in both groups, and the administration of clenbuterol at the start of surgery resulted in a transient, but statistically significant (P < 0.05), decrease in mean arterial blood pressure in the midazolam group during isoflurane anaesthesia. It is concluded that intravenous midazolam premedication did not adversely affect cardiovascular function during propofol induction, but intra-operative clenbuterol during isoflurane maintenance of anaesthesia may result in transient hypotension. Midazolam premedication may increase adverse respiratory effects when administered before propofol induction of anaesthesia.


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