scholarly journals Induction of oscillatory ventilation pattern using dynamic modulation of heart rate through a pacemaker

2008 ◽  
Vol 295 (1) ◽  
pp. R219-R227 ◽  
Author(s):  
Charlotte H. Manisty ◽  
Keith Willson ◽  
Justin E. R. Davies ◽  
Zachary I. Whinnett ◽  
Resham Baruah ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Cardiac Pacemaker ◽  
Breathing Patterns ◽  
Cardiac Pacemakers ◽  
Oscillatory Ventilation ◽  
Disease States ◽  
Ventilation Pattern ◽  
End Tidal ◽  
Respiratory Gases

For disease states characterized by oscillatory ventilation, an ideal dynamic therapy would apply a counteracting oscillation in ventilation. Modulating respiratory gas transport through the circulation might allow this. We explore the ability of repetitive alternations in heart rate, using a cardiac pacemaker, to elicit oscillations in respiratory variables and discuss the potential for therapeutic exploitation. By incorporating acute cardiac output manipulations into an integrated mathematical model, we observed that a rise in cardiac output should yield a gradual rise in end-tidal CO2 and, subsequently, ventilation. An alternating pattern of cardiac output might, therefore, create oscillations in CO2 and ventilation. We studied the effect of repeated alternations in heart rate of 30 beats/min with periodicity of 60 s, on cardiac output, respiratory gases, and ventilation in 22 subjects with implanted cardiac pacemakers and stable breathing patterns. End-tidal CO2 and ventilation developed consistent oscillations with a period of 60 s during the heart rate alternations, with mean peak-to-trough relative excursions of 8.4 ± 5.0% ( P < 0.0001) and 24.4 ± 18.8% ( P < 0.0001), respectively. Furthermore, we verified the mathematical prediction that the amplitude of these oscillations would depend on those in cardiac output ( r = 0.59, P = 0.001). Repetitive alternations in heart rate can elicit reproducible oscillations in end-tidal CO2 and ventilation. The size of this effect depends on the magnitude of the cardiac output response. Harnessed and timed appropriately, this cardiorespiratory mechanism might be exploited to create an active dynamic responsive pacing algorithm to counteract spontaneous respiratory oscillations, such as those causing apneic breathing disorders.

Ventilatory responses to cardiac output changes in patients with pacemakers

1981 ◽  
Vol 51 (5) ◽  
pp. 1103-1107 ◽  
Author(s):  
P. W. Jones ◽  
W. French ◽  
M. L. Weissman ◽  
K. Wasserman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Oxygen Uptake ◽  
Blood Gas ◽  
Cardiac Pacemakers ◽  
Ventilatory Responses ◽  
Mean Delay ◽  
Arterial Blood ◽  
End Tidal

Cardiac output changes were induced by step changes of heart rate (HR) in six patients with cardiac pacemakers during monitoring of ventilation and gas exchange, breath-by-breath. Mean low HR was 48 beats/min; mean high HR was 82 beats/min. The change of oxygen uptake immediately after the HR change was used as an index of altered cardiac output. After HR increase, oxygen uptake (V02) rose by 34 +/- 20% (SD), and after HR decrease, Vo2 fell by 24 +/- 11%. There was no change in arterial blood pressure. After HR increase, ventilation increased, after a mean delay of 19 +/- 4 s; after HR reduction, ventilation fell, after a mean delay of 29 +/- 7 s. In the period between HR increase and the resulting increase in ventilation, end-tidal PCO2 (PETCO2) rose by 2.6 +/- 2.0 Torr, and in the period between HR decreases and the fall in ventilation, PETCO2 dropped by 2.9 +/- 2.2 Torr. The response time and end-tidal gas tension changes implicate the chemoreceptors in the reflex correction of blood gas disturbances that may result from imbalances between cardiac output and ventilation.

Pet CO2 inversely affects MSNA response to orthostatic stress

2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orthostatic Intolerance ◽  
Muscle Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Burst Frequency ◽  
Head Up Tilt ◽  
End Tidal ◽  
Combined Data

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.

scholarly journals The Cardiovascular Effects of Pancuronium in the Dog during Pentobarbitone Anaesthesia

1976 ◽  
Vol 4 (2) ◽  
pp. 135-137 ◽  
Author(s):  
J. M. Gibbs ◽  
A. R. Tait ◽  
M. K. Sykes
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Body Weight ◽  
Cardiac Output ◽  
Muscle Relaxation ◽  
Cardiovascular Effects ◽  
End Tidal Carbon Dioxide ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Cardiac Output Measurements

The effect of pancuronium on the cardiovascular system of the dog was studied in 12 greyhounds who were anaesthetized with pentobarbitone 30–40 mg/kg body weight. During the study, the animals were artificially ventilated to give an end-tidal carbon dioxide in the range 4·0–4·5 per cent. Duplicate cardiac output measurements were made before and ten minutes after the intravenous administration of pancuronium (0·18 mg/kg). There was a slight (but statistically insignificant) fall in cardiac output. Heart rate, aortic and pulmonary arterial pressures remained substantially unaltered. It is suggested that pancuronium should be used in the dog when muscle relaxation is required during pentobarbitone anaesthesia. In this way cardiovascular changes related to the drugs themselves will be minimized.

Dynamics of cardiac, respiratory, and metabolic function in men in response to step work load

1982 ◽  
Vol 52 (5) ◽  
pp. 1198-1208 ◽  
Author(s):  
Y. Miyamoto ◽  
T. Hiura ◽  
T. Tamura ◽  
T. Nakamura ◽  
J. Higuchi ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Time Constant ◽  
Minute Ventilation ◽  
Initial Period ◽  
Work Load ◽  
Work Intensity ◽  
Control Value ◽  
End Tidal

Stroke volume, heart rate, cardiac output, tidal volume, respiratory frequency, minute ventilation, end-tidal tensions of O2 and CO2, O2 uptake, CO2 output, and respiratory exchange ratio were measured simultaneously in healthy male volunteers before, during, and after upright bicycle exercise from 0 to 360 and 720 kpm/min. The circulatory variables were determined continuously once per 20 cardiac cycles and the respiratory variables breath by breath using separate computer-based systems in which an impedance pneumograph and an impedance cardiograph were incorporated. Stroke volume, heart rate, and cardiac output started to increase without measurable delay at the onset of exercise. Stroke volume increased by 20% from resting control value in response to the mildest exercise and essentially leveled off with a further increase in work load. Time constant for cardiac output increased with the increasing work load. Time constant for minute ventilation was much longer than that for cardiac output and independent of work intensity. A good synchronization between the ventilation and cardiac output responses at an initial period of transitions from rest to exercise and from exercise to rest seems to support the concept of cardiodynamic hyperpnea.

Mixed-effects Modeling of the Influence of Alfentanil on Propofol Pharmacokinetics

2004 ◽  
Vol 100 (4) ◽  
pp. 795-805 ◽  
Author(s):  
Martijn J. Mertens ◽  
Erik Olofsen ◽  
Anton G. L. Burm ◽  
James G. Bovill ◽  
Jaap Vuyk
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Venous Blood ◽  
Compartment Model ◽  
Volume Of Distribution ◽  
Mixed Effects ◽  
Pharmacokinetic Parameters ◽  
Population Pharmacokinetic ◽  
Elimination Clearance ◽  
End Tidal

Background The influence of alfentanil on the pharmacokinetics of propofol is poorly understood. Therefore, the authors studied the effect of a pseudo-steady state concentration of alfentanil on the pharmacokinetics of propofol. Methods The pharmacokinetics of propofol were studied on two occasions in eight male volunteers in a randomized crossover manner with a 3-week interval. While volunteers breathed 30% O2 in air, 1 mg/kg intravenous propofol was given in 1 min, followed by 3 mg.kg(-1).h(-1) for 59 min (sessions A and B). During session B, a target-controlled infusion of alfentanil (target concentration, 80 ng/ml) was given from 10 min before the start until 6 h after termination of the propofol infusion. Blood pressure, cardiac output, electrocardiogram, respiratory rate, oxygen saturation, and end-tidal carbon dioxide were monitored. Venous blood samples for determination of the blood propofol and plasma alfentanil concentration were collected until 6 h after termination of the propofol infusion. Nonlinear mixed-effects population pharmacokinetic models examining the influence of alfentanil and hemodynamic parameters on propofol pharmacokinetics were constructed. Results A two-compartment model, including a lag time accounting for the venous blood sampling, adequately described the concentration-time curves of propofol. Alfentanil decreased the elimination clearance of propofol from 2.1 l/min to 1.9 l/min, the distribution clearance from 2.7 l/min to 2.0 l/min, and the peripheral volume of distribution from 179 l to 141 l. Scaling the pharmacokinetic parameters to cardiac output, heart rate, and plasma alfentanil concentration significantly improved the model. Conclusions Alfentanil alters the pharmacokinetics of propofol. Cardiac output and heart rate have an important influence on the pharmacokinetics of propofol.

Cardiopulmonary readjustments in passive tilt

1979 ◽  
Vol 47 (3) ◽  
pp. 503-507 ◽  
Author(s):  
S. V. Matalon ◽  
L. E. Farhi
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Random Sequence ◽  
Upright Position ◽  
Alveolar Ventilation ◽  
Gravity Effect ◽  
Threshold Values ◽  
Ample Evidence ◽  
Residual Capacity ◽  
End Tidal

There is ample evidence that posture affects many cardiorespiratory variables, but the extent to which secondary reflex mechanisms complement or oppose the primary gravity effect is not clear. We have addressed ourselves to this problem by studying five normal volunteers, passively tilted from the supine to the upright position in 15 degrees increments, in random sequence, determinging cardiac output (Q), heart rate (HR), stroke volume (SV), minute and alveolar ventilation (VE and VA), functional residual capacity (FRC), and arterial-end-tidal PCO2 pressure difference. In each position, four to five measurements were obtained by noninvasive techniques. Changes in Q and in FRC were linearly related to the sine of the tilt angle, indicating that reflexes were either absent or that their net effect was proportional to the effects of gravity; this was clearly not the case for other variables (HR, SV, VE, VA) in which it was possible to demonstrate threshold values for the appearance of secondary changes.

Cardiovascular and Metabolic Responses to Electrical Stimulation-Induced Leg Exercise in Spinal Cord Injury

1997 ◽  
Vol 36 (04/05) ◽  
pp. 372-375 ◽  
Author(s):  
J. R. Sutton ◽  
A. J. Thomas ◽  
G. M. Davis
Keyword(s):  
Spinal Cord ◽  
Heart Rate ◽  
Spinal Cord Injury ◽  
Cardiac Output ◽  
Electrical Stimulation ◽  
Knee Flexion ◽  
Flexion Extension ◽  
Cord Injury ◽  
Leg Exercise ◽  
Leg Muscle

Abstract:Electrical stimulation-induced leg muscle contractions provide a useful model for examining the role of leg muscle neural afferents during low-intensity exercise in persons with spinal cord-injury and their able-bodied cohorts. Eight persons with paraplegia (SCI) and 8 non-disabled subjects (CONTROL) performed passive knee flexion/extension (PAS), electrical stimulation-induced knee flexion/extension (ES) and voluntary knee flexion/extension (VOL) on an isokinetic dynamometer. In CONTROLS, exercise heart rate was significantly increased during ES (94 ± 6 bpm) and VOL (85 ± 4 bpm) over PAS (69 ± 4 bpm), but no changes were observed in SCI individuals. Stroke volume was significantly augmented in SCI during ES (59 ± 5 ml) compared to PAS (46 ± 4 ml). The results of this study suggest that, in able-bodied humans, Group III and IV leg muscle afferents contribute to increased cardiac output during exercise primarily via augmented heart rate. In contrast, SCI achieve raised cardiac output during ES leg exercise via increased venous return in the absence of any change in heart rate.

Diastolic pressure and peripheral resistance during stellate ganglion stimulation

1963 ◽  
Vol 204 (1) ◽  
pp. 71-72 ◽  
Author(s):  
Edward D. Freis ◽  
Jay N. Cohn ◽  
Thomas E. Liptak ◽  
Aristide G. B. Kovach
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Total Peripheral Resistance ◽  
Diastolic Pressure ◽  
Stellate Ganglion ◽  
Peripheral Resistance ◽  
Resistance Vessels ◽  
Left Stellate Ganglion ◽  
Increased Blood Flow

The mechanism of the diastolic pressure elevation occurring during left stellate ganglion stimulation was investigated. The cardiac output rose considerably, the heart rate remained essentially unchanged, and the total peripheral resistance fell moderately. The diastolic rise appeared to be due to increased blood flow rather than to any active changes in resistance vessels.

End-tidal CO2 pressure in the monitoring of cardiac output during canine hemorrhagic shock

1990 ◽  
Vol 5 (1) ◽  
pp. 42-46 ◽  
Author(s):  
Arnaldo Dubin ◽  
Carlos Silva ◽  
Gladys Calvo ◽  
Javier Valli ◽  
Osvaldo Fariña ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Hemorrhagic Shock ◽  
End Tidal ◽  
End Tidal Co2

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

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