scholarly journals 779 Blood Pressure and Heart Rate do not Reflect Cardiac Output in Critically ill Children

2012 ◽  
Vol 97 (Suppl 2) ◽  
pp. A224-A224
Author(s):  
A. Nusmeier ◽  
P. Gooskens ◽  
J. v. d. Hoeven ◽  
J. Lemson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Critically Ill ◽  
Critically Ill Children

scholarly journals Heart Rate and Blood Pressure Centile Curves and Distributions by Age of Hospitalized Critically Ill Children

2017 ◽  
Vol 5 ◽  
Author(s):  
Danny Eytan ◽  
Andrew J. Goodwin ◽  
Robert Greer ◽  
Anne-Marie Guerguerian ◽  
Peter C. Laussen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Critically Ill ◽  
Critically Ill Children

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.

Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson
Keyword(s):  
Heart Failure ◽  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Peripheral Resistance ◽  
Open Loop ◽  
Ventricular Pacing ◽  
Baroreflex Control ◽  
Rapid Ventricular Pacing ◽  
Reflex Control

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.

Development of a Heart Rate Variability Risk Score to Predict Organ Dysfunction and Death in Critically Ill Children

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Colleen M. Badke ◽  
Lauren E. Marsillio ◽  
Michael S. Carroll ◽  
Debra E. Weese-Mayer ◽  
L. Nelson Sanchez-Pinto
Keyword(s):  
Heart Rate ◽  
Heart Rate Variability ◽  
Critically Ill ◽  
Organ Dysfunction ◽  
Risk Score ◽  
Critically Ill Children

The effect of Trendelenburg and modified trendelenburg positions on cardiac output, blood pressure, and oxygenation: a preliminary study

1994 ◽  
Vol 3 (5) ◽  
pp. 382-386 ◽  
Author(s):  
CL Ostrow ◽  
E Hupp ◽  
D Topjian
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Critically Ill ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Critically Ill Patients ◽  
Hemodynamic Parameters ◽  
Trendelenburg Position ◽  
Dependent Variables ◽  
Preliminary Study

BACKGROUND: Although we have insufficient knowledge about the effects of Trendelenburg positions on various hemodynamic parameters, these positions are frequently used to influence cardiac output and blood pressure in critically ill patients. OBJECTIVES: To determine the effect of Trendelenburg and modified Trendelenburg positions on five dependent variables: cardiac output, cardiac index, mean arterial pressure, systemic vascular resistance, and oxygenation in critically ill patients. METHODS: In this preliminary study subjects were 23 cardiac surgery patients (mean age, 55; SD, 8.09) who had a pulmonary artery catheter for cardiac output determination and who were clinically stable, normovolemic and normotensive. Baseline measurements of the dependent variables were taken in the supine position. Patients were then placed in 10 degrees Trendelenburg or 30 degrees modified Trendelenburg position. The dependent variables were measured after 10 minutes in each position. A 2-period, 2-treatment crossover design with a preliminary baseline measurement was used. RESULTS: Five subjects were unable to tolerate Trendelenburg position because of nausea or pain in the sternal incision. In the 18 who were able to tolerate both position changes, no statistically significant changes were found in the five dependent variables. Changes in systemic vascular resistance over time approached statistical significance and warrant further study. CONCLUSIONS: This preliminary study does not provide support for Trendelenburg positions as a means to influence hemodynamic parameters such as cardiac output and blood pressure in normovolemic and normotensive patients.

The Chanages of Blood Pressure , Heart Rate and Cardiac Output During Awake Fiberoptic Nasotracheal and Orotracheal Intubation

1991 ◽  
Vol 24 (3) ◽  
pp. 505
Author(s):  
Young Jin Lim ◽  
Jae Hyon Bahk ◽  
Kook Hyun Lee ◽  
Jin Kyu Park ◽  
Kwang Won Yum
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Orotracheal Intubation

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.

Cardiovascular functions in the dog rewarmed rapidly and slowly from deep hypothermia

1960 ◽  
Vol 198 (2) ◽  
pp. 333-335 ◽  
Author(s):  
H. E. D'Amato ◽  
Suzanne Kronheim ◽  
B. G. Covino
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Superior Vena ◽  
Vena Cava ◽  
Deep Hypothermia ◽  
Cardiovascular Collapse ◽  
Cardiovascular Failure ◽  
Myocardial Failure ◽  
Cardiovascular Functions

Heart rate, blood pressure, cardiac output and cardiac minute work were measured in pentobarbitalized dogs prior to induction of hypothermia, at rectal temperatures of 25°C or 20°C and following rapid rewarming in warm water or slow rewarming by wrapping in heated sheeting. During rapid rewarming from either 25°C or 20°C no consistent failure in recovery of normal cardiovascular function was observed, although 1 out of 10 dogs did suffer cardiovascular collapse during rapid rewarming. Slow rewarming from 25° and 20°C resulted in consistent failure of some or all of these functions to recover to prehypothermic levels. Moreover, 5 out of 15 slowly rewarmed dogs suffered cardiovascular collapse during the rewarming process. In five dogs slowly rewarmed from 20°C saline was infused into the superior vena cava. This procedure resulted in moderate increases in blood pressure but dramatic increases in cardiac output and minute work (200% and 270%, respectively), thereby negating myocardial failure as the primary cause of the occasionally observed cardiovascular failure.

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