Application of the thermodilution technique for measuring cardiac output and assessing cardiac stroke volume in crabs

1. Dogfish were acclimated to 7, 12 or 17 degrees C and exposed to progressive hypoxia at the temperature to which they had been acclimated. During normoxia, the Q10 values for oxygen uptake, heart rate, cardiac output and respiratory frequency over the full 10 degrees C range were: 2.1, 2.1, 2.1 and 2.5 respectively. Increased acclimation temperature had no effect on cardiac stroke volume or systemic vascular resistance, although there was a decrease in branchial vascular resistance, pHa and pHv. 2. Progressive hypoxia had no effect on heart rate or oxygen uptake at 7 degrees C, whereas at 12 degrees C and 17 degrees C there was bradycardia, and a reduction in O2 uptake, with the critical oxygen tension for both variables being higher at the higher temperature. Cardiac stroke volume increased during hypoxia at each temperature, such that cardiac output did not change significantly at 12 and 17 degrees C. Neither pHa nor pHv changed significantly during hypoxia at any of the three temperatures. 3. The influence of acclimation temperatures on experimental results from poikilotherms is pointed out. Previously-published results show quantitative differences. 4. The significance of the present results with respect to the functioning and location of oxygen receptors is discussed. It is argued that as the metabolic demand and critical oxygen tension of the whole animal are increased at high acclimation temperatures the same must be the case with the oxygen receptor. This would raise the stimulation threshold and could account for the bradycardia seen during hypoxia becoming manifest at higher values of PI,O2, Pa,O2 and Pv,O2 as the acclimation temperature is raised.

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Haemodynamic changes due to delayed sternal closure in newborns after surgery for congenital cardiac malformations

Cardiology in the Young ◽

10.1017/s1047951109991065 ◽

2009 ◽

Vol 19 (6) ◽

pp. 573-579 ◽

Cited By ~ 2

Author(s):

Pavel Vojtovič ◽

Oleg Reich ◽

Marek Selko ◽

Tomáš Tláskal ◽

Jiří Hostaša ◽

...

Keyword(s):

Cardiac Output ◽

Stroke Volume ◽

Transpulmonary Thermodilution ◽

Lung Compliance ◽

Volume Index ◽

Thermodilution Technique ◽

Sternal Closure ◽

Delayed Sternal Closure ◽

Haemodynamic Changes ◽

Transpulmonary Thermodilution Technique

AbstractBackgroundDelayed sternal closure is used to prevent low cardiac output syndrome in selected newborns shortly after cardiac surgery for congenital cardiac defects. Sternal closure itself often causes haemodynamic and ventilatory instability that cannot be entirely assessed by standard monitoring means. Therefore, we used transpulmonary thermodilution technique for an exact evaluation of the haemodynamic changes.Patients and methodsBetween April, 2006, and December, 2008, 23 neonates aged from 1 to 30 days, with a median of 7 days, and weighing from 1.9 to 4.2 kilograms, with a median of 3.25 kilograms, were studied after biventricular corrections. Residual intracardiac shunts were excluded by echocardiography. Haemodynamic and ventilatory parameters, along with those obtained by the transpulmonary thermodilution technique, were recorded before and immediately after the sternal closure, and then at 0.5, 1, 2, 6, 12, 24, and 48 hours.ResultsChest closure caused significant decrease in systolic arterial pressure from 80.04 ± 11.48 to 69.48 ± 9.63 mmHg (p < 0.001), cardiac index from [median (25th/75th centile)] 2.640 (2.355/2.950) to 2.070 (1.860/2.420) l/min/m2 (p < 0.001), stroke volume index from 18.50 (16.00/20.00) to 14.00 (11.00/17.00) ml/m2 (p < 0.001), and dynamic lung compliance from 2.45 (2.31/3.00) to 2.30 (2.14/2.77) ml/cmH2O (p = 0.007). Stroke volume variation increased from 14.00 (9.25/16.75) to 18.00 (15.00/21.00) % (p < 0.001). The oxygenation index transitorily increased from 2.50 (2.14/3.15) to 3.36 (2.63/4.29) (p < 0.001). Serum lactate decreased from 1.40 (1.12/2.27) to 1.0 (0.8/1.3)mmol/l, p < 0.001 in coincidence with a haemodynamic stabilisation at a later time after chest closure. Cardiopulmonary instability caused by the sternal closure necessitated therapeutic intervention in 18 of 23 patients (78.3%).ConclusionDelayed sternal closure causes a significant transitory decrease in stroke volume, cardiac output and arterial blood pressure. Also lung compliance and blood oxygenation are temporarily significantly compromised.

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Respiratory pump maintains cardiac stroke volume during hypovolemia in young, healthy volunteers

Journal of Applied Physiology ◽

10.1152/japplphysiol.01009.2017 ◽

2018 ◽

Vol 124 (5) ◽

pp. 1319-1325 ◽

Cited By ~ 9

Author(s):

Maria Skytioti ◽

Signe Søvik ◽

Maja Elstad

Keyword(s):

Cardiac Output ◽

Stroke Volume ◽

Healthy Volunteers ◽

Negative Pressure ◽

Spontaneous Breathing ◽

Positive Pressure Ventilation ◽

Control Mode ◽

Positive Pressure ◽

Beneficial Effects ◽

Cardiac Stroke Volume

Spontaneous breathing has beneficial effects on the circulation, since negative intrathoracic pressure enhances venous return and increases cardiac stroke volume. We quantified the contribution of the respiratory pump to preserve stroke volume during hypovolemia in awake, young, healthy subjects. Noninvasive stroke volume, cardiac output, heart rate, and mean arterial pressure (Finometer) were recorded in 31 volunteers (19 women), 19–30 yr old, during normovolemia and hypovolemia (approximating 450- to 500-ml reduction in central blood volume) induced by lower-body negative pressure. Control-mode noninvasive positive-pressure ventilation was employed to reduce the effect of the respiratory pump. The ventilator settings were matched to each subject’s spontaneous respiratory pattern. Stroke volume estimates during positive-pressure ventilation and spontaneous breathing were compared with Wilcoxon matched-pairs signed-rank test. Values are overall medians. During normovolemia, positive-pressure ventilation did not affect stroke volume or cardiac output. Hypovolemia resulted in an 18% decrease in stroke volume and a 9% decrease in cardiac output ( P < 0.001). Employing positive-pressure ventilation during hypovolemia decreased stroke volume further by 8% ( P < 0.001). Overall, hypovolemia and positive-pressure ventilation resulted in a reduction of 26% in stroke volume ( P < 0.001) and 13% in cardiac output ( P < 0.001) compared with baseline. Compared with the situation with control-mode positive-pressure ventilation, spontaneous breathing attenuated the reduction in stroke volume induced by moderate hypovolemia by 30% (i.e., −26 vs. −18%). In the patient who is critically ill with hypovolemia or uncontrolled hemorrhage, spontaneous breathing may contribute to hemodynamic stability, whereas controlled positive-pressure ventilation may result in circulatory decompensation. NEW & NOTEWORTHY Maintaining spontaneous respiration has beneficial effects on hemodynamic compensation, which is clinically relevant for patients in intensive care. We have quantified the contribution of the respiratory pump to cardiac stroke volume and cardiac output in healthy volunteers during normovolemia and central hypovolemia. The positive hemodynamic effect of the respiratory pump was abolished by noninvasive, low-level positive-pressure ventilation. Compared with control-mode positive-pressure ventilation, spontaneous negative-pressure ventilation attenuated the fall in stroke volume by 30%.

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Cardiac stroke volume during exercise measured by Doppler echocardiography: comparison with the thermodilution technique and evaluation of reproducibility.

Heart ◽

10.1136/hrt.58.5.455 ◽

1987 ◽

Vol 58 (5) ◽

pp. 455-459 ◽

Cited By ~ 31

Author(s):

H Ihlen ◽

K Endresen ◽

S Golf ◽

S Nitter-Hauge

Keyword(s):

Stroke Volume ◽

Doppler Echocardiography ◽

Thermodilution Technique ◽

Cardiac Stroke Volume

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Chronic fatigue syndrome: comments on deconditioning, blood volume and resulting cardiac function

Clinical Science ◽

10.1042/cs20090327 ◽

2009 ◽

Vol 118 (2) ◽

pp. 121-123 ◽

Cited By ~ 8

Author(s):

Julian M. Stewart

Keyword(s):

Cardiac Output ◽

Chronic Fatigue Syndrome ◽

Stroke Volume ◽

Blood Volume ◽

Sedentary Lifestyle ◽

Orthostatic Intolerance ◽

Bed Rest ◽

Chronic Fatigue ◽

Fatigue Syndrome ◽

Cardiac Stroke Volume

Cardiovascular and autonomic dysfunction have been suggested to underlie the symptoms accompanying CFS (chronic fatigue syndrome). In the present issue of Clinical Science, Hurwitz and co-workers have investigated whether deficits were present in cardiac output and blood volume in a cohort of patients with CFS and if these were linked to illness severity and sedentary lifestyle. The results clearly demonstrate reduced cardiac stroke volume and cardiac output in more severely afflicted patients with CFS, which is primarily attributable to a measurable reduction in blood volume. Similar findings are observed in microgravity and bed rest deconditioning, in forms of orthostatic intolerance and, to a lesser extent, in sedentary people. The circulatory consequences of reduced cardiac output may help to account for many of the findings of the syndrome.

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Elevated Pericardial Pressure And Cardiac Output In The Leopard Shark Triakis Semifasciata During Exercise: The Role Of The Pericardioperitoneal Canal

Journal of Experimental Biology ◽

10.1242/jeb.147.1.263 ◽

1989 ◽

Vol 147 (1) ◽

pp. 263-277 ◽

Cited By ~ 2

Author(s):

N. CHIN LAI ◽

JEFFREY B. GRAHAM ◽

WILLIAM R. LOWELL ◽

RALPH SHABETAI

Keyword(s):

Heart Rate ◽

Cardiac Output ◽

Stroke Volume ◽

Pericardial Fluid ◽

Fluid Loss ◽

Primary Role ◽

Pericardioperitoneal Canal ◽

Pericardial Pressure ◽

Triakis Semifasciata ◽

Cardiac Stroke Volume

Changes in pericardial pressure, pericardial fluid volume, cardiac stroke volume and heart rate induced by swimming were monitored for Triakis semifasciata (Girard). Maximum pericardial pressure (Pmax, 0.07±0.03 kPa) in resting sharks was typically above ambient, whereas minimum pressure (Pmin, −0.08±0.03 kPa) was slightly subambient. During swimming, both Pmax (0.23±0.03 kPa) and Pmin (−0.02±0.03 kPa) became elevated, as did heart rate (51±2 to 55±2 beats min−1) and fractional cardiac stroke volume (0.49±0.03 to 0.65±0.04ml). After swimming, all variables fell, except fractional cardiac stroke volume. Estimates of total cardiac output from fractional cardiac stroke volume data during rest, exercise and recovery were 33.1, 56.2 and 60.4 ml kg ‘1 min’ 1, respectively. The occurrence of both elevated pericardial pressure and cardiac output during swimming argues against a primary role for pericardial-induced vis a fronte filling as the principal mechanism responsible for increasing cardiac output with exercise. Pericardial fluid loss via the pericardioperitoneal canal (PPC) occurs during swimming as a result of steady-state elevation of pericardial pressure, a series of transient high pericardial pressures, or both. Good general agreement seen for net pericardial fluid loss (0.6 ml kg−) and the net increase in cardiac stroke volume (0.45 ml kg−) during swimming establishes fluid displacement as a mechanism for increasing cardiac stroke volume and suggests that this is the primary function of the PPC.

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Differences between directly measured and calculated values for cardiac output in the dogfish: a criticism of the Fick method

Journal of Experimental Biology ◽

10.1242/jeb.99.1.255 ◽

1982 ◽

Vol 99 (1) ◽

pp. 255-268

Author(s):

J. D. Metcalfe ◽

P. J. Butler

Keyword(s):

Cardiac Output ◽

Oxygen Uptake ◽

Stroke Volume ◽

Complete Control ◽

Fick Principle ◽

Scyliorhinus Canicula ◽

Respiratory Surface ◽

Significant Difference ◽

Cardiac Bypass ◽

Cardiac Stroke Volume

Cardiac output has been measured directly, and calculated by the Fick method, during normoxia and hypoxia in six artificially perfused dogfish (Scyliorhinus canicula) in an attempt to estimate the accuracy of this method in fish. The construction and operation of a simple extra-corporeal cardiac bypass pump is described. This pump closely mimics the flow pulse profiles of the fish's own heart and allows complete control of both cardiac stroke volume and systolic and diastolic periods. During normoxia (PO2 = 21 kPa) there was no significant difference between directly measured and calculated values for cardiac output. However, some shunting of blood past the respiratory surface of the gills may have been obscured by cutaneous oxygen uptake. In response to hypoxia (PO2 = 8.6 kPa) there is either a decrease in the amount of blood being shunted past the respiratory surface of the gills and/or an increase in cutaneous oxygen uptake such that the Fick calculated value for cardiac output is on average 38% greater than the measured value. It is proposed that the increase in the levels of circulating catecholamines that is reported to occur in response to hypoxia in this species may play an important role in the observed response to hypoxia. The results are discussed in terms of their implications for the calculation of cardiac output by the Fick principle in fish.

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