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Thirty-two mongrel dogs were used in a comparative study to assess the effect of normal saline solution, metrizamide and Cardioconray on serum osmolality, haematocrit and cardiac output. The study demonstrated that the higher the osmolality of the test substance, the greater the reduction in haematocrit and the higher the increase in cardiac output.
This study aimed to explore the 24-h patterns of stroke volume, cardiac output, and peripheral vascular resistance along with other correlated variables, such as left ventricular ejection time, ejection velocity index, thoracic fluid index, heart rate, and blood pressure. The study was performed on 12 clinically healthy subjects by means of a noninvasive beat-to-beat monitoring using the thoracic electric bioimpedance technique associated with the automated sphygmomanometric recording. Time data series were analyzed by means of chronobiological procedures. The results documented the occurrence of a circadian rhythm for all the variables investigated, giving relevance to the beat-to-beat bioperiodicity of cardiac output and peripheral vascular resistance. Temporal quantification of the investigated variables may be useful for a better insight of the chronophysiology of the cardiovascular apparatus.
In patients with acute lung injury, high levels of positive end-expiratory pressure (PEEP) may be necessary to maintain or restore oxygenation, despite the fact that 'aggressive' mechanical ventilation can markedly affect cardiac function in a complex and often unpredictable fashion. As heart rate usually does not change with PEEP, the entire fall in cardiac output is a consequence of a reduction in left ventricular stroke volume (SV). PEEP-induced changes in cardiac output are analyzed, therefore, in terms of changes in SV and its determinants (preload, afterload, contractility and ventricular compliance). Mechanical ventilation with PEEP, like any other active or passive ventilatory maneuver, primarily affects cardiac function by changing lung volume and intrathoracic pressure. In order to describe the direct cardiocirculatory consequences of respiratory failure necessitating mechanical ventilation and PEEP, this review will focus on the effects of changes in lung volume, factors controlling venous return, the diastolic interactions between the ventricles and the effects of intrathoracic pressure on cardiac function, specifically left ventricular function. Finally, the hemodynamic consequences of PEEP in patients with heart failure, chronic obstructive pulmonary disease and acute respiratory distress syndrome are discussed.
The authors compare two methods of simple measures of cardiac output which may be achieved using "bedsides procedures": the thermodilution and the isotopic embolism. The correlation of both series of measures is statistically significant. Besides, each method shows certain constraints. It brings different complementary hemodynamic informations.
Doppler technique of measuring cardiac output was evaluated during pregnancy. In a study of accuracy Doppler technique correlated well with thermodilution, (r = 0.95, y = 1.05x - 0.35). In a study of interoperator variability, the technique was found to be reproducible, (r = 0.92, y = 0.91x + 0.74).
BACKGROUND: A new Doppler echocardiographic technique has been developed for automated cardiac output measurement (ACOM) that assumes neither a flat flow profile nor collinearity with the scan line, but clinical validation of this method is lacking. METHODS AND RESULTS: In 165 subjects (50 intensive care patients, 10 dobutamine echocardiography patients, and 105 normal volunteers; age, 49.4 +/- 19.3 years; 92 men), ACOM was performed in the left ventricular outflow tract (LVOT), with the color baseline shifted to avoid aliasing. ACOM was also tested in a pulsatile in vitro model. Stroke volume was calculated by double integration of Doppler signals in space (across the LVOT) and in time (through the systolic period), assuming hemiaxial symmetry: integral of integral of pi r v(r,t) dr dt, where v(r,t) is the velocity at a distance r from the center of the LVOT at time t during systole. Stroke volume from ACOM was compared with thermodilution (TD), aortic valve pulsed-wave Doppler (PWAO), and left ventricular echocardiographic (two-dimensional [2D]) methods. There was good correlation between ACOM and PWAO (r = .93). TD (r = .86), and 2D (r = .74), with close agreement seen. ACOM had higher correlation and agreement with TD than did either PWAO (P < .02) or 2D (P < .01). ACOM was also able to track accurately the changes in cardiac output with dobutamine infusion in comparison with PWAO (r = .94). In vitro assessment demonstrated excellent correlation (r = .98, y = 1.0x + 1.94) with little impact of pulse repetition frequency or misalignment up to 30 degrees. Gain dependency was noted but could be optimized by visual inspection of the color image. CONCLUSIONS: Automatic integration of numerical data within color Doppler flow fields is a feasible new method for quantifying flow. It is simpler and faster, requires fewer assumptions, and uses only one apical view. ACOM is a promising new approach to echocardiographic quantification that deserves further study and refinement.
To investigate the combined effect of water immersion (WI) and lean body mass on cardiac output (Q), 12 healthy young men, 6 lean (fat less than 9%) and 6 fat (fat greater than 18%), were studied at rest and during steady state exercise approximating 30-40% Vo2 max under three experimental conditions. There were on land at 24 degrees C (LND), and immersed in water at 33-34 degrees C to hip level (HIP), and to the xiphoid (XIP). Metabolic measures were determined during 30-s periods from the average breath measurements. Mixed venous PCO2 (PVCO2) was estimated using rebreathing equilibration technique. Cardiac output was calculated by the indirect Fick's principle. In the lean individuals the average Q rose from a resting value of 5.43 +/- 0.43 (LND) to an exercise value of 7.25 +/- 0.40 L/min (XIP), and from resting value of 5.62 +/- 0.40 to an exercise 6.47 +/- 0.5 L/min in the fat individuals. During exercise, the associated increase in Q with increasing WI was significantly (p less than 0.05) higher compared with the land experiments. Inspection of the mean profile corresponding to this increase indicated that an increase in the level of immersion results in a significant (p less than 0.05) increase in the average Q for the lean group. For the fat group, the average Q was significantly (p less than 0.05) larger only at XIP level. At rest, heart rate dropped from 67 +/- 3.36 (LND) to 60 +/- 4.13 (XIP), and from 79 +/- 3.73 to 73 +/- 4.10 BPM for the lean and fat group, respectively. MANOVA analysis showed a significant (p less than 0.05) interaction between WI and group membership, indicating that the effect of WI is significantly different between the two groups. These data indicate that the change in central blood volume with WI depends, in part, on the lean mass of the body.
After a Fontan operation pulmonary blood flow is heavily dependent on respiration. Two patients with a Fontan and normal sinus rhythm developed episodes of collapse with loss of cardiac output secondary to the tonic phase of an epileptic fit. The forced expiratory effort during the tonic phase severely compromised systemic venous return and led to collapse due to loss of cardiac output.
BACKGROUND: When single-ventricle physiology is established acutely (ie, after a Norwood procedure), the combination of limited cardiac output and hypoxemia could result in limited oxygen transport to systemic organs. This study investigates the regional distribution of cardiac output and oxygen delivery after creation of single-ventricle physiology. METHODS: Single-ventricle physiology was created in 8 piglets, and 8 other piglets served as sham control animals. Aortopulmonary shunt, echocardiography-guided atrial septostomy, tricuspid valve avulsion, and pulmonary artery occlusion allowed the left ventricle to support systemic and pulmonary circulations. Physiologic parameters and regional blood flow were determined at baseline and at 30 and 120 minutes after conversion to single-ventricle physiology. Parameters were compared by means of 1-way and 2-way analysis of variance. RESULTS: Single-ventricle physiology resulted in lower diastolic arterial pressure, oxygen saturation, and arterial oxygen saturation (P < .05), whereas hemoglobin was unchanged. Cerebral blood flow increased markedly in control animals (P = .04). In contrast, in single-ventricle physiology regional blood flow was unchanged in the brain, higher in the myocardium (P = .1), and mildly reduced in low-priority organs (liver, kidneys, and bowel). Cerebral oxygen delivery increased in control animals, whereas in animals with single-ventricle physiology, oxygen delivery decreased in the brain, liver, kidneys, and bowel (P < .05) and was unchanged in the myocardium. Total-body oxygen delivery decreased in animals with single-ventricle physiology (P < .001) but not in control animals. Total-body oxygen consumption was unchanged in both groups. CONCLUSIONS: This study shows that in acute single-ventricle physiology hypoxemia and limited regional blood flow reduce oxygen transport to low-priority organs and partly to the brain. These findings might contribute to the understanding of gastrointestinal and neurologic complications in children with single-ventricle physiology.
The authors determined the correction factor (Ct) for three sizes of commonly available central venous catheters. These catheters are used as the injectate catheter when a 2.5 Fr transthoracic thermistor is used to determine cardiac output by thermodilution. The valves for Ct were highly reproducible. These determinations can be used conveniently in children to determine cardiac output by thermodilution.
Organ blood flow and distribution of cardiac output (CO) were determined in awake resting swine, using radionuclide-labeled 15-micrometer diameter microspheres. Absolute values of blood flow (per 100-g basis) were determined for various organs and peripheral tissues. Internal organs of the swine, which constituted 8.25 +/- 0.79% of the total body mass, received 45.46 +/- 2.64% of the resting CO. The fraction of CO received by brain, heart, kidneys, liver (via hepatic artery), and gastrointestinal tract was 1.13%, 3.04%, 12.95%, 4.27%, and 18.71%, respectively.
To evaluate cardiac function with various tracers to be used for radionuclide scintigraphy, we examined the validity of a simplified method to measure cardiac output (CO) by modifying the equation of Stewart-Hamilton in the radionuclide study. After a bolus injection of I-123 or Tc-99m tracer, the total injection dose and count in the pulmonary artery during the first transit of the tracer were measured to calculate the CO Index. The CO Index was obtained from the integral of the first transit of radiotracers in the pulmonary artery divided by the total injected count. CO was estimated from the regression formula which was obtained by comparing the CO Index with CO measured by the Doppler echocardiographic method. There were close correlations between the CO Index and CO measured by Doppler echocardiography both in the study with I-123 (n = 13, r = 0.85, p < 0.001) and with Tc-99m (n = 17, r = 0.88, p < 0.001). The regression formula varied according to the radionuclide used for the study (CO = 2.29 x (CO Index)(0.634) for I-123 and CO = 3.18 x (CO Index)(0.518) for Tc-99m). CO measured by this method is useful for the assessment of cardiac function with various tracers in routine clinical studies, and this simple method may be utilized for assessment of organ blood flow on the basis of the microsphere model.
Sodium pentobarbital (PB), 30 mg/kg, iv, was administered to 30 conscious dogs instrumented for measurement of cardiac output and regional blood flow distribution, left ventricular (LV) diameter, LV pressure, dP/dt, and dD/dt, i.e., velocity of myocardial fiber shortening. Ventilation was controlled during anesthesia to maintain arterial blood gases at control values for conscious dogs. The anesthetic produced an initial transient, peripheral vasodilation but the steady state effects 15-30 minutes later were characterized by slight reductions in mesenteric flow and cardiac output and increases in mesenteric and systemic resistances, whereas iliac and renal resistances were not significantly different from control. When heart rate rose, PB increased end-systolic diameter and decreased coronary resistance, LV end-diastolic diameter, dP/dt/P (42%), and shortening velocity (36%). When heart rate was controlled, PB still increased end-systolic diameter and decreased shortening velocity and dP/dt/P, as occurred during spontaneous rhythm, but end-diastolic diameter rose instead of falling and coronary resistance did not change. After recovery from bilateral cervical section of both carotid sinus and aortic nerves, PB failed to elicit tachycardia. Thus, PB affects systemic and regional hemodynamics only slightly, but depresses the myocardium markedly. The tachycardia associated with PB anesthesia in intact, trained dogs appears not to be only vagolytic, as previously thought, but is predominantly mediated through the arterial baroreceptor reflex.
In order to prove definitely that echocardiography is a noninvasive and safe method that can be used in the perioperative period to assess cardiac function and evaluate the effects of pharmacologic agents on the heart, we have carried out further sonographic studies concerning cardiac output and the effects of volatile anesthetics on left ventricular contractility. In series A (n = 12), we compared different sonographic techniques (uni-dimensional, two-dimensional, pulse Doppler echocardiography) with invasively measuring cardiac output by thermodilution in ICU patients and in the immediate preoperative phase before CABG with a Swan Ganz catheter that was already inserted. M-mode echocardiography proved to be best and correlated well with invasively gained values (y = 0.57 + 0.96x, r = 0.795, p less than 0.01). Use of the Teichholtz formula to estimate left ventricle volumes seems to be imperative. The two-dimensional technique yielded less favorable results, the pulse Doppler method being least informative. In series B (n1 = n2 = n3 = 6) the effects of halothane, enflurane and isoflurane MAC 1.0 and 1.5 on left ventricular performance were assessed in patients undergoing cholecystectomy or gastrectomy under standard anesthetic conditions. The results support the already well-known pharmacologic effects of these drugs, with minimal decrease in contraction with isoflurane. Critical interpretation of the different sonographic parameters, however, is just as important as considering various existing interdependances. Finally, when comparing our numerical values with other 1.0 MAC effects reported in the literature, there was also very good agreement.(ABSTRACT TRUNCATED AT 250 WORDS)
In pithed rats, but not in pithed cats, the alpha 2-/dopamine agonist B-HT 920 (10-300 micrograms kg-1) increased cardiac output. The increase was inhibited by yohimbine (1 mg kg-1), but not by sulpiride (0.3 mg kg-1) and nifedipine (1 mg kg-1). Both in pithed rats and cats, the alpha 1-adrenoceptor agonist methoxamine (30-300 micrograms kg-1 and 30-1000 micrograms kg-1, respectively) increased cardiac output. This increase (rats) was inhibited by prazosin (0.1 mg kg-1). The results indicate the existence of functional venous alpha 2-adrenoceptors in pithed rats, and their absence in pithed cats. Furthermore, alpha 2-adrenoceptor-mediated venoconstriction appears independent of extracellular calcium.
The effects of large doses of angiotensin II on the rabbit kidney and heart and or the ability of perfused canine kidney to inactivate angiotensin II were examined to clarify the role of angiotensin II in the low cardiac output syndrome after open-heart surgery. Intravenous infusion of angiotensin II at a rate of 1.1 to 1.4 microgram/Kg/min for 48 hours caused multifocal myocardial necrosis and renal mononuclear cell infiltration and necrosis. Isolated canine kidney preparations inactivated 76% of angiotensin I and 79% of angiotensin II. The results indicates that the kidney can inactivate angiotensin and that high doses of angiotensin II can produce myocardial and renal lesions. It is suggested that an increased concentration of angiotensin II may result in the low cardiac output syndrome through myocardial damage, and that decreased inactivation of angiotensin II by the kidney accelerates the myocardial damage.
The kinetics of oxygen uptake (VO2), cardiac output (Q), and heart rate (HR) were studied in three healthy male subjects during onset of exercises up to 750 kpm/min. VO2 was measured on a single breath basis, Q by CO2-N2 rebreathing method at 30" intervals from time 0 to 6 min of exercise, and HR beat by beat. In the transition from rest to exercise, the increase of Q and VO2 follows a single exponential function, while h. r. a double exponential. Average half times of Q and VO2 during the onset of exercise are about 18" and 26" respectively. Q changes seem to anticipate VO2 changes at the first 15-45 s of exercise, while thereafter a proportional increase is observed. This non-linear increase of Q to VO2 at the beginning of exercise may presumably be due to a neurogenic control of h.r. and hence of Q from receptors at muscular level.
Many observers remain sceptical with regards to the utilization of Doppler-echocardiographic measurements of intracardiac outputs for the quantification of shunts and regurgitations. In this context, we evaluated the feasibility and validity of measuring output at the level of the four cardiac valves in a population of 35 normal subjects (24 M, 12 F) aged from 23 to 37 years (mean +/- SD = 28 +/- 4). Measurement of stroke volume and output using predetermined criteria was possible in the aortic position in 35 (100%) subjects, in the mitral position in 34 (97%), in the pulmonary position in 20 (57%) and in the tricuspid position in 10 (29%). In 14 subjects (40%), measurement was possible at 2 sites, in 14 (40%) at 3 sites and in 7 (20%) at 4 sites. Inability to measure output was most often due to poor visualization of valvular annulus. There are excellent correlations between aortic stroke volume on the one hand and the mitral (r = 0.97, SEE = 3.41 cc), pulmonary (r = 0.97, SEE = 3.69 cc) and tricuspid (r = 0.96, SEE = 2.77 cc) stroke volumes respectively on the other. These results suggest that reliable measurements of output are feasible in a majority of cases in the aortic and mitral positions but to a much more limited extent in the pulmonary and tricuspid positions; given the small SEE's, they should be useful to quantitate shunts and regurgitations, when feasible.