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The measurement of cardiac output by the indicator dilution method is reviewed. Theoretical and practical problems relating to the direct and indirect Fick methods and the continuous and bolus injection methods are considered in detail. Choice of indicator is also discussed. Problems remain with all of these methods, but reasonable accuracy and consistency may be achieved if attention is paid to detail.
Impedance cardiography was compared with thermodilution cardiography in the measurement of cardiac output serially during maintenance hemodialyses in ten chronic uremic patients. Measurements were carried out pre-dialysis and post-dialysis as well as hourly during dialysis. The results demonstrated statistical identity between impedance and thermodilution cardiography at all times of measurement. The study confirms the validity of the non-invasive technique in measuring cardiac output in the uremic patient.
In the Cooperative New Scandinavian Enalapril Survival Study (CONSENSUS II), in which enalapril treatment was initiated intravenously within 24 h after acute myocardial infarction, there was a neutral effect on 6-month mortality, whereas a beneficial effect on the progression of congestive heart failure was noted. We studied the effect of enalapril on left ventricular systolic function in terms of cardiac output and mean acceleration time measured by pulsed-wave Doppler in the left ventricular outflow tract and peripheral resistance. Early angiotensin-converting enzyme inhibition after acute myocardial infarction did not result in a general improvement of cardiac output. However, a small increase in cardiac output was observed in a subgroup of enalapril-treated patients with ejection fraction > or = 45%, probably due to a reduction in peripheral resistance in these patients.
Data published by this laboratory indicated that the beta adrenergic blocking drugs timolol and propranolol exerted equivalent beta blocking and antihypertensive actions in patients with mild essential hypertension, but that whereas cardiac output fell acutely with both drugs, it returned to normal after 5 wk of treatment with timolol, but remained depressed after propranolol. This preliminary observation needed further confirmation in a larger series of patients. In this study, 11 patients with initial diastolic blood pressures between 90 and 125 mm Hg were given timolol for 5 wk. Hemodynamic measurements were made before and at the end of treatment. Mean heart rate fell from 76.8 to 64.3 bpm (p less than 0.001), and blood pressure was reduced from 179.4/99 mm Hg to 167.4/93.3 mm Hg (less than 0.02). Cardiac output averaged 6.29 L/min before timolol, and fell to 5.95 L/min (NS) after treatment. Stroke volume increased significantly, while total peripheral resistance was unchanged. These results confirm our earlier observations that timolol is an effective beta adrenergic blocking drug with antihypertensive action that does not reduce cardiac output significantly when given chronically. This drug merits further evaluation in other cardiovascular disorders since it may have advantages over other beta adrenergic blocking drugs.
BACKGROUND: Studies of the hemodynamic effects associated with the pneumoperitoneum have had controversial results. We set out to investigate the effect of increased intraabdominal pressure (IAP) on cardiac output and tissue blood flow in various intraabdominal and extraabdominal organs using the color-labeled microsphere (CLM) technique. METHODS: IAP was induced by CO2 insufflation in anesthetized pigs; 0, 5, and 10 mmHg was used in the low-pressure group and 0, 15, and 24 mmHg in the high-pressure group. Tissue blood flow (ml.min-1.g-1) and cardiac output (CO) (ml/min) were determined by the CLM technique. RESULTS: CO decreased at IAP > or = 15 mmHg. Arterial PaCO2 and hydrogen ion concentration increased in response to all levels of IAP. Arterial PaO2, oxygen saturation, and bicarbonate ion concentration remained unchanged. Low IAP did not influence tissue blood flows in most of the organs. However, in the spleen, pancreas, esophagus, and gastric mucosal specimens, tissue blood flow was significantly decreased at 24 mmHg. CONCLUSION: The level of IAP used in current practice (10-12 mmHg) appears to be safe with regard to hemodynamic variables and tissues blood flow; however, higher levels may induce a decrease in cardiac output and tissue blood flow.
Sympathetic overdrive in acute low cardiac output syndrome, diverts blood from cutaneous and visceral circulation centripetally. Microcirculation in general, and renal circulation in particular, deteriorates during these circulatory adjustments leading to multi-organ failure (MOF). Decreased afferent glomerular arteriolar blood flow, increased renal sympathetic nerve discharge and a resultant decreased sodium chloride delivery around macula densa stimulates the Juxta-glomerular apparatus (JGA) and triggers renin-angiotensin-aldosterone mechanism. This, along with increased ADH production results in a state of vasoconstriction, increased after-load, and continued fluid retention, further compromising the visceral microcirculation. Initially the fluid retention under the effect of aldosterone and ADH is iso-osmotic, but later under inappropriate ADH action more water than salt is retained, as evidenced by the presence of hyponatraemia and 'water-logging' in the endstage of this condition.The author hypothesizes that: although physiological, the persistent stimulation of the JGA during the low cardiac output state plays an important role in perpetuating a negative cardiovascular vicious cycle and further aggravating it into MOF. Furthermore, by infusing hypertonic saline and hence increasing the sodium chloride delivery to the distal tubules and the macula densa, the JGA could be inhibited. This strategy should work like angiotensin-converting-enzyme-inhibitor drugs in chronic cardiac failure, except by acting at the root cause and inhibiting Renin production at its source. It should further help by stimulating atrial natriuretic peptide secretion.
The influence of the lung time constant (tc) and preset volume on a ventilator-cardiac output ratio (Vv/Q) on the decrease in the oxygenation of blood (PaO2/FiO2) due possibly to mechanical controlled ventilation, was examined with special reference to the time of passive expiration in 18 patients. The degree of deterioration of oxygenation appeared to depend mainly on the time following FRC, during which the blood continued to perfuse the lungs until the next active insufflation by the ventilator. The characteristics of the negative exponential function indicated that the lungs theoretically were passively evacuated by 98% at tc x 4 (= TC) sec. The value for the expiratory time-TC/TC was 3. 7 +/- 1.3 before reduction of this expiratory time. Following reduction, 11 subjects showed improved oxygenation while no change was noted in the other 7. In the former Vv/Q was 1.19 +/- 0.21 and in the latter 0.94 +/- 0.03 before reduction, showing significantly smaller values in the latter (p less than 0.01). Within each of the four [(expiratory time-TC)/TC]/Vv/Q zones between 1.0 and 5.0 (1.0-2.0, 2.0-3.0, 3.0-4.0, 4.0-5.0), Vv/Q of those who showed no change in oxygenation was always less than Vv/Q of those who showed improved oxygenation (p less than 0.01). Thus, it is possible that a relatively prolonged exhalation time compared to the lung time constant, under the conditions of cardiac output dominance in Vv/Q, could be one of the causes of deterioration of oxygenation which occurs frequently during mechanically controlled ventilation.
The accuracy of cardiac output (C.O.) measurements by the thermodilution method was evaluated in an in vitro model within a flow range from 1 to 5 liters/min. For C.O. determinations, a 5F Swan-Ganz balloon-tipped thermodilution catheter and a 9520 Edwards computer were used. We made 420 measurements at known flow rates. In serial determinations, we achieved an overall accuracy of 86 to 93% compared to the reference flow; for single determinations, the accuracy ranged from 75 to 85%. The indicator volume (3, 5, or 10 cc) had no influence on the results. The thermodilution determinations at each flow rate were reproducible at between 2.5 and 8.5%. There was no difference in accuracy or reproducibility when ice-cold or room temperature saline was used. Caution in the interpretation of single C.O. determinations in low-flow states, i.e., in pediatric patients, is recommended.
Cardiac output (CO) is a fundamentally important haemodynamic parameter and its continuous measurement has the potential to enable early recognition of haemodynamic trends and earlier therapeutic response. A method of continuous cardiac output (CCO) monitoring is now available for clinical use. The accuracy and reliability of this method has been confirmed in clinical trials but not, to our knowledge, in the presence of abnormal heart rhythms. A comparison was made between CCO and bolus thermodilution methods, to determine if there is a greater difference between their respective determinations of CO when heart rhythm is abnormal. A convenience sample of 38 intensive care patients was used to obtain 410 comparisons of CCO and bolus CO determinations. Heart rhythm associated with each comparison was determined. The comparison produced a measurement bias of -0.07 l/min and limits of agreement of -1.77 to 1.63 l/min. The bias of the two measurements was -0.35 l/min for sinus rhythm, -0.19 l/min for sinus tachycardia and -0.12 l/min for atrial flutter/fibrillation. Increased temperature and heart rate did not affect measurement agreement. In conclusion, the agreement between the bolus and continuous methods is clinically acceptable and is unaffected by the heart rhythms of sinus rhythm, sinus tachycardia and atrial flutter/fibrillation.
Changes in resting cardiac output (CO), stroke volume (SV), and systemic vascular resistance (SVR) during neonatal growth were studied in chronically instrumented lambs from the 1st to 5th wk of age; adult nonpregnant sheep values measured simultaneously were used as standard reference. Neonatal responses to autonomic agonists and antagonists were also investigated. Total CO increased linearly with neonatal growth, but decreased strikingly when expressed per weight unit; at 5 wk of age, CO/kg was still significantly higher than the adult value. SV also increased with neonatal growth but did not change when related to body weight; at 5 wk of age, SV/kg values were still higher than those of adult sheep. SVR changed reciprocally to CO. The decrease in CO/kg during neonatal growth paralleled the progressive decline in heart rate (HR). Beta receptor stimulation increased neonatal CO markedly and the increment was the same from the first through the fifth neonatal week. Beta blockade had insignificant effects, but cholinergic blockade produced moderate CO increases.
The acute circulatory effects of asthma have been studied in two groups of children, having an average age of 13.2 and 14.7 years, respectively. Asthma was provoked by exercise (EIA group) and histamine inhalation (HIA group). The latter group was also studied after subsequent inhalation of a beta 2 receptor agonist. Cardiac output was measured by dye dilution and intraarterial blood pressure was recorded. During attacks of asthma cardiac output and heart rate increased in both groups (p less than 0.05). The stroke volume decreased in the EIA group (p less than 0.01) but remained unchanged in the HIA group. The systemic vascular resistance (SVR) did not change. After salbutamol inhalation, the cardiac output and stroke volume increased and the SVR decreased (all p less than 0.05). The hemodynamic response during exercise was normal. Thus asthmatic children have normal cardiovascular function during moderate asthma. The decrease in stroke volume in the EIA group depended presumably on the preceding exercise test. The response to the beta 2-stimulation was similar to that seen in healthy adults.
To evaluate the blood flow distribution during exercise, 51 patients with chronic heart failure underwent ergometer exercise testing measuring cardiac output and leg blood flow. At the given workrate (10 watts and 25 watts) cardiac index (L/min/m2) was significantly lower in NYHA class III patients than class I patients (at 10 watts, 4.08 +/- 1.05 in class I, 4.01 +/- 1.29 in class II and 3.00 +/- 0.89 in class III, p less than 0.05; I vs III), while leg blood flow (L/min/m2) was similar among 3 groups (at 10 watts, 1.19 +/- 0.32, 1.29 +/- 0.25 and 1.16 +/- 0.29, ns). Consequently, residual blood flow (L/min/m2) was significantly lower in class III than class I (at 10 watts, 2.89 +/- .92 and 2.78 +/- 1.27 and 1.84 +/- 0.71, p less than 0.05: I vs III). The results at 25 watts were similar. Serum noradrenaline was significantly higher in class III patients than class I patients at both 10 and 25 watts. We concluded that in severe heart failure, agreater blood flow is distributed to the working leg muscle as compared with less severe heart failure. And such an increased distribution of blood flow to working leg plays a role to compensate an insufficient cardiac output response in patients with severe heart failure.
Cardiac output (Q) determination using the equilibrium CO2-rebreathe indirect Fick technique (Equil) to estimate mixed venous PCO2 (Pv-CO2) has been validated during steady state (SS) exercise in subjects with lung disease. A modification of the exponential method using a low concentration of CO2 with an exponential rise in PEt-CO2 (Ex) during rebreathing to estimate Pv-CO2 has been validated during nonsteady state exercise. The purpose of the present study was to validate the Ex method in subjects with lung disease. Q was measured by Ex at every second work load during Prog. Q was measured after 5 min of SS exercise by both Ex and Equil. Arterial PCO2 was estimated from PEtCO2. There was no significant difference in the Q-VO2 relationship during Prog exercise between the combined control and mild (FEV1 > 70%) CF subjects or the moderate and severe CF subjects. Q can be determined in the nonsteady state using the exponential CO2-rebreathe indirect Fick technique in subjects with CF, allowing for noninvasive examination of cardiopulmonary interaction during exercise at a wide range of work loads.
We experienced a plasma cell leukemia (PCL) patient complicated with high output cardiac failure (HOCF), proved as his elevated cardiac index and pulmonary artery wedge pressure and decreased systemic vascular resistance index in a hemodynamic study. We found no possible causes of HOCF. Interestingly, HOCF was improved as PCL responded to intensive chemotherapy. On the other hand, he showed consciousness disturbance, and had frequent attacks of generalized seizure. His electroencephalogram showed slow waves, and a spike and wave complex. Hyperammonemia and abnormal amino acid distribution were also found. This abnormal serum amino acid distribution, especially elevated glycine level, was different from that seen in chronic liver failure, and he had no hepatic disease. After intensive chemotherapy, the serum ammonia level and glycine level decreased. In this patient, PCL seemed to be responsible for HOCF, hyperammonemia, and abnormal amino acid distribution. We experienced two more cases of multiple myeloma (MM) with HOCF, hyperammonemia, abnormal serum amino acid distribution, and consciousness disturbance of unknown origin. Those two cases showed slow waves in the electroencephalogram. Improvement was seen in their HOCF, hyperammonemia, and abnormal amino acid levels after chemotherapy. The possibility of MM as a cause of HOCF is discussed.
Cardiac output (CO), arterial blood pressure (ABP), heart rate (HR), blood gases and blood flow (BF) to the brain, heart, kidney and skeletal muscles and other cephalic tissues in five dogs were studied before and at 30 minutes of betahistine infusion (0.12 to 0.2 mg per minute per kilogram). The particle distribution method using radioactive labeled 141Ce (15 mu) and 85Sr (15 mu) microspheres was utilized to quantitate and assess BF and CO. In the five dogs, the increase in CO averaged 20.8%, ABP remained constant, and HR increased in all but one exception where it decreased slightly concomitant with a decrease in Paco2. Brain BF increased (+ 29.6%) in the dogs whose Paco2 reamined constant. The BF increased to the heart (25.4%) and skeletal muslce (80%), while BF to the kidney and other tissues did not change. The change in HR appears to account for the change in CO. The dilating effect of betahistine on blood vessels, in the skeletal muscle, brain and heart could reduce peripheral resistance and decreace ABP. Thus, the increase in HR may be mediated through baroreceptor mechanisms rather than by a direct effect of betahistine. In addition, a decrease in Paco2, is more effective for decreasing cerebral BF than betahistine is for increasing blood flow.
The cardiac-output (Q) of seven young healthy Indians with common physical characteristics at rest and after a single bout of exercise of 600 kpm for 10 min on a bicycle ergometer was ascertained by the Indirect Fick Principle. The end tidal alveolar Co2 pressure was obtained at the end of a normal expiration and PvCo2 was obtained by the help of the exponential rise (Defares method) in Co2 concentration during rebreathing from an initially low Co2 in O2 mixture (3-4%). The standard Co2 dissociation curve of oxygenated blood was used to find out the corresponding arterial and venous Co2 content, assuming the Hb content of these individuals to be normal. The mean value of the Cardiac-Output so obtained during rest is 4.21 liters/min when Co2 rebreathing time does not exceed 10 secs, and 17.33 litres/min., 2 to 3 breaths after exercise, when rebreathing time did not exceed 5 to 7 secs. Repeated studies and better training of the subjects will perhaps improve the resting values, while after exercise and during recovery our values are better reproducible.
Continuous cardiac output (CO) and mixed venous oxygen saturation (SvO2) determined through the pulmonary artery catheter may be helpful in monitoring hemodynamic conditions in critically ill patients. This study aimed to evaluate CO and SvO2 in a model of acute normovolemic hemodilution (ANH), analyzing the accuracy of the continuous versus intermittent method for CO and SvO2 measurement in pigs. Twenty-three pigs were enrolled to three groups: control, ANH with 6% hydroxyethyl starch (HES), or ANH with lactated Ringer's (LR) solution. After hemodilution, we showed that SvO2 was reduced in both groups, mainly in LR animals (P < 0.05). Regarding the evaluation of CO, we showed an increase in both groups submitted to ANH (P < 0.05). Through Bland-Altman analysis, we showed that the continuous CO catheter presented lower values than the intermittent method after hemodilution, mainly with HES (P < 0.001), and there was no difference in the measurement of SvO2. The ANH promoted a decrease in SvO2 and an increase in CO values, mainly in animals submitted to hemodilution with HES. The use of continuous and intermittent (laboratory) measurement of SvO2 showed clinical applicability and good agreement, an effect not reproduced by the CO measurement. New studies are needed to further investigate the agreement between the continuous and intermittent methods for the measurement of CO in adverse hemodynamic conditions such as ANH.
The variability of the interpretation by two individuals of a combined echocardiographic and Doppler method of calculating output was studied in 30 normal adults. In each subject three separate cardiac cycles were recorded to calculate maximal mitral valve orifice, the ratio of mean to maximal mitral valve leaflet separation, and the mean flow velocity through the mitral valve. The recordings were digitised twice by two independent observers. Estimates of cardiac output ranged from 3.2 to 8.11 1/min. Analysis of variance showed that interobserver and intraobserver variability for these measurements was 5.8% and 6.1% respectively. It is concluded that the reproducibility for interpreting this non-invasive method is adequate for clinical use in adults with cardiac outputs within the normal range.