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Controversy exists regarding whether "Decreased Cardiac Output" is really a nursing, or instead, a medical diagnosis. These authors clarify the importance of this diagnosis for nursing care.
This study determined whether noninvasive electrical impedance cardiography accurately measures systemic blood flow (cardiac output) in children with congenital heart defects. A total of 37 patients ranging in age from 2 to 171 months underwent complete right- and left-sided heart catheterizations that included simultaneous Fick and impedance measurement of cardiac output. Based on the diagnosis, 4 groups were formed consisting of a control group (n = 11) with no shunts, a group with intracardiac left-to-right shunting and an atrial septal defect (n = 7), another with a ventricular septal defect (n = 12) and an extracardiac left-to-right shunting with patent ductus arteriosus group (n = 7). Impedance values for systemic blood flow were compared with systemic and pulmonary blood flow obtained by the direct Fick method with measured oxygen consumption. The difference between impedance and Fick systemic blood flow was less than or equal to 5% in each of the 4 groups. The highest correlation between impedance and Fick systemic blood flow was with the atrial septal defect group (r = 0.89) and lowest with the ventricular septal defect and control (r = 0.69) groups. Fick pulmonary blood flow was significantly greater than impedance or Fick systemic flow in all 3 shunt groups. Impedance cardiography accurately measured systemic blood flow in children without shunts or valvular insufficiency. Likewise, systemic blood flow was accurately measured by impedance in the presence of intracardiac left-to-right shunts (atrial and ventricular septal defects) and extracardiac left-to-right shunts (patent ductus arteriosus).(ABSTRACT TRUNCATED AT 250 WORDS)
The specific aim of this exploratory, descriptive study was to demonstrate that the nursing diagnosis, decreased cardiac output, contains at least seven separate and specific components. Forty critical care nurses completed a questionnaire about seven different case studies, or vignettes. Each vignette reflected one of the following: myocardial injury, arrhythmias, decreased preload, myocardial ischemia, increased afterload, drug effects, and cardiac surgery alterations. Mean scores were used to validate the specific subcategories. Analyses of variance were used to demonstrate statistically significant differences among them. Six of the labels were supported, providing preliminary evidence for the validity of these components of decreased cardiac output.
BACKGROUND: Removal of one kidney during the period of nephrogenesis in the sheep leads to offspring with elevated blood pressure and reduced glomerular filtration rate (GFR) at 6 and 12 months of age. The mechanisms underlying the hypertension and the degree of renal impairment are not known. METHODS: Changes in GFR were measured in response to an infusion of amino acids and cardiac output was measured by thermal dilution in female offspring at 2 years of age in eight control (sham-operated) and seven animals that had been unilaterally nephrectomized at 100 days of gestation. RESULTS: Animals uninephrectomized as fetuses had significantly higher blood pressure (91 +/- 2 mm Hg) compared to control animals (86 +/- 2 mm Hg) (P < 0.05). Cardiac output was significantly higher in the uninephrectomized group (148 +/- 10 mL/kg/min) compared to the control group (124 +/- 6 mL/kg/min) (P < 0.05). Heart rate and stroke volume were similar in the two groups although both parameters tended to be higher in the uninephrectomized group. Uninephrectomized animals had a lower basal GFR (P < 0.05). An infusion of amino acids caused a significantly different response in GFR in the two groups (P < 0.01 between the groups) with the uninephrectomized animals having significantly lower GFRs during the infusion period. CONCLUSION: The increased blood pressure observed after fetal uninephrectomy is due to an increase in cardiac output. Thus, formation of a low number of nephrons in utero may predispose an individual to later renal failure and elevated blood pressure.
The purpose of the study was to evaluate the role of insulin in glucose kinetics after glucose administration using an insulinogenic index to indicate the magnitude of insulin response. The initial distribution volume of glucose (IDV-G) was calculated with a one-compartment model from repeated measurements of plasma glucose concentration three to seven minutes after administration of 100 mg.kg-1 glucose. The IDV-G was compared with the insulin response and the thermodilution assessments of cardiac output, measured simultaneously both before and after induced haemorrhage (30 ml.kg-1 over 30 min) in 12 adult mongrel dogs. The plasma insulin concentration was measured during the procedure and insulinogenic indices were calculated. There was no correlation between the IDV-G and insulinogenic indices, but there was a correlation between the IDV-G and thermodilution cardiac output before and after induced haemorrhage (r = 0.85, n = 24, P < 0.001). We conclude that the initial distribution volume of glucose is an indication of cardiac output in normo- and hypovolaemic dogs. Modification of glucose kinetics by the insulin response to glycaemic stimuli was negligible in that short period of time.
Inductance cardiography (thoracocardiography) non-invasively monitors changes in stroke volume by recording ventricular volume curves with an inductive plethysmographic transducer encircling the chest at the level of the heart. Clinical application of this method has been hampered, as data analysis has not been feasible in real time. Therefore a novel, real-time signal processing technique for inductance cardiography has been developed. Its essential concept consists in performance of multiple tasks by several, logically linked signal processing modules that have access to common databases. Based on these principles, a software application was designed that performs acquisition, display, filtering and ECG-triggered ensemble averaging of inductance signals and separates cardiogenic waveforms from noise related to respiration and other sources. The resulting ventricular volume curves are automatically analysed. Performance of the technique for monitoring cardiac output in real time was compared with thermodilution in four patients in an intensive care unit. The bias (mean difference) among 76 paired thoracocardiographic and thermodilution derived changes in cardiac output was 0%; limits of agreement (+/- 2 SD of the bias) were +/- 25%. It is concluded that the proposed signal processing technique for inductance cardiography holds promise for non-invasive, real-time estimation of changes in cardiac output.
BACKGROUND: Accumulation of lung fluid in the critically ill patient is believed to attenuate impedance cardiac output (CO(IC)) measurements. However, this phenomenon has never been shown experimentally. METHODS: In eight anaesthetized and ventilated dogs (weight 15-22 kg) a high-precision flow probe was placed on the ascending aorta via a left thoracotomy incision and the direct cardiac output (CO(FP)) was measured. Simultaneous CO(IC) measurements were made using a RheoCardioMonitor (ACMA, Singapore). Lung oedema was induced by intravenous oleic acid 0.1 mg kg(-1). Lung fluid was assessed by the decrease in basal thoracic impedance (Z(b)). Percentage errors between the two methods (CO(IC)-CO(FP)) were calculated and compared as Z(b) decreased at 1 Omega intervals. RESULTS: During the experiment mean Z(b) decreased from 35.9 (sd 5.2) to 27.8 (6.5) Omega (P=0.0037). This occurred over a period of 225 (range 112-338) min and Z(b) decreased by 1 Omega every 51 (22-68) min. The presence of excessive lung fluid was confirmed at post-mortem. Before lung oedema was induced, CO(IC) was 1.5 (0.6) litre min(-1) and the corresponding value of CO(FP) was 1.5 (0.7) litre min(-1) (data from eight dogs). As Z(b) decreased, and lung fluid accumulated, the error between CO(IC) and CO(FP) widened (P<0.0001, anova for repeated measures). Eventually, CO(IC) decreased to 0.7 (0.3) litre min(-1) and the corresponding value of CO(FP) was 1.2 (0.3) litre min(-1) (DeltaZ(b)=5 Omega, data from six dogs). Mean arterial pressure, central venous pressure and systemic vascular resistance were kept constant. CONCLUSION: The presence of lung fluid attenuates CO(IC) measurements with respect to CO(FP).
PURPOSE: To illustrate the multiple causes of hypoxemia to be considered following cardiopulmonary bypass and how therapy given to improve oxygen delivery may have contributed to a decrease in arterial oxygen saturation to life-threatening levels. CLINICAL FEATURES: A 61 yr old man with severe mitral regurgitation and chronic obstructive lung disease underwent surgery for mitral valve repair. A pulmonary artery catheter with the capacity to measure cardiac output and mixed venous oxygen saturation (SvO2) continuously was used. Two unsuccessful attempts were made to repair the valve which was finally replaced, requiring cardiopulmonary bypass of 317 min. Dobutamine 5 micrograms.kg-1.min-1 and sodium nitroprusside 1 microgram.kg-1.min-1 were used to increase cardiac output. Soon after, the SvO2 decreased progressively from 55 to 39%. The patient became cyanotic with a PaO2 of 39 mmHg. Sodium nitroprusside was stopped and amrinone 100 mg bolus followed by 10 micrograms.kg-1.min-1 was given in addition to adding PEEP to the ventilation. With these measures PaO2 could be maintained of safe levels but PEEP and high inspired oxygen concentrations were needed postoperatively until the trachea could be extubated on the third postoperative day. CONCLUSION: The profound hypoxemia in this case was likely due to a combination of intra- and extrapulmonary shunt, both augmented by sodium nitroprusside. The desaturation of mixed venous blood amplified the effect of these shunts in decreasing arterial oxygen saturation. The interaction of these factors are analyzed in this report.
OBJECTIVE: To evaluate cardiac position, left ventricular (LV) mass, and distribution of fetal cardiac output in infants with congenital diaphragmatic hernia (CDH) who required extracorporeal membrane oxygenation (ECMO), and in control subjects. STUDY DESIGN: Echocardiograms were performed on 23 neonates with CDH shortly after birth, and repeated within 5 days of repair on ECMO in 21 infants,aand on 12 infants receiving ECMO for other diagnoses, and on 10 healthy, term neonates. Cardiac angle between the midline saggital plane and the interventriculak septum was measured, and deviation from normal (45 degrees) was determined. The ratio of cross-sectional areas (proportional to flows) across the pulmonary (PV) and aortic (AV) valves was determined (PV2/AV2) in 19 infants with CDH and in the healthy control subjects. RESULTS: Thirteen (57%) infants with CDH survived and 10 (43%) died, with no difference in cardiac deviation before surgical repair (35 +/- 13 degrees vs Cardiac deviation persisted after repair in nonsurvivors (27 +/- 14 degrees vs 800.01 and LV mass was significantly less (1.68 +/- 0.39 vs 3.05 +/- 1.20 gm/kg, p00.0005). Neonates requiring ECMO for other diagnoses and well term babies did not have cardiac angle deviations; both these groups had a greater LV mass than did the infants with CDH. The PV2/AV2 flow ratios were higher in infants with CDH (median, 1.73; range, 1.25 to 16.50) compared with those of the healthy infants (0.96, 0.79 to 1.69, p < 0.0002). CONCLUSIONS: Cardiac malposition persisted despite CDH repair in nonsurvivors with low LV mass, and fetal cardiac output was redistributed away from the left ventricle. Lung hypoplasia with reduced pulmonary flow returning to the left atrium and altered left atrial hemodynamics may result in LV hypoplasia
1. Dose-response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2-5% (w/w) or 0-007% (w/w) sodium and administered in various sequences. 2. Dose-response curves were shifted to the left in rats on a high-, compared with a low-, sodium intake. This response was maintained for 7 days on changing from high to low sodium. 3. There was no difference in the relation between the fall of cardiac output and the rise of blood pressure in any of the experimental groups. 4. Dose-response curves for peripheral resistance showed the same directional change as seen for the pressor response in rats on high- and low-sodium diets. Since depression of cardiac output was proportional to the pressure rise, the absolute change in peripheral resistance was greater than the blood pressure response. The proportional changes were similar. 5. It is concluded that alterations in the pressor response to angiotensin caused by changes in sodium loading are attributable to changes in peripheral resistance and not to changes in the cardiac output response to the acute rise in blood pressure.
The comparative hemodynamic effects of dobutamine and dopamine were studied in 6 patients with low cardiac output resulting from acute myocardial infarction. Plasma levels of noradrenaline and renin were measured before and during a 5 microgram/kg/min infusion of each of the drugs. Dobutamine had a more pronounced chronotropic effect, increased the systolic arterial pressure more and decreased the systemic vascular resistance less than dopamine at doses which had comparable effects on cardiac output. Dobutamine stimulated renin release, which might partly be the cause of the increased systolic arterial pressure. The drug reduced the plasma level of noradrenaline, which might be explained as a reflex reduction in sympathetic tone. Dopamine, however, did not stimulate renin release but it did enhance the plasma level of noradrenaline, which might be due mainly to the release of endogenous noradrenaline.
Tracking changes in stroke volume or cardiac output (CO) can be useful in the diagnosis and treatment of various cardiac illnesses. Existing arterial pressure waveform based pulse contour CO algorithms perform poorly during altered systemic hemodynamics. In this study, a right ventricular pressure waveform based pulse contour CO algorithm was developed to estimate the amplitude and duration of a hypothetical triangular flow waveform in the pulmonary artery. This algorithm was tested against gold standard blood flow measurements in ten canines during acute perturbations to preload (inferior vena caval occlusion (IVCO), rapid saline infusion), afterload (descending aortic occlusion (DAO), serotonin, angiotensin II, sodium nitroprusside infusion), and cardiac contractility (dobutamine and propranolol infusion). The algorithm correctly predicted the changes in CO (r2 = 0.82) that varied from - 45 to 31% of the baseline levels. To explain this finding both the pulmonary arterial (PA) and the ascending aortic (AA) input impedances were modeled as three element windkessels. In the AA the peripheral resistance (from - 61 to 191%), characteristic impedance (from - 59 to 20%) and total arterial compliance (from - 49 to 34%) varied significantly with these perturbations. In contrast, these parameters in the PA changed little. In particular, except serotonin infusion, the characteristic impedance of the PA deviated only 6% (SD/mean) from baseline values. This suggests right ventricular pressure waveform based estimate of CO is possible during acute changes in left ventricular hemodynamics.
Theoretically, if the cardiac output were increased in the presence of a given intrapulmonary shunt, the arterial haemoglobin oxygen saturation (SaO2) should improve as the venous oxygen extraction per ml of blood decreases. To test this hypothesis, eight pigs were subjected to one-lung ventilation and adrenaline and isoprenaline infusions used to increase the cardiac output. The mixed venous oxygen, shunt fraction and oxygen consumption were measured. With both adrenaline and isoprenaline, although there was a small rise in mixed venous oxygen content, there was a fall in SaO2. With adrenaline, the mean shunt rose from 48% to 65%, the mean oxygen consumption rose from 126 ml/min to 134 ml/min and the mean SaO2 fell from 86.9% to 82.5%. With isoprenaline, the mean shunt rose from 45% to 59%, the mean oxygen consumption rose from 121 ml/min to 137 ml/min and the mean SaO2 fell from 89.5% to 84.7%. It is concluded that potential improvement in SaO2, which might occur from a catecholamine-induced increase in mixed venous oxygen content during one-lung ventilation, is more than offset by increased shunting and oxygen consumption which reduce SaO2.
1. The effects of daily administration of propranolol on the distribution of cardiac output were studied in the late pregnant guinea-pig. 2. The animals were given either saline, 5 or 50 mg/kg per day of l-propranolol for 15 days during the last trimester of gestation. 3. Blood flow responses were assessed by injecting 15 microns microspheres into the conscious animal one to two days prior to parturition. 4. The fraction of cardiac output reaching the placentas was significantly reduced in both groups (P less than 0.5 and P less than 0.001, respectively), while flow to all other organs studied remained unaltered. 5. It is suggested that propranolol exerts a selective effect on the placental vascular bed in the guinea-pig.
BACKGROUND AND AIM OF THE STUDY: The non-invasive evaluation of mitral valve area is often used in the assessment of patients with mitral stenosis. The pressure half-time method is commonly used to calculate valve area, but is inaccurate in many clinical scenarios. We sought to quantify the effects of changing cardiac output on the accuracy of mitral valve area determination. METHODS: Thirteen patients with mitral stenosis underwent routine stress echocardiography with resting and peak exercise results compared. A previously described and clinically validated mathematical model of the cardiovascular system was used to validate the clinical results. Seven different loading conditions for each of four different stenotic valve areas were modeled. RESULTS: In patients, with increasing cardiac output, pressure half-time decreased (-30.6+/-35.3 ms/l/min) and calculated valve area increased by 0.25+/-0.30 cm2/l/min. By continuity, it appeared that approximately half of this increase was due to actual valve orifice stretching, the remainder reflecting fundamental changes in the relationship between half-time and valve area. Mathematical modeling resulted in similar changes in pressure half-time and calculated valve area (0.06 to 0.12 cm2/l/min, p = 0.20 versus clinical results). CONCLUSION: Changes in cardiac output result in predictable changes in pressure half-time, and should be considered when performing serial examinations in patients with mitral stenosis.
OBJECTIVE: To compare two transesophageal echocardiographic methods of cardiac output and stroke volume measurement in mechanically ventilated patients. DESIGN: Prospective clinical study. SETTING: Operating room (group I) and intensive care unit (group II) in two university hospitals. PATIENTS: Fifteen deeply anesthetized patients undergoing gynecological laparoscopy for sterility (group I) and 40 patients with septic shock (group II). INTERVENTIONS: Transesophageal echocardiography with modification of hemodynamic conditions. MEASUREMENTS AND RESULTS: Left ventricular (LV) volumes, cardiac (CI) and stroke index (SI) were measured with two methods using either LV volumes or aortic Doppler. These values were significantly lower in group I compared to group II. Using ANOVA and paired t-tests, there were no significant differences between the two methods of measurement. Correlation between these methods was better in group II than in group I, although not significantly so. In group I, bias for CI measurements was low (0.05 l/min per m(2)), with a weak agreement in terms of the 95% confidence interval (-1.17; 1.06 l/min per m(2)) compared to the mean values obtained with both methods (1.3 l/min per m(2)). In group II, bias for CI measurements was lower (0.2 l/min per m(2)). Agreement was weak, regarding 95% confidence intervals (-1.7; 1.3 l/min per m(2)) compared to the mean values (3 l/min per m(2) with the LV volumes method and 3.2 l/min per m(2) and with the Doppler method). CONCLUSIONS: Cardiac output and stroke volume can be measured from LV volumes in mechanically ventilated patients, yielding relevant information. However, the accuracy of LV volume measurements is not excellent compared to the aortic Doppler method. Thus, this latter technique should still be considered as the gold standard.
The adjustment of pulmonary oxygen uptake (VO2) following a step increase in work rate has been characterized as consisting of an early "cardiodynamic" component with unchanged mixed-venous O2-content ("phase 1") and a subsequent "metabolic" component ("phase 2") starting when venous blood from the muscle arrives at the lungs. The aim of the present study was to investigate whether the onset of phase 2 actually indicates the arrival of blood influenced by the altered muscle metabolism. Parallel measurements of cardiac output (Doppler technique) and VO2 (breath-by-breath measurements at the mouth) were performed in eight subjects during step increases in exercise intensity (from a 20 W baseline to either 80 W, 120 W, 160 W or 200 W). To vary the absolute cardiac output values for given muscle VO2 the subjects exercised both in upright and supine position. Individual time-courses of the arterio-venous O2 difference (a-v delta O2) were computed from cardiac output and VO2 data. Independent of body position two clear-cut phases of similar duration were seen both in VO2 and in the computed a-v delta O2. The duration of the first component with unchanged a-v delta O2 was about 20 s at the lowest step amplitudes (20-80 W and 20-120 W). It decreased to about 15 s for the 20-160 W and 20-200 W steps. At the lower exercise intensities the duration of phase 1 appears too long to be entirely due to the transit time of venous blood from the exercising muscles to the lungs.(ABSTRACT TRUNCATED AT 250 WORDS)
The largest decrease in cardiac output in patients undergoing aortoiliac bypass grafting for peripheral arterial occlusive disease occurs when the aorta is cross-clamped, not when it is declamped. This decrease was reduced in four patients who received 2 liters of Ringer's lactate preoperatively. Postoperatively, as peripheral resistance decreases, a large volume of fluid may be necessary to maintain homeostasis. By knowing when changes in cardiac hemodynamics can be expected to occur during aortoiliac surgery, it may be possible to prevent cardiac complications.