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Biomedical subjects

R W Gotshall

Publications and source records attributed to R W Gotshall.

At least 55 records · Page 3Linked to original sources

Accuracy of electrical impedance cardiography for measuring cardiac output in children with congenital heart defects.

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)

Blood Circulation↗

Single-breath DLCO maneuver causes cardiac output to fall during and after cycling.

The purpose of this study was to evaluate the influence of the single-breath pulmonary diffusing capacity (DLCO) breath-hold maneuver on central hemodynamics. Ten men (mean age 24 yr) were studied at rest, during 40 min of cycling at 40 and 60% of peak O2 uptake, and 10 min into recovery. DLCO was measured in the seated position during a 10-s breath hold at total lung capacity. At rest the breath hold caused a significant fall in stroke volume (SV, -16%) and an increase in heart rate (HR, +20%) with no change in cardiac output (Q). The resting DLCO of 36.5 ml.min-1.mmHg-1 increased by 28 and 48%, respectively, during the low- and moderate-intensity cycling. The breath hold while cycling caused a significant decrease in SV and Q, but HR did not change. Likewise, during recovery SV and Q fell with the breath hold but again HR did not change. A significant fall in systolic (-17%), diastolic (-12.5%), and mean arterial pressure (-15%) occurred during the breath hold at rest and during and after the exercise. The reduction observed in SV and blood pressure most likely reflected a decrease in venous return. The differences observed in the HR response before, compared with during and after exercise, were consistent with a resetting or shift in the operating point of the arterial baroreflex. Because blood flow fell during the exercise and recovery breath-hold maneuver, the "true" DLCO may have been underestimated during and after cycling.

Adult↗

Central and peripheral hemodynamics during maximal leg extension exercise.

The purpose of this study was to examine the central and peripheral hemodynamic adaptations to maximal leg extension exercise. Seventeen men (X = 25 years, 84 kg) performed leg extension exercise (Universal equipment) for 12 repetitions (90s) to fatigue. Each repetition consisted of a 3s lifting motion, 1s pause, and 3s lowering motion. Impedance cardiography was used to measure stroke volume (SV), cardiac output (Q), systolic time intervals, and impedance contractility indices on a beat-by-beat basis. There were significant increases in systolic, diastolic, mean arterial pressure, total peripheral resistance, and HR during exercise. The mean Q remained similar throughout the protocol. SV decreased even though indices of myocardial performance indicated an enhancement of contractility. The magnitude of Q and SV were dependent upon the phase of leg extension. SV and Q during the lifting portions of the exercise were smaller than the lowering portions. The differences in SV and Q during the concentric and eccentric phases of the exercise most likely reflect the large static forces in exercising muscle which impeded venous return and increased afterload.

Adolescent↗

Cardiac output in adult and neonatal rats utilizing impedance cardiography.

Impedance cardiography (IC) has the potential to be applied to very small animals for the measurement of cardiac output (Q). To evaluate this, Q measured by impedance (ZQ) and thermal dilution (TDQ) were compared in adult Sprague-Dawley rats. Absolute values for TDQ were comparable with ZQ (e.g., 29.7 vs. 26.0 ml.min-1.100 g-1), and both equally followed the change in Q caused by hemorrhage and reinfusion of blood. IC was also evaluated in neonatal rats (1 and 7 day old). Control ZQ values were 113 ml.min-1.100 g-1 for the 1-day-old rats, and 104 ml.min-1.100 g-1 for 7-day-old rats. Both stroke volume and Q decreased with head-up tilt and increased with head-down tilt for both ages. Therefore, in the neonate, ZQ decreased appropriately with age and with preload reduction. From these results, it is concluded that IC can be utilized to evaluate cardiac function in neonatal and adult rats.

Animals↗

Evaluation of impedance cardiography in the canine pup.

This study evaluated the use of the noninvasive technique of impedance cardiography to assess central hemodynamics in an animal model similar in size to the neonate. Seven canine pups 5-6 wk of age, with an average weight of 2.2 kg, were studied. To alter cardiac output (Q), the pups were given 12 and 8% O2 to breathe, which produced an arterial PO2 of 30 and 21 Torr, respectively. Q was obtained simultaneously by impedance and thermal dilution under both normoxic and hypoxic conditions. The average Q measured by impedance and thermal dilution were within 10% agreement and moderately correlated (r = 0.76). Impedance Q and stroke volume (SV) averaged 201 ml X min-1 X kg-1 and 2.8 ml, respectively. Thermal dilution Q and SV averaged 212 ml X min-1 X kg-1 and 2.9 ml, respectively. Individual responses to the hyoxemia were variable, but the impedance technique appeared to measure these individual responses as well as the thermal-dilution technique. These findings demonstrate that impedance cardiography may be suitable to assess either the absolute or relative changes in central hemodynamics. The use of this technique in critical care neonatal and pediatric medicine seems justified.

Animals↗

Oscillatory cardiopulmonary effects of high-frequency jet ventilation.

The cardiovascular effects of high-frequency jet ventilation (HFJV) were compared with conventional volume ventilation in the anesthetized dog. A unique effect of HFJV on stroke volume and cardiac output was observed when stroke volume was analyzed on a beat-by-beat basis with impedance cardiography. A pronounced amplitude modulation of stroke volume, as well as of pulmonary and arterial pressure, occurred when the frequency of the HFJV approached the heart rate. The beat frequency of these amplitude oscillations was equal to that predicted based upon the frequency of the HFJV and the heart rate. Cardiac outputs obtained by techniques which average several beats will not detect these oscillations in cardiac output. These findings suggest that HFJV can generate an oscillation in thoracic hemodynamics which affects ventricular output in a similar manner.

Animals↗

The combined effects of hypoxemia and mechanical ventilation on renal function.

The combined effects of hypoxemia and mechanical ventilation on renal function were investigated in anesthetized dogs. Spontaneously breathing dogs (S) and dogs mechanically ventilated with a volume-ventilator (V) were made hypoxemic by breathing hypoxic gas to achieve PaO2 values of 35 and 22 mm Hg. At a PaO2 of 35 mm Hg, urine output and sodium excretion were increased in both groups. These responses closely followed the blood pressure response, which was greater in the V group. Renal blood flow (RBF), glomerular filtration rate (GFR), and fractional sodium excretion (FNA) were unchanged. At a PaO2 of 22 mm Hg, both groups demonstrated a reduction in urine flow, sodium excretion, FNA, RBF, and GFR. However, the mechanism involved was different and ventilator-dependent. At this low PaO2, arterial blood pressure was reduced in the S group with no change in renal resistance, while blood pressure increased in the V group with a marked increase in renal resistance as a result of the modification of the cardiovascular effects of lung inflation reflexes by mechanical ventilation. These results indicate that renal function is well-maintained at low PaO2 values (35 mm Hg) and reduced at more severe hypoxemia, mainly in response to systemic hemodynamics.

Animals↗

Canine renal vascular response to bilateral carotid occlusion during hypoxia.

Chloralose-urethane anesthetized dogs were utilized to determine if hypoxemic potentiation of the baroreceptor-mediated increase in renal sympathetic nerve activity (RSNA) results in sufficient renal vascular vasoconstriction to reduce renal blood flow (RBF) during bilateral carotid occlusion (BCO). Additionally, hypercapnia and mechanical ventilation were randomly combined with hypoxemia during BCO to determine if further augmentation of renal vasoconstriction could be accomplished. BCO resulted in a similar increase in blood pressure (renal perfusion pressure) in all periods. RBF was not reduced significantly by BCO during any period even though renal vascular resistance was significantly increased by BCO during each period. When hypoxemia was combined with hypercapnia and mechanical ventilation simultaneously, there was a greater percentage increase in renal resistance with BCO. During BCO, when renal perfusion pressure was returned to control values by suprarenal aortic constriction, RBF remained unchanged and renal resistance decreased to control values. These results indicate that the BCO-induced increase in RSNA is relatively moderate and, even when potentiated by hypoxemia, hypercapnia, and mechanical ventilation, is not sufficient to reduce RBF in the presence of an increase in blood pressure and renal autoregulation.

Animals↗

Pulmonary and systemic vascular responses to tolazoline in neonatal and mature calves.

Tolazoline was infused intravenously (2 mg/kg over 2 minutes) in awake neonatal and mature calves. In normoxic pulmonary normotensive neonatal calves, tolazoline induced minimal hemodynamic changes, except for an immediate bradycardia. Tolazoline caused increases in systemic arterial pressure and vascular resistance and a bradycardia in normoxic normotensive mature calves. Calves were also made hypoxic, by breathing 12% O2 by facemask, in order to produce pulmonary hypertension. In hypoxic pulmonary hypertensive neonatal calves, tolazoline induced transient pulmonary vasodilation, a reduction in systemic arterial pressure, and marked bradycardia. Similarly, tolazoline caused reductions in pulmonary and systemic arterial pressure and bradycardia in hypoxic pulmonary hypertensive mature calves. Pentobarbital anesthesia in neonatal calves induced marked hemodynamic changes but did not alter the cardiovascular responses to tolazoline. A significant correlation was found between the baseline pulmonary arterial pressure and the magnitude of the pulmonary depressor response to tolazoline when all interventions were evaluated. Thus, tolazoline induced transient pulmonary vasodilation in pulmonary hypertensive calves but simultaneously caused profound transient bradycardia, particularly in neonatal calves.

Aging↗

Metabolic, hemodynamic, and respiratory responses to performing cardiopulmonary resuscitation.

The purpose of this study was to evaluate the cardiorespiratory demands inherent to the maintenance of continuous one- and two-man cardiopulmonary resuscitation (CPR) for 10 min. Ten male paramedics (X age = 26 yrs) certified to perform CPR participated. Each subject assumed the three possible roles for administering CPR: ventilator, compressor, and one-man technique. Cardiorespiratory responses were determined by impedance cardiography and open-circuit spirometry at 2 min intervals while performing CPR with a resuscitation manikin. Left ventricular performance was evaluated by impedance ventricular function indices (VFI) and systolic time intervals (STI). All three roles elicited an increase in oxygen uptake compared to kneeling rest, with the roles of one-man and compressor being the most demanding. There were moderate increases in cardiac output and heart rate during the exercise roles, but stroke volume remained similar to resting values. Pulmonary ventilation increased during exercise, with the greatest increase occurring for the one-man role. STI and impedance VFI reflected an enhanced ventricular performance while performing the roles of one-man and compressor. These findings suggest that the energetic demands placed on the rescuer depend upon the specific role assumed. Properly trained and experienced individuals can perform CPR efficiently for at least 10 min while eliciting only moderate physiological stress.

Adult↗

Changes in pulmonary diffusing capacity and closing volume after running a marathon.

The purpose of this study was to evaluate changes in lung function after running a marathon. Pulmonary function tests were administered to 8 men before, immediately after, and the day following competition (mean run time = 3 hr 30 min). Subjects completed maximum expiratory flow volume maneuvers breathing air and 80% He/20% O2. Lung volumes were determined by N2 washout and single breath He dilution. Closing volumes (CV) were determined using a single breath O2 test. Pulmonary diffusing capacity (DLCO), pulmonary capillary blood volume (Vc), and membrane diffusing capacity (DM) were measured with the single breath technique. There were no changes in lung volumes or flow rates, except for an increase in FEV1, after the marathon. The He/O2 delta Vmax50, delta Vmax25, and isoflow values were similar pre- compared to post-race. There were significant decreases, however, in DLCO, DM and increases in CV post-race. Vc remained similar to pre-race values. These results suggest that small airways obstruction does not occur after a marathon. The significant increase in alveolar-capillary membrane resistance, however, may reflect the occurrence of subclinical edema. Such a change would decrease lung elastic recoil and could explain the increase in CV.

Adult↗

Canine renal vascular response to hyperoncotic dextran in kidneys with or without glomerular filtration.

The effect of intrarenal arterial infusion of hyperoncotic dextran on renal hemodynamics and excretion was studied in anesthetized dogs. To examine the role of glomerular filtration and tubular flow in the hemodynamic response, several kidney models were employed. Nonfiltering kidneys (NFK) were produced by combined ischemia and ureteral obstruction (UO). Additionally, kidneys with only UO and a lack of filtration as well as kidneys with only ischemia and glomerular filtration were studied. Renal blood flow in normal kidneys was increased by hyperoncotic dextran from 357 +/- 47 to 486 +/- 65 ml X min-1 X 100 g-1, with a corresponding decrease in renal vascular resistance. Ischemic kidneys responded likewise to the dextran infusion, increasing renal blood flow from 261 +/- 31 to 339 +/- 29 ml X min-1 X 100 g-1. Glomerular filtration rate was reduced by the dextran infusion from 80.1 +/- 7.9 to 60.7 +/- 6.6 in normal kidneys and from 31.8 +/- 9.6 to 20.2 +/- 5.8 ml X min-1 X 100 g-1 in ischemic kidneys. Urine flow and sodium excretion were also reduced in these kidneys. In contrast, both NFK and UO, which lacked filtration and tubular flow, did not vasodilate in response to dextran. Renal blood flow remained unchanged from control values (NFK: 146 +/- 6, UO: 111 +/- 22 ml X min-1 X 100 g-1) in these kidneys. These experiments show that the renal vascular response to hyperoncotic dextran is not due to a change in blood volume or viscosity nor to a direct pharmacologic action of dextran. The most likely explanation is that hyperoncotic dextran alters tubuloglomerular feedback control of renal vascular resistance by decreasing filtration and altering tubular flow and/or composition. However, the involvement of another intrarenal vasodilatory system cannot be discounted.

Animals↗

Renal oxygen delivery and consumption during progressive hypoxemia in the anesthetized dog.

The relationship between renal oxygen delivery (RDO2) and function was evaluated during progressive hypoxemia. Seven anesthetized, spontaneously breathing dogs were given progressively lower oxygen concentrations to breathe while monitoring renal O2 consumption (RVO2), renal hemodynamic and excretory function. In addition, basal RVO2 was determined in three models of kidneys without filtration. RDO2 averaged 3648 mumole O2/min/100 g during normoxia. Basal RVO2 averaged 100 mumole O2/min/100 g kidney while total RVO2 was 466 mumole O2/min/100 g kidney during normoxia, leaving 366 mumole O2/min/100 g consumed by those processes involved in tubular transport. During hypoxemia, all renal parameters were well maintained until the lowest PaO2 (24.2 Torr). At this level, total RVO2 and RDO2 were significantly reduced. However, RDO2 remained well above RVO2 throughout hypoxemia. The reduction in RVO2 was a direct result of decreased O2 demand, as glomerular filtration and tubular load were also reduced. This associated decrease in O2 demand and RVO2 was indicated by the fact that the renal (a - v)O2 difference remained low and unchanged (1.9 vol%), fractional sodium excretion was unchanged, and the ratio of tubular sodium reabsorption to RVO2 also remained unchanged (30.8 meq Na/mmole O2). It was concluded that hypoxemia, while reducing both RDO2 and RVO2 at the lowest PaO2 (24.2 Torr), did not functionally impair renal excretory function by limiting RDO2 to the tubular transport processes. A reduction in RBF is far more likely to compromise the RDO2 needed to sustain basal and active transport processes than hypoxemia itself.

Animals↗

Evaluation of myocardial performance during wheelchair ergometer exercise.

Since a relatively high incidence of cardiovascular disease is associated with wheelchair confinement, exercise stress testing techniques should be utilized to assess myocardial performance of wheelchair-dependent individuals. Therefore, the purpose of this study was to apply the techniques of impedance cardiography to graded wheelchair-type exercise. For this, 9 wheelchair-dependent volunteers completed a progressive intensity, discontinuous test on a wheelchair ergometer (WERG) at power outputs (PO) of 10, 20, and 30 watts. An impedance cardiogram (ZCG), electrocardiogram (ECG), and phonocardiogram (PCG) were recorded for 15 sec immediately following steady state exercise. Stroke volume (delta V) calculated from the ZCG was multiplied by steady state heart rate (HR) to estimate cardiac output (Q). The simultaneous recording of the ZCG, ECG, and PCG permitted calculation of systolic time intervals and impedance cardiography contractility indices. Values for delta V, HR, Q, arteriovenous oxygen difference, systolic and diastolic blood pressure, mean systolic ejection rate, the first derivative of the impedance change, and the Heather Index increased with increments in PO. The Q-S2 interval, left ventricular ejection time (LVET), the pre-ejection period (PEP), the ratio of PEP to LVET, and the R-Z interval decreased with increases in exercise intensity. A linear relationship was found between Q and oxygen uptake which was similar to that reported by other investigators for arm exercise. These data indicate that impedance cardiography may be used in conjunction with electrocardiography and phonocardiography for the non-invasive assessment of myocardial performance during wheelchair exercise testing.

Adult↗

Evidence for an intrarenal beta receptor in control of renin release.

Infusion of isoproterenol intravenously in normal dogs at rates of 0.10 or 0.018 mug/min per kg body wt increased renin secretion; at the lower infusion rate arterial pressure (AP) and renal blood flow (RBF) were unchanged. Isoproterenol was also infused into the renal artery in normal dogs at 0.10 mug/min per kg; renin secretion increased in association with an increase in RBF but AP was unchanged. Plasma K concentration was consistently decreased in all three of the above experiments and because hypokalemia is known to increase renin release isoproterenol was not infused intrarenally at the lower rate; the decrease in plasma K level precluded relating the entire response in renin release to isoproterenol. Intrarenal infusion of propranolol at 0.05 mg/kg per h in Na-depleted dogs decreased renin secretion whereas intravenous infusion at the same dose failed to alter renin release. Intrarenal infusion of propranolol at this rate in Na-depleted dogs with a denervated, nonfiltering kidney also decreased renin release. In contrast, intrarenal infusion of phentolamine or phenoxybenzamine in normal dogs failed to alter renin secretion in doses that blocked alpha-adrenergic receptors. These experiments provide strong evidence for an intrarenal beta-adrenergic receptor that mediates renin release, and it seems likely from the experiment in the denervated, nonfiltering kidney that the receptor is located in the juxtaglomerular cells.

Animals↗