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Biomedical subjects

S M Scharf

Publications and source records attributed to S M Scharf.

At least 55 records · Page 3Linked to original sources
PubMed1995

Effects of CPAP on cardiac output in pigs with pacing-induced congestive heart failure.

Continuous positive airway pressure (CPAP) may improve left ventricular (LV) function in patients with congestive heart failure (CHF). To understand mechanisms involved, in nine sedated, unanesthetized pigs with pacing-induced CHF we measured cardiac index (CI), heart rate (HR), LV pressures and volumes, ejection fraction (LVEF), and maximal rate of LV pressure rise (dp/dtmax). LV end-systolic transmural pressure (afterload) was estimated as LV end-systolic pressure (LVESP)-CPAP. Measurements were taken at CPAP 0, 5, 10, and 15 cm H2O and during recovery. At CPAP 5 cm H2O, CI increased from 4.23 +/- 1.00 to 4.99 +/- 0.88 L/min/m2 (p < 0.005), LV end-systolic volume decreased from 82.3 +/- 32.1 to 72.7 +/- 30.3 ml (p < 0.04) and LVEF increased from 0.30 +/- 0.09 to 0.36 +/- 0.12 (p < 0.02), and dp/dtmax increased. LVESP-CPAP was unchanged. After CPAP was discontinued, there was a rise in CI (p < 0.03), HR (p < 0.03), LVESP (p < 0.02), dp/dtmax (p < 0.02) and a decrease in total peripheral resistance (p < 0.03). We conclude that in CHF, low levels of CPAP improved CI, at least partly by improving contractility. Increased CI after discontinuing CPAP may be due to sympathoadrenal stimulation or withdrawal of alpha-adrenergic tone.

Animals↗
PubMed1995

Intravenous magnesium sulfate as an adjunct in the treatment of acute asthma.

STUDY OBJECTIVE: This study was conducted to determine whether intravenous magnesium sulfate (MgSO4), when used as part of a standardized treatment protocol, can improve pulmonary function and decrease admission rate in patients presenting to the emergency department with exacerbations of asthma. DESIGN: In this randomized double-blind placebo-controlled study, patients with acute asthma were treated with inhaled beta-agonists at regular intervals and intravenous (IV) steroids. At 30 min after entry, patients received either 2 g IV MgSO4 or IV placebo. Patients were monitored for up to 4 h with regular measurements of pulmonary function. Patients who were discharged from the emergency department were contacted at 1 day and 7 days for follow-up. SETTING: Emergency departments of a university-affiliated, voluntary hospital and municipal hospital. PARTICIPANTS: Asthmatics aged 18 to 65 years during acute exacerbation with FEV1 less than 75% predicted both before and after a single albuterol treatment. INTERVENTIONS: Patients were given 2 g of MgSO4 or placebo as an adjunct to standardized emergency department procedure for acute asthma. MEASUREMENTS AND RESULTS: One hundred thirty-five patients were studied. Hospital admission rates were 35.3% for placebo-treated group and 25.4% for the magnesium-treated group (p = 0.21). FEV1 measured at 120 min was 56% predicted for the placebo-treated group and 55% predicted for the magnesium-treated group. (p = 0.92) For subgroup analysis, patients were divided into "severe" (baseline FEV1 < 25% predicted on presentation) or "moderate" (baseline FEV1, 25 to 75% predicted on presentation). For the severe group, admission rates were 78.6% (11/14) for the placebo-treated group and 33.3% (7/21) for the magnesium-treated group (p = 0.009). For the moderate patients, admission rates were 22.4% (11/49) for the placebo-treated group and 22.2% (10/25) for the magnesium-treated group (p = 0.98). There was no significant improvement in FEV1 in the moderate group for magnesium-treated patients. However, in the severe group, there was a significant improvement in FEV1 at 120 min and 240 min (p = 0.014 and 0.026, respectively). CONCLUSION: Intravenous MgSO4 decreased admission rate and improved FEV1 in patients with acute severe asthma but did not cause significant improvement in patients with moderate asthma.

Acute Disease↗
PubMed1995

Sleep quality in Lyme disease.

Complaints of chronic fatigue as well as sleep disturbances are prevalent in Lyme disease. We compared polysomnographic measures of sleep in patients with documented Lyme disease with those of a group of age-matched normal control subjects. Eleven patients meeting Centers for Disease Control criteria for late Lyme disease with serologic confirmation by enzyme-linked immunosorbent assay and Western blot without a history of other medical or psychiatric illness and 10 age-matched control subjects were studied. Lyme disease patients and controls underwent 2 nights of polysomnography. Multiple sleep latency testing (MSLT) was performed in the patients. Sleep was staged by standard criteria, and continuity of sleep was assessed for each stage of frequency analysis of consecutive epochs. All patients studied reported sleep-related complaints, including difficulty initiating sleep (27%), frequent nocturnal awakenings (27%), excessive daytime somnolence (73%) and restless legs/nocturnal leg jerking (9%). Greater sleep latency, decreased sleep efficiency and a greater arousal index were noted in Lyme patients. The median length of uninterrupted occurrences of stage 2 and stage 4 non-rapid eye movement (NREM) sleep was less in Lyme patients (6.3 +/- 3.0 epochs in patients vs. 11.4 +/- 4.4 epochs in controls for stage 2, p < 0.01, and 4.3 +/- 4.4 epochs in patients vs. 11.2 +/- 6.3 epochs in controls for stage 4, p < 0.01), indicating greater sleep fragmentation. Mean sleep onset latency during the MSLT was normal (12.7 +/- 5.6 minutes). Three patients demonstrated alpha-wave intrusion into NREM sleep. These sleep abnormalities may contribute to the fatigue and sleep complaints common in this disease.

Adult↗
PubMed1994

Mechanisms of myocardial depression after bolus injection of sodium bicarbonate.

PURPOSE: The classic model for the effects of NaHCO3 on myocardial function predicts transient myocardial depression after an intravenous bolus of sodium bicarbonate in association with myocardial acidosis. METHODS: Five anesthetized, paralyzed, and ventilated dogs underwent midline sternotomy. Myocardial global function was assessed by cardiac output, left ventricular (LV) dp/dt, LV end-systolic, and LV end-diastolic pressures. Regional myocardial function assessed by measuring the LV regional end-systolic, LV end-diastolic lengths, and LAD coronary blood flow. Coronary sinus, intramyocardial and arterial pH were measured as was free serum Ca++. Animals were made acidemia by infusion of 0.3 N HCl and then given a bolus of sodium bicarbonate. This produced transient depression followed by recovery of myocardial function. RESULTS: During the depression phase there was no significant decrease in interstitial pH or an increase in A-VCO2 difference as predicted by the current model. However, there was a significant decrease in the serum free Ca++ that coincided with myocardial depression. CONCLUSION: We could not confirm the predictions of the classic model and hypothesize that myocardial depression may be caused by decreased availability of free Ca++ of decreased Ca++ flux rather than intracellular acidosis.

Acidosis↗
PubMed1994

Hemodynamic effects following injection of venom from the scorpion Leiurus quinquestriatus.

PURPOSE: The present study tested the hypothesis that scorpion sting induces left ventricular (LV) hypokinesia and myocardial ischemia shortly after injection due to reduction of coronary blood flow (CBF) and increased oxygen demand. METHODS: In 5 mechanically ventilated, open-chest dogs, we measured LV function following i.v. injection of venom (0.05 mg/kg) obtained from the scorpion Leiurus quinquestriatus. Hemodynamic responses to the venom were followed up for 90 minutes. RESULTS: The venom induced significant combined respiratory and metabolic acidosis (arterial pH progressed from 7.35 +/- 0.03 at baseline to 7.10 +/- 0.06 at 90 minutes). There were large increases in blood pressure, LV end systolic pressure, stroke work, and velocity of contraction. Twenty minutes following venom injection, cardiac output (CO) increased by 37% but then declined to 36% below baseline by 90 minutes (P < .05). CBF increased significantly in proportion to increased perfusion pressure; hence, there was no change in coronary vascular resistance. There was no evidence of myocardial ischemia or LV dysfunction because there was no change in myocardial pH, percentage fiber shortening, or LV end-diastolic pressure. Despite the fact that some variables returned to baseline at 90 minutes, they did not reach steady state; thus, the preparation would have continued to deteriorate. CONCLUSIONS: Myocardial ischemia does not occur in this dog model immediately following administration of scorpion venom. There are significant peripheral circulatory effects of the venom, which account for many of the hemodynamic changes.

Animals↗
PubMed1994

Cardiovascular effects of periodic obstructive and central apneas in dogs.

Patients with sleep apnea may experience two types of apnea, central and obstructive. We compared cardiovascular effects of these two types of apnea matched for changes in arterial blood gas tensions and periodicity. In 12 anesthetized, closed chest dogs, obstructive apneas were induced by completely occluding the endotracheal tube at end-expiration for 1 min and allowing 1 min of spontaneous ventilation. Central apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on with the same periodicity as obstructive apneas. During both types of apnea, changes in arterial PO2 and PCO2 were approximately the same. During obstructive apneas, mean blood pressure (BP) and cardiac output (CO) did not change significantly, heart rate (HR) decreased by 27% (p < 0.001), and stroke volume increased by 7.8 ml (p < 0.005). During central apnea, BP did not change, but HR and CO decreased by far more than with obstructive apneas: 44% (p < 0.001) and 27% (p < 0.05) respectively, and stroke volume increased by 5.0 ml (p < 0.05). During obstructive apneas, right atrial pressure increased, as did right heart blood volume. During central apneas, both right atrial pressure and left atrial pressure increased, as did pulmonary blood volume. We conclude that: (1) HR decreases are more severe during central apnea, most likely due to lack of respiratory mechanoreceptor input; (2) CO decreases more with central compared with obstructive apnea due to the heart rate response; (3) HR-induced cardiac dysfunction with central apnea could lead to pulmonary vascular congestion.

Animals↗
PubMed1994

Effects of continuous positive airway pressure on cardiac output in normal and hypervolemic unanesthetized pigs.

Continuous positive airway pressure (CPAP) has been used to increase cardiac index (CI) in patients with congestive cardiomyopathy in the presence of elevated pulmonary wedge pressure. We hypothesized that with normovolemia, CPAP would decrease CI because of decreased left ventricular (LV) preload, whereas in hypervolemia CPAP would increase CI because of a decrease in afterload. We tested this hypothesis on nine sedated, unanesthetized pigs instrumented 5 to 10 d before study. We measured CI, heart rate, stroke volume, LV end-diastolic and end-systolic pressures, and LV dimensions at CPAP levels 0, 5, 10, 15, and 20 cm H2O before and after volume expansion with hetastarch (35 ml/kg). From LV dimensions, LV end-diastolic (LVEDV) and LV end-systolic volumes (LVESV) and LV ejection fraction (LVEF) were calculated. With normovolemia, CI and LVEDV decreased with increased CPAP. Volume infusion produced mild cardiac dysfunction as evidenced by increased LV volumes, decreased LVEF, and decreased contractility. With hypervolemia, CPAP produced an increase in CI, decrease in LVEDV and LVESV, and an increase in LVEF. At higher values of CPAP, we observed decreased CI and LVEDV as with normovolemia. We conclude that with normovolemia, CPAP's effects are mainly related to changes in preload. Hypervolemia produced mild cardiac dysfunction. The improvement in CI with CPAP appears predominantly to be secondary to decrease in LV afterload, but a mild preload effect, which parallels the effect seen with normovolemia, was superimposed on afterload changes at higher CPAP values.

Analysis of Variance↗
PubMed1993

Nortriptyline-induced depression of ventilatory control in a patient with chronic obstructive pulmonary disease.

Psychiatric disorders occur frequently in patients with COPD, but therapy with psychotropic drugs is often limited by concomitant depression of ventilatory drive. We present a patient with COPD and major depression who developed hypercapnic respiratory failure while receiving nortriptyline and oxazepam. Because of known respiratory depressant effects of the latter drug, nortriptyline alone was resumed upon recovery. Depression of CO2 sensitivity and ventilatory load compensation with a concomitant increase in exercise tolerance with decreased dyspnea was observed while she was receiving nortriptyline. These results demonstrate a previously unreported depressant effect of nortriptyline on ventilatory control, and they suggest the need for further investigation of the ventilatory effects of this drug in patients with pulmonary disease.

Aged↗
PubMed1993

Effects of periodic obstructive apneas on venous return in closed-chest dogs.

With sleep apnea syndrome, mean cardiac output (CO) may fall. This implies a fall in venous return (VR) that is equal to the product of the pressure gradient for VR (GVR)--mean circulatory pressure (MCP)--right ventricular end-diastolic pressure and the conductance for VR (Gv). During airway obstruction there could also be shifts of blood volume between central and peripheral circulatory compartments. We studied these parameters in anesthetized closed-chest, spontaneously breathing dogs when hypoxia occurred (room air [RA] breathing) and when hypoxia was prevented (100% O2 breathing). Obstructive apneas were induced by completely occluding the endotracheal tube at end expiration for 1 min and allowing 1 min of spontaneous ventilation. During RA apneas, arterial PO2 decreased to 32.7 +/- 6.1 mm Hg (p < 0.01). Apnea reduced respiratory effort rate by 22.0 to 37.0% and was associated with inspiratory airway pressure swings in both RA and O2 of approximately -16.0 mm Hg. During apnea, on RA and O2 heart rate and mean arterial pressure decreased by 20 to 30 beats/min and by 8 to 12 mm Hg, respectively. On RA, CO decreased by 7.0% (not significant). In contrast, on O2, CO increased by 21.0% (p < 0.01). With RA apneas, GVR and MCP increased by 55% (p < 0.05) and Gv decreased by 63% (p < 0.05). On O2, there were no changes in GVR or Gv, and changes in CO were predictable from the baseline VR curve. With O2 there was an increase in central blood volume by 21.0% (p < 0.01) during the apneic phase.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Chronic upper airway obstruction produces right but not left ventricular hypertrophy in rats.

With airway obstruction there is a decrease in inspiratory intrathoracic pressure. This could lead to increased venous return to the right ventricle (RV) and increased afterload imposed on the left ventricle (LV). Chronic upper airway obstruction, caused by either upper airway lesions or obstructive sleep apnea, is a cause of congestive heart failure because of a chronic resistive load imposed on the respiratory system. To determine the effects of chronic upper airway obstruction on RV and LV in adolescent rats, we chronically obstructed the trachea so as to considerably increased inspiratory esophageal pressure excursion (-3.7 +/- 2.2 to -29.4 +/- 10.1 cm H2O). Rats were studied at 7 wk (Group 1) and at 1 yr (Group 2) after tracheal banding. Sham-operated time-matched rats served as controls. In neither group was there evidence of arterial hypoxemia, but in both groups there was chronic hypercapnia (PCO2, approximately 51 mm Hg; bicarbonate, 27 to 28 mEq/ml). Hemoglobin was also normal in both groups, confirming the absence of chronic hypoxia. There were no significant differences between obstructed and control rats in lung, liver, and LV weight to body weight ratio. However, RV weight to body weight ratio was increased in obstructed rats compared with that in control rats in both groups by approximately 50% (p < 0.005). Thus, chronic normoxic airway obstruction leads to evidence of RV but not LV hypertrophy. We conclude that the mechanical effects of airway obstruction impose a chronically increased afterload on the RV, probably caused by venous return effects, but they have relatively little effect on the LV.

Animals↗
PubMed1993

Depressed ventilatory load compensation in sleep apnea. Reversal by nasal CPAP.

Abnormal inspiratory load compensation may be one factor leading to development of obstructive sleep apnea (OSA). Alternatively, abnormalities in ventilatory load compensation may be a consequence of the manifestations of OSA. This investigation was designed to determine if impairment of awake inspiratory load compensation exists in OSA and to determine if abnormalities in this parameter are reversible by nasal CPAP therapy. A new technique for assessment of awake inspiratory load compensation was devised to standardize the degree of ventilatory stimulation applied during load compensation assessment in each subject. This eliminates intersubject differences in degree of ventilatory stimulation during testing, which are inevitable with standard techniques and which have been shown to affect the measurement of load compensation. Inspiratory load compensation was assessed during resting room air ventilation and during steady state CO2 and exercise stimulation titrated to provide similar degrees of ventilatory stimulation in each subject. Impairment of awake inspiratory load compensation was found during all conditions in the patients with moderate to severe OSA studied compared with that in weight-matched control subjects. Normalization of awake inspiratory load compensation was observed after 4 wk of nasal CPAP therapy in five patients. These results indicate that impairment of awake inspiratory load compensation is a reversible consequence rather than a cause of OSA.

Carbon Dioxide↗
PubMed1992

Ventilatory and P0.1 response to hypercapnia in quadriplegia.

Unlike individuals with comparable degrees of respiratory muscle weakness from other causes, quadriplegic patients have a blunted ventilatory and P0.1 response to hypercapnia. This suggests that the diminished response in quadriplegia is due, in part, to an alteration in respiratory drive. We measured the hypercapnic response in 9 subjects with chronic quadriplegia (Q) and 8 normal controls (N). Ventilatory muscle strength, maximum voluntary ventilation (MVV), and lung volumes were measured in all subjects. The ventilatory response (HCVR) in Q was significantly less than in N (0.73 +/- 0.37 vs 2.95 +/- 0.4 L.min-1.mmHg-1; P less than 0.001), even when normalized for indices of respiratory muscle performance (e.g., vital capacity, MVV). There was no significant change in the HCVR in Q after the administration of naloxone. We also serially studied 2 subjects with acute quadriplegia, and found that despite progressive improvement in respiratory muscle performance, there was no accompanying increase in the response to hypercapnia. These data suggest that muscle weakness alone cannot explain the blunted hypercapnic response in quadriplegia, and are consistent with the hypothesis that these subjects have a reduced ventilatory drive.

Adult↗
PubMed1992

Effects of inspiratory loading on left ventricular myocardial blood flow and metabolism.

With airways obstruction, mean pleural pressure decreases. It has been postulated that associated increases in left ventricular afterload increase myocardial O2 demand (MvO2) and coronary blood flow (CBF). We tested this hypothesis in 12 anesthetized mixed-breed dogs. Through a median sternotomy, dogs were instrumented for the measurement of mean arterial pressure, cardiac output, and left anterior descending CBF. A catheter placed in the coronary sinus allowed sampling of left ventricular venous blood. MvO2 was calculated as CBF x (arteriovenous content difference), and coronary resistance was calculated as (mean arterial pressure)/CBF. After closure of the thoracotomy, animals were studied before and during inspiratory threshold loading (IL) of -20 to -25 cmH2O while breathing 100% O2 before and after bilateral cervical vagotomy. During IL, heart rate fell [approximately 20 beats/min (NS prevagotomy, P less than 0.05 postvagotomy)], arterial PCO2 increased [45 to 66 Torr prevagotomy, 45 to 50 Torr postvagotomy (P less than 0.01)], and arterial O2 content was unchanged. CBF increased with IL:41% prevagotomy (P less than 0.01), 18% postvagotomy (P less than 0.02). However, with IL, MvO2 did not increase significantly either pre- or postvagotomy. Coronary resistance decreased with IL [30% prevagotomy, 24% postvagotomy (P less than 0.01)]. In eight dogs, PCO2 was increased by increasing dead space while the animals were mechanically ventilated and paralyzed. Although there was little change in CBF, heart rate fell by an amount equal to that with IL. We conclude that 1) IL causes coronary vasodilation not related to changes in MvO2, PCO2, or vagal tone; 2) MvO2 does not increase with IL; and 3) decreased heart rate with IL is related to hypercapnia and/or acidosis.

Airway Obstruction↗
PubMed1992

Oxygen cost of resistive-loaded breathing in quadriplegia.

We hypothesized that, in quadriplegia, chest wall distortion would increase the energy cost of ventilation. To assess this, we measured the oxygen cost of breathing (VO2 resp) and changes in chest wall configuration during inspiratory resistive-loaded breathing tasks in five quadriplegic and five normal subjects. Each subject performed three breathing tasks that spanned a range of work rates (Wtot). Configurational changes of the abdomen and upper, lower, and transverse rib cage were assessed with magnetometers. We found that 1) in both groups, VO2resp increased linearly with Wtot over the range of tasks performed, 2) the mean slope of the regression line of VO2resp vs. Wtot was greater for quadriplegic than for normal subjects (3.7 +/- 0.8 vs. 2.0 +/- 0.7 ml O2/J, P less than 0.01), 3) efficiency of breathing (Wtot/VO2resp) was less for quadriplegic than for normal subjects (1.9 +/- 0.6 vs. 3.5 +/- 1.4%, P less than 0.001), 4) during inhalation, upper and lower rib cages behaved similarly in the two groups, but the quadriplegic subjects had a decrease in transverse rib cage and a much greater increase in abdomen than normal subjects, and 5) functional residual capacity decreased in normal but not in quadriplegic subjects during the breathing tasks. We conclude that the lesser efficiency of breathing in quadriplegia may be related to the elastic work of chest wall distortion, shorter mean operational diaphragm length, and possibly differences between normal and quadriplegic subjects in mechanical advantage of available inspiratory muscles.

Adult↗
PubMed1992

Respiratory phasic effects of inspiratory loading on left ventricular hemodynamics in vagotomized dogs.

Exaggerated inspiratory swings in intrathoracic pressure have been postulated to increase left ventricular (LV) afterload. These predictions are based on measurements of LV afterload by use of esophageal or lateral pleural pressure. Using direct measurements of pericardial pressure, we reexamined respiratory changes in LV afterload. In 11 anesthetized vagotomized dogs, we measured arterial pressure, LV end-systolic (ES) and end-diastolic transmural (TM) pressures, stroke volume (SV), diastolic left anterior descending blood flow (CBF-D), and coronary resistance. Dogs were studied before and while breathing against an inspiratory threshold load of -20 to -25 cmH2O compared with end expiration. Relative to end expiration, SV and LVES TM pressures decreased during inspiration and increased during early expiration, effects exaggerated during inspiratory loading. In all cases, LV afterload (LVES TM pressure) changed in parallel with SV. LV end-diastolic TM pressure did not change. CBF-D paralleled arterial pressure, and there were no changes in coronary resistance. In two dogs, regional LVES segment length paralleled calculated changes in LVES TM pressure. We conclude that 1) LV afterload decreases during early inspiration and increases during early expiration, changes secondary to those in SV; 2) changes in CBF-D are secondary to changes in perfusion pressure during the respiratory cycle; and 3) the use of esophageal or lateral pleural pressure to estimate LV surface pressure overestimates changes in LV TM pressures during respiration.

Animals↗
PubMed1992

Cardiovascular effects of periodic occlusions of the upper airways in dogs.

Hypoxemia and decreased intrathoracic pressure have been postulated as contributing causes of cardiovascular morbidity in obstructive sleep apnea syndrome (OSAS). Because of the difficulty of manipulating experimental conditions in humans, we developed an anesthetized closed-chest dog model, simulating the periodic airway occlusions of OSAS by periodic occlusions of the endotracheal tube (PUO). Using a periodicity of 60 s occluded, followed by 60 s ventilation for five to seven cycles, we measured heart rate (HR), cardiac output (CO), arterial pressure (Pa); left ventricular (LV) end-diastolic and end-systolic transmural pressure; dp/dt of LV pressure; left anterior descending (LAD) coronary blood flow (CBF), and regional myocardial contractility and intramyocardial pH. Four experimental conditions were studied: room air (RA) breathing (PO2 = 40); 100% O2 breathing (O2), and RA and O2 breathing with critical LAD stenosis (CS). Under all conditions PUO produced decreases in CO (10 to 30%) and proportional decreases in Pa. HR decreased, and in all but RA conditions stroke volume was unchanged. During the obstructed phase, indices of LV preload decreased. Indices of LV afterload also decreased except for LAD-perfused myocardium under RACS conditions. This latter was shown to be associated with regional ischemia (decreased regional pH and shortening). Regional ischemia was also demonstrated in two of nine dogs even under O2CS conditions. Among our major conclusions: (1) decreased Pa during PUO is due to decreased CO; (2) LV afterload does not increase during PUO; (3) with limited coronary flow reserve (CS), PUO can lead to myocardial ischemia. This is mostly but not solely due to hypoxia.

Animals↗