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Biomedical subjects

M R Pinsky

Publications and source records attributed to M R Pinsky.

154 records · Page 9Linked to original sources
PubMed1984

Respiratory augmentation of left ventricular function during spontaneous ventilation in severe left ventricular failure by grunting. An auto-EPAP effect.

A patient with severe congestive cardiomyopathy demonstrated involuntary forceful expiratory grunting that was associated with an elevated intrathoracic pressure and stable hemodynamics. Face-mask administration of 20 cm H2O as continuous positive-airway pressure (CPAP) abolished the grunting without hemodynamic compromise. However, loss of CPAP by mask leak resulted in rapid hemodynamic deterioration and resumption of grunting. Endotracheal intubation with 20 cm H2O of positive end-expiratory pressure restored hemodynamic stability. This suggests that spontaneous ventilatory efforts can augment the failing myocardium.

Adult↗
PubMed1983

Cause-specific management of shock.

Any condition that decreases blood volume, cardiac output, or peripheral vasomotor tone sufficiently to impair tissue perfusion can cause shock. The cause should be established so that specific therapy can be given, but in the meantime, general measures should be directed at shock itself. Besides fluid resuscitation, these include correction of acid-base imbalance and maximization of tissue oxygenation. If hypotension persists after adequate fluid replacement, vasopressor therapy is indicated. Various drugs are available, and the choice depends on the pharmacologic characteristics of the agent and the pathophysiologic process involved.

Acid-Base Imbalance↗
PubMed1983

Augmentation of cardiac function by elevation of intrathoracic pressure.

We studied the cardiovascular effects of increasing intrathoracic pressure in an acute pentobarbital-anesthetized canine model of acute ventricular failure induced by large doses of propranolol. Left ventricular (LV) function curves were generated by volume loading from LV filling pressures of 5-20 Torr. The animals were ventilated by using intermittent positive-pressure ventilation with large tidal volumes (30 ml/kg). Chest and abdominal pneumatic binders were used to increase intrathoracic pressure. When compared with the control state, acute ventricular failure was associated with a decrease in the slope of the LV function curves (P less than 0.01). After binding the increase in intrathoracic pressure (1.1 +/- 1.6 to 12.1 +/- 2.4 Torr, P less than 0.01) was associated with an improvement in both right ventricular and LV function. Our study demonstrates that in this model of acute ventricular failure, increasing intrathoracic pressure improves cardiac function. We postulate that this observed improvement with increased intrathoracic pressure is due to reduced LV wall stress in a manner analogous to that seen with arterial vasodilator therapy in congestive heart failure.

Acute Disease↗
PubMed1983

Cardiac augmentation by phasic high intrathoracic pressure support in man.

Left ventricular performance can be significantly influenced by changes in intrathoracic pressure. In man, sustained increases in intrathoracic pressure unload the left ventricle, but since venous return decreases, increased intrathoracic pressure is associated with a decreased cardiac output. In a canine model of acute ventricular failure, it has been shown that phasic increases in intrathoracic pressure, which do not decrease venous return, improve steady-state cardiac output. We thus studied the cardiovascular effects of phasic high intrathoracic pressure support (PHIPS) in seven patients with shock in our intensive care unit whose condition was not responsive to conventional types of therapy. The PHIPS was generated by abdominal and chest wall binding during positive-pressure ventilation. As compared to the state before PHIPS, the PHIPS was associated with an increase in esophageal pressure (6.6 +/- 1.1 mm Hg; p less than 0.01) and in mean arterial pressure (43.0 +/- 6.1 to 51.0 +/- 7.7 mm Hg; p less than 0.01) while not changing arterial pressure relative to esophageal pressure. Cardiac output also increased from 3.6 +/- 0.5 to 4.2 +/- 0.6 L/min (p less than 0.05), while left ventricular filling pressures remained constant. In one subject a gated cardiac blood pool scan demonstrated a PHIPS-associated increase in ejection fraction and decreased end-diastolic volume. These results are consistent with the hypothesis that PHIPS, by increasing intrathoracic pressure, augments left ventricular performance by reducing left ventricular afterload. This appears to be a promising area for future research.

Bandages↗
PubMed1982

Effects of antihistamines and indomethacin on hyperosmolar-induced vasodilation.

The circulatory effects of iv injections of hyperosmolar solutions were studied both in intact dogs with aortic flow probes and in dogs using a standard right heart-bypass preparation. Serial iv injections of 20 ml of 10% NaCl or 50 ml of 25% mannitol produced reproducible episodic vasodilation characterized by falls in mean aortic pressure from 99 +/- 10 (SE) to 61 +/- 6 Torr and increases in aortic flow from 2.20 +/- 0.06 1/min to 3.12 +/- 0.28 (P less than 0.01). Systemic vascular resistance decreased (P less than 0.01) with each injection and serum osmolarity increased (P less than 0.01); however, there was a poor correlation between these two variables (r = -0.24). Because the mechanism of these physiological changes is unclear, the following experiments were performed to determine whether they were due to the release of vasoactive chemical mediators. We measured arterial and venous plasma histamine, a mediator released systemically in IgE-mediated anaphylactic reactions, but found no changes in histamine levels. Furthermore, pretreatment with both H1 and H2 blockers (diphenhydramine and cimetidine), agents that blocked histamine-induced hypotension, did not prevent hyperosmolar vasodilation. Also, indomethacin (a cyclooxygenase pathway inhibitor of prostaglandin synthesis) did not affect hyperosmolar vasodilation or the fall in systemic vascular resistance. Therefore, hyperosmolar vasodilation is not caused by the systemic release of histamine or by the effects of prostaglandins. The mechanism of these reactions is unknown, but it may be due to direct local effects of hyperosmolar solutions on vascular smooth muscle, perhaps mediated by local fluid and electrolyte shifts.

Animals↗
PubMed1979

Effect of intrathoracic pressure on left ventricular performance.

Left ventricular dysfunction is common in respiratory-distress syndrome, asthma and obstructive lung disease. To understand the contribution of intrathoracic pressure to this problem, we studied the effects of Valsalva and Müller maneuvers on left ventricular function in eight patients. Implantation of intramyocardial markers permitted beat-by-beat measurement of the velocity of fiber shortening (VCF) and left ventricular volume. During the Müller maneuver, VCF and ejection fraction decreased despite an increase in left ventricular volume and a decline in arterial pressure. In addition, when arterial pressure was corrected for changes in intrapleural pressure during either maneuver it correlated better with left ventricular end-systolic volumes than did uncorrected arterial pressures. These findings suggest that negative intrathoracic pressure affects left ventricular function by increasing left ventricular transmural pressures and thus afterload. We conclude that large intrathoracic-pressure changes, such as those that occur in acute pulmonary disease, can influence cardiac performance.

Cardiac Output↗
PubMedDate not supplied

Two-dimensional echocardiographic automated border detection accurately reflects changes in left ventricular volume.

The objective of this study was to determine the relationship of on-line measurements of left ventricular cavity area generated by echocardiographic automated border detection to true volume measured by an intraventricular balloon in an isovolumically contracting isolated canine heart preparation. Seven excised dog hearts had placement of an intraventricular balloon and were perfused in an ex vivo apparatus. Left ventricular area data from the midventricular short-axis plane and pressure data were recorded on a computer through a customized hardware and software interface with the ultrasound system. Left ventricular volumes were varied from 5 ml to maximal values (30 to 40 ml) at 1-milliliter increments. Three increasing and decreasing volume ramps were analyzed on each of seven hearts for a total of 1260 simultaneous measurements. Linear regression analysis correlated mean automated border detection area with absolute volume from each preparation. A predominantly linear relationship was observed with an average correlation of r = 0.97 (y = 0.16x-0.69, SEE = 0.31 cm2, p < 0.01). Left ventricular area measures for six of seven dogs varied little during isovolumic contraction (< 0.4 cm2) but did show a systematic cardiac cycle-related variability in one dog (28% change in area, maximum to minimum, over all volumes). In conclusion, the relationship between cross-sectional area and left ventricular volume was predominantly linear and varied little during isovolumic contractions in the normal canine left ventricle. Echocardiographic automated border detection appears to be a promising method to reflect changes in left ventricular volume.

Animals↗
PubMedDate not supplied

Dynamic biventricular response to alterations in preload in patients undergoing left ventricular device implantation.

Ventricular interdependence is important for the successful use of a left ventricular assist device (LVAD) because the filling of the device depends on right ventricular (RV) function as well as the interactions between the ventricles. The pulmonary arterial (PAP) and systemic arterial (AP) response to inferior vena caval (IVC) occlusion before and after insertion of an LVAD in 15 patients was used to "dissect out" the determinants of these interactions. PAP and AP were recorded during each IVC occlusion and peak systolic values calculated for each beat. Linear regression analysis was used to calculate the slope (k) between peak systolic AP values and peak systolic PAP values. k, a measure of preload responsiveness of the heart, is predominantly linear. k is relatively "flat" in selected LV failure patients pre-LVAD but increases significantly (P < 0.001) after LVAD (0.67 +/- 0.55 vs. 2.71 +/- 1.39). The increase in this parameter after LVAD suggests that the loss of RV-to-LV ventricular interdependence in patients with congestive heart failure appears to recover somewhat once an LVAD is inserted.

Adolescent↗
PubMedDate not supplied

Long-term outcome of critically ill elderly patients requiring intensive care.

OBJECTIVE: To evaluate the long-term mortality and morbidity of critically ill elderly patients requiring intensive care. DESIGN: Prospective comparison of outcome of critically ill patients aged 75 years and older with patients aged 65 to 74 years. PATIENTS: Critically ill patients aged 65 years and older who required intensive care and who were recruited during a 3-month period. MAIN OUTCOME MEASURES: Duration of hospitalization, hospital charges, procedures used in the intensive care unit, mortality in the hospital and during the follow-up period, and quality of life of survivors during the follow-up period. RESULTS: Ninety-seven patients were included in the study; 54 were 75 years or older and 43 were aged 65 to 74 years. No significant difference was noted between the two groups for length of stay in the hospital, hospital charges, or mortality at 1 year. Severity of illness, as assessed by Acute Physiology and Chronic Health Evaluation score at the time of intensive care unit admission, was a better predictor of survival than age. Quality of life, as assessed by activities of daily living, perceived quality of life, and Center for Epidemiologic Studies-Depression score, were not significantly different in either group at 1, 6, and 12 months after discharge from the hospital. Most patients in both groups described their quality of life as adequate and were willing to receive intensive care again, if necessary. CONCLUSION: Age alone is not an adequate predictor of long-term survival and quality of life in critically ill elderly patients.

Aged↗