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M Hausknecht

Publications and source records attributed to M Hausknecht.

7 recordsLinked to original sources
PubMed1989

Dependence of left ventricular twist-radial shortening relations on cardiac cycle phase.

Cardiac models have proposed tight coupling between the systolic twisting motion of the left ventricle about its longitudinal axis and muscle shortening. Whether a similar relationship holds during diastole is unknown. The present study determined the dynamic twist-radial shortening relationship throughout the cardiac cycle in six in situ canine left ventricles. Radiopaque markers (15-26) were implanted throughout the myocardial midwall in six canine left ventricles. Three-dimensional marker location was determined by computer analysis of biplane cineradiograms (60 frames/s), and the results were transformed to cardiac cylindrical coordinates. Mean chamber twist was defined as the gradient along the long axis of circumferential rotation relative to end diastole. Changes in chamber dimension were indexed by average radial shortening, normalized to span from 0 at end diastole to 1.0 at end systole. During systole, ventricular twist and radial shortening were linearly related with an average slope of -0.058 radians (r = 0.99). However, during early diastolic relaxation there was substantial untwist (48 +/- 20% of total) despite only an approximately 15% increase in mean radial dimension resulting in a much steeper twist-percent shortening relationship (-0.24 radians, r = 0.96). During most of the remainder of diastolic filling, the twist-shortening relation was shallower (-0.02, r = 0.91) than the corresponding systolic relation (P less than 0.05). Thus the twist-radial shortening relation depends on the phase of the cardiac cycle. These data suggest that models of chamber mechanics that incorporate twisting motion need to account for the matrix surrounding the muscles in addition to the shortening and lengthening of the muscle fibers.

Animals↗
PubMed1986

Longitudinal distribution of vascular compliance in the canine lung.

With an isolated perfused canine lung, the compliance of pulmonary circulation was measured and partitioned into components corresponding to alveolar and extra-alveolar compartments. When the lungs were in zone 3, changes in outflow pressure (delta Po) affected all portions of the vasculature causing a change in lung blood volume (delta V). Thus the ratio delta V/delta Po in zone 3 represented the compliance of the entire pulmonary circulation (Cp) plus that of the left atrium (Cla). When the lungs were in zone 2, changes in Po affected only the extra-alveolar vessels that were downstream from the site of critical closure in the alveolar vessels. Thus the ratio delta V/delta Po with forward flow in zone 2 represented the compliance of the venous extra-alveolar vessels (Cv) plus Cla. With reverse flow in zone 2, delta V/delta Po represented the compliance of the arterial extra-alveolar vessels (Ca). The compliance of the alveolar compartment (Calv) was calculated from the difference between Cp and the sum of Ca + Cv. When Po was 6-11 mmHg, Cp was 0.393 +/- 0.0380 (SE) ml X mmHg-1 X kg-1 with forward perfusion and 0.263 +/- 0.0206 (SE) ml X mmHg-1 X kg-1 with reverse perfusion. Calv was 79 and 68% of Cp with forward and reverse perfusion, respectively. When Po was raised to 16-21 mmHg, Cp decreased to 0.225 +/- 0.0235 (SE) ml X mmHg-1 X kg-1 and 0.183 +/- 0.0133 (SE) ml X mmHg-1 X kg-1 with forward and reverse perfusion, respectively. Calv also decreased but remained the largest contributor to Cp. We conclude that the major site of pulmonary vascular compliance in the canine lung is the alveolar compartment, with minor contributions from the arterial and venous extra-alveolar segments.

Animals↗
PubMed1986

Modifications of cardiopulmonary resuscitation based on the cough.

The ability of cardiopulmonary resuscitation (CPR) to provide adequate vital organ blood flow during prolonged resuscitation has long been questioned, as has the mechanism of blood flow during CPR. Because coughing during cardiac arrest has been shown to produce adequate anterograde flow to maintain consciousness in man without compressing the heart, cough CPR has been used as a model of a pure "thoracic pump" mechanism on which to base modifications of CPR. In the thoracic pump mechanism, the left heart is a passive conduit for blood expressed from the pulmonary vasculature to the aorta, and there is selective flow to the brachiocephalic vascular bed because of its low pressure veins, which are protected by closure of thoracic inlet venous valves. Right heart flow from systemic veins to the lungs occurs between applications of pressure. Four alternative modalities exploiting the thoracic pump concept were studied in dogs during ventricular fibrillation with angiographic and pressure recordings: cough CPR, simultaneous chest compression and lung inflation, abdominal compression with lung inflation, and inflation of a vest and binder. The latter technique was associated with successful defibrillation and recovery after more than 30 min of circulatory support during ventricular fibrillation. Preliminary studies in a primate preparation indicate that this technique might be useful for prolonged circulatory support in man when defibrillation is not initially available or successful.

Animals↗
PubMed1980

Cough-CPR: documentation of systemic perfusion in man and in an experimental model: a "window" to the mechanism of blood flow in external CPR.

Maintenance of arterial pressure and consciousness by vigorous coughing during ventricular fibrillation has been previously documented. Observations in 4 additional patients with unstable rhythms and in fibrillating dogs confirm that coughing: (1) produces an arterial pulse; (2) produces opening of the aortic valve; (3) generates forward blood flow; and (4) can maintain consciousness during circulatory arrest. The authors speculate that cough-induced systemic perfusion results from compression of the pulmonary vascular beds by a rise in intrathoracic pressure, the left heart acting only as a one-way conduit to the lower pressure extrathoracic vascular outlets. Recent data suggest that conventional CPR likewise produces blood flow by compression of the pulmonary vascular blood pool, and not by cardiac compression as previously thought.

Adult↗