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L Hannemann

Publications and source records attributed to L Hannemann.

11 recordsLinked to original sources

Reversible decrease of oxygen consumption by hyperoxia.

The hemodynamic and metabolic effects of 90 minutes normobaric hyperoxia were studied in 20 critically ill patients (11 septic, 9 nonseptic) requiring mechanical ventilation with inspired O2 fraction (FIO2) less than 0.40. Thirty minutes after increasing the FIO2 to 1.0, arterial PO2 had increased from about 100 to about 400 mm Hg, and whole body oxygen uptake (VO2) was decreased 10 percent (p less than 0.05) due to an 18 percent decrease in O2 extraction ratio. During the subsequent 60 minutes of hyperoxia, there was no further significant change in VO2. Cardiac index did not change in hyperoxia, but it increased 10 percent (p less than 0.05) in recovery as systemic vascular resistance decreased. VO2 returned to baseline after 30 minutes recovery at original FIO2 due to increased O2 extraction as well as the increased cardiac output. The decrease in VO2 without a decrease in O2 delivery may reflect maldistribution of blood flow and functional O2 shunting to protect tissue from unphysiologically high PO2. While brief oxygenation is advisable before periods of hypoventilation, the present data suggest that hyperoxic ventilation in these patients with already adequate O2 delivery was counterproductive.

Bacterial Infections

[Oxygen transport and tissue oxygenation in critically ill patients--value of volumes and vasoactive substances].

The primary function of the cardio-respiratory system is to meet the oxygen demands of the various organs and tissues and to remove metabolic wastes. The cellular O2 supply in the critically ill patient afflicted with severe infection, sepsis or ARDS is impaired not only by reduced O2 transport to the tissue due to myocardial depression caused by inadequate preloading and depressed contractility, but also by inadequate blood flow at the regional and microcirculatory levels. To obtain adequate tissue oxygenation despite derangements of the microcirculation, it is useful to aim for a hyperdynamic circulatory state that provides a supramaximal O2 transport. The best way to achieve this goal is first to optimize cardiac filling pressures, i.e. to the upper range of normal, and then to improve cardiac output using inotropic support. Only when the arterial pressure remains too low despite these measures is the use of vasopressors indicated.

Blood Volume

[The clinical assessment of tissue oxygenation. The significance of hemodynamic and oxygen transport-related parameters].

Adequate matching of the tissue O2 supply to the cellular O2 demands depends on the integrity of all components of the O2 transport system. The quality of O2 uptake by the lungs as well as O2 transport to the tissues can be assessed nowadays in the clinical setting. However, even if O2 uptake by the lungs and O2 transport to the tissues are normal cellular O2 supply may nevertheless be inadequate, if gas and substrate exchange are impaired on the tissue level. This may occur when nutritive blood flow is disturbed, as in patients with sepsis and ARDS. The hemodynamic monitoring parameters that are available in the clinical setting (i.e. systemic blood pressure, heart rate, cardiac filling pressures and art. blood gases) are only poor reflectors of the adequacy of tissue oxygenation. This review attempts to evaluate the extent to which the commonly measured hemodynamic variables relate to O2 transport and tissue oxygenation.

Hemodynamics

Optimal oxygen delivery in critically ill patients.

Standard hemodynamic support in septic shock is to increase pulmonary capillary wedge pressure to above 15 mmHg by volume replacement and to give inotropic support if the mean arterial pressure (MAP) is not adequate. In an attempt to decrease mortality in critically ill patients, oxygen delivery (DO2) was increased by switching inotropic support from dobutamine alone or in combination with norepinephrine to dopamine alone, or by adding dopexamine, prostacyclin, or hypertonic saline to the treatment. DO2 increased significantly in all patients, but the increase in DO2 was accompanied by only a 10% increase in oxygen consumption (VO2). The increase in VO2 was similar in survivors and nonsurvivors and in patients with and without septic shock. The results indicate that if adequate volume and inotropic support is provided for critically ill patients, the detectable oxygen debt is small and has little effect on patient outcome. When DO2 is adequate, factors other than a tissue oxygen deficit seem to determine patient outcome.

Cardiotonic Agents

[Early recognition of malignant hyperthermia using capnometry].

Although malignant hyperthermia is still a potentially fatal disease that was marked by a high mortality until recently, lasting damage to the patient can now be prevented by early diagnosis and treatment. The following case demonstrates the special value of capnometry in diagnosing this condition. A 34-year-old man admitted for oral surgery showed symptoms of malignant hyperthermia 5 h after induction of anesthesia. Neuroleptanalgesia had been conducted. The patient had received thiopental and fentanyl for induction of anesthesia and alcuronium and succinylcholine for intubation. The first symptom noticed was an elevation of the end-tidal pCO2 as monitored by capnometry. Additional symptoms, such as a pronounced rise in temperature, blood pressure, and heart rate did not develop until 20-25 min later. The end-tidal oxygen concentration decreased from 30 vol.-% to 26 vol.-%. The patient had to be ventilated with a volume of 25 l/min to keep end-tidal pCO2 under 6 kPa. Treatment with dantrolene was started immediately. Not until 3 h after the onset of the first symptoms did the patient's body temperature and the minute volume needed for ventilation return to normal. Postoperative laboratory findings showed only a slight elevation of creatine kinase and serum lactate. Myoglobin was not detected in serum or urine. This case indicates that capnometry permitted immediate adaptation of controlled ventilation to the patient's increased metabolic rate and early initiation of dantrolene treatment, thus preventing more severe disorders and possible consequences for the patient. Other studies have also suggested the special importance of capnometry. Since the patient refused to give his consent, the diagnosis could not be ascertained by muscle biopsy, and had to be based on symptoms.

Adult

Comparison of central-venous to mixed-venous oxygen saturation during changes in oxygen supply/demand.

Because central venous O2 saturation (superior vena cava, ScvO2) can be monitored with less patient risk than mixed venous O2 saturation (pulmonary artery, SvO2), we examined the correlations between SvO2 and ScvO2 over a broad range of cardiorespiratory conditions, including hypoxia, hemorrhage, and resuscitation in anesthetized dogs. The correlation coefficient (r) between SvO2 and ScvO2 in 179 simultaneously drawn blood samples from 22 dogs was 0.97. In another nine dogs, the two sites were continuously and simultaneously monitored with fiberoptic catheters; r was 0.96 with a mean difference of 3.7 +/- 2.9 percent (SD) saturation. In each dog the changes in ScvO2 closely paralleled the changes in SvO2. Although absolute values of ScvO2 are not sufficiently identical to SvO2 to calculate O2 uptake or pulmonary shunt precisely, close tracking of changes in the two sites across a wide range of hemodynamic conditions warrant further consideration of ScvO2 for patient monitoring of trends in O2 supply/demand.

Animals

[Catheter induced rupture of a proximal pulmonary artery caused by vigorous coughing in a spontaneously breathing patient].

A complication is occurred during insertion of a pulmonary artery catheter in a 73-year-old woman with class III NYHA cardiac failure. After easy insertion of the catheter, massive haemoptysis developed as the patient coughed while the balloon of the catheter was inflated. Despite prompt emergency measures, the patient did not survive. Autopsy revealed a 2.7-cm perforation of the proximal pulmonary artery with penetration into the right lower lobe bronchus. This complication and its prevention are discussed.

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