Marcia Kemper

Cardiovascular changes during transport of critically ill and postoperative patients

We examined cardiovascular changes in 37 patients transported to an ICU after major general or vascular surgery (n = 14), open heart surgery (n = 13), or carotid endarterectomy (n = 10). Cardiovascular variables were also measured in a control group of 11 patients transported from an ICU for diagnostic or therapeutic procedures. All patients were followed for 30 min before transport until approximately 30 min after they arrived at their destinations. During this period, systolic BP and heart rate significantly increased only in patients recovering from major general/vascular surgery or carotid endarterectomy. These changes were apparently related to acute emergence from inhalational anesthesia (isoflurane plus nitrous oxide), since the other surgical patients were anesthetized with narcotic anesthesia, and the control group did not receive any anesthesia.

Modulating effects of propofol on metabolic and cardiopulmonary responses to stressful intensive care unit procedures.

OBJECTIVE Patients in the intensive care unit (ICU) undergo acute increases in metabolic and cardiopulmonary demands in response to routine care interventions, such as chest physical therapy. This study examined whether the short-acting drug, propofol, could blunt the responses to chest physical therapy. DESIGN Prospective, randomized, crossover (placebo vs. drug) study. SETTING University hospital surgical ICU. PATIENTS Postoperative ICU patients being ventilated in the synchronized intermittent mandatory ventilation mode. INTERVENTIONS Two groups of 16 patients were studied. Each patient received two successive sessions of chest physical therapy. In random fashion, one was preceded by the administration of placebo and the other by an intravenous bolus of propofol (0.75 mg/kg in one group and 0.35 mg/kg in the other group). Each session was preceded and followed by a period of rest. MEASUREMENTS AND MAIN RESULTS The increases in oxygen uptake, CO2 elimination, oxygen delivery, heart rate, and systolic blood pressure associated with chest physical therapy were attenuated with the low dose and suppressed with the high dose of propofol. The Paco2 concentration was slightly increased during both placebo and drug administration. CONCLUSIONS Propofol, in the doses administered in this study, significantly reduced the hemodynamic and metabolic stresses caused by chest physical therapy.

Caloric requirements and supply in critically ill surgical patients.

ObjectiveTo compare the caloric intake with the caloric requirements in postoperative patients being fed enterally via nasoenteric tubes, parenterally, or by both enteral and parenteral methods. DesignDescriptive study. SettingSurgical ICU in a university teaching hospital. PatientsSample of 22 mechanically ventilated postoperative patients, mean age 62 ± 17 yrs, selected from among those patients routinely scheduled to receive enteral or parenteral nutrition or both, for ≥4 days. The patients were studied for a total of 144 study days. InterventionEight patients received total parenteral nutrition, eight patients received enteral nutrition, and six patients received both parenteral and enteral nutrition. MeasurementsResting energy expenditure was measured by using indirect calorimetry, and daily nutritional intake was quantitated. ResultsThe patients who received parenteral, or enteral plus parenteral nutrition received an average of 80% of their caloric requirements, while those patients who received only enteral nutrition received only 68% of their caloric requirements. There was more day-to-day variation in nutrient intake in the enteral group (40% ± 56%) than in the parenteral group (12.2% ± 24%, p <.001). ConclusionsEnteral nutrition delivered via nasoenteric tubes as the sole delivery method in postoperative critically ill patients resulted in an inadequate and inconsistent nutrient supply. The use of parenteral or parenteral plus enteral nutrition resulted in more stable and adequate feeding than feeding byenteral nutrition alone.

Insights into the increased oxygen demand during chest physiotherapy

OBJECTIVES To determine the mechanism responsible for the increase in oxygen consumption (VO2) during chest physical therapy. Specifically, to examine the hypothesis that muscular activity is the major contributor to the increase in oxygen demand. DESIGN Prospective, observational study. SETTING University hospital surgical intensive care unit. PATIENTS Phase one included 13 patients who were mechanically ventilated after coronary artery bypass surgery. Phase two involved seven mechanically ventilated patients who had undergone major vascular or abdominal surgery. INTERVENTIONS Phase one involved turning patients to the lateral decubitus position. During the second phase, patients were given midazolam (0.15 microg/kg) 2 mins before an initial chest physiotherapy session and midazolam plus vecuronium (0.7 mg/kg) before a subsequent session. Physiologic measurements were made during the resting periods before and following each session, as well as at the completion of the intervention. MEASUREMENTS AND MAIN RESULTS Turning patients to the lateral position resulted in significant increases in oxygen uptake and CO2 elimination (VCO2). VO2 increased from 219 +/- 21 (SD) mL/min at rest to 324 +/- 58 mL/min (p <.05) with turning. These increases in oxygen demand were met by increases in both oxygen delivery (852 +/- 238 mL/min at rest to 1116 +/- 430 mL/min, p < .05) and extraction (0.27 +/- 0.7 at rest to 0.32 +/- 0.09, p < .05). There were associated increases in hemodynamic and respiratory variables including heart rate and systolic blood pressure. The administration of vecuronium completely suppressed the 50% increases in VO2 and VCO2 seen without the use of a muscle relaxant. The increases in systolic blood pressure were unaffected by vecuronium. The magnitude of the increase in PaCO2 (32 +/- 5 torr [4.3 +/- 0.7 kPa] at rest to 36 +/- 5 torr [4.8 +/- 0.7 kPa] during therapy, p < .05), was not accentuated by vecuronium (30 +/- 4 torr [4.0 +/- 0.5 kPa] to 35 +/- 6 torr [4.7 +/- 0.8 kPa], p < .05) despite a lack of any increase in minute ventilation or respiratory rate. This change was due to the parallel suppression of VCO2. CONCLUSIONS The increase in metabolic demand during chest physiotherapy is the result of increased muscular activity as evidenced by the suppression of VO2 following the administration of the muscle relaxant and the observation that turning a patient into the lateral decubitus position produces similar increases in VO2. The increases in blood pressure and cardiac output are due to another mechanism, most likely enhanced sympathetic output. The increase in physiologic activity produced by chest physiotherapy is thus secondary to both exercise-like and stress-like responses.

Variation in the Resting Metabolic Rate of Mechanically Ventilated Critically Ill Patients

There has been increasing interest in the nutritional support of the critically ill patient. The day-to-day variation in resting energy expenditure (REE) was studied over a 35-day period in 17 postoperative mechanically ventilated critically ill patients to gain insight as to how often caloric intake should be reassessed, whether changes observed over 3–5 days are of sufficient magnitude to make frequent adjustments in caloric intake, and what factors are associated with large alterations in metabolic rate. REE was measured daily for 3–5 days, and the percent variation in REE [(highest REE - lowest daily REE)/(lowest daily REE) × 100] calculated. The variation ranged from 4 to 56%, and on further analysis two distinct groups were identified, one with a mean variation of 12 ± 4% (sD) (range 4–18%) and the other with a mean variation of 46 ± 8% (range 37–56%). The former group was clinically stable, whereas the latter was not. Clinically stable patients need less frequent measurements than those who are more ill, but when designing a nutritional regimen for them, at least 20–25% should be added to the REE, 15% to account for day-to-day variation and 5–10% for activity.

An in vitro evaluation of an instrument designed to measure oxygen consumption and carbon dioxide production during mechanical ventilation

Objective: To determine the ability of the Puritan‐Bennett 7250 metabolic monitor to measure CO2 production and oxygen consumption (&OV0312;o2) under simulated clinical conditions. Design: An in vitro validation study. Setting: Laboratory of a large university medical center. Methods: An in vitro evaluation was performed by adding precise amounts of CO2 and nitrogen to a lung model to simulate CO2 production and &OV0312;o2. CO2 production and &OV0312;o2 values measured by the metabolic monitor were compared with simulated values at various Fio2 values (0.21 to 0.80), levels of positive end‐expiratory pressure (0 to 20 cm H2O), and flow‐by mode flow rates (0 to 20 L/min). This comparison was also made at increased peak airway pressures (60 cm H2O). The effects of various concentrations of oxygen on the accuracy of the CO2 production measurements were also examined. Results: The measurements made by the instrument were within 7% of values predicted from the CO2 and nitrogen infusions. There was no effect of various oxygen concentrations on the accuracy of CO2 production measurements. Conclusion: Under the in vitro conditions tested, the metabolic monitor provided accurate measurements of &OV0312;2 and CO2 production. (Crit Care Med 1994; 22:1995–2000)

RESPONSE OF CRITICALLY ILL PATIENTS TO INCREASED OXYGEN DEMAND : HEMODYNAMIC SUBSETS

Objective: To ascertain how patients with different abnormalities of oxygen transport at rest respond to an acute increase in oxygen demand. Design: Observational study with retrospective assignment to subgroups, based on resting oxygen extraction ratio or increased cardiac output. Setting: University hospital surgical intensive care unit (n = 96). Patients: Postoperative, mechanically ventilated, critically ill patients (n = 96). Intervention: Chest physical therapy. Measurements and Main Results: Metabolic, hemodynamic, and respiratory measurements were made during an initial rest period and then during chest physical therapy. During chest physical therapy, patients (n = 10) having low resting oxygen extraction ratios (≤0.20) increased oxygen extraction, without changing oxygen delivery (&U1E0A;o2); while those patients (n = 19) with high resting oxygen extraction ratios (≥0.30) increased &U1E0A;o2, but not oxygen extraction. Patients (n = 46) with oxygen extraction ratios between 0.2 and 0.3 had an intermediate response; both &U1E0A;o2 and oxygen extraction increased. The group (n = 19) with increased resting cardiac output (>9 L/min) and associated low resting oxygen extraction ratios and high &U1E0A;o2 values, increased their extraction of oxygen during chest physical therapy. Conclusions: The response to an acute increase in oxygen demand was influenced by resting conditions and was characterized by the use of “reserve” capacity. Patients with a resting hyperdynamic state (high &U1E0A;o2 and low oxygen extraction) were able to further increase oxygen extraction during the increase in oxygen demand. (Crit Care Med 1994; 22:1809–1816)

Stressing the critically ill patient: The cardiopulmonary and metabolic responses to an acute increase in oxygen consumption

Critically ill patients frequently have compromised respiratory and hemodynamic function. Chest physical therapy has been previously shown to increase oxygen demand and therefore was used to examine how postoperative mechanically ventilated patients responded to an increased oxygen demand. We found that during chest physical therapy, oxygen consumption increased 52% +/- 37% (SD) over baseline values. There was a 35% +/- 32% increase in oxygen extraction and a 17% +/- 33% increase in oxygen delivery. Arterial and pulmonary artery pressures also increased. The cardiac output increase was due to increased heart rate with no change in stroke volume. The increases in minute ventilation and alveolar ventilation were not sufficient to eliminate the greater quantity of carbon dioxide produced, resulting in a small increase in PaCO2. There was no significant change in systemic vascular resistance. The increase in oxygen demand caused by chest physical therapy triggered an integrated physiological response that resulted in increased respiratory and cardiac performance. This in some ways, such as the lack of increase in systemic vascular resistance, resembles the response to exercise.

Alfentanil Attenuates the Cardiopulmonary Response of Critically 111 Patients to an Acute Increase in Oxygen Demand Induced by Chest Physiotherapy

Critically ill patients often are subjected to interventions that acutely increase oxygen demand and require increased output of the cardiac and respiratory systems. This study explored whether alfentanil could attenuate the response to chest physical therapy, a procedure that increases oxygen consumption by 40%-50%. Patients were examined during two consecutive therapy sessions. In random order, they received either a placebo or alfentanil (30 or 60 micrograms/kg) 2 min before treatment. In Group 1 (n = 11, 30 micrograms/kg alfentanil) only the arterial blood pressure increases induced by chest physical therapy were attenuated. In Group 2 (n = 12, 60 micrograms/kg) alfentanil attenuated the increases in heart rate, central venous pressure, and pulmonary artery systolic pressures as well as systemic blood pressure. Neither dose of alfentanil altered the increases in oxygen consumption, carbon dioxide elimination, oxygen delivery, or extraction ratio. Thus alfentanil attenuated the hemodynamic responses to chest physiotherapy in a dose-dependent fashion. This was likely due to its vagotonic actions. In contrast, alfentanil had no effect on the balance between oxygen demand and delivery during chest physiotherapy. There was thus a dissociation between the hemodynamic and metabolic responses.

MIDAZOLAM ATTENUATES THE METABOLIC AND CARDIOPULMONARY RESPONSE TO AN ACUTE INCREASE IN OXYGEN DEMAND

Critically ill patients are subjected to routine clinical activities that increase oxygen demand. This results in increased heart rate, blood pressure, minute ventilation, and oxygen delivery in patients with often already compromised cardiopulmonary systems. This study examines whether the benzodiazepine, midazolam, could attenuate the increase in metabolism, respiration, and circulation seen during chest physical therapy. Two groups of mechanically ventilated postoperative patients were studied. One group (n = 15) received, in random order, 0.015 mg/kg of midazolam and placebo prior to two consecutive chest physical therapy sessions, while the other (n = 13) received 0.030 mg/kg and placebo. Both doses of midazolam significantly attenuated the increases in oxygen consumption, heart rate, and systemic blood pressure observed during placebo administration. The cardiac output increase was also attenuated. Although midazolam reduced minute ventilation and respiratory rate, no excess CO2 retention occurred when the drug was administered likely as the result of reduced CO2 production. The administration of midazolam (0.015 mg/kg and 0.030 mg/kg) prior to chest physical therapy reduces metabolic, hemodynamic, and ventilatory responses to chest physical therapy.