Functional hemodynamic parameters do not reflect volume responsiveness in the immediate phase after acute myocardial ischemia and reperfusion.

OBJECTIVE: Functional preload parameters such as stroke-volume variation (SVV) and pulse-pressure variation (PPV) are superior to filling pressures when assessing volume responsiveness in mechanically ventilated patients. This investigation studied their application in the setting of acute myocardial ischemia and reperfusion (I/R). DESIGN AND SETTING: Experimental animal study in a university laboratory. PARTICIPANTS: Twenty anesthetized and ventilated pigs. INTERVENTIONS: A temporary reduction of preload was obtained by ventilation with a positive end-expiratory pressure of 10 cmH(2)O. Ischemia was induced by temporary occlusion of the left anterior descending coronary artery for 60 minutes and was followed by 30 minutes of reperfusion. MEASUREMENTS AND MAIN RESULTS: Animals were instrumented with an ultrasonic aortic flow probe to monitor stroke volume (SV) and SVV. Arterial pressure and PPV were recorded with a microtip catheter; left ventricular volume and pressure were registered by a conductance catheter. Respective hemodynamic measurements were made before, during, and after PEEP; before and after the induction of I/R. Eleven animals survived I/R and were analyzed. Before I/R, SVV (r = 0.87, p < 0.001) and PPV (r = 0.75, p < 0.05) during PEEP correlated significantly with relative changes in SV caused by the release of PEEP. Changes in SVV (r = 0.82, p < 0.01) and PPV (r = 0.67, p < 0.05) correlated significantly with relative changes in SV. After I/R, neither the relations between changes in SV to SVV or PPV during PEEP nor the relations between changes in SVV or PPV to changes in SV reached significance. CONCLUSIONS: SVV and PPV did not reflect volume responsiveness in an experimental model of acute myocardial I/R.

Systolic pressure variation and pulse pressure variation during modifications of arterial pressure.

OBJECTIVE: This study was performed to investigate the effect of vasopressor therapy on systolic pressure variation (SPV) and pulse pressure variation (PPV) compared to experimentally measured left ventricular stroke volume variation (SVV). DESIGN AND SETTING: Prospective study in a university laboratory. SUBJECTS: Twelve anesthetized and mechanically ventilated pigs. INTERVENTIONS: Increase in mean arterial pressure (by 100%) using phenylephrine and decrease (by 38%) using adenosine. MEASUREMENTS AND RESULTS: SPV and PPV were calculated and compared to SVV derived from aortic blood flow measurements. SPV was significantly affected by changes in arterial pressure [4.6% (1.5) vs. 6.3% (2.1), p < 0.05, increased vs. decreased arterial pressure], whereas PPV did not change during modifications of arterial pressure. During baseline conditions and decreased afterload, correlation with SVV was good both for SPV (r =0.892 and r = 0.859, respectively) and for PPV (r = 0.870 and r = 0.871, respectively) (all p < 0.001). Correlation with SVV was only moderate during increased arterial pressure (r = 0.683 for SPV and r = 0.732 for PPV, p < 0.05). CONCLUSION: For guiding fluid therapy in patients under vasopressor support, PPV seems superior to SPV.

Positive end-expiratory pressure does not compromise myocardial contractility in myocardial ischemia/reperfusion.

Therapy for severe myocardial ischemia/reperfusion sometimes necessitates intermittent positive pressure ventilation, which may impair left ventricular function by reduction of ventricular loading. It is unknown today whether positive airway pressure also affects contractile force after myocardial ischemia/reperfusion. The authors tested whether positive end-expiratory pressure (PEEP) impairs myocardial contractility in acute ischemic heart failure. In 11 anesthetized mechanically ventilated pigs (28 +/- 3 kg), cardiac output (CO, aortic flow probe), load-independent parameters of left ventricular contractility (conductance method: preload recruitable stroke work [PRSW] and end-systolic elastance [E(es)]) and preload (end-diastolic volume [EDV] conductance) were assessed before and after myocardial ischemia and reperfusion (left anterior descending artery occlusion, 60 min). Data were taken during PEEP 0, 5, and 10 cm H2O. Before myocardial ischemia, both PEEP 5 and 10 cm H2O reduced CO (P < 0.05) because of a reduction of EDV (P < 0.05, PEEP 10 cm H2O). The PRSW remained unchanged (not significant [NS]) and E(es) increased (P < 0.05, PEEP 10 cm H2O). After myocardial ischemia/reperfusion, CO and PRSW, but not E(es) (NS), deteriorated markedly. At the same time, PEEP 10 cm H2O reduced CO (P < 0.05) and, slightly, EDV (NS). Now, both PRSW (P < 0.05, PEEP 5 cm H2O) and E(es) (P < 0.05, PEEP 10 cm H2O) improved upon ventilation with PEEP. In our model, the administration of PEEP impaired global left ventricular function before and after myocardial ischemia/reperfusion. The observed impairment is not attributable to compromised contractility.

Inhalative and intravenous stimulation of soluble guanylate cyclase reduces pulmonary vascular resistance and increases cardiac output in experimental septic shock.

The effects of inhaled and intravenous application of a guanylate cyclase stimulator (BAY 41-8543) on pulmonary vascular resistance (PVR) and cardiac output (CO) were investigated in an experimental model of septic shock. Following induction of septic shock, anaesthetized pigs (n=31) were randomly place into two groups receiving different interventions. Animals in the first group received intravenous BAY 41-8543 (0.6 mg), inhalative BAY 41-8543 (6 mg) or a placebo. In the second group, the dosage of BAY 41-8543 was increased two-fold or combined with inhalation of nitric oxide (iNO). Intravenous and inhaled administration of BAY 41-8543 resulted in a significantly (P<0.05) reduced PVR and increased CO compared with the placebo. Increasing the dosage of BAY 41-8543 or combining it with iNO did not further decrease PVR. The results of the present study indicate that BAY 41-8543 effectively reduces PVR and increases CO in septic shock, through inhaled or intravenous routes of administration.

The influence of positive end-expiratory pressure on stroke volume variation and central blood volume during open and closed chest conditions.

OBJECTIVE: Intermittent positive pressure ventilation and positive end-expiratory pressure (PEEP) affect cardiac preload. Their effect is dependent on chest wall compliance. This study compares the effects of intermittent positive pressure ventilation and PEEP on stroke volume variation and central blood volume during open and closed chest conditions. MATERIALS AND METHODS: Fourteen anesthetized and mechanically ventilated pigs (25-40 kg) were studied. Central blood volume was assessed using global end-diastolic volume and right ventricular end-diastolic volume measured by thermodilution. Further, left and right ventricular stroke volume variations were determined with ultrasonic flow probes placed around the pulmonary artery and ascending aorta, respectively. Measurements were performed during mechanical ventilation without and with PEEP (15 cmH(2)O) in open and closed chest conditions. RESULTS: With the chest closed mean arterial pressure, cardiac output, stroke volume, global end-diastolic volume, and right ventricular end-diastolic volume were significantly lower when compared to open chest conditions. Concomitantly, right ventricular, but not left ventricular stroke volume variation increased significantly. Applying PEEP led to a significant reduction of cardiac output, stroke volume and right ventricular end-diastolic volume, with a concomitant increase in left and right ventricular stroke volume variation both during open and closed chest conditions (all P-values<0.05). CONCLUSIONS: We conclude that PEEP increases right and left ventricular stroke volume variation both during open and closed chest conditions. The concomitant reduction of right ventricular end-diastolic volume further indicates that PEEP has a preload reductive effect during open chest conditions, too.