Positive end-expiratory pressure-induced hemodynamic changes are reflected in the arterial pressure waveform

Pizov, Reuven; Cohen, M. L.; Weiss, Yoram; Segal, Eran; Cotev, Shamay; Perel, Azriel

doi:10.1097/00003246-199608000-00018

Cited by 70 publications

(47 citation statements)

References 30 publications

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“…These results were in accordance with those of Pizov and colleagues (26) who found that systolic pressure variations in dogs increased mostly when cardiac output decreased with PEEP. In preload-sensitive subjects, it may be assumed that the further increase in pleural pressure with PEEP would have produced a greater decrease in both expiratory LVSV and mean cardiac output.…”

Section: Discussionsupporting

confidence: 93%

“…These findings are consistent with the respiratory pattern of arterial pressure previously described in animal and clinical studies during positive pressure ventilation (9)(10)(11)(12)(19)(20)(21)(22)(23)(24)(25)(26). The respiratory changes in PP have been shown related to the cyclic changes in LVSV that followed after a delay the respiratory changes in RVSV (10).…”

Section: Discussionsupporting

confidence: 90%

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Clinical Use of Respiratory Changes in Arterial Pulse Pressure to Monitor the Hemodynamic Effects of PEEP

Michard

Chemla

Richard

et al. 1999

Am J Respir Crit Care Med

335

189

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In ventilated patients with acute lung injury (ALI) we investigated whether respiratory changes in arterial pulse pressure ( ⌬ PP) could be related to the effects of PEEP and fluid loading (FL) on cardiac index (CI). Measurements were performed before and after application of a PEEP (10 cm H 2 O) in 14 patients. When the PEEP-induced decrease in CI was Ͼ 10% (six patients), measurements were also performed after FL. Maximal (PPmax) and minimal (PPmin) values of pulse pressure were determined over one respiratory cycle and ⌬ PP was calculated: ⌬ PP (%) ϭ 100 ϫ {(PPmax In ventilated patients with acute lung injury (ALI), positive end-expiratory pressure (PEEP) may improve pulmonary gas exchange. However, it may also decrease cardiac output and thus offset the expected benefits in terms of oxygen delivery. The PEEP-induced decrease in cardiac output is assumed to be mainly due to a decrease in systemic venous return secondary to the increased pleural pressure (1-3). Impairment of right ventricular (RV) ejection related to increased transpulmonary pressure (i.e., alveolar minus pleural pressure) could also play a role in some patients (4, 5). The adverse hemodynamic effects of PEEP are not easily predictable in clinical practice, although they have been shown to be more likely to occur in patients with low left ventricular (LV) filling pressure (6-8).Mechanical ventilation induces cyclic changes in LV stroke volume (SV) characterized by a lower LVSV during expiration than during insufflation (9-12). This respiratory pattern is mainly explained by the expiratory decrease in LV filling that followed after a delay (caused by the long pulmonary transit time of blood) the decrease in RVSV occurring during insufflation (10). The inspiratory decrease in RVSV has been shown to result essentially from a decrease in RV filling caused by the effects of increased pleural pressure on systemic venous return (9) and from transient impairment of RV ejection related to increased transpulmonary pressure on pulmonary circulation (13,14).Interestingly, the decrease in mean cardiac output induced by PEEP and the decrease in RVSV induced by mechanical insufflation share the same mechanisms, i.e., the negative effects of increased pleural pressure on RV filling and of increased transpulmonary pressure on RV ejection. Thus, it is reasonable to expect that the magnitude of the expiratory decrease in LVSV would correlate with the PEEP-induced decrease in mean cardiac output.Finally, the negative effects of increased pleural pressure on RV filling should be more pronounced in patients with low cardiac preload (15, 16). Thus, the beneficial effect of fluid loading on cardiac output might be expected to correlate with the magnitude of the inspiratory decrease in RVSV and hence of the expiratory decrease in LVSV before fluid loading.Aortic pulse pressure is directly proportional to LVSV and inversely related to aortic capacitance (17). Respiratory changes in peripheral pulse pressure ( ⌬ PP) during mechanical ventilation have been shown to close...

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 90%

Clinical Use of Respiratory Changes in Arterial Pulse Pressure to Monitor the Hemodynamic Effects of PEEP

Michard

Chemla

Richard

et al. 1999

Am J Respir Crit Care Med

335

189

View full text Add to dashboard Cite

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“…The study included eight domestic pigs (mean [ 22,23 all affect PPV and SVV, these parameters were kept within strict ranges throughout the entire study.…”

Section: Resultsmentioning

confidence: 99%

Impact of epinephrine and norepinephrine on two dynamic indices in a porcine hemorrhagic shock model

Giraud

Siegenthaler

Arroyo

et al. 2014

Journal of Trauma and Acute Care Surgery

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BACKGROUND: Pulse pressure variations (PPVs) and stroke volume variations (SVVs) are dynamic indices for predicting fluid responsiveness in intensive care unit patients. These hemodynamic markers underscore Frank-Starling law by which volume expansion increases cardiac output (CO). The aim of the present study was to evaluate the impact of the administration of catecholamines on PPV, SVV, and inferior vena cava flow (IVCF). METHODS:In this prospective, physiologic, animal study, hemodynamic parameters were measured in deeply sedated and mechanically ventilated pigs. Systemic hemodynamic and pressure-volume loops obtained by inferior vena cava occlusion were recorded. Measurements were collected during two conditions, that is, normovolemia and hypovolemia, generated by blood removal to obtain a mean arterial pressure value lower than 60 mm Hg. At each condition, CO, IVCF, SVV, and PPV were assessed by catheters and flow meters. Data were compared between the conditions normovolemia and hypovolemia before and after intravenous administrations of norepinephrine and epinephrine using a nonparametric Wilcoxon test. RESULTS:Eight pigs were anesthetized, mechanically ventilated, and equipped. Both norepinephrine and epinephrine significantly increased IVCF and decreased PPV and SVV, regardless of volemic conditions ( p G 0.05). However, epinephrine was also able to significantly increase CO regardless of volemic conditions. CONCLUSION: The present study demonstrates that intravenous administrations of norepinephrine and epinephrine increase IVCF, whatever the volemic conditions are. The concomitant decreases in PPV and SVV corroborate the fact that catecholamine administration recruits unstressed blood volume. In this regard, understanding a decrease in PPV and SVV values, after catecholamine administration, as an obvious indication of a restored volemia could be an outright misinterpretation. (J Trauma Acute Care Surg. 2014;77: 564Y569.

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“…These variations during a defined interval have proven to be useful parameters of cardiac preload (12). But the ventilatory issues, such as tidal volume (13), positive end-expiratory pressure (14), and chest and lung compliance (15) may also have effects on SVV. SVV could predict fluid responsiveness in patients undergoing thoracoscopic lobectomy during OLV only when tidal volume is at least 8 mL/ kg (13) and with PEEP (14).…”

Section: Fluid Responsiveness To Fluid Therapymentioning

confidence: 99%

“…But the ventilatory issues, such as tidal volume (13), positive end-expiratory pressure (14), and chest and lung compliance (15) may also have effects on SVV. SVV could predict fluid responsiveness in patients undergoing thoracoscopic lobectomy during OLV only when tidal volume is at least 8 mL/ kg (13) and with PEEP (14). Another study showed that PPV could predict fluid responsiveness in patients who received protective OLV with tidal volume of 6 mL/ kg, FIO 2 of 0.5 and positive end-expiratory pressure (PEEP) of 5 cm H 2 O for lung surgery using thoracotomy, but not in patients who received conventional OLV with tidal volume of 10 mL/ kg, FIO 2 of 1.0 and no PEEP ( 16 ).…”

Section: Fluid Responsiveness To Fluid Therapymentioning

confidence: 99%

Stroke volume variation fail to predict fluid responsiveness in patients undergoing pulmonary lobectomy with one-lung ventilation using thoracotomy

Fu¹,

Zhao²,

Mi³

et al. 2014

BST

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Positive end-expiratory pressure-induced hemodynamic changes are reflected in the arterial pressure waveform

Cited by 70 publications

References 30 publications

Clinical Use of Respiratory Changes in Arterial Pulse Pressure to Monitor the Hemodynamic Effects of PEEP

Clinical Use of Respiratory Changes in Arterial Pulse Pressure to Monitor the Hemodynamic Effects of PEEP

Impact of epinephrine and norepinephrine on two dynamic indices in a porcine hemorrhagic shock model

Stroke volume variation fail to predict fluid responsiveness in patients undergoing pulmonary lobectomy with one-lung ventilation using thoracotomy

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