Cardiopulmonary Research Laboratory, Department of Critical Care Medicine, University of Pittsburgh Medical Center, 606 Scaife Hall, 3550 Terrace Street, Pittsburgh, PA 15261, USA.
Intensive Care Med. 2011 Oct;37(10):1672-9. doi: 10.1007/s00134-011-2304-3. Epub 2011 Jul 8.
We evaluated the impact of increasing tidal volume (V (t)), decreased chest wall compliance, and left ventricular (LV) contractility during intermittent positive-pressure ventilation (IPPV) on the relation between pulse pressure (PP) and LV stroke volume (SV(LV)) variation (PPV and SVV, respectively), and intrathoracic blood volume (ITBV) changes.
Sixteen pentobarbital-anesthetized thoracotomized mongrel dogs were studied both before and after propranolol-induced acute ventricular failure (AVF) (n = 4), with and without chest and abdominal pneumatic binders to decrease chest wall compliance (n = 6), and during V (t) of 5, 10, 15, and 25 ml/kg (n = 6). SV(LV) and right ventricular stroke volume (SV(RV)) were derived from electromagnetic flow probes around aortic and pulmonary artery roots. Arterial pressure was measured in the aorta using a fluid-filled catheter. Arterial PPV and SVV were calculated over three breaths as (max - min)/[(max + min)/2]. ITBV changes during ventilation were inferred from the beat-to-beat volume differences between SV(RV) and SV(LV).
Arterial PP and SV(LV) were tightly correlated during IPPV under all conditions (r (2) = 0.85). Both PPV and SVV increased progressively as V (t) increased and with thoraco-abdominal binding, and tended to decrease during AVF. SV(RV) phasically decreased during inspiration, whereas SV(LV) phasically decreased 2-3 beats later, such that ITBV decreased during inspiration and returned to apneic values during expiration. ITBV decrements increased with increasing V (t) or with thoraco-abdominal binding, and decreased during AVF owing to variations in SV(RV), such that both PPV and SVV tightly correlated with inspiration-associated changes in SV(RV) and ITBV.
Arterial PP and SV(LV) are tightly correlated during IPPV and their relation is not altered by selective changes in LV contractility, intrathoracic pressure, or V (t). However, contractility, intrathoracic pressure, and V (t) directly alter the magnitude of PPV and SVV primarily by altering the inspiration-associated decreases in SV(RV) and ITBV.
我们评估了在间歇正压通气（IPPV）期间增加潮气量（V（t））、降低胸壁顺应性和左心室（LV）收缩力对脉搏压（PP）和左心室射血分数（SV（LV））变化之间关系的影响（分别为 PPV 和 SVV），以及胸腔内血容量（ITBV）的变化。
16 只戊巴比妥钠麻醉开胸杂种犬在普罗帕酮诱导急性心室衰竭（AVF）前后（n=4）、使用和不使用胸部和腹部气动约束器降低胸壁顺应性（n=6）以及在 V（t）为 5、10、15 和 25 ml/kg 时（n=6）进行研究。SV（LV）和右心室射血分数（SV（RV））通过电磁流量探头在主动脉和肺动脉根部得出。动脉压通过充满液体的导管在主动脉中测量。在三次呼吸中计算动脉 PPV 和 SVV，公式为（最大值-最小值）/[（最大值+最小值）/2]。在通气过程中，通过 SV（RV）和 SV（LV）之间的每搏体积差异推断 ITBV 的变化。
在所有条件下，在 IPPV 期间，动脉 PP 和 SV（LV）之间存在紧密的相关性（r（2）=0.85）。随着 V（t）的增加和胸廓腹部的束缚，PPV 和 SVV 逐渐增加，并在 AVF 期间趋于下降。SV（RV）在吸气时瞬间下降，而 SV（LV）在 2-3 个心跳后瞬间下降，因此 ITBV 在吸气时下降，并在呼气时恢复到无呼吸值。随着 V（t）或胸廓腹部束缚的增加，ITBV 减少，而由于 SV（RV）的变化，AVF 期间的 ITBV 减少，使得 PPV 和 SVV 与 SV（RV）和 ITBV 相关的吸气变化密切相关。
在 IPPV 期间，动脉 PP 和 SV（LV）之间存在紧密的相关性，LV 收缩力、胸腔内压力或 V（t）的选择性变化不会改变它们之间的关系。然而，收缩力、胸腔内压力和 V（t）直接通过改变与吸气相关的 SV（RV）和 ITBV 的下降来改变 PPV 和 SVV 的幅度。
