Hemodynamic Deterioration Following Local Compression of the Heart: an Animal Experiment Mimicking Local Compression of the Heart Resulting from Postoperative Bleeding and an Associated Blood Clot

日常所見的心包膜填塞（cardiac tampo-nade）由於液體蓄積於心包膜內壓迫心臟，多有低心輸出量，脈博壓狹窄，心跳加速，中央靜脈壓及肺鍥壓昇高，常有心臟四腔等壓（pressure equilibration）現象的發生。同時也有奇異脈（paradoxical pulse）之出現。但是在接受心臟手術之病人於手術後發生之心包膜填塞往往不能有明顯之血液力學變化。根據推論，這是由於手術後之殘存血塊（blood clot）呈固體堆積於心包膜內造成與一般滲出液（effusion）呈液體堆積於心包膜內有截然不同之血液力學之表現。現今模擬臨床之血塊堆積，本實驗利用10隻狗在麻醉下給予心臟局部壓迫觀察其血液力學之變化。令人驚訝的是，實驗中可見在心輸出量（low cardiac output）呈劇變之際，整個血液力學指標（hemodynamic indices）卻沒有一個明顯變化。這種隱匿性心包膜填塞（concealed cardiac tamponade）會在不明的過程裏逐漸損毀心臟的輸出功能，引發心臟衰竭。由於少量血塊堆積於心包膜內常見於手術後超音波（echocardiography）檢查，但是這種少量之血塊堆積對心臟功能之影響不易由超音波檢查得到明確之結論，往往拖延之結遂導致不可逆之心肌損傷。由本實驗之結果，我們認為在心臟手術之後，如果經由超音波檢查或Swan-Ganz導管查知有不明原因之低心輸出量（low cardiac output）的發生。再度探查手術（surgical ex-ploration）是明智的。事實上，清除這些血塊提升心輸出量必然會減少不必要之手術罹病率（morbidity）及提昇病人日常之生活功能（functional class）。

關鍵字

心包膜填塞；局部壓迫；低心輸出量

並列摘要

Cardiac tamponade is an important complication after operation under cardiopulmonary by-pass. Occasionally, a residual blood clot in the pericardial space or mediastinum may be local-ized, compressing one side of the heart or one cardiac chamber. The so-called “localized cardiac tamponade” may result in deterioration of the hemodynamic status. In this animal experiment, 10 mongrel dogs were used to pass through a condition which mimicked the status of “localized cardiac tamponade”, to assess the effect of local compression of the heart. The results demon-strated that the value of cardiac output shifted from 2.185 ± 0.317 L/min at the preconditioned state to 0.798 ± 0.0733 L/min at 10 minutes, 0.849 ± 0.0798 L/min at 20 minutes, 0.853 ± 0.0797 L/min at 30 minutes, 0.844 ± 0.0800 L/min at 45 minutes and 0.866 ± 0.771 L/min at 60 minutes (P＜0.001), and returned to 2.150 ± 0.313 L/min immediately with the removal of the compression. However, it was interesting that the other hemodynamic indices, such as central aortic pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, central venous pressure and intrapericardial pressure, remained little changed (P＞0.05). Severe hemodynamic deterioration occurred with the value of cardiac output being 0.753 ± 0.159 L/min, the heart rate being 86.4 ± 13.780 L/min, the highest systolic pressure being 78 ± 7.888 mmHg, the mean pulmonary arterial pressure being 21.7 ± 2.540 mmHg, the central venous pressure being 13.6 ± 2.221 mmHg, the pulmonary capillary wedge pressure being 13.6 ± 1.897 mmHg and intrapericardial pressure being 6.1 ± 1.523 mmHg when heavy compression of the heart was administrated. Severe heart failure was most likely. The experimental results showed that (1) heavy compression of the ventricle may result in acute heart failure, which is easily detected from hemodynamic indices, and (2) mild local compression of the ventricle may induce low cardiac output in spite of the hemodynamic indices remaining little changed. According to the results from this experiment, we strongly suggest that surgical exploration is fully justified whenever inexplicable low cardiac output is detected during the postoperative period after open heart surgery.

並列關鍵字

cardiac tamponade ； local compression ； low cardiac output

國際替代計量

Hemodynamic Deterioration Following Local Compression of the Heart: an Animal Experiment Mimicking Local Compression of the Heart Resulting from Postoperative Bleeding and an Associated Blood Clot

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