Cano A E, Meaney E
Arch Inst Cardiol Mex. 1975 May-Jun;45(3):344-56.
The heart and the lung make up an inseparable anatomic and functional unit. The changes in one affect the other and vice versa. In acute myocardial infarction a heart failure syndrome develops. This syndrome is characterized by passive pulmonary congestion, which leads to hypoxemia. This hypoxemia indicate the functional disturbance of the lung, and the hemodinamic evolution of the disease. Arterial gases determination is the best way to assess the sickness progression. A certain paralelism exists among the central venous saturation, cardiac insufficiency and the degree of pulmonary disfunction. Such a procedure is not very appreciable and does not substitute the direct analysis of the arterial PO2. The pulmonary complications in the myocardial infarction shock are directly responsable of death in 50% of the patients. To heart failure and shock, hipperfusion and hypoxia are added. Many vessels close due to the decrease in the pulmonary flow. This brings about the release of substances that are toxic to the vessel causing an inflammatory vascular reaction. The decrease in the flow harms the lung cell and for this reason atelectasia or alveolar colapse occur; besides inducing the formation of shunts. Under these conditions the lung compliance decreases. The areas that are badly ventilated and hypoperfused can easily become infected and pneumonitis and abscesses cause even more harm to the tissue. The decrease in the speed of circulation and hematologic changes of shock, induce a diseminated intravascular coagulation. What was stated before leads to an important reduction of the lung as a depurating organ and makes the shock irreversible. As far as therapy is concerned in the prevention of vascular colaps and the improvement of the oxemia, oxygen is very useful when there is a venous congestion (clinically, X rays, and oxemia). When the concentration of O2 is lower than 50% in the cases with slight cardiac failure; do not use oxygen in higher concentrations unless the hypoxia is associated to acute pulmonary edema and shock. Mechanic ventilators, and intermitent possitive pressure are recommended even though they have a posenous effect on the cardiac output. Always keep the air ways permeable: changing position, breathing exercises, humidifications, aspiration of secretions, intubation, or traqueostomy depending upon the various cases.
心脏和肺构成一个不可分割的解剖和功能单元。一方的变化会影响另一方，反之亦然。在急性心肌梗死时会出现心力衰竭综合征。该综合征的特征是肺被动充血，进而导致低氧血症。这种低氧血症表明肺的功能紊乱以及疾病的血液动力学演变。测定动脉血气是评估疾病进展的最佳方法。中心静脉饱和度、心脏功能不全和肺功能障碍程度之间存在一定的平行关系。但这样的操作不太可行，也不能替代对动脉血氧分压的直接分析。心肌梗死休克中的肺部并发症直接导致50%的患者死亡。除了心力衰竭和休克外，还会出现高灌注和缺氧。由于肺血流量减少，许多血管关闭。这会导致释放对血管有毒的物质，引发炎症性血管反应。血流量减少损害肺细胞，因此会发生肺不张或肺泡塌陷；此外还会诱导分流的形成。在这些情况下，肺顺应性降低。通气不良和灌注不足的区域很容易感染，肺炎和肺脓肿会对组织造成更大的损害。休克时循环速度减慢和血液学变化会引发弥散性血管内凝血。上述情况会导致肺作为净化器官的功能大幅下降，使休克不可逆。就治疗而言，在预防血管塌陷和改善氧血症方面，当出现静脉充血（临床、X线和氧血症表现）时，氧气非常有用。在轻度心力衰竭患者中，当氧浓度低于50%时；除非缺氧与急性肺水肿和休克相关，否则不要使用更高浓度的氧气。尽管机械通气和间歇正压通气对心输出量有不良影响，但仍建议使用。始终保持气道通畅：根据不同情况改变体位、进行呼吸锻炼、湿化、吸痰、插管或气管切开。
