【经验】右心衰竭的临床处理方法

匹兹堡大学医学院Marc A. Simon教授

右心衰竭是许多疾病发生时出现的一组病情复杂、难以处理的综合征。当急性发作时，我的处理方法需要首先评估3个问题：①患者的血容量如何？②患者右心的收缩功能如何？③导致患者出现右心衰竭的潜在病因是什么？

血容量

血容量的正确管理对右心衰竭患者很关键。右心超负荷，收缩功能下降，并通过房室间隔的转换（心室间相互作用），使左心（LV）充盈度及功能下降。静脉压力增大与肾功能下降相关。应考虑逐步采用利尿剂：

1 初始间歇使用IV呋塞米（≥门诊剂量）。

2 呋塞米逐渐增量至80 mg，3次/天；剂量可以高于80 mg，但应逐步增加剂量，或对危重患者，应考虑持续静脉滴注。

3 使用布美他尼的患者，静脉滴注应采用与呋塞米相同的剂量，因为尽管布美他尼口服生物利用度高，但容量超负荷的右心衰竭患者可能有肠壁水肿，从而影响有效吸收。也可以使用等剂量的呋塞米进行间歇或持续性静脉滴注。

4 当持续静脉滴注布美他尼时，也可添加噻嗪类利尿剂。

5 一项很好的经验是留意患者的医疗记录。避免重复使用过去无效的利尿剂，应采用过去有效的药物作为用药指导。

6 多次给予利尿剂可改善肾功能。不过，对于尿量低和/或进行性肾功能衰竭患者，如果心输出量低（参见下文）和/或采用血液透析/超滤机械去除水分（若患者病情危重和/或全身血压过低，可能需要持续而非间歇去除水分），应考虑加用一种血管活性药物。

7 检查患者钠和液体的摄入。

右心收缩功能

初步的患者评估应包括以审慎的态度评估心输出量是否充分。尽管答案“是”或“否”很简单，但症状与体征却很复杂。在病史方面，心输出量低的警戒症状包括食欲差、体重下降（可能会被体液增加而掩盖），以及乏力。在体格检查方面，警戒症状包括四肢冰凉、发绀、尿量减少，以及肝淤血与肝功能衰竭（特别是巩膜黄染、黄疸明显；肝肿大/搏动可能仅反映了血容量增加）。多数RV衰竭患者会有一定程度的长期低血压，但长期血压低于正常可能提示心输出量低。

如果症状和体征提示心输出量低，则应立即使用血管活性药物。我喜欢使用米力农，因为它还是肺动脉扩张剂，有助于降低RV后负荷。要警惕血管扩张和室性心律失常，采用或改用多巴酚丁胺。根据所在医疗机构，血管活性药物的使用也许需要将患者移至ICU。

如果有明显的低血压，则需要开始使用血管加压药物。这一步的关键在于判断何时为血压太低；首推的评估方法是收缩压低于患者平常的20%。我更喜欢采用多巴胺，但是选择加压素也不错，也可采用去甲肾上腺素（该药也有一些正性肌力作用）或去氧肾上腺素。患者应在ICU接受治疗。

右心衰竭的病因

导致右心衰竭的潜在原因有很多，这一点可以用于个体化评估与治疗。应考虑收缩期左心衰竭/心肌疾病（心衰治疗如上所述；视情况考虑心脏移植评估）、冠状动脉疾病（右心梗死；应考虑冠状动脉造影和干预）、先天性心脏病（对于右心扩大但肺动脉压力正常的患者，应考虑房间隔缺损，各种年龄段都可出现）、肺动脉高压（包括肺栓塞）、肺原发病变、肝功能衰竭和原发性肌肉疾病。

具体到因肺动脉高压所致的右心衰竭患者，有几项特殊的治疗措施可供选择。采用机械通气的ICU患者可以吸入一氧化氮，但费用可能过高；因此，急性期就开始可以考虑使用前列环素。

前列环素（依前列醇）（或者通过IV，或者通过呼吸机吸入）可迅速增量，但需要注意的是，这些患者预后极差，应该向患者和（或）家属交代这些事情。开始采用肺血管扩张剂时应该警惕两方面问题。第一，缺乏有创性血流动力学记录到的肺动脉高压（平均肺动脉压＞25 mmHg，左侧充盈压≤15 mmHg）时，不应该使用肺血管扩张剂。第二，危重患者除了在ICU继续治疗，出院后持续药物治疗的保险审批需要几周时间，直到能够明确患者出院后仍可继续治疗，才该开始治疗。

何时进行有创性血流动力学检查

如果进行有创性血流动力学检查，需要问自己两个问题：这一检查手段如何改变或指导治疗？导管应立即移除还是继续保留一段时间（在ICU中）以进一步指导治疗？在以下情况下应采用有创性血流动力学检查：①对危重患者充盈压和心输出量的了解能影响治疗时；②对症状/体征和（或）治疗反应有临床困惑时；③一旦达到等容进行评估时。例如，肺动脉高压患者，考虑开始或改变治疗措施，或对于心衰患者，确认其的确达到等容及心输出量充足。

Right ventricular (RV) failure is a complex and difficult-to-treat syndrome occurring in the setting of many diseases. In the acute setting, my approach involves three fundamental questions:

1. What is the patient’s volume status?
2. What is the patient’s RV contractility?
3. What is the patient’s underlying etiology for RV failure?

Volume status

Appropriate management of volume status is crucial for the patient with RV failure. The volume-overloaded RV has reduced contractility and may also reduce LV filling and function via septal shifting (ventricular interaction). High venous pressure is associated with decreased renal function. Consider a stepwise approach to diuretics:

• Start with intermittent IV furosemide (same or greater than the outpatient dose).
• Up-titrate furosemide to 80 mg three times daily; one can go higher, but, generally beyond this dose or in the critically ill patient, continuous IV drip should be considered.
• In the patient on bumetanide, use the same dose IV (although oral bioavailability is high, the volume-overloaded RV failure patient is likely to have bowel wall edema preventing effective absorption). The equivalent IV dose of furosemide intermittently or a continuous IV drip can also be used.
• Adding a thiazide diuretic is another option, as is continuous IV bumetanide.
• A good rule of thumb is to keep in mind the patient’s medical records. Avoid repeating past diuretic failures, and use what has worked in the past as an effective guide.
• Renal function will improve with diuresis at a surprising frequency. However, in the patient with poor urine output and/or progressive renal failure consider adding an inotrope if low cardiac output is suspected (see below) and/or mechanical removal of fluid with hemodialysis/ultrafiltration (which may need to be continuous instead of intermittent if the patient is critically ill and/or systemic blood pressure is too low).
• Review sodium and fluid restrictions with patients.

RV contractile state

 Initial assessment of the patient should include a critical eye toward sufficient cardiac output. While a simple yes or no question, the signs and symptoms can be subtle. On history, warning signs of low output include poor appetite, weight loss (may be masked by fluid weight gain), and fatigue. In the physical exam, warning signs include cool extremities and cyanosis, poor urine output, and signs of hepatic congestion and failure (scleral icterus, overt jaundice, in particular; enlarged/pulsatile liver may just reflect volume overload). Most patients with RV failure will have somewhat low systemic blood pressure chronically but a pressure lower than their usual may indicate low cardiac output.

If signs and symptoms suggest low cardiac output, then prompt institution of inotropes are indicated. I prefer to use milrinone because it is also a pulmonary vasodilator, which will decrease RV afterload. Be alert for vasodilation and ventricular arrhythmias. In the case of vasodilation, use or switch to dobutamine. Depending on your institution, inotropes may require the patient to be moved to the ICU.

If there is significant hypotension, then start a vasopressor as needed. The key to this is to determine when blood pressure is too low; a good rule of thumb is systolic blood pressure 20% below the patient’s usual. I prefer dopamine, but vasopressin can be a good option, as can norepinephrine (which may also have some positive inotropic effect) or phenylephrine. These patients should be in an ICU.

Etiology of RV failure

There are many potential underlying causes of RV failure that lead to individualized evaluation and treatment. Think about systolic LV heart failure/cardiomyopathies (heart failure treatment as above; consider heart transplant evaluation depending on circumstances), coronary artery disease (RV infarction; consider coronary angiography and intervention), congenital heart disease (consider atrial septal defects in those with an enlarged RV but normal pulmonary pressures, which can present at any age), pulmonary hypertension (including pulmonary embolus), intrinsic lung disease, hepatic failure, and primary myopathies.

With specific regard to the patient with RV failure from pulmonary hypertension, there are several unique therapeutic options. Inhaled nitric oxide can be used in the mechanically ventilated ICU patient, but the cost can be prohibitive; so, acute start of a prostacyclin should be considered. Epoprostenol (administered either IV or inhaled through a ventilator) can be rapidly up-titrated, but note that these patients have a very poor prognosis, which should be communicated with the patient and/or family. Caution should be advised in starting pulmonary vasodilators in two regards. First, pulmonary vasodilators should never be started without invasive hemodynamics documenting pulmonary arterial hypertension (mean pulmonary arterial pressure >25 mmHg, with a left-sided filling pressure ≤15 mmHg). Second, outside of the critically ill patient in the ICU, insurance approval for continuing the medications on discharge can require several weeks, and therapy should not be started until it can be confirmed that it will continue when the patient is discharged.

When to check invasive hemodynamics

If checking invasive hemodynamics, ask yourself two questions: how will this change or guide therapy, and will the line be removed immediately or kept in for a period of time (in the ICU) to further guide therapy? Invasive hemodynamics should be checked in the following circumstances:

1. Critically ill patients in whom knowledge of the filling pressures and cardiac output can influence your therapy
2. Clinical confusion between signs/symptoms and/or response to therapy
3. Assessment once euvolemia is reached (ie, pulmonary hypertension if considering starting or changing treatment or confirming true euvolemia and adequate cardiac output in the heart failure patient)

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