Low cardiac output syndrome
Low cardiac output syndrome (LCOS) was first introduced by Dietgman in 1969, which refers to severe hemodynamic abnormalities such as hypotension and even shock due to a significant decrease in cardiac output after cardiac surgery, and is one of the main causes of death in postoperative patients.
Etiology and mechanism of occurrence
Cardiac output is related to ventricular end-diastolic transmural pressure (ventricular end-diastolic transmural pressure), myocardial diastolic (distensibility), myocardial contractility (contractility) and ventricular wall stress during ventricular systole with some of the following factors, etc.
1, myocardial contractility: the heart circulation is blocked during surgery, and myocardial contractility is caused by ischemia, hypoxia and reperfusion injury. The degree of damage is closely related to the duration of block, the use of measures to protect the myocardium and prevent reperfusion injury. Factors such as excessive cardiac incision, excessive myocardial resection and huge atrial and ventricular septal defects or flow ratio tract widening patch can affect myocardial contractility and compliance.
2, blood volume deficiency and acidosis: acidosis with low myocardial contractility, postoperative blood volume balance without close attention, no timely blood replenishment according to central venous pressure or left atrial pressure.
3, arrhythmia: third degree conduction block due to hypoxic or surgical trauma is a common cause of LCOS, and all kinds of tachycardia or bradycardia can affect atrial diastolic insufficiency.
4, heart compression: heart compression, tightly bound heart after pericardial suture affects ventricular filling is a common cause of LCOS.
5, inadequate coronary artery supply, myocardial infarction and myocardial infarction due to coronary artery air embolism are occasionally seen.
6.Other: unsatisfactory surgical correction of malformation, vasodilator malfunction and pulmonary embolism, etc.
7.About half of them occur for unknown reasons.
In general, mitral valve surgery and Fallow tetralogy LCOS occur more often than after aortic valve surgery, and occur earlier and have a higher mortality rate. The reasons may be related to abnormal function of the left ventricle itself after mitral valve lesion, hypovolemic tricuspid regurgitation, papillary muscle resection and caged ball valve inertia is larger.
Clinical manifestations
The cardiac index is slightly lower than normal and is often clinically unrecognizable, with symptoms beginning if it falls below 2.0-2.5 L/(min/m2).
The disease is characterized by postoperative shock, cold extremities, cyanosis, oliguria (less than 30 ml/hour), low blood pressure (may be normal), low heart sounds, possible arrhythmias, jugular venous anger, wet rales at the base of the lungs, ST-T changes in the electrocardiogram, prolonged Q-T interval, and decreased blood carbon dioxide binding capacity. Although central venous pressure is relatively high and left atrial and left ventricular diastolic pressures are moderately increased, there are often no obvious signs of pulmonary edema.
Diagnosis
LCOS can be diagnosed when the CI is less than 2.0-2.5 L/min/m2 with inadequate tissue perfusion, excluding recurrent heart failure, myocardial infarction, pericardial hemorrhage, infectious toxic shock, cardiogenic shock, hypovolemic shock, etc. In the absence of CI monitoring, the presence of elevated central venous pressure (CVP), decreased arterial pressure, poor peripheral circulation and hyponatremia can also be diagnosed. The diagnosis of LCOS can also be made in the presence of elevated central venous pressure (CVP), decreased arterial pressure, poor peripheral circulation, and decreased urine.
The following diagnostic criteria can be used for reference.
1. Systolic blood pressure decreases by more than 20% of the operative basal blood pressure for 2 hours or more;
2, urine output of 0.5 ml/kg per hour for 2 hours or more;
3, central venous pressure >13mmHg for 2 hours or more;
4.The difference between central body temperature and surface temperature >5℃ for 2 hours or more, resulting in chills in the extremities;
5.CI <2.5 L/min/m2 (infants and children <2.0 L/min/m2). LCOS is diagnosed when two or more of the above events occur.
Prevention and treatment The disease focuses on prevention, and once it occurs, the main focus is on the treatment of the cause and intensive symptomatic treatment.
1.Adequate sedation.
2.Postoperative blood volume should be replenished and central venous pressure should be raised to 12-15 mmHg. correct acidosis, maintain water and electrolyte balance.
3.Ventilation therapy for hypoxemia: under normal conditions of cardiac return, ventilation with large tidal volume (12-15 ml/kg), high oxygen concentration (>45%), low frequency (12-14 times/min) and long inspiration (1.5-2.0 s) is possible. Perform positive end-expiratory pressure ventilation (PEEP) in cases of intractable hypoxemia (moderate to severe pulmonary hypertension, respiratory failure, adult respiratory distress syndrome, etc.).
4.Increase cardiac output: Find the cause of heart failure and give active treatment. Use intravenous/arterial dilators or vasoconstrictors after peripheral resistance assessment. β-agonists or phosphodiesterase inhibitors are better choices in enhancing myocardial contractility.
5.Treat ischemia or coronary spasm. For cardiac compression, strive for open-heart hemostasis within 6 h after surgery, and for thoracic and abdominal effusion, prompt puncture or drainage.
6.Control cardiac arrhythmia.
7.Protect gastrointestinal function, gastrointestinal decompression, gastric mucosal protective agent and acid suppressant can be given.