Ali Dabbagh, Fardad Esmailian and Sary F. Aranki (eds.)Postoperative Critical Care for Cardiac Surgical Patients201410.1007/978-3-642-40418-4_7
© Springer-Verlag Berlin Heidelberg 2014
7. Cardiovascular Complications and Management After Cardiac Surgery
(1)
Cardiovascular Research Center, Shahid Beheshti University of Medical Sciences, Tehran, Iran
(2)
Perioperative Transesophageal Echocardiography Education, Division of Cardiothoracic Anesthesiology, Department of Anesthesiology, Cedars-Sinai Medical Center, Los Angeles, CA, USA
Mahnoosh Foroughi (Corresponding author)
Email: mahnoosh.foroughi@gmail.com
Email: m_foroughi@sbmu.ac.ir
Abstract
The essential principle in post-cardiac surgical care is ensuring optimal hemodynamic preservation and tissue perfusion through the utilization of continuous hemodynamic monitoring, adequate volume repletion, and, if necessary, use of inotropic agents and/or pressors. Cardiopulmonary resuscitation (CPR) for cardiac arrest after cardiac surgery is different from cardiac arrest in other settings as its causes are usually reversible with associated improved outcomes.
Due to aging of the cardiac surgical population and broader application of interventional cardiologic interventions before admission for cardiac surgery, the profile of patients has changed. Cardiac surgical patients in the twenty-first century are older and sicker, possess diminished physiologic reserve, manifest decreased ventricular function, are referred for more complex procedures, and are at high risk for postoperative major cardiac complications in comparison with other patient populations. The main insult sustained by the patient is related to inadequate myocardial contraction that results in a low cardiac output syndrome. Inability to wean from cardiopulmonary bypass created more emphasis in evaluating means of more prolonged supportive measures. Innovative techniques for circulatory support devices have developed, and different types are now available. Initially intra-aortic balloon pumps (IABP) and centrifugal pumps were developed, whereas now rapidly evolving technical changes have led to new and improved pneumatic and electrically driven internal assist devices. These devices are being increasingly inserted in an effort to provide supportive assistance to one or both ventricles with increased safety and durability.
7.1 Cardiac Monitoring
Upon arrival to the ICU, the post-cardiac surgical patient requires intense adequate hemodynamic monitoring; this is accomplished via continuous ECG, arterial blood pressure measurement via arterial catheter, frequent arterial blood gas sampling, central venous pressure (CVP) measurement via central venous catheter, pulse oximetry, and evaluation of chest tube drainage. The use of a pulmonary artery catheter is validated in pulmonary hypertension, severe low cardiac output, and partition of right and left ventricular failure; however, its use is associated with multiple risks and higher morbidity and mortality when inappropriately utilized.
The main aim in post-cardiac surgical care is to maintain optimal hemodynamics with resultant normal tissue perfusion achieved by sufficient intravascular volume and cardiac output. Although, during CPB there is increased weight gain due to water retention, it is distributed to the extravascular component. However, the hypovolemic condition postoperatively is common. CVP is considered an approximate indicator of preload status. It is recommended to keep CVP >10 mmHg by volume repletion; by the same respect, a CVP >20 mmHg may warrant diuresis. Before volume administration, hemodynamic response to increasing preload can be assessed by passive leg rising.
After cardiac surgery reduced myocardial function may be due to inadequate valve repair or insufficient revascularization, ischemic reperfusion injury, myocardial edema, reduced preload, and increased afterload. The adequacy of cardiac performance during the postoperative period in the ICU is assessed by cardiac index, arterial blood pressure, pedal pulses, skin temperature, mixed venous oxygen saturation level, urinary volume, and metabolic acidosis. Possible indicators of insufficient cardiac performance are:
Mean arterial pressure < 60 mmHg
Serum lactate > 2 mmol/L
Urinary output < 0.5 mL/h
Svo 2 < 60 % with Sao 2 > 95 %
Central-mixed venous oxygen saturation (SVO2) is a very accurate indicator of tissue perfusion, as it demonstrates the relationship between oxygen supply (determined by cardiac output) and demand (metabolic state).
Some causes of low cardiac output after cardiac surgery are evaluated by electrocardiogram, chest X-ray, hemodynamic data, and echocardiography. ECG changes may be suggestive of myocardial ischemia or infarction, significant chest tube drainage, and blood collection, or signs of tamponade may be noted through chest X-ray, and echocardiography can delineate new ventricular wall motion abnormalities, decreased ejection fraction (EF), and new or residual valvular pathology (Wasir et al. 2003; Joshi et al. 2005; Overgaard and Džavík 2008).
7.1.1 Cardiovascular Effects of Common Inotropic Agents
The primary treatment for low cardiac output states has been pharmacologic interventions. Catecholamines exert their cardiovascular effects through α-, β1−, β2−, and dopaminergic receptors. α-receptor activation causes arterial vascular smooth muscle contraction and rising in systemic vascular resistance (SVR). β1-receptor stimulation in myocardium causes increased contractility and conduction velocity. β2-receptor activation causes vascular smooth muscle relaxation and reduction in SVR. Dopaminergic receptor in kidney and splanchnic circulation causes vasodilation. Epinephrine in low dose acts in β1-receptors and in high dose acts in α-receptors. Norepinephrine is a potent α-receptor agonist, enhancing SVR via vasoconstriction. Phenylephrine as α-receptor agonist is used in bolus setting to correct hypotension.
Pharmacologic support in patients with low cardiac output may be obligatory in the postoperative period. However, before starting inotropes, improvement of preload status and SVR reduction must be considered because cardiac output is a function of myocardial contractility and hemodynamic conditions (afterload and preload).
7.2 Cardiac Complications
7.2.1 Postoperative Myocardial Ischemia
While a large majority of cardiothoracic surgery is performed in order to optimize vascular supply to the heart via coronary artery bypass grafting, postoperative myocardial ischemia (PMI) and associated myocardial infarct (MI) continue to remain a significant complication in the postoperative setting. The Society of Thoracic Surgeons (STS) maintains a clinical database for every cardiothoracic surgical procedure performed; the STS has defined perioperative ischemia as the occurrence of at least one of the following markers: (1) electrocardiographic changes consistent with ischemia, (2) elevation of serum markers (i.e., troponin), and (3) reduced systolic ejection fraction. The incidence of PMI in the STS database is 1 %.
7.2.1.1 Diagnosis
The diagnosis of postoperative myocardial ischemia is based upon detection of the aforementioned markers. The most common laboratory tool for assessment of PMI is measurement of troponin I or cardiac troponin. Patients who manifested elevated preoperative levels of troponin may not necessarily imply PMI in the postoperative period. In addition, patients who underwent coronary artery bypass grafting (CABG) with the use of cardiopulmonary bypass (CPB) were more likely to have elevated levels of troponin compared to patients who were “off-pump”; troponin levels were more apt to remain within normal limits if CPB during CABG is not utilized. Elevation of the MB fraction of creatine kinase may also be measured and may be indicative of PMI. Since the majority of PMI may occur while a postsurgical patient is still intubated, symptoms associated with angina may not be elicited; therefore, electrocardiographic detection with follow-up laboratory assessment is paramount.
The type of cardiac surgery performed may allow the clinician to more accurately assess the etiology for PMI. In cases where coronary artery bypass grafting has been conducted, patients may be prone to closure of newly created vascular coronary conduits, as well as residual myocardial injury secondary to poor myocardial protection. Patients having undergone valve repair or replacement, especially aortic valve replacement, as well as aortic root surgery may be prone to anatomic disturbances in coronary blood flow originating at the coronary ostia. Diagnosis may require invasive cardiac catheterization to rule out reocclusion or new occlusion of coronary ostia or their tributaries.
7.2.1.2 Management
Treatment of coronary myocardial ischemia is targeted at maneuvers to improve or restore coronary perfusion and resultant myocardial perfusion. In the absence of arterial hypotension, the initiation of intravenous venodilators (i.e., nitroglycerin) and arterial vasodilators (sodium nitroprusside) may yield significant improvement. In addition, the administration of calcium channel blockers (nifedipine, nicardipine) may ameliorate vasospasm in cardiac arterial blood vessels. The need to augment oxygen-carrying capacity may also require the administration of red blood cell transfusion. Patients not responding to restoration of arterial diastolic pressure concomitant with use of preferential vasodilators may necessitate further evaluation with cardiac catheterization or invasive assessment with a pulmonary artery catheter. Efforts should be made to initiate the appropriate treatment intervention as soon as possible.
7.2.2 Hemodynamic Instability
Patients undergoing cardiac surgery undergo significant alterations in temperature, circulating blood volume, initiation of cardiopulmonary bypass, myocardial protection with plegic solutions, and total circulatory arrest that render this patient population extremely susceptible to residual hemodynamic lability upon arrival in the intensive care unit.
7.2.2.1 Low Cardiac Output
Afterload, preload, and myocardial contractility are the main determinants of heart performance. Cardiac contraction cannot be considered independent from the vascular system, and manipulation of both afterload and preload is necessary for optimal cardiac function. Review of the Starling Curve is important in understanding this relationship. Low cardiac output is the most critical complication after cardiac surgery. It is defined as the need for inotropic infusion support (for longer than 30 min), IAPB, or both to achieve cardiac output >2.2 L/m2/min and preserve systolic blood pressure >90 mmHg despite afterload reduction, optimization of preload, and correction of electrolytes and blood gases. Low cardiac output plays an important role in morbidity and mortality after cardiac surgery.
Some causes of low cardiac output syndrome include incomplete myocardial revascularization, insufficient myocardial protection during aortic cross clamp, reperfusion injury, and systemic inflammatory response. During aortic cross clamp, myocardial perfusion is interrupted; a bloodless field is provided at the expense of potential myocardial ischemia. A cardioplegic solution is used to arrest the heart and decrease the ischemic damage of myocardium during these intervals. Although there is no consensus about type, time, temperature, route, and volume of cardioplegic solution, many studies had shown that inadequate myocardial preservation during surgery leads to postoperative low cardiac output. Therefore, improved ways of cardiac protection can minimize myocardial injury.
Studies have shown that there are multiple independent predictors of low cardiac output after aortic valve and mitral valve replacement. These include:
The most important predictor of low cardiac output after CABG is preoperative left ventricular dysfunction (EF < 20 %). Management of low cardiac output due to left heart failure consists of increasing contractility, afterload reduction, and preload limitation. For right heart failure, in addition to inotropic agents, adequate preload status and reduction in pulmonary vascular resistance are recommended. In low cardiac output states that do not respond to inotropic support and IABP, the use of a ventricular assist device as a bridge to recovery or transplantation may be advised.
Preoperative renal disease
Increasing age
Female sex
Redo surgery and small aortic valve
Urgency of the operation and CPB time
7.2.2.2 Diagnosis
The critical care team should accurately and efficiently review the patient’s preoperative hemodynamic and intraoperative hemodynamic history as well as noting significant events which may have deviated from the usual and customary management of a cardiothoracic surgical patient.
Diagnosis should include assessment of systolic and diastolic blood pressure trends as well as calculation of perfusion pressure, total peripheral resistance, and possible cardiac output or cardiac index. Changes in the patient’s cardiac rhythm and rate should also be conducted to determine if deviations from the intraoperative status have occurred. Loss of circulating blood volume should also be determined by assessing chest tube drainage or reductions in urinary output.
7.2.2.3 Management
The implementation of pressors, vasodilators, or inotropic agents may be necessary based upon the specific hemodynamic disturbance. However, definitive therapy should be aimed at determining the underlying etiology for the respective change (i.e., hypovolemia causing hypotension). Persistent hypotension despite pressor therapy may warrant further support such as administration of colloids or blood products. Hypertension may denote inadequate pain relief or lack of adequate sedation; therefore, opioids or sedatives may be warranted. Transesophageal echocardiography may be of assistance in delineating cardiac-specific pathology contributing to hemodynamic compromise.
Implementation of inotropic support should be based upon more specific findings delineated by use of a pulmonary artery catheter or echocardiogram. Low cardiac output states secondary to diminution of stroke volume can be augmented by the use of fluids or pharmacologic therapy (i.e., epinephrine, norepinephrine, dobutamine, dopamine, or milrinone). The insertion of an intra-aortic balloon pump should be reserved only for instances of refractory hemodynamic compromise unresponsive to pharmacologic support (Mair and Hammerer-Lercher 2005; Noora et al. 2005; Maganti et ak. 2010; Algarni et al. 2011 Hausenloy et al. 2012; Likosky et al. 2012).
7.2.3 Arrhythmias
Numerous rhythm disturbances may manifest themselves in patients’ status post-cardiac surgery. Electrophysiologic cardiac abnormalities may be secondary to manual manipulation of the heart, arrest with plegic solutions, anatomic/mechanical disruption of electrical pathways, and/or impaired cardiac perfusion resulting in ischemia. A more detailed discussion about arrhythmias could be found in this book in the related chapter.
7.2.3.1 Diagnosis
The diagnosis of rhythm disturbances is most accurately assessed with a minimal of two-lead electrocardiographic monitoring; however, more occult arrhythmias may necessitate 12-lead electrocardiographic evaluation. Arrhythmias may include but are not limited to bradyarrhythmias, tachyarrhythmias, malignant tachyarrhythmias, and multiple degrees of heart block.
The most common arrhythmia occurring in both the acute and later phases of postoperative recovery is the appearance of atrial fibrillation. A recent study of the STS database revealed an annual incidence of 20 % with the mean occurrence on postoperative day three, but the range was from 0 to 21 days after surgery. Predictors of atrial fibrillation during hospitalization include age greater than 65, history of intermittent atrial fibrillation, atrial pacing, and chronic obstructive pulmonary disease. Predictors after discharge were atrial fibrillation during hospitalization, valve surgery, and pulmonary hypertension. Patients with atrial fibrillation had almost twice the hospital mortality of patients without atrial fibrillation.
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