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Critical Care for the Adult Cardiac Patient
This chapter will familiarize providers with the expected management of patients following adult cardiac surgery using a systematic approach. The common and important side effects or complications of cardiac surgery are described, and their managements are reviewed. The provided references support evidence-based approaches to common postoperative conditions and represent important sources for more detailed analysis of individual topics. The chapter is not meant to be comprehensive but instead focuses on common conditions encountered by those caring for patients in the intensive care unit (ICU) following adult cardiac surgery.
Immediate Postoperative Care
Initial Evaluation
A systematic evaluation of the patient should be performed immediately on arrival in the ICU. The first step is a structured hand-off or debriefing, which occurs jointly between the surgical, anesthesia, and critical care teams and is critical for patient safety. This structured hand-off may be tailored to individual institutions but should provide a review of the relevant patient history, including comorbid conditions and allergies; pertinent details of the procedures performed; intraoperative hemodynamic management; discussion of lines, tubes, devices, and dressings; active/ongoing medications; and any expected deviations from routine postoperative care. Although attention may be focused initially on one aspect of the patient's condition (e.g., hypotension), a systematic approach to initial hand-off and evaluation is essential. Following the structured hand-off or briefing, a more detailed evaluation is undertaken by the critical care provider as follows.
Airway and Ventilation
The trachea should be palpated and confirmed to be in the midline, and breath sounds should be auscultated bilaterally. Adequacy of ventilation and absence of tension pneumothorax should be confirmed. The ventilator should be functioning normally and without alarms—if it is not, the patient should be immediately converted to hand-controlled ventilation. The peak inspiratory pressure should be noted. High inspiratory pressures may indicate a tension pneumothorax, inappropriate ventilator settings, or severe pulmonary or chest wall restriction. Pulse oximetry, mixed venous oximetry, and direct measurement of arterial gas tensions are used to confirm adequate oxygen delivery and CO 2 elimination.
Neurologic Examination
Evaluation of the patient's neurologic status should be performed frequently. Uncontrollable hypertension or extreme variability of peripheral vascular resistance may result from severe neurologic injury initially ascribed to residual anesthetic agent.
Initial Cardiac Auscultation and Electrocardiogram
The cardiac examination should document normal heart sounds and the character of any murmurs. The initial electrocardiogram (ECG) may be difficult to interpret because of lead placement changes related to surgical dressings, cardiac pacing, and the presence of conduction abnormalities. Right bundle branch block and first-degree atrioventricular (AV) block occur frequently but usually resolve within the first few postoperative hours. Maintaining a normal sinus rhythm with an adequate rate is important in the early postoperative period when cardiac output may be transiently impaired because of intraoperative ischemia or because of temporary diastolic dysfunction resulting from myocardial edema. First-degree AV block can result in substantial reduction in the instantaneous end-diastolic left ventricular (LV) volume, which determines stroke volume. The use of atrial or AV sequential pacing can overcome these transient derangements, and, in the latter case, it is common to see improved cardiac function with normalization of the AV interval despite abnormal ventricular activation with the ventricular pacing component.
Atrial fibrillation is poorly tolerated in the first postoperative day, and every effort should be made to maintain sinus rhythm, even in patients with preexisting chronic atrial fibrillation. Immediate cardioversion is often required in the ICU, although atrial fibrillation occurring on the third postoperative day or later is usually well tolerated.
Ventricular arrhythmias may result from early graft failure or coronary spasm, which should be ruled out. A malpositioned pulmonary artery catheter irritating the right ventricular (RV) outflow tract is more easily correctable. Arrhythmias may have many contributing factors (e.g., hypothermia, electrolyte derangement, acid-base imbalances, drug effects), which must be considered and addressed.
Abdominal and Genitourinary Examination
Abdominal examination will reveal the presence of a well-positioned nasogastric or orogastric tube. Exclusion of unexpected masses, organomegaly, pain, or abdominal distention should be documented. Correct placement and securing of the indwelling urinary catheter should be confirmed. Urine should be clear, not concentrated, and free of hemoglobin or frank blood. This is also the time for evaluation of groin or inguinal surgical sites, which are of particular importance when recovering patients following transcatheter and minimally invasive procedures.
Peripheral Perfusion
The adequacy of global and regional perfusion should be assessed by physical examination of the vascular system, including examination of accessible pulse character and the quality of skin and soft tissue perfusion. Intraoperative embolization, vascular injury, or low cardiac output in the setting of peripheral vascular disease may compromise limb perfusion. Special attention should be paid to perfusion distal to any intra-arterial cannulas or lines. This is also the time for evaluation of upper or lower extremity surgical sites as from vessel harvest or vascular cannulation.
Body Temperature
Initial hypothermia is best avoided by expeditious operation and adequate rewarming while the patient is on cardiopulmonary bypass. Hypothermia compromises cardiac function, impairs surgical site healing, causes shivering and increased metabolic demand, interferes with coagulation, and may aggravate or cause rhythm disturbances. Blankets, other auxiliary warming devices, and fluid warmers for intravenous infusions should be used, particularly in the bleeding patient. Fever is poorly tolerated in the early postoperative period and should be treated aggressively with antipyretics and possibly with intravenous steroids if there is associated hemodynamic compromise.
Hemodynamics
With appropriate cardiac rhythm, the patient should have a cardiac index of greater than 2 liter/min/m 2 with blood pressure adequate for systemic perfusion. This requires consideration of the patient's age, preoperative blood pressure, and renal function. The importance of generating adequate cardiac output has been established by several studies with mortality as the outcome variable. Acceptance of lower cardiac output occasionally results in good outcome when associated with reasonable mixed venous oxygen saturation (MV o 2 ) (>55%), adequate urine output (>20 mL/hr without stimulation), and evidence of good peripheral and central perfusion (physical examination, maintenance of acid-base balance). There is no evidence that supranormal cardiac output is beneficial.
Elevated central venous pressure (CVP), especially when associated with facial edema or facial discoloration, must be aggressively evaluated. Possible causes include cardiac tamponade, volume overload, right heart dysfunction, or technical errors that have compromised superior vena caval flow. Elevated pulmonary artery pressures may indicate LV dysfunction or cardiac tamponade, or may be related to preoperative changes in pulmonary vascular resistance. All central pressures should be related to initial values obtained during preoperative studies. Central pressure measurements are also quite sensitive to afterload, which can vary widely and rapidly in the early postoperative course in patients who are often hypovolemic. Elevation of intrathoracic pressure can frequently mimic cardiac failure in the patient with chest wall rigidity because of emergence from anesthetic effect and shivering. The latter process can also increase metabolic demand and reduce MV o 2 to very low levels.
Lines, Tubes, Devices, and Dressings
The type, size, and location at the incisors of the patient's endotracheal tube should be noted. A discussion of the ease of intubation is typically part of the initial debriefing/hand-off with the anesthesia team upon ICU arrival.
All indwelling lines must be confirmed to be functional, particularly those delivering vasoactive drugs. Transport of the patient can partially or completely dislodge intravenous lines. Hemodynamic instability resulting from failure of drug delivery and tissue injury resulting from drug infiltration must be avoided. Mediastinal and pleural space tubes (chest tubes) are placed to underwater seal and are usually set to have −20 cm H 2 O suction applied. Mediastinal tubes should be examined for the quantity and quality of drainage. The initial amount of drained blood should be less than 100 mL, and larger amounts should be explained by the surgical team. The initial rate of drainage may reflect drainage of blood or irrigation fluid that has accumulated, particularly in the left thoracic gutter. Nonetheless, an initial assessment of the bleeding rate, tube patency and clotting in the tubes, and correlation of drainage with intravascular volume replacement are critically important. When multiple chest tubes are present, good practice is the labeling of these tubes (e.g., mediastinal vs. pleural, right vs. left) by the operating room nurse to avoid errors and improve communication throughout the patient's recovery.
Pacemaker, intra-aortic balloon pump, or ventricular assist device settings should be recorded. Sutures and dressings securing these various devices at the skin should be confirmed to be intact.
Surgical site dressings are commonly kept intact during the first 48 hours for infection control. If dressings must be disturbed for diagnostic purposes or if they become saturated during this time, strict aseptic technique should be followed. If negative pressure dressings are used or special antimicrobial dressings for lines or devices, then the planned strategy for maintenance of these should be discussed at the initial hand-off upon ICU arrival.
Chest Radiograph
A portable chest radiograph should be obtained and interpreted immediately on arrival. Critical aspects include (1) position of the endotracheal tube, (2) pneumothorax or mediastinal shift, (3) lobar atelectasis, (4) pleural and extrapleural fluid collections, (5) size of the mediastinal silhouette, (6) correct intravascular location of lines, and (7) satisfactory position of radiopaque markers for any devices, sternal wires, or drainage tubes.
Cardiac Surgery with Cardiopulmonary Bypass
Cardiopulmonary bypass (CPB) induces many of the physiologic changes encountered in the postoperative patient, and its duration is a primary determinant of the rapidity of recovery. CPB nonspecifically activates the inflammatory system, a phenomenon that begins with the interaction of heparinized blood and the bypass circuit. Generalized complement activation is seen, with elevations in C3a and C5a anaphylatoxins after discontinuation of CPB. This activation can lead to pulmonary sequestration of leukocytes and the production of superoxides and other products of lipoxygenation. This causes further leukocyte activation and the generation of leukotactic circulating factors that increase the local inflammatory response, including elevations in tumor necrosis factor-α (TNF-α), interleukin (IL)-1, and prostaglandin E 1 . The generalized inflammatory reaction seen after CPB may change vascular permeability and cause pulmonary hypertension as well as bronchial hyperreactivity. Together with transient elevations in left atrial pressure, reduced oncotic pressure from hemodilution and increased vascular permeability also contribute to increased pulmonary shunt from the resultant extravascular water.
Cellular components that play a significant role in inflammatory response to CPB include circulating cells (platelets, neutrophils, monocytes) and regulatory cells (endothelial cells). Platelets are activated by shear forces, heparin, foreign surfaces, and activated thrombin, a potent platelet agonist. Despite full anticoagulation with heparin, thrombin continues to be generated. The clinical consequences of platelet activation include generation of microemboli, thrombosis, and bleeding from diminution of platelet number and function. Additionally, vasoactive substances may be liberated from platelets in response to CPB or protamine infusion, which can cause pulmonary hypertension and systemic hypotension.
Neutrophil activation occurs consequent to the complex interaction of blood with the CPB circuit. Proinflammatory mediators (e.g., IL-1, -2, -6, and -8, TNFα), complement anaphylatoxins (C3a and C5a), platelet activating factor (PAF), and leukotriene-B4 (LTB4) increase the number of cell surface adhesion molecules and promote neutrophil adhesion to the pulmonary endothelium. Neutrophil adherence and transmigration into the lung occurs under the influence of IL-8. Proteolytic enzyme and oxygen free radical release from activated neutrophils promote further tissue injury and inflammatory activation of endothelial cells.
Endothelial cells are a central player in inflammation and coagulation. Specific agonists responsible for endothelial activation have been characterized and include IL-1β, TNFα, C5a, and thrombin. Endothelial cell activation results in a procoagulant, vasoconstrictive, and proinflammatory response. Once activated, the anticoagulant properties of the endothelial cell are dramatically reduced, with loss of heparan sulfate proteoglycan, conformational changes in the endothelial cell resulting in increased exposure to tissue factor and von Willebrand factor in the cellular submatrix, increased expression of tissue factor and plasminogen activator inhibitor type 1, and loss of thrombomodulin. The vasoconstrictive effects occur through the production of endothelin-1 and thromboxane A2. Proinflammatory changes are seen with increased expression of P and E selectins and consequent recruitment and sequestration of inflammatory cells.
Cardiac Surgery without Cardiopulmonary Bypass
On-pump coronary artery bypass surgery has been demonstrated by randomized controlled trials to both reduce symptoms and prolong life in every decade since the first coronary artery bypass graft (CABG) procedures were performed in the 1960s. Despite the proven benefits and ever-increasing safety of this procedure, room for improvement remains with regard to neurocognitive complications, atrial fibrillation, transfusions, stroke, and death. Because CPB is perhaps the most invasive aspect of conventional coronary revascularization, and because much of the morbidity of coronary revascularization can be attributed to hypothermic cardiac arrest, aortic cannulation, cross-clamping, and the bypass circuit itself, surgeons may consider performing coronary anastomoses on the beating heart without CPB. Some individual surgeons or institutions perform most coronary revascularization procedures without CPB. The term off-pump coronary artery bypass (OPCAB) generally refers to multivessel coronary artery bypass performed off the CPB machine, through a standard sternotomy.
Here we will focus on those differences between OPCAB and conventional on-pump revascularization procedures that may substantially impact the patient's recovery. During OPCAB procedures, coronary arteries are individually snared proximally and occluded during the performance of the coronary anastomosis. Depending on whether intracoronary shunts are used, there may be periods of local ischemia without cardioplegic arrest. However, unlike in the conventional on-pump procedures, there are no periods of aortic cross-clamping and global cardiac arrest. For these reasons, the degree of myocardial stunting during OPCAB may be reduced relative to on-pump procedures. Furthermore, during OPCAB, normothermic pulsatile flow is maintained throughout the procedure, whereas conventional on-pump procedures include a period of nonpulsatile perfusion and generally some degree of systemic cooling and rewarming. Finally, although both techniques require anticoagulation with heparin, many centers practice reduced-heparin dosing for OPCAB. Despite multiple randomized controlled trials, the issue of off-pump versus on-pump myocardial revascularization remains an area of debate. The inflammatory response to CPB appears to be a nonspecific response that includes complement and leukocyte activation. Although the exact mechanism of activation is unclear, the strongest stimulant for the response is the blood–artificial surface contact that occurs with CPB. This response can be modified by coating the tubing and oxygenator surfaces with biological materials and by improving the hemodynamic performance of the system. Theoretically, by eliminating the heart-lung machine entirely, this response could be significantly reduced.
Several quality studies have investigated the inflammatory response during heart surgery, comparing groups in which coronary revascularization is performed with and without CPB. Angelini and colleagues looked at four important inflammatory markers: neutrophil elastase, an endopeptidase released with neutrophil activation; IL-8, a potent neutrophil chemotactic and activating factor; and C3a and C5a, fragments generated with activation of the common complement pathway. These markers were measured at four time-points within the first 24 hours postoperatively. Patients were randomized to two groups: standard coronary revascularization with CPB and OPCAB. The OPCAB group demonstrated significantly lower levels of all four markers and had reduced leukocyte, neutrophil, and monocyte counts. These findings support a reduced inflammatory response with OPCAB; however, the clinical significance of this difference remains unclear. It is interesting that by 4 hours into the recovery period, the activated complement components had decreased in the on-pump group to OPCAB levels.
OPCAB requires less intraoperative anticoagulation and avoids blood–artificial surface contact, which should reduce platelet activation and destruction. Furthermore, systemic cooling, which may further negatively impact coagulation function, can be avoided with OPCAB. Several studies have compared on-pump procedures to OPCAB and report significant reduction in postoperative bleeding, reduced need for perioperative transfusion, and reduced rate of take-back for bleeding. Indeed, when coagulation and fibrinolysis variables have been studied, marked changes in fibrinolytic and coagulation variables occur within the first 24 hours. Conventional on-pump revascularization causes a transient decrease in the platelet count, fibrinogen level, and activation of plasminogen with increased d -dimer formation, which only after 24 hours approximate the levels seen in OPCAB. Two contemporary multicenter randomized controlled trials have supported reduced need for blood transfusion and reoperation for bleeding following off-pump compared to on-pump CABG; however, rates of rate of death, myocardial infarction, stroke, or renal failure requiring dialysis were no different.
Pericardiotomy Syndrome
A specific manifestation of the inflammatory response in cardiothoracic surgery is the post-pericardiotomy syndrome. This syndrome, occurring in 10% to 30% of patients, is a self-limited condition beginning in the second or third week after surgery. It is associated with fever and pleuritic, precordial, or substernal chest pain. Chest radiographs in patients with post-pericardiotomy syndrome commonly show pleural and pericardial effusions ( Fig. 60-1 ). This syndrome has been associated with specific reactive antibodies and may be seen after any operation that violates the pericardium. It is treated with nonsteroidal anti-inflammatory agents, although corticosteroids may be necessary in severe cases.
Cardiac Dysfunction after Cardiac Surgery
Low Cardiac Output Syndrome
Output and Filling Pressure
Low cardiac output after CPB has historically been recognized as a cause of sudden death. Low cardiac output resulting from ventricular dysfunction causes a series of adaptive neurohumoral responses as well as geometric changes—dilation and hypertrophy—in the heart. Acute loss of 20% to 25% of functioning myocardium causes significant reduction in cardiac output and carries extremely poor short-term and long-term prognoses.
Measurement and therapeutic manipulation of both cardiac output and central filling pressures are critical to the postoperative care of cardiac surgical patients and are predictive of survival ( Fig. 60-2 ). Central pressures, cardiac output, and venous saturation are routinely measured by means of a flow-directed pulmonary artery catheter. The cardiac index, or cardiac output expressed as liters per minute per meter squared, has a normal range of 2.1 to 4.9 liter/min/m 2 . In adults, a cardiac index of at least 2.0 liter/min/m 2 during the immediate postoperative period is generally required for normal convalescence.
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