Using Vasoactive/Inotropic/Antiarrhythmic Drugs During the Adult Open-Chest Cardiac Procedure
J. Kirk Edwards, MD
Assistant Professor , Department of Anesthesiology, Emory University School of Medicine Atlanta, Georgia
Outline
I. Introduction
II. Preparation for the Open-Chest Cardiac Procedure
The Crucial Role of Standardization
Drug Preparation
The “Typical” Open-Chest Cardiac Procedure
The “High-Risk” Open-Chest Cardiac Procedure
Drug Administration: Technical Considerations
Access
Dead Space
Carrier Infusion
Intravenous Line Care
Medication Labeling
III. Pre-Cardiopulmonary Bypass
Pre-Induction of Anesthesia
Induction of Anesthesia
Maintaining an Adequate Level of Anesthesia
Post-Induction
Incision and Sternal Separation
Graft Harvest (for coronary artery bypass surgery)
Cannulation and Post-Cannulation
IV. Cardiopulmonary Bypass
Mean Arterial Pressure Goals
V. Deep Hypothermic Circulatory Arrest
Mean Arterial Pressure Goals with Selective Cerebral Perfusion
VI. Weaning from Cardiopulmonary Bypass
Rhythm
Rate
Chronotropy
Inotropy
Preload
Afterload
MAP
VII. Post-Cardiopulmonary Bypass
Decannulation
Post-Bypass Cardiac Manipulation
Chest Closure
Transport
VIII. Off-Pump Coronary Artery Bypass Graft Surgery
Distal Anastomoses
Proximal Anastomoses
IX. Intraoperative Pharmacotherapy and Treatment Algorithms for Specific Arrhythmias
Sinus Tachycardia
Sinus Bradycardia
Supraventricular Tachycardia
Ventricular Tachycardia
Ventricular Fibrillation
Asystole
X. Summary
XI. Sources
I. Introduction
II. Preparation for the Open-Chest Cardiac Procedure
The Crucial Role of Standardization
Drug Preparation
The “Typical” Open-Chest Cardiac Procedure
The “High-Risk” Open-Chest Cardiac Procedure
Drug Administration: Technical Considerations
Access
Dead Space
Carrier Infusion
Intravenous Line Care
Medication Labeling
III. Pre-Cardiopulmonary Bypass
Pre-Induction of Anesthesia
Induction of Anesthesia
Maintaining an Adequate Level of Anesthesia
Post-Induction
Incision and Sternal Separation
Graft Harvest (for coronary artery bypass surgery)
Cannulation and Post-Cannulation
IV. Cardiopulmonary Bypass
Mean Arterial Pressure Goals
V. Deep Hypothermic Circulatory Arrest
Mean Arterial Pressure Goals with Selective Cerebral Perfusion
VI. Weaning from Cardiopulmonary Bypass
Rhythm
Rate
Chronotropy
Inotropy
Preload
Afterload
MAP
VII. Post-Cardiopulmonary Bypass
Decannulation
Post-Bypass Cardiac Manipulation
Chest Closure
Transport
VIII. Off-Pump Coronary Artery Bypass Graft Surgery
Distal Anastomoses
Proximal Anastomoses
IX. Intraoperative Pharmacotherapy and Treatment Algorithms for Specific Arrhythmias
Sinus Tachycardia
Sinus Bradycardia
Supraventricular Tachycardia
Ventricular Tachycardia
Ventricular Fibrillation
Asystole
X. Summary
XI. Sources
I. Introduction
This chapter outlines the major vasoactive/inotropic/antiarrhythmic considerations during each stage of the open-chest cardiac procedure. While not all-inclusive, the discussions provide the science as well as the art behind medication management in this dynamic setting. Additionally, section IX details decision and treatment algorithms for the major arrhythmias, specifically from an intraoperative cardiac surgery perspective.
Although the primary focus of this chapter is drug management, modalities such as atrial, atrioventricular, or ventricular pacing, cardioversion, or defibrillation are sometimes necessary and must be used in conjunction with the appropriate drugs. Preoperative discussions, preoperative checklists and good team dynamics add additional layers of safety in managing patients during open-chest cardiac procedures
II. Preparation for the Open-Chest Cardiac Procedure
The Crucial Role of Standardization
Standardization of room setup for the open-chest cardiac procedure cannot be overemphasized, and chief among setup components is drug preparation. At every institution, all cardiac anesthesia practitioners should agree to a “baseline” list of drugs that should be immediately available for the “typical” cardiac case. More specifically, the exact location of the drugs in the operating room, drug concentrations, volume of each drug preparation, and intended method of administration (intravenous bolus versus infusion) should also be standardized.
This standardization provides the following benefits:
1. Reduces error in drug preparation
2. Provides smooth transition of care between staff members by homogenizing clinical practices
3. Facilitates expedient, emergent pharmacologic interventions
The accepted format should be diagramed and made readily available to all cardiac anesthesia practitioners for immediate reference.
There are several caveats to standardized drug preparation. The “baseline” drug preparation should be used as the universal foundation. Any additions or alterations needed for “non-typical” or “high-risk” cardiac surgeries should be clearly labeled and specifically discussed at every handover.
At institutions with high volumes of emergency open-chest procedures, consider having a “backup emergency” operating room (if available) prepared, incorporating the standardized drug preparation, which can be used the following day if not used for an emergency.
Cardiac surgeons, anesthesiologists, intensivists, ICU nurses, pharmacists, and others as appropriate should reach agreement on the institutional standard for drug concentrations and volumes. Having a common standard across the institution prevents errors after postoperative transfer of care and movement of patients to different locations within the hospital.
Drug Preparation
The following description of drug preparation is specific to the Emory University hospitals and serves as an example rubric for other institutions. The logic comprising specific aspects of the Emory rubric is detailed.
The “Typical” Open-Chest Cardiac Procedure
Syringe Medications:
During the “typical” open-chest cardiac procedure, the following vasoactive/inotropic/antiarrhythmic medications are used with enough frequency to warrant pre-emptive preparation in syringes. These are prepared in 10 mL syringes for all open chest cardiac cases:
Syringe Drug Name Concentration
Phenylephrine 100 mcg/mL
Ephedrine 5 mg/mL
Norepinephrine 16 mcg/mL
Epinephrine 16 mcg/mL
Vasopressin 2 U/mL
Esmolol 10 mg/mL
Nitroglycerine 50 mcg/mL
Nicardipine 100 mcg/mL
The specific uses of the above medications are detailed in this chapter. These drugs are used for their specific combination of effects on systemic vascular resistance (SVR), pulmonic vascular resistance (PVR), inotropy, and/or chronotropy.
Drug Name: Common Use [1]:
Phenylephrine: Increase SVR and/or trigger a reflex reduction in chronotropy
Ephedrine: Increase SVR, inotropy, and chronotropy, temporarily and to a mild/moderate degree
Norepinephrine: Increase SVR, while maintaining or slightly increasing chronotropy and inotropy, commonly leading
to increased cardiac output
Epinephrine: Increase SVR, inotropy, and chronotropy, to a moderate/high degree
Vasopressin: Increase SVR while avoiding increase in PVR, often used with other vasopressors
Esmolol: Reduce chronotropy, especially with supraventricular tachycardias, or relative tachycardia in setting of
ischemia
Nitroglycerine: Reduce preload, often to temporarily reduce mean arterial pressure (ultra-short acting)
Nicardipine: Reduce preload, often to temporarily reduce mean arterial pressure (half-life ~20 minutes)
These medications are prepared in concentrations that provide physiologically desirable effects when given as 0.5-2 mL boluses. The medication syringes are segregated and grouped by their effect on mean arterial pressure, with designated locations specified to facilitate quick access.
**Note: 10 mL syringes of epinephrine 100 mcg/mL are also present in the Emory operating room anesthesia carts, as part of the standardized cardiac arrest medication supplies.
Additionally, the appropriate dose of heparin (400 Units/kg at Emory) for the specific patient should be calculated and drawn into a labeled syringe, prior to induction, to allow for immediate use should the patient acutely decompensate requiring emergent surgery.
Infusion Medications:
Two infusion medications, phenylephrine and norepinephrine, are frequently used during the “typical” open-chest cardiac procedure. Phenylephrine is typically used more commonly pre-bypass and norepinephrine is typically used more often post-bypass. These vasoactive/inotropic medications are prepared in 250 mL crystalloid bags, usually saline, ready for immediate infusion:
Infusion bag and syringe medication concentrations are intentionally the same as to minimize provider confusion and dose administration errors. The one exception is nitroglycerine, which in syringes is 50 mcg/mL and as an infusion, is premixed in glass bottles with concentration of 200 mcg/mL). The desired physiologic effects are the same as with intravenous bolus, though infusions provide a steady-state response. A crystalloid volume of 250 mL should provide enough infusate to sustain a standard duration open chest cardiac surgery at typical dose rates (typically phenylephrine 0.1-1.5 mcg/kg/min; norepinephrine 0.04-0.1 mcg/kg/min). For all open chest cardiac procedures, given the frequency of their use, these infusion medications are placed in a pump, programmed for specific patient’s weight, pre-set to start at low end of typical dose, placed on standby mode, connected to the carrier manifold, which, prior to induction, is connected “in-line” to the patient’s dedicated infusion site ready to begin infusion whenever necessary.
Other Vasoactive/Inotropic/Antiarrhythmic Medications:
While used less frequently, the periodic and sometimes urgent necessity of the following medications warrants their immediate availability, either in the operating room, in an electronic medication dispenser, or in an operating room satellite pharmacy. Some of these medications have other indications during general anesthesia, which also may warrant their physical presence in the operating room.
The “High-Risk” Open-Chest Cardiac Procedure
Common factors associated with increased risk during open cardiac procedures [1,2]:
- Moderate to severely reduced function of one or both ventricles
- Redo-sternotomy
- Complex cardiac procedures (combination valve/revascularization procedures or repair/replacement of multiple valves)
- Long cardiopulmonary bypass time (>2 hours)
- Long circulatory arrest time (>1 hour)
- Coagulopathy
- Advanced age (>70 years old)
- Emergency procedure
Syringe Medications:
The drugs prepared in 10 mL syringes for the “high-risk” cardiac surgery are the same as those prepared for the “typical” open-chest cardiac procedure. The only difference is to have multiple syringes of each vasopressor/inotrope and to ensure immediate access to epinephrine 100 mcg/mL.
Infusion Medications:
As with the “typical” case, phenylephrine and norepinephrine infusions are prepared and connected “in-line” with the patient. The specific reason(s) that make a cardiac procedure “high-risk” will also dictate choices for additional infusion medications to be prepared in advance and connected to the patient’s dedicated infusion carrier manifold. These potential vasoactive/inotropic medications, prepared in 250 mL crystalloid bags, include the following:
The desired physiologic effects of vasopressin and epinephrine are the same as with intravenous bolus. However, infusions provide a steady-state response. The specific uses of the above medications are detailed in this chapter. Briefly, however, milrinone, dobutamine, and isoproterenol are prepared for the following purposes:
Drug Name: Common Use [1]:
Milrinone: Increase inotropy/lusitropy and decrease SVR/PVR
Dobutamine: Increase inotropy/chronotropy and small decrease in SVR
Isoproterenol: Increase inotropy/chronotropy and decrease in SVR
Most commonly used for heart transplants
Other Vasoactive/Inotropic/Antiarrhythmic Medications:
The list of less commonly used vasoactive/inotropic/antiarrhythmic medications is the same for the “typical” and the “high-risk” open-chest cardiac case. However, consider an augmented supply of calcium chloride in cases where high-anticipated transfusion volumes may result in citrate-induced hypocalcaemia.
Drug Administration: Technical Considerations
Access
Whenever possible, vasopressors and inotropes should be administered via central venous access, as peripheral administration can result in vein sclerosis or, in the event of extravasation, tissue necrosis [1]. However, short duration infusions and infrequent boluses pose a smaller risk to peripheral veins. Therefore, temporary peripheral administration is deemed permissible at Emory, as central access is obtained. This strategy is often implemented following induction of general anesthesia in those patients deemed stable enough for central access to be placed post-induction.
Vasodilators and antiarrhythmic drugs can usually be administered safely via peripheral venous access.
Peripheral venous access for temporary vasopressor/inotrope administration should be a large-bore (14-gauge or 16-gauge) angiocatheter, well placed into a large vein. This will minimize the chances of sclerosis or necrosis and expedite drug entry and circulation. Angiocatheter placement in the forearm or arm is preferable to insertion in the hand or wrist, as kinking is frequent in the latter locations.
Baseline hemodynamics, patient stability, and the severity of certain pathologies (ventricular dysfunction, coronary artery occlusion, valvular dysfunction) will determine the necessity of central access prior to the start of anesthesia. While peripherally inserted central catheters (PICC) offer dedicated central access, slow flows rates result in delayed onset of drug effects and are not recommended.
Subclavian or internal jugular veins are most often chosen for central access. These provide easy access to the anesthesiology team and have a lower line infection rate than femoral lines [1]. However, femoral venous access is a viable alternative, although intravenous dead space will be long (see Dead Space section below). Note that sternal retractors can occasionally kink subclavian lines, particularly left subclavian lines, which has caused inability to infuse and loss of monitoring of central pressures. During insertion of left internal jugular central lines, dilators should not be over-advanced, as they can puncture the far vein wall where the internal jugular and subclavian veins combine to form the innominate vein. The right internal jugular vein is most commonly used secondary to ease of venous puncture, vein anatomy which leads directly to the right atrium, low infection rates, and proximity to the anesthesia team.
Dead Space
In the context of medication infusions, “dead space” refers to the distance between the infusion’s attachment to a carrier and the carrier’s entry into the patient. The dead space length should be minimized by attachment of infusions to the carrier line as close to the patient as possible. This is important as dead space delays entry of drugs and onset of their effects.
Carrier Infusion
Vasoactive/inotropic/antiarrhythmic infusions should be administered with a “carrier” crystalloid infusion. Ideally, the crystalloid carrier should be placed onto an infusion pump, set at 50 to 100 mL/hour. This keeps the dead space clear, avoiding inadvertent bolusing of concomitant drug infusions. Having a carrier allows multiple infusions to be connected “in-line” at the same location, via a multiport manifold. Piggybacking multiple infusions onto one another is not recommended since that practice fills part of one medication’s intravenous tubing with another drug, which may lead to dose administration errors.
Maintaining a specific carrier infusion rate (typically 50-100 mL/hr) will allow continuous clearing of the dead space contents and ensure rapid delivery of medications to the patient.
Intravenous Line Care [5]
Intravenous lines should be kept clean from blood and contaminants. Access ports with stopcocks should be capped when not in use. Access ports with diaphragms should be wiped clean with antiseptic (alcohol, chlorhexidine, etc.) before use. Intravenous lines should not touch the floor.
Medication Labeling
All medications, either in syringes or infusion bags, should be clearly labeled with the drug name, concentration, and expiration date. Additionally, labeling infusion lines with the drug name at the point of their attachment to the carrier manifold helps to minimize confusion, especially when multiple medications are placed in tandem to a carrier manifold. One can easily remove an unnecessary drug without having to trace all the way back to the bag source. It is critical to be meticulous in ensuring the infusion is correctly labeled at the manifold.
III. Pre-Cardiopulmonary Bypass
Pre-Induction of Anesthesia
In the period preceding anesthesia induction, it is important to formulate a vasoactive/inotropic/antiarrhythmic management plan for the case. The sections below outline the key considerations that influence pharmacologic decisions during each stage of the open-chest cardiac procedure. In addition, several pathologies carry overarching pharmacologic implications that will affect medication choices. Briefly, the most common are listed below with general therapeutic goals [1]:
Induction of Anesthesia
The induction of general anesthesia can be a very challenging period. Specifically, at the time of induction, most patients have been NPO (no oral liquid or solid intake) for eight or more hours, resulting in a state of relative hypovolemia. In addition, many cardiac surgery patients have one or more of the following: depressed ventricular function, valvular dysfunction, significant coronary artery disease, or active ischemia. Anesthetics can cause a sympathectomy, vasodilation, myocardial depression, and preload reduction, each of which can exacerbate the above preexisting conditions. Finally, in the event of difficult mask ventilation or difficult intubation, hypercarbia or hypoxia may occur.
Because compounding of these effects may lead to hemodynamic collapse, the induction should be executed in a controlled, well-planned manner. The following induction checklist helps ensure an appropriate plan for vasoactive/inotropic/antiarrhythmic medications:
1. Reliable, continuous blood pressure monitoring: For the vast majority of open-chest cardiac procedures, patient acuity warrants continuous arterial waveform analysis [1]. Noninvasive blood pressure monitoring is periodic, and it is unreliable at low mean arterial pressures. Reliable arterial lines produce undamped waveforms, are easily aspirated for blood, and contain no bubbles. The arterial line transducer should be zeroed at the level of the patient’s heart.
2. Reliable, fast flowing venous access: Please see the above Access section. Briefly, a reliable large-bore peripheral (16- or 14-guage) angiocatheter or a central line should be available for induction. An intravenous line with easily accessible flow control should be connected to allow rapid medication administration.
3. Induction strategy that minimizes hemodynamic derangements: Several options exist, and while detailed discussion of anesthetics is beyond the scope of this chapter, these include one or a combination of the following [1]:
- Slow, titrated intravenous induction: Any intravenous anesthetics should be administered in divided, titrated doses with adequate time allowed for drug circulation and onset.This will ensure that induction is achieved with the smallest possible drug doses and that hemodynamic derangements are small and punctuated.
- High-dose narcotic induction: While narcotics cannot be used as sole induction agents, high dosages of fentanyl (>8) or sufentanil (>0.75) minimally depress mean arterial pressure (MAP) and minimize the dose of other anesthetics. After an adequate narcotic dose, propofol, typically 30-50 mg, is enough to induce unconsciousness, as is etomidate in comparable low doses. If additional propofol is needed, small, 20-30 mg bolus will typically induce unconsciousness. As a caution, chest wall rigidity may result with high narcotic loads, which can lead to difficult mask ventilation. The addition of an inhalation agent, typically 0.5-1% isoflurane maintains an adequate level of anesthesia, which can be monitored by the BIS.
- Etomidate induction: Etomidate causes less myocardial depression than propofol and is useful in states of significantly depressed ventricular function. It should be noted that in critically ill patients with no catecholamine reserve, the resulting sympathectomy from etomidate might still cause hemodynamic collapse.Additionally, even a single dose of etomidate may result in adrenal suppression, particularly detrimental to critically ill patients.
- Ketamine induction: Ketamine itself can cause myocardial depression and vasodilation, but this is normally counterbalanced by its sympathomimetic effects. MAP is usually maintained. Note that in critically ill patients, a state of catecholamine depletion may exist, in which case ketamine may cause a drop in MAP.Additionally, the increase in heart rate often seen with ketamine may be undesirable in certain disease states, such as with tight valve stenosis, on-going ischemia or dynamic outflow tract obstruction. Ketamine induction is most commonly used for significant, symptomatic cardiac tamponade.
- Inhaled anesthetic induction:Most inhaled anesthetics cause vasodilation and myocardial depression; however, effect onset is slower and usually less severe with a properly titrated inhaled induction. This allows time to counteract hemodynamic depressions. As a caution, the shallow and variable respiratory pattern that occurs with an inhaled induction (especially during stage 2 of anesthesia) can result in hypercarbia. Assisted ventilation is usually required.
4. Muscle relaxant for rapid control of ventilation [8]: Hypercarbia and hypoventilation can rapidly lead to right heart failure. When adequate anesthetic depth has been achieved, and in the setting of confirmed or anticipated easy mask ventilation, muscle relaxant should be given. Paralysis of the airway musculature will more easily allow ventilation to provide adequate tidal volumes for gas exchange. While the depolarizing agent succinylcholine has rapid onset, usually an adequate dose of a nondepolarizing muscle relaxant suffices, and it avoids succinylcholine’s risk of hyperkalemia in certain patients. Rocuronium (1-1.2 mg/kg) is a common choice for agent and dose due to its rapid onset. Cardiac surgical duration usually allows more than enough time for metabolism of the muscle relaxant. If the patient is well anesthetized, rarely is a second dose of muscle relaxant needed even during or after cardiopulmonary bypass. However, sugammadex, in the absence of renal failure, can now be used to reverse moderate muscle relaxation from rocuronium and vecuronium.
5. Vasopressor to counteract hypovolemia and vasodilation: Many anesthetic inductions require a vasopressor to maintain vascular tone. For stable patients with normal cardiac function, a decrease in MAP can be treated with the pure vasopressor phenylephrine (typically 50-200 mcg bolus). In states of hypovolemic shock, such as with ruptured aneurysms, vasopressin often provides stronger dose-response to maintain circulation while addressing the immediate problem.
6. Inotropy to counteract myocardial dysfunction: In patients with depressed ventricular function, with active ischemia, or in hemodynamically unstable patients, a combined inotrope/vasopressor is more appropriate to treat low mean pressures. Ephedrine (typically 5-10 mg) is useful for mild hypotension, while norepinephrine (typically 8-32 mcg) and epinephrine (typically 8-16 mcg) are more potent and appropriate for higher acuity patients.
7. Determination of medication onset time and effect: Once the appropriate drugs to supplement MAP have been chosen, it is useful to “test-bolus” a small dose of these medications immediately prior to or at the beginning of induction. While not perfectly correlative to later doses, the “test-bolus” will demonstrate the “lag-time” between drug administration and its effects, as well as the amplitude of pressure supplementation per drug dose administered. Low cardiac output states will result in longer “lag-times.”
8. Infusion versus intermittent bolus: In the setting of small “lag-times” and strong pressure augmentation, intermittent titrated vasopressor/inotrope bolusing during induction drug administration may be sufficient to maintain MAP. Conversely, in critically ill patients, hemodynamically unstable patients, or with a long “lag-time,” it is wise to begin a baseline infusion of inotrope/vasopressor prior to induction. This will provide a basal level of support, while drug boluses can be reserved for supplementation. Norepinephrine (typically 0.04-0.1 mcg/kg/min) and/or epinephrine (typically 0.04-0.1 mcg/kg/min) are the most commonly used infusions.
9. Have a planned strategy in event of profound hemodynamic depression:
- Supplemental inotropes/vasopressors readily available
- Epinephrine bolus 16-1000 depending on severity
- Chest compressions to circulate medications in pulseless or minimally pulsatile states
10. Adjuncts to counteract hypertension or tachycardia:
In patients with acute aortic syndrome (aortic trauma, aortic dissection, acute penetrating atherosclerotic ulcer, intramural hematoma), avoiding hypertension and tachycardia is paramount. Additionally, light anesthetic states and/or stimulation from airway instrumentation often lead to hypertension and/or tachycardia. A short acting vasodilator such as nitroglycerine (typically 50-200 mcg bolus) should be used to counteract pure hypertension. Nicardipine (typically 100-300 mcg bolus) is also effective, especially when patients have developed nitroglycerine tolerance from preoperative administration. Both the onset time and duration of nicardipine are longer than for nitroglycerine.
Tachycardia, especially high rates and with concomitant valvular stenosis, ischemia, or dynamic outflow tract obstruction, should be treated with a short acting β-blocker such as esmolol (typically 0.25-1 mg/kg bolus).
Maintaining an Adequate Level of Anesthesia
Ensuring that the patient is well anesthetized during the procedure is crucial. After induction and intubation, intraoperative analgesia is commonly provided with a narcotic infusion, typically fentanyl or sufentanil. An inhaled volatile anesthetic, delivered via the anesthesia machine prior to bypass and after bypass and via the bypass machine during cardiopulmonary bypass provides anesthesia. At Emory, an isoflurane vaporizer has been installed on all bypass machines and the standard is to have the perfusionist set the vaporizer to 1% for the duration of the bypass. Occasionally, to supplement anesthesia, the perfusionist will be asked to increase the vaporizer to 1.5% or occasionally to 0.5% to lessen anesthetic level.
Both volatile anesthetics and propofol can cause myocardial depression and vasodilation [1]. Even in hemodynamically stable patients with preoperative normal cardiac function, maintenance anesthesia often necessitates vasopressor supplementation (typically phenylephrine 0.1-1.5 mcg/kg/min). In the setting of hemodynamic instability and/or a severely reduced left ventricular function, significant support with multiple inotropes and vasopressors may be needed. In this latter setting, the anesthesia provider will often adjust the maintenance anesthesia regimen to minimize myocardial depression and vasodilation. Adjustment strategies include: a lower concentration of inhaled volatile anesthetic with high dose narcotic supplementation, a ketamine infusion, or high dose narcotic with benzodiazepine supplementation.
Regardless of the hemodynamic rationale for anesthetic decisions, maintaining adequate anesthesia remains paramount. For that reason, bispectral index (BIS) monitoring is useful to judge anesthetic depth. Additionally, neuromuscular blockade agents should be dosed cautiously and be guided by nerve twitch monitoring. Additional muscle relaxant, after induction is usually not necessary provided the patient is well anesthetized. If additional muscle relaxant is given, it is important to monitor the NMB to allow knowledge of depth of blockade to facilitate emergence and extubation in the intensive care unit.
Post-Induction
Once a maintenance level of anesthesia is achieved, and prior to surgical stimulation, an infusion of a vasopressor or a combination vasopressor/inotrope is ideal to correct hypotension. At this point, a steady-state infusion is preferable to bolus dosing medications to eliminate therapeutic variability during a relatively quiescent period. As with induction, inotropy is added in states of myocardial dysfunction. Echocardiography, cardiac index measurement and pulmonary artery pressures can help quantify the degree of primary cardiac dysfunction.
Maintaining normocarbia and adequate oxygenation is essential.
Phenylephrine infusion (typically 0.1-1.5 mcg/kg/min) is usually sufficient. For added inotropy, norepinephrine (typically 0.01-0.15 mcg/kg/min) and/or epinephrine (typically 0.01-0.15 mcg/kg/min) infusions are appropriate. In the setting of uncorrected coronary artery disease, severe valvular stenosis, or dynamic left ventricular outflow tract obstruction, avoiding excess heart rate increases is important.
Pure inotropes such as dobutamine, isoproterenol, or milrinone are less commonly used immediately post-induction. If these drugs are used, frequently a vasopressor will also be needed to maintain MAP. Additionally, milrinone has a relatively longer onset time and a long duration of action once the infusion is stopped making it less useful in the short period immediately preceding surgical incision [1].
In persistently severely hypertensive patients, a rapidly titratable infusion of nitroglycerine (typically 0.1-10 mcg/kg/min) or nicardipine (typically 1-5 mcg/kg/min) should be administered with a dosage increase immediately prior to incision. Persistent tachycardia should be evaluated for etiology (see Sinus Tachycardia section below). While the underlying etiology is being assessed and treated, short-term β-blockade can be provided with esmolol, while labetalol (typically 5-20 mg) or metoprolol (typically 1-5 mg), titrated to heart rate, will provide longer duration β-blockade. Of note, labetalol also has an α-blockade component [1]. Long acting β-blockers should be used with caution, as bradycardia post-bypass from stunning and ischemia is common.
Incision and Sternal Separation
Strong surgical stimulation from skin incision and sternal separation often allows a reduction in vasopressor/inotrope infusion dose or warrants an increase in vasodilator infusion dose. Severe hypertension can be temporized with a vasodilator bolus and/or deepening the level of anesthesia. Narcotics are not anesthetics and should be used in a dose that provides a good level of analgesia. If the plan it to extubate the patient within 4-6 hours of arrival in the ICU, excessive doses will delay extubation and should be avoided.
For redo sternotomy patients, because of the risk of right ventricular or right atrial perforation, blood checked and available in the room in a cooler or refrigerator will allow rapid transfusion should that be necessary.
Graft Harvest (for coronary artery bypass surgery)
The period of graft harvest for coronary artery bypass surgery is usually hemodynamically quiescent. Hypotension during this phase can be corrected with a vasopressor or vasopressor/inotrope infusion. For procedures necessitating cardiopulmonary bypass, fluid administration is kept to a minimum, as the bypass circuit crystalloid will cause moderate hemodilution.
Worsening ischemia may manifest with sudden myocardial dysfunction. Should the effective dose of vasopressor or vasopressor/inotrope increase substantially, one should evaluate for signs of ischemia, visual inspection of the heart, electrocardiogram (EKG) changes, new or worsening wall motion abnormalities on echocardiography or acute elevations in pulmonary artery pressures.) [1]. Going emergently onto cardiopulmonary bypass may be necessary.
Cannulation and Post-Cannulation
For most cardiopulmonary bypass procedures, cannulation is central.
Arterial cannulation is performed at the level of the mid-ascending aorta,
while venous cannulation is performed at the right atrium and vena cava.
Management of vasoactive/inotropic/antiarrhythmic medications usually occurs in the following order:
1. Pericardial separation and exposure: During this phase, electrocautery near and on the heart, can result in ectopic beats or arrhythmias. Consider a lidocaine bolus (typically 100 mg) or magnesium infusion (typically 2 grams over 10 minutes) upon opening of the pericardium when any of the following is present at baseline:
- Frequent premature atrial or ventricular contractions
- Ischemic EKG changes
- Electrolyte abnormalities, particularly hypokalemia, hyperkalemia, or hypomagnesaemia
- Moderate or severe acidosis
- Recent episode(s) of arrhythmia
Treatment of specific arrhythmias, especially supraventricular tachycardia (SVT), is addressed later in the chapter.
2. Central arterial cannulation: For aortic cannulation, a short-term reduced systolic arterial pressure (typically <100 mmHg) is desired to minimize the chances of aortic injury or bleeding. Consider the following interventions in stepwise fashion:
- Reverse Trendelenburg positioning
- Titrated vasodilator boluses (typically nitroglycerine 50-100 versus nicardipine 100-300
- Reduction in dose of vasopressor or vasopressor/inotrope infusions
Because aortic cannulation requires only a brief period of lower systolic pressures, the first two interventions are often more appropriate, as they produce immediate effects that are rapidly reversible.
3. Central venous cannulation: Temporary right atrial compression and manipulation reduces venous return during central venous cannulation. Usually, a short period of permissible hypotension, Trendelenburg positioning, or a small bolus of vasopressor/inotrope are all reasonable options. Sometimes atrial manipulation will trigger SVT or atrial fibrillation. See the section below for suggested treatment algorithm for SVT. In the event of refractory unstable SVT, cardiopulmonary bypass should be initiated to decompress and arrest the heart.
4. Retrograde autologous priming (RAP) of the cardiopulmonary bypass circuit: Once the arterial and venous cannula are in place, it is common practice for the perfusionist to backfill arterial and venous cannulas with patient blood, to minimize circuit-induced hemodilution. This process is called retrograde autologous priming [1]. “Rapping” is the commonly used slang term. To maintain an acceptable MAP during retrograde autologous priming, bolus doses of a vasopressor or vasopressor/inotrope (typically phenylephrine 100-200 mcg, norepinephrine 16 mcg, or vasopressin 0.5-2 units) are given. After “rapping,” the patient is in a state of moderate to severe hypovolemia. Vasopressor infusion dose requirement is often high, and pre-bypass manipulation of the heart can result in severe hypotension. Trendelenburg positioning, minimizing the periods of heart manipulation, vasopressor bolus dosing or the initiation of cardiopulmonary bypass are all treatments for hypovolemic hypotension during this period.
IV. Cardiopulmonary Bypass
Mean Arterial Pressure Goals
During cardiopulmonary bypass, inotropic infusions can often be discontinued, as the heart is usually decompressed and arrested. Maintaining the MAP within a target range is usually done using direct-acting vasopressors or vasodilators. The ideal MAP for cardiopulmonary bypass is controversial, though tailoring to the patient’s baseline pressure is often a sound approach. Generally, the target MAP is somewhere between 50-90 mmHg with the expectation that this will provide adequate perfusion to the vital organs, especially the kidneys and brain. Factors that influence what MAP range is acceptable include the following:
- Patient temperature: Basal metabolic rate decreases 10-14% with every 1C drop in core body temperature [8]. Therefore, due to the reduced total body oxygen consumption, lower range mean pressures (50-70 mmHg) are often accepted during mild-moderate hypothermia (28-32C).
- Patient co-morbidities: A higher target MAP (70-90 mmHg) is often chosen in the setting of uncontrolled baseline hypertension or high grade cerebrovascular, reno-vascular, or coronary artery stenosis, though the data is conflicting [1,2,3,4,5]. For coronary artery stenosis, the same logic applies to the period after removal of the aortic cross-clamp but prior to proximal coronary artery bypass grafting.
- Patient age: In patients > 80 years old, a higher target MAP (70-90 mmHg) is often chosen, due to the often higher number of co-morbidities and the reduced ability of organs to compensate/autoregulate from hypoperfusion.
- Physiologic indices: Certain measurements can help guide the adequacy of regional or global perfusion, including serum lactate level, cerebral saturation values, urine production, and venous oxygen saturation. High lactate levels, or low values for cerebral oxygen saturation, urine production, and/or venous oxygen saturation, suggest the need to evaluate for inadequate perfusion.
In the event of refractory hypotension, consider the causes listed below:
For persistent refractory vasoplegia, intravenous methylene blue (typically 2 mg/kg) can be infused as a nitric oxide inhibitor [1]. This medication will interfere with infrared hemoglobin saturation measurements. Methylene blue used in patients taking selective serotonin release inhibitors (SSRIs) or monoamine oxidase inhibitors (MAOIs) can lead to serotonin syndrome, where excessive serotonin leads to neuro-agitation (confusion, tremors, sweating, hyperreflexia), hyperthermia, and rarely, seizures [1]. Treatment of serotonin syndrome involves supportive care and the removal of offending agents. Controversially, some suggest the use of the serotonin antagonist cyproheptadine [1].
To decrease a persistently high mean arterial pressure, an infusion of nitroglycerine (typically 0.1-10 mcg/kg/min) or nicardipine (typically 1-5 mcg/kg/min) is standard. In the event of acutely elevated MAP, a bolus of nitroglycerine (typically 50-200 mcg) or nicardipine (typically 100-300 mcg) can be administered via the bypass oxygenator. Decreasing pump flow rate or increasing the inhaled volatile anesthetic concentration are temporary adjustments that should be made only in the event of severe hypertension and should be used briefly until control can be achieved with a vasodilator. Prolonged low flow rate causes poor tissues perfusion and acidosis.
V. Deep Hypothermic Circulatory Arrest
Mean Arterial Pressure Goals with Selective Cerebral Perfusion
Deep hypothermic circulatory arrest is often performed with selective cerebral perfusion via one of two routes: retrograde via the superior vena cava or anterograde via one carotid artery with subsequent contralateral perfusion through the Circle of Willis. Normally, the vasoconstriction from profound induced hypothermia (often as low as 23-25°C) eliminates the need for vasopressors. While controversial, cerebral oxygen saturation monitoring can be used to gauge the adequacy of cerebral perfusion [1]. During selective anterograde perfusion via one carotid artery, for example, a low cerebral oxygen saturation reading on the contralateral side may signal poor Circle of Willis flow. In this situation, a trial of vasopressor via the bypass oxygenator may help to augment flow beyond the Circle of Willis.
VI. Weaning from Cardiopulmonary Bypass
Weaning off cardiopulmonary bypass is a dynamic and individualized process. The combination and dosages of specific vasoactive/inotropic/antiarrhythmic medications is often variable during this period; however, when optimizing physiology during the bypass wean, certain important caveats exist that are elaborated upon below.
Rhythm
Termination of cardiopulmonary bypass requires a rhythm that will allow adequate perfusion. The rhythm can be an intrinsic sinus, an accelerated junctional, paced (atrial, ventricular, or atrioventricular), or occasionally, chronic baseline atrial fibrillation or atrial flutter. Restoration of coronary artery blood flow, normal-range electrolyte levels, an adequately rewarmed core body temperature, (36-37 degrees C), and correction of significant acid-base derangement must be addressed. Once these are optimized, a rhythm typically develops either: 1) spontaneously, 2) via cardioversion of a supraventricular tachycardia (SVT)/ventricular tachycardia (VT) 3) via defibrillation of ventricular fibrillation (VF), or 4) via pacing for asystole, significant or relative sinus bradycardia, or heart block with slow ventricular response. Persistent, recurrent ventricular fibrillation requiring multiple, unsuccessful defibrillation attempts may be related to persistent cardiac ischemia and requires a check of the newly re-vascularized vessels a to rule-out kinking or other causes of lack of adequate flow.
It is important to remember that, in the minutes following aortic cross-clamp removal and restoration of coronary artery blood flow, the myocardium is prone to arrhythmias. Delaying giving calcium (10 minutes at Emory) following unclamping allows time for myocardial washout of ischemic mediators. In patients with frequent ectopic beats or a varying rhythm during the bypass wean, the following pharmacologic interventions should be considered to help maintain stability:
For treatment of sustained arrhythmias that do not support adequate perfusion, specifically supraventricular tachycardia (SVT), ventricular tachycardia (VT), or ventricular fibrillation (VF), please refer to the below arrhythmia section.
Chronotropy
During cardiopulmonary bypass wean, the target heart rate for most open chest cardiac procedures falls within the range of 70-90 beats per minute. This target ensures both an adequate rate and adequate diastolic filling time and a reasonable myocardial workload. In situations where stroke volume potential is maximized, increasing cardiac output is achieved with higher target heart rates. Occasionally, the heart rate is targeted as high as 90-110 beats per minute for this reason. It should be noted, however, that heart rates above 120 beats per minute increasingly compromise diastolic filling time and subsequently decrease cardiac output.
Adequate Heart Rate and Rhythm
Pharmacologic heart rate augmentation is most often achieved with a β-agonist. Sometimes, when the heart rate slowly increases following cross-clamp removal, a single bolus of a short acting β-agonist (typically epinephrine 8-16 mcg) will expedite the process. B-agonist should be given after allowing for myocardial reperfusion, typically approximately 10 minutes after the aortic cross-clamp is removed.
Most commonly, a β-agonist infusion is started to augment the heart rate of a perfusable rhythm. Chronotropy is most specifically enhanced with dobutamine (typically 5-10 mcg/kg/min) and isoproterenol (typically 1-5 mcg/min), though these agents also augment inotropy. Of the two, dobutamine is the most β1 specific, with only limited β2 and α1 effects. Isoproterenol stimulates both β1 and β2 receptors [1]. Both dobutamine and isoproterenol require 5-10 minutes of administration before full effect develops. Additionally, both will result in some degree of vasodilation which can lead to hypotension especially if the patient is relatively hypovolemic [1]. A vasopressor infusion is commonly used to compensate for the vasodilation. Isoproterenol in large doses (> 10 mcg/min), commonly causes serious ventricular arrhythmias [6]. An alternative agent should be considered when β1 augmentation is required particularly in the setting of recurrent arrhythmias.
For combined chronotropy, inotropy, and vasopressor augmentation, epinephrine (typically 0.01-0.15 mcg/kg/min) is potent, rapidly titratable, and effective in all three domains. The use of epinephrine can simplify the patient’s medication profile, but separating the myocardial and vascular effects is not possible. It should be noted that epinephrine infusions frequently cause hyperglycemia and hypokalemia. While norepinephrine has both β and α effects, heart rate is usually unaltered [6]. In younger patients, however, a larger β effect is often seen with a mild dose-related increase in heart rate.
Inotropy
While some patients can be weaned off cardiopulmonary bypass without inotropic support, most require some degree of pharmacologic augmentation secondary to pre-existing ventricular dysfunction, myocardial stunning from surgical manipulation, or from bypass-induced ischemic injury. These factors will help formulate the plan for inotropic support. Consider the following pearls when deciding the number, order, and type of inotropic agents to administer for the bypass wean:
First Agent:
Combination drug therapy (norepinephrine, epinephrine, milrinone and vasopressin) is commonly used in patients who require significant support. If additional support is needed, an IABP or another type mechanical assist device is often placed.
Just prior to the beginning of bypass wean, approximately 10 minutes after aortic cross-clamp has been removed, calcium chloride is administered to correct hypocalcemia. This will also provide a short-duration boost in inotropy. During the bypass wean, choice(s) for inotropic support will be tested with real-time indices, including echocardiography, arterial waveform pulsatility, visual inspection of the heart, and venous oxygen saturation values from the pump. The choice to bolus inotropes to boost depressed contractility should be made carefully. In patients with preserved pre-bypass ventricular function and short bypass duration, a single bolus of epinephrine (typically 8-16 mcg) can restore normal contractility. Additionally, sudden myocardial stunning from coronary artery air entrainment is effectively treated with epinephrine (typically 16 mcg) and a vasopressor (typically vasopressin 1-2 units) bolus. In most situations, however, titration of infusions to achieve an acceptable baseline level of inotropy will ensure a more stable wean and reduce the chances of sudden post-bypass hypotension.
Preload
A successful cardiopulmonary bypass wean necessitates optimal preload (volume). Rarely are vasoactive/inotropic/antiarrhythmic medications used to manage preload during the wean. Communication between the anesthesiologist, perfusionist, and surgeon allows gradual filling of the ventricles as the pump flow is decreased while assessing the pulmonary artery pressures, the right atrial pressure and the mean arterial pressure. A slow bypass wean, particularly in patients with severely impaired ventricular function is optimal and can avert the need to rapidly go back onto bypass. Slowly weaning allows drugs to be added, effects to be seen and better control of MAP, PA pressures, RA pressure and cardiac function.
Overfilling or distending a ventricle is poorly tolerated which argues for a slow wean. Particularly at risk for over-distension is a poorly functioning right ventricle. Looking at the heart over the drapes and correlating with the pressures, PA, RA, and MAP as well as using echocardiography helps with proper filling of the heart and a continued wean from bypass.
Afterload
SVR:
Due to the inflammatory state commonly induced by cardiopulmonary bypass, optimal afterload usually requires a vasopressor infusion. The ideal MAP for termination of bypass is usually that of the patient’s physiologic baseline. This will ensure that organs are perfused within the range of intrinsic autoregulation. In the setting of pre-bypass ischemic myocardium, higher goal mean pressures may be warranted to ensure maximum perfusion and oxygen delivery to stunned or hibernating myocardial segments. Dynamic outflow tract obstructions also call for higher afterload [1]. Conversely, evaluation of suture line integrity or concern for aortic intimal integrity may warrant a lower goal mean arterial pressure, at least temporarily. Issues with significant impact on the optimal mean arterial pressure should be addressed by the surgeon and the anesthesiologist.
Vasopressor infusion requirements for the bypass wean are commonly predicted during the rewarming phase. Those patients necessitating large vasopressor dosages during rewarming will usually also needed high afterload support during wean and following cardiopulmonary bypass. Causes for refractory vasoplegia should be investigated and treated before the bypass wean (see “Cardiopulmonary Bypass” section for specific causes and therapies). Increased vasopressor requirements will also be needed should a vasodilating inotrope, such as milrinone, dobutamine, or isoproterenol, be used.
Phenylephrine is rarely used for bypass wean as some level of inotropic augmentation is also desired. The baseline vasopressor of choice is usually norepinephrine (typically 0.04-0.15 mcg/kg/min) due to its additional inotropic effect. Vasopressin (typically 0.04-0.1 units/minute) is often added as a second agent, but because it minimally affects the pulmonary vasculature, it may be an ideal first choice with pulmonary hypertension or right ventricular dysfunction. Because epinephrine (typically 0.04-0.15 mcg/kg/min) has potent chronotropic, inotropic, and vasoconstrictive properties, it is often added when additional support is needed.
Vasodilators are rarely needed for bypass wean, however patients with poorly controlled hypertension preoperatively and with good left ventricular function may require treatment. Typically, nitroglycerine (0.1-10 mcg/kg/min) with its very short half-life is the best vasodilator choice during this dynamic period. Patients with long standing uncontrolled hypertension or those with preserved left ventricular function after aortic valve replacement for aortic stenosis may have severe left ventricular hypertrophy and a poorly-compliant left ventricle, which puts them at risk for disproportionately large changes in mean arterial pressure with small changes in volume which can lead to significant hyper or hypotension.
As with determining inotropic support, choosing vasoactive support can be aided by comparing echocardiography, visual inspection of the heart and arterial waveform pulsatility, and with venous oxygen saturation values from the bypass machine. The decision to bolus vasoactive medications should be made carefully. When vasopressor infusion requirements have been overestimated and volume-loading results in significant hypertension, a vasodilator bolus can temporize hemodynamics while vasopressor infusions are down titrated. In most cases, taking the time (i.e. a slow bypass wean) to achieve steady state infusion dosages of inotrope and vasopressors, in lieu of medication boluses, will ensure a smoother bypass wean.
Sudden myocardial stunning from coronary artery air entrainment, usually associated with sudden ST segment elevation in inferior leads, is effectively treated with vasopressor and inotrope boluses.
Pulmonary Vascular Resistance:
(Right Ventricular Afterload)
Reducing PVR decreases right ventricular afterload and decreases right ventricular myocardial work. Pulmonary arteriolar constriction is minimized with adequate levels of anesthesia, analgesia, oxygen, and carbon dioxide. Additionally, in the setting of right ventricular compromise, vasopressin and milrinone are the preferred vasopressor and inotrope, respectively, as vasopressin minimally constricts and milrinone dilates the pulmonary vasculature [1].
For bypass wean, inhaled epoprostenol (typically 50 ng/kg/min) or inhaled nitric oxide (typically 0.5-80 ppm) should be added in the setting of baseline high pulmonary artery pressures and when the risk of post-bypass right ventricular failure is high. Both selectively dilate the pulmonary vasculature [1]. Inhaled nitric oxide is very expensive and requires a cumbersome delivery system that complicates patient transport. When using nitric oxide, having respiratory therapy support facilitates optimal patient care during a typically complex, dynamic, challenging hemodynamic state.
VII. Post-Cardiopulmonary Bypass
Decannulation
As with central aortic cannulation, central aortic decannulation requires a short-term reduced systolic arterial pressure (typically <100 mmHg) to minimize the chances of aortic injury or bleeding. Consider the following interventions in stepwise fashion:
Central venous decannulation necessitates surgical compression of the right atrium and/or caval veins. This will temporarily reduce venous return and may irritate conduction pathways. Patients with normal post-bypass function and adequate preload usually tolerate venous decannulation with minimal intervention. In less stable patients, prior to decannulation, consider Trendelenburg positioning and titrated boluses of a medication with a vasopressor component (typically norepinephrine 8-24 mcg, vasopressin 0.5-2 units, or epinephrine 8-16 mcg) to increase vascular resistance. With severe hypotension, release of atrial/caval pressure to allow hemodynamic recovery must occur as early as possible. Communication between the anesthesiologist and surgeon facilitates safer patient care and guides which maneuvers are necessary at that specific moment.
Sustained SVT from venous decannulation is usually treated with immediate synchronized electrical cardioversion rather than pharmacologically. Electrical cardioversion is the most rapid way to restore normal rhythm to an already compromised post-bypass heart.
Post-Bypass Cardiac Manipulation
Lifting and manipulation of the heart is common post-bypass for inspection of graft anastomoses and suture lines, and to identify and isolate bleeding sources. Optimization of preload, afterload, inotropy, and cardiac output and communication between the surgeon and anesthesiologist will help facilitate a smoother and less eventful process.
Clear communication between the surgical and anesthesia teams is paramount. By this point in the surgical procedure, the anesthesia team is familiar with the intervention needed to accommodate mild to moderate hemodynamic insults. Preemptive Trendelenburg positioning or vasopressor/inotrope boluses are preferred over reactionary post-manipulation treatment of hypotension. This latter scenario is particularly dangerous in patients with reduced right ventricular function who require high inotrope dosages. In those patients, hemodynamic collapse requiring emergent return to cardiopulmonary bypass can result from the concomitant effects of surgical manipulation, volume loading, and protamine administration.
Chest Closure
Sternal re-approximation may result in a variable degree of right-sided compression and a reduction in venous return. The anesthesia practitioner must carefully trend data from available monitors (echocardiography, electrocardiogram, pressure waveforms/values, cardiac index, and sometimes, venous saturation). Significant hemodynamic compromise can occur at this time from one or more of three etiologies:
1. Hypovolemia or relative hypovolemia: Occult hypovolemia can clinically manifest with sternal closure. Hypovolemia should be temporized with vasopressor bolus (typically norepinephrine 8-24 or vasopressin 0.5-2 units) and Trendelenburg positioning while volume is carefully loaded. In vasoplegic states, dilation of high capacitance vascular beds creates a relative hypovolemia and often necessitates high doses of vasopressors. Severe vasoplegia from a systemic inflammatory state may exist, either from the bypass circuit, from an allergic reaction, or from blood product administration [1].Empiric treatment of an inflammatory etiology should be considered (typically diphenhydramine 50mg, hydrocortisone 100mg, and/or titrated epinephrine
2. Global right ventricular failure: When post-bypass right ventricular function is severely reduced or dependent on high dose inotropic agents, even mild sternal compression can result in hemodynamic collapse. Additionally, hypoxia and hypercarbia from acute lung injury and pulmonary dysfunction are often exacerbated with sternal closure, which can also lead to right ventricular failure. A failing right ventricle necessitates a strong inotrope bolus (typically epinephrine 32-500 . Reverse Trendelenburg positioning will reduce right-sided pressures but will also reduce venous return, so the effect of this maneuver is mixed. Additionally, a low threshold should exist for sternal re-separation, as right ventricular failure can quickly result in circulatory arrest. Should a second attempt at sternal re-approximation be made following recovery of right ventricular function, it should be done after the following interventions:
3. Coronary artery graft compression: Bypass grafts that course along the anterior heart are at risk for kinking or compression upon chest closure. Hemodynamic compromise with concomitant ischemic electrocardiogram changes and new or worsening regional wall abnormalities should warrant sternal re-separation and graft inspection. Inotropic support should be increased to temporize hemodynamic instability. However, new onset ischemia will also lower the threshold for arrhythmias, and increasing β-agonists should be done with care. The providers should anticipate sudden onset SVT, VT, or VF. In this scenario, emergent chest re-separation to ensure graft patency must occur along, with electrical cardioversion/defibrillation.
Transport
Transport of the open-chest cardiac procedure patient from the operating room to the intensive care unit is highly tenuous. Practically, providers should confirm an adequate volume of vasoactive/inotropic/antiarrhythmic infusions and have syringes of, at minimum, norepinephrine (16 mcg/mL), epinephrine (16 mcg/mL), and vasopressin (1-2 units/mL) accessible for emergent bolusing. Intravenous lines should be easily accessible, clean and not touching the floor. A defined port to administer boluses should be easily accessible. The right atrial port of the pulmonary artery catheter is ideal and with easy access to the transducer flush system will ensure drug is delivered quickly and centrally. Transport should be executed only when hemodynamics are stable on vasoactive/inotropic/antiarrhythmic infusions and frequent boluses are not required.
Typically, mean arterial pressure most often increases during patient transport, as inhaled anesthetic gas is discontinued. An adequate level of intravenous sedative should already be achieved prior to leaving the operating room to prevent both awareness and the sometimes-sizeable accompanying increase in blood pressure. Sedative choice varies but either a propofol or dexmedetomidine infusion is most commonly used.
VIII. Off-Pump Coronary Artery Bypass Graft Surgery
Distal Anastomoses
Variable periods of coronary artery occlusion are required for distal bypass graft anastomosis. The severity and territory of subsequent tissue ischemia depends on the myocardium’s collateral blood flow. During distal grafting, mean arterial pressure should be maintained at the upper limit of the patient’s baseline to promote collateral flow to poorly perfused areas [10]. Norepinephrine infusion (typically 0.04-0.15 mcg/kg/min) is usually the first line, as it is easily titrated and its β-agonism provides some inotropic support while not significantly promoting ischemia-induced arrhythmias. Euvolemia is the goal during these procedures and should reduce the need for strong afterload support. However, norepinephrine’s vasopressor component augments blood pressure during periods of compromised myocardial function. Phenylephrine (typically 0.1-1.5 mcg/kg/min), vasopressin (typically 0.04-0.1 units/minute) dobutamine (typically 5-10 mcg/kg/min), isoproterenol (typically 1-5 mcg/min), or epinephrine (typically 0.04-0.15 mcg/kg/min) infusions are also options, though each carries a disadvantage. Specifically, phenylephrine lacks inotropic support [1]. Dobutamine, isoproterenol, and epinephrine, augment chronotropy but are more arrhythmogenic than norepinephrine [8]. Pacing, atrial or atrioventricular, can be a very useful adjunct if there is significant bradycardia or if the rhythm is nodal or if there is heart block.
Marginal and posterior coronary artery targets necessitate significant repositioning of the heart. The act of repositioning will result in a 2-4 beat duration of myocardial stunning that often is self-limited. However, markedly increased vasopressor/inotrope requirements are often needed for these targets [10]. Trendelenburg positioning and a high normal heart rate (80-90 beats per minute) can help support mean arterial pressure.
Coordination between the surgeon and the anesthesia practitioner is critical. Taking the time to position, assess impact on hemodynamics and to reposition with reassessment of hemodynamics best achieves the dual goal of optimizing both the position and the hemodynamics. Together the surgeon and the anesthesia practitioner can decide whether hemodynamics can be successfully maintained pharmacologically for the full duration of each distal anastomosis to prevent emergent repositioning during graft anastomosis. Lifting the heart as compared to compressing the heart is the key to success.
During distal bypass grafting, progressive hypotension, increasing inotrope requirements, diminishing inotropic effects with the need for inotrope/vasopressor boluses, worsening ischemic mitral regurgitation, ischemic electrocardiogram changes, and new frequent premature ectopic beats indicate potential cardiac arrest. If possible, a shunt should be placed past the anastomosis site, and the heart should be placed in its normal position as soon as feasible.
Proximal Anastomoses
Off-pump proximal bypass graft anastomoses require a partial aortic side clamp (C-clamp) or a clamp-less hemostatic seal. Conventionally, the systolic blood pressure goal is usually 90-100 mmHg to prevent disruption of aortic segment isolation, bleeding, and aortic tissue injury.
Immediately after the last distal anastomosis, the heart is placed into its usual position. The vasopressor/inotropic infusions needed to maintain mean arterial pressure through distal grafting now usually result in a supra-physiologic systolic pressure. Cessation of vasopressor and inotropic support, as well as reverse Trendelenburg positioning, help to lower systolic pressure. Vasodilator boluses (typically nitroglycerine 50 mcg or nicardipine 100 mcg) can expedite the process, but care should be taken to avoid significant hypotension.
Usually, the ventricular function is stunned from manipulation and temporary periods of ischemia during distal grafting. Even patients with normal preoperative function typically require some low level hemodynamic support to maintain a systolic pressure of 90-100 mmHg. One algorithm to achieve this tight blood pressure management is as follows:
Coordination between the surgeon and the anesthesia practitioner facilitates a smoother transition to a controlled systolic pressure of the required 90 to 100 mmHg. As the systolic pressure goal of 90-100 mmHg is below most patients’ physiologic baseline, monitoring for signs of ischemia is important.
IX. Intraoperative Pharmacotherapy and Treatment Algorithms for Specific Arrhythmias
Arrhythmias are common during the open-chest cardiac procedure secondary to a variety of factors, including myocardial ischemia from vaso-occlusive disease or cardiopulmonary bypass, preexisting cardiac pathology, maladaptive chamber remodeling, electrolyte abnormalities, hypothermia, and physical manipulation by the surgical team. Certain arrhythmias are more common during particular phases of the procedure, such as SVT during central venous cannulation or VT/VF following aortic cross-clamp removal.
Briefly, the major arrhythmias are listed below, each with an accompanying diagnostic/therapeutic algorithm that is applicable for most stages of the open-chest cardiac procedure. These algorithms involve components of the classic ACLS pathways [1], but are tailored to the intraoperative cardiac surgery setting. Hypoxia and hypercarbia should be immediately addressed since arrhythmias triggered by a failure of gas exchange are usually refractory to other therapies. Moreover, rapidly progressive hemodynamic instability and loss of pulsatility will occur with depleted oxygen stores or severe respiratory acidosis. Of note, the first few steps of each pathway are often executed simultaneously in the dynamic operating room setting.
Sinus Tachycardia
Note: Correcting sinus tachycardia revolves around etiology identification and correcting the underlying insult. Below is a suggested order for the sequential consideration of the differential diagnoses. Although much less common, time-sensitive gas exchange failure is addressed first, followed by the more common diagnoses of light anesthetic levels, hypovolemia and ischemia.
Differential Diagnoses and Treatment Algorithm
1. Gas exchange failure: Hypoxemia and/or hypercarbia
Treatments: Increase FiO2, confirm endotracheal tube position, increase minute ventilation, increase positive end expiratory pressure, perform recruitment maneuvers, suction the airway. Consider bronchospasm and treat with bronchodilators if appropriate. Usually one or more of those maneuvers will correct the problem. With continued gas exchange failure, consider using an ICU ventilator and change mechanical ventilation mode. Extracorporeal membrane oxygenation can be used if all else fails to improve the gas exchange.
2. Light anesthetic levels
Treatments: Increase inhaled anesthetic concentration, supplement intravenous anesthetic, (i.e., a small, 10-30 mg propofol bolus), give a narcotic bolus, and, if necessary, temporize using short-acting β1-blockade (esmolol).
3. Hypovolemia
Treatments: Volume administration, Trendelenburg positioning, temporizing vasopressor bolus/infusion.
4. Ischemia
Treatments: Vasopressor to increase perfusion pressure, rate control with β1-blockade (esmolol, metoprolol, labetalol), surgeon should check graft positioning and reassess graft flow. If ischemia persists, discussion with surgeon to determine if heparin should be given to counteract thrombogenesis, and if the culprit lesion should be bypassed.
5. Medication induced (glycopyrrolate, β-agonists)
Treatments: Cessation or dose reduction of offending agents, temporizing β1-blockade (esmolol).
6. Less common diagnoses: Malignant hyperthermia, serotonin syndrome, substance withdrawal.
Sinus Bradycardia
Treatment Algorithm
1. Correct hypoxia (especially if acute, severe, or progressive).
Treatments: Increase FiO2, increase positive end expiratory pressure, recruitment maneuvers, airway suctioning, endotracheal tube position reconfirmation, change mechanical ventilation mode, ICU ventilator use, extracorporeal membrane oxygenation, cardiopulmonary bypass.
(Often executed as steps 2-4 are being addressed)
2. Eliminate acute vagal stimulation.
Treatments: Pause in surgical manipulation.
3. Rapidly correct severe bradycardia (<40 beats per minute) or bradycardia causing hemodynamic instability.
Treatments: During cardiac surgery, pacing is usually readily available and is the first line choice. If pacing is not available, Atropine (typically 0.2-1 mg) and/or epinephrine (typically 16-32 mcg).
4. Temporize unwanted mild to moderate bradycardia.
Treatments: Pacing if available, Glycopyrrolate (typically 0.2-0.4 mg), ephedrine (typically 5-10 mg), epinephrine (typically 8-16 mcg).
5. Assess for other common causes: Deep anesthesia, ischemia, medication induced (β-blockade, central calcium channel blockade, phenylephrine, narcotics), sick sinus syndrome.
Supraventricular Tachycardia (Atrial Fibrillation/Atrial Flutter/Accessory Pathway SVT/Junctional Tachycardia)
Treatment Algorithm
1. Correct gas exchange failure (especially if acute, severe, or progressive).
Treatments: Increase FiO2, increase minute ventilation, increase positive end expiratory pressure, recruitment maneuvers, airway suctioning, endotracheal tube position reconfirmation, change mechanical ventilation mode, ICU ventilator use, extracorporeal membrane oxygenation, cardiopulmonary bypass.
(Executed as steps 2-4 are being addressed)
2. Pause surgical manipulation to promote cardioversion and ensure stability.
3. Assess for hemodynamic stability.
4. With hemodynamic instability, pulslessness, or worsening cardiac ischemia, initiate emergent electrical cardioversion (versus cardiopulmonary bypass, if readily available), and provide supportive measures.
Treatments: Synchronized electrical cardioversion (typically biphasic 10-200 joules or monophasic 100-200 joules) or cardiopulmonary bypass.
Supportive measures: Volume administration, vasopressor/inotrope bolus, sodium bicarbonate (typically 50 mEq, assuming adequate ability to eliminate carbon dioxide), chest compressions/cardiac massage (when pulseless), Trendelenburg positioning.
5. With hemodynamic stability and an accessory pathway rhythm, attempt chemical cardioversion and/or rate modulation with procainamide or amiodarone.
6. With hemodynamic stability and either a non-accessory pathway rhythm or a rhythm with an unknown conduction pathway, consider electrical or chemical cardioversion while investigating for etiology.
Treatments: Synchronized electrical cardioversion (typically biphasic 10-200 joules or monophasic 100-200 joules), adenosine (typically 6-12 mg bolus), esmolol (typically 10-40 mg bolus), phenylephrine (typically 100-300 mcg bolus), amiodarone (150 mg slow push).
(If refractory to above treatments, consider accessory pathway rhythm and address step 5)
7. Assess for and treat other common causes: Ischemia, hypotension, hypovolemia, electrolyte abnormalities, hypothermia, acid-base imbalance, light anesthesia.
8. In hemodynamically stable patients refractory to cardioversion, consider rate control while investigating for etiology.
Treatments: Esmolol (typically 50-200 mcg/kg/min)
Ventricular Tachycardia (Monomorphic/Long-QT polymorphic/Normal-QT polymorphic), Ventricular Fibrillation
Treatment Algorithm
1. Correct gas exchange failure (especially if acute, severe, or progressive).
Treatments: Increase FiO2, increase minute ventilation, increase positive end expiratory pressure, recruitment maneuvers, airway suctioning, endotracheal tube position reconfirmation, change mechanical ventilation mode, ICU ventilator use, extracorporeal membrane oxygenation, cardiopulmonary bypass.
(Executed as steps 2-4 are being addressed)
2. Pause surgical manipulation to promote defibrillation and ensure stability.
3. Assess for hemodynamic stability.
4. With hemodynamic instability, pulslessness, or worsening cardiac ischemia, deliver emergent unsynchronized electrical shocks (versus cardiopulmonary bypass, if immediately available), administer intravenous antiarrhythmics, and provide supportive measures.
Primary treatments:
Unsynchronized electrical shocks (typically biphasic 200 joules or monophasic 360 joules) or cardiopulmonary bypass.
Chest compressions/cardiac massage (when pulseless or with very low MAP)
Intravenous antiarrhythmics:
Lidocaine (typically 100 mg)
Amiodarone (typically 150-300 mg)
Magnesium sulfate (typically 2 gm) -- for suspected long-QT polymorphic VT
Supportive measures:
Vasopressor/inotrope bolus (typically epinephrine 100-1000 mcg)
Sodium bicarbonate to treat acidosis (typically 50 mEq, assuming adequate ability to eliminate carbon dioxide),
Trendelenburg positioning
5. With hemodynamic stability, deliver unsynchronized electrical shocks and administer intravenous antiarrhythmics
Treatments:
Unsynchronized electrical shocks (typically biphasic 200 joules or monophasic 360 joules)
Intravenous antiarrhythmics:
Lidocaine (typically 100 mg)
Amiodarone (typically 150 mg slow push)
Magnesium sulfate (typically 2 gm)--for suspected long-QT polymorphic VT
6. Assess for and treat other common causes: Ischemia, hypotension, hypovolemia, electrolyte abnormalities, hypothermia, acid-base imbalance
7. Following successful cardioversion of a polymorphic ventricular tachycardia, assess the QT interval. To prevent the recurrence of a long-QT polymorphic VT, perform maneuvers to shorten long-QT segments
Treatments:
Magnesium sulfate (typically 2 gm, if not already administered)
Chronotropic augmentation (atropine, isoproterenol, dobutamine, epinephrine, ventricular pacing)
Avoidance of medications that prolong the QT-interval
Asystole
1. Begin chest compressions/cardiac massage or initiate cardiopulmonary, bypass, if immediately available
2. For open chest cardiac procedures, pacing wires are immediately available and should be used to attempt to pace
3. Attempt transcutaneous/transvenous/epicardial ventricular pacing as soon as possible, e.g., via right ventricular port of the pulmonary artery catheter
4. Promote rhythm development with epinephrine (typically 1000 mcg every 3-5 minutes), and maintain SVR with vasopressin (typically 20-40 units)
5. Consider administration of sodium bicarbonate to treat acidosis (typically 50 mEq, assuming adequate ability to eliminate carbon dioxide),
6. Upon restoration of a perfusable rhythm, assess for and treat common causes: Gas exchange failure, ischemia, hypotension, hypovolemia, electrolyte abnormalities, particularly hyperkalemia, hypothermia, and acid-base imbalance
X. Summary
This chapter has presented comprehensive and detailed information designed to provide scientific basis for managing adult patients having cardiac surgery, as well as rationale for selection of different inotropes, vasopressors, and combinations of drugs to provide optimal outcomes while minimizing drug side effects. Doing this well requires scientific knowledge, experience, and finesse akin to art. Knowledge of drugs’ pharmacodynamics and pharmacokinetics, the typical doses used, potential side effects, and when to consider adding a second, third and/or more drugs is critical. Of utmost importance is well-defined and clear communication between all the operating room team members. Standardization in communication pathways and supplemental checklists for critical times, such as going onto and weaning from cardiopulmonary bypass, helps reduce errors and morbidities. Additionally, having all team members aware of potential issues, and where and when in the process to anticipate certain complications, requires each team member to be able to communicate freely and to ask questions when unsure.
To decrease a persistently high mean arterial pressure, an infusion of nitroglycerine (typically 0.1-10 mcg/kg/min) or nicardipine (typically 1-5 mcg/kg/min) is standard. In the event of acutely elevated MAP, a bolus of nitroglycerine (typically 50-200 mcg) or nicardipine (typically 100-300 mcg) can be administered via the bypass oxygenator. Decreasing pump flow rate or increasing the inhaled volatile anesthetic concentration are temporary adjustments that should be made only in the event of severe hypertension and should be used briefly until control can be achieved with a vasodilator. Prolonged low flow rate causes poor tissues perfusion and acidosis.
V. Deep Hypothermic Circulatory Arrest
Mean Arterial Pressure Goals with Selective Cerebral Perfusion
Deep hypothermic circulatory arrest is often performed with selective cerebral perfusion via one of two routes: retrograde via the superior vena cava or anterograde via one carotid artery with subsequent contralateral perfusion through the Circle of Willis. Normally, the vasoconstriction from profound induced hypothermia (often as low as 23-25°C) eliminates the need for vasopressors. While controversial, cerebral oxygen saturation monitoring can be used to gauge the adequacy of cerebral perfusion [1]. During selective anterograde perfusion via one carotid artery, for example, a low cerebral oxygen saturation reading on the contralateral side may signal poor Circle of Willis flow. In this situation, a trial of vasopressor via the bypass oxygenator may help to augment flow beyond the Circle of Willis.
VI. Weaning from Cardiopulmonary Bypass
Weaning off cardiopulmonary bypass is a dynamic and individualized process. The combination and dosages of specific vasoactive/inotropic/antiarrhythmic medications is often variable during this period; however, when optimizing physiology during the bypass wean, certain important caveats exist that are elaborated upon below.
Rhythm
Termination of cardiopulmonary bypass requires a rhythm that will allow adequate perfusion. The rhythm can be an intrinsic sinus, an accelerated junctional, paced (atrial, ventricular, or atrioventricular), or occasionally, chronic baseline atrial fibrillation or atrial flutter. Restoration of coronary artery blood flow, normal-range electrolyte levels, an adequately rewarmed core body temperature, (36-37 degrees C), and correction of significant acid-base derangement must be addressed. Once these are optimized, a rhythm typically develops either: 1) spontaneously, 2) via cardioversion of a supraventricular tachycardia (SVT)/ventricular tachycardia (VT) 3) via defibrillation of ventricular fibrillation (VF), or 4) via pacing for asystole, significant or relative sinus bradycardia, or heart block with slow ventricular response. Persistent, recurrent ventricular fibrillation requiring multiple, unsuccessful defibrillation attempts may be related to persistent cardiac ischemia and requires a check of the newly re-vascularized vessels a to rule-out kinking or other causes of lack of adequate flow.
It is important to remember that, in the minutes following aortic cross-clamp removal and restoration of coronary artery blood flow, the myocardium is prone to arrhythmias. Delaying giving calcium (10 minutes at Emory) following unclamping allows time for myocardial washout of ischemic mediators. In patients with frequent ectopic beats or a varying rhythm during the bypass wean, the following pharmacologic interventions should be considered to help maintain stability:
- Limit the dose of arrhythmogenic agents whenever possible, especially -agonists
- Antiarrhythmic medication bolus, such as lidocaine (typically 100 mg, for ventricular arrhythmias), esmolol (typically 10-40 mg, for supraventricular arrhythmias), or amiodarone (typically 150-300 mg over 5-10 minutes, for ventricular and supraventricular arrhythmias)
- Antiarrhythmic medication infusion, such as lidocaine (typically 2-4 mg/min, for ventricular arrhythmias), esmolol (typically 50-20 , or amiodarone (after bolus of 150-300 mg, the infusion is 1 mg/min for six hours then 0.5mg/min for six hours, then re-ealuation, typically by cardiologist in ICU), for ventricular and supraventricular arrhythmias)
For treatment of sustained arrhythmias that do not support adequate perfusion, specifically supraventricular tachycardia (SVT), ventricular tachycardia (VT), or ventricular fibrillation (VF), please refer to the below arrhythmia section.
Chronotropy
During cardiopulmonary bypass wean, the target heart rate for most open chest cardiac procedures falls within the range of 70-90 beats per minute. This target ensures both an adequate rate and adequate diastolic filling time and a reasonable myocardial workload. In situations where stroke volume potential is maximized, increasing cardiac output is achieved with higher target heart rates. Occasionally, the heart rate is targeted as high as 90-110 beats per minute for this reason. It should be noted, however, that heart rates above 120 beats per minute increasingly compromise diastolic filling time and subsequently decrease cardiac output.
Adequate Heart Rate and Rhythm
- May occur spontaneously once re-warmed
- May require defibrillation
- May require drugs
- May require pacing
Pharmacologic heart rate augmentation is most often achieved with a β-agonist. Sometimes, when the heart rate slowly increases following cross-clamp removal, a single bolus of a short acting β-agonist (typically epinephrine 8-16 mcg) will expedite the process. B-agonist should be given after allowing for myocardial reperfusion, typically approximately 10 minutes after the aortic cross-clamp is removed.
Most commonly, a β-agonist infusion is started to augment the heart rate of a perfusable rhythm. Chronotropy is most specifically enhanced with dobutamine (typically 5-10 mcg/kg/min) and isoproterenol (typically 1-5 mcg/min), though these agents also augment inotropy. Of the two, dobutamine is the most β1 specific, with only limited β2 and α1 effects. Isoproterenol stimulates both β1 and β2 receptors [1]. Both dobutamine and isoproterenol require 5-10 minutes of administration before full effect develops. Additionally, both will result in some degree of vasodilation which can lead to hypotension especially if the patient is relatively hypovolemic [1]. A vasopressor infusion is commonly used to compensate for the vasodilation. Isoproterenol in large doses (> 10 mcg/min), commonly causes serious ventricular arrhythmias [6]. An alternative agent should be considered when β1 augmentation is required particularly in the setting of recurrent arrhythmias.
For combined chronotropy, inotropy, and vasopressor augmentation, epinephrine (typically 0.01-0.15 mcg/kg/min) is potent, rapidly titratable, and effective in all three domains. The use of epinephrine can simplify the patient’s medication profile, but separating the myocardial and vascular effects is not possible. It should be noted that epinephrine infusions frequently cause hyperglycemia and hypokalemia. While norepinephrine has both β and α effects, heart rate is usually unaltered [6]. In younger patients, however, a larger β effect is often seen with a mild dose-related increase in heart rate.
Inotropy
While some patients can be weaned off cardiopulmonary bypass without inotropic support, most require some degree of pharmacologic augmentation secondary to pre-existing ventricular dysfunction, myocardial stunning from surgical manipulation, or from bypass-induced ischemic injury. These factors will help formulate the plan for inotropic support. Consider the following pearls when deciding the number, order, and type of inotropic agents to administer for the bypass wean:
First Agent:
- Norepinephrine (typically 0.04-0.15
- Dobutamine Isoproterenol . While there are subtle differences between these two agents (
- Milrinone (typically 0.25-0.5 mcg/kg/min; loading dose of 50 mcg/kg over 10 minutes)- Milrinone is useful when longer-term inotropic support is anticipated, as is often the case with elderly patients, markedly reduced baseline left ventricular function, and long bypass durations.Milrinone’s vasodilating properties also help reduce PVR in the setting of pulmonary hypertension and right ventricular dysfunction [1]. Additionally, milrinone is ideal in patients prone to arrhythmias, as it is less arrhythmogenic than β-agonists [21]. Unfortunately, the systemic vasodilation often necessitates significant vasopressor dosages. The loading dose of milrinone can markedly reduce mean arterial pressure. As an alternative, starting a milrinone infusion as rewarming is begun can minimize sudden shifts in blood pressure while allowing enough time for adequate drug levels to be achieved. Another alternative is to administer the loading dose, prior to discontinuing CPB in divided portions to minimize the dilating effects.
- Epinephrine (typically 0.04-0.15 Epinephrine is usually required for bypass wean in high morbidity patients who have pre-bypass hemodynamic instability, severe left ventricular dysfunction and/or an anticipated unstable post-bypass period.As a “pan-agonist” catecholamine (chronotropy, inotropy, and vasopressor), it addresses all areas of the sympathetic nervous system that may require augmentation. Failure of an inotropic response to high dose epinephrine usually signals sympathetic exhaustion and is a poor prognostic sign.
Combination drug therapy (norepinephrine, epinephrine, milrinone and vasopressin) is commonly used in patients who require significant support. If additional support is needed, an IABP or another type mechanical assist device is often placed.
Just prior to the beginning of bypass wean, approximately 10 minutes after aortic cross-clamp has been removed, calcium chloride is administered to correct hypocalcemia. This will also provide a short-duration boost in inotropy. During the bypass wean, choice(s) for inotropic support will be tested with real-time indices, including echocardiography, arterial waveform pulsatility, visual inspection of the heart, and venous oxygen saturation values from the pump. The choice to bolus inotropes to boost depressed contractility should be made carefully. In patients with preserved pre-bypass ventricular function and short bypass duration, a single bolus of epinephrine (typically 8-16 mcg) can restore normal contractility. Additionally, sudden myocardial stunning from coronary artery air entrainment is effectively treated with epinephrine (typically 16 mcg) and a vasopressor (typically vasopressin 1-2 units) bolus. In most situations, however, titration of infusions to achieve an acceptable baseline level of inotropy will ensure a more stable wean and reduce the chances of sudden post-bypass hypotension.
Preload
A successful cardiopulmonary bypass wean necessitates optimal preload (volume). Rarely are vasoactive/inotropic/antiarrhythmic medications used to manage preload during the wean. Communication between the anesthesiologist, perfusionist, and surgeon allows gradual filling of the ventricles as the pump flow is decreased while assessing the pulmonary artery pressures, the right atrial pressure and the mean arterial pressure. A slow bypass wean, particularly in patients with severely impaired ventricular function is optimal and can avert the need to rapidly go back onto bypass. Slowly weaning allows drugs to be added, effects to be seen and better control of MAP, PA pressures, RA pressure and cardiac function.
Overfilling or distending a ventricle is poorly tolerated which argues for a slow wean. Particularly at risk for over-distension is a poorly functioning right ventricle. Looking at the heart over the drapes and correlating with the pressures, PA, RA, and MAP as well as using echocardiography helps with proper filling of the heart and a continued wean from bypass.
Afterload
SVR:
Due to the inflammatory state commonly induced by cardiopulmonary bypass, optimal afterload usually requires a vasopressor infusion. The ideal MAP for termination of bypass is usually that of the patient’s physiologic baseline. This will ensure that organs are perfused within the range of intrinsic autoregulation. In the setting of pre-bypass ischemic myocardium, higher goal mean pressures may be warranted to ensure maximum perfusion and oxygen delivery to stunned or hibernating myocardial segments. Dynamic outflow tract obstructions also call for higher afterload [1]. Conversely, evaluation of suture line integrity or concern for aortic intimal integrity may warrant a lower goal mean arterial pressure, at least temporarily. Issues with significant impact on the optimal mean arterial pressure should be addressed by the surgeon and the anesthesiologist.
Vasopressor infusion requirements for the bypass wean are commonly predicted during the rewarming phase. Those patients necessitating large vasopressor dosages during rewarming will usually also needed high afterload support during wean and following cardiopulmonary bypass. Causes for refractory vasoplegia should be investigated and treated before the bypass wean (see “Cardiopulmonary Bypass” section for specific causes and therapies). Increased vasopressor requirements will also be needed should a vasodilating inotrope, such as milrinone, dobutamine, or isoproterenol, be used.
Phenylephrine is rarely used for bypass wean as some level of inotropic augmentation is also desired. The baseline vasopressor of choice is usually norepinephrine (typically 0.04-0.15 mcg/kg/min) due to its additional inotropic effect. Vasopressin (typically 0.04-0.1 units/minute) is often added as a second agent, but because it minimally affects the pulmonary vasculature, it may be an ideal first choice with pulmonary hypertension or right ventricular dysfunction. Because epinephrine (typically 0.04-0.15 mcg/kg/min) has potent chronotropic, inotropic, and vasoconstrictive properties, it is often added when additional support is needed.
Vasodilators are rarely needed for bypass wean, however patients with poorly controlled hypertension preoperatively and with good left ventricular function may require treatment. Typically, nitroglycerine (0.1-10 mcg/kg/min) with its very short half-life is the best vasodilator choice during this dynamic period. Patients with long standing uncontrolled hypertension or those with preserved left ventricular function after aortic valve replacement for aortic stenosis may have severe left ventricular hypertrophy and a poorly-compliant left ventricle, which puts them at risk for disproportionately large changes in mean arterial pressure with small changes in volume which can lead to significant hyper or hypotension.
As with determining inotropic support, choosing vasoactive support can be aided by comparing echocardiography, visual inspection of the heart and arterial waveform pulsatility, and with venous oxygen saturation values from the bypass machine. The decision to bolus vasoactive medications should be made carefully. When vasopressor infusion requirements have been overestimated and volume-loading results in significant hypertension, a vasodilator bolus can temporize hemodynamics while vasopressor infusions are down titrated. In most cases, taking the time (i.e. a slow bypass wean) to achieve steady state infusion dosages of inotrope and vasopressors, in lieu of medication boluses, will ensure a smoother bypass wean.
Sudden myocardial stunning from coronary artery air entrainment, usually associated with sudden ST segment elevation in inferior leads, is effectively treated with vasopressor and inotrope boluses.
Pulmonary Vascular Resistance:
(Right Ventricular Afterload)
Reducing PVR decreases right ventricular afterload and decreases right ventricular myocardial work. Pulmonary arteriolar constriction is minimized with adequate levels of anesthesia, analgesia, oxygen, and carbon dioxide. Additionally, in the setting of right ventricular compromise, vasopressin and milrinone are the preferred vasopressor and inotrope, respectively, as vasopressin minimally constricts and milrinone dilates the pulmonary vasculature [1].
For bypass wean, inhaled epoprostenol (typically 50 ng/kg/min) or inhaled nitric oxide (typically 0.5-80 ppm) should be added in the setting of baseline high pulmonary artery pressures and when the risk of post-bypass right ventricular failure is high. Both selectively dilate the pulmonary vasculature [1]. Inhaled nitric oxide is very expensive and requires a cumbersome delivery system that complicates patient transport. When using nitric oxide, having respiratory therapy support facilitates optimal patient care during a typically complex, dynamic, challenging hemodynamic state.
VII. Post-Cardiopulmonary Bypass
Decannulation
As with central aortic cannulation, central aortic decannulation requires a short-term reduced systolic arterial pressure (typically <100 mmHg) to minimize the chances of aortic injury or bleeding. Consider the following interventions in stepwise fashion:
- Reverse Trendelenburg positioning
- Titrated vasodilator boluses.
- Nitroglycerine (25-50 mcg boluses) is most commonly used due to very short duration of action.
- Nicardipine (100-200 mcg boluses) with its longer duration of action is not commonly used during aortic decannulation.
- Reduction in dose of vasopressor or vasopressor/inotropic infusions.
Central venous decannulation necessitates surgical compression of the right atrium and/or caval veins. This will temporarily reduce venous return and may irritate conduction pathways. Patients with normal post-bypass function and adequate preload usually tolerate venous decannulation with minimal intervention. In less stable patients, prior to decannulation, consider Trendelenburg positioning and titrated boluses of a medication with a vasopressor component (typically norepinephrine 8-24 mcg, vasopressin 0.5-2 units, or epinephrine 8-16 mcg) to increase vascular resistance. With severe hypotension, release of atrial/caval pressure to allow hemodynamic recovery must occur as early as possible. Communication between the anesthesiologist and surgeon facilitates safer patient care and guides which maneuvers are necessary at that specific moment.
Sustained SVT from venous decannulation is usually treated with immediate synchronized electrical cardioversion rather than pharmacologically. Electrical cardioversion is the most rapid way to restore normal rhythm to an already compromised post-bypass heart.
Post-Bypass Cardiac Manipulation
Lifting and manipulation of the heart is common post-bypass for inspection of graft anastomoses and suture lines, and to identify and isolate bleeding sources. Optimization of preload, afterload, inotropy, and cardiac output and communication between the surgeon and anesthesiologist will help facilitate a smoother and less eventful process.
Clear communication between the surgical and anesthesia teams is paramount. By this point in the surgical procedure, the anesthesia team is familiar with the intervention needed to accommodate mild to moderate hemodynamic insults. Preemptive Trendelenburg positioning or vasopressor/inotrope boluses are preferred over reactionary post-manipulation treatment of hypotension. This latter scenario is particularly dangerous in patients with reduced right ventricular function who require high inotrope dosages. In those patients, hemodynamic collapse requiring emergent return to cardiopulmonary bypass can result from the concomitant effects of surgical manipulation, volume loading, and protamine administration.
Chest Closure
Sternal re-approximation may result in a variable degree of right-sided compression and a reduction in venous return. The anesthesia practitioner must carefully trend data from available monitors (echocardiography, electrocardiogram, pressure waveforms/values, cardiac index, and sometimes, venous saturation). Significant hemodynamic compromise can occur at this time from one or more of three etiologies:
1. Hypovolemia or relative hypovolemia: Occult hypovolemia can clinically manifest with sternal closure. Hypovolemia should be temporized with vasopressor bolus (typically norepinephrine 8-24 or vasopressin 0.5-2 units) and Trendelenburg positioning while volume is carefully loaded. In vasoplegic states, dilation of high capacitance vascular beds creates a relative hypovolemia and often necessitates high doses of vasopressors. Severe vasoplegia from a systemic inflammatory state may exist, either from the bypass circuit, from an allergic reaction, or from blood product administration [1].Empiric treatment of an inflammatory etiology should be considered (typically diphenhydramine 50mg, hydrocortisone 100mg, and/or titrated epinephrine
2. Global right ventricular failure: When post-bypass right ventricular function is severely reduced or dependent on high dose inotropic agents, even mild sternal compression can result in hemodynamic collapse. Additionally, hypoxia and hypercarbia from acute lung injury and pulmonary dysfunction are often exacerbated with sternal closure, which can also lead to right ventricular failure. A failing right ventricle necessitates a strong inotrope bolus (typically epinephrine 32-500 . Reverse Trendelenburg positioning will reduce right-sided pressures but will also reduce venous return, so the effect of this maneuver is mixed. Additionally, a low threshold should exist for sternal re-separation, as right ventricular failure can quickly result in circulatory arrest. Should a second attempt at sternal re-approximation be made following recovery of right ventricular function, it should be done after the following interventions:
- Reconfirm euvolemia
- Maximize support with inotropic agents
- Addition of an inhaled pulmonary vasodilator (epoprostenol or nitric oxide), if not already being administered
- Optimize gas exchange (consider using an ICU ventilator that delivers more accurate tidal volumes and allows additional ventilation modes.)
- Reverse Trendelenburg positioning to reduce right-sided pressures, if tolerated
3. Coronary artery graft compression: Bypass grafts that course along the anterior heart are at risk for kinking or compression upon chest closure. Hemodynamic compromise with concomitant ischemic electrocardiogram changes and new or worsening regional wall abnormalities should warrant sternal re-separation and graft inspection. Inotropic support should be increased to temporize hemodynamic instability. However, new onset ischemia will also lower the threshold for arrhythmias, and increasing β-agonists should be done with care. The providers should anticipate sudden onset SVT, VT, or VF. In this scenario, emergent chest re-separation to ensure graft patency must occur along, with electrical cardioversion/defibrillation.
Transport
Transport of the open-chest cardiac procedure patient from the operating room to the intensive care unit is highly tenuous. Practically, providers should confirm an adequate volume of vasoactive/inotropic/antiarrhythmic infusions and have syringes of, at minimum, norepinephrine (16 mcg/mL), epinephrine (16 mcg/mL), and vasopressin (1-2 units/mL) accessible for emergent bolusing. Intravenous lines should be easily accessible, clean and not touching the floor. A defined port to administer boluses should be easily accessible. The right atrial port of the pulmonary artery catheter is ideal and with easy access to the transducer flush system will ensure drug is delivered quickly and centrally. Transport should be executed only when hemodynamics are stable on vasoactive/inotropic/antiarrhythmic infusions and frequent boluses are not required.
Typically, mean arterial pressure most often increases during patient transport, as inhaled anesthetic gas is discontinued. An adequate level of intravenous sedative should already be achieved prior to leaving the operating room to prevent both awareness and the sometimes-sizeable accompanying increase in blood pressure. Sedative choice varies but either a propofol or dexmedetomidine infusion is most commonly used.
VIII. Off-Pump Coronary Artery Bypass Graft Surgery
Distal Anastomoses
Variable periods of coronary artery occlusion are required for distal bypass graft anastomosis. The severity and territory of subsequent tissue ischemia depends on the myocardium’s collateral blood flow. During distal grafting, mean arterial pressure should be maintained at the upper limit of the patient’s baseline to promote collateral flow to poorly perfused areas [10]. Norepinephrine infusion (typically 0.04-0.15 mcg/kg/min) is usually the first line, as it is easily titrated and its β-agonism provides some inotropic support while not significantly promoting ischemia-induced arrhythmias. Euvolemia is the goal during these procedures and should reduce the need for strong afterload support. However, norepinephrine’s vasopressor component augments blood pressure during periods of compromised myocardial function. Phenylephrine (typically 0.1-1.5 mcg/kg/min), vasopressin (typically 0.04-0.1 units/minute) dobutamine (typically 5-10 mcg/kg/min), isoproterenol (typically 1-5 mcg/min), or epinephrine (typically 0.04-0.15 mcg/kg/min) infusions are also options, though each carries a disadvantage. Specifically, phenylephrine lacks inotropic support [1]. Dobutamine, isoproterenol, and epinephrine, augment chronotropy but are more arrhythmogenic than norepinephrine [8]. Pacing, atrial or atrioventricular, can be a very useful adjunct if there is significant bradycardia or if the rhythm is nodal or if there is heart block.
Marginal and posterior coronary artery targets necessitate significant repositioning of the heart. The act of repositioning will result in a 2-4 beat duration of myocardial stunning that often is self-limited. However, markedly increased vasopressor/inotrope requirements are often needed for these targets [10]. Trendelenburg positioning and a high normal heart rate (80-90 beats per minute) can help support mean arterial pressure.
Coordination between the surgeon and the anesthesia practitioner is critical. Taking the time to position, assess impact on hemodynamics and to reposition with reassessment of hemodynamics best achieves the dual goal of optimizing both the position and the hemodynamics. Together the surgeon and the anesthesia practitioner can decide whether hemodynamics can be successfully maintained pharmacologically for the full duration of each distal anastomosis to prevent emergent repositioning during graft anastomosis. Lifting the heart as compared to compressing the heart is the key to success.
During distal bypass grafting, progressive hypotension, increasing inotrope requirements, diminishing inotropic effects with the need for inotrope/vasopressor boluses, worsening ischemic mitral regurgitation, ischemic electrocardiogram changes, and new frequent premature ectopic beats indicate potential cardiac arrest. If possible, a shunt should be placed past the anastomosis site, and the heart should be placed in its normal position as soon as feasible.
Proximal Anastomoses
Off-pump proximal bypass graft anastomoses require a partial aortic side clamp (C-clamp) or a clamp-less hemostatic seal. Conventionally, the systolic blood pressure goal is usually 90-100 mmHg to prevent disruption of aortic segment isolation, bleeding, and aortic tissue injury.
Immediately after the last distal anastomosis, the heart is placed into its usual position. The vasopressor/inotropic infusions needed to maintain mean arterial pressure through distal grafting now usually result in a supra-physiologic systolic pressure. Cessation of vasopressor and inotropic support, as well as reverse Trendelenburg positioning, help to lower systolic pressure. Vasodilator boluses (typically nitroglycerine 50 mcg or nicardipine 100 mcg) can expedite the process, but care should be taken to avoid significant hypotension.
Usually, the ventricular function is stunned from manipulation and temporary periods of ischemia during distal grafting. Even patients with normal preoperative function typically require some low level hemodynamic support to maintain a systolic pressure of 90-100 mmHg. One algorithm to achieve this tight blood pressure management is as follows:
- Allow the systolic pressure to decrease to 85-90 mmHg as the effects of discontinued vasopressor/inotropic infusion wear off.
- Bolus norepinephrine 2-8 mcg to increase systemic pressures by 5-10 mmHg and restore the systolic pressure to 95-100 mmHg.
- After the initial bolus, initiate a low dose norepinephrine infusion (typically 0.02-0.03 mcg/kg/min).
- Repeat low-dose norepinephrine boluses (2-8 mcg) as necessary when the systolic pressure decreases below 90 mmHg.
- After each norepinephrine bolus, increase the background norepinephrine infusion by 0.01-0.02 mcg/kg/min until boluses are no longer required.
Coordination between the surgeon and the anesthesia practitioner facilitates a smoother transition to a controlled systolic pressure of the required 90 to 100 mmHg. As the systolic pressure goal of 90-100 mmHg is below most patients’ physiologic baseline, monitoring for signs of ischemia is important.
IX. Intraoperative Pharmacotherapy and Treatment Algorithms for Specific Arrhythmias
Arrhythmias are common during the open-chest cardiac procedure secondary to a variety of factors, including myocardial ischemia from vaso-occlusive disease or cardiopulmonary bypass, preexisting cardiac pathology, maladaptive chamber remodeling, electrolyte abnormalities, hypothermia, and physical manipulation by the surgical team. Certain arrhythmias are more common during particular phases of the procedure, such as SVT during central venous cannulation or VT/VF following aortic cross-clamp removal.
Briefly, the major arrhythmias are listed below, each with an accompanying diagnostic/therapeutic algorithm that is applicable for most stages of the open-chest cardiac procedure. These algorithms involve components of the classic ACLS pathways [1], but are tailored to the intraoperative cardiac surgery setting. Hypoxia and hypercarbia should be immediately addressed since arrhythmias triggered by a failure of gas exchange are usually refractory to other therapies. Moreover, rapidly progressive hemodynamic instability and loss of pulsatility will occur with depleted oxygen stores or severe respiratory acidosis. Of note, the first few steps of each pathway are often executed simultaneously in the dynamic operating room setting.
Sinus Tachycardia
Note: Correcting sinus tachycardia revolves around etiology identification and correcting the underlying insult. Below is a suggested order for the sequential consideration of the differential diagnoses. Although much less common, time-sensitive gas exchange failure is addressed first, followed by the more common diagnoses of light anesthetic levels, hypovolemia and ischemia.
Differential Diagnoses and Treatment Algorithm
1. Gas exchange failure: Hypoxemia and/or hypercarbia
Treatments: Increase FiO2, confirm endotracheal tube position, increase minute ventilation, increase positive end expiratory pressure, perform recruitment maneuvers, suction the airway. Consider bronchospasm and treat with bronchodilators if appropriate. Usually one or more of those maneuvers will correct the problem. With continued gas exchange failure, consider using an ICU ventilator and change mechanical ventilation mode. Extracorporeal membrane oxygenation can be used if all else fails to improve the gas exchange.
2. Light anesthetic levels
Treatments: Increase inhaled anesthetic concentration, supplement intravenous anesthetic, (i.e., a small, 10-30 mg propofol bolus), give a narcotic bolus, and, if necessary, temporize using short-acting β1-blockade (esmolol).
3. Hypovolemia
Treatments: Volume administration, Trendelenburg positioning, temporizing vasopressor bolus/infusion.
4. Ischemia
Treatments: Vasopressor to increase perfusion pressure, rate control with β1-blockade (esmolol, metoprolol, labetalol), surgeon should check graft positioning and reassess graft flow. If ischemia persists, discussion with surgeon to determine if heparin should be given to counteract thrombogenesis, and if the culprit lesion should be bypassed.
5. Medication induced (glycopyrrolate, β-agonists)
Treatments: Cessation or dose reduction of offending agents, temporizing β1-blockade (esmolol).
6. Less common diagnoses: Malignant hyperthermia, serotonin syndrome, substance withdrawal.
Sinus Bradycardia
Treatment Algorithm
1. Correct hypoxia (especially if acute, severe, or progressive).
Treatments: Increase FiO2, increase positive end expiratory pressure, recruitment maneuvers, airway suctioning, endotracheal tube position reconfirmation, change mechanical ventilation mode, ICU ventilator use, extracorporeal membrane oxygenation, cardiopulmonary bypass.
(Often executed as steps 2-4 are being addressed)
2. Eliminate acute vagal stimulation.
Treatments: Pause in surgical manipulation.
3. Rapidly correct severe bradycardia (<40 beats per minute) or bradycardia causing hemodynamic instability.
Treatments: During cardiac surgery, pacing is usually readily available and is the first line choice. If pacing is not available, Atropine (typically 0.2-1 mg) and/or epinephrine (typically 16-32 mcg).
4. Temporize unwanted mild to moderate bradycardia.
Treatments: Pacing if available, Glycopyrrolate (typically 0.2-0.4 mg), ephedrine (typically 5-10 mg), epinephrine (typically 8-16 mcg).
5. Assess for other common causes: Deep anesthesia, ischemia, medication induced (β-blockade, central calcium channel blockade, phenylephrine, narcotics), sick sinus syndrome.
Supraventricular Tachycardia (Atrial Fibrillation/Atrial Flutter/Accessory Pathway SVT/Junctional Tachycardia)
Treatment Algorithm
1. Correct gas exchange failure (especially if acute, severe, or progressive).
Treatments: Increase FiO2, increase minute ventilation, increase positive end expiratory pressure, recruitment maneuvers, airway suctioning, endotracheal tube position reconfirmation, change mechanical ventilation mode, ICU ventilator use, extracorporeal membrane oxygenation, cardiopulmonary bypass.
(Executed as steps 2-4 are being addressed)
2. Pause surgical manipulation to promote cardioversion and ensure stability.
3. Assess for hemodynamic stability.
4. With hemodynamic instability, pulslessness, or worsening cardiac ischemia, initiate emergent electrical cardioversion (versus cardiopulmonary bypass, if readily available), and provide supportive measures.
Treatments: Synchronized electrical cardioversion (typically biphasic 10-200 joules or monophasic 100-200 joules) or cardiopulmonary bypass.
Supportive measures: Volume administration, vasopressor/inotrope bolus, sodium bicarbonate (typically 50 mEq, assuming adequate ability to eliminate carbon dioxide), chest compressions/cardiac massage (when pulseless), Trendelenburg positioning.
5. With hemodynamic stability and an accessory pathway rhythm, attempt chemical cardioversion and/or rate modulation with procainamide or amiodarone.
6. With hemodynamic stability and either a non-accessory pathway rhythm or a rhythm with an unknown conduction pathway, consider electrical or chemical cardioversion while investigating for etiology.
Treatments: Synchronized electrical cardioversion (typically biphasic 10-200 joules or monophasic 100-200 joules), adenosine (typically 6-12 mg bolus), esmolol (typically 10-40 mg bolus), phenylephrine (typically 100-300 mcg bolus), amiodarone (150 mg slow push).
(If refractory to above treatments, consider accessory pathway rhythm and address step 5)
7. Assess for and treat other common causes: Ischemia, hypotension, hypovolemia, electrolyte abnormalities, hypothermia, acid-base imbalance, light anesthesia.
8. In hemodynamically stable patients refractory to cardioversion, consider rate control while investigating for etiology.
Treatments: Esmolol (typically 50-200 mcg/kg/min)
Ventricular Tachycardia (Monomorphic/Long-QT polymorphic/Normal-QT polymorphic), Ventricular Fibrillation
Treatment Algorithm
1. Correct gas exchange failure (especially if acute, severe, or progressive).
Treatments: Increase FiO2, increase minute ventilation, increase positive end expiratory pressure, recruitment maneuvers, airway suctioning, endotracheal tube position reconfirmation, change mechanical ventilation mode, ICU ventilator use, extracorporeal membrane oxygenation, cardiopulmonary bypass.
(Executed as steps 2-4 are being addressed)
2. Pause surgical manipulation to promote defibrillation and ensure stability.
3. Assess for hemodynamic stability.
4. With hemodynamic instability, pulslessness, or worsening cardiac ischemia, deliver emergent unsynchronized electrical shocks (versus cardiopulmonary bypass, if immediately available), administer intravenous antiarrhythmics, and provide supportive measures.
Primary treatments:
Unsynchronized electrical shocks (typically biphasic 200 joules or monophasic 360 joules) or cardiopulmonary bypass.
Chest compressions/cardiac massage (when pulseless or with very low MAP)
Intravenous antiarrhythmics:
Lidocaine (typically 100 mg)
Amiodarone (typically 150-300 mg)
Magnesium sulfate (typically 2 gm) -- for suspected long-QT polymorphic VT
Supportive measures:
Vasopressor/inotrope bolus (typically epinephrine 100-1000 mcg)
Sodium bicarbonate to treat acidosis (typically 50 mEq, assuming adequate ability to eliminate carbon dioxide),
Trendelenburg positioning
5. With hemodynamic stability, deliver unsynchronized electrical shocks and administer intravenous antiarrhythmics
Treatments:
Unsynchronized electrical shocks (typically biphasic 200 joules or monophasic 360 joules)
Intravenous antiarrhythmics:
Lidocaine (typically 100 mg)
Amiodarone (typically 150 mg slow push)
Magnesium sulfate (typically 2 gm)--for suspected long-QT polymorphic VT
6. Assess for and treat other common causes: Ischemia, hypotension, hypovolemia, electrolyte abnormalities, hypothermia, acid-base imbalance
7. Following successful cardioversion of a polymorphic ventricular tachycardia, assess the QT interval. To prevent the recurrence of a long-QT polymorphic VT, perform maneuvers to shorten long-QT segments
Treatments:
Magnesium sulfate (typically 2 gm, if not already administered)
Chronotropic augmentation (atropine, isoproterenol, dobutamine, epinephrine, ventricular pacing)
Avoidance of medications that prolong the QT-interval
Asystole
1. Begin chest compressions/cardiac massage or initiate cardiopulmonary, bypass, if immediately available
2. For open chest cardiac procedures, pacing wires are immediately available and should be used to attempt to pace
3. Attempt transcutaneous/transvenous/epicardial ventricular pacing as soon as possible, e.g., via right ventricular port of the pulmonary artery catheter
4. Promote rhythm development with epinephrine (typically 1000 mcg every 3-5 minutes), and maintain SVR with vasopressin (typically 20-40 units)
5. Consider administration of sodium bicarbonate to treat acidosis (typically 50 mEq, assuming adequate ability to eliminate carbon dioxide),
6. Upon restoration of a perfusable rhythm, assess for and treat common causes: Gas exchange failure, ischemia, hypotension, hypovolemia, electrolyte abnormalities, particularly hyperkalemia, hypothermia, and acid-base imbalance
X. Summary
This chapter has presented comprehensive and detailed information designed to provide scientific basis for managing adult patients having cardiac surgery, as well as rationale for selection of different inotropes, vasopressors, and combinations of drugs to provide optimal outcomes while minimizing drug side effects. Doing this well requires scientific knowledge, experience, and finesse akin to art. Knowledge of drugs’ pharmacodynamics and pharmacokinetics, the typical doses used, potential side effects, and when to consider adding a second, third and/or more drugs is critical. Of utmost importance is well-defined and clear communication between all the operating room team members. Standardization in communication pathways and supplemental checklists for critical times, such as going onto and weaning from cardiopulmonary bypass, helps reduce errors and morbidities. Additionally, having all team members aware of potential issues, and where and when in the process to anticipate certain complications, requires each team member to be able to communicate freely and to ask questions when unsure.
XI. Sources
1. Katzung B, Trevor A. Basic and Clinical Pharmacology. 13th ed. McGraw-Hill; 2015.
2. Dupuis J, Wang F, Nathan H, et al. The Cardiac Anesthesia Risk Evaluation Score: A Clinically Useful Predictor of Mortality and Morbidity afterCardiac Surgery. Anes. 2001; 94(2): 194-204.
3. Tuman K, McCarthy R, March R, et al. Morbidity and Duration of ICU Stay after Cardiac Surgery: A Model for Preoperative Risk Assessment. Chest. 1992; 102(1): 36-44.
4. Loubani O, Green R. A systematic review of extravasation and local tissue injury from administration of vasopressors through peripheral intravenous catheter and central venous catheters. J Crit Care. 2015; 30(3).
5. Practice Guidelines for Central Venous Access: A Report by the American Society of Anesthesiologists Task Force on Central Venous Access. Anes. 2012; 116(3): 539-573.
6. Hensley F, Martin D, Gravlee G. Cardiac Anesthesia. 4th ed. LWW; 2007.
7. Moffitt E, Tarhan S, Lundborg R. Anesthesia for Cardiac Surgery: Principles and Practice. Anes. 1968; 29(6): 1181-1205.
8. Butterworth J, Mackey D, Wasnick J. Morgan and Mikhail's Clinical Anesthesiology. 5th ed. McGraw-Hill; 2013.
9. Miller R, Eriksson L, Fleisher L, et al. Miller’s Anesthesia. 8th ed. Saunders; 2014.
10. Hemmerling T, Romano G, Terrasini N, et al. Anesthesia for off pump coronary artery bypass surgery. Ann Card Anesth. 2013; 16(1): 28-39.
11. Trapp C, Schiller W, Mellert F, et al. Retrograde Autologous Priming as a Safe and Easy Method to Reduce Hemodilution and Transfusion Requirements during Cardiac Surgery. Thorac Cardiovasc Surg. 2015; 63(7): 628-634.
12. Azau A, Markowicz P, Corbeau JJ, et al. Increasing mean arterial pressure during cardiac surgery does not reduce the rate of postoperative acute kidney injury. Perfusion. 2014; 29(6): 496-504.
13. Kandler K, Jensen ME, Nilsson JC, et al. Arterial pressure during cardiopulmonary bypass is not associated with acute kidney injury. Acta Anesthesiol Scan. 2015; 59(5): 625-631.
14. Ono M, Brady K, Easley RB, et al. Duration and magnitude of blood pressure below cerebral autoregulation threshold during cardiopulmonary bypass is associated with major morbidity and operative mortality. J Thorac Cardiovasc Surg. 2014; 147(1): 483-489.
15. Hori D, Brown C, Ono M, et al. Arterial pressure above the upper cerebral autoregulation limit during cardiopulmonary bypass is associated with postoperative delirium. Br J Anaesth. 2014; 113(6): 1009-1017.
16. Pirraglia PA, Peterson JC, Hartman GS, et al. The efficacy and safety of a pharmacologic protocol for maintaining coronary artery bypass patients at a higher mean arterial pressure during cardiopulmonary bypass. J Extra Corpor Technol. 1998; 30(2): 64-72.
17. Lavigne D. Vasopressin and methylene blue: alternate therapies in vasodilatory shock. Semin Cardiothorac Vasc Anesth. 2010; 14(3): 186-189.
18. Ng BK, Cameron AJ. The role of methylene blue in serotonin syndrome: a systematic review. Psychosomatics. 2010; 51(3): 194-200.
19. Wilson L, Rooney T, Baugh RF, et al. Recognition and management of perioperative serotonin syndrome. Am J Otolaryngol. 2012; 33(3): 319-321.
20. Fischer GW, Lin HM, Krol M, et al. Noninvasive cerebral oxygenation may predict outcome in patients undergoing aortic arch surgery. J Thorac Cardiovasc Surg. 2011; 141(3): 815-821.
21. Shipley JB, Tolman D, Hastillo A, et al. Milrinone: basic and clinical pharmacology and acute and chronic management. Am J Med Sci. 1996; 311(6): 286-291.
22. Hensley N, Dietrich J, Nyhan D, et al. Hypertrophic cardiomyopathy: a review. Anesth Analg. 2015; 120(3): 554-569.
23. Wallace AW, Tunin CM, Shoukas AA. Effects of vasopressin on pulmonary and systemic vascular mechanics. Am J Physiol. 1989; 257(4): 1228-1234.
24. Omar S, Zedan A, Nugent K. Cardiac vasoplegia syndrome: pathophysiology, risk factors and treatment. Am J Med Sci. 2015; 349(1): 80-88.
25. ACLS Pathways. https://www.acls.net/aclsalg.htm. Accessed 1 March 2017.