(1)
Department of Anesthesiology, Vanderbilt University School of Medicine, Nashville, TN, USA
Keywords
Intraoperative problemsUnstable surgical patientEmergenceExtubationPost operative complicationsCardiac adverse eventsHypotensionHypertensionHypoxemiaFailure to ventilateHigh airway pressuresHypocarbiaAnaphylaxisTransfusion reactionHypothermiaHyperthermiaIntraoperative arhythmiasBradycardiaTachycardiaPremature ventricular contractionsVentricular tachycardiaPremature atrial contractionsAtrial fibrillationAtrial flutterAsystolePulseless electrical activity (PEA)Key Learning Objectives
Discuss a general approach to managing the unstable surgical patient, including formation of a differential diagnosis for the instability.
Be able to identify the most common intraoperative problems that occur in a systematic manner
Review management options for the common intraoperative problems encountered
Discuss an approach to emergence and extubation, including a differential diagnosis for failure to extubate.
General Concepts
Anesthesiologists and nurse anesthetists have the opportunity and challenge of caring for a wide array of patients ranging from the healthy ASA I patient to the moribund ASA 5 patient. Despite the complexity and uniqueness of each patient, there are many common problems that occur in the operating room of which you should be aware. It is important that you have a thorough understanding of both physiology and pharmacology in order to care for patients undergoing anesthesia, and in order to be able to recognize and confidently manage intraoperative events.
Additionally, it is imperative that members of the anesthesia care team act quickly to correct any problems that occur in order to prevent harm to the patient. As opposed to standard Advanced Cardiac Life Support (ACLS) that is primarily built for unwitnessed cardiopulmonary arrest, the problems that will be described in this chapter typically occur in a setting in which (a) the problem is witnessed from its onset, (b) the patient is extensively monitored (e.g. ECG, pulse oximeter, ETCO2), and (c) the past medical and surgical history of the patient is known. As such, while many of the underlying principles and goals of ACLS for assessment of patients in unstable, near-arrest, and arrest situations apply, numerous management steps are different. Table 17.1 lists the most common intraoperative problems that may occur during anesthesia. Almost all perioperative urgencies and emergencies will map to one of five areas of concern: cardiac, pulmonary, neurologic, metabolic/endocrine, or toxins. This is certainly true for all common intraoperative patient problems. The only additional category is that of machine or system failure (e.g. oxygen supply failure), which is not discussed in this chapter.
Table 17.1
Common intraoperative problems and differential diagnoses
Problem | Differential diagnosis | Remarks |
---|---|---|
Cardiovascular | ||
Hypotension | Hypovolemia | Common causes include blood loss or dehydration from preoperative fasting |
Relative anesthetic overdose | Minimal or a decrease in surgical stimulation can lead to relative anesthetic overdose and hypotension | |
Vasodilatation from medication | Opioids, sedatives, and most anesthetics reduce central sympathetic outflow and cause vasodilatation. Virtually every anesthetic induction or heavy sedation will be accompanied by this finding. Usually treated with phenylephrine, 40–100 mcg | |
Low cardiac output | Many anesthetics decrease cardiac output. Other causes include congestive heart failure, myocardial infarction, or tamponade | |
Severe bradycardia | This may cause low cardiac output (CO = HR × SV), leading to hypotension | |
Severe tachycardia or arrhythmias | If atrial fibrillation or flutter becomes too fast, hypotension may result | |
Pneumothorax | Uncommon, but may spontaneously arise during positive pressure ventilation | |
Anaphylactic reaction | Most commonly from reaction to muscle relaxants or antibiotics. Give epinephrine to treat | |
Sepsis | Sudden decreases in blood pressure may result from sepsis | |
Hypertension | Pain from surgical stimulus | Always consider “light” or insufficient anesthesia |
Essential hypertension | These patients may be adequately anesthetized, but still markedly hypertensive | |
Tourniquet pain | A tourniquet can produce a hard, recalcitrant kind of hypertension called “cuff hypertension | |
Light anesthesia | Check for empty vaporizers or medication infusors | |
Hypervolemia | Fluid overload from intravenous fluid or blood products; may lead to pulmonary edema and congestive heart failure in patients with heart disease | |
Pulmonary | ||
Hypoxemia Failure to ventilate | Low inspired oxygen (FiO2) Hypoventilation Disconnection of breathing circuit Atelectasis Bronchospasm Mucus Plugging Right main-stem bronchial intubation Pulmonary thromboembolism (PE) Venous air embolism Kinked endotracheal tube | Always start by increasing the FiO2, and then continue to look for other causes May be from opioids, benzodiazepines, or muscle relaxants, which decrease respiratory drive and muscle strength. If a patient is being ventilated, consider increasing respiratory rate or tidal volumes The most common cause of serious hypoxemic accidents Often a result of positive pressure ventilation, intubation and/or hypoventilation. Consider alveolar recruitment maneuvers Consider administering albuterol Perform suction and alveolar recruitment maneuvers Maximum depth for tracheal tubes measured at teeth: females 21 cm; males 23 cm. May visualize with bronchoscope or auscultate with stethoscope This may be diagnosed by a sudden drop in end-tidal CO2, and hypoxemia that does not improve with 100 % FiO2. Often accompanied by tachycardia and hypotension Also causes drop in end-tidal CO2, and an increase in end-tidal N2 Most likely during ENT or thoracic surgery |
Biting on endotracheal tube | May occur during “light” anesthesia or emergence; Can cause negative pressure pulmonary edema | |
Disconnection of endotracheal tube from circuit or adapter | The most common cause | |
Complete endotracheal tube obstruction from mucus or tissue | Can occur rapidly in infants/children whose ETT are narrow (especially when no humidification is used). Suction or replace tube | |
Hole in endotracheal tube or a punctured cuff | Most often during laser airway surgery or tracheostomy. Both surgeries also have ↑ risk of airway fire! | |
High airway pressures | Bronchospasm | (1) deepen anesthesia, (2) consider neuromuscular blockade, (3) administer beta-agonists, inhaled or intravenous corticosteroids, theophylline or epinephrine |
Kinked endotracheal tube | May require the use of an armored (metal spring reinforced) tube to prevent kinking | |
Biting on endotracheal tube | Consider placing a bite block or mouth gag | |
Mucus plugging | Common in patients with COPD, asthma and cystic fibrosis. This may require replacement of the ETT | |
Stacking or auto-PEEP of mechanical breaths | Occurs when the expiratory phase isn’t long enough to allow exhalation. Decrease the respiratory rate | |
Dynamic airway obstruction | May be from an airway tumor or mediastinal mass, especially after change in patient position | |
Obesity or chest wall rigidity | May be difficult to manage. High opioid dose can cause a “rigid chest syndrome | |
Acute Respiratory Distress Syndrome (ARDS) | A common cause of high mean pressures, especially in the ICU | |
Hypocarbia | Hyperventilation | May see in anxious (awake) or mechanically hyperventilated (anesthetized) patients |
Leak of CO2 in sampling tubing | This may also cause an abnormality in the capnograph waveform or envelope | |
Massive pulmonary embolus | Can impair gas exchange, manifesting as a sudden drop in expired CO2 | |
Hypothermia | Most evident in severe hypothermia as during cardiopulmonary bypass | |
Cardiac Arrest | Impaired circulation and CO2 elimination | |
Hypercarbia | Hypoventilation | Often from opioids, residual neuromuscular blockade, or low respiratory rate/ventilator tidal volumes |
CO2 insufflation during laparoscopy | May need to increase minute ventilation to overcome hypercarbia | |
Malignant hyperthermia | Uncoupling of calcium metabolism in mitochondria from a rare (1:15,000) genetic defect in the ryanodine receptor of the calcium channel | |
Toxins | ||
Anaphylaxis | Usually due to neuro-Muscular blockers, latex, or antibiotics | Stop offending agent, support hemodynamics |
Transfusion reaction | Many types | Stop agent, support pressure, report to blood bank |
Metabolic | ||
Hypothermia | Convective, conductive, radiative, evaporative losses | Convective losses are the #1 cause of heat loss in the OR (skin to air). Heat loss also occurs from wet drapes and sheets, exposed skin or body cavities, non-heated breathing circuits |
Anesthetic effects on hypothalamus | Anesthetics cause impaired central thermoregulation due to effects on the hypothalamus | |
Administration of unwarmed fluid or blood products | Fluids should be warmed by an FDA-approved device | |
Massive blood loss | Difficult to keep patients warm after ≥1 blood volume has been lost | |
Hyperthermia | Excessive warming | Use the air-warming blanket at a room-temperature setting to cool the patient |
Fever from sepsis or transfusion reaction | Give acetaminophen or ibuprofen in addition to a cooling blanket | |
Stroke | Sudden extreme hyperthermia (>105 °F) may be from a stroke to the hypothalamus | |
Neuroleptic malignant syndrome | Uncommon side effect of antipsychotic medications (chlorpromazine, haloperidol, olanzepine) | |
Malignant hyperthermia | (1) stop anesthetic, (2) give iv dantrolene, (3) call for help (see Appendix B, Malignant Hyperthermia) |
The goals of this chapter include providing you with a framework by which to think about the approach to the unstable patient, how you might construct a differential diagnosis for that instability, and the proper steps for initial management of common intraoperative problems. When there is a concern for an acute change in patient condition under anesthesia, having a structured approach to the patient will be of benefit. First, you should start by assessing the general hemodynamic state of the patient and proceed through a series of decision nodes to define the initial course of action. This should start with the steps of defining whether the patient has a pulse. If not, proceed with advanced cardiac life support (ACLS) management while noting the differences in the operative setting [10, 13]. If the patient has a pulse, then one should define whether there is an acute hemodynamic instability to be addressed. If so, following the steps outlined in the cardiovascular section below is indicated. If the patient appears to have adequate cardiac output, then an assessment can proceed to the other four areas of concern noted above, with pulmonary being most important in order to ensure that adequate oxygenation and ventilation are present. A progression of thought through the other possible major categories should be undertaken in sequence. At each step, one should ask the questions outlined in Fig. 17.1, which will aid in constructing a differential diagnoses, picking a leading diagnosis, and then proceeding with initial management plan. Of note, the initial diagnosis may simply be a patient state (e.g. severe hypoxemia) rather than a particular known cause. Thus, in the acute care setting the first step is to ensure that cardiopulmonary function is at a level that meets basic metabolic requirements in order to avert patient harm and then proceed to defining an exact etiology.
Figure 17.1
Approach to the unstable patient
Cardiovascular
The cardiovascular system is often the source of many intraoperative problems as there are numerous forces at play that can effect normal homeostasis in preload, afterload, chronotropy, and inotropy. Disturbances of the cardiovascular system can be thought of originating from the following etiologies: pipes (systemic vessels), pump (RV/LV inotropy), preload, valves, vessels (coronary arteries), and voltage (conduction system). Systematically reviewing these six categories provides structure within the cardiovascular system to critically evaluate the patients condition, formulate a differential diagnosis, and quickly identify and treat the problem. Below is a brief overview of the six key components of cardiovascular integrity. For a more in-depth discussion of cardiovascular physiology, please see Chap. 18.
Pipes are the peripheral vessels (aorta – >arteries – > arterioles) that carry oxygen and nutrients to the tissues for exchange at the capillary level. They then carry CO2 and waste back to the liver, for detoxification, and heart by the venous system (venules – > veins – > IVC and SVC). This complex system of vessels in series and in parallel accounts for the majority of afterload as systemic vascular resistance. The heart is a pump that provides cardiac output to the body. The effectiveness of the heart as a pump is affected by heart rate, stroke volume, contractility, and afterload, which is the pressure the heart must contract against to generate forward flow. Preload can be thought of as the volume of blood in the right and left ventricles at the end of diastole. This volume is important for determining the strength of contraction, which is due to myocardial stretch at the beginning of systole, according to the Frank-Starling law. The extremes of preload (severe hypovolemia and hypervolemia) both result in reduced cardiac output, but by different mechanisms. The heart has four chambers, thus there are four valves, which are responsible for both allowing forward flow of blood and halting backward flow, depending on which part of the cardiac cycle is occurring. These include the tricuspid, pulmonic, mitral, and aortic valves. The coronary arteries are the vessels that supply blood and oxygen to the myocardium. They consist of the left and right coronary arteries, which become the left anterior descending, left circumflex, and posterior descending arteries, along with a number of smaller branched arteries. Voltage refers to electrical conduction through the heart during the cardiac cycle. Normal sinus rhythm is important because it produces maximal atrio-ventricular coupling for effective filling and ejection of blood to produce a stable cardiac output. The most common problems of the cardiovascular system will be discussed below. For an extensive list with many other problems, please refer back to Table 17.1.
Dysrhythmias and Cardiac Arrest
As an extension of what was discussed above, the following steps are helpful during the initial assessment and management of an acute cardiovascular disturbance related to cardiac arrest or acute rhythm disturbance:
1.
Pulse: present or absent?
2.
Stability: is patient stable (adequate C.O.) or unstable (signs/symptoms of poor perfusion – angina, SOB, altered mental status, etc)
3.
Rate: tachycardic (>150, >120 in afib) or bradycardic (<50)
4.
Rhythm: assess the QRS and rhythm strip
(a)
wide or narrow?
(b)
regular or irregular?
(c)
is a dysrhythmia causing instability?
5.
Diagnosis
(a)
6.
Treatment: as per ACLS protocols for rhythm disturbances
In order for blood to be delivered in an efficient fashion to the peripheral circulation, it is important for the heart to be in normal sinus rhythm. Severe bradycardia and tachycardia can negatively affect the ability of the heart to pump oxygenated blood to tissues. In the community and non-operative health care settings, ACLS algorithms are standardized and followed by all health care professionals [13]. However, the operating room presents a unique setting for the performance of ACLS, which is often modified to a tailored approach for each patient because the anesthesia provider usually witnesses the event, knows the patient’s medical comorbidities, and understands the surgical pathophysiology that may have led to the event [10]. See Table 17.2 for common causes of intraoperative dysrhythmias and Fig. 17.2 for the comprehensive anesthesia-centric ACLS algorithm that should be followed.
Table 17.2
Common intraoperative dysrhythmias
Problem | Differential diagnosis | Remarks |
---|---|---|
Bradycardia | β-blockers | Probably the most common cause |
Hypoxia | Occurs with severe hypoxia | |
Myocardial infarction | Likely if the right coronary artery and sinus node are involved in the infarction | |
Increased vagal tone | Surgical stimulus on the gut, bladder, or other organs may increase vagal tone. Atropine and, later, deepening anesthesia may be indicated. May also be seen in athletes | |
Third degree heart block | The ECG rhythm strip will provide the diagnosis | |
Calcium channel blockers | Especially caused by diltiazem (used for this purpose in atrial fibrillation and flutter) | |
Reversal of neuromuscular blockade with cholinesterase inhibitors such as edrophonium or neostigmine | Co-administration of an anticholinergic medication (atropine or glycopyrrolate) is standard practice, so this happens rarely. However, edrophonium may be used alone to try to convert SVT or a slow heart rate, during testing for myasthenia gravis | |
Tachycardia | Total spinal Increased pain or surgical stimulus | Support hemodynamics and administer vasopressors as needed The most common cause at the start of the surgical procedure. May suggest insufficient anesthesia |
Vasopressors or inotropes | Ephedrine, epinephrine, norepinephrine, isoproterolol can all cause tachycardia | |
Myocardial infarction | The most common dysrhythmia associated with MI | |
Arrhythmias | Atrial fibrillation, Ventricular Tachycardia
Stay updated, free articles. Join our Telegram channelFull access? Get Clinical TreeGet Clinical Tree app for offline access |