Treatment of Medical Emergencies

Introduction

The interventional suite plays host to a wide variety of patient types and procedures. Some of the patients who arrive into the suite are in good baseline health, while others are severely ill. In either case, patients can experience a life-threatening emergency during any interventional procedure. Unlike the operating room, where an anesthesiologist is routinely present to handle any non–procedure-related emergency, the level of support in the interventional suite is variable. When medical emergencies occur, it is not uncommon for interventionalists to have only their complement of nurses and technologists as support staff. In this brief chapter, we endeavor to provide a framework that will help mitigate the medical emergencies that can occur in patients undergoing interventional procedures.

The lion’s share of medical emergencies can be placed into five categories: (1) oversedation, (2) airway compromise, (3) respiratory distress, (4) cardiac/hemodynamic emergencies, and (5) contrast reactions. The response to these medical emergencies often requires an anesthesiologist, an intensivist, and/or a surgeon. However, there are concrete steps and planning by the interventionalist and staff that can help lessen these emergencies and may prove life saving while appropriate personnel and resources are mobilized. This chapter will focus on these bridging and moderating techniques.

Oversedation

Procedural sedation/analgesia is a common and important component of interventional procedures. Appropriate patient positioning and maintaining patient comfort are facilitated by proper sedation. However, reaching the perfect balance of sedation and comfort without oversedating the patient can be challenging. Striking the right balance can be particularly difficult in patients with underlying lung disease and in patients with unpredictable metabolism of common sedatives. In addition, patients with a marginal circulatory status may be prone to hemodynamic effects. The oversedated patient can experience hypercarbia, hypoxemia, and/or hypotension either related to the sedative itself or due to secondary effects. Prevention of oversedation and hypercarbia can be prevented with close patient monitoring and the use of pulse oximetry; the patient’s response to verbal commands; observation of ventilation, blood pressure (BP), and heart rate every 5 minutes; electrocardiography for patients with significant cardiovascular disease; and use of exhaled capnography. When patients become oversedated, it is common for minute ventilation to decrease, which is often associated with a rise in end-tidal CO₂ (ETCO₂). This elevation typically precedes apnea and can alert the physician that the level of sedation is excessive. ETCO₂ above 50 mmHg, an absolute change of over 10 mmHg, or an absent waveform may detect subclinical respiratory depression not detected by pulse oximetry alone.¹ This is vitally important, since many patients have a variable response to hypnotic drugs. The choice of drugs that have minimal hemodynamic and respiratory depression may be considered (e.g., etomidate,² ketamine,³ ketamine-propofol combination⁴).

In this section, we will focus on airway and respiratory management of the oversedated patient. Management of hypotension and arrhythmia is covered in the circulatory management section of the chapter. When patients become oversedated, their airway and respiratory centers can be compromised. The mechanisms by which this occurs are multiple:

• Use of narcotics can cause vomiting and aspiration.

• Narcotic and benzodiazepine use decreases respiratory drive and can cause central apnea.

• Muscle relaxation caused by sedatives can cause upper airway obstruction.

Typically the response to the oversedated patient is cessation of the sedative agent, increasing the inspired oxygen (e.g., placing a 100% Fio₂ face mask), and some form of stimulation (e.g., sternal rub) in an attempt to arouse the patient to stimulate breathing while the sedative wears off. This approach is often unsatisfactory owing to the half-life of the sedating agent. In addition, if the airway or respiratory center is compromised, subsequent hypercarbia may spiral toward complete respiratory arrest.

The approach to the oversedated patient should be managed in a more airway-centered manner. Once oversedation is recognized, a staff member in the interventional suite should be detailed to the head of the bed to manage the airway. Noninvasive airway management should be sufficient in most cases. If stimulation of the patient (e.g., calling the patient’s name loudly, sternal rub) fails to immediately correct the compromise in oxygenation or respiratory effort, the airway should be assessed and optimized (Fig. 16-1; also see Airway Management and Optimization, later). At this point, if the sedative used has an antidote (e.g., flumazenil for benzodiazepines or, naloxone for narcotics), that antidote should be drawn up (Table 16-1).

TABLE 16-1

Sedative Antidote Administration

Antidote	Dosage and Comments	Side Effects
Naloxone	0.4-2 mg at a time; maximum dose 10 mg For typical doses used for conscious sedation, a dose of 0.2-0.4 mg should be sufficient Can be given as an infusion (2 mg/100 mL) 0.1 mg/min⁷	As narcotic reverses, elevated blood pressure, tachycardia, nausea, and vomiting can occur
Flumazenil	0.2-1 mg dose Each 0.2-mg increment should be given over 1 minute In clinical trials, 75% of patients responded to a dose of 1-3 mg	Frequent side effects (≈10%): nausea, vomiting, headache, blurred vision Major side effect (<1%): seizure⁶

Optimization of the airway often requires repositioning the patient’s head and neck. A simple understanding of the anatomy allows anyone to place the patient’s head in more favorable position for gas exchange. The tongue is the most common cause of upper airway obstruction. A head-tilt/chin-lift or jaw-thrust maneuver (Fig. 16-2) also called the sniffing position may establish an airway. If proper positioning fails to establish a viable airway, however, more invasive maneuvers such as using a nasopharyngeal/oropharyngeal airway or a laryngeal mask airway (LMA) may be necessary and will be discussed in a later section.⁵

FIGURE 16-2 A, Chin lift into sniffing position. B, Jaw thrust. C, Good mask position with one hand. D, Good mask position with two hands.

Both benzodiazepines and narcotics have reversal agents that if used correctly could save an oversedated patient from having a respiratory arrest. Flumazenil antagonizes the action of benzodiazepines on the central nervous system and inhibits activity at γ-aminobutyric acid/benzodiazepine receptor sites. It is contraindicated in patients with serious tricyclic overdoses.⁶ Available in injectable 0.1 mg/mL, flumazenil can be given undiluted or in D₅W, lactated Ringer’s solution, or 0.9 normal saline. The initial intravenous (IV) dose is 0.2 to 0.4 mg over 15 seconds. If ineffective, a repeat dose can be given every 60 seconds. Maximum initial dose is 1 mg. If the patient becomes oversedated, a repeat dose can be given, and a drip may have to be started if the half-life of the offending benzodiazepine is longer than the half-life of flumazenil (41-79 minutes). Adverse effects include seizures, dizziness, headache, blurred vision, diplopia, visual field deficit, hyperventilation, nausea, and vomiting.⁶

Naloxone hydrochloride is a pure narcotic antagonist. It reverses the respiratory depression, sedation, and hypotensive effects of opioids. In the absence of narcotics, naloxone has no activity. Caution must be used in narcotic addiction, cardiac disease, and use of cardiotoxic drugs. Rapid reversal of narcotic depression may also cause nausea, vomiting, diaphoresis, and circulatory stress. The initial dose is 0.1 to 2 mg IV at 2- to 3-minute intervals until the desired effect of reversal is reached. It can be given undiluted as a bolus or as an IV infusion with D₅W or 0.9 normal saline. As with flumazenil, a drip may have to be started owing to a longer half-life of the offending agent. Naloxone has a half-life of 30 to 81 minutes. As an infusion, use 3.7 µg/kg/h. Adverse effects include seizures, ventricular tachycardia, ventricular fibrillation, acute narcotic abstinence syndrome, and return of pain.⁷

If stimulation, airway optimization, and reversal agents fail to rectify the situation, airway compromise may be the underlying problem, in which case the clinician should continue down the airway management algorithm (see Fig. 16-1).