Heart rate dropped to 40 during surgery

Sustained Bradycardia

A sustained fetal heart rate of less than 120 beats/min represents fetal bradycardia and merits further evaluation. In contrast, fetal bradycardia related to deep transducer pressure or a particular maternal lie might represent a normal fetal response. In such cases, if the fetal heart rate normalizes after relief of transducer pressure or change in maternal or fetal position, no further cardiac evaluation may be necessary.

The differential diagnosis of fetal bradycardia includes sinus bradycardia, atrial bradycardia, blocked atrial bigeminy, atrial flutter with high-degree block, and complete heart block. Treatment approaches and prognosis depend on the precise diagnosis. Sinus bradycardia, manifesting with a slow rate but with physiologic variability and with 1 : 1 conduction between the atria and ventricles, may represent fetal distress and therefore should prompt a thorough evaluation of fetal well-being and placental function. Particularly if it is associated with second- or third-degree heart block, fetal sinus bradycardia may be the first sign of long QT syndrome.247 Affected fetuses and newborns are at risk for ventricular tachycardia. For this reason, fetuses in good health that demonstrate unexplained sinus bradycardia without fetal distress should undergo electrocardiographic evaluation after delivery. In addition, because long QT syndrome may run in families, a family history of long QT syndrome, recurrent syncope, or sudden infant death syndrome should be sought. In contrast, atrial bradycardia may appear identical to sinus bradycardia, but it actually represents the normal rate of an accessory atrial pacemaker in the absence of an effective sinus node. Such an atrial bradycardia commonly occurs in conjunction with polysplenia, so the suspicion of this rhythm should prompt evaluation for the cardiac and abdominal abnormalities seen with polysplenia.126,130,186

Occasionally, fetal sinus bradycardia represents blocked atrial bigeminy, in which normal sinus beats alternate with blocked PACs. In atrial bigeminy the premature beats may be blocked if they occur very early, when the atrioventricular node is still refractory. In such cases, only sinus beats conduct, generating a uniform ventricular rate exactly half of the atrial rate. No specific therapy is warranted other than close observation and maternal avoidance of caffeine, decongestant medications, and tobacco. Prognosis is excellent.

In some cases, atrial flutter may conduct consistently 3 : 1 or 4 : 1, and such fetuses may present with bradycardia. Close inspection of the heart with 2D, M-mode, or spectral Doppler imaging can diagnose the arrhythmia and assess the degree of conduction. Although atrial flutter usually has an atrial rate of 300 to 500 beats/min, high degrees of atrioventricular block may lead to fetal bradycardia; for example, atrial flutter with a flutter rate of 300 beats/min and a 3 : 1 conduction would present with a fetal ventricular rate of 100 beats/min. Unlike SVT, atrial flutter rarely manifests as intermittent tachycardia; flutter is typically incessant, although the ventricular response rate may vary. Like other fetal arrhythmias, fetal atrial flutter may be associated with structural heart disease. Treatment of atrial flutter, typically with pharmacologic therapy (e.g., digoxin, sotalol, amiodarone) administered orally to the mother, can slow the ventricular response rate and decrease the likelihood of development of fetal CHF or hydrops. Some investigators believe that sotalol has emerged as a potential first-line agent for the treatment of atrial flutter.248

Risk Assessment

Bradyarrhythmias can arise from either intrinsic myocardial causes or external influences, such as increased vagal tone or electrolyte imbalance. Implanted artificial pacemakers (see Chapter 97) are indicated for patients with symptomatic bradyarrhythmias (e.g., easy fatigability, near or true syncope) without reversible causes.

Resolution and Consequences of Apnea, Bradycardia, and Intermittent Hypoxia

Apnea of prematurity generally resolves by 36-40 weeks’ postconceptional age. Cardiorespiratory events in most preterm infants return to baseline “normal full-term” levels by 43-44 weeks’ postconceptional age.43 In infants ≤26 weeks’ gestation, resolution may take longer. For a subset of infants, the persistence of cardiorespiratory events can delay hospital discharge despite having achieved other physiologic developmental milestones. In these infants, apnea longer than 20 seconds is rare; rather, these infants exhibit frequent bradycardia to less than 70 or 80 beats per minute with short respiratory pauses.13 As mentioned earlier, bedside nursing observations are known to be an unreliable measure of apnea and bradycardia and do not correlate with electronic recordings of events; however, they may be beneficial when trying to determine which episodes are clinically significant. A 2016 Clinical Report from the Committee on Fetus and Newborn emphasizes the lack of consistent definitions for apnea, bradycardia, and desaturation and recognizes that monitoring practices vary among NICUs. These inconsistencies have major implications on length of stay (Box 67.3).17 To assess the maturation of respiratory control in premature infants and better inform discharge planning, Lorch and colleagues examined the success rates (the percentage of infants who had no additional events) following various event-free intervals. They found that the risk of recurrence of apnea or bradycardia depends on both the gestational age and postmenstrual age at the time of the last event. For the entire cohort in this retrospective study, a 95% success rate was achieved with a 7-day apnea- or bradycardia-free interval.29

Because of the growing concern over the consequences of intermittent hypoxia and recognition that intermittent hypoxia persists after discontinuation of caffeine for the treatment of apnea of prematurity, extended caffeine dosing until term-adjusted age has recently been proposed and is under investigation.15,44

Correlating apnea and its consequences with an unfavorable neurologic outcome is problematic, because apnea and brain injury may coexist in premature infants, making it challenging to determine causality. However, evidence is mounting and there are data that suggest a link between delayed apnea resolution and the severity of the apnea course with impaired neurodevelopmental outcome.40 A high number of cardiorespiratory events recorded after discharge via home cardiorespiratory monitoring also appear to correlate with a less favorable neurodevelopmental outcome.23 A 2014 retrospective chart review in extremely low birth weight infants found an association between a greater frequency and severity of bradycardia and worse language development in the first 2 years of life after adjusting for neonatal and social variables.21 And finally, in a post hoc analysis of the Canadian Oxygen Trial, prolonged hypoxemic episodes in the first 2-3 months of life were associated with adverse 18-month outcomes.42 Former preterm infants appear to be at greater risk of later sleep-disordered breathing. Recurrent episodes of desaturation during early life and resultant effects on neuronal plasticity related to peripheral or central respiratory control mechanisms may serve as the underlying mechanisms for such a putative relationship.

Abstract

Bradyarrhythmias encompass a number of rhythm disturbances including sinus node dysfunction (SND) and atrioventricular block (AVB). Bradyarrhythmia may be asymptomatic and detected during routine electrocardiographic (ECG) examination or presented with dizziness, fatigue, syncope, presyncope, exercise intolerance, and poor concentration. Symptomatic SND is called sick sinus syndrome (SSS). ECG presentations of SND are sinus bradycardia, sinus pause or arrest, sinoatrial exit block, chronotropic incompetence, and tachy-brady syndrome. Symptom–rhythm correlation is highly important in SSS diagnosis. The initial clues to the diagnosis of SSS are most often gleaned from the patient's history, and the diagnosis is confirmed by a 12-lead surface ECG, ambulatory ECG recording, or exercise stress testing. In SND, treatment should be limited to those patients with a good symptom–rhythm correlation. Asymptomatic patients do not need any treatment. AVB is traditionally classified as first-, second-, or third-degree (complete) AV block. On the basis of intracardiac recordings, supra-, intra-, or infra-Hisian block can be differentiated. Diagnosis of AVB can be established in most cases noninvasively by the 12-lead ECG. In intermittent AVB, ambulatory ECG monitoring and exercise testing are important to establish a symptom–rhythm correlation. Except for asymptomatic first-degree AVB, type 1 second-degree AVB, and reversible types, other types of AVBs need a pacemaker, irrespective of associated symptoms.

Hypotension and Bradycardia

Hypotension can be caused by myocardial depression, inadequate heart rate, or peripheral vasodilation. Atropine may be used for bradycardia but is rarely effective. We recommend atropine at the doses noted earlier for a heart rate of less than 50 beats per minute with concomitant hypotension and symptoms of severe bradycardia such as weakness, drowsiness, or obtundation. Atropine's effect has often been minimal and short-lived, and it is at best a temporizing intervention. A bolus of crystalloid fluid (20 to 40 mL/kg or more) should also be infused early; however, care should be taken to avoid fluid overload given the additional risk of pulmonary edema with calcium channel blocker poisoning particularly in older patients. Calcium salts, HDI, vasopressors, and inotropes should be administered in the same fashion as noted earlier for beta-blocker toxicity with one exception—we do not recommend glucagon in calcium channel blocker poisoning. It has no mechanistic advantage over epinephrine, and no good evidence exists to support its use in calcium channel blocker poisoning.

IFE (eg, Intralipid) has been described in the use of calcium channel blockers. The proposed mechanisms are discussed earlier with beta-blockers. Animal evidence exists that IFE may be effective especially for the treatment of verapamil toxicity. Human case reports exist of successful resuscitation of toxicity from diltiazem and verapamil. Dosing and indications are identical to those for beta-blocker toxicity. We recommend that IFE be used in patients with hypotension refractory to calcium, HDI, and three vasopressors.

Methylene blue is an emerging therapy for calcium channel blocker poisoning.24 Although traditionally used as a reducing agent for the treatment of methemoglobinemia, methylene blue is also a vasoconstrictor. Specifically, it inhibits the enzyme guanylyl cyclase, resulting in decreased production of cyclic guanosine monophosphate (cGMP) and inhibition of endothelial smooth muscle relaxation, causing an increase in systemic vascular resistance.25 Methylene blue is particularly intriguing to use in the treatment of amlodipine poisoning, because amlodipine specifically causes an increase in nitric oxide production, which leads to increased cGMP and vasodilation as noted earlier. Data are limited to a small number of animal studies and human case reports, and thus far suggest improvements more in hemodynamic parameters as opposed to mortality. We recommend the use of methylene blue only as an alternative salvage therapy to ECMO when HDI, catecholamines, and IFE have failed. Dosing involves a 1- to 2-mg/kg bolus of a 1% methylene blue solution followed by an infusion of 1 mg/kg for up to 6 hours.

Bradycardia.

Bradycardia may result from vagotonic stimulation due to prolonged laryngoscopy and, in severe and prolonged hypoxemia, during failed intubations. Patients with intrinsic atrioventricular (AV) nodal disease and those on AV nodal blocking drugs—such as β-blockers, calcium channel blockers, and amiodarone—are prone to bradycardia. High-dose opiates (such as fentanyl) or sedatives (such as dexmedetomidine) may also predispose to bradycardia by drastically reducing the sympathetic tone. Hypoxemia is the primary cause of bradycardia in the pediatric population, especially infants. Bradycardia results in reduced CO and, therefore, hypotension. Several database analyses have noted that bradycardia preceded cardiac arrest in 90% of cases.50,54 With the aggressive implementation of the ASA difficult airway algorithm and the availability of rescue devices, such as the LMA and fiberoptic bronchoscopy, the incidence of bradycardia and cardiac arrest following intubation has decreased by up to 50%.55

Bradyarrhythmias

Bradyarrhythmias are relatively rare after noncardiac thoracic surgery. In most cases, they consist of transitory episodes of low ventricular heart rate resulting from (usually preexisting) sick sinus syndrome or various degrees of atrioventricular blocks. Bradyarrhythmias may be hemodynamically relevant because of a decrease in cardiac output. Atropine can reverse symptomatic bradycardia. It is prudent to stop all unnecessary medications that can cause increased AV block like beta blockers or calcium channel blockers. Temporary electrical pacing may be required in symptomatic bradycardias not responding to atropine. In some cases, when the conduction defect does not revert, permanent pacing may be necessary.

Terminology

Bradycardia is a very vague term, and thus to be more exact, one must try to examine the site of bradycardia, the degree of bradycardia, and hemodynamic consequences in order to better communicate its importance or severity. A classification scheme of bradycardia location and degree is shown in Figure 31.19. Essentially, the classification scheme requires that the site of bradycardia be localized to the level of either the sinus node or the AV junction (including the AV node and His–Purkinje system). Once location and degree of bradycardia have been identified, it is important to determine whether the bradycardia has resulted in any hemodynamic compromise. Generally, if bradycardia has caused hemodynamic compromise in the absence of reversible causes, then pacemaker implantation is indicated.

Sinus node (SA) dysfunction manifests as sinus bradycardia, sinus pauses, or prolonged periods of asystole and is usually transient, readily treatable, and rarely causes serious compromise. Examples of SA dysfunction are shown in Figure 31.20. Conversely, the diagnosis of AV block requires differentiation of physiologic block from pathologic block; the latter usually occurs in the presence of severe AV node or His–Purkinje disease and almost universally requires pacing. Examples of AV block are shown in Figure 31.21.

In the following sections, several important scenarios of bradycardia that may be encountered in the critically ill patient are discussed.