Perioperative Cardiac Complications

Major cardiac complications presenting as myocardial infarction, myocardial ischemia, cardiac failure, or life-threatening dysrhythmias contribute significantly to perioperative morbidity and mortality. Preventive strategies are of major importance since even despite adequate treatment these events are associated with poor outcome.

Myocardial Ischemia

According to Poldermans and Boersma (2005), the incidence of a perioperative myocardial infarction is 0.185% in the United States. Approximately 50,000out of 27 million patients who are given anesthesia for surgical procedures annually suffer perioperative myocar-dial infarction. The cause is a prolonged mismatch between myocardial oxygen demand and supply owing to the stress of surgery or as the result of a sudden rupture of a vulnerable plaque followed by thrombus formation and coronary artery occlusion.

Beta-blockers decrease the myocardial oxygen demand by reducing heart rate and myocardial contractility. Additionally they modulate the adrenergic activity leading to decreased levels of fatty acids, thus resulting in a shift in myocardial metabolism toward glucose uptake (Schouten et al. 2006). To identify patients who might benefit from a perioperative beta-blocker therapy, Lindenauer et al. (2005) conducted a retrospective cohort study on 782,969 patients using the validated Revised Cardiac Risk Index (RCRI) (Lee et al. 1999) to stratify patients as low cardiac risk (RCRI 0 and 1) and as high cardiac risk (RCRI 2, 3, 4 or more). The study demonstrated that perioperative beta-blocker therapy is associated with a reduced risk of in-hospital death among high risk, but not low-risk patients undergoing major noncardiac surgery.

According to the meta-analysis of Schouten et al. (2006), in 1,077 patients with noncardiac surgeries, perioperative administration of beta-blockers lowers the risk of myocardial ischemia by 65% (p< 0.001), the risk of myocardial infarction by 56 % (p = 0.04), and the surrogate risk of cardiac death and nonfatal myocardial infarction by 67% (p = 0.002). Administration of beta-blockers should be commenced prior to surgery, a dose-titration has to be carried out up to the induction of anesthesia, and a lifelong continuation of beta-blocker therapy is recommended in high-risk patients. The optimum time interval to start treatment with beta-blockers before surgery has not yet been defined by studies. The choice of the beta-blocker is of minor importance, since no specific beta-blocker demonstrated a superior effect in the perioperative setting. The side effects of perioperative administration of beta-blockers are a 4.3-fold increased risk of bradycardia (p = 0.006), but hypotension, atrioventricular block, pulmonary edema, and bronchospasm are not significantly associated with perioperative beta-blocker therapy. The following contraindications should be kept in mind prior to commencement of beta-blocker therapy: bradycar-dia, second or third degree atrioventricular block, sick sinus syndrome, and acute heart failure. Patients with asthma bronchiale have to be carefully evaluated as to whether they may benefit from primary protective cardiac effects or are harmed by side effects.

For a practical pathway concerning the perioperative beta-blocker therapy, please refer to Fig. 3.1.


Cardiac arrhythmias contribute significantly to morbidity and mortality in the perioperative period. Although the knowledge on antiarrhythmic drug use in nonsurgical settings is expanding rapidly, data on the use of these agents perioperatively are still scarce.

Antiarrhythmic pharmacology is focused on the cardiac ion channels and adrenergic receptors for management of arrhythmias in adults during surgery and anesthesia. Virtually all drugs that modulate heart rhythm work through the adrenergic receptor/second messenger system through one or more ion channels. Generally three classes of ion channels have to be considered based on the cation they conduct: sodium (Na+), calcium (Ca2+), and potassium (K+) channels. Although ion channels as molecular targets are distinctive, the drug receptor sites are highly homologous, causing some class overlap associated with antiar-rhythmic therapy. Table 3.1 lists the molecular targets of antiarrhythmic agents used perioperatively.

Table 3.1. Classification of antiarrhythmic drugs




Na+, K+ channels


Amiodarone, procainamide, aj-maline, quinidine

Na+ channels


Lidocaine, phenytoin, mexileti-nea, tocainidea





Esmolol, amiodarone, proprano-lol, atenolol, sotalola

K+ channels


Bretylium, ibutilide, sotalola, do-fetilidea

Ca2+ channels


Verapamil, diltiazem, amiodarone

Orally (only commercially available form)

Orally (only commercially available form)

Risk factors:

- Diabetes mellitus

- Art. Hypertension ■ Abuse at nicotine

- Renal insufficiency

- Hyperlipoproteinemia

Préexistent coronary artery disease

Risk factors:

- Diabetes mellitus

- Art. Hypertension ■ Abuse at nicotine

- Renal insufficiency

- Hyperlipoproteinemia

Préexistent therapy with p-b lock ere

No therapy with p-blockers

>2 Risk factors

<2 Risk factors

Fig. 3.1. Perioperative therapy with |3-blockers. Patients with good left-ventricular function (LVF) receive meto-prololsuccinate 95 mg once per day; patients with impaired LVF receive 47.5 mg once per day. For contraindications and further explanations see text. Modified from Teschendorf 2006

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