Anesthetic considerations

The primary goal of anesthesia in the patient with MR is to maintain forward aortic flow while minimizing regurgitant flow and development of pulmonary edema (Box 36.1). The volume of regurgitant flow across the mitral valve is related to the size of the regurgitant orifice (which is related to ventricular size), the time available for retrograde flow, and the pressure gradient across the dysfunctional valve [22]. Patients with chronic, compensated MR will be sensitive to changes in ventricular loading conditions and preload should generally be maintained during anesthesia [23]. Overzealous fluid administration should be avoided; however, to avoid ventricular distension and resultant changes in regurgitant flow. Maintenance fluid rates of 2–4 mL/kg/h are generally recommended. Preload reduction may be helpful in some cases. Heart rates should be maintained at a normal or slightly above normal rate to help maintain smaller left ventricular volumes and minimize MR secondary to annular dilation. Bradycardia also increases the duration of systolic contraction and the time available for regurgitant flow.

Most patients with MR benefit greatly from afterload reduction. By reducing afterload, the left ventricular systolic pressures required for ejection from the ventricle to the aorta and arterial vasculature decrease, optimizing forward flow. This, in turn, decreases the pressure gradient from the left ventricle to the left atrium during systole and decreases regurgitant flow. Adequate depth of anesthesia and anesthetic agents that promote arteriolar dilation and maintenance of heart rate are generally recommended. In contrast, administration of drugs that cause increases in systemic blood pressure and afterload (e.g., α₂‐adrenergic receptor agonists) can impair forward flow, increase regurgitant flow, and cause rapid deterioration of patients with MR. In early compensated MR, LV contractility may be preserved, but patients with significant MR may benefit from inotropic support with a drug such as dobutamine (5–15 μg/kg/min) (Table 36.4).

Premedication may be required in some cases to decrease the anxiety of the animal and stress during patient handling, minimizing catecholamine release, tachycardia, and increased myocardial work. Ideally, patients should receive supplemental oxygen after receiving sedative medication, but the stress of restraint for oxygen administration should be considered. If preoperative sedation is necessary, opioid receptor agonists are generally the drug class of choice since they usually cause minimal cardiovascular depression at clinically useful doses, with left ventricular contractility, CO, and systemic blood pressure being well maintained. In healthy animals, opioids cause behavioral changes ranging from sedation to excitement; however, in depressed or critically ill patients, opioids usually cause sedation. Opioids may cause dose‐dependent bradycardia by stimulation of the vagal nerve [24]. Heart rate should be monitored and an anticholinergic drug such as glycopyrrolate or atropine administered if beneficial. Some animals with MR may also have pulmonary hypertension (PHT) and right heart failure. Increased carbon dioxide secondary to opioid‐induced hypoventilation can increase pulmonary pressures and may be of concern in those animals with PHT.

A combination of an opioid receptor agonist (e.g., fentanyl, methadone, or hydromorphone) or agonist/antagonist (e.g., butorphanol and buprenorphine) and a benzodiazepine tranquilizer (diazepam or midazolam) may be used to sedate patients for chest radiographs or echocardiography. This combination provides sedation with minimal cardiovascular depression [25–27]. The use of fentanyl may be more likely to cause clinically significant bradycardia. Reversal may be accomplished by using an opioid receptor antagonist such as naloxone and/or a benzodiazepine antagonist such as flumazenil. Phenothiazine tranquilizers such as acepromazine in low doses may be beneficial in some patients with MR because they calm the patient, decrease afterload, and decrease the incidence of arrhythmias. Acepromazine should only be used after careful consideration; however, since α₁‐adrenergic receptor antagonism may cause hypotension, not only by decreasing SVR, but also by causing venodilation and decreased preload. In conscious dogs, intravenous acepromazine (0.01–0.05 mg/kg) decreased mean arterial pressure (MAP) and stroke index, but did not significantly change SVR, heart rate, or cardiac index [28].

In general, a carefully titrated anesthetic induction is preferred in the cardiac patient with continuous monitoring of cardiovascular parameters. Although no one best technique exists, a high‐dose opioid technique including an opioid and a benzodiazepine tranquilizer with or without low‐dose propofol, etomidate, and/or alfaxalone is often advocated for induction to maintain systolic function in patients with severe myocardial dysfunction. Premedicaton with maropitant 30–60 min prior to induction is helpful in preventing emesis if hydromorphone or etomidate are being used [29]. MR patients with minimal systolic dysfunction may be anesthetized with other protocols using propofol or alfaxalone, (remembering to avoid excessive increases in SVR).

The primary advantages of opioids are lack of myocardial depression and maintenance of hemodynamic stability. Most opioid receptor agonists, with the exception of meperidine, lack negative inotropic effects with clinically used doses. Hydromorphone, methadone, fentanyl, or synthetic fentanyl derivatives such as remifentanil [30–34] are usually preferred. μ‐Opioid receptor agonists such as fentanyl and its analogs, although relatively free of direct cardiovascular effects, can cause a significant vagally mediated bradycardia that would result in decreased CO. The extent of the bradycardia is dependent on the dose and rate of drug administration, and the use of any opioid in high doses can produce excessive bradycardia. Some anesthesiologists prefer to administer anticholinergics such as glycopyrrolate prior to high‐dose opioids used during induction to avoid extreme swings in heart rate. Vagally mediated bradycardia induced by fentanyl (e.g., at 5 μg/kg IV) can sometimes be useful in ameliorating the sympathomimetic effects of other induction agents such as alfaxalone and help prevent significant changes in heart rate during induction. Other adjunctive drugs are commonly used, including benzodiazepine tranquilizers such as midazolam or diazepam.

A low dose of propofol given as a slow infusion is often used as an induction agent in patients with MR or other cardiac disease. Propofol acts as a vasodilator and can decrease afterload while maintaining heart rate. Rapid administration of large doses of propofol should generally be avoided owing to potentially profound cardiovascular effects, including vasodilation, decreased cardiac contractility, and hypotension [35–41]. In patients with poor systolic function, propofol induction requirements can be reduced by concurrent administration of other drugs in a balanced induction protocol, including an opioid, a benzodiazepine, and/or etomidate. Co‐administration of propofol and etomidate decreases the required doses of each individual drug. While one study found that midazolam co‐induction decreased the induction dose of propofol and improved the quality of induction, it did not improve cardiopulmonary variables in critically ill dogs [40]. Etomidate is a useful anesthetic induction agent in any animal with cardiac disease associated with poor systolic function [42–45]. Left ventricular pressures, mean aortic pressure, and coronary blood flow do not change significantly in healthy dogs receiving up to 2.5 mg/kg for induction. Etomidate is not arrhythmogenic and may also be useful in animals with cardiac conduction abnormalities. The addition of midazolam decreases the etomidate induction dose required with no change in cardiopulmonary function [45]. An opioid is also used as part of this induction protocol. Alfaxalone has a rather large therapeutic index and can also be used to induce animals with heart disease, although dose‐dependent adverse effects such as tachycardia can be seen after larger doses are given rapidly [46–51]. The administration of fentanyl prior to alfaxalone can decrease induction requirements and ameliorate changes in heart rate.

Maintenance of anesthesia can be achieved with an opioid (e.g., fentanyl or remifentanil), propofol infusion, and/or alfaxalone infusion (or some combination of these) with or without an inhalant agent. Etomidate infusions are not recommended owing to the potential for hemolysis associated with the high osmolality of the commercially available formulations and also concerns related to prolonged adrenocortical suppression [52–54]. A single bolus injection of 2 mg/kg etomidate reduces the adrenocortical response to anesthesia and surgery for 2–6 h, and longer infusions have been associated with prolonged adrenocortical suppression and higher mortality rates in critically ill multiple‐trauma patients [55].

The hemodynamic changes associated with dexmedetomidine administration include bradycardia and increased SVR and are generally to be avoided. When given as a constant rate infusion without a loading bolus, plasma concentrations are lower and may reduce cardiovascular side effects, although increased blood pressure and decreased heart rate still occur [56]. Use of vatinoxan (MK‐467), a peripheral α₂‐adrenergic receptor antagonist, in combination with medetomidine may reduce the increase in SVR and may expand the potential utility of α₂‐adrenergic receptor agonists in patients with myocardial disease. However, further research to establish the safety of this combination in patients with heart disease is needed.

Most of the commonly used inhalant agents (e.g., isoflurane, sevoflurane, and desflurane) tend to preserve myocardial contractility at light anesthetic planes. The advantages of inhalant anesthetics for maintenance of anesthesia include their dose‐dependent cardiovascular effects, the ability to rapidly adjust the depth of anesthesia, and their suppression of sympathetic responses associated with surgical stress. Disadvantages include myocardial depression, systemic hypotension (due to decreased contractility or vasodilation), and lack of postoperative analgesia. Mild decreases in SVR coupled with adequate systolic function may reduce regurgitant fraction and are goals of anesthetizing patients with MR. Decreased preload and decreased systolic function associated with deep planes of inhalant anesthesia are not recommended; therefore, multimodal “balanced” anesthetic techniques are often advocated.

Patients on medication for heart disease are generally continued on their medications (especially diuretics, calcium channel blockers, antiarrhythmics, and inotropic drugs) until the time of anesthesia. Pimobendan acts as both a positive inotrope (by increasing calcium binding to the myofibrils) and as a vasodilator (by acting as a phosphodiesterase 3 inhibitor) and is usually given on the day of anesthesia. However, hypotension may be more pronounced under anesthesia in patients receiving ACEIs such as enalapril and some anesthesiologists prefer to delay giving enalapril until after recovery. It is always prudent to have inotropic and venoconstrictor agents immediately available for the management of intraoperative hypotension since fluid administration is often contraindicated.

Anesthetic considerations

Anesthetic considerations for DCM patients are similar to those of animals with MR, with the added concerns of decreased systolic function (which may be severe), CHF, and increased incidence of cardiac arrhythmias. Additionally, dogs with cardiomyopathy often have a significant downregulation of β‐adrenergic receptors in the heart, although receptor affinity does not change [57], making these animals more resistant to treatment with a positive inotrope. Dogs with significant systolic dysfunction probably benefit from inotropic drug support (e.g., dobutamine or dopamine) during anesthesia.

Ventricular arrhythmias can be seen during anesthesia in animals with DCM. Antiarrhythmic drugs such as lidocaine and procainamide should be available but are often reserved for cases where the frequency of abnormal beats creates significant blood pressure or CO decreases. Although often unnecessary, esmolol, a short‐acting β‐blocker, may be given as an infusion as indicated (0.5 mg/kg loading bolus followed by an infusion of 0.01–0.2 mg/kg/min to reduce the frequency of ventricular premature contractions associated with sympathetic stimulation). The dose rate may be adjusted as needed to minimize any negative inotropic and bradycardic effects associated with β‐receptor blockade. In addition to blood pressure monitoring (direct or indirect), monitoring of end‐tidal CO₂ can be helpful under anesthesia, as a secondary means of monitoring CO.

In dogs with concurrent DCM and AF, electrocardioversion may be considered (if the patient is a candidate) at the beginning of anesthesia. The increased ventricular filling following resynchronization of the atria and ventricles can improve CO. Alternatively, drugs that slow the sinus rate and conduction through the AV node, such as fentanyl, can be used during anesthesia. Anticholinergic agents are to be avoided in dogs with AF but may be useful for dogs with DCM without AF that are bradycardic under anesthesia. Fentanyl at a dose of 5–40 μg/kg/h can be an effective anesthetic in sick dogs when used as a primary agent in combination with oxygen and ventilation in those animals that do not tolerate inhalant anesthetics. Remifentanil has an elimination half‐life shorter than that of fentanyl, with rapid recovery times regardless of the duration of infusion, although either opioid is suitable for an infusion technique. Infusion of remifentanil at 0.25–0.5 μg/kg/min with propofol at 0.2 mg/kg/min produces little change in mean arterial blood pressures in healthy dogs, although the heart rate decreases with increasing doses of remifentanil [34].

Anesthetic considerations

In animals with VSD or PDA, the degree and magnitude of shunt flow are dependent upon relative outflow resistances, which are determined by the size of the defect or ductus and the difference between systemic and pulmonary resistance. With simple left‐to‐right shunting, pulmonary blood flow is increased, and the right ventricle and pulmonary vasculature can be pressure or volume overloaded; some degree of pulmonary hypertension (PHT) may be present. Further increases in pulmonary blood flow are avoided by preventing increases in SVR. In addition, manipulations that decrease pulmonary vascular resistance (PVR) (hypocapnia, alkalemia, spontaneous ventilation, and deep anesthesia) can also increase the magnitude of left‐to‐right shunt flow.

In many cases, heart failure is not yet present, and the animal is relatively young and active and may become excited with restraint. Almost any anesthetic agent that does not significantly alter SVR may be used safely for premedication, induction, or maintenance. Drugs that significantly increase SVR, including the α₂‐adrenergic receptor agonists (e.g., dexmedetomidine) are generally avoided. Repair of PDA may be accomplished by surgical ligation or transvascular occlusion, with the rate of survival being similar between the two techniques [58], although arrhythmias and hypotension are commonly reported [59].

If not corrected within the first year, a significant percentage of dogs with PDA will develop CHF. For those cases in which some degree of CHF is present, considerations are similar to those for patients with volume overload (see earlier). An opioid‐based induction technique with benzodiazepine tranquilizer and etomidate, alfaxalone, or propofol followed by inhalant anesthesia or propofol infusion, or a combination of fentanyl/remifentanil and propofol infusion can all be used [33,58,59]. Propofol can result in clinically significant changes in cardiac shunt direction and arterial desaturation; however, due to a decrease in SVR [60]. This decrease is usually dependent on the dose and rapidity with which the propofol is given.

Diastolic pressures are often low in these patients owing to the shunting of blood from the systemic circulation to the lower resistance pulmonary circulation. A characteristic change in the arterial waveform may be seen with ligation of the PDA, including a decrease in the pulse pressure, increase in mean and diastolic pressures, and reappearance of a dicrotic (reflected) wave (Fig. 36.3). Hypotension may be pronounced in some patients due to the low diastolic pressures and is generally treated with the use of an inotrope such as dobutamine (see Table 36.4), which helps maintain myocardial function and heart rate while avoiding increases in SVR. However, significant decreases in SVR must also be avoided, especially in those patients with significant PHT in which shunt flows may reverse in the face of inhalant anesthetic‐associated arteriolar dilation. These patients will benefit from the administration of a vasoconstrictor (e.g., dopamine or phenylephrine; see Table 36.4) to maintain baseline SVR. A sudden decrease in arterial oxygen saturation due to venous admixture as monitored with a pulse oximeter or arterial blood gas may be an early indicator of shunt reversal.

If surgery is to be performed on a relatively young animal for repair of a congenital heart defect, the progressive maturation of the autonomic nervous system and cardiovascular responses must be taken into account. In puppies, the adrenergic vasoconstrictor response is not fully developed until after 8 weeks of age [61]. Similarly, although chronotropic responsiveness is apparent at 1 week, the inotropic response to sympathetic stimulation does not fully develop until after 8 weeks of age [62]. Neonatal patients typically have a higher heart rate and lower arterial blood pressure and SVR than adults. In addition, the cardiovascular response to sympathomimetic agents may be less pronounced in the neonatal or pediatric patient than the adult animals of similar species [63–65].

Anesthetic considerations

Goals of anesthesia for the patient with TF or other reverse shunt disorders are to maintain SVR and arterial pressures while minimizing changes in PVR and pulmonary pressures. As right‐to‐left shunting increases so does arterial oxygen desaturation. Patients with significant PHT can be sensitive to changes in preload. Hypotension secondary to hypovolemia or vasodilation should be avoided and treated immediately if it occurs.

Premedication with an intramuscular opioid may be useful as struggling and sympathetic stimulation with restraint can increase right‐to‐left flow. These drugs should, however, be used judiciously as hypoventilation can lead to hypercarbia and respiratory acidosis, which can increase PVR and reverse shunting. Hypoxemia and hypotension can occur quickly in these patients. Preoxygenation prior to induction of anesthesia is extremely important, not only to address the underlying chronic hypoxemia that occurs in these animals, but also as a means of decreasing PVR. Other manipulations that can help decrease PVR include lowering the hematocrit to < 60% prior to anesthesia and hyperventilation with the maintenance of relative hypocarbia and respiratory alkalosis during anesthesia. Care must be taken with controlled ventilation, as increases in intrathoracic pressure with mechanical ventilation or the use of positive end‐expiratory pressure can increase PVR and the magnitude of right‐to‐left shunt flow.

Patients with TF often have a dynamic component to the stenotic lesion and increases in heart rate may exacerbate the pulmonary outflow obstruction and reverse shunting [23]. An opioid‐based induction technique is often used with or without etomidate, although significant decreases in heart rates should be avoided, especially if fentanyl or remifentanil is used. All catheters and injection ports should be cleared of bubbles to avoid systemic air embolization.

SVR must be maintained in these patients, as excessive hypotension will increase the right‐to‐left flow. Phenylephrine, an α‐adrenergic receptor agonist that causes arterial and venous vasoconstriction, can be useful in reversing right‐to‐left shunting during anesthesia, although other pressor agents such as norepinephrine or dopamine may also be used.

Anesthetic considerations

Patients with SAS or PS often have poor ventricular compliance; thus, it is critically important to maintain adequate preload in these animals. Maintaining an adequate venous return by insuring a full intravascular volume to fill the non‐compliant ventricular chamber will help optimize diastolic filling and CO, although volume overload should be avoided. In addition, these patients are dependent on maintenance of a normal sinus rhythm and atrial “kick” to optimize ventricular filling. Tachycardia must be avoided to limit myocardial oxygen deficit (Box 36.2). The stenosis may also have a dynamic component, becoming more pronounced at rapid heart rates.