Anesthesia for the cardiac patient (Proceedings)


Anesthetizing a patient with cardiac disease requires a plan for the use of supportive measures to maintain adequate tissue perfusion. As in the case of left sided cardiac dysfunction patients, volume administration frequently is not an option to support blood pressure. In these cases, should a positive inotropic or pressor agent be indicated, the volume of the adjunctive agent required should be deducted from the volume of crystalloid administered to maintain a balanced hourly rate.

Adjunctive agents used to support blood pressure

Anesthetizing a patient with cardiac disease requires a plan for the use of supportive measures to maintain adequate tissue perfusion. As in the case of left sided cardiac dysfunction patients, volume administration frequently is not an option to support blood pressure. In these cases, should a positive inotropic or pressor agent be indicated, the volume of the adjunctive agent required should be deducted from the volume of crystalloid administered to maintain a balanced hourly rate.


Cardiomyopathies, or pathologically affected heart muscle can occur in a variety of ways. These diseases are functionally very different from one another, although ultimately the pathological effects on the body and treatment modalities are similar.

Dilated Cardiomyopathy

Dilated cardiomyopathy is most commonly seen in certain large breed dogs. This condition is characterized by elongation, weakening of the heart muscle, so that chamber size is increased, but contractility is compromised. Stroke volume is reduced and resulting in decreased blood pressure. Compensatory mechanisms for hypotension ensue. Chamber enlargement may alter the shape and function of the mitral valve, leading to valvular insufficiency. In addition, the chamber may be so enlarged as to affect cell communication and organized depolarization. Atrial fibrillation, premature ventricular contractions and ventricular tachycardia may develop. Whether heart failure is due to valvular insufficiency or cardiomyopathy, compensatory mechanisms in response to poor cardiac output are similar. The sympathetic nervous system, the renin-angiotensin-aldosterone system are activated. Secretion of antidiuretic hormone increases. Results are increased heart rate and vascular tone, and sodium and water retention.

Treatment of heart failure from either cause is also similar, as it is aimed at minimizing this compensatory mechanism which becomes harmful when they are chronic. Medications to decrease heart rate and improve contractility, decrease blood volume by diuresis, and decrease vascular resistance against which the heart must pump.

Digitalis and digitoxin are positive inotropes which increase the concentration of calcium within the myocardial cells thus increasing the force of contractions and decreasing heart rate. A relatively new addition to management is pimobendan which elicits calcium sensitization of the myofilaments. Anti-arrhythmics such as procainamide, quinidine or mexiletine may be used if indicated. Calcium channel blockers and beta blockers may be used to help control supraventricular arrhythmias.

Diuretics such as furosemide are used for decreasing circulating blood volume. ACE inhibitors cause relaxation of the blood vessels, thereby decreasing systemic vascular resistance. Anesthetic protocols for patients with dilated cardiomyopathy should aim to avoid drugs that would increase heart rate or decrease contractility. Fluids must be delivered with caution to avoid overload. Ideally central venous pressure would be monitored to determine how well the heart is able to handle the circulating volume and fluids may be regulated accordingly.

Hypotension may be corrected with the use of CRI opioid/benzodiazepines to reduce vaporizer setting thus avoiding the dose dependent peripheral vasodilation attributed to inhalant anesthetics. Positive inotropes or beta agonists such as dobutamine may be added if further support of adequate blood pressure is required. These drugs focus on improving contractility without increasing afterload. Dobutamine should be diluted and administered as a constant rate infusion, beginning at 2 micrograms per kilogram per minute, and increased as needed. The use of dobutamine is not benign as increased rate of administration may cause an increase in heart rate or arrhythmias may be noted as it acts as a positive inotrope as well at higher doses as a vasocontrictor. Dopamine as a CRI may also be used to support blood pressure and is calculated to be delivered at a starting rate of 2 mcg/kg/minute.

Ventricular arrhythmias may be exacerbated with the use of beta agonists; however, so close monitoring of the EKG is necessary.

Suggested protocols may include +/- glycopyrrolate at 0.011 mg/kg given subcutaneously, dependent on patient's heart rate

Hydromorphone or oxymorphone at 0.1 mg/kg or 0.05mg/kg given subcutaneously

Pre-medicants will be given 20-30 minutes prior to induction time

Should patients be of a brachycephalic breed where respiratory difficulties may be present, butorphanol at 0.2 mg/kg will be used in lieu of hydromorphone and the patient will be observed for any signs of distress.

pre-oxygenation will occur prior to induction unless the patient becomes distressed by mask placement.

Induction agents:

diazepam /midazolam at 0.2 mg/kg given IV followed by

etomidate at 1-2 mg/kg given IV to effect to facilitate placement of the endotracheal tube.

Anesthetic maintenance-

Inhalant gas anesthesia maintenance will be sevoflurane with oxygen.

Fentanyl at 0.8 mcg/kg/minute and midazolam at 8 mcg/kg/minute combined may be given IV via syringe pump as an anesthetic adjunct for a MAC sparing effect. This will allow the vaporizer setting to be reduced to between 0.25-1% if sevoflurane is the inhalant used. Contraindicated: Ketamine, any alpha 2 agonist, and precaution should be taken with propofol administration.

Hypertrophic Cardiomyopathy

While hypertrophic cardiomyopathy (HCM) is not commonly seen in dogs, it is the most common heart disease in cats.

Feline HCM is common sequelae of hyperthyroidism, but generally, its etiology is not considered genetic. The disease is considered a disease of diastole and is characterized by inability of the heart to fill adequately with blood, thickening of the left ventricular wall and decreased chamber size. Relaxation of the heart muscle during diastole and decreased filling due to chamber size is affected thereby reducing cardiac output.

Hypertrophic cardiomyopathy may also occur independent of hyperthyroidism. In these cases, increased wall thickness and decreased chamber size are still an issue. It is important to maintain heart rate within normal range in order to maintain cardiac output in the face of decreased stroke volume. Relaxation of the heart during diastole is important to promote optimal chamber filling, as well as perfusion to the heart muscle so that it may receive as much oxygen as possible to meet its increased demands. Anticholinergics should be avoided unless bradycardia occurs.

Mitral Valve Insufficiency

One of the most common cardiac disorders in dogs is mitral valve insufficiency. A normal mitral valve will close during ventricular contraction, thereby causing all blood to move forward to systemic circulation. A defective valve will allow some blood to be pumped back into the left atrium. This reduces forward flow, and thus cardiac output and systemic blood pressure. In addition, pressure in the left atrium will increase, making it more difficult for blood to enter it from the lungs. Resulting backpressure in the lungs may lead to pulmonary edema.

Compensatory mechanisms in response to lowered blood pressure will increase the total fluid volume in circulation and cause vasoconstriction. This, however, results in an increase in resistance against which the left ventricle must pump. Over time, the left ventricular muscle will may enlarge due to this "workout", but its efficiency continues to decline. Eventually, if left untreated, left-sided heart failure will result in life threatening pulmonary edema and inadequate tissue perfusion.

Treatment for significant mitral valve dysfunction consists of medications that cause relaxation of the blood vessels, such as ACE inhibitors, or other vasodilators making it easier for the left ventricle to pump blood forward. Diuretics (e.g. furosemide) are administered in order to reduce the volume load for the heart to pump, and remove fluid causing pulmonary edema. In addition, positive inotropes (e.g. digitalis) will increase contractility of the heart by increasing the concentration of calcium in heart muscle cells.

When anesthetizing a patient with mitral valve disease, one must be careful since the vasodilatory effects of many anesthetics may be exaggerated by the patient's existing medication. On the other hand, untreated mitral valve disease may benefit from the vasodilating effects of anesthetics. When pressors are needed, pure alpha agonists such as phenylephrine that cause vasoconstriction may exacerbate the back pressure and may result in pulmonary edema. Beta agonists such as dobutamine may be used to improve contractility. Fluids must be administered conservatively, to avoid overload and pulmonary edema. However, because these patients may have been on diuretics and also have the same issues a normal patient with regard to fluid needs, there is a balance that must be achieved. Currently, the most effective way to monitor this balance is by measuring central venous pressure (which approximates the pressure of the blood entering the right atrium).

Maintaining heart rate within the normal range for these patients is important. Tachycardia should be avoided as it will increase the oxygen needs of the heart, so an anticholinergic is usually not recommended prophylactically as in a pre-med. However, low doses can be used if indicated by bradycardia that is causing hypotension.

Opioids, benzodiazepines, and etomidate are considered good choices in an anesthesia protocol for these cases. Ketamine is usually avoided as it increases myocardial oxygen needs. Propofol should be avoided or used with extreme care due to its vasodilating andhypotensive effects. IV administration of an opioid/benzodiazepine combination immediately prior to induction with propofol can greatly reduce the amount of propofol required to capture the airway thus allowing the anesthetist to use this agent while avoiding the majority of the myocardial depressive effects.

Aortic stenosis

Aortic stenosis is usually a congenital abnormality. Stenoses may be subvalvular, valvular, or supravalular and is caused by the development of extra fibrous tissue sometime during the first few months in life. The result is a partial obstruction of flow from the left ventricle through the aortic valve and out the aorta to systemic circulation. This obstruction causes increased left intraventricular pressure and subsequent thickening of the left ventricular walls. Other sequelae include cardiac ischemia, arrhythmias, aortic or mitral regurgitation, and left-sided congestive failure.

Diagnosis is usually made at an early age due to a murmur caused by the increased turbulence of blood flow in the affected area, but the degree of disease may or may not correlate with the loudness of the murmur. Mildly affected dogs may lead fairly long lives, whereas severely affected animals develop CHF or may die suddenly of ventricular arrhythmias.

Surgical correction requiring open heart surgery and cardiac bypass is usually not an option and carries a poor prognosis.

Medical management usually begins with the administration of beta blockers in order to limit myocardial oxygen consumption, prevent tachycardia and ventricular arrhythmias. However, as heart failure ensues, increased heart rate is necessary for maintaining cardiac output and beta blockers become counterproductive.

As the heart walls thicken and the muscle becomes less compliant cardiac output is dependent ofn adequate filling pressure. Thus, diuretics and venodilators must be used with caution. ACE inhibitors, calcium channel blockers, or other arteriolar dilators may also negatively affect the ability of the heart to produce adequate cardiac output due to worsening of the obstruction. Positive inotropes may also exacerbate outflow obstruction and ventricular arrhythmias.


     • Will cause an increase in heart rate, contractility, cardiac output and myocardial oxygen consumption.

     • Often there will be no change in blood pressure and a decrease in right atrial pressure

Phenothiazines –

     • Main cardiovascular effect = peripheral vasodilation

     • Consequence – decreased blood pressure

     • Some boxers – fainting/syncope seen due to vasovagal response (bradycardia and peripheral vasodilation)

Midazolam and diazepam:

     • Cause little or no myocardial depressant effects

     • May see increase in heart rate due to excitation with inadequate use of adjunctive agent

     • i.e. mu opioid

     • When combined with an opioid as a CRI can be utilitized to decrease MAC of inhalant agent.

     • No analgesia provided

Alpha 2 agonist

     • Significant cardiovascular effects

     • Vasoconstriction

     • Bradycardia

     • Decreased cardiac output


     • Reduction in blood pressure – peripheral vasodilation is the main action

     • Commonly associated with ventricular arrhythmias – bigeminy rhythm not uncommon

     • Contraindications:

     • Patient with known cardiac disease – paricularly those with existing arrhythmias

     • Trauma patients – think of traumatic myocarditis!

Etomidate: hypnotic agent with no direct myocardial depression. Safe to use with cardiac, critical and septic patients.

     • Cardiovascular stability may be better due to maintained barorecptor mediated responses.

Propofol: hypnotic agent that does cause direct myocardial depression as well as decrease in systemic vascular resistance

     • Decrease in contractility leads to increase in heart rate – will be transient – lasting several minutes

     • Profound bradycardia has been noted (dose dependent)

     • Use cautiously in patients with heart disease and hypovolemia

Mu opioids

     • Fentanyl

     • Causes dose dependant bradycardia (increase in vagal tone)

     • Bradycardia is responsive to anticholinergics – atropine/glycopyrrolate

     • Hydromorphone:

     • morphine-like agonist, primary activity at the mu receptors.

Cardiovascular effects:

     • bradycardia due to central vagal stimulation,

     • alpha-adrenergic depression causing peripheral vasodilation, decreased peripheral resistance

     • baroreceptor inhibition.

     • Morphine

     • No direct myocardial effect

     • Dose dependent bradycardia – responsive to anticholinergics

Mixed agonist/antagonist agents

     • Buprenorphine: a partial mu agonist/antagonist. Slow onset of action, duration of 6-8 hours.

     • Cardiovascular depression and respiratory depression not as profound as pure mu agonists.

     • Butorphanol: partial agonist/antagonist. Similar to buprenorphine in cardiovascular/respiratory effects.

     • Faster onset of action, shorter duration that buprenorphine.

     • Recommended in multiple texts for premedication for cardiac patients due to minimal cardiac effects.


     • Will indirectly stimulate the cardiovascular system by increasing sympathetic tone

     • cause an increase in heart rate, cardiac output, mean arterial pressure, pulmonary arterial pressure and central venous pressure.

     • Increase in rate causes an increase in myocardial work and oxygen demand/consumption

One of the key points that should be remembered when providing anesthesia/analgesia to a patient with cardiac disease should be to carefully monitor all of the patient parameters. It is wise to induce patients with ECG and non-invasive blood pressure monitoring in place in order to have real time information. This allows the nurse anethetist to provide appropriate interventions in a timely manner vs trying to "chase" hypotension, heart rate and/ or arrhythmias seen following induction and instrumentation. Feline patients often do not permit application of ECG patches or leads prior to induction but if at all possible, a blood pressure cuff should be in place with readings available prior to inducton.

Anesthesia for the cardiac patient dictates that you know your patient, know your drugs and know how to monitor!

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