Anesthetic management of patients with cardiovascular disease (Proceedings)


Our patient population has changed fairly dramatically in the last 10 years as our medical skills have progressed and we have become capable of supporting patients with advanced disease and advancing age. Now we must hone our anesthesia skills in order to support patients that largely don't fit into the 'young, healthy' category and it is no longer appropriate to think that safe anesthesia means recovering as many patients as we anesthetize.

Our patient population has changed fairly dramatically in the last 10 years as our medical skills have progressed and we have become capable of supporting patients with advanced disease and advancing age. Now we must hone our anesthesia skills in order to support patients that largely don't fit into the 'young, healthy' category and it is no longer appropriate to think that safe anesthesia means recovering as many patients as we anesthetize. Patients with cardiovascular disease often require anesthesia and it is imperative that we understand the medical implications of the cardiovascular disease as well as the pharmacologic implications of the anesthetic drugs.


The ultimate goal of the cardiovascular system is to provide adequate cardiac output (Q) and subsequent oxygen delivery (DO2) to the working cells. Physiologic responses occur in an attempt to maintain adequate Q, even in the face of progressive cardiac disease. Cardiac output is a product of heart rate (HR) and stroke volume (SV), which is comprised of preload, afterload and myocardial contractility (inotropy).

Heart rate is affected by sympathetic and parasympathetic nervous system balance and by the anesthetic drugs themselves. Arrhythmias change HR and can decrease SV if their rate or timing results in inadequate cardiac filling. Obviously, since HR is an integral determinant of Q, bradycardia can result in inadequate flow. Conversely, tachycardia can be as hazardous as bradycardia, especially as cardiac disease becomes more severe. During tachycardia, diastolic filling time is decreased, resulting in decreased SV. In addition, ventricular relaxation time is decreased. Since the myocardium receives most of its blood flow during diastole, myocardial oxygen delivery is decreased at a time when myocardial oxygen consumption is increased, resulting in inadequate oxygen delivery to the myocardium. In fact, tachycardia in itself can result in myocardial ischemia and heart failure. Myocardial oxygen delivery is often inadequate in patients with hypertrophic cardiomyopathy since the large myocardial mass consumes a significant amount of oxygen and blood supply is limited. Tachycardia in these patients can cause decompensation and overt cardiac failure.

Preload, or cardiac filling, is dictated in part by blood flow and blood volume. Afterload, or resistance to ejection, is dictated primarily by vascular tone. Ideally, an appropriate preload will cause stretch of the myocardium which will improve contractility and increase SV (due to Starling's Law). Also ideally, the arterial tree should provide minimal resistance to ejection so that adequate SV is ejected with minimal cardiac work. However, failing hearts may not be able to accommodate (hypertrophic cardiomyopathy) or eject (dilatative cardiomyopathy) the blood delivered to it, in which case stroke volume is decreased and cardiac output will decrease unless the heart rate can increase to compensate. Also, afterload may increase to the point that cardiac output is limited and cardiac work is excessive, often leading to hypertrophic cardiomyopathy. Contractility is severely impaired in patients with dilatative cardiomyopathy and drugs that improve or support contractility (positive inotropes) should be administered perioperatively. Conversely, hypertrophic cardiomyopathy produces a hyper-contractile state and drugs that increase cardiac work in any manner should be avoided.

Patient preparation

A thorough physical exam, complete blood count (CBC) and serum chemistry are imperative. Mucous membrane color, capillary refill time, cardiac sounds, thoracic radiographs and an electrocardiogram (ECG) should be carefully evaluated. Depending on the severity of the disease, a more thorough cardiac workup including advanced techniques such as cardiac ultrasound may be necessary. A detailed and exhaustive history with emphasis on evidence of cardiovascular dysfunction such as exercise intolerance, syncope, recurrent coughing, etc... is important. All current medications should be noted and concurrent diseases evaluated.

Stabilization of patients with cardiovascular disease is crucial and the first goal of the anesthesiologist is to attempt to return cardiovascular function to as close to normal as possible. Heart rate should be normalized and arrhythmias should be treated. Myocardial contractility should be supported with positive inotropic drugs (eg, pimobendin). Adequate blood volume is essential and the judicious use of fluids may be warranted, especially in hypovolemic patients. However, since pump function is impaired, overhydration should be avoided at all costs. Whole blood should be administered if anemia is present. Oxygen should be administered for 5-10 minutes prior to administering induction drugs ("preoxygenate"). Patient support should continue throughout anesthesia and recovery.


Circulation becomes "centralized" in patients with moderate to severe cardiac disease, resulting in greater delivery of blood, and drugs carried by the blood, to highly perfused tissues, including the brain. However, cardiac output may be decreased in these patients, resulting in slower drug delivery to the brain. Thus, the dosage of anesthetic drugs administered to patients with cardiac disease should be decreased and drugs should be administered slowly and with ample time between doses for delivery to the brain.

In addition to the cardiovascular depression caused by the disease itself, most anesthetic drugs cause some degree of cardiovascular depression. The second goal of the anesthesiologist is to choose anesthetic drugs that will have minimal impact on the patient's disease. Furthermore, the cardiovascular effects caused by anesthetic drugs are generally dose dependent and selection of the appropriate DOSE is even more important than selection of the appropriate drug.


Excitement, struggling and fear cause tachycardia and increased peripheral resistance, arterial blood pressure, cardiac work and cardiac oxygen consumption. These changes are generally well-tolerated in patients with a normal cardiovascular system but are extremely dangerous in a patient with cardiovascular disease, possibly resulting in decompensation and cardiac failure. Pain causes the same sympathetic response as excitement, struggling and fear. Therefore, these stressors must be avoided in patients with cardiovascular disease and a low-dose tranquilizer and preemptive analgesic drug are recommended.

Opioid agonists (eg, fentanyl, hydromorphone, morphine), agonist-antagonists (eg, butorphanol), and partial agonists (buprenorphine) cause minimal depression of the cardiovascular system when used in low doses. As previously stated, pain is a stressor that will cause an increase in heart rate with a subsequent increase in myocardial oxygen consumption. Thus, opioid-induced analgesia is an extremely valuable means of alleviating or eliminating pain-induced cardiac complications. Opioids should also be used during the maintenance phase to decrease the dosage of concurrently used maintenance drugs. Thus, ALL patients with cardiovascular disease should receive an opioid as a premedicant, even if the procedure for which the patient is being anesthetized isn't painful. Opioids alone may not provide adequate sedation in young, healthy patients but are often effective in older, compromised patients. Opioid effects can be reversed with the opioid agonist, naloxone, or partially reversed with the opioid agonist-antagonist, butorphanol.

The benzodiazepines (e.g., diazepam and midazolam) are commonly used as mild tranquilizers and muscle relaxants in debilitated patients because they produce minimal to no cardiovascular or respiratory depression. Sedation following the administration of a benzodiazepine alone IS NOT adequate for healthy, young animals but is generally satisfactory when combined with an opioid for compromised patients. Drug effects can be reversed with the benzodiazepine antagonist, flumazenil. Acepromazine causes vasodilation secondary to alpha-adrenergic blockade. In low doses, this is generally manifest as decreased peripheral resistance or "afterload", which allows increased cardiac output without increased cardiac work. Thus, a low dose of acepromazine might be an appropriate tranquilizer choice in a patient with increased afterload and/or hypertrophic cardiomyopathy. However, moderate to high doses of acepromazine can cause systemic hypotension. Acepromazine does not provide analgesia and is not reversible.

Anticholinergics increase heart rate and myocardial oxygen consumption and can increase the possibility of cardiac arrhythmias and decrease the threshold for ventricular fibrillation. Since patients with cardiovascular disease may not tolerate excessive increases in heart rate and myocardial oxygen consumption, anticholinergics should not be a routine component of the anesthetic protocol but should be reserved for the treatment of bradycardia that limits cardiac output.


Etomidate is generally the drug of choice for patients with severe cardiac disease because the drug causes minimal to no changes of myocardial contractility, heart rate, stroke volume or cardiac output. However, etomidate can also produce excitement and involuntary movement following injection. The use of premedicant tranquilizers such as diazepam reduces these side effects. Etomidate is fairly expensive and has a fairly short shelf-life. Fortunately, etomidate is not necessary for anesthesia of most patients, and many patients with cardiovascular disease have been safely anesthetized with other induction agents, like propofol or ketamine/diazepam.

Ketamine and tiletamine cause direct stimulation of the sympathetic nervous system leading indirectly to increased heart rate, afterload, cardiac output and arterial blood pressure. These traits can be beneficial in disease states marked by impaired myocardial contractility (eg, dilatative cardiomyopathy), however, if the myocardium is already contracting maximally or beating at maximal rates (eg, hypertrophic cardiomyopathy and/or hyperthyroid disease), sympathetic nervous system stimulation can cause excessive cardiac work and precipitate heart failure. Also, in patients with no sympathetic reserve, as may occur in end-stage cardiac disease, ketamine and tiletamine are unable to improve cardiac function and, in fact, will cause direct myocardial depression. Thus, these drugs are often a good choice for the induction of patients with dilatative cardiomyopathy but may not be ideal for patients with hypertrophic cardiomyopathy and/or extreme tachycardia. However, the stimulatory effects of the drugs are blunted by the prior administration of tranquilizers (eg, benzodiazepines, acepromazine), thus improving their safety in patients with hyperdynamic cardiac disease.

Propofol causes myocardial depression and hypotension that is comparable to that caused by barbiturates, however, this effect is extremely short-lived and generally well-tolerated in patients without profound cardiovascular disease. Propofol is easily titrated "to effect", thus attenuating the likelihood of over dosage. A dose of diazepam can be used immediately prior to the propofol injection to further decrease the dose. Also, propofol is rapidly cleared from the body by multiple routes. Recoveries are rapid and complete, thereby minimizing the duration of anesthesia- induced physiological depression.

Mask induction with inhalant anesthetics IS NOT ACCEPTABLE. Stress and struggling with subsequent tachycardia and increased oxygen consumption should absolutely be avoided in patients with cardiovascular disease. Furthermore, high dosages of inhalants are required for mask induction and these high dosages can contribute to cardiac dysfunction. Thus, patients should be sedated, induced to anesthesia with injectable agents and then should receive inhalant anesthetics for the maintenance period ONLY.


Inhalant anesthetic agents are the drugs of choice for long-term anesthesia and both isoflurane and sevoflurane are good choices. However, all inhalant anesthetic agents cause DOSE DEPENDENT myocardial depression. Regardless of which inhalant anesthetic is used, the concentration of the anesthetic must be maintained as low as possible in order to limit myocardial depression. The use of premedicants, including analgesic agents, will greatly decrease the amount of inhalant anesthetic necessary for maintenance. In addition, the concurrent administration of a constant-rate infusion of an opioid (eg, morphine, hydromorphone or fentanyl) will allow the concentration of inhalant anesthetic to remain at a minimum. Opioid boluses can be used if a CRI is not possible and local anesthetic blockade should be used whenever possible.

Diligent monitoring and patient support are imperative for successful anesthetic outcome. Blood pressure, ECG, SPO2 and ETCO2 should all be monitored. The patient should be constantly evaluated for appropriate anesthetic depth and anesthetic drugs should be delivered to effect. Support includes the judicious delivery of appropriate IV fluids (eg, crystalloids, colloids, blood products) and support of cardiac function. The latter may require the use of positive inotropic drugs like dopamine. Blood pressure should be maintained with a mean arterial blood pressure (MAP) >60 mmHg and a systolic arterial pressure (SAP) >90 mmHg. The patient should also be kept warm as hypothermia can further contribute to cardiac dysfunction and can delay recovery from anesthesia. Furthermore, shivering can increase oxygen consumption by up to 200%. Analgesia should be readdressed.


Patient support and monitoring MUST continue well into the recovery period. Oxygen and fluids should be administered, aggressive warming should be continued and all appropriate drugs should be continued (eg, dopamine, anti-arrhythmic drugs, etc...) Analgesia should be readdressed. If the patient experiences excitement or fear, a low dose of a sedative drug should be administered.


  • Preanesthesia: KEEP THE PATIENT CALM, premedicate with opioids ± benzodiazepines or low-dose acepromazine, preoxygenate (if possible) patients with moderate to severe disease

  • Induction: Induce with low-dose diazepam-propofol or diazepam-ketamine

  • Maintenance: Maintain on inhalants at lowest dose possible, monitor carefully & use supportive drugs like dopamine, use a judicious amount of fluids and consider using colloids, keep the patient warm

n Recovery: Continue support, monitoring and analgesia in recovery. Sedate if necessary.

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