Introduction
The cardiovascular system is comprised of the heart, the vasculature, and the blood. Dysfunction of any or all of these components can occur in patients with cardiovascular disease, disease that secondarily affects the cardiovascular system (e.g., hyperthyroidism), and in patients that are hypovolemic, anemic, or in vasoactive states (e.g., vasodilatory shock). Unfortunately, anesthetic drugs and events (e.g., recumbency, positive pressure ventilation) can exacerbate this dysfunction and contribute to the demise of the patient. Because of the vast number of diseases that affect the cardiovascular system, one anesthetic protocol may not be appropriate for all patients in this category but an understanding of cardiovascular physiology and the cardiovascular effects of the anesthetic drugs will promote appropriate anesthetic protocol selection. Anesthetic considerations for some of the more commonly encountered diseases that affect the cardiovascular system are described in this chapter.
In every cell of the body, oxygen is required for normal cellular function and it is delivery of oxygen that drives the cardiovascular system. Regulation of cardiac output, vascular tone, production of red blood cells, and hemoglobin loading and unloading all occur in response to tissue oxygen needs. Sophisticated physiological changes occur in an attempt to regulate these processes, even in the face of progressive cardiac disease.
Most of the changes that occur with cardiac disease, and many of the effects of anesthetic drugs, ultimately affect cardiac output. Cardiac output (Q) is the amount of blood pumped by the left ventricle into the aorta each minute and it is a product of heart rate (HR) and of stroke volume (SV), which is comprised of preload, afterload, and myocardial contractility (inotropy). Most of the drugs associated with sedation and anesthesia cause some degree of dose-dependent cardiovascular depression, which may be manifest as changes in HR, SV, or both.
Obviously, since HR is an integral determinant of Q, bradycardia can result in inadequate flow if SV does not increase to compensate for decreased HR. Conversely, tachycardia can be as hazardous as bradycardia, since an increase in HR causes a decrease in diastolic filling time, resulting in a reduction in SV. Also, tachycardia reduces ventricular relaxation time, which decreases the time for myocardial perfusion (which occurs during diastole) and causes an increase in myocardial oxygen consumption. Oxygen debt occurs if oxygen demand is not met by oxygen supply and myocardial ischemia can result. In fact, severe tachycardia in itself (i.e., in the absence of underlying cardiac disease) can result in myocardial ischemia and heart failure.1
Preload, or cardiac filling (or venous return), is dictated by blood flow, blood volume, and venous capacitance. Ideally, an appropriate preload volume will fill the ventricle just enough to cause a slight stretch of the myocardium, which will improve contractility and increase SV (due to Starling’s law). The volume of venous return is extremely important because: (1) the heart can only eject the amount of blood that is returned to it, making cardiac output highly dependent on preload, and (2) the heart must eject the amount of blood returned to it or congestion will occur. Excessive or even moderate vasodilation causes hypotension and may lead to “pooling” of the blood in the vasculature with minimal cardiac return and inadequate preload. Afterload, or resistance to ejection of blood from the left ventricle, is dictated primarily by arterial tone. The arterial tree must maintain some degree of tone in order to support the flow of blood from the aorta through the vascular tree to the capillaries. However, excessive tone will increase the amount of cardiac work needed to eject blood from the left ventricle and this will decrease cardiac output. Myocardial contractility is impaired by most cardiac diseases and many anesthetic drugs. Clearly, a decrease in myocardial contractility will cause a decrease in cardiac output.
Pharmacology of anesthetic drugs
An overview of the effects of anesthetic drugs on cardiovascular function is listed in Table 11.1.
Sedatives, tranquilizers, and anticholinergics
Excitement, fear, and pain can cause a sympathetic response marked by tachycardia, hypertension, and increased myocardial oxygen consumption, and this response can exacerbate concurrent cardiovascular disease. Thus, most patients with cardiovascular disease should receive a low dose of sedative and analgesic drugs prior to anesthesia. All of the sedatives and tranquilizers listed below are “MAC sparing,” meaning that they decrease the minimum alveolar concentration (MAC) of inhalant anesthetic gases required to maintain anesthesia. Because the inhalant gases can cause profound dose- related cardiovascular side effects, decreasing the dose of the inhalant should increase anesthetic safety.
Opioid agonists (e.g., fentanyl, hydromorphone, morphine), agonist-antagonists (e.g., butorphanol), and partial agonists (buprenorphine) causes minimal cardiovascular effects when used in low doses and are the mainstay for sedation and analgesia in patients with cardiovascular disease.2 The opioids do not cause myocardial depression or arrhythmias and cause only a minimal decrease in blood pressure in recumbent patients.3 In fact, opioids can be cardioprotective and induce pharmacological preconditioning of the myocardium2 and a slight decrease in afterload.3 A mild vagally mediated bradycardia can occur after the administration of most opioids.3 Morphine can cause histamine release and subsequent hypotension, but this effect is associated solely with rapid intravenous (IV) delivery of the drug and is not seen subsequent to intramuscular (IM) injections or IV constant rate infusions (CRIs).3 Many opioids are also somewhat sedating, especially in dogs. Opioids used alone may not provide adequate sedation in young, healthy patients but are often sufficient for compromised patients. Opioid effects can be reversed with the opioid agonist naloxone, or partially reversed with the opioid agonist3antagonist butorphanol. Reversal of side effects associated with opioid analgesics will also antagonize analgesia.4 Rapid IV administration of naloxone has been associated with development of cardiac dysrhythmias and even sudden death.5,6
Table 11.1. Overview of the most common cardiovascular effects of some frequently used anesthetic drugs. Effects are typical of drugs used at clinically relevant dosages
Source: Adapted from: Muir W.W. Anesthesia of dogs and cats with cardiovascular disease. Part II. Compend Pract Vet 20(4): 473–484, 1998.
↑, increased; ↓, decreased; —, no change; +, potentially arrhythmogenic.
The benzodiazepines (e.g., diazepam and midazolam) produce minimal cardiovascular effects. Diazepam produces minimal decreases in systemic blood pressure, cardiac output, and systemic vascular resistance that are similar to that produced by natural sleep.7 Midazolam produces a greater decrease in systemic blood pressure and increase in HR than diazepam produces, but the effects are short33ived and generally of little clinical significance. Midazolam decreases systemic vascular resistance and this may improve cardiac output in patients with congestive heart failure (CHF).7 Sedation following the administration of a benzodiazepine alone is generally not adequate for healthy, young animals but is often satisfactory when combined with an opioid for compromised patients. However, the combination of diazepam and fentanyl causes a decrease in systemic vascular resistance and systemic blood pressure that does not occur when fentanyl is used alone.7 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 mitral valve insufficiency (MVI). However, moderate to high doses of acepromazine will cause a 20–25% decrease in SV, cardiac output, and mean arterial pressure,8 and these effects can be extremely detrimental in a patient with cardiovascular disease. Acepromazine increases the dose of epinephrine required to induce ventricular arrhythmias, possibly due to alpha1 blockade.8 Acepromazine does not provide analgesia and is not reversible.
Alpha2 agonists (e.g., medetomidine and dexmedetomidine) cause profound vasoconstriction and increased cardiac work and are thus not appropriate for patients with cardiovascular disease.
Anticholinergics increase HR 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 HR 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.
Induction drugs
Etomidate is generally the drug of choice for patients with severe cardiac disease because the drug causes minimal to no changes in myocardial contractility, HR, SV, or cardiac output at clinically relevant dosages.9 Systemic vascular resistance often decreases, resulting in a decrease in arterial blood pressure. At supraclinical dosages, etomidate is a negative inotrope.10 Etomidate can produce excitement, muscle twitching, and vocalization but these effects are minimized or eliminated by the administration of a benzodiazepine or acepromazine prior to injection of etomidate.
Ketamine and tiletamine are unique among anesthetic drugs in that they cause an increase in HR, afterload, cardiac output, and arterial blood pressure.9 These are indirect effects caused by the direct stimulation of the sympathetic nervous system by ketamine and tiletamine. These effects can be beneficial in disease states marked by impaired myocardial contractility (e.g., dilatative cardiomyopathy), hypotension, or bradycardia, but may be detrimental in patients with hypertrophic disease, hypertension, or tachycardia. Ketamine and tiletamine also cause an increase in myocardial oxygen consumption that could precipitate myocardial ischemia.9 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.9 Both the positive and negative effects of these drugs are blunted by the prior administration of tranquilizers (e.g., benzodiazepines, acepromazine), thus improving their safety in patients with cardiac disease.
Propofol causes dose-dependent myocardial depression and hypotension that is comparable to that caused by barbiturates.9 However, this effect is extremely short-lived and is blunted by the prior administration of sedative drugs with minimal cardiovascular effects, like the opioids and benzodiazepines. Propofol is easily titrated “to effect,” thus attenuating the likelihood of overdosage and dose-related side effects. Also, propofol is rapidly cleared from the body by multiple routes, thereby minimizing the duration of anesthesia-induced physiological changes.
Inhalant anesthetics are associated with a moderate to profound dose-dependent decrease in arterial blood pressure that is primarily caused by systemic vasodilation.9 Thus, high dosages of inhalant gases should usually be avoided in patients with cardiovascular disease. Induction of anesthesia by mask or chamber is often accompanied by stress and struggling with subsequent tachycardia and increased oxygen consumption, which can further exacerbate cardiac disease. The use of inhalant gases alone to induce and maintain anesthesia increases the risk of anesthesia-induced mortality in dogs and cats.11
Maintenance drugs
Inhalant anesthetic gases are the drugs of choice for long-term anesthesia; however, as stated, isoflurane, sevoflurane, and desflurane all cause dose-dependent cardiovascular changes and the concentration of the anesthetic must be maintained as low as possible in order to limit hypotension. The use of premedicants, including analgesic drugs, and the use of analgesic drugs during the maintenance phase of anesthesia (e.g., locoregional blockade or CRIs of analgesic drugs) will allow the concentration of inhalant anesthetic gases to remain at a minimum. Although not proven in dogs and cats, sevoflurane may be less likely than isoflurane or desflurane to cause tachycardia and may be preferable in patients prone to myocardial ischemia.9
Analgesic drugs
Pain is a stressor that will cause an increase in HR and blood pressure with a subsequent increase in myocardial oxygen consumption. Thus, all attempts should be made to alleviate or eliminate pain in the patient with cardiovascular disease. The positive effects of opioids have already been stated. Local and regional analgesia can be used in patients with cardiovascular disease and may decrease morbidity.12,13 The nonsteroidal anti-inflammatory drugs (NSAIDs) are appropriate in many patients with cardiovascular disease but NSAIDs can cause or contribute to hypertension and may interfere with diuretic therapy and should not be used in patients with hypertensive disease. 14 Some NSAIDs can contribute to myocardial complications in humans but these are unlikely to occur in dogs and cats due to differences in myocardial perfusion.
Circulation becomes “centralized” in patients with moderate to severe cardiac disease, resulting in greater delivery of blood, and drugs carried by the blood, to the vessel-rich group of 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. Furthermore, the cardiovascular effects caused by anesthetic drugs are generally dose dependent and selection of the appropriate dose may be even more important than selection of the appropriate drug.
Monitoring and support of the patient with cardiovascular disease should begin prior to the induction of anesthesia and should continue until the patient is fully recovered from the effects of the anesthetic drugs. Clearly, arterial blood pressure and cardiac rate and rhythm should be monitored in all patients. Support should include the use of IV fluids (including crystalloids, colloids, plasma, packed red cells, and whole blood), antiarrhythmic drugs, and positive inotropic drugs, as appropriate. In most instances, normothermia should be actively and aggressively maintained as hypothermia can have a negative impact on cardiovascular function15 and shivering can greatly increase metabolic oxygen consumption.16
Anesthesia for patients with specific cardiovascular disease
The most commonly encountered cardiovascular diseases in dogs and cats include MVI, dilated cardiomyopathy (DCM), and hypertrophic cardiomyopathy (HCM).
MVI
MVI is the most common cardiac valvular disease in dogs17 but is uncommon in cats. MVI is usually caused by a progressive degeneration of the atrioventricular valves that allows regurgitant flow of blood into the left atrium during left ventricular systole. Valvular regurgitation causes further pathology, including dilation of the left atrium and eccentric hypertrophy of the left ventricle. Myocardial contractility decreases as the disease worsens. Depending on progression of the disease, patients can present with a wide variety of signs that range from a soft systolic murmur with no signs of cardiac disease to complications from end-stage heart failure.17
The anesthetic goals are to maintain adequate HR and myocardial contractility while minimizing afterload. In patients with MVI, a slightly increased HR (not tachycardia) is advantageous since increased ventricular filling and distention may occur when the HR is slow. In a normal ventricle, increased distension is generally met with increased force of contraction. In patients with MVI, increased distention may cause additional enlargement of the AV orifice and further increase of the regurgitant volume. Systemic vascular resistance or afterload should be kept to a minimum in order to promote more flow forward into the systemic vasculature rather than backward through the regurgitant valve.18 The benzodiazepines or low3dose acepromazine can be used to decrease afterload and opioids should be included to allow a decrease in the MAC of the inhalant drugs. The choice of the opioid will depend on the severity of expected pain from the surgical procedure. Etomidate, propofol, and valium/ ketamine are all suitable induction drugs and both isoflurane and sevoflurane are appropriate for maintenance.
Hypotension is common because of the decreased myocardial contractility, and drugs that increase contractility without increasing SVR (e.g., dobutamine) should be utilized, while drugs that promote an increase in vascular resistance (e.g., phenylephrine, ephedrine) are not recommended.18 Treating hypotension with fluid therapy can be somewhat difficult since adequate preload is necessary for appropriate cardiac output but excessive fluid loading can cause ventricular stretch and increased regurgitant volume.
DCM
DCM is the most common myocardial disease in the dog, with adult medium and large-breed dogs most commonly affected. 19 With the discovery and correction of taurines deficient diets, DCM has become uncommon in cats. DCM is characterized by cardiac enlargement and impaired systolic function of one or both ventricles (most commonly the left ventricle). A progressive decrease in myocardial contractility with impaired systolic ventricular function occurs in patients with DCM and the clinical presentation is highly variable depending on the stage of the disease.
Measures of pump function such as ejection fraction, fractional shortening, rate of ejection, and rate of ventricular pressure development are all reduced, while end-diastolic ventricular volume is increased.18 Ventricular relaxation is also impaired. Contractility, SV, and cardiac output continue to decline as the disease progresses, and mitral and tricuspid valve insufficiency, ventricular arrhythmias, and/or atrial fibrillation occur in a significant number of patients. Patients with advanced DCM are at high risk for anesthetic complications and stabilization prior to anesthesia is critical. The anesthetic goals are to maintain or improve contractility (e.g., with positive inotropic drugs) and to avoid drugs that increase afterload.18
Opioids should be used as premedicants, and an induction of either IV fentanyl or a benzodiazepine followed in 1–2 minutes with etomidate to effect is the induction protocol of choice. The same premedicants followed by low-dose ketamine is the second choice as ketamine may cause some improvement in cardiac function through stimulation of the sympathetic nervous system. A low dose of propofol is also acceptable in patients with mild to moderate disease. Either isoflurane or sevoflurane can be used during maintenance but maintaining the patient at the lowest possible dose of inhalant is imperative. Thus, additional analgesia will almost certainly be required during maintenance.
IV fluids should be administered intraoperatively but fluid balance can be difficult to achieve in advanced stages of the disease. Adequate circulation and appropriate preload volume is critical since an adequate preload is necessary to compensate for decreased pump function. Yet, since pump function is poor, the heart cannot eject excess fluid load and the volume of fluids should be low to prevent overhydration. Also, poor pump function means that increased afterload can severely limit cardiac output so vasoconstrictive drugs should be avoided. Hypotension can be treated with drugs that have a primary inotropic function, like dobutamine.
HCM
HCM is the most commonly diagnosed myocardial disease in cats but is uncommon in dogs.20 This disease is characterized by concentric hypertrophy of the ventricles (primarily the left ventricle) with small ventricular chamber size. Atrial enlargement may also occur. The cardiac chambers become stiff, resulting in increased pressure for any given volume during diastolic filling and this will eventually lead to CHF with pulmonary edema and pleural effusion. Myocardial oxygen delivery is often inadequate in patients with HCM since the large myocardial mass consumes a significant amount of oxygen and blood supply to all parts of the muscle may not be adequate. Tachycardia in HCM patients can further tax myocardial oxygen supplies and can cause decompensation and overt cardiac failure. Coronary circulation to the thickened myocardium decreases, predisposing the patient to myocardial ischemia. Thromboembolism may develop. Myocardial relaxation is impaired but contractility is normal. The clinical presentation is highly variable depending on the stage of the disease, and the prognosis of severe HCM is poor and sudden death is not uncommon.
In patients with HCM, myocardial contractility or pump function is adequate but decreased cardiac output and perfusion occur because of inadequate diastolic ventricular volume secondary to the decreased ventricular chamber size. A slightly decreased HR is generally beneficial in these patients. Anesthetic goals include prevention of tachycardia, which will decrease ventricular filling time and increase cardiac work, and prevention of increases in myocardial contractility.18 Thus, drugs that increase rate or force of contraction (e.g., anticholinergics, ketamine, dobutamine, dopamine) are not generally used.18 Also, vasodilation (e.g., as occurs with acepromazine, propofol and the inhalant gases) may cause marked hypotension because of a limited ability of the heart to increase SV.
Opioids should be used as premedicants and an induction of either IV fentanyl or a benzodiazepine followed in 1–2 minutes with etomidate to effect is the induction protocol of choice. A benzodiazepine followed by propofol is also acceptable and a benzodiazepine with ketamine can be used in patients with mild disease. Either isoflurane or sevoflurane can be used during maintenance but maintaining the patient at the lowest possible dose of inhalant is imperative. Thus, additional analgesia will almost certainly be required during maintenance.
Hypotension is difficult to treat in patients with HCM. Appropriate (but judicious) fluid therapy both before and during anesthetic drug administration is required for adequate preload. Hypotension that is unresponsive to fluid therapy may be treated with a CRI of phenylephrine,18 which will promote adequate filling but is not ideal in that the drug will also increase afterload and decrease tissue perfusion.
Revised from “Cardiovascular Disease” by Ralph C. Harvey and Stephen J. Ettinger in Lumb and Jones’ Veterinary Anesthesia and Analgesia, Fourth Edition.
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