Anaesthesia of Cardiac Patients, including Haemodynamically Unstable Cases

Louise O’Dwyer

MBA BSc(Hons) VTS(Anaesthesia/Analgesia & ECC)

DipAVN(Medical & Surgical) RVN

Dogs and cats with cardiac disease commonly present for anaesthesia in general practice. While in some cases this may be for management of the primary cardiac disorder (e.g. ligation of a patent ductus arteriosus), more commonly, they are being anaesthetised for some unrelated condition (e.g. dentistry in the older Cavalier with mitral endocardiosis). While it would be extremely convenient to be able to utilise a ‘one anaesthetic protocol for all’ tactic when dealing with these cases, the varying pathophysiology of the cardiac disorders dictates differing approaches to the anaesthesia for each of the individual conditions, although there are some generalisations that are appropriate ‘across the board’.

Essentially, the aim in all cases is to optimise cardiac output while maintaining myocardial oxygen supply (mDO2) in excess of myocardial oxygen demand (mVO2). The major factors increasing mVO2 include an increase in heart rate, increased afterload and increased contractility. Factors decreasing mDO2 include anaemia and hypoxaemia, tachycardia and hypotension. Based on this, it becomes obvious that it is essential to maintain blood oxygenation, and also to prevent periods of severe tachycardia in patients with heart disease (given that tachycardia both increases myocardial oxygen demands while simultaneously decreasing supply). Tachycardia should, therefore, be avoided by provision of adequate reflex suppression (analgesia) during noxious procedures.

Anaesthetic management of the ‘generic’ high risk cardiac patient

a) Premedication Unlike the situation with high risk respiratory cases, most high risk cardiac cases benefit from adequate sedative premedication, to reduce stress associated with the procedure. Both the opioids and benzodiazepines (BZPs) are relatively cardiostable, and are extremely useful when dealing with high risk cardiac cases. The opioid chosen should be based on the procedure being undertaken: partial agonists (butorphanol, buprenorphine) may be suitable for mildly to moderately noxious procedures, but full opioid agonists (methadone, pethidine, morphine) are more appropriate if noxious stimulation is likely to be severe. In terms of benzodiazepines, diazepam is poorly absorbed and relatively painful when given intramuscularly, so midazolam (@~0.2mg/kg) is preferable. This can be mixed in the same syringe as the opioid drug and given by IM injection.

b) Induction Most of the commonly used induction agents (propofol; alfaxalone) cause hypotension even in healthy patients, and this can be profound in the high risk cardiac case. For this reason, these agents are generally not recommended by themselves for anaesthetic induction in patients with poor cardiovascular reserve. Alfaxalone appears to have lesser effects on the cardiovascular system (in healthy laboratory animals, at least), but there is currently insufficient data on its effects in clinical patients with pre-existing cardiovascular pathology to recommend it as a panacea. Although ketamine/diazepam is commonly used for IV induction in high risk canine and feline patients in North America, with the belief that ketamine normally maintains or increases arterial blood pressure, there is little guarantee that it exerts the same actions in animals with cardiac disease as it does in patients with normal cardiovascular function; indeed, the tachycardia that ketamine may induce is likely to be detrimental in many cases. Consequently, there is little to recommend ketamine induction techniques over any other agent in patients with cardiac disease. Etomidate is an IV induction agent that has been widely used in human anaesthesia for patients with cardiovascular disease, as it has minimal effects on cardiac output and arterial blood pressure. It is not licensed for animal use, but has been extensively used in our clinic for patients with significant pre-existing arrhythmias, cardiac pathology or ongoing hypovolaemia. Due to the high osmolarity of the solution, etomidate can cause pain on injection and thrombophlebitis. As a result, it is probably best administered into a free-flowing IV fluid line so it is suitably diluted before it enters the patient’s vein; this is probably more important in cats due to the small vein size. Etomidate can also cause myoclonus (twitching) at induction, so is best preceded immediately beforehand by a benzodiazepine (diazepam or midazolam IV) or a potent opioid (e.g. fentanyl), to offset this effect. Etomidate causes suppression of cortisol production, so should only be administered as a single IV induction dose or acute hypoadrenocorticism may be observed.

BZP/opioid induction techniques are also useful in high risk canine cardiac cases (although it can be used in cats, it is generally less effective). Because both groups of drugs are relatively cardiostable, they can be given in fairly high doses to achieve induction of anaesthesia. This author typically uses a combination of fentanyl and diazepam. A dose of 10mcg/kg fentanyl and 0.5mg/kg diazepam are drawn up into separate syringes. Following an adequate period of preoxygenation by facemask, half the fentanyl (5mcg/kg) is administered IV, and then followed by half of the diazepam (0.25mg/kg). The patient is observed for a few minutes (this technique results in slower induction than traditional IV induction agents), and, if inadequately anaesthetised for endotracheal intubation, further increments of the 2 drugs are delivered until unconsciousness is achieved. The use of the two drugs in this manner is referred to as a co- induction technique. It is important to realise that these patients will often appear quite ‘awake’ (eyes still central and staring) but will still tolerate intubation of the trachea. If inadequate hypnosis is achieved after the full doses of diazepam and fentanyl have been given, unconsciousness can then be achieved with an IV induction agent such as propofol or alfaxalone. Only tiny doses of these agents will be required due to the anaesthetic sparing effects of both fentanyl and diazepam. High doses of fentanyl can result in bradycardia; this can usually be avoided if the drug is given very slowly (several minutes), but it is wise to have an antimuscarinic (atropine or glycopyrrolate) drawn up ready to administer, if necessary.

c) Maintenance of anaesthesia All of the volatile anaesthetic agents cause cardiovascular depression, either by direct effects on myocardial contractility (halothane) or by vasodilation (isoflurane, sevoflurane), and these effects are dose-dependent, so it is important to use as low a vaporiser setting as possible. Nitrous oxide, on the other hand, has minimal effects on CV function, and allows a reduction in the concentration of volatile agent required to maintain anaesthesia. Consequently, inclusion of nitrous oxide will generally allow better preservation of cardiac output and arterial blood pressure, and has a definite role in anaesthetic maintenance of the majority of high risk cardiovascular cases. Similarly, the use of potent short-acting opioids by intermittent IV bolus injection (fentanyl) or by constant rate IV infusion (fentanyl, alfentanil, remifentanil) is also extremely useful in reducing the requirement for volatile anaesthetics, and since the opioids are relatively cardiostable, will also allow better maintenance of cardiovascular function during anaesthesia. Although having little effect on cardiac output and arterial blood pressure, these short-acting opioids can cause profound bradycardia and, occasionally, ventricular asystole if given by bolus IV injection, particularly if high doses are used; this appears more common with alfentanil and remifentanil than with fentanyl, but can occur with all three. This can be avoided in several ways:

  • avoid giving IV boluses, and just use CRIs (constant rate infusions), bearing in mind that it will take some time for a CRI to achieve therapeutic blood levels if not preceded by a bolus dose
  • pre-administer atropine or glycopyrrolate immediately before these drugs (more important prior to alfentanil or remifentanil boluses than fentanyl), and probably unnecessary if only using them by CRI
  • probably most importantly, if giving by IV bolus, titrate very slowly over several minutes with careful monitoring of the pulse rate during administration

The downside to the relative cardiostability of the short-acting opioids is that they can cause marked respiratory depression, so intermittent positive pressure (IPPV) is likely to be required. Appropriate doses for these agents during maintenance of anaesthesia are given in Table 1. Where these short-acting agents are not available, liberal use of longer-acting agents, such as methadone, should be considered.

Table 1. Doses of short-acting opioids.

At all times when dealing with cardiovascularly compromised patients, attention should be paid to support of oxygenation.

It is important to recognise that the ‘generic’ description above of anaesthesia for cardiac patients applies to the ‘high risk’ animal (e.g. that which may be in heart failure). For the majority of cases presented in practice, the above technique is likely to be overkill, and simpler anaesthetic protocols are likely to be suitable.

In choosing anaesthesia for patients with cardiac disease, it is important to recognise that different drugs and techniques may be required for the individual cardiac diseases, but the principles described previously of optimising cardiac output while maintaining the balance between mDO2 and mDO2 still apply.

For all cardiac cases, secure IV access should be achieved before induction of anaesthesia, and pre-oxygenation of the patient should be carried out for 3-5 min. Intravenous induction agents should be titrated slowly to effect, as circulation times may be prolonged. In addition, emergency drugs should be readily available, and appropriate doses calculated in advance. It is important to remember that many of these animals may already be receiving drug therapy for management of the cardiac disease, and the potential side-effects of these drugs may be of importance for the anaesthesia. For example, furosemide may lead to hypokalaemia which can cause cardiac arrhythmias during anaesthesia; potassium levels should, therefore, be checked and corrected if necessary, before anaesthesia is undertaken. ACE-inhibitors may lead to marked hypotension when combined with anaesthetic agents, and most anaesthetists (though not all) recommend omitting the dose on the day of anaesthesia.

Congenital cardiac disease

i) Patent Ductus Arteriosus (PDA) Although many centres now accomplish closure of PDA using a coil embolization technique, this is usually unavailable in general practice, where it is still more common to manage the condition by thoracotomy and ligation. In most cases, the PDA shunts blood from the aorta to the pulmonary artery (i.e. a left-to-right shunt), and this results in arterial hypotension, as a consequence of ‘loss’ of some of the left ventricular output entering the pulmonary circulation. The systemic diastolic pressure, in particular, is usually very low. Over time, biventricular hypertrophy will usually occur due to the increased volume load on the left ventricle, and pressure load on the right ventricle.

In some cases, if pulmonary arterial pressure is higher than aortic pressure, the PDA will reverse and be in a right-to-left direction. These cases can usually be recognised clinically due to the presence of ‘differential’ cyanosis, i.e. the mucous membranes of the caudal half of the animal will be cyanosed, while those of the cranial half are normal. Right-to-left shunting can be confirmed by echocardiography. Surgery should not be undertaken in animals with right- to-left shunts, as right heart failure will then occur.

In young, asymptomatic animals, the risk associated with ligation of a left-to-right shunting PDA is relatively low. However, some cases will present already in heart failure, where the risk of anaesthesia will be greater. Essentially, the main aims of anaesthesia for PDA ligation are to maintain cardiac output, while avoiding altering the magnitude or direction of the shunting blood; this involves maintaining the pressure gradient between the aorta and pulmonary artery.

For premedication of PDA cases, because of the low diastolic blood pressure in these patients, the use of drugs causing vasodilation (e.g. acepromazine) is inadvisable; in addition, the reduction in systemic vascular resistance (SVR) induced, may cause reversal of the shunt to a right-to-left direction. Alpha2-agonists will cause vasoconstriction which - on initial consideration - may appear desirable to offset the low diastolic pressure; however, by increasing systemic vascular resistance, these drugs may worsen the degree of left-to-right shunting. Opioids and benzodiazepines are generally considered relatively cardiostable, as they have minimal effects on cardiac output. They also tend to minimally alter vascular tone, so are beneficial agents for PDA cases. Although any opioid could be used, if closure of the ductus is to be performed by thoracotomy (as opposed to coil embolization), this will be associated with a significant degree of post-operative pain, and a full opioid agonist (such as methadone) would be the best choice. On occasion, a midazolam/opioid combination may provide inadequate restraint for IV access in the bouncy asymptomatic PDA puppy or kitten; in these cases, addition of a low dose of acepromazine (i.e. no more than 0.02mg/kg) may be administered ‘on top’ of the midazolam/opioid; higher doses should be avoided due to the effects on SVR.

For induction of anaesthesia, provided the animal is not in heart failure, slow IV titration of propofol or alfaxalone to effect, is suitable. If heart failure is already present, a BZP/opioid induction technique may be preferable.

Both isoflurane and sevoflurane would be suitable for maintenance, but, because of their vasodilatory effects, the concentration should be minimised, preferably by co-administration of an opioid (fentanyl, alfentanil or remifentanil) CRI. Marked bradycardia may occur when the PDA is ligated (a baroreceptor response to the sudden rise in diastolic pressure), so atropine should be available (it is rarely required provided the ligation is undertaken gradually).

ii) Aortic / sub-aortic stenosis (AS) This condition is especially common in Boxers, and is often an incidental finding in asymptomatic animals. However, it is still of importance, as sudden death can occur in these patients, particularly with a badly managed anaesthetic. The problem occurs because the stenosis limits cardiac output, resulting in hypertrophy of the left ventricle and an increase in contractility, which increases mVO2. However, mDO2 is compromised because the reduced diastolic arterial pressure which occurs in AS, limits coronary perfusion; tachycardia is, therefore, particularly problematic, as the low coronary perfusion cannot keep pace with the increased oxygen demands. Stroke volume is relatively ‘fixed’ in these patients, so they also tolerate bradycardia poorly, as cardiac output cannot be maintained.

Dogs with AS are unable to compensate for vasodilation, thus acepromazine should generally be avoided for premedication. A BZP/opioid combination is probably most suitable. However, this is unlikely to pacify a very excitable or aggressive Boxer, and, in this case, it may be necessary to utilise an alpha2-agonist, but only low doses should be used. This is probably preferable to the use of ACP, as the alpha2-agonist will maintain/increase SVR.

In terms of induction and maintenance of anaesthesia, similar considerations apply as to those described above for PDA.

Acquired cardiac disease

i) Mitral regurgitation Probably the commonest heart disease we encounter in veterinary practice is that of acquired mitral valve degeneration due to endocardiosis. Often, this is an incidental finding on physical examination of an older patient presenting for routine anaesthesia (for dentistry, for example), and, provided appropriate care is taken, the anaesthetic risk should not be significantly increased in these animals. If the animal is already receiving medication for the condition, then this should generally be continued and given at the usual times before the anaesthetic. Controversy exists, however, with regard to continuation of ACE-inhibitors in relation to anaesthesia, since there is some evidence that they can lead to marked hypotension during anaesthesia that is relatively non-responsive to conventional management. For this reason, some anaesthetists (including this author) recommend that ACE-inhibitors are not given on the morning of anaesthesia.

Mitral regurgitation is worsened by reductions in heart rate and by increased afterload; thus, the main aims with anaesthesia are to maintain or slightly increase heart rate, and to induce mild vasodilation. This means that alpha2-agonists are contraindicated in this condition, since they induce both bradycardia and an increase in vascular resistance. Low doses of acepromazine are suitable for premedication (vasodilation) in combination with opioids - pethidine (meperidine) may be the drug of choice as it mildly increases heart rate, although other opioids would be acceptable provided high doses are avoided. Induction can generally be carried out with propofol or alfaxalone, provided the drugs are titrated very slowly to effect.

Both isoflurane and sevoflurane are suitable for maintenance

ii) Hypertrophic cardiomyopathy (HCM) This is a relatively common condition in cats, and it is often necessary to either sedate or anaesthetise animals suffering from this complaint. As a result of the ventricular hypertrophy, a muscular sub-aortic stenosis may be present in some individuals, and this can result in left ventricular outflow obstruction. This is worsened by high heart rates and increases in contractility, as well as reductions in afterload.

In terms of sedation/premedication, acepromazine would not be recommended because of its vasodilatory effects. There are theoretical reasons why alpha2-agonists may be useful, in that they will reduce heart rate and myocardial contractility, while concomitantly increasing SVR; indeed, one echocardiographic study in cats with HCM demonstrated better cardiac output when the animals were sedated with medetomidine, as compared to the conscious state. Thus, alpha2-agonists would appear to be suitable drugs in these cases, although they should not be used if the animal is in heart failure. To achieve synergistic sedative effects, they are best combined with an opioid.

Although many people use ketamine as an induction agent in HCM cats, this drug is contraindicated as it increases both heart rate and myocardial contractility; slow IV administration of propofol or alfaxalone would be preferred.

Both isoflurane and sevoflurane are suitable for maintenance.

iii) Dilated cardiomyopathy (DCM) DCM is common in large breed dogs, and may cause significant anaesthetic-related issues, including sudden death. The left ventricle becomes flabby and dilated, and is incapable of effective pumping.