The prevalence of anaesthetic complications in cardiac patients is high (Brouwer, 2000; Bagshaw-Wright, 2018) as these animals have a decreased ability to regulate their heart rate and cardiac output (Bednarski et al., 2011; Ohad, 2014), putting them at risk of altered drug distribution, hypotension, hypothermia, cardiac arrhythmias, reduced tissue perfusion and death (Dugdale, 2010). The type and severity of cardiac disease present will impact heavily on how the anaesthetic protocol is designed and how the case is managed (Hughes, 2008).
Mitral valve disease
Mitral valve disease (MVD) is an acquired cardiac disease, common in old and small-breed dogs and most prevalent in the Cavalier King Charles Spaniel and the Dachshund (Mattin et al., 2015). MVD is the most common cause of dilated cardiomyopathy (DCM) in the dog, which in severe cases results in congestive heart failure (CHF). It is thought to be genetic in origin; however, the ageing process is also thought to play a role (Suh et al., 2016; Robertson, 2018).
The disease occurs when the mitral valve becomes defective, and allows backflow of blood into the left atrium, reducing the amount pumped into the aorta and therefore the systemic circulation (Pablo, 2011a); cardiac output and systemic blood pressure are subsequently affected and the body must use compensatory mechanisms to maintain these parameters. By increasing blood volume in combination with vasoconstriction, this can be temporarily achieved, however places the left ventricle under increased pressure to contract against. Ultimately if untreated, the left ventricular wall becomes thickened and ineffective and left-sided heart failure develops; this life-threatening condition causes pulmonary oedema and perfusion of the body tissues to become inadequate (Waddlel, 2010).
The physiology of MVD creates a challenge for the anaesthetist, and will unavoidably place strain on an already diseased heart, which must be managed by careful planning of an appropriate anaesthetic protocol. This should aim to reduce preload whilst avoiding increases in afterload, maintaining contractility of cardiac muscle whilst avoiding increases in myocardial oxygen demand. Avoiding tachycardia, maintaining sinus rhythm and minimising stress, excitement and sympathetic stimulation are essential to a good outcome (Hughes, 2008).
Hypotension and tachycardia are the most common complications (45 percent and 36 percent respectively) and it is vital that these are avoided. Many drugs used in anaesthesia have profound effects on the cardiovascular system which healthy hearts are able to compensate for; however, an anaesthetised patient with MVD is highly likely to decompensate and there is a risk of CHF developing. The overall anaesthesia risk is dependent on the stage and severity of disease; how-ever, these patients can be anaesthetised safely, if extreme caution is used (Steinbacher and Dorfelt, 2012).
An eight-year-old Miniature Dachshund with MVD presented for anaesthesia for surgical excision of a mammary gland mass. The patient was diagnosed four years before, and progressed into an acute period of CHF six months previously. The patient was stabilised with pimobendan 0.5mg/kg BID; frusemide 2.5mg/kg SID; and benazepril/spironolactone 0.25mg/kg SID.
History and clinical examination
It is essential to take a thorough patient history to assess the stability of the patient’s condition and anaesthesia risk (Hughes, 2008); exercise tolerance and history of general well-being, including development or worsening of coughing or wheezing, are important indicators of the stability of the cardiovascular system and effectiveness of cardiac medications and are an essential part of the preoperative assessment, in combination with the physical examination and bloodwork.
The patient presented normally hydrated, normothermic (rectal temperature: 38.5°C) and normotensive (mean arterial pressure: 100mmHg oscillometric measurement). Thoracic auscultation revealed a grade 5 murmur over the mitral valve, unchanged from the previous exam three months prior; breath sounds were equally normal. There were no recent changes in exercise tolerance and the patient had not developed any coughing or wheezing.
Cardiac medications were administered as normal; stress and excitement of the patient was kept to a minimum. Blood was drawn for biochemistry, electrolyte and haematology values. ALT and BUN were found to be mildly elevated. Cardiac disease can alter renal and hepatic perfusion so elevated enzymes are usually a result of congestion of these organs (Waddlel, 2010). A reduction in glomerular filtration rate is common as animals age and, combined with poor perfusion, puts the patient at risk of reduced kidney function. SDMA was checked and found to be normal.
Despite this, the kidneys are likely to be challenged during anaesthesia, and the patient was therefore placed on a balanced, isotonic crystalloid solution (Hartmann’s) for maintenance requirements (2ml/kg/hr), to support perfusion and maintain normal electrolyte levels and hydration (Davis et al., 2013). It was essential to administer fluids conservatively, avoiding increased preload which could lead to pulmonary oedema (Waddlel, 2010).
Acepromazine was chosen for this case and is an excellent choice of premedication for MVD. If used at low doses (0.01 to 0.02mg/kg) mild vasodilation occurs, reducing afterload and providing good sedation whilst providing protection against dysrhythmias and minimising unwanted side effects (Pablo, 2011a).
Drugs that are more “anaesthetic sparing”, such as alpha-2 agonists, were available for premedication, which may have decreased the volume of injectable and inhalation anaesthesia required. However, these are contraindicated in MVD due to vasoconstriction and potential for devel-opment of pulmonary oedema, due to increased preload (Waddlel, 2010). A midazolam-ketamine combination could be used for future cases (0.24mg/kg and 5mg/kg respec-tively), which will act to maintain heart rate and reduce the required dosage of induction agent (Pablo, 2011a).
Methadone 0.3mg/kg was injected intramuscularly (IM) and was selected because of its availability, familiarity for staff and anaesthetic sparing properties; a low dose was used due to its potential to cause bradycardia (Pablo, 2011a). Buprenorphine was available; however, it was thought this would not provide adequate analgesia for the procedure.
The patient was pre-oxygenated and the abdomen clipped prior to induction to reduce anaesthetic time.
Propofol at 2mg/kg was injected IV over two minutes. Endotracheal intubation was performed using a lubricated 6.0mm silicone endotracheal tube; the cuff was not inflated as no leak was audible.
Bradycardia and hypotension are the most common side effects of propofol; in this case, a period of sinus bradycardia was experienced shortly after induction. The patient was found to be normotensive and was treated with oxygen therapy only. Treatments for bradycardia were available, such as anticholinergics (atropine); however, it was feared that administration may result in tachycardia, which is highly contraindicated for MVD patients (Haskins, 2011). Furthermore, anticholinergics are only indicated if bradycardia is causing hypotension due to the risk of reduced organ perfusion (Waddlel, 2010).
Propofol is acceptable for MVD; however, etomidate (0.5 to 1mg/kg) is the gold standard induction agent and, although very expensive, is the drug of choice for any patient with cardiac dysfunction because of its haemodynamic stability (Pablo, 2011a). Propofol should be avoided if possible due to its profound vasodilatory effects. The addiction of benzodiazepines as co-induction agents are useful to reduce induction agent dosages, which is advantageous, especially if propofol is the only drug available, as in this case (Hughes, 2008).
Maintenance and monitoring
Once stabilised, the patient received isoflurane delivered in 100 percent oxygen via a coaxial Bain breathing system. The fresh gas flow was set to 3l/min.
Additional monitoring equipment was connected in the following order: capnography (sidestream) for ETCO2 and capnogram; pulse oximetry (lingual probe) for SPO2 and graphical pleth; NIBP measurement using the left pedal artery; and oesophageal temperature monitoring.
A period of sinus tachycardia (170bpm) during surgery was attributed to pain and methadone 0.2mg/kg was repeated slow IV. HR slowly decreased to normal over seven minutes (100bpm). There were no surgical complications.
Tachycardia should be avoided in MVD as it increases myocardial oxygen demand; common causes include stress, excitement and painful stimuli. In this case, the tachycardia was attributed to a sympathetic response from the patient and more analgesia was administered. This may have been prevented by administering multimodal analgesia, such as the addition of ketamine or a non-steroidal anti-inflammatory drug, which will be considered for future cases. Higher doses of opioids should be used with caution due to the risk of bradycardia (Pablo, 2011a).
Recovery was overall uneventful; the patient was placed into sternal recumbency and oxygen was administered until the patient was able to sit up. The patient was eating and drinking within 90 minutes post-extubation.
Methadone 0.2mg/kg was repeated IM four hours post premedication for continued analgesia. The patient was discharged later that day and there were no postoperative complications.
The physiology of MVD creates a challenge for the anaesthetist, and referral of these cases is common (Pablo, 2011b; Steinbacher and Dorfelt, 2012). Anaesthetic plans and protocols must be designed taking into account the complex physiological disease abnormalities present within the patient and aim to maintain normal parameters whilst preventing further compromise of the cardiovascular system. With careful planning, good knowledge of the physiology of MVD, appropriate drug choices and excellent perioperative monitoring, it is possible to safely anaesthetise the MVD patient successfully in general practice and achieve good patient outcomes (Brouwer, 2000; Steinbacher and Dorfelt, 2012).