Anaesthesia in Patients Suffering a Heart Murmur

Heart murmurs diagnosed on precordial auscultation are a significant finding that warrant further clinical investigation. The clinical implications of the murmur requires consideration to determine the anaesthetic risk.
2 Patient signalment, presenting complaint, presence of concurrent diseases, exercise tolerance and current medication are important considerations to address during a pre-anaesthetic evaluation. A heart murmur
per se is not a contraindication, but rather a caution for general anaesthesia in a patient not showing clinical signs. The drug selection to achieve general anaesthesia and analgesia may require a patient tailored approach, especially if the murmur is due to cardiac pathology.
• Murmurs are audible evidence that there is turbulent blood flow through the heart. The murmur is graded according to how loud the murmur is compared to the lub-dub sounds heard during the cardiac cycle. 4 The lower the grade of the murmur (III and less) the less reliable it is to indicate the severity of the pathology. 4, 9 Therefore, on detecting a heart murmur, further investigation is required to determine the severity of the
pathology and if the murmur is cardiac in origin or not.

Post-murmur-detection clinical investigation

Two critical clinical investigation aims need to be achieved. First, is to determine if the pathology is due to cardiac or non-cardiac processes. Second, is to determine if the patient is otherwise clinically affected by the presence of the murmur. 1, 2
• Cardiac related pathologies include valve stenosis or insufficiency (disease or traumatic), atrial or ventricular septal defects, or complex cardiac malformations (e.g. tetralogy of Fallot). Non-cardiac pathologies include vascular anomalies (e.g. patent ductus arteriosus), altered viscosity (e.g. anaemia), altered flow velocity (e.g. hyperdynamic flow), or obstruction to flow through the heart (e.g. thrombus, air emboli). 4
• Exercise tolerance is considered an excellent marker to gauge cardiovascular fitness and risk for general anaesthesia, whereby, the more tolerant the patient is to exercise the lower the risk of general anaesthesia. Perceptive questioning could clarify the patient’s exercise tolerance.
• The clinician should be suspicious if the patient presents with a murmur and tachycardia, delayed capillary refill time, pale mucous membranes and a history of being “sleepy” or mostly inactive during the day. These findings could suggest that the patient is not cardiovascular stable and thus of a higher anaesthetic risk. The resultant pathophysiology is invariably related to a decrease in cardiac output which translates into a ecrease in perfusion of oxygen to metabolically active tissues.
Oxygen is chiefly transported to the tissue via haemoglobin and delivery is dependent on the cardiac output. Cardiac output is the product of the stroke volume per beat multiplied by the heart rate. The stroke volume is generally decreased in patients suffering cardiac murmurs. The heart rate is increased to preserve the cardiac output. Thus heart rate can be an indicator of clinical stability. Arterial blood pressure (figure 1) is the product of cardiac output multiplied by the systemic vascular resistance. During low cardiac output states, systemic vasoconstriction is often present in order to preserve
an adequate arterial blood pressure (activation of the sympathetic nervous system and the renin-angiotensin-aldosterone axis). Therefore, patients presenting with pallor and tachycardia with an audible murmur require pre-anaesthetic stabilisation.

Pre-anaesthetic stabilisation

A functional or innocent heart murmur in an otherwise healthy patient may not require any special pre-anaesthetic stabilisation. 4 Patients which are already on cardiovascular supporting drugs (pimobendin, digoxin, angiotensin converting enzyme inhibitors, diuretics etc.) but are otherwise stable and compensating may also not require stabilisation. Serum electrolytes (potassium, sodium and calcium) should be measured in atients undergoing long term diuretic or digoxin therapy, as they may present with low potassium or calcium concentration which would prolong the recovery. Sodium is important to maintain the intravascular fluid volume (water shifts according to the sodium gradient between the blood and tissue) of circulating blood. If the sodium level is high it could indicate that there is a decrease in the circulating volume and that fluid bolusing may be required. While a low sodium level may indicate caution with fluid management as it would be easier to inadvertently fluid overload these patients. Furthermore, routine haematology and serum creatinine and total serum proteins (albumin of most interest) should be measured for baseline readings in all patients. Collecting this data prior to general anaesthesia may assist in managing patients suffering unexpected post-recovery complications. 6, 11

• Patients presenting with cardiovascular instability should be managed medically prior to general anaesthesia (Table 1). Patients that are cardiovascularly unstable and requiring emergency intervention carry a high risk for general anaesthesia. The presenting pathology will indicate the appropriate emergency medical intervention to improve the cardiac output, blood pressure and tissue oxygenation prior to general anaesthesia.
• Murmurs due to anaemia have serious implications and will require pre-anaesthetic stabilisation. It is imperative to understand that oxygen transport is heavily dependent (97% of all transport) on the amount of functioning haemoglobin available. Pre-oxygenation with 100% oxygen prior to general anaesthesia in an anaemic patient is inadequate to compensate for a low haemoglobin concentration, especially during low cardiac output states. The generally accepted guideline is to ensure a haematocrit level of greater than 0.2 to 0.25 (20 to 25%) in dogs and cats, even in patients suffering chronic anaemia (e.g. chronic renal failure in cats) prior to general anaesthesia. 6, 11
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Anaesthetic management

General anaesthesia should be kept to the shortest time period possible. Therefore, a decisive plan on all procedures that need to be completed must be decided on and prepared for prior to induction.
• A general principle for a cardiac safe general anaesthesia is to not change the heart rate or vascular tone from that in the pre-anaesthetic clinical exam in a stable patient. Therefore monitoring of the heart rate and blood pressure during general anaesthesia is paramount. Other indicators of peripheral perfusion such as capillary refill time and mucous membrane colour may be helpful in monitoring cardiac output. A pulseoximeter (figure 2) is useful to monitor peripheral perfusion (machine must detect a pulse) and oxygen haemoglobin saturation. 10 Capnography (measuring the end tidal carbon dioxide) should also be used to monitor these patients. The capnograph is a useful tool to detect respiratory depression and poor cardiovascular performance. 6, 11 Other indirect markers of perfusion are heart rate, mucous membrane colour and CRT.
• Patient anxiety and stress should be managed in patients with cardiac disease. Management interventions such as: 1) allowing the patient to be dropped off on the day of the procedure prior to the general anaesthesia, 2) having the owner pre sent during the premedication, 3) keeping the patient in a quiet, warm cage where the patient can be regularly observed, 4) treating for existing pain (injured animals or those suffering osteoarthritis) will all decrease the level of anxiety and stress. Patients suffering from extreme anxiety during visits to the veterinarian may benefit from an oral dose of a benzodiazepine 15 minutes prior to leaving home. Oral alprazolam (0.01 to 0.1 mg/kg) or diazepam (0.2 to 0.5 mg/kg) usually suffices.

• Acepromazine, a phenothiazine derivative psychotropic drug, is a frequently used sedative drug. It causes a dose dependent reduction of the stroke volume and the cardiac output. Due to alpha1-adrenergic blocking effects on the vascular walls, vasodilation occurs and arterial blood pressure decreases. 12 Acepromazine desensitizes the myocardium to the potentially arrhythmogenic effect of catecholamines. Due to its effect on the myocardial alpha1-receptors, it prevents the development of ventricular arrhythmias which may be advantageous in certain cases. 13
• Patients already on cardiovascular supportive medication should continue their medication as prescribed. Pre-anaesthetic fasting should be 6 to 8 hours. However, water should not be withheld until the administration of the premedication.
• A conservative cardiovascular sparing drug combination should always be used in a patient presenting with a murmur (Table 2). The most common cardiovascular sparing premedication drugs are the pure mu-agonist opioids and benzodiazepines (midazolam and diazepam). Histamine release that causes vasodilation is a common side-
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effect of pethidine administration, and to lesser extent with morphine. Morphine induces vomiting (increases patient anxiety and stress) more commonly compared to fentanyl and methadone. Therefore, pre-emptive treatment with an antiemetic (e.g. maropitant) prior to morphine administration is advised. Buprenorphine, a partial mu-agonist, should only be reserved for minor painful procedures or as a post-surgical analgesic
when pain levels have subsided to a mild to moderate pain level (e.g. gonadectomy procedures). Butorphanol, a mixed mu-antagonist-kappa-agonist, is usefully to partially antagonise undesirable effects of pure-mu opioids (e.g. dysphoria, delayed recovery, hypoventilation) while maintaining some analgesia.
• Induction agents that can be used include potent opioids of the fentanyl group (e.g. fentanyl, sufentanil), propofol or alfaxalone. Patients suffering a murmur of cardiac origin may have a decreased cardiac output and thus the perfusion to the central nervous tissue may be decreased. Therefore, careful titration of intravenous induction agents is always advised as there will be a delay in the onset of action. Volatile inhalation anaesthetics (isoflurane, sevoflurane) are the preferred maintenance agents because they provide good myocardial perfusion and rapid recovery. 6, 11
• The routine use of alpha2-adrenoceptor agonists (xylazine, medetomidine, dexmedetomidine) are contraindicated in most cardiovascular cases and should only be used in cases where the pathophysiology of the disease process is well understood. These drugs cause a profound peripheral vasoconstriction, increase in blood pressure and reflex bradycardia during the initial phase of drug administration. Once the drug moves more centrally (central nervous system) there is a decrease in sympathetic tone which causes a decrease in vasoconstriction and relative increase vagal tone to the heart which maintains the bradycardia. 8 Both the initial peripheral and delayed centrally mediated drug effects are not desirable in most patients suffering cardiac disease due to alterations in the systemic vascular resistance and heart rate. However, in certain cardiac pathologies where a murmur may be heard, such as hypertrophic cardiomyopathy in cats, medetomidine has been shown to decrease the dynamic outflow obstruction of the left ventricle and is useful in maintaining cardiac output.
• Making use of a familiar protocols to induce and maintain general anaesthesia is considered safer than using an unfamiliar protocol. However, there are physiological derangements which manifest from inappropriate drug selection which may be detected over time, such as an early cardiac patient presenting with acute renal failure, a stable patient rapidly deteriorating weeks after the general anaesthesia. Thus the immediate post- operative recovery for a poorly planned anaesthetic does imply that no “harm” has been done to the patient. Examples of less desirable anaesthetic protocols would include: xylazine-atropine premedication, thiopentone induction and maintenance, and protocols with no-premedication or analgesics.
• Always provide enough analgesia during the procedure using a multimodal approach where possible. Maintenance agents are designed to keep the patient asleep in an appropriate surgical plane (or lighter for diagnostic investigations such as radiographs). If the patient awakens often during surgical stimulation it is indicated to increase the analgesia and not the anaesthesia depth. In patients with cardiac disease a combination of opioids, local anaesthetics and judicial use of non-steroidal-anti-inflammatory (NSAIDs) drugs are preferred. Whereas healthy patients without other organ failure, a combination of opioids, local anaesthetics and routine use of NSAIDs should suffice.7
• Fluid management in patients with cardiac disease requires titration to individual needs. Ensuring that the intravascular volume is maintained throughout the general anaesthetic is important however fluid overloading is a real post-anaesthetic risk in patients suffering from cardiac disease. An early indicator of fluid overloading is an increase in the respiratory rate of at least 20% which is not due to surgical stimulation or depth of general anaesthesia. The effort of breathing will also be increased and referred breath sounds can be auscultated due to the increased sound carrying capacity of the lung tissue due to interstitial fluid accumulation. Late indicators of fluid overloading are jugular distension, increase in central venous pressure, auscultating for changes in respiratory sounds (crackles) and pleural effusions (especially in cats).
• A fluid rate of 10 mL/kg/hour could be started just after induction and titrated downwards to 5 mL/kg/hour during routine surgical procedures where minimal fluid loss and evaporation is anticipated. 5 Patients not on diuretic therapy often benefit from a low dose furosemide (1-2 mg/kg) twice daily for one or two days.

• Maintaining normothermia throughout the general anaesthetic and recovery is paramount and may be achieved by using blankets, forced warm air devices, warm water or electric (Hot Dog) blankets (figure 3). Recovery should be observed and be done in a quiet, warm environment where emergency drugs and equipment are at hand in case the patient crashes. The recovery period has the highest risk of death, especially in cats.
During recovery from anaesthesia hypoxia is common and one of the main reasons for unexpected deaths and this necessitate vigilant monitoring until patient is fully recovered and conscious. The reasons for this are 1) functional residual capacity is reduced, 2) dampened ventilation response to carbon dioxidelevel, 3) decreased respiratory response to hypoxia at even sub- anaesthetic concentrations of anaesthetic argents (0.1MAC), 4) depression of the hypoxic pulmonary vasoconstriction reflex (this is the major reflex that matches blood flow to the ventilation of each alveoli), 5) CNS depression (residual drug in the system), 7) residual anaesthetic causes reduced strength in the diaphragm and intercostal muscles resulting in hypoventiliation, 8) reduction in compliance as a consequence of reduced FRC and the development of lung tissue atelectasis. 9) CNS depression (residual drugs) 10) Hypotension and decreased cardiac output, 11) hypothermia induced shivering which increases O2 consumption, 12) Pain, 13) Sympathetic nervous response and stress response both act to increase circulating catecholamines, 14) No sigh reflex (collapsed lung), 15) No voluntary changes in body position.

6 “MUST KNOW ” facts to consider in murmur patients undergoing general anaesthesia

1. A murmur is not necessarily a contraindication for general anaesthesia – it depends if the patient’s cardiovascular system is stable. Differentiate between cardiovascular disease and cardiovascular failure.
2. The risk of general anaesthesia increases if the patient presents with concurrent disease processes and/or requires stabilisation prior to general anaesthesia.
3. Plan and prepare your procedures – this will keep your general anaesthesia to the shortest time possible.
4. Be patient with your patient – decreased cardiac output states delay the onset of action of the drugs, allow enough time for the drugs to reach clinical effect before administering additional boluses.
5. Fluid administration requires titration – even in stable patients.
6. Analgesia is paramount – Use opioids and local anaesthetics with judicial use of NSAIDs

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