"Heart disease" in dogs and cats comes in a lot of different versions and even if a specific diagnosis is made, each patient is different depending on the severity of their disease and how well they have compensated for it. The primary problem may be electrical in origin (e.g., atrio-ventricular conduction blocks and ventricular tachycardia) or mechanical (e.g., mitral insufficiency and pulmonic stenosis). Each abnormality presents different challenges and requires a different anesthetic approach. The dog or cat may undergo anesthesia so that the defect can be repaired (e.g., correction of a patent ductus arteriosus), or it may have some degree of heart failure (e.g., mitral regurgitation) but require anesthesia for a dental procedure. In many cases it is possible to stabilize the patient prior to anesthesia (e.g., treat pulmonary edema and improved contractility in cases of congestive heart failure). Assigning a risk factor (e.g., using the American Society of Anesthesiologist's physical status classification system)¹ is recommended and the risks related to anesthesia should be discussed with the owner.

When developing a plan for a patient with heart disease, it is a good idea to remind yourself of the heart's primary function and how a normal healthy heart works, then consider what is different about your patient and how you will avoid further compromise. Some basic physiologic equations are always worth remembering.²

The most critical function of the heart is to continuously deliver oxygen to tissues and this depends on adequate carriage of oxygen by hemoglobin and a functional cardiovascular system.

Oxygen delivery (DO₂) = cardiac output (CO) x oxygen content (CaO₂)

DO₂ is the milliliters (ml) of oxygen delivered per minute, cardiac output is a product of stroke volume (SV; ml per beat) and heart rate (HR; beats per minute) and is the liters of blood ejected per minute. Stroke volume depends on preload (venous return to the heart), afterload (resistance to systolic ejection) and contractility (inotropy or strength of contraction). Preload is an important concept: in a healthy heart an increase in preload will increase SV (Frank-Starling Law of the heart), but an unhealthy heart dos not respond in the same way. A major determinant of preload is circulating blood volume and an adequate preload is required to produce a good CO. However, when dealing with a failing heart there is a fine balance; an increased fluid load will increase the myocardial workload to a point that may not be sustainable, resulting in a negative effect on CO. Until recently, fluid administration rates during anesthesia were not evidence based and have been, in most cases, excessively high especially in cats. Accurate delivery of appropriate fluid rates are essential in the face of cardiac disease; excellent guidelines for perioperative fluid administration have been provided by the American Animal Hospital Association and American Association of Feline Practitioners.³ These are available along with an accompanying implementation toolkit for download at: http://www.catvets.com/guidelines/practice-guidelines/fluid-therapy-guidelines.

Oxygen content is the ml of blood carried per dL of blood:

Oxygen content (CaO₂) = Hemoglobin concentration (Hb) x 1.34 x oxygen saturation of hemoglobin (SaO₂) + 0.003 x partial pressure of oxygen dissolved in blood (PaO₂)

Measuring blood pressure is easy to do in clinical practice but it is important to know that this is a reflection of CO and systemic vascular resistance (SVR; dynes•s•cm^-5). SVR is a measure of the degree of vasodilation or vasoconstriction.

Mean arterial pressure (MAP) is important for tissue and organ perfusion:

Mean arterial pressure = CO x SVR

A MAP of > 60 mm Hg or a systolic arterial pressure of > 90 mm Hg have historically been the numbers to aim for to ensure adequate oxygen delivery. Note however that MAP may be a "good number" but a low CO and high SVR may be present and perfusion may not be adequate. For this reason it is important to use several different parameters when monitoring the anesthetized patient.

From these equations it becomes clear that many variables can be affected by disease processes or can be manipulated by the anesthesiologist.

Table 1. Examples of common causes of changes in cardiovascular variables

* Intermittent Positive Pressure Ventilation

General Principles

If the patient is receiving cardiac medications these should not be stopped prior to anesthesia. Reducing stress is a high priority in patients with cardiac disease as catecholamine release will result in vasoconstriction (increased systemic vascular resistance), tachycardia and increased myocardial oxygen demands. Stress can be decreased by judicious use of sedatives, tranquilizers, opioids and correct handling and restraint. Due to decreased cardiac reserve and intolerance to hypoxemia pre-oxygenation for 3 minutes, using a face mask, is recommended to increase the time taken to desaturation.⁴ So-called "anesthetic sparing" techniques should be embraced; induction agents and inhalant anesthetics have profound cardiorespiratory depressant effects so their use should be reduced as much as possible by good premedication protocols, preemptive analgesia and supplemental infusions during procedures (e.g., opioids). Co-induction is a technique where one drug is used to decrease the requirements of another; for example, the induction dose of propofol can be significantly reduced by using drugs with minimal negative cardiovascular effects such as midazolam or diazepam (0.25 mg/kg IV). Induction drugs should also be given slowly and to effect. Mask induction with inhalant agents cannot be recommended due to the stress this causes and the high dose of inhalant agent required to achieve unconsciousness; this technique has been documented to increase mortality in dogs.⁵ Preventing and treating hypothermia is also important in these patients; hypothermia causes bradycardia that is not responsive to anticholinergic drugs, decreases cardiac contractility, increases viscosity of blood, increases bleeding and during rewarming, shivering dramatically increases oxygen requirements. Patients should receive supplemental oxygen until they are normothermic.

Armed with knowledge of the basic principles outlined above a plan can be devised for most animals even with complex cardiac diseases. The basic principles should be applied to all patients undergoing anesthesia. A common disease of the cat is discussed in more detail below.

Feline Hypertrophic Cardiomyopathy (HCM)

Hypertrophic cardiomyopathy is a common disease in cats. Several studies suggest that approximately 15% of all cats are affected.^6,7 The challenge of this disease is that apparently healthy young cats may be affected and it is subclinical until they are challenged by anesthesia. Auscultating a heart murmur does not necessarily mean a cat has functional cardiac disease and 50% of cats with HCM do not have a murmur. Echocardiography is required for diagnosis; therefore, we often anesthetize a cat with HCM thinking it is normal. Affected cats have a thickened and stiff left ventricle which fails to relax normally and a decreased internal ventricular volume. In some cases there is left ventricular outflow obstruction. The goals of anesthesia are to maintain a normal heart rate and avoid tachycardia, maintain preload, increase afterload and avoid increased myocardial contractility. Ketamine should be avoided as it causes tachycardia, increased contractility and myocardial oxygen demand. Acepromazine can cause vasodilation and worsen outflow obstruction. Opioids should be utilized and bradycardia is beneficial. Alpha-2 agonists can be used.⁸ Induction should be with a benzodiazepine plus propofol or alfaxalone. The maintenance requirements for inhalant agents can be minimized by using opioid infusions (e.g., fentanyl).

References

1.  Bednarski R, Grimm K, Harvey R, et al. AAHA anesthesia guidelines for dogs and cats. J Am Anim Hosp Assoc. 2011;47(6):377–385.

2.  Congdon JM. Cardiovascular disease. In: Snyder LBC, Johnson RA, eds. Canine and Feline Anesthesia and Co-Existing Disease. Ames, Iowa: Wiley-Blackwell; 2014.

3.  Davis H, Jensen T, Johnson A, et al. 2013 AAHA/AAFP fluid therapy guidelines for dogs and cats. J Am Anim Hosp Assoc. 2013;49(3):149–159.

4.  McNally EM, Robertson SA, Pablo LS. Comparison of time to desaturation between preoxygenated and nonpreoxygenated dogs following sedation with acepromazine maleate and morphine and induction of anesthesia with propofol. Am J Vet Res. 2009;70(11):1333–1338.

5.  Brodbelt DC, Pfeiffer DU, Young LE, Wood JL. Results of the confidential enquiry into perioperative small animal fatalities regarding risk factors for anesthetic-related death in dogs. J Am Vet Med Assoc. 2008;233(7):1096–1104.

6.  Paige CF, Abbott JA, Elvinger F, Pyle RL. Prevalence of cardiomyopathy in apparently healthy cats. J Am Vet Med Assoc. 2009;234(11):1398–1403.

7.  Cote E, Manning AM, Emerson D, Laste NJ, Malakoff RL, Harpster NK. Assessment of the prevalence of heart murmurs in overtly healthy cats. J Am Vet Med Assoc. 2004;225(3):384–388.

8.  Lamont LA, Bulmer BJ, Sisson DD, Grimm KA, Tranquilli WJ. Doppler echocardiographic effects of medetomidine on dynamic left ventricular outflow tract obstruction in cats. J Am Vet Med Assoc. 2002;221(9):1276–1281.