Patients vary and accidents occur. This truth emphasizes the need for patient monitoring.
Patients vary and accidents occur. This truth emphasizes the need for patient monitoring. One only need visit the exhibit hall of a major veterinary meeting to appreciate the advancements made in veterinary patient monitoring. Historically, human monitors were refurbished and sold to veterinarians at reasonable prices. However, human monitors had limitations (especially with respect to blood pressure) when used on smaller patients with relatively high heart rates. More recently, monitors designed specifically for veterinary patients have been made widely available resulting in an improved level of monitoring in veterinary practices.
Monitoring is simply the process of collecting of data. These data are used by the anesthetist to formulate or modify the anesthetic plan to avoid or minimize risks to the patient. Obviously, anesthetic risk is directly related to the adequacy and accuracy of data collection and the knowledge and skill of the anesthetist to utilize the information. Automated monitoring (pulse oximetry, ECG, arterial blood pressure, end tidal CO2, arterial blood gases) provide more complete information and usually facilitate earlier detection of problems than manual monitoring alone (pulse palpation, mucous membrane color, respiration rate). Specialized situations often require specialized monitoring techniques and as veterinary surgery advances, so must veterinary anesthesia monitoring. When considering purchasing monitoring equipment, thought should be given to the training of the people using it. While the owner's manual and salespersons are able to guide in the application of the monitor to the patient, interpretation of the data and formulating a correct and timely response is equally important. Veterinary anesthesiologists are usually very willing to train staff in the proper use of monitoring equipment.
Arterial blood pressure is determined by several interacting factors. Simplistically, Ohm's Law can be used to describe the interrelationship.
Pressure = Flow x Resistance (Eq. 1)
It is important to recognize that an increase in blood pressure is not necessarily associated with an increase in blood flow (either tissue blood flow or cardiac output). Cardiac output is determined by heart rate and stroke volume.
Cardiac Output = Heart rate x Stroke volume (Eq. 2)
Blood pressure is not the same as blood flow and it is possible to have high blood pressure and very low blood flow.
Several methods of measuring arterial blood pressure are available. Arterial catheterization is routinely performed by many anesthesiologists. Arterial catheterization can be associated with a small risk of infection and requires training before use, but it can provide essential information about cardiac function and tissue perfusion pressure as well as allow easy access for intraoperative blood gas analysis.
Non-invasive methods include oscillometric and Doppler methods. These methods are usually less accurate than arterial catheterization and only provide intermittent readings, but are easy for technicians and veterinarians to perform.
Low blood pressure is a common complication of anesthesia and may lead to tissue hypoperfusion and ischemia. General recommendations for adequate pressures can be found in almost any anesthesia text, but it should be remembered disease processes can alter "acceptable" ranges. Additionally, as perioperative NSAID use becomes common in veterinary medicine, tissue hypoperfusion is a major concern. Normal blood pressure is not a guarantee of normal tissue perfusion, but significant hypotension will likely result in tissue hypoperfusion and may increase the risk of NSAID-associated toxicity.
Treatments for hypotension depend on the cause. The more common causes include hypovolemia and anesthetic-associated myocardial depression and vasodilation. Reduction of anesthetic dose may resolve the hypotension. Increased fluid administration may also be beneficial, but knowledge about the patient's cardiovascular function is important to avoid fluid overload. If blood loss is significant, blood products may be required to restore adequate intravascular volume. Pharmacotherapy (e.g., ephedrine, dopamine, dobutamine) can be beneficial when myocardial depression and/or low vascular resistance are present. Dose titration is important to avoid unwanted effects such as arrhythmias. Most anesthesia texts have detailed discussions about causes and treatments for hypotension.
Intravenous fluid therapy is usually associated with minimal risk and a large benefit and is therefore probably warranted in most patients. One common misconception is that administration of fluids assures adequate blood pressure and cardiac output. While it probably helps improve intravascular volume and cardiac preload, other causes of hypotension can also occur (anesthetic drug associated myocardial depression). Proper fluid selection will depend upon underlying abnormalities and preoperative blood work may be useful to guide selection. Recommended fluid rates vary, but generally healthy patients will tolerate 10 ml/kg/h. If hypovolemia is suspected, a bolus of fluid may help restore cardiac output. If severe heart disease is present (e.g., mitral regurgitation) excess fluid may induce congestive heart failure. Thoracic radiographs and possible echocardiography may be warranted prior to anesthesia if cardiac disease is suspected. Several studies have been published questioning the need for intraoperative fluid administration in dogs and cats. However, if one approaches anesthesia from the perspective of reducing patient risk, unless contraindicated fluid therapy is probably warranted.
Epinephrine is the prototype catecholamine and it is used clinically for the treatment of a variety of conditions. In vivo epinephrine is released from the adrenal medulla and is involved in the regulation of cardiac, vascular, glandular, and metabolic processes. It is more potent at α1 and α2-adrenergic receptors than NE or isoproterenol, but has similar potency at β1 receptors. Oral administration is not effective due to first pass hepatic metabolism and epinephrine is rapidly metabolized when administered parenterally so its effects are short-lived. Subcutaneous absorption is slow because of local epinephrine-induced vasoconstriction. Therefore, it is best administered intravenously when used as an emergency treatment for cardiovascular collapse or arrest.
Epinephrine is used clinically as: 1) an additive to local anesthetic solutions to prolong the duration of effect and decrease toxicity by slowing absorption, 2) treatment of life-threatening allergic reactions and bronchospasm, 3) during cardiopulmonary resuscitation (CPR), and 4) occasionally as a continuous infusion to improve myocardial contractility. Epinephrine is still the drug of choice for use during cardiopulmonary resuscitation. The mechanism of action of epinephrine during CPR appears to be primarily through α-adrenergically mediated vasoconstriction resulting in improvement of diastolic myocardial perfusion. However, following successful resuscitation with epinephrine, tachycardia and increased myocardial oxygen demand occur and may predispose the heart to subsequent ischemia. The administration of other vasoconstrictors including vasopressin (ADH) and phenylephrine has been associated with similar or better resuscitation success rates without subsequent β1-mediated tachycardia.
The cardiovascular effects of epinephrine result from a dose dependant stimulation of α1, β1, and β2-adrenergic receptors. When administered intravenously to adult humans 1-2 µg/kg/min stimulates principally β2-adrenergic receptors resulting in vasodilation and a slight decrease in mean arterial blood pressure. Stimulation of β1- adrenergic receptors at around 4 µg/kg/min directly increases cardiac output through increased myocardial contractility, increased heart rate, and increased preload. As the dose increases α1-adrenergic receptors are stimulated and vasoconstriction in tissues containing large amounts of α1-adrenergic receptors (e.g., skin and renal cortex) occurs resulting in redistribution of cardiac output to muscle and tissues vital for life.
Epinephrine administration may cause hypotension and significant tachycardia when administered following pretreatment with a α1-adrenoceptor antagonist. This paradoxical effect of epinephrine is called epinephrine reversal and is a clinical concern in veterinary patients given acepromazine, a nonspecific sedative with α1-adrenoceptor antagonist activity. After blockade of α1-adrenoceptor mediated vasoconstriction, β2-adrenergic receptor activation will cause unopposed vasodilation in skeletal muscle and other vascular beds resulting in hypotension. However, the antagonism of the α1-adrenoceptor is likely competitive and the observed effect on blood pressure may be a function of timing, dose, and route of administration.
Dopamine is a major neurotransmitter in the central and peripheral nervous systems. Dopamine1 receptors located postsynaptically mediate vasodilation of renal, mesenteric, coronary, and cerebral blood vessels. Dopamine is rapidly metabolized and must be given as a continuous rate infusion to maintain therapeutic plasma concentrations. Like norepinephrine, dopamine will cause tissue necrosis if administered perivascularly.
Dopamine is used clinically for increasing urine output in patients with renal failure, and as a treatment for hypotension during anesthesia and in the intensive care unit. Traditionally dopamine has been administered at renal, cardiac, and vasoconstrictive doses. 1-3 µg/kg/min is commonly believed to act predominately on DA1 receptors resulting in renal and splanchnic vasodilation and diuresis. 3-10 µg/kg/min is believed to cause more pronounced β1-adrenergic receptor mediated cardiovascular effects including increased heart rate and myocardial contractility. If greater than 10 µg/kg/min is administered, α1-adrenergic receptor effects occur resulting in vasoconstriction and further increases in blood pressure.
The above dosing regimen has been challenged based on several arguments. First, the effectiveness of the renal dose of dopamine to prevent or reverse renal insult has not been established and is largely based on clinical impression, and second, Habuchi et al. observed the cardiac effects of dopamine at clinically relevant concentrations (< 1 µM) result almost exclusively from the indirect effect of β adrenoceptor stimulation, mediated by the release of norepinephrine from sympathetic nerve terminals. The roles of the direct stimulation of β adrenoceptors by dopamine at these concentrations and the stimulation of post-junctional DA1 receptors seem negligible. Regardless of the mechanism, dopamine administration can cause diuresis and improved blood pressure in many patients and it is a useful drug in many species.
Dobutamine is a relatively selective agonist at β1 adrenergic receptors. Like most other catecholamines, dobutamine undergoes rapid biotransformation and must be given by a continuous intravenous infusion in order to be effective. Typical doses of dobutamine are between 1-20 µg/kg/min and dobutamine may be co-administered with low doses of dopamine to improve splanchnic perfusion. Experimental evidence substantiating the effectiveness of this combination is lacking. High doses of dobutamine may predispose the patient to tachycardia and cardiac dysrhythmias.
Clinical uses of dobutamine include short-term treatment for heart failure and as a way to maintain cardiac output and tissue perfusion during anesthesia. Dobutamine is most effective when preload is adequate and metabolic disease hasn't altered the ability of the myocardium to respond to catecholamines. Dobutamine is effective during anesthesia, but some animals may respond better if adequate volume replacement occurs before or during drug administration to improve preload. Clinical and experimental evidence would suggest that at this time dobutamine is the drug of choice for equine anesthesia to improve cardiac output and muscle perfusion.
Ephedrine has historically been used as a chronic oral treatment for asthma in people. Ephedrine is resistant to MAO metabolism and can be effective when administered orally. It causes bronchodilation via nonspecific β2-adrenergic receptor agonism but its use has been replaced by more specific cholinergic antagonists and β2-adrenergic receptor agonists.
Intravenous ephedrine administration results in a mild to moderate increase in heart rate and an increase in blood pressure. The observed effect is similar to norepinephrine, but the intensity is less and the duration longer. Some of the hemodynamic response is due to direct agonist activity at adrenergic receptors, but much of the effect is due to ephedrine-induced release of epinephrine and norepinephrine from adrenergic nerve terminals. It is useful treatment for hypotension due to vasodilation and myocardial depression associated with inhalant and injectable anesthetics. Ephedrine also is useful for counteracting hypotension associated with sympathetic blockade following spinal or epidural anesthesia. Ephedrine usually must be administered intravenously every 10-30 min (0.1-0.3 mg/kg) and administration may be effective initially, but decrease with repeated doses. Tachyphylaxis associated with repeated administration can be explained by the depletion of catecholamines from the adrenergic nerve terminals or long term binding to and deactivation of presynaptic adrenergic receptors. Ephedrine has minimal effects on uterine blood flow and may be a good choice for improving blood pressure and cardiac output in pregnant patients.