= increased; ↓ = decreased; — = no change; + = potentially arrhythmogenic. If the myofibrils can respond, this initially leads to improved contractility via the Frank‐Starling law.It eventually leads to over‐distension of the ventricle, which impairs contractility and increases myocardial O2 demand.
Circulation becomes “centralized” in patients with moderate to severe cardiac disease, resulting in greater delivery of blood (and drugs carried by the blood) to highly perfused tissues, including the brain.However, cardiac output is often decreased in these patients, resulting in slower drug delivery to the brain.Thus, the dosage of anesthetic drugs administered to patients with cardiac disease should be decreased and drugs should be administered slowly and with ample time between doses for delivery to the brain.
Congestion of blood and lack of forward flow leads to the development of edema.Pulmonary edema can seriously impair gas exchange.
Myocardial O2 demand increases (due to tachycardia, increased afterload and overdistended or hypertrophic myocardium) yet O2 supply decreases (due to decreased myocardial perfusion), possibly resulting in O2 debt and further myocardial injury.
VIII Cardiovascular disease in horses presented for anesthesia
A Diseases of the conducting system
Include irregularities of the SA node (e.g. sinus tachycardia and vagally‐mediated bradycardia), the atrial conduction system (e.g. atrial fibrillation), the AV node (e.g. first‐, second‐, or third‐degree AV block) and the bundle branch or His‐Purkinje system (e.g. bundle branch block).
Because the equine atrial muscle mass is large, the equine heart is predisposed to the development of re‐entrant rhythms like atrial fibrillation.
Atrial fibrillation
The most common pathologic arrhythmia encountered in horses.
Atrial contribution to ventricular filling may be significant during anesthesia.
Some anesthetic drugs are arrhythmogenic and should be avoided.
Patients may need to be converted to normal sinus rhythm prior to anesthesia, although conversion is not always achieved with current options.
B Congenital disease
Includes patent ductus arteriosus, ventricular septal defects and tetralogy of Fallot.
Patent ductus arteriosusThe most commonly encountered congenital disease in horses.The ductus arteriosus may be patent for up to 72 hours in normal foals.Anesthetic‐induced hypotension may reverse blood flow through the PDA and create pulmonary hypertension.
C Primary myocardial disease
Rare in horses.
Congestive heart failure (CHF) is associated with limited cardiac output, increased neurohumoral activity, sodium retention, edema in tissues and transudation of fluid into body cavities.Valvular disease is the most common cause of (CHF) in the horse.Horses with CHF are at an extremely high anesthetic risk.
D Secondary cardiovascular compromise
Common in horses presented for anesthesia.
Causes include circulatory shock (e.g. severe hemorrhage), sepsis (e.g. colic) and profound electrolyte imbalance (e.g. uroabdomen in foals).
Cardiovascular changes that occur in sepsis include:Decreased cardiac output resulting from a direct decrease in cardiac contractility and a decrease in preload due to splanchnic pooling and vascular leakage.Pulmonary hypertension (with subsequent hypoxemia).Complex alterations in systemic BP (initial hypertension followed by hypotension with loss of vascular tone).Drastic alterations in hematologic function, including hypercoagulability followed by hypocoagulability.
IX Anesthetic plan for horses with cardiovascular disease
A Patient preparation
All patients scheduled for anesthesia should have a thorough physical examination.
Because anesthetic drugs can drastically alter cardiovascular function, techniques to evaluate the cardiovascular system should be emphasized, especially in patients with primary cardiovascular disease or cardiovascular compromise secondary to other systemic disease (e.g. sepsis).Laboratory tests should include serum chemistry and a complete blood count.
Regardless of the cause of cardiovascular compromise, the patient must be stabilized prior to anesthesia. This includes:Restoration of circulating blood volume (use of whole blood if necessary).Intravenous fluids must be used judiciously in horses with heart failure.Restoration of electrolyte balance.Serum [Ca++] and [K+] are often decreased.Promotion of cardiovascular function (e.g. IV fluids, positive inotropes, and analgesics).
B Sedation and induction
Following stabilization, the patient should be sedated with low dosages of sedatives (e.g. alpha2 agonists, acepromazine).
Pre‐emptive analgesic drugs should be utilized (e.g. opioids, alpha2 agonists, NSAIDs) to decrease the horse's stress and to decrease the dosages of induction and maintenance drugs.
A balanced induction technique should be used (e.g. guaifenesin + ketamine) and low dosages of the drugs should be administered to effect.
Intubation and oxygen administration should occur as soon as possible.
C Maintenance
Inhalational anesthetics are generally used for maintenance but dosages should be kept as low as possible to minimize the hypotensive effects of the drugs.Balanced anesthesia (e.g. inhalational agent plus a ketamine and/or lidocaine infusion) should be considered.
Analgesia is imperative and can be supplied via systemic administration of drugs or by the use of local anesthetic blockade, or ideally, by using both techniques.
Monitoring is extremely important and should include arterial BP, ECG, and arterial blood gases.A cardioselective inotrope (e.g. dobutamine) is recommended for correction of hypotension.
Fluid therapy should include evaluation and support of PCV, total protein (TP), acid–base balance and electrolyte concentrations.
D Recovery
Is as critical as the other steps of anesthesia.
Patient support (including monitoring, fluid administration, oxygen administration and provision of analgesia, should be maintained, when possible, throughout the recovery period.
