Manual of Equine Anesthesia and Analgesia. Группа авторов

       Describes the intrinsic capability of the heart to increase its force of contraction in response to an increase in venous return.This response occurs in isolated hearts indicating that it is independent of humeral and neural factors.

       Preload directly determines cardiac output when the HR is constant.

       An increase in preload, up to a certain point, increases cardiac output.

       At the end‐diastolic volume, cardiac output will not increase further and may actually decrease.

       As stated, the ultimate responsibility of the cardiovascular system is to provide adequate oxygen to the working cells.

       CaO2 = ([Hb] × SaO2% × 1.36) + (PaO2 × 0.003)[Hb] = concentration of hemoglobin in the blood in gr/dlSaO2 = percent saturation of hemoglobin with oxygen1.36 = a constant (Hüfner's) describing the amount of oxygen bound by 1 g of HbPaO2 = the partial pressure of oxygen in arterial blood0.003 = the solubility coefficient of oxygen in blood (ml/mmHg of oxygen/dL of blood)

       Normal [Hb](15 g/dl) and normal SaO2 (SaO2 98%, PaO2 95 mmHg):

       Normal [Hb](15 g/dl) and decreased SaO2 (SaO2 85%, PaO2 60 mmHg):

       Decreased [Hb] (6 g/dl) and normal SaO2 (SaO2 98, PaO2 95 mmHg):

       Most drugs used for sedation/tranquilization and anesthesia cause some degree of dose‐dependent cardiovascular changes which may manifest as changes in HR, preload, afterload, contractility or a combination of these factors.

       Regardless of which drugs are used, drug dosages in compromised patients should almost always be reduced.Most adverse effects, like the cardiovascular depression caused by inhalational anesthetic gases, are dose‐dependent.A greater percentage of administered drug may reach the brain (see below).

       Depending on the severity of the cardiovascular disease, changes in HR, preload, afterload and contractility can range from barely noticeable to life threatening.

       SV decreases due to decreased contractility and increased afterload.

       Decreased contractility due to:Direct effects of the disease (e.g. myofibril damage from ischemia).Indirect effects of electrolyte imbalance (e.g. decreased ionized calcium), acid–base imbalance, or sepsis.

       Increased afterload due to:A hypotension‐mediated increase in sympathetic activity, which results in excessive vasoconstriction in an attempt to maintain BP in the face of decreased cardiac output.A hypotension‐mediated decrease in arterial baroreceptor inhibition of autonomic centers in the brain stem, which stimulates the release of renin, which increases vascular resistance and promotes salt and water retention through release of aldosterone.

       Decreased SV due to decreased contractility and increased afterload.This causes cardiac output to become more HR dependent.HR generally increases, thereby increasing myocardial O2 consumption.

       Increased preload due to reduced SV, accumulated venous return and an increase in fluid retention secondary to activation of the renin/angiotensin system.Table 3.3 Cardiovascular effects of some commonly used anesthetic drugs.Source: Adapted from Muir (1998).DrugHeartHeart rhythmPre‐loadAfter‐loadContractilityCardiacrateoutputAcepromazine↑−↓↓− or ↓↑or ↓Alpha2 agonists↓↓+↑↑− or ↓↓Benzodiazepines−−−−−−Opioids− or↓−↓−− or ↓− or ↓Thiopental↑+↓↓↓↓Ketamine and Tiletamine↑+↑↑↑ or ↓↑ or ↓ or −Propofol− or↓±↓↓↓↓Halothane↓+↓↑↓↓↓Isoflurane↓−↓↓↓↓Sevoflurane↓−↓↓↓↓↑ = 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.

       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.

       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.

       Includes patent ductus arteriosus, ventricular septal defects and tetralogy of Fallot.

       Patent ductus arteriosusThe most commonly encountered congenital disease in horses.The