Читать книгу Manual of Equine Anesthesia and Analgesia - Группа авторов - Страница 106

 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.