Anaesthesia For Cardiac Disease.pptx

SRI VENKATESWARA VETERINARY UNIVERSITY College of veterinary science Tirupati Tracking programme: ANESTHESIOLOGY(SURGERY) Topic:• ANESTHESIA FOR CARDIAC FAILURE PATIENTS • Submitted to: • Dr.Veena, • Professor, • Dept.of surgery & radiology Submitted by: • M.Muni Chaitanya, • Tv/2015-64, • IV-year BVSC&AH. •

Anaesthesia for cardiac disease

INTRODUCTION  The anesthetic mangement of a patient with cardiovascular dysfunction can be very challenging, because most preanesthetic and anesthetic agents capable of depressing the central nervous system can also produce cardiovascular depression. Patients with cardiovascular dysfunction may be more prone to fluid overload and dysrhythmias

 Extremes in heart rate may cause severe problems, including heart failure.  Patients with cardiovascular dysfunction may lack sufficient cardiac reserve to compensate for anesthetic-induced depression.  Appropriate patient monitoring with arterial blood pressure, central venous pressure, ECG, end-tidal carbon dioxide, pulse oximetry and other parameters is essential to reduce anesthetic and surgical risk.

Commonly used drugs for premedication , induction and maintenance of anaesthesia  Midazolam-Oxymorphone(20%)  Thiopental or Etomidate(30%)  Isoflurane (64%)

ISOFLURANE Provides cardiac stability Reduction in blood pressure is noticed during isoflurane anaesthesia due to reduction in peripheral vascular resistance not due to myocardial depression as in halothane It increases the myocardial perfusion by reducing the caronary vascular resistance

It has little or no action on sensitivity the myocardium for the actions catecholomines .  Hence it is recommended in patients with cardiac disease.

Anaesthesia of Patients with Atrioventricular Valve Regurgitation • Decreases in heart rate cause a greater fraction of the stroke volume to regurgitate into the atrium, while a mild increase in heart rate may improve the forward flow at the expense of regurgitation fraction, as will arteriolar-dilating anesthetics. Preanesthetic Sedation • Whereas an anesthetic protocol which mildly decreases the force of myocardial contraction and vascular resistance may be beneficial, extreme bradycardia should be avoided

• Pethidine and oxymorphone are opioids that mildly decrease contraction and mildly increase heart rate, while morphine and fentanyl will preserve cardiac function and give better analgesia when necessary, but may cause too severe a bradycardia, which would warrant anticholinergic support. • A very low dose(i.e., 0.02 mg/kg or less) of acepromazine (ACP) may provide adequate tranquilization. • However, ACP, a dopamine antagonist, reduces the efficacy of dopamine as a vasopressor in isofluraneanesthetized animals.

Mitral valve regurgitation

Induction • Induction can be performed with conservatively dosed propofol or thiopental • Etomidate maintains relatively normal cardiovascular function and is considered a good choice in severe valvular insufficiency

Maintenance with Inhaled Anesthetics • Maintenance with inhaled anesthetics may be a good choice for these patients but a balanced protocol with an opioid or benzodiazepine constant rate infusion (CRI) may be necessary to minimize their dose, and inotropic and arrhythmogenic side effects.

Anaesthetizing Patients with Cardiomyopathy • Dilated cardiomyopathy (DCM) therapy is aimed at improving myocardial contraction and decreasing both preload and afterload. Using pimobendan, a positive inotrope and an arteriolar dilator, is the current standard. • It should not be discontinued as it may attenuate the myocardial depression caused by anesthetics.

• A benzodiazepine-opioid combination is a good choice for sedation of pets withDCM. • Of the opioids, pethidine should be avoided as it is a strong negative inotrope. • Acepromazine may add sedation when necessary and decreases afterload by arteriolar dilation, but at high doses may also cause excessive and prolonged hypotension.

Cardiomyopathy

• Alpha-2-agonists are contraindicated in patients with DCM due to bradycardia, conduction disturbances, myocardial depression, and arrhythmogenicity. • Propofol and thiopental, despite having a short duration of action, may depress myocardial contraction dramatically.

• Ketamine as a positive inotrope and etomidate as a minor cardiovascular depressant are a reasonable combination for induction in DCM patients. • The main disadvantage of ketamine is potential excitation, increasing oxygen demand, which, especially in the already compromised myocardium, potentially triggers myocardial ischemia with lifethreatening ventricular arrhythmia.

• Adequate sedation, therefore, is essential. • Inhaled maintenance anesthetics cause a dose-dependent depression of myocardial contraction and should be used judiciously. • To avoid high concentrations a balanced protocol is advised, for example with a CRI of low-dose ketamine, a benzodiazepine, and an opiate.

Anaesthesia of Patients with Hypertrophic Cardiomyopathy (HCM) • As in other cardiomyopathies, a decreasing ventricular compliance gradually builds high diastolic pressures even with low filling volumes, leading to elevation of left atrial and pulmonary venous pressures that may trigger pulmonary edema.

• This risk is especially important in HCM cats with a documented gallop. When accompanied by a dynamic left ventricular outflow tract obstruction (HOCM), the risk may be exacerbated by positive inotropes, excessive arteriolar dilation, hypovolemia (e.g.,following overzealous diuretic therapy), or excessive tachycardia.

• An opioid-benzodiazepine combination (e.g., butorphanol and midazolam, or morphine and midazolam, according to the amount of analgesia necessary) offers a good choice for premedication. • Acepromazine offers good tranquilization but also causes vasodilation which may overly decrease preload. • Therefore, if ACP is being used, doses should be low (e.g., 0.02 mg/kg or less).

• Alpha 2 agonists initially cause vasoconstriction and bradycardia and may therefore be beneficial. • Ketamine should not be used in patients with HCM as it increases heart rate, cardiac oxygen consumption, and possibly arrhythmogenicity.

• Animals with HCM should receive only judicious fluid supplementation at a rate only enough to maintain adequate filling pressures, but overload should be avoided; monitoring CVP can help fine-tune intravenous fluid administration rate and duration.

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