**5.1. Pathophysiology**

Tachycardia, arrythmias, and decreases in afterload will exacerbate LVOTO and may cause haemodynamic deterioration. In addition to this, increases in contractility (chronotropy) and decreases in preload will accentuate LVOTO. Therefore, the principle of treatment for hypotension is volume expansion (including increasing preload in the Trendelenburg position) and use of drugs that increase systemic vascular resistance without a positive inotropic or chronotropic response (e.g. phenylephrine and vasopressin). Sympathetic response secondary to patient anxiety, intubation process, and surgical site incision and acute changes in preload, afterload, and contractility secondary to the pharmacological effects of anaesthetic agents, blood loss during surgery, and postoperative pain can precipitate haemodynamic collapse. DC cardioversion may be necessary in case of sudden onset of atrial fibrillation that is

Although both general and neuraxial anaesthesia can be used, it is important to have a clear understanding of the haemodynamic changes associated with each option. Depending on the route of the anaesthetic drugs chosen, close monitoring and titration of the medications affecting heart rate, preload, afterload, contractility of myocardium, and sympathetic activity are important. Neuraxial techniques may also be considered. In general, a slow controlled titration of medication via an epidural is preferred over a single dose spinal anaesthesia with the aim of maintaining preload and afterload and avoiding sympathetic stimulation. Regional anaesthesia can be an invaluable tool to manage postoperative pain and in turn prevent the

In addition to the standard American Society of Anaesthesiologists monitoring requirements, an intra-arterial catheter and/or non-invasive pulse plethysmographic variability (PPV) index monitor and central venous pressure (CVP) monitoring may be considered. The overall haemodynamic goals include maintaining the mean arterial blood pressure at >65–70 mm Hg to maintain coronary perfusion pressure to the subendocardium in the hypertrophied heart. The most useful monitoring tool for patients undergoing high-risk surgery is TEE. TEE can determine whether haemodynamic alterations are caused by hypovolemia, increased LVOTO

**Postoperative management:** Patient with HCM should be continuously monitored in the postoperative room. All factors that activate a sympathetic response like pain, hypothermia, shivering, anxiety, hypoxia, and hypercarbia should be immediately addressed. The mainte-

Restrictive cardiomyopathy (RCM) is a disorder of the myocardium that occurs due to increased myocardial stiffness (decreased compliance) that leads to impaired ventricular filling. Size of both ventricle chambers and systolic function usually remains normal or near-normal until later stages of the disease. RCM may arise as a result of either inherited or acquired predispositions and diseases or a combination of the both, and can broadly be classified as infiltrative, non-infiltrative, storage disease, and endomyocardial fibrosis. Restrictive

nance of euvolemia and prompt treatment of hypotension is very important.

haemodynamically unstable.

116 Current Topics in Intensive Care Medicine

activation of sympathetic response in these patients.

or SAM, or LV systolic dysfunction.

**5. Restrictive cardiomyopathy**

RCM is characterised by contracted stiff ventricles with progressive impairment of diastolic filling, leading to the haemodynamic problem of a low preload but high ventricular filling pressure. This pattern of diastolic dysfunction leads to dilation of the atria and elevation of mean atrial pressures, resulting in biventricular "backward heart failure" manifesting itself as pulmonary venous congestion leading to dyspnea as well as systemic venous pressure elevation resulting in peripheral oedema. Systolic function is preserved in most cases. However, in spite of intact systolic function, the restrictive pathology on true ventricular preload limit the stroke volume, resulting in low cardiac output and ultimately hypoperfusion of the tissues.
