**3.4. Prognosis**

Symptomatic patients with DCM who are referred to tertiary medical centres for care have a high 5-year mortality rate (50%). If the cardiomyopathy involves both the right and left ventricles, the prognosis is very poor. Haemodynamic abnormalities that predict a poor prognosis include:


#### **3.5. Anaesthetic management for non-cardiac surgery**

Any major surgeries on these patients can be associated with morbidity and mortality, therefore, requires planning. Optimisation of congestive heart failure (CHF) at least for a week before the planned surgery is advisable. In critically ill or patients undergoing a high-risk procedure or those in which CHF is not appropriately managed, intra-arterial BP line should be inserted preoperatively. Premedication should be tailored according to the patient's requirement and may include short acting anxiolytic and/or sedative. Regional anaesthesia or nerve blocks alone or in combination with general anaesthesia can help us achieve the set goals of anaesthesia with a minimal haemodynamic compromise. However, the ongoing anticoagulation therapy may limit the option of regional anaesthesia. American Society of Regional Anaesthesia (ASRA) guidelines must be strictly followed if the patient is on an anticoagulation therapy.

The goals of anaesthesia are to [4]:

pulmonary capillary wedge pressure, high systemic vascular resistance, and a low cardiac output. Additional laboratory tests carried out may reveal raised brain natriuretic peptide

Management of DCM begins with lifestyle modifications such as adequate rest, weight control, low sodium diet, fluid restriction, stopping alcohol intake and smoking, and less physical

*Medical management*: The patients of DCM are at increased risk of pulmonary and systemic thromboembolisation due to stasis of blood in the dilated hypokinetic cardiac chambers. Anticoagulation therapy with warfarin or dabigatran is often indicated in these patients. The risk of embolisation is the highest in patients with atrial fibrillation, severe left ventricular dysfunction, a previous history of thromboembolism, or echocardiographic evidence of a mural thrombus. Other medications like angiotensin-converting enzyme inhibitors and angiotensin antagonists, diuretics, beta blockers, vasodilators, digoxin, antiarrhythmics, and statins can

Patients with a LVEF <30% and an intraventricular conduction defect with wide QRS complex ≥130 ms may lack synchronised contraction of both ventricles. Resynchronisation of right and left ventricle with biventricular pacing using a cardiac resynchronisation therapy device (CRT-D) can restore synchronous contraction of both ventricles, shorten the QRS interval, decrease left ventricular size and improve systolic function, stroke volume and the overall

Heart transplantation is the definitive treatment and the most common indication for transplantation in patients with DCM for both adults and children. Patients that are likely to benefit highly from a heart transplant include patients who were previously very active, <60 years of age who show intractable symptoms of congestive heart failure despite optimal medical

Symptomatic patients with DCM who are referred to tertiary medical centres for care have a high 5-year mortality rate (50%). If the cardiomyopathy involves both the right and left ventricles, the prognosis is very poor. Haemodynamic abnormalities that predict a poor prog-

levels.

**3.3. Treatment**

110 Current Topics in Intensive Care Medicine

survival rate of patients.

therapy.

**3.4. Prognosis**

nosis include:

• an ejection fraction <25%,

• cardiac index <2.5 L/min/m<sup>2</sup>

• an increased central venous pressure.

• pulmonary hypertension, • systemic hypotension, and

• pulmonary capillary wedge pressure > 20 mm Hg,

,

activity during periods of cardiac decompensation.

be prescribed to keep the condition under control.


These patients can become haemodynamically unstable due to the depressant effect of anaesthetic agents, fluid shifts and ongoing blood loss, which add to the already poor myocardial function due the cardiomyopathy. Propofol, thiopentone and inhalational agents cause vasodilation and myocardial depression. Benzodiazepines like midazolam and nitrous oxide may cause cardiovascular depression. Etomidate, ketamine, and narcotics like opioids are the ones that have minimal adverse haemodynamic response. We need to use a balanced anaesthetic technique. Slow induction should be carried out. Response of induction agents may be delayed due to prolonged circulation time, so slow and titrated doses of anaesthetic agents should be administered. Additional doses may not be required.

Optimal pain management helps to maintain haemodynamic stability. Regional anaesthesia may be a source of excellent postoperative pain relief, reducing the episodes of sympathetically mediated tachycardia, and afterload increases.

*Monitoring*: In addition to basic monitoring, central venous pressure (CVP) monitoring allows us to measure preload and central venous saturation (ScVO<sup>2</sup> ). It provides for an access to administer inotropes and vasoconstrictors if needed. Direct intra-arterial pressure monitoring enables early identification of haemodynamic alterations by beat-to-beat measurement of BP. Pulmonary artery pressure monitoring is useful in patients undergoing high-risk or emergency surgery or those in whom large fluid shifts are anticipated. The role of noninvasive methods to estimate cardiac output as well as estimate global end-diastolic volumes, the extravascular lung water, and other indices if available are invaluable for assessing cardiac function.

Transesophageal echocardiography (TEE) is also helpful as it identifies causes of hypotension, response to fluid therapy or inotrope support, estimates preload, cardiac output, diastolic dysfunction, valve function, and regional wall motion abnormalities.

Myocardial ischaemia is present in patients with HCM, irrespective of the presence or absence of coronary artery disease. Myocardial ischaemia is precipitated by several factors including

Current Perspectives on Cardiomyopathies http://dx.doi.org/10.5772/intechopen.79529 113

• the presence of a metabolic derangement regarding the utilisation of oxygen at the cellular

Supraventricular or ventricular dysrhythmias are relatively common in these patients due to the presence of disorganised cellular architecture, expanded interstitial matrix and myocardial scarring. They are the cause of incidence of sudden arrest in this group of cardiomyopathy.

The clinical presentation of HCM varies widely. These patients can present early in their life with debilitating symptoms or can live for decades asymptomatically while some others die suddenly. The most frequent symptoms include dyspnea, dizziness, exercise intolerance,

Physical examination may be normal at rest but may reveal a double apical impulse, gallop rhythm, a systolic murmur and thrill in the presence of functional LVOTO. It is rare, but some people with hypertrophic cardiomyopathy can suffer sudden cardiac arrest during a vigorous physical workout. The physical activity can trigger dangerous arrhythmias leading to sudden

Electrocardiography (ECG) changes include left atrial (LA) enlargement, pathologic Q waves, high QRS voltage complexes, ST segment depression, and inverted T waves in at least two or

Echocardiography can easily demonstrate the presence of myocardial hypertrophy. Ejection fraction is usually >80%, reflecting the increase in force of contraction of the heart. Echocardiography can also assess the mitral valvular apparatus, the presence of mitral regurgitation, and the

• a mismatch between ventricular mass and coronary artery size,

• increased oxygen consumption due to hypertrophy,

• increased LVEDP compromising coronary perfusion, and

• abnormal coronary arteries,

**4.2. Signs and symptoms**

angina, syncope, and/or sudden death.

• a family history of sudden death;

• unexplained syncope;

more consecutive leads.

The major risk factors for sudden cardiac death are:

• non-sustained ventricular tachycardia (VT)

• extreme hypertrophy of the left ventricular wall (0.30 mm);

level.

death.

• decreased diastolic filling time,
