High CPK Levels – Causes, Symptoms, Side Effects, Treatment

In acute myocardial infarction, CPK rises by 3-12 hours and return to normal levels by 48-72 hours.

• Acute Myocardial Infarction (heart attack)
• Congestive Cardiac Failure
• Acute Myocarditis (Inflammation and damage of middle layer of cardiac muscles)

ECG along with an assessment of cardiac enzymes is done for each patient presenting with chest pain.

Often shows CPK levels higher than 1000U/L

• Medicines – statins, anti-psychotics, diuretics
• Toxins – snake venom, heavy metals
• Drug abuse
• Crush injury
• Electrical injury
• Heart stroke
• Infections
• Prolonged immobilization
• Lack of blood supply to a particular limb

The medications cause the release of stored calcium within the muscles causing them to contract and generate heat.

• Chest pain described as tightness or squeezing
• Chest pain radiating to the left shoulder, arm, and jaw. Rarely it radiates to the back or abdomen
• Sweating
• Occasionally nausea and vomiting
• Palpitations and loss of consciousness

• Excess fatigue
• Shortness of breath
• Swelling over ankles and feet
• Swelling of abdomen
• Distension of jugular vein – can be seen prominently on the neck

• Chest pain
• Shortness of breath
• Irregular heart rate
• Fever

Complications include cardiac failure, cardiac arrest, the involvement of heart valves and sudden death.

• Muscular pain and tenderness
• Muscular weakness
• Swelling of affected muscle

Complications include low blood pressure and hypovolemic shock, electrolyte disturbances and abnormal heart rate and rhythm and disseminated intravascular coagulation (DIC).

• Progressive muscle wasting
• Inability to stand, walk or maintain posture
• Scoliosis – curvature of the spine
• Muscle spasms
• Limited range of movements
• Respiratory difficulties
• Cardiomyopathy

The intensity of signs and symptoms depend upon the extent of muscular damage.

• Muscular rigidity
• Rapid heart rate
• Rapid breathing or respiratory rate
• High-grade fever

Rhabdomyolysis and metabolic acidosis are common complications.

• Sedentary lifestyle and physical inactivity
• Diabetes mellitus
• High cholesterol levels
• Cigarette smoking
• High blood pressure
• Diet rich in fats

Treatment includes avoidance of causative factors and lifestyle modifications.

• Management of high blood pressure and heart rate
• Anti-coagulant drugs
• Fibrinolysing agents to disintegrate the thrombus (clot)

• Weight loss
• Increase in physical activity
• Curbing smoking and alcohol
• Limited intake of oily food
• Including fresh fruits and vegetables in diet which provide anti-oxidants

Treatment includes:

• Management of blood pressure and heart rate
• Maintaining airway, breathing and circulation
• Implantable cardiac defibrillator may have to  be used in severe cases

• Anti-viral or antibiotics for infections
• Management of abnormal heart rate by anti-arrhythmic drugs
• Diuretics may be used to prevent cardiac failure
• Intravenous immunoglobulins and corticosteroids may have to used
• Implantable cardiac defibrillator may be recommended in severe cases

• Correction of low blood pressure and hypovolemic shock with intravenous saline.
• Enhance urine production in order to prevent myoglobin from depositing into the kidneys.
• Correction of acidosis and electrolyte imbalance
• Hemodialysis or peritoneal dialysis to manage acute kidney failure

• Corticosteroids and creatinine supplements are the only pharmacological therapy available
• Physiotherapy
• Occupational therapy
• Surgical therapy to improve the quality of life of patients.
• A cardiac pacemaker may be required if cardiomyopathy is severe.

• Prophylactic intravenous use of dantrolene
• Discontinuation of triggering medicine
• Supportive therapy including correction of acidosis and hyperthermia