Chest pain caused by build-up of lactic acid caused by ischaemia of the cardiac muscle. Pain may also be referred (jaw, left arm etc). Two types, stable angina and unstable angina.

Pathophysiology:

1. Impaired blood flow to the myocardium

2. Reduced oxygen supply to the myocardium

3. Cellular metabolism changes from aerobic to anaerobic

4. Lactic acid is a bi-product of anaerobic metabolism

5. Lactic acid irritates pain receptors in the myocardium More than 20 minutes of ischaemia causes myocyte necrosis which leads to infarction

Stable angina:

Pain occurring with increased activity and decreasing with rest Unstable angina: more frequent, lasts longer or occurs at rest.

Risk factors: diet, smoking and atherosclerosis

Treatment:

• Short acting nitrates (e.g. nitro-glycerine GTN) are the first-line therapy for the treatment of angina.

• MoA: (relaxation of vascular smooth muscles) converted by mitochondrial aldehyde dehydrogenase to nitric oxide, an active substance which then activates the enzyme guanylate cyclase. The activation of guanylate cyclase is followed by the synthesis of cyclic guanosine 3’, 5’ monophosphate (cGMP), activating a cascade of protein kinase-dependent phosphorylation events in smooth muscles. This process eventually leads to the dephosphorylation of the myosin light chain of smooth muscles, causing relaxation and increase blood flow.

Adverse effects: postural hypotension, throbbing headache, dizziness, nausea Important notes: provided as a short acting sublingual spray (occasionally dissolvable tablets), 400-800mcg per spray, repeated once after 5 minutes if necessary. Headache is a very common adverse effect and indicates it is likely working.

Complications: myocardial infarction and dysthymias.

Nursing care: important to distinguish weather the patient is having a MI or true angina through diagnostic testing (usually ECG). Monitor vital signs frequently especially blood pressure.