Patho & Pharmo 2 Cardiac Ishemia Wk 2

In adequate blood supply to tissues

Coronary Artery Disease

Coronary heart Disease - is normally responsible for heart failure, Angina or myocardial infarction.

Tissue is dying off

Hypoxia pain in the myocardial muscle, causing Angina. The O2 deficit if <20 mins ischemic episode if >20 mins myocardial infarction.

• Myocardial ischemia due to inadequate oxygen supply for supply the metabolic demands of the heart.
• Build up of latic acid (anaerobic respiration) & waste in the cells.
• Makes the cells swell resulting in Angina pain

Angina Pectoris

• Stable angina - a small AS plaque has formed but Ischemic pain would only occur if heart is excerted ie running for a bus.
• Unstable angina - once a thrombus has formed a MI is likely Antithrombus medication will be needed and soon.

It is a vasodilator and operates on the veins. Beware that it will reduce the load going back to the heart so may cause Orthostatic Hypotension.

Unstable Angina

Silent Angina

• 1st Episode - Assume MI = Hospital: Antithrombolytic therapy increases the chances of MI if applied quickly.
• Previously diagnosed - rest - cease activity, take medication, monitor vital signs and pain resolution.

• Thrombus formation in the coronary arteries
• Embolisation of a coronary thrombus
• Severe vaso-spasm

STEMI is when there is a transmural infartion of the myocardium - which just means that the entire thickness of the myocardium has undergone necrosis - resulting in ST elevation. Usually due to a complete block of a coronary artery (occlusive thrombus). This requires the use of thrombolytics like Streptokinase to lyse the thrombus. Evidence has proven that it is very effective but risky.

UA or NSTEMI is when there is a partial dynamic block to coronary arteries (non-occlusive thrombus). There will be no ST elevation or Q waves on ECG, as transmural infarction is not seen. The main difference between NSTEMI and unstable angina is that in NSTEMI the severity of ischemia is sufficient to cause cardiac enzyme elevation.

Restoring the balance between myocardial oxygen supply and demand.

• Peripheral vasodilators - Both arterial and venous vasculture reducing the workload of the heart
• Selective Coronary vasodilators - A prophylactic agent
• Beta adrenergic antagonists - B1 blockers reduce HR and force of contraction
• Calcium Channel blockers - This will reduce the contractiability of the heart muscles.
• Combined A & B antagonists - Reduces heart workload and indirectly by peripheral vasodilation as a result of A receptor blockade.
• Potassium channel openers - Opening potassium channels in the muscle membrane blocking calcium therefore inhibiting muscle contraction producing arterial vasodilation.

• Glyceryl Trinitrate
• Isosorbide Dinitrate
• Isosorbide Moninitrate
• These are all organic nitrates, the nitrates are NO (Nitric Oxide) donors which at a intracellular level alters availibilty of Calium ions. Hindering the activity of contractile protein.

• Excessive vasodilation
• Reflex tachycardia - Because this tachycardia occurs reflexly in response a hemodynamic situation
• Facial Flushing
• Syncope - Loss of consciousness (Fainting)
• Migraine like headache - Due to cerebal vasodilation

Dipyridamole - Inhibits phosphodiesterase elvating cAMP which is a selective vasodilator promoting BF and O2 delivery to the myocardium.

• Bradycardia
• Dizziness
• GI distress
• Atrioventricular block