Lecture 17 – Pharmacology of the CVS Flashcards
What is Angina Pectoris? Where does it originate from? 3
• Chest pain
• Angina pain originates from heart muscle and is caused by the lactic acid produced during anaerobic respiration.
• Irritated/stimulated myocardial pain receptors which message via cardiac nerves and upper posterior nerve roots to the brain.
originates from cardiac point
symptoms of angina pectoris 5
Feeling of cramping and severe constriction in the chest.
• Referred pain jaw, shoulders, nerve and arms.
• May be associated with shortness of breath, sweating, nausea and increased heart rate.
• Strangulation in the chest.
• Originates from the cardiac point.
Treatment Aims 3
Treatment Aims:
• To enhance quality of life through reduction of symptoms.
• To improve prognosis and prevent complications such MI and premature death.
• Well tolerated and cause minimal side effects.
• Successful treatment improves prognosis and prevent complications such MI and premature death.
3 types of classification 3
• Typical angina
o Substernal chest discomfort of characteristic quality and duration.
o Provoked by exertion or emotional stress.
o Relieved by rest and/or nitrates within minutes.
o This is the older definition - duration/provoked by exercise and relieved. If there is chest, but without the symptoms, it can be classified as non-anginal.
• Atypical angina
o Presentation of two of the above characteristics.
• Non-anginal
o Presentation of only one or none of the chest pain characteristics.
• The different types of angina have different treatments.
Pathophysiology
• Pathophysiology is in between aetiology (the cause) and symptoms and provides the rational for pharmacological treatment and other approaches to management.
Angina Pectoris: Stable angina - Classic (8)
- Predictable
- Short Duration 2-5 mins
- Radiation to left arm, neck, jaw or
- Precipitated by Exertion /increase in cardiac O2 demand
- Not life-threatening
- Relived by rest or taking medications
- Most common form.
- It occurs when the heart is working harder than usual.
Angina Pectoris: Stable angina - Classic - Pathophysiology
Narrowed CA lumen Restricted BF to area of myocardium, O2 received is insufficient when the heart has to work harder anaerobic respiration pain.
Angina Pectoris: Unstable angina (8)
- Unpredictable
- Pain symptoms more severe, can persist and lasts longer
- Happens at rest with little exertion
- May not have a trigger
- Not usually relieved by rest and medications
- Serious, regarded as emergency, patients are advised to go to hospital
- Potentially dangerous needs treating quickly.
- The discomfort is more severe than with stable angina and last for longer. It starts to happen when resting.
Angina Pectoris: Unstable angina - Pathophysiology
- Clot occludes artery (plaque rupture) critical reducation to BF so oxygen supply is iadequate even at rest transient (lasts for a short time).
- Unstable angina is transient formation and dissolution of a blood clot (thrombosis) within a coronary artery.
- Endothelium is unable to produce nitric oxide and prostacyclin that inhibit platelet aggregation and clot formation.
- If the clot completely occludes the coronary artery for a sufficient period of time, the myocardium supplied by the vessel may become infarcted (acute myocardial infarction) and become irreversibly damaged.
Angina Pectoris: Prinzmetal Angina (9)
- Usually occurs while resting and during the night or early morning hours.
- Episodes tend to last around 5 to 15 mins (longer in some cases)
- Rare (1 in 100 Angina cases)
- Younger patients present with this kind of angina
- Attacks are usually severe described as very painful
- Pain may spread from the chest to the head, shoulder, or arm
- Associated symptoms heart burn, nausea, sweating, dizziness and palpitation migraines and Raynaud’s phenomenon.
- Usually due to a spasm in the coronary arteries and tend to come in cycles.
- Can be relieved by taking medication.
Angina Pectoris: Prinzmetal Angina - Pathophysiology 2
- Coronary artery vasospasm (can be caused by drugs like cocaine) Critical reduction in BF so that O2 supply is inadequate (can occur at rest).
- Causes include enhanced sympathetic activity (e.g. during emotional stress), especially when coupled with a dysfunctional coronary vascular endothelium (i.e. reduced endothelial production of the vasodilators nitric oxide and prostacyclin) can precipitate vasospastic angina.
Types of angina pectoris – summary 3
Stable angina – Fixed stenosis = IN O2 requirement = DEMAND ISCHAEMIA = Angina.
Unstable – Thrombus/blockage
Printzmetal Angina – Vasospasm
Both 2 and 3 have DE coronary BF = SUPPLY ISCHAEMIA = Angina.
Angina - define
An imbalance between demand and supply of oxygen to the heart.
Precipitating factors 3
IN S activity
IN HR, Less diastolic time so less CA perfusion (occurs in systole).
IN Contractility
Exercise, emotion, stress (greater O2 demand)
IN VC
Angina treatment strategy (3 = 1,5,5) on FC
FC
