Coronary heart disease Flashcards
When does CHD occur?
CHD occurs when the blood flow to the heart muscle is impeded by one of the following:
- atheroma
- thrombosis
- spasm of the coronary arteries
The main clinical manifestations of CHD
Angina and myocardial infarction
Define Angina pectoris
Medical term referring to chest pain caused by reduced blood flow to the heart muscle.
The ischaemia caused by the lack of blood flow and oxygen to the cardiac tissue results in this chest pain or ‘anginal’ pain.
Angina can broadly be divided in to two categories:
- Stable or chronic stable angina, and
- Unstable angina (which comes under the umbrella term ‘Acute Coronary Syndromes’)
Pathophysiology of angina
Angina occurs where there is myocardial ischaemia without any corresponding tissue necrosis.
Myocardial ischaemia occurs when the supply of oxygen to the heart cannot meet the demands of the heart muscle (or myocardium).
Under normal conditions, arterial oxygen saturation and myocardial oxygen demand are relatively constant and myocardial oxygen supply is in balance.
However, myocardial oxygen supply can be reduced if coronary blood flow is reduced, for example when the cross section of a coronary artery or the tone of a coronary artery is reduced. Atherosclerotic plaques can affect both of these.
Narrowed coronary arteries can upset the balance between arterial oxygen saturation and myocardial oxygen demand.
Management of stable angina
Stable angina is a chronic condition which has a lower incidence of acute coronary events, such as heart attack, and mortality. Management is aimed at the following:
The aims of the management of stable angina are to:
Preventing or limiting the symptoms b y reducing the number, severity and severity of the angina attacks.
Reducing the long term morbidity of the condition. This includes reducing the risk of progression of atherosclerosis.
Reducing the risk of mortality. This includes protecting against events such as unstable angina, myocardial infarction, cardiogenic shock and sudden death (NICE CG126).
Management options of stable angina will include:
- Lifestyle advice
- Drug therapy
- Revascularisation procedures
Lifestyle advice
Discussion should be undertaken with the patient regarding their needs in relation to activities, physical activity and exercise, diet and smoking cessation. Discussion should also involve the impact of stress, anxiety and depression which may have an effect on their angina.
Smoking cessation
Smoking still remains one of the most significant causes of preventable disease and early death in the UK. Giving up smoking is therefore one of the most important lifestyle changes a patient can undertake to prevent or limit heart disease and to improve their overall health. Pharmacists have a significant public health role to play in assisting patients to give up smoking.
Both non-pharmacological and pharmacological treatments are available. First-line pharmacological treatment available is nicotine replacement therapy (NRT) of which several formulations exist e.g. transdermal patches, chewing gum, inhalators, lozenges. Choice of treatment will depend on patient preference, previous treatments tried and success rate/s. Other interventions include the use of drugs such as bupropion and varenicline. E-cigarettes are another increasingly popular option to aid smoking cessation although they are not currently classed as licensed medicines.
Drug therapy
The initial drug therapy for the management of stable angina includes offering the patient one or two anti-anginal drugs as needed for regular treatment.
The patient should also be offered drug therapy for secondary prevention of cardiovascular disease.
A short acting nitrate is offered to prevent and treat angina episodes or attacks.
A suggested mnemonic for remembering key factors fundamental to management of angina is the ABCDE approach:
A Aspirin and anti-anginal drugs B Blood pressure lowering therapy C Cholesterol and smoking cessation D Diet and diabetes control E Education and exercise
Anti-anginal drug therapy is aimed at the following:
A reduction of cardiac afterload thereby decreasing oxygen demand on the heart
A reduction of blood pressure and heart rate, thereby decreasing oxygen demand on the heart
Dilation of coronary arteries, reducing preload thereby decreasing oxygen demand on the heart
A reduction in angina pain. [ The pain experienced by the patient increases sympathetic drive leading to an increase in blood pressure and heart rate. This increases the oxygen demand on the heart]
Percutaneous coronary intervention (also known as PCI)
This procedure was formerly known as ‘coronary angiography with stenting’. It involves inserting a catheter via the groin or arm and threading it through the blood vessels and into the coronary artery or arteries which have narrowing. A contrast dye is used to enhance visibility of the arteries and the catheter on the imaging screen which the surgeon then uses as a guide for the procedure. When the catheter tip is in place a balloon tip which is covered with a stent is inflated. This compresses the arterial plaque and expands the stent to widen the artery. Once the stent is in place and the plaque compressed the balloon tip is deflated and withdrawn. The purpose of the procedure is to open up the narrowed artery, restore blood flow and improve symptoms of chest pain and breathlessness.
Coronary artery bypass grafting (CABG)
This is a surgical procedure in which a healthy artery is taken from another part of the body, usually chest, leg or arm, and is attached above and below the narrowed part of the diseased coronary artery. One or more grafts may be needed depending on how many diseased arteries there are and the severity. It is a significant procedure lasting several hours and requires the patient to remain in hospital for several days afterwards. patients usually experience significant improvement in their chest pain symptoms and breathlessness however lifestyle improvements should still be the mainstay of recovery and future health.
Acute coronary syndromes - definition and classification
Acute coronary syndromes, also known as ACS, occur when the blood supply to the myocardium suddenly becomes blocked. ACS tend to have a high associated morbidity and mortality. The spectrum of acute coronary syndromes has a common causality, namely, a sudden reduction in blood flow to part of the heart muscle (or myocardium).
ACS is an umbrella term and includes the following:
- Unstable angina
- Non-ST elevation myocardial infarction (known as an NSTEMI)
- ST elevation myocardial infarction (known as a STEMI)
The term ‘ST’ refers to
The term ‘ST’ refers to the ST segment in the section of an ECG trace. It is a key marker in the determination that myocardial ischaemia / infarction has taken place. Click on the link below for an explanation of the ST segment.
Acute Coronary Syndromes - pathophysiology
Myocardial necrosis (cardiac cell death), which occurs during a STEMI or an NSTEMI results in the release of intracellular proteins. For diagnostic purposes the troponins (I and T) are used as a marker of cardiac cell death. In a STEMI a large part of the myocardium is affected possibly involving the full thickness of the ventricular wall. The tissue necrosis is often a result of prolonged myocardial ischaemia. NICE states that nearly half of salvageable myocardium is lost within an hour of occlusion of the coronary artery and two thirds lost within 3 hours.
In an NSTEMI there is often incomplete or temporary occlusion of the coronary blood vessel/s and so the degree of ischaemia and myocardial necrosis may be less. It is usually limited to cardiac tissue surrounding the smaller distal blood vessels.
In unstable angina the coronary obstruction is limited in its extent and time of exposure. This is still enough to cause ischaemia and the symptoms thereof but there is usually no detectable myocardial necrosis present.
Unlike stable angina, the symptoms of unstable angina can come on very suddenly, become more frequent, prolonged and severe, and/or may occur at rest.
Risk factors for ACS include
Non modifiable
- Increasing age
- Male gender
- Family history
- Ethnicity
Modifiable
- Smoking / tobacco use
- Diet
- High cholesterol
- Low daily consumption of fruit and vegetables - Hypertension
- Physical inactivity
- Obesity
- Stress
- Alcohol intake
ACS has a common set of clinical symptoms, not all of which are present in each affected patient. These include:
- Crushing pain which originates at chest, radiates to neck, jaw and/or left arm
- Nausea and vomiting
- Sweating
- Shortness of breath
Management of ACS
Before any diagnosis can be made prompt stabilisation and management of the symptoms are needed.
In nearly 25% of acute myocardial infarction cases death will occur before reaching hospital however this can be preveneteed by rapid access to a defribillator (BMJ, 2015). If medical help does arrive in time, typically the following drugs are used to stabilise the patient:
♥ Morphine or diamorphine intravenously. To treat the pain and also relax the patient.
♥ Anti-emetic e.g. prochlorperazine. To prevent nausea and vomiting which may also be caused by the opioid drug.
♥ Oxygen (only if oxygen saturation levels in the blood are below 94% as per NICE guidance).
♥ Sublingual glyceryl trinitrite (GTN). Used as a vasodilator to decrease heart rate, decrease stress and oxygen demand on the myocardium.
♥ Aspirin 300 mg chewable tablet. Prevents further platelet aggregation and extension of the existing thrombus.
Diagnostics should include:
- Resting 12 lead ECG, a first priority
- Physical examination including pulse, blood pressure and signs of complications e.g. pulmonary oedema.
- Detailed clinical history including cardiovascular history and previous treatments
- Pain characteristics and onset
- Determination of cardiovascular risk factors
