Cardiovascular E-book Flashcards
The main clinical manifestations of CHD
Angina and myocardial infarction.
Angina can be divided broadly in to two categories:
stable or chronic stable angina, and
unstable angina (which comes under the umbrella term ‘Acute Coronary Syndromes’)
Pathophysiology
Angina
- Angina occurs when 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.
The classic symptoms of stable angina include
The classic symptoms of stable angina include retrosternal heaviness or pain. The pain may radiate to the jaw, neck, shoulders, central abdomen or the arms (usually the left arm).
Some patients may experience atypical features such as gastrointestinal discomfort or indigestion, breathlessness or nausea (NICE CG 126). Symptoms are usually brought on by exertion or emotional stress and are relieved by rest.
The symptoms are relieved, typically after several minutes, following rest. Relief may be much quicker with the use of sublingual glyceryl trinitrate (GTN). Most patients will suffer an average of two attacks per week and will start to avoid the activities that bring on their
symptoms.
chest pain is classified by one or more of the following:
- The pain is described as a constricting discomfort in the front of the chest, or in the neck, shoulders, the jaw, or the arms.
- The pain is precipitated by physical exertion.
- The pain is relieved by rest or by the use of sublingual GTN within about five minutes.
- Typical angina = all three features present
- Atypical angina = two features present
- Non-anginal pain = one feature or no features present
The severity of angina is graded using a system
I Ordinary physical activity does not cause angina; symptoms with strenuous, rapid or prolonged exertion only.
II Slight limitation of ordinary activity; angina during activities such as walking or climbing stairs rapidly or walking uphill; symptoms may also be experienced during cold weather, when under emotional stress or during the first few hours after awakening only, or after meals.
III Marked limitation of ordinary physical activity; angina when walking one or two blocks on a flat surface, or one flight of stairs at a normal pace under normal conditions.
IV Inability to carry out any physical activity without discomfort, or angina at rest.
Risk factors which increase the likelihood of developing angina include:
Hypertension Diabetes Family history of CHD Hyperlipidaemia Chronic kidney disease Smoking
Management of stable angina
o Preventing or limiting the symptoms by reducing the number and the severity of angina attacks
o Reducing the long term morbidity of the condition. This includes reducing the risk of progression of atherosclerosis.
o Reducing the risk of mortality. This includes protecting against events such as unstable angina, myocardial infarction, cardiogenic shock and sudden death.
Management options will include:
Lifestyle advice
Drug therapy
Revascularisation procedures
Drug therapy (ABCDE)
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 mnemonic for remembering key factors fundamental to the management of angina is the ABCDE approach as follows:
A Aspirin and antiplatelets B Blood pressure lowering therapy C Cholesterol and smoking cessation D Diet and diabetes control E Exercise and education
Antianginal 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 the coronary arteries, reducing preload thereby decreasing oxygen demand on the heart
A reduction in anginal 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 (PCI)
This procedure was formerly known as ‘coronary angiography with stenting’. It involves inserting a catheter via the groin or arm and threading it up through the blood vessels and into the coronary artery or arteries which have narrowing. A contrast dye is used to enhance the 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 plaque and expands the stent to widen the artery. Once the stent is in place and the plaque is 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 a mainstay of recovery and future health.
Acute coronary syndromes (ACS) - Definition
Acute coronary syndromes, also known as ACS, occur when the blood supply to the myocardium becomes suddenly 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 ST segment in the section of the ECG trace. It is a key marker in the determination of whether myocardial ischaemia or infarction has taken place.
Pathophysiology ACS
Myocardial necrosis, 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 (necrosis). 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 coronary blood vessels and so the degree of ischaemia and myocardial necrosis may be less. It is usually limited to cardiac tissue surrounding smaller distal blood vessels.
The symptoms of acute myocardial infarction (STEMI) generally occur very suddenly and are very severe. The symptoms of an NSTEMI tend to develop over a period of 24-72 hours.
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
Non-modifiable Increasing age Male gender Family history Ethnicity
Modifiable Smoking / tobacco use Diet o High cholesterol o Low daily consumption of fruit and vegetables Hypertension Physical inactivity Obesity Stress Alcohol intake
- Risk factors are classified as either modifiable (e.g. blood pressure control and exercise) or non-modifiable (e.g. age)
Symptoms
ACS
ACS has a common set of clinical symptoms, not all of which are present in each affected patient. These include:
Crushing pain which originates in the chest and radiates to the neck, jaw and/or left arm
Nausea and vomiting
Sweating
Shortness of breath
Management of ACS
Morphine or diamorphine intravenously. To treat the pain and also relax the patient.
Anti-emetic e.g. intravenous prochlorperazine. To prevent nausea and vomiting which may also be caused by the opioid drug.
Oxygen (only if oxygen saturation levels are below 94% as per NICE guidance)
Sublingual glyceryl trinitrate (GTN). Used as a vasodilator to decrease heart rate, decrease stress and oxygen demand on the myocardium.
Aspirin 300mg chewable tablet. Prevents further platelet aggregation and extension of the existing thrombus.
Diagnostics ACS
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
Simple algorithm showing diagnosis and treatment pathway for NSTEMI and
STEMI
Confirm diagnosis
(ECG and troponins)
1- Stemi –> Thrombolysis or Primary angioplasty
- NSTEMI –> Risk stratification
Management of a STEMI (ST elevation myocardial infarction)
The aim of treatment in the case of a STEMI is to reperfuse the occluded blood vessel/s supplying the myocardium as soon as possible. This can be done either by thrombolysis or by physical intervention.
The most effective way to reperfuse the heart is through primary angioplasty. This involves inserting a fine wire into the coronary artery which positions a catheter with a balloon tip at the site of the occlusion. The balloon is then inflated to 10-20 times the atmospheric pressure which forces the atheroma back into the blood vessel wall and opens the lumen of the blood vessel. The balloon is surrounded by a wire meshwork known as a stent which
when inflated prevents the collapse of the vessel wall. The process of angioplasty and stent insertion is known as ‘percutaneous coronary intervention’ or PCI.
Thrombolytic (fibrinolytic) agents
There are several thrombolytic agents available for the treatment of a STEMI. These include streptokinase, and the tissue plasminogen activators (tPAs) such as alteplase, reteplase and tenecteplase. Choice of thrombolytic may vary depending on local policy however tPAs are generally preferred to streptokinase.
Further management of ACS
One an episode of ACS has been treated the risk of a second episode occurring should be assessed. This should be undertaken before risk assessment strategies, intervention treatments and rehabilitation begin.
Assessing risk is formally known as ‘risk stratification’. There are several scoring systems available however NICE CG 94 recommends the use of an established scoring system such as the Global Registry of Acute Cardiac Events (GRACE) tool. The GRACE tool predicts the 6 month mortality risk for the patient following their myocardial infarction.
Secondary prevention of myocardial infarction (NSTEMI and STEMI)
A programme of cardiac rehabilitation is offered to patients following an MI in order to help prevent any further MIs occurring in the future. The programme includes health education advice, stress management and an exercise component. Patients are encouraged to attend. Advice on lifestyle modification includes the following: Physical activity Diet Safe alcohol consumption Smoking cessation Weight management
Drug treatment for secondary prevention
All patients who have had an acute myocardial infarction should be offered the following combination of drugs:
ACE inhibitor (or ARB if intolerant of ACE inhibitor)
Dual antiplatelet therapy consisting of aspirin and a second antiplatelet drug
Beta blocker
Statin
ACE inhibitors and beta blockers should titrated carefully to their target doses with close monitoring.
The most common cause of strokes are:
Arterial embolism from another site (e.g. heart, carotid artery)
Arterial thrombus
Haemorrhage (intracranial or subarachnoid)
Less common causes of stroke include:
Venous infarction Fat or air embolisms (e.g. from scuba diving) Multiple sclerosis Carotid or vertebral artery dissection Brain tumours
risk factors for the development of a stroke
Hypertension Smoking / tobacco use Excess alcohol intake Raised lipids Poor diet Physical inactivity Atrial fibrillation Obesity Diabetes Sleep apnoea
Symptoms of a stroke include:
Numbness Weakness or paralysis of the face, arm and leg (usually only one side of the body) Slurring or loss of speech Confusion Blurring of vision Severe headache (uncommon)
NSTEMI (Non-ST elevation myocardial infarction) and unstable angina – management
The initial stabilisation therapy for patients presenting with an NSTEMI or unstable angina is the same as for a STEMI.
Patients who considered to have a high mortality risk should be considered for PCI
Unfractionated heparin or low molecular weight heparin along with antiplatelet therapy is indicated.
As an example of antiplatelet therapy, aspirin and clopidogrel both at 75mg once daily, are given for 12 months. Typically, a loading dose of 300mg of each drug is given on presentation of the condition.
Which treatment cannot be using in NSTEMI or unstable angine
Thrombolysis (using thrombolytics) is never indicated for NSTEMI or unstable angina.
The GRACE tool
The GRACE tool predicts the 6 month mortality risk for the patient following their myocardial infarction.
The risk score obtained from the GRACE ACS risk and mortality indicator tool is based on the following:
Age
Heart rate
Systolic blood pressure
Serum creatinine renal function)
The presence of congestive heart failure
ST segment deviation on the ECG
Cardiac arrest at admission
Abnormal cardiac enzymes (e.g. elevated troponins)
Why are tPA’s generally preferred to streptokinase’s
This is due to streptokinase’s lack of fibrin specificity and its antigenicity. Patients can produce antibodies to streptokinase after a first administration thereby reducing the drug’s potency if it should it ever be administered for a second time.
