Cardiology is one of the most commonly tested subjects in undergraduate medicine.
Cardiology is one of the most tested specialties in undergraduate examinations. This is because cardiac diseases are common and seen all the time in clinical practice.
There are many different conditions that affect the heart. Some of these are common whereas others are rare.
Conditions that are common are more likely to be tested and the depth of knowledge required will be higher. Therefore, you should put your time into learning these common diseases well. Here are five really common conditions that are vital to know in depth:
In these notes, we cover the pertinent information required to help you understand each disease process. For more detailed information, check out our Cardiology section.
We can approach learning cardiology by dividing diseases into their site of pathology.
Dividing and categorising diseases is useful to be able to conceptualise what you need to learn within the specialty. You can use this as a type of mental checklist to ensure you have covered the major diseases in each category when studying or revising for exams.
Cardiac diseases can be divided based on their site of pathology:
The pericardium is a double-walled sac that contains the heart and roots of the great vessels.
The pericardium is composed of a tough, outer fibrous layer and an inner, serous layer. The combined thickness of these layers is 1-2mm. The fibrous pericardium is a tough sac, which completely surrounds the heart but remains unattached.
The serous pericardium is composed of two membranes that line the heart. These are the parietal and visceral pericardium. Between these two membranes is a small volume of fluid.
The pericardium has three main physiological functions:
Pericardial diseases may be isolated or form part of a systemic disease process such as a connective tissue disease (e.g. systemic lupus erythematosus). The two main pericardial disease processes are pericarditis and effusions.
In pericarditis, there is infiltration of the pericardium with immune cells. This may be due to direct invasion of microorganisms or due to deposition of immune proteins and cells as part of a systemic inflammatory response. If the inflammation is chronic it can lead to scarring and loss of the normal pericardial elasticity. This can impede normal cardiac filling leading to raised pressures and features of heart failure with fluid overload, fatigue and shortness of breath. This chronic process is known as constrictive pericarditis.
Practically any condition that affects the pericardium can lead to an effusion. Effusions may be a manifestation of pericarditis or they may occur in isolation. Effusions are often asymptomatic, but if they become very large or develop acutely they can have haemodynamic effects on the heart because they increase pericardial pressure leading to compression of the heart's chambers.
Acute pericarditis is the most common pericardial disease.
Acute pericarditis is the most common pericardial disease. It is estimated to be present in 1% of adults who present with ST-elevation changes on an ECG to accident & emergency.
In developed countries, acute pericarditis is most commonly secondary to a viral aetiology (e.g. influenza, echovirus, adenoviruses, enterovirus).
A wide range of other conditions can cause pericarditis:
The cardinal feature of acute pericarditis is chest pain. Chest pain is typically described as sharp, pleuritic (worse on inspiration) and better on leaning forward and sitting up. Other features can include:
A formal diagnosis of acute pericarditis is based on finding two of the following four features:
Patients with suspected acute pericarditis require formal assessment, blood tests (e.g. troponin, full blood count, U&E, CRP), ECG, chest x-ray and echocardiogram. It is important to exclude other causes of chest pain as part of the work-up.
The characteristic ECG findings are widespread saddle-shaped ST elevation with PR depression.
The mainstay of treatment for acute pericarditis is the use of NSAIDs, aspirin or colchicine. These drugs are used to reduce inflammation. Specific causes of acute pericarditis should be treated appropriately.
For more information see our notes on Acute pericarditis.
Chronic pericarditis refers to long-standing inflammation (>3 months) of the pericardium that usually follows an acute episode.
Chronic pericarditis refers to pericardial inflammation that has lasted > 3 months. Incessant pericarditis is essentially the middle ground between acute and chronic. It refers to an episode of acute pericarditis lasting > 4-6 weeks but < 3 months.
Chronic inflammation can occur after virtually any pericardial disease process. However, it rarely occurs after an episode of acute idiopathic pericarditis (1%) and is more likely in patients with an aetiology consistent with bacterial or TB.
The main clinical consequence of chronic inflammation of the pericardium is development of constrictive pericarditis. This causes scarring and loss of the normal fibroelastic pericardial tissue that impedes normal cardiac filling and causes features of right heart failure (raised JVP, peripheral oedema, exercise intolerance).
The development of constrictive pericarditis can be categorised into three clinical phenotypes:
These phenotypes represent a spectrum of pericardial disease following an acute episode:
Patients characteristically present with features of right heart failure.
The diagnosis of chronic constrictive pericarditis is made through imaging of the heart using an echocardiogram, CT or cardiac MRI. This shows impaired filling of the heart chambers during diastole and there may be features of chronicity including calcification.
The treatment of chronic pericarditis is specialist and depends on the extent of fibrosis and phenotype of constrictive pericarditis. Pericardiectomy is generally considered for patients with chronic constrictive pericarditis and severe symptoms of heart failure. This involves surgically removing the pericardial sac.
A pericardial effusion essentially refers to excess fluid (or other substances) within the pericardial space.
The normal pericardial sac contains 20-50 mL of pericardial fluid. This acts to prevent friction between the pericardial layers. If excess fluid (or other substances such as blood or exudate) occur within the pericardial space then an effusion develops.
Pericardial effusions can be classified by four major factors:
Excess fluid may accumulate in the pericardial sac due to three major mechanisms:
Pericardial effusions may be asymptomatic. Symptoms often depend on the speed of development. Fluid that accumulates quickly can lead to haemodynamic compromise and shock. Fluid that accumulates slowly may cause symptoms over weeks or months.
Typical features include:
Classic features can develop due to compression of surrounding structures:
A pericardial effusion is confirmed on imaging with echocardiography that is also able to assess the degree of haemodynamic compromise on ventricular filling.
Small, asymptomatic effusions may be monitored with serial imaging (e.g. echocardiogram). Large or symptomatic effusions may require drainage with pericardiocentesis.
An effusion can lead to increased pericardial pressure that compresses all chambers of the heart. If accumulation occurs acutely, it can lead to the rapid development of haemodynamic compromise (i.e. hypotension) due to inadequate filling even with small amounts of fluid. This presentation with shock is known as cardiac tamponade.
Cardiac tamponade may present clinically with ‘Beck’s triad’ that is a combination of hypotension, venous distension (i.e. raised JVP), and muffled heart sounds. Cardiac tamponade is diagnosed through echocardiography and without urgent needle pericardiocentesis it can lead to cardiac arrest.
For more information see our notes on Cardiac tamponade.
Vascular disease refers to damage to blood vessels.
Vascular diseases essentially refer to damage of blood vessels that may be venous or arterial.
Vascular disease, especially arterial disease, can be categorised according to the site of pathology:
The term peripheral arterial diseases (PAD) encompasses all arterial diseases other than disease of the coronary arteries, aorta and intracranial vessels. This should not be confused with the term peripheral artery disease that is often used to refer to vascular disease affecting the arteries of the lower limbs.
Depending on the site of the disease, different specialties are involved in patient management.
Coronary artery disease refers to the development of atherosclerotic plaques within the coronary vessels.
Coronary artery disease (CAD) is the predominant mechanism of both angina and acute coronary syndrome (discussed below). It occurs due to the formation of atherosclerotic plaques within the coronary vessels.
The development of atherosclerosis is a complex process that involves lipids, macrophages and smooth muscle. Atherosclerosis leads to the formation of an atheroma, which contains a hard plaque on its surface. Plaques may be obstructive or non-obstructive:
These plaques limit blood flow and can lead to ischaemia (i.e. lack of oxygen) of cardiomyocytes. Ischaemia causes the typical central pressing, squeezing, or constricting chest discomfort referred to as angina. This typically occurs on exertion because the oxygen demand of cardiomyocytes increases but cannot be met by increased blood flow due to the narrowed coronary vessels.
The major concern with CAD is the risk of one of these plaques rupturing. Rupture of an atheromatous plaque exposes a collagen-rich cap. Platelets aggregate on this exposed collagen forming a thrombus that may occlude or severely narrow the vessel. Occlusion can lead to a complete absence of oxygen and subsequent death of cardiomyocytes. Cell death secondary to ischaemia is known as infarction. This forms the basis of a heart attack, otherwise known as myocardial infarction (death of cardiac tissue due to lack of oxygen through the coronary vessels).
The identification and treatment or CAD is important in patients with chest pain to prevent a major cardiac event (e.g. myocardial infarction, cardiac arrest, death).
Angina refers to classic cardiac pain that is felt when there is a reduction in blood supply to the heart.
Angina refers to the central pressing, squeezing, or constricting chest discomfort that is experienced when there is a reduction in blood flow through the coronary arteries. There may be typical radiation to the arm, jaw or neck and it is bought on by physical or emotional exertion and relieved by rest. It typically lasts < 10 minutes.
Angina is the main symptom of myocardial ischaemia, which is usually secondary to coronary artery disease (CAD). However, other conditions can cause angina such as coronary spasm, severe ventricular hypertrophy or severe aortic stenosis.
The three classic features of angina include:
Based on these classical features, angina can be differentiated into three types:
Angina is a clinical diagnosis. Patients with suspected angina usually need referral to a ‘Rapid Access Chest Pain Clinic’ where they undergo further testing to determine the likelihood of coronary artery disease and need for intervention
All patients with angina should be offered a short-acting nitrate PRN (e.g. sublingual GTN) to relieve episodes of angina. Nitrates cause smooth muscle dilatation and help to increase coronary blood flow. Other interventions can include:
For more information see our notes on Angina.
ACS is an umbrella term for three conditions according to clinical features, ECG findings and cardiac enzymes.
ACS is a medical emergency requiring urgent admission. It is classified into three types:
A myocardial infarction (MI), which is more colloquially known as a 'heart attack', refers to the death of cardiac tissue (i.e. myocardial necrosis). MI is defined as 'evidence of myocardial necrosis in a clinical setting consistent with acute myocardial ischaemia’.
ACS is most commonly due to rupture of an atheromatous plaque leading to complete or partial obstruction of a coronary vessel. This type is often referred to as a type 1 myocardial infarction (i.e. plaque rupture).
Other causes include conditions that lead to obstruction of the coronary vessels (e.g. dissection, vasospasm) or those that cause an oxygen supply/demand mismatch for long enough that myocardial necrosis occurs (e.g. anaemia, sepsis, valvular disease). When there is damage secondary to an oxygen supply/demand mismatch it is known as a type 2 myocardial infarction.
The hallmark feature of ACS is central, crushing chest pain that may radiate to the arm or jaw and is associated with sympathetic symptoms (e.g. sweating, palpitations, nausea & vomiting). Patients may present in cardiac arrest or develop life-threatening arrhythmias with possible syncope (transient loss of consciousness).
The diagnosis of ACS is based on characteristic changes on an electrocardiogram (ECG) and cardiac enzymes. ECG changes reflect alteration in electrical activity in the ischaemic/necrotic segment and cardiac enzymes (e.g. troponin) are released when there is death of cardiac tissue.
The three key parts of the work-up for a patient presenting with suspected ACS include:
The changes observed on an ECG and the rise in troponin can be used to differentiate the three causes of ACS:
The management of ACS is complex and depends on the subtype. Here, we briefly summarise the management.
The management of patients with STEMI can be remembered using the mnemonic 'TAAP':
Emergency coronary angiography +/- primary percutaneous coronary intervention (PCI) should be offered within 120 minutes of a diagnosis of STEMI if patients present within 12 hours of chest pain.
The management of patients with NSTEMI or UA can be remembered using the mnemonic 'BATMAN':
Myocardial infarction is associated with many serious complications including death. These can be remembered with the mnemonic 'DREAD':
For more information see our notes on Acute coronary syndrome.
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