Learning & Test Objectives with Description 

The student is examined on cadaveric specimens of the heart in oral format. Each student is required to correctly orientate the heart; they must demonstrate it's correct position in the body, its surfaces and surrounding structures. Following this the examiner presents the student with questions from the following subtopics:

1. Chambers of the heart

The student is asked to identify and describe one of the chambers of the heart.

2. Vessels of the heart

The student answers several questions on the arteries and veins of the heart.

3. Other features of the heart

1.    Topography and projections

2.    Valves and auscultation points

3.    Cardiac skeleton

4.    Cardiac conduction system

5.    Foetal circulation

6.    Pericardium

4. Clinical correlations and curiosities

The examiner may ask questions regarding clinical correlations and curiosities of the heart, the majority of which are listed below.

5. Radiological images

The student may be examined radiological images of the heart.

The test is held by the general rules of oral examination (see Continuous Testing – Organisation).

Clinical correlations

Cardiac tamponade is a pathological disorder in which fluid accumulates in the pericardial cavity causing the heart to be unable to adequately distend during diastole. The pericardial cavity can expand to contain 1000 ml of fluid. If the increase of fluid occurs slowly over a long period time, there may be no clinical manifestations. An acute tamponade is caused by a sudden increase of fluid, by approximately tens of millilitres (max. 200 ml) and is a medical emergency. This may occur due to rupture of free myocardial wall over a post-ischemic scar or as a result of rupture or dissection of the aorta.

Right heart failure results in blood congestion in the systemic circulation and an elevation in central venous pressure. This condition manifests with oedema, which accumulates around the ankles (perimalleolar oedema) due to gravity and elevated jugular venous pressure detected by increased filling of the external jugular veins. Blood also accumulates in the portal circulation, which leads to enlargement of the liver and spleen (hepatosplenomegaly) and an accumulation of fluid in the peritoneal cavity (ascites).

Left-sided heart failure leads to congestion of blood and elevated blood pressure in the pulmonary circulation. This results in lung oedema presenting as dyspnoea that is most prominent when lying down. Dyspnoea is relieved when the patient sits or stands up (orthopnoea).

Atrial fibrillation is a heart rhythm disorder in which the atria contract irregularly, chaotically, and thus ineffectively. This causes a change of blood flow in the atrial auricle from laminar to turbulent with an increased risk of blood clot formation. Blood clots may be released into the systemic circulation and obstruct an arteries supplying the brain and/or other organs (thromboembolism), leading to a complete or partial loss of blood supply (ischaemia).

Mitral regurgitation (insufficiency) leads to the reverse of blood flow from the left ventricle to the left atrium during systole. It is one of the most common acquired valve defects, usually caused by degeneration of the valve. Mitral regurgitation often results in left-sided heart failure.

Aortic valve stenosis is a narrowing of the orifice of the aortic valve, usually caused by degenerative calcification (a process similar to atherosclerosis), thus presenting most frequently in older age. It is a common acquired valve defects.

A heart block is a block in the conducting system of the heart, which prevents the propagation of action potentials through certain parts of the heart. Heart blocks are differentiated by their ECG profiles and clinical manifestations.

Ischemic heart disease is the result of coronary artery disease on the heart. Coronary artery disease results from atherosclerosis obstructing the lumen of the coronary arteries. The extent of the obstruction leads to variable range of clinical entities: stable angina, unstable angina, myocardial infarction, sudden cardiac death and heart failure.

Angina pectoris is a form of ischaemic heart disease that classically presents with chest pain or discomfort.

Myocardial infarction is caused by an obstruction of blood flow in the coronary artery (usually by a thrombus) leading to ischemia and necrosis of the given segment of myocardium. Acute chest pain is the typical presenting symptom. However, it may be absent in some cases. 

In myocardial infarction, pain radiates to the Head's zones of the T1–T4 spinal cord segments (the thoracic wall and the left side of the upper limb, including the little finger).

Transoesophageal echocardiography: as the left atrium lies right in front of the oesophagus, an ECHO probe can be inserted into the oesophagus. This provides better view of the left atrium than a transthoracic probe.


Other curiosities

The thickness of the wall of the right ventricle is 3–4 mm. The left ventricular wall can be up to three times thicker (7–11 mm).

Atrial natriuretic peptide/factor (ANP/ANF) is a hormone created by the cardiomyocytes of the atria of the heart, which function as baroreceptors. They release ANF on increased blood pressure. ANF acts on the kidneys to increase the excretion of sodium in urine. 

Viscerosensory nerve fibres in the heart are found only in the pericardium. They arise as branches of the phrenic nerve.

The blood supply of the pericardium is derived from the pericardiacophrenic artery, which travels in a neurovascular bundle with the phrenic nerve through the mediastinum to the heart.

Frequency of sinoatrial node excitation is 60–80 bpm. The atrioventricular node has a slower autonomic rhythm of 30–40 bpm.

The sinoatrial node is sets the rate and rhythm of heart contraction, and thus is known as the pacemaker of the heart.

The coronary arteries are located subepicardially. They follow a curved course on the surface of the heart in a wave, which allows them to stretch during contractions of the heat


Radiological images

Heart and vessels

Created: 13. 3. 2017 / Modified: / Responsible person: MUDr. Azzat Al-Redouan