2. Myocardial blood supply

Arterial supply: the heart is supplied by the right and left coronary arteries; these originate from the ascending aorta (anterior and posterior aortic sinuses, located just above the cusps of the aortic valve)

Right coronary artery: this passes between the pulmonary trunk and the right atrial appendage to descend in the anterior atrioventricular groove. It gives off atrial and ventricular short branches to supply those structures. At the inferior border of the heart, it effectively divides into the marginal branch which travels along the right ventricle towards the apex and the posterior interventricular artery which continues in the groove of the same name to anastomose with the circumflex artery (the corresponding branch of the left coronary artery). This anastomosis is variable

The right ventricle and right atrium, part of the interventricular septum, the sinoatrial node, SAN (in 65%), the bundle of His, the atrioventricular node, AVN (80%) and the conducting system (80%). It also supplies a small diaphragmatic part of the left ventricle.

Left coronary artery: this is larger than the right and, after arising from the posterior aortic sinus, passes between the left atrial appendage and the pulmonary trunk. It divides shortly into the anterior interventricular (also known as the left anterior descending, LAD) artery, which passes down the interventricular groove giving off anterior ventricular branches, and into the circumflex artery. This continues in the atrioventricular groove to anastomose with the inferior interventricular artery.

coronary artery or its branches supply the left ventricle and left atrium, part of the interventricular septum, the SAN (in 35%), the AVN (20%) and the conducting system (20%).

The innermost part of the endocardium receives oxygen directly from the blood within the ventricle.

Venous drainage: as much as a third of cardiac venous blood drains directly into the cardiac chambers via the venae cordis minimae (a network of small veins). The remainder is drained by larger veins which tend to accompany the coronary arteries.
Most of the remaining venous blood drains into the right atrium via the coronary sinus, which is located to the left of the opening of the inferior vena cava, and which lies in the posterior atrioventricular groove. Great - lad middle inferior groove and small cardiac vein marginal RCA

250 ml min @ rest X5 during excericse Flow - driving pressure In the presence of a fixed coronary stenosis, this pressure gradient is crucial. In the absence of a stenotic lesion, the main variable that determines flow is the calibre of the blood vessels. Vasodilatation occurs mainly in response to the presence of local metabolites such as hydrogen ions, adenosine potassium, phosphate, carbon dioxide and prostaglandins. Autonomic control of vascular tone is present but is a negligible influence in comparison

Myocardial tissue has a high oxygen extraction ratio (80%), which limits its capacity for anaerobic metabolism. Increased oxygen demand has to be met by an increase in coronary perfusion.
During systole, the subendocardial pressure in the left ventricle exceeds that in the outer part of the myocardium, and so, in the main, arterial flow occurs through the arteries only in diastole. There is, however, some flow to the outer areas of the left ventricle throughout the cardiac cycle. In the right side of the heart, which is a lower pressure system, coronary perfusion persists throughout systole and diastole. At an average heart rate of 72 beats per minute, about 0.3 seconds will be spent in systole and 0.5 in diastole. High heart rates can compromise ventricular perfusion as well as ventricular filling.

Supply: This is dependent on coronary blood flow, O2 content of blood (dependent on haemoglobin concentration and SpO2) and the position of the oxygen– haemoglobin dissociation curve.
Demand: This is dependent on systolic arterial pressure (afterload), left ventricular end-diastolic pressure (preload), myocardial contractility and heart rate.

Acute coronary syndrome. This defines any cardiac problem secondary to acutely restricted blood flow to the myocardium, and so includes unstable angina pectoris and myocardial infarction (both NSTEMI and STEMI)

NSTEMI follows partial blockage of a major artery or complete occlusion of one of the minor arteries. Typically, this is with a platelet-rich thrombus or so-called white clot. STEMI accounts for around 65–70% of all cases of myocardial infarction and is due to complete occlusion of one of the major coronary arteries. Typically, this is with a fibrin-rich thrombus or so-called red clot often superimposed on white clot.

Clinical presentation is similar, with the typical symptoms of central chest pain, dyspnoea, diaphoresis and nausea. The different ECG changes reflect the degree of myocardial damage, with a STEMI causing full-thickness and an NSTEMI only partial-thickness damage to the ventricular wall. As a result, the biochemical markers of myocardial injury are less elevated. The typical STEMI ECG shows ST segment elevation, q waves in the affected distribution and T-wave inversion. The NSTEMI ECG shows ST segment depression and/or T-wave inversion.

inversion. If percutaneous coronary intervention (PCI) is not available within 2 hours, then thrombolysis is indicated in STEMI, but it is contra-indicated in NSTEMI because of the risk of reinfarction, which in any event is higher post-hospital discharge (15–25% vs. 5–8%).

NICE have produced detailed guidelines for the immediate management of NSTEMI. Following diagnosis, it is suggested that aspirin and antithrombin therapy should be ‘offered’ (as if a patient with crushing central chest pain is going to want to embark on a discussion of the risks and benefits of treatment) and a formal assessment of the risk of future events should be made. (The Global Registry of Adverse Cardiac Events, GRACE, is one such scoring system, which predicts 6-month mortality. See under ‘Scoring Systems’ in Chapter 5.) The level of predicted risk (low, medium, high) determines further treatment, which can range from conservative management to coronary angiography, PCI and coronary revascularization.

Coronary occlusion and the ECG. Acute thrombotic occlusion of the left anterior descending artery will result in an anterior or anteroseptal myocardial infarction. Occlusion of the posterior interventricular branch of the right coronary artery can result both in inferior and posterior infarction. The right coronary artery supplies the SA and the AV nodes in most individuals, so occlusion will result in conduction abnormalities.