2. Myocardial blood supply Flashcards
Arterial 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)
RCA
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
Supply
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.
LCA
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.
LCA supply
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
The innermost part of the endocardium receives oxygen directly from the blood
within the ventricle.
Venous drainage:
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
The Physiology of Coronary Perfusion
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
Do2
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.
Myocardial Oxygen Supply and Demand
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 Myocardial Ischaemia
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)
STEMI and NSTEMI (ST segment elevation myocardial infarction and non-ST
segment elevation myocardial infarction).
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.
ACS clin features and ecg
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.
Thrombolysis?
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 guidelines for NSTEMI.
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.
