Abstract
The oxygen extraction ratio (OER) is the ratio of oxygen consumption, V̇O2, to oxygen delivery, ḊO2 (see Chapter 17). At around 60%, the OER of the heart is near maximal. This is in contrast to the lower OERs of the liver (around 50%), the kidney (around 15%) and skeletal muscle (between 10% and 100% depending on activity).
How does the oxygen extraction ratio of the heart compare to other organs?
The oxygen extraction ratio (OER) is the ratio of oxygen consumption, V̇O2, to oxygen delivery, ḊO2 (see Chapter 17). At around 60%, the OER of the heart is near maximal. This is in contrast to the lower OERs of the liver (around 50%), the kidney (around 15%) and skeletal muscle (between 10% and 100% depending on activity).
During exercise, myocardial V̇O2 increases by up to fivefold. Normally, coronary blood flow increases to match the increase in V̇O2 through coronary vasodilatation (see Chapter 27). However, when the flow of blood is limited by coronary arterial stenosis, a mismatch between V̇O2 and ḊO2 occurs, resulting in myocardial ischaemia.
What is meant by the term ‘acute coronary syndrome’?
Acute coronary syndrome encompasses a range of conditions that are due to an acute interruption of myocardial perfusion. It includes:
ST-segment elevation myocardial infarction (STEMI);
Non-ST-segment elevation myocardial infarction (NSTEMI);
Myocardial ischaemia without evidence of myocyte necrosis (e.g. unstable or crescendo angina).
How is a myocardial infarction diagnosed?
The diagnosis of myocardial infarction (MI) requires evidence of myocardial necrosis in a clinical setting consistent with acute MI. In practice, this usually means a rise in measured serum cardiac troponin (either troponin T or troponin I isoform) above the upper reference range, with at least one of:
Typical anginal symptoms;
New significant ST-segment or T-wave changes on the electrocardiogram (ECG), which may be dynamic in nature, or new left bundle branch block (LBBB);
Development of pathological Q-waves on the ECG in established infarct;
New regional wall abnormality on echocardiography.
Describe the typical symptoms associated with MI
The most common symptom of myocardial ischaemia is severe central chest pain: tightness, pressure or squeezing. The pain may classically radiate to the left arm, neck or lower jaw, but also to the right arm, shoulder, back or upper abdomen. Other associated symptoms include autonomic features (sweating, nausea or vomiting), dyspnoea, syncope and fatigue. In a significant proportion of cases, patients experience no symptoms of MI – this is termed a ‘silent MI’. Presentation in women is more likely to be atypical, which may delay presentation and diagnosis.
Anaesthetised patients cannot complain of chest pain. The anaesthetist must instead rely on clinical signs to detect myocardial ischaemia: ECG changes, cardiovascular instability, arrhythmias, hypoxia and increased airway pressures due to pulmonary oedema, as well as (if transoesophageal echo is being used) regional wall abnormalities.
What is the physiological mechanism for referred cardiac pain?
Visceral pain is often referred to (i.e. perceived as coming from) the surface of the body. In addition to efferent sympathetic and parasympathetic neurons (see Chapter 59), the heart is innervated by unmyelinated afferent sympathetic neurons. Myocyte ischaemia triggers these afferent neurons to transmit action potentials, through the cardiac plexus, to synapse in the dorsal horn of the spinal cord. It is thought that when the spinal cord is bombarded with sensory information from a viscus, the signal is instead interpreted as pain originating from a dermatome whose afferent sensory neurons also synapse in the same spinal cord segment.
Up to half of all MIs occur either without any symptoms or with atypical symptoms, and as a result these patients often miss the opportunity for early treatment. Many of these patients develop pathological Q-waves on their ECG. Silent MI is as significant a clinical event as recognised MI, and both carry a similar mortality rate.
Two groups of patients at particular risk of silent MI are:
Diabetics. As a result of autonomic neuropathy, there may be abnormal transmission of action potentials along the afferent sympathetic neurons.
Heart transplant recipients. As the donor heart is completely denervated, there is no pathway for the afferent transmission of ischaemic pain signals. This is of real significance in heart transplant recipients, as the graft coronary arteries undergo accelerated atherosclerosis.
How is MI classified?
MI is classified into five types:
Type 1 refers to a primary coronary event, such as atherosclerotic plaque rupture or coronary dissection.
Type 2 is myocardial ischaemia due to either increased oxygen demand or decreased supply in the context of another acute illness.
Type 3 is unexpected cardiac death with symptoms suggestive of MI.
Type 4 is associated with percutaneous coronary intervention (PCI).
Type 5 is associated with cardiac surgery.
The majority of cases of MI are due to spontaneous rupture of an atheromatous plaque. Thrombus rapidly forms around the damaged vascular lumen. Complete occlusion of a coronary artery results in a full-thickness MI (with ST-segment elevation on the ECG), while partial occlusion of a coronary artery results in a partial thickness or subendocardial MI (with ST-segment depression and/or T-wave inversion on the ECG).
