of the ventricles.
QT interval – from the start of the QRS complex to the end of the T wave. This interval represents the time for ventricular activation and recovery. Heart rate variability occurs and therefore a corrected QT interval (QTc) can be calculated (normal value is <0.44 s).
ECG changes associated with acute coronary syndromes and myocardial infarction
Acute coronary syndromes – include non-ST-elevation myocardial infarction and unstable angina. The primary ECG changes observed are ST segment depression and T wave flattening or inversion.
Myocardial infarction – early evidence of transmural ischaemia and myocardial infarction includes hyperacute T waves followed by ST elevation. Q wave formation may begin within 1 hour of infarction. Inverted T waves are a later sign within 72 hours of cell death. Stabilization of the ST segment usually occurs within 12 hours, although ST elevation may persist for more than 2 weeks.
1.1.11
Electrocardiogram – cardiac axis and QTc
Division of the hexaxial reference system into four quadrants allows further interpretation of the cardiac ventricular axis (for calculation see Section 1.1.8 – Einthoven triangle).
The normal QRS axis ranges from −30° of left axis deviation (LAD) to +90°.
LAD is defined as an axis between −30° and −90°. This may be an isolated finding or can be associated with pathology. Causes include: left ventricular hypertrophy, left bundle branch block (LBBB), left anterior fascicular block, myocardial infarction, and mechanical shifts of the heart (i.e. pneumothorax).
Right axis deviation (RAD) is defined as an axis between +90° and +180°. Causes include: physiological variant in infants and children, right ventricular hypertrophy, myocardial infarction, left posterior fascicular block, chronic lung disease, dextrocardia, and ventricular arrhythmias.
Extreme right axis deviation (ERAD) is defined as an axis of −90° to +180°. This is a rare finding associated with dextrocardia, ventricular arrhythmias or a paced rhythm.
Precordial axis
Assessment of the precordial leads, V1–V6, enables determination of the precordial axis as described by R wave progression. Normal R wave progression is characterized by a primarily negative QRS complex in V1 and a primarily positive QRS complex in V6. Transition between negative and positive complexes occurs between the V2 and V4 leads.
Early R wave progression is characterized by much more positive QRS complexes in leads V1 and V2. This observation is always pathological and may be due to posterior myocardial infarction (with the positive QRS complexes representing reciprocal Q waves), right ventricular hypertrophy, RBBB, or Wolff–Parkinson–White syndrome.
Poor R wave progression is characterized by a predominance of negative QRS complexes through the transitional precordial leads. This late transition can be a normal variant but may also be associated with anterior myocardial infarction, left ventricular hypertrophy, LBBB, or lung disease.
1.1.12
Fick method for cardiac output studies
Q = VO2Ca – Cv
Q = cardiac output (ml.min–1)
VO2 = volume of oxygen consumed (ml.min–1)
Ca = oxygen content of arterial blood (ml O2.ml blood–1)
Cv = oxygen content of venous blood (ml O2.ml blood–1)
The Fick principle states that blood flow to an organ may be calculated using a marker substance if the amount of the marker taken up by the organ per unit time and the arteriovenous difference in marker concentration are known. This principle has been applied to the measurement of cardiac output (CO) where the organ is the entire body and the marker substance is oxygen.
Direct Fick method – a minimum of 5 minutes of spirometry is required to determine resting oxygen consumption. During this time a peripheral arterial blood sample is obtained to calculate arterial oxygen content. Cardiac catheterization is required to calculate mixed venous oxygen content using a blood sample from the right ventricle/pulmonary trunk. A peripheral venous sample is insufficient because peripheral oxygen content varies markedly between tissues. This method is therefore time consuming and invasive. Validity is limited to the steady-state, prohibiting the use of this method during periods of changing CO such as exercise or other physiological stress.
Indirect Fick method – application of the Fick principle through carbon dioxide rebreathing avoids invasive measurement of mixed venous oxygen content. Rebreathing techniques estimate arterial and venous carbon dioxide content through measurements of end-tidal partial pressure of carbon dioxide during normal breathing and intermittent rebreathing. Automated systems have eliminated much of the technical difficulty in performing this method.
Thermodilution – based on the Fick principle, thermodilution is a minimally invasive method for CO measurement. The marker substance is a cold bolus of fluid and the arteriovenous difference is determined by a change in temperature. Thermodilution methods have been studied extensively and shown to correlate well with the direct Fick method. In addition to the minimally invasive nature of this method, other advantages over the direct method include validity during exercise and improved time resolution.
1.1.13
Frank–Starling curve
The Frank–Starling curve is used to represent the Frank–Starling law. It states that the ability of the cardiac muscle fibre to contract is dependent upon, and proportional to, its initial fibre length.
As the load experienced by the cardiac muscle fibres increases (within the heart this is the end-diastolic pressure, or preload) so the initial fibre length increases. This results in a proportional increase in the force of contraction due to the overlap between the muscle filaments being optimized. This intrinsic regulatory mechanism occurs up to a certain point. Past this, regulation is lost and contractility does not improve despite increasing fibre length, with eventual muscle fibre failure occurring.
A change in end-diastolic pressure (preload) will cause a patient to shift along the same curve. Increasing preload will cause the patient to shift up along the curve, resulting in increased cardiac output with each contraction. A reduction in preload will cause the opposite.
The whole curve can also be shifted as a result of inotropy or failure of the myocardium. An increased inotropy will cause a greater cardiac output for any given preload and therefore will shift the curve up and to the left. Failure of the myocardium will result in the curve shifting downwards and to the right, demonstrating that for any given preload the cardiac output will be reduced. There is a more exaggerated fall in cardiac output at higher preloads as the fibres become overstretched, with the curve falling off towards the baseline at the far right.
1.1.14
Oxygen flux
O2 flux (ml.min−1)
