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) = CO × [(1.34 × [Hb] × SpO2) + (PaO2 × 0.0225)]
CO = cardiac output
[Hb] = haemoglobin concentration (g.dl–1)
1.34 = maximal O2 carrying capacity of 1 g of Hb measured in vivo (Hüfner’s constant) (ml.g–1)
SpO2 = arterial haemoglobin oxygen saturation (%)
PaO2 = arterial oxygen tension (kPa)
0.0225 = ml of O2 dissolved per 100 ml plasma per kPa
Oxygen flux is defined as the amount of oxygen delivered to the tissues per unit time. Oxygen delivery to the tissues is governed by two fundamental elements: cardiac output and arterial oxygen content. Arterial oxygen content comprises the sum of oxygen bound to haemoglobin and oxygen dissolved in plasma. The normal clinical range for oxygen flux is 850–1200 ml.min–1, with measurement requiring pulmonary artery (PA) catheter insertion.
Oxygen flux may be optimized, without invasive PA pressure measurement, if the modifiable variables are considered.
Cardiac output (CO) – determined by heart rate, preload, contractility and afterload. These factors may be negatively affected by pathological states and drugs (i.e. anaesthetic agents, vasopressors). Optimization may include heart rate control, correction of volume status and administration of vasoactive medications. Direct treatment of disease states should also be implemented.
Haemoglobin concentration – correction of anaemia will result in an increase in arterial oxygen content. Paradoxically, this may have a deleterious effect on oxygen flux due to the changing rheology of blood in the vascular compartment.
Haemoglobin oxygen saturation (SpO2) – may be adversely affected by hypoxia due to hypoventilation, diffusion impairment and ventilation/perfusion inequality. Carbon monoxide poisoning and methaemoglobinaemia should be considered where appropriate. Optimization should focus on the use of supplemental oxygen to maximize alveolar oxygen tension (although the effect will be minimal in shunt) and specific treatment of the cause.
Arterial oxygen tension – influences SpO2 and volume of oxygen dissolved in plasma. Increasing PaO2 has a finite effect on SpO2 once maximal saturation is reached. Dissolved arterial oxygen increases proportionally with an increase in PaO2. This increase becomes clinically significant at hyperbaric pressures.
1.1.15
Pacemaker nomenclature – antibradycardia
The pacemaker code has five positions.
Position I – chamber paced.
Position II – chamber sensed (detection of spontaneous cardiac depolarization).
Position III – response to sensing on subsequent pacing stimuli.
Position IV – presence or absence of an adaptive-rate mechanism in response to patient activity. The previous pacemaker code included a programmability hierarchy (i.e. simple vs. multi), which is now deemed unnecessary.
Position V – presence and location of multisite pacing. This is defined as stimulation sites in both atria, both ventricles, more than one stimulation site in a single chamber or any combination of these.
Pacemakers and diathermy
If possible, diathermy should be avoided in patients with pacemakers. However, if diathermy is required, bipolar is safer (as the current travels between the two instrument electrodes). This should be used in short bursts at the lowest energy settings.