in the gradient of the slope of phase 4 will reduce the amount of time taken for the cell to reach threshold potential, causing depolarization to occur more rapidly. This occurs with sympathetic stimulation (red trace) via β1 adrenoreceptors which results in an increase in cyclic-AMP levels, allowing the opening of calcium channels and thereby increasing the discharge rate of the cell.
Conversely, a decrease in the slope of phase 4 will increase the time taken to reach threshold potential and depolarization, causing a reduced discharge rate. This occurs with parasympathetic stimulation (blue trace). The vagus nerve acts to slow the discharge rate by hyperpolarizing the cell membrane through increased permeability to potassium. The membrane potential is therefore more negative so will take longer to reach threshold potential and to discharge.
1.1.4
Cardiac cycle
The diagram depicts events that occur during one cardiac cycle. It is a graph of pressure against time and includes pressure waveforms for the left ventricle, aorta and central venous pressure (CVP), with the electrocardiogram (ECG) and heart sound timings superimposed.
There are five phases.
Phase 1 (A). Atrial contraction – ‘P’ wave of the ECG and ‘a’ wave of the CVP trace. Atrial contraction (or ‘atrial kick’) contributes to about 30% of ventricular filling.
Phase 2 (B). Ventricular isovolumetric contraction (IVolC) – marks the onset of systole and coincides with closure of the mitral and tricuspid valves (first heart sound). The pressure in the ventricle rises rapidly from its baseline, while blood volume remains constant, since both inlet and outlet valves are closed. The ‘c’ wave of the CVP trace represents tricuspid valve bulging as the right ventricle undergoes IVolC.
Phase 3 (C). Systole – as the ventricular pressure exceeds that in the aorta and pulmonary arteries, the aortic and pulmonary valves open and blood is ejected. The aortic pressure curve follows that of the left ventricle, but at a slightly lower pressure, depicting the pressure gradient needed to allow forward flow of blood. At the end of this phase, ventricular repolarization is represented by the ‘t’ wave on the ECG.
Phase 4 (D). Ventricular isovolumetric relaxation (IVolR) – once the aortic and pulmonary valves close (second heart sound), the ventricular pressure rapidly falls to baseline with no change in volume. Aortic valve closure is seen on the aortic pressure trace as the dicrotic notch, after which the pressure in the aorta exceeds that in the ventricle.
Phase 5 (E and F). Ventricular filling – passive filling of the ventricle during diastole. As ventricular pressure falls below atrial pressure (and CVP), the tricuspid and mitral valves open allowing forward flow of blood. This filling is initially rapid (E), followed by a slower filling phase known as diastasis (F), before atrial contraction occurs and the cycle starts again. The ‘y’ descent on the CVP trace occurs as the atrium empties.
1.1.5
Cardiac output equation
Q = HR × SV
Q = cardiac output (ml.min–1)
HR = heart rate (beats.min–1)
SV = stroke volume (ml.beat–1)
Cardiac output (CO) is defined as volume of blood pumped by the heart per minute; it is equal to the product of heart rate and stroke volume. In considering this equation there are four determinants of CO: heart rate, preload, afterload and contractility. Changes in each variable do not occur in isolation but will impact the remaining variables. Therefore, depending on the magnitude of change, each variable may positively or negatively impact CO.
CO monitoring is frequently used as a means of optimizing tissue oxygenation and guiding treatment. Historically, the gold standard for CO measurement was invasive pulmonary artery catheterization. However, due to the specialist skill required for insertion and the potential for complications, its use has been superseded by less invasive methods.
Pulse contour analysis (i.e. PiCCO, LiDCO) – algorithms relate the contour of the arterial pressure waveform to stroke volume and systemic vascular resistance. Research demonstrates good agreement with the gold standard. Limitations include the necessity for an optimal arterial pressure trace and potential for error (arrhythmias, aortic regurgitation).
Oesophageal Doppler – estimates CO through measurement of blood velocity in the descending aorta (see Section 5.5 – Doppler effect).
Transpulmonary thermodilution – based on the classical dilution method (dilution of known concentration of indicator injectate is measured within the arterial system over time) and is coupled with pulse contour analysis in the PiCCO system. Thermodilution is utilized to calibrate the PiCCO system and to provide measurements of volumetric parameters (i.e. global end-diastolic index) and extravascular lung water.
Thoracic electrical bioimpedance (TEB) – a small electrical current is passed through electrodes applied to the neck and chest. The pulsatile flow of blood leads to fluctuations in current allowing calculation of CO from the impedance waveform. Studies have shown poor correlation between CO values derived via TEB and those dervived via thermodilution methods.
1.1.6
Central venous pressure waveform
The central venous pressure (CVP) waveform reflects the pressure at the junction of the vena cavae and the right atrium. It consists of three peaks and two descents:
‘a wave’ – the most prominent wave, represents right atrial contraction
‘c wave’ – interrupts ‘a wave’ decline, due to bulging of the tricuspid valve into the right atrium during right ventricular isovolumetric contraction (IVolC)
‘x descent’ – decline of right atrial pressure during ongoing right ventricular contraction
‘v wave’ – increase in right atrial pressure due to venous filling of the right atrium during late systole
‘y descent’ – decline of right atrial pressure as the tricuspid valve opens.
Alignment with the ECG trace may aid identification of the CVP waveform components.
Onset of systole marked by ECG R wave; onset of diastole marked by end of ECG T wave.
Three systolic components – ‘c wave’, ‘x descent’ and ‘v wave’.
Two diastolic components – ‘y descent’ and ‘a wave’.
Potential errors in CVP measurement
Sampling errors: positioning of both the central venous catheter and the pressure transducer are important for accurate and precise measurement. Due to the narrow clinical range of CVP, small variations in the transducer reference point may have a disproportionally large effect on CVP measurement.
Interpretation errors: the effects of ventilation on CVP measurement must be considered. All vascular pressures should be measured at end-expiration, because pleural pressure is closest to atmospheric pressure. In
