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 However, due to the specialist skill required for insertion and the potential for complications, its use has been superseded by less invasive methods.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 positive pressure ventilation, low PEEP results in minimal error by only increasing the observed value by 1–2 mmHg. With high PEEP, error may be more difficult to predict.
1.1.7
Central venous pressure waveform – abnormalities
Examination of the CVP waveform may aid diagnosis of various pathophysiological conditions.
Cardiac arrhythmias
A – Atrial fibrillation is characterized by an absent ‘a wave’. The ‘c wave’ is more prominent due to a greater than normal right atrial volume at the end of diastole.
B – In isorhythmic AV dissociation, the atria and ventricles beat independently of each other but at the same rate. As such, the atria contract against a closed tricuspid valve producing an enlarged ‘a wave’ termed a ‘cannon a wave’.
Other arrhythmias also affect the CVP waveform. Sinus tachycardia is characterized by a shortening of diastole and therefore alters the diastolic waveform components (shortening of ‘y descent’ with merger of the ‘v’ and ‘a’ waves). In contrast, sinus bradycardia leads to increased distinction between the three waves.
Valvular disease
C – Tricuspid stenosis is a diastolic abnormality impeding right atrial emptying. As the right atrium contracts against a narrowed tricuspid valve, a prominent ‘a wave’ is produced. Right atrial pressure remains elevated for longer than normal, attenuating the ‘y descent’.
D – In tricuspid regurgitation, systolic flow of blood back into the right atrium through an incompetent valve leads to a persistent elevation of right atrial pressure. As such, the ‘c’ and ‘v’ waves gradually merge over time with subsequent loss of the ‘x descent’.
Elevation of CVP may be observed with raised intrathoracic pressure (positive-pressure ventilation), cardiac dysfunction (cardiac tamponade, cardiac failure) and circulatory overload.
Reduction in CVP may occur in association with reduced venous return (hypovolaemia, vasodilatation) and a reduction in intrathoracic pressure (spontaneous inspiration).
1.1.8
Einthoven triangle