from experiments looking at isolated muscle fibres in vitro, allowing individual definitions to be produced. In vivo, these factors are interlinked, being dependent upon and affected by each other, making measuring them individually more difficult.
The stroke volume is determined by all three variables: preload, contractility and afterload. These, together with the heart rate, determine myocardial performance. Preload can also give an indication of how well a myocardium is performing. A heart requiring a higher preload to generate a cardiac output is not performing as well as one that is generating the same cardiac output with a lower preload.
In vivo, direct measurement of initial myocardial fibre length is not possible and therefore preload cannot be determined. As such, various surrogate markers have to be used. The volume in the ventricle at the end of diastole gives an indication of fibre stretch just before the onset of contraction. This can be measured by echocardiography and is called the end-diastolic volume.
The pressure generated in the heart chambers for a given volume is dependent on the chamber’s compliance, with the end-diastolic pressure often being referred to as the ‘filling pressure’. The right atrial pressure can be inferred from the CVP giving an indication of the filling pressure of the right side of the heart. The left-sided pressures are more difficult to measure and require a pulmonary artery catheter to obtain their values.
Contractility is difficult to define in isolation, being affected by all the factors that affect myocardial performance. Most factors that increase contractility do so by increasing the intracellular calcium concentration. Inotropy is often used synonymously with contractility.
Afterload can be represented by the mean arterial pressure during systole, or by measurement of the end-systolic pressure.
1.1.18
Pulmonary artery catheter trace
A pulmonary artery catheter is a balloon-tipped, flow-directed multi-lumen catheter, initially inserted through a central venous introducer sheath. During its placement a trace is produced demonstrating the pressures as the catheter moves through the chambers of the right heart and into the pulmonary circulation. The pulmonary capillary wedge pressure (PCWP) is used as a surrogate for the left atrial pressure.
Continuous pressure monitoring is used, via the distal lumen of the catheter, to guide correct insertion and produce the trace seen above. The balloon is inflated once the catheter has reached the right atrium and is allowed to float with the flow of blood to reach the pulmonary circulation. The right atrium pressure waveform is similar to the CVP waveform. On reaching the right ventricle the wave will oscillate between 0–5 mmHg and 20–25 mmHg. The catheter will then pass through the pulmonary valve and enter the pulmonary artery. The systolic pressure will remain the same as the right ventricle, but the diastolic pressure will rise to about 10–15 mmHg owing to the presence of the pulmonary valve. A PCWP is obtained by allowing the catheter’s balloon to occlude a pulmonary vessel. The trace will look similar to the CVP waveform, but with a range of 6–12 mmHg. The measurement should ideally be taken in West Zone 3 of the lung (where the pulmonary artery pressure is greater than both the alveolar and pulmonary venous pressures, ensuring a continuous column of blood to the left atrium) and at the end of expiration.
Pulmonary artery catheters can also be used to measure cardiac output (by means of an integral thermistor), mixed venous oxygen saturations, right-sided heart pressures and the right ventricular ejection fraction. It can also be used to derive systemic and pulmonary vascular resistances and the cardiac index.
1.1.19
Systemic and pulmonary pressures
The heart consists of two pumps in parallel: the low pressure right side that pumps into the pulmonary circulation, and the higher pressure left side that pumps into the systemic circulation.
The CVP approximates to the pressure in the right atrium and oscillates between 0 and 5 mmHg. In the right ventricle, the systolic pressure increases to 20–25 mmHg, with the diastolic pressure remaining similar to that in the right atrium. The presence of the pulmonary valve increases the diastolic pressure in the pulmonary artery to 10–15 mmHg, while the systolic pressure remains the same. The pulmonary capillary pressures are 6–12 mmHg, creating a pressure gradient that allows forward flow of blood from the pulmonary artery into the pulmonary circulation. The pulmonary capillary (wedge) pressure is often used as a surrogate for left atrial pressure and, in the presence of a normal mitral valve, left ventricular end-diastolic pressure. A pulmonary artery catheter allows accurate measurement of these pressures (see Section 1.1.18 – Pulmonary artery catheter trace).
The pressures in the left side of the heart are higher than the right due to the higher vascular resistance in the systemic circulation. To generate these higher pressures it therefore has a larger muscle bulk than the right. Left atrial pressure measures between 1 and 10 mmHg. During systole, the left ventricular pressure will rise to about 120 mmHg to generate forward flow. As blood passes through the aortic valve, the diastolic pressure will rise to about 60–80 mmHg with the systolic pressure remaining the same. Arterial cannulation can be performed to measure systemic pressures continuously. Peripheral cannulation will produce higher peak systolic and lower diastolic pressures than more central cannulation due to the differences in impedance and harmonic resonance. However, mean arterial pressure will remain broadly similar.
1.1.20
Valsalva manoeuvre
A Valsalva manoeuvre is performed by attempted expiration against a closed glottis. This results in an abrupt but transient increase in intrathoracic pressure and vagal tone. The normal physiological response to this manoeuvre consists of four phases.
Phase I – sudden rise in intrathoracic pressure compresses capacitance thoracic vessels, increasing return of blood from the lungs to left atrium. A sudden, but transient, increase in systemic blood pressure is observed in accordance with the Frank–Starling law of the heart, coupled with direct compression of the thoracic aortic arch. Aortic arch baroreceptors are activated, initiating a compensatory reduction in heart rate.
Phase II – venous return of systemic blood is impeded by sustained increase in intrathoracic pressure. This reduction in preload leads to a fall in cardiac output, once again, in accordance with the Frank–Starling law. A progressive reduction in blood pressure is observed. Baroreceptor activity is reduced, resulting in a sympathetically mediated gradual increase in heart rate, systemic vasoconstriction and a restoration of blood pressure.
Phase III – sudden release of the intrathoracic pressure leads to an abrupt reduction of systemic blood pressure as compression of the aortic arch and thoracic capacitance vessels ceases. Baroreceptor activity is reduced, thereby maintaining heart rate elevation.
Phase IV – an increase in blood pressure occurs with rapid restoration of the cardiac output as venous return suddenly increases. Systolic blood pressure exceeds the resting value (‘overshoot’) as blood is ejected into a constricted peripheral vascular system, as mediated by sympathetic activation in phase II. This rise in blood pressure results in baroreceptor activation and a compensatory bradycardia. Phase IV is not considered complete until the blood pressure has stabilized at its resting value. This may take up to 90 seconds and an ‘undershoot’ of blood pressure is often observed.
1.1.21
Valsalva
