Graphic Anaesthesia. Tim Hooper

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 manoeuvre – clinical applications and physiological abnormalities