● ECG monitoring provides no indication of the adequacy of the circulation and can lead to a false sense of security.
● ECG should be used in conjunction with other forms of monitoring that indicate the presence and adequacy of the circulation.
● A normal-looking ECG is no guarantee that the patient is not profoundly hypoxic or hypo- volaemic or that the patient even has a pulse. It is quite possible to have normal electrical activ- ity without adequate contractility (e.g. in pulseless electrical activity, PEA).
■ KEY POINT
ECG should be used in conjunction with other forms of monitoring that indicate the presence and adequacy of the circulation.
●
CENTRAL VENOUS PRESSURE
The measurement of CVP involves inserting a catheter into a central vein, connecting the catheter to a transducer (a device that converts one form of energy to another) via a fluid-filled (heparinised saline) column, and zeroing the transducer so that it is at the level of the right atrium
Figure 4.9 ● PR and QRS intervals of an electrocardiogram (ECG). PR interval 0.2s (normal 0. 12–0.2) QRS 0.08s (normal 1.0 or less)
CARDIOVASCULAR MONITORING 46
(mid-axillary line at the level of sternal angle). The transducer is connected to a monitor, which displays the waveform and the numerical values in terms of millimetres of mercury (mmHg).
Normal CVP values are 5–10 cmH2O (or a very similar value in mmHg, since specific grav- ity of mercury is 13.6, and 10 mm = 1 cm).
Methods of insertion of a CVP catheter are shown in Figure 4.11.
The CVP trace has three positive and two negative waveforms (Figure 4.12):
● The a wave corresponds to atrial systole (and the P wave on ECG).
● The c wave corresponds to isovolumetric contraction of the right ventricle, causing a bulge of the tricuspid valve into the right atrium (correlates with the end of QRS on ECG).
● The v waves are due to filling of the right ventricle leading to a lifting of the tricuspid valve (cor- relates with the end of the T wave on ECG).
● The x descent is due to ventricular contraction pulling down the tricuspid valve.
● The y descent is due to ventricular diastole (opening of the tricuspid valve). The relationship between ECG and CVP is shown in Figure 4.13.
Left atrial pressure is measured indirectly by using a pulmonary artery catheter (Swan– Ganz). This is a multi-lumen balloon floatation catheter introduced through a central vein and advanced until the tip of the catheter is in the pulmonary artery. The inflated balloon wedges
Isovolumic relaxation Ejection Isovolumic contraction Aortic valve opens a R Q S T c v A-V valve closes 50 90 130 0 20 40 60 80 Pressure (mm Hg) Volume (ml) 100 120 Rapid inflow Diastasis Atrial systole Aortic pressure Atrial pressure Ventricular pressure Ventricular volume Electrocardiogram Phonocardiogram Systole Diastole Systole
Events of the cardiac cycle for left ventricular function, showing changes in left atrial pressure, left ventricular pressure, aortic pressure, ventricular volume, the electrocardiogram, and the phonocardiogram.
1st 2nd 3rd A-V valve opens Aortic valve closes P
Cardiac output 47
against the pulmonary artery and gives a wedge pressure, which indicates the left atrial pres- sure. This technique has been largely replaced by less invasive methods.
The saline used to fill the pressure tubing and transducer assembly is anticoagulated (heparin 1– 2 units/mL) to prevent thrombus formation. The measurement is both analogue (in the form of a pressure wave) and digital (numbers indicating systolic, diastolic and mean arterial pressures).
●
CARDIAC OUTPUT
Cardiac output is the volume of blood pumped by the heart per minute. For an average adult (70 kg) at rest, cardiac output is about 5 L/min. During severe exercise, cardiac output can increase to over 30 L/min (although not unfit people).
The three main determinants of cardiac output are preload, cardiac contractility and after- load.
(a) insert into vein
(a) insert wire through needle in vein
(b) remove needle
(b) remove needle
(c) pass catheter over wire (d) remove wire
Different methods of insertion
A. Catheter over needle
B. Catheter over guidewire (Seldinger technique)
Figure 4.11 ● Insertion of a central venous pressure catheter.
Ventricular Systole Jugular pulse Diastole y y v v x c a x c a Figure 4.12 ● Waves associated with central venous pressure trace.
CARDIOVASCULAR MONITORING 48
Preload reflects ventricular filling and is determined chiefly by venous return.
Contractility is determined by the force of ventricular contraction and in the normal heart is determined largely by the initial fibre length, which is determined by the ventricular filling (preload). Within physiological limits, greater initial ventricular filling (preload) results in greater contractility and hence increased cardiac output.
When the ventricular filling exceeds the ability of the heart to increase its contractility, decreased cardiac output results. This is believed to be due to stretching of the sarcomeres beyond their optimal length, such that actin and myosin do not overlap enough in order to produce an effective contraction.
Afterload is the resistance that comes into play after the onset of cardiac contraction and is determined largely by the systemic vascular resistance (SVR) and the pulmonary vascular resistance (PVR) for the left and right sides of the heart, respectively.
The stroke volume is the volume of blood pumped out of each ventricle during each contrac- tion. It increases as the initial fibre length increases, within physiological limits. This initial fibre length of the heart muscle is represented as ‘filling pressure’ on the x-axis of the graph in Figure 4.14 and corresponds to the filling of the heart or ‘preload’.
Cardiac output is often divided by body surface area to take into account the size of the sub- ject. Cardiac output is then expressed as L/min/m2and is known as the ‘cardiac index’. This is much more accurate, since there is a large variation in individual values of cardiac output, which can create a wrong impression of its true significance.
Oxygen delivery is the product of the cardiac output and the arterial oxygen content and represents the amount of oxygen delivered to the tissues in the arterial supply.
Oxygen flux is the volume of oxygen delivered by the left ventricle per minute and is usually about 1000 mL/min. This includes the volume of oxygen carried by the Hb and plasma and is influenced by the amount of Hb present, the per cent saturation of Hb and the cardiac output.