The Fick principle
According to the Fick principle:
Cardiac output = oxygen consumption/arteriovenous oxygen content difference The original method described by Fick in 1870 is difficult to carry out. Several variants of the basic method have been devised, but usually they are less accurate. There are many other methods of measuring cardiac output nowadays, but the most accurate are those that use some form of indicator dilution.
Bio-impedance
This method was described by Kubicek and colleagues in 1966 and has been reviewed by Critchley and Critchley (1999).
A small, high-frequency current is passed through the thorax from a pair of spot electrodes stuck to the skin. Sensing electrodes are used to measure the changes in impedance within the thorax; the normal value for an adult is 20–48 Ω at a frequency of 50–100 Hz. Contraction of the heart produces a cyclical change in transthoracic impedance. Although the method has been reported to give accurate results in normal subjects, several studies show some inaccuracy in critically ill patients.
Echocardiography
Transoesophageal echocardiography (TOE) provides diagnosis and monitoring of a variety of structural and functional abnormalities of the heart. It can be used to derive cardiac output from measurement of blood flow velocity by recording the Doppler shift of ultrasound reflected from the red blood cells.
The instantaneous blood flow velocity during one cardiac cycle is obtained for the blood flow in the left ventricular outflow tract (other sites can also be used). This is multiplied by the cross-sectional area and the heart rate to give cardiac output.
12 RV Str oke volume (ml) LV Isolated dog heart 6 0 0 20 Filling pressure (mmHg) 40
Figure 4.14 ● Starling’s curve for the heart.
CARDIOVASCULAR MONITORING LiDCO
The LiDCOTM
system is a bolus indicator dilution method of measuring cardiac output. A small dose of lithium chloride is injected via a central or peripheral venous line; the resulting arterial lithium concentration–time curve is recorded by withdrawing blood past a lithium sensor attached to the patient’s existing arterial line.
The LiDCOTM
plus haemodynamic monitor is intended for monitoring continuous blood pressure and cardiac output in patients with pre-existing peripheral arterial line access.
The PulseCOTM
algorithm computes the heart beat period and stroke volume from the entire blood pressure waveform.
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ORGAN AND TISSUE PERFUSION
Organ and tissue perfusion is the ultimate goal of the cardiovascular system and blood circula- tion. Vital organs have autoregulatory mechanisms to regulate their blood flow, e.g. the renin– angiotensin–aldosterone mechanism in the kidneys. Autoregulation occurs within a range of mean arterial pressures (MAP) and maintains organ perfusion. Myogenic and metabolite theo- ries are the most commonly postulated mechanisms for autoregulation.
Direct and indirect assessment of organ perfusion can be achieved by assessment of blood flow to the organs and by assessment of organ function. Simple measurements such as urine output give an idea of adequate hydration, MAP and adequate perfusion to the kidneys.
Adequate oxygen should be carried by blood to the tissues. This depends on the amount of Hb (g/100 mL of blood) available, the percentage of Hb fully saturated with oxygen, the inspired concentration of oxygen and an adequate circulation of the blood for it to reach the tissues.
Control of the blood pressure is central, via the vasomotor centre, and peripheral, via the feedback mechanism from the baroreceptors in the carotid sinus and aortic arch (Figure 4.15). 50 Right interior carotid Right exterior carotid Left interior carotid Left exterior carotid Carotid sinus receptors Ascending aorta Aortic arch receptors
Carotid sinus nerve to nerve IX
Vagus nerve X
References 51
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SUMMARY
● Based on the baseline parameters of the individual patient, the urgency and the complexity of the planned surgical procedure, monitoring, particularly for the cardiovascular system, needs to be established sufficiently early.
● The goal is to optimise the patient’s preoperative status to the best extent possible in the time available for surgery, without causing further deterioration to the patient’s pathophysiology. This may involve wide-bore peripheral intravenous access, monitoring of fluid intake and output, CVP monitoring if required, and occasionally direct arterial pressure monitoring.
● In more complex cases, cardiac output monitoring is also established before surgery.
● The main determinants of cardiac output are preload, contractility and afterload. These are opti- mised by adequate volume replacement and, if required, pharmacological agents. This optimisa- tion is continued throughout and after the surgical procedure so that the patient has the best chance of coming through the surgery and anaesthesia successfully.
● Induction of general anaesthesia and regional blocks, e.g. for epidural (sympathetic blockade), can affect the venous return (preload), contractility (some anaesthetic agents are myocardial depressants) and afterload (sympathetic blockade, vasodilation).
● General anaesthesia can result in arrhythmias, which, if severe, can affect cardiac function.
● Splanchnic circulation may be decreased during general anaesthesia.
● Prolonged hypotension can lead to vital organ dysfunction, particularly of the kidneys.
● Blood loss is a common cause of hypovolaemia. Blood loss should be assessed carefully and replaced with fluids and, if severe, blood and blood products.
● The patient’s regular medications, e.g. angiotensin-converting enzyme (ACE) inhibitors, beta- blockers and calcium channel blockers, can not only aggravate the hypotension produced by anaesthetic agents but also make the hypotension more difficult to correct.
● The chief goal of patient management is to maintain the cardiovascular parameters around 15–20 per cent of their baseline values (Tables 4.1. and 4.2).
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QUESTIONS
1 How is cardiac output controlled?
2 How is central venous pressure measured?
3 How is arterial blood pressure regulated?
4 How is left atrial pressure measured?
5 What is shock?
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REFERENCES
Association of Anaesthetists of Great Britain and Ireland (2000). Recommendations for Standards of Mon- itoring During Anaesthesia and Recovery. London: Association of Anaesthetists of Great Britain and Ire- land.
Critchley LAH, Critchley JAJH (1999). A meta-analysis of studies using bias and precision statistics to com- pare cardiac output measurement techniques. J Clin Monit 15: 85–91.
Kubicek WG, Karnegis JN, Patterson RP (1966). Development and evaluation of an impedance cardiac output system. Aerosp Med 37: 1208–12.
CARDIOVASCULAR MONITORING 52
Table 4.2 Oxygenation parameters (adult)
Parameter Equation Normal range
Partial pressure of arterial oxygen (PaO2) 80–100 mmHg Partial pressure of arterial CO2(PaCO2) 35–45 mmHg
Bicarbonate (HCO3) 22–28 mEq/L
pH 7.38–7.42
Arterial oxygen saturation (SaO2) 95–100%
Mixed venous saturation (SvO2) 60–80%
Arterial oxygen content (CaO2) (0.0138× Hgb × SaO2) + 17–20 mL/dL (0.0031× PaO2)
Venous oxygen content (CvO2) (0.0138× Hgb × SvO2) + 12–15 mL/dL (0.0031× PvO2)
AV oxygen content difference (C(av)O2) CaO2– CvO2 4–6 mL/dL
Oxygen delivery (DO2) CaO2× CO × 10 950–1150 mL/min
Oxygen consumption (VO2) (C(av) O2)× CO × 10 200–250 mL/min Table 4.1 Normal haemodynamic parameters (adult)
Parameter Equation Normal range
Arterial blood pressure (BP) Systolic (SBP) 90–140 mmHg Diastolic (DBP) 60–90 mmHg Mean arterial pressure (MAP) SBP + [(2 × DBP)/3] 70–105 mmHg Right atrial pressure (RAP) (corresponds to CVP) 2–6 mmHg Right ventricular pressure (RVP) Systolic (RVSP) 15–25 mmHg
Diastolic (RVDP) 0–8 mmHg Pulmonary artery pressure (PAP) Systolic (PASP) 15–25 mmHg
Diastolic (PADP) 8–15 mmHg Mean pulmonary artery pressure (MPAP) [PASP + (2 × PADP)]/3 10–20 mmHg
Pulmonary artery wedge pressure (PAWP) 6–12 mmHg
Left atrial pressure (LAP) 6–12 mmHg
Cardiac output (CO) HR × SV/1000 4.0–8.0 L/min
Cardiac index (CI) CO/BSA 2.5–4.0 L/min/m2
Stroke volume (SV) End diastolic volume (EDV) 60–100 mL/beat – end systolic volume (ESV)
Systemic vascular resistance (SVR) 80× [(MAP – RAP)/CO] 800–1200 dynes s/cm5 Pulmonary vascular resistance (PVR) 80× [(MPAP – PAWP)/CO] < 250 dynes s/cm5