Intensive care

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Chapter 7 Intensive care

Acute Respiratory Distress Syndrome (ARDS)

First described in Denver, Colorado, in 1967 by Ashbaugh. North American–European consensus group has changed the definition to ‘acute’ (as opposed to ‘adult’) respiratory distress syndrome, since the syndrome can occur in children. It is often the pulmonary component of the systemic inflammatory response syndrome (SIRS) and is characterized by severe hypoxia refractory to oxygen, low compliance, high airway pressure, bilateral diffuse alveolar infiltrates and microscopic atelectasis. It has an annual incidence of about 3.5:100 000.

Causes

Table 7.1 Causes of ARDS

Direct injury	Indirect injury
Pulmonary contusion	Septicaemia
Gastric aspiration	Major trauma
Fat and amniotic fluid embolus	Cardiopulmonary bypass
Infection	Massive blood transfusion
Cytotoxic drugs	Prolonged hypotension
Smoke inhalation	Hepatic and renal failure
Oxygen toxicity	Disseminated intravascular coagulation

Pathophysiology

Activated neutrophils adhere to endothelial cells and release inflammatory mediators, including oxygen-free radicals and proteases, to cause lung damage. Direct lung damage or endotoxins alone are sufficient to damage endothelial cells with cytokine release and an inflammatory cascade (Fig. 7.1).

Figure 7.1 Pathophysiology of systemic inflammatory response syndrome (SIRS).

Endothelial damage results in increased capillary permeability and formation of protein-rich alveolar exudate rich in neutrophils. Type I alveolar cells are damaged and type II cells proliferate. As the disease progresses, fibroblast infiltration and collagen proliferation cause microvascular obliteration and widespread fibrosis. Areas of lung involvement are not fixed but shift to dependent areas. Within areas of reduced lung volume, some alveoli remain open and capable of gas exchange, whereas others are filled with alveolar exudate.

IPPV may cause damage more through excess volume (‘volutrauma’) than through pressure itself. The significance of oxygen toxicity is controversial.

Treatment

Cardiovascular System

Inotropes

If shock persists despite adequate volume replacement and vital organ perfusion is jeopardized, inotropic drugs may be required to improve blood pressure and cardiac output (Table 7.2).

Table 7.2 Receptor actions of inotropes

Cardiogenic shock. Characterized by low cardiac output, high filling pressures and increased systemic vascular resistance (SVR). Inodilators (dobutamine, enoximone, milrinone, dopexamine) improve cardiac contractility and decrease SVR. Specific vasodilators (nitroprusside, GTN) may reduce afterload further, increasing stroke volume and decreasing cardiac work by decreasing systolic wall tension.

Septic shock. Characterized by high cardiac output (if hypovolaemia corrected) and decreased SVR. Vasoconstrictors (noradrenaline) reduce SVR. Dobutamine or adrenaline may be required to improve myocardial contractility.

Adrenergic receptor function

Arterioles and veins contain α₁ and α₂ receptors which cause vasoconstriction. Vessels in skeletal muscle are rich in β₂ receptors which cause vasodilation. Myocardium is rich in β₁ and β₂ receptors which are pro-chronotropic and pro-inotropic.

α₁ receptors activate phospholipase C which cleaves phosphoinositol 4,5-biphosphate (PIP₂) to diacylglycerol (DAG) and inositol triphosphate (IP₃). DAG activates protein kinase C to release arachidonic acid which increases cGMP synthesis (Fig. 7.2). Activation of β₁, β₂ and dopamine (D₁) receptors triggers the conversion of ATP to cAMP, activating protein kinase C and triggering protein phosphorylation which causes tachycardia and increases contractility (Fig. 7.3).

Figure 7.2 Activation of α₁ receptors.

Figure 7.3 Activation of β₁, β₂ receptors.

Pulmonary artery catheters

Although a recent meta-analysis concluded that PAC did not affect mortality, intensive care unit or hospital length of stay, analysis of the National Trauma Data Bank in 2006 (53 312 patients) has demonstrated improved outcomes when used for major trauma. Although there is limited evidence to show improved outcome with PAC use, the general consensus is that their use in appropriate patients by clinicians skilled in their insertion and data interpretation is of benefit.

Pressure changes during PAC insertion (Fig. 7.4)

Place catheter so that it does not wedge until at least 1.2 mL air is in the balloon (1.5 mL max.). Greatest degree of accuracy if tip of catheter is placed in West’s zone III. Zone I tends to measure airway pressure, particularly with hypovolaemia. Measure wedge from ‘a’ wave at end of expiration.

Figure 7.4 Pressure changes during pulmonary artery catheter insertion. RA, right atrium; RV, right ventricle; PA, pulmonary artery; PCW, pulmonary capillary wedge.

Complications

Table 7.3 Complications of pulmonary artery catheter insertion

Associated with insertion	Associated with catheter presence
Pneumothorax/haemothorax	Infection of catheter or site
Haematoma	Pulmonary thrombosis/infarct
Cardiac arrhythmias	Cardiac arrhythmias
Arterial puncture	Valve damage/endocarditis
Pulmonary artery perforation	Pulmonary artery erosion
Catheter knotting	Thrombocytopenia
Cardiac valve damage

Cardiac output monitoring

Invasive techniques

• Intermittent thermodilution. Change in temperature of blood following injection of iced saline. Calculated from the Stuart–Hamilton equation:

where:

CO = cardiac output

VI = volume of injectate

BT = blood temperature after injection

BT₀ = blood (pulmonary artery) temperature before injection

IT = injectate temperature.

• Continuous thermodilution. Change in temperature of blood warmed by heating coil on pulmonary artery catheter. Calculated from a modified Stuart–Hamilton equation.

• Indocyanine green dilution (historical)

• Fick calculated cardiac output

• Pulse contour cardiac output (PiCCO). Calculates cardiac output continuously from pulse contour analysis of the aortic waveform via an arterial catheter. Requires central venous access to perform a thermodilution cardiac output measurement for calibration (analysed by a thermistor present in the arterial catheter tip).

• Combined lithium dilution and pulse contour analysis (LiDCO). Uses lithium dilution curve for initial calibration followed by a pulse contour algorithm to determine beat-to-beat stroke volume from a mathematical analysis of the peripheral arterial waveform.

Non-invasive techniques

• Transthoracic/oesophageal Doppler ultrasonography. Measurement of aortic cross-sectional area and blood flow velocity allows calculation of cardiac output. Acceleration and peak velocity indicate myocardial performance, while flow time is related to circulating volume and peripheral resistance.

• Transthoracic impedance. Can be measured across externally applied electrodes. Small changes in impedance (<1Ω) occur with the cardiac cycle as the blood volume in the heart increases during diastole and decreases during systole. Rate of change of impedance can be used to estimate cardiac output.

• Pulse contour analysis. Analyses the arterial waveform to calculate cardiac output by using an estimated compliance of the arterial tree to calculate the stroke volume needed to increase the blood pressure by a given amount. Accuracy limited by non-linear vascular compliance, damped waveforms and aortic wall pathology.

Transoesophageal echocardiography (TOE)

Increasing use in critical care. Uses the physical principle that sound is reflected from tissue interfaces. Piezoelectric crystals transmit and receive acoustic signals to build a two-dimensional image. TOE provides better cardiac views than transthoracic echocardiography, particularly of valves, contractility and filling status.

TOE is of particular use in the assessment of:

• left ventricular systolic function

• left ventricular filling

• wall motion abnormalities

• cardiac tamponade

• valve function

• chest trauma (limited views of ascending aorta).

TOE has shown a poor relationship between PCWP and left ventricular end-diastolic volume, particularly in septic patients and those on high doses of inotropes. In these patients, mean pulmonary capillary pressure may be a more accurate measure.

Bibliography

American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization. Practice guidelines for pulmonary artery catheterization. Anesthesiology. 2003;99:988-1014.

Antonelli M., Levy M., Andrews P.J., et al. Hemodynamic monitoring in shock and implications for management. International Consensus Conference. Intensive Care Med. 2007;33:575-590.

Dawson S., Jhanji S., Pears J.R.M. Cardiac output monitoring: basic science and clinical application. Anaesthesia. 2008;63:172-181.

Jhanji S., Dawson J., Pearse R.M. Cardiac output monitoring: basic science and clinical application. Anaesthesia. 2008;63:172-181.

Klein A.A., Snell A., Nashef S.A., et al. The impact of intra-operative transoesophageal echocardiography on cardiac surgical practice. Anaesthesia. 2009;64:947-952.

Moppett I., Shajar M. Transoesophageal echocardiography. BJA CEPD Rev. 2001;1:72-75.

Van Lieshout J.J., Wesseling K.H. Continuous cardiac output by pulse contour analysis? Br J Anaesth. 2001;86:467-469.

Fluid and Electrolyte Balance

The neonate has a greater proportion of body water and in a different distribution than the adult (Fig. 7.5). More fluid is distributed within the extracellular compartment (interstitial and plasma volume) compared with the adult, resulting in a larger volume of distribution for water-soluble drugs. A large proportion of interstitial fluid is excreted within the first few weeks after birth and adult levels are attained by adolescence.

Figure 7.5 Body water distribution in the neonate and adult.

A 70 kg male has about 42 kg of water distributed through three body compartments.

• extracellular fluid – 20% (plasma volume 4%, interstitial fluid 16%)

• intracellular fluid – 40%

Plasma volume expansion is least effective with fluids that are distributed throughout all body compartments and most effective with those that remain within the intravascular compartment. Therefore:

• 1000 mL 5% dextrose (plasma, interstitial and intracellular compartments) expands plasma by 1000 × 4/60 = 67 mL

• 1000 mL normal saline (plasma and interstitial compartments) expands plasma by 1000 × 4/20 = 200 mL

• 1000 mL colloid (plasma only) expands plasma by 1000 × 4/4 = 1000 mL.

Homeostatic control

A rise in serum osmolality stimulates osmoreceptors in the anterior hypothalamus to release ADH from the supraoptic nuclei. ADH release is also stimulated by volume receptors in the left atrium and carotid sinus baroreceptors in response to hypovolaemia.

ADH increases permeability of the distal collecting ducts, resulting in more fluid reabsorption and a reduction in the osmolality of body fluids.

Aldosterone is produced by the adrenal cortex in response to ACTH, renin, hyponatraemia or hyperkalaemia. It acts on the distal tubules and collecting ducts to increase Na⁺ resorption and K⁺ excretion.

Renin is secreted by the juxtaglomerular apparatus in response to a fall in extracellular volume or BP and acts on angiotensinogen to form angiotensin I which is converted to angiotensin II by passage through the lungs. Vasoconstriction produced by angiotensin II produces a marked rise in both systolic and diastolic blood pressures.

Normal fluid requirements

Fluid and electrolyte requirements per 24 h

• Water: 35 mL.kg⁻¹

• Na⁺: 2 mmol.kg⁻¹

• K⁺: 1 mmol.kg⁻¹

Loss

• Insensible loss (skin and lungs) 500–1000 mL.24 h^−1.

• Urine (minimum) 300 mL.24 h^−1.

• Faeces 500 mL.24 h⁻¹.

Assessment of hydration

Thirst, skin turgor (loss of turgor at >10% fluid deficit), hydration of mucous membranes, core–peripheral temperature gradient, pulse rate and volume, postural hypotension (>20% fluid deficit), urine output and osmolality and fluid balance.

Postoperative fluid requirements

Intravenous fluids administered perioperatively during minor gynaecological surgery reduce morbidity, particularly nausea and dizziness. However, blood coagulation appears to be accelerated by haemodilution with saline, and in patients undergoing elective abdominal surgery, the incidence of DVT was four times greater than in the fluid-restricted group (Janvrin et al 1980).

Despite this latter study, it is generally agreed that the advantages of perioperative fluids outweigh any disadvantages. Hartmann’s 15 mL.kg⁻¹.h⁻¹ has been suggested for major surgery; a rate shown to improve postoperative renal function. Septic patients or those with lung trauma have raised extravascular lung water, and lesser rates may be necessary to avoid pulmonary oedema. In addition, give blood to maintain Hb >8.5–9.0 g.dL⁻¹.

Surgical stress causes release of ADH, renin and aldosterone, resulting in sodium and water retention, potassium excretion and an inability to excrete a hypotonic urine. Postoperative catabolism increases the minimum metabolic demand for water from 20 to 30 mL.kg⁻¹ per day, i.e. 2000 mL.day⁻¹. The addition of 100 g.day⁻¹ of glucose reduces nitrogen loss by up to 60%. Therefore, give maintenance fluids of 2000 mL 5% dextrose.24 h⁻¹ postoperatively with 30 mmol KCl added to each 1 L bag to provide daily K⁺ requirements. Hidden losses are difficult to judge so titrate fluids according to urine output (>0.5 mL.kg⁻¹.h⁻¹). Sodium retention is greatly reduced by 48 h so then add Na⁺ to maintenance fluids and reduce KCl supplements.

Albumin

Single polypeptide of 585 amino acids. Synthesized in the endoplasmic reticulum of hepatocytes at 9–12 g/day but can increase 2–3 times in states of maximum synthesis. Stimulus to production is colloid osmotic pressure, osmolality of the extravascular liver space, insulin, thyroxine and cortisol. Catabolized by vascular endothelium. 5% of albumin is removed from the intravascular space per hour. Clinical properties of albumin include:

• Binding and transport – strong negative charge binds Ca²⁺ (40%), Cu²⁺, thyroxine, bilirubin and amino acids; also binds warfarin, phenytoin, NSAIDs and digoxin

• Maintenance of colloid osmotic pressure (COP) – contributes to 80% of COP

• Free radical scavenging – thiol groups scavenge reactive oxygen and nitrogen species

• Platelet inhibition and antithrombotic effects

• Effects on vascular permeability – may bind within the subendothelium to alter capillary membrane permeability.

Serum albumin decreases due to dilutional effects with crystalloid/colloid solutions, redistribution due to altered capillary permeability (five-fold increase during sepsis), decreased synthesis in septic patients, and increased loss from kidney or gut.

Correlation between COP and serum albumin is poor. Therefore, oedema associated with hypoalbuminaemia is not necessarily related and may be related more to lymphatic dysfunction. The acute-phase response is initially associated with a decrease in albumin synthesis, possibly due to IL-6-mediated inhibition of synthesis. A later hypermetabolic phase results in increased albumin synthesis.

Benefits of correcting hypoalbuminaemia are unclear. A prospective randomized study of 475 ICU patients comparing albumin and gelatin solutions failed to show any benefit (Stockwell et al 1992). In 70 children with burns, albumin supplementation failed to improve morbidity or mortality (Greenhalgh et al 1995). In septic patients, albumin infusions will only increase COP for a relatively short period. Increased capillary permeability results in >60% of albumin leaving the intravascular compartment within 4 h, potentially worsening oedema.

A controversial systematic review by the Cochrane Group of 23 randomized controlled trials found that the risk of death was 6% greater in the group treated with albumin compared with those receiving crystalloids or no treatment (Cochrane Injuries Group 1998). The Committee on Safety of Medicines now advises doctors to restrict the use of, and take special care when using, human albumin, but states that there is ‘insufficient evidence of harm to warrant withdrawal of albumin’. Hypoalbuminaemia in itself is not an appropriate indication. Risks of hypervolaemia and cardiovascular overload warrant monitoring in patients receiving albumin.