Controversy has since existed regarding how tight the glucose control should be, with some advocating a 5 \200\2238mmol/L target range to reduce the risk of potentially injurious hyp oglycaemia, particularly as regular testing introduces a signi \201 cant nurse workload. T he introduction of (semi-) con- tinuous, (semi-) automated blood glucose monitoring devices should facili- tate closer maintenance of normoglycaemia. Protocol Several protocols and algorithms have been devised by different groups. None are p erfect, but suit the particular circumstances of their units in terms of staf \201 ng leve ls and expertise. TIGHT GLYCAEMIC CONTROL/INTENSIVE INSULIN THERAPY 133 Key papers Van den Berghe G, Wouters P, Weekers F, et al. (2001) Intensive insulin therapy in critically ill patients. N Engl J Med 345: 1359 \200\22367. Van den Berghe G, Wilmer A, Hermans G, et al. (2006) Intensive insulin therapy in the medic al ICU. N Engl J Med 354: 449 \200\22361. Brunkhorst FM, Engel C, Bloos F, et al. (2008) Intensive insulin therapy and pentastarch re suscita- tion in severe sepsis. N Engl J Med 358: 125 \200\22339. See also: Hypoglycaemia, p506. This page intentionally left blank 135 Chapter 7 Wound and pressure area management Wound management principles 136 Dressing techniques 138 Special support surfaces 140 136 CHAPTER 7 Wound and pressure area management Wound management principles Wound management attempts to promote wound healing, prevent con - tamination and wound breakdown, and reduce pain and discomfort. A wound heals through the phases of haemostasis, in \202 ammation, granu- lation, and maturation. The \201 rst two processes arrest bleeding and help remove contamination. Granulation inv olves rebuilding of the tissues, angiogenesis contraction, and epithelialisation. This proc ess normally takes about 21 days, but may be delayed by age, infection, dehydration, or poo r nutrition. Maturation may take several years and involves remodeling of the dermis to inc rease the strength of the healed wound. A wound that fails to go through these process steps may become chronic. It is important to keep the wound warm and moist since all human cells (with the exception of the dead, kerat inised, super \201 cial skin cells) require moisture to survive, and warmth to grow and di vide. An exudate provides the best environment for healing by supporting cells involved in wound repair with nutrients. Although angiogenesis is increased in a low oxygen environment (e.g. under occlusive dressings), most large, randomized trials show reduction in post-ope rative wound infection from administering supplemental oxygen. Wound cleansing Wounds should be cleaned by irrigation with isotonic saline. Soaps irritate the wound but may be useful on the surrounding skin. Both iodine and peroxide irritate the wound, are unnecessary, and best avoided. Wound infection The hallmarks of wound infection are: \200 \200 \200 \200 \200 \200 \200 Pain. Redness. Increased warmth. Tenderness. Oedema. Purulent discharge. Foul odor. Systemic or spreading signs of infection (e.g. cellulitis) may be present and mandate syste mic antibiotic therapy. The wound should be swabbed prior to treatment. Otherwise, local tr eatments may be suf \201 cient, e.g. silver preparations, iodine-based preparations, and t opical antibiotic (e.g. silver sulfadiazine). The latter should only be used for short-term treatment in mild cases. Surgical debridement may occasionally be needed. Pressure sores Pressure sores occur due to compression of tissue between bone and the suppo rt surface, and due to shearing forces, friction, and maceration of tissues against the sup port surface. A pressure sore requires cleansing, debridement of eschar or necrotic tissue, staging (see table opposite), and packing if there is crater formation. Packing should occ lude the ulcer, but should be loose to avoid adding to the pressure damage. Dressings shoul d keep the ulcer moist. WOUND MANAGEMENT PRINCIPLES 137 Staging of pressure sores Stage 1 Stage 2 Stage 3 Stage 4 Skin intact with persistent redness due to pressure Ulcer involving the epidermis or dermis . Ulcer involving subcutaneous tissue layer. May be undermined. Ulcer extends through the f ascia to muscle, tendon, or bone. Undermining and tunneling may be present. Ulcer bed canno t be visualized due to slough or eschar. Unstageable Modi \201 ed from the National Pressure Ulcer Advisory Panel, February 2007. See also: Dressing techniques, p138; Special support surfaces, p140. 138 CHAPTER 7 Wound and pressure area management Dressing techniques Wound dressings serve to reduce pain, protect the wound from further in jury and infection, and reduce moisture loss. Dressings should be non- adherent, sterile, a nd cover the wound completely. Adherent dressings delay wound healing. When dressings are applied to wounds, an aseptic technique must be used. Bio-occlusive dressings These allow air and water vapor to permeate, thus accelerating heal ing; they are transparent to allow wound assessment and are waterproof. Calcium alginate Calcium exchanges with sodium from the wound to convert exudates to a gel. This reduces moisture loss. They are not effective for dry wounds since they depend on abs orption of exudates to be active. Foam dressing Foam dressings absorb excessive exudates while allowing air and vapor permeat ion to accelerate healing. They require absorption of exudates to be effective. They are th ermally insulating and non-adherent. Hydrocolloids Hydrocolloid dressings provide slow absorption of exudates to create a soft, non-adherent gel which occludes the wound and retains moisture. They are effective when exu dates are low volume. They should not be used in infected wounds as growth of anaerobes may be encouraged by their occlusive properties. Hydrogels Hydrogels have hydrophilic sites to enable absorption of excess exudates. They re tain moisture. Vacuum-assisted closure (VAC) A foam dressing is placed in the ulcer absorbing excessive ex udates. The ulcer is sealed with an adhesive drape and negative pressure is applied for up to 24h per day. The VAC dressing reduces oedema and improves local blood supply while remov ing surface debris and exudate. Intermittent treatment may be more effective than continuou s. Use of VAC dressing is advantageous in perineal pressure sores because the vacuum helps keep the dressing in place. DRESSING TECHNIQUES 139 Properties of wound dressings \200 \200 \200 \200 \200 \200 Maintain warmth. Maintain moisture. Remove exudates. Allow vapor and gas permeation. Minimi ze contamination. Non-adherent. See also: Wound management principles, p136. 140 CHAPTER 7 Wound and pressure area management Special support surfaces The use of special support surfaces attempts to reduce the pressur e at the contacting skin surface to a level below capillary occlusion pressure. In most cas es, it is suf \201 cient to use postural changes to minimize the time the support surface contacts with any one area of skin. Factors suggesting need for special support surfaces \200 Patients with severely restricted mobility due to external traction or cardiorespiratory in stability cannot be turned frequently, if at all. Patients with decreased skin integrity, e .g. burns, pressure sores already present, chronic corticosteroid use, diabetes mellitus. P atients on vasoactive drug infusions and/or poor tissue perfusion. Types of special support surface Air mattress This either replaces or is placed on top of a standard hospital bed mat- tress. Although providing minimum reduction in contact pressure , they should be considered as minimum support for patients with any of the above factors. Low air loss bed These purpose-built, pressure-relieving beds allow easier patient mobility than other support surfaces. Contact pressure may still be higher than capillary occlusion pressure so positioning is still required. Patients who are haemodynamically unstable shou ld usually be managed on a low air loss bed, particularly if receiving vasoconstrictor drug s. The presence of pressure sores with intact skin is an indication for a low air loss bed. Rotational low air loss beds allow automated lateral rotation at variable time intervals t o facilitate chest drainage. These may also be useful where manual positioning is impractic al. Air \202 uidised bed This is the only support surface that consistently lowers contact pr es- sure to below capillary occlusion pressure. Consequently, most bene \201 t is seen in patients with severe cardiorespiratory instability who cannot be turned, and those with pre ssure sores and broken skin. The additional ability to control temperature of the immediate environment is advanta- geous in hypothermic patients and those with large surface area bu rns. Any exudate from the skin is adsorbed into the silicone beads on which the patient \202 oats. This drying effect is particularly useful in major burns (although it must be ta ken into account for \202 uid replacement therapy). The air \202 uidised bed also has a role in pain relief. Rotation therapy Rotation therapy beds continuously change the pressure with the con- tacti ng surface by lateral turning to each side. This reduces shear and mini- mises pain and dis comfort associated with manual turning. SPECIAL SUPPORT SURFACES 141 See also: Wound management principles, p136. This page intentionally left blank 143 Chapter 8 Respiratory monitoring Pulse oximetry 144 CO2 monitoring 146 Pulmonary function tests 148 Volume-pressure relation ship 150 Blood gas machine 152 Blood gas analysis 154 Extravascular lung water measurement 156 Respiratory imaging 158 144 CHAPTER 8 Respiratory monitoring Pulse oximetry Continuous, non-invasive monitoring of arterial oxygen saturation by placeme nt of a probe emitting red and near-infrared light over a pulse on a digit, ear lobe, cheek , or bridge of the nose. It is unaffected by skin pigmen- tation, hyperbilirubinaemia, or a nemia (unless profound). Physics The color of blood varies with oxygen saturation due to the optical properties of t he haem moiety. As the hemoglobin molecule gives up O2, it becomes less permeable to red li ght and takes on a blue tint. Saturation is determined spectrophotometrically by measuring the \200\230blueness \200\231, utilizing the ability of compounds to absorb light at a spe ci \201 c wavelength. The use of two wavelengths (650 and 940nm) permits the relative quan tities of reduced and oxyhaemoglobin to be calculated, thereby determining satu- ration. Th e arterial pulse is used to provide timepoints to allow subtrac- tion of the constant absor ption of light by tissue and venous blood. The accuracy of pulse oximetry is 9 2% at values above 70% SaO2. Indications \200 Continuous monitoring of arterial oxygen saturation. Cautions \200 As only two wavelengths are used, pulse oximetry measures functional rather than fractional oxyhaemoglobin saturation. Erroneously high readings are given with carboxyhaemoglobin and methaemoglobin. With poor peripheral perfusion or intense vasoconstriction, the reading ma y be inaccurate ( \200\230fail soft \200\231) or, in newer models, absent ( \200\230fail ha rd ). Motion artifact and high levels of ambient lighting may affect readings. Erroneous si gnals may be produced by signi \201 cant venous pulsation from tricuspid regurgitation or venous congestion. Venous pulsatility accounts for differences between ear and \201 nger SpO2 in the same subject. Ensure a good LED signal indicator or a pulse waveform (if availa ble) is seen on the monitor. Vital dyes, e.g. methylthioninium chloride (methylene blue) an d indocyanine green, may affect SpO2 readings as may nail varnish. \200 PULSE OXIMETRY 145 See also: Oxygen therapy, p38; Ventilatory support \200\224indications, p44; IPPV \200\224a djusting the ventilator, p50; Vasopressors, p268. 146 CHAPTER 8 Respiratory monitoring CO2 monitoring Capnography For capnography, respiratory gasses must be sampled continuously and measured by a rapid response device attached to (sidestream sampling) or within the br eathing circuit (mainstream sampling). As CO2 has an absorp- tion band within the infrared spectrum, CO2 tension is usually measured by infrared absorption. Other gasses can interfer e, but this may be over- come by calibrating the instrument with known concentrations of CO 2 in the required measurement range, i.e. diluted with a gas mixture similar to exhaled gas . The capnogram The CO2 concentration of exhaled gas consists of four phases (see \201 gure 8.1). The presence of signi \201 cant concentrations of CO2 in phase 1 implies rebreathin g of exhaled gas. Failure of an expiratory valve to open is the most likely cause of rebrea thing during manual ventilation, although an inadequate \202 ow of fresh gas into a rebre athing bag is a common cause. The slope of phase 3 is dependent on the rate of alveolar gas exchange. A steep slope may indicate ventilation-perfusion mismatch since alveoli that are poorly ventilated but well-perfused discharge late in the respira- tory cycle. A steep slo pe is seen in patients with signi \201 cant auto-PEEP. Colorimetric devices The underlying principle is that the change in pH produced by differen t CO2 concentrations in solution will change the color of an indicator. These are small dev ices that \201 t onto an ET tube or the ventilator circuit and respond rapidly (up to 60 breaths/min). They can be affected by excessive humidity and generally only work in the ran ge 0 \200\2234% CO2. They are useful to con \201 rm tracheal intubation during patient tra nsfer and in the cardiac arrest situation. End-tidal PCO2 End-tidal PCO2 approximates PaCO2 in patients with normal lung func- tion. I n ICU patients, pulmonary function is rarely normal, thus end-tidal PCO2 is a poor approxim ation of PaCO2. Large differences may represent an increased dead space to tidal volume rat io, poor pulmonary perfusion or intra-pulmonary shunting. A progressive rise in end-tidal P CO2 may represent hypoventilation, airway obstruction, or increased CO2 produc- tion due to increased metabolic rate. End-tidal PCO2 falls with hyper- ventilation and in low cardiac output states. It is absent with ventilator disconnection and during cardiac arrest, but ri ses with effective CPR or restoration of a spontaneous circulation. Dead space to tidal volume ratio The arterial to end-tidal PCO2 difference may be used to c alculate the physiological dead space to tidal volume ratio via the Bohr equation: \216\233 \216\234 \216\235 \216\236 \216\237 \216 \200\223 PaCO PetCO 2 PaCO V D V T = 2 2 In health, a value between 30 and 45% should be expected. CO 2 MONITORING 147 PCO2 Phase 3 Phase 4 Phase 2 Phase 1 Time Fig. 8.1 The components of the normal capnogram. Phase 1 During the early part of the exhaled breath, anatomical dead space and sampling dev ice dead space gas are sampled. There is negligible CO2 in phase 1. Phase 2 As alveolar gas begins to be sampled, there is a rapid rise in CO2 concen- tration. Phase 3 Phase 3 is known as the alveolar plateau and represents the CO2 concen- tration in mixed expired alveolar gas. There is normally a slight increase in PCO2 during phase 3 as a lveolar gas exchange continues during expira- tion. Airway obstruction or a high rate of CO 2 production will increase the slope. End-tidal PCO2 will be less than the PCO2 of ideal al veolar gas since the sampled exhaled gas is mixed with alveolar dead space gas. Phase 4 As inspiration begins, there is a rapid fall in sample PCO2. See also: Endotracheal intubation, p42; Ventilatory support-indications, p44; IPPV \200\224 adjusting the ventilator, p50; Tracheotomy, p80; Blood gas analysis, p154. 148 CHAPTER 8 Respiratory monitoring Pulmonary function tests Few of the numerous pulmonary function tests available currently i mpact upon clinical management of the critically ill, particularly if the patient has to be moved to a laboratory. A number of other tests require highly specialized equipment and fu l \201 l a predominant research role. Clinically relevant tests Measurement PaO2, SaO2, PaCO2 SpO2 End-tidal PCO2 Vital capacity, tidal volume (see \201 gure 8.2) Test Arterial blood gasses Pulse oximetry Capnography Spirometry, electronic \202 owmetry Common clinical use Serial measurement of borderline function (VC <10 \200\22315mL/kg) e.g. Guillain \200\223Ba rr syndrome (Spontaneous ventilation) asthma Peak expiratory \202 ow rate FEV1, FVC (see \201 gure 8.2) Wright peak \202 ow meter Spirometry, electronic \202 owmetry (Spontaneous ventilation) asthma, obstructive/restrictive disease Ventilator adjustments, m onitoring disease progression Ventilator adjustments Lung/chest wall compliance The change in pressure liter increase in volume above FRC Pneumotachograph, manometry Flow-volume loop, pressure-volume loop Notes \200 The alveolar \200\223arterial oxygen difference (A \200\223aDO2) is <2kPa in youth and <3.3 kPa in old age. The Bohr equation calculates physiological deadspace (VD). The normal value is <30%. The shunt equation estimates the proportion of blood shunted past poorly ventilat ed alveoli (QS) compared to total lung blood \202 ow (QT). The normal range is <15%. PULMONARY FUNCTION TESTS 149 Equations Alveolar gas equation \216\233 \216\235 \216\234 \216\236 \216 \216\237 ) PaCO RQ ( \227 FIO 94.8 2 = 2 \200\223 P O A 2 Respiratory quotient (RQ) is often approximated to 0.8. Alveolar \200\223arterial oxygen di fference (A \200\223aDO2) ) ) ( \227 FIO 94.8 2 ( \210\222 = \200\223 \200\223 A aDO PaCO RQ PaO 2 2 2 Dead space to tidal volume ratio (Bohr equation) \216\233 \216\234 \216\235 \216\236 \216\237 \216 \200\223 PaCO PetCO 2 PaCO V D V T = 2 2 Shunt equation \216\233 \216\234 \216\235 \216\236 \216\237 \216 \200\223 CcO CaO \200\223 CcO CvO Q Q = S 2 2 T 2 2 CcO2 = end-capillary O2 content, a = arterial, v = mixed venous. TLC Total lung capacity VC Vital capacity FRC Functional residual capacity VT Tidal volume RV Residual volume TLC VC VT FRC RV Fig. 8.2 Lung volumes and capacities. See also: Pulse oximetry, p144; CO2 monitoring, p146. 150 CHAPTER 8 Respiratory monitoring Volume-pressure relationship This is determined by the compliance of the lungs and chest wa ll. The inspiratory volume-pressure relationship contains three components: an initial incr ease in pressure with no signi \201 cant volume change; a linear increase in volume as pre ssure increases (the slope of which repre- sents respiratory system compliance); and a furt her period of pressure increase with no volume increase. These three phases are separated b y two in \202 exion zones, the lower representing the opening pressure of the system after \202 ow resistance has been overcome in smaller airways, and the upper approximating to total lung capacity. The expiratory pressure- volume relationship should normally approxima te the inspiratory curve, returning to functional residual capacity. In patients with small airway collapse, separation of the inspiratory and expiratory curves occurs (hysteresis) a s gas is trapped in smaller airways at the end of expiration. Dynamic measurement A pressure-volume loop may be viewed on most modern mechanical ventilat ors. A square wave inspiratory waveform (constant \202 ow) and no inspiratory pause are n ecessary for waveform interpretation. Static measurement Small, incremental lung volumes (200mL) are delivered with a calibrated syringe. The pressure measurement after each increment is taken under zero \202 ow condit ions, allowing construction of a pressure-volume curve. A quasi-static curve can be constru cted by setting incremental tidal volumes (e.g. between 100 and 1000mL) for successive vent ilator breaths and measuring the pressure during an inspiratory pause. Use of volume-pressure curves Since respiratory muscle activity can alter intrathoracic pre ssure, the volume-pressure curve is more easily obtained in the relaxed, fully venti- lated patient (see \201 gure 8.3). Both static and dynamic respiratory system compliance can b e determined as the slope of the linear portion of the curve, i.e. where incremental pressu re in \202 ates the lungs. Below the lower in \202 exion zone the small airways are close d and expiration does not reach functional residual capacity. Therefore, the lower in \202 exion zone represents the appropriate setting for external PEEP to avoid gas trapping. Abo ve the upper in \202 exion zone, the lungs cannot in \202 ate further. Therefore, the upp er in \202 exion zone represents the maximum setting for peak airway pressure. VOLUME-PRESSURE RELATIONSHIP 151 Volume Upper inflection zone Compliance Hysteresis Lower inflection zone Pressure Fig. 8.3 Volume-pressure curve. Compliance: calculations Lung compliance (L/cmH2O) = \224VL/ \224PL where L, the liter abo ve FRC, is the slope of the linear portion of the curve. Total respiratory system compliance is derived from the equation: (1/total compliance) = (1/lung compliance) + (1/chest wall compliance) Total compliance can be calculated in well-sedated, ventilated patients as: tidal volume/(e nd-inspiratory pause pressure \200\224 PEEP). See also: IPPV \200\224adjusting the ventilator, p50; Positive end expiratory pressure (1), p66; Positive end expiratory pressure (2), p68. 152 CHAPTER 8 Respiratory monitoring Blood gas machine A small amount of heparinised blood is either injected from a syringe or aspirated from a capillary tube into the machine. The blood comes into contact with three e lectrodes which measure pH, PO2, and PCO2. \200 pH \200\224measured by the potential across a pH-sensitive glass membrane separating a samp le of known pH and the test sample. PO2 \200\224the partial oxygen pressure, is measured by applying a polarizing voltage between a platinum cathode and a silver anode (Clark electro de). O2 is reduced, generating a current proportional to the PO2. PCO2 \200\224the partial pressure of carbon dioxide, utilizes a pH electrode with a Te \202 on membrane (Severingha us electrode) that allows through uncharged molecules (CO2), but not charged ions (H+). CO2 alone thus changes the pH of a bicarbonate electrolyte solution, the change being linearly related to the PCO2. Hb \200\224estimated photometrically; this is not as accurate as co-o ximetry (see below). Bicarbonate \200\224calculated by the Henderson \200\223Hasselbach equ ation. Actual HCO3 \200\223 includes bicarbonate, carbonate, and carbamate. \216 \200\223 arterial HCO \216 3 PaCO 0.03 2 \216 \216 = + pH 6.1 log \227 10 Actual base excess (de \201 cit) \200\224the difference in concentration of strong base (a cid) in whole blood and that titrated to pH 7.4, at PCO2 5.33kPa and 37*C. Standard base ex cess (de \201 cit) \200\224a calculated in vivo base excess (de \201 cit). Standard bicar bonate \200\224the plasma concentration of hydrogen carbonate equilibrated at PCO2 5.33kPa, PO2 13.33kPa, and temperature 37*C. \200 Blood gas values can be given either as \200\230pHstat \200\231 or \200\230alphastat \200 \231, the former correcting for body temperature by shifting the calculated Bohr oxyhae- mo globin dissociation curve (hyperthermia to the right, hypothermia to the left). Alphastat m easures true blood gas levels in the sample. Co-oximeter This differs from a blood gas machine in that the blood is haemolysed to calcul ate: (i) total Hb and fetal Hb, and (ii) oxyHb, carboxyhaemoglobin (COHb), methaemoglobin, and sulphaemoglobin by utilizing absorbance at six wavelengths (535, 560, 577, 622, 636, 67 0nm). Taking a good blood gas sample Use a 1mL syringe containing preferably a dry heparin salt ( if not, liquid sodium heparin 1000IU/mL solution just \201 lling the hub). Take sample, e xpel air, mix sample thoroughly, and insert without delay. Cautions \200 \200 \200 \200 Too much heparin causes dilution errors and is acidic. Nitrous oxide or halothane anesthesi a may give unreliable PO2 values. Intravenous lipid administration may affect pH values. Ab normal (high/low) plasma protein concentrations affect base de \201 cit. BLOOD GAS MACHINE 153 See also: Blood gas analysis, p154. 154 CHAPTER 8 Respiratory monitoring Blood gas analysis A heparinised (arterial, venous, capillary) blood sample can be inserted into a blood gas machine and/or co-oximeter for measurement of gas ten- sions and saturati ons, and acid-base status. Measurements \200 Identi \201 cation of arterial hypoxaemia and hyperoxia, hypercapnia and hypocapnia \200 \224enabling monitoring of disease progression and ef \201 cacy of treatment. Ventilator a nd FIO2 adjustments can be made precisely. pH, PaCO2 and base de \201 cit (or bicarbonate) values can be reviewed in parallel for diagnosis of acidosis and alkalosis, whether it is respiratory or metabolic in origin, and whether any compensation has occurred. (see \201 gure 8.4). Using a co-oximeter, accurate measurement can be made of hemoglobin oxygen satur ation and also the total Hb level. The more sophisticated co-oximeters permit measurement o f the fraction of metHb, COHb, deoxyHb, and fetal Hb. Measurement of mixed venous oxygen sa turation \200\224for calculation of oxygen consumption and monitoring of \200\230oxygen su pply:demand balance \200\231. Causes of acid-base disturbances pHd, PaCO2i Excess CO2 production and/or inadequate excretion, e.g. hypoventilation, excess narcotic. R eduction in PCO2 due to hyperventilation Usually lactic, keto, renal, or tubular. Consider tissue hypoperfusion, ingestion of acids (e.g. aspirin), loss of alkali (e.g. diarrhea, ren al tubular acidosis), diabetic ketoacidosis, and hyperchloraemia (e.g. from excess normal s aline administration). Consider excess alkali (e.g. bicarbonate or buffer infusion), loss o f acid (e.g. large gastric aspirates, renal), hypokalaemia, drugs (e.g. diuretics). Respiratory acidosis pHi, PaCO2d Respiratory alkalosis Metabolic acidosis pHd, PaCO2 l or d pHi, PaCO2 l or i Metabolic alkalosis BLOOD GAS ANALYSIS 155 Normal values pH PCO2 PO2 HCO3 ABE Arterial O2 saturation Mixed venous oxygen saturation 7.35 \200\2237.45 4.6 \200\2236kPa 10 \200\22313.3kPa 22 \200\22326mmol/L \200\2232.4 to + 2.2 95 \200\22398% 70 \200\22375% \200\223 pH 7.0 Metabolic acidosis Acute respiratory acidosis 7.2 Chronic respiratory acidosis Normal 7.4 Metabolic alkalosis Metabolic alkalosis 7.6 Respiratory alkalosis 0 2 4 6 8 10 PaCO2 (kPa) Fig. 8.4 Relationship between PaCO2 and pH in various acid-base disturbances. See also: Oxygen therapy, p38; Ventilatory support \200\224indications, p44; IPPV \200\224a djusting the ventilator, p50; Pressure and stroke volume vatriation, p190; Respiratory fail ure, p350; General acid-base principles, p500; Metabolic acidosis, p502; Metabolic alkalosi s, p504. 156 CHAPTER 8 Respiratory monitoring Extravascular lung water measurement Standard methods of assessing pulmonary oedema are ind irect. The chest X-ray allows only a qualitative assessment and is slow to change in respon se to clinical treatment. Assessment of cardiac \201 lling pressures does not take into a ccount the degree of capillary permeability or lymphatic adaptation. Consequently, a relati vely low CVP or PAWP may be associated with pulmonary oedema formation. High \201 lling p ressures in chronic heart failure may be associated with no oedema and be entirely appropri ate. Extravascular lung water (EVLW) measurement provides a technique for quantifying pulmo nary oedema and monitoring the response to treatment. Measurement technique The normal value of 4 \200\2237mL/kg for extravascular lung water has been derived by gravimetric techniques performed post-mortem. A double indicator technique can be used in patients whereby two indicators are injected vi a a central vein; one distributes within the vas- cular space and the other throughout the intra- and extra-vascular space. The volume of distribution of the indicators is derived fr om the dilution curves detected at the femoral artery. Cooled 5% glucose is used as a therm al indicator for intravascular and extravascular volume, and indocya- nine green bound to a lbumin as a colorimetric indicator for intravascular volume. Detection at the femoral arter y is by a \201 breoptic catheter with a thermistor tip. The cardiac output is measured by thermodilution at the femoral artery. The rate of exponential decay of the thermodilution curve allows deri- vation of the volume of distribution between the injection and detection sites (the heart and lungs). Pulmonary thermal volume = thermodilution cardiac output x rate of exponential decay of the rmodilution curve (intravascular and extravascular volume) Similar principles may be applied to the dye dilution curve produced on injection of indocy anine green which is assumed to distribute within the vascular space only. Pulmonary blood volume = dye dilution cardiac output x rate of exponential decay of dye dil ution curve (intravascular volume) EVLW may be calculated by subtracting pulmonary blood volume from pulmonary thermal volume. Limitations of EVLW measurement Since albumin can exchange across capillary membranes, pulm onary blood volume is over-estimated by this technique, and therefore, extravascular lung w ater is under-estimated. However, the corresponding error is small and not clinically signi \201 cant. A more serious drawback is in the limitation of treatment options. Treatment o f pulmonary oedema by diuresis and ultra \201 ltration have been shown to be less effectiv e at reducing EVLW in capillary leak from in \202 ammatory conditions compared to congesti ve heart failure. Similarly, the strategy of preventing oedema formation by diuresis while maintaining the circulation with catecholamine infusions appears to be futile; the vasocons triction so produced increases EVLW. EXTRAVASCULAR LUNG WATER MEASUREMENT 157 See also: Cardiac output \200\224central thermodilution, p178; Cardiac output \200\224perip heral thermodilution, p180; Acute respiratory distress syndrome (1), p360; Acute respirator y distress syndrome (2), p362. 158 CHAPTER 8 Respiratory monitoring Respiratory imaging Chest X-ray The chest X-ray has the advantage that it can be performed at the bedside of a critically ill patient. It yields much useful information on pathologie s within and outside the lung parenchyma (e.g. consolidation, pulmonary oedema, collapse, p leural effusion, pneumothorax); con \201 rmation of suitable positioning of intra-tracheal , intravascular, and naso-gatric/oesophageal tubes and catheters; soft tissue and bony abno rmalities; cardiac contour and size; vascular abnormalities (e.g. aortic diameter, oligaemi c lung \201 eld suggestive of a pulmonary embolus); and free air under the diaphragm. There are certain pitfalls that need to be appreciated: The position of the patient is usua lly supine (AP image) over- estimating ventricular dimensions and camou \202 aging the pre sence of a pneumothorax that sits in front of (or behind) normal lung tissue. Look for an \200\230inverted diaphragm \200\231 and increased lucency compared to the other lung. Under estimation of the size of pleural effusions or pneumothoraces. Lateral chest X-rays may be useful in diagnosing a pneumothorax that is not obviously appar ent on a supine \201 lm. Ultrasound Ultrasound can detect pleural or pericardial effusions, peripheral areas of cons olidated lung, and peripheral pneumothorax. It can also assist with intravascular line plac ement to minimize risk of arterial or lung puncture and drainage of \202 uid collections. CT scan CT scan is the de \201 nitive imaging procedure for pathology within the thorax. I njection of contrast highlights vascular structures and the pres- ence of pulmonary emboli in sub-segmental arteries (with high resolu- tion scanning). It enables improved discrimina tion of pulmonary shadows, e.g. \202 uid, \201 brosis, consolidation, atelectasis, absc ess, empyema, and can be used to guide drainage procedures of air and \202 uid collection s. RESPIRATORY IMAGING 159 See also: Airway obstruction, p348; Atelectasis and pulmonary collapse, p352; Acute chest i nfection (1), p356; Acute respiratory distress syndrome (1), p360; Asthma \200\224general m anagement, p364; Pneumothorax, p368; Haemothorax, p370; Pulmonary embolus, p376; Heart fail ure \200\224assessment, p392; Intrahospital transportation, p644. This page intentionally left blank 161 Chapter 9 Cardiovascular monitoring ECG monitoring 162 Blood pressure monitoring 164 Arterial cannulation 166 Central venous ca theter \200\224insertion 168 Central venous catheter \200\224use 170 Central venous cathete r \200\224complications 172 Pulmonary artery catheter \200\224insertion 174 Pulmonary arter y catheter \200\224use 176 Cardiac output \200\224central thermodilution 178 Cardiac output \200\224peripheral thermodilution 180 Cardiac output \200\224indicator dilution 182 Cardia c output \200\224Doppler ultrasound 184 Cardiac output \200\224pulse contour analysis 186 C ardiac output \200\224other techniques 188 Pressure and stroke volume variation 190 Echocar diography 192 Tissue perfusion monitoring 194 Gut tonometry 196 162 CHAPTER 9 Cardiovascular monitoring ECG monitoring Continuous ECG monitoring is routinely used in every Critical Care Unit. The standard technique is to display a three-lead ECG (commonly lead II). Other limb leads may be used although the electrodes are placed at the shoulders and left side of the abdomen. Other lead con \201 gurations can be used for speci \201 c purposes: \200 \200 \200 Chest \200\223shoulder \200\223V5: Early detection of left ventricular strain. Chest \200 \223manubrium \200\223V5: Early detection of left ventricular strain. Chest \200\223back \200\223V5: p wave monitoring. Modern monitors include alarm functions for bradycardia and tachycardia monitoring, and sof tware routines for arrhythmia detection or ST segment analysis. Causes of changes in heart rate or rhythm Changes in heart rate or rhythm may be an indicat ion of: \200 Increased sympathetic/parasympathetic activity: \200 \200 \200 \200 \200 \200 A dverse drug effects: \200 Antiarrhythmics. \200 Sedatives. Electrolyte imbalance. Fever . Circulatory insuf \201 ciency. Pain. Anxiety. Hypoxaemia. Hypercapnia. Sepsis. \200 ECG MONITORING 163 See also: Tachyarrhythmias, p384; Bradyarrhythmias, p386; Acute coronary syndrome (1), p388 ; Acute coronary syndrome (2), p390. 164 CHAPTER 9 Cardiovascular monitoring Blood pressure monitoring Non-invasive techniques Non-invasive techniques are intermittent but automated. They include oscillotonometry (detection of cuff pulsation as the systolic p ressure), detection of arterial turbulence under the cuff, ultrasonic detection of arterial wall motion under the cuff, and detection of blood \202 ow distal to the cuff. Any cuff system should use a cuff large enough to cover two thirds of the surface of the upper arm. Invasive (direct) arterial monitoring Blood pressure is most usefully monitored from larger limb arteries, e.g. femoral or brachial. However, because of the potential risk of damage to these arteries compromising the distal limb, it is generally safer to use radial, ulnar, or dorsalis pedis arteries. Pressure measured in a distal artery is higher than from a cen tral vessel. The arterial cannula is connected to an appropriate transducer system via a sh ort length of non-compliant manometer tubing. The transducer should be matched to the monit or, i.e. as recommended by the manufacturer of the monitor. The transducer must be zeroed t o atmospheric pressure and be positioned at the level of the 4th intercostal space in the m id-axillary line. The transducer, mano- meter tubing, and cannula should be continuously \202 ushed with 3mL/h saline or heparinised saline (1000IU/L). Damping errors A correctly damped system will return immediately to the pressure wave- form after \202 ushing. Return is slow in an over-damped system, and there is often resonance around the baseline before return to the pressure wave- form in an under-damped system. An under-damped system will over-esti- mate systolic and under-estimate diastolic blood press ure. The converse is true for an over-damped system. Waveform shape cannot be correctly int erpreted unless damping is correct. Interpretation of waveform The shape of the arterial pressure waveform gives useful qualita tive infor- mation about the state of the heart and circulation (see \201 gure 9.1): Shor t systolic time Hypovolaemia High peripheral resistance Hypovolaemia Pericardial effusion Airways obstructi on High intrathoracic pressure Poor myocardial contractility High peripheral resistance Marked respiratory swing Slow systolic upstroke Limitations of blood pressure monitoring It is important not to rely on arterial blood pres sure monitoring alone in the critically ill. A normal blood pressure does not guarantee ade quate organ blood \202 ow. Conversely, a low blood pressure may be acceptable if perfusio n pressure is adequate for all organs and blood \202 ow is high. Measurement of cardiac o utput and markers of organ perfusion, in addition to blood pressure, is necessary where the re is doubt about the adequacy of the circulation. BLOOD PRESSURE MONITORING 165 Normal arterial waveform BP Systolic time Short systolic time BP Systolic time Slow systolic upstroke BP Fig. 9.1 Examples of arterial waveform shape. See also: Arterial cannulation, p166; Hypotension, p380; Hypertension, p382. 166 CHAPTER 9 Cardiovascular monitoring Arterial cannulation Indications Performed correctly, arterial cannulation is a safe techni que allowing con- tinuous monitoring of blood pressure and frequent sampling of blood. It i s indicated in any patient with unstable or potentially unstable haemodynamic or respirator y status. Radial artery cannulation The radial artery is most frequently chosen because it is accessi ble and has good collateral blood \202 ow. Allen \200\231s test, used to con \201 rm the ulnar blood supply, is not reliable. Technique of cannulation Use aseptic technique. Hyperextend the wrist and abduct the thumb. After skin cleansing, local anesthetic (1% plain lidocaine) is injected into the skin and sub- cutaneous tissue over the most prominent pulsation. The course of the artery is noted and a 20G Te \202 on cannula inserted along the line of the vessel. The vessel is usually entered in similar fashion to an intravenous cannula. There is usually some resistance to s kin puncture. To avoid accidentally puncturing the poste- rior wall of the artery, the skin and artery should be punctured as two distinct maneuvers. Alternatively, a small skin nick may be made to facilitate skin entry. In the case of elderly patients with mobile, atherom atous vessels, a tech- nique involving deliberate trans \201 xation of the artery may be u sed. The cannula is passed through the anterior and posterior walls of the vessel, thus imm obilizing it. The needle is removed and the cannula withdrawn slowly into the vessel lumen before being advanced. Seldinger-type kits are available for arterial cannulation. A guidewire is \201 rst inser ted through a rigid steel needle. The indwelling plastic cannula is then placed over the gu idewire.