Humidi \201 cation during spontaneous breathing and mechanical ventilation With natural ai rways The upper airways ensure that inspired gasses are heated or cooled to body temperatur e (37 C) and humidi \201 ed to an RH of 100% at body temperature. More speci \201 cally , when inspired gasses arrive at the con- chae, turbulent \202 ow is created. The archite cture of the conchae consists of three turbinates covered by a folded mucous membrane, repr esenting a volume of only 20ml but a surface area of 160cm2. Therefore, each gas molecule i s likely to come into contact with the surface area of the vascular nasal mucous membrane. The moist mucous membrane heats inspired gasses to body temperature and, producing up 650 \200\2231000ml of H2O per day, brings inspired gasses to an RH of 80% on leaving the nose t o enter the nasopharynx. Mucus produced in the nasal cavity is also responsible for the hum idi \201 cation of inspired gasses Heat and moisture exchangers (HMEs) This system, which is placed close to the patient at th e end of the dead space, preserves the water vapor contained in the gas exhaled by the pati ent. During the subsequent inspiration, the water maintained in the HME is used to humidify the inspired gas. There are two types of HME: hygroscopic and hydropho- bic. The ef \201 ciency of these two types of HME is quite simi- lar, close to 70%. Hydrophobic HMEs can \201 lter bacteria. Contraindications of HME \200 \200 Thick, copious or bloody secretions Leaks in the circuit creating an expired tidal volume < 70% of the inspired tidal volume. Patients with a body temperature <32 C High minute volum es (>10l/min) With arti \201 cial airways The gas arriving from the ventilator is cold (15 C) and dry ( 2% RH), and the ETT bypasses the physiological humidi \201 - cation and heating of inspire d gasses. Absence of humidi \201 ca- tion induces alterations in mucus transportation, dec reased mucus clearance, lesions of the epithelium and mucosa, and changes in ventilatory pa rameters (decreased compli- ance and functional residual capacity, increased resistance). T herefore, artificial devices must be installed during mechanical ventilation. There is a re lationship between air- way mucosal dysfunction and the combination of inspired gas humidit y and temperature with exposure time to a given humidity An arti \201 cial humidi \201 er replaces the humidifying function of the upper airways by increasing the water vapor conte nt of a dry gas. \200 Comparison between active and passive humidi \201 ers Le Bourdell s et al. observed a sig ni \201 cant decrease in alveolar ventilation with HMEs (as indicated by an increase in mi nute ventilation and respiratory rate, but an increase in PaCO2) in comparison with heated humidi \201 ers during weaning from mechanical ventilation in a pressure support mode. The se observations should be taken into account during dif \201 cult weaning . Other authors reached the same conclusions. HME sin- crease work of breathing (WOB), respiratory rate and minute ventilation in pressure support in comparison with heated humidi \201 ers. On the basis of these observations, one may recommend increasing the level of pressure sup- port ( by 5 \200\22310cm H2O) to maintain the WOB constant. For all these reasons, HME is not reco mmended for patients with COPD. In non-COPD patients receiving prolonged mechanical ventila tion, Ricard et al. compared a group of patients where the HME was changed every 48h with a group with a change after 7 days. There was no difference in resistance Humidi \201 ers There are two types of humidi \201 er: active and passive. Active humidi \201 ers add water vapor to inspired gasses, whereas passive humidi \201 ers exchange hea t and moisture by preserving the moisture and heat in the gas exhaled by the patient. Active humidi \201 ers Active humidifiers consist of a humidity generator (or water reserv oir) and humidity delivery system (or 47 CHAPTER 1.21 Humidi \201 cation During weaning from mechanical ventilation in pressure support mode and in NIV, HMEs are no t recommended because of increases in dead space, PaCO2 and WOB, unless one signi \201 can tly increases the pressure support level. Passive and active devices seem to be equivalent in terms of ef \201 cacy and prevention of infection. in the ETT or in infection, indicating that the HME can be changed only once a week, which represents a substantial cost saving. Nevertheless, few studies have studied the problem of the reduction in diameter of the ETT. Two different methods have been used (measurement of internal pressure and \202 ow along the tube, and an acoustic re \202 ection method), a nd both concluded that there was a progressive reduction in ETT patency with active and pas sive humidi \201 cation, but this occurred to a greater extent with HMEs than with active humidi \201 ers. The effect of these systems on the incidence of VAP is con- troversial. T hree recent reviews or meta-analyzes reached different conclusions: Ricard et al. and Ni l -Weise et al. concluded that the type of humidi \201 cation device does not in \202 uence the incidence of VAP. If an active humidi \201 er is used, Ni l-Weise et al. recommended using a heated wire circuit because less condensate reduces colonization. On the other han d, Kola et al. reported a signi \201 cant reduction in the occurrence of VAP with HMEs, pa rticularly for patients ventilated for >7 days, but they excluded patients at high risk of airway occlusion (COPD). Finally, in NIV, if humidi \201 cation is mandatory (i.e. with an ICU ventilator using cold and dry gasses), a heated humidi- \201 er is recommended over HMEs because HMEs decrease the bene \201 cial effects of NIV on WOB. Further reading Jaber S, Pigeot J, Fodil R, et al. Long-term effects of different humid- i \201 cation systems on endotracheal tube patency: evaluation by the acoustic re \202 ecti on method. Anesthesiology 2004; 100: 782 \200\2238. Kola A, Echmanns T, Gastmeier P. Ef \201 cacy of heat and moisture exchangers in preventin g ventilator-associated pneumonia: meta- analysis of randomized controlled trials. Intensiv e Care Med 2005; 31: 5 \200\22311. Le Bourdell s G, MierL, Fiquet B, et al. Comparison of the effects of heat and moisture ex changers and heated humidi \201 ers on ventila- tion and gas exchange during weaning trial s from mechanical ventilation. Chest 1996; 110: 1294 \200\2238. Ni l-Weise BS, Wille JC, van den Broeck PJ. Humidi \201 cation policies for mechanically ventilated intensive care patients and prevention of ventilator-associated pneumonia: a sys tematic review of rand- omized controlled trials. J Hosp Infect 2007; 65: 285 \200\22391. Ricard JD, Boyer A, Dreyfuss D. The effect of humidi \201 cation on the incidence of venti lator-associated pneumonia. Respir Care Clin N Am 2006; 12: 263 \200\22373. Ricard JD, Le Mi re E, Markowicz P, et al. Ef \201 ciency and safety of mechanical ventil ation with a heat and moisture exchanger changed only once a week. Am J Respir Crit Care Me d 2000; 161: 104 \200\2239. Conclusions Regardless of their type, humidifiers are essential for mechanically ventilated patients. For at risk patients (e.g. COPD, copious secretions, etc.), one may prefer activ e humidi \201 ers with heated wire circuits. Villafane MC, Cinnella G, Lofaso F, et al. Gradual reduction of endotracheal tube diameter during mechanical ventilation via different humidification devices. Anesthesiology 1996; 85 : 1341 \200\2239. 48 M PINSKY Heart \200\223lung interactions Introduction The respiratory system and the cardiovascular systems are not separate, but ti ghtly integrated. ARF can directly alter cardiovascular function, and vise versa. Many of t hese effects are predictable from knowledge of cardiovascular function. Both lung underinfl ation and hyperinflation increase pulmonary vascular resistance, heart \200\223lung inter- actions and the work of breathing. Both spontaneous inspiratory efforts during acute bronch ospasm and acute lung injury induce markedly negative swings in intratho- racic pressure (I TP). Arti \201 cial ventilatory support increases ITP during inspiration, in contradistinc tion to spontaneous ventilation which will decrease ITP for the same tidal breath. Heart \200\223lung interactions involve four basic concepts: inspiration increases lung volume, s pontaneous inspiration decreases ITP, positive pressure ventilation increases ITP, and vent ilation is exercise, i.e. it consumes O2 and produces CO2. transpulmonary pressure more than pulmonary artery pressure. Reversing hyperin \202 ation by any means decreases pulmonary arterial pressure, improving RV ejection. The use of small er tidal volumes and less positive end-expira- tory pressure has reduced the incidence of a cute cor pul- monale seen in critically ill patients. LV end-diastolic volume (preload) can be altered by ventilation by decreasing venous return, RV dilation-induced decreased LV di astolic compliance (ventricular interdependence) and by cardiac compression by the expandin g lungs. Haemodynamic effects of changes in intrathoracic pressure The heart within the chest is a pressure chamber within a pressure chamber. Changes in ITP affect the pressure gra- dients for systemic venous return to the RV and systemic outflow f rom the LV independent of the heart itself. Increases in ITP reduce these pressure gradient s decreas- ing intrathoracic blood volume. Decreases in ITP augment venous return and imped e LV ejection, increasing intratho- racic blood volume. Variations in right atrial pressure rep- resent the major factor determining the \202 uctuation in pressure gradient for sys temic venous return during venti- lation. Increases in ITP with positive-pressure ventilati on or hyperin \202 ation during spontaneous ventilation decrease venous return, whereas de creases in ITP during spontane- ous inspiration increase venous return. LV afterload or sys tolic wall tension is proportional to the product of transmural systolic LV pressure and LV volume. Thus, increasing ITP will decrease transmural LV pressure if arterial pressure is constant; increases in ITP unload the LV, whereas decreases in ITP have the opposite effect . Increases in ITP actually may increase cardiac output in congestive heart failure states. Spontaneous ventilatory efforts against a resistive (bronchospasm) or elastic (acute lung injury) load decrease LV stroke volume manifest as pulsus paradoxus by ventricular interdep endence and increased LV afterload. Increases in ITP have the opposite effect, decreasing L V afterload. Although increases in ITP should augment LV ejection by decreasing LV afterloa d, this effect is limited because of the obligatory decrease in venous return. There is no difference from a mechanical perspective between increasing ITP from a basal end-expiratory level Haemodynamic effects of changes in lung volume Lung in \202 ation alters autonomic tone an d pulmonary vascu- lar resistance, and, at high lung volumes, compresses the heart, limitin g \201 lling, similar to cardiac tamponade. The associated diaphragmatic dissent increase s abdominal pressure, compressing the liver and altering venous return. Each of these proce sses may predominate in determining the \201 nal cardiovascular state. Small tidal volume (<10ml/ kg) inspiration increase heart rate by vagal withdrawal, called respiratory sinus arrhythmia. Larger tidal volumes (>15ml/kg) decrease heart rate, arterial tone and cardiac contractility by sympathetic withdrawal. The major determinants of the haemodynamic respons e to increases in lung volume are mechanical in nature. Lung in \202 ation, independently of changes in ITP, primarily alters right ventricular (RV) preload and afterload and left v entricular (LV) preload. First, inspiration induces diaphrag- matic dissent which increases abdominal pressure. Venous return is a function of the ratio of the pressure difference be tween the right atrium and the systemic venous reser- voirs and the resistance to venous re turn. Since a large proportion of the venous blood volume is in the abdomen, abdominal pres sure increases should augment venous blood \202 ow. Diaphragmatic descent also compresses the liver, increasing hepatic out \202 ow resistance thus decreasing venous blood \202 ow. Thus, inspiration shifts venous \202 ow from high resistance splanchnic circuits drai ning through the liver, to low resistance systemic venous circuits, making venous return gr eater for the same blood volume. Thus, increasing lung volume may increase or decrease veno us return depending on which factors predominate. Usually, inspiration increases venous ret urn in volume-overloaded states and decreases venous return in hypovolaemic and hepatic cir rhotic states. End-expiratory lung volume also determines alveolar stability. Alveolar coll apse increases pulmonary vasomotor tone by hypoxic pulmonary vasoconstriction. Alveolar rec ruitment reverses this process, although during the recruitment maneuvers, the associated h yperin \202 ation may impair RV function. Increasing lung volume above the FRC also increa ses RV out \202 ow resistance by increasing ESPVR Increased LV ejection pressure ITP ) g H m m Decreased LV ejection pressure ( e r u s s e r p V L ITP Increased LV preload Decreased LV preload Diastolic compliance LV volume (mL) Fig 1.22.1 Normal cardiac function. 49 CHAPTER 1.22 Heart \200\223lung interactions to interpose venous return (end-diastolic volume) and afterload (end-systolic volume). Thus , performing an endotracheal intubation in patients with obstructive breathing abolishes th e markedly negative swings in ITP without reducing venous return. and eliminating negative end-inspiratory ITP swings seen in spontaneous ventilation. Removi ng negative swings in ITP may be more clinically relevant than increasing ITP for many reas ons. First, many pulmonary diseases are associ- ated with exaggerated decreases in ITP duri ng inspiration. In restrictive lung disease states, such as interstitial \201 brosis or a cute hypoxaemic respiratory failure, ITP must decrease greatly to generate a large enough t ranspulmonary pressure to ventilate the alveoli. Similarly, in obstructive diseases, such a s upper airway obstruction or asthma, large decreases in ITP occur owing to increased resis tance to inspiratory air \202 ow. Secondly, exaggerated decreases in ITP require increased respiratory efforts that increase the work of breathing, taxing a potentially stressed cir culation. Finally, the exaggerated decreases in ITP can only increase venous blood \202 o w so much before venous collapse limits blood \202 ow. The level to which ITP must decrea se to induce venous \202 ow limitation is different in different circulatory conditions b ut occurs in most patients below an ITP of \200\223 10cm H2O. Thus, further decreases in I TP will further increase only LV afterload without increasing venous return. Abolishing the se markedly negative swings in ITP reduces LV afterload more than venous return (LV preload ). These concepts of a differential effect of increasing and decreasing ITP on cardiac func tion are illustrated for both normal and failing hearts in Figs 1.22.1 and 1.22.2 using the LV pressure \200\223volume relationship during one cardiac cycle Ventilation as exercise Spontaneous ventilatory efforts are exercise, requiring increased b lood \202 ow and O2, and produce CO2. In lung disease states where the work of breathing is increased, the work cost of breathing may increase to 25% or more of total O2 delivery, limiting exercise capacity, inducing coronary ischaemia and leading to weaning failure. Sta rting arti \201 cial ventilation will decrease O2 extraction, increasing SvO2 for a consta nt cardiac output and CaO2. Under conditions in which \201 xed right-to-left shunts exist , the obligatory increase in SvO2 will result in an increase in the PaO2, despite no change in the ratio of shunt blood \202 ow to cardiac output. Further reading Buda AJ, Pinsky MR, Ingels NB, et al. Effect of intrathoracic pressure on l eft ventricular performance. N Engl J Med 1979; 301: 453 \200\2239. Butler J. The heart is in good hands. Circulation 1983; 67: 1163 \200\2238. Kaneko Y, Flora s JS, Usui K, et al. Cardiovascular effects of continu- ous positive airway pressure in pat ients with heart failure and obstructive sleep apnea. N Engl J Med 2003; 348: 1233 \200\223 41. Nielson J, Ostergaard M, Kjaegaad J, et al. Lung recruitment maneu- ver decreases central h aemodynamics in patients after cardiac surgery. Intensive Care Med 2005; 31: 1189 \200\2239 4. Pinsky MR, Matuschak GM, Klain M. Determinants of cardiac augmentation by increases in intr athoracic pressure. J Appl Physiol 1985; 58: 1189 \200\22398. ESPVR Increased LV ejection pressure ) g H m m Taylor RR, Covell JW, Sonnenblick EH, et al. Dependence of ventricular distensibility on \201 lling the opposite ventricle. Am J Physiol 1967; 213: 711 \200\2238. Decreased LV ejection pressure ( e r u s s e r p V L Van den Berg P, Jansen JRC, Pinsky MR. The effect of positive- pressure inspiration on veno us return in volume loaded post- operative cardiac surgical patients. J Appl Physiol 2002; 92: 1223 \200\22331. Increased LV preload ITP Decreased LV preload Diastolic compliance Viellard-Baron A, Schmitt JM, Augarde R, et al. Acute cor pulmonale in acute respiratory di stress syndrome submitted to protective ventilation: incidence, clinical implications, and prognosis. Intensive Care Med 2001; 29: 1551 \200\2238. LV volume (mL) Fig. 1.22.2 Congestive heart failure. This page intentionally left blank 51 Chapter 2 Cardiovascular therapy techniques Chapter contents De \201 brillation 52 Temporary cardiac pacing 54 Intra-aortic balloon counterpulsation pu mp 56 Cardiac assist devices 58 Therapeutic cooling 60 52 J NOLAN De \201 brillation De \201 brillation is the delivery of suf \201 cient electrical current to depolarize a c ritical mass of myocardium and enable restoration of coordinated electrical activity. All d e \201 brilla- tors have three features in common: \200 \200 For ventricular arrhythmias, place electrodes (either pads or paddles) in the conventional sternal \200\223apical (AP) position. Anteroposterior electrode placement may be more effec tive than the AP position in elective cardio- version of atrial \201 brillation (AF). Sel f-adhesive de \201 brillation pads are preferable to stand- ard de \201 brillation paddle s. a power source capable of providing direct current a capacitor that can be charged to a pre -determined energy level two electrodes which are placed on the patient \200\231s chest thr ough which the capacitor is discharged. CPR vs de \201 brillation as the initial treatment After out-of-hospital cardiac arrest, i f response times exceed 4 \200\2235min, a period of 2min of CPR before shock delivery may i mprove survival compared with immediate de \201 brillation. After in-hospital cardiac arre st, response times should be much less than 5min \200\224if a shockable rhythm is identi \201 ed, give a shock immediately. De \201 brillation is de \201 ned as the termination of \201 brillation or, more precis ely, the absence of ventricular \201 brillation/ven- tricular tachycardia (VF/VT) at 5s a fter shock delivery; however, the goal of attempted de \201 brillation is to restore spont aneous circulation. De \201 brillation is a key link in the chain of survival and is one o f the few interventions that have been shown to improve outcome from VF/VT cardiac arrest. The likelihood of suc- cessful de \201 brillation diminishes rapidly with any delay in sho ck delivery. Automated external de \201 brillators (AEDs) have microprocessors that analyz e several features of the ECG, including frequency and amplitude \200\224the user does not need to be able to interpret the ECG. Manual de \201 bril- lators rely on the user interpr eting the rhythm and deter- mining if a shock is appropriate. One-shock vs three-shock sequence There are no published human studies comparing a single- shock protocol with a three-stacked-shock protocol for treatment of VF cardiac arrest. The 2005 CPR guidelines included a single-shock protocol followed by immediate resumption of CP R for the following reasons: \200 The time taken to deliver three shocks (up to 1min) results in prolonged interruptions to c hest compres- sions, which affects outcome adversely. Modern, biphasic de \201 brillators have a \201 rst shock ef \201 cacy of >90% \200\224failure to de \201 brillate implies that the quality of VF is poor. Two minutes of high-quality CPR may make the VF \200\230mo re shockable \200\231. Immediately after a successful shock, despite ROSC (return of sponta neous circulation), the pulse may not be palpable \200\224at this stage, 2min of CPR will m aintain some coronary and cerebral blood \202 ow while the myo- cardial contractility pic ks up. If the shock has not been successful, any time spent feeling for a pulse represents a period of zero blood \202 ow. Quality of CPR By incorporating a force transducer in a sternal compres- sion pad and measu ring transthoracic impedance, some de \201 brillators can provide real-time feedback on co mpression depth and rate, and ventilation volume and rate. This improves the quality of CPR and may improve outcome. Strategies before de \201 brillation Safe use of oxygen during de \201 brillation In an o xygen-enriched atmosphere, sparking from poorly applied de \201 brillator paddles can caus e a \201 re. This can be minimized by taking the following precautions. \200 Waveforms and energy levels \200 All modern defibrillators deliver a biphasic shock: the current direction is reversed midwa y through shock delivery. First-shock ef \201 cacy for long duration VF/VT is greater with biphasic (86 \200\22398%) than monopha- sic waveforms (54 \200\22391%); however, a long-te rm survi- val advantage with biphasic de \201 brillators has yet to be demonstrated. Bipha sic devices have smaller capacitors and need less battery power. They are smaller, lighter and easily portable. Many biphasic de \201 brillators are impedance-compensat- ing. i.e. t he output is adjusted depending on the tran- sthoracic impedance. Although energy levels ar e selected for de \201 brillation, it is the transmyocardial current \202 ow that achiev es de \201 - brillation. Current correlates well with the successful de \201 brillation a nd cardioversion. The optimal current for de \201 brillation using a monophasic waveform i s in the range of 30 \200\22340amps. Indirect evidence from measure- ments during cardiover sion for AF suggests that the cur- rent during de \201 brillation using biphasic waveforms is in the range of 15 \200\22320amps. Optimal energy levels for both monophasic and biphas ic waveforms are unknown. The recommended energy levels vary between manufacturers, partly because the Take off any oxygen mask or nasal cannulae and place them at least 1m away from the patient \200\231s chest. Leave the ventilation bag connected to the tracheal tube or disconnect an d remove it at least 1m from the patient \200\231s chest during de \201 brillation. If the patient is connected to a ventilator, leave the ven- tilator tubing connected to the trach eal tube unless chest compressions prevent the ventilator from deliver- ing adequate tidal volumes. Minimize the risk of sparks during defibrillation. Theoretically, self-adhesive de \201 brillation pads are less likely to cause sparks than manual paddles. The technique for electrode contact with the chest An optimal de \201 brillation technique aims to deliver current across the \201 brillating myocardium in the presence of mini- m al transthoracic impedance. Transthoracic impedance varies considerably with body mass, but is 70 \200\22380 \204 in adults. \200 A very hairy chest may cause poor electrode \200\223skin elec- trical contact and high impe dance \200\224with minimal delay, rapidly shave off excess hair. If using manual paddles, a pply \201 rm force (8kg) to reduce impedance. 53 CHAPTER 2.1 De \201 brillation CHAPTER 00 Chapter title Cardioversion If electrical cardioversion is used to convert atrial or ven- tricular tachya rrhythmias, the shock must be synchronized to occur with the R wave of the electrocardiogra m rather than with the T wave: VF can be induced if a shock is deliv- ered during the relat ive refractory portion of the cardiac cycle. Synchronization can be dif \201 cult in VT be cause of the wide-complex and variable forms of ventricular arrhyth- mia. If synchronizatio n fails, give unsynchronized shocks to the unstable patient in VT to avoid prolonged delay in restoring sinus rhythm. precise waveform varies between different de \201 brillators. Although higher energy level s might cause more myo- cardial injury, the earlier conversion to a perfusing rhythm may ou tweigh this risk. In general, the energy level for the \201 rst shock with a biphasic de \201 brillator should be 150 \200\223200J. If using a mono- phasic de \201 brillator, del iver the \201 rst and subsequent shocks at 360J. Subsequent shocks can be given at the sa me energy level ( \201 xed) or at a higher (escalating) energy level. The strat- egy used will depend on the manufacturer \200\231s recommen- dations and the setting available on th e de \201 brillator. Both strategies are acceptable; however, if the \201 rst shock is n ot successful and the de \201 brillator is capable of deliv- ering shocks of higher energy , it is rational to increase the energy for subsequent shocks. Atrial \201 brillation Biphasic waveforms are more effective than monophasic waveforms fo r cardioversion of AF. \200 When using a monophasic de \201 brillator for cardioversion of AF, start with 200J, and in crease stepwise as neces- sary. With a biphasic de \201 brillator, use an initial shock of 120 \200\223 150J, escalating if necessary. Manual de \201 brillation The sequence for using a de \201 brillator in manual mode is de scribed. Because of the interruption in chest compres- sions caused by automatic rhythm ana lysis, shock advisory or AED mode should be used only by those unfamiliar with rhythm inter pretation. 1 Con \201 rm cardiac arrest clinically and con \201 rm VF from the monitor or from adhesive pads or the de \201 brillator paddles. Atrial \202 utter and paroxysmal supraventricular tachycardia Atrial \202 utter and par oxysmal supraventricular tachycardia generally require less energy than AF for cardioversio n. Give an initial shock of 100J monophasic or 70 \200\223120J bipha- sic waveform. Give su bsequent shocks using stepwise increases in energy. 2 Place self-adhesive pads or de \201 brillator gel pads on patient \200\231s chest \200 \224one below the right clavicle and one in the V6 position in the midaxillary line. If usi ng de \201 brilla- tor paddles, place them \201 rmly on gel pads. Ventricular tachycardia The energy required for cardioversion of VT depends on the morpholo gical characteristics and rate of the arrhyth- mia. \200 3 Select correct energy level: 150 \200\223200J biphasic (360J monophasic) for \201 rst s hock and 150 \200\223360J biphasic (360J monophasic) for subsequent shocks. Ventricular tachycardia with a pulse responds well to cardioversion using initial monophasi c energies of 200J. Use biphasic energy levels of 120 \200\223150J for the initial shock. I ncrease stepwise if the \201 rst shock fails to achieve sinus rhythm. 4 Ensure that high \202 ow oxygen is not passing across the zone of de \201 brillation 5 Charge self-adhesive pads or de \201 brillator paddles. 6 Warn everyone to \200\230stan d clear \200\231 and deliver shock. 7 Without reassessing the rhythm or feeling for a pulse , start CPR using a ratio of 30:2, starting with chest com- pressions. Further reading Anonymous. 2005 International Consensus on Cardiopulmonary Resuscitation an d Emergency Cardiovascular Care Science with Treatment Recommendations. Part 3: de \201 br illation. Resuscitation 2005; 67, 203 \200\22311. 8 Continue CPR for 2min, then pause brie \202 y to check the monitor. Deakin CD, Nolan JP. European Resuscitation Council guidelines for resuscitation 2005. Sect ion 3. Electrical therapies: automated external de \201 brillators, de \201 brillation, c ardioversion and pacing. Resuscitation 2005; 67 Suppl 1: S25 \200\22337. 9 If VF/VT, deliver a second shock. 10 Continue CPR for 2min, then pause brie \202 y to ch eck the monitor. 11 If VF/VT persists, give adrenaline 1mg IV followed by a third shock and 2min CPR. If the adrenaline is not ready, do not delay the shock \200\224the adrenaline can be given after the shock. Nolan J, Soar J, Lockey A, et al Advanced life support, 5th edn. Resuscitation Council (UK), London, 2006. Wik L, Hansen TB, Fylling F, et al. Delaying de \201 brillation to give basic cardiopulmon ary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized t rial. JAMA 2003; 289: 1389 \200\22395. 12 Repeat this sequence if VF/VT persists. 13 Give further adrenaline 1mg IV after alternat e shocks (i.e. approximately every 3 \200\2235min). 14 After three shocks, consider amiodarone 300mg IV. 15 If organized electrical activity is seen during the pause to check the monitor, feel for a pulse. a. If pulse is present, start post-resuscitation ca re. b. If no pulse is present, continue CPR and switch to the non-shockable algorithm. 16 If asystole is seen, continue CPR and switch to the non- shockable algorithm. 54 D HAUSENLOY Temporary cardiac pacing \200 Put on a lead apron, and a sterile gown and gloves. Obtain central venous access (see Chapt er 7.3). The right internal jugular vein offers easiest access to the right ventricle and i s the recommended approach. The right subclavian vein is the most comfortable for the patie nt. The right femoral vein should be considered if the above fail. Insert a venous sheath t hat is one size larger than the pacing wire, which is usually 5F or 6F in size. Right ventr icular lead placement: from the right atrium, advance the pacing wire across the tricuspid valve and into the right ventricle. If it does not cross the tricuspid valve, rotate it so that it faces the lateral wall of the right atrium and forms a loop, and then prolapse the loop into the right ventricle. Entering the right ventricular out \202 ow tract and then w ithdrawing the pacing wire will allow the tip to position in the apex. Maintain some slack in the pacing wire. Right atrial lead placement: on entering the right atrium, the pre-form ed \200\230J \200\231 shape of the atrial pacing wire should reform. Rotate the pacing wir e and position the tip in the right atrial appendage. Connect the pacing wire(s) to the pac ing box and check for stability of the pacing wire(s) by asking the patient to cough, sniff and take some deep breaths. Exclude dia- phragmatic pacing. Obtain a CXR to exclude a pneu mothorax and check the position and integrity of the pacing wire(s). The atrial pacing wire should face anteriorly and loop upwards on a lateral CXR. The ventricular pacing wire shou ld resemble the outline of a \200\230sock \200\231 on a postero-anterior (PA) CXR. Temporary cardiac pacing provides a potentially life-saving measure for supporting the hear t in patients with haemo- dynamic compromise due to a disturbed conducting sys- tem. Depend ing on the particular indication for temporary cardiac pacing and the availability of suita ble equipment and skilled personnel, there exist several types of tempo- rary cardiac pacin g. Indications for temporary cardiac pacing The setting of an acute myocardial infarction (AMI ) \200 \200 Asystole, 2nd or 3rd degree atrioventricular (AV) block with symptoms , New trifascicular b lock,. 2nd or 3rd degree AV block without symptoms but fol- lowing an anterior AMI. \200 Not related to an AMI \200 \200 \200 \200 Asystole. 2nd or 3rd degree AV block with symptoms. Sinus or junctional bradycardia with sy mptoms. Tachyarrhythmias secondary to bradycardia. Overdrive suppression of tachyarrhythmias \200 To prevent or treat Torsade de Pointes. Prophylactic temporary cardiac pacing Pre-operative patient with symptoms and: \200 \200 Sinus node disease or 2nd degree AV block (type I). Bifascicular/trifascicular block. Pre-operative patient without symptoms and: \200 2nd degree (type II) or 3rd degree AV block. Complications of transvenous pacing These include pneumothorax, haemothorax, infection, ina dvertent arterial puncture, non-sustained VT as the pac- ing wire is maneuvered across the tricuspid valve, throm- boembolism with pulmonary embolism, and myocardial perforation with cardiac tamponade. The setting of cardiac surgery \200 \200 Valvular surgery (especially tricuspid and aortic). Ventricular septal defect (VSD) closure or ostium pri- mum repair. Biatrial pacing to reduce post-operative AF. Temporary transoesophageal cardiac pacing This approach obviates the requirement for centra l venous access or sterile precautions, and may be considered when \202 uoroscopy is unav ailable. It comprises a transoesophageal pulse generator and gelatine bipolar pill electrod es (for the oral route) or transoesophageal pacing catheters (for the nasal route). During the replacement of a permanent pacemaker and rarely for right coronary artery angiop lasty. Types of temporary cardiac pacing Temporary transcutaneous cardiac pacing This non-invasive approach is used if temporary trans- venous cardiac pacing is not immediately available. S elf- adhesive electrode pads are placed on the left anterior chest between the xiphoid proc ess and the left nipple, and posteriorly below the left scapula and spine. These are attach ed to the external pulse generator. Conscious patients should be given sedation to minimize discomfort. Temporary epicardial cardiac pacing This involves directly stimulating the epicardium of th e atria and/or ventricle using electrodes sutured to the epi- cardium at the time of cardia c surgery. The pacing wires are pulled through an incision in the skin and secured to the e xternal chest wall. By convention, the atrial wires and the ventricular wire exit from the right and left side of the sternum, respectively. Infection, myocardial damage and/or perfo ration, tamponade and disruption of coronary anas- tomoses are the recognized complications . Temporary transvenous cardiac pacing This procedure requires suitable equipment and skilled personnel as stipulated by American Heart Association guidelines. Cannulation of a central vein allows a pacing wire to be placed in the right ventricle and/or the right atrium unde r \202 uoroscopic guidance. Where \202 uoroscopy is unavailable, pacing wires can be pl aced using balloon- tipped catheters. Setting the pacemaker up \200 Check the pacemaker box has a fresh battery and ensure the connections are secure and corre ct. Turn the pacemaker box on and set the pacing rate at 90 \200\223110bpm for cardiac surg ery, 50bpm for sinus rhythm and 70 \200\22390bpm for heart block or bradycardias. The procedure \200 Check that the \202 uoroscopy equipment, pacemaker box and de \201 brillator are functio ning properly. 55 CHAPTER 2.2 Temporary cardiac pacing Troubleshooting The absence of pacing spikes on the ECG This may be due failure to pace whe n the intrinsic rate is less than the pacing rate. Or it may be because the intrinsic rate is greater than the set pacemaker rate. Determine the capture threshold Capture describes the ability of the electrical impulse to initiate a myocardial depolarization. \200 Turn the pacemaker rate to 10bpm above the intrinsic rate and increase the pacemaker output to 3V. Slowly decrease the output until loss of capture occurs, then increase it until cap ture reoccurs after every pacer spike. This is the capture threshold (aim for <1.0 and <1.5 V for ventricular and atrial wires, respectively). Set output at 2 \200\2233 times the thre shold or at 3V, whichever is higher. Reset the pacemaker to the prescribed rate. Failure to pace This describes the failure of the pacemaker box to deliver an electrical im pulse, and is indicated by the absence of pacing spikes when the intrinsic heart rate is le ss than the pacemaker rate. See checklist below. Failure to capture This describes the failure of an electrical impulse to initiate a myocar dial depolarization, and is revealed by the failure of an appropriately timed pacing spike to be followed by either a \200\230P \200\231 wave or a widened \200\230QRS \200\231 comp lex. The capture threshold often doubles in the \201 rst few days due to endo- cardial oe dema. Therefore, try increasing the output to restore capture. Determine the sensitivity threshold Sensitivity refers to the ability of the pacemaker to d etect intrinsic myocardial activity. The sensitivity dial indicates the minimum voltage tha t the pacemaker is able to sense. Therefore, decreasing the sensitivity dial actually incre ases pacemaker sensitivity, and vise versa. \200 \200 Set the pacing rate at 10bpm below the intrinsic rate. Lower the pacemaker output to 0.1V t o prevent com- petitive pacing. Increase the sensitivity dial until the sense indicator sto ps \202 ashing and the pace indicator starts \202 ashing. Slowly decrease the sensitivi ty dial until the sense indica- tor \202 ashes continuously. This value is the sensing th resh- old. Set the sensitivity dial at half the sensitivity threshold value. If there is no underlying rhythm and sensitivity cannot be determined, set the sensitivity dial at 2mV. R eset pacemaker to prescribed rate. Failure to sense or undersensing This describes the failure of the pacemaker to detect intr insic myocardial activity. It is indicated by regular pacing spikes unrelated to the intrin sic rhythm, which may or may not capture. Try decreasing the sensitivity dial (thereby incr easing pacemaker sensitivity). Inappropriate or oversensing This describes the situation where the pacemaker is misin- ter preting skeletal activity or \200\230P \200\231 and \200\230T \200\231 waves as \200\230 QRS \200\231 complexes, and is inhibiting pacemaker activity, causing bradycardic episodes. Try increasing the sensitivity dial (thereby decreasing pacemaker sensitivity). Pacemaker mode and variables \200 VVI for ventricular pacing only. \200 DDD for dual-ch amber pacing, allowing AV sequential pacing, which may bene \201 t patients with a low car diac output state or those patients with a \200\230stiff \200\231 left ventricle. The thre e letter code corresponds to the chamber paced ( \200\230V \200\231 for ventricle and \200 \230D \200\231 for dual chamber), the chamber sensed and the response to sensing ( \200\230 I \200\231 means pacing is inhibited on sensing intrinsic myocar- dial activity). AV interv al ( 150ms): this is the time interval between a paced or sensed event in the atrium and a paced event in the ventricle. Upper rate limit ( 135bpm): this is the maximum rate the vent ricles will pace at, as determined by tracking the atrial rate. PVARP (post-ventricular atr ial refractory period, 300ms): this time interval limits how early after a paced or sensed ventricular beat an atrial event can trigger a ventricular paced event.