Non-pulmonary Critical Care - part 3 ppsx

and PR intervals. MAT is most often associated with hypoxia in the setting of pulmonary disease but may occasionally be due to use of theophylline, metabolic derangements, and end-stage cardiomyopathy. Treat- ment consists of correcting hypoxia by either or both treating underlying pulmonary disease and correcting electrolyte abnormalities. 26 AV nodal blockers are some- times useful to control the ventricular response in the interim. WIDE COMPLEX TACHYCARDIA The most frequently reported tachyarrhythmia in the ICU setting is a wide complex tachycardia. The first step in treatment is establishing the diagnosis because VT is more ominous than SVT with aberrancy. VT is defined by three or more consecutive ventricular beats. Sustained VT is defined as more than 30 seconds of ventricular beats at a rate of more than 100 bpm. 27,28 Initial evaluation should include obtaining a 12-lead ECG, and measurement of serum potassium, calcium, and magnesium. The ECG should be examined and compared with prior ECGs with attention to QRS width in sinus rhythm, prior Q waves that may indicate prior myocardial infarction (MI), the presence of delta waves, as well as the QT interval. A careful review of medications is para- mount in excluding iatrogenic causes of VT. VT can be diagnosed using some clinical and electrocardiographic clues, as outlined following here: 1. Play the odds. VT is approximately four times more common than SVT with aberrancy. In one study of 200 consecutive patients with a wide QRS tachycardia, 164 were ventricular, 30 were SVT with aberrancy, and six were SVT with antegrade conduction. 29 2. Ask the right qu estions. VT is much more common in patients who have a history of MI or heart failure. 3. Do not rely on hem odynamics alone . C irculatory col- lapseismorecommonwithVTthanwithSVT,but patients with VT may maintain a normal blood pressure. 4. Do not count on AV dissociation. This is present in less than 50% of cases of VT and is difficult to identify at faster heart rates. 5. Do not count on irregularity. Regularity was identified in 90% of patients with SVT versus 78% with VT. 30 Other clues are useful in distinguishing VT from SVT. A QRS width of more than 0.14 seconds with right bundle branch block or 0.16 seconds during left bundle branch bloc k favors VT. 31 Comparison of QRS morphology during the tachycardia with the morphology of ventricular premature beats in sinus rhythm can be helpful. Other diagnostic clues suggestive of VT are fusion and capture beats, but these are seen in only 20 to 30% of cases of VT. 32 Fusion beats, a hybrid of the supraventricular and ventricular complexes, occur when two impulses, one supraventricular and one ventricular, simultaneously activate the same territory of ventricular myocardium. The implication is that the wide complexes are ventricular. Capture beats are occasional beats con- ducted with a narrow complex, and such beats rule out fixed bundle branch block. It is better to err on the side of overdiagnosis of VT. The potential consequences of misdiagnosis were demonstrated in a study analyzing adverse events in- curred by patients with VT misdiagnosed as SVT and given calcium channel bloc kers. 33 Many of the patients promptly decompensated and some required resuscitation. Interestingly, all of these patients were hemody- namically stable when first seen in VT. NONSUSTAINED VENTRICULAR TACHYCARDIA This common clinical problem, occurring equally in women and men, is usually asymptomatic, with an incidence of 0 to 4% in the general population. 34,35 A major determinant of prognosis is the presence or absence of underlying structural heart disease. The Baltimore Longitudinal Study of Aging screened patients aged 60 to 85 years old for cardiovascular disease and followed them for 10 years; nonsustained ventricular tachycardia (N SVT) did not predict coronary events in this population. 36 Therefore, in asymptomatic patients with NSVT, a thorough history and physical examina- tion, echocardiography, and stress testing are usually sufficient to exclude prognostically significant structural heart disease. Patients with symptoms of palpitations, syncope, or presyncope should undergo further evaluation to exclude episodes of sustained VT or other arrhythmias. Patients who have NSVT with structural heart disease (coronary heart disease, dilated cardiomyopathy, or valvular heart disease) require more comprehensive evaluation and management. As will be discussed here, the prognosis of NSVT following a myocardial MI is dependent upon the timing of onset of VT in relation to the incident MI. NSVT occurring in the first 48 hours of an MI is most likely related to reperfusion or ischemia and has no prognostic significance. However, NSVT occurring more than 1 week after MI doubles the risk of sudden cardiac death (SCD) in patients with preserved left ventricular function. 37 The risk of SCD is increased more than fivefold in patients with left ventricular dysfunction (ejection fraction less than 40%). 38 The risk of SCD is greatest in the first 6 months post-MI and persists for up to 2 years. NSVT is present in up to 80% of patients with an idiopathic dilated cardiomyopathy (ejection fraction [EF] < 40%). 39 The current American College of Cardiology/American Heart Association guidelines CARDIAC ARRHY THMI AS I N THE I CU /TARDITI, HOLLENBERG 225 recommend implantation of an internal cardiac defibrillator (ICD) for nonsustained VT in patients with coronary disease, prior MI, LV (left ventricular) dysfunction, and inducible VF or sustained VT at electrophysiological study that is not suppressible by a class I antiarrhythmic drug. 40 Initial treatment of NSVT in the setting of dilated cardiomyopathy should include correction of electrolyte abnormalities, removal of exacerbating factors (hypoxia, dehydration, medications, vasopressors, etc.), and up titration of b-blockers. Mitral and aortic valve disease is associated with NSVT, occurring in up to 20% of patients with mitral valve prolapse (MVP) and $ 5% of patients with aortic stenosis. In both severe mitral regurgitation and aortic stenosis, NSVT does not appear to be associated with increased risk of SCD. 41–43 In patients at high risk as already described, further evaluation is warranted. This may include cardiac catheterization, electrophysiological testing, and/or sig- nal-averaged ECG. MONOMORPHIC VENTRICULAR TACHYCARDIA Monomorphic VT in the setting of a normal QT interval usually occurs from a fixed substrate (i.e., scar) rather than acute ischemia. The importance of m onomorphic VT depends on the clinical milieu in which it occurs and on the presence of underlying structural heart disease. Sustained monomorphic VT, either with or without acute ischemia, portends a worse prognosis even after hospital discharge. 44 The approach to treatment of sustained monomorphic VT is based on the presence of hemodynamic instability and/or other clinical factors (heart failure, pulmonary congestion, shortness of breath, decreased level of consciousness, or myocardial ischemia). If any are present, then synchronized cardioversion is indicated. Stable or recurrent monomorphic VT can be treated with lidocaine, procainamide, or amiodarone. The next step in evaluation and management of the patient is dependent on left ventricular function. If left ventricular function is normal and the patient is not in heart failure, treatment with procainamide, amiodarone, lidocaine, or sotalol is recommended. The choices are limited to amiodarone or lidocaine in those with impaired left ventricular function (EF < 40%). Amiodar- one can be given as a 150 mg IV bolus over 10 minutes followed by an infusion of 360 mg (1 mg/min) over 6 hours, and then 540 mg (0.5 mg/min) over the remain- ing 18 hours. The maximum total dose is 2.2 g over 24 hours. Bradycardia and hypotension can result from IV amiodarone, in which case the rate of the infusion should be decreased. Lidocaine is administered by IV bolus of 0.5 to 0.75 mg/kg, followed by continuous infusion at 1 to 4 mg/min. Procainamide is administered at 20 mg/ min IV for a loading dose of 17 mg/kg, then continued as an infusion at 1 to 4 mg/min. The infusion should be stopped if the patient becomes hypotensive or the QRS widens by 50% above baselin e. The most serious side effects of pro cainamide are hypotension and proarrhythmia (most commonly torsades de pointes), both of which increase in frequency in patients with renal insufficiency because of decreased excretion. If the QTc is longer than 500 msec the drug should be stopped immediately and the QTc followed closely. Cimetidine and amiodarone can increase levels of procainamide and its metabolite N- acetyl procainamide. 45 Measurement of serum levels may be useful, especially in patients with renal insufficiency. In patients with transvenous or epicardial pacemakers, overdrive antitachycardia pacing is an option. The ventricular pacing rate should be $10 to 20 bpm faster than the VT. Absent a reversible cause, an implantable cardioverter-defibrillator (ICD) should be considered in patients with recur rent monomorphic VT and an ejection fraction less than 40% or a history of syncope. POLYMORPHIC VENTRICULAR TACHYCARDIA Polymorphic VT with a normal QT interval is considered to be an ischemic rhythm that typically degenerates into VF. It is almost never asymp tomatic and thus DC synchronized cardioversion is the initial recommended treatment. Polymorphic VT with a normal QTc is a more ominous sign than monomorphic VT in patients with myocardial ischemia. Medications that might pre- dispose to ischemia, such as inotropes or vasopressors, should be stopped or tapered, if possible, and b-blockers started if blood pressure permits. Intraaortic balloon pumping may be useful as a supportive measure, but revascularization is usually required. If withdrawal of vasopressors is contraindicated on a clinical basis, IV infusion of lidocaine or amiodarone should be initiated. TORSADES DE POINTES Torsades de pointes is a French term translated as ‘‘twist- ing of the points.’’ It is a syndrome composed of polymorphic VT and a prolonged QTc interval (by definition ! 460 millisecondsec). This may be due to various medications, including procainamide, disopyra- mide, sotalol, phenothiazines, quinidine, some antibi- otics (erythromycin, pentamidine, ketoconazole), some antihistamines (terfenadine, astemizole), and tricyclic antidepressants. Other etiologies include hypokalemia, hypocalcemia, subarachnoid hemorrhage, congenital prolongation of the QTc interval, and insecticide poisoning. 46 A key to treatment is correction of any exacerbating factors and normalization of electrolyte disturbances, particularly hypomagnesemia, hypocalcemia, and hypokalemia. Magnesium should be given 1 to 2 g IV push over 30 to 60 minutes. Other potential treatments may include overdrive pacing or isoproterenol to increase heart rate and thus shorten QTc. Admin- istration of sodium bicarbonate IV can be useful to 226 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006 antagonize the proarrhythmic effects of class I antiarrhythmics. 47 WOLFF-PARKINSON-WHITE SYNDROME (VENTRICULAR PREEXCITATION) AVRT using an accessory bypass tract, WPW, occurs in 0.1 to 0.3% of the general population. An accessory pathway bypass tract (bundle of Kent), bypass es the AV node and can activate the ventricles prematurely in sinus rhythm, producing the characteristic delta wave. The diagnosis of WPW is reserved for patients with both preexcitation and tachyarrhythmias. In AVRT conduction can go down the bypass tract and back up the AV node, producing a wide QRS complex (antidromic) or down the AV node and back up the bypass tract, producing a narrow QRS complex (orthodromic). AVRT should be suspected in any patient whose heart rate exceeds 200 bpm. AF is a potentially life-threat- ening arrhythmia in patients with WPW syndrome because it can generate a rapid ventricular response with subsequent degeneration into VF. This is important because one third of patients with WPW syndrome have AF. 48 Adenosineshouldbeusedwithcautioninany young patient suspected of having WPW because it may precipitate AF with a rapid ventricular response rate down an antegrade accessory pathway. Procaina- mide, ibutilide, and flecainide are preferred agents because they slow conduction through the bypass tract. The long-term treatment of choice for symptomatic patients is radiofrequency catheter ablation of the accessory pathway. ELECTRICAL STORM The definition of an electrical storm is more tha n three distinct episodes of VT/VF within a 24-hour period. 49 In patients with ventricular arrhythmias requiring ICD implantation, the incidence of ventricular storm ranges from 10 to 30%. 50,51 According to one study, the event occurred at an average of 133 Æ 135 days after ICD implantation. Precipitating factors (hypokalemia, myocardial ischemia, and heart failure) were identified in only 26% of the patients in one study. Evaluation should include measurement of serum electrolytes, obtaining an ECG, an d further evaluation for ischemic heart disease, which may include coronary angiography. Proarrhythmia secondary to antiarrhythmic drugs that prominently slow conduction velocity, such as flecainide, propafenone, and moricizine, should be excluded. 52,53 Treatment for proarrhythmia is hemodynamic support until the drug is excreted. If exacerbating factors (acute heart failure, electrolyte abnormalities, proarrhythmia, myocardial ischemia, and hypoxia) are corrected, repeated doses of IV amiodarone should be given, even if the patient is already on oral amiodarone. 54 Deep sedation can help reduce sympathetic activation. Mechanical ventilatory support and IV b-blockers can be used in conjunction, but IV amiodarone is the pharmacological treatment of choice for this condition. If pharmacological therapy and antitachycardia pacing are unsuccessful, electro- physiology mapping–guided catheter ablation can be considered, although this is often difficult in unstable patients. 55 The prognosis of patients with electrical storm after ICD implantation is poor, with a 2.4-fold increase in the risk of subsequent death, independent of ejection fraction. The risk of SCD is greatest 3 months after an electrical storm. BRADYARRHYTHMIAS AND PACING Asymptomatic bradyarrhythmias do not carry a poor prognosis and in general no therapy is indicated. 56 Recommended initial therapy for bradycardia inducing end organ perfusion problems is atropine IV 1.0 mg. The presence of syncope, heart failure, or other symptoms accompanying bradycardias is an indication for pacemaker implantation. Third degree or advanced heart block with either symptomatic bradycardia, pauses ! 3 sec, or heart rate < 40 bpm is also an indication for pacemaker insertion. Class I indications (general agree- ment that a treatment is beneficial) for temporary transvenous pacing after an acute MI are listed here: 1. Asystole 2. Symptomatic bradycardia 3. Bilateral bundle branch block (BBB) a. Alternating BBB or right BBB (RBBB) with alternating left anterior fascicular block (LAFB)/ left posterior fascicular block (LPFB) 4. New or indeterminate age bifascicular block with first-degree AV block a. RBBB with LAFB or LPFB b. Left BBB (LBBB) 5. Mobitz type II second-degree AV block REFERENCES 1. Imrie JR, Yee R, Klein GJ, Sharma AD. Incidence and clinical significance of ST segment depression in supraventricular tachycardia. Can J Cardiol 1990;6:323–326 2. Tebbenjohanns J, Pfeiffer D, Schumacher B, Jung W, Manz M, Luderitz B. Intravenous adenosine during atrioventricular reentrant tachycardia: induction of atrial fibrillation with rapid conduction over an accessory pathway. Pacing Clin Electrophysiol 1995;18:743–746 3. Pelleg A, Pennock RS, Kutalek SP. 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Interventions on prevention of postoperative atrial fibrillation in patients undergoing heart surgery: a meta-analysis. Circu- lation 2002;106:75–80 24. Stebbins D, Igidbashian L, Goldman SM, et al. Clinical outcome of patients who develop atrial fibrillation after coronary artery bypass surgery [abstract]. PACE 1995;18:798 25. Gage BF, Waterman AD, Shannon W, Boechler M, Rich MW, Radford MJ. Validation of clinical classification schemes for predicting stroke: results from the National Registry of Atrial Fibrillation. JAMA 2001;285:2864–2870 26. Wang K, Goldfarb BL, Gobel FL, Richman HG. Multifocal atrial tachycardia. Arch Intern Med 1977;137:161–164 27. Wagner G. Marriott’s Practical Electrocardiography. Phila- delphia, PA: Lippincott Williams and Wilkins; 2001 28. Shenasa M, Borggrefe M, Haverkamp W, Hindricks G, Breithardt G. Ventricular tachycardia. Lancet 1993;341: 1512–1519 29. Wellens HJ, Brugada P. Diagnosis of ventricular tachycardia from the 12-lead electrocardiogram. 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Cardiac arrhythmias in a healthy elderly population: detection by 24-hour ambulatory electrocardiography. Chest 1982;81:302–307 37. Anderson KP, DeCamilla J, Moss AJ. Clinical significance of ventricular tachycardia (3 beats or longer) detected during ambulatory monitoring after myocardial infarction. Circula- tion 1978;57:890–897 38. Buxton AE, Marchlinski FE, Waxman HL, Flores BT, Cassidy DM, Josephson ME. Prognostic factors in nonsustained ventricular tachycardia. Am J Cardiol 1984;53:1275– 1279 39. Larsen L, Markham J, Haffajee CI. Sudden death in idiopathic dilated cardiomyopathy: role of ventricular arrhythmias. Pacing Clin Electrophysiol 1993;16:1051–1059 40. Gregoratos G, Abrams J, Epstein AE, et al. ACC/AHA/ NASPE 2002 guideline update for implantation of cardiac pacemakers and antiarrhythmia devices: summary article: a report of the American College of Cardiology/American 228 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006 Heart Association Task Force on Practice Guidelines (ACC/ AHA/NASPE Committee to Update the 1998 Pacemaker Guidelines). Circulation 2002;106:2145–2161 41. Kligfield P, Levy D, Devereux RB, Savage DD. Arrhythmias and sudden death in mitral valve prolapse. Am Heart J 1987; 113:1298–1307 42. Kligfield P, Hochreiter C, Niles N, Devereux RB, Borer JS. Relation of sudden death in pure mitral regurgitation, with and without mitral valve prolapse, to repetitive ventricular arrhythmias and right and left ventricular ejection fractions. Am J Cardiol 1987;60:397–399 43. Wolfe RR, Driscoll DJ, Gersony WM, et al. Arrhythmias in patients with valvar aortic stenosis, valvar pulmonary stenosis, and ventricular septal defect: results of 24-hour ECG monitoring. Circulation 1993;87:I89–101 44. Newby KH, Thompson T, St ebbins A, Topol EJ, Califf RM, Natale A. Sustained ventricular arrhythmias in patients receiving thrombolytic therapy: incidence and outcomes. The GUSTO Investigators. Circulation 1998;98:2567– 2573 45.TrujilloTC,NolanPE.Antiarrhythmicagents:drug interactions of clinical significance. Drug Saf 2000;23:509– 532 46. Kossmann CE. Torsade de pointes: an addition to the nosography of ventricular tachycardia. Am J Cardiol 1978;42: 1054–1056 47. Banai S, Tzivoni D. Drug therapy for torsade de pointes. J Cardiovasc Electrophysiol 1993;4:206–210 48. Campbell RW, Smith RA, Gallagher JJ, Pritchett EL, Wallace AG. Atrial fibrillation in the preexcitation syndrome. Am J Cardiol 1977;40:514–520 49. Exner DV, Pinski SL, Wyse DG, et al. Electrical storm presages nonsudden death: the antiarrhythmics versus implantable defibrillators (AVID) trial. Circulation 2001;103: 2066–2071 50. Greene M, Geist M, Paquette M, et al. Long-term follow-up of implantable defibrillator therapy in patients with electrical storm [abstract]. Pacing Clin Electrophysiol 1997;20:1207 51. O’Donoghue S, Patia EV, Waclawski S, et al. Transient electrical storm: prognostic significance of very numerous automatic defibrillator discharges [abstract]. J Am Coll Cardiol 1997;17:352A 52. Passman R, Kadish A. Polymorphic ventricular tachycardia, long Q-T syndrome, and torsades de pointes. Med Clin North Am 2001;85:321–341 53. Tschaidse O, Graboys TB, Lown B, Lampert S, Ravid S. The prevalence of proarrhythmic events during moricizine therapy and their relationship to ventricular function. Am Heart J 1992;124:912–916 54. Kowey PR. An overview of antiarrhythmic drug management of electrical storm. Can J Cardiol 1996;12(Suppl B):3B–8B; discussion 27B–28B 55. Brugada J, Berruezo A, Cuesta A, et al. Nonsurgical transthoracic epicardial radiofrequency ablation: an alternative in incessant ventricular tachycardia. J Am Coll Cardiol 2003; 41:2036–2043 56. Gregoratos G, Cheitlin MD, Conill A, et al. ACC/AHA guidelines for implantation of cardiac pacemakers and antiarrhythmia devices: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Pacemaker Implanta- tion). J Am Coll Cardiol 1998;31:1175–1209 CARDIAC ARRHY THMI AS I N THE ICU /TARDITI, HOLLENBERG 229 Evaluation and Management of Shock Olivier Axler, M.D., Ph.D., F.C.C.P. 1 ABSTRACT Shock is one of the most frequent situations encountered in the intensive care unit (ICU). Important new concepts have emerged for shock management in recent years. The concept of early goal-directed therapy has evolved from the basic management concepts for septic shock delivered in a structured fashion. Numerous cardiovascular techniques, methods, and strategies have been developed as novel alternatives to the use of the pulmonary artery catheter. Among these techniques, echocardiography, esophageal Dop- pler, and arterial pulse contour analysis show great promise. Prediction of responsiveness to fluid administration is a key component of the management of shock, as is assessing cardiovascular performan ce. The intensivist has several options to evaluate and treat shock. Further research should yield additional important advances. KEYWORDS: Shock, cardiovascular protocols, cardiovascular techniques; central venous pressure; pulmonary arterial catheter Shock is a common cause of admission in any intensive care unit (ICU) and also occurs frequently during the course of critical illness. Shock is associated with significant morbidity and mortality and represents a medical emergency. Early, targeted therapy is crucial; the first hour of care may be key to a successful outcome. 1,2 Therefore, it is important that physicians are aware of updated concepts and management guidelines for treating patients with shock. Although the principles of shock management are well established, there is consid- erable heterogeneity of bedside management. This heterogeneity is apparent not only with accurate clinical identification of a shock state 3 but also in regard to evaluation and therapy. Critical care societies and other experts have published evidence-based guidelines for diagnostic criteria and therapeutic strategies 4–8 ; however, these recommendations generally fo- cus on severe sepsis and septic shock. This article reviews the traditional criteria and current guidelines for management of shock, the traditional and newer diagnostic and monitoring techniques, and therapeutic strategies. OVERVIEW, DEFINITIONS, AND DIAGNOSIS OF SHOCK Shock is traditionally defined by multisystem organ hypoperfusion, whatever its specific cause, leading to common physical signs. It can also be defined as an inability to assure adequate cellular and tissue oxygen supply and removal of waste products of cellular metab- olism, thus overwhelming the compensatory mechanisms of the organism. The presentation of shock may be obvious but can also be latent and incomplete, leading to a delayed diagnosis, potentially worsening the prognosis and de- creasing chances of reversal. The clini cian must be familiar with different clinical patterns of shock and the pathophysiological aspects of shock, including cardiovascular (ven tricular pressure–volume curves, cardiac function curves), biochemical (oxygenation cascades), and immunological (mediators and cytokine cascades) features. The clinical signs and symptoms of shock have been known for years 9 and have been presented in 1 Cardiology Department, Centre Hospitalier Territorial Gaston Bourret, Noumea, New Caledonia, France. Address for correspondence and reprint requests: Olivier Axler, M.D., Ph.D., F.C.C.P., Cardiology Department, CHT Gaston Bourret, 98800 Noumea, New Caledonia, France. E-mail: olivier. axler@canl.nc. Non-pulmonary Critical Care: Managing Multisystem Critical Illness; Guest Editor, Curtis N. Sessler, M.D. Semin Respir Crit Care Med 2006;27:230–240. Copyright # 2006 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. DOI 10.1055/s-2006-945526. ISSN 1069-3424. 230 comprehensive reviews. 1,10 Several points are worthy of emphasis. First, the diagnosis must be made quickly, followed by classification of type of shock. Second, the sensitivity and specificity of each sign are highly variable. Third, the quantitative aspects of these signs are useful but vary depending upon the clinical circumstances. The first step is to begin the correct resuscitation measures, not only to achieve therapeutic goals but also to confirm the diagnosis. Depending on the response to the therapeutic intervention, the diagnos is can be confirmed or corrected, allowing adjustment of treatment. In its complete clinical presentation, shock classically includes: tachypnea; tachycardia; low systolic, diastolic, and mean blood pressures (BPs); diaphoresis; poorly perfused skin and extremities; cyanosis; mottling of cool and moist extremities; altered mental status (ranging from decreased state of consciousness to agi- tation); and decreased urine output. Joly and Weil emphasized the role of the ‘‘cold great toe,’’ 11 whereas we have not ed that cold knees have an excellent diagnostic specificity and sensitivity for shock (unpub lished data). However, these signs are not always present con- comitantly, and some of these features may be absent or borderline. For instance, in classical shock, BP is decreased, and a commonly accepted threshold for a resuscitation goal in septic shock is 65 mm Hg for mean arterial pressure (MAP). 6 However, not all hypotensive states are associated with shock, and not all shocks present with hypotension. In fact, some shock states present with high BP at the onset because of the adaptive adrenergic response. Early septic shock is classically ‘‘hyperdynamic,’’ with increased pulse pressure and warm extremities. In addition, low BP is relative to the baseline BP for a given patient. Invasively measured BP using an intra-arterial catheter is more accurate than cuff measuremen ts. 12 Chronotropic medications, or sinus or atrioventricular dysfunction, can blunt the tachycardic response. Oliguria is often defined as urine output less than 0.5 mL/kg/hr. 6 From a laboratory standpoint, blood lactate is a robust clue of shock arising from cellular and tissue hypoxia, 3 and precedes acidemia. This was recently confirmed, 2 with a threshold of 4 mmol/ L consistent with shock. However, the specificity of blood lactate is imperfect because any condition exceeding the aerobic threshold leads to increased lactate levels, and some metabolic conditions increase lactate levels without shock (i.e., any sympathetic activation). 13 Tissue hypercapnia is known to correlate well with decreased blood flow. 14 The first organ to be studied was the gastric mucosa, but this technique has largely been abandoned. Sublingual PCO 2 has emerged as a good predictor of shock (irrespective of cause), and in some studies was superior to blood lactate levels and mixed venous oxygen saturation (SVO 2 ) or central venous oxygen saturation (SCVO 2 ). 15,16 TRADITIONAL AND NEWER METHODS AND TECHNIQUES TO ASSESS MECHANISMS OF SHOCK Several simple tools used in the initial management of shock (e.g., electrocardiogram; chest radiographs; routine hospital chemistries; blood gases) are well known and will not be further discussed here. In this section, invasive and noninvasive techniques to assess hemodynamics are discussed. Measurement of central venous pressure (CVP) or pulmonary artery pressure (PAP) may be useful to classify the mechanism of shock. Further, measurement of SCVO 2 [via a catheter in the superior vena cava (SVC)] or mixed SVO 2 (via a pulmonary arterial catheter) may be useful to diagnose and monitor the impact of therapeutic interventions in patients with shock. 17 Arterial pulse contour techniques are used to measure cardiac output (CO), and requires arterial access. 18,19 This technique is incorporated in more sophisticated devices, measuring other parameters as preload with an estimation of fluid responsiveness for the LiDCO plus System (LiDCO Ltd., Cambridge, UK) via a pulse power analysis. 18–20 Another system, PiCCO (Pulsion Medical Systems AG, Munich, Germany) also measures intrathoracic volumes and extravascular lung water from transpulmonary indica- tor dilution. 21,22 This latter technique mandates fem- oral arterial and central venous access, whereas the former requires only a radial artery and a peripheral vein. Analysis of the systemic systolic pressure, pulse pressure and stroke volume (SV), and their respiratory variations, provides an excellent assessment of preload and estimation of fluid responsiveness. 19 Ultrasound techniques that are useful to assess fluid status and cardiac function include esophageal Doppler 23 and echocardiography (transthoracic and transesophageal). 24 Methods such as monitoring splanch- nic blood flow or monitoring the microcirculation with videomicroscopy have been utilized in research investiga- tions but have no or limited clinical utility. Traditional Methods CENTRAL VENOUS PRESSURE MONITORING Although CVP was recently shown to be somewhat inaccurate to assess preload, 25,26 CVP, when integrated into an algorithm, was a useful parameter to guide volume administration in a cohort of septic patients. 2 However, CVP measurements should be interpreted with caution, even at low or high values, when the value is used in isolation. 10,25–28 Some authors emphasize the need to incorporate the cardiac and venous return curves for a correct interpretation of CVP. 29,30 Indeed, the basic concept espoused is to use CVP with simultaneous measurement of cardiac output. In a study of 33 ICU patients, the right atrial pressure (RAP) decreased at least 1 mm Hg EVALU A TION AN D MANAGE M ENT OF SHOCK/AXLER 231 with inspiration [with a decreased pulmonary artery oc- clusion pressure (PAOP) of at least 2 mm Hg with inspiration] and increases in CO of  250 mL/min. 30 This analysis can differentiate ‘‘relative hypovolemia’’ (or more accurately a fluid responsive state) from euvolemia. This concept was discussed in a recent excellent review. 31 Despite the low reliability of CVP to assess preload, this parameter continued to be widely measured by 93% of a cohort of European intensivists in 1998. 32 CENTRAL VENOUS OXYGEN SATURATION (SCVO 2 ) The O 2 saturation in a central vein (most often the SVC) was recently shown to be a key component of early goal- directed therapy in the emergency department (ED) 2 ; values < 70% are consistent with incomplete resuscitation. This parameter is less useful after several days of severe critical illness and severe tissue oxygenation defi- cit. 17,33,34 A low SVO 2 generally reflects low CO because oxygen extraction by the tissues is greater in cardiac failure. 34,35 Low SCVO 2 is also associated with a poor prognosis 34 and often appears earlier than any other clinical sign of shock. 2 In a cohort of patients with septic shock, Rivers and colleagues demonstrated mortality reduction of 15% by maintaining a therapeutic algorithm that maintained the following parameters: SCV O 2 > 70%; CVP > 8 to 12 mm Hg; MAP > 65 mm Hg; urine output > 0.5 mL/kg/h. 2 SCVO 2 and SVO 2 are usually similar but can diverge in some cases, particularly in severe sepsis, due to greater O 2 extraction in the hepatosplanchnic circulation. However, SCVO 2 is preferred to SVO 2 because it can be measured more simply from a central venous catheter rather than a pulmonary artery catheter (PAC). 36–38 SCVO 2 can be continuously monitored using a special catheter or intermittently by direct repeated samples. SCVO 2 correlates with outcome in all kinds of shock, even during cardiopulmonary resuscitation. 17,33,34 The research by Rivers and colleagues addressed very early shock, 2 and studies have not demonstrated benefit for patients later in the course of shock when oxygen extraction may be impaired and SCVO 2 exceeds 80%. 17,33,34 PULMONARY ARTERY CATHETERS The PAC has been used to differentiate various mechanisms of shock since the early 1970s, but utilization of data from PACs has many pitfalls. First, hemodynamic values are frequently misinterpreted, leading to incorrect treatment. 37,38 Second, recent studies found that the use of PAC did not confer any benefit compared with no PAC use 36,39,39a,39b ; further, some studies suggested deleterious effects of PACs, particularly in patients presenting with acute respiratory distress syndrome (ARDS) or shock. 35,36,39 However, PAC-directed therapy was shown to be cost effective in the preoperative period. 40–43 In North America, there continues to be relatively wide- spread use of PACs, 6 whereas newer techniques such as ICU echocardiography 24,44 and pulse contour analysis techniques (PiCCO and LiDCO) 18,19,21,22 have sup- planted PACs in most European ICUs. Despite the limitations of PACs, recent guidelines (e.g., the Survival Sepsis Campaign) continue to recommend PACs for the assessment of severe sepsis and septic shock. 6 More- over, a recent paper focusing on ‘‘practice parameters for hemodynamic support of sepsis in adult patients’’ favors the use of PACs, and states that ‘‘echocardiography may also be useful to assess ventricular volumes and cardiac performance.’’ 7 Several measured and derived values are available from a PAC to deter mine the mechanism of shock: PAP, PAOP, right ventricular pressure (RVP) and RAP, CO by thermodilution, and its modified deriva- tives: (1) semicontinuous cardiac output (using a thermal coil in the right ventricular portion of the PAC; (2) calculation of right ventricular end-diastolic volume (RVEDV) from measurement of right ventricular ejection fraction (RV EF); SVO 2 and related oyge nation variables; oxygen consumption (VO 2 ); oxygen delivery (DO 2 ); and O 2 extraction ratio (O 2 ER). Measurement of PAP is a very important parameter to diagnose pulmonary arterial hypertension (PAH) as may be seen in ARDS, pulmonary embolism, right ventricular infarction, obstructive lung disease, left heart diseases, and primary PAH. Its measurement is generally easy and its interpretation is the least problematic of all PAC-derived data. Using the PAOP is one of the most controversial issues related to PAC. Classically, hypovolemic shock has low right and left heart filling pressures, whereas left ventricular cardiogenic shock is associated with elevated PAOP and RAP. Historically, PAOP has been considered to provide information regarding preload and the presence or absence of pulmonary edema. However, measurement and interpretation of PAOP may be difficult. 37,38,45 The utility of PAOP to assess volume status has recently been challenged 25,26,46 ; this is also true for RAP. 25,26,46 This can be explained by a frequent absence of linearity between left ventricular end-diastolic volume (LVEDV) and left ventricular end-diastolic pressure (LVEDP); second, disparity between LVEDP and PAOP may exist. The LVEDV/LVEDP relationship can be profoundly modified by LV compliance factors such as left ventricular hypertrophy (LVH), myocardial ischemia, positive end-expiratory pressure (PEEP), and active exhalation. Further, PAOP can overestimate LVEDP if mitral stenosis or mitral regurgitation are present, and conversely underestimates LVEDP when diastolic dysfunction or hypervolemia exist. These conditions are frequent in patients presenting with shock but are often not appreciated. Thus PAOP should be interpreted cautiously. 45 Notwithstanding these pitfalls, 58% of European intensivists continued to measure PAOP as part of monitoring critically ill ICU patients in 1998. 32 232 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006 Measurement of CO is one of the most important issues in the management of shock. 1,47–49 Thermodilu- tion is the gold standard method for measuring CO for clinical use because measurement is relatively straight- forward and does not present the same technical diffi- culties as PAOP. Additionally, the thermodilution technique was validated against electromagnetic flow, Fick, and dye dilutions techniques. However, thermodilution has important limitations. Specifically, thermodilution can overestimate CO in low output states, whereas significant tricuspid regurgitation leads to underestimation of CO. Other confounding issues include intracardiac shunts and temperature issues. 47 In this context, echocardiography is helpful. Recently, the left ventricular outflow tract (LVOT) pulsed Doppler method has been employed as an alternative method to measure CO. 49,50 Some authors believe that this should become the new gold standard 49,50 unless significant aortic valve disease exists. Cardiac output can be monitored with a modified PAC. This PAC incorporates a thermal coil in the right ventricular portion of the catheter, and conti nuous CO measurement is based on the delivery of electrically generated heat to the blood near the right atrium and ventricle and the resulting temperature change in the PA. This technique avoids performing an intermittent injection and yields a continuous CO display. The accuracy is good compared with thermodilution, provided regular calibration is performed. 51 Recent refinements of the PAC allow calculation of RVEF. This catheter has a rapid-response thermo ‘‘slur’’ and intracardiac electrocardiogram electrode, allowing the calculation of RVEF. Combined with SV, the RVEF allows the calculation of right ventricular end diastolic volume (RVEDV). This parameter has been extensively studied in circulatory shock, 52,53 but in the most important studies comparing RVEDV before and after a fluid challenge, significant difference was found in only one of 15 studies. 53 Intraindividual changes in RDEDV with various treatments are more useful than absolute values. 25,52,54 Continuous fiberoptic measurement of SVO 2 , coupled with traditional PAC parameters, is available with some catheters. Finally, the relationship of oxygen delivery/consumption ratio (DO 2 /VO 2 ) has been used for both research and clinical indications among critically ill patients for more than 3 decades. 55 However, awareness and incorporation of these variables into clinical protocols have not been shown to influence outcome. 55 Newer Methods ECHOCARDIOGRAPHY-DOPPLER Cardiac ultrasound (echocardiography) has increasingly been utilized in ICUs within the past few years. Trans- thoracic echocardiography (TTE) is noninvasive and relatively easy to perform after an adequate training. Transesophageal echocardiography (TEE) is modestly invasive and requires some degree of sedation for patient comfort but is safe and highly accurate. Echocardiog- raphy provides an excellent assessment of cardiac fun c- tion and estimates left and right heart filling pressures and can be useful to determine the cause of shock. 56 Echocardiography provides acceptable estimates of most parameters gleaned from pulmonary artery catheters (PACs) (i.e., CO; right arterial pressure (RAP) from inferior vena cava (IVC) size and ventilatory variations, systolic pulmonary artery pressure (SPAP); left and right ventricular filling pressures; ejection fraction; ventricular interdependence; right heart function; diastolic dysfunction; left ventricular hypertrophy (LVH); ischemic heart disease, valvular diseases, and so on). Recent publications emphasized the value of echocardiography to predict fluid responsiveness using heart–lung interactions ba- sics. 57–65 Many studies have shown that echocardiography (either TTE or TEE) may be invaluable to monitor therapeutic interventions or hemodynamic changes in critically ill patients. 62–80 TEE is more useful than TTE for this purpose. 66–79 In most of the studies, TEE provided clinically useful information in 60 to 90% of cases. More importantly, TEE had a direct favorable impact on the acute care management. 79 Our recent experience with TTE has been favorable (unpublished data). The value of TTE was recently underscored in a study by Joseph et al, who noted clinically useful and reliable information in 70 to 80% of critically ill ICU patients who had TTE. 80 Recent improvement in imaging, software, and electronic systems have improved the quality and utility of images gleaned from TTE. Transthoracic echocardiography is useful as a diagnostic tool for critically ill patients in shock (or impending shock) but in some cases, TEE is necessary for a more accurate assessment. 79 Specific indications for TEE include: aortic dissection (when computed tomographic angiography is inconclusive, or to complete it if necessary); endocarditis (especially when a valvular prosthesis is present); complicated cardiac surgery; marked obesity; poor echogenicity with TTE; intracavitary thrombi; and cardiac sources of emboli. TEE is the preferred method to assess the SVC size and its ventilatory variations, a new powerful parameter to predict fluid volume responsiveness. 64 In a patient with shock, echocardiography (usually TTE) can provide prompt (within 15 minutes) assessment of critical variables, including size of cardiac chambers; left and right systolic function; cardiac output (49); wall motion abnormalities; valvular pathology; LV filling pressures from a combination of parameters ob- tained from mitral flow, Doppler tissue imaging (DTI), pulmonary venous flow (PVF), early diastolic mitral flow propagation velocity (Vp), PA pressures; RV filling EVALU A TION AN D MANAGE M ENT OF SHOCK/AXLER 233 pressures; and pericardial imaging. Echocardiography can estimate fluid volume responsiveness using heart– lung interactions. This concept assumes that the measurement of some parameters before fluid loading can predict a significant increase of cardiac ouput in hemo- dynamically unstable patients. 54 This estimation uses inferior vena cava (IVC) 62,63 or SVC, 64 size and ventilatory variations, as well as the respiratory variations of the LVOT. 57–59 These parameters correlated strongly in these 5 studies with the concept of ‘‘fluid responsiveness.’’ The measurement of left heart filling pressures requires more sophisticated echo devices. These two new steps represent one of the major advances in the management of shock. Some echocardiographists prefer to use TTE first, and then TEE if necessary, and some always use directly TEE. This is an ongoing discussion, and this choice depends upon the ability of each echocardiographist. Published data regarding the assessment of preload using echocardiography are disappointing. Preload was initia lly assessed by measuring left ventricular end- diastolic diameters, areas, or volumes; close correlations were found with blood loss or expansion in normal subjects 81 or perioperative conditions. 82 However, in ICU settings, recent studies found that the left ventricle end-diastolic area (LVEDA) failed to accurately predict fluid requirement or fluid overload status, particularly when compared with newer methods to assess fluid responsiveness. 57,83–85 Therefore, echocardiographic measurements of LV and RV size are no longer used to assess volume status. However, diameter of the IVC and its ventilatory variations are invaluable to predict fluid responsiveness. This measurement is simple to assess, with a short learning curve (1 hour). The IVC diameter and its ventilatory variations are measured with TTE, on a subcostal view, in M mode. Measurement parameters include IVC diameter (D) at end-exp iration (Dmin) and at end-inspiration (Dmax); distensibility index of the IVC (dIVC) calculated as the ratio of Dmax-Dmin:Dmin and expressed as a percentage, or ((Dmax-Dmin:Dmax þ Dmin):2 ). 62,63,86 Measurement of IVC size and respiratory variation is useful to predict response to a flu id challenge. 62,63,65 The useful threshold was 12% of variability, with a positive and negative predictive value of 93% and 92% in one study of septic patients requiring mechanical ventilation (MV). 62 An- other group studied 23 patien ts in septic shock requiring MV. 63 The size and ventilatory variation of the IVC (IVCVV) predicted a positive response to a fluid challenge [ 15% increase of the cardiac index (CI) following a 7 mL/kg fluid challenge]. IVCVV was defined in this study by Dmax-Dmin:Dmin. There was an excellent correlation (r ¼ 0.9) between an 18% IVCVV at baseline and  15% increase in CI after a fluid loading, with 90% specificity and 90% sensitivity. 63 Importantly, baseline CVP did not accurately predict fluid responsiveness. Additionally, in a cohort of septic patients on MV, measurement of the SVC by TEE, and ventilatory collapsibility of the SVC predicted the cardiac response to fluid challenge. 64 The 36% threshold of variability (Dmax-Dmin:Dmax) could define responders and non- responders in CO, with 90% sensitivity and 87% specificity. 64 Although measurement of IVC diameter ventilatory variations was studied only in septic patients on MV, we use it in every patient in acute circulatory or acute respiratory failure, even among patients not requiring MV. However, outcomes data in these other patient populations are lacking. The second important new parameter in assessing shock is the ventilatory variation of left ventricular outflow tract (LVOT) (called also aortic) Doppler velocities. Two studies found that this parameter was a strong predictor of preload responsiveness: one in septic patients on MV (using TEE), 57 and one with a rabbit model. 58 The first study defined the respiratory variation as the ratio of the difference between maximal velocities to the mean of these two velocities. A ventilatory variation of LVOT blood flow velocity > 12% was associated with a 15% increase of CI with a 91% positive predictive value. A ventilatory variation < 12% had a 100% negative predictive value. This could imply that no volume expansion was necessary with a high degree of confidence. There was a high degree of correlation between baseline ventilatory variation and degree of CI increase after volume expansion. 57 This important study can be extended to TTE. We regularly use this method in all patients in shock to assess potential fluid responsiveness. Patients must be on MV and well adapted to their ventilator, and must be free of arrhythmias. Slama et al found similar results in a rabbit model, using TTE, with progressive blood withdrawal. 58 In these two studies, this parameter was more powerful than all other parameters (CVP, PAOP, left ventricular end-diastolic area) that had been used for the past several years. The most recent studi es showed that ‘‘static’’ echocardiographic parameters failed to consistently predict response to fluid loading. 57–59,83–85 The second important advance is the ability of echocardiography to estimate LV and RV filling pressures (LVFP and RVFP). These measurements were extensively studied over the past 10 years in the cardio- logical arena 86–90 but were only recently applied to the critically ill (noncardiac) patients in ICUs. 91–93 These measurements do not accurately measure preload, but may predict fluid responsiveness. An algorithm is now available to determine if LVFP are predictive of PAOP as ‘‘high’’ (> 15 mm Hg) or ‘‘not hig h’’ ( 15 mm Hg). This analysis is usually applied when the LVEF is decreased (< 45%). This algorithm is determined by the analysis of the combination of pulsed Doppler of mitral flow, tissue Doppler imaging, color M-mode of mitral flow, pulmonary venous flow (PVF), left atrial 234 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 2006 [...]... Principles of Critical Care 3rd ed New York: McGraw Hill; 2005:249–265 2 Rivers E, Nguyen B, Havstadt S, et al Early goal therapy in the treatment of severe sepsis and septic shock N Engl J Med 2001 ;34 5: 136 8– 137 7 3 Weil MH Defining hemodynamic instability In: Pinsky MR, Payen D, eds Functional Hemodynamic Monitoring Update in Intensive Care and Emergency Medicine No 42 New York: Springer-Verlag; 2005:9–17... Surviving Sepsis Campaign for management of severe sepsis and septic shock Crit Care Med 2004 ;32 :858–8 73 7 Hollenberg SM, Ahrens TS, Annane D, et al Practice parameters for hemodynamic support of sepsis in adult patients: 2004 update Crit Care Med 2004 ;32 :1928– 1948 8 Annane D, Belissant E, Cavaillon JM Septic shock Lancet 2005 ;36 5: 63 78 9 Weil MH, Shubin H Shock following acute myocardium infarction: current... American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference: definitions of sepsis and organ failure and guidelines for the use of innovative therapies in sepsis Crit Care Med 1992;20:864–874 5 Levy MM, Fink MP, Marshal JC, et al 2001 SCCM/ ESICM/ACCP/ATS/SIS International Sepsis Definition Conference Crit Care Med 20 03; 31:1250–1256 6 Dellinger RP, Carlet JM, Masur H,... determined, and a prediction of an increased CO can be tested with volume expansion.94,95 In interpreting these tests, it is important to note that a positive fluid 235 236 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 27, NUMBER 3 responsiveness test does not imply that there is an indication for giving fluids, because a normal heart will increase CO with any volume expansion By contrast, even... cardiovascular drugs, antiarrhythmic drugs, inotropic, vasoconstrictor, or vasodilator agents; adequate fluid loading, etc.).1 COST-EFFECTIVENESS OF EACH METHOD AND STRATEGY Data comparing morbidity, mortality, and cost of therapeutic interventions are critical. 43 Regarding cost-effectiveness, only the PAC has been extensively studied Esophageal Doppler and EVALUATION AND MANAGEMENT OF SHOCK/AXLER echocardiography... technique in high-risk surgical patients. 23 VENOUS AND TISSUE PCO2 Venous and tissue PCO2 have been used for more than 3 decades to manage shock, but sublingual PCO2 has emerged as the simplest and most reliable technique to assess venous and tissue PCO2 In patients in the ED and in the ICU, sublingual PCO2 indicates the presence of shock but does not allow any classification of shock .3, 15,16 ARTERIAL... respiratory variations provides ancillary information.94–96 Values above 10 to 13% indicate with a high sensitivity and specificity that a volume expansion will increase CO.94–96 Perel and colleagues developed a respiratory systolic variation test (RSVT) that uses three consecutive incremental pressure-controlled (10, 20, and 30 cm H2O) breaths to test the response of venous return, left ventricular stroke... the past few years First, the major scientific critical care societies have defined quantitative parameters (primarily for septic shock) to allow a faster and a more unified diagnosis not only at the bedside but also for common inclusion criteria in clinical studies.2,8,98,99 Second, early management of patients in shock must be aggressive and orchestrated This critical time has been called ‘‘the golden... other parameters help to determine LVFP These parameters are (1) the maximal early diastolic velocity (Ea) of the mitral annulus at the lateral- or septal most basal point, measured from DTI; (2) early flow (LV flow propagation velocity) Vp using M-mode color Doppler; (3) PVF, where the systolic fraction is measured: this fraction is the ratio between the velocity time integral (VTI) of the systolic component... volumetric parameters such as the global end-diastolic volume index (GEDVI) and the intrathoracic blood volume index (ITBVI) by transcardiopulmonary thermodilution These parameters are more accurate than left and right cardiac filling pressures to estimate preload in critically ill patients but do not reliably assess fluid responsiveness.19,25 The noninvasive Modelflow-Finapress (Finapress Medical Systems, . 2006 by Thieme Medical Publishers, Inc., 33 3 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 58 4-4 662. DOI 10.1055/s-200 6-9 45526. ISSN 106 9 -3 424. 230 comprehensive reviews. 1,10 Several points. France. E-mail: olivier. axler@canl.nc. Non-pulmonary Critical Care: Managing Multisystem Critical Illness; Guest Editor, Curtis N. Sessler, M.D. Semin Respir Crit Care Med 2006;27: 230 –240. Copyright. J 1976;52(Suppl 7) :32 38 36 . Fleg JL, Kennedy HL. Cardiac arrhythmias in a healthy elderly population: detection by 24-hour ambulatory electrocardiography. Chest 1982;81 :30 2 30 7 37 . Anderson KP,

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