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(BQ) Part 2 book The NeuroICU book has contents: Cardiovascular problems, pulmonary diseases, renal and electrolyte disorders, hamatology, infectious disease, nutrition and endocrinology, ethics and end of life issues.
SEctIon cardiovascular Problems Section Editor: Joseph E Parrillo, MD, FCCP Chapter 31 Acute Coronary Syndrome Joanne Mazzarelli, MD Steven Werns, MD 543 cardiovascular Problems A 67-year-old man with a history of hypertension, hyperlipidemia, and tobacco use was found by family members with left-sided paralysis, rightward eye deviation, and change in mental status and was brought to the emergency department (ED) Computed axial tomography (CAT) of the brain performed in the ED (Figure 31-1) showed a large acute nonhemorrhagic right hemispheric infarct within the vascular territory of the right middle cerebral artery The infarct involved large portions of the frontal, temporal, and parietal lobes as well as underlying basal ganglia structures The proximal right middle cerebral artery was hyperdense, consistent with thrombosis within the vessel The patient was not administered thrombolytic therapy because of the unknown onset of symptoms The local ED physicians decided to transfer the patient immediately to the nearest tertiary medical center On arrival to the intensive care unit, the patient was awake and alert but with a left hemiparesis and left hemineglect Upon admission he complained of dyspnea but no chest pain Heart rate (HR) was 77 bpm and regular, blood pressure (BP) 89/55 mm Hg, respiratory rate (RR) 15 breaths/min, temperature (T) 36.5°C (97.7°F), and arterial oxygen saturation (SaO2) 98% on L oxygen Cardiovascular examination was notable for jugular venous distention with an estimated jugular venous pressure of cm H2O The first and second heart sounds were noted to be normal and regular There was a III/VI holosystolic murmur at the apex The lungs were clear to auscultation bilaterally Initial laboratory test results were notable for a blood urea nitrogen (BUN) of 65 mg/dL, creatinine of 1.5 mg/dL, white blood cell (WBC) count of 16,700/µL, hemoglobin (Hb) of 12.2 g/dL, and platelets of 413,000/µL Cardiac biomarkers were elevated with a creatinine kinase of 821 U/L, a troponin T of 4.33 ng/mL, and a creatine kinase MB (CK-MB) of 12.0 ng/mL An electrocardiogram (ECG) and chest x-ray were performed on admission (Figures 31-2 and 31-3) 544 SEctIon • d e Figure 31-1 Computed axial tomography (CAT) scan of the brain Figure 31-2 Chest x-ray cHAPtER 31 • Referred by: e n nd e 545 Unconfirmed I aVR V1 V4 II aVL V2 V5 III aVF V3 V6 V1 II V5 40 Hz 25.0 mm/s 10 mm/mV by 2.5 s + rhythm Ids MAC5K 008A 12SL v235 Figure 31-3 Twelve-lead electrocardiogram What should be the first step in managing this patient? This patient presents with acute ischemic stroke and myocardial infarction There is evidence of hemodynamic deterioration; therefore, a decision regarding management of acute coronary syndrome (ACS) must be made quickly Management of acute ischemic stroke is discussed in Chapter How would you classify this patient’s clinical presentation? How you define acute coronary syndrome? This patient presents with ECG and laboratory evidence of myocardial infarction The initial ECG showed ST depressions anteriorly, which should alert the clinician to the possibility of posterior wall ST-segment elevation myocardial infarction In this clinical scenario it would be appropriate to place “posterior” ECG leads, which can be accomplished by placing three electrodes—V7, V8, and V9—in the left posterior axillary line at the fifth interspace, at the left midscapular line at the fifth interspace, and at the left paraspinal border at the fifth interspace, respectively Significant ST elevation in leads V7 through V9 is defined as at least 0.5 mm in two or more of the leads, based on the increased distance between the posterior chest wall and the heart Q waves wider than 0.04 second or deeper than one-quarter of the amplitude of the succeeding R wave are considered pathologic in leads V7 through V9.1,2 Acute coronary syndrome is a spectrum of clinical syndromes and includes unstable angina (UA), non–ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment-elevation myocardial infarction (STEMI) Variant angina, also known as Prinzmetal angina, can manifest as ST-segmentelevation on the electrocardiogram and elevated serum troponin levels but is pathologically distinct from acute coronary syndrome Although the pathogenesis and clinical presentation of UA and NSTEMI are similar, the presence of serum cardiac biomarkers, troponin I, or troponin T distinguishes NSTEMI from UA In patients with NSTEMI, the degree of myocardial injury is severe enough to cause detectable serum levels of troponin I, troponin T, or CK-MB the Pathogenesis of AcS cardiovascular Problems It is well established that coronary atherosclerosis is by far the most common cause of acute myocardial ischemia, with thrombosis as the trigger for myocardial infarction Less common causes of myocardial ischemia include coronary artery dissection, coronary arteritis, coronary artery vasospasm, emboli, and rarely myocardial bridging Until recently, the majority of our understanding of the mechanisms of conversion from chronic to acute coronary artery disease had largely been limited to postmortem data In 1912, Dr James Herrick published an autopsy study that associated the clinical presentation of acute infarction with a thrombotic coronary occlusion.3 Coronary artery occlusion 546 SEctIon • d e resulting in acute coronary syndrome occurs by three mechanisms: thrombosis, plaque erosion, or plaque rupture Plaque morphology described angiographically or via intravascular ultrasound or angioscopy has been instrumental in identifying atherosclerotic plaques that were more likely to cause acute coronary syndrome, the so-called vulnerable plaque However, our understanding of the cellular and molecular mechanisms of how a vulnerable plaque develops is far from being complete Histopathologic and angioscopic studies have demonstrated that both plaque rupture and erosion leading to thrombosis are the most common causes of acute coronary syndrome Plaques that are more likely to rupture are termed vulnerable plaques or thin-cap fibroatheromas They are characterized as being eccentric, with a larger lipid core, fewer smooth muscle cells, and a greater number of macrophages.4-6 Plaque with a lipid core often contains oxidized lipids and macrophage-derived tissue factor, which makes the plaque highly thrombogenic when its contents are exposed to blood This in turn activates the clotting cascade, as well as platelet adhesion, activation, and aggregation.7 It is thought that plaque rupture accounts for > 70% of fatal acute myocardial infarctions and/or sudden cardiac death The smaller concentration of smooth muscle cells is thought to weaken the mechanical resistance of the plaque Plaque rupture generally occurs where the plaque is thinnest and has the highest degree of inflammatory cells (ie, foam cells) In an eccentric plaque this typically occurs at the shoulder region, which is the junction between the plaque and the area of the vessel wall that is less diseased.8 Plaque erosion refers to a thin-cap fibroatheroma that literally develops a fissure or defect in the fibrous cap, thereby exposing the thrombogenic core to flowing blood.9 Erosions occur over plaques that are rich in smooth muscle cells and proteoglycans Luminal thrombi occur in denuded areas lacking surface endothelium Unlike plaques prone to rupture, plaques prone to erosion typically lack a necrotic core of lipid but rather are composed of macrophages and lymphocytes Lastly, calcified nodules are plaques with luminal thrombi showing calcified nodules protruding into the lumen through a disrupted thin fibrous cap There is absence of endothelium at the site of the thrombus as well as lack of inflammatory cells (macrophages and T lymphocytes) There is little or no necrotic core and typically there is no obvious rupture of the lesion However, there are superficial, dense, calcified nodules within the intima, which appear to be erupting through fibrous tissue into the lumen, possibly causing the thrombus.10 Numerous postmortem studies have identified ruptured plaque as the cause of thrombosis in acute myocardial infarction Richardson et al studied 85 coronary thrombi postmortem and found a disrupted atheromatous plaque beneath 71 (84%) of the thrombi.11 Studies comparing coronary angiograms before and after the onset of the acute coronary syndrome confirmed that the majority of culprit lesions demonstrate a luminal stenosis of 70% on the initial angiogram However, the lesions with a less severe degree of luminal stenosis ( 50%) on the initial angiogram were more likely to be the cause of acute coronary syndrome.12-16 The composition and vulnerability of plaque rather than its volume or the consequent severity of stenosis produced have emerged as being the most important determinants of the development of the thrombus-mediated acute coronary syndromes.8 In addition, both angiographic studies and intravascular ultrasound of plaque morphology in patients presenting with acute coronary syndrome have shown that multiple complex or ruptured plaques exist simultaneously This implies a systemic process in the pathogenesis of plaque rupture.17 The relationship between systemic markers of inflammation and the acute coronary syndromes is beyond the scope of this chapter.18 The clinical presentation and outcome depend on the location, severity, and duration of myocardial ischemia Unstable angina and NSTEMI are typically caused by partial coronary artery obstruction by a thrombus, while STEMI is caused by complete coronary artery obstruction The clinical presentation can, of course, be mediated by other factors such as vascular tone or the presence of collaterals.19 It is noteworthy that many coronary arteries apparently occlude silently without causing myocardial infarction, probably because of a well-developed collateral circulation at the time of occlusion.20 Morphological studies suggest that plaque progression beyond 40% to 50% cross-sectional luminal narrowing may occur secondary to repeated asymptomatic plaque ruptures, which may lead to healing with infiltration of smooth muscle cells.7,18 cHAPtER 31 • e n nd e 547 Are there triggers to pla ue rupture that could explain this patient’s simultaneous ischemic stroke and myocardial infarction? Acute coronary syndrome is not likely to occur at random The first study that looked at external triggers of ACS such as time of day, occupation of the patient, and physical effort was published by Masters in 1960 It was a retrospective review of 2600 patients Although the study lacked formal statistical analysis, it concluded that there was no link between such external triggers and the onset of ACS.21 In 2006, Strike et al performed a prospective observational study of 295 patients with electrocardiographic and biochemically verified ACS Ten percent of patients reported physical exertion hour before symptom onset, whereas 17.4% of patients reported anger in the hours prior to symptom onset Both types of triggers were more commonly associated with STEMI than with other forms of ACS.22 The possible link between physical or emotional stress and acute coronary syndrome is not well understood Physical exertion and mental stress may have similar effects on cardiovascular functioning in that both can trigger an increase in heart rate, blood pressure, coronary vasoconstriction, plasma catecholamine levels, and platelet activation.23 During exercise or periods of stress, there is activation of the sympathetic nervous system with subsequent release of norepinephrine from myocardial sympathetic nerves in addition to circulating epinephrine and norepinephrine Sympathetic stimulation leads to α1-mediated vasoconstriction and 2mediated vasodilatation The net physiologic response is dilation of the epicardial coronary arteries and microvessels.24 Patients with impaired endothelial function and clinical risk factors for coronary artery disease exhibit an enhanced α-adrenergic vasoconstriction When nitric oxide endothelium–dependent vasodilatation is impaired, vasoconstriction predominates, which in turn increases shear stress at the atherosclerotic plaque A possible consequence is plaque rupture at the shoulder region.25-27 What are some examples of acute coronary syndrome with normal epicardial arteries? cardiovascular Problems What has been described above is the pathogenesis of acute coronary syndrome due to plaque disruption However, coronary angiography may demonstrate normal coronary arteries in patients with chest pain, ECG abnormalities, and/or positive cardiac biomarkers There are five major causes of ACS: thrombus, mechanical obstruction, dynamic obstruction, inflammation, and increased oxygen demand.28 Takotsubo syndrome, also known as broken heart syndrome, is defined as transient reversible left ventricular (LV) apical ballooning of acute onset without coronary artery stenosis that clinically mimics acute coronary syndrome It is associated with typical chest pain and ECG changes consistent with ischemia or infarction Tsuchihashi et al performed a multicenter retrospective review of 88 patients (12 men and 76 women), aged 67 ± 13 years, who fulfilled the following criteria: (1) transient LV apical ballooning, (2) no significant angiographic stenosis, and (3) no known cardiomyopathies Chest pain occurred in 67% of patients, and 56% of patients had a significant elevation in creatine kinase; of the 43 patients who had troponin T measured, 72% of them had a significant elevation Electrocardiogram findings included ST elevation (90%), Q waves (27%), T-wave inversion (44%) Fifteen percent of patients developed cardiogenic shock All patients had angiogram-confirmed nonobstructive epicardial coronary arteries (stenosis 50%) During cardiac catheterization, only 10 patients were found to have coronary vasospasm Based on chart review, the authors concluded that 20% of patients had a recent psychological stressor, 7% had an associated neurogenic condition, and 33% had a recent minor or major physiologic stress such as surgery.29 It has been proposed that stress-induced cardiomyopathy is a catecholamine-driven process Wittstein et al performed a prospective study on 19 patients who presented with stress-induced cardiomyopathy On hospital day or 2, plasma levels of catecholamine among patients with stress cardiomyopathy were to times the values among patients with Killip class III myocardial infarction and to 34 times the published normal values.30 Other causes of acute coronary syndrome with normal coronary arteries include coronary artery embolism (eg, in patients with atrial fibrillation or prosthetic heart valves)31; coronary artery spasm 548 SEctIon • d e table 31-1 Nonatherosclerotic Causes of acute Myocardial nfarction In e e end n d e d e end e d e e ed e e n n e e n In ne n x e n n n e d d e e e n e e e e ed n d n n n n ne nd ed n e d e n (eg, in patients who abuse cocaine)32; and spontaneous coronary artery dissection (eg, in pregnant and postpartum women).33 See Table 31-1 Patients with coronary artery spasm (CAS), also known as variant or Prinzmetal angina, present with chest pain and concomitant ST-segment elevation Prolonged vasospasm can result in frank myocardial infarction It is commonly seen in young people who abuse cocaine However, more recent reviews suggest that vagal withdrawal is most often the mechanism leading to spontaneous CAS Other mechanisms responsible for CAS include increased sympathetic tone, abnormal nitric oxide synthase in dysfunctional endothelium, and enhanced phospholipase C enzyme activity inducing focal smooth muscle cell sensitivity.34-36 Established therapies include calcium channel blockers, long-acting nitrates, and in rare intractable cases internal mammary artery grafting CAS may be associated with life-threatening ventricular arrhythmias, which may be an indication for implantation of an automated defibrillator.37 this patient denied chest pain before or during his presentation Is this typical in patients presenting with AcS? Does lack of chest pain in this patient’s clinical presentation have clinical significance? Acute coronary syndrome can present in varying ways High-risk or probable high-risk chest pain is described as prolonged, lasting for more than 30 minutes, a pressure-like sensation, or chest heaviness with radiation to or both shoulders or arms It often occurs on exertion and is associated with nausea, vomiting, or diaphoresis.38 However, a considerable proportion of patients who present with ACS not have chest pain The National Registry of Myocardial Infarction (NRMI) is a database to which 1674 US hospitals contribute data Among patients with confirmed MI who were enrolled in the NRMI between 1994 and 1998, 33% (n 142,445) had chest pain at the time of presentation to cHAPtER 31 • e n nd e 549 the hospital Older patients, women, and diabetic patients were more likely to lack chest pain Only 23% of patients without chest pain had ST elevation on the initial ECG.39 Patients without chest pain but with myocardial infarction were less aggressively treated and had a 23.3% in-hospital mortality rate compared with 9.3% among patients with chest pain.39 Other atypical symptoms such as dyspnea, nausea and vomiting, and syncope can be associated with ACS Describe the EcG changes seen on the patient’s initial EcG How does one differentiate an injury pattern from an infarct pattern on a 12-lead EcG? What are the EcG criteria for StEMI? This patient has ST-segment depressions in V1 through V5 All patients with chest discomfort, anginal equivalent, or other symptoms consistent with ACS should have a 12-lead ECG within 10 minutes of arrival to the emergency department An experienced physician should interpret the ECG immediately Either serial ECGs at 5- to 10-minute intervals or continuous ST-segment monitoring should be performed in a patient with a nondiagnostic initial ECG if the patient remains symptomatic and there is high clinical suspicion for ACS In patients with inferior STEMI, right-sided ECG leads should be obtained to screen for ST elevation suggestive of right ventricular infarction.40 See Table 31-2 Normally the ST segment on the ECG is at approximately the same baseline level as the PR segment or the TP segment If coronary artery blood flow is sufficient to satisfy metabolic demands, then there is minimal alteration, if any, of the ST segment on the surface ECG If there is partial obstruction of a coronary artery that prevents blood flow from increasing enough to meet the increased metabolic demand, the resulting ischemia is manifested by horizontal or downsloping ST-segment depression This is typically called subendocardial ischemia Often the ST segments return to normal once the metabolic demand has ceased Hyperacute T waves might be the first manifestation of myocardial injury due to complete arterial occlusion If the arterial occlusion persists without reperfusion, a myocardial infarction occurs and is represented as ST-segment deviation on the surface ECG This patient’s electrocardiogram is consistent with posterior wall infarction An ECG utilizing leads V7, V8, and V9, which are placed on the posterior torso, would likely show ST-segment elevation The standard 12-lead electrocardiogram is a relatively insensitive tool for detecting posterior infarction because these leads not face the posterior wall of the left ventricle Using leads V7, V8, and V9, ECG criteria for ST elevation of the posterior wall is defined as an elevation of at least 0.5 mV in two or more of the leads This lower voltage can be explained by the increased distance between the posterior chest wall and the heart.2,41 Currently, the indications for thrombolytic therapy or percutaneous coronary intervention require identification of ST elevation on the standard 12-lead electrocardiogram However, ST elevation may not be seen in up to 50% of patients with an MI because of occlusion of the left circumflex coronary artery.4,42,43 Suspicion of left circumflex–related infarction should table 31-2 eC Manifestations of acute Myocardial schemia in the absence of L h or LBBB ee e n de e e n n ee n en n e d e n nd n e d e d n n n nd ≥ n n e d e e d e n n ≥ n en ≥ n e n nen de e e n≥ n n ≥ e d nd ne n≥ n Contiguous leads refer to lead groups such as anterior leads (V1-V6), inferior leads (II, III, and aVF), or lateral leads (I and aVL) a (Adapted from Thygesen K, Alpert JS, White HD, et al Universal definition of myocardial infarction on behalf of the joint ESC/ ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction J Am Coll Cardiol 2007;50:2173-2219.) cardiovascular Problems Abbreviations: LBBB, left bundle branch block; LVH, left ventricular hypertrophy SEctIon • 550 d e occur if the standard 12-lead ECG shows an abnormal R wave in lead V1, which may be defined as ≥ 0.04 seconds in duration and/or an R-to-S wave ratio of ≥ in lead V1 in the absence of preexcitation or right ventricular hypertrophy In addition, the presence of anterior ischemia with ST-segment depression in leads V1 and V2 may suggest reciprocal electrical phenomena in the presence of a posterior infarction Posterior wall infarction rarely occurs in isolation but rather is almost always associated with inferior or posterior lateral infarction The term posterior to reflect the basal part of the LV wall that lies on the diaphragm is no longer recommended It is preferable to refer to this territory as inferobasal.44 In patients with ECG evidence of inferior wall MI, right-sided precordial leads should be recorded to detect ST-segment elevation in leads V3R or V4R, signs of right ventricular infarction.45 The location of the infarcted area can usually be determined by the standard 12-lead electrocardiogram and includes the left anterior descending artery (LAD), left circumflex artery (LCX), and right coronary artery (RCA) The LAD and its branches usually supply the anterior and anterolateral walls of the left ventricle and the anterior two-thirds of the septum The LCX and its branches usually supply the posterolateral wall of the left ventricle The RCA supplies the right ventricle, the inferior and true posterior walls of the left ventricle, and the posterior third of the septum The usual ECG evolution of an STEMI is variable depending on the size of the MI, how quickly reperfusion is restored, and the location of the MI See Table 31-3 The first finding of ischemia on a 12-lead electrocardiogram can be hyperacute T waves, which appear as tall-amplitude primary T-wave abnormalities These typically occur in the first 15 minutes of a transmural MI and therefore are rarely recorded If transmural ischemia persists for more than a few minutes, the peaked T waves evolve into ST-segment elevation The ST-segment elevation of myocardial infarction is usually upward convex As acute infarction continues to evolve, the STsegment elevation decreases and the T waves begin to invert The T wave usually becomes progressively deeper as the ST-segment elevation subsides Pathologic Q waves develop within the first few hours to days after an infarction They are defined as having a duration ≥ 0.04 seconds or > 25% of the R-wave amplitude However, ST-segment elevation that persists beyond weeks is usually associated with the presence of a ventricular aneurysm.46 See Table 31-3 table 31-3 Occluded Coronary artery and ts relationship to anatomic Location and eC Findings Category anatomic location x ne e nd n e e d eC finding I x nd e e ne d e e x nd n e ed n I ne e nd ex d ed n n x e e ne ex II III > n e n e I en n ne II III n Abbreviations: LAD, left anterior descending artery; LCX, left descending circumflex artery; RCA, right coronary artery (Adapted from Topol EJ, Van De Werf F Acute myocardial infarction: early diagnosis and management In: Topol EJ, Califf RM, Prystowsky EN, et al, eds Textbook of Cardiovascular Medicine 3rd ed Philadelphia, PA: Lippincott Williams & Wilkins; 2007:283-284; and Sgarbossa EB, Birnbaum Y, Parrillo JE Electrocardiographic diagnosis of acute myocardial infarction: current concepts for the clinician Am Heart J 2001;141:507-517.) cHAPtER 31 • e n nd e 551 Describe causes of St elevation on a 12-lead EcG that are not associated with acute myocardial infarction Typically the degree of ST elevation is determined by comparing it to the end of the PR segment In certain populations, ST-segment elevation can be a normal finding or a normal variant Early repolarization is an ECG finding that frequently occurs in young men and is described as an elevated takeoff of the ST segment at the junction between the QRS and ST segment (J point) It most commonly involves V2 through V5 but can be seen in II, III, and aVF The ST segment is usually concave.47,48 Other causes of ST elevation not associated with acute myocardial infarction include left bundle branch block, left ventricular hypertrophy, acute pericarditis or myocarditis, Brugada syndrome, hyperkalemia, and arrhythmogenic right ventricular cardiomyopathy (Figure 31-4) A 2-D echocardiogram was performed and revealed a severe abnormality of segmental wall motion and moderate to severe mitral regurgitation Is echocardiography a useful tool in the diagnosis of acute coronary syndrome? What are the indications for echocardiography in AcS? In the acute setting it is appropriate to consider 2-D echocardiography for the following indications: evaluation of acute chest pain with suspected myocardial ischemia in patients with nondiagnostic laboratory Tracing Lead V1 Lead V2 Lead V3 Lead II cardiovascular Problems Figure 31-4 ST-segment elevation in various conditions Tracing 1, left ventricular hypertrophy Tracing 2, left bundle branch block Tracing 3, acute pericarditis; note the PR depression in lead II Tracing 4, hyperkalemia Tracing 5, acute anteroseptal infarct Tracing 6, acute anteroseptal infarction with right bundle branch block Tracing 7, Brugada syndrome (Reprinted with permission from Wang K, Asinger RW, Marriot HJ ST-segment elevation in conditions other than acute myocardial infarction N Engl J Med 2003;349:2128-2135.) 552 SEctIon • d e markers and ECG and in whom a resting echocardiogram can be performed during pain; and evaluation of suspected complications of myocardial ischemia or infarction, including but not limited to acute mitral regurgitation, hypoxemia, abnormal chest x-ray, ventricular septal rupture, free wall rupture, cardiac tamponade, shock, right ventricular involvement, heart failure, or thrombus.49 A 2-D echocardiogram alone should not be used to diagnose an acute coronary syndrome However, there are several echocardiographic findings that may support the diagnosis of an acute coronary syndrome In the setting of acute ongoing ischemia the echocardiogram may demonstrate hypokinesis of the affected wall, referred to as a segmental wall motion abnormality Often the contralateral wall will appear hyperkinetic However, if a segment is akinetic, dyskinetic, or severely hypokinetic, a single echocardiogram cannot differentiate ischemia with myocardial stunning from irreversible damage due to myocardial necrosis A transesophageal echo may be helpful in differentiating acute myocardial infarction from aortic dissection Mitral regurgitation commonly occurs in the setting of acute myocardial infarction Color Doppler echocardiography was performed within 48 hours of admission in a series of 417 consecutive patients with acute MI.50 Mild mitral regurgitation was present in 29% of patients, moderate mitral regurgitation in 5%, and severe mitral regurgitation in 1% Echocardiography performed in a cohort of 773 patients 30 days after an acute MI revealed that 50% of patients had mitral regurgitation.51 Among 30-day survivors of an MI, during a mean follow-up period of 4.7 years, moderate to severe mitral regurgitation detected by echocardiography within 30 days of MI was associated with a 55% increase in the relative risk of death independent of age, gender, left ventricular ejection fraction, and Killip class.51 Initial labs on this patient revealed a troponin I of 11.6 ng mL, creatinine kinase of L, and c -M fraction of 12.6 ng mL How are biomarkers used in the diagnosis and management of acute coronary syndrome? What other processes can cause an elevation in cardiac biomarkers that are not related to AcS? Myocardial infarction is defined as myocardial cell death as a result of prolonged myocardial ischemia Cardiac troponin I and cardiac troponin T are the preferred biomarkers to confirm myocardial ischemia The cardiac troponin elevations begin to hours after onset of symptoms and may persist for several days beyond the initial event (Figure 31-5) Myoglobin and CK isoforms Troponin (large MI) Multiples of the AMI cutoff limit 50 20 10 CKMB 10% CV/99th percentile Troponin (small MI) 0 Days after onset of AMI Figure 31-5 Timing of serum cardiac biomarkers in acute coronary syndrome (ACS) AMI, acute myocardial infarction; CK, creatine kinase; CV, coefficient of variation (Reprinted with permission from Jaffe AS, Babuin L, Apple FS Biomarkers in acute cardiac disease: the present and the future J Am Coll Cardiol 2006;48(1):1-11.) Index neuromuscular junction disease, 130 neuromuscular weakness See weakness neuronal injury, CBF and, 229, 230t neuropathy(ies) acute, differential diagnosis, 129t cranial, brainstem disease with, 130 underlying, 130 neurophysiologic decision support systems See also clinical decision support system benefits of, 316 commercial options available for, 321–322 cart-based all-in-one systems, 321 dashboard systems, 322 hybrid systems, 321 ICU-wide enterprise systems, 321 creation of, 317–318 EHR and, 319–320 neurotoxic fish poisoning, 128, 130 neurotrauma spinal cord injury, 85–87 cardiac system and, 87 classification of, 85, 86f DVT prophylaxis and, 87 infectious complications and, 87 respiratory system and, 86–87 steroids after, 85 surgical decompression for, 87 traumatic brain injury, 77–85 antibiotics for, 80 cervical spine clearance and, 82 CPP goal for, 80–81 craniotomy after, 82 CT scan of, 78f–79f DVT prevention and, 82–83 hypertonic saline for, 83–84 hypothermia after, 81 ICP monitoring after, 80 management of, 77–78 mannitol for, 83 osmotic agents for, 83–84 PbtO2 and, 80 prophylactic AED for, 78–80 steroids after, 80 sympathetic storming after, 84–85 transfusions and, 84 ventilation and, 84 New York Islands Arteriovenous Malformation Study, 365 nicardipine, 41t, 801t NICE-SUGAR trial, 838 961 NIHSS See National Institutes of Health Stroke Scale nimodipine, for bacterial meningitis, 151 nitrates, for acute coronary syndrome, 555–556 nitroglycerin, 621, 801t nitroprusside, 41t non aortic great vessel injury, stab wounds and, 489 noncontinuous status epilepticus (NCSE), 64–66, 65f acute brain injury and CT scan of, 66–67, 67f diagnostic tests for, 66–67 evolving seizure, 67, 68f–69f treatment protocol for, 68t criteria for, 65, 66t semiologic spectrum of, 65, 66t nonconvulsive seizures (NCSs), 229, 229t, 230f, 230t nonconvulsive status epilepticus (NCSE), 229, 229t, 230f, 230t qEEG for, 229–233, 232f–234f nonhemorrhagic stroke, 802t non-ST-segment elevation myocardia infarction (NSTEMI), 565–566, 565f, 573–574, 574f differential diagnosis of, 574 management of, 565–566 treatment algorithm for, 569f nonthrombolytic treatment, for acute ischemic stroke, 107–108 norepinephrine, 144, 144t, 624, 833t normal pressure perfusion breakthrough, AVMs and, 404 normothermia, therapeutic core temperature monitoring location during, 350–351 discontinuation of, 355 infection development tracking during, 351 North American Symptomatic Carotid Endarterectomy Trial (NASCET), 429, 435 NovoSeven, 37 NSM See neurogenic stunned myocardium NSTEMI See non-ST-segment elevation myocardia infarction nutrition artificial, complications of, 903–904 for bacterial meningitis, 150 death and, 908 962 Index nutrition (Cont.): enteral tolerance, evaluation of, 901f ICH and, 43 parenteral, complications of, 904t nutritional status, medications affecting, 905t O obesity, tracheostomy and, 730 obstruction See small bowel obstruction OHCA See out-of-hospital cardiac arrest open repair, of aneurysms, 487 operating room (OR) EPs in, 304–305 medications and, 305 EVD placement in, 415 opioids See also specific opioids pain management and, 326 organ donor specialists, brain death and, 927–928 organ injuries AAST Organ Injury Severity Scale bladder injury classification by, 519, 519t renal injury classification by, 516, 516t ureteral injury classification by, 518, 518t urethral injury classification by, 520, 520t blunt trauma and, 483 penetrating trauma and, 483 organophosphate toxicity, 128, 130 ORx See oxygen reactivity index osmotherapy, intracranial hypertension treatment and, 222 osmotic agents for intracranial hypertension, 10 for TBI, 83–84 osteomyelitis, subdural empyema and, 447 out-of-hospital cardiac arrest (OHCA), 189, 191 oxygen for acute coronary syndrome, 555 delivery devices, 658t deprivation to brain, 189 oxygen reactivity index (ORx), autoregulatory status and, 264, 266f oxygenation, 680–681 brain improvement of, 14 PbtO2 monitoring system for, 13–14 cerebral, 680 failure of, 657–659 goal setting, 680 systemic, 680 P PAI See penetrating aortic injury pain bleeding and, 493t in chest acute coronary syndrome and, 548–549 ECG with, 565f, 566 ECG without, 565f, 566 control of for pneumothorax, 457, 458f for rib fractures, 457, 458f management of, with opioids, 326 scrotal causes of, 524 evaluation of, 524–525 PAMORAs See peripherally acting mu opioid receptor antagonists pancreatic injury, from abdominal trauma, 479–480 pancreatitis, 503 acute coronary syndrome and, 504 surgical decompression for, 504 enteral feeding and, 503 head of bed elevation and, 503 papillary muscle rupture, MR and, 575–576 paraneoplastic neurologic diseases, causing encephalitis, 183, 183t parenchymal hematoma type (PH-1), 99, 99f parenchymal hematoma type (PH-2), 99, 99f parenteral agents, for hypertensive emergencies, 801t parenteral nutrition, complications of, 904t parenteral tube feeding, 899–900 partial pressure of brain tissue oxygen tension (PbtO2) monitoring system, 683–684 for brain oxygenation, 13–14 DO2 and, 13–14, 13f SjvO2 and, 13–14, 13f TBI and, 80 traumatic brain injury (TBI), 80, 256–257 blood transfusion and, 261–262 brain glucose decrease and, 266, 269f brain metabolism and, 266 cardiac performance optimization and, 262, 264f CO2 and, 259, 259f CPP correlation with, 259–260, 260f, 261f decrease in, 257, 259 FiO2 increase and, 260 Index partial pressure of brain tissue oxygen tension (PbtO2) monitoring system, traumatic brain injury (TBI) (Cont.): LPR increase and, 266, 269f treatment to increase, 257, 258f, 262, 262f, 263f passive leg raise test, 534 Patient State Index, 242 PAV See proportional assist ventilation PbtO2 See partial pressure of brain tissue oxygen tension monitoring system PCC See prothrombin-complex concentrate PCI See percutaneous coronary intervention PE See plasmapheresis; pulmonary embolism PEA See pulseless electrical activity peak pressures, 678f PEDs See periodic epileptiform discharges PEEP See positive end expiratory pressure pelvic fractures, retroperitoneal bleed from, 480 penetrating aortic injury (PAI), stab wounds and, 489 penetrating cardiac trauma, stab wounds and, 488–489 penetrating trauma solid organ injuries and, 483 vascular injuries and, 483 penicillin, 855t penicillin/tazobactam, 855t pentobarbital, intracranial hypertension treatment and, 222–223 Penumbra System, 107, 373–374 peptic ulcer, bleeding, 494 ICU management of, 495, 496f medical consultation for, 495 percutaneous coronary intervention (PCI), 563 delayed, 563–564, 564f percutaneous dilational tracheostomy, technique for, 746t percutaneous tracheostomy, 726–727 bronchoscopy for, 745 pericallosal aneurysm, 415, 416f EVD for management after, 416–418, 417f rebleeding risk and, 415 settings for, 417–418 peri-infarct depolarization (PID), 279, 281 periodic epileptiform discharges (PEDs), 63–64, 63f, 65t, 229, 229t peripherally acting mu opioid receptor antagonists (PAMORAs), 336 peritoneal dialysis, 769–770 963 permissive hypercapnia, 705 persistent electrographic seizures, cEEG for, 55, 58f PES See postextubation stridor PH-1 See parenchymal hematoma type PH-2 See parenchymal hematoma type phenobarbital, 11, 55, 59, 59t phenobarbital bolus, for TBI, cEEG of, 239, 241, 241f phenylephrine, 144, 144t, 833t phenytoin, 54t, 55, 79–80, 156 valproic acid and, 61 Philips InnerCool RTx Endovascular System, 348f PICCO, 289, 291 PID See peri-infarct depolarization pituitary adenoma, 165 pituitary apoplexy adrenal crisis and, 166 brain tumors and, 165–168, 166f EVD for, 166, 168 hydrocephalus and, 166 MRI of, 167, 167f postoperative goals, 168 surgical decompression of, 167–168 plaque rupture, 547 plasma arginine vasopressin concentration, 777–778, 778f plasma osmolality, 777–778, 778f plasmapheresis (PE) for ADEM, 181 for neuromuscular diseases, 138t plateau pressures, 678f plateau waves See Lundberg A waves pleural effusion, chest ultrasonography of, 537, 537f PML See progressive multifocal leukoencephalopathy pneumonia, 457, 459, 460 health care-associated, 736 hospital-acquired, 878–879 antibiotic therapy for, 880–882, 881f, 882f risk reduction for, 884 ventilator-associated, 736, 878–879 antibiotic therapy for, 880–882, 881f chest radiograph of, 295f risk reduction for, 884 pneumothorax, 456, 457, 458f chest ultrasonography of, 538–539, 539f after CPB, 463 intercostal nerve block for, 457, 458f pain control for, 457, 458f 964 Index poisoning, neurotoxic fish, 128, 130 polymorphic ventricular tachycardia, 611, 612f polyneuropathies, 128 portable monitoring solution, 317–318, 317f positioning, for bacterial meningitis, 149 positive end expiratory pressure (PEEP), 681–683 ICP and, 709 postcraniotomy complications, 438–440, 440t, 442t risk factors for, 439 seizures, 443, 444f hemorrhage prevention, 444–445 hydrocephalus and, 450 monitoring, 440–443 blood pressure, 442 hypertension, 442 hypotension, 442 nausea, 443, 443f neurologic examination, 440, 441t subgaleal hematoma, 444, 445f posterior fossa surgery, craniotomy and, 439t posterior reversible encephalopathy syndrome (PRES), 797, 799f postextubation stridor (PES), bronchoscopy and, 743–745 prasugrel, 568, 570 prednisone, for neuromuscular diseases, 138t PRES See posterior reversible encephalopathy syndrome pressure microsensors, for ICP monitoring, 219 pressure natriuresis, 800 pressure reactivity index (PRx), 263–264, 265f pressure-regulated volume control (PRVC), 692 pressure-volume (PV) curve, 678f primary abdominal compartment syndrome, 497t primary survey, 476 for vascular injuries, 482 Prinzmetal angina See coronary artery spasm PRIS See propofol infusion syndrome PROACT See Prolyse in Acute Cerebral Thromboembolism study progressive multifocal leukoencephalopathy (PML), 180 prolonged QT intervals, 611, 613t Prolyse in Acute Cerebral Thromboembolism (PROACT) study, 106 prone positioning, for ARDS, 706 prophylactic antibiotics for EVD infections, 418, 419t subdural empyema and, 446–449, 447f propofol, 10, 11, 58, 59t, 143 initial changes with, 333 propofol infusion syndrome (PRIS), 335 proportional assist ventilation (PAV), 693–694 propranolol, 608t protected specimen brush (PSB), 736–737 BAL vs., 737 sample handling after, 737 prothrombin-complex concentrate (PCC), for warfarin-induced coagulopathy, deep brain hemorrhage and, 814, 814t proton pump inhibitor, for GIB, 493 PRVC See pressure-regulated volume control PRx See pressure reactivity index PSB See protected specimen brush pseudoaneurysm, 486 Pseudomonas aeruginosa, 868t pulmonary artery catheter, for acute heart failure, 625–626 pulmonary contusion, 457 chest radiograph of, 459f complications of, 459–460, 460f CT scan of, 460f pulmonary embolism (PE), 714–717, 714t, 716f after acute ischemic stroke, 114 V/Q scan and, 717 pulmonary system, complications after acute ischemic stroke, 114 pulseless electrical activity (PEA), CA and, 194–196, 195t putaminal hemorrhage, CEA after CHS and, 433–434 PV See pressure-volume curve pyridostigmine, for neuromuscular diseases, 138t pyridoxine hydrochloride, 62 pyruvate concentration variation, 272–273, 274f pyuria, 887 Q qEEG See quantitative electroencephalography QT prolongation, 613t quantitative electroencephalography (qEEG), 277, 279, 279f, 280f IVH and, 239, 240f–241f for nonconvulsive status epilepticus, 229–233, 232f–234f Index R radiocontrast-induced nephropathy (RCIN), 757–759 preventive measures for, 758t risk factor for, 757t radiograph of pulmonary contusion, 459f of SBO, 506f Randomized Controlled Trial of Brain Tissue Oxygenation Monitoring, 257 rapid coronary revascularization, 643–645 rapid sequence intubation (RSI), for ICH, 39 RASS See Richmond Agitation-Sedation Scale rCBF See regional cerebral blood flow monitoring RCIN See radiocontrast-induced nephropathy rebleeding risks clipping of UIAs and, 396, 397t from EVD, for pericallosal aneurysm, 415 SAH and, 288 due to ruptured aneurysms, 388 recombinant activated factor VII (rFVIIa), for warfarin-induced coagulopathy, deep brain hemorrhage and, 814 recombinant tissue plasminogen activator (r-tPA), for acute ischemic stroke, 97t refractory status epilepticus (RSE), 56 causes of, 60, 61t CSF test for, 61t fecal test for, 61t immunomodulatory agents for, 62 mechanism for, 57 surgery for, 63 therapeutic hypothermia for, 62 treatment for, 58–60, 59t, 61–63, 62t regional anticoagulants, 773 regional cerebral blood flow (rCBF) monitoring, 273–275 remifentanil, 326 remodeling, 629, 629f renal injuries causes of, 516 classification of, 516, 516t evaluation of, 517 nonsurgical management of, 517–518 postoperative complications for, 517 surgical indications for, 517 renal replacement therapy (RRT), 768–769, 768f, 769f anticoagulant for, 772 dialysate, 772 965 renal replacement therapy (RRT) (Cont.): dialysis and, 768 continuous dialysis/hemofiltration therapies, 771–772 intermittent hemodialysis/hybrid therapies, 770–771, 770f, 771f peritoneal, 769–770 ICP increase during, 774 indications for, 767t initiation of, 766–768 replacement fluid, 772 renal salt wasting, 781 reperfusion therapy, for STEMI, 558, 561 repetitive stimulation, acute bilateral weakness and, 131, 133t residual volumes, increased, differential diagnosis for, 504–505, 505t respiratory failure, tracheostomy and, 730 respiratory system mechanics, 677–679 SCI and, 86–87 resuscitation after, after SAH, 3–4 reteplase, 558 retroperitoneal bleed, from pelvic fractures, 480 reversible posterior leukoencephalopathy syndrome, 797 rFVIIa See recombinant activated factor VII rib fractures intercostal nerve block for, 457, 458f pain control for, 457, 458f Richmond Agitation-Sedation Scale (RASS), 329, 330t RIFLE (Risk, Injury, Failure, Loss, and End-stage) staging, 752–753, 752t Riker Sedation-Agitation Scale (SAS), 330 Risk, Injury, Failure, Loss, and End-stage (RIFLE)staging, 752–753, 752t RRT See renal replacement therapy RSE See refractory status epilepticus RSI See rapid sequence intubation r-tPA See recombinant tissue plasminogen activator ruptured aneurysms craniotomy for, 439t endovascular therapy for, 358–360 SAH due to antifibrinolytic therapy and, 388 DSA for, 386, 387f management of, 385–386 medications for, 387 rebleeding risks and, 388 966 Index ruptured aneurysms, SAH due to (Cont.): surgical clipping for, 388–389 third nerve palsy and, 387–388, 388t treatment strategy for, 386–387 ruptured arteriotomy closure, after CEA, 432 S Safar, Peter, CA approach, 189, 190t SAFE See Saline versus Albumin Fluid Evaluation study SAH See subarachnoid hemorrhage SAINT See Stroke Acute Ischemic NXY-059 Trial Saline versus Albumin Fluid Evaluation (SAFE) study, 832 Saline versus Albumin Fluid Evaluation trial, 77 SAS See Riker Sedation-Agitation Scale SBO See small bowel obstruction scalp electroencephalography, depth electrode monitoring as component of, 242–243, 242f–247f Scandinavian Candesartan Acute Stroke Study, 108 SCI See spinal cord injury scrotal pain, acute causes of, 524 evaluation of, 524–525 SE See status epilepticus seashore sign, lung pattern on chest ultrasonography, 535–536, 536f, 539f secondary abdominal compartment syndrome, 497t secondary survey, 478–479 second-degree atrioventricular block, 590–591, 591f treatment of, 592–593, 593t–594t sedation, 327t for acute ischemic stroke, 111 analgesia vs., 325–326 interdependence, 326, 328, 328f assessment of, 329–330, 330t bacterial meningitis and, 150 CMR and, 328 daily interruption of, with intracranial hypertension, 335 depth of, BIS and, 334 goals for, 328 for ICH, 42 ICP and, 328 intracranial hypertension and, 10 sedation (Cont.): intracranial hypertension treatment and, 220–221 lab monitoring with, 335 management of, 326 monitoring level of, 242 scales, 329–30, 330t seizure threshold and, 328 therapeutic hypothermia and, 331–332 pharmacologic algorithm for, 331f seizures See also generalized convulsive status epilepticus; noncontinuous status epilepticus; refractory status epilepticus acute brain injury and, 69–70, 71f analgesia and, 328 cardiac arrest and, 70–72, 71f cEEG interpretation, 71 treatment of, 71, 72, 72f cEEG monitoring and, 230, 231f detection time, 229, 230f control of, 60 etiology of, 57t evolving, acute brain injury and, 67, 68f–69f intracranial hypertension treatment and, 219–220 persistent electrographic, cEEG for, 55, 58f postcraniotomy complications, 443, 444f precipitants of, 57t prevention of, ICH and, 43 sedation and, 328 sensory nerve action potentials (SNAPs), 301 sensory weakness, differential diagnosis for, 123, 124t–126t SENTIS, randomized controlled trial, 22 sepsis, 824–825 antibiotic therapy and, 830–831 bundles, 829t diagnostic criteria for, 827t host response modulation and, 836–837 lactate increase and, 830 management bundle, 829t management of, 826–830 model, 828f organ failure in, 828f recombinant human activated protein C in, 837t resuscitation bundle, 829t source control techniques, 831t supportive therapies for, 838t treatment approach, 828f Index sepsis hemodynamic support protocol, 835f septic shock corticosteroids and, 836 host response modulation and, 836–837 hypotension and, 832–835 supportive therapies for, 838t vasoactive drugs for, 833t serology studies, for neuromuscular diseases, 134t serum glucose, brain glucose and, 271, 273f shivering, 194 BSAS for, 353, 353t buspirone and, 354 dexmedetomidine and, 355 importance of, 352–353 magnesium and, 354 meperidine and, 333, 355 stepwise protocol for control of, 353, 354t treatment of, 353–355 SHOCK See SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK Trial Registry shock CA and, 196 cardiogenic AMI and, 638, 640–641, 642t, 643 causes of, 642t pathogenesis of, 643f categories of, 641f septic corticosteroids and, 836 host response modulation and, 836–837 hypotension and, 832–835 supportive therapies for, 838t vasoactive drugs for, 833t SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK (SHOCK) Trial Registry, 640 SIADH See syndrome of inappropriate antidiuretic hormone sick euthyroid syndrome, 910–911 sick sinus syndrome (SSS), 588, 589, 590f singed hair, of nares, intubation and, 457 sinus bradycardia, 587 causes of, 588, 588f treatment of, 588, 589f sinus node dysfunction (SND), permanent pacing recommendations in, 589t sinus tachycardia, 596, 597f SIRPIDs See stimulus-induced rhythmic periodic, or ictal discharges 967 SIRS See systemic inflammatory response system SjvO2 See jugular venous oxygen saturation small bowel obstruction (SBO) appendicitis vs., 508 complications of, 506–507 epidemiology of, 507f etiology of, 507f, 507t management of, 507–508, 508t, 509f radiograph of, 506f surgery for, 505–506 systemic inflammatory response and, 508 terminology of, 506t snake venom, 127 SNAPs See sensory nerve action potentials SND See sinus node dysfunction sodium nitroprusside, 801t solid organ injuries blunt trauma and, 483 penetrating trauma and, 483 somatosensory evoked potentials (SSEPs), 301, 302, 302f, 303 after CA, 305–306 therapeutic hypothermia and, 306 normal values, 302t TBI and, 308, 309, 309f Spetzler and Martin Grading System, 368t, 400t spinal cord disorders, 130 lesions, 130 surgery, minimize bleeding during, 815–816, 816t spinal cord injury (SCI) cardiac system and, 87 cervical, tracheostomy and, 730 classification of, 85, 86f DVT prophylaxis and, 87 fever control after brain injury and, 349 infectious complications and, 87 respiratory system and, 86–87 steroids after, 85 surgical decompression for, 87 splenic injury, from abdominal blunt trauma, 483–484 sputum, carbonaceous, in nares, intubation and, 457 SSEPs See somatosensory evoked potentials SSS See sick sinus syndrome ST elevation, changes on ECG, 551, 551f, 553–555, 555f, 567t 968 Index stab wounds abdominal trauma from, 475–479 for, 477 abdominal compartment syndrome due to, 478 antibiotics for, 478 blood transfusion for, 477 FAST examination for, 476, 477 fluid administration for, 477 IAH due to, 478 liver injury and, 479, 479t primary survey for, 476 secondary survey for, 478–479 staging of, 479 tertiary survey for, 477 to mediastinum, 488 BAI, 489 blunt cardiac trauma, 488–489 management of, 488 non aortic great vessel injury, 489 PAI, 489 penetrating cardiac trauma, 488–489 STA-MCA See superficial temporal artery/ middle cerebral artery bypass Staphylococcus aureus, 447f Staphylococcus epidermidis, 447f statins, for bacterial meningitis, 151 status epilepticus (SE) See also generalized convulsive status epilepticus; noncontinuous status epilepticus; refractory status epilepticus benzodiazepine trial for, 64t myoclonic, 71 prognosis of, 71–72 STEMI See ST-segment elevation myocardial infarction stenting for acute ischemic stroke, 107 for ICAD, 374–377 steroids for ARDS, 707 after SCI, 85 after TBI, 80 STICH See Surgical Trial in Intracerebral Hemorrhage study stimulus-induced rhythmic periodic, or ictal discharges (SIRPIDs), 69 streptokinase, 558 stress-induced cardiomyopathy, 547, 575 stroke acute, 371–374, 372f stroke (Cont.): fever control after brain injury and, 349–350 hemorrhagic, 802t ischemic acute See stroke, acute ischemic carotid angioplasty and stenting for, 429 CEA for, 429, 429f, 430–431, 430t ECG abnormalities and, 577 management of, 427–428 MRI for, 178 plaque rupture and, 547 workup for, 427–428 nonhemorrhagic, 802t stroke, acute ischemic biomarkers for, 95 complications after, 113–114 cardiovascular events, 113–114 death, 114 infections, 113 neurologic, 113 pulmonary, 114 CT scan for, 93–95, 93f, 94f, 95f CTP for, 94, 94f diagnosis of, 92–93, 93f DVT after, 114 DWI for, 95 EPs and, 310 evaluation and, 112–113 flow sheet for, 92f hemorrhages and, 99–100 classification of, 99, 99f ICP management clinical pathway, 109, 110f magnetic-resonance perfusion for, 95, 95f MRI for, 95, 95f prevalence of, 91 public health burden of, 91 pulmonary embolism after, 114 risk factors for, 91–92 symptomatic intracerebral hemorrhage after, 99 TCD for, 95 treatment of after hours onset, 101–102, 101f under hours onset, 96, 96f, 104 antithrombotics, 101, 103 carotid angioplasty and stenting for, 108–109 carotid revascularization, 108–109 CEA, 108–109 clinical pathways, 96f, 101f clinical trials, 104t Index stroke, acute ischemic, treatment of (Cont.): complications, 99 heparin, 106 hyperventilation, 111 ICP elevation, 109, 110f, 111 intra-arterial, 103, 106–107 intravenous thrombolysis, 96, 98, 102–103 NeuroFlo, 113 nonthrombolytic, 107–108 pharmacology, 103 r-tPA contraindications, 97t sedation, 111 stenting, 107 surgical decompression, 111 vasopressors, 112–113 Stroke Acute Ischemic NXY-059 Trial (SAINT), 108 Stroke Council of American Heart Association guidelines, 395–396 stroke volume variation (SVV), 289 ST-segment elevation myocardial infarction (STEMI), 638, 639f anticoagulant therapy in, 561t antiplatelet therapy for, 562 CA and, 196 criteria, ECG and, 545f, 549–550 emergency management of, 644f fibrinolytic contraindications for, 560t fondaparinux for, 562 glycoprotein IIb/IIIa and, 562 reperfusion therapy for, 558, 561 treatment algorithm for, 564, 564f subarachnoid hemorrhage (SAH) See also aneurysmal subarachnoid hemorrhage aneurysmal endovascular treatment for, 360–362 morbidity rates of, 358 mortality rates of, 358 brain oxygenation and, PbtO2 monitoring system for, 13–14 computed angiographic scan of, 390f CT scan of, 1, 2f, 253, 254f, 289, 289f, 386f, 390f DSA of, 390f due to ruptured aneurysms antifibrinolytic therapy and, 388 DSA for, 386, 387f management of, 385–386 medications for, 387 rebleeding risks and, 388 surgical clipping for, 388–389 969 subarachnoid hemorrhage (SAH), due to ruptured aneurysms (Cont.): third nerve palsy and, 387–388, 388t treatment strategy for, 386–387 EPs and, 310 external ventricular drain for, 3–4 fever control after brain injury and, 346, 349 fluid resuscitation and, 288 grading systems for, 4–8 with hydrocephalus, 411, 412f EVD placement for, 411–414, 412f, 414f management algorithm for, 413f ventriculostomy for, 411–412 ICH and, 392, 392f surgery for, 392 intracranial hypertension in See intracranial hypertension intracranial pressure treatment and, 9–12 jugular bulb oximetry monitoring for, 275, 275f rebleeding and, 288 resuscitation after, 3–4 treatment of, 390 vasospasm after, 292, 294 ventriculomegaly and, 391, 391f subdural empyema, 448t CT of, 446f infection and, 446–449 brain abscess, 449, 449t meningitis, 448, 448t osteomyelitis, 447 prophylactic antibiotics and, 446–449, 447f of surgical site, 447 subfulminant hepatic failure, 206 subgaleal hematoma, postcraniotomy, 444, 445f succinylcholine, 143 superficial temporal artery/middle cerebral artery (STA-MCA) bypass, 435 suprapubic catheters, for acute urinary retention, 523, 524t supratentorial tumor resection, craniotomy for, 439t supraventricular tachycardia, 611–612 with aberration, 608–612, 609f–610f, 610t supraventricular tachycardias, 595f surface electroencephalo-cardiogram, aSAH and, 235, 236f surgery for ICH, 392 970 Index surgery (Cont.): minimally invasive, 45 posterior fossa, craniotomy and, 439t for RSE, 63 for small bowel obstruction, 505–506 of spinal cord bleeding and, 815–816, 816t minimize bleeding during, 815–816, 816t surgical aneurysmal repair, postoperative complications with, 440t surgical decompression for acute ischemic stroke, 111 for intracranial hypertension, for SCI, 87 Surgical Trial in Intracerebral Hemorrhage (STICH) study, 44, 392 Surviving Sepsis Campaign, 827, 829 SVV See stroke volume variation sympathetic storming, after TBI, 84–85 syndrome of inappropriate antidiuretic hormone (SIADH), 24–25, 780–781 causes of, 782t systemic anticoagulants, 773–774 systemic inflammatory response system (SIRS), 826 SBO and, 508 T T3 syndrome, 911 T4 syndrome, 911 tachycardias atrial, 600–601, 601f multifocal, 601, 602f junctional, 599–600, 601f narrow complex, 595–606 adenosine for, 602–603, 603f atrial flutter, 596–597, 597f atrial tachycardia, 600–601, 601f, 602f AV reciprocating tachycardia, 598–599, 599f–600f AVNRT, 597–598, 598f, 599f causes of, 601–602 differential diagnosis of, 595 on ECG, 595–601, 596f junctional tachycardia, 599–600, 601f management of, 603–604 maneuvers to differentiate, 602–603, 602f medications to differentiate, 602–603, 602f, 603f precipitants of, 601–602 sinus tachycardia, 596, 597f tachycardias (Cont.): sinus, 596, 597f supraventricular, 595f ventricular, significance of, 614, 615f wide complex, 606–616, 608f accelerated idioventricular rhythm, 611, 611f differential diagnosis for, 606–608 management of, 614–616 monomorphic ventricular tachycardia, 610 polymorphic ventricular tachycardia, 611, 612f prolonged QT intervals, 611, 613t supraventricular tachycardia, 611–612 supraventricular with aberration, 608–612, 609f–610f, 610t of ventricular origin, 608–612, 609f–610f, 610t Takotsubo cardiomyopathy, 27, 28f Takotsubo syndrome, 547 TBI See traumatic brain injury TCD See transcranial Doppler temperature See body temperature Temperature-modulation devices, FDA approved, 345, 346f–348f tenecteplase, 559 tertiary survey, 477 testicular torsion, management of, 525 TEVAR See thoracic endovascular aortic repair therapeutic normothermia core temperature monitoring location during, 350–351 discontinuation of, 355 infection development tracking during, 351 thiazides, 621 third nerve palsy, SAH due to ruptured aneurysms and, 387–388, 388t third-degree atrioventricular block, 590–591, 592f treatment of, 592–593, 593t–594t thoracic endovascular aortic repair (TEVAR), 488 thoracic trauma ARDS, 460–462, 460f chest radiograph of, 461f ECMO for, 460–462, 461f burn injury, 457 life-threatening complications of, 455–457, 456f hemothorax, 456 pneumothorax, 456, 457, 458f Index thoracic trauma (Cont.): pneumonia, 457, 459, 460 pulmonary contusion, 457, 459 chest radiograph of, 459f complications of, 459–460, 460f CT scan of, 460f rib fractures, 457, 458f thrombolysis for ICH, 45 intravenous, for acute ischemic stroke, 96, 98, 102–103 thrombosis, risk reduction for, 377 thrombotic thrombocytopenic purpura, 807 thymectomy, for neuromuscular diseases, 139t thyroid crisis, 908–909 thyroid storm, 909–910 ticagrelor, 570 tick paralysis, 127 ticlopidine, 568, 570 TIMI risk score calculation, 566t tobramycin, 855t torsades de pointes, 613t torsemide, 620 toxicity, organophosphate, neuromuscular diseases, 128, 130 tracheostomy, 723 after acute brain injury, 724t anatomical considerations for, 724 cervical spine injury and, 730 coagulopathy and, 729 complications of, 728–729, 728t indications for, 724t intracranial hypertension and, 729–730 obesity and, 730 percutaneous dilational, 726–727 bronchoscopy for, 745 technique for, 746t programmatic approach to, 731 severe respiratory failure and, 730 tube selection for, 725–726 transcranial Doppler (TCD) for acute ischemic stroke, 95 of symptomatic vasospasm, 14–16 Transfusion Requirements in Critical Care (TRICC) trial, 84 transfusions for abdominal trauma, 480 for stab wounds, 477 TBI and, 84 PbtO2 and, 261–262 971 trauma brain injury, 77–85 antibiotics for, 80 cervical spine clearance and, 82 CPP goal for, 80–81 craniotomy after, 82 CT scan of, 78f–79f DVT prevention and, 82–83 hypertonic saline for, 83–84 hypothermia after, 81 ICP monitoring after, 80 management of, 77–78 mannitol for, 83 osmotic agents for, 83–84 PbtO2 and, 80 prophylactic AED for, 78–80 steroids after, 80 sympathetic storming after, 84–85 transfusions and, 84 ventilation and, 84 spinal cord injury, 85–87 cardiac system and, 87 classification of, 85, 86f DVT prophylaxis and, 87 infectious complications and, 87 respiratory system and, 86–87 steroids after, 85 surgical decompression for, 87 trauma, abdominal from automobile collision, 470–471 blood transfusion for, 480 CT scan for, 471–472, 473, 473t DPL for, 471–473, 473t FAST examination for, 471–472, 472f, 473, 473t, 474f fluid administration for, 471 higher level of care transfer indications for, 474, 475t, 476t intraperitoneal bleeding and, 474 retroperitoneal bleed from pelvic fractures, 480 blunt penetration hepatic injury from, 484 splenic injury from, 483–484 exploratory laparotomy indications in, 477, 478t from gunshot wounds, 477 pancreatic injury from, 479–480 from stab wounds, 475–479 abdominal compartment syndrome due to, 478 972 Index trauma, abdominal, from stab wounds (Cont.): antibiotics for, 478 blood transfusion for, 477 FAST examination for, 476, 477 fluid administration for, 477 IAH due to, 478 laparotomy for, 477 liver injury and, 479, 479t primary survey for, 476 secondary survey for, 478–479 tertiary survey for, 477 trauma, blunt to abdomen hepatic injury from, 484 splenic injury from, 483–484 cardiac, stab wounds and, 488–489 compression forces in, 483 deceleration forces in, 483 solid organ injuries and, 483 vascular injuries and, 483 trauma, cardiac, stab wounds and blunt, 488–489 penetrating, 488–489 trauma, penetrating solid organ injuries and, 483 vascular injuries and, 483 trauma, thoracic ARDS, 460–462, 460f chest radiograph of, 461f ECMO for, 460–462, 461f burn injury, 457 life-threatening complications of, 455–457, 456f hemothorax, 456 pneumothorax, 456, 457, 458f pneumonia, 457, 459, 460 pulmonary contusion, 457, 459 chest radiograph of, 459f complications of, 459–460, 460f CT scan of, 460f rib fractures, 457, 458f traumatic brain injury (TBI), 77–85, 802t antibiotics for, 80 BAEPs after, 310 cEEG and, 241 on phenobarbital bolus, 239, 241, 241f cervical spine clearance and, 82 CPP goal for, 80–81 CPP management and, 294–295 craniotomy after, 82 CT scan of, 78f–79f traumatic brain injury (TBI) (Cont.): DVT prevention and, 82–83 EPs after, 309 fever control and, 350 hypertonic saline for, 83–84 hypothermia after, 81 ICP monitoring after, 80 jugular bulb oximetry monitoring for, 275, 275f ketamine and, 328–329 management of, 77–78 mannitol for, 83 osmotic agents for, 83–84 PbtO2 and, 80, 256–257 blood transfusion and, 261–262 brain glucose decrease and, 266, 269f brain metabolism and, 266 cardiac performance optimization and, 262, 264f CO2 and, 259, 259f CPP correlation with, 259–260, 260f, 261f decrease in, 257, 259 FiO2 increase and, 260 LPR increase and, 266, 269f treatment to increase, 257, 258f, 262, 262f, 263f prophylactic AED for, 78–80 SSEPs and, 308, 309, 309f steroids after, 80 sympathetic storming after, 84–85 transfusions and, 84 ventilation and, 84 TRICC See Transfusion Requirements in Critical Care trial triggering, in mechanical ventilation, 673–674, 674t triple-H therapy, for symptomatic vasospasm, 18–20 troponin See biomarkers tumors of brain acoustic neuroma, 174–175, 174f, 175f CT scan of, 155, 156f, 159f, 162f DWI of, 157, 158f hemangioblastoma, 161–162 hemorrhagic brain lesions, 168–172 hydrocephalus and, 161 hyperosmolar therapy, 156 ICP and, 155, 156, 157 malignant glioma, 172–173, 172f, 173f management of, 155–157 Index tumors, of brain (Cont.): MRA of, 157, 157f MRI of, 157, 157f, 161f, 163f operative resection of, 158, 159 pituitary adenoma, 165 pituitary apoplexy and, 165–168, 166f cerebellopontine angle, postoperative complications with, 440t supratentorial resection, craniotomy for, 439t T-wave, changes on ECG, 567t U UA See unstable angina UFH See unfractionated heparin UIAs See unruptured intracranial aneurysms ultrasonography, chest, 534, 535f for acute severe dyspnea, 539–540, 540f of air bronchograms, 537, 538f of alveolar consolidation, 537–538, 538f clinical scenarios for, 539–540 limitations of, 540 lung pattern on, 535–536, 536f, 537f, 539f pathologic process suspicion on, 537–539, 537f, 538f, 539f of pleural effusion, 537, 537f of pneumothorax, 538–539, 539f role for performing, 534 scanning zones for, 534–535, 535f ultrasound, volume responsiveness assessment by, 528, 529f, 539 IVC variation measurement, 530, 532–533, 532f, 533f, 534 measurement location, 530, 532–533, 533f passive leg raise test and, 534 requisite images, 530, 531f, 532–533, 532f unfractionated heparin (UFH), 150, 714 unruptured intracranial aneurysms (UIAs) craniotomy for, 439t DSA of, 393, 393f hydrocephalus and, 396 management of, 393, 394 myocardial infarction and, 398 neurologic deficits and, 388t rupture rates for, 394t rupture risk for, 393–394 surgical clipping for, 396 complications from, 397t diagnostic modalities in NICU status post, 398 perioperative management, 396 postoperative management, 398 973 unruptured intracranial aneurysms (UIAs), surgical clipping for (Cont.): rebleeding after, 396, 397t symptoms of, 395 unstable angina (UA), 545 treatment algorithm for, 569f upper gastrointestinal bleeding See gastrointestinal bleed (GIB) ureteral injury causes of, 518 classification by, 518, 518t evaluation of, 518 management of, 518 urethral catheters, for acute urinary retention, 523, 524t urethral injury causes of, 519–520 classification of, 520, 520t evaluation of, 520 management of, 520 urinalysis, in intrinsic renal disease, 756t urinary catheter, urine specimen and, 887 urinary retention, acute See acute urinary retention urinary tract infection (UTI), 884–885, 885f urine osmolality, 777–778, 778f UTI See urinary tract infection V VA-ECMO See veno-arterial extracorporeal membrane oxygenation valproate, 54t valproic acid, phenytoin and, 61 vancomycin, 80, 147t, 855t VAP See ventilator-associated pneumonia variceal bleeding, 493t VAS See Verbal or Visual Analog Scale vascular injuries acute coronary syndrome, 485 aneurysm dissection formation, 486–487 mechanism of, 486–487 mesenteric ischemia from, 488 open repair of, 487 surgical options for, 487–488 TEVAR for, 488 blunt trauma and, 483 carotid artery dissection, 484–485 carotid bruit, 484–485 interventional radiology role in, 484 from motor vehicle accident, 482 974 Index vascular injuries (Cont.): penetrating trauma and, 483 primary survey for, 482 stab wounds See stab wounds vasculitis, serologic evaluation of, 756t vasodilators, intravenous, 621 vasogenic edema, 159, 159f, 160 vasopressin, 144, 144t, 833t vasopressors, 624 for acute ischemic stroke, 112–113 cerebral circulation and, 144t vasospasm cerebral angiography of, 269f, 293f multimodality pattern seen during, 268, 269f after SAH, 292, 294 treatment of, 271, 272f vasospasm, symptomatic approach to, 14–18 cEEG, 18 CTA, 16–17, 17f CTP, 16–17, 17f transcranial Doppler, 14–16 therapy for, 18–22 basal cistern implants of calcium channel blockers, 21–22 blood pressure management, 19–20 cerebral angiography, 21, 21f intra-aortic balloon counterpulsation therapy, 22 intrathecal infusion of calcium channel blockers, 21–22 NeuroFlo device, 22, 23f, 24f triple-H, 18–20 volume management, 19–20 veno-arterial extracorporeal membrane oxygenation (VA-ECMO), 461–462 venous blood compartment, 684–686, 685f venous thromboembolism (VTE), 712–713 incidence of, 713t veno-venous extracorporeal membrane oxygenation (VV-ECMO), 461–462 ventilation failure of, 657–659 high-frequency, ARDS and, 706 mechanical, 672, 703 airway pressures, 677–679 approach to, 705–706 for ARDS, 703 cerebral blood flow and, 684–686 controlled ventilation vs., 676–677 ventilation, mechanical (Cont.): cycling, 674–676, 674t expiration, 676 hypoxemia mechanisms, 680t indications for, 673, 673t inspiration, 674, 674t mode of, 676 respiratory system mechanics, 677–679 triggering, 673–674, 674t TBI and, 84 weaning from, weakness and, 135, 137 ventilation perfusion (V/Q ) scan, pulmonary embolism and, 717 ventilator-associated pneumonia (VAP), 736, 878–879 antibiotic therapy for, 880–882, 881f chest radiograph of, 295f risk reduction for, 884 ventilator-induced lung injury (VILI), 687–688 brain and, 688–689 ventricular arrhythmias, 606–616, 608f See also wide complex tachycardias development of, 612, 614 ventricular septal rupture, 576 ventricular tachycardia, significance of, 614, 615f ventriculitis, 418 ventriculomegaly, CT of, 391, 391f ventriculoperitoneal shunt (VPS) placement, in EVD for hydrocephalus, 422–423 ventriculostomy, for SAH with hydrocephalus, 411–412 ventriculostomy-related infections (VRIs), 418 VEPs See visual evoked potentials verapamil, 608t Verbal or Visual Analog Scale (VAS), 330 Veterans Administration Cooperative Study, 556 VHL See Von Hippel–Lindau disease Vigileo, 289 VILI See ventilator-induced lung injury VINDICATE mnemonic, weakness and, 124t–126t Virchow triad, 713f visual evoked potentials (VEPs), 301 vitamin K, for warfarin-induced coagulopathy, deep brain hemorrhage and, 813 volume management, for symptomatic vasospasm, 19–20 volume responsiveness assessment, by ultrasound, 528, 529f, 539 IVC variation measurement, 530, 532–533, 532f, 533f, 534 Index volume responsiveness assessment, by ultrasound (Cont.): measurement locations, 530, 532–533, 533f passive leg raise test and, 534 requisite images, 530, 531f, 532–533, 532f Von Hippel–Lindau (VHL) disease, 162 VPS See ventriculoperitoneal shunt placement VQ See ventilation perfusion scan VRIs See ventriculostomy-related infections VTE See venous thromboembolism VV-ECMO See veno-venous extracorporeal membrane oxygenation W Wake up and Breathe trial, 135 warfarin, ICH and, 37, 38t Warfarin Versus Aspirin Symptomatic Intracranial Disease Study for Stroke (WASID), 375 warfarin-induced coagulopathy, deep brain hemorrhage and, 813–814 FFP, 813–814 PCC, 814, 814t rFVIIa and, 814 vitamin K and, 813 WASID See Warfarin Versus Aspirin Symptomatic Intracranial Disease Study for Stroke waveforms, ICP, 3f, 214–216, 216f, 217f, 418– 419, 420t intracranial compliance and, 215, 216f weakness See also acute bilateral weakness bedrest and, 133, 135 mobilization and, 133, 135 975 weakness (Cont.): motor, differential diagnosis for, 123, 124t–126t sensory, differential diagnosis for, 123, 124t–126t ventilator weaning and, 135, 137 VINDICATE mnemonic and, 124t–126t Wenckebach See second-degree atrioventricular block West Haven Criteria, 205–206, 205t WFNS See World Federation of Neurosurgical Societies Scale wide complex tachycardias, 606–616, 608f accelerated idioventricular rhythm, 611, 611f differential diagnosis for, 606–608 management of, 614–616 monomorphic ventricular tachycardia, 610 polymorphic ventricular tachycardia, 611, 612f prolonged QT intervals, 611, 613t supraventricular tachycardia, 611–612 supraventricular with aberration, 608–612, 609f–610f, 610t of ventricular origin, 608–612, 609f–610f, 610t Wolff-Parkinson-White (WPW) syndrome, 598, 599f, 604 World Federation of Neurosurgical Societies (WFNS) Scale, 5, 6t WPW See Wolff-Parkinson-White syndrome Z Zoll Intravascular Temperature Management System, 348f ... conditions other than acute coronary syndrome and heart failure Clin Chem 20 09;55( 12) :20 98 -21 12; and Jaffe AS, Babuin L, Apple FS Biomarkers in acute cardiac disease: the present and the future JACC 20 06;48(1):1-11.)... the 20 05 guideline and 20 07 focused update]: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines Circulation 20 09; 120 ;22 71 -23 06.)... posterolateral wall of the left ventricle The RCA supplies the right ventricle, the inferior and true posterior walls of the left ventricle, and the posterior third of the septum The usual ECG evolution