Ebook The neuro ICU book: Part 2
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Ebook The neuro ICU book: Part 2
SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2-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 per-e ED (Figure 31 Ebook The neuro ICU book: Part 2-1) showed a large acute nonhemorrhagic right hemisphericinfarct within the vascular territory of the right middle cerebral artery. The infarct involvEbook The neuro ICU book: Part 2
ed large portions of the frontal, temporal, and parietal lobes as well as underlying basal ganglia structures. The proximal right middle cerebral arteSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2 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.He Ebook The neuro ICU book: Part 2art 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 arteEbook The neuro ICU book: Part 2
rial oxygen saturation (SaO2) 98% on 6 L oxygen. Cardiovascular examination was notable for jugular venous distention with an estimated jugular venousSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2lungs 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/pl, hemoglobin (Hb) of 12.2 g/dl, and platelets of 413,000/pl. Cardiac biomarkers were elevated with Ebook The neuro ICU book: Part 2 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-raEbook The neuro ICU book: Part 2
y were performed on admission (Figures 3 1-2 and 31-3).CardiovascularProblems543544 SECĨION6 • Cdroiũvôsculôr ProblemsFigure 31-1. Computed axial tomoSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2 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 strok Ebook The neuro ICU book: Part 2e is discussed in Chapter 5.How would you classify this patient's clinical presentation? How do you define acute coronary syndrome?This patient presenEbook The neuro ICU book: Part 2
ts with ECG and laboratory evidence of myocardial infarction. The initial ECG showed ST depressions anteriorly, which should alert the clinician to thSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2 leads, which can be accomplished by placing three electrodes—v_, Vg, 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 V Ebook The neuro ICU book: Part 2, 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 heartEbook The neuro ICU book: Part 2
. 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 V, through VySECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2), and ST-seginent-elevation myocardial infarction (STEMI). Variant angina, also known as Prinzmetal angina, can manifest as ST-segment-elevation on the electrocardiogram and elevated serum troponin levels but is pathologically distinct from acute coronary syndrome. Although the pathogenesis and cli Ebook The neuro ICU book: Part 2nical presentation of ƯA and NSTEMI are similar, the presence of serum cardiac biomarkers, troponin I, or troponin T distinguishes NSTEMI from ƯA. InEbook The neuro ICU book: Part 2
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 PathogSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2 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 a Ebook The neuro ICU book: Part 2cute coronary artery disease had largely been limited to postmortem data. In 1912, Dr. James Herrick published an autopsy study that associated the clEbook The neuro ICU book: Part 2
inical presentation of acute infarction with a thrombotic coronary occlusion.’ Coronary artery occlusionCardiovasculaProblems546 SECTION 6 • CỏrdíOvàsSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2bed 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 vulner Ebook The neuro ICU book: Part 2able plaque develops is far from being complete.Histopathologic and angioscopic studies have demonstrated that both plaque rupture and erosion leadingEbook The neuro ICU book: Part 2
to thrombosis are the most common causes of acute coronary syndrome. Plaques that are more likely to rupture are termed vulnerable plaques or thin-caSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2.4 '’ 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 though Ebook The neuro ICU book: Part 2t that plaque rupture accounts for > 70% of fatal acute myocardial infarctions and/or sudden cardiac death. The smaller concentration of smooth muscleEbook The neuro ICU book: Part 2
cells is thought to weaken the mechanical resistance of the plaque. Plaque rupture generally occurs where the plaque is thinnest and has the highest SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2plaque and the area of the vessel wall that is less diseased.8Plaque erosion refers to a thin-cap flbroatheroma 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 a Ebook The neuro ICU book: Part 2nd proteoglycans. Luminal thrombi occur in denuded areas lacking surface endothelium. Unlike plaques prone to rupture, plaques prone to erosion typicaEbook The neuro ICU book: Part 2
lly lack a necrotic core of lipid but rather are composed of macrophages and lymphocytes. Lastly, calcified nodules are plaques with luminal thrombi sSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2s 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 Ebook The neuro ICU book: Part 2lumen, possibly causing the thrombus.10Numerous postmortem studies have identified ruptured plaque as the cause of thrombosis in acute myocardial infaEbook The neuro ICU book: Part 2
rction. Richardson et al studied 85 coronary thrombi postmortem and found a disrupted atheromatous plaque beneath 71 (84%) of the thrombi." Studies coSECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67- Ebook The neuro ICU book: Part 2inal 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.1210 The composition and vulnerability' of plaque rather than its volume or the consequent Ebook The neuro ICU book: Part 2severity of stenosis produced have emerged as being the most important determinants of the development of the thrombus-mediated acute coronary' syndroEbook The neuro ICU book: Part 2
mes.8 In addition, both angiographic studies and intravascular ultrasound of plaque morphology in patients presenting with acute coronary' syndrome haGọi ngay
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