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Ebook The NeuroICU book (1/E): Part 2

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Ebook The NeuroICU book (1/E): Part 2

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): 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 dev

iation, 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 NeuroICU book (1/E): Part 2

-1) showed a large acute nonhemorrhagic right hemisphericinfarct within the vascular territory of the right middle cerebral artery. The infarct involv

Ebook The NeuroICU book (1/E): Part 2

ed large portions of the frontal, temporal, and parietal lobes as well as underlying basal ganglia structures. The proximal right middle cerebral arte

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): Part 2 symptoms. The local ED physicians decided to transfer the patient immediately to the nearest tertiary medical center. On arrival to the intensive car

e 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 NeuroICU book (1/E): Part 2

art 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 arte

Ebook The NeuroICU book (1/E): Part 2

rial oxygen saturation (SaO2) 98% on 6 L oxygen. Cardiovascular examination was notable for jugular venous distention with an estimated jugular venous

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): 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 NeuroICU book (1/E): 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-ra

Ebook The NeuroICU book (1/E): Part 2

y were performed on admission (Figures 3 1-2 and 31-3).CardiovascularProblems543544 SECĨION6 • Cdroiũvôsculôr ProblemsFigure 31-1. Computed axial tomo

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): Part 2 be the first step in managing this patient?This patient presents with acute ischemic stroke and myocardial infarction. There is evidence of hemodynam

ic deterioration; therefore, a decision regarding management of acute coronary syndrome (ACS) must be made quickly. Management of acute ischemic strok Ebook The NeuroICU book (1/E): Part 2

e is discussed in Chapter 5.How would you classify this patient's clinical presentation? How do you define acute coronary syndrome?This patient presen

Ebook The NeuroICU book (1/E): Part 2

ts with ECG and laboratory evidence of myocardial infarction. The initial ECG showed ST depressions anteriorly, which should alert the clinician to th

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): 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 NeuroICU book (1/E): 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 heart

Ebook The NeuroICU book (1/E): 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 Vy

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): Part 2), and ST-seginent-elevation myocardial infarction (STEMI). Variant angina, also known as Prinzmetal angina, can manifest as ST-segment-elevation on t

he electrocardiogram and elevated serum troponin levels but is pathologically distinct from acute coronary syndrome. Although the pathogenesis and cli Ebook The NeuroICU book (1/E): Part 2

nical presentation of ƯA and NSTEMI are similar, the presence of serum cardiac biomarkers, troponin I, or troponin T distinguishes NSTEMI from ƯA. In

Ebook The NeuroICU book (1/E): 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 Pathog

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): 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 NeuroICU book (1/E): Part 2

cute coronary artery disease had largely been limited to postmortem data. In 1912, Dr. James Herrick published an autopsy study that associated the cl

Ebook The NeuroICU book (1/E): Part 2

inical presentation of acute infarction with a thrombotic coronary occlusion.’ Coronary artery occlusionCardiovasculaProblems546 SECTION 6 • CỏrdíOvàs

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): 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 NeuroICU book (1/E): Part 2

able plaque develops is far from being complete.Histopathologic and angioscopic studies have demonstrated that both plaque rupture and erosion leading

Ebook The NeuroICU book (1/E): 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-ca

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): Part 2.4 '’ Plaque with a lipid core often contains oxidized lipids and macrophage-derived tissue factor, which makes the plaque highly thrombogenic when it

s 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 NeuroICU book (1/E): Part 2

t that plaque rupture accounts for > 70% of fatal acute myocardial infarctions and/or sudden cardiac death. The smaller concentration of smooth muscle

Ebook The NeuroICU book (1/E): 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 NeuroICU book (1/E): 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 d

efect 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 NeuroICU book (1/E): Part 2

nd proteoglycans. Luminal thrombi occur in denuded areas lacking surface endothelium. Unlike plaques prone to rupture, plaques prone to erosion typica

Ebook The NeuroICU book (1/E): 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 s

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): 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 o

f the lesion. However, there are superficial, dense, calcified nodules within the intima, which appear to be erupting through fibrous tissue into the Ebook The NeuroICU book (1/E): Part 2

lumen, possibly causing the thrombus.10Numerous postmortem studies have identified ruptured plaque as the cause of thrombosis in acute myocardial infa

Ebook The NeuroICU book (1/E): Part 2

rction. Richardson et al studied 85 coronary thrombi postmortem and found a disrupted atheromatous plaque beneath 71 (84%) of the thrombi." Studies co

SECTION 6Cardiovascular ProblemsSection Editor: Joseph E. Parrillo, MD, FCCPAcute Coronary SyndromeJoanne Mazzaretli, MDSteven Werns, MDformed inA 67-

Ebook The NeuroICU book (1/E): 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 w

ere 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 NeuroICU book (1/E): Part 2

severity of stenosis produced have emerged as being the most important determinants of the development of the thrombus-mediated acute coronary' syndro

Ebook The NeuroICU book (1/E): Part 2

mes.8 In addition, both angiographic studies and intravascular ultrasound of plaque morphology in patients presenting with acute coronary' syndrome ha

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