Cardiac abnormalities ischemia

CNS disorders CNS adverse reactions including decreased mental status, gait disturbance, and dizziness have been observed, particularly in patients receiving doses greater than 250 mcg/m /day. Most of these abnormalities were mild and reversible within a few days upon dose reduction or discontinuation of therapy. Exercise caution in patients with seizure disorders and compromised CNS function. Cardiac disease Use with caution in patients with pre-existing cardiac disease, including symptoms of ischemia, CHF, or arrhythmia. 

Many factors can precipitate or exacerbate arrhythmias ischemia, hypoxia, acidosis or alkalosis, electrolyte abnormalities, excessive catecholamine exposure, autonomic influences, drug toxicity (eg, digitalis or antiarrhythmic drugs), overstretching of cardiac fibers, and the presence of scarred or otherwise diseased tissue. However, all arrhythmias result from (1) disturbances in impulse formation, (2) disturbances in impulse conduction, or (3) both. 

Eliminate the cause. Precipitating factors must be recognized and eliminated if possible. These include not only abnormalities of internal homeostasis, such as hypoxia or electrolyte abnormalities (especially hypokalemia or hypomagnesemia), but also drug therapy and underlying disease states such as hyperthyroidism or cardiac disease. It is important to separate this abnormal substrate from triggering factors, such as myocardial ischemia or acute cardiac dilation, which may be treatable and reversible. 

S100B Overexpression Female specific hyperactivity, lack of habituation to novelty, reduced T-maze spontaneous alternation rate, abnormal exploratory behavior Enhanced astrocytosis and neurite proliferation Impaired learning and memory, increased dendrite density, enhanced age-related loss of dendrites Inhibitory effect on cardiac hypertrophy Increased susceptibility to hypoxia-ischemia Increased apoptosis after myocardial infarction Enhanced neuroinflammation and neuronal dysfunction induced by amyloid-(3... 

Several disease states can result from abnormal blood clots. For example, strokes were mentioned previously. However, the most common and deadliest thrombotic disease is myocardial infarction (MI). Atherosclerosis has long been associated with reduced cardiac function and elevated mortality due to rupture of atherosclerotic plaques. The rupture of an atherosclerotic plaque usually results not only in blockage due to the plaque itself but also in the immediate formation of an occlusive blood clot, which results in an MI. Immediately after the initiation of an MI, a zone of necrosis begins to develop around the area as ischemia proceeds. It is during this early phase of ischemia (several hours) that therapeutic intervention not only can be life-saving but also can minimize the amount of necrotic heart tissue formed. 

The authors of a review of the cardiac toxicity associated with paclitaxel in a number of studies concluded that the overall incidence of serious cardiac events is low (0.1%) (20). Heart block and conduction abnormalities occurred infrequently and were often asymptomatic. Sinus bradycardia was the most frequent, occurring in 30% of patients. The causal relation of paclitaxel to atrial and ventricular dysrhythmias and cardiac ischemia was not entirely clear. There did not appear to be any evidence of cumulative toxicity or augmentation of acute cardiac effects of the anthracydines. 

ECHO is the use of ultrasound to visualize anatomic structures such as the valves within the heart and to describe wall motion. Clinically, ECHO is the most frequently used noninvasive cardiovascular test, aside from the ECG. It competes well with invasive techniques such as cardiac catheterization with angiography for the evaluation of ischemia and valvular abnormalities. ECHO is... 

Dobutamine, a synthetic catecholamine, increases heart rate and cardiac output, resulting in an increase in myocardial oxygen demand. Ischemia develops in areas where stenosis prevents the increase in oxygen demand from being met with increased blood flow. Ischemia is detected by ECHO as regional wall motion abnormalities or with thallium scanning. 

Patients with diastolic heart failure are typically dependent upon preload to maintain adequate cardiac output. While patients with symptomatic volume overload will benefit from careful modulation of intravascular volume, volume reduction should be accomplished gradually and treatment goals reassessed frequently. In addition to cautious volume management, it is important to maintain synchronous atrial contraction in such patients, which maintains adequate left ventricular filling during the latter phase of diastole. Cardiac function is often severely impaired if patients with diastolic heart failure develop atrial fibrillation, particularly in the context of sub-optimal ventricular rate control. Meticulous control of the ventricular rate with drugs that slow AV conduction is mandatory (see Chapter 34) and restoration of sinus rhythm should be considered. It is also important to evaluate and treat conditions that are associated with dynamic abnormalities of diastolic function, such as myocardial ischemia and poorly controlled systemic hypertension. 

Enhanced automaticity may occur in cells that normally display spontaneous diastolic depolarization— the sinus andAVnodes and the His-Purkinje system. [) Adrenergic stimulation, hypokalemia, and mechanical stretch of cardiac muscle cells increase phase 4 slope and so accelerate pacemaker rate, whereas acetylcholine reduces pacemaker rate both by decreasing phase 4 slope and by hyperpolarization (making the maximum diastolic potential more negative). In addition, automatic behavior may occur in sites that ordinarily lack spontaneous pacemaker activity e.g., depolarization of ventricular cells by ischemia) may produce such abnormal" automaticity. 

If hypertension is accompanied by a focally abnormal neurologic examination (eg, hemiparesis), perform a computed tomography (CT) scan as quickly as possible. In a patient with a cerebrovascular accident, hypertension should generally not be treated unless specific complications of the elevated pressure (eg, heart failure or cardiac ischemia) are present. Consult a neurologist. 

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