Hypoxia myocardial

The goal of treatment is to prevent myocardial hypoxia either by raising blood flow (oxygen supply) or by lowering myocardial blood demand (oxygen demand) (A). 

Angiogenesis driven by myocardial hypoxia may permit collateral formation, relief of angina, and minimize tissue damage during myocardial infarction. On the other hand, hypoxic drive to retinal neovascularization can contribute to retinal hemorrhage and blindness. 

Ng CK, Sisanus AJ, Zaret BL, Soufer R. Kinetic analysis of technetium-99m-labeled nitroimidazole (BMS-181321) as a tracer of myocardial hypoxia. Circulation 1995 92 1261-1268. 

Ventricular premature depolarizations occur with variable frequency, depending on underlying comorbid conditions. The prevalence of complex or frequent VPDs is approximately 33% and 12% in men with and without CAD, respectively 34 in women, the prevalence of complex or frequent VPDs is 26% and 12% in those with and without CAD, respectively.35 Ventricular premature depolarizations occur more commonly in patients with ischemic heart disease, a history of myocardial infarction, and HF due to LV dysfunction. They may also occur as a result of hypoxia, anemia, and following cardiac surgery. 

From earlier times when it has first been established that ischemia and hypoxia are the potential causes of coronary heart disease and myocardial infraction [50,51], antioxidants... 

Acidosis occurs during cardiac arrest because of decreased blood flow and inadequate ventilation. Chest compressions generate only about 20% to 30% of normal cardiac output, leading to inadequate organ perfusion, tissue hypoxia, and metabolic acidosis. Furthermore, the lack of ventilation causes retention of carbon dioxide, leading to respiratory acidosis. The combined acidosis reduces myocardial contractility and may cause arrhythmias because of a lower fibrillation threshold. 

Anxiety is common among the elderly but the literature regarding the assessment, diagnosis, and treatment of these illnesses in older individuals is sparse (Blazer 1997). Most often anxiety does not present for the first time in late life. If that is the case one should suspect an underlying condition or other external cause. These causes could be medications such as digitalis, antipsychotics but also conditions as anaemia, chronic obstructive lung disease with hypoxia or myocardial infarction. 

An anginal pain attack signals a transient hypoxia of the myocardium. As a rule, the oxygen deficit results from inadequate myocardial blood flow due to narrowing of larger coronary arteries. 

T.R. de Grado, M.T. Kitapci, S. Wang, J. Ying, Validation of F-fluoro-4-thia-palmitate as a PET probe for myocardial fatty acid oxidation Effects of hypoxia and composition of exogenous fatty acids, J. Nucl. Med. 47 (2006) 173-181. 

T.R. DeGrado, M.T. Kitapci, S. Wang, J. Ying, G.D. Lopaschuk, Validation of F-fluoro-4-thia-palmitate as a PET probe for myocardial fatty acid oxidation Effects of hypoxia and composition of exogenous fatty acids, J. Nucl. Med. 47 (2006) 173-181. T.M. Shoup, D.R. Elmaleh, A.A. Bonab, A.J. Fischman, Evaluation of trans-9- F-fluoro-3,4-methyleneheptadecanoic acid as a PET tracer for myocardial fatty acid imaging, J. Nucl. Med. 46 (2005) 297-304. 

Cyanide toxicity, overshoot hypotension, and myocardial ischaemia. Hypoxia caused by increased ventilation-perfusion mismatch due to pulmonary vasodilatation and inhibition of hypoxic pulmonary vasoconstriction. Rebound hypertension after discontinuation of SNP infusion. 

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. 

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