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Related Concept Videos

Secondary Spinal Cord Injury llI: Pathophysiology01:25

Secondary Spinal Cord Injury llI: Pathophysiology

Early Ischemia and Ionic ImbalanceWithin minutes of spinal cord injury, a secondary cascade begins, progressing over hours to weeks. Vascular damage reduces blood flow, causing ischemia and mitochondrial dysfunction. ATP depletion leads to ion pump failure, membrane depolarization, sodium influx, potassium efflux, and water accumulation, resulting in cellular swelling. Increased intracellular calcium further disrupts mitochondria and accelerates cellular injury.Excitotoxicity and Neuronal...
Spinal Cord Injury ll: Pathophysiology01:14

Spinal Cord Injury ll: Pathophysiology

Spinal cord injury progresses through two interconnected phases: primary injury and secondary injury.Primary InjuryPrimary injury happens at the moment of trauma and involves immediate mechanical damage to the spinal cord.Compression happens when broken vertebrae, herniated discs, or accumulating blood (such as a hematoma) press directly against the spinal cord, distorting its normal shape and function. In cases of contusion, the cord is bruised by a blunt force (like penetrating injuries or...
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An ischemic stroke occurs when a cerebral blood vessel becomes obstructed, most often by a thrombus or embolus, interrupting the delivery of oxygen and glucose to brain tissue. Because neurons rely on continuous aerobic metabolism, energy failure begins within minutes of reduced perfusion. The region receiving the least blood flow becomes the infarct core, an area of irreversible cellular death. Surrounding this core lies the penumbra, a zone of hypoperfused but still viable tissue that is...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
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Cellular injury is any process that disrupts a cell’s ability to maintain homeostasis, leading to structural or functional changes. It is broadly classified based on etiology (cause) and mechanism of damage.Classification by EtiologyCellular injury may result from several causes. Hypoxic injury happens due to reduced oxygen delivery, most commonly from inadequate blood supply, such as arterial obstruction; for example, coronary artery thrombosis can cause myocardial infarction. Chemical injury...
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Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.

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Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
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Published on: November 19, 2012

Alterations in arterial function after high-voltage electrical injury.

Kyoung-Ha Park1, Woo Jung Park, Min-Kyu Kim

  • 1Department of Cardiology, Hallym University Hangang Sacred Heart Hospital, 94-200, Yeongdeungpo-dong, 150-030 Seoul, Korea. pkhmd@naver.com

Critical Care (London, England)
|February 14, 2012
PubMed
Summary

High-voltage electrical injury (HVEI) significantly impairs arterial endothelial and smooth muscle function for at least six weeks. Long-term monitoring is crucial for HVEI survivors due to potential risks of thrombosis and stenosis.

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Area of Science:

  • Vascular Biology
  • Trauma Medicine
  • Cardiovascular Physiology

Background:

  • High-voltage electrical injury (HVEI) can cause significant vascular damage.
  • Assessing endothelial and smooth muscle function is critical for understanding post-injury vascular health.

Purpose of the Study:

  • To evaluate functional changes in arterial endothelium and smooth muscle post-HVEI.
  • To compare flow-mediated dilation (FMD) and nitrate-mediated dilation (NMD) in injured versus healthy individuals.

Main Methods:

  • Twenty-five male patients with upper extremity HVEI were assessed for brachial artery FMD and NMD within 48 hours and at six weeks post-injury.
  • A control group of 25 healthy individuals was used for comparison.
  • Follow-up FMD in the uninjured contralateral arm was also assessed in a subset of patients.

Main Results:

  • HVEI patients showed significantly reduced initial FMD compared to controls (2.1% vs 13.6%).
  • FMD improved at six weeks but remained lower than controls (5.1% vs 13.6%).
  • Nitrate-mediated dilation (NMD) was significantly lower in HVEI patients both initially and at follow-up compared to controls.

Conclusions:

  • HVEI leads to significant, lasting impairment of brachial artery endothelial and smooth muscle function for at least six weeks.
  • HVEI survivors may have an increased risk of thrombosis or stenosis, necessitating long-term cautious care.