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Case Report
- Neurogenic-stunned Myocardium and Pulmonary Edema Following a Ruptured Cerebral Aneurysm: A Case Report
- Sung Ha Mun, Won Joon Choi, Jeong Min Mok, Jae Young Yang, Chul Ho Woo
- Korean J Crit Care Med. 2010;25(2):93-97.
- DOI: https://doi.org/10.4266/kjccm.2010.25.2.93
- 2,520 View
- 22 Download
- 1 Crossref
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Abstract
PDF - We report a case of neurogenic cardiopulmonary instability with pulmonary edema occurring after an aneurysmal subarachnoid hemorrhage. The patient's pre-operative Glasgow coma scale score was 6 and the PA chest radiograph showed increased diffuse haziness in the right lung field. The patient presented with severe hypotension and low oxygen saturation during surgery. Cardiac damage was documented by increased CK-MB troponin-T levels, and ischemic ECG findings. Reversible cardiac failure associated with subarachnoid hemorrhage may be due to a neurogenic-stunned myocardium. The patient underwent clipping of the aneurysm and recovered with minimal neurologic impairment and normal cardiac function.
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Citations
Citations to this article as recorded by
- A Retrospective Study about Characteristics of Out-of-hospital Cardiac Arrest Caused by Non-traumatic Subarachnoid Hemorrhage
Min Seob Sim, Ki Dong Sung, Mun Ju Kang, Ji Ung Na, Tae Gun Shin, Ik Joon Jo, Hyoung Gon Song, Keun Jeong Song, Yeon Kwon Jeong
The Korean Journal of Critical Care Medicine.2011; 26(3): 151. CrossRef
- A Retrospective Study about Characteristics of Out-of-hospital Cardiac Arrest Caused by Non-traumatic Subarachnoid Hemorrhage
Original Article
- The Direct Myocardial Depressant Effect of Naloxone in Vitro: Mechanical and Electrophysiological Actions
- Ki Jun Kim, Haeng Cheol Lee, Ki Young Lee, Ji Young Kim, Sueng Teck Joo, Wyun Kon Park
- Korean J Crit Care Med. 2002;17(2):107-118.
- 1,496 View
- 13 Download
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Abstract
PDF
- BACKGROUND
Naloxone,an opioidant agonist, has been s hown t o have a c ar di ovascular pressor effect in states of hemorrhagic and endotoxic shock.We determined the direct inotropic effect of naloxone using guinea pig right ventricular papillary muscles.
METHODS
With institutional approval,isometric contractile force was measured in normal and 26mM K+ Tyrode's solution at various stimulation rates.Normal and slow action potentials (APs) were measured with conventional microelectrode technique.The effects of naloxone on sarcoplasmic recticulum function were evaluated by measuring rapid cooling contractures (RCCs)in normal Tyrode 's solution and rested-state (RS)contraction in low Na+ (25 mM)Tyrode's solution.Patch clamp study was performed to examine the direct effect on Ca2+ current in myocytes.
RESULTS
Naloxone (50,100,200 micro M)caused dose-dependent depression of peak force and maximal rate of peak force (dF/dt-max)by 30,50 and 70%,respectively.Modest depression was shown in RS contraction in low Na+ Tyrode's solution.In 26 mM K+ Tyrode's solution,100 micro M naloxone markedly depressed late force development.100 micro M naloxone depressed RCCs by 20%. While 100 micro M naloxone did not alter amplitude or dV/dt-max in normal and slow APs at 0.25 Hz, AP duration was prolonged significantly.In patch clamp study,50 micro M naloxone depressed Ca2+ current by 50%.
CONCLUSIONS
Naloxone depresses contractile force.Myocardial depressant effect partly seems to be caused by depressed Ca2+ influx through cardiac membrane.Rapid release of Ca2+ from the sarcoplasmic reticulum by depolarization and release by rapid cooling seems to be minimally affected.
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