ventricular muscle
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Folia Medica ◽  
2021 ◽  
Vol 63 (6) ◽  
pp. 981-984
Author(s):  
Feridoun Sabzi ◽  
Aghigh Heydari ◽  
Reza Heidari Moghaddam ◽  
Atefeh Asadmobini

Bentall operation is considered a gold standard of surgery in the treatment of ascending aortic aneurysm. This operation with en-bloc resection of ascending aorta and aortic valve requires aortic valve with two coronary bottoms re-replacements in a prepared composite graft. The four important locations for the pseudoaneurysm include proximal and distal composite graft anastomosis and two coronary bottom sites. However, many complications have been reported with this technique but the most serious complication associated with this operation is defined as pseudoaneurysm. We report an exceedingly rare case of subaortic ring pseudoaneurysm in retro composite graft position enclosed by infected surgical that was used to control bleeding in this location. Dehiscence occurred between the aortic ring and the underlying left ventricular muscle. The aortic ring was separated from the underlying muscle by the high tensile strength of sewing ring sutures. The pseudoaneurysm compressing the left atrium without communicating with any cardiac chamber and presenting with high fever (39°C), chills, a few months after Bentall operation. The patient underwent redo operation and repair of the dehiscence’s site. The 6-month follow-up revealed no recurrence of a pseudoaneurysm. The uniqueness of this case report is related to the site of pseudoaneurysm between the aortic ring and underlying left ventricular muscle that have not been reported in the medical literature so far.


Author(s):  
Ronald F. Coburn

The major goal of this article was to quantify relationships of the carboxyhemoglobin % saturation, a calculated tissue PCO and tissue hypoxia to the binding of carbon monoxide (CO) to canine skeletal and heart ventricular muscle extravascular (EV) tissue under normal conditions and during CO poisoning scenarios. These data are relevant to CO poisoning because CO bound to EV cellular hemoproteins evoke metabolic changes that produce toxic effects. Skeletal and heart muscle EV CO contents were calculated from data obtained from biopsies performed on living anesthetized dogs reported in previous publications (4, 6). Results include normal values of EV CO contents of resting skeletal muscle and heart ventricular muscle, effects of increasing COHb% saturation and a calculated mean tissue PCO on skeletal muscle EV CO binding, and effects of tissue hypoxia evoked by arterial hypoxemia on EV CO binding in both of these tissues. This study is the first that shows that tissue hypoxia-induced CO shifts out of blood resulting in increased EV CO binding are a mechanism that causes CO toxicity. Projections of results to tissue PCO levels occurring during different severe CO toxicity scenarios predict that skeletal muscle EV CO contents could increase as much as 100 to 300 fold.


2020 ◽  
Vol 192 ◽  
pp. 111359
Author(s):  
Kevin Boldt ◽  
Venus Joumaa ◽  
Graham MacDonald ◽  
Jaqueline Lourdes Rios ◽  
Walter Herzog

Author(s):  
Tamás Árpádffy-Lovas ◽  
Zoltán Husti ◽  
István Baczkó ◽  
András Varró ◽  
László Virág

Increased transmural dispersion of repolarization is an established contributing factor to ventricular tachyarrhythmias. In this study, we evaluated the effect of chronic amiodarone treatment and acute administration of dofetilide in canine cardiac preparations containing electrotonically coupled Purkinje fibers (PFs) and ventricular muscle (VM) and compared the effects to those in uncoupled PF and VM preparations using the conventional microelectrode technique. Dispersion between PFs and VM was inferred from the difference in the respective action potential durations (APDs). In coupled preparations, amiodarone decreased the difference in APDs between PFs and VM, thus decreasing dispersion. In the same preparations, dofetilide increased the dispersion by causing a more pronounced prolongation in PFs. This prolongation was even more emphasized in uncoupled PF preparations, while the effect in VM was the same. In uncoupled preparations, amiodarone elicited no change on the difference in APDs. In conclusion, amiodarone decreased the dispersion between PFs and VM, while dofetilide increased it. The measured difference in APD between cardiac regions may be the affected by electrotonic coupling; thus, studying PFs and VM separately may lead to an over- or underestimation of dispersion.


2020 ◽  
Vol 4 (3) ◽  
pp. 438-446
Author(s):  
Setiawidayat Sabar ◽  
Aviv Yuniar Rahman ◽  
Ratna Hidayati

In each cycle of the Heart on the Electrocardiogram there are generally P waves as a presentation of Atrial Muscle Depolarization, QRS waves as a presentation of Ventricular Muscle Depolarization and T waves as a presentation of Ventricular Muscle Repolarization. Some types of electrocardiographs only represent wave morphology and some other types of electrocardiographs are equipped with duration and amplitude information but are limited. This limitation of information is calculated manually using small boxes on ecg paper measuring 40 ms for duration and 1 mV for amplitude. The consequences of this manual calculation will require time and accuracy of the calculation results. This study aims to obtain the QRS wave duration along with the amplitude value in each cycle of cardiac examination results. Discrete data from the sampling results of the ECG continuous signal in the maximum filter amplitude to get peak R values. The position of integer peak R with the next peak R is the duration of the cycle. PQRST algorithm is used to obtain peak Q and peak S, so the duration of QS can be obtained by subtracting the position of integer peak S with integer position Q. 10 samples of discrete ecg Sinus Rhythm data from Physionet and 5 samples from ECG-UWG were used in this study. The results showed that all sample data in 3 cycles had a value of QRS duration and peak amplitude values ​​Q, R and S. Peak amplitude R max values ​​and R min physionet sample records were obtained in record 16273 which was 3,485 mV and record 16795 was 0.805 mV. The QRS duration for Bradicardia and Tachicardia is shown in record 16483 which is 40 ms and record 17052 which is 144 ms.


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