زكاة العلم الدكتور محمد البيضاني

حياكم الله ودكم نحجي على sudden cardiac death هيج لمحات بسيطه باوقات مختلفه بس اريد تكونون متفاعلين

First comment

something about digoxin toxicity : - Lidocaine is a useful agent for treating arrhythmias due to digitalis excess - Second- and third-degree atrioventricular blocks in this setting often respond to atropine - Recurrence of digitalis toxicity may occur 24 to 48 hours after the administration of antidigoxin immunotherapy - Direct-current cardioversion may precipitate ventricular arrhythmias in patients with digitalis intoxication and should be avoided - Dialysis is not effective in cases of massive overdose. - hypokalemia and hypomagnsemia can lead to digoxin toxicity at low toxic dose

First comment

Old age male with history of smoking, Presented with SOB. He looks COPD get well on O2 and ventulin neubilizer. During examination there is irregularity in the radial pulsation. I sent him for ECG and the results revealed - sinus rhythm - frequent supranodal ectopic beat 1- come early 2- same shape of preceded beats 3- post ectopic pause 4- abnormal p wave or absent P wave if the focus of ectopic beats located at or near to the Junctional area. These beats occur due to irritation of atrium by pressure and hypoxia And consider pre AF state.

Young age presented with fainting attacks? ECG show - sinus rhythm with short PR interval - delta wave appear clearly in avF - slightly wide QRS - negative delta wave and R in V1 Conclusion: WPWS type B

النمط الجديد من النشر عاجبكم لو لا!

مرات يجيك مريض عنده جلطه قويه بالقلب او شاب يكبسل و وكف كلبه ورجع بالانعاش وقلبه تعب وخل بعجز قلب ورا اسبوعين اموره تحسنت و وضيفه القلب زينه من sever LV dysfunction صار very mild mild LV dysfunction اقرا 👇🏻 1- Myocardial stunning represents prolonged myocardial dysfunction that follows a brief episode of severe ischemia, with gradual return of contractile activity. 2- myocardial hibernation is the term applied to myocardial dysfunction resulting from chronic hypoperfusion. Notes - Myocardial stunning affects both systolic and diastolic function and may occur in globally as well as regionally ischemic myocardium. - Clinically, stunning is most frequently seen in patients recovering from ischemic arrest during cardiopulmonary bypass. - It is also observed in ischemic regions adjacent to infarcted zones and in territories that are severely ischemic in patients with unstable angina. - There are three likely mechanisms of myocardial stunning: (1) generation of oxygen-derived free radicals. (2) calcium overload. (3) reduced sensitivity of myo filaments to calcium.

Somethings to Know 1- The level of C-reactive protein (CRP), an acute-phase reactant, is approximately five times higher in patients with an ACS compared with those with stable coronary disease, and patients with the highest levels of CRP have an increased risk of death, even if cardiac troponin levels are not elevated. 2- The white blood cell count is a simpler but nonspecific marker of inflammation. Patients with unstable angina/non-ST-seg-ment elevation myocardial infarction (MI) and elevated white blood cell counts have higher mortality and recurrent MI rates. This association is independent of CRP levels. 3- Elevated levels of B-type natriuretic peptide, a neuro-hormone released in response to ventricular wall stress, are associated with a two- to three-fold higher risk of death by 10 months.

Left ventricular (LV) aneurysms 1- arise in less than 5% of patients who survive acute ST-segment elevation myocardial infarction (MI). 2- Formation of the aneurysm is presumed to occur when intraventricular tension leads to expansion of the noncontracting, infarcted myocardial tis-sue. 3- An anterior MI complicated by LV aneurysm occurs due to total occlusion of a poorly collateralized left anterior descending artery. The presence of multivessel disease, extensive collateral vessels, or a nonoccluded left anterior descending artery makes the development of an aneurysm much less likely. 4- Aneurysms occur approximately four times more often at the apex and in the anterior wall than in the inferoposterior wall and, in general, range from 1 to 8 cm in diameter. 5- True LV aneurysms, in contrast to pseudoaneurysms, rarely rupture. 6- the presence of an LV aneurysm increases the rate of mortality up to six times compared with patients without aneurysm. Death in such patients is often sudden and presumed to be secondary to a high incidence of associated ventricular tachyarrhythmias. 7- The diagnosis of an aneurysm is best made by echocardiography, magnetic resonance imag-ing, computed tomography, or left ventriculography. 8- The"classic" evidence of aneurysm on the ECG--persistent ST-segment elevation in the area of the infarction- -actually indicates a large infarct but does not necessarily imply an aneurysmal segment

Atrial fibrillation in acute myocardial infarction 1- usually transient and occurs more commonly in patients with left ventricular failure, infarct-associated pericarditis, or ischemic injury to the atria. 2- Atrial fibrillation is more common during the first 24 hours after infarction than later. 3- It is associated with increased mortality, in part because it occurs more frequently with extensive anterior wall infarctions. 4- The rapid ventricular response and loss of atrial contribution to ventricular filling may lead to an important reduction in cardiac output. 5-In patient who are hemodynamically stable, a beta blocker is typically appropriate to slow the ventricular rate. However, cardioversion is the treatment of choice in patients with evidence of hemodynamic decompensa-tion. 6- Patients with recurrent episodes of atrial fibrillation should be anticoagulated.

Smoking : 1- Cigarette smoking is one of the strongest risk factors for coronary artery disease. 2- smoking increases platelet aggregation, serum fibrinogen, and oxidation of low-density lipoprotein cholesterol. 3- Patients who continue to smoke after a myocardial infarction have twice the mortality rate of those who stop. 4- Observational studies show that smoking cessation reduces the risk of a coronary event by 50% within 2 years, compared with patients who continue to smoke. 5- The cardiovascular risk equal to a person who never smoked after 3 to 5 years of smoking cessation.

Alcohol and IHD : - Moderate alcohol intake (1 or 2 drinks daily) is associated with a lower incidence of coronary heart disease than is no alcohol intake - Alcohol consumption reduces platelet aggregation - Heavy alcohol intake is associated with increased cardiovascular mortality Alcohol not affect the low-density lipoprotein levels - Alcohol raises high-density lipoprotein levels

65 years old male DM and smoker Presented frequent attacks of dyspnea and chest tightness after walking upstairs. she also reported history of pitting odema and attack of palpitations. He had family history of IHD. Echos study show moderate LV systolic dysfunction . ECG show - sinus rhythm with heart rate 100bpm - regular with normal P and PR interval - widespread ST depression ( lead I,II,III avF، avL and V2–6). - ST elevation in avR Conclusion: this patient had LV dysfunction due to three vessel disease as appear clearly in catheterisation. His brother had CABG at age 55 years old

ECG (1) : - wide complex tachycardia - irregular and heat rate 214 bpm - No p wave - delta wave appear clear in pericardial lead - if look carefully to the base of QRS you see different morphology Conclusion:( irregular wide complex tachycardia, heart rate more than 200bpm , no. p wave , delta wave and different morphology of QRS ) this is typical Picture of atrial fibrillation with pre excitation ( AF with WPWS ) . Treatment: - if the patient hemodynamically stable 1- IV procainamide is the drug of choice ( Class Ia antiarrhythmia) 2- IV amidarone is alternative especially in patient with structural heart disease If the patient unstable Cardioversion 200 J Long term treatment is sotalol , flecanide , amidarone Definite treatments: ablation of accessory pathway ECG (2): after 200 J cardioversion show - sinus rhythm with normal heat rate - short PR interval - delta wave - slightly wide QRS - prominent R and delta wave in V1 This is sinus with WPWS type B

27 years old male with negative past medical history of IHD,SHD and congenital heart disease. Presented with palpitations Vital signs wave with normal range.

الجواب على WPWS حتى عندي كيس حلو اشرحه الكم بعده احجي الي بخاطركم بدون تقيد

#wellen syndrome type A.

56 years old male with history of hypertension and smoking present with frequent attacks of chest pain. ECG SHOW - P wave present, regular and heart rate 60 bpm - left axis deviation - there is ST and T wave change in pericardial leads has the following features 1- not preceded by Q wave 2- normal progression of R wave 3- biphasic T wave ( initial positive and then negative. This is wellen syndrome type A which means there is critical stenosis in left anterior descending coronary artery. The condition treat as acute coronary syndrome as a medication and need urgent PCI. But if the patient develop Stemi or Positive troponine >>> emergent PCI. If you want to read more about wellen syndrome you can review previous posts in the channel by searching wellen syndrome.

احد المنشورات السابقه 56 years old male presented with intracranial haemorrhage That manifested by T wave inversion in the ECG. Other ECG findings - sinus bradycardia or junctional rhythm - prolonged QT - widespread ST depression or elevation.