BloodPressure

A comprehensive summary on the effects of elevated blood pressure during pregnancy and pre-eclampsia.  

Easy tutorial for a basic physics concept, simply explained. Electrical engineering overlaps with neuroscience and cardiophysiology. Learn why fat increases blood pressure and antagonists decrease signal transmission! Please SUBSCRIBE for new videos: More cool stuff coming as we get more Hippo Helpers! http://www.helphippo.com - for more video tutorials organized by topic/year.  

http://www.handwrittentutorials.com - This tutorial explores the Renin-Angiotensin-Aldosterone System, its role in Blood Pressure, the enzymes, involved, and how drugs act upon the system. For more entirely FREE medical tutorials visit http://www.handwrittentutorials.com  

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Doctors get their patients' blood pressure soaring, while nurses don't, findings suggest.  

ADH (/vasopressin) is synthesised in the hypothalamus. From there it migrates in neurosecretory granules along axonal pathways to the posterior pituitary gland. Secretion of ADH is principally in response to changes in plasma osmolality. It acts on the collecting duct of the kidney to cause water reabsorption via the translocation of aquaporin channels in the CD lumen, and is therefore stimulated when we need to conserve water volume. It is stimulated by large falls in blood pressure or volume. At high concentrations, ADH also causes vasoconstriction.  

Pre-eclampsia and eclampsia are different stages of the same condition. Pre-eclampsia can result in eclampsia at any time. Eclampsia is immediately life-threatening and often symptomatic.   Pre-eclampsia is a condition characterised by increased blood pressure, proteinuria and often oedema during pregnancy. It is typically asymptomatic, and occurs after 20 weeks, although it rarely presents before 32 weeks – but when it does, it is associated with a worse prognosis.  

Adrenaline (epinephrine) has been an integral component of advanced resuscitation algorithms since the early 1960s. Initial guidelines for the treatment of cardiac arrest recommended the use of intracardiac adrenaline (0.5 mg) or high dose intravenous adrenaline (10 mg), repeating with larger doses if required.1 The mechanism of action for adrenaline in cardiac arrest is attributed to stimulation of α2 receptors in vascular smooth muscle, causing vasoconstriction. This increases aortic diastolic pressure, which in turn leads to increased coronary perfusion pressures, which improves short term survival. Experimental studies, however, suggest that adrenaline impairs cerebral macrovascular2 and microvascular blood flow,3 4 increases ventricular arrhythmias, and increases myocardial dysfunction after return of spontaneous circulation.5 This creates the paradox of better short term survival but at the potential cost of worse long term outcomes.  

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An overview of how to approach calls regarding elevated blood pressure while cross-covering on inpatient medicine. The distinction between hypertensive emerg...  

This animation focuses on the renin angiotensin aldosterone system (RAAS), a classic endocrine system that helps to regulate long-term blood pressure and ext...  

Figure out how all of those physiology terms: end-systolic, end-diastolic, pulse pressure, stroke volume, and ejection fraction, can be easily figured out us...  

Learn about how the arteries use nerve impulses to help regulate blood pressure.