11 Matching Annotations
  1. Mar 2019
    1. SBP, DBP, RR, and weight did not change following T3 administration

      Liothyronine does not raise blood pressure despite the rise in heart rate. The reason that respiratory rate (RR) was not changed may be because the increased cardiac output compensates for the increased oxygen demand.

  2. Feb 2019
    1. Office-based devices that permit multiple automated measurements after a pre-programmed rest period produce blood pressure readings that are independent of digit preference bias and the “white coat” phenomenon (where blood pressure is elevated in the clinic but normal at home)

      This is a great recommendation.

  3. Aug 2018
    1. CONCLUSIONS: These findings suggest that higher standing BP is a biomarker that helps identify persons with combat PTSD who are likely to benefit from prazosin. These results also are consistent with α1AR activation contributing to PTSD pathophysiology in a subgroup of patients.

      This is precisely the results I would expect. However, I completely disagree with their interpretation.

      People with high blood pressure (BP) can tolerate a reduction in BP without instigating compensatory mechanisms. People with normal or low BP would invoke compensation by the sympathetic nervous system in response to alpha blockade. This would counteract the depressant effects of adrenergic antagonism. Indeed, adrenaline and noradrenaline elevate in response to standing, which I find to be an obvious prediction. Thus, the lack of benefit from prazosin in these subjects may be mediated by an increase in adrenergic receptor activation other than the apha1-adrenoreceptor; in particular, the beta-adrenergic receptors are likely at fault. Propranolol, a beta-blocker, is used for PTSD, so this mechanism seems well substantiated.

      The study apparently found benefit for patients with BP over 110 (with more benefit for higher BP). Thus, I would conclude that systolic pressure below 110 induce compensation.

    1. Graph 2 shows the trend for the diastolic pressure.

      Post-exercise, diastolic pressure is higher than baseline; compression garments exaggerate this effect

    2. Graph 1 shows the systolic pressure data (x-axis in mmHg). It can be noted that the test subjects start from an equal baseline condition, but after performing the swimming test the athletes not wearing the costume in the first control (20-30 mins) have an average systolic pressure that has dropped to approximately 90 mmHg.

      Thus, compression garments may prevent circumstantial hypotension. In this case, one possibility is that the compression is delivering blood to the heart that would otherwise be shunted to the skin for heat dissipation.

    1. Table 2

      These trained athletes have a BP of about 100/60 at rest. This is substantially lower than the roughly 120/80 BP that I've seen elsewhere. This likely limits the drop in BP seen post-exercise.

    1. Hypertension also affects brain capillary density. Similar to the peripheral microcirculation, hypertension causes rarefaction (decrease in number) of capillaries and impaired microvessel formation that can increase vascular resistance

      This is important because it implies that syncope or incomplete syncope as a result of vasodilators may not be dependent on actual blood pressure. It means that it is theoretically possible that vasodilators will acutely increase blood flow despite a drop in BP, depending on the body's level of compensation via increased cardiac output.

    1. Although atenolol had no effect on subjective measures of sleep this hydrophilic drug also reduced REM frequency, suggesting that either it has some central effect, or that REM reduction is due to a peripheral 'shielding' effect.

      Alternatively, it could have been nocturnal hypotension that was causing the sleep disruption.

  4. Nov 2017
    1. While the title of this report does not really imply anything to contradict the results of the testing of the theory, the content of the report itself leaves room for interpretation as to what these results mean and who it applies to. The main study referenced conducted by the University of Rome (Loffredo) does show that the participants who were given dark chocolate showed a higher acute result than those who were given milk chocolate, their study was made up of a small group of 20. It could also be pointed out that they did not establish a portion of their group who were tested without the ingestion of chocolate to establish a better baseline for their results. Participants endurance on a treadmill was used to measure the effects of the chocolate, but there is no indication of how or if the participants increase in ambulatory movement, or having “warmed up” with their baseline test day may have contributed to the improved results after the chocolate was administered. Another point to note is where the author mentions a previous report she submitted (Aubrey) covering the similarity of the results of the chocolate study to a study on the affects of meditation on the body. While the result may be considered similar, the way the results were achieved were very different. The wording in the studies referenced for the benefits of meditation reflect a psychological improvement as a means for a physical response, while the chocolate experiment was testing a chemical application for a physiological response. This article, although not wrong or misrepresenting the study, simplifies much of the work and applies it to the general public. The author does manage to address that the study is incomplete, as an afterthought and could easily be interpreted as having less weight than the argument for chocolate treatment by simply being under represented or under explained. Further investigation is definitely needed to understand the “how and why” of the affects of chocolate/polyphenols on our bodies before we can set any sort of prescription in place. The study would need to be much more comprehensive or added to others that test this same result on other demographics to determine if the affects can be replicated on everyone, or to narrow down if they only get this result with those who have PAD.

      Aubrey, A. (2008, August 21). To Lower Blood Pressure, Open Up And Say 'Om'. Retrieved November 09, 2017, from https://www.npr.org/2008/08/21/93796200/to-lower-blood-pressure-open-up-and-say-om MPH, M. G. (2014, March 01). Meditation for Psychological Stress and Well-being. Retrieved November 09, 2017, from https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1809754 Loffredo, L., Perri, L., Catasca, E., Pignatelli, P., Brancorsini, M., Nocella, C., . . . Violi, F. (2014, August 21). Dark Chocolate Acutely Improves Walking Autonomy in Patients With Peripheral Artery Disease. Retrieved November 09, 2017, from http://jaha.ahajournals.org/content/3/4/e001072

  5. Oct 2017
    1. Beta blockers have long been associated with sleep disturbances such as difficulty falling asleep, staying asleep, and insomnia. They have been shown to reduce the production of melatonin via specific inhibition of beta-1 adrenergic receptors. Melatonin is a hormone secreted by the pineal gland in the brain, and helps in maintaining normal circadian rhythms.6,20-21 People with hypertension already have a lower melatonin production rate than those with normal blood pressure.22

      The question becomes, then, do beta blockers impair sleep when exogenous melatonin is administered concurrently?

  6. Mar 2017
    1. In patients receiving diuretic therapy symptomatichypotension may occur following the initial dose of proposed FDC, particularly due to volume/salt depletion with diuretic therapy

      We have found different results in the research that we have done.