3 WAY FMLY MWAD 45RWN X 1ASHK AVE TO 45 RWN AVE A JRNY

 AUTOCRACY V CORRUPT ELCTORAL DEMOCRACY V LIB DEMOCRACY

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SCI LT V MYS RT

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SN CNMA STILLWATER 2021

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SHAWSHANK ACCEPTANCE

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FRANKL LINE

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TIME FOR HOPE V ACCEPTANCE

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HAS NOT ACCEPTED HER SENTENCE

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Where is the seat of awareness, can one become more aware and by what means?

You are awareness. All of you, not an organ, or a spot, or a place. All you are is awareness and this awareness can grow and expand as you grow and expand.

Meditation is a practice of awareness. Practicing awareness tends to stretch and expand it.

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Hmm, why does it seem it so much in our heads?

Pausha Foley

 · 7mo

Because in your head there is a brain that produces thoughts, and thoughts is what you think you are, what you identify with, what you identify as.

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Your awareness is your third eye middle of eyebrows ficus there abs it’s easy because that’s where the soul resides

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There is a seat of awareness in our brain. This seat or minutes organ is called Reticular formation which is present in the brain stem. And the awareness can be expanded by only regular practice of mindfulness meditation. The insight or Vipassana meditation will help you in better way.

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Another’s awareness of awareness could be the empty stillness of ultimate silence. … Stillness. … In the mental world there would be a potential tension between ‘stretchy’ … and ‘stillness’.

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NOT ABT JUSTICE- ITS ABT FINDING PEACE

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The entity known as John likes understanding the text it has chosen to read. So far as John knows there is no knowing pure awareness as a sensory experience only. There is, instead, realising awareness is nothing - no thing, the only quality being the quality of awareness. But awareness knows all things. John doesn’t see awareness as needing to expand or stretch when it just is - awareness of all and nothing. What does Pausha mean when Pausha states the actions of expansion and elasticity are qualities of awareness? Is it possible for there to be more light shed on these interesting - and as yet not understood, (to John’s mind) -attributes?

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I am looking for an example from the human, physical world that would illustrate this, but I can’t find any because awareness doesn’t work the way matter does.

So it will be an imaginary example: imagine that awareness is water. Endless, limitless expanse of water. In this water there is an organism - Pausha - that is limited and contained, but that also is water. Like a bubble of water in the water. This bubble of water can expand through water limitlessly, endlessly, because the bubble of water is the same water as the water it is submerged within. The only limit to this bubble, that which makes it in a bubble, that makes it separate and distinct, is that it thinks it is separate and distinct. In truth there is no bubble, there is only water. But there is an idea that there is a bubble, that there is a limitation, and this idea creates a separation.

Pausha is both the water,and the bubble in the water, because the water and the bubble of water are truly one and the same.

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IISB JVW

 When passing through doorways, our brains ‘file’ memories away, making it difficult to recall what we were doing, research finds.

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"If you're walking down the right path and you're willing to keep walking, eventually you'll make progress."

-- Barack Obama

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FOW 

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• Published: 11 March 2019

Respiratory management during therapeutic hypothermia for hypoxic-ischemic encephalopathy

• Eniko Szakmar, 
• Agnes Jermendy & 
• Mohamed El-Dib 

Journal of Perinatology volume 39, pages763–773 (2019)Cite this article

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In summary, PPHN is commonly associated with HIE, particularly when lung disease (such as MAS and pulmonary hemorrhage), postnatal acidosis, culture-positive sepsis, systemic hypotension and cardiac dysfunction are present.

J Pediatr. 2018 May; 196: 45–51.e3.

Published online 2018 Mar 1. doi: 10.1016/j.jpeds.2017.12.055

PMCID: PMC6052458

NIHMSID: NIHMS948779

PMID: 29502880

Pulmonary Hypertension Associated with Hypoxic-Ischemic Encephalopathy—Antecedent Characteristics and Comorbidities

Satyan Lakshminrusimha,1 Seetha Shankaran,2 Abbot Laptook,3 Scott McDonald,4 Martin Keszler,3 Krisa Van Meurs,5 Ronnie Guillet,6 Sanjay Chawla,2 Beena G. Sood,2 Sonia Bonifacio,5 Abhik Das,7 and Rosemary D. Higgins8

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COOLING X HYPOTHERMIA CONNECTION 

Asphyxia and PPHN: Fetal hypoxia (secondary to in-utero asphyxia and meconium aspiration) causes pulmonary vascular remodeling, which down regulates iNO signaling pathways and causes PPHN. In infants with perinatal hypoxia, the combination of hypoxia and acidosis increases the risk of PPHN. 

Preexisting PPHN may be exacerbated by therapeutic hypothermia. 

Errors in PaCO2 measurement secondary to body temperature changes may result in fluctuations in PCO2 leading to changes in cerebral and pulmonary vascular resistance (see text for details). (copyright Satyan Lakshminrusimha).

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Abstract Hypoxic-ischemic encephalopathy (HIE) can have both transient and long-lasting effects on the neonate, including neurologic, renal, cardiac, hepatic, and hematologic. 

Both the disease process and the treatment option of therapeutic hypothermia can result in hemodynamic instability

. Understanding the effects of HIE on the neonatal myocardium, pulmonary vascular bed, and the cardiac dysfunction that can occur is key to managing infants with HIE. This article focuses on causes of hemodynamic instability in neonates following perinatal asphyxia and how to recognize hemodynamic compromise. It reviews the underlying pathophysiology and associated management strategies to improve hemodynamics and potentially improve outcomes. Keywords: cardiovascular status; hypoxic-ischemic encephalopathy (HIE); hemodynamics; neurology

Hemodynamic Instability in Hypoxic Ischemic Encephalopathy: More Than Just Brain Injury—Understanding Physiology, Assessment, and Management Sharifa Habib, RN(EC), MN, NP-Pediatrics, NNP-Dip Jennie Saini, RN(EC), MN, NP-Pediatrics, NNP-Dip Stephanie Amendoeira, RN(EC), MN, NP-Pediatrics, NNP-Dip Carol McNair, RN(EC), MN, PhD(c), NNP-BC, NP-Pediatric 2020

https://torontocentreforneonatalhealth.com

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Persistent pulmonary hypertension of the newborn Vinay Sharma1*, Sara Berkelhamer2 and Satyan Lakshminrusimha2

Sharma et al. Maternal Health, Neonatology, and Perinatology DOI 10.1186/s40748-015-0015-4

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ABSTRACT Therapeutic hypothermia in neonates with perinatal asphyxia may increase the risk of PPHN. This potentially affects outcome. Objectives: (1) To investigate whether neonates with perinatal asphyxia and therapeutic hypothermia more often developed PPHN compared to a control group with perinatal asphyxia not treated with hypothermia; (2) To identify risk factors for severe PPHN during hypothermia and evaluate short-term outcome. Methods: This single-center retrospective cohort study included (near-)term neonates with perinatal asphyxia admitted between 2004 and 2016. Neonates with perinatal asphyxia and hypothermia were compared to a historical control group without hypothermia. Primary outcome was PPHN, defined as severe hypoxemia requiring mechanical ventilation and inhaled nitric oxide, confirmed by echocardiography. Short-term adverse outcome was defined as mortality within one month and/or severe brain injury on MRI. Results: Incidence of PPHN was 23% (26/114) in the hypothermia group and 11% (8/70) in controls. In multivariate analysis, PPHN was 2.5 times more common among neonates with hypothermia. Neonates developing PPHN during hypothermia often had higher fraction of inspired oxygen at baseline. PPHN was not associated with a higher risk of severe brain injury. However, early mortality was higher and three infants died due to severe refractory PPHN during hypothermia. Conclusions: In this study PPHN occurred more often since the introduction of therapeutic hypothermia. This was usually reversible and did not lead to overall increased adverse outcome. However, in individual cases with PPHN deterioration occurred rapidly. In such cases the benefits of hypothermia should be weighed against the risk of a complicated, fatal course.

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Persistent pulmonary hypertension in neonates with perinatal asphyxia and therapeutic hypothermia: a frequent and perilous combination 

Vijverberg Joanna R. G.a , Enrico Lopriorea , Arjan B. te Pasa , Monique Rijkena , Erik W. van Zwetb , Francisca T. de Bruinec and Sylke J. Steggerdaa a Department of Neonatology, Leiden University Medical Center, Leiden, The Netherlands; b Department of Medical Statistics, Leiden University Medical Center, Leiden, The Netherlands; c Department of Neuroradiology, Leiden University Medical Center, Leiden, The Netherlands

THE JOURNAL OF MATERNAL-FETAL & NEONATAL MEDICINE https://doi.org/10.1080/14767058.2021.1873941

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Cardiovascular Changes During Mild Therapeutic Hypothermia and Rewarming in Infants With Hypoxic–Ischemic Encephalopathy 

Marianne Thoresen, MD;

 

Andrew Whitelaw, MD

Pediatrics (2000) 106 (1): 92–99.

Reprint requests to (A.W.) Division of Child Health, University of Bristol, Medical School, Southmead Hospital, Bristol, BS10 5NB, England. E-mail: andrew.whitelaw@bristol.ac.uk

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Background.

Clinical trials of mild cooling to 35°C or below in infants with early hypoxic–ischemic encephalopathy are under way. The objective of this study was to systematically document cardiovascular changes associated with mild therapeutic hypothermia and rewarming in such infants.

Patients and Methods.

Nine infants with gestational ages of 36 to 42 weeks, with 10-minute Apgar scores of 5 or less, clinical encephalopathy, and an abnormal electroencephalogram before 6 hours were cooled by surface cooling the trunk (n = 3) or by applying a cap perfused with cooled water (n = 6) for a median of 72 hours. The target core temperature was 34.0°C to 35.0°C for head-cooled infants and 33.0°C to 34.0°C for surface-cooled infants. Maintenance heating and rewarming were provided by an overhead heater.

Results.

Mean arterial blood pressure increased by a median of 10 mm Hg during cooling and fell by a median of 8 mm Hg on rewarming. Heart rate decreased by a median of 34 beats/minute on cooling and increased by a median of 32 beats/minute on rewarming. A large increase in the output of the overhead heater decreased mean arterial blood pressure in 5 infants. Anticonvulsant drugs, sedatives, or intercurrent hypoxemia also produced falls in temperature. The inspired oxygen fraction had to be increased by a median of .14 to maintain oxygenation during cooling with 2 infants requiring 100% oxygen, an effect probably attributable to pulmonary hypertension, which was reversible with rewarming.

Conclusions.

Therapeutic cooling produces changes in heart rate and blood pressure that are not hazardous, but the combination of inadvertent overcooling and inappropriately rapid rewarming, together with sedative drugs that can impair normal thermoregulatory vasoconstriction, can cause hypotension in posthypoxic newborn infants.

 Infants who already require 50% oxygen should be cooled cautiously because pulmonary hypertension may develop. Knowledge of these cardiovascular changes, careful monitoring, anticipation, and correction should help to avoid potential adverse effects in the upcoming clinical trials.

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0320-0520  -NONE OF THESE ABN ONES NOTED

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WHT HPPNED- STTMNT

WHY DECISIONS MADE SENSE AT THAT TIME- 

WHT WAS HAPPENING AROUND U-WHAT WERE U FEELING - ZIG ZAG PATTERN , NO CATASTROPHIC DETERIORN TILL COOLING STARTED

- CONS X SORT DISCUSSN REASSURED - BOLUS THERAPY-STEP WISE RX - NO DXTIC PATTERN IN EARLY CFAM V ARTEFACT-AWAY FROM WARD TO PAEDS CALL

HOW CAN MINIMISE LIKELIHOOD OF SAME HAPPENING- NEED 1-1 STAFFING FOR 1 UNWELL BABY - WILL CALL AGAIN BEFORE COOLING AN ACIDOTIC BABY WITH SUSPECTED PPHN WITHOUT INO ON SITE 

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