Wednesday, 27 March 2019
Wednesday, 13 March 2019
Sameer's Personal Story
Sameer's Personal Story
From sleep deprivation to the life-saving PAP device
My name is Sameer and this is a true story. In fact, it is my personal journey into years of suffering, pain and anguish owing to an undiagnosed condition called obstructive sleep apnea. Many years of incorrect diagnosis and treatment by a number of well-meaning doctors prevented me from getting the proper treatment for my condition. I tell my story in the hope that physicians and other health workers will recognize the urgency of their learning about sleep apnea and prescribing testing for this most under-diagnosed condition. I hope as well that people with the symptoms of sleep apnea will take this condition very seriously. It could save lives, possibly yours.
My story concerning sleep apnea is a rather long. At first, I wanted to give long, detailed information going back to the 1980s, or even before that, in the military in the 1970s. There are so many heart episodes throughout these years that I will only highlight some of them for you. I thought it prudent to begin at an event in August 1991, an event that changed everything about my life, and for the next 10 years almost ended it.
From 1989 to 1993 I was a radio host of a live-talk program on radio station KKLA in Los Angeles, CA. My program was from midnight to 2 a.m. Monday through Friday. I enjoyed my work and it was some of the greatest times in my life on radio.
My wife was with me that particular evening. After the program, we were driving home to Santa Ana, a bit more than an hour from the studio. About five miles from the house, I felt my heart began to beat uncontrollably, both in the rhythm and speed. Since I was driving, I was very concerned that I might be having a heart attack or stroke. This was the first time that something this serious had happened to me and I immediately awakened my wife and told her of my condition and that I was going to the hospital. We went to Fountain Valley Regional Hospital. There I was seen by the on-call physician. By then it was 3:30 in the morning. In those years my normal pulse was probably 70. At the hospital that morning it was over 150. I spent the next day there before I was transferred to Kaiser Permanente. I spent the next two days there. The main objective was to get the heart rate down to normal, which my caregivers managed to do that late in the evening of the first day. I was kept overnight for observation. I asked the doctor what was the reason for my condition. His answer was surprising. He said that he had no idea what caused it. This answer would be repeated over and over again for the next nine years!
I was referred to a specialist two days later and they ran an electrocardiogram and sent me away with medication. Since they did not know the cause, this began the journey of many disappointing “treatments” of different medications. I was prescribed a drug called atenolol. Atenolol is called a “beta blocker.” Beta blockers are drugs that lower blood pressure by reducing the amount of blood pumped by the heart. This treatment brought about fatigue, nausea, drowsiness, and dizziness. I was taken off this medication after two days. What is interesting about this “treatment” was that none of the doctors ever told me what was wrong. Every one of them said that they could not pinpoint what was wrong, but that they would treat me for what they think the problem could be. What they did not tell me was that atenolol is given for those who have had a heart attack! Certainly, I didn’t have a heart attack. This medication was replaced by one called, verapamil, which is a calcium or channel blocker. Calcium blockers relax blood vessel walls, thereby lowering blood pressure. I was on verapamil for about a year. It was more tolerable than atenolol, but I stopped taking it because of the side effects. It also did not maintain a reasonable blood pressure.
From 1991 until 2001, my life began to nosedive. I began to suffer off and on from massive headaches, usually in the summer, but not exclusively. These headaches lasted up to two weeks and no treatment would stop them. I was prescribed Tylenol with codeine, as well as extra strength over-the-counter medications. None of them worked. I was also having horrible nightmares, but until I began CPAP treatment many years later, I had no thought that the nightmares and sleep apnea were related.
As the headaches increased, so did the heart episodes. In 1995, again stricken while driving, I was taken to the same Fountain Valley Hospital, and again spent three days there and heard the same conclusion from the doctor that he could not tell me exactly what was the cause of the heart problem. This time, though, different medications were prescribed. I was put on Toprol, another beta blocker, along with Zestril. Toprol is given to patients who have had mild heart failure. Zestril is one of the newer medications called angiotensin-converting enzyme inhibitors. ACE inhibitors expand blood vessels and decrease resistance. This allows blood to flow more easily and makes the heart’s work easier. Zestril is prescribed for patients with congestive heart failure. Keep in mind that no doctor has ever told me the direct cause of why my heart was suffering. Heart episodes continued, from one doctor to another with the same conclusion, urging me to take stronger doses of the medicine.
July 1999 saw one of the most traumatic episodes to date. My wife again rushed me to Fountain Valley Hospital and the on-call doctor who this time inverted me and injected me with nitroglycerine. It was the most frightening and excruciating pain and fear that I have ever experienced. My rapid heart rate dropped so fast that I was disoriented. My hands and legs were flailing and I had no control over my body. My hearing was gone and I was on the verge of vomiting and passing out. All of this was done in an attempt to force the heart back to a regular rhythm. Two days after that I was sent home; not only with the same drugs I was already taking, but with nitroglycerine tablets.
In 2000, I wanted off the Topril because it made me sick. I was also prescribed hydrochlorothiazide, a diuretic. Zestril, or lisinopril, is now the only medication that I am taking.
I had been told that I had cardiac arrhythmias (irregular heart beat), atrial fibrillation, etc,. but no firm diagnosis was offered as to the cause of any of these alleged conditions. Not only that, but a heart ultrasound performed in July 1999 showed no heart abnormalities. I had been treated for heart disease; but there was never a connection between the cause and cure.
During all this time I was increasingly irritable, fatigued, gaining weight, losing the ability to concentrate, lethargic, sickly, and the list goes on. I could never get enough sleep and never get to sleep! I took two naps some days and still never felt rested. It was at this time that I progressed to the worst state of my life, with all of these symptoms climaxing in October 2001. That was the day I was subjected to electrical cardioversion to reset my heart rhythm. An intravenous anesthetic was injected and patches were placed on my chest. After I was completely anesthetized, a small electrical charge was delivered over the hear. The charge caused a momentary electrical discharge of all the cardiac cells and allowed the primary pacemaker to take control of the rhythm, thus stopping the atrial fibrillation and resetting the heart.
This was it. I had no more solutions. The emergency room doctor told me that unless I lost weight I was going to die. I told my wife that I feared the next time I would be in a hospital concerning my heart I would have a heart attack or stroke. I was resolved to face the fact that I was probably going to die.
In November 2000, I met (again) Alex. At this time he was working at St. John’s Medical Center. He had been prodding me to come to a “sleep study.” I had no idea what he was talking about and thought the entire matter of sleep being the cause of my issues was foolishness. I told him that all I needed to do was to lose weight and I would be just fine. In December 2001, he prodded me again with the idea that I might have the disease called “sleep apnea.” Frustrated, cranky, overmedicated, and with a blistering headache, I went to St. John’s to prove to Alex that his studies concerning me were all wrong. On New Year’s Eve 2001, swerving all over the 405 freeway, I finally got to St. John’s and there he explained to me exactly what sleep apnea was and I began to get more curious as he explained to me that my life was characteristic of someone with sleep apnea. He wired me up, prepared the bed and CPAP machine, and away I went to sleep.
When I woke up on New Year’s Day 2002, it was a rude awakening. The study showed thatduring sleep my oxygen levels steadily decreased from a percentage in the high 90s to the low 70s. That was serious. Not only that, but he showed me how many times I stopped breathing! It was quite a shock. The very first words from my mouth after I saw the results was, “Hook me up!”
The result of using the CPAP machine was nothing short of astonishing! The next day, I had tremendous energy! I also noticed that I actually slept throughout the night. The position that I lay down in bed was the same position I was in when I rose from sleep. I noticed immediately that I had no more headaches, no more fatigue, no more snoring, no more nightmares, no more sleepless nights and no more heart episodes! The proper treatment corrected all of the horrific symptoms that plagued my life for many years. From the day of my delivery from this ill-health bondage, I have been telling people I know, especially those who have similar symptoms that I had, to get tested. I know that for me, the proper diagnosis of my medical condition literally saved my life. I now can fulfill one of my lifelong desires; weight training and cardio. My exercise program has never been better. I am training better at 50 years old, than I did in my 20s! Whenever I speak of Alex, I always refer to him as “the man God used to save my life.
Tentabs.in
Online Medical Accessories And CPAP and BiPAP Machines
Visit Us : https://tentabs.in/
From sleep deprivation to the life-saving PAP device
My name is Sameer and this is a true story. In fact, it is my personal journey into years of suffering, pain and anguish owing to an undiagnosed condition called obstructive sleep apnea. Many years of incorrect diagnosis and treatment by a number of well-meaning doctors prevented me from getting the proper treatment for my condition. I tell my story in the hope that physicians and other health workers will recognize the urgency of their learning about sleep apnea and prescribing testing for this most under-diagnosed condition. I hope as well that people with the symptoms of sleep apnea will take this condition very seriously. It could save lives, possibly yours.
My story concerning sleep apnea is a rather long. At first, I wanted to give long, detailed information going back to the 1980s, or even before that, in the military in the 1970s. There are so many heart episodes throughout these years that I will only highlight some of them for you. I thought it prudent to begin at an event in August 1991, an event that changed everything about my life, and for the next 10 years almost ended it.
From 1989 to 1993 I was a radio host of a live-talk program on radio station KKLA in Los Angeles, CA. My program was from midnight to 2 a.m. Monday through Friday. I enjoyed my work and it was some of the greatest times in my life on radio.
My wife was with me that particular evening. After the program, we were driving home to Santa Ana, a bit more than an hour from the studio. About five miles from the house, I felt my heart began to beat uncontrollably, both in the rhythm and speed. Since I was driving, I was very concerned that I might be having a heart attack or stroke. This was the first time that something this serious had happened to me and I immediately awakened my wife and told her of my condition and that I was going to the hospital. We went to Fountain Valley Regional Hospital. There I was seen by the on-call physician. By then it was 3:30 in the morning. In those years my normal pulse was probably 70. At the hospital that morning it was over 150. I spent the next day there before I was transferred to Kaiser Permanente. I spent the next two days there. The main objective was to get the heart rate down to normal, which my caregivers managed to do that late in the evening of the first day. I was kept overnight for observation. I asked the doctor what was the reason for my condition. His answer was surprising. He said that he had no idea what caused it. This answer would be repeated over and over again for the next nine years!
I was referred to a specialist two days later and they ran an electrocardiogram and sent me away with medication. Since they did not know the cause, this began the journey of many disappointing “treatments” of different medications. I was prescribed a drug called atenolol. Atenolol is called a “beta blocker.” Beta blockers are drugs that lower blood pressure by reducing the amount of blood pumped by the heart. This treatment brought about fatigue, nausea, drowsiness, and dizziness. I was taken off this medication after two days. What is interesting about this “treatment” was that none of the doctors ever told me what was wrong. Every one of them said that they could not pinpoint what was wrong, but that they would treat me for what they think the problem could be. What they did not tell me was that atenolol is given for those who have had a heart attack! Certainly, I didn’t have a heart attack. This medication was replaced by one called, verapamil, which is a calcium or channel blocker. Calcium blockers relax blood vessel walls, thereby lowering blood pressure. I was on verapamil for about a year. It was more tolerable than atenolol, but I stopped taking it because of the side effects. It also did not maintain a reasonable blood pressure.
From 1991 until 2001, my life began to nosedive. I began to suffer off and on from massive headaches, usually in the summer, but not exclusively. These headaches lasted up to two weeks and no treatment would stop them. I was prescribed Tylenol with codeine, as well as extra strength over-the-counter medications. None of them worked. I was also having horrible nightmares, but until I began CPAP treatment many years later, I had no thought that the nightmares and sleep apnea were related.
As the headaches increased, so did the heart episodes. In 1995, again stricken while driving, I was taken to the same Fountain Valley Hospital, and again spent three days there and heard the same conclusion from the doctor that he could not tell me exactly what was the cause of the heart problem. This time, though, different medications were prescribed. I was put on Toprol, another beta blocker, along with Zestril. Toprol is given to patients who have had mild heart failure. Zestril is one of the newer medications called angiotensin-converting enzyme inhibitors. ACE inhibitors expand blood vessels and decrease resistance. This allows blood to flow more easily and makes the heart’s work easier. Zestril is prescribed for patients with congestive heart failure. Keep in mind that no doctor has ever told me the direct cause of why my heart was suffering. Heart episodes continued, from one doctor to another with the same conclusion, urging me to take stronger doses of the medicine.
July 1999 saw one of the most traumatic episodes to date. My wife again rushed me to Fountain Valley Hospital and the on-call doctor who this time inverted me and injected me with nitroglycerine. It was the most frightening and excruciating pain and fear that I have ever experienced. My rapid heart rate dropped so fast that I was disoriented. My hands and legs were flailing and I had no control over my body. My hearing was gone and I was on the verge of vomiting and passing out. All of this was done in an attempt to force the heart back to a regular rhythm. Two days after that I was sent home; not only with the same drugs I was already taking, but with nitroglycerine tablets.
In 2000, I wanted off the Topril because it made me sick. I was also prescribed hydrochlorothiazide, a diuretic. Zestril, or lisinopril, is now the only medication that I am taking.
I had been told that I had cardiac arrhythmias (irregular heart beat), atrial fibrillation, etc,. but no firm diagnosis was offered as to the cause of any of these alleged conditions. Not only that, but a heart ultrasound performed in July 1999 showed no heart abnormalities. I had been treated for heart disease; but there was never a connection between the cause and cure.
During all this time I was increasingly irritable, fatigued, gaining weight, losing the ability to concentrate, lethargic, sickly, and the list goes on. I could never get enough sleep and never get to sleep! I took two naps some days and still never felt rested. It was at this time that I progressed to the worst state of my life, with all of these symptoms climaxing in October 2001. That was the day I was subjected to electrical cardioversion to reset my heart rhythm. An intravenous anesthetic was injected and patches were placed on my chest. After I was completely anesthetized, a small electrical charge was delivered over the hear. The charge caused a momentary electrical discharge of all the cardiac cells and allowed the primary pacemaker to take control of the rhythm, thus stopping the atrial fibrillation and resetting the heart.
This was it. I had no more solutions. The emergency room doctor told me that unless I lost weight I was going to die. I told my wife that I feared the next time I would be in a hospital concerning my heart I would have a heart attack or stroke. I was resolved to face the fact that I was probably going to die.
In November 2000, I met (again) Alex. At this time he was working at St. John’s Medical Center. He had been prodding me to come to a “sleep study.” I had no idea what he was talking about and thought the entire matter of sleep being the cause of my issues was foolishness. I told him that all I needed to do was to lose weight and I would be just fine. In December 2001, he prodded me again with the idea that I might have the disease called “sleep apnea.” Frustrated, cranky, overmedicated, and with a blistering headache, I went to St. John’s to prove to Alex that his studies concerning me were all wrong. On New Year’s Eve 2001, swerving all over the 405 freeway, I finally got to St. John’s and there he explained to me exactly what sleep apnea was and I began to get more curious as he explained to me that my life was characteristic of someone with sleep apnea. He wired me up, prepared the bed and CPAP machine, and away I went to sleep.
When I woke up on New Year’s Day 2002, it was a rude awakening. The study showed thatduring sleep my oxygen levels steadily decreased from a percentage in the high 90s to the low 70s. That was serious. Not only that, but he showed me how many times I stopped breathing! It was quite a shock. The very first words from my mouth after I saw the results was, “Hook me up!”
The result of using the CPAP machine was nothing short of astonishing! The next day, I had tremendous energy! I also noticed that I actually slept throughout the night. The position that I lay down in bed was the same position I was in when I rose from sleep. I noticed immediately that I had no more headaches, no more fatigue, no more snoring, no more nightmares, no more sleepless nights and no more heart episodes! The proper treatment corrected all of the horrific symptoms that plagued my life for many years. From the day of my delivery from this ill-health bondage, I have been telling people I know, especially those who have similar symptoms that I had, to get tested. I know that for me, the proper diagnosis of my medical condition literally saved my life. I now can fulfill one of my lifelong desires; weight training and cardio. My exercise program has never been better. I am training better at 50 years old, than I did in my 20s! Whenever I speak of Alex, I always refer to him as “the man God used to save my life.
Tentabs.in
Online Medical Accessories And CPAP and BiPAP Machines
Visit Us : https://tentabs.in/
Thursday, 7 March 2019
Which Dialyser to choose..?
Introduction
Trades through dialyser films point: (I) at the expulsion of uraemic solutes that are held due to renal disappointment (for example urea) and (ii) at the rebuilding of exhausted mixes (for example bicarbonate).
The initially utilized cellulosic layers were gotten from cotton and in this manner named 'regular'. They initiated supplement and leukocytes, prompting a provocative response as one of the records of 'bioincompatibility' [1]. Later on, artificially created 'manufactured' polymers seemed to relieve this actuation [2]. Besides, veiling hydroxyl gatherings, which are in charge of the supplement initiation with cellulosic films, likewise brought about greater biocompatibility [3]. Subsequently, cuprophan and its analogs were called 'unmodified cellulosic' versus the more biocompatible, later created 'changed/recovered cellulosic' films.
Numerous engineered layers have extensive pore sizes permitting higher rates of water motion and allowing a higher ultrafiltration limit just as a superior evacuation of high sub-atomic weight 'uraemic solutes' than films with littler pore estimate. Consequently, in spite of the fact that a high ultrafiltration rate and the ability to expel expansive atoms don't entirely keep running in parallel, extensive pore layers are for the most part alluded to as 'high-motion', as opposed to 'low-transition' layers with little pores. Five general sorts of films are accessible at present (Table 1).
Kinds of layers with some examples
Unmodified cellulose (low-flux)b
Cuprophan
Cellulose diacetate
Cuprammonium rayon
Adjusted/recovered cellulose (low-transition)
Hemophan
Manufactured (low-transition)
Polysulfone
Polycarbonate
Adjusted/recovered cellulose (high-transition)
Cellulose triacetate
Manufactured (high-transition)
Polysulfone
Polyamide
Polyethersulfone
Polyacrylonitrile
Polymethylmethacrylate
not comprehensive.
bUnmodified cellulosic films are bioincompatible; every single other layer are moderately biocompatible.
In this audit, the most significant film qualities permitting a levelheaded decision for treatment are talked about. Increasingly broad pertinent information can be found in the European Best Practice Guidelines for hemodialysis, part I [4,5].
Significant film qualities
Biocompatibility towards leukocytes and the supplement framework
Biocompatibility depicts materials, which cause just minor biochemical and natural impacts. In this audit, we will focus on leukocyte and supplement actuation, which happen prevalently when unmodified cellulosic films are utilized.
Benchmark actuation of leukocytes results in aggravation, which is identified with vascular infection, the main source of death in dialysis patients [6]. C-responsive protein, a marker of aggravation that is identified with mortality [7,8], is lower when engineered, biocompatible, high-transition polysulfone is utilized, contrasted and unmodified cellulose [9]; this distinction is available both pre-dialysis, as a continuing impact of past dialyzes, and is additionally emphasize a few hours after dialysis [9].
Along these lines, useful debilitation of leukocytes creates also, for example, the debilitated capacity of invigorated granulocytes and monocytes, of phagocytosis, of chemotaxis and of surface particle articulation. All these useful imperfections incline to contamination [10], the second most continuous reason for death in dialysis patients [6]. The biocompatibility concerning supplement and leukocytes isn't so solid when engineered and adjusted cellulosic layers are utilized [11,12].
Impermeability against dialysate pollutions
Dialysate might be polluted by microscopic organisms, which discharge lipopolysaccharides, peptidoglycans, DNA and other star incendiary items when they navigate the layer and enter the circulation system. The hazard for aggravation is much higher when backfiltration happens, for example at the point when dialysate enters the blood by convection in the distal piece of the dialyzer to make up for net ultrafiltration, which happens in the more proximal pieces of the dialyzer. Incomprehensibly, bacterial items infiltrate all the more effectively crosswise over little pore cellulosic films into the blood compartment than crosswise over substantial pore engineered layers, which adsorb such bacterial items. Because of this exchange of bacterial items, leukocytes are actuated [13]. Applying as unadulterated dialysate as conceivable is the ideal way to deal with keep away from the exchange of polluting influences. By and by, utilizing a manufactured film as an extra precautionary measure will offer additional insurance.
Adsorption
Adsorption onto the film, a normal for engineered layers, adds to the evacuation of toxic mixes, for example, interleukin-1, tumor corruption factor, peptides, interleukin-6 and β2-microglobulin (β2-M) [14]. Not every manufactured film have the equivalent adsorptive limit. Adsorption is most articulated for polymethylmethacrylate and AN69.
Because of the confined surface territory of dialysers, adsorption limit will quickly be immersed. Adequate rates of net evacuation by adsorption must be accomplished if the surface zone is radically expanded by the advancement of explicit gadgets that have adsorption as just point. These gadgets should then contain globules to which all around characterized adsorptive properties are presented.
Pore estimate
As of late, an expanding number of bigger mixes (supposed center atoms, >500 Da), which are bioactive and may add to the uraemic disorder have been perceived (Table 2) [15]. Amplifying pore measure and expanding motion permit high rates of the evacuation of these solutes.
β2-M has been embroiled at the beginning of uraemic amyloid infection [16]; the convergence of β2-M diminishes dynamically when patients are treated on high-transition layers [17]. A further reduction in the convergence of β2-M can be accomplished by changing the span and key idea of dialysis sessions, for example by embracing day by day-long moderate medium-term on-line haemodiafiltration [18].
As a further case of a 'center particle', the centralization of leptin, which causes diminished hunger and lack of healthy sustenance [19], is decreased just amid high-transition dialysis [20].
Propelled glycation finished results (AGEs) are engaged with the beginning of a provocative state and cardiovascular illness [21]. Their focus is essentially diminished amid dialysis with super-transition films, another age of gadgets, which have a considerably higher ability to evacuate center atoms than high-motion layers [22].
Homocysteine, a little protein bound compound, is identified with vascular harm [23]. Its focus is diminished when patients are changed from high-transition to super-motion dialysis [24]. In like manner, pre-dialysis indoxyl sulfate focus is likewise diminished by super-transition dialysis (R. De Smet, unpublished information). The two investigations have been directed with cellulosic super-motion films, which are additionally progressively flawed for egg whites. This trademark may clarify the high rate of expulsion of the two protein bound mixes.
Synopsis
The by and by accessible layers spread a wide range from unmodified cellulose low-transition to engineered high-motion films (Tables 1 and 3). Unmodified low-motion cellulose: (I) is bio-inconsistent (for example initiates supplement), (ii) does not keep the infiltration of contaminations from the dialysate into the circulation system, (iii) does not adsorb unwelcome mixes and (iv) does not expel center atoms.
High-motion engineered layers are bio-perfect, reflect dialysate debasements, adsorb mixes and evacuate center particles.
All other film types show halfway qualities.
Clinical outcomes
A few controlled examinations propose the predominance of high-motion layers for separated parts of the uraemic disorder, for example, β2-M amyloidosis [25], loss of lingering renal capacity [26], dyslipidemia [27], polyneuropathy [28] and disease [10], albeit different investigations stayed uncertain [5,17,29,30].
As to, something like eight observational examinations demonstrated the prevalence of high-transition dialysis [5, 31– 38], and somewhere around two investigations recommended that this advantage was to a limited extent identified with the evacuation of center particles [37,38].
Interestingly, the main controlled mortality think about, the HEMO examine, neglected to report the prevalence of high-transition contrasted and slow-motion films. The auxiliary investigation demonstrated a pattern, which could be good with a specific predominance [39], since an advantage as for cardio-vascular occasions was appeared high-transition films. The deficiencies of this examination were, in any case, that generally short dialysis times and reuse, which may unpredictably affect layer transition, were permitted. Likewise, pervasive dialysis patients were selected with the goal that the result may have been perplexed by morbidities, which had been gained in the pre-ponder treatment period.
Thus, in spite of the fact that there may be a pattern for the predominance of high-motion layers in regards to mortality, this finding must be affirmed by further examinations, before clear ends can be drawn. The information recommending prevalence in regards to dreariness are additionally persuading.
Conclusion
On hypothetical grounds, dialysis layers with the best organic properties ought to be biocompatible, bar polluting influences in the dialysate and have a substantial pore measure. A high adsorptive limit is less basic, yet may build the aggregate sum of solutes expelled. Clinical contentions supporting the thought of prevalence of high-transition manufactured layers identify with specific aspects of the uraemic disorder, for example, the personal satisfaction, yet whether they beneficially affect mortality remains an uncertain issue.
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