Reply to Karthik Viswanathan: What is the link between psychologic stress, caffeine, sympathetic activity and ventricular ectopics?
Mohan Shanmugam, Anesthesia & Intensive Care, Abertawe Bro Morgannwg University NHS Trust, Swansea, UK; E-mail: mohan at intubator dot co dot uk
Received, accepted and published 27 April 2008
There appears to be adequate clinical, laboratory and cellular evidence that suggests that psychologic stress is arrhythmogenic. It is presumably related to the sympathetically mediated catecholamine surge [1-3]. Essentially, the mechanism is related to the activation of sodium-potassium-ATPase pump causing redistributional hypokalemia. The resulting hyperpolarisation of cardiac muscle cells predisposes to ventricular arrhythmias.
While a relationship between caffeine intake and ventricular ectopics is anecdotally presumed, there is inconsistent evidence in this area. It seems caffeine, when consumed in moderate amounts (~200 mg/day), causes a relatively insignificant increase in catecholamines [4].
The clinical management of ventricular ectopics and the current evidence base is very well summarised in a recent paper by Ng [5].
Conflict of interests: none declared.
References:
1. Tisdale JE, Patel RV, Webb CR, Borzak S, Zarowitz BJ. Proarrhythmic effects of intravenous vasopressors. The Annals of Pharmacotherapy. 1995; 29: 269-281 available online at http://www.theannals.com/cgi/content/abstract/29/3/269, accessed 27 April 2008
2. Clausen T and Everts ME. Regulation of the Na, K pump in skeletal muscle. Kidney International 1989; 35: 1–13. Full text article at http://www.nature.com/ki/journal/v35/n1/pdf/ki19891a.pdf accessed 27 April 2008
3. Macdonald JE and Struthers AD. What is the optimal serum potassium level in cardiovascular patients? Journal of the American College of Cardiology 2004; 43: 155-161; full text at http://content.onlinejacc.org/cgi/content/full/43/2/155 accessed 27 April 2008
4. Myers MG. Caffeine and cardiac arrhythmias. Chest 1988; 94: 4–5, full text at http://www.chestjournal.org/cgi/reprint/94/1/4.pdf accessed 27 April 2008
5. Ng GA. Treating patients with ventricular ectopic beats. Heart 2006; 92:1707-1712; extract at http://heart.bmj.com/cgi/content/extract/92/11/1707 accessed 27 April 2008
Reviewed by E.S.Prakash, Editor, Medical Physiology Online
Showing posts with label Letters to the Editor. Show all posts
Showing posts with label Letters to the Editor. Show all posts
27 April 2008
24 January 2008
Surface-potential theory for explaining the increase in sodium permeability seen in hypocalcemia
Type of article: Letter to the editor
Anand Bhaskar, Department of Physiology, Christian Medical College, Vellore, 632002, India. E-mail: anandbhaskar [at] sify [dot] com.
Received 23 January 2008; accepted 24 January 2008.
We are aware that hypocalcemia decreases the activation threshold of sodium channels. How does this happen? It can be explained on the basis of the surface-potential theory [1]. According to this theory, the outer surface of cells has a net negative charge. When calcium levels are high, these charges get neutralized by calcium and the electric field in the membrane is purely due to the resting potential. When there is low or zero calcium, the outer surface has a net negative charge and hence, a local negative potential or surface potential is created. The voltage sensor in the sodium channel will sense this change in electric field as depolarization. This results in the opening of sodium channels and thereby an increase in excitability.
Reference:
[1] Hille B. Chapter 13. Modifiers of gating; In: Ionic channels of excitable membranes, 1st edition, Sinauer Associates Inc, Sunderland, Massachusetts, 1984.
Conflict of interests: none declared.
Please cite this letter as Bhaskar A. Surface-potential theory for explaining the increase in sodium permeability seen in hypocalcemia. Medical Physiology Online, article 3.6, volume 1, 2008, available from http://medicalphysiologyonline.blogspot.com [Link]
Reviewed by E.S.Prakash, Editor, Medical Physiology Online.
Anand Bhaskar, Department of Physiology, Christian Medical College, Vellore, 632002, India. E-mail: anandbhaskar [at] sify [dot] com.
Received 23 January 2008; accepted 24 January 2008.
We are aware that hypocalcemia decreases the activation threshold of sodium channels. How does this happen? It can be explained on the basis of the surface-potential theory [1]. According to this theory, the outer surface of cells has a net negative charge. When calcium levels are high, these charges get neutralized by calcium and the electric field in the membrane is purely due to the resting potential. When there is low or zero calcium, the outer surface has a net negative charge and hence, a local negative potential or surface potential is created. The voltage sensor in the sodium channel will sense this change in electric field as depolarization. This results in the opening of sodium channels and thereby an increase in excitability.
Reference:
[1] Hille B. Chapter 13. Modifiers of gating; In: Ionic channels of excitable membranes, 1st edition, Sinauer Associates Inc, Sunderland, Massachusetts, 1984.
Conflict of interests: none declared.
Please cite this letter as Bhaskar A. Surface-potential theory for explaining the increase in sodium permeability seen in hypocalcemia. Medical Physiology Online, article 3.6, volume 1, 2008, available from http://medicalphysiologyonline.blogspot.com [Link]
Reviewed by E.S.Prakash, Editor, Medical Physiology Online.
20 January 2008
Is hyperphosphatemia an independent cause of tetany?
Type of article: Letter to the Editor
Harsha Halahalli, Department of Physiology, KS Hegde Medical Academy, Mangalore, India
Received 20 January 2008; accepted 20 January 2008.
Singh has rightly pointed out [1] that hyperphosphatemia could also trigger muscular spasms. Hyperphosphatemia could result from several causes such as impaired renal function, tissue necrosis, rhabdomyolysis, tumor lysis syndrome, and exogenous administration of phosphate commonly in the form of laxatives. If phosphate builds up rapidly in such situations, it may be associated with features of tetany. However, in such cases the tetany is due to the hypocalcemia that results from the excess phosphate levels and in that sense, hyperphosphatemia may not be an independent cause for tetany [2].
Milk-alkali syndrome is not always accompanied by hyperphosphatemia [4]. Unfortunately, in the case report by Goetz [3], serum phosphate levels at the time of admission are not reported and those reported for the sixth day after admission are within normal limits. The tetany observed in this case despite the hypercalcemia could be attributed to the accompanying alkalosis which is known to reduce ionized calcium levels. It is possible that the level of ionized calcium which modulates membrane excitability is sufficiently low so as to cause tetany even though total serum calcium is moderately elevated.
Thus, my interpretation is that hyperphosphatemia could be associated with tetany only if it were also accompanied by reduced serum levels of ionized calcium.
Was the tetany in the case report by Goetz [3] due to hyperphosphatemia? Well, it is questionable.
Conflict of interests: none
References:
[1] Singh S. Milk alkali tetany. Medical Physiology Online 2008 [Link], accessed 20 January 2008
[2] Domico MB, Huynh V, Anand SK, Mink R. Severe hyperphosphatemia and hypocalcemic tetany after oral laxative administration in a 3-month-old infant.
Pediatrics. 2006; 118: e1580-1583.
[3] Goetz AA. Milk-alkali syndrome with jaundice and tetany. California Medicine 1958; 89: 136-139
[4] Felsenfeld AJ and Levine BS. Milk alkali Syndrome and the dynamics of calcium homeostasis. Clin J Am Soc Nephrol 2006; 1: 641–654.
Reviewed by E.S.Prakash, Editor, Medical Physiology Online.
Harsha Halahalli, Department of Physiology, KS Hegde Medical Academy, Mangalore, India
Received 20 January 2008; accepted 20 January 2008.
Singh has rightly pointed out [1] that hyperphosphatemia could also trigger muscular spasms. Hyperphosphatemia could result from several causes such as impaired renal function, tissue necrosis, rhabdomyolysis, tumor lysis syndrome, and exogenous administration of phosphate commonly in the form of laxatives. If phosphate builds up rapidly in such situations, it may be associated with features of tetany. However, in such cases the tetany is due to the hypocalcemia that results from the excess phosphate levels and in that sense, hyperphosphatemia may not be an independent cause for tetany [2].
Milk-alkali syndrome is not always accompanied by hyperphosphatemia [4]. Unfortunately, in the case report by Goetz [3], serum phosphate levels at the time of admission are not reported and those reported for the sixth day after admission are within normal limits. The tetany observed in this case despite the hypercalcemia could be attributed to the accompanying alkalosis which is known to reduce ionized calcium levels. It is possible that the level of ionized calcium which modulates membrane excitability is sufficiently low so as to cause tetany even though total serum calcium is moderately elevated.
Thus, my interpretation is that hyperphosphatemia could be associated with tetany only if it were also accompanied by reduced serum levels of ionized calcium.
Was the tetany in the case report by Goetz [3] due to hyperphosphatemia? Well, it is questionable.
Conflict of interests: none
References:
[1] Singh S. Milk alkali tetany. Medical Physiology Online 2008 [Link], accessed 20 January 2008
[2] Domico MB, Huynh V, Anand SK, Mink R. Severe hyperphosphatemia and hypocalcemic tetany after oral laxative administration in a 3-month-old infant.
Pediatrics. 2006; 118: e1580-1583.
[3] Goetz AA. Milk-alkali syndrome with jaundice and tetany. California Medicine 1958; 89: 136-139
[4] Felsenfeld AJ and Levine BS. Milk alkali Syndrome and the dynamics of calcium homeostasis. Clin J Am Soc Nephrol 2006; 1: 641–654.
Reviewed by E.S.Prakash, Editor, Medical Physiology Online.
Ill-conceived questions
Type of article: Letter to the Editor
Harsha Halahalli, Department of Physiology, KS Hegde Medical Academy, Mangalore, India.
Received 20 January 2008; accepted 20 January 2008.
I agree with the author [1] that, from a mechanistic point of view, little is achieved by differentiating the terms "tetanus" and "tetany". Tetany is best thought of as a clinical feature that may be seen in a variety of conditions including Clostridium tetani infections and hypocalcemia. The line of questioning that is referred to by the author does lead to the erroneous conclusion that tetany is a distinct condition that is attributable solely to hypocaclcemia. This is just one example of how ill-conceived and poorly framed questions could create flawed concepts in students. Having said this, it may however be noted that there is a difference in the pathogenesis of tetany resulting from tetanotoxin and hypocalcemia. While the site of action of tetanotoxin is pre-synaptic to the alpha-motorneurons in the spinal cord, hypocalcemia affects the motor neuronal membrane itself [2]. But the consequence of both is the increase in the firing rate of alpha-motoneurons resulting in the features of tetany.
Conflict of interests: none
References:
[1] Prakash ES. What is the difference between tetanus and tetany? Medical Physiology Online, article 3; volume 1: 2008; available from http://www.medicalphysiologyonline.org, accessed 17 January 2008
[2] Kandel ER, Schwartz JH and Jessel MT. Chapter 14: Transmitter Release; In: Principles of Neural Sciences, 4th Edn, Mc Graw Hill Co., New York, 2000.
Editor's note: I commissioned and reviewed this letter.
E.S.Prakash, Editor, Medical Physiology Online
Harsha Halahalli, Department of Physiology, KS Hegde Medical Academy, Mangalore, India.
Received 20 January 2008; accepted 20 January 2008.
I agree with the author [1] that, from a mechanistic point of view, little is achieved by differentiating the terms "tetanus" and "tetany". Tetany is best thought of as a clinical feature that may be seen in a variety of conditions including Clostridium tetani infections and hypocalcemia. The line of questioning that is referred to by the author does lead to the erroneous conclusion that tetany is a distinct condition that is attributable solely to hypocaclcemia. This is just one example of how ill-conceived and poorly framed questions could create flawed concepts in students. Having said this, it may however be noted that there is a difference in the pathogenesis of tetany resulting from tetanotoxin and hypocalcemia. While the site of action of tetanotoxin is pre-synaptic to the alpha-motorneurons in the spinal cord, hypocalcemia affects the motor neuronal membrane itself [2]. But the consequence of both is the increase in the firing rate of alpha-motoneurons resulting in the features of tetany.
Conflict of interests: none
References:
[1] Prakash ES. What is the difference between tetanus and tetany? Medical Physiology Online, article 3; volume 1: 2008; available from http://www.medicalphysiologyonline.org, accessed 17 January 2008
[2] Kandel ER, Schwartz JH and Jessel MT. Chapter 14: Transmitter Release; In: Principles of Neural Sciences, 4th Edn, Mc Graw Hill Co., New York, 2000.
Editor's note: I commissioned and reviewed this letter.
E.S.Prakash, Editor, Medical Physiology Online
17 January 2008
Milk and alkali tetany
Type of article: Letter to the Editor
Satendra Singh, Department of Physiology, Pt Bhagwat Dayal Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, 124001, India. E-mail: dr.satendra [at] gmail [dot] com
Received 14 January 2008; accepted 16 January 2008
In agreement with the author [1], I would like to add that though hypocalcemia is a common cause of tetany, an excess of phosphate (high phosphate-to-calcium ratio) could also trigger muscular spasms. Milk-and-alkali tetany is an example of this imbalance. [2]
References:
[1] Prakash ES. What is the difference between tetanus and tetany? Medical Physiology Online [serial online] article 3; volume 1: 2008; available from http://www.medicalphysiologyonline.org, [link to the article] accessed 14 January 2008.
[2] Goetz AA. Milk-alkali syndrome with jaundice and tetany. California Medicine 1958; 89: 136-139.
Conflict of interest: none
Please cite this letter as: Singh S. Milk and alkali tetany. Medical Physiology Online [serial online] article 3.1; volume 1: 2008; available from http://medicalphysiologyonline.blogspot.com [Link]
Reviewed by E.S.Prakash, Editor, Medical Physiology Online.
Satendra Singh, Department of Physiology, Pt Bhagwat Dayal Sharma Postgraduate Institute of Medical Sciences, Rohtak, Haryana, 124001, India. E-mail: dr.satendra [at] gmail [dot] com
Received 14 January 2008; accepted 16 January 2008
In agreement with the author [1], I would like to add that though hypocalcemia is a common cause of tetany, an excess of phosphate (high phosphate-to-calcium ratio) could also trigger muscular spasms. Milk-and-alkali tetany is an example of this imbalance. [2]
References:
[1] Prakash ES. What is the difference between tetanus and tetany? Medical Physiology Online [serial online] article 3; volume 1: 2008; available from http://www.medicalphysiologyonline.org, [link to the article] accessed 14 January 2008.
[2] Goetz AA. Milk-alkali syndrome with jaundice and tetany. California Medicine 1958; 89: 136-139.
Conflict of interest: none
Please cite this letter as: Singh S. Milk and alkali tetany. Medical Physiology Online [serial online] article 3.1; volume 1: 2008; available from http://medicalphysiologyonline.blogspot.com [Link]
Reviewed by E.S.Prakash, Editor, Medical Physiology Online.
The difference between tetanus and tetany
Type of article: Letter to the Editor
Selvakumar Balakrishnan, Final year undergraduate medical student, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry 605006, India. E-mail: selvasriram87 [at] gmail [dot] com
Received 17 January 2008; accepted 17 January 2008.
The message from this article [1] is clear enough for anyone to understand; i.e., the terms “tetanus” and “tetany” are not as different as we assume them to be. This deeper understanding is a refreshing experience and inspires us to stop and assimilate medical literature rather than reading it as such, a common practice these days. But it is also true that both the terms are not the same. In my opinion, “tetany” is a state of hyperexcitability in which a muscle can contract non-stop, and this is the final pathogenetic mechanism by which Clostridium tetani causes the disease “tetanus”. Maybe that is why the disease was named tetanus in the first place!
Acknowledgment: I am a student advisor for Medical Physiology Online.
Reference:
[1] Prakash ES. What is the difference between tetanus and tetany? Medical Physiology Online article 3; volume 1: 2008; available from http://www.medicalphysiologyonline.org, [link to the article] accessed 16 Jan 2008
Editor’s note: I commissioned and reviewed this contribution from Selvakumar. We have learnt a lot together and have recently published an article together.
Please cite this letter as:
Balakrishnan S. The difference between tetanus and tetany. Medical Physiology Online [serial online] article 3.2; volume 1: 2008, available from http://medicalphysiologyonline.blogspot.com [Link]
Submit a response to Balakrishnan's letter
Selvakumar Balakrishnan, Final year undergraduate medical student, Jawaharlal Institute of Postgraduate Medical Education and Research, Pondicherry 605006, India. E-mail: selvasriram87 [at] gmail [dot] com
Received 17 January 2008; accepted 17 January 2008.
The message from this article [1] is clear enough for anyone to understand; i.e., the terms “tetanus” and “tetany” are not as different as we assume them to be. This deeper understanding is a refreshing experience and inspires us to stop and assimilate medical literature rather than reading it as such, a common practice these days. But it is also true that both the terms are not the same. In my opinion, “tetany” is a state of hyperexcitability in which a muscle can contract non-stop, and this is the final pathogenetic mechanism by which Clostridium tetani causes the disease “tetanus”. Maybe that is why the disease was named tetanus in the first place!
Acknowledgment: I am a student advisor for Medical Physiology Online.
Reference:
[1] Prakash ES. What is the difference between tetanus and tetany? Medical Physiology Online article 3; volume 1: 2008; available from http://www.medicalphysiologyonline.org, [link to the article] accessed 16 Jan 2008
Editor’s note: I commissioned and reviewed this contribution from Selvakumar. We have learnt a lot together and have recently published an article together.
Please cite this letter as:
Balakrishnan S. The difference between tetanus and tetany. Medical Physiology Online [serial online] article 3.2; volume 1: 2008, available from http://medicalphysiologyonline.blogspot.com [Link]
Submit a response to Balakrishnan's letter
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