Hypo-/Hyperkaliämie Hypokalziämie bei den "vier H" bei Reanimation

Uns wurde in der Schule beigebracht: "Wenn ihr nicht gerade rein zufällig in einer Dialysepraxis reanimiert, hat dieser Faktor wenig Relevanz."

Zitat von tansamalaja

Bei den "vier H" scheint ja die Hypoglykämie zu Gunsten der Hypo-, Hyperkaliämie, Hypokalziämie rausgeflogen zu sein. Frage hierzu: Kann man diese Parameter präklinisch bei einer Reanimation überhaupt irgendwie ausschließen?

Die H's und die SHIT's sind ja nicht nur für die Präklinik gemacht worden.

Zitat von tansamalaja

Bei den "vier H" scheint ja die Hypoglykämie zu Gunsten der Hypo-, Hyperkaliämie, Hypokalziämie rausgeflogen zu sein. Frage hierzu: Kann man diese Parameter präklinisch bei einer Reanimation überhaupt irgendwie ausschließen? Gerade bei einer asystolen Reanimation ohne wirklich erkennbare EKG-Hinweise?

Quelle u.a.:
http://www.der-mensch.at/4h_hits.php

Da ist gar nichts "rausgeflogen". Es heißt weiterhin "Hyperkalämie, Hypokalämie, Hypokalzämie, Acidose und andere metabolische Störungen werden durch laborchemische Untersuchungen diagnostiziert oder können anhand der Krankengeschichte des Patienten erfragt werden". (Im Original "Hyperkalaemia, hypokalaemia, hypocalcaemia, acidaemia
and other metabolic disorders [...]").

Zum einen wurde ja schon vollkommen richtig gesagt, dass das Vorgehen nicht nur für die Präklinik gilt, zum anderen sollte man auch immer daran denken, dass die Suche nach reversiblen Ursachen auch für die Prä- und Postreanimationsphase geboten ist. Hier kann dann z.B. (Fremd)Anamnese, EKG und Co auch präklinisch den ein oder anderen Hinweis geben.

VG

Seit ich das Schema kenne war die Hypoglykämie sowieso nie Bestandteil. Somit wäre es zumindest nicht neu.

Das die Hypo-/ Hyperkaliämie in der Präklinik nicht verifiziert werden kann wurde ja bereits gesagt. Aber über eine Anamnese könnte man zumindest den Verdacht äußern.

Resuscitation. 2007 Sep;74(3):573-4. Epub 2007 Jun 20.
Hypoglycaemia--one of the 'H's or not!
Whiticar R, Smith S, Wathen C.

PMID:
17583408
[PubMed - indexed for MEDLINE]

und weiter

Sir,

It came to our attention, on a recent Advanced Life Support (ALS) course, that a lot of the emphasis on teaching is placed on ensuring the candidates are able to remember and recite the reversible causes of cardiac arrest (the “4H's and 4T's”), and treat them appropriately. The 4th ‘H’ as stated in the 5th edition of ALS manual is “Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders.”1 There is no doubt that hyperkalaemia/hypokalaemia can cause arrhythmias which can precipitate a Pulseless Electrical Actvitity arrest.

However, a debate has been started recently in our emergency department between the medical physicians and the emergency physicians as to whether hypoglycaemia should be listed as part of the metabolic disorders ‘H’! We are all aware that hypoglycaemia can result in irreversible neurological damage but is it a potentially reversible cause of cardiac arrest?

There is a general consensus that tight control of blood glucose (range 80–110 mg dl or 4.4–6.1 mmol) with insulin reduces hospital mortality in critically ill patients,2, 3 and after myocardial infarction.4 This has yet to be shown in a randomised controlled study in post-arrest patients. However, an animal study in rats has shown that glucose and insulin improves cerebral outcome after asphyxial cardiac arrest.5

There has been little research which suggests how, if at all, hypoglycaemia causes cardiac arrest. Two studies from Sheffield have hypothesized that clinical hypoglycaemia can cause abnormal cardiac repolarization and is therefore an attendant risk for cardiac arrhythmia. They studied the effect of hypoglycaemia in patients with type 1 diabetes and found that there is a significant lengthening of the QT interval during hypoglycaemia, the clinical relevance of this is uncertain but would be potentially consistent with their hypothesis.6, 7

However there has been some research, comparing the neuro-radiological changes in the brains of patients after hypoglycaemic coma, with those after cardiac arrest. It is interesting to note that not only were major radiological differences observed on magnetic resonance (MR) images between the two groups but also that these differences were attributed to a different patho-physiology between ischaemia and hypoglycaemia. In particular, cerebral intracellular acidosis accompanies cerebral ischaemia, resulting in minor haemorrhages in the MR images. We also know that acidosis appears to contribute to cell death and leads to poor outcome in patients after cardiopulmonary resuscitation. In contrast, profound hypoglycaemia causes tissue alkalosis, resulting from the ammonia formation from deamination of amino acids, the consumption of metabolic acids and the absence of lactic acid formation. This results in differences on the MR images post-hypoglycaemic episode versus a period of cerebral ischaemia—with no minor haemorrhages seen.8

ALS states that one of the potentially reversible metabolic states in PEA arrest is acidaemia, but as noted above hypoglycaemia results in alkalosis, not acidosis as is a common finding post-arrest.

This is obviously a controversial issue and raises the point of whether we should still be teaching that hypoglycaemia is a reversible cause of cardiac arrest when there seems to be not enough evidence to support this. Current evidence would suggest that patients may suffer cardio-respiratory arrest with hypoglycaemia, but not because of it.

In ALS teaching, surely the greatest emphasis on hypo/hyperglycaemia should be placed in the post-arrest and critically ill patient, where we know that good glycaemic control can affect mortality rates, and that a persistently high blood glucose after resuscitation from cardiac arrest can result in poor neurological outcome?9
References

Resuscitation Council (UK). Advanced Life Support Manual. 5th Edition. Resuscitation Council: London, UK; 2006.
View in Article
Van Der Berghe, G., Wilmer, A., Hermans, G. et al. Intensive insulin therapy in the critically ill patient. N Engl J Med. 2001; 345: 1359–1367
View in Article
| CrossRef
| PubMed
| Scopus (5712)
Krinsley, J.S. Effect of an intensive glucose management protocol on the mortality of critically ill adult patient. Mayo Clin Proc. 2004; 79: 992–1000
View in Article
| PubMed
Malmberg, K., Ryden, L., Hamsten, A. et al. Randomized trial of insulin-glucose infusion followed by subcutaneous insulin treatment in diabetic patients with acute myocardial infarction (DIGAMI study): effects on mortality at 1 year. J Am Coll Cardiol. 1995; 26: 56–65
View in Article
| Scopus (1135)
Katz, L.M., George, E., and Peacey, S.R. Glucose plus insulin infusion improves cerebral outcome after asphyxial cardiac arrest. Neuroreport. 1998; 9: 3363–3367
View in Article
| CrossRef
| PubMed
Marques, J.L., Wang, Y., Ebmeyer, U., Radovsky, A., and Safar, P. Altered ventricular repolarization during hypoglycaemia in patients with diabetes. Diabet Med. 1997; 14: 648–654
View in Article
| CrossRef
| PubMed
| Scopus (128)
Robinson, R.T., Harris, N.D., Ireland, R.H., Macdonald, I.A., and Heller, S.R. Changes in cardiac repolarization during clinical episodes of nocturnal hypoglycaemia in adults with type 1 diabetes. Diabetologia. 2004; 47: 312–315
View in Article
| CrossRef
| PubMed
| Scopus (58)
Fujioka, M., Okuchi, K., Hiramatsu, K.I., Sakaki, T., Sakaguchi, S., and Ishii, Y. Specific changes in human brain after hypoglycaemic injury. Stroke. 1997; 28: 584–587
View in Article
| CrossRef
| PubMed
ERC CoSTR Document; 2005. http://www.erc.edu/index.php/guidelines_download_2005/en/; accessed 28th April 2007.
View in Article

Resuscitation. 2009 Jun;80(6):624-30. doi: 10.1016/j.resuscitation.2009.02.011. Epub 2009 Mar 18.
Derangements in blood glucose following initial resuscitation from in-hospital cardiac arrest: a report from the national registry of cardiopulmonary resuscitation.
Beiser DG1, Carr GE, Edelson DP, Peberdy MA, Hoek TL.
Author information
Abstract
STUDY AIMS:

Hyperglycemia is associated with poor outcomes in critically ill patients. We examined blood glucose values following in-hospital cardiac arrest (IHCA) to (1) characterize post-arrest glucose ranges, (2) develop outcomes-based thresholds of hyperglycemia and hypoglycemia, and (3) identify risk factors associated with post-arrest glucose derangements.
METHODS:

We retrospectively studied 17,800 adult IHCA events reported to the National Registry of Cardiopulmonary Resuscitation (NRCPR) from January 1, 2005 through February 1, 2007.
RESULTS:

Data were available from 3218 index events. Maximum blood glucose values were elevated in diabetics (median 226 mg/dL [IQR, 165-307 mg/dL], 12.5 mmol/L [IQR 9.2-17.0 mmol/L]) and non-diabetics (median 176 mg/dL [IQR, 135-239 mg/dL], 9.78 mmol/L [IQR 7.5-13.3 mmol/L]). Unadjusted survival to hospital discharge was higher in non-diabetics than diabetics (45.5% [95% CI, 43.3-47.6%] vs. 41.7% [95% CI, 38.9-44.5%], p=0.037). Non-diabetics displayed decreased adjusted survival odds for minimum glucose values outside the range of 71-170 mg/dL (3.9-9.4 mmol/L) and maximum values outside the range of 111-240 mg/dL (6.2-13.3 mmol/L). Diabetic survival odds decreased for minimum glucose greater than 240 mg/dL (13.3 mmol/L). In non-diabetics, arrest duration was identified as a significant factor associated with the development of hypo- and hyperglycemia.
CONCLUSIONS:

Hyperglycemia is common in diabetics and non-diabetics following IHCA. Survival odds in diabetics are relatively insensitive to blood glucose with decreased survival only associated with severe (>240 mg/dL, >13.3 mmol/dL) hyperglycemia. In non-diabetics, survival odds were sensitive to hypoglycemia (<70 mg/dL, <3.9 mmol/L).

Die letzte conclusion sagt:
BZ macht doch n Unterschied, nur nicht immer...

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