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ERC Guidelines 2005 Cardiac Arrest in Special Circunstances

ERC Guidelines 2005 Cardiac Arrest in Special Circunstances

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Resuscitation (2005)
67S1
, S135—S170
European Resuscitation Council Guidelines forResuscitation 2005Section 7. Cardiac arrest in special circumstances
Jasmeet Soar, Charles D. Deakin, Jerry P. Nolan, Gamal Abbas,Annette Alfonzo, Anthony J. Handley, David Lockey,Gavin D. Perkins, Karl Thies
7a. Life-threatening electrolytedisorders
Overview
Electrolyte abnormalities can cause cardiacarrhythmias or cardiopulmonary arrest. Life-threatening arrhythmias are associated commonlywith potassium disorders, particularly hyper-kalaemia, and less commonly with disorders ofserum calcium and magnesium. In some casestherapy for life-threatening electrolyte disordersshould start before the laboratory results becomeavailable.The electrolyte values for definitions have beenchosen as a guide to clinical decision-making.The precise values that trigger treatment deci-sions will depend on the patient’s clinical con-dition and the rate of change of the electrolytevalues.There is little or no evidence base for the treat-ment of electrolyte abnormalities during cardiacarrest. Guidance during cardiac arrest is basedon the strategies used in the non-arrest patient.There are no major changes in the treatment ofthese disorders since the International Guidelines2000.
1
Prevention of electrolyte disorders
Treat life-threatening electrolyte abnormalitiesbefore cardiac arrest occurs.
After initial treatment, remove any precipitatingfactors (e.g., drugs) and monitor electrolyte lev-els to prevent recurrence of the abnormality.
Monitor renal function in patients at risk of elec-trolyte disorders.
In haemodialysis patients, review the dialy-sis prescription regularly to avoid inappropriateelectrolyte shifts during treatment.
Potassium disorders
Potassium homeostasis
Extracellular potassium concentration is regulatedtightly between 3.5—5.0mmoll
1
. A large con-centration gradient normally exists between theintracellular and extracellular fluid compartments.This potassium gradient across the cell membranescontributes to the excitability of nerve and mus-cle cells, including the myocardium. Evaluationof serum potassium must take into considerationthe effects of changes in serum pH. When serumpH decreases, serum potassium increases because
0300-9572/$ — see front matter © 2005 European Resuscitation Council. All Rights Reserved. Published by Elsevier Ireland Ltd.doi:10.1016/j.resuscitation.2005.10.004
 
S136 J. Soar et al.potassium shifts from the cellular to the vascularspace. When serum pH increases, serum potassiumdecreases because potassium shifts intracellularly.We therefore anticipate the effects of pH changeson serum potassium during the therapy for hyper-kalaemia or hypokalaemia.
Hyperkalaemia
This is the most common electrolyte disorder asso-ciated with cardiopulmonary arrest. It is usuallycaused by increased potassium release from thecells or impaired excretion by the kidneys.
Definition.
There is no universal definition,althoughwehavedefinedhyperkalaemiaasaserumpotassium concentration higher than 5.5mmoll
1
;in practice, hyperkalaemia is a continuum. Asthe potassium concentration increases above thisvalue, the risk of adverse events increases and theneed for urgent treatment increases. Severe hyper-kalaemia has been defined as a serum potassiumconcentration higher than 6.5mmoll
1
.
Causes.
There are several potential causes ofhyperkalaemia, including renal failure, drugs(angiotensin converting enzyme inhibitors (ACEI),angiotensin II receptor blockers (ARB), potassium-sparing diuretics, non-steroidal anti-inflammatorydrugs (NSAIDs), beta-blockers, trimethoprim, tis-sue breakdown (rhabdomyolysis, tumour lysis,haemolysis), metabolic acidosis, endocrine disor-ders (Addison’s disease), hyperkalaemic periodicparalysis, or diet, which may be the sole causein patients with established renal failure. Abnor-mal erythrocytes or thrombocytosis may cause aspuriously high potassium concentration. The riskof hyperkalaemia is even greater when there isa combination of factors, such as the concomi-tant use of ACEI and NSAIDs or potassium-sparingdiuretics.
Recognition of hyperkalaemia.
Exclude hyper-kalaemia in patients with an arrhythmia or car-diac arrest.
2
Patients may present with weaknessprogressing to flaccid paralysis, paraesthesia ordepressed deep tendon reflexes. The first indica-tor of hyperkalaemia may also be the presence ofECG abnormalities, arrhythmias, cardiopulmonaryarrest or sudden death. The effect of hyper-kalaemiaontheECGdependsontheabsoluteserumpotassium as well as the rate of increase. Mostpatients will have ECG abnormalities at a serumpotassium concentration higher than 6.7mmoll
1
.
3
The ECG manifestations of hyperkalaemia are usu-ally progressive and include:
first-degree heart block (prolonged PR interval)>0.2s;
flattened or absent
waves;
tall, peaked (tented)
waves, larger than
R
wavein more than one lead;
ST segment depression;
S
and
waves merging;
widened QRS >0.12s;
ventricular tachycardia (VT);
bradycardia;
cardiac arrest, i.e., pulseless electrical activity(PEA), ventricular fibrillation (VF), asystole.
Treatment of hyperkalaemia.
The five key stepsin treating hyperkalaemia are:1. cardiac protection by antagonising the effects ofhyperkalaemia;2. shifting potassium into cells;3. removing potassium from the body;4. monitoring serum potassium for rebound hyper-kalaemia;5. prevention of recurrence of hyperkalaemia.When hyperkalaemia is strongly suspected, e.g.,in the presence of ECG changes, start life-savingtreatment even before laboratory results are avail-able. The management of hyperkalaemia is the sub-ject of a recent Cochrane review.
4
Patient not in cardiac arrest.
If the patientis not in cardiac arrest, assess fluid status;if hypovolaemic, give fluid to enhance urinarypotassium excretion. The values for classificationare an approximate guide. For mild elevation(5.5—6mmoll
1
), remove potassium from the bodywith:
potassium exchange resins, i.e., calcium reso-nium 15—30g or sodium polystyrene sulfonate(Kayexalate
®
) 15
30g in 50
100ml of 20% sor-bitol, given either orally or by retention enema(onset in 1
3h, maximal effect at 6h);
diuretics, i.e., furosemide 1mgkg
1
IV slowly(onset with the diuresis);
dialysis; haemodialysis is more efficient thanperitoneal dialysis at removing potassium (imme-diate onset, 25
30mmolpotassiumh
1
removedwith haemodialysis).For moderate elevation (6—6.5mmoll
1
) with-out ECG changes, shift potassium into cells with:
dextrose/insulin: 10 units short-acting insulinand 50g glucose IV over 15—30min (onset in15—30min, maximal effect at 30
60min; mon-itor blood glucose). Use in addition to removalstrategies above.
 
European Resuscitation Council Guidelines for Resuscitation 2005 S137For severe elevation (
6.5mmoll
1
) withoutECG changes, shift potassium into cells with:
salbutamol, 5mg nebulised. Several doses maybe required (onset in 15
30min);
sodium bicarbonate, 50mmol IV over 5min ifmetabolic acidosis present (onset in 15
30min).Bicarbonate alone is less effective than glucoseplus insulin or nebulised salbutamol; it is bestused in conjunction with these medications;
use multiple shifting agents in addition toremoval strategies above.For severe elevation (
6.5mmoll
1
) with toxicECG changes, protect the heart
first
with:
calciumchloride,i.e.,10ml10%calciumchlorideIV over 2—5min to antagonise the toxic effects ofhyperkalaemia at the myocardial cell membrane.This protects the heart by reducing the risk ofVF, but does not lower serum potassium (onset in1—3min). Use in addition to potassium removaland shifting strategies stated above.
Patient in cardiac arrest.
If the patient is incardiac arrest, there are no modifications to BLSin the presence of electrolyte abnormalities. ForALS, follow the universal algorithm. The generalapproach to treatment depends on the degree ofhyperkalaemia, rate of rise of serum potassium andthe patient’s clinical condition.In cardiopulmonary arrest, protect the heartfirst, then apply shifting and removal strategiesusing:
calcium chloride: 10ml of 10% calcium chlorideIV by rapid bolus injection to antagonise the toxiceffects of hyperkalaemia at the myocardial cellmembrane;
sodium bicarbonate: 50mmol IV by rapid injec-tion (if severe acidosis or renal failure);
dextrose/insulin:10unitsshort-actinginsulinand50g glucose IV by rapid injection;
haemodialysis: consider this for cardiac arrestinduced by hyperkalaemia, which is resistant tomedical treatment.
Indications for dialysis.
Haemodialysis is themost effective method of removal of potassiumfrom the body. The principal mechanism of actionis the diffusion of potassium ions across thetransmembrane potassium ion gradient. The typ-ical decline in serum potassium is 1mmoll
1
inthe first 60min, followed by 1mmoll
1
over thenext 2h. Consider haemodialysis early for hyper-kalaemia associated with established renal fail-ure, oliguric acute renal failure (<400mlday
1
urine output) or when there is marked tissuebreakdown. Dialysis is also indicated when hyper-kalaemia is resistant to medical management.Serum potassium frequently rebounds after ini-tial treatment. In unstable patients, continuousveno-venous haemofiltration (CVVH) is less likelyto compromise cardiac output than intermittenthaemodialysis.
Hypokalaemia
Hypokalaemia is common in hospital patients.
7
Hypokalaemia increases the incidence of arrhyth-mias, particularly in patients with pre-existingheart disease and in those treated with digoxin.
Definition.
Hypokalaemia is defined as a serumpotassium <3.5mmoll
1
. Severe hypokalaemia isdefined as a K
+
<2.5mmoll
1
and may be associ-ated with symptoms.
Causes.
Causes of hypokalaemia include gas-trointestinal loss (diarrhoea), drugs (diuretics,laxatives, steroids), renal losses (renal tubulardisorders, diabetes insipidus, dialysis), endocrinedisorders (Cushing’s syndrome, hyperaldostero-nism), metabolic alkalosis, magnesium depletionand poor dietary intake. Treatment strategies usedfor hyperkalaemia may also induce hypokalaemia.
Recognition of hypokalaemia.
Exclude hypoka-laemia in every patient with an arrhythmia orcardiac arrest. In dialysis patients, hypokalaemiaoccurs commonly at the end of a haemodialysissession or during treatment with continuous ambu-latory peritoneal dialysis (CAPD).As serum potassium concentration decreases,the nerves and muscles are predominantlyaffected, causing fatigue, weakness, legcramps and constipation. In severe cases(K
+
<2.5mmoll
1
), rhabdomyolysis, ascendingparalysis and respiratory difficulties may occur.ECG features of hypokalaemia comprise:
U
waves;
-wave flattening;
ST segment changes;
arrhythmias, especially if patient is takingdigoxin;
cardiopulmonary arrest (PEA, VF, asystole).
Treatment.
Treatment depends on the severity ofhypokalaemia and the presence of symptoms andECG abnormalities. Gradual replacement of potas-sium is preferable but in emergency intravenouspotassiumisrequired.The maximumrecommendedIV dose of potassium is 20mmolh
1
, but more rapidinfusion, e.g., 2mmolmin
1
for 10min followed by10mmol over 5—10min is indicated for unstable

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