Manejo de la Hiperkalemia

Dr. Pavel González Guzmán

• Medicina Interna/Endocrinología
• Alta Especialidad en Enfermedades del Metabolismo
mineral
Introducción
• No existe un consenso universalmente aceptado sobre las mejores prácticas para la monitorización de la
hiperpotasemia

• La hiperpotasemia, definida como una concentración sérica elevada de potasio (K+) superior a 5,0 o 5,5
mEq / L (mmol / L)

• La hiperpotasemia tiene efectos despolarizadores en el corazónà provocando potenciales de acción

acortados y aumentando el riesgo de arritmias.

• La hiperpotasemia causa síntomas neuromusculares, acidosis metabólica y supresión de la

amoniagénesis.
• La concentración exacta de K+ que los médicos deben considerar potencialmente mortal sigue siendo
controvertida
• Disminución gradual en el riesgo de mortalidad a medida que empeoraba el estadio de la ERC

Clinical Management of Hyperkalemia,Biff F. Palmer, MD, 2020 Mayo Foundation for Medical Education and Research.
 s,
1.0
i-
Predicted probability of mortality
0.9
e- 0.8
en 0.7 HF, CKD, DM
se 0.6
ed CKD
0.5 HF
th 0.4
ty 0.3 DM
0.2 Control group
ng
HF 0.1
0
n-
2.5 3.0 3.5 4.0 4.5 5.0 5.5 6.0 6.5 7.0 7.5 8.0
ts
Baseline serum potassium level (mEq/L)
or
ia Clinical Management of Hyperkalemia,Biff F. Palmer, MD, 2020 Mayo Foundation for Medical Education and Research.
Factores de riesgo

• Ciertas poblaciones de pacientes tienen un mayor riesgo de morbilidad y mortalidad asociadas: ERC,
IC, hipertensión resistente, diabetes, infarto de miocardio (IM) y / o combinaciones de estas
afecciones.

• Factores de riesgo adicionales : RAASi, edad avanzada, y fármacos heparina, betabloqueantes,

antiinflamatorios no esteroideos, inhibidores de la calcineurina, trimetoprima, pentamidina y
diuréticos ahorradores de K

Clinical Management of Hyperkalemia,Biff F. Palmer, MD, 2020 Mayo Foundation for Medical Education and Research.
FIGURE 1. Regulation of potassium (Kþ) homeostasis. Absorbed Kþ is largely redistributed from the blood to the intracellular space
Clinical
by active transport (Naþ/Kþ-ATPase), which Management of Hyperkalemia,Biff
is stimulated F. Palmer, MD, 2020InMayo
by insulin and catecholamines. Foundation
individuals withfornormal
Medicalkidney
Education and Research.
function, Kþ
þ
Tratamiento

• Al decidir cómo para tratar los episodios de hiperpotasemia, puede ser útil centrarse en la
hiperpotasemia con impacto clínico, así como en las fluctuaciones rápidas del K sérico, en lugar
de los umbrales de K sérico rígidos y algo arbitrarios.

• Los umbrales de concentración de potasio para la clasificación de hiperpotasemia leve, moderada

y grave son útiles; sin embargo, la clasificación basada en el riesgo y el impacto clínico del
paciente también puede orientar la intervención clínica.

Clinical Management of Hyperkalemia,Biff F. Palmer, MD, 2020 Mayo Foundation for Medical Education and Research.
 Dépret et al. Ann. Intensive Care (2019) 9:32
https://doi.org/10.1186/s13613-019-0509-8

Raro: Modificación inespecífica del segmento ST o el síndrome

REVIEW Open Access
pseudo-Brugada (con QRS ancho, elevación del segmento ST,
Management of hyperkalemia in the acutely
elevación del punto J, inversión de la onda T). ill patient
François Dépret1,2,3, W. Frank Peacock5, Kathleen D. Liu6, Zubaid Rafique5, Patrick Rossignol4,7
and Matthieu Legrand1,2,3,4*

Abstract
Purpose: To review the mechanisms of action, expected efficacy and side effects of strategies to control hyper-

Rara vez pueden presentar debilidad que progresa a parálisis flácida, parestesias o reflejos tendinosos
kalemia in acutely ill patients.
Methods: We searched MEDLINE and EMBASE for relevant papers published in English between Jan 1, 1938, and July

profundos deprimidos.
1, 2018, in accordance with the PRISMA Statement using the following terms: “hyperkalemia,” “intensive care,” “acute
kidney injury,” “acute kidney failure,” “hyperkalemia treatment,” “renal replacement therapy,” “dialysis,” “sodium bicarbo-
nate,” “emergency,” “acute.” Reports from within the past 10 years were selected preferentially, together with highly
relevant older publications.
Results: Hyperkalemia is a potentially life-threatening electrolyte abnormality and may cause cardiac electrophysi-
ological disturbances in the acutely ill patient. Frequently used therapies for hyperkalemia may, however, also be
associated with morbidity. Therapeutics may include the simultaneous administration of insulin and glucose (associ-
ated with frequent dysglycemic complications), β-2 agonists (associated with potential cardiac ischemia and arrhyth-

• Los hallazgos electrocardiográficos de hiperpotasemia clásica incluyen signos de hiperexcitabilidad

mias), hypertonic sodium bicarbonate infusion in the acidotic patient (representing a large hypertonic sodium load)
and renal replacement therapy (effective but invasive). Potassium-lowering drugs can cause rapid decrease in serum
potassium level leading to cardiac hyperexcitability and rhythm disorders.

como ondas T puntiagudas (que reflejan una disminución en el umbral de despolarización rápida).
Conclusions: Treatment of hyperkalemia should not only focus on the ability of specific therapies to lower serum
potassium level but also on their potential side effects. Tailoring treatment to the patient condition and situation may
limit the risks.
Keywords: Hyperkalemia, Intensive care, Emergency, Renal replacement therapy, Acute kidney injury

Background abnormalities [7, 8]. However, the actual causes of death

Hyperkalemia is a potentially life-threatening electro- in patients with hyperkalemia are poorly described, and

• Prolongación de PR, pérdida de ondas P, ensanchamiento del QRS, bradicardia y, en última instancia,
lyte abnormality [1–3]. Although there is no interna- the causal relationship between hyperkalemia and out-
tionally agreed upon definition for hyperkalemia, the come remains controversial.
European Resuscitation Council defines hyperkalemia The aim of this review is first to describe mecha-

un ritmo de onda sinusoidal debido al acortamiento del potencial de acción y prolongación de la

as a plasma level > 5.5  mmol/L and severe hyperkalemia nisms and the risk–benefit ratio of different strategies
as > 6.5  mmol/L [4]. Hyperkalemia is associated with of hyperkalemia treatment and second, to propose a
poor outcomes in many different settings, including the tailored treatment strategy. This will include a discus-

despolarización diastólica. acutely ill patient [5, 6]. In acute hyperkalemia, the pri-
mary mortality risks are cardiac rhythm or conduction
sion of the effectiveness as well as complications of renal
replacement therapy, limiting the risk of hypoglycemia
with judicious insulin and glucose administration, and
*Correspondence: matthieu.legrand@aphp.fr
the potential benefit and risks of hypertonic sodium
1
GH St-Louis-Lariboisière, Department of Anesthesiology and Critical bicarbonate.
Care and Burn Unit, St-Louis Hospital, Assistance Publique-Hopitaux de
Paris, Paris, France
Full list of author information is available at the end of the article

• Es importante destacar que la correlación entre la elevación de potasio y los cambios © The Author(s) 2019. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License
(http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium,
provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license,
and indicate if changes were made.

electrocardiográficos (ECG) es pobre.

Table 1 Mechanisms contributing to  the  development show its efficacy and its ind
of hyperkalemia opinion [34]. The effect sh
Mechanisms contributing to the development of hyperkalemia 5 min) when any hyperkalem
identified or suspected [33]
Increased extracellular K+ Decreased K+ elimination
last between 30 and 60  mi
Tissue injury AKI tion in the case of hyperca
Hemolysis Hypovolemia It also increased toxicity w
Rhabdomyolysis Sepsis
Tumor lysis syndrome Acidosis treatment
mal models [34]. However,
K+ shift in extracellular space RAAS inhibitor nonphysiologically high calc
Mineral acidosis (i.e., hyperchoride Calcineurine inhibitor use of calcium in cases of h
acidosis) Cardiac glycosides
Succinylcholine
digoxin toxicity was not ass
Inability to enter into myocyte dysrhythmias or mortality
Diabetes mellitus Finally, calcium may cause t
Hyperglycemia
Hypertonicity
sis) in case of extravasation [
β2-receptor antagonists is 10–20 mL of a 10% calciu
Aldosterone blockers nate or chloride).
Cardiac glycosides
High acute iatrogenic K+ load
Increased dietary intake Hypertonic sodium
Blood transfusion Infusion of hypertonic sodiu
Error of injection
potential rising velocity in i
K+ potassium, RAAS renin–angiotensin–aldosterone system In 1960, Greenstein et al. [43
lactate, sodium bicarbonat
 Hyperkalemia

Acute Chronic

Dietary K+ counseling
IV calcium
(avoid salt substitutes)
Monitor: (10 mL of 10%)
Monitor:
• K+ trajectory • Serum K+ ¾2 times/year
• ECG changes • Comorbidities
• Other symptoms Manage RAASi therapy
IV insulin/glucose (reinitiate and titrate to optimal dose after
• Medications (OTC NSAIDs
(10 U + 50 mL dextrose) serum K+ stabilizes) and herbal supplements)
• Exclude pseudohyperkalemia
Educate:
• Health care professionals
Nebulized salbutamol Effective diuretic therapy • Patients
(20 mg in 4 mL) (loop diuretics with eGFR <30 mL/min)
Multidisciplinary care:
• Dietitian input
• Pharmacist input
IV sodium
Diureticsb Hemodialysisc Oral sodium bicarbonatea
bicarbonatea

Consider K+ binders
Consider K+ binders
(may facilitate RAASi dose optimization)

aIn patients with metabolic acidosis Stabilize myocardial cell membrane

bIn patients with hypervolemia (nonoliguric)
cIn patients with oliguria or ESRD K+ redistribution into intracellular space
Total body K+ elimination
Reduction of K+ intake
Identification/removal of medications that inhibit renal K+ excretion

FIGURE 3. Treatment options for the management of acute and chronic hyperkalemia. In patients with acute hyperkalemia, intravenous
Clinical Management of Hyperkalemia,Biff F. Palmer, MD, 2020 Mayo Foundation for Medical Education and Research.
(IV) calcium reduces membrane excitation in cardiac tissue within 1 to 3 minutes, while insulin and b-agonists redistribute potassium (Kþ)
to the intracellular space (30 to 60 minutes) but do not reduce total body Kþ. b-Agonists have a short duration of effect (2 to 4 hours),
 pret et al. Ann. Intensive Care
Table 2 Treatments of hyperkalemia
Type of treatment Effect on potassium plasma Administration Potential side effects Population at risk Preferred population
level

Myocardial protection
Calcium salt
Hypertonic sodium (e.g.,
sodium bicarbonate)
None 10–20 mL of calcium gluconate Hypercalcemia Digitalis intoxication or hyper- Hyperkalemia with ECG modifica-
10% i.v within 5 min calcemia tions
− 0.47 ± 0.31 mmol/L at 30 min 10–20 mL of sodium chloride Venous toxicity, increasing Hypervolemia, patients with Hyperkalemia with ECG modifica-
20% i.v within 5 min or PaCO2 (due to bicarbonate) heart failure, hypernatremia, tions, patient with metabolic

(2019) 9:32
100 mL of 8.4% i.v sodium patient with respiratory insuf- acidosis or AKI
bicarbonate ficiency (due to bicarbonate)
Intracellular potassium transfer
Insulin dextrose − 0.79 ± 0.25 mmol/L at 60 min 5 UI of rapid insulin + 25 grams Hyperglycemia and hypogly- All patients Severe hyperkalemia with hourly
of dextrose over 30 min or cemia Critically ill patients at monitoring of plasma glucose
10 of rapid insulin + g of increased of hyperglycemia- possible
dextrose or 0.5 U/kg of body related side effects
weight
Patients with acute neurologi-
cal disease
β2 mimetics − 0.5 ± 0.1 mmol/L at 60 min 10 mg nebulized salbutamol Tachycardia, arrhythmias, myo- Patients with ischemic cardi- Patient without heart failure,
cardial ischemia opathy angina or coronary disease
Increase plasma lactate level Patient under β blockers Spontaneously breathing patient
therapy
Elimination
Renal replacement therapy − 1 mmol/L within minutes High blood flow and dialysate Complications related to cath- Low availability of the tech- Severe renal failure, multiple
flow in hemodialysis, high eter (i.e., infection, thrombo- nique organ failure
ultrafiltration rate in hemo- sis, hemorrhage) Delay to initiate the treatment
filtration
Loop diuretics Unpredictable Variable Hypovolemia, hypokalemia, Hypovolemic patients Hypervolemic patients with
hypomagnesemia normal or moderately altered
renal function
Absorption
Sodium polystyrene sulfonate Unpredictable (no randomized 15 g one to four times per day Digestive perforation, hypocal- Patients with abnormal transit, Treatment of chronic hyper-
controlled trial in acute cemia, hypomagnesemia critically ill patients kalemia
hyperkalemia)
Patiromer 0.21 ± 0.07 mmol/L within 7 h 8.4–25.2 g per day Potential interaction with Patients with abnormal transit Treatment of chronic hyper-
(no randomized controlled co-administered drugs, kalemia
trial in acute hyperkalemia) hypomagnesemia, potential
long-term calcium disorder
ZS-9 0.6 ± 0.2 mmol/L within 2 h 10 g one to three times per day Edema Patients with abnormal transit Treatment of chronic and poten-
tially acute hyperkalemia

Pag
Fig. 1 Suggested algorithm for hyperkalemia treatment in the acutely ill. *In case of Digitalis intoxication or hypercalcemia. **Sodium zirconium
cyclosilicate and patiromer when available, kayexalate if not available. ESKD end-stage kidney disease, AKI acute kidney injury, CKD chronic kidney
disease, RRT renal replacement therapy
 Fig. 3 Action mechanisms of plasma lowering treatments by intracellular transfer. β-2 agonist (i.e., salbutamol) binds the β-2 receptor, insulin binds
insulin receptors and sodium bicarbonate (NaHCO3) induces an intracellular entrance of sodium through the Na+/H+ exchanger (NHE), all activate
the sodium–potassium adenosine triphosphatase (NaK+ ATPase) leading to a potassium transfer from the extracellular space to the intracellular
space

of hypoglycemia may induce severe hyperglycemia, and insulin resistance. We propose insulin–glucose as
Fig. 4 Action mechanisms of hypokalemic treatments by intracellular transfer. a Potassium dialysance, flux and plasma kinetic under short high
 Fig. 5 First-line treatment of hyperkalemia. During hyperkalemia with ECG modifications, first-line therapy should consist on cardiomyocyte
Las estrategias que aumentan
stabilization laorexcreción
using calcium salt hypertonic sodium (redrenal de line
panel), second potasio disminuyen
therapy on treatment el pool
leading to a fast transfer total
of potassium from de potasio (es decir,
extracellular to intracellular space using either insulin–glucose i.v, aerosol of β2 agonist and/or sodium bicarbonate (in case of metabolic acidosis
opLmización hemodinámica
and hypovolemic ypatient)
corrección
depending of thede lacomorbidities
patient’s lesiónand renal aguda
clinical status. o diuréLcos
Insulin–glucose is recommended asde asatreatment
the first-line
in severe hyperkalemia (i.e., above 6.5 mmol/L) but close glucose monitoring is mandatory. β2 agonists can be used in spontaneously breathing
de Henle en pacientes con
patients but with safety concerns in patients withsobrecarga defailure.
unstable angina or cardiac líquidos)
Hypertonic sodium bicarbonate should probably be restricted
to hypovolemic patients with metabolic acidosis (blue panel). Strategies increasing potassium renal excretion decreases the total potassium
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