Dynamics of serum potassium change during acute respiratory alkalosis

Sánchez, Muñoz; Finlayson, Donald C.

doi:10.1007/bf03007412

Cited by 9 publications

(2 citation statements)

References 20 publications

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“…, may be explained by more effective re-uptake in our study, associated with greater catecholamine release and/or by uptake associated with respiratory alkalosis (see values above and Sanchez & Finlayson, 1978). Assuming [K+] .…”

Section: Methodsmentioning

confidence: 66%

Interactions between K+ and beta 2‐adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia

Mian¹,

Marshall²,

Kumar³

1990

Experimental Physiology

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SUMMARYIn spontaneously breathing anaesthetized rats, both moderate and severe hypoxia caused increases in [K+] in venous efflux from hindlimb muscle, from 4-3 to 4.6 and from 3-8 to 4.4 mM respectively; the increases were accentuated to 5.2 and 5*7 mM after fl-receptor blockade with I.V. sotalol. Sotalol also potentiated the vasodilatation evoked in hindlimb muscle by moderate hypoxia, but reduced that evoked by severe hypoxia. We propose that K+ released from muscle during hypoxia contributed to the local vasodilatation. Further, we suggest that this effect was enhanced in moderate hypoxia by blockade of the h2-mediated uptake mechanism for K+ in skeletal muscle, but outweighed in severe hypoxia by blockade of the 02~-mediated dilator action of circulating catecholamines on vascular muscle.

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Section: Methodsmentioning

confidence: 66%

Interactions between K+ and beta 2‐adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia

Mian¹,

Marshall²,

Kumar³

1990

Experimental Physiology

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“…As per patient's initial lab and ABG, she had severe primary respiratory alkalosis with mild high anion gap metabolic acidosis which was considered to be from patient's elevated lactate level from her tachypnea. Voluntary hyperventilation in normal healthy patients has been found to be associated with severe respiratory alkalosis, increase in anion gap from lactic acidosis, and significant change in serum K + level [9, 10]. Severe alkalemia resulting from hyperventilation and hypocapnia has been shown to cause perioral numbness, cardiac arrhythmias, seizure, and tetany [11–13].…”

Section: Discussionmentioning

confidence: 99%

Opiate Withdrawal Complicated by Tetany and Cardiac Arrest

Kugasia

Shabarek

2014

Case Reports in Critical Care

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Patients with symptoms of opiate withdrawal, after the administration of opiate antagonist by paramedics, are a common presentation in the emergency department of hospitals. Though most of opiate withdrawal symptoms are benign, rarely they can become life threatening. This case highlights how a benign opiate withdrawal symptom of hyperventilation led to severe respiratory alkalosis that degenerated into tetany and cardiac arrest. Though this patient was successfully resuscitated, it is imperative that severe withdrawal symptoms are timely identified and immediate steps are taken to prevent catastrophes. An easier way to reverse the severe opiate withdrawal symptom would be with either low dose methadone or partial opiate agonists like buprenorphine. However, if severe acid-base disorder is identified, it would be safer to electively intubate these patients for better control of their respiratory and acid-base status.

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Hypokalemia After Resuscitation From Out-of-Hospital Ventricular Fibrillation

Thompson¹

1982

JAMA

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Dynamics of serum potassium change during acute respiratory alkalosis

Cited by 9 publications

References 20 publications

Interactions between K+ and beta 2‐adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia

Interactions between K+ and beta 2‐adrenoreceptors in determining muscle vasodilatation induced in the rat by systemic hypoxia

Opiate Withdrawal Complicated by Tetany and Cardiac Arrest

Hypokalemia After Resuscitation From Out-of-Hospital Ventricular Fibrillation

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