A case of severe hypokalaemia with stupor, skeletal muscle and heart muscle damage is reported. An initial infusion of glucose-insulin and potassium (GIK) produced a temporary clinical improvement with reduction of creatine kinase (CKMB) and elevation of serum K+. On the 4th day of treatment, neuromuscular and cardiovascular deterioration occurred accompanied by a further rise of CKMB. This deterioration was coincident with a serum phosphate of 0.26 mmol/l. The impaired left ventricular (LV) function was measured using echocardiography and detecting the ejection fraction (EF). GIK was stopped and a potassium phosphate infusion commenced. As the phosphate and potassium deficiencies were corrected, the neuromuscular and cardiac abnormalities resolved, CKMB fell to normal and LVEF rose from 40% to 72%. We suggest that additional cardiac damage due to hypophosphataemia may have occurred in this patient, who already had cardiac impairment as a result of profound hypokalaemia. Possible mechanisms are discussed.
Myocardial damage due to hypokalaemia and hypophosphataemia / Frustaci, Andrea; Pennestri, ; C., Scoppetta. - In: POSTGRADUATE MEDICAL JOURNAL. - ISSN 0032-5473. - STAMPA. - 60:708(1984), pp. 679-681.
Myocardial damage due to hypokalaemia and hypophosphataemia.
FRUSTACI, ANDREA;
1984
Abstract
A case of severe hypokalaemia with stupor, skeletal muscle and heart muscle damage is reported. An initial infusion of glucose-insulin and potassium (GIK) produced a temporary clinical improvement with reduction of creatine kinase (CKMB) and elevation of serum K+. On the 4th day of treatment, neuromuscular and cardiovascular deterioration occurred accompanied by a further rise of CKMB. This deterioration was coincident with a serum phosphate of 0.26 mmol/l. The impaired left ventricular (LV) function was measured using echocardiography and detecting the ejection fraction (EF). GIK was stopped and a potassium phosphate infusion commenced. As the phosphate and potassium deficiencies were corrected, the neuromuscular and cardiac abnormalities resolved, CKMB fell to normal and LVEF rose from 40% to 72%. We suggest that additional cardiac damage due to hypophosphataemia may have occurred in this patient, who already had cardiac impairment as a result of profound hypokalaemia. Possible mechanisms are discussed.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.