Congestive heart failure (CHF) is a clinical syndrome that features a failing heart together with signs and symptoms arising from renal retention of salt and water, mediated by attendant neurohormonal activation, and which prominently includes the renin-angiotensin-aldosterone system. More than this cardiorenal perspective, CHF is accompanied by a systemic illness whose features include an altered redox state in diverse tissues and blood, an immunostimulatory state with proinflammatory cytokines and activated lymphocytes and monocytes, and a wasting of tissues that includes muscle and bone. Based on experimental studies of aldosteronism and clinical findings in patients with CHF, there is an emerging body of evidence that secondary hyperparathyroidism is a covariant of CHF. The aldosteronism of CHF predisposes patients to secondary hyperparathyroidism because of a chronic increase in Ca 2+ and Mg 2+ losses in urine and feces, with a fall in their serum ionized levels and consequent secretion of parathyroid hormone. Secondary hyperparathyroidism accounts for bone resorption and contributes to a fall in bone strength that can lead to nontraumatic fractures. The long-term use of a loop diuretic with its attendant urinary wasting of Ca 2+ and Mg 2+ further predisposes patients to secondary hyperparathyroidism and attendant bone loss. Aberrations in minerals and micronutrient homeostasis that includes Ca 2+ , Mg 2+ , vitamin D, zinc and selenium appear to be an integral component of pathophysiologic expressions of CHF that contributes to its systemic and progressive nature. This broader perspective of CHF, which focuses on the importance of secondary hyperparathyroidism and minerals and micronutrients, raises the prospect that dietary supplements could prove remedial in combination with the current standard of care.

No abstract

No abstract

No abstract

A woman in her 50s with a history of hypertension, hyperlipidemia, diabetes, neuropathy, smoking, asthma, and previous stroke presented with altered mental status and respiratory distress necessitating intubation in the field. An electrocardiogram (ECG) was recorded on presentation (Figure 1). On arrival, she was found to have 1 episode of nonsustained ventricular tachycardia but otherwise remained in normal sinus rhythm. Home medications included lisinopril, amitriptyline hydrochloride, and insulin. On physical examination, she was nonresponsive, with blood pressure of 113/70 mm Hg and pulse of 59 beats per minute with 100% oxygen saturation with mechanical ventilation. Examination including the cardiovascular system had normal results.Question: What does this ECG suggest and what would you do next? Interpretation