K+ and Mg2+ Dyshomeostasis in Acute Hyperadrenergic Stressor States.

Acute stressor states are linked to neurohormonal activation that includes the adrenergic nervous system. Elevations in circulating epinephrine and norepinephrine unmask an interdependency that exists between K+ and Mg2+ based on their regulation of a large number of Mg2+-dependent Na+-K+-ATPase pumps present in skeletal muscle. The hyperadrenergic state accounts for a sudden translocation of cations into muscle with the rapid appearance of hypokalemia and hypomagnesemia. The resultant hypokalemia and hypomagnesemia will cause a delay in myocardial repolarization and electrocardiographic QTc prolongation raising the propensity for supraventricular and ventricular arrhythmias. In this review, we focus on the interdependency between K+ and Mg2+, which is clinically relevant to acute hyperadrenergic stressor states found in patients admitted to intensive care units.

Pleural effusion leading to right atrial collapse.

Rapid accumulation of pericardial fluid can lead to tamponade, resulting in cardiac chambers' collapse, which can lead to hemodynamic and clinical instability, potentially needing emergent pericardiocentesis. Pleural effusion should also be considered as a potential, if rare, cause of cardiac chambers' collapse and possibly cardiac tamponade. This phenomenon has clinical implications because hemodynamically unstable patients with moderate to large pleural effusion may actually need thoracentesis instead of massive volume resuscitation, inotropic agents, or pericardiocentesis.

Disturbances in calcium metabolism and cardiomyocyte necrosis: the role of calcitropic hormones.

A synchronized dyshomeostasis of extra- and intracellular Ca(2+), expressed as plasma ionized hypocalcemia and excessive intracellular Ca(2+) accumulation, respectively, represents a common pathophysiologic scenario that accompanies several diverse disorders. These include low-renin and salt-sensitive hypertension, primary aldosteronism and hyperparathyroidism, congestive heart failure, acute and chronic hyperadrenergic stressor states, high dietary Na(+), and low dietary Ca(2+) with hypovitaminosis D. Homeostatic responses are invoked to restore normal extracellular [Ca(2+)](o), including increased plasma levels of parathyroid hormone and 1,25(OH)(2)D(3). However, in cardiomyocytes these calcitropic hormones concurrently promote cytosolic free [Ca(2+)](i) and mitochondrial [Ca(2+)](m) overloading. The latter sets into motion organellar-based oxidative stress, in which the rate of reactive oxygen species generation overwhelms their detoxification by endogenous antioxidant defenses, including those related to intrinsically coupled increments in intracellular Zn(2+). In turn, the opening potential of the mitochondrial permeability transition pore increases, allowing for osmotic swelling and ensuing organellar degeneration. Collectively, these pathophysiologic events represent the major components to a mitochondriocentric signal-transducer-effector pathway to cardiomyocyte necrosis. From necrotic cells, there follows a spillage of intracellular contents, including troponins, and a subsequent wound healing response with reparative fibrosis or scarring. Taken together, the loss of terminally differentiated cardiomyocytes from this postmitotic organ and the ensuing replacement fibrosis each contribute to the adverse structural remodeling of myocardium and progressive nature of heart failure. In conclusion, hormone-induced ionized hypocalcemia and intracellular Ca(2+) overloading comprise a pathophysiologic cascade common to diverse disorders and that initiates a mitochondriocentric pathway to nonischemic cardiomyocyte necrosis.

Streptococcus pneumoniae-associated pneumonia, meningitis, and endocarditis: a case of Austrian syndrome.

Streptococcus pneumoniae is the leading cause of hospitalization in cases of community-acquired pneumonia and meningitis in adults. It is also an uncommon cause of endocarditis in the antibiotic era. The occurrence of these three entities in one individual is rare, forming a triad termed Austrian syndrome.

A dyshomeostasis of electrolytes and trace elements in acute stressor states: impact on the heart.

Acute stressor states are associated with a homeostatic activation of the hypothalamic-pituitary-adrenal axis. A hyperadrenergic state follows and leads to a dyshomeostasis of several intra- and extracellular cations, including K, Mg, and Ca. Prolongation of myocardial repolarization and corrected QT interval (QTc) of the ECG are useful biomarkers of hypokalemia and/or hypomagnesemia and should be monitored to address the adequacy of cation replacement. A dyshomeostasis of several trace elements, including Zn and Se, are also found in critically-ill patients to compromise metalloenzyme-based antioxidant defenses. Collectively, dyshomeostasis of these electrolytes and trace elements have deleterious consequences on the myocardium: atrial and ventricular arrhythmias; induction of oxidative stress with reduced antioxidant defenses; and adverse myocardial remodeling, including cardiomyocytes lost to necrosis and replaced by fibrous tissue. To minimize such consequences during hyperadrenergic states, systematic surveillance of electrolytes and trace elements, together with QTc, are warranted. Plasma K and Mg should be maintained at > or =4.0 mEq/L and > or =2.0 mg/dL, respectively (the 4 and 2 rule).