The natriuretic system consists of the atrial natriuretic peptide (ANP) and four other similar peptides including the wrongly named brain natriuretic peptide (BNP). Chemically they are small peptide hormones predominantly secreted by the cardiac myocytes in response to stretching forces. The peptide hormones have multiple renal, hemodynamic, and antiproliferative effects through three different kinds of natriuretic receptors. Clinical interest in these peptide hormones was initially stimulated by the use of these peptides as markers to differentiate cardiac versus noncardiac causes of breathlessness. Subsequently work has been done on using these peptides to prognosticate patients with acute and chronic heart failure and those with acute myocardial infraction. Synthetic forms of both atrial- and brain-natriuretic peptides have been studied and approved for use in acute heart failure with mixed results. This review focuses on the biochemistry and physiology of this fascinating hormone system and the clinical application of these hormones.
Thyroid disorders and primary hyperparathyroidism have been known to be associated with increases in blood pressure. The hypertension related to hypothyroidism is a result of increased peripheral resistance, changes in renal hemodynamics, hormonal changes and obesity. Treatment of hypothyroidism with levo-thyroxine replacement causes a decrease in blood pressure and an overall decline in cardiovascular risk. High blood pressure has also been noted in patients with subclinical hypothyroidism. Hyperthyroidism, on the other hand, is associated with systolic hypertension resulting from an expansion of the circulating blood volume and increase in stroke volume. Increased serum calcium levels associated with a primary increase in parathyroid hormone levels have been also associated with high blood pressure recordings. The mechanism for this is not clear but the theories include an increase in the activity of the renin–angiotensin–aldosterone system and vasoconstriction. Treatment of primary hyperparathyroidism by surgery results in a decline in blood pressure and a decrease in the plasma renin activity. Finally, this review also looks at more recent evidence linking hypovitaminosis D with cardiovascular risk factors, particularly hypertension, and the postulated mechanisms linking the two.
Pulmonary arterial hypertension (PAH) is a heterogeneous, hemodynamic, and pathophysiological state which is commonly found throughout the world, but the disease burden is greater in India and in other developing countries. It is a disease characterized by vascular obstruction and vasoconstriction leading to progressive increase in pulmonary vascular resistance and right ventricular failure. PAH is a progressive disorder carrying a poor prognosis; however, dramatic progress has occurred in our knowledge of its pathogenesis and consequently, its treatment over the last two decades. In this article, we attempt to provide an overview of the etiology, pathophysiology, and current therapeutic modalities in the treatment of PAH. Patients suspected to have PAH should be submitted to a battery of investigations which help in establishing the diagnosis, identifying the etiology, guiding in treatment and informing the prognosis. All patients should be considered for standard therapy with oxygen, anticoagulation, and diuretics for right heart failure. Oral calcium channel blockers should be used in patients with a favorable response to acute vasodilator challenge. Disease targeted therapies include prostacyclines, endothelin receptor blockers, and phosphodiesterase-5 inhibitors. A brief mention of new and potential therapeutic strategies is also included.
BACKGROUND Residual neuromuscular blockade (RNMB) after the use of neuromuscular blocking agents (NMBAs) increases postoperative morbidity and mortality. The incidence of RNMB associated with the unmonitored use of NMBAs in our population has not been ascertained. We undertook this study to determine the occurrence of RNMB, defined as train of four (TOF) ratio less than one and to identify the risk factors associated with it. METHODS This was a prospective observational study consisting of patients who received NMBAs and underwent elective surgeries under general anaesthesia. They were monitored with TOF-Watch® SX for RNMB in the post anaesthesia care unit (PACU). RNMB was recorded and confirmed. Demographic and clinical data related to anaesthesia care, surgical procedure and post anaesthesia adverse effects were analysed. RESULTS A total of 195 patients who underwent elective surgeries under general anaesthesia were included in the study. The incidence of residual neuromuscular blockade was 31% with a TOF ratio of <0.9 and 51% with a TOF ratio of <1. RNMB occurred more frequently among the female gender, body mass index (BMI) >25 and hypothermic patients. Residual neuromuscular blockade was shown to be associated with increased use of airway adjuncts in the PACU and commonly used clinical tests were not sensitive to pick up RNMB. CONCLUSIONS The significant incidence of RNMB in the PACU emphasizes the need for anaesthesiologists to be mindful of this potentially serious event. Use of neuromuscular monitor can aid in the detection of RNMB and should be considered especially for the high-risk group. Detection will allow appropriate interventions before serious adverse events occur.
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