on 10-Sep-2016 (Sat)

In addition, a variety of protein and nonprotein mediators are produced at the site of injury as part of the inflammatory response, and they act as afferent impulses to induce a host response. These mediators include histamine, cytokines, eico- sanoids, and endothelins, among others

Hemorrhage results in diminished venous return to the heart and decreased cardiac output. This is compensated by increased cardiac heart rate and contractility, as well as venous and arterial vasoconstriction. Stimulation of sympathetic fibers innervating the heart leads to activation of β 1 -adrenergic receptors that increase heart rate and contractility in this attempt to increase cardiac output. Increased myocardial O 2 consumption occurs as a result of the increased workload; thus, myocardial O 2 supply must be maintained or myocardial dysfunction will develop. The cardiovascular response in hemorrhage/hypovolemia differs from the responses elicited with the other etiologies of shock.

Direct sympathetic stimulation of the peripheral circula- tion via the activation of α 1 -adrenergic receptors on arterioles induces vasoconstriction and causes a compensatory increase in systemic vascular resistance and blood pressure. The arte- rial vasoconstriction is not uniform; marked redistribution of blood flow results. Selective perfusion to tissues occurs due to regional variations in arteriolar resistance, with blood shunted away from less essential organ beds such as the intestine, kid- ney, and skin. In contrast, the brain and heart have autoregu- latory mechanisms that attempt to preserve their blood flow despite a global decrease in cardiac output. Direct sympathetic stimulation also induces constriction of venous vessels, decreas- ing the capacitance of the circulatory system and accelerating blood return to the central circulation.

Catecholamine effects on peripheral tissues include stimulation of hepatic glycogenolysis and gluconeogenesis to increase circulating glucose availability to peripheral tissues, an increase in skeletal muscle glycogenolysis, suppression of insulin release, and increased glucagon release.

Increased sympathetic output induces catecholamine release from the adrenal medulla. Catecholamine levels peak within 24 to 48 hours of injury and then return to baseline. Persis- tent elevation of catecholamine levels beyond this time suggests ongoing noxious afferent stimuli. The majority of the circulating epinephrine is produced by the adrenal medulla, while norepi- nephrine is derived from synapses of the sympathetic nervous system.

The stress response includes activation of the ANS as discussed earlier in the Afferent Signals section, as well as activation of the hypothalamic-pituitary-adrenal axis.

Shock stimulates the hypothalamus to release corticotropin- releasing hormone, which results in the release of adrenocorti- cotropic hormone (ACTH) by the pituitary. ACTH subsequently stimulates the adrenal cortex to release cortisol. Cortisol acts synergistically with epinephrine and glucagon to induce a catabolic state. Cortisol stimulates gluconeogenesis and insu- lin resistance, resulting in hyperglycemia as well as muscle cell protein breakdown and lipolysis to provide substrates for hepatic gluconeogenesis. Cortisol causes retention of sodium and water by the nephrons of the kidney. In the setting of severe hypovolemia, ACTH secretion occurs independently of cortisol negative feedback inhibition.

The renin-angiotensin system is activated in shock. Decreased renal artery perfusion, β-adrenergic stimulation, and increased renal tubular sodium concentration cause the release of renin from the juxtaglomerular cells. Renin cata- lyzes the conversion of angiotensinogen (produced by the liver) to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) produced in the lung. While angiotensin I has no significant functional activ- ity, angiotensin II is a potent vasoconstrictor of both splanchnic and peripheral vascular beds, and also stimulates the secretion of aldosterone, ACTH, and antidiuretic hormone (ADH). Aldo- sterone, a mineralocorticoid, acts on the nephron to promote reabsorption of sodium and, as a consequence, water. Potassium and hydrogen ions are lost in the urine in exchange for sodium.

Dyspnea is a term used to characterize a subjective experience of breathing discomfort that is comprised of qualitatively distinct sensations that vary in intensity. The experience derives from interactions among multiple physiological, psychological, social and environmental factors, and may induce secondary physiological and behavioral responses.

Common
• Status asthmaticus
• Acute exacerbation of COPD
• Pneumonia (especially in immunocompromised or immunodeficiency patients such as HIV disease and alcoholics)
• Acute laryngotracheobronchitis (Croup)
• Acute LVF (due to MI, pericarditis, cardiac tamponade, fulminant myocarditis)
• Arrhythmias (VT, AF, VF)
• Psychogenic (hyperventilation syndrome).

Occasional
• Spontaneous or tension pneumothorax
• Massive pleural effusion (tubercular, malignant)
• Massive lobar collapse (traumatic, post-
operative)
• Massive pulmonary embolism(PE)
• Metabolic acidosis (DKA, uremia, salicylate
overdose)
• Anaphylaxis (angioneurotic edema)
• Severe acute respiratory syndrome (SARS).
Rare
• Foreign body aspiration
• Drug induced (NSAIDs, beta blockers)
• Acute respiratory distress syndrome (ARDS)
• Neurologic (CVA, Guillain-Barré syndrome,
Bulbar polio)
• Pacemaker syndrome.

RBI act does not directly deal with the regulation of the banking system except for Section 42 and Section 18

last major amendment to the Act by the RBI(Amendment) Act, 1997. Recently a provision was inserted by the IT Act, 2000 for enabling the Reserve Bank to make regulations for regulating payment systems of banks and financial institutions

Reserve Bank is a body corporate having perpetual succession and common seal and shall sue and can be sued by others

The Government holds the entire capital of the Reserve Bank and appoints the Governor and the members of the Central Board and has power to remove them