Norepinephrine causes predominately vasoconstriction with a mild increase in heart rate, whereas epinephrine predominately causes an increase in heart rate with a small effect on the vascular tone; the combined effect results in an increase in blood pressure. The renin–angiotensin axis is activated, and arginine vasopressin (anti-diuretic hormone) is released to conserve fluid by reducing its excretion via the renal system. These hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production. However the effects of the renin–angiotensin axis take time and are of little importance to the immediate homeostatic mediation of shock. Progressive/decompensated
The Progressive stage (stage 3) results if the underlying cause of the shock is not successfully treated. During this stage, compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells in the body, sodium ions build up within the intracellular space while potassium ions leak out. Due to lack of oxygen, cellular respiration diminishes and anaerobic metabolism predominates. As anaerobic metabolism continues, the arteriolar smooth muscle and precapillary sphincters relax such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.
Combined hyperlipidemia (or -aemia) is a commonly occurring form of hypercholesterolemia (elevated cholesterol levels) characterised by increased LDL and triglyceride concentrations, often accompanied by decreased HDL. : 534  On lipoprotein electrophoresis (a test now rarely performed) it shows as a  hyperlipoproteinemia type IIB. It is the most commonly inherited lipid disorder, occurring in around one in 200 persons. In fact, almost one in five individuals who develop coronary heart disease before the age of 60 have this disorder. The elevated triglyceride levels (>5 mmol/L) are generally due to an increase in very low density lipoprotein (VLDL), a class of lipoproteins prone to cause atherosclerosis. Cause
Hereditary factors are the most common cause. A diet high in saturated fat and cholesterol increases blood cholesterol and triglyceride levels. Other disorders, such as diabetes mellitus, kidney disease, and hypothyroidism, may promote hypertriglyceridemia. Certain drugs, such as estrogen, corticosteroids, retinoids, protease inhibitors, thiazide diuretics, and beta-blockers, may cause hypertriglyceridemia. Obesity increases the risk of hyperlipidemia. Chronic, excessive alcohol use increases the risk of hypertriglyceridemia. Smoking and not exercising may lead to hyperlipidemia. Steroid uses, alcoholism, hypothyroidism, oral contraceptives, chronic kidney failure, hypopituitarism, and nephritic syndrome are other contributors to hyperlipidemia. Diagnosis
Types
The two forms of this lipid disorder are:

Familial combined hyperlipidemia (FCH) is the familial occurrence of this disorder, probably caused by decreased LDL receptor and increased ApoB. Acquired combined hyperlipidemia is extremely common in patients who have other diseases from the metabolic syndrome ("syndrome X", incorporating diabetes mellitus type II, hypertension, central obesity and CH).