Neurohumoral responses are an integrated response to maintain blood pressure and blood volume. A neurohumoral response is initiated that includes increased sympathetic nervous system activity with direct cardiac stimulation and peripheral vasoconstriction, increased pituitary release of adrenocorticotropic hormone (ACTH) and antidiuretic hormone (ADH), increased adrenocortical release of epinephrine and cortisol, and increased renin-angiotensin-aldosterone secretion.

These compensatory mechanisms are ineffective with severe hypovolemia. During shock, catecholamines (vasoactive agents) and  immune system factors producing inflammation are released into the circulation . The result alters myocardial function, clotting mechanisms, and increase inflammatory response to name just a few.

Shock is divided into several terms : hypovolemic shock, cardiogenic shock, septic  shock, obstructive shock, anaphylatic shock.

Hypovolemic Shock

Hypovolemic shock is characterized by marked decreases in cardiac filling pressures and a consequent decrease in stroke volume. Reflex increases in peripheral vascular resistance and myocardial contractility initially maintain perfusion to the brain and heart. Treatment must focus on restoring volume, red cells, and perfusion.

Cardiogenic Shock

Cardiogenic shock is marked by peripheral vasoconstriction, pulmonary congestion, and oliguria. Cardiac rupture into the pericardial sac can produce classic signs of tamponade. Septal rupture can produce the classic murmur and thrill of a ventricular septal defect. Papillary muscle or chordae tendineae rupture can produce fulminant mitral regurgitation and pulmonary edema.

Septic Shock

The Infectious agents or their products in the blood stream cause septic shock. A useful definition of septic shock is: sepsis-induced hypotension despite adequate fluid challenge with systolic blood pressure less than 90 mm Hg or reduction of more than 40 mm from baseline along with organ perfusion abnormalities.

Obstructive Shock

Several causes of shock present with signs of elevated right-sided cardiac filling pressures but no evidence of pulmonary edema, suggesting normal left-sided filling pressures. These include right ventricular infarction (see previous description), pulmonary embolus, tamponade, and tension pneumothorax.

Anaphylactic  Shock

The hemodynamic manifestations of anaphylactic shock include decreased blood pressure, cardiac output, preload (primarily from venodilation), and occasionally systemic vascular resistance. Parenterally administered drugs, especially penicillins, cephalosporins, and iodinated contrast media, are common offenders