Some indications for shock treatment

2021-04-30 08:24 PM

Because the main detrimental effect of most types of shock is too little oxygen delivery to the tissues, giving the patient oxygen may be beneficial in some cases.

Treatment is with a bow position

When the pressure drops too low in most types of shock, especially haemorrhagic and neurological shock, placing the patient with the head at least 25cm lower than the leg will help promote venous return, thus also. increases cardiac output. This low head position is a necessary first step in treating many types of shock.

Oxygen therapy

Because the main detrimental effect of most types of shock is too little oxygen delivery to the tissues, giving the patient oxygen may be beneficial in some cases. However, this intervention is often less beneficial than one might expect, because the problem in most types of shock is not that the lungs are getting enough oxygen to the blood, but the transport of the blood. sufficient after oxygen is supplied.

Glucocorticoid treatment

Glucocorticoids - adrenocortical hormones that control glucose metabolism - are often used in patients with severe shock for a number of reasons: (1) experiments have shown empirically that glucocorticoids often increase heart strength during the period. the end of shock; (2) glucocorticoids stabilize lysosomes in the tissue cell and thus prevent the release of lysosome enzymes into the cytoplasm of the cell, thereby preventing quality deterioration from this source; and (3) glucocorticoids may aid in the glucose metabolism of severely damaged cells.

 

MOST VIEW

Pathophysiology of cardiogenic shock

Urine formation: Reabsorbed glomerular filtration

Air in and out of the lungs: pressure causes the movement of air

Mechanism of urine concentration: osmotic pressure changes in different segments of the renal tubule

Absorption and excretion of potassium through the kidneys

Prothrombin activation: initiates blood clotting

Pulmonary capillary dynamics: capillary fluid exchange and pulmonary interstitial fluid dynamics

Graphical analysis of high-volume heart failure

Calculate the glomerular filtration rate (GFR): the forces that cause the filtration process

Estimated renal plasma flow: PAH clearance

Nephron: The functional unit of the kidney

Reduced sodium chloride, dilates arterioles, increases Renin release.

Ammonia buffering system: excretes excess H + and creates new HCO3

Red blood cells: differentiation and synthesis

Concentrated urine formation: urea contributes to increased osmotic pressure in the renal medullary

Extracellular fluid distribution between interstitial space and blood vessels

The proximal tubule reabsorption: active and passive reabsorption

Origin of lymphocytes: the body's resistance to infection

The endocrine regulates tubular reabsorption

Acidosis causes a decrease in HCO3- / H + in renal tubular fluid: compensation mechanism of the kidney

Sodium channel blockers: decrease the reabsorption of sodium in the manifold

Physiological anatomy of the kidneys and urinary system

Self-regulation of glomerular filtration rate and renal blood flow

Pathophysiology of fever

The kidneys excrete sodium and fluid: feedback regulates body fluids and arterial pressure