geriatric shock
Introduction
Introduction to senile shock Shock is a syndrome of neuro-humoral factors and acute microcirculation disorders caused by various pathogenic factors, resulting in insufficient blood perfusion in tissues and organs, cell damage, and organ dysfunction. basic knowledge The proportion of the disease: the incidence rate of the elderly over 50 years old is about 0.01%-0.02%, more common in patients with cardiovascular disease Susceptible people: the elderly Mode of infection: non-infectious Complications: disseminated intravascular coagulation
Cause
Causes of senile shock
(1) Causes of the disease
1. Hypovolemic shock due to severe water loss or massive blood loss caused by insufficient blood volume, such as bleeding, vomiting, diarrhea, extensive burns, fractures, etc.
2. Traumatic shock due to trauma caused by massive loss of blood and plasma, plus shock caused by the involvement of central nervous system trauma factors.
3. Septic shock is caused by pathogenic microorganisms including bacteria, viruses, rickettsia, protozoa, fungi and other metabolic products (endotoxin, exotoxin, etc.).
4. Cardiogenic shock caused by myocardial contractility caused by various cardiovascular diseases, cardiac ejection disorders or large blood flow disorders leading to severe pump failure.
5. Anaphylactic shock is caused by an allergen antibody reaction.
Elderly shock is more common in cardiogenic shock, septic shock and hypovolemic shock.
(two) pathogenesis
Although the causes of shock are different, all types of shock show the same pathophysiological characteristics to a certain stage, and there are many absolute or relatively effective circulating blood volume reduction; tissue perfusion is low; in vivo nerve, body fluid regulation compensation and loss Reimbursement process; metabolic disorders, microcirculatory disorders, etc., if not timely prevention and treatment, eventually leading to important organs such as heart, brain, kidney, lung and other functional failure, cell necrosis.
1. The regulation of sympathetic and parasympathetic nerves In order to compensate for the insufficient circulating blood volume, the sympathetic nerve activity in the body is rapidly enhanced, the catecholamines are released in large amounts, the venules and venules are contracted, the blood volume is increased, the myocardial contractility is enhanced, and the heart rate is increased. In order to improve left ventricular discharge, but increased sympathetic activity can increase the resistance of the systemic circulation to increase left ventricular afterload and increase myocardial oxygen consumption, which will in turn aggravate the heart's ischemia and hypoxia, affecting the heart's blood circulation function, Therefore, during the shock period, the application of exogenous vasopressors has fewer disadvantages.
Experiments have shown that the vagus nerve is also involved in the shock process, a large amount of acetylcholine accumulates in the synaptic cleft, exciting M-cholinergic receptors, inhibiting myocardial contraction, and slowing heart rate; acetylcholine makes venule contraction more pronounced, but makes skeletal muscle The opening of the arteries and veins destroys the body's ability to compensate for the insufficient circulating blood volume.
2. Influence of body fluid factors, media and metabolites on shock With the continuous development of shock research, it was found that certain humoral factors, media and metabolites participate in the pathophysiological process of shock.
(1) Shock factor: When shock occurs, the stability of the lysosomal membrane is reduced, and the lysosomal enzyme enters the cytoplasm in large quantities, causing the cells to digest themselves, decompose the tissue proteins, produce myocardial inhibitory factor (MDF), reticuloendothelial inhibitors and Intestinal factors, etc., aggravate the development of shock, the application of glucocorticoids in shock can stabilize the lysosomal membrane to reduce the production of shock factor.
(2) Prostaglandins: In shock, intracellular Ca2+ overload activates phospholipase A2, releases membrane phospholipids, converts to arachidonic acid, produces prostacyclin (PGI2), thromboxane (TXA2) and leukotriene's , LT), TXA2 has strong vasoconstriction and platelet aggregation. It is found that plasma TXB2 (the metabolite of TXA2) increases in the early stage of shock, and its increase is parallel with the severity of shock. PGI2 has vasodilator effect and platelet inhibition. Accumulation, treatment shock is better, can now be artificially synthesized, indomethacin can inhibit the formation of prostaglandins, may be beneficial to shock, but these drugs reduce renal blood perfusion, acute renal failure can occur.
(3) Renin-angiotensin: low perfusion of the kidney and sympathetic nerve stimulation increase the release of renin, transform into angiotensin I through the liver, and then transform into angiotensin II through the lungs, causing the blood vessels to contract strongly, which can aggravate the circulation. obstacle.
(4) Histamine: shock, allergies, inflammation can release histamine from tissue mast cells and blood eosinophils, and histamine continues to release a large amount of vasodilatation, increase permeability, increase plasma permeability, and aggravate shock development. This adverse effect may be related to the action of histamine on the H1 receptor, so it is advocated to use H1 blockers in shock.
(5) Endogenous opioids: It has been found that endogenous opioids (such as endorphins) have the effect of lowering blood pressure and myocardial contractility, and also confirm the increase of endorphin release during shock. The opiate receptor blocker naloxone is used for hemorrhagic and septic shock, has the effect of improving blood pressure and improving myocardial perfusion, and is now clinically used to treat various types of shock.
(6) Oxygen free radicals: Increased oxygen free radicals during shock, can damage cells with intracellular fatty acids or sulfhydryl groups, damage capillary endothelium, increase capillary permeability, participate in the onset and development of shock, therefore, people try to use freedom Base scavengers such as superoxide dismutase, reduced glutathione, vitamin E, etc. to prevent shock.
(7) Ca2+: Ca2+ flows from the extracellular to the cell when the cell or cell membrane is damaged, the ability to regulate the intracellular Ca2+ concentration is lost, a large amount of Ca2+ accumulates in the cell, causing cell damage or death, and the Ca2+ channel blocker can prevent Ca2+ is used as a vasodilator in the transmembrane of small arterial smooth muscle cells. It has also been used as an experimental treatment of shock. It has been found that verapamil can significantly improve the survival rate and reduce myocardial damage in dogs with hemorrhagic shock. And hemorrhagic necrosis of the small intestine; in the cat's hemorrhagic shock, not only can increase blood pressure, but also reduce the release of lysosomal enzymes and the production of myocardial inhibitory factor (MDF), but clinical application of calcium antagonists often occur myocardial inhibition And hypotension, so the treatment of shock remains to be further evaluated.
(8) Others: such as tumor necrosis factor (TNF), interleukin and fibronectin (FN) are also considered to play an important role in shock.
3. Microcirculatory dysfunction In the early stage of shock, the sympathetic nervous system excites the common arteries of the arterioles, venules, etc., and the arteriovenous short circuit is open, which reduces the microcirculation blood perfusion, compensates for the reduction of blood volume, and enables Maintain the needs of important organs such as the central nervous system.
Sympathetic excitation causes contraction of the anterior capillaries of the capillaries, tissue perfusion is reduced, and the tissue cells are hypoxic and the acidic products are increased, which is very unfavorable to the body. If the perfusion is still not improved, the hypoxia is continued, and the microcirculatory vessels are maintained. Will lose the sensitivity to endogenous catecholamines, combined with the effects of mediators and metabolites such as histamine, increase the volume of capillary bed, more fluid stagnant in capillaries, slow blood flow, increased hydrostatic pressure; plus capillary Endothelial injury, increased permeability of the blood vessel wall, tissue edema, effective circulation of blood loss, further reduction of blood flow to the heart, blood pressure decreased significantly, and then entered the decompensation period of shock.
The blood flow stagnates in the microcirculation, the acidic products increase, the venules also expand, the vascular endothelial damage promotes platelet aggregation, forms diffuse capillary intravascular coagulation (DIC), causes tissue necrosis, and after DIC, the fibrinolysis system in the body acts, a large number The blood coagulation factor is consumed, and the blood is in a hypocoagulable state, which tends to be easy to hemorrhage. For example, only a small amount of cell necrosis can be repaired in the organ. If a large amount of necrosis occurs, the organ is depleted and the body is dead. Therefore, in the shock treatment, frequent attention should be paid. The state of the microcirculation and its response to treatment to prevent the occurrence of DIC.
4. Metabolic changes
(1) Hyperventilation: During shock, the body is compensated for metabolic acidosis, often with spontaneous hyperventilation, breathing deep and fast, resulting in a decrease in PaCO2, ie, respiratory alkalosis, which is particularly prominent in the early stages of septic shock.
(2) Reduced oxygen uptake and utilization capacity: As a result, the oxygen consumption is reduced. Due to the disorder of oxygen transmission in the lung, the tissue blood perfusion is less, the erythrocyte oxygenation at the cellular level is reduced, the peripheral arteriole-venous short circuit is open, and the cells take up oxygen and oxygen. The ability to decline, so the performance of the arteriovenous oxygen partial pressure difference is significantly reduced.
(3) Energy metabolism disorder: tissue ischemia and hypoxia during shock, decreased ATP synthesis, increased consumption, cell membrane dysfunction, Na+, H2O enter cells, and K+ escapes cells, leading to cell edema, affecting the function of various organs, intracellular Ca2+ overload further aggravates the energy metabolism disorder of cells.
(4) abnormal glucose metabolism: early in shock due to sympathetic stimulation, glucagon release, and inhibition of insulin release gluconeogenesis and increased glycogen decomposition, etc., so that blood sugar is elevated, low blood sugar can occur in the late stage, the main reason is Exhaustion of glycogen, liver failure.
(5) Metabolic acidosis: poor perfusion of tissue during shock, insufficient oxygen supply and anaerobic metabolism, producing a large amount of lactic acid; late hypoglycemia stimulates gluconeogenesis, the body uses decomposition of fats and amino acids to make fatty acids and certain Increased acid amino acids, combined with the liver's ability to use lactic acid and kidney to remove acidic substances, resulting in metabolic acidosis, acidosis brings a series of evil consequences to the body: such as aggravating red blood cell aggregation, triggering DIC; weakening myocardial contractility; inhibiting the surrounding The reaction of blood vessels and myocardium to catecholamines; the expansion of microcirculation capacity; the extracellular K+ shift, causing hyperkalemia.
5. Important organ dysfunction
(1) Heart: effective circulating blood volume during shock, myocardial ischemia and hypoxia, open Ca2+ channel of myocardial cells and coronary smooth muscle cell membrane, Ca2+ cell internal flow, causing coronary artery spasm and myocardial tonic contraction, increase myocardial oxygen consumption, myocardial Hypoxia aggravation, contractility is weakened, MDF release inhibits myocardial contractility, and toxic myocarditis caused by bacterial toxins is more prone to cardiac insufficiency. The elderly are based on the original chronic coronary heart disease, heart enlargement, cardiovascular The system has low compensatory ability and can easily cause acute heart failure.
(2) Lung: In the shock, due to the release of various vasoactive substances and intracellular Ca2+ accumulation, the pulmonary blood vessels continue to paralyze, increasing the right ventricular afterload, making the blood flow perfusion less abnormal, the arterial oxygen partial pressure is reduced, due to The action of bioactive substances damages the vascular endothelium, promotes platelet aggregation, thrombosis in the pulmonary blood vessels, and further decreases PaO2. In addition, in the late stage of shock, type II cells of the alveolar epithelium are damaged, affecting the formation of alveolar surfactants, resulting in large alveolar Collapse, the formation of ARDS (adult respiratory distress syndrome) pathological changes, increased pulmonary capillary pressure or increased permeability can cause pulmonary interstitial or alveolar pulmonary edema, is another cause of PaO2 decline, the elderly often have Chronic bronchitis, emphysema ventilation function and gas exchange function decline, often increased PaCO2, acute respiratory failure is more likely to occur in shock.
(3) Brain: The cerebral vasomotor range is small, the self-regulation function is poor, the cerebral arteriosclerosis is common in the elderly, the blood pressure is significantly decreased during shock, the cerebral perfusion is insufficient, the brain tissue oxygen consumption is increased, and cerebral edema and brain cell damage are prone to occur. Therefore, the elderly often show signs of central nervous system function inhibition in the early stage of shock.
(4) Kidney: The renal arterioles contract during shock, renal perfusion is reduced, early oliguria or no urine, and acute renal failure can occur in renal tubular thrombosis caused by late renal microthrombus.
(5) Liver: Hepatic ischemic necrosis, impaired function can increase serum GPT and GOT, manifested as metabolic dysfunction, phagocytic function, and detoxification.
(6) Gastrointestinal tract: Stress ulcers, erosion, bleeding, bacteria and toxins can easily enter the blood circulation through the intestinal mucosa, and the "intestinal factor" can cause irreversible shock.
In the elderly, due to the existence of cardiac dysfunction, decreased circulating blood volume, increased capillary permeability, progression of organ atherosclerosis, and other conditions of shock onset, coupled with the regulation of the nervous and humoral factors from imbalance to balance in the elderly The ability is limited, so there are many complications and high mortality rate in shock. There are often heart and lung, heart and kidney, brain and lung, lung and kidney failure and acid-base water and electrolyte disorders. The key problem is early diagnosis and early treatment.
Prevention
Elderly shock prevention
Older shock patients with low organ function, decreased immune function, combined with a variety of chronic diseases, long-term use of various drugs, so the treatment is more difficult, often encounter a variety of difficult contradictions in the clinic, such as hemorrhagic The contradiction between hemostasis and possible cerebral vascular occlusive disease during shock, correcting the contradiction between hypovolemia and heart failure, applying antibiotics to control the contradiction between infection and dysbacteriosis, broad-spectrum antibiotics, dehydration drugs and liver and kidney dysfunction Contradictions, the use of hormones and gastrointestinal stress ulcers, bleeding and infection spread, and so on, these problems, in the specific treatment should be based on the patient's specific circumstances, comprehensive analysis and comparison, properly handled, to prevent this loss, Shock pre-existing symptoms should be detected early, early treatment, in addition, rapid replenishment of blood volume, correction of electrolyte and acid-base imbalance, early and rapid, adequate, short-term application of glucocorticoids and active treatment of important comorbidities, rescue shock, improvement The prognosis is also very important.
Complication
Geriatric shock complications Complications, disseminated intravascular coagulation
Severe shock complications are common DIC-type vital organ failure and acid-base hydroelectric mediator disorder.
Symptom
Symptoms of senile shock common symptoms shock unconsciousness coma skin wet and cold irritability disorder consciousness expression indifferent skin pale red blood cell pressure high pulse rate increase
Mental state
The patient's mental state often reflects the brain tissue perfusion status. The early shock patients show irritability, reluctance to answer questions or multilingualism, and later turn into apathy and unresponsiveness, indicating that shock has entered decompensation, and when it is serious, it is unconscious. Even deep coma, the elderly due to cerebral arteriosclerosis, brain tissue tolerance to ischemia and hypoxia, early can appear disturbance of consciousness, and sometimes become the first symptoms of senile shock.
2. Skin changes
The color of the skin, the temperature often reflects the blood perfusion of the body surface, the skin and anus temperature difference of 1 ~ 3 ° C shows severe shock, skin small blood vessels contraction caused pale skin, cold, skin pressure pale time extended, pressure and then refill Slow time (> 2s), sympathetic excitation makes the sweat glands secrete hyperthyroidism, so the skin is wet and cold.
3. Pulse speed
It often occurs before the blood pressure drops. It is the performance of the body's compensation response to the reduction of circulation. The pulse rate increases by 100/min or more. Even if the blood pressure is not low, the shock should be watched and the pulse becomes weak. Peripheral arterioles contracted, peripheral vascular resistance increased cardiac output decreased, elderly patients often have degenerative lesions and dysfunction of sinus node tissue, sometimes even if shock has occurred, but its pulse rate does not increase.
4. Blood pressure drops
It is an important indicator for the diagnosis of shock. However, in the early stage of shock, due to the compensatory mechanism of the body, the sympathetic excitement causes the surrounding small arteries to contract, so that the systolic blood pressure is maintained within the normal range, the peripheral vascular resistance increases, and the diastolic blood pressure increases. The pulse pressure becomes small. When the pulse pressure is 2.67 kPa (20 mmHg), shock should be considered.
Systolic blood pressure reduced to 10.7kPa (80mmHg) or below is one of the diagnostic conditions of shock. Patients with elderly or pre-existing hypertension, although their blood pressure is within the normal range, cannot be denied the existence of shock. According to the change of blood pressure, if the systolic blood pressure decreases by 30%, combined with other performances (such as pulse speed, skin wetness, etc.), the presence of shock should still be judged.
5. Changes in urine volume
Urine volume is an indicator of renal blood flow. Early mild shock, normal urine volume, blood pressure as low as 10.7/6.6kPa (80/50mmHg), renal blood flow decreased, vascular resistance increased, urine output began to decrease, blood pressure to 6.6 At /0kPa (50/0mmHg), renal blood flow is almost stopped, urine volume is very small, and even no urine, late shock can also cause anuria due to acute renal insufficiency. Increased urine output in elderly shock patients sometimes does not mean kidney Good work, on the contrary, it may be a manifestation of a decline in concentration.
6. Respiratory changes
Early shock patients often have hyperventilation, which may be the body's performance on ischemic hypoxia compensation. In septic shock, bacterial endotoxin directly affects the respiratory center is another reason, when blood gas analysis results often show breathing Alkalosis, with the development of shock, metabolic acidosis occurs in the body, the respiratory performance is deep and fast, the elderly often have emphysema and pulmonary insufficiency, which can make the breathing shallow, respiratory depression, and may have respiratory Acidosis.
Examine
Elderly shock examination
The following tests are important for diagnosis and treatment.
1. Hematology examination blood routine, hematocrit, bleeding tendency or shock for more than 12h should be used for platelet count, prothrombin time and fibrinogen concentration determination.
2. Bacteriological examination of patients with septic shock or other causes of shock co-infection should be bacteriologically checked according to the condition.
3. Biochemical examination
(1) Determination of lactate concentration: not only reflects the degree of hypoxia in microcirculatory cells, but also indicates the severity of acidemia. The normal value is 0.5-1.5mmol/L, but some septic shock microcirculation should be noted. When there is focal tissue necrosis in thrombosis, the concentration of lactic acid in the blood is low, which is easy to give people an illusion.
(2) Electrolytes such as blood K+, Na+, Cl-, Mg2+, etc. may be disordered.
(3) blood transaminase, lactate dehydrogenase, creatine phosphokinase, urea nitrogen, creatinine and the like.
(4) blood gas analysis: shock itself and concurrent or combined cardiopulmonary dysfunction often have hypoxemia and respiratory and metabolic double or triple acid-base imbalance, blood gas analysis for accurate diagnosis, guiding treatment and prognosis are helpful .
4. ECG and ECG monitoring.
5. Chest X-ray examination.
The electrocardiogram of patients with cardiac dysfunction can be abnormal, and the X-ray of elderly patients with pneumonia can be abnormal.
Diagnosis
Diagnosis of senile shock
diagnosis
According to the medical history, clinical symptoms and signs, combined with changes in blood pressure, diagnosis is not difficult.
Differential diagnosis
Mainly should be differentiated from chronic hypotension. Some elderly people may have lower blood pressure due to physical fitness, body position, endocrine dysfunction, chronic consumption or severe aortic valve or mitral stenosis, but the systolic blood pressure is generally not lower than 10.7kPa. (80mmHg), more than no cold sweat, fine pulse, reduced urine output and other clinical manifestations of shock.
