-, cardiac arrest
refers to the sudden onset of the state of the raw cardiac effective blood output of zero, most often seen in heart disease, but also in other systemic diseases such as asphyxia asthma, acute cerebrovascular disease, poisoning, electrolyte disorders, positive trauma and other patients.
Diagnostic basis:
Sudden onset of loss of consciousness.
Loss of aortic pulse.
Respiratory arrest.
Electrocardiogram showing VF, VT, or severe bradycardia or an isoelectric line (cardiac arrest).
Principles of treatment:
I. Ventricular fibrillation
1. If ventricular fibrillation persists, three consecutive electric shocks are delivered: energy increments of 200, 200-300, and 360J, during which the electrode plates do not leave the skin. If the electrocardiogram shows tissue electrical activity or a straight line after the shock, there is no need for another shock.
2 . Open the airway or tracheal intubation.
3. Artificial respiration with a portable respirator.
4. Standard chest compressions.
5. Open venous access, intravenous epinephrine lmg/dose, l every 3-5 minutes.
6. Continuous electrocardiographic monitoring
7. Amiodarone 150-300mg, lidocaine 1.0-1.5mg/kg, magnesium sulphate 1-2g may be applied as appropriate. electroconvulsive shock, administration of medication, and compression are carried out cyclically.
II. Pulseless electrical activity (PEA) and cardiac arrest
1. Open the airway or tracheal intubation.
2. Artificial respiration with portable respirator.
3. Standard chest compressions.
4. Open intravenous access, intravenous epinephrine 1mg/dose or intravenous atropine lmg.
5. Continuous cardiac monitoring.
Note:
After each administration, inject 20m1 of 0.9% saline intravenously, elevate the injected limb by 20° to 30° for several seconds to accelerate the drug's arrival in the central circulation, and apply uninterrupted chest cardiac compression. Drugs such as epinephrine and atropine can be given intratracheally at double the dose, diluted with 10 ml of saline and injected into the trachea, followed by immediate forceful extrusion of the air sac 3 to 5 times.
In the absence of an electric defibrillator, immediately tap in the precordial area to reset the rhythm and immediately begin cardiac compression.
Transfer precautions:
1. Transportation should be done immediately after recovery of spontaneous heartbeat, or if on-site resuscitation has exceeded 30 minutes.
2. When resuscitating cardiac arrest in a public ****situation, it should not take too long, and can be transported while resuscitating.
3. Timely notification of the emergency department of the hospital to be delivered.
yzszgr 2004-12-17 05:55
Two, acute myocardial infarction
Diagnosis based on:
1. Most have a history of angina pectoris.
2. Severe angina lasts for more than half an hour and is not relieved by containing nitroglycerin tablets.
3. The electrocardiogram showed hyperacute T wave, ST segment elevation, T wave inversion and pathologic Q wave in the corresponding leads.
Principles of treatment:
1. Oxygen intake.
2. Vital signs monitoring (ECG, blood pressure, pulse, oxygen saturation).
3. Open intravenous access.
4. In the absence of hypotension, intravenous nitroglycerin 15 μg/minute.
5. Morphine sulfate 3~5mg intramuscularly or added to 25% GS20m1 slowly intravenously or diazepam 5~10mg intravenously. Pay attention to the toxic side effects of morphine. Arrhythmia, heart failure, cardiogenic shock when the corresponding rescue treatment.
6. Chewing aspirin 150mg.
Transfer precautions:
1. Prompt treatment of fatal arrhythmia.
2. Continuous vital signs and ECG monitoring.
3. Forecast to the receiving hospital
yzszgr 2004-12-17 05:56
Three, acute left heart failure
Heart failure is due to the primary cardiac machine diastolic dysfunction, cardiac overload or cardiac diastolic limitation, so that in the case of sufficient venous return and normal vasodilatory function, the cardiac output can not meet the A clinical syndrome characterized by venous stasis and inadequate perfusion of the arterial system and tissues. Impaired left heart function leads to pulmonary venous stasis, which in turn causes pulmonary edema, sometimes reaching its peak within minutes. It is commonly seen in large myocardial infarctions or acute exacerbations of chronic cardiac conditions.
Diagnostic basis:
1. History: exertional dyspnea, history of nocturnal paroxysmal dyspnea, history of cardiac disease.
2. Clinical manifestations: sudden onset of respiratory distress, coughing, wheezing, cackling of white or pink foamy sputum, or even constant gushing. The patient is forced to sit up, face cyanosis. Early rales can be heard in both lungs, and wet rhonchi appear late. The third or fourth heart sound may be present. The heart rate is accelerated and in a gallop rhythm. Arrhythmias such as atrial fibrillation or premature ventricular contractions may be present. Initially, blood pressure may be elevated, and alternating veins may be detected.
Principles of treatment:
1. Pure oxygen mask inhalation, so that arterial oxygen saturation reaches more than 95%. For those with blurred consciousness or respiratory weakness, they can be intubated by trachea or even given mechanically assisted breathing (CPAP) or transnasal BiPAP (bi-level positive airway pressure ventilation).
2. Put the patient in a semi-sitting position with both calves hanging down.
3. 0.5mg of nitroglycerin should be taken every 3-5 minutes, and then nitroglycerin should be dripped intravenously, starting from 10μg/min, and increasing by 5μg-15μg/min in 10 minutes-15 minutes until 250pg/min. The systolic blood pressure should be maintained at 90-100mmHg, and for the patients with intractable hypertension or those who are not responsive to nitroglycerin, the drip of sodium nitroprusside can be dripped intravenously. Sodium nitroprusside is started from 2.5μg(min.kg).
4. Intravenous furosemide 40mg, if the patient is taking this drug can be given 80mg first, after 30 minutes of ineffectiveness can be doubled.
5. Intravenous morphine sulfate 2mg, note that this drug can inhibit respiration, in the elderly or COPD, patients with caution.
Transfer precautions:
1. Keep the airway open.
2. Continuous oxygenation.
3. Keep intravenous access open.
4. Make the patient semi-sitting position, calf down, as comfortable as possible
yzszgr 2004-12-17 05:58
Four, hypertension emergency
refers to the hypertension patient due to emotional fluctuations, overfatigue and other factors, the cerebral circulation of its own regulation is dysfunctional, the peripheral arteries of the small temporary intense spasms, the blood pressure increases dramatically, resulting in heart , brain, kidney and other target organs progressive damage and a series of performance.
Diagnostic basis:
1. There may be a history of hypertension, nephritis, and pregnancy poisoning.
2. Diversified clinical symptoms, patients have sudden onset of severe headache, dizziness, nausea, vomiting, palpitations, irritability, blurred vision, skin flushing, fever and other symptoms or even coma, convulsions, but also palpitations, dyspnea, acute left heart failure, pulmonary edema, hemianesthesia, hemiparesis, aphasia and other symptoms.
3. Blood pressure rises sharply, with systolic blood pressure exceeding 26kPa (200mmHg) or diastolic blood pressure exceeding 17.3kPa (130mmHg).
Principles of treatment:
Stabilization of the condition and timely transfer to the hospital are the basic goals in pre-hospital emergency. Hypertensive emergency prehospital only deal with symptoms (such as hypertensive encephalopathy symptoms), do not deal with the original disease.
1. Comfort the patient and his family to stabilize his mood. Give diazepam (Valium) etc. if necessary.
2. Administer oxygen. Closely monitor changes in consciousness, pupils, vital signs, etc., and keep the airway open.
3. Control of blood pressure: pre-hospital conditions are limited and short-lived, and gentle antihypertensive drugs can be used if they are not accompanied by other comorbidities or diseases. But the blood pressure should not be reduced too quickly, so that the blood pressure is gradually reduced to 160/90mmHg up and down. Nitrophenylpyridine tablets can be selected sublingual, nitroglycerin or sodium nitroprusside intravenous drip.
4. Reduce intracranial pressure: with cerebral edema, 20% mannitol can be used intravenous drip, or furosemide, dexamethasone static injection, the above drugs can be used in conjunction.
5. Control convulsions and other symptoms, the use of phenobarbital, diazepam and so on.
Transfer precautions:
1. Monitor ECG and vital signs.
2, Oxygen administration en route.
yzszgr 2004-12-17 06:01
V. Arrhythmia
Diagnostic basis:
(-) Clinical manifestations
1. Symptoms:
Can be palpitations, weakness, dizziness. In ventricular tachycardia or atrial fibrillation, syncope may occur with heavy.
2. Signs:
①If there is organic heart disease or systemic disease, there may be corresponding signs.
②Changes in heart rate (fast or slow) and/or rhythm (irregular), and pulse shortening in atrial fibrillation.
(2) Electrocardiogram
Conventional electrocardiogram, or ambulatory electrocardiogram, etc. are of great value in diagnosis.
Principles of treatment:
(-) Tachyarrhythmias
1. Paroxysmal supraventricular tachycardia:
Includes atrioventricular nodal area refractory tachycardia and atrioventricular refractory tachycardia.
(1) Excitation of the vagus nerve, e.g., holding the breath after deep inspiration, pressure on the eyes, or carotid sinus massage.
(2) Verapamil 5mg pushed slowly intravenously (5 minutes), or cediran 0.2-0.4mg plus 25% or 50% GS in 20ml pushed slowly intravenously, or ATP 10-20mg injected rapidly intravenously in 1-2 seconds.
2. Ventricular tachycardia:
(1) hemodynamically unstable ventricular tachycardia:
immediately synchronized electrical resuscitation with an energy of 10 J. If pulseless ventricular tachycardia can be asynchronized with 200 J electrical shock resuscitation. This applies to other perceived QRS wave tachycardias.
(2) Hemodynamically stable ventricular tachycardia:
Amiodarone 150 mg IV over 10 minutes, followed by 1 mg/min IV drip for 6 hours, then 0.5 mg/min IV drip. If ineffective, give another 150 mg/min intravenously once if necessary, with a maximum dose of no more than 2 doses in 1 day. Lidocaine, propafenone, vimipar, diltiazem should not be used in those with organic heart disease or cardiac insufficiency.
(3) Tip-twisting ventricular tachycardia:
①Magnesium sulfate is preferred, with the first dose of 2 to 5 g, administered intravenously over 3 to 5 minutes.
②Isoproterenol helps to control this type of ventricular tachycardia, but it can worsen some of the ventricular tachycardia into ventricular fibrillation, and should be used with caution.
3. Ventricular fibrillation/ventricular flutter
(1) Immediate asynchronous direct-current defibrillation. 200-360J
(2) Find and correct the causes or triggers of the disease, such as electrolyte disorders (low potassium/low magnesium), myocardial ischemia, digitalis toxicity, or arrhythmogenic antiarrhythmic drugs.
4. Atrial fibrillation / flutter
(l) slow down the ventricular rate Cediran 0.2 ~ 0.4mg diluted slow intravenous injection, such as Cediran is ineffective can be used for Diltiazem 5 ~ 10mg, slow intravenous injection, and then 5 ~ 10mg / h intravenous drip. In most atrial flutter, sildenafil is ineffective, need to use Diltiazem.
(2) Rhythm restoration
①Drugs Isolated atrial fibrillation in patients with normal heart or combined atrial fibrillation in patients with hypertension, intravenous propafenone 2mg/kg, 7-10 minutes intravenous push, or a single tonic propafenone 450-600mg. myocardial infarction, heart failure patients should be selected to use amiodarone.
②Hemodynamic instability, synchronized direct current resuscitation. Atrial fibrillation 100 to 200 J, atrial flutter 25 to 50 J.
(3) Pre-excitation syndrome containing concomitant atrial fibrillation, partially or wholly transmitted down to the ventricle via the atrioventricular bypass.
(1) Drugs that act on the AV node, such as cediran, verapamil, and beta-blockers, are not used, as they may worsen to ventricular fibrillation.
②Ventricular rate >200 beats / min, hemodynamic instability, immediately synchronized direct current resuscitation, energy as above.
③ Ventricular rate >200 beats/min, hemodynamic stability, intravenous procainamide or propafenone.
(2) Slow-rate arrhythmias
(1) Asymptomatic sinus bradycardia with a heart rate of ≥45 beats requires no treatment.
(2) Sick sinus syndrome causing syncope, especially slow-fast syndrome, first temporary pacing, and then permanent buried pacemaker implantation at a later stage.
(3) Atrioventricular block
1) I degree and II degree Wen block can be observed, find and correct the cause of the disease, generally do not need emergency treatment.
②Type II and II or complete atrioventricular block, should be immediate temporary pacing. Complete atrioventricular block with a clear etiology or causative factor that can be corrected, such as lower wall myocardial infarction, acute myocarditis, digitalis toxicity, or antiarrhythmic drugs (B-blockers, verapamil, diltiazem, etc., especially when they are included in their use), should be corrected. Most of such patients do not need buried pacemakers without etiology and causative factors.
If the cause can be corrected, an implantation of a buried pacemaker should be performed at a later date.
In the above treatment, pacing is safe and reliable, and temporary pacing should be performed as soon as possible, or atropine or isoproterenol may be used if pacing is not available or before satisfactory pacing is achieved.
Conditions for referral:
1. Improved or better condition. Those who need pacing and electrical resuscitation are referred to the hospital for treatment as early as possible.
2. Oxygen inhalation on the way to keep the airway open.
3. Open the venous channel.
4. Do a good job of cardiac monitoring on the way
yzszgr 2004-12-17 06:04
Six, bronchial asthma
Bronchial asthma is caused by sensitizing factors or non-sensitizing factors acting on the body, causing reversible bronchial smooth muscle spasm, mucosal edema, mucus secretion and other pathological changes, the clinical manifestations of the episodic expiratory The clinical manifestations are episodes of expiratory dyspnea and bilateral rales. Asthma that persists for 24h without relief is called persistent asthma.
Diagnosis is based on:
(-) History
1. There may be a history of recurrent asthma attacks or allergen exposure.
2. There may be a history of hormone dependence and long-term application of beta2 agonists.
(2) Symptoms and signs
1. Expiratory dyspnea, sitting breathing, sweating, nervousness and even coma.
2. Physical examination Shortness of breath, frequency >30 times/min, auxiliary respiratory muscles involved in respiratory movements, lip cyanosis, prolonged expiratory time of both lungs, full of expiratory rales or rales disappeared (silent lung).
Principles of treatment:
(I) Oxygen inhalation The flow rate is 1~3L/min.
(II) Bronchodilatation
1. Nebulized inhalation of β2 agonist: salbutamol and/or anticholinergic drug ipratropium.
2. Aminophylline 0.25-0.5g added to 5% or 10% dextrose liquid 250ml intravenous drip or astringent 0.25g added to 25% or 50% dextrose liquid 20ml slow intravenous injection.
3. 0.1% epinephrine 0.3~0.5m1 subcutaneous injection, if necessary, can be repeated after an interval of 10~15 minutes 1~2 times.
(3) Glucocorticoid:Dexamethasone 10~20mg or methylprednisolone 40~80mg intravenously.
(D) pay attention to the treatment of factors that induce and aggravate the disease: timely detachment from the sensitizing environment, timely detection of pneumothorax and other concomitant conditions.
(E) assisted respiration If there is no improvement after the above treatment, the heart rate is >140 beats/min or there is a drop in blood pressure, tracheal intubation should be carried out in a timely manner, and a ventilator should be applied.
Note
Subcutaneous injection of epinephrine is sometimes effective in patients with critical bronchial asthma, less than 40 years of age, and no history of heart disease. However, it is contraindicated in coronary artery disease, cardiogenic asthma, hypertension, and hyperthyroidism.
Referral precautions:
1. Oxygen inhalation
2. Maintain open venous access.
3. Closely observe the changes of consciousness, respiration, blood pressure, heart rate and heart rhythm on the way.
yzszgr 2004-12-17 06:05
VII. Acute Stroke
Stroke is a neurological impairment caused by abnormalities in the local blood supply to the brain and can lead to brain damage. Stroke can be divided into two categories: ischemic stroke and hemorrhagic stroke, and about 85% are ischemic strokes. Ischemic strokes are caused by occlusion of cerebral blood vessels and usually include transient ischemic attack (TIA), embolism and thrombosis. Hemorrhagic strokes are mostly caused by rupture of cerebral arteries with vasospasm. This includes cerebral hemorrhage and subarachnoid space hemorrhage.
Diagnosis is based on:
1. Medical history: most of the patients have a history of hypertension, heart valve disease or long-term cerebral atherosclerosis symptoms or transient ischemic attack. Some patients have a history of headache attacks in the past. The disease is more common in middle-aged and elderly people. Some patients have headache, dizziness, limb numbness, weakness, vomiting and other prodromal symptoms. Cerebral hemorrhage and subarachnoid hemorrhage mostly occur during activity (e.g., agitation, exertion). Cerebral infarction often occurs during sleep or quiet rest, and there is often an aggravation of symptoms a few days after the onset of the process.
2. Symptoms and signs:
(1) The severity of the disease varies, with only headache and vomiting in the mild cases, and significant brain symptoms in the severe cases. These depend on the primary site of hemorrhage and ischemia, the amount of hemorrhage, the direction of hematoma expansion, the extent of ischemic wave, as well as cerebral edema, elevated brain pressure and other pathological changes.
(2) Most patients have sudden headache as the first symptom, followed by vomiting, paralysis, and impaired consciousness.
(3) Some patients show vertigo, nystagmus, diplopia, dysphagia, dysarthria, dysarthria, hoarseness, ergotism, homonymous hemianopsia, cortical blindness, oculomotor paralysis, limb ****jet disorders, sensory deficits, and so on.
(4) The patient may have vital signs, pupillary changes, and signs of meningeal irritation.
The main points of treatment:
It is difficult to distinguish the specific type of stroke in the prehospital period, so the condition should be stabilized, appropriate symptomatic treatment and timely transfer to the hospital. The key points of stroke management can be memorized as 7 "Ds": detection, dispatch, delivery, door, data, decision, and drug. Each of these should be handled skillfully and effectively.
1. Keep the airway open and administer oxygen.
2. Closely monitor changes in consciousness, pupils, and vital signs.
3. Control blood pressure: reactive hypertension may occur in stroke, and due to the limited pre-hospital conditions and short duration, antihypertensive drugs should not be used. When the blood pressure is too high or too low, the use of mildly elevating drugs or antihypertensive drugs can be appropriate, so that the blood pressure can be gradually reduced to 160/90mmHg up or down.
4. Reduce intracranial pressure: in acute stage with cerebral edema, 20% mannitol can be used intravenously, or furosemide (tachycardia), dexamethasone static injection, the above drugs can be used in conjunction.
Note
1. Timely referral to the hospital is very important. Emergency medical services systems (EMSS) should prioritize the management and transport of patients with signs and symptoms of acute ischemic stroke so that thrombolytic therapy can be administered within one hour of onset.
2. During the application of osmotic dehydrating agents such as mannitol, the dosage and drip rate of the medication should depend on cardiac function.
3. The identification of the etiology of cerebrovascular accidents often requires CT to determine, pre-hospital should not be hastily use of hemostatic drugs or vasodilators.
Transfer precautions:
1. Monitor vital signs during transfer.
2. Ensure that the airway is open and oxygen is administered.
yzszgr 2004-12-17 06:06
Eight, diabetic ketoacidosis
Diabetic ketoacidosis is a disorder of sugar and fat metabolism due to the lack of insulin in the body and the increase of insulin counter-regulatory hormone. It is a clinical syndrome characterized by hyperglycemia, hyperketosis and metabolic acidosis.
Diagnostic points:
1. History of diabetes mellitus, especially type I diabetes mellitus.
2. Presence of causative factors, such as acute infection, drug interruption or inadequate treatment, mental stimulation, stress, eating disorders, complication of other diseases, pregnancy and childbirth.
3. The onset of the disease is rapid, with a sharp increase in diabetic symptoms as the early manifestations, such as nausea, thirst, polyuria (or oliguria), loss of appetite, nausea, vomiting, abdominal pain, and even drowsiness, coma and so on.
3. Dehydration and peripheral circulatory failure, acidosis as a distinctive feature: ① severe dehydration: dry skin, elasticity, sunken eyes, dry mouth and lips red (cherry red), deepening of the respiration accelerated, part of the patient's expiratory breath in the smell of rotten apples, etc.; ② peripheral circulatory failure: cold extremities, weak pulse, decreased blood pressure, oliguria, anuria, or even shock; ③ psychiatric disorders: delirium, The patient's body will be in a state of shock, and the patient will be in a state of drowsiness.
The main points of treatment:
1. Immediately establish intravenous access, and start rehydration as soon as possible.
2. Rehydration: depending on dehydration and cardiac function, decide the rate of rehydration and the amount of rehydration. If there is no cardiac or renal insufficiency, it should be replenished according to the principle of first fast and then slow, and the first two hours of replenishment should be 1000-2000ml, and the rest of the time, according to the patient's blood pressure, heart rate, urinary output, and the state of peripheral circulation, to decide the amount and speed of fluid replenishment. Saline should be given intravenously first. If there are conditions, human insulin should be added, and the dose is 4~6U per hour.Generally, acidosis is not serious, no need to replenish alkali. Usually, potassium supplementation is not necessary before hospitalization, if there are the following indications before treatment: ① K+<3.5mmol/L; ② urine volume per hour>50ml; ③ EKG indicates that there is low potassium, then potassium supplementation will be given at the same time as the start of rehydration. For those who can be taken orally, 10%KCL10~20m1 should be taken orally, otherwise, 10%KCL10ml can be added into 500ml of liquid for intravenous drip.
3. Patients can be encouraged to take light saline orally.
4. Transfer to hospital in time.
Transfer precautions:
1. Monitor vital signs during the transfer.
2. Keep the venous channel open.
3. Oxygen inhalation if necessary.
yzszgr 2004-12-17 06:07
Nine, allergic reaction
The human body is exposed to a variety of physical and chemical, biological and other allergens caused by the body of the rapid-onset metamorphosis.
Diagnosis is based on:
1. A history of contact with allergens (certain foods, drugs, chemicals, etc.) or suspected contact with allergens.
2. Acute onset.
3. itchy skin, rash, panic, wheezing, and in severe cases, dyspnea, decreased blood pressure, and impaired consciousness.
Principles of treatment:
1. Allergens are clearly identified and quickly removed.
2. Oxygen inhalation should be given to those with signs of hypoxia.
3. Open the airway, maintain effective ventilation, nasal mask or tracheal intubation if necessary, use of respiratory resuscitation airbag or portable ventilator for respiratory support.
4. Use Benadryl, Isoprozine, Calcium Gluconate, Glucocorticoids and other drugs as appropriate, intramuscular or intravenous anti-allergy.
5. For anaphylactic shock that is the scale of subcutaneous injection of epinephrine 0.5 ~ 1mg, at the same time choose the above treatment.
6. Cardiac arrest, respiratory arrest immediately in cardiopulmonary resuscitation.
7. Other symptomatic treatment.
Transfer precautions:
1. Maintain effective ventilation.
2. Establish intravenous access and use necessary antiallergic drugs.
3. Monitor vital signs.
yzszgr 2004-12-17 06:08
X. Electrocution
The pathological process by which electric current passes through the human body and causes tissue damage.
Diagnosis based on:
1. History of electrocution.
2. There may be one or more tissue necrosis, charring, or charring scars on the body surface due to electrical burns.
3. There may be nervousness, dizziness, weakness, palpitations, convulsions, cyanosis, cardiac arrhythmia, impaired consciousness or even cardiac arrest.
Principles of treatment:
1. Quickly disengage from the power source.
2. Give oxygen to those who have hypoxia indication.
3. Cardiopulmonary resuscitation for cardiac and respiratory arrest.
4. Protect the body surface electric burn wound.
5. Symptomatic treatment.
Transfer precautions:
1. Cardiac respiratory arrest should establish effective ventilation and oxygenation. The heartbeat is restored or transferred to the hospital at the same time as effective cardiac compression.
2. Establish intravenous access for critically ill patients.
3. Check for the presence of other comorbid trauma, such as trauma from a fall from a height after an electrocution injury resulting in a fracture.
4. Monitor vital signs.
yzszgr 2004-12-17 06:09
XI. Drowning
Diagnosis is based on:
1. History of drowning.
2. There may be facial bruising, swelling, cold and wet limbs, abdominal distension, impaired consciousness or even cardiac and respiratory arrest.
Principles of treatment:
1. Remove foreign bodies from the mouth and respiratory tract, open the airway and maintain effective ventilation. Use nasal mask or tracheal intubation if necessary, and use respiratory resuscitation airway or portable ventilator for respiratory support.
2. Quickly pour out the water in the airway and stomach.
3. Oxygen inhalation is given to those with signs of hypoxia.
4. Cardiac arrest, respiratory arrest immediately be cardiopulmonary resuscitation.
5. Establish intravenous access to maintain effective circulation. Fresh water drowning people choose 0.9 ~ 3% sodium chloride solution drip, seawater drowning people choose 5% dextrose solution drip.
6. Other symptomatic treatment.
Transfer precautions:
1. Critical patients to establish intravenous access.
2. Monitor vital signs.
yzszgr 2004-12-17 06:10
XII, heatstroke
Diagnosis based on:
1. A history of working in a high-temperature environment or exposure to the hot sun.
2. There may be thirst, dizziness, excessive sweating or dry and hot skin, elevated body temperature, muscle cramps, and impaired consciousness.
Principles of treatment:
1. Make the patient quickly get out of the hot environment.
2. Oxygen inhalation should be given to those who have signs of hypoxia.
3. Give the body surface physical cooling. High fever at the same time drug cooling, selection of chlorpromazine 25 ~ 50mg plus 0.9% sodium chloride solution intravenous drip.
4. Circulatory failure of intravenous rehydration at the same time as appropriate selection of dopamine, scopolamine intravenous drip.
5. 20% mannitol and glucocorticoid are used for cerebral edema.
6. Cardiac arrest, respiratory arrest immediately be cardiopulmonary resuscitation.
7. Other symptomatic treatment.
Transfer precautions:
1. Ensure that the venous channel is unobstructed.
2. Cardiac and respiratory arrest should establish an effective airway and oxygen administration, and be transferred to the hospital under the condition of effective cardiac compression.
3. Monitor vital signs.
yzszgr 2004-12-17 06:11
Thirteen, acute poisoning
This refers to a variety of plant and animal toxins, chemicals, toxic gases and other poisons invade the human body, resulting in organism tissue damage, organ dysfunction of the pathological process.
Diagnostic basis:
1. History of exposure to poisons (via respiratory tract, digestive tract, skin, etc.).
2. Clinical manifestations of dysfunction of the damaged organs as well as poisoning manifestations specific to the exposed poison.
3. There may be abnormal changes in pulse, respiration, blood pressure, mental state and even cardiac and respiratory arrest.
Principles of treatment:
1. Make the patient get out of the poisonous environment or poison quickly, such as taking off the clothes contaminated by poison.
2. Oxygen inhalation should be given to those who have hypoxic indications, such as high-flow oxygen inhalation for carbon monoxide poisoning.
3. Open the airway, maintain effective ventilation, if necessary, nasal mask or tracheal intubation, the use of respiratory resuscitation airbag or portable ventilator for respiratory support.
4. Establish intravenous access, drip 5% to 10% glucose injection, while the intravenous use of tachycardia to promote the excretion of toxic substances. Organophosphorus poisoning according to the degree of poisoning static injection of appropriate amount of atropine and chlorophosphamide and other special antidotes.
5. Cardiac arrest, respiratory arrest immediately in cardiopulmonary resuscitation.
Transfer precautions:
1. Frequent vomiting and unconsciousness, the patient's head to the side, to prevent asphyxiation due to aspiration of vomit.
2. Ensure the airway is open and monitor vital signs.
yzszgr 2004-12-17 06:13
Fourteen, animal injuries
(a), venomous snake bites
China has found more than 40 kinds of venomous snakes, of which about 10 kinds are common. According to the nature of the venom secreted, the venomous snakes are roughly classified into 3 categories: neurotoxicity-based, such as the golden ringed snake, silver ringed snake; blood venom-based, such as the bamboo leaf green, five-step snake; mixed venomous, such as pit vipers, cobras and so on.
Diagnostic basis:
1. History of venomous snake bite with localized tooth marks, pain and swelling.
2. Neurotoxicity is absorbed quickly and dangerously, the symptoms are mild and easily ignored, but the consequences are serious and can cause respiratory muscle paralysis and muscle paralysis.
3. Hematotoxicity produces early and severe symptoms, with strong histolytic, hemolytic and anticoagulant effects, can cause blood pressure drop and shock.
4. In addition to the poisoning characteristics of the above two toxins, mixed poison also produces synergistic effects of toxins. But the main cause of death is neurotoxicity.
Principles of treatment:
1. The aim is to prevent continued absorption of the venom and to minimize local damage.
2. Prevent the spread of toxin ① Tie the proximal end of the injured limb to block venous blood and lymphatic reflux, it should be relaxed once every 10-20 minutes to avoid tissue necrosis; ② Brake the injured limb and lower it.
3. Herbal medicine has the effect of detoxification, anti-inflammatory, hemostatic, cardiac, diuretic, anti-hemolytic, etc., there are two kinds of drugs used externally and internally. Commonly used drugs are snake medicine tablets.
4. If possible, as soon as possible intramuscular injection of tetanus antitoxin injection 1500 units (2 ml).
5. Injection of antivenom when possible.
Transfer precautions:
1. Oxygen inhalation on the way.
2. Close observation of vital signs.
(2) Human and animal bites
1. History of human and animal bites.
2. The bite is localized with teeth marks, extensive tissue edema, subcutaneous hemorrhage, hematoma, and may be accompanied by muscle or soft tissue lacerations.
3. Usually the wound is heavily contaminated.
Principles of treatment:
Shallow wounds can be treated with iodine and alcohol.
1. deeper wounds, disinfection and attention to stop bleeding.
2. It is recommended to go to an epidemic prevention station for further treatment.
3. Intramuscular injection of tetanus antitoxin when available.
(C) Bee stings
1. History of bee stings.
2. Localized redness, swelling and pain, which will subside after a few hours, mostly without systemic symptoms.
3. Bee stings can cause a systemic reaction, similar to serum sickness.
Principles of treatment:
1. Early use of ice cold compresses to reduce swelling.
2. Elevate the affected limb.
3. Oral antihistamines are effective in producing urticaria.
4. Intravenous corticosteroids reduce the delayed inflammatory response.
5. When anaphylactic shock occurs, 1:1000 epinephrine 0.5-1.0m1 intramuscular injection can be given, and other antiresorptive drugs can be given as appropriate.
yzszgr 2004-12-17 06:14
Fifteen, trauma
By mechanical, chemical, thermal, electric current, nuclear and other two or more factors caused by the injury is called a compound injury; by the mechanical factors caused by the injury is greater than the two parts of the injury, one of the parts of the damage to reach the severity of the degree of damage is known as multiple injuries. If the parts are not serious, it is called multiple injuries. Trauma has a high incidence both in wartime and in peace. If the prehospital time is not too long, basic life support is the mainstay of on-site resuscitation; urban prehospital advanced life support is not necessarily better than basic life support in terms of ultimate salvage.
Trauma patient deaths show three peaks in distribution, the first peak in 1h, the number of immediate deaths accounted for 50% of trauma deaths, mostly serious craniocerebral injuries, high spinal cord injury, rupture of the heart, the aorta, or other large blood vessels, and respiratory obstruction, etc. These patients basically die in the field. These patients basically die at the scene, known as on-site death, only a very small number of patients may be saved, which is the difficulty of pre-hospital emergency care. The second peak of death occurs within 2~4h after injury, called early death, the number of deaths accounted for 30% of trauma deaths, the cause of death is mostly brain, chest or abdominal blood vessels or substantial organs rupture, serious multiple injuries, severe fractures and other causes of massive blood loss. These patients are the focus of pre-hospital emergency care. The first hour after critical multiple injuries is called "golden hour", and the first 10 minutes of this hour is the decisive time, which is called "platinum 10 minutes", more valuable than gold, if the bleeding is controlled during this time, and asphyxiation does not occur, it can avoid the death of many trauma patients. If bleeding is controlled and asphyxia does not occur during this time, many deaths of trauma patients can be avoided. The goal of the "Platinum 10" period is to minimize or avoid cardiac arrest and gain time for subsequent resuscitation. In order to achieve improved trauma outcomes, prehospital EMS response times need to be geared toward the "platinum 10 minutes".
Diagnostic basis:
1. A history of trauma with a clear causative factor, and pain at the site of the injury in a conscious person.
2. One or more injuries all over the body.
3. Dyspnea, shock, and coma in severe cases.
Principles of treatment:
1. Rapidly detach the injury-causing factor, and determine whether the injured person has any life-threatening signs. If cardiac arrest, immediately implement cardiopulmonary resuscitation. For those who are in shock, they should be treated with anti-shock therapy.
2. Keep the airway open, oxygen intake, tracheal intubation if necessary.
3. Wound treatment: use sterile gauze or dressings to bandage the wound, for open pneumothorax or chest wall collapse to abnormal respiration need to use large cotton pads to fill the wound, and be fixed.
4. Those with suspected cervical spine injury should be immobilized with neck brace, and those with thoracolumbar spine injury should be carried on flat or shovel stretcher to avoid any twisting of the spine.
5. Fractures need to be properly immobilized, and various kinds of splints or local materials are commonly used to replace them.
6. For those with combined thoracic and abdominal hemorrhage, blood volume needs to be replenished quickly, and it is recommended that
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