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polo shirts outlet Acute cardiac insufficiency _26
with heart failure in-depth basic and clinical research, are concerned about dysfunction pathophysiology and clinical treatment of the traditional concept of a new awareness of change was defined as cardiac insufficiency of different causes of cardiac systolic and diastolic dysfunction caused by , the development of the cardiac output in the circulating blood volume and vasomotor function of normal blood flow can not meet the needs of the whole body metabolism, resulting in a hemodynamic abnormalities and neurohormonal system activation characteristics of both the clinical syndrome. Determined to dysfunction syndrome or heart failure syndrome, said. Pump failure in Acute myocardial infarction originally referred to the left heart failure,Zhang Shan set battle _974, are caused by different causes dysfunction of the heart pumping, it was called the pump system failure, the traditional concept that heart failure patients had symptoms of organ blood stasis, which is also called congestive heart failure. New concept that heart failure can be divided into two stages of asymptomatic and symptomatic, the former is objective evidence of ventricular dysfunction (left ventricular ejection fraction decreased as the heart), but without typical symptoms of congestive heart failure, heart function is still is NYHA (New York Heart Association) I level, there is the early stage of heart failure symptoms, if not effectively treated, sooner or later develop into heart failure symptoms. According to the priority of heart failure occurred, the extent of the difference between compensatory circulatory system, there is clinical Acute heart failure, chronic heart failure decompensated heart failure and various manifestations.
cardiac ejection according to the degree of dysfunction, the different speed and duration, and the compensatory function of the difference between any of the following four different expression.
(a) of the faint heart itself ejection dysfunction, cardiac output decrease caused by cerebral ischemia, transient loss of consciousness occurred, called cardiac syncope (cardiogenicsyncope). Fainting episode may have a few seconds the limbs continue to twitch, apnea, cyanosis, such as performance, known as A - Adams syndrome (Adams-Stokessyndrome). Episodes were short, often immediately after the onset of consciousness recovery. Mainly observed in Acute obstruction or severe cardiac arrhythmia ejection.
(b) of the shock due to cardiac dysfunction caused ejection of insufficient cardiac output due to shock, cardiogenic shock is called (cardiogenicshock). Sudden and cardiac output decreased significantly, the body too late to be compensated by increasing blood circulation, but through reflex peripheral and visceral blood vessels can make a significant contraction in order to maintain blood pressure and ensure the blood supply of the heart and brain. In addition to general clinical manifestations of shock, a number associated with cardiac insufficiency, venous stasis circulation, such as venous hypertension, jugular vein engorgement and other performance.
(c) Acute pulmonary edema and Acute left heart failure or Acute left ventricular failure of the main performance. More serious due to sudden left ventricular ejection of left atrial ejection inadequate or obstructed pulmonary venous and pulmonary capillary pressure caused by a sharp rise due. When the pulmonary capillary pressure is increased more than plasma colloid osmotic pressure, the liquid leakage from the capillaries to the pulmonary interstitial and alveolar or airway, causing pulmonary edema. Typical hair as a sudden, severe shortness of breath; breath per minute up to 30 ~ 40, orthopnea, coughing, looking pale, lips cyanosis, sweating, and often spit up foamy sputum, severe oral and nasal cavity from pouring a lot of pink foam. Onset heart rate, faster pulse, blood pressure can be increased at the start, later reduced to normal or below normal. The two lungs and a wide range of blisters can be heard wheezing tone. Apical gallop may be heard, but often obscure lung sounds blisters. The typical X-ray shadow of a large butterfly-shaped extension from the hilar to the peripheral. Acute pulmonary edema (acutepulmonaryedema) early stage of interstitial pulmonary edema can be no such typical clinical and X-ray, while only shortness of breath, coughing, heart rate, apical gallop and pulmonary wheeze, X ray shown on the pulmonary vein filling, hilar vascular obscure markings thickening and lung interlobular septal thickening, such as the timely diagnosis and treatment measures can prevent the development into the alveolar pulmonary edema.
(d) of cardiac arrest for the performance of severe heart failure, cardiac arrest or cardiogenic sudden death of the clinical course can be divided into four periods: the prodromal period, the incidence of, cardiac arrest and death period.
prodromal period: many patients before cardiac arrest occurred a few days or weeks or even months of prodromal symptoms, such as angina, shortness of breath or palpitations of the increase, easy fatigue, and other non-specific complaint. These prodromal symptoms are not specific to cardiogenic sudden death, but common to any prior heart attack. Data shows that 50% of cardiogenic sudden death in patients sudden death has been within the previous month, but the chief complaint often is not necessarily heart-related. In hospital cardiac arrest survivors, 28% in cardiac arrest prior to the aggravation of angina or shortness of breath. However, only suggestive of prodromal symptoms of cardiovascular disease risk, but does not recognize the occurrence of cardiogenic sudden death that is a sub-group.
incidence of: that led to cardiac arrest before the period of Acute cardiovascular changes, usually not more than 1 hour. Typical manifestations include: prolonged chest pain of angina or Acute myocardial infarction, Acute respiratory distress, sudden heart palpitations, sustained tachycardia, or dizziness and so on. If the moment of cardiac arrest occurred without warning in advance warning, the 95% of cardiogenic, and coronary artery disease. Sudden cardiac death were obtained from the continuous ECG records can be seen in a few hours or minutes before death often changes in electrical activity of the heart, in which heart rate and ventricular premature deterioration of the most common upgrade. Sudden death in ventricular fibrillation who are often the first burst of sustained or non sustained ventricular tachycardia. The incidence of patients with arrhythmias, most clearly before the onset of illness and in their daily activities, the onset phase (from onset to cardiac arrest) short. Most of the ventricular fibrillation ECG abnormalities. Another part of the incidence of patients with circulatory failure, cardiac arrest is not active before, or even unconscious, the incidence of long. Before a change in the dying often have non-cardiovascular heart disease. ECG with ventricular asystole more common than ventricular fibrillation.
of cardiac arrest: complete loss of awareness of the characteristics of the period. If not immediately rescue, generally within a few minutes into the death phase. Those rare spontaneous reversal.
cardiac arrest is a sign of clinical death, the symptoms were there as follows: ① heart sounds disappeared; ② no palpable pulse, blood pressure measurement could not; ③ sudden loss of consciousness or associated with paroxysmal convulsions. Often generalized convulsions, cardiac arrest occurred in the 10 seconds, sometimes accompanied by eye deviation; ④ breathing intermittent, was like a sigh, after the stop. After cardiac arrest occurred within 20 to 30 seconds; ⑤ coma, cardiac arrest occurred in 30 seconds; ⑥ dilated pupils, mostly in cardiac arrest occurred after 30 to 60 seconds. However, this period has not yet to the biological death. As to the timely and appropriate emergency treatment, the possibility of recovery. The success rate of recovery depends on: ① recovery started sooner or later; ② place of occurrence of cardiac arrest; ③ type of abnormal electrical activity of the heart (ventricular fibrillation, ventricular tachycardia, ventricular cardiac mechanical separation suppression pause); ④ in the heart arrest before the patient's clinical condition. If cardiac arrest occurs in cardiopulmonary resuscitation may be the place immediately, the recovery of a high success rate. In a hospital or intensive care unit immediately under the conditions of the rescue, recovery depends largely on the success rate of patients in cardiac arrest prior to the clinical situation: the case of temporary Acute cardiac conditions or metabolic disorders, the prognosis is better; if chronic advanced heart disease or serious non-cardiac conditions (such as kidney failure, pneumonia, sepsis, diabetes, or cancer), the recovery success rate no better than hospital cardiac arrest occurred in the recovery success rate. The latter depends on the success rate of cardiac arrest when the heart's electrical activity of the type, of which the best prognosis of ventricular tachycardia (success rate 67%), followed by ventricular fibrillation (25%), ventricular standstill, and electro-mechanical separation of poor prognosis. The impact of age is also an important factor in successful resuscitation.
of biological death: cardiac arrest from the death of the biological evolution of cardiac arrest depends on the type of cardiac electrical activity and cardiac recovery timeliness. Ventricular fibrillation or ventricular arrest,polo shirts outlet, as in the first 4 to 6 minutes were not cardiopulmonary resuscitation, the prognosis is poor. If were not in the first 8 minutes, resuscitation, except in special circumstances such as low temperature, or almost no survival. From the statistics, the witness immediately DNR and early defibrillation is the key to prevent biological death. Hospitalized after cardiac resuscitation most common cause of death is the central nervous system damage. Hypoxic brain damage and secondary infection in long-term mechanical ventilation account for 60% of the cause of death. Low cardiac output accounted for 30% of the cause of death. And because the recurrence of fatal arrhythmia accounted for only 10%. Acute myocardial infarction complicated by cardiac arrest, the prognosis depends on the primary or the secondary: the former cardiac arrest occurs there is no hemodynamic instability; the latter system secondary to an unstable hemodynamic state. Thus, primary cardiac arrest resuscitation immediately if the success rate should be 100%; and secondary poor prognosis of cardiac arrest, the recovery success rate of about 30%.
following a variety of reasons, so that cardiac output fell sharply in a short time, and even loss of ejection function, which can cause Acute heart failure (acutecardiac insufficiency).
1. Caused by diffuse myocardial damage in Acute myocardial contraction, weakness, such as Acute myocarditis, diffuse myocardial infarction.
2. Taiwan stay in the mechanical obstruction caused by increased cardiac load resistance, ejection blocked, such as severe valvular stenosis, ventricular outflow tract obstruction, atrial ball valve thrombus or myxoma-like incarceration, the Director-General or large branch artery embolism.
3. Taiwan stay in the heart of increased volume load, such as trauma, Acute myocardial infarction or valvular endocarditis caused by damage to chordae rupture, papillary muscle dysfunction, perforation intervals, aortic sinus aneurysm rupture into the heart chamber, and venous blood transfusion or type too fast or too much liquid sodium.
4. Taiwan stay ventricular diastolic restricted, such as Acute large pericardial effusion or hemorrhage, ectopic rhythm so fast.
5. Serious arrhythmias such as ventricular fibrillation (VF) and other serious ventricular arrhythmia, ventricular pause, significant bradycardia, so that the heart of suspension or discharge of blood significantly reduced cardiac output.
according to typical symptoms and signs, the diagnosis of Acute heart failure is not difficult, primarily with other reasons (especially vascular dysfunction) caused by syncope, shock, and differentiated from pulmonary edema. Syncope At the time, heart rate, heart rate was too slow, too fast, missing or suspended, nor cause Acute heart failure based on heart disease, can be ruled out cardiogenic syncope. Cardiogenic shock venous pressure and ventricular end-diastolic pressure is increased, and other causes of shock are different. Pulmonary edema with pulmonary wheezing with asthma should be identified, this time in favor apical gallop diagnosis of pulmonary edema. Other causes of pulmonary edema, chemical or physical factors such as pulmonary vascular permeability changes (infection, hypoproteinemia, allergic, toxic and radioactive gas inhalation pneumonia),polo shirts outlet, poor lymphatic drainage of interstitial pulmonary (lung lymphoid tissue cancer infiltration, etc.) or chest negative pressure increased (pleural paracentesis too fast or too much), bronchial poor drainage (liquid or inhalation of bronchial cough reflex, etc.), according to the appropriate medical history and symptoms of Acute cardiac function is not difficult Identification failure caused by pulmonary edema. However, patients with heart disease caused by non-cardiogenic pulmonary edema, and other causes of pulmonary edema with cardiogenic pulmonary edema are not uncommon. Should take into account and make judgments.
First, given the appropriate treatment according to etiology.
(a) the treatment of cardiogenic syncope, cardiogenic syncope attack most of the more short-lived,polo shirts outlet, but there may be recurrent. Treatment should include the prevention of attacks. Syncope occurred in the cardiac ejection were blocked by the supine or knee-chest position to rest, warmth and oxygen, are often can be alleviated. The atrioventricular valve orifice obstruction by blood clots or tumors, seizures may change the position block to reduce or stop seizures. Caused by a severe arrhythmia, should be promptly controlled arrhythmia (see Thorough treatment is to remove the cause, such as surgery to lift outflow tract obstruction, removal of blood clots or tumors, control arrhythmia episodes.
(b) the treatment of cardiogenic shock, see the
(c) the treatment of Acute pulmonary edema Acute pulmonary edema as a medical emergency, one in critical condition, the treatment must be timely and have quick results.
1. Principle of treatment ① lower left atrial pressure and (or) left ventricular filling pressure; ② increased left ventricular stroke volume; ③ reduced circulating blood volume; ④ reduce infiltration of alveolar fluid to ensure gas exchange.
2. Specific measures
(1) the patient was sitting or semi-supine, legs down, to reduce venous return.
(2) oxygen therapy: pulmonary congestion and reduced lung compliance, the work of breathing in patients with pulmonary edema, and oxygen consumption increased, and mucosal congestion, edema and prevents gas exchange in the terminal respiratory unit. Oxygen mask oxygen effect than the nasal catheter. Oxygen pressure can not only correct the hypoxia, but also by increased alveolar and intrathoracic pressure,polo shirts outlet, reduce the liquid into the alveoli and lower venous blood Rhodobryum. Venous obstruction while the surrounding venous pressure also increased in favor of liquid leakage from blood vessels into the interstitial space, thereby reducing blood circulation. But alveolar pressure is too high may affect right ventricular stroke volume, stroke volume caused by decreased blood pressure. At this point the pressure of oxygen should be adjusted to shorten the time for oxygen pressure to extend the interval of time, to obtain satisfactory results.
(3) sedation: intravenous injection of 3 ~ 5mg of morphine, can be rapidly expanding body of veins, reducing venous change thy blood, lower left atrial pressure. Can also reduce irritability, and difficulty breathing, reduce peripheral arterial resistance, thereby reducing left ventricular afterload and increase cardiac output. Subcutaneous or intramuscular injection in the peripheral blood vessels of patients significantly, can not guarantee the whole amount of absorption.
(4) sublingual or intravenous nitroglycerin can rapidly reduce pulmonary wedge pressure or left atrial pressure, the effect of relieving symptoms often very significant, but may cause hypotension. Determine the systolic blood pressure in 13.3kPa (100mmHg) or more after the first dose sublingual 0.3mg, 5min after the review of blood pressure, to give 0.3 ~ 0.6mg, 5 minutes after the re-measurement of blood pressure. Such as systolic blood pressure decreased to 12kPa (90mmHg) or less, stop administration. Initial intravenous dose of nitroglycerin 10μg/min, measured in the blood pressure monitored every 5min increased 5 ~ 10μg/min, until the symptoms ease or systolic blood pressure decreased to 12kPa (90mmHg) or less. Continue to maintain the effective dose intravenous drip in a stable condition after the gradual reduction to the disabled, a sudden stop may cause symptoms of intravenous anti-jump.
(5) intravenous injection of furosemide or by Thani 40mg sodium 50mg (50% glucose solution diluted), the former before the start of the diuretic effect can be reduced through the expansion of the left atrial pressure venous system, reducing dyspnea. Urine after administration began to increase 15 ~ 30min, 60min peak, a large number of diuretic to reduce blood volume, further to the left atrial pressure decreased. Low blood pressure patients, especially Acute myocardial infarction or pulmonary edema caused by aortic stenosis should be used with caution in order to avoid hypotension or shock.
(6) other adjuvant therapy: ① intravenous aminophylline 0.25g (dilute 40ml of 50% glucose, 15 ~ 20min end note) can relieve bronchospasm and reduce breathing difficulties. Also may enhance myocardial contraction, expansion of the surrounding blood vessels, reducing pulmonary artery and left atrial pressure. ② digitalis preparations on supraventricular tachycardia caused by pulmonary edema and a significant effect. Digitalis slows atrioventricular conduction, the room rate and to improve left ventricular filling, decreased left atrial pressure. Intravenous lanatoside C or digoxin, and within a week who have not used the first dose of digoxin lanatoside C0.6mg, digoxin 0.5 ~ 0.75mg; week who used digoxin are advised to start small. Intravenous digitalis preparations can drag vasoconstriction, increased afterload, and thus less for patients with pulmonary edema were in sinus rhythm. ③ hypertensive heart disease caused by pulmonary edema, intravenous infusion of sodium nitroprusside, can be quickly and effectively reduce the heart before and after the load, reducing blood pressure. Usage 15 ~ 20μg/min, every 5min increased 5 ~ 10μg/min, until symptom relief, or systolic blood pressure reduced to 13.3kPa (100mmHg) or less. Effective dose to maintain a stable condition, after the gradual reduction and withdrawal. Sudden withdrawal can cause rebound. Long-term medication can cause cyanide and thiocyanate poisoning, which in recent years has gradually been replaced by nitroglycerin. Phentolamine infusion 0.1 ~ 1mg/min, but also the rapid blood pressure and reduce the role of afterload, but can cause tachycardia and reduce the role of pre-load less, in recent years has been less used. ④ pulmonary edema in patients with low blood pressure are advised to intravenous infusion of dopamine 2 ~ 10μg/kg/min, maintaining systolic blood pressure 13.3kPa (100mmHg), and then to vasodilator therapy. ⑤ vein blood 300 ~ 500ml, can be used for the treatment fails in patients with pulmonary edema, especially in a large number of rapid infusion or transfusion-induced pulmonary edema.
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