Cardiac asthma lung edema is a form of acute failure
Clinical Characteristics acute heart failure
Acute congestive heart failure - one of the most serious violationsblood circulation. It can develop as a result of prolonged oxygen starvation (hypoxia) due to blood loss or respiratory depression, traumatic shock, heart defects (mitral stenosis, hypertension, myocardial infarction, poisoning with toxic substances).
When acute heart failure the heart muscle loses its contractility, so the heart can not pump the blood flowing to it. The cardiac output sharply decreases, blood stasis arises.
If left ventricular insufficiency prevails, the blood stagnates in the lungs, there is an overflow of the small circle of blood circulation, cardiac asthma develops, pulmonary edema develops.
If the right-ventricularinsufficiency, the blood stagnates in a large circle of blood circulation, edema develops, the liver is enlarged, the rate of blood flow and supply of oxygen to various tissues and organs decreases.
So, acute cardiovascular failure -Pathological condition due to the incompetence of the heart as a pump that provides adequate blood circulation.
Typical examples of acute cardiacleft ventricular failure are cardiac asthma and pulmonary edema, which is usually converted to cardiac asthma. These are paroxysmal forms of severe shortness of breath caused by the effusion of serous fluid into the pulmonary tissue with the formation of either an interstitial edema in cardiac asthma or alveolar edema with foaming of a protein-rich transudate (with pulmonary edema).
The causes of cardiac asthma and pulmonary edema areprimary acute left ventricular failure (myocardial infarction, hypertensive crisis, left ventricular failure in patients with myocardiopathy, etc.) or acute manifestations of chronic left ventricular failure (mitral or aortic defect, chronic cardiac aneurysm, other chronic forms of ischemic heart disease). Acute weakness of the left ventricle of the heart leads to the main pathogenetic syndrome - an increase in hydrostatic pressure in the pulmonary capillaries. There are such provocative additional moments as physical or emotional tension, hypervolemia (hyperhydration, fluid retention), an increase in blood flow to the system of a small circle of circulation during the transition to a horizontal position, and other factors. Accompanying attack excitement, blood pressure rise, tachycardia, tachypnea, increased work of respiratory and auxiliary muscles increase the burden on the heart. Hypoxia of the tissues and acidosis due to poor heart function are accompanied by a further deterioration of its work, a violation of central regulation, increased permeability of the alveoli, a decrease in the effectiveness of drug therapy.
• Harbinger and erased forms: increased dyspnea, the patient can not lie down. Suffocation, coughing or just sadness behind the sternum with a little physical exertion, weakened breathing and scanty wheezing below the scapula.
• Cardiac asthma: suffocation with a cough, wheezing. Forced rapid breathing, orthopnea (forced sitting position). Excitement, fear of death. Cyanosis, tachycardia, often - increased blood pressure. Auscultatory: against the background of weakened breathing - dry, often finely bubbling rales. In severe cases - cold sweat, "gray" cyanosis, swelling of the cervical veins, prostration. The differential diagnosis with bronchial asthma is very important here, since drugs are contraindicated and adrenalytics are shown.
• Pulmonary edema occurs more or less suddenlyor with the increase in the severity of cardiac asthma. The appearance in the heart of asthma of abundant small and medium bubbling rales extending to the anterolateral lungs points to the developing pulmonary edema. The appearance of a foamy, usually pink sputum is a reliable sign of pulmonary edema. Chryps are clearly audible from a distance. Other signs - as in severe cardiac asthma (see above). When swelling of the lungs are distinguished: lightning current (death within a few minutes), acute (from 30 minutes to 3 hours), prolonged (up to a day or more).
Emergency treatment is already at the stage of harbingers. For a paramedic, the sequence of therapeutic measures is largely determined by their accessibility, time. If possible, you should call for a team of cardiac recovery.
• relief of emotional stress, it should be possible to calm the patient;
• Sick the patient with his legs down;
• nitroglycerin 2-3 tablets under the tongue every5-10 minutes under the control of arterial pressure before the onset of a noticeable improvement (less abundant rales, subjective improvement) or until blood pressure decreases. In a number of cases, this set of measures is sufficient, a noticeable improvement occurs in 5-15 minutes.
If there is no improvement or it is ineffective:
• 1-2 ml of a 1% solution of morphine is injected intravenously slowly, on isotonic sodium chloride solution;
• furosemide - from 2 to 8 ml of a 1% solution intravenously (do not use at low blood pressure);
• inhalation of oxygen through the mask;
• cardiac glycosides-digoxin solutions of 0.025%-1-2 ml or strophantin 0.05% in a dose of 0.5-1 ml are slowly injected into the vein with a 0.9% solution of sodium chloride;
• Prednisolone (30-60 mg) or hydrocortisone (60-125 ml) intravenously to prevent or treat damage to the alveolar membrane; the introduction of hormones is especially indicated for mixed asthma;
• for mixed asthma with bronchospasm, a 2.4% solution of euphyllin in a quantity of 10.0 ml is slowly injected intravenously. As "defoamer" is used inhalation of vapors of ethyl alcohol.
Patients are subject to emergency hospitalization incardiorespiratory department after relief of signs of left ventricular failure or with improvement of the condition. It should be reiterated that the paramedic who must carry out the above measures should be called upon to take care of the cardio-recreational ambulance.