Cardiac asthma and pulmonary edema

Cardiac asthma (CA) and pulmonary edema (AL) are paroxysmal forms of severe breathing difficulty caused by sweating serous fluid in the lung tissue with the formation of an edema (interstitial edema) and alveolar edema, with foaming of protein-rich transudate (with pulmonary edema ).

Etiology, pathogenesis . The causes of CA and AL are primary acute left ventricular failure (myocardial infarction, other acute and subacute forms of IBO, hypertensive crisis and other paroxysmal forms of arterial hypertension, acute nephritis, acute 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 IVO, etc.). To the main pathogenetic factor - the increase in hydrostatic pressure in the pulmonary capillaries, additional provoking attacks are usually added: physical or emotional tension, hypervolemia (hyperhydration, fluid retention), increased blood flow to the system of the small circle when moving to a horizontal position and violation of central regulation during sleep and Other factors. Accompanying attack excitement, lifting blood pressure, tachycardia, tachypnea, increased work of the respiratory and auxiliary muscles increase the load on the heart and reduce the effectiveness of its work. The sucking action of the forced inspiration leads to an additional increase in the blood filling of the lungs. Hypoxia and acidosis are accompanied by further deterioration of the heart, a violation of central regulation, increased permeability of the alveolar membrane and reduce the effectiveness of drug therapy.

Symptoms, course .

  • Precursors worn-out forms: strengthening (appearance) of dyspnea, orthopnea. Choking, coughing, or just sighing behind the sternum with little physical exertion or moving to a horizontal position. Usually - weakened breathing and poor wheezing below the scapula.

  • Cardiac asthma (CA): choking with a cough, wheezing. Ortopnoe, forced rapid breathing. Excitement, fear of death. Cyanosis, tachycardia, often - increased DD. Auscultatory - against the background of weakened breathing, dry, often - lean little bubbling rales. In severe cases - cold sweat, "gray" cyanosis, swelling of the cervical veins, prostration. Swelling of bronchial mucosa may be accompanied by a violation of bronchial patency ("mixed asthma"). Differential diagnosis with bronchial asthma (see) is very important, since in the case of bronchial asthma (as opposed to CA), narcotic analgesics are contra-indicated (dangerous) and (-adrenergic drugs are indicated. Pay attention to the complicated, elongated exhalation (with bronchial asthma).

  • Pulmonary edema (AL): occurs more or less suddenly, or as a result of the increase in severity of OA. Appearance in OA of abundant small- and medium bubbling rales extending to the anterolateral regions of the lungs indicates a developing ("AND degree") OL. Appearance of frothy, usually pink sputum (an admixture of erythrocytes) is a reliable sign of OL. Chryps are clearly audible at a distance ("And! Degree"). Other objective and subjective signs both in severe CA (see above). For the 1 st stage of the OL, heavy orthopnea, cold sweat is characteristic. There are lightning fast (death within a few minutes), acute (duration of attack from 0, b to 2 - 3 hours) and prolonged (up to a day or more) course. Frozen sputum for OL should be distinguished from frothy, often colored blood, saliva secreted by epileptic seizure and with hysteria. The "clotting" breathing in extremely hard (agonizing) patients is not a specific sign of AL.

    Treatment - emergency already at the precursor stage (possible fatal outcome). The sequence of therapeutic measures is largely determined by their availability, the time that will be required to implement them.

  • Coping of emotional stress. Significant in this pathology, the role of the emotional factor determines the increased demands on the manner of the doctor's actions. With OA and its precursors, attempts to calm the patient, assessing his condition as relatively innocuous, lead to the opposite result. The patient should make sure that the doctor takes seriously his complaints and condition, acts resolutely and confidently.

  • The patient is seated (with his legs flat).

  • Nitroglycerin 1 - 1.5 mg (2 to 3 tablets or 5 to 10 drops) under the tongue every 5 to 10 minutes under the control of blood pressure until noticeable improvement (rales become less abundant and cease to be heard at the patient's mouth, subjective relief) or to decrease HELL. Possible intravenous nitroglycerin at a rate of 5 - 0 mg per 1 min. In a number of cases, monotherapy with nitroglycerin is sufficient, a noticeable improvement occurs after 5 to 1 5 minutes. If the effectiveness of nitroglycerin is insufficient or impossible, the treatment is carried out according to the scheme below.

  • 1% morphine solution from 1 to 2 ml is injected under the skin or into a vein (slowly, in an isotonic solution of glucose or sodium chloride). If contraindications to the appointment of morphine (respiratory depression, bronchospasm, cerebral edema) or relative contraindications in elderly patients - 2 ml of 0.25'1 ~ solution of droperidol IM or IV under the control of blood pressure are administered.

  • Furosemide - 2 to 8 ml of 1'b solution of IV (do not use with low blood pressure, hypovolemia); At a low diuresis - the control of efficiency by means of a urinary catheter.

  • Apply inhalation of oxygen (nasal catheters or a mask, but not a pillow). In severe cases, AL is breathing under high blood pressure (IVL, anesthesia apparatus).

  • Digoxin solutions 0.025% in a dose of 1 - 2 ml or strofantina - 0.05% in a dose of 0.5 - 1 ml are injected into the vein simultaneously or drip in an isotonic solution of sodium chloride or glucose. According to the indications, they are re-introduced in a half dose after 1 and 2 hours. Limited indications for acute forms of ischemic heart disease.

  • When the alveolar membrane is affected (pneumonia, allergic component) and hypotension, prednisolone or hydrocortisone is used.

  • With mixed asthma with a bronchospastic component, prednisolone or hydrocortisone is administered; Perhaps a slow introduction into the vein of 10 ml of a 2.4% solution of euphyllin (bear in mind the possible threat of tachycardia, extrasystole).

  • According to the indications - suction of foam and liquid from the tracheobronchial tree (electric pump), inhalation of the defoamer (10% solution of antifosilane), antibiotics.

    The treatment is carried out under constant (with a 1-min interval) control of systolic blood pressure, which should not decrease by more than 1/3 from the initial or below 100-110 mm Hg. Art. Particular caution is required when combined with drugs, as well as elderly streets and with high arterial hypertension in the anamnesis. With a sharp decrease in systolic blood pressure, emergency measures (lowering the head, raising legs, starting the introduction of mezaton with the help of a pre-prepared reserve system for drip infusion) are necessary. With low blood pressure, the greatest value in therapy for OL has a long (up to 1 - 2 days or more) administration of large doses (up to 1.5 g / day) of prednisolone and in some cases ventilation under high blood pressure.

    Venous tourniquets on the limbs (alternately for 15 min) or venous bloodletting (200-300 ml) can be recommended as an involuntary replacement of the "internal bloodletting" of redistribution of blood filling, carried out with nitroglycerin, furosemide or (and) ganglioblokatorov. Inhalation of ethyl alcohol vapors is ineffective and is accompanied by undesirable irritation of the mucosa of the respiratory tract. The volume of infusion therapy and the introduction of sodium salts should be limited to the necessary minimum.

    Indications for hospitalization may occur in the precursor stage and after withdrawal from the CA attack.

    The withdrawal from the OL is carried out on site by the specialized resuscitation cardiac ambulance brigade. After removal from the OL, hospitalization is carried out by the same brigade (threat of recurrence of AL).

    For the treatment of SA and OL, see also Myocardial infarction, Heart failure and (in the chapter "Diseases of the respiratory organs"), the AL is not cardiac.

    The prognosis is serious in all stages and is largely determined by the severity of the underlying disease and the adequacy of therapeutic measures. Especially serious is the prognosis with the combination of developed AL with hypotension.