Cardiac asthma and pulmonary edema

CARDIAC ASTHMA (CA) AND LUNG Edema (OL) – is a paroxysmal form of severe breathing difficulty due to sweating in the lung tissue of serous fluid with the formation (intensification) of edema – interstitial (with cardiac asthma) and alveolar, with foaming of a protein-rich transudate (with pulmonary edema) )
Etiology, pathogenesis. The causes of SA and OL 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 heart aneurysm, other chronic forms of IVO, etc.). The main pathogenetic factor – the increase in hydrostatic pressure in the pulmonary capillaries is usually joined by additional attacks that provoke an attack: physical or emotional stress, hypervolemia (hyperhydration, fluid retention), an increase in blood flow to the small circle system when moving to a horizontal position, and a violation of central regulation during sleep and other factors. Accompanying an attack, arousal, a rise in blood pressure, tachycardia, tachypnea, increased work of the respiratory and auxiliary muscles increase the load on the heart and reduce its efficiency. The suction effect of forced inspiration leads to an additional increase in blood supply to the lungs. Hypoxia and acidosis are accompanied by a further deterioration of the heart, a violation
central regulation, increased permeability of the alveolar membrane and reduce the effectiveness of drug therapy.
Symptoms, course.
1. Harbingers of worn-out forms: intensification (appearance) of shortness of breath, orthopnea. Choking, coughing or only soreness behind the sternum with little physical exertion or when moving to a horizontal position. Usually weakened breathing and scanty wheezing below the shoulder blades
2. Cardiac asthma (SA): choking with coughing, wheezing. Orthopnea, forced rapid breathing. Arousal, fear of death. Cyanase, tachycardia, often – increased DD. Auscultatory – against the background of weakened breathing, dry, often – scanty small-bubbling rales. In severe cases – cold sweat, “gray” cyanosis, swelling of the cervical veins, prostration. Swelling of the bronchial mucosa may be accompanied by a violation of bronchial obstruction (“mixed asthma”). A differential diagnosis with bronchial asthma (see) is very important, because with bronchial asthma (as opposed to SA) narcotic analgesics are contraindicated (dangerous) and (-adrenergic drugs are indicated. Anamnesis (heart or lung disease, effectiveness (-adrenergic drugs) and to pay attention to a difficult, elongated exhalation (with bronchial asthma) 3. Resistance to lungs (OL): occurs more or less suddenly, or as a result of an increase in the severity of OA. of wheezing that spreads to the anteroposterior regions of the lungs indicates the developing (“And degree”) OL. The appearance of foamy, usually pink sputum (an admixture of red blood cells) is a reliable sign of OL. Wheezing is clearly audible at a distance (“And! degree”). Other objective and subjective signs as in severe SA (see above). For the 1H stage of AR, severe orthopnea, cold sweat are characteristic. Lightning fast (death within a few minutes), acute (duration of attack from O, b to 2 – 3 hours) and prolonged (up to a day or more) course. Foamy sputum in patients with AR should be distinguished from foamy, often stained blood, saliva secreted during an epileptic seizure and hysteria. Bubbling breathing in extremely difficult (agonizing) patients is not a specific sign of OL.
Treatment – emergency is already at the precursor stage (possible fatal outcome). The sequence of therapeutic measures is largely determined by their availability, the time it takes to implement them. 1. Stopping emotional stress. The significant role of the emotional factor in this pathology determines the increased requirements for the physician’s actions. With OA and its precursors, attempts to reassure the patient, evaluating his condition as relatively harmless, lead to the opposite result. The patient must make sure that the doctor takes his complaints and condition very seriously, acts decisively and confidently. 2. Patient to sit down (with legs down). 3. Nitroglycerin 1-1.5 mg (2-3 tablets or 5-10 drops) under the tongue every 5-10 minutes under the control of blood pressure until a noticeable improvement (wheezing becomes less profuse and ceases to be heard at the patient’s mouth, subjective relief) or to lower blood pressure. Perhaps intravenous administration of nitroglycerin at a rate of 5 – 0 mg per 1 min. In some cases, nitroglycerin monotherapy is sufficient, a noticeable improvement occurs after 5 – 1 5 minutes. With insufficient effectiveness of nitroglycerin or the impossibility of its use, treatment is carried out according to the scheme below. 4. 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 there are contraindications to the use of morphine (respiratory depression, bronchospasm, cerebral edema) or relative contraindications in elderly patients, 2 ml of 0.25’1 ~ solution of droperidol vlm or iv is administered under the control of blood pressure. 5. Furosemide – from 2 to 8 ml of a 1’B iv solution (do not use with low blood pressure, hypovolemia); at low diuresis – control of efficiency with the help of a urinary catheter. 6. Apply oxygen inhalation (nasal catheters or mask, but not a pillow). In severe cases, OL – breathing under high pressure (mechanical ventilation, anesthesia apparatus). 7. Digoxin solutions of 0.025% in a dose of 1 – 2 ml or strophanthin – 0.05% in a dose of 0.5 – 1 ml are injected into a vein simultaneously or dropwise in an isotonic solution of sodium chloride or glucose. According to the indications, they are reintroduced in half dose after 1 and 2 hours. Limited indications in acute forms of coronary heart disease. 8. With damage to the alveolar membrane (pneumonia, allergic component) and with hypotension, prednisone or hydrocortisone is used. 9. In mixed asthma with a bronchospastic component, prednisone or hydrocortisone is administered; perhaps a slow introduction into the vein of 10 ml of a 2.4% solution of aminophylline (keep in mind the possible threat of tachycardia, extrasystopia). 10. According to indications – suction of foam and fluid from the tracheobronchial tree (electric suction pump), antifoam inhalation (10% antifomsilan solution), antibiotics.
Treatment is carried out under constant (with an interval of 1 min) systolic blood pressure control, which should not decrease by more than 1/3 of the original or below 100 – 110 mm Hg. Art. Particular caution is required with the combined use of drugs, as well as elderly streets and with a high history of hypertension. With a sharp decrease in systolic blood pressure, emergency measures are necessary (lowering the head, raising legs, starting the introduction of the mesatone using a previously prepared backup system for drip infusion). With low blood pressure, long-term (up to 1–2 days or more) administration of large doses (up to 1.5 g / day) of prednisolone and, in some cases, mechanical ventilation under high pressure is of greatest importance in the treatment of AL.
Venous tourniquets on the extremities (alternately 15 minutes each) or venous bloodletting (200-300 ml) can be recommended as a compulsory replacement for “internal bloodletting” redistribution of blood supply using nitroglycerin, furosemide or (and) ganglion blockers. Inhalation of ethyl alcohol vapor is ineffective and is accompanied by undesirable irritation of the respiratory tract mucosa. The volume of infusion therapy and the introduction of sodium salts should be limited to the necessary minimum.
Indications for hospitalization may occur at the precursor stage and after withdrawal from an attack of SA.
Withdrawal from the AR is carried out on site by a specialized resuscitation cardiological emergency team. After withdrawal from OL, hospitalization is carried out by the same team (the threat of relapse of OL).
For the treatment of SA and OL, see also Myocardial infarction, Heart failure, and (in the chapter “Respiratory diseases”) OL is not cardiac.
The prognosis is serious at all stages and is largely determined by the severity of the underlying disease and the adequacy of treatment measures. Especially serious is the prognosis with a combination of advanced OL with hypotension.

Leave a Reply

Your email address will not be published. Required fields are marked *