Cardiac and pulmonary edema

Pulmonary edema - acute severe left ventriculardeficiency with pulmonary venous hypertension and alveolar edema. With swelling of the lungs there are pronounced dyspnea, sweating, wheezing and sometimes foamy sputum stained with blood. Diagnosis is established clinically and based on chest radiography data. The treatment uses inhalation of oxygen, intravenous nitrates, diuretics, morphine, sometimes endotracheal intubation and artificial ventilation.

If the filling pressure of the left ventricleincreases suddenly, there is a rapid movement of blood plasma from the pulmonary capillaries into the interstitial space and the alveoli, which causes pulmonary edema. Approximately half of all cases are due to acute coronary ischemia, and a quarter due to decompensation of severe pre-existing heart failure, including heart failure due to diastolic dysfunction due to hypertension. The remaining cases are associated with arrhythmia, acute valve dysfunction, or acute volume overload, often due to intravenous fluids. As reasons, there are also violations of medication and dietary errors.

Patients complain of intense dyspnoea,fussiness and anxiety, a sense of lack of air. Often there is a cough with sputum stained with blood, pallor, cyanosis and severe sweating; some patients have a foam from their mouth. Pronounced hemoptysis is rare. The pulse becomes fast, with low filling, the BP changes. The emerging arterial hypertension indicates a significant cardiac reserve; Arterial hypotension is a threatening sign. Heard crepitation on the breath, scattered on the front and back surfaces over all the pulmonary fields. There may be pronounced wheezing (cardiac asthma). Sound breathing noises often make auscultation difficult. The rhythm of the canter can be determined due to the combination of III (S3 ) and IV (S4 ) of cardiac tones. There are signs of a lack of right ventricle (for example, swelling of the veins of the neck, peripheral edema).

Diagnosis and treatment of pulmonary edema

Exacerbation of COPD can mimic pulmonary edemabecause of the lack of a left ventricle or both ventricles in the event that the patient has a pulmonary heart. Pulmonary edema may be the first clinical manifestation in patients without a history of heart disease, while COPD patients with such severe manifestations have a long history of COPD, although they may suffer from too much shortness of breath, which prevents this complication. The pattern of interstitial edema on emergency chest radiographs usually helps to establish a diagnosis. The content of the brain natriuretic peptide was increased with pulmonary edema and did not change with exacerbation of COPD. Perform also ECG, pulse oximetry and blood tests (examine cardiac markers, electrolytes, urea, creatinine, and in severe patients - gas composition of arterial blood). Hypoxemia can be severe. CO2 delay is a late, threatening sign of secondary hypoventilation.

Initial treatment includes inhalation of 100%oxygen through a mask with a unilateral intake of gas, elevated position of the patient, intravenous administration of furosemide in a dose of 0.5-1.0 mg / kg of body weight. Nitroglycerin 0.4 mg is given under the tongue every 5 minutes, then intravenously dripped at 10-20 μg / min with an increase in dose of 10 μg / min every 5 minutes, if necessary up to a maximum speed of 300 μg / min or systolic BP 90 mm Hg. Art. Intravenous morphine is administered 1-5 mg 1 or 2 times. With severe hypoxia, non-invasive respiratory support with independent breathing and constant positive pressure is used, however, if there is a delay of CO2 or a patient without consciousness, endotracheal intubation and ventilation are used.

Specific complementary therapy depends on the etiology:

  • thrombolysis or direct percutaneous coronary angioplasty with or without stenting with myocardial infarction or other variant of acute coronary syndrome;
  • vasodilators with severe arterial hypertension;
  • cardioversion with supraventricular or ventricular tachycardia and intravenous beta-blockers;
  • digoxin intravenously or with cautionintravenous administration of calcium channel blockers to slow the ventricular rhythm with frequent atrial fibrillation (preference is given to cardioversion).

Other treatment options, eg intravenousthe introduction of MNUG (nesiritide) and new inotropic drugs are under investigation. With a sharp drop in blood pressure or the development of shock, intravenous dobutamine and intra-aortic balloon counterpulsation are used.

After stabilizing the condition, further treatment for heart failure is performed as described above.