Cardiogenic pulmonary edema is a pathological condition characterized by perfusion of fluid from the pulmonary vessels into the interstitial space and alveoli. It is a consequence of acute heart failure. At the initial stage of the disease, the patient is diagnosed with acrocyanosis, tachycardia, shortness of breath. As the pathology develops, white or pinkish foam begins to stand out from the respiratory tract. Signs of hypoxia are determined. The diagnosis is made on the basis of the clinical picture and anamnestic data. Treatment includes oxygen passed through 70% ethyl alcohol, ventilators, narcotic analgesics, loop diuretics, nitrates. According to the indications, cardiotonics and bronchodilators are used.
I50.1 Left ventricular failure
Cardiogenic pulmonary edema (CPE) is the accumulation of fluid in the pulmonary vesicles or interstitial space. It is usually observed in patients with a cardiological history. It occurs in the form of a transient complication, which can sometimes be stopped at the pre-hospital stage. Regardless of the results of first aid, the patient is subject to hospitalization in the ICU. The frequency of occurrence in men is slightly higher than in women, the ratio is about 7:10. This is due to the somewhat later development of atherosclerosis and coronary pathology in female representatives. Cardiogenic PE can be observed in heart failure of any origin, however, it is more often diagnosed with a weakening of the function of the left ventricle.
Disorders in the work of the heart occur with organic changes in the organ, a significant increase in CBV, under the influence of non-cardiogenic factors. Determining the root cause is an important diagnostic step, since the treatment regimen depends on the etiology of the condition. Among the diseases in which edema of cardiac origin develops are:
- Left ventricular failure (LVF). It is a true deterioration of the contractility of the heart, most often it causes hydrothysation of the lungs. It is observed in myocarditis, acute myocardial infarction localized in the corresponding zone, aortic stenosis, coronary sclerosis, hypertension, aortic valve insufficiency, arrhythmias of various origins, coronary artery disease.
- Increase in CBV. It is noted in acute renal failure, against the background of a violation of the water balance. The liquid injected into the patient intravenously or consumed by him through the mouth is not excreted from the body, a CPE is formed. A similar situation is created with an incorrectly selected volume of infusion therapy, thyrotoxicosis, anemia, cirrhosis of the liver.
- Pulmonary venous obstruction. The reason is organic malformations of the venous system. It is determined with mitral stenosis, abnormal confluence of pulmonary veins, their hypoplasia, formation of vascular membranes, fibrosis. In addition, this condition occurs in the presence of postoperative scars, compression of the vessel by a mediastinal tumor.
- Non-cardiac causes. Cardiac disorders and, accordingly, pulmonary edema can result from acute poisoning with cardiotoxic poisons, disorders of cerebral circulation with damage to areas responsible for the work of the heart and vascular tone, skull injuries. Pathology is often a symptom of shock of any etiology.
Cardiogenic pulmonary edema has two mechanisms of development. With true left ventricular insufficiency, the contractility of the left ventricle weakens. The heart is unable to pump all the blood coming from the pulmonary veins. In the latter, stagnation occurs, hydrostatic pressure increases. The second pathogenetic mechanism occurs during hyperhydration. At the same time, the left ventricle works normally, but its volume is insufficient to accommodate all the incoming blood. The further development of the process does not differ from the true variety of LVF.
There are three stages of the formation of cardiogenic pulmonary edema. At the first stage, there is stretching of large pulmonary vessels, active involvement of venules and capillaries in the process. Then the liquid begins to accumulate in the interstitial space. Interstitial J-receptors are irritated, persistent cough appears. At a certain point, the connective tissue of the lungs overflows with fluid, which begins to sweat into the alveoli. Foaming occurs. Up to one and a half liters of foam is formed from 100 ml of plasma, which is separated outwards through the respiratory tract when coughing.
The attack often begins at night. The patient wakes up with a feeling of suffocation, takes a forced semi-sitting or sitting position with his hands resting on the bed. This position promotes the connection of auxiliary muscles and somewhat facilitates breathing. There is a cough, a feeling of lack of air, shortness of breath more than 25 breaths per minute. In the lungs, dry whistling wheezes, distinguishable from a distance, are heard, breathing is hard. Tachycardia reaches 100-150 beats/min. Upon examination, acrocyanosis is detected.
The transition of interstitial cardiogenic pulmonary edema to alveolar edema is characterized by a sharp deterioration in the patient’s condition. Wheezing becomes moist, large-bubbled, breathing bubbling. When coughing, pinkish or white foam is released. The skin is bluish or marbled, covered with a large amount of cold sticky sweat. There is anxiety, psychomotor agitation, fear of death, confusion, dizziness. The pulse gap between systolic and diastolic blood pressure is decreasing.
The pressure level depends on the pathogenetic variant of the disease. With true insufficiency of the left ventricle, systolic blood pressure decreases to less than 90 mm Hg. Compensatory tachycardia develops above 120 beats per minute. The hypervolemic variant proceeds with an increase in blood pressure, while the increase in heart rate remains. There are compressive pains behind the sternum, which may indicate a secondary attack of coronary heart disease, myocardial infarction.
Complications are mainly associated with hypoxia and hypercapnia. With a prolonged course of the disease, ischemic damage to brain cells (stroke) occurs, which further leads to intellectual and cognitive disorders, somatic disorders. Insufficient oxygen content in the blood causes oxygen starvation of internal organs, which often ends with partial or complete cessation of their activities. The most dangerous is myocardial ischemia, which can result in the development of a heart attack, ventricular fibrillation, asystole. Against the background of cardiogenic edema, sometimes there is the addition of a secondary infection and the occurrence of pneumonia.
A preliminary diagnosis is established by the ambulance team. Differentiation is carried out with pulmonary edema of non-cardiac origin. It is difficult to determine the cause of the disease at the first contact with the patient, since the clinical signs of CPE and pathology of another genesis practically do not differ. The criterion for diagnosis is the presence of a history of chronic heart disease, arrhythmia. In favor of a non-cardiac cause, the presence of thyrotoxicosis, eclampsia, sepsis, massive burns, injuries indicates. In the hospital, the list of diagnostic measures is expanding, the patient is shown the following examinations:
- Physical. During auscultation, dry or wet wheezes are detected, with percussion, the appearance of a “box” sound is noted. With preserved consciousness, the patient takes a forced position, with psychomotor agitation, rushes, does not realize what is happening.
- Laboratory. Signs of hypoxemia and hypercapnia are found in the blood. SpO2 less than 90%, PaO2 less than 80 mmHg, pH less than 7.35, lactate more than 2 mmol/liter. With hyperhydration, the level of CVP exceeds 12 mm of water column. If the cause of the pathology is a heart attack, the concentrations of cardiospecific troponin, CPK and CPK MB increase in the blood.
- Instrumental. ECG shows signs of paroxysmal disorders, acute coronary syndrome, myocardial ischemia (coronary t-wave, ST segment elevation). Radiography indicates a decrease in the pneumatization of the lung fields by the type of a snowstorm, with the alveolar variety, a butterfly-like blackout is visible. On ultrasound of the heart, signs of hypokinesia of the left ventricle are determined.
Therapy at the stage of medical evacuation and in the hospital as a whole does not differ. Outside of the medical facility, some treatment methods may be ignored due to the lack of technical feasibility of their implementation. The purpose of first aid is to eliminate the clinical manifestations of the disease, stabilize the condition, transport to the cardiological intensive care unit. In a medical institution, the complete elimination of pneumonic hyperhydration and the cause that caused it is carried out. The number of therapeutic techniques include:
- Oxygen therapy. During transportation, oxygen passed through 70% alcohol is injected through nasal cannulas. In a hospital setting, it is possible to transfer the patient to artificial ventilation with 100% O2. Alcohol or typhomsilane is used as a defoamer. An invasive ventilator method with tracheal intubation is preferred. Ventilation through the mask is not used due to the high risk of aspiration. To increase the efficiency of the device, the airways are cleaned of foam using an electric pump.
- Dehydration. To relieve the small circle of blood circulation and reduce the CBV, the patient receives loop diuretics in high doses. Furosemide and its analogues are prescribed. The use of mannitol is contraindicated, since at first it increases the flow of fluid into the vascular bed, which leads to an aggravation of the situation. According to the indications, ultrafiltration of blood can be carried out with the selection of the required volume of liquid fraction.
- Analgesia. The drug of choice is morphine. It is administered intravenously under respiratory control. It helps to eliminate pain and anxiety, dilate the vessels of the large circle, reduce the load on the pulmonary veins. With severe psychomotor agitation or pain syndrome, neuroleptanalgesia is used – a combination of a narcotic analgesic with an antipsychotic agent. With SAD below 90 units, drugs and neurotropic drugs are contraindicated.
- Stimulation of the heart. Cardiotonic drugs are used only for true LVF. The drug of choice is dopamine, which is supplied titrated through a syringe pump or an infusion system with a dispenser. To achieve an inotropic effect, doses of less than 5 mg/kg/hour are required. To increase blood pressure, dosages should exceed the specified value. Instead of pressor amines, cardiac glycosides (corglycone, strophanthin) can be prescribed.
- Reduction of OPSS. Nitrates (nitroglycerin) are shown. Medicines of this group contribute to the expansion of peripheral and coronary arteries, facilitate the work of the heart, help reduce blood flow to the lungs. At the stage of transportation, tablet sublingual forms are used, intravenous administration is performed in the hospital.
Cardiogenic edema is treated by a resuscitator. If necessary, the patient is prescribed consultations with a cardiologist or cardiac surgeon, therapist, pulmonologist. During the patient’s stay in the ICU, blood pressure, heart rate, RR, SpO2, and body temperature are monitored around the clock. The biochemical composition of blood is analyzed daily, ABB and electrolytes are determined, markers of acute coronary pathology are measured, if necessary, CVP is measured.
Prognosis and prevention
With the timely start of treatment, the prognosis is favorable, cardiogenic pulmonary edema can be stopped in 95% of cases. Long-term prospects depend on the disease that caused the edema. In the absence of medical care, the patient is highly likely to die from acute circulatory disorders, shock, ischemia of the brain and heart. There are no specific preventive measures. It is necessary to diagnose vascular and heart diseases in a timely manner, use all existing possibilities of their treatment, observe the therapeutic and protective regime recommended by the doctor.