Acute pulmonary heart
- Embolism fat, gas, tumor
- Thrombosis of the pulmonary veins
- Valvular pneumothorax, pneumomediastinum
- lung infarction
- Lobar or total pneumonia
- Severe asthma attack, status asthmaticus
- Cancer lymphangitis of the lungs
- Hypoventilation of central and peripheral genesis (botulism, poliomyelitis, myasthenia gravis)
- Arteritis of the pulmonary artery
- Lung resection
- Massive lung atelectasis
- Multiple rib fractures, sternum fracture (floating chest)
- Rapid accumulation of fluid in the pleural cavity (hemothorax, exudative pleurisy, massive infusion of fluid through a subclavian catheter falsely inserted into the pleural cavity). Risk factors
- Thrombophlebitis of deep veins of the lower extremities
- Postoperative or postpartum period
- Bronchopulmonary pathology.
- Acute development of pulmonary hypertension
- Severe bronchoconstriction
- Development of pulmonary-cardiac, pulmonary-vascular and pulmonary-coronary reflexes – a sharp decrease in blood pressure, deterioration of coronary blood flow
- Acute respiratory failure.
The clinical picture is a sudden deterioration in the patient’s condition within a few minutes or hours against the background of half-way well-being or a stable course of the underlying disease. Sometimes develops at lightning speed
- Sharp shortness of breath, feeling of suffocation, fear of death
- Severe cyanosis, acrocyanosis
- Chest pain
- With PE – pain in the side associated with breathing, hemoptysis
- Swelling of the neck veins
- motor excitation
- Tachycardia 100-160 per minute
- Emphasis of the II tone over the pulmonary artery, increased cardiac impulse, not often arrhythmia (atrial and ventricular extrasystole, atrial fibrillation), sometimes systolic murmur, gallop rhythm
- Decreased blood pressure up to the collaptoid state
- There may be sharp pains in the right hypochondrium due to liver enlargement with the rapid development of right ventricular failure
- Auscultation of the lungs – signs of the pathological process that caused ALS: weakening, absence of breath sounds or bronchial breathing, dry and / or moist rales, pleural rub
- Sometimes there is a discrepancy between the severity of the patient’s condition and the normal results of percussion and auscultation of the lungs.
- In subacute cor pulmonale, the clinical picture differs little from that in ALS, but the increase in symptoms occurs over several days or weeks.
- Hypoxia (decreased p02)
- Hyperventilation (determined by falling pCO2)
- Moderate acute respiratory alkalosis (low pCO2 and elevated pH). Special Studies
- X-ray examination of the organs of the chest cavity
- Signs of pneumothorax, the presence of fluid in the pleural cavity, total pneumonia, atelectasis
- Even with massive embolism, x-ray changes in the lungs may be absent.
- Angiography of the pulmonary vessels – determination of the localization of the thrombus in case of need for emergency embolectomy.
- ECG (especially informative in dynamics)
- Signs of ALS can be mistaken for MI of the posterior wall of the left ventricle Wide and deep Q wave and negative T wave in II, III standard leads, aVF, V, -V2, an increase in R wave amplitude in lead V,, a decrease in the ST segment in standard and chest leads
- Signs of overload or hypertrophy of the right heart: EOS deviation to the right, deep S wave in standard lead I, V5-V6, high R in aVR, shift of the transition zone to the left, P-pulmonale, partial or complete blockade of the right bundle of His bundle
- Arrhythmia (extrasystoles, atrial fibrillation). The differential diagnosis is acute right ventricular failure with right ventricular myocardial infarction.
Treatment: etiological. Treatment is focused on the prevention and treatment of cor pulmonale, focusing on the correction of hypoxia and acidosis, control of hypervolemia and correction of right ventricular failure (if any).
- Oxygen therapy. The initial steps in the treatment of cor pulmonale should include the administration of oxygen and improvement of the patient’s lung ventilatory capacity by correcting the underlying lung disease. Since many patients are sensitive to oxygen, it will be necessary to avoid high concentrations and maintain saturation at 90%.
- Diuresis. Fluid retention is typical and can interfere with pulmonary gas exchange and increase pulmonary vascular resistance. Improved oxygenation and salt restriction
quite enough, but diuretics will not often be needed.
- Phlebotomy provides a short-term effect and may be useful at Ht levels above 55-60%.
- Cardiac glycosides do not give a good effect in the absence of left ventricular failure.
- Vasodilators are widely used, especially in cases mediated by obliterating vascular lesions or pulmonary fibrosis. However, the effectiveness of the products is being questioned.
See also Pulmonary embolism, Chronic pulmonary heart, Secondary pulmonary hypertension, Primary pulmonary hypertension, Bronchial asthma
- ALS — acute pulmonary heart of ICD. 126.0 Pulmonary embolism with mention of acute cor pulmonale