Myocardial infarction with pulmonary edema

Myocardial infarction with pulmonary edema is the death of cells in a section of the heart muscle as a result of their necrosis, which develops due to a sharp disruption of intracellular metabolism with a critical decrease or complete cessation of blood circulation in the coronary arteries (ischemia), which is accompanied by the accumulation of blood plasma that has left the vessels in the alveoli and lung tissues. That is, acute heart failure in patients is complicated by a decrease in the respiratory functions of the lungs.

Acute myocardial infarction has the code according to ICD 10 (the latest version of the International Classification of Diseases) – 121; its current complications are assigned the code I23. Acute pulmonary edema in left ventricular failure (cardiac asthma) is coded 150.1.

[ 1 ], [ 2 ], [ 3 ], [ 4 ], [ 5 ]

Causes of myocardial infarction with pulmonary edema

In clinical cardiology, the pathogenesis of myocardial infarction with pulmonary edema (cardiogenic pulmonary edema) is associated not only with sudden blockage or narrowing of the lumen of the coronary artery due to progressive atherosclerosis, but also with increased pressure in the left ventricle of the heart in the presence of diastolic dysfunction.

The heart pumps blood in cycles through alternating rhythmic contractions and relaxations of the heart muscle (myocardium) of the "pumping chambers" - the ventricles. During relaxation (diastole), the ventricle must fill with blood again in order to release it into the bloodstream during the next contraction (systole).

During a heart attack, as well as ischemic heart disease, high blood (arterial) pressure, aortic stenosis, hypertrophic cardiomyopathies, the ventricles become "stiff", i.e. they cannot fully relax during diastole. This occurs due to pathological changes, and in the case of myocardial infarction - partial focal necrosis of muscle fiber cells, which, due to ischemia, lose glycogen, magnesium, potassium, phosphorus and simultaneously accumulate lipids, sodium, calcium and water.

Cardiogenic pulmonary edema, as a result of acute decompensated heart failure, is expressed in blood stagnation in the pulmonary circulation and pulmonary capillaries, increased hydrostatic pressure in them, as well as in the penetration and accumulation of blood plasma "squeezed" from the vessels in the tissue and interstitial space of the lungs. This is a potentially fatal cause of acute respiratory failure in general and in myocardial infarction in particular.

[ 6 ], [ 7 ], [ 8 ], [ 9 ]

Symptoms of myocardial infarction with pulmonary edema

The first signs of myocardial infarction with pulmonary edema noted by doctors are manifested in the form of:

• severe pain behind the breastbone, in the heart area and under the spoon;
• disturbances in heart rate up to paroxysmal ventricular tachycardia (180-200 or more beats per minute);
• increasing general weakness;
• increased blood pressure;
• difficulty breathing (feeling short of breath) when lying down;
• inspiratory dyspnea (when inhaling air);
• dry and then wet wheezing in the lungs;
• cough with sputum production;
• the appearance of cold sweat;
• blue discoloration of the mucous membranes and skin (cyanosis).

After a few hours or a day, the patient’s body temperature rises (not higher than +38°C).

When extravasation of blood cells and subsequent edema affects all lung tissue, which often occurs in left ventricular acute heart failure and myocardial infarction, dyspnea rapidly increases and the disturbance of alveolar gas exchange develops into suffocation.

Then, from the interstitial tissues, the transudate can penetrate directly into the alveolar and bronchial cavities. In this case, the alveoli stick together, and patients experience strong moist rales in the lungs; when exhaling, pinkish foamy sputum appears from the mouth, which can block the bronchi and cause hypoxia with a fatal outcome. And the more foam that forms, the greater this threat.

Consequences

If help arrived in time and was provided correctly, sudden death can be avoided, which occurs due to atrial fibrillation (fibrillation) of the ventricles of the heart or asphyxia. And often the consequences of myocardial infarction with pulmonary edema are manifested by the return of severe chest pain, acute heart failure and interruptions in the work of the heart with tachycardia.

As a result of this type of myocardial infarction, the following may develop:

• cardiogenic shock with a drop in blood pressure, threadlike pulse and subsequent cardiac arrest;
• post-infarction cardiosclerosis – replacement of dead myocardial tissue with scar tissue;
• acute fibrinous pericarditis is an inflammation of the fibrous-serous membrane of the heart, which can progress to exudative pericarditis (leakage of extracellular fluid into the pericardial cavity) and ultimately lead to cardiac tamponade - the accumulation of excessive fluid volume inside the pericardium;
• partial disruption or complete cessation of the conduction of intracardiac electrical impulses (atrioventricular block 2-3 degrees);
• protrusion of the damaged section of the wall of the left ventricle (post-infarction aneurysm) - occurs after several months in approximately 15% of cases;
• pulmonary embolism or pulmonary infarction - obstruction of one of the pulmonary arteries, as a result of which the normal blood supply to the lung tissue stops and their necrosis occurs (with minor areas of damage, over time, the dead tissue is replaced by scar tissue);
• embolic cerebral infarction (cardioembolic stroke).

The prognosis of myocardial infarction with pulmonary edema, given its lethal consequences in 25-30% of cases, cannot be considered favorable. Death occurs as a result of external and internal ruptures of the cardiac muscle tissue of various localizations, which occur with extensive areas of myocardial necrosis, very high blood pressure, untimely (or ineffective) medical care, and in older patients.

[ 10 ], [ 11 ], [ 12 ], [ 13 ], [ 14 ], [ 15 ]

Diagnostics

In most cases, the primary diagnosis of myocardial infarction with pulmonary edema is carried out by emergency physicians based on a fairly pronounced clinical picture of this disease (symptoms are described above).

Hardware or instrumental diagnostics of myocardial infarction with pulmonary edema is carried out by listening to the heart rhythm with a stethoscope and taking ECG readings - electrocardiogram.

After the patient is admitted to hospital (often this is the cardiac intensive care unit), echocardiography (ultrasound of the heart and lungs) or X-ray of the lungs may be performed.

Tests for myocardial infarction with pulmonary edema help determine the extent of the necrotic focus in the myocardium and include a biochemical blood test, based on which doctors determine the level of leukocytes, platelets, fibrinogen in the blood, ESR and pH. The content of specific proteins is determined: albumin, A2-, Y- and G-globulins, myoglobin and troponins. The level of serum creatine phosphokinase-MB (MB-CPK) and transaminases: aspartate aminotransferase (AST) and lactate dehydrogenase (LDH) is also determined.

Differential diagnosis of myocardial infarction with pulmonary edema should be carried out taking into account the similarity of some symptoms in severe internal bleeding, pulmonary embolism, aortic dissection, pneumothorax, acute pericarditis, acute attack of pancreatitis, perforation of gastric ulcer or duodenal ulcer.

[ 16 ], [ 17 ], [ 18 ], [ 19 ]

Treatment of myocardial infarction with pulmonary edema

It should be taken into account that the treatment of myocardial infarction with pulmonary edema is urgent, combining intensive therapy for vital indications (indicatio vitalis) with the simultaneous use of pharmacological drugs that help improve the functioning of the heart muscle and the circulatory and respiratory systems.

Everyone should know that before the ambulance arrives, at the first signs of a heart attack, a person should not be laid down, but placed in a semi-sitting position, and to expand the coronary vessels, 1-2 Nitroglycerin tablets should be placed under the tongue, doing this every 10-15 minutes. It is also necessary to take orally (be sure to chew!) at least 150-160 mg of Aspirin (acetylsalicylic acid).

Doctors also begin providing assistance with intravenous (jet) administration of Nitroglycerin (1% solution, up to 20 mcg per minute). Nitroglycerin acts not only as a vasodilator, but also helps to reduce the return of venous blood to the heart and the need of the heart muscle for oxygen, and also enhances its contractions. To relieve pain, a neuroleptic with anti-shock, antiarrhythmic and adrenolytic effects, Dehydrobenzperidol (Droperidol, Inapsin), is administered intravenously in combination with the powerful analgesic Fentanyl (or their ready-made mixture - Thalamonal). Morphine and Promedol, used to relieve pain, have a depressing effect on breathing.

The relief of pulmonary edema in myocardial infarction (after intravenous administration of Nitroglycerin and narcotic painkillers) is continued by administering humidified oxygen to the patient's respiratory tract (using a mask, nasal cannula or by intubation). To suppress the formation of foam in pulmonary edema, oxygen is administered through gauze moistened with medical alcohol (60-70%); the liquid drug Antifomsilan is used for the same purpose. And intravenous administration of diuretics - Furosemide (Lasix), Bumetanide, Pyretamide or Uregit - allows to reduce the volume of fluid circulating in the body, but they are used only for high blood pressure.

In case of obvious threat or onset of development of cardiogenic shock, emergency therapy includes injections of: Dopamine or Dobutamine (stimulates myocardial contraction, supporting coronary and general circulation), as well as Metoprolol, Isoproterenol, Enalapril, Amrinone - to maintain the rhythm and conduction of the heart.

In resuscitation cardiology, the following medications are used for myocardial infarction with pulmonary edema:

• Anticoagulants (Heparin, Neodicoumarin, Sinkumar) and thrombolytics (Streptokinase, Anistreplase, Alteplase, Urokinase) - to reduce blood clotting, dissolve the thrombus and restore blood flow through the coronary vessels.
• Ganglionic blockers (Nitroglycerin, Sodium Nitroprusside, Pentamin, Benzohexonium) - to reduce the load on the pulmonary circulation.
• Antiarrhythmic drugs (reduce heart rate) - Propafenone, Mexitil, Procainamide, and the anesthetic Lidocaine.

Beta-blockers (Metoprolol, Propranadol, Amiodarone, Atenolol, Solatol) – also have an antiarrhythmic effect.

• Glucocorticosteroids (Prednisolone, Hydrocortisone) - to stabilize cellular and lysosomal alveolar-capillary membranes.
• ACE (angiotensin-converting enzyme inhibitors) - Enalapril, Captopril, Lisinopril, Ramipril - improve blood flow to the myocardium and reduce cardiac stress.
• Antiplatelet agents (Aspirin, Warfarin) - to reduce platelet aggregation and thrombus formation.

If the above medications are ineffective, defibrillation is performed - cardiopulmonary resuscitation using electrical impulses on the heart.

Surgical treatment

Today, surgical treatment of myocardial infarction with pulmonary edema and left ventricular failure involves opening the blocked blood vessel by installing an intra-aortic balloon counterpulsator (balloon coronary angioplasty).

A special catheter equipped with a polyurethane balloon is inserted into the patient's aorta through the femoral (or radial) artery, into the area of atherosclerotic narrowing of the lumen. Using a pump (adjusted by a computer based on ECG readings), helium is pumped into the balloon (at the diastolic phase of the heart's contractile cycle), the balloon inflates, and diastolic pressure in the aorta increases. This increases coronary blood flow, the heart continues to work, but with a much lower load.

When the balloon is deflated, diastolic and systolic pressures, as well as resistance to blood flow, decrease. As a result, the load on the left ventricle and damaged myocardium is significantly reduced, as is its need for oxygen.

To prevent the vessel lumen from narrowing again after the balloon is removed, a stent is installed on the damaged section of the vascular wall – a metal mesh “prosthesis” that holds the vessel from the inside, preventing it from narrowing.

To create a new vessel instead of one blocked by a thrombus and restore coronary blood flow, aortocoronary bypass surgery is performed (no later than 6-10 hours after the infarction, before irreversible changes in the myocardium occur). During this operation, an autoimplant is implanted around the damaged vessel – a section of the subcutaneous vein from the patient’s leg. Another approach is mammary-coronary bypass surgery, in which the internal mammary artery (on the left side) is used as a bypass. As cardiac surgeons note, in case of complete occlusion of the vessel, stent installation is sometimes impossible and then only bypass surgery is performed.

The decision to perform an urgent surgical intervention is made based on the clinical picture of myocardial infarction, ECG data and X-ray examination of the heart pulsation (electrokymography), as well as taking into account the indicators of a biochemical blood test for serum enzymes. But cardiologists consider the results of an X-ray contrast examination of the heart (coronary angiography), which makes it possible to assess the condition of all intracardiac vessels, to be the decisive factor.

Being the method of choice, coronary artery bypass grafting cannot be performed in cases of obliterating coronary endarteritis (atherosclerosis of several coronary arteries), diabetes mellitus, acute inflammatory and oncological diseases.

Folk remedies

What can folk treatment for myocardial infarction with pulmonary edema consist of?

When a person is in intensive care, often on the verge of life and death, no herbal treatment for myocardial infarction with pulmonary edema is simply impossible...

Over time, in the post-infarction period - but only on the recommendation of a doctor - this is acceptable. As a rule, in phytotherapy for cardiological problems, decoctions of the herb motherwort, stinging nettle, marsh cudweed, medicinal sweet clover, fruits and flowers of hawthorn, roots of elecampane are used. Traditional healers advise drinking carrot juice, eating nuts with honey,

As practice shows, homeopathy is not used for myocardial infarction with pulmonary edema.

Although it can be used as an auxiliary method - again, on the recommendation of an experienced physician - during traditional drug treatment of heart disorders, for example, arrhythmia.

[ 20 ], [ 21 ], [ 22 ], [ 23 ]

Prevention

If you ask any cardiologist what the prevention of myocardial infarction with pulmonary edema consists of, the specialist’s answer will consist of several simple points:

• regular physical activity,
• normalization of body weight (i.e. revision of the nutrition system and the range of food products consumed),
• quitting smoking and drinking alcohol,
• timely detection and treatment of atherosclerosis, arterial hypertension, angina pectoris, renal failure and other diseases.

For example, elderly Americans take aspirin to avoid heart attacks, and overseas doctors claim that this reduces the risk of heart attacks by almost a quarter.

They also believe that the main factor of cardiovascular risk is a positive family history of myocardial infarction (including those accompanied by pulmonary edema). Although it has not been possible to identify the genes responsible for the hereditary component of infarction to date. And many researchers have focused on finding new approaches to the prevention and treatment of myocardial infarction with pulmonary edema based on available genetic information.