Killip classification of heart failure

Acute coronary syndrome (ACS) is a complex of clinical signs and symptoms that suggest a patient has a myocardial infarction (MI) or unstable angina (UA). This means that the diagnosis is collective in nature. Establishing a diagnosis of “acute coronary syndrome” requires the initiation of urgent therapeutic and diagnostic measures without waiting for a nosological diagnosis. All forms of ACS are based on the same pathophysiological process: insufficient blood supply to the myocardium due to occlusion of varying degrees of severity of the coronary vessels. The most common cause of occlusion is atherosclerosis.

• Diagnostics
• Electrocardiography
• Heart rhythm disturbances
• Myocardial infarction and its types
• Unstable angina
• Treatment of myocardial infarction with ST segment elevation
• Antiplatelet and anticoagulant therapy in the postoperative period

Myocardial infarction occurs due to rupture or rupture of an atherosclerotic plaque in a coronary artery, which leads to activation of platelets and the formation of a blood clot. Thrombotic coronary artery occlusion with undeveloped collateral arteries usually leads to ST-segment elevation myocardial infarction. A non-occlusive thrombus in the lumen of a large coronary artery, occlusion of a small-caliber coronary artery (diameter 1-2 mm), the presence of unstable atherosclerotic plaques (uneven contours, undermined edges) lead to the development of myocardial infarction without ST-segment elevation or angina. Other causes of occlusion: inflammatory diseases of the coronary arteries, thromboembolism (including iatrogenic ones - during interventions on the coronary arteries), coronary spasm.

OKS includes:

• ST elevation myocardial infarction (STEMI);
• myocardial infarction without ST elevation (STEMI);
• MI diagnosed by changes in enzymes, biomarkers, and late ECG signs;
• Unstable angina.

Diagnostics

ACS should be considered in men over 30 years of age and women over 40 years of age if the main symptom is chest discomfort or pain. Since the pathogenesis of all forms of ACS is similar and differs mainly in the extent and degree of myocardial damage, then clinically (in terms of symptoms) different forms of ACS have similar manifestations, mainly anginal pain.

Pain during ACS must be distinguished from pain during pulmonary embolism, pneumonia, pericarditis, pneumothorax, myocarditis, rib fractures, hypertensive crisis, esophageal spasm, diaphragmatic hernia, renal colic, acute aortic dissection, osteochondrosis. In most cases, anginal pain has obvious characteristic features, which makes it possible to confidently make a preliminary diagnosis:

• According to the patient's description, the pain is of a compressive, sometimes burning nature;
• The pain is most often localized behind the sternum - in its middle and lower parts.
• The pain is diffuse and has a large area on the front surface of the chest.

A well-remembered description of coronary pain is given in his wonderful book “The ABCs of ECG” (author Yu.I. Zudbinov):

“If you combine the above properties of coronary pain and ask the patient to show it, then the patient will describe a circle or several circles at the level of the middle and lower part of the sternum with an open palm, and then clench the spread fingers into a fist. The patient seems to subconsciously indicate a feeling of constriction, compression in the middle lower part of the sternum and diffuse pain. This is the “clenched fist” symptom described by Yushar - one of the reliable signs of coronary pain.”

When it comes to angina, there is an alternation of attacks of pain and periods when the pain goes away completely. Sublingual nitroglycerin (a tablet under the tongue) quickly stops the pain or significantly reduces it. The attack itself has a wave-like character - at first the pain becomes more and more intense, and then subsides. Typically, the duration of an angina attack is 2-7 minutes. Stereotypy is also characteristic - each subsequent attack is practically no different from the previous one.

Myocardial infarction (MI) is characterized by severe pressing or squeezing pain in the chest, often radiating to the left arm and accompanied by fear of death. In general, in terms of its characteristics and localization, pain is similar to angina pectoris, but is more severe, lasts >20 minutes and does not go away with rest or after taking nitroglycerin.

Be sure to ask the patient if he has experienced such pain before, and if so, how did it end? Were there any warning signs such as discomfort in the chest or increased frequency of angina attacks? A gradual increase in pain is characteristic of myocardial infarction.

With pulmonary embolism and dissecting aortic aneurysm, the pain generally occurs abruptly. If there is tearing or stabbing pain radiating to the back, resistant to narcotic analgesics, a dissecting aortic aneurysm should be suspected. Sometimes the patient feels pain during MI only in places of irradiation, and not behind the sternum. For example, quite often epigastric pain is mistaken for gastrointestinal disorders.

Painless forms of MI occur in approximately 20% of patients. They are typical: for elderly patients, patients with diabetes mellitus and in the case of intraoperative development of MI. Other signs of myocardial infarction are shortness of breath, sweating, weakness, dizziness, palpitations, abdominal pain, confusion, nausea, vomiting. Complaints reminiscent of gastrointestinal diseases are especially common with lower infarction.

Causes of AHF

The loss of the heart's ability to contract can be caused by overload of the heart muscle, for example, due to increased blood pressure, a decrease in the number of functioning muscle fibers, heart rhythm disturbances, or the inability to adapt to physical and emotional stress.
The leading causes of AHF are cardiac, associated with pathologies of the heart itself:

1. Acute coronary syndrome (ACS) is a condition caused by a sudden disruption of the blood supply to the heart. It develops with thrombosis of the arteries that supply blood to the heart muscle, narrowing of the heart vessels caused by the presence of atherosclerotic plaques or spasm. It manifests itself as myocardial infarction - irreversible necrosis of the heart muscle and a pre-infarction state, which is not accompanied by a complete cessation of blood supply to the myocardium, but can result in a heart attack. The leading symptoms of ACS are severe chest pain and specific changes in the electrocardiogram (ECG).
2. Hypertensive crisis. It is caused by a persistent increase in blood pressure (BP) and is accompanied by certain symptoms: headache, nausea and vomiting, shortness of breath, visual disturbances, sometimes convulsions, chest pain due to insufficient blood supply to the myocardium.
3. Sudden arrhythmias and heart blocks. The following are considered life-threatening: complete inability to conduct a cardiac impulse to the ventricles of the heart from the atria, when each of them contracts in its own rhythm (AV block), a decrease in the heart rate (HR) to 40 beats/min and below, paroxysmal tachycardia, cardiac arrest . “Precursors” of dangerous arrhythmias are heart rate less than 50 and more than 110 beats/min, frequent extraordinary heart contractions, atrial fibrillation.
4. Severe heart valve defects. They appear against the background of rheumatism and other connective tissue pathologies, atherosclerosis, coronary artery disease (IHD) and severe infections. Various defects lead to overload of the heart with pressure or volume, which creates an obstacle to the release of blood into the circulatory system. With myocardial infarction, ruptures of the tendon structures of the mitral and tricuspid valves are possible with the formation of valvular insufficiency.
5. Acute myocarditis. These are severe inflammatory lesions of the heart muscle caused by viruses or bacteria.
6. Cardiac tamponade. This is the accumulation of blood or other fluid between the layers of the outer lining of the heart, which prevents adequate heart contractions and filling the heart with blood. Tamponade occurs with wounds and trauma to the heart, dissection and rupture of an aortic aneurysm (protrusion), myocardial infarction with rupture of the heart wall (transmural infarction), pericarditis due to infections and cancer. The accumulation of 500 ml of fluid in the pericardial cavity leads to cardiac arrest.
7. Chronic heart failure (CHF) in the stage of decompensation.

Extracardiac causes of AHF are:

1. Thromboembolism of the pulmonary artery (PE) and its branches. The source of pulmonary embolism is thrombosis of the veins of the lower extremities with thrombophlebitis, in the postoperative period, with prolonged immobility of the body and limbs due to injuries (most often).
2. Acute circulatory disorders of the brain, in which the release of vasoactive hormones occurs (they maintain high pressure in the vessels of the lungs).
3. Pneumothorax is the accumulation of air in the chest cavity due to lung diseases and due to chest injuries. With tension pneumothorax, with each inhalation and exhalation, the volume of air in the chest increases, the lung on the affected side collapses, and the heart moves to the opposite side. In this case, the venous return to the heart and the contractile function of the myocardium are disrupted.

Risk factors

Factors that increase the risk of developing acute heart failure include:

• failure to comply with recommendations for the treatment of CHF;
• physical stress and emotional stress;
• severe acute infections and pneumonia;
• an increase in BCC (circulating blood volume) with excessive intravenous drips of drugs (for kidney disease, in patients with CHF);
• renal failure;
• alcohol abuse;
• overdose of drugs with cardiotoxic effect;
• bronchial asthma.

Other diagnostic tests for ACS

• X-ray of the chest organs;
• EchoCG for atypical course. If possible, echocardiography should be performed in all patients with acute MI in order to assess the contractile function of the left ventricle, papillary muscle dysfunction, detect a left ventricular aneurysm, signs of myocardial hypokinesia, etc.;
• Determine: urea, glucose, creatinine, sodium, potassium, blood magnesium, general blood count, prothrombin time, platelet count, fibrinogen, INR, APTT;
• Cholesterol, low-density lipoproteins (LDL) in the blood. This study should be performed within the first 24 hours after MI. When performing analysis at a later date, the results obtained are not counted.

monitoring
, non-invasive blood pressure, pulse oximetry (from the moment of admission) - for 1 day in case of uncomplicated myocardial infarction, and until the condition stabilizes - in case of complicated myocardial infarction. In complicated forms of MI (heart failure, cardiogenic shock), it is possible to use invasive methods of hemodynamic control.

Determining the risk of death

Modern recommendations for the diagnosis and treatment of ACS recommend that, early after the patient’s admission, it is mandatory to determine the probability of the risk of his death, using at least three gradations - high, intermediate, low risk. First of all, this makes it possible to identify patients for whom an invasive strategy for treating ACS would be most effective. But even if the medical institution does not have the appropriate capabilities, it is always useful to know the estimated prognosis, at least in order to determine the correct strategy in communicating with the patient’s relatives.

GRACE scale

Quite a lot of risk stratification scales have been proposed, which have their own advantages and disadvantages (PURSUIT, TIMI, SCORE). They can help the doctor determine the degree of risk and choose the right treatment strategy. Russian recommendations suggest using the GRACE rating scale to assess the risk of death in non-ST segment elevation ACS.

Calculation of points on the GRACE scale can be done manually using the corresponding table, or using a calculator on the website. Risk assessed using the GRACE scale is usually interpreted as:

1. Low risk - mortality less than 1% (when calculated using an automatic calculator), the number of points (when performing manual calculations) is less than 109;

2. Average risk – mortality from 1% to 3% (when calculated using an automatic calculator); number of points (when performing manual calculations) from 109 to 140;

3. High risk – mortality rate more than 3% (when calculated using an automatic calculator); the number of points (when performing manual calculations) is more than 140.

Killip scale

The Killip classification, which characterizes the severity of heart failure (acute or chronic), is a reliable predictor of mortality in patients with ACS.

Classification of acute heart failure according to Killip (Killip T, Kimballe J, 1967)

In most cases, and especially if thrombolytic therapy is planned, central venous catheterization is contraindicated. Morphine has an analgesic, anti-anxiety effect and reduces myocardial oxygen consumption. To reduce the likelihood of side effects (respiratory depression, hypotension), doctors dilute 10 mg of morphine in 10 ml of 0.9% sodium chloride and administer 2-3 ml intravenously at 5-minute intervals, or use a dispenser. Due to the risk of side effects (respiratory depression, hypotension, vomiting), do not administer morphine more than 20 mg/hour. For concomitant obstructive pulmonary diseases, preference is given to fentanyl or promedol.

Non-steroidal anti-inflammatory drugs (NSAIDs) cannot be used for pain relief - they slow down the regeneration of damaged myocardium, increase the risk of its rupture and increase coronary vascular resistance.

Killip classification of heart failure – Wise Doctor

1. Acute left ventricular failure:

• Interstitial pulmonary edema or cardiac asthma:
• Alveolar pulmonary edema.

• Acute right ventricular failure.
• Acute biventricular failure.

According to severity, the following stages of AHF are distinguished (Killip classification):

Stage I – no signs of heart failure.

Stage II – mild AHF: there is shortness of breath, moist fine rales are heard in the lower parts of the lungs.

Stage III – severe AHF: severe shortness of breath, a significant amount of moist rales over the lungs.

Stage IV – a sharp decrease in blood pressure (systolic blood pressure 90 mmHg or less) up to the development of cardiogenic shock. Severe cyanosis, cold skin, clammy sweat, oliguria, blackout.

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Etiology of acute left ventricular heart failure:

1. IHD: acute coronary syndrome (protracted anginal attack, painless widespread myocardial ischemia), acute myocardial infarction (AMI).
2. Mitral valve insufficiency caused by avulsion of the papillary muscle (in AMI) or avulsion of the mitral valve chord (in infective endocarditis or chest trauma).
3. Stenosis of the left atrioventricular orifice associated with a tumor in any of the chambers of the heart (most often left atrial myxoma), thrombosis of the mitral valve prosthesis, or damage to the mitral valve due to infective endocarditis.
4. Aortic valve insufficiency due to rupture of the aortic valves, with dissecting aneurysm of the ascending aorta.
5. Acutely increased heart failure in patients suffering from chronic heart failure (acquired or congenital heart defects, cardiomyopathy, post-infarction or atherosclerotic cardiosclerosis); this may be associated with a hypertensive crisis, paroxysmal arrhythmia, fluid volume overload as a result of inadequate diuretic or excessive infusion therapy.

Etiology of acute right ventricular heart failure:

1. AMI of the right ventricle.
2. Pulmonary embolism (PE).
3. Stenotic process in the right atrioventricular orifice (as a result of a tumor or vegetative growths in infective endocarditis of the tricuspid valve).
4. Asthmatic status.

Etiology of acute biventricular heart failure:

1. AMI involving the right and left ventricles.
2. Rupture of the interventricular septum during AMI.
3. Paroxysmal tachycardia.
4. Acute severe myocarditis.

Pathogenesis . Basic development mechanisms:

Acute left ventricular heart failure.

The main pathogenetic factor is a decrease in the contractility of the left ventricle with preserved or increased venous return, which leads to an increase in hydrostatic pressure in the pulmonary circulation system.

When the hydrostatic pressure in the pulmonary capillaries increases more than 25 - 30 mm Hg. transudation of the liquid part of the blood occurs into the interstitial space of the lung tissue, which causes the development of interstitial edema.

One of the important pathogenetic mechanisms is the foaming of the liquid that enters the alveoli with each breath, which rises upward, filling the bronchi of a larger caliber, i.e. alveolar pulmonary edema develops. So, from 100 ml of sweated plasma, 1 - 1.5 liters of foam are formed.

Foam not only disrupts the patency of the airways, but also destroys the surfactant of the alveoli, which causes a decrease in lung compliance and increases hypoxia and edema.

Clinical picture:

Cardiac asthma (interstitial pulmonary edema) most often develops at night with a feeling of lack of air and a dry cough. The patient is in a forced position of orthopnea. Cyanosis and pallor of the skin, cold sticky sweat. Tachypnea, moist rales in the lower parts of the lungs, muffled heart sounds, tachycardia, accent of the second tone over the pulmonary artery.

Alveolar pulmonary edema is characterized by the development of a sharp attack of suffocation, a cough with the release of foamy pink sputum, “bubbling” in the chest, acrocyanosis, profuse sweating, and tachypnea. There are various moist rales in the lungs. Tachycardia, accent of the second tone over the pulmonary artery.

Acute right ventricular heart failure is a consequence of a sharp increase in pressure in the pulmonary artery system. Given the low prevalence of isolated right ventricular AMI and infectious lesions of the tricuspid valve, as a rule, in clinical practice, acute right ventricular failure occurs in combination with left ventricular failure.

Clinical picture: gray cyanosis, tachypnea, acute enlargement of the liver, pain in the right hypochondrium, swelling of the jugular veins, peripheral and cavitary edema.

Acute biventricular heart failure: symptoms of left and right ventricular failure appear simultaneously.

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Classification of heart failure according to killip

Acute heart failure is one of the most common causes of death in cardiovascular diseases. Very often it develops against the background of another disease and is accompanied by acute clinical manifestations. In the absence of qualified medical care, this condition quickly leads to death.

The classification of acute heart failure is based not only on symptoms, but also on the location of the lesion, the speed and mechanism of development.

The most common causes of AHF are the following diseases and conditions:

• Myocardial infarction. During a heart attack, the blood supply to the myocardium is disrupted, as a result of which the tissue begins to partially die. The most common cause of heart attack is thrombosis. A common consequence of a heart attack is heart failure. Due to myocardial necrosis, the heart cannot sufficiently perform its functions.
• Myocarditis. This is inflammation of the myocardium, which, if left untreated, can also lead to AHF. In acute and severe myocarditis, heart failure develops quickly, which can lead to the death of the patient.
• Trauma and heart surgery. In some cases, surgery and serious chest injuries can lead to the development of acute heart failure.
• Hypertonic disease. Severe hypertension can lead to hypertensive crisis, a condition that is accompanied by a sharp and strong jump in blood pressure. This condition is considered life-threatening and can lead to tissue damage to the heart and brain, severe AHF, and death.
• Pulmonary embolism. In this disease, blood clots block the pulmonary artery, which leads to a sharp increase in arterial and venous pressure and acute heart failure.
• It is worth remembering that AHF can also be caused by a non-cardiac disease, for example, a pulmonary infection, brain injury, or stroke.

The symptoms of AHF differ depending on which ventricle is affected. The most common symptoms are shortness of breath and dry cough, swelling, bluish skin, wheezing in the chest, and foam at the mouth. AHF develops very quickly, so when the first signs appear, it is necessary to take the patient to the hospital as quickly as possible.

Classification according to Killip and clinical severity

The Killip classification is based on the severity of AHF. There are several stages on this scale, which allows you to make a forecast.

The Killip scale is most often used in acute heart failure secondary to myocardial infarction, but can also be used in other forms of AHF.

According to the Killip classification, there are 4 stages of acute heart failure:

• Stage 1. This stage is asymptomatic. In the acute form of the disease, it does not last long, since the rate of development of the disease is high and the first signs begin to appear quite quickly.
• Stage 2. At the second stage, pulmonary circulation disturbances are observed, that is, wheezing appears in the chest, which is clearly audible, and shortness of breath. But at this stage, the symptoms of the disease are still weakly expressed, so AHF can easily be confused with another disease.
• Stage 3. Pulmonary wheezing is heard more clearly, shortness of breath becomes stronger. Moist rales are present in more than half of the lung fields, and pulmonary edema begins.
• Stage 4. At the last stage, cardiogenic shock occurs, when an extreme degree of left ventricular failure is observed, the functioning of not only the heart, but also other organs is disrupted, the blood vessels narrow, blood pressure drops, and the excretory function of the kidneys worsens.

To clarify the stage, not only the clinical picture is often used, but also radiographic data. The prognosis largely depends on the stage of the disease, age and individual characteristics of the patient.

There is another classification, which is based on the development of symptoms of AHF. This is a classification according to Vasilenko, Strazhesko, Lang. There are 3 stages of the disease: the first, initial or hidden, the second pronounced and the third dystrophic.

At the first stage, only mild shortness of breath and rapid heartbeat appear. In the second stage, shortness of breath becomes stronger and is observed even at rest. At the third stage, irreversible changes begin in the internal organs due to circulatory problems.

The classification is based on the clinical manifestations of the pathology and its radiological signs. Based on these data, four stages of pathology are distinguished according to increasing severity:

• I – signs of heart failure do not appear;
• II – in the lower parts of the pulmonary fields, moist rales are heard, signs of pulmonary circulation disorders appear;
• III – moist rales are heard in more than half of the lung fields, severe pulmonary edema;
• IV – cardiogenic shock, signs of peripheral vasoconstriction, cyanosis appear, systolic blood pressure is reduced to 90 mm Hg. Art. and below, sweat appears, the excretory function of the kidneys is impaired.

Consequences and prevention of AHF

Since AHF occurs at lightning speed, the most dangerous consequence is death, which can occur within a few hours or within a few minutes. A prognosis can be given only after resuscitation measures have been provided.

Heart failure itself is already a complication of many heart diseases. In severe form, AHF leads to cardiogenic shock, pulmonary edema and death. The prognosis is almost always unfavorable. About 50% of all cases of AHF result in sudden death. About 17% of all hospitalized patients with AHF die within a year.

This condition is difficult to treat because the consequences are often irreversible. Therefore, doctors recommend not to neglect preventive measures:

1. Regular examination. Twice a year you need to undergo a preventive examination, donate blood, check the condition of the heart and blood vessels, monitor cholesterol levels and blood pressure.
2. Rejection of bad habits. Alcohol and smoking negatively affect the condition of the heart and blood vessels. Bad habits can lead to a number of diseases, so it is advisable to limit them or eliminate them altogether.
3. Proper nutrition. The diet should be balanced and contain enough protein and vitamins to maintain normal heart function. It is also important to monitor your cholesterol levels. If it is consistently elevated, you need to stop eating fatty meat.
4. Moderate physical activity. The development of heart failure is affected not only by physical inactivity, but also by excess weight. It is necessary to move enough, but not to overload. It is recommended to constantly include cardio training in your daily routine, appropriate for your age and health status.
5. Lack of emotional overload. It is advisable to avoid stress and long-term depression.

Examples of diagnostic reports:

1. IHD, large-focal Q-myocardial infarction in the area of ​​the anterolateral wall of the left ventricle dated January 5, 2004. Severity class III (according to Killip). Complications: alveolar pulmonary edema. Concomitant diseases: stage III hypertension, stage III, risk 4. Stage II obesity.

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Heart rhythm disturbances

A wide variety of cardiac arrhythmias occur in ACS and MI. 70% of patients with myocardial infarction die in the first 6 hours! Ventricular fibrillation, ventricular tachycardia, is the most common cause of death. After 12 hours, ventricular fibrillation rarely develops. In case of ventricular fibrillation, defibrillation is carried out with an initial discharge power of 150-200 J for a biphasic defibrillator, and 360 J for a monophasic one. And, if necessary, extensive CPR is carried out according to accepted rules.

To prevent recurrence of fibrillation, amiodarone 150-300 mg is administered intravenously over 20-30 minutes. The daily dose of the drug is 800-1200 mg orally or intravenously. Usually used in combination with beta-blockers. Frequent (more than 5 per 1 minute) polytopic extrasystoles, especially early ones, can lead to ventricular fibrillation. In such cases, amiodarone can be used according to the above scheme.

When should you see a doctor?

In case of acute heart failure, you need to urgently consult a cardiologist to receive help in a hospital setting.

You should not expect dangerous complications from diseases that can lead to AHF. Dyspnea on exertion and at rest, increased blood pressure, any heart rhythm disturbances, chest pain, cough, peripheral edema should alert anyone who has not sought medical help for a full examination and treatment (Fig. 1).

Patients with cardiovascular pathologies and concomitant respiratory infections also need to consult a doctor to prevent severe complications.

Figure 1. When to suspect heart failure and see a doctor. Source: MedPortal

Myocardial infarction and its types

As mentioned above, the diagnosis of MI is made based on the clinical manifestations of the disease, ECG data and the determination of biochemical markers in the blood that reflect necrotic changes in cardiomyocytes. In typical cases, clinical manifestations are quite characteristic:

• Pain suddenly appears behind the sternum and (or) in the heart area of ​​a pressing, squeezing or burning nature;
• Often the pain radiates (“gives”) to the upper limbs, neck, lower jaw, back, epigastric region;
• The duration of pain exceeds 20 minutes. Many patients experience a feeling of fear and cold sweat. Unlike ordinary angina, nitroglycerin does not stop these attacks, or brings only short-term relief.

It is worth noting that modern invasive methods of treating ACS have not only improved treatment outcomes, but also greatly diversified the causes that lead to the development of MI.

Types of myocardial infarction

Thrombolysis is not indicated in patients without ST segment elevation.

Severity classes of patients with myocardial infarction

AHF is a condition that can be life threatening!

Acute heart failure is one of the most common causes of death in cardiovascular diseases. Very often it develops against the background of another disease and is accompanied by acute clinical manifestations. In the absence of qualified medical care, this condition quickly leads to death.

The classification of acute heart failure is based not only on symptoms, but also on the location of the lesion, the speed and mechanism of development.

The most common causes of AHF are the following diseases and conditions:

• Myocardial infarction. During a heart attack, the blood supply to the myocardium is disrupted, as a result of which the tissue begins to partially die. The most common cause of heart attack is thrombosis. A common consequence of a heart attack is heart failure. Due to myocardial necrosis, the heart cannot sufficiently perform its functions.
• Myocarditis. This is inflammation of the myocardium, which, if left untreated, can also lead to AHF. In acute and severe myocarditis, heart failure develops quickly, which can lead to the death of the patient.
• Trauma and heart surgery. In some cases, surgery and serious chest injuries can lead to the development of acute heart failure.
• Hypertonic disease. Severe hypertension can lead to hypertensive crisis, a condition that is accompanied by a sharp and strong jump in blood pressure. This condition is considered life-threatening and can lead to tissue damage to the heart and brain, severe AHF, and death.
• Pulmonary embolism. In this disease, blood clots block the pulmonary artery, which leads to a sharp increase in arterial and venous pressure and acute heart failure.
• It is worth remembering that AHF can also be caused by a non-cardiac disease, for example, a pulmonary infection, brain injury, or stroke.

The symptoms of AHF differ depending on which ventricle is affected. The most common symptoms are shortness of breath and dry cough, swelling, bluish skin, wheezing in the chest, and foam at the mouth. AHF develops very quickly, so when the first signs appear, it is necessary to take the patient to the hospital as quickly as possible.

Unstable angina

Unstable angina (UA) is acute myocardial ischemia due to decreased coronary blood flow, the severity and duration of which is insufficient for the development of myocardial necrosis. But at any time, NS can transform into myocardial infarction. Based on symptoms and ECG data, early treatment clinicians are often unable to distinguish between UA and non-ST-segment elevation MI.

With NS, attacks of coronary pain increase in frequency, duration and intensity, exercise tolerance sharply decreases, and the effectiveness of nitroglycerin decreases. Along with this, ECG changes appear that were previously unnoted. NS also includes post-infarction (recurrent) angina (PS) - the occurrence or increase in frequency of angina attacks within 24 hours and up to 8 weeks after the development of MI.

It is divided into early (up to two weeks) and late post-infarction angina . In the presence of early PS, patient mortality; after myocardial infarction, increases from 2 to 17-50% over the course of 1 year. The main complication directly related to PSC is the expansion of the necrosis zone, observed in 20-40% of such patients.

ECG signs of unstable angina recorded during an attack include depression of the ST segment, less often - its rise above the isoelectric line, the appearance of tall T waves in the chest leads, their inversion, or a combination of these changes. Signs of ischemia are unstable and disappear either soon after the cessation of the attack of pain, less often - over the next 2-3 days.

In fairly common cases, the ECG remains within normal limits. In fact, angina pectoris differs from non-ST segment elevation myocardial infarction (NSTEI) only by the absence of an increase in blood biomarkers of myocardial necrosis in quantities sufficient for the diagnosis of myocardial infarction.

Recently, with the advent of highly sensitive tests (troponins, H-FABP) for markers of myocardial necrosis, the frequency of diagnosing non-ST segment elevation myocardial infarction has increased significantly. This suggests that the difference between these two forms of ACS is quite relative. Treatment of UA and non-ST segment elevation MI, at least with medication, should be the same.

Classification of acute heart failure - severity of the disease

Acute heart failure, AHF, is a polyetiological syndrome in which profound disturbances in the pumping function of the heart occur.

The heart loses its ability to provide blood circulation at the level necessary to maintain the functioning of organs and tissues.

Let's take a closer look at the classification of acute heart failure.

Main types

In cardiology, several methods are used to classify the manifestations of acute cardiovascular failure. Based on the type of hemodynamic disturbance, a distinction is made between congestive and hypokinetic acute heart failure (cardiogenic shock).

Depending on the location of the lesion, the pathology is divided into right ventricular, left ventricular and mixed (total).

Left ventricular

With lesions of the left ventricle, stagnation occurs in the pulmonary circulation. The pressure in the pulmonary artery system increases, and as pressure increases, the pulmonary arterioles narrow. External breathing and oxygen saturation of the blood are difficult.

The liquid portion of the blood begins to leak into the lung tissue or into the alveoli, interstitial edema (cardiac asthma) or alveolar edema develops. Cardiac asthma is also a form of acute failure.

Difficulty breathing is manifested by shortness of breath, increasing to suffocation; in some patients, Cheyne-Stokes breathing is observed (intermittent breathing with periodic stops).

In the lying position, shortness of breath intensifies , the patient tries to sit (orthopnea). In the early stages, moist rales are heard in the lower parts of the lungs, turning into fine rales.

Increasing obstruction of the small bronchi is manifested by dry wheezing, prolongation of exhalation, and symptoms of emphysema. Alveolar edema is indicated by ringing moist rales over the lungs. In the severe stage, the patient's breathing becomes bubbling.

The patient is tormented by a dry cough ; as the pathological condition progresses, scanty sputum is released, turning into foamy sputum. The sputum may be pink in color.

Oxygen starvation provokes an acceleration of myocardial contractions, and the patient develops tachycardia. The skin turns pale, profuse sweat appears, and pronounced cyanosis is observed in the peripheral parts of the body.

Blood pressure levels remain within normal limits or decrease . The left ventricular form develops as a complication of coronary heart disease, myocardial infarction, aortic disease, and arterial hypertension.

Right ventricular

Acute right ventricular failure develops with pneumothorax, decompression sickness, embolism of the trunk or branches of the pulmonary artery, and total pneumonia. When the functions of the right ventricle are impaired, stagnation occurs in the systemic circulation. The patient develops shortness of breath, and upon inhalation, swelling of the jugular veins is noticeable.

The liver enlarges and thickens due to stagnation of blood in the portal system, and becomes painful.

Profuse cold sweat appears, acrocyanosis and peripheral edema appear.

As the swelling progresses, it spreads higher, and effusion of the liquid part of the blood into the abdominal cavity begins - ascites.

In some patients, the functioning of the stomach is disrupted - congestive gastritis develops . Blood pressure drops sharply until cardiogenic shock develops. In response to the progressive lack of oxygen in the tissues, the respiratory rate and heart rate increase.

In total heart failure, symptoms of both forms are observed.

Killip classes

The classification is based on the clinical manifestations of the pathology and its radiological signs. Based on these data, four stages of pathology are distinguished according to increasing severity:

• I – signs of heart failure do not appear;
• II – in the lower parts of the pulmonary fields, moist rales are heard, signs of pulmonary circulation disorders appear;
• III – moist rales are heard in more than half of the lung fields, severe pulmonary edema;
• IV – cardiogenic shock, signs of peripheral vasoconstriction, cyanosis appear, systolic blood pressure is reduced to 90 mm Hg. Art. and below, sweat appears, the excretory function of the kidneys is impaired.

The Killip classification of acute heart failure is designed to assess the patient's condition during myocardial infarction, but can be used in cases of pathological conditions arising for other reasons.

According to clinical severity

Proposed in 2003 to assess the condition of patients with acute decompensation of chronic heart failure. It is based on symptoms of peripheral circulatory disorders and auscultatory signs of congestion in the pulmonary circulation. According to these criteria, four classes of severity of the condition are distinguished:

• I – congestion is not detected, peripheral blood circulation is normal. The skin is dry and warm.
• II – symptoms of blood stagnation in the pulmonary circle are detected, there are no visible signs of impaired venous outflow. The skin is warm and moist.
• III – failure of peripheral circulation is determined without concomitant disturbance of venous outflow in the pulmonary circle. The skin is dry and cold.
• IV – signs of peripheral circulatory failure are accompanied by congestion in the lungs.

There are several possible clinical options for the course of the pathology:

• Decompensated , develops as a complication of a chronic form of pathology or for other reasons. The patient's symptoms and complaints correspond to the typical clinical picture of moderate AHF.
• Hypertensive heart failure . Blood pressure is highly elevated with relatively preserved left ventricular function. There are no signs of pulmonary edema on x-rays. The patient's symptoms and complaints are typical for AHF.
• Pulmonary edema . It manifests itself as disturbances in the rhythm and frequency of breathing, wheezing, orthopnea are heard in the lungs, gas exchange in the lungs is difficult. X-rays confirm fluid accumulation in the lungs.
• Cardiogenic shock . An extreme manifestation of low cardiac output syndrome. Systolic blood pressure drops to critical values, the blood supply to tissues and organs is severely impaired. The patient exhibits symptoms of progressive renal dysfunction.
• Increased cardiac output syndrome . Accompanied by manifestations of blood stagnation in the pulmonary circulation. The patient's extremities are warm, and blood pressure may decrease.
• Right ventricular . Cardiac output is reduced, arterial pressure is increased. The pressure in the jugular veins increases, congestion in the portal system of the liver leads to the development of hepatomegaly.

Any possible classification is, to one degree or another, conditional and is intended to simplify diagnosis and choice of treatment tactics in emergency situations.

Learn more about heart failure in this video:

Source: https://oserdce.com/serdce/serdechnaya-nedostatochnost/ostraya/osnovnaya-klassifikaciya.html

Emergency PCI

Emergency PCI, performed within the first two hours of hospital admission, is indicated in the following group of patients with non-ST segment elevation acute coronary syndrome:

1. The presence of ongoing or recurrent myocardial ischemia;

2. Dynamic changes in the ST segment (depression more than 1 mm or transient elevation (less than 30 minutes) more than 1 mm from the isoline);

3. The presence of deep ST segment depression in leads V2-V4, indicating ongoing transmural damage to the posterior myocardium of the left ventricle;

4. Acute heart failure (III-IV class according to Killip);

5. The presence of life-threatening arrhythmias (ventricular fibrillation, ventricular

tachycardia);

Prevention

Primary prevention includes the prevention of major diseases that can lead to heart failure: coronary artery disease, hypertension, atherosclerosis. In addition to a healthy lifestyle, prophylactic low-dose aspirin and statins may be recommended for people at high risk.

In case of cardiovascular diseases, it is important to carry out secondary prevention measures:

• strictly follow the doctor’s recommendations for the treatment of rhythm disturbances, hypertension, coronary artery disease, correction of heart defects and other causative pathologies;
• reduce excess weight;
• normalize or compensate for impaired types of fat and carbohydrate metabolism with the help of diet therapy, rational physical activity and medications;
• carry out adequate monitoring of target blood pressure, lipid and blood sugar levels, blood coagulation system;
• give up alcohol;
• avoid excessive physical activity and emotional stress.

Emergency prevention includes preventing the occurrence of AHF in patients with cardiovascular diseases: with ARVI, anemia, upcoming surgical interventions, before emotional and physical stress.

All such patients should learn about self-care measures from their healthcare provider.

Later PCI

Late PCI, which is performed within the first 72 hours from the patient’s admission to the hospital, is indicated in the following group of patients with acute coronary syndrome without ST-segment elevation:

• GRACE score <140 but >108 (if calculated manually), estimated mortality rate less than 3% but >1% (if calculated using an automatic calculator);
• Patients without multiple other high-risk criteria who experience relapse of symptoms during intensive drug therapy or who experience the appearance of induced myocardial ischemia during stress testing.

Why is heart failure dangerous? Complications

AHF is a life-threatening condition. The risks of death are especially high with cardiogenic shock (about 80%). If the patient survives after the development of acute heart failure, his quality of life may deteriorate: poor exercise tolerance occurs, any excessive emotions can provoke a heart attack, and severe arrhythmias are possible. To prevent repeated decompensation of cardiac activity, the need for medications usually increases, which increases the drug load on the body. In some cases, serious surgical interventions are required, which are also accompanied by life-threatening risks.

Treatment of myocardial infarction with ST segment elevation

The most common cause of ST elevation infarction is acute myocardial ischemia and necrosis due to coronary artery thrombosis. Two main methods have been developed to restore myocardial perfusion: thrombolytic therapy and surgical myocardial revascularization (using a balloon, or using angioplasty, excimer laser, coronary stenting or coronary bypass surgery).

Percutaneous coronary intervention (PCI) is the preferred method of reperfusion in the first 2 hours after the initial contact of doctors with a sick person. If PCI is not available within these periods for some reason, then thrombolysis must be performed (either in the hospital or at the prehospital stage).

Note that successful reperfusion does not at all mean achieving success in the treatment of MI and can itself contribute to the development of reperfusion damage in the form of:

• Microembolization of the microvasculature with impaired blood flow - the “no reflow” phenomenon;
• Fatal damage to cardiomyocytes that were viable until reperfusion;
• Stunned (stunned) myocardium, i.e. long-term contractile dysfunction of cardiomyocytes;
• A variety of arrhythmias, including potentially fatal ones - fibrillation or ventricular tachycardia.

Doctors need to prepare in advance for the most likely reperfusion complications - cardiac arrhythmias and worsening heart failure. Doctors make sure that the defibrillator is accessible, ready and in working order. Next, you need to draw 10-20 ml of 0.9% sodium chloride and 1 mg of adrenaline into the syringe.

Treatment

AHF is an indication for emergency hospitalization. At the prehospital stage, before the ambulance arrives, it is important to provide assistance on the spot and eliminate additional stress. The patient needs to be seated comfortably, make sure there is an influx of fresh air, and measure blood pressure. When blood pressure is not lower than 100 mm Hg. Art. Give a nitroglycerin tablet under the tongue. To reduce venous return and stress on the heart, you can immerse your legs and arms in hot water. It will be useful to chew an aspirin tablet, and in case of a hypertensive crisis, take an antihypertensive drug.

In a hospital setting, treatment is carried out under constant monitoring of blood pressure, pulse, respiratory rate, saturation, ECG, diuresis, temperature until the condition stabilizes. Monitoring of many indicators in intensive care conditions is carried out through a special device - a cardiac monitor.

The approach to the treatment of AHF is always individual and depends on the form, cause and severity of heart failure, as well as pressure, pulse, saturation, heart rate and other important parameters. In case of cardiac arrest, cardiac massage and defibrillation are performed - “starting” the heart muscle using a high-voltage hardware current pulse.

Oxygen therapy for AHF

Oxygen therapy is the use of oxygen in treatment. It is indicated for insufficient saturation of blood and tissues with oxygen (hypoxia), which is often present in various forms of AHF. In this case, a moistened oxygen-air mixture is used, the composition and flow rate of which is determined by the doctor. In case of pulmonary edema, oxygen is supplied through alcohol or special substances that suppress foaming.

Drug treatment of AHF

Medicines are administered primarily intravenously. Medications used:

1. Narcotic analgesics and sedatives. Suppress pain in acute myocardial ischemia, eliminate panic and fear, promote varicose veins and reduce preload on the heart.
2. Vasodilators. They reduce pre- and afterload on the heart by dilating the veins and small arterioles of the capillary bed, and improve blood supply to tissues. These drugs are not used to lower blood pressure.
3. Diuretics. They have a diuretic effect. They are able to quickly expand veins, eliminate pulmonary edema and reduce pressure in the arteries of the pulmonary and systemic circulation.
4. Fibrinolytic agents for thrombolysis (dissolution of blood clots). Used for myocardial infarction. They are effective during the first 4–6 hours of the development of a heart attack (maximum - up to 12 hours).
5. Anticoagulants prevent blood clots. Indicated for acute ischemia, rhythm disturbances, and risks of pulmonary embolism.
6. Cardiotonic agents and vasopressors. Prescribed to stabilize pressure and increase myocardial contractility. Indicated for severe hypotension, used short-term. They can cause constriction of peripheral blood vessels and impair oxygenation of tissues; they can increase the need for oxygen in the heart muscle.
7. Antiarrhythmic drugs.
8. Beta blockers are used for certain conditions with persistent increases in blood pressure and tachycardia.

If AHF develops against the background of severe diseases of the respiratory system, blood, kidneys, or septic conditions, appropriate treatment of the causative pathology is required.

Indications for reperfusion therapy

Reperfusion therapy should be carried out if no more than 12 hours have passed since the onset of an anginal attack, and the electrocardiogram shows ST segment elevation ≥0.1 mV in at least two consecutive chest leads or in 2 limb leads, or blockade appears LNPG.

The administration of thrombolytics or PCI should be done at the same time when ECG signs of true posterior myocardial infarction (high R waves in the right precordial leads and ST segment depression in leads V1-V4 with an upward T wave). It is recommended to consider the feasibility/possibility of reperfusion even if more than 12 hours have passed since the onset of symptoms (according to the patient), but there is clinical and/or electrocardiographic evidence of ongoing myocardial ischemia. Performing PCI on a completely occluded infarct-causing artery after 24 hours from the onset of clinical symptoms in stable patients is not recommended.

Diagnostic measures

1. Taking anamnesis (simultaneously with diagnostic and therapeutic measures);
2. Examination by an emergency medical technician (paramedic) or a medical specialist from a visiting emergency medical team of the appropriate profile;

1. Registration of an electrocardiogram, decoding, description and interpretation of electrocardiographic data;

For inferior and posterior diaphragmatic infarctions, additionally:

• V2R and V3R registration;

1. Monitoring of electrocardiographic data;

1. If there are atypical ECG signs of myocardial infarction or an atypical clinical picture and the duration of clinical manifestations of the disease is > 2 hours:

• Express examination of troponin levels in the blood;

1. Pulse oximetry;
2. For anesthesiologists and resuscitators:

• Control of central venous pressure (in the presence of central venous access);

1. General thermometry;
2. Diuresis control.

Monitoring

Standard monitoring should be established (non-invasive blood pressure, heart rate, respiratory rate, blood saturation, electrocardiography, body temperature).

Antiplatelet and anticoagulant therapy during percutaneous coronary interventions:

1. As soon as doctors have decided to perform percutaneous coronary intervention (PCI), the patient should be given an oral loading dose of drugs:

• Acetylsalicylic acid – 325-500 mg, chew;
• Plus one of the P2Y12 receptor inhibitors:

— Ticagrelor 180 mg;

— Clopidogrel – 600 mg.

2. The effect of another class of antiplatelet agents, GP IIb/IIIa platelet receptor blockers, develops many times faster. If for some reason a person has not received clopidogrel or ticagrelor in advance, or the effect of these drugs does not have time to manifest itself before the start of PCI, doctors should prescribe abciximab. It is administered as an intravenous bolus of 0.25 mg/kg, followed immediately by an infusion of 0.125 mcg/kg/min (maximum 10 mcg/min). Administration should begin 10-60 minutes before the procedure, continue during it, and for the next 12 hours.

The combination of absiximab with ASA and UFH has advantages over the combination of ASA and UFH during primary transluminal balloon angioplasty (TBA) in patients with STEMI. Monofram has the same mechanism of action as abxiximab, but has a longer half-life and can therefore be administered as a single bolus of 0.25 mg/kg body weight.

3. For patients receiving acetylsalicylic acid and P2Y12 receptor inhibitors who are referred for primary PCI, maintenance therapy with anticoagulants is recommended in the following regimens:

Bivalirudin is the drug of choice as a maintenance anticoagulant during primary PCI. The recommended dose of bivalirudin for adults, including the elderly, is 0.75 mg/kg, administered intravenously as a bolus, followed by an immediate intravenous infusion at a rate of 1.75 mg/kg/hour throughout the entire period of the revascularization procedure.

Heparin (UFH) is administered intravenously as a bolus at a dose of 70-100 IU/kg if the patient is not receiving GP IIb/IIIa platelet receptor blockers, and 50-70 IU/kg if therapy includes drugs of this group.

4. After PCI, long-term use of antiplatelet agents is recommended.

First aid

Instructions for first aid for AHF instruct the patient to act in the following order:

1. Call an ambulance.
2. Open the window (window).
3. Sit in a chair, lean your forearms on the armrests.
4. Measure blood pressure.
5. Take 0.5 mg of nitroglycerin tablets under the tongue. If the nitrate-containing product is a spray, then inhalation is done under the root of the tongue. Capsulated nitrates bite and quickly move the contents under the tongue. If nitroglycerin helps and the symptoms begin to disappear, then it is used every 5-7 minutes until the ambulance arrives. If the result is negative, the medicine is not taken again.

Cardiac glycoside is not used as an emergency self-help drug for acute heart failure. A short-acting drug (glycoside of strophanthus or lily of the valley) can, but not necessarily, be administered intravenously by a visiting cardiologist.

In severe cases and/or when nitroglycerin is ineffective, in a patient with normal or high blood pressure, before the ambulance arrives, the superficial arteries on both thighs can be pulled. This can be done conveniently using waist belts or tourniquets to stop bleeding.

Thigh constriction for AHF should be shallow, not blocking the deep veins

This manipulation will reduce blood flow to the heart, thus making it easier to work with. The constriction can be replaced with a hot foot bath (up to the level of the middle of the shins).

Attention! A patient with AHF is strictly prohibited from standing, moving, drinking water and alcohol, smoking, eating, including liquid food. This can be done only after special permission from the doctor.

It is also worth remembering that nitrates should not be taken if the upper blood pressure is below 100 mmHg, the pulse is less than 50 beats/min, the presence of severe headache and dizziness, as well as with pronounced disturbances in speech, vision and coordination of movements.

Therefore, people with hypertension and coronary artery disease should receive instructions from their treating cardiologist about first medical aid (FAM) for acute heart failure, namely, what medications they should have not only at home, but always with them.

Antiplatelet and anticoagulant therapy in the postoperative period

In the postoperative period, it is recommended to prescribe enoxaparin or fondoparinux for 2-8 days.

Antiplatelet therapy in case of implantation of bare metal stents

Acetylsalicylic acid – 75-100 mg for life;

Clopidogrel – 75 mg once a day or ticagrelor 90 mg twice a day for 12 months.

Antiplatelet therapy in case of implantation of drug-eluting stents

• Acetylsalicylic acid – 160-325 mg 1 time/day for the first 3 months. Starting from the 4th month, the drug is prescribed in a dosage of 75-100 mg 1 time/day for life;
• Clopidogrel – 75 mg once a day or ticagrelor 90 mg twice a day for 12 months.

Thrombolytic therapy

Today, thrombolytic therapy is not the method of choice for the treatment of myocardial infarction. It is performed if primary angioplasty cannot be performed in a given medical institution.

Thrombolysis is also recommended if the patient’s delivery time to the vascular center is more than 2 hours, or the person has signs of pulmonary edema or cardiogenic shock. The sooner therapy is started from the minute symptoms appear, the better the results of thrombolytic therapy will be.

The best time to start thrombolysis is the first half hour after coronary artery thrombosis. Acceptable time is up to 6 hours from the onset of the disease, maximum is up to 12 hours.

ECG indications for thrombolysis : ST segment elevation greater than or equal to 0.1 mV in at least 2 consecutive chest leads or 2 limb leads, or left bundle branch block appears. It is advisable to administer thrombolytics at the same time when there are ECG signs of true posterior myocardial infarction (high R waves in the right precordial leads and ST segment depression in leads V1-V4 with an upward T wave).

Prescription of antiplatelet agents during thrombolysis

Before starting thrombolysis:

Acetylsalicylic acid (ASA) is given to the patient in a dosage of 150-350 mg, it must be chewed. The next day and thereafter, the same remedy is indicated, 75-150 mg 1 time per day. The drug is prescribed for all types of MI. Simultaneously with ASA, it is recommended to use P2Y12 receptor inhibitors - clopidogrel or ticagrelor - to enhance the antiaggregation effectiveness of therapy.

In case of myocardial infarction in patients under 75 years of age, in order to accelerate the development of drug effects on the first day, it is recommended to increase the dose of clopidogrel to 300 mg/day, then switch to the standard dose of 75 mg/day.

For patients over 75 years of age, clopidogrel 75 mg is indicated. A loading dose of the drug is not indicated. Ticagrelor (loading dose 180 mg, then 90 mg twice daily) is prescribed instead of clopidogrel. The duration of taking clopidogrel or ticagrelor is at least 6 months.

Anticoagulant therapy during thrombolysis

Simultaneously with the administration of the thrombolytic drugs listed below, with the exception of streptokinase, the administration of unfractionated or low molecular weight heparin is prescribed.

Depending on the situation, you need to choose one of the options:

• Fondaparinux, a synthetic factor Xa inhibitor, is administered 2.5 mg intravenously before the start of thrombolytic administration. Next, doctors administer a dose of 2.5 mg once a day for 5-8 days. The drug should not be prescribed if the glomerular filtration rate is <30 ml/min;
• Enoxaparin (Clexane):
• If the patient's age is less than 75 years, 30 mg intravenously 15 minutes before administration of the thrombolytic. Then 1 mg/kg subcutaneously (but not more than 100 mg) every 12 hours for 5-8 days;
• If the patient's age is more than 75 years - 0.75 mg per 1 kg of human body subcutaneously every 12 hours for a course of 5-8 days.
• If the glomerular filtration rate is less than 30 ml/min – 1 mg/kg once a day for 5-8 days;
• Doctors administer heparin intravenously with a bolus of 5000 units, and then infusion at a rate of 1000-1200 units/hour for 24-48. Then heparin is prescribed at a dose of 5000 units 3 times a day for a course of 5-8 days with monitoring of the activated partial thromboplastin time.

Symptoms of AHF

The symptoms of acute left ventricular and right ventricular failure are different.

Symptoms of left ventricular AHF

Acute left ventricular failure almost never occurs in healthy people. It is preceded by undetected or inadequately treated hypertension, heart defects, ischemic heart disease with cardiosclerosis, arrhythmias, and myocardial infarction.

Provoking factors may be physical activity, stress, intravenous infusion of an excess volume of dissolved drugs. In some cases, symptoms develop at night due to increased pulmonary congestion or heart rhythm disturbances.

The main manifestations of left ventricular AHF are cardiac asthma, pulmonary edema and cardiogenic shock. These conditions are a consequence of severe stagnation of venous blood in the lungs. They can develop sequentially, accompanied by the following symptoms:

• severe shortness of breath, which can cause suffocation;
• fear of death, dizziness, weakness;
• persistent chest pain;
• forced sitting position with support on hands to facilitate breathing - orthopnea;
• cough is dry, then wet, with foamy pink sputum;
• the skin is pale, covered with cold sweat, there may be a bluish discoloration of the lips, ears, nose;
• pulse is frequent (more than 90 beats/min), weak filling, often arrhythmic;
• Blood pressure may be elevated or normal and decreases as symptoms progress.

Symptoms of right ventricular AHF

With this pathology, “acute cor pulmonale” (ACP) develops. Causes of ULS:

• acute severe diseases of the bronchopulmonary system - a prolonged attack of bronchial asthma, extensive acute pneumonia, total right-sided pleurisy, tension pneumothorax;
• blockage of large branches of the pulmonary artery by blood clots, fat and tumor cells, and air;
• extensive infarction of the interventricular septum with transition to the right ventricle.

Symptoms of acute right ventricular failure include:

• signs of causative diseases;
• sudden shortness of breath and an increase in respiratory rate of more than 20 in one minute;
• pain in the right hypochondrium (when pressure is applied to the liver, the neck veins dilate);
• cyanosis of the skin, rapidly developing swelling of the legs;
• frequent weak pulse, possible bradycardia and decreased blood pressure.