Tests Diagnosis, Treatment and Drugs for Acute Subacute Chronic Constrictive Pericarditis

Diagnosis Treatment and Drugs for Acute Subacute Chronic Constrictive Pericarditis

Pericarditis is an inflammatory lesion of the visceral and parietal layers of the pericardium, and is often part of a systemic disease. It can also be caused by the spread of inflammation in adjacent tissues such as the pleura, myocardium, mediastinum, lymph nodes or damage.

According to the clinical process, it can be divided into three categories:

  1. Acute
  2. Subacute
  3. Chronic Constrictive pericarditis

The course of disease is acute within 6 weeks, subacute within half a year, and chronic over six months. Acute patients are often accompanied by exudate, and chronic patients are prone to pericardial constriction.

 

What is the Cause of Pericarditis?

Most of them are secondary to systemic diseases. Clinically, tuberculosis and non-specificity are common, followed by rheumatism, purulent and viral.

I. Infectiousness of Pericarditis

(i) Tuberculous: Dysentery is more common in children and young people. It often spreads directly from tuberculosis, mediastinal lymphatic tuberculosis and pleural tuberculosis. Or it spreads from blood and lymph. But some can’t find TB lesions.

(ii) Purulent rashes are often secondary to sepsis or sepsis, and bacteria invade the pericardium from bloodstream or lymph. Or the direct spread of purulent inflammation from adjacent tissues such as the lungs, pleura and mediastinum. Pleural surgery, trauma or penetration of foreign bodies into the pericardium can also cause secondary infections. Staphylococcus aureus is the most common pathogenic bacteria, and others such as pneumococcus, hemolytic streptococcus, E. coli and Pseudomonas aeruginosa can cause disease.

(iii) Viral: Coxsackie virus and influenza virus (types A and B) are more common. In recent years, some cases of non-specific pericarditis have been thought to be viral infections.

(iv) Mycotic tadpoles are more common in capsular tissue cytoplasmic bacteria, often secondary to infection in adjacent lungs or hilar lymph nodes, and rarely spread by blood. In addition, there are actinomycetes, candida, and fungi.

(v) The left lobe liver abscess caused by parasitic tadpole amoeba often penetrates into the pericardium and develops acute pericarditis. In addition, occasional infections of microfilaria, schistosomiasis, toxoplasma, etc.

II. What is Non-infectious Pericarditis?

(i) Acute non-specific pericarditis is very common in foreign countries and is also increasing in Asia. The cause may be related to a viral infection, and there is also a manifestation of allergies or autoimmune reactions. Onset is rapid and about half of the patients had upper respiratory tract infections 1 to 8 weeks before the onset. The course of the disease is mostly self-healing from several days to two weeks. A few patients can relapse. Very few patients develop pericardial tamponade or constrictive pericarditis.

(ii) Rheumatic diseases associated with pericarditis. Acute rheumatic fever is often accompanied by pericarditis. This is often part of rheumatic pancarditis and accompanied by other manifestations of rheumatic activities. These are more common in adolescents. Pericarditis can also be found in other rheumatic diseases, such as systemic lupus erythematosus, rheumatoid arthritis, scleroderma, nodular polyarteritis and dermatomyositis, which are often a clinical manifestation of the disease.

(iii) Uremic disease is more common in the late stage of chronic renal failure, often caused by uremia stimulating the pericardium, and its appearance indicates a serious prognosis. If pericardial friction sounds occur in uremic patients undergoing induction therapy, attention should be paid to whether Systemic heparinization measures result in the presence of intrapericardial hemorrhage.

(iv) Myocardial infarction: Acute myocardial infarction under the visceral layer of the pericardium can involve reactive inflammation in the pericardium, which usually occurs in the first 2-3 days after infarction.

(v) Allergic dysentery appears after pericardial trauma, cardiac surgery, heart contusion, or two weeks or more after myocardial infarction. It may be caused by the injury of the pericardial myocardial tissue into an antigen-antibody reaction.

(vi) Tumorous dysentery is often caused by metastatic pericardium of lung cancer, breast cancer and lymphoma, and leukemia can occasionally invade the pericardium.

(vii) Radiation-damaged thoracic breasts receive a radiation dose of more than 1500 Rads, which can cause pericardial inflammatory reactions in the pericardium. The greater the dose, the earlier the pericarditis appears. There are also clinical manifestations of cardiac damage 3 months or even 6 years after irradiation, and myocardium and endocardium can also be damaged and fibrosis.

 

What is the Pathology for Pericarditis?

Can be divided into 2 stages:

  1. Fibrinou
  2. Serous fibrinous

 In the early stage of pericarditis, the parietal and visceral pericardium is hyperemic, swollen and exuded with fibrin, leukocytes and several endothelial cells. Thick exudates can be confined to a single pericardium or cover the entire surface of the heart, making the pericardium. The film becomes rough.

If the exudate increases, a serous fibrinous exudate is formed. The amount of exudate can range from 100ml to 2-3 liters.

The myocardium under the epicardium often has inflammatory changes. When healed, the exudate can be reabsorbed within 2-3 weeks or less, but there is also exudate. Remains for days or years, such as tuberculous pericarditis.

After the pericardial inflammation has dissipated, adhesions of varying degrees may remain. Some two layers of pericardium have a marked thickening and adhesion that completely closes the pericardial cavity, forming a thick scar, compressing the heart and the roots of large blood vessels, affecting the diastole of the heart and becoming chronic contraction, narrow pericarditis.

 

What is the Pathophysiology of Pericarditis?

There is 15-30ml of fluid in the normal pericardial cavity, which plays a lubricating role. When the amount of fluid in the pericardial cavity of pericarditis is not large, it will not affect the heart function. Although a large amount of exudate or the amount of exudate is not too much, such as only 200-300ml, but when the speed is very high. It can also cause the pressure in the pericardial cavity to rise significantly, compress the left and right ventricles, and restrict the diastole and filling of the ventricle. As a result, signs of venous return obstruction, increased venous pressure, insufficient ventricular filling, decrease in systolic blood volume, and decrease in arterial blood pressure are called cardiac tamponade.

In patients with chronic pericardial tamponade, venous congestion is prominent, while in patients with acute pericardial tamponade, arterial pressure is reduced or even shocked.

 

What is Acute Pericarditis?

Acute pericarditis is an acute inflammation of the pericardial visceral and parietal layers. Most of the causes are secondary to systemic diseases. Clinically, non-specific, tuberculosis, rheumatism, myocardial infarction, uremia and tumors are more common. In recent years, due to the widespread use of antibiotic drugs, bacterial and rheumatic sexually decreased, while acute non-specific pericarditis is increasing.

 

What are the Clinical Manifestations of Pericarditis?

Symptoms: Mild and mild can be asymptomatic, so it is easy to be ignored, but generally shows the following performance.

(1) Systemic symptoms: According to different causes and individual reactions, systemic symptoms vary widely. People with infective pericarditis often have symptoms of toxic blood, such as fever, chills, sweating, sleepiness and loss of appetite. The symptoms of non-infective pericarditis are mild, and those with tumor may have no fever.

(2) Pain in the precardiac region is mainly seen in the stage of fibrinous pericarditis. The pain is located in the anterior region of the heart or behind the sternum. It can also be released to the left arm, left shoulder, left scapular region, or upper abdomen. It presents sharp acute pain or heavy stuffiness, which can be exacerbated by breathing, coughing, swallowing and changes in posture.

The pericardial visceral layer has no painful nerves. Only the parietal pericardium below the fifth and sixth intercostal levels on the left has pain fibers. Therefore, pain occurs when pericarditis involves the part or with iliac pleurisy.

Heterosexual pericarditis is often accompanied by pleurisy and is particularly painful. In tuberculous and uremic pericarditis, the pain is mild.

(3) Symptoms of pericardial dysfunction during pericardial tamponade, epigastric swelling, vomiting, and lower extremity swelling may occur due to vena cava stasis. Pulmonary stasis may cause breathing difficulties. Shock symptoms such as paleness and irritability can be seen when the arterial blood pressure drops significantly. A large number of pericardial hydraulic forced airways can cause irritating coughs, such as compression of the lungs or bronchi, which can make breathing difficult. When the recurrent laryngeal nerve and phrenic nerve are compressed, hoarseness and hiccups may appear, and esophageal compression may have difficulty swallowing.

Diagnosis Treatment and Drugs for Acute Pericarditis

What are the Signs of Acute Fibrinous Pericarditis?

(1) Pericardial friction is a typical sign of acute fibrinous pericarditis. The two layers of pericardium are rough due to inflammation and fibrin oozing out. When the heart beats, they rub against each other. Friction sounds often appear on the third edge of the sternum The space between four, five, and five ribs can also cover the front of the heart.

It is easier to hear when sitting and holding your breath after taking a deep breath. Loud friction sounds can be felt in the percussion area.

It usually lasts for a short time. It can exist for several hours, several days, and a few can reach several weeks.

When the pericardial effusion increases and the two layers of pericardium are separated, the friction sound can be weakened or even disappeared.

(2) Pericardial effusion: When the volume of pericardial effusion exceeds 300ml or the effusion occurs rapidly, the following signs may appear:

1. The pericardial effusion, the body’s signs of dullness, expand rapidly to both sides and can change with the body position, such as the lower boundary widens when sitting, the second and third intercostal spaces at the bottom of the heart widen, and the apical pulsation is weakened or disappear.

Heart sounds are distant and heart rate increases. Sometimes early diastolic additional sounds are also heard in the third and fourth intercostal spaces on the left margin of the sternum, also known as pericardial throbbing sounds, forming a three-tone rhythm with the first and second heart sounds. This is because the ventricular dilatation is limited, and blood flow into the ventricle is suddenly blocked. The formation of vortices is produced by impacting the ventricular wall.

2. Pericardial tamponade sign: In acute pericardial tamponade, the cardiac output decreases significantly, the heart rate increases, the pulse is weak, the arterial systolic pressure decreases, and the pulse pressure decreases. In severe cases, shock may occur.

During chronic pericardial tamponade, signs of venous congestion are obvious, jugular veins may be swollen but not pulsating, and are more obvious during the inspiratory phase (Kussmaul sign).

Hepatic jugular vein reflux sign is positive, liver enlargement with tenderness and ascites, and lower limb edema.

Strange pulses can be found, that is, the pulse weakens or disappears during inspiration. The pulse increases or pays attention during expiration, and when auscultation of blood pressure it can be found that the systolic pressure during expiration is higher than that during inspiration by 1.33 kpa.

3. Pericardial effusion of the left lung is mostly from the pericardial cavity on the diaphragm. When the pericardial cavity is filled after the sternum, the expanded pericardial cavity can compress the lungs and bronchi. The left iliac crest can be found during physical examination. There is a dullness zone on the inner and lower side of the ear, accompanied by enhanced tremor and bronchial breathing sounds, also known as Ewart’s sign.

 

What are the Laboratory and other Inspections for of Pericarditis?

I. Laboratory tests to check whether the white blood cell count is increased or not, depending on the disease, the white blood cell count and neutrophils of purulent pericarditis are significantly increased, and the pericardial puncture and fluid extraction can further confirm that the pericardial fluid is exudative, purulent or bloody. Smear and culture may detect the infectious agent, tumor pericardial effusion can detect tumor cells.

II. When X-ray examination of adult pericardial effusion is less than 300ml, there are not many X-ray signs and it is difficult to find. When the effusion reaches 300-500ml or more, the heart shadow will generally expand to both sides, and the heart shadow shape may be changes due to different body positions.

There was obvious dilatation of superior vena cava and blunt palpation angle. When the pericardial effusion exceeds 1000 ml, the heart shadow expands significantly, and the shape is triangular or flask-shaped.

The normal boundaries of each heart marginal bow disappear, and the pulsation of the heart can be seen to weaken or disappear, and the lung field is often clear. X-ray metering or electrocardiography can show that the heart beat is weakened or disappeared.

III. Echocardiographic examination: When the volume of pericardial effusion exceeds 50 ml, M-mode echocardiography shows that when the ventricle contracts, there is a liquid dark area between the posterior wall of the left ventricle and the posterior pericardial wall; if the dark area is in diastole It can also be seen that the volume of effusion is in the range of 400-500ml. Two-dimensional echocardiography.

When there is a moderate volume of effusion in the pericardium, it can be seen that the dark liquid area is evenly distributed on the periphery of the heart. The echocardiographic examination is fast, reliable and easy. Yes, non-invasive, can be repeated at the bedside.

 

What is the Diagnosis and Differential Diagnosis for Pedricarditis?

I. Determine the presence or absence of pericarditis. Acute fibrinous pericarditis can be established based on typical pericardial friction sounds. Exudative pericarditis is based on the above-mentioned pericardial fluid signs. It is generally not difficult to combine the symptoms and signs of pericardial stuffing with X-rays and ECG The diagnosis, especially after the widespread use of echocardiography, is extremely accurate in diagnosing pericardial effusion.

II. The cause of diagnosis different causes of pericarditis, its clinical manifestations and treatment methods are different, so after the diagnosis of pericarditis is determined, the etiology should be further determined.

Tuberculous purulent non-specific rheumatic

Onset is slow and  rapid with rheumatic activity

Primary lesions often have extracardiac tuberculosis, sepsis or internal suppuration, most often upper respiratory infections, often with myocarditis or valvular signs.

Systemic reactions often have symptoms such as low fever, weakness, night sweats, high fever, obvious symptoms of toxemia, low fever or high fever, mild or moderate irregular fever

Chest pain often no often severe cough or chest pain often

Signs: Pericardial friction sounds are rare, may have acute or chronic pericardial tamponade signs Pericardial friction sounds may occur, acute pericardial tamponade signs are likely to be present, pericardial friction sounds are rare. Pericardial tampons are likely to occur.

Blood test Rapid erythrocyte sedimentation Total white blood cells and neutrophils are significantly increased Hematology is normal

  • ESR Normal
  • ESR Increased

Pericardial fluid examination often has a large amount of bloody exudate less grass yellow, concentrated or cultured can be found acid-fast bacillus purulent, smear or culture can be found pathogenic bacteria in small or medium amount. Blood color is often small volume yellow.

Course and Prognosis: Antipyretic drugs have good curative effects, and are easy to form constrictive pericarditis. Timely treatment, good prognosis, untimely treatment, and easy to cause constrictive pericarditis.

 

What is the Pathology for Pericarditis?

Can be divided into 2 stages:

  1. Fibrinous
  2. Serous fibrinous

 In the early stage of pericarditis, the parietal and visceral pericardium is hyperemic, swollen and exuded with fibrin, leukocytes and several endothelial cells.

Thick exudates can be confined to a single pericardium or cover the entire surface of the heart, making the pericardium. The film becomes rough.

If the exudate increases, a serous fibrinous exudate is formed. The amount of exudate can range from 100ml to 2-3 liters.

The myocardium under the epicardium often has inflammatory changes. When healed, the exudate can be reabsorbed within 2-3 weeks or less, but there is also exudate. Remains for days or years, such as tuberculous pericarditis.

After the pericardial inflammation has dissipated, adhesions of varying degrees may remain. Some two layers of pericardium have a marked thickening and adhesion that completely closes the pericardial cavity, forming a thick scar, compressing the heart and the roots of large blood vessels, affecting the diastole of the heart and becoming chronic contraction, narrow pericarditis.

 

What is the Pathophysiology of Pericarditis?

There is 15-30ml of fluid in the normal pericardial cavity, which plays a lubricating role. When the amount of fluid in the pericardial cavity of pericarditis is not large, it will not affect the heart function.

Although a large amount of exudate or the amount of exudate is not too much, such as only 200-300ml, but when the speed is very high, it can also cause the pressure in the pericardial cavity to rise significantly, compress the left and right ventricles and restrict the diastole and filling of the ventricle.

As a result, signs of venous return obstruction, increased venous pressure, insufficient ventricular filling, decreased systolic blood volume, and decreased arterial blood pressure are called cardiac tamponade.

In patients with chronic pericardial tamponade, venous congestion is prominent, while in patients with acute pericardial tamponade, arterial pressure is reduced or even shocked.

 

 What is Acute Pericarditis?

Acute pericarditis is an acute inflammation of the pericardial visceral and parietal layers. Most of the causes are secondary to systemic diseases.

Clinically, non-specific, tuberculosis, rheumatism, and myocardial infarction, uremia and tumors are more common.

In recent years, due to the widespread use of antibiotic drugs, bacterial and rheumatic sexually decreased, while acute non-specific pericarditis is increasing.

 

What are the Clinical Manifestations of Acute Pericarditis?

1. Symptoms: Mild and mild can be asymptomatic, so it is easy to be ignored, but generally shows the following performance.

(1) Systemic symptoms: According to different causes and individual reactions, systemic symptoms vary widely. People with infective pericarditis often have symptoms of toxic blood, such as fever, chills, sweating, sleepiness, and loss of appetite. The symptoms of non-infective pericarditis are mild, and those with tumor may have no fever.

(2) Pain in the precardiac region is mainly seen in the stage of fibrinous pericarditis. The pain is located in the anterior region of the heart or behind the sternum. It can also be released to the left arm, left shoulder, left scapular region, or upper abdomen.

It presents sharp acute pain or heavy stuffiness, which can be exacerbated by breathing, coughing, swallowing, and changes in posture.

The pericardial visceral layer has no painful nerves. Only the parietal pericardium below the fifth and sixth intercostal levels on the left has pain fibers. Therefore, pain occurs when pericarditis involves the part or with iliac pleurisy. Heterosexual pericarditis is often accompanied by pleurisy and is particularly painful. In tuberculous and uremic pericarditis, the pain is mild.

(3) Symptoms of pericardial dysfunction during pericardial tamponade, epigastric swelling, vomiting, and lower extremity swelling may occur due to vena cava stasis. Pulmonary stasis may cause breathing difficulties. Shock symptoms such as paleness and irritability can be seen when the arterial blood pressure drops significantly.

A large number of pericardial hydraulic forced airways can cause irritating coughs, such as compression of the lungs or bronchi, which can make breathing difficult. When the recurrent laryngeal nerve and phrenic nerve are compressed, hoarseness and hiccups may appear and esophageal compression may have difficulty swallowing.

 

What are the Signs of Acute Fibrous Pericarditis?

(1) Pericardial friction is a typical sign of acute fibrinous pericarditis. The two layers of pericardium are rough due to inflammation and fibrin oozing out. When the heart beats, they rub against each other. Friction sounds often appear on the third edge of the sternum The space between four, five, and five ribs can also cover the front of the heart. It is easier to hear when sitting and holding your breath after taking a deep breath. Loud friction sounds can be felt in the percussion area. It usually lasts for a short time, it can exist for several hours, several days, and a few can reach several weeks. When the pericardial effusion increases and the two layers of pericardium are separated, the friction sound can be weakened or even disappeared.

(2) Pericardial effusion: When the volume of pericardial effusion exceeds 300ml or the effusion occurs rapidly, the following signs may appear:

1. The pericardial effusion, the body’s signs of dullness, expand rapidly to both sides, and can change with the body position, such as the lower boundary widens when sitting. The second and third intercostal spaces at the bottom of the heart widen, and the apical pulsation is weakened or disappear. Heart sounds are distant and heart rate increases.

Sometimes early diastolic additional sounds are also heard in the third and fourth intercostal spaces on the left margin of the sternum, also known as pericardial throbbing sounds, forming a three-tone rhythm with the first and second heart sounds. This is because the ventricular dilatation is limited, and blood flow into the ventricle is suddenly blocked. The formation of vortices is produced by impacting the ventricular wall.

2. Pericardial tamponade sign: In acute pericardial tamponade, the cardiac output decreases significantly, the heart rate increases, the pulse is weak, the arterial systolic pressure decreases, and the pulse pressure decreases. In severe cases, shock may occur.

During chronic pericardial tamponade, signs of venous congestion are obvious, jugular veins may be swollen but not pulsating, and are more obvious during the inspiratory phase (Kussmaul sign).

Hepatic jugular vein reflux sign is positive, liver enlargement with tenderness and ascites, and lower limb edema. Strange pulses can be found, that is, the pulse weakens or disappears during inspiration, the pulse increases or pays attention during expiration. When there is auscultation of blood pressure, it can be found that the systolic pressure during expiration is higher than that during inspiration by 1.33 kpa.

3. Pericardial effusion of the left lung is mostly from the pericardial cavity on the diaphragm. When the pericardial cavity is filled after the sternum, the expanded pericardial cavity can compress the lungs and bronchi. The left iliac crest can be found during physical examination. There is a dullness zone on the inner and lower side of the ear, accompanied by enhanced tremor and bronchial breathing sounds, also known as Ewart’s sign.

 

What are Tests for Acute pericarditis?

IV. ECG examination of Acute pericarditis: As the inflammation often spreads to the epicardial myocardium, and extensive myocardial injury-type ECG changes occur, typically early, except for the AVR lead. The ST segment of each lead was generally elevated with the arched back down and recovered after several days to several weeks. Followed by a low or flat T wave, it can last for weeks or days, and it can be restored after the pericarditis disappears. After the occurrence of pericardial effusion, in addition to T changes, there may also be QRS complex low voltages in the limb leads. This may be related to the “short circuit” of the ECG caused by the pericardial fluid.

When there is a large amount of pericardial effusion, the phenomenon of “electrical alternation” may also occur. This is mostly related to the increase of mechanical activity caused by the heart suspended in the pericardial cavity. In addition, sinus tachycardia is often present.

V. Nuclide scan: 125 vein albumin is injected into the iliac vein for blood pool scan.

The nuclide can show the true size of the heart cavity. If the heart shadow in the X-ray film is larger than the scan, it indicates that the part of the blood is increased.

 

What is the Treatment for Pericarditis?

The principle of treatment is: treat the primary disease, improve symptoms and relieve circulation disorders.

i. The general treatment acute stage should be bed rest, breathing difficulties in the semi-recumbent position, oxygen, chest pain can be given analgesics, if necessary, can use codeine or dulandine. There is need to strengthen supportive therapies.

ii. The cause of treatment tuberculous pericarditis is given treatment, the method and course of treatment are the same as tuberculous pleurisy, can also be added prednisone 15-30mg daily to promote the absorption of exudate and reduce adhesions. Rheumatic patients should strengthen anti-rheumatic treatment. Non-specific pericarditis is generally treated symptomatically.

Those with severe symptoms may consider corticosteroids. In addition to the use of sensitive antibacterial drugs, purulent pericarditis should be repeatedly pumped during the course of treatment, or through the trocar into the pericardial cavity A thin plastic catheter is placed for drainage, and antibacterial drugs can be injected into the pericardial cavity if necessary.

If the effect is not good, pericardial incision and drainage should still be performed as soon as possible to control the infection in time to prevent the development of constrictive pericarditis. For uremic pericarditis, dialysis therapy or peritoneal dialysis should be strengthened to improve uremia. At the same time, indomethacin 25-50 mg can be taken 2-3 times a day.

Prednisone 10 mg can be administered orally for 3 days. 4 times. It should be gradually reduced before stopping to prevent recurrence.

  • There is Exudative Pericarditis Heart enlargement.
  • Apical pulsation is located in the heart dullness zone or not obvious
  • Heart dullness world Moves dullness with body position Does not change with body position
  • Heart sounds are low and distant. Except for rheumatics, which may be accompanied by murmurs, generally no murmurs. Heart sounds are often clear and often accompanied by murmurs.
  • X-ray examination Heart shadow is triangular or flask-shaped Lung field is clear Heart shadow is spherical or boot-shaped, lung field is congested
  • Electrocardiogram Low voltage, multi-lead T-wave inversion or flatness with ventricular hypertrophy
  • Echocardiography: Dark dark areas around the heart showing enlarged or enlarged atrioventricular space
  • Contraction time interval normal abnormal

iii. The release of pericardial tamponade, a large amount of exudate or symptoms of pericardial tamponade, can be performed with pericardial puncture and convulsive fluid decompression. Ultrasound should be performed before puncture to understand the needle insertion path and the thickness of the effusion layer that penetrates the pericardium.

 

The puncture sites are:

i. Often in the left fifth intercostal space, about 1-2 cm inside the heart dullness, (or at The needle is inserted at 1-2cm outside the cusp) The puncture needle should be advanced inward and backward, pointing towards the spine, and the patient should take a sitting position.

ii. At the angle formed by the sternal process of the sternum and the left costal margin, the needle point should be upward and slightly backward , Advancing closely behind the sternum, the patient takes a semi-seated position.

iii. For those with suspected right or posterior enveloping effusion, consider using the right 4th intercostal sternal margin for vertical penetration or the 7th or 8th rib of the right back a puncture is performed at the midline of the interscapular shoulder.

To avoid puncturing the heart muscle, the chest lead of the electrocardiograph can be connected to the puncture needle during puncture.

Under the monitoring of ECG oscilloscope and cardiac B ultrasound, if the needle tip touches the ventricular muscle, the ST segment is elevated, but the insulation must be closely checked to prevent the patient from electric shock.

In addition, a “hole ultrasound probe” is used. The puncture needle is inserted through the probe hole.

The puncture can be performed under ultrasonic monitoring, and the position and movement of the puncture needle tip in the fluid cavity can be observed, and the use is completely reliable.

What is the Prognosis for Constrictive Pericarditis?

Rheumatic and non-specific pericarditis rarely cause pericardial tamponade and constrictive pericarditis. Tuberculous, purulent, and radiation-damaged pericarditis are more likely to develop into constrictive pericarditis. Therefore, early diagnosis and timely treatment are needed to prevent development.

 

What is Subacute Exudate Constrictive Pericarditis (Subacute effusive-constrictivepericanditis)?

Subacute osmotic constrictive pericarditis is a special type of lesion with narrowing of the pericardial viscera accompanied by a large amount of pericardial exudate. It can be caused by tuberculosis, recurrent non-specific pericarditis, trauma, radiation, rheumatoid arthritis, uremia, scleroderma and the like. Part of the reason is unknown. Clinical manifestations include both pericardial tamponade and constriction. Odd pulses are more common than constrictive pericarditis.

The X-ray shows that the heart shadow was significantly enlarged, and pericardial calcification was rarely seen. After pericardial injection of gas, the pericardial wall was thickened and the heart shadow was normal or reduced.

ECG diagram QRS low voltage, T wave low or inverted, after pericardial puncture and drainage, the central venous pressure and right atrial pressure remained at the original high level. In the right atrial pressure curve, X tilt or Y tilt are equal. After draining, Y tilt deepened.

The disease often progresses to constrictive pericarditis within a year.

Although treatment with hormones and pericardial puncture can achieve temporary effects, it cannot prevent it from developing into constrictive pericarditis, so the treatment mainly depends on pericardial dissection.

 

 What is Constrictive Pericarditis?

Constrictive pericarditis is a clinical practice of a series of circulatory disorders, such as pericardial inflammation, in which the heart is surrounded by a thick, stiff, fibrotic pericardium, which affects normal ventricular filling, reduces returning blood volume, causes a decrease in cardiac output and venous pressure Performance. The incidence rate is of about 1.6% of the total number of heart disease.

 

What is the Cause of Constrictive Pericarditis?

Partly caused by tuberculosis, purulent, and nonspecific pericarditis. It is also seen in patients with pericardial trauma or rheumatoid arthritis. There are many patients with constrictive pericarditis who have not been able to determine the cause even after a pericardial pathological examination. Pericardial tumors and radiation therapy can occasionally cause the disease.

 

What is the Pathology and Pathophysiology for Constrictive Peicarditis?

In constrictive pericarditis, the visceral and parietal layers of the pericardium are widely adhered, thickened, and calcified, and can be as thick as 0.5 cm. The pericardial cavity is occluded into a fibrous scar tissue shell, which tightly encloses and compresses the entire heart and large blood vessel outlet Office.

Sometimes the lesion is particularly serious at a certain site, such as the atrioventricular sulcus, the superior vena cava entrance, or extensive adhesions to the chest wall and diaphragm.

Some patients can find tuberculous suppurative infection in the pericardial tissue of some patients, and the granulation tissue is hard, thickened and constricted pericardial scars compress the heart, restricting the expansion of the ventricle during diastole, reducing the amount of blood entering the ventricle, thus lowering cardiac output.

Reduced cardiac output can lead to kidney retention of salt and water, which increases blood volume. At the same time, the narrowing of the pericardium makes it difficult for the diastolic blood to flow back into the heart, resulting in increased venous pressure, venous bulging, liver enlargement, ascites, pleural effusion, and lower extremity edema.

The left heart, especially the left atrium, is affected by constriction, which can cause pulmonary congestion and dyspnea.

 

What are the Clinical Manifestations of Constrictive Pericarditis?

Onset is hidden, and pericardial constriction often occurs months to years after acute pericarditis. Patients have varying degrees of dyspnea, abdominal distension, fatigue, dizziness, decreased appetite, cough, weight loss, and pain in the liver area.

Common signs are that the apex beats are not easy to reach, the heart dullness is normal or slightly increased, the first heart sound is reduced, and sometimes an extra diastolic early sound is heard in the third and fourth ribs of the left margin of the sternum.

The loudness changes, sometimes The flapping sound is called the pericardial throbbing sound. Mainly because the ventricle is not fully relaxed, the atrial blood quickly enters the ventricle in the early stage of ventricular diastole, and then the sound caused by the sudden stop of vibration.

The heart rate is fast, and there may be premature beats, atrial flutter, or atrial fibrillation. Heart compression and venous return obstruction can occur. Jugular veins are flared, and flaring is more pronounced during inhalation, with collapse only seen early in diastole (Friedreich sign).

Hepatomegaly, ascites, lower extremity edema, ascites appear earlier and more obvious than lower extremity edema, arterial systolic pressure is reduced, pulse pressure is small, and odd pulses are present.  There is significant increase in venous pressure measurement, often exceeding 2.45kpa (250mmH2O)

 

What are the Laboratory and other inspections for Constrictive Peicarditis?

i. The X-ray examination shows that the size of the heart shadow is normal or slightly larger. The enlarged heart may be due to thickening of the pericardium or accompanied by pericardial effusion. The normal arch of the left and right heart edges disappears. Some patients have calcification in the pericardium in the shape of an eggshell. In addition, the atrium can be seen to be enlarged.

ii. Most of the ECGs have low voltage, sinus tachycardia, a few may have atrial fibrillation, and multiple lead T waves are flat or inverted. Sometimes the P wave is widened or increased as “mitral valve P wave” or “pulmonary P wave” showing left and right atrium enlargement and right ventricular hypertrophy.

iii. Echocardiography: The amplitude of the anterior wall of the right ventricle or the posterior wall of the left ventricle becomes smaller. If there is pericardial effusion at the same time, the thickness of the pericardial wall can be found.

iv. Cardiac catheter examination shows that the average right atrial pressure is elevated, and the pressure curve is “M” or “W” shape. The pressure of the right ventricle is increased. Also elevated.

 

What is the Diagnosis for Constrictive Pericarditis?

If there is a history of acute pericarditis with symptoms and signs of large and small circulation congestion, without significant heart enlargement, small pulse pressure, odd pulses, X-rays show pericardial calcification and the diagnosis is not difficult.

 

What is the Differential Diagnosis for Constrictive Peicarditis?

The disease should be distinguished from portal cirrhosis and congestive heart failure. Cirrhosis has ascites and edema in the lower extremities, but there is no increase in venous pressure and jugular vein distension. Patients with congestive heart failure often have valvular heart disease and characteristic murmurs, and the heart enlarges significantly without singular pulses. Echocardiography and X-ray examination can help identify them.

The hemodynamic changes of constrictive cardiomyopathy are similar to those of constrictive pericarditis, so its clinical manifestations are very similar to those of calcified constrictive pericarditis, which is difficult to identify.

 

What is the Treatment for Constrictive Pericarditis?

Once diagnosed, pericardial detachment surgery should be considered early after the acute symptoms have subsided, so as to avoid myocardial atrophy and affect the efficacy of the operation. Bed rest should be performed before surgery.

Low-salt diet, diuretics as appropriate, supportive therapy should be given to those with anemia and decreased serum protein, and patients with active tuberculosis should be actively treated with anti-TB before and after surgery.

For those with a longer course of disease and more pronounced decrease in cardiac function, a heart-strengthening agent, a small dose of cedilan or digoxin can be given before or after surgery to prevent atrophic heart muscle from developing heart failure after an increased burden.

 Those with pericardial calcification alone without increased venous pressure do not need special treatment, and those with poor response to cardiac tonics or poor liver and kidney function are not suitable for surgery.

  • The disease is treated early with early treatment and better after administration.
  • Constrictive pericarditis Restrictive cardiomyopathy
  • Symptoms and signs progress more slowly and quickly
  • Extra heart sounds and percussive pericardial sounds can be heard
  • Mitral or tricuspid regurgitation incomplete murmurs None More commonly heard
  • X-ray examination Slightly enlarged heart with pericardial calcification in 50% of cases The heart is often significantly enlarged without pericardial calcification

Electrocardiogram Hypotension is more common with T-wave changes and may have atrial fibrillation. Hypotension, T-wave changes and sometimes pathological Q waves. In addition to atrial fibrillation, other arrhythmias are common, such as atrioventricular block, indoor block, visible ventricular hypertrophy or strain.

Echocardiography without ventricular hypertrophy or smaller ventricular cavity.

 

 

 

See Also:

Cardiology

Telemedicine

 

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