Pathogenesis and Pathology for Syphilitic Cardiovascular Disease

Syphilitic Cardiovascular Disease and Cardiogenic Sudden Death

Syphilitic Cardiovascular Disease: It is caused by Treponema pallidum entering the aortic adventitia to nourish blood vessels and cause chronic inflammation and vascular occlusion. Later, aortic middle elastic fibers and muscle layer necrosis and fibrotic scars occur, leading to aortic inflammation, aortic aneurysm, coronary artery stenosis and main coronary arterial valve insufficiency and other lesions appear corresponding clinical manifestations. A few cases can also invade the heart muscle. The disease is an acquired infection, and most of the clinical symptoms and signs of cardiovascular disease begin to appear 10-25 years after infection.


Pathogenesis and Pathology for Syphilitic Cardiovascular Disease

After Treponema Pallidum enters the human body through localized infections, it enters lymph nodes and organs such as liver, spleen, heart and brain through lymphatic vessels.

Due to the ascending aortic lymphoid tissues, the part of Treponema pallidum passes through hilar lymphatic vessels to enter the aortic adventitia. Blood vessels, causing chronic inflammation, hypertrophy and hyaline degeneration of vascular endothelial cells, occlusion of the lumen, fibrosis of the adventitia of the arteries, destruction of middle layer muscles and elastic fibers, and infiltration of plasma cells and local necrosis.

Subaortic fibrous thickening, often accompanied by atherosclerosis in the later stage.

Lesions occur in the ascending aorta and aortic arch, and rarely involve the descending thoracic aorta, common carotid arteries, and abdominal aorta.

The intima of syphilitic aortic inflammation can be smooth or have bark-like wrinkles. Most patients have the main Atherosclerosis. Because the lesion often involves the ascending aortic root, the aortic valve can be enlarged, the aortic valve leaflet is separated, and aortic valve insufficiency occurs.

 The aortic valve leaflet is involved, and the valve leaflet thickens, curls and causes the main. The insufficiency of the aortic valve is further exacerbated, and the aortic middle elastic fibers and muscle layers are necrotic.

The elasticity of the arterial wall disappears and bulges outward, forming an aortic aneurysm. If the lesion involves the aortic sinus, aortic wall fibrous disease can cause coronary artery stenosis. Because the narrowing of the coronary arteries occurs slowly, collateral circulation is often formed, which causes less myocardial infarction, but angina still occurs from time to time.

Treponema pallidum rarely invades the heart directly. Myocardial disease is mainly due to aortic valve insufficiency or coronary artery stenosis caused by myocardial hypertrophy or fibrosis. If accompanied by coronary atherosclerosis, it can often cause myocardial infarction and myocardial gum-like changes. It is extremely rare. Such lesions are mostly confined to the left side of the interventricular septum, the His bundle, and the bundle branch. Diffuse gum-like changes are rare.


Clinical Manifestations of Syphilitic Cardiovascular Disease

According to the site of cardiovascular disease and its characteristics, it can be divided into the following five types clinically:

I. Simple syphilitic aoritis (syphilitic aortitis)

It is generally asymptomatic, with occasional mild chest discomfort, so it is difficult to detect it early in the clinic. Examination revealed that the second heart sound in the aortic valve area was accompanied by a mild jet systolic murmur. X-rays show that the ascending aorta is locally widened and bulging, the aortic contraction and beating are enhanced, and linear calcification is sometimes seen on the aortic wall. With aortic atherosclerosis, calcification often occurs in the aortic arch and is massive.

II. Syphilitic aortic regurgitation

Syphilitic heart disease usually develops symptoms and signs 10-25 years after infection. Aortic valve insufficiency is the most common clinical type. After aortic valve insufficiency, it can remain asymptomatic for 5-6 years or more, or only mild palpitation, shortness of breath, or angina pectoris, the latter Often due to coronary stenosis. Once heart failure occurs, the condition often progresses rapidly, recurrent pulmonary edema, and severely threaten life.

On physical examination, the dullness of the heart dullness often widens to the left, the dullness of the second and third intercostal spaces of the right margin of the sternum widens, and the apex pulse increases.

Auscultation in the second right margin of the sternum, the third intercostal space and the third and fourth intercostal spaces of the sternum may have systolic ejection and diastolic water-repellent murmurs that can be transmitted to the left axilla.

Lighter rumbling diastolic murmur can often be heard in the apical region, which is caused by the relative mitral stenosis due to the aortic insufficiency regurgitation impacting the anterior leaflet of the mitral valve that is opening. This murmur is also called Austin-Flint murmur, which is different from rheumatic mitral stenosis. The former is not accompanied by the first apical hyperthyroidism or valvular sound in the apical region, and there is no pre-systolic enhancement.

The systolic jet murmur heard in the auscultation area of ​​the aortic valve is mainly due to the aortic dilation, which often increases in the early stage of systole. While the murmur caused by rheumatic aortic valve stenosis combined with insufficiency is mostly contracting Late enhancement, often accompanied by a second intercostal systolic tremor of the neck or right edge of the sternum.

The second heart sound in the aortic valve area is hyperactive, weakened or disappeared depending on the extent of the involvement of the aortic valve disease. Inflammation only affects the aortic annulus, the second heart sound in the aortic valve area is hyperactive.

The lesion involves the fibrosis of the aortic valve or the leaflet activity is weakened, the second heart sound in the aortic valve area weakens or disappears, and the apical area in heart failure. We can hear that the diastolic horse runs.

When the aortic insufficiency is severe, the pulse pressure is often increased and the surrounding arteries may have signs of peripheral blood vessels such as gunshots, capillary pulsations and murmurs at the aorta (Duroziez sign).

X-ray examination showed that the heart shadow increased to the lower left and rear, the heart could be in the shape of a boot, the ascending aorta showed a localized enlargement, the electrocardiogram showed left ventricular hypertrophy, and the left chest lead could have ST segment decline and T wave inversion.

III. Syphilitic coronary artery stenosis (Syphilitic Stenosis of Coronary Ostia)

Often accompanied by aortic valve insufficiency. Due to the slow onset of coronary artery stenosis, the coronary arteries often have abundant collateral circulation; therefore, early patients may have no obvious symptoms. Coronary arterial stenosis occurs slowly, angina pectoris may occur in patients with severe coronary stenosis, and some patients may die shortly after the onset of symptoms. The incidence of myocardial infarction is low, but if it is complicated by coronary atherosclerosis, the incidence of myocardial infarction is higher.

IV. Syphilitic aortic aneurysm

Syphilitic aortic aneurysms have different clinical manifestations due to their different locations. The following clinical types are more common:

(1) Ascending aortic aneurysm is also called physical aortic aneurysm. Because aortic ascending aneurysm often enlarges forward, right and upper, it can be asymptomatic during the aortic aneurysm enlargement, although there are obvious signs, But the symptoms are still not very significant. The ascending aortic aneurysm expands forward, which can cause local bulges and pulsations in the first and second intercostal spaces of the right margin of the sternum. Expansion of the aneurysm to the right can compress the superior vena cava and cause facial, upper limb edema and bruising, and thoracic vein distension and compression.

There is shortness of breath and copper-tone cough occur in the right bronchus and right lung, often accompanied by pulmonary infections, and occasional pulmonary arterial compression with symptoms and signs of pulmonary artery stenosis. Ascending aortic aneurysms such as compression of nerves, ribs, or sternum can cause chest pain. The ruptured aneurysm ruptures.

If the aneurysm breaks into the pulmonary artery, a continuous murmur similar to that of an open arterial catheter may appear. If it breaks into the pericardial cavity, symptoms and signs of acute pericardial tamponade may occur, and if it breaks into the chest cavity, sudden death may occur.

(2) Aortic arch aneurysms are called symptomatic aortic aneurysms. Symptoms occur because aortic arch aneurysms can compress the surrounding tissue structure at an early stage. If an aneurysm compresses the esophagus, dysphagia may occur. Facial, upper extremity edema and thoracic vein bulge may appear on the upper vena cava.

On the sympathetic nerve plexus, pupils may shrink on one side and / or the skin may be sweatless on the other side. Hoarseness may occur. Compression of the phrenic nerve may cause perversion and chest pain. Compression of the left bronchus can cause asthma and copper-like cough, and atelectasis and recurrent lung infections due to bronchoconstriction.

If the aneurysm protrudes toward the thorax, a physical examination of the aneurysm shows pulsations in the chest. The heart is generally not enlarged significantly, systolic murmurs can be heard at the site of the ascending aortic aneurysm, and pleural effusion signs can occur when the pulmonary veins and sacral veins are compressed.

 A few patients with aortic arch aneurysms also ruptured into the trachea causing massive hemoptysis and suffocation to death.

(3) Aortic sinus aneurysms Aneurysms and tumors can grow in the three aortic sinuses and grow into the heart, gradually increasing, which can compress nearby tissues and cause narrowing of the right ventricular outflow tract, aortic valve insufficiency, Atrioventricular block or coronary embolism.

When the tumor is not broken, there are usually no obvious symptoms, and it can have palpitations, chest pain, angina, atrioventricular block or aortic valve insufficiency and right ventricular outflow stenosis. The tumor wall becomes thinner and can rupture into the right atrium, right ventricle, pulmonary artery, left atrium, left ventricle or pericardial cavity. Among them, the right aortic sinus aneurysm is most commonly broken into the right ventricle.

When the tumor breaks into the pulmonary artery, right ventricle or right atrium, a loud continuous machine sound-like murmur can be heard in the third and fourth ribs of the left margin of the sternum, which can touch fine tremors, increase the heart dullness, and relax the arterial pressure. The pressure decreases, the pulse pressure increases and water pulses and capillary pulses appear.

(4) Early aortic aneurysms may be asymptomatic or signs early. Large aneurysms such as oppression of the esophagus can cause difficulty swallowing, oppression of the bronchus can cause cough, shortness of breath, and repeated respiratory infections, oppression of the ribs or thoracic spine can cause severe chest pain and pulse can be seen in the posterior chest wall.

(5) Abdominal aortic aneurysms are rare. Compression of the spine or other organs by an aneurysm may cause persistent or paroxysmal epigastric pain. On examination, pulsations and fine tremors were palpable at the tumor site.

V. Myocardial syphilitic tumor (syphilitic gumma of myocardium)

Mainly myocardial gum-like changes, more common are localized lesions, located in the left ventricular septum, without symptoms. If the tumor is located in the bundle of Heath\’s bundle or bundle branch, the ECG may have left bundle branch block, larger myocardial gum-like swelling, which can cause pseudo mitral valve stenosis, corresponding symptoms and signs may appear, and diffuse gum-like changes Can make the heart significantly larger, and eventually, refractory heart failure can occur.


Diagnosis of Syphilitic Cardiovascular Disease

According to the clinical manifestations, there is a history of metallurgical or sexually transmitted diseases, and syphilis is seropositive, and a diagnosis can be made. If there are typical clinical manifestations, but those with negative serotypes, can be used for the treponema pallidum antibody test (borrelia inhibitory activity test, borrelia fluorescent antibody adsorption test). Those who are positive for the above test and have cardiovascular signs should be highly suspected of having syphilitic cardiovascular disease.

Differential Diagnosis of Syphilitic Cardiovascular Disease

1. Syphilitic aortic valve insufficiency needs to be distinguished from rheumatism, arteriosclerosis and other reasons. Rheumatism is younger, and often accompanied by changes in murmur and heart sounds caused by mitral valve disease. In aortic atherosclerosis, the aorta is widely enlarged and often involves the abdominal aorta.

2. Syphilitic thoracic aortic aneurysms need to be distinguished from mediastinal tumors. Thoracic aortic aneurysms are easier to identify if pulsating. However, when there is a large blood clot in the aneurysm, the pulsation is not obvious, and a selective aortic angiography is needed to confirm the diagnosis.

Prognosis of Syphilitic Cardiovascular Disease

If simple syphilitic aorticitis can be treated in time to prevent the disease from progressing, the prognosis is still good. Syphilic aortic valve insufficiency can be asymptomatic before heart failure occurs. Once heart failure occurs, the condition deteriorates rapidly, and the mortality rate is within 3 years. Up to 70%. Those with angina symptoms have a worse prognosis and are at risk of sudden death.


Treatment of Syphilitic Aorticitis

I. Plum Blossom Treatment

(1) Simple syphilitic aorticitis can be administered with 400,000-800,000 units / day of penicillin, intramuscular injection, 10-15 days; those who are allergic to penicillin can take 2-3 g / day of erythromycin, once every 10-20 days Course of treatment.

(2) For syphilitic aortic valve insufficiency accompanied by angina pectoris or heart failure, bismuth preparation should be given before priming. Commonly used bismuth salicylic acid oil 0.1-0.2g / time, intramuscular injection, once every 4 days, and then penicillin treatment after 8-10 times.

The starting dose of penicillin should be small. The first 200,000 intramuscular injection, 2-3 After a day of no response. The dose was gradually increased, 1 million units / day. A course of treatment on the 10th.

 The treatment process should pay attention to the Jarisch-Herxheimer reaction, such as exacerbation of angina pectoris, obvious deterioration of ST-T of the electrocardiogram. You should reduce the dose or suspend the plum-driving treatment.

II. Symptomatic treatment of angina pectoris and heart failure, see relevant sections.

III. Surgical treatment of syphilitic aortic

Syphilitic aortic aneurysm can be performed by tumor resection and blood vessel transplantation. Aortic valve insufficiency can be performed by artificial valve replacement. Coronary stenosis can be treated by coronary endometrial ablation or coronary artery bypass surgery.



Pathology Cause Treatment drugs for Cardiogenic Sudden Death

Section 13:    Cardiogenic Sudden Death

Sudden death is a clinical syndrome. Refers to those who generally appear to have recovered or stabilized their health or illness, and suddenly have an unexpected non-human death. Most occur within 6 hours after the acute onset, and the longest time is less than 6 hours. The main reason is that the heart suddenly stops effectively contracting function due to primary ventricular fibrillation, ventricular arrest or electromechanical separation.


Cause of Cardiogenic Sudden Death

1. Coronary heart disease is the most common cause of sudden cardiac death. Multiple coronary arteries are severely affected. Small coronary arteries have diffuse proliferative lesions. Fresh thrombi form in the coronary arteries, and within the first hour of acute myocardial infarction. Or there may be psychogenic factors such as excessive tension, sadness, fear, etc. All cases have a high incidence of sudden death. More men than women, the incidence rate is also higher in the 30-39 and 40-49 age groups

2. In addition to myocarditis lesions, in addition to myocardial cell edema and necrosis, invasion of the conduction system can cause severe arrhythmias, invasion of coronary arteries can cause stenosis and ischemia, and severe myocarditis can have diffuse myocardial lesions, leading to cardiogenic shock and sudden death.

3. Primary cardiomyopathy includes myocardial hypertrophy, myocardial fibrosis, and scar formation. The lesions mainly invade the ventricle and can also involve the cardiac conduction system. The incidence of ventricular arrhythmias is high. The disease is prone to heart failure.

Digitalis: Many applications, due to myocardial degeneration there are scars and other changes. There is reduced tolerance to digitalis, prone to digitalis toxic arrhythmias, multi-source premature ventricular contractions, ventricular tachycardia, ventricular fibrillation causes sudden death.

More than half of the sudden deaths of hypertrophic cardiomyopathy occur before the age of 20, but can also occur at any age. The risk of sudden death is increased in patients with ventricular septal hypertrophy ≥25mm.

4. Rheumatic heart disease and aortic stenosis can cause sudden death in about 25% of patients, which may be related to ventricular fibrillation caused by insufficient coronary blood supply, cardiac block, and cardio-cerebral ischemia syndrome.

5. The QT interval prolongation syndrome includes congenital deafness, prolonged QT interval, syncope, and is prone to sudden death. The common causes of secondary cases are hypokalemia, quinidine, amiodarone, prolonged QT interval, prolonged vulnerability period, premature ventricular contraction and easy reentry in the vulnerable period to form torsional ventricular tachycardia. .

6. Mitral valve prolapse syndrome is due to mitral valve itself or / and tendon, papillary muscle disease caused by prolapse of one or two leaves of the mitral valve, forming mitral regurgitation, and the corresponding systole.

The clinical syndrome consisting of murmurs and karales, due to increased myocardial stress, often causes tachyarrhythmias, such as short-term atrial fibrillation or ventricular tachycardia, about 1% of sudden deaths occur, and the following signs are often present before sudden death, and ventricular Premature beats, T-wave abnormalities, late or full systolic murmurs, syncope and most often die of ventricular tachycardia or ventricular fibrillation.

7. Congenital heart disease-coronary artery malformation, such as the left coronary artery originates from the right coronary sinus or is connected to the right coronary artery. Fallot’s quadruple symptoms can cause sudden death in severe pulmonary stenosis before surgery.

8. Pre-excitation syndrome with atrial fibrillation. The shorter the bypass refractory period, the more likely it is to become malignant arrhythmia-ventricular fibrillation and sudden death.

9. Sick sinus node syndrome mostly due to coronary disease, myocarditis, cardiomyopathy, sinus node artery ischemia, degenerative changes, sinus node ischemia, necrosis, fibrosis. Severe slow arrhythmia can cause ventricular fibrillation.


Pathology for Cardiogenic Sudden Death

I. Histological changes in the heart of sudden death from coronary heart disease

(1) Chronic lesions include the formation of myocardial scars, which can have reticular, dendritic, flaky, and stellate forms. In addition, thickening of the intima of the intermuscular arterioles is rare, especially in cases with hypertension.

(2) Acute myocardial infarction. Rissenan pointed out that half of the sudden death patients had early myocardial infarction. Lie proposed that autopsy confirmed that acute death with acute myocardial infarction was about 10-30% in recent years.

(3) Pre-infarct lesions include:

i. Significant microcirculation disorders such as arteriolar dilatation, stasis, bleeding, and edema, and arterial spasm causing microthrombosis.

ii. Disorders of myofibrillar contraction, the most common of which is wavy degeneration. This kind of change is characterized by thinning and stretching of muscle fibers, forming a wavy shape in parallel arrangement. Another type of change is myofibrosis and myocardial rupture.

2. Pulmonary embolism is a typical cardiovascular disease that causes sudden death. Larger emboli mechanically block the pulmonary artery and its larger branches, causing right ventricular dysfunction and insufficient coronary perfusion. At the same time, pulmonary embolism causes vagus nerve excitement, as well as pulmonary artery, Coronary and bronchial artery smooth muscles have spasms that exacerbate asphyxia and myocardial ischemia. In addition, catecholamine and serotonin are released in large quantities, which promotes vasospasm and myocardial ischemia.


Pathogenesis for Cardiac Sudden Death

1. Myocardial infarction and sudden death In the sudden death of coronary heart disease, most of the coronary arteries may have more serious lesions. The detection rate of acute, especially old myocardial infarction is high. The compensatory function of such myocardium is on the verge of failure. At this time, if some incentives occur, such as excessive fatigue, mental stress, and the release of large amounts of catecholamines to increase myocardial oxygen consumption, it will suddenly make the blood demand and blood supply incompatible, leading to acute circulatory failure sudden death, such a situation in sudden death of coronary heart disease More common.

2. Metabolic dysfunction and sudden death. Such patients often have no obvious history of heart disease or clinical symptoms, and no obvious damage and necrosis of the myocardium. The coronary arteries are occasionally mildly sclerotic, but the presence of this mild disease makes the arteries sensitive. Sexual increase, easy to cause reflex convulsions due to various inducements.

i. Due to spasm and ischemia, stress intracardiac and epicatecholamines are released in large amounts, and a large amount of Ca2 + influx in the myocardium, which significantly strengthens the slippage of myofibril filaments, causing a large amount of ATP in the myocardium and spasm of myofibrils. Simultaneous contraction causes ventricular fibrillation and morphologically, It shows wavy degeneration, contraction band formation, and even myocardial rupture.

ii. After severe myocardial ischemia in coronary artery spasm, the metabolism of the myocardial well-perfused area and the ischemic area are significantly different, showing lactic acid accumulation in the ischemic area, local acidosis, K + outflow, potassium deficiency and membrane potential in myocardial cells in the ischemic area decrease. When it reaches -60mv, the fast Na + channel is inactivated and the slow channel activates Ca2 + inflow. This reaction makes the myocardial cell polarization rate in the ischemic area much slower than normal and the ECG activity is delayed.

Intermittent and asynchronous electrical activity occurs between ischemic myocardium and healthy myocardium, as well as between myocardium with different degrees of ischemia. For example, when the adjacent area has repolarized, the ischemic area is still activated, and as a result, the adjacent myocardium is activated.

It causes frequent repeated reentry excitement, causing localized small ventricular fibrillation in the area of ​​ischemic myocardium with increased autonomy, which directly causes the entire ventricular fibrillation, or the rapid and repeated reentry of this ischemic area and adjacent tissue areas, causing frequent Ventricular premature beats, ventricular tachycardia and even ventricular fibrillation. Some people call it “heart self-killing” or “cardiac instability” and “cardiac failure”.

Variant angina pectoris, reperfusion after coronary artery occlusion, reperfusion after coronary artery spasm disappears, myocardial collateral circulation is established, and coronary reperfusion can cause ventricular fibrillation or sudden death due to this mechanism.


3. Platelet microthrombosis and sudden death Haxerem found most platelet microthrombosis in small arteries and veins in the myocardium of the sudden death group, especially in the transient death group. It is believed that platelets aggregated to form a large number of microthrombs during acute stress.

The latter affects myocardial microcirculation, causing myocardial ischemic dysfunction and sudden death. Some people have confirmed that thromboxane A2 (Thromboxane (R) A2), which is synthesized and released by platelets, has a strong role in promoting blood coagulation and vasoconstriction, and can increase myocardial ischemia and necrosis.

Normal vascular intima can synthesize prostacyclin PGI2, which has the opposite effect of thromboxane A2, is a strong platelet aggregation inhibitor, and has the effect of expanding coronary arteries.

At present, it is believed that secondary to certain causes cause normal coronary arteries. Imbalance of systolic and diastolic balance, such as atherosclerosis, decreased PGI2 synthesis in the intima of arteries, weakened antithrombin A2 effect, vasoconstriction, myocardial ischemia, promote platelet adhesion and aggregation, resulting in microthrombosis of vascular intima.

This microemboli formation can also be seen in the large amount of catecholamines injected into the arteries. This proves that catecholamines are strong guides for platelets. This can degranulate and agglutinate platelets, which exacerbates spastic contraction of myocardial ischemia.


4. The conduction system lesions and sudden death causes of the conduction system lesions are:

i. Acute necrosis and inflammatory cell infiltration; seen in myocardial infarction, myocarditis or cardiomyopathy.

ii. Conductive fiber atrophy and fibrosis are seen in chronic coronary heart disease, primary double bundle branch fibrosis, or severe aortic and mitral valve disease.

iii. The sclerosis and occlusion of the blood supply arteries of the conduction system occur in coronary heart disease and polyarteritis.

iv. The ectopic, dysplasia and degeneration of the conduction system are seen in congenital heart malformations and sudden cardiac death in infants.

v. The degenerative changes of the peripheral nervous tissues of unknown conduction system are seen in the QT interval prolongation syndrome. When the pathological changes of the conduction system are sufficient to cause severe complete atrioventricular block, the ventricular rhythm can be unstable, and ventricular fibrillation can easily occur due to various reasons.

5. Non-arrhythmic sudden cardiac death, also known as “electromechanical separation”

i. Preload reduction; seen in the heart or aorta rupture.

ii. Afterload is too heavy, for example, acute outflow tract obstruction caused by pulmonary embolism.

iii. Pump failure or sympathetic reflex inhibition, such as large myocardial infarction or severe cardiomyopathy, can cause mechanical separation.


Clinical Manifestations of Cardiogenic Sudden Death

Sudden death may occur without any warning. Some patients have mental stimuli and / or emotional fluctuations before sudden death. Some patients may have pain in the precardiac area, which may be accompanied by dyspnea, palpitations, extreme fatigue, or acute myocardial infarction. Premature ventricular contractions.

When sudden death occurs, the heart loses effective contraction for 4-15 seconds, and fainting and convulsions can occur. The breathing slows down, becomes shallow, and stops. Heart sounds disappeared, blood pressure side was not reached, pulse could not be touched, cyanosis appeared on the skin, pupils dilated, and reaction to light disappeared.

Some patients may make unusual snoring noises before death, but some may die quietly during sleep. If the ECG is performed in time, the following three manifestations can occur:

i.                  Ventricular fibrillation (or flutter) wave pattern.

ii.               Ventricular arrest, ECG straight or only atrial wave.

iii.            ECG mechanical separation, the ECG showed a slowly deformed QRS wave, but did not produce effective myocardial mechanical contraction.

Diagnosis of Cardiogenic Sudden Death

The diagnosis of sudden death and cardiac arrest can be based on the following clinical manifestations:

i.             Sudden onset of syncope or convulsions.

ii.             First appeared wheezing-like dyspnea with cyanosis, and then stopped breathing.

iii.           The aortic pulse disappears

iv.            The heart sound disappears

v.             Dilated pupils. Make a diagnosis.

Rescue of Sudden Death

Once a diagnosis of sudden death is made, rescue should be carried out immediately.


I.                  Cardiopulmonary Resuscitation

(1) Tap the anterior region of the heart. Use the fist to strike three times in the anterior region of the heart. For patients who have just suffered a cardiac arrest, some of them can be re-beated. If they do not re-beat, they can immediately perform chest heart compression.

(2) Chest compression on the patient lies on a hard bed or on the floor. The operator places the root of the left hind palm on the second half of the lower half of the patient’s sternum, places the right palm on the back of the left hand, and presses rhythmically with both hands. With the help of the body’s pressing force, you can press 60-70 times per minute rhythmically to avoid excessive rib fractures.

(3) Mouth-to-mouth respirators hold the neck of the patient with one hand to tilt the head back as far as possible to keep the airway open; hold the patient’s nostril with the other hand, and blow deeply into the patient’s mouth after deep breathing. Press the heart 4-5 times, and make artificial mouth-to-mouth respiration.

(4) ECG examination and establishment of venous channel and ECG examination to clarify arrhythmia for symptomatic treatment.

1. Treatment of ventricular fibrillation:

i. External non-synchronous DC defibrillation, generally 300WS (watt-second).

ii. Drug defibrillation; 300 mg of procaine hydrochloride, or 100-200 mg of lidocaine plus 1 mg of epinephrine, and 1 mg of atropine can also be added. Those who cannot defibrillate should continue to press the heart, and can use 250mg bromobenzylamine in 40ml of 5% glucose solution and intravenous injection (5min). Procainamide can also be used repeatedly.

2. Ventricular arrest and ventricular autonomic rhythm can be injected intracardiacly with 1 mg of epinephrine or 0.3-0.5 mg of isoproterenol, and continue cardiac compression.

Those who fail the above treatments can use artificial heart pacing.

(5) Correction of acidosis: At the same time of cardiac compression, 100ml of 5% sodium bicarbonate should be injected intravenously quickly, and basic drugs should be given according to the blood gas analysis results.

(6) Respiratory stimulants: When spontaneous respiration is restored, respiratory stimulants such as sylvia, colamine, etc. may be given.

Management after CPR


(I) Recovery of Heart Rhythm, Blood Pressure and Heart Work

1. Management of arrhythmia: Patients with repeated ventricular arrest or abnormally slow ventricular rate, or recurrent ventricular tachycardia or ventricular fibrillation should be treated in time. Paroxysmal ventricular tachycardia can be converted by synchronous DC first.

Drug therapy can be given by intravenous bolus of lidocaine and procainamide, which can be maintained by intravenous drip after heart rhythm recovery. Severe sinus bradycardia associated with cardiac arrest can be treated with atropine or isoproterenol. When drug treatment fails, artificial heart pacing can be used. Specific dose, method see arrhythmia section.

2. Treatment of hypotension: Hypotension occurs after resuscitation for many reasons, such as severe acidosis, insufficient blood volume, weak myocardial contraction, and respiratory insufficiency. For hypotension itself, m-hydroxylamine or dopamine or hydrocortisone can be administered intravenously.

3. Management of heart failure: Pay attention to the patient\’s heart function. Sudden cardiac death patients often have heart failure and heart failure. During the resuscitation, heart failure worsens or pulmonary edema occurs. Depending on the condition and the availability of digitalis preparations, cedilan or digoxin can be given. For doses and usage, see Heart Failure .

(II) Prevention and treatment of pulmonary infection: To keep the airway open, to clear the secretions of the respiratory tract, to prevent lung infections, and to give antibiotics if there are signs of lung infections.

(III) Prevention and treatment of cerebral hypoxia To reduce the damage of cardiac arrest to brain tissue, cerebral edema should be prevented as soon as possible.

Specific method: Try to protect the brain with ice cap as early as possible (within 5 minutes) for selective head cooling. If the patient is unconscious, artificial hibernation can be given to keep the temperature low and maintain circulation. Protect the heart, brain, kidneys, and prevent brain edema. At the same time, dehydration therapy can be given.

 After recovery of heartbeat, intravenous injection of 20% mannitol 250ml and dexamethasone 5-10mg can be given every 8 hours, and medication can be adjusted after 3 days or when cerebral edema improves.

(4) Prevention and treatment of renal insufficiency: Correct shock or hypotension as soon as possible, correct acidosis, and apply diuretic and dehydrating agents such as mannitol and furosemide in the early stage.


Prevention of Cardiogenic Sudden Death

I. Prediction of risk factors for sudden cardiac death

The risk factors of coronary heart disease are: hypercholesterolemia, hypertension, smoking, diabetes, obesity, and the ST segment of the ECG down at rest. Sudden death is often caused by ventricular fibrillation, so arrhythmia is inferred as a risk factor for sudden death. Holter ECG monitoring showed that 90% of patients with sudden death had ventricular premature beats.

(1) Clinical Significance of Ventricular Premature Beat Classification

Class 0: No ventricular premature beats

Level 1: Ventricular premature beats <30 beats / hour

Level 2: Ventricular premature beats> 30 beats / hour

Level 3: Multi-source premature ventricular contractions

Grade 4A continuous paired ventricular premature beats

Grade 4B has more than 3 consecutive ventricular premature beats (ie, short array ventricular tachycardia)

Grade 5 R R


Ruberman et al. Monitored patients with complex ventricular premature beats (Grade 3, 4, 5) at three times the risk of sudden death than those without such arrhythmias. It was observed that 2035 patients with acute myocardial infarction and ventricular premature beats had higher mortality rates during the first three years than those without ventricular premature beats. The more ventricular premature beats, the greater the risk of sudden death.

(2) Multiple lesions of coronary heart disease, severe stenosis (> 70%), obvious myocardial ischemia, and high incidence of sudden death.

(3) unstable angina pectoris, premature ventricular contractions during angina pectoris.

(4) Repeated ventricular beats during electrophysiological examinations are sensitive indicators of ECG instability. If continuous ventricular tachycardia can be induced, the chance of sudden death will increase.

(5) Left ventricular dysfunction, increased end-diastolic pressure, decreased cardiac index, decreased ejection fraction, EF <40%. It can also be manifested as segmental or multiple segmental dysfunction or generalized reduced heart beat or papillary muscle dysfunction. Sudden death is more likely.

(6) Positive Ventricular Late Potential Examination: Simson reported 66 cases. The positive rate of late potential was 7% in those without ventricular tachycardia. The positive rate was 92% in those with ventricular tachycardia.

(7) The Q-T interval is prolonged with ventricular premature beats, especially those with R riding across T waves.

(8) For pre-excitation syndrome, the bypass refractory period is shorter than 250ms or patients with atrial fibrillation.

(9) Certain factors that can reduce the threshold of ventricular fibrillation, such as heavy smoking or Significantly increased blood pressure.


II. Prevention of sudden cardiac death

(1) Application of antiarrhythmic drugs

Most sudden cardiac death is caused by primary ventricular fibrillation. Therefore, it is a reasonable way to actively manage and prevent ventricular arrhythmias. However, after a large number of observations and studies by clinical cardiologists, It is found that patients who have been using anti-arrhythmic drugs for a long time have not shown a reduction in sudden death rate.

Moreover, most anti-arrhythmic drugs can have arrhythmogenic effects. Therefore, it is not recommended to use anti-arrhythmic drugs for patients with ventricular arrhythmia.


At present, most scholars believe that:

i. Patients with a risk of sudden death should be detected by electrophysiological tests, for example, such patients can induce ventricular fibrillation or persistent ventricular tachycardia.

ii. Select anti-arrhythmic drugs that are effective for this patient’s arrhythmia through the electrophysiological drug test, and observe whether the drug has an arrhythmogenic effect.


(2) The prevention of sudden cardiac death from coronary heart disease

1. Application of β-blockers in a European research center in 1970 pointed out that β-blockers can reduce the mortality of myocardial infarction. Large-scale clinical trials with a control group observed the use of β-blockers after acute myocardial infarction. Delayed patients, the survival rate within one year increased compared with the control group. Most scholars advocate long-term application, because β-blockers can reduce myocardial oxygen consumption and reduce the area of ​​myocardial infarction. At the same time, they have membrane stability and reduce the occurrence of ventricular arrhythmias.

2. Coronary endoluminal surgery or coronary artery bypass surgery, for patients with severe coronary artery stenosis leading to myocardial ischemia, perform coronary angioplasty, using a balloon to expand the stenosis, and significantly improve coronary blood supply. Coronary artery bypass surgery and ventricular aneurysm resection in patients with left main coronary artery stenosis or severe stenosis of more than three coronary arteries and acute myocardial infarction complicated by ventricular aneurysm can reduce the incidence of sudden cardiac death.

3. Embedded automatic heart defibrillator: This is a new method, which has achieved initial results. When ventricular tachycardia or ventricular fibrillation occurs, the electrodes of the automatic heart defibrillator can send out according to the sensed electrocardiogram. 25 joules of electrical energy for cardioversion, which can both treat ventricular fibrillation and prevent sudden death.


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