Brain-heart syndrome in the elderly

Introduction to the elderly brain-heart syndrome Because acute encephalopathy is mainly cerebral hemorrhage, subarachnoid hemorrhage (SAH), acute craniocerebral trauma involving the hypothalamus, brainstem, autonomic nerve center caused by similar AMI, subendocardial hemorrhage, myocardial ischemia, arrhythmia or A general term for heart failure, when the brain disease becomes more stable or better, the heart disease symptoms and ECG abnormalities will improve or disappear. basic knowledge The proportion of illness: 0.07%-0.1% Susceptible people: the elderly Mode of infection: non-infectious Complications: paroxysmal supraventricular tachycardia hypertensive cerebral hemorrhage cerebral hemorrhage in the elderly

The cause of brain syndrome in the elderly

(1) Causes of the disease

Mainly caused by acute encephalopathy such as stroke, cerebral hemorrhage, cerebral infarction, and various types of brain trauma.

(two) pathogenesis

The brain and its structure are governed by the sympathetic, parasympathetic innervation of the heart.

1. The ventral nucleus of the lower thalamus emits descending fibers to the ventral side of the brainstem containing catecholamine cell population, blue spot, vagus dorsal nucleus and spinal cord.

2. The solitary tract nucleus emits fiber-induced lateral angles of the spinal cord and suspected nucleus, from the nucleus to the heart; the lateral angle of the spinal cord receives fibers from the blue-spotted noradrenergic neurons, the ventral nucleus of the brainstem, and the fibers are re-emitted from the lateral corners. The sympathetic ganglia descends and the fibers innervate the heart.

3. Suspected nucleus, dorsal nucleus of the vagus nerve, the nucleus of the nucleus of the nucleus of the nucleus to form the parasympathetic nervous system

4. Receiving cardiac baroreceptors, the chemoreceptor fibers pass through the vagus nerve and the ninth and tenth pairs of cranial nerves reach the solitary tract nucleus, and the ventral nucleus of the brain stem returns to the thalamus.

The mechanisms of brain-derived cardiac function and ECG abnormalities are multifaceted. Basic and clinical studies in recent years have confirmed that the specific mechanism can be formed by the following aspects.

1 hypothalamic-pituitary-adrenal system.

2 sympathetic - adrenal medulla system.

3 Heart disease and ECG abnormalities after stroke.

4 through the vagus nerve cortex representative area and brain stem related to the vagus nerve nucleus and vagus ganglion.

Hypothalamic-pituitary-adrenal cortical system (43%):

The lower part of the thalamus includes the anterior nucleus, the supraoptic nucleus, the paraventricular nucleus, the gray nodule, the funnel, the nipple body, and the latter are the main parts; the acute cerebrovascular disease often involves the hypothalamus, and the brainstem important nucleus leads to sympathetic and parasympathetic The neurological imbalance, which affects the heart, has been confirmed by experiments. The above-mentioned damages are easily caused by autonomic nerves, visceral function and metabolic disorders, and are closely related to ECG abnormalities. When the main pathological changes in the lower thalamus are located in the funnel, the papillary body is covered by blood. The third ventricle expands, the papillary body shifts downward, the cerebral edema, the nucleus cells become bad, leading to perivascular hemorrhage and cerebral infarction. After the hypothalamus is damaged, the blood corticosteroid is increased through the pituitary-adrenal axis. Increased heart rate, elevated blood pressure; excessive corticosteroids lead to electrolyte imbalance, especially the decrease of serum potassium causes myocardial repolarization process disorder, ECG ST-T changes and U wave appear, serum potassium drop can lead to increased myocardial excitability , easy to cause premature contraction, severe cases may have ventricular tachycardia or ventricular fibrillation, and other cerebral vasospasm after SAH, especially the lower thalamus through the artery trunk and branches The twin-induced ischemic ECG abnormalities caused.

Sympathetic-adrenal medulla system (27%):

After the hypothalamus is involved, through the sympathetic-adrenal medulla system, ACTH affects the synthesis of catecholamines, which can promote the synthesis of catecholamines directly or through corticosteroids. Excessive catecholamines can produce toxic effects, causing subendocardial damage, and SAH can cause sympathetic nerve function. Excitement, hyperactivity, increased plasma concentrations of epinephrine and norepinephrine lead to systemic hypertension, aggravation of myocardial ischemia and hypoxia, myocardial fibrosis and subendocardial ischemia, left ventricular strain and QT interval prolongation, arrhythmia or Various ECG abnormalities such as conduction disorders.

The heart itself changes after SAH (14%):

It has been controversial whether the heart itself has histological damage after SAH. At present, a few scholars believe that it is "inhibitable", but most scholars believe that ECG abnormalities and cardiac damage are consistent, there is a close relationship between them, SAH patients have serum CPK Elevated, myocardial isoenzymes and myocardial creatine kinase increased, histology showed focal myocardial lysis and subendocardial ischemic necrosis, inflammatory cells around myocardial fibers, affecting myocardial depolarization and repolarization, which led to ECG is abnormal.

Area 13 of the frontal lobe (6%):

There is a representative region of the vagus nerve cortex in the 13 area of frontal lobe, which is stimulated by ECG abnormalities. In the anterior middle cranial fossa, the anterior middle cerebral artery ischemia affects the marginal system and the ECG amplitude is low; Can cause sinus tachycardia, transient premature contraction or myocardial ischemia; damage to the lower part of the brain stem can cause sinus bradycardia or myocardial ischemia; deep brain, ventricle or midbrain hemorrhage has obvious ECG abnormalities, In the animal test, stimulate the third ventricle or the cerebral artery ring (sensory reflex zone) may have ECG and arrhythmia. Intraventricular hemorrhage necropsy half of the myocardial morphology has subendocardial or extensive interstitial hemorrhage, left ventricular myocardial multifocal necrosis, myocardial capillarity Vasodilatation with RBC stasis, perivascular edema, myocardial fibrosis or hyaline degeneration. In summary, brain-heart syndrome is characterized by multiple levels of neuro-humoral regulation of the nervous system, with neurological mechanisms leading.

Prevention of brain and heart syndrome in the elderly

1, first of all should actively treat the primary disease and protect the heart function.

2. Control cholesterol intake. Studies have shown that people with high cholesterol have a five-fold higher incidence of coronary heart disease than normal people. Therefore, patients with cardiovascular disease should eat less cholesterol-rich foods such as animal brain, internal organs, egg yolk, and crab yellow.

3. Control the quality and quantity of fat intake. Saturated fatty acids can raise blood cholesterol, while polyunsaturated fatty acids can lower cholesterol. Therefore, it is necessary to control the intake of saturated fatty acids such as lard and tallow in the diet.

4, eat more foods rich in vitamin C, such as: vegetables, fruits. Vitamin C increases blood vessel elasticity and protects blood vessels.

5. Increase dietary fiber intake. Dietary fiber can absorb cholesterol and prevent cholesterol from being absorbed by the body.

Complications of elderly patients with brain and heart syndrome Complications Paroxysmal supraventricular tachycardia hypertensive cerebral hemorrhage in elderly patients with cerebral hemorrhage

The power generation medium is disordered, supraventricular tachycardia, cardiac insufficiency, ventricular fibrillation, and the like.

Symptoms of brain syndrome in the elderly Common symptoms High heat conduction block arrhythmia edema tachycardia sudden cardiac arrest Brachiol cerebral hemorrhage ventricular fibrillation ganglia hemorrhage

Diagnosis of this syndrome requires differentiation of the disease with both the brain and the heart. Combined with the clinical studies reported in the literature and long-term clinical observations, the syndrome has the following characteristics:

Central arrhythmia

It must occur during stroke, and there is no organic history of heart valve and myocardium, and there is no arrhythmia before CVD. In addition, there is a need for infection secondary to acute CVD, heart disease caused by water and electrolyte disorders and ECG. The abnormalities are different, and the latter can be restored to normal after the above points are corrected.

2. Types of arrhythmia

ECG monitoring and Holter ECG examination showed that 91% of patients with arrhythmia observed by Htolter ECG after 48 hours of SAH, including life-threatening ventricular or supraventricular tachycardia, ventricular fibrillation is one of the main causes of sudden death, among which QT Prolongation syndrome is extremely important, 0.4-0.43 s at normal time; foreign literature reports that prolongation of QT at fatal torsade ventricular tachycardia (Tdp) is the greatest risk factor for Tdp, so ECG monitoring is essential for early detection. Need to exclude low potassium, calcium, magnesium and secondary, but often incentives, can disappear after correction.

3. The occurrence and duration of ECG anomalies

The abnormality of ECG occurs from 80% to 90% after 12h to 2 days after onset. Later, the waveform of the acute phase is abnormal. The waveform abnormality lasts for 1 to 2 weeks, the elderly can reach 4 weeks, and the arrhythmia is mostly 2 It disappeared within ~7 days, and most of the patients with arrhythmia after the acute phase were considered to be caused by cardiogenicity.

4. The relationship between ECG abnormalities and disease severity

There are many abnormal ECG cases in severe cases, but the ECG changes and the degree of disease are not completely consistent. In some cases, the ECG is improved but the symptoms are aggravated. The following situations should be noted:

1 severe sinus bradycardia or overspeed, ventricular arrhythmia, conduction block, abnormal Q wave is a poor prognosis factor.

2 obvious QT prolongation needs to be alert to the danger of Tdp.

The change of 3ST-T wave, especially the ST segment elevation, is more dead.

4 tachycardia and P wave increase are more common in high fever, ventricle, brain stem hemorrhage or central pulmonary edema.

5. Relationship between brain lesions and ECG abnormalities There is a relationship between animal experiments and clinical observations, but there are few data:

1 cerebral hemisphere stroke ventricular, atrial premature contraction and atrial fibrillation more than brain stem stroke.

2 Left frontal lobe hematoma often accompanied by QT interval prolongation and T wave abnormalities.

3 apical hematoma associated with sinus bradycardia and ventricular premature contractions are more common.

4 Thalamic and basal ganglia hemorrhagic sinus bradycardia is more common.

5 brain stem hemorrhage often occurred in paroxysmal atrial fibrillation or atrial premature contraction.

6 Stimulate the tachycardia induced by the left side of the left island cortex, stimulate the tail to cause bradycardia, and prolong the stimulation time to induce atrioventricular or indoor conduction block.

In the 7-line MCA obstruction (McAo) surgery group, 61% died, the sympathetic activity increased significantly, and the QT interval prolonged most prominently, which was a prelude to the fatal rhythm.

8 About 40% of patients with carotid artery disease have asymptomatic coronary heart disease, and increase with age, so these patients are more likely to cause ECG abnormalities in acute CVD.

According to the medical history and clinical features, the ECG features can be diagnosed.

Examination of brain syndrome in the elderly

1. ECG waveform abnormalities have significant U waves in the characteristic changes of acute CVD; the incidence of early occurrence is 30%, the appearance or disappearance of U wave is not related to hypokalemia, and the U wave is not prominent in AMI.

2. QT interval prolongation: The positive rate in SAH with U wave is as high as 50% to 60%. Significant QT prolongation can lead to fatal torsade ventricular tachycardia (TorsP), unlike CVD in AMI. Secondary is obvious.

3. T wave inversion: more common in severe SAH, a huge inverted T wave of more than 10mm can be seen in the chest lead, which is difficult to distinguish from the inferior infarct, but the T wave rising slope caused by the former is slow and asymmetrical.

4.P wave increase (II>2mm): high-point P wave increases with T wave, and is associated with brain stem hemorrhage or infarction, sympathetic over-excitation, central pulmonary edema, and cardiac dysfunction in SAH. Accounted for 30% to 70%.

Diagnosis and diagnosis of brain and heart syndrome in the elderly

Differential diagnosis

ECG abnormalities in CVD are differentiated from other heart diseases.

1. AMI ST segment depression or elevation, inverted T wave, abnormal Q wave is more common in myocardial ischemic lesions, may have serum CK, LDH and other enzyme activity abnormal value identification, CVD serum enzyme value increase rate is slower than AMI, but need to combine Clinical history and symptoms.

2. Heart and stroke without chest pain, stroke-like AMI is unique to senile AMI. Teng reports that the incidence of AMI and CVD is 5% to 10%, so it is difficult to diagnose when not at the same time.

3. Acute reversible myocardial infarction: Features:

1 Abnormal Q waves are more common in V1 ~ V3 leads, ST segment elevation, coronary T wave and other typical AMI waveforms.

2 The duration can be changed to normal after 1 to 2 weeks.

3 myocardial enzymes escape light.

4 necropsy showed AMI changes in the naked eye, myocardial histology showed wall thrombus, small blood vessel thrombus and scattered necrosis of surrounding myocardial tissue.

5 combined with DIC, coagulation and other factors such as coronary microvascular dysfunction.

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