Cold breasts and chest

As for people, their hands and feet will feel cold in winter, and they are particularly afraid of cold. Men are much more resistant to cold, so women need to wear one more piece of clothing than men in this regard. Especially women may experience cold breasts and chests. To improve this situation, you can regulate your diet or take Chinese medicine. Feeling cold indicates weakness, which can also be seen in the pulse.

, which is generally a symptom of premature beats.

Premature beat is also called premature contraction, extrasystole, or simply premature beat. It is a premature ectopic heart beat.

Clinical manifestations

Premature beats may be asymptomatic or may cause palpitations or a feeling of cardiac arrest. Frequent premature beats can cause symptoms such as fatigue and dizziness (due to reduced cardiac output). For people with existing heart disease, this can induce or aggravate angina pectoris or heart failure. Auscultation may reveal irregular heart rhythm and a long compensatory interval after premature beats. The first heart sound of premature beats is often enhanced, while the second heart sound is often weakened or disappeared. When premature beats are in a binomial or tripeminic rhythm, a long pause can be heard after every two or three heartbeats. Premature beats are inserted between two regular heartbeats and may appear as three consecutive heartbeats. Palpation of the pulse may reveal intermittent absence of pulses.

Pathogenesis

It may occur in a variety of ways.

(I) Abnormal impulse formation caused by abnormal autonomy ① Under certain conditions, such as when the sinus impulse reaches the ectopic pacemaker, the threshold potential at that point is lowered and the diastolic depolarization slope is changed due to the Weidensky phenomenon, causing premature beats. ② The permeability of the diseased atrium, ventricle or pulsatile fiber cell membrane to different ions changes, causing the fast-response fibers to transform into slow-response fibers, thereby accelerating the automatic depolarization during diastole, enhancing autonomy, and producing premature beats.

(ii) Reentry phenomenon: Circular reentry or focal microreentry: If the reentry pathway is the same, the morphology of the premature beats will be consistent; if the conduction velocity during the reentry is consistent, the pairing time of the premature beat with the previous beat will be fixed.

(III) Parallel contraction

(IV) Triggered

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Etiology and pathology

Etiology

Premature beats can occur in normal people. But it is more likely to occur in patients with cardiac neurosis and organic heart disease. Emotional excitement, nervous tension, fatigue, indigestion, excessive smoking, drinking or drinking strong tea can all cause attacks. There may also be no obvious triggers. The toxic effects of digitalis, barium, quinidine, sympathomimetic drugs, chloroform, cyclopropane anesthetics, potassium deficiency, and heart surgery or cardiac catheterization can all cause attacks. Coronary heart disease, advanced mitral valve disease, heart disease, myocarditis, hyperthyroidism heart disease, mitral valve prolapse, etc. are prone to premature beats.

Treatment and prevention

The treatment principles should be determined based on the presence or absence of organic heart disease, whether it affects cardiac output, and the possibility of developing serious arrhythmias.

Most premature beats without organic heart disease do not require special treatment. Those with symptoms should reassure themselves. Sedatives and beta-blockers can be tried for premature beats induced by tension, excessive excitement, or exercise.

For patients with frequent attacks, obvious symptoms or organic heart disease, it is advisable to find out the causes and triggers of premature beats as soon as possible and give corresponding treatment for the causes and triggers. At the same time, the potential fatality should be correctly identified, and the causes and symptomatic treatment should be actively treated.

In addition to etiological treatment, antiarrhythmic drugs can be used for treatment. Atrial and atrioventricular junction premature beats are mostly treated with Class IA, Ic, II, and IV drugs that act on the atria and atrioventricular junction, while ventricular premature beats are mostly treated with Class I and III drugs that act on the ventricles (see the drug classification above, and also see Chapter 7 "Introduction to Clinical Pharmacology"). Potentially fatal premature ventricular contractions often require emergency intravenous medication. Class Ib is preferred. Intravenous lidocaine is still often the first choice in the early stages of acute myocardial infarction. Beta-blockers are often used to treat myocardial infarction unless there are contraindications. Class I drugs are contraindicated in patients with primary or secondary long QT syndrome. For primary patients, beta-blockers, phenytoin, or carbamazepine can be used as an alternative. For secondary cases, the cause should be removed and treatment should be with isoproterenol or atrial or ventricular pacing.

Recent studies (CAST 1989) suggest that antiarrhythmic therapy increases the risk of mortality. Even if patients with heart disease control ventricular premature beats, there is no evidence that the sudden death rate is reduced (except for the use of beta-blockers after myocardial infarction). Therefore, the pros and cons of using antiarrhythmic drugs should be weighed. There have been large series of multicenter trials and long-term follow-up in China on patients with non-myocardial infarction arrhythmias (mainly premature beats). The use of propafenone and moricizine for supraventricular arrhythmias and propafenone, moricizine, and mexiletine for ventricular arrhythmias have shown certain therapeutic effects, and no serious cardiac events have been found. However, close follow-up is still required during the use of the medication to monitor its effects and possible adverse reactions. Patients with heart failure should be especially cautious.