Mix natural acne skin and shine

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Ingredients:


Teaspoon honey
Half a teaspoon milk
Quarter teaspoon of lemon


The way:



Mix all ingredients and put them on the face evening before going to sleep ..
For a period of 10 to 15 minutes. Then wash the face with warm water. And drying the face with a towel thin
And lack of pressure on the skin. Of course, I am with natural herbs.
  Because it is from God

source:heaalthy

How to get rid of acne forever ?

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Lettuce and milk mask to treat acne:


Taken 10 lettuce leaves and green in addition to a glass of low fat milk and then boiled lettuce and milk over low heat for a few minutesand taken lettuce leaves and placed on the face, For a period of 20 to 30 minutes later still compresses and wash the face. Mixing milk with water when washing the face, it helps to sterilize the skin and prevent the emergence of a new grain
Avoid anxiety and stress because it will increase the acne.

Avoid cosmetics in this particular period.


Avoid washing with ordinary soap and replace it with  soapmedical or children.
Avoid the use of oils and creams for hair because it has an indirect effect on acne.


source:heaalthy

Acne treatment natural herbal !

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If the limited effectiveness of pharmaceutical medicine in the treatment of acne, The natural medicine has more hope.
There are many qualities and praised by the experimenters and specialists in herbal medicine as an effective treatment for acne, Among them the following recipes:


Mint juice:


Squeeze a set of mint leaves, and uses the resulting juice to the facepiece of cloth in the paint .... And repeat this every day.


Boiled plum:

Boil the fruits of plum in the water, then mash well so that they areabout 8 teaspoons, And add to it a teaspoon of oil geese .. Place this mixture on the faceevery day. 


Chrysanthemum:


Mash the range of Chrysanthemum leaves. And placed on the face.


Treatment of red pimples:


Leaf juice is used to paint trees, camphor skin every day, then rinseface with warm water..

Camphor helps to clear pimples red, and resistance to infection andinflammation and speed healing.
As well as mint juice from the above-mentioned works in the holderand rinsed every evening after it dries. And repeat this every day.


Cataplasm onion:


Peel onion 2 to 3. And cut well and boil on low heat and when cooledonion wrapped with gauze and placed on medical places pimples,and repeat this every day twice a day at least.


Treatment of blackheads:


The most important way to treat blackheads is a commitment toclean the face. For this purpose, can do the following.:
Face wash with soap and water, preferably sulfur soap or soap-freeherbal chemicals three times a day, and be the last time with warm water before going to sleep.
Action mask cleaner skin of masks already mentioned, preferablymask almond kernels. And duplicate the work of the mask weekly.
Lemon juice and benefit from cleaner good for the skin layer by placing it on the place of injury, two to three times
Day and not less and not more than once every ten minutes.


Facial steam bath

Operates a steam bath for the face for 10 minutes, to softenblackheads, allowing remove them after that, and this is the surrounding tissue juice until you come out blackheads from the pores of the sebaceous glands with slots to avoid try to extract themwith violence.
source:heaalthy

Coronary heart disease. ECG in ischemic heart disease

Previously been described electrocardiographic pattern of ischemia, and myocardial lesion, its electrophysiological basis and differential diagnosis. The articles examined the diagnostic value and indications for VCG, ECG exercise test, Holter monitoring and electrophysiologic study of intracavitary (VEFI) for coronary heart disease. This article will describe the changes observed at different stages of coronary heart disease, certain aspects of the correlation between coronary heart disease and clinical features, angiographic data, etc., and the common value of electrocardiography in the diagnosis and evaluation of heart disease.

Angina can be diagnosed on the basis of the pathophysiology and development. In terms of pathophysiology distinguish primary and secondary angina. The most characteristic manifestation of primary angina, the ECG (usually occurs at rest) is an electrocardiographic phenomenon of Prinzmetal. In this type of angina, ischemia is the result of a sharp decline in blood supply due to coronary artery spasm unchanged or, more rarely, organically modified coronary artery in this type of angina is not always observed preceding an increase in oxygen consumption. Secondary angina corresponds to the classical angina, and ischemia is due to the fact that critically stenosed coronary artery can not adapt to increased blood flow in the increased needs (increased oxygen consumption).

Increasingly there are reports that one and the same patient observed primary and secondary attacks of angina at various stages of the disease (a type of mixed angina).

From an evolutionary perspective can be stable angina (stable ischemic heart disease), and unstable.

Coronary heart disease. ECG in ischemic heart disease

ECG in ischemic heart disease

These include post-infarction patients with stable clinical picture and patients with all types of stable angina without previous myocardial infarction. Patients with angina usually have angina, although they may have bouts of angina in primary dormant (mixed angina). Less commonly, seizures occur only at rest.

A. ECG at rest. ECG at rest remains normal in almost 50% of patients without previous myocardial infarction and in 5-30% of patients with prior myocardial previously]. Therefore, the ECG alone is not a very sensitive method. The specificity of its slightly higher but similar ECG changes were observed in other clinical situations. On the other hand, in patients with anginal attacks of the same gravity, and there are different and similar ECG signs.

a. Changes in repolarization. If angina or angina with negative or mixed flattened T waves or ST segment depression observed in approximately 50% of patients with prior myocardial previously, especially with anterior wall infarction, ST-segment elevation persists and in some cases there is a negative spike U, which often indicates lesion anterior descending coronary artery. In patients with predominantly or exclusively of primary angina (Prinzmetal angina) ECG alone is not changed in almost 50% of cases.

b. Abnormal Q waves detected in 30-40% of patients with angina or mixed angina. However, 15% of patients with abnormal Q waves were observed before signs of a heart attack. On the other hand, the tooth of Q, indicating a heart attack, not 25% of patients with lesions of the three vessels and 20% of patients with a history of heart attack.

a. Arrhythmias. The incidence of arrhythmias on the ECG at rest in all types of coronary heart disease is relatively small. However, patients with premature ventricular beats, registiruemymi ECG at rest, have a poor prognosis. It is obvious that the frequency of arrhythmias is much higher in holteovskom monitoring.

Patients with recurrent sustained ventricular tachycardia in the chronic stage podostroi or heart attack often have asinergicheskie area and a poor prognosis, because the onset of sudden death is possible. Currently, they represent one of the most difficult categories of patients, requiring the use of large doses of antiarrhythmic agents for the prevention of sudden death and / or non-pharmacological treatments (surgery, fulguration, defibrillator Mirovska). There are three prognostic indicator of electrical instability in patients with myocardial infarction:
- Identification of arrhythmias using Holter ECG and exercise;
- Programmed electrical stimulation with imposed by ventricular arrhythmias.
- Registration of late potentials ryamaya depolarization, which was considered by some authors as an indicator of propensity to malignant ventricular arrhythmias reentry. It was shown that the disappearance of late potentials after surgery for ventricular tachycardia observed in cases in which it helped to avoid a recurrence of arrhythmia, but not marked with the introduction of anti-arrhythmic drugs.

ECG during an attack of coronary artery disease. ECG phenomenon of Prinzmetal

The ECG of patients with stable angina may occur only ventricular conduction disturbances (5-10%, based on some studies), increased left ventricular (5-25%) and P wave abnormalities (especially in coronary patients with changes in contractile function).

On the other hand, the ECG in patients with stable angina may remain unchanged for a long time or it may be subject to change without any connection with the development pattern of the disease in this patient.

In contrast, a small number of patients with significant ECG changes may be absent. Arrhythmia, usually ventricular extrasystoles often appear or are enhanced, but in patients with stable angina are more common primary ventricular fibrillation during the attacks and AV block than in patients with angina pectoris. Arrhythmias in all types of anginal attacks may be the result of ischemia associated with reperfusion. The latter is often observed in the remission phase of the attack, when the ST segment is reduced, which is observed in patients with primary angina in patients undergoing thrombolysis.

In 1959, Prinzmetal described a picture of atypical angina pectoris, which he called an inverted (or variant) angina (angina in the primary result of spasm described above). The main features of such a angina are:

ECG during an attack of coronary artery disease. ECG phenomenon of Prinzmetal

a) pain in prekardialnoy of prevailing in a state of rest, and sometimes occur at the same time every day;
b) The pain is often accompanied by a pronounced rise of the segment 57, and sometimes, when an intense ischemic ST segment changes and / or TQ. ST-segment elevation disappears within a few minutes or even seconds after the cessation of the attack (ECG phenomenon of Prinzmetal);
c) during the attack indicated a high incidence of serious ventricular arrhythmias and, rarely, significant AV block;

d) ergometric test is usually normal;
e) the ischemia that occurs as a result of coronary spasm. Only rarely observed transient abnormal Q waves in Prinzmetal angina. The diagnosis of variant angina, confirmed the existence of pain attacks in the resting state, accompanied by transient ST-segment elevation on ECG. Currently, many researchers prefer to use the term "ECG phenomenon of Prinzmetal '(transient-segment elevation ST) t instead of Prinzmetal angina.

In practice, at one and the same patient may occur this ECG phenomenon (segment elevation ST) suitable cases and segment depression ST - in other ac expression of various degrees of ischemia. On the other hand, some attacks in the resting state there is a steady rise in the ST segment is not necessarily as a result of spasm. In some patients with stable angina, the primary, usually with a spasm of distal vessels, which do not segment elevation ST, and noted his depression, there are minimal changes in T wave or negative T wave psevdonormalizatsiya However, it was confirmed that some minor changes of the T wave are the only ECG changes in patients with spasm of the anterior descending coronary artery.

Echocardiographic studies have shown that mechanical changes precede ECG signs of myocardial ischemia and allow us to understand the original, sometimes minimal, electrical changes, which may be the only pas all subsequent ECG.

Methods of diagnosis of ventricular tachycardia. QRS complex tachycardia with more than 0.12

The possibilities of other methods electrocardiological: previously mentioned the use of Holter monitoring, stress tests and intracavitary programmed electrophysiological studies for ventricular tachycardia study. However, the true testimony to the EPE in a patient with ventricular tachycardia is controversial.

Most authors, including the Committee of NASPE, believe that the EPS should not be performed during unstable ventricular tachycardia, especially if it is asymptomatic and the patient do not have heart disease. According to many authors, EPS and pharmacological tests for the selection of the most effective therapy (ie, a drug that prevents imposed tachycardia) should be performed in patients with:

a) with sustained ventricular tachycardia;
b) with sustained tachycardia and decompensated hemodynamic disturbances;
c) with ventricular tachycardia resistant to therapeutic treatment, especially in patients with heart disease.
However, there are still doubts as to whether it is the best scheme, and there are many differences between the results of clinical tests and elektrofarmakologicheskih reaction. NASPE Committee recommends that EPS in patients with ventricular tachycardia in patients with heart failure in the community, as well as in patients with syncope. More recently, Wellens, Brugada and Stevenson studied the relationship between ventricular arrhythmias and hyperactive, and EPS reached the following conclusion:

a) the value of an unstable ventricular tachycardia is not known;
b) Commencement of polymorphic ventricular tachycardia during EPS is not a specific feature;
c) during the EPS ventricular fibrillation can occur in patients with heart disease or not. The frequency of this disorder is similar to that observed in patients after myocardial infarction with significant ventricular arrhythmias or without them, as well as in patients after sudden cardiac arrest;
d) the occurrence of sustained ventricular tachycardia in postinfarction patients does not mean that they are at high risk of sudden death in contrast to what is stated in Sec. 3 and 10. Other authors are of the same opinion;
d) In terms of therapy, has a value of preventing the occurrence of sustained ventricular tachycardia after administration of the drug, but the stability of the arrhythmia after antiarrhythmic treatment does not preclude the clinical use of this drug.

Methods of diagnosis of ventricular tachycardia. QRS complex tachycardia with more than 0.12

QRS complex tachycardia with more than 0.12

These types of tachycardia occur infrequently. Tachycardia occurs. beams (the trunk, right leg, left leg or the trunk of the two beams), so called beam tachycardia. According Elisari, Munoy et al., There may be a pattern of ventricular blockade of I degree, in particular the blockade of right bundle branch block in combination with or without gemiblokom and ECG pattern of isolated gemibloka. QRS complex tachycardia at some of the beam can be up to 0.13. AQRS strongly rejected by the left or right, and HV interval is short or negative. AV dissociation occurs frequently, there may be pulses of capture or drain systems.

Differential diagnosis of supraventricular tachycardia or atrial flutter with some aberrant difficult with a single surface ECG, because the blockade of the right bundle branch block I degree may be the result of aberrant or momentum generated in the upper part of the intraventricular conducting system (in the branching left bundle branch block in the case), and gives a similar picture. The following signs may help in diagnosis:

a) a drain complexes suggests the emergence of ventricular tachycardia;
b) signs AB dissociation strongly suggest ventricular tachycardia. Active fibrillation should be carefully studied, it is often difficult to do using the surface ECG;

c) if there is no pattern of ventricular conduction disorders of I degree in sinus rhythm, it is likely that there is a beam ventricular tachycardia, supraventricular tachycardia, but not with an aberrant, since aberrant supraventricular tachycardia is usually represented by a picture of complete ventricular block (QRS complex more than 0,12 c). The problem is that the ECG sinus rhythm is often missing. However, it should be remembered that in paroxysmal reentry nodal tachycardia circuit intranodalnym prong P1 often (30%) occurs after the complex QRS, although it is close by reminding the blockade of right bundle branch block I degree (prong r 'in lead V1 and / or II, III, aVF). If a picture is reminiscent of an aberrant pattern of tachycardia blockade of the right bundle branch block first degree, you should consider this possibility;
d) electrophysiological signs of retrograde aktivaschii bundle branch block.

According to some authors, such arrhythmias are often poorly tolerated. Forecast is similar to that seen with classical ventricular tachycardia.

Characteristics such as ventricular tachycardia pirouette. Pleomorphism of ventricular tachycardia

These are typical characteristics of ventricular tachycardia type of pirouette observed when it occurs in patients with prolongation of the interval Q-T, usually as a result of changes in metabolism (hypoxemia, hypokalemia, etc.) or losle administration of various drugs (quinidine, prenylamine liters etc ..) However, there are an increasing number of patients with ventricular tachycardia and complex configuration of the QRS, typical of "pirouette" who have heart disease, the coronary patients who often lack a long Q-T interval (up to 70% in some studies), a long interval coupling, a slow basic rhythm, metabolic or electrolyte changes or effects associated with taking anti-arrhythmic drugs. For this reason, all characteristics, except for the configuration of the complex QRS, characteristic polymorphic ventricular tachycardia, similar to those of classical monomorphic ventricular tachycardia, in which she transformed.

Thus, it can be assumed on the basis of clinical data and results of treatment, this subgroup of polymorphic ventricular tachycardia (the configuration of the complex QRS, indicating a "pirouette" and the rest electrocardiographic features - a classic ventricular tachycardia) is a variant of the classical ventricular tachycardia, and ventricular not an option tachycardia type "pirouette."

It is necessary to distinguish tachycardia type "pirouette" mainly from ventricular fibrillation. "Pirouette" is a typical configuration, and a slower rate than ventricular fibrillation, it responds to stimulation of the heart and is usually self-limiting. As was described, the configuration of the QRS complex is identical to that observed in ventricular tachycardia of the "pirouette", but without additional traits, such cases must be regarded as a classic of ventricular tachycardia and ventricular tachycardia is not a type of "pirouette."

Characteristics such as ventricular tachycardia pirouette. Pleomorphism of ventricular tachycardia

Ventricular tachycardia of "pirouette" is a severe arrhythmia, which can sometimes lead to ventricular fibrillation, and is often the cause of sudden death among ambulatory patients (15%), according to Leclerq and Coumel, as a result of the introduction of certain medications or electrolyte imbalance, often no signs of apparent heart disease.

Other types (pleomorphism). Completely block the picture ha near the right and left bundle branch block alternate. Such changes may be sudden or gradual, transient or prolonged, usually accompanied by changes in cycle length. Tachycardia may be uneven, at least for such changes. In any case, the usual duration of a few minutes the ECG may not reveal changes in the regular, rhythm. In this case it is impossible to identify the differences between classical monomorphic ventricular tachycardia, tachycardia, and this: why it is appropriate to recall that one can be mistaken for areas of tachycardia, relying only on the configuration. Using Holter monitoring confirmed that the volleys of ventricular tachycardia are sometimes polymorphic.

Other types of polymorphic ventricular tachycardia have also been described, although in most cases they represent variants of tachycardia type "pirouette" or specific morphological changes, which are based on mechanisms similar to those that were described earlier. Some classical ventricular tachycardia with frequent seizures or drainage complexes of the ECG may show different pictures, though rarely observed (see above). Finally, if ventricular tachycardia is converted to ventricular fibrillation, it may have an atypical configuration.

Ventricular flutter. Ventricular fibrillation

It is poorly tolerated and is characterized by QRS complexes of the same height and no isoelectric line between them and the T wave is absent. Differences between the QRS and ST-T can not be identified. The ups are the same as ups, which means that the ECG can be inverted. The frequency is 200-250 h 1 min. If it persists through defibrillation, it usually leads to ventricular fibrillation. In rare cases, it terminates itself.

The more damaged myocardium, the lower the amplitude of the flutter of teeth, though it usually exceeds 10 mm in some leads. In a healthy heart ventricular flutter teeth are the same as in ventricular fibrillation.

Ventricular fibrillation and atrial flutter often exist together or one violation goes to the other. By analogy with atrial flutter can talk about a typical or atypical flutter or ventricular fibrillotrepetanii ventricles. On the other hand, there may be an intermediate situation between ventricular tachycardia and atrial flutter before they will be well established atrial flutter. From the clinical and prognostic point of view of ventricular flutter is an emergency situation that must be addressed in the same way as ventricular fibrillation.

Ventricular flutter. Ventricular fibrillation

Ventricular fibrillation. If for any reason (electrolyte imbalance, ischemia), there is an asynchronous repolarization of myocardial fibers, is the ventricular premature complex, usually premature, and often two or more, unless there is severe disease of the heart can cause ventricular fibrillation in the most vulnerable period of the ventricles. The mechanisms responsible for atrial flutter and ventricular fibrillation and in the ventricles, are basically the same as in atrial fibrillation: repetitive micro-reentry or the formation of pulses in multiple foci. Data in favor of repeating micro-reentry etiology more.

ECG records the uneven teeth of various shapes and heights, as well as an increased frequency (300-500 in 1 min), QRS complex and ST-T segment is becoming indistinguishable from each other. If the teeth are relatively broad and frequent, the outlook for the elimination of ventricular fibrillation with defibrillation is much better than when they are slow and low. However, it was experimentally shown that a significant fibrillation is not a greater synchronization of electrical activity in comparison with fine fibrillation.

Ventricular fibrillation is characterized by partial, unsynchronized contractions of the ventricles, which are not accompanied by efficient pumping activity of the heart, which leads to heart failure.

Most susceptible to such disruption, patients with ischemic heart disease, especially in the acute phase of myocardial infarction, and patients with frequent or repetitive ventricular premature reentry and significant cardiomegaly with poor ventricular function, who already had a ventricular fibrillation outside the hospital or have some electrolyte imbalance and metabolism. It was believed that patients with acute myocardial infarction and primary ventricular fibrillation (ventricular fibrillation in the absence of violations of the pumping function) in the acute phase does not have a more favorable prognosis than patients without atrial fibrillation. However, recent studies have shown that infarct with primary ventricular fibrillation occurring in the first few hours, is characterized by a higher hospital mortality and could happen again, as a harbinger of heart failure. Moreover, patients who had ventricular fibrillation during acute anterior wall infarction have a poorer prognosis than patients with inferior wall infarction.

In the study of hospitalized coronary patients, mostly with myocardial infarction, ventricular fibrillation was detected in almost 50% of patients with the phenomenon of R / T, 25% of cases - with late arrhythmia and almost 10% with stable ventricular tachycardia. Other studies have shown the close relationship between the primary ventricular fibrillation, and the phenomenon of R / T. Ventricular fibrillation causes sudden death in nearly 70% of outpatients, and it often develops as a result of ventricular tachycardia. In the remaining 30% half of the deaths were caused by the rhythm of the "pirouette" and the other half - underactivity arrhythmias.

Ventricular fibrillation may occur with a favorable clinical course or the terminal stages of any disease. In very rare cases, ventricular fibrillation terminated by itself. In general, it causes cardio-pulmonary failure and death of the patient, if not immediately taken care (intensive care, cardiovascular events).

Patients in whom ventricular tachycardia was eliminated, not associated with acute myocardial infarction should continue to be treated to prevent new attacks with the help of drugs, implants minidefibrillyatora (if required), or surgery, but if the ejection fraction is very low, eliminating the possibility of such violations is limited . According to some authors, in individuals with arrhythmia Lown type II or IV, but without the occurrence of sustained ventricular tachycardia or fibrillation, ventricular tachycardia, in response to programmed stimulation is an indicator of poor prognosis, especially in cases where the ejection fraction is less than 40%. However, other researchers have reported contradictory results. In terms of these conflicting data, the current practice in post-MI patients with EPS can not be recommended.

Patients with heart failure, which happened outside the hospital and, most often due to ventricular fibrillation, should be thoroughly examined (coronary angiography, ECG, exercise, EPS). The choice of treatment depends on the results of the survey, there is currently no consensus as to what treatment or the treatment system of choice are preferred.

Chaotic ventricular rate. The term "chaotic ventricular rate" applies to those cases in which more or less simultaneously, there are ventricular tachycardia, ventricular flutter, atrial rhythms, and pop-up as a result of various sinus dysfunction or AV block. This rhythm is often observed in moribund states, and usually leads to heart failure (apparent isoelectric line).

The prognosis for sinus bradycardia. Sinoatrial block

The prognosis of sinus bradycardia is usually good, but if it is intense, particularly in the elderly, it is necessary to assume sick sinus syndrome (SSS). Pacemaker implantation reduces the incidence of recurrent symptoms, but does not increase life expectancy. Sinus arrhythmia in children, although significant, are not associated with poor prognosis. About 20% of cases of sudden death in an outpatient setting as a result of hypoactivity nastupayug rhythm, usually caused by a decrease in sinus automaticity or the blockade of the SA and AV block do not.
In this case, the blockade occurs in the region located between the sinus node and atria, and AV relationship remains unchanged (R-QRS).

If there is a blockade of the I level, it can not be detected by conventional ECG.
If there is a degree of block II, a fixed 2: 1 type, the frequency of ventricular contractions in 2 times less than the frequency of sinus rhythm, and if it does not register on the ECG, it can exist in the form of bradycardia caused by depression, the SA node. During exercise, or it increases slightly (if previously it was 80/2 = 40 in 1 min, and then it increases to 100/2 = 50 to 1 min), or, if the blockade of 2: 1 disappears, the heart rate immediately increases by more than 2 times (for example, 80/2 = 40 min in 1 - to 100/1 in 1 minute - after). Intermittent blockade of 2:1 creates a pause in 2 times the basic rhythm.

Sinoatrial Wenckebach type of block can also be observed, and if it is a blockade of the type 3:2, it is paired complexes that are difficult to distinguish from atrial arrhythmia with bigeminy arising near the sinus node with the P wave ', is almost equal to the sinus P wave when atrial bigeminy R-R interval of basic rhythm is approximately equal to the long interval of R-R coaxial rhythm, and when sinoatrialioy blockade of type 3-2 R-R interval of basic rhythm is approximately equal to the short interval of R-R coupled rhythm.

The prognosis for sinus bradycardia. Sinoatrial block

If there is a sinoatrial block III level, the atrial depolarization is absent, and the electrical state of fibrillation depends on the pop-up rhythms.

Sinoatrial (upper atrial) blockade without blockade intrasite arises where there is intranodalnaya conductivity of the conductive system, but the sinoatrial conduction in atrial myocardium is slowed down. QRS complex occurs at a time that is normal, but the P wave is delayed and usually leads to a short interval of R-R. It's interesting, because in some cases short interval P-R does not occur as a result of excitation of the ventricles, and the blockade of the SA. This disorder, which can be intermittent, voznikaeg very rare. He was seen in some versions of myocardial infarction, and valvular lesions with significant fibrillation.

When hyperkalemia sinoatrial transfer to the ventricles may be normal with delayed ventricular activation (short-range P-R) or even with the P wave, QRS complex, or a hidden log after it (sinoventrikulyarnaya conductivity). This phenomenon explains one of the causes of sinus rhythm in the absence of P wave (the other reason is the fibrosis of the atrium, which prevents the registration of P wave on surface ECG, although it exists).

The prognosis of CA blockade worse than sinus bradycardia due to decreased automaticity, usually not occurring or arising as a side effect of a drug. It is part of the sinus node syndrome, and often require pacemaker implantation.