The left ventricle is longer and more conical than the right ventricle.Its cross section also presents an oval or nearly circular outline.The sternocostal plane, the front of the heart, is mainly composed of the right ventricle, while a small part is composed of the left ventricle.However, the left ventricle not only constitutes the apex, but also most of the septal plane of the heart, which is the side where the organ contacts the diaphragm.In order to pump blood out at a high blood pressure, the muscles of the left ventricle are thicker and more developed than those of the right ventricle.
Starting from teenagers, the left ventricular wall will become thicker, making it three to six times thicker than the right ventricle.This also reflects that the left ventricle will create five times more pressure than the right ventricle in the process of pumping blood.In each heartbeat, the left ventricle receives from the pulmonary vein at about 80Bracket(equivalent to nearly 11000PascalAnd then push the blood pressure up to about 120 torr (equivalent to 16.3 kPa) to send it into the great arteries.(All pressure values are measured when the heart is at rest, and are also relative values to the surrounding atmospheric pressure of the reference pressure set as zero).
For a normal heart, the muscles of its left ventricle must relax immediately after each contraction to allow the oxygenated blood from the pulmonary vein to rapidly fill, which is the relaxation and filling of the heart in diastole.Rapid intense contraction to push a large amount of blood into the great arteries, overcome the very high pressure of the great arteries and provide additional pressure to extend the great arteries and other main arteries and provide enough space for the sudden rise of blood volume, which is the contraction and efflux of the heart in the systolic period.At the centerSystem controlThe pumping capacity can be increased or decreased rapidly.A normal adult heart can pump about five liters of blood per minute when it is at rest.The maximum output capacity can be increased from about 25 per minute for non athletes toOlympicsThe level of athletes is about 45 liters per minute.
Simple rheumatic mitral regurgitation is rare, and it is often combined withRheumatic mitral stenosis。On auscultation, the apex of the heart can hear 2/6 or more systolic blow like murmurs, rough, and the first heart sound can be concealed.
The causes of aortic regurgitation include rheumatism and syphilis.The former has a younger onset age, mostly between 10 and 40 years old, may have a history of rheumatic fever, have a longer period of cardiac function compensation, and are often associated with mitral valve orAortic valve stenosis；The latter is usually 34-50 years old, and has a history of sexually transmitted diseasesangina pectorisSeizures.
It is common in men, and the symptoms appear later. In the late stage, syncope and angina pectoris are prominent symptoms, and syncope may lead to sudden death.
The patient had long-termHypertensionShi, the heart boundary expands to the left and down.The second tone in aortic valve area is enhanced due to relativityMitral insufficiencySystolic murmurs were heard at the apex of the heart.
It is characterized by angina pectorismiocardial infarction, which can also be expressed asArrhythmia、heart failureIt can also have no clinical symptoms, or sudden death after the first attack.
Aortic coarctation is the narrowing of the active pulse cavity. Its clinical feature is that lower limb blood pressure is significantly lower than upper limb blood pressure, while upper limb blood pressure, especially systolic blood pressure, is significantly higher than normal blood pressure.Patients often have fatigue, cold and numbness of lower limbs.
It shows angina pectoris ormiocardial infarction, similar to coronary heart disease.If the lesion involves the kidney, it can cause hypertension, thus aggravating the degree of heart damage.
X-ray manifestations
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① The apex extends downward to the left. ②Opposite pulsation point moves upward. ③The left heart segment was extended, rounded and extended to the left. ④The left ventricle overlaps the spine. ⑤In the left position, the posterior cardiac space narrowed or even disappeared, and the anterior esophageal space at the lower posterior edge of the heart disappeared.
ECG performance
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The normal left ventricle is located in the left rear of the heart, and the left ventricular wall is significantly thicker than the right ventricle, so the ventricular depolarization complex vector in normal conditions shows the characteristics of left ventricle predominance.Left ventricular hypertrophyIt can make the left ventricular advantage more prominent, and the following changes can appear on the electrocardiogram: 1QRS complexVoltage increase: Rv5 or Rv6 of chest lead ＞ 2, 5mV;Rv5+Sv1 ＞ 4, 0mV (male) or ＞ 3, 5Mv (female).In limb lead,R1＞1、5Mv；RaVL＞1、2Mv；RaVF＞2、0Mv；RI+SIII＞2、5Mv.
In recent years, some scholars have established Cornell voltage standards: RaVL+Sv3>2, 8mV (male) or 2, 0V (female).It is reported that this standard can improve the sensitivity of detecting left ventricular hypertrophy and improve the accuracy of ECG diagnosis.
2. Left deviation of frontal ECG axis may occur.
3. QRS complex time was prolonged to 0, 10~0, 11 s, but generally<0, 12 s
4. In the R wave dominated lead, the ST segment was depressed to more than 0, 05 mV in a downward slope, and the T wave was low, flat, bidirectional, or inverted.In the lead dominated by S wave (such as lead V1), upright T wave can be seen instead.WhenQRS complexLeft ventricular hypertrophy with strain is said to be associated with increased voltage and ST-T changes.
On the basis of meeting one or more QRS voltage increase criteria, combined with one of other positive indicators, the diagnosis of left ventricular hypertrophy can generally be established.The more conditions are met, the greater the reliability of diagnosis.If only QRS voltage is increased, but no other person has any positive indicators, the diagnosis of left ventricular hypertrophy should be cautious.
treatment
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Left ventricular hypertrophy is divided into primary and secondary, primary refers toHypertrophic cardiomyopathy, medication includes beta blockers andCalcium channel blockerChemical ablation can achieve good results.The secondary disease is mainly secondary to hypertension, valve disease, etc., mainly to treat the primary disease.
Left ventricular hypertrophy is generally compensatory hypertrophy of the heart caused by hypertension.Failure to actively treat blood pressure may eventually lead to heart failure.Hypertension should be actively controlled in treatment.Life should be low salt, low-fat diet, take antihypertensive drugs. If the diet of blood lipids is not well controlled, you need to take drugs.
In general, attention should be paid to not be impatient but stable during work. The selection of antihypertensive drugs should be based on the principle of individualization, and drugs should be selected according to the patient's age, blood biochemical changes, target organ damage, blood pressure and its complications. ①Among the patients with hypertension without target organ damage, most of the young patients belong to high dynamic type, increased cardiac output, high pulse pressure, high blood pressure fluctuation with tachycardia and other sympathetic excitatory states, so beta blockers should be the first choice.Elderly patients should choose ACEI or calcium antagonist or angiotensin II because of the increased vascular resistance for external useReceptor antagonist；②Not suitable for people with hyperlipidemia, diabetes and goutBeta blockerAnd thiazide diuretics; ③For patients with left ventricular hypertrophy and angina pectoris, beta blockers and calcium antagonists can be selected; ④Patients with hypertension and heart failure should choose ACEI or angiotensin Ⅱ receptor antagonist or diuretic; ⑤mergeArrhythmiaincludeVentricular extrasystole. Patients with supraventricular tachyarrhythmia should choose beta blocker orVerapami；③For patients with renal insufficiency, loop diuretics or calcium antagonists should be selected, and ACEI or angiotensin Ⅱ receptor antagonists can be selected when serum creatinine is less than 3mg/dl; ①The deceased with cerebral infarction should choose calcium antagonist or ACEI or angiotensin Ⅱ receptor antagonist.
