Acute right heart failure

Introduction to acute right heart failure Acute right heart failure, that is, acute right heart failure, is a clinical syndrome caused by a sharp decrease in right ventricular contraction force due to a sharp decrease in right ventricular myocardial contractility or a sudden increase in right anterior and posterior load. . basic knowledge The proportion of the disease: the rate of the disease in the population over 50 years old is about 0.001% -0.002%, more common in patients with pre-existing hypertension Susceptible people: no special people Mode of infection: non-infectious Complications: shock

Acute right heart failure

(1) Causes of the disease

Common causes are:

1. Acute right ventricular myocardial damage: acute large-area right ventricular infarction.

2. Acute right ventricular afterload increased: such as acute massive lung infarction.

3. Acute right ventricular preload increase: such as a large number of rapid intravenous blood transfusion, infusion.

(two) pathogenesis

1. Normal right ventricular function

The maintenance of the pulmonary circulation depends on normal left ventricular function. The main function of the right ventricle is not to maintain the pulmonary circulation. The right ventricle only acts as an auxiliary pump. The normal left ventricular function can maintain a lower left atrial pressure, so that the blood is in the right ventricular auxiliary pump. Under the action, through the low resistance, short path, low pressure pulmonary circulation reaches the left ventricle to maintain a low central venous pressure and reflux of the systemic venous system.

2. Pathophysiology of acute right heart failure

1 Acute right heart failure can cause insufficient left ventricular filling, causing a decrease in left ventricular output resulting in hypotension or shock.

2 due to a sharp drop in arterial pressure, reflex can cause pulmonary vasoconstriction, pulmonary circulation resistance increases, thereby further reducing left ventricular filling pressure, forming a vicious circle.

3 Acute right ventricular dilatation in acute right heart failure: due to the thin right ventricular wall and high compliance, when the contractile force is sharply reduced or the acute right ventricular anterior and posterior load is increased, the right ventricle can be expanded to 2 times the original capacity. Maintain its normal end diastolic pressure.

4 When the right ventricular compensation is incomplete, right ventricular end-diastolic pressure and peripheral venous pressure may increase, and systemic venous congestion may occur.

Acute right heart failure prevention

1. To correct the cause and cause

According to foreign data, 80% to 90% of patients with pulmonary embolism are complicated by deep venous thrombosis (DVT) of the lower extremities, while the predisposing factors of DVT and long-term bed rest and inactivity, surgery and other traumas cause blood stasis, venous injury and It is related to hypercoagulable state. Therefore, for patients with long-term bed rest and older age, it is necessary to increase activities and actively treat trauma. For the prevention of acute right ventricular infarction, it is necessary to actively prevent coronary heart disease and control the risk factors of coronary heart disease.

2. In the treatment of diseases that may cause right heart failure in clinical practice, it is necessary to closely observe changes in the condition, early detection of symptoms and signs of right heart failure, and give active and effective treatment.

Acute right heart failure complications Complications

Acute right heart failure can be complicated by complications such as cardiogenic shock, multiple organ system failure and electrolyte and acid-base balance disorders.

Acute right heart failure symptoms Common symptoms Heart failure Circulatory failure Shock hypotension Cold sweat sorrow biliary colic right heart failure response Dull hair

The clinical manifestations of right heart failure are significantly different from acute left heart failure.

1. Low perfusion signs of the arterial system

(1) hypotensive state: hypotension and tachycardia, there is no manifestation of peripheral circulatory failure.

(2) Cardiogenic shock: a significant decrease in blood pressure with less urinary (<20ml/h) and peripheral circulatory failure, such as wet limbs, cold sweat, convulsions, irritability or unresponsiveness.

2. Acute signs of right ventricular dilatation

(1) Functional tricuspid regurgitation: 3 to 4 intercostal systolic murmurs on the left sternal border. This murmur can be significantly attenuated or disappeared after right heart failure control.

(2) When the right ventricle contracts, the blood flows back to the right atrium, and there is a positive jugular vein pulsation and an advanced systolic pulsatile pulsation. However, when the right ventricular contractility is significantly reduced, the sign is not obvious.

3. Peripheral venous congestion signs

(1) jugular vein engorgement, large liver tenderness, positive liver-jugular regurgitation.

(2) Kussmaul sign positive: jugular vein engorgement is more obvious when inhaling.

(3) Acute liver congestion causes pain in the right upper quadrant, sometimes resembling biliary colic.

(4) Cyanosis: Peripheral cyanosis caused by blood stasis, and mixed cyanosis in pulmonary infarction with significant hypoxemia.

Acute right heart failure examination

According to its primary disease, there may be corresponding performance:

Acute pulmonary infarction

(1) Soluble fibrin complex (SFC) and FDP: SFC suggests that thrombin is newly produced. FDP suggests fibrinolytic activity, and the positive rate in pulmonary embolism is 55% to 75%. At the time, it is conducive to the diagnosis of pulmonary embolism, but the level of FDP is affected by liver, kidney, and disseminated intravascular coagulation. Free FDP in plasma can be measured 1 to 2 days after onset, lasting about 10 days. Faster, can increase the specificity and sensitivity of the diagnosis, but also positive when the patient has vasculitis or central nervous system damage.

(2) Arterial blood gas analysis and pulmonary function: 85% of patients with pulmonary embolism have hypoxemia, and are related to the degree of embolism, alveolar oxygen partial pressure and arterial oxygen partial pressure difference (PA-aDO2) are significantly increased; The gas/tidal volume ratio (VD/VT) increased during embolization. When the patient had no restrictive or obstructive ventilatory dysfunction, a ratio of >40% suggested a pulmonary embolism, and <40% without clinical embolism may exclude pulmonary embolism.

2. Acute right ventricular infarction

(1) leukocytosis, increased neutrophils, and accelerated erythrocyte sedimentation rate.

(2) Serum myocardial enzymes (CPK, CPK-MB, AST, LDH, etc.) are increased.

Acute pulmonary infarction

(1) Chest X-ray: showing pulmonary congestion, pulmonary artery segmentation and hilar dance, heart shadow gradually enlarged, heart-thorax ratio, severely increased, if there is a large pulmonary infarction, X-ray examination may have large pulmonary artery shadow and surrounding The blood vessels become thinner. In some cases, there is no ischemia due to no bleeding in the infarct area. Because of the ischemia in the infarct area, the transmittance of the lung increases, and the chest radiograph can not exclude the pulmonary embolism.

(2) Electrocardiogram: Temporary changes often occur, but the changes are very inconsistent, mainly manifested as acute right ventricular dilatation and pulmonary hypertension, showing a significant right deviation of the ECG axis, extreme clockwise transposition, right bundle branch block, There is a typical S1QIITIII wave pattern (I lead S wave depth, III lead Q wave significant and T wave inversion), sometimes pulmonary P wave, or lung-crown reflex induced myocardial ischemia.

(3) Right heart catheterization and selective indicator dilution curve measurement: can be found in the right atrium, right ventricular or pulmonary artery level left to right shunt, and the heart chamber pressure increased.

(4) pulmonary perfusion imaging and pulmonary ventilation/perfusion (V/Q) imaging: pulmonary radionuclide perfusion imaging can improve the correctness of pulmonary embolism diagnosis, can show radioactive defects of the lung lobe or segment, but it is not highly specific Sex, such as emphysema, can also produce lung perfusion imaging defects, therefore, combined with radionuclide 99mTc aerosol imaging, local ventilation function test can improve the correctness, the combination of the two called V / Q imaging, there are the following 3 Type:

1Vn/Qn: ventilation and perfusion are normal, excluding pulmonary embolism;

2Vn/Qo: normal ventilation with perfusion imaging defect of lung segment or lung lobe, such as typical clinical symptoms, can confirm pulmonary embolism;

3Vo/Qo: Partial lung ventilation and perfusion imaging are defective. At this time, pulmonary embolism cannot be diagnosed. It must be combined with clinical and pulmonary angiography if necessary.

(5) Pulmonary angiography: Selective pulmonary angiography is the most accurate method for diagnosing pulmonary embolism. The positive rate is 85% to 90%. The location and extent of obstruction can be determined. If supplemented with partial enlargement and oblique imaging, An embolus with a diameter of 0.5 mm is shown as a basis for diagnosis of pulmonary embolism. X-ray signs of pulmonary angiography must have filling defects or vascular interruptions in the pulmonary lumen. Other meaningful signs such as localized lobes and vascular texture of the lung segments Reduce or slow blood flow and reduced blood flow.

(6) Digital subtraction angiography: Compared with V/Q imaging, the coincidence rate is 83.5%. This method is applicable to patients with high V/Q imaging suspiciousness or estimated embolization in the main branches of pulmonary artery, especially those with chronic obstructive pulmonary disease. Can not accept pulmonary angiography.

(7) Magnetic resonance imaging technology: an effective method for diagnosing pulmonary hypertension and pulmonary emboli.

2. Acute right ventricular infarction

(1) Electrocardiogram: V3R, V4R and CR4R (the fifth intercostal midline of the right clavicle) are QS type, ST segment elevation is 1mm, and there may be temporary right bundle branch block.

(2) Echocardiography: the increase of the right heart cavity diameter >25mm and RVED/LVED>0.7 can be used as the diagnostic criteria for right ventricular infarction.

(3) Chest X-ray: no pulmonary congestion; due to right ventricular dilatation, there is an increase in cardiothoracic index in the early stage of infarction.

(4) Radionuclide examination: The localized wall of the right ventricular wall disappeared and the right ventricular ejection fraction decreased.

Diagnosis and diagnosis of acute right heart failure

Diagnostic criteria

1 clinical cause of acute right heart failure;

2 clinical manifestations of acute right heart failure;

3 hemodynamic examination: visible right ventricular filling pressure (RVFP) increased and left ventricular filling pressure (LVFP) normal or low, or a disproportionate increase in the two (RVFP / LVFP> 0.65).

Differential diagnosis

The disease needs to be differentiated from patent ductus arteriosus, aortic pulmonary artery septal defect, supraventricular ventricular septal defect with aortic valve prolapse, such as acute pulmonary embolism and acute myocardial infarction, pulmonary edema, acute asthma , atelectasis, pericarditis, spontaneous pneumothorax and inter-wall aneurysms are confused, should pay attention to identification.

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