Sudden right heart failure

Introduction Sudden right heart failure, that is, acute right heart failure, is a clinical result of a sharp decrease in right ventricular output due to a sharp decrease in right ventricular myocardial contractility or a sudden increase in right and left anterior and posterior loads for some reasons. Syndrome. Acute right heart failure is more common in acute massive pulmonary infarction and acute right ventricular infarction. Because acute right heart dysfunction has its unique characteristics, there is a significant difference in clinical management and left ventricular dysfunction, so early clinical diagnosis and correct treatment of right heart failure have important significance.

Cause

Common causes of sudden right heart failure 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.

4. Acute left heart failure mainly manifests as: sudden dyspnea, especially paroxysmal dyspnea at night, the patient can not sit flat, can only sit and breathe. Shortness of breath, frequent, up to 30 to 40 beats / min, while the patient has a feeling of suffocation, pale complexion, cyanosis, irritability, sweating, cold skin, coughing, coughing out of serous foam, severe coughing Red foam sputum, and even respiratory depression, suffocation, and mental disorder.

an examination

Related inspection

Two-dimensional echocardiography electrocardiogram M-mode echocardiography (ME)

diagnosis:

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

Identification of sudden right heart failure:

Acute pulmonary infarction

(1) Soluble fibrin complex (SFC) and FDP: SFC suggests that thrombin is newly produced, and FDP suggests fibrinolytic activity. The positive rate in pulmonary embolism is 55% to 75%. When both are positive, it is conducive to the diagnosis of pulmonary embolism. However, 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. This test is faster and can increase the specificity and sensitivity of the diagnosis, but when the patient has vasculitis or central nervous system damage, Positive.

(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, neutrophil increased; ESR accelerated.

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

Acute left heart failure mainly manifests as: sudden dyspnea, especially paroxysmal dyspnea at night, the patient can not sit flat, can only sit and breathe. Shortness of breath, frequent, up to 30 to 40 beats / min, while the patient has a feeling of suffocation, pale complexion, cyanosis, irritability, sweating, cold skin, coughing, coughing out of serous foam, severe coughing Red foam sputum, and even respiratory depression, suffocation, and mental disorder.

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