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Abstract: The patient complained of shortness of breath after activity for 5 years, aggravated with cough, and inability to lie down at night for 4 days. He had a 30-year history of hypertension and was taking intermittent oral antihypertensive medication, which was usually poorly controlled. The patient had a history of smoking for 20 years. The diagnosis of cardiac insufficiency, pulmonary edema and hypertension was confirmed by relevant investigations. The patient’s condition was clinically controlled by aggressive treatment of the primary disease, such as correction of cardiac insufficiency and anti-inflammation.
Basic information】Female, 70 years old
Disease Type】Cardiac insufficiency, pulmonary edema, hypertension
Hospital】The Second Hospital of Harbin Medical University
Date of consultation】January 2019
Treatment plan】Medication (nifedipine controlled-release tablets + amiodarone hydrochloride injection + deacetyl trichothecene injection + furosemide injection + amoxicillin capsule) + oxygen absorption
[Treatment Period] 10 days of hospitalization
Treatment effect】The condition has been controlled and all indicators are improving
I. Initial consultation
The patient was wheeled from the emergency room to the ward. The family reported shortness of breath after intermittent activities for 5 years, aggravated by cough, and inability to lie down at night for 4 days. The patient was diagnosed with hypertensive heart disease and cardiac insufficiency in a local hospital five years ago when he developed shortness of breath after activity due to a cold, and his symptoms were relieved after he was given blood pressure control and improvement of cardiac function. The patient came to the hospital for further treatment and was admitted to our department with respiratory distress and pulmonary infection. On examination: heart rate was 135 beats/min, blood pressure was 182/95 mmHg, lips and mouth were slightly cyanotic, jugular veins were filled, hepatic neck reflux (-), dry and wet rales were heard in both lower lungs, the heart border was enlarged under the left, the first heart sound was unequal in strength, pulse was short, and there was no sunken edema in both lower limbs. Electrocardiogram showed atrial fibrillation. Cardiac ultrasound: enlarged bilateral atria, moderate regurgitation in the mitral valve area, mild regurgitation in the aortic valve area and tricuspid valve area, chest X-ray suggested: enlarged cardiac shadow, pulmonary edema. Liver function: glutamic aminotransferase and glutamic oxalacetic aminotransferase were elevated, cardiac enzyme profile was normal, troponin was slightly elevated, and blood glucose electrolytes were normal. Consider: cardiac insufficiency, pulmonary edema, hypertension. Previous history of hypertension for 30 years, intermittent oral antihypertensive drugs, usually poorly controlled, while the patient has a history of smoking for 20 years.
II. Treatment history
After admission, close monitoring (ECG, BNP, blood gas analysis, etc.); active treatment of the primary disease: control of blood pressure, nifedipine controlled-release tablets orally; administration of intravenous amiodarone hydrochloride injection to divert atrial fibrillation and control ventricular rate; for cardiogenic pulmonary edema: cardiac strengthening (deacetyl trichothecene injection), diuresis (furosemide injection pumped in); for fever: administration of amoxicillin capsules to control infection; improvement of hypoxia and Tissue oxygen supply: oxygenation; fluid management (restrict fluid intake as much as possible, control intake and output according to patient’s symptoms, urine output, BNP). Repeat lung CT: increased cardiac shadow and exudative lesions in the hilar region of both lungs with a small amount of bilateral pleural effusion.
III. Treatment effect
For cardiogenic pulmonary edema, the patient’s dyspnea was reduced after 2 days of cardiac stimulation (deacetyl trichothecene injection), tachypnea pumping and vasodilation; blood pressure was controlled with nifedipine controlled-release tablets taken orally, and blood pressure gradually returned to 145/85 mmHg, and atrial fibrillation returned to sinus rhythm with intravenous amiodarone; body temperature returned to normal after 4 days of amoxicillin capsules for infection control; fluid intake was restricted as much as possible to reduce The patient’s symptoms of inability to lie down at night were gradually relieved, and all the indexes of the patient were effectively improved at the 10th day of hospitalization, and he was discharged immediately.
IV. Notes
I am glad that the patient’s symptoms improved after treatment, but patients who continue to pay no attention to control the primary disease in general can lead to recurrent attacks like this patient, so in order to avoid recurrent pulmonary edema and prevent disease progression, the following should also be noted.
1, control blood pressure, prevent and control arrhythmias, and try to reverse recurrent tachyarrhythmias once they occur, and actively control the frequency of ventricular beats if they cannot be reversed.
2, in addition to quitting smoking, patients should also pay attention to is a light diet, such as do not eat too spicy and oily food.
3, actively increase resistance, including appropriate daily exercise, as well as in the winter and spring season when the climate changes quickly, reminded by opening windows to keep indoor air circulation to avoid colds.
V. Personal insight
Through the treatment of this patient, it can be realized that pulmonary edema is a relatively serious disease with a high mortality rate, which is clinically divided into cardiogenic and non-cardiogenic pulmonary edema, and sometimes even pulmonary imaging changes are easily misdiagnosed as pulmonary infection and admitted to the respiratory department. Cardiogenic pulmonary edema is usually caused by a large amount of blood accumulation in the pulmonary circulation due to a sharp increase in the amount of return blood and right heart expulsion or a sudden decrease in left heart expulsion, resulting in pulmonary circulation stasis and increased permeability of the pulmonary capillary wall. Clinically, it is commonly seen in acute, or chronic pulmonary edema caused by hypertensive heart disease, coronary artery disease, severe arrhythmias, heart valve disease, and various precordial diseases.
In addition, non-cardiogenic pulmonary edema is commonly seen in ARDS, i.e. acute respiratory distress syndrome, as well as inhalation of harmful gases, allergic reactions, radiation pneumonia, uremia, hepatic and renal diseases causing hypoproteinemia, diplopia pulmonary edema, plateau pulmonary edema, neurogenic pulmonary edema, etc. Note the differentiation.