For Patients With Chronic Kidney Disease And Acute Heart Failure, The Acute Treatment Method Is Here!

A middle-aged male patient was admitted to the hospital mainly because of "heart fatigue, shortness of breath and dyspnea for 1 day". One day before admission, the patient began to experience heart fatigue and shortness of breath after being exposed to a cold. Dyspnea, chest tightness, cough, sputum discomfort, yellow purulent sputum, especially at night, accompanied by abdominal distension, anorexia, orthopnea, and other discomforts, without chest pain, fever and night sweats, and other discomforts.

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There was no treatment outside the hospital, and the symptoms did not improve but gradually worsened. I came to our hospital for treatment today. The outpatient was admitted to our department with "heart failure". There was no change in body weight.

History: There was a history of type 2 diabetes for more than 10 years. He did not take hypoglycemic drugs and insulin injections regularly. He had a history of hypertension for many years. The systolic blood pressure was as high as 180mmhg. The dialysis treatment in our hospital denies a history of "hepatitis, tuberculosis" and other infectious diseases, no history of drug allergy, no history of food allergy, no history of trauma, no history of surgery, no history of blood transfusion, and no history of vaccination.

Specialist examination: jugular vein filling, rough breath sounds in both lungs, wet and dry sounds, enlarged heart circle, heart rate: 50 beats/min, regular heart rhythm, no murmurs heard in each valve area, flat and soft abdomen, small liver and spleen, tenderness under the sword, no rebound tenderness and muscle tension, normal bowel sounds, mild edema of both lower extremities.

Auxiliary inspection:

Electrocardiogram prompts: sinus rhythm, complete left bundle branch block;

Three items of myocardial infarction: troponin I 0.02 ng/ml;

Electrolytes: Potassium 7.60 mmol/L, Calcium 1.44 mmol/L; five types of blood cell analysis: white blood cells 7.65×109/L, percentage of neutrophils 86.10%, red blood cells 2.75×1012/L, hemoglobin 94 g/L.

17 items of liver function + myocardial enzyme spectrum: total protein 53.8 g/L, globulin 17.7 g/L, total bilirubin 3.0 μmol/L, lactate dehydrogenase 305.0 U/L, α-hydroxybutyrate dehydrogenase 232.0 U/L, creatine kinase isoenzyme 25.0 U/L.

Cardiac color Doppler ultrasound: in line with coronary heart disease changes with mild mitral regurgitation, normal high line on the left ventricular wall, it is recommended to observe blood pressure; mild tricuspid regurgitation, aortic valve degeneration with mild regurgitation, pericardial effusion.

Chest CT:

1. There are scattered patches and streaks in both lungs, and some interlobular septa are thickened. Pulmonary edema and a little inflammation may be considered. It is recommended to re-examine after treatment.

2. The left atrium and left ventricle are enlarged; the density of each cardiac chamber is reduced, suggesting anemia; a small amount of pericardial effusion; punctate calcification of the aortic wall and aortic valve.

initial diagnosis:

Coronary atherosclerotic heart disease? Enlarged heart circle, sinus rhythm, cardiac function grade IV, total heart failure, acute exacerbation of chronic heart failure;

community-acquired pneumonia;

Type 2 diabetes;

Grade 3 hypertension (very high risk);

Chronic renal failure uremic phase (mild renal anemia);

Hyperkalemia;

Hypocalcemia.

After admission, he was given continuous oxygen inhalation, ECG monitoring, methylprednisolone sodium succinate for injection for anti-inflammation, ceftazidime for anti-infection, nitroglycerin for dilating blood vessels and lowering blood pressure, furosemide injection for diuresis to improve heart function, and immediate dialysis.

Question Discussion

★ 1. The patient has a medical history of hypertension and diabetes. What causes chronic renal failure?

The history of hypertension in hypertensive nephropathy is preceded by kidney damage. Proteinuria occurs after persistent hypertension for more than 5 years. Mild to moderate proteinuria and hematuria are rare. The early stage mainly manifests as nocturia and urine concentration. Reduced, the damage to the renal tubular function is the most severe and precedes the damage to the glomerulus, and there are fewer formed elements such as blood cells in the urine. And often combined with multiple organ damage: left ventricular hypertrophy, fundus vascular disease, cerebrovascular disease, etc., in the late stage, B-ultrasound can show that both kidneys shrink, and CT examination can show granular unevenness on the kidney surface. The main pathological changes.

Diabetic nephropathy has a clear history of diabetes, and microalbuminuria, early diabetic nephropathy should be suspected, because when type 2 diabetes is combined with diabetic retinopathy, it can be diagnosed; when the medical history does not match or there is no medical history, it should rely on renal biopsy; clinically Urinary albumin excretion rate, renal function, and glomerular filtration rate are used as the grading standard of diabetic nephropathy. Glomerular function damage is the main cause, and B-ultrasound can also be used in some patients in the stage of chronic renal failure. Kidneys appear normal in size.

★ 2. The patient had sudden dyspnea during the dialysis period, and he had long-term maintenance hemodialysis treatment in our hospital (twice a week, 4 hours each time). During the dialysis period, his weight increased a lot, and he had a history of coronary heart disease, Is it caused by an acute exacerbation of chronic heart failure or metabolic acidosis caused by renal failure?

Acute heart failure often manifests as dyspnea, forced sitting, pale complexion, cyanosis, irritability, etc., a sustained drop in blood pressure or even shock, and when it is combined with pulmonary edema, it may manifest as continuous wheezing, irritability, and a sense of fear, accompanied by shortness of breath. The frequency increases and some will cough up pink foamy phlegm.

In chronic renal failure, GFR decreases, metabolites such as phosphoric acid, sulfuric acid, and other acidic substances are retained due to renal excretion dysfunction, and hyperchloremia (or positive chloride) high anion gap acidosis may occur.

There may be no obvious abnormality in the respiratory state of mild metabolic acidosis; when the degree of acidosis is aggravated, the respiratory rate may be accelerated and its amplitude may be deepened; when severe metabolic acidosis occurs, Kussmaul breathing may appear, which is manifested as when inspiratory Deepen and slow down and speed up when exhaling. The principle is that when acidosis is stimulated by the central and surrounding receptors, the respiratory center is excited to increase the removal of carbon dioxide and reduce the partial pressure of carbon dioxide to obtain a certain compensation.

When the patient did not undergo blood gas testing, how to judge the cause of dyspnea?

At the beginning of the patient's onset, the heart rate was significantly accelerated (150-180 beats/min), shortness of breath, orthopnea, distended jugular veins, blood pressure as high as 180mmHg, accompanied by edema of both lower extremities, and chest CT showed pulmonary edema, so coronary heart disease was considered Combined with acute heart failure, nitroglycerin was given to dilate blood vessels to lower blood pressure, furosemide injection diuretic and other treatments. However, the patient did not excrete urine 6 hours after diuresis; the patient had hyperkalemia, combined with his medical history, there is a high probability that he was complicated with metabolic acidosis, and he could be treated with acid correction, diuresis, hypertonic sugar, calcium, etc., but this The patient indicates acute dialysis.

★ 3. What kind of arrhythmia did the patient experience, and what was the reason?

At first glance, the QRS is wide and deformed in the electrocardiogram, and the first reaction is ventricular arrhythmia, but if you look carefully, there is no ventricular fusion wave and ventricular capture, and it is not a sine wave. The heart is slightly relaxed. After consulting the superior, consider: the complete left bundle branch block, but why is this arrhythmia found? Is it because of hyperkalemia?

What should be the next step in treatment?

The effect of high potassium on the heart is manifested as changes in ion permeability and membrane potential under high potassium conditions, resulting in changes in its automaticity, conduction, and excitability.

There are three kinds of ion channels, Na+, K+, and Ca2+ in the environment of cardiomyocytes. Only their opening and closing are discussed. The following table lists the corresponding relationship between the action potential of the heart and the process of depolarization and repolarization of the heart.

Common hyperkalemia mainly manifests as decreased myocardial systolic function, low and blunt heart sounds, slowed heart rate, atrioventricular block, ventricular fibrillation, and even cardiac arrest.

Hyperkalemia first affects repolarization, and the potassium outflow increases rapidly at the end of the rapid repolarization period, causing T wave peaks, and the potassium outflow increases in the early and plateau stages of rapid repolarization, causing ST-segment depression; then it further affects the initial depolarization, Elevated blood potassium increases the absolute value of the resting potential of the membrane, which leads to the slowing down of depolarization and the reduction of self-discipline, conduction, and sexual self-discipline. Decreased cell conductance prolongs PR, even conduction block, and working cells can manifest as widening, shortening, and equalization of P waves and QRS waves.

Different blood potassium levels have different ECG manifestations. When the blood potassium is >6mmol/L, there will be a narrow and sharp T wave at the base. When the blood potassium is 7-9mmol/L, the PR interval will be prolonged, the P wave will disappear, and the R wave will appear. Decrease, etc.; when the blood potassium is 9-10mmol/L, a sine wave appears, the QRS complex is prolonged, and the T wave is high and sharp.

Combined with the medical history, it was preliminarily inferred that it was caused by hyperkalemia. After hemodialysis, the patient's symptoms of heart fatigue and shortness of breath were significantly improved, and when the blood potassium recovered, the QRS gradually recovered in the electrocardiogram, and finally, he was discharged from the hospital.

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