HISTORY, CURRENT ILLNESS AND PHYSICAL EXAMINATION

History
85 year old male admitted from outpatients for poor outpatient control of congestive signs and symptoms in the context of decompensation of heart failure.
No drug allergies.
Cardiovascular risk factors (CVRF): essential hypertension, no diabetes mellitus (DM) or dyslipidaemia.
Toxic habits: ex-smoker since the age of 65, previously smoked about ten cigars a day for 48 years.
Cardiological history: permanent atrial fibrillation CHAD2DS2-VASc 4 with controlled ventricular response and on anticoagulant treatment with apixaban. Congestive heart failure labelled as hypertensive aetiology, with preserved ejection fraction.
Other history: chronic kidney disease of probable origin due to nephroangiosclerosis, stage 3a KDIGO (usual creatinine 1.3 mg/dl). Rigid-kinetic syndrome of right predominance. Chronic iron deficiency anaemia due to digestive losses.
Benign prostatic hyperplasia and chronic open-angle glaucoma in both eyes.
Usual treatment: furosemide 40 mg 2-2-0; apixaban 2.5 mg 1-0-1; nebivolol 5 mg 0-0.5-0; spironolactone 25 mg 0-2-0; dutasteride 0.5 mg 1-0-0; carbidopa/levodopa 25/100 mg 2-2-2; allopurinol 100 mg 0-1-0; pantoprazole 40mg 1-0-0; brimonidine+timolol eye drops 1-0-1.


Present illness
The patient reports oedema in the lower limbs and dyspnoea on moderate exertion since his last admission for heart failure in a private centre a few months ago. He also reports two-pillow orthopnoea. Symptomatology has not improved despite high doses of oral diuretics and weekly boluses of intravenous furosemide in a day hospital.
He denies paroxysmal nocturnal dyspnoea, chest pain or palpitations. No infectious symptoms. She admits frequent dietary transgressions.

Physical examination
On arrival he was in good general condition, conscious and oriented, normohydrated, normoperfused and normal colour. Weight 58 kg. Blood pressure 115/83 mmHg, heart rate 75 bpm, basal oxygen saturation 93% and temperature 36.8 oC. Jugular venous engorgement up to the mandibular angle. Cardiac auscultation: arrhythmic, no murmurs or friction rubs.
Pulmonary auscultation: coarse crackles and hypophonesis up to midfields. Abdomen: normal hydro-aerial sounds, soft and depressible. No masses or visceromegaly. No pain on palpation, no evidence of peritoneal irritation or wall oedema. Lower extremities: oedema with fovea up to the middle of both legs.

COMPLEMENTARY TESTS
Electrocardiogram (ECG) on admission: atrial fibrillation (AF) at about 60 bpm, normal axis, complete right bundle branch block (RBBB) with secondary repolarisation alterations.
Chest X-ray on admission: bilateral pleural effusion of left predominance. Evidence of vascular redistribution. Aortic calcification. Spondyloarthrosis.
Blood tests on admission:
Haemogram: red blood cells 3.85 million/mm3. Haemoglobin 11.6 gr/dl. Haematocrit 36.6%. MCV. 95.1 fl, MCH 30.1 pg. MCHC 31.7 g/dl. RDW-CV 16.3%. Normoblasts (%) 0.0%. Platelets 275
Thousands/mm3. Leukocytes 7.45 thousands/mm3. Neutrophils 59.1%. Lymphocytes 23.9%. Monocytes 14.1%.
Eosinophils 0.9%. Basophils 0,3%. Granulocytes Imm. 1.7%, ESR 88 mm/h.
Coagulation study: INR 1.61. Prothrombin activity 52%. Cephalin time 31.9 seconds, Prothrombin time 18.0 s.
Biochemistry: glucose 83 mg/dl, urea 107 mg/dl, creatinine 2.09 mg/dl, estimated glomerular filtrate CKD-EPI 28.02 ml/min/1.73 m2, sodium 137 mEq/l, potassium 4.6 mEq/l, chlorine 94 mEq/l, total protein 7.2 g/dl, albumin 3.9 g/dl, total bilirubin 1.80 mg/dl, direct bilirubin 1.05 mg/dl, indirect bilirubin 0.75 mg/dl, GOT/AST 18 U/l, GPT/ALT 5 U/l, GGT 143 U/l, alkaline phosphatase 217 U/l, cholesterol 116 mg/dl, uric acid 8.3 mg/dl, total calcium 9.0 mg/dl, magnesium 2.71 mg/dl, inorganic phosphorus 2.3 mg/dl, iron 333 ug/dl, transferrin 190 mg/dl, ferritin 1409 ng/ml, transferrin saturation 138%, C-reactive protein 2.77 mg/dl, folic acid 5.6 ng/ml, vitamin B12 401 pg/ml, Natriur peptide. pro-BNP of 2300 pg/ml.
ECG on the fifth day of admission (rhythm strip): blocked atrial fibrillation, ventricular escape rhythm with QRS morphology different from baseline, at about 30 bpm.

Urgent laboratory tests on the fifth day of admission:
Haemogram: red blood cells 3.64 million/mm3, haemoglobin 11.0 g/dl, haematocrit 34.7%, MCV 95.3 fl, MCH 30.2 pg, MCHC 31.7 g/dl, RDW-CV 16.6%, platelets 233 thousands/mm3, leukocytes 7.05 thousands/mm3, neutrophils 68.2% 4.81, lymphocytes 19.9% 1.40, monocytes 11.1% 0.78, eosinophils 0.7% 0.05, basophils 0.1% 0.01.
E. Coagulation: INR 2.06, prothrombin activity 38%, cephalin time 32.8 seconds.
Biochemistry: glucose 141 mg/dl, urea 114 mg/dl, creatinine 2.08 mg/dl, sodium 134 mEq/l, potassium 4.4 mEq/l, chlorine 92 mEq/l, venous blood gases pH 7.45 pCO2 40 mmHg pO2 110 mmHg, bicarbonate 27.8 mmol/l, methaemoglobin 0.9% L-Lactate 1.9 mmol/l, ionic calcium (Calc) 4.40 mg/dl Ions in gas sample: k+ =4.3 mmol/l Na+ = 129 mmol/l.
ECG at discharge (image 5): AF with RV at 60 bpm. HR-CDBHR similar to the admission ECG.

CLINICAL EVOLUTION
After decompensation of HF refractory to oral and intravenous diuretics, the patient was admitted to cardiology with high-dose intravenous loop diuretics in combination with oral thiazide.
The ECG performed on admission showed atrial fibrillation at about 60 bpm, normal axis, HRBBB with secondary repolarisation alterations, and chest X-ray showed bilateral pleural effusion, predominantly on the left, with evidence of vascular redistribution, aortic calcification and spondyloarthrosis. Laboratory tests on admission showed worsening renal function in the context. The transthoracic echocardiogram showed a non-dilated left ventricle with moderate concentric hypertrophy, preserved ejection fraction with impaired relaxation, no significant valvular heart disease, normal estimated PSAP, dilated inferior vena cava (IVC). Good diuretic response and marked improvement in decongestion.
On the fifth day of admission, the patient had an episode of dizziness, bradycardia and BP of 85/60 mmHg. The nurse notified the doctor on duty, who found that the patient was conscious, although drowsy and sleepy, and reactive to verbal stimuli. On physical examination he was cold, bradycardic, rhythmic, with no murmurs and no signs of congestion at the time. AC: bradycardic, rhythmic, no murmurs. ECG: atrial fibrillation with complete atrioventricular block (AVB) with ventricular escape, with a different morphology to the baseline, at about 30 bpm (image 4). Urgent laboratory tests were requested to rule out ionic alterations, but the ions were in range and his renal function was stable with no worsening with respect to previous years. Blood pressure improved after infusion of 1000 cc of physiological saline. The patient was transferred to the coronary unit for monitoring.
After ruling out ionic aetiology, in view of a possible pharmacological trigger, it was decided to suspend doses of beta-blocker (nebivolol 2.5 mg) and eye drops (brimonidine/timolol).
However, a comparison of the medication administered showed that two tablets of carbidopa/levodopa 25/250 mg (plus formulation) were accidentally administered every eight hours, instead of the usual dose of carbidopa/levodopa 25/100 mg. After discontinuation of all three drugs, without the need for implantation of pacing devices, the patient showed improvement of atrioventricular conduction disturbance, recovering 1:1 conduction in less than 24 hours. Subsequently, the patient remained in AF with controlled VR and after 48 hours (in the presence of elevated HR) nebivolol could be reintroduced at its previous doses without incident. The patient is discharged with improved renal function and congestive data in AF with controlled VR under treatment with a well-tolerated beta-blocker.

DIAGNOSIS
Complete AVB due to accidental carbidopa/levodopa overdose.
Decompensated heart failure with preserved ejection fraction.
Permanent atrial fibrillation CHAD2DS2-VASc 4.
Exacerbation of stage 3a chronic kidney disease.
Stiff-kinetic syndrome on treatment with carbidopa/levodopa.
