Hypertensive emergency secondary to atropine / Emergencia hipertensiva secundaria a atropina

Atropine, a competitive antagonist of acetylcholine muscarinic receptors, is commonly used to treat severe bradycardia by blocking parasympathetic activity. We present a rare case of hypertensive emergency following atropine administration, with only one previous report in the literature. A 78-year-old woman with essential hypertension and hypercholesterolemia was admitted to the cardiac intensive care unit for non-ST segment elevation myocardial infarction. During coronary angiography, an occlusion of the right coronary artery was identified. While removing the diagnostic catheter through the right radial artery, the patient experienced intense pain and discomfort, accompanied by a vasovagal reflex characterized by bradycardia and hypotension. Intravenous atropine (0.5mg) was administered, leading to a rapid rise in heart rate with frequent ventricular ectopy. Subsequently, a progressive and exaggerated elevation in arterial blood pressure occurred, peaking at 294/121mmHg approximately 10min after atropine administration. The patient developed hypertensive acute pulmonary edema, successfully treated with intravenous nitroglycerine (10mg) and furosemide (60mg). Blood pressure normalized after approximately 14min. The exact mechanism of atropine-induced hypertensive emergency remains unknown. While hypertensive emergencies with atropine are exceedingly rare, healthcare professionals should be aware of this potential effect and be prepared for prompt intervention.(AU)

La atropina, un antagonista competitivo de los receptores muscarínicos de acetilcolina, se utiliza comúnmente para tratar la bradicardia severa al bloquear la actividad parasimpática. Presentamos un caso raro de emergencia hipertensiva después de la administración de atropina, con solo un informe previo en la literatura. Una mujer de 78 años con hipertensión esencial e hipercolesterolemia fue ingresada en la unidad de cuidados intensivos cardíacos por infarto agudo de miocardio sin elevación del segmento ST. Durante la angiografía coronaria, se identificó una oclusión de la arteria coronaria derecha. Mientras se retiraba el catéter diagnóstico a través de la arteria radial derecha, la paciente experimentó un intenso dolor y malestar, acompañado de un reflejo vasovagal caracterizado por bradicardia e hipotensión. Se administró atropina intravenosa (0,5 mg), lo que provocó un rápido aumento de la frecuencia cardíaca con frecuente ectopia ventricular. Posteriormente, ocurrió una elevación progresiva y exagerada de la presión arterial, alcanzando un máximo de 294/121 mmHg aproximadamente 10 minutos después de la administración de atropina. La paciente desarrolló edema pulmonar agudo hipertensivo, tratado con éxito con nitroglicerina intravenosa (10 mg) y furosemida (60 mg). La presión arterial se normalizó después de aproximadamente 14 minutos. El mecanismo exacto de la emergencia hipertensiva inducida por atropina sigue siendo desconocido. Aunque las emergencias hipertensivas con atropina son excepcionalmente raras, los profesionales de la salud deben estar al tanto de este efecto potencial y estar preparados para intervenir rápidamente.(AU)

Hypertensive emergency secondary to atropine.

Atropine, a competitive antagonist of acetylcholine muscarinic receptors, is commonly used to treat severe bradycardia by blocking parasympathetic activity. We present a rare case of hypertensive emergency following atropine administration, with only one previous report in the literature. A 78-year-old woman with essential hypertension and hypercholesterolemia was admitted to the cardiac intensive care unit for non-ST segment elevation myocardial infarction. During coronary angiography, an occlusion of the right coronary artery was identified. While removing the diagnostic catheter through the right radial artery, the patient experienced intense pain and discomfort, accompanied by a vasovagal reflex characterized by bradycardia and hypotension. Intravenous atropine (0.5mg) was administered, leading to a rapid rise in heart rate with frequent ventricular ectopy. Subsequently, a progressive and exaggerated elevation in arterial blood pressure occurred, peaking at 294/121mmHg approximately 10min after atropine administration. The patient developed hypertensive acute pulmonary edema, successfully treated with intravenous nitroglycerine (10mg) and furosemide (60mg). Blood pressure normalized after approximately 14min. The exact mechanism of atropine-induced hypertensive emergency remains unknown. While hypertensive emergencies with atropine are exceedingly rare, healthcare professionals should be aware of this potential effect and be prepared for prompt intervention.

ARNIs: balancing "the good and the bad" of neuroendocrine response to HF.

BACKGROUND: A new class of drugs-angiotensin receptor, neprylisin inhibitors, ARNI-has shown to be prognostic superior in HFrEF to the sole inhibition of the renin-angiotensin axes with enalapril. The ultimate mechanism of action of ARNIs is unknown. AIM: We have considered that ARNI exerts a positive modulation of the neuroendocrine balance, with enhancement of the physiological diuresis and dilatation due to neprylisin inhibition by sacubitril. This represents a shift in HF medical therapy always directed to counteract (with inhibitors of the renin-angiotensin system, beta blockers or inhibitors of aldosterone) the so-called "bad" neuroendocrine response. Development of ARNI, on the contrary, has led to consider the neuroendocrine response to HFrEF from a different angle, which is to say that the activation is not always deleterious, but it could also be beneficial. This concept is highlighted by the enhancement of the activity of atrial natriuretic peptide, induced by sacubitril/valsartan in the PARADIGM trial, and found as proof from early studies on untreated patients with constrictive pericarditis. The possibility that sacubitril inhibition of neprylisin acts by enhancing substance P and gene-related calcitonin peptide is also considered, as well as the negative effect of neprylisin inhibition. CONCLUSIONS: The beneficial effects of ARNI are related, in part at least, to a positive modulation of the neuroendocrine response to the disease, resulting in an increase of physiological diuresis and dilatation.