Rebound hyperkalemia in a dog with albuterol toxicosis after cessation of potassium supplementation.

OBJECTIVE: To describe the presentation of rebound hyperkalemia as a delayed side effect of albuterol toxicity in a dog. CASE SUMMARY: A 3-year-old female neutered mixed-breed dog was presented for albuterol toxicosis that led to a severe hypokalemia, hyperlactatemia, and hyperglycemia. The dog also experienced sinus tachycardia and generalized weakness. Treatment was instituted with intravenous fluid therapy and potassium supplementation, and the dog was monitored with a continuous electrocardiogram. Resolution of hypokalemia was documented 12 hours after initial presentation, at which time fluid therapy and potassium supplementation were discontinued. There were no further periods of sinus tachycardia, but instead the dog developed ventricular ectopy with rapid couplets (instantaneous rates of 300/min). An echocardiogram revealed normal cardiac size and function. Twenty-four hours after presentation, the patient developed severe hyperkalemia, despite discontinuation of fluids and potassium supplementation for 12 hours. Serial venous and urinary electrolytes were performed for determination of the fractional excretion of electrolytes. These data confirmed rebound hyperkalemia (7.0 mmol/L), consistent with a markedly increased fractional excretion of potassium, and secondary to the release of potassium from inside the cells. Fluid therapy with dextrose supplementation was provided until 36 hours postpresentation. The hyperkalemia resolved, and the dog was discharged after 44 hours of hospitalization. NEW OR UNIQUE INFORMATION PROVIDED: This case documents rebound hyperkalemia following treatment of albuterol toxicosis in a dog. This case highlights the importance of understanding the distribution of total body potassium when treating serum hypokalemia. Transcellular shifts of potassium, as in the case of albuterol toxicosis, can lead to rebound hyperkalemia even after discontinuation of potassium supplementation. This case further explores the utility of fractional excretion of electrolytes in elucidating the etiology and management of electrolyte disturbances.

Heart rate control with landiolol hydrochloride in infants with ventricular dysfunction and pulmonary hypertension.

AIMS: Sinus tachycardia potentially leads to a deterioration of cardiac function in critically ill infants. The ultrashort-acting beta-blocker landiolol hydrochloride is a new pharmacological option for a selective heart rate (HR) control in patients with sinus tachycardia and heart failure. METHODS AND RESULTS: This study was a monocentric retrospective medical chart review study at the University Children's Hospital Bonn (Germany) from 01 January 2018 until 30 June 2020. This study included a cohort of 62 term and preterm infants with a diagnosis of ventricular dysfunction and/or pulmonary hypertension (PH), in combination with preexisting tachycardia and treatment with landiolol hydrochloride. Infants were allocated to subgroups according to weeks of gestational age (GA): born at <35 weeks of GA (Group A) and born at >35 weeks of GA (Group B). Tachycardia was defined depending on GA (<35 weeks of GA: >170 b.p.m.; ≥ 35 weeks of GA: >150 b.p.m.). The primary endpoint was defined as percentage of patients achieving HR normalization during the first 24 h of landiolol treatment. Twenty-nine infants were allocated to Group A and 33 infants to Group B. The overall median GA of the infants was 35.3 (23.3/41.3), with 53% female infants. The primary endpoint was achieved in 57 patients (91.9%). The median time to reach target HR was 1.8 (0.3-24) h. The median starting dose of landiolol was 8.8 (3.9-25.3) µk/kg/min, with a median dosing during the first 24 h of landiolol treatment of 9.9 (2.8-35.4) µk/kg/min. The median landiolol dose while achieving the target HR was 10 (2.4-44.4) µk/kg/min. The right ventricular dysfunction improved significantly in both groups 24 h after onset of landiolol infusion (P = 0.001 in Group A and P = 0.045 in Group B). The left ventricular and biventricular dysfunction improved significantly 24 h after onset of landiolol infusion in infants of Group B (P = 0.004 and P = 0.006, respectively). The severity of PH improved significantly after 24 h in infants of Group A (P < 0.001). During landiolol treatment, no severe drug-related adverse event was noted. CONCLUSIONS: The use of landiolol hydrochloride for HR control of non-arrhythmic tachycardia in critically ill infants is well tolerated. Reduction of HR can be guided quickly and landiolol treatment is associated with an improvement of ventricular dysfunction and PH.

Sympathetic toggled sinus rate acceleration as a mechanism of sustained sinus tachycardia in chronic orthostatic intolerance syndrome.

BACKGROUND: The role of sympathetic nerve activity to maintain sinus rate acceleration remains unclear. OBJECTIVE: The purpose of this study was to test the hypothesis that sustained (>30 seconds) sinus rate acceleration can be associated with either a sympathetic driven or a sympathetic toggled mechanism. METHODS: We used a patch monitor to record skin sympathetic nerve activity (SKNA) and electrocardiogram over 24 hours. Study 1 included chronic orthostatic intolerance (OI) (n = 18), atrial fibrillation (n = 7), and asymptomatic normal control (n = 19) groups. Study 2 included 17 participants with chronic OI not treated with ivabradine, pyridostigmine, or ß-blockers. RESULTS: While a majority of sinus rate acceleration was driven by persistent SKNA in study 1, some episodes were toggled on and off by SKNA bursts without persistent SKNA elevation. The sympathetic toggled sinus rate acceleration episodes were found in 7 of 18 participants with chronic OI (39%), 2 of 7 participants with atrial fibrillation (29%), and 6 of 19 normal control participants (32%) (P = .847) and were faster and longer in the chronic OI group than in other groups. In study 2, there were a total of 11 episodes of sinus rate acceleration that persisted for >200 seconds. Among these episodes, 6 (35%) were toggled on and off by SKNA bursts. CONCLUSION: Sustained sinus rate acceleration (may be toggled on or off) is associated with SKNA bursts in participants with chronic OI, participants with atrial fibrillation, and normal controls. Patients with OI had more frequent and longer episodes than did other groups.

The spectrum and prevalence of arrhythmia in different clinical pulmonary hypertension groups in Chinese population.

BACKGROUND: Arrhythmia is not uncommon among pulmonary hypertension (PH) population, and may be associated with disease severity. HYPOTHESIS: To investigate different spectrums and prevalence of arrhythmias in different clinical PH groups in Chinese population. METHODS: Patients diagnosed with PH between April 15, 2019, and August 2, 2021, were enrolled prospectively. The prevalence of different types of arrhythmias in PH patients were calculated. Logistic regression analyses were conducted to determine independent predictors for arrhythmia. RESULTS: One thousand patients were enrolled. The prevalence of any arrhythmia, sinus node dysfunction, sinus tachycardia, atrial fibrillation, atrial flutter, other types of atrial tachycardia, atrioventricular block, and ventricular tachycardia is 44.4%, 12.2%, 15.2%, 8.1%, 4.1%, 10.2%, 7.1%, and 2.5%. Logistic regression analyses revealed that older age and larger right ventricle (odds ratio: 1.111 and 1.095, p < .05) were independently related with higher probability of supraventricular arrhythmia; Complicating with coronary artery disease, larger right ventricle, and increased left ventricular end-diastolic diameter (odds ratio: 19.540, 1.106, and 1.085, p < .05) were independently correlated with sinus node dysfunction/atrioventricular block in patients with pulmonary arterial hypertension. CONCLUSIONS: Nearly half of PH patients experienced at least one type of arrhythmia. The most common seen arrhythmias were supraventricular arrhythmia, sinus tachycardia, and sinus node dysfunction. Older age and larger right ventricle were independently related with higher probability of supraventricular arrhythmia; Complicating with coronary artery disease, larger right ventricle and increased left ventricular end-diastolic diameter were independently correlated with higher probability of sinus node dysfunction/atrioventricular block in patients with pulmonary arterial hypertension.

Síndrome de Tako-Tsubo tras intento de homicidio a una anciana de 89 años / Tako-Tsubo syndrome after homicide attempt on an 89 year-old woman

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Respiration driven excessive sinus tachycardia treated with clonidine.

A 26-year-old man presented to our syncope service with debilitating daily palpitations, shortness of breath, presyncope and syncope following a severe viral respiratory illness 4 years previously. Mobitz type II block had previously been identified, leading to a permanent pacemaker and no further episodes of frank syncope. Transthoracic echocardiography, electophysiological study and repeated urine metanepherines were normal. His palpitations and presyncope were reproducible on deep inspiration, coughing, isometric hand exercise and passive leg raises. We demonstrated rapid increases in heart rate with no change in morphology on his 12 lead ECG. His symptoms were resistant to fludrocortisone, flecainide, ß blockers and ivabradine. Initiation of clonidine in combination with ivabradine led to rapid resolution of his symptoms. We suggest that an excessive respiratory sinus arrhythmia was responsible for his symptoms and achieved an excellent response with the centrally acting sympatholytic clonidine, where previous peripherally acting treatments had failed.

Epilepsia y síndrome de Brugada / Epilepsy and Brugada syndrome

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Downgrading mitral regurgitation in the echo laboratory: a case of rheumatic mitral restricted motion unmasked by emotional stress.

We report the case of a 76-year-old woman with mild-to-moderate mitral regurgitation due to rheumatic disease, severe dyspnoea, pulmonary hypertension and a recent episode of heart failure with paroxysmal atrial fibrillation. Transthoracic echocardiography at rest showed a mild-to-moderate mitral regurgitation, which was unable to justify the acute worsening of heart failure symptoms. During transesophageal echocardiography (TEE), deep anxiety induced sinus tachycardia and high SBP followed by pulmonary subedema. The TEE study ascertained a new-onset transient severe mitral regurgitation induced by stress and tachycardia. We speculate that the mechanism underlying the increasing of mitral regurgitation was related to the restricted motion of the posterior leaflet worsened by tachycardia. A further TEE, performed in the operating room under general anesthesia, thus without the emotional involvement of the patient, was not able to provoke a heart failure, even after dobutamine infusion, thus, downgrading the anatomical and functional mitral regurgitation severity.

Managing the patient with episodic sinus tachycardia and orthostatic intolerance.

Patients with episodic sinus tachycardia and associated orthostatic intolerance present a diagnostic and management dilemma to the clinician. We define this group of disorders to include sinus node reentrant tachycardia (SNRT), inappropriate sinus tachycardia (IAST), and postural orthostatic tachycardia syndrome (POTS). After a brief review of the current understanding of the pathophysiology and epidemiology of this group of disorders, we focus on the diagnosis and management of IAST and POTS. Our approach attempts to recognize the considerable overlap in pathophysiology and clinical presentation between these two heterogeneous conditions. Thus, we focus on a mechanism-based workup and therapeutic approach. Sinus tachycardia related to identifiable causes should first be ruled out in these patients. Next, a basic cardiovascular and autonomic workup is suggested to exclude structural heart disease, identify a putative diagnosis, and guide therapy. We review both nonpharmacologic and pharmacologic therapy, with a focus on recent advances. Larger randomized control trials and further mechanistic studies will help refine management in the future.

Shock anafiláctico prolongado de 4 días de duración / Anaphylactic shock lasting 4 days

Se presenta el caso de un varón de 62 años programado para una cistectomía radical que a los 10 min de comenzar la cirugía presentó hipotensión arterial severa, taquicardia sinusal y un aumento de las presiones en la vía aérea. No se obtuvo respuesta a la administración de diversos fármacos vasoactivos (efedrina, fenilefrina, dopamina, noradrenalina). Tras descartar otras posibles etiologías se valoró la posibilidad de que se tratara de una reacción de anafilaxia y se inició la administración de adrenalina, con lo que se consiguió estabilizar hemodinámicamente al paciente. En la unidad de reanimación fue preciso mantener la perfusión de adrenalina y la ventilación mecánica durante 4 días (AU)

We present a case of a 62 year-old male scheduled for radical cystectomy, who, ten minutes into the surgery, presented with severe hypotension, tachycardia and increased airway pressure. There was no response to the administration of vasoactive drugs such as, ephedrine, phenylephrine, dopamine and norepinephrine. After ruling out several causes, we evaluated the possibility of an anaphylactic reaction. Adrenaline was given, and the patient stabilized. An adrenaline infusion and mechanical ventilation was required for four days in the critical care unit (AU)