Heart Rate Recovery in Adult Individuals with Asthma

Background. Slow heart rate recovery (HRR) after exercise is predictor of overall mortality in individuals with and without cardiovascular or respiratory disorders. No data on adults with asthma are available. Aim. To evaluate the prevalence of slow HRR in these individuals as compared with those with chronic obstructive pulmonary disease (COPD).Methods. Retrospective analysis of baseline characteristics and physiological response to the six-minute walking distance test of stable individuals with asthma or COPD. Slow HRR was defined as HRpeak - HR at 1 minute after end exercise < 12 bpm.Results. Individuals with asthma walked significantly longer (median (IQR): 455 (385-512) vs 427 (345-485) meters; p= 0.005) with a lower prevalence of slow HRR (30.3% vs 49.0%, respectively: p<0.001) than those with COPD. Individuals with asthma and slow HRR were older and walked less than those with normal HRR, without any difference in airway obstruction or in disease severity. Multivariate analysis showed that only the difference HRpeak - baseline HR (∆HR), was predictor of slow HRR in both groups.Conclusion. More than 30% of adult individuals with asthma may show slow HRR. Only exercise ∆HR but no baseline characteristic seems predict the occurrence of slow HRR.

Not-so-typical typical atrioventricular nodal re-entrant tachycardia in an adolescent

Dysrhythmias are commonly encountered in the Emergency Department (ED). Timely management and recognition of dysrhythmia in the ED is essential and crucial. Physicians working in the ED should be familiar with atypical presentation of common dysrhythmias. This case report illustrates atrioventricular nodal re-entrant tachycardia (AVNRT) with an unusually slow heart rate in an adolescent. A 16-year-old male presented to the ED twice for palpitations. His electrocardiograms showed narrow complex tachycardia with absent P waves. Electrophysiology studies confirmed typical slow-fast AVNRT which was treated successfully with radiofrequency ablation of the slow pathway. Diagnosing rare dysrhythmias or common dysrhythmias which manifest atypically can be challenging for non-cardiologists. Although AVNRT generally occurs with a heart rate of >130 bpm, emergency physicians should be aware that AVNRT can take place with a relatively slower rate in both the elderly and young.

Confinement, partial sleep deprivation and defined physical activity–influence on cardiorespiratory regulation and capacity

Introduction Adequate cardiorespiratory fitness is of utmost importance during spaceflight and should be assessable via moderate work rate intensities, e.g., using kinetics parameters. The combination of restricted sleep, and defined physical exercise during a 45-day simulated space mission is expected to slow heart rate (HR) kinetics without changes in oxygen uptake ($${\dot{\text{V}}\text{O}}_{{2}}$$ V ˙ O 2 ) kinetics. Methods Overall, 14 crew members (9 males, 5 females, 37 ± 7 yrs, 23.4 ± 3.5 kg m−2) simulated a 45-d-mission to an asteroid. During the mission, the sleep schedule included 5 nights of 5 h and 2 nights of 8 h sleep. The crew members were tested on a cycle ergometer, using pseudo-random binary sequences, changing between 30 and 80 W on day 8 before (MD-8), day 22 (MD22) and 42 (MD42) after the beginning and day 4 (MD + 4) following the end of the mission. Kinetics information was assessed using the maxima of cross-correlation functions (CCFmax). Higher CCFmax indicates faster responses. Results CCFmax(HR) was significantly (p = 0.008) slower at MD-8 (0.30 ± 0.06) compared with MD22 (0.36 ± 0.06), MD42 (0.38 ± 0.06) and MD + 4 (0.35 ± 0.06). Mean HR values during the different work rate steps were higher at MD-8 and MD + 4 compared to MD22 and MD42 (p < 0.001). Discussion The physical training during the mission accelerated HR kinetics, but had no impact on mean HR values post mission. Thus, HR kinetics seem to be sensitive to changes in cardiorespiratory fitness and may be a valuable parameter to monitor fitness. Kinetics and capacities adapt independently in response to confinement in combination with defined physical activity and sleep.

Pharmacodynamic and pharmacokinetic behavior of landiolol during dobutamine challenge in healthy adults

Background To study the pharmacokinetic and -dynamic behavior of landiolol in the presence of dobutamine in healthy subjects of European ancestry. Methods We conducted a single-center, prospective randomized study in 16 healthy subjects each receiving an infusion of dobutamine sufficient to increase heart rate by 30 bpm followed by a 60 min infusion of 10 μg/kg/min landiolol. Results Dobutamine-induced increases in heart rate were stable for at least 20 min before a 60 min landiolol- infusion was started. The dobutamine effects were rapidly antagonized by landiolol within 16 min. A further slight decrease in heart rate during 20–60 min of the landiolol infusion occurred as well. Upon termination of landiolol infusion, heart rate and blood pressure recovered rapidly in response to the persisting dobutamine infusion but did not return to the maximum values before landiolol infusion. The pharmacokinetic parameters of landiolol in presence of dobutamine showed a short half-life (3.5 min) and a low distribution volume (0.3 l/kg). No serious adverse events were observed. Conclusion Landiolol can antagonize the dobutamine-induced increases in heart rate and blood pressure in a fast way. A rapid bradycardic effect until steady-state plasma levels is followed by a slow heart rate reduction. The latter can be attributed to an early desensitization to dobutamine. Consequently, after termination of landiolol, the heart rate did not achieve maximum pre-landiolol values. The pharmacokinetics of landiolol during dobutamine infusion are similar when compared to short- and long-term data in Caucasian subjects. Landiolol in the given dose can thus serve as an antagonist of dobutamine-induced cardiac effects. Trial registration Registration number 2010–023311-34 at the EU Clinical Trials Register, registration date 2010-12-21.

BRADYCARDIA IN ATHLETES: DOES THE TYPE OF SPORT MAKE ANY DIFFERENCE? – A SYSTEMATIC REVIEW

ABSTRACT Bradycardia in athletes can range from moderate to severe, and the factors that contribute to slow heart rate are complex. Studies investigating the mechanisms associated with this condition are controversial, and may be linked to the form of exercise practiced. A systematic literature review was conducted to discuss bradycardia mechanisms in athletes who practice different forms of sport. The databases consulted were Pubmed (MEDLINE), Clinical Trials, Cochrane, Scopus, Web of Science, SciELO, Sport Discus and PEDro. The search included English language articles published up to January 2019, that evaluated athletes who practiced different forms of sport. One hundred and ninety-three articles were found, ten of which met the inclusion criteria, with 1549 male and female athletes who practiced diverse forms of sport. Resting heart rate and cardiac structure were studied in association with the form of sport practiced, through heart rate variability, electrocardiogram, echocardiogram and pharmacological blockade. The studies suggest that a slow resting heart rate cannot be explained by increased vagal modulation alone, but also includes changes in cardiac structure. According to the studies, different sports seem to produce different cardiac responses, and the bradycardia found in athletes can be explained by non-autonomic and autonomic mechanisms, depending on the type of effort or the form of sport practiced. However, the mechanism underlying the slow heart rate in each form of sport is still unclear. Level of evidence II; Prognostic studies - Investigating the effect of a patient characteristic on the outcome of disease.

Molecular basis of signaling specificity between GIRK channels and GPCRs

Stimulated muscarinic acetylcholine receptors (M2Rs) release Gβγ subunits, which slow heart rate by activating a G protein-gated K+ channel (GIRK). Stimulated β2 adrenergic receptors (β2ARs) also release Gβγ subunits, but GIRK is not activated. This study addresses the mechanism underlying this specificity of GIRK activation by M2Rs. K+ currents and bioluminescence resonance energy transfer between labelled G proteins and GIRK show that M2Rs catalyze Gβγ subunit release at higher rates than β2ARs, generating higher Gβγ concentrations that activate GIRK and regulate other targets of Gβγ. The higher rate of Gβγ release is attributable to a faster G protein coupled receptor – G protein trimer association rate in M2R compared to β2AR. Thus, a rate difference in a single kinetic step accounts for specificity.

In-Hospital Initiation of Guideline-Directed Heart Failure Pharmacotherapy to Improve Long-Term Patient Adherence and Outcomes

Heart failure is a burdensome cardiovascular condition associated with high rates of morbidity and mortality. The 3-month period after hospitalization is a vulnerable phase in which patients are at high risk for mortality and rehospitalization. To reduce risk during this period, patients with heart failure and reduced ejection fraction should receive guideline-directed pharmacological therapies—the right drugs at the right doses—before hospital discharge. Optimal pharmacotherapies for these patients include agents that suppress the renin-angiotensin-aldosterone system, suppress the sympathetic nervous system, enhance vasodilation, slow heart rate when needed, and reduce excess volume. Because optimal prescription and adherence are both necessary to ensure the best clinical outcomes, nurses need to participate in interventions that optimize prescription and drug use over time. Collaboration with pharmacists and advanced practice acute care nurses may help ensure that medication selection and dosing are consistent with national guidelines. Use of a predischarge order set and electronic medical records checklist can enhance collaborative care.