Perioperative Point-of-Care Ultrasound in Children

Anesthesiologists and other acute care physicians perform and interpret portable ultrasonography—point-of-care ultrasound (POCUS)—at a child’s bedside, in the perioperative period. In addition to the established procedural use for central line and nerve block placement, POCUS is being used to guide critical clinical decisions in real-time. Diagnostic point-of-care applications most relevant to the pediatric anesthesiologist include lung ultrasound for assessment of endotracheal tube size and position, pneumothorax, pleural effusion, pneumonia, and atelectasis; cardiac ultrasound for global cardiac function and hydration status, and gastric ultrasound for aspiration risk stratification. This article reviews and discusses select literature regarding the use of various applications of point-of-care ultrasonography in the perioperative period.

Cardiovascular magnetic resonance in cardiac resynchronization therapy

Cardiovascular magnetic resonance (CMR) can inform on the aetiology of heart failure, global cardiac function, and myocardial viability, all of which are essential in cardiac resynchronization therapy (CRT). Late gadolinium enhancement (LGE)-CMR allows quantification of myocardial scarring and characterization of the pattern of scar, both of which may be useful in risk stratification. In addition, the ability of CMR to localize myocardial scar and provide reliable measures of segmental motion and deformation is being applied to targeting left ventricular lead deployment. The development of CMR-compatible devices may permit the use of CMR in the optimization of CRT after implantation.

Sex-specific cardiovascular susceptibility to ischaemic myocardial injury following exposure to prenatal hypoxia

Cardiovascular diseases (CVDs) are the leading cause of mortality and hypertension contributes substantially to the incidence of stroke, coronary artery disease, heart failure, atrial fibrillation and peripheral vascular disease. The origin of hypertension is clearly multifactorial, and a complex and multifaceted approach is necessary to decrease its incidence. The most recognizable factors involved in reducing the incidence of hypertension are prevention, early diagnosis and treatment; however, the importance of the foetal environment and early postnatal development has recently been considered. In clinical practice, these factors are still frequently overlooked, probably because of a lack of knowledge about the underlying mechanisms and effective treatment or prevention. Pathophysiological mechanisms underlying the prenatal programming of CVDs were investigated in the study by Shah et al. published recently in Clinical Science (2017) 131(17), 2303–2317. The study explored cardiac susceptibility of adult male and female rat offspring to ischaemic myocardial injury due to prenatal exposure to hypoxia. The results demonstrated significant changes in global cardiac function and left ventricular dilatation following myocardial infarction in rat offspring prenatally exposed to hypoxia. The effects were gender specific and occurred only in males, whereas females were protected. These findings are important from several perspectives. First, they point to the fact that an inadequate foetal environment can increase susceptibility to death from myocardial infarction. Second, during their reproductive life, females are better protected from cardiovascular insult than males, but it is not known if they lose this advantage after menopause, and can be equally at risk as males.

Obesity-metabolic derangement exacerbates cardiomyocyte loss distal to moderate coronary artery stenosis in pigs without affecting global cardiac function

Obesity associated with metabolic derangements (ObM) worsens the prognosis of patients with coronary artery stenosis (CAS), but the underlying cardiac pathophysiologic mechanisms remain elusive. We tested the hypothesis that ObM exacerbates cardiomyocyte loss distal to moderate CAS. Obesity-prone pigs were randomized to four groups ( n = 6 each): lean-sham, ObM-sham, lean-CAS, and ObM-CAS. Lean and ObM pigs were maintained on a 12-wk standard or atherogenic diet, respectively, and left circumflex CAS was then induced by placing local-irritant coils. Cardiac structure, function, and myocardial oxygenation were assessed 4 wk later by computed-tomography and blood oxygenation level dependent (BOLD) MRI, the microcirculation with micro-computed-tomography, and injury mechanisms by immunoblotting and histology. ObM pigs showed obesity, dyslipidemia, and insulin resistance. The degree of CAS (range, 50–70%) was similar in lean and ObM pigs, and resting myocardial perfusion and global cardiac function remained unchanged. Increased angiogenesis distal to the moderate CAS observed in lean was attenuated in ObM pigs, which also showed microvascular dysfunction and increased inflammation (M1-macrophages, TNF-α expression), oxidative stress (gp91), hypoxia (BOLD-MRI), and fibrosis (Sirius-red and trichrome). Furthermore, lean-CAS showed increased myocardial autophagy, which was blunted in ObM pigs (downregulated expression of unc-51-like kinase-1 and autophagy-related gene-12; P < 0.05 vs. lean CAS) and associated with marked apoptosis. The interaction diet xstenosis synergistically inhibited angiogenic, autophagic, and fibrogenic activities. ObM exacerbates structural and functional myocardial injury distal to moderate CAS with preserved myocardial perfusion, possibly due to impaired cardiomyocyte turnover.

High inborn aerobic capacity does not protect the heart following myocardial infarction

Maximal oxygen uptake (V̇o2max) is a strong prognostic marker for morbidity and mortality, but the cardio-protective effect of high inborn V̇o2max remains unresolved. We aimed to investigate whether rats with high inborn V̇o2max yield cardio-protection after myocardial infarction (MI) compared with rats with low inborn V̇o2max. Rats breed for high capacity of running (HCR) or low capacity of running (LCR) were randomized into HCR-SH (sham), HCR-MI, LCR-SH, and LCR-MI. V̇o2max was lower in HCR-MI and LCR-MI compared with respective sham ( P < 0.01), supported by a loss in global cardiac function, assessed by echocardiography. Fura 2-AM loaded cardiomyocyte experiments revealed that HCR-MI and LCR-MI decreased cardiomyocyte shortening (39%, and 34% reduction, respectively, both P < 0.01), lowered Ca2+ transient amplitude (37%, P < 0.01, and 20% reduction, respectively), and reduced sarcoplasmic reticulum (SR) Ca2+ content (both; 20%, P < 0.01) compared with respective sham. Diastolic Ca2+ cycling was impaired in HCR-MI and LCR-MI evidenced by prolonged time to 50% Ca2+ decay that was partly explained by the 47% ( P < 0.01) and 44% ( P < 0.05) decrease in SR Ca2+-ATPase Ca2+ removal, respectively. SR Ca2+ leak increased by 177% in HCR-MI ( P < 0.01) and 67% in LCR-MI ( P < 0.01), which was abolished by inhibition of Ca2+/calmodulin-dependent protein kinase II. This study demonstrates that the effect of MI in HCR rats was similar or even more pronounced on cardiac- and cardiomyocyte contractile function, as well as on Ca2+ handling properties compared with observations in LCR. Thus our data do not support a cardio-protective effect of higher inborn aerobic capacity.