Intra-operative patient monitoring
Daniel Cottle, Shondipon Laha, Peter Nightingale in Anaesthetics for Junior Doctors and Allied Professionals, 2018
In order to use cardiac output monitors it is useful to first review your cardiac physiology. Cardiac output = stroke volume × heart rate.Blood pressure = cardiac output × systemic vascular resistance.Stroke volume is dependent on preload (ventricular filling), contractility and afterload (ventricular outflow resistance including systemic vascular resistance).Oxygen delivery = cardiac output × arterial O2 content.Indexes (e.g. cardiac index) are the value in question divided by the body surface area (m2).
Ion Channels in Immune Cells
Shyam S. Bansal in Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
A clinical study in 1953 demonstrated that 30 out of 40 heart failure (HF) patients showed the presence of C-reactive protein in their blood, indicating the involvement of inflammatory components to the complexity related to HF155. Since then, many cardiac pathophysiological conditions such as atherosclerosis, atrial fibrillation (AF), myocarditis, endocarditis, arrhythmia, and myocardial infarction (MI) have also been associated with defects in immune cell function156,157. The immune cell populations, including macrophages, mast cells, eosinophils, neutrophils, monocytes, and B and T cells, reside in the heart or infiltrate the cardiac tissue upon a variety of stimuli158. The resident immune cells are not distributed homogeneously, as they localize to different locations in the heart158. The differential localization of resident immune populations in the heart defines their distinct interaction with the various other cells, including cardiomyocytes, endothelial cells, and fibroblasts. These interactions are important because the non-leukocytes send signals in the form of cytokines, chemokines, and growth factors, to which the leukocytes respond and initiate the inflamma-tory signaling cascade. Similarly, non-leukocytes contain receptors that are specific to leukocyte products and upon binding activate the downstream signaling pathway. These interactions serve as one of the important regulatory mechanisms that aids in maintaining the structure and function of the heart. Interestingly, there are also studies focused on how the ion channel proteins in immune cells, namely, connexins and KCa3.1, influence these interactions and regulate cardiac physiology and pathophysiology. The structure-function properties of these channels and their specific role in maintaining cardiac physiology will be discussed briefly in this section.
Cardiac regeneration in a newborn: what does this mean for future cardiac repair research?
Published in Expert Review of Cardiovascular Therapy, 2018
Bernhard J Haubner, Thomas Schuetz, Josef M Penninger
Besides the elucidation of the underlying mechanism for neonatal cardiac repair, one key question remained: Can one translate these models to the human heart considering the fundamental differences in basic cardiac physiology? Talking to pediatric cardiologists we learned from their experience that human neonatal hearts still possess an enormous cardiac plasticity and can even recover functions after removal of the causative harmful conditions. For instance, the ALCAPA syndrome (Anomalous Left Coronary Artery From the Pulmonary Artery) designates a congenital pediatric heart disease that causes myocardial ischemia [20]. Currently, the only curative approach is cardiac surgery with correction of the coronary malformation. Whereas early correction within the first year of age leads to complete recovery of the heart, delayed diagnosis most often ends in damage and ultimately ischemic cardiomyopathy [20]. Encouraged by the clinical experience, we found a handful of documented cases of human neonatal myocardial infarctions. Perinatal cardiac infarction is a very rare clinical event, primarily due to malformation of the heart or coagulation diseases. Since such events are accompanied with high mortality, all the clinical case reports focused on the description of diagnosis and emergency, and critical care treatment in the acute setting. In the discussions, the authors hinted at a good outcome as long as the baby survived the initial ischemic event, without further descriptions (References within Reference [20])
Valsartan-mediated chronotherapy in spontaneously hypertensive rats via targeting clock gene expression in vascular smooth muscle cells
Published in Archives of Physiology and Biochemistry, 2022
Jiajie Luan, Kui Yang, Yanyun Ding, Xiaotong Zhang, Yaqin Wang, Haiju Cui, Deixi Zhou, Lu Chen, Zhangqing Ma, Wusan Wang, Wen Zhang, Xiaoyun Liu
Diastole and contraction of the heart regulate BP levels, and clock genes in cardiomyocytes control cardiac physiology and pathophysiology (Martino et al. 2015). The oscillations of clock genes determined in the present study were decreased in SHRs compared with those in WKY rats. This suggests that non-dipper BP patterns might disrupt heart clock-gene rhythms. However, we found that VSA restored circadian BP rhythms but did not restore heart-clock rhythms compared with that of VWA. In addition, we have reported a review that clock genes control liver homeostasis and pathology (Zhou et al. 2016). In our present work, VSA significantly recovered liver clock-gene expression rhythms, which suggests that VSA might exert a liver-protective effect. Moreover, both VSA and VWA significantly increased clock gene expression in the kidney, which might accompany kidney injury. Our previous work has compared the effects of VSA and VWA on target organ damage in SHRs in detail (Yang et al. 2019). Thus, our present research further elucidates the safety and effectiveness of valsartan chronotherapy.
Dobutamine effects on systolic and diastolic left ventricular long-axis excursion and timing – significance for the interpretation of s′ and e′
Published in Scandinavian Cardiovascular Journal, 2023
Roger E. Peverill, Om Narayan, James D. Cameron
The increases in EDExc which occurred during low-dose dobutamine infusion for both walls and in both groups in the present study reflected the concomitant increases in SExc, and this relationship was also similar for the increases in EDExc and SExc for the lateral wall during the moderate dobutamine dose in both groups. However, there was no increase in EDExc or SExc for the septal wall in either group at the moderate dobutamine dose. Thus, the effects of dobutamine on EDExc did not occur in parallel with the changes in the timing of the onset or end of early diastolic motion, which in most cases decreased progressively with dobutamine at each dose level. The relationship of EDExc with SExc was not unexpected given that increases in SExc with dobutamine reflect an increase in contraction due to its inotropic effect, and an increase in systolic motion must be accompanied by a subsequent increase in diastolic motion. Thus, it is a fundamental aspect of normal cardiac physiology that the annulus returns to the same position at the end of every cardiac cycle, and SExc will be approximately equal to the sum of EDExc and AExc on a beat-to-beat basis. In the present study there was no consistent change in AExc during dobutamine infusion, this finding also implying the presence of a close relationship between any changes in SExc and EDExc.