Continuing Education Activity High-output cardiac failure is a less common form of heart failure, and although it may sound contradictory at first, in the simplest form, it is still the heart's inability to provide sufficient blood for the body's demand. Most patients with heart failure are either classified as a systolic or diastolic dysfunction with increased systemic vascular resistance, however, patients with high output cardiac failure have normal cardiac function and decreased systemic vascular resistance, either secondary to diffuse arteriolar dilation or possible bypass of the arterioles and capillary beds, leading to activation of neurohormones. This activity reviews the cause, pathophysiology, and presentation of high output heart failure and stresses the role of the interprofessional team in its management Continue reading →

Cardiac asthma Purpose diagnosis of congestive heart failure Cardiac asthma is the medical condition of intermittent wheezing, coughing, and shortness of breath that is associated with underlying congestive heart failure (CHF).[1] Symptoms of cardiac asthma are related to the heart's inability to effectively and efficiently pump blood in a CHF patient.[2] This can lead to accumulation of fluid in and around the lungs (pulmonary congestion), disrupting the lung's ability to oxygenate blood.[3] Cardiac asthma carries similar symptoms to bronchial asthma, but is differentiated by lacking inflammatory origin.[1][4] Because of the similarity in symptoms, diagnosis of cardiac versus bronchial asthma relies on full cardiac workup and pulmonary function testing.[2][5] Treatment is centered on improving cardiac function, maintaining blood oxygen saturation levels, and stabilizing total body water volume and distribution.[1][5] The most common findings of cardiac asthma are the presence of wheeze, cough, or shortness of breath (predominantly occurring at night or when laying down) in a patient that possesses signs of congestive heart failure.[5][6][7][8] Additional findings consist of production of frothy or watery sputum and presence of water in the lungs that can be heard via stethoscope.[3] In severe cases, a patient can experience multiple night time episodes of breathlessness, changes in skin coloration, and episodes of bloody sputum.[1] The underlying causes for cardiac asthma stem from the eventual back up of fluid into the pulmonary vasculature as a result of the heart's, particularly left sided, inability to effectively and efficiently pump blood.[2] The accumulation of fluid in the heart creates a higher than normal pressure system that places increasing pressure demands on the pulmonary venous system in order for appropriate oxygenation of blood to occur.[5] This results in what is called pulmonary venous hypertension (PVH), and results in distention and recruitment of pulmonary capillaries to help distribute the increased pressure gradient.[2][5] At the capillary, there is a microvascular barrier that helps regulate fluid status via molecular pressure forces such as forces that push outward from vessels and pressures that pull or attract into vessels.[2] With increasing PVH, pressure outward overcomes pressure inward, and fluid is distributed to the lung interstitium, preserving oxygen exchange at the capillary.[2] Fluid is transported to the hilum and pleural space, and removed via the lymphatic system.[2][8] At first, the body is capable of handling excess water. Later, the capillary vasculature is overwhelmed by increased pressure and fluid backs up into the alveolar sac, resulting in pulmonary edema and decreased oxygenation capability.[2] Additionally, increased pressure demands on capillary vasculature result in increases in vascular tone to include remodeling of pre-capillary vessels such as medial wall hypertrophic changes.[2] Overtime, the remodeling efforts of the vessels can progress to hyperplastic changes of the vessels' wall construction, and results in increased pulmonary vascular resistance.[2] There is ongoing interest into establishing connections of cardiac asthma to abnormalities in bronchiole anatomy.[1][5] Current evaluation has proposed multiple mechanisms for increased airway resistance, and focus is on four alternate explanations: The diagnosis of cardiac asthma is accomplished through workup of congestive heart failure, complete with: As well as evaluation of lung function via: Treatment of asthma symptoms in CHF patients is directed towards optimizing the patient's cardiovascular status and correcting potential oxygen deficit.[5] Current recommendations in acute asthma symptoms are utilization of diuretics such as furosemide, venodilators such as nitroglycerin, and morphine.[1] The initial strategy should focus on decreasing patient fluid retention with diuretic therapy, thereby decreasing cardiac preload and overall fluid load in pulmonary circuit (pulmonary congestion).[1] Next, if aggressive diuresis is not adequately correcting symptoms, venodilators can be used to distribute blood and fluid to the venous system, thereby decreasing cardiac preload and left heart pressures contributing to pulmonary congestion.[1] Lastly, morphine can be utilized for assistance in improving ease of breathing through a presumed mechanism similar to venodilation, as well as reducing patient anxiety.[1] Additionally, applications of supplemental oxygen and repositioning to upright or standing positions in events of low blood oxygen saturation and difficulty breathing can be utilized as needed.[1][3] Chronic management of cardiac asthma is directed at optimizing therapy of heart failure Continue reading →

Introduction Myocardial fibrosis, characterized as interstitial fibroblast proliferation and excessive collagen deposition, is the structural basis of myocardial stiffness and the key process of cardiac function transformation from the compensatory phase to heart failure.1 Thus, it is imperative to understand the mechanisms involved in inhibition of myocardial fibrosis. Cardiac fibroblasts are generally the primary effector cells of fibrosis and have been reported to be partly derived from cardiac endothelial cells through the endothelial to mesenchymal transition (EndMT) process.2 EndMT is a process by which endothelial cells lose a portion of their cellular features and obtain the mesenchymal phenotype, including the loss of tight junctions and increased production of extracellular matrix. Continue reading →

Introduction As scholars have been studying tissue engineering more and more, oral bone regeneration which is of fundamental importance in the dentistry field has become a hot research topic.1 Mesenchymal stem cells (MSCs) are undifferentiated cells known for their self-renewal and differentiation properties, and they can secrete immunomodulatory factors, leading to the creation of a regenerative microenvironment, and trans-differentiate into cells of the different germ layers: mesoderm lineage cells, as well as ectoderm and endoderm lineage cells.2 The capacity of MSCs is useful for osteogenic differentiation and tissue regeneration.3 Some clinical studies have demonstrated that MSCs from different sources may have the ability to repair, replace, and regenerate cells, tissues, and bones.4 MSCs can be extracted from different tissues such as bone marrow, skeletal muscle, cartilage, dental organ, adipose tissue, synovium, and cardiac tissue.5 BMSCs were the first to be discovered.6 Bone is formed via endochondral and intramembranous ossification.7 MSCs play a vital role in bone formation. On the one hand, MSC-driven condensation occurs firstly, and then, MSCs differentiate into chondrocytes during the process of formation of growth plates, which are replaced by new bone in longitudinal-endochondral bone growth.8 On the other hand, MSCs can also directly differentiate into osteoblasts in bone formation such as skull, facial bones, and pelvis, generated by intramembranous ossification without a cartilaginous template.9,10 Transverse maxillary constriction often manifests a typical vertical skeletal pattern, with long anterior lower facial height, high palatal vault, low tongue posture, incompetent lip muscles, and mouth-breathing.11 Previous studies indicated that approximately 18% of mixed-dentition patients had a transverse maxillary constriction,12 which led to dentofacial deformities such as anterior deep overbite, posterior reverse overbite, and dental crowding Continue reading →