Pulmonary Arterial Hypertension (PAH)

In epicardial vessels there is not enough resistance to blood flow in healthy heart. Due to the presence of atherosclerotic plaques in the arteries or vessels, blood flow is slow down, but autoregulation process can pay off to a certain degree. Autorgulation is the process of myocardial vessel dilation in response to diminish supply of oxygen. By autoregulation process, there are rapid changes in blood flow to heart because of increase in demand. Adenosine which is potent vasodilator, are the key mediators that are involved in myocardial perfusion. Other mediators are nitric oxide (NO), prostaglandins (PGE2), carbon dioxide (CO2) and hydrogen ions. Obstruction as result of atherosclerosis can be fixed to coronary blood flow, or dynamics as with coronary

Systemic vasoconstriction - increases left ventricular afterload and myocardial oxygen consumption and may produce tissue ischemia.

Chronic hypoxic events during pregnancy associated with mild to moderate maternal hypertension have shown however to sometime accelerate fetal lung maturity and surfactant production leading to a decrease in neonatal respiratory complications. (Kim, Vohr, & Oh, 39) This due to cortical steroid secretion that stimulate an increased production of surfactant in response to the stresses of hypoxic events. (Porth, 1306)

Hemodynamic Changes: Contractility is influential in cardiac output and can be compromised due to myocardial infarction, ischemia, cardiomyopathy, and increased cardiac workload, to name a few. Inflammatory, immune, and neurohumoral changes can mediate ventricular remodeling, which will alter myocardial cellular structure resulting in myocardial dilation and further dysfunction of myocyte contractility over time. The decreased contractility will result decreased stroke volume and increased left ventricular end-diastolic volume, which results in dilation of the heart and increased preload. Increased afterload can be caused by increased pulmonary vascular resistance (PVR). This can result from hypertension or aortic valvular disease. The PVR results in resistance to ventricular emptying, increasing the work load of the LV, thus causing hypertrophy of the myocardium. Sustained elevated afterload results in pathologic hypertrophy, caused by angiotensin II and catecholamines. The increase in cardiac muscle mass causes an increase in the heart’s oxygen and energy demands. Thus, more energy from ATP is needed and when demand is greater than supply, cardiac contractility suffers. Ventricular remodeling continues, further

SHealth is one thing I think we take for granted when we are young. We eat what we want, sleep when we want and do what we want. I’ve learned your body is only as good to you to you as you are to it. Yes, I love the times overseas drinking at all hour and eating grease foods thinking it was the cure for a hangover. But I had no idea how it was affecting my body. I was first diagnosed with high blood pressure at the age of twenty-three. I laughed at it because I did not understand the seriousness of it. It took family members including my mother to pass to see how dangerous the life I was living was and or will be. So I want to change. In this essay, I am going to outline how I am going to change my behavior by Describe the expected outcome

The mechanism for fall in arterial pressure after intravenous induction is multifactorial. The fall in arterial pressure after the propofol is associated with both, vasodilatation with reduced preload and afterload and myocardial depression because of the negative inotropic effect.2,14-16 This hypotension is caused by inhibition of sympathetic nervous system and impairement of baroreceptor regulatory mechanism.17 Similar to our results, Saricoaglu et al14 found that propofol was associated with significant fall in arterial blood pressure as compared to etomidate and attributed this hypotension to the negative ionotropic effect of propofol. Conversely, etomidate distinctively have the capacity to bind and stimulate peripheral alpha-2 beta adrenergic receptors with subsequent vasoconstriction18 and its lack of effect on sympathetic nervous system and baroreceptor function.2,19 These unique effects may be responsible for the haemodynamic stability after the

Pulmonary Arterial Hypertension (PAH) belong to group 1 in the classification of Pulmonary Hypertension (PH). It is a chronic progressive disease caused by narrowing of the minor pulmonary arteries due to vascular proliferation and remodeling.

Further research into the Protein Kinase C and its association with voltage-activated potassium channels (BKCa) in pulmonary arterial smooth muscle cells (PASMC) will hopefully proved a clear answer as to why idiopathic pulmonary arterial hypertension (IPAH) occurs, its mechanism, and the synthesis of a new medication in the future that could manipulate the mechanism to reverse

About seventy million American Adults have hypertension or high blood pressure. Hypertension increases the risks for a cerebral vascular accident, heart failure/disease/attack, and kidney disease, which are leading causes of death (Mann, 2012). The treatment for hypertension includes lifestyle changes and Drug therapy. There are four drug categories involved in the treatment of hypertension two of which are Calcium channel blockers and Sympatholytics (Mann, 2012). This paper will assess the various aspects of the different calcium channel blockers and the specific contraindication with beta-blockers, which pertain to the sympatholytic class. As mentioned above, calcium channel blockers or CCB’s

As a result of continuous activation of these mechanisms make adaptive changes in ventricles known as “LV remodeling”. (Mann, D. L., & Bristow, M. R. (2005). Myocardial fibrosis is one of the important mechanisms in heart failure explains myocardial contractile dysfunction. Fibrosis makes heart muscle stiff and decreases in compliance of ventricles could be the reason for left ventricle dilation in ventricles remodeling. Aldosterone, Endothelin and Angiotensin ll cause excessive fibrosis in heart muscle. (Weber KT) Various mechanisms of heart failures such as stretching, remodeling, fibrosis and activation of neurohormonal system related with some cardiac biomarkers and their role might be helpful in diagnosis and predicting outcomes of heart

Hypoxia has been reported to be associated with fibrosis in other organs of the body as it has been shown that renal fibroblasts reduce their turnover and upregulate matrix production when exposed to hypoxia (6). Another study revealed that lung fibroblasts produce augmented levels of TGF-b and enhanced accumulation of collagen during hypoxia (7) . In addition, molecules which are upregulated by hypoxia such as Hypoxia Induced Factor-1α (HIF-1 α) are said to be associated with malignant transformation of epithelia in other

Vascular endothelium plays a role in both vasoconstriction and relaxation, while hypercholesterolemia by modulating arterial tone adversely affects this process. However, endothelial function is improved by statin therapy due to production of the vasodilator nitric oxide.

The study induced EIB using eucapnic voluntary hyperpnea (EVH) and tested fall in FEV1 and measurement of other biomarkers associated with EIB; first with a placebo, and then with beclomethasone.

Ca2+-sensitive K+ channel current is increased in hypertension. Experiments by Liu, Pleyte, Knaus, and Rusch (1997) were aimed at discovering the molecular pathway by which the KCa efflux is stimulated. Two conclusions

Doxazosin is an alpha-1 adrenergic receptor blocker that inhibits the binding of norepinephrine (released from sympathetic nerve terminals) to the alpha-1 receptors on the membrane of vascular smooth muscle cells. The primary effect of this inhibition is relaxed vascular smooth muscle tone (vasodilation), which decreases peripheral vascular resistance, leading to decreased blood pressure. Selective alpha-1 blocking agents, such as prazosin, terazosin, and doxazosin, have more favorable adverse effect profiles and are used when long-term therapy is required (metastatic pheochromocytoma). These medications are not used to prepare patients for surgery, because of their incomplete alpha