Pulmonary Hypertension

Pulmonary hypertension is a lung disorder. The arteries that carry blood from the heart to the lungs become narrowed, making it very hard for the blood to get through the vessels, this then causes the pressure in the arteries to increase more than usual (high blood pressure). Scientists think that the procedure starts with injury to the layer of cells that line the small blood vessels of the lungs.

Voltage gated channels are necessary components of life processes, in many organisms. One in particular, is the calcium voltage gated ion channel. Often lodged within the phospholipid bilayer, the imbalance of the calcium, or, the inside vs outside concentration, creates a gradient. The channel proteins often undergo conformations, states that which allow or block calcium ions from passing through. As ions move inside the cell, this creates a depolarization, or surge in the voltage. Clinically, this is associated with the heart and how it allows the heart to contract, which can be read in the

The cardiac muscle cells can be affected by heart disease through the inability to maintain its homeostasis through the calcium pump. If there is excess calcium within the heart it results in the in ability of the heart muscle to relax. As a result, the ADP/ATP ratio increases, phosphocreatine decreases, and energy stores are depleted. Furthermore, this imbalance affects the energy needed to relax the left ventricle. Secondly, diastolic heart failure can occur from changes in preload, afterload, renin-angiotension-aldosterone system, and the sympathetic nervous system. These changes affect the fibrillar collagen within the extracellular matrix that affects the ability of the ventricular to relax. These changes along with those compensatory mechanisms results in continuous resistance that results in increased in left ventricular end-diastolic pressure (McCance & Huether, 2010).

It inhibits Na+K+ ATPase active transport raising cytosolic Na+ concentrtion and leading to the increasement of Ca2+ concentration in the sarcoplasmic reticulum by the reversival exchange of Na+ and Ca2+ in the myocardial cell. This increase in the contraction of the heart (32) and improve cardiac outpur , left ventricualr ejection fraction, stroke volume, pulmonary capilary wedge pressure and exercise tolerance (33). Secondly, digoxin produce vagus activation showing negavite chronotropic action in SA node and negative dromotropic action in AV node. This lead to a shift in automatic balance by dominating the positive iontropic action of the drugs digoxin (33). In this way digoxin is cosinder as a only available inotropic drug which increase cardiac output and decreae pulmoary capillary wedge preure with our increasing heart rate and without decreasing blood pressure

13 Boron, W. F., & Boulpaep, E. L. (2009). Medical physiology: a cellular and molecular approach (2nd ed.). Philadelphia, PA: Saunders/Elsevier.

the expression of a gene for cardiac contractile proteins, causing increased protein synthesis, a reduction in arterial contractility and a reduction in atrial energy demands. There is an action potential prolongation of the Ca+ current at a cellular level, which prolongs the time taken for myocytes to contract and relax [ncbi.nlm.nih 1998].

Vascular remodeling of the vessel layers of the pulmonary arteries from smooth muscle cell proliferation and inflammation results in reducing the size of the arterial lumen (Lundgren & Ladegran, 2014). As pulmonary hypertension progresses, this vascular remodeling leads to a further reduction in the size of the arterial lumen, increased peripheral vascular resistance, increased right ventricular load, and right ventricular hypertrophy (Lundgren & Ladegran, 2014). Eventually, the right ventricle is unable to compensate for the increased pressure causing it to dilate resulting in the symptoms associated with the disease and eventual death (Lundgren & Ladegran, 2014; Weber et al.

Heart growth can also be regulated by the pathological response to volume or pressure overload in a disease setting (1,3).

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

Pulmonary Edema is a condition caused by excess of fluid in the lungs. This fluid collects in the numerous air sacs in the lungs, making it difficult to breathe. Pulmonary edema is caused by heart problems. The fluid can accumulate for other reasons, including pneumonia, exposure to certain toxins and medications, trauma to the chest wall, and exercising or living at high elevations. Treatment for Pulmonary Edema varies depending on the cause but generally includes supplemental oxygen and medications. Depending on the cause, Pulmonary Edema symptoms may appear suddenly or develop over time. Pulmonary Edema can be fatal if not treated.

The human body is a very complex organism composed of different types of systems and functions. All the functions that each system has, is what makes possible for the body to obtain life. One of the most important systems in one’s body is the circulatory system, where the heart, the lungs, and the blood vessels work together to form the circle part of the circulatory system. The pumping of the heart forces the blood on its journey. The body’s circulatory system really has three parts: pulmonary circulation, coronary circulation, and systemic circulation. Each part must be working independently in order for them to all work together. However, when one of the parts of the circulatory system does not

One of the main problems that occur from the maintaining of pulmonary resistance is bidirectional hemodynamic shunting at the ductus arteriosus or at the patent foramen ovale (Razzaq et al, 2013). Starting with the ductus arteriosus this duct usually closes due to the oxygen saturation increase, which leads to the lesser circulation of PGE2 which is Prostaglandin E2. PGE2 binds and activates the prostaglandin E2 receptor which leads to the duct being held open (Rang et al, 2007). Due to the lower blood flow of the PGE2 stays circulating in greater amounts and leaves the duct open which causes increased blood pressure on the vasculature of the lungs. This increased pressure doesn’t allow the blood to enter the vasculature of the lungs and shunts it back. This then results in less gas exchange than necessary for survival. Next, we need to look at the foramen ovale. It should close off at birth when the

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

Acute cardiogenic pulmonary oedema (ACPO) is a life threatening condition requiring rapid emergency care. ACPO occurs as a result of rapid fluid collection in the lungs interstitial and alveolar spaces (Pinto & Kociol, 2018). Consequently, gas exchange and lung compliance diminishes as the lungs are unable to cope with the rapid fluid accumulation (Purvey & Allen, 2017). ACPO is most commonly seen on a background of left ventricular failure which causes reduced cardiac contractility. This results in a lack of forward pressure leading to pooling of blood in the pulmonary vasculature. Left ventricular dysfunction is triggered by a variety of cardiac diseases such as myocardial infarction, chronic heart failure, cardiomyopathy, new onset arrhythmias

These effects which make your heart work harder to pump blood through your pulmonary arteries and lungs. For a long time, the pressure on arteries inclines. Surely, the