The major health problem selected for this project was hypertension (Harrison et al, 2011). It is identified as a cardio vascular disease risk factor such as dementia, chronic kidney disease, coronary heart disease, and stroke (NICE, 2011). It can be missed easily, as in various instances it is asymptomatic as well as it is also known as a silent killer. The Hypertension is thought to be a disease of vascular regulation ensuing from arterial pressure control mechanisms malfunction (extracellular fluid volume, rennin-angiotensin-aldosterone system, and CNS) that results in elevation of BP by means of enhanced peripheral vascular resistance, and cardiac output. There are 2 basic hypertension types. Around 90 to 95 percent of the individuals have primary hypertension which is linked with change in lifestyle as well as needs medical treatment. On the other hand, 5-10% has secondary hypertension which is linked with various other diseases for instance pregnancy, thyroid, and renal (Haslam and James, 2005). It is estimated that around 1 in 20 adults will have increased BP of 160/100 mmHg and above that results in either more than one predisposing aspects (Gemmell et al, 2006).
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
Blood pressure in our blood vessels is monitored by the baroreceptors. These receptors send messages to the cardio regulatory center of the medulla oblongata to regulate our blood pressure every minute. In order for blood to be delivered to all organs and tissues, our cardiovascular system must always maintain adequate blood pressure. If the blood pressure drops too low, these organs will not receive an adequate of nourishing blood. Also if the pressure goes too high, the walls of the arteries will stretch and increased activity within the baroreceptor, information will then be sent through the nerves to the cardio regulatory center within the medulla which will responds by initiating the mechanisms that decrease the blood pressure to a normal
Aldosterone and Hormone Replacement Therapy Aldosterone falls in the class of hormone called mineralocorticoids, produces by the adrenal glands and is found near the kidneys. It sustains blood pressure, water and salt balance within the body. This procedure is assisting the kidneys to preserve sodium and excrete potassium in order to maintain a balance. If Aldosterone production falls, there isn’t enough regulation of salt and water balance (as aldosterone is being lost through urination) triggering blood pressure and blood volume to decline as a result of the kidneys not functioning properly. If body is in need of salt, water is not retained and adrenals release more Aldosterone and salt is reabsorbed from the tubule.
According to the blood pressure in the assessment, M.K. has stage one hypertension. It was noted that she is currently being prescribed Lasix and Lotensin to help with her high blood pressure. Lotensin, also known as Benazepril, is an ACE-inhibitor, or angiotensin-coverting enzyme inhibitor. These types of drugs play an important role in the RAAS (which stands for renin-angiotensin-aldosterone system). Arterial blood pressure is regulated and accomplished through neural, hormonal, and renal interaction and is in tune with the homeostatic fluid volume of one’s body. The balance of sodium and water is performed by the kidneys and the renin-angiotensin-aldosterone system is the main regulator of fluid volume in the body. An increase of extracellular fluid increases vascular resistance, which in turn leads to increased arterial blood pressure. The kidneys will then sense this pressure change and in order to compensate, will promote sodium and water loss through micturition. Sodium intake is directly proportional to arterial blood pressure and since the kidneys cannot get rid of sodium as fast as water, higher levels are expected. As sodium increases serum osmolality triggering the hypothalamus to act as the regulator by signaling the posterior pituitary gland to
While RAAS can be good for blood pressure maintenance there are some drawbacks. Angiotensin II can cause structural changes of the heart and blood vessels. It can be implicated hypertrophy and remodeling within the heart. Aldosterone also has adverse effects. Like angiotensin II, aldosterone can cause cardiac remodeling as well as a decreased reuptake of norepinephrine in the heart. This can increase the chances of dysrhythmias (Burchum 472). In a healthy heart these adverse effects would not be seen, but in a heart already in dysfunction, it can cause further complications. The mechanism of action several drugs is to control the outcome of this system.
There is a complex interrelationship among the cardiovascular system, the central nervous system (Na+, appetite and thirst regulation), the kidneys, and the tissue capillary beds distribution of extracellular fluid volume). Any change at any of these sites affects the function at other sites. There is a basic law of kidneys that Na+ excretion is directly proportional to mean arterial blood pressure (MABP). A marginal increase in MABP causes significant increase in Na+ excretion.
Angiotensin constricts the blood vessels, maintain blood pressure and the fluid in our body. Renin keep the blood pressure at a normal level by intaking more water and solutes so that the filtration in our bodies can balance out. The juxtaglomerular apparatus cell answer to low blood pressure when angiotensin one is converting to angiotensin two.
Pathophysiology of the underlying process The pathophysiology of hypertension (HTN) is best explained clearly if you have an understanding of how blood pressure (BP) works in the body. BP is seen as the function of both cardiac output (CO) in the human system and systemic vascular resistance (SVR). Cardiac output (CO) is made up of both heart rate (HR) and stroke volume (SV). SV in turn depends on contractility and preload of the system. SVR relies on contractility and afterload. There is literature that supports molecular and cellular levels relating to effects on blood pressure in terms of genetic make-up. Changes in any of these processes have the ability to alter CO or SVR, causing BP alteration and HTN.
When the heart begins to fail, mechanisms are activated to compensate for the impaired function and maintain the cardiac output. The primary compensatory mechanisms are Frank –Starling mechanism, neuroendocrine responses including activation of the sympathetic nervous system and the renin- angiotensin-aldosterone system, and ventricular hypertrophy. Decreased cardiac output initially stimulates aortic baroreceptors, which in turn stimulate the SNS. SNS stimulation produces both cardiac and vascular responses through the release of norepinephrine. Norepinephrine increases heart rate and contractility by stimulating cardiac beta- receptors. Cardiac output improves as both heart rate and stroke volume increase. Norepinephrine also causes arterial
The cardiovascular system is formed by the heart and the vasculature, a close system of vessels, which include arteries, arterioles, capillaries, venules, veins and lymph vessels.
Renin inhibitors are effective in treating hypertension because they block the activity of an enzyme secreted within the kidney called renin. Renin inhibitors blocks the activation of angiostensinogen. Without the activation of angiostensinogen, blood vessels will relax and widen. This will cause a decrease in blood pressure. The blood volume decrease as well through the diuretic and natriuretic effects with helps treat hypertension.
A Schwartz criterion is used for diagnosing SIADH which is mentioned below: Diagnostic Criteria for SIADH:Schwartz diagnostic criteria [5,13] ESSENTIAL CRITERIA Decreasing measured serum ACEI causes hyponatremia by blocking the conversion of angiotensin I to angiotensin II in the peripheral circulation but not in the brain where angiotensin I gets converted to angiotensin II [16]. Angiotensin II is known to stimulate the release of ADH resulting in hyponatremia [18].
Angiotensin-Converting Enzyme Inhibitors (ACE Inhibitors) are a group of drugs that belong to the antihypertensive drug class. There are currently 10 ACE inhibitors that are available. ACE inhibitors can be taken either by themselves or can be combined with a calcium channel blocker or a thiazide diuretic to enhance the treatment This group of drugs is often used as a first line of treatment to treat both heart failure and hypertension. Some of these drugs include; benazepril (Lotensin), captopril (Capoten), enalapril (Vasotec), and fosinopril (Monopril) (Lilley, p. 348).
Heart disease, commonly known as cardiovascular disease, consists of various conditions that affect an individual’s heart. The biological system involved in heart disease is the circulatory system, which delivers oxygen and food to all the cells of the body in order to remove waste and carbon dioxide (“Heart Disease”, N.d.). The circulatory system consists of the heart, lungs, blood, and blood vessels. These conditions affect blood vessels by narrowing or blocking their passage way to the heart, which can lead to numerous types of heart conditions. There are 3 major types of blood vessels, which are the arteries, capillaries, and veins. Once any of these blood vessels are affected, many heart conditions can arise. The various conditions include: