Renin Angiotensin Aldosterone System Analysis

Alpha- adrenergic are receptors that generally stimulate the sympathetic nervous system. The sympathetic nervous system is responsible for flight or flight response, which includes, mobilizing energy, dilating the pupils, diverting blood flow from organs to the skeletal muscle, and increasing the heart rate. The alpha-adrenergic receptor make the heart beat faster causing the blood vessels to constrict. This combination can lead to high blood pressure. The more stress we intake, the more our bodies go into this risky

ACE inhibitors are important and useful in the medication and treatment for KH due to their effectiveness in treating hypertension. ACE inhibitors will help treat KH by slowing the angiotensin converting enzyme (ACE). Angiotensin II is produced by the body that can cause vasoconstriction of the blood vessels. Angiotensin II is made from Angiotensin I by the ACE. If the production of Angiotensin II is slowed by the ACE inhibitor, the blood vessels will be able to dilate, and blood pressure is able to be lowered (Copstead and Banasik). Thus, it is important for KH to stay on the ACE inhibitors due to his blood pressure readings. KH’s blood pressure is 135/96. His systolic blood pressure is in the pre-hypertensive range, however, his diastolic blood pressure is in the hypertensive range and therefore, his blood pressure is hypertensive. Since his blood pressure is high, it is important for KH to remain taking the

John’s long standing Hypertension causes his heart to work harder, putting more strain on his heart and arteries. In order to achieve a gradient in pressure by which blood flows from an area of higher pressure to one of lower pressure, the left ventricle must exceed the increased pressure in the arterial system (Ref).

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).

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

The sympathetic nervous system is controlled by the hypothalamus and transmits signals down the spinal cord to the periphery through alpha and beta receptor sites. Alpha receptor stimulation induces smooth muscles contraction in blood vessels and bronchioles. Beta receptors respond with smooth muscle relaxation in blood vessels and bronchioles. Controls the “fight or flight” response which controls sweating, pupil dilations, and temperate regulation. Loss to the sympathetic nervous system can disrupt homeostasis. The parasympathetic nervous system carries signals to the organs in the abdomen, heart, lungs, and skin above the waist. The parasympathetic nerves attempt to control a rapidly increasing blood pressure by slowing heart rate, this may happen when the sympathetic nervous system is

Heart rate and blood pressure can change with many different stimuli; any stimuli that result in an increase in sympathetic nervous system activity, such as emotional stress or physical exercise, should result in an increase in heart rate and/or blood pressure, assuming there are no other health problems at play. Similarly, activities that inhibit sympathetic nervous system activity help to decrease both heart rate and blood pressure (Powers and Howley, 2009, p. 178). However, there are extrinsic factors that can affect the two: for example, beta-blockers will stimulate vasodilation and thus a decrease in blood pressure (Powers and Howley, 2009, p. 183). The kidneys also plays a large role in cardiac regulation: secretion of norepinephrine by the adrenal glands leads to a more rapid heart rate, and higher levels of water retention by the kidneys leads to increased blood volume and thus increased blood pressure (Powers and Howley, 2009, p. 178).

Baroreceptors activate the sympathetic nervous system, with an increase in heart rate and blood pressure and vasoconstriction, causing beta receptor downregulation, and further increased adrenergic tone with pathological activation of the renin-angiotensin-aldosterone-system (Johnson, 2014). Angiotensin II releases catecholamine and stimulates renin release, which raises tone and pressure on the heart, and leads to aldosterone secretion, also increasing the pressure load on the heart; water and sodium retention through the presence of vasopressin and aldosterone add to preload (Johnson, 2014). This model is used to explain the compensatory mechanisms employed to maintain cardiac reserve, the ability of the heart to respond to increased needs; additional neurohormonal changes involve natriuretic peptides, atrial natriuretic peptide, brain natriuretic peptide and endothelin 1 (Johnson, 2014; Porth,

Body: the regulation tof blood pressure. When your blood pressure increases, it is detected by the recepters in your blood vessels that sence the resistance of blood flow against the walls if the vessel. The receptors send a message to your brain, which sends a message to your heart and blood vessels. Your heart rate decreases and your blood vessels expand in diameter, which together decreases your blood

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 are three systems that play an essential part in homeostatic response to intravascular volume reduction, these include; sympathetic nervous system, cardiovascular system, and neuroendocrine system. Adrenaline, noradrenaline, angiotensin II, and antidiuretics hormones assist to sustain cardiac output (CO) and sufficient tissue perfusion to the brain and the heart. Compensated, decompensated and irreversible are the 3 phases of hypovolaemic shock. Compensated shock phase is when there is a decrease in blood pressure identified by baroreceptors located in the aortic arch and carotid sinus that stimulate sympathetic output. Increased levels of catecholamines create an effect of increased heart rate, myocardial contractility, and vasoconstriction

The kidneys play a part in the regulation of blood volume and blood pressure. The kidneys Juxtaglomerular cells are the primary site for renin storage and release, the renin responses to the body’s low and high blood pressure (Jenkins & Tortora, 2013). If the renin angiotensin aldosterone system (RAAS) is interrupted due to the formation of AVAs in the kidneys this could cause renal hypertension. This is the result from the narrowing and weakening of the kidneys arteries thus resulting in kidney failure because blood is not delivered to kidney tissue (Jenkins & Tortora,

(White 2007) If there is an increased amount of angiotensin II circulating in the capillaries there will be net dis-inhibition of sympathetic nervous system outflow causing an inappropriately high blood pressure. ACE inhibitors are used to counteract increased angiotensin II levels and prevent high blood pressure or hypertension.

Reduction of the risk of MI, stroke and death from cardiovascular disease in patients at risk. ACE inhibitors block the conversion of angiotensin I to the vasoconstrictor angiotensin II. ACE inhibitors also increase plasma renin levels and decrease aldosterone levels. Nursing Considerations: Monitor BP and pulse frequently. Assess patient for signs of angioedema. Monitor BUN, creatinine, and electrolyte levels

Basically, arterial blood pressure (BP) is directly proportional to the product of blood flow (cardiac output, CO) and the resistance to passage of blood through pre-capillary arterioles (peripheral vascular resistance, PVR) Hypertension can be caused by either an increase in Cardiac Output (CO) or by an increase in Peripheral Resistance (PR)