Unlike their friend Jemima, the other patients have all experienced a drop in blood pressure (Hypotension) and have an elevated heart rate (125-135 bpm) Hypertension occurs when blood pressure drops below 90 mm Hg systolic or 60 mm Hg diastolic number. Due to the girls all consuming substances that affect their bodies to normally retain water, they have all suffered similar symptoms but to different degrees. Dehydration causes the volume of blood circulating through the body to decrease in volume and become more viscous.
To compensate, the heart beats faster, increasing the heart rate and potentially causing conditions such as tachycardia (increased heart palpitations) to occur. In addition when the body is exposed to high temperatures, it requires a larger amount of blood to be transported toward the surface of the skin for thermoregulation and to regulate metabolic heat, increasing the requirements on the heart rate even more. Substantial cardiovascular stress can occur as a result of dehydration and being just 5-6% dehydrated can lead to symptoms of fatigue and tachycardia.
The heart rate of an individual can change an average of three beats per minute for every one-percent change in body-weight resulting from dehydration. Also if the blood volume continued to drop the patients would be at risk of hypovolemic shock, which occurs when low blood volume causes a drop in blood pressure and a significant reduction in the amount of oxygen reaching your tissues. If untreated, severe hypovolemic shock can cause death within a few minutes or hours.
The body tracks circulatory system pressures through specialised sensory neuron cells (a type of mechanoreceptor) called baroreceptors in the walls of major blood vessels in the chest and neck (Carotid sinus and aortic nerve). These baroreceptors measure how much the vessel walls are stretching. If blood volume is too high, vessels are strained; if volume is too low, vessels stretch minimally, or not at all. When dehydration occurs, the blood volume decreases due to lack of water, so vessel walls do not stretch as much as they normally should.
Baroreceptors relay this information to the cardioregulatory and vasomotor centres in the medulla oblongata through a reflex mechanism called the Baroreflex, which acts as a rapid negative feedback loop (taking place in milliseconds), and regulates blood pressure . Through nerves such as glossopharyngeal nerve (IX cranial nerve) and vagus nerve (cranial nerve X), action potentials are sent to these centres increase/decreases parasympathetic stimulation of the heart. . During low blood pressure, a decrease in action potentials occurs and affects the cardioregulatory center of the medulla.
Therefore, to raise blood pressure, the body firstly will create an increase in sympathetic nerve response in the SA node, causing it to fire more frequently, increasing the heart rate. Due to the increase in heart rate the muscles in the heart are also prompted to pump with more exertion, increasing the stroke volume, which also increase cardiac output. Increasing the cardiac output and increasing the sympathetic input to the blood vessels through vasoconstriction of the heart will eventually increase the blood pressure and restore it back to a normal level.
In normal circumstances the baroreflex would cause a rapidly readjustment of heart rate to restore blood pressure quickly. In the case of these three patients, however, their significant dehydration (hence substantial loss of blood volume) would render this process slower and they would remain below a normal blood volume levels with the heart rate increased, until they the fluid in body is restored to healthy homeostasis levels. Question #6 The first step in creating urine is glomerular filtration.
This is the system the kidneys use to filter out excess water and waste products in the blood, and into the urine collecting tubules of the kidney, so they may be expelled from the body. The rate at which kidneys filter blood is called the Glomerular Filtration Rate (GFR), specifically the rate of which fluid moves between the glomerular capillaries and the Bowman’s capsule, and is measured in milliliters per minute. A GFR test estimates how much blood passes through the glomeruli each minute and is used to check how well the kidneys are functioning.
Several factors such as age, gender, body type, etc, are used to calculate your normal estimated GFR (eGFR, typically measured primarily by serum creatinine, urea and electrolyte levels). The healthy eGFR for Indigo would be around 125, while hers has dropped to a low 85, indicating that the kidneys are struggling and there is a low volume of blood being filtered. For reference an eGFR of 85 would be typical for a woman in her 60s.
A persistently low eGFR such as this over several months could indicate chronic kidney disease, however in this instance her circumstances and consumption of the seawater are the cause. It is normal for blood pressure to fluctuate throughout a period of time in the body, due to many internal and external factors, however, this usually has no effect on your glomerular filtration rate. This is because under normal circumstances, your body can precisely control it through both intrinsic and extrinsic mechanisms.
Renal autoregulation is an intrinsic mechanism where the kidney alone can adjust the dilation or constriction of the afferent arterioles, which counteracts changes in blood pressure. This intrinsic mechanism works over a large range of blood pressure, but can malfunction if the kidneys are under severe stress, such as severe dehydration. Extrinsic mechanisms such as neural controls and hormonal controls can override renal autoregulation and decrease the glomerular filtration rate when needed.
In the case of low blood pressure, which Indigo is experiencing due to her rapid dehydration due to factors such as her diarrhea and lack of water consumption, the nervous system will stimulate contraction of the afferent arteriole, reducing urine production, as an attempt to try and regulate blood volume levels. If this is not enough to help regain homeostasis, the nervous system will also activate the hormonal control, the renin-angiotensin-aldosterone system (RAAS), that also regulates blood pressure and fluid balance (as mentioned in question 3).
The hormone responsible for maintaining electrolyte concentrations in extracellular fluids is called aldosterone, a steroidal hormone that is produced within the adrenal cortex. In contrast to ADH, which stimulates the reabsorption of water to maintain proper water balance, aldosterone maintains water balance by amplifying sodium reabsorption and potassium secretion from extracellular fluid of the cells in kidney tubules.
Because aldosterone is produced in the cortex of the adrenal gland and affects the concentrations of both minerals Na+ and K+, it is referred to as a mineralocorticoid, a type of corticosteroid that affects the balance of ion and water. Aldosterone release is triggered by a decrease in blood sodium levels, blood volume, or the blood pressure, or an increase in blood potassium levels. It also prevents the loss of Na+ from sweat, saliva, and gastric juice. The reabsorption of sodium also results in the osmotic reabsorption of water, which alters blood volume and blood pressure.
Aldosterone production can be prompted by low blood pressure, which triggers a sequence of chemical releases . When the blood pressure decreases, the renin-angiotensin-aldosterone system (RAAS) is initiated. Cells in the juxtaglomerular apparatus, which controls the functions of the nephrons of the kidney, specifically measuring GFR, identify this and release an enzyme called Renin. Renin circulates in the blood, reacting with a plasma protein produced by the liver called angiotensinogen. When angiotensinogen is divided by renin, it produces angiotensin I, which is then further converted into angiotensin II in the lungs.
Angiotensin II operates as a hormone, causing the release of the hormone aldosterone by the adrenal cortex, resulting in increased sodium reabsorption, water retention, and an increase in blood pressure. Angiotensin II, in addition to being a potent vasoconstrictor, also influences an rise in ADH and increases thirst, both of which help to raise blood pressure back to healthy level. In situations where the blood pressure lowers further due severe fluid loss, like Indigo is experiencing, then the sympathetic nervous system response will supersede the usual renal autoregulation.
Here, sympathetic nerves stimulate the afferent arterioles of the kidneys causing vasoconstriction. This has occurred through: loss of the extracellular fluid volume (due to Indigo’s acute dehydration) causing a decrease in her mean arterial pressure (MAP: her systolic/diastolic blood pressure results were 75/40). A lowered MAP was identified by her arterial baroreceptors, which then lead to sympathetic nervous system stimulation, afferent arteriole narrowing, decreasing the blood flow into the glomerulus and ultimately reducing her GFR.