1) Secretion and absorption of fluids and electrolytes normally takes place in the gastrointestinal tract. The stomach is its first segment to start the process of digestion. Thus, special mechanisms to digest are present in the stomach. This is the acidic solution, which meets food first and begins to take it down. Early fluid loss evidently affects extracellular compartment. Normally, in the stomach, 0,5-2 liters of highly acidic liquid content is produced. Most of this volume is reabsorbed. In vomiting, this extracellular solution is evacuated, followed by depletion in plasma volume. Then, water will move from tissues to the intravascular space to keep the electrolytes and circulating blood volume within the normal range. However, on the late stage, the interstitial and intracellular potential fails to meet the requirements.
2) Sodium composes 90% of extracellular cations. In isotonic dehydration, as described in Case A, the fluid rich both in potassium and in water is lost. Water and electrolytes (mainly sodium) are lost in equal amounts. Thus, the level of potassium will be stable. It must be kept in mind that after the stomach is empty; it is to be refilled with sodium. Sodium in the stomach space forces water to follow from plasma to the third space.
3) Mr. K.B. is thirsty and this is an early symptom of dehydration, can be explained by elevated osmotic pressure of the plasma. Dry mucous membranes correspond to sunken eyes, which in combination point to water deficit.
4) Normally, the pH of gastric fluid may be as low as 1,0 (Gennari & Weise, 2008), meaning the concentration of Hydrogen cations is very high. In early vomiting, the Hydrogen ions are lost, thus shifting pH to the alkalosis. The second electrolyte that contributes to alkalosis is chloride. Loss of chloride demands that another anion replaces chloride. Namely, bicarbonate from intracellular space moves from the red blood cells into the plasma space to elevate pH. Activated compensation mechanisms include water and sodium reabsorption in the kidneys, and hydrogen and potassium excretion, which also contributes to alkalosis. The normal range of blood pH is within 7,35-7,45. Alkalosis is pH higher than 7,45.
5) Fluid loss will result in activation of hypothalamic center for thirst, which elevates the level of vasopressin (antidiuretic hormone). This hormone retains water in the body by increasing its reabsorption in the kidneys and constricts peripheral vessels to support circulation with diminished circulating blood volume. Second, renin-angiotensin-aldosterone system is activated to increase reabsorption of sodium and water in the tubules of the kidneys. However, these mechanisms are effective in mild deteriorations only.
6) Mr. K.B. is 81 years old, supposing he is suffering from other diseases too. The age and male gender of the patient make ischemic heart disease most likely co-morbidity in this case. Thus, the heart function might be compromised and will not be able to meet the new requirements to support circulation. Other possible concomitant diseases include diabetes (consider glucose level to worsen dehydration), renal failure (in case of arterial hypertension history) or pulmonary disease (inability to support oxygen supply). In the elderly, the percentage of water in the body is lower comparing to the younger and children, so the potential for compensation is limited.
7) Elevated sodium level suggests water losses are more prominent than sodium losses. Water losses activate renin-angiotensin-aldosterone system, of which angiotensin II activates Na+/H+ exchanger to reabsorb sodium, and aldosterone acts on the tubules to reabsorb sodium at the expense of potassium excretion. Considering the advanced age and serious condition of the patient, his inability to drink water must add to hypernatremia. The neighbor reported his respirations are rapid – the observation that explains additional water losses to be more considerable than sodium loss.
8) High sodium levels mean elevated osmotic blood pressure. Following the osmotic gradient, water leaves cells to the extracellular spaces. The cells, in turn, shrink and may destruct. Attempts to rehydrate the cells meet the obstacle of extracellular edema: the extracellular space is high in sodium concentration, and the amount of water increases in this place.
9) a. Continued fluid loss is likely to reduce the circulating blood volume. The liquid part is affected most, and the elevated hematocrit level points to this fact. Moreover, as there is hypovolemia, the blood pressure is decreased, because there is no enough volume to fill the vessels. To support the cardiac output, the heart develops tachycardia so that minute circulation volume could be supported by heart rate, not the stroke volume.
b. Cell function may be severely compromised. The fluid is mobilized from the cells to support the circulating blood volume. However, the compensation mechanisms are not enough to support the homeostasis. The oxygen delivery is depleted and mitochondrial ATP-producing chains fail to produce high-energy phosphates. Thus, all energy-dependent actions within the cell diminish. For example, Na+/K+ exchanger is inhibited and will not support the electrolyte gradient through the cell membrane; therefore, the membrane potential decreases. Calcium influx into the mitochondria further inhibits respiration and contributes to cellular damage. Intracellular lysosomes lose their structure and enzymes may contribute to cell death.
c. During hypovolemia, the decrease in cardiac output is partially supported by systemic vasoconstriction. The vessels in kidneys constrict only at the late stages of hypovolemic shock. Renal ischemia decrease glomerular filtration rate, while compensatory systems (like renin-angiotensin-aldosterone) reabsorb water, the two in combination result in oliguria or even anuria. Local hemodynamic shifts decrease cortical perfusion and cortical ischemia ultimately develops. Severe or prolonged ischemia may result in necrosi.
10) Cardiac history means potassium imbalance may have serious effects on the patient. Potassium is essential to maintain cardiac rhythm, low potassium levels may contribute to atrial fibrillation and other rhythm disturbances. Potassium depletion may provoke bradycardia. In hypokalemia, PR and QT prolong, and U appears, contributing to possible heart arrest. Hypokalemia decreases myocardium sensitivity to digoxin and may result in digitalis intoxication.
11) Mr. K.B. evidently experiences low minute volume cardiac output, because his circulating volume is depleted. The central venous pressure is probably close to zero. Therefore, his oxygen delivery index is low. All body tissues and organs are under distress, including the brain. High hematocrit level and acidosis suggest severe microcirculation impairment, so oxygen extraction ration is probably low. The arteriovenous oxygen difference had been measured, it would appear to be decreased. Due to systemic compensatory vasospasm, the systemic vascular resistance is increased and obscures adequate tissue perfusion. All components explain lethargy and weakness.
12) Mr. K.B. is tachypneic . Rapid breathing takes out carbon dioxide due to its washout from the alveoli. Hence, carbon dioxide level decreases, like less than 35 mmHg. Bicarbonate had been lost during vomiting and used to compensate acidic chemicals that develop from tissue malperfusion, thus HCO3 decreases too, like less than 21 (22 venous) mmol/L.
13) Severe hemodynamic compromise certainly leads to hypovolemic shock and decompensated metabolic acidosis. Renal failure may develop and contribute to the condition.
14) According to Quinn et al. (2009), the patient might complain of head, eyes, ears, nose, throat (tinnitus, blurred vision), visual disturbances (dimming, photophobia, scotomata), cardiovascular findings (palpitations, chest pain), neurologic findings (headache, visual changes, mental confusion), pulmonary findings (dyspnea from the patient's observation of hyperventilation), GI findings (abdominal pain), musculoskeletal findings (generalized muscle weakness, bone pain). Note the findings are non-specific and engage most organs and systems.
15) Acidosis causes hyperkalemia due to its shift from the cells. The plasma potassium concentration rises by 0,6 mmol/L for every 0,1 unit reduction in extracellular pH (Adrogue & Madias, 1981)
16) It is an extremely important isuuse to replase both water and electrolyte losses in dehydration. Suppose, the patient is 65kg, so that his extracellular volume was approximately 13 liters, and sodium concentration 140 mmol/L. Gastric secretion with low pH contain 45mmol/L sodium. Suppose, he lost 5% of his body weight (5%*65 kg=3,25 L of water) and respective amount of sodium (45 mmol/L*3,25=146,25 mmol). In this case, if he is replenished with water only (or 5% dextrose) his sodium concentration waill be (140 mmol/L*13L – 146,25 mmol)/13= 128,75 mmol/L. These simple calculations show how the patient may develop severe hyponatriemia. The same may happen with potassium if ignored in fluid therapy.