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43 Cards in this Set
- Front
- Back
- 3rd side (hint)
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Push |
At the arterial end of capillary, hydrostatic pressure is higher than oncotic pressure in the capillary so fluid moves - or is pushed - out into the interstitial space |
Outside ==> inside |
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Pull |
Towards venous end of the capillary, fluid moved into interstitial space leaving solute (plasma protein) behind. Creates higher capillary osmotic pressure which pulls fluid from interstitial space back into the vessel. |
Inside ==> outside |
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Increased Capillary Hydrostatic Pressure |
Can cause higher amounts of fluid to leave the capillary. Net fluid movement will be OUT of the capillary if pressure is continuously high at the venous end. Pressure also increased if there is any back up of blood flow. Ex.; DVT obstructing blood flow |
HTN or increase in fluid volume |
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Decreased Capillary Colloidal Osmotic Pressure |
Lack of sufficient capillary oncotic pressure to pull fluid back into the interstitial space - into the capillary - at the venous end. Albumin is most prevalent colloid or solid in plasma any decrease in albumin will lead to decreased pressure |
Burns, Liver disease, malnutrition, and excessive wound drainage. |
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Increased Interstitial Colloidal Osmotic Pressure |
Third mechanism that causes fluid imbalance. When solutes escape from the vessel into the interstitial fluid, they will take fluid with them and hold the fluid in the interstitial space. Permeability increases in response to chemical mediators of the inflammatory processes. |
Leaky Capillaries. |
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Increased Tissue Hydrostatic Pressure |
Fourth mechanism. This can happen when lymphatics are obstructed and do not remove excess fluid and is complicated by increased tissue oncotic pressure which continues to pull fluid from the vessel. Lymphatic obstruction can occur in liver disease or because of physical obstruction from surgery. |
Lymphatic obstruction. |
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Edema |
Represents an increase in fluid in the interstitial space. Sometimes fluid becomes trapped in another compartment. |
Fluid trapping. |
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Causes of Edema |
1. Increased capillary hydrostatic pressure - causing movement of fluid into the tissue. 2. Decrease in plasma proteins results in decreased capillary oncotic pressure. (The lack of "pull") 3. Increased capillary permeability results in the loss of intravascular proteins and other solids to the interstitial space. This movement is accompanied by fluid keeping it in the space. 4. Lymphatic obstruction results in decreased absorption of interstitial fluid and therefore Edema. |
Including the 4 mechanisms of fluid imbalance. |
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Third-Spacing |
Transcellular compartment is a small division of the extra cellular fluid compartment. it includes various body spaces such as joint spaces, the pericardial and pleural cavities, the peritoneum and ocular fluid. When fluid shifts and is unable to be pushed or pulled or lymphatic obstruction, fluid becomes trapped in the transcellular space. |
Joint spaces |
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Manifestations of Edema (BRAIN) |
- Increased Intracranial pressure = headache, altered level of consciousness or coma - Abnormal pupil size or reflective response, changes in pattern of respiration and changes in muscle tone and abnormal posturing. |
Associated with infections or trauma. |
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Manifestations of Edema (Airway) |
Swelling (acute) = may result in difficulty swallowing, anxiety, stridor and possible airway obstruction and asphyxia. |
Appearances. |
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Manifestations of Edema (Lungs) |
- Decrease in gas exchange - Decrease in the ability of the lungs to inflate. - Dyspnea - May also have anxiety and restlessness, diminished breath sounds, and/or crackles on auscultation. |
Breathing. |
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Manifestations of Edema (Abdomen) |
Fluid collecting in the peritoneal cavity is ascites. (Third-spacing)
- Due to increased intravascular hydrostatic that results when portal vein is affected by liver cirrhosis - Abdominal tumour or pancreatitis - Increase in abdominal girth and a protruding umbilicus. - Abdominal discomfort or SOB (sometimes) |
Fluid impeding diaphragm. |
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Manifestations of Edema (Peripheral) |
- Increases capillary hydrostatic pressure - Can occur in the lower extremities in ambulatory patients - Sacral area for bedridden patients - Salt retention is usually pitting edema |
Soft tissues and pit is evident. |
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Treatment of Edema |
- Lack of albumin = consume adequate amounts of protein - When there is a lack of albumin intravascularly = would require transfusions of albumin to increase capillary oncotic pressure. - Diuretic therapy commonly used when there is an increased extracellular fluid volume. (HTN) - Pregnant women with edema = should elevate her legs and avoid standing for long periods of times |
Supportive measures or compensate for the loses. |
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Maintaining Na+ & H2O Balance |
Movement of body fluids between the intracellular and extracellular fluid compartments depends on the levels of water and sodium.
The major regulator of sodium and water balance is the amount of circulating blood volume.
Body continues to strive to maintain adequate vascular volume to effectively perfuse tissues, supplying with nutrients and removing wastes. |
Compensating water and sodium |
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Osmoreceptors |
Located in the hypothalamus. Keep track of the osmolality or the concentration of the blood. Sodium is predominant osmotically active in the blood. |
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Baroreceptors |
Sensors located in blood vessels walls and in the kidneys. It measures the stretch in the vessel walls that is produced by blood volume and blood pressure. |
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THIRST |
Primary regulator of water intake. If you eat a lot of salty food, your thirst mechanism will prompt you to drink more. Thirst develops with even a small change in fluid volume or osmolarity. |
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ADH |
When hypothalamus senses low blood volume or increased osmolality, it sends signals to the posterior pituitary to release ADH. It acts on the kidney tubules to retain water and therefore increases blood volume and reduced serum osmolality. |
Stops cycle when hypothalamus gets the message. |
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R-A-A-S |
=> Circulating blood volume drops => less renal perfusion => juxtaglomerular cells sense reduced stretch of afferent arteriole => increase in renin release which acts as an enzyme => convert angiotensinogen to angiotensin 1 => Angiotensin 1 converted to 2 (by ACE) => Stimulates the production of aldosterone in the adrenals => Sodium is reabsorbed and potassium is lost and brings water with it, resulting in an increase in circulating blood volume. |
The system. |
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Natriuretic Peptide |
Provides counter balance to the activity of baroreceptors, ADH and the R-A-A-System.
These cells cause the kidney to increase sodium and water excretion by: - suppressing renin levels - decreasing aldosterone release - causing vasodilation
ANP & BNP - respond to increased blood pressure/volume - counter-regulatory: excretion of Na+ and water. |
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Risk for Fluid imbalances |
- Infants have more than half of their total body water in the extracellular compartment. Daily fluid exchange is greater in infants because of their higher metabolic rate. - Infants have immature kidneys therefore have greater loss of fluid through skin compared to adults because of their body surface! - Elderly have decrease kidney functioning and a decrease in GFR. There is a decrease in the ability to concentrate urine. Slower to respond to sodium and water imbalances. - Obese individuals have a percentage of total water that is much less than a leaner individual therefore they will have less body water to lose. - Sick individuals are also at risk especially when they have vomiting, fever or diarrhea. |
Think normal natural risk factors. |
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Assessing Fluid Balance |
Thirst, Mucous membranes, Turgor, tearing - Dry mouth (deficit), - Skin turgor - skin flattens more slowly after a pinch is released. - Obese might maintain their skin turgor even with a fluid deficit. - In infants, tearing is considered a indicator of dehydration
Pulse and BP - Tachycardia - Alterations in pulse rate
Edema - Excessive amounts of interstitial fluid - Pulmonary edema = crackles and dyspnea - increased abdominal girth.
Weight - Losing weight at an abnormal rapid rate
Intake/Output - Decreased urine output - Increased urine concentration
Neuromuscular Signs - headache, anxiety, changes in level of consciousness + twitching.
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6 Factors! |
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Isotonic Fluid Volume Deficit: CAUSES |
Both sodium and water is lost. Plasma concentrations remain unchanged but circulating fluid volume is decreased.
Fluid intake has decreased or because fluids are not available or intentionally being withheld.
OR, there is abnormally large output of fluid. Fluid can be lost through skin due to fever, due to exposure to heat, or due to wounds or burns.
Fluid lost from drug therapy (diuretics), to circulation when it gets trapped in third spacing such as peritoneum. |
Medium - midline |
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Isotonic Fluid Volume Deficit: MANIFESTATIONS |
- Initiating thirst response - Decrease in body weight (but watch out for third spacing) - Baroreceptors will sense a decrease in vascular volume and will send a message to initiate compensatory secretion of ADH. It increased reabsorption of water and sodium. - Eyes look sunken and skin or tissue turgor decreases (not reliable indicators in dehydration for elders) - Decrease in tearing for infants - Decrease in blood volume, there is a decrease in blood pressure then heart rate will increase and pulse will become weak and thread. - RBC and BUN become more concentrated. |
Think about dehydration! |
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Isotonic Fluid Volume Deficit: TREATMENT |
Hypovolemia = replace lost fluid promptly
Isotonic losses are replaced with isotonic fluids such as normal saline or lactate ringers solution. |
Think hypovolemia
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Isotonic Fluid Volume Excess: CAUSES |
Sodium and water retained in proportion.
Both extracellular fluid compartments expand. Hypervolemia can occur when body is unable to eliminate appropriate amounts of fluid due to poor kidney function.
If excessive amounts of IV were given, the body maybe unable to manage the the increase in circulating volume. |
Think hypervolemia |
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Isotonic Fluid Volume Excess: MANIFESTATIONS |
Changes in body weight can indicate fluid overload.
Increase in vascular volume can be seen in distended neck veins and in full, bounding pulse.
Listen for crackles and watch for a productive cough.
BUN and Hematocrit levels will decrease when both are diluted. |
Increased Hydrostatic pressure - hypervolemia results in edema. |
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Isotonic Fluid Volume Excess: TREATMENT |
Stop increasing the fluid volume by restricting fluid intake and restricting sodium intake.
Help decrease the excess fluid volume - diuretics can be given to increase sodium (+water) elimination
Determine the reason behind the volume excess and treat accordingly |
Hypervolemia |
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Hyponatremia |
Plasma Concentration of sodium less than 135 mmol/L.
Too little sodium in the ECF or there is too much water.
Deficiency of sodium can be the result of too little sodium intake.
Can be lost through diuretic use. Sodium is also lost through sweating and gastrointestinal losses such as vomiting, diarrhea or nasogastric suction.
High levels of ADH result in too much water retention. Which can also be caused by some medications. |
Renal Problems |
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Hyponatremia: Manifestations
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Depend on the cause and the speed of the onset.
Fluid shifts from the extracellular space into the cells which causes the cells to swell = headaches.
With further swelling, there will be changes in level of consciousness and coma.
Diarrhea, muscle cramping, weakness, fatigue and tremors.
Decreased serum osmolarity, hematocrit and BUN - dilution of these substances by the fluid. |
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Hyponatremia: Treatment |
Water excess = fluid restrictions. Medication should be stopped if its causing the problem.
May be necessary to limit water and sodium intake until the problem ceases.
Might order oral or IV supplements. Avoid any huge shifts of fluid.
Monitor Vitals, neurological status, intake/output, and daily weight. |
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Hypernatremia |
Serum concentration of more than 145 mmol/L. High levels of sodium can be caused by to much sodium in the ECF or by too little water.
Increased sodium creates an increase in osmolality of blood, which stimulates thirst.
Commonly caused by water loss. Through fever, heat stroke or respiratory illnesses, diarrhea.
Loss of particles in the filtrate will cause a related loss of water. |
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Hypernatremia: Manifestations |
Shrunken cells - client will be restless, confused and weak due to a shift in fluid from the intracellular compartment to the vasculature because of the osmotic pull.
If not corrected symptoms will worsen: stupor, seizure, and coma. Should look out for twitching.
Dry mucous membranes and orthostatic hypotension
Increase in Sodium concentration and osmolality and thirsty. |
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Hypernatremia: Treatment |
Either add water or remove salt.
Oral rehydration solution is available. Contains glucose and electrolytes along with water and is recommended for treating dehydration. IV solutions can also be used. |
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Hypokalemia |
Decrease in plasma potassium levels below 3.5 mmol/L.
People on fad diets may not eat sufficient potassium-rich foods.
May be caused by excessive losses of potassium. When aldosterone levels are high or, because of diuretic use. Many thiazide and loop diuretics increase the loss of potassium in the urine.
Potassium lost due to vomiting, diarrhea or GI suctioning.
Insulin promotes movement of potassium into the cell - bronchodilators and decongestants. |
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Hypokalemia: Manifestations |
Most clients will not show signs until potassium levels fall below 3.0 mmol/L, and signs are gradual in onset.
Urine output increases and therefore plasma osmolality increases and the client will experience thirst.
Client may have anorexia, nausea or vomiting. Decrease in smooth muscle activity can cause constipation or in severe cases, paralytic ileus.
Abnormal muscle contractility in skeletal muscles can cause fatigue, weakness and muscle cramping.
Patients may experience postural hypotension and cardiac arrhythmias. |
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Hypokalemia: Treatment |
Best treatment is prevention. Should be taught to ingest foods with high concentration.
Clients are prescribed oral potassium supplements, which will slowly correct the problem.
When deficit is severe, potassium may be added to an IV solution. |
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Hyperkalemia |
Plasma levels of potassium in excess of 5.0 mmol/L.
Clients with impaired kidney function and are administered rapid potassium containing solutions - hyperkalemia can result.
Most common cause is decreased renal function. Decrease in aldosterone will cause elimination of sodium with a decrease in elimination of potassium.
Movement of potassium out of the cells and into the plasma will also cause hyperkalemia. In response to tissue injury, body tries to compensate for high number of hydrogen ions by shifting them into the cells - in periods of acidosis. |
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Hyperkalemia: Manifestations |
Often not noticeable until plasma levels exceed 6.0 mmol/L.
Nausea and vomiting, cramping and diarrhea.
Clients will have weakness, dizziness and muscle cramps but might also have abnormal sensation or paresthesia.
The heart rate may slow, ECG changes will occur, and if severe, ventricular fibrillation and cardiac arrest may occur. |
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Hyperkalemia: Treatment |
Depends on how quickly the potassium rate has risen and how high it is.
Treatment can be limited to restricting dietary potassium - particularly in salt substitutes - or discontinuing medications that promote potassium retention. (Sparring diuretics)
Aggressive treatment = oral solutions which will remove potassium by exchanging sodium for potassium in the intestinal tract.
In severe cases, when there are neuromuscular or ECG changes, need more aggressive treatment that helps move potassium back into the cells or promote renal excretion. |
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Calcium, Phosphorus & Magnesium Imbalances |
Very important cations in the body. Not much of each of these three ions are available in the ECF levels of these substances. Calcitonin removes calcium from the extracellular fluid.
- Regulated by Vitamin D, parathyroid hormone and calcitonin - Normal Ca2+ = 2.1 - 2.6 mmol/L. - Neuromuscular and cardiovascular manifestations of imbalances |
Just know the gist of it. |
