| Flap 1 | Flap 2 |
| S/Sx of FVE? | Edema, JVD, anorexia, V&N, dyspnea, orthopnea couch, moints sounds. increased BP, bounding pulse, pitting |
| S/Sx of FVD? | chng in LOC, thirst, headache, v&N, dry skin, decreased turgor, diarrhea, soncstipation, muslce weakness, parathesias, tetany. postural hypotention, change in rate of resp, pulse and depth of resp. |
| When edema is great it is called______. | Anasarca |
| ABG's give infor about what 3 things? | oxygenation, ventilation and acid base. |
| When drawing blood for an ABG what should you note? | Temperature |
| Level of HCO3 ? | 22-26 |
| Level of pH? | 7.35 - 7.45 |
| Level of PaCO2? | 35-45 |
| Acids release what? | H |
| Bases bind what? | H |
| As H increases pH does what? | Decreases |
| Lungs excrete carbonic acid as what? | CO2 |
| When pH decreases ( becomes acidic) the rate and epth of resp does what? | Increases to create greater excretion of CO2. |
| When pH increases ( alkalosis), the rate of resp does what? | Decreases to retain CO2 (which will join with H2O to create carbonic acid.) |
| CO2 is constantly being formed by what? | metabolism so the resp system is contantly balancing the amount of CO2 in the ECF |
| The kidney usually excretes______ urine and retains _______ | acidic, bi-carbonate |
| What is the main point of excretion of CO2? | The lungs |
| With Alkalosis, what is the kidney going to do? | Bi-carb will be combined with Na in the tubules and excreted |
| With Acidosis, what will the kidneys do? | Excrete excess H |
| What is the major effect of acidosis? | CNS depression |
| What does Alkalosis do to the CNS? | Over excites it |
| When ventilation decreases, what heppens? | The amont of CO2 and H increases creating resp acidosis. |
| Hypercapnia ( too much CO2) causes what? | CO2 Narcosis |
| Acidosis makes ______move out of cells, creating _______. | K, creating hyperkalemia of the blood |
| what happens if you have too much blood K? | Ventricl fibrilation. |
| What are the basic causes of Resp acidosis? | Anything blocking airway, poor ventilation, decression of respirations(COPD most common), COPD, pneumothorax, atelectasis, pneumonia |
| What causes respiratory alkalosis? | Excessive ventilation. |
| What is the common cause of resp alkalosis? | Hyperventilation from anxiety, pain, hypozia, brain lesions, over ventilation on mechanical ventilator |
| Metabolic Acidosis is a deficit of what? | Bi-Carbonate |
| What does metabolic acidosis come from? | Losing bi-carb or too much organic acid is added to the body. |
| What are common causes of Metabolic Acidosis? | DM and starvation. |
| Why idoes DM create metabolic acidosis problems? | If glucose can't be used (or there is none) the body uses fat creating ketone acids. Plasma bi-carb is used to try to buffer the ketones acids so you get metab. acidosis or keto acidosis. |
| Metabolic acidosis also can be created by lactic acid? | Excess lactic acid is caused by prolonged exercise or oxidation without O2 from heart failure, shock, or a bicarb deficit from diarrhea or draining fistula. |
| What is the relationship between metabolic acidosis and kidney failure? | The acids accumulate because they cannot be filtered out of the blood. |
| In a normal Kidney with acidosis, what happens? | The excess H will be released, retain K and create hyper K along with the acidosis. |
| Metabolic Alkalosis is an excess of what? | Bi-carb or lactate |
| What are some common causes of Metabolic alkalosis? | loss of acids from vomit, suction, drainage, loss of K from fistulas and diarrhea, iinjestion of sodium bicarb, antacids, bicarb or lactate IV infusion, diuretics. |
| In metabolic acidosis, what happens with the K? | It enters the cell and HypOkalemia results. |
| What do you assess for with Metabolic Alkalosis? | HypOkalemia, dizziness and tingling. |
| What is the Tx for Resp Acidosis? | enhance ventilation, TCDB, remove blockage |
| What is the Tx for Resp Alkalosis? | treat cause, watch for dysrythmias, Ca gluconate for tetany, help renal function to help compensation |
| What is the Tx for metabolic acidosis? | Treat Cause ( Dm, Starvation, lactic acid) give Na bi-carb, dialysis if from renal failure, beware hypo K as K moves back into cell. |
| What is the Tx for metabolic alkalosis? | Treat cause(vomit, suction, drainage, antacids, fistualas, diarrhea) dc NGtube, dc antacids, give Na Cl or amonium Cl, diuretics to excrete excess bi-carb. keep resp function going to help compensation. |
| Elderly and COPDers are at an increased risk for______? | Acid Base disorders |
| Acid Base disorders in elderly may lead to? | Respiratory depression. |
| Normal pH distrubances are due to? | Aging |
| Name some ore-existing conditions that can lead to Acid Base disorders? | Renal, cardiac, endocrine and pulmonary. |
| Once an acid base disorder has occured, elders are less able to compensate because of what? | Age related changes to the kidney. |
| the amount of diuresis produced is in direct proportion to.. | The amont of Na and Cl blocked from reabsorption. |
| High ceiling diuretics produce the most and work even when... | Glomerular filtration is low. |
| High ceiling diuretics can cause? | dehydration, hypOtension, hearing loss ( ototoxity) and hypOkalemia |
| Thiazides produce les and are ineffective with.... | lower glomerular filtration rate but aren't ototoxic. |
| K sparing diuretics cause what rate of diuresis? | Modest |
| K sparing diuretics are use to counteract what? | K loss from high ceiling / thiazide diuretics |
| K sparing can cause what electrolyte disorder? | HyperKalemia |
| Don't comine K sparing diuretics with what? | K supplements or with each other. |
| High ceiling and Thiazide diuretics are used for? | HTN and Edema associated with CHF, cirrhosis and renal disease., |
| Name a high ceiling diuretic. | Furosimide / Lasix |
| Name some Thiazide diuretics. | HCTZ and HydroDiuril |
| Name a K sparing diuretic. | Spironolactone |
| When is comes to electrolyte, what is is really all about? | Shrinking and swelling of the brain. |
| Aldosterone is a ______secreted by the ________. | Hormone, Adrenal cortex. |
| Aldosterone secretion is stiumlated by____ | FVD |
| Aldosterone site of action is.. | Kidney |
| Aldosterone reabsorbs____ and secretes _____ | Na, K |
| If a patient has hypo-aldosteroneism what will happen to BP and volume status? | Low BP and dehyration |
| ADH is produced by the ? | Hypothalamus |
| ADH is secreted by the ? | Posterior Pituitary. |
| ADH is released in response to | FVD or high osmolarity and thirst. |
| The site of ADH action? | Kidney |
| ADH re-abropbs what? | H2O |
| ADH allows for the excretion of what? | concentrated urine |
| Three conditions that can trigger ADH are? | stress, anasthesia and narcotics. |
| What is SIADH | Syndrome of Inappropriate ADH |
| If a pt has SIADH what would you expect the volume status to be? | FVE or normal. Na will be low, water is trying to move back into the cell. |
| What is the Tx for SIADH with a head injury? | monitor I and O, fluid restriction, any fluid should be hypertonic to draw fluid away from brain, and check LOC |
| What is diabetes insipidus? | Too little ADH |
| What happens with diabetes insipidus? | H2O moves out of the cell, volume status is low, frequent urination. |
| Tx for diabetes insipidus? | Give ml for ml urinated, replace with hypotonic fluids, give vasopressin, |
| What is vasopressin? | Synthetic ADH |
| Types of Dehydration | Isotonic, Hypotonic, Hypertonic |
| What is Isotonic dehydration? | Fluid has the same osmolarity as plasma, from bleeding. Lose fluid and electros in equal amounts. |
| What is Hypotonic dehydration? | Fluid has fewer solutes than plasma, from heatstroke |
| What is Hypertonic dehydration? | Fluid has more solutes than plasma, Dm, DKA, hyperglycemia and DI |
| What are neuro manifestations of FVD? | decreased lov , restless, dissy from low circulating blood vol. and confusion. |
| Whare are the cardiovascular manifestations of FVD? | decreased BP and tachycardia |
| What are the Pulmonayr manifestations of FVD? | increase respirations trying to pump blood around |
| What is the renal manifestation of FVD? | increased specific gravity |
| what is the manifestation of FVD in the extremities? | poor turgor, muscle cramps, dry skin, cold, clammy |
| What are the "general" manifestations of FVD? | weight loss, shrunken eyeballs, thirsty |
| What are some causes of FVD? | diuretics, third spacing, vomiting |
| What are neuro manifestations of FVE? | confusion, seizures ( from increased ICP and decreased Na) |
| What are cardios signs of FVE? | increase dystolic, decreased diastolic (widening pulse pressure) |
| What are pulmonary signs of FVE? | crackles, SOB |
| What are some abdominal signs of FVE? | aceites and enlarged liver |
| what are some signs in the extremities of FVE? | edema, dependant or sacral |
| What are some general signs of FVE? | weight fain, prone to bed sores |
| What are some causes of FVE? | Disease processes or overhydration. |
| What are some causes of Hyper natremia? | DI ( not enough ADH), excessive Na intake, fever, heatstroke, pulmonary infections, burns, diarrhea. |
| Hypernatremia may come from ____in the elderly? | Decreased thirst response so they do not drink enough water. |
| The basic symptom rule of hyperNatremia? | Everything is jacked up. Reflexes, blood pressure, CNS, thirst, heart rate |
| S/Sx of Hyper Natremia? | Hyper reflexes, thirst, low urine output, HTN seixures, increased HR |
| Nsg Interventions Hyper Na? | treat cause, monitor I & O, Hypotonic fluids ( D5), monitor labs ( blood sugar and Osmo), watch LOC , seizure precautions. |
| Why do you infuse IV slow with hyper Na? | to avoid a rapid shift in fluid which will swell cells and create cerebral edema |
| What is the most important Nsg intervention for Hyper Na? | Monitor I and O |
| What does hypO Na do? | Pulls H2O from intravascular into the intracellular |
| HypO Na creates a potential for what? | Cerebral Edema |
| What are some causes of HypO Na? | Diuretics, vomiting sweating renal failure, over admin. of hypotonic fluids |
| S/Sx of Hyponatremia? | Confusion, headache, nausea, vomit, muscle weakness, fatique, apathy, anorexia. |
| What are late s/sx of HypO Na? | shock and coma |
| What are the Nsg Interventions for HypO Na? | I & O, weigh daily, vital signs, check for postural hypotension. |
| Why do you need to correct the HypO Na before giving fluids? | Use Isotonic to raise the Na level without the fluid so the cells don't draw the H20 in first. |
| Kidneys excrete K in echanges for___, controlled by ________. | Na, Aldosterone |
| The cause of HyperK is? | use of supplements, , movement of K due to hypoxia or acidosis, sepsis, trauma, crushing |
| S/sx of Hyper K? | Diarrhea, apathy, confusion, brady cardia and cardiac arrhythmias, cardiac arrest, numbness hands/feet. |
| Nsg Interventions for Hyper K? | Cardiac monitor, Kayexalate, Ca gluconate, IV insulin and IV D50, sodium Bicarb. |
| why do you use Calcium gluconate Iv in hyperK? | Offsets the effects of K on the heart. |
| Why do you use insulin and dextrose for Hyper K? | Promotes the uptake of K into the cells. K follows the insulin/dextrose. |
| If a patinet has refractory hyperkalemia what do you do? | Dialysis. It means that nothing else is working. |
| What happens with K and acidosis? | K move out of the cell where K and H are xchanged and H goes into the cell. |
| If you are using K in a peripheral line what do you use with it? | Lidocane for the pain. |
| What is the Iv rage for K in a peripheral line? | 10 mEq / hr, no more. |
| What are the s/sx of Hypo K | N&V, weak, hypOtension, elevated HR, dysrythmias, lethargy, confusion,( constipation and paralytic ileus with GI losses) |
| What happens with K and the kidney during metabolic alkalosis? | K is lower as K is moving into the cells during the alkaline state, then excreted by kidneys which hold onto the K because of the alkalitic state. |
| What are common causes of HypO k? | Starvation, increased aldosterone ( re-sorbs Na and rids of K), GI loss, laxatives and diuretics. |
| Most common causes of Hypo K? | Diuretics and laxatives. |
| What are some Nsg Interventions for HypO K? | Cardiat monitor, watch for dig toxicity, make sure you have urine output b/4 giving K, oral supplements |
| How do you administer intravenous K? | Dilute K, add lidocane and give no faster than 10mEq/hr. ( perpiheral line) |
| What does digitalis do? | Slow down the heart and increases contractility. |
| Why do you need to watch digitalis with K? | Potentiates the Digitalis and risk of toxicity. |
| What is Mag use for? | Protects against over excitability of muscles. |
| Mag has a sedative effect on?? | the neuromuscular junction by inhibiting acetylcholine (ATC) release and diminishes nmuscle cell excitability |
| Mag also helps with? | nerve conduction, DNA and PRO synthesis, ATP production, vasodilation. |
| have Torsseauds? Need more______> | Magnesium |
| What are causes of HypO Mag? | Malnutrition, alcoholism ( don't eat) steriods, diuretics ( lose K lose mag) diarrhea. |
| If you have HypO Mag you probably also have_______. | HypO Ca, mag effects parathyroid hormone. |
| S/Sx of Hypo Mag? | Tachycardia , Toursedes, paresthesis, muscle spasm, tremors, tetany, loc changes, seizures |
| What is Toursedes ? | Life Threathening cardia dysrymthias. |
| Low magnesium makes for muscular irritability. What are some signs of that? | Tetany, muscles spasms, tremors. |
| What are some Nsg Interventions for HypOMag? | Watch Dig ( mag enhances), cardiac monitor, seizure prec. replacement. |
| How do you administer IV Mag? | 1 gm to 20 ml of NS to dilute. |
| What is a common side effect of IV Mag admin? | Flushed, sweating, bradycardia, hypOtension. |
| What do you need to have before administering Mag? | A urine output. |
| S/Sx of Hyper Mag? | Bradycardia, hyporeflexia, resp. depress. lethary leading to coma |
| What are Nsg interventions for Hyper Mag? | Volume admin, diuretics, insulin and glucose admint, hemodialysis, seizure precautions, watch loc |
| Why use unsuling and glucose admint with hyper mag? | Mag follows K into the cells which is drawn there by the insulin/gluc. |
| why use diuretics with Hyper Mag? | K wasting diuretics ( loops especially) will take the mag with the K. |
| Ca is for.... | Transmission of nerve pulses, cardiac contractility, activation of clotting mech. |
| HypO Ca is related to what acid base problem? | Alkalosis |
| Hyper Ca is rrelated to what acid base problem? | Acidosis |
| HypO Ca is relate to _____Phosphate? | Hyperphosphate = HypO Ca |
| Causes of HypO Ca? | Multiple blood transfuions, dkined diseas and draining fistufals, diet, decrease GI absorb, decrease bone reabsorb, alkalosi, alcholism |
| Why does blood transfusion contribute to Hypo Ca? | the citrate binds with the Ca |
| Why does kidney disease contribute to Hypo Ca? | the kidney loses it's ability to excrete phos and retain Ca |
| The S/Sx of HypO Ca is caused by.. | increased muscle irritability. |
| The s/sx of HypO Ca are? | Numbness, tingling, muscle weakness, twitching tetan seizures. |
| What are two nsg tests you can do for HypO Ca? | Chvostek's sign and Trousseau's. |
| What are nsg interventions for HypO Ca? | cardia montior, seizure precaution, replacement. |
| What are the IV Ca replacements | Emerg- Ca Chloride, non emerg- Ca gluconate |
| What type of line is used for Ca chloride? | Central line |
| What is the rate that Ca Chloride is given? | 1gm/hr. |
| S/Sx of Hyper Ca? | depressed deep tendon reflex, lethary coma, decrease GI motility, dysrythmias, fractures. |
| Interventions for Hyper Ca? | cardia monitor, watch lOV, increase volume, diuretics, drugs calcitono and mithrimycin |
| Causes of Hyper Ca? | bone loss, immobilization, intake, antacids, increase PTH and Vit D. |
| Everywoman will be slightly ______Calcemia? | HypOcalcemic. |
| Phosphorus has an inverse relationship with? | Calcium |
| Phosphorus is absorbed where? | Jejunem of the intestine |
| S/sx of HypO phos? | Muscle weakness, low energy, confusion, memory loss, slurred speech, HTN and decreased C.O. |
| What are the cardiac effects of HypO Phos? | decreased contractility so they are HTN and decreased cardiac output, anemia, resp failure. |
| What are the resp effects of HypO Phos? | weak muscles lead to resp failure |
| Phos effects the structure and functino of what? | RBCs and Leukocytes, creating anemia |
| What does CHEMO stand for ( in hyperphophatemis?) | Cardiac irregularites, Hyperreflexia, Eat poor, Muscle weakness, Oliguria |
| PaO2 tells you about.. | Oxygenation |
| SaO2 tells you about | Hemoglobin. Giving O2 doesn't help if you don't have the hemoglobin to carry it. |
| PaCO2 tells you about | if they are breathing effectively. |
| HCO3 reflects the _______component of ABGs | Renal |
| Causes of Hyperphosphatemia? | Impaired renal function, acid base imbalance, thyroid or parathyroid surgery. |
| Tx of Hyper-Phospate | Drug therapy, Iv therapy, diuretics and Hemodialysis |
| What type of drug therapy is used for Hyper Phos? | Aluminum, Mag and Ca all will bind Phos |
| Fo Iv and Diuretic therapy for hyper phos what do you need? | Functioning kidneys so you can promote renal excretion. |
| What are the three chemical buffer systems? | Carbonic acid/bi-carb, Phosphate buffer and protein buffer. |
| How do you assess Resp Acidosis? | 1. headache then2. confusion, then hyperkalemia |
| If CO2 is high what signs will the pt exhibit? | Obtunded, sleepy, difficulty arousing. |
| What does compensation tell you? | That the problem has been around long enough for the body to want to compensate. |
| esp Alkalosis is always due to?? | Hyperventilation, blowing off too much CO2 |
| Who is at risk for Resp Alkalosis? | those with anxiety, fear, asthma, head injury, pulmonary edema due to hypervent trying to get O2 |
