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Test 2 Review
| Question | Answer |
|---|---|
| bicarbonate (HCO3) | 22-26 mEq/L |
| chloride (Cl) | 96-106 mEq/L |
| phosphate (PO4) | 2.4-4.4 mg/dL |
| Anions | bicarbonate, chloride, phosphate |
| Cations | potassium, magnesium, sodium, calcium (total), calcium (ionized) |
| potassium (K) | 3.5-5.0 mEq/L |
| magnesium (Mg) | 1.5-2.5 mEq/L |
| sodium (Na) | 135-145 |
| calcium (Ca) total | 8.6-10.2 mg/dL |
| calcium (Ca) ionized | 4.6-5.3 mg/dL |
| CM of ECF volume deficit | restless, drowsy, lethargy, confused, thirsty, dec. skin turgor, dec. cap refill, postural hypotension, inc. BP, dec. CVP, dec. UO, inc. RR, weak, weight loss, seizures, coma |
| CM of ECF Volume Excess | headache, confusion, lethargy, per. edema, JVD, bounding pulse, inc BP, inc CVP, polyuria, dyspnea, crackles, pulmonary edema, muscle spasms, weight gain, seizures, coma |
| causes of excess sodium intake | IV fluids: hypertonic NaCl, excessive isotonic NaCl, IV sodium bicarb, hypertonic tube feedings w/o water supplements, near-drowning, in salt water |
| causes of hypernatremia (>145) | excessive sodium intake, inadequate water intake, excessive water loss (inc. Na concentration), disease states |
| causes of excessive water loss (inc. Na concentration) | inc insensible water loss (high fever, heatstroke, prolonged hyperventilation), osmotic diuretic therapy, diarrhea |
| CM of hypernatremia w/decreased ECF volume | restless, agitation, twitching, seizures, coma, intense thirst, dry, swollen tongue, stick mucous membranes, postural hypotension, dec. CVP, weight loss, inc. pulse, weakness, lethargy |
| CM of hypernatremia w/normal or increased ECF volume | restless, agitation, twitching, seizures, coma, intense thirst, flushed skin, weight gain, peripheral and pulmonary edema, inc. BP, inc. CVP |
| causes of hyponatremia (<135) | excessive sodium loss, inadequate sodium intake (fasting diets), excessive water gain (dec. Na concentration), disease states |
| What disease states can cause hypernatremia? | diabetes insipidus, primary hyperaldosteronism, Cushing syndrome, uncontrolled DM |
| What disease states can cause hyponatremia? | SIADH, heart failure, primary hypoaldosteronism |
| CM of hyponatremia w/decreased ECF volume | irritable, apprehension, confusion, dizzy, personality changes, tremors, seizures, coma, dry mucous membranes, postural hypotension, dec CVP, dec jug. venous filling, inc pulse, thready pulse, cold & clammy skin |
| CM of hyponatremia w/increased ECF volume | headache, apathy, confusion, muscle spasms, seizures, coma, N/V/D, abdominal cramps, weight gain, inc BP, inc CVP |
| causes of hyperkalemia (>5.0) | excess K intake, shift of K out of cells, failure to eliminate K |
| causes of excess K intake | excessive or rapid parenteral administration, K containing drugs (K penicillin), K containing salt substitute |
| causes of shift of K out of cells | acidosis, tissue catabolism (fever, sepsis, burns), crush injury, tumor lysis syndrome |
| causes of failure to eliminate K | renal disease, K-sparing diuretics (amiloride-Midamor), adrenal insufficiency, ACE inhibitors, NSAIDS |
| CM of hyperkalemia | irritable, anxiety, abdominal cramping, diarrhea, weakness of lower extremities, paresthesias, irregular pulse, cardiac arrest (if hyperkalemia sudden or severe) |
| causes of hypokalemia (<3.5) | K loss, shift of K into cells, lack of K intake |
| causes of K loss | GI losses: diarrhea, vomiting, fistulas, NG suction; renal losses: diuretics, hyperaldosteronism, Mg depletion, skin losses, diaphoresis, dialysis |
| causes of shift of K into cells | increased insulin (IV dextrose load), alkalosis, tissue repair, increased epinephrine (stress) |
| causes of lack of K intake | starvation, diet low in K, failure to include K in parenteral fluids if NPO |
| CM of hypokalemia | fatigue, muscle weakness, leg cramps, N/V, paralytic ileus, soft, flabby muscles, paresthesias, decreased reflexes, weak, irreg pulse, polyuria, hyperglycemia |
| ECG changes in hyperkalemia | tall, peaked T waves; prolonged PRI; ST segment depression; loss of P wave; widening QRS, Vfib; ventricular standstill |
| ECG changes in hypokalemia | ST segment depression; flattened T wave; presence of U wave; prolonged QRS; ventricular dysrhythmias (PVCs); bradycardia |
| causes of increased Total calcium | multiple myeloma, malignancies w/bone metastasis; prolonged immbolization; hyperparathyroidism; Vit D overdose; thiazide diuretics; milk-alkali syndrome |
| cause of increased ionized calcium | acidosis |
| causes of hypercalcemia (>10.2) | increased total calcium; increased ionized calcium |
| CM of hypercalcemia | lethargy, weakness, depressed reflexes, decreased memory, confusion, personality changes, psychosis, anorexia, N/V, bone pain, fractures, polyuria, dehydration, nephrolithiasis, stupor, coma |
| causes of hypocalcemia (<8.6) | decreased total calcium; decreased ionized calcium |
| causes of decreased total Ca | CKD, elevated phosphorus, primary hypoparathyroidism, Vit D deficiency, Mg deficiency, acute pancreatitis, loop diuretics (furosemide-Lasik), chronic alcoholism, diarrhea, dec albumin |
| causes of decreased ionized Ca | alkalosis, excess administration of citrated blood |
| CM of hypocalcemia | easy fatigability; depression, anxiety, confusion, numbness & tingling in extremities & around mouth; hyperreflexia, muscle cramps; Chvostek & Trousseau sign; laryngeal spasm, tetany, seizures |
| ECG changes in hypercalcemia | shortened ST segment; shortened QT interval, ventricular dysrhythmias; increased digitalis effect |
| ECG changes in hypocalcemia | elongation of ST segment, prolonged QT interval, ventricular tachycardia |
| causes of hyperphosphatemia (>4.4) | renal failure; chemo drugs; enemas containing phosphorus (fleet enemas); excess ingestion (milk, phosphate laxatives); hypoparathyroidism; sickle cell anemia |
| CM of hyperphophatemia | hypocalcemia; numbness & tingling in extremities & around mouth; hyperreflexia, muscle cramps; tetany, seizures, deposition of calcium-phosphate precipitates in skin, soft tissue, cornea, viscera, blood vessels |
| causes of hypophosphatemia (<2.4) | malabsorption syndromes; recovery from malnutrition or refeeding; glucose or insulin therapy; TPN; alcohol withdrawal; phosphate binding antacids; recovery from DKA; respiratory alkalosis |
| CM of hypophosphatemia | CNS depression (confusion, coma); muscle weakness, including respiratory muscle weakness & difficult weaning from vent.; polyneuropathy, seizures, cardiac problems (dysrhthmias, dec. SV); osteomalacia; rhabdomyolysis |
| causes of hypermagnesemia (>2.5) | renal failure; adrenal insufficiency; excess administration of Mg, esp for tx of eclampsia; tumor lysis syndrome; DKA |
| CM of hypermagnesemia | lethargy, drowsiness, N/V, diminished DTRs, flushed, warm skin; dec. pulse; dec. BP; muscle weakness; dyshphagia |
| causes of hypomagnesemia | diarrhea; vomiting; chronic alcoholism; malabsorption syndrome; prolonged malnutrition; inc. UO; NG suction; poorly controlled DM; hyperaldosteronism |
| CM of hypomagnesemia | confusion; tremors; seizures; hyperactive DTRs; insomnia; inc. pulse; inc. BP; muscle cramps |
| Classification of burn injury | Partial thickness skin destruction: Superficial (1st degree), deep (2nd degree), Full thickness skin destruction: 3rd and 4th degree burns |
| Appearance of superficial 1st degree burns | erythema, blanching on pressure, pain and mild swelling, no vesicles or blisters (may blister or peel after 24 hrs) |
| Causes of 1st degree burns | superficial sunburn, quick heat flash |
| Appearance of deep 2nd degree sunburn | fluid filled vesicles that are red, shiny, wet (if vesicles have ruptured). severe pain caused by nerve injury. Mild to moderate edema. |
| Appearance of 3rd and 4th degree burns | Dry, waxy, white, leathery, or hard skin, visible thrombosed vessels. Insensitivity to pain bc of nerve destruction. Possible involvement of muscles, tendons, and bones. |
| Causes of 2nd degree burns | flame, flash, scald, contact burns, chemical, tar, electric current |
| Causes of 3rd and 4th degree burns | flame, scald, chemical, tar ,electric current |
| Rule of Nines chart to calculate percentage of burns on the body. | Each leg front and back is 9%, each arm front and back is 4.5%, the chest and back are 18%, the head front and back is 4.5%, and the genital region is 1% |
| Phases of burn management | emergent (resuscitative), acute (wound healing), and rehabilitative (restorative) |
| What is the primary concern during the emergent phase of burns? | The onset of hypovolemic shock and edema formation. |
| When does the emergent phase of burns end? | when fluid mobilization and diuresis begin |
| Care of burns during the emergent phase | Fluid therapy (assess & begin IV fluids, insert cath, monitor UO), wound care (shower, debride, assess), pain & anxiety, PT & OT, nutritional therapy, respiratory therapy (assess, provide O2, monitor) , psychosocial care |
| Care of burns during the acute phase | Continue replacing fluids; continue daily shower & wound care, debridement, assess wound for infections; early excision & grafting, assess pain, PT &OT (ROM, splints), nutritional therapy, cont to assess oxygenation & resp status, monitor for pneumonia; |
| Care of burns during the rehabilitation phase | Continue to counsel & teach pt; continue to encourage & assist pt in resuming self care; continue to prevent or minimize contractures & assess for scarring; discuss possible reconstructive surgery; prepare for discharge home or transfer to rehab hospital. |
| In the emergent phase of burns, a patient with burns to the face and then neck require this within 1 to 2 hours after injury. | intubation |
| What fluid is usually given to burn patients? | Lactated ringers (usually); colloids (albumin - watch for FVE), or combo of the two |
| Parkland (Baxter) Formula | 4 mL LR/kg of body weight per percent of TBSA burned = total fluid requirements for first 24 hours after burn. 1/2 of total in first 8 hrs; 1/4 of total in 2nd 8 hrs; 1/4 of total in 3rd 8 hrs |
| Parkland (Baxter) formula example: For a 70 kg pt with a 50% TBSA burn. | 4x70x50 = 14,000 mL/24 hrs. 1/2 of total in 1st 8 hrs = 7000 mL (875 ml/hr). 1/4 of total in 2nd 8 hours = 3500 ml (437 ml/hr). 1/4 of total in 3rd 8 hours = 3500 ml (437ml/hr) |
| When caring for or exposing a patient's burn wounds what kind of equipment should the nurse wear? | disposable hats, masks, gowns, and gloves; use sterile gloves if applying ointment or sterile dressings; use nonsterile gloves when removing the contaminated dressings & washing the dirty wound. |
| glomerulus | selective filtration |
| proximal tubule | reabsorption of 80% of electrolytes and water, glucose, amino acids, HCO3. Secretion of H and creatinine. |
| Loop of Henle | Reabsorption of Na and Cl in ascending limb and water in descending loop. Concentration of filtrate. |
| Distal tubule | Secretion of K, H, ammonia. Reabsorption of water (regulated by ADH) and HCO3. Regulation of Ca and PO4 by parathyroid hormone. |
| Collecting duct | Reabsorption of water (ADH required). |
| creatinine clearance | 70-135 mL/min |
| BUN | 6-20 mg/dL |
| creatinine | 0.6-1.3 mg/dL |
| BUN/creatinine ratio | 12:1 - 20:1 |
| uric acid | F: 2.3-6.6 mg/dL; M: 4.4-7.6 mg/dL |
| potassium | 3.5-5.0 mEq/L |
| calcium (total) | 8.6-10.2 mg/dL |
| phosphorus | 2.4-4.4 mg/dL |
| bicarbonate | 22-26 mEq/L |
| What is an intravenous pyelogram (IVP? | Visualizes urinary tract after IV injection of contrast media. Presence, position, size, & shape of kidneys, ureters, & bladder can be evaluated. Pt w/significantly decreased renal function should not have IVP b/c of contrast media can be nephrotoxic. |
| How should you prepare a patient for an IVP? | Evening before, give cathartic or enema to empty colon. Before procedure assess pt for iodine sensitivity. Inform pt that they will be lying on table & have serial x-rays taken. May feel warmth, a flushed face, & salty taste when injecting contrast. |
| What is a renal arteriogram (angiogram) used for? | Visualizes renal blood vessels. Assist in diagnosing renal artery stenosis, addl or missing renal blood vessels, & renovascular HTN. Differentiate renal cyst & tumor. Done for potential renal transplant donor. |
| Describe how an angiogram is done. | A catheter is inserted into the femoral artery and passed up the aorta to the level of the renal arteries. Contrast media is injected to outline the renal blood supply. |
| What should you do for the patient before an angiogram? | Prepare pt the prior evening by giving cathartic or enema. Before injection of contrast, assess for iodine sensitivity. Pt may experience a transient warm feeling along blood vessel when injection contrast media. |
| What should you do for the patient after an angiogram? | A pressure dressing over fem artery inject site. Observe for bleeding. Maintain bed rest w/affected leg straight. Take per. pulses in involved leg q30-60 mins for occlusion caused by thrombus. Observe for thrombus, embolus, local inflammation, hematoma. |
| With any type of diagnostic test involving contrast media (-gram), what should before the procedure, especially in patients with renal failure? | Always check for iodine sensitivity to avoid anaphylaxis. Should not be done with renal patients as the contrast media is nephrotoxic and can worsen renal failure. |
| urine specific gravity | 1.003-1.030 |
| What does a low urine specific gravity (<1.003) indicate? | Dilute urine, excessive diuresis, diabetes insipidus |
| What does a high urine specific gravity (>1.030) indicate? | dehydration, albuminuria, glycosuria |
| What does a fixed (at about 1.010) urine specific gravity indicate? | Renal inability to concentrate urine, end-stage kidney disease. |
| osmolality | 300-1300 mOsm/kg |
| What does a low osmolality (<300) or high osmolality (>1300) indicate? | Tubular dysfunction, kidney lost ability to concentrate or dilute urine |
| pH (urine) | 4.0-8.0 (avg = 6.0) |
| What does a high urine pH (>8.0) indicate? | UTI, urine allowed to stand at room temp (bacteria decompose urea to ammonia). |
| What does a low urine pH (<4.0) indicate? | Respiratory or metabolic acidosis |
| An inflammation of the renal parenchyma and collecting system (including renal pelvis). Usually begins w/colonization & infection of the lower urinary tract via the ascending urethral route. | pyelonephritis |
| What causes pyelonephritis? | Most common cause is bacterial infection, but fungi, protozoa, or viruses can also infect the kidney. |
| What bacteria normally found in the intestinal tract frequently cause pyelonephritis? | E.Coli, Proteus, Klebsiella, or Enterobacter species |
| What are the CM of pyelonephritis? | mild fatigue, chills, fever, vomiting, malaise, flank pain, characteristics of cystitis - dysuria, urgency, & frequency; CVA pain on affected side. |
| What diagnostics are done for acute pyelonephritis? | Hx & physical; urinalysis; urine culture & sensitivity; imaging studies - US, CT, IVP, CT/IVP, VCUG, radionuclide imaging; CBC ct w/WBC diff; blood culture; percussion for flank (CVA) pain |
| How do you treat acute pyelonephritis with mild symptoms (uncomplicated infection)? | Outpatient mgmt. antibiotics - ampicillin, vanc. combine w/aminoglycoside (tobramycin, gentamicin), cipro; adequate fluid intake; NSAIDS or antipyretics; f/u urine culture & imaging studies. |
| How do you treat acute pyelonephritis with severe symptoms? | Hospitalization; parenteral antibiotics - ampicillin, vanc; oral antibiotics when pt tolerates; adequate fluid intake (parenteral then switch to oral when N/V/D subsides); NSAIDs, urinary analgesics, f/u urine culture & imaging studies |
| The kidneys become small, atrophic, and shrunken and lose function due to fibrosis (scarring). Is usually the result of recurring infections involving the upper urinary tract, but can occur in absence of infection, recent infection, or hx of UTIs. | chronic pyelonephritis |
| What tests are used to diagnose chronic pyelonephritis? | radiologic imaging reveal small, fibrotic kidney; the collecting system may be small or hydronephrotic & a biopsy result's indicate loss of functioning nephrons, infiltration of the parenchyma w/inflammatory cells, and fibrosis |
| What is glomerulonephritis? | Inflammation of the glomeruli, which affects both kidneys equally & is the third leading cause of ESKD. Can be acute or chronic. |
| What are some causes or risk factors for glomerulonephritis? | poststrep glomerulonephritis; inf. endocarditis; viral infections; SLE; scleroderma; Goodpasture syndrome; IgA nephropathy; polyarteritis; Wegeners granulomatosis; diabetic nephropathy; HTN; focal segmental glomerulosclerosis; amyloidosis; illegal druguse |
| This is a common type of acute glomerulonephritis, most common in children & young adults, develops 5-21 days after an infection of the tonsils, pharynx, or skin. | acute poststreptococcal glomerulonephritis (APSGN) |
| What are the CM of APSGN? | general body edema, HTN, oliguria, hematuria w/a smoky or rusty appearance (due to bleeding in upper urinary tract), & proteinuria; fluid retention due to dec. glomerular filtration, periorbital edema progresses to total body edema; HTN; flank pain |
| How is APSGN diagnosed? | Dipstick urinalysis & urine sediment microscopy reveal erythrocytes in significant numbers. Erythroctye casts are highly suggestive of APSGN. Mild to severe proteinuria. Blood tests include BUN & serum creatinine to assess renal impairment. |
| How is APSGN treated? | Symptomatic relief. Rest for inflammation & HTN. Restrict Na & fluid intake, & diuretics for edema. Antihypertensives for HTN. Restrict protein if increase of wastes (inc. BUN). Antibiotics only if strep infection is present. |
| A syndrome that reflects the end stage of glomerular inflammatory disease. | chronic glomerulonephritis |
| What are the CM of chronic glomerulonephritis? | Varying degrees of hematuria & urinary excretion of various formed elements, including RBCs, WBCs, & casts. Proteinuria & elevated BUN & creatinine levels. Fatigue may be present. |
| How is chronic glomerulonephritis diagnosed? | Pt history & exam, ultrasound, CT scan, or a renal biopsy may be performed to determine the exact cause. |
| This results when the glomerulus is excessively permeable to plasma protein, causing proteinuria that leads to low plasma albumin and tissue edema. | nephrotic syndrome |
| What are the CM of nephrotic syndrome? | Per. edema, massive proteinuria, HTN, hyperlipidemia, & hypoalbuminemia, ascites and anasarca develop if there is hypoalbuminemia |
| What are the characteristic lab findings for nephrotic syndrome? | Dec. serum albumin, dec. total serum protein, & elevated serum cholesterol |
| What is responsible for the massive excretion of protein in the urine? | the increased glomerular membrane permeability |
| What are some causes of nephrotic syndrome? | primary glomerular diseases; multisystem disease (SLE, DM, amyloidosis), infections -bacterial strep, viral (hepatitis, HIV); neoplasms -Hodgkins lymphoma, tumors, leukemia; allergens - bee stings, pollen; drugs - NSAIDs, heroin, captopril, penicillamine |
| What are the goals for treatment of nephrotic syndrome? | To cure or control the primary disease and relieve the symptoms. |
| How is nephrotic syndrome treated? | Corticosteroids & cyclophophamide, prednisone, mgmt of diabetes & tx of edema - ACEIs, NSAIDs, & low Na (2-3g/day), mod. protein (1-2g/kg/day) diet, salt restrict (thiazide or loop diuretics); statins for high cholesterol; anticoags if thrombosis detected |
| What are some important interventions when treating nephrotic syndrome? | Assess edema, weigh pt daily, monitor I&Os, measure abdominal girth or extremity size, clean edematous skin carefully, monitor effectiveness of diuretics; avoid exposure to people w/infections; encourage dietary intake. |
| Characterized by a rapid loss of kidney function. Accompanied by a rise in serum creatinine &/or a reduction in UO. Severity can range from a small increase in serum creatinine or reduction in UO to the development of azotemia. Potentially reversible. | acute kidney injury (AKI) |
| An accumulation of nitrogenous waste products (urea nitrogen, creatinine (in the blood). | azotemia |
| Most commonly, AKI follows severe prolonged _____ or ______ or exposure to a neprhotoxic agent. | hypotension; hypovolemia |
| Comparison of onset of AKI & CKD | AKI - sudden; CKD - gradual, often over many years |
| Comparison of most common cause of AKI & CKD | AKI - acute tubular necrosis; CKD - diabetic nephropathy |
| Comparison of diagnostic criteria of AKI & CKD | AKI - Acute reduction in UO &/or elevation in serum creatinine; CKD - GFR <60 mL/min for > 3 months &/or kidney damage >3 months |
| Comparison of reversibility of AKI & CKD | AKI - potentially; CKD - progressive and irreversible |
| Comparison of primary cause of death of AKI & CKD | AKI - infection; CKD - cardiovascular disease |
| The causes of AKI can be grouped into these 3 categories. | prerenal, intrarenal, and postrenal |
| Prerenal causes of AKI | hypovolemia, decreased cardiac output, decreased peripheral vascular resistance, decreased renovascular blood flow |
| What are some prerenal causes of hypovolemia of AKI? | dehydration, hemorrhage, GI losses (D/V), excessive diuresis, hypoalbuminemia, burns |
| What are some prerenal causes of decreased CO of AKI? | cardiac dysrhythmias, cardiogenic shock, heart failure, MI |
| What are some prerenal causes of decreased peripheral vascular resistance in AKI? | anaphylaxis, neurologic injury, septic shock |
| What are some causes of decreased renovascular blood flow in AKI? | bilateral renal vein thrombosis, embolism, hepatorenal syndrome, renal artery thrombosis |
| Intrarenal causes of AKI | nephrotoxic injury, interstitial nephritis, other causes |
| What are some intrarenal causes of nephrotoxic injury that can cause AKI? | Drugs: aminoglycosides (gentamicin, amikacin), amphotericin B; contrast media, hemolytic blood transfusion rx; severe crush injury; chemical exposure: ethylene glycol, lead, arsenic, carbon tetrachloride |
| What are some intrarenal causes of interstitial nephritis that can cause AKI? | Allergies: antibiotics (sulfonamides, rifampin), NSAIDs, ACEI; Infections: bacterial (acute pyelonephritis), viral (CMV), fungal (candidiasis) |
| What are some Other intrarenal causes of AKI? | prolonged prerenal ischemia, acute glomerulonephritis, thrombotic disorders, toxemia of pregnancy, malignant HTN, SLE |
| What are some postrenal causes of AKI? | benign prostatic hyperplasia; bladder cancer; calculi formation; neuromuscular disorders; prostate cancer; spinal cord disease; strictures; trauma (back, pelvis, perineum) |
| This is the most common intrarenal cause of AKI and is primarily the result of ischemia, nephrotoxins, or sepsis. | acute tubular necrosis (ATN) |
| RIFLE Classification for staging AKI | R - Risk: serum creatinine increased >1.5 OR GFR decreased by 25%; UO <0.5 mL/kg/hr for 6 hrs |
| RIFLE Classification for staging AKI | I - Injury: serum creatinine increased x2 OR GFR decreased by 50%; UO <0.5 mL/kg/hr for 12 hrs |
| RIFLE Classification for staging AKI | F - Failure: serum creatinine increased x3 OR GFR decreased by 75% OR serum creatinine >4 mg/dL w/acute rise >= 0.5 mg/dL; UO <0.3 mL/kg/hr for 24 hrs (oliguria) OR anuria for 12 hrs |
| RIFLE Classification for staging AKI | L - Loss: persistent acute kidney failure, complete loss of kidney function >4 wks |
| RIFLE Classification for staging AKI | E- End stage kidney disease: complete loss of kidney function >3 months |
| What are the phases of AKI? | oliguric, diuretic, and recovery phase |
| A reduction in UO to less than 400 mL/day. | oliguria |
| This phase usually occurs within 1-7 days after injury to the kidneys but can occur as early as 24 hrs. Lasts on average about 10-14 days but can last months in some cases. The longer this phase lasts the less likely to recover. | oliguric phase |
| What are the urinary CM of AKI? | Urinary changes: oliguria commonly seen w/prerenal etiologies, anuria usually seen w/urinary tract obstruction, & nonolguria is seen w/acute interstitial nephritis & ATN. UA may show casts, RBCs, & WBCs. Urine specific gravity fixed at 1.010 |
| What CM are associated with fluid volume in AKI? | Hypovolemia has potential to worsen AKI. Reversed w/fluid replacement. When UO decreases, fluid retention occurs. Neck veins may become distended w/bounding pulse. Edema & HTN develop. FVE lead to HF, pulm edema, & pericardial & pleural effusions. |
| Metabolic acidosis usually occurs in kidney failure b/c kidneys can't synthesize ammonia or excrete acid products of metabolism. With severe acidosis the patient may develop what and why? | Kussmaul respirations (rapid, deep respirations) in an effort to compensate by increasing the exhalation of carbon dioxide. |
| What occurs to the sodium balance in AKI? | Damaged tubules can't conserve Na so urinary excretion of Na may increase resulting in normal or below normal levels of Na. Excessive intake of Na should be avoided b/c it can lead to volume expansion, HTN, & HF. |
| Uncontrolled hyponatremia or water excess can lead to what? | cerebral edema |
| What happens to the potassium levels in AKI? | Kidneys normally excrete the body's K but in AKI the K levels increase b/c kidneys are impaired. |
| Hyperkalemia is more of a risk if AKI is caused by what and why? | Caused by a massive tissue trauma b/c the damaged cells release add'l K into the extracellular fluid. Add'l bleeding & blood transfusions may cause cellular destruction, releasing more K into ECF. |
| Why does acidosis worsen hyperkalemia? | B/c hydrogen ions enter the cells and K is driven out of the cells into the ECF. |
| What would hyperkalemia look like on an ECG? | Peaked T waves, widening of the QRS complex, and ST segment depression. |
| Why is treatment essential whenever hyperkalemia develops? | B/c cardiac muscle is intolerant of acute increases in K (dysrhythmias) |
| What is the most common cause of death in AKI? | infection |
| What are the most common sites of infection in AKI? | the urinary and respiratory systems |
| What is urea? | an end product of protein metabolism |
| What is creatinine? | an end product of endogenous muscle metabolism |
| BUN and serum creatinine levels are what in kidney failure? | elevated |
| An elevated BUN must be interpreted w/caution b/c it can also be caused by what? | dehydration, corticosteroids, or catabolism resulting from infections, fever, severe injury, or GI bleeding |
| What is the best indicator of AKI and why? | Creatinine b/c it is not significantly altered by other factors. |
| What are the CM of neurologic changes that can occur in AKI? | Can be as mild as fatigue & difficulty concentrating, & escalate to seizures, stupor, and coma. Asterixis is common w/liver failure but can occur w/advanced or severe kidney dysfunction. |
| Flapping tremor when the wrist is extended. Resembles a bird flapping its wings when the hands and wrists are extended outward. | asterixis |
| What does the daily UO look like in the diuretic phase of AKI? | Usually 1-3 L, but may reach 5 L or more. |
| What causes the high urine volume during the diuretic phase of AKI? | Though UO is increasing, the nephrons are still not fully functional. The high urine volume is caused by osmotic diuresis from high urea concentration in glom. filtrate & inability of tubules to concentrate urine. |
| In this phase the kidneys have recovered their ability to excrete wastes, but not concentrate the urine. | diuretic phase |
| What can occur in the diuretic phase from massive fluid losses? | hypovolemia & hypotension |
| In the diuretic phase, b/c of the large losses of fluid & electrolytes, the pt must be monitored for what? | hyponatremia, hypokalemia, and dehydration |
| How long can the diuretic phase last? | 1-3 wks |
| What occurs during the end of the diuretic phase? | The pts acid-base, electrolytes, and waste product (BUN, creatinine) values begin to normalize. |
| When does the recovery phase of AKI begin? | When the GFR increases, allowing the BUN and serum creatinine levels to plateau and then decrease. |
| How long does the recovery phase of AKI last? | Major improvements occur in the first 1-2 wks of this phase, but kidney function may take up to 12 months to stabilize. |
| What influences the outcome of AKI? | The pt's overall health, the severity of kidney failure, & the number & type of complications. Some pts don't recover & progress to ESKD. |
| The nurse should consider prerenal causes when there is a history of what? | dehydration, blood loss, or severe heart disease |
| The nurse should suspect intrarenal causes if the patient has a history of what? | Exposure to potentially nephrotoxic drugs or a recent history or a blood transfusion, or a study using contrast media. |
| The nurse should suspect postrenal causes if the patient has a history of what? | Hx of changes in the urinary stream, stones, BPH, or cancer of the bladder or prostate. |
| What are some diagnostic tests that can be done with AKI? | Hx & physical exam; identify precipitating cause; creatinine & BUN levels; electrolyte levels; UA; renal US; renal scan; CT scan |
| Treatment for AKI | Tx of prec. cause; fluid restrict. (600 mL+prev. 24 hr fluid loss); nut'l therapy - adequate protein (0.6-25g/kg/day), K restrict, phos. restrict, Na restrict; lower K if elevated; Ca supple. or phos.-binding agents; par/enteral nut.; dialysis/CRRT PRN |
| Treatment for elevated K levels | Regular insulin w/glucose to prevent hypoglycemia; sodium bicarb (corrects acidosis); calcium gluconate IV (protects heart); hemodialysis; kayexelate, dietary restriction (40 mEq/day) |
| Diuretic therapy is often administered in AKI but not recommended in high doses. What diuretics are usually used? | loop diuretics (furosemide-Lasiks), bumetanide (Bumex), or an osmotic diuretic (mannitol) |
| What is the general rule for calculating the fluid restriction in AKI? | Add all losses for the previous 24 hrs (e.g. urine, diarrhea, emesis, blood) plus 600 mL for insensible losses (e.g. respiration, diaphoresis) |
| Example: if a patient excreted 300 mL of urine on Tuesday w/no other losses, what would the fluid allocation be on Wednesday? | 300 (previous loss in 24 hrs) + 600 (insensible loss) = 900 mL |
| What are the two treatments for hyperkalemia that actually remove K from the body? | kayexelate and dialysis |
| What is the primary nutritional goal in AKI? | Maintain adequate caloric intake (30-35 kcal/kg & 0.8-1.0 g of protein/kg/body weight) to prevent further breakdown of body protein for energy purposes. |
| In AKI, adequate enegy should be primarily from what and why? | From carbohydrates and fat sources to prevent ketosis from endogenous fat breakdown and gluconeogenesis from muscle protein breakdown. |
| What should never be given to a hyperkalemic patient that has an ileus? | kayexelate |
| Acute interventions for AKI | Manage f&e balance, observe & record I&O; watch for infections (swelling, redness, pain, fever, malaise, leuokocytosis), careful dosage for antibiotics; perform skin (for edema) & oral care (prevents stomatitis) |
| Involves progressive irreversible loss of kidney function. The presence of kidney damage or a decreased GFR less than 60mL/min for longer than 3 months. | chronic kidney disease (CKD) |
| This occurs when the GFR is less than 15 mL/min. | end stage kidney disease (ESKD) - the last stage of kidney failure |
| In ESKD, this is required to maintain life. | RRT(dialysis or transplantation) |
| What are the two leading causes of CKD? | diabetes (50%) and HTN (25%); less common - glomerulonephritis, cystic diseases, & urologic diseases |
| Stage 1 of CKD | Kidney damage w/normal or elevated GFR >=90; Diagnosis & treatment, CVD risk reduction, slow progression |
| Stage 2 of CKD | Kidney damage w/mild decreased GFR b/t 60-89; estimation of progression |
| Stage 3 of CKD | Moderate decreased GFR b/t 30-59; Evaluation and treatment of complications |
| Stage 4 of CKD | Severe decrease GFR b/t 15-29; Preparation to RRT (dialysis, kidney transplant) |
| Stage 5 of CKD | Kidney failure; GFR <15; RRT (if uremia present & pt desires tx) |
| What are the psychologic CM of CKD? | anxiety, depression |
| What are the cardiovascular CM of CKD? | HTN, HF, CAD, pericarditis, PAD |
| What are the gastrointestinal CM of CKD? | anorexia, N/V, GI bleeding, gastritis |
| What are the endocrine/reproductive CM of CKD? | hyperparathyroidism, thyroid, abnormalities, amenorrhea, erectile dysfunction |
| What are the metabolic CM of CKD? | carbodydrate intolerance, hyperlipidemia |
| What are the hematologic CM of CKD? | anemia, bleeding, infection |
| What are the neurologic CM of CKD? | fatigue, headache, sleep disturbances, encephalopathy |
| What are the ocular CM of CKD? | hypertensive retinopathy |
| What are the pulmonary CM of CKD? | pulmonary edema, uremic pleuritis, pneumonia |
| What are the integumentary CM of CKD? | pruritus, ecchymosis, dry, scaly skin |
| What are the musculoskeletal CM of CKD? | vascular and soft tissue calcification, osteomalacia, osteitis fibrosa |
| What are the peripheral neuropathy CM of CKD | paresthesias, restless leg syndrome |
| In CKD, as GFR decreases what happens to the BUN and serum creatinine levels? | increase |
| What happens to potassium levels in CKD? | increase |
| What happens to sodium levels in CKD? | may be elevated, normal, or low |
| If large quantities of water are retained what can occur with sodium levels? | dilutional hyponatremia |
| In CKD sodium levels are usually restricted to how much? | 2g/day |
| What electrolyte should CKD patients not ingest? | magnesium products (milk of magnesia, magnesium citrate, antacids containing magnesium) |
| What are the CM of hypermagnesemia? | absence of reflexes, decreased mental status, cardiac dysrhythmias, hypotension, & respiratory failure |
| What causes anemia in CKD? | Due to decreased production of erythropoietin by the kidneys. |
| What is the function of erythropoietin? | Stimulates precursor cells in the bone marrow to produce RBCc (erythropoiesis). |
| Besides decreased erythropoietin, what other factors cause anemia in CKD? | nutritional deficiencies, decreased RBC life span, increased hemolysis of RBCs, frequent blood samplings, and bleeding from the GI tract |
| What type of breathing may occur in CKD due to metabolic acidosis? | Kussmaul breathing to try and remove carbon dioxide |
| What is the function of Vitamin D and what occurs to Vitamin D in CKD? | It is necessary to optimize absorption of calcium from the GI tract, thus low levels of active Vitamin D result in decreased serum calcium levels. |
| What can be seen on the skin with extremely elevated BUN levels? What is this? | Uremic frost is a rare condition in which urea crystallizes on the skin. |
| What is usually the first indication of kidney damage? | persistent proteinuria |
| What diagnostics are done for CKD? | Hx & physical; id of reversible kidney disease, renal US, renal scan, CT scan, renal biopsy, BUN, creatinine, & creat. clearance levels, electrolytes, lipid profile, protein-to-creatinine ratio in 1st morning void, UA, H&H levels |
| Although serum creatinine is a good indicator of kidney function, what is the preferred measure to determine kidney function? | GFR |
| What are some risk factors for CKD? | diabetes, HTN, age>60 yr, CVD, family hx of CKD, exposure to nephrotoxic drugs, ethnic minority (e.g. Afr.-Amer, Native-Amer) |
| What could occur if you gave a patient kayexelate and they also have an ileus? | Fluid shift could lead to bowel necrosis. |
| What antihypertnesive drugs are used in CKD? | diuretics, CCBs, ACEI, ARBs |
| T/F: Phosphate binder should be given before bed. | False. Phosphate binders should be given with food. |
| Examples of phosphate binders. | Calcium based binders: calcium acetate (Phoslo), calcium carbonate (Caltrate); Noncalcium based binders: lanthanum carbonate (Fosrenol), sevelamer carbonate (Renvela) |
| What is a frequent side effect of phosphate binders and how can this be fixed? | constipation, fix w/stool softeners |
| How can anemia be treated in CKD? | with exogenous erythropoietin (EPO) such as epoetin alfa (Epogen, Procrit), or darbepoietin alfa (Aranesp) |
| For CKD patients, what is the recommended protein intake? | at least 1.2 g/kg of ideal body weight (IBW) per day |
| In CKD, how much sodium is a patient usually allowed? | 2-4 g/day |
| What are some high sodium foods that patients with CKD should be taught to avoid? | cured meats, pickled foods, canned soups and stews, frankfurters, cold cuts, soy sauce, and salad dressings |
| How much potassium are CKD patients allowed? | 2-3 g |
| As kidney function diminishes phosphate elimination deteriorates which can lead to hyperphophatemia. By ESKD, phosphate should be limited to? | 1 g/day |
| What foods are high in phosphate? | meat, dairy products (e.g. milk, ice cream, cheese, yogurt), and foods containing dairy products (e.g. pudding) |
| What are some high potassium fruits that CKD patients should avoid? | raw apricot, avocado, banana, cantaloupe, dried fruit, grapefruit juice, honeydew, orange, orange juice, prunes, raisins |
| What are some vegetables that are high in potassium and should be avoided in CKD? | baked beans, butternut squash, refried beans, black beans, broccoli - cooked, raw carrots, greens except kale, canned mushrooms, white & sweet potatos, cooked spinach, tomatoes & tomato products, veg. juices |
| What are some other foods that are high in potassium and should be avoided in CKD? | bran or bran products, chocolate, granola, milk (all types), nutritional supplements, nuts and seeds, peanut butter, salt substitutes, salt-free broth, yogurt |
| What are the advantages of peritoneal dialysis (PD)? | immediate initiation in any hospital; less complicated than HD; portable system; fewer dietary restrictions; short training time; usable in pt w/vasc. access problems; less cardiovascular stress; home dialysis possible; prefer for diabetic pts |
| What are the disadvantages of PD? | bacterial or chemical peritonitis; protein loss in dialysate; exit site & tunnel infections; hyperglycemia; surgery for cath placement; contraindicated in pt w/multiple abdomen surgery, traume, unrepaire hernia; catheter can migrate; requires edu. program |
| What are the advantages of hemodialysis (HD)? | rapid fluid removal; rapid removal of urea & creat.; effective K removal; less protein loss; lowering of serum triglycerides; home dialysis possible; temporary access can be placed at bedside |
| What are the disadvantages of HD? | Vasc. access problems; dietary & fluid restrictions; heparinization may be necessary; extensive equipment nec.; hypotension during dialysis; added blood loss contributes to anemia; surgery perm. access place.; special train personnel; self-image problems |
| Why is automated peritoneal dialysis (APD) a popular form of PD? | It can be done while they sleep. |
| T/F: Continuous ambulatory peritoneal dialysis (CAPD) is done during the day when the patient is awake. | true |
| What are some complications w/PD? | Exit site infections; peritonitis; hernia; lower back problems; bleeding; pulmonary complications; protein loss; |
| CM of exit site infections with PD | redness at the site, tenderness, & drainage |
| This results from contamination or from progression of an exit site or tunnel infection. | peritonitis |
| What is the most frequent cause of peritonitis? | Improper technique in making or breaking connections for exchanges. |
| What is a less common way that periotonitis can occur? | Bacteria in the intestine crossing over into the peritoneal cavity. |
| Peritonitis is usually caused by what? | S. aureus or S. epidermidis |
| What are the primary CM of peritonitis? | abdominal pain, cloudy peritoneal effluent w/a WBC count >100 (more than 50% neutrophils), or demonstration of bacteria in the peritoneal effluent by gram stain or culture |
| What are the GI manifestations of peritonitis? | diarrhea, vomiting, abdominal distention, hyperactive bowel sounds, fever (may or may not be present) |
| What diagnostics are done to confirm peritonitis? | cultures, gram stain, and WBC differential |
| Repeated infections in PD may require what? | Removal of the peritoneal catheter and termination of PD. Change to HD. |
| In PD, after catheter placement, is it normal for the first few exchanges to be pink or slightly bloody? | Yes it can be secondary to trauma associated with catheter placement. |
| In PD, bloody effluent over several days or the new appearance of blood in the effluent can indicate what? | intraperitoneal bleeding |
| If intraperitoneal bleeding occurs what should be checked? | BP and hematocrit |
| What pulmonary complications can occur with PD? | atelectasis, pneumonia, and bronchitis may occur from repeated upward displacement of the diaphragm, resulting in decreased lung expansion |
| What can be done to help or prevent these pulmonary problems? | frequent repositioning, and deep breathing exercises can help; elevate the head of the bed to prevent these problems |
| What is the most difficult problem associated with HD? | obtaining vascular access |
| To perform HD, a very rapid blood flow is required, and access to a large blood vessel is essential. What are the types of vascular access? | arteriovenous fistualas (AVFs), arteriovenous grafts (AVGs), and temporary vascular access |
| This is usually created in the forearm or upper arm with an anastomosis b/t an artery and a vein (usually cephalic or basilic). | subcutaneous arteriovenous fistula |
| What should always be checked for with AVFs? | A thrill can be felt by palpating the area of anastomosis, and a bruit (rushing sound) can be heart with a stethoscope. |
| What causes a bruit and a thrill? | Created by arterial blood moving at a high velocity through the vein. |
| AVFs are more difficult to create with what kind of patients? | Patients w/a history of severe PVD, those w/prolonged IV drug use, and obese women |
| These are made of synthetic materials and form a "bridge" b/t the arterial and venous blood supplies. They are placed under the skin and are surgically anastomosed b/t an artery (usually brachial) & a vein (usually antecubital). | arteriovenous graft (AVGs) |
| Because AVGs are made of artificial materials, they are more likely to do what compared to AVFs? | To become infected, and they also have a tendency to be thrombogenic. |
| What should never be done in the extremity with the vascular access and why? | Never peform BP measurements, insert IV lines, and venipunctures in the extremity w/the vascular access. These precautions are to prevent infection and clotting of the vascular access. |
| Catheterization of the internal jugular or femoral vein is performed when vascular access needs to be done immediately. | temporary vascular access |
| Patients with a temporary vascular catheter are recommended not to be discharged from the hospital. Why? | These catheters have high rates of infection, dislodgement, and malfunction. |
| This type of catheter provides temporary access while the patient is waiting for fistula placement or as long term access when other forms of access have failed. | long-term cuffed HD catheters |
| Before beginning HD treatment what should always be done first? | Complete an assessment that includes fluid status (weight, BP, peripheral edema, lung, and heart sounds), condition of vascular access, temperature, and general skin condition. |
| What determines the ultrafiltration or the amount of weight (from fluid) to be removed in HD? | The difference b/t the last postdialysis weight and the present predialysis weight. |
| While the patient is on dialysis, what should the nurse do? | Take vital signs at least every 30-60 minutes b/c rapid BP changes may occur. |
| What are some complications of HD? | hypotension, muscle cramps, loss of blood, hepatitis |
| Hypotension that occurs during HD results from what? | Rapid removal of vascular volume (hypovolemia), decreased CO, and decreased SVR. |
| What are the CM of hypotension during dialysis? | lightheadedness, N/V, seizures, vision changes, and ches pain from cardiac ischemia. |
| What is the usual treatment for hypotension during dialysis? | decrease the volume of fluid being removed and infusion of 0.9% NS |
| Muscle cramps are usually seen in the first month after inititation of dialysis, how is it treated? | Reduce the ultrafiltration rate and administer fluids (saline, glucose, mannitol). Hypertonic saline is NOT recommended but hypertonic glucose IS preferred. |
| Continuous venovenous hemofiltration (CVVH) | Removes both fluid and solutes. Replacement fluid required. |
| Slow continuous ultrafiltration (SCUF) | Removes fluid. N fluid replacement required. |
| Continuous venvenous hemodialysis (CVVHD) | Removes both fluids and solutes. Requires both dialysate and replacement fluid. |
| Continuous venovenous hemodiafiltration (CVVHDF) | Removes both fluids and solutes. Requires both dialysate and replacement fluid. |
| This is an alternative or adjunctive method for treating AKI. It provides a means by which uremic toxins and fluids are removed, while acid-base status & electrolytes are adjusted slowly & continuously in a hemodynamically unstable patient. | continuous renal replacement therapy (CRRT) |
| What patients are usually selected for CRRT? | Those who do not respond to dietary interventions & drug therapy. |
| What is the principle of CRRT? | To dialyze the patients in a more physiologic way over 24 hours, just like the kidneys. |
| When is CRRT contraindicated? | If a patient has a life-threatening manifestations of uremia (hyperkalemia, pericarditis) that require rapid resolution. CRRT can be used in conjunction with HD. |
| What are some features of CRRT that differ from HD? | It's continuous vs intermittent. Lg. volumes of fluid removed over days vs. 3-4 hrs. Solute removal occurs by convection (no dialysate req.), osmosis & diffusion. Less hemodynamic instability. No constant monitoring or complicated HD equipment. |
| What are some specific nursing interventions for CRRT? | Obtain weights; monitor & document labs daily; assess I&O hourly, vitals, & hemodynamics. Reductions in CVP & PAWP expected but no change in MAP or CO. Assess & maintain patency of CRRT, monitor pts vasc. access site. |
| Complications of PD | exit site infection; peritonitis; abdominal pain; cath. outflow; hernias; lower back pain; CVD; pulm. problems: atelectasis, pneumonia, bronchitis; protein loss; carb. abnormalities; lipid abnorms; encap. sclerosing peritonitis |
| Complication of HD | hypotension; muscle cramps; exanguination; hepatitis; infection, including sepsis; disequilibrium syndrome; CVD |
| Syndrome characterized by decreased tissue perfusion & impaired cellular metabolism that results in an imbalance b/t the supply of & demand for O2 & nutrients. | shock |
| four main categories of shock | cardiogenic, hypovolemic, distributive, & obstructive |
| Relationship of shock, SIRS, and MODS | Shock (all types) can lead to SIRS which can lead to MODS which can lead to dysfunction of any and all systems (CV, Lungs, GI, liver, CNS, renals, skin) |
| What causes cardiogenic shock? | Systolic dysfunction: inability of the heart to pump blood forward; diastolic dysfunction: inability of heart to fill; dysrhythmias; structural factors |
| Examples of systolic dysfunction that can cause cardiogenic shock. | MIs, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary htn, myocardial depression from metabolic problems |
| Examples of diastolic dysfunction that can cause cardiogenic shock. | cardiac tamponade, ventricular hypertrophy, cardiomyopathy |
| Examples of dysrhythmias that can cause cardiogenic shock. | bradydysrhythmias and tachydysrhythmias |
| Examples of structural factors that can cause cardiogenic shock. | valvular stenosis or regurgitation, ventricular septal rupture, tension pneumothorax |
| Causes of hypovolemic shock | Absolute hypovolemia: external fluid loss of whole blood, loss of other body fluids; Relative hypovolemia: pooling of blood or fluids, fluid shifts, internal bleeding, massive vasodilation |
| Examples of external loss of whole blood that can cause hypovolemic shock. | hemorrhage from trauma, surgery, GI bleeding |
| Examples of loss of other body fluids that can cause hypovolemic shock. | vomiting, diarrhea, excessive diuresis, DI, DM |
| Examples of relative hypovolemia that can cause hypovolemic shock. | Pooling of blood or fluids (bowel obstruction); fluid shifts (burn injuries, ascites); internal bleeding (fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis); massive vasodilation (sepsis) |
| Types of distributive shock | neurogenic shock, anaphylactic shock, septic shock |
| Causes of neurogenic shock | hemodynamic consequence of spinal cord injury or disease at or above T5 (severe pain, drugs, hypoglycemia, injury); spinal anesthesia; vasomotor center depression |
| Causes of anaphylactic shock | hypersensitivity (allergic) rx to a sensitizing substance (contrast media, blood or products of, drugs, insect bites, anesthetic agents, food or additives, vaccines, environmental agents, latex) |
| Causes of septic shock | infection (pneumonia, peritonitis, urinary tract, invasive proc., indwelling lines/caths; At-risk pts: older adults, pts w/chronic diseases (DM, CKD, HF, immunosuppressed pts, malnourished or debilitated pts) |
| Causes of obstructive shock | physical obstruction impeding the filling or outflow of blood resulting in reduced CO (cardiac tamponade, tension pneumo, superior vena cava syndrome, abdominal compartment syn., PE) |
| Systolic dysfunction primarily affects what side of the heart and why? | Left ventricle, since systolic pressure is greater on the left side of the heart. |
| When systolic dysfunction affects the right side of the heart, what occurs? | Blood flow through the pulmonary circulation is reduced. |
| Diagnostic studies: Lab changes in shock: Increased | WBC, FSP, PTT, PT, INR, thrombin time, D-dimer, creatine kinase, troponin, BUN, creatinine, lactate levels, liver enzymes (ALT, AST, GGT) |
| Diagnostic studies: Lab changes in shock: Decreased | Fibrinogen level, platelet count |
| Diagnostic studies: Lab changes in shock: Normal, Increased, or Decreased | RBC count, Hgb, Hct, glucose, sodium, potassium |
| Diagnostic studies: Lab changes in shock: ABGs | Respiratory alkalosis: Occurs in early shock due to hyperventilation; Metabolic acidosis: Occurs later in shock when lactate accumulates in blood from anaerobic metabolism. |
| What type of fluid is used for initial volume in most types of shock? | Isotonic fluids: 0.9% NaCl (NSS); Lactated Ringer's (LR) |
| What should you monitor when administering isotonic fluids during shock? | Monitor pt closely for circulatory overload. Don't use LR in pts w/liver failure. LR may be used if hyperchloremic acidosis develops from use of NSS in fluid resuscitation. |
| This fluid may be used for initial volume expansion in hypovolemic shock? | Hypertonic fluids: 1.8%, 3%, 5% NaCl |
| What should you monitor when administering hypertonic fluids in hypovolemic shock? | Montior pts for signs of hypernatremia (disorientation, convulsions). Central line preferred for infusing saline solutions >=3% since these may damage veins. |
| This type of fluid can be used for all types of shock EXCEPT cardiogenic and neurogenic shock. | Colloids: Human serum albumin (5% or 25%); 5% for hypovolemic pts; 25% for pts w/fluid & sodium restrictions; (more expensive than crystalloids) |
| What should you monitor when giving albumin in shock? | Monitor for circulatory overload. Mild SE of chills, fever, and urticaria may develop. |
| This type of fluid can be given in ALL types of shock. | Blood or blood products: packed RBCs, fresh frozen plasma, platelets |
| What are some drugs used in cardiogenic shock? | dobutamine (Dobutrex); dopamine (Intropin); epinephrine (Adrenalin); norepinephrine (Levophed); nitroglycerin (Tridil); sodium nitroprusside (Nipride); |
| What are some drugs used in septic shock? | dobutamine (Dobutrex); epinephrine (Adrenalin); hydrocortisone (Solu-Cortef); norepinephrine (Levophed); vasopressin (Pitressin, Pressyn) |
| What are some drugs used in anaphylactic shock? | epinephrine (Adrenalin) - low dose; hydrocortisone (Solu-Cortef) |
| What drug can be used in neurogenic shock? | phenylephrine |
| A decreased platelet count (thrombocytopenia) is present in? | HIT |
| An increased fibrin splint products (FSP) is present in? | DIC |
| Respiratory CM of SIRS/MODS | severe dyspnea; tachypnea; PaO2/FIO2 ratio <200; bilateral fluffy infiltrates on chest xray; PAWP <18 mmHg; ventilation perfusion (VQ) mismatch; pulmonary HTN; inc. minute vent.; dec. compliance; refractory hypoxemia |
| Cardiovascular CM of SIRS/MODS | Myocardial depression; massive vasodilation; dec. SVR, BP; dec. MAP; inc. HR, stroke volume; inc. CO; systolic, diastolic dysfunction; biventricular failure |
| CNS CM of SIRS/MODS | acute change in neuro status; fever; hepatic encephalopathy; seizures; confusion; disorientation; delirium; failure to wean, prolonged rehabilitation |
| Endocrine CM of SIRS/MODS | hyperglycemia can lead to hypoglycemia |
| Renal CM of SIRS/MODS | Prerenal: renal hypoperfusion: BUN/creat ratio>20:1, dec. urine Na<20 mEq/L, inc. urine spec. grav., inc. urine osmolality; Intrarenal: ATN: BUN/creat ratio<10:1-15:1, inc. urine Na>20, dec. urine osmolality, urine spec. gravity 1.010 |
| GI CM of SIRS/MODS | mucosal ischemia: dec. intramucosal pH, potential translocation of gut bacteria, potential abdominal compartment sydnrome; Hypoperfusion lead to dec. peristalsis, ileus; mucosal uleration on endoscopy; GI bleeding |
| Hepatic CM of SIRS/MODS | Bilirubin>2 mg/dL; inc. liver enzymes (ALT, AST, GGT); inc. serum NH3; dec. serum albumin, prealbumin, transferrin; jaundice; hepatic encephalopathy |
| Hematologic CM of SIRS/MODS | Inc. bleeding times, inc. PT, inc. PTT, dec. platelet count (thrombocytopenia)=HIT; inc. FSP=DIC; inc. D-dimer |
| What is the best position to place a patient in SIRS/MODS? | prone |
| In SIRS/MODS, what should be given to prevent hypoglycemia? | Provide continuous infusion of insulin and glucose to maintain blood glucose 140-180 |
| What should be given in SIRS/MODS to manage the renals? | diuretics: loop-furosemide (Lasik), may need to inc. dosage due to dec. GFR; CRRT |
| How should GI CM be managed? | Stress ulcer prophylaxis: antacids (Maalox), PPIs (omeprazole-Prilosec), sucralfate (Carafate); monitor intraabdominal distention, intraabdominal pressures; enteral feedings: stimulate mucosal activity, provide essential nutrients & optimal calories |
| How should the hematologic CM of SIRS/MODS be managed? | Observe for bleeding from obvious &/or occult sites; replace factors being lost (platelets); minimize traumatic interventions (IM injections, multiple venipuncture) |
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