Hurst Review Notes for NCLEX PDF

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Hurst Review notes for NCLEX (2021)....

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HURST REVIEW FLUID + ELECTROLYTES 1. HORMONAL REGULATION OF FLUID VOLUME a. ALDOSTERONE (steroid, mineralocorticoid) i. Stored in adrenal glands—on top of kidneys ii. When blood volume gets low (vomiting, hemorrhage, etc.): 1. Aldosterone secretion ↑  RETAIN SODIUM/WATER  blood volume goes UP ↑ a. **Diseases w/ TOO MUCH aldosterone: retain sodium + water i. Cushing’s—too much of ALL steroids ii. Hyperaldosteronism / Conn’s b. **Diseases w/ TOO LITTLE aldosterone: losing sodium + water i. Addison’s—hypovolemia b. ADH (anti-diuretic hormone) i. Normally makes you RETAIN WATER—ADH = H2O ii. Found in pituitary iii. Another name for ADH = vasopressin (Pitressin) or desmopressin (DDAVP) 1. Utilized as ADH replacement in Diabetes Insipidus (DI) iv. 2 ADH Problems: 1. TOO MUCH ADH NOT ENOUGH ADH -

RETAIN water Fluid volume EXCESS

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LOSE/diurese water Fluid volume DEFECIT

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SIADH—too many letters = too much water

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DI = diuresis (can go into shock)

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Urine = concentrated + ↓ Blood = dilute

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Urine = dilute Blood = concentrated

i. **Concentrated makes #s go UP  Urine specific gravity, sodium, hematocrit ii. **Dilute makes #s go DOWN 2. Key words to make you think potential ADH problem: a. Craniotomy b. Head injury c. Sinus surgery d. Transsphenoidal hypophysectomy e. Any condition that can lead to increased ICP can lead to ADH problem i. **ADH problems = 2/2 something else

2. HYPERVOLEMIA—FLUID VOLUME EXCESS a. Too much fluid in vascular space b. Causes: i. Heart Failure (HF)—heart = weak  ↓ cardiac output, ↓ kidney perfusion, ↓ urinary output 1. Volume stays in vascular space ii. Renal failure (RF)—kidneys aren’t working iii. 3 things w/ lots of sodium: 1. Effervescent soluble meds  Alka-Seltzer 2. Canned/processed foods **sodium makes us retain water— 3. IVF w/ sodium stays in vascular space** c. S/S: i. Distended neck veins / peripheral veins  vessels = FULL ii. Peripheral edema / third spacing  vessels can’t hold anymore—start to LEAK iii. Lungs sound wet /crackles 1. May be SOB, heard first in bases/low lungs iv. Polyuria  kidneys trying to help get rid of excess fluid  DIURESE CVP NORMAL v. HR ↑  want fluid to go forward 2-6 mmHg 1. If fluid doesn’t go forward—it’s going to go backwards into lungs 2. Can lead to HF + pulmonary edema 5-10 cmH2O vi. BP ↑  MORE VOLUME = MORE PRESSURE vii. CVP ↑  MORE VOLUME = MORE PRESSURE (measured in right atrium) viii. Weight ↑  any acute gain or loss = fluid…NOT fat TESTING STRATEGY: d. TX: Fluid retention  think HEART i. Low-sodium diet + restrict fluids PROBLEMS FIRST ii. I&O + daily weights iii. Diuretics 1. Loop diuretics—furosemide (Lasix) a. Bumetanide (Bumex) may be given when furosemide (Lasix) doesn’t work 2. Hydrochlorothiazide (Thiazide) a. Watch lab work w/ all diuretics for dehydration + electrolyte problems 3. Potassium sparing diuretics—spironolactone iv. Bed rest (induces diuresis v. Physical assessment—focus on pertinent s/s vi. Give IVFs SLOWLY to elderly/very young + pt. w/ Hx heart or kidney problems 1. Monitor for fluid volume excess ** TESTING STRATEGY: Anytime you see assessment or evaluation on the NCLEX—you should be looking for the presence or absence of pertinent S/S

3. HYPOVOLEMIA—FLUID VOLUME DEFICIT a. Big time deficit = SHOCK  problem w/ supply (O2) + demand (cellular metabolism) b. Causes: i. Loss of fluid from ANYWHERE 1. Vomiting, diarrhea, hemorrhage, thoracentesis, paracentesis ii. Third spacing—when fluid is in a place that does you no good 1. Burns (interstitial space / tissues) 2. Ascites (fluid in abdomen / peritoneum  can develop breathing problems) a. Measure abdominal girth daily b. Worry about hypotension—check BP iii. Diseases w/ polyuria  ex. Diabetes Mellitus 1. Polyuria—THINK SHOCK FIRST 2. Polyuria  Oliguria  Anuria (worry about renal failure) c. S/S: i. Weight ↓ ii. Decreased skin turgor ↓ iii. Dry mucous membranes iv. Peripheral veins / neck veins vasoconstrict (become very tiny) v. Cool extremities  peripheral vasoconstriction to shunt blood to vital organs vi. Urine output ↓ vii. Urine specific gravity ↑  if putting out any urine, it will be very concentrated viii. BP ↓  LESS VOLUME = LESS PRESSURE ix. CVP ↓ x. HR ↑, pulse = weak + thready  heart trying to pump what little fluid is left xi. RR ↑  to improve hypoxia d. TX: i. Prevent further losses ii. Replace volume: 1. Mild deficit—PO fluids 2. Severe deficit—IV fluids iii. Safety precautions: 1. Higher risk for FALLS  hypotension, mental status changes 2. Monitor for OVERLOAD w/ IV fluid replacement

4. MAGNESIUM + CALCIUM—act like sedatives a. Causes: HYPERMAGNESMIA -

Renal failure

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Antacids -

HYPERCALCEMIA

Hyperparathyroidism: too much PTH o When serum calcium gets low, PTH kicks in + pulls Ca from bone + puts it in blood  serum Ca goes UP Thiazides (retain calcium) Immobilization

b. S/S: HYPERMAGNESMIA -

HYPERCALCEMIA

Flushing + warmth Mg causes vasodilation (↓ BP, prevent seizures)

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Bones = brittle Kidney stones (bc serum Ca ↑)

c. S/S common in HYPERMAGNESMIA + HYPERCALCEMIA—act like sedatives 1. DTRs ↓ 2. Weak, flaccid muscle tone 3. Arrhythmias 4. ↓ LOC 5. ↓ pulse 6. ↓ respirations d. TX: HYPERMAGNESMIA -

Ventilator

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Dialysis

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Calcium gluconate— antidote for Mg toxicity

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Safety precautions

HYPERCALCEMIA -

Move! Fluids (prevent kidney stones) Protein to diet o Ca has inverse relationship w/ phosphorus Steroids (↓ Ca) Safety precautions Meds: ↓ serum Ca o Biphosphates (etidronate) o Calcitonin (Tx osteoporosis—drives Ca back to bones

e.

NORMAL LAB VALUES TESTING STRATEGY: Magnesium: 1.3 – 2.1 Mg & Ca questions  think MUSCLES FIRST

Calcium: 9.0 – 10.5

5. MAGNESIUM + CALCIUM—not enough sedative a. Causes: HYPOMAGNESMIA -

HYPOCALCEMIA

Diarrhea (lots of Mg in intestines) Alcoholism Alcohol suppresses ADH + it’s hypertonic o Not eating o Not drinking + diuresing

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Hypoparathyroidism Radical neck Thyroidectomy o ALL = not enough PTH o Serum Ca ↓

b. S/S common in HYPOMAGNESMIA + HYPOCALCEMIA—not enough sedative 1. Rigid + tight muscle tone 2. Stridor / laryngospasm 3. + Chvostek’s sign—tap cheek  twitches (C = cheek) 4. + Trousseau’s sign—pump up BP cuff  hand starts to shake 5. Arrhythmias (heart is a muscle) 6. DTRs ↑ 7. Mind changes 8. Swallowing problems c. TX: HYPOMAGNESMIA -

Give some Mg Check kidney function (before + during IV Mg) Seizure precautions Eat Mg

HYPOCALCEMIA -

PO calcium IV Ca  GIVE SLOWLY + always make sure pt. on heart monitor Vitamin D Phosphate binders: phos ↓, Ca ↑ o Sevelamer hydrochloride (Renagel) o Calcium acetate (PhosLo)

a. ** pt. reports flushing + sweating after starting IV Mg  STOP infusion d. Foods high in magnesium: i. Spinach, mustard greens, broccoli, turnip greens, green beans ii. Squash, halibut, pumpkin seeds iii. Peppermint iv. Kale, cucumber, celery v. Sunflower seeds, sesame seeds, flax seeds

6. SODIUM—think neuro changes a. Sodium level in blood = totally dependent on how much water in the blood

b. HYPERNATREMIA = dehydration i. Too much sodium; not enough water ii. Causes: 1. Hyperventilation 2. Heat stroke 3. Diabetes insipidus 4. Vomiting diarrhea

v. S/S: 1. 2. 3. 4. i. Tx: 1. 2. 3. 4. 5.

NORMAL LAB VALUE Sodium: 135 – 145

HYPONATREMIA = dilution c. Too much water; not enough sodium d. Causes: i. Drinking water for fluid replacement (vomiting, sweating) ii. Psychogenic polydipsia iii. D5W (sugar & water) iv. SIADH—retaining water S/S: e. Headache f. Seizure g. Coma

Dry mouth Thirsty Swollen tongue Neuro changes Restrict sodium Dilute pt. w/ IV fluids (Na ↓) Daily weights I&O Lab work a. **feeding tube pt. tend to become dehydrated**

Tx: h. Pt. needs sodium; doesn’t need water i. Neuro problems  hypertonic saline i. “packed w/ particles” ii. 3% or 5% NS = sodium

TESTING STRATEGY: Neuro changes—the brain doesn’t like when sodium is messed up **neuro changes common w/ hypernatremia or hyponatremia**

7. POTASSIUM a. Excreted by the kidneys b. If kidneys not working well  serum potassium will go UP ↑ c. HYPERKALEMIA i. Causes: 1. Kidney trouble 2. Spironolactone (Aldactone) —makes you retain potassium

NORMAL LAB VALUE Potassium: 3.5 – 5.0

HYPOKALEMIA d. Causes: i. Vomiting ii. NG suction* (lots of K+ in stomach) iii. Diuretics iv. Not eating

e. S/S: i. Begins w/ muscle twitching ii. Proceeds to muscle weakness iii. Then flaccid paralysis iv. Life-threatening arrhythmias

f.

g. TX: i. ii. iii. iv.

h. TX: i. Give potassium ii. Spironolactone iii. Eat more potassium (causes GI upset— give w/ food)

Dialysis—kidneys not working Calcium gluconate (↓ arrhythmias) Glucose + insulin Sodium polystyrene sulfonate (Kayelexate) – given w/ hyperkalemia + push fluids

S/S: i. Muscle cramps ii. Muscle weakness iii. Life threatening arrhythmias

TESTING STRATEGY: Sodium + potassium have an INVERSE RELATIONSHIP

TESTING STRATEGY: ECG changes w/ HYPERKALEMIA: bradycardia, tall + peaked T waves, prolonged PR intervals, flat or absent P waves, widened QRS, conduction blocks, ventricular fibrillation ECG changes w/ HYPOKALEMIA: U waves, PVCs, ventricular tachycardia

i.

Miscellaneous Info: i. Major problem w/ oral potassium  GI upset—give w/ food ii. Assess urinary output before + during IV potassium iii. Always put potassium on a pump iv. Mix well! (shake bag) v. NEVER give potassium IV push  has to be diluted in something vi. Burns during infusion 1. Watch IV site

IV FLUIDS

1. ISOTONIC SOLUTIONS a. Goes into vascular space + stays there i. Makes BP ↑, vascular volume ↑ b. Ex: NS, LR, D5W, D5¼ NS c. Uses: pt. who has lost fluids thru N/V, burns, sweating, + trauma i. NS = basic solution when administering blood d. DO NOT USE in pt. w/: i. Hypertension ii. Cardiac disease  Isotonic solutions can cause FVE, HTN, or hypernatremia iii. Renal disease 1. Hypernatremia = alert only when administering isotonic solutions that contain sodium

2. HYPOTONIC SOLUTIONS a. Goes into vascular space + then shifts out into cells to replace cellular fluid i. Rehydrate but do not cause hypertension b. Ex: D2.5W, ½ NS, 0.33% NS c. Uses: i. Hypertension ii. Renal or cardiac disease iii. Needs fluid replacement bc N/V, burns, hemorrhage, etc. iv. Dilution when pt. has hypernatremia or cellular dehydration d. ALERT: i. Watch for cellular edema  fluid moving out to the cells  could lead to fluid volume deficit + ↓ BP 3. HYPERTONIC SOLUTIONS a. Volume expanders that draw fluid into vascular space from the cells  return fluid volume to vascular space b. Ex: D10W, 3% NS, 5% NS, D5LR, D5½ NS, D5 NS, TPN, Albumin c. Uses: i. Hyponatremia ii. Pt. who has shifted large amounts of vascular volume to a 3rd space iii. Severe edema, burns, or ascites d. ALERT: i. Watch for fluid volume excess ii. Monitor in ICU setting w/ frequent BP, pulse, + CVP (esp. if receiving 3% or 5% NS)

Isotonic Solutions

Hypotonic Solutions

Hypertonic solutions

“Stay where I put it”

“Go Out of the vessel”

“Enter the vessel”

ACID BASE BALANCE

Acid-Base Balance represents homeostasis of hydrogen (H+) ion concentration in body fluids  pH—indirect measurement of H+ concentration—result of respiratory + kidney compensation function  pH = balance b/w carbon dioxide (CO2) (regulated by lungs) + bicarbonate (HCO3-) (regulated by kidneys) o Hydrogen shifts = acid-base imbalances o Greater H+ concentration  more acidic + lower pH o Lower H+ concentration  more alkaline + higher pH  ABGs—used to evaluate acid-base balance What is the role of the kidney’s in regulating acid-base balance?  Kidneys regulate bicarbonate level in ECF  REGENERATE + REABSORB HCO3- TO MAINTAIN STABLE pH o Ex: respiratory + metabolic acidosis  kidneys excrete H+ + conserve HCO3- to help restore balance o Ex: respiratory + metabolic alkalosis  kidneys retain H+ + excrete HCO3- to help restore balance  High H+ (low pH)—bicarbonate reabsorption + production  Low H+ (high pH)—bicarbonate excretion  Regulate normal electrolyte levels in the ECF by selective electrolyte retention + excretion  Excrete metabolic wastes and toxic substances How might renal failure affect ABGs?  Failure of the kidneys would result in multiple fluid and electrolyte abnormalities  They would not be able to regulate pH by excreting or reabsorbing H+ or HCO3 Kidneys cannot compensate for metabolic acidosis caused by kidney injury Causes of Metabolic Acidosis  Kidneys have a problem  lungs compensate o Too little HCO3 (bicarb) o Too much Hydrogen  Excess production H+ ions o Diabetic Ketoacidosis (DKA) o Starvation o Lactic acidosis (exercise, seizures, hypoxia)  Renal failure  Excess elimination HCO3-: diarrhea  Chronic metabolic acidosis—seen w/ CKD Causes of Metabolic Alkalosis  Kidneys have problem  lungs compensate o Too much HCO3 (bicarb) o Too little Hydrogen  Loss of upper GI contents—losing acid: o Vomiting / hyperemesis gravidum o Gastric suctioning (loss of gastric fluid) o Diuretic use (potassium depletion) o Laxative overuse  Antacids (excessive ingestion of bases)  Blood transfusions, TPN, sodium bicarbonate (venous admin. of bases)  Hyperaldosteronism, Cushing’s syndrome

**S/S of Metabolic Acidosis: low pH (↑ H+) + low HCO3 ↑ RR (causing more CO2 elimination to ↓ acid load)  Kussmaul respirations (deep, rapid + labored)  ↓ BP / hypotension  Arrhythmias—caused by ↑ potassium  Muscle twitching + weakness, flaccid paralysis  Diagnostics: ABGs o pH < 7.35 o HCO3- < 22 mEq/L o CO2 ↓ (r/t hyperventilation) o Hyperkalemia (K+ shift out of cells)

S/S of Metabolic Alkalosis: high pH (↓ H+) + high HCO3 ↓ RR (causing CO2 retention to ↑ acid load)  Arrhythmias / Atrial Tachycardia  Tingling of fingers + toes  Muscle cramps  Hyperactive reflexes  Hypoventilation—more in un/semiconscious  Tetany  Confusion, convulsion  Diagnostics: o pH > 7.45 o HCO3- > 26 mEq/L o Hypokalemia o Hypocalcemia (s/s = predominant)

TESTING STRATEGY:

TESTING STRATEGY:

Metabolic Acidosis = Hyperkalemia Metabolic Alkalosis = Hypokalemia

Acidotic person = lethargic Alkalotic person = excitable

METABOLIC

RESPIRATORY

Causes of Respiratory Acidosis  Hypoventilation (too much CO2)  Respiratory depression opioids, anesthetics)  Emergency situations: o Asthma o Aspiration of foreign object o Atelectasis o Pulmonary edema o Pneumothorax  Sleep apnea assoc. w/ morbid obesity  Pneumonia, ARDS (resp. effort affected)  Muscular dystrophy, MS, myasthenia gravis, Guillain-Barré syndrome (impaired resp. muscles)  Chronic resp. acidosis—chronic emphysema + bronchitis, COPD, OSA, + obesity

Causes of Respiratory Alkalosis  Hyperventilation (excess “blowing off” CO2) o Too little CO2 / losing CO2  Hypermetabolic states (fever, anemia, septicemia)  Extreme anxiety  Acute aspirin overdose  Excessive mechanical ventilation o Pt. breathing too fast  removing CO2  Chronic resp. alkalosis—from chronic hypocapnia

S/S Respiratory Acidosis: low pH + high PaCO2 (↑ CO2)  Sudden hypercapnia (↑ PaCO2) – can cause:  Confusion, headache  ↓ LOC  V-fib (1st s/s in anesthetized pt.)  Ineffective, shallow, rapid breathing  Pale / cyanotic  Acidosis worsens: o Bradycardia (↓ RR), Hypotension ( ↓ BP) o Lethargy, possible coma  Diagnostics: o pH < 7.35 o PaCO2 > 45 ( ↑ CO2) o Variation in HCO3-

S/S Respiratory Alkalosis: high pH + low PaCO2 (↓ CO2)  Lightheadedness (↓ cerebral blood flow)  Inability to concentrate  Numbness + tingling (r/t ↓ calcium ionization)  Sometimes loss of consciousness  Diagnostics: o pH > 7.45 o PaCO2 < 35 ( ↓ CO2) o Hypokalemia o Hypocalcemia

TESTING STRATEGY: TESTING STRATEGY: Metabolic Acidosis = Hyperkalemia Metabolic Alkalosis = Hypokalemia

NORMAL LAB VALUE pH: 7.35 – 7.45 PaO2: 80 – 100 PaCO2: 35 – 45 HCO3/bicarb: 22 – 26

Acidotic person = lethargic Alkalotic person = excitable

TESTING STRATEGY: ↑ CO2 = ↓ LOC ↑ CO2 = ↓ O2 CO + O2 have an INVERSE RELATIONSHIP

Alkalosis = EXCITEABLE: pH goes up  systems get more irritable Hyperreflexia (+3, +4), tachypnea, tachycardia, borborygmi, seizure Suction bag at bedside  could seize and aspirate Acidosis = LETHARGIC: pH goes down  everything shuts down Hyporeflexia, bradycardia, lethargy/obtundent, coma, paralytic ileus, respiratory arrest, urinary retention Need ambu bag at bedside BURNS

1. PATHO a. ↑ capillary permeability  plasma seeps out into the tissue b. ↑ pulse  because of fluid volume deficit c. ↓ CO  less volume to pump out d. ↓ urine output  kidneys either trying to hold onto fluid or not being perfused adequately e. Epinephrine secreted  epi + norepi secretion make you peripherally vasoconstrict  blood shunted to vital organs + ↑ BP f. ADH + aldosterone secreted: i. Aldosterone—retain sodium + water  blood volume will go UP ↑ ii. ADH—retain water 2. DEPTH a. Partial thickness burns—first + second degree burns b. Full thickness burns—third + fourth degree burns 3. TX a. Stop burning process: i. Wrap pt. in blanket to stop burning process ii. Cool water  soak area (no more than 10 minutes) 1. Blanket will help hold in body heat + keep out germs iii. Remove jewelry bc swelling will occur iv. Clothing—remove non-adherent clothing + cover burns w/ clean, dry cloth 1. Clothing stuck to skin  leave it b. Inhalation injury: i. #1 cause of death = inhalation injury ii. CARBON MONOXIDE POISONING: 1. Normally O2 binds w/ hemoglobin 2. Carbon monoxide travels much faster than O2 (200x)  gets to hemoglobin first + binds 3. Oxygen cannot bind now 4. Pt. = hypoxic 5. Tx = 100% O2 iii. HYDROGEN CYANIDE: 1. Tx = 100% O2 2. An antidote may be given at hospital 3. Determine if burn occurred in open or closed space  burned in closed space = inhaled more carbon monoxide and/or hydrogen cyanide a. Risk of complications ↑ iv. S/S inhalation injury: 1. Singed nose hair + facial hair, soot on face 2. Coughing up secretions w/ dark specks, wheezing 3. Difficulty swallowing 4. Blisters found on oral/pharyngeal mucosa 5. Hoarseness 6. Substernal/intercostal retractions + stridor = bad signs c. Burns to neck/face/chest  focus on their AIRWAY d. Prophylactic TX? Intubate or trach (least invasive first)

4. FLUID REPLACEMENT

a. Giving large volumes of fluid  pt. will need at least 2 large bore IVs b. Crystalloids (LR) + colloids (albumin) = used c. Important to know what time burn occurred i. Fluid replacement therapy—for first 24 hrs.—based on time injury occurred, not when Tx started ii. Common rule: calculate total amount of fluid needed for first 24 hrs. then give half of the amount during the first 8 hours 1. 1st 8 hours = ½ of total volume 2. 2nd 8 hours = ¼ of total volume 3. 3rd 8 hours = ¼ of total volume d. If pt. restless  could suggest 3 problems: i. Inadequate fluid replacement ii. Pain—**pain never killed anyone** iii. Hypoxia—PRIORITY—pick killer answer e. Determine if fluid volume adequate: i. URINE OUTPUT—needs to be minimum 0.5-1 mL/kg/hr. 1. 30-50 mL/hr. adult 2. 1 mL/kg/hr. children 5. MEDICATIONS a. Albumin (colloid): i. Administered after first 24 hrs. (capillary permeability normal) ii. Holds onto fluid in vascular space iii. ↑ vascular volume iv. ↑ kidney perfusion v. ↑ BP, ↑ CO vi. Helps correct fluid volume deficit  putting more fluid in vascular space vii. Vascular volume will ↑ + workload of the heart will ↑ b. ALERT: i. If you stress...