AH1 Exam #1

what factors affect amount and distribution of body fluids

age, gender, and fat

what routes do fluid loss occur through (outtake)

kidney, skin, lungs, intestinal tract

describe ECF

extracellular fluid that contains Na+, Cl-, Ca2+, and K+ in small numbers

describe ICF

intracellular fluid that contains K+, phosphate, proteins, and Na+ in small numbers

describe fluid intake

regulated by thirst, should be around 2300 mL/dose

what parts of the body regulate fluid balance

kidneys (juxtaglomerular cells and adrenal cortex), hypothalamus, heart

describe how the juxtaglomerular cells of the kidneys regulate fluid balance

RAAS system:

juxtaglomerular cells sense low sodium (Na+) or low blood volume --> release renin --> renin converts angiotensinogen (from the liver) to angiotensin I --> ACE (angiotensin-converting enzyme) converts angiotensin I to angiotensin II --> angiotensin II constricts blood vessels (increase BP) and stimulates the release of aldosterone from the adrenal cortex of the kidneys

what are the effects of aldosterone on the body

causes resorption of water and sodium (Na+) in isotonic/equal proportion in the distal renal tubules --> this returns sodium and water to the blood to increase extracellular volume

describe how the adrenal cortex of the kidneys regulate fluid balance

adrenal cortex senses low serum osmolarity or low Na+ --> this releases aldosterone, causing resorption of Na+ into the blood, increasing K+ excretion in the urine --> this increases serum osmolarity

describe how the hypothalamus regulates fluid balance

the hypothalamus senses high serum osmolarity or high Na+ --> stimulates the thirst sensation --> triggers the release of ADH/vasopressin from the posterior pituitary --> ADH causes renal cells to resorb water back into the blood, concentrating urine, constricting blood vessels, and decreasing serum osmolarity

describe how the heart regulates fluid balance

the heart senses high blood volume through stretch receptors in the right atrium --> it then secretes ANP and BNP --> these inhibit ADH and stop the RAAS system, increasing Na+ and water excretion in the urine --> this dilates blood vessels and decreases serum osmolarity

what are the functions of electrolytes

- maintain fluid balance

- contribute to acid/base regulation

- facilitate enzyme reactions

- transmit neuromuscular impulses

what is the normal range of sodium (Na+)

136-145 mEq/L

what is the normal range of potassium (K+)

3.5-5.0 mEq/L

what is the normal range of calcium (Ca2+)

9.0-10.5 mg/dL

what is the normal range of magnesium (Mg2+)

1.3-2.1 mEq/L

what is the normal range of chloride (Cl-)

98-106 mEq/L

what is the normal range of phosphorous

3.0-4.5 mEq/L

describe sodium

normal range: 136-145 mEq/L

"where sodium goes, water follows"

often enters the body through foods and fluids

describe potassium

normal range: 3.5-5.0 mEq/L

major cation of intracellular fluid (ICF)

highest in meat, fish, some vegetables and fruits

describe calcium

normal range: 9.0-10.5 mg/dL

enters the body via dietary intake and undergoes absorption through the intestinal tract (this requires the active form of vitamin D)

stored in bone

describe the compensation of calcium

when more calcium is needed = parathyroid hormone (PTH) is released

when excess calcium is present = thyroid gland secretes thyrocalcitonin (TCT)

describe magnesium

normal range: 1.3-2.1 mEq/L

stored mostly in bones and cartilage

assists with skeletal muscle contraction, carbohydrate metabolism, generation of energy stores, vitamin activation, blood coagulation, and cell growth

describe dehydration

fluid intake/retention doesn't meet body's fluid needs, resulting in fluid volume deficit

what are the clinical manifestations of dehydration

dry skin, skin tenting, increased thirst, confusion, oliguria, decreased weight, capillary refill >4 secs, increased HR, postural hypotension, restlessness, lethargy/weakness, decreased CVP, increased respirations

what are the lab results for dehydration

increased urine specific gravity

increased BUN

increased Hct to Hgb ratio

increased RBCs

describe fluid overload

excess of body fluid (hypervolemia) with failure to eliminate

- severe overload can lead to heart failure and pulmonary edema

what are the clinical manifestations of fluid overload

neurologic: changes in LOC, confusion, headaches, seizures

respiratory: pulmonary congestion

cardiovascular: bounding pulse, increased BP, JVD, presence of S3, tachycardia

gastrointestinal: anorexia, nausea

edema: dependent and pitting

what are the labs of fluid overload

decreased Hct

describe the clinical manifestations of hypernatremia (>145 mEq/L)

flushed skin, restlessness, confusion, increased BP, fluid retention, edema, decreased urine output, dry skin, agitation, low-grade fever, thirst

describe the treatment/interventions of hypernatremia (>145 mEq/L)

IV fluid replacement, drug therapy, nutrition therapy, diuretics, adequate water intake, sodium restriction

describe the assessment of hypernatremia (>145 mEq/L)

irritability (overresponse to stimuli), altered cerebral function, muscle twitching, decreased cardiac contractility

describe the assessment of hyponatremia (

excitable cellular activity, cerebral, neuromuscular, intestinal, and cardiovascular changes

describe the treatment/interventions of hyponatremia (

determine the cause 1st --> IV drug therapy and nutrition therapy, reducing diuretics, IV fluids, oral Na+ intake, oral fluid restrictions

describe the clinical manifestations of hyponatremia (

stupor/coma, anorexia, lethargy, tachycardia, muscle weakness, orthostatic hypotension, seizures/headache, stomach cramping

describe the assessment of hyperkalemia (>5.0 mEq/L)

cardiac irregularities, palpitations, skilled heartbeats, muscle twitching, leg weakness/tingling/numbness, diarrhea

describe some interventions/treatment of hyperkalemia (>5.0 mEq/L)

decrease serum potassium, prevent recurrence, ensure patient safety (high fall risk), K+ binding medicines, K+ excreting diuretics, hypotonic IV fluids, nutrition

describe the clinical manifestations of hyperkalemia (>5.0 mEq/L)

muscle twitches, cramps and paresthesia, irritability and anxiety, decreased BP, EKG changes, dysrhythmias, abdominal cramping, diarrhea

describe assessment for hypokalemia (

may have no symptoms with gradual K+ loss

may have dramatic function changes with rapid K+ loss

describe some interventions/treatment for hypokalemia (

prevent K+ loss, increased serum K+, ensure patient safety (fall risk), regular repiratory assessment K+ supplements and nutrition

CAUTION WITH IV POTASSIUM

describe the clinical manifestations of hypokalemia (

alkalosis, shallow respirations, irritability, confusion, drowsiness, weakness, fatigue, arrythmias, lethargy, thready pulse, decreased intestinal motility

describe assessment for hypercalcemia (>10.5 mg/dL)

cardiovascular changes, severe muscle weakness, decreased DTRs, decreased peristalsis

describe the interventions/treatment for hypercalcemia (>10.5 mg/dL)

decrease Ca2+ levels, drug therapy, rehydration, dialysis, cardiac monitoring --> stop Calcium meds, isotonic IV fluids

describe the manifestations of hypercalcemia (>10.5 mg/dL)

can be asymptomatic, nausea and vomiting, abdominal discomfort, excessive thirst, frequent urination, muscle weakness, bone pain

what are some causes of hypercalcemia (>10.5 mg/dL)

hyperparathyroidism, excessive intake of Ca2+, cancers, medicines

describe assessment for hypocalcemia (

frequent painful muscle spasms, paresthesia, cardiac, intestinal, and skeletal cramps

describe some interventions/treatments for hypocalcemia (

restore normal Ca2+ levels, drug/nutritional therapy, decreased environmental stimuli, prevent injury, oral or IV Ca2+ replacement with vitamin D, nutrition

describe the manifestations of hypocalcemia (

can be asymptomatic, muscle cramps, dry skin, tingling, seizures

what are some causes of hypocalcemia (

hypoparathyroidism, vitamin D deficit, renal failure, medications

describe assessment for hypermagnesemia (>2.1 mEq/L)

cardiac changes, depressed nerve impulse transmission, respiratory insufficiency

describe the intervention/treatments for hypermagnesemia (>2.1 mEq/L)

decrease serum magnesium levels, correct underlying problems, Mg-free IV fluids, loop diuretics

describe the manifestations of hypermagnesemia (>2.1 mEq/L)

LOW EVERYTHING: decreased DTRs, decreased energy, decreased HR and BP, decreased respiratory rate, decreased bowel sounds

describe some interventions/treatments for hypomagnesemia (

correct the imbalance, manage the cause, drug therapy, IV magnesium sulfate

describe clinical manifestations of hypomagnesemia (

HIGH EVERYTHING: increased DTRs, increased HR and BP, shallow respirations, twitches, paresthesias, tetany seizures, irritability, confusion

describe assessment for hypomagnesemia (

cardiac changes, inhibited nerve impulse transmission, GI symptoms

describe interventions/treatment for hypomagnesemia (

correct the imbalance, manage the cause, drug therapy (IV magnesium sulfate)

what is the goal of acid-base balance

maintenance of arterial blood pH between 7.35 and 7.45 ensures optimal body function

what is pH

the concentration of hydrogen ions (H+)

what are acids

substances with a pH

what are bases

substances with a pH >7

- ex: bicarbonate (HCO3-)

what are buffers

1st line of defense against changes in free hydrogen ion levels (changes in pH)

- ex: phosphate, proteins, albumin, globulins, hemoglobin

what is the respirator system

2nd line of defense against changes in pH (quick but less powerful)

- hypoventilation: increases CO2 retention, decreases blood pH

- hyperventilation: decreases CO2 retention, increases blood pH

describe how the kidneys regulate pH

3rd line of defense, release bicarbonate into blood

- strong but slow (takes around 24-48 hours to respond to pH changes)

describe how potassium regulates pH

plays an exchange role with H+

- high hydrogen ion concentration in the blood = H+ moves into the cells and K+ goes out (this causes hyperkalemia)

- low hydrogen ion concentration in the blood = H+ moves out of the cells and K+ goes in (this causes hypokalemia)

what is the normal range for PaO2

80-100 mmHg

what does a PaO2 < 80 mmHg mean

hypoxemia

what does a PaO2 < 60 mmHg mean

hypoxemia, may be see in patients with chronic lung disorders

what does a PaO2 < 50 mmHg mean

life-threatening hypoxemia

what is the normal range for SaO2

93-100%

what is hypoxia

decreased oxygen in the tissues

what is hypoxemia

decreased oxygen in the blood

what is PaCO2 and what is its normal range

partial pressure of CO2 dissolved in the arterial plasma (regulated in the lungs)

- 35-45 mmHg

what does PaCO2 >45 mmHg mean

primary respiratory problem: RESPIRATORY ACIDOSIS

- more carbon dioxide = more acidic

- bicarbonate levels will be normal

what does PaCO2

primary respiratory problem: RESPIRATORY ALKALOSIS

- less carbon dioxide = less acidic

- bicarbonate levels will be normal

what is HCO3- and what is its normal range

bicarbonate (regulated by the kidneys)

- 21-28 mEq/L

what does HCO3-

primary metabolic/renal disorder = METABOLIC ACIDOSIS

- less bicarbonate = more acidic

- PaCO2 levels will be normal

what does HCO3- >26 mEq/L mean

primary metabolic/renal disorder = METABOLIC ALKALOSIS

- more bicarbonate = less acidic

- PaCO2 levels will be normal

describe the patho of respiratory acidosis

impaired gas exchange (hypoventilation) leads to retention of CO2

- increased CO2 = lowered pH, low PaO2, and hyperkalemia

what are the manifestations of respiratory acidosis

rapid and shallow respirations, decreased BP, pale/cyanotic skin/mucosa, headache, hyperkalemia, dysrhythmias (due to increased K+), drowsiness, dizziness, disorientation, muscle weakness, hyerreflexia

what causes respiratory acidosis

respiratory depression (anesthesia, overdose, increased intracranial pressure), airway obstruction, decreased alveolar capillary diffusion (pneumonia, COPD, ARDs, PE)

what are some interventions for respiratory acidosis

monitor respiratory status, oxygen therapy, hydration, bronchodilators, mucolytics, anti-inflammatories

describe the patho of respiratory alkalosis

excessive loss of CO2 (hyperventilation) leads to an increased pH and PaCO2

- bicarbonate should be within normal range unless compensation is occuring

what are the manifestations of repiratory alkalosis

seizures, tetany/confusion, deep/rapid breathing, lightheadedness, nausea and vomiting, hyperventilation, tachycardia, decreased or normal BP, hypokalemia, numb/tingling extremities

what are the causes of respiratory alkalosis

hyperventilation (anxiety, PE, fear), mechanical ventilation

what are some interventions for respiratory alkalosis

monitor respiratory status, emotional support, monitor K+ and Ca2+, calcium gluconate (for tetany)

describe the patho of metabolic acidosis

low bicarbonate levels = low pH (acidic), normal PaO2 and PaCO2, high K+

what are the manifestations of metabolic acidosis

headache, decreased BP, hyperkalemia, changes in LOC (confusion, drowsiness), Kussmaul respirations (compensatory hyperventilation), muscle twitching, warm/flushed skin (vasodilation), nausea and vomiting, diarrhea

what causes metabolic acidosis

DKA, severe diarrhea, renal failure, shock

what are some interventions for metabolic acidosis

correct the cause, rehydration, bicarbonate administration if pH

describe the patho of metabolic alkalosis

high bicarbonate levels due to loss of acids leads to a high pH, normal PaCO2 and PaO2

what are the manifestations of metabolic alkalosis

restlessness followed by lethargy, confusion (decreased LOC, dizziness, irritability), dysrhythmias (tachycardia), nausea and vomiting, diarrhea, tremors, muscle cramps, tingling of digits, hypokalemia, compensatory hypoventilation

what are some causes of metabolic alkalosis

severe vomiting, excessive GI suctioning, diuretics, excessive sodium bicarbonate

what are some interventions for metabolic alkalosis

administer fluids, electrolyte replacement, treat causes

describe compensation

- if pH abnormality is due to a respiratory problem, the metabolic system (aka the kidneys) will compensate

- if pH abnormality is due to metabolic problems, the respiratory system (lungs) will compensate

who are some patients at risk for VTE

obese patients, 40 years old or older, history of cancer, decreased cardiac output, decreased mobility, history of VTE/PE/varicose veins/edema, oral contraceptives, smoking, hip fracture/surgery

describe malignant hyperthermia

inherited muscle disorder; an acute life-threatening complication of certain drugs for anesthesia causing inadequate thermoregulation

what are some signs and symptoms of malignant hyperthermia

increased Ca2+ and K+, metabolic acidosis, cardiac dysrhythmias, high body temp

describe informed consent

includes explanation of risks, benefits, alterations, and answers

- the surgeon obtains consent, the nurse verifies it

- patients must be competent and voluntary (exceptions for minors, emergencies)

- patients have the right to refuse/withdraw consent

- is NOT general consent

what is general consent

consent that covers routine care; informed consent is required for procedures!

what are the parts of a time-out

verifies:

1. correct patient identity

2. correct procedure

3. correct side and site

4. agreement on procedure to be done

5. availability of implants, special implants, or special requirements

6. correct position