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NUR 516 > Fluid, Electrolytes, and Acid-Base Disorders (complete) > Flashcards

Fluid, Electrolytes, and Acid-Base Disorders (complete) Flashcards

1
Q

How much of the human body is fluid?

A

60%; it acts as a solvent

Can be as low as 45% in older adults due to decreased muscle mass

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2
Q

Why is fluid important in the body overall?

A

It plays a vital role in maintaining homeostasis
- regulation of various bodily functions
- electrolytes are the mechanisms that help control cellular function

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3
Q

What is intracellular fluid?

A
  • fluid found within cells
  • approximately 2/3 of the total body fluids
  • water diffuses out of the ICF and can cause cell shrinkage or cellular dehydration
  • water can enter the cell and lead to swelling of the cell or cellular edema
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4
Q

What is extracellular fluid?

A
  • most ECF is found within the intravascular compartment of the blood vessels
  • contains electrolytes, oxygen, glucose, and nutrients
  • cellular waste
  • fluid found outside cells (intravascular, interstitial and transcellular fluid spaces)
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5
Q

What is the interstitial space?

A
  • is filtrate from the blood
  • located between the cells and blood
  • contains electrolytes (mostly Na+) and water
    – no proteins because they are too big; except in inflammation when membrane becomes more permeable
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6
Q

What is diffusion?

A

Passive spread of molecules from an area of high concentration to an area of low concentration until equilibrium is reached
(passive diffusion)

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7
Q

What is the rate of diffusion determined by?

A
  • concentration gradient
  • molecular weight of the substance
  • temperature of the solution
  • the electrical charge
  • the availability of a carrier molecule
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8
Q

What is osmosis?

A
  • molecules of the solvent to pass through the semi-permeable membrane from less concentrated to more concentrated
  • water and electrolytes can move
    – larger proteins like albumin should not be able to move from ECF
  • the greater the number of particles on one side, the greater the osmotic (attractive) force
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9
Q

What is filtration?

A

Occurs when water moves across membrane due to hydrostatic pressure

albumin plays a role – if too low, results in edema

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10
Q

What is the sodium-potassium pump?

A

Uses active transport to move molecules from a high concentration to a low concentration

3 sodium out, 2 potassium in

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11
Q

What is facilitated transport?

A

Passing of certain molecules through the membrane with assistance of carrier proteins

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12
Q

What is active transport?

A
  • substance needs energy to pass through against a concentration gradient
  • sodium and potassium require ATPase to keep potassium inside and sodium on the outside
    – sodium potassium pump
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13
Q

What is hydrostatic pressure?

A

Pushing force by water in the bloodstream
- causes by the heart pumping blood against the capillary tends to push fluid from vascular to the interstitial space
– important for filtration

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14
Q

What is osmotic pressure?

A

Pressure exerted by the solutes; in the blood it comes from the electrolytes like sodium and plasma proteins
- pulls water into the bloodstream from the ICF and ISF
- solution with greater number of particles has higher osmotic pressure
- when pressure is high in the blood, it increases movement from the ICF and ISF to the blood
- when pressure is low, it moves fluid out of the blood and into the ICF and ISF

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15
Q

What is oncotic pressure?

A
  • type of osmotic pressure exerted solely by albumin
  • main colloidal protein in blood and maintains oncotic pressure
  • attracts water and helps keep it inside the blood vessle
    – if too low, fluid goes into the tissues and causes edema
  • albumin is an indicator of nutrition
    – when albumin is low, there is reduced oncotic pressure which raises hydrostatic pressure and pushes fluid into the ISF and ICF
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16
Q

What is Starling’s Law of Capillary Forces?

A

Explains the movement of fluid that occurs at every capillary bed
Two major opposing forces:
- hydrostatic pressure (generated by fluid in the capillary)
- osmotic pressure (includes oncotic pressure)
– in each capillary, the blood contains the electrolytes and proteins which exert osmotic pressure

Oppose each other to balance each other out and lead to homeostasis

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17
Q

What is the lymphatic system responsible for in the regulation of fluid and electrolytes?

A

Accessory system which returns small proteins and fluid from the interstitial space back into the general circulation
- helps to keep pressures relatively constant

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18
Q

What is the renal system responsible for in the regulation of fluid and electrolytes?

A

kidneys regulate concentrations of most substances in the body by filtering plasma and then reabsorbing needed substances back into the vascular system

what we don’t need is excreted

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19
Q

What is osmolality?

A

concentration of solutes per kg of solvent
– based on 1 mole dissolved in 1 kg of water

  • evaluate hydration based on concentration of fluids to particles
    – normal is 282-295 milliosmoles/kg of water
    – low means few particles in solutions (lower than normal means well hydrated)
    – high means less solution to particles (higher normal means dehydrated)
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20
Q

What is osmolarity?

A

Number of osmoles of solutes in 1 liter of solution

Solutes:
- albumin
- sodium: major ECF fluid balance
- potassium: major ICF neuromuscular excitability and acid-base
- PO4: ICF negative anion
- magnesium: enzyme systems; stored in bone
- calcium: neuromuscular irritability, blood clotting, bones
- HCO3: acid-base
- glucose

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21
Q

What is tonicity?

A

Concentration (amount) of solutes in solution compared with the bloodstream

Also used to describe 3 types of IV solutions:
- isotonic
- hypertonic
- hypotonic

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22
Q

What is an isotonic IV solution?

A

Same tonicity as blood
- no fluid shifts and no change in cell size
- standard is 0.9% NSS
- volume expander and to maintain access

Ex: 0.9% NSS, LR

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23
Q

What is a hypertonic IV solution?

A

Higher concentration than the blood
- water moves from area of lower to higher solute concentration
- monitor for fluid overload; but used to treat hypovolemia and replace fluid and electrolytes
- don’t want to dehydrate cells (water moves from cells into ECF)

Ex: 5% dextrose in 0.9% NS, 5% dextrose in LR

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24
Q

What is a hypotonic IV solution?

A

Lower concentration than the blood
- water moves from lower concentration to higher solute concentration
- administer slowly to prevent cellular edema (causes cells to swell)
- used for dehydration

Ex: 0.45% NSS

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25
Q

What is the role of kidneys in maintaining fluid and electrolyte balance?

A
  • removal of waste
  • regulation of blood pressure
  • regulation of electrolytes
  • acid-base balance
  • reabsorption of amino acids, glucose, and water
  • RBC, hormone, and enzyme production
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26
Q

Kidney: Routes of gains and losses

A
  • daily urine volume of fluid in adults is typically 1.5L
  • output is approx 0.1-1 mL of urine per kg of body weight per house
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27
Q

Skin: routes of gains and losses

A
  • sensible perspiration
  • chief solutes of sweat are sodium, chloride, and potassium
  • sweat loss varies from 0-1000mL or more every hour
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28
Q

Lungs: routes of gains and losses

A
  • water vapor (insensible loss) is about 400mL per day
  • amount is increased with increased respiratory rate and depth; or dry climate
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29
Q

GI Tract: routes of gains and losses

A
  • fluid loss via GI tract is about 100mL per day even though about 8L circulates through daily
  • bulk of fluid is reabsorbed
  • need certain amount of fluid for a bowel movement
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30
Q

What is insensible fluid loss and what are examples?

A

Can not be measure
Ex: fever, skin, respirations

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31
Q

What is sensible fluid loss and what are examples?

A

Can be measured

Examples:
- urine
- feces
- wound/surgical drains
- NGT
- emesis

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32
Q

What is hypovolemia (fluid volume deficit)

A
  • loss of extracellular fluid
  • decrease in tissue perfusion
  • can be loss of sodium and water
    – hemorrhage
    – vomiting
    – diarrhea
    – CHF
    – drains
    – poor PO intake
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33
Q

What is dehydration?

A

Loss of water
- without equal loss of sodium
- decrease in size of body cells
- results in hypovolemia and hypernatremia

  • monitor I/O and weight
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34
Q

What happens when volume is low?

A
  • thirst reflex (in hypothalamus; decreases as we age)
  • ADH: antidiuretic hormone
    – kidneys
    – stops excretion and reabsorbs water
    – helps maintain osmotic pressure
  • RAAS (renin-angiotensin-aldosterone system)
    – when activated, increases blood volume and increases blood pressure
  • SNS (sympathetic nervous system)
    – increases HR
    – leads to vasoconstriction
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35
Q

Examples of fluid overload

A
  • edema
  • pulmonary edema
  • edema from low albumin
  • other causes
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36
Q

What is edema and causes?

A
  • develops when there is excess fluid in the interstitial space and intracellular fluid

Caused by:
- increased hydrostatic pressure in the blood
- OR by osmotic pressure being low (low amount of solutes in the blood)

Can occur in the inflammatory response because of increased vascular permeability allowing fluid to get into the tissues

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37
Q

What is pulmonary edema?

A

Increase in the volume in the blood
- backs up into the pulmonary circulation
– leads to respiratory distress, lungs can’t expand fully, impaired gas exchange
- increases in the hydrostatic pressure (pressure of water) forces the blood out into the alveolar spaces

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38
Q

What is edema from low albumin?

A
  • oncotic pressure should equal hydrostatic pressure
  • when oncotic pressure is low, hydrostatic pressure increases
    – albumin is allowed to leak from the ECF to the ISF and ICF, edema can occur

occurs from low albumin:
- malnutrition
- renal disease

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39
Q

What is dependent edema?

A
  • occurs from venous disease
  • standing and compromised circulation, blood pools in legs
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40
Q

Sodium intake and fluid overload

A
  • causes pulling of fluid from the cells into the ECF
  • cells begin to shrink
  • stimulates the thirst reflex in healthy patients
  • stimulates RAAS
  • increased hydrostatic pressure overwhelms the osmotic pressure
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41
Q

What are natriuretic peptides?

A

Compensatory mechanism for intravascular changes
- natriuresis

Four types:
- Atrial (ANP)
- Brain (BNP)
- C-type (CNP)
- DNP

BNP and ANP: promote natriuresis at the glomerulus by increasing GFR

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42
Q

What is natriuresis?

A

Excretion of sodium and water by the kidneys as a response to ECF overload

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43
Q

What is the function of electrolytes?

A

Neuromuscular balance (Na, Mg, K, Ca):
- mentation, muscles, cardiac rhythm, GI motility

Enhance energy utilization (Na, K, Phos):
- sodium-potassium pump
- removal of wastes
- enhance growth and repair

Regulation of fluid balance (Na, Cl)
- encourage or diminish fluid shifts

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44
Q

What happens with electrolyte imbalances?

A

alterations affect many functions
- muscle contraction
- nerve transmission

45
Q

Action potentials

A

Action potentials are triggered by changes in sodium and potassium ions
- sodium goes into the cell, potassium leaves the cell
- the positive ions of sodium cause depolarization
– sodium closes at the peak of the action potential
- potassium continues to leave the cell

46
Q

What is sodium?

A

Main extracellular electrolyte in blood
Normal serum level: 135-145 Meq/L

  • maintains the cell membrane potential (important for cellular communication and muscle contraction)
  • maintains fluid balance of blood
  • maintain osmolality of blood
  • can move from ECF to ICF
47
Q

What is the pathophysiology of hyponatremia?

A

less than 135 meq/L
can be caused by overhydration or body losses of salt water take is replaced by just watere

48
Q

Etiologies of hyponatremia

A
  • due to decrease blood volume (non-renal): vomiting, diarrhea, excessive sweating, burns, NGT suctioning, diuretics
  • due to increased or normal blood volume: SIADH, CHF, hypotonic IV fluid, cirrhosis, excessive fluid intake, diarrhea, hyperglycemia
  • causes a hypo-osmolality
49
Q

What are the clinical manifestations of hyponatremia?

A
  • depend on cause, magnitude, and speed of deficit
  • hypovolemia:
    – thirst, dry mouth, orthostatic BP, tachycardia, renal insufficiency
  • dilutional hyponatremia:
    – N/V, headache, confusion, muscle weakness, cramps and spasms

Severe (sodium <115 meq/L):
- neurologic: altered mental status, lethargy, seizures, coma

50
Q

Medical and nursing management for hyponatremia

A
  • treat underlying cause
  • volume replacement
    – can’t go too fast or will cause brain to swell
    – sodium replacement (PO or IV)
    – LR or isotonic saline (0.9%)
  • dilutional hyponatremia:
    – water restriction (SIADH)
    – diuretics (loop; prevent fluid overload)
    — not thiazide b/c can worsen hyponatremia
  • monitor I/O, weight, GI, and neurological status
51
Q

Pathophysiology of hypernatremia

A

Sodium level greater than 145 meq/L
- occurs when there is a gain of sodium in exces of water
– or by loss of water in excess to sodium
- can occur in euvoluemic patients or existing fluid volume depletion or excess

Common causes: inadequate fluid intake, diabetes, hypertonic fluid or feeding administration, excessive use of sodium bicarbonate

52
Q

Clinical manifestations of hypernatremia

A
  • primarily neurologic symptoms: disorientation, delusions, hallucinations, fatigue, irritability, behavioral changes
  • thirst
  • specific gravity and osmolarity are increased (urinary test)
53
Q

More clinical manifestations for hypernatremia

A
  • if kidneys are damaged: ADH issue causing kidneys not to reabsorb water
  • too much sodium
  • low volume cause stimulation of aldosterone causing reabsorption of water
    – cells become dehydrated
    – respond by transporting electrolytes across cell membrane and alter action potential
    – body tries to fix by making more solutes so need to be careful not to hydrate too quickly or brain will swell
    – shrunken neurons do not work as well because of altered action potential and CNS symptoms are the issue
54
Q

Medical and nursing management for hypernatremia

A
  • treat underlying cause
  • use of hypotonic solution OR a non-isotonic solution (D5W or .45%NaCl)
  • diuretics
  • be aware of food and medications high in sodium
  • monitor neurologic status
  • monitor I/O
55
Q

What is potassium?

A

Major intracellular electrolyte
Normal level: 3.5-5.5 meq/L

  • transported into cells via sodium-potassium pump
  • moves from ICF to ECF (can be affected by insulin, pH, epinephrine)
  • kidneys are primary regulator
  • bulk is in the muscle
    – changes in concentration has neuromuscular effects
56
Q

What does potassium play a role in?

A
  • nerve impulses in cardiac, smooth, and skeletal muscle
  • acid-base
  • ATP synthesis
  • osmotic balance
  • urine concentration
57
Q

What is the pathophysiology of hypokalemia?

A

Level less than 3.5 meq/L

Caused by: diuretics!, vomiting, diarrhea, sweating, CHF, NGT suctioning, cirrhosis, GI suctioning, ileostomy, decreased PO intake, metabolic alkalosis, DKA, hypomagnesemia

58
Q

What are the clinical manifestations of hypokalemia?

A
  • typically do not occur until level is below 3.0
  • symptoms include:
    – decreased bowel sounds
    – fatigue
    – anorexia
    – N/V
    – muscle weakness
    – leg cramps
    – decreased bowel motility
    – arrhythmias
59
Q

What is the medical and nursing management for hypokalemia?

A
  • treat underlying cause
  • increase PO intake of potassium
  • IV replacement
    – never give IV push
    – very irritating to veins
    – infuse slowly
  • correct magnesium deficit
  • monitor I/O
  • monitor CV and GI status

ideally need a 2nd nurse to check before giving IV replacement because can cause cardiac or respiratory arrest

60
Q

What is the pathophysiology of hyperkalemia?

A

Level more than 5.5 meq/L

Caused by: increased intake, certain medications, cell injuries, intravascular hemolysis, insulin deficiency, DKA, renal disease, metabolic acidosis

61
Q

What are the clinical manifestations of hyperkalemia?

A
  • typically do not occur until level above 6.5, but may be sooner
  • symptoms include:
    – fatigue
    – N/V
    – colic
    – weakness
    – ventricular arrythmias
    – cardiac arrest
    – metabolic acidosis
62
Q

What is the medical and nursing management for hyperkalemia?

A
  • decrease PO intake of potassium
  • restrict potassium-sparing medications
  • administration of kayexalate or patiromer (laxative)
  • emergency therapy:
    – IV calcium gluconate, insulin, sodium bicarbonate, hypertonic dextrose solution, beta-2 agonist
  • dialysis (more common in renal impairment)
  • monitor I/O
  • monitor CV, GI, and renal status
63
Q

Effects of hyperkalemia on heart (sorry i drew on this in class)

A
64
Q

What are foods high in potassium?

A
  • many fruits and veggies
  • beans and legumes
  • whole-grain bread
  • meat
  • fish
  • oranges/orange juice
  • milk
  • eggs
  • coffee/tea
  • cocoa
65
Q

What is acid-base?

A

Acid: substance which donates H+ to a base
- HCl, nitric acid, acetic acid
Base: substance which accepts or binds H+
- ammonia, bicarbonate (HCO3)

pH reflects the overall H+ concentration in body fluids
- low concentration H+ ions: increases pH
- high concentration H+ ions: decreases pH

66
Q

What is the normal pH range?

A

7.35-7.45

67
Q

What do abnormal processes cause with acid-base balance?

A
  • the blood to become more acidic (acidosis)
  • the blood to become more alkaline (alkalosis)

Can be metabolic or respiratory

68
Q

What is acid-base regulated by?

A
  • lungs
  • kidneys
  • buffer systems
    – bicarbonate/carbonic acid system
    – buffers up to 90% of hydrogen ions in ECF
69
Q

What is the carbonic acid buffering system?

A

Is working all the time to maintain acid base balance
- carbonic acid has reversible dissociation and releases bicarbonate ions and hydrogen
– response to increase in pH
– response to increase in pH

Used by lungs and kidneys to compensate for changes in pH

70
Q

The respiratory system and acid-base

A
  • regulates Co2 in the blood by combining with H20, making carbonic acid
  • immediate response but temporary
  • receptors in the brain sense changes in the pH and vary the rate/depth of respiration to regulate CO2 level
    – faster deep breathing: eliminates CO2 from lungs, pulls H+ from the blood and reduces acid pH increases
    – slower shallow breathing: retention of CO2, increases acid in blood so pH decreases
71
Q

What does the renal system do in acid-base?

A
  • adjust the amount of HCO3- that is reabsorbed or excreted in the urine
  • kidneys produce HCO3 and eliminates H+ ions

Decreased pH: kidneys reabsorb HCO3- and excrete H+
Increased pH: excrete HCO3- and retain H+

takes at least 24 hours to take effect

72
Q

What is compensation?

A

the process by which the lungs and kidneys attempt to adjust to pH disturbances

73
Q

Potassium and hydrogen

A
  • both are positively charged and move freely in and out of cell
  • when H+ is high (acidosis) in the blood (ECF), it trades hydrogen for potassium in the cell (ICF)
    – potassium goes to blood causing hyperkalemia
  • when H+ is low (alkalosis) in the blood (ECF), it trades potassium for H+
    – leads to more H+ in the blood, causing hypokalemia
  • potassium shifts are more pronounced in acidosis than alkalosis
  • greater in metabolic than respiratory
74
Q

What is metabolic acidosis?

A
  • excess acid production OR loss of HCO3-
  • occur when the cellular metabolism rate increases
    – increased production of acids
    – decreased excretion of acids
    – loss of HCO3
  • will see an initial respiratory compensation

Low pH (<7.35) and low HCO3- (<22)

potassium will increase by 0.5 mew for every 0.1 drop in pH
- cardiac arrythmias are common
- hypotension
- insulin will not work as well
- decreased ATP

75
Q

Potassium change in relation to metabolic acidosis

A

potassium will increase by 0.5 mew for every 0.1 drop in pH
- cardiac arrythmias are common
- hypotension
- insulin will not work as well
- decreased ATP

76
Q

How to recognize metabolic acidosis on labs?

A

Low pH (<7.35) and low HCO3- (<22)

77
Q

Possible causes of metabolic acidosis (from image)

A
  • ketoacidosis (diabetics)
  • shock
  • severe diarrhea
  • impaired kidney function (esp. seen in end-stage renal disease)
78
Q

Warning signs and symptoms of metabolic acidosis

A
  • headache
  • lethargy
  • anorexia
  • deep, rapid respirations (Kussmaul)
  • nausea
  • diarrhea
  • abdominal discomfort (in severe acidosis)
  • coma and dangerous dysrhythmias)

Watch potassium level, it will go up

79
Q

Causes of metabolic acidosis according to lecture

A

Anything that causes increased acid and decreased bicarbonate
- anaerobic metabolism (cardiac arrest, severe hypoxemia, ischemia)
- ketoacidosis
- renal failure (unable to regulate bicarbonate)
- salicylate (ASA) intoxication
- severe sepsis
- starvation
- TPN (hyperalimentation)
- diarrhea (loss of bicarb)
- fistulas (loss of bicarb)
- liver failure (not able to make bicarbonate)

80
Q

Compensation and treatment for metabolic acidosis

A
  • will see immediate respiratory changes like Kussmaul
  • will see hyperkalemia which could become hypokalemia as treatment begins
  • correct underlying metabolic defect:
    – fix hypoxemia
    – restore fluid balance
    – bicarbonate
    – alkalizing agent
    – stop ketosis
    – manage chronic disease
    – treat infection/sepsis
81
Q

What is metabolic alkalosis?

A

Caused by excessive loss of acids
Most common acid-base disturbance occurring in hospitalized patients
- usually kidneys and GI tract are affected and easy to lose H+ ions when there is dysfunction
- loss of gastric secretions in severe vomiting or NGT suctioning
- occurs in hypokalemia (diuretic therapy, hyperaldosteronism Cushing’s disease)

High pH (>7.45) and High HCO3- (>36)

82
Q

What are the lab values to recognize metabolic alkalosis?

A

High pH (>7.45) and High HCO3- (>36)

83
Q

What are the causes of metabolic alkalosis?

A

Loss of acids:
- nasogastric suction
- hypokalemia
- hypochloremia
- loop or thiazide diuretics
- steroids
- uncontrolled vomiting
Increase in HCO3-:
- excessive ingestion of antacids
- excessive use of bicarbonate
- lactate administration in dialysate

84
Q

Warning signs and symptoms of metabolic alkalosis

A
  • cardiac dysrhythmias as a result of dropping potassium
  • physical weakness
  • muscle cramping
  • hyperactive reflexes
  • tetany because of decreased calcium
  • convulsions
  • confusion

hydrogen, calcium and potassium all drop

85
Q

Treatment for metabolic alkalosis

A
  • treat underlying cause
  • restore fluid volume
  • fix electrolyte imbalance
    – replace potassium
86
Q

What is respiratory acidosis?

A

Pulmonary ventilation decreases and CO2 is retained; CO2 combines with H2O to increase carbonic acid
- excessive carbonic acid causes drop in pH
- respiratory rate stimulated by medulla to increase to rid CO2
- increase CO2 and H_ ions causes cerebral vessels to dilate and leads to cerebral edema and depressed CNS activity

High PCO2 causes kidneys to hold onto HCO3 (probably the compensatory action)

Low pH (<7.35) and High PCO2 (>45)

87
Q

What are the lab values to recognize respiratory acidosis?

A

Low pH (<7.35) and High PCO2 (>45)

88
Q

What are clinical manifestations of respiratory acidosis?

A
  • sudden hypercapnia (elevated PaCO2)
  • symptoms: increased HR and RR, mental cloudiness, headache, weakness, cyanosis, arrhythmias
89
Q

Causes of respiratory acidosis from image

A
  • over sedation
  • brainstem trauma
  • immobility
  • respiratory muscle paralysis
  • pneumonia
  • emphysema
  • bronchitis
  • COPD
90
Q

Medical or nursing treatment for respiratory acidosis

A
  • correct underlying cause
  • bronchodilators
  • fluid hydration
  • oxygen
  • mechanical ventilation (worst case)
91
Q

Causes of respiratory acidosis from powerpoint

A

anything that causes hypoventilation and a rise in CO2 levels (hypercapnia)
- acute pulmonary edema
- CNS depression
- chronic respiratory disease
- disorders of respiratory muscles and chest wall inadequate mechanical ventilation
- oversedation (OD)
- severe pulmonary infections like pneumonia or COVID

92
Q

Physical exam of respiratory acidosis

A
  • respiratory distress, accessory muscle use, high RR, barrel chest, changes in LOC
  • hyperresonance on percussion
  • lung sounds may have wheezing, crackles or rhonchi
  • increased HR and RR
93
Q

Compensation for respiratory acidosis

A
  • kidneys reabsorb HCO3 and excrete H+

those with chronic high CO2 (like in COPD) have normal pH often b/c of kidneys compensating but is very fragile

94
Q

Treatment for respiratory acidosis

A
  • improve ventilation

fix the problem:
- bronchodilators
- oxygen
- steroids
- sedative
- antibiotics
- diuretics
- naloxone (narcan)
- mechanical ventilation

95
Q

What is respiratory alkalosis?

A

Ventilation increases above what is needed to maintain normal CO2 levels

Excessive amounts of CO2 are exhaled (hypocapnia):
- causes reduction in carbonic acid
- loss of H+ and increased bicarbonate ions
- leads to increased pH
- body compensates by pulling HCO3 into the blood which converts to carbonic acid to lower pH

high pH (>7.45) and low PCO2 (<35)

96
Q

What are the lab values to recognize respiratory alkalosis?

A

high pH (>7.45) and low PCO2 (<35)

97
Q

Effects of hypocapnia

A

Stimulates carotid/aortic bodies; leads to increased HR

Cerebral vasoconstriction leads to blood flow
- causes anxiety, diaphoresis, tingling in fingers, toes and around mouth
- hyperventilation: overexcitation of medulla and pons
- may experience anxiety, irritability
- can have changes in potassium and calcium
– reduced blood level
– as H+ moves out of blood, potassium moves back into cell
– leads to palpitations, dysrhythmias, seizures

98
Q

Causes of respiratory alkalosis

A

Anything that causes hyperventilation or decreased PCO2 (hypocapnia)
- anxiety
- early sepsis
- excessive mechanical ventilation (rate is too high)
- exercise
- fear
- hypermetabolic states like fever
- hypoxemia
- liver failure
- pain

99
Q

Compensation for respiratory alkalosis

A

If symptoms continue for over 6 hours:
- kidneys increase excretion of HCO3
- reduce excretion of H+ and pH begins to fall

100
Q

Treatment of respiratory alkalosis

A
  • treat underlying cause
  • SLOW THE BREATHING
    – reduce anxiety
    – sedation
    – oxygen
    – breathe into paper bag
    – lower fever
101
Q

Chart for resp/met alk/ac

A
102
Q

Respiratory compensation for acid-base imbalances and medical interventions: chart

A
103
Q

Renal compensation in acid-base imbalances and medical intervention: chart

A
104
Q

PH OF 7.25, CO2 OF 60MM HG, AND HCO3 22: what is this showing

A

respiratory acidosis

105
Q

PH OF 7.5, CO2 OF 45MM HG, AND HCO3 40: what is this showing

A

metabolic alkalosis

106
Q

PH OF 7.4, CO2 OF 40MM HG, AND HCO3 25: what is this showing

A

normal

107
Q

PH OF 7.25, CO2 OF 50MM HG, AND HCO3 22: what is this showing

A

respiratory acidosis

108
Q

PH OF 7.55, CO2 OF 24MM HG, AND HCO3 22: what is this showing

A

respiratory alkalosis

NUR 516 (6 decks)

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