Acid/Base Flashcards

1
Q

Allen’s test

A

before an arterial blood gas test, looks at indicators for acid/base imbalance

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2
Q

Hydrogen Ions (H+)

A

vital to life

expressed as pH

pH of 7 is neutral, small is acidic

low concentration in body

circulate as carbonic acid (H2CO3) = (CO2+H2O) (fixed)
(governed by lungs)

circulate has nonvolatile for of hydrogen and organic acids (governed by kidneys)

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3
Q

Acids

A

Produced as end products of metabolism

create muscle aches (build up of lactic acid - anaerobic glycolysis)

Contain H+ ions (lower pH scale)

Strength of acid determined by # of H+ ions

Fewer H+ = weaker acid, or form weak base

Lungs to bulk of work in acid /base balance, kidneys fine tune

RR increase, removal of metabolic acids (CO2)

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4
Q

Bases

A

Contain NO H+ ions at all, but they accept H+ ions from acids: will neutralize or decrease strength of the base or form weak acid

HCO3- Bicarb is most important base

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5
Q

pH and Acids in the blood

A

Blood pH 7.34-7.45

reflects H+ ion concentration, greater concentration, the lower the pH, the more acidic the blood

the lower the H+ the higher the pH and the more alkalotic the blood

Acids form from metabolic activity (Duh)

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6
Q

Regulation on Blood pH: Blood Buffers

A

Buffer: A weak acid/base that can combine with strong acid/base to minimize changes in pH

goal: to try and fix what the body sense is wrong, keep blood pH in normal range

MAJOR buffer systems:
(Intracellular)
-Potassium-Hydrogen ion exchange (in and out of cell)

/\ H+ > H+ moves into cells & K+ moves out
\/ H+ > H+ moves out of cells & K+ moves in

(Extracellular)
Protein buffers, hgb (80%)
Albumin and plasma globulins (20%)

Bicarbonate buffer: most important

phosphate buffer: 2nd most

bone buffer

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7
Q

Buffers: Regulatory systems for H+ concentration in blood

A

Fast acting

immediate protection against changes in H+ ion concentration

Function to keep pH within narrow limits of stability

Absorb or release H+ as needed

transport to carry H+ ions to lungs

Once primary buffer systems react, they are consumed, body less able to manage correcting pH in blood. so MORE stress, less of ability to compensate.

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8
Q

Intracellular buffer system: Potassium

A

Alkalosis: cells release H+ ions into blood to increase acidity of blood and combat alkalosis. K moving into cell and the K level goes down

Blood: HIGH H+, HIGH pH

End result: Normal pH (bc HIGH H+) but low serum K level

Acidosis: body protects itself from acid state by moving H+ ions into the cell and K moves out to make room for H+ ions. H+ and the K level goes up

Blood: HIGH H+ and LOW pH

End Result: LOW H+ , Normal pH, HIGH serum K

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9
Q

Major buffer systems: Extracellular Fluid

A

Hemoglobin System* (80% of extracellular buffer system)

  • in RBCs
  • maintains acid/base balance
  • Chloride exchange with Bicarbonate*** in response to level of O2 in the blood

for each Chloride ion that leave, a Bicarb enters and visa versa

Anion exchange for Anion

Low pH, more acidic: Bicarb OUT, Cl IN = low serum chloride aka HYPOCHLOREMIA

High pH, more basic: Bicarb IN, Cl OUT = high serum chloride aka HYPERCHLOREMIA

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10
Q

Plasma Proteins system and Calcium example

A

Albumin/ Globulins - responsible for wound healing, oncotic pressure

functions with LIVER (made in liver) can vary H+ ions in protein

ex: Total calcium, unbound calcium, bound calcium

UNBOUND = Ionized calcium (metabolic active) can give s/s but bound cannot give s/s bc not metabolic active

Low Ca is lower threshold for firing nerves, tingling

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11
Q

Phosphate buffer system

A

Present in cells and body fluids

especially active in kidneys

(acts like bicarb) clears spare H+ Ions in order to bring pH to normal range

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12
Q

Major Buffer system: Carbonic acid / Bicarbonate system

A

Carbonic acid: IN THE LUNGS

its the only acid the lungs can breathe out (Co2) and water (H20)

Bicarbonate system: KIDNEYS

whole system maintains pH of 7.4 with

20:1 ratio
bicarb:carbonic acid

(when ratio out of sync - buffer systems kick in)

Carbonic acid concentration controlled by excretion of Co2 by lungs, RR will change to control this

Bicarbonate concentration selectively retain or secrete bicarb in response to body needs

DKA - produces ketoacids, deplete bicarb and make more carboinc acid, this increases RR and give kusmal respirations

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13
Q

Carbonic Anhydrase

A

Carbonic acid dissociates with help of enzyme Carbonic Anhydrase

HIGH acid: HIGH RR and Depth

BASE: LOW RR and low depth

Carbonic acid is volatile bc it is in gas form (continual buffer regulation required in lungs)

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14
Q

Lungs

A

2nd defense (1st blood buffer) with respirations and depth rate

Alkalosis: pH goes up, and RR and depth go DOWN, to neutralize excess bicarb

in Acidosis: pH goes down and RR and depth go UP to blow off acids

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15
Q

Activation of Lungs

A

reversible in controlling excess or deficit

take 10-30 seconds to occur (really fast)

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16
Q

Kidneys

A

Final correction of Acid/Base disturbances. Rental excretion of acids and alkali occur more slowly

takes hours or days

in acidosis: pH goes down and excess H+ secreted into tubules and combine with buffers for excretion in urine

in alkaosis: pH is UP and bicarb ions move into tubules combine with Na and are excreted into urine

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17
Q

Renal excretion of Acid

A

selective regulation of bicarb in kidneys: 3 ways

  • kidney restore bicarb by release of H+ ion and holding bicarb
  • extra H+ ions excreted in urine AS phosphoric acid
  • alteration of amino acids in renal tubules, and diffuses into ammonia and is excreted in urine

takes HOURS to DAYS

end result is fine tuning we need

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18
Q

Ratio of buffer system

A

Fixed ratio of HCO3 (base) to H2CO3 (acid) 20:1

increase base: 30:1
result: HIGH blood pH, alkalosis

decrease base: 13:1
result: LOW blood pH, acidosis

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19
Q

BMP*

A

Basic Metabolic Panel

**CO2 from VENOUS blood is actually a measure of HCO3 (Bicarb) **

High value = alkalosis
low value = acidosis

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20
Q

Metabolic Acidosis

A

Total concentration of buffer base is lower than normal with a relative increase in H+ concentration

occurs as a result of losing too many bases and holding too many acids without sufficient bases

lose base with severe diarrhea

gain acid with DKA

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21
Q

Causes: Metabolic Acidocis

A

DKA (#1 reason) - can be life threatening. Not enough insulin, glucose builds up in system (not in cell) so cell function goes to fat metabolism, ketones build up, makes person acidotic. Bicarb becomes exhausted, increase RR and depth

Renal insufficiency/ Failure:
results from the inability of kidneys to metabolize proteins and remove acids as a result of protein metabolism. Bicarb cannot sustain. PT needs to be on dialysis.

Carbohydrates: not enough O2 for proper burning of Carbs, glucose and water. Lactic acid builds up, lactic acid acidosis

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22
Q

Causes: Metabolic Acidocis Pt II

A

Excessive ingestion of Aspirin:
causes increase in H+ concentration

Severe Diarrhea: loss of base leads to acidosis.

Malnutrition: improper nutrients causes fat catabolism leading to build of up ketones and acids

High Fat diet: too much rapid accumulation of waste products leading to ketone and acids (Ex: Atkins Diet)

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23
Q

Anion Gap

A

Lab that describes concentration of unmeasured anions

only look at for metabolic acidosis. Do they have too much acid or loss of base

elevation results from accumulation of acids (unmeasured anions of acids)

LOW AG result from:
Low in unmeasured anion or
High in unmeasured cation

24
Q

High Anion gap vs Low Anion Gap

only applicable with acidosis

A
HIGH:
high acids
excessive production of metabolic acids
-DKA, starvation, Alcoholic intoxication
-Aspirin poisoning , rental Failure
NORMAL: 
low bicarb, low base
loss of intestinal secretions
diarrhea, pancreatic fistulas
- renal losses, tubular acidosis
-HYPOaldosteronism 
-increased CL levels
25
Q

Assessment of metabolic acidosis

A

In attempt to blow off extra CO2 and compensate for acidosis, hyperpnea and Kussmaul respirations (high RR and depth)

headache, vomiting, diarrhea, fruity smelling breath, twitching, mental dullness**, drowsiness, stupor, coma, convulsions

26
Q

Manifestations of metabolic acidosis

A

Neutral:
weakness, lethargy, malaise, confusion, stupor, coma

cardio:
decrease HR, dysrhythmias, vasodilation

GI:
Anorexia, abdominal pain

Skeletal:
Bone disease

Skin:
Flushed warm dry

COMPENSATION:
RR and depth INCREASE (Kussmaul)

Hyperkalemia

Acid Urine: increase in ammonium in urine

27
Q

intervention of metabolic acidosis

A

determine cause

maintain airway

asses LOC for CNS depression

Monitor electrolytes

maintain I&O, assist with fluids

safety for confusion and coma

administer IV, isotonic saline, 5% dextrose ect

monitor K carefully

28
Q

intervention of metabolic acidosis PT II

A

In DKA - GIK mechanism - insulin given so K can go into cell with K. Decreases ketoacidosis

monitor for circulatory collapse, moving lots of fluids. make sure they have enough fluid to maintain BP

in Renal failure:

dialysis may be sued to remove protein and waste products.

maintain better diet to lessen acidosis.

29
Q

metabolic acidosis treatment

A

monitor patients at risk (DM, sepsis, shock)

monitor BP and RR
monitor ABGs
Monitor K+ levels
Administer sodium bicarbonate
cardiac monitor for low serum K+ levels

correct underlying cause of acidosis

administer IV fluids with lactase

for lactic acidosis: IV fluids and O2

for renal fluid, drug OD or poisoning: Dialysis

Chronic: Increase Carbs and decrease Fat

30
Q

Metabolic Alkalosis

A

Kidneys

deficit of carbonic acid and decrease in hydrogen ion concentration

results from accumulation base or loss of acid without a comparable loss of base in body fluids

pH>7.45

31
Q

Metabolic Alkalosis Causes

A

Malfunction of metabolism, leading to increased amount of basic solution in the blood and decrease in available acids in blood

Can happen with:
Ingestion of excess sodium bicarbonate (more base in blood)

THAT LEADS TO

Excessive vomiting (leads to loss of acids)

32
Q

Metabolic Alkalosis Causes Pt. II

A

Also gastrointestinal suctioning: most common cause IN HOSPITALS

Diuretics - wash out Hydrogen and potassium ions. Increases Bicarb

Hyperaldosteronism - increases tubular sodium reabsorption, Hydrogen ions leave

Massive blood transfusion - Citrate anticoagulant used for storage of blood is metabolized to bicarb

33
Q

Metabolic Alkalosis Etiologies

A

Excess gain on bicarb (alka-seltzer)

TPN - for ppl who cannot maintain nutritional status orally. Has acetate, not good

solutions with lactate, or citrate

NaHCO3 in CPR

Loss of acid, increased bicarb

vomiting, bulimia
potassium deficit

volume contraction (loss of fluids, diuretic therapy)

mechanical ventilation, respiratory acidosis

34
Q

Metabolic Alkalosis Assessment

A

In an attempt to compensate, RR and depth go down to conserve CO2

nausea
vomiting
diarrhea
numbness and tingling
restlessness and twitching
hypokalemia
hypocalcemia
sinus tachycardia
dysrhythmias
35
Q

Metabolic Alkalosis Manifestation

A

Neural: association with hypocalcemia

confusion
convulsion
paraesthesia

Cardio:
hypotension
dysrhythmias

Compensation:
RR and depth decrease
urine ph increase

36
Q

Metabolic Alkalosis Treatment

A

Monitor patients at risk (GI fluid loss)

Monitor Vs (respiration rate and depth)

correct underlying cause

supply Cl to enable renal reabsorption of NaCl

MONITOR CARDIAC for hypocalcemia

Teach: new method for indigestion

37
Q

Respiratory Acidosis

A

lower pH and High PaCO2

Too much acid, too little base

total concentration of buffer base is lower than normal, but increased Hydrogen concentration

due to defective function in the lungs or changes in normal respiratory patterns due to secondary problems

anything that obstructs airway can cause respiratory acidosis

38
Q

Respiratory Acidosis Causes

A

Hypoventilation - not breathing effectively (ex. drug OD)

Co2 is retained and H ions increase leading to acid state. carbonic acid is retained and Ph goes down

can cause infection dude to inflammation and bacterial agents. Airways can become obstructed

meds:
sedatives, narcotics, anesthetics depress respiratory center lead to hypoventilation

39
Q

Respiratory Acidosis Causes pt II

A

Pneumonia - secretions obstruct airway passages, limits gas exchange (common cause)

Atelectasis - excessive mucus production , infection drainage, collapse of alveolar sacs, decreased respiration

Brain trauma - too much pressure of respiratory center of brain

emphysema - part of COPD, loss of avelolar sacs, more energy to breathe in and out, increased Co2

Asthma, Bronchitis, Pulmonary Edema, Bronchiectasis

40
Q

Respiratory Acidosis Etiologies

A
Acute** VERY TROUBLESOME
lung disease
acute pulmonary edema
aspiration
atelectasis
pneumothorax
pneumonia
depression of respiration center
narcotic OD
head injury
Chronic conditions:
Chronic bronchitis 
Asthma
cystic fibrosis
COPD
Chest wall and respiratory muscles:
Obesity
post op pain
abdominal ro thoracic incisions
Abdominal distention (bowel obstruction)
41
Q

Respiratory Acidosis Assessment

A
in attempt to compensate, RR and depth increase**
headache
mental status change
confusion
drowsiness
restless
visual disturbances 
diaphoresis
cyanosis
hyperkalemia
rapid and irregular pulse, dysrhythmias
42
Q

Respiratory Acidosis Manifestations

A
Neural:
Dilation of cerebral vessels
fullhead
headache
behavior changes
confusion
depression
paranoia
tremors
paralysis
stupor 
coma

SKIN: warm and flushed
Head is tachy
Respiratory: dyspnea and cyanosis

Compensation:
Acid Urine

43
Q

Respiratory Acidosis Interventions

A
Maintain airway
improve ventilation 
administer o2
semi-fowlers
turn, cough, breath deep
hydrate
suction if necessary
TCDB - turn cough deep breath

NEVER USE SEDATIVE

44
Q

Respiratory Alkalosis

A

pH is high, Co2 is low

(hyperventilation - panic attack)

deficit of carbonic acid and decrease in hydrogen ion concentration

results from accumulation of base or from loss of acid without a comparable loss of base in the body fluids

45
Q

Respiratory Alkalosis Cause

A

conditions that cause over stimulation of respiratory system

(hyperventilation - panic attack)
blowing off too much co2

Hysteria - often neurogenic in nature, can lead to vigorous breathing

Over ventilation by mechanical ventilators ( ventilated TOO quickly)

46
Q

Respiratory Alkalosis Causes Pt II

A

condition that increase metabolism

Pain or brain trauma

Salicylates - aspirin poisoning , causes hyperventilation

Hypoxia - causes respiratory stimulation with result of carbonic acid deficit

47
Q

Respiratory Alkalosis Etiologies

A
Excessive ventilation
anxiety
hypoxemia
high fever
Excessive mechanical vent
(same as causes)

Pregnancy (increased sensitivity to Co2)

48
Q

Respiratory Alkalosis assessment

A

initial hyperventilation and respiratory stimulation will cause abnormal rapid respiration***RR and depth go down to compensate

headache
Mental status changes
vertigo
lightheaded
paresthesias
hypokalemia
hypocalcemia
tetany
convulsions
49
Q

Respiratory Alkalosis Manifestations

A
cerebral vasoconstriction
(head fog)

neuromuscular irritability

  • hypocalcemia
  • electrolyte imbalances

cardio: dysrhythmias

hyperventilation

GI epigastric pain

50
Q

Respiratory Alkalosis

A
manage anxiety 
maintain airway
control breathing
rebreather mask
monitor 
monitor electrolyte values 
emotional support

administer calcium gluconate for tetany if necessary

51
Q

Obtaining an Arterial Blood Gas Specimen

A
get Vs
determine if they have arterial line
do allens test
asses factors impacting results
prepare heparinized syringe
emotion support
pressure to puncture for 5 min
label specimen and put on ice
document 

COPD is different - careful bc the co2 sensors are worn out, respond to low o2, so giving o2 can shut down respiratory system

52
Q

Major forms of acid/base imbalances

A

primary imbalance:
acute condition or chronic condition
cause of the problem

compensated imbalances:
respiratory compensated by renal system**
metabolic compensated by the respiratory**

combined imbalance:
both respiratory and metabolic both acidic or basic, both of everything

53
Q

Analyzing blood gas resutls

A
  1. look at ph (up -alkolosis, down -acidosis)
  2. look at PCO2,
  3. look at bicarb (does it correspond with pH? if so, metabolic imbalance)
  4. remember compensation has occurred is ph is in normal range, if not , look at respiratory and metabolic indicators)
54
Q

Acid base imbalances summary

A

Respiratory acidosis:
In respiratory acidosis, the pH is down

In respiratory acidosis, the PCO2 is up
Respiratory alkalosis

In respiratory alkalosis, the pH is up

Metabolic acidosis:
In metabolic acidosis, the pH is down

In metabolic acidosis, the HCO3 is down

Metabolic alkalosis:

In metabolic alkalosis, the pH is up

In metabolic alkalosis, the HCO3 is up

55
Q

Compensation: pH within normal limits

A

Respiratory acidosis & respiratory alkalosis:

When compensation has occurred, the pH will be within normal limits

The blood gas result reflects partial compensation if the HCO3 is abnormal

The blood gas result reflects an uncompensated condition if the HCO3 is normal

______________-

Metabolic acidosis & alkalosis:

When compensation has occurred, the pH will be within normal limits

The blood gas result reflects partial compensation if the PCO2 is abnormal

The blood gas result reflects an uncompensated