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
Assessment of metabolic acidosis
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
Manifestations of metabolic acidosis
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
intervention of metabolic acidosis
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
intervention of metabolic acidosis PT II
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
metabolic acidosis treatment
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
Metabolic Alkalosis
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
Metabolic Alkalosis Causes
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
Metabolic Alkalosis Causes Pt. II
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
Metabolic Alkalosis Etiologies
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
Metabolic Alkalosis Assessment
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
Metabolic Alkalosis Manifestation
Neural: association with hypocalcemia confusion convulsion paraesthesia Cardio: hypotension dysrhythmias Compensation: RR and depth decrease urine ph increase
36
Metabolic Alkalosis Treatment
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
Respiratory Acidosis
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
Respiratory Acidosis Causes
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
Respiratory Acidosis Causes pt II
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
Respiratory Acidosis Etiologies
``` 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
Respiratory Acidosis Assessment
``` 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
Respiratory Acidosis Manifestations
``` 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
Respiratory Acidosis Interventions
``` 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
Respiratory Alkalosis
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
Respiratory Alkalosis Cause
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
Respiratory Alkalosis Causes Pt II
condition that increase metabolism Pain or brain trauma Salicylates - aspirin poisoning , causes hyperventilation Hypoxia - causes respiratory stimulation with result of carbonic acid deficit
47
Respiratory Alkalosis Etiologies
``` Excessive ventilation anxiety hypoxemia high fever Excessive mechanical vent (same as causes) ``` Pregnancy (increased sensitivity to Co2)
48
Respiratory Alkalosis assessment
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
Respiratory Alkalosis Manifestations
``` cerebral vasoconstriction (head fog) ``` neuromuscular irritability - hypocalcemia - electrolyte imbalances cardio: dysrhythmias hyperventilation GI epigastric pain
50
Respiratory Alkalosis
``` manage anxiety maintain airway control breathing rebreather mask monitor monitor electrolyte values emotional support ``` administer calcium gluconate for tetany if necessary
51
Obtaining an Arterial Blood Gas Specimen
``` 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
Major forms of acid/base imbalances
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
Analyzing blood gas resutls
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
Acid base imbalances summary
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 In respiratory alkalosis, the PCO2 is down ---------------------- 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
Compensation: pH within normal limits
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