Module 3 - Alterations in Acid-Base Balance Flashcards
How many acid base disturbances are important to us?
4
How does ABG help us with acid base imbalances?
Gives us numbers from arterial blood that can indicate any acid base disturbances and imbalances
What needs to be done before each ABG?
An Allens Test
Hydrogen Ions (H+)
Ions vital to life with low concentration in the body compared to Na, K, etc, but equally as important
Has 2 forms
How are H+ ions expressed
They are expressed as pH (logarithmic form)
What are the 2 forms of Hydrogen Ions in the Body
- Volatile Hydrogen of Carbonic Acids
- Nonvolatile form of Hydrogen and Organic Acids (Fixed)
Carbonic Acid
Most important acid in the body
H2CO3
It breaks down into and is made up of CO2 and H2O (think of breathing!)
What two areas of the body control acid base balance?
Lungs
Kidneys
What area of the body controls volatile forms of hydrogen ions?
Lungs
What area of the body controls nonvolatile forms of hydrogen ions?
Kidneys
What is the normal pH range for the body?
7.35 to 7.45 (slightly alkalotic)
Acids
produced as the end products of metabolism (ex: Lactic acids cause achy muscles from anaerobic glycolysis)
Contain H+ Ions
Acids are Hydrogen Ion ___
Donors
they give up H+ to neutralize or decrease the strength of an acid or to form a weaker base (makes acid weaker giving away H+)
Strength of an acid is determined by …
the number of hydrogen ions it contains
The number of hydrogen ions in body fluid determines…
acidity, alkalinity, or neutrality of the body fluid
More H+ = More ____ = ___ pH
More H+ = More acidic = lower pH
Discuss Lung excretion of acids
Lungs excrete 13000-30000 mEq of volaile hydrogen per day in the form of carbonic acid (H2CO3) as CO2
The respiratory rate increases to get rid of the acids make things more alkalotic/neutral
The fast workhorse of acid base balance
Discuss Kidney excretion of acids
Kidneys excrete 50mEq of nonvolatile acids per day
The kidney releases a lot less than the lungs but the difference they make could be what determines the difference between life and death
The slow fine tuners of acid base balance
Bases
contain no Hydrogen ions (H+)
Most important Base in the body?
Bicarb (HCO3-)
Bases are hydrogen ion (H+) ____
acceptors
they accept H+ from acids to neutralize or decrease the strength of a base or to form a weaker acid
What is pH
it reflects the hydrogen ion concentration (H+) in a fluid
The greater the concentration of H+ ions, the ___ the pH and the more ___ the blood
lower the pH; the more acidic the blood
The lower the concentration of H+ ions, the ___ the pH and the more ___ the blood
higher the pH; the more alkalotic the blood
Acids are formed from …
Metabolic activity (or other substances)
ex: Glucose –> Carbonic Acid (H2CO3)
ex: incomplete oxidation of fats –> Ketoacids
What is the normal ratio of alkali (bicarbonate) to acid (H2CO3) ?
20:1
1 part acid to 20 part alkali
What balance situations lead to acidosis?
Increased acid with normal alkali
Normal acid with decreased Alkali
What balance situations lead to alkalosis?
Normal acid with increased alkali
Decreased acid with normal alkali
What is the acidosis (non death) range of pH
<7.35 but > 6.80
What is the alkalosis (non death) range of pH
> 7.45 but <7.80
What is the acidosis (death) range of pH
< 6.80
What is the alkalosis (Death) range of pH
> 7.80
What is an example of acidosis?
DKA
What is an example of alkalosis
Hyperventilation (blowing off a lot of CO2 and Water (which makes up carbonic acid) which raises pH and you become more numb, tingling, etc)
Buffer
a weak acid/base that can combine with strong acids/bases to minimize changes in pH of the blood
they sense what is wrong in the body and try to keep pH in a healthy range
End Goal - keep pH 7.35 to 7.45
Major Intracellular Buffer System
Potassium - Hydrogen Ion Exchange
H+ increase (acidic)–> H+ moves into cells and K+ moves out
H+ decreases (alkalotic) –> H+ moves out of cells and K+ moves in
Major Extracellular Buffer Systems
Protein Buffers
Bicarbonate Buffers
Phosphate Buffers
Bone Buffers
What makes up 80% and 20% of Protein Buffers Respectively?
80% - Hgb
20% - Albumin and plasma globulin
Bicarbonate Buffer
ECF Buffer
Exchange of Carbonic Acid in the Lungs w/ breathing (Fast) and Bicarbonate from the Kidneys (Slow)
Bone Buffer
ECF Buffer
More common in chronic conditions
Exchanges of pH between bones and blood
Causes kidney stones and demineralization of bones)
Where else can buffer systems take place?
Cells
Blood
interstitial Tissue
Bones
Etc
What are the 3 most important things to know for Buffers as a Regulatory System of H+ Concentration in the Blood?
- Fast Acting
- Reacts Immediately - protection against H+ changes in ECF
- Functions to keep pH in narrow limits of stability where there is too much acid or base released
What other things do Buffer Systems do?
Absorb or release H+ as needed
Serve as a transport mechanism that carries excess hydrogen ions (H+) to the lungs
What is important to know about what happens after a primary buffer system reacts?
Once they are consumed, the body is less able to withstand further stress until the buffers are replaced (autonomic process)
What is the major intracellular buffer and how does it shift pH?
Potassium
The K level changes to compensate for H+ level changes
There is tons of K+ in cells
How does the Potassium Buffer work with Acidosis?
The body protects itself from the acid state by moving H+ INTO cells –> K+ then moves out to make room for the H+ in the cells and serum potassium levels rise
This is when Serum H+ is high and pH is low
How does the Potassium Buffer work with Alkalosis?
Cells release hydrogen ions (H+) into the blood in an attempt to increase acidity of the blood and combat alkalinity –> K+ then moves into the cells and serum K+ levels decrease
This is when Serum H+ is low and pH is high
The body prioritized what balance?
pH balance before electrolyte balance (so temporary imbalances can occur)
What can happen regarding potassium and alkalosis? Acidosis?
Hypokalemia/ Hyperkalemia can occur making people not feel well for a little while
Ex: cardiac arrhythmias, GI issues with innervation
What is the Major Buffer System of ECF and how does it balance pH?
HG Systems (80%)
Acid Base balance is maintained with chloride exchanges for bicarbonate between the RBCs/HGB
Chloride shifts in and out of cells in response to level of O2 in the blood
A cation must be exchanged for a ___ and an anion must be exchanged for a ___
cation; anion
How does the HGB buffer fix low serum bicarbonate (Acidosis)?
Less base = acidic –> pH is lower –> RBC will let HCO3 out and Cl- in –> Serum chloride decreases
How does the HGB buffer fix high serum bicarbonate (Alkalosis)?
More base= alkalotic –> pH is higher –> RBC lets HCO3- in and Cl- out –> Serum Chloride increases
The benefit of the HGB system is what?
You do not feel symptoms of hypo or hyperchloremia unless it is extreme
Hyper - Fluid Volume Excess
Hypo - Dehydration, Fluid Loss, Vomiting, Diarrhea
Plasma Protein Systems
ECF Buffer
Functions in conjunction with the liver (via albumin, globulin, etc) to vary the amount of hydrogen ions (H+) in the chemical structure of protein
What special acid base function does plasma proteins have?
they have the ability to attract or release H+ ions
What would the action be of the Plasma Protein Buffer System if there is Metabolic Alkalosis?
H+ ions release from plasma proteins and enter serum to increase acidity –> H+ will then bind to unbound calcium and decrease total ionized calcium –> nL pH with Hypocalcemia occurs
ex: Hyperventilation –> Alkalosis –> Correction –> Serum Ionized Levels Drop –> Hypocalcemia w/ dizziness, tingling, etc because of lowered threshold
What would the action be of the Plasma Protein Buffer System if there is Metabolic Acidosis?
Too many serum H+ –> H+ goes into a plasma protein and calcium unbinds and enters the blood –> Increase in ionized Ca and decrease in bound Ca –> Hypercalcemia and nL pH
ex: DKA –> Acidosis –> Correction –> Serum ionized levels rise –> hypercalcemia w/ longer distance to firing and slowing of muscle and nerve innervation
Phosphate buffer system
ECF Buffer
present in cells and body fluids
especially active in the kidneys
acts like bicarb and clears spare H+ ions by exchanging phosphorous with calcium at the level of the kidneys
The only acid that the lungs can get rid of, unlike the kidneys which can get rid of many, is what?
Carbonic Acid
What does the Carbonic Acid/Bicarbonate System do?
it is a buffer system for ECF
it maintains a pH of 7.4 with a 20 bicarb to 1 carbonic acid ratio (20:1)
The 20:1 ratio determines what?
Hydrogen ion (H+) concentration of body fluid
Carbonic acid concentration is controlled by what?
The excretion of CO2 by the LUNGS
The rate and depth of respiration changes then in response to the changes in CO2
Bicarbonate concentration is controlled by what?
the KIDNEYS which selectively retain or secrete bicarb in response to body needs
How does DKA cause Kussmaul breathing?
DKA occurs with productions of ketoacids which lower pH and deplete bicarb while creating carbonic acid. The buildup leads to an increase in rate and depth of respiration by the lungs to try and raise the pH
In what directions/areas can Carbonic Acid go
To the lungs: H2CO3 H2O and CO2
To the Kidney H2CO3 H+ and HCO3-
What is needed for carbonic acid to turn into bicarb and hydrogen or carbon dioxide and water?
Carbonic Anhydrase - an enzyme that breaks down carbonic acid into these components
If blood buffer systems are the first defense for acid base balance, what are the second and third/final?
second - lungs
third/final - Kidneys
What occurs during Acidosis regarding the lungs and pH?
pH decreased so RR and Depth increase to try and blow off acids
Carbonic acid can be carried to the lungs and reduced to CO2 and Water to be exhaled, thus H+ ions are inactivated and excreted
What occurs during Alkalosis regarding the lungs and pH?
pH increased so RR and Depth decrease to try and blow off acids
CO2 is retained and carbonic acid builds up (CO2 + H2O) to neutralize and decrease the strength of excess bicarbonate
How do the lungs mechanically compensate for acidosis and alkalosis?
Acidosis: increase RR and Depth
Alkalosis: decrease RR and depth
How fast are the lungs in fixing excess or deficit?
The action of the lungs is reversible and only takes 10-30 seconds to correct
Why is Bicarbonate considered volatile?
it is in a gaseous form - in lungs 30,000 mEq of volatile acids are removed with only 50 mEq removed via kidneys so we do need constant buffering
What occurs with acid base balance, buffering, and diarrhea?
Diarrhea gets rid of bases, letting the body get acidotic. So respiration rate and depth increase to blow off carbonic acids and raise pH. This only takes 10-30 seconds to correct.
The lungs can only deal with ___ ___, everything else is handled by the ___
deal with CARBONIC ACID
handled by the KIDNEYS
Why can the lungs only deal with carbonic acid?
the lungs can only inactivate H+ carried by carbonic acid, excess H+ on other carriers and from other problems need to be excreted by the kidneys
How does the lungs exactly retain or get rid of H+ ions
Lungs can either hold H+ with CO2 and making Carbonic acid until deficit is corrected
Or it can inactivate H+ and turn them into water molecules to be exhaled as CO2 to correct excess
How long does acid base compensation by the kidneys take?
Few hours to several days, but this is more selective and thorough than other regulators as its the ultimate correction
What is the action of correcting acidosis for the kidneys?
pH has gone down, so excess H+ are secreted into the tubules and combine with buffers for excretion in the urine
the urine is outside normal pH and more acidic but we only care about blood pH at the moment so this is ok
What is the action of correcting alkalosis for the kidneys?
pH has gone up, so bicarbonate ions move into the tubules, combine with sodium, and are excreted in the urine
this urine is outside normal pH and more alkalotic but we only care about blood pH at the moment so this is ok
What are the 3 methods for the kidneys to selectively regulate bicarbonate and rid of acids?
- Conservation of bicarbonate that is filtered by releasing H+ and holding onto Bicarb ions
- Extra H+ is turned into phosphoric acid (using phosphorous) and is excreted in urine
- Amino Acid alteration in renal tubules diffuses ammonia into the kidneys which then combines with excess H+ (into ammonium) and is excreted in the urine
Respiratory: ___ + ___ Carbonic Acid __ + __ :Renal
Respiratory: CO2 + H2O Carbonic Acid (via Carbonic Anhydrase) H+ + HCO3- :Renal
In health there is a ratio of what?
20 bicarb (base) for 1 part Carbonic acid (acid) (or CO2)
20b:1a –> pH of 7.4 (within 7.35 to 7.45)
What happens if the ratio of bases:acids increases?
ex: 30:1 –> blood pH increases –> alkalosis
What happens if the ratio of bases:acids decreases?
ex: 13:1 –> blood pH decreases –> Acidosis
Slower and shallower breathing leads to …
retention of CO2 –> production of acid
can correct alkalosis
Faster and deeper breathing leads to …
elimination of CO2 –> elimination of acid
can correct acidosis
Response difference between the lungs and kidneys?
Lungs: Rapid response occurring within minutes with a maximum of 12-24 hours (with effect declining thereafter)
Kidney: Slow response occurring within 1 to 2 days
Decreased pH (acidosis) leads to what occurring in the kidneys?
decreased pH –> secrete more H+ (and less K+) and phosphate –> reabsorb more bicarbonate (and less Cl-)
this can raise the pH
Increased pH (alkalosis) leads to what occurring in the kidneys?
increased pH –> secrete less H+ (and more K+) –> Reabsorbs less bicarb (and more Cl-)
this can lower the pH
BMP
Basic Metabolic Panel
Drawing venous blood (rather than arterial for ABG) to check electrolyte and acid base balance
A BMP CO2 levels comes from what type of blood and represents what?
venous blood
Venous CO2 is actually a measure of Bicarbonate
so, high CO2 values means alkalosis, and low CO2 levels means acidosis
Metabolic Acidosis
Total concentration of buffer base (Bicarbonate) is lower than normal with a relative increase in H+ concentration
Metabolic means what?
it is dealing within the body
so in the case of metabolic acidosis, there is a kidney problem and the lungs must compensate
When does Metabolic Acidosis occur?
as a result of losing too many bases (ex: diarrhea) and holding too many acids without sufficient bases (ex: DKA)
Potential causes for Metabolic Acidosis
Diabetes and DKA
Renal Insufficiency or Failure
Insufficient Metabolism of Carbohydrates
Excessive ingestion of Acetylsalicylic Acid (Aspirin)
Severe Diarrhea
Malnutrition
High Fat Diet
The most common and main reason for Metabolic Acidosis is?
DKA and Diabetes
Why are kidneys the problem for Metabolic Acidosis?
kidneys will hold back bicarbonate, but eventually this system is exhausted. The lungs will then blow off carbonic acid to try and compensate
How does DKA and Diabetes lead to Metabolic Acidosis
insufficient insulin causes increased fat metabolism because the glucose cannot get into cells
this leads to accumulation, in excess, of ketones and other acids that exhaust the bicarbonate system
How does Renal Failure/Insufficiency cause Metabolic Acidosis
Increased waste products of protein metabolism are retained because the kidney cannot metabolize them and rid of the acids
excessive acid build up thus overpowers bicarbonates ability to maintain balance
How does Insufficient metabolism of carbohydrates cause Metabolic Acidosis
insufficient supplies of O2 are available for proper burning of CHO, glc, and H2O –> this leads to lactic acid buildup, and insufficient metabolism of carbs causes Lactic Acidosis
What must the lungs do when there is Lactic Acidosis causing Metabolic Acidosis?
It cannot blow off lactic acid, so it must blow off Carbonic acid
How does excessive ingestion of acetylsalicylic acid (aspirin) cause Metabolic Acidosis?
excessive ingestion of acetylsalicylic acid causes an increase in H+ concentration because it metabolizes into H+
This is a mixed imbalance though
How is Acetylsalicylic Acid causing a mixed imbalance of Metabolic Acidosis?
Aspiring poisoning in the early stages is associated with respiratory alkalosis -d/t aspirin impact on resp centers - so they will breath fast, but once aspirin is metabolized the acids will build up and metabolic acidosis occurs
How does severe diarrhea cause Metabolic Acidosis
intestinal and pancreatic secretions are normally alkaline so excessive loss of base in this case causes MA
faster and deeper respirations occur as a result
How does malnutrition lead to Metabolic Acidosis
improper metabolism of nutrients causes fat catabolism leading to excess build up of ketones and acids (like DKA a little)
How does a High fat Diet lead to metabolic acidosis
high intake of fat causes a much too rapid accumulation of waste products of fat metabolism leading to a build up of ketones and acids
think Atkins diet
Anion Gap
Lab that describes the difference between the serum concentration of the major measured cation, Sodium (Na+), and the sum of measured major anions, Chloride and Bicarbonate.
The difference between the major measured cation and the major measured anions represents the concentration of unmeasured anions (like phosphates, sulfates, ketone bodies, lactic acid, and proteins)
AG = [Na+] - ([HCO3-]+[Cl-])
This will tell us whether they have too much acid or loss of bases
Anion Gap is only looked at in the case of …
metabolic acidosis
Normal Anion Gap range?
12 +/- 2 mEq/L
What does elevated anion gap mean?
elevation is occurring from accumulation of acids (these are the unmeasured anions of acids)
ex: lactate in lactic acidosis, acetoacetate in ketoacidosis, sulfates and phosphates in RF - unmeasured anions of acids
What does a Normal Anion Gap represent?
a loss of base (bicarb)
What does a lowered anion gap mean?
It is a rare occurrence
It occurs from a decrease in proteins like in cancer and cirrhosis
it either comes from a decrease in unmeasured anions or an increase in unmeasured cations
ex: low albumin, hyperkalemia, hypercalcemia, hypermanesemia
What are the etiologies for a High anion gap?
- Excess production of metabolic acids (lactic acidosis, DKA, starvation, alcoholic intoxication, aspirin poisoning)
- Impaired elimination of metabolic acids (ex: RF)
What are the etiologies for a Normal anion gap?
- Loss of intestinal secretions (diarrhea, intestinal suction, biliary or pancreatic fistula)
- increased renal losses (renal tubular acidosis, tx with carbonic anhydrase inhibitors, HYPOaldosteronism)
- Increased chloride levels (excess reabsorption of chloride by the kidney, sodium chloride infusion, ileal conduit)
Ileal Conduit
placed for bladder cancer
ureter attached to Small intestine instead of emptying urine via the bladder
urine then mixes with feces causing chloride absorption allowing for a normal anion gap and thus loss of bases
Assessment of Metabolic Acidosis shows what?
Headache
Nausea
Vomiting (low pH stims vomit centers)
Diarrhea
Fruit smelling breath from improper fat metabolism
Twitching
Mental Dullness (!!)
Drowsiness
Stupor
Coma
Convulsions
Hyperpnea with Kussmaul Breathing - due to an attempt to blow off extra CO2 and compensate for the acidosis
Neural Manifestations of Metabolic Acidosis
Weakness
Lethargy
General Malaise
Confusion
Stupor
Coma
Cardiovascular Manifestations of Metabolic Acidosis
Peripheral Vasodilation (Decreased HR and BP)
Decreased HR
Cardiac Dysrhythmias
GI Function Manifestations of Metabolic Acidosis?
Anorexia
Nausea and Vomiting
Abdominal Pain
Non Cardiac, GI, or Neural Manifestations of Metabolic Acidosis?
Skeletal - bone disease if MA is chronic
Skin - flushed warm and dry (from peripheral vasodilation)
What is the Stupor, Coma, and Confusion related to in metabolic acidosis manifestations?
An increase in ionized calcium from the plasma protein buffer system (H+ moves to proteins but those proteins release Ca2+)
The most important Metabolic Acidosis manifestations are?
Neural
Cardiovascular
GI Function
How does the Body compensate for Metabolic Acidosis?
Respiratory: Kussmaul breathing - increased RR and depth
Hyperkalemia
Acidic Urine
Increased Ammonium in Urine
*kidneys are trying, but they are also the issue, so lungs are the compensatory part
General Interventions for Metabolic Acidosis
Determine the Cause of the Acidosis!!!
Maintain a patent airway
Assess LOC for CNS depression - a chance of seizure exists if the body is acidotic
Monitor Lyte values
maintain I and O and assist with fluid and lyte replacement as prescribed
Initiate safety precautions for convulsions and coma
Prepare to administer IV solutions like isotonic saline, 5d1/2NS (hypertonic to pull fluid from cells to return circulating volume), sodium lactate or bicarbonate to increase the buffer base
Monitor K level very closely (as K moves with GIK for example)
Why do Potassium levels need to be monitored very closely in Metabolic Acidosis?
When acidosis is being treated, K will move back into the cell and blood levels will drop rapidly
Metabolic Acidosis Interventions if it is caused by DKA
Insulin (GIK) is given to hasten movement of serum glucose into cells –> decreases concurrent ketosis (making ketone acids)
When glc is being properly metabolized, body will stop making fats into glucose
Monitor for circulatory collapse d/t polyuria which may come from the hyperglycemic state, as polyuria or diuresis may lead to ECF volume deficit
Metabolic Acidosis Interventions if it caused by Renal Failure
Dialysis may be used to remove protein and waste products thereby lessening the acidosis state - potential primary need / main treatment
Diets low in protein and high in calories will lessen the amount of protein waste products d/t protein catabolism; this in turn will lessen acidosis - but this is slower and not the main fix in the end
Treatments for Metabolic Acidosis
Monitor patients at risk (DM, sepsis, shock)
Monitor VS (esp RR and depth)
Monitor ABGs and K+ levels
Administer Sodium Bicarb (NaHCO3)
Cardiac Monitoring for low serum K+ levels
CORRECT UNDERLYING CAUSE OF ACIDOSIS
Administer IV fluids with lactate (unless contraindicated)
Treatment for DKA Metabolic Acidosis?
Insulin + Normal Saline
Treatment for Lactic Acidosis Metabolic Acidosis
IV fluids and oxygen
Treatment for Renal Failure, Drug Overdose, or Drug Poisoining Metabolic Acidosis
Dialysis
Treatment for CHRONIC Metabolic Acidosis
Increase in Carbohydrates and Decrease in Fat diet
Why is DKA Metabolic Acidosis treatment so serious?
Metabolic acidosis compensation is making K+ move into cells which then is lost in urine, while DKA GIK treatment moves it in so we are at double risk for low potassium levels that could lead to arrhythmias (higher resting membrane to reach)
Define Metabolic Acidosis
Fixed Acid Excess - too much acid
Causes of Metabolic Acidosis
- Acid Accumulation - excessive Metabolic acids
- Loss of bicarbonate base (HCO3-)
This is a problem via the KIDNEYS
What compensates for Metabolic Acidosis
Respiratory excretion of H2CO3 (CO2 + H2O)
the LUNGS ARE COMPENSATORY
What are normal PaCO2 levels?
35-45 (thinks of 7.35-7.45)
PaCO2 is the respiratory marker and partial pressure of CO2
What are normal HCO3- levels?
22-26
HCO3- is the renal/metabolic marker
What are the pH, PaCO2, and HCO3- levels like in uncompensated Metabolic Acidosis?
pH - «_space;7.35 (ex: 7.3)
PaCO2 - normal range (35-45)
HCO3- -<22 (low)
What are the pH, PaCO2, and HCO3- levels like in partially compensated Metabolic Acidosis?
pH - <7.35 (slightly low)
PaCO2 - <35 (slightly lower now)
HCO3- - No change (still <22)
What are the pH, PaCO2, and HCO3- levels like in compensated Metabolic Acidosis?
pH - low normal (ex: 7.35 exactly)
PaCO2 - «_space;35 (much lower)
HCO3- - No change (still <22)
Why are the pH, PaCO2, and HCO3- levels like an elevator?
the levels never increase or decrease compared to one another, they either decrease together, increase together, or they may increase or decrease with some having no change (all going in same direction)
Why does PaCO2 decrease and HCO3- stay relatively the same in Metabolic Acidosis compensation?
PaCO2 decreases because the compensatory system for MA (lungs) will blow it off fast to correct/raise pH
Bicarbonate stays largely the same (low) because the kidneys are the problem here, not the compensatory mechanism
Why does the body allow such a drop in PaCO2 for metabolic acidosis compensation?
Because it cares more about correcting pH than the Co2 amount
How may the ratio of bases:acids be in normal, uncompensated, and compensated Metabolic Acidosis?
Normal: 20:1 with ex: 24 mEq/L of Bicarb and 40 mmHg of PaCO2 and a pH of 7.4
Uncompensated: 13:1 with ex: 16 mEq/L of Bicarb and 40 mmHg of PaCO2 with a pH of 7.2
Compensated: 20:1 with an ex: 18 mEq/L of bicarb (largely the same but slightly corrected since kidneys are still working) and 30 mmHg of PaCO2 with a pH of 7.38
Metabolic Alkalosis
Issue with the kidneys, compensated by the lungs
Deficit of carbonic acid (H2CO3) and a decrease in hydrogen ion concentration
pH > 7.45
2nd most common acid base disorder in hospital patients
opposite effect of metabolic acidosis
What can result in metabolic alkalosis?
Results from the accumulation of base or from a loss of acid without a comparable loss of base in body fluids
What are 2 potential causes for the increase in available basic solution in the blood and decrease in available acids in the blood in Metabolic Alkalosis?
- Ingestion of excess sodium bicarbonate (ex: excessive ingestion of sodium bicarb like in Alka-Seltzer or baking soda causes an increase in the amount of base in the blood
- Excessive Vomiting (leads to an excessive loss of acids)
What are some examples of events/disease that cause Metabolic Alkalosis?
- GI Suctioning - leads to an excessive loss of acids from the suctioning
- Diuretics - loss of H+ ions and K+ ions causes a compensatory increase in the bicarbonate in the blood
- Hyperaldosteronism - increased renal tubule reabsorption of sodium occurs with the resultant loss of H+
- Massive Transfusion of Whole Blood - citrate, and anticoagulant in the whole blood, metabolizes into bicarb
What is the most common reason for causing Metabolic Alkalosis
Gastrointestinal Suctioning
How does Hyperaldosteronism cause Metabolic Alkalosis?
The increased reabsorption of sodium causes Na to stay and H+ to leave in the urine
Also called Conns Syndrome
General Etiologies for Metabolic Alkalosis
Excess gain of bicarb.
Increased bicarb retention
Excessive H+ loss
Volume contraction
Abrupt correction of respiratory acidosis by mechanical ventilation
What are some ways a person with metabolic alkalosis ended up with excess gain of bicarbonate
- Administration/Ingestion of HCO3 (e.g. alka seltzer)
- Adminsitration of TPN containing ACETATE, solutions with LACTATE, or CITRATE in whole blood - all will metabolize into Bicarb
- NaHCO3 administration during CPR
Why is bicarbonate retention increased in Metabolic Alkalosis?
d/t a loss of chloride
How can H+ be lost in excess leading to Metabolic Alkalosis?
- NG Suctioning (most common reason)
- Vomiting
- Bulimia
- Potassium Deficit d/t diuretic therapy or hyperaldosteronism
What does volume contraction mean as an etiology for metabolic alkalosis
loss of body fluids through something like diuretic therapy
Things that can be seen on assessment for Metabolic Alkalosis
DECREASED RR AND DEPTH OF BREATHING (conserve volatile acid CO2)
Nausea and Vomiting
Diarrhea
Numbness and Tingling in the extremities
Restlessness and twitching in the extremities
Hypokalemia
Hypocalcemia
Sinus Tachycardia
Dysrhythmias
What is causing the twitching/neuro excitability and hypocalcemia in Metabolic Alkalosis?
Low H+ leads to calcium attaching to plasma proteins to release H+ which lowers the unbound amount of calcium. There is then hypocalcemia occurring which lowers the threshold for firing allowing for neuro excitability
Important Areas of Manifestations in Metabolic Alkalosis?
Neural
Cardiovascular
GI Function
Compensatory
Neural Manifestations of Metabolic Alkalosis?
Confusion
Hyperactive DTR
Tetany
Paresthesias in the Fingers and Toes
Circumoral Paresthesias (tingling around the mouth)
Carpopedal Spasm
*All of this d/t hypocalcemia lowering threshold
Cardiovascular Manifestations of Metabolic Alkalosis?
Hypotension
Dysrhythmias
What are the compensatory manifestations of Metabolic Alkalosis?
Respiratory rate decreases and depth decreases
Urine pH increases because the kidneys are trying to get rid of some bicarb - but these areas are the problem still and cannot do too much
Interventions for Metabolic Alkalosis?
Maintain a patent airway (may have spasms)
Monitor vitals, I&O, Lyte values, muscle weakness
Institute safety precautions for tetany and convulsions
Prepare K and Cl– as prescribed, to administer meds as prescribed to promote kidney excretion of excess bicarb, and to administer acidifying solutions as ammonium chloride and arginine chloride as prescribed
Treatments for Metabolic Alkalosis?
Monitor pts at risk (ex: those with GI fluid loss)
Assess I&O
Monitor VS (esp., RR and Depth)
Monitor ABGs
Correct the underlying cause of imbalance
IV fluids (NS) and lyte supplements to replace fluid volume and K+ and Cl- losses
Supply sufficient Cl- to enable renal reabsorption of NaCl and renal excretion of excess Bicarb
Cardiac monitor for hypokalemia
teach about excess sodium bicarb ingestion and supplemental KCl for thiazide and loop diuretic therapy
What is the hallmark/most important treatment for Metabolic Alkalosis behind treating the underlying cause?
Teaching them about other methods of treating dyspepsia (not alka seltzer or baking soda)
Definition of Metabolic Alkalosis
Fixed acid deficit
Causes for Metabolic Alkalosis
Base Accumulation
Loss of Acids
Compensation Mechanism for Metabolic Alkalosis
Respiratory retention of H2CO3 (CO2+H2O)
What would pH, PaCO2, and HCO3- levels look like in Uncompensated Metabolic Alkalosis?
pH»_space; 7.45 (ex: 7.5)
PaCO2 = normal range (35-45)
HCO3- > 26 (high like 32)
What would pH, PaCO2, and HCO3- levels look like in Partially compensated Metabolic Alkalosis?
pH > 7.45 (slightly lower now - maybe 7.48)
PaCO2 > 45 (retention of CO2 is occurring to lower pH)
HCO3- = No change (still greater than 26 since this is not really the compensatory thing)
What would pH, PaCO2, and HCO3- levels look like in Compensated Metabolic Alkalosis?
pH = High normal (ex: pH = 7.45 - compensated)
PaCO2 »_space; 45 (much greater because it was retained to lower pH)
HCO3- = no change (still greater than 26, maybe a little lower like 28-30, but this is not the compensatory mechanism)
Respiratory Acidosis
Total concentration of buffer base is lower than normal with a relative increasing H+ concentration - a greater number of H+ ions are circulating in the blood than can be absorbed by the buffer system (too much acid not enough base)
In this case respiratory is where the problem is at with metabolic/kidney being the compensator
Root Mechanical Cause for Respiratory Acidosis
Defects in the function of the lungs or by changes in normal respiratory patterns due to secondary problems (like lack of perfusion)
Any condition that causes an obstruction of the airway or depresses respiratory status can cause respiratory acidosis
What is pH and PaCO2 like in (uncompensated) respiratory acidosis?
pH < 7.35 and PaCO2 >45
Potential Causes for Respiratory Acidosis
Hypoventilation
Infection
Medications
Pneumonia
Atelectasis
Brain Trauma
emphysema
asthma
bronchitis
pulmonary edema
bronchiectasis
How does Hypoventilation cause Resp Acidosis
CO2 is retained and H+ increase causing an acidic state
Carbonic acid is retained d/t slow and shallow breaths making pH lower
How does Infection cause Resp Acidosis
inflammation and bacterial agents can decrease aeration in the lungs from obstruction leading to acid buildup
How do Medications and what Medications cause Resp Acidosis
Sedatives, narcotics, anesthetics
They depress the respiratory center leading to hypoventilation –> increase in H+ then leads to CO2 narcosis
Narcosis
stupor or unconsciousness due to medication impact
How does Pneumonia cause Resp Acidosis
infection, irritants, and immobility lead to pneumonia which causes obstruction of airway passages leading to inadequate oxygenation from fluid accumulation
COVID pneumonia leads to consolidation that decreases lung volume potentially even
How does Atelectasis (lung collapse) cause Resp Acidosis
Excessive mucus collection with the collapse of alveolar sacs d/t mucus plugs, infectious drainage, or anesthetic medication causes decreases respiration or no exchange occurring
How does Brain trauma cause Resp Acidosis
excessive pressure on the respiratory center or medulla oblongata depresses respiration ability/rate
How does Emphysema cause Resp Acidosis
Loss of elasticity of alveoli sacs restricts air flow in and out, mostly out, leading to an increased CO2 level
How does Asthma cause Resp Acidosis
spasms from allergens, irritants, or emotions can lead to smooth muscles of the bronchioles constricting causing decreased oxygenation and loss of CO2
How does Bronchitis cause Resp Acidosis
Inflammation causes airway obstruction
How does Pulmonary Edema cause Resp Acidosis
Extracellular accumulation of fluid in acute CHF causes disturbances in alveolar diffusion and perfusion (plus it is more difficult to expand the lungs)
How does bronchiectasis cause Resp Acidosis
Bronchi become dilates from inflammation; destructive changes and weakness of the bronchi then occur which leads to decreased and hindered perfusion and less effective bronchiole walls
this is a part of COPD
Acute Etiologies of Respiratory Acidosis
Lung Disease - Acute pulmonary edema, aspiration, atelectasis, pneumothorax, severe pneumonia
Depression of respiratory center - sedative or narcotic overdose, head injury
Chronic Etiologies of Respiratory Acidosis
Chronic lung diseases - chronic bronchitis, asthma, cystic fibrosis, emphysema, COPD
Chest wall and respiratory muscle issues - obesity, post op pain, high abdominal or thoracic incisions, abdominal distension from ascites or bowel obstruction (all of these prevent lung expansion)
Why are acute problems particularly/especially dangerous for Respiratory Acidosis in comparison to chronic issues?
Acute happens quickly, but the compensatory mechanisms of the kidneys are very slow - therefore we may need to give outside help in the hospital because of the low speed
With chronic, the kidneys have time to compensate, so while lyte balance may be abnormal, it can still be compensated for efficiently
Things assessed and found for Respiratory Acidosis?
RR and depth drop
headaches and mental status changes (ex: confusion, drowsiness, restlessness, visual disturbances)
Diaphoresis
cyanosis as hypoxia becomes mroe acute
hyperkalemia
rapid and irregular pulse leading to dysrhythmias and ventricular fibrillation
The nervous system is depressed, much like Metabolic Acidosis in many ways
___ leads to restlessness in people
hypoxemia
Important group Manifestations of Respiratory Acidosis
Neural
Cardiac
Skin
Respiratory
Neural Manifestations of Respiratory Acidosis
Dilation of cerebral vessels and depression of neural function (to get oxygen to the brain)
Feeling of fullness in the head
headache
weakness
behavior changes like confusion, depression, paranoia, hallucinations
tremors
paralysis
depressed DTR
*neural depression from hypercalcemia
Skin Manifestations of Resp Acidosis
warm and flushed from dilation of vessels to get more O2 and get rid of more CO2
Cardiac Manifestation of Resp Acidosis
Tachycardia
Respiratory Manifestations of Resp Acidosis
Dyspnea
Cyanosis
How does the kidney compensate for Resp Acidosis
Makes the urine more acidic by getting rid of acids (H+)
Interventions for Respiratory Acidosis
Maintain patent airway
improve ventilation and aeration based on the clinical manifestations
Monitor for signs of respiratory distress
administer O2 as prescribed
place in semi fowlers unless contraindicated since they may have orthopnea
encourage and assist client to turn cough and deep breath
prepare to administer chest physiotherapy and postural drainage as prescribed
encourage hydration to thin secretions unless excess fluid intake is contraindicated
What needs to be reduced, monitored, avoided, and administered with Respiratory Acidosis
Reduce - restlessness by improving ventilation rather than by administering sedatives or narcotics
Monitor - lyte values
Avoid - tranquilizers, narcotics, hypnotics because they depress respiration
Administer - antibiotics for infection as prescribed
Treatment for Respiratory Acidosis
TCDB (turn cough deep breathing) every 2 hours
IS - incentive spirometer use
chest PT
suctioning
semi fowlers or orthopneic position
encourage fluids (unless contraindicated)
supplemental O2 to treat hypoxemia
Monitor VS, ABGs, Serum K+
use bronchodilators
give antibiotics for pneumonia
administer sedatives with caution
be prepared for intubation and mechanical ventilation
Why do we need to be careful giving supplemental O2 to treat hypoxemia in respiratory acidosis for COPD patients?
it may cause a loss of hypoxemic stimulus to breath
Definition of Respiratory Acidosis
Carbonic Acid (H2CO3) excess
Cause of Respiratory Acidosis
Altered alveolar ventilation leading to retention of CO2
Compensation for Respitaory Acidosis
Occurs in the kidneys
Renal retention of HCO3- occurs slowly
acidic urine is excreted
If Metabolic Acid-Base issues are like an elevator, what are Respiratory Acid-Base issues like?
A see saw/ teeter totter
because values move in opposite directions rather than together
What is the respiratory and metabolic markers for Respiratory acid base disturbances and what is the marker we are most concerned with?
Resp - PaCO2
Metabolic - HCO3-
We are most concerned with the PaCO2 since it is what is causing this issue (and the lungs)
pH, PaCO2, and HCO3- values in uncompensated Respiratory Acidosis
pH «_space;7.35 (very low)
PaCO2 > 45 (very high)
HCO3- normal range (22-26)
pH, PaCO2 and HCO3- values in partially compensated Respiratory Acidosis
pH < 7.35 (still low but slight increase/H+ decreases to make it more basic)
PaCO2 - no change (slightly lower but not much)
HCO3- >26 (increased)
pH, PaCO2, and HCO3- values in compensated Respiratory Acidosis?
pH = low normal (7.35 ish)
PaCO2 - not much change (slight decrease)
HCO3-»_space; 26 (much higher)
Respiratory Alkalosis
deficit of carbonic acid (H2CO3) and a decrease in H+ concentration
results from the accumulation of base or from loss of acid without a comparable loss of base in body fluids
What are the pH and CO2 levels like in Respiratory Alkalosis
pH»_space; 7.45
CO2 <35
Causes for Respiratory Alkalosis Occurring
Conditions that cause over stimulation of the respiratory system:
Hyperventilation
Hysteria
Overventilation by Mechanical Ventilators
Conditions that increase metabolism such as
Fever
Pain or Brain Trauma
Salicylates
Hypoxia
What happens calcium levels in Respiratory Alkalosis?
they drop (hypocalcemia) since calcium binds to plasma proteins to release H+
This leads to neuromuscular excitability and cardiac issues
How does Hyperventilation cause Respiratory Alkalosis
rapid respiration causes blowing off of CO2 –> leads to a decrease in carbonic acids
How does Hysteria cause Resp Alkalosis
often neurogenic in nature and related to psychoneurosis, but this conditions causes hyperventilation and excessive exhaling of CO2
How does Over-Ventilation by mechanical ventilators cause Resp Alkalosis
administration of O2 and the depletion of CO2 can end up occurring and the patient may be hyperventilated by the mechanical ventilator
What do we commonly do in regard to acid-base balance if a patient has cranial swelling?
We want to vasoconstrict to prevent too increased ICP so we might keep them slightly alkalotic on a ventilator to cause vasodilation
What stimulates change in blood vessel tone?
pH O2 and CO2 levels
What levels will cause vasoconstriction?
high pH, high O2, low CO2
What levels will cause vasodilation?
low pH, low O2, high CO2
How does Pain or Brain Trauma cause Resp Alkalosis
overstimulation of the resp center in the brain stem with a resultant carbonic acid deficit due to the changes
How do Salicylates cause Resp Alkalosis?
They stimulate the respiratory center causing hyperventilation initially
What is unique about acid base changes and Salicylates/Aspiring?
It will cause initial Resp Alkalosis by stimulating the respiratory center in the brain to lead to hyper ventilation
Later on though it will cause Metabolic Acidosis as more acids are absorbed and then the lungs need to try and compensate
How does hypoxia cause resp Alkalosis?
causes resp stimulation with resultant carbonic acid deficit
Main Etiologies of Resp Alkalosis
Excessive Ventilation
Excessive Mechanical Ventilation
Pregnancy
Hyperventilation during Labor and Delivery
Examples of Excessive Ventilation leading to Resp Alkalosis?
Extreme Anxiety (most common)
Hypoxemia
Stimulation of Resp Center d/t high fever, early salicylate poisoning, encephalitis, CNS lesions affecting resp center, increased blood ammonia
Why may excessive mechanical ventilation be deliberate?
to cause vasoconstriction to prevent cerebral edema
Why does pregnancy and labor and delivery sometimes cause respiratory alkalosis
Pregnant women are more sensitive to CO2 and are stimulated to breath more
L&D causes hyperventilation potentially when pushing
What is seen on Assessment of Resp Alkalosis
Initially hyperventilation and resp stimulation will cause abnormal rapid respiation (Tachypnea), in an attempt to compensate, resp rate and depth will then go down!
headache
Mental status changes
vertigo
lightheadedness
paresthesias as tingling of the fingers and toes
Hypokalemia
Hypocalcemia (lowers threshold)
tetany
convulsions
Manifestations of Resp Alkalosis?
Cerebral Vasoconstriction from pH and O2 increases and CO2 decreases
Neuromuscular Irritability
Cardiovascular Dysrhythmias
Hyperventilation (high RR and depth)
Dry mouth
GI function problems like pain
Cerebral Vasoconstriction manifestations for Respiratory Alkalosis?
lightheadedness, syncope
inability to concentrate
blurred vision, vertigo
loss of consciousness
Neuromuscular Irritability manifestations for Respiratory Alkalosis
paresthesias
tinnitus
carpopedal spasms (Trousseaus sign)
Spasms (chvostek))
tetany and twitching
hyperactive DTR
seizure, convulsion, coma
Interventions for Respiratory Alkalosis
Emotional support and reassurance
Maintain patent airway
encourage appropriate breathing patterns
assist with breathing techniques and apply breathing aids as prescribed
voluntary holding of breath
rebreathe exhaled CO2
rebreathing mask as prescribed
CO2 breaths as perscribed
provide cautious care with ventilator clients so that the client is not forced to take breaths too deeply or rapidly
monitor lyte values
administer meds as ordered
prepare to administer calcium gluconate for tetany as prescribed
Calcium Gluconate for tetany treats the underlying issue of ___
hypocalcemia
Treatments for Respiratory Alkalosis
Monitor VV especially RR and Depth
Encourage slow breathing and less deep breathing
Breathe into paper bag
use rebreather mask
administer sedatives (FOR ANXIETY NOT RESP DEPRESSION)
correct underlying cause (pain, anxiety)
monitor ABGs
adjust mechanical ventilator settings
monitor serum K+ levels
provide emotional support
Definition of Respiratory Alkalosis
Carbonic Acid (H2CO3) deficit
Cause of Respiratory Alkalosis
Hyperventilation leading to excessive elimination of CO2
Compensation for Respiratory Alkalosis
Renal Excretion of HCO3-
What does pH, PaCO2, and HCO3- looks like in uncompensated Resp Alkalosis
pH»_space; 7.45 (high, up)
PaCO2 <35 (low, down)
HCO3- Normal
What does pH, PaCO2, and HCO3- looks like in partially compensated Resp Alkalosis
pH >7.45 (still up)
PaCO2 No change (it is the problem)
HCO3- <22 (lower now, down)
What does pH, PaCO2, and HCO3- looks like in compensated Resp Alkalosis
pH High Normal (7.45) (this is now corrected)
PaCO2 - no change - may be slightly higher but not by much since its not the compensator
HCO3- «22 (very low, down to correct pH)
What to do before obtaining an Arterial Blood Gas Specimen?
Obtain VS
Determine if there is an Arterial Line
Performed Allen’s Test
Assess factors that may impact accuracy
Assist with specimen draw by having a heparinized syringe
Provide emotional support
Apply pressure
Label specimen and transport on ice to Lab
Record clients Temp, and type of supplemental O2 that client is receiving on lab form
What does an Allen Test do?
it determines the presence of collateral circulation
What must be done to take an ABG Specimen after a suctioning or client activities?
Wait 20 minutes
How long must you put pressure on an ABG site after getting a specimen?
apply pressure for 5 to 10 minutes (since anticoagulants)
How to do an Allen’s Test
- Ask client to make a tight fist
- Occlude ulnar and radial arteries
- tell them to open their hands with occlusion still occurring
- let go of one artery and check for color return
- Do it again for the other side
Normal H+ concentration
7.35-7.45
pH range that leads to acidosis
<7.35
pH range that leads to Alkalosis
> 7.45
pH ranges that are deadly?
<6.8 or >7.8
Normal PaCO2 level (partial pressure of CO2 in arterial blood)
35-45 mmHg
A PaCO2 <35 indicates what
hypocapnia/hypocarbia and Respiratory Alkalosis
A PaCO2 >45 indicates what
Hypercapnia/Hypercarbia and Respiratory Acidosis
What is the normal PaO2 (partial pressure of O2 in arterial blood)
80-100 mmHg
What does PaO2s of <80, <60, and <40 indicate?
<80 - mild hypoxemia
<60 - moderate hypoxemia
<40 - severe hypoxemia
What is the normal HCO3- Concentration
22-26 mEq/L
% Hgb molecules saturated with O2 in a normal healthy person is..
> 95%
HCO3- concentration <22 indicates?
Metabolic Acidosis
HCO3- concentration >26 indicates?
Metabolic Alkalosis
What are the 3 important indicators on an ABG to look at
pH, PCO2, and HCO3- concentration
Why is PaO2 not a good thing to know, but a non-used indicator for acid base imbalance on an ABG?
You can have normal PaCO2 and be hypoxemic or have normal O2 with Hypercarbia
The levels depend on what is wrong with the person. Such as a COPD patient can get O2 in (normal) but cannot get CO2 out (Hypercarbia)
So the level changes do not necessarily mean much for acid base
Major Forms of Acid Base Imbalances
Primary Imbalance
Compensated Imbalances
Combined or Mixed Imbalances
Primary imbalance
Primary cause of the problem
originates from an acute condition
either respiratory or metabolic in origin
Compensated Imbalances
Respiratory imbalances compensated by the renal system
Metabolic imbalances compensated by the respiratory system
Combined or Mixed Imbalances
involve both respiratory and metabolic imbalances at the same time (both acidosis, both alkalosis, or one acidosis and one alkalosis)
ex: Salicylate Poisoning causes initial Respiratory Alkalosis followed by Metabolic Acidosis
Steps for Analyzing ABG Results
- Look at blood gas report
- look at pH, is it up or down? if up then its alkalosis, if down then its acidosis
- Look at PCO2, is it up or down? If it is an opposite response/direction to pH then it is d/t a respiratory imbalances. if not reflecting opposite response as pH then move to next step
- Look at HCO3-, does it reflect a corresponding/same direction response with the pH? If so, then condition is metabolic imbalance
- Keep in mind compensation has occurred if pH in 7.35 to 7.45 range (low and high ends), and if the pH is not in normal limits it is important to look at the resp or metab function indicators to determine if partially compensated (pH starting to go in normal direction) or uncompensated
In Respiratory Acidosis, pH is ___ and PCO2 is ___
pH down, PCO2 up
In Respiratory Alkalosis, pH is __ and PCO2 is ___
pH is up and PCO2 is down
In Metabolic Acidosis, pH is ___ and HCO3 is ___
pH is down and HCO3 is down
In Metabolic Alkalosis, pH is ___ and HCO3 is ___
pH is up and HCO3 is up
When compensation has occurred for Respiratory Acidosis and Alkalosis, what occurs to the ABG levels
compensation -pH is in normal limits
partial compensation if HCO3 is abnormal
Uncompensated if HCO3 is normal
When compensation has occurred for Metabolic Acidosis and Alkalosis, what occurs to the ABG levels
Compensation - pH in normal limits
Partial - PCO2 is abnormal
Uncompensated - PCO2 is normal
In acidosis, pH is ___
down
In alkalosis, pH is __
UP
The respiratory function indicator is the ___
PCO2
The metabolic function indicator is the ___
HCO3
What sort of thing could cause a Mixed Imbalance of Metabolic and Respiratory Acidosis
Cardiopulmonary Arrest
- the hypoxemia –> lactic acidosis and CO2 retention
What sort of thing could cause a Mixed Imbalance of Metabolic and Respiratory Alkalosis
Vomiting during pregnancy
- out of breath/hyperventilate + losing acids
What sort of thing could cause a Mixed Imbalance of metabolic acidosis and respiratory alkalosis?
Salicylate/ASA poisoning
- first Aspirin stimulates resp centers to cause respiratory alkalosis
- second the metabolism of the aspirin causes acids leading to metabolic acidosis (which increases breathing yet again)
