Pulm Content; Final Exam Flashcards

(101 cards)

1
Q

Atmospheric Pressure is a Result of What?

A

Gravity and the weight of the atmosphere between us and outer-space

Sea level: 760mmHg
Outer Space: 0mmHg

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2
Q

What is the highest point of altitude on earth?
How do hikers acclimatize to this?
What are short-term & long-term compensation methods?

A

Highest point of altitude on Earth
Summit of Mount Everest: ~9km (8848m)
PB: 243mmHg
PIO2: 43.1mmHg
* This PO2 can typically only be tolerated by a human for ~2 hours.
* Fractional concentration of atmospheric pressures should remain the same.
* PIH2O will remain 47mmHg

  • Base camps are used to acclimatize hikers to the high altitude
  • Hyperventilation typically occurs as a short-term compensation to the high altitude
  • After a few days: EPO is increased in response to hypoxia –> increases HCT in order to facilitate increased oxygen carrying capacity
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3
Q

Barometric pressure is the amount of pressure available to….?

A

Push oxygen and other inspired gases into the blood

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4
Q

What is different about the body if a person has grown up in a high-altitude area?

A
  • Increased surface area in the lungs as a function of an increased number of alveoli
  • More surface area for gas exchange
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5
Q

How does descending in altitude into a body of water affect the body?

What is the make-up of the O2 tank used in low altitudes?

A
  • Descending in altitude into a body of water significantly magnifies the amount of atmospheric pressure that is felt
  • Descending 500ft below sea level causes the atmospheric pressure to be as high as 16x the PB at sea level
  • If the body is subjected to this high of a pressure, the source you are breathing from needs to be highly pressurized as well
    • Typically the contents of the tank is the same composition as air. Eliminating the N2 would eliminate the risk associated with sudden decompression; however, O2 is explosive
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6
Q

Lowest Altitude on Earth?

A

Death valley

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7
Q

Sudden Decompression

A
  • The gases in the blood increase in proportion to the increase in atmospheric pressure
  • N2 partial pressure is the main concern in people who are diving —> if there is a sudden decompression of the body, the pressures will adjust by the gas coming out of solution
    • This is essentially boiling your blood. Taking N2 in a liquid form in the blood and releasing it in gas form
    • This causes air emboli to form

The best way to avoid this is to decompress gradually.

Arnold Schwarzennegar Movie- Total Recall

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8
Q

Which camp do people tend to figure out they can’t handle altitude?

Altitude Sickness & Mt. Everest

A
  • Some people are genetically prone to altitude sickness
  • Typically Camp #3 is when people discover whether they can handle the altitude or not
    -PB: 317mmHg
    -PIO2: 56.5mmHg
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9
Q

Standard vs military, hyperbaric rooms? Benefits? Michael Jackson?

Hyperbaric Chamber Therapy

A

Standard Hyperbaric Chamber
* Can simulate up to 3x ATM
* Usually seen in large, academic hospitals
* Single or multiperson
* Can be mobile

Military Hyperbaric Chambers
* Expensive
* Dangerous
* Can significantly increase the ATM pressure

Oil rigs have hyperbaric “rooms” so that people that are constantly diving very deep for work can live in a high-pressure environment

Benefits
* Decompression treatment
* Wound healing

Michael Jackson had one in his house

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10
Q

How do we increase dissolved PaO2?

A
  • O2 is relatively insoluble
  • Travels via Hb so that it doesn’t have to dissolve in solution
  • In order to increase PaO2 –> PAO2 must be increased by:
    - Increase FIO2
    - Increase ATM (hyperbaric chamber)
  • Any of the additional O2 being pushed into the blood will have to be in the dissolved form
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11
Q

Why do we give a higher FIO2 in the OR?

A

General anesthetics interfere with normal physiologic functions such as HPV and airway reactivity

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12
Q

Dangerous Oxygen Molecules

A

O2- Superoxide
- O2 molecule with an extra, unpaired e- that is very reactive and degrade many different compounds

OONO- Peroxynitrite
- “Oh no!”
- Very bad. Interacts with and mutates/destroys DNA (Cancer)
- Need Superoxide & NO in large amounts to form this compound

H2O2 Hydrogen Peroxide
-ROS used as an aseptic cleaning substance

NO Nitric Oxide
- Toxic if there is a high concentration of NO in the presence of other dangerous oxygen molecules

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13
Q

How are dangerous oxygen molecules used and contained in the body?

A

Macrophages and immune killer cells can release these compounds in order to destroy harmful things in the body

Superoxide dismutase
- Degrades superoxide

Peroxidases
- Degrades H2O2

Catalases
- Can degrade or form H2O2

Acetylcysteines
- Excellent at scavenging excess ROS
- N-Acetylcysteine used for APAP overdose
- Can get OTC, FDA wants to regulate it because it’s effective

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14
Q

What was this used for? And how does it work?

A
  1. Postive pressure valve
  2. Negative pressure valve
  3. Leather Diaphragm
  • Used heavily for Polio victims in the 1960’s.
  • Polio destroys the ability of the CNS to communicate with skeletal muscles
  • Can be used long-term

How does it work?
- Leather diaphragm is fitted around the patient’s neck or upper body in order to create a seal between the iron-lung and the environment
- Leather diaphragm on the distal end pulls the diaphragm outward causing the pressure inside the iron-lung to become negative/reduced —> allowing for air to be pulled into the patient

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15
Q

Negative Pressure Breathing vs PPV

A

Negative pressure breathing
- Diaphragm contracts –> PPl is reduced –> outer lung is pulled closer to the chest wall bringing air into the lungs evenly
- Alveoli closest to superficial lung tissue will fill first
- Allows for deeper alveoli to fully-fill and stretch (mechanical stretch is important for surfactant)

PPV
- PP pushes air into the lungs
- Alveoli closest to the large airways fill first (deep alveoli)
- Deeper alveoli compress alveoli between the deep areas and the border of the lung
- Loss of mechanical stretch

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16
Q

Iron Lung Guy vs Christopher Reed

A

Irong Lung Guy
- Used the iron lung for 50+ years
- Became a lawyer while in the iron lung
- Had to source spare parts for the iron-lung when they wore out
- Not mobile, so inconvenient

Christopher Reed
- Did not live 50 years with the PPV (trach)
- Died from pulmonary complications
- Mobile, but not normal ventilation for the lung

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17
Q

Which patient population is affected by this?

Airplanes: Altitude & Pressurization

A
  • Planes fly at high altitude (40,000ft) because the air is thinner and they better gas mileage
  • Modern planes are pressurized to mimic the atmosphere of ~8,000ft
    - Sick lungs, a sick right heart will be affected by this atmosphere
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18
Q
A
  1. 760mmHg
  2. 523mmHg
  3. 349mmHg
  4. 226mmHg
  5. 141mmHg
  6. 87mmHg
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19
Q

What happens if a plane depressurizes?

A
  • O2 masks are connected to a container, once pulled from the container, an exothermic chemical reaction is set off (heat)
  • Chemicals combine –> produce a higher concentration of oxygen
  • Masks contain just enough O2 to keep you conscious until the pilot takes the plane down to a safer altitude
  • This is not sufficient O2 for the pilots. They keep their own tanks with 100% O2
  • With sudden depressurization at an altitude of 40,000ft, the PO2 of the air in the airplane will become 29mmHg. Because this is lower than the PO2 in the lungs, gas exchange will begin to work in reverse —> O2 leaves the lungs to move into the environment
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20
Q

The acidity of a solution is dependent on…

A

⍺ represents acidity

⍺ H+
- the acidity of a solution is dependent on hydrogen ion activity (directly related to concentration)

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21
Q

Volatile, Non-Volatile, & Pathologic Acids in the body

A

Volatile Acids
Means this acid can take the form of a gas
- CO2

Non-Volatile Acids
Because these are non-volatile, they cannot turn into a gas (CO2) and be removed from the body. Must be removed by the kidney or liver
- Typically formed from dietary protein metabolism
- Sulfuric acid (sulfate)
- HCl
- Lactic acid (lactate)
- Phosphoric acid (phosphate)

Pathologic Acids
- Acetoacedic acid (acetone):
- produced in poorly managed DM
- produced by the liver after large amount of ETOH metabolism

  • Butryic acid:
    - produced in poorly managed DM
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22
Q

Why is CO2 considered a weak acid?

A
  • CO2 & H2CO3 are considered weak acids in the body
  • CO2 can combine with H2O to form H2CO3
    • CO2 +H2O ⇌ H2CO3

CO2 is considered a weak acid because:
- H2O & CO2 are largely present throughout the body, meaning that CO2 can rapidly combine with H2O to form H2CO3
- Since CO₂ indirectly causes an increase in free H⁺ ions, it’s effectively considered an acid

CO2:H2CO3 Ratio –> 1000:1

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23
Q

Why Does CO₂ ≈ H₂CO₃ in Physiology?

A

Extremely Fast Equilibrium:
- The enzyme carbonic anhydrase, especially abundant in red blood cells, catalyzes the CO₂ ⇌ H₂CO₃ reaction almost instantaneously.
- Because of this, any change in CO₂ rapidly affects [H⁺], influencing pH.

H₂CO₃ is Hard to Measure:
- In clinical practice, we don’t measure H₂CO₃ directly.
- Instead, we estimate it using the partial pressure of CO₂ (PaCO₂), since:
[H2CO3] ≈ 0.03 × PaCO2

So physiologically, changes in PaCO₂ directly imply changes in H₂CO₃.

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24
Q

Acid Dissociation Equation: What is it?
What makes a component of the equation a conjugate base?

A

HA ⇌ H+ + A-

  • H+ is the weak acid
  • A- is a conjugate base

When an acid dissociates, and in the process a base is produced, that base is called a conjugate base.

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25
Strong Bases vs Weak Bases: What are the differences? Examples of Each?
**Strong Bases** - dissociates fully & easily in solution to form OH- ions - accepts H+ well - forms weak conjugate acids - Ex: NaOH -main component in drain cleaner **Weak Bases** - partially dissociates in solution - does not accept H+ as well - forms strong conjugate acids - Ex: Flouride in toothpaste & **HCO3-**
26
Strong Acids vs Weak Acids: What are the differences? Examples of each?
**Strong Acids** - dissociate very easily in solution and are prone to donating H+ - generate weak conjugate bases - Ex: HCL ⇌ H+ + Cl- - Cl- is a weak conjugate base because it does like to accept protons after dissociation **Weak Acids** - do not dissociate as easily in solution - generate strong conjugate bases - Ex: H2CO3⇌ H+ + HCO3- - HCO3- is a strong conjugate base because it will accept protons
27
Protein Structure & Acid/Base Balance: How do changes in pH affect structure? Specific examples?
**Protein Structure Depends on pH** - Proteins rely on ionic interactions to maintain their 3D shape (tertiary/quaternary structure). - Changes in pH can alter the charge on amino acid side chains (especially histidine, lysine, arginine, glutamate, and aspartate). - This can disrupt folding, causing denaturation or loss of function. **Acidosis or Alkalosis Can Impair Protein Function** - Acidosis → more H⁺ binds to proteins → altered charge and conformation → impaired function (decreased Hb affinity for O2 in the presence of too many H+ ions) - Alkalosis→ fewer H⁺ ions → abnormal ionization → impaired protein binding (decreased Ca²⁺ binding to albumin in alkalosis).
28
# Na+/K+/ATPase and ATPases? Enzyme Activity & Acid/Base Balance
- Every enzyme has an optimal pH - Deviations from this range reduce catalytic efficiency or inactivate the enzyme entirely. - Changes in pH can alter the charge and shape of the active site **Na+/K+ATPase Pump:** - Extra H+ ions reduce effectiveness and efficiency of the pump - K+ is no longer pumped into the cell --> hyperkalemia **ATPase Enzyme** - Produces ATP - Located in mitochondria - Extra H+ reduces effectiveness of pump ---> decreasing ATP production --> further increasing hyperkalemia
29
Additives in prescription meds? Super basic drug example given in class?
- Usually a HCl salt to promote absorption or distribution of the drug - Sodium pentobarbitol: very painful if infused too fast
30
What kind of scale is pH? How do we calculate pH and [H+]? How is [H+] measured (units)?
- pH is a logarithmic scale - a pH difference in 1 will give us a 10x change: pH of 8: [H+] =10 nmol/L pH of 7: [H+] = 100 nmol/L pH of 6: [H+] = 1000 nmol/L **How do we calculate pH?** pH= -log[H+] **How do we calculate [H+]?** 1 x 10 -pH [H+] concentration is measured in moles/L .**000**000000 = milimole .000**000**000 = micromole .000000**000** = nanomole
31
Gastric & Pancreatic pH: How is acid/base balance affected with pathologic conditions affecting these organs?
**Gastric pH: 1** - Acidity facilitates degradation of food products - Intestinal obstruction or vomitting stomach contents will cause a significant loss of acid --> can cause alkalosis **Pancreatic pH: 8** - Most alkaline pH in the body - Neutralize the acid found in the stomach before it moves into the intestines - High volume of pancreatic secretions/enzymes needed to neutralize the significant acid load - Very high intestinal motility will cause acidosis because HCO3- produced by pancreas is lost
32
33
# Functionality of these buffers rely on what? Buffers Present in the Body: What are they? What is their funtion?
- HCO3- (extracellular) - Hb (and other proteins) - Phosphate (intracellular) -ATP storage, ATP is released when pulled from adenosine, phosphorylates & dephosphorylates things Reduce the overall concentration of H+ Can donate protons if they have to Can acquire protons Both are dependent on the composition of the buffer and it's pKa The functionality of these buffers largely rely on Hb concentration
34
Small changes in pH equate to....
**Small changes in pH = drastic changes in [H+]**
35
How do the lungs act as a buffer?
The lungs are able to rid the body of CO2 quickly, acting as a buffer The lungs removing CO2 from the body allow the physiologic buffers in our blood to function optimally
36
What does this graph show?
- This graph shows us how well we are able to buffer protons with varying levels of Hb - The steepness of the buffering line slope correlates to blood buffering capacity **High Hb Levels:** - Higher amount of Hb inside the RBC - Increased buffering capacity - Steep buffering line on graph **Low Hb Levels:** - Lower amount of Hb inside the RBC - decreased buffering capacity - Flatter buffering line on graph
37
What is this graph showing? Based on what equation? Main patterns we will see?
This graph shows us how different systems behave under normal & abnormal conditions - Isobars are lines of constant PCO₂ - Based on the Henderson–Hasselbalch equation: - pH=6.1+log [(HCO3-) / (0.03 × PCO2)] **Main Patterns Seen** - pH and bicarbonate move in the same direction in metabolic disorders. - pH and PCO₂ move in opposite directions in respiratory disorders
38
Acid/Base Disturbances: Uncompensated Respiratory Acidosis
CO₂: Increased (hypercapnia). HCO₃⁻: Slightly elevated as a byproduct of CO2 levels. pH: Decreased (acidosis). **CO2** + H2O ↔ H2CO3 ↔ **H+ + HCO3−** More CO₂ drives the reaction to the right → more H⁺ → slightly elevated HCO₃⁻ → lower pH (acidosis). In uncompensated respiratory acidosis, HCO₃⁻ may be slightly elevated due to CO₂-driven H₂CO₃ dissociation, but this small rise is not considered true compensation
39
Acid/Base Disturbances: Uncompensated Respiratory Alkalosis
CO₂: Decreased (hypocapnia). HCO₃⁻: Slightly decreased as a byproduct of having less CO2 pH: Increased (alkalosis). **CO2** + H2O ↔ H2CO3 ↔ **H+ + HCO3−** Mechanism: Less CO₂ shifts the reaction to the left → fewer H⁺ ions → slightly less HCO₃⁻ → higher pH (alkalosis).
40
Nomogram- Acute: Uncompensated Chronic: Compensation
41
# Kyphoscoliosis is abnormal curvature in which planes? Causes of Respiratory Acidosis (long list, mostly common sense)
Anything that can decrease VE or decrease chest wall compliance - Kyphoscoliosis is abnormal curvature in the sagital and coronal plane. Surgical correction actually decreases chest wall compliance - Barbituates, such as pentobarbitol, cause significant respiratory depression
42
Phrenic Nerve?
C3, C4, C5 This becomes a problem with regional blocks in the shoulder/interscalene area if you block the phrenic nerve
43
pH Formulas (including HA & A-)
-log [H+] = -logK + log (A-/HA) or pH = pK + log(A-/HA)
44
Base Dissociation Formula: What is considered the conjugate acid?
HB ⇌ B- + H+ When a base dissociates, it breaks down into the base (B-) and conjugate acid (H+)
45
Buffer Formula? How does this formula apply to our blood buffer system? Two examples?
Buffer + H+ ⇌ HBuffer - In solution, buffers are ionized in order to better combine with a H+ - If the environment becomes more acidic, the buffer soaks up some of those hydrogen ions to form HBuffer. - If the environment becomes less acidic, the reaction can go backward: HBuffer can release H⁺ back into the solution **Deoxy Hb buffering the blood** Hb− +H + ↔ HHb **Bicarb buffering the blood** HCO3− +H + ↔ H2CO3
46
Kidney based buffer briefly mention in class?
Ammonia-based buffer- buffers the urine so it is not acidic
47
# pK of HCO3-? What is pK? How does this apply to buffers?
- pK is the pH at which a buffer is equal parts ionized and unionized - A buffer is best at buffering when the pH is at it's pK value pK of HCO3-? 6.1; meaning HCO3- is most effective at a pH of 6.1
48
What is the Isohydric Principle?
- The different buffer systems in the body respond to changes in H⁺ concentration at the same time and in the same way — so the pH stays coordinated across all the buffers - If the H⁺ concentration in the blood changes, it affects every buffer instantly. - Buffers don’t act in isolation — they’re all reacting to the same "pool" of H⁺ ions. ✅ So a shift in H⁺ → all buffers shift their reactions together → one consistent blood pH.
49
Why is albumin not considered a major buffering protein?
- Albumin is a protein in the *plasma* - This protein is more important for oncotic pressure, and keeping the plasma within in the cardiovascular system - Hb is in high concentrations *inside* the RBC, allowing for Hb to be a more potent H+ buffer - The Hb that is dissolved in plasma is hematocrit, and that is not nearly as effective as Hb inside the RBC
50
As Hb increases --> Buffering capacity increases --> Causing the PCO2 Isobars become compressed or move closer towards "normal." This allows for a greater variability in the HCO3- response to changes in pH: - Larger availability of HCO3- to buffer an increase in H+ - Faster response to decrease HCO3- in the presence of alkalosis
51
As Hb decreases ---> decreased buffer capacity --> isobars are stretched further from the point of "normal." Less variability in HCO3- response, meaning we will not see as much of a change in HCO3- levels in response to a change in pH.
52
What is the gain of a control system?
How strongly a system is able to respond to change - High gain: Large correction - Low Gain: Small correction
53
What role do the kidneys place in acid/base balance?
- **Reabsorbs HCO₃⁻ to preserve base** - The kidneys reabsorb almost all filtered bicarbonate in the proximal tubule. - **Secretes H⁺ to eliminate acid.** - The kidneys actively secrete hydrogen ions into the urine, mainly in the proximal tubule, distal tubule, and collecting duct. - **Generates new HCO₃⁻ during acidosis.** - **Acidifies urine to safely excrete H⁺** - H+ ions are buffered in the urine by phosphate and ammonia, allowing the urine to become very acidic while protecting kidney tissues
54
Why do we not see major differences between acute vs chronic metabolic acid/base disorders?
* In metabolic acidosis, lungs increase ventilation → blow off CO₂ → partially compensate almost immediately * In metabolic alkalosis, lungs decrease ventilation → retain CO₂ → partially compensate almost immediately Because the respiratory system compensates so quickly, acute and chronic metabolic disorders don't look dramatically different in terms of the basic acid-base measurements like pH, CO₂, and HCO₃⁻. (At least not nearly as different as respiratory problems do.)
55
Common Causes of Respiratory Alkalosis
Congenital Hyperventilation Syndromes Inflammation in brain Brainstem Tumor Salicylates: ASA Toxicity Progesterone: "Breathing for two" Acute asthma- basically anxiety induced alkalosis
56
Common Causes of Metabolic Acidosis
Losing HCO3- Producing too many H+ Inability to excrete H+ Consuming acids in diet or drugs - Methanol: byproduct of fermentation. In moonshine. Can make you go blind - Ethanol: methanol & ethanol stimulates the pancreas - Ethylene Glycol: Component of antifreeze. Smells sweet, make sure pets and kids are not around a leak -Blue if european car. Green if japanese or american - Ammonium chloride: Component of fertilizer
57
Net production of ATP from one molecule of glucose under normal conditions? What about in hypoxemia?
- 30 ATP - 2 ATP in anaerobic metabolism
58
Common Causes of Metabolic Alkalosis
Loss of H+ ions Ingestion of excess HCO3- Gastric Fistula: Causes loss of stomach acid Overproduction of steroids- aldosterone or cortisol
59
- Uncompensated respiratory acidosis - Uncompensated respiratory alkalosis - Uncompensated metabolic acidosis - Uncompensated metabolic alkalosis - Both are uncommon. Respiratory system usually compensates quickly - Partially compensated respiratory acidosis - Partially compensated respiratory alkalosis - Partially compensated metabolic acidosis - Partially compensated metabolic alkalosis - Ventilation can only be reduced so much to compensate for alkalosis without compromising oxygenation
60
# What is it? What does this do for the blood? Anion Gap
* (Cations+) = (Anions-) * Blood needs to be electrically neutral. Cations should equal Anions * Normal value should 12 mEq/L , +/- 4 mEq/L * The normal anion defecit is due to the unmeasured proteins that are negatively charged
61
Values? Which components are cations and which are anions?
**Cations/Unmeasured Cations** Na: 142 mEq/L K: 4 mEq/L Ca: 1.3 mEq/L Mg: 0.8mEq/L **Anions/Unmeasured Anions** Cl: 106 mEq/L HCO3: 24 mEq/L HPO4, H2PO4: 2 mEq/L SO4 2-: 0.5mEq/L
62
Anion Gap- Full Equation: How does the body maintain electrical neutrality?
[Na+] + [unmeasured cations] = [Cl-] + [HCO3-] + [unmeasured anions] or [Na+] - ([Cl-] + [HCO3-]) = [unmeasured anions] - [unmeasured cations]
63
Causes of metabolic acidosis w/ normal anion gap?
**Loss of HCO3:** - Diarrhea - Pancreatic fluid loss **Cl retention:** - Renal tubular acidosis - Anion gap is normal because the kidney can maintain the charge balance by increasing/decreasing HCO3- or Cl- as necessary - Children cannot maintain this balance as well as adults
64
# MUDPILEES Causes of metabolic acidosis w/ an increased anion gap?
Overproduction of non-volatile acids **Presence of unmeasured metabolic anions:** * DKA from DM, ETOH, starvation * Lactic acidosis from hypoxemia, anemia, CO, hypovolemia, ARDS, shock, strenous exercise * Renal insufficiency **Presence of ingested drugs or toxic substances:** * Methanol * Ethanol * Salicylates * Ethylene glycol * Ammonium chloride MUDPILEES: Methanol, Uremia, DKA, Propylene glycol, Iron/Isoniazide, Lactic acidosis, Ethylene Glycol/ETOH, Salicylates
65
A strong/loud cough moves how much air?
- About 2 liters of air - As the cough becomes more muffled, the less air that's moved
66
What are each of the components of this negative feedback? Changes in metabolism cause what? How are regulated variables ranked in order of response by the sensors?
**Sensors** - Looking at levels of PO2, pH, PCO2 - Peripheral chemoreceptors; carotid body - Secondary peripheral chemoreceptors; aortic body - Central chemoreceptors in brain stem are mostly responsive to fluctuations in H+ - Respond fastest to H+ changes as a function of changes in PCO2 - Non-volatile acids do not cross the BBB, central chemoreceptors will have a delayed response to a buildup of these **Controller** - Pons/Medulla react to information from sensors, monitor for disturbances, and react to maintain a normal pH - If we have a plan to exercise in a healthy system, our ventilation increases as needed almost instantly **Control System** - Alveolar ventilation: - Changes in metabolism cause an increase or decrease in VE, first by adjusting Vt, secondly by adjusting RR **Regulated Variables** - pH: illicit the strongest response from chemoreceptors - PaCO2: Second to [H+] - PO2: Chemoreceptors do not usually respond to a decrease in PO2 until it is ~70mmHg
67
# What kind of nerve fibers? How does the body increase Vt during an increase in metabolism?
Central respiratory sends stronger inspiratory signals → recruitment of A⍺ skeletal muscle motor neurons (very large, myelinated nerve fibers) → increased motor unit size → frequency of motor neuron firing increases → more force generated
68
How is RR determined by the body?
Governed by the duration of the respiratory cycle and time in between each of the events
69
Which nerve fibers are harder to block?
A⍺ motor neurons are the hardest to block because of their size Pain neurons are easier to block because they are smalled Rule of thumb: if motor function is blocked, pain is likely blocked as well
70
Organization of respiratory cycle
**Higher Order Control Centers** - Frontal Lobe - Motor Cortex - Allows for voluntary control of breathing **Cycle of inspiration and expiration** - Automatic control of breathing in the central respiratory center **Reflexes** - Response from sensors - Baroreceptors are also included **Lung Sensors** - Irritant sensors; cough - Stretch (volume) sensors: Inhibits inspiration at a certain volume **Airway Sensors** - Irritant sensors; cough - Trachea **Other sensors that affect breathing** - Pain sensors **Main muscles of breathing** - Diaphragm - External intercostal - Internal intercostal - Accessory: sternocleidomastoid, scalene, abdominal, pec minor - Coordination of these muscles is organized by the brainstem; duration of inspiration and expiration are affected
71
Pons: - Pontine respiratory group (bottom of pons, top border of medulla) Medulla: - Dorsal respiratory group (posterior) - Ventral respiratory group (anterior) All considered nuclei because they are bundles of nerves/cell bodies within the CNS
72
**1. PRG** **2. DRG** **3. VRG** **4. Decussation of the pyramids:** cross-over point at the distal border of medulla or most superior border of the spinal cord **5. Phrenic nerve** **6. Nucleus tractus soltarius** **7. Nucleus ambiguus** **8. Botzinger/Prebotzinger Complex:**
73
Reciprocal Inhibition
The process where inspiratory and expiratory neurons in the brainstem alternate activity by inhibiting each other, creating a smooth breathing rhythm without overlap between inhalation and exhalation
74
What do central chemoreceptors detect, and how do they influence breathing?
Central chemoreceptors in the medulla detect increased CO₂ (via H⁺) in cerebrospinal fluid and stimulate the DRG to increase respiratory rate and depth.
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What do peripheral chemoreceptors detect, and where are they located?
Peripheral chemoreceptors in the carotid and aortic bodies detect low PaO₂, high PaCO₂, and low pH. They send signals via CN IX and X to the DRG to increase ventilation.
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Which chemoreceptor is more sensitive to changes in PaCO₂: central or peripheral?
Central chemoreceptors are more sensitive to PaCO₂ (H+ primarily) changes and are the primary drivers of respiratory rate under normal conditions.
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What is the function of the Dorsal Respiratory Group (DRG)?
- It receives sensory input ([H+, PaCO2, PO2]) from the vagus (X) and glossopharyngeal nerves (IX) - Receives input indirectly from baroreceptors via NTS - **Sends inspiratory signals via phrenic nerve to the diaphragm and external intercostals** - Sends forced/labored expiratory signals to abdominal and internal intercostal muscles - Located within the NTS
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What is the function of the Ventral Respiratory Group (VRG)?
- It regulates motor output in the pharyngeal constrictor muscles to maintain an open upper airway - Located within the VRG is the Botzinger & Prebotzinger Complex
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How does the PRG affect timing of the respiratory cycle?
**Phase-Switching** - The PRG helps smooth transitions between inspiratory and expiratory phases - It adjusts the duration of inspiration by inhibiting or stimulating the DRG/VRG, ensuring adaptive breathing patterns during different physiological conditions Primary function is limiting inspiratory time
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1. Decussation of the pyramids 2. Trigeminal nerve (V) 3. Glossopharyngeal nerve (IX) 4. Vagus Nerve (X) 5. Hypoglossal nerve (XII) 6. Accessory nerve (XI)
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What is the role of the trigeminal nerve (CN V) in respiration?
It provides sensory input from the face and nasal mucosa, helping trigger reflexes like sneezing and altered breathing in response to nasal irritation.
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What is the role of the glossopharyngeal nerve (CN IX) in respiration?
It carries afferent signals from carotid body chemoreceptors, relaying information about PaO₂, PaCO₂, and pH to the DRG to adjust ventilation.
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What is the role of the vagus nerve (CN X) in respiration?
It transmits sensory input from pulmonary stretch receptors, aortic bodies, and lung irritant receptors, and mediates the Hering-Breuer reflex to prevent overinflation.
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Reticular Formation: A broad term that describes a swath of tissue in the brainstem Portion of the reticular formation that is considered the "Medullary Area" or "Medullary Respiratory Center" Contains inspiratory and expiratory neurons
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What is the function of Nucleus Tractus Soltaris? Where is it located?
- Located within the reticular formation - DRG is located within the NTS - Primary function is to generate inspiratory signals, but also inhibits expiratory signals when the NTS is active - Receives input from baroreceptors - Sends inspiratory signals via phrenic nerve - Crosses over at pyramidal decussation
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Which cranial nerves carry baroreceptor input to the brainstem?
- Glossopharyngeal nerve (CN IX) from the carotid sinus - vagus nerve (CN X) from the aortic arch.
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Where do baroreceptor signals first synapse in the brainstem?
Nucleus tractus solitarius (NTS) in the medulla.
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Where is the Bötzinger complex located?
In the rostral portion of the ventral respiratory group (VRG) in the ventrolateral medulla.
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What type of neurons are primarily found in the Bötzinger complex?
Expiratory neurons.
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What is the main function of the Bötzinger complex?
→ Inhibits inspiratory neurons to help terminate inspiration and allow the transition to expiration **Sends inhibitory signals to:** - Dorsal respiratory group (DRG) - Pre-Bötzinger complex (the rhythm generator) This action "turns off" inspiratory neurons, promoting passive expiration and setting the rhythm for breath-to-breath cycling. - Controls **respiratory rhythmogenesis**
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# What happens if there is a lesion to this region? How does the PRG contribute to modulation of inspiratory cut-off?
The pneumotaxic center tells the DRG to limit inspiratory time based on sensory feedback Lesions to this region cause prolonged inspirations (apneustic breathing) and short expirations (terribly awful)
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How does the PRG integrate information from the pulmonary stretch receptors?
**Stretch/irritant receptors → CN X → PRG → DRG/VRG → Phrenic motor output** - PRG interprets information --> sends signals to the DRG: - When to stop inspiration - How long inspiration should last - Adjusting rhythm to match sensory context **Reflex: Hering-Breuer Inflation Reflex** - Inhibits inspiration when lungs are overly inflated. - The PRG uses this input to terminate inspiration sooner, helping regulate tidal volume and prevent overinflation.
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How does the PRG integrate sensory information from the irritant receptors?
**Stretch/irritant receptors → CN X → PRG → DRG/VRG → Phrenic motor output** Trigger protective reflexes such as: - Coughing - Bronchoconstriction - Rapid shallow breathing The PRG adjusts the breathing pattern (e.g., shortening inspiration, increasing rate) to minimize further exposure.
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Central chemoreceptor response time: CO2 vs non-volatile acids
**CO2** - Increase in peripheral CO2 leads to and increase in CO2 in the brain; - Can easily diffuse across the BBB and central chemoreceptors respond almost instantaneously **Non-Volatile Acids** - Non-volatile acids have a harder time crossing the BBB due to their charged nature - Sometimes need a carrier protein - Delay in brainstem response to non-volatile acids
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Conditions in the CSF
**Conditions in CSF** - Clear - Minimal protein - pH: 7.31-7.32 - Contains it's own buffering system - Produces HCO3- (HCO3- cannoted cross BBB) - Glial cells act as a buffer - PCO2: 50mmHg - Higher than PaCO2 due to neurons producing CO2 as a byproduct of metabolism - CO2 (all gasses) must move down a pressure gradient --> needs to be higher in the brain to reach the lungs
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How does [CO2] affect cerebral blood flow?
↑ CO2 → vasodilation → ↑CBF ↓ CO2 → vasoconstriction → ↓ CBF
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- Apneustic center in the PRG - Responsible for apneustic breathing - Can limit activity of pneumotaxic center
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Location of peripheral chemoreceptors: What specifically are they monitoring?
**Aortic bodies** - Group of 3-5 aortic bodies located on the aortic arch - Monitors gas concentration of blood coming from the LV - Transmit info to medullary brainstem via vagus **Carotid Bodies** - Carotid body on each side of the neck located between the internal and external carotid arteries - Monitors gas concentration going to the brain - Transmit info to medullary brainstem via glossopharyngeal
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# Respiratory vs Cardiac Peripheral Chemoreceptor Reflexes
**Respiratory** ↑CO2 or ↓pH: - Vt is increased first - RR increased second if needed **Cardiac** ↑CO2 or ↓pH: - CO is increased - BP is increased - Allows for more blood to be pumped through the lungs --> increased surface area in the lungs for gas exchange --> blow off more CO2
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What is the problem with blowing off too much CO2 in someone with heart problems?
- Albumin/ proteins are negatively charged and attract H+ - If too much H+ is removed from the body, Ca++ takes it's place - Leads to decreased serum ionized Ca++ → heart cannot properly contract
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When do peripheral chemoreceptors respond to PO2?
~70mmHg