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Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
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Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
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Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
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Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
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ABG interpretation alication me uuu.pptx
1.
2. Dr. Ahmed Tantawy
Lecturer of chest diseases,
Faculty of medicine,
Cairo university
Arterial Blood Gas (ABG) Interpretation
3. If you are given this ABG:
pH (7.38)
PaCO2 (41 mmHg)
PaO2 (95 mmHg)
HCO3 (23 mmol/L)
Na+ (143 mg/dl)
Cl− (98 mg/dl)
These values are all normal but the patient has significant
acid base disturbances that may be fatal, if untreated.
How would you
interpret it?
4. DEFINITIONS
• Acidosis: is a disturbance that lowers the extra-cellular fluid pH.
• Alkalosis: is a disturbance that raises the extra-cellular fluid pH.
• Acidemia: is a reduction of the extra-cellular fluid pH of the blood. Accordingly an
acidemia may result from a combination of different types of acidosis or a combination
of acidosis and alkalosis.
• Alkalemia: is an elevation of the extra-cellular fluid pH of the blood.
• Base Excess (BE): is the amount of acid (+) or base (−) (in mEq/liter) required to
restore the pH of a liter of blood to the normal range at a PaCO2 of 40 mmHg.
6. HENDERSON EQUATION
• This equation represents the relationship between the components of the ABG
and may be written in different ways:
A simple way is:
By substituting PaCO2 for [H2CO3] that is measured from ABG, the equation can
be written in a more practical way :
[H+] is the Hydrogen ion (proton) concentration, and it can be easily calculated
from pH
7. [H+] is the Hydrogen ion (proton) concentration, and it
can be easily calculated from pH
8. The purpose of this equation is:
• To ensure that the ABG values are accurately recorded.
Solving the equation should result in equalization of its two
sides.
• If one of the ABG values is missing, the equation can be
solved to determine that missing value.
9. Approach to ABG interpretation
1. Determine whether the ABG data are accurate by quickly applying Henderson
equation
2. Look at the pH and determine whether it is normal, acidemic or alkalemic
3. Determine the most likely primary disturbance (by looking at HCO3 and
PaCO2 and determining which one is largely responsible)
4. If the primary disturbance is respiratory, determine whether it is acute or
chronic
5. If the primary disturbance is metabolic, determine whether an appropriate
respiratory compensation is present
6. Calculate the AG
7. Calculate the corrected HCO3, if applicable
11. Approach to metabolic acidosis
Quickly apply the Henderson equation ( Validity)
Look at the pH (normal, acidemia or alkalemia).
If the reduction in HCO3 is the predominant abnormality → primary metabolic
acidosis
Calculate the AG (AG = Na+ − (Cl− + HCO3))
• If normal (~ 12) → non-anion gap metabolic acidosis (NAGMA)
• If high (>12) → anion gap metabolic acidosis (AGMA). Calculate the corrected
HCO3, (corrected HCO3 = ΔG + measured HCO3; as ΔG = AG − 12):
– If within normal range of HOC3 (21–26) → no other metabolic disturbance
– If >26 → primary metabolic alkalosis
– If <21 → primary non-anion gap metabolic acidosis
12. Look at PaCO2:
•If normal or high → primary respiratory acidosis.
•If low → calculate the (expected PaCO2 range) which
equals ( 1.5 × HCO3 + (8 ± 2) )
– If the patient’s PaCO2 is within this range → no respiratory
disturbance
– If patient’s PaCO2 is above the range → primary respiratory
acidosis
– If patient’s PaCO2 is below the range → primary respiratory
alkalosis
13. Interpret the following ABG :
pH (7.32); PaCO2 (24); HCO3 (12); Na+ (135); K− (5.4); Cl− (101)
• Interpretation:
1. Applying the Henderson equation:
[H+] = K × (PaCO2/ [HCO3]) ↔ 48 = 24 × (24/12) = 48
– So, the equation proves that the values are accurate.
2. pH is ↓, so this is an acidemia.
The predominant abnormality is the ↓ HCO3 → so this is primary metabolic acidosis.
3. By calculating the AG = Na+ − (Cl− + HCO3) = 22 (↑). It is >12 → so this is an anion
gap metabolic acidosis (AGMA).
4. Corrected HCO3 = ΔG + measured HCO3 (as ΔG = AG – 12 = 10) = 10 + 12 = 22; it
is within the normal range of HCO3 (21–26), so there is no other metabolic
disturbance.
5. PaCO2: is low, so we should calculate the expected PaCO2 range:
Expected PaCO2 Range = 1.5 × HCO3 + (8 ± 2)= 24–28; the patient’s PaCO2 lies
within this range, so there is no primary respiratory disturbance.
pure anion gap
metabolic acidosis
14. Interpret the following ABG:
pH (7.11); PaCO2 (16); HCO3 (5); Na+ (133); Cl− (118)
• Interpretation:
1. – Applying Henderson equation indicates accurate results.
2. ↓ pH → so this is an acidemia.
↓ HCO3 → so this is a primary metabolic acidosis
3. AG = Na+ − (Cl− + HCO3) = 10 (normal) → so this is a non
anion gap metabolic acidosis (NAGMA).
4. Expected PaCO2 Range = 1.5 × HCO3 + (8 ± 2) = 13.5– 17.5 →
the patient’s PaCO2 lies within this range, so there is no primary
respiratory disturbance.
Non-anion gap
metabolic acidosis
15. Interpret the following ABG:
pH (6.88) ; PaCO2 (40) ; HCO3 (7) ; Na+ (135) ; Cl− (118)
• Interpretation:
1. Applying Henderson equation indicates accurate results.
2. ↓ pH → so this is acidemia.
↓ HCO3 → so this is primary metabolic acidosis.
3. AG = Na+ − (Cl− + HCO3) = 10 (normal) → so this is a non anion gap
metabolic acidosis (NAGMA).
4. PaCO2 is normal (it should be low in the face of a very low pH) → so, there is a
primary respiratory acidosis.
Apply the Expected PaCO2 Range = 1.5 × HCO3 + (8 ± 2) = 16.5–20.5 → the
patient’s PaCO2 is higher than this range so there is primary respiratory
acidosis.
Combined non-anion
gap metabolic
acidosis
and respiratory
acidosis
17. Approach to metabolic alkalosis
Quickly apply the Henderson equation ( Validity)
Look at the pH (normal, acidemia or alkalemia).
The increase in HCO3 is the predominant abnormality → primary metabolic alkalosis
Calculate the AG (AG = Na+ − (Cl− + HCO3))
• If normal (~ 12) → no primary metabolic acidosis
• If high (>12) → primary anion gap metabolic acidosis (AGMA)
Look at PaCO2:
• If normal or low → primary respiratory alkalosis.
• If high → calculate the (expected PaCO2 range = 0.9 × HCO3 + (9 to 16)):
– If patient’s PaCO2 is within this range → no respiratory disturbance
– If patient’s PaCO2 is above the range → primary respiratory acidosis
– If patient’s PaCO2 is below the range → primary respiratory alkalosis
18. Interpret this ABG:
pH (7.55) ; PaCO2 (49) ; HCO3 (42) ; Na+ (148) ; Cl− (84)
• Interpretation:
1. Applying Henderson equation indicates accurate results.
2. ↑ pH → so there is an alkalemia.
↑ HCO3 → so there is a metabolic alkalosis.
3. AG = Na+ − (Cl− + HCO3) = 22 (↑) → so there is an anion gap metabolic
acidosis.
4. ↑ PaCO2 (same direction as HCO3) → Expected PaCO2 Range = 0.9 × HCO3
+ (9-to-16) = 47–54 → the patient’s PaCO2 (49) lies within this range → so, there
is no primary respiratory disturbance.
Combined anion
gap metabolic
acidosis and
metabolic
alkalosis with an
alkalemic pH
19. RESPIRATORY ACIDOSIS
Types:
Acute respiratory acidosis: for every 10 mmHg rise in PaCO2 :
pH drops by 0.08
HCO3 increases by 1 mmol/L; maximum level of HCO3 is ~32 mmol/L.
Chronic respiratory acidosis : for every 10 mmHg rise in PaCO2:
pH drops by 0.03
HCO3 increases by 3 mmol/L; maximum level of HCO3 is ~45 mmol/L.
21. Approach to respiratory acidosis
Quickly apply the Henderson equation.
Look at the pH (normal, acidemia or alkalemia)
The increase in PaCO2 is the predominant abnormality → primary respiratory
acidosis
Determine whether acute or chronic
• Acute: pH ↓ by 0.08 for every 10 mmHg ↑ in PaCO2. HCO3 ↑ by 1 mmol/L (max
~32)
• Chronic: pH ↓ by 0.03 for every 10 mmHg ↑ in PaCO2. HCO3 ↑ by 3 mmol/L (max
~45)
22. Calculate the AG (AG = Na+ − (Cl− + HCO3))
• If high (>12) → primary anion gap metabolic acidosis (AGMA)
If applicable, calculate the corrected HCO3, as in metabolic acidosis
• If normal (~ 12) → look at HCO3
If ↓ or N → primary non-anion gap metabolic acidosis
If ↑ → look at HCO3 and determine the type of respiratory acidosis:
(HCO3 ↑ by 1 (acute) OR 3 (chronic) for each 10 mmol/L ↑ in PaCO2)
If within the expected → no primary metabolic disturbance
If lower → non-anion gap metabolic acidosis
If higher → metabolic alkalosis
23. Interpret the following ABG :
pH (7.34); PaCO2 (60); HCO3 (31); AG (11)
• Interpretation:
1. Applying Henderson equation indicates accurate results.
2. pH is slightly low indicating a mild acidemia.
3. ↑ PaCO2, so this is a primary respiratory acidosis.
4. Metabolic compensation indicates a chronic respiratory acidosis: PaCO2
increased by 20 mmHg which corresponds to a drop in pH by ~ 0.6 and an increase
in HCO3 by ~ 6 .
5. AG is normal and HCO3 is adequately increased, therefore no metabolic
disturbances.
6. The A-a gradient = (150 – PaCO2 × 1.25) – PaO2 = 11 (normal)
Chronic primary
respiratory acidosis
related to COPD
24. The patient in the previous case became drowsy and unresponsive 4 hours after presentation.
A repeated ABG showed: pH (7.15); PaCO2 (96); PaO2 (169) HCO3 (33); AG (10).
• Interpretation:
1. Applying Henderson equation indicates accurate results.
2. ↓ pH → acidemia.
3. ↑ PaCO2 → so this is primary respiratory acidosis.
4. Metabolic compensation indicates an acute respiratory acidosis in addition to the
chronic respiratory acidosis.
5. AG is normal and HCO3 is adequately increased, therefore no metabolic disturbances.
Conclusion: Acute primary respiratory acidosis and a chronic
respiratory acidosis. This COPD patient was given a high flow O2
(indicated by the high PaO2) unnecessarily resulting in CO2
elevation
25. RESPIRATORY Alkalosis
Types:
Acute respiratory alkalosis: for every 10 mmHg drop in PaCO2 :
pH rises by 0.08
HCO3 drop by 2 mmol/L.
Chronic respiratory alkalosis : for every 10 mmHg drop in PaCO2:
pH rises by 0.03
HCO3 increases by (5-7) mmol/L.
27. Approach to respiratory Alkalosis
Quickly apply the Henderson equation.
Look at the pH (normal, acidemia or alkalemia)
The drop in PaCO2 is the predominant abnormality → primary
respiratory alkalosis
Determine whether acute or chronic
• Acute: pH ↑ by 0.08 (and HCO3 ↓ by 2 mmol/L) for every 10 mmHg ↓ in
PaCO2
• Chronic: pH ↑ by 0.03 (and HCO3 ↓ by 5–7 mmol/L) for every 10 mmHg ↓ in
PaCO2
28. Calculate the AG (AG = Na+ − (Cl− + HCO3))
• If high (>12) → primary anion gap metabolic acidosis (AGMA)
If applicable, calculate the corrected HCO3, as in metabolic acidosis
• If normal (~ 12) → look at HCO3
If ↑ or N → primary metabolic alkalosis.
If ↓ → look at HCO3 and determine the type of respiratory alkalosis:
(HCO3 ↓ by 2 (acute) OR (5-7) (chronic) for each 10 mmol/L ↓ in
PaCO2)
If within the expected → no primary metabolic disturbance
If lower → non-anion gap metabolic acidosis
If higher → metabolic alkalosis
29. Interpret the following ABG: pH (7.55); PaCO2 (44); HCO3 (45); Na+ (144); Cl−
(112).
• Interpretation:
Applying Henderson equation:
[H+] = K × (PaCO2/ [HCO3]) ↔ 28 ≠ 24 × (44/45) = 21
So, the equation indicates that the values are incorrect.
Repeat ABG sampling is advised or check with the lab to ensure accurate
calculation of HCO3 and recording of results.
31. • Applying Henderson equation indicates accurate results.
• – Normal pH → so no acidemia or alkalemia.
• – Normal HCO3 → so no obvious metabolic abnormality.
• AG = Na+ − (Cl− + HCO3) = 22 (↑) → so there is an anion gap metabolic
acidosis.
• – Corrected HCO3 = ΔG + measured HCO3 (ΔG = 22–12 = 10). = 10 + 23 =
33; So, the corrected HCO3 = 33 → it is higher the normal range of HCO3
(21–26) → so there is an additional metabolic alkalosis.
• – PaCO2 is normal
• – Expected PaCO2 Range = 1.5 × HCO3 + (8 ± 2) = 41–45 → the patient’s
PaCO2 (41) lies within this range → so, there is no primary respiratory
disturbance.
ABG 1:
pH (7.38), PaCO2 (41 mmHg), PaO2 (95 mmHg), HCO3 (23 mmol/L),
Na+ (143 mg/dl), Cl− (98 mg/dl)
32. ABG 2:
pH (6.88) , PaCO2 (40), HCO3 (7), Na+ (142), Cl− (100)
• Applying the Henderson equation indicates accurate results.
• – ↓ pH → so this is an acidemia.
• – ↓ HCO3 → so this is a primary metabolic acidosis.
• – AG = Na+ − (Cl− + HCO3) = 35 (↑) → so this is an anion gap metabolic
acidosis.
• – Corrected HCO3 = 30; it is higher than the normal range of HCO3 (21–26),
so there is an additional primary metabolic alkalosis.
• – PaCO2 is normal (it should be low) → there is a primary respiratory
acidosis.
33. EFFECT OF A LOW ALBUMIN LEVEL ON AG
Because albumin is one of the unmeasured anions in the blood, a drop in its
level (e.g. secondary to a critical illness or liver disease) will influence the AG
level.
In this case, the calculated AG should be adjusted for albumin:
Adjusted AG = Calculated AG + [2.5 × (4.5 – alb in g/dl)]
If this adjustment is ignored with a low albumin, the calculated anion gap
will be underestimated and a significant AGMA may be missed.
34. THE ALVEOLAR—ARTERIAL (A-a) GRADIENT AND ALVEOLAR
GAS EQUATION
This equation allows us to estimate the O2 tension in the alveoli
(PAO2):
• PatmO2 :
• PIO2 :
• PAO2:
35. PaO2: is the arterial O2 tension that is measured in the ABG.
FIO2: is the Fractional Inspired O2, i.e. the percentage of O2 in the inspired air.
If breathing room air at sea level, it equals 0.21. This value changes if the
patient is breathing through a nasal cannula or a face mask.
RQ: is the Respiratory Quotient and represents the amount of CO2 produced
for a given amount of O2 consumed by our bodies. It equals 0.8 at rest, in a
normal individual (because we produce 0.8 mole of CO2 for each mole of O2 we
consume while at rest). The RQ increases with exercise .
36. A-a Gradient (P(A-a)O2) It is the difference between the alveolar and
the arterial O2 tension.
P(A-a)O2 is normally ≤15 mmHg and increases with age.
Different formulas are used to determine the normal P(A-a)O2 in
relation to age, the following is a popular one:
• Normal P(A-a)O2 = 2.5 + (0.21 × age in years)
37. MECHANISMS OF HYPOXEMIA
These mechanisms can be classified into hypoxemia with a wide A-a gradient and
hypoxemia with a normal A-a gradient:
1. Hypoxemia with a wide A-a gradient (P(A-a)O2 > 15)
Shunting, like intra-cardiac shunts or pulmonary AV malformation.
VQ mismatch, as in atelectasis
Decreased mixed venous O2 tension PvO2 .
Diffusion limitation (reduced gas tranfer) (seen in severe ILD).
2. Hypoxemia with a normal A-a gradient (P(A-a)O2 ≤ 15)
Low inspired O2 (↓ FIO2), as in case of high altitude.
Hypoventilation, as in obesity hypoventilation syndrome.