Final MCQs Physiology - ANZCA Flashcards
PH01 [1986] At an altitude of 14,000 feet (4,200m), ambient pressure is 450mmHg. Breathing air, a normal man has an alveolar pO2 of: A. 40 mmHg B. 50 mmHg C. 55 mmHg D. 60 mmHg E. 80 mmHg
PiO2 = FiO2 × (Pb - 47) PiO2 = 0.21 × (450-47) = 84
PAO2 = PiO2 - (PaCO2 / R) PAO2 = 84 - (35 / 0.8) = 40mmHg (Assuming PaCO2 lower because of hyperventilation)
A is the BEST answer
Disagree. read Nunn ch.16 on altitude. Graph shows how R value changes with altitude, and compares alveolar PO2 and PCO2 values. PCO2 at this altitude (acclimatised) is somewhere between 26 and 30mmHg NB. FIO2 and SVP H20 at body temp constant regardless of altitude (ie. 0.21 and 47mmHg respectively) Thus, substituting -> 84 - (28/0.8) = 49 -> thus B is the best answer
For some rough values to remember (alveolar values)
19000m atm P equals H20 P -> PO2 and PCO2 become zero
>8000m - alveolar PO2 remains relatively stable at about 36mmHg (and PCO2 is about 8!)
6000m - PO2=40 PCO2=18
3000m - PO2=64 PCO2=30
1500m - PO2=80 PCO2=35 (remember these are rough values from the graph)–Spud 15:42, 12 Feb 2006 (EST)
But who can really say what the RR and PaCO2 will be. Also wrt to the graph in Nunn, if you look back a page at the barometric pressure relative to altitude table, these pressure are inconsistent with those in the question (ie the question gives a higher pressure). Isn’t there also some discussion from the UK everest expedition which notes that the PO2 was consistently higher than predicted from the fireplace chairs of those at sea level.
PH02 Peripheral cyanosis appears when: A. Hb exceeds 17G% B. MetHb level exceeds 0.1G% C. SulpHb level exceeds 0.1G% D. MetHb level exceeds 1.5G%
“MetHb and SulfHb produce detectable cyanosis at concentration as low as 2.0 gm and 0.5 gm/dl respectively” Lee et al (eds) Wintrobe’s Clinical Hematology. 10th ed. Philadelphia: Lippincott Williams & Wilkins 1999: p1046-53.
This is further supported by Nunn’s 5th edition p. 293:
“It is generally found that cyanosis can be detected when arterial blood contains greater than
1.5g/dL of reduced haemoglobin, or at an arterial oxygen saturation of 85-90%, although there
is much variation.”
and on p294:
“Non-hypoxic cyanosis has several causes, all of which are rare but worth considering in a patient
who seems cyanosed yet displays no other evidence of cyanosis. Sulphhaemoglobin and, more
importantly, methaemoglobin (at concentrations of 1.5g.dl-1 cause a blue-grey appearance.”
D the best answer
PH03 [1988] [Aug93] [Mar94] If breathe 100% oxygen, marked increase in paO2 occurs in: A. Hypoventilation B. V/Q abnormality C. Moderate diffusion problems D. True shunt
Answer: A, B, and C are true. Only true shunt is not amenable to an increased FiO2.
PH04 In a healthy person lying quietly on his back, the intracranial pressure (referred to the level of the interventricular foramen) is in the range: A. 0-5 cmH2O B. 5-15 cmH2O C. 15-30 cmH2O D. 2-3 mmHg E. 15-18 mmHg
Answer: B
conversion: 10.2cm H2O = 7.3mmHg, so 5-15cm H20 would be 3.5-11mmHg
PH05 [1986] [1987] Normal maternal blood gases: A. pH 7.4 B. Bicarbonate 31mmol/l C. pCO2 50mmHg D. Metabolic alkalosis E. None of the above
A. True: as stated in the Physiology Viva Book the arterial pH is normal at term. This is the one example of complete compensation in normal physiology.
B. False: the HCO3 is lowered
C: False: pCO2 is ~32mmHg due to maternal hyperventilation
D: False: respiratory alkalosis with (complete) metabolic compensation
PH06 [1988] [Mar92] What is the main lung function derangement in pregnancy? A. Decreased tidal volume B. Decreased VC C. Decreased FRC D. Decreased airway resistance E. ? (Related Q PH21)
The respiratory changes in pregnancy include: Increased Respiratory Rate 15% Decreased FRC 20% (decreased ERV & RV) Increased Tidal Volume 30-40% Increased Minute Volume 50% Increased Alveolar Ventilation 70% decreased ariway resistance etc... Disagree(slightly)
Nunn 5th ed Table 13.1
increase TV and alveolar vent 40%, no change RR.
decreased FRC 27%, RV 26%, VC 15%
which gives closest answers 06 -C, and 06b - E
PH06b [Mar93] Typical physiological changes in pregnancy at term, compared to the non-pregnant state include a twenty percent A. Increase in alveolar ventilation B. Increase in tidal volume C. Increase in vital capacity D. Reduction in arterial pH E. Reduction in functional residual capacity
The respiratory changes in pregnancy include: Increased Respiratory Rate 15% Decreased FRC 20% (decreased ERV & RV) Increased Tidal Volume 30-40% Increased Minute Volume 50% Increased Alveolar Ventilation 70% decreased ariway resistance etc... Disagree(slightly)
Nunn 5th ed Table 13.1
increase TV and alveolar vent 40%, no change RR.
decreased FRC 27%, RV 26%, VC 15%
which gives closest answers 06 -C, and 06b - E
PH07 [1986] [Apr96] Which of the following is NOT a normal pressure measurement? A. Pulmonary artery: 25/10 mmHg B. Aortic root: 120/0 mmHg C. Right ventricle 25/8 mmHg D. Right atrium: 5 mmHg E. Left atrium: 3 mmHg
Answer: B. Aortic root pressure typically 120/80mmHg
–BassBoyDave 02:38, 31 Mar 2010 (EDT)
Hang on- the DBP in the RV should be zero, shouldn’t it? The figures I remember are
RAP 5-10/0 RVP 25/0 PAP 25/8 LAP 5-10/0 LVP 120/0 MAP 120/80
So I think B and C are both wrong.
PH08 [1986] [Mar93]
The cardiovascular response to rise in intrathoracic pressure to 40 mmHg include:
1. Reduced venous return
2. Increased peripheral vascular resistance (vasoconstriction)
3. Arterial hypotension
4. Bradycardia
This is obviously a question about the Valsalva manoeuvre. It does not specify the acuity of the change. Taken directly from the Physiology Viva book: There are 4 phases:
pulse rate steady. Small increase in blood pressure (augmented VR).
increased HR. Vasoconstriction. Slight decrease in BP (diminished VR).
Steady HR. Drop in BP.
Increase in BP, with compensatory bradycardia.
Hence, all changes listed do occur.
I’ll go for 1 and 3, probably just 1 if type A.
Nunn 5th ed, fig 31.10 and text explains the changes well, though neglects to mention the reflex bradycardia
secondary to the overshoot increase MAP when the valsalva is released and the VR improves in the presence of increased SVR.
Answer is 1, 2, 3. you only get braycardia with release of pressure…..spooky
–BassBoyDave 02:40, 31 Mar 2010 (EDT)
Indeed, remember the Valsalva diagram-bradycardia only occurs after the termination of increased ITP.
PH09 [1988] Carboxyhaemoglobin: A. Due to CO2 combining with Hb B. Can be 2% in non-smokers C. Can be up to 15% in smokers D. ? E. ?
Answer: B. Nunns seems to suggest levels up to 10% being found in smokers
Clinical Evidence suggests up to 5% is normal in urban non-smokers and up to 15% can be found with heavy smokers [1]
PH10 [1988] Time constant of lung is: A. Resistance x compliance B. Resistance / compliance C. ? D. ?
Answer A: TC = R x C
PH11 [1988] [Aug91] With which of the following vessels are the following results compatible? pO2 15, SO2 26%, O2 5 vols% A. Umbilical artery B. Umbilical vein C. Uterine vein D. ?
Answer: A
Umbilical artery: pH 7.21, p02 = 18, pCO2 = 55, Sa02 = 45%, Ca02 = lOmlldl
Umbilical vein: pH 7.32, pO2 28, pC02 = 40, Sa02 = 70%, CaO2 = 16 mlldl
PH12 [1988] [Mar91] [Mar92] In non-shivering thermogenesis: A. Vessels and muscles of neck are involved B. Perinephric & periadrenal fat C. Interscapular mass D. Gluteal muscles
Brown fat is localised around the adrenal glands, kidneys, nape of the neck, inter-scapula area, and the axillary region.
Note that recently (1995) halothane was shown to inhibit non-shivering thermogenesis (in animal studies) in response to noradrenaline challenge. This is important and may explain why neonatal temperature regulation is lousy under anaesthetic.
With respect to respiration in neonates (as compared to young adult): Which is true:
A. Diaphragmatic respiration
B. O2 consumption (mls/kg) x 3 times that of an adult
C. Specific compliance much the same
D. pO2 is 20 mmHg less than adult (on room air)
E. Larger VD/VT ratio
F. Lack of type I fibers
G. Alveolar ventilation (mls/kg) roughly the same
H. Increased alveolar ventilation to FRC ration
Lung Volumes/Capacities Neonate vs Adult in (mL/kg or mL/kg/min as appropriate) Lower TLC 60 vs 80 "Low end of normal" FRC 30-35 vs 32-50 Same Vt = 6.5 Vd = 2.2 Higher Vm = 220 vs 100 Va = 140 vs 60 Va/FRC ratio = 5:1 vs 1.5:1
O2 Consumption (mL/kg/min) around doubled 7-10 vs 3-4
Blood Gases on room air (mmHg) PO2 68 vs 98 PCO2 34 vs 40 pH "in normal range" PO2 increases to adult levels over childhood, "much of it in the 1st year"
PH13b ANZCA version [2001-Apr] Q105
Pulmonary function values which are significantly different
between normal infants and normal adults include
1. tidal volume as ml.kg-1
2. tidal volume to FRC ratio
3. physiologic dead space to tidal volume ratio
4. O2 consumption as ml.kg-1.min-1
PH13b ANZCA version [2001-Apr] Q105 Pulmonary function values which are significantly different between normal infants and normal adults include
- tidal volume as ml.kg-1 -
- tidal volume to FRC ratio -
- physiologic dead space to tidal volume ratio - false: All ages 0.3 according to Table 84-4 in Miller
- O2 consumption as ml.kg-1.min-1 - true: Infants have a higher oxygen consumption per kg per minute than adults (around 6.0 compared to 3.5ml/kg/min in adults) according to Miller Table 84-4
PH13c ANZCA version [2002-Aug] Q100, [2003-Apr] Q17
Compared to an adult, in the neonate:
A. FRC is a more efficient buffer to changes in partial pressures of inspired gases
B. closing volume in ml/kg is lower
C. oxygen consumption in ml/kg is similar
D. FRC in ml/kg is higher
E. the ratio of alveolar ventilation to FRC is higher
PH13c ANZCA version [2002-Aug] Q100, [2003-Apr] Q17 Compared to an adult, in the neonate:
A. FRC is a more efficient buffer to changes in partial pressures of inspired gases - false
B. closing volume in ml/kg is lower - false: closing volume is higher
C. oxygen consumption in ml/kg is similar - false: higher O2 requirement per Kg
D. FRC in ml/kg is higher - false: FRC is lower per kg
E. the ratio of alveolar ventilation to FRC is higher - true: Using table 84-4 from Miller, ratio in neonate is 385/80 cf 3100/3000 for adults.
PH13d [1997]
Compared to an adult, in the neonate:
1. Subglottis is the narrowest portion of the airway
2. The diaphragm contains relatively fewer type I fibres
3. The brainstem is sensitive to opioid-induced respiratory depression
4. The breathing pattern is sinusoidal with no expiratory pause
(A related but different MCQ is PH24)
?
PH14a [1988] [Aug93] [Apr97] [Jul97] [Apr98] [Jul98] (type K)
Neonatal respiratory system different as:
1. Diaphragmatic breathing
2. Decreased type I fibres in diaphragm
3. Increased sensitivity to opioids
4. Sinusoidal breathing with no expiratory pause
5. Increased chest compliance
Laryngospasm Says: PH14a:
- A - True. “The respiration is irregular and mainly diaphragmatic.” Power & Kam. p 360.
- B - True. “There are also fewer Type I muscle fibres (slow contracting and highly oxidative fibres used for sustained contractions) in the diaphragm and intercostal muscles and hence these respiratory muscles fatigue easily.” Power & Kam. p 359-360.
- C - True. “Yet, the fact that apparent toxicity occurred with a maternal dose as low as 0.63 mg/kg/day of codeine should serve as a reminder that the higher sensitivity of neonates to the CNS-depressing effects of opioids may put some infants at risk even with an apparently small maternal dose.” Pharmacogenetics of Neonatal Opioid Toxicity Following Maternal Use of Codeine During Breastfeeding: A Case–Control Study. Clinical Pharmacology & Therapeutics (2008); 85, 1, 31–35 doi:10.1038/clpt.2008.157.
- D - True. “The respiratory pattern is sinusoidal with no expiratory pause seen.” Asian Intensive Care: problems & solutions.
- E - ? True “Lung compliance increases during the first few hours after birth. Specific compliance is similar in the neonate, infant and adult. The chest wall is very compliant because of the soft rib cage of the infant.” Power & Kam. p 360.
PH14b ANZCA version [2001-Apr] Q134
In an infant
1. the chest wall is more compliant than in an adult
2. the diaphragm lacks type 1 muscle fibres
3. oxygen consumption (in ml.kg-1.min-1) is twice that of an adult
4. anatomical deadspace volume (in ml.kg-1) is larger than in an adult
PH14b Version
1. True
2. False - There are fewer type I fibres, not a lack.
From Kam p359 “There are (also) fewer Type I muscle fibres in the diaphragm and intercostal muscles, hence these respiratory muscles fatigue easily.”
From Miller p2369 “These muscles do not achieve the adult configuration of type I muscle fibers until the child is approximately 2 years old”
3. True - two to three times
4. False - relatively smaller
Reference - Miller 6th ed p 2369
4. is true infant has larger anatomical dead space despite normal total. (Nunn 5th ed, p178)
http://jap.physiology.org/cgi/content/abstract/80/5/1485
Anatomic dead space in infants and children (Abstract)
A. H. Numa and C. J. Newth Division of Pediatric Critical Care, Children’s Hospital Los Angeles, University of Southern California 90027, USA.
In adults, anatomic dead space is 2.2 ml/kg. Because of the relatively large head size of infants and children, we hypothesized that extrathoracic and, therefore, total dead space would be relatively larger in pediatric subjects. Extrathoracic dead space was measured by a “water displacement” technique in 40 patients aged 7 days to 14.2 yr who were intubated with cuffed endotracheal tubes. Intrathoracic dead space was measured by continuous analysis of end-tidal and mixed-expired PCO2 and minute ventilation in 10 patients, aged 18 days to 14.7 yr. Extrathoracic dead space per kilogram decreased exponentially with increasing age, ranging from 2.3 ml/kg in early infancy to 0.8 ml/kg in children older than 6 yr. Mean intrathoracic anatomic dead space was 1.03 ml/kg and was not related to age. The following relationship between total anatomic dead space (DStotal; in ml/kg) and age (in yr) is derived: DStotal = 3.28 - 0.56 [ln(1 + Age)], with r = 0.95 and P = 0.0001. Anatomic dead space is age dependent and is > 3 ml/kg in early infancy.
J Appl Physiol 80: 1485-1489, 1996 –Stmz 21:09, 6 Jul 2008 (EDT)
PH15 [1988] [Mar91] [Aug91] [Aug93]
Neonates:
A. Oxygen stored in brown fat
B. Baroreceptors are more sensitive than in an adult
C. Cardiac output same as adult on a weight basis
D. Heart has less compliance than adult
Answer: D
Brown Fat: contains many fat glubule and many large mitochondria. It is specialised for non-shivering thermogenesis through a higher concentration of thermogenin or uncoupling protein 1, which provides an alternative return route for the proton motive force (H+ gradient) produced by the electron transport chain, uncoupling oxidative phosphorylation and releasing the energy as heat. It consumes more oxygen and has a rich capillary supply, but does not contain oxygen.
Baroreceptors In infants: Baroreceptor responsiveness increase with post conception age in neonates and pre-term infants.
PH16 [1988] [Mar91] [Aug91] P50 is increased by a fall of: A. 2,3 DPG B. ATP C. Temperature D. pH
Decreased pH (ie increased [H+]) causes a RIGHT shift in ODC, which is an increase in P50. The other options cause a left shift.
PH17 [1985] [Aug92]
Regarding the coagulation cascade:
A. Factor XI activates factor X
B. Factor VIII is involved in the extrinsic pathway
C. Factor VII is involved in the extrinsic pathway
D. Factor XIII and fibrinogen together activate the intrinsic pathway
E. Activated IX acts VIII which acts on X
C & E correct
I disagree. IXa and VIIIa combine to form “tenase” which activates Factor X to Xa.
VIIIa levels rise under the influence of IIa (aka Thrombin) by conversion of VIII to VIIIa.
This would only leave C as correct. See good old Wikipedia for details…[1]–Groundhog 01:00, 12 Aug 2008 (EDT)
PH18 Immune mechanisms: which are TRUE? A. IgE activates complement B. IgM involved in wheal and flare C. Ab/Ag complex involved in haemolytic reaction D. ?
Answer: C
PH19 Umbilical artery: A. pO2 .... mmHg B. ? C. ? D. ?
see page 129 West. Respiratory Physiology, 6th Edition
–BassBoyDave 03:02, 31 Mar 2010 (EDT)
but jsut for the record, it’s about 15mmHg
PH20
A child inhales a marble into the left main bronchus. At that instant, compliance is:
A. Halved
B. Unchanged
C. Doubled
D. No constant relation
The above comments are misleading.
To gain an understanding of how compliances are related, first consider how to determine the total compliance of the lung and chest wall together. As these are in series, the compliances are related by their reciprocals as follows:
1/CT = 1/CL + 1/CCW
This means that if we measure the compliances of the lung (CL) and chest wall (CCW) individually, we can determine the total respiratory compliance (CT), by substituting in the above formula.
Now, consider just the lungs:
The compliance of the lung (CL) is determined by the individual compliances of the left lung (CLL) and that of the right lung (CRL). As the lungs are in parallel, the compliances are related as follows:
CL = CLL + CRL
Now, if a main bronchus were suddenly occluded, then the occluded lung now cannot contribute to determining the compliance of the lung. There can be no change in volume there so the compliance is zero. Pressure can change so the denominator is not zero. Thus, at that sudden instant of occlusion of the LEFT main bronchus:
CL = CRL + 0
Now, we have to make an assumption here and that is that the compliances of both left and right lung are about the same. Obviously not EXACTLY true but still pretty close so the assumption is an acceptable one to make.
Thus CL being now equal to the compliance of one lung only, so it is (approximately) halved. That is the correct answer.
In anaesthetics, more common than inhaling marbles is the problem of endobronchial intubation. This results in a situation exactly analogous to the sudden marble obstruction. So the answer is directly relevant to anaesthetic practice. With endobronchial intubation, the lung compliance is decreased.
How about this….
C = change in volume / change in pressure
One lung = half the volume, therefore Compliance is halved.
See, that wasn’t that difficult now, was it!?! –Groundhog 01:17, 12 Aug 2008 (EDT)
PH21a Pregnancy: A. Decreased FRC B. Increased alveolar ventilation C. Increased AP and transverse diameters of chest expansion on inspiration D. Diaphragm up 4 cms
Answer- A-true B-true by 70% C-true D-true
PH21b ANZCA version [2004-Aug] Q48
Typical physiological changes in pregnancy at term, compared to the non-pregnant state include a twenty percent
A. increase in alveolar ventilation
B. increase in tidal volume
C. increase in vital capacity
D. reduction in arterial pH
E. reduction in functional residual capacity
E Answer-E A-increase by 70% B-increase by 40% C-unchanged D-unchanged
PH21b ANZCA version [2004-Aug] Q48 Typical physiological changes in pregnancy at term, compared to the non-pregnant state include a twenty percent
A. increase in alveolar ventilation - false: minute volume increased 40-50%
B. increase in tidal volume - unspecified
C. increase in vital capacity
D. reduction in arterial pH - false There is another MCQ that states pH remains the same.
E. reduction in functional residual capacity - true: See Table 1 Physiological changes of pregnancy in “Anesthesia, minimally invasive surgery and pregnancy” Best Practice Reseach Anesthesiology 2002, 16:1; 131
PH21c [Mar91]
Physiological changes of pregnancy include:
A. Increased O2 consumption by 40% ( ? 20% )
B. Increased alveolar ventilation by 40%
C. Increased circumference of thorax
D. Increased fibrinogen by 20%
E. Decreased expiratory reserve volume
A-increase by 60% B-increase by 70% C-true D-true, increases E-increase by 20% Shnider and Levinson pp3-6: MV increased 50% VA increased 70% VC unchanged FRC decreased 15-20% Tidal volume increased 40%
The hyperventilation that occurs during pregnancy is probably due in part to progesterone stimulating the respiratory center. Lung volume changes and altered compliance may also contribute. The effect is a chronic respiratory alkalosis which is compensated by renal excretion of bicarbonate. Typical blood gases results in the third trimester are: pH 7.43 pCO2 33mmHg [HCO3] 21mmHg pO2 104 mmHg.
The reduction in bicarbonate results in a slightly reduced ability to buffer a metabolic acid load. The lower pCO2 would shift the oxygen dissociation curve to the left but the minimal change in pH and the increased 2,3 DPG levels during pregnancy mean the ODC is little altered in position.
Miller: Maternal blood volume up 45%. Red cell mass up 30%. Physiological anemia 11.6g/dl. Cardiac output increases 40%, half in first trimester, mainly by increasing SV. By start fo 3rd trimester it’s maxed out.
Earl;y in pregnancy there is a reduction in the Aa gradient but as pregnancy progresses and the mechanical effects of the uterus become more significant, the FRC can fall below CC. FRC down by up to 20%. MV up by 40%. Increased Tidal volume by 45%. Increased dependence on the diaphragm. Dissociation curve right by 2,3 DPG according to Miller.
PH21d [Mar92]
Pregnancy:
A. Oxygen dissociation curve shifted to right
B. Decreased red cell mass
C. C.O. max in third stage
D. Decreased SVR
E. Increased 2,3 DPG in maternal red cells
?
PH21e ANZCA version [2001-Aug] Q135
Respiratory changes associated with full-term pregnancy include
1. reduction in functional residual capacity
2. reduction in arterial carbon dioxide
3. increased alveolar-arterial oxygen gradient
4. rightward shift of the P50 of the oxygen-haemoglobin dissociation curve
1, 2, 3 - true
4 - false (low CO2 and high pH will lead to left shift)
From the CEACP review: “Increased minute ventilation leads to a decrease in PaCO2 producing a respiratory alkalosis and a left shift of the oxyhaemoglobin dissociation curve. A 30% increase in 2,3-DPG has the opposite effect on the oxyhaemoglobin dissociation curve with an increase of the P50 from 3.5 kPa to 4 kPa. The respiratory alkalosis is compensated by increased renal bicarbonate excretion so that plasma hydrogen ion concentrations remain essentially unchanged.
The increase in 2,3-DPG and the fact that the pH stays the same means that you actually get a R shift - and baby is very glad of this! They are all true.–lovethedrugs 16:30, 21 Jun 2008 (EDT)
PH21e ANZCA version [2001-Aug] Q135 Respiratory changes associated with full-term pregnancy include
- reduction in functional residual capacity - true
- reduction in arterial carbon dioxide - true
- increased alveolar-arterial oxygen gradient
- rightward shift of the P50 of the oxygen-haemoglobin dissociation curve
PH22 Normal pCO2 of CSF? (In mmHg) A. 36 B. 40 C. 44 D. 48 E. 52
Ganong 16th ed p 553: pH 7.33, pCO2 50.2 mmHg
Also the same as per good ol Kerry-
The CSF has a composition identical to that of the brain ECF but this is different from plasma. The major differences from plasma are:
* The pCO2 is higher (50 mmHg) resulting in a lower CSF pH (7.33)
* The protein content is normally very low (0.2g/l) resulting in a low buffering capacity
* The glucose concentration is lower
* The chloride concentration is higher
* The cholesterol content is very low
PH23 Cerebral blood flow changes by how much per mmHg change in pCO2? A. 0.4% B. 1% C. 4% D. 10% E. 12%
4% (SEE KERRYS BOOK - the physiology viva 4% is correct answer)
Cerebral blood flow in an adult = 750 mls/min = 50-54 mls/100g/min (15% of cardiac output).
Over a wide range (eg from 20-80mmHg pCO2) the relationship between arterial pCO2 and CBF is linear, changing by 4% per mmHg change in arterial pCO2.
Unfortuneately there is a major flaw in both the concept and wording of this question (and answer)
pCO2 vs CBF describes a sigmoid curve across the entire pCO2 range
As stated it is roughly linear between 20 - 80 mmHg of pCO2
In this case one can not state a percentage change of the y axis (CBF) of itself for each change in the x axis (pCO2), not in a linear fashion at any rate.
In this case CBF = k0 + k1.pCO2 (linear between 20 - 80 mmHg)
however the question phrases the problem as CBF = k0 + k1 e ^ (k2.pCO2)
Lets assume for a minute that the answer is C=4% and that at pCO2 of 40mmHg CBF = 55ml/100g/min
Then at pCO2 of 80mmHg (with an increase CBF of 4% per mmHg increase of pCO2)
we have CBF = 55 x (1.04)^(80-40) = 264! ml/100g/min ~ 3.6 l /min for an adult brain or ~ 75% CO!!!
Clearly this can not be correct
I submit (within the flawed framework of the question) that the anwswer is B=1% then
CBF = 55 x (1.01)^(80-40) = 81ml/100g/min which is in keeping with the published material
Interestingly the curve may not be even linear. Sigmoid curve much more narrower than 20-80mmHg. Max 6-8%/Torr. See http://jap.physiology.org/cgi/reprint/102/3/870 Michael
For the purposes of the exam:
The CBF vs pCO2 curve is pseudosigmoid, with a flat upper limit of max cerebral vasodilation of >2xnormal CBF at pCO2 of 80mmHg,
and a flat lower limit of 1/2 normal CBF at pCO2 20. The latter is because of hypoxic vasodilation restricting further fall.
Between these is an almost linear relationship where at the physiological pt of pCO2 40 and CBF 54ml/100gm/min,
a 1mmHg change in pCO2 elicits a 2ml/100gm/min change in CBF which is a 4% change. LouM
Increase in CBF -1ml/100g/min for every 1mmHg increase in PaCO2 REF-Stoelting Page 238
PH24 Neonates have higher respiratory rates than adults because of: A. Increased airway resistance B. Decreased thoracic compliance C. Immature chemoreceptors D. Non-respiratory acidosis E. ? (Related Q PH13)
Comment
Answer: A??.
The neonate has high airways resistance and low lung compliance. A high airways resistance alone would tend to increase the time constant, slow alveolar filling and thus require a decreased resp rate so A cannot be correct.
Alternate : Its usually said that the neonate has a high respiratory rate to “minimise work of breathing”; perhaps that is the missing option E.
Comment
I am pretty sure the answer is B. West has some nice work of breathing curves to show this.
High Raw -> slow deep breaths (CAL, asthma) because WOB inc. with inc Raw
Low compliance -> rapid breathing (Fibrosis) because of extra woek needed to stretch lung/chest wall.
When the two curves are overlaid vs RR WOB is lowest for a child at faster resp rates than an adult
Comment
I’m confused, but Kam says “The high respiratory rate is the optimal frequency for the minimal work of breathing to overcome the compliance of the respiratory system.” And Nunn doesn’t explain why resp rate is high, but says, “Compliance is about one-twentieth that of an adult and resistance is about 15 times greater.” So I would put B first, then A.
Answer maybe B This reference is from Mitchell’s notes-Anaesthesia UK website-links at the end of the article
Fiona Macfarlane
Consultant Anaesthetist Mater Children’s Hospital, Brisbane, Australia e-mail: Fiona.Macfarlane@mater.org.au
Paediatric anatomy, physiology and the basics of paediatric anaesthesiato
Horizontal ribs prevent the ‘bucket handle’ action seen in adult breathing and limit an increase in tidal volume.Minute ventilation is rate dependant as there is little means to increase tidal volume.
Laryngospasm says:
A - Part of the answer - as it influences the time constant. The neonate is trying to maintain FRC by having a respiratory rate fast enough for expiration time to be less than the time constant - and thus to prevent lung collapse.
B - Does not seem true as it refers to thoracic compliance which is actually increased in the neonate as compared to the adult / older child and not decreased.
COMMENT
ANSWER A
increased resistance of elastic and airway result in increased RR to minimize WOB
Nunn figure 6.11
PH25 [Mar93]
Normal intracranial pressure is:
A. 10-15 mmHg
B. 5-15 cmsH2O
C. Maintained independently of arterial systolic pressure
D. Maintained independently of alterations of arterial pCO2
Answer: B.
Um, sorry, but no. CSF has a hydrostatic pressure of 5-15 mmHg or 6.5 - 20 cmH20. (Trivial, i agree) (Ref Kam p41)
–BassBoyDave 03:38, 31 Mar 2010 (EDT)
A-Z quotes normal range as 7-17mmHg, which equates to 9.2-22.4 cmH2O. It’s not trivial at all-remember the brain compliance curve?
PH26 [Apr96] The oxygen dissociation curve is moved to the left by: A. Acidosis B. Hypothermia C. Increase in 2,3 DPG D. Blood storage prior to transfusion E. Sickle cell anaemia
The ODC is shifted to the right by: decrease in pH increased pCO2 increasing temperature increased 2,3 DPG This leaves the correct answer as B
Sickle cell anemia shifts it to the right favouring sickling by deoxygenating Hb.
Left shift of ODC by decreased temperature, 2,3 DPG, pCO2; increased pH. Opposite for right shift.
Storage of blood depletes 2,3 DPG, shifting ODC to left. p50 17 by 2 to 3 weeks. Hypothermia would enhance, acidosis
oppose.
Foetal Hb shifts ODC to left,
sickle Hb shifts it to right, enabling offload in anemia but making vulnerable to sickle crisis.
PH27
An increase in 2,3 DPG:
A. Shifts ODC to same side as does metabolic acidosis
B. Shifts curve in same direction as hypothermia
C. Increases storage life of red blood cells
D. Decreases oxygen consumption in vivo
The ODC is shifted to the right by: decrease in pH increased pCO2 increasing temperature increased 2,3 DPG The answer is A.
Free fatty acids:
A. Can be used as an energy source by heart and skeletal muscle
B. Are bound to albumin
C. Can be used by the brain once they are changed to ketones
D. Can be changed to glucose
A, B, and C are correct.
PH29 [1987] [Mar92] [Mar93] [Aug93]
Mixed venous blood oxygen saturation:
A. Is measured from blood sampled from the right atrium
B. Is accurately calculated from mixed venous pO2 measurements
C. Is used in the calculation of cardiac output
C. Assesses peripheral circulation
D. Has no effect on the A-a oxygen gradient
E. Is normally in the range of 40%
Mixed venous blood can ONLY be sampled from the pulmonary artery. It cannot be sampled from the right atrium (or right ventricle) as there is not adequate mixing of the 3 contributing blood streams (SVC, IVC, coronary sinus). So option A is wrong.
Saturation can be calculated from pO2 but for accurate results you have to know the position of the oxygen dissociation curve and not just use the standard curve. A blood gas machine gives a fairly good estimate by (effectively) correcting the curve for pH and pCO2 but this is still an estimate. So for option B then it depends on the weight placed on the word “accurately” (Of cousre the the actual version of the question may have slightly different wording so we cannot be sure about this). So before accepting this option we have to check to see if there is a better one.
SvO2 measurements with the SAT-2 Oximeter have a correlation of 0.92 with measurements obtained via standard laboratory cooximetry for an oxygen saturation range of 39% to 96%. The reliability of the system is ± 3.5% oxygen saturation for the range of 40% to 92% saturation. However, this is a measurement of saturation not partial pressure so not really relevant here.
When using Fick’s law to calculate cardiac output using oxygen, we need to measure total body oxygen consumption, mixed venous oxygen content, and arterial oxygen content. One way to measure oxygen content is directly using either the Lloyd-Haldane volumetric method or the van Slyke manometric method. However, mixed venous oxygen content can be calculated as equal to the product of [Hb], SVO2 and a value for the amount of oxygen that binds to one gram of Hb (eg 1.34). Because of variations in this last value the accuracy is slightly affected. (Also need to add in a calculated value -usually small- for dissolved oxygen). So C is correct and the best option so far.
SvO2 does provide a measure of total oxygen extraction, but the usefulness of this alone is limited unless you also know the [Hb] and the arterial SO2 and the cardiac output. Afterall if the arterial saturation is low (say 80%) then a low mixed venous saturation will result but that really doesn’t mean the same as when a reduced SVO2 is coupled with a normal SaO2. So I don’t think option D is as good as option C
Because pulmonary capillary blood is easily oxygenated in the lung (equilibrium in one third of the usual 0.75 seconds spent in the pulmonary capillary, a low SVO2 is readily converted to a high SaO2. However, for abnormal lungs with significant V/Q mismatch (esp shunt) then a low SvO2 will impair arterial oxygenation. So to say that SVO2 has “no effect” on A-a gradient is wrong.
SvO2 is related to the A-a gradient through the shunt equation, where, Qs/Qt = (Cc’O2 -CaO2) / (Cc’O2-CvO2) and CvO2 = 1.3 x Hb x SvO2 + 0.003 x PvO2.
SvO2 is normally in the range of 75% with an extraction ratio of around 25%, so option E is wrong. This option uses the numerical value of the mixed venous pO2 as a distractor.
PH30 [Mar92]
Brown fat stores involve all of these EXCEPT:
A. Between scapula
B. Peri-nephric & around adrenals
C. Gluteal region
D. Involves muscles & blood vessels of neck
E. Around great vessels in root of neck / thoracic inlet
Answer C Brown Fat is largely in the: Interscapular region Mediastinum Perinephric tissues Axillae Near major blood vessels in neck
PH31 ANZCA version [2003-Apr] Q64, [2003-Aug] Q81
A morbidly obese patient is to have an open cholecystectomy. Compared with a patient of normal weight the
A. risk of thromboembolism is increased by 20%
B. dose of patient controlled intravenous analgesia is increased and is related more closely to body
surface area than weight
C. recovery time from atracurium is unchanged
D. increased volume of distribution of some drugs may prolong the elimination half-life even though clearance
may be unchanged or increased
E. volume of the central compartment is significantly changed
PH31 ANZCA version [2003-Apr] Q64, [2003-Aug] Q81
A morbidly obese patient is to have an open cholecystectomy. Compared with a patient of normal weight the
A. risk of thromboembolism is increased by 20% - unsure if 20%: Definitely increased risk. “Obese patients are at increased risk of venous thromboembolism; appropriately sized compression stockings, low molecular weight heparin, and dynamic flow boots should be used from arrival in theatre until full postoperative mobilization.”(Continuing Education in Anaesthesia, Critical Care & Pain 2008 8(5):151-156)
B. dose of patient controlled intravenous analgesia is increased and is related more closely to body surface area than weight - false: “Propofol is highly lipid-soluble, but also has a very high clearance. Its volume of distribution at steady state and clearance are proportional to total body weight. Therefore, when using total i.v. anaesthesia, the infusion rate should be calculated on total body weight, not ideal body weight.” (Continuing Education in Anaesthesia, Critical Care & Pain 2008 8(5):151-156)
C. recovery time from atracurium is unchanged - maybe: Atracurium differs from the other muscle relaxants. It needs a higher initial dose based on total body weight. If dosed on ideal body weight like other muscle relaxants, recovery time will probably be shorter. However, if the higher dose according to TBW is used, then recovery time will be the same as the non-obese.
“Neuromuscular blockers are polar and hydrophilic. Vecuronium, rocuronium and cisatracurium should be dosed using IBW [58–60]. Atracurium is unique amongst neuromuscular blockers because there is a clinically observed hyposensitivity to the drug among obese patients that necessitates dosing based upon TBW to ensure adequate effect” (Current Opinion in Anaesthesiology Issue: Volume 20(2), April 2007, p 113–118)
“Although atracurium concentrations were consistently higher in obese patients than in nonobese patients, there was no difference in the time of recovery from neuromuscular blockade between the two groups. Consequently, the median effective concentration was higher in obese than in nonobese patients” (Clinical Pharmacology and Therapeutics (1990) 48, 18–25)
D. increased volume of distribution of some drugs may prolong the elimination half-life even though clearance may be unchanged or increased - true: “An increase in Vd prolongs the elimination half-life, despite increased clearance (Table 3).” (Continuing Education in Anaesthesia, Critical Care & Pain 2008 8(5):151-156)
E. volume of the central compartment is significantly changed - false: “The volume of the central compartment is largely unchanged, but dosages of lipophilic and polar drugs need to be adjusted due to changes in volume of distribution (Vd).” (Continuing Education in Anaesthesia, Critical Care & Pain 2008 8(5):151-156)
Comments
Answer is C: Atracurium—unchanged pharmacokinetics. A–Thromboembolism can also be true. As per the article above, obese have 48% risk of TE compared to 23% in non obese. This is a 20% increase.
Suggestions welcome.maverick
I think that a 25% absolute increase is a >100% relative increase and that is what makes that option wrong. –SteveW 19:55, 6 Sep 2007 (EDT)
GL: I agree with Steve. The risk of deep-vein thrombosis in obese patients undergoing non-malignant abdominal surgery is approximately twice that of lean patients (48% vs 23%) - so risk is twice that of non=obese pts - sorry can’t work out if this makes it 100% increase (I think so?) or 200%, but def more than 25%.
C is certainly right, although D seems right to me as well as stated in ‘Anesthesia in the obese patient: Pharmacokinetic considerations’, Journal of Clinical Anesthesia (2005) 17, 134-145:
“…these changes in tissue distribution produced by obesity can markedly affect the apparent volume of distribution of the anaesthetic drugs.” and “…hepatic clearance is usually normal or even increased in the obese patient. Renal clearance increases in obesity because of the increase in kideny weight, renal blood flow, and GFR.”
This review article is quite extensive and and detailed, and looks at different anaesth. drugs.
Nevertheless, I’d go for C
Just to put the cat amongst the pigeons: “We conclude that the duration of action of atracurium block is prolonged in obese patients, and that atracurium dose in milligrams per kilogram of total body weight should be reduced in these patients” From: “Anthropometric variables as predictors for duration of action of atracurium-induced neuromuscular block”, Anesthesia & Analgesia, Vol 83, 1076-1080, 1996. I’m for D now. –iatrophobe 21:03, 14 Apr 2008 (EDT)
The answer is C. A-thromboembolism risk doubled-Stoelting Page 448 B,D,E-false
Referece for B,C,D,E-Anaesthesia and Intensive Care,Vol.5,Issue 3,Pages 92-95
What a crap question. A is true if they mean absolute risk increase. C is true according to most (but not all) sources. D, with its ‘may’, is definitely true too. Yet another case of the examiner not being too sharp that day. I hope that if they put this one in again, they fix it. –lovethedrugs 16:54, 21 Jun 2008 (EDT)
Couldn’t agree with above comment more. Really tempted by D. Definite evidence that obesity assoc with increased abs BVol, CO and RBF thus increasing clearance of renally excreted drugs. Also the double “may” giveaway and doubt cast upon validity of C. Unless anyone can find proof that it’s wrong, I’m going with D. Reckon A deals with rel risk. Tortis 18Oct08
The volume of the central compartment is largely unchanged, but dosages of lipophilic and polar drugs need to be adjusted due to changes in volume of distribution (Vd). An increase in Vd prolongs the elimination half-life, despite increased clearance. CEACCP Vol 8, No5 2008 - Anaesthesia and morbid obesity
PH32 [Mar93] The lower limit of normal blood glucose concentration (mmol/l) in an infant more than 3 days old is: A. 4.3 mmol/l B. 3.2 C. 2.2 D. 1.1
Cord blood 45–96 mg/dL 2.5–5.3 mmol/L
Premature 20–60 1.1–3.3
Neonate 30–60 1.7–3.3
Newborn
Nelson - Textbook of Pediatrics
After the first few hours of life plasma glucose less than 2.2mmol/l (40mg/dl) equals hypoglycaemia. - Rudolph’s Pediatrics.
From primary short course notes- in first few hours of life rapid fall in BSL,
lower limit normal Term infant 1.6mmol/l, preterm 1.1 mmol/l
PH33 [Mar93] [Aug99] The normal Hb (gm/dl) for age during infancy is: A. 16 at 3 months B. 12 at 3 months C. 11 at 12 months D. 10 at 8 months E. 9 at 4 months
A False B True - BEST answer C True - lower end of normal D ?True - lower end of normal E False Comments Infant Term (cord blood) 135-195 g/L 3-6 months 95-135 g/L Child 1 year 105-135 g/L 3-6 years 105-140 g/L 10-12 years 115-145 g/L Adult Male 130-180 g/L Female 115-165 g/L
Manual of Paediatric Anesthesia has different no. that make C a better answer
Nelson - Textbook of Pediatrics agrees with B being the better answer
The nadir in Hb for infants is around 3-4 months with a median of 11.4g/dl. My guess is that this is the knowledge being checked in the several questions on this topic.
Also:
Power & Kam state: “A week after birth the haemoglobin concentration returns to 18 g/dL, and then decreases steadily to about 11-12 g/dL at 4-8 weeks due to a decrease in red cell mass.”
PH34 [Mar93] [Mar00] (type K) Hyperventilation to two times normal (?alveolar ventilation) causes: 1. Vasoconstriction in skin 2. Increased arterial pH 3. Decreased cardiac output 4. Decrease in free Ca++ 5. Increased SVR 6. Decreased coronary perfusion (Related Q: PH43)
hyperventilation : alveolar (therefore arterial) CO2 is inversely related to alveolar ventilation.
Double the alv vent will halve the alv and art CO2. - West resp physiol
effects - decreased HCO3, increased pH (resp alkalosis),
decreased cerebral blood flow leading to symptoms of lightheadedness, dizziness, paraesthesia,
increased cardiac output
direct vasoconstriction, but depressed vasomotor centre means BP unchanged or only slightly elevated,
alkalosis leads to normal total Ca, but fall in free Ca causing tetany/carpopedal spasm. - Ganong
1, 2, 4, 5 true
Laryngospasm says:
6 also true: True. “Hypocapnia adversely impacts on myocardial O2 supply/demand balance and may increase the risk of myocardial ischemia. Experimental hypocapnia increases coronary vascular resistance, reduces coronary blood flow and myocardial O2 delivery and left ventricular performance and reduces collateral flow in experimental myocardial ischemia.” Perioperative control of CO2, Kavanagh B. CAN J ANESTH 2003 / 50: 6 / pp R1–R6[1]
PH35a ANZCA version [Mar93] [Aug93] [Aug94] [Jul00] [2001-Aug] Q61, [2002-Aug] Q72
Normal features of changing physiology with age include
A. increased lean body mass
B. increased adrenal-cortical function
C. earlier onset of shivering
D. increased plasma albumin
E. decreased gastric pH
A False - ↓ 6kg muscle mass by 80 B True - see the article below C False - ↓BMR and ↓ thermogenic responsiveness D False - 4g/dl at 40, 3.6g/dl at 80 E False - Aging itself is associated with slowing of gastric emptying, diminished gut wall function, and an increase in gastric pH [1] A False B False C True - see the abstract below D False E False
PH35a ANZCA version [Mar93] [Aug93] [Aug94] [Jul00] [2001-Aug] Q61, [2002-Aug] Q72
Normal features of changing physiology with age include
A. increased lean body mass - false: “Changes in body composition with aging reflect a decrease in lean body mass, an increase in body fat, and a decrease in total body water. We might infer that a decrease in total body water could lead to a smaller central compartment and increased serum concentrations after bolus administration of a drug. In addition, the increase in body fat might result in a greater volume of distribution, with the potential to prolong the clinical effect of a given medication” (Miller 7th Ed Ch 71)
B. increased adrenal-cortical function - false: “Production of androgens by the adrenal gland progressively decreases with age (also see Chapter 71 ). This decrease in androgen activity has no known implications for anesthesia. Plasma levels of cortisol are unaffected by increasing age. Levels of CBG are also unaffected by age, which suggests that a normal fraction of free cortisol (1% to 5%) is present in elderly patients. Several investigators have noted a progressively impaired ability of aged patients to metabolize and excrete glucocorticoids. In normal individuals, the quantity of 17-hydroxycorticosteroids excreted is reduced by half by the seventh decade. This decreased excretion undoubtedly reflects the reduced renal function that occurs with aging. When excretion of cortisol metabolites is expressed as a function of creatinine clearance, the age difference disappears.” (Miller 7th Ed Ch 35)
Note that adrenaline and noradrenaline are secreted by the adrenal medulla
C. earlier onset of shivering - false: The shivering set point is decreased in the elderly so shivering occurs later. “the vasoconstriction threshold is about 1°C less in patients aged 60 to 80 years than in those between 30 and 50 years… Shivering is rare at surgical levels of general anesthesia, which is consistent with its threshold being roughly 1°C less than the vasoconstriction threshold.” (Miller 7th Ed Ch 48)
D. increased plasma albumin - false: “The circulating level of albumin decreases with age, whereas α1-acid glycoprotein levels increase.” (Miller 7th Ed Ch 71)
E. decreased gastric pH
PH35b ANZCA version [2003-Aug] Q142, [2004-Apr] Q84
Normal physiological changes with ageing
A. Increased lean body mass
B. Earlier onset of shivering
C. Increased resting levels of catecholamines
D. decreased gastric pH
E. increased plasma albumin
PH35b ANZCA version [2003-Aug] Q142, [2004-Apr] Q84
Normal physiological changes with ageing
A. Increased lean body mass
B. Earlier onset of shivering
C. Increased resting levels of catecholamines - true: That’s why they get hypertension and why beta blockers work.
D. decreased gastric pH
E. increased plasma albumin
PH35a ANZCA version [Mar93] [Aug93] [Aug94] [Jul00] [2001-Aug] Q61, [2002-Aug] Q72
Normal features of changing physiology with age include
A. increased lean body mass - false: “Changes in body composition with aging reflect a decrease in lean body mass, an increase in body fat, and a decrease in total body water. We might infer that a decrease in total body water could lead to a smaller central compartment and increased serum concentrations after bolus administration of a drug. In addition, the increase in body fat might result in a greater volume of distribution, with the potential to prolong the clinical effect of a given medication” (Miller 7th Ed Ch 71)
B. increased adrenal-cortical function - false: “Production of androgens by the adrenal gland progressively decreases with age (also see Chapter 71 ). This decrease in androgen activity has no known implications for anesthesia. Plasma levels of cortisol are unaffected by increasing age. Levels of CBG are also unaffected by age, which suggests that a normal fraction of free cortisol (1% to 5%) is present in elderly patients. Several investigators have noted a progressively impaired ability of aged patients to metabolize and excrete glucocorticoids. In normal individuals, the quantity of 17-hydroxycorticosteroids excreted is reduced by half by the seventh decade. This decreased excretion undoubtedly reflects the reduced renal function that occurs with aging. When excretion of cortisol metabolites is expressed as a function of creatinine clearance, the age difference disappears.” (Miller 7th Ed Ch 35)
Note that adrenaline and noradrenaline are secreted by the adrenal medulla
C. earlier onset of shivering - false: The shivering set point is decreased in the elderly so shivering occurs later. “the vasoconstriction threshold is about 1°C less in patients aged 60 to 80 years than in those between 30 and 50 years… Shivering is rare at surgical levels of general anesthesia, which is consistent with its threshold being roughly 1°C less than the vasoconstriction threshold.” (Miller 7th Ed Ch 48)
D. increased plasma albumin - false: “The circulating level of albumin decreases with age, whereas α1-acid glycoprotein levels increase.” (Miller 7th Ed Ch 71)
E. decreased gastric pH
PH36 [Mar93] [Aug93] [Aug99] (type K MCQ)
In a normal person, cerebral blood flow is increased by:
1. Administering propofol
2. Head-down position
3. Systolic increase from 100 to 130mmHg
4. Increase in arterial pCO2 to 60 mmHg
Propofol causes cerebral vasoconstriction and a decreased cerebral blood flow (CBF). All IV anaesthetics agents EXCEPT for ketamine, decrease CBF.
Head-down has no effect
The increase in systolic BP will not affect CBF as the change is still on the plateau of the cerebral auotregulation curve.
CBF increases very markedly with increases in arterial pCO2. This increase is 4% per mmHg rise in arterial pCO2
Answer: 4.
It is a K type question. Answers - B and D Reference- Oxford’s handbook pages 398-401
Head down decreases venous drainage but I’m not convinced that it increases blood flow…. any other opinions?
I believe that the CBF will not change with head down. Think about what happens - increased venous pressure and increased ICP. Arterial pressure increases by the same amount, but the pressure difference (what drives flow) will be the same. In fact, if the ICP rises more than the venous pressure, your blood flow will likely decrease. Can’t be bothered finding a reference sorry –lovethedrugs 18:25, 21 Jun 2008 (EDT)
Spot on LTD. Basic physiology says only a few things affect CBF.
CMRO2
PCO2
PO2
MAP
Viscosity (normal CBF at Hct 30-50%) - if you believe OHA 2nd edn p387
MAP and CVP rise equally. In this situation CBF should remain constant.
But if venous congestion causes ICP to rise, then CBF may decrease viz…
CBF = CPP/CVR
Higher MAP is causing an increased CVR due to pressure autoregulation whilst CPP is being reduced (or returned to normal) by a rising ICP. This means that a lower or normal CPP divided by a higher CVR will cause a reduced CBF. –Groundhog 03:44, 12 Aug 2008 (EDT)
PH37 [Aug94] [Mar95] [Jul98]
Pressure volume loop for the left ventricle:
Which of the labelled points (A,B,C,] [MAR95] corresponds to mitral valve opening?
(incl: E. None of the above)
Left ventricular pressure-volume (PV) loops are derived from pressure and volume information found in the cardiac cycle diagram (see left panel of figure below). To generate a PV loop for the left ventricle, the left ventricular pressure (LVP) is plotted against left ventricular (LV) volume at multiple time points during a complete cardiac cycle. When this is done, a PV loop is generated (right panel of figure and animated figure).
To illustrate the pressure-volume relationship for a single cardiac cycle, the cycle can be divided into four basic phases: ventricular filling (phase a; diastole), isovolumetric contraction (phase b) , ejection (phase c) , and isovolumetric relaxation (phase d) . Point 1 on the PV loop is the pressure and volume at the end of ventricular filling (diastole), and therefore represents the end-diastolic pressure and end-diastolic volume (EDV) for the ventricle. As the ventricle begins to contract isovolumetrically (phase b), the LVP increases but the LV volume remains the same, therefore resulting in a vertical line (all valves are closed). Once LVP exceeds aortic diastolic pressure, the aortic valve opens (point 2) and ejection (phase c) begins. During this phase the LV volume decreases as LVP increases to a peak value (peak systolic pressure) and then decreases as the ventricle begins to relax. When the aortic valve closes (point 3), ejection ceases and the ventricle relaxes isovolumetrically - that is, the LVP falls but the LV volume remains unchanged, therefore the line is vertical (all valves are closed). The LV volume at this time is the end-systolic (i.e., residual) volume (ESV). When the LVP falls below left atrial pressure, the mitral valve opens (point 4) and the ventricle begins to fill. Initially, the LVP continues to fall as the ventricle fills because the ventricle is still relaxing. However, once the ventricle is fully relaxed, the LVP gradually increases as the LV volume increases. The width of the loop represents the difference between EDV and ESV, which is by definition the stroke volume (SV). The area within the loop is the ventricular stroke work.
The filling phase moves along the end-diastolic pressure-volume relationship (EDPVR), or passive filling curve for the ventricle. The slope of the EDPVR is the reciprocal of ventricular compliance. The maximal pressure that can be developed by the ventricle at any given left ventricular volume is defined by the end-systolic pressure-volume relationship (ESPVR), which represents the inotropic state of the ventricle. The pressure-volume loop, therefore, cannot cross over the ESPVR, because that relationship defines the maximal pressure that can be generated under a given inotropic state. The end-diastolic and end-systolic pressure-volume relationships are analogous to the passive and total tension curves used to analyze muscle function.
Kerry Brandis also has good figures on PV loops.
PH38 [Mar95] [Apr96] [Aug96]
A 32 week 2000g infant born premature will have the following differences
compared to a normal term infant of the same size:
A. Hb higher
B. HbF higher
C. P50 lower
D. Increased 2,3 DPG
A ? False - prem’s are anaemic relative to their term counterparts - Hb conc may rise by 1-2g/dl in the first days of life as a result of excretion of fluids (Kam p361)
B True - 90% HbF until 35/40, 75% at birth, replaced by HbA at 6/12
C True - HbF has P50 of 19, HbA P50 is 26 ∴ P50 lower because ↑ HbF
D False - a characteristic of HbF is its lower 2,3 DPG (thus left shift ODC/lower p50
PH39 [Aug95] What is the optimum haematocrit for maximal cerebral ?perfusion/?oxygenation ? A. 15% B. 20% C. 25% D. 30% E. 35%
Haemodilution and oxygen carrying capacity: As the haematocrit and viscosity decrease, the cerebrovascular resistance also decreases and CBF increases. One argument against haemodilution is that the oxygen carrying capacity also decreases. Experimental studies and clinical experience suggest that a haematocrit of 30–33% is optimal.
References
Current controversies in neuroanaesthesia, head injury management and neuro critical care CEACP 2006
Laryngospasm says:
Answer: ? D > E
“CBF can be influenced by blood viscosity, of which haematocrit is the single most important determinant. Studies suggest that a haematocrit of 30–34% may result in optimal oxygen delivery.” Notes in Neuroanaesthesia and critical care. 2001. p. 21.
“The optimum haematocrit value for cerebral perfusion / O2 delivery is 30-40%” Fundamental principles and practice of anaesthesia By Peter Hutton et al. p. 432, Published by Informa Health Care, 2002
“Experimental studies and clinical experience suggest that a haematocrit of 30–33% is optimal.” Current controversies in neuroanaesthesia, head injury management and neuro critical care: CEACP 2006
“Blood viscosity increases logarithmically with increasing haematocrit and the optimal level is probably about 35%. Cerebral blood flow is reduced with haematocrit levels above 50% and increased with haematocrit levels below 30%.” Accident and Emergency: Theory Into Practice By Brian Dolan, Lynda Holt, p. 72. Edition: 2, Published by Elsevier Health Sciences, 2008
PH40 [Apr96] [Aug96] [Jul98] [Apr99]
With regard to CVP trace:
A. The a wave is caused by atrial contraction & occurs at the same time as
the p wave on the ECG
B. The c wave is caused by isovolumetric contraction & occurs after QRS
C. The x descent is caused by relaxation of the ventricle
D. The v wave relates to venous filling & peaks after T wave
E. The y descent corresponds with isovolumetric relaxation
(see also MC60)
(April99: type K with first 4 options above)
A ?False - strictly speaking it follows immediately the p wave
B True
C False - downward movement with ventricular contraction
D True
E False - tricuspid opens ∴ not isovolumetric relaxation
cvpwave.gif
+ a wave : This wave is due to the increased atrial(a) pressure during right atrial contraction. It correlates with the P wave on an ECG.
+ c wave : This wave is caused by a slight elevation of the tricuspid valve into the right atrium during early ventricular contraction(c). Correlates with the end of the QRS segment on an ECG
- x descent : This wave is probably caused by the downward movement of the ventricle during systolic contraction. (atrial rela(x)ation mid- systole) It occurs before the T wave on an ECG.
+ v wave : This wave arises from the pressure produced when the venous(v) filling of the right atrium comes up against a closed tricuspid valve. It occurs as the T wave is ending on an ECG.
- y descent : This wave is produced by the tricuspid valve opening in diastole with blood flowing into the right ventricle. It occurs before the P wave on an ECG.
PH41a [Apr97]
The elderly have:
A. Increased serum creatinine B. Decreased hepatic & renal function of 1% per year from the age of 30 yrs. C. Decreased FRC D. Decreased resting cardiac output E. Increased LV stiffness
L - E - Stiff V wall.
A. CI stays about the same but decreased reserve
B. Falseish increased according to COA 2001 maybe because the absolute value decreases as does TLC but the ratio to TLC actually increases
C. False… hypoxic drive decreases
D. False decreased production is matched by decreased excretionFalse
E. True
Kam p368:
“Progressive decline in hepatic clearance of certain substances due to reduced liver size. Hepatic blood flow decreases, but hepatic enzyme function does not change with age”. This means that hepatic function does not decrease, therefore B is False
See Nunn 5th ed p52 for discussion of C
Resting cardiac output is decreased 1%/yr after 30yrs old and cardiac index 0.8%/yr due to decreased body surface area. But I would still go for E. Michael
according to OHA, maximal CO decreases.. didnt mention resting CO. did say reduce ventricular compliance.p690
Renal function loss of 10%/decade after 50y. By 8th decade: an additional 10-30% nephrons sclerotic.
–BassBoyDave 21:36, 31 Mar 2010 (EDT)
About cardiac output- surely we see the effects of a low cardiac output on a daily basis-what else explains longer arm-brain circulation times?
PH41b ANZCA version [2005-Apr] Q150, [2005-Sep] Q48
During adulthood, ageing results in
A. a decline in resting cardiac output
B. a decrease in functional residual capacity (FRC)
C. an increase in hypoxic ventilatory drive
D. an increase in serum creatinine
E. an increase in ventricular wall stiffness
PH41b ANZCA version [2005-Apr] Q150, [2005-Sep] Q48
During adulthood, ageing results in
A. a decline in resting cardiac output - probably false: “Ageing affects cardiac function in many ways. Stiffening of large arteries increases afterload on the heart, while myocardial stiffening impairs early diastolic filling.53 114 The beta-adrenergic responsiveness of the heart decreases. Contractility does not change (despite prolongation in duration26), but the resulting increase in end-diastolic volume plays an important role in preserving maximal cardiac output during exercise.” (British Journal of Anaesthesia, 2001, Vol. 87, No. 4 608-624)
B. a decrease in functional residual capacity (FRC) - probably false: “COPD, pneumonia, and sleep apnoea are common in the elderly. Closing capacity increases with age,24 and forced expiratory volume in 1 s (FEV1) declines 8–10% each decade because of decreased compliance of the pulmonary system and of muscle power.82 Arterial blood oxygen tension decreases progressively with age-induced ventilation/perfusion mismatch, diffusion block, and anatomial shunt.” (British Journal of Anaesthesia, 2001, Vol. 87, No. 4 608-624)
Note that anaesthesia does decrease FRC: “Anaesthesia has profound effects on pulmonary function and gas exchange, resulting in decreased functional reserve capacity (FRC), increased closing volume (CV), and impaired hypoxic pulmonary vasoconstricton (HPV).” (British Journal of Anaesthesia, 2001, Vol. 87, No. 4 608-624)
C. an increase in hypoxic ventilatory drive - false: “In the elderly, reduced respiratory reserve leads to a lower baseline PaO2 and an increased risk of peri- and postoperative hypoxaemia. There are reduced central ventilatory responses to both hypoxaemia and hypercapnia.” (Perioperative care of the elderly CEACCP, Dec 2004; 4: 193 - 196.)
D. an increase in serum creatinine - false: “Despite this, the serum creatinine concentration remains within normal limits in a healthy elderly patient. This paradox is primarily due to the loss in muscle mass that accompanies the previous termageingnext term process.” (Anaesthesia & Intensive Care Medicine Volume 8, Issue 9, September 2007, Pages 361-364)
E. an increase in ventricular wall stiffness - true: See A with regard to myocardial stiffening.
Comments r
PH42a [Jul97] [Jul98]
Thyroid hormones: (type A)
A. Mainly release T4 which is converted to rT3 in the periphery
B. Mainly releases T4 which is converted to T3 (which is the active form)
in the periphery
C. Peripherally converted to T3 and reverse T3 in equal proportions
D. Releases equal amounts of T3 & T4
E. Converted peripherally to T2 & reverse T2
F. Converted peripherally to T3 in larger amounts during surgical stress
G. T3 & rT3 are released in equal amounts
GL - A, equal amounts
The Thyroid gland releases three hormones.
T4 - majority
T3 - minority
Reverse T3 - relative minority
Reverse T3 is pharmacologically inactive, whilst T4 and T3 have activity. T3 is more active than T4.
In the periphery, T4 is converted to T3 and Reverse T3, by two enzymes - 5’-deiodinase and 5-deiodinase. Note the naming convention - the presence of absence of the prime indicates which portion of T4 is affected by each respective enzyme.
Figures vary, but approximately:
40-60% of T4 converted to T3 by 5’-deodinase
40-60% of T4 converted to reverse T3 by 5-deodinase.
Ie. Essentially in equal parts.
During times of surgical stress, the activity of 5’-deodinase is inhibited. Hence more T4 is converted to reverse T3.
Corticosteroids (either endogenous or exogenous) will also suppress the conversion to of T4 to T3 and enhance rT3 production.
–Phishy 22:52, 29 Jan 2008 (EST)
Answer for Black bank version
Option C is correct.
T3 and RT3 are converted in approximately equal portions.
Answer for March 2002 version
Option A is correct.
Option B incorrect. T4 is converted approximately equally to T3 and RT3.
Option C incorrect. T4 is converted equally.
Option D incorrect. Greater proportion of reverse T3 during times of surgical stress.
Option E is clearly made up. T2 will only become a reality when the robots from the future come back in time (grin)..
(actually T3 is converted to T2, the main reason that rT3 increases at times of stress is actually due to decreased breakdown to 3,3’ T2 by 5’monodeiodination - not sure about the robots). ref Harrisons
GL: OK now I am getting mad. Ganong plus this good article http://www.encyclopedia.com/doc/1G1-65068470.html - Under normal conditions, 45-50 percent of the daily production of T4 is transformed into rT3 - say that T4 -goes to T3 (33%) and RT3 (45%). So not equal amounts. But the rest are wrong also. THought maybe last one was right, there IS a T2 (see article) but no mention of RT2. So I guess I will go with A.
References
Ganong 16th Ed - p292.
Ganong 20th ed pg 312 now says 33% of T4 –> T3 and 45% –> RT3.
PH42b ANZCA version [2002-Mar] Q40
Tetra-iodothyronine (T4) is converted peripherally in the tissues to
A. equal quantities of tri-iodothyronine (T3) and reverse T3
B. mainly reverse T3 since this is the biologically active hormone
C. mainly T3
D. a greater proprtion of T3 during periods of surgical stress
E. equal quantities of di-iodothyronine (T2) and reverse T2
PH42b ANZCA version [2002-Mar] Q40 Tetra-iodothyronine (T4) is converted peripherally in the tissues to
A. equal quantities of tri-iodothyronine (T3) and reverse T3 - true
“T4 is degraded at a rate of about 10 percent per day. Approximately 80 percent is deiodinated, 40 percent to form T3 and 40 percent to form rT3.” (Uptodate)
B. mainly reverse T3 since this is the biologically active hormone - false: “RT3 is not biologically active.” (Ganong)
C. mainly T3 - false: Either equal or less. “One third of the circulating T4 is normally converted to T3 in adult humans, and 45% is converted to RT3.” (Ganong)
D. a greater proprtion of T3 during periods of surgical stress - probably false as T3 looks like it falls with surgical stress: “We therefore studied the relation of the endogenous serum IL-6 and TNF rise early in the course of nonthyroidal illness syndrome to the early decline in serum T3 in 19 apparently healthy individuals, aged 43 ± 16 yr, who underwent elective abdominal surgery for cholelithiasis or gastroplasty. Serum T3, free T3, T4, free T4, rT3, TSH, IL-6, and TNF were measured before and at various time intervals up to 42 h after skin incision. We observed a prompt decline in serum T3 30 min before skin incision, which continued to decline throughout the observational period. The magnitude of the decline reached 20% from the baseline value at 2 h. The early decline of T3 was attenuated and lasted from the 2–8 h, probably due to the sharp increase in serum TSH that started immediately after the entrance to the operating room and lasted for 2 h. In contrast, serum T4 and free T4 concentrations were increased soon after skin incision and remained elevated during the first postoperative day. Serum rT3 increased approximately 6 h after the initiation of surgery and remained elevated thereafter. Serum IL-6 remained essentially undetectable for 2 h after skin incision, whereas serum T3 was low.” (The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 9 4198-4205. Abstract here[1]
E. equal quantities of di-iodothyronine (T2) and reverse T2
PH43 [Apr98] Hyperventilation: A Causes vasoconstriction in intra-cranial vessels only B Is relatively contraindicated in severe ischaemic heart disease C ? D ? E ? (Related Q: PH34)
B is BEST answer
Apparently proven in dogs, ↓ PCO2 → ↓ coronary blood flow
Reference?
Surely flow metabolism coupling would overcome this??
er… that’s the flow metabolism coupling, ie response to CO2. (CO2 Inc with > metabolism!!) in this case, CO2 brought down by hyperventilation.
Addit: Above point has been proven in humans. See Ref Nakao K., Ohgushi M., Yoshimura M., Morooka K., Okumura K., Ogawa H., Kugiyama K., Oike Y., Fujimoto K., Yasue H.: Hyperventilation as a specific test for diagnosis of coronary artery spasm. Am J Cardiol 80. 545-549.1997; who state in conclusion that “These findings imply that hyperventilation is a highly specific test for the diagnosis of coronary artery spasm, and that hyperventilation test-positive patients are likely to have life-threatening arrhythmias during attacks and multivessel spasm.” See also Am J Cardiol 65. 417-421.1990; and Am J Cardiol 99. 322-324.2007.
PH44 [Apr99]
Spinal cord perfusion pressure:
A. Equal to mean distal aortic pressure minus CVP
B. ?Has same control as cerebral autoregulation
C. Increased pCO2 >60mmHg increases cord blood flow
D. Thoracic aortic surgery decreases perfusion pressure because of decreased CVP
E. Different blood flow (mls/100g/min) compared to brain due to differences in
proportion of grey & white matter
Answer B and C
Spinal Cord Perfusion Pressure = MAP - ICP
Autoregulation of SCBF is similar to CBF
Since CSF pressure increases with aortic cross clamp (from 10 to 20-25 mmHg)
Society of Cardiovascular Anaesthesiologists [[1]]
Sodium nitroprusside during thoracic aortic cross-clamping reduces spinal cord perfusion pressure and increases the incidence of neurological deficits. The decrease in cord perfusion pressure is owing to a decrease in the distal aortic pressure beyond the clamp and an increase in CSF pressure. The increase in CSF pressure occurs from cerebrovasodilatation. Pharmacological efforts to reduce proximal aortic pressure ideally should possess minimal cerebrovasodilating properties. [[2]]
Laryngospasm says:
A - False. Spinal cord perfusion pressure is equal to mean arterial pressure minus CSF pressure.
B - True. “Three concepts which have been proposed for brain blood flow can now be extended to the regulation of spinal cord blood flow. They are as follows: 1. Autoregulation maintains regional as well as total spinal cord blood flow constant during moderate alterations in system pressure.” Regulation of total and regional spinal cord blood flow, Marcus M et al., Circ. Res. 1977;41;128-134 AND “Our study, which measured cerebral and spinal cord blood flows simultaneously, demonstrated that there was essentially no difference in the autoregulatory capacities of these two tissues. Autoregulation was functional between MAP of 60-120 mm Hg in both brain and spinal cord. Regional blood flows demonstrated similar autoregulatory patterns.” Hickey R, Autoregulation of spinal cord blood flow: is the cord a microcosm of the brain?, Stroke 1986;17;1183-1189[3]
C - True. “Hypercapnia caused a marked increase in spinal cord blood flow and hypocapnia caused a marked decrease in spinal blood flow to all regions (cervical, thoracic, and lumbosacral) of the spinal cord in both dogs and sheep” Regulation of total and regional spinal cord blood flow, Marcus M et al., Circ. Res. 1977;41;128-134[4]
D - False. “Cross-clamping the thoracic aorta decreases anterior spinal artery pressure and increases CSF pressure.” And from A - a decrease in arterial pressure, and an increase in CSF pressure will reduce spinal cord blood flow.
E - False. “Autoregulation of the spinal cord mirrored that of the brain, with an autoregulatory range of 60 to 120 mm Hg for both tissues. Within this range, cerebral blood flow (CBF) was 59.2 ± 3.2 ml/100 g/min (SEM) and spinal cord blood flow (SCBF) was 61.1 ± 3.6.” Hickey R, Autoregulation of spinal cord blood flow: is the cord a microcosm of the brain?, Stroke 1986;17;1183-1189
PH45 [Aug99] (type K) Methaemoglobinaemia: A. Clinically obvious if >30% B. Hypoxia if >60% C. Not caused by nitrates D. ?
A True
B ?
C False
Definition
Methaemoglobinaemia = ↑ ferric form of iron in haem (Fe3+)
Normal levels 20% but rate of formation is also important
Treatment
Methylene blue (1-2mg/kg over 5 minutes) (except in patients with G6PD because it causes severe haemolysis)
Ascorbic acid
B is true if you accept Slovakian references “The level above 10% of MetHb causes peripheral cyanosis. The level of MetHb higher than 35% causes general symptoms which are results of the tissue hypoxia.” [1]
PH46a [Aug99] [Mar00] (type A) The (?most important) factor controlling the production of albumin is: A. Serum thyroid hormone B. Serum growth hormone C. Colloid osmotic pressure D. Serum cortisol E. Insulin
Colloid osmotic pressure is the primary driver which increases hormone levels of:
Insulin
Cortisol
Thyroid hormones
See this reference from BJA that may have prompted the question? - did the question appear earlier than this? - Yes, it was on a 1999 paper
‘Albumin will be synthesized only in a suitable nutritional, hormonal and osmotic environment. The colloid osmotic pressure (COP) of the interstitial fluid bathing the hepatocyte is the most important regulator of albumin synthesis.’
The role of albumin in critical illness British Journal of Anaesthesia, 2000, Vol. 85, No. 4 599-610 http://bja.oxfordjournals.org/cgi/content/full/85/4/599
I have found the reference article for this question. –Phishy 23:13, 29 Jan 2008 (EST)
Anaesthesia, Volume 53 Issue 8 Page 789-803, August 1998. Serum albumin: touchstone or totem? M. P. Margarson & N. Soni
Synthesis occurs in the polysomes bound to the endoplasmic reticulum of hepatocytes at a rate of 9–12 g.day−1 in a healthy adult [2, 3]. Only 20–30% of hepatocytes seem to produce albumin at any one time; it is not stored in the liver and there is, therefore, no reserve for release on demand. In states of maximal stimulus the synthesis of albumin can only be increased two to three fold. The primary factor controlling the rate of production is a change in the colloid osmotic pressure and the osmolality of the extravascular liver space [4]. Synthesis is also stimulated by raised concentrations of insulin, thyroxine and cortisol [5]. Growth hormone, despite its effects on reducing total urinary nitrogen loss, has no measurable effect on albumin synthesis in patients [6].
PH46b ANZCA version [2001-Apr] Q60, [2003-Apr] Q95
The primary factor controlling the rate of production of albumin is
A. colloid osmotic pressure
B. serum atrial natriuretic factor concentration
C. serum cortisol concentration
D. serum growth hormone concentration
E. serum sodium concentration
PH46b ANZCA version [2001-Apr] Q60, [2003-Apr] Q95 The primary factor controlling the rate of production of albumin is
A. colloid osmotic pressure - true
B. serum atrial natriuretic factor concentration
C. serum cortisol concentration
D. serum growth hormone concentration
E. serum sodium concentration
PH46c ANZCA version [2001-Aug] Q10 The primary factor controlling the rate of production of albumin is A. serum insulin concentration B. serum thyroxine concentration C. colloid osmotic pressure D. serum cortisol levels E. serum growth hormone levels
PH46c ANZCA version [2001-Aug] Q10 The primary factor controlling the rate of production of albumin is
A. serum insulin concentration
B. serum thyroxine concentration
C. colloid osmotic pressure - true: “The primary factor controlling the rate of production is a change in the colloid osmotic pressure and the osmolality of the extravascular liver space” (Anaesthesia, Volume 53 Issue 8 Page 789-803)
D. serum cortisol levels
E. serum growth hormone levels
PH47 [Aug99] [Mar00]
Albumin:
A. Produced at 12G/day
B. Interstitial fluid concentration is 7G%
C. Mostly intravascular
D. Leaks out of intravascular space at ?1.5g/day
E. ? half-life of 18 hours
Answer is A
A True - 9-12g/day (120-300mg/kg/day Kam)
B IV concentration is 30-40g/l = 30mg/ml = 3%. Lower concentration in interstitium. Think4% albumex.
C False
* Although albumin is perceived as intravascular protein, the total extravascular albumin actually
exceeds the total intravascular amount by 30%.
* The ratio of albumin to water is, however higher in the intravascular space (the extracellular
fluid is 2/3 interstitial and 1/3 intravascular), hence the colloidal effect.
D ?
Albumin cyclically leaves the circulation, through the endothelial barrier at the level of the
capillaries, passes into the interstitium and returns to the bloodstream through the lymph
system via thoracic duct.
* The circulation half time for this process is 16 -18 hours.
* 4 - 5% of total intravascular albumin extravascates in this way per hour
ie D false. 0.05 x 30g/L = 1.5g/h
E False - Half life is 20 days (Kam)
I have found the reference article for this question. –Phishy 23:17, 29 Jan 2008 (EST)
Anaesthesia, Volume 53 Issue 8 Page 789-803, August 1998. Serum albumin: touchstone or totem? M. P. Margarson & N. Soni
Synthesis occurs in the polysomes bound to the endoplasmic reticulum of hepatocytes at a rate of 9–12 g.day−1 in a healthy adult
The serum concentration of albumin is normally around 40 g.l−1, and in an average adult with a 3-l plasma volume there is an intravascular mass of ~ 120 g. The interstitial concentration is lower, at around 14 g.l−1, and varies in different areas of the interstitium;
In man, albumin is predominantly an extravascular protein.
The trans-capillary escape rate (TER) is defined as the percentage of intravascular albumin leaving the intravascular compartment per hour, and in healthy volunteers has been measured as some 4–5%.
This movement across the capillary wall has been measured and can be described in terms of a circulation half-life (normally held to be 16–18 h)
PH48 [Aug99] [Mar00] Reduced PaO2 is seen with: A. Anaemia. B. Left to right shunt. C. 5% carboxyhaemoglobin D. (Alveolar) hypoventilation E. Methaemoglobinaemia F. Left shift ODC
Answer is D
‘Reduced’ is an unfortunate term to have in this MCQ as there are two common uses of the word when referring to haemoglobin, and neither are intended here.
Firstly, reduced haemoglobin is a term used for deoxy haemoglobin
Secondly, methaemoglobin can be reduced (ie the chemical process known as reduction) back to normal haemoglobin by some drugs (eg methylene blue)
The MCQ does not mean either of this uses. Reduced just means decreased.
Also, it is talking about PaO2 and not Hb. –Phishy 23:22, 29 Jan 2008 (EST)
There are several processes that can lead to a decreased arterial pO2. The 5 most commonly quoted ones are:
Hypoventilation (or more specifically alveolar hypoventilation)
Low inspired inspired pIO2
Shunt
V/Q mismatch
Diffusion block
Anaemia and methaemoglobinaemia do not affect paO2.
The position of the ODC does NOT affect paO2 as pO2 refers to dissolved oxygen
The options L->R shunt (a form of ‘true’ shunt) and alveolar hypoventilation can both decrease arterial pO2.
Note that a right to left shunt causes decreased PaO2, not a left to right shunt.
PH49a [Jul00] Most sensitive haemodynamic parameter indicating hypovolaemia: A. Systolic pressure variability/swing B. PAOP C. CVP D. Hypotension E. Tachycardia
GL - A
Systolic pressure variation is the most sensitive of the above methods.
Δdown is a more accurate indicator of the response to stroke volume than pulmonary artery occlusion pressure.
A Δdown of more than 5mmHg indicates that stroke volume index would increase in response to a subsequent fluid challenge.
“Systolic pressure variation has not become popular in the UK, despite the fact that it correlates with hypovolaemia more closely than any other measured variable, including central venous pressure, pulmonary artery occlusion or diastolic pressure, pulse pressure, cardiac output or systolic arterial pressure.” British Journal of Anaesthesia 83 (4): 550–1 (1999)[1]
PH49b ANZCA version [2003-Apr] Q54 In a mechanically ventilated patient the haemodynamic parameter that correlates most closely with hypovolaemia is A. systolic pressure variation B. central venous pressure C. pulmonary artery occlusion pressure D. pulse pressure E. cardiac output
GL - A
Systolic pressure variation is the most sensitive of the above methods.
Δdown is a more accurate indicator of the response to stroke volume than pulmonary artery occlusion pressure.
A Δdown of more than 5mmHg indicates that stroke volume index would increase in response to a subsequent fluid challenge.
“Systolic pressure variation has not become popular in the UK, despite the fact that it correlates with hypovolaemia more closely than any other measured variable, including central venous pressure, pulmonary artery occlusion or diastolic pressure, pulse pressure, cardiac output or systolic arterial pressure.” British Journal of Anaesthesia 83 (4): 550–1 (1999)[1]
PH51 ANZCA version [2001-Apr] Q149
Changes in cardiovascular physiology associated with advanced age include
1. blunted beta-adrenoreceptor mediated modulation of inotropy, chronotropy
and vasomotor tone
2. decreased stroke volume
3. autonomic reflex dysfunction
4. reduced atrial contribution to left ventricular filling
Apr2001
True - ↓ responsiveness of the cardiac β-adrenergic agonists due to either ↓ receptor numbers or affinity or ↓ generation of cAMP after β-receptor activation
True - Maximum stroke volume that can be achieved is reduced (but no decline in cardiac output in healthy subjects between 25-79 years)
True (see 1)
False - progressively dependent on atrial contractions for diastolic filling
I disagree with 2, I think it is false. At rest, the elderly have a normal stroke volume. With exercise/stress, I agree it is altered.
Agree with above. Also autonomic dysfunction is seen but autonomic reflex dysfunction is a broader term. I would go for A. Michael
I disagree with this comment- I think there is autonomic reflex dysfxn (Stoelting pg 740)–Gord 15:11, 20 Nov 2008 (EST)
Hang on. Option 4 does NOT say reduced dependence on atrial contractions, (which is true) - it says reduced atrial CONTRIBUTION to diastolic filling. I’ve just read Stoelting p740 and it says AF is the most common supraventricular dysrhythmia in the elderly (>65yrs) The wording is vauge on this option. What the option should have said is: increased dependence on atrial contractions for diastolic filling. As it’s currently worded I would almost consider it correct. –Groundhog 05:41, 12 Aug 2008 (EDT)
I agree groundhog but the question refers to physiology and AF is not strictly physiological (I’m sure i have see a few elderly patients in sinus rhythm) thus we have to assume they are referring to a patient in sinus.
PH53 ANZCA version [2001-Aug] Q59
In assessing the adequacy of oxygen delivery to meet the body’s oxygen demands the best indicator is
A. arterial PO2
B. arteriovenous oxygen content difference
C. oxygen flux calculation
D. mixed venous PO2
E. cardiac output
D
ESA refresher course Saturday April 1, 2000
“Mixed venous oxygenation is probably the best single indicator of the adequacy of whole body oxygen transport since it represents the amount of oxygen in systemic circulation that is left after passage through the tissues. Accordingly, it represents the “oxygen reserve”, or the balance between oxygen delivery and consumption.”
AV content difference is going to be constant for varying cardiac outputs and so would not be useful. The mixed venous will go up and down with changing delivery.
Disagree B best answer AV difference will increase with low CO or incresed demand not be constant. Mixed ven Po2 doesn’t account for Hb and thus content.
Disagree with the disagree Answer D
If I gave somebody just the A-V oxygen content difference and ask them to make a rational decision of ongoing management of a patient it will have very little value. This is because it does not not reflect tissue oxygen tension. Goal directed therapy relies on mixed venous saturation for good reasons. It does reflect low CO state, low Hb etc. i.e. low CO will lead to more O2 extraction and therefore lower mixed venous saturation. …etc I will add more to this later.
To guage the importance of SVO2 please look at the NEJM “Early Goal-Directed Therapy in the Treatment of Severe Sepsis and Septic Shock”http://content.nejm.org/cgi/content/abstract/345/19/1368
rg–Macglu 04:08, 16 Jun 2007 (EDT)
This extract is from respiratory section of Anaesthesia UK website-D seems the best choice. Oxygen delivery is the amount of oxygen delivered to the peripheral tissue, and is obtained by multiplying the arterial oxygen content (CaO2) by the cardiac output (Q). For CaO2 = 20.1 ml/100 ml and Q = 5 l/min:
Oxygen delivery (DO2) = 1005 ml/min
The oxygen returned is given by the product of the mixed venous oxygen content (CvO2) and the cardiac output. For CvO2 = 15.2 ml/100 ml and Q = 5.0 l/min:
Oxygen return = 760 ml/min
Oxygen uptake is the amount of oxygen taken up by the tissues that can be calculated from the difference between oxygen delivery and the oxygen returned to the lungs in the mixed venous blood.
Thus
Oxygen uptake (VO2) = (oxygen delivery) – (oxygen return) = 1005 – 760 = 245 ml/min
To Summarise:
The primary goal of the cardio respiratory system is to deliver adequate oxygen to the tissues to meet their metabolic requirements, a balance between VO2 and DO2. The balance between oxygen uptake by the body tissues and oxygen delivery to them is assessed by:
The oxygen content of mixed venous blood CvO2, which is normally about 15 ml/100 ml
The extraction ratio, which is the ratio of VO2 to DO2 expressed as a percentage. Normally the extraction ratio is about 25% but can double to 50% if tissue demand increases.
PH54 ANZCA version [2003-Apr] Q147 The partial pressure of oxygen in the blood of the fetal umbilical vein is A. 27 mmHg B. 33 mmHg C. 40 mmHg D. 45 mmHg E. 70 mmHg
A is nearest to the correct answer
pH PO2 PCO2 SaO2
Umbilical artery 7.21 18 55 45%
Umbilical vein 7.32 28 40 70%
References
KB has 28mmHg in UV, 18mmHg in UA.
West has 30mmHg in UV, 22mmHg in UA.
[1] decent diagram of fetal circulation with pO2 and sats
PH55 ANZCA version [2003-Aug] Q122 The oxygen saturation of fetal haemoglobin in the fetal umbilical vein is A. 50% B. 60% C. 70% D. 80% E. 90%
KB physiology viva says 70%, take your chances
Power and Kam (p356) and Ganong both say 80%. As does Berne and Levy 8th ed P. 266. And Yentis A-Z Fig. 63 p206.
CEACCP Review 2005 5(4):107-112 ([1]) says 89-90%
Hmmm, I think you have misquoted CEACCP, it does however say 80-90%, with the picture stating 80%. I guess the bottom line is whether KB made the question? Everybody else says 80% plus, KB’s stuff is not referenced.–Boris 21:37, 8 Jan 2008 (EST)
Response from Kerry
My reference for the 70% figure is Fig 21 on p29 of “Obstetric Analgesia and Anesthesia” by John Bonica (published by the “World Federation of Societies of Anaesthesiologists” in 1980).
I have checked the CEACCP article by Murphy and this quotes a pO2 of 4.7 kPa (about 35mmHg) and a saturation of 80%. As noted this 80% also appears in fig 1. Incidentally, in fig 2 of his oxygen dissociation curve (on p109), if you plot a pO2 value of 4.7 on the x-axis, then the corresponding saturation value on the y-axis is 70%!! - so the article is internally inconsistent.
When I wrote the section in my book (p253-6), the problem was finding suitable source material. I made a comment about this on p255. I could not find a single reference with a consistent set of values. The Bonica book was the closest I could find. The Bonica data is a least complete and thus allows one to calculate the oxygen balance across the placenta. The problem though was two-fold:
he has more O2 leaving the placenta than being delivered to it - which is absurd
he does not account for O2 consumption by the placenta (which has a large O2 consumption - 10 mls/kg/min) and this important fact should be noted.
No other source provided enough data to allow calculation of the O2 balance and I sought out all the primary articles I could locate (all non-human). This is why in my text I actually provided a complete and fairly representative set of values which actually work - and I did the calculations to prove it - and accounted for placental O2 consumption.
This is a poor question as more than one answer could be given and judged correct. My overall view though is that they were expecting the 80% value given that it is quoted in Ganong.
References
In vitro perfusion of human placenta. V. Oxygen consumption - This is the ref for the 10mls/kg/min figure in humans:
“. . . oxygen consumption approximated 10 ml. per minute
per kilogram. This rate of 02 consumption is similar to those
obtained from studies of animal placentas in vivo and is more
consistent with that of an active metabolic organ. If one were to
accept estimates of 02 consumption by the human fetus in utero,
the present studies indicate that approximately one fifth of
maternal oxygen supplied to the conceptus is diverted to support
placental metabolism.”
This UK ref says 75-80% saturated)
The First Breath of Life:»_space;
“Oxygen and nutrients are delivered to the fetal circulation by the
umbilical vein. Levels of oxygen in the umbilical vein are
measured at 28-30 mmHg, with an oxygen saturation of 70%.”
Placental Compared With Umbilical Cord Blood to Assess Fetal Blood Gas and Acid-Base Status Obstetrics & Gynecology 2005;105:129-13 - Values from women at delivery (i.e. actual human data): UV pO2 28.7 +/- 5.9 mmHg; sats 63.3 +/- 13.9% (+/- SD)
“Introductory Maternity Nursing”»_space; - says 80% in umbilical vein (p107)
Ganong p628
“The blood in the umbvilical vein in humans is believed to be about
80% saturated with O2…”
Fetal circulation
“Average oxygen saturation of blood is 80% in the umbilical vein
before it mixes with unoxygenated blood in the ductus venosus.
After mixing, the oxygen saturation is approximately 67%.”
Growth, Maturation, and Physical Activity
“Blood of the umbilical vein has an oxygen saturation of about 70%”
This ref says single umbilical vein (80% saturation)
From Child Development (1950):
“In the fetus, oxygenated blood coming from the umbilical vein may
have an oxygen saturation of 60-80 per cent of its capacity”
Fetal development Fig 3.1 on p28 says 80% in umbilical vein (Note that the Bohr effect is ignored in this book and figure so there is no consideration of the double Bohr effect)
Fetal & Neonatal Physiology:
Diagram on p3 says sats of 80% for pO2 of 29mmHg in Um vein -BUT-
if you look at the fetal ODC on p5 and plot in pO2 29mmHg you find a
sats value of 70%!! The typical problem of quoting/using figures and
graphs from different sources uncritically.
Power & Kam - “Principles of Physiology for Anaesthetists”:-
“The oxygen partial pressure of the blood returning to the fetus
in the umbilical vein is about 30mmHg(4 kPa).” (p354)
AND
“In the fetus, oxygenated blood with a pO2 of about 30mmHg (4kPa)
and an oxygen saturation of 80%” (p356)
HOWEVER: If you look at Fig 14.12 on p354, and draw in lines on
the oxygen dissociation curve labelled ‘umbilical vein’, then a pO2
of 30mmHg plots to a saturation of 70% (NOT 80%) so the book is
internally inconsistent.
PH56 ANZCA version [2003-Aug] Q145
Physiological changes of ageing include all except
A. decreased intracellular water
B. decreased total lung capacity
C. diminished baroreceptor responsiveness
D. lower maximum heart rate in response to stress
E. increased CSF volume
Aug 2003. B is the best answer.
Intra-cellular water decreases with age from approx 42% at 25 years to 33% at 75 years. Of interest extracellular water does NOT change. (Anaesthesia in the elderly by Davenport, pg 22).
Total lung capacity is NOT decreased but remains relatively stable. Both inspiratory and expiratory reserve volumes (and hence vital capacity) reduce with age. FRC increases. Lung compliance increases, chest wall compliance decreases, total compliance decreases. (Anaesthesia in the elderly by Davenport, pg 23).
There is both diminished baroreceptor responsiveness (due to damage from stiffened blood vessel walls) to changes in blood pressure as well as reduced responsiveness of the heart to catcholamines which predisposes to postural hypotension. (Anaesthesia in the elderly by Davenport, pg 14)
Maximal heart rate in response to stress declines with age (remember the formula for maximal heart rate is approx 220-age). Anaesthesia in the elderly by Davenport, pg 13.
As we age our brains shrink due to neuronal loss. This volume is replaced by CSF to maintain a normal ICP. (Anaesthesia in the elderly by Davenport, pg 6).
A - True - TLC ↓ 10% due to ↑ chest wall rigidity
B - False - FRC increases
C - False - usually ↓ catecholamine levels but also have ↓ responsiveness of the cardiac β-adrenergic agonists due to either ↓ receptor numbers or affinity or ↓ generation of cAMP after β-receptor activation
C - ? True - 15% ↓ Adrenal mass, but ↑ Adrencortical activity, with 2-4x circulating Adr & NA levels
Given this cannot be a Type K, I’d presume it’s an ‘All True EXCEPT…’ type question [with the other option being False
Another suggestion- B is false. Notwithstanding Kam’s diagram to suggest otherwise, he does not specifically state it goes down. One source (ASA) suggests no change or modest increase. [1]
Ratio of FRC/TLC increases while FRC decreases mildly… COA 2001
This statement from an article in the European Respiratory Journal 2005;26:563-565 [2] These studies established that the maximum size of the lungs (total lung capacity) did not change with age, but functional residual capacity (FRC) and residual volume (RV) both increased so that inspiratory capacity and vital capacity (VC) both declined. The increase in FRC was due to an increase in relaxation volume of the respiratory system, which arose from changes in the static recoil pressure of both the chest wall and the lungs - suggests that B is incorrect
Also this article - admittedly a little old suggests that E is a physiological change with ageing [3]: “The results show a strong correlation between increased intracranial CSF volume and increasing age” This page also links to a 1996 article that confirms increased CSF, (particularly extraventricular) with age. [4]
Regarding the ANZCA question:
A, B, C are all stated explicitly to be true by Kam on pages 367-8
D. -Elderly have same resting heart rate but reduced maximal heart rate so this option is as expected
E. -Increased CSF volume is also a physiological change as a consequence of decreased brain volume (1400->1200g)
So if a college examiner can’t get it right in their textbook, what chance do we have? –Phil 22:33, 18 Jul 2007 (EDT)
Sorry to muddy the water.
But a few extra quotes.
Body water spaces and cellular hydration during healthy aging.Ritz P.
Service de Médecine B, Centre Hospitalier Universitaire, Angers, France. paritz@chu-angers.fr
Ann N Y Acad Sci. 2000 May;904:474-83. Links
Age-related changes in the proportions of intracellular or extra-cellular water to total body water and in the ratio of total body water to fat-free mass are debatable. These are important issues both for medical reasons (dehydration is a threat in the diseased elderly) and for methodological reasons (most techniques for assessing of body composition assume constant hydration of the fat-free mass). This study compared hydration in young and elderly (60 years) people. In the first part of the study, we analyzed the literature and computed the ratio of total body water over fat-free mass, Hf. Eligible studies involved independent measurements of fat-free mass and total body water. Hf did not appear to change with age. The second part of this study computed Hf in 103 individuals studied in our laboratory. The mean values were not different in young (73.2 +/- 2.4%) and elderly people (73.4 +/- 2.4%). At all ages, the proportion of intracellular or extracellular water (as measured by bromide dilution) to total body water (as measured by oxygen 18 dilution) was similar. The same finding holds for the proportion of intracellular water to fat-free mass. We conclude that hydration of fat-free mass and cellular hydration are not affected in healthy aging.
May be the brain changes are related to apoptosis rather than loss of brain water. My bichem PhD mate thinks loss of cellular water also sounds doubtful. What with the potential for the cell to fill with debris as you get older why would the cell water decline at least for oncotic reasons? (Just a theory of mine.)
From: Syllabus on Geriatric Anesthesiology: Aging and the Respiratory System by Brian K. Ross
The total lung capacity (TLC) grows with age until puberty, where it reaches an average value of 6 to 7 liters, after which a slow loss of volume begins. With the age-related loss in total lung capacity (TLC), plus the very modest increase in FRC, the ratio of FRC to TLC tends to increase with age.
If you read Kam you would go with B.
If you try to read a few abstracts you may go with A.
I personally hope they do not ask this question again.
References
Kam and Power, Physiology for the Anaesthetist p366-367
Merck - Aging and the Nervous System
Anaesthesia in the elderly. Harold T Davenport, 1986, London.
Anesth Analg 2003;96:1823–36
PH57 ANZCA version [2001-Apr] Q126
Serum creatinine levels
1. are affected by muscle mass
2. are affected by renal tubular secretion of creatinine
3. may be reduced by fluid loading.
4. can be used to detect small (less than 25%) reductions in glomerular filtration rate
True
?True - but only a minor factor mostly dependent on filtration. (Other comment) Secretion of creatinine increases as GFR falls as increased concentration delivered to prox tubule.
True - increases filtration
False - only rises once 25-50% renal function lost
–BassBoyDave 22:08, 31 Mar 2010 (EDT)
remember from primary physiology: creatinine is used to measure renal blood flow, not GFR.
For those as simple as I… Creatinine clearance rate (CCr or CrCl) is the volume of blood plasma that is cleared of creatinine per unit time and is a useful measure for approximating the GFR. Creatinine clearance exceeds GFR due to creatinine secretion which can be blocked by cimetidine. Creatinine clearance or estimates of creatinine clearance based on the serum creatinine level are used to measure GFR. Creatinine is produced naturally by the body (creatinine is a break-down product of creatine phosphate, which is found in muscle). It is freely filtered by the glomerulus, but also actively secreted by the peritubular capillaries in very small amounts such that creatinine clearance overestimates actual GFR by 10-20%.from google. http://en.wikipedia.org/wiki/Creatinine_clearance. Disco.
PH58 ANZCA version [2003-Aug] Q112, [Mar06] Q66, [Jul06] Q26
When intravenous magnesium sulphate is administered in the management
of severe pre-eclampsia, deep tendon reflexes are lost at a serum
Mg2+ level of
A. 2 mmol.1-1 B. 3.5 mmol.1-1 C. 5 mmol.1-1 D. 8 mmol.1-1 E. 12 mmol.l-1
Therapeutic 4-6mEq/L (=2-3 mmol/l)
Loss of deep tendon reflex and widened QRS at 10mEq/L (= 5 mmol/l)
Respiratory arrest 15mEq/L (=7.5 mmol/l)
Asystole 20mEq/L (=10 mmol/l)
Note: Difference between mEq/L (commonly quoted in US sources) and mmol/L
ANZCA version: The classic teaching is that deep tendon reflexes are LOST when [Mg+2] EXCEEDS 5 mmol/l (ie 10 mEg/l) so C is the best answer
For a local reference, see the RWH Protocol which says LOSS of DTR occurs at >5 mmol/l.
Mg conc (mmol/L)
0.8 - 1.0 normal plasma level
1.7 - 3.5 therapeutic range
2.5 - 5.0 ECG changes (P-Q interval prolongation, widen QRS complex)
4.0 - 5.0 reduction in deep tendon reflexes
> 5.0 loss of deep tendon reflexes
> 7.5 sinoatrial and atrioventricular blockade. Respiratory paralysis and CNS depression
> 12 cardiac arrest
Other sources such as the “Up-to-date” reference below quote a range of 3-5mmol/l so this would lead to some uncertainty between B & C.
From Up-to-Date article on “Symptoms of hypermagnesemia”
OVERVIEW
Hypermagnesemia is an uncommon problem in the absence of magnesium administration or renal failure.
When it occurs, the elevation in the plasma magnesium concentration is usually mild ( 5
PH59 ANZCA version [Jul 06] Q58
In a normal pregnant woman laboratory tests would show:
A. an arterial pH of 7.4 B. an increase in functional residual capacity (FRC) C. decreased oxygen consumption D. an arterial base excess of +5mmol.l-1 E. a PaCO2 of 50 mmHg
In a normal pregnant woman laboratory tests would show:
A. an arterial pH of 7.4 - true
B. an increase in functional residual capacity (FRC)
C. decreased oxygen consumption
D. an arterial base excess of +5mmol.l-1 (wrong -I found an Google reference from 1972 for normal Base excess in pregnancy as -3 mmol/l)
E. a PaCO2 of 50 mmHg
Answer= A (see K.B’s book p248-9)
To quote KB: “This is the only example of full acid-base compensation in normal physiology.”
pH increases to 7.41-7.46 A&IC 33:2 p168 table (2005).
FRC decreased during pregnancy
pCO2 decreased to 30-32 mmHg
PH60 [Apr07] [Jul07] What raises intra-ocular pressure (IOP)? A. metabolic acidosis B. respiratory acidosis C. miosis D. reverse trendelenberg (head up) E. carbonic anhydrase inhibitor
ANSWER IS B
B true D False
From http://www.cja-jca.org/cgi/reprint/33/2/195.pdf
resp acidosis increases ICP
metab acidosis decreases! ICP
miosis also decreases ICP –amyhsk 10:03, 14 Nov 2007 (EST)
C is false, answer B. --drstitch 18:41, 19 Nov 2007 (EST) Yeah, Mydriasis will change the angle and increase IOP, not Miosis and thus I'm with Drstitch =B And in answer to the exclamation mark, it is all about CO2/ HCO3 Me too (!), AND it's all about: IOP = aqueous production = choroidal blood flow = cerebral blood flow = pCO2 which is raised in resp acidosis. B
Agree resp acidosis increases IOP. Jamesj
Factors that affect ICP are the same as IOP… -> disagree.
Not sure what the difference between metabolic and respiratory acidosis is… Perhaps Aqueous humor formation is an active process. Perhaps metabolic acidosis = inadequate respiration at a tissue level = reduced cellular function = reduced humor production. Respiratory acidosis = increased blood flow which does not necessarily = increased production of humor although is less likely to = tissue level dysfunction.
ANZCA Version Intra-ocular pressure is increased by A. head-up B. hypothermia C. metabolic acidosis D. miosis E. respiratory acidosis
Intra-ocular pressure is increased by A. head-up B. hypothermia C. metabolic acidosis D. miosis E. respiratory acidosis - true
PH61 [Jul07]
In a 140kg obese patient, compared to a 70 kg person
A. cardiac output >20% lower B. cardiac output 10% lower C. cardiac output no different D. cardiac output 10% higher E. cardiac output >20% higher
Definitely increased, but can’t find a source to say whether it is 10% or >20%. My guess is >20%.–drstitch 23:41, 7 Nov 2007 (EST)
Consider that blood flow to fat is something like 1-2 ml/min/100g. Therefore if 70 kg of extra fat that is a blood low of around a litre/min extra. If the normal cardiac output is around 5l/min than an increase of 20% is very reasonable.
A Google search revealed a link to a 2003 book ‘Obesity: Mechanisms and Clinical Management by Robert H. Eckel’,
stating that ‘…both stroke volume and cardiac output are higher (…) in overweight, than in normal-weight, individuals (about 9%).
The author’s explanation:
Although CO increases with total fat mass, perfusion per unit of adip. tissue decreases by about 35% with incr. obesity.
concomitant incr. in lean body mass may account for some of incr. CO
Reference from the book which I cannot access: Collis et al, ‘Relations of stroke volume and cardiac output to body composition: the strong heart study’ Circulation 2001; 103:820-5
So D should be right?!–Anaestralia 02:48, 28 Dec 2007 (EST)
D from Circulation ref “…Overweight individuals were younger, heavier and had higher adipose mass, % body fat, & waist/hip ratio than normal weight participants. Fat free mass was higher, by a mean of 14%, & SV & CO were approx 9% higher in overweight individuals…”–GCS3 20:42, 22 Jan 2008 (EST)
I think it is > 20% - this BJA paper suggests CO increases 20-30 ml per kilogram - meaning this person’s CO could be increased by 2L/min. BJA: British Journal of Anaesthesia Volume 85, Number 1 Pp. 91-108
Here is the link [1] –Drip 06:35, 18 Feb 2008 (EST)
Stoelting says that CO increases by 0.1 L/kg for each kg extra fat - this may be a bit excessive(!) but considering the above BJA ref as wellsuggests that this morbidly obese 140kg person could conceiveably have double the CO. This is why they get systemic hypertension and cardiomegaly and ultimately cardiomyopathy. I think it’ll be E. –nic b 22:28, 1 Mar 2008 (EST)
Miller 6th edition says CO increases by 0.01L/min for each kg of adipose tissue. If this is true, a 10% increase in CO represents 50kg extra adipose tissue, whilst a 20% increase in CO represents 100kg extra adipose tissue (ie, more than 140kg!). Furthermore, not all the extra weight in the 140kg person is adipose tissue, some will be due to increased plasma, red cells and interstitial fluid. I’d go with option D.–Seaslug 01:16, 10 Mar 2008 (EST)
I had a look at one of the “9%” articles and the overweight people were only about 95 kg. Schneider and Levinson back up the more generous increase in CO, saying in contrast to the 35-45% increase seen in pregnancy, in obesity the CO can almost double. I also had a look at this issue from another perspective, because there are lots of articles saying that the cardiac index doesn’t change for obese vs non-obese subjects. So looking at a 70kg vs 140kg person with a normal CI and plugging in both a short and a tall height just to double check things, there was a huge difference in CO between the two. I won’t note all the calculations here, do it for yourself, but as one example using a CI of 3 and a height of 170cm, the CO at 70kg is 5.46L/min and the CO at 140kg is 7.71L/min so like a 40% increase. That convinces me it’s E. Jo, May 09.
Although fat increases there is a concomitant increase in lean body weight. LBW is what most closely corresponds to CO so therefore despite a reduced proportion of CO that goes to fat there is an overall increase to LBW which comprises up to 40% the increased mass of an obese person. Option E
PH61 ANZCA version [Jul07]
A morbidly obese 140kg, 40-year-old male is scheduled for cholecystectomy. He has no history of
cardiac disease. His ideal body weight is 70kg. Compared to his resting cardiac output at ideal
body weight, his resting cardiac output at his weight of 140 kg would be
A. decreased by 20% or more
B. decreased by 10%
C. unchanged
D. increased by 10%
E. increased by 20% or more
Definitely increased, but can’t find a source to say whether it is 10% or >20%. My guess is >20%.–drstitch 23:41, 7 Nov 2007 (EST)
Consider that blood flow to fat is something like 1-2 ml/min/100g. Therefore if 70 kg of extra fat that is a blood low of around a litre/min extra. If the normal cardiac output is around 5l/min than an increase of 20% is very reasonable.
A Google search revealed a link to a 2003 book ‘Obesity: Mechanisms and Clinical Management by Robert H. Eckel’,
stating that ‘…both stroke volume and cardiac output are higher (…) in overweight, than in normal-weight, individuals (about 9%).
The author’s explanation:
Although CO increases with total fat mass, perfusion per unit of adip. tissue decreases by about 35% with incr. obesity.
concomitant incr. in lean body mass may account for some of incr. CO
Reference from the book which I cannot access: Collis et al, ‘Relations of stroke volume and cardiac output to body composition: the strong heart study’ Circulation 2001; 103:820-5
So D should be right?!–Anaestralia 02:48, 28 Dec 2007 (EST)
D from Circulation ref “…Overweight individuals were younger, heavier and had higher adipose mass, % body fat, & waist/hip ratio than normal weight participants. Fat free mass was higher, by a mean of 14%, & SV & CO were approx 9% higher in overweight individuals…”–GCS3 20:42, 22 Jan 2008 (EST)
I think it is > 20% - this BJA paper suggests CO increases 20-30 ml per kilogram - meaning this person’s CO could be increased by 2L/min. BJA: British Journal of Anaesthesia Volume 85, Number 1 Pp. 91-108
Here is the link [1] –Drip 06:35, 18 Feb 2008 (EST)
Stoelting says that CO increases by 0.1 L/kg for each kg extra fat - this may be a bit excessive(!) but considering the above BJA ref as wellsuggests that this morbidly obese 140kg person could conceiveably have double the CO. This is why they get systemic hypertension and cardiomegaly and ultimately cardiomyopathy. I think it’ll be E. –nic b 22:28, 1 Mar 2008 (EST)
Miller 6th edition says CO increases by 0.01L/min for each kg of adipose tissue. If this is true, a 10% increase in CO represents 50kg extra adipose tissue, whilst a 20% increase in CO represents 100kg extra adipose tissue (ie, more than 140kg!). Furthermore, not all the extra weight in the 140kg person is adipose tissue, some will be due to increased plasma, red cells and interstitial fluid. I’d go with option D.–Seaslug 01:16, 10 Mar 2008 (EST)
I had a look at one of the “9%” articles and the overweight people were only about 95 kg. Schneider and Levinson back up the more generous increase in CO, saying in contrast to the 35-45% increase seen in pregnancy, in obesity the CO can almost double. I also had a look at this issue from another perspective, because there are lots of articles saying that the cardiac index doesn’t change for obese vs non-obese subjects. So looking at a 70kg vs 140kg person with a normal CI and plugging in both a short and a tall height just to double check things, there was a huge difference in CO between the two. I won’t note all the calculations here, do it for yourself, but as one example using a CI of 3 and a height of 170cm, the CO at 70kg is 5.46L/min and the CO at 140kg is 7.71L/min so like a 40% increase. That convinces me it’s E. Jo, May 09.
Although fat increases there is a concomitant increase in lean body weight. LBW is what most closely corresponds to CO so therefore despite a reduced proportion of CO that goes to fat there is an overall increase to LBW which comprises up to 40% the increased mass of an obese person. Option E
