Cardio-respiratory (
A morbidly obese, non-smoking patient who is otherwise well is likely to have a significant reduction in:(18)
1. Functional Residual Capacity (FRC).
2. Forced Expiratory Volume in 1 second (FEV1).
3. Expiratory Reserve Volume (ERV).
4. Diffusing Capacity for Carbon Monoxide (DLCO).
Ans:1,2,3
Biring et al have recently examined pulmonary physiological changes of morbid obesity and concluded that "Forced vital capacity, forced expiratory volume in 1 second, expiratory reserve volume, functional residual capacity, maximum voluntary ventilation, and forced expiratory flow during midexpiratory phase were all significantly reduced." However, no abnormality in DLCO was found.
Biring MS, Lewis MI, Liu JT, Mohsenifar Z. Pulmonary physiologic changes of morbid obesity. Am J Med Sci. 1999 Nov;318(5):293-7.
An acclimatised mountaineer, breathing air on the summit of Mount Everest (barometric pressure 253 Torr), will have an arterial PCO2 (PaCO2) of approximately: (30)
A. 24 mm Hg.
B. 20 mm Hg.
C. 16 mm Hg.
D. 12 mm Hg.
E. 8 mm Hg.
Ans:E
See the classic study by West. - "Pulmonary gas exchange was studied on members of the American Medical Research Expedition to Everest at altitudes of 8,050 m (barometric pressure 284 Torr), 8,400 m (267 Torr) and 8,848 m (summit of Mt. Everest, 253 Torr). Thirty-four valid alveolar gas samples were taken using a special automatic sampler including 4 samples on the summit. Venous blood was collected from two subjects at an altitude of 8,050 m on the morning after their successful summit climb. Alveolar CO2 partial pressure (PCO2) fell approximately linearly with decreasing barometric pressure to a value of 7.5 Torr on the summit. For a respiratory exchange ratio of 0.85, this gave an alveolar O2 partial pressure (PO2) of 35 Torr. In two subjects who reached the summit, the mean base excess at 8,050 m was -7.2 meq/l, and assuming the same value on the previous day, the arterial pH on the summit was over 7.7. Arterial PO2 was calculated from changes along the pulmonary capillary to be 28 Torr. In spite of the severe arterial hypoxemia, high pH, and extremely low PCO2, subjects on the summit were able to perform simple tasks. The results allow us to construct for the first time an integrated picture of human gas exchange at the highest point on earth."
West JB, Hackett PH, Maret KH, Milledge JS, Peters RM Jr, Pizzo CJ, Winslow RM. Pulmonary gas exchange on the summit of Mount Everest. J Appl Physiol. 1983 Sep;55(3):678-87.
A patient in an intensive care unit has the following haemodynamic measurements made:
Mean Systemic Arterial Pressure (MAP) 80 mm Hg.
Mean Central Venous Pressure (CVP) 10 mm Hg.
Cardiac Output (CO) 5.0 l/min.
Mean Pulmonary Arterial Pressure (MPAP) 35 mm Hg.
Pulmonary Artery Occlusion Pressure (PAOP) 20 mm Hg.
The pulmonary vascular resistance (PVR) is: (31)
A. 14 dynes.sec.cm-5.
B. 120 dynes.sec.cm-5.
C. 240 dynes.sec.cm-5.
D. 400 dynes.sec.cm-5.
E. 1120 dynes.sec.cm-5.
Ans:C
PVR= 80 x (MPAP-PAOP)/CO.
This equation is the hydraulic equivalent of Ohm's Law ie: Flow = Driving pressure / Resistance. The constant '80' being a conversion factor to convert the pressures (in mm Hg) to SI units. (More accurately the value is 79.9).
The normal range for PVR in an adult is 150 - 250 dynes.sec.cm-5.
The MAP and CVP are not needed for calculation of the PVR but can be used in the calculation of systemic vascular resistance according to the equation:
SVR= 80 x (MAP-CVP)/CO.
In the left lateral position, blood flow to the non-dependant lung is:(94)
A. 25%.
B. 35%.
C. 45%.
D. 55%.
E. 65%.
Ans:C
The distribution of perfusion in the lungs varies regionally and is under the influence of posture, mode of ventilation, and type of anaesthesia. In general, a hydrostatic head of pressure exists which decreases with vertical height above the heart. In the upright position, the absolute pressure in the pulmonary artery decreases by 1 cm water/cm vertical distance up the lung.
Distribution of blood flow can be summarized as follows: Normally, in the upright position, the right lung receives 55% of blood flow and the left receives 45%. In the lateral decubitus position, when the right lung is up, it receives 45% and the dependant left lung receives 55%. When the left lung is up, it receives 35% and the right dependant lung receives 65%.
These values are for an awake, spontaneously breathing patient. With respect to the left lateral position only, blood flow to the non-dependant lung is:
(1) 41% in an awake, spontaneously breathing patient.
(2) 43% in an anaesthetised, spontaneously breathing patient.
(3) 44% in a paralyzed patient, ventilated with IPPV.
(4) 70% in a paralyzed patient, ventilated with IPPV, with the chest wall open.
MARTIN, J; Positioning the Patient for Anaesthesia and Surgery, 1978, p138.
ROGERS, M.C ET AL (EDS); Principles and Practice of Anesthesiology, Mosby, 1993, pp 1748.
What is the rate of rise of PaCO2 during breath holding?(96)
A. 1 mmHg/min.
B. 3 mmHg/min.
C. 5 mmHg/min.
D. 7 mmHg/min.
E. 10 mmHg/min.
Ans:B
The rise of PaCO2 is most rapid in the first minute of breath holding. This felt to be due to the additional effects of equilibration between the venous and arterial blood. Thereafter a steady rise of ~ 3mmHg/min occurs.
NUNN, J; Applied respiratory Physiology,3rd Ed., Butterworths, 1987.
Which of the following are true with respect to increasing oxygen reserves through preoxygenation with 100% oxygen:(97)
1. It is well reflected by the arterial oxygenation saturation.
2. It requires longer when using a Bain circuit.
3. It is achieved equally as well with 4 vital capacity breaths or 3 minutes of tidal volume breathing.
4. Oxygen reserves are reduced in pregnancy.
Ans:4
Arterial oxygen saturation does not reflect the amount of oxygen contained within the functional residual capacity- the major reservoir utilized during preoxygenation. This is reflected by the end-tidal N2. Non-rebreathing circuits generally achieve denitrogenation rapidly. Vital capacity breathing reduces end-tidal N2O to 6% as compared with conventional tidal volume breathing in which it is reduced to 1%. In ASA I patients, this will still prevent desaturation for up to 6 minutes of apnoea, but may cause significant reductions in the tolerated apnoeic intervals in obstetric or elderly patients.
Arterial oxygen saturation falls to a mean of 75% within 1 minute of suxamethonium when oxygen is not administered prior to induction of anaesthesia. Maximizing oxygen reserve has been advocated as a means of delaying this event. The major oxygen stores of the body are shown after equilibration when breathing 21% and 100% oxygen:
21% 100%
functional residual capacity = 0.21 x 2.4 L ~450 mls ~3000 mls
chemical combination with haemoglobin ~850 mls ~950 mls
dissolved in plasma ~50 mls ~100 mls
chemical combination with myoglobin ~200 mls ~200 mls
Thus, increasing oxygen reserve by " preoxygenation " is achieved predominantly through denitrogenation of the FRC and to a lesser extent through increasing saturation of arterial blood. This will be manifested using pulse oximetry as an elevation of baseline SAO2 and a delayed fall in SAO2 during apnoea.
The best method of preoxygenation has been studied. The options include:
(1)Preoxygenation with tidal volume breaths for 2-10 minutes.
(2) " 4 vital capacity breaths.
(3)Postoxygenation by assisted ventilation after apnoea has occured.
(4)Any combination of the above.
(1)Recommendations vary between 2 and 10 minutes. Earlier studies showed that in normal subjects, breathing 100% achieved > 98% denitrogenation in 7 minutes. Reducing alveolar N2 to 4% was felt to be acceptable however, and allowed 5-6 minutes of apnoea without desaturation. The difference in oxygen stores at 0% and 4% N2 were negligible (2.53L v 2.61L). More recently, it has been shown that in ASA I patients, tidal breathing of 100% oxygen reduced alveolar N2 to 1% after 3 minutes, and to 6% after 2 minutes.
The time required will however vary with different breathing circuits. Circuits using low fresh gas flows require longer to complete denitrogenation. Non-rebreathing systems generally achieve this rapidly.
Three minutes has been recommended with the Magill (Mapleson A) system using 8 L/min flow rate. One minute using 10 L/min will allow 3 minutes of apnoea before desaturation > 6% SAO2 occurs. When a circle system is used with 5 L/min flow rate, an adequate level of denitrogenation is achieved within 5 minutes.
Note that these times assume a tight seal with the face mask.
(2)More recently, it has been shown that four voluntary, maximal breaths of 100% oxygen over 30 seconds produced a similar level of oxygenation as 3 minutes of tidal breathing. It would appear that this technique would require a non-rebreathing circuit with a large reservoir bag and a large fresh gas flow. Satisfactory results have been obtained however, with a circle system with 5 L/minute flows and a Magill circuit with 8 L/min flows despite this observation. Here, the patient was instructed to inhale slowly to prevent the reservoir bag from collapsing.
A study published in 1989 has challenged the second method on the basis that most studies performed measured oxygen content of the blood rather than actual N2 content of the lungs. This was following an earlier study which showed the maximal breath technique to be associated with a significantly shorter time to desaturation than tidal breathing for 3 minutes.The implication was that whilst they both fully saturate haemoglobin, only the latter provides adequate denitrogenation. One of the reasons suggested was that the maximal breath method was assumed to represent vital capacity breathing where in reality, many patients achieved inspiratory capacity or smaller volumes. In the study cited, 3 minutes of tidal breathing was compared with eight inspiratory capacity breaths (TLC with passive exhalation) and four vital capacity breaths (exhaling to residual volume then maximal breaths). The study showed that N2 washout to 1% was achieved with 3 minutes of tidal breathing and to 6% with 2 minutes of tidal breathing, 8 inspiratory breaths or 4 vital capacity breaths.
It should be noted that whilst 6% residual N2 may be adequate in an ASA I patient, it may only allow a shorter apnoeic time before desaturation in a patient with a less favourable relationship between closing capacity and FRC as seen in pregnancy, obesity and age > 44.
(3)Oxygenation after induction is practiced widely however is felt to be less effective than preoxygenation because the volume of the reservoir bag is limited and the FRC is often reduced.
LATTO, I.P & ROSEN, M (EDS); Difficulties in Tracheal Intubation, Balliere Tindall, pp 20-23.
Which of the following typically result from the application of an aortic cross clamp?(130)
1. Stroke volume decreases.
2. Systemic blood pressure increases.
3. Myocardial contractility decreases.
4. Venous return decreases.
Ans:1,2,3,4
The anticipated consequences of application of an aortic cross-clamp include an increased ventricular afterload, a decreased venous return, and a decreased velocity and shortening of myocardial muscle fibres. Clinical reports consistently report a 15-35% reduction in stroke volume and cardiac index, coupled with an increased arterial blood pressure and up to 40% increase in systemic vascular resistance. The effect of cross-clamping on venous return is a composite of complimentary and opposing factors- diminished venous return due to exclusion of blood flow to the pelvis and lower extremities; a possible redistribution of blood flow from the inferior vena cava to the superior vena cava; and an increase in left ventricular end systolic and end-diastolic volumes.
CUNNINGHAM, A.J; " Anaesthesia for abdominal aortic surgery- a review (Part 1) ", Can J Anaesth, vol 36, no 4, 1989, pp 426-44.
Pulmonary Surfactant:(183)
1. Is produced by type II alveolar cells.
2. Is turned over so rapidly that a reduction in pulmonary blood flow can cause a decrease in surfactant production.
3. Synthesis is stimulated by thyroxine and glucocorticoids.
4. Is partly recycled by endocytosis into the synthesising cell.
Ans:1,2,3,4
The role of surfactant in the aetiology of respiratory distress syndrome has been recently reviewed.
ARDS includes a complex series of events leading to alveolar damage, high permeability pulmonary edema, and respiratory failure. The endogenous pulmonary surfactant system is crucial to maintaining normal lung function, and only recently has it been appreciated that alterations in the surfactant system significantly contributed to the pathophysiology of the lung injury of patients with ARDS. Through a combination of analyzing broncho-alveolar lavage samples from patients with ARDS and extensive animal studies, there have been significant insights into the variety of surfactant abnormalities that can occur in injured lungs. These include altered surfactant composition and pool sizes, abnormal surfactant metabolism, and inactivation of alveolar surfactant by serum proteins present within the airspace. Positive effects of exogenous surfactant administration on acute lung injury have been reported. There is now a prospective, randomized clinical trial evaluating the efficacy of aerosolized exogenous surfactant in patients with ARDS. This trial has demonstrated improvements in gas exchange and a trend toward decreased mortality in response to the surfactant. Despite these encouraging results, there are multiple factors requiring further investigation in the development of optimal surfactant treatment strategies for patients with ARDS. Such factors include the development of optimal surfactant delivery techniques, determining the ideal time for surfactant administration during the course of injury, and the development of optimal exogenous surfactant preparations that will be used to treat these patients. With further clinical trials and continued research efforts, exogenous surfactant administration should play a useful role in the future therapeutic approach to patients with ARDS.
NUNN, J.F; Applied Respiratory Physiology, 3rd edition , Butterworths, 1987.
LEWIS. J.F; Am Rev Respir Dis, vol 147, no 1, Jan. 1993, pp 218-33.
The carotid body chemoreceptors are:(272)
1. Stimulated by a decrease in pO2 of arterial blood
2. Stimulated in an hypotensive subject at rest
3. Subject to a blood flow of over 50ml/100g per minute
4. Inhibited by a decrease in pH of arterial blood
Ans:1,3
Effect of arterial oxygen tension on Chemoreceptor Activity.
Changes in arterial oxygen content have no direct stimulatory effect on the respiratory center itself but when the oxygen partial pressure in the arterial blood falls below normal, the chemoreceptors become strongly stimulated. The receptors are particularly sensitive to changes in arterial PO2 in the range between 60 and 30 mm Hg, which is the range in which the arterial haemoglobin saturation vith oxygen decreases rapidly.
Effect of Carbon Dioxide and Hydrogen Ion Concentration on Chemoreceptor Activity.
An increase in either carbon dioxide concentration or hydrogen ion concentration also excites the chemoreceptors and in this way indirectly increases respiratory activity. However, the direct effects of both these factors in the respiratory center itself are so much more powerful than their effects mediated through the chemoreceptors that for most practical purposes the indirect effects through the chemoreceptors do not need to be considered. In the case of oxygen, on the other hand, this is not true because diminished oxygen in the arterial blood can affect the respiration significantly only by acting through the chemoreceptors.
Basic Mechanism of Stimulation of the Chemoreceptors by Oxygen Deficiency.
The blood flow through the carotid and aortic bodies is extremely high, as high as that for almost any tissue in the body. Because of this, the A-V oxygen difference is less than 1 volume per cent, which means that the venous blood leaving the carotid bodies still has a PO2 nearly equal to that of the arterial blood. It also means that the PO2 of the tissues in the carotid and aortic bodies remains at all times almost equal to that of the arterial blood. Therefore, it is the arterial PO2, not the venous PO2, that normally determines the degree of stimulation of the chemoreceptors. Occasionally, though, serious hypotension can sufficiently decrease the blood flow through the carotid and aortic bodies to stimulate the chemoreceptors even when the arterial PO2 is normal. The exact means by which low PO2 excites the nerve endings in the carotid and aortic bodies is still unknown. However, these bodies have two different, highly characteristic glandular-like cells in them. Therefore, some investigators have suggested that these cells might function as chemoreceptors and then in turn stimulate the nerve endings. However, other studies suggest that the nerve endings themselves are directly sensitive to the low PO2
Acidosis may result in:(284)
1. Potassium retention
2. A rise in plasma chloride
3. A low pCO2
4. Tetany
Ans:1,2,3
Alkalosis enhances and acidosis depresses renal potassium secretion, probably by inducing corresponding changes in tubular cell potassium.
Chloride is required for bicarbonate secretion in the collecting duct via a bicarbonate-chloride exchanger.
In acute metabolic acidosis, hyperventilation is usual and may be intense (Kussmaul respiration).
Alkalosis directly enhances neuromuscular excitability; this effect, rather than the modest decrease in ionized plasma calcium induced by alkalosis, is probably the major cause of tetany.
Concerning the membrane potential of cardiac muscle:(324)
1. Phase 2 is associated with efflux of calcium ions
2. Phase 3 is produced by an efflux of potassium ions
3. Slowing of phase 3 decreases the QT interval
4. Verapamil blocks slow calcium currents
Ans:2,4
Phase 2 is the plateau phase of the action potential. The slow calcium channel is open during this time. During phase 3 membrane repolarisation occurs as a result of the continued flow of potassium out of the cell.
The gas transfer (DLCO) depends on:(325)
1. The volume of the pulmonary capillary bed.
2. Ventilation perfusion matching
3. Haemoglobin concentration
4. Residual volume
Ans:1,2,3
The ability of gas to diffuse across the alveolar-capillary membrane is ordinarily assessed by the diffusing capacity of the lung for carbon monoxide (DLCO). In this test, a small concentration of carbon monoxide (0.3%) is inhaled, usually in a single breath that is held for approximately 10 s. The carbon monoxide is diluted by the gas already present in the alveoli and is also taken up by haemoglobin as the erythrocytes course through the pulmonary capillary system. The concentration of carbon monoxide in exhaled gas is measured, and DLCO is calculated as the quantity of carbon monoxide absorbed per minute per mmHg pressure gradient from the alveoli to the pulmonary capillaries.
The value obtained for DLCO depends on the alveolar-capillary surface area available for gas exchange and on the pulmonary capillary blood volume. In addition, the thickness of the alveolar-capillary membrane, the degree of ventilation-perfusion ratio mismatching, and the patient's haemoglobin level will affect the measurement. Because of this effect of haemoglobin levels on DLCO, the measured DLCO is frequently corrected to take the patient's haemoglobin level into account. The value for DLCO can then be compared with a predicted value, based either on age, height, and gender or on the alveolar volume (VA) at which the value was obtained. Alternatively, the DLCO can be divided by VA and the resulting value for DLCO/VA compared with a predicted value.