Memory Master Flashcards

Question

"What is the normal range of values for pulmonary artery occlusion pressure (PAOP), also called pulmonary capillary wedge pressure (PCWP)?"

Answer 1

"Normal PAOP:::: 5-15 mmHg. When stated as wedge pressure, PCWP""""' 2-12 mmHg. [Miller & Stoelting, Basics. 5e. 2007 pp53, 310: Morgan, et a!., Clin. Anesth. 4e. 2006 pp136f; Dunn, eta!., Mass. Gen. 7c. 2007 pp402t)"

Answer 2

"Normal mean arterial pressure ranges from 80-120 mmHg. [Barash, Handbook. 5e. 2006 pp510, 972["

Answer 3

Normal mean arterial pressure ranges from 80-120 mmHg. [Barash, Handbook. 5e. 2006 pp510, 972[

Answer 4

Use the l, 2, 3 rule. MAP~ (1 x SBP + 2 x DBP)/3. Alternatively, MAP can be calculated as follows: MAP~ DBP + (113) (pulse pressure)~ DBP + (l/3) (SBP-DBP). Either equation gives the correct answer. Note: SBP ~ systolic blood pressure; DBP ~diastolic blood pressure. [Morgan, eta!., Clin. Anesth. 4e. 2006 pp429; Barash, Handbook. Se. 2006 pp972]

Answer 5

Using tl1e 1, 2, 3 rule, MAP~ [ 1 x 150 + (2 x 90)]/3 = [150 + 180]/3 = 330/3:::::: II0mmHg.Theansweristhesameifthealternateequationis used: MAP= 90+(1/3) 60 = 90 + 20 ~ 110 mmHg. [Authors]

Answer 6

Altered preload (altered venous return) is most responsible for a change in blood pressure when the patient is re-positioned. [Barash, Clinical Anesthesia, 1997, pp595-597]

Answer 7

The two determinants ofsystemic arterial blood pressure are systemic vascular resistance (SVR) and cardiac output (CO). This is an application of Ohm's law. [Barash, Clinical Anes. 5e. 2006 pp856, 878; Stoelting, PPAP. 4e. 2006 pp725]

Answer 8

Systemic vascular resistance (SVR) is determined by the tone (degree of constriction} of arterioles and small arteries. [Guyton, TMP. lle. 2006 ppl68; Morgan, eta!., Clin. Anesth. 4e. 2006 pp424]

Answer 9

The normal range for SVR is 1200-1500 dynes•sec•cm-s. [Barash, Hand- book. 5e. 2006 pp510, 972; Miller, Anesthesia. 6e. 2005 ppl328t]

Answer 10

SVR ~ [(MAP-CVP)/CO] x 80, where MAP is mean arterial pressure, CVP is centra! venous pressure, and CO is cardiac output. The units for SVRaredynes-sec-cm-5. [Barash,Handbook.5e.2006pp510,972;Miller, Anesthesia. 6e. 2005 ppl328t]

Answer 11

SVR ~ [(MAP-CVP)/CO] x 80 ~ [(80-8)/9] x 80 = 640 dynes•sec-cm 5• [Authors]

Answer 12

The resistance to blood flow is greatest in the arterioles, accounting for about half the resistance in the entire systemic circulation. The greatest decrease in blood pressure in the arterial tree occurs in the arterioles. [Stoelting, PPAP. 4e. 2006 pp719-720; Guyton, IMP. lie. 2006 ppl62- 163]

Answer 13

Elastic recoil of arterial blood vessels during diastole keeps systemic arte- rial blood pressure from fa!ling precipitously during diastole. [Guyton, TMP. lie. 2006 ppl09]

Answer 14

Pulse pressure is the difference between the systolic and diastolic arterial pressures during the cardiac cycle. The patient with a blood pressure of 160/90 has a pulse pressure of 160-90 = 70 mmHg. [Guyton, TMP. lle. 2006 ppl73]

Answer 15

The two determinants of pulse pressure are stroke volume and arterial compliance. Pulse pressure is determined by the ratio of stroke volume to arterial compliance. Pulse pressure increases when either cardiac output increases or arterial compliance decreases. Pulse pressure decreases when either cardiac output decreases or arterial compliance increases. [Guyton, TMP. lle. 2006 ppl73-l74]

Answer 16

Compliance is defined as a change in volume for a given change in pres- sure. When compliance of arterial vessels decreases, pulse pressure in- creases. [Guyton, TMP. lle. 2006 ppl72-173]

Answer 17

Baroreceptors are located in the aortic arch and carotid sinus. The aortic and carotid baroreceptors respond to stretching caused by mean arterial pressure greater than 90 mmHg. [Guyton, 1MP. lie. 2006 pp209; Stoelt- ing, PPAP. 4e_ 2006 pp726]

Answer 18

When stretched, the baroreceptors fire and reflexly inhibit the sympathet~ ic nervous system outflow resulting in a decrease in myocardial contrac- tility, a decrease in heart rate, a decrease in venous tone, a decrease in SVR, and a decrease in blood pressure. Parasympathetic outflow is simul- taneously increased, which also decreases heart rate. [Barash, Clinical Anes. Se. 2006 pp877; Guyton, TMP. !!e. 2006 pp209-2!0]

Answer 19

Venous baroreceptors are located in the right atrium and great veins. They produce an increase in heart rate when the right atrium or great veins are stretched by increased vascular volume. This reflex is called the Bainbridge reflex. [Barash, Handbook. Se. 2006 pp!SO]

Answer 20

Heart rate increases with inspiration and decreases with expiration. Dur- ing inspiration, the pressure within the thorax decreases (becomes more negative) and venous return increases. The increased venous return stretches the right atrium leading to a reflex increase in heart rate. The opposite occurs during expiration. This is the Bainbridge reflex. [Guyton, TA1P. !!e. 2006 pp2!2; Stoelting, PPAP. 4e. 2006 pp728]

Answer 21

When the great veins and right atrium are stretched by increased vascular volume, stretch receptors send afferent signals to the medulla via the vagus nerve. The medulla then transmits efferent signals via the sympa- thetic nerves to increase heart rate (by as much as 75%) and myocardial contractility. The Bainbridge reflex helps prevent clamming up ofblood in veins, the atria, and the pulmonary circulation. [Guyton, TMP. llc. 2006 pp2!2l

Answer 22

Arterial blood pressure normally decreases several mmHg during inspira- tion. With inspiration, pulmonary venous capacitance increases and venous return to the left heart decreases. According to Starling's law, with a decrease in venous return (preload) to the left ventricle, stroke volume, cardiac output, and arterial blood pressure all decrease (even though heart rate may increase because of the Bainbridge reflex). [Barash, Cliui~ cal Anes. Se. 2006 pp878]

Answer 23

Pulse pressure undergoes a natural amplification during transit through the arterial tree. Compared with the aortic pressure waveform, systolic pressure is greater and diastolic pressure is lower in the dorsalis pedis. Pulse pressure is, therefore, greater in the dorsalis pedis than in the aorta. [Miller, Anesthesia. 6e. 2005 ppl282-l283; Barash, Clinical Anes. Se. 2006 pp878]

Answer 24

Angiotensin I is converted to angiotensin II in the pulmonary vasculature of the lung. [Guyton, TMP. lie. 2006 pp224; Barash, ClinicalAnes. 5e. 2006 pp88l, ll37]

Answer 25

Antidiuretic hormone~also called vasopressin-is even more powerful than angiotensin II as a vasoconstrictor. Barash states that angiotensin II is the more potent vasoconstrictor; realize that textual discrepancies exist. [Barash, Clinical Anes. 5e. 2006 ppll37; Guyton, TMP. lie. 2006 pp202]

Answer 26

The arterial blood vessels contain 13% of the total blood volume, and the capillaries contain 7% of the total blood volume. 64% of the total blood volume is found in the venous side of the systemic circulation. [Guyton, TMP. lie. 2006 ppl62]

Answer 27

Capillaries allow exchange of oxygen, fluid, nutrients, electrolytes, hor- mones, and other substances between the blood and the interstitial space. [Guyton, TMP. lie. 2006 ppl6l]

Answer 28

Oxygen and nutrients are delivered from the capillary to the cell by diffu- sion. Diffusion supplies all oxygen required for metabolism. Pick's law of diffusiou applies. [Authors, MM. !9. 2010 ppO; Guyton, TMP. lie. 2006 ppl83-l84]

Answer 29

Peripheral edema may result from one or more of the following: (1) de- creased plasma colloid osmotic pressure (hypoalbuminemia, liver dis- ease), (2) increased capillary hydrostatic pressure (usually secondary to increased central venous pressure, sometimes secondary to heart failure), (3) increased interstitial protein (lymphatic obstruction), and (4) in- creased permeability in the capillary wall. [Guyton, TMP. lie. 2006 pp302-304]

Answer 30

The colloid osmotic pressure of albumin is 22 nunHg. Albumin is respon- sible for approximately 80% of the total colloid osmotic pressure in the plasma. [Guyton, TMP. lie. 2006 ppl88]

Answer 31

Approximately 75% of resting cardiac output is delivered to the vessel- rich organs, although they constitute only 10% of total body mass. [Stoelt- ing, PPAP. 4e. 2006 ppS-6]

Answer 32

The two determinants of blood flow are pressure gradient (pressure dif- ference, liP) and resistance (R). Blood flow= (P,-P,)/R. Blood flow to any tissue is directly proportional to the hydrostatic pressure gradient (P1-P2) and inversely proportional to vascular resistance (R). (P1-P2) is usually (PaneriaJ-Pvcnou1) . This is an application of Ohm's law. [Guyton, TMP. 1le. 2006 pp164]

Answer 33

Blood flow to a tissue or organ is generally directly related to tissue me- tabolism. Metabolites (local factors) dilate the vasculature, and blood flow to the tissue increases. [Guyton, TMP. 11e. 2006 pp196]

Answer 34

Cardiac output and arterial blood Oz content. Arterial blood oxygen con- tent is determined by the blood hemoglobin concentration and percent saturation. [Guyton, TMP, 1996, p516]

Answer 35

Hypercapnia causes dilatation of both the cerebral vasculature and the systemic vasculature. An increase in COz concentration in the arterial blood perfusing the brain decreases cerebral vascular resistance and increases cerebral blood flow. Hypercapnia also relaxes systemic vascular smooth muscle causing decreased systemic vascular resistance (SVR). [Guyton, TMP, 1996, pp 200-201, 783; Miller, Anesthesia, 1994, pp 129- 130]

Answer 36

Pulmonary vascular resistance increases in response to hypercarbia. The pulmonary vasoconstrictor response to hypercarbia is opposite that ob- served in the systemic and cerebral vasculature. [Miller, Anesthesia, 1994, pp128-130J

Answer 37

Both hypertension and hypotension may occur with hypercapnia. Hyper- capnia appears to cause direct depression of both cardiac muscle and vascular smooth muscle, but at the same time it causes reflex stimulation of the sympathoadrenal system. Thus, hypercapnia, like hypoxemia, may cause increased myocardial 0 2 demand (tachycardia, early hypertension) and decreased myocardial 02 supply (tachycardia, late hypotension). [Miller, Anesthesia, 5th ed. 2000, p613]

Answer 38

Acidosis increases pulmonary vascular resistance (PVR) and decreases systemic vascular resistance (SVR). [Longnecker eta!., PPA, 1998, p961; Barash, Clinical Anesthesia, 2001, p878]

Answer 39

Coronary flow is greatest during diastole. During diastole, ventricular muscle relaxes completely, and blood flow through the ventricular capil- laries is not obstructed. [Guyton, TMP. lle. 2006 pp250]

Answer 40

During early systole, the compression of the vasculature in the left ventri- cle causes a brief cessation of flow in the left ventricle. On the other hand, flow through the right ventricle is sustained during both systole and diasto- le. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p33l-332]

Answer 41

Coronary blood flow is 225-250 mL/minute, or about 4-5% of cardiac output. [Stoelting, PPAP. 4e. 2006 pp753; Guyton, TMP. lOe. 2000 pp226]

Answer 42

The venous saturation of coronary blood is 30% (P02 :;;:; 18-20 mmHg). Therefore, the oxygen extraction level of coronary blood is 7096 ( l 00% - 30%, assuming 100% saturation for coronary arterial blood). [Barash, Clinical Anesthesia, 4e, 2001, pp865-866; Stoelting, PPAP. 4e, 2006, p752 [Stoelting, PPAP. 4e. 2006 pp752; Barash, Clinical Anes. 4e. 2001 pp865- 866]

Answer 43

Coronary blood flow is autoregulated when coronary perfusion pressure ranges between 60 nun Hg and 160 mmHg. We assume 60-160 mm Hg is the normal range for coronary perfusion pressure. [Kaplan, Cardiac Anes- thesia, 1999, p95; Authors]

Answer 44

Coronary perfusion pressure (CorPP) is the difference between the aortic diastolic pressure (AoDP) and the left ventricular end-diastolic pressure (LVEDP). CorPP ~ AoDP- LVEDP. Usually, PCWP is used to estimate LVEDP, so CorPP ~ AoDP- PCWP. [Morgan and Mikhail, Clinical Anes- thesiology, 1996, p331]

Answer 45

CorPP ~ AoDP- LVEDP. Since PCWP reflects l.VEDP, AolJP ~ 80-30 ~ 50 mmHg. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p333]

Answer 46

Since coronary perfusion pressure (CorPP) equals aortic diastolic pres- sure (AoDP) minus left ventricular end-diastolic pressure (LVEDP), a decrease in AoDP or an increase in LVEDP will decrease coronary perfu- sion pressure. Note: LVEDP is reOected by pulmonary capillary wedge pressure (PCWP), so CorPP will decrease when PCWP increases. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp331-332; Authors]

Answer 47

Myocardial metabolism is the major determinant of coronary blood flow. Normally, coronary blood fiow and myocardial metabolism are closely matched. [Guyton, TMP. 11e. 2006 pp250]

Answer 48

Usually changes in coronary blood flow are entirely due to changes in metabolism. Local factors are produced when metabolism increases, and these local factors decrease coronary vascular resistance. Hence, coronary dilation in response to increased metabolic demand produces the increase in myocardial flow when work load increases. [Morgan and Mikhail, Clinical A11esthesiology, 1996, p333]

Answer 49

The vasodilation theory of blood flow regulation states that the greater the rate of metabolism or the lower the availability of oxygen, the greater becomes the rate of accumulation of vasodilator substances such as aden- osine, carbon dioxide, lactic acid, histamine, potassium ions, and hydro- gen ions. With vasodilation, blood flow is increased to meet the metabolic demands of the myocardium. [Guyton, TMP .lle. 2006 pp250-251]

Answer 50

The most potent vasodilator substance released by cardiac cells is adeno- sine (Stoelting). In general, the most important regulators of coronary vascular tone are metabolic and involve multiple pathways. Most if not all references list adenosine first in the metabolites that control coronary vascular tone. NB: Miller has the most extensive discussion of this topic. [Stoelting, PPAP, 4th ed. 2006, p754; Barash, Clinical Anesthesia, 4th ed. 2001, p866; Miller, Anesthesia, 5th ed. 2000, p643 [Stoelting, Handbook. 2e. 2006 pp754; Barash, Clinical Anes. 4e. 2001 pp866; Miller, Anesthesia. Se. 2000 pp643]

Answer 51

The oxygen consumption rate of the heart ranges from 8-10 mL 0,/1 DOg/minute. (NB: Miller gives a larger range: 6-10 mL 0 2/100 g/minute.) [Barash, Clinical Anesthesia, 4th ed. 2001, p873; Stoelting, PPAP, 4th ed. 2006, p753; Miller, Anesthesia, 5th ed. 2000, p642 [Stoelt- ing, PPAP. 4e. 2006 pp753; Barash, Cli11ical Anes. 4e. 2001 pp873; Miller, Anesthesia. Se. 2000 pp642]

Answer 52

Myocardial oxygen demand is determined by (1) heart rate, (2) diastolic wall tension (preload), (3) systolic wall tension (afterload), and (4) con- tractility (determined by chemical environment). An increase in each of these parameters will increase myocardial oxygen consumption. Con- versely, a decrease in each of these parameters will decrease myocardial oxygen consumption. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp333-334]

Answer 53

Heart rate> afterload >preload. Increases in heart rate are likely to in- crease oxygen consumption more than increases in blood pressure (after- load). Increasing venous return (increasing preload) increases oxygen consumption less than either increases in heart rate or afterload. Inct·eas- ing preload is the least costly means of increasing cardiac output. Stoelt- ing, PPAP, 2006, p754 [Stoelting, PPAP. 4e. 2006 pp754]

Answer 54

Heart rate. [Stoelting, PPAP. 4e. 2006 pp754]

Answer 55

Myocardial oxygen supply is determined by (1) aortic diastolic pressure (perfusion pressure), (2) left ventricular end-diastolic pressure (high LVEDPs compress the subendocardium and decrease flow), (3) heart rate (high heart rates may decrease perfusion because the time in diastole, the time when coronary flow occurs, is decreased), (4) oxygen content of arterial blood(% saturation), and (5) oxygen extraction. [Davison, Eck- hardt, and Perese, Mass General, 1993, ppl4-15]

Answer 56

Alpha-l and beta-2 receptors are found throughout the coronary vascula- ture. Epicardial blood vessels have mostly alpha receptors, which promote vasoconstriction. Intramuscular and subendocardial blood vessels have mostly beta-2 receptors, which promote vasodilation. [Guyton, l'MP. lie. 2006 pp25l]

Answer 57

The subendocardium (the muscle just inside the endocardial lining of the left ventricle) has the densest network of capillaries. This capillary net- work is referred to as the subendocardial plexus. During diastole, blood Oow in the subendocardium is considerably greater than blood Oow to the mid-wall or subepicardial regions. This higher blood Oow reflects the greater oxygen requirements of the subendocardium. During systole, the subendocardium of the left ventricle is compressed and subendocardial blood flow is zero. [Guyton, TMP. lle. 2006 pp250]

Answer 58

The subendocardium is most vulnerable to ischemia because it has the greatest metabolic demands and is most compressed (no blood flow) during systole. [Stoelting, PPAP. 4e. 2006 pp753; Guyton, TMP. lle. 2006 pp250]

Answer 59

Myocardial preconditioning is a short-term rapid adaptation to brief ischemia such that during a subsequent, more severe ischemic insult, myocardial necrosis is delayed. The infarct -delaying properties of ischem- ic preconditioning have been observed in all species studied. Five minutes of ischemia is sufficient to initiate preconditioning, and the protective period lasts for 1 to 2 hours. [Stoelting, PPAP. 4e. 2006 pp !71; Cote, PAlC. 4th. 2009 pp343]

Answer 60

Pharmacological activation ofadenosine receptors (particularly al and a2 subtypes) initiates preconditioning via intracellular signal transduction mechanisms involving protein kinase C and adenosine triphosphate (ATP)-dependent potassium channels (KATP). Other factors involved include including the sodium: hydrogen exchanger, inhibitory G proteins, and tyrosine kinase. [Stoelting, PPAP. 4e. 2006 ppl7!; Cote, PAIC. 4th. 2009 pp343; Barash, C/in. Anes. 6th. 2009 pp430]

Answer 61

The volatile anesthetics mimic ischemic preconditioning and trigger a similar cascade of intracellular events resulting in myocardial protection that lasts beyond the elimination of the anesthetic. Adenosine or opioid agonists delivered into the coronary circulation may also mimic precondi- tioning. Ketamine antagonizes the protective effect of preconditioning and thus should be used with caution in the patient at risk for myocardial infarction in the perioperative period. [Stoelting, PPAP. 4e. 2006 ppl71; Cote, PAIC. 4th. 2009 pp343; Barash, Clin. Anes. 6th. 2009 pp430]

Answer 62

Excitability is the ability of a cell (cardiac, nerve, or muscle cell) tore~ spond to a stimulus by depolarizing and firing an action potential. [Guy~ ton, TMP, 1996, pp68-70]

Answer 63

Depolarization occurs when there is a decrease in polarity across the cell membrane (a reduction in both the number of positive charges on the outside surface of the membrane and the number of negative charges on the inside surface of the membrane). [Guyton, TMP. lle. 2006 pp61-65]

Answer 64

Hyperpolarization occurs when there is an increase in the polarity across the cell membrane (an increase in both the number of positive charges on the outside surface of the membrane and the number of negative charges on the inside surface of the membrane). [Guyton, IMP, 1996, pp67-68]

Answer 65

Conductivity is the ability to transmit action potentials from cell to adja- cent cell. [Bullock and Rosenthal, Pathophysiology, 1992, pp436-439]

Answer 66

Depolarization occurs if the membrane potential decreases from -70 mV to -60 mV. [Guyton, TMP, 1996, pp63-65]

Answer 67

Hyperpolarization occurs if the membrane potential increases from -70 mV to -80 mV. [Guyton, TMP, 1996, pp67-68]

Answer 68

Rhythmicity is the ability of cells to generate action potentials automati- cally on a rhythmic, or regular, basis. [Guyton, TMP. 11e. 2006 pp116- 117]

Answer 69

The impulse must traverse the atrioventricular (AV) node to pass from the atria to the ventricles. Normally, the pause at the AV node is 100 milliseconds. [Guyton, TMP. 11e. 2006 pp 118-1!9]

Answer 70

Conduction is slowest through the atrioventricular node and fastest in the Purkinje fibers. Purkinje fibers are larger-diameter fibers that transmit impulses at a velocity 6 times that of cardiac muscle and 150 times faster than nodal tissues. [Guyton, TMP. !Oe. 2000 pp 1!0-111]

Answer 71

The Purkinje system synchronizes right and left ventricular contractions. This occurs because the Purkinje fibers allow very rapid transmission of the cardiac impulses from the atrioventricular node (AV node) to the ventricles. [Guyton and Hall, TMP, 2000, pill)

Answer 72

Phase 4 depolarization is fastest in the SA node, somewhat slower in the AV node and slowest in the terminal Purkinje fibers. Because phase 4 depolarization is fastest in the sinoatrial node, the sinoatrial node is the dominant pacemaker of the heart. [Guyton, TMP. I ! e. 2006 pp!IS-!21)

Answer 73

Intrinsic firing rates are: SA node, 60-100 per min; AV node, 40-60 per min; Purkinjesystem, 15-40 perr11in. [Guyton, TMP. lie. 2006 ppl20- l2l I

Answer 74

The heart is not equally innervated by the sympathetic and parasympa- thetic divisions of the autonomic nervous system. In general, the sympa- thetic system innervates both the atria and ventricles and the conduction system (SA & AVnodes), whereas parasympathetic innervation is mainly to the SA & A V nodes and atria, with minor input to the ventricles. Stoelt- ing, PPAP, 4th ed. 2006, p752, 752f; Miller, Anesthesia, 5th ed. 2000, p533 [Stoelting, PPAP. 4e. 2006 pp752; Miller, Anesthesia. Se. 2000 pp533j

Answer 75

The parasympathetic innervation of the heart arises from the dorsal motor nucleus of the vagus nerve in the medulla of the brain. (Remember: the parasympathetic division is also known as the craniosacral division). [Boron and Boulpaep, Med. Physiol., 2003, p38l; Authors)

Answer 76

The P wave occurs when the atria depolarize. The T wave occurs when the ventricles repolarize. [Guyton, TMP. lie. 2006 pp !24-!25)

Answer 77

The action potential is passing through the atrioventricular (AV) node. [Guyton, TMP. lie. 2006 ppl25)

Answer 78

The ventricular action potential is in phase 2, the plateau phase. The duration of the QT segment is determined by the duration of the plateau. Ventricular contraction is occurring during this time. [Guyton, TMP. lle. 2006 ppl25-l26; Barash, Clin. Anes. 6th. 2009 pp2!7j

Answer 79

Potassium ions control the resting potential, and calcium ions control threshold. [Guyton, 1MP. lie. 2006 pp59-65j

Answer 80

Hypokalemia decreases excitability (increases stability). The resting membrane becomes more polarized (hyperpolarized). The difference between the resting and threshold potentials increases thereby making the tissue Jess excitable. [Stoelting, PPAP. 4e. 2006 pp654; Barash, Hand- book. Se. 2006 pp92; Guyton, 1MP. !Ie. 2006 pp69-70j

Answer 81

Hyperkalemia increases excitability (decreases stability). The resting membrane becomes less polarized (depolarized). The difference between the resting potential and threshold potential decreases, thereby making the tissue more excitable. [Leaf and Cotran, Renal Pathophysiology, 1980; Guyton, TMP, !996, pp67-68; Barash, Clinical Anesthesia, !997, pp814- 815]

Answer 82

Hypocalcemia increases membrane excitability (decreases stability). The threshold potential increases (becomes more negative). Thus, the resting and threshold potentials approach each other, and nerves and cardiac cells become more excitable. Recognize that the excitability of nerve and muscle is increased when hypocalcemia is present. [Guyton, TMP. lle. 2006 pp64-65; 371; 979-980]

Answer 83

ypercalcemia decreases excitability (increases stability). The threshold potential decreases (becomes less negative). Thus, the resting and thresh- old potentials diverge from each other, and nerves and cardiac cells be- come less excitable. [Guyton, TMP. lle. 2006 pp37!, 980]

Answer 84

An increase in concentration of magnesium (Mgl+-) decreases excitability (increases stability) of cardiac cells. Calcium ions and magnesium ions are membrane potential stabilizers. [Barash, Clinical Anesthesia, 1997, pp179, 183; Authors]

Answer 85

Bradycardia, punctuated by episodes of supraventricular tachycardia, most often observed in the elderly patient, characterize sick sinus syn- drome. [Stoelting Handbook, Co-Existi11g, !993, p69]

Answer 86

The refractory period of an accessory pathway determines the ventricular rate, which may exceed 300 beats per minute in the patient in atrial fibril- lation with Wolff-Parkinson-While syndrome. Syncope or congestive heart failure, or both, could result from the rapid ventricular rate [Hines, Stoelting's Co-existing. 5e. 2008 pp72]

Answer 87

If rapid ventricular response during atrial fibrillation results in life- threatening hypotension, electrical cardioversion is necessary. If the atrial fibrillation is tolerated, give IV procainamide, which prolongs the refrac- tory period of accessory fibers. Avoid verapamil or digitalis because either may accelerate conduction through the accessory pathway. [Hines, Stoelt- ing's Co-existing. Se. 2008 pp72]

Answer 88

first degree heart block and Mobitz type I second degree heart block ordinarily do not require treatment. Mobitz type II second degree heart block has a serious prognosis and may require pacemaker insertion prior to major surgical procedures. IMiller, Anesthesia, !994, ppl244-!248]

Answer 89

With severe pulmonary hypertension, right ventricular output will de- crease; right atrial pressure and CVP will increase; hence, CVP will he greater than PCWP. [West, Respiratory Pathophysiology, 1990, pl26]

Answer 90

Concentric hypertrophy develops in response to a chronically elevated afterload (referred to as a pressure overload). Two conditions that cause concentric left ventricular hypertrophy are (1) systemic arterial hyperten- sion, and (2) aortic valve stenosis. Two conditions that cause concentric right ventricular hypertrophy are (l) pulmonary artery hypertension and (2) pulmonic valve stenosis. [Stoelting, Co-Existing, 1993, p88; Authors]

Answer 91

The ventricular wall and septum thicken, which permits the ventricle to develop more tension and eject blood more effectively against an in- creased afterload. The chamber size remains unchanged with a chronical- ly elevated aflerload. This is concentric hypertrophy. [Morgan and Mi- khail, Clinical Anesthesiology, 1996, pp325-327; Barash, Clinical Anesthesia, 1997, p841]

Answer 92

Yes. According to the version of the law of Laplace that assumes a struc- ture with a finite wall thickness (T:::: Pr/2h), the tension (T) in the wall decreases with wall thickness (h). You can see from the equation that as thickness (h) increases, tension (T) decreases (an inverse, or reciprocal, relationship). The thickening of the ventricular wall associated with con- centric hypertrophy produces a substantial decrease in wall tension, at rest. Concentric hypertrophy may be one of the best ways to decrease wall tension. Note: r = radius of ventricular chamber. [Kaplan, Cardiac Anes· thesia, 1999,p222;Morgan,eta!.,ClinicalAnesthesiology,3'"ed.2002, pp369-370]

Answer 93

In mitral stenosis, the left ventricle is subjected to neither a pressure nor a volume overload. The increase in left atrial pressure, however, is reflected back through the pulmonary circulation leading to right ventricular pres- sure overload and right ventricular concentric hypertrophy. [Barash, Clini- cal Anesthesia, 1997, p845]

Answer 94

Volume overload (chronically increased preload) stimulates the ventricu- lar free wall to dilate. The chamber enlarges and can accommodate a larger volume of blood. Three factors that promote left ventricular eccen- tric hypertrophy are (l) excessive intravascular volume, (2) aortic regurgi- tation, and (3) mitral regurgitation. [Stoelting, Co-Existing, 1993, p88; Authors]

Answer 95

Diastolic function of the !eft ventricle is assessed by examining left ven- tricular compliance. The best indicator of diastolic dysfunction is a de- crease in left ventricular compliance. [Morgan and Mikhail, Clinical Anes- thesiology, 1996, p91; Authors]

Answer 96

The use of invasive monitoring such as central venous pressure (CVP) or pulmo- nary artery catheter (PAC) may be indicated in managing the patient with a history of congestive heart failure secondary to diastolic dysfunction. [Miller & Stoelting, Basics. Se. 2007 pp526]

Answer 97

Aortic stenosis. With aortic stenosis, there is a midsystolic ejection mur- mur that peaks in late systole. "There is often a faint diastolic murmur of minimal aortic regurgitation." [Hurst's The Heart, 200!, p1671]

Answer 98

Aortic regurgitation. The very low diastolic pressure and wide pulse pres- sure suggest aortic regurgitation as the primary problem. With severe and prolonged aortic regurgitation, the dilation of the ventricle (eccentric hypertrophy) may be associated with a secondary mitral regurgitation. Hence, there is a diastolic murmur (aortic regurgitation) and a systolic murmur (mitral regurgitation). [Hines, Stoelting's Co-existing. 5e. 2008 pp38-39]

Answer 99

Maintenance of cardiac output is desired. Phenylephrine, with its pre- dominant alpha actions, will serve to increase blood pressure and SVR while decreasing heart rate (reflexively) to allow better flow through the stenotic opening. Dopamine may be used for inotropic support. [Stoelt- ing, Co-Existing, 1993, p25]

Answer 100

(1) Heart rate, (2) rhythm, (3) preload, (4) afterload (determined by SVR), and (5) contractility. [Kirby and Gravenstein, Clinical Anesthesia Practice, !994, pp117l-1173]

Answer 101

(1) Keep heart rate low (50-70 beats per minute) to reduce myocardial oxygen consumption and prevent myocardial ischemia, (2) maintain or increase preload, (3) maintain or increase afterload (SVR), (4) maintain sinus rhythm (very important), (5) maintain contractility. Slow,full, tight, regular and not too strong. lKirby and Gravenstein, Clinical Anesthesia Practice, 1994, pl171]

Answer 102

Afterload is kept relatively fixed to maintain coronary perfusion pressure. Maintaining corona1y perfusion pressure prevents a cycle of hypotension- induced ischemia, ventricular dysfunction, and worsening hypotension. [Barash, Clinical Anesthesia, 1997, p842]

Answer 103

(I) Keep heart rate slow to allow lime for blood to ilow through the mitral valve into the left ventricle during diastole, (2) maintain sinus rhythm (very important), (3) maintain preload, (4) maintain aflerload (SVR), and (5) maintain contractility. Slow, regular, not too full, rwt too tight, not too strong. [Kirby and Gravenstein, Clinical Anesthesia Practice, 1994, ppll?l-!172]

Answer 104

Remember: slow (low heart rate), regular (maintain sinus rhythm), not too full (maintained preload), not too tight (maintained afterload (SVR), and not too strong (maintained contractility) . [Kirby and Gravenstein, Clinical Anesthesia Practice, 1994, pll71; authors)

Answer 105

Yes. Important for both groups of patients is a low heart rate (slow) and maintenance ofsinus rhythm (regular). [Kirby and Gravenstein, Clinical Anesthesia Practice, 1994, pp1!71-1172]

Answer 106

(1) Increase heart rate, (2) decrease afterload (decrease SVR- very im- portant), (3) maintain sinus rhythm, (4) increase preload, and (5) main- tain contractility. Fast,full,forward, regular, not too strong. [Kirby and Gravenstein, Clinical Anesthesia Practice, 1994, p1172]

Answer 107

(1) Maintain or increase heart rate (avoid bradycardia), (2) maintain sinus rhythm, (3) decrease afterload (decrease SVR) to increase forward ilow, (4) maintain or slightly increase preload, and (5) maintain or slight- ly increase contractility. [Kirby and Gravenstein, Clinical Anesthesia Practice, 1994, pll72]

Answer 108

Both strategies are appropriate for managing tlw patient with mitral stenosis, but decreasing afterload (SVR) is the most important of the two. [Authors]

Answer 109

Yes. Keep heart rate high and decrease SVR while maintaining or increas- ing preload are the important goals for each group of patients. [Kirby and Gravenstein, Clinical Anesthesia Practice, 1994, pl172; Authors]

Answer 110

The principle is to avoid agents that alter cardiovascular status. Agents that increase heart rate (pancuronium and gallamine) are inappropriate and so are agents that release histamine and decrease systemic vascular resistance (d-tubocurarine). Select a nondepolarizing muscle relaxant that lacks significant circulatory affects (cisatracurium, vecuronium). [Stoelt- ing, Co-Existing, 1993, p30; Barash, Clinical Anesthesia, 1997, p845]

Answer 111

The cause of an idiopathic disorder is unknown. II-ISS may be caused by heredity or may occur sporadically. IHSS was formerly known as hyper- trophic obstructive cardiomyopathy. [Morgan and Mikhail, Clinical Anes- thesiology, 1996, p365; Stoelting, Co-Existing, 1993, p99]

Answer 112

Hemodynamic management of the patient with IHSS is directed toward minimizing the systolic pressure gradient between the left ventricle and the aorta. When this gradient (LV systolic pressure minus aortic systolic pressure) is minimized, the outflow tract obstruction is also minimized. The LV-aortic systolic pressure gradient reflects the severity of the out- flow tract obstruction. [Miller, Anesthesia, 1994, p1775J

Answer 113

The outflow obstruction is increased when there is increased contractility, or increased heart rate, or decreased preload or decreased afterload. [Ba- rash Handbook, Clinical Anesthesia, 1997, pp842-843]

Answer 114

Vasoconstrictors (e.g., phenylephrine), beta-adrenergic receptor blockers (e.g., esmoloi, propranolol), and myocardial depressant anesthetics (e.g., enflurane, halothane) are acceptable for use in the patient with IHSS. These agents reduce the outflow tract obstruction which is reflected by a reduction in the LV-aortic systol- ic pressure gradient. [Miller, Anesthesia, 1994, p1775; Stoelting, Anesthesia and Co-Existing Disease, 1993, p99; Morgan and Mikhail, Clinical Anesthesiology, !996, p365; Kaplan, Cardiac Anesthesia, 1999, p749; Barash, Clinical Anesthesia, p843j

Answer 115

( l) Volume is first line treatment for IHSS: full full full; (2) The next pre- scription is administration of an alpha-adrenergic vasoconstrictor such as phenylephrine; (up, up, up). [Barash, Clinical Anesthesia, 1997, p843; Miller, Anesthesia, 1994, p1775; Kirby and Gravenstein, Clinical Anesthe- sia Practice, 1994, p138]

Answer 116

Vasodilators (nitroglycerin, nitroprusside), positive inotropes (digitalis, calcium), beta adrenergic agonists, and diuretics are avoided in the pa- tient with idiopathic hypertrophic subaortic stenosis. These agents can worsen the left ventricular outflow obstruction. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p365; Barash, Clinical Anesthesia, p843]

Answer 117

Explain your answer. Fentanyl. Fentanyl does not provide the beneficial effects (depressed myocardial contractility or increased systemic vascular resistance) offered by the other agents such as halothane, phenylephrine, or propranolol. [Stoelting, Anesthesia and Co-Existing Disease, 1993, p99; Morgan and Mikhail, Clinical Anesthesiology, 1996, p365; Kaplan, Cardiac Anesthesia, 1999, p749; Barash, Clinical Anesthesia, p843; Authors]

Answer 118

Unstable angina, angina that occurs during rest, is the most ominous sign of coronary artery disease. It is ominous if severity and/or frequency of attacks increase. Unstable angina is poorly controlled by medication and carries significant risk of myocardial ischemia. [Davison, Eckhardt, and Perese, Mass General, 1993, p16]

Answer 119

The question is asking for the test that rules in coronary artery disease. Thus, the test with the highest specificity will provide the answer. (Re- member SpPin: if a diagnostic test is highly specific, and the patient is positive by the test, then the disease or condition can be ruled in). The stress (exercise) ECG has a high specificity of90%. [Morgan and Mildlail, Clinical Anesthesiology, 1996, p352; Authors]

Answer 120

On the ECG, ST segment depression of greater than l mm provides evi- dence of myocardial ischemia. [Stoelting and Miller, Basics, 1994, p254J

Answer 121

The primary goal is to maintain cardiovascular stability, which involves avoiding hypotension, hypertension, and tachycardia. [Stoelting, Co- Existing, 1993, p13]

Answer 122

Tachycardia. Tachycardia increases myocardial metabolism and may also decrease coronary blood flow. [Stoelting, Co-Existing, 1993, pl3]

Answer 123

Increase anesthetic depth. If deepening anesthesia is inappropriate or does not correct the problem) give a beta blocker such as esmolol. [Barash, Clinical Anesthesia, 1997, p835-838]

Answer 124

The hypertension appears to be due to an increased systemic vascular resistance (SVR). When SVR increases, blood pressure rises, cardiac output falls, and preload (reflected by PCWP) increases. Increase anes- thetic depth and give nitroglycerin. [Barash Handbook, Clinical Atlesthe- sia, 1997, p448]

Answer 125

The Goldman Cardiac Risk Index for noncardiac surgery identified myo- cardial infarction and 53 gallop as the most significant risk factors. [Barash, Clinical Anesthesia, 1997, p444]

Answer 126

0-3 months: 27-37%; 3-6 months: ll-16%; greater than 6 months: 5-6%. (Two different studies account for the variability in the ranges.) [Stoelting and Miller, Basics, 1994, p250]

Answer 127

Six months. If a prior myocardial infarction occurred more than 6 months before, a reinfarction will occur within 1 week of anesthesia with non- cardiac surgery in about 5-6% of cases. If the myocardial infarction is recent (within six months), there is much greater risk. [Thomas, Manual ofCardiacArzesthesia, p153]

Answer 128

Intrathoracic or intra-abdominal operations lasting longer than 3 hours. [Stoelting and Miller, Basics, 1994, p250]

Answer 129

The probability that a patient will have his or her first myocardial infarc- tion in the perioperative period is less than IO%. [Barash, Clinical Anes- thesia, 1997, p878j

Answer 130

Labile hemodynamics (labile blood pressure). Although perioperative reinfarction is higher within the first six months of a myocardial infarc- tion, normalization of hemodynamics appears to reduce perioperative morbidity. [Miller, Anesthesia, 1994, pp939-940; Morgan and Mikhail, Clinical Anesthesiology, 1996, p351]

Answer 131

Most of the final stages of recovery are achieved within 5 to 12 weeks, though some recovery continues for 6 months. [Guyton, TMP, 1996, pp260-262; Barash Handbook, Clinical Anesthesia, 1997, p23]

Answer 132

f the patient has good ventricular function, volatile agents are generally used. If the patient has poor ventricular function (ejection fraction

Answer 133

Myocardial depression may be seen in a patient with coronary artery disease with N20 use, especially if opioids are also used. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pl!Sj

Answer 134

Systemic venous congestion, peripheral edema, and congestive hepato- megaly are signs of poor RV function. Pulsating neck veins indicate ve- nous congestion secondary to right-sided heart failure. [Hines, Stoelting's Co-existing. 5e. 2008 pp!05j

Answer 135

A decrease in left ventricular compliance is the general cause of left ven- tricular diastolic dysfunction. Reductions in left ventricular compliance can be seen with myocardial ischemia, shock, or pericardia! effusion. [Longnecker eta!., PPA, !998, p1667; Barash, Clinical Anesthesia, !997, p775; Authors]

Answer 136

Left ventricular compliance, the best indicator of diastolic function, can be assessed clinically by Doppler electrocardiography. Doppler electrocar- diography assesses left ventricular compliance. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p329; Longnecker eta!., PPA, 1998, p159]

Answer 137

Decreased cardiac output and increased preload are signs ofleft heart failure. The Swan-Ganz catheter data for the patient in heart failure would show cardiac index 15-18 mmHg. [Yao and Artusio, Yao & Artusio's POPM. Se. 2003 ppl50j

Answer 138

The hallmark of decreased cardiac reserve and low cardiac output is fa- tigue at rest with minimal reserve (Stoelting). Cardiac reserve should be estimated through questioning the patient about their usual physical activities and exertiona[ tolerance. Both perioperalive and long-term cardiac risks are increased in a patient who is unable lo achieve a level of expenditure of about 4 METs (metabolic equivalents). A level of 4 METs corresponds to: taking a flight of stairs without fatigue, walking at a 4

Answer 139

Four major compensatory mechanisms participating in the response to cardiac failure are (1) increased left ventricular preload, (2) increased sympathetic tone, (3) activation ofthe rettiu-angioteusitt-aldosteroue system, (4) release of AVP (arginine vasopressin, antidiuretic hormone), and (5) ventricular hypertrophy. These mechanisms initially compensate for cardiac failure, but with increasing severity of the disease, they may actually contribute to the cardiac impairment. The RAA and sympathetic nervous system contribute to the progressive structural changes in the peripheral vasculature and in the remodeling of the left ventricle. [Mor- gan, eta!., Clin. Anesth. 4e. 2006 pp433-434; Hines, Stoelting's Co- existing. 5e. 2008 pp106-!07j

Answer 140

The hallmark of decreased cardiac reserve and low cardiac output is fa- tigue at rest with minimal reserve (Stoelting). Cardiac reserve should be estimated through questioning the patient about their usual physical activities and exertiona[ tolerance. Both perioperalive and long-term cardiac risks are increased in a patient who is unable lo achieve a level of expenditure of about 4 METs (metabolic equivalents). A level of 4 METs corresponds to: taking a flight of stairs without fatigue, walking at a 4 mph pace, ability to run a short distance, or participation in recreational sports such as bowling, golf, tennis, or dancing. [Stoelting & Dierdorf, Co- Existing, 4th ed. 2002, p109; Miller, Anesthesia, 5th ed. 2000, p1754; Kirby, Clinical Anesthesia Practice, 2"' ed. 2002, p135t]

Answer 141

Cardiac tamponade is accumulation of fluid in the pericardia! space caus- ing increased external intracardiac pressure and decreased ventricular filling (preload). Stroke volume and blood pressure decrease secondary to the decrease in preload. [Miller, Anesthesia, 1994, p1777; Barash Hmul- book, Clinical Anesthesia, 1997, pp769-770]

Answer 142

The principal hemodynamic feature of cardiac tamponade is a decrease in cardiac output due to a reduced stroke volume, secondary to an increased central venous pressure and thus reduced venous return to the heart. The diagnosis of postoperative cardiac tamponade should be considered whenever hemodynamic deterioration is encountered, particularly when reductions in CO or BP or both are not readily resolved by conventional management. Becks triad is the constellation of hypotension, jugular venous distension, and distant, muffled heart sounds. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 4e, 2006, p526; Yao & Artusio, Yao & Artusio's POPM, Se, 2003, p361; Barash, Clinical Anesthesia, Se, 2006, p926]

Answer 143

A decrease in arterial blood pressure (hypotension) with reflex tachycar- dia. [Stoelting and Miller, Basics, 1994, p267]

Answer 144

Normally, systolic blood pressure decreases 6 mmHg or less during inspi- ration. A prominent decrease(> 10 mmHg} in systolic blood pressure usually occurs during inspiration in the patient with cardiac tamponade. This exaggerated decrease in systolic blood pressure during inspiration in the patient with cardiac tamponade is called pulsus paradoxus. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p687; Barash, Clinical Anes- thesia, 1997, p827]

Answer 145

(1) Administer fluids (maintain ventricular fdling); (2) administer a posi- tive inotrope (beta-1 adrenergic receptor agonist) to increase contractility; and (3) correct metabolic acidosis. [Stoelting, Co-Existing, 1993, pp110- 112]

Answer 146

Right and left atrial pressures and right ventricular end-diastolic pressure equalize at about 20 mm Hg. [Stoelting, Co-Existing, 1994, pplOS-109]

Answer 147

Pericardiocentesis is the treatment. [Stoelting, Co-Existing, 1993, pliO; Davison, Eckhardt, and Perese, Mass General, 1993, p266]

Answer 148

If intrapericardial injury is confirmed, general anesthesia can be induced with ketamine (0.5 mglkg) and 100 percent oxygen after decompression of thepericardia!space.[Kaplan,CardiacAnesthesia, 1999,p935]

Answer 149

(1) Large bore intravenous access is mandatory; (2) use anesthetic tech- nique that maintains high sympathetic tone until the tamponade is re- lieved (ketamine is the induction agent ofchoice, and pancuronium is the muscle relaxantofchoice aftersuccinylcholinefor intubation); and (3) generous intravenous fluid administration is useful in maintaining ve- nous return and filling pressures. [Morgan and Mikhail, Clinical Anesthe- siology, 1996, p400]

Answer 150

Fast (increase heart rate),full (increase preload), and forward (decrease afterload, decrease SVR). Fast, full and forward. These three interventions increase forward flow from the heart. [Kirby and Gravenstein, Clinical Anesthesia Practice, 1994, pp1171-1172; AuthorsI

Answer 151

Avoid vasodilation or cardiac depression. [Barash Handbook, Clinical Anesthesia, 1997, pp458-459]

Answer 152

Avoid drugs or manipulations that decrease: (1) venous return; (2) heart rate; (3) arterial blood pressure; or (4) ventricular contractility. [Miller, Anesthesia, !994, pl777]

Answer 153

Hypertension. [Barash Handbook, Clinical Anesthesia, 1997, p447]

Answer 154

20-25% of hypertensive patients become hypertensive upon intubation. The goal for managing induction of the hypertensive patient is to main- lain blood pressure within 20-30% of the patient's usual level. [Barash Handbook, Clinical Anesthesia, 1997, pp296-297]

Answer 155

A small oral dose of a beta-adrenergic antagonist, such as labetalol (Nor- modyne, Trandate), atenolol (Tenormin), or oxprenolol (Trasicor) given preoperatively to the asymptomatic, mildly hypertensive patient may effectively attenuate tachycardia with tracheal intubation or upon emer- gence. [Yao & Artusio, Yao & Artusio's POPM, 5e, 2003, p;350-35l]

Answer 156

The goal during maintenance of anesthesia is to avoid wide fluctuations in blood pressure. A useful technique includes a volatile agent so rapid ad- justments in anesthetic depth can be made in response to changes in blood pressure. [Stoelting, Co-Existing, 1993, p84]

Answer 157

Severe hypertension that occurs during a surgical procedure is most frequently due to inadequate anesthesia. Treat the hypertension by deep- ening the inspired concentration of inhaled agent if it is in use. If deepen- ing the anesthesia is ineffective, add a continuous infusion of phentola- mine (10 mg/250 mL) in normal saline or nitroprusside (1-2 meg/kg/ min). [Yao and Artusio, Problem Oriented Patient Management, 1993, p253]

Answer 158

Takayasu's arteritis is also called pulseless disease because of the absence of palpable peripheral pulses. Chronic inflammation of the aorta and its major branches is the cause of the lack of peripheral pulses. Takayasu 's arteritis primarily affects young Asian females. [Stoelting, Co-Existing, 1993, p123]

Answer 159

Most of the signs and symptoms ofTakayasu's arteritis reflect decreased perfusion of organs secondary to occlusive inflammatory and thrombotic processes. [Stoelting, Co-Existing, 1993, p123-124]

Answer 160

Central nervous system signs and symptoms owing to involvement of the carotid arteries include: (1) vertigo, (2) visual disturbances, (3) syncope, (4) seizures, and (5) cerebral ischemia or infarction. [Stoelting, Co- Existing, 1993, p123-124]

Answer 161

Cardiovascular system signs and symptoms ofTakayasu's arteritis in- clude: ( 1) multiple occlusions of peripheral vessels, (2) ischemic heart disease, (3) cardiac valve dysfunction, (4) cardiac conduction defects, and (5) renal artery stenosis. [Stoelting, Co~Existing, 1993, pl23-124]

Answer 162

Patients with Takayasu's arteritis may exhibit (l) pulmonary hyperten- sion and (2) ventilation-to-perfusion mismatch. [Stoelting, Co-Existing, 1993, p123-124]

Answer 163

Ankylosing spondylitis and rheumatoid arthritis may accompany Takaya- su's arteritis. [Stoelting, Co-Existing, 1993, p123-l24]

Answer 164

Takayasu's arteritis is treated with corticosteroids. [Stoelting, Co-Existi11g, !993, pl23]

Answer 165

(1) Supplemental exogenous corticosteroids may be needed during the perioperative period because chronic corticosteroid therapy can suppress adrenocortical function; (2) regional anesthesia may be controversial if the patient is anticoagulated; (3) musculoskeletal changes (ankylosing spondylitis and rheumatoid arthritis) can make it difficult to perform lumbar epidural or spina! anesthesia. [Stoelting, Co-Existing, 1993, pl23- 124]

Answer 166

(I) Blood pressure may be difficult to measure noninvasivety in the upper extremities; (2) if carotid blood flow is compromised, electroencephalo- gram monitoring may be useful in detecting cerebral ischemia; (3) hyper- extension of the neck during laryngoscopy for tracheal intubation may compromise blood flow through the carotid arteries, which may have shortened because of the vascular inflammat01y process. [Stoelting, Co- Existing, t993, pl23-l24]

Answer 167

Maintaining an adequate perfusion pressure is the goal in the intraopera- tive period for the patient with Takayasu's arteritis. Hence, drug induced decreases in blood pressure should be avoided. [Stoelting, Co-Existing, 1993, p123-I24]

Answer 168

Avoid excessive hyperventilation, which would promote cerebral vaso~ constriction secondary to a decrease in PaC02, and use a volatile agent (volatile agents increase cerebral blood flow). [Stoelting, Co-Existing, 1993, pp!23-!24j

Answer 169

The glossopharyngeal nerve (cranial nerve IX) provides sensory innerva- tion of the posterior one-third of the tongue and carries taste sensations. [Guyton, TMP .lle. 2006 pp665-666]

Answer 170

The facial nerve (cranial nerve VII) provides sensmy innervation of the anterior two-thirds of the tongue and carries taste sensations. [Guyton, TMP. !!e. 2006 pp665]

Answer 171

The primary function of the larynx is to protect the lungs from aspiration of foreign material. The larynx also functions in respiration and in phona- tion. [Barash Handbook, Clinical Anesthesia, 1997, p283; Davison, Eck- hardt, and Perese, Mass General, !993, pl7]

Answer 172

In the awake subject, the cricopharyngeus muscle is the primary muscular barrier to regurgitation. [Nagelhout & Zaglaniczny, NA, yd eel., 2004, p409j

Answer 173

The 3 unpaired laryngeal cartilages are the epiglottis, thyroid, and cricoid. The 3 paired laryngeal cartilages are the arytenoids, cuneifonns, and corniculates. The 9laryngeal cartilages encountered from superior to inferior are: epiglottis, thyroid, cuneiform (paired), corniculate (paired), arytenoids (paired), and cricoid. [Nagelhout & Zaglaniczny, NA, y

Answer 174

The aryepiglottic muscle pair closes the laryngeal inlet-they are sphinc- ters of the laryngeal vestibule. [Nagelhout & Zaglaniczny, NA, y

Answer 175

The posterior cricoarytenoids abduct (open) the cords; the lateral cricoa1ytenoids adduct (close) the cords. [Miller, Anesthesia, 1994, pp2!83-2184j

Answer 176

The key to answering this question is interpreting the word "dilates". If "dilates" means that the space between the cords widens (the cords ab- duct), the answer is the posterior cricoarytenoids. [Snell, Clinical Anato- my. 4e. 2004 pp34j

Answer 177

The cricothyroid muscle lengthens (tightens or tenses) the vocal cords. The voice will go up in pitch when the cords are tensed. [Hollinshead, Textbook of Anatomy, 1974, p943; Guyton, TMP, 1996, p488]

Answer 178

The thyroarytenoid relaxes the cords. [Ellis & Feldman, Anatomy for Anaesthetists. 8e. 2004 pp35]

Answer 179

The recurrent laryngeal nerve, which is a branch of the vagus, provides sensation below the cords. The internal branch of the superior laryngeal nerve, which also is a branch of the vagus, provides sensations above the cords. [Barash Handbook, Clinical Anesthesia, 1997, p283]

Answer 180

The internal branch of the superior laryngeal nerve supplies sensory fibers to the anterior and posterior surfaces of the epiglottis. [Miller, Anesthesia, 1994, p2184]

Answer 181

Stimulation of the superior laryngeal nerves may cause laryngospasm. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 4e, 2006, p938]

Answer 182

The cricothyroids are the muscles involved in laryngospasm. The crico- thyroids adduct and tense the true vocal cords. Laryngospasm is mediated by the external branch of the superior laryngeal nerve. The external branch of superior laryngeal nerve provides motor innervation to the cricothyroid muscle. [Miller, Anesthesia, 1994, pp 140S-1406, 2184]

Answer 183

When the recurrent laryngeal nerve is damaged, the paralyzed vocal cord assumes a position intermediate between the abducted and adducted states. The paralyzed cord cannot adduct. The lateral cricoarytenoid causes adduction of the cords. [Ellis & Feldman, Anatomy for Anaesthe- tists. Se. 2004 pp38; Hines, Stoelting's Co-existing. Se. 2008 pp388]

Answer 184

The muscles of inspiration are the diaphragm and the external inter- costals. The diaphragm is the most important muscle of inspiration. [Guyton, TMP. 11e. 2006 pp471; Ellis & Feldman, Anatomyfor Anaesthe- tists. Se. 2004 pp308]

Answer 185

The answer is controversial. Stoelting states that the diaphragm accounts for approximately 75% of air that enters the lung during spontaneous respiration, without respect to position. Levitzky states that when a per- son is in the upright position, the diaphragm contributes one-third to one-half (33% to SO%) of the tidal volumed uring eupnea. Levitzky also states that the action of the diaphragm is responsible for about two-thirds (66%) ofridal volume during eupnea when supine. Summa!}': ifbody positional orientation is not given, assume about 67% to 75% of tidal volume enters the lungs due to the action of the diaphragm during eup- nea. [Stoelting, PPAP, 4e, 2006, p774 (Chapter SO); Levitzl

Answer 186

The diaphragm is innervated by the phrenic nerve originating from C3, C4, C5. The phrenic nerve arises chiefly from the 4th cervical nerve with contributions from the yd and 5th cervical nerves. Remember: C3, C4, C5 keeps the diaphragm alive. [Morgan and Mildrail, 1996, p411]

Answer 187

The vertical dimension of the chest cavity is lengthened or shortened and the anteroposterior diameter is increased and decreased during ventila- tion. [Guyton, TMP. lle. 2006 pp471]

Answer 188

The most important muscles that raise the rib cage to increase the A/P diameter are the external intercostals, but others that help are the (1) sternocleidomastoid muscles, which lift upward on the sternum; (2) ante- rior serrati, which lift many of the ribs; and (3) scaleni, which lift the first two ribs. [Guyton, TMP. 11e. 2006 pp471]

Answer 189

Contraction of the diaphragm most contributes to the increase in the vertical (up and down) dimension of the chest wall. [Guyton, TMP. lie. 2006 pp471; Ellis & Feldman, Anatomy for Anaesthetists. Be. 2004 pp308]

Answer 190

The muscles that pull the rib cage downward during expiration are main- ly the (1) abdominal recti, which have the powerful effect of pulling downward on the lower ribs at the same time that they and other ab- dominal muscles also compress the abdominal contents upward against the diaphragm, and (2) internal intercostals. [Guyton, TMP. 11e. 2006 pp471]

Answer 191

Dead space is that portion of the tidal volume that does not participate in gas exchange. [Barash Handbook, Clinical Anesthesia, 1997, pp309, 407- 408]

Answer 192

Anatomic dead space is the volume of air in the conducting airways. 50% of anatomic dead space is contained in the upper airway. The anatomic dead space remains relatively constant throughout life. Note: Conducting airways are airways where gas exchange does not occur. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p423]

Answer 193

Alveolar dead space is that volume of inhaled gas that enters non- perfused or poorly perfused alveoli. Inadequate perfusion of ventilated alveoli causes alveolar dead space. [Guyton, TMP. 11e. 2006 pp477-478]

Answer 194

Physiologic dead space is the sum of the anatomic and alveolar dead spaces. [Guyton, TMP. 11e. 2006 pp478]

Answer 195

In a normal, healthy adult in whom nearly all alveoli are functional, alveo- lar dead space is minimal. In this situation, physiologic dead space is nearly equal to anatomic dead-space. [Guyton, TMP. 11e. 2006 pp478]

Answer 196

Physiologic dead space is the sum of the anatomic dead space and alveolar dead space. Physiologic dead space minus anatomic dead space is, there-fore, alveolar dead space. Alveolar dead space is caused by unperfused or poorly perfused alveoli. Hence, the difference between physiologic dead space and anatomic dead space is unperfused or under-perfused alveoli. [Guyton, TMP. lle. 2006 pp477-478j

Answer 197

2 ml.ikg is the normal adult anatomic dead space. For an 80 kg adult, anatomic dead-space is 2 ml.ikg x 80 kg~ 160 mL. [Barash, Clinical Anes- thesia, 1997, p759; Morgan and Mil

Answer 198

Dead space increases: (1) with age, (2) during positive-pressure ventila- tion, (3) when there is pulmonary embolism, and (4) in the patient with lung disease. [Morgan and Mild1ail, Clinical Anesthesiology, 1996, p423j

Answer 199

Dead space is 20-40% (average, 33%) of tidal volume in a spontaneously breathing adult and 40-60% in a paralyzed, mechanically ventilated pa- tient. [Barash Handbook, Clinical Anesthesia, 1997, pp407-408)

Answer 200

About two-thirds of the inspired gas in each breath mixes with alveolar gases, because one-third is dead space. [Miller, Anesthesia, 1994, p594

Answer 201

Normally, anatomic dead space is almost equal to physiologic dead space (alveolar dead space is small), and V,/V,. is about 0.33 (33%). (Recall that dead space averages 33% of tidal volume in the spontaneously breathing healthy young adult.) With lung disease, the physiologic dead space in- creases and the VD/VT ratio increases. In the patient with obstructive airway disease, VD/V·r may increase to 0.6 to 0.7 (60-70%). [Guyton, TMP. lle. 2006 pp478]

Answer 202

The carina. [Guyton, "IMP. Ile. 2006 pp480)

Answer 203

Goblet cells secrete mucus. [Guyton, 1MP. lie. 2006 pp480]

Answer 204

Compliance is the change in volume that occurs in response to a change in pressure. Resistance is the change in pressure along a tube divided by flow. Compliance is a measure of the ease with which a structure such as an alveolus is distended. Resistance is a measure of the ease with which a fluid (gas, liquid) fiows through a tube (such as a bronchus). [Guyton, TMP. lle. 2006 pp473-474j

Answer 205

An alveolus with a large compliance will have a large increase in volume for a small increase in pressure. Alveoli with large compliances are easy to distend. [Barash, Clinical Anesthesia, 1997, pp762-763; Authors]

Answer 206

Surfactant is secreted by type II alveolar epithelial cells. Surfactant is a lipoprotein mixture. Dipalmitoyllecithin is the major phospholipid of surfactant. [Guyton, TMP. lie. 2006 pp474]

Answer 207

Surfactant: (1) acts like a detergent to decrease surface tension, so pul- monary compliance is increased and the work of breathing is reduced, (2) permits alveolar stability by keeping small alveoli from collapsing into larger alveoli, and (3) helps keep alveoli dry. [Guyton, TMP. lie. 2006 pp474-475]

Answer 208

Normally, surface tension decreases as alveoli become smaller. (The sur- face tension of surfactant decreases as surface area decreases.) I t is this property of surfactant that keeps pressure equalized among alveoli and prevents small alveoli from collapsing and emptying into larger ones. The law ofLaplace applies. [Guyton, TMP. lie. 2006 pp474]

Answer 209

Functional residual capacity is the volume of gas left i n the lungs after a normal exhalation. [Guyton, TMP. lie. 2006 pp476; Barash, Clin. Anes. 6th. 2009 pp247]

Answer 210

The chest wall (thorax) naturally recoils outward, and the lungs naturally recoil inward. At functional residual capacity (FRC), the outward chest recoil equals the inward lung recoil. [Guyton, 1MP. lie. 2006 pp471-475]

Answer 211

More than two-thirds of the work of quiet breathing is used to overcome elastic recoil of the lungs and the thorax. [Stoelting, PPAP. 4e. 2006 pp774]

Answer 212

Passive elastic recoil of the lungs is responsible for exhalation during normal tidal breathing. [Guyton, TMP. !!e. 2006 pp471]

Answer 213

Intrapleural pressure is negative at the onset of inspiration and becomes more negative during inspiration. During expiration, intrapleural pres- sure becomes less negative. [Guyton, TMP. lie. 2006 pp472]

Answer 214

Intrapleural pressure is never positive, it is always negative (subatmos- pheric) during a normal inspiratory-expiratory cycle. [Guyton, TMP. lle. 2006 pp472]

Answer 215

Intrapulmonary pressure becomes negative (subatmospheric) during inspiration and positive (above atmospheric pressure) during expiration. Intrapulmonary pressure is zero at end-expiration and at end-inspiration. [Guyton, TMP. lie. 2006 pp472]

Answer 216

Intrapleural pressure is greater (less negative) in dependent lung and lower (more negative) in non-dependent lung. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p423)

Answer 217

Intrapleural pressure has the greatest magnitude (is most negative) in the apex and has the least magnitude {is least negative) at the base. Intrapleu- ral pressure is minimal (least negative) in the dependent lung which is the base in the standing or sitting (upright) person. [Barash, Clinical Anesthe- sia, 1997, p750)

Answer 218

The intrapleural pressure is the same at the base as at the apex in the supine, prone, and lateral decubitus positions. Intrapleural pressure changes in the vertical direction, not in the horizontal direction. [West, Respiratory Physiology, 1990, p97)

Answer 219

No, the gradient in intrapleural pressure does not change when the awake, spontaneously breathing patient is anesthetized and paralyzed. Intrapleural pressure is greater (less negative) in dependent lung com- pared with nondependent lung regardless of whether the patient is awake or anesthetized/paralyzed. [Barash, Clinical Anesthesia, 1997, p575; Au- thors]

Answer 220

During inspiration, intrapleural pressure increases (becomes less negative and may become positive) if the patient is on a positive pressure ventila- tor. [Miller, Anesthesia, 1994, p578)

Answer 221

he Valsalva maneuver is accomplished by performing a forced expira- tion with the glottis closed. All intrathoracic pressures, including intra- pleural and intrapulmonary pressures, increase; intrapleural pressure changes from negative to positive, so venous return to the right ventricle decreases; consequently, cardiac output and blood pressure decrease; the decrease in blood pressure results in a reflex increase in heart rate (baro- receptor reflex). [Barash, Clinical Anesthesia, 1997, p263; Miller, Anesthe- silr, 1994, p644)

Answer 222

Total lung capacity is inspiratory capacity plus functional residual capaci- ty. Total lung capacity is inspiratory reserve volume plus tidal volume plus expiratory reserve volume plus residua! volume. [Guyton, TMP. lle. 2006 pp476)

Answer 223

Residual volume is norma!ly 20-25% of total lung capacity. [Guyton, TMP. lie. 2006 pp475-476)

Answer 224

Closing volume is the volume of gas that can be exhaled during a force expiration after airways begin to dose. [West, Respiratory Pathophysiolo- gy, 1990, pl6)

Answer 225

Functional residual capacity (FRC) is the sum of the expiratory reserve volume (ERV) and residual volume (RV). [Guyton, TMP. lie. 2006 pp476--477; Barash, Clin. Anes. 6th. 2009 pp248)

Answer 226

Dependent lung is the region oflung that is closest to the ground and non-dependent lung is located farthest from the ground. The bases of the lung are dependent in the upright (sitting or standing) individual. The apices of the lung are non-dependent in the upright (sitting or standing) individual. Dependent lung is dependent on gravity and upon support from the base ofthe structure. [Authors, MM. 19. 2010 ppO]

Answer 227

Alveolar ventilation is minute ventilation minus dead space ventilation. Alveolar ventilation= (tidal volume- dead space) x ventilation rate. For a healthy patient, dead space is 2 mL/kg. Alveolar ventilation for the 65 kg 30-year-old is: (450 mL- 65 kgx 2mL!kg) x 12/min = (450 mL- 130 mL) x 12/min =320 mL x 12/min =3,840 mL =3.84liters. [Guyton, TMP. 11e. 2006 pp478]

Answer 228

An increase in tidal volume will improve alveolar ventilation more than will an increase in ventilation rate. An increase in tidal volume increases alveolar ventilation without increasing dead space ventilation. An in- crease in ventilation rate increases both alveolar and dead space ventila- tion. [Barash, Clinical Anesthesia, 1997, pp758-759, 1524; Authors]

Answer 229

End-tidal C02 decreases. With high fresh gas flows, ETC02 is dependent on minute ventilation. [Dorsch and Dorsch, UAE, 1984, pp175-176]

Answer 230

Tidal volume and thus minute ventilation (respiratory rate x tidal vol- ume) will increase due to high flows of fresh gas within the bellows and the anesthetic circuit to the patient. [Dorsch and Dorsch, UAE, 1984, pp256-258; Authors]

Answer 231

PaC02 and ETCOz are inversely proportional to alveolar ventilation. When alveolar ventilation increases, both PaC02 and ETC02 decrease, and vice versa. Note: ETCO, is average alveolar PCO, (P,CO,). [Stoelting and Mil- ler, Basics, 1993, pp230-231]

Answer 232

If dead-space ventilation increases without a change in total minute venti- lation, alveolar ventilation decreases, and PaC02 and ETC02 increase. [Stoelting and Miller, Basics, 1994, pp230-231]

Answer 233

Alveolar ventilation would decrease, so there would be increased PaC02 and decreased P,O,. [Guyton, TMP. l1e. 2006 pp478]

Answer 234

Carbon dioxide production and alveolar ventilation are the two determi- nants of PaC02• The anesthetist alters the patient's l \ ( 0 2 by decreasing or increasing ventilation (by changing tidal volume or ventilatory rate). [Barash, Clinical Anesthesia, 1997, p759j

Answer 235

The alveolar partial pressure of 0 2 (P,\02) is higher in the apex and lower in the base, and the alveolar partial pressure of CO, (P,CO,) is lower in the apex and higher in the base. [West, Respiratory Physiology, 1990, p62]

Answer 236

Zone I (non-dependent lung) has the highest P,O,. Zone Ill (dependent lung) has the highest P,co,. [Miller, Anesthesia, !994, pp577-579]

Answer 237

The most negative intrapleural pressure is found in Zone I (non- dependent lung) and the least negative intrapleural pressure is found in Zone Ill (dependent lung). [West, Respiratory Physiology, 1990, p98]

Answer 238

Water has a higher concentration in the airway compared with atmos- pheric air. Alveolar air is 100% humidified at 37 degrees C. Air becomes 100% humidified as it Oows into the respiratory tract. 02 and Nz are dilut- ed slightly by the water vapor. [Gnyton, TMP. lie. 2006 pp480]

Answer 239

The gas everywhere in the airway is saturated wilh water vapor (relative humidity~ !00%). [Guyton, IMP. lie. 2006pp492]

Answer 240

ETC0 2 = 38 mmHg (0.05 x 760 mmHg). Note:% concentration/100 x atmospheric pressure yields the partial pressure. Dalton's law of partial pressures permits this calculation to be made. [Authors]

Answer 241

Approximately 450 mL, or 9%, of the total blood volume is in the pulmo- nary circuit. Of this 450 mL, 70 mL is in the capillaries and the remainder (380 mL) is divided equally between arteries (!90 mL) and veins (!90 mL). [Guyton, TMP. lie. 2006 pp484; Stoelting, PPAP. 4e. 2006 pp743]

Answer 242

West's zone 1 is non-dependent lung whereas West's zone 3 is dependent lung. [Authors]

Answer 243

Intrapulmonary pressure exceeds pulmonary arterial blood pressure in Zone 1. Zone I is not perfused because pulmonary artery pressure is less than alveolar pressure. The alveolar capillaries are collapsed. [Guyton, TMP. lie. 2006 pp486j

Answer 244

Pulmonary arterial blood pressure is higher than alveolar pressure in Zone II. Zone II is perfused. The perfusion pressure gradient in Zone II is pulmonary arterial blood pressu!'e minus alveolar pressure. !Guyton, TMP. lie. 2006 pp486]

Answer 245

West zone 2 shows the greatest increase in blood flow over the distance of the zone; blood flow is zero at the nondependent start of zone 2 and in- creases with dependency over the distance of zone 2. Reminder: zone 2 is the "waterfall zone" of intermittent bloodflow, where Pt>A> PA> Ppv. [West, Pulm. Physiol. Be. 2008 pp43-44; Barash, Clinical Anes. Se. 2006 pp82lf; Guyton, TMP. lle. 2006 pp485-486; Stoelting, PPAP. 4e. 2006 pp746)

Answer 246

Pulmonary arterial and venous pressures exceed alveolar pressure in Zone III. The perfusion pressure gradient in Zone III is the difference between the pulmonary arterial blood pressure and the venous blood pressure. [Guyton, TMP. lie. 2006 pp486)

Answer 247

West zone 3 possesses the maximal pulmonary blood flow of any zone (region). Reminder: zone 3 is the "distension zone" with continuous blood flow, where PPA> Ppv> PA.

Answer 248

A right-to-left shunt occurs when some portion of the right heart's output is shunted past the alveoli to the left ventricle. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p425)

Answer 249

An intrapulmonary shunt is present when blood passes from the pulmo- nary artery to the pulmonary vein through capillaries of unventilated or poorly ventilated alveoli. This is a right-to-left shunt. [Morgan and Mi- khail, Clinical Anesthesiology, 1996, pp424-425)

Answer 250

Marked right-to-left intrapulmonary shunting (shunt flow> 15%) is asso- ciated with radiographically discernable findings such as pulmonary atelectasis, parenchymal infiltrates, or a large pneumothorax. [Morgan, et a!., Ciin. Anesth. 4e. 2006 pp1012)

Answer 251

A shunt causes a decrease in Pa02• Hypoxemia and tissue hypoxia result if a shunt develops and the patient is breathing room air and possibly also when breathing a high inspired oxygen concentrations. [Barash, Clinical Anesthesia, 1997, pp758, 760)

Answer 252

An increase inl\C02 is a consequence of mild deadspacing. With severe deadspacing, 1\02 will also decrease. [Barash, Clinical Anesthesia, 1997, p758)

Answer 253

In response to alveolar hypoxia, the pulmonary vessels constrict so that there is reduced blood flow to the unoxygenated alveoli. This is hypoxic pulmonary vasoconstriction (HPV). [Barash, Clinical Anesthesia, 1997, pp785-787; Miller, Anesthesia, 1994, p609[

Answer 254

Hypoxic pulmonary vasoconstriction (HPV) decreases shunt. HPV reduc- es perfusion to unventilated or poorly ventilated alveoli, and reduces the severity of the shunt. [Stoelting and Miller, Basics, 1993, p51)

Answer 255

The PAOz-1\0z gradient is normally about 5-15mmHg (up to 25 mmHg is acceptable) when breathing room air. The P110rPa02 gradient is normally

Answer 256

The P110 2-PaOz gradient reflects the degree of right-to-left shunt. There normally is a small right-to-left shunt, which is reflected by a small P11 0 2- Pa02 gradient of 5-15 mrnHg. The l\C02-P 11C02 gradient reflects dead- spacing. Normally, there is a small PaC02-P11C02 gradient of2-IO mmHg, when breathing room air. [Barash Handbook, Clinical Anesthesia, 1997, p408; Morgan and Mikhail, Clinical Anesthesiology, 1996, pp429, 431]

Answer 257

The PAOrPa02 gradient increases any time shunting increases. The P,C02- p11C0z gradient also increases when deadspacing or shunting increases. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp429, 431; Barash Handbook, Clinical Anesthesia, 1997, p408]

Answer 258

A pathological right-to-left shunt (intrapulmonary or intracardiac). [Ba- rash Handbook, Clinical Anesthesia, 1997, p408]

Answer 259

The Pa02/PAo2, ratio. [Miller, Anesthesia, 1994, pl257]

Answer 260

Lung regions where PPA>P1s1:> Ppv> PA are termed zone 4 regions. Blood flow in zone 4 is reduced by gravitational compression of the lung paren- chyma or by interstitial edema formation. [Stoelting, PPAP. 4e. 2006 pp746; Hagberg, Benumofs Airway Management. 2e. 2007 pp116-117]

Answer 261

Greater. Perfusion (blood flow) is best in dependent lung. The base of the lung is dependent in the upright (sitting or standing) individual. [Barash, Clinical Anesthesia, 1997, p757]

Answer 262

Gravity. [Authors]

Answer 263

Greater. Total ventilation is best in dependent lung. [Barash, Clinical Physiology, 1997, p757]

Answer 264

In the awake spontaneously breathing patient in the lateral decubitus position, ventilation is best in dependent (lower) lung and perfusion is best in dependent (lower) lung. [Miller, Anesthesia, 1994, pp1681,1685- l687]

Answer 265

When the patient in the lateral decubitus position is anesthetized and paralyzed, perfusion is best in the dependent (lower) lung, but ventilation is best in the nondependent upper lung. [Miller, Anesthesia, 1994, ppl68l, 1685-1687]

Answer 266

4 l/min is the alveolar ventilation rate (V). Sl/min is the pulmonary blood flow (Q). Normally, V/Q = 0.8 [(4L/min)/(5 L/min) =V/Q =0.8]. [Guy- ton, TMP. 11e. 2006 pp244, 495, 499]

Answer 267

A normal ventilation-to-perfusion relationship is required to keep PaC02 and Pa02 in the normal range. [Barash, Clinical Anesthesia, 1997, pp757- 758]

Answer 268

In a lung unit that exhibits absolute shunt, V/Q = 0 because V = 0; perfu- sion (Q) may be decreased somewhat because of hypoxic pulmonary vasoconstriction. [Barash, Clinical Anesthesia, 1997, pp757-758]

Answer 269

A V/Q ratio between zero and unity (0

Answer 270

A V/Q > l indicates deadspacing. [Morgan and Mikhail, Clinical Anesthe- siolagy, 1996, pp424,425]

Answer 271

V/Q =infinity if the lung unit is ventilated and completely unperfused, because Q ~ 0. [Barash, Clinical Anesthesia, 1997, p758]

Answer 272

With absolute dead-space, V/Q = infinity (V/0) and with absolute shunt, V/Q ~ 0 (0/Q). [Kirby, Gravenstein, Lobato and Gravenstein, Clinical Anesthesia Practice, 2002, p857, Authors]

Answer 273

At end-expiration, dependent alveoli are smaller than non-dependent alveoli. [Barash, Clinical Anesthesia, 1997, p757; Morgan and Mikhail, Clinical Anesthesiology, 1996, pp423, 424]

Answer 274

Lower. The V/Q ratio is high in nondependent lung and low in dependent lung. [Barash, Clinical Anesthesia, 1997, pp757; Morgan and Mikhail, Clinical Anesthesiology, 1996, p425]

Answer 275

An intrapulmonary shunt develops i f a bronchus is clipped and the vascu- lature is left intact. When a shunt develops, PaOz decreases. [Barash, Clirli- cal Anesthesia, 1997, p779]

Answer 276

There is a large shunt when one lung is nonfunctionaL Pa02 decreases possibly/probably resulting in arterial hypoxemia. If the lung is removed, there is no shunt and hence there is no arterial hypoxemia. [Authors]

Answer 277

P1102 can be estimated by multiplying% inspired 0 2 by 6 (P"02""% in- spired(), x 6). When F,O, =50%, P ,O, = 50 x 6 = 300 mmHg. When F,O, = 100%, P,O, = 100 X 6 = 600 mmHg. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p428]

Answer 278

Pa0 2 can be estimated by multiplying% inspired 0 2 by 5 (P"02 = % i n - s p i r e d O z x 5 ) . W h e n F 10 2 i s 5 0 % , P a 0 2 = 5 0 X 5 : : : 2 5 0 m m H g . W h e n F 10 z is 100%, P,O, = 100 x 5 = 500 mmHg. [Barash, Clinical Anesthesia, 1997, p760]

Answer 279

PA O2 - Pa O2 , = 4 0 x 6 - 4 0 x 5 = 2 4 0 - 2 0 0 = 4 0 mm H g . [ A u t h o r s ]

Answer 280

The maximall\02 for a young person breathing room air is 104 rnm Hg (Guyton). The best achievable P,02 is 100-105 mm Hg (Authors). [Guy- ton, TMP. lie. 2006 pp502-503]

Answer 281

Normal P.02 ranges from about 78 mmHg in elderly persons to 105 mmHg in young individuals (P,02 = 102-Age/3). [Miller, Anesthesia, 1994, p597; Morgan and Milchail, Clinical Anesthesia, 1996, p429]

Answer 282

The difference between P

Answer 283

Normal Sa02 is 90-97%. [Guyton, TMP. lie. 2006 pp506]

Answer 284

When oxygen saturation is 90%, P02 is 60 mrnHg. This is arterial blood. [Stoelting and Miller,Basics, l993, p204l

Answer 285

When oxygen saturation is 70%, P02 is 40 mmHg. This is mixed venous blood. [Morgan and Mikhail, Clinical Anesthesiology, l996, pp432, 433]

Answer 286

When the P02 is 60 mm Hg, oxygen saturation is 90%. When the P02 is 40 mm Hg, oxygen saturation is 70%. [Barash Handbook, Clinical Anesthesia, 1997, p313]

Answer 287

5 mL 0 2/100 mL blood. This says that 5 mL 02 are extracted from each 100 mL of blood by tissues as blood flows from the arterial to the venous side of the systemic circulation. [Morgan and Mild1ail, Clinical Anesthesi- ology, 1996, p434]

Answer 288

A decrease in Sv02 can occur if there is: (1) a decrease in oxygen delivery (decreased cardiac output, decreased hemoglobin concentration, abnor- mal hemoglobin) with a resulting increased extraction of 0 2 from the blood, or (2) an increase in Oz consumption (fever, shivering, malignant hyperthermia, thyroid storm). [Morgan and Mikhail, Clinical Anesthesiol- ogy, 1996, p430; Miller, Anesthesia, 1994, p597-599]

Answer 289

Multiply P02 x0.003, and your answer will be the amount of oxygen dissolved in blood. The units are mL 0 2/100 mL blood. Henry's law per- mits this calculation to be made. [Guyton, TMP. 11e. 2006 pp492; Stoelt- ing, PPAP. 4e. 2006 pp787]

Answer 290

Pa02s while breathing 50%02 and 100% 0 2 are estimated to be 250 {50 x 5) and 500 (100 x 5) mmHg, respectively. The amounts of O, dissolved are 0.75 (250 x 0.003) and 1.5 (500 x 0.003) mL 0 1/100 mL blood when breathing 50%02 and 100%02, respectively. [Authors]

Answer 291

The amount of dissolved Oz increases 0.9 mL OilOO mL blood. When P0 2 is 100 nunHg, dissolved o, = 0.003 x 100 mmHg= 0.3 mL 0,/100 mL blood. When PO, is 400 mmHg, dissolved 0 2 = 0.003 x 400 mmHg = 1.2 mL 0 1/100 mL blood. Therefore, the dissolved oxygen increased by 0.9 mL 0 2/100 mL blood (1.2- 0.3 = 0.9). ]Morgan and Mikhail, 1996, p431; Authors]

Answer 292

P 0 2 and the amount of hemoglobin are the two factors that determine the amount of oxygen carried by hemoglobin. ]Guyton, TMP. 11e. 2006 pp505-506]

Answer 293

1.34 mL of 0 2is carried by each gram of saturated hemoglobin. [Guyton, TMP. lle. 2006 pp506]

Answer 294

Hemoglobin (Hgb)-bound O, = (1.34 mL 0 1/gm Hgb)(15 gm Hgb/100 mL blood)= 20.1 mL 0,/100 mL blood. Dissolved O, = (100 mmHg)(.003) = 0.3 mL 0,/100 mL blood. Total o, = Hgb-bound 0 2 +dissolved o, = 20.1 + 0.3 = 20.4 mL 0,1100 mL blood.]West, Respiratory Physiology, 1990, p71]

Answer 295

The flat portion o f the oxyhemoglobin dissociation curve facilitates the loading of oxygen by the blood because, in the flat portion of this curve, large changes in the partial pressure of oxygen in arterial blood (Pa02) produce only small changes in oxygen saturation (Sa02). [Stoelting and Miller, Basics, 1994, p230]

Answer 296

The steep portion of the oxyhemoglobin dissociation curve facilitates unloading of oxygen at tissues because large amounts of oxygen are un- loaded from hemoglobin (large decrease in oxygen saturation) in re- sponse to a small change in the partial pressure of oxygen. [Stoelting and Miller, Basics, 1994, p232]

Answer 297

When Pa02 falls below 60 mmi-lg, large reductions in Sa02 occur with small decreases in Pa02. [Barash Handbook, Clinical Anesthesia, 1997, p3!3]

Answer 298

The P50 is the 0 2 partial pressure at which hemoglobin (Hgb} is SO% satu- rated. The normal PSD = 26-27 mmHg. [Barash Handbook, Clinical Anes- thesia, !997, p313; Morgan and Mikhail, Clinical Anesthesiology, !996, p432; Miller, Anesthesia, !994, pp595-597]

Answer 299

The P50 increases when the oxyhemoglobin dissociation curve shifts to the right and decreases when the oxyhemoglobin dissociation curve shifts to the left. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p432]

Answer 300

(1) Increased temperature, (2) increased H+ concentration (decreased pH), (3) increased partial pressure of C02, (4) increased 2,3-DPG, and (5) siclde cell disease. In general, increased metabolism promotes a rightward shift of the oxyhemoglobin curve, facilitating unloading of oxygen at the tissues. [Guyton, TMP. lle. 2006 pp508; Morgan, eta!., Clin. Anesth. 4e. 2006 pp562-563]

Answer 301

(1) Decreased temperature, (2} decreased B:- concentration (increased pl-l), (3) decreased partial pressure of C02, (4) decreased 2,3-DPG, (5) presence of fetal hemoglobin, (6) presence of carboxyhemoglobin, and (7) presence of methemoglobin. [Morgan, eta!., Clin. Anesth. 4e. 2006 pp562-563]

Answer 302

The oxyhemoglobin curve shifts to the right when PC02 increases; this rightward shift, which occurs

Answer 303

The oxyhemoglobin curve shifts to the left when PC02 decreases; this leftward shift occurs in pulmonary capillaries as C0 2 is blown off; 0 2 loading by hemoglobin is favored in pulmonary capillaries when the oxyhemoglobin dissociation curve shifts left. [Guyton, TMP. lle. 2006 pp508]

Answer 304

The shift in the oxyhemoglobin dissociation curve caused by carbon diox- ide entering or leaving the blood is the Bohr effect. As you know, the increase in PC02 in systemic capillaries is partly responsible for shifting the oxyhemoglobin dissociation curve rightward, which facilitates the unloading ofoxygen from hemoglobin. The decrease in PC02 in pu!mo-nary capillaries, on the other hand, helps shift the oxyhemoglobin curve to the left, which facilitates the loading of oxygen onto hemoglobin. Stoelting, PPAP, 2006, p789 [Stoelting, PPAP. 4e. 2006 pp789j

Answer 305

Normal hemoglobin (Hgb) has iron in the ferrous (Fe'') state. Oxygen carriage by normal Hgb is excellent. Met-Hgb has iron in the ferric (Fel+) state. The oxygen carrying capacity in patients with methemoglobinemia is poor. [Stoelting, Co-Existing, 1993, p403j

Answer 306

5 grams ofHgb per 100 mL blood must be in reduced form (without 0,) for cyanosis to develop. [Guyton, TMP. 11e. 2006 pp531j

Answer 307

The polycythemic patient will most easily become cyanotic. Cyanosis develops when there is 5 g/100 mi. of reduced Hgb. The polycythemic patient, not the anemic patient, is most likely to have this much reduced Hgb. [Guyton, TMP. 11e. 2006 pp531; Stoelting, PPAP. 4e. 2006 pp789- 790j

Answer 308

The anemic patient is not likely to become cyanotic. With low levels of Hgb, it is difficult to reduce enough Hgb to turn the patient cyanotic. Note that it is much easier for the polycythemic patient to become cyanotic. [Miller, Anesthesia, 1994, p980; AuthorsJ

Answer 309

Administration of inhalational or IV anesthetics may cause the oxyhemo- globin dissociation curve to shift to the right because respiratory depres- sion permits PaC02 to increase. [Barash, Clinical Anesthesia, 1997, pp191- 192; Stoelting and Miller, Basics, 1993, pp48, 230j

Answer 310

250 mL!min of02 is normally delivered to, and used by, the tissues. This is 3-4 mL OJ!kglmin. Note: Oxygen delivery matches oxygen consumption. [Guyton, TMP, 1996, pp516-517j

Answer 311

Oxygen consumption is normally 250 mL 02/min. This is a value you should have memorized. To get your answer in mL Oikg/min, assume the average person weighs 70 kg, and divide 250 mL 0 2/min by 70 kg as follows: [250 m1 0 2/minj![70 kgj ~ 250/70 mL 0,/kg/min ~ 3.57 mi. 0 2/kg/min. To get the answer in mL 0 2/lOOg/min, convert kg to 1000 g; 3.57 mi. 0 2/kg/min ~ 3.57 mi. 0,11000 g/min ~ 0.357 mL 0 21100 g/min. Note: You may expect to be asked to convert a normal value to a per kg or per 100 g basis. [Morgan and Mild1ail, Clinical Anesthesiology, 1996, p124; Authors!

Answer 312

The most probable cause ofa decrease in Sr02 is a decrease in cardiac out- put. An increase in oxygen consumption could also be a likely cause. [Barash Handbook, Clinical Anesthesia, 1997, pp86-87j

Answer 313

Mixedvenousoxygencontent(Mv02) isdeterminedby:(1)oxygendeliv- ery to the tissues (cardiac output, hemoglobin concentration, abnormal hemoglobin), and (2) oxygen consumption (malignant hyperthermia, thyroid storm, fever, shivering). For example, a decreased cardiac output, or anemia, or increased oxygen consumption wilt decrease Mv02. Note: The question could ask, "What determines mixed venous oxygen satura¥ tion (S,02) " , and the answer would be the same. ]Miller, Anesthesia, 1994, pp597-599; Morgan and Mikhail, Clinical Anesthesiology, 1996, p430]

Answer 314

The mixed venous oxygen tension (or saturation) is the best measurement for determining adequacy ofcardiac output. Adecrease in mixed venous oxygen saturation in response to increased demand usually reflects inad* equate tissue perfusion. Thus, in the absence of hypoxia or severe anemia, the mixed venous oxygen tension (or saturation) is the best measurement for detecting adequacy of cardiac output. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 3'" eel., 2002, p366]

Answer 315

Venous blood oxygen saturation monitoring provides inforrnation on the relationship between oxygen delivery and oxygen consumption. [Barash, Clinical Anesthesia, 1997, pp631-632]

Answer 316

enous blood oxygen saturation monitoring uses fiberoptic technology similar to pulse oximetry. Carboxyhemoglobin absorbs red and infrared light in a fashion similar to oxyhemoglobin. When carboxyhemoglobin is present, oxygen saturation readings will be falsely high. [Davison, Eck- hardt, and Perese, Mass General, 1993, p7]

Answer 317

The functional residual capacity (FRC) serves as a reservoir for 02. The 02 in the r:Rc diffuses into the blood during a brief period of apnea. [Morgan and Mild1ail, Clinical Anesthesiology, !996, p434]

Answer 318

The carbon dioxide content of room air is 0.03%. According to Daltons law, the partial pressure of C02 in room air is 0.23 mm Hg. [Authors]

Answer 319

Multiply PC02 by 0.067 and the result is the mL of C02dissolved in each 100 mL of solution. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p435]

Answer 320

The amount of C0 2 that dissolves in solution is 0.067 x PC0 2• 2.68 mL C02 (0.067 x 40) dissolves in each !00 mL arterial blood, and 3.08 mL CO, (0.067 x 46) dissolves in each !00 mL of venous blood. [Morgan and Mikhail, Clinical Anesthesiology, !996, p435]

Answer 321

C02 is approximately 20 times more soluble thatCh The solubility coeffi- cients for C0 2 and 0 2 are 0.067 mL C0,/100 mL blood/mm Hg and 0.003 mL 0,/!00 mL blood/mm Hg, respectively. [West, Respiratory Physiology, 1990, p75; Morgan and Mikhail, Clinical Anesthesiology, 1996, p435]

Answer 322

Carbon dioxide is produced and eliminated at a rate of200 mL/min or 2.4-3.2 mL!kg/min. Note: (200 mL/min)/70 kg= 2.9 mL/kg/min. [Da· vison, Eckhardt, and Perese, Mass General, 1988, p569; Stoelting, PPAP, 1991, p733]

Answer 323

Normally, C02 excretion is 200 mL/min. Since cardiac output is Sliters/ min, or 5,000 mL/min, the CO, excretion per 100 mL blood is 200 mL C0,/5000 mL blood= 4 mL C0,/100 mL blood. Stoelting, PPAP, 2006, p790; Morgan and Mikhail, Clinical Anesthesiology, 1996, p436 [Stoelting, PPAP. 4e. 2006 pp790]

Answer 324

C02intimally accumulates at a rate of 200 mL/min. [Stoelting and Miller, Basics, 1993, p23l]

Answer 325

When P02 decreases, the C02 dissociation curve shifts to the left, so more co, is carried by the blood. This leftward shift occurs as oxygen diffuses out of capillaries of systemic tissues. This left shift of the C02 dissociation curve facilitates the loading of COz into the blood. [Guyton, TMP. llc. 2006 pp508l

Answer 326

When P02increases, the C02 dissociation curve shifts to the right, so less COz is carried by the blood. This rightward shift occurs as blood flows through pulmonary capillaries in the lungs. This right shift of the C0 2 dissociation curve is important because it facilitates the unloading of C0 2 from the pulmonmy capillaries. [Guyton, TMP. 11e. 2006 pp508]

Answer 327

The Haldane effect describes how changes in P02 in the blood alter the amount of carbon dioxide carried by the blood. In the lungs, the increase in P02 in the pulmonary capillaries causes the carbon dioxide blood dis- sociation curve to shift to the right, which facilitates the unloading of carbon dioxide by the blood. In systemic capillaries, the decrease in P02 causes the carbon dioxide blood dissociation curve to shift leftward, which facilitates the loading of carbon dioxide by the blood. Stoelting, PPAP, 2006, p790 [Stoelting, PPAP. 4e. 2006 pp790J

Answer 328

The arterial blood C02 content is approximately 48 mL C02/100 mL blood. The venous blood C02 content is approximately 52 mL C02/100 mi. blood. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p435 (see graph)]

Answer 329

The normal venous-arterial carbon dioxide content difference (CvCOr CaC02) is4mLC02/100mLblood.Hence,4mLC02areeliminatedfrom each 100 mL of venous blood. [Morgan and MikhaH, Clinical Anesthesiol- ogy, 1996,p436]

Answer 330

Approximately 20 mL 0 2are carried in each I00 mL of arterial blood. The amount of C0 2 carried in each 100 mL of arterial blood of 48 mL C0 2 is almost 2 1/2 times greater than the amount of02 carried. [Morgan and

Answer 331

Carbon dioxide is carried: (1) physically dissolved in solution, 5%; (2) as carbonic acid (H2C03),

Answer 332

Carbonic anhydrase is an enzyme in red blood cells that accelerates the conversion ofH20 and COz to carbonic acid (H2C03) and then to bicar- bonate ions. Carbonic anhydrase is responsible for converting C02 to bicarbonate ions. [Guyton, TMP, 1996, p521]

Answer 333

Normal bicarbonate (HC03) values will rule out C02 retention. For every 10 mmHg increase in PC02, serum [HC03] will increase by I mmol!L. [Barash, Clinical Anesthesia, 2001, p522; Kirby, et al., Clinical Anesthesia Practice, 2002, p793]

Answer 334

Bicarbonate diffuses out of red blood cells in exchange for chloride ions. This is the chloride shift. It is also known as the Hamburger shift. [Mor- gan and Mikhail, Clinical Anesthesiology, 1996, p435; Guyton, TMP, 1996, p52l)

Answer 335

The primary respiratory centers (dorsal and ventral respiratory groups) are located in the medulla of the brains tern. Secondary respiratory centers (apneustic and pneumotaxic centers) are located in the pons of the brain- stem. [Guyton, TMP, 1996, pp525-527]

Answer 336

All opioids cause dose-dependent depression of respiration through direct mu2-receptor stimulation at the brainstem respirato1y centers located superficially in the floor of the 4th ventricle (i.e., medulla ar1d pons). [Miller, Anesthesia, 5th ed. 2000, pp294, 2331]

Answer 337

Hydrogen ions (H'") in the cerebrospinal fluid directly stimulate central chemoreceptors. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p436)

Answer 338

C02 that diffuses into the CSF is converted by carbonic anhydrase first to carbonic acid (I-hC03) and then to If' and bicarbonate ions (HC0.1-). [Authors]

Answer 339

Peripheral chemoreccptors (carotid body and aortic body) respond to Pa02, P,C01, and pH. Peripheral chemoreceptors are most sensitive to P,02, but not until P.,(h

Answer 340

In addition to Pa02, PaC02, and pH, peripheral chemoreceptors are also stimulated by cyanide, doxapram, and nicotine. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 3'' ed. 2002, p507j

Answer 341

The ventilatory response to an increased PaC02 is mediated primarily by central chemoreceptors. The effect of C02 on central chemoreceptors is seven times more powerful than it is on peripheral chemoreceptors. Point: central chemoreceptors are normally more important than periph- eral chemoreceptors in controlling ventilation. [Guyton, TMP, 1996, p525; Barash, Clinical Anesthesia, 1997, pp753-754j

Answer 342

C02 normally drives ventilation. COz is the physiological respiratory stimulant. The single most important regulator ofalveolar ventilation is P,C02• [Guyton, TMP, 1996, p527-529; Morgan and Mikhail, Clinical Anesthesiology, 1996, p437j

Answer 343

Pathological stimulants are low P.02 or acids (hydrogen ions). [Guyton, TMP, 1996,pp529-530j

Answer 344

An increase in PaC02 produces a far greater increase in ventilation than does a decrease in arterial blood pH. An increase in PaC02from 40 to 60 or from 40 to 90 mm Hg produces a six-fold or lO~fold increase in ventila- tion, respectively. In contrast, a decrease in blood pH from 7.4 to 7.0 produces a four-fold increase in ventilation. [Guyton, TMP, 1996, p528]

Answer 345

Four causes of hypocapnia are: (1) voluntary hyperventilation, (2) iatro~ genic hyperventilation (mechanical ventilation), (3) decreased C0 2 pro- duction (hypothermia, deep anesthesia, hypotension), and (4) decreased dead space ventilation (change from mask airway to endotracheal tube airway, decreased PEEP, decreased rebreathing). By far the most common cause of hypocapnia is hyperventilation by mechanical means. [Miller, Anesthesia, 1994, p6I2j

Answer 346

Four causes of hypercapnia are: (1) hypoventilation (depression of venti- lation by drugs such as opioids), (2) increased dead space ventilation, (3) inadvertently switching offC02absorber, and (4) increased C02 pro- duction. [Miller, Anesthesia, 1994, p6Ilj

Answer 347

The partial pressure of the inspired C0 2 is 23-53 mmHg if one breathes 3-7% CO, (0.3% X 760 = 0.03 X 760 = 22.80 = 23 mmHg; 7% X 760 = 0.07 x 760 =53.20 =53 mmHg). Thus, hypercapnia (increased !',C02) will occur. Ventilation will increase dramatically in an attempt to compensate. [Miller, Anesthesia, 1994, pp611-614j

Answer 348

Lung inflation triggers the Hering-Breuer reflex. When the Hering-Breuer reflex is triggered by lung inflation, inspiration is inhibited. The Hering- Breuer reflex plays a minor role in normal ventilation in the adult. It is mainly a protective mechanism that is probably not activated until the tidal volume increases to greater than l.Sliters. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p437; Guyton, TMP, 1996, p527j

Answer 349

The vagus nerve carries sensory (afferent) impulses of the Hering-Breuer reflex.[Miller,Anesthesia, 1994,pl!Sj

Answer 350

Juxtapulmonary-capillary receptors(! receptors) are located in the walls of the pulmonary capillaries or in the interstitium, hence the name. Jrecep- tors appear to be stimulated by pulmonary vascular congestion or an increase in pulmonary interstitial fluid volume, leading to tachypnea. The Jreceptors may also be responsible for the dyspnea encountered during pulmonary vascular congestion and edema secondary to left ventricular failure.[Levitzky, Pulm. Physiol. ?e. 2007 pp199-200; Lumb & Nunn, Nrmn's Applied Resp. Physiol. 6e. 2005 pp60-61)

Answer 351

C-fibers lie in close relationship to the pulmonary microcirculation and appear to innervate the pulmonary Jreceptors. The afferent pathway from the Jreceptors is the slow-conducting nonmyelinated (C) fibers in the vagal nerves.[Levitzky, Pulm. Physiol. ?e. 2007 pp199-200; Lumb & Nunn, Numz's Applied Resp. Physiol. 6e. 2005 pp60-61)

Answer 352

In chronic smokers, closing volume is increased. This means that during expiration, air trapping will be greater in the smoker compared with the nonsmoker.[Miller,Anesthesia, 1994,pp603-604;Authors!

Answer 353

The beneficial effects of cessation of smoking include: (1) improvement of ciliary function, (2) improvement of closing volume, (3} increase in mid- maximal expiratory flow, and (4) reduction in sputum production. These changes usually occur within 2-3 months following the cessation of smol

Answer 354

Smoking should be stopped for more than six weeks before the surgery. [Barash, Clinical Anesthesia, 1997, p448j

Answer 355

Smokers polycythemia is the increase ill hematocrit seen with chronic smoking. Smoking generates carbon monoxide (CO) which binds with high affinity to hemoglobin, forming carboxyhemoglobin. Elevated levels of carboxyhemoglobin lead to tissue hypoxia which stimulates erythro- poietin production from the kidneys. Elevated RBC production in re- sponse to increased erythropoietin, coupled with decreased plasma vol- ume, increases the hematocrit, leading to polycythemia. Fortunately, cessation of smoking for about 5 days usually restores plasma volume levels to near normal, which alleviates the polycythemia. [Stoelting & Dierdorf, Co-Existing, 4e, 2002, p485; Authors!

Answer 356

Cessation of smoking 12-24 hours preoperatively reduces carboxyhemo- globin levels and nicotine levels. Within 12 hours of cessation of smoking Pso increases from 23 mmHg to 26 mmHg and plasma carboxyhemoglo- bin are reduced from 6.5% to 1.1%. Unfortunately, short-term cessation of smoking does not decrease the incidence of postoperative morbidity and mortality. [Stoelting & Dierdorf, Co-Existing, 4e, 2002, p184-185]

Answer 357

The difference between ETCO, and P,CQ, (the ETCO,- P,CO, gradient) becomes larger in the chronic smoker. The increased difference between ETC0 2 and PaC02 reflects the degree of ventilation:perfusion mismatch- ing, in this case dead space ventilation. The greater the ETCOz- P~C02 gradient, the greater the ventilation:perfusion mismatch. [Barash, Clinical Anesthesia, 1997, p759; Authors]

Answer 358

The normal ETC02 - P,C02 gradient is 2-10 mm Hg. The larger than normal ETC02 - PaC02 gradient occurs because this long~time smoker has a ventilation:perfusion (V/Q) mismatch. [Barash, Clinical Anesthesia, 1997, p623; Authors]

Answer 359

Pulmonary compliance increases. Proteolytic enzymes are uninhibited and loss of elastic recoil (increased compliance) occurs over time in the smok- er. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p445]

Answer 360

Cough and copious amounts of sputum suggest chronic bronchitis. Cough with exertion and scant sputum could suggest emphysema. Chronic bron- chitis and emphysema are components of chronic obstructive pulmonary disease and require special considerations on the part of the anesthetist. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p445]

Answer 361

The diaphragm, which is innervated by the phrenic nerve, normally de- scends upon inspiration. The ipsilateral half-diaphragm innervated by the damaged phrenic nerve would ascend paradoxically during inspiration. [Miller, Anesthesia, 1994, p1714]

Answer 362

Mast cells. Human cutaneous mast cells can degranulate and release his- tamine; histamine, as you know, can trigger bronchoconstriction. [Ba- rash, Clinical Anesthesia, 1997, p1210; Morgan and Mikhail, Clinical Anesthesiology, 1996, p44]

Answer 363

Pa02 always falls because of the presence of an intrapulmonary shunt during one-lung anesthesia. If the patient has an F10 2 of 1.0, Pa02 might fall from 400 to 150 mmHg when the nondependent lung becomes unven- tilated. The Pa02 did not fall in this example into the hypoxemic range (the patient's hemoglobin is saturated), but it did fall. The P,C02 can generally be prevented from increasing by increasing ventilation, unless the shunt is severe. PaC02 may increase if the shunt is severe. When the diseased lung is excised, I\02 increases because shunt is decreased. [Miller, Anesthesia, 1994, pl705]

Answer 364

Colloid osmotic pressure of28 mmHg, the force holding water in the pulmonary capillaries, greatly exceeds hydrostatic pressure of 6-8 mmHg, which is the force driving water out of capillaries. This high colloid os- motic pressure provides a large safety factor for preventing pulmonary edema. [Stoelting, PPAP. 4e. 2006 pp743]

Answer 365

Pulmonary edema usually results from: (1) an increase in pulmonary hydrostatic pressure in the capillaries (left ventricular failure), or (2) an increase in permeability of the alveolar-capillary membrane. The most common cause of acute pulmonary edema is increased hydrostatic pres- sure secondary to left ventricular failure (cardiogenic pulmonary edema). [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp817-818; Stoelt- ing, PPAP. 4e. 2006 pp747]

Answer 366

Plasma proteins are diluted, so (I) colloid osmotic pressure in plasma decreases. In addition, (2) the hydrostatic pressure in capillaries will increase. Each change promotes the movement of water out of capillaries into tissues, thereby causing edema. [Guyton, TMP, 1996, pp306-307]

Answer 367

The detection of basilar crackles on auscultation is the traditional hall- mark of early pulmonary edema. A "butterfly" appearance or "whited- out" areas on chest radiographs support the diagnosis of pulmonary edema. [Nagelhout & Zaglaniczny, NA, 3'' ed., 2004, p550]

Answer 368

Acute airway obstruction such as lmyngospasm can lead to negative- pressure pulmonary edema. As the patient breathes against a closed glot- tis during laryngospasm, a more negative (greater magnitude) intratho- racic pressure is created. The increased intrathoracic pressure is transmit- ted to interstitial tissue, creating a greater hydrostatic pressure gradient between the interstitial space and the pulmonary circulation. The in- creased hydrostatic pressure gradient from blood to tissue will promote movement off1uidfrom the blood to the tissue and into the alveoli. [Stoelting & Miller, Basics, Se, 2007, p470; Nagelhout & Zaglaniczny, NA, 3'' ed., 2004, p421; Authors]

Answer 369

Negative-pressure pulmonary edema (NPPE) is treated by positive end- expiratoiy pressure (PEEP) ventilation. Diuretics and fluid restrictions are not required as the condition is self-correcting. [Yao & Artusio, Yao & Artusio's POPM, Se, 2003, p956l

Answer 370

It is true that diverse insults can trigger adult respiratory distress syn- drome (ARDS). Causes of ARDS include (l) shock, (2) fat or air embolus, (3) aspiration, (4) burns, (5) sepsis, (6) drug ingestion, (7) trauma, (8) uremia, (9) pancreatitis, (10) massive blood transfusion, (11) head injury, (12) cardiopulmonary bypass, (13) radiation of thorax, (14) drowning. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p818j

Answer 371

Hypoxemia is the major manifestation of Arms. Hypoxemia develops secondary to atelectasis and a right· to-left intrapulmonary shunt. [Stoelt- ing, Co-Existing, 1993, pl6l; Morgan and Mikhail, Clinical Anesthesiology, l996,pp818-819j

Answer 372

In ARIJS, (1) pulmonary compliance decreases, (2) work of breathing increases, and (3) edema develops. [Stoelting, Co-Existing, 1993, pl60; West, Respiratory Physiology, 1990, pi 59]

Answer 373

(l) Hypoxic hypoxia: P,O, is abnormally low (diffusional hypoxia is a form of hypoxic hypoxia); (2) anemic hypoxia: hemoglobin concentration is reduced, so 0 2 carriage by blood is inadequate; (3) hypoxia secondary to venous-to-arterial cardiac shunts; (4) histotoxic hypoxia: 02 delivery to tissues is adequate, but 0 2 use by cell is impaired (cyanide poisoning, toxicity, vitamin poisoning). (5) hypoxia secondary to pulmonary disease. [Guyton, TMP, 1996, p542]

Answer 374

Cyanide poisoning is the most common cause. [Guyton, TMP, 1996, p542]

Answer 375

Signs and symptoms of aspiration are: (I) wheezing, (2) coughing, (3) cyanosis, (4) pulmonary edema, (5) shock, and (6) hypoxemia. Hypox- emia is the earliest and most reliable sign of aspiration. [Miller, Anesthe- sia, 1994, ppl445-1446]

Answer 376

When (1) intragastric volume is greater than25 mL, and (2) intragastric pH is less than 2.5, the risk of aspiration pneumonitis increases. [Barash, Clinical Anesthesia, 1997, p976]

Answer 377

Adult respiratory distress syndrome (ARDS), also known as aspiration pneumonitis (Mendelson's syndrome), is the most serious complication ofaspiration.[Miller,Anesthesia, 1994,ppl441-1442]

Answer 378

Fluffy infiltrates may appear on the chest x-ray film immediately or with- in 24 hours of an event. [Barash, Clinical Anesthesia, 1997, p1294]

Answer 379

The affinity of carbon monoxide for hemoglobin is 200-250 times greater than that of oxygen. [Stoelting, Co-Existing, 1993, p536; Stoelting, PPAP. 4e. 2006 pp789]

Answer 380

The elimination half-time of carboxyhemoglobin is 250 minutes. 100% oxygen increases the dissociation of carbon monoxide from hemoglobin and decreases the elimination half-time to about 50 minutes. [Stoelting, Co-Existing, 1993, p536]

Answer 381

Carbon monoxide causes tissue hypoxia, despite high POz, because CO binds to hemoglobin with 200-times greater affinity than oxygen, thus reducing the oxygen-carrying capacity of the blood. That fraction of he- moglobin that is carboxyhemoglobin is unable to bind and transport oxygen, so this is a functional anemia. West, in fact, calls carbon monox- ide poisoning "anemic hypoxemia." [Longnecker, Tinker, and Morgan, PPA, 2e, 1998, p2166; Barash, Clinical Anesthesia, 4e, 2001, pl275; West, Respiratory Physiology, 6e, 2000, p76]

Answer 382

Loss ofsurfactant (due to prolonged exposure to oxygen radicals), leading to AIUJS (adult respiratory distress syndrome). [Miller, Anesthesia, 1994, p614]

Answer 383

There is a right-to-left shunt. Right-to-left shunts are quite refractory to oxygen therapy. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p425]

Answer 384

This is a shift of the heart and other mediastinal contents, usually after a pneumothorax or hemothorax. The mediastinum moves toward the side opposite the problem. [Miller, Anesthesia, 1994, p1684]

Answer 385

The shift occurs because the pneumothorax causes the intrapleural pres- sure to increase from a negative (subatmospheric) value to zero mmHg. This increased pressure forces the mediastinum away from the side with the pneumothorax and toward the side of the chest with a normal nega- tive intrapleural pressure. [Miller, Anesthesia, 1994, pl684]

Answer 386

There wil! be a doubling of the size of the pneumothorax when 50% ni- trousoxideisadministered.[Miller,Anesthesia, 1994,pp112-113J

Answer 387

Atelectasis most commonly occurs when pulmonary blood Oow absorbs air from unventilated alveoli. This is absorption atelectasis and occurs when secretions plug bronchi. [Stoelting, PPAP. 4e. 2006 pp747]

Answer 388

During spontaneous ventilation with an open pneumothorax, the collapse of the lung is accentuated during inspiration and, conversely, the col- lapsed lung expands during expiration. This is paradoxical breathing. [Miller, Anesthesia, 1994, p1684; Morgan and Mikhail, Clinical Anesthe- siology, 1996, pp454, 455]

Answer 389

Sarcoidosis is a systemic granulomatous disorder that can involve many tissues. It has a marked predilection for the thoracic lymph nodes and lungs. Restrictive lung disease is associated with the lung involvement. [Stoelting, Co-Existing, 1993, p163)

Answer 390

The patient with sarcoidosis can have his or her airway obstructed be- cause of the presence or hyperplastic lymphoid tissue. [Miller, Anesthesia, 1996, p1407J

Answer 391

The concern is the very thick mucus secretions. Retained secretions cause problems with pulmonary infections and airway obstruction and collapse. Cystic fibrosis patients may develop COPD with reduced vital capacity, lower l\02 and higher !\C02• FEV1 is reduced. They may have hyperactive cough. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p738; Stoelt- ing, Co-Existing, 1993, p147]

Answer 392

Intraoperatively, give higher F10 2, humidify gases, and use inhalation agents; keep patient normocarbic. Make sure patient is well hydrated preoperatively and post-operatively. Bleeding may occur because these patients do not absorb vitamin K well. It is a good idea to check liver enzymes pre-operatively. [Stoelting, Co-Existing, 1993, p147]

Answer 393

Avoid glycopyrrolate and atropine because they may make secretions thicker and harder to remove. [Stoelting, Co-Existing, 1993, pl47]

Answer 394

Obstruction of medium-sized airways. [Barash, Anesthesia, 1997, pp75l- 752]

Answer 395

The initial symptom of an asthma attack is a decrease in expiratory flow, as reflected by a decrease in forced expiratory volume in one second (FEV 1) or forced expiratory flow 25-75 (FEhs-7s), also known as midmaximal expiratory flow (MMEF). This decrease in expiratory flow is due to bron- choconstriclion and may be seen in otherwise symptomless asthmatics. Asymptomatic individuals may have an FEV1 of 60-80% of predicted and an FEF25 . , of 60-75% of predicted. [Longnecker et al., PPA, 1998, p237; Stoelting, Anesthesia and Co-existing Diseases, 1993, pl51; Authors]

Answer 396

Wheezing is the most common physical finding associated with an acute asthma attack. Cough and dyspnea may also be present. [Stoelting and Miller, Basics, 1994, p276; Stoelting, Anesthesia and Co-existing Diseases, 1993, p151]

Answer 397

Hypoxemia is a universal arterial blood gas finding during an asthma attack. Frank ventilatory failure with C02 retention (hypercarbia) is un- common; hypocarbia and respiratory alkalosis are also typical ABG find- ings during an asthma attack. co?. retention is a late finding indicating severe and prolonged airway obstruction, such as in status asthmaticus. [Yao & Artusio, Yao & Arlllsio's POPM, Se, 2003, p14; Stoelting & Dierdorf, Co-Existing, 4e, 2002, pl95]

Answer 398

Intubate the asthmatic patient if his or her FEV1 or peak expiratory flow rate is decreased to less than 25% of normal. Patients with these spirome- try results are at risk ofhypercarbia. The presence ofhypercarbia (PaCOz greater than 50 mmHg) despite aggressive bronchodilator and anti- inflammatory (corticosteroid) therapy may require tracheal intubation and mechanical support of ventilation. [Stoelting, Co-Existing, 1993, p154]

Answer 399

Drugs with beta-2 blocking actions such as propranolol and labetalol and drugs that release histamine such as trimethaphan, curare, atracurium, mivacurium, and morphine. [Morgan and Mikhail, Clinical Anesthesiolo- gy, 1996, pp350, 444; Stoelting, Co-Existing, 1993, ppl54-t57]

Answer 400

The goal is to depress hyperactive airway reflexes. Volatile anesthetics, synthetic opioids, and local anesthetics can be used to achieve this goal. [Barash Handbook, Clinical Anesthesia, 1997, pp233, 411-412]

Answer 401

The combination of (1) obstruction of small airways, (2) enlargement of air sacs (alveoli), (3) destruction oflung parenchyma, (4) loss of elasticity, and (5) closure of small airways is called COPD, which is a mixture of chronic bronchitis and emphysema. In COPD, there is progressive alveo- lar destruction with excessive mucous secretion accompanied by bron- choconstriction. [Hines, Stoelting's Co-existing. Se. 2008 pp168]

Answer 402

COPD is often seen in patients with a history of cigarette smoking. Ciga- rette smoking is the major predisposing factor to the development of COPD. [Stoelting Handbook, Co-Existing, 1993, p137; Morgan and Mi- khail, Clinical Anesthesiology, 1996, p445]

Answer 403

Physical examination of the patient reveals the "barrel chest". This term refers to the increased antero-posterior dimensions. This antero-posterior dimension may equal or exceed the lateral diameter. The anterior- poste- rior:lateral ratio may exceed 1.0. The sternum becomes prominent. There is kyphosis of the thoracic spine. The ribs remain elevated even after exhalation. There is little motion to the thoracic cage even after forced breathing. [Young and Crocker, 2e, p61; Morgan and Mikhail, Clinical Anesthesiology, 1996, pp445-447; Price and Wilson, Pathophysiology, 1992, p553l

Answer 404

In the patient with COPD, airway resistance increases because ofbronchi- ole obstruction, and pulmonary compliance increases. [Morgan and Mi- khail, Clinical Anesthesiology, !996, pp445-447; Stoelting, Co-Existing, !993, p137]

Answer 405

he primary mechanism of hypoxemia in obstructive pulmonaty disease is regional mismatch of ventilation and perfusion (V/Q mismatch). [Dunn, et al., Mass Gen Handbook, 7e, 2007, p35]

Answer 406

Blue bloaters are COPDers with severe chronic bronchitis. Blood oxygena- tion is not maintained. Cor pulmonale with resultant peripheral edema, heart failure, and pulmonary hypertension develop. [Morgan and Mi- ldJail, Clinical Anesthesiology, 1996, p445; Stoelting, Co-Existing, 1993, p138]

Answer 407

Chronic respiratory acidosis (increased H.. ) causes the patient to rely on peripheral chemoreceptor oxygen drive for breathing. [Barash, Clinical Anesthesia, !997, pl61]

Answer 408

Oxygen therapy can elevate PaC02 to dangerous levels in patients with C02 retention. Raising Pa02 > 60 mmHg can precipitate respiratory failure in these patients. Key concepts: patients with chronically elevated PaC02 have increased bicarbonate levels in the CSF; the elevated CSF bicarbonate ions reset the central medullary chemoreceptors and decrease the centralrespiratory drive sensitivity to C02• IfPa0 2 > 60, peripheral chemoreceptor respiratory drive diminishes and the patient will hypoventilate. Know and understand these concepts. [Morgan, Mikhail, and Murray, Clinicrd Anesthesiology, 3'' ed., 2002, p517; Barash, Clinical Anesthesia, 4e, 2001, p814; Authors]

Answer 409

Pink puffers (pursed~lip breathers) are COPDers with severe emphysema. Pulmonary emphysema is characterized by destruction of the lung tissue that results in loss of elastic recoil of the lungs. When dyspneic, these people often purse their lips to delay closure of the small airways. Note: compliance of the lungs increases when elastic recoil diminishes. [Morgan and Mll

Answer 410

An FEV1 ofless than 50% or carbon dioxide retention indicate the COPD patient is at increased risk for postoperative complications. [Barash Handbook, Clinical Anesthesia, 1997, p409; Morgan and Mikhail, Clinical Anesthesiology, 1996, p443]

Answer 411

Extubate the COPD patient while the depth of anesthesia is still sufficient to suppress hyperreactive airway reflexes. If it is unsafe to extubate prior to being fully awake because of the presumed presence of gastric contents, administer lidocaine IV to decrease airway stimulation. [Stoelting and Miller, Basics, 1994, p278]

Answer 412

Criteria for extubating the COPD patient are: (1) l\C02 less than 50 mmHg, (2) Pa02 greater than 60 mmHg on 50% F10 2, (3) maximal inspira" tory effort greater than 20 em H20, (4) normal pH (7.35-7.45), (5) respir- atory rate less than 30 breaths per minute, and (6) vital capacity greater than IS mL/kg. [Stoelting, Co-Existing, 1993, p178]

Answer 413

In the patient with obstructive lung disease, different lung units have their nitrogen diluted at different rates. Fast, well~ventilated alveoli cause a rapid decrease in expired nitrogen, whereas slow, poorly ventilated areas produceaprolongedwashoutofnitrogen.[Miller,Anesthesia, 1994, pp591-592,960-961]

Answer 414

Preoperative evaluation of the patient with (kypho)scoliosis should in- clude (1) pulmonary function tests, (2) arterial blood gases, and (3) elec- trocardiography (ECG). [Morgan eta!., Clinical Anesthesiology, 3"1 ed. 2002, p869; Yao, POPM, 5th ed. 2003, ppll00-1104]

Answer 415

Chronic bronchitis history includes chronic cough with production of sputum on most days for three months a year for at least two years. These patients are usually smokers. Chronic cough and sputum production are diagnostic for chronic bronchitis. [Miller, Anesthesia, 1994, pp958-959]

Answer 416

Tracheal stenosis is an extreme example of chronic obstructive pulmonary diseas- es (COPD). Tracheal stenosis typically develops after mechanical ventilation of the lungs that included prolonged translaryngeal tracheal intubation or tracheostomy. Tracheal stenosis becomes symptomatic when the lumen of the trachea (adult) becomes less than 5 mm diameter. [Hines, Stoelting's Co-existing. Se. 2008 ppl77]

Answer 417

Tracheal stenosis is an example of afixed extrathoracic obstruction. A representative flow-volume loop of fixed, extra thoracic obstruction is found in the reference text (Yao). [Yao & Artusio, Yao & Artusio's POPM, Se, 2003, p701; Authors.]

Answer 418

Pulmonary restrictive disease may be due to: (l) acute intrinsic restrictive lung disease such as ARDS, aspiration, or congestive heart failure; (2) chronic intrinsic restrictive lung disease such as sarcoidosis or drug- induced pulmonary fibrosis; (3) chronic extrinsic restrictive lung disease such as obesity, ascites, pregnancy, kyphoscoliosis, or neuromuscular disorders; and (4) disorders of the pleura and mediastinum. [Hines, Stoelting's Co-existing. Se. 2008 ppl80t]

Answer 419

Because scoliosis and kyphoscoliosis affect the vertebral column and thus the thoracic cage, they are restrictive diseases. The hallmark of restrictive pulmonary diseases from pulmonary function tests is a normal to slightly elevated FEV1/FVC, even though both FEV, and FVC are reduced ("re- stricted") from normal. [Hines, Stoelting's Co-existing. Se. 2008 ppl80- 18l]

Answer 420

With restrictive disease there is/are: (l) reduced lung volumes (decreased vital capacity, total lung capacity, functional residual capacity, etc.), (2) decreased chest wall or lung compliance, (3) decreased l\02 and increased PaC02 (with severe disease) secondary to ventilation:perfusion mismatch, and (4) pulmonary hypertension secondary to increased pulmonary vascular resistance from chronic hypoxia. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p739]

Answer 421

Restrictive disease. Twenty percent of patients with rheumatoid arthritis have pulmonary fibrosis. Pulmonary function tests show a restrictive disease pattern: decreased lung volumes, hypocapnia, and hypoxia. [Katz, Anesthesia and Uncommon Disease, p320]

Answer 422

unipolar neuron has a single, large extension from its ceH body (cell body= soma). A bipolar neuron has a short axon process arising from one side of the soma, and a short dendritic process arising from the oppo- site side. A pseudo-unipolar neuron has one short branch from the soma which splits into the axon and dendritic processes. Multipolar neurons comprise one axon and multiple dendritic processes. Multipolar neurons are the most common type in the brain and nervous system overall. [Au- thors]

Answer 423

Motor neurons are multipolar neurons. Recall that the majority of neu- rons in humans are multipolar. Sensory neurons, for example dorsal root ganglion nerves, are pseudo-unipolar neurons. Special sense neurons-·- those found in the eyes, ears, and nose-are bipolar neurons. NB: unipo- lar neurons are found in lower invertebrates, never in humans. [Nagel- hout & Zaglaniczny, NA, 3'" ed., 2004, p59l: Authors!

Answer 424

(1) The presence of a resting membrane potential, and (2) the presence of voltage-gated sodium channels permit neurons to respond to stimuli. [Guyton, TMP, !996, pp57-65]

Answer 425

lnside: potassium, 140 mM; Outside: sodium, 142 mM. [Guyton, TMP, 1996, p60]

Answer 426

The resting membrane potential of nerve and muscle is due primarily to the diffusion of potassium ions (K') out of cells through potassium leak channels. [Guyton, TMP, !996, p60-61; Barash, Clinical Anesthesia, 1997, p699]

Answer 427

The nerve action potential is associated first with opening of voltage- gated sodium channels (Na+ diffuses inward and produces massive depo- larization) when threshold is reached, which is followed quickly by open- ing of voltage-gated potassium channels (KI- diffuses out and the nerve repolarizes). [Guyton, 1MP, 1996, pp61-62; Barash, Clinical Anesthesia, 1997, p699]

Answer 428

The voltage-gated sodium channels snap open when the membrane of the axon depolarizes to threshold. [Guyton, TMP, 1996, p62]

Answer 429

The absolute refractory period is the time period following stimulation of an excitable tissue during which no additional action potential can be evoked no matter how intense the stimulus. Voltage-gated Na+ channels are closed in the inactivated state during the absolute refractory period. [Guyton, TMI', 1996, p70]

Answer 430

onduction speed is greater in fibers with larger diameters and in fibers that are myelinated. Thus, the most rapidly conducting fibers are those that are myelinated and have large diameters. [Guyton, TMP, 1996, p68]

Answer 431

Potassium (K+. [Guyton, TMP, !996, p62]

Answer 432

The necessary actor in causing both depolarization and repolarization of the nerve membrane during the action potential is the voltage-gated sodium channel. A voltage-gated potassium channel also plays an im~ portant role in increasing the rapidity of repolarization of the membrane. Repolarization begins with the closing of the voltage-gated sodium chan- nels, followed by opening of the voltage-gated potassium channels. Dur- ing early repolarization, the sodium channels are in the dosed, inactive conformation causing the cell to be absolutely refractory to stimulus. During the latter stages of repolarization, the voltage-gated sodium chan- nels have returned to the closed, resting conformation, and the cell is relatively refractory to stimulus. [Guyton, TMP. lle. 2006 pp62; Nagel- hout & Plaus, NA. 4th. 2009 pp660; Authors]

Answer 433

Glutamate is the most common excitatoty neurotransmitter in the central nervous system (CNS). Glutamate is an excitatory amino acid neuro- transmitter. [Stoelting, PPAP. 4e. 2006 pp674; Miller, Anesthesia. 6e. 2005 pp330]

Answer 434

The three ligand-gated ionotropic glutamate receptors of the CNS are: (1) N-methyi-D-aspartate = NMDA, (2) AMPA, and (3) kainate. When the ligand glutamate binds to these ionotropic receptors, a transmembrane, cation-selective channel opens, permitting influx ofNa+ and Ca2+ and efflux ofK+. Sodium is the main ion permeating the channel, leading to membrane depolarization. [Stoelting, PPAP. 4e. 2006 pp674; Guyton, TMP. 11e. 2006 pp601; Miller, Anesthesia. 6e. 2005 pp330]

Answer 435

Acetylcholine (ACh) is the transmitter of the efferent ann of the somatic nervous system. Efferent nerves of the somatic nervous system innervate skeletal muscle. [Guyton, TMP, 1996, pp87-90, 572]

Answer 436

Release of neurotransmitter from nerve terminals requires entry of calci- um ions. "Calcium comes in, neurotransmitter goes out." [Guyton, TMP, 1996, p570; Morgan and Mil

Answer 437

he release of neurotransmitter from nerve terminals increases with hypercalcemia or hypomagnesemia and decreases with hypocalcemia or hypennagnesemia. [Miller, Anesthesia, 1994, pp464,1603-1605]

Answer 438

Synthesis of acetylcholine (ACh) occurs in the cytoplasm of nerve tenni- nals. Choline acetyltransferase (ChAT) catalyzes the formation of ACh from the precursors (substrates) choline and Acetyl-CoA (from mito- chondria). [Stoelting, PPAP. 4e. 2006 pp701; Guyton, TMP. 11e. 2006 pp563J

Answer 439

The action of acetylcholine released from neurons is terminated by me- tabolism. Acetylcholinesterase, located in postsynaptic membranes near- by cholinergic receptors, breaks down acetylcholine to choline and ace- tate, and the enzyme is regenerated for further use. [Guyton, TMP. lie. 2006 pp87; Miller & Stoelting, Basics. Se. 2007 pp 136; Stoelting, PPAP. 4e. 2006 pp253]

Answer 440

Muscarinic receptors and nicotinic receptors are the two types of cholin- ergic receptors. Muscarinic receptors are found on target tissues opposite the parasympathetic postganglionic nerve endings. Nicotinic receptors at located at autonomic ganglia and at the neuromuscular junction. [Barash Handbook, Clinical Anesthesia, 1997, p120]

Answer 441

Up regulation is an increase in the number of receptors when the prevail- ing concentration of agonist is decreased. [Barash Handbook, Clinical Anesthesia, 1997, p121]

Answer 442

Denervation or trauma to skeletal muscle causes cholinergic nicotinic receptors to up-regulate. The nicotinic receptors spread beyond the motor end-plate and are called extrajunctional receptors. [Barash Handbook, Clinical Anesthesia, 1997, p152]

Answer 443

Down regulation is a decrease in the number of receptors occurring in response to an increased concentration of agonist. [Barash Handbook, Clinical Anesthesia, 1997, p121]

Answer 444

The first step in the termination of the adrenergic receptor stimulation by norepinephrine is the diffusion ofnorepinephrine awayfrom the adrener- gic receptor. [Authors]

Answer 445

The efficacy of norepinephrine is lost (the effects of norepinephrine are terminated) by: (1) reuptake (which accounts for 80% of the loss of effica- cy); (2) by metabolism (monoamine oxidase in tissues and catechol-0- methyltransferase in blood and liver); and (3) diffusion away from recep- tors. Note: The action of norepinephrine is terminated primarily by reuptake. [Stoelting and Miller, Basics, 1994, p35; Barash, Handbook. Se. 2006 pp796-797]

Answer 446

Norepinephrine accounts for 20% and epinephrine 80%, although the relative proportions can change under different physiologic conditions. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p643; Guyton, TMP, 1996, p776]

Answer 447

Monoamine oxidase (MAO) metabolizes amines within terminals of nerves. Neurotransmitter amines include norepinephrine, dopamine, and serotonin (5-hydroxytryptamine). [Guyton, TMP, 1996, p772]

Answer 448

Catechol-0-methyltransferase (COMT) degrades norepinephrine and epinephrine primarily as they circulate through the liver. [Guyton, TMP, 1996, p772J

Answer 449

(1) Sympathetic denervation, and (2) treatment with a sympathetic com- petitive antagonist (e.g., beta blockade) causes adrenergic receptors to up regulate). [Barash Handbook, Clinical Anesthesia, !997, p121]

Answer 450

The GABAA {gamma aminobutyric acid) receptor is a major channel for chloride ion movement. Because the opening of the channel is promoted by binding ofGABA-a chemical, the GABAA receptor is called a ligand- gated receptor. [Guyton & Hall, TMP, !Oe, 2000, pp517, 523; Nagelhout & Zaglaniczny, NA, 3'" ed., 2004, p106; Authors]

Answer 451

Chloride concentration, as you know, is greater in the serum (104-114 mEq/L) than in the cytoplasm (15-25 mEq/L). Movement through ion channels occurs by passive diffusion, down a concentration gradient. Therefore, chloride will move from serum to cytoplasm ("out to in") usual- ly resulting in an inhibitory postsynaptic potential. [Authors]

Answer 452

The ?ligand binding sites on the GABAA receptor are for: (1) GABA, (2) barbiturates, (3) benzodiazepines, (4) propofol, (5) steroids, (6) anesthet- ic/alcohol, and (7) picrotoxin. Notice that 5 of the 7 sites involve anesthet- ic agents! [Nagelhout & Zaglaniczny, NA. 3e. 2005 pp106-l07: Barash, Clinical Anes. 5e. 2006 pp336]

Answer 453

The C-1 vertebra is the atlas; the C-2 vertebra is the axis. [Ellis & Feldman, Anatomyfor Anaesthetists. 8e. 2004 pp99-100]

Answer 454

The spinal cord of the neonate ends at L3, while the spinal cord of most adults ends at Ll. In 30% of adults the spinal cord ends at Tl2 while in 10% it may extend to L3. [Barash, Clinical Anesthesia, !997, p647; Black and Chambers, Essential Anatomy for Anesthesia, 1997, ppll6~117]

Answer 455

The conus medullaris is the blunt, tapering tip of the spinal cord. The pia alone continues from the conus medullaris and after piercing the dural sac, continues with a covering of dura to the coccyx, forming the filum terminalis. The filum tenninalis is comprised of the pia and dura matere. [Ellis & Feldman, Anatomy for Anaesthetists. 8e. 2004 ppl20; Authors]

Answer 456

L3 is the highest; T6 is the lowest. [Barash, Clinical Anesthesia, 1997, p646l

Answer 457

The anterior longitudinal ligament runs along the front of the vertebral bodies from C2 to the upper sacrum and the posterior longitudinal liga- ment extends along the posterior surfaces of the vertebral bodies. These ligaments link the individual vertebrae together and confine the interver- tebral discs as well. [Ellis & Feldman, Anatomy for Anaesthetists. Se. 2004 ppl15-116]

Answer 458

Canal width is greatest at about L5. Canal width is about 17 mm in the thoracic region and increases to 25 mm in cervical canaL Canal width is about 22 mrn at Ll and enlarges progressively to 27 mm at LS. !Brown, Regional Anesthesia and Analgesia, 1996, p52]

Answer 459

The cauda equina (horse's tail) is the collection of nerves that travel down the vertebral canal below the termination of the spinal cord. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p212]

Answer 460

Afferent (sensory) nerves enter the spinal cord via the dorsal (posterior) root. Efferent (motor) nerve fibers exit the spinal cord via the ventral (anterior) root. [Stoelting, PPAP. 4e. 2006 pp669]

Answer 461

The anterior horn of the spinal cord (gray matter) contains the cell bodies of alpha and gamma motor neurons, which innervate skeletal (voluntary) muscle. Main Point: Motor neurons arise from the anterior horn of the spinal cord. [Ellis & Feldman, Anatomyfor Anaesthetists. Be. 2004 ppl29]

Answer 462

The principle inhibitory neurotransmitter in the spinal cord is glycine. Recall that the major inhibitory neurotransmitter in the CNS in general is gamma-amino butyric acid (GABA). Read each and every word carefully in a question about this topic. [Stoelting, PPAP, 4e, 2006, p675 [Stoelting, PPAP. 4e. 2006 pp675]

Answer 463

Cerebrospinal fluid (CSF) has a positive pressure. The epidural space has a negative (subatmospheric) pressure. [Ellis & Feldman, Anatomy for Anaesthetists. Be. 2004 pp122, 125]

Answer 464

The hydrostatic pressure of cerebrospinal fluid is positive (5-15 mmHg), which means that fluid should leak out of a needle when its tip is placed in the subarachnoid space. [Guyton, TMP, 1996, p7B7]

Answer 465

The epidural space is filled with loose connective tissue, adipose tissue, nerve roots, blood vessels and lymphatics. [Ellis & Feldman, Anatomyfor Anaesthetists. Be. 2004 ppl21]

Answer 466

The epidural space lies between the meninges and the sides of the verte- bral canal. The epidural space is bounded cranially by the foramen mag- num, caudally by the sacrococcygeal ligament, anteriorly by the posterior longitudinal ligament, laterally by the vertebral pedicles, and posteriorly by the liganzentum jlavum. [Barash, Clinical Anesthesia, 4e, 2001, p689j

Answer 467

The epidural space between the ligamentum flavum and the dura mater is largest at L2-L3, approximately 4-6 mm. [Barash, Clinical Anesthesia, 200!, p6B9]

Answer 468

The potential space between the dura mater and arachnoid mater is called the subdural space. (Cf. MemoryMaster 2005, IIIH6:Q29) [Barash, Clini- cal Anesthesia, 4e, 200!, p691]

Answer 469

The subarachnoid space lies between the arachnoid and pia maters. The subarachnoid space is filled with cerebrospinal fluid. [Barash, Clinical Anesthesia, 4e, 2001, p691, 69!0

Answer 470

The spinal nerves and rootlets course through the subarachnoid space. [Barash, Clinical Anesthesia, 4e, 2001, p69I]

Answer 471

Myelinated A-beta fibers carry touch and pressure, as well as propriocep- tion modalities. Some texts also state that A-beta fibers are motor to muscle spindles, and some texts omit proprioception, but these state- ments are controversial.[Nagelhout & Zaglaniczny, NA, 3rd ed., 2004, p982t; Guyton & Hall, TMP, 11e, 2005, pp576-577; Stoelting, PPAP. 4e. 2006 pp672-673]

Answer 472

Bfibers (preganglionic sympathetic motor nerves) and sympathetic C fibers (postganglionic sympathetic nerves) cany vasomotor, visceromo- tor, sudomotor, and pilomotor signals. A-gamma fibers are efferents to the muscle spindle of skeletal muscle. [Barash, Clinical Anesthesia, 1997, pp415, 421]

Answer 473

A-alpha and A-beta nerves carry both afferent and efferent information to skeletal muscle and joints. [Barash, Clinical Anesthesia, 1997, p415]

Answer 474

A-alpha fibers carry both motor and sensory information. lBarash, Clini- cal Anesthesia, t997, p415]

Answer 475

The hypothalamus plays a major role in activating the sympathetic nerv- ous system. The posterior and lateral nuclei of the hypothalamus are sympathetic and their stimulation results in the discharge of the sympa- tho-adrenal system. [Collins, Physiologic and Pharmacologic Bases of Anesthesia, 1996, p281]

Answer 476

Sympathetic preganglionic nerves originate in the lateral horns (specifi- cally, the intermediolateral horns of the gray matter) of the thoracolumbar ('fl-L3} segments of the spinal cord. Preganglionic sympathetic nerves, which arise in the intermediolateral horn of the gray matter, pass out o f the spinal cord via the anterior roots. [Guyton, TMP, 1996, pp769-770; Black and Chambers, Essential Anatomy for Anesthesia, 1997, pl46]

Answer 477

Tl-L2 (adults) or Tl-L3 (neonate to adolescence). Because of these cord segment origins, the sympathetic system is also known as the thoracol- umbar system. ]Stoelting, PPAP. 4e. 2006 pp696; Barash, Clinical Anes. Se. 2006 pp2770

Answer 478

he adrenal (suprarenal) meduHa is the only organ innervated by sympa- thetic preganglionic neurons. [Guyton, 1MP. 1le. 2006 pp750; Ellis & Feldman, Anatomyfor Anaesthetists. Be. 2004 pp22l]

Answer 479

The sympathetic ganglia are the: (I) paravertebral, including superior, middle and inferior cervical, (2) celiac, (3} superior mesenteric, and (4) inferior mesenteric. [Miller, Anesthesia, 1994, p528]

Answer 480

The pelvic viscera in men and women-the urogenital organs, the colon, and the rectum-are supplied by afferent fibers from the lumbar sympa- thetic chain. The superior hypogastric plexus is a retroperitoneal structure that isformed by confluence ofthe bilateral lumbar sympathetic chains; it is situated between the bodies of the LS and Sl vertebrae. The pelvic pain caused by either inflammatory diseases or cancer can be relieved by inter- ruption of bilateral sympathetic pathways, which can be achieved with a superior hypogastric plexus block. [Miller, Anesthesia. 6e. 2005 pp2201; Barash, Clinical Anes. 5e. 2006 pp739]

Answer 481

Postganglionic sympathetic neurons arise from autonomic ganglia. Most sympathetic postganglionic neurons arise from the paravertebral ganglia. [Stoelting, PPAP. 4e. 2006 pp696]

Answer 482

Together, the inferior cervical ganglion and the first thoracic ganglion form the stellate ganglion. In 80% of the population, the inferior cervical and first thoracic ganglia are fused. [Miller, Anesthesia, 1994, p528]

Answer 483

Motor (efferent). [Miller, Anesthesia, 1994, p528, 531-33]

Answer 484

Sympathetic nerves arising from TS-'1'12 innervate organs in the abdomen including most of the intestinal tract, liver, kidneys, and adrenal medulla, Sympathetic nerves arising from Ll and L2 innervate the bladder, colon and rectum. [Guyton, TMP, 1996, p770; Miller, Anesthesia, 1994, p528]

Answer 485

Norepinephrine is the transmitter released from sympathetic postgangli- onic neurons to viscera, heart, lungs, smooth muscle, salivary glands; acetylcholine is released from sympathetic postganglionic neurons to sweat glands and piloerector muscles. [Miller, Anesthesia, 1994, pp528, 531-533; Guyton, 1MP, 1995, p771]

Answer 486

Preganglionic parasympathetic nerves arise from nuclei of cranial nerves III, VII, IX and Xin the brainstem and also from sacral segments 2-4 (S2- S4) of the spinal cord. Owing to these origins, the parasympathetic system is also known as the craniosacral division. [Ellis & Feldman, Anatomyfor Anaesthetists. 8e. 2004 pp215, 229-230; Stoelting, PPAP. 4e. 2006 pp696]

Answer 487

About 75% of all parasympathetic nerve fibers are found in the vagal nerves (cranial nerve X), which passes to the entire thoracic and most abdominal regions of the body. [Guyton, TMP, 1996, p771]

Answer 488

Those fibers that release acetylcholine are cholinergic. These are the sym- pathetic and parasympathetic preganglionic neurons, the parasympathet- ic postganglionic neurons and the sympathetic postganglionic neurons that innervate sweat glands and piloerector muscles. [Guyton, TMP, 1996, p77l]

Answer 489

Acetylcholine (ACh) produces simultaneous bradycardia and hypoten- sion. [Miller, Anesthesia, 5th ed. 2000, pp533]

Answer 490

Muscarinic receptors, one of two types of cholinergic receptors, are found in tissues innervated by the parasympathetic postganglionic neurons. [Stoelting, PPAP. 4e. 2006 pp701]

Answer 491

The antimuscarinic drugs, also commonly referred to as anticholinergics (atropine, scopolamine, and glycopyrrolate} interrupt muscarinic trans- mission at tissues innervated by the parasympathetic nervous system. [Stoelting, PPAP. 4e. 2006 pp266]

Answer 492

Nicotinic receptors, the second type of cholinergic receptors, are found on cell bodies of sympathetic and parasympathetic postganglionic neurons, on chromaffin cells of the adrenal medulla, and on the motor end-plate of the skeletal neuromuscular junction. [Guyton, TMP, 1996, p773j

Answer 493

Nondepolarizing neuromuscular blockers interrupt nicotinic receptor transmission at the neuromuscular junction. The ganglionic blocker, trimethaphan (Arfonad}, as well as two nondepolarizing neuromuscular blockers (d-tubocurarine and metocurine} interrupt nicotinic receptor transmission at the autonomic ganglia. [Stoelting, PPAP. 4e. 2006 pp215]

Answer 494

Blockade of the stellate ganglion with local anesthetic produces Horner's syndrome. In some cases, Horner's syndrome is a side-effect of intersca- lene or supraclavicular approaches to the brachial plexus. [Barash, Clini- cal Anesthesia, 1997, p679]

Answer 495

Ptosis, miosis, anhydrosis, nasal congestion, vasodilation, and increased facial temperature are signs and symptoms of Horner's syndrome. They occur on the ipsilateral (same) side. [Barash, Clinical Anesthesia, 1997, p679]

Answer 496

Reuptake. [Barash Handbook, Clinical Anesthesia, 1997, p120]

Answer 497

The two known forms of monoamine oxidase (MAO) are type A (MAO- A) and type B (MAO-B). MAO-A metabolizes serotonin, dopamine, epi- nephrine, and norepinephrine. MAO-B metabolizes tyramine (found in cheeses, red wine, and beer) and phenylethylamine. Dopamine is metabo- lized by both MAO-A and MAO-B. [Goodman and Gilman, PBT, 1996, p250; Morgan and Mikhail, Clinical Anesthesiology, 1996, p512]

Answer 498

Monoamine oxidase type A (MAO-A} is an enzyme present in the central nervous system, adrenergic nerve endings, liver and gastrointestinal tract. This enzyme is involved in metabolic degradation (by oxidative deamina- tion} of epinephrine, serotonin (5-hydroxytryptamine, 5-HT), dopamine, and norepinephrine. [Stoelting, PPAP. 4e. 2006 pp701]

Answer 499

The olfactory (I) and optic nerve (II) are not true cranial nerves. [Ellis & Feldman, Anatomyfor Anaesthetists. 8e. 2004 pp235-236]

Answer 500

Superior rectus: Supraduction of orbit ("look up"); innervation by CN III (oculomotor}. Inferior rectus: Infraduction of orbit ("look down"); inner- vation by CN III- oculomotor. Medial rectus: Adductiun of orbit ('look inward'); innervation by CN III- oculomotor. Lateral rectus: Abduction of orbit ('look outward"}; innervation by CN V I - abducens Superior oblique: Intorsion, depression or orbit ("look in and down"); innervation by CN I V - trochlear. Inferior oblique: Extorsion, elevation or orbit ("look out and up"}; innervation by CN III- oculomotor [Nagelhout & Plaus, NA. 4th. 2009 pp943; Authors]

Answer 501

The trigeminal nerve (CN V) provides sensory innervation to the face. The trigeminal nerve has three branches: the ophthalmic, the maxillary, and the mandibular. The ophthalmic and maxillary are purely sensoiy, where- as the mandibular nerve is a mixed (motor & sensory) nerve. [Barash, Clinical Anesthesia, Se, 2006, pp721-722; Morgan, Mikhail, and Murray, Clinical Anesthesiology, 4e, 2006, pp375-376]

Answer 502

The anterior branch of the mandibular nerve provides motor innervation to the muscles of mastication (chewing, "moves the mandible"). The posterior branch of the mandibular ne1ve provides sensory innervation to the lower teeth and gums ("feels the mandible, inside and out"). [Barash, Clinical Anesthesia, Se, 2006, pp721-722; Morgan, Mikhail, and Murray, Clinical Anesthesiology, 4e, 2006, pp375-376; Authors]

Answer 503

The trigeminaluerve (cranial nerve V). [Guyton, TMP, 1996, p487]

Answer 504

The facial nerve (VII) supplies the muscles of facial expression. [Ellis & Feldman, Anatomyfor Anaesthetists. 8e. 2004 pp267]

Answer 505

The facial nerve (CN VII) provides special sens01y innervation to the anterior two-thirds of the tongue (taste} and general sensory innervation to the tympanic membrane, external auditory meatus, soft palate, and part of the pharynx. [Morgan, Mikhail, and Murray, Clhzical Anesthesiolo- gy,4e,2006,p378]

Answer 506

The vestibular branch of cranial nerve VIII controls equilibrium. [Guyton, TMP, 1996, p705)

Answer 507

Motor innervation to the tongue is provided by the hypoglossal nerve (cranial nerve XII). [Ellis & Feldman, Anatomy for Anaesthetists. 8e. 2004 pp283-284]

Answer 508

The hypoglossal nerve is a motor nc1ve controlling the extrinsic and intrinsic muscles of the tongue. Damage to the nerve can relax the tongue causing it to fall back and obstruct the airway. [Hollinshead, Textbook o[ Anatomy, 1974, p875]

Answer 509

Found also in the medulla are centers for vomiting, coughing, and swal- lowing. [Price and Wilson, Pathophysiology, 1992, p731l

Answer 510

Stimulation of the reticular activating system (RAS) increases alertness. Diffuse electrical stimulation of the RAS causes immediate and marked activation of the cerebral cortex and will even cause a sleeping individual to awaken instantaneously. [Guyton, TMP, 1996, p706l

Answer 511

Delta waves are seen during deep sleep or deep anesthesia. Theta waves are seen during physiologic sleep, during general anesthesia in adults, and during hyperventilation in awake children. [Barash Handbook, Clinical Anesthesia, 1997, p381I

Answer 512

Alpha waves are seen during the resting awake state with eyes closed or during sedation. Most beta waves appear during activation of the central nervous system (during mental concentration) and during light anesthe- sia. [Guyton, TMP, 1996, p764: Barash Handbook, Clinical Anesthesia, 1997, p381l

Answer 513

Delta waves occur during deep anesthesia. [Barash Handbook, Clinical Anesthesia, 1997, p381l

Answer 514

Cerebral blood flow is 750 mL!min, 50 mL/100 g/min, and 15% percent of cardiac output. [Guyton, IMP, !996, p783: Barash, Clinical Anesthesia, 1997, p702: Morgan and Mikhail, Clinical Anesthesiology, 1996, p477l

Answer 515

EEG evidence of cerebral ischemia appears when cerebral blood flow has fallentoabout50%ofnormal.[Miller,Anesthesia, !994,p7l3I

Answer 516

The two determinants of cerebral blood Oow are cerebral vascular re- sistance and cerebral perfusion pressure. Cerebral blood flow (CBF) is inversely proportional to cerebral vascular resistance (CVR) and directly proportional to cerebral perfusion pressure (CPP). CBF = CPP/CVR. [Barash, Clinical Anesthesia, 1997, p702l

Answer 517

Cerebral perfusion::: MAP-ICP. Note: MAP is mean arterial pressure and ICP is intracranial pressure. [Morgan and Mikhail, Clinical Anesthesiolo- gy, 1996, p478l

Answer 518

If right atrial pressure (RAP) is abnormally elevated and greater than intracranial pressure (ICP), cerebral perfusion pressure"" MAP-RAP, not MAP-lCP. [Faust, !99!, p327: Stoelting and Miller, Basics, !994, p332)

Answer 519

95 rnmHg. Cerebral perfusion pressure in this case is MAP-ICP. Thus, cerebral perfusion pressure= 110- 15 = 95 rnrnHg. [Authors]

Answer 520

Changes in PaC02> Pa02 or temperature alter cerebral vascular resistance. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p478]

Answer 521

l\C02• Cerebral blood flow is proportional to PaC02 when PaC02 varies between20 and 80 rnrnHg. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p478]

Answer 522

Cerebral blood flow is increased by hypercarbia (the cerebral vasculature dilates) and is decreased by hypocarbia (the cerebral vasculature con- stricts). [Barash, Clinical Anesthesia, 1997, p702]

Answer 523

Hypocapnia associated with hyperventilation causes constriction of cere- bral blood vessels and a decrease cerebral blood flow. Hypercapnia associ- ated with hypoventilation causes dilatation of cerebral blood vessels and an increase in cerebral blood flow. [Guyton, TMP, 1996, p783; Stoelting, Co-Existing, 1993, p185]

Answer 524

The relationship between cerebral blood flow and l\C02 is nearly linear for PaC02;?.20 mmHg. Thus a cerebral blood flow will decrease 1 mL! IOOg/min for each mmHg decrease in PaC02 down to about 20 mmHg. Accordingly, cerebral blood flow will increase 1 mL!lOOg/min for each 1 mmHg increase in P,CO,. [Stoelting & Dierdorf, Co-Existing, 4e, 2002, p238]

Answer 525

CO2. IGuyton, TMP, 1996, p783]

Answer 526

Ketamine dilates the cerebral vasculature and increases cerebral blood flow by 50-60%. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 3'" ed. 2002, p560]

Answer 527

Cerebral blood flow and cerebral metabolism vary directly with tempera- ture. An increase in temperature causes an increase in cerebral blood flow and cerebral metabolism. A decrease in temperature causes a decrease in cerebral blood flow and cerebral metabolism. [Morgan and Mikhail, Clinical Anesthesiology, 1996, pp478, 479]

Answer 528

There is a 7% decrease in cerebral blood flow for each one degree centi- grade decrease in temperature. [Morgan and Mikhail, Clinical Anesthesi- ology, 1996, p478]

Answer 529

Cerebral metabolic rate (CMR) decreases by 6 to 7percent for each I°C decrease in temperature. [Miller, Arwsthesia, 2000, p697]

Answer 530

No. Alterations in cerebral vascular resistance occur when pH of the cerebrospinal fluid is altered (which occurs quickly with changes in Pa. C02). Since ions including H+ and HCQ3- do not cross the blood-brain barrier, neither acute metabolic acidosis nor acute metabolic alkalosis alters cerebral blood now. [Morgan and MikhaiL Clinical Anesthesiology, 1996, p478]

Answer 531

Cerebral blood now will increase substantially only when P,O, falls below 50 mmHg. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p478]

Answer 532

Changing perfusion pressure does not normally alter CBF, because CBF is auto regulated over the range of mean arterial pressure from about 50 to 150 mmHg. [Barash, Clinical Anesthesia, 1997, p703; Morgan and Mi· khaiL Clinical Anesthesiology, 1996, p478]

Answer 533

Autoregulation of CBF ceases when mean arterial pressure (MAP) falls below 50 mmHg or rises above a mean arterial pressure (MAP) of 150 mmHg. The range for autoregulation of cerebral blood flow is 50 to 150 mrnHg. Note: Miller emphatically emphasizes that the autoregulatory range for cerebral blood flow is 70 to 150 mmHg. Morgan and Mikhail suggest the autoregulatory range is 50-175 mmHg. [Barash, Clinical Anesthesia, 1997, p703; Miller, Anesthesia, 2000, p699]

Answer 534

The range of pressures for autoregulation increases. Whereas the normal autoregulatory range for cerebral blood flow is about 50-150 mmHg, the autoregulatory range may be 90-190 in the hypertensive patient. Point: The range of pressures for autoregulation increases in the patient with hypertension. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p478]

Answer 535

Autoregulation may be absent in diseased or traumatized regions of brain. For example, autoregulation is absent in tissue surrounding brain tumors, in the acute phase of subarachnoid hemorrhage, and after brain trauma. [Miller, Anesthesia, 1994, p1492]

Answer 536

Global ischemia occurs when the entire brain is unperfused, such as would occur during cardiac arrest. In focal ischemia, which may occur with a stroke or a trauma (blow to the head), there are three zones of brain tissue: ( l) an inner zone, which is ischemic and the tissue is necrotic (dead), (2) the penumbra, a zone of tissue which surrounds the ischemic core of tissue (the penumbra is perfused by collateral vessels and is par- tial! y, not completely, starved for blood), and (3) normally perfused tis· sue. Inverse steal (Robin Hood effect) can increase blood flow to, and survival of, tissue in the penumbra. [Barash, Clinical Anesthesia, 1997, p705]

Answer 537

Focal ischemia develops when intracranial pressure is between about 25 and 55 mm Hg. Global ischemia occurs whep intracranial pressure ex- ceeds approximately 55 mm Hg. [Miller, Anesthesia, 1994, pl910]

Answer 538

The anesthetist can hyperventilate the patient or reduce metabolism by giving an agent such as a barbiturate. [Barash, Clinical Anesthesia, 1997, p703]

Answer 539

A shunting of blood from adequately perfused cerebral tissues to com- promised, potentially ischemic areas is referred to as the Robin Hood effect. Other names for the Robin Hood effect are reverse steal and inverse steal. [Barash, Clinical Anesthesia, 1997, p702]

Answer 540

Hypocarbia. Hypocarbia constricts cerebral vessels in nonischemic tis~ sues. Blood is diverted from nonischemic to ischemic (maximally dilated} regions. [Davison, Eckhardt, and Perese, Mass General, 1993, p364]

Answer 541

Hyperventilation decreases l\C02• Decreased PaC02 produces increased cerebrovascular tone, which decreases blood flow to nonischemic areas of the brain. Blood vessel diameters in ischemic areas remain unchanged; they remain maximally dilated because of the presence of local metabolic factors so blood flow to ischemic tissue increases (inverse steal, reverse steal or Robin Hood effect). [Barash, Clinical Anesthesia, 1997, p702]

Answer 542

Increased PaC02 in a hypoventilated patient causes a decreased cerebro- vascular tone and a corresponding increase in blood flow in nonischemic regions of the brain. Cerebrovascular tone in ischemic areas remains unchanged, but blood flow decreases because blood is diverted to non- ischemic regions (steal effect or luxUJy perfusion). [Barash, Clinical Anes- thesia, 1997, p702]

Answer 543

The Circle of Willis provides collateral blood flow to the brain if a major vessel carrying blood to the brain becomes obliterated. [Authors]

Answer 544

Intracranial pressure varies directly with cerebral blood flow: the greater the cerebral blood flow, the greater the intracranial pressure. [Stoelting and Miller, Basics, 1993, p333]

Answer 545

Normally, intracranial pressure is less than IS mmHg (range: 5-15 mmHg). [Stoelting and Miller, Basics, 1994, p333]

Answer 546

Intracranial volume is: (1) 80% brain matter and intracellular water; (2) 12% blood; and (3) 8% cerebrospinal fluid. A change in the volume of any of these compartments will cause a pressure change. [Morgan and Mikhail, Clinical Anesthesiology, !996, p480]

Answer 547

erebrospinal fluid passes through the foramen magnum into the spinal cord.[Miller,Anesthesia, 1994,pl909]

Answer 548

Papilledema is edema and hyperemia of the optic disk. It is usually associ- ated with an increased intracranial pressure (ICP). [Guyton, TMP, 1996, pp787-788; Stoelting, PPAP. 4e. 2006 pp68l]

Answer 549

Papilledema involves cranial nerve II (optic nerve). The dura of the brain extends as a sheath around the optic nerve. When the pressure increases in the cerebrospinal fluid, it also increases in the optic nerve sheath. [Guy- ton, TMP, 1996, p787]

Answer 550

There are three ICP waveforms: (1) A waves, which are also known as plateau waves; (2) B waves; and (3) C waves. Band C ICP waves are of lesser magnitude than A (plateau} waves, are related to the respiratory pattern and blood pressure, and are not useful in guiding therapy or predicting outcome. [Barash, Clinical Anesthesia, 1997, p636; Miller, Anesthesia, 1994, pl9!1]

Answer 551

The plateau ICP waveform (A waveform) is found in patients with elevat- ed ICP. The plateau waveform consists ofan additional increase in ICP for 5 to 20 minutes. The plateau waveform (A waveform) results from an abrupt increase in cerebral blood volume in regions where cerebral blood flow is decreased. The decrease in regional cerebral blood flow is due to brain swelling, venous obstruction, or obstruction of cerebrospinal fluid (CSF) flow. [Barash, Clinical Anesthesia, 1997, p636; Miller, Anesthesia, 1994, pl9ll]

Answer 552

The frontal lobe rests on the anterior cranial fossa. The temporal lobe rests on the middle cranial fossa. The brainstem and cerebellum rest on the posterior cranial fossa. The brainstem herniates when intracranial pressure becomes excessive. [Hollinshead, Textbook of Anatomy, 1994, p804]

Answer 553

When intracranial pressure (ICP} exceeds 30 nun-flg, cerebral blood flow progressively decreases and a vicious cycle is established: ischemia pro- duces cerebral edema, which in turn increases ICP, and further precipi- tates ischemia. If this cycle remains unchecked, progressive neurologic damage or catastrophic herniation may result. [Nagelhout & Plaus, NA. 4th. 2009 pp67!]

Answer 554

Signs and symptoms of increased intracranial pressure (ICP} include: (1} headache, (2} nausea and vomiting, (3} blurred vision, (4) unilateral pupillary dilation, (5) papi!ledema, (6) cranial nerve III (oculomotor nerve) paralysis (inability to adduct the eye), (7) cranial nerve VI (abdu- cens nerve) paralysis (inability to abduct the eye), (8) hypertension, (9) bradycardia, (lO) irregular respirations, (11) altered level of con- sciousness (somnolence to unconsciousness), and (12) seizures. Note: The combination of hypertension, bradycardia, and irregular respirations is referred to as Cushing's triad. Cushing's triad (hypertension, bradycardia, irregular respirations) is a late sign of an elevated intracranial pressure. [Miller, Anesthesia, 2000, p1895; Barash, Clinical Anesthesia, 1997. p717; Stoelting and Miller, Basics, 1994, p334]

Answer 555

Thirty-five mm Hg is substantially higher than the upper limit for normal intracranial pressure of 15 mm Hg. You will see any or all of the signs of increased intracranial pressure including Cushing's triad (hypertension, bradycardia, irregular respirations). [Miller, Anesthesia, 2000, p 1895; Barash, Clinical Anesthesia, 1997, p717; Stoelting and Miller, Basics, 1994, p334; Miller, Anesthesia, 1994, p644; Authors]

Answer 556

Dehydrate the brain rapidly with mannitol (0.25-1 g/kg IV) or furo- semide (0.5-1 mg/kg IV alone or 0.15-0.3 mg/kg IV in combination with mannitol); (2) administer a corticosteroid such as dexamethasone, which is effective for localized cerebral edema surrounding tumors; (3) hyper- ventilate to a P,C02 of25-30 mm Hg; (4) restrict fluids; (5) elevate the head to 30 degrees to facilitate cerebral venous drainage; (6) administer a potent cerebral vasoconstrictor such as thiopental, etomidate, or propofol; (7) control blood pressure; (8) cool the patient to 34 degrees C to protect the brain during surgery. [Barash Handbook, Clinical Anesthesia, 1997, pp387-388]

Answer 557

( 1) Hyperventilation has an intermediate onset for reducing ICP, and may last up to 4-6 hours. (2) Mannitol rapidly decreases elevated intracranial pressure, acting within 10-15 minutes and lasting up to 2 hours. (3) Furosemide also acts rapidly, but is less effective than mannitol, requiring up to 30 minutes for effective reduction of elevated ICP. (4) Corticosteroid treatrnent of increased ICP may require many hours or days before re- duced ICP is apparent. The advantage of corticosteroids is that they may restore the blood-brain barrier. [Hurford, Mass Gen Handbook, Ge, 2002, pp404-406; Morgan, Mikhail, and Murray, Clinical Anesthesiology, yJ ed., 2002, pp568-569; Barash, Handbook, 4e, 2001, pp396-397]

Answer 558

Mannitol is the osmotherapeutic agent of choice for decreasing intracra- nial pressure (ICP) and reducing brain swelling. [Miller, Anesthesia, 1994, p1914; Stoelting, Handbook. 2e. 2006 pp508-509]

Answer 559

Mannitol, a sugar similar to glucose, effectively reduces intracranial pres- sure because it cannot permeate the cerebral capHlary. Mannitol is thus capable of exerting a high osmotic pressure across the cerebral capillary wall. [Stoelting, PPAP. 4e. 2006 pp49l-492]

Answer 560

A dose of mannitol of0.25-l.O g/kg is especially effective in rapidly decreasing intracranial pressure. 0.25-1.0 g/kg is the initial dose. Larger doses do not reduce intracranial pressure more effectively than this dose. [Morgan and Mikhail, Clini- cal Anesllwsiology, 2c, 1996, p492; Stoelting, Handbook. 2e. 2006 pp509]

Answer 561

Mannitol may cause: (1) pulmonary edema and cardiac decompensation (in patients with poor left ventricular function) due to mannitol-induced increase in intravascular fluid volume; (2) rebound increase in intracrani- al pressure (ICP), if the blood-brain barrier is not intact; (3) hypovolemia; (4) hypernatremia; (5) hyponatremia (yes, both hyper- and hypo- natremia); (6) hyperkalemia; [controversial] (7) acidosis; (8) dehydration; and, (9) acute hemodilution. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 3'" ed., 2002, p674; Omoigui, The Anesthesia Drugs Hand- book, 3"1ed., 1999, p253]

Answer 562

No. Mannitol is an inert 6-carbon sugar that is neither metabolized nor converted, so it should not alter blood glucose levels. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 3'" ed., 2003, pp250-253]

Answer 563

Hyperventilation of the lungs to maintain PaC02 between 25 and 30 mmHg is the mainstay therapy for acute or subacute management of increased intracranial pressure. [Barash Handbook, Clinical Anesthesia, 1997, pp718-719]

Answer 564

No. Cerebral vascular resistance and cerebral blood flow normalize (half- life is about 6 hours) during sustained hyperventilation and hypocapnia in normal subjects and stroke victims; therefore, the efficacy of continu- ous hyperventilation to a fixed PaC02 for decreasing the intracranial pres- sure diminishes as its use is prolonged. [Miller, Anesthesia, 1994, pl915]

Answer 565

Suitable agents are those that constrict the cerebral vasculature, thereby decreasing cerebral blood flow and intracranial pressure. Barbiturates, benzodiazepines, propofol, and etomidate have this action. Opioids also decrease intracranial pressure so long asPaC02 is not pennitted to in- crease. [Stoelting and Miller, Basics, 1993, p334]

Answer 566

DSW or any other dextrose-containing solution should be avoided. Hy- perglycemia has been shown in animals to exaggerate neurological defi- cits after incomplete neurological ischemia. Give 2 mL of isotonic crystal- loid (preferably 0.9% sodium chloride) for each 3 mL of urine formed. [Davison, Eckhardt, and Perese, Mass General, 1993, p379]

Answer 567

Do not administer ketamine to a patient with an elevated intracranial pressure. Ketamine increases cerebral blood flow and intracranial pres- sure. [Barash Handbook, Clinical Anesthesia, 1997, pp379-382]

Answer 568

The specific gravity of cerebrospinal fluid is 1.005 (range: 1.003-1.009). [Stoelting and Miller, Basics, 1993, p168; Stoelting, PPAP. 4e. 2006 pp680]

Answer 569

Compared with plasma, CSF has: (1) 7% more sodium; (2) 30% less glu- cose; (3) 40% less potassium; (4) much less protein; (5) higher magnesi- um; (6) higher chloride, and (7) higher W (lower pH). [Stoelting, PPAP. 4e. 2006 pp680j

Answer 570

The rate of formation of cerebrospinal fluid is 0.35 mL/min, or 21 mL!hour, or 500-700 mL!day. [Barash, Clinical Anesthesia, 1997, p703; Morgan and Mikhail, Clinical Anesthesiology, 1996, p480]

Answer 571

Cerebrospinal fluid is formed by the choroid plexus (highly vascular folds of pia). [Barash, Clinical Anesthesia, 1997, p703; Morgan and Mikhail, Clinical Anesthesiology, 1996, p480]

Answer 572

The choroid plexus is composed of blood vessels located in the lateral, third, and fourth ventricles. Specifically, the choroid plexus is found in the temporal horn of each lateral ventricle, the posterior portion of the third ventricle, and the roof of the fourth ventricle. [Ellis & Feldman, Anatomy for Anaesthetists. 8e. 2004 pp124]

Answer 573

This channel is the aqueducl of Sylvius, or cerebral aqueduct. [Guyton, TMP, 1996, p780]

Answer 574

CFS leaves the fourth ventricle through the single foramen of Magendie (found medially) and the two foramina ofLuschka (located laterally) and enters the cerebral and spinal subarachnoid space. Remember: "m" for Magendie and medial, "l" for Luschka and lateral. [Ellis & Feldman, Anatomyfor Anaesthetists. Be. 2004 ppl24; Authors]

Answer 575

CSF is found between the pia and the arachnoid. [Miller, Anesthesia, 1994, p15061

Answer 576

The structures that reabsorb most of the cerebrospinal fluid are the arachnoid villi. [Guyton, TMP, 1996, p786]

Answer 577

The volume of cerebrospinal lluid is 150 mL. [Guyton, TMP, 1996, p787j

Answer 578

The volume of cerebrospinal fluid (CSF) in the subarachnoid space is 25- 35 mL. [Hurford, Mass Gen Handbook, 6e, 2002, p234; Cousins & Bridenbaugh, Neural Blockade, 3'' ed., 1998, p208]

Answer 579

Interference with cerebral spinal fluid drainage results in hydrocephalus, or water in the cranial vault. [Stoelting, PPAP. 4e. 2006 pp680]

Answer 580

The aqueduct ofSylvius is the most common site of obstruction leading to hydrocephalus. [Guyton, TMP, 1996, p786]

Answer 581

In communicating hydrocephalus, cerebrospinal fluid (CSF) flows readily through the cerebral ventricles into the subarachnoid space, but reabsorp- tion ofCSF is blocked so CSF volume and pressure increase; in non- communicating hydrocephalus, fluid does not flow out of one of the cerebral ventricles because the exit is blocked, so CSF volume and pres- sure increase behind the block. [Guyton, TMP, 1996, p788]

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