Memory Master Flashcards
“What causes the first (Sl) heart sound?
What causes the second (S2) heart sound?”
“The first heart sound is caused by closure of the mitral and tricuspid
valves at the beginning of systole. The second heart sound is caused by
closure of the aortic and pulmonic valves (semilunar valves”
“An S3 heart sound is an indicator of what
condition?”
“An S3 heart sound (gallop rhythm) during mid-diastole is most often
heard in the context of congestive heart failure. [Duke, Secrets. 2e. 2000
ppl94]”
“What is the postulated mechanism(s) that
produces an S3 heart sound?”
“The third heart sound (S3) is thought to reflect a flaccid and inelastic
condition of the heart during diastole (Stoelting). Guyton says: ““a logical
but unproven explanation of this sound (S3) is oscillation of blood back
and forth between the walls of the ventricles initiated by inrushing blood
from the atria.”” We favor Guyton’s explanation. [Guyton, TMP. lle. 2006
pp270; Stoelting, PPAP. 4e. 2006 pp755]”
“Describe the murmurs heard, and specify
the stethoscope location where they are best
heard, if the patient has mitral stenosis. If
the patient has mitral regurgitation.”
“Mitral stenosis is recognized by the characteristic opening snap that occurs
early in diastole and by a rumbling diastolic murmur, best heard with
the chest piece placed over the cardiac apex. The cardinal feature of mitral
regurgitation is a blowing holosystolic (heard throughout systole) murmur,
best heard with the chest piece placed over the cardiac apex. The
murmur typically radiates into the axilla as well. [Hines, Stoelting’s Coexisting.
Se. 2008 pp32, 24]”
“;I Describe the murmurs heard, and specify
the stethoscope location where they are best
heard, if the patient has aortic stenosis. If the
patient has aortic regurgitation.”
“Aortic stenosis is recognized by its characteristic systolic murmur, best
heard in the second right intercostal space (over the aortic arch) with
transmission into the neck. Aortic regurgitation is recognized by its diastolic
murmur, best heard along the left sternal border. [Hines, Stoelting’s
Co-existing. Se. 2008 pp37, 39]”
How is aortic valvular regurgitation graded?
“The severity of aortic valvular regurgitation is graded angiographically
after contrast injection into the aortic root as follows: 1 +,small amount of
contrast material enters left ventricle during diastole, but is cleared from
left ventricle during systole; 2+, left ventricle is faintly opacified by contrast
media during diastole and not cleared during systole; 3+, left ventricle
is progressively opacified; 4+, left ventricle is completely opacified
during the first diastole and remains so for several beats. Note: recognize
there are four grades for aortic valvular regurgitation reflecting the severity
of the problem. [Miller, Anesthesia, 2000, pl770]”
“What is the problem if the newborn has a
systolic and a diastolic murmur?”
“The patient with patent ductus arteriosus has both a systolic and diastolic
murmur. The murmur is more intense during systole than during diastole,
so that the murmur waxes and wanes with each beat of the heart, creating
a machinery murmur. [Guyton, TMP. lle. 2006 pp275]”
“A patient is in congestive heart failure, and
you are listening to the heart sounds. What
should be heard? Where on the chest should
this be heard?”
“An S3 gallop should be heard if the patient is in congestive heart failure.
Left-sided S3 is best heard with the bell piece of the stethoscope at the left
ventricular apex during expiration and with the patient in the left lateral
position. Right-sided S3 is best heard at the left sternal border or just beneath the xiphoid and is increased with inspiration. [Miller, Anesthesia,
1994, pl760; Waugaman, PPNA, p584; Harrison’s Principles oflnternal
Medicine, lle, pp868-869]”
“What dysrhythmia is most commonly observed
in the patient with a mitral valve
lesion, either stenosis or regurgitation?”
“Atrial fibrillation. [Barash, Clinical Anes. Se. 2006 pp903; Hines, Stoelting’s
Co-existing. Se. 2008 pp33-34]”
“With atrial flutter, atrial fibrillation, or
junctional rhythms a portion of! eft ventricular
Oiling is lost; what percent of! eftventricular
end-diastolic volume is normally
contributed by atrial contraction (““kick”” or
““priming””)?”
“Passive diastolic filling usually accounts for 75% ofleft-ventricular filling,
with atrial contraction causing an additional25% filling of ventricles.
Stoelting states: ““During the latter portion of diastole, the atria contract to
deliver about 30% of the blood that normally enters the ventricle during
each cardiac cycle.”” [Guyton, TMP. lle. 2006 ppl07-108; Stoelting,
PPAP. 4e. 2006 pp75l]”
“What is the normal range for stroke volume
in mL in a 70 kg male? Write the formula for
stroke index (SI). What is the normal range
for stroke volume index?”
“The normal range for stroke volume is 60-90 mL. Stroke index is stroke
volume (SV) divided by body surface area (BSA) in meters squared. SI =
(SV)/(BSA). The normal range for stroke volume index is 40-60
mL!beat/m2• [Barash, Clinical Anes. Se. 2006 pp86l]”
“Define ejection fraction, and state its normal
range.”
“Ejection fraction (EF) is the ratio of stroke volume (end-diastolic volume
minus end-systolic volume) to end-diastolic volume. EF::: SV/EDV =
(EDV -ESV)/EDV. The normal range is 0.6-0.8, or 60-80%. [Barash,
Clinical Anes. Se. 2006 pp86It]”
“What are the two determinants of cardiac
output? If stroke volume is 70 mL and heart
rate is 70 beats/min what is the cardiac
output?”
“Stroke volume and heart rate are the two determinants of cardiac output.
Cardiac output::: stroke volume x heart rate. With a stroke volume of 70
mL and a heart rate of70 beals/min, cardiac output is 70 mL/beat x 70
beats/min= 4,900 mL/min::: 4.91iters/min. [Authors; Barash, Clinical”
“What is cardiac index? What is the normal
range for cardiac index?”
“Cardiac index (CI) is cardiac output (CO) divided by body surface area
(BSA) in meters squared. CJ:::CO/BSA. Normal cardiac index ranges from
2.5-4.0 I!min/m2
• [Barash, Clinical Anes. Se. 2006 pp86lt; Guyton, TMP.
lle. 2006 pp232]”
“When the ventricle fills more during diastole,
more blood is ejected during systole.
Whose law is this?”
“Starling’s (or Frank-Starling’s) law of the heart. [Guyton, TMP, 1991,
pl06]”
“Starling’s law of the heart relates ventricular
filling during diastole to what?”
“Starling’s law of the heart relates ventricular filling during diastole to the
amount of blood ejected during systole. The greater the ventricular filling
during diastole (i.e., the greater the preload), the greater the quantity of
blood pumped into the aorta during systole. [Guyton, 1MP. lle. 2006
ppll2]”
"Describe the process that causes ventricular myocyte relaxation (lnsitropy)."
“Ventricular myocyte contraction requires increased intracellular calcium.
Thus, for the ventricular myocyte to relax, intracellular calcium must be
reduced back to resting levels. Calcium is sequestered in the sarcoplasmic
reticulum (SR) through energy-dependent processes. [Guyton, TMP. 1le.
2006 pp106)”
“Name the organs in the vessel rich group
(VRG). What percent of cardiac output goes
to each of these organs?”
“The brain, kidney, liver, lungs, heart. digestive tract, and endocrine tissues
are organs of the vessel rich group (VRG). These are the wellperfused
organs. 25% of the cardiac output goes to the liver; 4-5% (225
mL!min) to the heart; 15% to the brain; 20% to the kidneys; and 100% to
the lungs. [Guyton, TMP. lle. 2006 pp196t; Stoelting, PPAP. 4e. 2006
pp31; Morgan, eta!., Clin. Anesth. 4e. 2006 pp158)”
“What percent of the right heart’s cardiac
output traverses the pulmonary circulation?
Bronchial circulation?”
“One-hundred percent (100%) of the blood pumped by the right heart
traverses the pulmonary circulation and 0% traverses the bronchial circulation.
[Guyton, TMP. lie. 2006 pp485: Stoelting, PPAP. 4e. 2006 pp741)”
“What percent of the left heart’s output
traverses the bronchial circulation? Vessels
delivering blood to the bronchial circulation
arise from what arteries?”
“1-2% of the left heart’s output traverses the bronchial circulation. The
bronchial circulation arises from the thoracic aorta and intercostal aiteries.
[Stoelting, PPAP. 4e. 2006 pp741; Guyton, TMP. 11e. 2006 pp483)”
“In words, describe where isovolumetric
relaxation occurs on the left ventricular
pressure-volume loop.”
“Isovolumetric relaxation occurs from closure of the aortic valve to opening
of the mitral valve on the left ventricular pressure-volume loop. [Nagelhout
& Zaglaniczny, NA. 3e. 2005 pp436)”
”;(In words, describe where isovolumetric
contraction occurs on the left ventricular
pressure-volume loop.”
“lsovolumetric contraction occurs from closure of the mitral valve to opening
of the aortic valve on the left ventricular pressure-volume loop.
[Nagelhout & Zaglaniczny, NA. 3e. 2005 pp436)”
“What is the range of normal pressures in
each chamber of the heart?”
“Right atrium, 1-8 mmHg; right ventricle, !5-30/0-8 mmHg: left atrium,
2-12 mmHg: left ventricle, 100-140/0-12 mmHg. [Dunn, eta!., Mass.
Gen. 7e. 2007 pp402t)”
“What is the normal value for mean pulmonary
artery pressure? For pulmonary artery
systolic and diastolic pressures?”
“Mean pulmonary artery pressure normally is about 16 mmHg. Systolic/
diastolic pressures average 25/8 mm Hg. [Guyton, TMP. lle. 2006
pp484)”
“What is the normal range of values for pulmonary
artery occlusion pressure (PAOP),
also called pulmonary capillary wedge pressure
(PCWP)?”
“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)”
“What is the normal value for mean systemic
arterial pressure?”
“Normal mean arterial pressure ranges from 80-120 mmHg. [Barash,
Handbook. 5e. 2006 pp510, 972[”
What is the normal value for mean systemic arterial pressure?
Normal mean arterial pressure ranges from 80-120 mmHg. [Barash, Handbook. 5e. 2006 pp510, 972[
How do you estimate mean arterial pressure (MAP)?
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]
- If arterial blood pressure is 150/90, what is themeanarterialpressure(MAP)?
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]
What causes a change in blood pressure when d1anging the patient’s position?
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]
What are the two determinants ofarterial blood pressure? What law applies?
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]
- What most determines systemic vascular resistance?
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]
- What is normal range of values for systemic vascular resistance (SVR)?
The normal range for SVR is 1200-1500 dynes•sec•cm-s. [Barash, Hand- book. 5e. 2006 pp510, 972; Miller, Anesthesia. 6e. 2005 ppl328t]
How do you calculate systemic vascular resistance (SVR)?
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]
If mean arterial pressure is 80 mmHg, cardi- ac output 91iters/min, and central venous pressure 8 mmHg, calculate SVR.
SVR ~ [(MAP-CVP)/CO] x 80 ~ [(80-8)/9] x 80 = 640 dynes•sec-cm 5• [Authors]
In what segment of the systemic circulation is resistance greatest? The greatest decrease in blood pressure in the arteria! tree occurs where?
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]
What maintains systemic arterial blood pressure during diastole?
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]
What is pulse pressure? The patient’s arteri- al blood pressure is 160/90 mmHg: calculate the patient’s pulse pressure.
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]
What are two determinants of pulse pres~ sure? What changes can increase pulse pressure? Decrease pulse pressure?
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]
Define compliance. When peripheral vessels become less compliant (as would occur in the patient with atherosclerosis), does pulse pressure increase or decrease?
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]
Where are arterial baroreceptors located? To what do the baroreceptors respond?
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]
When blood pressure increases and the baroreceptors are stimulated, what happens reflexly (baroreceptor reflex) to myocardial contractility, venous tone, heart rate, sys~ temic vascular resistance (SVR), and blood pressure?
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]
Where are venous haroreceptors located, how do they work, and what is the reflex called?
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]
What happens to heart rate during inspira~ tion and during expiration in the spontane- ously breathing individual? Explain.
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]
What nerves carry the afferent and effer~ ent signals of the Bainbridge reflex? What does the Bainbridge reflex help prevent?
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
What happens to arterial blood pressure during inspiration in the spontaneously breathing individual? Why?
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]
How does a normal dorsalis pedis arterial waveform differ from the waveform found in the aorta in the supine or prone patient?
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]
Angiotensin I is converted to angiotensin II in what organ?
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]
Which is the more potent vasoconstrictor, angiotensin II or antidiuretic hormone (ADH)?
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]
The arterial system contains what percent of the total blood volume? The capillary system contains what percent of the total blood volume? What percent of total blood volume is found in the venous segment of the circu- lation?
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]
What is the function of the capillaries?
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]
How are oxygen and nutrients delivered from capillary blood to the tissues? What law applies?
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]
Changes in any of what four factors may promote peripheral edema?
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]
What is the colloidal osmotic pressure in mml-Ig of albumin? How much does albu- min contribute to the total colloid osmotic pressure of the plasma?
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]
What percentage of cardiac output is delivered to the highly-perfused organs (heart, lungs, brain, kidneys, and liver)?
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]
What determines blood flow through an organ or tissue? This is an application of what law?
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]
In genera!, blood flow to a tissue or organ is most directly related to what? Explain.
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]
What are the two most important determi- !Hnts of oxygen delivery to the tissues?
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]
Describe the effect of hypercapnia on the cerebral vasculature and on the systemic vasculature.
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]
How does hypercarbia affect pulmonary vascular resistance?
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
With hypercapnia is there hypertension or hypotension?
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]
How does severe acidosis alter pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR)?
Acidosis increases pulmonary vascular resistance (PVR) and decreases systemic vascular resistance (SVR). [Longnecker eta!., PPA, 1998, p961; Barash, Clinical Anesthesia, 2001, p878]
When during the cardiac cycle is blood flow lhrough the coronary arteries greatest? Explain.
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]
Describe the flow pattern in the left and right coronary arteries during systole and diastole.
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]
State the resting coronary blood flow in: (I) mL/minute, (2) as a percent of cardiac out- put.
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]
What is the venous saturation of coronary blood? In other words, what is the oxygen extraction level of coronary blood?
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]
What is the normal range for coronary perfusion pressure?
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]
How is coronary perfusion pressure (CorPP) calculated?
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]
A patient has a blood pressure of 130/80 mm Hg, heart rate of 120, and PCWP of30 mm Hg. What is his coronary perfusion pres- sure?
CorPP ~ AoDP- LVEDP. Since PCWP reflects l.VEDP, AolJP ~ 80-30 ~ 50 mmHg. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p333]
Changes in either of what two parameters will decrease coronary perfusion pressure?
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]
What most determines coronary blood ilow?
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]
Explain how an increase in coronary blood flow is achieved when the work of the heart increases?
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]
What theory relates to the metabolic control of the coronary circulation?
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]
What is the most potent local vasodilator substance released by cardiac cells?
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]
State the oxygen consumption rate of the heart.
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]
What four factors determine myocardial oxygen demand?
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]
Arrange afterload, preload, and heart rate in an order that shows greatest to least effect on myocardial oxygen consumption?
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]
What cardiovascular parameter correlates
best with myocardial oxygen consumption?
Heart rate. [Stoelting, PPAP. 4e. 2006 pp754]
What five factors determine myocardial oxygen supply?
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]
Describe the distribution of alpha·! and beta-2 receptors in the coronary vasculature. What responses do these receptors mediate?
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]
In the left ventricle, where is the density of capillaries greatest: base, apex, subepicardi- um, or subendocardium? What is the signif- icance of this?
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]
What layer of ventricle, the subendocardium (inner layer) or the subepicardium (outer layer), is most vulnerable to ischemia? Why?
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]
escribe myocardial preconditioning.
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]
escribe the cellular mechanisms mediat- ing myocardial preconditioning.
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]
What anesthetic agents can trigger or modu- late the myocardial preconditioning response? Wbat anesthetic agent can antagonize the effect?
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]
Define excitability.
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]
Define depolarization.
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]
Define hyperpolarization.
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]
Define conductivity.
Conductivity is the ability to transmit action potentials from cell to adja- cent cell. [Bullock and Rosenthal, Pathophysiology, 1992, pp436-439]
Does a change in membrane potential from -70 mV to -60 mV represent depolarization or hyperpolarization?
Depolarization occurs if the membrane potential decreases from -70 mV to -60 mV. [Guyton, TMP, 1996, pp63-65]
If the membrane potential becomes more negative (e.g., if the membrane potential shifts from -70 mV to -80 mV) has depolar- ization or hyperpolarization occurred?
Hyperpolarization occurs if the membrane potential increases from -70 mV to -80 mV. [Guyton, TMP, 1996, pp67-68]
Define rhythmicity.
Rhythmicity is the ability of cells to generate action potentials automati- cally on a rhythmic, or regular, basis. [Guyton, TMP. 11e. 2006 pp116- 117]
Rhythmicity is the ability of cells to generate action potentials automati- cally on a rhythmic, or regular, basis. [Guyton, TMP. 11e. 2006 pp116- 117]
Identify the only site through which cardiac impulses can be transmitted from the atria to the ventricles. Normally, the pause at this site is how long?
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]
In what segment of the cardiac conduction system is the action potential conducted slowest? Fastest?
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]
What is the function of the Purkinje system? How is this function accomplished?
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)
Tissues in the conduction system of the heart depolarize spontaneously in phase 4. What tissue in the heart’s conduction system has the fastest phase 4 depolarization? In~ termediate? Slowest? What is the im- portance of a fast phase 4 depolarization?
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)
What are the intrinsic firing rates of the sinoatrial (SA) node, atrioventricular (AV) node, and the Purkinje network?
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
Compare and contrast the parasympathetic and sympathetic innervation of the heart. Is the heart equally innervated by both auto- nomic divisions?
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
Where does the parasympathetic innerva- tion of the heart arise?
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)
What cardiac electrical event is represented by the P wave? The T wave?
The P wave occurs when the atria depolarize. The T wave occurs when the ventricles repolarize. [Guyton, TMP. lie. 2006 pp !24-!25)
What cardiac electrical event is represented by the PR interval?
The action potential is passing through the atrioventricular (AV) node. [Guyton, TMP. lie. 2006 ppl25)
What cardiac electrical event is represented by the QT segment?
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
What ion controls the resting membrane potential, and what ion controls threshold?
Potassium ions control the resting potential, and calcium ions control threshold. [Guyton, 1MP. lie. 2006 pp59-65j
Does acute hypokalemia increase or de- crease the excitability of nerve and cardiac muscle? Explain.
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
Does acute hyperkalemia increase or de- crease the excitability of nerve and cardiac muscle? Explain.
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]
Does hypocalcemia increase or decrease the excitability of nerve and cardiac muscle? Explain.
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]
Does hypercalcemia increase or decrease the excitability of nerve and cardiac muscle? Explain.
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]
An increase in calcium concentration de- creases excitability, or stabilizes, the cardiac cell? An increase in concentration of what other ion decreases excitability of, or stabi- lizes, the cardiac cell?
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]
What are the characteristics of sick sinus syndrome?
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]
Why is atrial fibrillation particularly dan- gerous in a patient with Wolff-Parkinson- White (WPW) syndrome?
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]
The patient has Wolff-Parkinson-White syndrome. Atrial fibrillation develops. How should the atrial fibrillation be treated? What drugs should be avoided in this situa- tion?
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]
Is it necessary to treat any of the following before surgery: First degree heart block; Mobitz type I (Wenckebach) second degree heart block; Mobitz type II second degree heart block?
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]
How does central venous pressure (CVP) compare with pu!monaty capillary wedge pressure (PCWP) if pulmonary hypertension is present?
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]
What promotes concentric hypertrophy? Identify two conditions that cause concen- tric left ventricular hypertrophy. Identify two conditions that cause concentric right ventricular hypertrophy.
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]
What happens to the ventricular wall with a chronically elevated afterload? What is the advantage of this adaptation? What happens to chamber size?
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]
Does concentric hypertrophy decrease wa!l tension?
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]
s left ventricular hypertrophy associated with mitral stenosis? Is right ventricular hypertrophy associated with mitral stenosis?
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]
What promotes eccentric hypertrophy? What happens to the size of the left ventricu- lar chamber when there is eccentric hyper- trophy? Identify three factors that will pro- mole left ventricular eccentric hypertrophy.
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]
How is diastolic function of the left ventricle assessed? What is the BEST indicator of left ventricular diastolic dysfunction
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]
What monitoring is indicated for managing the patient with a history of congestive heart failure secondary to diastolic dysfunction?
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]
What valve problem (aortic stenosis, aortic regurgitation, mitral stenosis, mitral regur~ gitation) may be associated with both a systolic and a diastolic murmur?
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]
What valve problem (aortic stenosis, aortic regurgitation, mitral stenosis, mitral regur- gitation) may be associated with both a systolic and a diastolic murmur if the patient has a heart rate of 100 and a blood pressure of 135/45?
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]
A patient with mitral valve stenosis presents with: HR of 100; blood pressure 80/50; PCWP, 18; and CVP, 12. How is this treated?
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]
Hemodynamic goals for a patient with val- vular heart disease involve consideration of what five cardiac parameters?
(1) Heart rate, (2) rhythm, (3) preload, (4) afterload (determined by SVR), and (5) contractility. [Kirby and Gravenstein, Clinical Anesthesia Practice, !994, pp117l-1173]
What are five hemodynamic goals for the patient with aortic stenosis?
(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]
Why is it important to maintain afterload in the patient with aortic stenosis?
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]
What are five hemodynamic goals for the patient with mitral stenosis?
(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]
State the hemodynamic goals for the patient with mitral stenosis in a way that is easy to remember.
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)
Are the hemodynamic goals for the patient with aortic stenosis similar to those for the patient with mitral stenosis?
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]
What are the hemodynamic goals for the patient with aortic insufficiency (regurgitaH tion)?
(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]
What are the hemodynamic goals for the patient with mitral insufficiency (regurgita- tion)?
(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]
- What is more important in the patient with mitral regurgitation: (a) maintaining or slightly increasing preload, or (b) decreasing afterload (SVR)?Both strategies are appropriate for managing tlw patient with mitral stenosis, but decreasing afterload (SVR) is the most important of the two. [Authors]
Both strategies are appropriate for managing tlw patient with mitral stenosis, but decreasing afterload (SVR) is the most important of the two. [Authors]
Are the hemodynamic goals for the patient with aortic insufficiency (regurgitation) similar to those for patients with mitral insufficiency (regurgitation)?
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]
- What muscle relaxants should be given to the patient with mitral valve prolapse?
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]
What is the cause of ll·ISS (idiopathic hyper- trophic subaorlic stenosis)? IHSS was for- merly known as what?
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]
- What is the goal for hemodynamic man- agement of the patient with idiopathic hy- pertrophic subaortic stenosis (IHSS)?
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
What four changes increase the outflow obstruction in the patient with idiopathic hypertrophic subaortic stenosis (IHSS)?
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]
What drugs are acceptable for maintaining hemodynamic status of the patient with idiopathic hypertrophic subaortic stenosis (IHSS)? Why?
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
What is the first treatment for hypotension in the patient with idiopathic hypertrophic subaortic stenosis (IHSS)? Second treat- ment?
( 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]
What drugs are avoided in the patient with idiopathic subaortic stenosis?
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]
Which of the following agents would most likely not be used in the patient with idio- pathic hypertrophic subaortic stenosis: fentanyl, halothane, phenylephrine, or pro- pranolol?
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]
What is the most ominous sign of coronary artery disease?
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]
- Of the following diagnostic tests, which is best for determining coronary artery dis- ease: resting ECG, Holter monitor ECG, stress (exercise) ECG, stress (exercise) thai- limn testing?
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]
What identifies myocardial ischemia during surgery?
On the ECG, ST segment depression of greater than l mm provides evi- dence of myocardial ischemia. [Stoelting and Miller, Basics, 1994, p254J
What is the primary goal of anesthesia in the patient with coronary artery disease (CAD)?
The primary goal is to maintain cardiovascular stability, which involves avoiding hypotension, hypertension, and tachycardia. [Stoelting, Co- Existing, 1993, p13]
What hemodynamic change (hypotension, hypertension, or tachycardia) is most detri- mental in the patient with coronary artery disease? Why?
Tachycardia. Tachycardia increases myocardial metabolism and may also decrease coronary blood flow. [Stoelting, Co-Existing, 1993, pl3]
During surgery the patient, whose angina has been controlled with antianginal medi- cation such as nitroglycerin, suddenly be- comes hypertensive and tachycardic. There is no ECG evidence of myocardial ischemia. What actions should be taken?
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]
A patient with coronary artery disease un- dergoes non-cardiac surgery. Blood pressure gradually increases to 155/115, cardiac output is 3.0 Llmin, and PCWP is 22 mmHg. What would be an appropriate antihyper- tensive medication?
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]
What are the two most significant risk fac- tors identified by the Goldman Cardiac Risk Index for noncardiac surgery?
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]
What is the incidence of peri-operative reinfarction for non-cardiac surgery at 0-3 months, 4-6 months, and after 6 months for a patient with a history of myocardial infarc- lion?
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]
Elective surgery is best not performed until how much time has elapsed after a myocar- dial infarction? Why?
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]
Which types of surgery cause the biggest risk of perioperative reinfarction?
Intrathoracic or intra-abdominal operations lasting longer than 3 hours. [Stoelting and Miller, Basics, 1994, p250]
A patient has not had a previous myocardial infarction. What is the likelihood that this patient will experience an infarction in the perioperative period?
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
Your patient experienced a myocardial infarction three months ago and now re- quires non-cardiac related surgery requiring a general anesthetic. Which of the following wil! most increase his/her chances of rein- farction: labile hemodynamics; moderate increase in heart rate over baseline; stable angina?
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]
How long does it take an infarcted area of the heart to fully heal?
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]
Identify appropriate maintenance agents for a patient with coronary artery disease. What agent would you avoid?
f the patient has good ventricular function, volatile agents are generally used. If the patient has poor ventricular function (ejection fraction
What is the concern aboul using nitrous oxide on a patient with coronary artery disease?
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
What are three signs of poor right ventricu- lar function?
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
In general, what causes left ventricular diastolic dysfunction? What specific events can cause left ventricular diastolic dysfunc- tion during anesthesia and surgery?
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]
How is left ventricular compliance assessed?
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]
What Swan-Ganz catheter data suggest left ventricular failure?
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
What is the hallmark of decreased cardiac reserve (poor ventricular function)? What is the best indicator of a person’s cardiac re- serve?
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
ist five (5) compensatory responses in the patient with cardiac failure.
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
What is the hallmark of decreased cardiac reserve (poor ventricular function)? What is the best indicator of a person’s cardiac re- serve?
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]
What is cardiac tamponade? Is the hypoten- sion that accompanies cardiac tamponade due to a change in preload, or afterload, or contractility?
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]
What is the principal hemodynamic alteration with cardiac tamponade~ What is Becks triad?
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]
What are the first signs of cardiac tam- ponade?
A decrease in arterial blood pressure (hypotension) with reflex tachycar- dia. [Stoelting and Miller, Basics, 1994, p267]
What happens to arterial blood pressure during inspiration in the patient with canii- ac tamponade? What is this ca!led and why?
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]
List three temporary measures that can be taken to maintain stroke volume in the patient with cardiac tamponade.
(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]
Which cardiac pressures equalize in cardiac tamponade?
Right and left atrial pressures and right ventricular end-diastolic pressure equalize at about 20 mm Hg. [Stoelting, Co-Existing, 1994, pplOS-109]
What is the treatment for cardiac tam- ponade?
Pericardiocentesis is the treatment. [Stoelting, Co-Existing, 1993, pliO; Davison, Eckhardt, and Perese, Mass General, 1993, p266]
If the patient with cardiac tamponade needs to be induced, what agent should be select- ed?
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]
List three anesthetic considerations for the patient with cardiac tamponade.
(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]
What three hemodynamic goals are proba- bly most important to achieve if the patient has aortic insufficiency?
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
What should be the goals for the patient with pericardia! tamponade?
Avoid vasodilation or cardiac depression. [Barash Handbook, Clinical Anesthesia, 1997, pp458-459]
What drugs should be avoided during anes- thesia for the patient with cardiac tam- ponade?
Avoid drugs or manipulations that decrease: (1) venous return; (2) heart rate; (3) arterial blood pressure; or (4) ventricular contractility. [Miller, Anesthesia, !994, pl777]
What is the most common circulatory dis- order?
Hypertension. [Barash Handbook, Clinical Anesthesia, 1997, p447]
What percent of hypertensive patients be- come hypertensive upon intubation? What is the goal when anesthetizing the medically controlled hypertensive patient?
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]
What class of drugs may be given preopera- tively to the untreated, asymptomatic, mild- ly hypertensive patient to attenuate tachy- cardia with tracheal intubation and tachycardia on emergence?
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]
What is the goal during maintenance of anesthesia for the patient who has chronic hypertension? What anesthetic technique may be useful for achieving this goal?
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]
- The blood pressure of the chronically hyper- tensive patient increases substantially dur- ing the case. What is the most likely cause? What should you do?
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]
What is another name for Takayasu’s arteri- tis? What is the underlying disease process in Takayasu’s arteritis? What segment of the population is primarily affected by this disease?
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]
What do most of the signs and symptoms of Takayasu’s arteritis reflect?
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]
What are five central nervous system signs and symptoms ofTakayasu’s arteritis?
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]
What five cardiovascular system signs and symptoms are seen in the patient with Taka~ yasu’s arteritis?
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]
he impact ofTakayasu’s arteritis on the pulmonary system results in what two signs and symptoms?
Patients with Takayasu’s arteritis may exhibit (l) pulmonary hyperten- sion and (2) ventilation-to-perfusion mismatch. [Stoelting, Co-Existing, 1993, p123-124]
What problems of the musculoskeletal sys- tem may be found in the patient with Taka- yasu’s arteritis?
Ankylosing spondylitis and rheumatoid arthritis may accompany Takaya- su’s arteritis. [Stoelting, Co-Existing, 1993, p123-l24]
What is the primary treatment for Takaya- su’s arteritis?
Takayasu’s arteritis is treated with corticosteroids. [Stoelting, Co-Existi11g, !993, pl23]
There are six concerns for the management of anesthesia in the patient with Takayasu’s arteritis. Identify three of them. (You will be asked to identify the other three concerns in the next question).
(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]
List three other concerns for managing the patient with Takayasu’s arteritis.
(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]
What is the goal during anesthesia of the patient with Takayasu’s arteritis? What should be avoided in this patient?
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]
What two actions can you take to maintain cerebral perfusion during anesthesia for the patient with Takayasu’s arteritis?
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
What cranial nerve innervates the posterior one-third of the tongue and carries the sensation of taste?
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]
What cranial nerve innervates the anterior two-thirds of the tongue and carries the sensation of taste?
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]
What is the primary function of the larynx? What are two other functions?
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]
What muscle acts as a barrier to regurgi- tation in the conscious subject?
In the awake subject, the cricopharyngeus muscle is the primary muscular barrier to regurgitation. [Nagelhout & Zaglaniczny, NA, yd eel., 2004, p409j
here are 91aryngeal cartilages, three paired, three unpaired (single). Identify and group the 9laryngeal cartilages by paired and single. Can you list the cartilages en- countered, in order from superior to inferi- or, from an anterior view?
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
Which intrinsic muscles close the laryngeal inlet (laryngeal vestibule)?
The aryepiglottic muscle pair closes the laryngeal inlet-they are sphinc- ters of the laryngeal vestibule. [Nagelhout & Zaglaniczny, NA, y
Identify the muscles that abduct and adduct the vocal cords.
The posterior cricoarytenoids abduct (open) the cords; the lateral cricoa1ytenoids adduct (close) the cords. [Miller, Anesthesia, 1994, pp2!83-2184j
What intrinsic laryngeal muscle dilates the cords?
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
Which muscle tenses the vocal cords? Will the voice go up or down in pitch when the cords are tensed?
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]
What muscle relaxes the vocal cords?
The thyroarytenoid relaxes the cords. [Ellis & Feldman, Anatomy for Anaesthetists. 8e. 2004 pp35]
What nerve provides sensation below the cords? What nerve provides sensation above the cords?
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]
What nerve provides sensation to the ante- rior and posterior surfaces of the epiglottis?
The internal branch of the superior laryngeal nerve supplies sensory fibers to the anterior and posterior surfaces of the epiglottis. [Miller, Anesthesia, 1994, p2184]
aryngospasm is caused by stimulation of which nerve?
Stimulation of the superior laryngeal nerves may cause laryngospasm. [Morgan, Mikhail, and Murray, Clinical Anesthesiology, 4e, 2006, p938]
What muscles are involved in laryn- gospasm? What motor (efferent) nerve is involved?
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]
Injury to what nerve wiU prevent the vocal cords from coming together? What intrinsic laryngeal muscles are involved?
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]
What are the muscles of inspiration? What is the most important muscle of inspiration?
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]
hat percentage of a tidal volume breath is contributed by the diaphragm in the upright subject during quite breathing (eupnea)?
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
he diaphragm is innervated by what nerve arising from what segments of the spinal cord?
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]
In what lwo directions are the thoracic dimensions altered during ventilation?
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]
Contraction of what muscles increase the antero-posterior (A/P) diameter of the thor- ax?
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]
Contraction of what muscle is most respon- sible for increasing the vertical (up and down) dimension of the thorax?
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]
Identify the two groups of muscles that may be employed to force expiration.
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]
Define dead space.
Dead space is that portion of the tidal volume that does not participate in gas exchange. [Barash Handbook, Clinical Anesthesia, 1997, pp309, 407- 408]
Define anatomic dead space. What percent of anatomical dead space is contained in the upper airway? Does anatomic dead space remain relatively constant throughout life?
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]
Define alveolar dead space. What causes alveolar dead-space?
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]
Define physiologic dead space.
Physiologic dead space is the sum of the anatomic and alveolar dead spaces. [Guyton, TMP. 11e. 2006 pp478]
When are anatomic dead space and physio- logic dead space almost equal?
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]
What is the difference between physiologic and anatomic dead space?
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
What is the anatomic dead space in mL!kg in the adult? Calculate the anatomic dead space in an 80 kg adult?
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
Identify four situations that are associated with a significant increase in dead space.
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
What percent of the tidal volume in a spon- taneously breathing adult is dead space? In a paralyzed, mechanically ventilated patient?
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)
With each breath in the spontaneously breathing healthy individual, what fraction of the tidal volume mixes with alveolar air?
About two-thirds of the inspired gas in each breath mixes with alveolar gases, because one-third is dead space. [Miller, Anesthesia, 1994, p594
What is the normal dead space to tidal vol- ume (Vn/VT) ratio, and what happens to this ratio when physiologic dead space increases?
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]
What site in the trachea produces the strongest cough reflex when stimulated?
The carina. [Guyton, “IMP. Ile. 2006 pp480)
What respiratory cells secrete mucus?
Goblet cells secrete mucus. [Guyton, 1MP. lie. 2006 pp480]
efine compliance. Define resistance. Con- trast airway compliance and airway re- sistance.
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
Describe the relationship between volume and pressure for an alveolus with a large compliance. Are alveoli with large compliances easier or harder to distend?
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]
What cells secrete surfactant? Describe the composition of surfactant.
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]
Discuss the three primary functions of sur- factant.
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]
As alveolar size decreases, what happens to surface tension in healthy individuals? What is the significance of this? What law applies.
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]
Define functional residual capacity (FRC).
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]
In what direction does the chest wall natu- rally recoil? In what direction do the lungs naturally recoil? When is the chest wall recoil exactly balanced by the lung recoil?
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]
More than two-thirds of the work of breath- ing is used to overcome what?
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]
What is the cause ofexhalation during the normal respiratory cycle?
Passive elastic recoil of the lungs is responsible for exhalation during normal tidal breathing. [Guyton, TMP. !!e. 2006 pp471]
How does the intrapleural pressure fluctuate during normal tidal breathing?
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]
During a normal respiratory cycle, when is the intrapleural pressure positive?
Intrapleural pressure is never positive, it is always negative (subatmos- pheric) during a normal inspiratory-expiratory cycle. [Guyton, TMP. lle. 2006 pp472]
- What happens to intrapulmonary pressure during normal inspiration? Expiration? When is intrapulmonary pressure zero?
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]
Compare intrapleural pressure in the de- pendent versus non-dependent lung?
Intrapleural pressure is greater (less negative) in dependent lung and lower (more negative) in non-dependent lung. [Morgan and Mikhail, Clinical Anesthesiology, 1996, p423)
How does intrapleural pressure vary from apex to base at end-expiration in the upright position?
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)
What is the intrapleural pressure in the base to apex direction in the supine position? Prone position? Lateral decubitus position?
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)
