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284 L.M. Walke and R.A. Rosenthal
11. I am going to tell you a story. Please listen carefully because afterwards, I’m going to ask you some questions about it
Jill was a very successful stockbroker. She made a lot of money on the stock market. She then met Jack, a devastatingly handsome man. She
married him and had three children. They lived in Chicago. She then stopped work and stayed at home to bring up her children. When they
were teenagers, she went back to work. She and Jack lived happily ever after
What was the female’s name?
2 points
What work did she do?
2 points
When did she go back to work?
2 points
What state did she live in?
2 points
Scoring
High school education Less than high school education
27–30 Normal 20–30
20–27 Mild cognitive impairment 14–19
1–19 Dementia 1–14
Source:
Available at http://www.medschool.slu.edu/agingsuccessfully/pdfsurveys/slumsexam_05.pdf. (See also 64)
Appendix
22.3
Michigan Alcoholism Screening Test: Geriatric Version (MAST-G)
1. After drinking have you ever noticed an increase in your heart rate or beating in your chest? Ye s No
2. When talking with others, do you ever underestimate how much you actually drink? Ye s No
3. Does alcohol make you sleepy so that you often fall asleep in your chair? Ye s No
4. After a few drinks, have you sometimes not eaten or been able to skip a meal because you didn’t feel hungry? Ye s No
5.
Does having a few drinks help decrease your shakiness or tremors? Yes No
6. Does alcohol sometimes make it hard for you to remember parts of the day or night? Yes No
7. Do you have rules for yourself that you won’t drink before a certain time of the day? Ye s No
8. Have you lost interest in hobbies or activities you used to enjoy? Ye s No
9. When you wake up in the morning, do you ever have trouble remembering part of the night before? Ye s No
10. Does having a drink help you sleep? Ye s No
11.
Do you hide your alcohol bottles from family members? Ye s No
12. After a social gathering, have you ever felt embarrassed because you drank too much? Ye s No
13. Have you ever been concerned that drinking might be harmful to your health? Ye s No
14. Do you like to end an evening with a nightcap? Ye s No
15. Did you find your drinking increased after someone close to you died? Ye s No
16.
In general, would you prefer to have a few drinks at home rather than go out to social events? Ye s No
17. Are you drinking more now than in the past? Ye s No
18. Do you usually take a drink to relax or calm your nerves? Ye s No
19. Do you drink to take your mind off your problems? Ye s No
20.
Have you ever increased your drinking after experiencing a loss in your life? Ye s No
21. Do you sometimes drive when you have had too much to drink? Ye s No
22. Has a doctor or nurse ever said they were worried or concerned about your drinking? Ye s No
23. Have you ever made rules to manage your drinking? Ye s No
24.
When you feel lonely, does having a drink help? Ye s No
Scoring:
Five or more “Yes” responses are indicative of an alcohol problem
Source:
from [67]
Appendix 22.2 (continued)
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Appendix 22.4 The Geriatric Depression Scale (Short Form)
https://t.me/med1917
Choose the best answer for how you felt over the past week.
28522 Preoperative Evaluation of the Older Surgical Patient
Answers in bold indicate depression and receive one point. Scores greater than five suggest the presence of
depression.
Source: material available at http://www.chcr.brown.edu/GDS_SHORT_FORM.PDF. See also Sheik and
Yesavage [70]
286 L.M. Walke and R.A. Rosenthal
Need for emergency
noncardiac surgery?
Step 1
Yes
Perioperative surveillance and
postoperative risk stratification
and risk factor management
Step 2
Active cardiac
conditions
Yes
Consider operating room
Step 3
Low risk surgery
Yes
Proceed with planned
surgery
Step 4
Good functional capacity (MET
level ≥4) without symptoms
Yes
Proceed with planned
surgery
Step 5
No or unknown
3 or more clinical
risk factors
1 or 2 clinical risk factors
Vascular
surgery
Consider treating if it
will change
management
Intermediate risk
surgery
Vascular
surgery
Intermediate
risk surgery
No clinical
risk factors
Proceed with planned surgery with heart rate control or
consider noninvasive testing if it will change management
Proceed with
planned surgery
No
No
No
Evaluate and treat
per ACC/AHA
guidelines
Operating
room
Appendix 22.5 Cardiac Evaluation and Care Algorithm
Reprinted from Fleischer et
al. [43]. Copyright 2007, with permission from Elsevier
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al (2006) Risk assessment
Chapter 23
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Invited Commentary
Jerry G. Reves
Practice of surgery and anesthesiology has changed
immensely over time. I can best comment on the field of
anesthesiology from my vantage point as a cardiac anesthesiologist, but obviously, I have admired the progress and
development of all anesthesiology during my professional
time in the field since 1969.
I became a cardiac anesthesiologist because of my interest in the cardiovascular system and the ability to rapidly
alter it with acute pharmacologic intervention during surgery. This preoccupation with cardiac surgery and anesthesia
began in 1965 with my pharmacology research as a medical
student and continues till today. Over this near half-century,
we have witnessed great changes and improvements in the
operative care of patients which merit commentary.
Of the many things that have changed over time, none is
greater than patient selection and operative procedure. In
early cardiac anesthesiology practice, virtually all patients
had congenital heart disease or acquired valvular disease.
The most morbid cardiovascular disease, coronary artery
disease, was not amenable to the surgical approach until the
latter half of the past century. At the same time, the age of the
adult population with the disease has been steadily increasing. I recall the days when we were doing our initial investigations into the anesthetic effects of patients undergoing
coronary bypass surgery and the average age was almost
always 55 years. Today, the average age is much higher for
patients undergoing coronary artery bypass surgery than in
the past. Reasons for this include less smoking among
patients, multiple available drugs such as statins that prevent
cardiac events, and greater variety of nonsurgical medical
interventions that delay surgery.
Older patients present a variety of problems to cardiac
anesthesiologists. For example, as patients age, there is
increased sensitivity to the central nervous system drugs that
J.G. Reves (*)
Department of Anesthesia and Perioperative Medicine,
Cell and Molecular Pharmacology & Experimental Therapeutic,
Medical University of South Carolina, Charleston, SC, USA
e-mail: revesj@musc.edu
anesthesiologists use for sedation, sleep, analgesia, and
anesthesia. Awareness of this is critical in prevention of
“overdosing” the patients that results in unwanted hemodynamic problems and prolonged somnolence after surgery.
There is no question that the tissue of older patients is not the
same as younger patients, and this leads to surgical hemostasis issues that can be challenging for the anesthesiologist as
well as surgeon. The entire coagulation system is also less
functional as patients age, again raising management problems around coagulation for the anesthesiologist and surgeon. Although no organs function in the very old as they do
in the young patient, the lungs and liver seem to be resilient
to the aging process, and this is important in the all important
areas of oxygenation and drug metabolism, respectively.
However, renal function tends to decline, and some of the
drugs administered by the anesthesiologist depend on good
renal clearance including some muscle relaxants and some of
the antiarrhythmic medications. Awareness of these potential
problems can avoid postoperative complications.
The greatest organ of concern to the cardiac anesthesiologist caring for elderly patient is the brain. All central nervous
system complications are increased with age. These complications vary in severity from temporary confusion to proven
susceptibility to cognitive impairment that can prohibit
patients from returning to preoperative functional levels.
Stroke is the most profound and dreaded of the neurologic
consequences of cardiac surgery. The causes of neurologic
adverse events are still largely unknown but probably are a
combination of compromised cerebral vascular perfusion,
emboli from the aorta, air and other debris when the heart or
aorta are opened, thrombi from the atria in patients with
atrial fibrillation, and many other possible causes. It is devastating to anesthesiologist, surgeon, family, and patient when
a surgery patient is never quite the same after the procedure,
especially when the heart or aorta has been “fixed.”
Despite the risks with cardiac surgery and the additional
risk that age confers on these patients, the results over the
years have steadily improved even as we have cared for older
and more complicated patients. This is a result of many innovations and improvements. The first of these is the education
R.A. Rosenthal et al. (eds.), Principles and Practice of Geriatric Surgery,
DOI 10.1007/978-1-4419-6999-6_23, © Springer Science+Business Media, LLC 2011
289
290 J.G. Reves
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of the cardiac anesthesiologist. Many of the anesthesiologists today who practice cardiac anesthesia have had formal
education and a fellowship. There are journals, textbooks,
and a whole new field of cardiac anesthesiology that has
emerged over the past 30 years. Evidence-based knowledge
guides the cardiac anesthesiologist today. The many drugs
used today by anesthesiologists are better than years ago,
and the anesthesiologist has an array of compounds to tailor
to the needs of the patient. Technology is vastly improved as
well. Monitoring allows the anesthesiologist to assess the
patient on virtually a beat-to-beat basis and to look at the
heart’s function with echocardiography. The anesthesiologist
now is diagnostician of the heart’s anatomy and physiology,
as well as pharmacology. The development of better pump
oxygenators and many other life-assist devices has made it
possible to get through surgery for patients who would not
have been able to in the past. Finally, a major development,
in my experience, was the introduction of myocardial protection with cardioplegia in the 1970s. This permitted prolonged
periods of safe heart stoppage to allow the surgeon to perform a more perfect operation. We are still searching for
other organ protective strategies.
Cardiac surgery has vastly improved as has cardiac anesthesiology over the past half-century. The two disciplines are
complementary approaches to improve patient outcomes
even in the very old. The same is true for all of our many
surgical fields. Neither the surgeon nor the anesthesiologist
can justifiably claim to have improved surgery for the patient
alone; it has been a marvelous team effort unmatched in all
medicine.
Chapter 24
Pulmonary physiology: effects of anesthesia and aging
Physiologic effects of anesthesia Physiologic effects of aging
Combined effects of anesthesia and
aging and their clinical implications
Shunt Hypoxic pulmonary vasoconstriction
inhibited, atelectasis, V/ ·Q mismatching
V/ ·Q mismatching, increased closing
capacity, increased PA pressures
Increased A-a gradient
Neuromodulation Decreased response to hypoxia and
hypercarbia
Decreased response to hypoxia and
hypercarbia
Susceptible to hypercapnea
Susceptible to hypoxemia
Susceptible to residual anesthetic
respiratory depressant effects
Mechanics Decreased TV, ·V
E
, FRC (anesthetized
and supine)
Decreased muscle mass, Loss of lung
elasticity
Decreased chest wall compliance
Increased work of breathing
Increased dead space ventilation
Susceptible to residual muscle relaxant
Protection Impaired cough
Impaired mucociliary clearance
Dysphagia, decreased cough reflex,
decreased esophageal motility
Greater aspiration risk
Organ specific effects of anesthesia and aging
Physiologic effects of anesthesia Physiologic effects of aging Clinical implications
Neurologic Inhibition of neurotransmitter function Decrease in neurotransmitters Increased postoperative delirium and
cognitive dysfunction
Renal Decreased blood flow and glomerular filtration rate Decreased renal mass Decreased drug clearance; Susceptible
to acute renal failure
Hepatic Decreased blood flow Decreased clearance of drugs with
high hepatic extraction ratios
Endocrine Impaired glucose tolerance Impaired glucose tolerance Hyperglycemia: Infection
Thermoregulation Vasodilatation; decreased shivering threshold Decreased muscle mass Hypothermia: Infection
Coagulopathy
Intraoperative arrhythmia
Postoperative myocardial infarction
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Physiologic Response to Anesthesia in the Elderly
Aaron N. LacKamp and Frederick E. Sieber
Cardiovascular physiology: effects of anesthesia and aging
Physiologic effects of
anesthesia Physiologic effects of aging
Venous Slight dilation Less compliant venous system Decrease in preload Greater fluctuation in preload for a
Arterial Dilation Decreased sympathetic response,
Heart Decreased contractility Diastolic dysfunction
Baroreceptor Response impaired Response impaired Response greatly impaired Greater susceptibility to hypotension
stiffening of arterial system
Left ventricular hypertrophy
Combined effects of
anesthesia and aging Clinical implications
Decreased systemic vascular
resistance
Higher filling pressures
needed to maintain
cardiac output
Possible hypotension, increased
Possible hypotension
Susceptible to volume overload,
given volume challenge
vasopressor requirements
dependant on late ventricular
filling from atrial contribution
A.N. LacKamp (*)
Department of Anesthesiology and Critical Care Medicine, Johns
Hopkins Bayview Medical Center, Baltimore, MD, USA
e-mail: alackam1@jhmi.edu
R.A. Rosenthal et al. (eds.), Principles and Practice of Geriatric Surgery,
DOI 10.1007/978-1-4419-6999-6_24, © Springer Science+Business Media, LLC 2011
291
292 A.N. LacKamp and F.E. Sieber
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Introduction
This chapter focuses on the physiologic components of aging
and anesthesia that are likely to increase perioperative complications. The approach entails a separate description of
anesthetic and aging physiology, followed by a discussion of
how the two interact. Only the physiologic changes invoked
by aging that provide important interactions with anesthesia
are discussed. The reader is encouraged to consult relevant
chapters contained in this textbook on preoperative assessment and specific organ systems for a more comprehensive
discussion of the physiologic changes with aging.
Cardiovascular Implications of Anesthesia
in the Elderly
Cardiovascular Effects of Anesthesia
Anesthetics decrease blood pressure by decreasing left ventricular contractility, decreasing systemic vascular resistance,
and inhibiting baroreceptor function (Fig. 24.1).
Decreased ventricular contractility occurs with intravenous anesthetic agents. Propofol is the most common induction agent used today and is generally thought to be a direct
myocardial depressant. The negative inotropic effect of
++
propofol is mediated by a decrease in intracellular Ca
[1]. In
fact, propofol is a greater myocardial depressant than the
inhalational anesthetics [2]. Even ketamine, which produces a
sympathetically mediated increased heart rate and blood pressure, causes some direct myocardial depressant effect [3, 4].
It appears that opioids have minimal effects on contractility
[3]. It has been suggested that etomidate is the induction agent
of choice in elderly patients with limited cardiovascular
reserve [5]. In fact, hemodynamic stability after induction
with this agent in severely compromised patients can be
remarkable. Etomidate can cause transient adrenal depression
[6,7], although the effect is of questionable significance.
In comparison to the intravenous agents, inhaled anesthetic
agents are associated with less myocardial depression. Volatile
anesthetics decrease inotropy by means of their effects on the
L-type Ca++ channels, the sarcoplasmic reticulum, and the
contractile apparatus [8]. Older drugs, such as halothane and
enflurane, cause greater decreases in myocardial contractility
than the modern agents isoflurane, sevoflurane, and desflurane [9–12]. Cardiac output is generally maintained under the
modern agents because the myocardial depression is accompanied by afterload reduction [10, 13, 14].
Most anesthetic agents reduce afterload by decreasing
arteriolar tone (Fig. 24.2). Propofol is a potent vasodilator
[15]. Opioids are also vasodilators, though this effect is small
when compared to propofol or the inhalational agents [16].
Fi g u r e 24.1 The effects of increasing concentrations (MAC) of halothane,
isoflurane, desflurane, and sevoflurane on mean arterial pressure (mmHg)
when administered to healthy volunteers. MAC is a means of defining
dose of inhaled volatile anesthetics, higher MAC values representing
higher anesthetic dose. One MAC equals the minimum alveolar concentration at which 50% of subjects aged 40 would not move in response to a
surgical stimulus (used with permission from Calahan [121]).
Fi g u r e 24.2 The effects of increasing concentrations (MAC) of halothane,
isoflurane, desflurane, and sevoflurane on systemic vascular resistance
(dynes/s/cm
defining dose of inhaled volatile anesthetics, higher MAC values representing higher anesthetic dose. One MAC equals the minimum alveolar concentration at which 50% of subjects aged 40 would not move in response to
a surgical stimulus (used with permission from Calahan [121]).
5
) when administered to healthy volunteers. MAC is a means of
29324 Physiologic Response to Anesthesia in the Elderly
https://t.me/med1917
Anesthetic agents blunt baroreceptor function. The degree
of inhibition depends on the anesthetic agents administered.
As a result, tachycardia may not be observed in response to
hypotension. Inhalational agents blunt baroreceptor function
in a dose-dependent manner [17]. Although both opioids and
propofol alter baroreceptor function, the effect is much less
than observed with the inhalational agents [2]. Significant
bradycardia can occur, however, because of the direct vagotonic effect of the opioids, especially fentanyl.
Anesthetic effects on venous pooling have been an area of
intense investigation because of the possible causal relationship
to deep vein thrombosis. However, the impact of general anesthetics on venous blood flow of the lower extremities is insignificant. Rather it seems that surgical stress is the primary
mediator of perioperative decreases in venous blood flow [
18].
Cardiovascular Changes with Aging That Effect
Anesthetic Physiology
Cardiovascular aging is characterized by increased sympathetic
tone, diminished b-adrenergic response, and stiffening of the
left ventricle and venous and arterial systems. The increased
sympathetic tone and arterial stiffening have several important
long-term effects. Arterial stiffening causes hypertension late
in systole, and this in turn causes an increased vascular load by
means of increased pulse wave velocity and wave reflection
[19]. This elevated vascular load is thought to be associated
with the development of left ventricular hypertrophy [20].
With ventricular hypertrophy comes delayed relaxation
and myocardial stiffening. Delayed relaxation impairs early
diastolic filling [21]. This enhances the importance of late
diastolic filling in maintaining cardiac output [22]. Late diastolic filling, however, must now overcome ventricular stiffness and that requires higher preload. The contribution of the
atrial contraction to ventricular filling becomes critical and
creates greater susceptibility to hypotension should atrial
fibrillation occur. Thus, the combination of chronic hypertension and left ventricular hypertrophy contribute to a higher
incidence of diastolic dysfunction in the elderly. To boost
cardiac output in the setting of increased ventricular stiffness, elderly patients may depend on higher diastolic filling
pressures. This impaired diastolic filling increases preload
requirements. Elderly patients may be thereby predisposed
to volume overload as they become increasingly reliant on
preload to maintain cardiac output.
Another factor that affects diastolic filling of the ventricle is
the relative time the heart spends in systole versus diastole. In
the aging heart, length of diastole is shortened and systole is
lengthened as a compensatory mechanism to maintain ejection
fraction [23, 24]. Increased left ventricular filling does increase
inotropy by means of the Starling forces, but the compensation
for the systolic function is at the expense of higher diastolic
pressures and greater time in systole [25–28]. Shortened dia-
stolic time also affects coronary perfusion [27, 28].
Stiffening of the vessel walls occurs in the venous system
with aging. Rigid veins fail to function as a preload buffer.
The venous system normally contains 80% of blood volume,
so low venous capacitance means that the aging venous system cannot accommodate excess volume or adapt to low volume states without a comparatively large change in filling
pressure [29]. This loss of venous compliance may be associated with impairment in diastolic filling.
Conduction abnormalities occur in the elderly. Dilation
and fibrotic change in the atria predispose the elderly to
atrial fibrillation. Bradycardia is the second most common
initiating rhythm after premature atrial contractions [30] and
may increase the incidence of new onset atrial fibrillation.
The high incidence of sinus bradycardia may be related to
drop-out of sinus node pacemaker cells to as little as 10% of
levels seen in young adults [23]. New onset atrial fibrillation
during the perioperative period in the elderly frequently
results in significant blood pressure changes. The cell populations in the aging AV node are maintained. AV conduction
slows with aging, however, resulting in lengthened P–R
interval [31, 32].
Cardiovascular responsiveness in the elderly is impaired.
For instance, maximal heart rate decreases with aging, and
can be estimated by the formula: maximum predicted heart
rate = 220 – age [33]. As a consequence, the ability to increase
cardiac output by means of an increase in heart rate is limited
[20]. There is reduced adrenergic responsiveness [34], affecting both the b-adrenergic [5, 35] absolute heart rate [36]
response and inotropy [37] and a-adrenergic mediated arteriolar tone [38].
Rapid response to hypotension is mediated by baroreceptor function. The stiffening of arterial walls in the elderly
may contribute to the well-documented decrease in baroreceptor response. There is a decrease in baseline vagal tone
[39] and consequently diminished carotid sinus baroreceptor
response to hypotension in the elderly [40, 41].
The aging of the autonomic nervous system is characterized by progressively limited capacity to adapt to stress. A
main concern of the anesthesia provider in evaluating the
elderly patient is the response to acute hemodynamic challenges in which the autonomic nervous system and its
effectors may play an important role. The preoperative
history can provide some indication of the competence of
the autonomic nervous system. The patient should be specifically questioned concerning signs and symptoms of
exercise intolerance, orthostatic hypotension, temperature
intolerance, and unusual patterns of sweating (especially
increased upper body sweating). If the history suggests that
autonomic nervous system responses are attenuated, one
has good reason to suspect that blood pressure lability will
occur perioperatively.
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