Anesthesia For High Risk Patients

Physiologic Changes of Aging
Cardiovascular
Arteries stiffen with age
pulse pressure waveform augmented early diastole to late systole
faster propagation
diastolic, systolic pressure pulse pressure
Slower myocardial relaxation and ventricular hypertrophy
late diastolic filling
diastolic dysfunction
Reduced venous capacitance
vascular reserve volume available to buffer hemorrhage
Reduced baroreceptor reflexes
sympathetic tone
parasympathetic tone
baroreceptor sensitivity
responsiveness to -adrenergic stimulation
Decreased maximal heart rate with age while stroke volume remain constant
Decreased maximal oxygen consumption
reduction in arteriovenous oxygen tension differences
Hypotension:
volume, position
anesthetic depth
RA-induced sympathetic block
Respiratory
Parenchymal changes
30% of alveolar tissue is lost between ages 20 and 80
diminishing elastic recoil and parenchymal fraction airway patency
Residual volume, Closing volume and FRC
VC and FEV
1

progressive V/Q mismatching age-dependent decrease in arterial O
2
tension
Physiologic dead space
Diffusing capacity
Chest wall changes
Stiffer chest wall
respiratory muscles
Depressed ventilatory response to hypoxia and hypercarbia
Decreased protective airway reflexes
aspiration risk
Renal
Serum creatinine remains stable
age-associated decreases of creatinine clearance offset by reduced creatinine production
normal creatinine level absence of renal impairment ?
Progressive atrophy of renal parenchyma and sclerosis of vasculature structures
RBF
GFR
Reduced ability to correct alteration :
electrolyte concentrations
intravascular volume
free water
Reduced GFR
delayed renal drug excretion
Physiologic changes of aging
Central Nervous System
Progressive loss of neurons
Decreased neurotransmitter activity
Cerebral autoregulatory response to BP, CO
2
and O
2
maintained
anesthetic requirement
Hepatic
Liver mass
proportional reduction of sphlancnic and hepatic blood flow
hepatic drug clearance
Activity of some cytochrome P-450 isoforms
Phase 1 and phase 2 reactions
Body composition and thermoregulation
Basal metabolism and heat production
skeletal muscle atrophy
adipose tissue
propensity of hypothermia
blunted central thermoregulation
body composition changes
muscle mass and total body water, body fat
Vd of water-soluble drugs
Vd of lipid-soluble drugs
Pharmacologic Implications of Aging
binding site for most lipophilic basic drugs
alpha
1
-acid glycoprotein
frequency and severity of adverse drug reactions
MAC for inhalational anesthetic
Anesthetic Considerations In The Elderly
Age-related coexisting disease is a major predictor for perioperative morbidity and mortality
age alone is a minor predictor
Major risk factors:
emergency surgery
operative site : major body cavity or vascular
ASA physical status
No significant difference:
specific anesthetic agent
RA vs GA
functional reserve capacity
therapeutic index of anesthetic interventions
highly variable
unpredictable
may be manifest only under severe stress
vigilance
preparation for contingencies

The leading cause of death

Risk factor identified to predict perioperative cardiac morbidity:
Recent myocardial infarction
The presence of congestive heart failure
Understanding the pathophysiology of the disease process
Careful selection of :
anesthetic drugs
monitors
Coronary artery disease
Often asymptomatic
A common accompaniment of aging
40% will either have or be at risk
morbidity and mortality
Routine preoperative cardiac evaluation:
history
PE
ECG
ambulatory ECG monitoring (Holter monitoring)
exercise stress testing
transthoracic or transesophageal echocardiography
radionuclide ventriculography
dypiridamole-thallium scintigraphy
cardiac catheterization
angiography
Selected
patients
Best medical condition possible
before elective cardiac or non-cardiac surgery
Patient History
Cardiac reserve
limited exercise tolerance in the absence of significant pulmonary disease
Characteristic of angina pectoris
stable : no change for at least 60 days in precipitating factors, frequency and duration
unstable
variant or prinzmetals : due to spasm of coronary arteries, may occurs at rest
dyspnea following the onset of angina acute left ventricular dysfunction due to MI
HR and/or SBP HR > SBP
The presence of a prior myocardial infarction
incidence of reinfarction in the perioperative period 48 72 hrs postoperatively
related to the time elapsed since the previous MI
delay the elective surgery for about 6 mos after MI (5 6%), 50 x (n: 0.13%)
intrathoracic or intra-abdominal operations lasting longer than 3 hours
Potential drug interactions
Coexisting non-cardiac disease
Patient can remain asymptomatic despite 50 70% stenosis of a major coronary artery
ECG
Myocardial ischemia
S-T segment depression > 1 mm
Prior myocardial infarction
Cardiac hyperthrophy
Abnormal cardiac rhythm and/or conduction
Electrolyte abnormalities
Exercise ECG
stimulates SNS
direct laryngoscopy
tracheal intubation
surgical incision
Resting ECG in the absence of angina pectoris may be normal despite extensive CAD
Management of anesthesia
Modulation of SNS responses
Provide for the rigorous control of hemodynamic variables

Based on:
preoperative evaluation of left ventricular function
Maintenance of a favorable balance between myocardial O
2
requirement and delivery
tachycardia
systolic hypertension
arterial hypoxemia
diastolic hypotension
more important than the specific technique or drugs
Preoperative medication
to produce sedation
to allay anxiety
if unopposed catecholamine secretion
myocardial O
2
requirements
SBP
HR
benzodiazepine
scopolamine + morphine
transdermal nitrogycerine
Induction of anesthesia
Rapidly acting IV drugs
Ketamine associated with HR and SBP
not popular
Tracheal intubation
facilitated by Succhinylcholine or Nondepolarizing MR

MI may accompany hypertension and tachycardia
brief duration (<15 sec)
to minimize the magnitude of circulatory changes
Lidocaine
laryngotracheal (2 mg/kg)
IV (1.5 mg/kg)
short-acting opioid
Fentanyl 1 3 g/kg/IV, 2 to 4 mins before DL
Esmolol (200 g/kg/min IV)
Maintenance of anesthesia
Choice of anesthesia
based on left ventricular function

CAD, but normal left ventricular function
SBP, HR in response to stimulation
volatile anesthetic with/without N
2
O
to control myocardial depression
N
2
O opioid + volatile anesthetic
to treat acute in SBP
drug-induced in SVR > drug-induced myocardial depression
isoflurane
sevoflurane
desflurane

Low blood solubility
rapid
Impaired left ventricular function

may not tolerate myocardial depression produced by volatile anesthetics
high dose opioid technique
opioid + N
2
O technique
N2O, when combined with opioid
may produce undesirable in SBP and CO
Regional anesthesia
Flow through critically narrowed coronary arteries is pressure-dependent
SBP associated with RA > 20% of the pre-block
should be treated
fluids infusion
sympathomimetic
ephedrine
phenylephine
Monitoring
Complexity of the operative procedure
Severity of the coronary artery disease
ECG
non-invasive
balance between myocardial O
2
requirement and myocardial O
2
delivery
myocardial ischemia S-T depression
V5 left ventricle
TEE
ventricular wall motion abnormality
most sensitive indicator for MI
invasive and not practical
Pulmonary artery catheter
Central venous pressure
may not reliably reflect left heart filling pressure
in the presence of left ventricular dysfunction
For selected high risk patients
recent MI
CHF
unstable angina
Signs of MI
aggressive treatment of adverse changes in HR and/or SBP
tachycardia
propanolol
esmolol
SBP
nitropruside
nitroglycerine
more appropriate choice when MI is associated with normal SBP
hypotension
sympathomimetics
to rapidly restore pressure-dependent perfusion
intravenous infusion of fluids
myocardial O
2
requirements for volume work < pressure work

pulmonary artery catheter
for monitoring responses of ventricular function
Monitoring
Postoperative care
Analgesia
Sedation
To blunt excessive SNS activity
Facilities vigorous control of hemodynamic variables

intensive and continuous monitoring
to detect myocardial ischemia, which is often asymptomatic

! Identification and treatment
cardiac morbidity
Temperature
hypothermia shivering
abrupt in myocardial O
2
requirement
minimize in body temperature
O
2
supplementation
Congestive Heart Failure
should not be performed as an elective surgery
Associated with postoperative morbidity
optimally treated
when surgery can not be delayed
chose of drugs/techniques
goal : optimizing cardiac output

GA: induction : ketamine
maintenance: volatile anesthetic is not recommended
potential for cardiac depression
high dose opioid may be justified
positive pressure ventilation may be beneficial
pulmonary congestion
improving oxygenation
invasive monitoring
continuous infusion of dopamine and/or dobutamine
maintenance of cardiac contractility
RA: for peripheral surgery
SVR secondary to peripheral SNS blockade
facilitate left ventricular stroke volume
Essestial Hypertension
Sustained increases in systemic blood pressure independent of any known cause
systolic blood pressure > 160 mmHg
diastolic blood pressure > 90 mmHg
Tx with appropriate drugs
incidence of stroke and congestive heart failure

incidence of hypotension and MI on ECG during maintenance of anesthesia
in patient who remain hypertensive before the induction of anesthesia

SBP during intraoperative period
more likely to occur in patient with history of essential hypertension
regardless of the degree of pharmacology control of SBP preoperatively
no evidence of postoperative cardiac complications
as long as preoperative diastolic BP is not higher than 110 mmHg
Preoperative evaluation
adequacy of SBP control
drug therapy
!!! maintain current therapy throughout the perioperative period
extent of the disease
major organ dysfunction influences drug selection
assumed to have coronary artery disease until proven otherwise
evidence of peripheral vascular disease

Consideration of the implications of exaggerated SBP responses
elicited by painful intraoperative stimulation

Shift to the right of the curve for the autoregulation of cerebral blood flow
more vulnerable to cerebral ischemiashould perfusion pressure decrease
Exaggerated decrease in SBP may occur
unmasking of decrease intravascular fluid volume due to chronic hypertension
particularly if hypertension is present preoperatively

Ketamine rarely selected

Exagerated increase in SBP during direct laryngoscopy are predictable
MI
ensure maximal attenuation of SNS responses evoked by DL
volatile anesthetics
IV opioids
lidocaine
limit the duration of DL < 15 sec, if possible
Undesirable hypotension
Adjust the concentration of anesthetic drugs
to minimize wide fluctuations in SBP
more important than preoperative control of hypertension

N
2
O + volatile anesthetic
for rapid adjustment in the depth of anesthesia in response to or SBP
attenuating SNS, which is responsible for pressor responses

desflurane
sevoflurane

N2O + Opioid
the addition of a volatile anesthetic is often necessary to control undesirable SBP
particularly during periods of maximal surgical stimulation

Nitroprusside
-Blockers : esmolol or labetalol
Low blood solubilities
Hypotension that occurs during maintenance of anesthesia:
the concentration of volatile anesthetics
IV fluids infusion
to intravascular fluid volume
sympathomimetics
to restore perfusion pressure until underlying cause can be corrected
ephedrine
Regional anesthesia
Questionable choice
when high levels of SNS blockade would be associated with the sensory level
necessary for planned surgery
possibility of excessive decreases in SBP
vasodilatation unmasks a decreased intravascular fluid volume
associated with chronic hypertension
Choice of intra-operative monitors
Influenced by the complexity of the surgery

ECG
goal: recognizing changes suggestive of MI

invasive monitors: arterial and/or pulmonary catheters
if major surgery is planned
evidence of left ventricular dysfunction pre-operatively

Transesophageal echocardiography
an alternative to placement of a pulmonary artery catheter
Postoperative management
Hypertension in the early postoperative period
frequent
adequate analgesia
pharmacologically decrease SBP
nitroprusside, continuous IV
labetalol (0.1 0.5 mg/kg/IV

A challenge :
Intraoperative management
Regardless of the operative site
particular risk:
thoracic
upper abdominal
Co-existing disease:
coronary artery disease
essential hypertension
OBSTRUCTIVE AIRWAY DISEASE
Most frequent cause of pulmonary dysfunction
Chronic Obstructive Pulmonary Disease (COPD)
a group of disorders characterized by a persistent decrease in the maximum rate of exhalation
despite aggressive therapy
regional differences in airway resistance
areas of ventilation-to-perfusion mismatching
arterial hypoxemia
CO
2
retention respiratory acidosis
cough and sputum production

Symptom: dyspnea work of breathing

PE : wheezing during exhalation turbulence gas flow through narrowed airways

Chest X-ray : hyperinflated lung, radiolucency pulmonary blood flow
flattened diaphragm

Pulmonary function studies : expiratory flow rates airway resistance
FEV
1
< 80%
Bronchial asthma
Classic example of obstructive airway disease
Most common chronic inflammatory disease of the airway
characterized by acute and reversible increases in airway resistance
irreversible COPD

Chronic inflammatory changes in the submucosa of the airway
Increased airway responsiveness (hyper-reactivity) to various stimuli
Reversible expiratory airflow obstruction
Bronchial asthma
Clinical symptoms:
during periods of normal to near normal pulmonary function
no physical findings
acute bronchial asthma attack
wheezing
cough
non productive production of copious amount of tenacious sputum
dyspnea
parallel to the severity of expiratory airflow obstruction
FEV
1
: 25 75% vital capacity
the flow-volume loop
downward scooping of the expiratory limb of the loop
Bronchial asthma
Estimation of the severity of bronchial asthma
Expiratory airflow FEV
1
PaO
2
PaCO
2

Obstruction (% predicted) (mmHg) (mmHg)

Mild (asymptomatic) 65 80 > 60 < 40
Moderate 50 64 > 60 < 45
Marked 35 49 < 60 > 50
Severe (status asthmaticus) < 35 < 60 > 50
Bronchial asthma
Preoperatively
absence of : dyspnea
wheezing
PFT indicated for a thoracic or abdominal operation
before and after bronchodilator therapy
ABG adequacy of ventilation or arterial oxygenation

persistent symptoms
treated with glucocorticoids (inhaled or systemic)
continue throughout perioperative period
supplementation with cortisol
if suppresion of the hypothalamic-pituitary-adrenal axis is suspected
anticholinergics individualized
airway resistance
viscosity of the secretions
H
2
antagonists
antagonism of H
2
-mediated bronchodilation
unmask H
1
-mediated bronchoconstriction

No acute exacerbation of bronchial asthma
Regional anesthesia
an attractive choice
superficial or extremities surgery

General anesthesia
induction
maintenance
Suppression of airway reflexes
avoid bronchoconstriction of hyperreactive airways
in response to mechanical stimulation
Rapid IV induction
Thiopental
Etomidate
Propofol may blunt tracheal intubation-induced bronchospasm
Ketamine sympathomimetic effects on bronchial smooth muscle
airway resistance
secretions
Before intubation sufficient depth should be established
Lidocaine (1 to 2 mg/kg/IV)
to blunt bronchoconstriction reflex
Sevoflurane
Isoflurane

Halothane
Depress airway reflexes
Do not sensitize the heart to the cardiac dysrhythmic effects of SNS stimulation
produced by -agonist and aminophylline
Bronchodilation effects NO production
Bronchodilator
Associated with cardiac dysrhythmias in the presence of SNS stimulation
Neuromuscular blocking drugs
not associated with endogenous histamine release
PaO
2
PaCO
2
Maintained at normal levels
slow RR (6 to 10)
to allow adequate time for passive exhalation
high inspiratory flow rate
PEEP may not be ideal
adequate exhalation may be impaired
Liberal IV fluid administration
ensuring the presence of less viscous secretions
At the conclusion of elective surgery
deep extubation
anesthesia depth still sufficient to suppress hyperreactive airway reflexes
bronchospasm does not predictably follow administration of anticholinesterases
Lidocaine/IV may decrease the likelihood of airway stimulation
Intraoperative Bronchospasm
Deepening of anesthesia with volatile anesthetic
-2 agonist
Corticosteroids
Mechanical obstruction
Insufficient anesthetic concentration
Pulmonary aspiration
Endobronchial intubation
Pneumothorax
Pulmonary embolus
Acute bronchial asthma
?
Pulmonary emphysema
Loss of elastic recoil of the lung
collapse of airways during exhalation
airway resistance
Severe dyspnea
work of breathing
Determine the severity of the disease
Elucidate any reversible components
infections
bronchospasm
PFT
Do not always correlate with postoperative outcome
dyspnea
cough
sputum production
exercise tolerance
ABG
may be normal (pink puffer)
high minute ventilation
to overcome airway resistance
PaCO
2
> 50 mmHg
risk of post operative respiratory failure
Risk of postoperative respiratory failure:
vital capacity < 50% of the predicted value
FEV
1
< 50% of the predicted value
FEV
1
< 2 liters
Arterial hypoxemia and/or hypercarbia is present

!!!
preoperative detection and treatment of cor pulmonale
supplemental O
2
Does not dictate the use of specific drugs or techniques
Susceptible to the development of acute respiratory failure
in the postoperative period
continue tracheal intubation andmechanical ventilation of the lungs
General anesthesia
humidified inhaled gases to prevent drying of secretions, systemic hydration?
mechanical ventilation of the lung small tidal volumes
small breathing rates

N
2
O:
limitation of the inhaled concentration of oxygen
passage of this gas into bullae from emphysema
enlargement and rupture
tension pneumothorax

Opioids:
less ideal for maintenance of anesthesia to ensure amnesia
need high concentration of N
2
O
substituting a low concentration of volatile anesthetic for N
2
O
postoperative ventilatory depression
chronic hypercarbia should not be abruptly corrected
difficult to wean from mechanical ventilation
inspiratory flow rates
Chronic Bronchitis
Chronic or recurrent secretion of excess mucus into the bronchii
resistance to gas flow through the airways
Tend to develop:
Arterial hypoxemia (blue bloaters)
Hypercarbia
Cor pulmonale
early
Small airway account to only a minor proportion of total airways resistance
chronic bronchitis must be advanced before dyspnea become apparent
Restrictive Pulmonary Disease
Lung compliance
lung volume

vital capacity in the presence of a normal FEV
1
Dyspnea
work of breathing necessary to expand the poorly compliant lungs
Rapid and shallow breathing
to minimize the work of breathing in the presence of lung compliance
PaCO
2
hyperventilation
usually maintained at a decreased to normal value, until far advanced
Severe Pulmonary hypertension
Acute restrictive pulmonary disease
leakage of intravascular fluid into the interstitium and alveoli of the lungs
pulmonary edema
Acute Respiratory Distress Syndrome
Aspiration pneumonitis
Neurogenic pulmonary edema
Opioid-induced pulmonary edema
High-altitude pulmonary edema
Chronic restrictive pulmonary disease
presence of pulmonary fibrosis (sarcoidosis)
processes that interfere with expansion of the lungs
Effusions
Kyphoscoliosis
Obesity
Ascites
Pregnancy
RA
appropriate for peripheral surgery
sensory level above T10
associated with the impairment of respiratory muscle activity

GA
does not influence the choice of drugs used for induction or maintenance
mechanical ventilation is useful
high inflation pressures may be necessary
minimize ventilatory depression that may persist into postoperative period
vital capacity < 15 mL/kg
PaCO2 > 50 mmHg
difficult to generate effective cough

preoperatively
Effect of Anesthesia And Surgery on Renal Function
Important variable:
Type of surgical procedure
Fluid administration
Preexisting cardiac function
Preexisting renal function
Reversible decreases in RBF, GFR, urinary flow, and sodium excretion (RA & GA)
Changes are generally less marked during RA
Most of these changes are indirect
mediated by autonomic and hormonal influences
These effect can be at least partially overcome
by maintenance of an adequate intravascular volume and a normal BP
Only few anesthetics in high doses can cause specific renal toxicity
Effect of Anesthesia on Renal Function
Indirect effects
Cardiovascular effects
inhalational and intravenous agents
cardiac depression
vasodilatation
RA
sympathetic block
Neural effects
sympathetic activation
light anesthesia
intense surgical stimulation
tissue trauma
anesthetic-induced circulatory depression
Endocrine effects
stress response
surgical stimulation
circulatory depression
hypoxia
acidosis
BP, Below the limit of autoregulation:
RBF, GFR, urinary flow, Na
+
excretion
IV fluid administration
Renal vascular resistance
Activates hormonal system
RBF, GFR, UO
Catecholamines
Renin, Angiotensin II, Aldosterone
ADH
ACTH, Cortisol
Direct effects minor
Volatile agents
Methoxyflurane polyuric renal failure
defect in urinary concentrating ability
dose-related 1 MAC for 2 hrs
release of fluoride ions ( > 50 mol/L )

Enflurane, Sevoflurane (possible)
prolonged administration
fluoride excretion: GFR dependent
preexisting renal impairment more susceptible
Compound A: breakdown product of sevoflurane
FGF > 2 L/min

Halothane, Isoflurane, and Desflurane negligible
Intravenous agents
opioids and barbiturate minor effect when used alone
+ N2O volatine agents
ketamine
minimally affect renal function
preserve renal function during hemorrhagic hypovolemia
-adrenergic blocking agents (droperidol)
prevent catecholamine-induced redistribution of RBF
antidopaminergic agents (metoclopramine, phenothiazines, droperidol)
impair renal response to dopamine
NSAIDs (ketorolac)
prevent renal production of vasodilatory prostaglandins
ACE inhibitors
block the protective effects of angiotensin II GFR
Other drugs
antibiotics
aminoglycosides, amphotericine B
imunosupressive agents
cyclosporin
radiocontrast dyes

renal arterial vasospasm
direct cytotoxic properties
renal microvascular or tubular obstruction

preexisting renal dysfunction!
Effect of Specific Surgical Procedures on Renal Function
Laparoscopy procedures
Pneumoperitoneum
abdominal compartement syndrome-like state
intraabdominal pressure insufflation pressures
central venous compression (renal vein and vena cava)
renal parenchymal compression
cardiac output
plasma renin, aldosterone and ADH
oliguria/anuria

Cardiopulmonary bypass
Cross-clamping of the aorta
Dissection near the renal arteries
Neurosurgical procedure ADH
Management of Anesthesia
Pathophysiologic changes
Hemodialysis requirement
preoperative hypertension due to fluid overload
elective surgery
Electrolyte concentrations
unexpected hyperkalemia can occur rapidly
if surgery cannot be delayed
hyperventilation
10 mmHg PaCO2 0.1 unit pH
glucose-insulin mixture
25 50 g glucose + 10 20 u RI/IV
IV calcium
Bic. Nat
if accompanied by metabolic acidosis
Management of Anesthesia
Tracheal intubation

CRF (regardless of hydration status)
hypovolemic

risk of hypotension
if SNS function is attenuated by antihypertensive therapy
impairs compensatory peripheral vasoconstriction
small decrease in blood volume
positive pressure ventilation
sudden change in body position
common IV drugs
Muscle relaxants
Succinyl choline
acceptable assuming preexisting hyperkalemia is not present
Non-depolarizing MR
not dependent on renal clearance
intermediate and short acting

atracurium and cisatracurium
laudanosine clearance delayed

initial dose
Administer subsequent dose based on the response to PNS
Consider drug interaction
antibiotics, acidosis, electrolyte imbalance
N
2
O
FiO
2
?
Volatile anesthetics
controlling intraoperative hypertension
dose of MR
Desflurane
Isoflurane
Opioid
CV depression
avoid hepatotoxicity and nephrotoxicity
unreliable for controlling intraoperative hypertension
prolonged CNS & respiratory depression
accumulation of pharmacologically active metabolites
Ventilation
Normocapnia is desirable
Hyperventilation
respiratory alkalosis oxyhemoglobin dissociation curve
Hypoventilation
respiratory acidosis K+
Fluid Management
Hemodialysis dependent
narrow margin of safety :insufficient vs excessive fluid administration
replacement of insensible losses (including UO)
0.9% saline

potassium-containing fluids
should not administered to anuric patients

CVP measurement
guiding fluid replacement

ECG monitoring
for recognizing signs of hyperkalemia

AV shunts
must be carefully protected
Postoperaive period
Hypertension
frequent problem
hemodialysis is the best treatment if fluid excess is the cause
Opioid for postoperative analgesia
possibility of exagerated CNS and respiratory depression

regional analgesia
adequacy of coagulation?
presence of uremic neuropathies?
metabolic acidosis?
seizure threshold for local anesthetics

A challenge :
Regardless of the operative site
particular risk:
thoracic
upper abdominal
Co-existing disease:
essential hypertension
OBSTRUCTIVE AIRWAY DISEASE
Most frequent cause of pulmonary dysfunction
Chronic Obstructive Pulmonary Disease (COPD)
a group of disorders characterized by a persistent decrease in the maximum rate of exhalation
despite aggressive therapy
regional differences in airway resistance
areas of ventilation-to-perfusion mismatching
arterial hypoxemia
CO
2
retention respiratory acidosis
cough and sputum production

Symptom: dyspnea work of breathing

PE : wheezing during exhalation turbulence gas flow through narrowed airways

Chest X-ray : hyperinflated lung, radiolucency pulmonary blood flow
flattened diaphragm

Pulmonary function studies : expiratory flow rates airway resistance
FEV
1
< 80%
Bronchial asthma
Classic example of obstructive airway disease
Most common chronic inflammatory disease of the airway
characterized by acute and reversible increases in airway resistance
irreversible COPD

Chronic inflammatory changes in the submucosa of the airway
Increased airway responsiveness (hyper-reactivity) to various stimuli
Reversible expiratory airflow obstruction
Bronchial asthma
Clinical symptoms:
during periods of normal to near normal pulmonary function
no physical findings
acute bronchial asthma attack
wheezing
cough
non productive production of copious amount of tenacious sputum
dyspnea
parallel to the severity of expiratory airflow obstruction
FEV
1
: 25 75% vital capacity
the flow-volume loop
downward scooping of the expiratory limb of the loop
Bronchial asthma
Estimation of the severity of bronchial asthma
Expiratory airflow FEV
1
PaO
2
PaCO
2

Obstruction (% predicted) (mmHg) (mmHg)

Mild (asymptomatic) 65 80 > 60 < 40
Moderate 50 64 > 60 < 45
Marked 35 49 < 60 > 50
Severe (status asthmaticus) < 35 < 60 > 50
Bronchial asthma
Preoperatively
absence of : dyspnea
wheezing
PFT indicated for a thoracic or abdominal operation
before and after bronchodilator therapy
ABG adequacy of ventilation or arterial oxygenation

persistent symptoms
treated with glucocorticoids (inhaled or systemic)
continue throughout perioperative period
supplementation with cortisol
if suppresion of the hypothalamic-pituitary-adrenal axis is suspected
anticholinergics individualized
airway resistance
viscosity of the secretions
H
2
antagonists
antagonism of H
2
-mediated bronchodilation
unmask H
1
-mediated bronchoconstriction

No acute exacerbation of bronchial asthma
Regional anesthesia
an attractive choice
superficial or extremities surgery

General anesthesia
induction
maintenance
Suppression of airway reflexes
avoid bronchoconstriction of hyperreactive airways
in response to mechanical stimulation
Rapid IV induction
Thiopental
Etomidate
Propofol may blunt tracheal intubation-induced bronchospasm
Ketamine sympathomimetic effects on bronchial smooth muscle
airway resistance
secretions
Before intubation sufficient depth should be established
Lidocaine (1 to 2 mg/kg/IV)
to blunt bronchoconstriction reflex
Sevoflurane
Isoflurane

Halothane
Depress airway reflexes
Do not sensitize the heart to the cardiac dysrhythmic effects of SNS stimulation
produced by -agonist and aminophylline
Bronchodilation effects NO production
Bronchodilator
Associated with cardiac dysrhythmias in the presence of SNS stimulation
Neuromuscular blocking drugs
not associated with endogenous histamine release
PaO
2
PaCO
2
Maintained at normal levels
slow RR (6 to 10)
to allow adequate time for passive exhalation
high inspiratory flow rate
PEEP may not be ideal
adequate exhalation may be impaired
Liberal IV fluid administration
ensuring the presence of less viscous secretions
At the conclusion of elective surgery
deep extubation
anesthesia depth still sufficient to suppress hyperreactive airway reflexes
bronchospasm does not predictably follow administration of anticholinesterases
Lidocaine/IV may decrease the likelihood of airway stimulation
Intraoperative Bronchospasm
Deepening of anesthesia with volatile anesthetic
-2 agonist
Corticosteroids
Mechanical obstruction
Insufficient anesthetic concentration
Pulmonary aspiration
Endobronchial intubation
Pneumothorax
Pulmonary embolus
Acute bronchial asthma
?
Pulmonary emphysema
Loss of elastic recoil of the lung
collapse of airways during exhalation
airway resistance
Severe dyspnea
work of breathing
Determine the severity of the disease
Elucidate any reversible components
infections
bronchospasm
PFT
Do not always correlate with postoperative outcome
dyspnea
cough
sputum production
exercise tolerance
ABG
may be normal (pink puffer)
high minute ventilation
to overcome airway resistance
PaCO
2
> 50 mmHg
risk of post operative respiratory failure
Risk of postoperative respiratory failure:
vital capacity < 50% of the predicted value
FEV
1
< 50% of the predicted value
FEV
1
< 2 liters
Arterial hypoxemia and/or hypercarbia is present

!!!
preoperative detection and treatment of cor pulmonale
supplemental O
2
Does not dictate the use of specific drugs or techniques
Susceptible to the development of acute respiratory failure
in the postoperative period
continue tracheal intubation andmechanical ventilation of the lungs
General anesthesia
humidified inhaled gases to prevent drying of secretions, systemic hydration?
mechanical ventilation of the lung small tidal volumes
small breathing rates

N
2
O:
limitation of the inhaled concentration of oxygen
passage of this gas into bullae from emphysema
enlargement and rupture
tension pneumothorax

Opioids:
less ideal for maintenance of anesthesia to ensure amnesia
need high concentration of N
2
O
substituting a low concentration of volatile anesthetic for N
2
O
postoperative ventilatory depression
chronic hypercarbia should not be abruptly corrected
difficult to wean from mechanical ventilation
inspiratory flow rates
Chronic Bronchitis
Chronic or recurrent secretion of excess mucus into the bronchii
resistance to gas flow through the airways
Tend to develop:
Arterial hypoxemia (blue bloaters)
Hypercarbia
Cor pulmonale
early
Small airway account to only a minor proportion of total airways resistance
chronic bronchitis must be advanced before dyspnea become apparent
Restrictive Pulmonary Disease
Lung compliance
lung volume

vital capacity in the presence of a normal FEV
1
Dyspnea
work of breathing necessary to expand the poorly compliant lungs
Rapid and shallow breathing
to minimize the work of breathing in the presence of lung compliance
PaCO
2
hyperventilation
usually maintained at a decreased to normal value, until far advanced
Severe Pulmonary hypertension
Acute restrictive pulmonary disease
leakage of intravascular fluid into the interstitium and alveoli of the lungs
pulmonary edema
Acute Respiratory Distress Syndrome
Aspiration pneumonitis
Neurogenic pulmonary edema
Opioid-induced pulmonary edema
High-altitude pulmonary edema
Chronic restrictive pulmonary disease
presence of pulmonary fibrosis (sarcoidosis)
processes that interfere with expansion of the lungs
Effusions
Kyphoscoliosis
Obesity
Ascites
Pregnancy
RA
appropriate for peripheral surgery
sensory level above T10
associated with the impairment of respiratory muscle activity

GA
does not influence the choice of drugs used for induction or maintenance
mechanical ventilation is useful
high inflation pressures may be necessary
minimize ventilatory depression that may persist into postoperative period
vital capacity < 15 mL/kg
PaCO2 > 50 mmHg
difficult to generate effective cough

preoperatively
The leading cause of death

Risk factor identified to predict perioperative cardiac morbidity:
Recent myocardial infarction
The presence of congestive heart failure
Understanding the pathophysiology of the disease process
Careful selection of :
anesthetic drugs
monitors
Often asymptomatic
A common accompaniment of aging
40% will either have or be at risk
morbidity and mortality
Routine preoperative cardiac evaluation:
history
PE
ECG
ambulatory ECG monitoring (Holter monitoring)
exercise stress testing
transthoracic or transesophageal echocardiography
radionuclide ventriculography
dypiridamole-thallium scintigraphy
cardiac catheterization
angiography
Selected
patients
Best medical condition possible
before elective cardiac or non-cardiac surgery
Patient History
Cardiac reserve
limited exercise tolerance in the absence of significant pulmonary disease
Characteristic of angina pectoris
stable : no change for at least 60 days in precipitating factors, frequency and duration
unstable
variant or prinzmetals : due to spasm of coronary arteries, may occurs at rest
dyspnea following the onset of angina acute left ventricular dysfunction due to MI
HR and/or SBP HR > SBP
The presence of a prior myocardial infarction
incidence of reinfarction in the perioperative period 48 72 hrs postoperatively
related to the time elapsed since the previous MI
delay the elective surgery for about 6 mos after MI (5 6%), 50 x (n: 0.13%)
intrathoracic or intra-abdominal operations lasting longer than 3 hours
Potential drug interactions
Coexisting non-cardiac disease
Patient can remain asymptomatic despite 50 70% stenosis of a major coronary artery
ECG
Myocardial ischemia
S-T segment depression > 1 mm
Prior myocardial infarction
Cardiac hyperthrophy
Abnormal cardiac rhythm and/or conduction
Electrolyte abnormalities
Exercise ECG
stimulates SNS
direct laryngoscopy
tracheal intubation
surgical incision
Resting ECG in the absence of angina pectoris may be normal despite extensive CAD
Modulation of SNS responses
Provide for the rigorous control of hemodynamic variables

Based on:
preoperative evaluation of left ventricular function
Maintenance of a favorable balance between myocardial O
2
requirement and delivery
tachycardia
systolic hypertension
arterial hypoxemia
diastolic hypotension
more important than the specific technique or drugs
Preoperative medication
to produce sedation
to allay anxiety
if unopposed catecholamine secretion
myocardial O
2
requirements
SBP
HR
benzodiazepine
scopolamine + morphine
transdermal nitrogycerine
Rapidly acting IV drugs
Ketamine associated with HR and SBP
not popular
Tracheal intubation
facilitated by Succhinylcholine or Nondepolarizing MR

MI may accompany hypertension and tachycardia
brief duration (<15 sec)
to minimize the magnitude of circulatory changes
Lidocaine
laryngotracheal (2 mg/kg)
IV (1.5 mg/kg)
short-acting opioid
Fentanyl 1 3 g/kg/IV, 2 to 4 mins before DL
Esmolol (200 g/kg/min IV)
based on left ventricular function

CAD, but normal left ventricular function
SBP, HR in response to stimulation
volatile anesthetic with/without N
2
O
to control myocardial depression
N
2
O opioid + volatile anesthetic
to treat acute in SBP
drug-induced in SVR > drug-induced myocardial depression
isoflurane
sevoflurane
desflurane

Low blood solubility
rapid
Impaired left ventricular function

may not tolerate myocardial depression produced by volatile anesthetics
high dose opioid technique
opioid + N
2
O technique
N2O, when combined with opioid
may produce undesirable in SBP and CO
Regional anesthesia
Flow through critically narrowed coronary arteries is pressure-dependent
SBP associated with RA > 20% of the pre-block
should be treated
fluids infusion
sympathomimetic
ephedrine
phenylephine
Isoflurane
more potent coronary arteriole vasodilator than sevoflurane or desflurane
could divert blood flow
from ischemic areas to non-ischemic area of myocardium
coronary artery steal
Volatile anesthetics
myocardial O
2
requirement
SBP
coronary perfusion pressure
coronary artery steal
Monitoring
Complexity of the operative procedure
Severity of the coronary artery disease
ECG
non-invasive
balance between myocardial O
2
requirement and myocardial O
2
delivery
myocardial ischemia S-T depression
V5 left ventricle
TEE
ventricular wall motion abnormality
most sensitive indicator for MI
invasive and not practical
Central venous pressure
may not reliably reflect left heart filling pressure
in the presence of left ventricular dysfunction
For selected high risk patients
recent MI
CHF
unstable angina
Signs of MI
aggressive treatment of adverse changes in HR and/or SBP
tachycardia
propanolol
esmolol
SBP
nitropruside
nitroglycerine
more appropriate choice when MI is associated with normal SBP
hypotension
sympathomimetics
to rapidly restore pressure-dependent perfusion
intravenous infusion of fluids
myocardial O
2
requirements for volume work < pressure work

pulmonary artery catheter
for monitoring responses of ventricular function
Monitoring
Postoperative care
Analgesia
Sedation
To blunt excessive SNS activity
Facilities vigorous control of hemodynamic variables

intensive and continuous monitoring
to detect myocardial ischemia, which is often asymptomatic

! Identification and treatment
cardiac morbidity
Temperature
hypothermia shivering
abrupt in myocardial O
2
requirement
minimize in body temperature
O
2
supplementation
Congestive Heart Failure
should not be performed as an elective surgery
Associated with postoperative morbidity
optimally treated
when surgery can not be delayed
chose of drugs/techniques
goal : optimizing cardiac output

GA: induction : ketamine
maintenance: volatile anesthetic is not recommended
potential for cardiac depression
high dose opioid may be justified
positive pressure ventilation may be beneficial
pulmonary congestion
improving oxygenation
invasive monitoring
continuous infusion of dopamine and/or dobutamine
maintenance of cardiac contractility
RA: for peripheral surgery
SVR secondary to peripheral SNS blockade
facilitate left ventricular stroke volume
Essestial Hypertension
Sustained increases in systemic blood pressure independent of any known cause
systolic blood pressure > 160 mmHg
diastolic blood pressure > 90 mmHg
Tx with appropriate drugs
incidence of stroke and congestive heart failure

incidence of hypotension and MI on ECG during maintenance of anesthesia
in patient who remain hypertensive before the induction of anesthesia

SBP during intraoperative period
more likely to occur in patient with history of essential hypertension
regardless of the degree of pharmacology control of SBP preoperatively
no evidence of postoperative cardiac complications
as long as preoperative diastolic BP is not higher than 110 mmHg
adequacy of SBP control
drug therapy
!!! maintain current therapy throughout the perioperative period
extent of the disease
major organ dysfunction influences drug selection
assumed to have coronary artery disease until proven otherwise
evidence of peripheral vascular disease

Consideration of the implications of exaggerated SBP responses
elicited by painful intraoperative stimulation

Shift to the right of the curve for the autoregulation of cerebral blood flow
more vulnerable to cerebral ischemiashould perfusion pressure decrease
Exaggerated decrease in SBP may occur
unmasking of decrease intravascular fluid volume due to chronic hypertension
particularly if hypertension is present preoperatively

Ketamine rarely selected

Exagerated increase in SBP during direct laryngoscopy are predictable
MI
ensure maximal attenuation of SNS responses evoked by DL
volatile anesthetics
IV opioids
lidocaine
limit the duration of DL < 15 sec, if possible
Undesirable hypotension
Adjust the concentration of anesthetic drugs
to minimize wide fluctuations in SBP
more important than preoperative control of hypertension

N
2
O + volatile anesthetic
for rapid adjustment in the depth of anesthesia in response to or SBP
attenuating SNS, which is responsible for pressor responses

desflurane
sevoflurane

N2O + Opioid
the addition of a volatile anesthetic is often necessary to control undesirable SBP
particularly during periods of maximal surgical stimulation

Nitroprusside
-Blockers : esmolol or labetalol
Low blood solubilities
Hypotension that occurs during maintenance of anesthesia:
the concentration of volatile anesthetics
IV fluids infusion
to intravascular fluid volume
sympathomimetics
to restore perfusion pressure until underlying cause can be corrected
ephedrine
Regional anesthesia
Questionable choice
when high levels of SNS blockade would be associated with the sensory level
necessary for planned surgery
possibility of excessive decreases in SBP
vasodilatation unmasks a decreased intravascular fluid volume
associated with chronic hypertension
Choice of intra-operative monitors
Influenced by the complexity of the surgery

ECG
goal: recognizing changes suggestive of MI

invasive monitors: arterial and/or pulmonary catheters
if major surgery is planned
evidence of left ventricular dysfunction pre-operatively

Transesophageal echocardiography
an alternative to placement of a pulmonary artery catheter
Hypertension in the early postoperative period
frequent
adequate analgesia
pharmacologically decrease SBP
nitroprusside, continuous IV
labetalol (0.1 0.5 mg/kg/IV

Disorder of endocrine gland function:
May be the primary reason for surgery
May co-exist in patient requiring operation unrelated to the disorder
Preoperative evaluation of endocrine function:
Absence of glucose in the urine
SBP and HR normal
Body weight unchanged
Sexual function normal
No history of relevant drug therapy
Diabetes Mellitus
The most common endocrine disease in surgical patients
Broad range of severity
The manifestation can be altered in response to stress
Chronic systemic disease
An array of abnormalities, the most notable of which is
disturbed glucose metabolism resulting inappropriate hyperglycemia
Anesthetic Management
Principle goal:

to mimic normal metabolism as closely as possible by avoiding:
hypoglycemia adequate supply of exogenous glucose
excessive hyperglycemia
ketoacidosis
dehydration
electrolyte imbalance
Exogenous insulin
Pre-operative
Should be in the best state of metabolic control that is possible preoperatively
History and PE
detect symptoms of CVD, CAD, peripheral neuropathy
Laboratory test
ECG
blood glucose, creatinine and potassium levels
urinalysis (glucose, ketones, albumin)
Evidence of stiff joint syndrome
difficult to perform laryngoscopy
Evidence of cardiac autonomic nervous system neuropathy
resting tachycardia, orthostatic hypotension, absent variation in HR w/ deep breathing
prevent development of angina pectoris (painless MI)
risk of sudden death, cardiovascular lability
Evidence of vagal autonomic nervous system neuropathy
gastroparesis risk of aspiration of gastric content
Evidence of peripheral neuropathy
more susceptible to compression injury

Preoperative evaluation and treatment
hyperglycemia
ketoacidosis
electrolyte imbalance
Hba1c

manifestation of :
cerebral vascular disease
renal dysfunction

Should be scheduled for surgery early in the morning
Well controlled, diet treated NIDDM
does not require special treatment before and during surgery

Well controlled IDDM
brief, out-patient surgery
Subcutaneous RI may not require any adjustment
oral sulfonylurea may be continued until the evening before surgery
delayed hypoglycemia in the absence of any caloric intake
biguanide
less risk of hypoglycemia
metformin
risk of lactic acidosis

Poorly controlled IDDM
preoperative admission

Intra-operative
Anesthetic plan depend on the presence of end organ disease
heart disease invasive monitoring
renal disease fluid management and drug selection
gastroparesis aspiration consideration
Blood glucose levels
preoperative + postoperative
intraoperative
the duration and magnitude of surgery
the stability of the diabetes
Dehidration
may be presence
osmotic diuresis
Intra-operative
Glucose administration
avoid an overdose
standard glucose dose for adult:
5 10 g/hr or 100 200 mL of 5% glucose/hr
Positioning of patient
peripheral nerve may already be partly ischemic
susceptible to pressure or scratch injury
Intra-operative
The choice of drugs or techniques for induction or maintenance of anesthesia
less important than monitoring of blood glucose concentration
treatment of potential physiologic derangement
associated with diabetes
GA
tracheal intubation w/ cuffed tube

RA
preserve glucose tolerance
high incidence of peripheral neuropathy
diabetic sensory neuropathy could be erroneously attributed to RA
Management of diabetes
To prevent hypoglycemia
To accept mild hyperglycemia
can be corrected gradually in the postoperative periode
Monitoring blood glucose concentration
more important than selection of formula
5% glucose/IV
Regiments for exogenous insulin replacement
Subcutaneous insulin administration
administer to the usual daily intermediate-acting dose of insulin on the morning of surgery
initiate infusion of glucose (5 10 g/hr) with initiation of insulin infusion

Continuous intravenous infusion of insulin
Regular insulin (50 units in 500 mL NS) at 0.5 1 unit/hr
initiate infusion of glucose (5 10 g/hr) with initiation insulin infusion
measure blood glucose concentration as necessary (usually every 1 2 hours)
and adjust insulin infusion accordingly

<80 mg/dL discontinue insulin infusion
administer 25 mL of 50% glucose
remeasure blood glucose concentration in 30 minutes
80 120 mg/dL decrease insulin infusion rate by 0.3 unit/hr
120 180 mg/dL no change in insulin infusion rate
180 220 mg/dL increase insulin infusion rate by 0.3 unit/hr
>220 mg/dL increase insulin infusion rate by 0.5 unit/hr
Diabetic Emergencies
Hyperosmolar non-ketotic coma
Diabetic ketoacidosis
Hypoglycemia
Hyperosmolar non-ketotic coma
Elderly patients with impaired thirst mechanism
Minimal or mild diabetes
Profound hyperglycemia (>1000 mg/dL)
Absence of ketoacidosis, normal arterial pH
Hyperosmolarity (> 330 mOsm/L seizures, coma, venous thrombosis)
Osmotic diuresis (hypokalemia)
Hypovolemia
Seizures and coma (decreased intracellular brain water due to hyperosmolarity)
Diabetic ketoacidosis
Metabolic acidosis
Hyperglycemia (300 500 mg/dL)
Dehydration (osmotic diuresis and vomiting)
Hypokalemia
Skeletal muscle weakness (hypophosphatemia with correction of acidosis)
insufficient insulin to block the metabolism of fatty acids
resulting in the accumulation of acetoacetate and -hydroxybutyrate
Management
Regular insulin U/IV
followed by a continuous IV infusion
insulin in U/hr = blood glucose/150)
Intravenous fluids (isotonic)
as guided by vital signs and urine output
Potassium Chloride 10 40 mEq/hr/IV
when urine output exceeds 0.5 mL/kg/hr
Glucose 5%
100 mL/hr, when serum glucose concentration drops below 250 mg/dL
Consider Sodium Bicarbonate IV
to correct pH < 7.1
Hypoglycemia
Produces signs of SNS stimulation
tachycardia
hypertension
diaphoresis

in anesthetized patient may be:
masked
misdiagnosed
as an inadequate level of anesthesia relative to surgical stimulation
If renal disease prolongs the action of insulin or oral hypoglycemic agents
Avoidable !
Thyroid Gland
Thyroid metabolism and function
Thyroxine (T
4
) and Tri-iodothyroxine (T
3
)
major regulator of cellular metabolic activity

Thyroid gland is solely responsible for the dayly secretion of T
4
80% of T
3
is produced by extrathyroidal deiodination of T
4
mediated most of the excess effects of thyroid hormones (hyperadrenergic state)
Effect of T
3
on receptor concentration:
number of receptors
number of cardiac cholinergic receptors
Tests for the diagnosis of thyroid gland dysfunction
T
4
T
3
TSH

Hyperthyroidism Normal
Primary hypothyroidism
Secondary hypothyroidism
Hyperthyroidism
A hypermetabolic state
nervousness
heat intolerance
muscle weakness
tremors
weight loss
cardiovascular signs
arrhythmias (ST, AF)
systolic murmurs
high output
CHF
Etiologies:
Graves disease
Toxic multinodular goiter
Subacute thyroiditis
Toxic adenoma
Ovarian tumor secreting thyroid hormone (struma ovarii)
TSH or -HCG overproduction
Hyperthyroidism
Anesthetic consideration:

Preparation
proppylthiouracil
inhibit synthesis and peripheral conversion of T
4
to T
3
inorganic iodine
inhibits hormone release
-adrenergic antagonists
HR to < 90 beats/min
glucocorticoids
hormone release and peripheral conversion of T
4
to T
3

Goal:
to achieve a depth of anesthesia that prevents an exaggerated SNS response
to surgical stimulation
avoid administration of drugs that stimulate SNS
GA
Thiopental
thiourea structure antithyroid activity
Ketamine can stimulate SNS
N
2
O not reliably suppressing SNS activity
Inhaled anesthetic do not MAC
CO accelerates uptake of inhaled anesthetic
need to increase the inspire concentration
to achieve brain partial pressure euthyroid patient
temp. MAC
muscle relaxant drug that lack of cardiovascular effect
co-existing muscle weakness initial dose, close monitoring
RA
epinephrine should not be added to the local anesthetic solution
Monitoring
Early recognition of activity of the thyroid glands
suggests the onset of thyroid storm

temperature
ECG

Exophthalmus
corneal ulceration
drying
eye protection
Treatment of thyrotoxicosis crisis
Block sympathetic response
Propanolol: 1 2 mg/IV, repeat as needed
40 80 mg/PO, repeat q6h
Verapamil: 5 10 mg/IV, repeat as needed
Block thyroid hormone synthesis
Propylthiouracil (PTU) : 250 mg/PO q4-6h
Methimazole : 30 mg/PR q8h
Block thyroid hormone release
Sodium iodide (SSKI): 10 drops/PO q12h
Ipodate: 1g/PO qd
Dexamethasone: 2 mg/PO q6h
Block T
4
to T
3
conversion
-adrenergic blockade
Ptu
Ipodate
Dexamethasone
Supportive therapy
Fluids and electrolyte replacement
Cooling
Plasmapheresis
Hypothyroidism
Lethargy
Intolerance to cold
Facial edema with an enlarged tongue
Bradycardia, diminished barereceptor reflexes
Reversible cardiomyopathy
Decreased cardiac output
Pericardial effusion, ascites
Peripheral vasoconstriction
Constipation and an adynamic ileus with delay gastric emptying
Atrophy of adrenal cortex
dilutional hyponatremia, decreased water excretion

Hypothyroidism
Myxedema coma
Profound hypothyroidism
decrease mental status associated with hyporesponsiveness to CO
2

congestive heart failure
hypothermia
exaggerated symptoms of hypothyroidism
decompensated state
surgery
drugs
trauma
infections
Anesthetic consideration
Elective surgery should be postponed in severe hypothyroidism
Preoperative sedative should be administered with caution
Cortisol supplementation may be necessary
Hypovolemia may be present
Anemia should be corrected
Airway and respiratory difficulties may be due:
enlarged tongue
relaxed oropharyngeal tissue
CO
2
insensitivity
poor gastric emptying
increased sensitivity to all depressant medications
Complications following thyroid surgery

Thyroid storm
A state of physiologic decompensation in severe thyrotoxicosis
surgical stress 6 18 hr postoperatively
diarrhea
vomiting
hyperpyrexia (38 41
O
C)
hypovolemia, irritable, delirium or coma
DD/ : malignant hyperthermia
pheochromocytoma
inadequate anesthesia
sepsis
hemorrhage or transfusion/drug reaction
Airway obstruction
CT of the neck
Reccurent laryngeal nerve damage
unilateral hoarseness
bilateral aphonia
Hypoparathyroidism
develop in 24 48 hr, include laryngospasm
INITIAL ASSESSMENT
Primary survey
ABC sequences suggested for CPR
Secondary survey
A more comprehensive survey follows the primary surveys
PRIMARY SURVEY
A = Airway
assumed all multiple trauma patients have
a cervical spine injury initial stabilization before airway manipulation
manual or sand bags or collar
neutral position
a full stomach
hypovolemic
remove all secretions, blood, vomitus and any existing foreign bodies
If the airway is patent and ventilation is adequate
supplemental O
2
monitor closely
initiate other resuscitative measures
Endotracheal intubation
Awake patient
nature of injury
ability to cooperate
general stability
awake nasal or orotracheal intubation
blind nasal intubation
rapid sequence intubation
awake tracheostomy
Combative patient
hypoxemia must always be excluded
rapid sequence induction and orotracheal intubation
Unconscous patient
orotracheal intubation
Intubated patient
verify the position of the endotracheal tube
B = Breathing
Most critically ill trauma patients require assisted if not controlled ventilation
bag-valve device
immediately after intubation
during period of transport
deliver 100% O
2

until oxygenation is assessed by ABG

Patient with head trauma
hyperventilation
ICP

Ventilation may be compromised by
pneumothorax
flail chest
ET obstruction
direct pulmonary injury
C = Circulation
Hemodynamic
initially assessed by palpating pulses

Intravenous access
at least 2 large (min: 16-G) catheters are required
injury of the abdomen (and with potential for major venous disruption)
above the level of diaphragm
obstruction or disruption of the superior vena cava is suspected
below the level of the diaphragm
Peripheral venous cannulation failure
percutaneous
subclavian or femoral vein
internal or external jugular vein
surgical cutdowns
saphenous vein at the ankle or thigh
intraosseous infusion
pediatric patients
Volume resuscitation
rapid infusion of warmed crystalloids
colloids?
transfusion of type-specific blood
non-cross-matched blood
universal donor : type-O-non-cross-matched PRC

Vasopressor infusions
should not substitute for adequate volume replacement
as temporary measure
if perfusion pressure is clearly inadequate during ongoing volume resuscitation
History
Patient, family members, and prehospital care personel
Abbreviated history
Fasting
Mechanism of injury
blunt trauma
widespread energy transfer to the body
multiple injury in various anatomic locations
penetrating trauma
injury confined to the penetration tract
high velocity gunshot wounds
tissue disruption in area adjacent to the penetration track
Physical Examination
Frequent monitoring of vital signs
mandatory
provides an ongoing assessment
airway, neurologic, cardiovascular and pulmonary stability
Assess obvious sites of hemorrhage as well as less obvious sites
Investigate neurologic deficits and vascular compromise
Diagnostic Studies
Laboratory studies
blood type and cross-matching
CBC, platelet count
PT, APTT
Electrolytes
glucose
BUN, Creatinine
Urinalysis
Radiographic studies
lateral cervical spine, must include C7 T1 interface
sufficient quality to delineate the structures of interest (soft tissue and bones)
CXR
minimum for penetrating injury of the trunk
Pelvis, AP view
12-lead ECG
on all major trauma patients
to evaluate the presence of myocard injury
contusion, tamponade, ischemia and arrhythmias
Monitoring
Dictated by :
severity of the injuries
pre-existing medical problems

Arterial line
hemodynamic instability
respiratory failure
Central venous pressure line
to assess volume status
to administer vasoactive drugs
ventricular dysfunction
severe coronary artery disease
valvular heart disease
multiple organ system involvement
PATIENT SELECTION
ASA I
ASA II
ASA III
ASA IV
who are stable medically
Admission and complications correlate with:
type of procedure
duration of surgery
use of general anesthesia
patient age
INAPPROPRIATE FOR OUTPATIENT SURGERY
Pediatric
formerly premature infants < 46 wks post-conceptual age
risk of post anesthesia apnea
infants with respiratory disease
infants with cardiovascular disease
children with fever, cough, sore throat, coryza or other signs of recent
onset or worsening upper respiratory infection
Adult
Expected to have major blood loss or undergoing major surgery
ASA III and IV who require complex or extended monitoring or
postoperative treatment
Morbidly obe patients with significant respiratory disease
Need a complex pain management
Significant fever, wheezing, nasal congestion, cough or other symptom of
a recent upper respiratory infection
PATIENT PREPARATION
Preoperative testing
Minimal
CBC starting at age 50 yrs
ECG starting at age 40
Creatinine & BUN starting at 65 yrs
others performed as indicated
Pre-hospital instructions
diet guidelines
medications
preanesthetic visit
healthy patients immediately prior to the planned procedure
Premedication
Anxiolytics
Psychological reassurance
if necessary Midazolam 1 2 mg/IV
Aspiration prophylaxis
Non particulate antacids Na citrate 30 mL just before the procedure
H
2
-receptor antagonist Ranitidine 150 mg PO the night before surgery
Metoclopramide 10 mg PO or IV prior to surgery
Opioids
Fentanyl 50 100 g IV may be given
if preoperative pain is present
Intravenous access
small IV catheter

Standard monitoring
Bispectral index monitor
to allow more accurate titration of hypnotic agents
speed recovery
GENERAL ANESTHESIA
Induction
Propofol
short duration
depression of pharyngeal reflex
reduced incidence of postoperative emesis
Sevoflurane
Airway management
Face mask, LMA or tracheal intubation
Muscle Relaxant
Succinylcholine or Mivacurium
Maintenance
Volatile anesthetic
sevoflurane with or without N
2
O
Propofol
Alfentanil or Remifentanil
supplemental local anesthesia
N2O
REGIONAL ANESTHESIA
Ideal agents
Rapid onset
to minimize case delay
Short duration
to facilitate quick recovery and discharge

Patient selection
the benefits of RA will be negated if heavy sedation is required

Separate areas for RA
decrease time in the OR waiting for onset of anesthesia
should be fully equipped with the usual monitoring and resuscitative device
Monitored anesthesia care
For some patient with complex medical problems
Operation would be done under local anesthesia
to monitor the patient
to provide medications
sedatives or opioids

POSTOPERATIVE CARE
PACU
awake, oriented, stable VS, - PONV, minimal pain/discomfort,
able to sit without assisstance
phase II
fast track
Pain
pain on admission to PACU IV
awake, no pain PO
Nausea and vomiting (PONV)
predisposing factors
history of PONV
history of severe motion sickness
use of large doses of opioids
pelvic procedures in female
gastric distention
severe postoperative pain
Discharge criteria
operative site: no hematoma or active bleeding
ability to urinate after spinal/epidural anesthesia
adequate pain control
discharge instruction

Anesthesia For High Risk Patients

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