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Physiologic Changes of Aging
Cardiovascular
Arteries stiffen with agepulse pressure waveformaugmentedearly diastole to late systole
faster propagation
diastolic,systolic pressurepulse 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 b
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Respiratory
Physiologic Changes of Aging
Parenchymal changes
30% of alveolar tissue is lost between ages 20 and 80
diminishing elastic recoil and parenchymal fractionairway patency
Residual volume, Closing volume and FRC
VC and FEV1progressive V/Q mismatchingage-dependent decrease in arterial O2tensio Physiologic dead space
Diffusing capacity
Chest wall changesStiffer chest wall
respiratory muscles
Depressed ventilatory response to hypoxia and hypercarbiaDecreased protective airway reflexes
aspiration risk
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Physiologic Changes of Aging
Renal
Serum creatinine remains stable
age-associated decreases of creatinine clearance offset by reduced creatinine productio
normal creatinine levelabsence of renal impairment ?
Progressive atrophy of renal parenchyma and sclerosis of vasculature structuresRBF
GFR
Reduced ability to correct alteration :
electrolyte concentrations
intravascular volume
free waterReduced GFR
delayed renal drug excretion
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Physiologic changes of aging
Central Nervous System
Progressive loss of neurons
Decreased neurotransmitter activity
Cerebral autoregulatory response to BP, CO2and O2maintained
anesthetic requirement
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Physiologic Changes of Aging
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
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Physiologic Changes of Aging
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
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Pharmacologic Implications of Aging
binding site for most lipophilic basic drugs
alpha1-acid glycoprotein
frequency and severity of adverse drug reactions
MAC for inhalational anesthetic
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Anesthetic Considerations In The Elderly
Age-related coexisting disease is a major predictor for perioperative morbidity and mortaliage 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 capacitytherapeutic index of anesthetic interventions
highly variable
unpredictable
may be manifest only under severe stress
vigilance
preparation for contingencies
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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 drugsmonitors
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Coronary artery disease
Often asymptomatic
A common accompaniment of aging40% will either have or be at risk
morbidity and mortality
Routine preoperative cardiac evaluation:
historyPE
ECG
ambulatory ECG monitoring (Holter monitoring)
exercise stress testing
transthoracic or transesophageal echocardiography
radionuclide ventriculography
dypiridamole-thallium scintigraphy
cardiac catheterization
angiography
Select
patien
Best medical condition possible
before elective cardiac or non-cardiac surge
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Coronary artery disease
Patient History
Cardiac reservelimited 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 MIHR and/or SBPHR > SBP
The presence of a prior myocardial infarction
incidence of reinfarction in the perioperative period 4872 hrs postoperatively
related to the time elapsed since the previous MI
delay the elective surgery for about 6 mos after MI (56%), 50 x (n: 0.1
intrathoracic or intra-abdominal operations lasting longer than 3 hoursPotential drug interactions
Coexisting non-cardiac disease
Patient can remain asymptomatic despite 5070% stenosis of a major coronary arte
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Coronary artery disease
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 O2requirement and deliv
tachycardia
systolic hypertension
arterial hypoxemia
diastolic hypotension
more important than the specific technique or drugs
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Coronary artery disease
Induction of anesthesia
Rapidly acting IV drugs
Ketamineassociated with HR and SBP
not popular
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Coronary artery disease
Tracheal intubation
facilitated by Succhinylcholine or Nondepolarizing MR
MI may accompany hypertension and tachycardia
brief duration (
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Coronary artery disease
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/withoutN2O
to control myocardial depression
N2Oopioid + volatile anesthetic
to treat acute in SBP
drug-inducedin SVR > drug-induced myocardial depressisoflurane
sevoflurane
desflurane
Low blood solubility
rapid
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Impaired left ventricular function
may not tolerate myocardial depression produced by volatile anesthetics
high dose opioid techniqueopioid + N2O 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 infusionsympathomimetic
ephedrine
phenylephine
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Monitoring
Complexity of the operative procedure
Severity of the coronary artery disease
ECG
non-invasive
balance between myocardial O2requirement and myocardial O2delivery
myocardial ischemiaS-T depression
V5 left ventricleTEE
ventricular wall motion abnormality
most sensitive indicator for MI
invasive and not practical
Pulmonary artery catheter
Central venous pressuremay not reliably reflect left heart filling pressure
in the presence of left ventricular dysfunction
For selected high risk patients
recent MI
CHF
unstable angina
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Signs of MI
aggressive treatment of adverse changes in HR and/or SBP
tachycardia
propanolol
esmolol
SBP
nitropruside
nitroglycerinemore appropriate choice when MI is associated with normal S
hypotension
sympathomimetics
to rapidly restore pressure-dependent perfusion
intravenous infusion of fluids
myocardial O2requirements for volume work < pressure work
pulmonary artery catheter
for monitoring responses of ventricular functio
Monitoring
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Postoperative care
Analgesia
Sedation
To blunt excessive SNS activity
Facilities vigorous control of hemodynamic variables
intensive and continuous monitoringto detect myocardial ischemia, which is often asymptomatic
! Identification and treatment
cardiac morbidity
Temperature
hypothermiashiveringabruptin myocardial O2requirement
minimize in body temperature
O2supplementation
Congestive Heart Failure
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Congestive Heart Failure
should not be performed as an elective surgery
Associated with postoperative morbidity
optimally treated
when surgery can not be delayedchose of drugs/techniques
goal : optimizing cardiac output
GA: induction : ketamine
maintenance: volatile anesthetic is not recommended
potential for cardiac depressionhigh dose opioid may be justified
positive pressure ventilationmay be beneficial
pulmonary congestion
improving oxygenation
invasive monitoring
continuous infusion of dopamine and/or dobutaminemaintenance of cardiac contractility
RA: for peripheral surgery
SVR secondary to peripheral SNS blockade
facilitate left ventricular stroke volume
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Essestial Hypertension
Sustained increases in systemic blood pressure independent of any known cau
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 preoperat
no evidence of postoperative cardiac complications
as long as preoperative diastolic BP is not higher than 110 mmHg
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Management of anesthesia
Preoperative evaluation
adequacy of SBP controldrug therapy
!!! maintain current therapy throughout the perioperative period
extent of the disease
major organ dysfunctioninfluences 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
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M i t f th i
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Maintenance of anesthesia
Adjust the concentration of anesthetic drugs
to minimize wide fluctuations in SBPmore important than preoperative control of hypertension
N2O + volatile anestheticfor 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
particularly during periods of maximal surgical stimulation
Nitroprusside
-Blockers : esmolol or labetalol
Low blood solubilities
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Maintenance of anesthesia
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
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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 volumeassociated with chronic hypertension
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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
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Postoperative management
Hypertension in the early postoperative period
frequent
adequate analgesia
pharmacologically decrease SBP
nitroprusside, continuous IVlabetalol (0.10.5 mg/kg/IV
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A challenge :
Intraoperative managementPostoperative management
Regardless of the operative site
particular risk:
thoracic
upper abdominal
Co-existing disease:
coronary artery disease
essential hypertension
OBSTRUCTIVE AIRWAY DISEASE
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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 exhala
despite aggressive therapy
regional differences in airway resistance
areas of ventilation-to-perfusion mismatching
arterial hypoxemia
CO2retentionrespiratory acidosis
cough and sputum production
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Symptom: dyspnea work of breathing
PE : wheezing during exhalationturbulence gas flow through narrowed airw
Chest X-ray : hyperinflated lung, radiolucencypulmonary blood flow
flattened diaphragm
Pulmonary function studies : expiratory flow ratesairway resistance
FEV1< 80%
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Bronchial asthma
Classic example of obstructive airway diseaseMost common chronic inflammatory disease of the airway
characterized by acute and reversible increases in airway resistanc
irreversibleCOPD
Chronic inflammatory changes in the submucosa of the airwayIncreased airway responsiveness (hyper-reactivity) to various stimuli
Reversible expiratory airflow obstruction
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Bronchial asthma
Clinical symptoms:during periods of normal to near normal pulmonary function
no physical findings
acute bronchial asthma attack
wheezing
cough
non productiveproduction of copious amount of tenacious sput
dyspneaparallel to the severity of expiratory airflow obstruction
FEV1: 2575% vital capacity
the flow-volume loopdownward scooping of the expiratory limb of the loop
B hi l th
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Bronchial asthma
Estimation of the severity of bronchial asthma
Expiratory airflow FEV1 PaO2 PaCO2Obstruction (% predicted) (mmHg) (mmHg
Mild (asymptomatic) 6580 > 60 < 40
Moderate 5064 > 60 < 45
Marked 3549 < 60 > 50
Severe (status asthmaticus) < 35 < 60 > 50
Bronchial asthma
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Management of anesthesia
Preoperatively
absence of : dyspneawheezing
PFT indicated for a thoracic or abdominal operation
before and after bronchodilator therapy
ABG adequacy of ventilation or arterial oxygenation
persistent symptomstreated with glucocorticoids (inhaled or systemic)
continue throughout perioperative period
supplementation with cortisol
if suppresion of the hypothalamic-pituitary-adrenal axis is suspec
anticholinergicsindividualized
airway resistanceviscosity of the secretions
H2antagonistsantagonism of H2-mediated bronchodilation
unmask H -mediated bronchoconstriction
No acute exacerbation of bronchial asthma
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R id IV i d ti
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Rapid IV inductionThiopental
Etomidate
Propofol may blunt tracheal intubation-induced bronchospasm
Ketamine sympathomimetic effects on bronchial smooth muscleairway resistance
secretions
Before intubationsufficient 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 effectsNO production
Bronchodilator
Associated with cardiac dysrhythmias in the presence of SNS stimulation
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Neuromuscular blocking drugs
not associated with endogenous histamine release
PaO2PaCO2
Maintained at normal levels
slow RR (6 to 10)
to allow adequate time for passive exhalationhigh inspiratory flow rate
PEEPmay not be ideal
adequate exhalation may be impaired
Liberal IV fluid administration
ensuring the presence of less viscous secretions
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At the conclusion of elective surgery
deep extubationanesthesia depth still sufficient to suppress hyperreactive airway reflexes
bronchospasm does not predictably follow administration of anticholinestera
Lidocaine/IV may decrease the likelihood of airway stimulation
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Intraoperative Bronchospasm
Deepening of anesthesia with volatile anesthetic
-2 agonist
Corticosteroids
Mechanical obstructionInsufficient anesthetic concentration
Pulmonary aspiration
Endobronchial intubation
Pneumothorax
Pulmonary embolusAcute bronchial asthma
?
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Pulmonary emphysema
Loss of elastic recoil of the lung
collapse of airways during exhalation
airway resistance
Severe dyspnea
work of breathing
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Preoperative evaluation
Determine the severity of the disease
Elucidate any reversible components
infections
bronchospasm
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PFTDo not always correlate with postoperative outcome
dyspnea
coughsputum production
exercise tolerance
ABGmay be normal (pink puffer)
high minute ventilation
to overcome airway resistance
PaCO2> 50 mmHgrisk of post operative respiratory failure
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Risk of postoperative respiratory failure:
vital capacity < 50% of the predicted value
FEV1< 50% of the predicted value
FEV1< 2 liters
Arterial hypoxemia and/or hypercarbia is present
!!!
preoperative detection and treatment of cor pulmonalesupplemental O2
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Management of anesthesia
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 lun
Management of anesthesia
General anesthesia
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General anesthesia
humidified inhaled gases to prevent drying of secretions, systemic hydration
mechanical ventilation of the lung small tidal volumes
small breathing rates
N2O:
limitation of the inhaled concentration of oxygen
passage of this gas into bullae from emphysema
enlargement and rupturetension pneumothorax
Opioids:
less ideal for maintenance of anesthesia to ensure amnesia
need high concentration of N2O
substituting a low concentration of volatile anesthetic for N2O
postoperative ventilatory depression
chronic hypercarbia should not be abruptly corrected
inspiratory flow
Chronic Bronchitis
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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 pulmonaleearly
Small airway account to only a minor proportion of total airways resistancechronic bronchitis must be advanced before dyspnea become appare
Restrictive Pulmonary Disease
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y
Lung compliance
lung volume
vital capacity in the presence of a normal FEV1
Dyspneawork 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
PaCO2hyperventilation
usually maintained at a decreased to normal value, until far advance
Severe Pulmonary hypertension
Acute restrictive pulmonary disease
l k f i t l fl id i t th i t titi d l li f th l
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leakage of intravascular fluid into the interstitium and alveoli of the lu
pulmonary edema
Acute Respiratory Distress Syndrome
Aspiration pneumonitisNeurogenic 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
KyphoscoliosisObesity
Ascites
Pregnancy
Management of anesthesia
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Management of anesthesia
RA
appropriate for peripheral surgery
sensory level above T10
associated with the impairment of respiratory muscle activity
GAdoes 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 mmHgdifficult to generate effective cough
preoperatively
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Effect of Anesthesia on Renal FunctionIndirect effects
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Cardiovascular effects
inhalational and intravenous agents
cardiac depressionvasodilatation
RA
sympathetic block
Neural effects
sympathetic activation
light anesthesiaintense 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+excret
IV fluid administration
Renal vascular resistanceActivates hormonal system
RBF, GFR, UO
Catecholamines
Renin, Angiotensin II, Aldosterone
ADH
ACTH, Cortisol
Effect of Anesthesia on Renal Function
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Direct effects minor
Volatile agents
Methoxyfluranepolyuric renal failure
defect in urinary concentrating ability
dose-related1 MAC for 2 hrs
release of fluoride ions ( > 50 mol/L )
Enflurane, Sevoflurane (possible)prolonged administration
fluoride excretion: GFR dependent
preexisting renal impairmentmore susceptible
Compound A: breakdown product of sevoflurane
FGF > 2 L/min
Halothane, Isoflurane, and Desfluranenegligible
Effect of Anesthesia on Renal Function
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Direct effects minor
Intravenous agents
opioids and barbiturate minor effect when used alone
+ N2O volatine agents
ketamineminimally 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 IIGFR
Effect of Anesthesia on Renal Function
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Direct effects minor
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 Functio
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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 arteriesNeurosurgical procedureADH
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Management of Anesthesia
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Induction 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
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Succinyl choline
acceptableassuming preexisting hyperkalemia is not present
Non-depolarizing MRnot dependent on renal clearance
intermediate and short acting
atracurium and cisatracuriumlaudanosineclearance delayed
initial dose
Administer subsequent dose based on the response to PNSConsider drug interaction
antibiotics, acidosis, electrolyte imbalance
Maintenance of anesthesia
N O
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N2O
FiO2?
Volatile anestheticscontrolling intraoperative hypertension
dose of MR
Desflurane
Isoflurane
Opioid
CV depression
avoid hepatotoxicity and nephrotoxicity
unreliable for controlling intraoperative hypertension
prolonged CNS & respiratory depressionaccumulation of pharmacologically active metabolites
V til ti
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Ventilation
Normocapnia is desirable
Hyperventilation
respiratory alkalosisoxyhemoglobin dissociation curve
Hypoventilationrespiratory acidosisK+
Fluid Management
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Hemodialysis dependent
narrow margin of safety :insufficient vs excessive fluid administration
replacement of insensible losses (including UO)0.9% saline
potassium-containing fluidsshould not administered to anuric patients
CVP measurementguiding fluid replacement
ECG monitoringfor recognizing signs of hyperkalemia
AV shuntsmust be carefully protected
Postoperaive period
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Postoperaive period
Hypertension
frequent problem
hemodialysis is the best treatment if fluid excess is the cau
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
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A challenge :
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A challenge :
Intraoperative management
Postoperative management Regardless of the operative siteparticular risk:thoracic
upper abdominal
Co-existing disease:coronary artery disease
essential hypertension
OBSTRUCTIVE AIRWAY DISEASE
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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 exhala
despite aggressive therapy
regional differences in airway resistanceareas of ventilation-to-perfusion mismatching
arterial hypoxemia
CO2retentionrespiratory acidosis
cough and sputum production
S t d k f b thi
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Symptom: dyspnea work of breathing
PE : wheezing during exhalationturbulence gas flow through narrowed airw
Chest X-ray : hyperinflated lung, radiolucencypulmonary blood flow
flattened diaphragm
Pulmonary function studies : expiratory flow ratesairway resistance
FEV1< 80%
Bronchial asthma
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Classic example of obstructive airway diseaseMost common chronic inflammatory disease of the airway
characterized by acute and reversible increases in airway resistanc
irreversibleCOPD
Chronic inflammatory changes in the submucosa of the airwayIncreased airway responsiveness (hyper-reactivity) to various stimuli
Reversible expiratory airflow obstruction
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Bronchial asthma
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Estimation of the severity of bronchial asthma
Expiratory airflow FEV1 PaO2 PaCO2Obstruction (% predicted) (mmHg) (mmHg
Mild (asymptomatic) 6580 > 60 < 40
Moderate 5064 > 60 < 45
Marked 3549 < 60 > 50
Severe (status asthmaticus) < 35 < 60 > 50
Management of anesthesia
Bronchial asthma
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Preoperativelyabsence of : dyspnea
wheezing
PFT indicated for a thoracic or abdominal operation
before and after bronchodilator therapy
ABG adequacy of ventilation or arterial oxygenation
persistent symptomstreated with glucocorticoids (inhaled or systemic)
continue throughout perioperative period
supplementation with cortisol
if suppresion of the hypothalamic-pituitary-adrenal axis is suspec
anticholinergicsindividualized
airway resistanceviscosity of the secretions
H2antagonistsantagonism of H2-mediated bronchodilation
unmask H -mediated bronchoconstriction
No acute exacerbation of bronchial asthma
Choice of anesthesia
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Regional anesthesia
an attractive choice
superficial or extremities surgery
General anesthesiainduction
maintenanceSuppression of airway reflexes
avoid bronchoconstriction of hyperreactive airways
in response to mechanical stimulation
Rapid IV inductionThiopental
Et id t
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Etomidate
Propofol may blunt tracheal intubation-induced bronchospasm
Ketamine sympathomimetic effects on bronchial smooth muscle
airway resistance
secretions
Before intubationsufficient 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 effectsNO production
BronchodilatorAssociated with cardiac dysrhythmias in the presence of SNS stimulation
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At the conclusion of elective surgery
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At the conclusion of elective surgery
deep extubation
anesthesia depth still sufficient to suppress hyperreactive airway reflexes
bronchospasm does not predictably follow administration of anticholinestera
Lidocaine/IV may decrease the likelihood of airway stimulation
Intraoperative Bronchospasm
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Deepening of anesthesia with volatile anesthetic
-2 agonist
Corticosteroids
Mechanical obstructionInsufficient anesthetic concentration
Pulmonary aspiration
Endobronchial intubation
Pneumothorax
Pulmonary embolusAcute bronchial asthma
?
Pulmonary emphysema
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Loss of elastic recoil of the lung
collapse of airways during exhalation
airway resistance
Severe dyspnea
work of breathing
Preoperative evaluation
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Preoperative evaluation
Determine the severity of the disease
Elucidate any reversible components
infections
bronchospasm
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Risk of postoperative respiratory failure:
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s o postope at ve esp ato y a u e:
vital capacity < 50% of the predicted value
FEV1< 50% of the predicted value
FEV1< 2 liters
Arterial hypoxemia and/or hypercarbia is present
!!!
preoperative detection and treatment of cor pulmonale
supplemental O2
Management of anesthesia
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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 lun
Management of anesthesiaGeneral anesthesia
humidified inhaled gases to prevent drying of secretions, systemic hydration
h i l til ti f th l ll id l l
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mechanical ventilation of the lung small tidal volumessmall breathing rates
N2O:
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 N2O
substituting a low concentration of volatile anesthetic for N2Opostoperative ventilatory depression
chronic hypercarbia should not be abruptly corrected
inspiratory flow
Chronic Bronchitis
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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 pulmonaleearly
Small airway account to only a minor proportion of total airways resistancechronic bronchitis must be advanced before dyspnea become appare
Restrictive Pulmonary Disease
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Lung compliance
lung volume
vital capacity in the presence of a normal FEV1
Dyspnea
work of breathing necessary to expand the poorly compliant lungsRapid and shallow breathing
to minimize the work of breathing in the presence of lung compliance
PaCO2hyperventilation
usually maintained at a decreased to normal value, until far advance
Severe Pulmonary hypertension
Acute restrictive pulmonary disease
leakage of intravascular fluid into the interstitium and alveoli of the lu
pulmonary edema
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p y
Acute Respiratory Distress Syndrome
Aspiration pneumonitisNeurogenic pulmonary edema
Opioid-induced pulmonary edema
High-altitude pulmonary edema
Chronic restrictive pulmonary diseasepresence of pulmonary fibrosis (sarcoidosis)
processes that interfere with expansion of the lungs
Effusions
Kyphoscoliosis
Obesity
Ascites
Pregnancy
Management of anesthesia
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RAappropriate 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
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The leading cause of death
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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
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y p
A common accompaniment of aging
40% will either have or be at riskmorbidity and mortality
Routine preoperative cardiac evaluation:
history
PEECG
ambulatory ECG monitoring (Holter monitoring)
exercise stress testing
transthoracic or transesophageal echocardiography
radionuclide ventriculography
dypiridamole-thallium scintigraphycardiac catheterization
angiography
Select
patien
Best medical condition possible
before elective cardiac or non-cardiac surge
Coronary artery diseasePatient History
Cardiac reser e
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Cardiac reservelimited exercise tolerance in the absence of significant pulmonary disease
Characteristic of angina pectorisstable : 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 anginaacute left ventricular dysfunction due to MI
HR and/or SBPHR > SBP
The presence of a prior myocardial infarction
incidence of reinfarction in the perioperative period 4872 hrs postoperatively
related to the time elapsed since the previous MI
delay the elective surgery for about 6 mos after MI (56%), 50 x (n: 0.1
intrathoracic or intra-abdominal operations lasting longer than 3 hours
Potential drug interactionsCoexisting non-cardiac disease
Patient can remain asymptomatic despite 5070% stenosis of a major coronary arte
Coronary artery disease
ECG
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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
Coronary artery disease
Management of anesthesia
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g
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 O2requirement and deliv
tachycardia
systolic hypertension
arterial hypoxemia
diastolic hypotension
more important than the specific technique or drugs
Coronary artery disease
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Preoperative medication
to produce sedation
to allay anxiety
if unopposedcatecholamine secretion
myocardial O2requirements
SBPHR
benzodiazepine
scopolamine + morphine
transdermal nitrogycerine
Coronary artery disease
Induction of anesthesia
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Rapidly acting IV drugs
Ketamineassociated with HR and SBP
not popular
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Coronary artery disease
Maintenance of anesthesia
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Choice of anesthesiabased on left ventricular function
CAD, but normal left ventricular function
SBP,HR in response to stimulation
volatile anesthetic with/withoutN2O
to control myocardial depression
N2Oopioid + volatile anesthetic
to treat acute in SBP
drug-inducedin SVR > drug-induced myocardial depress
isofluranesevoflurane
desflurane
Low blood solubilityrapid
Impaired left ventricular function
may not tolerate myocardial depression produced by volatile anesthetics
hi h d i id t h i
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high dose opioid technique
opioid + N2
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
sympathomimeticephedrine
phenylephine
Isoflurane
more potent coronary arteriole vasodilator than sevoflurane or desflurane
ld di bl d fl
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could divert blood flow
from ischemic areas to non-ischemic area of myocardiumcoronary artery steal
Volatile anestheticsmyocardial O2requirement
SBP
coronary perfusion pressure
coronary artery steal
Monitoring
Complexity of the operative procedure
Severity of the coronary artery disease
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ECG
non-invasive
balance between myocardial O2requirement and myocardial O2delivery
myocardial ischemiaS-T depression
V5 left ventricle
TEEventricular 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 pressurein the presence of left ventricular dysfunction
For selected high risk patients
recent MI
CHF
unstable angina
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Postoperative care
Analgesia
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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
hypothermiashivering
abruptin myocardial O2requirementminimize in body temperature
O2supplementation
Congestive Heart Failureshould not be performed as an elective surgery
Associated with postoperative morbidity
optimally treated
when surgery can not be delayed
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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 ventilationmay be beneficial
pulmonary congestion
improving oxygenation
invasive monitoring
continuous infusion of dopamine and/or dobutamine
maintenance of cardiac contractilityRA: 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 cau
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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 preoperatno evidence of postoperative cardiac complications
as long as preoperative diastolic BP is not higher than 110 mmHg
Management of anesthesia
Preoperative evaluation
d f SBP l
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adequacy of SBP control
drug therapy!!! maintain current therapy throughout the perioperative period
extent of the disease
major organ dysfunctioninfluences 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 flowmore vulnerable to cerebral ischemiashould perfusion pressure decrease
Induction of anesthesia
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Exaggerated decrease in SBP may occur
unmasking of decrease intravascular fluid volume due to chronic hypertensionparticularly if hypertension is present preoperatively
Ketamine rarely selected
Exagerated increase in SBPduring direct laryngoscopy are predictableMI
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
Maintenance of anesthesia
Adjust the concentration of anesthetic drugs
to minimize wide fluctuations in SBP
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to minimize wide fluctuations in SBP
more important than preoperative control of hypertension
N2O + volatile anestheticfor rapid adjustment in the depth of anesthesia in response to or SBP
attenuating SNS, which is responsible for pressor responses
desfluranesevoflurane
N2O + Opioid
the addition of a volatile anesthetic is often necessary to control undesirable
particularly during periods of maximal surgical stimulation
Nitroprusside
-Blockers : esmolol or labetalol
Low blood solubilities
Maintenance of anesthesia
Hypotension that occurs during maintenance of anesthesia:
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the concentration of volatile anestheticsIV fluids infusion
to intravascular fluid volume
sympathomimetics
to restore perfusion pressure until underlying cause can be corrected
ephedrine
Regional anesthesia
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Questionable choicewhen 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
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Postoperative management
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Hypertension in the early postoperative periodfrequent
adequate analgesia
pharmacologically decrease SBP
nitroprusside, continuous IV
labetalol (0.10.5 mg/kg/IV
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Disorder of endocrine gland function:
May be the primary reason for surgery
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y p y g y
May co-exist in patient requiring operation unrelated to the disorder
Preoperative evaluation of endocrine function:
Absence of glucose in the urineSBP and HR normal
Body weight unchanged
Sexual function normal
No history of relevant drug therapy
Diabetes Mellitus
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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
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Pre-operative
Should be in the best state of metabolic control that is possible preoperative
History and PE
detect symptoms of CVD, CAD, peripheral neuropathy
Laboratory test
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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 neuropathyresting tachycardia, orthostatic hypotension, absent variation in HR w/ deep breath
prevent development of angina pectoris (painless MI)
risk of sudden death, cardiovascular lability
Evidence of vagal autonomic nervous system neuropathy
gastroparesisrisk of aspiration of gastric contentEvidence of peripheral neuropathy
more susceptible to compression injury
Preoperative evaluation and treatment
hyperglycemia
ketoacidosis
electrolyte imbalance
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Hba1c
manifestation of :
coronary artery disease
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
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Well controlled IDDMbrief, out-patient surgery
Subcutaneous RI may not require any adjustment
oral sulfonylureamay be continued until the evening before surgery
delayed hypoglycemia in the absence of any caloric intake
biguanideless risk of hypoglycemia
metformin
risk of lactic acidosis
Poorly controlled IDDM
preoperative admission
Anesthetic Management
Intra-operative
Anesthetic plan depend on the presence of end organ disease
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p p p g
heart diseaseinvasive monitoringrenal diseasefluid management and drug selection
gastroparesisaspiration consideration
Blood glucose levels
preoperative + postoperativeintraoperative
the duration and magnitude of surgery
the stability of the diabetes
Dehidrationmay be presenceosmotic diuresis
Anesthetic Management
Intra-operative
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Glucose administration
avoid an overdose
standard glucose dose for adult:
510 g/hr or 100200 mL of 5% glucose/hr
Positioning of patient
peripheral nerve may already be partly ischemic
susceptible to pressure or scratch injury
Anesthetic Management
Intra-operative
The choice of drugs or techniques for induction or maintenance of anesthesi
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The choice of drugs or techniques for induction or maintenance of anesthesi
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
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To prevent hypoglycemia
To accept mild hyperglycemia
can be corrected gradually in the postoperative periode
Monitoring blood glucose concentration
more important than selection of formula5% glucose/IV
Regiments for exogenous insulin replacement
Subcutaneous insulin administration
administer to the usual daily intermediate-acting dose of insulin on the morning of surg
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ad ste to t e usua da y te ed ate act g dose o su o t e o g o su g
initiate infusion of glucose (510 g/hr) with initiation of insulin infusion
Continuous intravenous infusion of insulin
Regular insulin (50 units in 500 mL NS) at 0.51 unit/hr
initiate infusion of glucose (510 g/hr) with initiation insulin infusion
measure blood glucose concentration as necessary (usually every 12 hours)
and adjust insulin infusion accordingly
220 mg/dL increase insulin infusion rate by 0.5 unit/hr
Diabetic Emergencies
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Hyperosmolar non-ketotic comaDiabetic ketoacidosis
Hypoglycemia
Hyperosmolar non-ketotic coma
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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
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Hyperglycemia (300500 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
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followed by a continuous IV infusioninsulin in U/hr = blood glucose/150)
Intravenous fluids (isotonic)
as guided by vital signs and urine output
Potassium Chloride 1040 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
If renal disease prolongs the action of insulin or oral hypoglycemic agents
Avoidable !
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Produces signs of SNS stimulation
tachycardia
hypertensiondiaphoresis
in anesthetized patient may be:
masked
misdiagnosed
as an inadequate level of anesthesia relative to surgical stimula
Thyroid Gland
Thyroid metabolism and function
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Thyroxine (T4) and Tri-iodothyroxine (T3)
major regulator of cellular metabolic activity
Thyroid gland is solely responsible for the dayly secretion of T480% of T3is produced by extrathyroidal deiodination of T4
mediated most of the excess effects of thyroid hormones (hyperadrenergic stat
Effect of T3on receptor concentration:
number of receptors
number of cardiac cholinergic receptors
Tests for the diagnosis of thyroid gland dysfunction
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T4 T3 TSH
Hyperthyroidism Normal
Primary hypothyroidism
Secondary hypothyroidism
Hyperthyroidism
A hypermetabolic statenervousness
heat intolerance
muscle weakness
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tremorsweight 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:
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Preparation
proppylthiouracil
inhibit synthesis and peripheral conversion of T4to T3inorganic iodine
inhibits hormone release
-adrenergic antagonistsHR to < 90 beats/min
glucocorticoids
hormone release and peripheral conversion of T4to T3
Intraoperative management
Goal:
to achieve a depth of anesthesia that prevents an exaggerated SNS respo
to surgical stimulation
avoid administration of drugs that stimulate SNS
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g
GA
Thiopental
thiourea structureantithyroid activity
Ketamine can stimulate SNS
N2O not reliably suppressing SNS activity
Inhaled anestheticdo not
MACCO accelerates uptake of inhaled anesthetic
need to increase the inspire concentration
to achieve brain partial pressure euthyroid patie
temp.MAC
muscle relaxantdrug that lack of cardiovascular effect
co-existing muscle weaknessinitial dose, close monit RA
epinephrine should not be added to the local anesthetic solution
Monitoring
Early recognition of activity of the thyroid glands
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suggests the onset of thyroid storm
temperature
ECG
Exophthalmuscorneal ulceration
drying
eye protection
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Hypothyroidism
Lethargy
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Intolerance to coldFacial 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
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Profound hypothyroidism
decrease mental status associated with hyporesponsiveness to CO2
congestive heart failure
hypothermia
exaggerated symptoms of hypothyroidism
decompensated statesurgery
drugs
trauma
infections
Anesthetic consideration
Elective surgery should be postponed in severe hypothyroidism
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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
CO2insensitivity
poor gastric emptying
increased sensitivity to all depressant medications
Complications following thyroid surgery
Thyroid storm
A state of physiologic decompensation in severe thyrotoxicosis
surgical stress618 hr postoperatively
diarrhea
vomiting
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hyperpyrexia (3841OC)
hypovolemia, irritable, delirium or coma
DD/ : malignant hyperthermia
pheochromocytoma
inadequate anesthesia
sepsishemorrhage or transfusion/drug reaction
Airway obstruction
CT of the neck
Reccurent laryngeal nerve damage
unilateralhoarseness
bilateral
aphoniaHypoparathyroidism
develop in 2448 hr, include laryngospasm
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INITIAL ASSESSMENT
Primary survey
ABC sequences suggested for CPR
S d
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Secondary surveyA more comprehensive survey follows the primary surveys
PRIMARY SURVEY
A = Airway
ass med all m ltiple tra ma patients ha e
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assumed all multiple trauma patients havea cervical spine injuryinitial stabilization before airway manipulati
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 O2monitor closely
initiate other resuscitative measures
Endotracheal intubation
Awake patient
nature of injury
ability to cooperate
general stability
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general stabilityawake 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 assistedif not controlledventilation
bag-valve device
immediately after intubation
during period of transport
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during period of transportdeliver 100% O2 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 =C
irculation
Hemodynamic
initially assessed by palpating pulses
Intravenous access
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Intravenous accessat 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 failurepercutaneous
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
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non-cross-matched blooduniversal 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 resuscitatio
History
Patient, family members, and prehospital care personel
Abbreviated history
Fasting
Mechanism of injury
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Mechanism of injury
blunt trauma
widespread energy transfer to the body
multiple injury in various anatomic locations
penetrating trauma
injury confined to the penetration tracthigh velocity gunshot wounds
tissue disruption in area adjacent to the penetration track
Physical Examination
Frequent monitoring of vital signs
mandatory
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mandatoryprovides 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
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Electrolytes
glucose
BUN, Creatinine
Urinalysis
Radiographic studies
lateral cervical spine, must include C7T1 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
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pre existing medical problems
Arterial line
hemodynamic instability
respiratory failure
Central venous pressure line
to assess volume statusto administer vasoactive drugs
Pulmonary artery catheter
ventricular dysfunction
severe coronary artery disease
valvular heart disease
multiple organ system involvement
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INAPPROPRIATE FOR OUTPATIENT SURGERY
Pediatricformerly premature infants < 46 wks post-conceptual age
risk of post anesthesia apnea
infants with respiratory disease
infants with cardiovascular disease
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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 surgeryASA 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 symptoma recent upper respiratory infection
PATIENT PREPARATION
Preoperative testing
MinimalCBC t ti t 50
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aCBC 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 patientsimmediately prior to the planned procedure
Premedication
Anxiolytics
Psychological reassuranceif
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y gif necessary Midazolam 12 mg/IV
Aspiration prophylaxis
Non particulate antacids Na citrate 30 mL just before the procedure
H2-receptor antagonist Ranitidine 150 mg PO the night before surgery
Metoclopramide 10 mg PO or IV prior to surgery
Opioids
Fentanyl 50100 g IV may be given
if preoperative pain is present
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GENERAL ANESTHESIA
Induction
Propofol
short duration
depression of pharyngeal reflex
reduced incidence of postoperative emesisSevoflurane
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Sevoflurane
Airway management
Face mask, LMA or tracheal intubation
Muscle Relaxant
Succinylcholine or Mivacurium
Maintenance
Volatile anesthetic
sevoflurane with or without N2O
Propofol
Alfentanil or Remifentanil
supplemental local anesthesia
N2O
REGIONAL ANESTHESIA
Ideal agents
Rapid onset
to minimize case delay
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Short duration
to facilitate quick recovery and discharge
Patient selectionthe benefits of RA will be negated if heavy sedation is required
Separate areas for RAdecrease 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 patientto provide medications
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to provide medications
sedatives or opioids
POSTOPERATIVE CAREPACU
awake, oriented, stable VS, - PONV, minimal pain/discomfort,
able to sit without assisstance
phase II
fast trackPain
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Pain
pain on admission to PACUIV
awake, no painPO
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 distentionsevere postoperative pain
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