Download Management of Anesthesia

Cardiovascular
Anesthesia
neurosurgery requires
Ali Mohammadian Erdi, MD
Assistant Professor of Anesthesiology &
Fellow of Pain Medicine
Ardabile-Iran
91/07/10
Management of anesthesia
 (I) Understanding of the pathophysiology of the
disease process
 (2) Appropriate preoperative testing
 (3) Application of perioperative risk reduction
strategies
 (4) Careful selection of anesthetic, analgesic, and
neuromuscular and autonomic blocking drugs
 (5) Monitors to match the needs created by this
disease.
 MI, presence of CHF & AS are the highest risk factors.
Patient History
 History from patients with CAD before noncardiac
surgery :
 (1) Evaluation of cardiac reserve :
 exercise tolerance :
 Inability to lie flat,
 awakening from sleep with angina or shortness of
breath,
 or angina at rest or with minimal exertion)
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Patient History
 (2) Characteristics of their angina pectoris:
- Stable and unstable
- Prinzmetals,
- Silent myocardial ischemia
- 70% of ischemic episodes are not associated with angina
pectoris and as many as 15% of acute MI are silent.
- Females and individuals with DM are more likely to have
painless myocardial ischemia and infarctions.
- An increased HR is more likely than systemic hypertension to
produce signs of myocardial ischemia .
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Patient History
 (3) Previous occurrence MI:
- delay elective surgery, especially thoracic,upper abdominal, or
other major procedures, for a period (2 to 6 months) after a MI.
- but the exact period of suggested delay is not clear.
 After 6 months: incidence of MI is about 50 times
greater than in patients undergoing similar operations
but in the absence of a previous MI.
 Most myocardial reinfarctions occur in the first
48 to 72 hours postoperatively.
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FACTORS THAT INCREASE THE RISK FOR PERIOPERATIVE MI
 The site of the previous MI
 A history of prior (CAB G) surgery
 Intrathoracic or intra-abdominal operation > 3 hours
 Techniques used to produce anesthesia.
 Perioperative betablockade and clonidine reduces the risk for
mortality .
 Perioperative betablocker started 7 to 30 days before surgery
and continued for 30 days postoperatively has been shown to
reduce the risk for cardiac morbidity by 90%.
 if started before surgery and continued for 7 days reduces the
risk for by 50%.
 Close hemodynamic monitoring and prompt pharmacologic
intervention with fluid infusion decrease the risk for peri
operative cardiac morbidity in high-risk patients.
Patient History
 (4) Medical, interventional cardiology, and cardiac
surgical therapy for these conditions.
 Interactions of medications of CAD with anesthesia
drugs.
 Coexisting noncardiac diseases:
 Hypertension
 peripheral vascular disease
 COPD
 Renal dysfunction associated with chronic hypertension
 DM
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CURRENT MEDICATIONS
 Drugs encountered in patients with CAD are beta antagonists,
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nitrates, CA blockers,ACE inhibitors, lipid-lowering agents,
diuretics, and platelet inhibitors.
Pharmacology and adverse interactions with anesthetics.
All patients with known CAD, peripheral vascular disease, or 2
risk factors for CAD (age > 60 years, HTN, DM, smoking history,
cholesterol>240 mg/dL) should receive perioperative betablockers
unless there is a specific contraindication.
Reactive asthma, but not COPD is a contraindication to
perioperative betablock.
Despite the potential for adverse drug interactions, cardiac
medications should be continued .
Discontinuation increases peri operative morbidity and
mortality.
Risk Stratification versus Risk Reduction
 One of the standard approaches to the peri operative care of
patients with cardiac disease is risk stratification.
 Consists of a preoperative history and physical examination,
followed by a series of tests thought to predict perioperative
cardiac morbidity and mortality.
 The results of these tests ( thalliumscintigraphy, echocardiography,
Holter monitoring, dobutamine stress echocardiography, angiography) can
justify subsequent angioplasty with or without an intracoronary
stent or CABG .
 There is no evidence suggesting that preoperative risk
stratification with invasive testing is superior to a careful history
and physical examination, followed by prophylactic medical
therapy.
PERIOPERATIVE CARDIAC RISK REDUCTION THERAPY
 Recommendations have been established for the
administration of prophylactic medical therapy to
stable patients with known CAD or at risk for such
disease .
 All patients who either have CAD, peripheral vascular
disease, or 2 risk factors for coronary artery disease
should receive perioperative beta blockers unless they
have a specific intolerance to these drugs .
 If a patient has an absolute contraindication to
perioperative betablockers, clonidine may be used as
an alternative.
Protocol for
perioperative
cardiac risk
reduction :
Evaluation of Left Ventricular Function
Determinants of Myocardial Oxygen
Requirements and Delivery
Management of Anesthesia
 Intraoperative anesthetic management, as well as postoperative
pain management in patients with CAD, should permit
modulation of sympathetic nervous system responses and
provide for rigorous control of hemodynamic variables.
 Anesthesia based on preoperative evaluation of LV function and
maintenance of a favorable balance between myocardial oxygen
requirements and delivery so that myocardial ischemia is
prevented.
 Any event associated with persistent tachycardia, systolic
hypertension, arterial hypoxemia, or diastolic hypotension can
adversely influence this delicate balance.
 A common recommendation: maintain HR and systemic BP
within 20% of awake values.
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Management of Anesthesia
 A single I-minute episode of myocardial ischemia detected by I-
mm segment elevation or depression on the ECG increases the
risk for cardiac events 10-fold and for death 2-fold.
- Tachycardia (> 105 beats/min) for 5 minutes in the
postoperative period can increase the risk for death 10-fold.
- The only clinically proven method to reduce the risk for
perioperative myocardial ischemia and associated death is
perioperative betablocker (atenolol or metoprolol) or alfa 2
agonist (clonidine) therapy.
- Vasoconstrictors, betaagonists, betablockers, anticholinergics,
and vasodilators should be immediately available
PREOPERATIVE MEDICATION
 Preoperative anxiety can lead to preoperative
myocardial ischemia.
 Preoperative beta-blocker therapy or clonidine
reduces the incidence of myocardial ischemia.
 Patients should receive their routine medications
except for oral hypoglycemic agents.
 Oral administration of benzodiazepines .
 Supplemental oxygen may be useful, especially if
opioids are combined with benzodiazepines for
sedation.
INDUCTION OF ANESTHESIA
 Etomidate is a popular induction drug( limited inhibition of the
sympathetic nervous system and minimal hemodynamic
effects).
 Propofol is popular( antiemetic effects and rapid recovery, but
the dose should be reduced to avoid undesirable degrees of
hypotension).
 Fentanyl plus midazolam in combination with an infusion of
phenylephrine and a NDNMB produces minimal changes
in systemic BP and HR.
- Ketamine is not popular.
- If desflurane is chosen, care should be taken to not increase the
dose rapidly to avoid sympathetic nervous system stimulation
TRACHEAL INTUBATION
 TI is facilitated by SCH or a NDNMB.
 Myocardial ischemia result from the stimulation of laryngoscopy
before tracheal intubation.
 A brief duration of direct laryngoscopy (preferably 15 seconds) is
important for minimizing the circulatory changes.
 If duration of direct laryngoscopy is not likely to be brief or
when systemic hypertension coexists, the addition of other
drugs to minimize the pressor response produced by direct
laryngoscopy may be a consideration( lidocaine 1- 2 mg/kg )
 Opioids and BetaBlockers before laryngoscopy reduce the
circulatory responses as.
MAINTENANCE OF ANESTHESIA
 Choice of anesthesia is often based on the patient's
LV function . patients with CAD but normal LV function,
tachycardia and systemic hypertension are likely to
develop in response to intense stimulation.
 Controlled myocardial depression produced by a
volatile anesthetic, with or without N2O may be
appropriate if the primary goal is to prevent increased
myocardial oxygen requirements.
 Equally acceptable for maintenance of anesthesia:
N2O - opioid technique with the addition of a volatile
anesthetic as necessary.
MAINTENANCE OF ANESTHESIA
 Avoiding tachycardia with the use of long acting betablockers is
more important than the choice of anesthetic.
- Impaired LV function:( previous MI), may not tolerate the direct
myocardial depression produced by volatile anesthetics. Then
short-acting opioids with N2O may be a more acceptable
selection.
- N2O + opioids may produce undesirable decreases in systemic
BP and cardiac output.
- High-dose fentanyl with benzodiazepines added to ensure
amnesia, has been advocated for patients who cannot tolerate
even minimal anesthetic-induced myocardial depression.
 There is no evidence to support the superiority of this
technique over moderate-dose opioids with an inhaled agent or
IV anesthetics.
MAINTENANCE OF ANESTHESIA
 RA may be an appropriate technique in selected
patients with CAD.
 It is important that flow through critically narrowed
coronary arteries is pressure dependent. Therefore,
decreases in systemic BP associated with a RA that are
greater than 20% of the pre block value should
probably be treated by the IV infusion or
vasoconstrictor or both.
 Perioperative betablockers or clonidine should be
administered to patients with known cardiac risk
factors who are undergoing surgery with RA.
NEUROMUSCULAR BLOCKING DRUGS
 The choice of NDNMB may be influenced by the
circulatory effects & myocardial oxygen requirements
and delivery.
 Vecuronium, rocuronium, and cisatracurium do not
evoke histamine even with the rapid IV administration
of large doses.
 Systemic BP –lowering effects of atracurium and
mivacurium are usually modest, especially if these
drugs are injected over a period of 30 to 45 seconds.
 It is unlikely that any of these drugs will adversely alter
myocardial oxygen requirements.
NEUROMUSCULAR BLOCKING DRUGS
 Pancuronium increases the HR and BP, but these changes are
usually less than 15% above predrug values . the circulatory
changes can be offset the negative inotropic and chronotropic
effects of anesthetic drugs.
 One of the common causes of postoperative myocardial
ischemia and MI is tachycardia after emergence, which may be
the result of the combination of emergence, surgical pain, and
reversal of drugs.
- Long- acting IV betablockers may be added to decrease the
incidence of tachycardia, which may lead to myocardial ischemia
in this period.
MONITORING
 The intensity of monitoring is influenced by the
complexity of the operative procedure and the severity
of the CAD.
 The five-lead ECG serves as a noninvasive monitor of
the balance between myocardial oxygen requirements
and delivery.
 V5 lead is for detecting ST-segment changes ( ischemia
of the LV).
 Intra-arterial pressure monitoring can speed the
identification and treatment of hemodynamic changes.
 Ventricular wall motion abnormalities observed by
transesophageal echocardiography.
MONITORING
 Tachycardia: is treated by atenolol, metoprolol,
propranolol, or esmolol.
 Excessive BP:may respond to opioids,
betablockers, vasodilators (nitroglycerin,
nitroprusside), or increased delivered volatile
anesthetics.
 Decreases in body temperature may predispose to
shivering on awakening and increases in myocardial
oxygen requirements.
Postoperative Care
 Is based on provision of peri operative anti-
ischemic drugs, analgesia, and if needed,
sedation to blunt excessive sympathetic
nervous system activity and facilitate rigorous
control of hemodynamic variables.
 Intensive and continuous postoperative
monitoring is useful for detecting myocardial
ischemia, which is often asymptomatic.
- It is more effective to prevent the occurrence
of myocardial ischemia than to detect it.
VALVULAR HEART DISEASE
 The most frequently forms of VHD produce:
pressure overload (MS, AS) or volume overload (MR,
AR) of the LV.
 Selection of anesthetic drugs and NMBD based on the
probable effects of drug-induced changes in cardiac
rhythm, HR, systemic BP, systemic vascular resistance
and pulmonary vascular resistance relative to
maintenance of CO in these patients.
VALVULAR HEART DISEASE
 Although no specific type of GA has been
shown to be superior, when cardiac reserve is
minimal, an anesthetic combination that
includes a high dose of a short-acting opioid, an
amnestic benzodiazepine, and a low dose of a
volatile anesthetic is common.
 Prophylactic infusion of a vasoconstrictor
(phenylephrine) may reduce hemodynamic
changes.
 Prophylactic AB for endocarditis.
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Mitral Stenosis
 MS : mechanical obstruction to LV diastolic filling
secondary to progressive decrease in the orifice of the
mitral valve.
 The obstruction produces an increase in left atrial and
pulmonary venous pressure.
 Distention of the left atrium predisposes to AF, which
can result in stasis of blood, the formation of thrombi,
and systemic emboli.
 Chronic anticoagulation or antiplatelet therapy (or
both) can reduce the risk for systemic embolic events .
Mitral Stenosis
 Patients with MS may be more susceptible to
the ventilatory depressant effects of the
sedative drugs used for preoperative
medication. If patients are given sedative drugs,
supplemental oxygen may increase the margin
of safety.
 Most medications except anticoagulants, anti
platelet drugs, and oral hypoglycemicdrugs,
should be continued throughout the
preoperative period.
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Mitral Stenosis
 Digitalis should continue until surgery.
 Adequate digitalis effect for heart rate control is generally
reflected by a ventricular rate less than 80 beats/min.
 Because diuretic therapy is common in these patients, the
serum potassium is often measured preoperatively.
 Management of anticoagulant or antiplatelet therapy should
be discussed with the surgeon and cardiologist.
 Patients should be switched from warfarin (Coumadin) to
heparin therapy preoperatively, depending on the type of
surgery.
Anesthetic Considerations in Mitral Stenosis
MANAGEMENT OF ANESTHESIA(MS)
 Intra-arterial pressure monitoring .
 Induction : with IV drugs ( possible exception of ketamine,
which increase the HR).
 Tracheal intubation : is facilitated by neuromuscular blocking
drugs with minimal effects on heart rate are commonly chosen.
 Drugs used for maintenance of anesthesia should cause
minimal changes in heart rate and systemic and pulmonary
vascular resistance. these drugs should not greatly decrease
myocardial contractility.
 No one anesthetic has been proved to be superior.
MANAGEMENT OF ANESTHESIA(MS)
 Combinations of an opioid and low concentrations of volatile
anesthetics or IV anesthetics, with or without N2O.
 Although N2O can increase pulmonary vascular resistance, this
increase is not sufficiently great to justify avoiding this drug .
 NDNMBD with minimal circulatory effects are useful.
 Pancuronium is less appropriate.
 Although there is no reason to avoid drug assisted antagonism of
NDNMBD, it is desirable to avoid the adverse effects of druginduced tachycardia .
 An option :Allow the neuromuscular blockade to wane
spontaneously with metabolism of the drug.
MANAGEMENT OF ANESTHESIA(MS)
 Intraoperative fluid : titrated ,susceptible to
intravascular volume overload and LV failure and
pulmonary edema.
 The head-down position may not be well tolerated.
 Monitoring intraarterial pressure and possibly right
atrial pressure is a helpful guide to the adequacy of IV
fluid replacement.
 An increase in right atrial pressure could also reflect
pulmonary vasoconstriction and thus suggests the
need to check for causes, which may include nitrous
oxide, desflurane, acidosis, arterial hypoxemia,
increased MR, or light anesthesia.
MANAGEMENT OF ANESTHESIA(MS)
 Postoperative: high risk for pulmonary edema
and right heart failure.
 Mechanical support of ventilation of the lungs
may be necessary, particularly after major
thoracic or abdominal surgery.
 The shift from controlled to spontaneous
ventilation with weaning and extubation of the
patient's trachea may lead to increased venous
return and increased central venous pressure
with worsening of CHF.
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A.Mohammadian
Mitral Regurgitation
 Mitral regurgitation : left atrial volume overload
and decreased left ventricular forward stroke
volume as a result of the backflow of part of
each stroke volume through the incompetent
mitral valve back into the left atrium.
 MR secondary to rheumatic fever usually has a
component of mitral stenosis.
 Dilated cardiomyopathy resulting from chronic
myocardial ischemia, repeated MI, or viral
infections may cause MR.
MANAGEMENTOF ANESTHESIA(MR)
 should be designed to reduce the
likelihood of decreases in forward left
ventricular stroke volume.
 Conversely, cardiac output can be
improved by mild increases in heart
rate and mild decreases in systemic
vascular resistance.
MANAGEMENTOF ANESTHESIA(MR)
 GA is the usual choice for patients with MR.
 Although decreases in systemic vascular resistance are
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theoretically beneficial, the uncontrolled nature of this response
with a RA may detract from the use of this technique.
Maintenance of GA with volatile anesthetics, with or without
N2O, or a continuous IV infusion of drugs.
NDNMB that lack significant circulatory effects are useful.
Pancuronium is acceptable because the increase in HR and
forward left ventricular strok volume.
IV fluid volume must be maintained by prompt replacement of
blood loss to ensure adequate venous return and ejection of an
optimal forward LV stroke volume.
Aortic Stenosis
 Aortic stenosis is characterized by increased left
ventricular systolic pressure to maintain the
forward stroke volume.
 The combination of clinical symptoms (angina,
congestive failure, fainting), signs (left
ventricular dysfunction, progressive
cardiomegaly), and reduced valve area suggests
the presence of critical aortic stenosis requiring
surgical replacemen.
MANAGEMENTOF ANESTHESIA(AS)
 Goals : maintenance of normal sinus rhythm and avoidance of
extreme and prolonged alterations in heart rate, systemic
vascular resistance, and intravascular fluid volume.
 Preservation of normal sinus rhythm is critical because the left
ventricle is dependent on properly timed atrial contractions to
ensure optimal left ventricular filling and stroke volume.
 Increases in HR (>100 beats/min) can decrease the time for LV
filling and ejection, whereas bradycardia (<60 beats/min) can
lead to acute overdistention of the LV.
 Tachycardia may lead to myocardial ischemia and ventricular
dysfunction.
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MANAGEMENTOF ANESTHESIA(AS)
The most important technique: intra-arterial pressure
monitoring with careful avoidance of hypotension.
GA may be preferred over a RA because sympathetic nervous
system blockade can lead to undesirable decreases in systemic
vascular resistance. However, if the surgical site is on an
extremity, a RA with intra-arterial pressure monitoring can be
equally successful.
Maintenance of GA can be achieved with volatile anesthetics,
with or without N2O, or with intravenous drugs.
A potential disadvantage of volatile anesthetics is depression of
sinus node automaticity.
IV fluid volume must be maintained by prompt replacement of
blood loss and liberal IV administration of fluids.
Defibrillator should be available because external cardiac
compressions are unlikely to generate an adequate stroke
volume across a stenosed aortic valve.
Aortic Regurgitation
 Decreased forward LV stroke volume as a result of
regurgitation of part of the ejected stroke volume
from the aorta back into the LV through an
incompetent aortic valve.
 Increased myocardial oxygen requirements
secondary to left ventricular hypertrophy, plus a
characteristic decrease in aortic diastolic pressure
that decreases coronary blood flow, can manifested
as angina pectoris in the absence of coronary
artery disease.
 Management of anesthesia: is the same as
described for patients with MR.
Anesthetic Considerations in Patients with
Mitral or Aortic Regurgitation
Ventricular Premature Beats(PVC)
 Recognized on the ECG by (1) premature occurrence, (2) the
absence of a P wave preceding the QRS complex, (3) a wide and
often bizarre QRS complex, (4) an inverted T wave, and (5) a
compensatory pause that follows the premature beat.
 Treatment:ed : lidocaine (1 to 2 mg/kg IV followed by 1 to 2
mg/min infusion)
when : (1) are frequent (more than six premature beats/min)
(2) multifocal
(3) occur in salvos of three or more, or
(4) take place during the ascending limb of the T wave (R on T
phenomenon).
 The primary goal should be to identify the underlying cause
(myocardial ischemia, arterial hypoxemia, hypercapnia,
hypertension, hypokalemia, mechanical irritation of the
ventricles) if possible and correct it.
NEUROANESTHETIC MAINTENANCE
ADEQUATE BRAIN RELAXATION
 Adequate oxygenation and ventilation (PaCO2 3335mmHg),, venous return, muscle relaxation,
anesthetic depth
 Furosmide 10-20mg iv, Mannitol 0.5-1.5g/kg iv, iv
thiopental, CSF drainage
NEUROANESTHETIC MAINTENANCE
STABLE ANESTHETIC STATE AND RAPID SMOOTH
EMERGENCE
 Low after the craniotomy (brain is devoid of sensation)
 Isoflurane, Sevoflurane or Desflurane 0.5MAC &
Propofol 50-150 ug/kg/min and Remifentanil 0.10.5ug/kg/min
 Muscle relaxant maintaining 2twitches (phenytoin may
increase requirment of muscle relaxants)
NEUROANESTHETIC EMERGENCE
 AVOID COUGHING STRAINING OR BP INCREASE
 Normalize gradually PaCO2
 Full reversal of muscle relaxant
 IV Lidocaine
 IV labetolol, Nicardpine, NTP, NTG
 Brief neurological Assessment before leaving OR
Pre emergence
 1-2 hr before end
 Gradual decrease anesth aiming for bis 80 at end
 Treat post op htn before hand, I aim for SBP 110
 Maintain solid reversible NMB!!
IMMEDIATE POSTOPERATIVE CARE IN
NEUROANESTHESIA
 ADEQUATE VENTILATION AND OXYGENATION
 HEAD OF BED (10-25C0
 NEUROLOGIC FUNCTION
 CEREBRAL DYNAMICS MONITORING AND CONTROL
 SERUM ELECTROLYTE: SIADH (↓Na, ↓serum osm, ↑urine osmo) Treatment restrict
water intake ‡meds
DI (polyuria, ↑Na, ↑serum osmo, ↓urine osmo) Treatment Aqueous vasopressin 510USP units sq or 3units iv OR desmporessin 1-2 ug iv sq q6-12hr. Plus adequate fluid
replacement
 SEIZURE (adequate oxygenation, ventilation and airway protection: midazolam (2-
4mg), thiopental (100-150mg), fosphenytoin 15-20mg/kg, 100 mg/min)
 POSTOPERATIVE IMAGING (CTScan, MRI, Angiography)
TRANSPORT FROM OPERATING ROOM
TRANSPORT FROM OPERATING ROOM TO NEURO-ICU OR PACU:
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PRIOR COMPLETE REPORT TO ACCEPTING UNIT WITH SET-UP NEEDED
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TRANSPORT ONLY WHEN PATIENT IS STABLE OR AS STABLE AS CAN BE
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DIRECT SUPERVISION OF ANESTHETIST
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HEMODYNAMIC AND RESPIRATORY SYSTEMS MONITORED AND CONTROLLED
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O2 SUPPLEMENT
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WORKING IV AND RUNNING INFUSION PUMPS
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BLANKETS AND HEAT LOSS PREVENTION
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EMERGENCY MEDS AND INTUBATION KIT
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ENDORSEMENT IS NOT COMPLETE UNTIL PATIENT IS STABLE AND COMPREHENSIVE REPORT HAS
BEEN DELIVERED
CAUSES OF POST-ANESTHETIC HYPOTENSION
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HYPOVOLEMIA
↑HR, RR, SKIN TURGOR, DRY MUCOUS MEMBRANE, OLIGURIA AND THIRST.
INADEQUATE FLUID REPLACEMENT, ONGOING LOSS, OSMOTIC POLURIA, FLUID SEQUESTRATION
(ASCITIS, INTESTINAL OBSTRUCTION
A MEANINGFUL VOLUME CHALLENGE AND FURTHER ASSESSMENT (CAUTIOUS IN IMPAIRED BBB)
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IMPAIRED VENOUR RETURN
JUGLAR VEIN DISTENTION, ↑CVP, ↓BREATH SOUNDS AND ↓HEART TONES.
POSITIVE PRESSURE VENTILATION, PEEP, PNEUMOTHORAX, PERICARDIAL TAMPONADE.
TREATED BY VOLUME AND THE CAUSE
CAUSES OF POST-ANESTHETIC HYPOTENSION
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VASODILATION
REWARMING, RESIDUAL INHALATION AGENTS, NEUROAXIAL ANESTHESIA, TRANSFUSION
REACTION, ANAPHYLAXIS, INFLAMMATION, SEPSIS, ADRENAL INSUFFICIENCY, LIVER FAILURE
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DECREASED CARDIAC OUTPUT
MYOCARDIAL ISCHEMIA, INFARCTION, CHF, NEGATIVE INOTROPIC DRUGS, SEPSIS,
HYPOTHYRODISM, MALIGNANT HYPERTHERMIA
DYSPNEA, DIAPHORESIS, CYANOSIS, JUGLAR VEIN DISTENTION, OLIGURIA, RHYTHM
DISTURBANCES, WHEEZING, DEPENDENT CRACKLES, AND S3 GALLOP
INOTROPIC AGENTS (e.g. DOPAMINE)
AFTERLOAD REDUCTION (e.g.Nitrate)
DIURESIS for fluid overload
ANTIDYSRHYTHMICS OR ELECTRICAL CARDIOVERSION
CAUSES OF
POST-ANESTHETIC DYSRHYTHMIAS
 INCREASED SYMPATHETIC OUTFLOW (PAIN)
 HYPOXEMIA, PE
 HYPERCARBIA
 HYPO-HYPERTHERMIA
 HYPOVOLEMIA
 ELECTROLYTE AND ACID-BASE IMBALANCE
 DRUG TOXICITY
 THYROTOXICOSIS
 MALIGNANT HYPERTHERMIA
 MYOCARDIAL ISCHEMIA, CHF
 ELEVATED ICP
COMMON TYPES OF POSTANESTHETIC
DYSRHYTHMIAS
SUPRAVENTRICULAR DYSRHYTHMIAS
 SINUS TACHYCARDIA
 SINUS BRADYCARDIA
 PAROXYSMAL SUPRAVENTRICULAR TACHYDYSRHYTHMIAS
VENTRICULAR DYSRHYTHMIAS; STABLE
 PVCS
 VENTRICULAR TACHYCARDIA (NON-SUSTAINED)
UNSTABLE VENTRICULAR TACHYCARDIA AND VENTRICULAR FIBRILLATION
GENERAL TREATMENT OF POST-ANESTHETIC DYSRHYTHMIAS
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O2 SUPPLEMENT
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INCREASE PERFUSION
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TREAT THE CAUSE (S)
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Pain: Opiods
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Bradycardia: Atropine 0.2-0.4mg or glycopyrrolate 0.2mg
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Synchronized cardioversion if unstable arrthymia
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Adenosine 6mg then 12mg rapid to convert PACS
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B-adrenergic blockers (labetalol 5-20mg -2mg/min, esmolol 10-100mg or 25-300ug/kg/min,
propranolol 0.5-1mg iv)
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Calcium-channel blockers (Verapamil 2.5-5mg increment, diltiazem 5-20mg iv or 0.25-0.35mg/kg
iv then 5-15mg/hr
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Amiodarone 150mg over 10min then 1mg/min for 6hrs then 0.5mg/min
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Digoxin 0.25mg increment 1.5mg
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Ibutilide, Procainamide 20-30mg/min iv up 17mg/kg 1-2mg/min, Lidocaine 1.5mg/kg then 14mg/min
PERIOPERATIVE FLUID MANAGEMENT IN
NEUROANESTHESIA
 Avoid infusion of water or dextrose in water (Water freely passes through
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BBB)
BBB is impermeable to most ions. Total osmolarity rather than oncotic
pressure determine osmotic gradient.
Maintenance of high serum osmolality decrease brain water content
Large, polar substances cross poorly BBB e.g albumin
If BBB is disrupted, permeability to mannitol, albumin, and saline increases
and edema formation
PERIOPERATIVE FLUID MANAGEMENT IN
NEUROANESTHESIA
 Physiologic mainenance fluid given hourly without replacement of overnight
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deficit
Third spacing is minimal during craniotomy surgery
2/3 of total intraoperative urine output is replaced with crystalloid
Iso-osmolar crystalloid sol (0.9NS, 309 mOsm. Large quantity may cause
metabolic acidosis)
Hypokalemia secondary to steriod, porassium-wasting diuretics,
hyperventilation.
Hyponatremia caused by SIADH and diuretic used
Brain Death
Determination
 Apnea test
 Disconnect the ventilator
 Deliver 100% FIO2 via t-piece/trach collar
 Monitor for ventilatory effort until ABG confirms a
PaCO2 greater than 60 mm Hg
 Reconnect ventilator
 If patient becomes unstable, terminate
apnea test
 Patient is considered apneic if PaCO2 is > 60
and there is no respiratory effort
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