PAIN PATHWAYS AND OPIOIDS

Peripheral Afferents Conducting Pain and Temperature
A-delta fibers

• free (naked) nerve endings
• Myelinated
• Diameter = 1-4 nm
• Transmit "fast pain" or "first pain"
• well-localized discriminative sensation (sharp, stinging, prickling)
• duration of pain coincides with duration of painful stimulus

C fibers

• free (naked) nerve endings
• Unmyelinated
• Diameter = 0.4-1.2 nm
• Transmits "slow pain" or "second pain"
• diffuse and persistent burning, aching, throbbing sensation - dull, chronic
• duration of pain exceeds duration of stimulus

Classification of Pain

1. Somatic
2. Superficial (cutaneous)
3. Deep (from muscles, tendons, joints, fascia) - generally involves both first and second pain.
4. Visceral (arising from either parietal peritoneum or viscera itself) - second pain from viscera is carried by C fibers.  First pain from parietal peritoneium is carried by A-delta fibers

Dual Pain Pathways
Entry of A-delta and C fibers into the Posterior Cord
The "fast" and "slow" pathways are activated in the periphery when the free nerve endings of the A-d and C fibers are stimulated (damaged; nociceptors details painful stimuli).  The cell bodies of the A-d and C fiber afferents are found in the dorsal root ganglion.  The A-d and C fibers enter the dorsal cord, divide and ascend or descent 1-3 segments in the tract of Lissauer. 
Pain pathways are contralateral - they crossover then go up spinal cord.
(touch, pressure and proprioception are ipsilateral).

Transmission of Pain Impulses Through the Dorsal Horn
Pathway for fast-sharp pain: After leaving the tract of Lissauer, the axons of the A-d fibers enter the dorsal horn and terminate in Rexed's lamina I and lamina V.  Second order neurons leaving lamina I or lamina V cross to the contralateral lateral spinothalamic tract and ascend to the brain.

Pathway for slow-chronic pain: The C fibers terminate primarily in lamina II and also lamina III. Interneurons transmit C fiber impulses to lamina V from laminae II and III.  Neurons leaving lamina V cross immediately to the contralateral lateral spinothalamic tract and ascend to the brain.

(pic)

***KNOW (Valley):

• Sources differ: some say lamina II is the substantia gelatinosa, other sources say it is lamina II and III.
• The major neurotransmitter released from A-d fibers is glutamate which binds to AMPA and NMDA receptors on the postsynaptic membrane.  The normal ligand for NMDA is glutamate.
• The major neurotransmitter released from C fibers is substance P, which binds to NK-1 (neurokinin-1) receptors on the postsynaptic membrane.

Spinal Cord Tracts for Transmitting and Modulating Pain
The ascending sensory spinal cord tract carrying pain and temperature is the lateral spinothalamic tract, which is a component of the anterolateral sensory. The dorsolateral funiculus shown in figure below is a descending tract.   The function of the dorsolateral tract is to modulate pain (stop pain at the spinal cord)

(pic)

Anatomy of the Lateral Spinothalamic Tract
The lateral spinothalamic tract carries pain and temperature modalities.  C fiber afferents enter the spinal cord via the dorsal horn.  The C fibers synapse just after entering the spinal cord with interneurons in lamina II or lamina III.  The interneurons from laminae II and III synapse with second order neurons in lamina V.  Second order neurons leaving lamina V cross immediately to the opposite (contralateral) side in the spinal cord and then ascend on the contralateral side.

QUESTION:
If the right spinothalamic tract is severed at C3, what sensations are lost where?
Pain & temperature deficits on contralateral side (L) at all levels below the injury (C3)

What sensations are blocked in the lateral columns by epidural or spinal anesthesia?
Pain and temperature bilaterally

(pic)

The Substantia Gelatinosa: The Side where Pain Impulses are Attenuated (decreased)
The body's natural Analgesia
(pic)
The first neuron in the slow-chronic pain pathway synapses with the interneurons in the substantia gelatinosa (Rexed's lamina II) and lamina III of the spinal cord and releases the excitatory transmitter, substance P (SP) to these interneurons.  Enkephalin-releasing interneurons synapse on the substance-P releasing nerve terminal.  When enkephalin is released to the nerve terminal of the primary pain C fiber afferent, the release of SP is decreased.  When the release of SP is decreased, the number of action potentials initiated in the interneuron of the pain pathway is reduced and, ultimately, the perception of pain is decreased.  Enkephalin may be considered the "gate" in the gate control theory of pain.  There are many other modulators of pain transmission in the substantia gelatinosa (not discussed here).

Enkephalin - a neurotransmitter that is a nateral endogenous opioid --> Endorpins, Dynorphins.  The Enkephalin receptor on the Presynaptic C-fiber is the opioid receptor: Mu1, Mu2, Kappa, Delta.  All are present but Mu2 dominates in the SG.  Signal transduction in Mu receptor decreases the release of substance P.

Mechanism of Analgesia Produced by Neuraxial Opioids
Narcotic (Rx) produced Analgesia
(pic)
Opioids (morphine, fentanyl, sufentanil, alfentanil, etc.) stimulate the same receptors that are stimulated by the body's endorphins and enkephalins.  After an opioid is injected into the intrathecal or epidural space, it diffuses into the substantia gelatinosa (Rexed's lamina II) and unites with opioid receptors on the nerve terminal of the primary pain afferent.  The release of substance P is reduced, and transmission of impulses through the SG is inhibited.  This is spinal analgesia.  Mu1, Mu2, kappa and delta receptors mediate spinal analgesia.  Spinal opioid analgesia is mediated primarily by Mu2 receptors.

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Neuraxial (Intrathecal or Epidural) Placement of Hydrophilic Opioids
Morphine, a hydrophilic opioid, crosses lipid membranes slowly

Intrathecal Placement - after intrathecal (spinal) placement, morphine diffuses out of the intrathecal space slowly.  Onset of analgesia is slow and duration of analgesia is prolonged.  Early depression of ventilation does not occur because uptake by systemic circulation is minimal, but rostral spread of significant quantities of morphine in CSF causes late (6-12 hours) depression of ventilation (morphine trapped in CSF circulates to brainstem)

Epidural Placement - after epidural placement of morphine, onset of analgesia is slow and duration of analgesia is prolonged.  Because systemic uptake is greater when morphine is injected into the epidural space, early depression of ventilation (within 2 hours) may occur, although unlikely.  Late depression of morphine, again d/t rostral spread in CSF, occurs.

(pic)

Neuraxial (Intrathecal or Epidural) Placement of Lipophilic Opioids
Lipophilic opioids (fentanyl, alfentanil, sufentanil) readily diffuse through lipid membranes

Intrathecal Placement - diffusion of lipophilic opioid out of the CSF is rapid.  For lipophilic opioids, onset of analgesia is rapid and duration of analgesia is short.  Early depression of ventilation (within two hours) occurs because of significant systemic uptake.  Because diffusion of lipophilic opioids out of CSF is substantial, rostral spread is minimal and late depression of ventilation does not occur.

Epidural Placement - Injecting a lipophilic opioid into the epidural space produces responses similar to those seen after intrathecal injection.

(pic)

Side-Effects of Neuraxial Opioids:

• Pruritus
• Neonatal morbidity
• Nausea
• Sexual dysfunction
• Urinary retention
• Ocular dysfunction
• Depression of ventilation
• Gastrointestinal dysfunction
• Sedation
• Thermoregulatory dysfunction
• CNS excitation
• Water retention

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Spinal Analgesia

Spinal analgesia occurs when transmission of pain impulses through the substantia gelatinosa (Rexed's lamina II) is suppressed. Mu1, Mu2, Kappa, and delta receptors mediate spinal analgesia, although the dominant receptor mediating spinal analgesia is the Mu2 Receptor.  The patient's perception of pain is diminished by spinal analgesia; this makes sense because fewer action potentials are relayed to the brain when spinal analgesia occurs.  Opioids acting in a region of brain referred to as the periventricular/periaqueductal gray produce spinal analgesia.  Spinal analgesia results from the action of opioids in the substantia gelatinosa (after epidural or intrathecal administration) or in the periventricular/periaqueductal gray (after IV administration).  *Narcotics work on different regions depending on how you administer them*.

Spinal analgesia can be produced starting in centers above the spinal cord (periventricular gray, periaqueductal gray, locus ceruleus, raphe magnus nucleus).  Do not call this supraspinal analgesia - the net action is analgesia at the spinal cord level (substantia gelatinosa).

Supraspinal Analgesia

Supraspinal analgesia occurs when opioids act in the brain at sites including the limbic system, hypothalamus, and thalamus.  Supraspinal analgesia is medited by Mu1, kappa and delta receptors, although the dominant receptor mediating supraspinal analgesia is Mu1.  With supraspinal analgesia, the patient's response to pain is altered, "I feel the pain, but I don't care"  Supraspinal analgesia develops after IV administration of opioids only.  Euphoria.

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Modulation of Pain - Brain Control of Substantia Gelatinosa (Spinal Analgesia)
Descending neurons originating in the periventricular and periaqueductal gray terminate on enkephalin-releasing interneurons in Rexed's lamina II (substantia gelatinosa).  The enkephalin released from the lamina II interneurons attaches to the receptors of the nerve terminal of the C fiber afferent and inhibits that release of substance P.  Spinal analgesia results. 
(pic)

Mechanisms of Modulation of Pain by Descending Spinal Cord Tracts
 (pic)



VASCULAR DISEASES

NAGELHOUT CH. 26: ANESTHESIA FOR VASCULAR SURGERY

Peripheral Vascular Disease:
Atherosclerosis
The most common cause of occlusive disease in arteries of lower extremities.  Degerenative process involves formation of atheromatous plaques that obstruct vessel lumen and cause reduction in distal blood flow.
Pathophysiologic process:

1. plaque formation, which obstructs the lumen (stenosis)
2. thrombosis, which results in acute ischemia
3. embolism from microthrombi or atheromatous debris which decreases distal blood flow
4. weakening of arterial wall with aneurysm formation

Most common risk factors:

• Hypercholesterolemia
• Elevated triglycerides
• Cigarette smoking**
• HTN
• Diabetes  mellitus**
• Obesity
• Genetic predisposition
• Sex (M>F)
• Impaired long-term glucose regulation
• Homocysteine
• C-reactive protein

Typical symptoms of peripheral occlusive disease include claudication, skin ulcerations, gangrene, impotence.  The extent of disability is primarily influenced by the development of collateral blood flow.  Initially, collateral blood flow sufficiently meets tissue oxygen demands.  As the disease progresses, supply is unable to meet demand, and limb ischemia becomes symptomatic, requiring therapeutic intervention.

Mortality rates a/w PVD are 30% at 5 years and 70% at 10 years.

Interest in relationship between inflammation and the development of atherosclerosis.  Platelet interaction with leukocytes and other cells that modulate the immune response play a major role in the development of atherosclerosis. 

Treatment:
Pharmacologic therapy or surgery.
Surgical therapy includes transluminal angioplasty, endarterectomy, thrombectomies, endovascular stenting and arterial bypass procedures.  Some common surgical maneuvers used for bypassing occlusive lesions are aortofemoral, axillofemoral, femorofemoral, and femoropopliteal bypass techniques.  Bypass techniques may be classified as inflow or outflow procedures, depending on levelo of obstruction, with the dividing axis being at the level of the groin.

Preoperative Evaluation:
Atherosclerotic process should also be expected to be present in coronary, cerebral and renal arteries.  More than half the mortality a/w PVD results from adverse cardiac events.  Cardiac pathology must be managed aggressively to optimize cardiac functioning and decrease morbidity and mortality from cardiac causes.

Advantages to B-blockade on factors that affect myocardial oxygen supply and demand - their use is recommended in pts at high risk for myocardial ischemia and MI.  10-fold decrease in cardiac morbidity in AAA surgery.  B-blockade should be instituted days to weeks before surgery and titrated to HR 50-60.  Vascular surgery patients with limited HR variability after B-blockade therapy exhibit less cardiac ischemia and troponin values postop and have decreased mortality from all causes 2 years postop.

Monitoring:
Extent of periop monitoring should be based on presence of coexisting disease processes.  The detection of myocardial ischemia should be the primary objective in patients with vascular disease. Routine use of PACs are not warranted.  Transesophageal echocardiography may be used.

D/t global nature of atherosclerotic disease, the anesthetist should assume some degree of systemic CV disease in patients with PVD.  Patients with HTN and angiopathology rely on increased MAP to perfuse their vital organs.  Thus cerebral and coronary autoregulation occurs at a higher than normal pressures.  Direct intraarterial blood pressure monitoring allows for near-real-time determination of blood pressure values and is warranted bc of dramatic fluctuations that can occur during anesthesia.

Anesthetic Selection:
Depends ont he types of surgery performed and presence of co-existing disease.  Regional anesthesia for surgery on lower extremities may decrease the overal morbidity and mortality a/w this population - although some studies showed higher frequency of CV complications.  Research still pending; no conclusive evidence suggesting superior anesthetic technique.

Benefits of Epidural Technique in Vascular Surgery:

• Endocrine:
• inhibits surgical stress response
• inhibits adrenaline and cortisol release
• inhibits hyperglycemia
• inhibits lymphopenia and granulocytosis
• causes nitrogen sparing
• blocks sympathetic tone
• Cardiovascular
• decreases myocardial O2 demand and afterload
• decreases myocardial infarct size
• increases endocardial perfusion at ischemic zone
• causes fewer sympathetic blood pressure swings
• causes less blood loss
• requires less general anesthesia depressant medication
• redistribures blood to lower extremities
• Pulmonary
• decreases FVC, FEV1, PEFR (peak expiratory flow rate)
• requires less shunting O2 consumption
• improves atrioventricular O2 differentiation
• causes fewer pulmonary infections
• causes fewer thromboembolisms
• Renal
• increases blood flow in the renal cortex
• causes less renovascular constriction
• Geriatric
• causes less cardiorespiratory trespass
• improves postop mental status
• Misc
• allows earlier extubation, ambulation, discharge
• achieves greater postop pain control

Postoperative Considerations:
Postop admin of narcotics provides patient comfort and contributes to cardiac stability.  Use of epidural opioid and local anesthetics in patients recovering from vascular surgery is an important component of postoperative case because pain can greatly enhance sympathetic nervous system stimulation.


Abdominal Aortic Aneurysms
Incidence increasing.  Increase may be results of detection of asymptomatic aneurysms by noninvasive diagnostic modalities (CT, MRI, ultrasound). M> F, white>black.  Occurence of AAAs increased d/t increased age of general population and vascular changes that occur as a result of aging.

Risk Factors:

• Atherosclerosis thought to be primary cause of AAA in over 90% of patients. 
• Other theories: aneurysmal development may result from proteolysis of elastin and collagen within a vessel wall and that atherosclerosis may be an incidental finding in the pathogenesis of aneurysm development.
• HTN is present in 60% of patients with aneurysmal lesions.
• Cigarette Smokers the incidence of AAA increases eightfold.  (Correlation but aneurysms are also observed in normotensive nonsmokers)
• Genetics may also contribute to the predisposition for aneurysmal development.
• obesity (not an independent risk factor) may mask S&S of AAA until complications arise

Mortality:
Decreased for elective AAA surgery. 5%
Advanced detection capabilities, earlier surgical intervention, extensive preop preparation, refined surgical techniques, better hemodynamic monitoring, improved anesthetic techniques, aggressive postop management have contributed to improvement in surgical outcomes. The risk for rupture is very low for AAA less than 4 cm, but risk dramatically increases for AAA with diameter of 5 cm or greater.   Surgical intervention is recommended for AAA 5.5 cm or greater.  Mortality for ruptured AAA vary from 35-94%.  5 year mortality rate for individuals with untreated AAA is 81%, and 10 year mortality rate is 100%.  Early detection and elective surgical intervention can be lifesaving.

Diagnosis:
Asymptomatic aneurysms are detected incidentally during routine exam or abdominal radiography.  Smaller aneurysms are often unetected on routine physical examination. Diagnostic techniques such as u/s, CT scan and MRI may identify vascular abnormalities in these patients. Digital subtraction angiography is the best method of evaluating suprarenal aneurysms because it provides superior definition of the aneurysmal relationship to the renal arteries.

Abdominal Aortic Reconstruction
Patient Selection:
Mortality a/w elective repair of AAAs is fairly low compared with nonsurgical management.  Most pts w abdominal aneurysms are considered surgical candidates.  Age is not a contraindication for elective aneurysmectomy.  Mortality rate for elective aortic reconstruction is 5% for those < 75 years old and 11% for those > 75 years old.  Physiologic age is more indicative of increased surgical risk than chronologic age. 

CI to elective repair include intractable angina pectoris, recent MI, severe pulmonary dysfunction, and chronic renal insufficiency.  Patients with stable CAD and coronary artery stenosis of greater than 70% who require nonemergent AAA repair do not benefit from revascularization if B-blockade has been established.  In most cases the presence of an AAA warrants surgical intervention.

Criteria for High risk patients in AAA repair:

• >85 years old
• Home O2, PaO2 < 50 mmHg, FEV1 < 1 L/s
• serum Creatinine > 3 mg/dL
• Class III-IV angina
• Resting LVEF < 30%
• Recent CHF
• complex ventricular ectopy
• Large L ventricular aneurysm
• severe valvular disease
• recurrent congestive failure or angina after CABG
• severe, noncorrectable CAD

The dimensions of an aneurysm can change over time.  AAAs grow approximately 4 mm/year.  Aneurysmal vessel dimensions correspond to the Law of Laplace. (T = P x r)    T = wall tension,  P = transmural pressure, r = vessel radius

As the radius of the vessel increases, the wall tension increases.  Therefore, the larger the aneurysm, the more likely the risk of spontaneous rupture.  Aneurysms measuring more than 4-5 cm in diameter generally require surgical intervention, but aneurysms measuring less than 4-5 cm should not be considered benign.  An aneurysm has the potentila to rupture regardless of size.

Patient Preparation
Preop fluid loading and restoration of intravascular volume are the most important techniques used to enhance cardiac function during AAA surgery.  Reliable venous access must be secured if volume replacement is to be accomplished.  Large bore IV lines and central lines can be used to infuse fluids or blood.  Massive hemorrhage is a threat so availability of blood and blood products should be ensured. Provisions for rapid transfusion and intraop blood salvage should be confirmed.

Routine Monitoring
Standard monitoring methods:
EKG (II for dysrhythmias and precordial V5 for analysis of ischemic ST segment changes)
Pulse Ox
ETCO2
Foley for continuous measurement of UOP and renal function
Neuromuscular function may also be monitored

Invasive Monitoring
Maintaining cardiac function is crucial for successful surgical outcome; cardiac function should be closely monitored during AAA reconstruction. 
A-line: Permits beat-to-beat analysis of BP, immediate ID of hemodynamic alterations r/t aortic clamping, and access for blood sampling.
PAWP: can be used for monitoring of Left sided filling pressures as a guide for fluid replacement. low sensitivity and low specificity in detecting MI when compared with EKG and TEE. No difference in cardiac morbidity with PAC vs. CVP monitoring.
TEE: provides a sensitive method for assessing regional myocardial perfusion  by detecting changes in ventricular wall motion.  Wall motion abnormalities also occur much sooner than EKG changes during periods of reduced coronary blood flow.  MI poses the greatest risk of mortality after AAA reconstruction.

Aortic Cross-Clamping
The most dramatic physiologic change occurs with the application of an aortic cross-clamp.  Temporary aortic occlusion produces various hemodynamic and metabolic alterations.

Hemodynamic alterations:

• Hemodynamic effects of aortic cross-clamping depend on the application site along the aorta, the patients preoperative cardiac reserve, and the patients intravascular volume
• The most common site for cross-clamping is infrarenal, because most aneurysms appear below the level of the renal arteries. 
• Less common sites of aneurysm development are the juxtarenal and suprarenal areas
• During aortic cross-clamping, hypertension occurs above the cross-clamp, and hypotension occurs below the cross-clamp.
• Organs proximal to the aortic occlusion may experience a redistribution of blood volume
• There is an absence of blood flow distal to the clamp in the pelvis and lower extremities.
• Increases in afterload cause myocardial wall tension to increase
• MAP and SVR also increase
• CO may decrease or remain unchanged.
• Pulmonary artery occlusion pressure may increase or display no change
• Patients with adequate cardiac reserve commonly adjust to sudden increases in afterload without the occurrence of adverse cardiac events.  However, patients with ischemic heart disease or ventricular dysfunction are unable to fully compensate ans a results of hemodynamic alterations.  The increased wall stress attributed to aortic cross-clamp application may contribute to decreased global ventricular function and MIschemia.  Clinically, these patients experience increases in PAOP in response to aortic cross-clamping.

Metabolic Alterations:

• After application of aortic cross-clamp, the lack of blood flow to distal structures makes these tissues prone to develop hypoxia.  In response to hypoxia, metabolites such as lactate accumulate.
• The reduction in CO during aortic cross-clamping might be partly the result of metabolic alterations, such as decreased oxygen consumption
• Plasma catacholamine levels increased significantly during application of aortic cross clamp
• Epi and Norepi stimulate myocardial B1-receptors that can increase HR and myocardial O2 demand.
• Release of arachidonic acid derivatives may contribute to cardiac instability observed during aortic cross-clamping. Thromboxane A2 synthesis (accelerated by aplication of aortic cross clamp) may be responsible for the decrease in myocardial contractility and CO that occurs.  Current studies on pretreatment with NSAIDS.
• Traction on mesentery is a surgical maneuver used for exposing the aorta.  Can lead to mesenteric traction syndrome a/w this procedure.  S&S include decreases in BP and SVR, tachycardia, increased CO, and facial flushing
• cause unknown
• a/w high concentrations of 6-ketoprostaglandin F1, the stable metabolite of prostacyclin
• NSAIDS may reduce mesenteric traction syndrome
• Neuroendocrine response to major surgical stress is mediated by cytokines such as interleukin (IL)-1B, IL-6, and tumor necrosis factor as well as plasma catecholamines and cortisol.
• these mediators are thought to be responsible for triggering the inflammatory response that results in increased body temperature, leukocytosis, tachycardia, tachypnea, and fluid sequestration.

Effects on Regional Circulation:

• structures distal to the aortic clamp are underperfused during aortic cross-clamping
• renal insufficiency and renal failure have been reported to occur after abdominal aortic reconstruction.
• Suprarenal and juxtarenal cross-clamping may be a/w a higher incidence of altered renal dynamics but reductions in renal blood flow can occur with any level of clamp application
• Infrarenal aortic cross clamping is w/e 38% decrease in renal blood flow and a 75% increase in renal vascular resistance; these effects may lead to acute renal failure which is fatal in 50-90% of patients who undergo AAA repair.
• Preop evaluation of renal function is the most significant predictors of postop renal dysfunction
• Spinal cord damage is a/w aortic occlusion.  Interruption of blood flow to the greater radicular artery (artery of Adamkiewicz) in the absence of collateral blood flow has been identified as the causative factor in paraplegia.
• the incidence of neurologic complications increases as the aortic cross-clamp is positioned in a higher or more proximal area.
• SSEP monitoring has been advocated as a method of identifying spinal cord ischemia.  However, SSEP monitoring reflects dorsal (sensory) spinal cord function and does not provide information regarding the integrity of the anterior (motor) spinal cord.
• Motor evoked potential (MEP) monitoring is capable of determining anterior cord function. Can't use muscle relaxant.
• Ischemic colon injury is a well-documented complication a/w AAA resections.  Most frequently attributed to manipulation of the inferior mesenteric artery, which supplies the primary blood supplies to the L colon.
• This vessel often sacrificed during surgery and blood flow to the descending and sigmoid colon depends on the presence and adequacy of collateral vessels.  Mucosal ischemia occurs in 10% of patients.
• In less than 1% of these patients, infarction of L colon requires surgical intervention.

Aortic Cross-Clamp Release:
Whilte the aorta is occluded, metabolites that are liberated as a result of anaerobic metabolism (lactate) accumulate below the aortic cross-clamp and induce vasodilation and vasomotor paralysis.  As the cross-clamp is released, SVR decreases and the blood is sequestered into previously dilated veins, which decrease venous return.  Reactive hyperemia causes transient vasodilation secondary to the presence of tissue hypoxia, release of adenine nucleotides, and liberation of an unnamed vasodepressor substance that acts as a myocardial depressant and peripheral vasodilator.  This results in decreased preload and afterload. The hemodynamic instability that may ensure after the release of an aortic cross-clamp is called declamping shock syndrome. Venous endothelin (ET)-1 may be responsible for hemodynamic alterations (has positive inotropic effect on heart and vasoconstricting/vasodilating action on vessels).

Most commonly observed hemodynamic response to aortic declamping:

• MAP decrease
• SVR decrease
• CO no change or increase
• PAOP decrease

Intravascular volume may influence the direction and magnitude of change in cardiac output.  The site and duration of cross-clamp application, as well as gradual release of the clamp, influence the magnitude of circulatory instability. Partial release of the aortic cross-clamp over time frequently results in less severe hypotension.

Surgical Approach
Transperitoneal incision - good exposure, but increased fluid losses, prolonged ileus, postop incisional pain, pulmonary complications

Retroperitoneal approach - excellent exposure (juxtarenal and suprarenal aneurysms), decreased fluid losses, less incisional pain, fewer postop pulmonary and intestinal complications.  Does not elicit mesenteric traction syndrome. Inaccessibility to distal R renal artery

Management of Fluid and Blood Loss
Evaporative losses and 3rd spacing.  Most blood loss occurs because of back bleeding from lumbar and inferior mesenteric arteries after vessels have been clamped and aneurysm is open.  Use of heparin contributes to EBL. Blood replacement is commonly administered during abdominal aortic resections.

Presence of Concurrent Disease
Preoperative Management
The presence of underlying CAD in patients with vascular disease exists in more than 50% of patients requiring AAA reconstruction and is the single most significant risk factor influencing long-term survivability.  MI is responsible for 40-70% of all fatalities that occur after aneurysm reconstruction.  Cardiac function must be optimized.
Stress test: dipyridamole thallium
HTN, COPD, DM, renal impairment and CAD is frequently observed in patients with AAA.

Intraoperative Management
Anesthetic Selection
A superior technique has not been identified. 
VAA: may depress myocardium; avoid high concentrations
Narcotics: high-dose narcotics with N2O can be used as the anesthetic for major vascular surgery.  Opioids provide CV stability.
Regional Anesthesia: epidural; may cause hypotension or hematoma formation (heparin)
Combo techniques: balanced technique of low-dose inhalation agents maintains CV hemodynamics and controls momentary autonomic responses to surgical stimulation. Epidural anesthesia combined with light general anesthesia

Fluid Management
Maintaining intravascular volume is a challenge
Crystalloids vs. Colloids
Crystalloids: may be used for replacing basal and 3rd-space losses at approximate rate of 10 ml/kg/hr
Blood losses initially can be replaced with crystalloid at ratio of 3:1.
Fluid replacement should be sufficient for the maintenance of normal cardiac filling pressures, cardiac output, and urine output of 1 ml/kg/hr
Patients with limited cardiac reserve can develop CHF if hypervolemia occurs.

Hemodynamic Alterations

Renal Preservation

Postoperative Considerations

Juxtarenal and Suprarenal Aortic Aneurysms

Ruptured AAA

Thoracic Aortic Aneurysms

Aortic Dissection

Descending Thoracic and Thoracoabdominal aneurysms

Endovascular Aortic Aneurysm Repair

Cerebrovascular Insufficiency and Carotid Endarterectomy

Carotid Artery Stenting

CARDIOMYOPATHIES

CARDIOMYOPATHIES

Joseph June 11, 2013

Readings:

Stoelting Ch. 8 pp 149-154

M&M 418-419

n  Definition of MYOPATHY:

   Any disease or abnormal condition of

   STRIATED MUSCLE.

   CARDIOMYOPATHY is a disease of the myocardium, primarily due to primary disease of the heart muscle.

There are various types of CARDIOMYOPATHIES

n  DILATED CARDIOMYOPATHY (congestive)

n  NONDILATED CARDIOMYOPATHY (restrictive)

n  HYPERTROPHIC CARDIOMYOPATHY

n  The classifications of cardiomyopathies are based on the LEFT VENTRICLE ejection fraction and ventricular volume (via ECHO or radionuclide studies of the ventricle)

             

n  Cardiomyopathies are disorders that directly affect either the right or left VENTRICLE resulting in CONGESTIVE HEART FAILURE.

n  The interesting thing about congestive heart failure related to cardiomyopathy is that the CHF cannot be attributed to CAD, any valve disease, pericardial disease, or even HTN.

DILATED CARDIOMYOPATHY

The ETIOLOGY is said to be idiopathic.

Specific etiologies include nutritional deficits, alcohol abuse, infections (viral, bacterial, and parasitic) causing myocarditis.

PATHOPHYSIOLOGY:

n  In order to maintain stroke volume as myocardial contractility progressively declines, LVEDP increases and the heart DILATES (Frank Starling mechanism).

n  Compensatory mechanisms in addition to cardiac enlargement include tachycardia to maintain CO and elevations in SVR to sustain blood pressure.

HEMODYNAMIC CHARACTERISTICS:

n  Marked decrease in LVEF (<0.4)

n  Marked increase in ventricular volume

n  Normal to increased ventricular filling pressures

n  Normal to decrease stroke volume

n  Cardiac output may be normal to low

n  Left atrial pressures may be normal to high

n  Ventricular dilation may be so MARKED that mitral or tricuspid regurgitation occurs.

n  EKG changes that you might see include LEFT BBB and evidence of  left ventricular hypertrophy, ST-segment and T wave abnormalities probably will be present.

n  PVCs and A fib may also be seen.

n  If there are Q waves, this may be indicative of a previous MI.

n  CXR will show pulmonary HTN and biventricular cardiac enlargement.

n  Mural or wall thrombi are likely to form in chambers of the heart that both dilated and hypokinetic.

n  It has been found that there is a HIGH incidence of systemic embolization in these patients (anticoagulation is NOT of proven benefit).

n  The clinical course of patients with dilated cardiomyopathy is characterized by intermittent CHF and systemic embolization.

n  Angina may be prominent in some of these patients.

n  The prognosis of these patients is POOR.

n  Sudden death may be attributed to acute cardiac dysrhythmias.

n  The most common cause of death is due to CHF

CLINICAL PRESENTATION:

n  Symptoms of right, left, or bi-ventricular failure include extreme fatigibility, marked decrease in exercise tolerance, and DOE or at rest.

n  Episodes of acute pulmonary edema may occur.

n  Common signs include JVD, hepatomegaly, peripheral edema, ascites, S3 gallop, and murmur of mitral insufficiency

n  Medications include digitalis, diuretics, and vasodilators.

n  Anti-arrhythmics are prescribed and regulated most effectively by 24-hour Holter monitor recordings.

n  Beta blockers and disopyramide are AVOIDED because of the likelihood of inducing further congestive failure.

ANESTHETIC IMPLICATIONS:

n  The MAIN GOAL is to optimize myocardial performance while providing adequate anesthetic depth.

n  Light premedication

n  Inhalationals should be avoided due to the cardiac depressant effects (this is not to say that they can’t be used in low doses)

n  A pure narcotic-oxygen technique offers the advantages of dense analgesia with minimal cardiac depression.

n  As much as possible, optimize ventricular performance.

n  Inotropic agents are required

n  Afterload reduction with nipride, hydralazine, or amrinone will often augment cardiac output.

n  Intraop hypotension is best treated with ephedrine

n  Alpha adrenergic stimulation by phenylephrine could produce adverse increases in ventricular afterload due to elevation of SVR

n  If preload optimization, inotropic support, and afterload reduction are inadequate, the insertion of an IABP should be considered.

n  And obviously a Swan-Ganz catheter is indicated for all of these patients undergoing general anesthesia.

n  If possible, regional anesthesia may be an attractive alternative to general anesthesia.

n  Epidural anesthesia produces changes in preload and afterload that mimic pharmacologic goals in the treatment of this disease.

n  A regional technique may not be the choice is a higher block is indicated.

NONDILATED (RESTRICTIVE) CARDIOMYOPATHY

n  Resembles constrictive pericarditis being characterized by marked increases in ventricular filling pressures, and often with reductions in CO.

n  Signs of right heart failure (hepatosplenomegaly and ascites) predominate.

n  The myocardium is non-compliant and diastolic filling is impeded, reflecting infiltration of the myocardium by abnormal material.

n  This disease can result from infiltrative diseases such as amyloidosis, hemochromatosis or glycogen storage diseases.

n  There is no effective treatment and death is usually due to cardiac dysrhythmias or irreversilble CHF.

n  Hemodynamic characteristics include:

n  Normal to decreased LVEF

n  Normal to decreased ventricular volume

n  Marked increase in ventricular filling pressures

n  Normal to decreased stroke volume

n  Management of anesthesia is similar to that for patients with cardiac tamponade.

n  General anesthesia and positive pressure ventilation is acceptable.

n  Induction and maintenance of anesthesia are often with ketamine, etomidate, and BNZ

n  Anesthetic-induced reductions in myocardial contractility, SVR, and HR must be avoided.

n  Ketamine tends to increase contractility, SVR, and HR.

n  Infusions of catecholamines such as isoproterenol, dopamine, and dobutamine may be required to maintain cardiac contractility.

HYPERTROPHIC CARDIOMYOPATHY (IHSS)

n  Also known as IHSS (idiopathic hypertrophic subaortic stenosis .

n  Currently, the preferred term is HYPERTROPHIC CARDIOMYOPATHY with or without LEFT VENTRICULAR OUTFLOW OBSTRUCTION.

n  A genetically transmitted disease.

n  The myocardial defect is related to the contractile mechanism (an increase in the density of calcium channels that gives rise to myocardial hypertrophy).

n  Assymetrical hypertrophy of the interventricular septum of the left ventricle occurs.

n  This causes a LEFT outflow tract obstruction, and therefore the hemodynamic consequences are similar to those that are characteristic of AORTIC STENOSIS.

n  The most common cause of SUDDEN DEATH in the pediatric and young adult population (eg. Athletes).

HEMODYNAMIC CHARACTERISTICS:

n  Marked increase in LVEF

n  Marked decrease in ventricular volume

n  Normal to increased ventricular filling pressures

n  Normal to increased stroke volume

PATHOPHYSIOLOGY:

n  Left ventricular myocytes are hypertrophic and their arrangement is chaotically arranged and in dissaray.

n  The walls of the coronary arteries are narrowed due to the presence of collagen

n  Diastolic compliance is reduced because the myocardium is stiffer than normal.

n  Ventricular filling pressures are usually elevated and vary markedly with small changes in ventricular volume.

n  Remember that ATRIAL systole may account for 40 to 50 percent of ventricular filling

n  Left ventricular function (LVEF) is supernormal and EFs of 80% are common.

n  The hypercontractility often results in cavitary obliteration during systole.

n  The rapid acceleration of blood traveling through the narrowed ventricular outflow tract creates a VENTURI EFFECT which pulls the anterior mitral valve leaflet into the outflow tract.

n  The anterior mitral valve leaflet further obstructs the left ventricular outflow.

n  Hypertrophic cardiomyopathy with obstruction is affected by three hemodynamic parameters.

n  These three parameters include preload, afterload, and contractility.

n  Increasing contractility exacerbates the obstruction by increasing septal wall contraction and decreasing CO.

n  Increased blood flow velocity causes a greater degree of systolic anterior motion of the mitral valve’s anterior leaflet, creating further obstruction.

n  Decreased preload changes the left ventricular geometry and brings the anterior leaflet of the mitral valve into closer proximity of the hypertrophied septum.

n  Increases in left ventricular contractility cause the LV to empty more completely and increase the degree of septal contractility, which results in a greater degree of obstruction.

CLINICAL PRESENTATION:

n  Chest pain, dyspnea, and exercise induced syncope.

n  EKG: LVH, Q waves, PACs, PVCs, supraventricular or ventricular tachycardia or fibrillation.

n  Treatment is directed at relief of symptoms, control of arrhythmias, and improvement of diastolic relaxation.

n  The arterial pressure waveform in patients with HC may be bifid or bisferiens pulse (2 beat pulse).

n  The initial rapid peak represents early un-obstructed ventricular ejection, while the subsequent decrease and second peak are due to dynamic obstruction.

PULSUS BISFERIENS

ANESTHETIC CONSIDERATIONS:

n  GOALS: preservation of adequate ventricular volume and prevention of left ventricular outflow obstruction.

n  Maintain LV preload by preventing hypovolemia and maintaining NSR.

n  Maintain left ventricular afterload

n  Reduce contractility

n  Adequate or slightly elevated left ventricular volume should be maintained.

n  Avoid decreased venous return (interferes with adequate preload)

n  Avoid increases in myocardial contractility.

n  Inadequate anesthesia results in SNS stimulation and this may be detrimental to the patient (hyperdynamic shifts)

n  In the event of hypotension, adequate perfusion should be maintained by increasing preload with fluids and increasing SVR with phenylephrine.

n  Pharmacologic agents used to treat patients with HC (beta blockers, calcium channel blockers) should be continued until the time of surgery.

n  Beta blockers can be used intraop to reduce HR and contractility.

n  Anesthetic management needs to focus on maintaining LV preload, decreasing contractility, and maintaining SVR.

n  Regional anesthesia can be a consideration in these patients

n  Treat hypovolemia immediately

n  Deep general anesthesia is preferred

n  Because Halothane is the most potent myocardial depressant inhaled agent in use today, it is the ideal choice of all the agents.

n  The PCWP  should be maintained 18-25 mm Hg.

n  If the hemodynamic status deteriorates and exaccerbation of outflow obstruction is suspected, labetalol or propanolol should be given.

CARDIOMYOPATHIES AND OTHER CONDITIONS

TYPE I DIABETES MELLITUS:

n  Patients with DM I may develop cardiomyopathy even in the absence of CAD.

n  Pathologic studies of the heart in patients with DM I who develop cardiomyopathy reveal

n  1. microvascular disease

n  2. hyaline thickening in the coronary arteries

n  3. fibrosis, degeneration, and fragmentation of

       myocytes.

n  The above changes are responsible  for diminished left ventricular compliance and ejection fraction.

HEART TRANSPLANTATION AND CARDIOMYOPATHY:

n  For those individuals in need of cardiac transplantation, idiopathic dilated cardiomyopathy (which is their underlying cause of CHF) accounts for 43% of all cardiac transplant candidates.

NEUROMUSCULAR DISORDERS

Neuromuscular Pathology and Anesthetic  Management

Julia May 28, 2013

Readings:

›  Nurse Anesthesia. J Nagelhout. Chapter 30, pp 737.

›  Readings: Anesthesia and Coexisting diseases; Hines & Marshall. Pg 505-549

›  Clinical Anesthesiology. Morgan & Mahkail.

SCLERODERMA

›  Is a condition characterized by inflammation, vascular sclerosis, and fibrosis of the skin and viscera.

 ›            Injury to the vascular endothelium results in obliteration and leaking of cell proteins.

›  The leaking proteins affects the interstitial fluids.

›  This will produce edema, lymphatic obstruction, and ultimately fibrosis.

CREST SYNDROME

›  Ina few patients the disease evolves into the Crest Syndrome.

›  Calcinosis

›  Raynaud’s

›  Esophageal hypomotility

›  Sclerodactyly (tightness of the skin)

›  Telangiectasis (dilation of small vessels of the skin)

SCLERODERMA

›  Prognosis is poor with this disease and there is no effective treatment.

›  Onset of the disease is between the ages of 20-40yrs old, with women being more affected then men.

›  Treatment may include the administration of corticosteroids.

Physiologic Changes:

›  Skin and muscular system

›  Initial mild thickening and non-pitting edema.

›  Eventually the skin becomes taught, limiting mobility.

›  Skeletal muscle may exhibit weakness.

›  Nervous system

›  Thickening of the nerve sheaths may lead to cranial or peripheral neuropathy.

›  Cardiovascular

›  Patients may develop sclerosing of the small coronary vessels, conduction system and cardiac muscle.

›  Systemic and pulmonary hypertension.

›  May develop arrhythmia, conduction abnormalities and congestive heart failure.

›  Raynaud’s phenomenon is often associated and is the initial presentation.

›  Pulmonary

›  Major cause of morbidity and mortality.

›  Patient may develop pulmonary hypertension and diffuse pulmonary fibrosis.

›  Pulmonary compliance is decreased with increased airway pressures.

›  Kidneys

›  Renal artery involvement can lead to deceased renal blood flow and systemic hypertension.

›  Gastrointestinal

›  Dryness of the oral mucosa

›  Hypomotility of the lower esophagus and small intestine.

›  Dysphagia

›  These patients are prone to reflux.

Anesthetic Management

›  Assessment of organ system involvement.

›  The skin may be taught making tracheal intubation difficult.

›  FOB

›  Oral and nasal telangiectosis may lead to severe bleeding of the airway on intubation.

›  Cannulation of the artery for blood pressure monitoring may face the same challenges of Raynaud’s phenomenon.

›  These patients may be intravascularly depleted leading to hypotension on induction.

›  Increase gastric PH with H2 blockers.

›  Intra-operatively

›  Adequate ventilation with positive pressure ventilation.

›  Avoid acidosis and hypoxemia because it increases PVR.

SYSTEMIC LUPUS ERYTHEMATOSUS

›  SLE is a multisystem chronic inflammatory disease.

›  Characterized:

›  Antinuclear antibody production.

›  Manifesting most often in women.

›  Stress such as pregnancy, surgery or infection can exacerbate the symptoms.

›  SLE may also be drug induced

›   progression is slower and milder than the spontaneous form.

›  Drugs causing SLE

›  Procainamide, hydralazine, isoniazide, D-penicillamide, alpha-methyldopa.

›  Susceptible individuals are thought to be slow metabolizers (Slow acetylators)of the drugs.

Diagnosis

›  Screening test for lupus- antinuclear antibody test.

›  95% of the patients will test for this.

›  The most common antibody is directed against the nucleosomal DNA- histone complex.

›  Diagnosis is likely when the patient exhibits 3-4 manifestations:

›  Antinuclear antibodies,

›  Rash

›  Thrombocytopenia

›  Serositis, or nephritis

›  The common presentations are:

›  Arthralgia or non specific pattern of arthritis,

›  Vague CNS symptoms

›  History of rash or Raynaud's.

›  Weakly positive anitnuclear test.

Systemic Manifestations of SLE

›  SLE of the CNS

›  Can affect any area of the CNS

›  Cognitive dysfunction, mood disorders, schizophrenia, and organic psychosis.

›  Pericarditis or pericardial effusions

›  Chest pain and pleural friction rub

›  Pulmonary SLE

›  Lupus pneumonia characterized by diffuse pulmonary infiltrates.

›  PFT’s show a restrictive type of disease.

›  Recurring atelectasis can result in “Shrinking Lung” syndrome.

›  Renal abnormalities

›  Glomerular nephritis with proteinuria.

›  Resulting in hypoalbuminemia

›  Severe forms can lead to oliguric renal failure.

Anesthetic Management:

›  Management is influenced by the drug treatment used.

›  Nsaids, corticosteroids, antimalaria drugs.

›  Magnitude of the organ involvement

›  Laryngeal involvement, such as cricoarytnoid arthritis, mucosal  ulcers and recurrent laryngeal nerve is present in 30% of the patients.

Review of MNT:

›  Muscle contraction:

›  Occurs when the electrical signal is transmitted between the presynaptic neuron and the post synaptic neuron.

›  The junction between the two is referred to as the Junctional (synaptic) cleft.

›  The motor neurotransmitter= ACh

What occurs presynaptic:

q  An action potential occurs.

q  Calcium is released.

q  This stimulates the release of Ach.

q  Breakdown and synthesis of Ach occurs here.

q   Enzyme choline acetyltrasnferase (CAT) catalyzes acetylcoenzyme A (Acetyl-coA) + Choline= Ach + Co-A

Neuromuscular Junction:

q  Fluid filled area.

q  Ach is released here.

q  Calcium is fused to Ach vesicles (Quanta) until it ruptures.

q  This is the site were drugs work.

Postjunctional Membrane:

q  Contain nerve endings that are closely approximated.

q   Also known as the motor end plate.

q   Calcium binds to the receptors here

q  You have an influx of NA+ and Calcium, outward K+.

q  The resting membrane potential becomes depolarized.

q  Action potential occurs.

›  1. Presynaptic( Eaton-lambert)

›  2. Sarcolemma

›  3. Synaptic vesicles

›  4. Ach nicotinic receptor (Myasthenia gravis)

›  5. Mitochondria

›  6. Synaptic cleft

›  7. Postjunctional membrane (NM blockers)

›  8. NMJ (Botox)

Skeletal Muscle Pathophysiology:

›  Causes of skeletal muscle disorders

›  Autoimmune

›  Defect in muscle protein

›  Pharmacologic effects.

›  Safety in anesthesia

›  Requires knowledge of Pathophysiology

›  Condition or state the patient is in.

›  Drug therapy being used

›  Preoperative

›  Perform thorough preop assessment

›  Know the degree of respiratory, cardiac and muscle involvement.

›  Intraop

›  How does the patient’s drug therapy affect the anesthetic

›  Post-op

›  May require post-op ventilation

›  Pain management

MYASTHENIA GRAVIS

›  Cause:

›  Autoimmune destruction or inactivation of the post-synaptic Ach receptor.

›  This leads to a decrease in the receptors and loss of the folds on the synaptic vesicles.

›  85% antibody to Ach receptors

›  65% Hyperplastic Thymus gland.

›  10%Thymus

›  10% other

›  Characteristics

›  Episodes of remission/exacerbation

›  Exacerbation can be generalized or confined to a muscle group.

›  Ocular muscles: Diplopia or Ptosis

›  Bulbar involvement: Laryngeal weakness, and dysphasia.

›  Characteristics

›  Proximal muscles (Severe ds): Involves the neck, shoulders & respiratory muscles.

›  With MG. Muscle strength improves with rest.

›  Exacerbation is enhanced: Stress, Pregnancy, surgery & infection.

Treatment:

›  Anticholinesterase

›  Pyridostigmine

›  Most common

›  Given Po and has a duration of 3-4hrs.

›  Side effects

›  Cholinergic crisis: Salivation, diarrhea, muscle weakness, miosis and bradycardia

How can you tell between myasthenic crisis and cholinergic crisis?

›  Edrophonium (Tensilon) Test

›  Used to determine whether weakness is caused from too much drug treatment or myasthenic crisis.

›  An increase in weakness with 10mg indicates cholinergic crisis

›  An increase in strength indicates myasthenic crisis.

Other medical treatments for MG:

›  Thymectomy

›  The thymus produces T-Lymphocytes which aids in immunity

›  Plasmaphoresis

›  Removal of anti-bodies from the blood stream

›  Medications

›  Azathioprine (Imuran): Immunosuppressant

›  Steroids

›  Anticholinesterase

Preop Evaluation:

›  What surgery are they having?

›  Thymectomy: Indicates deterioration of disease.

›  Other: the patient may be optimized or in remission

›  Determine how severe the disease is.

›  Consider pretreatment with H2 blocker for aspiration prevention.

›  Consider omitting sedatives.

›  Edrophonium test

Intraop Management:

›  May use standard inhalational agents.

›  Avoid muscle relaxants.

›  Consider deep inhalation technique.

›  May require increased doses of Sux for resistance, but duration will also be increased.

›  They will have a sensitivity to NDMR.

Postop Care:

›  Post-op ventilation criteria: Following Thymecotmy

›  If disease is > 6mn

›  Presence of pulmonary disease

›  VC < 40cc/kg

›  Pyridostigmine dose > 750mg/d

Babies of MG Mothers:

›  Babies will have symptoms of MG for 1-3 weeks

›  May require post-op ventilation.

EATON-LAMBERT SYNDROME: (Myasthenic Syndrome)

›  Paraneoplastic disorder affecting the lower extremities.

›  Usually associated with small cell carcinoma.

›  Other causes: Met. Ca, sarcoidosis or autoimmune.

›  Muscle weakness generally improves with exercise.

›  Unaffected by anticholinesterase drugs.

›  There is a  prejunctional deficit in the release of Ach, which is thought to be related to antibodies on the calcium channels.

Signs & Symptoms:

›  Autonomic deficits:

›  failure of nicotinic cholinergic synaptic transmission.

›  Patients may be prone to orthostatic hypotension and cardiac irritability.

›  Gastroporesis  and urinary retention

›  Muscle weakness

›  Usually the trunk, pelvic and legs

›  Fatigue and difficulty walking

Anesthetic Considerations:

›  These patients are sensitive to both depolarizers and nondepolarizers.

›  Consider using deep inhalationals anesthesia.

›  If MR is required you will need to decrease the dose.

›  May use reversal agents

›  Consider post-op ventilation support

DUCHENES MUSCULAR DYSTROPHY

›  (Pseudo Hypertrophic Muscular dystrophy).

›  Is the most common and most severe childhood progressive NMD

›  Affects 3 per 10,000 births

›  Caused by an X-linked recessive gene.

›  Becomes apparent in males 2-5 yrs of age

Signs & Symptoms:

›  Waddling gait

›  Difficulty climbing stairs

›  Frequent falls

›  Involves proximal skeletal muscles of the pelvis.

Characteristics:

›  Progressive skeletal muscle weakness to eventually being debilitated in a wheel chair by 8-11 yrs of age.

›  Kyphoscloiosis

›  Skeletal muscle atrophy can lead to long bone fracture.

›  Serum Creatinine Kinase is 30-300 times normal.

›  Death can occur by ages 15-25

›  Skeletal muscle cell shows necrosis and phagocytes of the muscle fiber.

›  Left-Normal  Right-Dystrophic cell

Anesthetic Considerations:

›  Cardiac function

›  Degenerative cardiac muscle

›  EKG shows tall R-waves in V1, deep Q waves in limb leads, Short PR and ST

›  Mitral regurg due to papillary muscle dysfunction.

›  Respiratory function.

›  Decreased function

›  Decreased cough ability

›  Loss of pulmonary reserve

›  Increased secretions

›  Kyphoscoliosis: Restrictive or obstructive lung ds?

›  Most common cause of death

›  Planned surgery

›  Sux is contraindicated

›  Rhabdo, Hyperkalemia, cardiac arrest.

›  NDMR

›  Prolonged effect

›  Dantroline

›  Should be readily available for these patients are at risk for MH.

›  Plan for regional anesthesia when possible.

›  Monitor for signs of M.H

›  Delayed respiratory depression for up to 36 hrs post-op.

›  Monitored unit

MALIGNANT HYPERTHERMIA

›  Life threatening uncommon hyper-metabolic state which is triggered by certain anesthetics.

›  Incidences.

›  Occurs in 52% of the patients under the age of 15 with a mean age of 18.3

›  Occurs in 1:50,000 adults, and 1:15,000. children

Pathophysiology:

›  Cause is unknown

›  Believed to be an inherited disorder.

›  There is a defect in calcium regulation.

›  Focus has been placed recently on the Ryanodine receptor which modulates calcium release from the SR.

What happens when a triggering agent is given?

›  Actin-myosin cross bridges are sustained.

›  Uptake of calcium requires energy and that energy increases muscle cell metabolism 2-3 fold.

›  ↑ metabolism = ↑ O2 consumption= ↑ Temp & CO2 → Depletion of ATP stores & ↑ lactic acid.

›  Triggering agents:

›  Sux

›  Inhalationals

›  K+ Salts

›  Non Triggering

›  Locals, Nitrous

›  Opioids, Barbiturates, Propofol & Ketamine

Neurological Diseases

›  Multiple Sclerosis (MS)

›  Amyotrophic Lateral sclerosis (ALS)

›  Guilliane Barre syndrome (Acute Demyelinating polyNeuropathy)

›  Myelin :

›  is an electrically-insulating dielectric phospholipid layer that surrounds only the axons of many neurons.

›  It main purpose is to increase the speed of impulses along the nerve cells.

›  In the brain the myelinated area is also known as the white matter.

›  Demyelination:

›  Refers to the loss of the myelin sheath insulating the nerve.

›  This is what is seen with disease such as, MS, ALS and Guiiliane Barre syndrome.

MULTIPLE SCLEROSIS

›  Demyelination of several sites of the brain and spinal cord with chronic inflammation and scarring.

›  DX

›  Early via MRI

Characteristics:

›  Autoimmune response initiated by a virus.

›  Occurs between the ages of 20-40yrs.

›  There are episodes of exacerbation and remission.

›  S/S: Motor weakness & Parasthesia, visual disturbances.

›  Increases in body temperature worsens symptoms.

Treatment:

›  Spasms:

›  Dantroline, Bachlofin & diazapam

›  Urinary retention:

›  Bethanechol

›  Decrease exacerbation:

›  ACTH, Gluccocorticois

›  Immunosuppressant:

›  Inteferon B, AZT, Cyclophosamide

Anesthetic Considerations:

›  Avoid elective surgery during relapse stages.

›  Council patients on the effects of stress on the disease.

›  Avoid sux

›  Avoid elevations in body temperature.

›  Increase in temp of 0.5 degree

›  Can decrease demyelinated nerve conduction.

›  Spinal anesthesia can exacerbate symptoms.

›  GA and epidural have not been shown to have e major effect.

AMYOTROPIC LATERAL SCLEROSIS

›  Most common and most rapidly progressing neurologic disease in adults.

›  Occurs during the 5^th and 6^th decade of life.

›  Muscle weakness, atrophy, fasciculation and spasms.

›  It progresses to involve the bulbar and skeletal muscles.

Anesthetic Management:

›  Aimed at keeping judicious respiratory care.

›  Avoid Sux

›  These patient's are more sensitive to NDMR.

›  Monitor respiratory status post-op.

›  Extubate fully awake.

GUILLIAN-BARRE SYNDROME:

›  (Acute demyelinating polyneuropathy).

›  Immune mediated.

›  Most common acute form of neuropathy.

›  Seen 2-4 weeks after a viral infection.

›  There is nerve infiltrated by lymphoid cells, with phagocytosis of myelin

›  The patient develops acute ascending paraysis.

›  Motor weakness and respiratory failure.

›  Bulbar involvement.

›  Remyelination occurs over 3-4 months, with full recovery in most cases.

Pathogenesis:

›  There is an immunologic response against myelin sheath of the PNS, especially the lower motor neurons.

›  Usually follows a viral infection.

›  Can also be seen in par-neoplastic disease such as:

›  Hodgkins lymphoma or HIV