Gyn Physiology

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Gyn Physiology

• Leigh Simpson, MD
• Resident Didactic Series
• November 11, 2004

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CREOG Educational Objectives

• Describe the hemodynamic changes associated with
  blood loss.
• Describe the physiology of thermoregulation in
  the anesthetized and postanesthetic patient

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CREOG Objective ONE

• Describe the hemodynamic changes associated with
  blood loss

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Acute Blood Loss

• Human CV system operates with small volume and
  steep Starling curve
• Energy efficient
• BAD for acute blood loss
• ½ fluid by weight(12-13 intravascular)
• Acute loss of 40 of blood stores can prove fatal
  ie, the loss of only 5 of total volume!!!

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Response to Mild Blood Loss

• Stage 1 (First hours) Transcapillary refill
• Movement of interstitial fluid into capillaries
• Helps maintain blood vol but leaves interstitial
  fluid deficit
• Stage 2 Dec body fluid activates RAAS
• Na conservation by kidneys?distributes in
  interstitial space ?retained Na replenishes
  deficit
• Stage 3 (Within few hours) Bone marrow begins to
  increase production RBCs
• SLOWCan take up to 2 months

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Pathophysiology

• Acute blood loss activates the four major
  physiologic systems
• Hematologic
• Cardiovascular
• Renal
• Neuroendocrine

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Hematologic

• Activates the coagulation cascade and stimulates
  contraction of bleeding vessels
• Stimulated by local Thromboxane A2 release
• Also activates platelets to form immature clot on
  bleeding source
• Damaged vessels expose collagen causing fibrin
  deposition and stabilization of clot
• Approx 24 hours needed to mature clot

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Cardiovascular

• Elevated HR, increased myocardial contractility,
  constriction peripheral blood vessels
• Due to incr NE, dec baseline vagal tone
  (regulated by baroreceptors in carotid arch,
  aortic arch, L atrium, pulm vessels)
• Redistribution of blood to brain, heart,
  kidneysAWAY from skin, muscles, GI tract

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Renal

• Elevated Renin secretion from juxtaglomerular
  apparatus
• Renin converts angiotensinogen to angiotensin I
• Angiotensin I ? Angiotensin II in lungs, liver
• Vasoconstriction of arteriolar smooth muscle
• Stimulates aldosterone by adrenal cortex?active
  Na resorption
• Subsequent H2O conservation

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Neuroendocrine

• Increased circulating ADH (from post pituitary)
  in response to
• dec BP (detected by baroreceptors)
• Dec serum Na conc (detected by osmoreceptors)
• ADH indirectly leads to increased resorption of
  water, salt by distal tubule, collecting ducts,
  and loop of Henle

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Clinical Consequences

• Determined by rapidity and magnitude of volume
  loss and patients responsiveness
• Hypovolemia may be clinically SILENT until the
  volume loss exceeds 30 of blood volume

Classification of Hemmorhage Based
on Extent of Blood Loss
American College of Surgeons, Committee on Trauma
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Amercian College of SurgeonsCategories of Acute
Blood Loss

• Class I (Loss of 15 or Less)
• Compensated by transcapillary refill
• Blood volume maintained
• Min/absent clinical manifestations
• Minimal Tachycardia
• Delay in capillary refill by gt3sec?Vol loss of
  10

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American College of SurgeonsCategories of Acute
Blood Loss

• Class II (15-30)
• Resting Tachycardia
• Orthostatic Changes in HR/BP
• Positive Tilt test Incr Pulsegt30 beats/min OR
  SBPgt30mm Hg from supine to uprightwait 1 minute
• Helps corroborate BUT Negative result has no
  meaning!!

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American College of SurgeonsCategories of Acute
Blood Loss

• Class III (30-40)
• Hypovolemic SHOCK
• Decreased SBP
• Decreased UOP (5-15cc/h)
• Profound Tachycardia/ Tachypnea
• Mental Status Changes?Confusion, Agitation
• Vasoconstrictor response to hemorrhage can be
  lost
• Decrease in BP is sudden and profound

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American College of SurgeonsCategories of Acute
Blood Loss

• Class IV (gt40 loss of volume)
• Circulatory collapse!!
• Lethargic mental status
• HR gt 140
• Usually fatal

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A Word on Hct

• Per ATLS Use of hematocrit to estimate acute
  blood loss is unreliable and inappropriate.
• WHY?
• Poor correlation with blood volume deficits /RBC
  volume deficits in acute hemorrhage
• Relative proportions of plasma RBC volumes
  unchanged in whole blood loss
• Hct drop occurs when kidney begins to conserve
  Na? 8-12 HOURS later!!!
• Hct drop also affected by administration of
  IV(asanguionous) fluids

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Resuscitation Strategies

• Universal Goal of Resuscitation Maintain Oxygen
  uptake to vital organs Sustain aerobic
  metabolism
• Factors posing risk to O2 uptake
• Cardiac Output
• Hemoglobin concentration
• Low CO far more threatening than consequences of
  anemia!
• THEREFORE First priority in acute blood loss is
  to preserve blood flow (cardiac output) while
  correcting erythrocyte deficits is a secondary
  goal

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Colloid vs Crystalloid

• Colloids
• Presence of large MW substances that do not
  easily pass from one fluid compartment to another
• Maintains volume of fluid compartment (plasma
  volume)
• Example Dextran-40
• Crystalloids
• Electrolyte solution devoid of large molecules
  that impede water movement
• Allow water to move freely from one fluid
  compartment to another (20 stays intravascular,
  80 to interstitial space
• Example LR

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What to give???

• Colloid fluids are superior to blood products and
  crystalloid fluids for promoting blood flow
• Erythrocyte concentrates (pRBCs) do NOT increase
  and can DECREASE blood flow and should never be
  used alone for resuscitation!!
• For equivalent effects on CO, vol of crystalloid
  infused must be 3X gt than volume of colloid
  infusion
• Crystalloid still more popular
• Cheaper
• Habit

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When to transfuse

• Begin with ONE unit pRBCs when 2 Liters of IV
  crystalloid does not stabilize BP
• Keep giving ONE unit pRBCs for each additional
  Liter of crystalloid transfused

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CREOG Objective TWO

• Describe the physiology of thermoregulation in
  the anesthetized and postanesthetic patient

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Background Information

• Why does the body try so hard to maintain body
  temperature around 37 degrees C?
• If the temperature deviates in either direction
  much at all, there are perturbations in metabolic
  functions
• How can we reliably check core body temperature?
• Pulmonary artery, tympanic membrane, distal
  esophagous and nasopharynx have been shown to be
  the most reliable
• Clinically, oral, rectal, bladder and axillary
  are close approximations

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Normal Thermoregulation

• How does the body regulate temperature?
• Afferent thermo sensing
• Cold (A-delta) and warm (C fibers)
• Central regulation
• Hypothalamus (central regulator in humans)
• Efferent response
• Behavioral (putting a coat on, turing on the A/C)
• Autonomic (shivering, vasodilation/constriction)

Note it takes only a few tenths of a degree to
activate sweating versus a full degree to
initiate shivering
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General Anesthesia
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General Anesthesia

• How is general anesthesia different?
• You cant put on your coat!
• In other words, you lose the normal behavioral
  responses and you are left with only autonomic
  responses
• So what?
• General anesthesia impairs vasoconstriction and
  shivering about 3 times as much as sweating --gt
  you get cold much easier
• Decreases basal metabolic rate
• Inhibits hypothalamic temperature
  regulation?vasodilation
• Use of muscle relaxants impair shivering to
  produce heat
• Spinal/Epidural anesthesia produce motor block
  and vasodilation-? May continue post-op if block
  is prolonged

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All Four Primary Mechanisms of heat loss are
affected

• Conduction transfer of heat from warmer object
  to cooler one by direct contact
• Cold OR table, Cold IVFs
• Convection heat loss in response to movement of
  fluid or gas
• Warming inhaled gases
• OR Ventilation Systems requireAir exchanges (min
  15/hr)
• Radiation heat loss through infrared emissions
• Cold ambient environment in OR
• Evaporation heat dependent phase change from
  liquid to vapor
• Humidifying inhaled gases
• Radiant and convective heat loss account for 90
  of pt heat loss in OR

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Anesthesia Induced Hypothermia(lt36 deg C)

• Again, the threshold for an autonomic response is
  much lower
• There is both a redistribution and a decrease in
  core temperature
• Redistribution
• Normally the body would close AV shunts (in the
  fingers and toes)
• Since these are left open, more heat is readily
  dissipated to the peripheral (venous system) the
  net result is a loss of 1-1.5 degrees C

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Anesthesia Induced Hypothermia

• Core Loss
• While the patient is asleep, there is constant
  radiation of heat into the room
• This typically exceeds the rate of metabolic
  production of heat
• Plateaus after reaching the autonomic threshold

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Malignant Hyperthermia

• Inherited myopathy
• Hypermetabolic state that is activated by some
  inhaled anesthetics (halothane)
• Not only seen in OR but 1-3 hours after patient
  is in RR!
• Due to reduction in Ca reuptake by sarcoplasmic
  reticulum which is necessary to stop muscle
  contractions
• Symptoms are acidosis, tachycardia, hypercarbia,
  hypoxemia and hyperthermia
• Mortality 10
• Treatment stop anesthetic and Dantrolene

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