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Shock/Ischemia/CPCR > Physiology/Pathophysiology > Flashcards

Physiology/Pathophysiology Flashcards

1
Q

What were the key preparedness and prevention recommendations in the RECOVER guidelines?

A
  • Organized, pre-stocked arrest stations improve CPR performance and should be located where animals are routinely anesthetized
  • Post-CPR debriefing is safe, easy and improves future performance
  • Standardized training programs have improved adherence to guidelines in human medicine and are needed in veterinary medicine
  • Leadership and team communication training increase effectiveness of CPR teams
  • High fidelity manikins for teaching CPR psychomotor skills are highly effective in human medicine and would be valuable in veterinary medicine.
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2
Q

What are the key BLS recommendations for canine and feline CPR made in the Recover guidelines?

A
  • Emphasis on rapid recognition of CPA and rapid initiation of CPR
  • Immediate initation of chest compressions with intubation and ventilation performed simultaneously
  • Ventilation rate of 10 breaths/min without interruptions to chest compressions
  • Chest compressions should aim to compress the chest by 1/3 to 1/2 its width in lateral recumbency, at a rate of at least 100 compressions/min allowing full recoil between compressions (“push hard and push fast”)
  • Utilization of 2 minute cycles of uninterrupted chest compressions with alternation of compressors between cycles. Intercycle interruptions in compressions should be kept to a minimum, only as long as required for rhythm diagnosis.
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3
Q

What are the key ALS reccomendations for canine/feline CPR as laid out in the RECOVER guidelines?

A
  • Standard dose epinephrine (0.01mg/kg) is the preferred dose for CPR
  • Rapid defibrillation is warranted in animals with observed progression to pulseless VT or VF, preferentially using a biphasic defibrillator
  • Defibrillation should follow a cycle of CPR in unwitnessed pulseless VT or VF
  • Open chest CPR might be considered in select cases with access to post cardiac arrest support
  • Reversal of anesthetic agents and correction of major acid-base and electrolyte disturbances is advisable
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4
Q

What are the key monitoring recommendations laid out by the RECOVER guidelines?

A
  • Time spent verifying an absent pulse may delay onset of CPR; chest compressions should be initiated immediately for apneic, unresponsive patients
  • ECG analysis of an unresponsive patient may help to rule out CPA or be used to evaluate for rhythms requiring specific therapeutic approaches (eg ventricular fibrillation–VF)
  • EtCO2 should not be used as the sole confirmation of ET intubation in cardiac arrest patients
  • Pauses in chest compressions to evaluate the ECG rhythm should be minimized
  • EtCO2 monitoring is useful to identify ROSC and may be prognostic for the liklihood of ROSC
  • Patient monitoring following ROSC should be directed at identifying abnormalities that may portend another CPA and should be individually tailored to each patient
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5
Q

What are the key post-cardiac arrest care guidelines recommended by the RECOVER analysis?

A
  • Based upon human studies that suggest hemodynamic optimization protocols during the PCA phase are clinically feasible an dpotentially useful, in hemodynamically unstable dogs and cats after cardiac arrest, a hemodynamic optimiazation strategy including fluid therapy adjusted according to criteria customary to veterinary SAECC is reasonable
  • Good evidence to advocate normoxemia versus hyper/hypoxemia in the early PCA period
  • THe evidence suggests a neuro benefit of mild hypothermia in the early postresuscitation period and that fast rewarming after induced/unintended hypothermia may be harmful
  • There is no evidence to support routine administration of corticosteroids, antiseizure prophylaxis, mannitol or metabolic protectants after cardiac arrest
  • Low-dose corticosteroid teratment of patients with perisstent hypotension requiring sympathomimetic support may be considered
  • Hypertonic saline may be considered in animals that are suspected of having cerebral edema as evidenced by coma or obtundation after cardiac arrest
  • Bundled therapy including hypothermia, hypertension and normocapnia and thiopental, methylprednisolone, phenytoin and perhaps antioxidants may have outcome benefit
  • More comprehensive PCA care in a specialty center wiht access to more advanced monitoring equipment and supportive care may have outcome benefit
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6
Q

Discuss the cardiac pump versus thoracic pump theory.

A
  • Cardiac Pump
    • During compressions, the ventricles are directly compressed between the ribs
    • Best for cats, small dogs
    • Can use in keel-chested dogs as well, placing hands directly over location of heart in lateral recumbency
  • Thoracic pump
    • During compressions, the overall intrathoracic pressure is increased, secondarily compressing the aorta and collapsing the vena cava, leading to blood flow out of the chest
    • During elastic recoil, subatmospheric intrathoracic pressure provides a pressure gradient that favors the flow of blood from the periphery back into the thorax/lungs where oxygen and Co2 exchange occurs
    • Best for medium, large dogs, placing hands over widest portion of chest
  • Provide compressions at 100-120bpm
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7
Q

What is the optimal ventilation strategy during a CPR event?

A
  • 10 breaths per minute
  • VT 10ml/kg
  • Inspiratory time of 1 second
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8
Q

Compare monophasic and biphasic defibrillators.

A
  • Monophasic defibrillator
    • Unidirectional current flows from one electrode to another
    • Requires higher energy
    • Initial dose 4-6J/kg
  • Biphasic defibrillator
    • Current initially flows in one direction, then reverses and flows in the other direction
    • Have been shown to more effectively terminate VF at lower defibrillation energy than monophasic defibrillators, in turn leading to less myocardial injury
    • initial dose 2-4 J/kg
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9
Q

After loss of perfusion, the ischemic heart is known to pass through what three phases?

A
  1. The electrical phase during which minimal ischemic damage occurs, lasting 4 minutes
  2. The circulatory phase during which reversible ischemic damage occurs, lasting 6 minutes
  3. The metabolic phase during which potentially irreversible ischemic damage begins to occur and which may necessitate more advanced techniques such as therapeutic hypothermia and cardiac bypass to reverse.

Immediate defibrillation is recommended in cases of CPA d/t pulseless VT of duration of 4 minutes or less.

If the patient is known/suspected to have been in VF/pulseless VT for >4 minutes (therefore beyond the electrical phase) energy substrates are likely depleted and the patient will most likely benefit from a 2min cycle of BLS before defibrillation.

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10
Q

What is the formula for myocardial perfusion pressure?

A
  • MPP=ADP-RADP (aortic diastolic minus right atrial diastolic)
  • The majority of myocardial perfusion during CPR occurs during the decompression phase of chest compressions and is determined predominantly by myocardial perfusion pressure
  • A higher MPP during CPR is associated with better success in both humans and dogs
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11
Q

What conditions essentially make external chest compressions futile and necessitate converstion to open chest CPR?

A

Pleural space disease, pericardial effusion, penetrating thoracic injuries

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12
Q

Following cardiac arrest, PCA brain injury results from global cerebral ischemia perfusion. Much of the mechanism of injury is poorly understood, however, list 4 key points that we do know…

A
  1. Most of the injury is sustained during the reperfusion event, not ischemia, giving the clinician time to intervene after ROSC is attained
  2. Cytosolic and mitochondrial calcium overload leads to activation of proteases that may lead to neuronal detah and production of ROS
  3. A burst of ROS occurs during reperfusion, leading to oxidative alterations of lipids, proteins, and nucleic acids, propagating injury of neuronal cell compnents and limiting the cells protective and repair mechanisms
  4. MIld thearpeutic hypothermia administered after ROSC is proven to reduce postresuscitation cerebral dysfuncion
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13
Q

How is mild therapeutic hypothermia proposed to exert its protective effects in increasing neurologically intact survival from OHCA?

A
  • Reduces mitochondrial injury and dysfunction
  • Decreases cerebral metbolism
  • REduces Ca inflow into cells and neuronal excitotoxicity
  • Reduced production of ROS and reduced apoptosis
  • Reduced seizure activity
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14
Q

Explain the term “myocardial stunning”.

A
  • Refers to reversible myocardial injury in the absence of cell necrosis that occurs following cardiac arrest
  • PCA myocardial dysfunction is characterized by:
    • increased CVP and pulmonary capillary wedge pessure
    • Decreased left and right sided systolic and diastolic ventricular function
    • Increased end diastolic and end systolic volume
    • Reduced left ventricular ejection fraction and cardiac output
  • Typically resolves within ~48 hours
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15
Q

What is a reactive oxygen species (ROS)?

A

A species that may cause oxidative injury; capable of reacting with all biological molecules including nucleic acids, proteins, carbohydrates and lipids

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16
Q

What molecules are most frequently damaged by ROS and what reaction happens?

A
  • Lipids
    • Mammalian cells are rich in PUFA’s which are highly susceptible to oxidative stress
  • Once an ROS is formed, it can either react with another radical to form a covalent bond or, more commonly, react with a non-radical
    • When a free radical reacts with a non-radical, the non-radical loses an electron and transforms into a free radical
    • This is the chain reaction that propagates extensive damage to cell membranes
    • The product can actually be more damaging than the original radical
      • NO combining with superoxide, creates peroxynitrite which is 2000 times more damaging than H2O2
  • The interaction of ROS with lipids in the presence of free iron results in lipid peroxidation
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17
Q

What are the two major free radicals that can initiate lipid peroxidation? What happens with lipid peroxidation?

A
  • Hydroxyl radical and peroxynitrite
  • Lipid peroxidation severely damages cell membranes, causing alterations in enzyme systems and receptors, alterations in ionic channels and increased permeability to calcium and other ions
  • The products of lipid peroxidation are also thought to initiate inflammation, apoptosis and activation of thiol-containing enzymes
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18
Q

What is an antioxidant? What are the main routes of antioxidant defense against cellular damage?

A
  • Antioxidants are substances that can delay or prevent oxidation of lipids, DNA or proteins.
  • Antioxidant proteins (albumin, haptoglobin, ferritin) abundant in plasma/ECF
  • Intracellular antioxidants
    • Glutathione: considered to be first line of defense against ROS
    • Superoxide dismutase
    • Catalase
  • Cell membranes contain tocopherols/beta-carotene in their lipid layer which can impede lipid peroxidation
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19
Q

Describe cold versus warm ischemia.

A
  • Cold ischemia
    • Occurs in organs outside the body
    • Endothelial cells and Kuppfer cells damaged first
  • Warm ischemia
    • Occurs in organs in the body
    • Hepatocyte death predominates
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20
Q

Several events combine during ischemia to set the stage for massive ROS formation. What are these key steps?

A
  • During hypoxia, cells degrade ATP into its components.
    • With continued ischemia, hypoxanthine accumulates.
  • Decreased ATP inactivates the ATP sensitive cell membrane pumps
    • Net efflux potassium, influx of sodium, calcium, chloride
    • Acute cellular swelling
  • The increased intracellular calcium is one of the earliest events in IR injury
    • Causes both apoptosis and necrosis of the cell
    • Activates a protein that leads to marked formation of xanthine-oxide (XO)
    • Continued accumulation of hypoxanthine and XO, which play a role in reperfusion
  • Activation of NFKB leads to increases in inflammatory mediators, adhesion molecules
    • Leads to increased leukocyte adhesion at the site of IR injury during reperfusion
  • Inactivation of NO leads to vasoconstriction
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21
Q

Reperfusion causes more injury than ischemia and is associated with severe endothelial dysfunction. What occurs during reperfusion to lead to this severe injury?

A
  • Massive ROS formation; first occurring at the interface between the endothelium and the blood upon reperfusion
    • Oxygen re-introduction combines with the already present XO and hypoxanthine which leads to superoxide release
    • Superoxide serves as a source for hydrogen peroxide
    • Hydrogen peroxide, in the presence of increased intracellular iron (due to ischemia), is converted via the Haber-Weiss reaction to the hydroxyl radical
  • Hydroxyl radical is a highly destructive/potent oxidizing agent
    • Chain reaction of lipid peroxidation leading to loss of membrane selective permeability, damage to DNA, degradation of structural proteins and membrane bound enzyme activity
  • During reperfusion, large bursts of ROS can bind to circulating NO
    • Loss of NO lets endothelin (potent vasoconstrictor) run unchecked
    • Also has anti-inflammatory activity
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22
Q

What role due neutrophils play in IR injury?

A
  • ROS cn initiate chemotaxis and subsequent neutrophil infiltration
  • Leukocyte infiltration is a crucial component of the IR cascade, with extravasation of the leukocytes from the vasculature a primary event.
    • Much of the tissue injurey occuring arises from the oxidants generated and the proteolytic enzymes released from the neutrophils after extravasation
  • Activated neutrophils can cause tissue injury by
    • ROS synthesis during respiratory burst
    • Release of intrinsic proteolytic enzymes
    • Physical obstruction of capillaries
  • Has been suggested the neutrophils mediate the majority of mucosal and microvascular injury subsequent to IR
    • Continual neutrophil chemotaxis and activation leading to additonal ROS formation, endothelial damage and capillary plugging
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23
Q

What is the no-reflow phenomenon?

A
  • Describes diminished or absent blood flow to an area of tissue after relief of vascular obstruction
  • Thought to be related to swollen endothelium, endothelial protrusions and platelet and fibrin thrombi.
  • Neutrophils likely to play a key role.
  • Longer periods of ischemia more likely to lead to no-reflow.
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24
Q

What are the initial goals of chest compressions?

A
  • Provide pulmonary blood flow for oxygen uptake and CO2 elimination
  • Tissue perfusion for oxygen delivery to restore cellular metabolic activity
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25
Q

Define shock.

A

Inadequate cellular energy production.

Most commonly arises secondary to poor tissue perfusion from low or unevenly distributed blood flow that causes a critical decreases in DO2 in relation to VO2.

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26
Q

What are the 5 functional classifications of shock?

A
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27
Q

What clinical signs are noted in compensatory shock?

A
  • Tachycardia
  • Normal to prolonged CRT
  • Normal blood pressure
  • Normal pulse quality
  • Normal mucous membrane color
  • Tachypnea
  • Normal body temperature
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28
Q

What clinical signs are noted in early decompensatory shock?

A
  • Tachycardia
  • Bounding pulses
  • Pale MM
  • Prolonged CRT
  • Mild to moderate hypotension
  • Mild to moderate hypothermia
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29
Q

What clinical signs are noted in late decompensatory shock?

A
  • Bradycardia
  • Poor pulse quality
  • Hypotension
  • Hypothermia
  • Pale MM with prolonged CRT
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30
Q

Compare the hyperdynamic and hypodynamic phases of septic shock.

A
  • Hyperdynamic
    • Early phase
    • Tachycardia, fever, bounding pulses, injected mm, rapid CRT
    • Secondary to cytokine mediated vasodilation (“vasodilatory shock”)
  • Hypodynamic
    • Late phase
    • Tachycardia, hypothermia, poor pulse quality, pale/icteric MM, prolonged CRT
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31
Q

What parameters must be met to consider a patient well perfused?

A
  • CVP 0-5cmH20
  • Urine 1ml/kg/hr
  • MAP 70-120mmHg
  • Normal HR, temperature, RR, pink mm, normal CRT
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32
Q

What is the breakdown of total body water (ICF/ECF, intravascular/interstitial)?

A
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33
Q

Define osmolarity versus tonicity.

A
  • Osmolarity:
    • Includes all osmoles in solution
  • Tonicity
    • Refers solely to effective osmoles that do not freely permeate most cell membranes
    • Changes in tonicity will drive fluid movement in/out of cells
    • Na=extracellular effective osmole
    • K=intracellular effective osmole
      *
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34
Q

What is normal plasma osmolarity for dogs? Cats?

A
  • Dogs:
    • 290-310mOsm/L
  • Cats
    • 311-322 mOsm/L
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35
Q

Compare hypotonic, isotonic, and hypertonic fluids.

A
  • Isotonic fluids
    • Similar osmolarity and sodium to plasma
    • Do not cause significant fluid shifts between intra/extracellular fluid compartments
    • Useful for treating hypovolemic shock, used for interstitial rehydration
  • Hypotonic fluids
    • Osmolarity/sodium concentration much lower in comparison to plasma
    • Replenish free water deficits
    • Useful for treating animals with hypernatremia secondary to hypotonic fluid loss
    • Distribute throughout both intra/extracellular fluid compartments with less remaining in the extracellular space than isotonic fluids
    • Large volume of distribution and free water content make them a safer choice for slowly treating animals with decreased ability to excrete excess sodium/tolerate an elevated intravascular volume
    • NEVER use for bolus therapy
  • Hypertonic fluids
    • High osmolarity and sodium concentration
    • Cause free water shift from the intracellular to extracellular space, expanding ECF volume be 3-5 times volume administered
    • Osmotic shifts from the interstitial into the intravascular space starts immediately
    • Free water from the intracellular fluid compartment moves into the ECF compartment as the interstitial fluid osmolarity rises
      *
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36
Q

What are the electrolyte compositions, buffers, and osmolality of the common isotonic and hypotonic crystalloids?

A
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37
Q

What does the labeling of a HES product mean?

I.e. 6% Hetastartch 650/0.7/12.4:1

A
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38
Q

What role does the concentration of a HES solution have on its clinical effects?

A
  • The concentration mainly influences the initial volume effect
  • The concentration of the HES solution and patient intravascular volume status and COP will play a role in how much vascular volume expansion occurs after IV infusion
  • Comes in 3,6 and 10%; 10% solution is hyperoncotic with a reported volume effect that exceeds the infused volume by 145%
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39
Q

What role does the molecular weight of a HES solution play in its kinetics?

A
  • Osmotic effectiveness of an HES solution depends on the number of particles in solution/unit volume
  • HES molecules with a MW below the renal threshold (45-60kDa) are excreted rapidly in the urine, reducing the number of circulating HES particles and decreasing the osmotic effect of the circulating HES
  • The higher MW molecules are broken down by alpha-amylase into smaller molecules–this continues, keeping up the osmotic support, until the molecules are hydrolyzed to a size below the renal threshold
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40
Q

What role does the molar substitution of a HES product play in its kinetics?

A
  • The MS represents the average number of HE residues per glucose subunit on the HES molecule
  • The number of sites of substitution will determine the shape and size of the specific HES molecule and ultimately what access alpha-amylase has to the bonds for degradation
  • HES with a higher MS will remain in the intravascular space for longer
  • 0.7=hetastarch; 0.6=hexastarch, 0.5=pentastarch, 0.4=tetrastarch
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41
Q

What does the C2C6 ratio of an HES solution mean?

A
  • Pattern of substitution describes the locations of HE residues on the glucose subunits
  • HE groups on the C2 atom will inhibit the access of alpha-amylase to the linking bonds more effectively than on the C6
  • A high C2C6 ratio will favor slower breakdown of the HES molecules
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42
Q

What are the most important factors determining the pharmacokinetics of an HES solution?

A

Pattern of substitution

Molar substitution

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43
Q

What is the elimination half life of hetastarch (6% HES 450/0.75) and how does that compare to humans?

A
  • 7.45 days in dogs compared to 12.8 days in people
  • Dogs have a higher alpha-amylase concentration than people
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44
Q

The majority of HES is excreted by the kidneys in the urine, however, other routes of elimination are possible, such as tissue storage. Which of the products have the highest level of tissue storage?

A
  • With increasing MS there is increased tissue storage of HES
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45
Q

What are 3 proposed mechanisms of HES induced renal injury?

A
  1. HES macromolecules are reabsorbed into proximal renal tubular cells causing an osmotic nephrosis
  2. “Hyperoncotic” AKI
    1. Increase in intravascular COP d/t unfiltered osmotically active colloid molecules coupled with low renal perfusion pressure in the glomerular arteries is proposed to cause alteration of intraglomerular colloid oncotic forces, leading to reduction/cessation of GFR
    2. Renal excretory function is proposed to be further compromised by back-leak of filtrate across damaged tubular epithelium
  3. Dilutional hypoalbuminemia
    1. Decreased levels of albumin d/t HES administration; albumin is renoprotective and decreases with dilution may predispose to AKI
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46
Q

What were the major findings of the CHEST study evaluating renal injury with use of HES (6% HES 130/0.4)?

A
  • In the HES group significantly more patients required RRT compared to those treated with NaCl
  • No significant difference in 28 and 90 day mortality
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47
Q

What reported coagulation abnormalities have been associated with HES products?

A
  • Platelet dysfunction
  • Decreased concentration of vWF
  • Decreased concentration of factor VIII coagulant (FVIII:C)
  • Enhanced fibrinolysis
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48
Q

What are proposed mechanisms of decreased platelet adhesion associated with HES administration?

A
  • Diminished circulating levels of vwF interfering with platelet binding to subendothelial collagen
  • Interference with platelet alphaIIb-Beta3 expression/activation
  • HES macromolecular binding to platelet surface
  • HES macromolecular nonspecific coating of platelet surface
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49
Q

What is a proposed mechanism for the development of decreased circulating levels of vWF secondary to HES administration?

A
  • vWF-FVIII binding with HES molecules leading to accelerated elimination in urine
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50
Q

What are proposed mechanisms of decreased FVIII secondary to HES administration?

A
  • Reduced half-life due to decreased circulating vWF
  • vWF-FVIII complex binding with HES molecules leading to accelerated elimination in urine
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51
Q

What is a proposed mechanism of increased fibrinolysis associated with HES administration?

A
  • Diminished thrombin-fibrinogen and FVIIIa-fiber polymer interactions via:
    • HES indcued efflux of coag factors fro IV to interstitium reducing physical contact of factors necessary for clot formation
    • Steric interactions of HES and fibrin polymers lessens transit of proteases, protease inhibitors, and/or FXIIa in forming clot matrix
    • HES molecule entrapment in microcompartments of developing clot prevents adequate intramuscular spacing of fibrin polymers for cross linking
    • Inhibits binding of TAFI
    • Poor alpha-2-antiplasmin-mediated protection of fibrin molecules from plasmin
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52
Q

Administration of large volumes of 0.9% NaCl has been associated with hyperchloremia induced AKI. What is the proposed mechanism for this development?

A
  • HIgh chloride levels inducing renal vasoconstriction, decreased GFR and subsequent ischemic renal tubular damage
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53
Q

What are proposed benefits of hypertonic saline administration?

A
  • Transiently improves cardiac output and tissue perfusion via arteriolar vasodilation (i.e. decreases afterload)
  • Volume loading (increasing preload)
  • Reduction of endothelial swelling
  • Weak positive inotrope effect
  • Immune-modulatory effects (suppression of neutrophil respiratory burst activity and cytotoxic effects)
  • Imporves CPP in head trauma patients by augmenting MAP and decreasing ICP
    *
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54
Q

What is normal COP in a dog? Cat?

A
  • Dog 15-26mmHg
  • Cat 17-33mmHg
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55
Q

What effect do colloidal molecules have on urine specific gravity?

A

Increase urine viscosity and USG measurement by the refractometer

Urine osmolality is a more accurate measure of urine concentration in animals receiving colloidal fluids

56
Q

How useful is plasma in providing colloid osmotic support?

A

Significantly less effective than hyperoncotic synthetic starch solutions

Requires 40-50ml/kg to raise plasma albumin by 1g/dL

57
Q

What are the 3 main natural colloid particles?

A

Albumin

Globulin

Fibrinogen

58
Q

Describe the changes that will happen in the ECF and ICF compartment with isotonic fluid loss.

A
  • Isotonic fluid loss occurs with vomiting, diarrhea, bleeding etc
  • Will lead to depletion of ECF compartment and dehydration; if losses severe, hypovolemia and perfusion deficits
  • Isotonic losses do not alter ECF osmolality so there is no movement of water from the ICF and the ICF will remain unchanged
59
Q

Describe the changes that will happen in the ECF and ICF compartment with hypotonic fluid loss.

A
  • Hypotonic fluid loss can occur with DI or excessive panting
  • Will cause a hypernatremia and an increase in ECF osmolality
  • Because of the increased ECF osmolality, fluid will move from the ICF into the ECF and cause depletion of both compartments
  • May need to administer free water as well as isotonic crystalloids to correct
60
Q

Describe the changes that will happen in the ECF and ICF compartment with hypertonic fluid loss.

A
  • Loss of hypertonic fluid occurs infrequently in small animals
    • Typically hyponatremia develops from excessive free water intake or retention
  • Hyponatremia/hyperoncotic fluid loss will cause a drop in ECF osmolality and water will move from the ECF compartment into the ICF, causing cellular swelling
61
Q

What is the formula for calculation of maintenance fluid needs (presumed to be the most accurate in animals <2kg or >40kg).

A

70(BWkg)0.75

62
Q

What is the formula for calculation of a free water deficit?

A

Free water deficit= ([current Na/normal Na]-1) x (0.6xbody weight in kg)

*Good starting point to lower by 1mEq/hr, rate of 3.7ml/kg/hr of free water is a good starting point….

63
Q

What is the formula for calculation of a patient’s albumin deficit?

A

Albumin Deficit (gms)= 10 x (desired albumin-patient album) x weight(kg) x 0.3

If were replacing with 25% HSA (remember significant adverse effects!), would replace over 6-12 horus

64
Q

Discuss end-point resuscitation/early goal directed therapy.

A
  • The amount of each fluid type administered is directed toward meeting specific cardiovascular goals targeted to the individual patient
  • According to the SSC, goals during the first 6 hours of resuscitation should be:
    • CVP of 8-12mmHg
    • MAP >/= 65mmHG
    • UOP >/= 0.5ml/kg/h
    • ScVO2 >/= 70%
65
Q

What is hypotensive resuscitation?

A
  • Restoration of a lower-than-normal systolic blood pressure helps facilitate control of hemorrhage and reduces the risk of rebleeding, but at the same time ensures preserved blood flow to the vital organs
  • Moderate under-resuscitation, aiming for a MAP or 60mmHg may be a compromise between increasing hemorrhage and maintaining tissue perfusion
  • SBP of 90mmHg target
  • Avoid dislodging clots….
66
Q

What comprises a small-volume resuscitation technique?

Large-volume?

A
  • Small volume: 10-15ml/kg crystalloid, 5ml/kg HES
    • Exclusively use in cats…
  • Large volume: 20-50ml/kg crystalloid, 5-15ml/kg HES
67
Q

Fill in the flow-chart regarding O2 delivery.

A
68
Q

Supply-dependent oxygen consumption is often seen in patients with shock. What is supply-dependent oxygen consumption?

A
  • In states of shock, decreased perfusion and subsequent decreased DO2 leads to an increase in cellular oxygen extraction (in an attempt to meet the body’s needs)–this will lead to a decrease in ScvO2 or SvO2
    • Once the increase in cellular oxygen extration exceeds 50-60%, anerobic metabolism ensues and lactate is produced
  • Under normal conditions, DO2 is determined by the O2 needs of the tissues. If no more O2 is needed in the tissue, increasing the O2 supplied will not increase DO2. This is the supply-independent portion of the curve.
  • If the tissues are starving for oxygen despite increasing the amount of oxygen extracted from the blood, consumption will begin to fall linearly with decreasing DO2=”critical point of DO2”
    • Below that point, cells are resorting to anaerobic pathways to survive and oxygen consumption will increase with increased supply
    • “Supply-dependent” oxygen consumption
  • This is not the case in all critically ill patients–sepsis, ARDS–oxygen consumption remains supply dependent to much higher levels than in a normal patient
69
Q

What has proven to be the single most significant prognostic indicator in states of shock/sepsis?

A

ScvO2/SvO2

70
Q

What is the difference between ScvO2 and SvO2? What are normal values?

A
  • ScvO2 is central venous oxygen saturation (from cranial vena cava) **much easier to measure**
  • SvO2 is mixed venous oxygen saturation (from pulmonary artery)
  • ScvO2 typially 72%, SvO2 >75%
  • Tissue hypoxia causes increased extraction of oxygen from venous blood which results in a decrease in ScvO2/SvO2.
    • Increased venous oxygen extraction and resulting venous desaturation is one of the major compensatory responses to help maintain DO2 to peripheral tissues in low flow states
  • Measurements of ScvO2/SvO2 reflect systemic oxygen balance and cumulative oxygen debt
71
Q

What is the formula for calculation of oxygen delivery?

A

DO2=CO x CaO2 x 10 (to convert to ml/min)

CO= cardiac output=HR x SV = HR x (preload+afterload+contractility)

CaO2=arterial O2 content=(1.34 x HgB x SaO2) + (PaO2 x 0.003)

CO would have to be calculated from a PA catheter or something to approximate the stroke volume

72
Q

Name 5 hemodynamic/laboratory parameters that have been used for goal-directed therapy.

A
  1. Lactate
  2. ScvO2/SvO2
  3. Urine output
  4. CVP
  5. BP
73
Q

What is the formula for calculation of MAP?

A

MAP= systolic BP + [(systolic-diastolic)/3]

74
Q

Fill in the blanks of the ABP waveform.

A
75
Q

What is the pulse pressure?

A

The difference between systolic and diastolic arterial blood pressure; responsible for the intensity of the peripheral palpated pulses.

76
Q

What is the dicrotic notch?

A

Elastic recoil of the arterial tree in the presence of a closed aortic valve causing a slight rebound/elevation of ABP

AKA incisura

77
Q

Explain what effect the respiratory cycle and hypovolemia have on systolic BP.

A
  • During spontaneous breathing, SAP is slightly lower during inspiration than expiration (opposite during mechanical ventilation)
    • Alterations in pleural pressure during respiration affect thoracic vasculature and cardiac function which in turn causes changes in stroke volume.
    • Pressure variation is normally quite small, <5mmHg
  • Hypovolemia magnifies this effect–during hypovolemia, the heart and thin-walled intrathoracic vessels are more collapsible
    • Changes in pleural pressure that occur during the respiratory cycle can have more significant hemodynamic impact and result in greater pressure variation
  • Respiratory cycle associated arterial pressure variation could be used as an indicator of volume responsiveness for patients undergoing PPV
    • Spontaneously breathing patients generally have a wide variation in tidal volume and variable changes in intrathoracic pressures, which makes respiratory effects on AP less consistent and interpretation challenging
78
Q

What is systolic pressure variation and how is it calculated? Does it have any correlation to hypovolemia?

A
  • The differnce between the maximum systolic pressure during inspiration and the minimum systolic pressure during expiration
  • SPV=SPmax-SPmin
  • SPV greater than 10mmHg has been shown to correlate fairly well to hypovolemia in human patients
79
Q

What is pulse pressure variation and how is it calculated? Does it correlate to hypovolemia?

A
  • PPV (%)=100 x (PPmax-PPmin)/[PPmax + PPmin/2]
  • Compared to SPV< PPV has the strongest correlation with hypovolemia and volume responsiveness, with higher PPVs correlating to greater degrees of volume responsiveness
80
Q

Describe damping as it applies to fluid filled monitoring systems. What is overdamping? Underdamping?

A
  • Damping is the inherent tendency for the system itself to alter the pressure signal as it is transmitted from the patient to the transducer
  • Underdamping
    • Occurs when the frquency of the monitoring system too closely matches the frequency of the waveform
    • SUmmation of the resonance of the two frequencies, amplification of the signal, overestimation of SAP and underestimation of DAP
    • Waveforms with points or sharp peaks are likely underdamped
  • Overdamping
    • Results in attenuation/muting of arterial pressure waveform
    • Falsely low SAP, falsely elevated DAP
    • Very smooth waveform with loss of most wave characteristics
    • Causes include air bubbles in the line, line occlusion from kinking/clotting, use of overly compliant tubing
81
Q

What phenomenon does this image represent?

A

Pulsus paradoxicus

Exaggeration in respiratory arterial pressure variation; most commonly occurs with pericardial effusion that has resulted in cardiac tamponade. The effective decrease in venous return results in an exaggeration of the difference between SAP during inspiration and expration.

Provided the patient is breathing spontaneously, SAP will be higher on expiration and lower on inspiration.

82
Q

What is the CVP?

A
  • Hydrostatic pressure in the intrathoracic vena cava; in the absence of vascular obstruction, is approximately equal to right atrial pressure
  • What is the normal range for CVP?
    • 0-5cm H20 (can be up to 10)
    • Convert to cmH20 from mmHg—cmH20=mmHg x 1.36
83
Q

How does the CVP vary with the respiratory cycle?

A
  • During inspiration, intrathoracic pressure decreases and CVP falls; vice-versa on expiration
  • If a patient has an upper airway obstruction and difficulty inspring, changes will be exaggerated
  • (Reversed with PPV)
84
Q

Label the CVP waveform and explain what each of the waves and descents correspond to.

A
  • A wave: increase in CVP caused by right atrial contraction
  • C wave: not always seen, caused by bulging of the tricuspid valve into the right atrium
  • X descent: sometimes labeled as X1 and X2, X and X’. decrease in atrial pressure during ventricular ejection.
  • Y descent: rapid emptying of the right atrium as tricuspid opens, allowing blood to flow into the right ventricle
85
Q

What does a low CVP reading suggest? A high CVP reading? What CVP level is typically present before cavitary efffusions/edema develops?

A
  • A low CVP indicates hypovolemia or peripheral vasodilation
  • A high CVP indicates volume overload, right sided heart failure or significant pleural effusion
  • A CVP of >16cm H20 wil lead to edema formation and cavitary effusion
86
Q

What is the utility of pulmonary artery pressure monitoring? What is pulmonary artery occlusion pressure and what is the normal value?

A
  • Requires placement of a central catheter through the right atrium and ventricle and into the pulmonary artery.
  • Allows for measurement of the systolic, diastolic and mean PAP and with a balloon, can measure PAOP (wedge pressure).
    • Inflation of the balloon eliminates PAP created by blood flow; measured pressure reflects left atrial filling pressure as it equilibrates across the pulmonary capillary bed
  • When the mitral valve is open, left atrial pressure equals LVEDP; provides the best measure of LV preload and is the best predictor of pulmonary edema secondary to fluid overload.
  • Normal PAOP in dogs is 5-12mmHg
87
Q

What is a normal cardiac output for a dog/cat?

A

120-200ml/kg/min

88
Q

What is the cardiac index?

A

Relates the volume of blood pumped over time to the animal’s body surface area (L/min/m2)

89
Q

What are the two primary methods for cardiac output monitoring?

A
  • Fick oxygen consumption method
  • Indictor dilution method (includes thermodilution technique)
90
Q

Briefly discuss the Fick method of oxygen consumption for measuring cardiac output. What are some drawbacks to this approach?

A
  • The Fick method states that the total uptake/release of a substance by the peripheral tissues is equal to the product of the blood flow to the peripheral tissues and the arteriovenous concentration difference (gradient) of the substance
    • “What went in minus what came out must equal what was left behind”
  • CO=O2 consumption/AV oxygen content difference
  • O2 consumption is classically determined by measuirng the O2 conentrationdifference in the inhaled air and exhaled air collected from the patient over time
  • Drawbacks
    • Not continuous real-time measure of CO and reliable collection of respiratory gases requires the patient be intubated
    • Also needs the patient to remain in a stable hemodynamic state throughout collection–the more unstable, the less reliable the method becomes.
    • Invalid in the presence of intracardiac/intrapulmonary shunting of blood
91
Q

Briefly discuss how the indicator dilution method for determining cardiac output works and list some of the options for indicator dilution.

A
  • Exogenous indicator is injected into the patient’s mixed venous blood via a PAC and the dilution of the indicator is followed. By calculating the concentration of the indicator against time, one can obtain a curve, with CO determined by taking the known amount of indicator and dividing it by the area under the curve.
  • Thermodilution method
    • Takes saline at a given temperature and measure the temperature of it using a thermocouple to follow the dilution of the sample in the larger blood pool of the patient
  • Lithium dilution method
    • Lithium ions can be tracked with an electrode inserted into an artery; inject small amounts of lithium into venous circulation and use the electrode to measure the dilution
    • “Minimally invasive”
92
Q

Describe some non-invasive/minimally invasive methods for CO monitoring.

A
  • Transesophageal echocardiography
    • Measurements of blood velocity using doppler and aortic diameter allow for estimates of stroke volume
    • Limited use in SA practice
  • Transthoracic bioimpedance
    • Uses four paired electrodes to measure changes in transthoracic impendance during the cardiac cycle and calculates an estimate of stroke volume
  • Pulse contour analysis
    • Calculate stroke volume from measured pulse pressure waveforms using specific algorithms
93
Q

List 5 things that can be measured with a balloon tipped PAC

A
  1. Cardiac output
  2. PCWP/PAOP
  3. Right ventricular end diastolic volume/index
  4. Systemic vascular resistance
  5. Pulmonary vascular resistance
94
Q

Define compartment syndrome.

A
  • Dysfunction of organs/tissues within a compartment that develops secondary to increased pressure within that compartment.
  • Increased pressure limits the blood supply resulting in reduced or absent perfusion to the tissues
95
Q

What are the 2 theorized pathways that may lead to cellular hypoxia resulting in compartment syndrome?

A
  • Arteriovenous pressure gradient theory
    • Increased pressure within the tissue resulting in an increase in pressure of the veins the compartment
    • This causes a decrease in the AV pressure gradient with that compartment
    • Decrease in pressure gradient results in decreased DO2, resulting in ischemia of the affected organs/tissues within the compartment
  • Ischemia-reperfusion injury
    • As pressure within the compartment incrases the interstitial fluid pressure rises above the capillary pressure and when this happens, there is an inability to perfuse the organs/tissues within that compartment
    • Ensuing reperfusion causes massive production of ROS
96
Q

Discuss primary versus secondary compartment syndrome.

A
  • Primary CS
    • Occurs as a result of an injury/disease process within the affected compartment
    • Causes include hemorrhage, edema, obstruction of blood supply (thrombosis), soft tissue/ortho injury to that compartment
  • Secondary CS
    • Injury/disease outside the compartment that is affected
    • “Secondary extremity compartment syndrome”–SECS
      • Fascial planes of muscle bellies form a compartment in the limb
      • Can develop following fluid resuscitation in patients with SIRS/shock
    • Most common cause of secondary CS is overaggressive fluid resuscitation; also can be d/t constrictive bandaging, improper surgical placement/positioning, inappropriately chosen surgical approach
97
Q

What is extremity or skeletal muscle CS?

A
  • Occurs with marked increases in the content or reduction in the volume of a muscle compartment resulting in increased pressure within the compartment.
  • Increased pressure results in ischemia of the affected muscle bodies and can lead to loss of muscle/limb fucntion, eventual muscle death
  • Most widely recognized CS entity in vet med
98
Q

Extremity compartment syndrome (ECS) can be the result of which three factors?

A
  1. Decreased compartmental volume within the extremity compartment
  2. Increased tissue/fluid volume within the compartment
  3. Externally applied pressure on the extremity

Ischemia/reperfusion plays a big role; neutrophil invasion into the area along with cytokine production during the ischemic/reperfusion phases of injury appear to have a significant impact on the severity of the syndrome.

99
Q

A normal intracompartmental pressure in human (and presumably dog) muscles is…

A

10-12mmHg (dogs 5.7 +/-5.1mmHg although not officially published)

100
Q

What type of dogs with injury to what muscle groups are at highest risk for developing ECS?

A

Athletic large breed dogs with injuries to their infraspinatus or supraspinatus muscles

101
Q

Surgery (fasciotomy) is the definitive treatment for ECS. When is it recommended?

A
  • When compartmental pressures are >30mmHg or when the compartmental pressure is within 30mmHg of the patient’s diastolic pressure if clinical signs are consistent with ECS (pain, paresthesia, paresis, pulselessness)
102
Q

Define abdominal compartment syndrome.

A

Syndrome in which increased intra-abdominal pressure (IAP) results in progressive intra-abdominal organ dysfunction as well as detrimental effects on the CV, respiratory and CNS systems.

103
Q

How is IAH defined? What are systemic consequences of IAH?

A
  • IAH is defined as sustained or repeated elevation in IAP >/= 12mmHg.
    • A normal IAP is 1.5-5mmHg in dogs
  • Consequences:
    • Secondary increase in intrathoracic pressure, resulting in decreased LV compliance and decreased ventricular filling due to decreased venous return associated with pressure on vena cava
    • Decreased diaphragmatic excursion, resulting in decreased FRC and impaired pulmonary function
    • Tertiary incease in ICP due to obsturction of cerebral venous blood outflow (associated with increased intrathoracic pressure)
    • More likely to develop kidney failure
    • Decreased to absent mesenteric lymph flow associated with gut wall edema which could further worsen IAH
104
Q

How is abdominal compartment syndrome diagnosed (i.e. what pressure etc–not tools for doing so…)?

A
  • Sustained IAP >20mmHg
  • With or without abdominal perfusion pressure of <60mmHG
  • Associated with new organ dysfunction or failure
105
Q

List 4 conditions (and examples of each) that are at risk for the development of IAH and subsequent ACS.

A
  1. Diminished abdominal wall compliance
    1. Counterpressure applied by belly wrap,positioning/imobility in critically ill
  2. Increased intra-luminal contents
    1. Ileus, GI obstruction
  3. Increased abdominal contents
    1. Fee gas, blood ascites, abdominal mass
  4. Any condition resulting in capillary leakage associated with fluid therapy
    1. SIRS, ARDS, pancreatitis
106
Q

Decompressive surgery is the definitive management recommendation for ACS, however, what are some non-surgical interventions that may help decrease IAP before ACS can develop?

A
  • NGT placement for decompression
  • Enemas
  • Changing body position
  • Diuretics to remove excess fluid/edema from tissues
  • Paracentesis to remove fluid from abdominal cavity
  • Hemodialysis
  • NMB
  • Epidural analgesia
107
Q

How is abdominal perfusion pressure calculated?

A

APP=MAP-IAP

108
Q

What is considered the gold standard for measurement of IAP? Instillation of saline is part of this method; how much infusate is recommended?

A
  • Placement of a sterile urinary catheter attached to a system of three-way stopcocks and a water manometer
  • Bladder needs to be emptied
  • Infuse 0.5-1ml/kg sterile saline into bladder
  • Zero water manometer to patient’s midline at symphisis pubis; keep patient in lateral recumbency
  • Fill manometer with sterile saline ; close stopckock to fluid source so meniscus in manometer can drop and equilibrate with pressure in the urinary bladder
  • Difference between the reading at the meniscus and the zero point is the IAP
109
Q

What is the formula for calculation of the renal filtration gradient (which will be affected with increased IAP)?

A

Filtration gradient=MAP-2IAP

(glomerular filtration pressure-proximal tubular pressure)

110
Q

Discuss the concept of damage control surgery.

A
  • The goal of DCS is to avoid the “triad of death” (coagulopathy, acidosis, hypothermia)
  • Focus placed on short operative times with concurrent and subsequent resuscitation
  • Phases of DCS:
    • Goal directed resuscitation
    • Identification of patient based on injury pattern
    • Abbreviated surgery to control bleeding or contamination
    • Reassessment of patient on operating table
    • Continued resuscitation in ICU
    • Definitive surgical repair
111
Q

Discuss the 2 hit theory of tissue injury.

A
  • First hit
    • Direct tissue damage resulting from trauma
    • Primary trauma force and impact severity determine the scope/significance of sold organ damage, soft tissue injury and fractures through mechanical disruption of traumatized tissue
  • Second hit
    • Sequelae of the inflammatory response
    • Endogenous second hits are direct complications of the initial tissue injury; hypoxia, hypovolemia, hypoperfusion, I&R, wound necrosis
    • Exogenous second hits generally result from attempts to treat the underlying disease

**Production of DAMPS secondary to injury, triggering of PRRs and initiation of inflammatory cascade, cytokine release. Trauma induced CARs occurs as well.**

112
Q

What are the 4 mechanisms of heat loss?

A
  1. Convection
    1. Transfer of heat from body surfaces to air surrounding the body
  2. Conduction
    1. Transfer of heat from body surfaces to objects that come in contact with the body
  3. Radiation
    1. Loss of heat to surrounding structures that do not come into contact with the body
  4. Evaporation
    1. Loss of heat from oisture on the body surfaces or through the respiratory tract to the environment
113
Q

What effects does hypothermia have on coagulation?

A
  • Primary hemostasis abnormalities
    • Sequestration of platelets in the liver/spleen
    • Decreased platelet aggregation (decreased production of thromboxane, platelet granule secretion, diminished expression of vWF receptor)
  • Secondary hemostasis abnormalities
    • Depressed enzymatic activity of the activated clotting factors during hypothermia
114
Q

What is cold diuresis?

A

Initial renal effect of diuresis seen with mild to moderate hypothermia. Can cause hypovolemia and subsequent hypotension.

Result of initially sensed increase in blood volume caused by peripheral vasoconstriction and begins before a drop in core body temp. As core body temp drops, there is a decreased response to vasopressin at the distal tubule, leading to an inability to reabsorb water and a loss of electrolytes.

In moderate hypothermia, GFR decreases secondary to decreases in CO and renal blood flow.

AKI seen in 40% of human patients with accidental hypothermia.

115
Q

Define heat cramp, heat exhaustion and heat stroke.

A
  • Heat cramp
    • Muscle spasm resulting from sodium and chloride depletion
  • Heat exhaustion
    • Fatigue, weakness, muscle tremors, vomiting, diarrhea
  • Heat stroke
    • Hyperthermia associated with systemic inflammatory response leading to a syndrome of multiorgan dysfunction in which encephalopathy predominates
116
Q

Briefly discuss the process of thermoregulation.

A
  • Hypothalamus maintains an almost constant core body temp through the balance of heat production and heat dissipation
  • Heat is produced from metabolism (endogenous) and gained from the environment (exogenous)
  • Heat is dissipated by 4 mechanisms
    • As body temp increases, dogs lose heat primarily via radiation and convection
  • Blood temperature elevations activate the heat receptors, which then activate the thermoregulatory center
    • Efferent responses such as constriction of renal/splanchnic blood vessles and cutaneous vasodilation cause increased delivery of blood to the body surface
    • Tachycardia and increases in CO and minute ventilation also occur
      *
117
Q

What is acclimitization?

A
  • PHysiologic process that allows the body to adapt to environmental or climatic changes
    • 10-20 days, but can take up to 60 days
  • Without this adaptive mechanism, hypovolemia and dehydration occur and lead to vasoconstriction and decreased cardiac output
118
Q

Briefly discuss the acute phase response as it relates to heat stroke.

A
  • APR initiated and modified by cytokines and cytokine modulators in response to heat stroke
  • Can be protective or destructive/inflammatory or anti-inflammatory
  • An exaggerated and inflammatory APR is involved in the development of heat stroke
119
Q

What role do the heat shock proteins play?

A
  • Produced by nearly all cells in response to sudden increases of temperature/other stressors
  • Protect the cellls and the body against further heat insults; protect against denaturation of intracellular proteins and help to regulate the baroreceptor response during heat stress, preventing hypotension and conferring cardiovascular protection
120
Q

Briefly discuss the proposed pathogenesis of heat stroke.

A
  • Initial production release of IL-1 and IL-6 from the muscles into circulation and an increase in systemic levels of endotoxin from the GI tract
  • Mediate excessive activation of leukocytes and endothelial cells, resulting in release of pro and anti-inflammatory cytokines as well as activation of coagulation and fibrinolysis
  • Direct endothelial cell injury due to heat, along with initial hypercoagulable state, results in microthrombosis and progressive tissue injury.
  • Proinflammatory, procoagulation processes and direct heat injury can lead to MODS
121
Q

Why may a dog with heatstroke have increased number of nRBCs present and what impact does this finding have on outcome?

A
  • nRBCs speculated to arise secondary to damage to the bone marrow due to direct heat resulting in premature release
  • Associated with a worse outcome
    • Value of 18+ nRBCs/100 leukocytes had senstivity of 91% and specificity of 88% for predicting death
122
Q

Why is renal failure a common sequelae of heat stroke?

A
  • Severe dehydration, hypotension, hyoxia, rhabdomylosis that causes myoglobinuria, direct thermal damage, acidosis and DIC all contribute to glomerular damage and tubular necrosis
123
Q

What benefit may lidocaine have in treating patients with heatstroke?

A
  • Decreases the release of intracellular calcium and glutamate in the neuronal tissue of the brain and by doing so, decreases the production of ROS
  • Also scavenges ROS, decreases leukocyte activation and adhesion, reduces cytokine release from macrophages and PMNs and decreases endothelial dysfunction
124
Q

What is electroporation?

A
  • The development of momentary holes in cellular membranes induced by electrical shock
  • Allow passage of macromolecules across membranes, causing osmotic damage to cells
125
Q

What is the most prominent pathologic feature in drowning victims?

A
  • Washout of surfactant from the alveoli, causing atelectasis, intrapulmonary shut and global hypoxia, which may then result in tissue injury, neurologic damage, cardiovascular collapse and death
126
Q

What is the dive reflex associated with cold water submersion and what role does it play in sumbersion victims?

A
  • With ice-cold water (<41F), reflex mediated by the trigeminal nerve sends impulses to the CNS that cause bardycardia, hypertension and preferential shunting of blood to the cerebral and coronary cirulcation
  • Protects the brain and heart from hypoxia induced injury
  • Also causes a decrease in metabolic need which protects the brain from injury
  • Effects of this response evidenced by good neurologic recovery in victims submerged in cold water despite the initial presence of coma or other negative neurologic prognostic indicators
127
Q

Compare “anyphylactic” versus “anaphylactoid”

A
  • Anaphylactic is reserved for reactions mediated by IgE
  • Anaphylactoid is for non-IgE mediated events

(The two are clinically indistinguishable!!!)

128
Q

What are the 3 classifications of anaphylactic reactions?

A
  1. Immunologic IgE mediated
    1. Insect stings/bites, reptile venom, food, medications
  2. Immunologic Non IgE mediated
    1. Immune aggregates (IVIg), IgG or IgM related, transfusion, complement system activation, coag system, autoimmune
    2. Non-immunologic
      1. PHysical facors (cold, water exposure, heat, exercise), some medications (opioids)
129
Q

Describe the pathogenesis of the classic, IgE mediated, pathway of anaphylaxis.

A
  • Initial phase of sensitization
    • IgE antibodies produced in response to initial antigen exposure
    • Bind to high-affinity IgE receptor–FceRI located in mast cells and basphils
    • IgE typically in low concentrations in the serum because of low production, short half life and sequestration on mast cells, basophils
    • Once recognized, antibodies bind to mast cells, basophiles allowing them to participate in immediate hypersensitivity reaction upon antigenic stimulation
  • Re-exposure
    • Allergen forms bridge across 2 cell-bound IgE antibody molecules, cross-liking them
    • Induces a membrane change that leads to Ca influx and triggering release of various substances
    • Releases histamine, PAF and upreugulates cytokine synthesis
  • Interaction of mediators with host target organs results in clinical manifestations of anaphylaxis
130
Q

Describe the pathogenesis of the alternative, IgE independent, pathway of anaphylaxis.

A
  • Systemic anaphylaxis induced by antigen binding to IgG molecules that cross-link low-affinity receptors for IgG on macrophages
  • Requires more antigen and antibody than the classic pathway
  • Releases PAF but NOT histamine
  • Studies in mice have demonstrated that IgG antibodies can block IgE dependent anphylaxis under conditions of high IgG antibody concentration and low allergen dose without causing anaphylaxis through the laternative pathway
131
Q

How does non-immunologic anaphylaxis develop?

A
  • Agents cause degranulation of mast cells and basophiles without help of immunoglobulins
132
Q

Discuss the role of histamine/its receptors in development of the signs associated with anaphylaxis.

A
  • Histamine release is rapid, measurable concentrations in plasma within 1 minute of an episode
  • H1 Receptors
    • Smooth muscel contraction and interaction with the endothelium, leading to vasodilatation and increased vascular permeability
    • Leads to rhinitis, pruritus, brochoconstriction, cornoary vasoconstriction, cardiac depression
    • Also stimulates endothelial cells to convert l-arginine into NO–>vasodilation!
  • H2 Receptors
    • Stimulate gastric acid secretion, produces coronary and systemic vasodilation, increases in heart rate, and ventricular contractility
  • H3 Receptors
    • Inhibit endogenous norepinephrine release from sympathetic nerves
    • Expected to accentuate the dgree of shock through prevention of compensatory adrenergic stimulation
133
Q

In anaphylaxis, downstream activation of phospholipase A2, followed by cyclooxygenases and lipoxygenases, produce mediators primarily derived from arachidonic acid metabolites. What are some of these mediators and their effects?

A
  • Prostaglandin D2
    • Bronchoconstriction, pulmonary and coronary vasoconstrictor, and vasodilation
    • ~10x more potent bronchoconstrictor than histamine
  • Lipooxygenase pathway produces “slow-reacting substances of anaphylaxis” (SRS-A)
    • 100 fold more potent when compared to histamine, slower onset but longer duration of action
    • Leukotriene D4; increases bronchoconstriction, vascular permeability and promotes airway remodeling
  • Cytokines, chemokines; TNF-alpha (activates neutrophiles, recruits other effector cells and increases chemokine synthesis)
    *
134
Q

The liver and the GI tract are the primarily affected organs during anaphylactic shock in the dog, with the severity of shock directly proportional to the degree of congestion to the liver and gallbladder. Discuss the pathogenesis of liver compromise during anaphylaxis.

A
  • Histmine released from the GI tract into the portal vein causing hepatic arterial vasodilation and concurrent increase in arterial hepatic blood flow
  • Marked increase in hepatic portal vascular resistance due to histamine induced hepatic venous outflow obstruction
  • Portal blood supply and venous return from the liver to the systemic circulation are severely compromised
  • Reduced venous return accounting for markedly suppressed CO

**Histamine acts primarily on hpeatic veins to raise intrahepatic pressure and produce massive infiltration of fluid, resulting in insufficienty return of blood to the heart**

135
Q

What are the four major categories of signs associated with anaphylaxis?

A
  • Gastrointsetinal
  • Cutaneous
  • Cardiovascular
  • Respiratory
136
Q

What type of shock is most commonly observed in anaphylaxis?

A
  • Mixed distributive-hypovolemic
  • Main cardiovascular changes are fluid extravasation and vasodilation
  • Increased vascular permeability (*key characteristic feature*) allows massive fluid shifts of up to 35% of intravascular volume into extravascular space within 10 minutes
  • Rapid hemodynamic collapse!
137
Q
A

Shock/Ischemia/CPCR (2 decks)

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