Shock and Stabilization, Venous Access

  1. Hypoxia
    Decrease in level of oxygen supplied to tissue
  2. Hypoxemia
    Inadequate oxygenation of arterial blood
  3. PaO2
    • Partial Pressure of O2
    • Measurement of O2 pressure in arterial blood
  4. PaO2 of ____ indicates hypoxemia
    < 80 mm Hg
  5. CaO2
    Arterial concentration of O2. Total number of O2 molecules in arterial blood
  6. Hypoxemia can be a result of (5)
    • 1. hypoventilation
    • 2. ventilation-perfusion mismatch
    • 3. diffusion impairment
    • 4. decreased O2 content of inspired air
    • 5. intrapulmonary shunt
  7. What disease can cause a reduction of global O2 deliver (4)
    • 1. sepsis
    • 2. sirs
    • 3. anemia
    • 4. acid-base imbalances
  8. SaO2
    oxygen saturation as measured by blood analysis
  9. Arterial O2 dependent on
    concentration of hemoglobin and degree of SaO2 of hemoglobin present
  10. How is majority of arterial O2 delivered to tissue
    bound to hemogobin
  11. How is a small fraction of O2 delivered to tissue
    Dissolved in plasma
  12. O2 supplementation is indicated when
    PaO2 ____
    SaO2 ____
    • PaO2 < 70 mm Hg
    • SaO2 < 93% on room air
  13. Why should O2 be humidified
    Avoids drying and irritation of nasal mucosa and airways
  14. Non-humidified O2 longer than several hours can cause (4)
    • 1. drying of nasal mucosa
    • 2. respiratory epithelial degeneration
    • 3. impaired mucociliary clearance
    • 4. increased risk of infection
  15. What should O2 be bubbled through
    Sterile H2O or saline
  16. Non-invasive means of O2 delivery (2)
    • 1. flow-by 
    • 2. face mask
  17. How far should flow-by O2 be held from pt
    2 cm
  18. O2 flow-rate of 2-3 L/min produces and FiO2 of what with flow-by O2
    25% - 40%
  19. Tight fitting face mask creates an FiO2 of _____ at 8-12 L/min
    50% - 60%
  20. Risk with tight fitting face mask
    Rebreathing of carbon dioxide. Should be periodically ventilated
  21. What flow rate should be used with a loose fitting face mask
    2-5 L/min
  22. Invasive O2 supplementation methods (3)
    • 1. nasal prongs
    • 2. nasal or nasopharyngeal catheters
    • 3. hyperbaric O2
  23. How to measure nasal catheter
    nose to level of lateral canthus of eye
  24. How to measure nasopharyngeal catheter
    Nose to ramus of mandible
  25. Desired flow rate for nasal catheters and resulting FiO2
    • 50-150 ml/kg/min
    • FiO2 30% - 70%
  26. At what nasal flow rate do patients often experience discomfort?
    >100 ml/kg/min
  27. Hyperbaric O2
    • administers 100% O2 under supra-atmospheric pressure (>750 mm Hg)
    • Dissolved O2 can readily diffuse into damaged tissues without adequate circulation
  28. How does hyperbaric O2 increase O2 in pts
    Increases % of dissolved O2 in pt bloodstream by 10% - 20%
  29. What injuries/conditions can hyperbaric chambers assist with? (7)
    • 1. severe soft tissue lesions
    • 2. burns
    • 3. shearing injuries
    • 4. infection
    • 5. osteomyelitis
    • 6. ruptured tympanum
    • 7. pneumothorax
  30. When does O2 toxicity occur
    O2 >60% for longer than 24-72 hrs
  31. Shock definition
    inadequate cellular energy production
  32. What is shock most commonly secondary to
    • Poor tissue perfusion
    • decrease O2 deliver compared to O2 consumption
  33. DO2
    O2 delivery
  34. VO2
    O2 consumption
  35. 3 leading causes of shock
    • decrease in DO2 secondary to:
    • 1. hypovolemia - loss of IV volume
    • 2. distributive - maldistribution of vascular volume
    • 3. cardiogenic - failure of cardiac pump
  36. 4 major types of shock
    • 1. obstructive
    • 2. distributive
    • 4. cardiogenic
    • 5. hypovolemic
  37. Hypovolemic shock
    Decrease in circulating blood volume
  38. common causes of hypovolemic shock (3)
    • 1. hemorrhage
    • 2. severe dehydration
    • 3. trauma
  39. Cardiogenic shock
    decrease in forward flow from heart
  40. common causes of cardiogenic shock (4)
    • 1. CHF
    • 2. arrhythmias
    • 3. tamponade - pressure on heart from pericardial effusion
    • 4. drug overdose
  41. Distributive shock
    decrease or increase in systemic vascular resistance or maldistribution of blood
  42. common causes of distributive shock (3)
    • 1. anaphylaxis
    • 2. sepsis
    • 3. neurogenic
  43. Obstructive shock
    caused by physical obstruction in blood flow
  44. Common causes of obstructive shock (3)
    • 1. GDV
    • 2. pulmonary embolism - saddle thrombus
    • 3. HW dz
  45. What activates renin-angiotensin-aldosterone system
    Decreased renal blood flow
  46. What does the renin-angiotensin-aldosterone system do in brief terms
    • Reaction designed to regulate BP. 
    • Upregulates SNS, causes NA and H2O retention via production of aldosterone and antidiuretic hormone
  47. What is compensated shock
    Increased IV volume, so initial signs of shock subtle
  48. Initial signs of compensated shock (5)
    • 1. Mild-mod depression
    • 2. tachycardia with normal or >CRT
    • 3. cool extremities
    • 4. tachypnea
    • 5. normal BP
  49. Signs of decompensated shock (4)
    • 1. pale mm
    • 2. poor pulse quality
    • 3. depressed mentation
    • 4. decrease in BP
  50. end result of untreated shock
    decreased organ perfusion and organ failure, death
  51. Signs of initial hyperdynamic phase of shock (4)
    • 1. tachycardia
    • 2. fever
    • 3. bounding pulses
    • 4. hyperemic mm secondary to cytokines (nitricoxide mediated peripheral vasodilation
  52. What else is hyperdynamic shock called
    vasodilatory shock
  53. shock organs in dogs
    GI tract
  54. Shock in dogs often leads to what due to it's effects on the GI tract? (4)
    • 1. ileus
    • 2. diarrhea
    • 3. hematochezia
    • 4. melena
  55. Hyperdynamic phase of shock is common in cats, true or false?
    false, it's rare
  56. what organ is vulnerable to damage with shock and sepsis in cats?
    Lungs, signs of respiratory dysfunction common
  57. Essential monitoring with shock (3)
    • 1. EKG
    • 2. BP
    • 3. Pulse ox
  58. What are often sign of successful return of cardiovascular stability in shock? (2)
    Gradual reduction of tachycardia and normalization of BP
  59. Best form of monitoring shock pt?
    Thorough physical exam
  60. Goal of shock treatment
    Optimizing O2 delivery and tissue perfusion
  61. Clinical signs of well-perfused pt (7)
    • 1. CVP between 0-5 cm H2O
    • 2. urine production of at least 1 ml/kg/hr
    • 3. MAP between 70-120 mm Hg
    • 4. normal body temp
    • 5. normal HR/rhythm
    • 6. normal RR
    • 7. moist pink mm with CRT <2 sec
  62. Why is monitoring lactate beneficial in shock pt?
    Indices of system O2 transport and mixed venous O2 saturation
  63. Hyperlactemia and acidemia are reflective of what?
    Reflective of severity of cellular hypoxia
  64. Normal lactate
    <2.5 mmol/L
  65. Severely elevated lactate
    > 7 mmol/L
  66. Lactate in neonatal and pediatric patients
    • may have higher levels
    • puppies 4 days old 1.07-6.59 mmol/L
    • 10-28 days 0.80 - 4.6 mmol/L
  67. Lactate samples with IDEXX analyzer (3)
    • 1. serum should not be used
    • 2. separate plasma within 5 mins
    • 3. restraint and prolonged occlusion can increase
  68. What is a good prediction of outcome with lactate?
    change in lactate concentrations/responsiveness to therapy
  69. PCWP
    • Pulmonary Capillary Wedge Pressure
    • indirect estimate of left atrial pressure (LAP)
  70. R-sided cardiac catheter (PAC) allows for measurement of (4)
    • 1. central venous and pulmonary artery pressure
    • 2. mixed venous blood gases (PvO2, SvOs)
    • 3. pulmonary capillary wedge pressure (PCWP)
    • 4. CO
  71. What other parameters of circulation and respiratory function can be derived from parameters supplied by PAC catheter? (9)
    • 1. stroke volume
    • 2. end-diastolic function
    • 3. systemic vascular resistance index
    • 4. pulmonary vascular resistance index
    • 5. arterial O2 content
    • 7. DO2 index
    • 8. VO2 index
    • 9. O2 extraction ration
  72. CO and Do2 should be optimized until PCWP approaches what?
    10-12 mmHg
  73. High PCWP levels and what does it promote?
    • >15-20 mm HG
    • Promotes pulmonary edema and further impairs DO2
  74. SvO2
    mixed venous O2 saturation (superior and inferior vena cava)
  75. ScvO2
    Central venous O2 saturation
  76. SvO2 and ScvO2
    Refers to O2 content of blood that returns to heart after meeting tissue needs. Requires PAC or central venous catheter
  77. If Vo2 constant, SvO2 determined by (3)
    • 1. CO
    • 2. hemoglobin concentration
    • 3. SaO2
  78. SvO2 decreased if (2)
    • 1. Do2 decreased (low CO, hypoxia, anemia)
    • 2. Vo2 increased (fever, sz)
  79. SvO2 increased if (2)
    • 1. hyperdynamic stages of sepsis
    • 2. cytotoxic tissue hypoxia (cyanide poisoning)
  80. Mainstay of therapy for shock
    rapid administration of fluids to restore circulating volume and tissue perfusion (except cardiogenic)
  81. Shock fluid dose
    • Up to 1 blood volume
    • k9 90 ml/kg
    • fel 50 ml/kg
  82. IV fluids rapidly distribute to _____________ fluid compartment
    extracellular
  83. How quickly do fluids rapidly distribute to fluid compartment?
    75% distributes to extracellular compartment after 30 mins
  84. How should resuscitation be done with active hemorrhage?
    Hypotensive resuscitation
  85. hypotensive resuscitation
    resuscitate slowly to MAP of 60 mm Hg to avoid worsening bleeding
  86. Fluids with coexisting head trauma
    0.9% NaCl - highest concentration of Na, least likely to contribute to cerebral edema
  87. Excessive fluid administration signs (2)
    • 1. pulmonary edema
    • 2. peripheral edema
  88. edema with excessive fluid administration caused by any combination of (3)
    • 1. increased hydrostatic pressure
    • 2. hypoalbuminemia
    • 3. increase in vascular endothelial permeability
  89. hydrostatic pressure
    the pressure of the blood against the vessel wall. It is the opposing force to oncotic pressure
  90. Additional fluid options for shock resuscitation (4)
    • 1. synthetic colloid solutions
    • 2. hypertonic saline
    • 3. blood products
    • 4. hemoglobin-based 02 carrying solutions (HBOC)
  91. Synthetic colloids
    • Hyperoncotic
    • pull fluid into intravascular space
    • cause increase in blood volume greater than infused volume and help retain it in intravascular space
  92. When are synthetic colloids used (2)
    • 1. acute hypoproteinemia (TP <3.5 g/dL)
    • 2. decreased colloid oncotic pressure
  93. hyperoncotic
    osmotic pressure exerted by colloids in solution
  94. Dog dose synthetic colloids
    10-20 ml/kg
  95. cat dose synthetic colloids
    • prevalence of heart dz, use more conservatively
    • 5-10 ml/kg
  96. Why are synthetic colloids avoided
    • evidence in humans for contribution to acute renal injury, especially in critically ill and septic pt
    • no evidence in dogs and cats
  97. Human albumin
    natural hyperoncotic and hyperosmotic colloid solution
  98. hypertonic saline
    • 7%-7.5%
    • after administration, transient (<30 min) osmotic shift of H2O from extravascular to intravascular compartment
  99. How is hypertonic saline administered
    • In small volumes over 10 mins
    • 3-5 ml/kg
  100. other actions of hypertonic saline (5)
    • 1. decreased endothelial swelling
    • 2. modulates inflammation
    • 3. increased cardiac contractility
    • 4. causes mild peripheral vasoconstriction
    • 5. decreases intracranial pressure
  101. How quickly are effects of hypertonic saline seen?
    decreased HR and improved pulses within 1-2 mins
  102. Why should hypertonic saline always be combined with other fluids? (2)
    • 1. osmotic diuresis
    • 2. rapid Na distribution
  103. How long will plts survive in fresh whole blood
    24 hrs
  104. What is Do2 dependent on (2)
    • 1. CO
    • 2. systemic vascular resistance
  105. Common vasopressors (3)
    • 1. catecholamines
    • 2. + inotropic agents
    • 3. phenylephrine
  106. Catecholamine drugs (3)
    • 1. epi
    • 2. norepi
    • 3. dopamine
  107. + inotropic agents do what?
    • Increase force of ventricular contraction
    • Increase strength of cardia muscle contraction by increasing quantity of intracellular Ca for binding by muscle proteins and/or increasing sensitivity of increased contractile proteins to Ca
  108. phenylephrine is what?
    • a sympathomimetic drug
    • Activates adrenergic receptors by increasing mediators of sympathoadrenal system levels (norepi and epi)
  109. Adjunctive pressor agents (3)
    • 1. vasopressin
    • 2. corticosteroids
    • 3. glucagon
  110. cardiogenic shock
    systolic or diastolic cardiac dysfunction
  111. What hemodynamic abnormalities does cardiogenic shock result in? (6)
    • 1. increase HR
    • 2. decreased stroke volume
    • 3. decreased CO
    • 4. decreased BP
    • 5. increased peripheral vascular resistance
    • 6. increase in right atria, pulmonary arterial, and pulmonary capillary wedge pressures
  112. What can help differentiate between causes of dyspnea in the cat?
    hypothermia secondary to decreased perfusion (CHF)
  113. what may excessive overhydration cause in shock? (2)
    • 1. dilutional coagulopathy
    • 2. pulmonary edema
  114. What type of catheters have potential for increased damage to vessel walls?
    Larger, rigid catheters
  115. Common materials for catheters (4)
    • 1. Teflon
    • 2. Polypropylene
    • 3. Polyurethane
    • 4. Silicone
  116. Less common IVC placement sites (3)
    • 1. Dorsal common digital veins
    • 2. Auricular veins
    • 3. Lingual veins
  117. What catheter placement sites may reach the heart faster?
    IVC placed centrally or in the cephalic region
  118. Movement of IVC within vein potentially causes what? (3)
    • 1. Increased damage to vessel wall
    • 2. Risk of thrombus formation
    • 3. Phlebitis
  119. Complications of surgical cut-down for IVC placement (6)
    • 1. Perforation of vascular wall
    • 2. Hematoma
    • 3. Thrombosis
    • 4. Venous transection
    • 5. Infection
    • 6. Cellulitis
  120. Advantages of central venous catheter over peripheral catheter (4)
    • 1. Longer dwell time
    • 2. Safer administration of hyperosmolar solutions such as TPN
    • 3. Measurement of CVP
    • 4. Blood sampling
  121. Why are certain catheters contraindicated in patients with head trauma or other CNS disturbances?
    Jugular vein catheters contraindicated, occlusion for placement may increase intracranial pressure
  122. Seldinger technique
    Placing catheter over guide wire
  123. Advantage of polyurethane catheters in central venous placement
    They are antithrombic and last longer
  124. What will thrombosis feel like around a catheter site
    "Ropey" feel to vessel
  125. Important thing to remember about parenteral nutrition connection
    Parenteral nutrition lines should NEVER be disconnected to decrease the risk of infection
  126. Ionized calcium levels should  be / not be  measured on heparanized samples
    Not be
  127. What vein closely approximates oxygenation of arterial blood, and how should sample be collected?
    Sublingual veins in anesthetized patients, should be punctured with 25 gauge needle and 5 minutes of pressure should be applied after
  128. Arterial catheter sites (5)
    • 1. Dorsal metatarsal (dorsal pedal)
    • 2. Radial
    • 3. Coccygeal
    • 4. Femoral
    • 5. Auricular
  129. What are the only things that should be injected into an arterial line? (2)
    • 1. Heparanized flush
    • 2. Sterile flush
  130. Ischemic complications are more common in what species, and why?
    Cats - they have poorer collateral circulation compared to dogs
  131. Nosocomial infection:
    Hospital-acquired
  132. Risks linked to nosocomial infections (3):
    • 1. Increased morbidity and mortality
    • 2. lengthen hospital stays
    • 3. added cost to pt. care
  133. Types of IVC material (4) and preferred materials*:
    • 1. Teflon*
    • 2. Polyurethane*
    • 3. polyvinyl chloride
    • 4. polyethylene
    • *Per CDC - reduces risk of infection
  134. Increased/Decreased IVC diameter increases risk of thrombi
    Increased
  135. What inactivates povidone-iodine
    Alcohol
  136. Topical antibiotic ointment Should/Should Not be applied to insertion site for IVC
    should not
  137. Thermoregulatory center
    Hypothalmus
  138. Why shouldn't topical antibiotic ointment be applied to insertion sites?
    • Promotes fungal growth
    • Encourages bacterial resistance
  139. How often should insertion sites be cleaned and with what?
    Cleaned with chlorhexidine and allowed to dry every time dressings are changed
  140. Phlebitis
    Inflammation of vessel
  141. Signs of Phlebitis (4)
    • 1. Redness around site
    • 2. Heat
    • 3. Swelling
    • 4. Pain on palpation of site or when flushing IVC
  142. Thrombosis
    • Thrombus formation at tip or along outer length of catheter.
    • Intravascular coagulation of blood in circulatory system
  143. Signs of thrombosis (5)
    • 1. Pain on palpation or when flushing IVC
    • 2. Vessel feels hard or "ropey"
    • 3. Vessel appears distended without being occluded
    • 4. Edema above or below site
    • 5. Becomes difficult to flush or aspirate
  144. Thrombosis increases risk of what?
    Pulmonary embolism
  145. Why may generalized edema be present when administering IVF?
    Due to compromise in vascular retention status due to low colloid osmotic pressure
  146. PICC
    Peripherally Inserted Central Catheter
  147. Why should multiple attempts not be made to place IO catheter in same site?
    • Fluid may leak from hole if replacing or attempting multiple placements in same bone.
    • Increases risk of compartment syndrome
  148. Compartment Syndrome IO catheter
    Fluids extravasate from IO site over long period of time. Pocket is formed in muscle, can cause necrosis
  149. What should be done with feeding tubes before feeding
    • Should be aspirated and checked for negative pressure
    • Gas aspirate back may be sign of line being in airway
  150. Hypotension
    Reduction in systemic arterial blood pressure
  151. Why does hypotension develop
    • Results from disruption of normal cardiovascular homeostasis
    • Only develops secondary to dz that has negatively affected regulation
  152. Systemic arterial blood pressure
    Force exerted by blood against any unit area of the vessel wall
  153. MAP
    Mean Arterial Blood Pressure
  154. What value plays biggest role in tissue perfusion (Systolic, Diastolic, MAP)
    MAP
  155. CO
    Cardiac Output
  156. SVR
    Systemic Vascular Resistance
  157. MAP is determined by what two functions
    CO and SVR
  158. Cardiac Output is function of
    SV times HR
  159. SV
    Stroke Volume
  160. Stroke Volume is
    volume of blood ejected with each contraction of heart
  161. HR
    Heart Rate
  162. Determinants of SV (3)
    • 1. Preload
    • 2. Contractility
    • 3. Afterload
  163. Preload
    Stretching of ventricle before contraction - function of venous return
  164. Contractility
    Force of ventricular contraction
  165. Afterload
    Force needed to overcome aortic pressure and achieve L ventricular outflow
  166. SV is directly related to
    Preload and Contractility
  167. SV is inversely related to
    Afterload
  168. HR is dictated by what
    balance between SNS and PNS
  169. SNS
    sympathetic nervous system
  170. PNS
    Parasympathetic nervous system
  171. Regulation of what is major factor in determining MAP?
    SVR
  172. Cardiogenic shock:
    Inadequate cellular metabolism secondary to cardiac dysfunction, despite adequate intravascular volume
  173. Aim of treatment for cardiogenic shock
    Restore cardiac output to normalize tissue perfusion
  174. 3 main causes of cardiogenic shock
    • 1. Systolic dysfunction
    • 2. Diastolic dysfunction
    • 3. Arrhythmias
  175. Most common cause of systolic dysfunction
    DCM
  176. Less common causes of systolic dysfunction (4)
    • Secondary to mechanical failure:
    • 1. subaortic stenosis
    • 2. hypertrophic obstructive cardiomyopathy
    • 3. Acute mitral regurge secondary to ruptured chordae tendinae
  177. Common causes of diastolic dysfunction (3)
    • 1. Secondary to cardiac tamponade
    • 2. hypertrophic cardiomyopathy
    • 3. tachyarrhythmias
  178. Common causes of severe bradyarrhythmias (2)
    • 1. 2nd and 3rd degree AV block
    • 2. Sick Sinus Syndrome
  179. Sick Sinus Syndrome
    sinus node (pacemaker) doesn't work properly, abnormally paced signals
  180. Shock
    inadequate cellular production
  181. Most common type of shock
    hypovolemic shock
  182. Forward flow failure = ___________ intravascular volume + Increased/decreased                  
    Forward flow failure = Adequate intravascular volume + decreased cardiac output
  183. ___ X ___ = CO
    SV X HR = CO
  184. Decreased SV = Increased/decreased HR in compensation
    Increased
  185. Clinical signs of cardiogenic shock
    • Consistent with global hypoperfusion
    • Change in mentation (depression, unresponsiveness, disorientation)
    • Cold peripheral extremeties
    • Pale MM
    • Increased CRT
    • Increased HR (Unless caused by bradyarrhythmia or pt moribund)
  186. Should tachycardia be treated with antiarrhythmics
    • Malignant tachycardia due to tachyarrhythmia should be treated to improve CO
    • Therapy for compensatory tachycardia contraindicated, fix underlying cause
  187. Compensatory respiratory Alkalosis/Acidosis can be seen in response to _________ with cardiogenic shock
    • alkalosis
    • lactic acidosis
  188. Reasons why cardiac sounds may be difficult to auscult (3)
    • 1. Pericardial effusion
    • 2. Severe hypovolemia
    • 3. Obesity
  189. What will you auscult with CHF
    • inspiratory crackles secondary to pulmonary edema
    • Or lungs my be quiet ventrally due to pleural effusion
  190. Venous blood gas often shows what with cardiogenic shock
    • Metabolic acidosis
    • Decreased cellular oxygen may cause anaerobic metabolism and lactic acidosis
    • Prerenal or renal azotemia may also contribute
    • Often see compensatory respiratory alkalosis
  191. If there is concurrent pulmonary edema with cardiogenic shock, what may be increased on arterial blood gas
    alveolar-arteriolar (A-a) gradient
  192. EKG on cardiogenic shock may show
    • 1. Sinus tachycardia
    • 2. bradyarrhythmias (AV block)
    • 3. tachyarrhythmias (a-fib, v-fib)
  193. CHF CXR will show
    • 1. Enlarge pulmonary veins
    • 2. Alveolar or interstitial pattern in perihilar region (K9s)
    • 3. Infiltrates often patchy or diffuse in felines
    • 4. pleural effusion
  194. Why can pulmonary arterial catheters help with diagnosis of cardiogenic shock
    Decreased CO + Increase in preload parameters of central venous pressure, pulmonary arterial pressure, and pulmonary arterial occlusion pressure will be seen
  195. Systolic dysfunction
    Decrease in cardiac contractility or decrease in flow through left ventricular outflow tract (mechanical failure)
  196. Common causes of failure of contractility with systolic dysfunction (4)
    • 1. DCM
    • 2. Sepsis
    • 3. Endomyocarditis
    • 4. Myocardial infarction
  197. Most common cause of cardiogenic shock from systolic dysfunction
    DCM
  198. Breeds commonly affected by DCM (5)
    • 1. Dobermann
    • 2. Boxer
    • 3. Great Dane
    • 4. Labs
    • 5. American Cocker Spaniel
  199. What is DCM
    • Progressive decrease in myocardial contractility over months or years.
    • Activation of renin-angiotensin system and SNS in compensation, renal retention of Na and H2O,
    • Increased intravascular volume produces increase end-diastolic volume
    • Eccentric hypertrophy secondary to myocardial stretch
  200. Eccentric hypertrophy
    Dilation of L ventricular chamber
  201. CXR for DCM may show
    • Enlarged heart
    • CHF if present
  202. EKG for DCM may show
    • +/- sinus tachycardia
    • +/- arrhythmias - afib or vtach
  203. Aim of tx for DCM
    • Increase CO by increasing SV
    • Preload parameters monitored closely
    • IVF only if necessary
    • Diuretics only if CHF
  204. Drugs for DCM tx (3)
    • Titrated to optimize SV
    • 1. Positive inotropic agents - dobutamine
    • 2. Phosphodiesterase inhibitors - Amrinone, Pimobendan
    • 3. Cardiac glycosides - Digoxin
  205. Why would sepsis potentially cause cardiogenic shock
    • Dysfunctional myocardium sometimes seen in humans and dogs.
    • During hyperdynamic phase of septic shock my see increase in CO and possible decrease in Ejection fraction
  206. Ejection fraction
    Percentage of blood L ventricle pumps out with each contraction
  207. Dysfunctional myocardium with sepsis caused by (3)
    • 1. Decrease in ventricular compliance
    • 2. Biventricular dilation
    • 3. Decrease in contractile function
  208. When will you see myocardial dysfunction with sepsis
    Will peak within days of onset, will resolve within 7-10 days with survival
  209. Do you see a change in CO with septic shock?
    Decreases in CO are rare with septic shock, usually due to end-stage decompensated myocardial depression
  210. What is endomyocarditis
    • Rare condition of cats, often seen several days after routine procedure like neuter.
    • Normal myocardial function pre-anesthesia, afterwards rapidly develop:
    • 1. Cardiac dysfunction
    • 2. Hypotension
    • 3. Pulmonary edema
    • 4. Interstitial pneumonia
  211. Echo with endomyocarditis
    Hyperechoic
  212. Histopath with endomyocarditis
    • Neutrophilic inflammation
    • Fibroplasia
  213. Prognosis with endomyocarditis
    Poor, even with PPV
  214. Two common causes of mechanical failure with cardiogenic shock
    • Forward flow decreased by obstruction to L ventricle outflow tract (aortic stenosis, Hypertrophic obstructive cardiomyopathy)
    • Severe acute retrograde bloodflow (Chordae tendinae rupture, causes acute and extensive MR)
  215. Diastolic failure
    Due to inadequate ventricular filling
  216. Common causes of diastolic failure (4)
    • 1. hypovolemia
    • 2. physical restriction (cardiac tamponade)
    • 3. Inability of myocardium to relax (HCM)
    • 4. inadequate time for filling (tachycardia)
  217. Most common cause of diastolic failure
    Hypovolemia - not truly cardiogenic shock
  218. Cardiac tamponade is secondary to
    pericardial effusion
  219. Cardiac tamponade
    pericardial effusion
  220. Most common causes of cardiac tamponade (5)
    • 1. neoplasia *most common
    • 2. coagulopathy
    • 3. trauma
    • 4. atrial tear
    • 5. idiopathic
  221. What may chronic pericardial effusion cause with bloodwork?
    increased potassium from reduced effective circulating volume induced pseudohypoadrenocorticism. Results from decreased preload
  222. Hypertrophic cardiomyopathy
    • Concentric hypertrophy of ventricular myocardium.
    • Failure of normal end-diastolic volume can occur secondary to inability of myocardium to relax
  223. concentric hypertrophy
    increased ventricular wall thickness
  224. what does decreased end-diastolic ventricular volume lead to
    decreased SV and decreased CO
  225. Pts with HCM typically have what flow failure
    backwards
  226. What happens to systolic function with end stage HCM
    May have severely impaired systolic function. Leads to decreased SV and cardiogenic shock
  227. Tx for HCM
    beta blockers or calcium channel antagonists. They enhance lusitropy and diastolic filling
  228. Lusitropy
    Rate of myocardial relaxation
  229. Increased heart rate affects ventricular filling how
    inadequate ventricular filling
  230. End diastolic volume is largely dependent on what?
    venous return
  231. How does atrial contraction contribute to preload
    Atrial contraction contributes little to normal preload
  232. How does tachycardia affect diastolic filling
    • Tachycardia leads to inadequate time for diastolic filling before systole.
    • Leads to decreased end diastolic filling which leads to decreased SV and decreased CO
  233. Most common cause of tachyarrhythmias that lead to cardiogenic shock
    Supraventricular tachycardia - caused by primary heart disease or cardiac manifestation of other systemic disease
  234. Tx for tachyarrhythmias
    • 1. vagal maneuvers
    • 2. calcium channel antagonists
    • 3. beta blockers to decrease HR
    • 4. management of underlying condition
  235. Most common bradyarrhythmias
    • 1. Severe high grade AV block
    • 2. Severe sick sinus syndrom
  236. 3rd degree AV block
    AV nodal conduction does not occur. Escape complexes from bundle of His, bundle branches, or purkinje fibers produce cardiac contractions
  237. HR with bundle of His escape complexes
    40-60 BPM
  238. HR with escape complexes from bundle branches or distal perkinje fibers
    20-40 BPM
  239. With 3rd degree AV block, what happens to SV
    SV increases secondary to increased preload (increased time for diastolic filling)
  240. Average cat HR with 3rd degree AV block
    • 100-140 BPM
    • Cardiogenic shock as a result rare in cats
Author
anubis_star
ID
357328
Card Set
Shock and Stabilization, Venous Access
Description
week 2-3
Updated