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VTS Studying > Silverstein Text (3rd ed) > Flashcards

Silverstein Text (3rd ed) Flashcards

1
Q

What is the primary survey?

A

A rapid assessment of an animal’s respiratory, cardiovascular and neurologic system

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2
Q

In the primary survey, what is the main focus of evaluating the respiratory system?

A

Determining the presence or absence of hypoxemia or hypoventilation

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3
Q

What can tachypnea indicate?

A

Presence of hypoxemia; hypovolemia, metabolic acidosis, pain, abdominal distension, etc.

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4
Q

In what circumstances is an upper airway obstruction more likely to occur?

A

Brachycephalic breeds, history of coughing/diagnosed or suspected tracheal or mainstem bronchial collapse, underlying laryngeal dysfunction, traumatic injury to neck/skull, secondary to orofacial surgery (secondary to bleeding/swelling)

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5
Q

Name 3 stabilization efforts in the event of an upper airway obstruction

A
  1. Sedatives
  2. Cooling if hyperthermic
  3. Antiinflammatory meds
    BONUS: intubation or tracheostomy
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6
Q

What are dull lung sounds associated with?

A

Pleural space disease or severe consolidation of lung parenchyma

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7
Q

What are increased lung sounds/crackles/wheezes associated with?

A

Development of pulmonary parenchymal disease (ie. aspiration pneumonia)

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8
Q

Why does pleural effusion develop?

A

Secondary to SIRS and endothelial damage resulting in fluid leakage, severe hypoalbuminemia, massive pulmonary thromboembolism, right sided heart failure, fluid overload in cats, blunt/penetrating thoracic trauma, post thoracic/diaphragm surgery, barotrauma from anesthesia/mechanical ventilation

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9
Q

What are some causes of pulmonary parenchymal disease?

A

Aspiration pneumonia, ALI, ARDS, fluid overload and CHF, pulmonary thromboembolism

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10
Q

What are the risk factors for developing ALI/ARDS?

A

SIRS, sepsis, infection, smoke inhalation, near drowning, severe trauma

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11
Q

What does a SpO2 <95% correlate to

A

PaO2 of <80 mmHg, hypoxemia

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12
Q

What is the difference between hypoxemia and hypoventilation?

A

Hypoxemia = SpO2 <95/PaO2 <80 mmHg while hypoventilation is PaCO2 >50 mmHg

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13
Q

What does a PaO2/FiO2 ratio indicate?

A

If <300 it is ALI, if <200 it is ARDS

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14
Q

Why does hypoventilation occur?

A

Post operatively, patients treated with opioids/benzos/other resp depressing meds, cervical myelopathy, tgoracic trauma or pain, secondary to intoxications, neuromuscular disease, CNS pathology

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15
Q

What can you do when hypoxemia is confirmed?

A

Provide supplemental O2 (even if SpO2 is >95% but RR/RE increased), administration of a diuretic or bronchodilator, antibiotics case by case

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16
Q

What can you do when hypoventilation is confirmed?

A

Underlying cause must be addressed (i.e. reverse medications, give pain medications)

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17
Q

What is the purpose of evaluating the cardiovascular system on primary survey?

A

To identify poor tissue perfusion resulting in decreased tissue oxygen delivery

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18
Q

What critical conditions may develop that result in poor tissue perfusion?

A

Hypovolemia secondary to GI dysfunction with fluid and electrolyte losses from V+/D+/R+, third space losses of fluid in systemic endothelial damage and vascular leak, massive urinary losses of fluid (post obstructive diuresis), hemorrhage, severe hypoalbuminemia, cardiac disease and ventricular dysfunction, cardiac arrhythmias, cardiac tamponade, vasodilatory states like sepsis/SIRS

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19
Q

What are the physical exam findings consistent with poor tissue perfusion?

A

Pale mucous membranes, prolonged CRT, tachycardia (bradycardia in cats), tall and narrow pulse profile, poor/absent peripheral pulses, hypothermia, cold extremities, dull mentation, quiet heart sounds

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20
Q

What are some indicates of a vasodilatory state?

A

Red mucous membranes (dogs) with shortened CRT, peripheral pulses widened due to lower diastolic pressure

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21
Q

What does an absence of peripheral pulses indicate?

A

Hypotension (SBP <90 mmHg)

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22
Q

What is a rectal interdigital temperature gradient and what does it indicate?

A

Rectal temperature is taken and compared to the temperature taken between the 3rd and 4th digit on a pelvic limb. If the gradient is -11.6 F, it is suggestive of shock in dogs

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23
Q

Why might cardiac arrhythmias develop?

A

Secondary to hyperkalemia, cardiac ischemia, intraabdominal disease, underlying cardiac disease, CNS disease

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24
Q

How is a shock index calculated?

A

Doppler BP/Heart rate

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25
Q

What does a shock index tell us?

A

> 1.0 in dogs and >1.6 in cats indicates possible presence of shock

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26
Q

When might a shock index be useful?

A

In patients with early compensatory shock where vital signs and systemic perfusion are not significantly abnormal

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27
Q

What is blood lactate?

A

A byproduct of anaerobic metabolism that occurs under conditions of hypoxia

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28
Q

What does blood lactate indicate?

A

> 2.5 mmol/L can indicate systemic hypo-perfusion, but conditions such as sepsis may lead to elevated lactate as well

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29
Q

What should the primary neurologic survey include?

A

Evaluation of mentation, brainstem reflexes (pupil size, PLR, nystagmus), motor ability, MGCS in critically ill patients with neuro disease allows for comparison over time

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30
Q

Why may seizures develop in patients with known/suspected intracranial disease?

A

Traumatic brain injury, meningoencephlitis, neoplasia

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31
Q

In critically ill patients without primary intracranial disease, why might seizures develop?

A

Rapid decreases in BG which causes cerebral edema (diabetic patients),rapid decreases in sodium concentration causing cerebral edema, brain hemorrhage or thrombosis, secondary to hepatic encephalopathy, following congenital portosystemic shunt ligation, secondary to med administration (enrofloxacin or dobutamine)

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32
Q

What are some intracranial and extracranial causes for increased intracranial pressure

A

Intracranial: TBI, neoplasia, inflammatory brain diseases
Extracranial: hepatic encephalopathy
Both should be considered in cases of severely altered mental state

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32
Q

Where has dysequilibrium syndrome been noted?

A

In animals following hemodialysis or relief of urinary tract obstruction due to rapid changes in plasma osmolality that result in cerebral edema and elevations in ICP

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33
Q

What is a cardiovascular sign of increased ICP?

A

Cushings reflex (bradycardia and hypertension)

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34
Q

What can prolonged increased ICP lead to?

A

Ischemia of the brain and herniation through the foramen magnum

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35
Q

What immediate interventions can be taken in animals with an altered mental state?

A

Administration of hyperosmotic agents (hyper NaCl or mannitol), placement on a slant board (head higher, 15-30 degrees) to decrease cerebral blood volume through increased venous drainage. Since seizures could be imminent, POC blood work/BG/electrolyres/ammonia. BP measurement as both hypo/hypertension can alter mental state

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36
Q

Why can hypotension lead to an altered mental state?

A

Severe hypotension = impending cardiac arrest due to cerebral hypoxia

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37
Q

Why can hypertension lead to an altered mental state?

A

Changes to mental state can occur secondary to cerebral hemorrhage, infarction, or edema

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38
Q

What are some signs of acute brain hemorrhage?

A

Decerebrate rigidity (stupor/coma with extended front and pelvic limbs)

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39
Q

What should be done (in addition to the usual interventions) to aid an animal with suspected brain hemorrhage?

A

Tracheal intubation and mechanical ventilation to temporarily lower arterial blood CO2 levels which will result in cerebral vasoconstriction leading to lower ICP (short term management of marked elevations in ICP)

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40
Q

What does the secondary survey consist of?

A

A more thorough assessment of patient history including past medical problems and chart review including medications, more formal physical exam of all body systems (i.e. abdominal palpation for acute abdominal pain, investigation or urine output to assess for oligoanuria or anuria)

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41
Q

How is metabolic acidosis defined?

A

pH <7.34, base deficit <-4 mmol/L in dogs or < -5 mmol/L in cats

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42
Q

What is metabolic acidosis often associated with?

A

Hyperlactatemia due to altered perfusion, DKA, renal failure, renal tubular acidosis, loss of bicarbonate from the GI tract (D+)

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43
Q

What may severe metabolic acidosis (pH <7.2) lead to?

A

Myocardial dysfunction, vasodilation, hypotension, decreased responsiveness to catecholamines

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44
Q

What is metabolic alkalosis?

A

pH >7.45

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45
Q

When do we see metabolic alkalosis?

A

Following furosemide therapy, animals with GI tract obstruction, gastric stasis, regurgitation, secondary to NGT suctioning (loss of chloride)

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46
Q

How cna you correct metabolic alkalosis?

A

Administration of 0.9% NaCl, correction of underlying hypokalemia, administration of prokinetics like metoclopramide

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47
Q

What is the safest rate to decrease blood sodium levels?

A

0.5-1 mEq/hr in animal with chronic hypernatremia

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48
Q

What ECG changes might be seen with hyperkalemia?

A

Tented T waves, bradycardia, widened QRS, atrial stand still

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49
Q

What conditions may cause hypokalemia?

A

DKA, administration of potassium deficient IVF, renal failure, albuterol toxicity, hyperalodsteronism

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50
Q

What indicates a pneumothorax on TFAST?

A

Lack of a glide sign in combination with reduced lung sounds

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51
Q

What indicates interstitial alveolar disease on TFAST?

A

Greater than 3 B- lines in more than one lung field

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52
Q

What indicates CHF or fluid overload on TFAST?

A

Left atrial enlargement with left atrial to aortic diameter of at least 1.5 to 1

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53
Q

What do pale/white mucous membranes suggest?

A

Anemia or a vasoconstrictive response to shock

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54
Q

What do red mucous membranes suggest?

A

Vasodilation, systemic inflammatory states, hyperthermia

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55
Q

What do cyanotic mucous membranes suggest?

A

Severe hypoxemia with normal PCV, cyanosis cannot be clinically evident without adequate hemoglobin levels

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56
Q

What do icteric mucous membranes suggest?

A

increased serum bilirubin levels resulting from hepatic disease, post hepatic disease, or hemolysis

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57
Q

What do brown mucous membranes suggest?

A

Methemoglobinemia

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58
Q

What do cherry red mucous membranes suggest?

A

Carbon monoxide poisoning

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59
Q

What is a normal CRT?

A

1 to 2 seconds

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60
Q

What does a CRT >2 sec mean?

A

poor perfusion due to vasoconstriction

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61
Q

What does a CRT <1 sec mean?

A

Hyperdynamic state (systemic inflammation, distributive shock, distributive shock) and vasodilation

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62
Q

How is venous distention visualized?

A

Patient is placed in lateral, lateral saphenous is visualized, if it seems distended the limb is raised higher than the level of the heart. If it remains distended, could indicate increased central venous pressure

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63
Q

What are some potential causes of increased central venous pressure?

A

Volume overload, pericardial effusions, right sided congestive heart failure

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64
Q

What can venous distention be a sign of?

A

Volume overload, right sided CHF, increased right sided filling pressure

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65
Q

What is pulse pressure?

A

The difference between the systolic and diastolic arterial pressures

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66
Q

What can stertor, wheezes and quiet crackles indicate?

A

fluid overload

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67
Q

When can inspiratory stridor be heard?

A

Laryngeal paralysis

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68
Q

When can expiratory wheezes be heard?

A

Small airway collapse and bronchitis

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69
Q

When can crackles be heard in the lungs?

A

Pneumonia, pulmonary edema, pulmonary hemorrhage and small airway disease

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70
Q

What lung fields does aspiration pneumonia normally affect?

A

Cranioventral lung fields

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71
Q

In what lung fields does pulmonary edema begin with?

A

Perihilar lung fields

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72
Q

When might you hear decreased lung sounds?

A

Pulmonary consolidation, pneumothorax, pleural effusion

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73
Q

Define stupor

A

A mentation level where a patient can be aroused only with painful stimuli

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74
Q

What is stupor a sign of?

A

Severe neurologic or metabolic derangements

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75
Q

What do coma and seizures indicate?

A

Abnormal cerebral electrical activity from either primary neurologic disease or severe metabolic derangements (hepatic encephalopathy)

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76
Q

What is third space fluid loss?

A

Fluid collection within a body cavity that does not contribute to circulation

77
Q

What is Kirby’s rule of 20?

A

A list of 20 parameters to monitor for septic small animal patients; provides an initial approach to monitoring most critically ill animals

78
Q

List Kirby’s rule of 20

A
  1. Fluid balance
  2. Oncotic pull
  3. Glucose
  4. Electrolyte and acid-base balance
  5. Oxygenation and ventilation
  6. Mentation
  7. Perfusion and blood pressure
  8. Heart rate, rhythm and contractility
  9. Albumin levels
  10. Coagulation
  11. RBC and hemoglobin concentration
  12. Renal function
  13. Immune status, antibiotic dose and selection, WBC count
  14. GI motility and mucosal integrity
  15. Drug dosage and metabolism
  16. Nutrition
  17. Pain control
  18. Nursing care and patient mobilization
  19. Wound care and bandage change
  20. TLC
79
Q

What is colloid osmotic pressure?

A

The osmotic pressure exerted by large molecules, serves to hold fluid within the vascular space

80
Q

What is a normal urine output?

A

1-2 mLkg/hr

81
Q

Define shock

A

A severe imbalance between oxygen supply and demand, leading to inadequate cellular production, cellular death, and multiorgan failure

82
Q

What are the 4 major mechanisms that can lead to reduction in delivery of oxygen?

A
  1. Loss of intravascular volume (hypovolemic shock)
  2. Maldistribution of vascular volume (distributive shock)
  3. Obstruction to diastolic filling (obstructive shock)
  4. Failure of the cardiac pump (cardiogenic shock)
83
Q

What are DAMPS? What do they do?

A

-Damage associated molecular patterns
-Consist of mitochondrial DNA, histones, heat shock proteins, and other mediators
-Released in response to damaged or dying cells
-Activate the innate immune system by interacting with pattern recognition receptors and triggering a pathologic systemic inflammatory response

84
Q

Describe hypovolemic shock

A

Occurs secondary to a loss of intravascular fluid volume causing inadequate organ perfusion. Insufficient oxygen delivery causes a shift from aerobic to anaerobic metabolism with accumulation of lactate, hydrogen ions, and oxygen free radicals

85
Q

What do baroreceptors do?

A

-Function to keep arterial blood pressure constant by communicating with the brain via the glossopharyngeal nerve and vagus nerve to the nucleus of the solitary tract in the brain stem
-decrease in impulse firing to the medulla oblongata in response to low pressure or stretch in the carotid sinuses or aortic arch disinhibits sympathetic activation while inhibiting parasympathetic activation

86
Q

Where are peripheral chemoreceptors located? What happens when they are stimulated?

A

-Located in the aortic and carotid bodies, respond to changes in CO2, hydrogen ions (decreased pH), paO2
-stimulation causes vasoconstriction and increased minute ventilation
-central chemoreceptors in the respiratory center of the medulla oblongata sense an increase in CO2 or decrease in pH in the cerebrospinal fluid and cause an increase in RR and tidal volume

87
Q

What is the purpose of the body releasing catecholamines and beta endorphins in response to severe hypotension?

A

Reduces pain perception

88
Q

What are the subclassifications of hypovolemic shock?

A
  1. hemorrhagic shock
  2. traumatic hemorrhagic shock
  3. hypovolemic shock without hemorrhage
  4. traumatic non-hemorrhagic shock
89
Q

What is distributive shock?

A

State of relative hypovolemia due to the pathologic redistribution of fluid caused by changes in vascular tone or increased vascular permeability

89
Q

What is the difference between hemorrhagic shock and traumatic hemorrhagic shock?

A

Both have acute drop in circulating RBCs causing tissue hypoxia; Traumatic hemorrhagic shock is further complicated by the inflammatory response that accompanies severe tissue injury resulting in worsened microvascular dysfunction, endothelial injury, and vasomotor tone derangements

89
Q

What are the subcategories of distributive shock?

A
  1. Septic
  2. Anaphylactic
  3. Neurologic
90
Q

Define sepsis

A

Life-threatening organ dysfunction in response to infection and persistent hypotension requiring vasopressor therapy indicates septic shock

91
Q

What does cytokine mediated endothelial damage cause?

A

Increased endothelial permeability and vasodilation which then causes a relative decrease in vascular filling and a shift from the intravascular to the interstitial space

92
Q

Why does vasodilation from neurogenic shock occur?

A

Traumatic brain injury or spinal cord injury
Results from abnormally low sympathetic tone and unopposed parasympathetic stimulation of vascular smooth muscle

93
Q

Define cardiovascular shock

A

-Characterized by systolic or diastolic cardiac dysfunction resulting in hemodynamic abnormalities that include increased heart rate, decreased stroke volume, decreased cardiac output, decreased BP, increased peripheral vascular resistance, increased right atrial/pulmonary arterial/pulmonary capillary wedge pressures
-These changes result in diminished tissue perfusion and increased pulmonary venous pressures, causing pulmonary edema and increased RE

94
Q

Define obstructive shock

A

Compression of the heart or a great vessel compromises venous return and cardiac preload (e.g. GDV)

95
Q

What is the shock organ in dogs?

A

The gastrointestinal system so shock will lead to ileus, diarrhea, hematochezie, and melena

96
Q

What is the shock organ in cats?

A

The lungs so shock will results in respiratory dysfunction

97
Q

What is a normal CVP?

A

0 to 6 mmHg

98
Q

What is a normal urine production?

A

At least 1 mL/kg/hr

99
Q

What is a normal lactate?

A

<2.5 mmol/hr (higher in neonates and pediatrics)

100
Q

Define hypoxia

A

A decrease in the level of oxygen supply to the tissues

101
Q

Define hypoxemia

A

Inadequate oxygenation of arterial blood
PaO2 less than 80 mmHg

102
Q

What is oxygen delivery to the tissues dependent on?

A

Cardiac output and the oxygen content of arterial blood (increase in CO can prevent tissue hypoxia)

103
Q

Why might hypoxemia occur?

A

REsult of hypoventilation, ventilation-perfusion mismatch, diffusion impairment, decrease oxygen content of inspired air, intrapulmonary shunt

104
Q

What FiO2 will 2-3 L/min of flow by O2 deliver?

A

25 - 40%

105
Q

Where is the measurement taken when placing a nasopharyngeal oxygen line?

A

The ramus of the mandible
When placing, nostril is pushed medially and the nose is pushed dorsally

106
Q

What are two complications of hyperbaric oxygen delivery?

A

Ruptured tympanum and pneumothorax

107
Q

When is hyperbaric oxygen delivery recommended?

A

Severe soft tissue lesions (burns), shearing ijuries, infections, osteomyelitis

108
Q

What is the benefit of hyperbaric oxygen delivery?

A

Administers 100% oxygen under supraatmospheric pressures (>760 mmHg) to increase the percent of dissolved oxygen by 10-20%
Oxygen can readily diffuse into tissues that may not have adequate circulation

109
Q

What are two complications of oxygen therapy?

A

“Blue bloater” syndrome and oxygen toxicity

110
Q

Describe “blue bloater” syndrome

A

In patients with chronic respiratory disease and hypercapnia, hypercapnic respiratory drive can be diminished/lost so the patient becomes largely dependent on hypoxia as a respiratory stimulant. The administration of supplemental oxygen to a chronically hypercapnic patient depresses the hypoxic respiratory drive and can leave to resp failure/severe hypoventilation

111
Q

What is oxygen toxicity?

A

O2 therapy can be directly toxic to pulmonary endothelium at prolonged exposure
FiO2 over 50% for more than 24-72 hours is not recommended

112
Q

What is the shock bolus rate for a dog?

A

80-90 mL/kg/hr

113
Q

What is the shock bolus rate for a cat?

A

50-60 mL/kg/hr

114
Q

What is the ROSE principle?

A

Describes the four phases of fluid administration
1. Resuscitation
2. Optimization
3. Stabilization
4. Evacuation

115
Q

What is the Eisenhower matrix of volume assessment?

A

Shows the application of different methods of volume assessment and fluid responsiveness, with some other factors in consideration

116
Q

How are wet lungs characterized?

A

The appearance of >3 B-lines

117
Q

What is a halo sign?

A

Gallbladder wall edema
commonly associated with anaphylaxis
can suggest hypervolemia

118
Q

What are clinical signs of hypovolemia on cardiac POCUS?

A

Smaller left ventricular and left atrial lumen sizes, thicker left ventricular walls

119
Q

What are isotonic crystalloids?

A

Fluids that have a composition similar to that of extracellular fluid
Principle component is NaCl

120
Q

What is hemorrhagic shock?

A

Impairment of oxygen delivery as a result of whole blood loss

121
Q

What is the lethal triad in hemorrhagic shock?

A

Hemorrhagic shock can rapidly result in coagulopathy, acidosis, and hypothermia which increase morbidity and mortality rates in humans. Each of these things perpetuates one another or further bleeding

122
Q

What is acute coagulopathy of of trauma shock?

A

A phenomenon where coagulopathy may be more pronounced in patients with major trauma due to direct anticoagulant and profibrinolytic and consumptive processes

123
Q

In severe hemorrhage, what is the risk with administering just pRBC?

A

Dilutional coagulopathy, hypofibrinogenemia, amd thrombocytopenia
Recommended to administer plasma and platelet products concurrently

124
Q

What can hypocalcemia result in?

A

Impaired coagulation, decrease in myocardial contractility and vascular tone

125
Q

What is hypotensive resuscitation?

A

Fluid resuscitation to a BP target that is subnormal btu sufficient to support major organ function, such as SBP of 90 mmHg or MAP or 60 mmHg to avoid disturbing fragile clots

126
Q

Define sepsis

A

A Life-threatening organ dysfunction caused by a dysregulated host response to infection

127
Q

Define septic shock

A

A subset of sepsis in which underlying circulatory and cellular/metabolic abnormalities are profound enough to substantially increase mortality

128
Q

How can you identify septic shock?

A

A patient with clinical construct of sepsis that experiences persistent hypotension requiring vasopressors to maintain a <AP of 65 mmHg and a lactate >2 mmol/L (18 mg/dL)

129
Q

How does the innate immune system perceive pathogens?

A

Recognizing pathogen-associated molecular patterns (PAMPs) that bind a host through pattern recognition receptors (PRRs)

130
Q

What is released from tissue during an infection or noninfectious injury?

A

Damage associated molecular patterns (DAMPs)/alarmins which are recognized and cause further activation of pattern recognition receptors

131
Q

What pathways are included along the afferent arm of the inflammatory response?

A

Afferent neuronal pathways
Cytokine transit across the blood-brain-barrier to influence the pituitary gland output
Cytokine production by the cells of the CNS

132
Q

How does the efferent arm of the inflammatory response effect immune modulation?

A

Affects immune modulation via the splenic nerve via the vagus nerve and coeliac plexus, resulting in norepinephrine and dopamine release that may enhance or suppress cytokine release depending on the receptors that are activated

133
Q

What mechanisms in sepsis cause a procoagulant state in sepsis?

A

Increase tissue factor-mediated thrombin production
Impaired fibrinolysis
Dysfunctional endogenous anticoagulant mechanisms

134
Q

What initiates the coagulation cascade?

A

Tissue factors binding to factor VIIa

135
Q

In sepsis, what factors are downregulated causing inhibition of natural anticoagulant and fibrinolytic processes?

A

Antithrombin, tissue factor pathway inhibitor (TFPI), tissue plasminogen activator (tPA), increased plasminogen activator inhibitor (PAI-1)

136
Q

What barriers are affected in sepsis?

A

Barrier between intravascular and interstitial compartments; endothelial and epithelial cells throughout the body; mitochondrial membranes

137
Q

What is cryptic shock?

A

Serious microcirculatory disturbances can occur prior to changes in macrohemodynamic variables like blood pressure – characteristic of septic patients

138
Q

What are the most common hematologic and chemistry abnormalities noted with sepsis in small animals?

A

Leukocytosis
Leukopenia
Increased % of bands
Toxic neutrophils
Thrombocytopenia
Coagulation abnormalities
Low albumin
High bilirubin
Ionized hypocalcemia
Metabolic acidosis secondary to poor tissue perfusion
Cats: anemic, metarubricytes
Dogs: elevated PCV caused by hemoconcentration secondary to volume depletion and/or splenic contraction

139
Q

What is a bundle of care?

A

A group of therapies that together result in better outcomes than if given alone

140
Q

What are some key strategies for treatment of a septic patient?

A

Judicious fluid resuscitation
Source control and acquisition of samples for C&S
Early empiric antimicrobial therapy
Vasopressor and/or inotropic therapy
Physiologic corticosteroid supplementation
Diligent vitals monitoring

141
Q

What are some common causes of sepsis in both cats and dogs?

A

Urosepsis
Bite wounds
Septic peritonitis
Pneumonia
Pleural space disease

142
Q

One negative side effect of vasopressors is that they can cause excessive vasoconstriction. Where is this of particular concern?

A

The splanchnic and renal circulation; results in GI and renal ischemia

143
Q

What is primary hypothermia?

A

Subnormal temperature caused by excessive exposure to low environmental temperatures

144
Q

What is secondary hypothermia?

A

A result of disease, trauma, surgery, drug induced ateration in heat production and thermoregulation

145
Q

What indicates mild hypothermia?

A

Thermoregulatory mechanisms like shivering and heat seeking behaviour are intact; there may be ataxia
32-37C

146
Q

What indicates moderate hypothermia?

A

Progressive loss of thermoregulatory system, with decreasing levels of consciousness and initial cardiovascular instability
28-32C

147
Q

What indicates severe hypothermia?

A

Complete loss of thermoregulatory system, inability to shiver, comatose states, susceptibility to ventricular fibrillation
20-28C
<20 is profound/critical

148
Q

What part of the brain is the primary thermostat of the body?

A

The hypothalamus
The preoptic region of the anterior hypothalamus contains primary temperature sensing neurons that allow immediate systemic responses to be directed to the body (the skin)
The posterior hypothalamus combines that input with additional core and peripheral temperature sensing receptor input to provide an integrate response (these are located in the spinal cord, abdominal viscera, surround great veins in abdomen and thorax)

149
Q

What are the four primary mechanisms of heat loss?

A
  1. Convection – transfer of heat from body surface to surrounding air
  2. Conduction - heat transfer from bod surface to object in contact with body
  3. Radiation- heat transfer by loss to surrounding structures that are not in direct contact with body
  4. Evaporative – heat transfer by loss of heat from moisture on the body surface or through respiratory tract to the environment

Usually about 70% lost via radiation and convection

150
Q

What is the primary effect of hypothermia on acid base status?

A

Acidemia – mixed5

151
Q

How does hypothermia affect coagulation?

A

Primary hemostasis
1. Sequestration of platelets by the liver and spleen
2. Decreased platelet aggregation secondary to decreased thromboxane B2 production
3. Decreased platelet granule secretion
4. attenuation of P selectin expression
5. Diminished expression of von Willebrand factor receptor
Secondary hemostasis
1. Prolonged pt/aptt

note: results for pt/ptt may appear normal because the machine warms the sample

152
Q

How much does HCT decrease per 1 degree decrease in body temp?

A

2%

153
Q

What is the initial renal affect of hypothermia?

A

In mild to moderate hypothermia, diuresis (called cold diuresis) which can result in hypovolemia and hypotension

154
Q

Describe the mechanism of cold diuresis

A
  1. Cold causes an initial vasoconstriction which is sensed as increase blood volume
  2. As CBT drops, there is a decrease in responsiveness to vasopressin at the distal tubule – inability to reabsorb water and loss of electrolytes
  3. in moderate hypotherm, GFR decreases secondary to decrease in cardiac output and renal blood flow - -causes reduction in renal clearance of glucose and H+ (hyperglycemia and acidosis)
155
Q

Why do we see hyperglycemia in hypothermia?

A
  1. REnal changes
  2. Catecholamine-induced gluconeogenesis
  3. Decreased insulin sensitivity and reduced insulin secretion from pancreatic islet cells
    will need more insulin than usual to correct
156
Q

What are the hepatic consequences of hypothermia?

A

Reduced drug clearance (fentanyl, pentobarbital, morphine, midazolam, phenobarbital, propofol, volatile anesthetics – all either increase potency or decrease clearance)

157
Q

What are the best ways to measure core body temperature?

A

Pulmonary artery and thoracic esophageal temperature

158
Q

What are the complications of active external rewarming?

A
  1. Surface rewarming causes peripheral vasodilation which can lead to hypovolemia and hypotension (rewarming shock)
  2. Core temperature afterdrop – cold peripheral blood is recirculated back to vital organs where CBT drops more, then colder blood and lactic acid are carried to the core causing rewarming acidosis
  3. AER can reduce shivering (but benefit outweighs risk)
159
Q

What is the maximum safe inhalation temperature?

A

45C

160
Q

How would you perform peritoneal lavage in active core rewarming?

A

Heated LRS or normal saline to 40-45 C via peritoneal catheter at 10-20 mL/kg. Dwell time of 20-30 minutes then aspirate fluid and repeat procedure

*Cons: invasive, can complicate ongoing coagulopathies, can cause electrolyte shifts

161
Q

What is the minimum necessary temperature for defibrillation?

A

28C

162
Q

What is anaphylaxis?

A

A severe, systemic, potentially fatal type I hypersensitivity reaction that may occur secondary to a variety of antigens

163
Q

What are the former and present classifications of anaphylaxis?

A

Former: anaphylactic - immunoglobulin-E (IgE) mediated versus anaphylactoid – non IgE mediated

Present: immune mediated (stings, bites, food, transfusions) and non-immune mediated (physical factors like exercise and extreme temperatures)

164
Q

What is the primary mediator in anaphylaxis?

A

Histamine

165
Q

What effect does histamine have in the lungs?

A

Smooth muscle contraction, bronchospasm, mucous secretion and edema formation

166
Q

What do the mediators of anaphylaxis lead to?

A

Smooth muscle contraction, increased vascular permeability, vasodilation

167
Q

What systems do the mediators of anaphylaxis affect?

A

Cutaneous
GI
Cardiovascular

168
Q

What are the main systems affected by anaphylaxis in dogs?

A

GI and portal circulation

169
Q

What are the main systems affected by anaphylaxis in cats?

A

Respiratory and GI

170
Q

Describe the GI consequences of anaphylaxis in dogs

A

Histamine alters circulatory flow to and from the liver which results in arterial vasodilation and venous congestion –> portal hypertension, transudation of fluid, decreased volume return to heart
Labs will show increased ALT, AUS will show hepatic venous congestion, free fluid (transudate or blood), gallbladder wall thickening (halo sign)

171
Q

What is biphasic anaphylaxis?

A

A patient may show signs of improvement and then relapse. Most commonly as cutaneous or respiratory signs hours to days later

172
Q

What conditions may have overlapping symptoms with anaphylaxis?

A

Sepsis
Heat stroke
Disseminated mast cell disease
Pericardial effusion with tamponade
Acute hemoabdomen
Sago palm ingestion

173
Q

Define hypotension

A

A SBP of less than 90 mmHg or a MAP of less than 60 mmHg

174
Q

What causes hypotension?

A

Decreased cardiac output secondary to reduced circulating volume
Myocardial failure
Severe bradyarrhythmia
Decreased systemic vascular resistance due to peripheral vasodilation secondary to sepsis/SIRS/anaphylaxis

175
Q

What are the two types of hypertension?

A

Primary (essential) – rare in small animals
Secondary – due to renal or hormonal disease

176
Q

True or False: Blood pressure varies slightly with variation

A

True; systolic pressure variation is the difference between maximum systolic pressure on inspiration and minimum systolic pressure on expiration

177
Q

What is systolic pressure variation?

A

the difference between maximum systolic pressure on inspiration and minimum systolic pressure on expiration

178
Q

What does a systolic pressure variation greater than 10 mmHg mean?

A

Hypotension

179
Q

How is pulse pressure variation calculated?

A

Dividing the difference between PP(max) and PP(min) over a single breath
PP(max) is the difference between systole and diastole that is greatest during that breath
PP(min) is the smallest difference
PPV greater than 13% indicates hypotension

180
Q

What does a pulse pressure variation >10% indicate?

A

Positive response to fluid therapy

181
Q

What is central venous pressure?

A

The hydrostatic pressure in the intrathoracic vena; it is approximately equal to right atrial pressure

182
Q

Does catheter size affect central venous pressure?

A

No

183
Q

How does tissue hypoxia affect mixed venous and central venous oxygen?

A

Tissue hypoxia causes and increased extraction of oxygen from venous blood which decreases both SvO2 and ScvO2

184
Q

What is cardiac output?

A

The volume per minute of blood delivered from the heart to systemic circulation. It is determined by heart rate and stroke volume which in turn is determined by preload, afterload, and contractility

185
Q

What is preload?

A

The stretching of the ventricle prior to contraction; largely a function of venous return

186
Q

What is afterload?

A

The force needed to achieve ventricular outflow; the amount of work the heart must do in order to move blood forward during systolic ejection

187
Q

What is contractility?

A

The ability of cardiac muscle fibers to develop tension at a given preload and afterload

188
Q

What is Fick oxygen consumption?

A

The first method described for assessing cardiac output; gold standard. Based on the notion that tissue oxygen consumption will be dictated by a product of cardiac output and the difference between arterial and venous oxygen content

189
Q
A

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