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VTS Studying > Norkus Text > Flashcards

Norkus Text Flashcards

1
Q

When will you see pale/grey/muddy/white mucous membranes?

A

Poor peripheral perfusion (vasoconstriction from shock or anemia)

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2
Q

When will you see red mucous membranes?

A

Carbon monoxide toxicity or states of vasodilation (sepsis, fever, anaphylaxis)

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3
Q

When will you see yellow mucous membranes?

A

Hyperbilirubinemia; may suggest hemolysis, bile duct obstruction, liver disease, feline sepsis

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4
Q

When will you see blue/purple mucous membranes?

A

Hypoxemia

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5
Q

When will you see brown mucous membranes?

A

Methemoglobinemia (i.e. acetaminophen toxicity)

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6
Q

When can you see CRT >2 sec?

A

During states of poor perfusion

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7
Q

When can you see CRT <2 sec?

A

Vasodilation (i.e. fever, sepsis, anaphylaxis)

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8
Q

Define lethargic

A

A patient who is mildly depressed with slightly decreased interaction with environment but patient is easily aroused

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9
Q

Define obtunded

A

Moderate to severely depressed demeanor and interaction with environment; patient is aroused with some difficulty

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10
Q

Define Stuporous

A

Patient responds only to vigorous or painful stimulus

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11
Q

Define comatose

A

Patient does not respond to any stimuli

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12
Q

What is the process by which ATP is produced (under normal conditions)?

A

Oxidative phosphorylation (of ADP)

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13
Q

Define cardiac output

A

The volume of blood pumped by the heart each minute

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14
Q

Define stroke volume

A

The volume of blood pumped by the heart each beat

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15
Q

What is critical oxygen delivery?

A

In the presence of marked decrease in oxygen delivery to tissue, the body is unable to maintain constant oxygen consumption and will therefore decrease consumption in proportion to delivery of oxygen

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16
Q

What happens below the critical oxygen delivery value?

A

The body undergoes anaerobic metabolism which results in increased formation of lactic acid

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17
Q

What are the 5 types of hypoxia?

A
  1. Hypoxemic hypoxia
  2. Hypemic hypoxia
  3. Stagnant hypoxia
  4. Histiotoxic hypoxia
  5. Metabolic hypoxia
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18
Q

What is hypoxemic hypoxia?

A

When inadequate oxygen delivery results from inadequate oxygen carrying capacity of blood secondary to hypoxemia from decreased PaO2 and SaO2

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19
Q

What is hypemic hypoxia?

A

Also called anemic hypoxia. Anemia causess a decrease in circulating Hb thus reducing CaO2 and DO2

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20
Q

What category of hypoxia does methemoglobinemia and carbon monoxide toxicity count as?

A

Hypemic hypoxia because although there is an adequate amount of Hb available, it is dysfunctional and unable to transport oxygen (hemoglobinopathy)

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21
Q

What is stagnant hypoxia

A

Circulatory hypoxia. Caused by low CO and low blood flow. Low DO2 because of low CO

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22
Q

What is stagnant hypoxia clinically referred to as?

A

Circulatory shock

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23
Q

What is histiotoxic hypoxia?

A

When there is adequate DO2 but the tissues are unable to extract and utilize the O2 appropriately (i.e. cyanide poisoning, carbon monoxide poisoning or mitochondrial dysfunction of sepsis)

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24
Q

What is metabolic hypoxia?

A

Increased oxygen consumption (i.e. in sepsis)

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25
Q

Define hypoxia

A

Inadequate oxygen delivery to meet tissue metabolic demand caused by inadequate tissue perfusion, metabolic disturbance, or lack of O2 supply

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26
Q

Define shock

A

A state of decreased CO leading to decreased perfusion and inadequate delivery of oxygen to tissue

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27
Q

What are the 4 classes of shock?

A
  1. Hypovolemic
  2. Obstructive
  3. Distributive
  4. Cardiogenic
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28
Q

Define hypovolemic shock

A

Most common form. Decreased intravascular volume from blood or fluid loss (V+/D+/third spacing). Inadequate circulating volume therefore decreased cardiac preload leading to decreased CO

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29
Q

Define obstructive shock

A

physical obstruction in the circulatory system (i.e. heartworm, pericardial effusion, gastric torsion). Decreased cardiac preload

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30
Q

Define distributive shock

A

Initiating cause such as sepsis, anaphylaxis and SIRS. Normal blood volume is present but so is vasodilation

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31
Q

Define cardiogenic shock

A

Results from the inability to eject blood and achieve normal cardiac output (i.e. heart failure). Decreased cardiac contractility, increased afterload, and increased preload

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32
Q

What activates the renin-angiotensin-aldosterone-system (RAAS)?

A

Decreased renal blood flow

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33
Q

What is the end result of RAAS?

A

Systemic vasoconstriction; water and sodium retention, which helps increase plasma volume/replace intravascular volume. Improve SV/CO/DO2

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34
Q

Where is renin released from?

A

juxtaglomerular cells in the kidney

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35
Q

What hormone initially activates RAAS?

A

Renin

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36
Q

What is the role of renin?

A

To cleave a peptide from the protein angiotensinogen (produced by the liver) which creates angiotensin 1

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37
Q

Where is angiotensinogen produced?

A

The liver

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38
Q

What converts angiotensin 1 to angiotensin 2?

A

ACE (angiotensin converting enzyme)

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39
Q

Where is angiotensin-converting enzyme produced?

A

Epithelial cells throughout the body

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40
Q

What does angiotensin 2 do?

A

vasoconstrictor; stimulates the secretion of adrenocorticotropic hormone (ACTH), aldosterone, and antidiuretic hormone (ADH)

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41
Q

What does adrenocorticotropic hormone (ACTH)?

A

Stimulates the adrenal cortex to release cortisol

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42
Q

What does cortisol do?

A

Works with epinephrine and glucagon to induce a catabolic state which allows the body to break down reserves for immediate energy needs, stimulates gluconeogenesis, and the generation of glucose from non-carbs (i.e. lactate), creates insulin resistance, and retains sodium and water through the kidneys

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43
Q

What is the body’s main mineralcorticoid hormone and where is it produced?

A

Aldosterone; in the zona glomerulosa of the adrenal cortex of the adrenal gland

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44
Q

What does aldosterone do?

A

Vasconstriction; Conservation of sodium in kidney (more water retentino), potassium excretion from kidney

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45
Q

What does antidiuretic hormone (ADH/vasopressin) do?

A

Vasoconstrictor; Increases water permeability within the kidney by insertion of aquaporin 2 channels within the cortical collecting duct of the kidney (decreases water losses)

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46
Q

What are the 3 stages of hypovolemic shock?

A

Compensatory, early decompensatory, late decompensatory

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47
Q

What is compensatory shock?

A

The bodies response to the initial injury; body tries to preserve vital organs by constricting the peripheral blood vessels (and the spleen)

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48
Q

What are the signs of compensatory shock?

A

PCV can be normal to high; cold extremities; tachycardia; injected mm with rapid CRT; bounding pulses; BP can be normal to slightly elevated

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49
Q

Do cats display compensatory shock?

A

No

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50
Q

What is early decompensatory shock?

A

The bodies response after moderate decreases in intravascular volume; the body’s reserves are being depleted and cytokines from hypoxic tissues are more pronounced

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51
Q

What are clinical signs of early decompensatory shock?

A

Tachycardia; weak pulses; hypotension; pale mm with prolonged CRT; hypothermia; cool extremities; increased RR/RE; decreased mentation

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52
Q

What treatment is important during early decompensatory shock?

A

Aggressive fluid resuscitation

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53
Q

What is late decompensatory shock?

A

Final and terminal stage of shock, brought on by prolonged and severe tissue hypoxia causing ATP depletion, anaerobic metabolism, and cell death

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54
Q

What are the clinical signs of late decompensatory shock?

A

Bradycardia; severe unresponsive hypotension; pale or cyanotic mm; undetectable CRT; weak or absent pulses; hypothermia; decreased or comatose mentation; cardiac arrest

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55
Q

Define hypoxemia

A

A low concentration of dissolved oxygen in the blood (i.e. an arterial partial pressure of oxygen below 80 mmHg)

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56
Q

What are the 5 causes of hypoxemia?

A
  1. Decreased inspired partial pressure of oxygen (PiO2)
  2. Hypoventilation
  3. Ventilation/perfusion (V/Q) mismatch
  4. Diffusion impairment (rare)
  5. Anatomical shunting
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57
Q

What is the fraction of inspired oxygen (FIO2) in room air?

A

21%

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58
Q

What are the oxygen flow rates for a patient with a standard nasal cannulae?

A

50-150 mL/kg/min

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59
Q

What can happen if you exceed the standard flow rates for patients with nasal cannulae?

A

Gastric distension, drying of mucous membranes, patient discomfort

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60
Q

What is the maximum flow rate of oxygen for a patient on intratracheal oxygen?

A

0.5 L/min

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61
Q

What are the consequences of exceeded the maximum oxygen flow rate for a patient on intratracheal oxygen?

A

the tube can oscillate and irritate the trachea; or over distension of the lungs

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62
Q

What is the FiO2 range for flow by oxygen?

A

30%-60%

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63
Q

What is the FiO2 maximum for high flow?

A

Almost 100%

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64
Q

What is rapid sequence intubation (RSI)?

A

Quickly inducing general anesthesia to facilitate intubation (i.e. using alfax or propofol). Can be used in cases where a resp distress patient has failed to respond to initial tranquilization with butorphanol

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65
Q

How many forms of lactate are there and what are they?

A

2; L- and D-lactate

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66
Q

Which stereoisomeric form of lactate does an in house plasma lactate measuring device measure?

A

Both L- and D-lactate

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67
Q

Which stereoisomeric form of lactate is more predominant and functioning?

A

L-lactate

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68
Q

Where is lactate produced?

A

Skeletal muscle, brain and adipose tissue, and circulating blood cells

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69
Q

Where is lactate metabolized?

A

Liver, kidney, myocardium

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70
Q

When will plasma lactate increase?

A

When its production by hypoxic tissues overwhelms its elimination by the liver

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71
Q

What is the normal range for plasma lactate in dogs and cats?

A

2.5 mmol/L in dogs and 2.5 mmol/L up to potentially 5 mmol/L in cats

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72
Q

What are the classes of hyperlactatemia?

A

Type A and type B

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73
Q

What is type A hyperlactatemia?

A

States of hypoxia and anaerobic metabolism (hypoperfusion, anemia, severe hypoxia, CO toxicity, seizures/tremors, patient struggling or exercise)

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74
Q

What is type B hyperlactatemia?

A

Results from systemic disease, drugs or toxins, or inborn congenital disease of lactate metabolism (type B1, B2, and B3 respectively)

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75
Q

What are examples of type B1 hyperlactatemia?

A

Systemic diseases like diabetes mellitus, neoplasia, hepatic failure, and sepsis/SIRS

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76
Q

What are examples of type B2 hyperlactatemia?

A

Drug or toxin exposure like corticosteroids, glucose, xylitol, endogenous or exogenous catecholamines like epinephrine, lactulose, and ACE-inhibitors

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77
Q

What are examples of type B3 hyperlactatemia?

A

Inborn congenital disease of lactate metabolism. Uncommon but have been seen in GSD, JRT, Old english sheepdogs, and spaniels

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78
Q

What is the shock index?

A

A bedside assessment of evaluating severyity of hypovolemic shock

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79
Q

Solutions of greater than how many milliosmoles should only be given through a central venous catheter?

A

> 600 mOsm

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80
Q

What is Virchow’s triad?

A

Proposes that all causes of thrombosis occur due to the presence of one or more of the following three factors:
1. endothelial damage
2. Blood stasis/turbulent blood flow
3. Hypercoagulability

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81
Q

What is another name for systemic vascular resistance?

A

Total peripheral resistance

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82
Q

What is arterial blood pressure?

A

The product of CO and SVR

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83
Q

What causes the doppler shift?

A

The re-entry of blood into the artery following deflation of the blood pressure cuff

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84
Q

What is the Beer-Lambert law?

A

Associates the intensity of light transmitted through a solution to the solution’s concentration. It is the principle that pulse oximetry works on.

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85
Q

What is SpO2?

A

The amount of light absorbed at both red and infrared wavelengths . This absorbance is expressed as a percentage of oxygenated hemoglobin to total hemoglobin

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86
Q

What is coronary perfusion pressure (CPP)?

A

The pressure gradient that drives coronary blood flow. It is the difference between diastolic aortic pressure (DAP) and right atrial diastolic pressure (RADP). An important variable associated with the likelihood of ROSC

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87
Q

What is the minimum presumed CPP for ROSC to occur?

A

15 mmHg

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88
Q

What are the 3 phases of CPR?

A
  1. Basic life support (BLS) = chest compressions
  2. Advanced life support (ALS) = meds, IV access, monitoring, defibrillation
  3. Postresuscitative care
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89
Q

What is the ideal compression depth during CPR?

A

1/3 to 1/2 the width of the chest

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90
Q

What is the cardiac pump theory in CPR?

A

Blood flow during compressions occurs due to physical compression of the ventricles which is only possible in patients under 7 kg

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91
Q

What is the thoracic pump theory?

A

In patients over 7 kg, compressions should be performed distal to the heart (where the chest is widest). The movement of blood occurs due to increased intra-thoracic pressure

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92
Q

What are interposed abdominal compressions (IAC)?

A

Compressions done over the liver by a second rescuer alternating with chest compressions to move blood out of the abdominal cavity. The rate should be 70-90 bpm

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93
Q

What is the purpose of an impedance threshold device (ITD)?

A

portable, non-invasive units that are place on the end of the ET tube. Decrease intrathoracic pressure during inspiration which allows for venous return and improved CO on the next compression

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94
Q

Why is the use of doxapram no longer recommended in CPR?

A

It increases the myocardial and cerebral oxygen demand and reduces cerebral perfusion which leads to worse neurological outcomes

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95
Q

Define Myocardium

A

The musculature and conducting system of the heart collectively

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96
Q

Where do the left ventricle and atrium receive blood from?

A

The lungs

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97
Q

Where do the right ventricle and atrium receive blood from?

A

All parts of the body (via venous circulation, including the heart)

98
Q

Where does blood go from the left side of the heart?

A

Pumps it through arterial circulation to all parts of the body

99
Q

Where does blood go from the right side of the heart?

A

Towards lungs for oxygen uptake

100
Q

What is the mediastinum?

A

A partition between the two pleural spaces (the heart is part of this)

101
Q

What ribs does the heart sit between (approximately)?

A

The third to the caudal of the sixth

102
Q

How much fluids is normally in the pericardium?

A

<1 mL of clear, light yellow fluid

103
Q

What is the purpose of the AV (atrioventricular) valves?

A

The intake valves to the ventricles; prevent blood from returning to the atria during the systolic phase of contraction

104
Q

What attaches and anchors the AV valves?

A

Chordae tendineae

105
Q

What is another name for right AV valve?

A

the tricuspid valve

106
Q

What is the function of the right AV valve?

A

Separates the right atrium from the right ventricle

107
Q

What happens with tricuspid valve lesions?

A

Heart murmurs that are heard loudest at the fourth right intercostal space (at the costochondral junction)

108
Q

What is another name for the left AV valve?

A

Mitral valve or bicuspid valve

109
Q

What is the function of the left AV valve?

A

Separates the left atrium from the left ventricle

110
Q

What happens with mitral/bicuspid valve lesions?

A

Heart murmurs that are most audible at the fifth left intercostal space above the middle of the lower 1/3 of the thorax

111
Q

What valve does blood pass through before leave the right ventricle and entering the lungs?

A

The pulmonic valve

112
Q

What happens with lesions of the pulmonic valve?

A

heart murmurs that are best heard at the third intercostal space more ventrally than the point of the shoulder

113
Q

What happens with lesions of the pulmonic valve?

A

heart murmurs that are best heard at the third intercostal space more ventrally than the point of the shoulder

114
Q

What valve does blood pass through before leaving the left ventricle and being pumped into the ascending aorta?

A

The aortic valve

115
Q

Where does blood go after the aortic valve?

A

The ascending aorta

116
Q

What happens with lesions of the aortic valve?

A

Heart murmurs that are loudest at the fourth left intercostal space slightly below the point of the shoulder

117
Q

What type of valves are the aortic and pulmonic valves?

A

Semilunar valves

118
Q

Do the aortic and pulmonic valves have chordae tendineae?

119
Q

What is the cardiac action potential?

A

A rapid change in membrane potential/voltage across the cardiac cell membrane that triggers muscle contraction

120
Q

What is a resting membrane potential?

A

When the cardiac cells of the ventricles are not electrically excited (-90 mV)

121
Q

What are the main ions found outside the cell at rest?

A

Sodium and chloride

122
Q

What is the main ion found inside the cell at rest?

123
Q

What is the threshold potential?

A

The critical level to which a membrane potential must reach to initiate an action potential

124
Q

What is depolarization (Phase 0)?

A

The action potential begins with the voltage becoming suddenly more positive; rapid opening of sodium channels that allows sodium into the cell

125
Q

What is repolarization (Phase 1)?

A

Potassium channels open, allowing potassium to leave the cell and a rapid inactivation of sodium channels causing the membrane potential to return to a negative state

126
Q

What is the plateau phase (Phase 2)?

A

Calcium ions move into the cell causing contraction of the heart (receptors located in the sarcoplasmic reticulum)

127
Q

What is the rapid repolarization phase (Phase 3)?

A

Calcium channels close and further potassium channels open yo create a more negative memnrane potential

128
Q

What happens in diastole to cause a state of rest (Phase 4)?

A

Cardiac cell has returned to it’s resting membrane potential

129
Q

How can hyperkalemia affect the membrane potential?

A

When there is an excessive of potassium in the blood, it will bring the resting membrane potential of a myocyte closer to the threshold potential which can make the cardiac cell more excitable

130
Q

How can intravenous calcium help during hyperkalemia?

A

Calcium will increase the threshold potential away from the resting potential (which has been increase by an excess of potassium) to protect the heart

131
Q

Describe electrical conductance?

A
  1. SA node (in R atrium) initiates the heart’s electrical activity
  2. Pulse spreads down both atria
  3. Atria contract (P wave)
  4. Electrical impulse continues down to the AV bundle (floor of R atrium)
  5. Electrical impulse depolarizing the heart is delayed to allow the atria to finish contracting (space between P and QRS)
  6. Impulse travels to the ventricles via the His-Purkinje system
  7. Ventricle contract
  8. His bundle divides into right and left bundle branches at apex which diverts electrical activity to the ventricles
  9. Depolarization of the ventricles is the QRS complex
  10. Atrial repolarization is hidden by the QRS
  11. Ventricular repolarization is the T wave
132
Q

What is the secondary function of the AV node?

A

Gatekeeper, preventing unwanted atrial impulses (APCs, a-fib) from crossing to and activating the ventricles

133
Q

Describe the cardiac cycle?

A
  1. Begins with blood returning to the R and L atrium from the body and lungs
  2. Blood accumulates in the atria until the atrial pressure increases until it exceeds the pressure in the ventricles
  3. AV valves open and blood passively flows into the ventricles
  4. The leftover atrial blood is pushed into the ventricles by the contraction of the atria (atrial kick, or atrial systole)
  5. Atrial contraction (systole) coincides with depolarization of the sinus node and the P wave
  6. As the ventricles fill and pressure rises, AV valves are displaced upward and ventricle contraction occurs (first part of ventricular contraction is isovolumic/isometric contraction)
  7. once the pressure exceeds that in the aortic and pulmonary arteries, the valves open and ventricular ejection occurs (this is the second part of ventricular contraction called period of rapid ventricular ejection)
  8. Pressure in the ventricles rapidly falls and ventricular diastole begins with closure of the pulmonic and aortic valves
  9. Initial period of ventricular rest/diastole consists of isovolumic/isometric relaxation phase = repolarization of the ventricular myocardium corresponding to the T wave
  10. ventricular pressure decreases until the pressure in the atria is higher and the cycle repeats
134
Q

Define arterial blood pressure

A

The pressure exerted by circulating blood on the walls of the blood vessels

135
Q

What is blood pressure made up of?

A

Systolic and diastolic components

136
Q

What is the systolic component of blood pressure?

A

Created at the end of the cardiac cycle when the ventricles are contracting, represents the peak pressure in the arteries

137
Q

What is the diastolic component of blood pressure?

A

The minimum pressure in the arteries which occurs at the beginning of each cardiac cycle when the ventricles are fully filled with blood

138
Q

What can systemic vascular resistance(SVR) also be called?

A

Total peripheral resistance (TPR)

139
Q

What is systemic vascular resistance?

A

The degree of peripheral resistance, mainly dilation or constriction of systemic blood vessels

140
Q

What is systemic vascular resistance?

A

The degree of peripheral resistance, mainly dilation and constriction of the vessel

141
Q

What is cardiac output?

A

The volume of blood being pumped by the heart each minute

142
Q

What is stroke volume?

A

The volume of blood being pumped by the heart at each pump

143
Q

What is cardiac index?

A

The cardiac output divided by the patient’s body surface area

144
Q

What is hypoxia?

A

Inadequate oxygen delivery to meet tissue metabolic demand caused by inadequate tissue perfusion, metabolic disturbances, or lack of oxygen supply. Can include cellular inability to extract valuable inability to extract available oxygen.

145
Q

What is the oxygen extraction ratio?

A

The ratio of oxygen consumption to oxygen delivery

146
Q

What is the approximate oxygen extraction ratio in dogs?

A

0.3 in most tissues but up to 0.6 in the brain

147
Q

True or False: Under normal conditions, VO2 is independent of VO2

148
Q

What is critical oxygen delivery?

A

The level at which the body is unable to maintain a constant VO2 and thus VO2 decreases in proportion to DO2

149
Q

What happens below critical oxygen delivery?

A

Anaerobic metabolism to ensure adequate energy production. Lactic acid is produced as a by-product

150
Q

What are the 5 types of hypoxia?

A
  1. Hypoxemic hypoxia
  2. Hypemic hypoxia
  3. Stagnant hypoxia
  4. Histiotoxic hypoxia
  5. Metabolic hypoxia
151
Q

What is hypoxemic hypoxia?

A

Occurs when inadequate oxygen delivery results from inadequate oxygen carrying capacity of blood (CaO2) secondary to hypoxemia from decreased partial pressure of oxygen and saturation of hemoglobin within oxygen

152
Q

What is hypemic hypoxia?

A

Also known as anemic hypoxia. Occurs when anemia causes a decrease in the circulating hemoglobin, thus reducing the CaO2, thereby decreasing the delivery of oxygen. Hemoglobinopathy caused by CO2 toxicity and methemoglobinemia occurs when there are adequate amounts of hemoglobin available but the available hemoglobin is dysfunctional and unable to transport oxygen normally

153
Q

What is stagnant hypoxia?

A

Also known as circulatory hypoxia, circulatory shock. Caused by low cardiac output and low blood flow. Low CO results in low DO2

154
Q

What is histiotoxic hypoxia?

A

There is adequate delivery of oxygen but the tissues are unable to extract and utilize it appropriately. Ex is cyanide poisoning and in mitochondrial dysfunction of sepsis

155
Q

What is metabolic hypoxia?

A

Occurs when there is an increased cellular consumption of oxygen (VO2). Transport/delivery/absorption are all appropriate but there is an increased need. Most common example is sepsis

156
Q

Define shock

A

A state of decreased cardiac output leading to decreased perfusion and inadequate delivery of oxygen to tissue

157
Q

What are 4 causes of shock?

A
  1. Hypovolemic shock
  2. Obstructive shock
  3. Distributive shock
  4. Cardiogenic shock
158
Q

Define hypovolemic shock

A

The most common form of shock. The result of decreased intravascular volume from blood loss or from fluid losses (vomiting, diarrhea, third spacing). Inadequate circulating volume causes decreased cardiac preload leading to decreased cardiac output

159
Q

Define obstructive shock

A

Physical obstruction in the circulatory system (heartworm, pericardial effusion, gastric torsion). Circulating volume may be normal but decreased cardiac preload returning to the heart

160
Q

Define distributive shock

A

Initiating cause of sepsis, anaphylaxis, SIRS. Normal circulating volume but systemic vasodilation

161
Q

Cardiogenic shock

A

Heart’s inability to eject blood and achieve normal cardiac output (seen during heart failure). Associated with decrease in cardiac contractility, increased afterload, and increased cardiac preload

162
Q

What is the most common form of shock in small animals?

A

Hypovolemic shock

163
Q

Describe the pathophysiology of hypovolemic shock

A
  1. initial fluid loss
  2. decrease in circulating intravascular volume (intravascular volume deficit)
  3. decreased venous return to the heart
  4. decreased ventricular filling and cardiac preload
  5. decreased stroke volume, cardiac output, and blood pressure
  6. decrease in cardiac output results in decreased delivery of oxygen to tissues
  7. failure of delivery of oxygen to meet consumption requirements
  8. critical oxygen delivery is reached
  9. anaerobic metabolism begins
164
Q

Describe Baroreceptor Reflex Inhibition

A

A decrease in blood pressure results in a decreased stretch/firing of baroreceptors in blood vessels (aortic arch/carotid sinuses). This results in the initiation of a neuroendocrine response which decreases autonomic parasympathetic stimulation and increases sympathetic stimulation. The increased sympathetic stimulation causes and activation of alpha 1 and beta 1 adrenergic receptions resulting in vasoconstriction, increased heart rate and increased cardiac contractility. This ultimately increases systemic vascular resistance and cardiac output

165
Q

What causes the activation of the renin-angiotensin-aldosterone system?

A

A decrease in renal blood flow

166
Q

What is the end result of the renin-angiotensin-aldosterone system?

A

Contribution to systemic vasoconstriction along with sodium and water retention, which helps increase circulating plasma volume and replace intravascular volume deficit, improves stroke volume, cardiac output, and delivery of oxygen to tissues

167
Q

What initially activates the renin-angiotensin-aldosterone system?

A

The release of renin from juxtaglomerular cells in the kidney in response the the macula densa sensing a drop in blood pressure

168
Q

What is renin’s job in the renin-angiotensin-aldosterone system?

A

Cleaves a peptide from the protein angiotensinogen to convert it to angiotensin I

169
Q

Where is angiotensinogen produced?

170
Q

What is the role of angiotensin-converting enzyme?

A

Made by epithelial cells in the body. converts angiotensin I to highly active angiotensin II

171
Q

What is the role of angiotensin II?

A

A potent vasoconstrictor. Stimulates secretion of adrenocorticotropic hormone (ACTH), aldosterone, and antidiuretic hormone (ADH)

172
Q

What does ACTH do?

A

Stimulates the adrenal cortex to release cortisol

173
Q

What does cortisol do in the renin-angiotensin-aldosterone system?

A

Works synergistically with epinephrine and glucagon to induce a catabolic state which allows the body to break down reserves for immediate energy needs, stimulates gluconeogenesis and the generation of glucose from non-carbohydrates (lactate), creates insulin resistance and retains sodium and water through the kidneys

174
Q

What is aldosterone and what is its role in the renin-angiotensin-aldosterone system?

A

The body’s main mineral corticoid, produced in the zona glomerulosa of the adrenal cortex of the adrenal gland. Vasoconstrictive properties, release further contributes to conservation of sodium and water, excretion of potassium. Helps restore cardiac preload, cardiac output, and blood pressure.

175
Q

What is antidiuretic hormone and what is its role in the renin-angiotensin-aldosterone system?

A

Also known as vasopressin. Vasoconstriction. Increases water permeability within the kidney by insertion of aquaporin 2 channels within the cortical collecting duct of the kidney, thus decreasing water losses and additionally conserving water and preserving intravascular volume.

176
Q

What are the stages of hypovolemic shock?

A
  1. Compensatory phase
  2. Early decompensatory phase
  3. Late decompensatory phase
177
Q

Describe the compensatory stage of hypovolemic shock

A

-starts at the initial insult
-body tries to preserve vital organs by constricting peripheral vessels and contracting the spleen to move RBC into the central arterial circulation (PCV will remain high to start)
-this causes reduced circulation to extremities so they’re cold, pale mm
-inflammatory cytokines build up in hypoxic tissues
-can be tachycardic, injected to start, bounding pulses, fast CRT, BP normal to hypertensive
-cats don’t show this

178
Q

Do cats exhibit compensatory hypovolemic shock?

179
Q

Describe early decompensatory hypovolemic shock

A

-2nd phase of hypovolemic shock
-body’s reserve are diminishing and the cytokines from hypoxic tissue are more pronounced
-sign are tachycardia, weak pulses, hypotension, pale mm, long CRT, hypothermia, cold extremities, increased RR/RE, decreased mentation
-need aggressive volume resusitation

180
Q

Describe the late decompensatory phase of hypovolemic shock

A

-final and terminal stage brought on by prolonged and severe tissue hypoxia causing ATP depletion, anaerobic metabolism, cell death
-even aggressive intervention may fail
-signs are bradycardia, severe unresponsive hypotension, pale to cyanotic membranes, undetectable CRT, weak to absent pulses, hypothermia, decreased to coma mentation, cardiac arrest

181
Q

How soon must antibiotics be started if there is concern for sepsis?

A

Within 1 hour

182
Q

If a patient is found to have life-threatening hyperthermia, to what temperature should they be cooled?

A

103.5 F (39.7C)

183
Q

What are 3 goals of initial stabilization?

A
  1. rapidly stabilize life threats
  2. meet oxygen delivery needs
  3. shut off the neuroendocrine and RAAS response
184
Q

What catheter type will result in the fastest fluid administration?

A

Short and fat

185
Q

What are the three major body fluid compartments?

A
  1. Intravascular
  2. Interstitial
  3. Intracellular
186
Q

What are the three broad categories of fluid therapy?

A
  1. Crystalloids
  2. Colloids
  3. Blood products
187
Q

Describe the contents of crystalloids

A

-electrolytes in various concentrations
-dextrose
-buffers to balance acid-base status
-free water

188
Q

How does hypertonic saline work?

A

Concentrated sodium and chloride solutions cause rapid shifts of fluid into the intravascular space because water follows sodium
-results in rapid expansion of intravascular volume, causing improved venous return/cardiac output/vasodilation,improved tissue perfusion
-also beneficial in cerebral edema TBI

189
Q

What are colloids?

A

-solutions in which large molecules >10,000 daltons are evenly suspended in liquid (does not settle)
-used for intravascular volume replacement
-falling out of favor due to concerns for kidney injury and increased mortality in septic/critical patients, alterations to coagulation and increased risk for blood loss and transfusion, tissue storage, cost, failure to reduce morbidity/mortality

190
Q

What is the full circulating blood volume for a dog?

191
Q

What is the full circulating blood volume for a cat?

192
Q

What is the shock dose of intravenous crystalloid fluid therapy for dogs and cats?

A

Dogs = 90 mL/kg/h
Cats = 55 mL/kg/h

193
Q

Do we give shock doses of IV crystalloid fluids?

A

No, generally start at 1/4 of the shock rate

194
Q

What are the risks of administering more fluids than the patients needs?

A
  1. Circulatory overload
  2. Damage to the glycocalyx
  3. Dilutional coagulopathy
195
Q

What are the cons of measuring central venous pressure?

A

It is a measure of pressure, not volume. It is influenced by factors other than just cardiac preload (like cardiac function, intrathoracic pressure)

196
Q

What is an adequate preload measurement

A

8-10 cmH2O

197
Q

What is the Pleth Variability Index (PVI)?

A

A measurement of the dynamic changes to the pleth waveform of a pulse oximeter throughout the respiratory cycle. Controlled ventilation is required for this but there appear to be a correlation between PVI values and fluid responsiveness (PVI decreased as hypovolemia is addressed)

198
Q

If hypotension is not resolved despite adequate volume being achieved, what must be causing it?

A

Decreased cardiac contractility (inotropy) or vasodilation

199
Q

What are positive inotropes used for?

A

To adjust cardiac contractility

200
Q

What are vasopressors used for?

A

To adjust vascular tone

201
Q

Can drugs be a substitute for adequate volume?

202
Q

Describe the action of dopamine

A

-mixed adrenergic effect
-lower doses (0.5-3mcg/kg/min) may help with renal mesenteric coronary and vascular beds (useful in oliguric renal failure?)
-5-13 mcg/kg/min can improve cardiac output and blood pressure – acts on beta-1 adrenergic agonist
-10-20 mcg/kg/min shift to alpha-a receptors (vasoconstricting)
-cats may need >15 mcg/kg/min for alpha-1
-short duration, take 5-10 min to see effect
-degraded by catechol-O-methyltransferases (COMT) and monoamine oxidases (MAO)

203
Q

Describe the action of dobutamine

A

-beta-1 adrenergic agonist
-most commonly used to improve cardiac contractility and cardiac output
-beta-2 adrenergic agonist effect – vasodilation
-very little alpha-1 adrenergic effect
-1-20 mcg/kg.min
-d/c or reduce if tachycardia or arrhythmias
-increasing cardiac output and delivery of oxygen but does not increase BP

204
Q

Describe the action of norepinephrine

A

-mixed adrenergic agonist with stronger alpha-1 receptor than beta-1
-common in distributive shock (sepsis, SIRS) to increase vasoconstriction
-may improve cardiac output in dogs
-will lower heart rate due to baroreceptor reflex when BP increases – large doses = profound bradycardia
-rapid clinical onset (<5 min)
-if too much vasoconstriction = increased afterload and decreased cardiac output = decreased DO2
-0.1-2 mcg/kg/min

205
Q

Describe the action of phenylephrine

A

-alpha-1 adrenergic agonist
-indicated for hypotension when beta adrenergic agonist effects are not desirable
-concern for too much vasoconstriction, marked increase in BP and bradycardia
-use with caution in bradycardic pets or heart disease
-0.1-2 mcg/kg/min

206
Q

Describe the action of vasopressin (ADH)

A

-causes vasoconstriction independent of adrenergic stimulation
-can be used as a stand alone drug but more often in combination for refractory hypotension
-0.01-0.04 U/kg/min

207
Q

Describe the action of epinephrine

A

-mixed adrenergic agonist with alpha-1 and beta-1 agonist properties
-low doses- beta = improved cardiac output and cardiac contractility
-higher doses - alpha = improved BP by vasoconstriction
-0.1-2 mcg/kg/min

208
Q

Does acidosis or alkalosis reduce the efficacy of adrenergic drugs?

209
Q

What does CIRCI stand for?

A

Critical Illness Related Corticosteroid Insufficiency

210
Q

Define hypoxemia

A

An arterial partial pressure of oxygen (PaO2) below 80 mmHg
low concentration of dissolved oxygen in the blood

211
Q

What does a pulse oximeter measure?

A

The partial pressure of oxygen through the oxygen dissociation curve

212
Q

What are the 5 causes of hypoxemia?

A
  1. Decreased inspired partial pressure of oxygen (PiO2)
  2. Hypoventilation
  3. Ventilation/perfusion mismatch (V/Q mismatch)
  4. Diffusion impairment (rare)
  5. Anatomical shunting
213
Q

What is the FiO2 of room air?

214
Q

What is the oxygen concentration of flow by O2?

215
Q

What rate should flow by be administered at?

216
Q

What are the oxygen flow rates with standard nasal cannulae?

A

50-150 mL/kg/min

217
Q

What are the risks of exceeding 150 mL/kg/min of O2 via nasal cannulae?

A
  1. Gastric distention
  2. Drying of the mucous membranes
  3. Patient discomfort
218
Q

What is the maximum flow rate for intratracheal oxygen?

A

0.5 L/min
higher rates an cause the tube to oscillate and irritate the trachea or lead to overdistension of the lung

219
Q

What are the advantages of high flow oxygen therapy?

A

Provides warm humidified oxygen at high flow rates close to 100% FiO2, provides low levels of PEEP

220
Q

How do opioids help with respiratory distress?

A

Helps reduce the feeling of breathlessness

221
Q

How does tranquilization help in upper airway obstructions?

A

Allows for deeper and slower respiratory rate that slows airflow and reduces airway resistance and work of breathing

222
Q

What is rapid sequence intubation (RSI)?

A

Quickly inducing general anesthesia to facilitate intubation, using agents like alfax or propofol

223
Q

What are the negative effects of NSAIDs and corticosteroid drugs?

A
  1. Immunosuppression
  2. GI bleeding
  3. Nephrotoxicity
224
Q

What is a normal lactate level?

A

<2.5 mmol/L (but new studies suggest up to 5 in cats)

225
Q

What are the types of lactate?

A

D-lactate and L-lactate. We care about L-lactate as it is the predominant biological and functioning form of lactate

226
Q

Where is lactate normally produced?

A
  1. Skeletal muscle
  2. Brain
  3. Adipose tissue
  4. Circulating blood cells
227
Q

Where is lactate metabolized?

A
  1. Liver
  2. Kidney
  3. Myocardium
228
Q

What are the types of hyperlactatemia?

A

Type A: States of hypoxia and anaerobic metabolism (hypoperfusion, anemia, severe hypoxemia, CO poisoning)
Type B: systemic disease, drugs or toxins, congenital disease of lactate metabolism (B1, B2, B3 respectively)

229
Q

What are mixed venous (SvO2) and central venous (ScvO2) oxygen saturation parameters used for?

A

Measure the saturation of oxygen returning to the right heart

230
Q

How is mixed venous oxygen saturation (SvO2) obtained?

A

Pulmonary artery catheter, reflects oxygen returning to the heart from both the cranial and caudal portions of the patient

231
Q

How is central venous oxygen saturation (ScvO2) obtained?

A

Sampling the jugular, reflects oxygen delivery in the cranial portion of the patient

232
Q

What SvO2/ScvO2 values are adequate?

A

Greater than 70% suggests adequate oxygen delivery, less that this suggest tissue oxygen debt

233
Q

What is Shock index?

A

A bedside assessment evaluating the severity of hypovolemic shock SI = HR/sBP
Values >1 can indicate small volume blood loss, >0.9-1 detects moderate to severe shock

234
Q

What concentration of hyperosmolar solution should be put through a PICC line?

A

> 600 mOsm

235
Q

What are common locations for IO catheters?

A

Flat medial surface of the proximal tibia, the throchanteric fossa of the femur, the greater tubercle of the humerus, the wing of the ilium, the ischium

236
Q

What are some complications of IO catheters?

A

Fat embolism, infection, nerve injury, bone fracture

237
Q

What are the contraindications for IO catheters?

A

Bone neoplasia, osteomyelitis, bone fracture

238
Q

What values do not correlate well from an IO sample?

A

BG and potassium

239
Q

What equation describes the flow through an intravenous catheter?

A

Hagen-Poiseuille law. States that the flow of fluid is related to a number of actors including viscosity of the fluid, the pressure gradient across the tubing, and the length and diameter of the tubing
Maximal flow of an IV catheter obtained by using shortest length and largest gauge

240
Q

How often should fluid bags and lines be changed?

A

Every 72 hours

241
Q

What is Virchow’s triad?

A

All causes of thrombosis occur due to the presence of one or more of the following?
1. Endothelial damage
2. Blood stasis/turbulent blood flow
3. Hypercoagulability (IMA, neoplasia)

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