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Exam 1 Flashcards

1
Q

What does blood pressure measure?

A

BP = CO x SVR

Systole (the pressure against arterial walls when ventricles contract/empty) and Diastole (the pressure against arterial walls when ventricles relax/fill)

CO = SVR x HR

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2
Q

Describe the flow of blood

A

Deoxygenated blood flows from the caudal and cranial vena cavae from peripheral veins to the right atrium -> tricupsid valve -> right ventricle -> pulmonic valve -> pulmonary trunk -> lungs -> oxygenated blood flows through pulmonary vein -> left atrium -> mitral valve -> left ventricle -> aortic valve -> aorta -> periphery vessels/tissues

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3
Q

What type of vessel has the greatest resistance and what is the significance?

A

Arterioles (systemic) - very small vessel diameter = increased resistance and decreased flow. Significance = vasoconstriction/dilation of arterioles play greater role in regulating BP than in any other vessel types

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4
Q

Describe vessel length, diameter, viscosity, resistance, and velocity of flow relationships

A
  • increased viscosity = increased resistance, decreased flow
  • increased vessel length = increased resistance, decreased flow
  • increased diameter = decreased resistance, increased flow

  • viscosity = hematocrit
  • increased diameter = less contact of blood to vessel wall = lower friction = lower resistance
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5
Q

What vessel holds greatest capacitance at rest?

A

systemic venous circulation

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6
Q

What vessel holds largest distribution?

A

aorta and large artery

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7
Q

What is Cardiac Output? What factors influence it?

A

CO = SV x HR, and measured in mL blood/min.

SV influenced by blood volume and vascular resistance. HR influenced by nervous system and hormones.

SV = vol. of blood ejected during systole

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8
Q

Blood pressures:
- RA
- RV
- PA
- PCW
- LA
- LV

A

RA = 2-8
RV = 15-30/2-8
PA = 15-30/4-12
PCW = 2-10
LA = 2-10
LV = 100-140/3-12

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9
Q

Systemic circulation is a ? pressure system than pulmonary circulation, and arteries are a ? pressure system than veins.

A

higher; higher

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10
Q

What is Dilated Cardiomyopathy? What happens to BP and HR in DCM patients?

A

a disease of systolic dysfunction that causes secondary dilation of chambers => decreased CO, hypotension (even though resistance in vessels is unchanged)
- body compensates for hypotension via increased HR -> increased CO, which may increase congestion

CO = SV x HR
BP = CO x SVR

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11
Q

What is the cardiovascular system?

A

A central muscular pump that is connected to vessels for the transport of blood; must maintain balanced CO and venous return

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12
Q

What are the two kinds of myocytes that makeup the CV system?

A
  1. Specialized Cardiomyocytes = conduction system: spread SA node depolarization -> AV node -> His-Purkinje System
  2. Working/Contractile Cardiomyocytes = contraction & pumping

specialized/conduction system = electrical events, working/contractile = mechanical events

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13
Q

Significance of sarcomere in striated cardiac muscle

A

is able to generate force and contractility in order to pump blood throughout the body

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14
Q

Significance of intercalated discs and gap junctions in cardiac muscle

A

allow for coordinate/united flow of electrical current between cardiomyocytes

AV node has reduced gap junctions -> slower conduction of electrical signal -> allows for atria to eject as much blood as possible into ventricles

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15
Q

Describe the relationship between myosin, actin and cross-bridge cycling

A

Myosin = thick filament, Actin = thin filament -> bind together and interact in presence of ATP to form cross bridge = sarcomere shortening/contraction

Sinus node initiaes depolarization –> action potential propagated and spreads across sarcolemma of cardiomyocytes –> opens Ca2+ voltage-gated channels in sarcolemma –> cardiac muscle contraction

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16
Q

What happens when sarcolemma calcium channels close in cardiac muscle?

A

calcium is pumped back into sarcoplasmic reticulum (where it is stored) and also pumped out of the cell -> cytosolic calcium is reduced and so are contractions –> sarcomeres return to resting length

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17
Q

What is the left ventricular pressure at early diastole/end-systolic volume versus late diastole/end-diastolic volume?

A

Early diastole/ESV = LOW (~10mmHg) so that blood flows from atrium to ventricle

Late diastole/EDV = HIGH (~80mmHg) so that oxygenated blood can be exerted into aorta

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18
Q

What effects do norepi and epi have on the heart? what receptor?

A

BOTH: *Beta-1 adrenergic -> increased sympathetic tone in cardiac muscle = increased SA node/AV node firing. Mostly favorable to epi than norepi.

Beta-2 = epi -> positive inotrope in the heart

Alpha 1 and 2 = increased vasoconstriction in peripheral vessels -> increased BP

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19
Q

What effect does acetylcholine have on the heart? Which receptor?

A

Decreased heart rate (- chronotrope) at cholinergic-muscarinic receptors

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20
Q

Dobutamine MoA // use:

A

Sympathomimetic / beta-1 adrenergic agonist, strong positive inotrope (increases contractility of cardiac muscle) and better relaxation.

Causes immediate increase in BP due to increased CO (BP = CO x R).

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21
Q

Lower dose vs higher dose effects of Dobutamine

A

Dobutamine = dose-responsive.

Lower: better inotrope effect

Higher: more effect on alpha receptors, which can lead to hypertension, tachycardia, and arrhythmias

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22
Q

Equation for Stroke Volume:

A

SV = EDV minus ESV

SV = change in volume from diastole to systole (mL)

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23
Q

3 determining factors of stroke volume?

A
  1. Pre-Load: sarcomere length of ventricle @ end-diastole / the ventricular wall stress (tension) from being filled. Higher pre-load = higher SV / directly related to CO.
  2. After-Load: the forces that ventricular myocytes must overcome during systole to open pulmonic and aortic valves. Higher after-load = lower SV / Inversely related to CO.
  3. Contractility: the measure of intrinsic contractile performance of cardiomyocytes, “the strength of the myocardium” independent of load. Increased ability of sarcomere to contract = increased CO.

BP = SVR * HR

CO = SV x HR

SV = EDV- ESV

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24
Q

What are 4 ways to increase CO?

A

CO = SV x HR

  1. increase preload
  2. increase contractility (e.g., dobutamine)
  3. increase HR (within physiological range)
  4. reduce afterload (e.g., vasodilators like nitroglycerin, amlodipine)
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25
Q

5 phases of cardiac cycle?

A
  1. atrial systole (atrial contracts small amt of additional blood into relaxed ventricles)
  2. isovolumetric ventricular contraction (AV valves close, pressure increases but volume stays the same)
  3. ventricular ejection (semilunar valves open, high pressure)
  4. early diastolic filling (ventricles begin to relax, semilunar valves close)
  5. late diastolic filling (all chambers relaxed and ventricles fill passively)
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26
Q

“Lub” vs “Dub”

A

S1 “Lub” = start of systole (AV closure, semilunar opening)

S2 “Dub” = end of systole (semilunar closure, AV opening)

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27
Q

What species can S3 and S4 be heard in?

A

Normal equine and bovine patients

S3 = early diastole
S4 = late diastole

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28
Q

How do venous return and systemic vascular resistance affect stroke volume when relaxed vs. stressed?

A

Relaxed: parasympathetic activation shifts systemic venous pool to peripheral vessels (away from heart) -> decreased SVR -> decreased CO and HR = decreased SV

Stressed: sympathetic activation shifts systemic venous pool centrally (towards heart) -> vasoconstriction and increased SVR -> increased CO and HR = increased SV (more filling)

parasymp influences HR and CO
symp influences SV, HR and CO

SVR = systemic vascular resistance

BP = CO x SVR
CO = SV x HR
SV = EDV - ESV

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29
Q

Which u/s view displays a 4-chamber view of the heart?

A

Right parasternal, long axis

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30
Q

What structures does the right parasternal, short axis view display?

A

LV (mushroom) and RV

LV @ level of papillary muscles

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31
Q

What structures does ther heart base, short axis view display?

A

Aortic valve (mercedes benz 3 cusps), and left atrium and its appendage (whale)

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32
Q

What structures does left parasternal apical view display?

apical = apex

A

all 4 chambers

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33
Q

Difference between 2-D and M-Mode echocardiography and benefits of each.

A

2-D = 2d place of u/s waves cross-sectioning the heart, either by long axis or short axis
- can visualize cardiac morphology and chamber dimensions

M-Mode = motion mode. single beam through the heart
- can visualize time-dependent measurements of the chambers (for dimensions, function)

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34
Q

Differences b/w Spectral versus Color Doppler Echocardiography

A

Both used to measure blood velocities

Spectral: blood velocities displayed on Y-axis (signal above x-axis = RBC towards probe, signal below x-axis = RBC away from probe)

Color: blood velocities displayed as colored pixels (BART)

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35
Q

Describe the pros/cons of each type of Spectral Doppler

A

Pulse Wave (PW)
- Higher spatial resolution
- Poorer measure of high velocities
Continuous Wave (CW)
- Lower spatial resoultion
- Better measure of high velocities

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36
Q

What does turbulent blood flow look like on Color Doppler?

A

mix of red/blue = ~orange-tinge color

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37
Q

Best uses of color doppler echocardiography

A
  • ID of turbulent blood flow (stenotic valves, valvular insufficiency)
  • determination of direction of blood flow through a shunt
  • assessment of severity of stenosis, shunt or valve regurg
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38
Q

Which echocardiography methods produce subjective vs. objective dimensions of the LV?

A

Subjective = 2D
Objective = M-motion; 2D using Simpson’s disc summation method for obtaining left ventricular ejection fraction

LVEF = [(EDV - ESV) / (EDV)] x 100%
normal = ~70%

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39
Q

How is echocardiogrpahy superior to radiology?

A

better for visualzing RA and RV

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40
Q

How can echocardiography be utilized to detect pressure gradients? Purpose?

A

change in pressure = 4V^2

Blood always flows from high pressure -> low pressure; detects pressure difference that generated the flow b/w chambers (e.g., in valve regurg)

Bernoulli equation

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41
Q

how can pulmonary hypertension lead to secondary tricupsid regurgitation?

A

increased pressure in lungs = greater pressure RV needs to overcome to force blood out into pulmonary trunk (increased after-load) -> pressure increases in RV to point where RV pressure is > RA pressure -> blood backflows into RA

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42
Q

Definition of heart failure and most common type in veterinary patients

A

“Clinical syndrome in which impaired systolic or diastolic events causes clinical signs of exercise intolerance and/or congestion.”

CHF = most common type

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43
Q

Left vs Right CHF

A

Left-sided CHF = backflow into lungs –> pulmonary edema (cardiogenic PE)

Right-sided CHF = backflow into systemic circulation –> ascites, +/- peripheral edema

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44
Q

Two most common causes of CHF in dogs

A

Mitral Valve Insufficiency/regurge

Dilated Cardiomyopathy

mitral valve regurg = volume overload

DCM = systolic myocardial dysfunction

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45
Q

4 stages of classifying heart disease

A

A: predisposed breeds
B: have heart disease, but not in failure yet
C: in CHF (current or past; even if CHF has been treated, you will almost never treat the disease that caused it)
D: refractory CHF (end-stage)

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46
Q

How do volume overload and pressure overload’s pathphysiological mechanisms differ with regards to their apperances on echocardiography?

A

Volume overload = eccentric hypertrophy: in-series replication of sarcomeres –> hypertroophy + dilation. Preserved wall thickness:lumen

Pressure overload = concentric hypertrophy: parallel replication of sarcomeres –> hypertrophy without dilation. Increased wall thickness:lumen

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47
Q

Identify the heart disease.

A

Volume overload: Eccentric hypertrophy – e.g., mitral valve regurgitation

(note hypertrophy + dilation and the preserved wall thickness:lumen ratio)

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48
Q

Identify the heart disease.

A

Pressure overload: Concentric hypertrophy – e.g., severe pulmonic stenosis

(note hypertrophy but NO dilation, and the INCREASED wall thickness compared to lumen)

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49
Q

Identify the heart disease.

most common acquired in cats.

A

Diastolic dysfunction - hypertrophic myopathy

causes impaired ventricular filling.

MUSHROOM = LEFT VENTRICLE
very difficult to assess non-invasively!

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50
Q

Identify the heart disease.

A

Systolic myocardial dysfunction: dilated cardiomyopathy (DCM)

dilation is secondary to systolic dysfunction!!

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51
Q

Identify the heart disease.

A

Arrhythmias

Top: 3rd degree AV block

Bottom: ventricular tachycardia

3rd degree AV block: all impusles are blocked at AV node –> bradycardia b/c HR generated entirely by slow-firing ventricles.

Ventricular tachycardia: significantly decreases CO and can worsen CHF

52
Q

What is ventilation and what are its determinants?

A

Ventilation: the movement of air in (inhalation) and out (exhalation) of alveoli.

Determinants:
- respiration rate
- tidal volume

also known as alveolar ventilation

inhalation: alveoli pressure less than atmosphereic
exhalation: alveoli presure greater than atmospheric

similar to CO = SV x HR

53
Q

difference b/w gas exchange and gas transport

A

Gas exchange = of O2/CO2 at the alveolar-pulmonary capillary interface

Gas transport = of O2/CO2 to/from systemic tissue capillary beds through the circulatory system

54
Q

Define respiration and what are its 3 associated components.

A

Repsiration: the transportation of O2 in the air to systemic cells and the transportation of CO2 in systemic cells back out into the atmosphere
- ventilation, gas exchange and gas transport

55
Q

How do chemoreceptors in the brain modulate respiratory rate?

A

by responding to the systemic blood levels of O2, CO2, and pH (acids)

decrease in pH (more acidic) -> brain stimulates deeper and faster breaths

56
Q

Explain Vt = Vdeadspace + Valveolus

A

Vt = Volume of air inhaled or exhaled into lungs during a normal breath

Vdeadspace = Volume of air in conducting airways (physiologic dead space) + volume of air in pathologic dead space

Valveolus = Volume of air in the alveoli

57
Q

Describe alveolar minute ventilation

A

Volume of air entering (or leaving) the alveoli per minute

AMV = (Vt - Vdeadspace)xRR

58
Q

3 causes of alveolar hypoventilation

A

reduced RR
reduced Vt
increased dead space

all decrease chances of air moving in/out of alveoli

59
Q

Conducting vs. Transitional vs Exchange Airways

A

Conducting Airway = transport air
- upper airway = nares to pharynx
- lower airway = trachea to bronchus
- physiologic dead space; warm/humidfy air and remove particulate matter

Transitional Airway = bronchioles

Exchange Airway = gas exchange
- alveolar duct to alveoli
- occurs b/w alveolus and pulmonary capillary beds

60
Q

What features of alveoli allow for gas exchange?

A
  1. single-cell thickness (0.5 um)
  2. surfactant (lowers surface tension / keeps alveoli open)
61
Q

What are 3 examples of impairments of the conducting airway?

A
  1. Brachycephalic Syndrome (stenotic nares, elongated soft palate, hypoplastic trachea)
  2. Laryngeal Paralysis (dogs; failure of cricoarytenoid muscle to contract during inhalation -> air cannot enter trachea)
  3. Dorsal Displacement of the Soft Palate (horses’ soft palate extends to epoglottis -> obligate nasal breathers)
62
Q

Define ‘glottis’ vs. ‘epiglottis’

A

Glottis: laryngeal orifice

Epiglottis: cartilaginous structure that prevents aspiration during swallowing

63
Q

Why is proper nasal dilation crucial for obligate nasal breathers?

A

radius is inversely proportional to airflow resistance. more nasal dilation = less airflow resistance = better ventilation

64
Q

Describe arytenoidal/vocal fold abduction and its effect on airway resistance.

A

During inspiration, the dorsal cricoarytenoid muscle contracts, -> abduction of vocal folds and arytenoid -> air can enter trachea

allows for decreased airway resistance so air can flow in

65
Q

Why does the pleural cavity always have negative pressure?

A

The lungs’ elastic recoil tends to collapse them, while chest wall’s elastic recoil allows for it to expand -> PLERUAL PRESSURE IS NEGATIVE B/C OF THESE OPPOSING FORCES

66
Q

When is intrapulmonary pressure negative, positive and equal to atmospheric pressure?

A

Negative: inspiration
Positive: expiration
Equal: in between inspiration and expiration

67
Q

What are 3 factors that prevent pulmonary collapse?

A
  1. Subatmospheric pleural space pressure
  2. High surface tension of pleural fluid (helps maintain position of lungs against thoracic wall)
  3. Alveolar surfactant (decreases surface tension, allowing lungs to inflate more easily)
68
Q

How does diaphragmatic contraction decrease intrapulmonary pressure during ‘quiet breathing’?

quiet = normal

A

Diaphragmatic contraction occurs during INSPIRATION and moves downward, while the external intercostal muscles pull the ribs upwards -> increases size of thoracic cavity and decreases the pressure within it

69
Q

Describe the importance of abdominal muscle recruitment during abnormal/heavy breathing.

A

necessary to help move the diaphragm back upwards to give more power to/enhance expiration

70
Q

Define inspiratory and expiratory reserve volume, and residual volume.

A

inspiratory RV = additional air volume resulting from deepst possibe breath

expiratory RV = additional air volume exhaled during maximally forceful exhalation

residual volume = volume remaining in lungs after maximally forceful exhalation

71
Q

What is the importance of ventilation/perfusion matching for gas exchange?

A

Alveolar ventilation needs to be adequate (determined by Vt and RR) and blood circulation through pulmonary capillary beds must be adequate (i.e., no blood clots, etc.) for this interface and gas exchange to occur

72
Q

What are the 4 necessarry components for gas exchange to occur at the alveolar-capillary interace in the lungs?

A
  1. Oxygen content of inspired air is 21%
  2. Effective alveolar ventilation
  3. Matching of ventilation and perfusion
  4. Diffusion of gas at this interface
73
Q

What are the 4 determinants of the diffusion of gas across the alveolar membrane?

A
  1. pressure gradient of the gases in the alveolus vs capillary
  2. diffusion coefficient (the solubility and MW of the gases)
  3. diffusion distance (b/w alveolus and capillary)
  4. membrane area (SA of alveolar epithelium and capillaries)

alveolar membrane thickness and fluid in interstitial space would increase diffusion distance

74
Q

Define hypoxemia and what can cause it.

A

Hypoxemia: reduced partial pressure of O2 in arterial blood, specifically reflecting oxyHb

Causes:
- reduced inspired oxygen (fire, failure of O2 turned on during anesthesia)
- alveolar hypoventilation
- ventilation/perfusion mismatch
- diffusion barrier

75
Q

What is the PaO2 and PaCO2 in pulmonary edema?

A

DIFFUSION ISSUE AND NOT VENTILATION ISSUE

PaO2 = decreased (O2 from alveoli cannot diffuse across the fluid into capillary bed)

PaCO2 = normal (CO2 has higher solubility and can still diffuse across the fluid and thus be breathed out)

pulmonary edema = diffusion issue, NOT ventilation

76
Q

What would decrease PaO2 and increase PaCO2?

A

hypoventilation (e.g., too deeply anesthesized)

77
Q

Compare the response of pulmonary arterioles to hypoxic conditions versus systemic arterioles.

A

Pulmonary arterioles: vasoconstriction - want to reduce/stop bloodflow to any hypoxic regions of the arterioles (decrease chances of deoxygenated blood flowing out of lungs)

Systemic arterioles: vasodilation: want to increase bloodflow to any hypoxic regions of systemic tissues (increase chances of oxygen reaching these tissues)

78
Q

What factors can alter perfusion and lead to ventilation/perfusion mismatch?

A

anything that alters flow thru the capillaries
- vasoconstriction
- physical obstruction (thromboembolism)
- shunt (blood skips lungs -> deoxygenated blood goes straight to systemic circ.)

recall: flow = pressure change / vascular resistance

79
Q

When is V/Q (ventilation and perfusion ratio) low vs high?

A

Low: shunt perfusion
High: dead space ventilation

80
Q

What is Brisket Disease in cattle?

A

In Pike’s Peak / regions of higher altitude, the partial pressure of inspired O2 is lower (still 21% but of a lower atmospheric pressure), leading to a lower drive of gas exchange in the lungs. This leads to hypoxic conditions in the alveolus which responds by vasoconstriction of pulmonary arterioles
-> pulmonic hypertension –> RV pressure increases due to increased afterload –> right-sided CHF

Bottle Jaw effect (subcutaneous edema from the CHF)

81
Q

What does PaCO2 reflect and why?

A

ventilation status b/c PaCO2 is only changed by hypoventilation (increases

82
Q
A
83
Q

What is the Resting Membrane Potential of the Sinoatrial Node versus Ventricular Working Myocytes? What is the genesis of the RMP?

A

SA Node = -65mV (spontaneously depolarizes w/ no plateau phase)

Ventricular Working Myocytes = -85mV (fixed w/ plateau phase)

at rest, cardiomyocyte in polarized (neg. inside, pos. outside)

Genesis of RMP:
- the Na+/K+ ATP-dependent pump (pumps Na+ out and K+ in)
- Donnan Effect (presence of large, impermeable anionic intracellular proteins)
- selective permeability membrane (K+ leakage channels allow it “leak” out w/out allowing Na+ in)

84
Q

What are the phases of the SA node action potential versus Ventricular Working Myocytes?

A

SA Node: 4 RMP -> 0 Spontaneous Depolarization -> 3 Repolarization

Ventricular Working Myocytes: 4 RMP -> 0 Non-Spontaneous Depolarization -> 1 Overshoot -> 2 Plateau -> 3 Repolarization

85
Q

What is meant by Spontaneous Depolarization of the SA Node?

A

SA node’s ability to become (+) whenever is due to its Funny (Na+) channels, Transient Ca2+ and Lasting Ca2+ channels.

Funny Na+ channels = activated on hyperpolarization during diastole and by phosphorylation by cAMP.

The ventricular working myocytes CANNOT depolarize spontaneously b/c they depend on a voltage-gated Na+ channel.

86
Q

What causes Plateau phase in ventricular working myocytes?

A

voltage-gated “slow” Ca2+ channels that allow for ventricular refill

87
Q

What anti-arrhythmic drug can cause a steeper RMP?

A

Atropine (parasympatholytic)

88
Q

Bipolar Leads vs Augmented Limb Leads of ECG

A

Bipolar Leads: detect positive (depolar.) and negative (repolar.) vectors
Augmented Limb Leads : only detect positive (depolar.) vectors

Size of deflection on ECG tracing always corresponds to size/magnitude of dipole in direction of electrode (leads)

89
Q

How much is the x-axis?

A

X-axis = 5mm

50mm = 1 sec -> 150mm = 3 secs
90
Q

What are the 5 ASA physical status classifications?

A

I = normal, healthy patient; elective procedure

II = slight-to-mild systemic disease with no obvious clincial signs

III = mild-to-moderate, under control systemic disease with clinical signs

IV = severe systemic disease, life-threatening, patient decompensated

V = morbund patient, not expected to survive >24h

Add ‘E’ if ER

American Society for Anesthesiologists (ASA) physical status: to quantify the amount of physiological reserve that a patient possesses at the time at which they are assessed for a surgical procedure, and which should also not be used as a sole predictor of operative risk to the patient.

91
Q

What are 3 factors in how you select your pre-anesthetic protocol?

A
  1. Any pre-existing diseases? (CV, resp, renal, CNS)
  2. What is the procedure to be performed? (elective, minimal vs. high risk, etc.)
  3. How will you choose the appropriate anesthetic drugs? (what are your desired effects, what side effects do they cause, etc.)
92
Q

What are two commonly used pre-anesthetic anti-cholinergic drugs and why are they used? What would be contrainindications?

A
  1. Atropine
  2. Glycopyrrolate

Use = parasympatholytic (prevent bradycardia)

Contrainindications: pre-exisiting tachycardia, narrow-angle glaucoma, equine colic

competitive antagonists of ACh @ muscarinic cholinergic receptors

93
Q

Major differences between Atropine and Glycopyrrolate?

A

Glycopyrrolate does NOT cross BBB or placenta, but it has a longer onset and duration than Atropine

94
Q

What are the most common tranquilizer/sedative drugs used in pre-anesthetic protocol?

A
  • Acepromazine
  • Benzodiazepines (diazepam, midazolam, zolazepam)
  • Alpha-2 agonists (xylazine, dexmed, romifidine)
95
Q

Which tranquilizer/sedative has the least sedative effect?

A

Benzodiazepines

96
Q

Which tranquilizer/sedative has the most profound cardiovascular effects?

A

Alpha-2 receptor agonists: biphasic BP effect: initial hypertension -> increased SVR -> reflex decr. CO -> prolonged, mild hypotension can then be more likely for decr. perfusion -> pale mm

97
Q

What is the reversal for benzodiazepines?

A

Flumazenil

competitve antagonism

98
Q

MoA of Benzodiazepines

A

increase affinity for GABA binding, potentiate GABA’s inhibitory effects

99
Q

Which tranquilizer/sedative would you choose in pre-anesthetic protocol if you wanted good sedation, antiarrhythmic effects and synergism with opioid?

A

Acepromazine

100
Q

What two drugs cause pain on injection due to their propylene glycol ingredient and therefore should be given slowly/titrated?

A

Diazepam (sedative agent, IM) and Etomidate (induction agent, IV)

101
Q

Which pre-anesthetic agent may cause paradoxical excitation?

A

Diazepam

102
Q

Which pre-anesthetic drugs provide NO analgesia?

A

Acepromazine and benzodiazepines

103
Q

Which opioids have little-to-no respiratory effects?

A

Buprenorphine (partial Mu agonist) and Butorphanol (Mu antagonist)

104
Q

What is one critical reason why we use pre-meds?

A

to decrease anesthetic requirements (aka decrease induction and maintenance drugs’ doses!)

105
Q

MoA of Propofol

A

increases duration of GABA receptor’s opening of Cl- channel -> hyperpolarization

106
Q

What are reasons why Propofol is a favorable induction agent?

A

smooth induction process
short-acting (rapid redistrib. to vessel-rich groups)
decreases ICP and IOP
safe for C-sections
easy/quick recovery

vessel-rich groups = brain, kidneys, liver

107
Q

What are precautions in using Propofol as an induction agent?

A

Profound CV and respiratory depressant
- decr. contractility -> hypotension
- potential apnea; titrate/give IV slow
- always provide supplemental O2 (poss. cyanosis)

108
Q

What is Propofol 28 and its extra-label use in cats?

A

single-use only as it has benzyl alcohol additive (no CRI b/c concern of buildup)

only use as induction agent in cats b/c they metabolize it very slowly (aka very prolonged recovery)

109
Q

Etomidate’s MoA and effects on the body

A

MoA = indirectly potentiates GABA, directly evokes Cl- currents in absence of GABA at high doses

-fast onset, short duration
- MINIMAL CV and RESP EFFECTS
- CAUSES ADRENAL SUPPRESSION -> DECREASES CORTISOL SYNTHESIS just after single dose (do NOT use in Addisonian pt or as a CRI)
- V+ @ induction
- no analgesia
- hematuria

110
Q

MoA of Ketamine and its effects on CNS, CVS and RS

A

MoA = non-competitive antagonist @ NMDAR (a glutamate receptor)

  • CNS = hallucinatory behavior (is a dissociative); increases ICP so don’t use in epileptic pts; eyes remain open but Palpebral and Corneal reflexes maintained!
  • CVS = increases HR, CO, BP
  • RS = no significant depression; “breath-holding”
111
Q

How are Ketamine and Tiletamine metabolized in dogs, cats and horses?

A

Dogs/horses = extensive hepatic metabolism

Cats = active metabolite (norketamine) eliminated unchanged in the urine

112
Q

MoA of Alfaxalone and its effects on the body.

A

MoA = synthetic neuroactive steroid that enhances agonist binding to GABA receptor; new version has preservative that extends shelf life and has NO histamine release

  • NO analgesia
  • smooth induction and recovery (like propofol)
  • minimal CV effects
  • decreases cerebral bloodflow and ICP
  • no cumulative effect
  • crosses placenta but STILL SAFE for C-sections
113
Q

What is a common concern in horses given sedative agents?

A

Ataxia

114
Q

Describe the 4 types of chemical restraint in large animals and when to use them.

A
  1. Recumbent = field procedures (wound debridement, dehorn, PE, BW)
  2. Recument with physical restraint = ruminants for surgical procedures requiring regional anesthesia
  3. Recumbent with back-up physical restraint, if needed = castration, small mass removal, hoof trim
  4. Standing (horses) = keep floor dry, cushion head, prevent dropping w/ sling, colic watch after long procedures

Regional anesthesia: Neuraxial Anesthesia (Spinal/Epidural/Combined), Peripheral Nerve Blocks

115
Q

Why should Acepromazine be used precautiously in stallions?

A

Can cause priaprism b/c it prolongs penile prolapse

priaprism = prolonged rigid ejection

116
Q

What drugs in horses…
1. increase their colic risk
2. cause paradoxical excitement in adult horses
3. cause severe ataxis on recovery

A
  1. opioids
  2. benzodiazepines
  3. guaifenesin
117
Q

What drug causes pulmonary edema and hypoxia in sheep?

A

Xylazine (alpha-2 agonist)

118
Q

What drug class can be used to “fine tune” your sedation protocol b/c of its modulatory properties?

A

Opioids

119
Q

MoA, uses, and precautions of Guaifenesin in large animals

A

MoA = central muscle relaxant with no analgesia

Uses: improve sedation/smooth induction agent (can be used as sole one in ruminants) with minimal CVS and RS depression

Precautions: perivascular tissue irritant (hemolysis and necrosis); severe ataxis on recovery

120
Q

What are some abnormal respiratory PE findings in horses?

A

Nostril flare, auscultation of crackles/wheezes or reduced thoracic sounds, SC emphysema, pain on thoracic palpation (broken rib), dull sounds on sinus percussion (fluid or mass)

121
Q

What are 4 methods of amplifying lung sounds in horses and what is the purpose of doing so?

A

Purpose = to ID where abnormal sound auscultated is originating from (i.e. upper or lower RT)

  1. Plastic bag method
  2. Exercise
  3. Doxapram (a potent respiratory stimulant)
  4. Obstruct the nares
122
Q

Equine Thoracic Ultrasound

What does each type line/lesion (A, B, C) indicate?

A

A: normal, air-filled lungs. The horizontal lines = reverebations caused by u/s waves traveling thru the air

B: indicate defect on pleural surface. “Comet Tails” = pleuritis, fibrin tags, SF abscesses (Rhodococcus equi)

C: abmormally large amt. of fluid present b/w the parietal and visceral membranes (inflammation, infection, hemorrhage)

123
Q

What is the use of endoscopy in collecting samples in sick horses with suspected respiratory disease?

A

Respiratory secretions/samples can be collected and/or visualized from several different locaitons along the RT

pharyngeal lymphoid hyperplasia, tracheal lesions (collapse, GCT, exercise-induced pulmonary hemorrhage)

124
Q

What are the methods of sampling from the equine lower/upper respiratory system? Which are sterile and non-sterile samples?

A

choose collection site closest to affected area / where infectious agent is most likely to be

  1. Nasal Swab or Wash - equires SEDATION; is a non-sterile sample -> PCR
  2. Trans-Tracheal Wash (TTW) - sterile sample -> C&S, PCR (can be percutaneous or trans-endoscopic)
  3. Bronchoalveolar Lavage (BAL) - non-sterile sample -> PCR
125
Q

Equine Respiratory Tract Diagnostics

What are the main differences between a TTW and a BAL

A

B&C (30 decks)

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