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Boards: Cardiovascular > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Write down the equation of systemic vascular resistance (SVR).

A

SVR = (MAP - CVP)/CO x 80

80 converts the unit from wood unit (mmhg/L/min) to metric (dynes/sec/cm-5)

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2
Q

Write down the equation of pulmonary vascular resistance (PVR).

A

PVR = (MPAP - PAWP)/CO x 80

80 converts the unit from wood unit (mmhg/L/min) to metric (dynes/sec/cm-5)

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3
Q

What is the terminal arterioles called?

A

Metarterioles

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4
Q

What are the two theories about acute local blood flow control in respond to metabolic need?

A

1) Vasodilator substance theory
When there is increased tissue metabolism or presence of oxygen deficiency, the tissue will release vasodilator substances (e.g. adenosine***, CO2, hydrogen ion, potassium ion, histamine). This substance will diffuse locally and cause local vasodilation

2) Oxygen demand theory
Smooth muscles need oxygen to contract. When there is increased metabolism and oxygen deficiency, vascular smooth muscle cannot constrict which lead to local vasodilation

*Reactive hyperemia vs Active hyperemia

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5
Q

Within a range of arterial blood pressure, the body is able to maintain local blood flow within a certain range. This is called Autoregulation. What are the two theories about autoregulation?

A

1) Metabolic theory
- Oxygen and nutrient deficiency → increase vasodilator substances → increase blood flow
- Too much oxygen & nutrient & blood flow → wash out vasodilator substances → vasoconstriction

2) Myogenic theory
- Stretch-induced vascular depolarization → Increase intracellular calcium…etc → vasoconstriction

  • Metabolic factors appear to override the myogenic mechanism in circumstances in which the metabolic demands of the tissues are significantly increased
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6
Q

What is NO synthesized from?

A

L-Arginine

O2 + L-Arginine → NO + L-Citrulline (via NOS)

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7
Q

What is the half-life of NO?

A

6 seconds

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8
Q

Explain how NO cause vasodilation.

A

NO activates guanylate cyclase → converts cGTP to cGMP (important second messenger) → cGMP activates cGMP-dependent protein kinase → vasodilation

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9
Q

What stimulates eNOS?

A

1) Shear stress
2) Vasoactive substances (e.g. acetylcholine, bradykinin, adenosine, substance-P)

  • Associated with increased intracellular Ca2+/calmodulin
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10
Q

True or False: Angiotensin II, a potent vasoconstrictor, can stimulate NO production.

A

True

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11
Q

What is iNOS?

A

It is inducible nitric oxide synthase. It does not express in resting cells and needs to be induced by cytokines or microbial products.

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12
Q

Does increased potassium level cause vasoconstriction or vasodilation?

A

Vasodilation

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13
Q

Does increased magnesium level cause vasoconstriction or vasodilation?

A

Vasodilaiton

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14
Q

Does increased calcium level cause vasoconstriction or vasodilation?

A

Vasoconstriction

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15
Q

Does increase plasma hydrogen ion concentration cause vasoconstriction or vasodilation?

A

Mild arterial vasodilation

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16
Q

Does increase plasma CO2 concentration cause vasoconstriction or vasodilation?

A

Moderate vasodilation peripherally, marked vasodilation in the brain

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17
Q

Define mean systemic filling pressure.

A

The pressure in the systemic circulation when there is no flow. It is composed of unstressed volume and stress volume.

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18
Q

What is the formula for venous return?

A

Venous return = [(Mean systemic filling pressure - right atrial pressure)/Venous resistance]

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19
Q

Describe Frank-Starling curve.

A

Within certain range, the increased left ventricular end diastolic volume will increase the stroke volume due to the stretch of the myocytes leading to more forceful contraction.

* The foundation concept of fluid responsiveness*

  • x axis: left ventricular end diastolic volume (preload)
  • y axis: stroke volume (or cardiac output)
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20
Q

What is the formula for shock index?

A

Shock index = HR/SBP

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21
Q

What is the shock index to differentiate shock and normal dog?

A

SI ≥ 0.9 → shock

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22
Q

Which electrolyte abnormality is associated with U wave?

A

Hypokalemia

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23
Q

True or False: Hypokalemia leaves the myocardium refractory to the effects of class I antiarrhythmic agents (e.g. lidocaine)

A

True

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24
Q

What is normal arterial oxygen content?

A

20 ml/dL

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25
Q

What is normal cardiac output in dogs and cats?

A

Dog: 125-200 ml/kg/min
Cat: 120 ml/kg/min

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26
Q

What is normal oxygen extraction ratio?

A

20-30%

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27
Q

What is normal DO2 and VO2?

A

DO2: 20-35 ml/kg/min
VO2: 4-11 ml/kg/min

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28
Q

What is the definition of hypotension?

A

SAP < 90 mmHg or MAP < 60 mmHg

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29
Q

What are the 4 organ systems affected by hypertension?

A

Renal
Eyes
Cardiovascular
CNS

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30
Q

When you are able to palpate the femoral pulses, what is the estimated SAP?

A

> 60 mmHg

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31
Q

What is the estimated SAP when you can palpate the dorsal pedal pulses?

A

> 90 mmHg

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32
Q

What blood pressure is Doppler measured? SAP, MAP or DAP?

A

SAP

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33
Q

During Doppler blood pressure measurement, if the limb with the cuff is below the RA, does that cause falsely lower or higher BP?

A

Falsely higher

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34
Q

What is the most reliable reading from standard oscillometry BP measuring?

A

MAP

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35
Q

What is the difference between High-definition oscillometry and standard oscillometry?

A

1) HDO can measure more accurately in a wider range
2) HDO can obtain a more accurate reading in the presence of arrhythmias
3) HDO can obtain SAP, MAP and DAP

HDO devices perform realtime analysis of arterial wall oscillations to obtain pressure wave amplitudes →

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36
Q

Fill in the pressure within each camber & vessel.

A
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37
Q

Describe how to set up a continuous arterial blood pressure monitoring system

A

1) Place an arterial line
2) Prepare a bag of 1L saline with heparin (1-2U/ml), a transducer, a monitor and non-compliant arterial line monitoring extension tube. Attach them together.
3) Fill the entire arterial monitoring system with heparinized saline.
4) Attach the arterial BP monitoring system to the arterial catheter and the monitor.
5) There should be a 3-way stopcock on the arterial BP monitoring system. Turn it to close the patient end and open the monitor end to the atmosphere. Keep the system at the level of RA and zero the system.
6) After the system is zero. Turn the 2-way stopcock to close the opening to the atmosphere and connect the monitor to the patient. You should be able to obtain the arterial waveform.
7) Perform a fast flush test to determine if it is necessary to adjust the system and optimize its dynamic’s response

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38
Q

What are the 3 important steps for arterial BP transducer setup?

A

1) Zeroing
2) Calibration
3) Leveling

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39
Q

Is CVP close to right ventricular systolic pressure or right ventricular diastolic pressure?

A

RV diastolic pressure (= filling pressure of right side of the heart)

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40
Q

What is normal CVP?

A

0 - 5 cmH2O

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41
Q

What are the 3 main factors that can affect CVP?

A

1) Venous return
- Circulating blood volume
- Venous wall compliance
2) Right-sided cardiac diseases
3) Intrathoracic/intraperitoneal pressure

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42
Q

When the CVP is low, what are the two main differential?

A

Vasodilation (venodilation)
Decreased systemic circulating blood volume

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43
Q

When the CVP is normal, beside normovolemia, what are the two other possibilities?

A

Compensated hypovolemia
Compensated hypervolemia

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44
Q

List 10 differentials for elevated CVP

A

1) Hypervolemia
2) Systemic hypertension or marked vasoconstriction
3) Occlusion of the catheter
4) Right sided cardiac disease (e.g. tricuspid regurgitation, right sided systolic dysfunction)
5) Pulmonary hypertension
6) Pericardial effusion
7) Pneumothorax
8) Marked ascitis
9) Pleural effusion
10) Mechanical ventilation (PEEP)
11) Intrathoracic mass

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45
Q

When we place an intravscular catheter for pressure measuring, ideally the catheter should not occupy more than ___% of the lumen. What is that number?

A

10

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46
Q

How many cmH2O equals 1 mmHg?

A

1.36 cmH2O = 1 mmHg

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47
Q

When the animal is in sternal recumbency, how do you estimate the height of RA during the leveling or CVP transducer?

A

Draw a vertical line from sternum to the top of spinous process caudal to the scapula. The RA is at about 40% of the height of the line.

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48
Q

Describe how is the arterial waveform generated?

A

When the pressure waves go through the vessels, the reflection will create multiple oscillating waves with different frequency and amplutide (Fourior series). The arterial waveform is the summation of those oscillating waves

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49
Q

This is arterial blood pressure waveforms. Name 1-6.

A

1: Systolic upstroke
2: Systolic peak pressure
3: Systolic decline
4: Dicrotic notch (incisura)
5: Diastolic runoff
6: End-diastolic pressure

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50
Q

Explain how Dicrotic notch is created.

A

The elastic recoil of the arteries with the closed aortic valves cause a slight and transient increase of the arterial blood pressure.

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51
Q

In an arterial BP waveform, which part indicate MAP?

A

The shaded area beneath the arterial pressure curve

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52
Q

List 5 factors that can affect the patient’s direct arterial BP monitoring reading.

A

1) System’s dynamic response
2) Presence of air bubbles in the tubing
3) Respiration
4) Arrhythmias
5) Catheter location/placement

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53
Q

What are the two major components when it comes to a ABP monitoring system’s dynamic response.

A

1) Natural frequency
2) Damping coefficient

  • They are determined by the system’s physical properties, specifically mass, elasticity, and friction
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54
Q

What happen when the natural frequency of the ABP monitoring system coincides with the natural ABP’s frequency?

A

The reading and the waveform will be exaggerated due to summation of the waveforms → higher SAP and lower DAP → overshooting, ringing

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55
Q

When the natural frequency of an ABP monitoring system is not adequate, it’s usually too low or too high?

A

Too low

  • Ideally need to > 12 Hz or as high as possible
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56
Q

What does damping mean in the ABP monitoring?

A

Loss of the pulse pressure energy when the waves travel from the catheter to the transducer.

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57
Q

List 4 causes of damping in ABP monitoring.

A

1) Friction resistance along the line
2) Absorption of energy by the tubing and system
3) Air bubbles
4) Line occlusion

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58
Q

Does the higher damping coefficient mean more likely to overdamp or underdamp?

A

Higher damping coefficient → more significant of the damping → overdamp

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59
Q

What can we see in overdamped and underdamped arterial waveforms?

A

Overdamped: loss of details (e.g. dicrotic notch), slurred waveform

Underdamped: falsely high SAP and falsely low DAP, extra spikes and details that are non-physiological

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60
Q

What is the natural frequency of this ABP monitoring system?

A

25/1.7 = 14.7 Hz

  • Note the number of blocks between oscillation peaks
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61
Q

Describe how to determine the damping coefficient with this figure.

A

17/24 = 0.71 (amplitude ratio)
According to the chart, the damping coefficient is 0.11

  • Measure the length of two successive oscillations (i.e., from peak to valley, and from that same valley to the next peak).
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62
Q

How many oscillations after the fast flush in the fast flush test will be considered underdamping?

A

> 2 oscillations

  • Normally should be 2 oscillations
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63
Q

Does air bubbles cause underdamp or overdamp?

A

Very small air bubble may cause underdamp
Large bubble will cause overdamp

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64
Q

As the arterial waveforms move from central to peripheral, does the systolic peak gets higher or lower? What about the end-diastolic pressure?

A

Initial upstroke becomes steeper
Systolic peak gets higher
End-diastolic pressure gets lower

  • The waveform is delayed; the dicrotic notch appears later and appears more slurred
  • distal pulse amplification
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65
Q

During mechanical ventilation, does the pulse pressure decrease or increase during inspiration?

A

Increase

  • The opposite during spontaneous ventilation
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66
Q

What are the three hallmarks for arterial waveforms in aortic stenosis?

A

1) Systolic upstroke becomes less steep
2) Loss of dicrotic notch
3) The systolic peak pressure may decrease in severe case

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67
Q

What are the three hallmarks for arterial waveforms in aortic regurgitation?

A

1) Very steep systolic upstrokes
2) Increased pulse pressure
3) Decreased end-diastolic pressure

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68
Q

Explain what Corrigan pulse is and list four conditions that we may observe it clinically.

A

Corrigan’s pulses is the rapid elevated and collapse pulse (increased pulse pressure but very short duration for each pules).

Aortic regurgitation, PDA, severe anemia, hypertension

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69
Q

When the ABP monitoring shows hypotension, list 5 steps you would do to check it.

A

1) Examine the patient to see if the patient’s clinical signs fit hypotension
2) Check the ABP tubing to see if there is any kink, blood clot or air bubbles
3) Check the pressured fluid bag to make sure the pressure is higher than 250 mmHg
4) Check if the arterial catheter is patent
5) Check if the patient’s position has change and if re-zeroing is needed.

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70
Q

Describe how to set up a CVP monitoring system (with water manometer).

A

1) Flush the patient’s central venous catheter with heparinized saline to make sure it’s patent
2) Keep the water manometer vertical (can use an IV pole). Collect the three way stopcock with manometer, fluid set and tubing toward the CVC (do not connect yet)
3) Close the manometer end. Fill the entire non-compliant tubing with normal saline. Connect the tubing to CVC.
4) Close the patient end. Fill the water manometer with 10-20 cm of normal saline.
5) Keep the zero marker of the water manometer at the level of right atrium.
5) Close the fluid set end. Allow the water manometer and patient’s end to equilibrate.

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71
Q

how many percentage of systemic blood volume is in the venous system?

A

65%

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72
Q

What is the formula for transmural pressure?

A

Transmural pressure = intravascular pressure - extravascular pressure

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73
Q

When using CVP to assess volume responsiveness, what is expected to see in euvolemic patient (i.e. how many cmH2O CVP will increase? how long does it take to return to baseline?)?

A

CVP usually will increase 2-4 cmH2O and will return to baseline after 15 min

  • Hypovolemic patient → CVP rises minimally or rapidly returns to baseline
  • CVP takes longer to return to baseline → volume overload, cardiac dysfunction, restrictive pericardial disease
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74
Q

Name which cardiac cycle/phase are those waves and descents represent and what happen to the heart during that cycle/phase.

A

a wave: end-diastolic; right atrial contraction
c wave: early-systolic; isovolumetric ventricular contraction; tricuspid valves are pushed toward RA
x descent: mid-systolic; right atrial relaxation
v wave: end-systolic; systolic filling of RA (venous return)
y descent: early-diastolic; early ventricular filling

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75
Q

What is the formula to estimate CVP from the waveform?

A

CVP = (a wave peak + x descent base)/2

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76
Q

What change of CVP waveform can we see in patient with VPCs?

A

Cannon “a” wave

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77
Q

What change of CVP waveform can we see in patient with atrial fibrillation?

A

Absence of a wave

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78
Q

What change of CVP waveform can we see in patient with tricuspid regurgitation?

A

Broad, tall systolic c-v wave, beginning in early systole and obliterating the systolic x descent in atrial pressure.

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79
Q

Name the function of the Swan-Ganz catheter ports from top to bottom.

A
  • Thermistor port
  • Measure CVP (blue; proximal)
  • Measure pulmonary artery pressure, collect sample for SvO2 (yellow)
  • Drug administration port
  • Balloon inflation port; measure PAWP (red)
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80
Q

Define preload and afterload.

A

Preload: a measure of the ventricular myocardium stretch at the end of diastole
Afterload: the force/resistance which the ventricles need to overcome to eject the blood

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81
Q

What is the formula for cardiac index?

A

Cardiac index (L/min/m2) = cardiac output/body surface area in m2

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82
Q

What is Fick’s principle and what is the formula modified from this principle to measure cardiac output?

A

Total uptake of the oxygen by the peripheral tissues equal the product of total blood flow through the tissues and the arteriovenous oxygen concentration difference.

  • it can also be used for CO2 production
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83
Q

What is the formula when using CO2 rebreathing method to measure cardiac output

A
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84
Q

When using thermodilution to measure cardiac output, where is the indicator (saline) injected and where is the dilution measured?

A

Injection: right atrium
Measurement: main pulmonary artery

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85
Q

What is transesophageal echocardiography measured to evaluate the cardiac output?

A

Cross-section area of left ventricular outflow tract & aortic blood velocity

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86
Q

What is mean pulmonary artery pressure in dogs?

A

10-20mmHg

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87
Q

What is normal cardiac index in dogs?

A

3.5 - 5.5 L/min/m2

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88
Q

What is normal stroke volume in dogs?

A

40-60 ml/beat/kg

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89
Q

What is normal SVR and Pulmonary vascular resistance?

A

SVR: 0.5-0.8 mmHg/kg/min
PVR: 0.04-0.06 mmHg/kg/min

10x difference!

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90
Q

What is normal pulmonary arterial wedge pressure in dogs?

A

5-12 mmHg

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91
Q

List 7 potential errors that can cause inaccurate CO measurement when using thermodilution method.

A
  • Arrhythmias
  • Respiration (ideally measure at end-expiration)
  • Intracardiac shunt
  • Thermistor probe problems (malfunction, got blood clote)
  • Severe hypotension
  • Inadequate indicator injection
  • Concurrent large volume fluid/med administration
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92
Q

For the CO measurement using CO2 rebreathing method, what is the name of the monitor? What is the formula used in this monitor to calculate CO?

A

NICO

  • The equation is for partial rebreathing technique
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93
Q

This is the graphs for thermodilution result. Which one indicates low cardiac output, and which one indicates high cardiac output?

A

b) indicates high cardiac output
c) indicates low cardiac output

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94
Q

List 4 possible complications for thermodilution method.

A

1) valve damage, endocarditis
2) rupture of RA or PA
3) blood clot formation, air embolism
4) arrhythmias

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95
Q

What technique does PICCO use to measure CO?

A

Transpulmonary thermodilution
- Inject a cold fluid bolus in jugular vein and measure its changes in femoral artery
- It can also analyze the pulse waveform contour and therefore obtain more information (e.g. preload, afterload…etc)

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96
Q

How does LiDCO measure CO?

A

Inject a fixed dose of lithium chloride and then has a lithium-selective electrode placed at the peripheral arterial catheter
- It can also analyze the arterial pulse waveform

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97
Q

What are the two CO monitor system that integrate arterial waveform?

A

PiCCO
LiDCO

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98
Q

True or False: When using Fick’s principle to measure CO, the result won’t be accurate if there is a shunt.

A

True

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99
Q

Describe how to place a Swan-Ganz catheter.

A

1) Attach ECG to the patient
2) Clip and aseptically prepare the jugular vein. Fill the introducer with heparinized saline and Insert the introducing catheter.
3) Attach distal catheter port to pressure transducer via a three-way stopcock and flush the system with heparinized saline.
4) Attach continuous flush line to the transducer and pressurize the bag to ≥200 mm Hg.
5) Zero the pressure transducer.
6) Insert the thermodilution catheter through the introducer catheter to about 20 cm and verify that the pressure tracing reflects a central venous pressure waveform.
7) Advance the catheter with the natural curve of the catheter aimed toward the sternum of the animal; watch for a typical ventricular waveform.
8) If the catheter advances to the 50-cm mark without entering the right ventricle, withdraw it to the 20-cm mark and start again.
9) If the pressure tracing becomes damped, flush the distal port with the transducer’s fast flush device; if the pressure tracing abruptly ceases followed by a rapid, linear increase, the end-hole has butted up against a vessel or heart chamber wall and should be withdrawn slightly and then reinserted.
10) Once the catheter tip has entered the right ventricle, inflate the balloon with 1 mL of air and advance it further until the pressure waveform indicates that the catheter tip has entered the pulmonary artery.
11) With the balloon inflated, advance the catheter until the pressure tracing reflects occlusion of a branch of the pulmonary artery; deflate the balloon and verify a good pulmonary artery tracing.
12) Bandage the catheter and introducer set aseptically and occlusively.

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100
Q

What is normal arterial and venous oxygen content in dogs?

A

Arterial: 17.8 ml/dL
Venous: 14.2 ml/dL

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101
Q

As the Swan-Ganz catheter enters the heart and advances slowly, what are the pressure waveform change do you expect to see? Order them from the beginning to the end.

A

C → D → A → B

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102
Q

Comparing the PAWP and CVP, the c wave is more difficult to discern in PAWP. List 2 reasons to explain why.

A
  • Damping when the waveform travels from LA to pulmonary artery
  • ## There is shorter time between LA contraction and LV contraction compared to RA & RV contraction → a & c waves may superimposed
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103
Q

List 4 ECG abnormalities that can be seen in hypokalemic patient.

A

1) Atrial/ventricular tachyarrhythmias
2) Prolonged QT interval
3) Decreased T wave amplitude
4) ST segment elevation/depression

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104
Q

What is the ECG abnormalities that can be seen in hypocalcemia?

A

Prolong QT interval

  • If hypercalcemia → shortening of QT interval
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105
Q

When patient experiences hypertension crisis, how fast shouldn’t the BP drop?

A

No more than 25% in 1 hour

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106
Q

What is the formula for Reynold’s number? What is it used for?

A

It is used to evaluate the tendency of turbulence to occur

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107
Q

What is the cutoff of Reynold’s number for the turbulence at the branch of vessels?

A

200-400

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108
Q

What is the cutoff of Reynold’s number for definitive turbulence no matter branch or smooth vessel?

A

> 2000

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109
Q

What is the formula for Poiseuille’s law?

A
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110
Q

In the systemic circulation, where do most of the systemic resistance occur?

A

Small arterioles (2/3 of total resistance)

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111
Q

Between what blood pressure range can the blood vessels maintain relatively constant flow rate via autoregulation?

A

75 - 175 mmHg

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112
Q

True or False: Pulse pressure = Stroke volume/arterial compliance.

A

True

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113
Q

Name 3 blood reservoirs.

A

1) Spleen
2) Liver
3) Large intra-abdominal veins
4) Venous plexus under the skin

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114
Q

True or False: Lymph from the entire body all flows into the thoracic duct, which empties the lymph into the venous system at the junction of left internal jugular vein and left subclavian vein.

A

False.

The lymph from right side of the neck and head, right arm, and parts of the right thorax flows into the right lymph duct → right subclavian vein and internal jugular vein

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115
Q

Where does vasomotor center locate?

A

Medulla and lower 1/3 of the pons

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116
Q

True or False: Under normal condition, there is continuous partial constriction of blood vessels caused by sympathetic nerve. This is called vasomotor tone.

A

True

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117
Q

True or False: The vasomotor center can not only control vascular tone but also the heart rate.

A

True

From Guyton: “The lateral portions of the vasomotor center tran mit excitatory impulses through the sympathetic nerve fibers to the heart when there is a need to increase heart rate and contractility. Conversely, when there is a need to decrease heart pumping, the medial portion of the vasomotor center sends signals to the adjacent dorsal motor nuclei of the vagus nerves, which then transmit parasympathetic impulses through the vagus nerves to the heart to decrease heart rate and heart contractility.”

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118
Q

True or False: The baroreceptors response is linear to the blood pressure.

A

False

When BP below 50-60 mmHg, baroreceptors at the carotid sinus do not respond.
When BP below 30 mmHg, baroreceptors at the aortic arch do not respond.

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119
Q

Explain how the circulatory reflex work after it is initiated by the activated baroreceptors.

A

The baroreceptor signal enters the vasomotor center → the secondary signal inhibits the vasoconstrictor center and stimulates the vagal parasympathetic center → vasodilation, decrease heart rate and contractility

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120
Q

List 3 conditions that will activate the chemoreceptors.

A

1) Low oxygen
2) High CO2
3) Increased H+ ion

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121
Q

Where do chemoreceptors locate?

A

2 carotid bodies locate at the carotid bifurcation; 1-3 aortic bodies locates adjacent to the aorta

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122
Q

List 3 mechanisms of how the low pressure baroreceptors (especially atrial receptors) regulate high blood volume.

A

1) Cause afferent renal vasodilation → increase GFR and fluid filtrated through the glomerulus
2) Decrease ADH release → decrease water reabsorption
3) Release atrial natriuretic peptide → decrease sodium and water reabsorption at the nephrons

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123
Q

Describe Bainbridege reflex.

A

Increased atrial pressure leads to increased heart rate and contractility.

  • The afferent limb of the reflex within this signal, when activated takes sensory information from the vagus nerve to medulla oblongata, and the efferent limb sends out inhibitory signals by reducing vagus nerve tone and increasing the sympathetic outflow.
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124
Q

What is the reflex associated with the respiratory sinus arrhythmia?

A

Bainbridge reflex vs vagal reflex?

Inspiration → increased HR
Expiration → decreased HR

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125
Q

What happen to heart rate and BP during CNS ischemic response?

A

Increased sympathetic tone → HR and BP elevate

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126
Q

How will the cardiac output curve and venous return curve change during sympathetic stimulation?

A
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127
Q

When does the S1 heart sound happen?

A

When the mitral and tricuspid valves close
Isovolumetric contraction

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128
Q

When does the S2 heart sound happen?

A

When the aortic and pulmonic valves close
Isovolumetric relaxation

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129
Q

Explain the splitting S2.

A

S2 heart sound is composed of closing of aortic valve and closing of pulmonic valve. Aortic valve usually close very slightly before pulmonic valve.
During inspiration, the intrathoracic pressure decreased → increased venous return → more blood in the RV → pulmonic valve open for a bit longer because more RV volume → less blood return to LA → slightly decreased LV volume → aortic valve closes earlier due to shortening emptying time

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130
Q

What is S3 heart sound and when does it usually happen?

A
  • It is also called ventricular gallop
  • When mitral or tricuspid valves open and the blood is passively filling the ventricular → S3 is the sound when the large volume of blood strikes a very compliant ventricle
  • Early diastole
  • Often heard in dogs with DVM
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131
Q

What is S4 heart sound and when does it usually happen?

A
  • It is also called atrial gallop
  • When atria contracts to force the blood into a very non-compliant ventricle
  • End diastole
  • Often heard in cats with HCM
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132
Q

What is the resting membrane potential for ventricular myocardium? What about SA nodal cells?

A

Ventricular myocardium: -85 mV
SA nodal cells: -55 ~ -60 mV

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133
Q

Which one is RBBB and which is LBBB?

A

A: LBBB
B: RBBB

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134
Q

List 3 differences between myocardium and skeletal muscles.

A

1) action potential of myocardium is caused by fast sodium channels and L-type calcium channels; AP of skeletal muscles is caused by fast sodium channels only
2) The source of Ca in myocardium is from extracellular space; while in skeletal muscles it’s from endoplasmic reticulum
3) There is no plateau phase in skeletal muscle AP

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135
Q

Name each phase and describe how electrolytes move in each phase.

A

0: depolarization; fast Na channel open
1: initial repolarization; fast Na channel close, transient outward K channel open
2: plateau; L-type Ca channel open, transient outward K channel close
3: rapid repolarization; L-type Ca channel close; slow K channel open
4: resting membrane potential; slow K channel closes, inward rectifier K channel open

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136
Q

Describe how excitation-contraction coupling happens.

A

1) Action potential reaches the T tubules system which leads to depolarization
2) The voltage change will be sensed by dihydropyridine (DHP) receptors which link to the ryanodine receptor channels (Ca release channels) on the sarcoplasmic reticulum
3) The Ca release channels open and release many Ca ions and cause contraction
4) Ca ions are re-uptaken by active calcium channels called SERCA (sarcoplasmic reticulum Ca2+-ATPase). Ca ions are bound with calsequestrin in the sarcoplasmic reticulum

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137
Q

What is the main difference between myocardium and skeletal muscle excitation-contraction coupling process?

A

The Ca storage in the myocardium sarcoplasmic reticulum is not as abundant as skeletal muscles. The Ca ion inflow during the plateau phase of AP triggers the Ca release from the sarcoplasmic reticulum and the Ca from both extracellular fluid and SR cause muscle contraction

  • Myocardial contractility is heavily dependent on the extracellular Ca ion concentration
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138
Q

During myocardial excitation-contraction coupling process, what are the two ways to lower Ca concentration in the cells?

A

1) SERCA2 (sarcoplasmic reticulum Ca2+-ATPase)
2) Na-Ca exchanger on the sacrolemma

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139
Q

Draw the Wigger’s diagram.

A
140
Q

How many percentage of blood in the ventricle is contributed by atrial filling?

A

20%

141
Q

What is ejection fraction (EF) and what is the formula? What is normal EF in dogs and cats?

A

Ejection fraction is the fraction of the blood in the ventricular chamber that is ejected during systole in relation to the total blood volume during end-diastole

EF = SV/LVEDV

Normal EF in dogs and cats: 50-70%

142
Q

What is the difference between LV and RV pressure.

A

RV is about 1/6 of LV

143
Q

On the heart, where do the parasympathetic nerves innervate?

A

atria

144
Q

How does SA node generate its self-excitation AP?

A

Slow Na channel is very leaky and can cause continuous slow Na inflow. When the membrane potential reaches -40 mV, L-type Ca channels open, causing depolarization and generation of AP.

145
Q

Compare the waveforms, different phases and electrolytes movement in each phases between ventricular and SA nodal AP.

A
146
Q

What is hepatojugular reflex and what does it indicate?

A

Hepatojugular reflex means when the pressure is applied on the liver, the jugular vein becomes distended.
Positive hepatojugular reflex means the heart cannot compensate with increased venous return.

147
Q

According to ACVIM Consensus Statement, systemic hypertension has three categories, what are them?

A

Situational hypertension
- White coat hypertension
Secondary hypertension (most common)
Idiopathic hypertension

148
Q

List 5 diseases process that can cause systemic hypertension in dogs and cats.

A

Cushing disease
Hyperthyroidism
Chronic kidney disease
AKI
Pheochromocytoma
DM
Primary hyperaldosteronism

149
Q

List 5 medications that can cause systemic hypertension in dogs and cats

A

Glucocorticoid
Vasopressin
Epinephrine
Phenylephrine
Minerocorticoid
EPO
Phenylpropranolamine

150
Q

True or False: ACVIM Consensus Statement recommends routine screening of systemic hypertension in dogs and cats.

A

False

  • Patients > 9yrs will be reasonable
151
Q

According to ACVIM Consensus Statement, SBP above what is considered severe hypertension?

A

> 180 mmHg

152
Q

According to ACVIM Consensus Statement, when the initial SBP is < 160mmHg, what is the recommended follow-up plan?

A

Recheck in 3-6 months

153
Q

According to ACVIM Consensus Statement, when the initial SBP is between 160-179mmHg without TOD, what is the recommended follow-up plan?

A

Recheck twice in 8 weeks & recheck for TOD
If the SBP is still persistently above 160mmHg, antihypertensive therapy is recommended.

154
Q

According to ACVIM Consensus Statement, when the initial SBP is > 180mmHg without TOD, what is the recommended follow-up plan?

A

Recheck twice in 14 days & recheck for TOD
If the SBP is still persistently above 160mmHg, antihypertensive therapy is recommended.

155
Q

According to ACVIM Consensus Statement, what are the two main goals for antihypertensive therapy

A

1) Minimize the risk of TOD (SBP ≤ 140 mmHg; optimal goal)
2) Maintain the SBP ≤ 160 mmHg (minimal goal)

156
Q

According to ACVIM Consensus Statement, when you start a anti-hypertensive therapy, what is the recommended follow-up plan?

A

Recheck BP in 7-10 days if no TOD
Recheck BP in 1-3 days if TOD presents

*If BP < 160 mmHg on recheck, the next recheck can be 4-6 months.

157
Q

Why calcium channel blocker should not be used as a monotherapy in dogs for hypertension management?

A

Because calcium channel blockers mainly cause renal afferent arteriole dilation → may increase the glomerulus capillary hydrostatic pressure

158
Q

What is the possible limitation of combining calcium channel blocker and ACE inhibitors or ARB for canine hypertension management?

A

Calcium channel blockers mainly cause renal afferent arteriole dilation; ACE inhibitors and ARB mainly cause renal efferent arteriole dilation → may not make much change of the glomerulus capillary hydrostatic pressure

159
Q

What is the first choice of antihypertensive drugs for dogs and cats, respectively?

A

Dogs: ACE inhibitor
Cat: calcium channel blocker (because of established efficacy)

160
Q

In cats with systemic hypertension, what is the key predictive factor for survival?

A

Proteinuria

  • As a result, ACEi is not the first line anti-hypertensive therapy in cats because it may worsen proteinuria
161
Q

According to ACVIM Consensus Statement, what is the recommended antihypertensive therapies for cats with hyperthyroidism?

A

Amlodipine
Beta blocker

162
Q

What are the two criteria for systemic hypertension that indicate emergency intervention?

A

1) SBP > 180 mmHg
2) Signs consistent with intracranial TOD

163
Q

What is the MOA for fenoldopam?

A

Dopamine-1 receptor agonist -> vasodilation

Dose: 0.1 μg/kg/min with careful (ie, at intervals of at least 10 minutes) monitoring of BP. The dosage can be titrated up by 0.1 μg/kg/min increments every 15 minutes to the desired SBP, to a maximal dosage of 1.6 μg/kg/min

164
Q

What is the MOA for hydralazine?

A

Direct smooth muscle relaxant

Dog: 0.1 mg/kg IV over 2 minutes, followed by a CRI of 1.5-5.0 μg/kg/min
Cat: 1.0-2.5 mg per cat SC

165
Q

What is the main difference between nitroprusside and nitroglycerin?

A

Nitroprusside: arterial and venous dilators
Nutroglycerin: mainly venodilator

166
Q

According to ACVIM Consensus Statement, what are the 5 types of cardiomyopathy phenotypes in cats?

A

1) Hypertrophic cardiomyopathy
2) Restrictive cardiomyopathy
- Endomyocardial form vs Myocardial form
3) Dilated cardiomyopathy
4) Arrhythmogenic cardiomyopathy
5) Nonspecific phenotype

167
Q

What are the two cardiomyopathy phenotypes that can be caused by hyperthyroidism?

A

HCM, RCM

168
Q

What are the staging and definition of cardiomyopathy in cats?

A

A: Predisposed
B1: Subclinical with low risk of developing CHF/ATE (normal, mild atrial enlargement)
B2: Subclinical with high risk of developing CHF/ATE (moderate, severe atrial enlargement)
C: Current/previous CHF/ATE
D: Refractory CHF

169
Q

What is the prevalence of HCM in cats?

A

15%

  • 29% in older cats
170
Q

What is the 5-year cumulative mortality rate in cats with HCM?

A

23%

171
Q

What are the breeds that are predisposed to HCM?

A

Maine Coon, Ragdoll, British Shorthair, Persian, Bengal, Sphynx, Norwegian Forest cat, Birman

172
Q

According to ACVIM Consensus Statement, in cats with HCM, what are the markers of increased risk of CHF/ATE?

A

Gallop sound or arrhythmia on PE
Moderate to severe LA enlargement
Decreased LA fractional shortening (LA FS%)
Extreme LV hypertrophy
Decreased LV systolic function
Spontaneous echo-contrast or intracardiac thrombus
Regional wall thinning with hypokinesis
Restrictive diastolic filling pattern

173
Q

True or False: Dynamic left ventricular outflow tract obstruction (DLVOTO) is a poor prognostic indicator in HCM cat.

A

False

174
Q

True or False: A loud systolic murmur (grade 3-4/6) is more common in cats with HCM than in normal cats, but an increase in heart murmur intensity over time does not necessarily indicate the presence or worsening of disease.

A

True

175
Q

What is the recommended treatment for cat with stage B1 HCM?

A

None

176
Q

What is the recommended treatment for cat with stage B2 HCM?

A

thromboprophylaxis (e.g. clopidogrel; 18.75 mg/cat PO q24h, with food)

  • If patient has rapid ventricular rate or AF → Diltiazem, atenolol or sotalol
177
Q

What is the recommended treatment for cat with stage C HCM?

A

Diuretic
Thromboprophylaxis
Pimobendan may be considered if patient has poor contractility and absent of DLVOTO (or dobutamine CRI)

178
Q

What is the recommended Torsamide dose in cats with CHF?

A

0.1-0.2 mg/kg PO q24h

179
Q

True or False: According to ACVIM Consensus Statement, thrombolytic treatment is not recommended in cats with ATE.

A

True

180
Q

In human, what is the definition of pulmonary hypertension?

A

PAP ≥ 25mmHg at rest

181
Q

What is Bernoulli Equation?

A

Pressure gradient = 4 x velocity^2 (m/s)

182
Q

How do you estimate PAP with echo?

A

Patient needs to have tricuspid regurgitation
Right atrial pressure + Pressure gradient

183
Q

What peak tricuspid regurgitation velocity make the probability of PH intermediate?

A

3.0 - 3.4 m/s

184
Q

According to ACVIM consensus statement, if you want to call the PH is secondary to left-sided heart disease, what are the two additional criteria?

A

1) Evidence of left-sided heart disease
2) Unequivocal LA enlargement

185
Q

What are the 6 classification of PH in dogs?

A

1) Pulmonary arterial hypertension
2) Left-sided heart disease
3) Respiratory disease, hypoxia or both
4) Emboli/thrombus/thromboembolism
5) Parasitic disease (e.g. heart worm)
6) Multifactorial or unclear mechanism

186
Q

What are the two breeds that are predisposed to PH secondary to interstitial lung diseases?

A

West Highland White Terriers
Pekingese dogs

187
Q

According to ACVIM consensus statement, if the PH is secondary to LHD, the use of phosphodiesterase 5 inhibitors (PDE5i) is not recommended as first line treatment.

A

True

188
Q

What is the MOA of sildenafil?

A

It is a phosphadiesterase type 5 inhibitor. Phosphadiesterase type 5 can degrade cGMP to 5’-GMP and decrease the NO vasodilatory function. By inhibiting cGMP degradation, it leads to vasodilation.

189
Q

True or False: Pimobendan is an PDE5 inhibitor.

A

False

Pimobendan is a PDE3 inhibitor

  • PDE3 → vascular smooth muscle
190
Q

What is an example of cause of forward heart failure?

A

DCM

191
Q

What is an example of cause of backward heart failure?

A

degenerative valve disease

192
Q

What kind of cardiac dysfunction can doxorubicin cause?

A

Systolic failure/dysfunction

  • toxic damage to the mitochondria of cardiomyocytes
193
Q

How to measure vertebral heart size (VHS)? What is normal reference in dogs and cats?

A

Compare the sum of cardiac long axis and short axis with vertebral lengths, starting at the cranial border of T4

Dog: < 10.7
Cat: < 8

194
Q

List 4 causes of mechanical systolic dysfunction.

A
  • Subaortic stenosis
  • Hypertrophic obstructive cardiomyopathy
  • Acute mitral regurgitation secondary to ruptured chordae tendineae
  • DCM
195
Q

List 3 causes of mechanical diastolic dysfunction.

A
  • HCM
  • Cardiac tamponade
  • Tachyarrhythmias
196
Q

What is the common histopathologic of endomyocarditis?

A

Neutrophilic inflammation
Fibroplasia

197
Q

How often is SAM detected in cats with HCM?

A

65%

198
Q

What is the normal end-diastolic thickness of the interventricular septum or left ventricular posterior wall?

A

< 6mm

199
Q

Which PE parameter is a prognostic indicator in FATE?

A

Hypothermia

200
Q

In dogs with CHF, what is the definition of diuretic resistance?

A

furosemide dose > 8mg/kg/d

201
Q

How does furosemide enter the renal tubule?

A

Because of a high degree of protein‐binding to albumin, furosemide is not filtered at the glomerulus, but rather is secreted from the blood into the proximal renal tubule by organic anion transporters.

  • NSAIDs can compete with these transporters, hypoalbuminemia can affect the transport

** once furosemide is transported into the nephron lumen, it must remain free of protein interactions so that it can bind to the NKCC transporters on the luminal side of the tubular epithelial cells of the loop of Henle. Diseases such as protein‐losing nephropathies can impair the availability of furosemide to bind to these transporters.

202
Q

Describe how to measure Vertebral left atrial score and what is the normal range in dogs?

A

1) Draw a line from the centro-ventral carina to the most caudal aspect of left atria where it intersects with dorsal border of caudal vena cave on the lateral view.
2) Transport the line to the cranial edge of T4 vertebral body.

VLAS ≥ 3 → likely h

203
Q

What is the cutoff of VLAS to diagnose dog with stage B2 MMVD?

A

VLAS ≥ 2.5 (sensitivity 100%)
VLAS ≥ 3 (specificity 100%)

Reference:Mikawa S, Nagakawa M, Ogi H, Akabane R, Koyama Y, Sakatani A, Ogawa M, Miyakawa H, Shigemoto J, Tokuriki T, Toda N, Miyagawa Y, Takemura N. Use of vertebral left atrial size for staging of dogs with myxomatous valve disease. J Vet Cardiol. 2020 Aug;30:92-99.

204
Q

In Doberman Pinscher, what kind of protein deficiency is a common cause for their DCM?

A

calstabin-2

205
Q

In Doberman Pinscher with DCM, What are the two poor prognostic indicators?

A

Atrial fibrillation
Bilateral CHF

206
Q

In Boxer, what kind of protein deficiency has been associated with the cause for their ARVC?

A

Striatin

207
Q

What is the common ECG findings in Boxers with ARVC?

A

Morphology of LBBB on lead I, II, III and aVF

208
Q

What are the two medications commonly used in Boxer ARVC treatment?

A

Sotalol (1.5-3 mg/kg PO q12h)
Mexiletine (5-8mg/kg PO q8h)

209
Q

What are the two main neurohormonal pathways involved in the CHF pathogenesis?

A

RAAS
SNS

  • Others: natriuretic peptides, endothelin, vasopressin systems
210
Q

Is endothelin a vasoconstrictor or vasodilator?

A

Vasoconstrictor

211
Q

In the pathogenesis of CHF, what is the main counterregulatory system?

A

Natriuretic Peptide system

Atrial natriuretic peptide (ANP) & B-type natriuretic peptide (BNP)

212
Q

List 3 factors that stimulate endothelin production and 3 factors that inhibits endothelin production.

A

Stimulation: shear stress, angiotensin II, epinephrine, vasopressin, thrombin (all the bad things causing vasoconstriction)

Inhibition: NO, atrial natriuretic peptide, prostacyclin, bradykinin, cGMP

213
Q

True or False: Endothelin 1 alters normal calcium cycling within muscle cells and is directly toxic to myocardiocytes.

A

True

214
Q

For concentric and eccentric hypertrophy, which is pressure overload and which one is volume overload?

A

Concentric hypertrophy: pressure overload
Eccentric hypertrophy: volume overload

215
Q

What is the function of phospholamban?

A

It is a SERCA inhibitor

216
Q

List 4 mechanisms of abnormal calcium handling during CHF development.

A

1) Myosin isoform switching
2) Impaired Ca2+ transients and ryanodine function
3) Phospholamban upregulation
4) SERCA downregulation

217
Q

What is the definition of P mitrale and P pulmonale?

A

P mitrale: P wave width >40 msec
- Usually seen in LA enlargement

P pulmonale: P wave height >0.5 mV
- Usually seen in RA enlargement

218
Q

True or False: In CHF management, mixed vasodilator theoretically provides both diuretic and inotrope effects

A

True

219
Q

What are the 4 criteria of cardiac remodeling in stage B2 MMVD?

A
  • Grade 3/6 systolic heart murmur
  • La:Ao ratio in right-sided short axis view in early diastole ≥ 1.6
  • Breed-adjusted VHS > 10.5
  • Left ventricular internal diameter in diastole, normalized by weight (LVIDDN) ≥ 1.7
220
Q

According to ACVIM consensus statement, at which stage of MMVD should the treatment be initiated?

A

Stage B2

221
Q

What is the recommended furosemide CRI rate for CHF?

A

0.66 - 1 mg/kg/hr

222
Q

What are the three most common arrhythmias reported after canine myocardial injuries?

A
  • premature ventricular contractions
  • ventricular tachycardia
  • nonspecific ST segment elevation or depression
223
Q

True or False: ECG abnormalities commonly are delayed in onset for up to 48 hours after blunt chest trauma.

A

True

224
Q

After myocardial injury, when is the earliest time the cTnI can be detected in the circulation? And how long does it last?

A

4-6 hr
7 days

225
Q

What is the dose (including CRI) for procainamide?

A

2-4 mg/kg
10-40 mcg/kg/min

226
Q

What is normal volume for pericardial effusion?

A

0.25 ml/kg

227
Q

What is pulsus paradoxus?

A

Left-ventricular output and systemic arterial pressure normally decrease slightly during inspiration.

Pulsus paradoxus is an exaggeration of this normal pressure difference with respirations; patients with pulsus paradoxus exhibit a fall in arterial pressure during inspiration of 10 mm Hg or more.

228
Q

What are the 5 causes for pericardial effusion?

A

Trauma
Neoplasia
Idiopathic
Coagulopathy
Infectious

229
Q

What is the difference on CVP waveform between constrictive pericardial disease and cardiac tamponade?

A

Both will show tall a and c wave.
In constrictive pericardial disease, the y descent will be tall
In cardiac tamponade, the y descent will be diminished

230
Q

How long of an asystolic pause can cause clinical syncopal episodes?

A

6-8 seconds

231
Q

What is the intrinsic ventricular heart rate for cats?

A

100-140 bpm

232
Q

What is the intrinsic ventricular heart rate for dogs?

A

15-40 bpm

233
Q

True or False: all the valves in the heart is supported by chordae tendinae

A

False

Aortic and pulmonary valves do not have chordae tendinae

234
Q

What dose the EDPVR imply?

A

End-diastolic ventricular pressure volume relationship

It implies ventricular compliance

235
Q

What does ESPVR imply?

A

End-systolic ventricular pressure volume relationship

It implies inotropic state of the heart

236
Q

Explain the mechanism of vagal reflex.

A

The acetylcholine released at the vagal nerve endings
→ Fiber membranes permeability to K+ ↑ ↑ ↑
→ Rapid leakage of K+ out of the conductive fibers
→ Membrane potential more negative
→ Hyperpolarization

237
Q

What is Bradycardia-tachycardia syndrome?

A

Periods of paroxysmal atrial tachycardia followed by a temporary failure of the sinus rhythm to resume when the tachycardia abruptly terminates → overdriven suppression

238
Q

What is Mobitz type I and Mobitz type II AV block?

A

Mobitz type I: progressive prolongation of PR interval before a complete block

Mobitz type II: unexpected irregular absence of QRS complex after P waves

239
Q

How long of the PR interval in dogs and cats will be considered first degree AV block?

A

Dog > 130 msec
Cat > 90 mec

240
Q

What is atropine response test?

A

To evaluate if the arrhythmias if vagal-induced

Atropine 0.04 mg/kg IV, the positive response = 50-100% increase in HR

  • Side effect: dry mouth, mydriasis, constipation, urinary retention
241
Q

List 7 mechanisms of SVT.

A

1) SA nodal reentry
2) Atrial reentry
3) Atrial fibrillation
4) Atrial automaticity
5) Atrioventricular reciprocating tachycardia
6) Junctional automaticity
7) AV nodal reentry

242
Q

What is multifocal atrial tachycardia usually associated with?

A

Pulmonary disease

243
Q

What is the emergency treatment for SVT in dogs?

A

Diltiazem 0.125-0.35 mg/kg slow IV over 2-3 minutes

244
Q

What type of SVT can the cardioversion covert?

A

Reentry

*Not automaticity

245
Q

True or False: Atenolol should be used cautiously in patient with kidney disease due to its renal clearance.

A

True

246
Q

What are the three arrhythmogenic mechanisms for ventricular arrhythmias?

A
  • Reentry
  • Enhanced automaticity
  • Triggered activities
247
Q

What is the definition of sustained VT?

A

VT > 30 sec

248
Q

What are the three most reliable diagnostic criteria of VT?

A

Atrioventricular dissociation
Fusion beats
Capture beats

  • Capture beats: A supraventricular impulse conducting through the normal conduction pathways to the ventricle during an episode of VT or AIVR. The PR interval can be longer than normal.
249
Q

What is E/A ratio used for?

A

It is used to evaluate the LV diastolic function

250
Q

What is normal E/A ratio?

A

0.8 ≤ E/A ratio < 2

251
Q

What does this E/A ratio and shape indicate?

A

Impaired relaxation (grade 1 diastolic dysfunction)

252
Q

If a patient has known diastolic dysfunction and this is the E/A ratio you see, what does it indicate?

A

Pseudonormal filling pattern (grade 2 diastolic dysfunction)

Progressive diastolic dysfunction causes LA pressure to rise. The latter increases the pressure gradient between the left atrium and the left ventricle and will act as a driving force to fill the ventricle during early diastole.

253
Q

If a patient has known diastolic dysfunction and this is the E/A ratio you see, what does it indicate?

A

Restrictive filling pattern (grade 3 diastolic dysfunction)

A further increase in filling pressure will increase the gradient between the left atrium and the left ventricle during early diastole. The E-wave will become even taller and the A-wave shorter. The E/A ratio will be ≥ 2. In severe forms the A-wave may be so small as to be nearly invisible, and the E/A ratio may reach very high values of 5 or more.

254
Q

What are the three places that have the highest concentration of L-type Ca channels?

A

Atria
Vascular smooth muscles
Skeletal muscles

255
Q

Define chronotropic, dromotropic, inotropic, and lusiotropic.

A

Chronotropic: HR
Dromotropic: AV conduction
Inotropic: contractility
Lusiotropic: myocardial relaxation

256
Q

Why does high dose Ca channel blocker cause hyperglycemia?

A

Pancreatic beta cells have L-type Ca channels

257
Q

Where do 𝜷1 receptors primary locate?

A

heart, kidney, adipose tissue

258
Q

How is esmolol metabolized?

A

erythrocyte esterases

259
Q

Why does 𝜷 blocker overdose cause hyperkalemia?

A

1) Inhibit 𝜷1 receptor at the juxtaglomerular cells → decrease renin release → decrease aldosterone formation
2) Inhibit 𝜷2 receptor on the cells membrane → inhibit Na/K-ATPase → decrease potassium uptake

260
Q

True or False: Both Ca channel blocker and 𝜷 blocker can inhibit pancreatic insulin release and cause hyperglycemia.

A

True

261
Q

For Ca channel blocker and 𝜷 blocker overdose, extracorporeal therapy is an option.

A

False

They are both high-protein bound and lipophilic (high Vd)

262
Q

What is the MOA of glucagon being used to treat Ca channel blocker and 𝜷 blocker overdose?

A

Glucagon can bypass 𝜷 receptors and directly activate Gs protein → activates adenylate cyclase (AC) → converts ATP to cAMP → activates protein kinase A (PKA) → enhancing the release of Ca2+ from the sarcoplasmic reticulum

  • Glucagon has inotropic, chronotropic, and dromotropic properties
263
Q

Which side of the aortic valve are most susceptible to infective endocarditis (ventricular vs aortic)? Which side of the mitral valve are most susceptible to infective endocarditis (atrial vs ventricular)?

A

Ventricular side of the aortic valve
Atrial side of the mitral valve

264
Q

What are the two common inciting causes for infective endocarditis?

A

Subaortic stenosis
Cardiac catheterization procedure

265
Q

How dose the cardiac valve get infected?

A

Mechanical damage/Inflammation → disruption of the endothelium → exposed extracellular matrix proteins, thromboplastin, tissue factor → activates coagulation cascade (fibrinogen, fibrin, platelet) → blood clot is formed and can bind bacteria → fibronectin binding triggers endothelial cell internalization and local pro- inflammatory and procoagulant responses → endothelial cell expression of integrins → bind bacterias and fibronectin to the extracellular matrix

266
Q

Staphylococcus and Streptococcus spp have a specific receptors which make them common organisms for infective endocarditis. What is that receptor?

A

Microbial surface components recognizing adhesive matrix molecules (MSCRAMMS)

267
Q

What are the two immune-mediated diseases that are commonly seen with infective endocarditis?

A

Polyarthritis
Glomerulonephritis

268
Q

In Bartonella infected endocarditis, which valve is primarily involved?

A

Aortic valve

269
Q

In infective endocarditis, what is the 4 mechanisms that the bacteria evade the host immune system?

A

1) Fibrinous vegetative lesion
- Shields bacteria from the blood stream and host defenses
- Provides a barrier for antibiotic penetration
2) Be resistant to platelet bactericidal protein
3) Internalize within the endothelial cells (e.g. S. aureus, Bartonella)
4) Colonize RBC without causing hemolysis (e.g. Bartonella)

270
Q

What are the three most common pathogens for infective endocarditis?

A

1) Staphylococcal spp (aureus, intermedius, coagulase positive, and coagulase negative)
2) Streptococcus spp (canis, bovis, and ß-hemolytic)
3) E. coli

271
Q

What is the most important Bartonella specie causing infective endocarditis in dogs?

A

Bartonella vinsonii ssp. berkhoffii

272
Q

What is the common murmur associated with infective endocarditis?

A

Diastolic murmur

273
Q

In infective endocarditis, which valve involvement indicates worse prognosis?

A

Aortic valve

274
Q

How long is the recommended treatment duration for infective endocarditis?

A

6-8 weeks

  • IV for the first 1-2 weeks
  • Higher end of the dose range
275
Q

True or False: Dogs with Bartonella IE have shorter survival times compared to other organisms.

A

True

276
Q

What are the three risk factors associated with higher mortality in infective endocarditis? What factor is associated with survival?

A

1) Thromboembolic event
2) AKI
3) CHF

1) administration of antithrombotic

Reagan KL, et al. Outcome and prognostic factors in infective endocarditis in dogs: 113 cases (2005-2020). J Vet Intern Med. 2022;36(2):429-440.

277
Q

Describe how to perform blood culture.

A

1) Three or four samples from different puncture sites should be clipped and aseptically prepared (e.g. cephalic vein, lateral saphenous vein, jugular vein)
2) The timing of sample collection should be at trough if patient is already on antibiotics
3)The person who performed venipuncture should wear sterile glove and the 5-10ml of blood should be collected from each site with 30 minutes to 1 hours apart.
4) The blood samples are aseptically put in the sealed vial for aerobic, anaerobic bacteria and Bartonella spp.

278
Q

In Modified Duke Criteria, what are the 4 major criteria and 7 minor criteria?

A

Major criteria
1) Positive echocardiogram - vegetative, oscillating lesion, erosive lesion, abscess
2) New valvular insufficiency
3) More than mild aortic insufficiency in the absence of subaortic stenosis
4) Positive blood culture
≤ 2 positive blood cultures
≥ 3 with common skin contaminant

Minor criteria
1) Fever
2) Medium to large dog (> 15 kg)
3) Subaortic stenosis
4) Thromboembolic disease
5) Immune-mediated disease
Polyarthritis
Glomerulonephritis
6) Positive blood culture not meeting major criteria
7) Bartonella serology ≥1:1024

279
Q

What is the definitive diagnosis for infective endocarditis according to Modified Duke Criteria? What is possible?

A

Definitive
1) Histopathology
2) Two major
3) One major + two minors

Possible
1) One major + one minor
2) Three minors

280
Q

What is normal MEA in dogs and cats?

A

Dog: +40 - +100
Cat: 0 - +160

281
Q

What is the difference between cardioversion and defibrillation?

A

Cardioversion: delivery the energy that is synchronized to the QRS complex

Defibrillation: Asynchronously deliver the energy to terminate the life-threatening arrhythmias

282
Q

When is the timing to deliver a shock during cardioversion?

A

The peak of R wave (absolute refractory period)

283
Q

What is the usual energy dose for cardioversion?

A

1-2 J/kg

284
Q

Which power source is effective at terminating ventricular fibrillation? AC or DC or both work?

A

DC

285
Q

What is the main complications of cardioversion?

A

V fib

286
Q

What are the 3 ways to perform temporal pacing?

A

Transvenous
Transesophageal
Transcutaneous

287
Q

What is the MOA for Digoxin?

A

1) positive inotropic (by inhibiting Na-K ATPase → increased intracellular Na → increased intracellular Ca
2) Decreased AV conduction: vagomimic effect

288
Q

Why does hypokalemia increase the risk of digoxin toxicity?

A

digoxin binds at the K site of Na-K ATPase
During hypokalemia, there are not that many potassiums competing with Dogoxin → increased toxicity

289
Q

What are the three subunits of cardiac troponin and what are their functions?

A

Cardiac troponin T: bind to tropomyosin and secure it to the thin filament
Cardiac troponin I: inhibitory the hydrolysis of ATP → inhibit myosin and actin interaction
Cardiac troponin C: binding site for calcium to remove the blockage of filament interaction

290
Q

Which troponin subunit is not a good biomarker for myocardial injury. Why?

A

Troponin C, because the skeletal and myocardium have very similar isoforms

291
Q

Are troponin intracellular or extracellular protein?

A

Intracellular protein

292
Q

If there is myocardial injury, how soon can the elevated cardiac troponin to be detected?

A

2-3 hours after injury
peak at 18-24 hours

293
Q

There are two pools for cardiac troponin, which are structural pool and cytosolic pool, which one contains the majority of troponin at normal state?

A

Structural pool

294
Q

After a cardiac insult, which cardiac troponin will have higher concentration in the circulation, troponin I or T?

A

Troponin I

295
Q

What are the 6 mechanisms of troponin release?

A

Dying cells
- Necrosis
- Apoptosis
- Cell turnover

Viable cells
- Increased permeability
- Formation of vesicles
- Increased proteolysis

296
Q

What are the two breeds that inherently have higher cTnI concentration?

A

Boxers
Greyhounds

297
Q

What are the two proposed pathways for troponin elimination?

A

Reticulo-endothelial system
Renal clearance

298
Q

True or False: Troponins have limited value in diagnosing primary heart diseases.

A

True

299
Q

True or False: Critically ill patients with noncardiac disease often have higher troponin concentrations than patients with severe primary cardiac disease.

A

True

Non-cardiac myocardial injury&raquo_space;> primary cardiac diseases

300
Q

True or False: CTnI can be elevated in dogs with renal diseases.

A

True

301
Q

What are the three conditions that may enhance lidocaine’s antiarrhythmic effect?

A

1) acidic environment
2) increased extracellular K+ concentration
3) partial depolarized cells

302
Q

Which class of antiarrhythmics does lidocaine belong to?

A

IB

303
Q

How is mexiletine metabolized?

A

renal excretion

304
Q

What are the different effect on QT interval between IA, IB and IC antiarrhythmic drugs?

A

IA (moderate): cause QT prolongation
- Because it cause moderate blockade of the rapid component of the delayed rectifier K+ current
IB (weak): cause QT shortening
IC (strong): no effect on QT interval

305
Q

What is the MOA of 𝜷-blocker as antiarrhythmic agent?

A

Inhibit the inflow Ca current
Inhibit the funny current

306
Q

Is Esmolol 𝜷1 or 𝜷2 blocker?

A

𝜷1

307
Q

Is Atenolol 𝜷1 or 𝜷2 blocker? How is it eliminated?

A

𝜷1, excreted by kidney

308
Q

Is Sotalol 𝜷1 or 𝜷2 blocker?

A

It is K channel blocker and also non-selective 𝜷 blocker

309
Q

How dose Class I antiarrhythmics work?

A

Sodium channel blocker,
Slows the rate and amplitude of initial rapid depolarization, reduces cell excitability, reduces conduction velocity.

310
Q

Why does sotalol have less negative inotrope effect than propanolol?

A

Because sotalol is also a K channel blocker → AP prolongation allows more Ca to enter the cell

311
Q

Which two classes of antiarrhythmics can slow AV nodal conduction?

A

Class II, IV

312
Q

What is the MOA of pimobendan?

A
  • Phosphodiesterase III inhibitor
  • Calcium sensitizing effect (increase phosphorylation of phospholamban, L-type Ca channels and Ryanodine calcium releasing channels)
313
Q

What are the two major categories of congenital heart diseases?

A

1) Shunting defect
2) Perivalvular defect

314
Q

What is the most common cause of congenital right-to-left shunt in dogs?

A

Tetralogy of Fallot

315
Q

What is Tetralogy of Fallot composed of?

A

Ventricular septal defect (VSD)
Overriding aorta
Pulmonary stenosis
Right ventricular hypertrophy

316
Q

What is the equation for palliative phlebotomy in patient with congenital heart disease and polycythemia? What is the cut-off to perform palliative phlebotomy? What is the target in ER textbook?

A

Volume of the blood remove = body weight x blood volume x (Current PCV-Desired PCV)/Current PCV

*Blood volume: 90 ml/kg (dog); 70 ml/kg (cat)

Cut-off: 70%
Target: 60%

317
Q

What are the three electrolyte imbalance and one endocrine disease that can potentiate digoxin toxicity?

A

1) Hypokalemia
2) Hypomagnesemia
3) Hypercalcemia
4) Hypothyroidism

318
Q

What kind of ECG change indicates procanamide toxicity?

A

25% prolongation of QRS complex

319
Q

True or False: The antiarrhythmic effect of Procanamide is increased by high potassium and decreased by low potassium.

A

True

  • Hyperkalemia strongly enhances procainamide-induced conduction slowing by increasing the interaction between the drug and sodium channels during the rested phase of the cardiac cycle
320
Q

What is the formula to calculate fraction shortening? What is considered normal in dogs and cats?

A

FS (%) = (LV internal diameter at end-diastole - LV internal diameter at end-systole)/LV internal diameter at end-diastole

Normal
- Dog: 25-45%
- Cat: 31-75%

321
Q

List 3 side effects of amiodarone.

A

1) Hepatic toxicity
2) Thyroid dysfunction
3) Arrhythmias

322
Q

What is a specific dermatological complication from spironolactone in cats?

A

Ulcerative facial dermatitis

323
Q

True or False: Hypothermia is a poor prognosis indicator in cats with ATE.

A

True

A rectal temperature of<98.9°F has been shown to predict a < 50% survival probability (in ER textbook)

324
Q

In dogs with heartworm infection, which pulmonary artery does the adult worms most often found?

A

Right caudal lobe artery

325
Q

Describe the current canine heartworm treatment guidelines

A

Day 1:
- Start on prednisone 0.5 mg/kg BID x 1 week, then 0.5 mg/kg SID x 1 week, then 0.5 mg/kg EOD x 2 weeks (if symptomatic)
- Start Doxycycline 10 mg/kg BID x 4 weeks
- Start regular prevention for mosquitos and heartworm

Day 30:
- Apply regular mosquitos and heartworm prevention

Day 31-60:
- A one-month wait period following doxycycline before administering melarsomine is currently recommended as it is hypothesized to allow time for the Wolbachia surface proteins and other metabolites to dissipate before killing the adult worms.

Day 61:
- Apply regular mosquitos and heartworm prevention
- Melarsomine 2.5 mg/kg IM
- Start on prednisone 0.5 mg/kg BID x 1 week, then 0.5 mg/kg SID x 1 week, then 0.5 mg/kg EOD x 2 weeks
- STRICT cage rest

Day 90:
- Apply regular mosquitos and heartworm prevention
- Melarsomine 2.5 mg/kg IM
- Start on prednisone 0.5 mg/kg BID x 1 week, then 0.5 mg/kg SID x 1 week, then 0.5 mg/kg EOD x 2 weeks
- STRICT cage rest

Day 91:
- Melarsomine 2.5 mg/kg IM
- Strict cage rest for 6-8 weeks

Day 120:
- Test for microfilaria

Day 360:
- Antigen test 9 months after last melarsomine injection
- screen for MF
- If still Ag positive, re-treat with doxycycline followed by two doses of melarsomine 24 hours apart

326
Q

What is Kussmaul’s sign?

A

Paradoxical rise in right atrial pressure (or right jugular venous pressure) during inspiration → decreased RV compliance for various reasons

327
Q

What is isoproterenol?

A

Non-selective 𝜷 adrenergic agonist

328
Q

For the temporary pacemaker, what does VVI mode?

A

Ventricle paced, ventricle sensed, pacing inhibited during a sensed event

329
Q

What is the difference between atrial fibrillation and atrial flutter?

A

Atrial fibrillation: irregular atrial contraction
Atrial flutter: regular but very rapid atrial contraction

330
Q

What is the main energy source for cardiomyocytes?

A

Fatty acid

331
Q

Does a tube that is too compliant cause overdamping or underdamping during arterial blood pressure monitoring?

A

Overdamping

332
Q

What is the vascular effect of D1 and D2 receptors?

A

D1 (post-synaptic): vasodilation
D2 (pre-synaptic): inhibit NE release from sympathetic nerve ending → less vasoconstriction

333
Q

Is dopamine receptor a G protein-coupled receptor or voltage-gated receptor?

A

G protein-coupled receptor

334
Q

What is the MOA of ephedrine?

A

increase the release of NE from sympathetic nerve ending

335
Q

Of the two determinants of arterial blood pressure—cardiac output and vascular resistance, which one is the main determinant of blood pressure?

A

Vascular resistance

336
Q

How does anemia cause vasodilation?

A

Decreased blood viscosity → increased shear stress → increased NO production → vasodilation

337
Q

Does ACEI decrease preload or afterload?

A

Both

Preload: decreased sodium and water retension
Afterload: vasodilaiton

338
Q

Does ACEI cause arterial or venous dilation?

A

Both

339
Q

Does Calcium channel blocker cause arterial or venous dilation?

A

Arterial

340
Q

Does hydralazine cause arterial or venous dilation?

A

Both

341
Q

Why ACEI cause hyperkalemia?

A

Inhibit aldosterone

342
Q

What type of drug is prazosin?

A

Competitive post-synaptic 𝜶1 receptor antagonist

343
Q

True or False: Aldosterone is pro-inflammatory and pro-fibrotic.

A

True

Aldosterone is considered proinflammatory and profibrotic and causes endothelial dysfunction secondary to vasoconstriction and vascular remodeling.

344
Q

True or False: Renin can be release when its 𝜷 adrenergic receptors are stimulated.

A

True

345
Q

What are the 5 functions of angiotensin II?

A

1) Increase aldosterone
2) Increase ADH
3) Cause vasoconstriction
4) Increase thirst drive within hypothalamus
5) Increase Na-H exchange at the proximal renal tubules

346
Q

What is the potential adverse effect when giving sodium nitroprusside to a patient with hepatic disease?

A

Cyanide toxicity

Sodium nitroprusside oxidizes sulfhydryl groups present in erythrocytes and cell membranes or reacts with hemoglobin to produce methemoglobin. This reaction results in the production of nitric oxide (as well as five cyanide groups), which leads to direct vasodilation through the action on vascular smooth muscle. Free cyanide is converted to thiocyanate by either thiocyanate oxidase within erythrocytes or a transsulfuration reaction with thiosulfate by the rhodanese enzyme in the liver.

347
Q

What do ESPVR and EDPVR imply?

A

ESPVR (End-systolic pressure volume relationship) - ventricular compliance
EDPVR (End-diastolic pressure volume relationship) - contractility

Boards: Cardiovascular (19 decks)

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