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Veterinary Physiology > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is heart failure

A

Inability to maintain cardiac output

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2
Q

What is homeostasis for the CV system

A

blood pressure (120/80)

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3
Q

The heart is connected in [SERIES or PARALLEL] through pulmonary circulation

A

Series

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4
Q

The heart is connected in [SERIES or PARALLEL] to the systemic circulation

A

Parallel

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5
Q

Why is the heart connected to the pulmonary circulation in series

A

Decreased resistance, lowers pressure requirements and work load on the heart

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6
Q

Why is the heart connected to the systemic circulation in parallel

A

Increased resistance; separate control of blood flow to individual vascular beds depending on physiological needs of the organs

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7
Q

Total body water is what % of body weight

A

60%

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8
Q

Total blood volume is what % of body weight

A

7%

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9
Q

What % of blood is in the venous system

A

70%

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10
Q

What % of blood is in the artery system

A

10%

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11
Q

What % of blood is in the capillaries

A

5%

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12
Q

Another name for veins is
a) capacitance vessels
b) resistance vessels
c) exchange vessels

A

a) capacitance vessels

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13
Q

Another name for arteries is
a) capacitance vessels
b) resistance vessels
c) exchange vessels

A

b) resistance vessels

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14
Q

Another name for capillaries is
a) capacitance vessels
b) resistance vessels
c) exchange vessels

A

c) exchange vessels

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15
Q

Flow steadily ____________ going from arteries -> arterioles -> capillaries

A

decreases (increased resistance and decreased blood volume)

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16
Q

Flow steadily _____________ going from capillaries -> venules -> veins

A

increases (decreased resistance and increased blood volume)

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17
Q

What vascular bed has the greatest total surface area

A

Capillaries

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18
Q

4 mechanisms for venous return

A
  1. some smooth mm contraction
  2. skeletal mm contraction
  3. respiratory inspiration
  4. valves
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19
Q

Blood flows _________ is exposed to the ____________ SA and experiences the _____________ diffusion distances in capillaries, where the _____________ exchange takes place

A

Blood flows SLOWEST is exposed to the GREATEST SA and experiences the SHORTEST diffusion distances in capillaries, where the MOST exchange takes place

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20
Q

The greatest resistance is in

A

arterioles (50% of total pressure drop); due to the decreasing volume of blood

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21
Q

What is the pressure when blood reaches the vena cava

A

0 mmHg

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22
Q

What is stroke volume? What is a normal value

A

Volume of blood ejected from the left ventricle by 1 beat of the heart; 30 mls

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23
Q

What is cardiac output

A

Volume of blood circulated in one minute (L/min)

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24
Q

How is cardiac output related to stroke volume (equation)

A

CO = hr x SV

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25
Q

what is the relationship between resistance, pressure and flow

A

R = ΔP/Q

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26
Q

What is another way to describe flow? (hint: L/min)

A

CO (where CO = hr x SV)

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27
Q

What is TPR and what is a typical value

A

Total peripheral resistance = resistance in the systemic circulation (17 mmHg/L/min)

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28
Q

What is the typical resistance in pulmonary circulation

A

1.7 mmHg/L/min (note: low pressure low resistance since it is in series)

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29
Q

If pressure increases what happens to resistance

A

Increases

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30
Q

If flow increases what happens to resistance

A

Decreases

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31
Q

What is PP

A

Systolic - diastolic pressure

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32
Q

What is MAP

A

MAP = diastolic + 1/3 PP

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33
Q

What are two ways to calculate map

A

1) MAP = diastolic + 1/3 PP
2) MAP = CO x TPR

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34
Q

How is CO measured experimentally
a) direct fick
b) dye/indicator diluation

A

a)

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35
Q

How is CO measured clinically
a) direct fick
b) dye/indicator diluation

A

b)

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36
Q

How does dye/indicator dilution work

A

Input dye (cardiogreen) into venous system and measure it coming back through the arterial system

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37
Q

How do you calculate CO using dye/indicator dilution (what is the equation)

A

CO = (known amount of dye injected x 60)/ AOC x DFC

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38
Q

Describe Poiseulle’s law

A

R = 8nl/πr^4); where n = viscosity; l = vessel length; r = vessel radius

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39
Q

What are the implications of Poiseulle’s law

A

R = 8nl/πr^4; small changes in radius have a large impact on resistance

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40
Q

If vessel radius decreases what happens to resistance? What about if vessel radius increases

A

If vessel radius decreases, resistance will greatly increase; if vessel radius increases; resistance will greatly decrease (greatly = four-fold change)

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41
Q

If blood flow increases what happens to blood pressure

A

Decreases (locally)

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42
Q

As a vessel dilates, blood flow _________, blood pressure __________ and resistance _____________

A

As a vessel dilates, blood flow INCREASES, blood pressure DECREASES and resistance DECREASES

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43
Q

Turbulent flow is related to vessel ________________ and _______________ of blood

A

Vessel diameter; viscosity of blood

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44
Q

T/F Hydrostatic pressure = MAP

A

FALSE; HP is a capillary filtration pressure of water

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45
Q

Starlings forces equation

A

Starling’s forces = (Pc-Pt) - (πc-πt)

46
Q

Is there net filtration or net reabsorption between arterial and venous ends

A

Typically net filtration

47
Q

Where does lymph empty

A

Subclavian veins

48
Q

What are the four causes of edema

A
  1. increased filtration pressure (HPc)
  2. decreased oncoticpressure gradient (πc)
  3. increased capillary permeability
  4. decreased lymphatic flow
49
Q

What is an example of an activity that increases VDMs and therefore triggers metabolic autoregulation

A

exercise (causes hyperthermia, hypoxia, acidosis and hypercapnia)

50
Q

What are the two types of autoregulation

A

metabolic and myogenic

51
Q

Humoral control mechanisms involve

A

Vasoconstrictor agents and vasodilator agents

52
Q

3(4) vasoconstrictors are

A

Epinephrine, norepinephrine, angiotensin II (-> aldosterone)

53
Q

Vasoconstrictors do what to flow and pressure

A

increase pressure, decrease flow

54
Q

Vasodilators do what to flow and pressure

A

decrease pressure, increase flow

55
Q

What are the three effects of stimulating a baroreceptor (ex. increased stretch due to bolus of blood entering aorta)

A
  1. decreased sympathetic output to blood vessels, heart and medulla (due to an inhibitory signal from the CVLM to the RVLM)
  2. increased parasympathetic output to the heart (due to a stimulatory signal from the NTS)
  3. increased stimulation of vagus (CNX) and glossopharyngeal (CNIX)

OVERALL: decreased hr and decreased bp

56
Q

How do we get hypo/hypertension

A

Resetting of baroreceptors due to changes in mean blood pressure

57
Q

What does the P wave represent

A

atrial depolarization

58
Q

What does the QRS complex represent

A

atrial repolarization/ventricular depolarization

59
Q

what does the T wave represent

A

ventricular repolarization

60
Q

What is systole

A

Contraction phase; ventricular emptying

61
Q

What is diastole

A

Relaxation phase; ventricular filling

62
Q

What makes the lub sound

A

Closing of the AV valves; systole

63
Q

What makes the dub sound

A

Closing of the aortic/pulmonic valves; diastole

64
Q

What is the equation for SV, EDV and ESV

A

SV = EDV - ESV

65
Q

What is diastasis

A

Period of diastole in which filling of the ventricles is almost at a standstill, before atrial contraction

66
Q

Is the ventricle ever fully empty

A

No; ESV dictates the emptiest the ventricle gets

67
Q

What causes the dicrotic notch

A

Backflow of blood in aorta prior to closure of the aortic valve

68
Q

What makes the third heart sound

A

When blood flows into almost empty ventricles during diastole

69
Q

What are the three types of myocardial cell fibres

A
  1. atrial
  2. ventricular
  3. excitatory/conductive
70
Q

What separates the atrial and ventricular syncytia

A

Valvular tissue

71
Q

What part of the conduction system is fastest

A

Purkinje

72
Q

What are three ways to control the SA node firing

A
  1. slope of pre-potential
  2. threshold for firing the AP
  3. change RMP
73
Q

T/F there is a prepotential in cardiac muscle

A

F

74
Q

T/F there is a prepotential in excitatory cardiac tissue

A

T

75
Q

What is the RMP of conducive cells

A

-55 mV

76
Q

Describe calcium-induced-calcium release

A

AP depolarizes the sarcolemma -> voltage-gated Ca channels in cytoplasm open and influx of calcium -> this calcium triggers release of Ca from the sarcoplasmic reticulum. NOTE: this is in addition to depolarization of sarcolemma -> AP travels down transverse tubules to sarcoplasmic reticulum -> release of calcium

77
Q

What is preload

A

equal to EDV; amount of filling of the ventricle before contraction

78
Q

What is afterload

A

resistance against ventricular emptying ; equal to the pressure in the vessel that the ventricle is trying to empty into (80 mmHg)

79
Q

What determines changes in SV

A

preload, afterload, ANS

80
Q

What determines the performance of the heart (CO)

A

Changes in hr; changes in SV

81
Q

chronotropic

A

affects heart rate

82
Q

inotropic

A

affects heart contractility

83
Q

how does the vagus nerve decrease hr/contractility

A

Ach acts through muscarinic receptors to increase K permeability; hyperpolarization of cells (LOWERS RMP)

84
Q

how does the SNS increase hr/contractility

A

NE acts through β-adrenergic receptors to increase permeability for Na and Ca; decreases conduction time (INCREASES RMP)

85
Q

What is the Frank Starling Law and what does it relate to

A

The greater the EDV, the greater the quantity of blood ejected during systole (due to being in an ideal state of overlap between filaments); has to do with preload and contractility

86
Q

With increased preload, stroke volume [increases/decreases]. Why?

A

increases; due to increased length of muscle fibers and maximal overlap

87
Q

What will happen to systolic pressure with increased preload

A

Will increase beyond 120 mmHg

88
Q

What happens to SV if afterload increases

A

If afterload increases, SV decreases initially, but then returns to normal due to increased EDV (which subsequently increases SV)

89
Q

syncope

A

collapse

90
Q

Which of the following can an ECG not be used to diagnose in LA species:

1) rhythm in a patient with abnormal rhythm or rate
2) chamber enlargement
3) electrolyte imbalances
4) myocardial ischemia/hypoxemia
5) drug intoxication
6) thoracic or pericardial effusion

A

2) chamber enlargement

91
Q

What is the standard position for an ECG

A

right lateral recumbancy (note: rhythm diagnosis can be done in any position)

92
Q

What lead is not always needed in an ECG

A

RL (always want RA, LA, LL)

93
Q

Arrhythmias are typically diagnosed with which lead

A

Lead II

94
Q

What does Lead I detect

A

RA - LA
- potential difference across SA node and atria
- top of the heart

95
Q

What does Lead II detect

A

RA - LL
- potential difference across atria, nodes, ventricles, conduction, valves
- whole heart

96
Q

What does Lead III detect

A

LA - LL
- electrical difference across ventricle

97
Q

T/F in all animals a negative T wave is normal

A

False; normal for small animals but indicates ischemia in horses or humans

98
Q

What does the PR interval represent

A

Conduction of AP from atria to ventricles

99
Q

What does the Q wave represent

A

Septal depolarization

100
Q

What does the QT interval represent

A

Duration of ventricular systole, including ventricular repolarization

101
Q

What is a normal sinus rhythm

A

Rhythm that arises from the sinus node and travels normally down to the ventricles

102
Q

Signs of normal sinus rhythm

A

P wave in front of every QRS
P wave positive on lead II
Regular PR interval

103
Q

What causes sinus arrhythmia

A

Hering-Breuer reflex: stretch receptors in lungs influence vagal innervation of sinus node

104
Q

On ECG you see no P wave, what does this indicate

A

SA node block

105
Q

On ECG you see a prolonged PR interval, what does this indicate

A

First degree AV block

106
Q

On ECG you see a prolonged PR interval and occasional drop beats (missing QRS complexes), what does this indicate

A

Second degree AV block

107
Q

On ECG you see no association between the P wave and QRS-T complexes, what does this indicate

A

Third degree AV block

108
Q

What causes 1st degree AV block

A

High vagal tone or conduction system disease (mild)

109
Q

What causes 2nd degree AV block

A

High vagal tone or conduction system disease (moderate)

110
Q

What causes 3rd degree AV block

A

Conduction system disease (severe)

111
Q

In third degree AV block what is responsible for ventricular contraction

A

Purkinje only (see a very slow heart beat)

112
Q

what is ventricular escape

A

strong vagal tone can completely stop signals from SA node, in which case AV and Purkinje take over

Veterinary Physiology (11 decks)

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