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MOD (year 3) > Cardiology and respiratory medicine > Flashcards

Cardiology and respiratory medicine Flashcards

1
Q

what are the common presenting problems that suggest cardiac or respiratory disease?

A 
cough
respiratory noise
increased RR or effort
lethargy/exercise intolerance
syncope
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2
Q

what cardiac disease are Cavalier King Charles Spaniels predisposed to?

A

myxomatous degenerative valvular disease (mitral valve disease)

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3
Q

what breeds are predisposed to dilated cardiomyopathy?

A

dobermans and other giant breed dogs

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4
Q

what cardiac disease are cats predisposed to?

A

hypertrophic cardiomyopathy

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5
Q

what should be found out about the history of a cough (if present)?

A

when it coughs
if it is productive
length of cough
when it started

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6
Q

what should be found out about the history of a rapid/laboured breathing (if present)?

A

if it is constant/intermittent
if the animal can lie down
if it has adopted a new sleeping position

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7
Q

what might a change in voice of an animal suggest?

A

problem with the larynx

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8
Q

what part of the respiratory tract does breathing noises suggest there is a problem with?

A

upper airway

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9
Q

what is it important to do before handling the patient in suspected cardio-respiratory cases?

A

get RR and pattern

note if animals is dyspnoeic

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10
Q

what is the normal RR of dogs/cats when calm?

A

20-30 respirations/minute

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11
Q

what are the two types of dyspnoeic patterns?

A

obstructive

restrictive

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12
Q

if an animal has cyanotic MM, what should be done?

A

avoid stress

give oxygen

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13
Q

what may a slow CRT be due to?

A

shock or reduced cardiac output

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14
Q

what can be checked on a clinical exam as a sign of cardiac output?

A

MM colour
CRT
femoral pulse quality
warmth of extremities

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15
Q

what two abnormalities can be seen with the femoral pulse?

A

weak or bounding

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16
Q

what is a possible cause of a bounding femoral pulse?

A

some congenital heart defects such as patent ductus arteriosus

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17
Q

what are some clinical signs off forward heart failure?

A 
lethargy
exercise intolerance
weak femoral pulse
pale MM and slow CRT
quiet heart sounds
cold extremities
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18
Q

what are the clinical signs of left sided congestive heart failure?

A 
tachypnoea
hyperpnoea
dyspnoea
restrictive breathing pattern
soft inspiratory crackles on auscultation
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19
Q

what is the major clinical sign of right sided congestive heart failure?

A

fluid accumulations in body cavities (ascites)

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20
Q

what are the clinical signs of right sided congestive heart failure?

A

ascites (abdominal distention) - wave on ballotment
hepatomegaly
distended jugular veins
pleural effusion

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21
Q

why is hepatomegaly a clinical sign of right sided congestive heart failure?

A

due to hepatic venous congestion

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22
Q

what reflex should be checked in animals with suspect right sided congestive heart failure?

A

hepatojugular

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23
Q

why does the hepatojugular reflex need checking in patients with suspected right sided congestive heart failure?

A

gentle cranial abdominal pressure will increase caudal vena cava flow to the heat to there will be increased distention of the jugular veins

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24
Q

what is the normal HR for a cat?

A

120-200bpm

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25
Q

what is a normal HR for a dog?

A

80-140bpm

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26
Q

what is a regularly irregular rhythm of the heart associated with in dogs?

A

sinus arrhythmias

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27
Q

how are heart tumours categorised?

A 
location
timing
grade 
character
radiation
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28
Q

how are murmurs characterised by location?

A

point of maximal intensity

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29
Q

what are the locations the valves of the heart can be auscultated on?

A 
left side
3rd intercostal space - pulmonic
4th intercostal space - aortic
5th intercostal space - mitral
left side
tricuspid valve
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30
Q

what can the location of murmurs be divided into in smaller patients?

A

basilar and apical

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31
Q

what are the three ways timing can be used to characterise murmurs?

A

systolic
diastolic
continuous

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32
Q

what are two examples of left basilar systolic murmurs?

A

aortic stenosis

pulmonic stenosis

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33
Q

what is a left apical systolic murmur often due to?

A

mitral regurgitation

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34
Q

what is a continuous murmur usually due to?

A

patent ductus arteriosus

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35
Q

where are continuous murmurs due to patent ductus arteriosus heard most intensely?

A

dorsally and cranially (push stethoscope into axilla)

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36
Q

what is a possible causes of a diastolic murmur?

A

aortic regurgitation

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37
Q

what is used to grade heart murmurs?

A

the loudness of them

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38
Q

how are heart murmurs graded?

A

I-VI

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39
Q

describe a grade I murmur

A

very quiet only heard in optimal conditions

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40
Q

describe a grade II murmur

A

less loud than heart sounds

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41
Q

describe a grade III murmur

A

as loud as heart sounds

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42
Q

describe a grade IV murmur

A

louder than heart sounds

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43
Q

describe a grade V murmur

A

loud heart murmur with precordial thrill

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44
Q

describe a grade VI murmur

A

very loud murmur with precordial thrill that can be detected with stethoscope lifted off the chest

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45
Q

what ways can the precise character of the murmur be described?

A

early systolic
mid systolic
holosystolic
pansystolic

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46
Q

what is a holosystolic murmur?

A

between the first and second heart sound

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47
Q

what does the radiation of a heart murmur describe?

A

describes where the murmur is the next loudest (eg. aortic stenosis radiates to the carotids and thoracic inlet)

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48
Q

what are murmurs due to?

A

turbulent flow of blood

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49
Q

what are innocent murmur in puppies/kittens?

A

usually left basilar and low grade that disappear by 20 weeks
(thought to be due to changes from foetal to adult haemoglobin)

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50
Q

what causes the S1 heart sound?

A

closure of the atrioventricular valves

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51
Q

what causes the S2 heart sound?

A

closure of semilunar valves

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52
Q

what heart sounds are heard in the healthy dog/cat?

A

S1 and S2

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53
Q

what heart sounds can sometimes be detected in dogs/cats?

A

diastolic sounds - S3 and S4

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54
Q

what is the best way of detecting the diastolic heart sounds in cats/dogs?

A

using the bell of the stethoscopes

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55
Q

what is S3 associated with?

A

early diastolic filling of the left ventricle

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56
Q

what causes the S3 to be louder than in normal animals?

A

high left atrial pressure

stiff poorly compliant left ventricle

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57
Q

what is S4 associated with?

A

late diastolic filling with atrial contraction

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58
Q

what causes S4 to be louder in some animals?

A

animals that are more dependant on atrial contraction to achieve ventricular filling

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59
Q

when are crackles usual heard in the lungs?

A

inspiration (when the airways open)

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60
Q

what does crackles in the lung field indicate?

A

indicates the presence of fluid

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61
Q

when are wheezes in the lung field heard?

A

during expiration

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62
Q

what are wheezes in the lung field associated with?

A

airway narrowing

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63
Q

what is thoracic percussion?

A

gently tapping on the chest wall checking for resonance

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64
Q

when is resonance normally heard in the lung?

A

air-filled lungs usually are

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65
Q

what might increased resonance of the lungs be evident of?

A

pneumothorax

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66
Q

what might cause decreased resonance of the lungs?

A

pleural effusion

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67
Q

what can cause reduced thoracic compressibility in cats?

A

cranial mediastinal mass

large pleural effusion

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68
Q

in the dog what is a good way to differentiate cardiac and respiratory disease?

A

heart rate and rhythm

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69
Q

in dogs with congestive heart failure what is reduced/absent?

A

vagal tone (compared to respiratory disease when the vagal tone is enhanced)

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70
Q

how is HR effected by cardiac disease?

A

normal or increased

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71
Q

how is HR effected by respiratory disease?

A

normal or decreased

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72
Q

how is the rhythm of the heart effected by cardiac disease?

A

sinus rhythm
sinus tachycardia
arrhythmias

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73
Q

how is the rhythm of the heart effected by respiratory disease?

A

sinus arrhythmia

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74
Q

what is a sinus arrhythmia?

A

an irregular heart rhythm/rate that originates from the SAN

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75
Q

when is coughing mainly seen in animals with cardiac disease?

A

at night

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76
Q

when is coughing mainly seen in animals with respiratory disease?

A

when excited/exerted

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77
Q

what are diastolic gallops?

A

S3 and S4

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78
Q

what is the ACVIM ABCD classification used for?

A

staging cardiac disease

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79
Q

what is the criteria for A in the ACVIM classification?

A

at risk but with no structural abnormalities (such as all CKCS)

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80
Q

what is the criteria for B in the ACVIM classification?

A

structural abnormalities detected but no clinical signs of congestive heart failure

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81
Q

what can the B criteria of the ACVIM be subdivided into?

A

B1 - no evidence of significant remodelling such as ventricular dilation
B2 - evidence of significant remodelling in response to volume overload

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82
Q

what is the criteria for C in the ACVIM classification?

A

congestive heart failure (acute or chronic)

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83
Q

what is the criteria for A in the ACVIM classification?

A

persistent endstage congestive heart failure

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84
Q

what is preload?

A

resistance that has to overcome for venous return to the heart

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85
Q

what is afterload?

A

resistance that has to be overcome for ventricular ejection during systole

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86
Q

define heart failure?

A

clinical syndrome caused by heart disease resulting in systolic/diastolic function severe enough to overwhelm the normal compensatory mechanisms of the heart resulting in poor cardiac output causing oedema and effusions

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87
Q

what are the four major consequences of congestive heart failure?

A

oedema/effusions
peripheral vasoconstriction
tachycardia/arrhythmias
remodelling/fibrosis of myocardium

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88
Q

what is the four major consequences of heart failure a result of?

A

neuro-hormonal activation

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89
Q

what does decreased cardiac output cause a decrease in?

A

blood pressure

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90
Q

where is a decreased blood pressure detected?

A

baroreceptors

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91
Q

what do the baroreceptors mediate when they detect a drop in blood pressure?

A

increase in sympathetic drive

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92
Q

what three things does increased sympathetic drive stimulate as a result of decreased blood pressure?

A 
increased HR (tachycardia)
activation of renin-angiotensin-alosterone-system (RAAS)
vasoconstriction
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93
Q

what is stimulated by the increased sympathetic drive to cause tachycardia?

A

cardiac beta1 adrenal-recepotors

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94
Q

why is tachycardia detrimental in the long term?

A

causes reduced coronary perfusion (blood to the heart muscle)

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95
Q

what is stimulated by the increased sympathetic drive due to decreased blood pressure to cause rennin to be released?

A

beta1 receptors on the juxtaglomerular apparatus

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96
Q

what are the two aims of vasoconstriction when associated with decreased blood pressure?

A

increased arteriole constriction - increases blood pressure

increased vena-constriction - increases venous return to the heart

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97
Q

what causes vasoconstriction when associated with increased sympathetic drive due to a drop in blood pressure?

A

alpha1 adrenal-receptors on the vascular smooth muscle cells

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98
Q

what cells release rennin?

A

juxtaglomerular cells

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99
Q

what triggers rennin release?

A

reduced kidney perfusion
reduced sodium concentration
beta1 stimulation

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100
Q

what is rennin?

A

an enzyme

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101
Q

what does rennin do?

A

converts angiotensinogen into angiotensin I in the liver

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102
Q

what is angiotensin I converted to?

A

angiotensin II

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103
Q

what converts angiotensin I to angiotensin II?

A

ACE (angiotensin converting enzyme)

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104
Q

what are the actions of angiotensin II?

A

vasoconstriction
potentiates sympathetic activity
release of vasopressin
hypertrophy and fibrosis of cardiomyocytes (myocardial remodelling)

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105
Q

where is vasopressin released from?

A

posterior pituitary

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106
Q

what is vasopressin?

A

an antidiuretic hormone

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107
Q

how does angiotensin II potentiate sympathetic activity?

A

enhances adrenergic tone
facilitates ganglionic transport
enhance release of noradrenaline from adrenergic neurons

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108
Q

where is aldosterone released from?

A

zona glomerulosa of adrenal cortex

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109
Q

what is the effect of aldosterone?

A

acts on the distal convoluted tubules of the nephron to cause sodium/water retention

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110
Q

what is the effect of vasopressin?

A

result in water retention leading to excessive retention causing oedema and effusions

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111
Q

other than sodium/water retention, what is an effect of aldosterone?

A

myocardial fibrosis and remodelling

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112
Q

what are the two types of natriuretic peptide?

A

atrial and brain

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113
Q

what are atrial natriuretic peptide released due to?

A

atrial stretch

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114
Q

what are brain natriuretic peptide released due to?

A

as a result of ventricular stretch

115
Q

what do natriuretic peptides do?

A

adverse effects of angiotensin II (counteract the RAAS - diuresis, natiuresis, vasodilation)

116
Q

what can be used to demonstrate the presence of heart failure?

A

atrial and brain natriuretic peptides

117
Q

what does endothelin cause?

A

vasoconstriction

118
Q

what mediates the release of endothelin?

A

elevated angiotensin II and endothelial damage

119
Q

other than vasoconstriction, what does endothelin have a role in?

A

myocardial fibrosis and remodelling

120
Q

what does volume overload of the heart chambers lead to?

A

chamber dilation and compensatory hypertrophy

121
Q

what is compensatory hypertrophy due to volume overload called?

A

eccentric hypertrophy

122
Q

what is compensatory hypertrophy due to pressure overload called?

A

concentric hypertrophy

123
Q

how do sarcomeres replicate in eccentric hypertrophy?

A

in series

124
Q

how do sarcomeres replicate in concentric hypertrophy?

A

in parallel

125
Q

what are some examples that pressure overload?

A

aortic stenosis
systemic hypertension
pulmonic stenosis
pulmonary hypertension

126
Q

define adaptive remodelling of the heart

A

changes in heart chamber and wall dimensions as a consequence of underlying lesions which normalise wall stress compensatory mechanisms

127
Q

define maladaptive remodelling of the heart

A

change in relative wall thickness or altered geometry of a heart chamber due to increased wall stress

128
Q

what mediates tachycardia and arrhythmias?

A

elevated catecholamine levels, increased sympathetic drive and reduced vagal tone

129
Q

what is the main immediate problem associated with congestive heart failure?

A

excessive sodium/water retention - oedema…

130
Q

what are three things the owner should be aware of when treating congestive heart failure?

A

it is palliative - not curable
it is life long treatment once started
aim is to improve animals quality of life

131
Q

what is left sided backwards congestive heart failure due to?

A

elevated filling pressures in the left side of the heart

132
Q

what is the primary sign of left sided backwards congestive heart failure?

A

pulmonary oedema

133
Q

why does pulmonary oedema occur in left sided backwards congestive heart failure?

A

increased left sided filling pressure is transmitted into the pulmonary vasculature leading to fluid leaving the pulmonary veins and capillaries

134
Q

what are the two types of pulmonary oedema?

A

interstial oedema - fluid in interstitium

alveolar oedema - air filled spaces of lungs

135
Q

what are the clinical signs of pulmonary oedema?

A

tachypnoea
dyspnoea
(inspiratory and expiratory)

136
Q

where is elevated right heart filling pressure transmitted to in right sided backward congestive heart failure?

A

great veins

137
Q

how may increased pressure in the great veins due to right sided backwards congestive heart failure be seen on a physical examination?

A

jugular vein distention

jugular pulsations seen cranial to thoracic inlet

138
Q

how do elevated central venous pressures effect the liver?

A

effects venous return from the liver so results in hepatomegaly

139
Q

what can cause ascites due to hepatomegaly?

A

sinusoids may leak fluid and some proteins into the abdominal cavity

140
Q

what type of reflex can may be identified in right sided backwards congestive heart failure?

A

positive hepatojugular reflex

141
Q

what effect can fluid leakage into pleural space have on lymphatics?

A

can overwhelm the lymphatics ability to return fluid to the cranial vena cava, this can result in pleural effusions

142
Q

what drugs are always indicated for congestive heart failure?

A

diuretics

143
Q

what diuretic is used for patients with severe pulmonary oedema?

A

furosemide

144
Q

what type of diuretics are most useful for treatment of oedema and effusions?

A

high ceiling loop diuretics

145
Q

what type of diuretic is furosemide?

A

high ceiling loop diuretics

146
Q

how is furosemide administered in life threatening pulmonary oedema cases?

A

IV

147
Q

what should be monitored when giving furosemide to cases of life threatening pulmonary oedema?

A

respiratory rate and urine production

148
Q

what effects does intravenous furosemide have?

A

diuretic

venodilator

149
Q

why should diuretics never be used as long term monotherapy for heart failure?

A

they result in further activation of the RAAS and accelerate the deterioration of congestive heart failure

150
Q

what are some common side effects of furosemide?

A

pre-reanl azotaemia

hypokalaemia

151
Q

what should be monitored when administering furosemide or patients with congestive heart failure?

A

renal function - urea and creatinine

electrolytes

152
Q

what conditions makes controlling congestive heart failure very difficult?

A

renal failure

153
Q

if furosemide is not adequately controlling congestive heart failure, what can be used?

A

a more potent loop diuretic with better/more reliable bioavailability (torasemide)

154
Q

if diuresis using furosemide or torasemide doesn’t control congestive heart failure, what can be done?

A

additional diuretic drugs can be used, normally ones that act on a different part of the nephron

155
Q

what is the use of two diuretics working on different parts of the nephron called?

A

sequential nephron blockade (synergistic effect)

156
Q

what are three diuretics that can be used alongside furosemide/torasemide in sequential nephron blockades?

A

spironolactone
hydrochlorothiazide
amiloride

157
Q

what is the mechanism of action of spironolactone when used as a diuretic?

A

competitively antagonises aldosterone - weak potassium sparing diuretic

158
Q

other than a diuretic, what additional effect does spironolactone have on congestive heart failure?

A

blocks aldosterone mediated myocardial remodelling and fibrosis (aldosterone antagonist)

159
Q

what type of diuretic is hydrochlorothiazide?

A

thiazide diuretic

160
Q

what type of diuretic is amiloride?

A

potassium sparing diuretic

161
Q

what should be done in cases of pleural effusion?

A

thoracocentesis (drain) - diagnostic and therapeutic benefit

162
Q

what should be done with abdominal effusions associated with congestive heart failure?

A

do not drain (unless very uncomfortable or breathing is compromised)

163
Q

why should abdominal effusions associated with congestive heart failure not e drained?

A

they are protein rich, therapies associated with reabsorption is preferred

164
Q

what should always be considered in animals with right sided congestive heart failure?

A

whether the animal has a pericardial effusion or not

165
Q

why does the possibility of pericardial effusion always need to be considered in animals with right sided congestive heart failure?

A

they will have cardiac tamponade which compromises preload and impairs cardiac output, giving diuretics can compromise preload further and may be fatal

166
Q

why do some patients on very high doses of furosemide not become azotaemic or have adequate control of their congestive heart failure?

A

may be diuretic resistant

167
Q

what clinical sign in patients being administered diuretics would make you suspect diuretic resistance?

A

no obvious PU/PD

168
Q

how can diuretic resistance possibly be bypassed?

A

IV/IM administration instead of oral

169
Q

what can chronic repeated diuretic administration lead to?

A

distal nephron tubular cell hypertrophy and increased sodium absorption (genuine diuretic resistance)

170
Q

what are the two licensed products of torasemide?

A

upcard

isemid

171
Q

why does care need to be given when administering torasemide?

A

can cause azotaemia (acute kidney injury)

172
Q

what can be used to counteract neurological-endocrine activation in congestive heart failure cases?

A

ACE inhibitors
angiotensin II blockers
anti-aldosterone drugs

173
Q

what are the favourable effects of ACE inhibitors?

A

vasodilators
reduce the release of aldosterone (counteracting sodium/water retention)
prevent angiotensin II mediated myocardial fibrosis and remodelling
reduce vasopressin release
prevents bradykinin breakdown
counteract increased glomerular filtration pressure

174
Q

what effect does bradykinin have, making the blocking of its breakdown by ACE inhibitors useful?

A

potent vasodilators (beneficial to renal function)

175
Q

what does bradykinin mediate its vasodilatory action through?

A

nitric oxide

vasodilatory prostaglandins

176
Q

how does aldosterone cause increased glomerular filtration pressure?

A

causes greater vasoconstriction in the efferent glomerular arteriole than the afferent

177
Q

what are the 4 ACE inhibitors licensed in dogs?

A

benazepril
enalapril
ramipril
imidapril

178
Q

when are ACE inhibitors indicated for use in congestive heart failure?

A

always (whatever the cause) - avoided when very hypotensive and shouldn’t be started until renal function is stable

179
Q

when may angiotensin II receptor blocker be indicated for use?

A

in cats that often show side effects when using ACE inhibitors

180
Q

what is an angiotensin II receptor blocker?

A

telmisartan

181
Q

what is the anti-aldosterone drug used in dogs?

A

spironolactone

182
Q

how does spironolactone work as an anti-aldosterone drug?

A

competitive aldosterone antagonist

183
Q

how should spironolactone be given?

A

with food (improves bioavailability)

184
Q

what is done to counteract vasoconstriction in congestive heart failure?

A

vasodilators given

185
Q

what do arteriodilators do to counteract vasoconstriction in congestive heart failure?

A

reduce mean arterial pressure which reduces the resistance against which the left ventricle has to pump

186
Q

what effect does reducing afterload have on controlling congestive heart failure?

A

reduce wall stress and myocardial oxygen consumption

187
Q

what effect do ventilators have on controlling congestive heart failure?

A

reduced preload which means left sided filling pressure is reduced and blood is diverted away from the cardiopulmonary circuit which alleviates pulmonary oedema

188
Q

what is used for emergency treatment of pulmonary oedema?

A

furosemide and nitroglycerine

189
Q

how does nitroglycerine work to control pulmonary oedema?

A

applied topically and results in venodilation

190
Q

what are balanced vasodilators?

A

drugs that effect with arteries and veins equally

191
Q

what are two examples of balanced vasodilators?

A

ACE inhibitors

pimobendan

192
Q

what can be used to improve mitral regurgitation?

A

arteriodilators

193
Q

how do arteriodilators help to improve mitral regurgitation?

A

reduce afterload so will improve the fraction of forward stroke volume (reduces left atrial size/pressure to alleviate pulmonary oedema)

194
Q

what are three arteriodilators used for mitral valve disease?

A

pimobendan
amlodipine
hydralazine

195
Q

what drug can be used to improve cardiac output in congestive heart failure cases?

A

pimobendan

196
Q

describe the mode of action of pimobendan

A

increases the sensitivity of the contractile apparatus to intracellular calcium levels

197
Q

what actions does pimobendan have?

A

positive inotrope

balanced vasodilator

198
Q

how should pimobendan be given?

A

orally on an empty stomach (absorption impaired by food)

199
Q

how fast does pimobendan act?

A

very quickly - in about 2 hours of oral administration

200
Q

what drug is used to counteract the high sympathetic drive of congestive heart failure?

A

digoxin

201
Q

when is digoxin use indicated in congestive heart failure cases?

A

atrial fibrillation and other supraventricular tachyarrhythmias
as an antiarrhythmic
patients with reduced systolic function (poor contractility)

202
Q

what are the effects of digoxin?

A

vagomimetic
favourable autonomic effects
mild positive inotrope

203
Q

how does digoxin do as a vagomimetic?

A

enhances vagal tone and reduces sympathetic drive

204
Q

how does digoxin act as a vagomimetic?

A

stimulating CNS vagal centres
sensitise baroreceptors to BP change
enhance cardiac pacemaker response to acetylcholine

205
Q

what do the vagomimetic effects of digoxin result in?

A

slowing the rate of discharge of SAN so slows the sinus rate
slows conduction through AVN and increased the refractory period
(negative chronotrope)

206
Q

what favourable autonomic effects does digoxin have?

A

can stop syncope episodes in animals with postural/tussive syncope

207
Q

what are some tips to avoid digoxin toxicity?

A

start with low oral dose rate
assess blood levels every week
warn owners of clinical signs

208
Q

what conditions is digoxin toxicity more likely to be seen with?

A 
cachexia
obesity
hypoproteinaemic
hypokalaemia
hypothyroidism 
renal dysfunction
209
Q

what are the clinical signs of digoxin toxicity?

A

dull
excessive stomach noises
inappetance
vomiting/diarrhoea

210
Q

what is the standard quadruple therapy for congestive heart failure in dogs?

A

furosemide
ACE inhibitor
pimobendan
spironolactone

211
Q

how are dobermans with preclinical dilated cardiomyopathy treated?

A

pimobendan

ACE inhibitors

212
Q

how are dogs with preclinical myxomatous degenerative mitral valve disease with cardiomegaly treated?

A

pimobendan

213
Q

what should never be used to counteract high sympathetic drive in patients with congestive heart failure?

A

beta blockers

214
Q

what does an ECG record?

A

changes in electrical potential difference in the heart occurring during depolarisation and repolarisation of the myocardium plotted against time

215
Q

what is the pacemaker of the heart?

A

SAN

216
Q

what is the P wave on an ECG?

A

atrial depolarisation

217
Q

what is the speed of the wave of depolarisation across the atria?

A

1m/s

218
Q

what happens to the speed of the wave of depolarisation when it reaches the AV node?

A

slows to 0.1m/s

219
Q

what does the P wave prompt?

A

atrial contraction

220
Q

what is the P-R interval?

A

the slowed wave passing through the AV node

221
Q

what does the P-R interval allow?

A

ventricular filling

222
Q

where does the wave reach after the AV node?

A

bundle of his which branches into purkinje fibres throughout the ventricles

223
Q

how fast do electrical impulses travel through the ventricles?

A

4m/s

224
Q

what does the QRS complex show?

A

ventricular depolarisation

225
Q

how fast is conduction during ventricular depolarisation?

A

1m/s

226
Q

what does the T wave show?

A

ventricular repolarisation

227
Q

what does an increase in the amplitude of a P wave indicate?

A

increased size of one/two atria

228
Q

what does an increase in the amplitude of a QRS complex indicate?

A

increased size of one/two ventricles

229
Q

what species is P wave and QRS complex amplitude associated with atria/ventricle size?

A

small animals and humans

230
Q

can ECG be used to determine which chamber is enlarged when increase P wave or QRS complex is increased?

A

no (need echocardiography)

231
Q

what colour is the right fore electrode?

A

red

232
Q

what colour is the left fore electrode?

A

yellow

233
Q

what colour is the left hind electrode?

A

green

234
Q

what colour is the earth lead of an ECG?

A

black

235
Q

what are the six leads (channels) of the ECG?

A

I, II, II, aVR, aVL, aVF

236
Q

what is the most important lead of an ECG?

A

II

237
Q

what does lead I of the ECG connect?

A

right fore (negative) to left fore (positive)

238
Q

what does lead II of the ECG connect?

A

right for (negative) to left hind (positive)

239
Q

what does lead III of the ECG connect?

A

left fore (negative) to left hind (positive)

240
Q

why is lead II of the ECG the most important in assessing the heart?

A

it is roughly parallel to the portion of the heart so has the largest QRS complex in the normal heart

241
Q

what should be checked when assessing an ECG?

A

paper speed and sensitivity

242
Q

what is assessed when looking at and ECG?

A

what the heart rate is
if the P:QRS ratio is 1:1
what is the predominant rhythm

243
Q

what does a wide and bizarre QRS complex indicate?

A

a rhythmic disturbance of ventricular origin or a conduction disturbance

244
Q

how can T waves look in a dog?

A

negative, positive or biphasic

asymmetrical

245
Q

what does a tall, spikey, symmetrical or a change in the T wave indicate?

A

underlying blood gas, acid-base or electrolyte disturbance

246
Q

what is the standard speed and sensitivity of an ECG?

A

50mm/s

1mV = 1cm

247
Q

what abnormality in lead II suggests left atrial enlargement?

A

prolonged P wave

248
Q

what abnormality in lead II suggests right atrial enlargement?

A

tall P wave

249
Q

what abnormality in lead II suggests left ventricular enlargement?

A

tall R wave

250
Q

what abnormality in lead II suggests ventricular enlargement/hypertrophy?

A

prolonged QRS complex

251
Q

what is the normal heart rhythm called?

A

sinus rhythm

252
Q

when can sinus rhythm vary slightly?

A

with respiration

253
Q

what is it called when sinus rhythm varies with respiration?

A

sinus arrhythmia

254
Q

is sinus arrhythmia normal?

A

yes its normal in dogs and indicates normal/high vagal tone

255
Q

describe how a sinus arrhythmia appear on an ECG?

A

R-R interval rhythmically decreases with inspiration and increases with expiration

256
Q

what is a sinus tachycardia?

A

normal ECG with a heart rate faster than normal

257
Q

what is sinus bradycardia?

A

normal ECG with a heart rate slower than normal

258
Q

what is sinus arrest?

A

ECG shows a gap with no electrical activity for a period exceeding two normal R-R intervals

259
Q

what are the types of AV block?

A

first degree
second degree
third degree

260
Q

what is an AV block?

A

AV node blocks/slows conduction of atrial depolarisation into the ventricles

261
Q

what is a first degree AV block?

A

the P-R interval is longer than normal for the species

262
Q

what does a second degree AV block look like on ECG?

A

some P waves aren’t followed by a QRS complex

263
Q

what can cause second degree AV block?

A

disease of AVN

normal/physiological (especially horses)

264
Q

what are the types of second degree AV block?

A

mobitz I

mobitz II

265
Q

what is a mobitz I AV block?

A

single non-conducted P waves in the ECG

266
Q

what is a mobitz II AV block?

A

multiple (every) non-conducted P wave

267
Q

are mobitz I or II AV blocks more serious?

A

II - usually represent pathology

268
Q

how does a third degree AV block appear on ECG?

A

one in which the P waves have no relationship to the QRS complex - they occur at their own normal rate

269
Q

what cause atrial fibrillation?

A

atria being large or stretched then normal cell to cell conduction is lost
they will randomly reach the AV node and be conducted into the ventricles

270
Q

what is seen on the ECG of animals with atrial fibrillation?

A

QRS and T waves are normal but the rate is fast and R-R interval is random (chaotic)
no P waves

271
Q

what is the most common rhythmic disturbance of the heart?

A

atrial fibrillation

272
Q

what is another name for supraventricular tachycardia?

A

supraventricular premature complexes

273
Q

what is a supraventricular tachycardia?

A

an ectopic focus in the atria or atrioventricular junction depolarises the atria prematurely then a complex with the appearance of a normal QRS complex is produced

274
Q

what is another name for ventricular tachycardia?

A

ventricular premature complex

275
Q

what is a ventricular tachycardia?

A

ectopic focus arise in the ventricular myocardium, this depolarisation spreads cell by cell (instead of by Purkinje fibres) causing a slow spread making a wide and bizarre complex

276
Q

what are the hallmarks of a ventricular tachycardia ECG?

A

wide bizarre complex that slurs into an oppositely directed T wave

277
Q

where does a ventricular premature complex with a positive T wave in leads I and II originate?

A

left ventricle

278
Q

where does a ventricular premature complex with a negative T wave in leads I and II originate?

A

right ventricle

279
Q

what is ventricular fibrillation?

A

complete loss of coordinated ventricular depolarisation/repolarisation
(chaotic ECG results)

280
Q

how does the autonomic nervous system influence an ECG?

A

vagal tone and sympathetic drive affects heart rate and rhythm

281
Q

how can electrolyte disturbances influence ECGs?

A

electrical activity of the heart depends on intra- and extra-cellular concentration gradients of electrolytes - potassium, sodium and calcium

282
Q

how can hyperkalaemia show on an ECG?

A

sinoventricular rhythm
no discernible P wave
relatively normal QRS complex
tall spikes T waves

283
Q

what is echocardiography?

A

cardiac ultrasound

MOD (year 3) (45 decks)

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