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Veterinary Medicine > Cardiology (SA) > Flashcards

Cardiology (SA) Flashcards

1
Q

What is #1?

A

SAN

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2
Q

What is #2?

A

AVN

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3
Q

What is #3?

A

Bundle of His (AV bundle)

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4
Q

What is #4?

A

Left Limb

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5
Q

What is #5?

A

Right Limb

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6
Q

What is #6?

A

Septomarginal Band

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7
Q

What is #7?

A

Left Bundle Branch

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8
Q

What is #8?

A

Right Bundle Branch

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9
Q

Label 1-9.

A
  1. Cranial VC
  2. Caudal VC
  3. Aorta
  4. Right Auricle
  5. Right Atrium
  6. Pulmonary Artery
  7. Right Ventricle
  8. Left Auricle
  9. Left Ventricle
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10
Q

Label 1-9.

A
  1. Cranial Vena Cava
  2. Caudal Vena Cava
  3. Aortic Arch
  4. Right Atrium
  5. Pulmonary Artery
  6. Left Atrium
  7. Left Ventricle
  8. Left Auricle
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11
Q

Label 1-7

A
  1. Right Cranial Lobe
  2. Right Middle Lobe
  3. Right Caudal Lobe
  4. Accessory Lobe
  5. Left Caudal Lobe
  6. Caudal portion of Left Cranial Lobe
  7. Cranial Portion of Left Cranial Lobe
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12
Q

Label 1-4. (Right Lung Lobes as L Lateral)

A
  1. Cranial Lobe
  2. Caudal Lobe
  3. Middle Lobe
  4. Accessory Lobe (need orthogonal views)
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13
Q

Label 1-3

A
  1. Cranial Portion of Left Cranial Lobe
  2. Caudal Portion of Left Cranial Lobe
  3. Left Caudal Lobe
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14
Q

Describe Starlings Law.

A

Hydrostatic pressure across the vessel wall and oncotic (protein) pressure within and outside the vessel balance to determine movement of fluid.

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15
Q

What is the Equation for Starlings Law?

A

Net pressure = (Pcapillary– Pinterstitium) – (Ocapillary– Ointerstitium)

P = Hydrostatic Pressure, O = Oncotic Pressure

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16
Q

What occurs if the result of a starlings equation is positive?

What about if it is negative?

A

+ = water moves out of capillary

  • = water moves into capillary
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17
Q

What is the equation for Cardiac Output?

A

CO = SV x HR

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18
Q

What is the equation for stroke volume?

A

EDVV - ESVV = SV

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19
Q

What causes an increased preload?

A

Increased EDVV

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20
Q

What causes an increased afterload?

A

Increased vascular presure

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21
Q

What is vascular resistance inversely proportional to?

What is the significance of this?

A

Radius4

Increased Radius = Decreased Vascular Resistance & vice-versa.

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22
Q

How is mean Aortic Pressure Calculated?

A

Total Peripheral Resistance x CO

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23
Q

What is the systolic pressure of the RV?

A

25mmHg

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24
Q

What is the systolic pressure of the LV?

A

120mmHg

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25
Q

What is the normal systolic pressure of the pulmonary arteries?

A

25mmHg

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26
Q

What is the normal systolic pressure of the systemic arteries?

A

120mmHg

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27
Q

How can we increase Cardiac Output?

A

Increase SV (Contractility or EDVV)

Increase HR

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28
Q

Sympathetic Drive increases HR but maintains CO - how?

A

Offsets severely reduced diastole with increase in:

Contractility

Lusitropy

(can also shorten systole to slightly inc diastole)

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29
Q

What is the adult remnant of the umbilical vein?

A

The round ligament of the liver

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30
Q

What is the adult remnant of the umbilical artery?

A

The round ligament of the bladder

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31
Q

Which 3 breeds of dog are predisposed to aortic stenosis?

A

Boxer

Newfoundland

Rottweiler

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32
Q

What structural change(s) may be caused by Aortic Stenosis?

A

LV dilation/hypertrophy

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33
Q

What are the clinical signs of Aortic stenosis?

A

Normally Asymptomatic - occasionally syncope.

Possibly also arrhythmia and sudden death.

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34
Q

Which dog breeds are commonly predisposed to pulmonic stenosis?

A

Bulldogs and Fox Terriers

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35
Q

What structural CV changes are caused by pulmonic stenosis?

A

dilation +/- hypertrophy of the RV

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36
Q

What are the clinical signs of pulmonic stenosis?

A

RHS heart failure

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37
Q

Which species most commonly suffers from PDA?

A

Dogs

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38
Q

Where does the blood travel in a PDA?

A

Aorta to Pulmonary Artery (L –> R)

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39
Q

What are the clinical signs of PDA?

A

LHS CHF - Pulmonary Oedema

Pulmoanry hypertension & shift to R > L flow = Differential Cyanosis (blue caudal MMs)

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40
Q

Desribe a PDA murmur.

A

Systolic + Diastolic

Rib Space 3/4

“Machinery Murmur”

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41
Q

Describe the murmur caused by Aortic Stenosis.

A

Sytolic.

4th ICS.

High-Pitched.

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42
Q

Describe the murmur caused by Pulmonic Stenosis.

A

Systolic

3rd ICS

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43
Q

Describe the murmur caused by a Small VSD.

A

Systolic

RHS - ICS 5

Loud, High-pitched.

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44
Q

Describe the murmur caused by a large VSD

A

Systolic

ICS 5 RHS.

Low, soft murmur.

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45
Q

Which 4 conditions encompass the Tetralogy of Fallot?

A

VSD

Dextraposed Aorta

Pulmonary Stenosis

RV Hypertrophy

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46
Q

Which cardiac defect may cause megaoesophagus?

A

Persistent right 4th Aortic Arch & L ductus arteriosus.

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47
Q

Which Cardiac Glycoside is used in Veterinary Medicine?

A

Digoxin

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48
Q

How do Cardiac Glycosides work?

A

Inhibit Na removal from cardiac myocytes.

Increases intracellular Ca & therefore SR Ca.

+ Inotrope

ALSO -ve Chronotrope via inhibition of Na Removal

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49
Q

Which receptors are present on cardiac myocytes?

A

ß1

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50
Q

Which ß1 agonist do we use in anaesthesia and why?

A

Dobutamine - to induce tachycardia.

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51
Q

What is the role of phosphodiesterase?

A

Degardes intracellular cAMP

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52
Q

What do PDE III inhibtors do to the heart? How?

A

Increase contractility.

Increased cAMP –> inc Ca channel opening –> increase Ca in myocyte.

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53
Q

Apart from increased contractility, what CV effects do PDE inhibitors have on?

A

Vasodilation

Tachycardia

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54
Q

What is the most common PDE III inhibitor used in veterinary practice and what are its major CV effects?

A

Pimobendan

+ inotrope, vasodilator

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55
Q

What are the potential adverse effects of PDE III inhibitors?

A

Inappetance

Lethargy

Dyspnoea

Azotaemia

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56
Q

What is the most appropriate treatment for a Bradyarrhythmia?

A

Pacemaker implantation

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57
Q

What can you use during anaesthesia to combat Bradycardia?

A

Anticholinergic - Atropine

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58
Q

What are the 4 classes of Vaughn-Williams?

A

I - Na blocker

II - Beta blockers

III - K blocker

IV - Ca blocker

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59
Q

How do Class I Vaughn-Williams drugs work?

A

Block fast Na channels and reduce heart rate.

K+ dependent: hypoK decreases fct, hyperK increases it.

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60
Q

Describe the Na blockade and effect on refractory period of VW class Ia drugs.

A

Na Blockade: Moderate

ERP: Increased

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61
Q

Describe the Na blockade and effect on refractory period of VW class Ib drugs.

A

Na Blockade: Weak

ERP: decreased

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62
Q

Describe the Na blockade and effect on refractory period of VW class Ic drugs.

A

Na Blockade: Strong

ERP = no change

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63
Q

Give an example of a VW class 1a drug.

A

Quinidine

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64
Q

Give an example of a VW class Ib drug.

A

Lidocaine

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65
Q

Give an example of a VW class Ic drug.

A

Flecainide

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66
Q

What is the route of administration for quinidine?

A

Oral

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67
Q

What are the 2 effects of quinidine?

A

Na blocking

Vagolytic (inc HR/conduction)

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68
Q

What is quinidine used to treat?

A

Atrial Fibrillation in horses

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69
Q

What are 4 possible side effects of quinidine?

A

Arrhythmia

GI signs

Behavioural - nervous/depression

Negative inotrope/vasodilation –> CHF

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70
Q

What is the route of administration for lidocaine when treating dysrhythmia?

A

SLOW IV!

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71
Q

On which cells does lidocaine have most effect?

A

Diseased cells

72
Q

What are the side effects of lidocaine?

A

CNS excitation

Disorientation/Nausea

Seizures

73
Q

What are the 4 ways beta blockers affect the CVS?

A

Slow pacemaker potential (slower Ca influx)

Slow AV conduction (inc refractory period)

Negative Inotrope

Reduced lusiotropy

74
Q

Which conditions (2) may we treat with Beta Blockers?

A

sVT/VT

Hypertension

75
Q

Give an example of a Beta blocker used in practice.

A

Atenolol (B1 selective)

76
Q

How do K channel blockers slow the HR?

A

Slows repolarization –> Increased refractory period

77
Q

Give an example of a VW class III drug.

A

Sotalol

78
Q

What are the two isomers of Sotalol?

A

I-Isomer: B1 and B2 blocker

D-Isomer: Blocks K+ Channels

79
Q

How do Ca channel blockers slow the HR?

A

Slows conduction at SA/AVN

Also negative inotrope and + lusiotrope

80
Q

Give and example of a class IV antidysrhythmic

A

Diltiazem

81
Q

Give an example of a “Class V Vaughn-Williams” drug.

A

Digoxin

82
Q

How does digoxin affect the CVS?

A

Slows AVN conduction (in refractory period) = -ve chronotrope

Vagomimetic.

NO negative inotropy!

83
Q

What are the 6 classes of DIRECT vasodilator?

A

Nitrates

Dopamine

Ca channel Blockers

PDE III inhibitors

Hydralazine

K+ channel activators

84
Q

How do nitrates cause vasodilation

A

NO converts GTP to cGMP

cGMP opens K+ and closes Na+ –> hyperpolarisation

cGMP also inhibits Ca entry to cell –> relaxation

85
Q

Give an example of a nitrate used in practice & when this would be.

A

Nitroglycerine - severe acute LHS CHF

86
Q

How is nitroglycerine administered to the patient?

A

Transdermally - ear/groin/axilla

87
Q

Which type of vessels are dilated by hydralazine?

A

Ateries - arteriodilator

88
Q

Circulation to which organ systems is most affected by Hydralazine?

A

Coronary

Cerebral

Renal

Splanchnic

89
Q

How does Hydralazine affect preload/afterload?

A

BIG drop in afterload

90
Q

What are the 3 major effects of hydralazine of vascular smooth muscle?

A

Reduced Ca release from SR

Hyperpolarisation of SM

NO release from endothelium

91
Q

What are the overall effects of hydralazine on the CVS?

A

Vasodilation –> Reflex tachycardia –> inc CO

92
Q

What are PDE III inhibitors used for?

A

CHF

93
Q

Give an example of a PDE V inhibitor.

A

Sildenafil (viagra)

94
Q

What is the most common use for sildenafil in veterinary practice?

A

Decrease pulmonary hypertension

95
Q

What are the two pathways INDIRECT vasodilators work on?

A

Sympathetic

RAAS

96
Q

Which two drugs may be used for a1 adrenoreceptor blockade? Which is non-selective?

A

Prazosin

Phenoxybenzamine (non-selective)

97
Q

What is a common use of prazosin in veterinary medicine?

A

Urinary Blockade - relaxes urtheral sphincter

CHF - reduce sympathetic drive

98
Q

How does the RAAS influence preload?

A

Retrains water and Na+

99
Q

Which conditions would benefit from RAAS blockade?

A

CHF

Hypertension

CKD

100
Q

How do ACE inhibitors affect the CVS?

A

Vasodilation & reduced circulating volume:

  • improved perfusion
  • reduced preload
  • reduced arterial pressure
101
Q

Which ACEI should be used in patients with renal compromise?

A

Benazepril - not renally excreted

102
Q

Name 3 commonly used ace inihibitors in veterinary medicine

A

Enalapril

Ramipril

Benazepril

103
Q

Which AII receptor antagonist is used in veterinary practice? What is it licenced for?

A

Telmisartan

Protein-losing nephropathy in cats

104
Q

How do Aldosterone antagonists work?

A

Reduce Na/H20 retention

Reduce K loss

Reduce Cardiac remodelling

105
Q

Give an example of an aldosterone antagonsit used in veterinary practice

A

Sprionolactone

106
Q

What are the 4 types of diuretic we can use to reduce preload? Give an example of each.

A

Loop - furosemide

Thiazide - Hydrochlorothiazide

K sparing - spironolactone

Osmotic - Mannitol

107
Q

A murmur caused by what is heard at the right apex?

A

VSD

108
Q

Where is a PDA murmur heard?

A

Dorsal to Aortic Valve

109
Q

Where is the PMI of a mitral valve murmur?

A

Left Apex

110
Q

Which murmur(s) has/have a PMI at the left base?

A

Pulmonic & Aortic

111
Q

Which left basillar systolic murmur has a crescendo-decrescendo pattern?

A

Pulmonic Stenosis

112
Q

Which murmur is often described as a machinery murmur?

A

PDA

113
Q

Why is s3 heard?

A

Poor LV compliance ie. DCM

114
Q

Why is s4 heard?

A

atrial contraction if abrnomal V relaxation ie. HCM

115
Q

When are crackles and wheezing head?

A

Crackles - inspiratory

Wheeze - expiratory

116
Q

What is class A heart Disease?

A

At risk - no strutctural abnormality

117
Q

What are class B1 and B2 cardiac Dz?

A

B: Structural abnormality w/o clinical signs.

1: no remodelling
2: remodelling

118
Q

What is class C 1 and 2 heart disease?

A

C: structural abnormality w/past or present signs of failure.

C1: CHF, hospitalisation needed

C2: Home Tx of CHF (poss after hospital)

119
Q

what is class D heart Dz?

A

Persistent/end-stage heart failure signs.

Refractory to standard Tx.

May be acute decompensation for CHF.

120
Q

Define Heart Failure

A

Clinical Syndrome caused by heart Dz resulting in poor systolic/diastolic function which is too severe for compensation.

Results in poor CO, Oedema and Effusion.

121
Q

What is ANP released in repsonse to?

A

Atrial stretch

122
Q

What is BNP released in response to?

A

Increased Ventricular Pressure

123
Q

How to Ace Inhibitors protect the heart from failure?

A

Counteract ANG II.

Reduce aldosterone release.

Reduce H20/Na retention.

Reduced BP

Reduce Cardiac Remodelling.

124
Q

Why is sipronolactone used in conjunction to ACE inhibitors in CHF?

A

Aldosterone levels can still increase w/Ace inhibition.

Therefore remodelling still present.

Spironolactone = Aldosterone Antagonist

125
Q

What is the cause of concentric hypertrophy?

A

Pressure overload

126
Q

What is the cause of eccentric hypertrophy?

A

Volume Overload

127
Q

Which diuretic is essential for controlling CHF?

A

Furosemide

128
Q

The dosage of which drug should be adjusted according to RR measured at home by the owners?

A

Furosemide

129
Q

What are the 2 major side effect of furosemide?

A

Pre-renal azotaemia

Hypokalaemia

130
Q

If Furosemide does not work for managing CHF at 3mg/kg q8h, what should be done? Any concerns?

A

MAX DOSE

change to torasemide (0.1mg/kg/day)

MAY CAUSE AKI- check renal fct 48h after each change in dose

131
Q

Which K sparing diuretic is often used in CHF?

A

Spironolactone

132
Q

What must be done before starting diuretics in a dog with RCHF?

A

Check for pericardial effusion!

133
Q

Name 4 ACE inhibitors used in veterinary medicine.

A

Enalapril

Benazepril

Ramipril

Imidapril

134
Q

In what type of heart disease are ace inhibitors contra-indicated?

A

Fixed outflow tract obstruction with no CHF

135
Q

Which CHF drug can cause venodilation, aiding in rapid control of pulmonary oedema?

A

Furosemide IV

(also topical nitroglycerine ointment)

136
Q

Which 3 arteriodilators may be of aid to mitral regurg?

A

Pimobendan

Amlopdipine

Hydralazine

137
Q

Name 2 balanced vasodilators.

A

ACE inhibitors

Pimobendan

138
Q

Which drugs sensitises cardiac myocytes to Ca and inhibits PDE?

A

Pimobendan

139
Q

What is the ideal drug protocol for a Doberman with DCM?

A

SPAF + Digoxin

140
Q

Which drug can be used to counteract sympathetic drive in heart failure by increasing vagal tone?

A

Low dose Digoxin

Negative Chronotrope

Partial + inotrope

141
Q

Name 5 signs of digoxin toxicity.

A

Cardiac arrthymias

Borborygmi

Depression

Anorexia/V+D+

142
Q

If an owner can’t afford the SPAF protocol - which 2 drugs must be prioritised?

A

Furosemide and Pimobendan

143
Q

When does sinus arrhytmia occur in the dog?

A

HR <140bpm - NORMAL

144
Q

When does sinus arrhytmia occur in the cat?

A

ABNORMAL inc vagal tone - asthma or compromised resp

145
Q

What causes a wandering pacemaker? (dog)

A

Varying vagal tone

146
Q

How can you tell if sinus arrest is vagally mediated?

A

Abolished by atropine - atropine response test

147
Q

Describe Sick Sinus Syndrome

A

A few normal beats, Then junctional escape complexes with NO P WAVE!

148
Q

What is the best treatment for sick sinus syndrome?

A

Pacemaker

149
Q

What causes wide, bizzare QRS complexes?

A

VPCs

150
Q

How is VTAC treated?

A

IV lidocaine

151
Q

What is the prognosis for VFIB?

A

DEATH

152
Q

Describe 1st degree AV block.

A

1:1 P:QRS

LONG P-R interval

153
Q

What are the 2 types of 2nd degree AV block?

A

Type I = Variable P-R interval with dropped P wave

Type II = constant P-R interval, fixed P:QRS but not 1:1

154
Q

What is the best treatment for MObitz type II AV block?

A

Pacemaker implantation

155
Q

What is 3rd degree AV block?

A

No association of P:QRS complexes

156
Q

What is a negative P wave with an early QRS complex called?

A

Supraventricular Premature complex

157
Q

How is AFIB controlled?

A

Slow AVN conduction - Digoxin?

158
Q

How is supraventricular tachycardia controlled?

A

Vagal manouvres - carotid massage and ocular pressure

Slow AVN conduction

159
Q

What are the 5 causes of a dampened QRS?

A

Giant Breed

Fat

Thoracic Mass

Pleural Effusion

Pericardial Effusion

160
Q

What is P Mitrale and what does it indicate?

A

Wide P wave - LA enlargement

161
Q

What is P Pulmonale and what does it indicate?

A

Tall P wave - RA enlargement

162
Q

What does a tall R wave indicate?

A

LV enlargement

163
Q

What does a prolonged QRS indiate?

A

LV enlargement

164
Q

What condition causes tall, wide WRS complexes with opposing T waves?

A

LBBB

165
Q

What causes deep, wide S waves (neg QRS) with positive T wave? (it would also have R axis deviation)

A

RBBB

166
Q

What causes + QRS in lead I but -ve QRS in lead, II, III and aVF, with a left axis deviation?

A

Left anterior fascicular block

167
Q

What may cause Tall/spiky T waves, no P waves, and sinus arrhythmia?

A

Hyperkalaemia - sinus bradycardia and atrial standstill

168
Q

What are the significant figures for changes in ST segment?

A

Elevation >0.15mV

Depression >0.2mV

169
Q

Which echocardiographic view will evidence MOST cardiac problems?

A

Right Parasternal Long Axis 4 chamber view

170
Q

What is M Mode used to measure?

A

Systolic Function

171
Q

What is the normal LA:Ao ratio?

A

<1.5

172
Q

Which equation is used to assess the severity of stenosis?

A

Modified Bernouilli Equation (PG = 4v2)

173
Q

What are the values for mild, moderate and severe aortic/pulmonic stenosis?

A

0-40mmHg Mild

40-80mmHg Moderate

>80mmHg Severe

174
Q
A
175
Q
A

Veterinary Medicine (68 decks)

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