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Clinical Veterinary Science and One Health 23/24 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the net result of cardiac disease?

A

Decreased cardiac output

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2
Q

How does activation of the sympathetic nervous system compensate for cardiac disease?

A

B receptors = tachycardia, contractility
a receptors = vasodilation (afterload)

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3
Q

How does renin-angiotensin-aldosterone system compensate for cardiac disease?

A

Kidneys detect a drop in blood pressure)

  • Sodium ion, water retention, increased blood volume = preload
  • Vasoconstriction = afterload
  • Vasopressin/ADH = afterload and preload
  • Remodelling = contractility
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4
Q

What happens in congestive heart failure?

A

Increased preload and afterload and decreased contractility lead to increased atrial pressures

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5
Q

What are the effects of congestive heart failure on the left and right atria?

A

LA – increased PV pressure causing pulmonary oedema

RA – increased systemic venous pressure causing pleural effusion and ascites

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6
Q

What are the goals of congestive heart failure therapy?

A
  • Decrease preload – diuretics, venodilators
  • Improve contractility – positive inotropes
  • Decrease afterload – arteriodilators
  • Address maladaptive compensatory mechanisms – RAAS modulators
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7
Q

Name the diuretic drugs.

A

Loop diuretics:
- Furosemide
- Torasemide

Thiazide diuretics: Hydrochlorothiazide

Potassium sparing diuretics:
- Mineralocorticoid (Aldosterone) receptor antagonists – spironolactone, eplerenone
- Renal epithelial Na+ channel inhibitors – Amiloride

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8
Q

Where do each of the diuretic drugs work in the nephron?

A

Acetazolamide = PCT
Osmotic diuretics = descending limb LOH
Loop diuretics = ascending limb LOH
Thiazides = Na+Cl- channel DCT
Potassium sparing = K+H+ channel DCT

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9
Q

What is the mechanism of action of loop diuretics?

A
  • Block sodium, potassium and chloride ion symport in the thick ascending LOH
  • Inhibit reabsorption of 25% of filtered sodium load
  • Marked natriuresis and diuresis
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10
Q

What is the net effect of loop diuretics?

A
  • Loss of sodium, potassium, chloride, calcium, magnesium and hydrogen ions with water
  • Hyponatraemia and extracellular volume depletion
  • Hypokalaemia
  • Hypochloraemic alkalosis
  • Hypocalcaemia and hypomagnesaemia
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11
Q

What are the indications for loop diuretics?

A

Congestive heart failure
Hypercalcaemia
Hyperkalaemia
Acute kidney injury
Exercise induced pulmonary haemorrhage
Udder oedema

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12
Q

Name the 2 loop diuretics used in congestive heart failure?

A

Furosemide
Torasemide

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13
Q

How does furosemide treat congestive heart failure?

A
  • Venodilatory effect
  • Mobilisation of oedema, prevents ongoing sodium/water retention, preload reduction, so monitor respiratory rate
  • RAAS activation
  • Active secretion into tubular lumen
  • 50-60% excreted unchanged in urine
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14
Q

How does torasemide treat congestive heart failure?

A
  • Longer half-life (8 hrs), duration of action (12 hrs)
  • Also blocks the mineralocorticoid receptor – anti-aldosterone effect
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15
Q

What are the possible adverse effects of loop diuretics to treat congestive heart failure?

A
  • Electrolyte balance
  • Ototoxicity in cats
  • GIT disturbances
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16
Q

What is the mechanism of action of thiazine diuretics?

A
  • Act in the distal convoluted tubule on sodium chloride symport
  • Increase delivery of sodium ion to distal tubule
  • Peak effect at 4 hours, duration of action 12 hours
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17
Q

What are the side effects of thiazine diuretics?

A

Hypokalaemia
Hypercalcaemia
Azotaemia

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18
Q

Which receptor do potassium sparing diuretics work via?

A

Mineralocorticoid receptor

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19
Q

What is the mechanism of action of potassium sparing diuretics?

A

Mineralocorticoid receptor antagonists – competitively block sodium potassium ATPase exchanger. Inhibitors of renal epithelial Na+ channel – mild increase in excretion NaCl, retention of potassium ions

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20
Q

Why is spironolactone a weak diuretic?

A

Weak diuretic effect – only when RAAS activated

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21
Q

What is the mechanism of action of spironolactone?

A
  • Peak effect 2-4 hrs, steady state reached by day 2
  • Acts on myocardium and vasculature to inhibit aldosterone-mediated fibrosis and remodelling
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22
Q

What are the indications of spironolactone use?

A
  • Congestive heart failure – used in combination with loop or thiazide diuretics, protective effects
  • Hyperaldosteronism
  • Hepatic disease
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23
Q

What are the adverse effects of spironolactone?

A
  • Hyperkalaemia
  • Hyponatraemia and reduced ECF volume
  • Non-specific binding to other steroid hormone receptors
  • Facial dermatitis
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24
Q

What are the indications of amiloride?

A

Congestive heart failure

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25
Q

What are the adverse effects of amiloride?

A

Hyperkalaemia
May be exacerbated by ACE inhibitors

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26
Q

What are the mechanisms of action of diuretic resistance?

A
  • Impaired absorption
  • Increased sodium ion absorption
  • Tubular hypertrophy
  • RAAS activation
  • Furosemide – variable bioavailability so doses can change but does not actually increase response past a point
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27
Q

How can the diuretic drugs, acetazolamide and dorzolamide, have other uses?

A
  • Glaucoma
  • Onset of action 30 mins, peak effect 5 hrs, duration of action 7 hrs
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28
Q

What are the adverse effects of the diuretic drugs, acetazolamide and dorzolamide?

A

Metabolic acidosis
Hypokalaemia

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29
Q

What is the mechanism of action of osmotic diuretics?

A
  • Increased intracranial pressure
  • Increases osmolality of blood and renal filtrate – draws fluid from tissues
  • Onset of action 30-60 mins, peak effect 1 hr, duration of action 6-8 hrs
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30
Q

Name 2 positive inotropic drugs.

A

Pimobendan
Dobutamine

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31
Q

What is the mechanism of action pimobendan?

A
  • Sensitizes troponin to calcium ions – positive inotrope
  • Phosphodiesterase 3 inhibitor (cAMP) – systemic vasodilation
  • Peak effect 2-4 hours
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32
Q

What are the indications of pimobendan use?

A

Congestive heart failure
Preclinical mitral valve disease
Dilated cardiomyopathy

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33
Q

What is the mechanism of action of dobutamine?

A
  • Beta adrenergic agonist
  • Max 72h. Plasma half-life very short
  • Potently increases contractility
  • Increases stroke volume, blood pressure, pulse strength, tissue perfusion
  • Increased heart rate, can provoke arrhythmias
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34
Q

What is the indication of dobutamine use?

A

Severe CHF with hypotension

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35
Q

Name the 2 classes of RAAS modulators.

A

ACE inhibitors
Aldosterone inhibitors

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36
Q

Name 3 ACE inhibitors.

A

Benazepril
Enalapril
Ramipril

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37
Q

What is the mechanism of action of ACE inhibitors?

A
  • Reduce Na+ and water retention
  • Vasodilation – reduces pre- and afterload
  • Anti-remodelling
  • Anti-adrenergic
  • Decrease blood pressure
  • Peak effect 2 hours, duration of action 30 hours
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38
Q

What are the adverse reactions of ACE inhibitors?

A

Azotaemia
Hyperkalaemia
Hypotension

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39
Q

Name an aldosterone inhibitors?

A

Spironolactone

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40
Q

How are veneodilators and arteriodilators used to treat severe congestive heart failure?

A

Veneodilators – reduce pre-load

Arteriodilators – reduce afterload

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41
Q

What is the effect of nitroglycerine ointment?

A

Dilates veins

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42
Q

What is the mechanism of action of sodium nitroprusside?

A
  • Dilates veins and arterioles
  • Converted to nitric oxide in circulation
  • Duration of action 1-10 minute
  • If used long term, accumulates cyanide metabolite
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43
Q

What is the mechanism of action of hydralazine?

A

Dilates arterioles via direct effect on vascular smooth muscle

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44
Q

What drug class are beta-blockers?

A

Sympatholytics

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45
Q

What is the mechanism of action of beta-blockers?

A
  • Blocks cardiac β1-adrenergic receptors – peak effect 3 hrs
  • Reduces heart rate and contractility
  • Reduces inappropriate tachycardia and arrhythmias
  • Prolongs diastole – improves coronary perfusion
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46
Q

When should beta-blockers be used and not be used?

A

Used in obstruction of ventricular outflow, such as severe aortic stenosis, hypertrophic obstructive cardiomyopathy

Do not use in heart failure

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47
Q

What are pulmonary arteriodilators used to treat?

A
  • Pulmonary hypertension
  • Increased left-sided filling pressures
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48
Q

Which drugs are used to manage chronic congestive heart failure in dogs?

A
  • Furosemide
  • Pimobendan
  • ACE inhibitors
  • Spironolactone – cardalis: benazepril + spironolactone
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49
Q

Which drugs are used to manage chronic congestive heart failure in cats?

A

Only furosemide and clopidogrel only for cats due to concern over thromboembolism

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50
Q

What is primary pathological myocardial hypertrophy?

A

Problem intrinsic to the myocardium. Cardiomyopathies on genetic and idiopathic basis.

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51
Q

What is secondary pathological myocardial hypertrophy?

A

Myocardial adaptive change (remodelling) secondary to another disease. Congenital or acquired CVS disease leads to volume overload or pressure overload and results in secondary myocardial hypertrophy.

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52
Q

How does volume overload lead to myocardial hypertrophy?

A
  • Volume overload (stress), cardiomyocyte hypertrophy
  • New sarcomeres added in series forming longer myofibrils
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53
Q

How does volume overload lead to hypertrophy of the ventricular myocardium?

A
  • The ventricle adapts to deal with increased blood volume at the end of diastole from excessive preload
  • Hypertrophy of the ventricular myocardium (increased mass)
  • Enlargement (dilation) of the ventricular chamber to accommodates increased end diastolic volume
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54
Q

What are 4 possible ventricular adaptive changes in response to volume overload?

A
  • Normal ventricular chamber
  • Ventricular wall thickness may appear mildly thickened or relatively normal thickness
  • Ventricular lumen radius (volume) is increased
  • Eccentric hypertrophy
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55
Q

What are the causes of volume overload?

A
  • Shunts causing abnormal patterns of blood flow between heart chambers or the great vessels, such as ventricular septal defect
  • Valvular insufficiencies – such as nodular swellings of the left atrioventricular valve leaflets – interfere with functional closure of the valve
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56
Q

How is ventricular hypertrophy caused by valvular insufficiencies/pathology?

A
  1. During systole some blood leaks/regurgitates back into the atrium from the ventricle
  2. During diastole the ventricle receives the venous return plus the blood that regurgitated back into the atrium
  3. Left atrial dilation and enlargement
  4. Left ventricular eccentric hypertrophy
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57
Q

What is pressure overload?

A
  1. Sarcomere and pressure overload
  2. Cardiomyocyte hypertrophy
  3. New sarcomeres added in parallel forming more myofibrils within cardiomyocytes to make them broader and wider in order to be able to apply more pressure.
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58
Q

What are the possible causes of ventricular pressure overload?

A
  • Increased pulmonary or systemic pressure (hypertension)
  • Stenosis of a ventricular outflow tract
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59
Q

What does ventricular pressure overload lead to?

A
  • Hypertrophy of the ventricular myocardium
  • Ventricular wall thickness is increased
  • The ventricular lumen may be normal or reduced in size
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60
Q

Explain pulmonic stenosis as an example of ventricular pressure overload.

A
  1. Narrowing of the pulmonary valve
  2. Increased afterload – the right ventricle has to generate higher systolic pressure to overcome the increased resistance to blood outflow
  3. Right ventricular wall undergoes hypertrophy and becomes thicker
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61
Q

How is concentric hypertrophy caused?

A
  1. Normal ventricular chamber
  2. Pressure overload
  3. Ventricular wall thickness is increased
  4. Ventricular lumen radius (volume) may be decreased or normal
  5. Concentric hypertrophy
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62
Q

Distinguish the causes of eccentric and concentric hypertrophy.

A

Normal ventricle > volume overload > eccentric hypertrophy

Normal ventricle > pressure overload > concentric hypertrophy

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63
Q

What is the consequence of myocardial hypertrophy?

A
  • Myocardial blood supply unable to meet metabolic demands of increased myocardial mass
  • Cardiomyocyte death and fibrosis
  • Reduced ventricular wall compliance (increased stiffness of the wall) – can impair ventricular relaxation and filling
  • Exhaustion stage – development of overt heart failure.
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64
Q

What are 3 possible types of congenital cardiac malformations?

A
  • Malformations causing left to right shunting of blood
  • Valvular or outflow tract malformations
  • Transposition of the great arteries, complex abnormalities, and other miscellaneous cardiac and vascular anomalies
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65
Q

What are some examples of malformations causing left to right shunting?

A

Patent ductus arteriosus (PDA)

Septal defects - atrial septal defect (ASD), ventricular septal defect (VSD

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66
Q

What is the ductus arteriosus?

A

Foetus has high resistance in lungs (uninflated). Blood flows through the ductus arteriosus from the pulmonary artery into the aorta.

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67
Q

What happens to the ductus arteriosus following birth?

A

Following birth, inflated lungs have low resistance to blood flow. Closure of the ductus arteriosus will form the ligamentum arteriosum and closure of the foramen ovale.

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68
Q

What is patent ductus arteriosus?

A

After 5 days of age, functional patency of the ductus arteriosus is considered abnormal.
After birth, patency of ductus arteriosus will allow blood to flow through the ductus arteriosus from the aorta into the pulmonary artery, left to right shunt.

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69
Q

What are 2 potential secondary effects of patent ductus arteriosus?

A
  • Reversal of flow – blood will bypass the lungs and so cyanosis
  • Severe pulmonary hypertension, lung disease
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70
Q

How can left to right shunting cause eccentric and concentric hypertrophy?

A
  1. Left to right shunt
  2. Heart murmur
  3. Increased blood volume within the pulmonary circulation - pulmonary over-circulation and oedema
  4. Increased volume of blood returning to left heart chambers causing volume overload: left atrial dilation/enlargement and left ventricular eccentric hypertrophy
  5. Increased pressure in the pulmonary artery can cause concentric hypertrophy of the right ventricle in order to eject increased volume of blood.
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71
Q

What factors determine the functional effects of VSD and the adaptive changes?

A
  • The size of the septal defect
  • Relative resistance in the pulmonary and systemic vasculature
  • Location of the defect in the septum – may have more of an effect lower down in a ventricle than near the top
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72
Q

Distinguish small and large ventricular septal defects.

A

Small defect = high resistance
Large defect = low resistance

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73
Q

In an uncomplicated case, what are the potential secondary effects of ventricular septal defects?

A
  1. Left to right shunt
  2. Heart murmur
  3. Pulmonary over-circulation
  4. Volume overload of left atrium and ventricle. Left atrial dilation/ enlargement and left ventricular eccentric hypertrophy
  5. Volume and pressure overload of right ventricle. Right ventricular hypertrophy and dilation (more prominent in large VSD or muscular region VSD)
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74
Q

What are aortic and pulmonary stenoses caused by?

A

Caused by malformation of the aortic or pulmonary valve or another part of the aortic or pulmonary outflow tract.

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75
Q

Distinguish pulmonic and aortic stenosis.

A

Pulmonic stenosis – valvular is most common. Valvular leaflet thickening fusion and/or hypoplasia of the valve annulus.

Aortic stenosis – subvalvular (subaortic) is most common. Caused by plaques, ridges or rings of excess connective tissue.

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76
Q

What can form on valves causing stenosis?

A

Band of fibrous tissue below the aortic valves causing stenosis.

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77
Q

What is tetralogy of fallot?

A
  • Ventricular septal defect
  • Overriding aorta
  • Pulmonic stenosis
  • Right ventricular hypertrophy
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78
Q

What is caused by tetralogy of fallot?

A
  1. Shunting of blood between ventricles
  2. Aorta receives some of the blood from the right ventricle in addition to blood from the left ventricle
  3. Causes right ventricular outflow tract obstruction
  4. Occurs secondary to the right ventricular outflow tract obstruction
  5. Cyanosis
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79
Q

What is involved in pericarditis?

A

Exudative effusions and fibrosis

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80
Q

What is fibrinous pericarditis?

A

Microvasculature endothelial cells and plasma proteins including fibrinogen. Inflammation increased vascular permeability and escape of fibrinogen, leading to fibrin polymerisation.

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81
Q

What is fibrous pericarditis?

A

Fibrin may be remodelled during healing and replaced by fibrous tissue.

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82
Q

What is fibrinous pericarditis most commonly present in?

A

In farm animals with bacterial septicaemias and haematogenous infections

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83
Q

What are some possible causes of fibrinous pericarditis in farm animals?

A
  • Coli-septicaemia
  • Mannheimia haemolytica in sheep and cattle
  • Blackleg/Clostridium chauvoei in cattle and sheep
  • Haemophilus parasuis in pigs
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84
Q

Describe fibrinous exudate in chronic cases of fibrinous pericarditis.

A

Undergone organisation to form fibrous tissue on the epicardial surface in more chronic cases.

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85
Q

What is suppurative/purulent/fibrinopurulent pericarditis?

A

Infection with pyogenic bacteria causing purulent or fibrinopurulent exudate. Most common in cattle due to traumatic reticulopericarditis/wire disease.

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86
Q

What is constrictive pericarditis?

A

Formation of severe adhesions and organising fibrous granulation tissue within the pericardium. May constrict the heart and cause impaired ventricular expansion and impaired diastolic filling.

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87
Q

What is hydropericardium?

A

Excess volume of clear fluid (transudate or modified transudate) on the pericardial space

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88
Q

What are the causes of hydropericardium?

A
  • Causes of generalised oedema – CHF, hypoproteinaemia
  • Toxaemia or uraemia – capillary endothelial injury
  • Pericardial or cardiac neoplastic disease
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89
Q

What is cardiac haemangiosarcoma?

A

Right atrial mass arising from the right auricle. Most common in dogs. Right atrium, especially the auricle is the most common site.

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90
Q

What is haemopericardium?

A

Accumulation of pure blood in the pericardial cavity. Should not be used to describe a mixture of serous fluid and blood.

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91
Q

What are the causes of haemopericardium?

A
  • Rupture of an atrium or blood vessel
  • Clotting defect
  • Neoplastic disease, such as cardiac haemangiosarcoma or heart base tumours
  • Idiopathic pericardial haemorrhagic effusion
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92
Q

What is cardiac tamponade?

A
  1. Rapid accumulation of fluid in pericardial sac
  2. Compression and restriction of heart expansion and inhibition of venous return
  3. Impaired cardiac filling and reduced cardiac output
    4.Heart failure and cardiogenic shock
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93
Q

What does atrial rupture lead to?

A

Atrial rupture > rapid accumulation > cardiac tamponade > shock > sudden death

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94
Q

What is caused by slow accumulation of pericardial fluid?

A

Fluid can stretch to accommodate large volume of fluid compared to when rapid accumulation of fluid occurs.

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95
Q

Distinguish primary and secondary cardiomyopathies.

A

Primary - idiopathic, genetic or suspected genetic cause, some breed dispositions

Secondary - nutritional deficiency, endocrine disorder, hypertension cause. May have similar morphological appearance to primary.

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96
Q

Name the 3 main pathological forms of cardiomyopathies.

A

Dilated cardiomyopathy (DCM)
Hypertrophic cardiomyopathy (HCM)
Restrictive cardiomyopathy (RCM)

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97
Q

What is dilated cardiomyopathy?

A

Reduced myocardial contractility and chamber dilation, affecting systolic function.

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98
Q

What is hypertrophic cardiomyopathy?

A

Ventricular hypertrophy, especially affecting the left ventricle. Reduces wall compliance, affecting diastolic function.

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99
Q

What is restrictive cardiomyopathy?

A

Characterised by pathological changes such as endocardial and/or myocardial fibrosis that reduce ventricular wall compliance, affecting diastolic function.

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100
Q

Which animals is dilated cardiomyopathy most common in?

A
  • Medium and large/giant dog breeds, often middle aged/older, more commonly males
  • Uncommon in cats – many cases in 90s linked to deficiency in dietary taurine.
  • Occasionally seen as an inherited condition in Holstein-Friesian and crosses.
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101
Q

What is the pathology of dilated cardiomyopathy?

A
  1. Impaired myocontractility
  2. Impaired systolic function in 1 or both ventricles
  3. Cardiac enlargement with progressive dilation of the heart chambers on 1 or both sides of the heart
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102
Q

What are the gross features of dilated cardiomyopathy?

A
  • Dilated ventricular chamber with thin ventricular walls with reduced contracting ability
  • Dilated atrium
  • Stretching of the AV valve annulus may cause valvular insufficiency
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103
Q

What are the potential consequences of dilated cardiomyopathy?

A
  • Impaired systolic function (pump failure) and reduced cardiac output
  • May have a heart murmur if valve insufficiency
  • Arrhythmias
  • Sudden death
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104
Q

Which animals is hypertrophic cardiomyopathy most common in?

A
  • Most common cause of heart disease in cats, some breed-specific genetic mutations
  • Uncommon/rare in dogs
  • Rare in cattle
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105
Q

What are the gross features of hypertrophic cardiomyopathy?

A
  • Left atrial enlargement is secondary
  • Hypertrophy of the left ventricular free wall and interventricular septum
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106
Q

What is the variability in the gross changes seen in hypertrophic cardiomyopathy?

A
  • Symmetrical hypertrophy affecting the ventricular septum and LV wall
  • Asymmetrical hypertrophy preferentially affecting the ventricular septum or the LV wall
  • Segmental hypertrophy particularly affecting the basal regions of the ventricular system
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107
Q

When should you consider hypertrophic cardiomyopathy in cats at post mortem examination?

A

Consider HCM or other causes of ventricular hypertrophy if the heart weighs over 20g.

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108
Q

What is the pathophysiology of hypertrophic cardiomyopathy?

A
  1. Abnormal cardiomyocyte hypertrophy and fibrosis affect cardiac function, especially the left ventricle
  2. Impaired diastolic relaxation and filling results in increased diastolic filling pressure
  3. Increased filling pressure lead to left atrial dilation and left sided congestive heart failure.
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109
Q

What are the other potential functional effects of hypertrophic cardiomyopathy?

A
  • Dynamic obstruction of the left ventricular outflow tract
  • Arrhythmias
  • Sudden death
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110
Q

What are the contributing factors of dynamic obstruction of the left ventricular outflow tract?

A
  • Narrowing of the outflow tract
  • Systolic anterior motion of the mitral valve
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111
Q

What are the clinical signs of feline aortic thromboembolism?

A

Forelimb will be pink and hind limb with be cyanotic – weak, painful, cold, lacking pulse, cyanosis or pallor of pad.

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112
Q

What are the functional effects and consequences of hypertrophic cardiomyopathy?

A
  • Diastolic dysfunction, atrial dilation, left sided congestive heart failure
  • Dynamic obstruction of the left ventricular outflow tract
  • Arrhythmias
  • Sudden death
  • Atrial thrombosis
  • Feline aortic thromboembolism
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113
Q

Which animals are seen with restrictive cardiomyopathy most commonly?

A

RCM is mainly seen in older cats and less commonly than HCM

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114
Q

What is the pathophysiology of restrictive cardiomyopathy?

A
  1. Extensive fibrosis of the endocardium and myocardium
  2. The fibrosis causes ventricular stiffness with impaired diastolic filling and increased diastolic pressure
  3. Can cause left atrial or bi-atrial dilation and heart failure
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115
Q

What is the most cardiovascular disease in dogs?

A

Myxomatous mitral valve disease

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116
Q

What is myxomatous mitral valve disease

A

Slowly progressive degenerative condition and not inflammatory. Chiefly affects the left atrioventricular (mitral) valve but can affect the right valve in 1/3 of cases.

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117
Q

What are the gross features of valvular endocardiosis?

A

Nodules or plaques, can coalesce. Particularly along the free margin, the valve leaflet is thickened with multiple, sometimes coalescing, bulging nodules with a smooth, red-pink opaque surface.

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118
Q

What are the microscopic features of valvular endocardiosis?

A

Should be nicely layered but is not but has nodule that has lots of blue staining due to too much production of interstitial matrix. Collagen starts to deteriorate.

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119
Q

What is the pathophysiology of valvulvar endocardiosis?

A
  1. Distortion of the valve leaflets can cause valvular insufficiency
  2. During systole, regurgitation of blood from the ventricle into the atrium
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120
Q

What secondary adaptive changes affecting the left ventricle and atrium might occur in myxomatous mitral valve disease?

A

Dilation of ventricles and undergo eccentric hypertrophy of the ventricle and atrial dilation or enlargement. Eventually may exceed ability of ventricle to adapt so walls start to get thinner.

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121
Q

Describe jet lesions as a consequence of valvular endocardiosis.

A

High pressure jets of blood squirting through the distorted valve leaflets (valvular insufficiency) can traumatise the atrial endocardium causing endocardial fibrosis.

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122
Q

Describe chordae tendinae rupture as a consequence of valvular endocardiosis.

A

Can below lax and elongated, leading to prolapse or rupture of the valve leaflet.

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123
Q

Describe atrial tear/rupture as a consequence of valvular endocardiosis.

A

Due to too much contraction or thinning, or jet lesions trauma, or chordae tendinae rupture and large volume of blood enter the atrium.

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124
Q

Distinguish valvular and mural endocardiosis.

A

Valvular endocarditis – inflammation affecting 1 or more of the heart valves

Mural endocarditis – inflammation of the endocardium lining the walls of the cardiac chamber

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125
Q

What is infective valvular endocarditis?

A

Farm animals, bacterial agents. May be one or multiple heart valves affected. Most species have left heart valves most commonly affected but in cattle, the right AV valve is most commonly affected.

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126
Q

What are the gross features of valvular endocarditis?

A

The atrial surface of the valve leaflets have multiple raised, irregular, pale yellow plaques due to fibrin build up. with rough/bumpy surfaces and multiple small red areas.

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127
Q

What is the pathogenesis of valvular endocarditis?

A
  1. Bacteraemia and disruption of the valve endothelium
  2. Bacterial invasion of the valve
  3. Inflammation and thrombus formation on the valve leaflet with blood, fibrin and bacteria. Layers build up forming ‘vegetive’ lesions.
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128
Q

What are the potential consequences of valvular endocarditis?

A
  • Stenosis > increases resistance through valve
  • Valvular insufficiency > allows regurgitation > atrial enlargement, volume overload and eccentric hypertrophy
  • Septic embolism > bacteraemia > brain/lung abscesses
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129
Q

What is the consequence of stenosis during systole?

A

Pressure overload causing concentric hypertrophy

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130
Q

What is the consequence of stenosis during diastole?

A

Increased diastolic filling pressure if blood cannot get through AV valve causing atrial enlargement

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131
Q

What is acute heart failure? What can it be the result of?

A

Rapid onset of new or worsening symptoms/signs of heart failure. Resulting from a new condition or acute decompensation of pre-existing chronic heart failure. Can result I cardiac syncope – profound changes in blood pressure and heart rate. Collapse and unconscious

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132
Q

What are the possible causes of chronic heart failure?

A
  • Pericardial disease
  • Myocardial disease
  • Arrhythmias and conductive disturbances
  • Valvular disease
  • Congenital shunts and anomalies
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133
Q

What is chronic congestive heart failure?

A

Loss of cardiac reserve > forward or backward failure

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134
Q

What is chronic congestive heart failure with backward failure?

A

Failure to deal with venous return, congestion of venous and capillary beds. Characterised by pulmonary and/or systemic vascular congestion and oedema.

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135
Q

What is chronic congestive heart failure with forward failure?

A

Inadequate cardiac output, decreased perfusion of peripheral tissues

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136
Q

What is the pathophysiology of left sided heart failure with backwards failure?

A

Pulmonary congestion and oedema. Clinical signs – dyspnoea, cough

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137
Q

What is the pathophysiology of left sided heart failure with forwards failure?

A

Reduced tissue/oxygen/organ perfusion resulting in hypoxia and ischaemia. Clinical signs – weakness, fatigue, hypotension and shock in severe cases

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138
Q

What is the pathophysiology of right sided heart failure with backwards failure?

A

Systemic tissue/organ congestion and oedema. Clinical signs – ascites, pleural effusion, peripheral oedema, visceral congestion.

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139
Q

What is the pathophysiology of right sided heart failure with forwards failure?

A

Reduced output to lungs and left heart

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140
Q

What are the species differences in backwards failure of right sided heart failure?

A
  • Ascites – especially in dogs
  • Pleural effusion – especially in cats
  • Peripheral oedema – dependent subcutaneous oedema, especially in ruminants and horses
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141
Q

What is the outcome of chronic congestive heart failure?

A

Reduced perfusion of tissues and cardiac output is perceived by the body as a drop in effective circulating blood volume. Occurs despite the fact that total blood volume is adequate or excessive.

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142
Q

How does the sympathetic nervous system attempt to increase plasma volume and maintain cardiac output in chronic congestive heart failure?

A
  • Increased heart rate and contractility and arteriolar constriction
  • Increased venous tone
  • Altered renal blood flow to promote sodium and water absorption
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143
Q

How does the RAAS attempt to increase plasma volume and maintain cardiac output in chronic congestive heart failure?

A
  • Angiotensinogen > renin > angiotensin I > ACE > angiotensin II
  • Vasoconstriction
  • Renal sodium and water retention
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144
Q

How may the neurohormonal responses to chronic congestive heart failure result in congestive heart failure?

A
  1. Sodium and water retention
  2. Systemic vasoconstriction
  3. Increased heart rate, increased contractility
  4. Venous/capillary bed congestion, oedema and reduced tissue perfusion
  5. Volume and/or pressure overload
  6. Maladaptive changes and reduced myocardial function
  7. Congestive heart failure
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145
Q

What are the clinical signs of left sided heart failure?

A

Pulmonary oedema
Tachypnoea
Dyspnoea

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146
Q

What are the clinical signs of right sided heart failure?

A

Distended peripheral veins
Ascites
Pleural effusion

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147
Q

What are the clinical signs of reduced cardiac output?

A

Weak peripheral pulses
Tachycardia

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148
Q

What is the effect of activation of the sympathetic nervous system on the cardiovascular system?

A

Tachycardia (β1) = contractility to increase CO

Vasoconstriction (α1) = afterload and blood pressure increase

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149
Q

What are the effects of the RAAS on the cardiovascular system?

A
  • Sodium, water retention, increase blood volume = preload, increased blood volume and blood pressure
  • Vasoconstriction = afterload
  • Vasopressin = preload and afterload
  • Remodelling
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150
Q

What is cardiovascular remodelling?

A

Contractility, eccentric hypertrophy in response to volume overload or pressure overload from increased afterload leading to concentric hypertrophy, development of fibrosis

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151
Q

What is the presentation of heart failure in small animals?

A
  • Cardiac cachexia (loses body condition as well as muscle tone)
  • Abdominal distension
  • Respiration rate over 35-40bpm
  • Tachypnoea or dyspnoea
  • Cough
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152
Q

What is the heart rate of in dogs and cats with congestive heart failure?

A

Dogs 80-160bpm
Cats 120-240bpm

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153
Q

Describe heart murmurs in horses.

A

It is easy to identify as anything between the slow lub and dub is systolic and anything in the long gap between the dub and the next lub is diastolic

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154
Q

Describe the 6 grades of heart murmurs.

A
  1. Very quiet, takes time to localise
  2. Quite, less loud then heart sounds
  3. Obvious, as loud as heart sounds
  4. Louder than heart sounds
  5. Very loud with precordial thrill
  6. Very loud, thrill, audible lifting stethoscope off chest
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155
Q

When is blood pressure classed as hypotensive?

A

Under 80mmHg

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156
Q

Distinguish dry and wet lungs on lung ultrasounds.

A

Dry lungs – reverberation artefacts (A lines)

Wet lungs – such as pulmonary oedema, pneumonia, haemorrhage

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157
Q

What are the 2 cardiac biomarkers?

A

Cardiac troponin I – cardiomyocyte damage

NT-proBNP – increased filling pressures

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158
Q

What is the aim of acute left sided heart failure?

A

Inotropic support
Pre and afterload reduction

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159
Q

How are the characteristics of acute left sided heart failure treated?

A

Hypoxia – oxygen
Pulmonary oedema – IV furosemide
Contractility – pimobendan
Minimise stress - sedation

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160
Q

How is the diuretic, furosemide, used to treat acute left sided heart failure?

A

Most important drug, NaKCL pump of ascending LOH, rapid and potent, IV vasodilation, IV (IM, SC, PO) 2mg/kg q1-4h

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161
Q

How is the diuretic, torasemide, used to treat acute left sided heart failure?

A

Longer half-life, more potent. Anti-aldosterone, initial drug, dose, PO

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162
Q

How does pimobendan treat acute left sided heart failure?

A
  • Phosphodiesterase 3 inhibitor (cAMP), Ca sensitiser
  • Inotropic, vasodilation, anti-remodelling
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163
Q

How are ACE inhibitors used to treat acute left sided heart failure?

A

Inhibits conversion Angiotensin I to II. Vasodilatation, inhibits sodium ion, water-retention, anti-remodelling

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164
Q

How is spironolactone used to treat acute left sided heart failure?

A

Aldosterone inhibitor, anti-remodelling, weak K-sparing diuretic

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165
Q

What are the life long treatments used in cats and in dogs for heart failure?

A

Dogs: furosemide, pimobendan, ACE inhibitor, spironolactone

Cats: furosemide, clopidogrel (pimobendan, ACE inhibitor, spironolactone)

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166
Q

What are ECGs the diagnostic test of choice for?

A

Bradycardia
Tachycardia
Irregular heart rhythm
Pulse deficits
Syncope, weakness

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167
Q

How are ECG electrodes attached to the animal?

A

Lead I: RA to LA
Lead II: RA to LL
Lead III: LA to LL

aVR: towards the right arm
aVL: towards the left arm
aVF: towards the feet

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168
Q

What is the purpose of ECG leads?

A
  • Leads which provide different views of the same electrical activity in the heart
  • Myocardial cells depolarise/repolarise and lead to vector
169
Q

What is the angle between adjacent ECG leads?

A

6 leads, 60˚

170
Q

What is P on ECG traces?

A

Atrial depolarisation

171
Q

What is PQ interval on ECG traces?

A

Time in AV node is slower for atrial filling

172
Q

What is the QRS complex on ECG traces?

A

Ventricular depolarisation

173
Q

What is T on ECG traces?

A

Ventricular repolarisation

174
Q

What is the structure of a sinus rhythm?

175
Q

What are the 5 steps of ECG analysis?

A
  1. Heart rate
  2. Overall rhythm
  3. P for every QRS, QRS for every P
  4. Complex morphology
  5. Final ECG diagnosis
176
Q

How is heart rate assessed from an ECG trace?

A

R waves in mm
50mm/s = 3000/number of small boxes
25mm/s = 1500/number of small boxes

Is heart rate normal, bradycardic, tachycardic, appropriate for the situation

177
Q

What is a regular ECG rhythm due to?

A

Slow - sinus bradycardia, 3rd degree AV block
Normal - sinus rhythm
Fast - supraventricular tachycardia, ventricular tachycardia

178
Q

What is a regularly irregular ECG rhythm due to?

A

Sinus arrhythmia

179
Q

What is an irregular ECG rhythm due to?

A

Atrial fibrillation

Slow - sinus arrhythmia, 2nd degree AV block
Normal - sinus arrhythmia
Fast - frequent supraventricular/ventricular premature complexes

180
Q

What is lack of consistency and relatedness in an ECG due to?

181
Q

Distinguish supraventricular and ventricular complexes on ECGs.

A

Supraventricular - use specialised condition system (fast) via AVN

Ventricular - conduct cell to cell (slow), slow = wide, abnormal direction of depolarisation = bizarre shape

182
Q

Distinguish premature supraventricular and ventricular ECG complexes.

A

Supraventricular – QRS narrow, sinus tachycardia, supraventricular premature complexes, supraventricular tachycardia (atrial fibrillation).

Ventricular – QRS wide and bizarre, ventricular premature complexes, ventricular tachycardia, accelerated idioventricular rhythm <180bpm.

183
Q

What is the ECG morphology with atrial fibrillation?

A

Irregular supraventricular rhythm, no P waves. In comparison, other supraventricular tachycardias are usually irregular and have present P waves but often hidden in QRS complexes

184
Q

What is the ECG morphology of accelerated idioventricular rhythm?

A

More than 3 ventricular escape complexes in a row, usually associated with systemic disease. Splenic mass/torsion, sepsis, so treat underlying cause.

185
Q

What is the ECG morphology of 1st degree AV block?

A

All P waves conducted, QRS for every P, increased PR interval

186
Q

What is the ECG morphology of 2nd degree AV block?

A
  • Some but not all P waves conducted
  • Type I – progressive increase in PR interval followed by a dropped QRS
  • Type II – fixed PR interval
187
Q

What is the ECG morphology of 3rd degree AV block?

A

No P waves conducted

188
Q

What are the clinical signs of arrhythmias?

A

Weakness
Collapse
Poor output signs

189
Q

What may cause bradyarrhythmia?

A

3rd degree AV block
High grade 2nd degree AV block

190
Q

How is bradyarrhythmia treated?

A
  • Vagolytics – atropine, glycopyrrolate
  • Sympathomimetics – terbutaline, theophylline
  • Permanent pacemaker implantation
  • Antiarrhythmic drugs
191
Q

What are the main 2 acquired cardiac diseases in dogs?

A

Myxomatous mitral valve disease – small breed dogs, adult onset, slow progression

Dilated cardiomyopathy – large breed dogs, adult onset, associated with ventricular arrhythmias

192
Q

What does the pulmonary vein being bigger than the artery indicate?

A

Congestion in the pulmonary veins

193
Q

How does blood pressure affect heart failure?

A
  • Low pressure in left atrium
  • Mitral regurgitation as the path of least resistance is to go the low pressure in the atrium down a pressure gradient. If pressure in the aorta is high, will make regurgitation worse.
  • So by treating the hypertension, can decrease the volume of blood going backwards into his atrium
  • Heart failure with reduced forwards stroke volume would have hypotension
194
Q

What are the 3 features of myxomatous mitral valve disease in dogs?

A

Valve prolapse
Valve thickening
Regurgitation of blood across the valve

195
Q

How is myxomatous mitral valve disease in dogs staged?

A

Stage A – at risk due to genetics mostly, healthy lifestyle is important though

Stage B1 – preclinical disease, no cardiomegaly on an echo

Stage B2 – preclinical disease, cardiomegaly on an echo

Stage C – congestive heart failure

Stage D – CHF refractory to standard therapy

196
Q

How is myxomatous mitral valve disease treated?

A
  • Pulmonary oedema – furosemide
  • Contractility – pimobendan
  • RAAS – ACE-inhibitor (and spironolactone)
  • Diuresis (and remodelling?) – spironolactone
197
Q

Distinguish stage B1 and B2 of myxomatous mitral valve disease?

A

No cardiomegaly = stage B1. No treatment, ACE inhibitors ineffective

Cardiomegaly = stage B2. Pimobendane, ACE inhibitors ineffective

198
Q

How is dilated cardiomyopathy treated?

A

Benazepril
Pimobendan

199
Q

What is the effect of increased ventricular stiffness in cats?

A

Diastolic dysfunction
Good/adequate systolic function

200
Q

What is the effect of left atrial dilation in cats?

A

Increased pressures causing left sided CHF, thrombus in left atrium that can break off causing arterial thromboembolism (unlike in dogs)

201
Q

What is the effect of left sided congestive heart failure in cats?

A

Pulmonary oedema, pleural effusion, pericardial effusion. Unlike dogs, cats also quite often develop right sided CHF at the same time

202
Q

Describe the genetic mutations in cats causing hypertrophic cardiomyopathy?

A

Myosin binding protein C, incomplete penetrance can have mutation without disease

203
Q

What are the possible causes of left ventricular hypertrophy in cats?

A
  • Systemic hypertension
  • Hyperthyroidism
  • Acromegaly
  • Dehydration – causes an optical illusion because the atria get smaller, called pseudohypertrophy
  • Aortic stenosis
204
Q

What are the characteristics of restrictive cardiomyopathy in cats?

A
  • Increased ventricular stiffness, myocardial thickness normal
  • Increased filling pressures, left atrial or bi-atrial dilation and enlargement
205
Q

Use Virchow’s Triad to explain how arterial thromboembolism forms in cats.

A
  • Endothelial disruption
  • Sluggish blood flow (‘smoke’)
  • Hypercoagulability
206
Q

What are the characteristics of arterial thromboembolism in cats?

A
  • Left atrial dilation
  • Aortic bifurcation
207
Q

What are the clinical signs of cardiomyopathies in cats?

A
  • Can have no clinical signs
  • Heart murmur/gallop
  • Arrhythmia, syncope
  • Sudden paresis/paralysis
  • Tachycardia, bradycardia if really severe
  • Tachypnoea, bradypnoea
  • Pulmonary oedema, pleural effusion
  • Weak peripheral pulses if poor CO
208
Q

What are the 5 Ps for the clinical signs of arterial thromboembolism in cats?

A
  • Pain
  • Paresis
  • Pulselessness
  • Pallor/cyanosis
  • Poikilothermy
209
Q

What are the features of a thoracic radiograph indicating heart disease in cats?

A
  • Vertebral heart sum/VHS > 9.3 heart disease likely
  • Pulmonary oedema
  • Pleural effusion
210
Q

What is hypertrophic obstructive cardiomyopathy in cats?

A

Dynamic obstruction left ventricular outflow tract. Systolic anterior motion of the mitral valve sucked towards the septum/outflow tract so does not close properly so mitral regurgitation. Outflow tract is narrowed, causing increased velocity of blood flow.

211
Q

Which diagnostic tests are used for acquired cardiac diseases in cats?

A
  • Biochemistry – electrolytes (RAAS, vasopressin), urea, creatinine, middle aged/older cats will have kidney problems so important to monitor
  • T4 – hyperthyroidism is common in middle aged/older acts and can lead to hypertrophy
  • Biomarkers
  • Blood pressure
212
Q

What is the treatment of preclinical acquired cardiac diseases in cats?

A
  • If increased risk of arterial thromboembolism – clopidogrel better than aspirin (stops platelets sticking together)
  • Left ventricular outflow tract obstruction – atenolol, diltiazem not proven
  • Decrease heart rate, reduces LVOTO, prolongs diastole (coronary circulation)
213
Q

In heart failure in cats, which drug must not be given?

214
Q

How is congestive heart failure treated in cats?

A
  • Check for pleural effusion – drain
  • Furosemide
  • Oxygen
  • Minimise stress
  • Pimobendan - not routine, care if outflow obstruction
  • ACE inhibitor - inhibits RAAS > vasodilation, inhibition of fibrosis
  • Spironolactone - inhibition of fibrosis and hypertrophy
215
Q

What are the anti-thrombotics used in cats?

A
  • Clopidogrel
  • Aspirin
  • Unfractionated or low molecular weight heparin
216
Q

List 6 congenital cardiac defects in dogs.

A

(Sub)aortic stenosis
Pulmonic stenosis
Patent ductus arteriosus
Mitral or tricuspid valve dysplasia
Ventricular septal defect
Tetralogy of Fallot

217
Q

List 4 congenital cardiac defects in cats.

A

Ventricular septal defect
Mitral or tricuspid valve dysplasia
Patent ductus arteriosus
Tetralogy of Fallot

218
Q

What does a left sided base heart murmur indicate?

A

Aortic stenosis – systolic
Pulmonic stenosis – systolic
Patent ductus arteriosus – continuous
Ventricular septal defect – systolic

219
Q

What does a left sided apex heart murmur indicate?

A

Mitral regurgitation – systolic

220
Q

What does a right sided base heart murmur indicate?

A

Ventricular septal defect – systolic

221
Q

What does a right sided apex heart murmur indicate?

A

Tricuspid regurgitation – systolic

222
Q

Describe heart murmurs in puppies and kittens.

A
  • No murmur over 6 months of age
  • No high grade murmur (more than 3/6)
  • No diastolic or continuous murmur
  • The louder the murmur, the more severe the disease, exception VSD
223
Q

What are the 3 forms of aortic stenosis in dogs?

A

Stenosis can be subvalvular, valvular and supravalvular

224
Q

What is the presentation of aortic stenosis?

A
  • Left sided systolic heart base murmur
  • Asymptomatic, exercise intolerance
  • Syncope on excitement/exercise
  • Ventricular arrhythmia, sudden death
  • Left sided congestive heart failure
225
Q

What is the outcome of aortic stenosis?

A
  1. Increased left ventricular pressure
  2. Left ventricular concentric hypertrophy
  3. Post stenotic dilation
  4. Left sided CHF
226
Q

Why does syncope occur in aortic stenosis?

A
  • Fixed obstruction limits cardiac output during exercise (vasodilation)
  • Increased LV pressures (from mechanoreceptor stimulation causing inappropriate bradycardia and vasodilation)
  • Inadequate myocardial blood supply – arrhythmias
227
Q

How is the pressure gradient in aortic stenosis calculated?

A

4 x velocity ^2

228
Q

Distinguish mild, moderate and severe aortic stenosis from pressure gradients.

A

Mild < 40 mmHg
Moderate 40-80 mmHg
Severe > 80 mmHg

229
Q

How is the beta blocker, atenolol, used to treated aortic stenosis?

A
  • If clinical signs, ventricular hypertrophy, ventricular arrhythmia
  • Reduces heart rate – tachycardia is inefficient
  • Prolongs diastole – myocardial perfusion
230
Q

What are the characteristics of pulmonic stenosis?

A
  • Leaflets fused
  • Pulmonary artery hypoplasia
  • No neonatal progression
  • Right ventricular hypertrophy, with/without dilation
  • Post stenotic dilatation
  • Right sided CHF
231
Q

How does pulmonic stenosis present?

A
  • Left sided systolic heart base murmur
  • Syncope on excitement/exercise
  • Right sided CHF
  • Tricuspid dysplasia/regurgitation
232
Q

How is pulmonic stenosis treated?

A
  • Atenolol, if clinical signs, ventricular hypertrophy
  • If severe PS, life expectancy is limited so intervene with balloon valvuloplasty
  • If in CHF, furosemide, ACE inhibitors, spironolactone
233
Q

What is a balloon valvuloplasty?

A

Place a balloon into the right heart across the valve and inflate and deflate very quickly, hopefully to decreased the pressure gradient enough

234
Q

When is balloon valvuloplasty not used?

A

With AS, as this is a fibromusculature ridge, cutting balloon with razer blades in to score this and using high pressure balloon to break it down is used in AS, but not used routinely/as salvage, as it is risky if you cut chordae tendinae and tends to scar over anyway

235
Q

What occurs in patent ductus arteriosus?

A
  1. Smooth muscle replaced with elastic fibres
  2. Left sided dilatation
  3. Increased LV strike volume, rapid run off of blood into pulmonary circulation
  4. Reduced myocardial contractility
  5. Left sided CHF
236
Q

How does patent ductus arteriosus present?

A
  • Asymptomatic, left sided CHF
  • Heart murmur – continuous, frequently palpable thrill (grade 5-6/6)
237
Q

What features of a thoracic radiograph indicate patent ductus arteriosus?

A
  • Overcirculation – both pulmonary artery and veins will be enlarged
  • 3 ‘knuckles’ – enlargement of the aortic arch, the pulmonary artery and the left auricle
238
Q

How is patent ductus arteriosus treated/cured?

A
  • Interventional device closure – amplatz canine duct occlude or coils
  • Surgical closure
239
Q

What is the presentation of ventricular septal defects?

A
  • 5/6 right sided systolic sternal murmur
  • Causes left sided volume overload
  • Small defect causes a very loud murmur
  • Common in cats, very small so have no clinical significance despite loud murmur
240
Q

Explain the pathology of tetralogy of fallot.

A

Septum is forming too far over to the right so end up with a small pulmonary artery and a large aorta and aorta staddles the ventricular septum and takes blood from both sides of the heart. Increased pressure in the right side of the heart, so may have right to left shunting across VSD, which would not normally expect without PS.

241
Q

What occurs during exercise with tetralogy of fallot?

A

Right to left shunting will get worse during exercise as this is when arteriodilation occurs to muscle and systemic vascular resistance decreases and blood can easily go right to left. So upon exercise, patient can go blue/bluer than they were at rest.

242
Q

Define arrhythmia.

A

An abnormality in heart rate, regularity of heart beat, site of impulse origin or sequence of activation (disruption of conduction).

243
Q

Describe the 4 phases of nodal cell action potentials in the heart.

A
  • Phase 4 is gradual increase in potential to minimum to threshold
  • Phase 0 at threshold caused by an inflex of calcium ions
  • Get peak and then repolarisation in stage 3. In myocardial cells you get a flat potential line at the bottom until the next impulse comes along and triggers an action potential
244
Q

What is pacemaker hierarchy?

A
  • Sino-atrial node 80-120 bpm
  • Atrioventricular node 60-70 bpm
  • Bundle of His 40-50 bpm
  • Purkinje fibres 30-40 bpm
244
Q

Which drugs decrease phase 0 in nodal tissue?

A

Calcium channel blockers:
- Used to slow conduction through the AVN
- Useful for arrhythmias originating above the AVN

245
Q

Describe the action potentials of myocardial cells.

A

Flat phase 4, rapid upstroke with phase 0, little decrease in phase 3 and fast repolarisation to baseline.

246
Q

What is the effect of sodium channel blockers on myocardial tissue?

A

Ventricular – class 1b, such as lidocaine

Atrial and ventricular – class 1a, such as procaine, class 1c, such as flecainide

247
Q

What are the causes of arrhythmias?

A
  • Structural remodelling - fibrosis will interfere with depolarisation wave across myocardium
  • Electrical remodelling
  • Haemodynamics
  • Endocrine disease causing electrolyte disturbances
  • Primary cardiac disease - structural remodelling
  • Non-cardiac diseases
248
Q

Which non-cardiac diseases can cause arrhythmias?

A
  • Electrolyte disturbances due to metabolic disease – hyperkalaemia in urethral obstruction cats or Addison’s disease
  • Systemic disease - gastric dilatation-volvulus or splenic neoplasia
249
Q

Name the 3 mechanisms of arrhythmias.

A

Abnormal automaticity
Triggered activity
Re-entry

250
Q

How does arrhythmia develop from abnormal automaticity?

A

Normal automaticity – spontaneous rhythmic depolarisation. Abnormal automaticity – spontaneous rhythmic depolarisation in cells outside the conduction system (outside the backup system), such as diseased myocardial cells may develop abnormal automaticity.

251
Q

How does arrhythmia develop from triggered activity?

A

Afterdepolarisations – oscillations during or just after repolarisation/phase 3 or 4 can trigger subsequent action potentials if big enough.

252
Q

How does arrhythmia develop from re-entry?

A

Abnormal circuit allows the impulse to self-perpetuate. Band of electrically conductive tissue separate from the AVN which allows the impulse to get through from the atrium to the ventricle.

253
Q

How do you investigate for underlying diseases that could cause arrhythmias?

A
  • Medical therapy for congestive heart failure will decreased sympathetic tone and so help control arrhythmia
  • Unblock a cat with urethral obstruction – hyperkalaemia
  • Surgery for gastric-dilation volvulus
254
Q

How does gastric-dilation volvulus cause arrhythmia?

A

Electrolyte abnormalities and cytokine release from a lot of neoplastic and inflammatory disease which affects the myocardium causing arrhythmia

255
Q

When should antiarrhythmic drugs be used and why?

A

Antiarrhythmic drugs can be proarrhythmic. Use only for haemodynamically significant arrhythmias

256
Q

What is the Vaughan Williams classification of antiarrhythmic drugs?

A

Class I – sodium ion channel blockers
Class II – beta blockers
Class III – potassium ion channel blockers
Class IV – calcium ion channel blockers
(Digoxin)

257
Q

What is the effect of amplodipine?

A

A vasodilator that work/block channels in the peripheral calcium ion channels vasculature so we use it for hypertension.

258
Q

Which class of drug is quinidine?

259
Q

What is the effect of quinidine?

A

Pro-arrhythmic, increases ventricular rate in atrial fibrillation, hypotension, sweat and are very unhappy, look very miserable

260
Q

When is quinidine used?

A

Horses – cardioversion of atrial fibrillation. Nowadays do transvenous electrical cardioversion instead

261
Q

Which drug class is procainamide?

262
Q

What is procainamide used to treat?

A

Supraventricular and ventricular arrhythmias in small animals

263
Q

Which class of drug is lidocaine?

264
Q

What is the use of lidocaine?

A
  • Life-threatening ventricular arrhythmias
  • Selective for diseased tissue, partially depolarised cells and cells with longer action potential duration
265
Q

What are the doses used for lidocaine?

A

Dogs: IV bolus 2mg/kg
Cats: 0.5-1mg/kg
Large animals 0.25-0.5 mg/kg

266
Q

What are the side effects of lidocaine?

A

Nausea
Depression
Seizures
Liver dysfunction

267
Q

Describe class Ic antiarrhythmic drugs.

A
  • Most potent sodium ion blockers
  • Not commonly used as there is risk of cardiac arrest
268
Q

What is the effect of beta-blockers?

A
  • Reduce pacemaker current – decreases the rate of spontaneous depolarisation
  • Slow sinus and AV node conduction
  • Inhibit afterdepolarisations, reducing triggered activity and so risk of tachyarrhythmias
  • Reduce intracellular Ca2+ overload
  • Reduce heart rate but are negative inotropy so a patient with active CHF then beta-blockers may make this worse
269
Q

When should beta-blockers be used?

A
  • Do not use in heart failure
  • Care if respiratory disease present as you can block B2 receptors and cause bronchoconstriction
270
Q

What is the effect of class III antiarrhythmic drugs?

A
  • Block K+ channels
  • Prolong refractory period and action potential duration
271
Q

Name 2 class III antiarrhythmic drugs and what they are used for?

A

Sotalol
Amiodarone

Ventricular and supraventricular arrhythmias

272
Q

What are the side effects of amiodarone?

A

GI, hepatotoxicity, thyroid changes

273
Q

What are the effects of class IV antiarrhythmic drugs?

A
  • Block calcium channels and inhibit inward movement of calcium ions
  • Slow phase 4
  • Slow AVN conduction
  • Decrease automaticity
  • Reduce contractility
  • Vasodilation
274
Q

When is diltiazem used?

A

Slow AVN conduction in supraventricular tachyarrhythmias. Combination with digoxin for rate control of atrial fibrillation

275
Q

What is the effect of digoxin?

A

Parasympathomimetic – decreases sinus node firing slows AVN conduction

276
Q

When is digoxin used?

A

Atrial fibrillation in combination with diltiazem for rate control

277
Q

How does digoxin affect rate control?

A

Inhibits sodium-potassium ATPase – increases intracellular calcium ion and increases contractility so has slight positive inotropic effect

278
Q

What are the adverse effects of digoxin?

A

GI
Arrhythmia

279
Q

Which drugs are used for emergency treatment of supraventricular tachyarrhythmias?

A

Diltiazem IV
Procainamide IV
Esmolol IV (care if cardiac dysfunction)
Amiodarone IV

280
Q

Which drugs are used to treat supraventricular tachyarrhythmias when there is no cardiac dysfunction?

A

Sotalol PO
Atenolol PO

281
Q

Which drugs are used to treat supraventricular tachyarrhythmias when there is associated cardiac disease or atrial fibrillation?

A

Diltiazem PO
Digoxin PO

282
Q

Which drugs are used to treat emergency ventricular tachycardia?

A

Lidocaine IV
Procainamide IV
Esmolol IV (care if cardiac dysfunction)
Amiodarone IV

283
Q

Which drug is used ventricular tachycardia with no cardiac dysfunction?

A

Atenolol PO

284
Q

Which drug is used ventricular tachycardia with associated cardiac disease?

A

Sotalol PO
Amiodarone PO

285
Q

Define oedema.

A

Accumulation of fluid in tissue, often in interstitial space

286
Q

Define effusion.

A

Abnormal accumulation of fluid in a body cavity

287
Q

Describe fluid transportation in the body.

A
  • 2/3 of fluid in the body is intracellular, 1/3 is extracellular
  • Filtration occurs at the arterial end of a capillary into the interstitium and then most of this fluid is reabsorbed
  • Small net filtration is mopped up by the lymphatic system and taken back to the heart
288
Q

What are the 4 factors affecting the movement of fluid?

A
  • Hydrostatic pressure
  • Colloid osmotic pressure
  • Endothelial permeability
  • Lymphatic function
289
Q

Why may there be accumulation of fluid?

A
  • Filtration > resorption
  • Increased capillary hydrostatic pressure
  • Wider oncotic pressure gradient
  • Increased endothelial permeability
  • Loss of effective lymphatic drainage
290
Q

What are the clinical signs of oedema and effusion based off location?

A
  • Peritoneal/ascites – abdominal distension and fluid thrill
  • Lungs or pleural effusion – dyspnoea, tachypnoea
  • Joint effusions – lameness
  • Lethargy
  • Inappetence
291
Q

What are the diagnostic tests for oedema and effusion?

A

Physical examination
Blood tests
Ultrasound
Radiographs
Urinalysis

292
Q

How is oedema and effusions investigated by taking effusion samples?

A
  • EDTA tubes – cell counts, cytology, PCV, PCR
  • Serum tubes – albumin, bilirubin, creatinine, K, triglyceride, glucose, lactate
  • Sterile tubes – culture (bacteria, fungi)
293
Q

How are effusions classified?

A

By total protein and cell count

294
Q

Distinguish transudate and exudate?

A

Transudate – pure or modified

Exudate – septic or non-septic (haemorrhagic, chylous, bilious, malignant)

295
Q

What are the properties of normal pleural/peritoneal fluid?

A
  • Low volume
  • Clear, straw coloured
  • Total protein less than 2.5g/dL
  • Nucleated cell count is low <1000/uL
  • Few cells – mesothelial, macrophages, lymphocytes, neutrophils
296
Q

Describe normal body cavity fluid.

A
  • Small volume because it has low protein so ultrafiltration of blood
  • Purpose is to lubrication between organ surfaces
297
Q

What are the properties of transudate?

A
  • Pale, straw-coloured
  • Specific gravity less than 1.017
  • Totally solids less than 2.5g/dL
  • Nucleated cell count low <1000/uL
  • Few cells
298
Q

Why do transudates form?

A
  • Increased hydrostatic pressure - systemic venous hypertension, pulmonary venous hypertension, hypoproteinaemia
  • Decreased osmotic pressure
  • No change in permeability
299
Q

What are the properties of modified transudate?

A
  • Yellow – serosanguinous
  • Specific gravity of 1.017-1.025
  • Total protein 2.5-5g/dL
  • Nucleated cells is higher at 1000-10000/uL
  • Low numbers of cells, mesothelial cells, macrophages, neutrophils, mature lymphocytes, RBC, atypical cells
300
Q

Why are modified transudates the most common type of effusion?

A

Because a chronic pure transudate will eventually create enough inflammation that some degree of increased permeability will occur so over time the transudate will become modified.

301
Q

In which patients do we see modified transudate?

A

Animals with increased hydrostatic pressure.

302
Q

What are the properties of exudate?

A
  • Turbid – red, yellow, white
  • Specific gravity is high at > 1.025
  • Total protein > 3g/dL
  • Nucleated cell count > 5000/uL
  • Mostly neutrophils and macrophages with/without atypical cells/neoplasia
  • If septic, bacteria
302
Q

Which conditions cause increased hydrostatic pressure causing modified transudate?

A

Right sided CHF
Vasculitis
Neoplasia
Post surgery
Organ torsions

303
Q

What is the effect of increased permeability in exudates?

A

Increased permeability causes inflammatory cells with decreased lymphatic drainage

304
Q

How do exudates form?

A
  1. Local inflammatory response to foreign material – exogenous, neoplastic, endogenous
  2. Cytokines, oxidants, proteases – increase mesothelial and endothelial permeability
  3. Influx of inflammatory cells
  4. Leak of protein into tissue
  5. Obstruction of lymphatics so decreases drainage
305
Q

What are the causes of septic exudates?

A
  • GI leakage
  • Foreign bodies
  • Urogenital tract
  • Respiratory tract
  • Haematogenous spread
  • Intracellular bacteria
306
Q

What are the causes of non-septic exudates?

A
  • Pancreatitis – intra-abdominal inflammation
  • Feline infectious peritonitis
  • Vessels – haemorrhagic effusion
  • Lymphatics – chylous effusion
  • Organ penetration – urine, bile
307
Q

What are the properties of haemorrhagic effusions?

A
  • Closely resemble peripheral blood – RBCs, neutrophils, lymphocytes
  • Specific gravity > 1.025
  • Total protein > 3.0g/dL
  • > 1000 cells/uL
  • PCV > 10%
308
Q

What are the causes of haemorrhagic effusions containing blood clots?

A

Splenic aspiration
Venipuncture
Acute severe haemorrhage

309
Q

What are the causes of haemorrhagic effusions without blood clots?

A
  • Secondary to blunt trauma
  • Coagulopathy
  • Neoplasia
310
Q

What are properties of chylous effusions?

A
  • Impaired lymphatic drainage from the GI tract into the caudal vena cava
  • Opaque – milky
  • Specific gravity > 1.017
  • Total protein > 2.5g/dL
  • Variable cell count
311
Q

Describe the triglyceride and cholesterol levels of effusions.

A

Effusion triglyceride greater than serum triglyceride

Effusion cholesterol is less then serum cholesterol

312
Q

What are the causes of chylous effusions?

A

Cardiac disease
Lung lobe torsion
Trauma
Mass lesions leading to compression of lymph drainage
Idiopathic

313
Q

Describe the creatinine and urea levels in effusions of uroabdomen.

A

Creatinine and urea effusion should be greater than in the blood

314
Q

Describe the properties of bilious effusions.

A
  • Green, orange, yellow fluid
  • Specific gravity > 1.025
  • Total protein > 3.0g/dL
  • Main cells are neutrophils, macrophages
  • Bilirubin in effusion is greater than bilirubin in serum
315
Q

What are the causes of bilious effusions?

A

Trauma
Cholangitis
Pancreatitis
Surgery
Concurrent bacterial infection

316
Q

What are the properties of effusions with exfoliation of cells?

A

Neoplastic or reactive mesothelial cells – highly cellular effusions

317
Q

What are the 4 audible heart sounds in the horse?

A

S1 and S2 always audible, S3 and S4 may be heard depending on the horse, the quality of the stethoscope and the experience of person listening.

318
Q

What is S1 heart sound?

A

Lub- turbulence at closure of mitral/tricuspid valves. Onset of systole

319
Q

What is S2 heart sound?

A

Dup- turbulence at closure of aortic/pulmonary valves. End of systole

320
Q

What is S3 heart sound?

A

D- Ventricular filling. Early diastole

321
Q

What is S4 heart sound?

A

Le- associated with atrial contraction. Just before S1

322
Q

How may cardiac disease present in the horse?

A

Weight loss
Ventral oedema
Weakness
Ataxia
Syncope
Exercise intolerance

323
Q

What are the clinical signs of reduced cardiac output/forward failure in the horse?

A
  • Exercise intolerance
  • Tachycardia
  • Pale mmbs
  • Weak arterial pulses
  • Cold extremities
  • Collapse/syncope
  • Cachexia/weight loss
324
Q

What are the clinical signs of pulmonary venous hypertension/left sided backwards failure in the horse?

A

Tachypnoea
Coughing
Crackles (pulmonary oedema)

325
Q

What are the clinical signs of systemic venous hypertension/right sided backwards failure in the horse?

A
  • Jugular vein distension
  • Pulsation of jugular vein extending beyond the caudal third of the neck
  • Pleural and peritoneal fluid (ascites) accumulation
326
Q

How is cardiac auscultation done in the left hemithorax of a horse?

A
  1. Mitral valve - S1 is loudest. Listen for systole and diastole, radiate
  2. Move cranially and dorsally, S2 becomes loudest
  3. Move over aortic valve, listen to systole and diastole, radiate
327
Q

How is cardiac auscultation done in the right hemithorax of a horse?

A

Move over tricuspid valve, radiate stethoscope around. Heart sounds on right are usually quieter

328
Q

Name 3 further diagnostic techniques used in horse cardiac diseases.

A

ECG
Echocardiography
Biomarkers

329
Q

What are 3 examples of ECG equipment used in horses?

A
  • AliveCor (smart phone) single lead
  • Televet has four leads
  • Lead II is the standard lead for equine interpretation, which records between the RA and LL electrodes
330
Q

What is the standard ECG configuration used in horses?

A

Base-apex configuration.
- Negative right arm electrode - cranial to right scapula
- Positive left leg electrode - caudal to cardiac apex

331
Q

Where are ECG leads placed in horses during ridden exercise?

A

All on the left side of the horse

332
Q

Why is echocardiography used in horses?

A

Identify congenital heart disease, valvular disease, to assess contractility and to obtain measures of heart size

333
Q

What is the most commonly used biomarker used in equine cardiac disease?

A

Cardiac troponin I
Identifying myocardial disease, however this is uncommon in horses

334
Q

Describe physiological murmurs in horses.

A

No cardiac pathology. Particularly associated with left ventricular ejection (blood flow into the aorta). Quieter, soft and localised, do not have precordial thrills and do not obscure heart sounds.

335
Q

Describe valvular regurgitation murmurs in horses.

A

Valvular disease in horses can be due to degenerative or inflammatory processes.

336
Q

Describe heart murmurs caused by congenital defects in horses.

A

Typically loud and often accompanied by precordial thrills, simple defects such as ventricular septal defects can be well tolerated and therefore not detected until the horse is mature.

337
Q

What are the causes of left sided systolic murmurs in horses?

A

Mitral regurgitation
Physiological ejection murmur

338
Q

What are the causes of right sided systolic murmurs in horses?

A

Tricuspid regurgitation
Ventricular septal defect

339
Q

What are the causes of diastolic murmurs in horses?

A

Aortic regurgitation
Functional early diastolic

340
Q

Distinguish holosystolic and pansystolic murmurs due to mitral regurgitation in horses?

A

With holosystolic murmurs (mitral/tricuspid regurgitation), the murmur is heard between the lub and dup

With pansystolic murmurs (mitral/tricuspid/VSD), murmur obscures the heard sounds

341
Q

Which valve regurgitation is most likely to lead to congestive heart failure in horses?

A

Mitral regurgitation

342
Q

When is echocardiography considered with mitral regurgitation in horses?

A

If grade 3/6 or higher

343
Q

What is the cause of physiological ejection murmurs in horses?

A

Turbulence caused by the high volume and velocity of blood flowing into the aorta

344
Q

Summarise the characteristics of mitral regurgitation in horses.

A
  • Point of max intensity = left apex
  • Timing = systolic - early, mid, late, pan, holo
  • Grade = 1 to 6
  • Radiation = localised to widely radiating
  • Exercise/sympathetic stimulation = no change with murmur
345
Q

Summarise the characteristics of physiological ejection murmurs.

A
  • Point of max intensity = left base
  • Timing = systolic - early to mid
  • Grade = typically 1 to 3
  • Radiation = localised
  • Exercise/sympathetic stimulation = murmur may disappear or be accentuated
346
Q

Describe ventricular septal defect in horses.

A
  • Commonest congenital defect in horses
  • The shunt direction is usually left to right
  • Causes a loud pansystolic coarse murmur over the right side
347
Q

Summarise the characteristics of tricupsid regurgitation in horses.

A
  • Signalment = common in TBs
  • Point of max intensity = right apex
  • Timing = systolic - early, mid, late, pan, holo
  • Grade = 1 to 6
  • Radiation = localised to widely radiating
348
Q

Summarise the characteristics of ventricular septal defects in horses.

A
  • Signalment = congenital predisposition in Welsh section A ponies, Shetlands, Arabs
  • Point of max intensity = ventral to right apex
  • Timing = systolic - pan, holo
  • Grade = 4 to 6
  • Radiation = cranial and ventral
349
Q

Describe the murmur produced from aortic regurgitation in horses.

A
  • Heard over the left hemithorax initially but as the murmur progresses, it may become audible to the right hemithorax
  • Holodiastolic decrescendo murmur (long)
  • Often musical quality, caused by vibration of the valve leaflet
350
Q

Describe aortic regurgitation in severe cases in horses.

A

Wide pulse difference which results in a very firm it short lasting pulse/waterhammer pulse

351
Q

What can the regurgitant jet in aortic regurgitation lead to in horses?

A

The regurgitant jet can lead to dilation of the left ventricle, which may lead to ventricular arrhythmias (risk of sudden death) so do ECG

352
Q

Describe the murmur produced from functional early systolic murmur in horses.

A
  • Short duration and occur just before S3
  • High pitched ‘whoop’
  • Ventral to the heart base and they can be heard on either side of the chest
  • Physiological
353
Q

Summarise the characteristics of aortic regurgitation in horses.

A
  • Point of max intensity = left base
  • Timing = diastolic - late, holo, pan
  • Grade = 1 to 6
  • Radiation = to the right
  • Characteristic = decrescendo, musical
  • Exercise/sympathetic stimulation = no change
354
Q

Summarise the characteristics of functional early diastolic in horses.

A
  • Point of max intensity = apex, ventral to heart base
  • Timing = diastolic - early
  • Grade = 1 to 3
  • Radiation = localised
  • Characteristic = musical, squeaking
  • Exercise/sympathetic stimulation = murmur may disappear or is accentuated
355
Q

What are the indications of echocardiography from heart murmurs in horses?

A
  • When a murmur other than physiological is heard
  • Aortic murmur greater than 3/6
  • Mitral above 3/6
  • Tricuspid, murmur over 4/6 in racehorse and over 3/6 in non-racehorse
356
Q

What are the other indications for echocardiography in horses?

A
  • In association with pyrexia
  • Other clinical signs of CHF
  • In association with atrial fibrillation or poor performance
357
Q

What are phsyiological arrhythmias in horses?

A

Physiological arrhythmias are 1st and 2nd degree AV block and sinus arrhythmia

358
Q

What are pathological arrhythmias in horses?

A

Pathological arrhythmias are atrial premature depolarisations, atrial tachycardia, atrial fibrillation, ventricular premature depolarisations, ventricular tachycardia and 3rd degree AVB.

359
Q

Describe sinus arrhythmias in horses.

A

Variations in RR interval. Not pathological. Uncommon but do see it occasionally after exercise. No treatment necessary.

360
Q

Describe 2nd degree AV block in horses.

A
  • Common
  • Occurs at low heart rates and disappears with exercise
  • On auscultation, hear a dropped beat in which the S4 sound is typically heard and is not followed by S1/lub or S2/dub
  • On ECG, dropped beats in which a P wave is not followed by a QRS complex
361
Q

Describe 3rd degree AV block in horses.

A
  • Complete conduction block between atria and ventricles
  • No relationship between P and QRS complexes
  • Present as recumbent, weakness, profound exercise intolerance
  • Heart rate very low
362
Q

Describe atrial fibrillation in horses.

A
  • Most frequent pathologic arrhythmia
  • Presents as exercise intolerance (wobbly, epistaxis) in athletic horses
  • Auscultation rhythm irregularly irregular and no S4
363
Q

What is the reason behind high incidence of atrial fibrillation in horses?

A

Due to high vagal tone and the large atrial size in horses. As large atria are more susceptible to maintain AF, large breed horses and horses with underlying cardiac disease that results in atrial dilatation (such as mitral valve regurgitation) are predestined to develop AF.

364
Q

What is the pathological mechanism of atrial fibrillation in horses?

A

Circus movement and re-entry of eaves of depolarisation

365
Q

How does atrial fibrillation in horses appear on ECG?

A

Baseline irregularity = f waves (no p waves), normal QRS complex but RR interval irregularly irregular.

366
Q

How does atrial fibrillation affect exercise in horses?

A

The loss of atrial contraction has minimal effect on cardiac output at rest, therefore, clinical signs are rarely noticed at rest. However, during exercise (high HR) the atrial contraction contribution to ventricular filling becomes important, therefore cardiac output is decreased resulting in exercise intolerance.

367
Q

How are horses with atrial fibrillation treated?

A
  • Oral quinidine sulphate is the pharmacological treatment available
  • Nowadays, transvenous electrical cardioversion (TVEC) is proving successful
  • Recurrence of AF is 30%
368
Q

What is the effect of quinidine sulphate in equine atrial fibrillation?

A
  • Prolongs the refractory period
  • 20mg/kg by nasogastric tube every 2 hours, until conversion, side effects or until 6 doses given
369
Q

6 year old racehorse that ran very badly in his last race. AF diagnosed post-race and confirmed present a few days later. Previous to thus was a good performer. Grade 1/6 left systolic murmur. Would you advise to attempt treatment in this horse with atrial fibrillation?

A

Yes – has left systolic murmur but only grade 1, echocardiography to confirm, unlikely to have atrial enlargement, owners would want to

370
Q

AF detected on annual vaccination in a 5 year old young event horse. Grade 2/6 right systolic murmur. Would you advise to attempt treatment in this horse with atrial fibrillation?

A

Yes – only 2/6 does not have impact on decision making, longer we leave horse in AF harder it is to treat, so must consider if it’s a candidate.

371
Q

AF detected at annual vaccination in a retired horse. No murmurs detected. Would you advise to attempt treatment in this horse with atrial fibrillation?

A

No – can live with AF and would not put horse through this.

372
Q

AF detected in a 8 year old eventer with recent history of exercise intolerance. Grade 5/6 left systolic murmur. Would you advise to attempt treatment in this horse with atrial fibrillation?

A

No – AF is impacting the horse but have a 5/6 murmur. Pursue in terms of murmur but not a good candidate for treatment. If LA is really big it is not fair to the horse, if not that big and owners knew risk, had money and wanted to do it, could do it but would only get 3 months before AF again. Chances are horse would not have a proper career.

373
Q

What are atrial premature depolarisations in horses?

A

Electrical impulses that originate too early/premature somewhere in the atrial myocardium/supraventricular premature depolarisations.

374
Q

What is the appearance of atrial premature depolarisations on ECGs in horses?

A

The P wave is occasionally abnormal in configuration, however, the QRS morphology is typically the same as normal sinus beats.

375
Q

When does atrial premature depolarisation become atrial tachycardia in horses?

A

4 or more APDs in a row are called atrial tachycardia

376
Q

Are atrial premature depolarisations pathological?

A
  • APDs are occasionally found in otherwise healthy horses but their presence is also associated with disease such as myocarditis and electrolyte imbalances.
  • APDs might increase the likelihood of AF
377
Q

What is a ventricular premature depolarisation?

A

A ventricular premature beat is caused by a depolarisation that originates, too early, from the ventricular myocardium. A VPD has a different morphology and usually longer duration than the normal supraventricular depolarisations

378
Q

When do ventricular premature depolarisations become ventricular tachycardia?

A

4 or more VPDs in a row is termed Ventricular tachycardia

379
Q

Are ventricular premature depolarisations pathological?

A
  • VPDs may suggest underlying pathology
  • Because VPDs may initiate VT or VF they carry the potential danger for syncope or sudden death
380
Q

Define collapse.

A

Sudden loss of postural tone. Sustained loss is also possible.

381
Q

Distinguish syncope and pre-syncope.

A

Syncope (fainting) – collapse with transient loss of consciousness

Pre-syncope – partial loss of consciousness, often associated with stumbling/ataxia.

382
Q

What are the characteristics of syncope?

A
  • Typically occur at wake/exercise
  • May be preceded by pre-syncopal event/ataxia
  • Typically flaccid collapse
  • No autonomic signs
  • Short (seconds to small number minutes)
  • Rapid recovery
383
Q

What are the characteristics of seizures?

A
  • Typically occur at rest
  • Loss of consciousness
  • Do not respond to environment
  • Tonic clonic movements
  • Jaw chomp/chatter/salivation with/without autonomic signs
  • Urination, defecation
  • Usually short (<2-5 minutes)
  • Post-ictal/longer recovery
384
Q

What are the body systems involved in collapse?

A

Cardiorespiratory, neuromuscular, metabolic. You need an intact neuromuscular system and postural tone to stand and co-ordinate ambulation. You brain cells need oxygen and glucose to function.

385
Q

What causes episodic collapse?

A

Transient failure of oxygen delivery causes episodic collapse. Most common cause of failure of oxygen delivery to cell, resulting in syncope is cardiac arrhythmias.

386
Q

What is syncope usually due to?

A

Intermittent (marked) hypotension

387
Q

What are the cardiac causes of syncope?

A
  • Tachyarrhythmias – impeded filling/impaired output
  • Bradyarrhythmias – impaired output
  • Neurocardiogenic reflexes
  • Myocardial/valvular disease rarely results in syncope
  • Right to left shunts
  • Pericardial effusion
388
Q

What is vasovagal syncope?

A

Combination of bradycardia/bradyarrhythmia with reflex vasodilation causing blood pressure to drop even further

389
Q

What is the mechanism behind vasovagal syncope?

A

Specific mechanism is unclear but is related to failure of autonomic function – abrupt increased vagal/parasympathetic tone and transient withdrawal of sympathetic tone

390
Q

What are the events that could trigger vasovagal syncope?

A

In apparent healthy dog, marked excitement, such as in young boxers.

391
Q

What are the physiological events that could cause neurocardiogenic syncope?

A

Coughing (tussive syncope)
Sneezing
Swallowing
Vomiting
Defecating
Urinating
Visceral pain

392
Q

How does coughing cause neurocardiogenic syncope?

A

There is increased intrathoracic pressure impeding venous return and vasovagal events – high vagal tone with respiratory disease and GI disease

393
Q

What are the characteristic sounds made by upper respiratory tract obstructions?

A

Stertor – pharyngeal
Stridor – laryngeal
Goose-honking – tracheal collapse

394
Q

Considering what you know so far about causes of syncope, in a syncopal patient, that is normal on examination, what 1 test is most likely to be useful?

A

ECG – dysrhythmias can be intermittent, can use a halter.

395
Q

How do metabolic causes lead to syncope?

A

Lack of energy/substrates required for cellular function

396
Q

What are the metabolic conditions leading to syncope?

A
  • Hypoglycaemia
  • Electrolyte derangements – required for muscle contraction/movement – hypokalaemia and hypocalcaemia
  • Endocrinopathies – hypoadrenocorticism, hypothyroidism (usually exercise intolerant – rarely episodic collapse)
397
Q

What are the possible differential diagnoses for hypoglycaemia?

A
  • Inadequate synthesis – hepatic dysfunction/portosystemic shunting, hypoadrenocorticism
  • Excessive consumption – sepsis
  • Excess hypoglycaemia agents – insulin (exogenous or insulinoma), xylitol toxicity, oral hypoglycaemics (diabetic owner)
  • Paraneoplastic – insulinoma, hepatomas, IGF2 producing tumours
398
Q

How is hypoglycaemia investigated?

A
  • Suspicion of hepatic dysfunction/portovascular anomaly – biochemistry, bile acid stimulation test, imaging
  • Rule out Addison’s disease – basal cortisol/ACTH stimulation test
  • Suspicious of sepsis – T-FAST/A-FAST
  • Suspicious of neoplasia – imaging, hepatoma, IGF-2 producing tumours
  • Suspicious of insulinoma – glucose, with insulin, at the time of hypoglycaemia, is glucose:insulin appropriate
399
Q

What is an insulinoma?

A

Tumour of pancreatic β-cells cause excessive, unregulated insulin production leading to hypoglycaemia and neuroglycopenia

400
Q

What are the clinical signs of insulinomas?

A

Disorientation
Ataxia
Lethargy
Weakness
Collapse
Seizures
Coma
Death

401
Q

How are the life threatening signs of insulinomas managed?

A
  • If IV available, IV glucose bolus
  • If no IV available, glucogel on mucous membranes
402
Q

How are the non-life threatening signs of insulinomas managed?

A
  • If anorexic, glucose continuous rate infusion
  • If eating, feed high-fibre complex-carbohydrate diet little and often
  • Restrict/gentle exercise
403
Q

How are insulinomas treated?

A
  • Surgical resection
  • Chemotherapy described but high expense/toxicity
  • Conservative management
404
Q

Bloods from a syncopal patient identify the following: Blood glucose 2.1mmol/l (ref. 3.5-5.0mmol/l) and serum insulin 18µU/ml (ref. 5-20µU/ml) Does this patient have an insulinoma?

A

Yes – low blood glucose with high insulin.

405
Q

What are neuromuscular diseases?

A
  • Neuropathy – junctionopathy to myopathy
  • Sodium, potassium, calcium are the principal electrolytes required for action potentials
406
Q

What are some examples of common neuromuscular causes of episodic collapse?

A
  • Myasthenia gravis
  • Exercise induced collapse
  • Paroxysmal movement disorders, such as epileptoid cramping syndrome
407
Q

What is myasthenia gravis?

A

Antibody-mediated destruction of the acetyl choline receptor – failure of sustained impulse conduction, rest and recover

408
Q

What are the 3 forms of myasthenia gravis?

A
  • Systemic, episodic collapse
  • Systemic, fulminant, sustained collapse
  • Focal – megaoesophagus/regurgitation, which can often lead to aspiration pneumonia
409
Q

What are the initial, non-invasive, rapid diagnostics for neuromuscular diseases?

A
  • Blood glucose and electrolytes (hypoglycaemia may be intermittent)
  • Systolic blood pressure
  • Peripheral oxygenation – SpO2 or arterial blood gas analysis with/without including during/post-exercise
410
Q

You are presented with a 5 year old Boxer with episodic, flaccid collapse on exercise. She is otherwise well and physical exam is normal. PCV, blood glucose and electrolytes are normal. What single next test is most likely to be diagnostically useful?

A

Electrocardiography

411
Q

You are investigating a 4 year old MN cross breed dog with collapsing episodes. He is underweight, with a picky appetite. Exam is otherwise normal. Haematology is normal, biochemistry shows low sodium and high potassium. What next test is most likely to be diagnostically useful?

A

ACTH stimulation test

412
Q

What are the possible aetiologies of pericardial effusion?

A
  • Idiopathic
  • Neoplastic
  • Coagulopathy
  • Trauma – penetrating vs non-penetrating
  • Ruptured left atrium – degenerative valvular heart disease
413
Q

How is a pericardiocentesis done?

A
  • Left lateral recumbency – right access 5th-6th ICS, avoid coronary artery, window (no lungs)
  • Prepare area 3rd-8th ICS
  • Echo to check incision point
414
Q

What is the prognosis of pericardiocentesis?

A

Can recur – redrain. If more than 3 times – pericardiectomy

415
Q

What is the pathophysiology of pericardial effusion?

A
  1. Fluid creates compression
  2. Right atrium begins to collapse because pressure is greater in atrium than ventricle
  3. Filling impaired
  4. Reduced cardiac output
  5. Ventricular interdependence – only so much room in the pericardium for ventricles to expand so may be the case that both ventricles cannot expand and fill
  6. Pulsus paradoxus
  7. Electrical alternans – swinging of heart backwards and forwards on ECG/QRS amplitude
416
Q

What is the use of sotalol?

A

Most effective for arrhythmogenic right ventricular cardiomyopathy

Clinical Veterinary Science and One Health 23/24 (36 decks)

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