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Year 3 MOD > Small Animal Cardiology and Respiratory Medicine: Examination, Pathophysiology and Management > Flashcards

Small Animal Cardiology and Respiratory Medicine: Examination, Pathophysiology and Management Flashcards

1
Q

What signs might a dog with respiratory or cardiac disease present with?

A

Cough
Respiratory noise
Increased respiratory rate or effort- dyspnoea
Lethargy/exercise intolerance
Collapse

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2
Q

What conditions are of the Resp/CV system are certain breeds predisposed to?

A

CKC spaniels and other small breeds- Mitral valve disease/MMVD

Dilated cardiomyopathy in Dobermans and large giant breeds of dog

Yorkshire terriers predisposed to tracheal collapse

Cats- hypertrophic cardiomyopathy

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3
Q

What history finddings may suggest cardiac/respiratory disease?

A
  • Coughing- when, productive?, length
  • Breathing rapidly, laboured, difficulty- constant/intermittent
  • Change in voice- laryngeal problem
  • Breathing noise
  • Nasal discharge- uni/bilateral
  • Excercise intolerance
  • Collapse/wobbly episodes- get a full description
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4
Q

How can CV/Resp diseases be physically examined for?

A

Observation- RR, (20-30 in dogs/cats)

Dyspnoeic patient- look for obstructive- inspiration/expiration/restrictive

MM- cyanosis, anaemic

CRT- <2 seconds

Cardiac output- femoral pulse quality

Warmth of extremities

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5
Q

What are signs of foward heart failure?

A
  • Lethargy, excercise intolerance
  • Weak femoral pulses
  • Pale mucous membranes
  • Quiet heart sounds- precordial impulse difficult
  • Cold extremities
  • Sometimes core temperature reduced
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6
Q

What are signs of left sided CHF?

A

Increased respiratory rate often with increased effort

Restrictive breathing pattern

Sometimes- soft inspiratory crackles

Radiographs- gold standard

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7
Q

What are the signs of right sided CHF?

A

Abdominal distension (ascites) most common in dogs, fluid wave on ballotment

Hepatomegaly- if liver is palpable, due to hepatic venous congestion

May have visibly congested, distended jugular veins

Heptaojugular reflex- gentle cranial abdominal pressure will increase caudal vena cava flow- increased distension of the jugular veins

Pleural effusion can sometimes be due to R-CHF or biventricular failure

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8
Q

What is the normal BPM of dogs and cats?

A

Dogs- 80-140

Cats- 120-200

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9
Q

What should be listened out for with respiratory auscultation?

A

Check larynx and trachea

Bronchovesicular sounds are normal

Adventitious lung sounds- crackles- smaller openings, wheezes- narrowing

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10
Q

What are the 5 ways a heart murur is categorised?

A

Location- point of maximal intensity (3rd, 4th, 5th intercostal space)

Timing- Systolic, diastolic, continuous

Grade

Character

Radiation

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11
Q

How are heart murmurs graded?

A

I/VI- very quiet- only detected in optimal conditions
II/VI- less loud then heart sounds
III/VI- as loud as heart sounds
IV/VI- louder then heart sounds
V/VI- loud heart murmur with precodial thrill
VI/VI- very loud with a precordial thrill

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12
Q

What are the four characters of murmurs?

A

Early systolic murmurs

Mid-systolic murmurs

Holosystolic murmus- between S1 and S2

Pansystolic murmurs- At point of maximal intensity only hear the murmur

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13
Q

What is radiation of a heart murmur?

A

Next loudest position of the murmur from PMI

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14
Q

What do the following point of maximal intensities tell you about the location of heart murmurs?:

Left apex

Left base

Left cranio dorsal

Right side

A

Left apex- mitral valve

Left base- pulmonic/aortic valve

Left cranio-dorsal- patent ductus arteriosis

Right side- tricupsid valve, ventricular septal defects

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15
Q

What is the reynolds number and how is it calculated?

A

The change from laminar to turbulent flow

Re ~ velocity of blood x diameter of blood vesels x density of blood / viscocity of blood

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16
Q

What is an innocent murmus in puppies and kittens?

A

Present initially- get less loud over time

Usually

Diminish with growth

Disappear by 16-20 weeks old due to change of foetal to adult haemoglobin

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17
Q

What creates S1, S2, S3 and S4?

A

S1- closure of atrioventricular valves

S2- closure of the semilunar valves

S3- sound associated with early diastolic filling

S4- late diastolic filling with atrial contraction

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18
Q

What causes an increased chance of S3 and S4 being heard?

A

S4 is heard when animals which depend on atrial contraction to achieve ventricular filling- hypertrophic cardiomyopathy

S3- when early diastolic filling is abruptly decelerated in a stiff, poorly compliant LV and filling pressures are high- dilated cardiomyopathy

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19
Q

How is the thorax percussed?

A

Percussing a cupped hand or directly on the chest wall checking for resonance- reduced with pleural effusion

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20
Q

How can thoracic compressability be assesed in cats?

A

Cranial to the heart- usually springy

With a mediastinal mass or large pleural effusion is is reduced

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21
Q

How can you distinguish between CV and Resp diseases with the following:

HR, Rythm, Coughing, Murmur, Diastolic gallops

A
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22
Q

How is heart disease classified with ACVIM?

A

ABCD

A- no risk/abnormality

B- structural abnormality, no clinical signs
B1- no evidence of remodelling, B2- evidence of significant remodelling

C- Congestive heart failre- acute or chronic
Moderate- home treatment, Severe- Hospitalisation

D- Persistent or end stage

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23
Q

How does ISAHC classify heart disease?

A

Class 1- no clinical signs
1a- no signs of compensation, 1b- mild chamber enlarmgent

Class 2- mild heart failure- signs only on strenuous excertion

Class 3- moderate- severe failure
3a- home treatment, 3b- hospital treatment

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24
Q

How does the NYHA classify heart disease?

A

Class 1- heart disease present

Class 2- heart disease- signs only after strenuous excertion

Class 3- comfortable at rest, signs on modest excertion

Class 4- Sever clinical signs even at rest

25
Q

What is the definition of preload?

A

The venous return to the heart

This influences the degree of end-diastolic stretch and cardiac output by the frank starling mechanism- stretch increases contraction- too an extent

26
Q

What is theh definition of afterload?

A

The resistance or impredance to ventricular ejection during systole

27
Q

What are the major consequences of congestive heart failure?

A

Oedema and effusions

Peripheral vasoconstriction

Tachycardia/Arrhythmias

Remodelling and fibrosis of the myocardium

These result from neuro-hormonal activation

28
Q

How does congestive heart failure increase sympathetic drive?

A

Fall in blood pressure due to low cardiac output causes baroreceptors mediated increase- stimulation of:

  • Cardiac B1 adreno-receptors results in increased HR to try and increase cardiac output
  • B1 receptors on the juxtaglomerular apparatus of nephron results in renin release
  • alpha 1 Adreno-receptors on vascular smooth muscle causes vasoconstriction
29
Q

How does congestive heart failure activate the RAAS system?

A
  • Renin is released from the JGA by B1 receptro stimulation, reduced perfusion of the kidney, reduced sodium concentration
  • Renin is an enzyme which converts angiotensin I in the liver
  • Angiotensin to angiotensin II by ACE
  • ACE also results in the breakdown of bradykinin
  • Angiotensin II acts on the zona glomerulosa of the adrenal cortex to stimulate aldosterone release
30
Q

How do the different components of the RAAS affect the CV system?

A

Angiotensin II-
Potent vasoconstrictor
Potentiates sympathetic activity- central activation enhancing adrenergic tone, facilitating ganglionic transport, enhances the release of noradrenaline
Causes vasopressin release from the posterior pituitary
Effects within cardiomyocytes resulting in hypertrophy and fibrosis

Aldosterone
Causes sodium and water retention
Causes myocardial fibrosis and remodelling

Vasopressin from An II release causes excessive sodium and water retention resulting in oedema and effusions

31
Q

What causes Atrial natriuretic peptide and Brain natriuretic peptide release and what do they cause?

A

ANP- is released due to atrial stretch

BNP is released due to increased LV pressures

These are natural opponents of the adverse effects of angiotensin II- causing diuresis, natriuresis and vasodilation

32
Q

How can heart failure be diagnosed?

A

ANP and BNP can be assayed to demonstrate the presence of heart failure but have a short half life

The inactive N-terminals are more stable and a longer half life and can be assayed by ELISA

33
Q

What causes endothelin release and what does it do?

A

Increases are mediated in part by elevated angiotensin II but also endothelial damage

Endothelin is a potent vasoconstrictor and plays a role in myocardial fibrosis and remodelling

34
Q

What is the La Place relationship?

A

Compensatory remodelling to attempt to normalise wall stress

Wall stress = radius x pressure / 2 x wall thickness

35
Q

What does volume overload lead to and what conditions can lead to this?

A

One or more chambers see and increased volume of blood leading to chamber dilation and usually compensatory hypertrophy- eccentric hypertrophy (wall thickness to chamber size preserved)

Mitral regurgitation
VSD- volume overload of RV, LA, LV
PDA- volume overload of pulmonary vasculature
Tricupsid regurgitation

36
Q

What does pressure overload lead to and what conditions can cause it?

A

Increased resistance results in concentric hypertrophy (thick walls)

Aortic stenosis

Systemic hypertension

Pulmonic stenosis

Pulmonary hypertension

37
Q

What is adaptive remodelling and maladaptive remodelling?

A

Adaptive- changes in heart chamber and all dimesions as a results of the underlying lesion which normalise wall stress

Maladaptive- change in thickness or geometry of a heart chamber and wall stress is increased

38
Q

Why does left sided backwards CHF lead to pulmonary oedema?

A

Elevate filling pressures in the left side of the heart

Increased pressures gets transmitted to the pulmonary vasculature causing fluid to leave the pulmonary circulation and capillaries to result in pulmonary oedema

39
Q

Why does right sided backwards CHF lead to ascites?

A

Elevated right heart filling pressures is transmitted to the great veins

The jugular veins may be distended, elevated central venous pressure affects venous return from the liver- hepatomegaly

Hepatic sinusoids may leak fluid and some protein into the abdominal cavity- Ascites

May result in pleural effusion if any fluid leaks into pleural space

40
Q

How can oedema and effusions be counteracted with CHF?

A

Diuretics- high ceiling loop diuretics- always indicated

e.g Furosemide

41
Q

Why should diuretics not be used as a monotherapy for heart failure long term?

A

They result in further activation of the RAAS and accelerated deterioration of congestive heart failure

Once diuretics are reuqired they are almost always required life long

42
Q

If one diuretic alone is not working (furosemide) as the total dose has reached a maximum what can be done?

A

Switch to a stronger ceiling loop diuretic- torasemide

If further diuresis is required, then additional diuretic drugs can be added, those which act on a different part of the nephron- synergistic effect

e. g spironolactone (competitive antagonist to aldosterone- weak potassium spearing diuretic)
e. g Hydrochlorothiazide and Amiloride

43
Q

Should pleural and abdmonial effusions be drained?

A

Pleural effusions should be drained

Abdominal effusions associated with CHF should not be drained, unless the patient is very uncomfortable or breathing is compromised
Re-absorption with assisted drug therapy is preferred

44
Q

How can neuro-endocrine activation in CHF be counteracted?

A

ACE inhibitors

Anti-aldosterone drugs

45
Q

What are the favourable effects of ACE inhibitor drugs for CHF?

A

Vasodilators- arteries and veins

Reduce release of aldosterone- counteract Na and H20 retention

Prevent Ang II myocardial fibrosis and remodelling

Reduce sympathetic activation

Reduce release of vasopressin

Prevents breakdown of bradykinin (vasodilator)

Ang II- Greater efferent glomerular arteriolar than afferent which results in increased glomerular filtration pressure- ACE inhib couteract this

46
Q

Why might Ang II receptor blockers be used insted of ACE inhibitors?

A

ACE inhibiors show side effects- seen in humans

47
Q

When are anti-aldosterone drugs indicated (spironlactone)?

A

In patients with adequate ACE inhibition, aldosterone levels can tend to rise despire inhibition of RAAS

48
Q

What different kinds of vasodilators can be used and what are there effects for CHF?

A

Arteriodilators- reduce mean arterial pressure, reducing resistance (afterload reducers), reduce wall stresss and myocardial oxygen consumption

Venodilators- increase the capacity of circulation- therefore preload is reduced- left sided filling pressures are reduced- therefore helps alleviate pulmonary oedema

49
Q

How can pulmonary oedema be controlled in an emergency?

A

Furosemide IV- potent diuretic and venodilator in IV

Nitroglycerine- topically- venodilation

This combination is used for rapid control of pulmonary oedema

50
Q

Which two drugs are ‘balanced’ vasodilators?

A

AVE inhibitors

Pimobendan- also positive inotropic effect

51
Q

What drugs are indicated with the treatment of mitral regurgiation and why?

For example MDD, ruptured chordae tendinae

A

Arteriodilators will improve the fraction of forward stroke volume by reducing afterload

52
Q

What drugs can be used for improving cardiac output and when is it indicated?

A

Pimobendan- positive inotrope by increasing sensitivty

Indicated in patients with systolic dysfunction- DCM
Haemodynamic improvments and arteriodilation- MMVD

53
Q

What drug can be used to conuteract the high sympathetic drive in CHF?

What are the indications?

A

Digoxin

Patients with atrial fibrillation

Antiarrythmic

Sinus tachycardia

Reduced systolic function

54
Q

How does digoxin reduce high sympathetic drive?

A

Vagomimetic

Enhances vagal tone and reduces sympathetic tone by:

Direct stimulation of CNS vagal centres
Sensitizes baroreceptors to blood pressure changes
Enhances cardiac pacemaker responses to acetylcholine

Results in- slowing rate of discharge of SAN, slows conduction through AVN

55
Q

Digoxin is a vagomimetic and enhances vagal tone and reduces sympathetic drive

What are its over all effects?

A

Negative inotrope- decreases HR

Favourable autonomic effects

Mild positive inotrope

56
Q

What is the risk of digoxin and what are the signs?

A

Toxicity- Digitoxity

Signs-

  • dull,
  • lethargic,
  • excessive borborygmi- gurgling from intestines
  • Anorexia
  • Vomiting/Diarrhoea
  • Arrythmias
57
Q

What is the standard quadruple therapy for CHF?

What additional drugs may be included?

A
  • Furosemide
  • ACE inhibitor
  • Pimobendan
  • Spironolactone

Additional- other diuretics, anti-arrythmics

58
Q

What is the minimum CHF therapy if there is economic constraints?

A

Furosemide and Pimobendan

Year 3 MOD (42 decks)

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