Sml an semtest

Question 1

Demonstrate a basic understanding of heart physiology ?

Answer 1

Cardiac physiology
(A closed system)

The ciiculatory system consists of two co-dependant pumps (each receives the same volume of blood).
- Left high pressure 120mmhg
- right low pressure 12mmhg
- the two pumps are in series

• the organ systems are in parallel, so one organs resistance dosen’t reduce blood flow through another organ system.

Question 2

Define cardiac output ?

Answer 2

Cardiac output = SV x HR L/min

• the cardiac output is physiologically regulated
• determines the function of CVS
• The CO is what begins to fail in cardiac failure
• the heart must always maintain cardiac output

Question 3

Define cardiac work, pre-load and after-load ?

Answer 3

Definitions heart topic

Cardiac work
- defined by volume, pressure and heart rate = work rate.
- these concepts are understood as pre-load and after-load
- important as both pre-load and after-load may fail during cardiac failure.
- both pre-load and after-load affect stroke volume, cardiac output and are involved in heart failure.

Pre-load
The amount of blood in the ventricle at the end of diastole (filling)

After-load
The pressure against which the heart has to pump

Question 4

Describe your understanding of cardiac regulation ?

Answer 4

Cardiac regulation

Pace maker fires at 100bpm
SA node is regulated “tweaked” depending on HR needs
- carotid sinus nerve and vagus nerve
- carotid receptors and aortic arch receptors

Question 5

Describe your technique for measurements of blood pressure ?

Answer 5

Measuring blood pressure

MAP
- mean arterial blood pressure
- MAP 90mmhg

CVP
- central venous pressure
- about 0mmhg

SVR
Systemic vascular resistance

Question 6

Describe what happens when cardiac reserve is exceeded ?

Answer 6

Cardiac reserve
A diseased heart will still function as long as the reserve is not exceeded.
- heart workload may be increased by about 400% = cardiac reaserve (used during exercise)

Compensation is initiated when cardiac out-put falls
- MAP falls
- Aortic and carotid receptors detect change
- initiates catecholamine release (adrenaline / noradrenaline)
- increased HR
- increased vasoconstriction
- increased contractility
- increased stroke volume
- increased systemic vascular resistance
- venoconstriction / increased pre-load

Question 7

Exam question

Describe intrinsic and extrinsic regulation of cardiac out-put ?

Answer 7

Regulation of cardiac out-put

Intrinsic
- The Frank-Starling law of the heart
- the heart pumps all the blood it receives

Extrinsic regulation
- Neurohormaonal
- Sympathoadrenal system (sympathetic nervous system)
- Renin Angiotensin aldosterone system (RAAS)

Question 8

Exam question

Describe how the sympathetic nervous system acts to regulate cardiac out-put ?

Answer 8

Sympathetic nervous system
(Adrenaline and noraadrenaline stimulated via hypoxia)

Acts upon Beta one receptors
- primarily located in the heart
- increases heart rate and stroke volume
- causes vasodilation to vital organs

Acts upon Beta two receptors
- also cause increased heart rate and stroke volume
- stimulation leads to vasodilation redirecting blood flow to organs important for a flight/ fight response

Stimulate alpha one receptors
- stimulation causes vasocontriction
- located in less vital organs eg GIT, cause vasodilation redirecting the majority of blood flow to where it is needed

Question 9

Exam question

Describe how the RAAS system works and its activation ?

Answer 9

RAAS = renin angiotensin aldosterone system.
Stimulated via
- decreased blood pressure
- reduced sodium to the macula denser
- increased sympathetic tone

Physiology
Angiotensinogen released via the liver
Renin released via the kidneys
- renin acts upon angitensinogen to angiotensin one (inactive)
- ACE from the lungs converts angiotensin one to angitensin two (active)
- Angiotensin two acts upon the adrenal gland (aldosterone) and the pituitary gland (vasopressin)

The overall effect of RAAS causes retention of sodium and thus fluid.

Question 10

Discuss how the RAAS system may act to exacerbate heart failure ?

Answer 10

RAAS activation
Angiotensin two = vasoconstriction and increased volume
Adosterone = Sodium retension

Overall effect
Increased blood volume
- increased CVP (central venous pressure)
- increased SVR
- CVP increase results in increased fluid extravasation

The overall effect increase cardiac work and may exacerabate heart failure

Question 11

Describe the difference between forward and backwards failure ?

Answer 11

Forward vrs backwards failure
**
Forward failure**
Heart fails to pump blood out at a high enough pressure to maintain BP
- fainting (syncope), collapse, pale mucous membranes, increased HR
- the afterload is too high or pre load to low
- cause blood loss, decreased contractility, increased systemic vascular resistance.

Backward failure
heart fails to pump out all the blood it receives
- more common
- congestion, lung oedema, ascites, anasarca, distended abdomen
- pre-load is too high or after load is too low
- causes volume retention, decreased contractility and poor filling.

Question 12

What is the consequences of congestive heart failure ?

Answer 12

Consequences of congestive heart failure.
Congestive heart failure = failure of the heart as a pump, concomitant activation of compensatory pathways, leading to volume retention, increased venous pressure with congestion and oedema.

Affects Starlings forces
- increases hydrostatic force
- forces promote fluid extrasation in capillaries
- Starling’s forces are affected in congestive heart failure; increased net pressure out

Question 13

A. What is concentric hypertrophy of the heart ?
B. Provide an example of concentric hypertrophy ?

Answer 13

Concentric hypertrophy = adaptive remodelling of the heart

A. Concentric hypertrophy
- occurs due to a pressure overload
- heart wall becomes thicker
- lumen of ventricles becomes smaller
- pressure overload, need to increase pressure of contraction (big strong muscle).

B.
- aortic stenosis (left ventricle)
- pulmonic stenosis (right ventricle)
- systemic hypertension may also cause pressure overload.

Question 14

A. What is eccentric hypertrophy of the heart ?
B. Provide examples of eccentric hypertrophy ?

Answer 14

A. Eccentric hypertrophy
- results from volume overload
- lumen becomes larger
- volume overload need to restore volume of SV to restore SV
- adaptive mechanism

B. Examples of eccentric hypertrophy
- CHF, mitral valve disease

Question 15

Answer 15

Answer

Aortic stenosis
Type of overload - afterload
which ventricle - right
adaptive response - pressure so concentric hypertrophy

Pulmonic stenosis
Type of overload - afterload
which ventricle - right
adaptive response - pressure so concentric hypertrophy

Patent ductus arteriosis
Type of overload - pre load
which ventricle - left (all recirculated back to left ventricle)
adaptive response - volume / eccentric hypertrophy

Question 16

Describe the clinical signs you would observe with right sided heart failure and left sided heart failure ?

Answer 16

Clinical signs

Right sided heart failure
- congestion of liver and abdominal organs
- increased pressure in capillaries
- hepatomegaly and ascites

Left sided heart failure
- pulmonary congestion and oedema
- increased respiratory rate
- crackles on auscultation
- dyspnoea (expiratory)

Question 17

What is acute heart failure and its causes ?

Answer 17

Acute heart failure
Not common in animals
- BP drops
- cerebral perfusion stops
- loss of consciousness
- death or recovery

Potential cause (very rare in animals)
- cardiomyopathy DCM or HCM
- Toxins cardiac glycosides, digitalis

Question 18

Describe how we could utilise signalment of dogs and cats to identify the most likely cardiac disease ?

Answer 18

Question 19

Describe what the heart sounds indicate during auscultation ?

Answer 19

Auscultation
(Quiet room, atleast 30sec, over all four heart valves PAM 345).

“Lub” S!
- closure of the mitral and tricupsid valve
- low pressure

“Dup”
- closure of the aortic valve
- high pressure

Question 20

What is a murmur, and identify its potantial causes ?

Answer 20

Murmur
Turbulent flow through the heart

In health blood flow through the heart is laminar.
Turbulent flow may be caused by;
- anemia (quiet murmur)
- valvular insufficiency (unable to close)
- valvular stenosis (unable to open)
- congenital malformation

Question 21

How do you identify a systolic and diastolic murmur, provide examples ?

Answer 21

Diastolic vrs systolic murmur

Diastolic (relaxation)
Heard outside the Lup dup sound
- occurs during relaxation
- insufficiency of aortic or pulmonary valve
- mitral or tricupsid stenosis

Systolic (contraction)
Heard between the Lub dup sound
- insufficiency of the mitral or tricupsid valve
- stenosis of pulmonary or aortic valve
- VSD

Question 22

What are the three things we can accurately identify on an X-ray of the heart ?

Answer 22

Radiographs of the heart
(probably the most valuable tool for cardiology).

1. Assessment of cardiac size
2. Shape - enlargement of the left atrium
3. Assessment of Congestive heart failure - cardiogenic oedema.

Question 23

What are the advantages and disadvantages of Xray ?

Answer 23

Radiographs

Advantage
- readily available and cheap
- can identify lung pathology; oedema, and thus CHF

Disadvanatge
- can not measure heart contractility
- can not assess chamber size
- less accurate to measure LA size
- unable to locate the source of murmur
- can not definitively diagnose the type of heart disease

Question 24

Identify the three ways we can assess cardiac size on X-ray ?

Answer 24

Cardiac size assessment on radiograph

1. Vertebral heart score
   - normal between 8.5-10.5
   - there is a large amount of variation between different breeds eg dachshund, dobberman (deep chested animals heart may appear larger).
   - objective measurement
2. VLAS (vertebral left atrial size).
   - objective measurement of the left atrial size
3. Subjective assessment
   - less than 2/3 of the width/ height of the thorax
   - dogs < 2.5-3.5 intercostal speces / cat >2 intercostal spaces
   -

Question 25

Describe how we assess shape in radiographs of the heart ?

Answer 25

Assessment in heart shape on rads Clock face anology - can only accurately assess MPA and LA on rads - left atrial bulge

Question 26

How can you assess congestive heart failure in your patient ?

Answer 26

Congestive heart failure This can only be assessed via visualisation of cardiac oedema in the lungs on radiograph.

Question 27

What are the main complications with assessment of cardiac disease on radiographs ?

Answer 27

Radiographs 1. Only visualises the silouette of the heart - can not differentiate soft tissue from fluid - unable to differentiate pericardial effusion from cardiomegaly - unable to differentiate between the chamber - unable to diagnose cause of cardioamegaly 2. Less sensitive - there is a large amount of variation between dogs in the shape of the chest - brachy, doberman deep chest may make the heart appear enlarged - this makes cardiac size more difficult to interpret

Question 28

Identify this pathology ?

Answer 28

Enlarged left atrium with pulmonary oedema. This animal has congestive heart failure.

Question 29

Identify this pathology of the heart, and identify its differentials ?

Answer 29

Cardiomegaly Differentials - pericardial effusion - myoxomatous mitral valve disease (usually has enlargement of the left ventricle) - globoid DCM - HCM

Question 30

What are the positives and negatives of echocardiography ?

Answer 30

Echocardiography Positives - can assess chamber size - can assess contractility - able to diagnose pathology Negatives - unable to predict the onset of congestive heart failure - unable to diagnose congestive heart failure

Question 31

What are the basic principles of echocardiography ?

Answer 31

The basic principles of echocardiography (best probe = phased array small point of beam) Ultrasound passed into the tissues, and bounces back to probe depending on the tissue acoustic properties. Hyperechoic - white/bright reflect the majority of ultrasound waves. Anechoic - black (fluid) hypoechoic - dark reflects some ultrasound waves.

Question 32

Describe the three parts to an echo exam ?

Answer 32

There are three parts to an echo exam 1. 2D (brightness) - mode of echo used to assess the structure of the heart, chamber size 2. M mode (motion) - echo mode to assess contractility and assess function of the heart. 3. Doppler - this is used to assess blood flow (regurgitant/ abnormal blood flow) - Colour doppler, blood flow through a colour depiction eg red away fast/ orange away slow etc - spectrral doppler plots blood movement in a graph

Question 33

Describe potential biochemical markers which could indicate cardiac disease ?

Answer 33

Only useful as an injury marker in humans.

Question 34

Describe the signalment and presentation of myxomatous mitral valve disease ?

Answer 34

**Myxomatous mitral valve disease.** This is the most common heart condition of dogs. Degeneration and break down of valvular tissue; previously called endocardiosis or mitral valve disease. Signalment - usually a small dog, however can present in any dog - predisposed breeds dushound, Cavielier King Charles Spaniel. Presentation - There is often no symptoms found, but a murmur is detected in routine examination - exercise intolerance - dyspnoea - acute collapse

Question 35

Identify the cause of MMVD ?

Answer 35

Myxomatous mitral valve disease There have been many factors identified which may cause MMVD; 1. Genetics - disease of small dogs + most of those dogs are related - gentic hitchhiking or causation - IGF, TGF - genes affecting cardiac development and animal size 2. Inflammatory mediators 3. serotonin 4. mechanical factors such as tensile stress

Question 36

Describe the pathophysiology underlying MMVD ?

Answer 36

Pathophysiology underlying Myxomatous mitral valve disease Degeneration and break down of valvular tissue (Valve becomes soft and edge dosen't seal properly). - most commonly mitral valve - leaks have been identified in other valves (tricupsid valve). - at the end of sytole ventricle pressure high 120mmhg, aorta pressure high 80mmhg but the left atrium low pressure - blood flows back into the atrium through the leaky valve This causes a decrease in cardiac out put. - sympathetic nervous system activated to compensate causing an increase in heart rate and systemic vasoconstriction. - RAAS system activated causing retention of fluid and salt thus volume - this results in increased workload on the heart which can eventually lead to Congestive heart failure. - pulmonary congestion and oedema - death The heart responds to the backflow of blood and increased volume through eccentric hypertrophy.

Question 37

What are the consequences of MMVD ?

Answer 37

Consequences - Myxomatous mitral valve disease 1. Volume overload leads to stretching of the left atrium and eventually left ventricle (eccentric hypertrophy) 2. pulmonary blood vessels become distended and eventually cardiogenic oedema forms.

Question 38

Describe the clinical presentation of MMVD

Answer 38

Clinical presentation Myoxomatous mitral valve - cardiac cough ? - tachypnoea / tachycardia - loss of sinus rhythm - exercise intolerance - syncope = collapse - systolic murmur - dyspnoea cyanosis

Question 39

Describe the gold standard of diagnosis for MMVD ?

Answer 39

**Diagnosing myxomatous mitral valve disease ** Routinely detected via a systolic murmur and nor presenting signs Thourough history - heart worm prophylaxis - typical clinical signs congestive heart failure - environment + duration of signs Physical examination - CBC and serum biochemistry - urinalysis to ensure health of the kidneys prior to treatment with diuretic - murmur - systolic, loudest over the mitral valve - heart rate - respiratory rate - pulse deficits **Radiograph** ( not all dogs with a murmur will develop CHF) - radiographs can be used to stage the disease - CHF = congestion lung oedema - VLAS size of the left atrium (staging) - pulmonary vein enlargement - never treat an animal for MMVD without the minimum of an X ray. Echcardiography - can be used to confirm diagnosis - mitral regurgitation and valve thickening - limited value to carry out serial echo measurements.

Question 40

Describe how you may utilise staging to manage MMVD ?

Answer 40

Staging to manage Myxomatous mitral valve disease ? ( not all murmurs develop into CHF 20% = Xray) A staging system has been developed to standardise management and treatment. **MMVD staging system and treatment Stage A** - at risk of heart failure, breed predisposition dush, Cavie - no detectable heart disease - no treatment reccomended. **Stage B1** - murmur can be heard on auscultation - no cardiac remodelling - no treatment recommended ** B2** - murmur detected on auscultation - cardiac remodelling evident (+enlarged left atrium / ventricle) - treatment = pimobendan - can delay the onset of CHF by as much as 15 months **Stage C - Congestive heart failure** - pulmonary oedema evident - frusimide - pimobendan - ACE inhibitor **Stage D - refractory to optimum treatment** - if kidneys are coping increase dosage of frusimide - 3rd dose of pimobendan - usually will die from heart disease faster than kidney disease.

Question 41

Describe your management of an animal with MMVD ?

Answer 41

Management of myoxamatous mitral valve disease. Emergency stabilise your patient priority - oxygen - frusemide - pimobendan - anxiolytics = diazepam - the patient must be staged onece stable + consider comorbidities. Radiograph Use staging to define your onging treatment - A - D

Question 42

Describe the effects of pimobendan and frusimide

Answer 42

Pimobendan - improves contractility of the heart - spares workload of the heart, making it more efficient - reduce afterload - inhibit RAAS - arterial dilator Frusemide - reduce congestion and fluid retention - requires healthy kidneys prior to treatment

Question 43

Describe the most effective strategy for onging monitoring of MMVD ?

Answer 43

Ongoing monitoring myxomatous mitral valve disease Best - Owner should collect sleeping respiratory heart rate (APP available) - accurate management of progression - <30 min = no treatment or change to treatment - >30 min needs increased frusimide For stages B1 and B2 recheck yearly For any dog with CHF recheck every 3-4 months

Question 44

Have an understanding of the prognosis of DCM

Answer 44

Prognosis of dilated cardiomyopathy Guarded to poor Indicators of poor prognosis - severity - ascites - atrial fibrillation - cardiac cachexia - outcome can be improved through the use of pimobendan - prevention can be carried out through genetic testing and echo examinations on potential breeders.

Question 45

Describe the common history and signalment of a patient presenting with DCM ?

Answer 45

Dilated cardiomyopathy Signalment - The second most common disease of dogs - most common heart condition of larger breed dogs - Doberman, Great Dane, Irish wolfhound, Portuguese water dogs History + Thourough physical exam - systolic murmur identified in consult - can auscultate the heart over a much larger area then expected - exercise intolerance - pale mucous membranes - tachycardia

Question 46

Describe the clinical signs of DCM in a patient ?

Answer 46

DCM Clinical signs -Most common heart condition of large breed dogs prognosis is generally poor Occult DCM - No obvious clinical signs - sudden death - of concern to owners (no good bye) Overt DCM - Exercise intolerance - Tachycardia - Tachypnoea - Syncope (collapse) - Ascites - Weight loss - Coughing is uncommon - jugular distension

Question 47

Discuss the potential causes of dilated cardiomyopathy ?

Answer 47

Dilated cardiomypathy The cause; The pathogenetic basis remains to be fully elucidated - genetics (many key loci identified) causation / association - taurine deficiency - idiopathic - myocarditis - doxorubicin

Question 48

Discuss the clinical consequences of DCM ?

Answer 48

What are the clinical consequences of DCM Unidentified insult (doxorubicin, taurin deficiency, or genetic) 1. The heart becomes dilated and thin walled - spherical or globoid - cardiac dysfunction - Left ventricular remodelling 2. This causes an increase in pre load and after-load with a subsequent decrease in cardiac out put. 3. This affects the myocardium of the left and right side of the heart 4. Neurohormonal activation RAAS - increases salt and water retention 5. Neurohormonal activation increase in catecholamine - causing tachycardia and vasoconstriction increasing cardiac workload 6. Fluid over load symptoms, morbity and death 7. Generally a poor prognosis

Question 49

Know and disscuss diagnosis of DCM

Answer 49

Diagnosis of dilated cardiac myopathy (history and thourough physical exam) - systolic murmur - can auscultate over a wider area then expected - pulmonary crackles - abdominal fluid wave - jugular distension Gold standard = Holter ECG (VPC per 24 hours) - no need to sedate, often used due to the risk of collapse - can be normal especially with occult cases - sinus tachycardia - large QRS complexes - atrial fibrillation Radiograpgh - pulmonary oedema indicates congestive heart failure (must be used to identify CHF) - globoid heart Echocardiography - dilated chamber and thin cardiac wall - tachycardia

Question 50

# 6 points of managemennt Describe the treatment principles of DCM ?

Answer 50

Dilated cardiomyopathy 1. relieve congestion - Frusimide 2. Promote contractility (positive ionotrope) dubutamine 3. Pimobendan - spares workload of the heart making it more efficient 4. Exercise retriction 5. Drain ascites and pleural effusion 5. Limit cachexia, Omega three fatty acids - reduces wastage along the spine and neck - thought to be related to beta receptors 6. Levosimendan - calcium sensitizer which improves cardiac function, reducing both pre-load and afterload - dilates bloods vessels