The Cardiac Patient Flashcards

1
Q

In a shelter population, non-selected and apparently healthy, what is the prevalence of congenital heart disease in both dogs and cats?

A

Reported at approximately 1 in 1000 dogs and cats [ 0.13% in dogs and 0.14% in cats]

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2
Q

For a young & juvenile patient, aside from congenital conditions, what other cardiovascular diseases have been reported?

A
  1. Dilated cardiomyopathy (DCM), such as in a Portuguese water dog which has been reported to be autosomal recessive.
  2. Myocarditis
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3
Q

What are some of the most commonly reported infectious etiologies reported to induce myocarditis, particularly in the young patient?

A

parvovirus, distemper virus, toxoplasma, neospora, spirochetes such as borrelia (Lymes disease), leptospirosis, and bartonella (cat scratch fever), and trypanosoma cruzi (Chagas disease).

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4
Q

Describe how a young patient diagnosed with myocarditis: (1) typically presents (e.g. clinical signs and features) and (2) if they survive, what echocardiogram features they display?

A

(1) presents as heart failure with marked arrhythmias.

(2) If they survive, they may present with a scarred, hypofunctional heart which has a “DCM phenotype”.

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5
Q

For the adult animal population, why are most heart diseases likely to present as acquired?

A

The short answer relates to “age-dependent penetrance”.

In other words, there is an underlying genetic substrate or predisposition, but compounding components related to epigenetics (e.g. other genes, environment, lifestyle, etc) increase the likelihood of that genotype being expressed.

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6
Q

In the REVEAL study by Fox et al. 2018, what is the median age in cats diagnosed with HCM?

A

According to the study, the median age of cats diagnosed with HCM is approximately 5 - 7 years of age. This means that 50% of the cats are older (30% were >10 years of age) and 50% were younger.

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7
Q

In the paper, “Prevalence of DCM in Doberman Pinschers in Various Age Groups” by Wess et al 2010, what is the reported age of this breed to be diagnosed with DCM?

A

According to the study, the prevalence of DCM in Doberman Pinschers is up to 6-years of age (e.g. <12%), but raises to >44% after 6+ years.

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8
Q

In the presumptive diagnosis of an acquired or congenital cardiac condition, what auscultation principles can be applied to suggest one or the other?

A

Most acquired cardiomyopathies present with a systolic, left apical murmur in dogs and a sternal murmur in cats.

However, if a diastolic, right-sided or basilar murmur is appreciated, congenital disease is considered more likely.

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9
Q

In the paper entitled, “Prevalence of and Risk Factors of degenerative MMVD in dogs attending primary care veterinary practices in England” by Mattin et al. 2015, what is the median age on onset of diagnosis with myxomatous mitral valve disease (MMVD)?

A

Mattin and colleagues report a diagnosis in dogs around 9.5 years.

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10
Q

In Stage A MMVD breeds, such as the Cavalier King Charles Spaniel, what is the reported prevalence in this breed to develop MMVD according to Darke 1987?

A

The study reported that CKCS first reported murmurs present in around half of the dogs over 4-years old, which increased to 100% of the population at age 10-years of more.

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11
Q

With regards to gender, which gender group (male or female) has a higher predisposition in the development of cardiac diseases?

A

Almost all heart disease has a male sex predisposition.

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12
Q

According to the REVEAL study Fox et al 2018 in the population of 1,730 cats with feline HCM, what is the reported proportion of affected MALE cats to develop HCM?

A

71% of affected cats with HCM are male.

To note, testosterone concentration is unlikely to be the primary factor because most cats are neutered at the time of becoming sexually mature.

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13
Q

What is the reported percentage of MALE dogs in the development of DCM?

A

60% of dogs with DCM are male.

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14
Q

What is the reported prevalence of the congenital cardiac condition, patent ductus arteriosus (PDA), with regards to gender?

A

Female sex predisposition to PDA is widely acknowledged, with around 3:1 (F:M) developing this congenital disease.

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15
Q

With regards to the Doberman Pinscher, DCM and gender, how do males typically die? What about females?

A

Male Doberman Pinschers diagnosed with overt DCM and heart failure

Female Doberman Pinschers diagnosed with DCM die suddenly, presumable to ventricular arrhythmias.

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16
Q

What other cardiac condition has been reported to be proportionally higher in females than males?

A

Sick sinus syndrome.

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17
Q

What is the most commonly reported congenital heart condition reported in dogs and what specific group of dogs report a higher frequency of this disease?

A

Pulmonic stenosis

It is common in brachycephalic breeds, but may also be diagnosed in the Cocker Spaniel and Terrier breeds

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18
Q

For conditions such as (sub)aortic stenosis, what breeds and size of dogs are typically reported?

A

SAS/AS tends to be diagnosed in larger breed dogs, but occasionally is identified in brachycephalic dogs.

Its worth noting that valvular aortic stenosis is much less common than SAS and seems to be almost exclusively described in the Bull terrier and Boxer Breeds.

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19
Q

What congenital heart condition is likely to be diagnosed in a non-pedigree dog?

A

PDA.

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20
Q

What dog breeds are overrepresented for the development of a VSD?

A

Labrador retrievers, GSDs, and French bulldogs.

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21
Q

What dog breeds are overrepresented for the development of Tetralogy of Fallot?

A

Beagles, Basenji, Keeshonds and French bulldogs.

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22
Q

What dog breeds are overrepresented for the development of tricuspid valve dysplasia?

A

Golden Retrievers, Labrador Retrievers

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23
Q

What dog breeds are overrepresented for the development of mitral valve dysplasia?

A

Bull terrier and springer spaniel.

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24
Q

What cat breed is overrepresented for the development of both: pericardio-peritoneal diaphragmatic hernias and VSDs?

A

Persians.

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25
Q

For myxomatous mitral valve disease (MMVD), what breeds are commonly diagnosed?

A

Small breed dogs, most commonly toy breeds, spaniels and terriers.

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26
Q

In the retrospective study by Martin et al. 2009 of 369 dogs diagnosed with DCM, what are the most commonly recognized breeds to develop the cardiomyopathy?

A

Doberman Pinschers, Boxers, and Great Danes were the most commonly diagnosed breed, followed by the Cocker Spaniel. Additional commonly affected breeds include Irish wolfhounds, Scottish Deerhounds, and Newfoundlands.

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27
Q

What is the gene identified for the development of DCM in Dobermans in the USA?

A

The PDK-4 gene.

28
Q

What breeds are more commonly affected by Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)?

A

Boxers and English Bulldogs.

In this disease fibrofatty infiltrates are present predominantly within the right ventricle, but not entirely exclusively, causing myocardial dysfunction and substrate for ventricular arrhythmias.

29
Q

In the United States, what particular mutated proteins have been implicated for the development of ARVC in Boxers?

A

A desmosomal protein called Striatin. Homozygous dogs are more likely to develop a DCM-phenotype, which chamber dilation and systolic dysfunction (Muers et al 2013) over dogs that are heterozygous carriers.

Additionally, autoantibodies to a protein called Desmoglein-2 were associated with the development of ARVC in humans and dogs.

30
Q

What are some unique features of ARVC in the English Bulldog?

A

ARVC in the English bulldog seems to be primarily localized to an area of the right ventricular outflow tract, causing aneurysmal dilation of this region on echo. Affected dogs are OLDER and there is a 3:1 MALE-to-female ratio in this breed.

31
Q

In cats, familial HCM has been reported in Sphynx, Bengal, British shorthair, and Norwegian Forest cats, all of which have what similar 3 traits?

A

(1) autosomal dominant inheritance pattern
(2) age-dependent penetrance
(3) male-sex bias

32
Q

In the Maine coon, what gene mutation encoding for HCM is present on what protein?

A

A breed-specific mutation in Maine coon cats, the A13P mutation is present on the sarcomere protein, myosin binding protein C3 (MYBPC3).

33
Q

Aside for the genetic mutation, what is the other cause for the predisposition of HCM in the Maine coon?

A

Maine coons demonstrate a phenomenon called incomplete dominance, where being heterozygous for the mutation seems to cause the disease is a proportion of cats but being homozygous for disease tends to have a worse expression.

Again, males and age-dependent penetrance are modifying factors to the disease.

34
Q

In the Ragdoll, what gene mutation encoding for HCM is present on what protein?

A

The R820W mutation is present on the sarcomere protein, myosin binding protein C3 (MYBPC3).

35
Q

What additional potential modifier gene present on a non-sarcomeric protein has been implicated in the development of HCM in Ragdolls?

A

Ragdolls homozygous for a polymorphism of the angiotensin converting-enzyme (ACE) receptor has greater left ventricular wall thickness than cats heterozygous or negative for this polymorphism.

36
Q

What nutritional deficiency has been implicated in the development of DCM in Golden retrievers and Newfoundland dogs?

A

Taurine.

37
Q

How does taurine deficiency in cats?

A

Taurine is an essential amino acid that cannot be manufactured from L-methionine like it is in dogs, thereby diets have to be rich in this amino acid.

In recent years, taurine deficient DCM in cats is almost exclusively diagnosed in those fed a non-commercial or home cooked diet.

38
Q

True or False. Mitral valve disease is most commonly diagnosed in large breed dogs.

A

False.

38
Q

True or False. Arrhythmogenic right ventricular cardiomyopathy is known to be a heritable in boxer.

A

True.

39
Q

True or False. DCM is commonly diagnosed in Great Danes.

A

True.

40
Q

Cough receptors located cranial to the carina respond to what kind of stimuli?

A

Mechanical (mechanoreceptors) and chemical (chemoreceptors) stimuli.

41
Q

Cough receptors located distal to the carina respond to what kind of stimuli?

A

Chemical (chemoreceptors) stimuli.

42
Q

The Expiratory reflex is defined as a strong expiratory push, often followed by a terminal retching sound. What stimuli (mechanical/chemical/both) activates the expiratory reflex and why?

A

The expiratory reflex is associated with mechanical stimuli of the more cranial receptors (cranial to the carina) and has evolved to push obstructions forward and out of the respiratory tract.

43
Q

The Deep “True” Cough is defined as a deep inspiration followed by a forced expulsion against a closed glottis which rapidly expels air from the respiratory tract. What stimuli (mechanical/chemical/both) activates the deep cough and why?

A

The deep cough is associated with chemical stimuli (e.g, smoke, allergens) of the deep cough receptors. This is evolved to clear the respiratory tract of airborne noxious stimuli.

44
Q

Describe the pathophysiology of a cough reflex?

A

Afferent pathways travel via the vagus nerve to the cough center located within the **medulla oblongata*, which are located adjacent to the centers which regulate normal cardiorespiratory function. This cough center is under high control from nuclei in the upper brain stem and pons. Efferent nerves from the medulla then travel via the vagus, phrenic and spinal motor nerves to the inspiratory and expiratory musculature.

45
Q

Does heart disease, notably left-sided failure, cause coughing?

A

Short answer: No.

Long answer: When considering the anatomic location of pulmonary edema, first beginning within the interstitial space (perivascular) and eventually extending into the alveolar space, we can see that there are no cough receptors present within that area.

Additionally, edema eventually would have to manage to extend to the first cough receptors located within the lowest bronchi and these receptors ONLY respond to chemical signaling, therefore would NOT respond to the mechanical stimulation for the airway fluid.

Ultimately, for pulmonary edema to produce a cough, the accumulation of fluid would have to be so severe that it would cause to alveoli, bronchioles, lower bronchi to be filled with fluid to the point that it reaches the level of the principle bronchi and trachea for the activation of mechanoreceptors to respond. This would thereby generate an expiratory reflex. In this case, the pulmonary edema would have incredibly severe.

46
Q

In the paper, “Bronchomalacia in Dogs with Myxomatous Mitral valve disease degeneration” by Singh et al 2012, small breed dogs that presented with chronic coughing episodes concluded what findings?

A

Small breed dogs that presented with a chronic coughing commonly have concurrent airway disease (e.g., both dynamic airway collapse and chronic bronchitis) BUT that left atrial dilatation is NOT the cause of airway collapse in all dogs.

47
Q

In the paper, “Risk factors for Coughing with Naturally Acquired Myxomatous Mitral Valve Disease” by Ferasin et al 2013, dogs with mitral valve disease were reviewed, along with concurrent imaging findings correlating with history, presenting clinical signs and other clinical data. What did they conclude with regards to left atrial enlargement and radiographic findings?

A

Ferasin and colleagues 2013 were able to conclude that coughing was associated with left atrial dilatation/enlargement and the presence of a radiographic bronchial pattern. This concept supports the idea that BOTH lower airway pathology and atrial enlargement are the processes which activate cough receptors in dogs with MMVD, NOT the presence of pulmonary edema.

48
Q

What are some possible reasons that pulmonary edema may elicit coughing?

A

Severe mechanisms have be speculated:

  1. Changes to air way mucus fluidity (increased water content being carried away via the mucocilliary escalator) causes increased airway inflammation
  2. High left atrial pressure can cause bronchial compression, which relieves after treatment.
  3. Furosemide has mild bronchodilatory effects alleviating the bronchoconstriction and inflammation associated with airway disease.
  4. Sudden increase in cardiac stretch activates pericardial cough receptors
49
Q

What is a normal sleeping respiratory rate?

A

Some publications suggest a sleeping respiratory rate <30 breaths per minute is considered normal in cats and dogs.

50
Q

How would you classify an abdominal push during expiration?

A

An abdominal push during expiration is typically indicative of lower airway disease

51
Q

How would you classify an abdominal motion in the opposite direction to the thoracic wall motion

A

An abdominal motion in the opposite direction to the thoracic wall motion, also known as “paradoxical breathing” indicates respiratory fatigue – where respiratory muscles are tired from the effort of breathing and abdominal muscles have had to be recruited to help ventilate the lungs.

This ultimately suggests that patient is unstable and prone to further deterioration.

52
Q

When we use the term “collapse” in veterinary medicine, various differentials may be implicated in this clinical sign. Can you list some?

A
  1. Syncope
  2. Seizure
  3. Weakness
  4. Ataxia
  5. Neuromuscular disorder
  6. Refusal to exercise.
53
Q

What pertinent information could be provided to us, as clinicians, that could help classify between the various differentials of collapse? List 2.

A
  1. timeline of the event
  2. association with recent events (e.g., exercise, respiratory signs, food intake, etc)
54
Q

Through the concept of neurocardiogenic syncope, when a patient is at rest and is suddenly excited which subsequently results in a collapse, describe the physiologic events that happened:

A

Whilst at rest (increased parasympathetic tone), the animal has a resting venous return.

Upon stimulation (sympathetic tone), the heart rate increases and there is now excessive ventricular motion which subsequently activates the mechanoreceptors present with the ventricles. As these specific receptors moderate ventricular loading conditions, they act to promote bradycardia and hypotension.

Therefore, from rest with decreased venous return to stimulation of the ventricular mechanoreceptors, ultimately “EMPTY VENTRICLE SYNDROME” occurs promoting bradycardia and hypotension leading to collapse (neurocardiogenic syncope).

55
Q

What are some typical features of syncope, which contrast to a seizure?

A
  1. Association with excitement
  2. Absent pre-episodic abnormalities/No preictal phase
  3. Collapse with a flaccid posture.
  4. A period of unresponsiveness with eyes open or glazed
  5. rapid recovery to normal WITHOUT abnormal behavior reported later in that day
56
Q

What are differentials associated with syncope outside of the cardiovascular and/or respiratory systems?

A
  1. reflex-mediated/vaso-vagal
  2. Systemic or metabolic conditions, notably insulinomas or pheochromocytomas
57
Q

List history points or clinical findings that are NOT suggestive of cardiovascular disease.

A

The following are responsible for collapsing episodes that are caused by neurological,, neuromuscular or musculoskeletal disease:

  1. Jaw clamping
  2. Salivation
  3. Nystagmus
  4. Pre-episodic abnormalities
  5. prolonged recovery
  6. Concurrent or persistent behavioral abnormalities
  7. Concurrent or persistent gait abnormalities
58
Q

List two useful history points that can distinguish syncopal vs. seizure:

A
  1. Every seizure will follow an almost identical pattern of activity.
  2. Epileptiform seizures are often associated with periods of rest or waking up from sleep.
59
Q

What are some useful history points, with regards to identifying exercise intolerance?

A
  1. Duration of exercise or distance covered.
  2. Frequency of exercise
  3. On lead vs. off-lead exercise
  4. Intensity of exercise
60
Q

Where are pure mechanoreceptors-type cough receptors located?

Larynx and nasopharynx
Carina and bronchi
Pericardium and diaphragm
Alveoli and pleural space

A

Where are pure mechanoreceptors-type cough receptors located?

Larynx and nasopharynx
Carina and bronchi
Pericardium and diaphragm
Alveoli and pleural space

61
Q

A 9-year-old female neutered Cavalier King Charles Spaniel presents with a history of chronic cough and the owner monitored sleeping respiratory rate is 28 breaths per minute. You are aware of a longstanding heart murmur. What differential do you consider likely?

Pulmonary oedema
Chronic bronchitis
Large pleural effusion
Interstitial fibrosis

A

A 9-year-old female neutered Cavalier King Charles Spaniel presents with a history of chronic cough and the owner monitored sleeping respiratory rate is 28 breaths per minute. You are aware of a longstanding heart murmur. What differential do you consider likely?

Pulmonary oedema
Chronic bronchitis
Large pleural effusion
Interstitial fibrosis

62
Q

A dog presents with episodes of falling over associated with exertion. The owner is uncertain about consciousness during the episode, but describe the following: no pre- or post- event behaviour changes; a duration of 1-2 minutes; and an unusual gait prior to falling. Which group of disorders seems most likely?

Neuromuscular
Cardiovascular
Respiratory
Neurological

A

A dog presents with episodes of falling over associated with exertion. The owner is uncertain about consciousness during the episode, but describe the following: no pre- or post- event behaviour changes; a duration of 1-2 minutes; and an unusual gait prior to falling. Which group of disorders seems most likely?

Neuromuscular
Cardiovascular
Respiratory
Neurological

63
Q

Describe the usefulness of the hepato-jugular reflex in the physical examination.

A

one observer looks at the jugular veins whilst another puts pressure on the liver – usually by gently increasing the pressure of palpation on the cranial abdomen. Here, we are effectively pushing blood cranial from the liver and into the thorax. In a normal heart, the blood will be taken into the ventricle and pulmonary circulation without incident, so the volume of blood in the cranial vena cava – and thus the jugular veins – will not increase. So, normal animals experience liver palpation without jugular distension. In an animal where the right heart is failing, there is no capacity to deal with the increase in venous return from the liver – here, the jugular veins distend upon palpation of the abdomen; a positive hepato-jugular reflux.

64
Q
A