Coughing with heart disease Flashcards

1
Q

What is the association between increased LA size and cough?

A

Limited evidence of association (although some)
Similar breeds get MVD and tracheal collapse/ chronic bronchitis, bronchomalacia etc
There is a possible association between VHS increases and differentiating between a cardiac and non cardiac cough

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2
Q

What is the association between CHF and cough?

A

The actual pulmonary oedema unlikely to be associated with the cough, likely to be the other bits of the disease causing coughing
There are not cough receptors in the alveoli so unless the whole lungs are flooded you shouldn’t see a cough

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3
Q

What are the main ddx for collapse?

A

circulatory - haemorrhage/ anaemia, cardiovascular, hyperviscosity, reflex syncope, reduced vascular patency
Endocrine - addisons, phaeochromocytoma, low BG, low Ca
Respiratory - URT obstruction, severe laryngeal paralysis, thoracic wall/ pleural space disease, haemoglobin abnormalities
Neuromuscular - Exercise induced collapose, myopathies, MG, neuropathies
Neurological - spinal disease, brain disease, epilepsy, hepatic encephalopathy, narcolepsy/ cataplexy

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4
Q

What is syncope?

A

Syncope: sudden transient loss of consciousness associated with loss of postural tone (collapse)
• Collapse into lateral recumbency (faint)
• +/‐ limb rigidity, opisthotonus,
• micturition, vocalisation
• Profound hypotension/ asystole – “hypoxic seizure” preceded by loss of muscle tone
• Presyncope – transient ataxia/weakness, esp HLs
• Rapid recovery

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5
Q

How can you identify a seizure?

A

• preceded by atypical limb/facial movement, staring,
prodromal “aura”
• persistent tonic/clonic motion, defecation,
• Post‐ictal aura/dementia, neurologic deficits
• Usually at rest
• Seizures during exercise/ excitement extremely rare
but reported occasionally

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6
Q

Outline reflex syncope

A

• Neurocardiogenic (vaso‐vagal)
Most common in small brachycephalic dogs, stimulated by excitement - get a reflex bradycardia and faint
• Situational – cough/ micturition/ vomit
• small breed dogs with DMVD (cough/ excitement),
• phaeochromocytoma, altered autonomic tone (GI
disease)
• Anaemia (viscosity?)

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7
Q

What are the standard ix done with collapse?

A
• CBC, biochem, urinalysis
• SBP +/‐ endocrine tests.
• ECG – especially if arrhythmia present
• Echo – r/o cardiac structural disease
• Ambulatory ECG (Holter monitoring)  +/‐ event 
recording
• ? Rectal temperature test
• Consider internal medicine/ neurology input!
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8
Q

What are the cardiac causes of collapse?

A
  1. Arrhythmias – tachy/brady DCM, ARVC
  2. Reduced cardiac output: DCM, DMVD, hypovolaemic
    shock
  3. Reduced cardiac filling – HCM, PE , cardiac neoplasia
  4. Cardiac outflow obstruction – SAS, PS, neoplasia/ thrombus, PHT, PTE, HOCM (cats), dynamic LVOT obstruction in young dogs (rare)
  5. Cyanotic disease (R‐L shunts) – R‐PDA, ToF, Eisenmengers
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9
Q

What are the componenets of BOAS?

A

combinations of stenotic nares, an overlong soft

palate, laryngeal or tracheal hypoplasia and eversion of the laryngeal saccules

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10
Q

What is suggestive of CO poisoning?

A

brick red mucous membranes

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11
Q

Outline methaemoglobinaemia

A

Methaemoglobin is formed as a result of oxidative damage to the haemoglobin caused by toxic oxidants such as nitrates, topical anaesthetics, and raw or cooked onions (and paracetamol in the cat). Mucous membranes may be cyanosed or tinged brown, but the presence of brown discoloration of blood spots collected on white filter paper is highly suggestive of methaemoglobinaemia

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12
Q

What can abruptly reduced cardiac output?

A

■ Obstructive lesions within the vasculature returning
blood to the right side of the heart;
■ Decreased right ventricular filling due to cardiac tamponade (usually caused by pericardial effusion);
■ Restrictive ventricular filling (eg, due to constrictive
pericarditis, constrictive myocardial disease);
■ Tricuspid stenosis;
■ Intracardiac neoplasia;
■ Heartworm disease;
■ Thromboembolism.

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13
Q

What suggests pericardial effusion?

A

Pericardial effusion may be suspected because of
poor peripheral pulse quality, muffled heart sounds on
auscultation, ascites, jugular venous distension and a
globoid cardiac silhouette on radiography, and can usually be diagnosed quite easily using two-dimensional ultrasound.

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14
Q

What are the most common arrhythmias causing collapse?

A

in dogs are sustained ventricular tachyarrhythmias, high grade second degree and third degree atrioventricular block, and periods of sinus arrest/asystole resulting from the ‘sick sinus’ syndrome

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15
Q

What are ventricular tachyarrhytmias associated with?

A

systemic disease states, electrolyte abnormalities, acidbase disturbances, hypoxaemia, severe abdominal disease (especially pancreatic and splenic) and neurological disease, or may be due to primary myocardial disease.

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16
Q

What are brady arrythmias associiated with?

A

may be provoked by states of high vagal tone,
which accompany some cases of respiratory or gastrointestinal disease, systemic electrolyte disturbances or metabolic disease, or may occur in cases of primary myocardial disease

17
Q

How can you test to see if a bradyarrhythmia is purely vagally mediated?

A

Test doses of atropine at 0·04 mg/kg subcutaneously or intramuscularly would be expected to ablate
purely vagally mediated bradyarrhythmias and result in
a reversion to sinus rhythm, usually accompanied by a
mild sinus tachycardia in the region of 130 to 170 bpm

18
Q

How an you treat AV block?

A

Some animals with atrioventricular block, particularly
if they are responsive to atropine administration, may
respond to oral medication with anticholinergic agents
(eg, propantheline and oral atropine if obtainable) or sympathomimetic agents (eg, terbutaline). In the majority of symptomatic patients, however, these medications are of limited efficacy and pacemaker implantation is ultimately required, probably because degeneration of conductive tissue is already advanced at the time of diagnosis.

19
Q

What are the clinical signs of hypernatraemia?

A

mostly neuro
Anorexia, v+, weakness
Rare if Na <170mmol/L
Due to neurocellular dehydration as water moves out of brain cells down osmotic gradient

20
Q

What are the clinical signs of hyponatramia?

A

Rare to get them

Can see hypovolaemia or cerebral oedema if occurs fast

21
Q

What are possible causes of hyponatramia?

A
Peritonitis
Hypoadrenocorticism
Diuresis
Psychogenic polydipsia
Syndrome of inappropriate
antidiuretic hormone
secretion (SIADH)
Hypotonic fluids
Liver disease
Renal disease
GI losses
CHF
Pancreatitis
22
Q

What are common clinical signs with hypokalaemia?

A

Occurs anywhere from >6mmol/L
Bradycardia
Ventricular fibrillaton
Sinus Arrest

23
Q

What can cause hyperkalaemia?

A
Blocked bladder/ UT
Reperfusion injury
Massive muscle/ tissue damage
UT rupture
Addisons
haemolysis
extreme trichuris infection
Acute renal failure
Acute tumour lysis syndrome
Acidosis
Drug-induced
24
Q

What are common clinical signs of hypokalaemia?

A

Weakness, respiratory muscle fatigue, ileus and arrhythmias

25
Q

What can cause hypokalaemia?

A
Starvation, especially if being fluid resuscitated
Diuretics
Hyperadrenocorticism
Hyperaldosteronism
Increased loss (GI or renal)
26
Q

What are the clinical signs of hypercalcaemia?

A

PUPD, weakness, v+,

27
Q

What are the clinical signs of hypocalcaemia?

A

Seizures, facial rubbing, twitching, cramps

28
Q

What can cause hypocalcaemia?

A
Acute tumour lysis syndrome
Acidosis
Drug-induced
Primary hypoparathyroidism
CKD
Pancreatitis
Puerperal tetany
29
Q

What are the ddx for hypoglycaemia?

A

puppy and hunting dog hypoglycaemia, hepatic insufficiency, congenital hepatic portovenous anomalies, sepsis, hypoadrenocorticism, pancreatic
beta cell neoplasia and paraneoplastic syndrome in some cases of extrapancreatic tumours.