Physiology/Pathophysiology and Tests

Question 1

4 causes of Heart disease (and examples)

Answer 1

Impaired filling (diastolic failure) - RCM, Pericardial disease

Resistance to Ejection (increased afterload) - outflow tract obstrucution from aortic/pulmonic stenosis, SAM MV; Large vessel thrombus; pulmonary hypertension

Impaired Ejection (volume overload of chamber) - myocardial disease (DCM, HCM); AV insufficiency (misdirection of flow); Left to right shunting through congenital defect; chronic high output failure (unable to meet demand such as hyperTH and anaemia)

Arrhythmia - sustained tachycardia, chronic bradycardia

Question 2

Classification and DDx for Syncope

Answer 2

Syncope = transient loss of consciousness due to reduce blood supply to brain
TRUE
Neurocardiogenic reflex: vasovagal (situational such as urination or defecation); tussive
Sudden sutonomic system failure causing sympathetic withdrawal and increased vagal tone.

Cardiogenic: intermittent profound hypotension due to poor CO
- marked bradycardia (asystole such as SSS, 3rd degree AV block)
- rapid tachycardia reducing SV (VT)
- Structural disease limiting CO on exertion (PHT, cardiomyopathy, HWD, pericardial effusion)

NON-SYNCOPAL COLLAPSE
- Systemic disease: addison’s, low BG, PSS, Shock
- Neurogenic: seizure, narcolepsy, neuromuscular disease
- Hypoxia: respiratory disease, airway obstruction

Question 3

Pathophys of maladaptive neurohormonal response in Heart disease (JVIM 2019 review)

Answer 3

INCREASED SNS TONE
- initial improvement in HR and contractility by B1 activation on myocytes
- Decompensates with reducing SV
- Also chronic activity reduces B1 receptor expression and responsiveness to activation

RAAS ACTIVATION
- SNS, hypovolaemia, hypotension, reduced Na all increase renal juxtaglomerular cell release of renin (rate limiting enzyme in RAAS activation)
- Renin cleaves angiotensinogen (produced constitutively from liver) in circulation to Ang1
- Ang1 is cleaved to Ang2 by ACE in lungs
- Ang2 acts on AT receptors 1 and 2
ATR1:
- Renal - Na retention, efferent vasoconstriction; fibrosis
- Cardiac - remodelling, fibrosis, increased HR, ionotropic, enhanced SNS effects
- Vasculature - endothelial dysfunction, remodelling, hypertrophy of smooth muscle.
ATR2:
- Adrenals - production of aldosterone that promotes K loss and is proinflammatory, and enhances Na retention and cardiac remodelling via mineralocorticoid activity
- Brain - increased production of ADH (also stimulated by reduced CO) - promotes water retention

Question 4

Main manifestations of increased RAAS activity

Answer 4

Fluid and Na retention

Cardiac remodelling and fibrosis

Vasculature remodelling and fibrosis
Pro-inflammatory

Renal damage and proteinuria

Question 5

Phases of cardiac remodelling and physiological vs pathological differences

Answer 5

Remodelling affects the size of myocytes as well as the volume of myocyte and non-myocyte components, the anatomy and the geometry of the cardiac chambers

Physiological:
With increased exercise/cardiac demand or reduced activity the heart weight may increase or decline through reorganisation of the interstitium and coordinated growth/atrophy of myocardial cells. These changes are all reversible

Pathological: irreversible
- starts with initial hypertrophy in response to increased wall stress (eccentric for volume, concentric for pressure)
- this compensates for the changes in fluid dynamics for a time
- then exhaustion occurs where myocytes die due to prolonged stress or reduced perfusion

Question 6

What causes vascular remodelling in heart disease and what are the consequences

Answer 6

SNS Adr and NAdr
ADH and AT2 from RAAS
Endothlelin from vessel walls that are constricted by above
All are vasoconstrictive, preferentially directing blood flow to organs in low CO
This maintains arterial BP but with chronicity causes vascular smooth muscle hypertrophy and myocardial hypertrophy due to increased afterload.

Reduced production of NO by the endothelial cells also contributes to further vasoconstriction.
Release of pro-inflammatory factors from endothelium

Question 7

Sensitivity of thoracic ultrasound for CHF (dogs and cat studies)

Answer 7

JVIM 2021 - Number of strong positive sites in a patient correlated positively with respiratory rate and x-ray oedema score.
Patterns of edema resolution differed between LUS and TXR, with cranial quadrants showing more significant reduction in B‐lines compared to TXR edema score

AJVH 2019 - On pericardial LUS, most control dogs (14/15) and dogs with DMVD but no CPE (13/15) had ≤ 2 B lines, whereas all dogs with DMVD and CPE had ≥ 3 B lines.
presence of ≥ 4 B lines had high sens 91%, spec 100% for diagnosis of CPE (compared to controls with and without MVD not resp dz)

JVIM 2018 - POC u/s in CATS: LUS criterion that maximized accuracy for CHF diagnosis was presence of >1 site strongly positive for B‐lines (>3 B‐lines per site), resulting in sensitivity of 78.8%, specificity of 83.3%
Subjective LA enlargement was 97.0% sensitive and 100% specific for CHF
Presence of PCEFF also was 100% specific, but only 60.6% sensitive

JVIM 2017 - Lung ultrasound examination detected PE with a sensitivity of 90%, specificity of 93%, and with positive and negative predictive values of 85.7 and 95.2%, respectively

Question 8

Role of Na in interstitial integrity, how is this disrupted in heart failure

Answer 8

GAGs in the interstitium bind excess Na in the body serving as a reservoir to release it as needed
Na-GAG complexes have increased rigidity and contribute to normal structural integrity of interstitium

In CHF the Na retention caused by RAAS -> overload of this reservoir and subsequent draw of H2O into the interstitial space along osmotic and hydrostatic gradients.

Question 9

What is diuretic responsiveness and how is it measured in vet med (and how could it be in future)

Answer 9

quantitative measures that relate the decongestive ability of a diuretic administered to a CHF patient through natriuresis and/or diuresis

In veterinary species diuretic responsiveness is qualitative or semi qualitative and based on relief of clinical signs, such as tachypnea and dyspnea, or resolution of radiographic pulmonary edema, rather than direct measures of the pharmacologic effects of the drug

Successful long-term decongestion of tissues primarily is achieved by removal of excess interstitial Na, without which any decrease in interstitial water content likely will be short-lived

Question 10

What is diuretic resistance

Answer 10

In dogs with chronic CHF, identification of diuretic resistance currently is based on the administered dosage relative to clinical signs, and is specifically defined as the need for >8 mg furosemide/kg/d (in conjunction with standard heart failure medications) to control clinical signs of congestion

In the acute setting,resistance can delay CHF resolution and increase duration of hospital stay

Question 11

Definition of Diuretic resistance:

Answer 11

JVIM 2023 review proposed
uNa <50-70mEq/L in spot sample at 2-3h
urinaryNa : K ratio <1
FeNa <0.2%
urine vol < 1.5ml/kg/h
weight loss <0.22kg/40mg frusemide at 5 days

Emerging evidence in humans and dogs suggests that serum chloride(Cl) concentration is also a marker and driver of diuretic resistance

Question 12

Causes of diuretic resistance with chronic therapy (5)

Answer 12

Decreased Na resorption in the loop of Henle. - secondary to increased NKCC transporter expression
- distal tubular hypertrophy
- increased activity of Na+/K+ ATPase

Diuretic braking -stimulation of the renin-angiotensin-aldosterone system(RAAS) and sympathetic nervous system, such that diuresis is quickly curtailed as the body attempts to mitigate intravascular volume depletion

Aldosterone breakthrough

Poor frusemide bioavailability - inadequate dose, delayed GI absorption
Impairment of active frusemide excretion - normal plasma levels but low urine levels (NSAIDs or low albumin can cause)

Polydipsia
Increased Na intake
Non-osmotic ADH release (corrected >measured Cl)

Question 13

Addressing Frusemide resistance

Answer 13

Poor frusemide bioavailability - give IV, or use torsemide

Resistance Associated with poor transport - discontinue other drugs. treat proteinuria

Post diuretic effect caused by rebound Na and water retention during intervals between dosing can be countered by increasing the dosing frequency

Intrarenal causes of resistance,such as distal tubular hypertrophy, sequential nephron blockade using distal tubule-specific drugs

serial measurements of uNa in patients being treated for chronic CHF might detect gradual loss of diuretic efficacy that can be addressed before an episode of congestion occurs

Question 14

Targets for treatment in CHF and drugs that adress these

Answer 14

Increased preload - diuretics (3 types); nitrates (venodilation)

Increased afterload - ACEi (?maybe); amlodipine; Nitroprusside

Poor contractility - ionotropes (dobutamine B1 agonist, pimobendan PDE3i increases calcium sensitivity of myocytes)

Low SV - occurs from poor diastolic filling
Improved by lusiotropes

HR - bradycardia impacting CO requires pacemaker if purely electrical. tachycardia can result in poor filling and paradoxical reduction in SV (address with antiarrhythmics)

Question 15

Impact of Heart disease on renal function

Answer 15

Overall decrease in CO -> arterial volume and sustained RAAS and SNS activation

Impaired renal perfusion and increased SNS activity -> REDUCED RENAL BLOOD FLOW –> more RAAS and reduces GFR

Increased RAAS activation is an expected physiological compensatory response to progressive loss of nephrons during CKd, as angiotensin ii works to increase single nephron glomerular filtration rate (GFR) via preferential constriction of the efferent arteriole

Fluid retention -> congestion of parenchyma, hypertensive damage to kidney

Enhanced fibrosis through AngII and proinflammatory effects of heart failure/RAAS

Ang2 mediated efferent vasoconstriction and reduced GFR

Question 16

ANP/BNP - source, physiological actions

Answer 16

Released from atrial storage granules in response to atrial stretch.

Balance the effects of RAAS/SNS activation by inhibiting renin release and impairing Na reabsorption. Also inhibit release of aldosterone from the adrenals.

Cleared from circulation by proteases (greater affinity for ANP to BNP), the N terminal fragments of which take a while to reduce and are primarily excreted renally.

Na retention can cause interstitial oedema which impairs normal renal function

Hypertension secondary to Na retention may result in glomerular damage

Vascular dysfunction causing vasoconstriction in end organs

Question 17

What is cardiovascular-renal disorders

Answer 17

disease, toxin or drug-induced structural and/or functional damage to the kidney and/or cardiovascular system, leading to disruption of the normal interactions between these systems, to the ongoing detriment of one or both

Question 18

Subgroups of CvRD

Answer 18

CvRDH - renal disease/dysfunction emanating from a disease involving the cardiovascular system (hypertension, cardiac shock, HW caval syndrome)
CvRDK - cardiovascular disease/ dysfunction secondary to renal disease (renal mediated SHT; volume overload; alterations in K+ causing arrhythmia; uraemic pericarditis)
and CvRDO to reflect concurrent impairment of both systems caused by concurrent primary cardiovascular and kidney disease or “other” disease processes, drugs, toxins or toxicants that affect both systems, respectively (septic or neoplastic emboli,

further subdivided into stable disease (S) or unstable disease (U) based on the patient’s clinical presentation.

Question 19

Ways kidney disease can cause heart damage

Answer 19

Anaemia - increasing cardiac work, may result in high output failure and myocyte oxygen deprivation

Increasing SNS activity through hypovolaemia resulting in tachycardia and increased work

Systemic hypertension -> ventricular remodelling from increased afterload

Increased oxidative stress due to uraemia and increased myocyte work

Question 20

Important considerations for CvRD from JSAP 2015 consensus

Answer 20

1) identification and treatment of elevated blood pressure as per IRIS recommendations;

2) stepwise titration of dosages of diuretics, ACEI, inotropes and/or fluids with frequent monitoring of renal function, body weight, hydration, electrolyte status, and systemic blood pressure (i.e. performed and rechecked within 3–5 days following initiation or dose adjustment of these drugs)

3) proper nutrition, with respect to reduced dietary sodium and phosphate and appropriate protein and caloric intake

Question 21

ECG interpretation steps

Answer 21

1. Determine heart rate - normal or abnormal
   50mm/sec - 10 heavy lines = 1sec
2. Regular or irregular rhythm
3. P wave for every QRS? QRS for every P wave?
4. Are all the P waves consistently related to the QRS
5. Do all the P waves look alike? Do all the QRS complexes look alike?
6. Determine the mean electrical axis

Question 22

Normal HR for dogs/cats

Answer 22

Giant breeds: 60-140
Adult dogs: 70-160
Toy breeds: 80-180
Puppies: Up-220

Cat: 100 (asleep)-240 (excited)

Question 23

What is and How to determine Mean electrical axis

Answer 23

the mean electrical axis is used to determine which chamber (the right ventricle or the left ventricle) is larger. Fairly insensitive unless severe.
Normally the left ventricle is much larger (3 times the mass) than the right ventricle. Consequently, the ECG primarily “sees” a wavefront of depolarization traveling caudally and to the left. This results in large R waves in leads I, II, III

identify the lead with the largest net QRS complex deflection, either positive or negative.

Left ventricular hypertrophy
Increase in size of the R wave. possibly prolonged QRS.

Right ventricular hypertrophy
Deep S wave - as the right ventricular mass exceeds left ventricular mas

Question 24

Diagnostic manipulations for ECG and when to use

Answer 24

Vagal manoeuvre (carotid massage or ocular pressure) - increases vagal tone.
Use to slow tachycardia and better evaluate ecg changes
Interrupts re-entrant circuits and pre-excitation syndromes

Atropine response test - decreases vagal tone
Differentiates physiological bradycardia (ie due to high vagal tone) from pathological (due to conduction block or reduced impulse formation)

Question 25

Causes of arrhythmia

Answer 25

disordered impulses conduction
- Blocks
- Re-entry: disease myocardium with slowed conduction causes early depolarisation of healthy tissue just after it has finished depol from first signal.

Disordered impulse formation
- depressed from increased PSNS tone, hyperkalaemia, hypoTH, SSS
- enhanced - tachycardia
- ectopy/abnormal: new site of automatic firing faster than SA node due to diseased tisse

Causes:
- structural heart disease
- cardiac trauma
- autonomic imbalance
- myocardial hypoaxia
- metabolic abnormalities
- inflammation
- drugs/toxins
- extremes of temp

Question 26

Causes of Atrial Tachycardia

Answer 26

Atrial dilation due to cardiac dz - most commmon
Structural disease of atria - myocardial, infiltrative, neoplasia, fibrosis
autonomic imbalance
hypokalaemia
Trauma - pericardiocentesis
Drugs (digoxin, quinidine, PDEi, sympathomimetics)

Question 27

Causes of pericardial effusion in cats vs dogs

Answer 27

CATS - CHF > infectious (FIP) > neoplasia
DOGs - Neoplasia (HSA) > idiopathic > mesothelioma > chemodectoma > thyroid gland neoplasia > infective pericarditis > lymphoma

Question 28

Most common congenital defects?

Answer 28

dogs are PDA, SAS and Pulmonic stenosis.

cats are VSD, PDA, TVD, MVD AVSD and AS.

Question 29

characteristics of physiologic/innocent murmur

Answer 29

murmurs that are encountered in young animals and are typically characterised as soft, systolic with a point of maximal intensity at the left base in the absence of clinical signs of heart disease

The presence of a soft,systolic left basilar murmur does not exclude CHD and can lead to delayed diagnosis of CHD in some animals if is incorrectly diagnosed as a non-pathologic murmur

Question 30

When to evaluate murmur (JSAP 2021 review)

Answer 30

If it is:
Continuous
Diastolic
Louder on the right side of the thorax
Greater than 3/6 at the left base
Radiates - increases in intensity or duration (especially in large breeds with predilection to SAS or TVD)
Presence of other heart sounds (arrhythmia or gallop)
Concurrent hyperkinetic pulses
Or if the murmur is present in a dog or cat with clinical signs, radiographic heart enlargement or elevated cardiac biomarker concentrations, in particular N-terminal pro-B-type natriuretic peptide
Erythrocytosis and HVS

Question 31

Utility of biomarkers in congenital heart disease

Answer 31

Elevations are more likely with severe disease and with cardiac enlargement
Normal concentrations are reported with mild and even severe disease. Normal results may not distinguish between a non-pathologic murmur and a murmur from CHD, and thus bio-markers are not recommended as a screening test to rule out CHD

Question 32

Pathophys of PDA (non-reversed)

Answer 32

PATENT DUCTUS ARTERIOSUS
Presistent left 6th aortic arch - foetal vessel that reduces blood flow to lungs in utero
At birth pulmonary vascular resistance falls and arterial oxygen tension rises → inhibition of PG release/also loss of supply from placenta → constriction of pulmonary vascular smooth muscle and closure in 7-10d

Left to right shunting during diastole → pulmonary circulation overload → LA volume overload from increase preload and LV eccentric hypertrophy to compensate
With time decompensates and develops myocardial failure on LEFT side → LSCHF if untreated

Genetic PRedisposition to failed closure exists - hypoplastic ductal smooth muscle interspersed by elastic tissue
Polygenic trait

Question 33

Features of tetralogy of fallot and pathphys

Answer 33

RVOT obstruction due to infundibular obstruction
Secondary RV hypertrophy
Large nonrestrictive VSD
Rightward positioned aorta

Severe RVOT obstruction → ↑ RV systolic pressure. Desaturated blood shunts from RV to LV via the VSD (right to left shunt) → arterial hypoxaemia → secondary erythrocytosis and hyperviscosity

Question 34

PAthogenesis and Phys of Infectious endocarditis

Answer 34

Micro-organism colonisation of defect in endocardium → platelet deposition → bacterial adhesion (expressing MSCRAMMS) resulting in proliferative and erosive lesions through inflammatory mediators and bacterial virulence properties.
Fibrinous vegetative lesions shields bacteria from host defences.
Requires a persistent or transient bacteraemia to have occurred. Often along with concurrent immune dysfunction, endothelial damage.
Factors affecting clinical presentation:
G- bac LPS can cause rapid sepsis
G+ more subacute/chronic disease,
degree of valvular destruction/alteration to valve function, production of endotoxins;
Immune interactions causing Ig production
Vegetation → thromboemboli or metastatic infections

Question 35

Diagnosis of Infectious endocarditis

Answer 35

Definitive 2 major; 1 major and 2 minor
Major: positive echo; new valvular insufficiency; 2 positive blood cultures (3 if skin contaminant)
Minor: fever, SAS, thromboembolic disease, IMPA; ICGN; <2 positive cultures; High Bartonella serology (>1:1024)

Question 36

Control of systemic venous return

Answer 36

Positive intravascular pressure behind
Negative intracardiac pressure ahead (preload)
Lateral forces from skeletal muscle contraction and relaxation
Autonomic traffic, hormonal influences, local vasoactive substances
Blood flow is assisted by one-way venous valves.

Question 37

Role/function of lymphatics

Answer 37

Lymphatics originate in the interstitium as specialised endothelial cell lined capillaries beginning blindly.
They transport fluid; solutes; macromolecules back into the venous system

Lymphatic vessels contain many junctions b/w endothelial cells and these are connected to surrounding ECM by reticular fibres and collagen.
The endothelial junctions open when tissue hydrostatic pressure increases (stretching the anchoring filaments), as fluid is cleared the anchoring fibres contract and the junctions close preventing backflow of lymph into the interstitium.

During transportation to larger lymphatics the lymph passes through one or more LNs. While at the LN the lymph is in contact with blood circulation and approximately half of the fluid is drained from here before leaving to larger ducts -> major role in immunosurveillance

The thoracic duct drains most of the body and returns the lymphatic fluid to the venous system via the brachycephalic vein or left subclavian vein.
While the right lymphatic duct drains the right side of the head and neck and the right FL

Question 38

Tests to evaluate lymphatics and venous system

Answer 38

Indirect lymphangiography - LN mapping procedure
(direct requires catheterisation of lymphatics)

Venography - eaasiest, can detect thrombi, neoplastic vascular invasion and venous stenosis

Question 39

Diseases of peripheral lymphatics

Answer 39

Lymphangitis/lymphadenitis - tends to be secondary to draining something inflammatory

Lymphoedema - accumulation of fluid in interstitium (protein rich - osmotic gradient created)
Primary = developmental abnormalities in lymphatics (fibrosis/aplasia/hypoplasia/
lymphangiectasia). Generally guarded prognosis
Secondary - trauma, surgery, radiation, parasites, infection. commonly related to combination of lymphatic and venous obstruction → inhibited venous return → increased tissue fluid accumulation → overloads lymphatic vessels

Lymphangioma - benign tumours of small calibre lymphatics

Lymphangiosarcoma - rare malignancy seen on ventral abdomen of cats. cause pitting oedema. Fast growing and unable to be resected in most cases due to infiltrative nature
Prognosis is guarded to poor.

Question 40

Differentials for oedema of: one limb, both HLs, both FLs and all limbs

Answer 40

DDx for oedema of one limb: inflammation, trauma, vascular obstruction, haemorrhage, cellulitis, phlebitis, AV fistula.

DDX for bilateral FL oedema : thrombosis/compression/invasion of cranial vena cava (often by mediastinal mass)

DDx for bilateral HL oedema: obstruction of sublumbar LNs by mass/thrombus (thighs and external genitalia affected), RSCHF, pericardial effusion, cause may not be identified.

DDx for oedema of all limbs: hypoproteinaemia, CHF, renal failure, portal hypertension, lymphatic neoplasm (lymphangiosarcoma).

Question 41

Diseases associated with venous thrombosus

Answer 41

nephrotic syndrome, hyperA, IMHA, thrombocytosis, HWD, sepsis, DIC and neoplasia

Often have multiple concurrent disorders.

Typically fibrin rich thrombi which are less dependent upon platelet number or function, but cell based model of coagulation posits platelets are integral to hemostasis thus the rationale for use of antiplatelet medications in VTE

Question 42

Clinical signs of venous occlusion depending on location

Answer 42

Obstruction of cranial vena cava → oedema of the head, neck and FLs. this may occur secondary to masses, indwelling central venous catheters or pacemaker leads.

Central venous obstruction → pleural effusion

Intra-abdominal or pelvic venous obstruction → ascites; abdominal pain; acquired PSS; hypovolemic shock; and oedema of HLs and external genitalia.

Aside from thrombosis, obstruction of the venous system may be caused by invasive malignancy, or compression by abscess, haematoma, tumour or lymphadenopathy.

Question 43

What are the receptors and effectors involved in BP maintenance

Answer 43

• Baroreceptors
• volume receptors
• macula densa flow receptors

Effectors
- SNS / PSNS
- RAAS
- ADH
- Endothelin

Question 44

Accurate blood pressure measurement

Answer 44

Calibrated doppler/NIBP
standardised procedure
isolated, quiet environment. Owner present
5-10 minutes to acclinmate
Gentle restraint, no sedation (ventral or lateral recumbency best)
Cuff width 30-40% of circumference
Single trained personnel
5-7 consecutive measurements - if trending down continue until plateaus/consistent values

ACVIM 2020

Question 45

Causes of Systemic Hypertension

Answer 45

Primary - rare in dogs/cats, though greyhounds reported to have higher reference than other breeds.

Secondary - most common
Kidney disease - RAAS, Aldosterone, SNS and contribute to vascular remodelling through ANgII
Proteinuria - independent assoc from renal disease/ increases inflammatory mediators
Hyperadrenocorticism - enhances vascular reaction to catecholamines, reduces vasodilation, off target mineralocorticoid activation
Diabetes - insulin loss associated reduced NO production by endothelium. contributes to renal dysfunction
Phaeochromocytoma
Hyperaldosteronism (Cohn’s adrenal tumour)
Hyperthyroidism

Question 46

Target organ damage for SHT

Answer 46

Ocular - breakdown of blood retinal barrier -> haemorrhage, vessel tortuosity, detachment or ocular nerve atrophy

Vascular - endothelial dysfunction and remodelling perpetuates disease. Reduced dilation ability

Cardiac - LV concentric remodelling, fibrosis from ANgII, coronary vascular remodelling may result in ischaemia and arrhythmia

Renal - causes glomerulosceloriss, results in proteinuria, vascular remodelling reduces GFR and causes further RAAS activation
AngII mediated fibrosis

CNS - acute increases cause vasogenic oedema in white matter through altered BBB
In chronic SHT vascular changes cause loss of regulatory tone in vessels –> ischaemia (cerebrum/white matter) -> hypertensive encephalopathy

Question 47

NT proBNP - what are they, test pros and cons, reported sens/spec

Answer 47

NPs modulate blood volume and pressure, antagonise the RAAS, induce bronchodilation and inhibit smooth muscle cell proliferation
BNP is released from atrial storage granules in response to increased stretch (same as ANP)

Both are broken down by proteases in circulation (ANP faster than BNP). The N terminal residues of this are measured as they take longer to clear (renal excretion, again BNP is slower)

NT-proBNP measured as a surrogate marker of atrial stretch (also production in ventricles increases with chronic heart disease)

Pros - POC test available (though not as accurate as lab)
- when used with other diagnostics (ie rads) can help differentiate cardiac from resp causes in dyspnoeic patients

Cons - kidney disease and recent exercise may interfere with results
- evidence of some breeds having different reference intervals

Useful in MMVD for B2 or C disease, PPV not known. Sens/Spec as screening for DCM in Dobermans is 79%.
Feline HCM for dx of CHF: 90% accuracy, 93% sensitive, 72-87% specific.
For HCM screening - poor sensitivity 50-70%

Not useful in ARVC and variable changes in congenital heart disease (only elevated once structural change)

Question 48

cTN1 - what are they, test pros and cons, reported sens/spec

Answer 48

Cardiac troponin T and troponin I are cardiac regulatory proteins that control the calcium mediated interaction between actin and myosin
These proteins are released into blood when myocyte damage occurs

PROS
Elevations may be associated with poorer outcome even in patients without clinical signs. So role in prognosis may be better

CONS
Non-cardiac disease can cause cardiac myocyte injury → release
Also affected by recent exercise
- not prognostic in non-cardiac disease
- external lab test only

Uses
- higher in B2 or C MMVD compared to control
- screening Dobermans for DCM: 84% sens and spec for all forms (improved since high senstivity test released)
- not enough info about ARVC
- feline HCM: A cutoff of 0.06 ng/mL provided good discrimination between healthy cats and cats with HCM (sensitivity, 91.7%; specificity, 95.4%)
Even for asymptomatic cats with HCM, sensitivity and specificity for a cutoff of >0.06 ng/mL remained high at 87.8% and 95.4%,