Cardiology Flashcards
1
Q
Does cardiac tamponade typically result in left or right-sided congestive heart failure?
A
Right side CHF
2
Q
What are the two locations for AV block?
A
AV node
Bundle of His (continues into the bundle branches)
3
Q
Why is high vagal tone a risk factor for development of atrial fibrillation?
A
In addition to depressing heart rate, AV conduction, excitability and contractility it also shortens the action potential and refractory period, making the myocytes more susceptible to other stimuli or re-entry.
4
Q
What are the dominant receptors in the heart and systemic vasculature?
A
Heart: B1 adrenergic
Systemic vasculature: α adrenoreceptors
5
Q
Which catecholamines and receptors augment vasoconstriction and vasodilation in general?
A
Vasoconstriction: post-synaptic α adrenergic receptors by adrenaline, noradrenaline or drugs such as phenylephrine
Vasodilation: stimulation of ß2 adrenergic receptors causes vasodilation in circulatory beds, as does locally produced nitric oxide, and dopaminergic receptors if present.
6
Q
Which main drugs/hormones enhance cardiac contractility?
And what decreases it?
A
Dobutamine and Digoxin (and other digitalis glycosides); catecholamines, Ca and phosphodiesterase inhibitors.
Decreased by anaesthetics and any drug that blocks or reduces Ca entry into cells.
7
Q
What is the pre-ejection period?
what is it an index of and what shortens it?
A
Delay between the onset of the QRS and the opening of the semilunar valves. This is an index of contractility/myocardial function.
It is shortened by inotropes or sympathetic activation.
8
Q
In what condition may pronounced splitting of the 2nd heart sound be heard, particularly if the pulmonic component is louder than the aortic?
A
Pulmonary hypertension.
9
Q
How do you calculate ejection fraction?
A
Ratio of stroke volume : end-diastolic volume
10
Q
List medications that decrease afterload primarily through arterial vasodilation.
A
Acepromezine
ACE-inhibitors
Hydralazine
11
Q
What might splitting of the first heart sound indicate?
A
May indicate abnormal ventricular electrical activity or VPCs
12
Q
When do you hear a systolic ejection murmur?
A
Starts after S1 and finishes before S2.
13
Q
In what circumstances might you palpate a thready or hypokinetic arterial pulse or a pulse deficit?
A
Thready/hypokinetic pulse: reduced stroke volume and peripheral vasoconstriction
Pulse deficit: LV pressure is not exceeding aortic pressure
14
Q
The recommended cuff width: tail ratio is 0.4-0.6 for the middle coccygeal artery. If the cuff width is too wide or too narrow the measurement is likely to be inaccurate. Does a wide or narrow cuff over or underestimate blood pressure values?
A
Wide cuff underestimates
Narrow cuff overestimates.
15
Q
What is the correction factor for blood pressure for height above the heart base?
A
0.77mmHg/cm above the heart base
16
Q
List normal MAP, SAP, DAP and pulse pressure for horses
A
MAP: 110 +/- 15mmHg
SAP: 135 +/- 15mmHg
DAP: 90 +/- 15mmHg
Pulse pressure 45 +/- 6mmHg
17
Q
What are the differentials for the following:
Pale MM
Dark red/Injected MM or greyish-blue
Prolonged CRT
A
Pale MM: anaemia, poor peripheral perfusion and vasoconstriction
Dark red/injected MM: septicaemia or endotoxaemia and peripheral vasodilation
Greyish-blue may indicate vasoconstriction (blue colour directly relates to absolute concentration of deoxygenated haemoglobin)
Prolonged CRT: poor CO, hypovolaemia, hypotension or peripheral vasoconstriction (CRT may be shortened with vasodilation)
18
Q
If you see isolated venous distention cranial to the thoracic inlet what conditions might you be suspicious of?
A
Cranial mediastinal or pulmonary mass putting pressure on/obstructing the cranial vena cava.
If jugular vein only, then CHF (right-sided), pericardial disease or hypervolaemia might be suspected.
19
Q
In a normal horse undergoing an exercise test, what heart rates would you expect to see at a trot, canter, gallop and during hard galloping/HR max? And what is the expected initial recovery period?
A
Trot: 70-140bpm
Canter: 120-160bpm
Gallop: 150-180bpm
Hard gallop: >180bpm
HR Max: 210-240bpm
Recovery: <100bpm within 2-5min
20
Q
How does spontaneous pacemaker activity work with respect to cellular depolarization in cardiac myocytes?
A
There is a background inward Na current and a time-related decrease in the membrane permeability to K efflux alongside a transient inward Ca current.
When the membrane potential is reached, ion flow across the long-lasting (slow) Ca channels predominates and leads to cell depolarization.
21
Q
What are the autonomic effects on automaticity?
A
Vagal activity opens K channels and hyperpolarised the membrane, depressing automaticity (harder for the cell to depolarise hence slower rate); sympathetic stimulation the depolarising “funny current” becomes activated, enhancing pacemaker activity.
22
Q
The left and right vagus have preferential innervation to the two nodes, and the parasympathetic activity is more extensive to certain regions - which ones is which?
A
Left vagus preferentially innervates the AV node
Right vagus preferentially innervates the SA node
Parasympathetic activity is more extensive to supraventricular than ventricular myocardium.
23
Q
What does the P-R interval tell you?
And what are changes in this interval often related to?
A
It is the time taken for conduction across the AV node and His-Purkinje system.
Changes often relate to changes in blood pressure and baroreceptor activation.
24
Q
In horses with hypovolaemia or shock myocardial ischaemia, myocardial hypoxia or hyperkalaemia can develop; what are the changes that you might see on the ECG to give you an indication of each of these abnormalities?
A
Myocardial ischaemia may show on ECG as S-T segment deviation.
Myocardial hypoxia and hyperkalaemia may be evident as enlargement of the T wave.
25
What are the requirements of an US probe for echo?
1.5-3.5mHz phased array sector transducer
Penetration 25-30cm
Frame rate of 20-40/sec or 40-90/sec for speckle tracking.
ECG leads.
26
In addition to LA diameter, what further measures should be taken for evaluation of chamber size and when in the cardiac cycle are these measurements best taken?
LA diameter and area should be measured.
Measurements taken at the end of systole, one frame before mitral opening.
27
A horse has severe mitral regurgitation and a normal fractional shortening. What are you suspicious of and what would you have expected instead?
**Myocardial failure.** With severe MR you expect to see increased FS% due to increased pre-load and decreased afterload.
28
Why is stroke volume and cardiac output of limited value in monitoring heart disease in horses?
CO is maintained in the failing heart until compensatory mechanisms are overwhelmed.
29
Tricuspid regurgitant flow above what velocity is suggestive of increased pulmonary artery pressure with PHT?
\>3.4m/s
30
A restrictive VSD has what characteristics?
Flow \>4.5m/s, (abnormally high velocity of driving blood through a restrictive orifice)
Shunt diameter \<2.8cm or less than 1/3 of the aortic root
31
When estimating right atrial pressure, what value would be used for normal and horses in CHF?
Right atrial pressure estimated to be 10mmHg in normal horses.
Estimated to be at least 20mmHg in horses with CHF.
Ideally, measure with a catheter!
32
What are the expected pressures in the pulmonary artery, aorta, central venous pressure?
PA pressure: systolic 35-45mmHg, mean 25-30mmHg, diastolic 20-25mmHg.
AO pressure: systole 110-130mmHg, diastolic 75mmHg
CVP: 5-10mmHg
33
What factors influence pulmonary artery pressure and how might these be influenced in different disease states?
PA pressure dependent on CO, pulmonary arteriolar resistance, pulmonary capillary resistance, and left atrium compliance/pressure.
Influenced by:
* pulmonary disease/changes (structural, vascular and parenchymal),
* alveolar hypoxia and acidosis (these can cause reactive vasoconstriction, increasing PA pressure),
* left ventricular function (LV failure leads to PHT and potentially biventricular failure)
34
How might you differentiate cardiac versus pulmonary causes of PHT?
Measurement of pulmonary wedge pressure - a near-normal wedge pressure is measured in the setting of elevated PA diastolic pressure if PHT is not caused by left heart failure/dysfunction. Hence you would be suspicious of increased vascular resistance across the small arteries due to pulmonary vasoconstriction or pulmonary vascular lesion.
One exception is a pressure gradient that develops between the PA diastolic pressure and pulmonary wedge pressure in normal horses with resting tachycardia.
35
How do you calculate vascular resistance?
(Mean arterial pressure-mean atrial pressure)/CO
For systemic vascular resistance use mean aortic and mean right atrial; for pulmonary vascular resistance use mean PA and mean pulmonary wedge.
(pressure measured in mmHg, CO in mL/min)
36
What is the half-life of cardiac troponin I and what significance does this have for diagnostic value and repeat measurements?
Half-life is \<1 hour.
A transient injury is easy to miss due to the short half-life.
A failure to decline over subsequent measurements indicates ongoing myocardial injury.
37
What are the stimuli for release of natriuretic peptides?
* Myocardial stretch due to volume overload
* Increases in intracardiac pressure
* Exercise
* Myocardial stretch due to dysfunction.
38
List causes/mechanisms of biventricular heart failure
1. Isolated LV failure leading to increased pulmonary venous pressure, pulmonary vascular remodelling and PHT and therefore increased pressure load on the RV
2. RV failure with marked ventricular dilation leads to leftward bulging of the IVS and impaired LV filling
3. Chronic pericarditis leads to impaired ventricular filling
4. Arrhythmias such as AF which are bilateral in the setting of structural heart disease can promote biventricular failure.
39
What are the common causes of PHT?
* Severe mitral disease
* Pulmonary overcirculation (eg left to right shunt)
* Chronic left-sided heart failure
* Asthma
* Reversion to foetal circulation in foals
40
What is a likely mechanism contributing to PHT in horses with asthma?
Low alveolar O2 tension is considered a potent trigger for reversible pulmonary vasoconstriction leading to increased vascular resistance. This likely plays a role in PHT with asthma.
41
What is cor pulmonale?
RV enlargement secondary to PHT due to pulmonary parenchymal or vascular disease in the absence of left ventricular failure or congenital abnormalities.
42
What is the treatment for cor pulmonale?
O2 therapy to reduce hypoxic vasoconstriction.
NO as a potent selective vasodilator (relevant in foals perhaps?).
Diuretics may be harmful due to decreased preload.
43
What are the common neurohormonal and renal responses to congestive heart failure?
* Increased sympathetic tone
* Activation of the renin-angiotensin-aldosterone system
* Release of antidiuretic hormone (vasopressin)
* Release of atrial natriuretic peptide
44
How does sustained AV dissociation cause CHF?
AV dissociation caused by junctional or ventricular tachycardia can lead to induced cardiomyopathy, reduced myocardial function, decreased CO and CHF.
45
List causes of per-acute CHF?
* Chordal rupture
* Papillary muscle ischaemia or infection
* Endocarditis
* Vascular rupture (eg aortocardiac fistula)
46
List the clinical findings in biventricular, left and right-sided CHF.
_Biventricular:_ Tachycardia, loud ventricular filling, sub-cut oedema, tachypnoea (secondary to pulmonary congestion and effusion), ascites, pleural effusion, pericardial effusion, jugular distension, abnormal jugular pulsation, lethargy and weight loss. Murmurs often include mitral, aortic and tricuspid.
_Right-sided:_ tachycardia, prominent 3rd heart sound, generalised ventral, preputial, pectoral and limb oedema, elevated venous pressures noted as jugular pulses, tricuspid murmur and tympanic pulmonic component to the 2nd heart sound.
_Left-sided_: pulmonary venous congestion, interstitial or more rarely alveolar oedema therefore signs of tachypnoea and respiratory distress predominate. Heart sounds may be obscured by pulmonary sounds. Resting tachycardia and loud 3rd heart sound are typical. Some cough.
47
List common treatments for CHF
* Antiarrhythmic Tx: lignocaine, MgSO4, quinidine, procainamide, propafenone, sotalol or amiodarone.
* Diuretic Tx: (only if not secondary to cardiac tamponade) furosemide or torsemide.
* Minimise stress: move to a quiet environment, sedate with ACP - anxiolytic and also vasodilatory (reduces afterload and hence reduces regurgitant fraction) and anti-arrhythmic effects. Titrate to effect and monitor BP to avoid hypotension
* Inotropes: dobutamine can be used in the acute setting but it is proarrhythmic and vasoconstrictive. Digoxin therapy is indicated in cases not associated with pericardial disease or ventricular ectopy - may be useful with AF as an underlying dysrhythmia. It also has baroreceptor sensitising effects and increases vagal tone, thereby reducing HR and controlling ventricular response rate to AF. Therapeutic monitoring is required for chronic use.
* ACE inhibitors: inhibit conversion of angiotensin I to angiotensin II thereby reducing Na and H2O reabsorption, reducing volume overload, blunting the mechanisms leading to diuretic resistance and causing vasodilation and decreased myocardial oxygen demand. They may also be cardioprotective by decreasing myocardial remodelling and fibrosis. Ramipril and quinapril suppress ACE activity and reduce indirect BP in healthy horses at rest and during exercise. Benazepril has superior ACE-I compared with other drugs and a good safety profile although is expensive.
48
Explain the foetal circulation in relation to the two foetal shunts and both cardiac and cerebral perfusion.
Desaturated blood from the foetal tissues is collected in the cardinal venous system and enters the sinus venosus and right atrium. It is mostly earmarked for the right ventricle and pulmonary artery but due to PHT it goes through the ductus arteriosus to the descending aorta, umbilical arteries, and placenta where it is oxygenated.
O2 saturated blood from the placenta (via the umbilical vein) is delivered to the caudal vena cava then right atrium where it preferentially crosses the foramen ovale to the left atrium, left ventricle and ascending aorta from where it is delivered to the foetal tissues. The heart and brain received well-oxygenated blood from the ascending aorta while the remainder of the body receives mixed blood from ascending and descending aorta.
49
What factors result in closure of the foetal shunts and at what age?
Foramen ovale: at birth, the lungs expand causing decreased pulmonary resistance and increased left atrial pressure and hence the foramen ovale closes by 24-48hrs
Ductus arteriosus: Inhibition by local prostaglandins cause functional closure of the ductus arteriosus by 72hrs.
50
At what ratio of pulmonary to systemic flow does a shunt typically result in clinical relevance such as LA/LV overload?
When the pulmonary to systemic flow exceeds 1.8 : 1.
51
What is the effect on shunt flow of a downstream right-sided obstruction? And list some examples
Reversion to a right to left shunt.
* Tricuspid atresia with an ASD may result in right-to-left shunting
* Pulmonic atresia with either an ASD or VSD may result in right-to-left shunting
* Chronic left to right shunting that then results in increased pulmonary vascular resistance and PHT may result in shunt reversion to a right-to-left.
52
With right-to-left shunting, which side of the heart will be enlarged and why, and what degree of hypoxia is expected?
The right ventricle will be hypertrophied to generate systemic blood pressure. The degree of hypoxia depends on the shunt fraction/volume and the degree of pulmonary blood flow.
53
With a VSD, in addition to PHT what is another possible cause of widened split of S2?
Disparate ventricular ejection times
54
With respect to murmurs, how might you differentiate a subpulmonic VSD from a paramembranous VSD?
Paramembranous VSD: Harsh holosystolic-pansystolic murmur loudest over tricuspid valve and a less intense ejection murmur over the left heart base due to increased flow across the right ventricular outflow.
Subpulmonic VSD: Harsh holosystolic-pansystolic murmur over tricuspid valve, but the left heart base murmur is louder, associated with high-velocity flow entering the main PA.
55
Differentiate the cause of PA dilation during systole versus during systole and diastole.
During systole alone, likely reflects pulmonary overcirculation (eg ASD causing right-sided volume overload and pulmonary overcirculation.
During systole and diastole, likely reflects pulmonary hypertension.
56
What are the typical components of an endocardial cushion defect?
* Large ASD involving the septum primum and AV septa
* Common AV valve leaflet
* Inlet VSD
* The ventricles may be partitioned normally, unequally with one rudimentary ventricular chamber or not at all, creating a single ventricle. In the most severe cases there is a common AV canal, a single common AV valve and a single ventricle from which both great vessels exit.
57
Which treatment/drug class given to the dam may predispose foals to development of PDA?
Prostaglandin inhibitors
58
List the 4 abnormalities associated with tetralogy of Fallot and the 5th abnormality that may occur with pentalogy of Fallot.
1. Large paramembraneous outlet VSD
2. Cranial dextro-positioning of the aorta with overriding VSD
3. RV outflow obstruction
4. RV hypertrophy.
5. PDA or ASD would classify as pentalogy of Fallot
59
What are the defects associated with pulmonary atresia and what is the common mistake with diagnosis?
1. Right ventricular outlet doesn't connect to the pulmonary artery
2. Right ventricle is hypertrophied
3. A large malalignment VSD is present
4. The foetal truncus arteriosus has been partitioned so unequally that the aorta is markedly dilated and the pulmonary trunk atretic or severely hypoplastic.
The main mistake with diagnosis is that the dilated aorta can be mistaken for a persistent truncus arteriosus. Pulmonary blood flow is derived from a PDA or the aorta (derived from systemic collaterals, usually bronchial arteries)
60
List clinical signs of pulmonary atresia
Cyanosis
Cardiac murmur
Stunting in a foal or weanling.
61
What is truncus arteriosus communis and what are the clinical features?
Failure of the foetal truncus arteriosus to partition into AO and PA. A large malalignment VSD enables communication of both ventricles with the truncus arteriosus.
If the PA origins are not stenotic and there isn't increased pulmonary vascular resistance the clinical features are of a left-to-right shunt with the exception of the right-to-left mixing of blood across the VSD; and hypoxia may be mild.
However, if there is high pulmonary vascular resistance or obstruction to flow of the PA you get arterial desaturation clinical signs of cyanosis, cardiac murmur and stunting of growth.
62
Atresia of the tricuspid valve has been associated with cyanotic heart disease in foals - what is the mechanism behind this?
Stenosis of the tricuspid valve leads to right-to-left shunting across either an ASD or FO. The result of this is that all venous return to the heart is mixed in the left atrium with minimal pulmonary flow (unless concurrent PDA or formation of collaterals via the bronchial arteries), hence marked cyanosis and hypoxaemia. To survive, these horses generally have to have a concurrent VSD that enables left to right shunting.
63
What is the common effect of MR on global left ventricular function in mild or more acute cases versus severe or chronic cases?
With mild MR the LV function is usually normal to increased.
With severe MR or MR that is associated with cardiomyopathy, LV function is usually normal to decreased.
64
With respect to MR, what would be indications for an exercising ECG?
* Mod-severe MR
* AF becoming established
* Progression of MR more rapidly than expected, in the absence of CHF.
65
What lesion typically results in aortic regurgitation?
Degeneration of the valve with nodular fibrotic bands.
66
How would you describe a clinically relevant aortic murmur?
Holodiastolic with PMI over the aortic valve and strong radiation to the right and towards the apex.
Character may be vibratory, musical, cooing, buzzing or "dive bomber" in quality. A precordial thrill may be palpable over the valve area.
67
What is the typical murmur of an aorto-cardiac fistula?
Holodiastolic or continuous murmur that is louder over the right side of the thorax. A continuous machinery type murmur is most common.
68
In reference to AR, what does the presence of bounding or hyperkinetic pulses suggest?
Increased pulse pressure (\>60mmHg) and moderate-severe AR with significant, but compensated LV volume overload (if the myocardium is failing the pulses become weak, pulse pressure decreases and tachycardia develops).
69
In reference to AR, what does premature (pre-systolic) mitral valve closure indicate?
Occurs with severe aortic regurgitation and is associated with elevated ventricular end-diastolic pressure (usually an ominous finding suggesting the myocardium is beginning to fail)
70
In general, what is the prognosis for horses with AR?
As it is slowly degenerative the prognosis is generally good with mild AR, particularly if unchanged at subsequent examinations. If it is moderate-severe or first recognised in a horse \<10yrs old the risk of reduced performance life and longevity are higher.
Flail aortic valve, endocarditis, moderate to severe LV volume overload or myocardial failure indicate a poor prognosis for life and performance.
71
Under what circumstances would an exercising ECG be indicated as part of investigation of AR?
* If AR is moderate-severe and/or volume overload is detected in the LV (due to increased risk of ventricular arrhythmias with ventricular dilation)
* If AF develops
* If progression is rapid
72
In which valve out of mitral or tricuspid is ruptured chordae tendinae tolerated better?
Generally tolerated better with the tricuspid valve.
73
The intensity of the tricuspid murmur often correlates with regurgitant volume but what factors does loudness depend on?
Pulmonary artery and right ventricular systolic pressure dictates the loudness of the murmur with TR.
74
What characteristics of the regurgitant jet are more likely to be associated with cardiomegaly in association with TR?
Jets that are wide at the origin, occupy a large area in the RA or project centrally or laterally into the RA are more likely to be associated with cardiomegaly.
75
What is the typical murmur associated with pulmonic valve regurgitation and what are the two most likely causes of this regurgitation?
Holodiastolic decrescendo murmur with PMI at the pulmonic valve area, radiating towards the right cardiac apex.
Most common causes of PR are left-sided heart failure with progression to biventricular failure from PHT; or PHT secondary to severe respiratory disease.
76
What are the most common sites for endocarditis?
Aortic and mitral valves.
77
What are the commonly reported sequelae of endocarditis?
* Valvular injury & regurgitation
* Chordal rupture
* Valvular stenosis (rare)
* Secondary cardiomegaly
* Myocarditis by extension of the infection or through coronary embolisation (if the latter, myocardial infarction is also a risk from emboli)
* Arrhythmias secondary to cardiomegaly, myocarditis or infarction
* Myocardial depression secondary to bacteraemia.
78
What are the common bacterial isolate from endocarditis lesions?
* Strep species
* Actinobacillus equuli
* Pasteuralla
79
Which viruses have been associated with pericarditis in equids?
* Equine influenza
* Equine viral arteritis
* Equine herpes virus
80
What are the main aetiologic differentials for pericarditis?
* Bacterial (Actinobacillus - part of mare reproductive loss syndrome - eastern tent caterpillars)
* Viral (EI, EVA, EHV) - poor evidence
* Neoplastic (mesothelioma & lymphoma most common)
* Idiopathic and/or immune-mediated
81
True or false, a history of upper or lower respiratory tract infection is common in cases of pericarditis?
True
82
What effects does pericardial effusion have on blood pressure and what is pulsus paradoxus?
Arterial blood pressure is often decreased with pericardial effusion and cardiac tamponade
Pulsus paradoxus is the pronounced inspiratory fall in blood pressure that is seen with cardiac tamponade.
83
What might you see on ECG with pericardial effusion?
Reduced amplitude of the QRS
84
When you see pericardial effusion on echo along with diastolic right ventricular collapse or systolic right atrial collapse what does this signify?
Cardiac tamponade.
85
What echocardiographic findings might you see with restrictive pericarditis?
* Thickened pericardium
* Atrial dilation
* Systemic venous dilation
* Exuberant movement of the ventricular septum - hyperkinetics
* Exaggerated inspiratory filling of the heart
86
What is the typical site for pericardiocentesis or drainage?
left side, 5th ICS above the lateral thoracic vein.
87
In addition to drainage, what is required to improve the prognosis with fibrinous pericarditis?
Repeated drainage and lavage.
50 mg rTPA in 300mL NaCl.
88
List differentials for myocardial injury/inflammation
* Drug or toxins induce (ionophores, antimicrobials cardiac glycosides, cantharidin, snake venom etc)
* Ischaemia and/or hypoxia
* Chronic/relentless tachycardia (junctional or ventricular)
* Endotoxins (Clostridial species or Salmonella, as well as post-colon torsion)
* Infection (fungal, bacterial, viral & parasites)
* Heavy metals
* Trauma
* Metabolic disease
* Nutritional deficiencies (vitamin E deficiency)
* Neoplasia (lymphoma, melanoma, lipoma, haemangioma, mesothelioma, carcinoma
* Amyloidosis
* 2ry systemic hypertension (chronic pain, laminitis CKD or EMS)
89
What are the general cardiac manifestations of myocarditis?
1. Decreased myocardial contractility and ejection fraction
2. Diastolic dysfunction with impaired filling
3. Mitral or tricuspid insufficiency due to dilation or papillary muscle dysfunction
4. Arrhythmias such as persistent VPCs, AF, APCs and atrial/ventricular tachycardia (later 3 are less common)
90
What are the clinical signs of myocarditis?
* Fever
* Persistent tachycardia +/- additional arrhythmias
* Murmur
* Pulmonary or ventral oedema
* Respiratory distress
* Sudden death
91
What clinicopathologic indices may be elevated to suggest myocardial injury?
* CK, specifically myocardial fraction of CK,
* lactate dehydrogenase,
* cardiac troponin I or T (normal values don't exclude it due to short half-life)
92
What are the recommended treatments for myocarditis?
* Rest (minimum 1 month; ensure cTnI and ECG returned to normal)
* Supplement with vitamin E and Se
* Antiarrhythmic therapy if indicated (potentially lignocaine, sotalol or MgSO4)
* ACE I to reduce myocardial remodelling (efficacy unknown)
* Corticosteroids (if non-infectious cause suspected)
* General supportive care (IVFT, correction of electrolyte derangements, anti-inflammatories, antibiotics if bacterial cause suspected)
93
What clinicopathologic and echocardiographic findings might you expect with monensin poisoning (or potentially other ionophores)
* Decreased Ca, K, Mg and P; increased cTnI and cTnT, urea, creatinine, unconjugated bilirubin, AST, CK and LDH (CK and LDH may be due to cardiac, skeletal and RBC damage).
* Decreased fractional shortening %, segmental wall motion artefacts/abnormalities, myocardial dyskinesis
94
What is dilated cardiomyopathy and what is the primary suspected cause?
A disease of global reduction in LV systolic function that cannot be explained by valvular, vascular, coronary or congenital heart disease. The cause is often unknown but myocarditis is often suspected.
Vitamin E and Se deficiency has been associated with a form of dilated cardiomyopathy mostly in fast-growing foals (~6mo) from deficient mares (white muscle disease).
95
What are the main features of dilated cardiomyopathy?
Biatrial and biventricular dilation with decreased FS%,
96
What is the treatment for dilated cardiomyopathy?
Digoxin and diuretics (furosemide) may help to stabilise the associated CHF and cause transient improvement, vitamin E and Se supplementation if deficiency is suspected (white muscle disease); however, most horses deteriorate within 3-12 months. Foals with white muscle disease often die within 24-48 hours of the onset of clinical signs.
97
What are the typical post mortem examination findings in foals with vitamin E/Se deficiency/white muscle disease? How can it be prevented in foals?
Pale streaking of the myocardium and intramuscular oedema, myodegeneration, myocardial necrosis and fibrosis or calcification.
Supplementation of the mares with Vit E/Se during gestation and importantly during lactation may help prevent the disease, as well as supplement the foal.
98
List the typical findings and suspected aetiopathogenesis for aortoiliac thrombosis.
Typical findings
* Multifocal in-growths of fibrous tissue
* Laminated thrombi
* Fibrous plaques
Suspected aetiology:
* Strongylus vulgaris migration
* Systemic infection
* Embolisation from a distant site
* Vasculitis
99
List commonly reported clinical signs of aortoiliac thrombosis.
Clinical signs are typically exercise-associated and often unilateral.
* Hindlimb lameness
* Ataxia
* Weakness or collapse
* Weak metatarsal arterial pulse
* Delayed saphenous refill
* Usually no change in limb temperature (unless complete arterial occlusion in which case the limb is cold and painful to touch, and may be oedematous)
100
List diagnostic methods for aortoiliac thrombosis
* TRP may identify fremitus, weak or absent pulse or aneurysmal dilation of the affected vessel
* US may show hyperechoic areas and an acoustic shadow suggestive of mature scar tissue and calcification or hypoechoic to echogenic mass protruding into arterial lumen.
101
List treatment options and prognosis for aortoiliac thrombosis
* Catheter-based thrombectomy or anticoagulation can be attempted in early cases and those occurring in the external iliac artery - if the thrombus is in the internal iliac artery femoral catheterisation is not successful for thrombectomy
* Medical treatment with pentoxifylline (improves abnormal erythrocyte deformability, reduces blood viscosity and reduces platelet adherence and plasma hypercoagulability) or aspirin for anti-platelet adhesion
* Prognosis reported in one study for US-guided thrombectomey was 65% regained athletic activity with 53% returning to previous level.
102
An association between occurrence of proximal aortic S. vulgaris lesions and focal ischaemic lesions in the myocardium has been described. What is the hypothesised reason for this?
Thought to be subsequent to microembolism from parasitic lesions.
103
What is the typical site of rupture/aneurysm for an aorto-cardiac fistula?
Typically the right sinus of valsalva into the right atrium, right ventricle, interventricular septum or pericardial space.
104
What are the potential causes implicated in rupture to form an aorto-cardiac fistula?
* Dystrophic changes in the media of the aorta
* Degenerative changes with aortic insufficiency
* Hypertension associated with breeding
* Congenital or acquired defects in the media of the aorta near the right coronary sinus (aneurysm of the right sinus of valsalva)
105
Which breed has been associated with aorto-pulmonary fistula, at which site, with what concurrent gross findings and associated with what hypothesised cause?
Friesians
Close to the arterial ligament and concurrent with a circumferential cuff of perivascular haemorrhage.
Possibly a defect in elastin or collagen of the aortic media.
106
What are the presenting clinical signs of aorto-pulmonary rupture and aorto-cardiac fistula?
Can be immediately fatal
Poor performance
Pain (often perceived as colic)
Cardiac murmur - continuous machinery
Arrhythmia (in particular if dissecting through the IVS)
Bounding arterial pulse
107
How are aorto-pulmonary and aorto-cardiac fistula/ruptures diagnosed?
Aorto-pulmonary: challenging views, particularly in Friesians where it tends to be quite cranial. Tilted image planes from the left 3rd or 4th ICS may be useful. Otherwise, cardiac catheterisation (right side) to measure increased right-sided and PA pressure with increased PaO2 in the distal PA indicating left to right shunting. Transoesophageal Echocardiography.
Aorto-cardiac fistula: usually these can be seen with standard imaging planes.
108
What are the types of AV block?
* 1°AV block: conduction is slowed but still proceeds, resulting in a prolonged P-R interval.
* 2°AV block: Some P waves are not conducted to the ventricle (complete block at the AV node) resulting in a P wave without a subsequent QRS. Mobitz I, the P-R interval progressively lengthens until the QRS-T segment is dropped. This is a normal finding in horses. Mobitz II the P-R interval is constant before and after the dropped QRS-T.
* 3°AV block: complete block of the AV node, resulting in a ventricular escape rhythm to develop below the AV node. There are often multiple P waves before the escape QRS (typically wide and bizarre and not associated with a P wave as it is originating from an idionodal or idioventricular pacemaker). If they all look the same as each other then they are escape complexes, but if there is multiple configurations then another ventricular ectopy should be suspected.
* Multiple 2°AV blocks consecutively is termed high grade and is considered pathological (technically 2 or more, although at this level if it still resolves with stimulation/exercise it is unlikely to be significant)
109
List procedures and physiological statuses that can depress sinus node function
* Anaesthetic drugs
* Hypoxia
* Traction on abdominal viscera
* Ocular manipulations
* Hypothermia
* Increased ICP
* Hypertension
110
What is the mechanism associated with the SA node, behind ectopic rhythms in anaesthetised horses
Depression of the SA node during anaesthesia with concurrent stimulation of latent pacemakers in the coronary sinus or AV junction can lead to ectopic rhythms.
111
Bradycardia is usually benign, however can lead to hypotension, particularly under anaesthesia. List treatment options to increase sinus rate.
* Catecholamines such as dobutamine, adrenaline, dopamine (dobutamine first choice due to reduced side effects)
* Anticholinergics (buscopan, atropine, glycopyrrolate)
112
List possible aetiologies for APCs
* Autonomic imbalance (high sympathetic or vagal tone)
* Hypokalaemia
* Catecholamines and anaesthetics
* Infection
* Fever
* Anaemia
* Hypoxia
* Colic
* Heart valve lesions
* Myocardial lesions
* Pericardial lesions
113
Why are APCs relevant clinically and at what rate are they considered relevant?
APCs may precipitate sustained atrial arrhythmias such as atrial tachycardia, atrial fibrillation and atrial flutter
In normal horses, APCs may be seen at a rate of 1-5/hr
114
What do you expect to see on the ECG with an APC?
With interpolated APCs there will be continuation of the regular sinus rhythm after the APC
Non-interpolated APCs there will be a pause after the APC if the sinus node is reset or if the APC is not conducted
The QRS is preceded by an abnormal premature P wave (P' wave) that is often buried within the preceding T wave. If the impulse arrives at the AV node too early, before complete repolarisation, the PR interval is longer than normal (physiologic first degree AV block); if the P' wave is not conducted, there will be a pause in the ventricular rhythm
115
When are APCs likely to be clinically relevant?
1. Frequent at rest
2. Associated with runs of atrial tachycardia
3. Related to poor performance (exclude other causes)
4. Precipitate paroxysmal atrial flutter or AF
5. Develop in conjunction with structural heart disease
116
When are you likely to see a wandering pacemaker and what can you do to check if this is benign?
During sinus arrhythmia such as sinus bradycardia you often get variation in the P-P interval with a wandering pacemaker, which is evident as an altered P-wave morphology. Exercise or stimulation should abolish this if it is a benign rhythm.
117
What is the reason for increased incidence of APCs in the post-exercise period?
Likely due to autonomic imbalance.
118
If you note increased frequency of APCs in a horse that has a history of intermittent poor performance for which you are suspicious of paroxysmal AF, what diagnostic and treatment options could you do?
Diagnostic: 24h Holter ECG, exercise ECG, ECO
Tx: Sotalol, ensure K+ and Mg++ are within normal limits.
119
What are the typical ECG features and the general precipitating factor to atrial tachycardia?
Can be sustained or paroxysmal
The atrial rate is rapid and regular however the AV node may block some of the P' waves so the ventricular response rate may be variable/irregular. Atrial rates of 120-250bpm are typical, often with 2:1 conduction - may be indistinguishable from atrial flutter.
120
When is sustained atrial tachycardia commonly seen?
During treatment of AF with quinidine, and it usually occurs before conversion to sinus rhythm. If it occurs in isolation an underlying structural or myocardial disease should be suspected.
121
What treatment is available for atrial tachycardia?
If the ventricular response rate is rapid (\>120bpm) consider treatment with digoxin to block AV node conduction or diltiazem.
If the ventricular response rate is not rapid, treatment is as for AF - TVEC, sotalol, quinidine.
122
What is the frequency of flutter waves with atrial flutter?
170-275/min
123
AF is typically well-tolerated at rest and during low-intensity exercise however exercise intolerance occurs with strenuous exercise - why?
At rest atrial contraction only contributes 15-20% to ventricular filling, so given the large cardiac reserve in horses the loss of this component doesn't significantly affect cardiac function.
During exercise, this increases to 45%, hence the influence on cardiac function becomes clinically significant and performance-limiting.
124
What is the difference between paroxysmal, persistent, Permanent/sustained and lone AF?
Paroxysmal resolves spontaneously within 24-48hrs
Persistent only resolves with treatment
Permanent/Sustained is resistant to treatment
Lone AF is AF in the absence of identifyable underlying structural heart disease.
125
Why does the duration of AF affect the prognosis for successful cardioversion?
AF can induce electrical, structural and functional remodelling making successful cardioversion less likely/reversion to AF more likely.
126
Horses with AF frequently have reduced FS%. Does this typically return to normal if they are converted back to sinus rhythm?
Yes as the reduction was likely due to reduced pre-load rather than pathology.
127
Development of broadened QRS and R-on-T phenomenon is associated with a poor prognosis - why?
It is considered a risk factor for development of ventricular arrhythmias which can lead to collapse and sudden cardiac death.
128
Atrial fibrillation is identified in a horse with CHF. Which condition do you prioritise with treatment and what should treatment entail?
Aim treatment at controlling CHF.
* Loop diuretics to reduce oedema, preload and afterload,
* Digoxin to reduce heart rate and
* ACE-I to reduce myocardial oxygen consumption, fibrosis/remodelling and circulating volume should be considered.
129
What type of drug is quinidine?
Type Ia Na channel blocker.
130
What is the conversion rate with TVEC and what percentage revert to AF after treatment?
98% conversion rate reported; approximately 25% revert.
Another study reported 36% first time recurrence; 43% overall recurrence rate.
131
Which features of AF, if present, are likely to make it more difficult to convert to normal sinus rhythm?
* Longer duration AF
* Shorter fibrillation cycle lengths
* Significant structural cardiac disease
132
What is the recommended treatment protocol for quinidine?
What can be done if this is not successful within 24hrs?
Loading dose of 22mg/kg q2h for 2-4 doses then q6h until cardioversion or toxic signs.
If not successful within 24hours Digoxin at 0.0055-0.011mg/kg orally q12h can be added for 24-48hrs. However, this effectively doubles the active availability of quinidine so toxicity is likely - monitor serum digoxin levels and have bicarb on hand!
133
What is the mechanism for use of NaHCO3 with quinidine toxicity?
And what other treatments should be implemented?
* Treatment is at 1mEq/kg and it works by:
* reversing the Na channel blocking effects of quinidine,
* alkalinizing ECF does increase Quinidine bind to protein,
* increase K intracellular and decrease Ca extracellular.
* Phenylephrine drip to restore blood pressure.
* IV MgSO4 (up to 25g) is the treatment of choice quinidine induced ventricular arrhythmias.
* Lignocaine can be used at 0.5-1.5mg/kg slowly if needed for arrhythmias.
* Digoxin may be indicated in some cases of quinidine toxicity to slow the ventricular response rate however it is contraindicated in horses with ventricular arrhythmias induced by quinidine.
* Diltiazem or α2 agonist to decrease ventricular tachycardia.
134
Why should flecainide not be used?
It causes dangerous arrhythmias and sudden death.
135
Where are the catheters placed for TVEC and at what point in the cardiac cycle is the shock delivered?
Left PA and right atrium. Shock delivered on the R-wave.
136
Shocking during which phase of the cardiac cycle could induce fatal ventricular arrhythmia and why?
Shock delivered on the T wave could induce fatal arrhythmia as this is the vulnerable period.
137
What is a potential complication of positioning the probe too close to the AV node?
Complete AV block
138
How long does it typically take for LV function to return to normal after TVEC?
3 days
139
Arrhythmias that originate in the AV conducting tissues, ventricular specialised conducting tissues or ventricular myocardium are classified as junctional (AV node and bundle of His) or ventricular in origin. What is characteristically seen on ECG with these?
A QRS without a preceding P wave is seen with these.
If they are junctional they are more likely to look like a normal, narrow morphology QRS as they likely follow the same pathway.
If they are ventricular in origin the morphology could be very different and is typically wider with an abnormal orientation due to slow conduction down an altered pathway.
140
What is AV dissociation and when does it occur?
When you have a normal atrial rhythm superimposed on an ectopic ventricular or supraventricular rhythm. It occurs with sustained junctional arrhythmias.
141
What are capture and fusion beats?
Capture beats are a normal P-QRS-T configuration occurring due to a normally conducted atrial beat resulting in ventricular activation.
Fusion beats are when both the conducted atrial impulse and the ectopic focus cause simultaneous ventricular activation - this results in a QRS morphology that is a summation of the normal and ectopic beat.
142
What treatment options are indicated in cases of AV dissociation?
* Lignocaine
* Procainemide
* Sotalol
* Quinidine
* IV digoxin or diltiazem, if the foci is clearly supraventricular, could be useful to either silence the rhythm or slow the response rate.
143
In a horse with junctional or ventricular arrhythmia secondary to bradycardia or AV block is an anti-arrhythmic medication indicated and if so which one?
No. Subsidiary pacemakers in the AV junctional and ventricular specialised tissues are rescue mechanisms. In cases of AV block and sinus bradycardia, these escape complexes are life-saving. The treatment should be aimed to resolve the cause of sinus bradycardia or AV block.
144
What is an accelerated idioventricular rhythm and what clinical conditions is this associated with most often?
When the subsidiary pacemakers discharge at a rate higher than that of the SA node, causing an accelerated idioventricular rhythm.
GIT (A/B and electrolyte imbalance) disease, anaesthesia and catecholamines are most often associated with the occurrence of these rhythms.
145
With idioventricular rhythms, the independent atrial and ventricular pacemakers can occasionally discharge at similar rates giving the impression of a P wave that marches in and out of the QRS complex. What is this called and when is it most likely to happen?
Isorhythmic AV dissociation.
Seen most commonly with inhaled anaesthesia.
146
True or false: ventricular arrhythmias are less common than atrial arrhythmias but are more likely to be associated with underlying structural cardiac disease, lesions of the myocardium or a multi-systemic disorder.
True
147
True or false: altered K, Mg, and Ca concentrations can affect myocardial electrophysiology, and electrolyte and A/B disorders can induce ventricular ectopy
True
148
List causes of ventricular arrhythmia
* Toxaemia
* Sepsis
* GIT disease (proximal enteritis, large bowel disease)
* Metabolic disease
* Hypoxia/ischaemia
* Toxins
* Systemic inflammation/SIRS
* Primary heart disease
* Occurrence in seemingly healthy horses
149
VPCs are typically manifest as a premature, widened QRS complex that is followed by a compensatory pause - why is there a pause?
Pause is due to the next sinus impulse being blocked by the refractory AV conduction system
150
What is the coupling interval and is it always the same?
Coupling interval is the relationship between a ventricular premature contraction and the preceding sinus beat and it can be fixed or variable. If it is very short, R-on-T phenomenon occurs.
151
Define bigeminy, couplets, triplets and runs with respect to VPCs
Bigeminy: alternating between a sinus beat and a VPC
Couplets: two VPCs in a row
Triplets: three VPCs in a row
Runs: 4 or more VPCs in a row (ventricular tachycardia).
152
True or false: many cases of frequent VPCs resolve spontaneously after a period of rest.
True
153
Ventricular tachycardia is runs of VPCs at a rate often exceeding 100bpm that may be regular or irregular. Multiform VT is more likely to be regular or irregular?
Irregular
154
In what circumstances do you see jugular pulses with VT?
AV dissociation.
155
What is Torsades de pointes?
A specific form of polymorphic ventricular tachycardia characterised by progressive changes in QRS direction leading to a steady undulation in the QRS axis (R-on-T).
156
What features of VT are considered "malignant" or associated with a poor prognosis?
* Haemodynamic instability
* Sustained VT
* Rapid ventricular rate
* Short coupling interval
* Multiform or polymorphic QRS morphology
157
What treatment is indicated for VT?
* Lignocaine (don't give too fast, CNS excitement)
* MgSO4 (effective even in horses without aberrations in Mg concentration)
* Quinidine (myocardial depressant and vagolytic plus GIT side effects)
* Procainamide (limited studies but well-tolerated, similar to quinidine but fewer GIT effects and less vagolytic)
* Amiodarone (only studied in small numbers, perhaps a second-line choice)
158
What is the protocol for recovery in horses with VT that respond to antiarrhythmic treatment?
* Period of rest (4-8wk)
* Repeat Holter ECG and exercise ECG
* Repeat ECO
* If the above examinations are within normal limits a slow return to exercise can occur. The exercising ECG should be repeated again once in full work but before return to competition/racing and then annually.
* Prognosis is favourable if no underlying structural disease/damage.
159
What are the features of an intraventricular conduction block and what distinguishes this from a VPC?
Widening of the QRS complex and axis deviation.
Distinguished from VPCs because they have a preceding P wave.
160
What conditions are intraventricular conduction blocks typically associated with and what is the underlying cause?
Commonly occur after APCs, post overdose with quinidine, from severe hyperkalaemia, secondary to supraventricular tachycardias with rapid ventricular response.
QRS broadening can be due to ectopic foci or aberrant intraventricular conduction.
161
What are the features on ECG of accelerated AV conduction and pre-excitation?
Accelerated AV conduction is seen as a shortened P-R interval due to an anomalous conduction pathway around the AV node.
Pre-excitation is seen as slurring of the initial QRS (a delta wave) and overall widening of the QRS complex.
162
What are the effects of hyperkalaemia on the heart?
Depression of AV, atrial and ventricular conduction, and shortened ventricular repolarisation.
163
What conditions can be associated with hyperkalaemia?
* Uroperitoneum
* Renal failure and oliguria
* Shock with severe metabolic acidosis
* K replacement IV
* Hyperkalaemia periodic paralysis
164
What ECG changes might you see with hyperkalaemia and at what K level?
Alterations usually start to be seen \>6mEq/L: broadening and flattening of the P wave is most consistently seen as well as prolonged P-R and bradycardia followed eventually by atrial standstill.
At \>8 mEq/mL inversion or/and enlargement of T waves, may marked widening of QRS (near to 10, near-lethal).
165
What is the treatment for hyperkalaemia and why?
* IVFT low in K - depending on cause Hartmann's or 0.45% NaCl (not in foals, use Hartmann's)
* Glucose to stimulate intracellular K movement
* Insulin (along with glucose facilitates intracellular shifts of K)
* ß2 agonists (clenbuterol, salbutamol to augment intracellular K movement)
* Calcium (stabilises resting cardiac membrane potential)
* NaHCO3 (for treatment of metabolic acidosis not usually indicated in foals, and ensure respiratory function is adequate to blow off the excess CO2 that will be produced) - NaHCO3 is given at 1-2mEq/kg depending on base excess. (mEq NaHOC3 = 0.3 x [-0.5] x BE x kgBW)
166
Describe the Eisenmenger physiology.
Chronic, high-volume left-to-right shunts can result in pulmonary vascular remodelling, increased pulmonary vascular resistance, and eventual right-to-left shunt flow if pulmonary vascular resistance exceeds systemic vascular resistance.
167
How to describe interventricular communications:
By Phenotypes
* Perimembranous is fibrous continuity between the aortic and tricuspid valve;
* Doubly committed (these are also commonly termed juxtaarterial), defect is fibrous continuity between the aortic and pulmonary valves; and
* Muscular is the one completely surrounded by muscular tissue;
By geography, meaning where does the interventricular communication open when viewed from the right ventricular perspective: centrally, apically, inlet, or outlet.
Last, the degree of septal alignment apparent at the borders of a VSD should be defined to fully categorize the defect.
168
Highlights additional features of VSD that have been associated with a worse prognosis in horses
**Physical Examination**
* Resting tachycardia
* Jugular venous distension
* Subcutaneous oedema bounding/hyperkinetic arterial pulse
* Pulmonary crackles
* Increased respiratory effort
**Echocardiography**
* Left atrial enlargement
* Left ventricular enlargement
* Moderate to severe pulmonary artery dilation
* Right ventricular hypertrophy
* Prolapse of the aortic root into the defect
* Malalignment of the aortic root (overriding aorta)
* Defect measures greater than 2.5 cm in a 450 to 500 kg horse
* Defect measures greater than 40% of aortic annular diameter
* Doppler velocity less than 4.5 m/s with good alignment to flow direction
* Moderate to severe aortic, mitral, or tricuspid regurgitation
* Concurrent congenital defects overload
169
Four forms of ASD are considered, classified by location relative to the interatrial septum
* Primum: Defects in the ventral interatrial septum above the tricuspid valve (1);
* Secundum: those in the area of the oval fossa (2);
* Sinus venosus: those high in the dorsal atrial septum near either cranial or caudal vena cava inflow (3) and;
* Unroofed coronary sinus: may be associated with anomalous pulmonary venous drainage (4).
170
Familiar risk for developing congenital cardiac anomalies in horses
Familial risk seems to be present with a disproportionate number of Arabians.
Familial risk for VSD in the Welsh Mountain pony and Standardbred
Prevalence de 0.5%
