Cardiology Flashcards
Does cardiac tamponade typically result in left or right sided congestive heart failure?
Right side CHF
What are the two locations for AV block?
AV node
Bundle of His (continues into the bundle branches)
why is high vagal tone a risk factor for development of atrial fibrillation?
In addition to depressing heart rate, AV conduction, exciteability and contractility it also shortens the action potential and refractory period, making the myocytes more susceptible to other stimuli or re-entry.
What are the dominant receptors in the heart and systemic vasculature?
Heart: B1 adrenergic
Systemic vasculature: Alpha adrenoreceptors
Which catecholamines and receptors augment vasoconstriction and vasodilation in general?
Vasoconstriction: post-synaptic alpha adrenergic receptors by adrenaline, nor adrenaline or drugs such as phenylephrine
Vasodilation: stimulation of B2 adrenergic receptors causes vasodilation in circulatory beds, as does locally produced nitric oxide, and dopaminergic receptors if present.
Which main drugs/hormones enhance cardiac contractility? And what decreases it?
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.
What is the pre-ejection period, what is it an index of and what shortens it?
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 ionotropes or sympathetic activation.
In what condition may pronounced splitting of the 2nd heart sound be heard, particularly if the pulmonic component is louder than the aortic?
Pulmonary hypertension.
How do you calculate ejection fraction?
Ratio of stroke volume : end-diastolic volume
List medications that decrease afterload primarily through arterial vasodilation.
Acepromezine
ACE-inhibitors
Hydralazine
what might splitting of the first heart sound indicate?
May indicate abnormal ventricular electrical activity or VPCs
When do you hear a systolic ejection murmur?
Starts after S1 and finishes before S2.
In what circumstances might you palpate a thready or hypokinetic arterial pulse, or a pulse deficit?
Thready/hypokinetic pulse: reduced stroke volume and peripheral vasoconstriction
Pulse deficit: LV pressure is not exceeding aortic pressure
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?
Wide cuff underestimates
Narrow cuff overestimates.
What is the correction factor for blood pressure for height above the heart base?
0.77mmHg/cm above the heart base
List normal MAP, SAP, DAP and pulse pressure for horses
MAP: 110 +/- 15mmHg
SAP: 135 +/- 15mmHg
DAP: 90 +/- 15mmHg
Pulse pressure 45 +/- 6mmHg
What are the differentials for the following:
Pale MM
Dark red/Injected MM or greyish-blue
Prolonged CRT
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)
If you see isolated venous distention cranial to the thoracic inlet what conditions might you be suspicious of?
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.
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?
Trot: 70-140bpm Canter: 120-160bpm Gallop: 150-180bpm Hard gallop: >180bpm HR Max: 210-240bpm Recovery: <100bpm within 2-5min
How does spontaneous pacemaker activity work with respect to cellular depolarisation in cardiac myocytes?
There is a background inward sodium current and a time-related decrease in the membrane permeability to K ion 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 depolarisation.
What are the autonomic effects on automaticity?
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.
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?
Left vagus preferentially innervates the AV node
Right vagus preferentially innervates the SA node
Parasympathetic activity more extensive to supraventricular than ventricular myocardium.
What does the P-R interval tell you? And what are changes in this interval often related to?
Time taken for conduction across the AV node and His-purkinje system.
Changes often relate to changes in blood pressure and baroreceptor activation.
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?
Myocardial ischaemia may show on ECG as S-T segment deviation.
Myocardial hypoxia and hyperkalaemia may be evident as enlargement of the T wave.
What are the requirements of an U/S 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.
In addition to LA diameter, what further measurement 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.
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.
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.
Tricuspid regurgitant flow above what velocity is suggestive of increased pulmonary artery pressure with PHT?
> 3.2-3.4m/s
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
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!
What are the expected pressures in the pulmonary artery, aorta, central venous pressure?
PA pressure: systolic 35-45mmHg, mean 25-30mmHg, diastolic 20-25mmHg.
Aortic pressure: systole 110-130mmHg, diastolic 75mmHg
CVP: 5-10mmHg
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, compliance and pressure in the left atrium.
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)
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.
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)
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
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.
List causes/mechanisms of biventricular heart failure
- Isolated LV failure leading to increased pulmonary venous pressure, pulmonary vascular remodelling and PHT and therefore increased pressure load on the RV
- RV failure with marked ventricular dilation leads to leftward bulging of the IVS and impaired LV filling
- Chronic pericarditis leads to impaired ventricular filling
- Arrhythmias such as AF which are bilateral in the setting of structural heart disease can promote biventricular failure.
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
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.
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.
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
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 naturietic peptide
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.
List causes of per-acute CHF?
Chordal rupture
Papillary muscle ischaemia or infection
Endocarditis
Vascular rupture (eg aortocardiac fistula)
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 distention, 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, intersitial 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.
List common treatments for CHF
- Antiarrhythmic Tx: lignocaine, MgSO4, quinidine, pracainamide, propafenone, sotalol or amiodarone.
- Diuretic Tx: (only if not secondary to cardiac tamponade) furosemide is the loop diuretic of choice and repeated boluses may be required, with increasing doses potentially necessary if renal function is compromised
- Minimise stress: move to 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
- Ionotropes: 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 dysrrhythmia. It also has baroreceptor sensitising eeffects 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.
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. Well 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.
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.
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.
What is the effect on shunt flow of a down-stream right sided obstruction? And list some examples
Reversion to a right to left shunt
Eg: 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.
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.
With a VSD, in addition to PHT what is another possible cause of widened split of S2?
Disparate ventricular ejection times
With respect to murmours, 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 murmour is louder, associated with high velocity flow entering the main PA.
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.
What are the typical components of an endocardial cushion defect?
Large ASD involving the primum and the 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.
Which treatment/drug class given to the dam may predispose foals to development of PDA?
Prostaglandin inhibitors
List the 4 abnormalities associated with tetralogy of fallot and the 5th abnormality that may occur with pentalogy of fallot.
- Large paramembraneous outlet VSD
- Cranial dextro-positioning of the aorta with overriding of the septal defect
- RV outflow obstruction
- RV hypertrophy.
(5) PDA or ASD would classify as pentalogy of fallot
What are the defects associated with pulmonary atresia and what is the common mistake with diagnosis?
- Right ventricular outlet doesn’t connect to the pulmonary artery
- Right ventricle is hypertrophied
- A large malalignment VSD is present
- 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)
List clinical signs of pulmonary atresia
Cyanosis
Cardiac murmur
Stunting in a foal or weanling.
What is truncus arteriosus communis and what are the clinical features?
Failure of the foetal truncus arteriosus to partition into aorta 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.
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 a foramen ovale. 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.
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.
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.
What lesion typically results in aortic regurgitation?
Degeneration of the valve with nodular fibrotic bands.
How would you describe a clinically relevant aortic murmour?
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.
