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RACP paeds Qld Group > Cardiology > Flashcards

Cardiology Flashcards

1
Q

what key event directly initiated myocardial contraction

A

release of stored calcium from sarcoplasmic reticulum (calcium induced calcium release)

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2
Q

most common congenital cardiac defect in t21

A

AVSD

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3
Q

Management of VSD/AVSD

A

In the neonatal period, pulmonary vascular resistance is high which limits the degree of left to right shunting. This shunting increases with age as the PVR and RV compliance decreases resulting in pulmonary vascular engorgement and symptoms of CCF.
Medical treatment is indicated for symptomatic CCF. This commonly involves a combination of captopril (for afterload reduction), frusemide (reduces pulmonary congestion) and digoxin (inotropic and deactivating effects).
Surgical management involves patch closure of the septal defects as well as valvular repair. It is usually performed in the first six months of life. In the setting of AVSDs, medical management is only indicated for symptomatic congestive cardiac failure, otherwise the treatment is surgery (and should be urgent once there are signs of pulmunary hypertension)

In small infants, pulmunary artery banding may be performed as this protects the pulmunary circuit from HTN until surgery can be performed

In babies with T21, surgery should be done before 6 months, as they are at risk of pulmunary hypertension

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4
Q

Cardiac embryology

A

Angiogenic cell clusters arise in the mesoderm
At 20 days, paired heart tubes fuse to form a single heart tube
By 24 days the cardiac loop is formed
The bulbus cordis becomes the right ventricle while the primitive ventricle becomes the left ventricle.

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5
Q

BMI weight criteria

A

Underweight: BMI <5th percentile for age
Normal weight: BMI 5th to <85th percentile
Overweight: BMI 85th to <95th percentile
Obesity: BMI ≥95th percentile

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6
Q

Epoprostenol

A

Prostaglandin analogue
Vasodilator
Treatment of pulmunary hypertension
Last line therapy while awaiting transplant

Epoprostenol is too unstable to be given orally. Its intravenous half-life is less than six minutes so it has to be given by continuous infusion.
Can be unstable at room temp so needs to be carried around on a backpack on ice.
The infusion should not be stopped suddenly as the patient can deteriorate within minutes- acute pulmunary hypertensive crisis (acute rise in pulmunary vascular resistance, resulting in R heart faiure and death) Adjustments to the infusion rate must be done under observation so that heart rate and blood pressure can be monitored for several hours.

Should use 2 + medications with differing mechanisms of action eg with endothelin receptor antagonist; thus less risk to child if infusion is suddenly ceased

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7
Q

Electrolyte abnormalities which cause prolonged QT interval

A

Hypokalemia
Hypocalcemia
Hypomagnesemia
Hypothermia

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8
Q

Major criteria of Rheumatic fever

A

Carditis
Polyarthritis (or monoarthritis if high risk)
Chorea
Erythema marginatum
Subcutaneous nodules

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9
Q

Minor criteria of rheumatic fever

A

Fever
Raised ESR/CRP
Polyarthralgia (oe monoarthralgia if high risk)
Prolonged PR interval on ECG

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10
Q

Pulsus paradoxus can be caused by ..

A

Cardiac tamponade

In healthy individuals, inspiration causes the systolic blood pressure to fall slightly as a result of the greater volume of blood accommodated by the pulmonary vascular bed. This occurs despite inspiratory increase in venous return to the right heart. In cardiac tamponade, right ventricular filling is maintained at the expense of restricted left ventricular filling, and the systolic blood pressure falls further (>10 mm Hg). This exaggerated fall in systolic blood pressure with inspiration is referred to as pulsus paradoxus.

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11
Q

Cardiac complication most likely with DMD

A

dilated cardiomyopathy

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12
Q

Qp Qs equation

A

(Aortic sat- MV sat)/ (pulmonary vein sat - pulmonary artery sat)

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13
Q

Cardiac anomalies associated with Noonans syndrome

A

Pulmunary artery stenosis
Hypertrophic cardiomyopathy
ASD

Superior axis on ECG

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14
Q

Drugs which cause QT prolongation

A

ntiarrhythmics e.g. amiodarone, TCAs, antipsychotics (haloperidol, quetiapine), anti-infectives (clarithromycin, fluconazole, erythromycin).

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15
Q

which anti arrythmics contraindicated in WPW

A

verapamil and digoxin

increase anterograde conduction

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16
Q

Class Ia antiarrythmics

A

Na channel blocker

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17
Q

Which drugs are effective in supraventricular arrythmias?

A

Adenosine
Digoxin
Verapamil (dont use in neonates!)

Both ventricular and supraventricular:
amiodorone
Quinidine
Flecanide

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18
Q

Class Ia antiarrythmics

A

Class 1- all sodium channel blockers
Procainamide
Quinidine

Lengthens the action potential

ECG effect: prolongs QT and QRS

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19
Q

Class Ib anti arrythmics

A

Lidocaine

only used for ventricular tachyarrythmias

shortens the action potential

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20
Q

Class Ic anti arrythmics

A

Flecanide
Strongest Na channel blocker
Causes widening of QRS

Prolongs slope of phase 0, doesnt affect the duration of the action potential

Pro arrythmic

Used for severe SVT and VT

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21
Q

Class II anti arrythmics

A

Beta blockers

Block the effects of catecholamines at B 1 adrenergic receptors and reduce conduction through the AV node

Selective: atenolol, metoprolol
Non selective: propranolol

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22
Q

Class III anti arrythmics

A

Potassium channel blockers
Prolong repolarisation/refractory period – prevents re entrant arrythmias

Amiodorone (also has class 1, 2, and 4 actions, lots of systemic side effects)
Sotalol (also non selective beta blocker)

Can cause QT prolongation

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23
Q

Class IV anti arrhythmic

A

Calcium channel blockers
Reduce condition through AV node, shorten the plateau and thus reduce the contractility of the heart

Verapamil
Diltiazam

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24
Q

Class V anti arrhythmic

A

Digoxin
- decreases condiction of impluses through the AV node –> reduces HR, extending the time of contraction
- increases contractility and stroke volume

Adenosine
-used to terminated SVT

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25
Q

which anti arrhythmic is contraindicated in WPW and infants

A

verapamil
class 4 anti arrythmic (ca channel blocker)
depresses contractility -> reduces cardiac output

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26
Q

management of SVT in infants

A

sotolol (class III)
flecanide (class Ic)

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27
Q

Truncus arteriosus

A

A single arterial trunk arises from the heart and supplies the systemic, pulmonary, and coronary circulations (total mixing lesion). VSD is always present, with truncus overriding the defect and receiving blood from both L + R ventricles. Both ventricles are at systemic pressure and both eject blood into the truncus.
Immediately after birth: pulmonary vascular resistance is still high, pulmonary blood flow can be normal. As pulmonary vascular resistance drops in the first month of life, blood flow to lungs is greatly increased and heart failure occurs. TA is a total mixing lesion with total mixture of pulmonary and systemic venous return: because of the large volume of pulmonary blood flow, clinical cyanosis is minimal initially –> as PVR increases over time (when untreated) and PBF reduces–> cyanosis more obvious
However in first 2 weeks of life, CHF develops as PVR reduces and there is increased pulmunary blood flow –> signs of heart failure (poor feeding, resp distress, tachycardia, hepatmegaly)

Exam:
full volume/bounding pulses
Mild cyanosis due to high pulmunary blood flow

Heart sounds: normal S1, single S2
Murmur: ESM (VSD) +/- apical mid diastolic murmur (increased flow through mitral valve)
ECG: biventricular hypertrophy (when PVR declines)
CXR: cardiac enlargement, plethoric lung fields

Must test for Di George!

Rx: ACE-I, diuretics, surgery in first few months

28
Q

Wide spitting S2

A

ASD (fixed)- Right volume overload, so RV needs to stay open longer to expel all blood
Pulmunary stenosis - needs to stay longer open to push blood through narrow opening
Ebstein anomaly - R volume overload
TAPVR - R volume overload
RBBB- R side takes longer to depolarise, so contracts after left side, so pulmunary valve stays open longer

29
Q

Narrow split S2

A

Pulmunary HTN (as pulmonary valve closes earlier due to high pulmonary resistance.
also pulm HTN causes increased intensity S2

30
Q

Single S2 occurs in …

A

a) If one of the semilunar valves is missing, as in pulmonary or aortic valve atresia, severe stenosis, truncus arteriosus, tricuspid atresia, hypoplastic left heart

b) If both valves close simultaneously as in double outlet single ventricle or in large VSD with equal ventricular pressures

c) In pulmonary hypertension with equal right and left ventricular pressures- Eisenmenger syndrome

d) If vessels are abnormally positioned- L transposition great arteries

31
Q

Paradoxical splitting of S2 (P2 before A2) occurs in

A

severe aortic stenosis
left bundle branch block

32
Q

L- TGA
Congenitally corrected

A

Morphologic LV is on the right side and connects to the PA-> lungs
Morphologic RV is on left and connects to aorta
Mitral and tricuspid valves are also on opposite sides

Theoreticaly no functional abnormality however assocuated with lots of other defects- conduction disturbances, arrythmias, valvular defects, VSD in 80%

ECG: Q waves V1
Upright T waves throughout precordium

33
Q

Mobitz type 1 (Wencheback)

A

Progressive prolongation of the PR intervalculminating in a non-conducted P wave:
* PR interval is longest immediately before dropped beat
* PR interval is shortest immediately after dropped beat

34
Q

Mobitz type 2

A

intermittent non-conducted P waveswithoutprogressive prolongation of the PR interval
* The PR interval in the conducted beats remains constant
* The P waves ‘march through’ at a constant rate
* The RR interval surrounding the dropped beat(s) is an exact multiple of the preceding RR interval (e.g. double the preceding RR interval for a single dropped beat, triple for two dropped beats, etc)

35
Q

Example of endothelium derived vasodilator

A

Prostacycin
Derived from arachedonic acid via the COX patheay
Inhibits platelet aggrefation and clot formation
Antagonises effect of thromboxane A2

Nitric oxide is another example

36
Q

Total anomalous pulmonary venous return

A

Complete anomalous drainage into the systemic venous circulation (ie all Left sided blood drains into right side, physiological L–> R shunt, then part of R sided blood flows through PFO/ASD into L heart (anatomical R–> L shunt –> cyanosis)
Total mixing lesion –> cyanosis
MUST HAVE INTRAATRIAL CONNECTION FOR SURVIVAL

Exam: if no obstruction: mild cyanosis at birth, signs pulmunary overcirculation, RVH and failure (resp distress, hepatomegaly, poor feeding, FTT)- ie similar to L-R shunt (may not actually look cyanotic)

If obstruction (usually infracardiac): increased pulmunary vascular resistance + pulmunary HTN.
If severe, will be a critically ill/shocked neonate with severe cyanosis due to severely reduced pulmunary venous return to heart, hypotension

Heart sounds: wide split S2 (due to right heart overload)
Murmur: SEM at LUSB from relative PS, mid diastolic murmur at LLSB from increased flow across tricuspid valve
ECG: RAD, RVH
CXR: snowman sign (supracardiac), plethoric lung fields, cardiomegaly (right sided)

37
Q

In a normal heart, increased splitting of S2 occurs during

A

Inspiration

During inspiration, negative intrathoracic pressure causes increased venous return to the right heart, with increased right ventricular filling and therefore a relative delay in closing of the pulmonary valve after systole

38
Q

Transposition of great arteries

A

Where the VSD is large and not restrictive to ventricular ejection, significant mixing of oxygenated and deoxygenated blood usually occurs and clinical manifestations of cardiac failure are seen.
CYANOSIS ALWAYS PRESENT
but its intensity is variable (most severe if intact ventricular septum, minimal with y restrictive VSD).
Can have ASD or PFO- if so will need urgen balloon atrial septostomy
Cyanosis can generally be recognised within the first month of life, but it may remain undiagnosed in some infants for several months. - can just be a well blue baby with no murmur
The murmur is holosystolic and generally indistinguishable from that produced by a large VSD in patients with normally related great arteries.

CXR: Cardiomegaly, a narrow mediastinal waist “EGG ON A STRING”, and increased pulmonary vascularity

ECG: upright T wav V1, isolated right ventricular hypertrophy or biventricular hypertrophy.
Usually RAD

Natural hx: progressive hypoxia, acidosis and heart failute (most sick if no VSD- less mixing; VSD most likley to develop CCF)

Rx: Prostaglandin E1 to improve mixing
Diuretcis, ACE-I if heart failure symptoms
Atrial switch at first 2 weeks of life

39
Q

Long QT syndrome types

A

All AD inheritance

type 1: KCNQ1 –> loss of function mutation of potassium channels –> prolonged repolarisation phase
T wave broad
type 2: KCNH2–> loss of function mutation of potassium channels
T wave low amp and notched

type 3: SCN5a–> gain of function mutation in sodium channels –> increase influx of sodium into cell during depolarisation
T wave pointy

40
Q

Symptoms long QT syndrome

A

torsade de pointes —> VF–> cardiac arrest –> sudden cardiac death
TdP is usually self-terminating, thus causing a syncopal event (most common symptom) or seizures
palpitations an uncommon presentation

Type 1: during exercise (esp swimming ) –> drowning
Type 2: during arousal (loud noises, emotional startle)
Type 3: during sleep

41
Q

Management inherited long QT syndrome

A

B blockers
Avoiding other QT prolonging medications and hypokalemia/hypomagnesemia

42
Q

ECGs in long QT syndrome

A

Type 1: broad, large T waves
Type 2: notched T waves, low amplitude
Type 3: prolonged isolectric ST segment with normal symmetrical T wave

43
Q

Drugs associated with QT prolongation

A

Class I and III anti arrythmics (quinidine, sotolol, amiodorone)
Antibiotics: azithromycine/clarithromycin/erythrmycin, metronidazole, moxifloxan
Antifungals: fluconazole (if cirrhosis), ketaconazole
Antimalarials: chrloroquine
Antidepressants: amitryptyline, imipramine
Antipsychotics: risperidone, haloperidol, clozapine, droperidol
Other: cisapride, ondansatron

44
Q

Catacholaminergic polymorphic VT

A

Inherited cardiac ion channelopathy
Life threatening arrythmias with catecholamines
Present with emotion or exercise induced syncope, seizures, or sudden cardiac death
usually present in childhood

Resting ECG normal
With exercise- VT /VF
Can do exercise stress test w sprint, adrenaline challenge test, and genetic testing to diagnose

Think of this if child is getting worse with adrenaline boluses

Rx: Beta blockers, flecanide, ICD, sympathectomy, avoid very strenuous exercise

45
Q

Brugada syndrome

A

Inherited channelopathy- sodium channel
Leading inherited cause of sudden death in people under 40 years

Type 1:
Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave.
This is the only ECG abnormality that is potentially diagnostic.
It is often referred to as Brugada sign.
This ECG abnormality must be associated with one of the following clinical criteria to make the diagnosis:

Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT).
Family history of sudden cardiac death at <45 years old .
Coved-type ECGs in family members.
Inducibility of VT with programmed electrical stimulation .
Syncope.
Nocturnal agonal respiration.

RX: ICD

46
Q

Pulmunary HTN values

A

mild - mean PAP 25-35 mmHg
moderate- mean PAP 35-45
severe- mean PAP >45 mmHg

Gradient from RV to PA > 10 = RVOTO

47
Q

Mixed venous sat equation

A

(3 x SVC sat + 1x IVC sat)/4

If only RA sat provided, use that instead

48
Q

cardiac output equation

A

CO= SV x HR

49
Q

Fick equation

A

CO= VO2 / AVD02
VO2= O2 consumption

AVD02= O2 content difference before and after lungs
= PV sat - PA sat x Hb x 1.36

50
Q

Qp Qs

A

L- R shunt Qp>1
R-L shunt Qp<1
Qs is always 1
so the ratio is always “something to 1”

Qp = VO2 / ((PV sat - PA sat ) x Hb x 1.36)

CO = Qp in a structurally normal heart

51
Q

Murmur or peripheral pulmunary stenosis

A

innocent
occurs in early infancy as PVR decreases
SEM
Heard at upper left sternal edge, radiates to axilla or back

52
Q

indications for antibiotic prophylaxis in CHD

A

prophylaxis is only ever recommended for cardiac lesions at highest risk of developing endocarditis, namely;
prosthetic cardiac valve or prosthetic material used for cardiac valve repair
previous infective endocarditis
congenital heart disease but only if it involves:
unrepaired cyanotic defects, including palliative shunts and conduits
completely repaired defects with prosthetic material or devices, whether placed by surgery or catheter intervention, during the first 6 months after the procedure (after which the prosthetic material is likely to have been endothelialised)
repaired defects with residual defects at or adjacent to the site of a prosthetic patch or device (which inhibit endothelialisation)
cardiac transplantation with the subsequent development of cardiac valvulopathy
rheumatic heart disease (in Indigenous Australians only)
Additionally, this group should only receive prophylaxis if undergoing a high risk procedure, or a prolonged procedure which would be expected to produce an protracted period of bacteria.

53
Q

Mechanism action nitric oxide

A

upregulation of cyclic GMP
Nitric oxide is endothelial derived relaxing factor. It is produced in the endothelium of blood vessels and diffuses out of the cells. It then enters vascular smooth muscle cells and activates guanalate cyclase which forms cyclic guanosine monophosphate (cGMP)(a smooth muscle relaxant).
Nitric oxide is bound to haemoglobin and inactivated instantly in the blood to nitosylhaemoglobins and methaemoglobin. The half life of NO is 3-6 seconds.

54
Q

risk of sibling having CHD

A

The incidence of congenital heart disease in the normal population is 0.8%.
This increases to 2-4% in the second pregnancy after the first birth of child with congenital heart disease, or if the parent is affected.

55
Q

how long to treat for ARF

A

National recommendations for secondary prophylaxis in ARF are IM benzathine penicillin every 28 days for 10 years or until 21 years old (whichever is longer). For ARF with moderate rheumatic heart diseases is is for 19 years or until 35 years old (whichever is longer). With severe rheumatic heart disease or post surgery it is up to 40 years or lifelong.

56
Q

coronary artery fistula

A

Coronary artery fistulae account for 50% of congenital coronary artery abnormalities. They involve a direct communication between a coronary artery and either a chamber of the heart (coronary-cameral fistula) or a segment of the systemic or pulmonary circulation (coronary arteriovenous fistula), bypassing the intervening myocardial capillary bed. Small fistulae do not cause any haemodynamic compromise ands are asymptomatic. The haemodynamic consequence of larger fistulae depends on the chamber or vessel in which the fistula drains into. 90% terminate into the right side of the heart. Fistulae that drain into the systemic veins or RA mimics an ASD. Those that drain into the pulmonary arteries have a physiology similar to a PDA, those into the LA produce a volume load into the LA mimicking MR and those that drain into the LV have a physiology similar to aortic valve regurgitation. Large fistulae that drain into low pressure systems may cause coronary artery steal with myocardial ischaemia of the distal arterial bed. As flow thorough this low pressure system increases over time, aneurysmal dilation of the proximal vessel may evolve. The majority of children with these fistulae are asymptomatic and are incidentally discovered on auscultation or during investigation of other lesions by echocardiogram or angiogram. The murmur is continuous, similar to a PDA, but is heard lower down on the sternal border and often peaks in mid-to-late diastole. Less commonly these lesions may present with angina, cardiac failure, endocarditis or arrhythmias.

57
Q

primary contibutor to oedema in CCF

A

sodium retention

Inadequate cardiac output results in decreased juxtaglomerular apparatus perfusion. This stimulates the release of renin, which in turn results in aldosterone secretion, leading to sodium (and water) retention via the kidneys. This effect is potentiated by poor hepatic blood flow and a subsequent decrease in catabolism of aldosterone. Sodium and water retention leads to an increase in plasma volume, elevated hydrostatic pressure in capillary beds, producing the end result of peripheral oedema. Hypoalbuminaemia is a dilutional effect secondary to the above-mentioned salt and water retention and does not significantly contribute to oedema. Likewise, thoracic duct drainage is not involved in its pathogenesis. In the early stages of CCF, ADH levels are elevated. However over time, retention of salt and water via the renin-angiotensin-aldosterone pathway results in an expansion in plasma volume, which inhibits the release of ADH and subsequent water retention.

58
Q

Transposition of great arteries with intact ventricular septum

A

Most common type
No murmur as no VSD - often well appearing blue baby
Mixing completely dependant on flow through ASD/PFO/PDA
Examination - marked cyanosis on D1 (but may not be obvious at birth) of life with sats <75% (higher if ASD). Split S2
May have higher sats on L arm compared to R
CXR- egg on a string
ECG: RAD, RVH (right side heart pumping to systemic circulation)
Rx: urgent PGE1, baloon atrial septostomy, arterial switch

59
Q

ECG findings in tricuspid atresia

A

left axis or superior axis deviation

60
Q

brain lesions in CHD

A

white matter injury
porencephalic cysts

61
Q

Ebsteins anomaly

A

Ebstein’s anomaly is a malformation of the tricuspid valve and right ventricle:

Tricuspid Valve: incompetent with downward displacement into the right ventricle
Right Ventricle: dilated and atrialized (thin walls)
With the dilated and atrialized RV and an incompetent tricuspid valve, the functional impairment of the right heart results from tricuspid regurgitation and decreased forward flow from the right heart.
Most have ASD or PFO
Associated with WPW syndrome

Presentation:
Varies widely depending on severity
If neonate- severe cyanosis and RHF (distended jugular veins, hepatomegaly)
Cyanosis improves as PVR drops

CXR: wall to wall heart (massive cardiomegaly, R>L, upturned apex)

ECG: tall peaked P waves (RAH), RBBB, low voltages on R sided chest leads

Rx: initial management is medical with diuretics, NO, digoxin

62
Q

Tricuspid atresia

A

Cyanotic lesions with reduced pulmonary blood flow ( as flow relies on PDA/VAD and ASD/PFO)
Agenesis of tricuspid valve–> complete lack of communication bw RA and RV
Must have ASD (and VSD or PDA) to be compatible with life
Presents as cyanosis and murmur on D1 of life if pulmunary blood flow is reduced, or first few days if large VSD and pulmunary blood flow is increased
Murmur: Single S2, murmur of VSD, PDA,ASD

ECG: LAD or superior axis (hypoplastic R ventricle), tall P waves (RAH), LV hypertrophy, diminished RV forces

CXR: right atrium enlargement with reduced pulmonary blood flow

Rx: medical, may need prostaglandin, BT shunt to improve pulm flow
Then need Glenn and Fontan to allow all systemic blood to return to pulmunary artery and bypass RA

63
Q

Pulmunary HTN

A

Definition: mean pulmunary pressures > 25 mmHg
Elevated PA pressures can lead to RV failure
Exam: loud, narrow split S2

64
Q

Tetralogy of fallot

A

May not be cyanotic if net L->R shunt through VSD and minimal obstrutction on R side
Cyanotic if elevated pressures on R side –> R to L shunt
If minimal obstruction, may only present as signs of heart failure or tet spells over 4-6 weeks
May have low ish sats but not appear Cyanotic
Severity of RVOT determines direction and magnitude of shunt through vsd
Mild stenosis- left to right shunt, clinical picture of Vsd, pink
Severe stenosis, leads to right to left shunt and Cyanotic TOF
- RV heave and thrill, horse ejection systolic murmur
Cxr- boot shaped heart
ECG- RAD, RVH, RAH

Rx: repair at 6-12 months. Closure of VSD with patch, widening of RVOT

65
Q

Tet spells

A

sudden profound cyanosis caused by increased RV outflow tract obstruction
Rx: knees to chest, supplemental O2, IV fluid bolus, morphine

66
Q

Which vascular ring can be managed conservatively

A

Anomalous innominate artery with evidence of tracheal compression, usually cause few or no symptoms, therefore surgical correction is not required. Only about 10% of patients with this lesion have severe symptoms (apnoea, severe stridor or respiratory infections) and require surgery.
A: Double aortic arch is corrected by ligation and division of the smaller arch.
B: Ligamentum or ductus is corrected with ligation.
C: Anomalous innominate causing few or no symptoms is managed conservatively.
D: Right aortic arch with left ligamentum arteriosum is corrected with surgical division of the left ligamentum arteriosum.
E: Pulmonary artery sling is managed by detaching the left pulmonary artery and re-anastomosing it to the main pulmonary artery anterior to the trachea.

67
Q

Mitral opening snap

A

Sign of mitral stenosis
Forceful opening of MV when pressure LA >LV
Occurs in early diastole

RACP paeds Qld Group (46 decks)

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