cardiology

Question 1

causes of Apical diastolic murmur

Answer 1

An apical diastolic rumble (Austin-Flint) may be heard at the apex. This is due to partial closure of the anterior leaflet of the mitral valve. The apex impulse becomes laterally displaced and sustained.

Question 2

causes of fixed split second heart sound

Answer 2

Dx: ASD (due to continuous blood flow from left side to right side leading lenthened cardiac cycle on the right side of the heart), Right heart failure, Pulmonary Hypertension

Question 3

loud first heart sound

Answer 3

extra volume out of the pulmonary pace

Question 4

loud second heart sound

Answer 4

DDx: pulmonary hypertension (most common), ASD will also increase P2

Question 5

widely split second heart sound

Answer 5

aortic something

Question 6

wide splitting

Answer 6

Anything that causes delayed conduction down the right bundle (RBBB, pre-excitation of left ventricle, pacing of left ventricle, premature LV beats), pulmonary stenosis, pulmonary arterial hypertension

Question 7

Paradoxical splitting: Reverse of normal physiology, splitting of second heart sounds during expiration, singular during inspiration

Answer 7

Anything that causes delayed conduction down the left bundle (LBBB, pre-excitation of right ventricle, right ventricular pacing, premature RV beats), aortic stenosis

Question 8

Single S2: Either from loss of A2 or loss of P2

Answer 8

DDx: Severe aortic stenosis, severe aortic regurgitation, congenital absence of pulmonary valve

Question 9

causes of RAD?

Answer 9

Right ventricular hypertrophy
Acute right ventricular strain, e.g. due to pulmonary embolism
Hyperkalaemia
Sodium-channel blockade, e.g. TCA poisoning
Wolff-Parkinson-White syndrome
Dextrocardia
Ventricular ectopy
Secundum ASD – rSR’ pattern
Normal paediatric ECG
Left posterior fascicular block – diagnosis of exclusion

Question 10

causes of LAD?

Answer 10

Left ventricular hypertrophy
Left bundle branch block
Inferior MI
Ventricular pacing /ectopy
Wolff-Parkinson-White Syndrome
Primum ASD – rSR’ pattern
conduction defect (pulm atresia with noonan)
HOCM/DORV/tricuspid atresia/Ebstein

Question 11

causes of extreme axis deviation?

Answer 11

Ventricular rhythms – e.g.VT, AIVR, ventricular ectopy/ AVSD
Hyperkalaemia
Severe right ventricular hypertrophy
Tricuspid Atresia

Question 12

common findings in differential causes of chest pain

Answer 12

Condition Findings
Myocardial ischaemia - Abnormal pulse or blood pressure, arrhythmia, ST segment elevation or depression, raised troponins

Pericarditis - Positional pain, pericardial rub, widespread ‘saddle-shaped’ ST elevation

Pericardial effusion- Hypotension, distended neck veins, muffled heart sounds, pulsus paradoxus, globular enlarged cardiac silhouette on CXR

Pulmonary embolus- Tachypnoea, tachycardia, hypoxia, haemoptysis, non specific ST and T wave changes in anterior chest leads most common ECG finding, ‘classical’ S1Q3T3 pattern is uncommon. May see minor CXR abnormalities - usually normal

Aortic dissection - Differential limb BP’s, CXR findings include: widened mediastinum, left pleural cap and deviated trachea and main stem bronchi. Signs of myocardial ischaemia or pericardial tamponade

Question 13

mechanism of action amiodarone?

Answer 13

Complex drug with a broad spectrum of activity. Predominately Class III antiarrhythmic drug but also has actions similar to antiarrhythmic classes Ia, II and IV. Main electrophysiological action is prolongation of the action potential and refractoriness of all cardiac structures resulting in reduction of membrane excitability in myocardial tissue.

prolongs the myocardial cell action potential in phase 3 (repolaristation) and refractory period of atrial, nodal and ventricular tissues

Increases the refractory period via sodium and potassium channel effects.

Slows the intracardiac conduction of the cardiac action potential via sodium-channel effects

Question 14

what is amiodarone used for?

Answer 14

reduces membrane excitability - Control of ventricular and supraventricular arrhythmias including those associated with Wolff Parkinson - White syndrome

Question 15

what is amiodarone used for?

Answer 15

reduces membrane excitability - Control of ventricular and supraventricular arrhythmias including those associated with Wolff Parkinson - White syndrome

Question 16

when to avoid amiodarone?

Answer 16

Sinus bradycardia, sino-atrial heart block
Unless pacemaker fitted avoid in severe conduction disturbances or sinus node disease
Thyroid dysfunction; iodine sensitivity

Avoid intravenous use in
Severe respiratory failure
Circulatory collapse or severe arterial hypotension
Avoid bolus injection in congestive heart failure or cardiomyopathy
Avoid rapid loading after cardiac surgery

Question 17

What is the consideration with amiodarone and drug interactions?

Answer 17

Amiodarone is a CYP 3A4 inhibitor, therefore has many drug interactions which can result in toxicity. Some important examples include:

Amiodarone and digoxin: reduce the digoxin dose to half maintenance. If loading digoxin, use full digoxin loading dose and half maintenance dose; take digoxin levels

Amiodarone and some QT prolonging drugs may induce torsades de pointes arrhythmias. These drugs should not be used with amiodarone: e.g. Class 1A antiarrhythmics, sotalol, erythromycin, mexiletine, citalopram

Amiodarone may interact with some drugs lowering heart rate or causing conduction disturbances. Caution is advised if also using: beta blockers or calcium antagonists

Amiodarone and drugs affecting electrolyte levels (especially potassium) should be used with caution: diuretics, corticosteroids, amphotericin, senna (stimulant laxative) are not recommended

Amiodarone may interact with other drugs leading to altered levels of those drugs e.g. warfarin, sildenafil, flecainide, phenytoin, cyclosporine, fentanyl, midazolam.

As amiodarone has a long half life (up to 60 days), these drug interactions may potentially occur some time after amiodarone treatment has stopped.

Question 18

adverse effects of amiodarone?

Answer 18

Negative inotropic effect

Prolongation of QT interval

Nausea, vomiting, taste disturbances, raised serum transaminases, jaundice, bradycardia, sleep disorders, corneal microdeposits, venous irritation (peripheral), photosensitivity

Pulmonary toxicity

Hypothyroidism and hyperthyroidism - due to iodine content of amiodarone.

Hepatotoxicity

Question 19

mechanism of action of dobutamine?

Answer 19

Dobutamine is a synthetic catecholamine and it is a direct acting inotropic agent whose primary activity results from stimulation of cardiac adrenergic receptors acting primarily on β 1 receptors. Dobutamine increases stroke volume and cardiac output and decreases ventricular filling pressure and total systemic and pulmonary vascular resistances. It produces comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilator effects. Like all inotropic agents, dobutamine hydrochloride increases myocardial oxygen consumption. Dobutamine hydrochloride also increases coronary blood flow and myocardial oxygen supply.

Question 20

indications for dobutamine

Answer 20

Administered to children with low-output hypoperfusion states resulting from decompensated heart failure, cardiac surgery, and cardiogenic and septic shock⁴.

Question 21

contraindications for dobutamine?

Answer 21

Impaired ventricular filling and ventricular outflow tract obstructions such as: left sided lesions, coarctation, critical aortic stenosis, hypertrophic obstructive cardiomyopathy.

Hypersensitivity to sodium bisulfite (metabisulphite) (more common in asthmatics)

Question 22

mechanism of action of dopamine in cardiac

Answer 22

Dopamine hydrochloride is a synthetic catecholamine which can stimulate alpha, beta and dopamine receptors via the sympathetic nervous system. The effects of dopamine are dose dependent. At low doses (infusion rates of 0.5 to 2 micrograms/kg/min), dopamine receptors are selectively activated with renal and mesenteric vasodilatation. Renal plasma flow, glomerular filtration rate and sodium excretion usually increase with increase in urine output. The blood pressure either does not change or decreases slightly.

At infusion rates of 2 to 10 micrograms/kg/min, beta1-receptors are activated causing increased myocardial contractility and conduction velocity and heart rate and results in increased cardiac output and systolic blood pressure. The total peripheral resistance is relatively unchanged because of peripheral vasoconstriction (alpha effect) and muscle vasodilatation (beta effect).
At higher infusion rates the alpha-receptors are activated, causing vasoconstriction, and increased peripheral vascular resistance resulting in increased blood pressure. However increasing cardiac output and increasing vascular tone will cause increased myocardial oxygen demand

Question 23

mechanism of action of milrinone

Answer 23

Milrinone is a positive inotrope and vasodilator, with little chronotropic activity. It is a phosphodiesterase inhibitor and acts by selectively inhibiting phosphodiesterase III in cardiac and vascular muscle resulting in increased levels of cAMP. The increased cAMP levels cause cAMP mediated increases in intracellular ionised calcium and contractile force in the myocardium and cAMP dependent contractile protein phosphorylation and relaxation in the vascular muscle. This combined effect increases myocardial contractility and causes vasodilatation, thus milrinone is known as an inodilator. It also lowers preload by increasing diastolic myocardial relaxation, lusitropy relaxant properties, this improves coronary perfusion¹.

Question 24

indicattions for milrinone?

Answer 24

Low output states following cardiac surgery including weaning from cardiopulmonary bypass pump.

Short-term therapy in severe congestive heart failure.

Question 25

adverse effects of milrinone?

Answer 25

Arrhythmia: Ectopic beats, ventricular tachycardia, supraventricular tachycardia.

Hypotension.

Hypokalaemia.

Thrombocytopenia - risk increases with increasing duration of therapy.

Headache.

Tremor.

Extravasation

Question 26

definition of pulmonary hypertension?

Answer 26

The definition of pulmonary hypertension, based on adult derived data, is a mean pulmonary artery pressure (mPAP) ≥25mmHg at rest, measured by cardiac catheterization.⁵,⁶ In paediatric patients, this definition has been revised to include pulmonary vascular resistance measurements.

Question 27

biventricular and univentricular differences?

Answer 27

In a biventricular circulation, it is defined as a mean pulmonary artery pressure ≥25mmHg AND a pulmonary vascular resistance index (PVRI) >3.0 Wood units m². In single ventricle patients following cavopulmonary anastomosis (Glenn or Fontan procedure) PVRI >3.0 Wood units m² OR transpulmonary gradient > 6mmHg are used.⁷

Question 28

what are the heritable forms of pulmonary hypertension?

Answer 28

1. 2.1 BMPR2

1. 2.2 ALK1, ENG, SMAD9, CAV1, KCNK3

Question 29

medication for PAH?

Answer 29

1. Sildenadfil
2. endothelin receptor antagonists
3. prostaglandin

Question 30

risk to nerves post cardiac surgery?

Answer 30

recurrent laryngeal nerve palsy: results in eating difficulties, a weak voice, poor cough and repeated chest infections because of aspiration pneumonia