Cardiology Flashcards
How do you calculate MAP
DBP + (1/3 x (SBP-DBP))
What is the normal blood pressure found in the
-Right ventricle
-Pulmonary artery
-Left atrium
-Left ventricle
-Aorta
RV: 25/8
PA: 25/8
LA: 8/0
LV: 110/8
Aorta: 110/65
What is FICKS equation
VO2 (volume oxygen consumption) = CO x (Arterial- venous oxygen consumption)
What are class I anti-arrhythmic drugs and name some examples
Class I anti-arrhythmic drugs= sodium channel blockers
-1a: Procainamide
-1b: Lidocaine
-1c: Flecanide
What are class II anti-arrhythmic drugs
B-blockers
Atenolol, Bisoprolol, Propanolol
What affect do Class I anti-arrhythmic drugs have on the ECG
Prolong QRS +/- QTc
What are class III anti-arrhythmic drugs and what affect do they have on the ECG
Class III- potassium channel blocking
Affect: Prolong re-polarisation - increased QT interval
Examples: Amiodarone
What class of anti-arrhythmic drug is amiodarone
Class III- potassium channel blocker
What class of anti-arrhythmic drug is Flecianide
Sodium channel blocker
What are class IV anti-arrhythmic drugs. Give an example and explain their effect on the ECG
Class IV drugs= calcium channel blockers
Examples: Diltiazem, Verapamil
ECG: slow SA and AV node conduction
Sotolol has properties of 2 classes of anti-arrhythmic drugs- what are they
Class II- B blocker + Class III- Potassium channel blocker- at higher doses
Name side effects of Amiodarone
Lung- ILD
Liver- hepatotoxicity
Thyroid- hyperthyroid
Skin- photosensitivity
Which valve opens at the end of isovolaemic contraction
Aortic valve
At what phase in the cardiac cycle does the aortic valve close
Isovolaemic relaxation
Heart sound S1 correlates to which phase of the cardiac cycle
Start of isovolaemic contraction
Which phase of the ECG represent isovolaemic contraction
QRS complex
Which phase of the ECG represents the ejection phase of the cardiac cycle
ST-segment
What causes prolonged splitting of the second heart sound
Prolonged RV ejection time e.g RV volume overload (ASD), Pressure overload (e.g. TOF, pulmonary stenosis), RV delayed conduction e.g. RBBB
What is a paradoxical splitting of S2 and what causes it
Splitting of the second heart sound during expiration (should split during inspiration)
Causes= LV sustained systole. Can be due to
-increased volume: R–> L shunt, heart failure
-increased ejection pressure: Aortic stenosis
-delayed conduction: LBBB
What do the following aspects of the sinus venous develop into
-common cardinal
-vitilline
-umbilical
Common cardinal; you have both a L and R sides. They both have anterior and posterior branches. The posterior branches regress.
-R) anterior cardinal branch- travels upwards to form the R) brachiocephalic vein containing the internal jugular vein and R) subclavian vein.
-L) anterior cardinal branch - travels upwards to form the left brachiocephalic vein.
-L) and R) brachiocephalic veins then fuse to form a shunt known as the SVC
-On the left side, any aspect of the left cardinal vein beneath this shunt is supposed to regress .
Vitilline duct: Travel to the yolk sac and form a GI venous plexus and hepatic plexus. Fuse to form the IVC
Umbilical: forms the ductus venous and drains into the IVC
What is formed by the following aortic arches
1-
2-
3-
4-
5-
6-
1- MAX (i.e. first is the MAX you can be)- Maxillary artery
2- “Second” = Stapedial artery
3- “C is the first letter in alphabet”- Carotids - becomes right and left common carotids
4- “4 limbs”- right and left subclavian arteries + aortic arch (which becomes descending aorta to supply blood to the feet)
5- degenerates
6- 96 = 2 lung= pulmonary arteries + ductus arteriosus
What is formed by the following aortic arches
1-
2-
3-
4-
5-
6-
1- MAX (i.e. first is the MAX you can be)- Maxillary artery
2- “Second” = Stapedial artery
3- “C is the first letter in alphabet”- Carotids - becomes right and left common carotids
4- “4 limbs”- right and left subclavian arteries + aortic arch (which becomes descending aorta to supply blood to the feet)
5- degenerates
6- 96 = 2 lung= pulmonary arteries + ductus arteriosus
How does the primitive pulmonary veins form
-Lung bud is formed from foregut
-Creates a splanchnic plexus which initially is connected to umbilical and vitilline venous system
-At day 28, left atrium forms a primordial invagination - common pulmonary vein
-Splanchnic plexus also differentiates into pulmonary vascular bed and grows down to connect to the new pulmonary vein
-Once connection is made, the cardinal and umbilicovitilline connection degenerates
What occurs to cause total anomalous pulmonary venous connection
-At day 28, left atrium forms a primordial invagination - common pulmonary vein
-Splanchnic plexus in the primitive lung also differentiates into pulmonary vascular bed and grows down to connect to the new pulmonary vein
-Once connection is made, the cardinal and umbilicovitilline connection is supposed to degenerate
-Failure to do so= TAPV
-If cardinal system is retained: connection of lung to the SVC, RA
-If umbilicovitilline system retain: connection to the IVC, hepatic or portal system
What SpO2 would there be before you detected clinical cyanosis in the below patients
-normal Hb
-anaemia
-polycythamia
-normal: 80%
-anaemia: 50%
-polycythaemia: 84%
What affect do the following conditions have on the oxygen-hb desaturation curve
-acidosis
-increased diphosphoglycerate
-increased fetal Hb
-Carbon monoxide
-Hypothermia
-Low pH shifts the curve to the Right, reducing affinity to Hb
-DPG made by cells in glycolysis during hypoxia. Increased level = increased hypoxia = shifts curve right
-fetal Hb= increased affinity for oxygen= shifts curve left
-CO= increased affinity for oxygen= shifts curve left
-Low temp= shifts curve left= increased affinity for oxygen
What murmur do you get with a
-secundum ASD
-primum ASD
-ASD= pulmonary flow murmur + fixed splitting of the second heart sound
-Primum = ASD close to the endocardial cushion which can affect the AV valves and result in MR. Murmur will be a pan systolic + pulmonary flow + fixed splitting of S2
What CHD is most associated with trisomy 21
AVSD
Indomethacin is used for PDA treatment. What is its Mechanism of action and side effects
COX 1+ 2 inhibitor - reduced circulating prostaglandins
SE- reduced urine output= fluid retention, thrombcytopenia, NEC, IVH
Indomethacin is used for PDA treatment. What is its Mechanism of action and side effects
COX 1+ 2 inhibitor - reduced circulating prostaglandins
SE- reduced urine output= fluid retention, thrombcytopenia, NEC, IVH
What is the Rastelli procedure and for what congenital heart defect is it performed
Performed for Truncus arteriosus
Involves sealing the VSD so that the LV pumps into the Truncus and then making a homograft connection from the RV to the main posterior pulmonary artery
What is the Rastelli procedure and for what congenital heart defect is it performed
Performed for Truncus arteriosus
Involves sealing the VSD so that the LV pumps into the Truncus and then making a homograft connection from the RV to the main posterior pulmonary artery
What is the difference between L-TGA and D-TGA
D-TGA: have parallel circuits. Right and left ventricles + atrium are normally positioned however aorta is connected to RV and pulmonary trunk to the left ventricle.
Need a PDA and ASD/VSD for mixing to survive
L-TGA: congenitally corrected TGA. Inlet and outlet vasculature is “normally” connected however LV and RV sites are switched
What is the classical CXR finding for Transposition of the great arteries
Egg on a string
Describe the Senning Procedure and when it is used
Used to correct Loop-TGA (where the ventricles are on opposite sides but the rest of the atrial and arterial aspects are normally placed
-PA band to build up strength of left ventricle which up to that point has been pumping to the pulmonary trunk
-Intra-atrial baffle placed to redirect systemic blood from the IVC+SVC –> Right atrium and visa versa for the pulmonary blood –> LA
-Arterial switch operation where great arteries transected and placed in correct anatomical positions
Describe the 3-step palliative cardiac pathway involved with a single ventricle e.g. severe tricuspid atresia
1) Blolock-Thaussig shunt- 1st week of life- shunt from subclavian to pulmonary artery to increased pulmonary blood flow
2) Bidirectional Glenn- SVC anastomosis to the pulmonary artery
3) Fontan- IVC anastomosed to the pulmonary artery
At end of Fontan have 2 separate circulations and single ventricle system where systemic blood bypasses the heart
What on a ECG would differentiate a VSD from tetralogy of fallot
VSD: get LVH
TOF: get RAD and RVH
Describe the 3 steps used in the palliative correction of HLHS
1) Norwood: aim to reconstruct the aorta and improve systemic circulation.
-ASD created
-Pulmonary trunk cut. Distal end is closed so the heart no longer directly supplies the pulmonary arteries
-Proximal end connected to native aorta with homograft material used to reconstruct its size
-BT shunt created to shunt blood from R) subclavian artery to the R) pulmonary artery.
-Sanno shunt may be created to direct some blood from the RV to the pulmonary arteries
2) Bidirectional Glenn- SVC cut and connected to the R) pulmonary artery
3) Fontann- IVC cut and connected directly to the R) pulmonary artery
END circulation: IVC + SVC directed via shunt to the pulmonary artery –> lungs –> pulmonary veins –> LA – (ASD) –> RA –> RV –> Neo-aorta –> circulation
What valvular lesion is Williams syndrome associated with
Supra valvular stenosis- aortic and pulmonary
What valvular lesion is Alagiles associated with
Peripheral pulmonary artery stenosis
What value issue is Turners associated with
Coarctation of the aorta + bicuspid aortic valve
What valve issues is Noonans associated with
Valvular pulmonary stenosis
How might an older child with Coarctation of the aorta present
Leg pain after exercise
Reduced ETT
Hypertension
On exam- ESM, LVH
CXR- 3 sign, rib notching
ECG: LAD, LVH
What murmur does mitral stenosis give you
Mid diastolic rumble
what murmur is associated with marfans syndrome
Aortic regurgitation (decrescendo diastolic murmur) due to aortic root dilatation
what murmur is associated with marfans syndrome
Aortic regurgitation (decrescendo diastolic murmur) due to aortic root dilatation
Name 3 clinical signs of aortic regurgitation
-decrescendo diastolic murmur
-wide pulse pressure
-collapsing pulse
-signs of left heart failure
Name 3 clinical signs of aortic regurgitation
-decrescendo diastolic murmur
-wide pulse pressure
-collapsing pulse
-signs of left heart failure
What is the risk to the next child is a
-parent
-sibling
is affected by congenital heart disease
Parent- 4-5%
Sibling 2-4%
Usual: 0.8%
What is patau syndrome, its features and what CHD is it associated with
Patau = trisomy 13
Sx; midline effects e.g. cleft lip and palate, microcephaly, coloboma, polydactyl, Holoprosencephaly
CHD: 80% have it- ASD, VSD- most common. Also seen with HLHS
What is Edwards syndrome
What are its clinical features
What CHD is it associated with
Edwards= trisomy 18
Clinical features: rocker bottom feet, hypertonia, arthrogryposis, omphalmocoele, reduced IQ
90-100% have CHD- ASD/VSD most common
Also get PDA, CoA, TOF, DORV
What are the symptoms of DiGeorge syndrome including what CHD is associated with it and was is the genetic abnormality
“CATCH-22”
-Cardiac abnormaliteis- conotruncal defects
-Abnormal facies: low set ears, long nose, short philtrium, micrognathia
-Thymic aplasia
-Cleft palate/ bifid uvula
-Hypocalcamia/ hypoparathyrodis,
-22q11 micro deletion
What is the most common CHD associated with 22q11 micro deletion
Tetralogy of Fallot- 35%
Followed by- interrupted aortic arch (20%) and Truncus arterioles (10%)
A child presents with hypertension and a ejection systolic murmur plus dysmorphic facial features- what is the likely syndrome
What electrolyte abnormality are they most likely to get
Williams
-supravalvular aortic or pulmonary stenosis
-renal artery stenosis causes hypertension
-facial feature: elfin like facies, long philtrum, broad forehead, short nose
-Hypercalcaemia
A child presents with jaundice, a triangular face and a systolic murmur. What is the likely diagnosis and CHD
Allagiles- peripheral pulmonary stenosis
What is the mutation in Marfans syndrome and what CHD does it cause
FBN1 mutation- for fibrillin
Aortic root dilatation
Noonan syndrome is inherited in what fashion, is a mutation of ..? and is associated with what CHD
AD - mutation in the RAs/mitogen activated protein signalling pathway
CHD- valvular pulmonary stenosis
(+HOCM)
Noonan syndrome is inherited in what fashion, is a mutation of ..? and is associated with what CHD
AD - mutation in the RAs/mitogen activated protein signalling pathway
CHD- valvular pulmonary stenosis
(+HOCM)
What are the criteria for infective endocarditis called and what are they
Dukes Criteria
-2 major OR 1 major 3 minor OR 5 minor
Major
-Microbiological evidence of IE
*1x PBC +ve for Coxiella
*2xPBC +ve for typical agent
*3x PBC +ve for atypical agent
-Echocardiogram evidence: new vegetation, lesion, regurgitation, abscesses, or dehisistance of a mechanical valve
Minor criteria
-Risk factors for IE: CHD, previous IE, RHD, CVC, Prosthetic valve, mitral valve prolapse
-Fever >38
-Immunological evidence: Oslers nodes, nephritis (haematuria/proteinuria), Rheumatoid factor +Ve, low complement
-Vascular phenomena: splinter haemorrhages, Janeway lesions, Roths spots
-+ve blood culture not meeting major criteria
Who receives IE prophylaxis before a dental procedure
-Previous IE, RHD, prosthetic valve
-CHD with stents or unrepaired/palliation
-CHD with repair <6 months ago
What are the criteria for diagnosis of rheumatic fever
JONES criteria
-2 major OR 1 major 2 minor = definitive
-1 major, 1 minor, preceding GAS = probable
Evidence of preceding GAS (ASOT and Anti-DNAse titres or throat swab)
PLUS
Major- JONES
-Joints- polyarthritis
-O-Carditis- new MR, AR, pericarditis, myocarditis, subclinical endocarditis on echocardiogram
-Nodules- subcutaneous nodules
-Erythema margiatum
-Sydenem chorea- can be used to diagnosis RF in isolation
Minor criteria
-Arthralgia
-Fever >38
-Elevated ESR and CRP
-Prolonged PR interval
How long do you give IM Benpen in RHD for
-minor MR
-moderate MR
-severe MR
minor: 10 years or until 21y/old which ever is longer
moderate: age 35
severe: age 40
Name features of Kawasaki disease
What investigations would you do
Fever > 5 days
Cervical lymphadenoapthy
Mucositis
Macular rash
Red hands/feet +/- desquamation
Non exudative conjunctivitis
Investigations:
-Increased ESR/CRP
-FBC: low/high WCC, thrombocytosis
-Electrolytes: low sodium and albumin
-LFTs; Increased
-Urine: sterile puria
-Echo: effusion, aneurysm, myocardial dysfunction, valvular issues
What medication is contraindicated in HOCM
Digoxin- increases contractility of the heart which can worsen the LVOTO
What glycogen storage disorder causes HOCM
Pompe disease
What dose of aspirin and IVIG do you give in Kawasaki Disease
IVIG- 2mg/kg
Aspirin- 7-12.5mg/kg QID until fever resolves
Then low dose (3-5mg/kg daily) for min 6/52
What genetic defect causes genetic HOCM
Autosomal dominant defect in cardiac B myosin
Describe aortic dissection types I, II and III
What conditions might they be seen in
Type I; ascending aorta and extending distally
Type II: ascending aorta and limited to the arch
Type III: beginning after L) subclavian artery
Ehlos Danlos + Marfan syndrome
Name the Mechanism of action of Digoxin
When is it contra-indicated
Inhibits membrane Na/K ATPas. Reverses the Na/Ca exchanger which would normally pump calcium out of the cell and sodium into the cell. Result = increased intra-cellular calcium to improve cardiac contractility.
Also releases myocardial norepinephrine –> affects the B1 receptors
C/I in HOCM + LVOTO
Name the MoA of action Dopamine and Dobutamine
dopamine: increases myocardial norepinephrine
dobutamine: B1 receptor agent
Dobutamine: synthetic catecholamine which acts as beta agonist –> positive inotropic and chronotrophic effect
What is the MoA of Enalapril and Captopril
ACE inhibitors- work for RAA pathway to reduce circulating Aldosterone –> reduce blood volume
Reduced angiotensin II also results in vasodilation therefore reduced PVR
What is the MoA of Enalapril and Captopril
ACE inhibitors- work for RAA pathway to reduce circulating Aldosterone –> reduce blood volume
Reduced angiotensin II also results in vasodilation therefore reduced PVR
What is the MOA of Frusemide
What electrolyte abnormality can it cause
Blocks Na/2Cl/K reabsorption in the Loop of Henle and distal tubule
Hypokalaemia
What is the MoA of Spironolactone
What is its advantage compared to other diuretics
Blocks Aldosterone - aldosterone agonist
Potassium sparing
What is the MoA of Chlorthiazide
Blocks Na/Cl resorption
in the distal convoluted tubule
Why are ACE inhibitors Contraindicated in LVOTO
Concerns about poor coronary artery perfusion if after load is reduced and diastolic coronary artery perfusion is impaired
What is the MoA of Milrinone
Phosphodiesterase inhibitor - prevents degradation of cAMP –> positive inotropy
note: cAMP= increased opening of L-calcium channels
What is the MoA of Milrinone
Phosphodiesterase inhibitor - prevents degradation of cAMP –> positive inotropy
note: cAMP= increased opening of L-calcium channels
What changes are seen in the ECG with hypokalaemia
Flattened T-waves with some inversion
U-waves
“long QT” due to fused T+U waves
What changes are seen in hyperkalaemia
Tall peaked T-waves
Shortened QT interval- faster repolarisation
Prolonged PR and QRS interval
What does hypocalcaemia do to the ECG and why
Prolongs the QT interval
L) voltage calcium channels only inactivated once intra-cellular calcium reaches a certain threshold. If low calcium levels, takes longer to do so = prolonged plateau phase of cardiac cycle = prolonged QTc
Describe the difference between Mobiz type I and II heart block
Mobiz I: progressive lengthening of PR interval until there is a drop of the p wave
Mobiz II: sudden non-conduction of a p-wave. Due to fibrosis at the AV node. At risk of progressing to type III block
Describe the difference between Mobiz type I and II heart block
Mobiz I: progressive lengthening of PR interval until there is a drop of the p wave
Mobiz II: sudden non-conduction of a p-wave. Due to fibrosis at the AV node. At risk of progressing to type III block
What is the key feature you see with focal atrial tachycardia on ECG and what is first line treatment
p-waves of variable morphology but still in sinus rhythm
B-blockers
May need Radiofrequency ablation
What do you see on ECG in atrial flutter
What causes it
What is the treatment
Sawtooth pattern
Re-entrant circuit contained to the atria. AV node prevents conduction this, resulting in a 2:1 or 3:1 block
TX= synchronised DC cardio version 0.5-2J/kg
May need Amiodarone + B-blocker
