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Flashcards in PT 1 Deck (30)
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Q. Name three features of foetal circulation that differ from adult circulation

A. Ductus venosus: bypasses hepatic circulation, blood flows from umbilical vein into IVC (to the heart). Why do these close after birth?
B. Foramen ovale: blood bypasses the heart by a hole from RA to LA, straight into the aorta
C. Patent ductus ateriosus: deoxygenated blood that enters the right ventricle goes into pulmonary arteries and into the descending aorta via this shunt (due to high foetal pulmonary resistance
D. Birth = Breath = Decreased Pulmonary Vasculature Resistance = Increased LA Press. > RA Press. = Foraman Ovale Close = Increased O2 (from respiration) & Decreased Prostaglandin (from placenta separation) = Ductus Arteriosus Close
E. Indomethacin (NSAID) used to help close PDA


Q. What are the most common R L shunts in congenital heart disease? How do these babies present and how should they be managed?

A. Truncus Arteriosus
B. Transposition of Great Vessels
C. Tricuspid Atresia
D. Tetralogy of Fallot
SIG: Cyanosis, Squatting (increases peripheral vascular resistance = increases preload = increases stroke volume), Clubbing, F to Thrive, Ejection Systolic Murmur
INV: CXR (boot-shaped), ECG (RBBB, RVH), ECHO
Tx: surgical tx


Q. What are the most common L R shunts in congenital heart disease? How do these babies present and how should they be managed?

A. Ventricular septal defect (VSD), (20% of all congenital heart defects)
LV > pressure than RV.
Pt: not blue, breathless, poor feeding, failure to thirive.
Signs: increased RR, tachycardia, breathless, failure to thrive, large heart, murmur my very in intensity

Tx: large may need require fixing in infancy.
Small: asymptomatic, but endocarditis risk.

Risk of Eisenmenger's syndrome (becomes cyanotic)

B. Atrial septal defect (ASD). Connection between Atria.
LA high pressure than RA. (L to R shunt), pt is not blue.
S&S: RH dilation, SOBOE, increased chest infections, pulmonary flow murmour, fixed split second heart sound (delayed closure of PV because more blood has to get out), big pulmonary arteries and big heart on CXR

C. Patent ductus arteriosus
Blood flows from aorta to PA\Signs: contious 'machinary' murmur, big heart, breathlessness, differential cyanosis (clubbed blue toes but pink not clubbed fingers).
May cause Eisenmenger's syndrome ---> CYANOTIC

Large ones need to be closed surgically.


Q. What is Eisenmenger Syndrome?

Eisenmengers syndrome: the process in which a long-standing left to right cardiac shunt caused by a congenital heart defect causes pulmonary hypertension and eventual reversal of the shunt into a cyanotic right to left shunt.

¥ High pressure pulmonary blood flow
¥ Damages to delicate pulmonary vasculature
¥ The resistance to blood flow through the lungs increases
¥ The RV pressure increases
¥ The shunt direction reverses
¥ The patient becomes BLUE


Q. What occurs in each of the heart sounds?

A. S1 = mitral and tricuspid valve closure
B. S2 = aortic and pulmonary valve closure
C. S3 = in early diastole during rapid ventricular filling, normal in children and pregnant women, associated with MR and HF
D. S4 = In late diastole, apex and patient left lateral, associated with LVH


Q. What is heard in Aortic stenosis and when?

A. Aortic valve = 2nd intercostal space, left of sternum, radiates to carotids. Open during systole, closes during diastole
B. Systolic: Crescendo-decrescendo Ejection Systolic Murmur, Loudest at Aortic Area, Radiates to Carotids.


Q. What is the commonest cause of aortic stenosis?

A. Calcific Aortic Valvular Disease (CAVD): mainly elderly, (T lymph, macrophages) results in thickening with fibrosis, lesions contain lipoproteins that calcify)
B. RF: old age, male, elevated lipoproteins, low LDL, HTN, DM, smoking
C. Bicuspid Aortic Valve (BAV): congenital – regular ECHO (associated with aortic coarctation, root dilation, aortic dissection)
D. Rheumatic Fever (progressive fusion and thickening)
E. Other: CKD, paget’s disease of bone, prev radiation exposure, homozygous familial hypercholesterolaemia)


Q. Name 4 symptoms and signs of aortic stenosis

A. Symptoms usually occur when aortic orifice reduced to 1/3rd normal size: exercise-induced syncope, angina, dyspnoea
B. Obstructed LV emptying LV hypertrophy ischemia angina, arrhythmias, LV failure
C. Signs: systolic, low pitched, ejection. Radiates to carotids, ejection click, palpable thrill


Q. What is heard due to mitral regurgitation and when?

A. Mitral valve = apex, radiating to axilla (MV prevents backflow of blood from LA during systole, opens during diastole)

B. Pansystolic High-Pitched “Blowing Murmur”, (Thrill is severe)
Mitral = Loudest at Apex and Radiates to Axilla (MR),
S3 = sudden rush of blood back in dilated LV

C. MR causes: degenerative, IHD, rheumatic heart disease, infective endocarditis (cardiomegaly, SLE, Marfan’s, Ehlers-danlos)

D. Pathology – regurg into LA = LA dilatation, LV/stroke volume must increase to compensate LV hypertrophy


Q. Name 4 symptoms of mitral regurgitation

A. Palpitation (often felt due to increase in SV), dyspnoea, orthopnoea (due to LV failure and pulmonary HTB), fatigue and lethargy (reduced CO)


Q. How would you diagnose mitral regurgitation, what would be seen? Describe the management

A. CXR: LA and LV enlargement, calcified mitral valve
B. ECG: Bifid P waves (due to LA delay), LV hypertrophy
C. ECHO: dilated LA and LV
D. Mx: mitral valve repair, prophylaxis against endocarditis


Q. Name 3 features of tetralogy of fallot

A. Pulmonary stenosis, RV hypertrophy, overriding aprta (boot shaped heart)
B. Most common congenital cyanotic disease, extreme hypoxia with cyanosis
C. Presents with: crying, clubbing, squatting, cyanosis, syncope


Q. What condition has saddle shaped (concave) ST elevation +- PR depression

A. Pericarditis
B. Sharp retrosternal chest pain, worse on movement, deep breathing and straining
C. Typically relieved on leaning forwards
D. A fever may also be present
E. (On auscultation there may be a pericardial friction rub)


Q. What is heard with a mitral valve prolapse and when?

A. Mitral valve = apex, radiating to axilla (MV prevents backflow of blood from LA during systole, opens during diastole)
B. At systole: Late Systolic Crescendo Murmur with Midsystolic Click, Loudest at Apex


Q. What is heard with Aortic regurgitation and when?

A. Diastolic: AR: High-Pitched “Blowing” Early Diastolic Decrescendo Murmur, Best Heard Sitting Forward
B. AE: acute (acute rheumatic fever, infective endocarditis, aortic dissection), chronic (rheumatic heart disease, syphilis, severe HTN, Marfan’s)
C. Signs: hyperdynamic circulation = bounding/collapsing pulse, Quinckle’s sign (capillary pulse in nail bed), De Musset’s sign (head nodding with heart beat)


Q. What is heard with Mitral stenosis and when?

A. (between LA/LV)
B. Mitral valve = apex, radiating to axilla (MV prevents backflow of blood from LA during systole, opens during diastole)
C. Diastolic: Opening Snap at apex & Delayed Rumbling Late Diastolic Murmur (decreasing interval between S2 and opening snap = increasing severity)
D. (opening snap occurs due to increased LA pressure, rumble occurs as blood is forced through the stenosed valve)
E. Commonest cause = rheumatic heart disease, secondary to rheumatic fever (group A strep) (inflammation valve thickening cusp fusion and calcium deposition, increased LA pressure = RA hypertrophy, PO, pulmonary HTN)


Q. How would you diagnose mitral stenosis, what would be seen? Describe the management

A. CXR: enlarged LA, calcified mitral valve, PO, (cardiomegaly)
B. ECHO: enlarged LA valve leaflet mobility, thickening, calcification
C. ECG: sinus rhythm, bifid P wave (LA activation)
D. Mx: valvotomy to widen the valve, mitral valve replacement if severe, treat AF (digoxin and anticoag), treat dyspnoea (lose dose diuretics)


Q. What symptoms are seen with mitral stenosis?

A. Severe dyspnoea and productive cough, RHF = weakness, fatigue, abdo/lower limb swelling, atrial fibrillation (due to enlarged LA = palpitations), systemic emboli/stroke


Q. What heart sounds are heard with patent ductus arteriosus?

A. Continuous Machine-Like Murmur, Loudest at S2, Beat Heard Infraclavicular Area


Q. Name some symptoms of acute end organ damage due to hypertension crisis (>200/120)

A. Symptoms of acute end-organ damage:
B. Neuro: headache, N+V, confusion, retinopathy, papilloedema, weakness
C. CVD: chest pain, SOB
D. Renal: oliguria/anuria
E. Emergency: High BP + Acute End-Organ Damage
F. Urgency: High BP (no end-organ damage)
G. Acute end-organ damage: pailloedema, encapalopathy, intracranial haemorrhage/stroke, aortic dissection, MI, PO, acute renal insufficiency
H. Mx: slow reduction of BP, beta-blockers (labetalol, IV/PR)
(LVF) = Nitroprusside/Hydralazine IV


Q. What are the criteria for rheumatic fever?

A. JONES CADE PAL, disease of children young adults <15 – group A strep
B. Major: Joint involvement, O- myocarditis, Nodules (subcutaneous), Erythema marginatum, Sydenham cholera
C. Minor: CRP increased, arthralgia, fever, elevated ESR
D. Minor: Prolonged PR interval, anamnesis of rheumatism, leucocytosis
E. Diagnosis: throat cultures growing GABHS or elevated anti-streptolysin O titres + 2 major or 1 major and 2 minor


Q. What is the management for rheumatic fever?

A. M: Bed Rest, IM Benzyl/PO Penicillin V, Aspirin (analgesia)
B. COMP: Chronic RF, Valvular Disease
C. Penicillin Prophylaxis


Q. What are the signs and symptoms of infection endocarditis?

B. Fever, Roth’s spots, Osler’s nodes, Murmur, Janeway lesions, Anemia, Nail hemorrhages (splinter haemorrhage), Emboli


Q. What are the criteria for infective endocarditis?

A. BE FEVEER * bacterial endocarditis
B. Major: Blood culture +ve X 2, 12 hours apart, Endocardial involvement from ECHO
C. Minor: Fever, ECHO findings, vascular findings, 2 X evidence of microbiological/immunology, Risk factors (e.g. drug abuse, valvular disease)


Q. Which bacteria are likely to cause infection endocarditis?

A. Acute: Staphylococcus aureus (IVDU)
B. Subacute: Streptococcus viridans (dental procedures)
C. Others: Enterococci, Staphylococcus epidermidis (prosthetic valves), diptheroids, candida, SLE (Libman-Sacks), malignancy


Q. How should infective endocarditis be treated?

A. (native valve) Amoxicillin + Gentamicin
B. (native valve + sepsis) Vancomycin + Gentamicin
C. (prosthetic valve) Vancomycin + Gentamicin + Rifampicin
D. Surgery


Q. What occurs in escape rhythms?

A. Normally, the SAN suppresses other pacemakers as it is faster. Escape rhythms occur when impulses from SAN are slower than that of own pacemaker rate capability
B. Pacemaker cells found at various points in conducting system with each site able to independently sustain rhythm:
C. SAN: 60-100bpm
D. Atria: <60bpm
E. AVN (junctional): 40-60bpm
F. Ventricles: 20-40bpm


Q. What is the definition of sinus bradycardia?

A. Def: <50bpm + sinus rhythm
B. (occurs in athletes, hypothermia, hypothyroidism, raised ICP)


Q. What are the different degrees of heart block?

A. 1st degree: benign and symptomatic – no tx required
AE: athletes (increased vagal tone), inferior MI, mitral valve surgery, AVN blocking drugs (beta blockers, CCB, digoxin)
B. 2nd degree – Mobitz type 1: progressive lengthening of PR interval until beat is “dropped”, excitation fails to pass through AVN/bundle of his
AE: AVN blocking drugs (betablockers, CCB, digoxin), increased vagal tone, inferior MI
C. 2nd degree – Mobitz type 2: PR interval is constant and QRS complex is dropped
Failure of conduction through HIS/PURKINJE. Associated with LBBB, bifascicular block, (may be symptomatic syncope)
AE: anterior MI, mitral valve surgery, SLE/RF/Lyme’s
D. 3rd degree/complete heart block: complete absence of AV conduction, rhythm is maintained by junctional or ventricular escape rhythm. There may be ventricular standstill = syncope/sudden cardiac death
AE: inferior MI, AVN blocking drugs (BB, CCB, digoxin)


1. Q. What is the definition of sinus tachycardia?

A. >= 100bmp + sinus rhythm
B. AE: exercise, pain, fever, hypovolaemia, anaemia, pregnancy, hyperthyroidism, vasodilators – atropine