Station 3: Cardio Flashcards
Approach to cardio exam?
Inspection
Syndromic features e.g. Down, Turner, Noonan, Holt-Oram (triphalangeal thumb, radial hypoplasia), Marfan
Previous central catheters (IE)
Surgical scars/midline sternotomy - look at legs for vein graft harvesting
Hands
Clubbing, splinter haemorrhages, Janeway lesions, Osler nodes, nail bed abnormality
Radial pulse - rate, rhythm, character, volume, radio-radial delay
Brachial pulse - collapsing character
Face
Eyes - anaemia, jaundice (haemolytic anaemia, cardiac cirrhosis)
Mouth - central cyanosis, dentition, glossitis, ulcers
Malar flush of MS
Neck
JVP - abnormal waves (absent a AF, cannon a CHB, large V TR)
Plucked chicken skin - pseudoxanthoma elasticum
Palpation **check again for scars before this (lateral chest, axilla, inframammary)
Apex beat - if unable to palpate, put into left lateral position but cannot comment on location, heaves
Mitral thrill
LSE - parasternal heave of RVH, thrill of TR/small VSD
Palpable P2, thrill of pulmonary/aortic valves
Auscultation
MV - bell first, then diaphragm -> 1st HS normal/loud (MS)/soft (MR), if systolic murmur - extending 2nd HS, radiation at axilla
TV - systolic murmur -> TR if accentuates with inspiration, if not VSD
PV - 2nd HS normal/loud (pulm HTN), splitting of 2nd HS (fixed wide splitting ASD), ESM accentuates with inspiration and radiates to the back (PS)
AV - ESM radiation at carotid (AS), soft EDM sitting up and pause after expiration (AR) *loud aortic murmur can be heard all over praecordium but does not radiate to axilla, or extend beyond 2nd HS
Lung bases for crepitations
Sacral and peripheral oedema
5 things to present in cardio?
- Which valve involved, or what lesion
- How severe, or if prosthetic valve - is it functioning
- Any signs of endocarditis (always assumed to be present until proven otherwise)
- Any signs of heart failure
- What is the possible cause
Scars in cardio?
Median sternotomy - bypass graft surgery, aortic/mitral valve replacement, TOF repair, TGA repair, Fontan procedure (blood flow reroute from IVC directly to pulmonary artery bypassing ventricle), correction surgery in Blalock-Taussig shunt
Right thoracotomy - Blalock-Taussig shunt, some ASD repair, pulmonary artery banding
Left thoracotomy - Blalock-Taussig shunt, mitral valve repair, coarctation of aorta repair, pulmonary artery banding, PDA ligation
Left upper chest - implantable device (pacemaker, defibrillator, resynchronisation device)
Right upper chest - minimally invasive surgey (tricuspid, aortic, mitral valve repairs, some septal defect repairs)
Inframmary - mitral valvotomy
Median LL - vein graft harvesting
Murmur grades?
1 - very faint, heard by experts, no thrill
2 - soft, no thrill
3 - moderately loud, no thrill
4 - loud, thrill
5 - very loud, heard with steth partially off chest, thrill
6 - loudest, heard with steth entirely off chest, thrill
What is physiologic split S2?
- Best heard at pulmonic area (P2 much softer than A2)
- A2 closes first before P2
- During inspiration when there is increased venous return to the right side of the heart
- Split disappears in expiration
What causes paradoxical/reversed splitting S2?
- Split occurs in expiration and disappears in inspiration
- Anything that causes delayed A2 closure
- Aortic stenosis, HOCM, LBBB
What causes widened splitting S2?
- Split occurs in both inspiration and expiration, but becomes greater with inspiration
- Anything that causes delayed P2 closure or early A2 closure
- Delayed P2 closure: RBBB, pulmonary hypertension, PS
- Early A2 closure: severe MR, VSD
What causes fixed splitting S2?
- Split occurs in both inspiration and expiration equally
- Fixed delay in P2 closure
- Pathognomonic of ASD
- > in inspiration, increased venous return to right side of heart and increased flow through PV hence delayed P2 closure
- > in expiration, reduced pressure in RA results in increased blood flow through ASD from LA to RA, hence increased flow through PV again and delayed P2 closure
Causes of reduced/absent radial pulse?
- Cervical rib
- Subclavian stenosis
- AVF
- Coarctation of aorta
- Takayasu arteritis
- Blalock-Taussig shunt surgery
- Radial artery harvesting for bypass graft surgery
- Radial artery injury
How to determine which is the predominant pathology in mixed valve disease?
APEX BEAT - location and character
-> The compensatory response of the ventricle is the final arbiter
AS
- Apex heaving, minimally displaced
- Pulse slow rising
- 2nd HS quiet
AR
- Apex thrusting, displaced
- Pulse collapsing
- HS normal
MS
- Apex tapping
- Pulse AF
- 1st HS loud
MR
- Apex displaced
- Pulse maybe AF
- HS normal, 1st HS maybe quiet
Coarctation of aorta - symptoms and signs?
Symptoms:
- Young, hypertension
- Fatigue, particularly the legs
- Leg claudication
- Endarteritis: fever, rigors etc
- Failure
- Chest pain (accelerated CAD or aortic dissection)
Signs:
- Turner: short stature, webbed neck, low posterior hairline, epicanthic folds, short 4th MCP, cubitus valgus, widely spaced nipples, lack of pubic hair, pigmented naevi, peripheral lymphoedema
- Left lateral thoracotomy scar for previous repair
- Lower body underdeveloped
- IE: Janeway lesion, Osler nodes, splinter haemorrhages
- Pulse: brisk and forceful (hypertension), radio-radial delay (prox subclavian), radio-femoral delay (check right radial and right femoral)
- Apex minimally displaced, heaving (hypertension or AS due to associated bicuspid AV)
- Systolic thrill at suprasternal notch, or thrill from AS
- HS: loud S1 (hypertension), loud S2, ESM from AS, possible EDM from AR, systolic murmur due to coarctation (loudest at thoracic spine or lower at abdomen - starts around 1/3 of systolic usually short)
- Failure signs
- > 20mmHg difference between left and right brachial systolic BP
Coarctation of aorta - associations?
- Turner’s syndrome
- Bicuspid aortic valve
- Aortic dissection
- VSD
- PDA
- MV prolapse
- Marfan syndrome
- Neurofibromatosis type 1
- Acromegaly
Coarctation of aorta - investigations?
- ECG: LVH
- CXR: indentation in aorta -> 3 shaped descending thoracic aorta
- TTE/TOE: anatomy of coarctation and functional effect to LV
- Cardiac MRI: more detailed, useful if preparing for surgery and monitoring outcome
- Coronary angiogram: might be considered before surgery given the high incidence of premature CAD
Coarctation of aorta - management and indications for intervention/surgery?
- General advice - avoid isometric exercises due to risk of aortic dissection, maintain other exercises to maintain good health and BP
- Medical - manage hypertension and risk factors given high incidence of premature CAD
- Percutaneous endovascular stenting - can also treat restenosis after primary surgical repair
- Surgical repair - resection of coarctation segment (if short) with end-to-end anastomosis, or bypass graft if longer segment
Indication for surgery:
- Symptomatic patients with gradient across coarctation > 30mmHg
- Asymptomatic patients in the presence of hypertension or LVH
- Patients undergoing other cardiac surgery e.g. bicuspid AV or aortic arch aneurysm
Coarctation of aorta - how to present?
- Distal or proximal to left subclavian artery (radial pulses equal: distal, left radial pulse diminished: proximal)
- Evidence of surgical repair - diminished left radial pulse (left subclavian artery used in repair), left thoracotomy scar, no radio-femoral delay
- Presence of bicuspid aortic valve: ejection click, with or without AS murmur
- Upper torso better developed than lower torso
Indications for endocarditis antibiotic prophylaxis?
Based on ESC Guideline 2015
Reserved for high-risk patients:
- Worse prognosis of IE
- Small number of these patients, so potential harm from abx use is reduced
- Uncertainties in the estimations of risk of IE
3 groups of patients:
- Prosthetic valve or any prosthetic material
- Previous Hx of IE
- Congenital heart disease - cyanotic or any type repaired with prosthetic materials
- If repaired with no residual defects - prophylaxis up to 1st 6 months
*AHA recommends prophylaxis in valve disease in transplanted heart - however not supported by strong evidence, so not recommended by ESC
Points against general endocarditis antibiotic prophylaxis?
- Low-grade bacteraemia occurs in the mouth from daily activities e.g. toothbrushing, flossing
- Estimated risk of IE following dental procedures is very low
- Most case control did not report association between invasive dental procedures and IE
- No RCT to prove efficacy of abx prophylaxis on occurrence of IE, only proven in animal model
- Risk of anaphylaxis from abx
- Risk of abx resistance from widespread use
Procedures indicated for endocarditis antibiotic prophylaxis?
- *In HIGH RISK PATIENTS
1. Dental - manipulation of gingival or periapical regions, perforation of oral mucosa (scaling, root canal)
2. Cardiac - prosthetic valve, defibrillator, pacemaker - Screen for staph aureus via nasal swab pre-op
- Eliminate source of sepsis > 2/52 before op
- Prophylaxis with IV cefazolin 1g pre-op and up to 48 hrs post-op
NO NEED: Braces, STO, LA injection, superficial caries, shedding of deciduous teeth, trauma to lips or oral mucosa Resp procedures GI or genitourinary procedures TOE Skin or soft tissue procedures
Choice of endocarditis antibiotic prophylaxis?
Single dose 30-60 mins before procedure:
No allergies to penicillin or ampicillin - IV or PO amoxicillin/ampicillin 2g OR IV cephalexin 2g OR IV cefazolin/ceftriaxone 1g
Allergies to penicillin or ampicillin - IV or PO clindamycin 600mg
VSD - how to present?
- Direction of shunt - cyanosis: R to L shunt
- Haemodynamic significance: pulmonary HTN and LV enlargement
- Important negatives: cyanosis, clubbing, pulmonary HTN, LV enlargement
Haemodynamic significance
Insignificant: small shunt, no clubbing/cyanosis, loud systolic murmur, parasternal thrill, apex undisplaced, S2 normal, no pulm HTN
Significant (L to R): large shunt, no clubbing/cyanosis, less loud murmur, apex displaced and thrusting, widened splitting S2 + loud P2, pulm HTN
Significant (R to L): large shunt, clubbing and cyanosis, no murmur, apex displaced and thrusting, single loud S2, pulm HTN
*Pulmonary HTN - raised JVP, parasternal heave, loud P2, functional TR murmur
VSD - symptoms and signs?
Symptoms
In adulthood usually asymptomatic and incidental finding
Or present with high output cardiac failure
Signs
Look for phenotypical features of congenital syndromes
Small: no clubbing/cyanosis, undisplaced apex, loud PSM/ESM at lower LSE, normal S2, parasternal thrill
Moderate to large: no clubbing/cyanosis, displaced apex and thrusting, less loud murmur, widened splitting S2 + loud P2, parasternal thrill
Large + Eisenmenger: clubbing and cyanosis, displaced apex and thrusting, no murmur, single loud S2, palpable P2
VSD - investigations?
- ECG: small normal, large LVH/RVH, bifid P wave lead II, biphasic P wave V1
- CXR: cardiomegaly, increased pulmonary vascular markings, enlarged LA (double right heart border)
- ECHO: direction of shunt
VSD - causes and types?
Maternal - PKU, diabetes, fetal alcohol syndrome
Congenital - Down, Edward, Patau, DiGeorge
Acquired - ischaemia (post MI rupture)
4 types:
- Perimembranous (commonest)
- Inlet
- Outlet
- Muscular
VSD - management?
Indications and contraindications for surgical repair?
- Small: reassurance
- Large: surgical or percutaneous repair
- No IE abx prophylaxis (unless prev Hx of IE)
Indication for surgical repair:
- Acute septal rupture post MI
- Significant shunting - pulmonary:systemic flow ratio > 2
- LV dysfunction
- Recurrent endocarditis
- Development of AR
Contraindication for surgical repair:
- Irreversible severe pulmonary HTN (tested via right heart catheterisation with vasodilators or lung biopsy)
VSD - complications?
- Infective endocarditis
- LV dysfunction
- Pulmonary hypertension
- Eisenmenger syndrome
VSD:
What is Maladie de Roger?
What is Gerbode defect?
Maladie de Roger:
Loud harsh systolic murmur at lower LSE, often with parasternal thrill -> indicating small VSD, does not need surgical correction
Gerbode defect:
Communication between LV-RA, in perimembranous type due to defect at the atrioventricular septum -> can cause RV failure
ASD - how to present?
- Direction of shunt: cyanosis R to L
- Haemodynamic significance: pulmonary HTN and presence of MDM at tricuspid region
- Important negatives: clubbing, cyanosis, presence of upper limb deformity, presence of pulmonary HTN
ASD - symptoms and signs?
Symptoms Lesions not recognized in childhood present in 3rd or 4th decade of life Recurrent resp tract infections Dyspnoea (pulmonary HTN or AF) Palpitations (AF or atrial arrhythmia) Peripheral oedema (RHF) Stroke (paradoxical embolism)
Signs
Look for phenotypical features of congenital syndromes
Down (epicanthic folds, low set ears, Brushfield spots of the iris, flat nasal bridge, excess nuchal fold, single simian crease)
Holt-Oram (triphalangeal thumb, radial hypoplasia)
Small (Haemodynamic insignificant, L to R)
Pulse normal, apex beat undisplaced, no thrill, grade 2/6 ESM at pulmonary area, S2 fixed wide splitting
Large (Haemodynamic significant, L to R)
Pulse may be AF, apex beat undisplaced, thrill at pulmonary area, ESM at pulmonary valve, MDM TV flow, S2 fixed wide splitting, loud P2/raised JVP/parasternal heave/PSM TR (pulm HTN), peripheral oedema (RV failure)
Large (Haemodynamic significant, R to L)
Clubbing and cyanosis, pulse may be AF, apex beat displaced, no thrill, no murmur, S2 fixed wide splitting, loud P2/raised JVP/parasternal heave/PSM TR (pulm HTN), crepitations (LV failure)
ASD - types?
4 types:
- Secundum: commonest, at foramen ovale area
- Primum: at AV septum
- Sinus venosus: at SVC, connection with pulmonary vein
- Coronary sinus: at wall between coronary sinus and LA
ASD - investigations?
- ECG: AF, RAD (secundum), LAD (primum), RVH (TWI and STD V1-V4, II, III, aVF)
- CXR: cardiomegaly, increased pulmonary vasculature and prominent pulmonary artery
- ECHO: direction of shunt, effect on RV function, pulmonary pressure
- cMRI: more detailed anatomy, shunt size, effect on RV function
- Right heart catheterization: determine reversibility of pulmonary hypertension with vasodilator therapy if surgical intervention is considered
- Lung biopsy: if reversibility with vasodilator is equivocal
ASD - management and indications for surgical/percutaneous repair?
Mainly observation and reassurance
Surgical or percutaneous repair:
- Symptomatic ASD
- After paradoxical embolism
- Asymptomatic ASD with significant shunt: pulmonary to systemic pressure ratio > 1.5
- Evidence of reversible pulmonary HTN: proven via right heart catheterisation with vasodilator therapy, or lung biopsy showing reversible pulmonary artery histopathological changes
ASD - complications?
- Recurrent chest infections
- Atrial arrhythmia (AF)
- Paradoxical embolism
- Pulmonary hypertension
- Eisenmenger syndrome
- Infective endocarditis
ASD - what is Lutembacher syndrome?
- Presence of secundum ASD with rheumatic mitral stenosis
- Due to puncture of IAS during percutaneous balloon mitral valvuloplasty - pass through IAS from RA to LA
PDA - how to present?
Similar to VSD
- Direction of shunt
- Haemodynamic significance: pulmonary HTN and LV enlargement
- Important negatives: clubbing (differential), cyanosis, pulmonary HTN, LV enlargement
PDA - symptoms and signs?
Symptoms
- Small: asymptomatic, incidental finding
- Large: endarteritis, failure, palpitations (AF)
Signs
Small: pulse normal, apex undisplaced, thrill and continuous machinery murmur at left infraclavicular
Moderate: large collapsing pulse, wide pulse pressure, apex beat displaced and thrusting, parasternal heave, thrill and continuous machinery murmur at left infraclavicular
Large: differential cyanosis and clubbing, no murmur or thrill, pulmonary HTN (raised JVP, parasternal heave, loud P2, TR murmur), lung congestion and leg oedema
PDA - aetiology?
- Congenital
- Prematurity
- Birth at high altitude
- Neonatal rubella syndrome
PDA - complications?
- Infective endocarditis
- LV failure
- Pulmonary HTN
- Eisenmenger’s syndrome
- Ductal aneurysm and rupture
