Summary Book Cardiology Flashcards
Which are the diastolic murmurs, early vs mid-late?
Early: aortic regurgitation and pulmonary regurgitation. Mid late: austin flint murmur and mitral stenosis.
Describe aortic stenosis
Ejection systolic, radiates to carotids, louder with expiration, narrow pulse pressure, LV enlarged with features of failure
Describe aortic coarctation
left third intercostal space
Describe aortic regurgitation
Heard in pulmonary area, louder with hand squeeze, early diastolic, have patient sit up / lean forward and breath out, water hammer pulse with wide pulse pressure
Describe pulmonary stenosis
Systolic, louder with inspiration, low volume pulse with narrow pressure, giant a waves, associated with tetralogy of Fallot (regurg post)
Describe patent ductus arteriosus
Pulmonary area, continuous with clubbing of only toes
Describe atrial septal defect
Pulmonary region, systolic, clubbed fingers and toes, S2 split
Murmurs of aortic region
Aortic stenosis, aortic coarctation
Murmurs of pulmonary region
Pulmonary stenosis, patent ductus arteriosus, atrial septal defect, aortic regurgitation
Describe tricuspid regurgitation
Tricuspid region, pan systolic, louder with inspiration, pulsatile liver, radiates to right lower sternal border
Describe HOCM murmur
Tricuspid region, increases with valsalva, systolic, doesn’t radiate, double or triple apex beat
Murmurs of tricuspid region
Tricuspid regurgitation, HOCM
Describe mitral stenosis
Mitral region, late diastolic, louder with expiration and left lateral position, associated with AF and pulmonary hypertension, narrow pulse pressure
Describe mitral regurgitation
Mitral region, louder with hand squeeze, pan systolic, louder with expiration and left lateral position, associated with AF, radiates to chest wall and axilla
Describe VSD
Mitral region, increased with hand squeeze, pansystolic, clubbed fingers and toes, radiates to back
Describe Mitral Valve Prolapse
Mitral region, mid systolic click with late systolic murmur
Mitral murmurs
Mitral stenosis, mitral regurgitation, VSD, mitral valve prolapse
Physiology of valsalva
Decreases preload and exacerbates HOCM and mitral valve prolapse
Physiology of hand squeeze
Increases afterload and exacerbates aortic regurgitation, mitral regurgitation, ventral septal defect
Regions of first hear sound
Mitral and tricuspid
Regions of second heart sound
Aortic and pulmonary
Causes of early systolic murmur
Acute severe mitral regurgitation
Causes of ejection systolic murmur
Aortic coarctation, aortic stenosis, flow murmur (anaemia, thyrotoxicosis), hypertrophic cardiomyopathy, pulmonary stenosis
Causes of late systolic murmur
Mitral valve prolapse
Causes of pan systolic
Mitral regurgitation, tricuspid regurgitation, ventricular septal defect
Cardiac findings for marfans
aortic regurgitation
Cardiac findings for turners syndrome
bicuspid aortic valve, coarctation (narrowing) of aorta; also short, square chest with webbed neck
Cardiac findings for down syndrome
atrioventricular septal defect, patent ductus arteriosus, tetralogy of fallot
Cardiac findings for ankylosing spondylitis
aortic regurgitation
Cardiac findings for Acromegaly
mitral and aortic regurgitation
If both young and cyanotic then consider
Eisenmenger Syndrome with atrial septal defect, ventricular septal defect, patent ductus arteriosus and aortopulmonary window
Causes of clubbing - cardiac / gastro / respiratory / other
cardiac: atrial myxoma, congenital cyanotic heart disease, infective endocarditis. gastro: coeliac, cirrhosis, IBD, lymphoma of GIT. respiratory: asbestosis, bronchial carcinoma, chronic suppurative lung disease (bronchiectasis, cystic fibrosis, empyema, abscess), idiopathic pulmonary fibrosis. other: hereditary, graves.
Causes of malor flush
Mitral and pulmonary stenosis
Carotid pulse - causes of slow rising, collapsing and alternans
Slow rising = aortic stenosis, Collapsing = aortic regurgitation, Alternans = left ventricular failure.
Apex beat - causes of pressure loaded, volume loaded, double impulse and tapping
Pressure (forceful and sustained) = aortic stenosis and hypertension, Volume (diffuse, displaced and non-sustained) = mitral regurgitation and dilated cardiomyopathy, Double impulse = HOCM, Tapping (palpable 1st heart sound) = mitral stenosis
Causes of S3
Early ventricular filling
Causes of S4
Atrial contraction against stiff ventricle
ECG findings for aortic stenosis
LVH (deep s in v2, tall r in v5) and LV strain (ST depression, TWI in 1, aVL and v5-6, left axis deviation)
CXR findings of aortic stenosis
LVH, calcified aortic stenosis
Markers to quantify severe aortic stenosis
valve area <1cm, gradient >40mmHg, velocity >4m/s
Aetiology of aortic stenosis
calcific, congenital bicuspid, rheumatic hear disease, systemic lupus erythematous, fabrys disease
Clinical findings of severe aortic stenosis
thrill, harsh murmur, prolonged murmur, split s2, s4, narrow pulse pressure, low volume late peaking pulse, left ventricular hypertrophy, left ventricular failure
ECG findings of aortic regurgitation
LVH (deep s in v2, tall r in v5)
CXR of aortic regurgitation
LV dilatation, aortic root dilatation
ECHO of aortic regurgitation
?stenosis, ?vegetations, aortic root pathology, increased left ventricular ejection fraction
Aetiology of aortic regurgitation - valvular vs aortic root
valvular = congenital, rheumatic heart disease, infective endocarditis, inflammatory rheumatologic disease, degeneration. aortic root = collagen disorders, aortitis (syphilis, vasculitis), dissection/aneurysms
Clinical findings of severe aortic regurgitation
Prolonged murmur, soft A2, s3, wide pulse pressure, water hammer pulse, left ventricular hypertrophy, left ventricular failure, austin flint murmurs
Management of chronic aortic regurgitation
Heart failure therapy (ACEi / ARB), MRA, B Blocker, diuretics, digoxin), balloon pump contraindicated, valve replacement if persistent symptoms, deteriorating ejection fraction and progressive left ventricular dilation
ECG of mitral stenosis
Afib, left atrial enlargement, right axis deviation, right ventricular hypertrophy (dominant tall R in v1, dominant deep s in v5/6)
CXR of mitral stenosis
Left atrial enlargement, mitral annular calcification
ECHO of mitral stenosis
Valve area <1cm is severe, posterior mitral valve leaflet maintains anterior during diastole)
Clinical signs of severe mitral stenosis
Early opening snap, narrow pulse pressure, diastolic thrill at apex, pulmonary hypertension
Clinical signs of pulmonary hypertension
prominent a wave, right ventricular heave, loud or palpable p2, pulmonary regurgitation, tricuspid regurgitation
ECG of mitral regurgitation
Afib, left atrial enlargement (p mitrale), LVH (deep s in v2, tall r in v5), left strain
CXR of mitral regurgitation
Cardiomegaly, left atrial enlargement, mitral annular calcification
ECHO of mitral regurgitation
prolapsed or thickened leaflets, decreased ejection fraction at late stage
Clinical signs of severe mitral regurgitation
early diastolic murmur, soft s1, early a2, s3, small volume pulse, pulmonary hypertension, left ventricular dilation, left ventricular failure
Aetiology of mitral regurgitation - structural vs functional
Structural = myxomatous (connective tissue degeneration), degeneration, rheumatic heart disease, papillary muscle dysfunction, infective endocarditis, connective tissue disease. Functional = LV dilation and LA dilation.
Commonest heart lesion
mitral valve prolapse
Mitral valve prolapse - murmur description / exacerbated by / ECHO findings
mid systolic click and late systolic murmur. Murmur prolonged by valsalva. prolapse of greater than 1cm into atrium.
ECG of tricuspid regurgitation
right acis deviation, right atrial enlargement (p pulmonale), right ventricular hypertrophy (dominant tall R in v1, dominant deep s in v5/6), right heart strain (ST changes and TWI in right precordial leads and inferior leads as well as right axis deviation, dominant R in V1, and dominant S in V5/6)
CXR of tricuspid regurgitation
Cardiomegaly, right ventricular enlargement (seen on lateral cxr)
Features of right ventricular failure
Right ventricular heave, hepatomegaly, ascites, lower limb oedema
Causes of Tricuspid Regurgitation - structural vs functional
Structural = myxomatous (tricuspid prolapse), degenerative, rheumatoid heart disease, infective endocarditis, connective tissue disease, trauma, congenital (ebsteins anomaly - septal and posterior leaflets displaced downward to apex). Functional = right ventricular dilation and pulmonary hypertension.
Pathophysiology of HOCM
obstruction of left ventricular blood flow
ECG of HOCM
LVH (deep s in v2, tall r in v5) and LV strain (ST depression, TWI in 1, aVL and v5-6, left axis deviation), deep Q waves inferiolaterally.
CXR of HOCM
LV enlargement
ECHO of HOCM
asymmetric septal hypertrophy, systolic anterior motion of the mitral valve, early aortic valve closure, prominent diastolic dysfunction
Exercise stress test and cardiac catheterisation of HOCM
Stress - induced outflow tract obstruction or ventricular arrhythmias. Cath - dynamic outflow tract obstruction
Epidemiology and aetiology of HOCM
Affects 1:1500 causing sudden death in young. Due to autosomal dominant mutations in sarcomeric proteins.
Management of HOCM
- Avoid diuretics, vasodilators and positive inotropes. 2. Aggressive management of tachyarrhythmias. 3. Negative inotropes and chronotropes. 4. Automatic implantable cardioverter defibrillator (required if ventricular arrhythmias, history of sudden cardiac death, unexplained syncope and LV ejection fraction less than 50%). 5. Surgical myomectomy or alcohol septal ablation.
ECG of pulmonary stenosis
R atrial enlargement (p pulmonale), right axis deviation, right ventricular hypertrophy (dominant tall R in v1, dominant deep s in v5/6)
CXR of pulmonary stenosis
right atrial enlargement, right ventricular hypertrophy on lateral
Clinical signs of severe pulmonary stenosis
late peak of systolic murmur, soft p2, s4, right ventricular failure, tricuspid regurgitation
Causes of pulmonary stenosis
Iatrogenic, congenital, carcinoid syndrome
ECG of pulmonary hypertension
R atrial enlargement (p pulmonale), right ventricular hypertrophy (dominant tall R in v1, dominant deep s in v5/6), right heart strain (ST changes and TWI in right precordial leads and inferior leads as well as right axis deviation, dominant R in V1, and dominant S in V5/6)
CXR of pulmonary hypertension
right sided cardiomegaly
ECHO of pulmonary hypertension
RA dilation, tricuspid regurg, pulmonary regurg, elevated right ventricle and pulmonary artery pressures
Diagnosis of pulmonary hypertension
right heart catheterisation with mean pulmonary pressure greater than 25mmHg
Management of pulmonary hypertension
- Medication: A. calcium channel blockers (nifedipine), B. endothelin receptor antagonists (bosentan), C. PDE 5-inhibitors (sildenafil), D. prostacyclin agonists (selexipag), E. guanylate cyclase inhibitors (riociguat). Also oxygen therapy, avoidance of pregnancy and heart lung transplant.
Aetiology of Pulmonary Hypertension
5 Groups. 1. primary pulmonary arterial hypertension (idiopathic, heritable), connective tissue disorders (scleroderma, RA, SLE, MCTD), HIV, congenital heart disease, drugs (chemotherapy, cocaine, meth). Group 2 (PCWP >15). left sided cardiac failure, elevated pulmonary capillary wedge pressure. Group 3. chronic hypoxic pulmonary disease (COPD, IPF). Group 4. chronic thromboembolic pulmonary hypertension. Group 5 - miscellaneous. sarcoidosis, chronic haemolytic anaemias, myeloproliferative disorders, glycogen storage disorders.
Symptoms of pulmonary hypertension
dyspnoea, chest pain, syncope
Clinical signs of congenital cyanotic heart disease
cyanosis, clubbing, pulmonary hypertension, right ventricular failure, dysmorphic features (down’s syndrome)
7 steps of management for cyanotic heart disease
- right heart catheterisation, 2. pulmonary hypertension medications, 3. oxygen therapy, 4. endocarditis prophylaxis, 5. avoidance of pregnancy, 6. do not close shunt if flow is right to left, 7. heart lung transplant
Tetrad of TOF
- pulmonary outflow tract obstruction. 2. overriding aorta. 3. VSD. 4. right ventricular hypertrophy
Post surgical complications of TOF
Pulmonary regurgitation (most common, needs replacement), endocarditis risk, right ventricular hypertrophy and failure, right ventricular and atrial arrhythmias, aortic root dilation with regurgitation
Endocrine investigations for systemic hypertension
TFT, parathyroid hormone, calcium, early morning cortisol, renin aldosterone ration, potassium, metanephrines/catacholamines
Pathophysiology of eisenmenger syndrome
Congenital pulmonary hypertension with left to right shunt, with associated cyanosis
ECG of eisenmenger
RBBB, right ventricular hypertrophy (dominant tall R in v1, dominant deep s in v5/6), right heart strain (ST changes and TWI in right precordial leads and inferior leads as well as right axis deviation, dominant R in V1, and dominant S in V5/6)
Management of eisenmenger
right heart catheterisation, pulmonary hypertension medications, oxygen therapy, endocarditis prophylaxis, avoidance of pregnancy, heart lung transplant
Complications of infective endocarditis
CCF, arrhythmia, valvular disease
Typical organisms for infective endocarditis
staph aureus, viridians strep, strep bovis, community acquired enterococcus, HACEK
Management of infective endocarditis
Current antibiotics, duration of treatment, PICC. Need for surgery if: moderate to sever heart failure, prosthetic valve involvement, uncontrolled infection, aortic root abscess, resistant organism, 1st degree heart block
Investigations for infective endocarditis
TOE, blood culture, ECG
Risk factors for infective endocarditis
IVDU, prosthetic valves, rheumatic heart disease, previous IE, immunosuppressants (transplant, chemotherapy)
Duke Criteria
2major, 1major and 3minor or 5minor. Major: persistently positive blood culture, ECHO demonstrate vegetation/abscess, new valvular regurgitation, Coxiella burnetii infection. Minor: predisposition heart condition or IVDU, fever, vascular = emboli or immuno (osler nodes, roths spots), positive blood culture which doesn’t meet criteria
Complications for IHD
CCF, arrhythmia, valvular disease, PVD
Management of IHD
Farmington Assessment Tool - cardiovascular risk. Adjust risk factors (diabetes HbA1c <6.5, HTN <130, smoking/EtOH cessation, regular exercise, weight loss, low salt/fat diet, total cholesterol <4, LDL <1.8, HDL <1.0, TG <1.7). Cardiac rehab. Long term drug MI treatment (anti-platelet, beta blocker, ACEi, statin). Previous treatment (stent vs meds). Cardiothoracic referral if >50% stenosis of left main, >70% of proximal LAD, triple vessel disease, 2 vessel disease with diabetes.
Investigations of IHD
CAG, ECG, stress testing, ECHO, MPS
IHD examination
cardio, fluid assessment, BMI, diabetes, stroke
Medical management of heart transplant
ciclosporin, diltiazem (reduce dose of ciclosporin), MMF/tacrolimus
Heart transplant investigations
last endometrial biopsy, angiogram, ECHO, also investigate for complications of immunosuppressants (inc. CMV load)
Presentation for heart transplant
Heart failure secondary to cardiomyopathy, rheumatoid heart disease, congenital heart disease. Requirement of inotropes or admission. Chest pain secondary to MI/pericarditis, acute CCF, ecg changes. Signs of previous rejection or surgery. Complications of immunosuppression.
When is a cardiac defibrillator required
if EF <35%, class 2 or 3, on optimal meds for 3 months, 40/7 since CABG or MI
Management of CCF
treat underlying condition, fluid + salt restriction with daily wt, optimise risk factors, medications (ACEi, beta blocker, spironolactone, diuretics), consider CRT-D if LBBB (QRS>120) and meds optimised, screening family if HOCM (autosomal dominant)
Investigations for CCF
CXR, BNP, ECHO, stress test, cardiac MRI
Risk factors for CCF
Ischaemic cardiomyopathy = hypertension, lipids, diabetes, smoking, obesity. Concurrent cardiac factors = MI, AF. Other causes = alcohol, congenital (HOCM), viral, amyloid, haemochromatosis.
Classes of New York Heart Association
Class 1 no symptoms. Class 2 strenuous activity. Class 3 limiting daily activities. Class 4 rest.
Indications for ICD
- CCF with LBBB (QRS > 120) w CRT. 2. VF/VT without acute MI. 3. VF/VT beyond medical management. 4. Symptomatic long QT sydrome.
Complications of AF
stroke, cardiomyopathy
Parts of CHADSVAS and HASBLED
CHF / HPT / AGE 75 / DM / Stroke / Vasc Disease / AGE 65 / Sex. HPT / Abnormal Renal or Liver / Stroke / Bleeding / Labile INR / Elderly >65 / Drugs + EtOH.
Management for AF
anticoag (CHADSVAS), anti-arrhythmic, DCCV, EPS
Management of SVT
adenosine, Valsalva
Management of bradycardia
PPM
Management of VF/VT
Defibrillator
Indications for PPM
Complete heart blocker with failure, type 2 second degree block, symptomatic sinus bradycardia, pauses over 3 seconds
Investigations for arrhythmias
ECG, holter, EPS, ECHO, MRI - amyloid
Risk factors for arrhythmias
drugs/alcohol, IHD, valvular disease (MS in AF), hypertension, thyroid, obesity, OSA, family history of sudden cardiac death (prolonged QT, Brugada)
Complications of hypertension
end organ damage - MI/stroke/LVF/PVD/CKD/retinopathy
Management of hypertension
Non-pharmacological = wt. loss, exercise, cease EtOH/smoking, reduce salt. Pharmacological = CCB, ACEi, thiazide - target < 120 if cardiac/diabetes/renal or <130 if general or <140 if elderly.
Investigations for hypertension
UEC, proteinuria, ECG, ECHO. Secondary causes = endocrine (conn’s, cushings, hyperthyroid, parathyroid, acromegaly), renal (CKD, renal artery stenosis), cardiopulmonary (OSA, aortic coarctation), drugs (NSAIDs, caffeine, amphetamines, steroids, CNI (tacrolimus/ciclosporin))
Risk factors for hypertension
obese, low exercise, alcohol, drugs
Risk factors for postural hypertension
BP/parkinson’s meds, diabetes, addisons, dialysis, amyloid, parkinson’s plus, shock
