Deck 1 Flashcards
Angina grading
Canadian cardiovascular society 1-4
1 is on strenuous, 2 is on mod exertion, 3 is on mild exertion and 4 is at rest
Angina causes
Reduced perfusion (atheroma, embolus, iflammation, hypotension, spasm, thrombosis), reduced oxygenation (anaemia, carboxyhaemoglobinaemia) or increased tissue demands (LVH)
CTCA
First choice in new onset angina pain. Looks at whole vessel, not just lumen (can adequately assess plaque burden)
Use in NICE probability 61-90%
CT-FFR
Computer modelling to assess functional impact (if <0.8 then haemodynamically significant)
Use in NICE probability 31-60%
Clinical diagnosis of angina
At NICE probability >90%
Looks at age and symptom type
Angina Tx
Address RF
GTN spray, BB (or rate limiting CCB)
Can add nicorandil for refractory disease (vasodilator)
Give statin and low dose aspirin
Surgery required if large area at risk (>10%) or left main stem, or 2-3 vessel disease.
CABG good for diffuse disease, reduced LV function, recurrent stent stenosis and in diabetes.
PCI good for 1 or 2 vessel, frailty, advanced age or varicose veins.
Acute MI
Can be regional (90%) or circumferential (10%)
See trop rise (if ECG change only then unstable angina)
If Trop rise + ST elevation/LBBB then STEMI (full thickness)
If trop rise and no ST elevation then NSTEMI (partial thickness)
RCA supplies
Type of MI
Which leads
RA, RV, posterior septum - often AVN and SAN
Gives posterior/inferior MI
Leads II, III, avF
LCA (main stem) MI
Massive anteriolateral MI
Seen on I, aVL, V1-V6
LAD supplies
Which leads
LV and anterior septum
V1-V4
Circumflex supplies?
Type of MI
Leads?
LA and LV
Lateral MI
I, aVL and V5/6
DDX for acute coronary syndrome
Coronary artery spasm, pericarditis/myocarditis, aortic dissection, PE, pneumothorax, oesophageal disease (worse on leaning forwards), mediastinitis, costochondritis, trauma
Troponin peak
24h
ECG MI progression
Tall T waves at 5 mins ST elevation at 30 minutes T wave inversion, Q waves (2h) ST segment normal (days) T wave may return to normal, Q wave remains (WEEKS)
ACS management
Morphine (5mg + antiemetic), GTN/IV nitrates (unless hypotensive), 300mg aspirin, oxygen if <94%
PCI within 90 minutes if STEMI
If NSTEMI then GRACE score
AMI complications
Short term:
Arrythmias, Pulmonary oedema (LVF), cardiogenic shock, thromboembolism, ventriculoseptal defect (due to intracardiac rupture), ruptured cordae tendinae (mitral valve incompetence), ventricular wall rupture (leads to haemopericadium, cardiac tamponade and death)
Long term: HF, dressler (immune mediated pericarditis wit raised ESR and myocardial antibodies), ventricular aneurysm formation (distended scar)
IE risks
Damaged endocardium (valve disease, prostetic valves, congenital disease), sustained bacteraemias (IVDU, infected intravascular device, untreated abscess/collection)
Vascular IE phenomenom
Splinter haemorrahage, janeway lesion
Immunological IE phenomenon
Osler node, Roth spot, glomerulonephritis (microscopic haematuria)
Native valve IE causes
Streptococcus viridans, Streptococcus mitis
S. aureus in IVDU
Prosthetic valve IE causes
coagulase negative staphylococcus (e.g. s epidermidis for first 2 month)
IE causes: - Bowel malignany -GI/GU disease If culture negative If non infectious
Streptococcus bovis in bowel malignancy
Enterococcus in GI/GU tract
Coxiella burnetii, bartonella, brucella, HACEK (haemophilus, actinobacilus, cardiobacterium, eikenella, kingella)
Non infectious cause is libman sacks lesions (SLE)
IE investigations
Echo (ideally TOE)
FBC, CRP, ESR, BCx3, Urinalysis, ECG, CXR
Dukes IE criteria
Major is: atypical organism on 2 separate BCs, echo findings or new valvular regurgitation (worsening of existing not enough)
Minor is predisposition, pyrexia, vascular phenomena, immunological phenomena, positive BC
Can diagnose if 2 major 1 minor, 1 major 3 minor or 5 minor
IE complications and managment
HF (sudden onset valve disease), perivascular abscess (aotic root abscess), septic emboli (stroke, discitis, splenic/renal infatct), metastatic abscess (lung) and mycotic aneurysm.
Manage with ABx, may need surgical involvement for valves or abscess. Prophylaxis is not routine.
Aortic stenosis Causes Features O/E O/I Management
Most common valvular disease.
Bicuspid valve, rheumatic fever, age related calcification.
Angina, arrythmias from remodelling, exertional syncope and LVF
O/E: small volume, slow rising, narrow pulse, chest wall heave, crescendo/decrescendo EJ murmur (?carotid radiation). Accentuate by sitting forward on expiration.
ECG shows LVH/arrythmia, cXR cardiomegaly, echo shows thickened valves/calcifications, cardiac catheterisation shows pressure gradient across valve
Management: balloon valvuloplasty or valve replacement
Aortic regurgitation Causes Features O/E O/I Management
HTN, aortic dissection tracking back, CT disorder, IE, Rh fever, bicuspid valve
SOB, fatigue, palpitations, angina
O/E: wide pulse volume, collapsing pulse, displaced apex, early diastolic (decrescendo) murmur. Quinke’s sign (nail bed pulse), De Musset’s sign (nod with heart beat), Duroziez’s sign (murmur on femoral with distal pressure)
O/I: ECG (LV hypertrophy), Echo (regurgitation), cardiac catheter shows wide pressure
Needs valve replacement as progresses to heart failure
Mitral stenosis causes
Features
O/E
O/I
Rheumatic fever (mainly), but congenital, degenerative and SLE
SOB, fatigue, AF, haemoptysis (pul. backflow)
Malar flush, small volume pulse, left parasternal heave (RVH), mid diastolic murmur at apex (rad lat), JVP distension, AF
ECG, CXR, Echo, cardiac catheter
Haemodynamic support, diuretic, PBV
Mitral regurgitation Causes Features o/e O/I Management
left ventricular dilatation, cardiomyopathy, degeneration, infection Rh, IE, CT disoders, autoimmune
SOB, fatigue, oedema, syncope,
AF (less common than MS), parasternal heay, PS murmur, displaced apex
ECG, CXR, echo, cardiac catheter
Haemodynamic support, ACEi, BB, surgical valve replacement
Infected valves
Tend to be mitral, bu IVDU tricuspid
Tricuspid/pulmonary mutmur
TS: mid diastolic murmur with RHF signs
TR: PS murmur and RHF signs (cor pulmonale)
PS: ES murmur, RV heave, RHF
PR: diastolic murmur, often asymptomatic
Valve replacement
Tissue replaced 10-15 years, but decreased clot risk (anticoag in weeks - months post surgery, but needs immunosuppression)
Mechanical last longer, but need lifelong anticoag.
If older, clot risk, or high bleed risk on warfarin/can’t take warfarin/limited life expectancy then tissue
Warfarin INRs
2-3 in AF
3-4 in mechanical heart valve
HF causes
IHD (most common), dilated cardiomyopathy, HTN, valvular, congenital, cor pulmonale, alcohol, drugs
EF HF classes
40-70% normal
40-50 is borderline
<40 is systolic HF
<35% is severe
HFrEF
Generally ischaemic heart disease, HTN, dilated cardiomyopathy, myocarditis. Systolic dysfunction, reduced EF
HEpEF
Insuffiicient filling of ventricle, reduced compliance.
Generally age, HTN, left ventricular hypertophy, restrictive cardiomyopathy, hypertrophic cardiomyopathy, fibrosis, amyloidosis, sarcoidosis, constrictive pericarditis, haemochromatosis, aging
left sided HF
Fatigue, restlessness, confusion, orthopnoea, tachycardia, exertional dyspnoea, paroxysmal noctural dyspnoea, elevated pulmonary capillary wedge pressure - can track back to give pulmonary HTN (cough, crackles, wheeze, blood tinged sputum, tachypnoea)
Can get crackles, gallop rhythm (3rd heart sound), displaced apex
RHF causes and signs
Can be via lung problem.
Fatigue, increased peripheral venous pressure, ascites, hepatosplenomegaly, JVP distention, anorexia, GI distress, weight gain, oedema
HF class
NYHA
1 is no limitations, 2 is slight, 3 is comfortable at rest but sig on activity, 4 is symptoms at rest
Pulmonary Oedema
Fluid in alveolar wall
Most common cause is LVF with backpressure (red cell leaks digested by macrophages - heart failure cells)
Generally increased capillary pressure (heart failure/fluid overload/pulmonary venous obstruction), can be increased capillary permeability (ARDS, infection, sepsis, DIC, inhaled toxin, protein loss, lymphatic obstruction (tumour)
Causes dyspnoea, paroxysmal noctural dyspnoea, orthopnoea. May get cheyne stokes on acute
CXR : batwing oedema, kerley B lines, upper vessel enlargement
HF management
In acute, sit patient up, give high flow oxygen and IV diuretics (consider IB nitrates, opiates, CPAP, ianotropic support, dervice therapy, assist device, transplant)
Cardiac resynch can be useful
In chronic: diuretic (symptom), ACEi (or ARB) + BB (not in acute decompensation or with asthma). Can add on others.
Digoxin in refractory HF.
Atheroma
Fatty streak (due to initial insult allowing LDL deposits)
Lipid plaque (damages media)
Fibrolipid plauqe
Complicated atheroma
Cardiac marker timeline
Initial rise is CK-MB, then myoglobin, then troponin. Peaks at 24h then has second peak at 4 days
ACS types1
Angina is demand ischaemia (no infarct)
Unstable angina is rupture of unstable plaque (ischaemia, no infarct - can get ECG change)
NSTEMI is plaque rupture. Top rise +/- ECG change
STEMI is trop and ST elevation
Histological infarct timeline
0-12h has limited evidence
12-24h has necrotic fibres and oedema
24-72h has acute inflammation (pale macroscopically)
3-14 days is macrophage removal and granulation occurs
14-21 days is fibrous granulation tissue
21-56 is scaring
MI sequalae
PE (thrombus in heard), stroke, arrythmia, cardiac tamponade, valvular problem, haemopericardium (myocardial rupture), fibrinous pericardium
Aortic dissection RF
CT disorder, vascular inflammation (inc. giant cell arteritis), trauma, surgery, HTN, age, smoking atheromas
Aortic dissection classes
De Bakey 1 is intimal tear on ascending that continues to descending
De bakey 2 is ascending only
De bakey 3 is descending only
Standard A is 1 and 2, B is 3
Dissection sequalae
Can occlude branches, can track back along and cause abscesses, valvular problems and haemopericardium
Can compress nearby structures
Can rupture into the vessel, or around the vessel
Left ventricle on CXR?
Not visible
Causes of hemidiaphragn elevation on CXR
Can be loss of lung volume pulling it up.
Also applies to hila
Can also be ipsilateral phrenic nerve palsy (malignancy invading/compressing nerve or C3, C4, C5 root.
Carina >90 on CXR
Atrial enlargement
Peaked P waves
RAH
Notched/broad P waves
LAH
PR interval
Start of P to start of QRS
AVN delay
3-5 squares
Longer is 1dHB
Increases then drops is wenckebach/mobitz 1
Intermittent drpo then mobitz 2 (pacing needed)
If p and QRS have no relationship then 3rd degree
QRS>120
ventricular origin or BBB
RV hypertrophy
R and S transition point (R and S equal) shifts from V3/4 to V5/6
LVHypertrophy
R in V5, or S depth in V1 and V5 <25mm
ST elevation
If all leads then ?pericarditis
>2mm chest
>1mm limb
ST depression
Ischaemia/digoxin
T wave inversion
aVR, III, V1/V2 (? V3 in black people)
Otherwise, ischaemia, ventricular hypertrophy, BBB, digoxin
Q waves are normal in
I, aVL, V5/V6
Can indicate old infarction elsewhere
Prolonged QT
Start of QRS to end of T
Should be <0.45s (2 large squares)
Can lead to VT
RBBB
M shape in V1
W in V6 with deep S
Consider underlying ASD/PE
LBBB
W in V1, M in V6. No further interpretation
If asymptomatic then ?aortic stenosis
If chest pain then ? MI
RAD
Can indicate PE
LAD
Can indicate conduction defect
aVR, V1, V2
Look at right ventricle
aVL, I
Left surface
V5/V6
Left ventricle
V3/V4
Septum
II, III and aVF
Inferior surface
WPW
Short PR interval
Slurred upstroke delta
RAD
Can cause paroxysmal tachycardia (re-entry circuit with no tachycardia)
Hypocalcaemia on ECG
Prolonged QT
Hypercalcaemia on ECG
QT shortening
Atrial flutter
> 250, no baseline between p waves. Tx as pre AF
AF causes
HTN, valvular heart disease, HF, IHD, chest infection, PE lung cancer, alcohol excess, thyrotoxicosis, electrolyte depletion, infection, DM
Tx with BB or rate limiting CCB. May use cardioversion if unstable
CHAD2DS2VASC
Assess stroke risk. Intervene is 1+ in men, 2+ in women
Ventricular tachycardia
Wide QRS in all leads. Can become VF so tx urgently (cardioversion if <90 systolic, chest pain, HF or rate >150. Otherwise amiodarone).
