Cardiology Flashcards
Secondary prevention MI
DAPT: aspirin + ticagreolor for 12 months if ACS, choice of ticagrelor or prasugrel if PCI, ACEi, BB, statin
Orthostatic hypotension tx
Fludrocortisone and midodrine
NSTEMI
: mx, mortality risk.
Aspirin, fondaparinux if no immediate PCI
Mortality risk: GRACE- age, ECG, troponin, renal function, CA, BP, HR
If <3%, ticagrelor. Otherwise, PCI, give prasugrel/ticag
Chronic HF Mx
1st line: ACEi/BB(Bisoprolol, Carvedilol)
2nd line Aldosterone antagonist(Spironolactone, Eplerenone)-monitor K as ACEi and spiro cause high K. Also, SGLT2 inhibitors- dapagliflozin, empagliflozin- increase urinary glucose excretion
3rd line: involve a specialist for
-Ivabradine(SR, HR>75+ EF<35%)
-Sacubitril-valsartan( EF <35%+ Symptoms despite ACEi/ARB)
-Digoxin( if coexistent AF)
- Hydralazine+Nitrate( in Afro-Caribbean)
-Cardiac resynchronization therapy( Widened QRS e.g. LBBB)
Acute mitral regurgitation cause + presentation
Infero-posterior infarction. Acute hypotension/plmonary oedema. Systolic murmur
Aortic stenosis features
Narrow pulse pressure
ejection systolic, louder on expiration
NSTEMI identified, aspirin given, 6-month mortality low (<3%)
Conservative management - give ticagrelor
Dresslers syndrome
2-6wks post MI, low grade fever, pleuritic CP, pericardial effusion, pericardial rub, raised ESR. Tx NSAIDs, sometimes steroids, pericardiocentesis if significant pericardial effusion to remove the fluid around the heart . (ECG global ST elevation, T wave inversion)
Aortic dissection features
Severe tearing CP, unequal BP in arms, false lumen on CT, widened mediastinum on CXR
a patient is noted to have a new early-to-mid systolic murmur 10 days after being admitted for a myocardial infarction
Ischaemia of the papillary muscle
Left ventricular free rupture presentation
sudden heart failure, raised JVP, pulsus parodoxus, recent MI
Mitral stenosis
mid-late diastolic, rumbling, malar flush, P mitrale on ECG -representing left atrial hypertrophy/strain
Aortic regurgitation
early diastolic, high pitched, blowing, collapsing pulse, Quinckes sign (nailbed), de mussets (head bobbing)
Beck’s triad
hypotension, raised JVP, muffled HS, electrical alternans on ecg: ACUTE CARDIAC TAMPONADE
Use of statin for primary prevention of CVD
20mg atorvastatin
-reduce cholesterol production in liver-inhibits HMG CoA reductase
-check lipids 3/12 after
-LFTs after 3/12 and at 12/12
-offered if QRISK>10%/ T1DM for 10 yrs/ CKD pts
Statin interaction with which abx
macrolides- clarithromycin, erythromycin
pericarditis ix
raised inflammatory markers
ECG: Widespread concave/saddle shaped ST elevation, PR depression (most specific marker)
Mx acute pericarditis
Mx: admit if fever>38/high troponin. NSAIDs + colchicine.
signs o/e acute HF
Raised respiratory rate
Reduced oxygen saturations
Tachycardia (fast heart rate)
3rd heart sound
Bilateral basal crackles (sounding “wet”) on auscultation of the lungs
Hypotension in severe cases (cardiogenic shock)
R HF
1) Raised jugular venous pressure (JVP), caused by a backlog on the right side of the heart, leading to an engorged internal jugular vein in the neck
2) Peripheral oedema of the ankles, legs and sacrum
acute LVF presentation
acute SoB (improves sitting up) , frothy sputum, looks unwell, type 1 RF (low O2, normal CO2)
causes of high BNP
HF, renal impairment, PE, tachycardia/sepsis, COPD
effects of LVF on the lungs
In the lungs LV failure will lead to dilatation of pulmonary vessels, leakage of fluid into the interstitium and the pleural space and finally into the alveoli resulting in pulmonary edema.
risk factors for infective endocarditis
Intravenous drug use
Structural heart pathology (see below)
Chronic kidney disease (particularly on dialysis)
Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
History of infective endocarditis
Structural pathology- valvular heart disease, congenital HD, hypertrophic cardiomyopathy, prosthetic valves, implantable cardiac devices
