Cardiology Flashcards
Definition of Pericarditis
Inflammation of Pericardium
Causes of Pericarditis
Idiopathic (most cases)
Infection - viral, bacterial, fungal or TB
Post MI - acute or late (Dressler’s syndrome)
Malignancy
Auto-immune
Drug induced
Post-surgical
Clinical features of Pericarditis
Chest pain - pleuritic, worse on movement, relieved by leaning forwards
Pericardial rub
Pericardial effusion
Investigations - Pericarditis
ECG - saddle shaped ST elevations
CXR - normal (effusion - pear shaped heart)
Bloods - FBC, U&Es, ESR, CRP, cardiac enzymes (normal usually)
Echocardiogram
Treatment of Pericarditis
Analgesia (e.g Ibuprofen 400mg/8h withfood). Treatment of the cause is indicated.
Consider Colchicine if relapsing or continuing symptoms or occur
Presentation of Pericardial Effusion
• Signs on examination:
○ Heart sounds soft & distant
○ Apex beat commonly obscured
○ Friction rub
• As the effusion worsens, signs of cardiac tamponade may become evident:
○ raised JVP with sharp x descent
○ Kussmaul’s sign (rise in JVP/increased neck vein distension during inspiration)
○ pulsus paradoxus (an exaggeration in the normal variation in pulse pressure seen with inspiration, such that there is a drop in systolic blood pressure of ≥10 mmHg)
reduced cardiac output.
Complications of Pericarditis
Pericardial effusion
Cardiac Tamponade
Cardiac arrhythmias
Risk factors for infective endocarditis
Infective organism in bloodstream - poor dental hygiene, IVDU, recent invasive procedures
Damaged endocardium - heart condition VSD/ASD, bicuspid valves
Clinical presentation of IE
Fever New murmur - tends to be regurgitative Malaise/lethargy Anorexia, weight loss Cardiac sx; SOB, chest pain, palpitations
Clinical signs of IE on examination
Cardiac murmur (85%): pansystolic murmur of mitral regurgitation or early diastolic murmur of aortic regurgitation classical
Features of heart failure: raised JVP, bilateral crackles on respiratory auscultation
Splinter haemorrhages: thin, red to reddish-brown lines of blood under the nails (microemboli)
Petechiae (20-40%): skin and mucous membranes (microemboli and immune complex deposition)
Janeway lesions: nontender erythematous macules on the palms and soles (microabscesses). Acute > subacute.
Osler nodes: tender subcutaneous violaceous nodules mostly on the pads of the fingers and toes (immune complex deposition). Subacute > acute.
Roth spots: exudative, oedematous hemorrhagic lesions of the retina with pale centre (immune complex deposition). Subacute > acute.
Splenomegaly: splenic abscess formation
Investigations for IE
Bloods inc FBC, WCC, ESR, CRP
Blood cultures - multiple
Echo
Dukes Criteria
Infective endocarditis
Definitive - 2 major or 1 major + 3 minor or 5 minor
Possible - 1 major + 1 minor or 3 minor
Major criteria - blood cultures micro suspicious, valvular evidence on echo/murmur
Minor - IVDU or known predisposing heart condition, fever >38, vascular features, immuno evidence, micro on blood cultures
Treatment of IE
Medical - prolonged targeted antibiotic therapy
Surgery - removal of infective tissue, VR
Types of MI
Type 1 - due to spontaneous atherosclerotic rupture in coronary artery
Type 2 - reduced oxygen supply or increased demand (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with PCI / coronary stunting / CABG
Differentials for ACS
• Cardiac - aortic dissection, angina, CA spasm, pericarditis
• Respiratory - infection, pleuritic chest pain, PE, pneumothorax
• GI - gastritis, reflux, PUD
Other - rib fracture, costochondritis
Investigations in ACS
• Initial A to E survey • Bloods - routine screen & cardiac troponins ○ FBC (Hb - anaemia) ○ U&Es (before ACEI) ○ LFTs (before statins) • ECG - looking for signs of ACS ○ ST depression or T wave inversion in US/NSTEMI ○ ST elevation in STEM Echo/coronary angiogram
Initial Management for MI
MONA - morphine, oxygen, nitrates & aspirin
Acute treatment for NSTEMI
BATMAN
beta blockers, aspirin, ticagrelor (180mg stat dose), morphine, anticoagulation (LWMH) & nitrates
Secondary prevention after MI
(6As)
Aspirin
Another anti platelet agent - clopidogrel
Atorvastatin
ACEI - Ramipril
Atenolol or another beta blocker
Aldosterone antagonist for those with HF e.g. eplerenone titrated to 50mg once daily
Management of STEMI
Primary PCI
Thrombolysis - streptokinase, alteplase and tenecteplase
Heart Failure - aetiology
• Valvular ○ Stenosis/Regurgitation • Vascular ○ Ischaemic Heart Disease ○ Hypertension • Muscular ○ Dilated or hypertrophic cardiomyopathy ○ Congenital heart disease • Electrical - Arrhythmias
Clinical features of HF
LHF - dyspnoea, orthopnoea, PND, fatigue, pleural effusions, cyanosis
RHF - peripheral oedema, ascites, hepatosplenomegaly, raised JVP
Investigations for HF
• Bedside: ECG, consider peak flow/spiro (causes of SOB)
• Bloods; routine (r/o other causes), cardiac enzymes, NT-proBNP
○ If BNP <400 ng/L - HF unlikely
○ If BNP 400-2000 ng/L - refer routinely (6 weeks)
○ If BNP >2000 ng/L - refer urgently
• Transthoracic echocardiogram - done in specialist centre
Checks for any valve abnormalities
Signs on examination for HF
• Hands; peripheral cyanosis
• Neck/Face; raised JVP
• Chest; displaced apex beat, creps, S3/4, crackles or pulmonary oedema
Body; peripheral oedema
Management of HF
• If symptomatic or retaining fluid - offer diuretics (symptomatic relief)
• Options (ABAL):
○ ACEI, Beta blockers, aldosterone antagonists & loop diuretics
• First line: ACEI + Beta blocker
○ ARB if not tolerated, hydralazine/nitrates if not ARB not tolerated
• 2nd line: + MRA (spironolactone)
3rd line: Replace ACEI with Sacubitril valsartan (specialist)
Stages of Hypertension
Stage 1 - >140/90
Stage 2 - >160/100
Stage 3 - >180/120
Causes of Hypertension
ROPEC Renal - renal artery stenosis, PKD, CKD Obesity Pregnancy Endocrine - hyperthyroid, Cushing's, Theo Cardiac - coarctation Drugs - sympathomimetics, steroids & OCP
Clinical features of Hypertension
Often asymptomatic; found on health checks or incidentally
Symptoms: headaches, visual disturbances, dizziness, syncope, epistaxis, angina
Investigations & Diagnosis of Hypertension
• Diagnosis - home BP monitoring or 3 clinic readings = diagnosis if average >135/85 (home) or >140/80 (clinic)
• Investigations - screening for end organ damage & r/o 2o causes
• Other investigations: HbA1c, lipids
In patients <35yrs consider 2o causes
• End organ damage checks: ○ Eyes - examine for papilledema ○ Kidneys - U&Es, urine dip, ACR ○ Cardiac - ECG to check for LV hypertrophy Stroke risk
Management of Hypertension
Options (ACD):
ACEI e.g. ramipril; inhibit conversion of angiotensin I to angiotensin II
Calcium Channel Blockers (CCB) e.g. amlodipine; block smooth muscle contraction of BV
Diuretics (thiazide-like) e.g. indapamide; inhibit Na/Cl co-transporter in DCT, prevents reabsorption of Na & water
Who & What:
Age <55yrs or any T2DM - ACEI (or ARB e.g. losartan if not tolerated)
Age >55yrs or black-afrocaribbean - CCB (or diuretic if not tolerated)
Aortic Stenosis - Causes
Degeneration & Calcification of valve - occurs in elderly patients Calcification of bicuspid aortic valve - occurs in middle age
Rheumatic fever
Aortic Stenosis - clinical features
- Often asymptomatic, only presents in severe disease when valve has been reduced to 1/3 of original size
- P/W: angina, dyspnoea, exertional syncope or dizziness, sx of heart failure
On examination:
• Harsh ejection systolic murmur, radiates to carotids
• Apex beat - undisplaced but may be thrusting
Investigations - Aortic Stenosis
ECG - signs of LV hypertrophy (left axis deviation)
CXR - normal heart size but may show dilatation of ascending aorta above stenosis & calcification of valve
Echocardiogram - diagnostic, visualises changes in valve & assessing LV function
Cardiac angiogram - allows differentiation of other causes of angina & assesses for concomitant CAD
Management of aortic stenosis
Surgical - valve replacement is recommended unless contraindicated, if unfit can have TAVI (balloon dilatation)
Medical - manage LV failure
Heart Block - Subtypes, Symptoms & Management
1st degree - CONSTANT prolonged PR interval >200ms, tends to be asymptomatic with no intervention needed
2nd degree Mobitz Type I - increasing prolonged PR interval followed by dropped QRS, tends to be asymptomatic with no intervention needed, stop AVN blocking drugs e.g. beta blockers
2nd degree Mobitz Type II - constant normal PR interval with occasional dropped QRS (Typically occurs with every 3 or 4 atrial beat (3:1, 4:1)), always pathological, sx inc syncope palpitations, management: Monitor & reverse any causes if possible, if not pacemaker, stop AV blocking drugs e.g. beta blockers
3rd degree - complete heart block, no electrical association between P waves & QRS, Symptoms inc chest pain, SOB, palpitations, syncope, pacemaker & temporary pacing needed
Mitral Regurgitation - Definition & Pathophysiology
Incompetence of mitral valve leading to backflow of blood into LA
Pressures/blood flows back into lungs & R side of heart, leads to S&S of heart failure
Mitral Regurgitation - S&S
Pulmonary Oedema Dyspnoea Fatigue Orthopnoea Palpitations MURMUR - high pitched systolic murmur, heard best at the Apex, which is displaced laterally, radiates to Axilla
Management of Mitral Regurgitation
If no symptoms - conservative, serial echos as follow up
OR
Surgery - replace/repair
Mitral Stenosis - pathophysiology
Left atrial enlargement occurs in the presence of chronically elevated atrial pressures predisposing patients to both atrial fibrillation and atrial thrombosis. Raised atrial pressures translate to raised pulmonary venous pressures and pulmonary hypertension which can eventually lead to right sided heart failure.
Mitral stenosis - causes
Rheumatic Heart Disease - MOST COMMON Rarer: Congenital MS Mitral annular calcification Radiation associated MS Carcinoid associated valve disease Fabry's disease
Mitral Stenosis - Clinical Features
Symptoms
Breathlessness
Haemoptysis
Chest pain
Signs Mid-diastolic murmur Atrial fibrillation Mitral facies (malar flush) Pulmonary hypertension: Right ventricular heave Prominent a-wave Right heart failure: Raised JVP Peripheral oedema Hepatomegaly
