Cardiology Flashcards

1
Q

Definition of Pericarditis

A

Inflammation of Pericardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Causes of Pericarditis

A

Idiopathic (most cases)
Infection - viral, bacterial, fungal or TB
Post MI - acute or late (Dressler’s syndrome)
Malignancy
Auto-immune
Drug induced
Post-surgical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical features of Pericarditis

A

Chest pain - pleuritic, worse on movement, relieved by leaning forwards
Pericardial rub
Pericardial effusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Investigations - Pericarditis

A

ECG - saddle shaped ST elevations
CXR - normal (effusion - pear shaped heart)
Bloods - FBC, U&Es, ESR, CRP, cardiac enzymes (normal usually)
Echocardiogram

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Treatment of Pericarditis

A

Analgesia (e.g Ibuprofen 400mg/8h withfood). Treatment of the cause is indicated.
Consider Colchicine if relapsing or continuing symptoms or occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Presentation of Pericardial Effusion

A

• 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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Complications of Pericarditis

A

Pericardial effusion
Cardiac Tamponade
Cardiac arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Risk factors for infective endocarditis

A

Infective organism in bloodstream - poor dental hygiene, IVDU, recent invasive procedures
Damaged endocardium - heart condition VSD/ASD, bicuspid valves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Clinical presentation of IE

A
Fever
New murmur - tends to be regurgitative
Malaise/lethargy
Anorexia, weight loss
Cardiac sx; SOB, chest pain, palpitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Clinical signs of IE on examination

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Investigations for IE

A

Bloods inc FBC, WCC, ESR, CRP
Blood cultures - multiple
Echo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Dukes Criteria

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Treatment of IE

A

Medical - prolonged targeted antibiotic therapy

Surgery - removal of infective tissue, VR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Types of MI

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Differentials for ACS

A

• Cardiac - aortic dissection, angina, CA spasm, pericarditis
• Respiratory - infection, pleuritic chest pain, PE, pneumothorax
• GI - gastritis, reflux, PUD
Other - rib fracture, costochondritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Investigations in ACS

A
• 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Initial Management for MI

A

MONA - morphine, oxygen, nitrates & aspirin

18
Q

Acute treatment for NSTEMI

A

BATMAN

beta blockers, aspirin, ticagrelor (180mg stat dose), morphine, anticoagulation (LWMH) & nitrates

19
Q

Secondary prevention after MI

A

(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

20
Q

Management of STEMI

A

Primary PCI

Thrombolysis - streptokinase, alteplase and tenecteplase

21
Q

Heart Failure - aetiology

A
• Valvular 
		○ Stenosis/Regurgitation
	• Vascular 
		○ Ischaemic Heart Disease
		○ Hypertension
	• Muscular 
		○ Dilated or hypertrophic cardiomyopathy
		○ Congenital heart disease
	• Electrical - Arrhythmias
22
Q

Clinical features of HF

A

LHF - dyspnoea, orthopnoea, PND, fatigue, pleural effusions, cyanosis
RHF - peripheral oedema, ascites, hepatosplenomegaly, raised JVP

23
Q

Investigations for HF

A

• 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

24
Q

Signs on examination for HF

A

• Hands; peripheral cyanosis
• Neck/Face; raised JVP
• Chest; displaced apex beat, creps, S3/4, crackles or pulmonary oedema
Body; peripheral oedema

25
Q

Management of HF

A

• 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)

26
Q

Stages of Hypertension

A

Stage 1 - >140/90
Stage 2 - >160/100
Stage 3 - >180/120

27
Q

Causes of Hypertension

A
ROPEC
Renal - renal artery stenosis, PKD, CKD
Obesity
Pregnancy 
Endocrine - hyperthyroid, Cushing's, Theo
Cardiac - coarctation 
Drugs - sympathomimetics, steroids & OCP
28
Q

Clinical features of Hypertension

A

Often asymptomatic; found on health checks or incidentally

Symptoms: headaches, visual disturbances, dizziness, syncope, epistaxis, angina

29
Q

Investigations & Diagnosis of Hypertension

A

• 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
30
Q

Management of Hypertension

A

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)

31
Q

Aortic Stenosis - Causes

A

Degeneration & Calcification of valve - occurs in elderly patients Calcification of bicuspid aortic valve - occurs in middle age
Rheumatic fever

32
Q

Aortic Stenosis - clinical features

A
  • 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

33
Q

Investigations - Aortic Stenosis

A

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

34
Q

Management of aortic stenosis

A

Surgical - valve replacement is recommended unless contraindicated, if unfit can have TAVI (balloon dilatation)
Medical - manage LV failure

35
Q

Heart Block - Subtypes, Symptoms & Management

A

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

36
Q

Mitral Regurgitation - Definition & Pathophysiology

A

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

37
Q

Mitral Regurgitation - S&S

A
Pulmonary Oedema
Dyspnoea
Fatigue
Orthopnoea
Palpitations
MURMUR - high pitched systolic murmur, heard best at the Apex, which is displaced laterally, radiates to Axilla
38
Q

Management of Mitral Regurgitation

A

If no symptoms - conservative, serial echos as follow up
OR
Surgery - replace/repair

39
Q

Mitral Stenosis - pathophysiology

A

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.

40
Q

Mitral stenosis - causes

A
Rheumatic Heart Disease - MOST COMMON
Rarer: Congenital MS
Mitral annular calcification
Radiation associated MS
Carcinoid associated valve disease
Fabry's disease
41
Q

Mitral Stenosis - Clinical Features

A

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