Cardiovascular Flashcards by Ehsen Mahmood

Make a not on NT-proBNP for heart failure

This is a hormone produced mainly by the left ventricule in response to strain)
Refer people with suspected heart failure and an NT‑proBNP level** >2,000** ng/litre (236 pmol/litre) urgently, to have specialist assessment and transthoracic echocardiogram within 2 weeks
Refer people with suspected heart failure and an NT‑proBNP level between 400 and 2,000 ng/litre (47 to 236 pmol/litre) to have specialist assessment and transthoracic echocardiogram within 6 weeks

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What is the management for chronic heart failure?

First line: an angiotensin-converting enzyme (ACE) inhibitor and a beta‑blocker
Second line: mineralocorticoid receptor antagonist - spironolactone
…
Specialist treatment:
- Ivabradine
Ivabradine should only be initiated after a stabilisation period of 4 weeks on optimised standard therapy with ACE inhibitors, beta‑blockers and aldosterone antagonists.
- Replace the ACEI with sacubitril valsartan if EF <35%
- Hydralazine in combination with nitrate
- Digoxin - used when there is co-existent AF
* Loop diuretics such as furosemide and bumetanide are used for symptomatic relief
* SGLT-2 inhibitors, such as dapagliflozin and empagliflozin
- Can be used in the management of heart failure with a reduced ejection fraction

All heart failure patients should be offered an annual influenza vaccine and a one-off pneumococcal vaccine

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Management of hypertension

If <55 years or type 2 diabetes
Step 1: ACE-inhibitor or angiotensin 2 receptor blocker
Step 2: ACE-inhibitor or angiotensin 2 receptor blocker + calcium-channel blocker OR ACE-inhibitor or angiotensin 2 receptor blocker + thiazide-like diuretic
Step 3: ACE-inhibitor or angiotensin 2 receptor blocker + calcium-channel blocker + thiazide-like diuretic
Step 4:
· If K ≤ 4.5 mmol/L add low-dose spironolactone
· If K > 4.5 mmol/L add an alpha or beta blocker
· If still not controlled, to refer to specialist
If ≥ 55 years and no type 2 diabetes or african-caribbean ethnicity
Step 1: calcium-channel blocker
Step 2: calcium-channel blocker + ACE-inhibitor or angiotensin 2 receptor blocker OR calcium-channel blocker + thiazide-like diuretic
Step 3: ACE-inhibitor or angiotensin 2 receptor blocker + calcium-channel blocker + thiazide-like diuretic
Step 4:
· If K ≤ 4.5 mmol/L add low-dose spironolactone
· If K > 4.5 mmol/L add an alpha or beta blocker
If still not controlled, to refer to specialist

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What is the main risk of atrial fibrillation?

Embolic stroke

(DOAC/ warfarin reduces this)

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What is the acute management for supraventricular tachycardia?

Vagal manoeuvres e.g. Valsalva manoeuvre; carotid sinus massage (5-10 seconds)
Rapid IV bolus of adenosine 6mg → 12mg → 18mg (adenosine terminates SVTs by binding to the AV node’s A1 receptors thereby ‘blocking’ the AV node; give verapamil for asthmatics)
Electrical cardioversion (go straight to this if the patient is haemodynamically unstable e.g. hypotension, low O₂ sats, drowsiness)

(adenosine is contraindicated in asthmatics and verapamil can be used instead)

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What is the management for ventricular tachycardia with no adverse features?

IV Amiodarone 300 mg over 10–60 mins (as a bolus, followed by a continuous infusion, ideally administered through a central line)

(other option includes IV lidocaine however use with caution)
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IF this fails:
Immediate cardioversion with synchronised DC shock up to 3 attempts

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What is the management for ventricular tachycardia with adverse features?

If an adverse feature in present (e.g. shock, syncope, myocardial ischaemia, heart failure), then prompt action to restore sinus rhythm is required and should usually be followed by prophylactic therapy:
1. Immediate cardioversion with synchronised DC shock up to 3 attempts
….
…
If unsuccessful:
2. IV Amiodarone 300 mg over 10–20 mins (as a bolus, followed by a continuous infusion, ideally administered through a central line)
3. Repeat synchronised DC shock

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If medical treatment for ventricular tachycardia fails, what can be done?

Implantable cardioverter-defibrillator (ICD)

(particularly indicated in patients with significantly impaired LV function)

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What are the causes of torsades de pointes?

QT-prolonging medications e.g. amiodarone, sotalol, erythromycin, clarithromycin, ciprofloxacin, SSRIs, TCAs, neuroleptic agents
Hypokalaemia (this prolongs repolarisation)
Hypomagnesaemia (this prolongs repolarisation)
Hypocalcaemia (this prolongs repolarisation)
Bradycardia
Congenital long QT syndrome

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What are the types of atrioventricular block?

1st degree atrioventricular block

2nd degree atrioventricular block: Mobitz I

2nd degree atrioventricular block: Mobitz II

3rd degree atrioventricular block

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Valve disease main aetiology:

MS →Rheumatic fever
MR → Mitral valve prolapse
AS →Calcific aortic valve, bicuspid aortic valve
AR → Non-valve: aortic root dilatation; valve: calcific, bicuspid, rheumatic

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Valve disease examination findings:

MS → Mid-diastolic murmur (heard best at the apex on expiration with the patient lying on their left side)
MR → Pan-systolic murmur (heard loudest at the apex and radiates to the axilla)
AS → Ejection-systolic murmur (loudest over the aortic area and radiates to the carotids)
AR → Early diastolic murmur (heard loudest over the left sternal edge, loudest with the patient sitting forward, with their breath held in expiration)
…
PS → Ejection-systolic murmur in the left sternal edge, ↑JVP with giant ‘a’ waves
TR → Pan-systolic murmur at the left sternal edge, ↑JVP with giant ‘v’ waves

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What are the causing organisms of infective endocarditis?

Staphylococcus aureus: leading cause of infective endocarditis. Usually occurs in IV drug abusers.
Streptococci viridans: second largest cause of infective endoscarditis. Mostly subacute infective endocarditis.
Enterococcal endocarditis - mainly with Enterococcus faecalis or Enterococcus faecium.
Streptococcus bovis - common in patients with colorectal cancer. Consider an endoscopy.

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What is the initial management for suspected infective endocarditis?

Blood cultures (1st line Ix): 3 sets, different sites, at intervals of ≥ 6 hours apart (to identify the organism that is the cause of the infection and to guide antibiotic therapy)
Start empirical antibiotics
a) IV Amoxicillin + (optional) low-dose IV Gentamicin for native valves
b) IV Vancomycin + low-dose IV Gentamicin for native valves and penicillin allergic
c) IV Vancomycin + low-dose IV Gentamicin + oral Rifampcin for prosthetic valves
Echocardiogram (Transthoracic (TTE) is usually the first line investigation. Transoesophageal (TOE) has a higher sensitivity than TTE for detecting IE; diagnostic becuase it shows valvular, mobile vegetations)

Other:

FBC (a normocytic normochromic anaemia, and leucocytosis are common)
U+E
ESR (may be raised)
CRP (may be raised)
Urinalysis (proteinuria may occur and non-visible haematuria is usually present)
ECG (may show the development of AV block due to aortic root abscess formation → PR interval > 0.2 s)
CXR (may show evidence of cardiac failure and cardiomegaly)

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What are the causes of myocarditis?

Viral infection is the most common cause: Coxsackie B, Adenovirus, HIV
Bacterial infection: Diphtheria, Clostridia
Spirochaetes: Lyme disease
Protozoa: Chagas’ disease, Toxoplasmosis
Autoimmune: SLE, Systemic Sclerosis. Rheumatoid Arthritis, Sarcoidosis
Drugs: Alcohol, Anthracyclines, Clozapine, Cocaine, Doxorubicin, Lithium

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What are the ECG findings for myocarditis?

ST segment elevation
T wave inversion

Hypertrophic cardiomyopathy is the leading cause of

Sudden cardiac death in the young

What is the inheritence pattern of hypertrophic cardiomyopathy?

Autosomal dominant

In which heart chamber would a myxoma most likely originate?

Left atrium

What are the causes of acute pericarditis?

Idiopathic

Secondary to:

Viruses e.g. Coxsackie A or B virus, echovirus
Bacteria e.g. TB
Fungi and parasites: very rare, usually in the immunocompromised
Malignancy
Trauma
Others: post-MI, chronic heart failure, Dressler’s syndrome, connective tissue disease. hypothyroidism

What investigations are done for acute pericarditis?

ECG (‘saddle-shaped’ ST elevation and PR depression which is the most specific ECG marker for pericarditis)
Troponin (may be elevated)
Other blood tests: FBC (↑WCC), ESR (may be elevated), CRP (may be elevated)
Blood culture (should order this due to presence of fever, it is positive if infectious cause)
Chest x-ray (may show a pericardial effusion)
Transthoracic echocardiogram (all patients should receive this; may show a pericardial effusion)

What are the ECG findings of acute pericarditis?

‘Saddle-shaped’ ST elevation
PR depression (which is the most specific ECG marker for pericarditis)

What is the treatment for idiopathic acute pericarditis?

A combination of:

NSAIDs

and

Colchicine

What are the examination signs of constrictive pericarditis?

Predominantly signs of right-sided heart failure

↑JVP, with prominent x and y descents
Kussmaul’s sign (a paradoxical rise in JVP during inspiration)
Auscultation: diastolic pericardial knock (audible, early S3 due to rapid ventricular filling into a stiff pericardial sac)
Hepatomegaly
Ascities
Oedema

What are the signs of cardiac tamponade?

Beck's triad: 1. **_↓BP_** (pericardial fluid accumulation =\> pressure on the outside of the heart =\> ↓maximum size the ventricles can stretch to =\> ↓EDV =\> ↓SV =\> ↓BP) 2. **_↑JVP_** with absent y descent (pressure from the expanding pericardial sac =\> backup of fluid into the veins draining into the heart) 3. **_Muffled heart sound_** (muffling effects of the fluid surrounding the heart) .... Pulsus paradoxus (a drop of at least 10 mmHg in arterial blood pressure with inspiration)

How do we manage a cardiac tamponade?

**Pericardiocentesis** (pericardial needle aspiration: drainage of the pericardial effusion) REMEMBER TO SEEK EXPERT HELP!

In a patient with bradycardia who has adverse signs that indicate haemodynamic compromise and atropine has been tried with an unsatisfactory response, what should be done next?

Atropine, up to maximum of 3mg (6 times in total) OR Transcutaneous pacing (a temporary means of speeding up a patient's heart during a medical emergency) OR IV Isoprenaline 5 mcg min^-1/ IV adrenaline 2–10 mcg min^-1 infusion titrated to response

In a patient with bradycardia who has adverse signs that indicate haemodynamic compromise and atropine or transcutaenous pacing or IV Isoprenaline/ IV adrenline have been tried, what should be done next?

**_Transvenous pacing_** (threading a pacing electrode through a vein into the right atrium, right ventricle, or both)

What are the symptoms of an aortic dissection?

- Sudden **_tearing_** anterior chest pain ± radiation to back suggests ascending aortic dissection - Interscapular back pain suggests descending aortic dissection (maximal at onset (unlike MI, which builds))

What investigations are done for an aortic dissection?

- ECG: may show left ventricular hypertrophy in patients with hypertension - CXR: may show a widened mediastinum - Cardiac enzymes: usually negative For diagnosis: **_CT angiography_** or MR angiography or Transoesophageal echocardiography (TOE) (more suitable for unstable patients who are too risky to take to CT scanner) Other: - CT aortogram (involves the placement of a catheter in the aorta and injection of contrast material while taking X-rays of the aorta)

Describe the DeBakey classification for aortic dissections

Type I: Ascending aorta, aortic arch and descending aorta Type II: Ascending aorta only Type III: Descending aorta only, distal to the left subclavian artery

What is the definitive management for a Standford type A aortic dissection?

Surgery

What is the definitive management for a Standford type B aortic dissection?

1. ↓Blood pressure 2. Beta blockers e.g. IV labetalol 3. Sodium nitroprusside (vasodilator; use with beta blockers; never use alone!) (note: use non-dihydropyridine calcium channel blockers if beta blockers are contraindicated e.g verapamil or diltiazem)

What special tests do we do for peripheral arterial disease?

1. Ankle brachial pulse index (ABPI: normal = 1-1.2, PAD = 0.5-0.9, critical limb ischaemia \<0.5) 2. Buerger’s test: The patient lies flat and lift the leg. angle of colour change = Buerger's angle, \< 20 degrees = severe ischaemia

What imaging investigations are done for peripheral arterial disease?

1. Duplex ultrasound (to assess location and degree of stenosis) 2. Magnetic resonance angiography/MRA (this should be performed prior to any intervention and can show stenosis and allows treatment planning)

What is the conservative management for peripheral arterial disease?

1. **_Supervised exercise programmes_** (reduce symptoms by improving collateral blood flow; 2 hours per week for 3 months; encourage patients to excercise to the point of maximal pain) 2. Management of risk factors/ secondary prevention: Prescribe an antiplatelet agent: 75 mg **_Clopidogrel_** (this is recommended as 1st-line in preference to aspirin) 80 mg **_Atorvastatin_** Risk factor modification: **_smoking cessation_**, management of blood pressure, diabetes

What investigations are done for acute limb ischaemia?

Bedside: 1. Handheld arterial Doppler examination (to show the extent and severity of the ischaemia by showing flow in smaller arteries) 2. IF Doppler signals are present → ankle brachial pressure index (ABPI) ... Imaging: 1. **CT/MR angiography** (gold standard for assessing occlusion) 2. Duplex ultrasound (useful in unstable patients)