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Cardiology Flashcards

The chambers and the valves pump the sentiment around...

1
Q

What dietary changes does NICE recommend to reduce risk of CVD? (%fat intake, frequency of food groups)

A

The NICE guidelines on cardiovascular disease (updated February 2023) recommend the following dietary changes:

Total fat is less than 30% of total calories (primarily monounsaturated and polyunsaturated fats)
Saturated fat is less than 7% of total calories
Reduced sugar intake
Wholegrain options
At least 5 a day of fruit and vegetables
At least 2 a week of fish (one being oily)
At least 4 a week of legumes, seeds and nuts

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2
Q

What dies NICE recommended in terms of exercise to reduce risk of CVD?

A

The NICE guidelines recommend (limited by co-morbidities):

Aerobic activity for a total of at least 150 minutes at moderate intensity or 75 minutes at vigorous intensity per week
Strength training activities at least 2 days a week

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3
Q

What is the difference between primary and secondary prevention in CVD?

A

Prevention of cardiovascular disease falls into two main categories:

Primary prevention for patients that have never had a diagnosis of cardiovascular disease.
Secondary prevention after a diagnosis of angina, myocardial infarction, TIA, stroke or peripheral arterial disease.

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4
Q

What does the QRISK score estimate?

A

The QRISK score estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years.

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5
Q

What QRISK3 score does NICE recommend as the threshold to commence medication? What medication would be offered?

A

The NICE guidelines (updated February 2023) recommend when the result is above 10%, they should be offered a statin, initially atorvastatin 20mg at night.

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6
Q

When is atorvastatin offered to patients as primary prevention of CVD? (Give 3 circumstances)

A
  • QRISK3 score >10%
  • Chronic kidney disease (eGFR less than 60 ml/min/1.73 m2)
  • Type 1 diabetes for more than 10 years or are over 40 years
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7
Q

What is the mechanism of action for statins?

A

Statins reduce cholesterol production in the liver by inhibiting HMG CoA reductase.

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8
Q

When does NICE recommend checking lipids after commencing statins? When should statin dose be increased?

A

NICE recommend checking lipids 3 months after starting statins and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol.

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9
Q

When does NICE recommend checking LFTs after starting statins and why?

A

NICE recommend checking LFTs within 3 months of starting a statin and again at 12 months. Statins can cause a transient and mild rise in ALT and AST in the first few weeks of use. They usually do not need to be stopped if the rise is less than 3 times the upper limit of normal.

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10
Q

Name some rare but significant side effects of statins.

A
  • Myopathy (causing muscle weakness and pain)
  • Rhabdomyolysis (muscle damage – check the creatine kinase in patients with muscle pain)
  • Type 2 diabetes
  • Haemorrhagic strokes (very rarely)
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11
Q

Which antibiotics interact with statins and would prompt withholding statins during the course?

A

Macrolide antibiotics e.g. clarithromycin, erythromycin

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12
Q

Name 2nd line cholesterol lowering drugs when statins are contraindicated.

A

Ezetimibe
PCSKg inhibitors (evolocumab, alirocumab)

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13
Q

Name the 4 A’s of secondary prevention in CVD

A

A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or an alternative beta blocker – commonly bisoprolol) titrated to the maximum tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the maximum tolerated dose

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14
Q

What medications are started after an MI? What is the duration?

A

After a myocardial infarction, patients are offered dual antiplatelet treatment initially, with:

  • Aspirin 75mg daily (continued indefinitely)
  • Clopidogrel or ticagrelor (generally for 12 months before stopping)
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15
Q

What is the inheritance pattern of familial hypercholesterolaemia?

A

autosomal dominant

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16
Q

What criteria can be used to make a clinical diagnosis of familial hypercholesterolaemia (2)? What level of serum cholesterol would be a sign?

A

Simon Broome criteria
Dutch Lipid Clinic Network Criteria

cholesterol of >7.5 mmol/L

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17
Q

What are the characteristics of stable angina?

A

Caused by exertion, relieved by rest or GTN spray

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18
Q

What investigation can be used to assess cardiac function?

A

Cardiac stress testing

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19
Q

What does cardiac stress testing involve?

A

Cardiac stress testing involves assessing the patient’s heart function during exertion. This can involve having the patient exercise (e.g., walking on a treadmill) or giving medication (e.g., dobutamine) to stress the heart. The options for assessing cardiac function during stress testing are an ECG, echocardiogram, MRI or a myocardial perfusion scan (nuclear medicine scan).

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20
Q

What investigations can be used to assess for coronary artery narrowing? Which is gold standard?

A

CT coronary angiography
Invasive coronary angiography (gold-standard)

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21
Q

What ECG changes may indicate ischaemia or previous MI?

A
  • Pathological Q waves (in particular).
  • Left bundle branch block (LBBB).
  • ST-segment and T-wave abnormalities (for example T-wave flattening or elevation, or T-wave inversion).
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22
Q

What are the 1st line treatments for stable angina?

A
  • GTN PRN - symptomatic relief
  • Beta-blocker (e.g. bisoprolol) OR CCB (e.g. diltiazem or verapamil C/I in HFREF)
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23
Q

What are some side effects of GTN?

A

headaches and dizziness caused by vasodilation

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24
Q

What is a contraindication of CCBs?

A

HFREF

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25
Q

What are some 2nd line treatments for stable angina?

A
  • Long-acting nitrates (e.g., isosorbide mononitrate)
  • Ivabradine
  • Nicorandil
  • Ranolazine
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26
Q

How much fluid is in the pericardium?

A

less than 50 mls

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27
Q

List causes of pericarditis (7). What is the most common?

A
  • Idiopathic (no underlying cause)
  • Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus and other viruses)
  • Autoimmune and inflammatory conditions (e.g., systemic lupus erythematosus and rheumatoid arthritis)
  • Injury to the pericardium (e.g., after myocardial infarction, open heart surgery or trauma)
  • Uraemia (raised urea) secondary to renal impairment
  • Cancer
  • Medications (e.g., methotrexate)
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28
Q

Which phase of the heart beat/function does pericardial effusion affect?

A

Diastole

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29
Q

Explain the process of the effect of pericardial tamponade on cardiac output.

A

Pericardial effusion => raised intra-pericardial pressure => reduced filling in diastole => lower cardiac output during systole => cardiac tamponade

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30
Q

Describe the chest pain in pericarditis.

A

Sharp, central/anterior, pleuritic (worse on inspo), orthopnoea (worse when lying down), improved on sitting forward

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31
Q

What sign can be elicited on auscultation in pericarditis?

A

Pericardial friction rub

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32
Q

What can be seen on a blood test in pericardial effusion

A

raised inflammatory markers

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33
Q

What can be seen on ECG in pericarditis?

A

Saddle-shaped ST elevation
PR depression

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34
Q

Diagnostic test for pericarditis?

A

Echo

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35
Q

Medical management of pericarditis?

A

NSAID (aspirin or ibuprofen)
Colchicine - longterm, 3 months, to reduce risk of recurrence

2nd line) steroids

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36
Q

Management of pericardial tamponade

A

Pericardiocentesis

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37
Q

Symptoms of pericarditis/cardiac tamponade

A

Pain - sharp, constant sternal pain relieved by sitting forward. Pain may radiate to the left shoulder and/or left arm and/or into the abdomen, and is worse when lying on the left side and on inspiration, swallowing, and coughing.
Fever
Cough
Arthralgia.

Cardiac tamponade may have associated breathlessness, dysphagia, cough, and hoarseness.

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38
Q

Signs of pericarditis

A

Auscultation - pericardial friction rub (high pitched scratching sound, best heard over the left sternal border during expiration).
Cardio exam - Signs of cardiac tamponade include pulsus paradoxus (decrease in palpable pulse and arterial systolic blood pressure of 10 mmHg on inspiration); and hypotension, muffled heart sounds, and jugular venous distention (Beck’s Triad).

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39
Q

What is cardiac output?

A

volume of blood ejected by the heart per minute

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40
Q

What is stroke volume?

A

volume of blood ejected during each beat

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41
Q

What is the formula for cardiac output and stroke volume

A

CO = SV x HR

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42
Q

How does left ventricular failure affect pulmonary circulation?

A

Blood is not flowing efficiently through the left side of the heart => backlog of blood in the left atrium, pulmonary veins and lungs => increased volume and pressure => pulmonary oedema

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43
Q

What is acute left ventricular failure caused by? What are the triggers?

A

Caused by decompensated chronic heart failure
Triggers:
- iatrogenic (e.g. aggressive IVI)
- MI
- arrhythmias
- sepsis
- hypertensive emergency

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44
Q

What is the typical presentation of acute LVF?

A

Acute shortness of breath, worse on lying flat, better with sitting up

  • Type 1 respirator failure
  • looking and feeling unwell
  • cough with frothy white or pink sputum
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45
Q

What is the nature of the cough in pulmonary oedema?

A

Cough with frothy white or pink sputum

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46
Q

What are some signs on examination in LVF?

A
  • raised RR
  • reduced O2 sats
  • inc HR
  • 3rd heart sound
  • b/l basal crackles
  • hypotension in severe cases (cardiogenic shock)
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47
Q

What is BNP?

A

B-type natriuretic peptide is a hormone released from ventricles when myocardium is stretched beyond normal , suggesting heart is overloaded.
It relaxes smooth muscle in blood vessels, reducing systemic vascular resistance. It also acts as a diuretic

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48
Q

Describe the sensitivity and specificity of BNP

A

BNP is sensitive (rules out) but not specific (rule in)

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49
Q

What is a normal ejection fraction?

A

Above 50%

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50
Q

How is cardiomegaly classified on CXR?

A

> 0.5 of cardiothoracic ratio

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51
Q

What is the management of LVHF (hint: mnemonic)?

A

SODIUM
Sit up
Oxygen
Diuretics
IVI stopped
Underlying causes stop
Monitor fluid balance

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52
Q

What management can be started by a specialist in severe cases of LVHF?

A
  • IV opioids = vasodilators
  • IV nitrates = vasodilators
  • Inotropes e.g. dobutamine = improve CO
  • Vasopressors e.g. noradrenalin = improve BP
  • NIV
  • invasive ventilation
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53
Q

How do inotropes work?

A

alter heart contractility
Positive inotropes increase the contractility => inc CO and mean arterial pressure

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54
Q

How do vasopressors work?

A

cause vasoconstriction => inc systemic vascular resistance => inc MAP => inc BP => inc tissue perfusion

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55
Q

What follow up is required for NT-pro-BNP >2000ng/L?

A

Urgent specialist assessment and echo in 2 weeks

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56
Q

What follow up is required for NT-pro-BNP 400-2000ng/L?

A

specialist assessment and echo within 6 weeks

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57
Q

What is the management of HF with reduced EF

A
  • Stop drugs that worsen HF
  • Diuretic
  • Offer ACE-i (exc valve disease) and B-b
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58
Q

What are symptoms of chronic heart failure?

A
  • SOBOE
  • cough
  • Orthopnoea
  • PND
  • peripheral oedema
  • fatigue
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59
Q

What are some signs of chronic heart failure?

A
  • tachycardia/pnoea
  • HTN
  • murmur or 3rd heart sound
  • b/l basal crackles
  • raised JVP
  • peripheral oedema
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60
Q

Describe the classifications in the New York Heart Association Classification (NYHA)

A

Class I: No limitation on activity
Class II: Comfortable at rest but symptomatic with ordinary activities
Class III: Comfortable at rest but symptomatic with any activity
Class IV: Symptomatic at rest

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61
Q

What is the 1st line medical treatment for chronic heart failure?

A

A – ACE inhibitor (e.g., ramipril) or ARB titrated as high as tolerated
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone)
L – Loop diuretics (e.g., furosemide or bumetanide)

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62
Q

When is ACE-i contraindicated in chronic heart failure? What medication can be used instead?

A

If due to valvular heart disease. Use ARB instead (candesartan)

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63
Q

What are some causes of secondary hypertension?

A

ROPED
Renal artery stenosis
Obesity
Pre-eclampsia
Endocrine (Cushing’s, Conn’s, Phaeochromocytoma)
Drugs (alcohol, NSAIDs, oestrogen, liquorice)

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64
Q

Name some complications of hypertension.

A
  • Ischaemic heart disease
  • cerebrovascular accident
  • vascular disease (PAD, aortic dissection, AAA)
  • HTN retinopathy
  • HTN nephropathy
  • vascular dementia
  • LV hypertrophy
  • HF
64
Q

What causes the 1st and 2nd heart sounds?

A

1st HS is caused by closure of the AV valves (tricuspid and mitral)
2nd HS is caused by closure of the semilunar valves (pulmonary and aortic)

65
Q

What is the 3rd heart sound?

A

heard 0.1 seconds after the 2nd HS
rapid ventricular filling causing chordae tendinae to pull
“gallop rhythm”
normal in 15-40y/o
can indicate heart failure in older people

65
Q

What is the 4th heart sound?

A

heard directly before S1
always abnormal, rare
indicates stiff or hypertrophic ventricles

66
Q

Describe how different valvular defects can affect chamber morphology?

A

When pushing against a stenotic valve, the muscle has to try harder, resulting in hypertrophy:
- Mitral stenosis causes left atrial hypertrophy
- Aortic stenosis causes left ventricular hypertrophy

When a leaky valve allows blood to flow back into a chamber, it stretches the muscle, resulting in dilatation:
- Mitral regurgitation causes left atrial dilatation
- Aortic regurgitation causes left ventricular dilatation

67
Q

What murmur is caused by aortic stenosis? Where does it radiate?

A

Ejection systolic, high-pitched, crescendo-decrescendo. radiates to the carotids

68
Q

What murmur is caused by aortic regurgitation?

A

early diastolic, soft murmur
Austin-Flint murmur - heard at the apex, “rumbling” sound

69
Q

Signs of aortic stenosis

A

thrill on aortic area
slow rising pulse
narrow pulse pressure
exertional syncope

70
Q

Signs of aortic regurgitation

A

thrill over aortic area
collapsing pulse/water hammer pulse
wide pulse pressure
heart failure and pulmonary oedema

71
Q

3 causes of aortic regurgitation

A
  • idiopathic age-related weakness
  • bicuspid aortic valve
  • connective tissue disorder - Ehlers-Danlos syndrome and Marfan syndrome
72
Q

What murmur is caused by mitral stenosis?

A

mid-diastolic, low-pitched “rumbling”

73
Q

Signs of mitral stenosis

A
  • tapping apex beat
  • malar flush
  • AF
74
Q

Causes of mitral stenosis

A
  • rheumatic heart disease
  • infective endocarditis
75
Q

What murmur is caused by mitral regurgitation?

A

pan-systolic, high-pitched “whistling”. radiates to the left axilla

76
Q

Signs of mitral regurgitation

A

-thrill over mitral area
- heart failure and pulmonary oedema
- AF

77
Q

Causes of mitral regurgitation

A
  • idiopathic weakening of the valve with age
  • ischaemic heart disease
  • infective endocarditis
  • rheumatic heart disease
  • connective tissue disorders - EDS, Marfans
78
Q

What murmur is caused by tricuspid regurgitation?

A

pan-systolic murmur, split second heart sound

79
Q

Signs of tricuspid regurgitation

A
  • thrill over tricuspid area
  • raised JVP
  • pulsatile liver
  • peripheral oedema
  • ascites
80
Q

Causes of tricuspid regurgitation

A
  • pulmonary HTN or left-sided heart failure
  • infective endocarditis
  • rheumatic heart disease
  • carcinoid syndrome
  • Ebstein’s anomaly
  • connective tissue disorders - EDS, Marfan’s
81
Q

What murmur is caused by pulmonary stenosis?

A

ejection systolic, widely split second heart sound

82
Q

Signs of pulmonary stenosis?

A
  • thrill over pulmonary area
  • raised JVP
  • pulmonary oedema
  • ascites
83
Q

Causes of pulmonary stenosis

A

usually congenital
- Noonan syndrome
- tetralogy of Fallot (VSD, OA, PS, RVH)

84
Q

What scar is usually associated with valve replacement surgery?

A

midline sternotomy scar

85
Q

Describe the differences between bioprosthetic and mechanical heart valves.

A

Bioprosthetic - lifespan of 10 years
Mechanical - lifespan >20 years but require lifelong anticoagulation with warfarin (INR 2.5-3.5 [AF is 2-3])

86
Q

Which mechanical valve has the lowest risk of thrombus formation?

A

St Jude valve

87
Q

Name 3 major complications of mechanical heart valves

A
  • thrombus formation
  • infective endocarditis
  • haemolysis causing anaemia
88
Q

When is a TAVI indicated?

A

Transcatheter Aortic Valve Implantation is indicates in severe aortic stenosis in patients at high risk for open valve replacement. catheter is inserted into the femoral artery

89
Q

What is the rate of infective endocarditis in valve replacement? What is the mortality rate? What organism usually causes it?

A

rate is 2.5%
mortality rate is 15%
caused by gram-positive cocci e.g. staph, strep, enterococcus

90
Q

Risk factors of infective endocarditis?

A
  • IVDU
  • structural heart pathology (valvular, congenital, HCM, heart valves, ICDs)
  • CKD (esp on dialysis)
  • immunocompromised (e.g. cancer, HIV)
  • prev IE
91
Q

Most common organisms causing of infective endocarditis?

A
  • strep, esp viridans
  • enterococcus
  • rare: pseudomonas, HACEK organisms and fungi
92
Q

How does infective endocarditis usually present?

A
  • fever, night sweats
  • fatigue
  • anorexia
  • muscle aches
93
Q

What can be found on examination in infective endocarditis?

A
  • New or “changing” heart murmur
  • Splinter haemorrhages (thin red-brown lines along the fingernails)
  • Petechiae (small non-blanching red/brown spots) on the trunk, limbs, oral mucosa or conjunctiva
  • Janeway lesions (painless red flat macules on the palms of the hands and soles of the feet)
  • Osler’s nodes (tender red/purple nodules on the pads of the fingers and toes)
  • Roth spots (haemorrhages on the retina seen during fundoscopy)
  • Splenomegaly (in longstanding disease)
  • Finger clubbing (in longstanding disease)
94
Q

What investigations are done for infective endocarditis?

A
  • blood cultures BEFORE antibiotics - 3 samples 6 hours apart from different sites
  • Echo - visualise vegetations
  • 18F-FDG PET/CT or SPECT-CT for prosthetic heart valves
95
Q

What criteria is used to diagnose infective endocarditis?

A

Modified Duke Criteria - 1 major + 3 minor, or 5 minor

Major criteria are:
- Persistently positive blood cultures (typical bacteria on multiple cultures)
- Specific imaging findings (e.g., a vegetation seen on the echocardiogram)

Minor criteria are:
- Predisposition (e.g., IV drug use or heart valve pathology)
- Fever above 38°C
- Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
- Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
- Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)

96
Q

What is the treatment of infective endocarditis?

A

IV broad-spec Abx until cultures identify an organism
- for 4 weeks with native heart valves
- for 6 weeks for prosthetic heart valves

Surgery if HF relating to valve pathology, large vegetations, or infection not responding to abx

97
Q

Complications of infective endocarditis

A
  • heart valve damage => regurgitation
  • heart failure
  • infective/non-infective emboli => abscesses, strokes, splenic infarction
  • glomerulonephritis
98
Q

What is hypertrophic cardiomyopathy? What specific structural issue does it cause

A

Hypertrophic obstructive cardiomyopathy (HOCM) is a condition where the left ventricle becomes hypertrophic, with thickening of the muscle. This tends to asymmetrically affect the septum of the heart, blocking the flow of blood out of the left ventricle. This is referred to as left ventricular outflow tract (LVOT) obstruction.
HOCM is an autosomal dominant genetic condition resulting from a defect in the genes for sarcomere proteins. It occurs in about 1 in 500 people.

99
Q

What does HOCM increase the risk of?

A

heart failure, myocardial infarction, arrhythmias and sudden cardiac death

100
Q

What is the genetic heritability of HOCM?

A

autosomal dominant
defect in genes for sarcomere proteins
in 1 in 500 people

101
Q

What examination findings can be found in HOCM?

A
  • ejection systolic murmur
  • 4th heart sound
  • thrill at lower left sternal border
102
Q

What may be seen on ECG in HOCM?

A

AF
LVH

103
Q

What can establish a diagnosis of HOCM?

A

Echo or Cardiac MRI
Genetic testing

104
Q

What is a medical management of HOCM? What are some surgical interventions?

A
  • beta blocker
  • surgical myectomy (to relieve the obstruction/LVOT)
  • alcohol septal ablation
  • implantable cardioverter defibrillator (ICD)
  • heart transplant
105
Q

Which drugs should be avoided in HOCM

A

ACE-inhibitors and nitrates
they can worsen LVOTO

106
Q

What are some complications of HOCM?

A
  • arrhythmias - AF
  • mitral regurgitation
  • heart failure
  • sudden cardiac death
106
Q

How much is the risk of ischaemic stroke higher in AF?

A

5 times higher

107
Q

What are some common causes of AF? (Hint: mnemonic)

A

SMITH
Sepsis
Mitral valve pathology (stenosis/regurg)
Ischaemic heart disease
Thyrotoxicosis
HTN

Alcohol and caffeine are lifestyle risk factors

108
Q

What are some symptoms of AF?

A
  • palpitations
  • SOB
  • dizziness/syncope
  • other conditions e.g. stroke, sepsis, thyrotoxicosis
109
Q

What are the ECG findings in AF?

A
  • irregularly irregular
  • absent p waves
  • narrow QRS complex tachycardia
110
Q

What investigation is considered in new AF? What conditions are investigated?

A

Echo
- valvular heart disease
- heart failure

111
Q

What is paroxysmal AF? How can it be investigated?

A

spontaneously resolve, last 30 seconds to 48 hours
24-hr ambulatory ECG. cardiac event recorder

112
Q

What are the 2 principles of treating AF? What is the most common choice for both?

A
  • rate or rhythm control - most likely bisoprolol rate control
  • anticoagulation - most likely DOAC
113
Q

What heart rate does rate control aim to achieve?

A

less than 100 bpm

114
Q

What are 3 options for rate control? Under what condition should they be used?

A
  1. beta blocker e.g. bisoprolol - FIRST LINE
  2. CCB e.g. diltiazem or verapamil - NOT in HF
  3. digoxin - only in SEDENTERY pts with persistent AF, requires monitoring and at risk of toxicity
115
Q

What are the 4 conditions that NICE recommends NOT to give rate-control?

A
  • reversible cause for AF
  • new onset AF (within last 48 hrs)
  • HF caused by AF
  • symptoms despite effective rate control

can do rhythm control instead

116
Q

What are the two main options for rhythm control? How can they be further split?

A
  • Cardioversion
    - immediate or delayed
  • Long-term rhythm control (medications)
117
Q

When is immediate cardioversion used? What are the 2 options for immediate cardioversion?

A

Used in AF:
- present for less than 48 hrs
- causing life-threatening haemodynamic instability

2 options:
- pharmacological cardioversion
- electrical cardioversion

118
Q

What are 2 examples of pharmacological cardioversion?

A
  • flecainide
  • amiodarone (esp in structural heart disease)
119
Q

What are the conditions for delayed cardioversion?

A
  • AF more than 48 hrs and pt is stable
  • pt should be anticoagulated for at least 3 weeks prior
  • pt should be rate-controlled in the meantime
120
Q

What can be used for long-term rhythm control?

A
  • beta blockers
  • dronedarone (after successful cardioversion)
  • amiodarone (in HF or LVF)
121
Q

What is the management of paroxysmal AF?

A

Flecainide as needed
if no structural heart disease

122
Q

What are the guidelines for anticoagulation in AF? What is the risk of serious bleeding? What is the reduction of stroke risk with anticoagulation?

A
  • DOAC 1st line (CHADSVASC of 2 or above)
  • warfarin 2nd line

2.5-8%

5% to 1-2%

123
Q

What is the mechanism of action for apixaban, edoxaban and rivaroxaban?

A

direct factor Xa inhibitors

124
Q

What is the mechanism of action for dabigatran?

A

direct thrombin inhibitor

125
Q

What is the mechanism of action of warfarin?

A

vitamin K antagonist, prolongs prothrombin time

126
Q

What is INR?

A

International normalised ratio, assesses prothrombin time compared to an average healthy adult. INR 1 is normal. INR 2-3 is the target in AF

127
Q

What can effect INR?

A

drugs that influence the activity of cytochrome P450
foods containing vitamin K e.g. leafy green veg
foods affecting P450 e.g. cranberry juice, alcohol

128
Q

What is CHA2DS2-VASc? What are the recommendation based on scores

A

assessing clot risk in AF

C – Congestive heart failure
H – Hypertension
A2 – Age above 75 (scores 2)
D – Diabetes
S2 – Stroke or TIA previously (scores 2)
V – Vascular disease
A – Age 65 – 74
S – Sex (female)

NICE (2021) recommends, based on the CHA2DS2-VASc score:

0 – no anticoagulation
1 – consider anticoagulation in men (women automatically score 1)
2 or more – offer anticoagulation

129
Q

Indications for a pacemaker

A

Symptomatic bradycardias(e.g., due tosick sinus syndrome)

Mobitz type 2 heart block

Third-degree heart block

Atrioventricular node ablationforatrial fibrillation

Severe heart failure(biventricular pacemakers)

130
Q

What is the role of SGLT2 inhibitors in heart failure?

A

SGLT2 inhibitors (e.g., dapagliflozin) are used as an additional specialist treatment to reduce heart failure symptoms and complications.

131
Q

What is a common side effect of ACE inhibitors, occurring in around 15% of patients?

A

Cough, possibly due to increased bradykinin levels.

132
Q

What serious side effect can ACE inhibitors cause, potentially up to a year after treatment?

A

Angioedema

133
Q

What electrolyte imbalance can ACE inhibitors cause?

A

Hyperkalaemia

134
Q

In what conditions are ACE inhibitors contraindicated?

A

Pregnancy and breastfeeding, renovascular disease, aortic stenosis, and patients with hereditary or idiopathic angioedema.

135
Q

What should be monitored before and during ACE inhibitor therapy?

A

Urea and electrolytes should be checked before starting treatment and after dose increases.
An increase in serum creatinine up to 30% from baseline and potassium up to 5.5 mmol/L is acceptable.

136
Q

What are the two categories of rhythms in cardiac arrest?

A

Shockable rhythms: Ventricular fibrillation (VF), Pulseless ventricular tachycardia (VT)

Non-shockable rhythms: Asystole, Pulseless electrical activity (PEA)

137
Q

What is the defibrillation protocol for VF/pulseless VT?

A

A single shock followed by 2 minutes of CPR.

138
Q

How should defibrillation be handled in a witnessed cardiac arrest in a monitored patient?

A

Consider up to three quick successive shocks (stacked shocks) instead of one shock followed by CPR.

139
Q

When should adrenaline be administered in non-shockable rhythms (asystole/PEA)?

A

1 mg adrenaline as soon as possible.

140
Q

When should adrenaline be administered in VF/pulseless VT?

A

1 mg adrenaline after the third shock, and then every 3-5 minutes during ALS.

141
Q

When should amiodarone be administered in VF/pulseless VT?

A

300 mg after 3 shocks.

150 mg after 5 shocks.

142
Q

What drug can be used as an alternative to amiodarone if it is unavailable?

A

Lidocaine

143
Q

How long should CPR be continued after administering thrombolytics for a suspected pulmonary embolism?

A

60-90 minutes.

144
Q

How should a patient with atrial fibrillation (AF) and haemodynamic instability be managed?

A

They should be electrically cardioverted as per the peri-arrest tachycardia guidelines.

145
Q

For haemodynamically stable patients with AF lasting less than 48 hours, what are the management options?

A

Either rate or rhythm control.

146
Q

What is the recommended management for AF lasting 48 hours or more, or if the duration is uncertain?

A

Rate control, and if long-term rhythm control is considered, delay cardioversion until therapeutic anticoagulation for at least 3 weeks.

147
Q

When is catheter ablation recommended for atrial fibrillation?

A

For patients with AF who have not responded to, or wish to avoid, antiarrhythmic medication.

148
Q

How long should anticoagulation be used before and during catheter ablation for AF?

A

At least 4 weeks before and during the procedure.

149
Q

What are the notable complications of catheter ablation?

A

Cardiac tamponade
Stroke
Pulmonary vein stenosis

150
Q

What are the common types of supraventricular tachycardia (SVT)?

A

Atrioventricular nodal re-entry tachycardia (AVNRT)
Atrioventricular re-entry tachycardia (AVRT)
Junctional tachycardias

151
Q

What is the acute management of SVT?

A

vagal manoeuvres:
- Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
- carotid sinus massage

intravenous adenosine
- rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg
- contraindicated in asthmatics - verapamil is a preferable option

electrical cardioversion

152
Q

What is the management of SVT in shock?

A

Synchronised direct current (DC) cardioversion

153
Q

What are the ECG features in hypokalaemia?

A

U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT

154
Q

What drug class can be used instead of ACE-i in HTN if not tolerated?

A

ARB e.g. losartan

155
Q
A

MSRA (16 decks)

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