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Cardiology Flashcards

1
Q

Name 3 non-modifiable risk factors for cardiovascular disease

A

Older age
Family history
Male

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2
Q

Name 4 modifiable risk factors for cardiovascular disease

A

Raised cholesterol
smoking
alcohol consumption
poor diet
lack of exercise
obesity
poor sleep
stress

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3
Q

State 4 medical co-morbidities which may increase the risk of cardiovascular disease

A

Diabetes
Hypertension
CKD
Inflammatory conditions e.g. rheumatoid arthritis
Atypical antipsychotic medications

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4
Q

What are 4 end results of atherosclerosis

A

Angina
Myocardial infarction
Transient ischaemic attacks
Strokes
Peripheral arterial disease
Chronic mesenteric ischaemia

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5
Q

What is the QRISK score and what does it guide

A

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

Atorvastatin should be offered to all patients as primary prevention with what co-morbidities?

A

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 statins

A

reduce cholesterol production in the liver by inhibiting HMG CoA reductase

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8
Q

What monitoring is required with statins

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
NICE also 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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9
Q

Name 4 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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10
Q

What can be done for the secondary prevention of cardiovascular disease

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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11
Q

What are 3 important features of familial hypercholesterolaemia

A

Family history of premature cardiovascular disease
Very high cholesterol (e.g., above 7.5 mmol/L in an adult)
Tendon xanthomata

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12
Q

What is the inheritance pattern of familial hypercholesterolaemia

A

autosomal dominant

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13
Q

When is angina defined as stable

A

when symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate

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14
Q

What baseline investigations should all patients with angina have

A

Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
ECG (a normal ECG does not exclude stable angina)
FBC (anaemia)
U&Es (required before starting an ACE inhibitor and other medications)
LFTs (required before starting statins)
Lipid profile
Thyroid function tests (hypothyroidism or hyperthyroidism)
HbA1C and fasting glucose (diabetes)

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15
Q

What investigations can be done for stable angina

A

Cardiac stress testing
CT coronary angiography
Invasive coronary angiography

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16
Q

What are the 5 principles of management in a patient with stable angina

A

R – Refer to cardiology
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
S – Secondary prevention

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17
Q

What is the medical management of stable angina

A

immediate symptomatic relief = GTN
long-term symptomatic relief = beta blocker, calcium channel blocker
Secondary prevention = aspirin, statin, ACEi, bblocker

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18
Q

What advice should you give a patient on using GTN

A

Take the GTN when the symptoms start
Take a second dose after 5 minutes if the symptoms remain
Take a third dose after a further 5 minutes if the symptoms remain
Call an ambulance after a further 5 minutes if the symptoms remain

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19
Q

What are 2 key side effects of GTN

A

headaches
dizziness

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20
Q

What are 2 surgical procedures a patient with severe angina may have

A

Percutaneous coronary intervention (PCI)
Coronary artery bypass graft (CABG)

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21
Q

Why is PCI usually preferred over CABG

A

Faster recovery
Lower rate of strokes as a complication
Higher rate of requiring repeat revascularisation

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22
Q

What are the 3 types of acute coronary syndromes

A

Unstable angina
ST-elevation myocardial infarction (STEMI)
Non-ST-elevation myocardial infarction (NSTEMI)

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23
Q

What areas of the heart does the right coronary artery supply

A

Right atrium
Right ventricle
Inferior aspect of the left ventricle
Posterior septal area

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24
Q

The left coronary artery branches into what

A

Circumflex artery
Left anterior descending (LAD)

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25
Q

What areas of the heart does the circumflex artery supply

A

Left atrium
Posterior aspect of the left ventricle

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26
Q

What areas of the heart does the left anterior descending artery supply

A

Anterior aspect of the left ventricle
Anterior aspect of the septum

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27
Q

What are the symptoms of acute coronary syndrome

A

central, constricting chest pain.

Pain radiating to the jaw or arms
Nausea and vomiting
Sweating and clamminess
A feeling of impending doom
Shortness of breath
Palpitations
Symptoms should continue at rest for more than 15 minutes.

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28
Q

What group of patients are particularly at risk of silent MIs

A

diabetics

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29
Q

What ECG changes are seen in a STEMI

A

ST-segment elevation
New left bundle branch block

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30
Q

What ECG changes are seen in an NSTEMI

A

ST segment depression
T wave inversion

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31
Q

What do pathological Q waves suggest

A

a deep infarction involving the full thickness of the heart muscle (transmural) and typically appear 6 or more hours after the onset of symptoms.

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32
Q

what leads of an ECG correlate to the left coronary artery and what heart area is this?

A

I, aVL, V3-6
Anterolateral

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33
Q

what leads of an ECG correlate to the left anterior descending artery and what heart area is this?

A

V1-4
Anterior

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34
Q

what leads of an ECG correlate to the Circumflex artery and what heart area is this?

A

I, aVL, V5-6
Lateral

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35
Q

what leads of an ECG correlate to the right coronary artery and what heart area is this?

A

II, III, aVF
Inferior

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36
Q

What investigations are done in suspected acute coronary syndrome

A

ECG
Troponin
Baseline bloods (FBC, U&E, LFT, lipids, glucose)
Echo

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37
Q

What are some alternative causes to ACS of a raised troponin

A

Chronic kidney disease
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism

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38
Q

How is a STEMI diagnosed

A

when the ECG shows either:

ST elevation
New left bundle branch block

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39
Q

How is a NSTEMI diagnosed

A

when there is a raised troponin, with either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

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40
Q

When is unstable angina diagnosed

A

when there are symptoms suggest ACS, the troponin is normal, and either:

A normal ECG
Other ECG changes (ST depression or T wave inversion)

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41
Q

What is the initial management for a patient presenting with symptoms of acute coronary syndrome

A

C – Call an ambulance
P – Perform an ECG
A – Aspirin 300mg
I – Intravenous morphine for pain if required (with an antiemetic, e.g., metoclopramide)
N – Nitrate (GTN)

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42
Q

How is a STEMI managed

A

discussed urgently with the local cardiac centre for either:

Percutaneous coronary intervention (PCI) (if available within 2 hours of presenting)
Thrombolysis (if PCI is not available within 2 hours) e.g. streptokinase, alteplase

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43
Q

How is a NSTEMI managed

A

B – Base the decision about angiography and PCI on the GRACE score
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel if high bleeding risk, or prasugrel if having angiography)
M – Morphine titrated to control pain
A – Antithrombin therapy with fondaparinux (unless high bleeding risk or immediate angiography)
N – Nitrate (GTN)

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44
Q

What is a GRACE score

A

gives a 6-month probability of death after having an NSTEMI.

3% or less is considered low risk
Above 3% is considered medium to high risk

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45
Q

What medications are given for secondary prevention following an MI

A

Aspirin 75mg once daily indefinitely
Another Antiplatelet (e.g., ticagrelor or clopidogrel) for 12 months
Atorvastatin 80mg once daily
ACE inhibitors (e.g. ramipril) titrated as high as tolerated
Atenolol (or another beta blocker – usually bisoprolol) titrated as high as tolerated
Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

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46
Q

State 5 complications of a myocardial infarction

A

D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

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47
Q

What is Dressler’s syndrome

A

occurs 2-3 weeks after an acute MI
localised immune response that results in inflammation of the pericardium
pleuritic chest pain, low grade fever, pericardial rub
managed with NSAIDS and steroids in severe cases
May cause effusion or tamponade

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48
Q

What are the 4 types of MI

A

Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (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 procedures such as PCI, coronary stenting and CABG

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49
Q

Name 4 causes of pericarditis

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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50
Q

what is pericardial tamponade

A

pericardial effusion is large and raises intra-pericardial pressure. Affects filling during diastole and decreases cardiac output during systole. Emergency drainage required

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51
Q

What two features are common in pericarditis

A

Chest pain
Low-grade fever

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52
Q

How would you describe the chest pain in pericarditis

A

Sharp
Central/anterior
Worse with inspiration (pleuritic)
Worse on lying down
Better on sitting forward

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53
Q

What would you hear on auscultation in pericarditis

A

pericardial rub

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54
Q

What investigations are done in pericarditis and what would they show

A

CRP + ESR + WBC = raised
ECG = saddle-shaped ST-elevation, PR depression

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55
Q

How is pericarditis managed

A

NSAIDS e.g. aspirin or ibuprofen
Colchicine longer term to reduce reoccurrence
2nd: steroids
treat underlying causes

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56
Q

how long does pericarditis take to resolve

A

most resolve within a month, may reoccur

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57
Q

what is the pathophysiology of acute left ventricular failure

A

acute event results in left ventricle being unable to pump blood efficiently through the left side of the heart, there is a backlog of blood waiting in the left atrium, pulmonary veins and lungs. As these areas experience an increased volume and pressure of blood, they start to leak fluid and cannot reabsorb excess fluid from the surrounding tissues, resulting in pulmonary oedema

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58
Q

What are some triggers of acute left ventricular failure

A

often result of decompensated chronic heart failure
may be triggered by: Iatrogenic e.g. too much IV fluids, MI, Arrhythmia, sepsis, hypertensive emergency

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59
Q

how does acute left ventricular failure present

A

acute shortness of breath (exacerbated by lying flat)
type 1 respiratory failure (dropping sats)
other: cough with frothy white/pink sputum

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60
Q

What signs on examination may be present in acute left ventricular failure

A

Raised respiratory rate
Reduced oxygen saturations
Tachycardia
3rd heart sound
Bilateral basal crackles (sounding “wet”) on auscultation of the lungs
Hypotension in severe cases (cardiogenic shock)

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61
Q

What are 2 key signs of right-sided heat failure

A

Raised JVP
Peripheral oedema

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62
Q

What investigations should be done in suspected acute left ventricular failure

A

ABCDE
ECG
Bloods - BNP, anaemia, infection, kidney function, consider troponin
ABG
CXR
Echo

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63
Q

What are some causes of a raised BNP that are no heart failure

A

Tachycardia
Sepsis
PE
renal impairment
COPD

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64
Q

what is an ejection fraction and what is considered normal

A

the percentage of blood in the left ventricle that is squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.

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65
Q

What x-ray findings may be seen in acute left ventricular failure

A

cardiomegaly
upper lobe venous diversion
bilateral pleural effusions
fluid in interlobar fissures
fluid in septal lines (Kerley lines)

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66
Q

How would you manage a patient with acute left ventricular failure

A

S – Sit up
O – Oxygen
D – Diuretics (IV furosemide)
I – Intravenous fluids should be stopped
U – Underlying causes need to be identified and treated (e.g., myocardial infarction)
M – Monitor fluid balance

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67
Q

What are some causes of chronic heart failure

A

Ischaemic heart disease
Valvular heart disease (commonly aortic stenosis)
Hypertension
Arrhythmias (commonly atrial fibrillation)
Cardiomyopathy

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68
Q

What are the key symptoms of chronic heart failure

A

Breathlessness, worsened by exertion
Cough, which may produce frothy white/pink sputum
Orthopnoea, which is breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
Paroxysmal nocturnal dyspnoea
Peripheral oedema
Fatigue

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69
Q

What are some signs of heart failure on examination

A

Tachycardia
Tachypnoea
Hypertension
Murmurs on auscultation indicating valvular heart disease
3rd heart sound on auscultation
Bilateral basal crackles
Raised jugular venous pressure
Peripheral oedema of the ankles, legs and sacrum

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70
Q

What investigations should be done to diagnose heart failure

A

N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
ECG
Echocardiogram

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71
Q

What is used to classify heart failure and what are the classes

A

The New York Heart Association (NYHA) classification system

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

72
Q

What guides the urgency of a heart failure referral

A

NT-proBNP
From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks

73
Q

What is the first line medical treatment of chronic heart failure

A

A – ACE inhibitor (e.g., ramipril) 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)

74
Q

Name 5 causes of secondary hypertension

A

R – Renal disease
O – Obesity
P – Pregnancy-induced hypertension or pre-eclampsia
E – Endocrine
D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)

75
Q

List 5 complications of hypertension

A

Ischaemic heart disease
Cerebrovascular accident
Vascular disease
Hypertensive retinopathy
Hypertensive nephropathy
Vascular dementia
Left ventricular hypertrophy
Heart failure

76
Q

what BP signifies stage 1 hypertension

A

clinic = >140/90
Ambulatory/home = >135/85

77
Q

what BP signifies stage 2 hypertension

A

clinic = >160/100
ambulatory/home = >150/95

78
Q

what BP signifies stage 3 hypertension

A

> 180/120

79
Q

What investigations for end organ damage should all patients with a new diagnosis of hypertension have

A

Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage
Bloods for HbA1c, renal function and lipids
Fundus examination for hypertensive retinopathy
ECG for cardiac abnormalities, including left ventricular hypertrophy

80
Q

Give 4 pieces of lifestyle advice that can be given to a patient with hypertension

A

stop smoking
reduce alcohol
healthy diet
reduce salt intake
reduce caffeine
regular exercise

81
Q

What are the stages of medical management of hypertension

A

step 1: ACEi (if <55, T2DM), Calcium channel blocker (if >55, black African)
step 2: ACEi (ARB if black african) + CCB
step 3: ACEi/ARB + CCB + thiazide-like diuretic
step 4: ACEi/ARB + CCB + thiazide-like diuretic + fourth agent (K<4.5 = potassium sparing diuretic, K>4.5 = alpha or beta blocker)

82
Q

What are the treatment targets of hypertension for under and over 80yrs

A

<80 = <140/90
>80 = <150/90

83
Q

What defines a hypertensive emergency

A

extremely high blood pressure, above 180/120, with retinal haemorrhages or papilloedema

84
Q

How is a hypertensive emergency managed

A

Intravenous options in a hypertensive emergency (guided by an experienced specialist) include:

Sodium nitroprusside
Labetalol
Glyceryl trinitrate
Nicardipine

85
Q

What are some indications for a pacemaker

A

Symptomatic bradycardias (e.g., due to sick sinus syndrome)
Mobitz type 2 heart block
Third-degree heart block
Atrioventricular node ablation for atrial fibrillation
Severe heart failure (biventricular pacemakers)

86
Q

What devices may be incompatible with a pacemaker

A

MRI
TENS
Diathermy

87
Q

What causes the first heart sound

A

closing of the atrioventricular valves (the tricuspid and mitral valves) at the start of the systolic contraction of the ventricles.

88
Q

What does a 3rd heart sound indicate

A

can be normal (15-40yrs)
heart failure

89
Q

What causes a 4th heart sound

A

stiff or hypertrophic ventricle

90
Q

What causes the second heart sound

A

closing of the semilunar valves (the pulmonary and aortic valves) once the systolic contraction is complete.

91
Q

Where should you auscultate to hear the 4 valve areas

A

Pulmonary area – in the 2nd intercostal space, left sternal border
Aortic – 2nd intercostal space, right sternal border
Tricuspid – 5th intercostal space, left sternal border
Mitral – 5th intercostal space, mid clavicular line (apex area)

92
Q

How can the patient be positioned to better listen to mitral stenosis

A

Position the patient on their left side

93
Q

How can the patient be positioned to listen to aortic regurgitation

A

sat up, leaning forward and holding exhalation

94
Q

mitral stenosis causes what type of hypertrophy

A

left atrial hypertrophy

95
Q

Aortic stenosis causes what type of hypertrophy

A

Left ventricular hypertrophy

96
Q

What is the most common valvular heart disease

A

Aortic stenosis

97
Q

What type of murmur does aortic stenosis cause

A

ejection-systolic, high pitched crescendo-decrescendo murmur
radiates to the carotids

98
Q

Apart from murmur what are some other signs of aortic stenosis

A

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

99
Q

3 causes of aortic stenosis

A

Idiopathic age-related calcification (by far the most common cause)
Bicuspid aortic valve
Rheumatic heart disease

100
Q

What are the characteristics of the murmur in aortic regurgitation

A

early diastolic, soft
may cause Austin flint murmur

101
Q

Apart from murmur what are some other signs of aortic regurgitation

A

Thrill in the aortic area on palpation
Collapsing pulse
Wide pulse pressure
Heart failure and pulmonary oedema

102
Q

What are some causes of aortic regurgitation

A

idiopathic age-related weakness
Bicuspid aortic valve
connective tissue diseases e.g. Ehlers-Danlos and Marfans

103
Q

what are the characteristic of the murmur heard in mitral stenosis

A

mid-diastolic, low pitched rumbling
loud S1

104
Q

Apart from murmur what are some other signs of mitral stenosis

A

Tapping apex beat, which is a palpable, prominent S1
Malar flush
Atrial fibrillation (irregularly irregular pulse)

105
Q

Name 2 causes of mitral stenosis

A

Rheumatic heart disease
Infective endocarditis

106
Q

What are the characteristics of the murmur heard in mitral regurgitation

A

pan-systolic, high-pitched whistling
radiated to left axilla
3rd heart sound may be heard

107
Q

Apart from murmur what are some other signs of mitral regurgitation

A

Thrill in the mitral area on palpation
Signs of heart failure and pulmonary oedema
Atrial fibrillation (irregularly irregular pulse)

108
Q

What are some causes of mitral regurgitation

A

Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective endocarditis
Rheumatic heart disease
Connective tissue disorders, such as Ehlers-Danlos syndrome or Marfan syndrome

109
Q

What are some signs of tricuspid regurgitation

A

pan-systolic murmur
split 2nd heart sound
Thrill in the tricuspid area on palpation
Raised JVP with giant C-V waves (Lancisi’s sign)
Pulsatile liver (due to regurgitation into the venous system)
Peripheral oedema
Ascites

110
Q

What are some signs of pulmonary stenosis

A

ejection systolic murmur loudest in pulmonary area with deep inspiration
widely split second heart sound
Thrill in the pulmonary area on palpation
Raised JVP with giant A waves (due to the right atrium contracting against a hypertrophic right ventricle)
Peripheral oedema
Ascites

111
Q

What are some pros and cons with bioprosthetic and mechanical valves

A

Bioprosthetic valves have a limited lifespan of around 10 years. “Porcine” bioprosthetic valves come from a pig.

Mechanical valves have a good lifespan (well over 20 years) but require lifelong anticoagulation with warfarin. The INR target range with mechanical valves is 2.5 – 3.5 (higher than the 2 – 3 target for atrial fibrillation).

112
Q

What are 3 major complications of mechanical heart valves

A

thrombus formation
infective endocarditis
haemolysis causing anaemia

113
Q

What can be used to treat severe aortic stenosis in patients with high risk of open valve replacement

A

Transcatheter Aortic Valve Implantation (TAVI)

114
Q

What are the risk factors for infective endocarditis

A

Intravenous drug use
Structural heart pathology e.g. prosthetic valves, congenital heart disease, pacemakers
Chronic kidney disease (particularly on dialysis)
Immunocompromised (e.g., cancer, HIV or immunosuppressive medications)
History of infective endocarditis

115
Q

What is the most common cause of infective endocarditis

A

Staphylococcus aureus.

116
Q

What are some presenting symptoms of infective endocarditis

A

Fever
Fatigue
Night sweats
Muscle aches
Anorexia

117
Q

What are some key examination findings in a patient with 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)

118
Q

What investigations should be done in suspected infective endocarditis

A

Blood cultures
Echo (transoesophageal more sensitive)

119
Q

What criteria can be used to diagnose infective endocarditis

A

Modified Duke Criteria

120
Q

What criteria are needed to diagnose infective endocarditis and what are some minor and major criteria

A

One major plus three minor criteria
Five minor criteria
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)

121
Q

How is infective endocarditis managed

A

IV broad spectrum antibiotics (4 weeks with native heart valves, 6 weeks for prosthetic)
Surgery

122
Q

What are some key complications of infective endocarditis

A

Heart valve damage, causing regurgitation
Heart failure
Infective and non-infective emboli (causing abscesses, strokes and splenic infarction)
Glomerulonephritis, causing renal impairment

123
Q

What is the inheritance pattern of hypertrophic obstructive cardiomyopathy

A

autosomal dominant affecting sarcomere proteins

124
Q

How may hypertrophic obstructive cardiomyopathy present

A

most patients asymptomatic
symptoms may come on during exertion
Shortness of breath
Fatigue
Dizziness
Syncope
Chest pain
Palpitations

125
Q

What are some examination findings in a patient with hypertrophic obstructive cardiomyopathy

A

Ejection systolic murmur at the lower left sternal border (louder with the valsalva manoeuvre)
Fourth heart sound
Thrill at the lower left sternal border

126
Q

What investigations can be done in suspected hypertrophic obstructive cardiomyopathy

A

ECG
CXR
Echo or cardiac MRI
Genetic testing

127
Q

How is hypertrophic obstructive cardiomyopathy managed

A

Beta blockers
Surgical myectomy (removing part of the heart muscle to relieve the obstruction)
Alcohol septal ablation (a catheter-based, minimally invasive procedure to shrink the obstructive tissue)
Implantable cardioverter defibrillator (for those at risk of sudden cardiac death or ventricular arrhythmias)
Heart transplant

128
Q

What should patients be advised to avoid if they have hypertrophic obstructive cardiomyopathy

A

intense exercise, heavy lifting, dehydration
ACE inhibitors and nitrates

129
Q

What are some complications of hypertrophic obstructive cardiomyopathy

A

Arrhythmias (e.g., atrial fibrillation)
Mitral regurgitation
Heart failure
Sudden cardiac death

130
Q

Name 5 common causes of atrial fibrillation

A

S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension

131
Q

What symptoms may a patient with atrial fibrillation have

A

Palpitations
Shortness of breath
Dizziness or syncope (loss of consciousness)
Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)

132
Q

what is the pulse like in atrial fibrillation

A

irregularly irregular pulse

133
Q

What are 3 key ECG findings in atrial fibrillation

A

Absent P waves
Narrow QRS complex tachycardia
Irregularly irregular ventricular rhythm

134
Q

What is paroxysmal atrial fibrillation

A

episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours

135
Q

Apart from a normal ECG what other investigations may be done in paroxysmal atrial fibrillation

A

24-hour ambulatory ECG (Holter monitor)
Cardiac event recorder lasting 1-2 weeks

136
Q

What options are available for rate control in atrial fibrillation

A

Beta blocker first-line (e.g., atenolol or bisoprolol)
Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)

137
Q

When would rhythm control be offered to patients with AF

A

A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled

138
Q

When is immediate cardioversion for AF considered

A

Present for less than 48 hours
Causing life-threatening haemodynamic instability

139
Q

What are 2 pharmacological options for immediate cardioversion in AF

A

Flecainide
Amiodarone (the drug of choice in patients with structural heart disease)

140
Q

how long should patients be anticoagulated for before delayed cardioversion

A

3 weeks

141
Q

what are long-term rhythm control options in AF

A

Beta blockers first-line
Dronedarone second-line for maintaining normal rhythm where patients have had successful cardioversion
Amiodarone is useful in patients with heart failure or left ventricular dysfunction

142
Q

how is paroxysmal atrial fibrillation managed

A

‘pill-in-pocket’ - Flecainide

143
Q

What are the 2 options for ablation in AF

A

Left atrial ablation
Atrioventricular node ablation and a permanent pacemaker

144
Q

what are the 1st and 2nd line options for anticoagulation in patients with AF

A

Direct-acting oral anticoagulants (DOACs) first-line
Warfarin second-line, if DOACs are contraindicated

145
Q

what are some advantages of DOACs over warfarin

A

No monitoring is required
No issues with time in therapeutic range (provided they have good adherence)
No major interaction problems
Equal or slightly better than warfarin at preventing strokes in atrial fibrillation
Equal or slightly lower risk of bleeding than warfarin

146
Q

What is the target range for INR in AF

A

2-3

147
Q

What is the CHA2DS2-VASc score

A

tool for assessing whether a patient with atrial fibrillation should start anticoagulation.

148
Q

what are the points in the CHA2DS2-VASc score

A

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)

149
Q

What should be recommended following calculating a CHA2DS2-VASc score

A

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

150
Q

What score can you use to assess risk of major bleeding in patients with AF taking anticoagulation

A

ORBIT score

151
Q

What does the ORBIT score stand for

A

O – Older age (age 75 or above)
R – Renal impairment (GFR less than 60)
B – Bleeding previously (history of gastrointestinal or intracranial bleeding)
I – Iron (low haemoglobin or haematocrit)
T – Taking antiplatelet medication

152
Q

What is a narrow complex tachycardia

A

fast heart rate with a QRS complex duration of less than 0.12 seconds.(<3 little squares)

153
Q

What are the 4 main differentials of a narrow complex tachycardia

A

Sinus tachycardia
Supraventricular tachycardia
Atrial fibrillation
Atrial flutter

154
Q

What is the extra pathway in Wolff-Parkinson-White syndrome called

A

Bundle of Kent

155
Q

What are some ECG changes in Wolff-Parkinson-white syndrome

A

Short PR interval, less than 0.12 seconds
Wide QRS complex, greater than 0.12 seconds
Delta wave

156
Q

What is the definitive treatment of Wolff-Parkinson-White syndrome

A

radiofrequency ablation of the accessory pathway

157
Q

What is the stepwise management of supraventricular tachycardia in patients without life-threatening features

A

Step 1: Vagal manoeuvres
Step 2: Adenosine
Step 3: Verapamil or a beta blocker
Step 4: Synchronised DC cardioversion

158
Q

How are patients with SVT and life-threatening features managed

A

synchronised DC cardioversion under sedation or general anaesthesia. Intravenous amiodarone is added if initial DC shocks are unsuccessful.

159
Q

Adenosine should be avoided in patients with what

A

Asthma
COPD
Heart failure
Heart block
Severe hypotension
Potential atrial arrhythmia with underlying pre-excitation

160
Q

State 2 shockable rhythms

A

(pulseless) Ventricular tachycardia
Ventricular fibrillation

161
Q

State 2 non-shockable rhythms

A

Pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
Asystole (no significant electrical activity)

162
Q

What does an ECG show in atrial flutter

A

saw-tooth pattern
narrow complex tachycardia

163
Q

Name 4 sub-types of broad complex tachycardia

A

Ventricular tachycardia or unclear cause (treated with IV amiodarone)
Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
Atrial fibrillation with bundle branch block (treated as AF)
Supraventricular tachycardia with bundle branch block (treated as SVT)

164
Q

what QT interval is prolonged

A

More than 440 milliseconds in men
More than 460 milliseconds in women

165
Q

Name 3 causes of prolonged QT

A

Long QT syndrome (an inherited condition)
Medications, such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia

166
Q

What is the acute management of torsades de pointes

A

Correcting the underlying cause (e.g., electrolyte disturbances or medications)
Magnesium infusion (even if they have normal serum magnesium)
Defibrillation if ventricular tachycardia occurs

167
Q

What does 1st degree heart block look like on ECG

A

PR interval greater than 0.2 seconds (5 small or 1 big square)

168
Q

What does Mobitz type 1 second degree heart block look like on ECG

A

increasing PR interval until a P wave is not followed by a QRS complex. The PR interval then returns to normal, and the cycle repeats itself.

169
Q

What does 3rd degree heart block look like on ECG

A

no observable relationship between the P waves and QRS complexes.

170
Q

What heart conditions increase the risk of asystole

A

Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds

171
Q

How are unstable patients and patients at risk of asystole managed

A

Intravenous atropine (first line)
Inotropes (e.g., isoprenaline or adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker, when available

172
Q

when is adrenaline given in cardiac arrest?

A

1mg ASAP for non-shockable
shockable rhythms given after 3rd shock
repeat every 3-5mins

173
Q

When is amiodarone given in cardiac arrest?

A

300mg in shockable rhythms after 3 shocks
further 150mg after 5 shocks

174
Q

For how long should you do CPR in cardiac arrest if thrombolytic drugs are given?

A

60-90 mins

175
Q

State 6 reversible causes of cardiac arrest

A

Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade - cardiac
Toxins

Finals (13 decks)

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