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Y3 medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Supraventricular tachycardias

A

Sinus tachycardia
Atrial tachycardia
Atrial flutter
Atrial fibrillation
Atrioventricular nodal re-entrant tachycardia (AVNRT)
Atrioventricular re-entrant tachycardia (AVRT)

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2
Q

Ventricular tachycardias

A

Ventricular tachycardia
Polymorphic ventricular tachycardia

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3
Q

Accessory pathway

A

Accessory pathway = abnormal connection between the atria and ventricles away from the AVN that allows electrical activity to pass through
If electrical activity is conducted via accessory pathway, it will take an abnormal slow route -> can lead to a broad QRS

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4
Q

Sinus tachycardia

A

Sinus rhythm with a HR > 100 bpm
Normal physiological response when the body is put under stress
-Exercise
-Intercurrent illness
-Underlying pathology
Management is dependent on the underlying cause

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5
Q

Atrial tachycardia

A

Occurs due a abnormal focus of activity undergoing rapid depolarisation in the atria
Different types depending on the origin: single foci, multiple foci & small re-entrant circuit
Usually a regular tachyarrhythmia but multi-focal atrial tachycardia may present with an irregular rhythm
ECG: tachyarrhythmia, with a narrow QRS and abnormal P waves
-Typically there is an abnormal P wave axis with inverted P waves in the inferior leads (II, III, aVF)
Treatment - medications (beta-blockers, calcium channel blockers), ablation (treats certain areas of your heart to stop them improperly conducting electricity) - very helpful in stopping focal atrial tachycardia

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6
Q

Atrial flutter

A

Specific type of atrial tachycardia - that occurs due to a rapid macro-reentrant circuit within the atria
ECG: typically sawtooth pattern, which is best visualised in the inferior leads
Due to fast atrial rate, the AVN causes a ‘block’ (some atrial activity is not conducted to the ventricles)
-Physiological response to allow time for ventricular filling
-Classically seen as a 2:1 block (two flutter waves to one QRS complex)

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7
Q

Atrial fibrillation

A

Occurs due to multiple waves of spontaneous depolarisation leading to fragmentation of normal electrical activity
Causes muscle fibres to contract independently leading to ‘fibrillation’ of the atrial muscle
Multiple waves of electrical activity (varying in strength) reach the AVN -> intermittently conducts these to the ventricles -> irregular rhythm
-Irregularly irregular rhythm
-Absence of P waves
-Irregular, fibrillating baseline

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8
Q

AF rate control

A

Rate control - first-line to many patients
Beta -blocker first-line: atenolol, bisoprolol
Calcium-channel blocker: diltiazem/verapamil
Digoxin: only in sedentary people with persistent AF, requires monitoring & has a risk of toxicity

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9
Q

AF rhythm control

A

Rhythm control - offered to patients with reversible cause for their AF, new onset AF, heart failure caused by AF, symptoms despite being effectively rate controlled
-Cardioversion - immediate and delayed cardioversion
–Immediate - pharmacological or electrical
—Pharmacological - flecainide or amiodarone
—Electrical - aims to shock the heart back into sinus rhythm, involves using a cardiac defibrillator to deliver controlled shocks
-Long-term rhythm control using medications - beta blockers, dronedarone, amiodarone

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10
Q

AF anticoagulation

A

Anticoagulation to prevent strokes
DOACs are first line

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11
Q

Supraventricular tachycardia

A

Can refer to the origin of a tachyarrhythmia or a subset of abnormally fast heart rhythms that are due to reentrant circuits involving the AVN
Clinical practice -> the term SVT is reserved for these reentrant arrhythmias
1) Atrioventricular nodal reentrant tachycardia
2) Atrioventricular reentrant tachycardia

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12
Q

AVNRT

A

Most common SVT - typically occurs in patients with a structurally normal heart
Due to additional conduction pathways within the AVN, which allows initiation of a reentrant circuit
Usually a rapid, narrow-complex tachycardia with absent P waves

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13
Q

AVRT

A

Second most common SVT, usually presents at a younger age than AVNRT & can occur in children
Due to an accessory pathway away from the the AVN
May enable electrical impulses to pass antegrade (atria to ventricles) or retrograde (ventricles to atria)
Difficult to distinguish AVRT from AVNRT on an ECG

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14
Q

Wolff-parkinson-white syndrome

A

Preexcitation syndrome that is characterised by a congenital accessory pathway & episodic tachyarrhythmias
Accessory pathway = usually referred to as the ‘Bundle of Kent’ & can allow conduction antegrade or retrograde
ECG pattern in WPW is due to preexcitation of the ventricles via the accessory pathway
-Short PR interval
-Early slurred upstroke in the QRS complex = delta wave
-Remaining QRS complex is normal - usual conduction via the AVN
Main concern is development of AF -> can deteriorate into ventricular fibrillation

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15
Q

Ventricular tachycardia

A

Occurs due to a focus of electrical activity in the ventricles undergoing rapid depolarisation
Commonly due to scarring of the ventricles following MI
ECG: rapid, broad-complex tachycardia
Life-threatening arrhythmia -> loss of consciousness, loss of CO and cardiac arrest
VT without a pulse is one of the ‘shockable’ cardiac arrest rhythms

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16
Q

Polymorphic VT

A

Particular types of VT that is due to depolarisation of multiple foci within the ventricles leading to variable QRS complexes
Usually secondary to MI

Torsades de pointes - subtype of polymorphic VT
-Characterised by ventricular tachycardia that ‘twists’ around the isoelectric line
-Subtype occurs secondary to a prolonged QT interval
-Management is aimed at shortening the QT interval with IV magnesium sulphate
-If unstable, they should undergo immediate DC cardioversion as with any unstable tachyarrhythmia

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17
Q

Ventricular fibrillation

A

Ventricular muscle fibres contract independently
ECG: coordinated electrical activity with a chaotic, fibrillating baseline
VF is incompatible with life & patients who develop this rhythm will go into cardiac arrest
One of the ‘shockable’ cardiac arrest rhythms that requires immediate DC cardioversion

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18
Q

Escape rhythm

A

Escape rhythm = SAN fails to undergo spontaneous depolarisation so electrical activity is initiated lower down
Can occur as a single beat or a sustained rhythm

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19
Q

Sinus pause/arrest

A

Failure of the SAN to initiate electrical activity
Sinus pause = transient absence of P waves that lasts from 2 seconds to several minutes
Dysfunction of the SAN may manifest as failed initiation of conduction/failed transmission of electrical activity

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20
Q

Sinus node dysfunction (‘sick sinus syndrome’)

A

Collective term that refers to conduction abnormalities affecting the SAN and surrounding tissue
Manifests as a variety of ECG abnormalities: sinus bradycardia, sinus pause/arrest, sinoatrial exit block, chronotropic incompetence
Also associated with atrial tachyarrhythmias
-Tachy-brady syndrome: presents with alternating bradyarrhythmias and tachyarrhythmias
Occurs due to depression of the normal autorhythmicity of the SAN and surrounding tissue

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21
Q

Heart block

A

Interference of the normal transmission of conduction within the AVN can lead to varying degrees of ‘block’
First-degree heart block - prolongation of PR interval > 200ms
Second-degree heart block - underlying conduction disease
Mobitz type I: progressive prolongation of PR interval, leading to dropped QRS
Mobitz type II: randomly dropped QRS
Third-degree heart block - complete dissociation between P waves and QRS complexes on ECG

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22
Q

Bradyarrhythmias clinical features

A

Asymptomatic
Fatigue, lethargy
Dizziness, pre-syncope
Syncope
Pulmonary oedema
Chest pain
Shock
Impaired consciousness

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23
Q

Four cardinal features that suggest an unstable arrhythmia

A

Syncope
Myocardial ischaemia (chest pain)
Heart failure
Shock

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24
Q

Bradyarrhythmias pharmacological management

A

Pharmacological therapy - used in an attempt to increase the heart rate
Atropine (antimuscarinic): reversible antagonist of muscarinic acetylcholine receptors, blocks the action of the vagus nerve on the SAN & AVN -> leads to increased SAN electrical activity and increased conduction through the AVN
Given as IV bolus, which can be repeated
Isoprenaline (non-selective beta-adrenoreceptor agonist): positive inotropic and chronotropic effects on the heart via beta-receptors, leads to an increase in HR and improved contractility
Given as IV infusion

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25
Q

Pacing

A

Delivers electrical stimuli to the heart via pacing leads
May be required in an emergency setting, following MI or a long-term option in patients with bradyarrhythmias
Temporary pacing - transcutaneous, epicardial & transvenous
Permanent pacing - permanent electronic device that is inserted under the skin (pacemaker box is attached to wires which are inserted into the heart via the transvenous route )

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26
Q

Permanent pacemakers

A

Three main types of pacemaker
Single chamber - single lead implanted into the right atrium/ventricle
Dual chamber - two leads implanted, one in the right atrium & one in right ventricle
Biventricular (cardiac resynchronisation) - left ventricular and right ventricular pacing
-Used in heart failure

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27
Q

Stable angina

A

Atherosclerosis affecting the coronary arteries, narrowing the lumen and reducing blood flow to the myocardium
Symptoms only come on with exertion and are always relieved by rest or glyceryl trinitrate (GTN)

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28
Q

Angina baseline investigations

A

Physical examination
ECG
FBC – anaemia
U&Es, LFTs – required before starting medications
Lipid profile
TFTs
HbA1C & fasting glucose (diabetes)

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29
Q

Angina specialist investigations

A

Cardiac stress testing – assessing the patient’s heart function during exertion, can involve having the patient exercise/giving medication (dobutamine)
- Options for assessing cardiac function = ECG, echo, MRI or myocardial perfusion scan
CT coronary angiography – involves injecting contrast and taking CT imaged timed with heart contractions (gives detailed view of coronary arteries, highlighting any narrowing)
Invasive coronary angiography – catheter is inserted into the patient’s brachial/femoral artery -> directed to coronary arteries under x-ray guidance, where contrast is injected to visualise coronary arteries = GOLD STANDARD

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30
Q

Angina principles of management

A

R – refer to cardiology
A – advice them about the diagnosis, management & when to call an ambulance
M – medical treatment
P – procedural or surgical interventions
S – secondary prevention
Referrals sent to rapid access chest pain clinic

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31
Q

Angina medical management

A

1) Immediate symptomatic relief
2) Long-term symptomatic relief
3) Secondary prevention of CVD

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32
Q

Angina immediate symptomatic relief

A

Sublingual glyceryl trinitrate in the form of spray/tablets
GTN causes vasodilation, improving the blood flow to the myocardium
Take GTN when symptoms start, take second dose after 5 mins if symptoms remain, take third dose after 5 mins if symptoms remain, call ambulance after a further 5 mins if symptoms remain
SE: headaches, dizziness

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33
Q

Angina long-term symptomatic relief

A

Beta blocker
Calcium-channel blocker (diltiazem/verapamil – both avoided in HFrEF)
Specialist may consider – long-acting nitrates (isosobide mononitrate), ivabradine, nicorandil, ranolazine

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34
Q

Angina secondary prevention

A

Aspirin 75mg once daily
Atorvastatin 80mg once daily
ACE inhibitor (if diabetes, HTN, CKD, HF present)
Already on a beta blocker for symptomatic relief

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35
Q

Angina surgical interventions

A

Percutaneous coronary intervention (PCI) – catheter into patient’s brachial/femoral artery & guided to coronary arteries, contrast injected, areas of stenosis can be treated by dilating a balloon to widen the lumen (angioplasty) & inserting a stent to keep it open
Coronary artery bypass graft (CABG) – involves opening the chest along the sternum, with a midline sternotomy incision, graft vessel is attached to the affected coronary artery, bypassing the stenotic area
- Saphenous vein
- Internal thoracic artery
- Radial artery
PCI: faster recovery, lower rate of strokes as a complication, higher rate of requiring repeat revascularisation (further procedures)

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36
Q

ACS

A

Result of a thrombus from an atherosclerotic plaque blocking a coronary artery
When a thrombus forms in a fast-flowing artery, it is formed mainly of platelets
3 types – unstable angina, STEMI, NSTEMI

37
Q

Coronary arteries

A

Two coronary arteries branch from the root of the aorta: right coronary artery & left coronary artery
Right coronary artery – curves around the right side and under the heart & supplies the right atrium, right ventricle, inferior aspect of the left ventricle, posterior septal area
Left coronary artery – circumflex artery, left anterior descending
Circumflex artery – curves around the top, left and back of the head & supplies the left atrium and posterior aspect of the left ventricle
Left anterior descending – travels down the middle of the heart & supplies the anterior aspect of the left ventricle, anterior aspect of the septum

38
Q

ACS presentation

A

Central, constricting chest pain
Pain radiating to the jaw/arms
N&V
Sweating and clamminess
Feeling of impending doom
SoB, palpitations
Symptoms should continue at rest for more than 15 mins

39
Q

Artery, heart area, ECG leads

A

Left coronary artery – anterolateral, I, aVL, V3-6
Left anterior descending – anterior, V1-4
Circumflex – lateral, I, aVL, V5-6
Right coronary artery – inferior, II, III, aVF

40
Q

ACS investigations

A

ECG
Troponin
Baseline bloods – FBC, U&E, LFT, lipids, glucose
CXR
Echo

41
Q

ACS initial management

A

CPAIN
C – call an ambulance
P – perform an ECG
A – aspirin 300mg
I – intravenous morphine for pain is required with anti-emetic
N – nitrate (GTN)

42
Q

STEMI management

A

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:
1) Percutaneous coronary intervention (PCI) if available within 2 hours of presenting
2) Thrombolysis (if PCI not available) – involves injecting a fibrinolytic agent, significant risk of bleeding, examples are streptokinase, alteplase & tenecteplase

43
Q

NSTEMI management

A

BATMAN
B – base the decision about angiography and PCI on 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)
Give O2 only if sats < 95%

44
Q

NSTEMI angiography

A

Unstable patients are considered for immediate angiography
GRACE score – 6-month probability of death after having an NSTEMI (above 3% is considered medium to high risk)
Patients at medium to high risk are considered for early angiography with PCI (within 72 hours)

45
Q

ACS ongoing management

A

Echo
Cardiac rehabilitation
Secondary prevention

46
Q

ACS secondary prevention

A

6 As
A – aspirin 75mg once daily indefinitely
A – another antiplatelet (ticagrelor or clopidogrel) for 12 months
A – atorvastatin 80mg once daily
A – ACEi titrated as high as tolerated
A – atenolol (or another beta-blocker, usually bisoprolol) titrated as high as tolerated
A – aldosterone antagonist for those with clinical HF

47
Q

MI complications

A

DREAD
Death
Rupture of the heart septum or papillary muscles
oEdema
Arrhythmia and aneurysm
Dressler’s syndrome

48
Q

Dressler’s syndrome

A

Post-myocardial infarction syndrome
Caused by a localised immune response that results in inflammation of the pericardium -> pericarditis
Presents with pleuritic chest pain, low-grade fever, pericardial rub on auscultation
Can cause a pericardial effusion & rarely a pericardial tamponade
Diagnosis can be made with ECG (global ST elevation & T wave inversion), echocardiogram (pericardial effusion) and raised inflammation markers
Management – NSAIDs and in more severe cases, steroids. Pericardiocentesis may be required to remove fluid from around the heart if there is significant pericardial effusion

49
Q

Pericarditis

A

Inflammation of the pericardium
Most common causes are idiopathic and viral

50
Q

Pericardial effusion

A

Potential space of the pericardial cavity fills with fluid
Creates an inward pressure on the heart, making it more difficult to expand during diastole

51
Q

Pericardial tamponade

A

Pericardial effusion is large enough to raise the intra-pericardial pressure
Increased pressure squeezes the heart -> reduces heart filling in diastole, decreasing CO during systole
Emergency and requires prompt drainage to relieve pressure

52
Q

Pericarditis presentation

A

Chest pain – sharp, central, worse with inspiration, worse on lying down, better on sitting forward
Low-grade fever
Pericardial friction rub on auscultation – rubbing, scratching sound that occurs alongside the heart sounds

53
Q

Pericarditis investigations

A

Blood tests – raised inflammation markers (WCCs, CRP & ESR)
ECG changes – saddle-shaped ST elevation, PR depression
Echo – diagnose a pericardial effusion

54
Q

Pericarditis management

A

NSAIDs – mainstay of treatment
Colchicine – taken longer-term to reduce the risk of recurrence
Steroids are taken second line
Underlying causes should be treated appropriately
Pericardiocentesis may be required to remove fluid from around the heart

55
Q

Acute left ventricular failure

A

Occurs when an acute event results in the left ventricle being unable to move blood efficiently through the left side of the heat & into systemic circulation
Backlog leading to pulmonary oedema

56
Q

Acute LVF triggers

A

Iatrogenic – aggressive IV fluids
MI
Arrhythmias
Sepsis
HTN emergency

57
Q

Acute LVF symptoms and signs

A

Symptoms – SoB, feeling unwell, cough with frothy white/pink sputum
Signs on examination – raised RR, reduced oxygen sats, tachycardia, 3rd heart sound, bilateral basal crackles, hypotension

58
Q

Acute LVF investigations

A

Clinical assessment – history and examination
ECG
Bloods – anaemia, infection, kidney function, BNP
ABG
CXR
Echo

59
Q

B-type natriuretic peptide

A

Hormone released from the heart ventricles when the cardiac muscle is stretched beyond normal range – raised BNP indicates the heart is overloaded beyond its normal capacity to pump effectively
BNP – acts to relax the smooth muscle in blood vessels (reduces systemic vascular resistance) & also acts on kidneys as a diuretic to promote water excretion in the urine
Sensitive but not specific, helps rule out HF when negative

60
Q

Acute LVF management

A

SODIUM
S – sit up
O – oxygen
D – diuretics
I – IV fluids should be stopped
U – underlying causes need to be identified and treated
M – monitor fluid balance
Inotropes & vasopressors

61
Q

Chronic heart failure

A

Refers to the clinical features of impaired heart function, specifically the function of the LV to pump blood out of the heart and around the body
HFrEF = ejection fraction < 50%
HFpEF = ejection fraction > 50%, result of diastolic dysfunction where there is an issue with the left ventricle filling with blood during diastole

62
Q

Chronic HF causes

A

Ischaemic heart disease
Valvular heart disease (aortic stenosis)
HTN
Arrhythmias
Cardiomyopathy

63
Q

Chronic HF presentation

A

Breathlessness, worsened by exertion
Cough
Orthopnoea – breathlessness when lying flat
Paroxysmal nocturnal dyspnoea
Peripheral oedema
Fatigue
Signs – tachycardia, tachypnoea, murmurs, 3rd heart sound, bilateral basal crackles, raised JVP, peripheral oedema

64
Q

Chronic HF investigations

A

Clinical assessment
NT-proBNP
ECG
Echo
Bloods – anaemia, renal function, thyroid function, liver function, lipids, diabetes
CXR and lung function tests to exclude lung pathology

65
Q

New York heart association classification

A

Used to grade the severity of symptoms related to heart failure
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

66
Q

Chronic HF management principles

A

RAMPS
R – refer to cardiology
A – advise them about the condition
M – medical treatment
P – procedural or surgical interventions
S – specialist heart failure MDT input eg. heart failure nurses
Flu, covid and pneumococcal vaccines, stop smoking, optimise treatment of co-morbidities, written care plan, cardiac rehabilitation

67
Q

Nt-proBNP referral criteria

A

400-2000 ng/litre = should be seen and have an echo within 6 weeks
>2000 ng/litre should be seen and have an echo within 2 weeks

68
Q

Chronic HF medical management

A

ABAL
ACE inhibitor
Beta blocker
Aldosterone antagonist
Loop diuretics
U&Es closely monitored – particularly ACEi and aldosterone antagonists (both can cause hyperkalaemia)
Additional specialist treatments – SGLT2 inhibitor, sacubitril with valsartan, ivabradine, hydralazine with a nitrate, digoxin

69
Q

Chronic HF procedural and surgical interventions

A

Implantable cardioverter defibrillators – continually monitor the heart and apply a defibrillator shock to cardiovert the patient back into sinus if they identify a shockable arrhythmia (used if patients who previously has VT/VF)
Cardiac resynchronisation therapy – involves biventricular (triple chamber) pacemakers, the objective is to synchronise the contractions in these chambers to optimise heart function
Heart transplant may be suitable in patients with severe disease

70
Q

Hypertensive emergency

A

Accelerated hypertension (malignant HTN) refers to BP > 180/120, with retinal haemorrhages/papilloedema
Recommended a same-day referral
Require a fundoscopy examination & assessed for secondary causes and end-organ damage
IV options include: sodium nitroprusside, labetalol, GTN, nicardipine

71
Q

Aortic stenosis murmur

A

Narrowing of the aortic valve, restricting blood flow from the left ventricle to the aorta
Causes an ejection-systolic, high-pitched murmur due to high blood flow velocity through the valve
Has a crescendo-decrescendo character
Murmur radiates to the carotids

72
Q

Aortic stenosis signs

A

Thrill in the aortic area on palpation
Slow rising pulse
Narrow pulse pressure (different between systolic and diastolic BP)
Exertional syncope

73
Q

Aortic stenosis causes

A

Idiopathic age-related calcification
Bicuspid aortic valve
Rheumatic heart disease

74
Q

Aortic regurgitation murmur

A

Incompetent aortic valve, allowing blood to flow back from the aorta into the left ventricle
Typically causes an early diastolic, soft murmur
Austin-flint murmur: heard at the apex as a diastolic ‘rumbling’ murmur – caused by blood flowing back through the aortic valve and over the mitral valve causing it to vibrate

75
Q

Aortic regurgitation signs

A

Thrill in the aortic area on palpation
Collapsing pulse – forcefully appearing and rapidly disappearing
Wide pulse pressure
HF and pulmonary oedema

76
Q

Aortic regurgitation causes

A

Idiopathic age-related weakness
Bicuspid aortic valve
Connective tissue disorders – EDS, Marfan syndrome

77
Q

Mitral stenosis murmur

A

Narrowed mitral valve restricting blood flow from the left atrium into the left ventricle
Mid-diastolic, low-pitched rumbling murmur, loud S1, opening snap after S2

78
Q

Mitral stenosis signs

A

Tapping apex beat
Malar flush – due to back pressure of blood into the pulmonary system, causing a rise in CO2 and vasodilation
AF

79
Q

Mitral stenosis causes

A

Rheumatic heart disease
Infective endocarditis

80
Q

Mitral regurgitation murmur

A

Incompetent mitral valve allowing blood to flow back from the left ventricle to the left atrium
Pan-systolic, high pitched whistling murmur, radiates to the left axilla, may heart a third heart sound

81
Q

Mitral regurgitation signs

A

Thrill in the mitral area on palpation
Signs of HF and pulmonary oedema
AF

82
Q

Mitral regurgitation causes

A

Idiopathic weakening of the valve with age
Ischaemic heart disease
Infective endocarditis
Rheumatic heart disease
Connective tissue disorders – EDS, Marfan

83
Q

Tricuspid regurgitation murmur

A

Incompetent tricuspid valve, allowing blood to flow back from the right ventricle to the right atrium during systolic contraction
Pan-systolic murmur, split second heart sound due to pulmonary valve closing earlier than the aortic valve

84
Q

Tricuspid regurgitation signs

A

Thrill in tricuspid area on palpation
Raised JVP with giant C-V waves (Lancisi’s sign)
Pulsatile liver
Peripheral oedema
Ascites

85
Q

Tricuspid regurgitation causes

A

Pressure due to left sided HF or pulmonary HTN
Infective endocarditis
Rheumatic heart disease
Carcinoid syndrome
Ebstein’s anomaly
Connective tissue disorders

86
Q

Pulmonary stenosis murmur

A

Narrowed pulmonary valve, restricting blood flow from the RV into the pulmonary arteries
Ejection systolic murmur loudest in the pulmonary area with deep inspiration, widely split secondary heart sound

87
Q

Pulmonary stenosis signs

A

Thrill in pulmonary area on palpation
Raised JVP with giant A waves
Peripheral oedema
Ascites

88
Q

Pulmonary stenosis causes

A

Usually congenital & may be associated with Noonan syndrome or tetralogy of Fallot

Y3 medicine (10 decks)

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