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Cardiology Flashcards

1
Q

What causes atherosclerosis?

A

Chronic inflammation and activation of the immune system-> lipid deposition-> atheromatous plaques

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2
Q

What do atherosclerotic plaques cause?

A
  • Stiffening of the artery wall (hypertension and heart strain)
  • Stenosis + reduced blood flow (angina)
  • Plaque rupture + thrombus (ischaemia)
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3
Q

Non-modifiable risk factors for atherosclerosis?

A

Older age, family history, male

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4
Q

Modifiable risk factors for atherosclerosis?

A

Smoking, alcohol, diet, low exercise, obesity, poor sleep, stress

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5
Q

Medical comorbidities that increase the risk of atherosclerosis?

A

Diabetes, HTN, CKD, inflammatory conditions (eg RA), atypical antipsychotics

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6
Q

Primary prevention of CVD?

A
  • When never had CVD before
  • QRISK 3 score
  • Give atorvastatin 20mg when-> 10% risk or more, CKD, T1DM
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7
Q

When should statins be stopped (in terms of LFT results)?

A

When ALT/AST rise to more than 3x upper limit of normal

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8
Q

Secondary prevention of CVD?

A

4A’s-> Aspirin (+clopidogrel for 12 months after event), Atorvastatin 80mg, Atenolol (or bisoprolol), ACE inhibitor (eg ramipril)

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9
Q

Side effects of statins?

A
  • Myopathy
  • Type 2 DM
  • Haemorrhagic strokes
  • Deranged LFTs
  • Rhabdomyolysis
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10
Q

What is stable angina?

A
  • When a narrowing of the CAs reduces blood flow to myocardium causing symptoms
  • Stable when symptoms relieved by rest or GTN spray
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11
Q

Gold standard investigation for stable angina?

A

CT coronary angiography

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12
Q

Baseline investigations in stable angina?

A

Examination, ECG, FBC, U+Es, LFTs, lipid profile, TFTs HbA1C, fasting glucose

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13
Q

General management for stable angina?

A

RAMP-> refer to cardio, advise about management, medical treatment, procedure/surgery

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14
Q

Medical management of stable angina?

A
  • Immediate relief-> GTN spray, repeat after 5 mins, call 999 if still pain
  • Long term-> beta-blocker or CCB, or long acting nitrate, ivabradine, nicorandil etc
  • Secondary prevention-> aspirin, atorvastatin, ACE inhibitor
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15
Q

What does primary PCI entail?

A
  • Percutaneous coronary intervention (PCI) with coronary angioplasty (dilate vessel with balloon and/or stent)
  • Catheter via brachial or femoral artery
  • Contrast injected
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16
Q

What is CABG?

A
  • Coronary artery bypass graft
  • Graft vein from leg (eg great saphenous vein) + sew onto CA to bypass stenosis
  • Leaves midline sternotomy scar
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17
Q

What does the RCA supply?

A

RA, RV, inferior of LV, posterior septal area

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18
Q

What does the circumflex artery supply?

A

LA and posterior LV

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19
Q

What does the LAD artery supply?

A

Anterior LV + anterior septum

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20
Q

Diagnosis of STEMI?

A

ST elevation or new LBBB on ECG

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21
Q

Diagnosis of NSTEMI?

A
  • ST depression, T wave inversion or pathological Q waves on ECG
  • Raised troponin levels
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22
Q

Diagnosis of unstable angina?

A

Symptoms but no ECG changes or raised troponin

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23
Q

Symptoms of ACS?

A
  • Central crushing chest pain, sweating, N+V, SOB, palpitations, pain radiating to jaw/arms
  • Symptoms usually last 20+ minutes at rest
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24
Q

What is a silent MI?

A

ACS in a diabetic patient-> might not get typical chest pain

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25
Q

What area of the heart would ECG changes in leads I, aVL and V3-6 suggest?

A

Left coronary artery (anterolateral)

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26
Q

What area of the heart would ECG changes in leads V1-4 suggest?

A

LAD (anterior)

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27
Q

What area of the heart would ECG changes in leads I, aVL, V5-6 suggest?

A

Circumflex (lateral)

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28
Q

What area of the heart would ECG changes in leads II, III, aVF suggest?

A

RCA (inferior)

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29
Q

When should troponin levels be taken?

A

Baseline, 6 hours and 12 hours after symptom onset

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30
Q

What might a raised troponin level suggest?

A
  • Myocardial ischaemia

- CKD, sepsis, myocarditis, aortic dissection, PE

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31
Q

Investigations for ACS?

A
  • Bloods-> FBC, U+Es, LFTs, lipid profile, TFTs HbA1C, fasting glucose
  • ECG
  • CXR
  • Echo-> functional damage
  • CT coronary angiogram
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32
Q

When is primary PCI an available treatment option for STEMI?

A

Within 2 hours of presentation

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33
Q

When is thrombolysis an available treatment option for STEMI?

A

Within 12 hours of symptom onset + PCI not available within 2 hours

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34
Q

What is thrombolysis?

A
  • Use of fibrinolytic medication to break down fibrin + dissolve clot
  • Can use streptokinase, alteplase or tenecteplase
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35
Q

Acute treatment of NSTEMI?

A

BATMAN-> beta-blockers, aspirin 300mg, ticagrelor (or clopidogrel), morphine, anticoagulant (eg fondaparinux), nitrates (eg GTN)

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36
Q

What is the GRACE Score for PCI in NSTEMI?

A
  • 6 month risk of death or repeat MI after NSTEMI

- If medium or high risk (5% risk or more) then considered for early PCI (within 4 days of admission)

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37
Q

Complications of MI?

A

DREAD-> Death, Rupture of heart septum/papillary muscles, Edema (HF), Arrhythmia, Aneurysm, Dressler’s Syndrome

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38
Q

What is Dressler’s syndrome?

A
  • Localised immune response + pericarditis 2-3 weeks post-MI
  • Pleuritic chest pain
  • Global ST elevation + T wave inversion on ECG
  • Raised inflammatory markers
  • Managed with NSAIDs + steroids + sometimes pericardiocentesis
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39
Q

Secondary prevention post-ACS?

A
  • Aspirin 75mg
  • Another antiplatelet-> clopidogrel or ticagrelor for 12 months
  • Atorvastatin 80mg
  • ACE-inhibitor
  • Atenolol or bisoprolol
  • Aldosterone antagonist (when clinical HF eg eplerenone)
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40
Q

What are the 4 types of MI?

A
  • 1-> traditional MI (acute coronary event)
  • 2-> ischaemia secondary to increased demand or reduced supply of oxyge
  • 3-> sudden cardiac death/arrest suggestive of ischaemic event
  • 4-> associated with PCI/stenting/CABG
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41
Q

Pathophysiology of acute LVF?

A

LV unable to move blood through to body-> backlog of blood in LA + pulmonary veins + lungs-> increased pressure in vessels + leak interstitial fluid (pulmonary oedema)-> interferes with gas exchange

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42
Q

Triggers of acute LVF?

A

Iatrogenic (eg IV fluids), sepsis, MI, arrhythmias

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43
Q

Symptoms of acute LVF?

A
  • Rapid onset breathlessness exacerbated by lying flat
  • Type 1 resp failure
  • SOB, unwell
  • Frothy white/pink sputum + cough
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44
Q

Examination findings in acute LVF?

A
  • Increased RR, reduced sats, tachycardia, 3rd heart sound, bilateral basal crackles, cardiogenic shock (severe)
  • If RVF present-> raised JVP + peripheral oedema
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45
Q

Investigations for acute LVF?

A
  • B-type Natriuretic Peptide (BNP) blood test
  • Bloods-> infection, kidney, troponin etc
  • ECG
  • ABG
  • CXR
  • Echo
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46
Q

What is the BNP blood test?

A
  • Hormone released from ventricles when myocardium stretched beyond normal range
  • Acts to relax smooth muscles in vessels + reduce systemic vascular resistance (easier for heart to pump blood)
  • Acts as diuretic
  • Can be raised in heart failure, tachycardia, sepsis, PE, renal impairment, COPD
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47
Q

What is ejection fraction and what level is considered as normal?

A
  • % of blood in LV squeezed out with contraction

- Normal-> >50%

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48
Q

Signs of heart failure on CXR?

A
  • Alveolar oedema-> Bat wing sign
  • Kerley B lines (fluid in septal lines)
  • Cardiomegaly-> >50% diameter of lung fields
  • DIlated upper lobe vessels-> venous diversion, larger diameter of upper lobe vessels
  • Effusions-> pleural
  • Fluid in interlobar fissures
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49
Q

Management of acute LVF?

A

Pour SOD->

  • Stop IV fluids + monitor balance
  • Sit up-> leave upper lobes clear for gas exchange
  • Oxygen
  • Diuretics-> IV furosemide 20-50mg stat

In severe->

  • IV opiates (vasodilators)
  • NIV eg CPAP
  • Inotropes-> noradrenaline, to strengthen contractions, in HDU/ICU
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50
Q

What is chronic heart failure?

A

Impaired LV contraction (systolic) or LV relaxation (diastolic) causing back-pressure of blood through left side of heart

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51
Q

Symptoms of chronic heart failure?

A
  • Breathless on exertion
  • Cough + frothy pink/white sputum
  • Orthopnoea-> SOB when lying flat
  • Paroxysmal nocturnal dyspnoea-> wake up in the night feeling SOB
  • Peripheral oedema
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52
Q

Investigations for chronic heart failure?

A
  • Clinical presentation
  • BNP
  • Echo
  • ECG
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53
Q

Causes of chronic HF?

A

IHD, valvular disease (eg aortic stenosis), HTN, arrythmias (AF)

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54
Q

Management of chronic HF?

A
  • Referral when BNP >2000ng/L
  • ACE-i (or ARB)
  • Beta-blocker
  • Aldosterone antagonist when not controlled (eg spironolactone)
  • Loop diuretics for symptoms
  • Surgical if underlying cause
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55
Q

What is cor pulmonale?

A
  • Right sided heart failure caused by respiratory disease
  • Increased pressure in pulmonary arteries (pulmonary HTN) -> RV unable to pump effectively-> back pressure to RA + VC + systemic venous system
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56
Q

Causes of cor pulmonale?

A

COPD, PE, interstitial lung disease, CF, primary pulmonary HTN

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57
Q

Symptoms and signs of cor pulmonale?

A
  • SOB, peripheral oedema, syncope, chest pain

- Cyanosis, raised JVP, oedema, 3rd heart sound, murmurs (eg pan-systolic in tricuspid regurg), hepatomegaly

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58
Q

Treatment of cor pulmonale?

A

Treat underlying cause + long term oxygen therapy

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59
Q

Diagnosis of hypertension?

A

BP above 140/90 (clinic) or 135/85 (home)

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60
Q

Most common cause of HTN?

A

Essential or primary HTN (ie no secondary cause) in 95%

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61
Q

Causes of secondary hypertension?

A

ROPE-> renal disease, obesity, pregancy induced/pre-eclampsia, endocrine (eg Conn’s syndrome)

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62
Q

Complications of HTN?

A

IHD, CVA, retinopathy, nephropathy, HF

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63
Q

When should blood pressure be measured to screen for HTN?

A
  • Every 5 years
  • More often when on borderline for diagnosis
  • Yearly in type 2 DM
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64
Q

What are the different stages of HTN?

A
  • Stage 1-> 140/90 or 135/85
  • Stage 2-> 160/100 or 150/95
  • Stage 3-> 180/120
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65
Q

Investigations for end organ damage in HTN?

A
  • Urine albumin:creatinine ratio + dipstick-> kidney damage
  • Bloods-> HbA1C, renal, lipids
  • Fundus exam
  • ECG
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66
Q

Management of HTN in aged <55 or non-black?

A
  • 1-> ACE i or ARB
  • 2-> ACE i or ARB + CCB or TLD
  • Step 3-> ACEi/ARB + CCB + TLD
  • Step 4-> add spironolactone (when K+ <4.5mmol/L) or alpha/beta blocker (when K+ >4.5mmol/L)
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67
Q

Management of HTN in aged >55 or black + any age?

A
  • 1-> CCB
  • 2-> CCB + ACE i or ARB or TLD
  • Step 3-> CCB + ACEi/ARB + TLD
  • Step 4-> add spironolactone (when K+ <4.5mmol/L) or alpha/beta blocker (when K+ >4.5mmol/L)

ARBs are preferred over ACEis in black patients

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68
Q

Treatment targets in HTN?

A
  • <80 years-> <140/90

- >80 years-> <150/90

69
Q

What causes the first heart sound (S1)?

A

Tricuspid + mitral valve closure at the start of systolic contraction of ventricles

70
Q

What causes the second heart sound (S2)?

A

Semilunar valve closure (pulmonary + aortic valves) when systolic contraction complete

71
Q

What causes a third heart sound (S3)?

A
  • Rapid ventricular filling causes chordae tendineae to pull + ‘twang’
  • Normal in 15-40 year olds
  • Can indicate heart failure as ventricles become stiff + weak
72
Q

What causes a fourth heart sound (S4)?

A
  • Directly before S1

- Stiff/hypertrophic ventricle + turbulent flow from atria to ventricle

73
Q

What are the four valve areas when listening for murmurs?

A
  • Pulmonary-> 2nd ICS left sternal border
  • Aortic-> 2nd ICS right sternal border
  • Tricuspid-> 5th ICS left sternal border
  • Mitral-> 5th ICS mid-clavicular line
  • Erb’s point-> 3rd ICS left sternal border (for S1 + S2)
74
Q

How to assess a murmur?

A

SCRIPT

  • Site-> where it’s loudest
  • Character-> soft, blowing, crescendo-descresendo etc
  • Radiation-> carotids (AS) or left axilla (MR)?
  • Intensity-> grade (1-6)
  • Pitch (indicates velocity)
  • Timing-> systolic or diastolic
75
Q

What effect does mitral stenosis have on the heart muscle?

A

LA hypertrophy-> as has to try harder to push blood out of stenosed valve

76
Q

What effect does aortic stenosis have on the heart muscle?

A

LV hypertrophy-> as has to try harder to push blood out of stenosed valve

77
Q

What effect does mitral regurgitation have on the heart muscle?

A

LA dilatation-> leaky valve allows backflow into chamber + stretches muscle

78
Q

What effect does aortic regurgitation have on the heart muscle?

A

LV dilatation-> leaky valve allows backflow into chamber + stretches muscle

79
Q

What type of murmur does mitral stenosis cause?

A
  • Mid-diastolic, low pitched, rumbling (low velocity)

- Loud S1-> thick valves need large force to shut

80
Q

What other features is mitral stenosis associated with?

A
  • Malar flush-> back pressure of blood to pulmonary system

- AF-> LA struggles to push blood

81
Q

Causes of mitral stenosis?

A

Rheumatic heart disease, infective endocarditis

82
Q

What type of murmur does mitral regurgitation cause?

A
  • Pansystolic + high pitched + whilstling-> high velocity
  • Radiates to left axilla
  • May have 3rd heart sound
83
Q

Causes of mitral regurgitation?

A

Idiopathic (age), IHD, infective endocarditis, rheumatic heart disease, Ehlers-Danlos, Marfan syndrome

84
Q

What does mitral regurgitation result in?

A

Congestive cardiac failure

85
Q

What murmur does aortic stenosis cause?

A
  • Ejection-systolic, high pitched, crescendo-decrescendo-> due to speed of blood flow during systole
  • Radiates to carotids
86
Q

Signs of aortic stenosis?

A
  • Slow rising pulse + narrow pulse pressure

- Exertional syncope

87
Q

Causes of aortic stenosis?

A

Idiopathic age-related calcification or rheumatic heart disease

88
Q

What murmur does aortic regurgitation cause?

A
  • Early diastolic, soft

- Austin-Flint-> diastolic rumbling murmur, heard at apex, as blood back through aortic + over mitral causing vibration

89
Q

What clinical sign is aortic regurgitation associated with?

A

Collapsing/Corrigan’s pulse-> rapid appear + disappearing pulse at carotids (blood out then back in)

90
Q

Causes of aortic regurgitation?

A

Idiopathic.age, connective tissue disorders

91
Q

What scars will someone with a valve replacement typically have?

A
  • Midline sternotomy (mitral/aortic/CABG)

- Right sided mini-thoracotomy (mitral)

92
Q

How long do bioprosthetic heart valves last?

93
Q

How long do mechanical valves last and what is needed to be prescribed alongside them?

A
  • 20+ years

- Warfarin therapy (lifelong) with INR target of 2.5-3.5

94
Q

Complications of mechanical heart valves?

A
  • Thrombus formation
  • Infective endocarditis
  • Haemolysis + anaemia (blood churned up in valve)
95
Q

Treatment for severe aortic stenosis?

A

TAVI (transcatheter aortic valve implantation)-> catheter in femoral, X ray guidance, implant bioprosthetic valve

96
Q

What organisms typically cause infective endocarditis?

A
  • Staphylococcus
  • Streptococcus
  • Enterococcus
97
Q

Pathophysiology of atrial fibrillation?

A
  • Disorganised electrical activity overrides that of SAN-> unco-ordinated + rapid atrial contraction
  • Blood tends to collect in atria + clot-> emboli + strokes
98
Q

Signs of atrial fibrillation?

A
  • Irregularly irregular ventricle contractions
  • Tachycardia
  • HF
  • No P waves on ECG
99
Q

Symptoms of AF?

A

None, palpitations, SOB, syncope, symptoms of other conditions (eg stroke)

100
Q

What is valvular AF?

A

When patient has AF alongside mitral stenosis or mechanical heart valve-> valve pathology leads to AF

101
Q

Causes of AF?

A

Mrs SMITH-> sepsis, mitral valve pathology, IHD, thyrotoxicosis, HTN

102
Q

When is rate control used 1st line in AF and what is the treatment aim?

A
  • All with AF-> onset >48 hours

- Aim to get HR <100

103
Q

When is rhythm control used 1st line in AF and what is the treatment aim?

A
  • Onset <48 hours, there is a reversible cause, the AF is causing heart failure, or symptoms despite rate control
  • Return to normal sinus rhythm
104
Q

What are the options for rate control in AF?

A
  • Beta blocker 1st line
  • CCB eg diltiazem (not in HF)
  • Digoxin (when sedentary)
105
Q

When is immediate cardioversion used for AF?

A

When AF present for <48 hours or haemodynamically unstable

106
Q

When is delayed cardioversion used in AF?

A
  • When stable + present for >48 hours

- Need anticoagulation for 3+ weeks before (prevent clots forming + mobilising + causing stroke)

107
Q

What is used for short-term pharmacological cardioversion in AF?

A
  • Flecainide

- Amiodarone-> when structural heart disease

108
Q

What does electrical cardioversion involve?

A
  • Rapid shock into sinus rhythm
  • Sedation or GA
  • Cardiac defibrillator
109
Q

What options are there for long-term medical rhythm control in AF?

A
  • Beta blockers
  • Dronedarone (when had successful cardioversion)
  • Amiodarone (HF or LV dysfunction)
110
Q

What is paroxysmal AF?

A
  • Episodes of AF lasting <48 hours
  • Anticoagulate based on CHADSVASc score
  • May have ‘pill in pocket’ approach when having episodes (flecanide)
111
Q

Why should flecanide be avoided in atrial flutter?

A

Can cause 1:1 AV conduction and significant tachycardia

112
Q

How much does anticoagulation affect risk of stroke in AF?

A

It reduces the risk by about 2/3rd

113
Q

How does warfarin work?

A
  • Vitamin K antagonist

- Prolongs the prothrombin time (ie takes longer to clot)

114
Q

What is the usual INR target for patients with AF taking warfarin?

115
Q

What may influence a patient’s INR level when on warfarin?

A
  • CYP450 inducers and inhibitors-> includes alcohol

- Foods containing vitamin K-> leafy green veg

116
Q

What can be used to reverse the effects of apixaban and rivaroxaban?

A

Andexanet alfa

117
Q

What can be used to reverse the effects of dabigatran?

A

Idarucizumab

118
Q

Why are DOACs preferred over warfarin?

A
  • No monitoring requirements
  • No major interactions
  • Equal or better risk of preventing stroke
  • Equal or less risk of bleeding
119
Q

What is the CHA2DS2-VASc scoring tool used for?

A
  • Assess whether a patient with AF should be put on anticoagulants
  • Risk of stroke/TIA
120
Q

What should be done when a patient has a CHA2DS2-VASc score of 1?

A

Consider anticoagulation

121
Q

What should be done when a patient has a CHA2DS2-VASc score of more than 1?

A

Offer anticoagulation

122
Q

What are the components of the CHA2DS2-VASc scoring tool?

A
  • Congestive heart failure
  • HTN
  • Age 75 + (scores 2)
  • Diabetes
  • Stroke or TIA previously (scores 2)
  • Vascular disease
  • Age 65-74
  • Sex (female)
123
Q

What is the HAS-BLED scoring tool used for?

A
  • Establish patient’s risk of major bleeding when on anticoagulation
  • Risk of stroke usually more than of bleed + is harder to treat
124
Q

What are the components of the HASBLED scoring tool?

A 
Hypertension
Abnormal renal or liver function
Stroke
Bleeding
Labile INRs (when on warfarin)
Elderly
Drugs or alcohol
125
Q

Which cardiac arrest rhythms are shockable?

A
  • ventricular tachycardia

- ventricular fibrillation

126
Q

Which cardiac arrest rhythms are non-shockable?

A
  • Pulseless electrical activity (ie any except VF + VT)

- Asystole

127
Q

Treatment for tachycardia (unstable patient)?

A
  • Consider 3 synchronised shocks

- Consider amiodarone infusion

128
Q

What rhythms may fall under the narrow complex tachycardia (QRS <0.12s) category?

A

AF, atrial flutter, supraventricular tachycardias

129
Q

Treatment for atrial flutter?

A
  • Rate control with beta-blocker or cardioversion
  • Radiofrequency ablation of re-entrant rhythm
  • Anticoagulation
130
Q

Acute treatment for SVT?

A
  • Vagal manouvres-> valsalva manouvre, carotid sinus massage
  • Adenosine rapid bolus-> slows cardiac condution through AVN + interrupt AVN/accessory pathway
  • Direct current cardioversion
131
Q

What rhythms may fall under the broad complex tachycardia (QRS >0.12s) category?

A
  • Ventricular tachycardia
  • SVT with bundle branch block
  • AF
132
Q

What is atrial flutter?

A
  • Re-entrant rhythm-> electrical signal re-circulates in atria due to extra electrical activity-> 300bpm atrial contraction
  • Signal to ventricles every 2nd lap-> 150bpm venticular rate
133
Q

What does atrial flutter look like on an ECG?

A
  • Ventricular rate of 150bpm

- Sawtooth appearance-> P waves repeating

134
Q

Causes of atrial flutter?

A

HTN, IHD, cardiomyopathy, thyrotoxicosis

135
Q

What causes supraventricular tachycardia?

A

Electrical signal re-entering the atria from ventricles-> self-perpetuating loop + cause narrow complex tachycardia

136
Q

What does SVT look like on an ECG?

A
  • QRS <0.12 seconds

- QRS the immediate T wave then repeats

137
Q

What are the different types of SVT?

A
  • AV nodal re-entrant tachycardia-> re-entry point back through AVN
  • AV re-entrant tachycardia-> WPW syndrome (accessory)
  • Atrial tachycardia-> signal starts somewhere other than SAN
  • Paroxysmal-> SVT recurs + remits over time
138
Q

What do you need to warn the patient about when giving them adenosine?

A

Will get a scary feeling of impending doom-> brief asystole or bradycardia

139
Q

Contraindications of adenosine?

A

Asthma, COPD, HF, heart block, severe hypotension

140
Q

Long term treatment of paroxysmal SVT?

A
  • Meds-> beta-blockers, CCBs, amiodarone

- Radiofrequency ablation

141
Q

What is Wolff-Parkinson White syndrome?

A

Extra pathway (Bundle of Kent) between atria + ventricles

142
Q

What ECG changes might be present in WPW syndrome?

A
  • Short PR interval (<0.12s)
  • Wide QRS (>0.12s)
  • Delta wave-> slurred upstroke of QRS complex
143
Q

Treatment of WPW syndrome?

A
  • Radiofrequency ablation of accessort pathway

- NOT antiarrhythmic meds-> may promote conduction through accessory

144
Q

When can radiofrequency ablation be used?

A

AF, atrial flutter, SVTs, WPW syndrome

145
Q

What is torsades de pointes?

A
  • Polymorphic ventricular tachycardia
  • QRS seems to twist around baseline
  • Can spontaneously resolve or cause VT + cardiac arrest
146
Q

Pathophysiology of torsades de pointes?

A

Prolonged QT interval-> repolarisation delayed so random depolarisation of some myocytes-> spread + cause recurrent contractions without normal repolarisation-> torsades de pointes

147
Q

Causes of prolonged QT interval?

A
  • Inherited-> long QT syndrome
  • Medications-> antipsychotics, citalopram, flecainide, sotalol, amiodarone, macrolide antibiotics
  • Electrolyte disturbances-> hypokalaemia, hypomagnesia, hypocalcaemia
148
Q

Acute management of torsades de points?

A
  • Correct underlying cause
  • Magnesium infusion
  • Defibrillation (when VT)
149
Q

Long term management of torsades de pointes?

A
  • Avoid medications that cause prolonged QT
  • Beta blockers (not sotalol)
  • Pacemaker or implantable defibrillator
150
Q

What are ventricular ectopics?

A

Premature ventricular beats caused by random electrical discharges from outside the atria

151
Q

Presentation of ventricular ectopics?

A
  • Random palpitations
  • All ages + can be in healthy patients
  • Common in IHD or HF
  • Random broad QRS complexes on normal ECG
152
Q

What is bigeminy?

A

Ventricular ectopics after every sinus beat (ie 1:1)

153
Q

Management of ventricular ectopics?

A
  • Bloods-> anaemia, electrolytes, thyroid
  • Reassurance
  • May need referral if other conditions
154
Q

What is 1st degree heart block?

A
  • Prolonged PR interval (>0.2s)

- Delayed conduction through AVN

155
Q

What is second degree heart block?

A

-Some instances of p waves not leading to QRS complexes

156
Q

What is second degree heart block (Mobitz Type I ie Wenckebach’s phenomenon)?

A
  • Atrial impulses gradually weaken till doesn’t pass through AVN
  • Increasing PR interval then absent QRS after a P wave
157
Q

What is second degree heart block (Mobitz type II)?

A
  • Intermittent failure or interruption of AV conduction
  • Usually set ratio
  • Risk of asystole
158
Q

What is 2:1 heart block?

A
  • 2 p waves for each QRS complex

- Can be Mobitz type I or II

159
Q

What is third degree heart block?

A
  • Complete heart block-> no relationship between P and QRS

- Risk of asystole

160
Q

Treatment for bradycardia or AVN blocks (when stable)?

161
Q

Treatment for bradycardia or AVN blocks (when unstable or risk of asystole)?

A
  • 1st-> atropine 500mcg IV
  • No improvement-> repeat atropine, inotropes, transcutaneous cardiac pacing
  • High risk of asystole-> temporary transvenous cardiac pacing or permanent pacemaker
162
Q

How does atropine work?

A

Antimuscarinic-> inhibits parasympathetic nervous system

163
Q

Side effects of atropine?

A

Antimuscarinic + pupil dilation

164
Q

What is a pacemaker?

A
  • Deliver controlled electrical impulses to the heart to restore normal activity
  • Pulse generator + pacing leads
  • Monitors activity + tailors function to that
165
Q

What interventions are contraindicated when a patient has a pacemaker?

A
  • MRI scan
  • TENS machine
  • Diathermy in surgery
  • Cremation
166
Q

What are the indications for a pacemaker?

A

Symptomatic bradycardias, Mobitz type 2 AV block, 3rd degree heart block, severe HF, hypertrophic obstructive cardiomyopathy

167
Q

What are the different types of pacemaker?

A
  • Single chamber-> in RA or RV
  • Dual chamber-> RA + RV
  • Biventricular (triple chamber aka cardiac resynch therapy)-> RA + RV + LV
  • Implantable cardioverter defibrillators-> cardiovert if identify shockable arrhythmia
168
Q

What ECG changes might be present in a patient with a pacemaker?

A
  • Line before P or QRS but not both-> single chamber

- Line before P and QRS-> dual chamber

Medicine (13 decks)

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