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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is cardiovascular disease

A

Chronic inflammation and activation of immune system in artery walls

Affects medium and large arteries

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2
Q

What do deposits of lipids in artery walls do

A

Stiffen (causing hypertension and putting additional strain on heart)

Stenose (reducing blood flow)

Rupture (give off thrombus that can lodge elsewhere)

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3
Q

What are the non-modifiable risk factors for cardiovascular disease

A

Older age

Family history

M>F

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4
Q

What are the modifiable risk factors for cardiovascular disease

A

Smoking

Alcohol

Poor diet (high in sugars and fats)

Low exercise

Obesity

Poor sleep

Stress

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5
Q

What are the co-morbidities associated with cardiovascular disease

A

Diabetes

Hypertension

CKD

Inflammatory conditions

Atypical antipsychotic medications

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6
Q

What are the end results of atherosclerosis

A

Angina

Myocardial infarction

Transient ischaemic attack

Stroke

Peripheral vascular disease

Chronic mesenteric ischaemia

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7
Q

What is the QRISK3 score

A

Percentage risk that a person will have a stroke or MI in the next 10 years

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8
Q

What should be done if a QRISK score is > 10%

A

Start a statin

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9
Q

What are the NICE statin use recommendations

A

Check lipids every 3 months

Check adherence before increasing dose

Check LFTs at 3 and 12 months (causes rise in ALT and AST, tolerate if up to 3 times normal)

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10
Q

What are the 4 As of secondary prevention of cardiovascular disease

A

Aspirin (plus a second antiplatelet)

Atorvastatin

Atenolol (or another beta blocker)

ACE inhibitor

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11
Q

What are the side effects of statins

A

Myopathy (check creatinine kinase if muscle pain/weakness)

T2DM

Haemorrhagic stroke

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12
Q

What is angina

A

Narrowing of coronary arteries causing reduced blood flow to myocardium

During exertion

Constricting chest pain

May radiate to arm/jaw

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13
Q

What are the 2 types of angina

A

Stable (relied by rest or GTN)

Unstable (come on at rest, considered an ACS)

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14
Q

What are the high risk factors for angina

A

Diabetes

Smoking

Hyperlipidaemia

Hypertension

Family history

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15
Q

What investigations are needed for angina

A

CT coronary angiograph (gold standard)

ECG

FBC, U&Es, LFTs, bone profile, TFTs, HbA1c

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16
Q

What are the appropriate investigations based on the likelihood of coronary artery disease

A

61-90%: invasive coronary angiography

30-60%: stress MRI, ECHO

10-29%: CT calcium scoring

Men over 70: assume likelihood >90%

Women over 70: assume likelihood 61-90%

Women at high risk and have typical symptoms: >90%

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17
Q

What is the medical management for stable angina that gives immediate relief

A

GTN

PRN, causes vasodilation.

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18
Q

What are the medical managements for stable angina that gives long term relief

A

Beta blockers

Calcium channel blockers

Second line: long acting nitrates (ivabradine, nicorandil)

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19
Q

What is the secondary prevention for stable angina

A

Aspirin (75mg OD)

Atorvastatin (80mg OD)

ACE inhibitors

Beta blockers

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20
Q

What is the surgical management for stable angina

A

Percutaneous coronary intervention (PCI) with coronary angioplasty

Coronary artery bypass graft (CABG)

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21
Q

What are the causes of non-cardiac chest pain

A

Costochondritis

GORD

PE

Pneumonia

Pneumothorax

Psychogenic/psychomotor

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22
Q

Which parts of the heart does the right coronary artery supply

A

Right atrium

Right ventricle

Inferior left ventricle

Posterior septal area

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23
Q

Which parts of the heart does the circumflex artery supply

A

Left atrium

Posterior left ventricle

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24
Q

Which parts of the heart does the left anterior descending artery supply

A

Anterior left ventricle

Anterior septal area

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25
Q

What are the 3 types of acute coronary syndrome

A

Unstable angina

STEMI

NSTEMI

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26
Q

What are the symptoms of acute coronary syndrome

A

Central, constricting chest pain

Nausea and vomiting

Sweating, clamminess

Feeling of impending doom

Shortness of breath

Palpitations

Pain radiating to jaw/arm

Symptoms continue for 20 mins at rest

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27
Q

What investigations are needed for acute coronary syndrome

A

ECG

Troponin

FBC, U&Es, LFTs, lipid profile, TFTs, HbA1c

CXR/CT coronary angiogram

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28
Q

What are the ECG signs of STEMI

A

ST elevation in 2+ leads from the same zone

New left bundle branch block

ST depression in V1-V4

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29
Q

What conditions can mimic STEMI on ECG

A

Pericarditis

Brugada syndrome

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30
Q

What are the ECG signs of NSTEMI

A

ST depression

Deep T wave inversion

Pathological Q waves

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31
Q

What are the ECG signs of unstable angina

A

ST depression

T wave inversion

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32
Q

How long after myocardial damage does troponin start to rise

A

3-4 hrs

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33
Q

What are some non-ACS causes of raised troponin

A

Chronic renal failure

Sepsis

Myocarditis

Aortic dissection

PE

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34
Q

What is the management for acute STEMI

A

Discuss with cardiac centre within 12 hours

Refer to cath lab (STEMI)

Morphine

Oxygen

Antiemetic

Aspirin, prasugrel, clopidogrel, ticagrelor

Primary percutaneous coronary intervention (PPCI)

Thrombolysis

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35
Q

What is the management for NSTEMI/unstable angina

A

Analgesia

Aspirin

LMWH

Repeat ECG

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36
Q

What is the GRACE score

A

Gives 6 month risk of death/repeat MI following an NSTEMI

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37
Q

What are the complications of MI

A

Death

Rupture of heart septum/papillary muscles

Oedema

Arrhythmias, aneurysms

Dressler’s syndrome

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38
Q

What is Dressler’s syndrome

A

2-3 days after MI

Get localised immune response

Get pericarditis

Presentation: pleuritic chest pain, low grade fever, pericardial rub

Can cause: pericardial effusion, pericardial tamponade

Diagnosis: ECG, ECHO, raised inflammatory markers

Management: NSAIDs, prednisolone, pericardiocentesis (remove fluid from around heart)

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39
Q

What is the secondary prevention for acute coronary syndrome

A

Aspirin

Another antiplatelet

Atorvastatin

ACE inhibitors

Atenolol

Aldosterone antagonist

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40
Q

What are the 4 types of MI

A

1: traditional MI, due to ACS

2: ischaemia due to increased demand/reduced oxygen

3: sudden cardiac death

4: associated with PCI/stunting/CABG

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41
Q

What are the causes of pulmonary oedema

A

Iatrogenic (aggressive fluids)

Sepsis

Myocardial infarction

Arrhythmias

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42
Q

How might pulmonary oedema present

A

Shortness of breath (exacerbated on lying flat)

Type 1 respiratory failure

Feeling unwell

Cough

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43
Q

What would you find on examination in pulmonary oedema

A

Increased respiratory rate

Reduced oxygen saturations

Tachycardia

3rd heart sound

Bibasal crackles

Cardiogenic shock

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44
Q

What investigations are needed for pulmonary oedema

A

ECG

ABG

CXR

ECHO

BNP, troponin

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45
Q

What is BNP

A

B-type natriuretic peptide

Released from ventricles when excessively stretched

Vasodilator, diuretic

Sensitive, but not specific

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46
Q

What is the management for pulmonary oedema

A

Pour SOD (stop IV fluids, sit up, oxygen, diuretics)

IV opiates (act as vasodilators)

NIV

CPAP

Inotropes (noradrenaline)

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47
Q

What is the NICE cutoff for hypertension

A

140-90 in clinic

135/85 at home

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48
Q

What are the secondary causes of hypertension

A

ROPE

Renal disease

Obesity

Pregnancy/pre-eclampsia

Endocrine (hyperaldosteronism)

49
Q

How might a patient with hypertension present

A

Asymptomatic

Headaches

50
Q

What are the complications of hypertension

A

Ischaemic heart disease

Cerebrovascular accident

Hypertensive retinopathy

Hypertensive nephropathy

Heart failure

51
Q

What are the 3 stages of hypertension

A

1: >140/90 (or >135/85 at home)

2: >160/100 (or >150/95 at home)

3: >180/110

52
Q

What investigations are needed for hypertension

A

Urine albumin:creatinine ratio

HbA1c

Fundus examination

ECG

ECHO

53
Q

What medications are used for hypertension

A

ABCD+

ACE inhibitors

Beta blockers

CCBs

Diuretics (thiazide-like)

ARBs (for people who do not tolerate ACE inhibitors and block population)

54
Q

Who should be offered hypertension management

A

Stage 2 hypertensives

Stage 1 hypertensives under 80 with: Qrisk > 10%, diabetes, renal disease, cardiovascular disease, end organ damage

55
Q

What are the steps of antihypertensive treatment

A

Step 1:
- <55 and non-black: A
- >55 or black: C

Step 2:
- A+C, A+D, C+D
- If black, give ARB rather than A

Step 3:
- A+C+D

Step 4:
- A+C+D+additional
- Diuretic, alpha blocker, beta blocker

56
Q

What are the treatment targets for hypertensives < 80

A

< 140
<90

57
Q

What are the treatment targets for hypertensives > 80

A

< 150
< 90

58
Q

What are the treatment targets for hypertensives with diabetes/stroke/MI/CKD

A

< 130
< 80

59
Q

What is systolic and diastolic heart failure

A

Systolic - impaired left ventricular contraction

Diastolic - ventricular relaxation

60
Q

How might chronic heart failure present

A

Breathlessness

Cough

Orthopnoea (breathless on lying flat)

Paroxysmal nocturnal dyspnoea (waking at night short of breath)

Peripheral oedema

61
Q

What features carry a worse prognosis for chronic heart failure

A

Severe fluid overload

Very high NT-pro-BNP

Severe renal impairment

Increasing age

Multiple comorbidities

62
Q

What investigations are needed for chronic heart failure

A

FBC, U&Es, LFTs, TFTs, BNP

CXR

ECG

ECHO (confirms diagnosis), cardiac MRI

63
Q

What might CXR show in chronic heart failure

A

Cardiomegaly

Pleural effusion

Perihilar shadowing/consolidation

Alveolar oedema

Air bronchograms

Increased width of vascular pedicles

64
Q

What are the causes of chronic heart failure

A

Ischaemic heart disease

Valvular heart disease

Hypertension

Arrhythmias

Chronic lung disease

Cardiomyopathy

Previous chemotherapy

HIV

65
Q

What is the main management for chronic heart failure

A

ACE inhibitors

Beta blockers

Aldosterone antagonists

Loop diuretics

Surgery (for severe stenosis/regurge)

66
Q

What are the additional management strategies for chronic heart failure

A

Yearly flu and pneumonia vaccines

Smoking cessation

Optimise co-morbidities

Exercise

Low salt diet

Fluid restriction

Ivabradine

Nitrates

Pacemaker insertion

67
Q

What is cor pulmonale

A

Right sided heart failure caused by respiratory disease

68
Q

What is the mechanism by which cor pulmonale happens

A

Increased pressure in pulmonary arteries

Ineffective pumping from right ventricle

Back pressure of blood into right atrium, vena cava, systemic venous system

69
Q

What are the respiratory causes of cor pulmonale

A

COPD

PE

Interstitial lung disease

Cystic fibrosis

Primary pulmonary hypertension

70
Q

How might cor pulmonale present

A

Often asymptomatic

Shortness of breath

Peripheral oedema

Syncope

Chest pain

71
Q

What might you find on examination in cor pulmonale

A

Hypoxia

Cyanosis

Raised JVP

Peripheral oedema

3rd heart sound

Murmur

Hepatomegaly

72
Q

What is the treatment for cor pulmonale

A

Treat underlying cause

Long term oxygen therapy

73
Q

What do S1 and S2 signify

A

S1: closing of tricuspid and mitral valves

S2: closing of pulmonary and aortic valves

74
Q

How is mitral stenosis best heard

A

Lie patient on left side

75
Q

How is aortic regurgitation best heard

A

Lean patient forward, holding exhalation

76
Q

How should murmurs be described

A

SCRIPT

Site

Character

Radiation

Intensity

Pitch

Timing

77
Q

What are the grades of murmurs

A

1: difficult to hear

2: quiet

3: easy to hear

4: easy to hear with a palpable thrill

5: hear with stethoscope barely touching chest

6: hear with stethoscope off chest

78
Q

Give an overview of mitral stenosis

A

Narrow mitral valve

Difficult for left atrium to push blood to ventricle

Causes: rheumatic heart disease, infective endocarditis

Associated with: malar flush, AF

79
Q

Give an overview of mitral regurgitation

A

Causes congestive heart failure (reduced ejection fraction)

Pan-systolic, high pitched, ‘whistling’ murmur

May have 3rd heart sound

Causes: idiopathic weakness of valve with age, ischaemic heart disease, infective endocarditis, rheumatic heart disease, connective tissue disorders

80
Q

Give an overview of aortic stenosis

A

Most common valve disease

Ejection-systolic, high pitched murmur

Crescendo-decrescendo

Other signs: radiates to carotids, slow rising pulse, narrow pulse pressure, exertional syncope

Causes: idiopathic age-related calcification, rheumatic heart disease

81
Q

Give an overview of aortic regurgitation

A

Early diastolic, soft murmur

Early diastolic, ‘rumbling’ murmur

Collapsing pulse

Causes: idiopathic age related weakness, connective tissue disorders

82
Q

What are the shockable cardiac arrest rhythms

A

Ventricular tachycardia

Ventricular fibrillation

83
Q

What are the non-shockable cardiac arrest rhythms

A

Pulseless electrical activity

Asystole

84
Q

How are different types of tachycardias treated

A

Atrial fibrillation: rate control with beta blockers or diltiazem (CCB)

Atrial flutter: rate control with beta blockers

Supraventricular tachycardia: valsalva manoeuvre and adenosine

Ventricular tachycardias: amiodarone infusion

85
Q

Give an overview of atrial flutter

A

Re-entrant rhythm in either atrium - self-perpetuating loop

Atria contact at around 300 bpm

Ventricles contract at around 150 bpm

Sawtooth appearance on ECG

Associated conditions: hypertension, ischaemic heart disease, cardiomyopathy, thyrotoxicosis

Treatment: rate/rhythm control (beta blockers, cardioversion), treat underling cause, radiofrequency ablation, anticoagulate

86
Q

Give an overview of supraventricular tachycardias

A

Electrical signals re-enter atria from ventricles

Treatment: ECG monitoring, valsalva manoeuvre, carotid sinus massage, adenosine, verapamil

Long term medications: beta blockers, CCBs, flecanide, sotalol, amiodarone

87
Q

Give an overview of Wolff-Parkinson-White syndrome

A

Extra electrical pathway connecting atria to ventricles

ECG changes: short PR, wide QRS, delta wave (slurred upstroke)

Definitive treatment: radiofrequency ablation of accessory pathway

88
Q

Give an overview of torsades de pointes

A

A polymorphic ventricular tachycardia

QRSs twisting around baseline

Can normalise spontaneously, or progress to ventricular tachycardia

Acute management: correct underlying cause, magnesium infusion, defibrillation

Long term management: avoid meds that prolong QTc, correct electrolyte imbalance, beta blockers, pacemaker, implantable defibrillator

89
Q

Give an overview of ventricular ectopics

A

Premature ventricular beats caused by random electrical discharge from outside atria

Random, brief palpitations

Management: general bloods, reassure

90
Q

Give an overview of first degree heart blocks

A

Delayed AV conduction through AV node

Every p wave leads to a QRS

PR > 0.2

No specific treatment needed

If symptomatic, do cardiac monitoring

91
Q

Give an overview of Mobitz 1 heart blocks

A

Increasing PR until QRS dropped

Repeating cycle

Can be found in young, healthy patients

No specific treatment needed

If symptomatic, look for other heart block

92
Q

Give an overview of Mobitz 2 heart blocks

A

Missed QRS complexes

Set ratio of p waves and QRS complexes

PR interval stays constant

Risk of asystole (consider pacemaker)

93
Q

Give an overview of third degree heart blocks

A

Complete heart block

No relationship between p waves and QRS complexes

Significant risk of asystole (need urgent permanent pacing)

Causes: digoxin toxicity, inferior MI, hyperkalaemia

94
Q

What is the treatment for bradycardias/AV node blocks

A

Stable: observe

Unstable: atropine, noradrenaline, transcutaneous cardiac pacing

High risk of asystole: temporary transvenous cardiac pacing, permanent implantable pacemaker

95
Q

What is atrial fibrillation

A

Uncoordinated, rapid, irregular contraction of the atria

Disorganised electrical activity overrides activity from SA node

Mostly in > 80s

Absent p waves

96
Q

How might atrial fibrillation present

A

Often asymptomatic

Palpitations

Shortness of breath

Syncope

97
Q

What can atrial fibrillation lead to

A

Haemodynamic instability

Acute coronary syndrome

Congestive heart failure

Cardioembolic stroke

98
Q

What will be seen on ECG in atrial fibrillation

A

Absent p waves

Narrow QRS complex tachycardia

Irregularly irregular ventricular rhythm

99
Q

What are the common causes of atrial fibrillation

A

SMITH

Sepsis

Mitral valve pathology

Ischaemic heart disease

Thyrotoxicosis

Hypertension

100
Q

What are the NICE guidelines for rate control in atrial fibrillation

A

All patients with AF should have rate control as 1st line unless:

There is a reversible cause

New onset (<48 hrs)

Causing heart failure

Remain symptomatic despite measures to control

101
Q

Give an overview of rate control methods for atrial fibrillation

A

Aim to extend diastole, to allow ventricles to fill up

Beta blockers, calcium channel blockers, digoxin

102
Q

Give an overview of rhythm control methods for atrial fibrillation

A

Aim to return patient to sinus rhythm

Cardioversion: electrical (flecanide, amiodarone), electrical

Long term: beta blockers, dronedarone, amiodarone

103
Q

What is paroxysmal atrial fibrillation

A

Comes and goes in episodes

Does not last > 48 hours

Can use pill in pocket approach (flecanide)

104
Q

Give an overview of warfarin

A

Vitamin K antagonist

Prolongs prothrombin time

Target INR 2-3

Half life 2-3 days

Reversible with vitamin K

105
Q

Give an overview of NOACs

A

Apixaban, dabigatran, rivaroxaban

Inhibit factor Xa or thrombin directly

Low bleeding risk

Renally excreted (monitor renal function annually)

106
Q

Go through CHA2DS2-VASc

A

Assess whether patients with AF should be started on anticoagulants

Anticoagulate if score 1+

Congestive heart failure

Hypertension

Age > 75 (2)

Diabetes

Stroke/TIA (2)

Vascular disease

Age 65-74

Sex (female)

107
Q

Go through HAS-BLED

A

Assess patient’s risk of major bleeding during anticoagulation

Hypertension

Abnormal renal/liver function

Stroke

Bleeding

Labile INR (whilst on warfarin)

Elderly

Drugs (aspirin, NSAIDs)

Alcohol abuse

108
Q

Which cardiac conditions predispose to infective endocarditis

A

Mitral valve prolapse

Prosthetic valves

Rheumatic heart disease

Degenerative aortic valve

Bicuspid aortic valve

Congenital heart disease

109
Q

Which organisms cause infective endocarditis

A

Staphylococcus viridans

Staphylococcus aureus

Enterococcus

110
Q

What is the diagnostic criteria for infective endocarditis

A

2 major, 1 major + 3 minor, 5 minor

Major: positive blood cultures, endocardial involvement, positive ECHO findings, new valvular regurg, dehiscence of prosthesis

Minor: predisposing valvular/cardiac abnormality, IV drug use, pyrexia > 38, embolic phenomenon, vasculitic phenomenon, suggestive blood cultures, suggestive ECHO findings

111
Q

What is the medical management for infective endocarditis

A

Streptococci: benzylpenicillin + gentamicin

Enterococci: amoxicillin + gentamicin

Staphylococci: flucloxacillin + gentamicin

112
Q

What are the indications for surgery in infective endocarditis

A

Moderate-severe cardiac failure

Valve dehiscence

Uncontrolled infection despite antibiotics

Relapse after medical therapy

Acute systemic embolus

Fungal infection

Paravalvular infection

Valve obstruction

113
Q

What are the indications for pacemaker insertion

A

Symptomatic bradycardia

Mobitz type 2 heart block

3rd degree heart block

Severe heart failure

Hypertrophic obstructive cardiomyopathy

114
Q

What is a hypertensive emergency

A

Increased blood pressure that will cause end organ damage within a few hours

115
Q

What is the difference between a hypertensive emergency and hypertensive urgency

A

Emergency: high BP associated with a critical event

Urgency: high BP without a critical illness

116
Q

What are the aims of treatment in hypertensive emergency/urgency

A

Reduce BP to 110 in:

3 - 12 hours (emergency)

24 hours (urgency)

117
Q

How is hypertensive emergency treated

A

Sodium nitroprusside

Labetalol

GTN

Esmolol

118
Q

How is hypertensive urgency treated

A

Amlodipine

Diltiazem

Lisinopril

ACE inhibitor + calcium antagonist

119
Q

Give an overview of pheochromocytoma

A

Triad of: episodic headaches, sweating, tachycardia

Diagnosis: measure urine and plasma fractionated metanephrines and catecholamines, 24 hr urine collection, CT/MRI pelvis (look for renal tumours)

Management: adrenal resection, control hypertension (alpha and beta blockers)

Medicine (9 decks)

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