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Phase 2a Stuff > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Define MI and the difference between STEMIs and NSTEMIs

A

MI occurs when cardiac myocytes die due to prolonged myocardial ischaemia. STEMIs show an ST elevation on ECG whereas NSTEMIs do not.

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2
Q

Causes of MI

A

ATHEROSCLEROSIS

Emboli, coronary spasm, vasculitis

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3
Q

MI risk factors

A

Age, males, FHx, smoking, HTN, obesity

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4
Q

Clinical manifestations of MI.

A

Crushing chest pain which may radiate to the arm/jaw.

Raised JVP, increased pulse and blood pressure changes, 4th heart sounds, signs of HF.

Anxiety, nausea, sweating, palpitatiions

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5
Q

First line investigations for MI

A

ECG - STEMI will show ST elevation and tall T waves

Troponin blood testing

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6
Q

Gold standard for investigating MI (often not needed)

A

Coronary angiography

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7
Q

Management of STEMI

A

Initially 300mg aspirin.

Hospital - aspirin +/- ticagrelor. Beta blcokers, CCBs

Other drugs used include GTN, antithrombins, statins, ACEi etc.

PRIMARY PCI IS THE TREATMENT OF CHOICE

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8
Q

Treatment of NSTEMI and unstable angina

A

Alleviate pain and secondary prevention (antiplatelets and antithrombotic)

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9
Q

Complications of MI

A

Cardiogenic shock, cardiac arrhythmias, pericarditis, emboli, aneurysms, ventricular rupture, papillary muscle rupture.

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10
Q

Can ACS occur without chest pain?

A

YES! This is called silent ACS and often occurs with elderly and diabetics.

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11
Q

Define angina

A

Chest pain caused by a mismatch between oxygen supply and demand by myocardial cells.

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12
Q

Main cause of stable angina

A

Atherosclerosis

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13
Q

Difference between stable and unstable angina.

A

Stable angina is a CCS induced by effort and relieved by rest. Unstable angina is an ACS which is not relieved by rest.

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14
Q

Investigations of angina

A

ECG, coronary angiography, perfusion MRI, bloods

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15
Q

Management of stable angina

A

Reassurance and lifestyle modifications

Medications

  • Secondary prevention (aspirin, statins, ACEi)
  • Anti-anginal drugs (beta blockers, CCBs)
  • Exacerbations (GTN spray)

Revascularisation

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16
Q

Key presentations of stable angina

A
  1. Heavy central chest pain which may radiate to jaw/arms
  2. Pain occurs with exercise
  3. Pain eases with rest or GTN

(classical angina has 3/3, atypical angina has 2/3 and non-anginal chest pain has 1/3)

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17
Q

Define heart failure

A

An inability of the heart to deliver blood (and oxygen) at a rate enough to meet with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.

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18
Q

Causes of heart failure

A

MYOCARDIAL DYSFUNCTION (usually from MI)

HTN, alcohol abuse, cardiomyopathy, valve disease, endocarditis, pericarditis

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19
Q

Different types of HF

A

HFREF (EF<40%) - commonly caused by IHD

HFPEF (EF>50%) - increased stiffness and decreased LV compliance leads to impaired diastolic filling

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20
Q

Key presentations of HF

A

Dyspnoea, fatigue, tachycardia, peripheral oedema

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21
Q

Signs of HF on examination

A

Displaced apex beat, tender hepatomegaly, cardiomegaly, pleural effusion, elevated JVP, 3rd an 4th heart sounds, ascites

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22
Q

1st line investigations for HF

A

ECG

NT-pro BNP blood test

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23
Q

Gold standard investigation for HF

A

Cardiac MRI

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24
Q

HF management

A

Prevention – lifestyle advice

Drug management – diuretics, ACEi, ARBs, beta blockers, aldosterone antagonists, vasodilators and nitrates

Revascularisation, myocardial stunning, transplantation

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25
Q

HF complications

A

AF, VF, kidney failure, anaemia, stroke

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26
Q

Define hypertension

A

An abnormally high blood pressure in the clinic (>140/90)

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27
Q

Causes of hypertension

A

Primary/Essential HTN = idiopathic

Secondary causes of HTN include pheochromocytoma, Conn’s and Cushing’s

Contributory lifestyle factors such as stress, smoking and obesity

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28
Q

1st line investigations for HTN

A

Clinical BP

Confirm with ambulatory or home BP

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29
Q

Other tests in patients with HTN

A

Bloods, urine dipstick, ECG, cholesterol, echo

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30
Q

HTN drug treatment for patients under 55

A
  1. ACEi (or ARB)
  2. ACEi + CCB
  3. ACEi + CCB + diuretic
  4. add beta blocker, alpha blocker or spironolactone
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31
Q

HTN drug treatment for patients over 55 or from an Afro-Caribbean background

A
  1. CCB
  2. CCB + ACEi
  3. CCB + ACEi + diuretic
  4. add beta blocker, alpha blocker or spironolactone
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32
Q

Thresholds for treatment of HTN

A

Low risk = 160/100

High risk = 140/90

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33
Q

BP targets for HTN

A

Routine = 140/90
Elderly = 150/90
PMH of stroke/CKD/diabetes = 130/80

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34
Q

Define atrial fibrillation and flutter

A

Tachyarrhythmia characterised by an irregularly irregular pulse, rapid HR and ECG changes. (Atrial flutter is chaotic beat but regularly irregular)

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35
Q

Causes of atrial fibrillation

A

IHD, HF, mitral valve disease, HTN, hyperthyroidism, alcohol induced

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36
Q

Pathophysiology of atrial fibrillation

A

Atrial ectopic beats (thought to originate in pulmonary veins) lead to dysfunction of the cardiac electrical signalling pathway. As a result, the atria no longer contract in a coordinated manner. Due to irregular contractions, the atria fail to empty properly. This may result in stagnant blood accumulating within the atrial appendage, increasing the risk of clot formation and embolic stroke.

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37
Q

Clinical manifestations of atrial fibrillation

A

Chest pain, dyspnoea, palpitations, fatigue, irregularly irregular pulse

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38
Q

1st line investigation

A

ECG

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39
Q

Tests other than ECG for atrial fibrillation

A

Blood tests, echo, TFTs, CXR

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40
Q

Differential diagnosis of atrial fibrillation

A

Tachycardias, ventricular atopic beats, Wolff-Parkinson-White

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41
Q

Management of atrial fibrillation

A

Beta blockers, rate-limiting CCBs, digoxin, amiodarone, anticoagulants

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42
Q

Complications of atrial fibrillation

A

STROKE, heart failure, sudden death

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43
Q

What is an electrical storm?

A

3 episodes of VF or VT during a 24-hour period

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44
Q

Arrhythmias other than atrial fibrillation

A
  • Supraventricular tachycardia
  • Ventricular tachycardia
  • Sinus tachycardia
  • AV blocks
  • LBBB
  • RBBB
  • Ventricular ectopic
  • Wolff-Parkinson-White
45
Q

Define acute pericarditis

A

An inflammatory pericardiac syndrome with or without pericardial effusion

46
Q

Causes of pericarditis

A

Viral, bacterial, autoimmune, neoplastic, metabolic, traumatic and iatrogenic, amyloidosis, aortic dissection

47
Q

What is a pericardial effusion and what can it lead to?

A

A collection of fluid within the potential space of the pericardial sac - can lead to cardiac tamponade

48
Q

Key presentations of pericardial effusion

A

Chest pain, pericardial chest rub, ECG abnormalities, pericardial effusion (2 of these required for diagnosis)

49
Q

1st line diagnosis for pericarditis

A

Clinical diagnosis based on signs and symptoms

50
Q

Other tests for pericarditis

A

ECG, CXR, echo, blood tests

51
Q

Management of pericarditis

A

Sedentary activity, NSAIDs or aspirin, colchicine

52
Q

Treatment of pericardial effusion

A

Pericardiocentesis

53
Q

Complications of pericarditis

A

Cardiac tamponade

Constrictive pericarditis

54
Q

Signs of cardiac tamponade

A

Pulsus paradoxus, muffled heart sounds, hypotension, increased JVP

55
Q

Treatment of cardiac tamponade

A

Pericardiocentesis, pericardiectomy, thoracotomy

56
Q

Define infective endocarditis

A

Infection of heart valves or other endocardial-lined structures within the heart.

57
Q

Types of IE

A

Left-sided native IE
Left-sided prosthetic IE
Right-sided IE
Device related IE

58
Q

Epidemiological changes in IE

A

Used to be a disease of the young affected by rheumatic heart disease. Now affects the elderly, drug abusers, those with congenital defects and prosthetic heart valves

59
Q

Causes of IE

A

Bacteraemia arising from poor dental hygiene, IV drug abuse and soft tissue infections.

60
Q

Pathophysiology of IE

A

Early microbial adherence is crucial. Bacterial adherence to a platelet-fibrin nidus. Hallmark of IE is vegetation.

61
Q

Clinical manifestations of IE

A

Signs of systemic infection.

Heart murmurs, splinter haemorrhages, Osler’s nodes, Janeway lesions, Roth spots on fundoscopy, petechiae

62
Q

1st line investigation for IE

A

Blood cultures - 3 samples from 3 peripheral sites

63
Q

Other investigations for IE

A

TRANSTHORACIC ECHO, urinalysis, CXR

64
Q

Management of IE

A

Antimicrobials
Treat complications
Surgery if antibiotics ineffective, complications occur or have a large vegetation needing removal

65
Q

Complications of IE

A

HF, arrhythmias, abscess formation in cardiac muscle, emboli formation (stroke, vision loss)

66
Q

Define aortic stenosis

A

Chronic progressive disease characterised by narrowing of the aortic valve area. Symptoms occur when the valve area is 1/4th of normal

67
Q

Causes of aortic stenosis

A

Calcific aortic valvular disease - most common
Bicuspid aortic valve
Rheumatic heart disease

68
Q

Pathophysiology of aortic stenosis

A

Narrowing of the aortic valve causes a pressure gradient to develop between LV and aorta (increased afterload)

LV function initially maintained by compensatory pressure hypertrophy. When these mechanisms are exhausted, LV function declines.

69
Q

Key presentations of aortic stenosis

A

Exertion dyspnoea, exertion syncope, ejection systolic murmur, slow rising carotid pulse, soft or absent second heart sound

70
Q

1st line investigations for aortic stenosis

A

Echocardiography

Doppler derived gradient and valve area

71
Q

Other investigations for aortic stenosis

A

CXR, ECG, cardiac CT

72
Q

Management of aortic stenosis

A

Surgical aortic valve replacement - definitive treatment
TAVI
Consider IE prophylaxis in dental procedures

73
Q

Factors that decrease survival rates for aortic stenosis

A

Angina, syncope, HF

74
Q

Define mitral regurgitation

A

Backflow of blood from the LV into the LA during systole due to abnormalities of the valves, chordae tendinea or papillary muscles

75
Q

Causes of mitral regurgitation

A 
Myxomatous degeneration
Ischaemic MR
Rheumatic heart disease
IE
Dilated and hypertrophic cardiomyopathy
Collagen diseases
76
Q

Pathophysiology of mitral regurgitation

A

Pure volume overload!

Compensatory mechanisms - LA enlargement (leading to pulmonary HTN), LV hypertrophy and dilation, increased contractility

77
Q

Key presentations of mitral regurgitation

A

Exertion dyspnoea, pansystolic murmur, displaced hyperdynamic apex beat, soft 1st heart sound, prominent 3rd heart sound, right heart failure

78
Q

1st line investigations for mitral regurgitation

A

Echocardiogram

79
Q

Other tests for mitral regurgitation

A

ECG, CXR, cardiac catheterisation

80
Q

Management of mitral regurgitation

A

Vasodilators, rate control for AF, anticoagulants, diuretics

Serial echocardiography

IE prophylaxis

Surgery if symptomatic, EF <60% or new onset AF

81
Q

Define aortic regurgitation

A

Leakage of blood into the LV from the aorta during diastole due to ineffective coaptation of aortic cusps

82
Q

Causes of aortic regurgitation

A

Bicuspid aortic valve
Rheumatic heart disease
IE
Aortic dissection

83
Q

Pathophysiology of aortic regurgitation

A

Combined pressure and volume overload

Compensatory mechanisms - LV dilation and hypertension - can lead to HF

84
Q

Key presentations of aortic regurgitation

A

Hyperdynamic and displaced apical pulse, wide pulse pressure. Systolic ejection murmur, diastolic blowing murmur.

Significant symptoms occur late - angina, dyspnoea, LV failure, palpitations

85
Q

How is aortic regurgitation diagnosed?

A

By physical exam. Then echocardiogram. Can also perform a CXR.

86
Q

Aortic regurgitation management

A

IE prophylaxis
Serial echocardiograms
Vasodilators
Surgery - definitive treatment

87
Q

Define mitral stenosis

A

Obstruction of LV inflow that prevents proper filling during diastole. Normal area is 4-6cm2 but symptoms arise at around <2cm2

88
Q

Causes of mitral stenosis

A

Rheumatic carditis is predominant cause
IE
Mitral annular calcification

89
Q

Pathophysiology of mitral stenosis

A

Progressive dyspnoea due to pulmonary congestion.

Increased trans-mitral pressure leads to LA dilation and AF

RHF due to pulmonary HTN

Haemoptysis

90
Q

Key presentations of mitral stenosis

A

Mitral facies, small-volume pulse, a-wave jugular venous pulse, diastolic murmur, loud opening heart sound

91
Q

1st line test for mitral stenosis

A

Echocardiogram

92
Q

Other tests for mitral stenosis

A

CXR, ECG, cardiac catheterisation

93
Q

Mitral stenosis management

A

IE prophylaxis

Serial echocardiogram

Diuretics, beta blockers/digoxin/CCBs

Percutaneous mitral balloon valvotomy

Mitral valve replacement in serious cases

94
Q

Define shock

A

Acute circulatory failure resulting in inadequate organ perfusion. Systolic BP <90 or MAP <65

95
Q

Types of shock

A 
Anaphylactic shock (IgE mediated allergic reactions)
Septic shock (uncontrolled infection)
Hypovolaemic shock (bleeding, burns, fluid loss)
Cardiogenic shock (arrhythmias, MI, PE, cardiac tamponade)

Other - tension pneumothorax, spinal cord injury, Addison’s, heat exhaustion

96
Q

Investigation and management of shock

A

ABCDE
IV Fluids!

Depending on cause may need adrenaline, antibiotics, reperfusion therapy etc.

97
Q

Definition of cardiomyopathy

A

A group of diseases of the myocardium that affect the mechanical or electrical function of the heart.

98
Q

4 main groups of cardiomyopathy

A 
Hypertrophic cardiomyopathy (HCM)
Arrhythmogenic cardiomyopathy (ARVC)
Dilated cardiomyopathy (DCM)
Restrictive cardiomyopathy (RCM)
99
Q

Causes of cardiomyopathy

A

GENETICS!!
HCM - sarcomeric protein gene mutations
DCM - cytoskeletal gene mutation
ARVC - desmosome gene mutations

100
Q

Pathophysiology of HCM

A

Hyperdynamic contraction of the heart which impairs diastolic relaxion. Causes chaotic myofibrillar disarray with features of ischaemia causing arrhythmias.

101
Q

Pathophysiology of DCM

A

Characterised by dilation of ventricles.

102
Q

Pathophysiology of ARVC

A

RV becomes thin and the muscle is replaced by fat and fibrous tissue leading to dilation

103
Q

Key presentation of cardiomyopathies

A

Arrhythmias!

Angina, SOB, palpitations, dizzy spells, syncope

104
Q

Gold standard investigation for cardiomyopathy

A

Cardiac catheterisation

105
Q

1st line tests for cardiomyopathy

A

ECG, echo, CMR

106
Q

Important investigation to do for cardiomyopathy

A

GENETIC ANALYSIS!

And should try to test family members.

107
Q

Management of cardiomyopathy

A

FAMILY EVALUATION
lifestyle modifications
Management of symptoms
HF management

108
Q

Complications of cardiomyopathies

A

HF, blood clots, valvular issues, cardiac arrest, sudden death

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