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GRACE Phase 2a Medicine > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Normal systolic ejection fraction? %

A

60

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2
Q

Plaque

A

endophytic mass of distorted endothelial surfaces containing lymphocytes, macrophages, smooth muscle cells

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3
Q

Foam cells

A

macrophages + oxidised LDLs

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4
Q

Aneurysm

A

enlargement of an artery caused by a weakness in an arterial wall

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5
Q

Complications of plaque rupture

A

occlusion due to thrombus, chronic narrowing of vessel lumen, aneurysm change, embolism of thrombus

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6
Q

Ischaemic heart disease

A

Angina, MI, chronic congestive cardiac failure, sudden death

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7
Q

Pathological complications of MI

A

arrhythmias, L ventricular failure, extension of infarction, rupture of the myocardium

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8
Q

aneurysm

A

dilation of part of the myocardial wall, usually associated with fibrosis and atrophy of myocytes, risk of subsequent embolism

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9
Q

Acute rheumatic fever

A

group A beta-haemolytic streptococcus infection, major factor with heart disease in the developing world

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10
Q

Clinical significance of acute rheumatic fever

A

chronically scarring and deformity produces contracture of the valve and chordae tendinae, may subsequently calcify and distort blood flow

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11
Q

Infective endocarditis

A

infective process involving the cardiac valves

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12
Q

Causes of infective endocarditis

A

rheumatic valvular heart, mitral valve prolapse, elderly pregnancy, diabetes

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13
Q

Characteristic microorganisms causing infective endocarditis

A

streptococci, staphylococci, fungi and atypical bacteria also

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14
Q

aortic stenosis increases the risk of ?

A

MI and infective endocarditis

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15
Q

Mitral stenosis is commonly associated with what disorders?

A

Connective tissue

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16
Q

Myocarditis

A

reflects inflammation of the myocardium, usually associated with muscle cell necrosis and degeneration, multiple causes but most common is viral myocarditis

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17
Q

Key types of cardiomyopathy

A

DCM (dilated), HCM (hypertrophic CM) , ARVCM (arrhythmogenic right ventricular CM)

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18
Q

cardiomyopathy

A

primary cardiac disease with contractile dysfunction and atypical morphology

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19
Q

DCM - dilated cardiomyopathy

A

most common type of CM, many causes, chronic ischaemia, MI, often end in cardiac failure

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20
Q

Pathological presentation of dilated cardiomyopathy

A

enlarged, heavy and dilated heart

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21
Q

HCM - hypertrophic cardiomyopathy

A

due to mutations of proteins in muscle cells, leads to progressive sarcomeric dysfunction, accounts for 5-10% of sudden deaths in young adults

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22
Q

ARVCM - arrhythmogenic right ventricular CM

A

thinning and fatty infiltration of right ventricular outflow tract with fibrosis and inflammation

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23
Q

Abdominal aortic aneurysm

A

almost always caused by atheroma, majority below renal arteries

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24
Q

Haemangioendothelioma

A

vascular tumour of endothelial cells of low grade malignancy

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25
Q

Rheumatic fever

A

Systemic infection common in developing countries from a Lancefield group A B-haemolytic streptococci, common cause of structural heart disease

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26
Q

Pathophysiology of rheumatic fever?

A

An antibody from the bacterial cell wall cross reacts with valve tissue, which can cause permanent damage to the heart valves

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27
Q

Rheumatic fever presentation

A

Fever, arthritis, chorea, fatigue, tachycardia, murmur, erythema marginatum (red rash with raised edges and clear centre on trunk)

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28
Q

Ix for rheumatic fever

A

Jones criteria - recent streptococcus infection + 2 major/1 major + 2 minor criteria
Major - carditis, arthritis, erythema marginatum
Minor - fever, raised ESR/CRP

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29
Q

Tx for rheumatic fever?

A

IV ABx, aspirin for analgesia, diazepam for chorea

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30
Q

Medications causing iatrogenic hyperkalaemia?

A

ACE-i, ARBs, potassium sparing diuretics, NSAIDs, digoxin

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31
Q

Renal causes of hyperkalaemia?

A

AKI, CKD - kidneys are responsible for 90% of the potassium excretion, therefore impaired renal function = hyperkalaemia

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32
Q

DKA and Addisons disease both cause

A

hyperkalaemia
DKA - lack of insulin, K+ moves out of the cell
Addisons - lack of aldosterone, therefore less K+ excretion

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33
Q

Typical ECG findings for hyperkalaemia?

A

Tall-tented T waves, flattened P waves, broad QRS complexes

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34
Q

Angina is caused by?

A

Narrowing of the coronary arteries - ischaemia

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35
Q

Sx of angina?

A

Constricting chest pain, may radiate to jaw/arms, worse after activity, relieved by rest or GTN within 5 minutes

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36
Q

Unstable angina

A

Part of acute coronary syndrome, symptoms of chest pain come on at rest, symptoms of angina acutely get worse

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37
Q

Why are plaques commonly formed in the coronary arteries?

A

Turbulent follow

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38
Q

GS investigation for assessing coronary arteries for px with angina?

A

CT coronary angiography (contrast to show narrowing in arteries)

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39
Q

Foam cells?

A

Injured endothelial cells attract macrophages, which engulf the LDLs that have accumulated, forming foam cells

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40
Q

Baseline tests for angina?

A

Bloods, ECG, echocardiography, CXR

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41
Q

Mx for angina

A
  1. Lifestyle - diet, limit alcohol/smoking, exercise, weight loss
  2. GTN spray
  3. Beta-blocker or CCB
  4. Revascularisation surgery
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42
Q

How does GTN spray work?

A

Stimulates endothelial cells to release NO which triggers vasoconstriction

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43
Q

ACS refers to 3 states of myocardial ischaemia:

A

unstable angina, NSTEMI, STEMI

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44
Q

How to make a dx in ACS?

A
  1. ECG - ST elevation = STEMI, no ST elevation = NSTEMI or unstable angina
  2. Troponin level - raised = NSTEMI, normal = unstable angina
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45
Q

Sx of ACS?

A

Central, constricting chest pain with…

  • Nausea/vomiting
  • Sweating
  • SOB
  • Palpitations
  • Pain radiating –> arm/jaw
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46
Q

What px might experience a silent MI?

A

diabetics

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47
Q

Why are troponins indicative of MI?

A

Released by myocytes after ischaemia

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48
Q

How to treat an acute STEMI?

A

Primary percutaneous coronary intervention, thrombolysis - should be treated within 12hrs

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49
Q

Example of thrombolytic agents?

A

Streptokinase

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50
Q

Complications of MI? DREAD

A 
Death
Rupture of heart septum
Edema (heart failure)
Arrhythmia, aneurysm
Dressler's syndrome
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51
Q

What is Dressler’s syndrome?

A

Post-myocardial infarction syndrome (2-3 weeks after MI) - localised immune response that causes pericarditis (presents with pleuritic chest pain, fever)

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52
Q

Most common cause of mitral stenosis?

A

rheumatic heart disease

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53
Q

sx of mitral stenosis

A

dyspnoea, reduced exercise tolerance, haemoptysis

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54
Q

What is rheumatic heart disease?

A

Infection by group A streptococcus pharyngitis

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55
Q

How might mitral stenosis –> AF? R heart failure?

A

Raised pressures in the L atrium –> atrial enlargement + increased pressure predisposes to AF and atrial thrombosis. Raised atrial pressures –> raised pulmonary HTN –> R sided heart failure

56
Q

What is the Q risk score?

A

Lifetime risk of cardiovascular disease development

57
Q

Who with HTN is offered treatment?

A
  1. Everyone with stage 2 (160/100mmHg)

2. Stage 1 (140/90) <80 and Q risk score >10%

58
Q

How does HTN mx differ for afro-caribbeans?

A

Similar to >55, 1st tx = CCBs

59
Q

Biggest rf for cardiac failure?

A

IHD

60
Q

Normal systolic ejection fraction? In systolic heart failure?

A

60-65%, <40%

61
Q

Categories of heart failure

A

Systolic/diastolic (impaired ejection/filling)
Left/right
Acute/chronic

62
Q

Px of heart failure

A

3 cardinal symptoms - SOB, fatigue, ankle swelling (peripheral oedema)
Fatigue, dyspnoea, orthopnoea, pulmonary oedema, raised JVP

63
Q

What are you looking for in a blood test with a patient with heart failure?

A

B-type NP - released due to myocardial wall stress –> systemic vasodilation –> less effort for heart

64
Q

MX of chronic heart failure - ABCD other

A 
ACE-I/ARBs - ramipril
Beta-blockers - bisprolol
CCBs- amlopidine
Diuretics - Indamapide
Other - Digoxin
65
Q

1st line test for cardiac failure

A

Blood test for BNP

66
Q

shockable cardiac arrest rhythms?

A

ventricular tachycardia and ventricular fibrillation (use defibrillation)

67
Q

Tx for tachycardia unstable arrhythmia?

A
  1. 3 synchronised shocks

2. amiodarone infusion

68
Q

Tx for stable tachycardia arrhythmia px –> narrow complex (QRS <0.12s)

A

AF - rate control with BB
Atrial flutter - “
Supraventricular tachycardias - treat with vagal manoeuvres and adenosine

69
Q

Tx for stable tachycardia arrhythmia px –> broad complex (QRS >0.12s)

A

Ventricular tachycardia - amiodarone infusion

SVT with bundle branch block - tx as normal SVT

70
Q

Atrial flutter

A

Re-entrant rhythm in either atria (electrical signals re-circulates due to extra electrical pathway) –> signal goes round and round the atria, atrial contraction at 300bpm. Each signal enters the ventricles every second lap (150bpm ventricular contraction) - ECG sawtooth appearance, P wave after P wave

71
Q

Supraventricular tachycardia

A

Caused by the signal from the ventricles, re-entering the atria, thus travelling through the AVN –> another ventricular contraction

72
Q

2 main types of SVT (based on source of signals)?

A
  1. Atrioventricular nodal re-entrant tachycardia (re-entry through AVN)
  2. Atrioventricular re-entrant tachycardia (extra accessory circuit)
73
Q

What does a SVT look like on an ECG?

A
  • Narrow QRS <0.12s

- QRS followed immediately by a T wave

74
Q

What is Wolff-Parkinson White syndrome?

A

Atrioventricular re-entrant tachycardia

75
Q

Px of AFib (PIS)?

A
  1. Palpitations, racing heart
  2. Irregularly irregular pulse
  3. SOB, lightheadedness
76
Q

ECG AF

A

Absent P waves

Irregular, rapid QRS complex

77
Q

TX for SVT

A
  1. Continuous ECG monitoring
  2. Valsalva manoeuvre
  3. Carotid sinus massage
  4. Adenosine/ verapamil
  5. Current cardioversion
78
Q

What is the valsalva manoeuvre?

A

Blowing really hard into a syringe in attempt to reset heart to sinus rhythm

79
Q

1st line drug for SVT?

A

Adenosine

80
Q

Wolf-Parkinson White syndrome

A

= arrhythmia that has an accessory electrical pathway that connects the atria and the ventricles

81
Q

tx for Wolf-Parkinson White syndrome

A

Radiofrequency ablation of the extra circuit

82
Q

ECG changes for Wolf-Parkinson White syndrome

A
  • Short PR interval
  • Wide QRS
  • Delta wave
83
Q

Causes of prolonged QT interval syndrome?

A

Idiopathic, drugs e.g. antipsychotics

84
Q

Prolonged QT interval

A

ECG finding of prolonged repolarisation, therefore in this period, random depolarisations occur called “afterdepolarisations”

85
Q

Prognosis of prolonged QT interval

A

Self-limiting, or will progress to ventricular tachycardia (can lead to cardiac arrest)

86
Q

Ventricular ectopics

A

Premature ventricular beats caused by random electrical discharges outside the area, often present of random brief palpitations

87
Q

Tx for ventricular ectopics?

A

In healthy people, no tx

In other heart conditions - expert advice

88
Q

ECG presentation for 1st AVN heart block

A

PR interval prolonged, >0.22s

89
Q

2nd degree AV heart block

A

SOME atrial impulses do not make it through

Mobitz type I (wenkebach) and type II

90
Q

Mobitz type I/Wenkebach block

A

Longer PR interval –> QRS dropped, repeat

91
Q

Mobitz type II

A

Constant prolonged PR –> drop

92
Q

3rd degree AV heart block

A

No impulses pass from atria –> ventricle, ventricular contractions are completely independent, risk of asystole

93
Q

Tx for bradycardias/stable AV block?

A

Observation

94
Q

Tx for unstable AV block

A

IV atropine (increase heart rate)

95
Q

AF

A

Contraction of atria is uncoordinated, rapid and irregular, due to disorganised electrical activity

96
Q

AF increases risk of?

A

Embolic stroke

97
Q

Differentials for irregularly irregular pulse?

A

AF, ventricular ectopics

98
Q

Tx for rate control in AF

A
  1. Beta-blockers
  2. CCBs
  3. Digoxin (if sedentary)
99
Q

When can rhythm control be offered to AF patients?

A

When the cause is reversible, is of new-onset, AF is causing heart failure - electrical or pharmacological cardioversion

100
Q

Anticoagulation for AF

A
  1. Warfarin

2. DOACs - apixaban, rivaroxaban

101
Q

How does acute LVF present?

A

Rapid onset breathlessness, worse lying down (orthopnoea), better sitting up

102
Q

Why might you have an enlarged vein in your neck with R sided heart failure?

A

raised jugular venous pressure

103
Q

Mx for L sided heart failure (Pour SOD)

A
  1. Pour away (stop) any IV fluids
  2. Sit up
  3. Oxygen
  4. Diuretics
104
Q

Risk factors for Infective endocarditis

A

Prosthetic valves, congenital cardiac defect, damage to valves from rheumatic heart disease, IV drug abuse, poor dental hygiene

105
Q

Pathophysiology of Infective endocarditis

A

characterised by formation of infected vegetations of heart valves, px has underlying cardiac disease allowing for the adherence of bacteria

106
Q

What is Infective endocarditis

A

Infection of the endocardial surface of the heart

107
Q

Infective endocarditis px

A

Fever, cardiac murmur, Janeway lesion, Oslers nodes, Splinter haemorrhages

108
Q

Ix for Infective endocarditis

A

Blood cultures and echocardiography

109
Q

Modified Dukes Criteria?

A

diagnostic tool for infective endocarditis

110
Q

Dx infective endocarditis?

A

Blood cultures, echocardiogram

111
Q

Tx infective endocarditis?

A

Antibiotics, cardiac surgery

112
Q

Pericarditis? late complication of PC?

A

inflammation of the pericardium, idiopathic, acute pericarditis can complicate into constrictive pericarditis (heart encased in rigid pericardium)

113
Q

Px of pericarditis?

A

Chest pain, better sitting up, fever, dyspnoea, pericardial rub

114
Q

ECG of pericarditis?

A

saddle shaped ST elevations

115
Q

Mx of pericarditis?

A

NSAIDs, colchicine

116
Q

Constrictive pericarditis

A

Complication of pericarditis, rigid pericardium, impedes diastolic filling, Kussmaul’s sign, ascites, oedema, R heart failure. Mx by pericardium resection

117
Q

All cardiomyopathies carry risk of?

A

arrhythmia

118
Q

What can pericardial effusion become?

A

cardiac tamponade - when fluid becomes so much it affects the filling

119
Q

Rheumatic fever

A

Systemic infection by streptococcal pharyngitis (throat inflammation), the antibodies produced by to the carbohydrate cell wall of the streptococcus cross-react with the valve tissue in the heart –> permanent valve disease
Px - tachycardia, murmurs, fever

120
Q

Px with abdominal or thoracic aneurysms need rigorous control of?

A

Blood pressure

121
Q

How does aortic dissection occur?

A

Tear in the intima, blood penetrates layers, forces the layers apart - medical emergency

122
Q

Px of aortic dissection

A

Sudden onset crushing chest pain (may radiate, mimicking an MI), HTN, shock, aortic regurgitation

123
Q

Mx of aortic dissection

A
  1. HTN drugs to reduce BP
  2. Analgesia
  3. Surgery to replace
124
Q

What defines aortic aneurysm?

A

Dilatation of the aortic to twice the normal diameter

125
Q

Dilated CM

A

dilated ventricles, genetic mutation, cardiac myocytes = weak, impairs contractility, reduces systolic function

126
Q

Hypertrophic CM

A

Interventricular septum in particular has hypertrophied –> filling issues, diastolic dysfunction (cause of sudden cardiac death in young people)

127
Q

Restrictive CM

A

Heart muscles –> stiff, infiltrative diseases cause stiffness

128
Q

Tx for CM

A

Same for cardiac failure (CCBs, Beta blockers) + AF, amiodarone - anti-arrhythmatic agents

129
Q

Px of dilated CM

A

SOB, fatigue, dyspnoea, (like heart failure), arrhythmias

130
Q

Dx for valvular disease?

A

echocardiogram

131
Q

examples of CCBs

A

Amlopidine, verapamil

132
Q

X-ray findings in heart failure - ABCDE

A 
A - alveolar oedema
B - Kerley B lines
C - cardiomegaly
D - dilation of upper lobe vessels
E - pleural effusions
133
Q

What would show an ST elevation on an ECG?

A

STEMI, prinzmetal angina, pericarditis

134
Q

Prinzmetal angina

A

spasm in the coronary artery recurrent angina at rest, transient ST elevations on ECG

135
Q

Difference between BNP and ANP

A

both indicative of HF, ANP released mainly from the atria in response to stretch, and BNP from ventricles

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