Cardiovascular Flashcards

1
Q

What is atherosclerosis?

A

Build up of fatty deposits within arteries.

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2
Q

What are the risk factors for atherosclerosis?

A
Age 
Smoking 
High cholesterol 
Obesity 
Diabetes
Hypertension 
Family history
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3
Q

What are the components of an atherosclerotic plaque?

A
Lipid 
Necrotic core 
Connective tissue 
Fibrous cap 
Lymphocytes and macrophages
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4
Q

Describe the pathogenesis of atherosclerotic plaques.

A

Injury occurs to the endothelium, inflammation occurs and a plaque progresses.

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5
Q

What is the first stage of an atherosclerotic plaque?

A

Fatty streak

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6
Q

What are the risks of an atherosclerotic plaque?

A

It will rupture and form thrombi which will occlude vessels.
Plaque erosion may occur and a platelet clot will form above the plaque and occlude a vessel.

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7
Q

What is ischaemic heart disease?

A

Heart problems caused by vessel obstruction where blood supply does not meet metabolic demand.

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8
Q

What are the risk factors for ischaemic heart disease?

A
Smoking 
Obesity 
Sedentary lifestyle 
Hypertension 
Diabetes 
Older age 
Male
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9
Q

Describe the pathophysiology of stable angina.

A

There is increased resistance in the blood vessels of the heart so microvascular blood vessels are dilated at rest. On exercise they cannot dilate further so myocardial ischaemia occurs with the increased demand.

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10
Q

Which two vessel types determine coronary blood flow?

A

Epicardial vessels - minimal resistance

Microvascular vessels - the major determinate of resistance.

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11
Q

What are the clinical features of stable angina?

A

Heavy, central, tight chest pain
Radiate to arms, jaw and neck
Precipitated by exercise
Relieved rapidly by rest

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12
Q

What are the differential diagnoses of stable angina?

A
GORD 
Pericarditis 
Aortic dissection 
Musculoskeletal injury - ie. broken rib 
Psychological - ie. anxiety
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13
Q

What investigations are carried out in angina?

A

Blood tests - risk of anaemia causing angina.
ECG
Chest X-Ray
Echocardiography - if a high risk is indicated
Angiography - if risk indicates so

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14
Q

What are the results of an ECG in stage angina?

A

Usually normal

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15
Q

What are the causes of stable angina?

A

Atherosclerosis - usually
Anaemia
Tachyarrhythmias

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16
Q

How do you stratify risk in a patient with angina?

A

Calculating the likelihood of CAD

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17
Q

How do you calculate the likelihood of CAD?

A

Patients age, gender and type of angina.

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18
Q

What is the initial management of angina?

A

Modify risk factors - stop smoking, exercise, weight loss, control hypertension and diabetes.

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19
Q

What can be used for symptomatic relief in angina?

A

GTN spray (causes vasodilation)

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20
Q

What other pharmacological therapies can be used?

A

Beta-blockers (ie. propranolol)
Calcium channel antagonists (ie. amlodipine)
Long acting nitrates

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21
Q

When may surgery be indicated in angina?

A

When symptoms persist on two anti - anginals.

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22
Q

What are the rarer forms of angina?

A

Prinzmetal angina - coronary artery spasm

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23
Q

What are the three forms of acute coronary syndrome?

A

Unstable angina
NSTEMI
STEMI

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24
Q

What are the causes of acute coronary syndrome?

A

Arterial thrombosis - most common
Coronary spasm
Emboli

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25
Q

What investigations should be carried out in acute coronary syndrome?

A

ECG
Bloods - FBC, U&E, glucose, lipids
Cardiac enzymes

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26
Q

What cardiac enzymes can you test for in ACS?

A

Troponin
Creatinine kinase
Myoglobin

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27
Q

What are the differential diagnoses of ACS?

A

Angina
Pericarditis
Myocarditis
Pulmonary embolism

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28
Q

How do you interpret troponin results?

A

Measure levels >6 hours after symptoms, if raised repear 3 hours later. If there has been a fall in troponin then an MI is indicated (STEMI or NSTEMI)

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29
Q

What other conditions can troponin be indicative for?

A

Pulmonary embolism
Myocarditis
Congestive heart failure

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30
Q

What is unstable angina?

A

Angina of increasing severity or frequency, occurs with minimal exercise. High risk of developing to an MI.

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31
Q

What are the ECG changes in unstable angina?

A

Usually normal

Or ST depression and T wave flattening.

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32
Q

What is an NSTEMI?

A

This is a myocardial infarct diagnosis made retrospectively after troponin results and other investigations.

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33
Q

What are the symptoms of a STEMI?

A
Acute central chest pain 
Radiating to jaw, arms and shoulder 
>20 minutes 
Nausea 
Dyspnoea 
Sweating 
Palpitations
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34
Q

Can a STEMI preset silently?

A

YES. This is most common in the elderly of diabetics.

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35
Q

What are the signs of a STEMI?

A

Distress, anxiety, pallor, sweatiness, raised pulse.

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36
Q

What are the ECG changes of a STEMI?

A

ST elevation, tall T waves, Q waves can develop later.

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37
Q

What are the ECG changes in a NSTEMI?

A

ST depression, Q waves can develop later.

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38
Q

What is the initial management of a STEMI?

A
M - morphine 
O - oxygen as needed 
N - nitrates 
A - aspirin 300mg
Restore coronary perfusion - PCI or thrombolysis
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39
Q

What are further pharmacological options offered to patients who have had a STEMI?

A

Beta blocker
ACE inhibitor
Aspirin 75mg daily
Statin

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40
Q

What lifestyle changes can be recommended following an MI?

A

Smoking cessation
Exercise
Healthy diet
Weight loss

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41
Q

What is heart failure?

A

An inability of the heart to deliver blood at a rate commensurate with the requirement of the metabolising tissues.

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42
Q

What are the types of heart failure?

A

HF with preserved ejection fraction (diastolic)

HF with reduced ejection fraction <40% (systolic)

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43
Q

What is the cause of systolic heart failure?

A

Myocyte death - IHD, MI, cardiacmyopathy

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44
Q

What is the cause of diastolic heart failure?

A

Muscle hypertrophy, cardiac tamponade, hypertension, constrictive pericarditis.

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45
Q

What is the body’s compensatory mechanisms when the heart begins to fail?

A

Sympathetic stimulation
RAAS activation
Myocardial remodelling - ventricular dilation and myocyte hypertrophy.

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46
Q

Describe the pathophysiology of sympathetic activation in heart failure.

A

In the short term this increases HR to maintain the required CO.
In the long term it reduced myocardial reserve and increases dysfunction.
Indication for beta blocker therapy.

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47
Q

Describe the pathophysiology of RAAS activation in heart failure.

A

It increases water and salt retention. This increases afterload and preload, the demand on the heart is increased and dysfunction is increased.

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48
Q

What are the causes of right sided heart failure?

A

Pulmonary stenosis
Left sided heart failure
Any lung disease that increases vascular resistance.

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49
Q

What are the symptoms of right sided heart failure?

A
Peripheral oedema 
Ascites 
Nausea
Anorexia 
Facial engorgement
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50
Q

What are the causes of left sided heart failure?

A

Ischaemic heart disease
Hypertension
Aortic/mitral valve disease

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51
Q

What are the symptoms of left sided heart failure?

A
Dyspnoea
Poor exercise tolerance 
Fatigue 
Wheeze 
Nocturia 
Cold peripheries
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52
Q

What is the term for both sides of the heart failing?

A

Congestive heart failure.

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53
Q

What are the signs of heart failure?

A
Cardiomegaly 
Cool peripheries 
Cyanosis 
Tachycardia 
Displaced apex beat 
Weight loss
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54
Q

What investigations should be carried out in heart failure?

A

Blood tests - b-type natriuretic peptide
ECG
Chest X-Ray
Echocardiography

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55
Q

What are the signs of heart failure on X-Ray?

A
Alveolar oedema
Kerley B lines
Cardiomegaly 
Dilated prominant upper lobe vessels 
Pleural effusion
ABCDE
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56
Q

What are the result of b-type natriuretic peptide in heart failure?

A

Raised. Released on myocyte stretch.

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57
Q

What is the classification system for heart failure?

A

New York Heart Association Classification

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58
Q

What are the categories in the NYHA Classification of HF?

A

I - no limitation, asymptomatic
II - mild limitation, comfortable at rest
III - marked limitation, gentle activity produced marked symptoms.
IV - significant limitation, symptoms at rest

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59
Q

Lifestyle advice for someone with heart failure?

A

Stop smoking
Dietary modification - less salt
Weight loss
Avoid exacerbating factors - NSAIDs

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60
Q

What drugs can be offered in heart failure and give an example?

A
Diuretics - frusomide
ACE inhibitors - lisinopril
Beta blockers - proranolol
Spironolactone 
Digoxin
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61
Q

What diuretics are used in heart failure?

A

Loop diuretics - frusomide

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62
Q

What are the side effect of diuretics?

A

Can cause hypokalaemia

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63
Q

What diuretics can be used if hypokalaemia occurs?

A

Spironolactone is a potassium sparing diuretic.

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64
Q

What are the possible side effects of ACE inhibitors?

A

Cough

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65
Q

How do ACE inhibitors work?

A

Inhibit the conversion of angiotensin I - angiotensin II. less vasoconstriction, less water retention, less sympathetic activity

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66
Q

In what condition are beta blockers contraindicated?

A

Asthma

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67
Q

How do beta blockers work?

A

Inhibit sympathetic activation - less vasoconstriction and lower HR.

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68
Q

What is the function of digoxin?

A

It is a rate control medication.

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69
Q

How do you treat acute heart failure?

A

Oxygen
Nitrates - GTN
Analgesia
IV frusomide

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70
Q

What are the possible complications of heart failure?

A

Renal dysfunction
Arrhythmias
Thromboembolism

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71
Q

What are the four main valvular problems in the heart?

A
Aortic stenosis 
Mitral regurgitation 
Aortic regurgitation 
Mitral stenosis 
ALL ON THE LEFT SIDE.
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72
Q

At what point in aortic stenosis are symptoms felt?

A

When the valve area is 1/4 of its normal.

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73
Q

What are the causes of aortic stenosis?

A

Degenerative calcification
Congenital bicuspid valve
Rheumatic heart disease

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74
Q

What is the most common valvular disease?

A

Aortic stenosis

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75
Q

What are the pressure changes in the heart for aortic stenosis?

A

Increased pressure gradient between LV and A.
LV pressure increases
A pressure decreases

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76
Q

What is the compensatory mechanism of the heart in aortic stenosis?

A

LV hypertrophy

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77
Q

What are the symptoms of aortic stenosis?

A

Exertional syncope
Angina
Exertional dyspnoea

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78
Q

What are the signs of aortic stenosis?

A

Slow rising carotid pulse - pulsus tardus
Decreased pulse amplitude - pulsus parvus
Ejectional systolic murmur - crescendo/decrescendo
Soft/absent second heart sound
Prominent 4th heart sound

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79
Q

What investigations to carry out in aortic stenosis?

A

Echocardiography - diagnostic test
ECG
Chest X-Ray - LVH and calcification visible

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80
Q

How do you diagnose aortic stenosis?

A

Severe - valve area <1.0cm2

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81
Q

What is the general management for aortic stenosis?

A

Dental hygiene/consider antibiotic prophylaxis

ANY symptom is an indication for surgical intervention

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82
Q

What is mitral regurgitation?

A

Backflow of blood from the LV->LA during systole.

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83
Q

What are the causes of mitral regurgitation?

A

Degenerative change
Ischaemic heart disease
Rheumatic heart disease Infective endocarditis

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84
Q

What are the compensatory changes of the heart in mitral regurgitation?

A
LA dilation (due to volume overload in systole) 
LV hypertrophy
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85
Q

What are the pressure changes in mitral stenosis?

A

Rise in LA pressure during systole.

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86
Q

What are the symptoms of mitral stenosis?

A

Exertional dyspnoea
Fatigue
Palpitations

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87
Q

What are the signs of mitral stenosis?

A

Soft first heart sounds (incomplete closure)
Pansystolic mumur at apex, radiating to axilla.
Displaced apex beat.

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88
Q

What investigations to carry out in mitral regurgitation?

A

Echocardiography - diagnostic test
ECG
Chest X-Ray - Enlarged LA + LV

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89
Q

What is the pharmacological management for mitral regurgitation?

A

ACE inhibitors
Rate control for AF - BBs CCBs digoxin
Anticoagulant for AF
Diuretics can help symptomatically

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90
Q

What are the indication for surgery in mitral regurgitation?

A

Any symptoms

EF <60%

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91
Q

What is aortic regurgitation?

A

Leakage of blood into the LV during diastole.

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92
Q

What are the causes of aortic regurgitation?

A

Bicuspid aortic valve
Rheumatic heart disease
Infective endocarditis

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93
Q

What are the compensatory heart changes seen in aortic regurgitation?

A

LV dilation and LV hypertrophy

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94
Q

What are the pressure changes seen in aortic regurgitation?

A

Aortic pressure drops during diastole.

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95
Q

What is the presentation of aortic regurgitation?

A

Exertional dyspnoea

Angina

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96
Q

What are the signs of aortic regurgitation?

A

Collapsing pulse
Wide pulse pressure
Displaced apex beat
Diastolic blowing murmur

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97
Q

What are the investigation is aortic regurgitation?

A

Echocardiogram
ECH
Chest X-Ray - LV dilation and hypertrophy

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98
Q

When is surgeyr indicated in aortic stenosis?

A

Any symptom

EF <50%

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99
Q

What is mitral stenosis?

A

Obstruction of flow from LA to LV that prevents proper filling during diastole.

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100
Q

What are the causes of mitral stenosis?

A

Rheumatic heart disease
Infective endocarditis
Mitral calcification

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101
Q

What compensatory changes are made in mitral stenosis?

A

LA hypertrophy and dilation

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102
Q

What are the pressure changes seen in mitral stenosis?

A

Increases LA pressure, can have a build up of back pressure onto the pulmonary circulation.
LA pressure decreases during diastole.

103
Q

What are the symptoms of mitral stenosis?

A

Progressive dyspnoea
Right heart failure symptoms eventually
AF

104
Q

What are the signs of mitral stenosis?

A

Low volume pulse
Malar flush on cheeks
Loud first heart sound
Rumbling diastolic murmur

105
Q

What are the indications for surgery in mitral stenosis?

A

Any symptoms

106
Q

What percentage of births have a cardia defect?

A

1%

107
Q

What are the defects in the tetralogy of Fallot?

A

Ventricular septal defect
Overriding aorta
Hypertrophy of the right ventricle
Right ventricular outflow tract obstruction/pulmonary stenosis.

108
Q

In what syndrome is tetralogy of Fallot very common?

A

DiGeorge syndorme

109
Q

Why do patients present cyanosed with tetralogy of Fallot?

A

Pulmonary stenosis leads to RV pressure increase. RvV pressure greater that LV and blood moves across via the VSD. Deoxygenated blood circulates.

110
Q

What intervention is needed in tetralogy of Fallot?

A

Blalock-taussing shunt - connects subclavian to pulmonary artery for further blood oxygenation.
VSD closure
Relief of pulmonary stenosis.

111
Q

What is the most common congenital heart defect?

A

Ventricular septal defect

112
Q

Is there cyanosis in a VSD.

A

No. The shunt is L-R as LV has a high pressure.

113
Q

What is the physiological consequence of a small VSD?

A

Small increase in pulmonary blood flow

114
Q

What are the symptoms of a small VSD?

A

Asymptomatic usually. Most close by 10 years old.

115
Q

What is the clinical sign of a VSD?

A

Large pansystolic murmur.

116
Q

What is the physiological consequence of a large VSD?

A

High pulmonary blood flow - can lead to Eisenmenger;s complex.
Significant LA and LV dilation.

117
Q

What is Eisenmenger’s complex?

A

Pulmonary hypertension - damages pulmonary vasculature - pulmonary resistance increases - RV pressure increases - eventually RV pressure>LV pressure - shunt reverses - CYANOSIS

118
Q

What is the treatment of a VSD?

A

Closure

119
Q

What is an atrial septal defect?

A

An abnormal connection between the two atria.

120
Q

Does the patient present cyanosed?

A

No. the shunt is from the L-R as the LA has a higher pressure.

121
Q

What are the clinical effects of a large ASD?

A

There is significant overload to the right heart. Dyspnoea and exercise tolerance.

122
Q

What are the clinical signs of an ASD?

A

Pulmonary flow murmur
Large pulmonary arteries on X-Ray
Possible cardiomegaly

123
Q

What are the heart changes as a result of a significant ASD?

A

Right sided dilation and hypertrophy.

124
Q

What is the treatment of an ASD?

A

Closure.

125
Q

What is an atrio-ventricular septal defect?

A

There is a large septal defect and one large atrioventricular valve.

126
Q

What is a patent ductus arteriosus?

A

The ductus arteriosus is a bypass from the pulmonary artery to aorta in order to bypass the lungs in a neonate.

127
Q

Where is the shunt is a patent ductus arteriosus?

A

From the aorta to the pulmonary artery.

128
Q

What is the effect of a patent ductus arteriosus?

A

Pulmonary hypertension
Left heart volume overload overload and hypertrophy
Possible Eisenmenger’s syndrome

129
Q

What the treatment of patent ductus arteriosus?

A

Closure.

130
Q

What is coarctation of the aorta?

A

Narrowing of the aorta at the site of the ductus arteriosus.

131
Q

What are the effects of coarctation of the aorta?

A

Hypertension
Murmur
Claudication
Headaches

132
Q

What is a bicuspid aortic valve?

A

A bicuspid valve made of two instead of three valves.

133
Q

What is the effect of a bicuspid aortic valve?

A

Is prone to becoming stetotic and regurgitant.

134
Q

What is pulmonary stenosis?

A

Narrowing of the pulmonary artery.

135
Q

What is the effect of pulmonary stenosis?

A

Right ventricular failure
Right ventricular hypertrophy
Poor pulmonary blood flow
Tricuspid regurgitation

136
Q

What are the cardiac causes of an arrhythmia?

A
MI 
Coronary artery disease
Mitral valve disease
Cardiomyopathy 
Pericarditis 
Myocarditis
137
Q

What are the non-cardiac causes of arrhythmia?

A
Caffeine 
Smoking 
Pneumonia
Drugs 
Metabolic imbalance ie. potassium
138
Q

What is the typical presentation of arrhythmias?

A
Palpitations 
Chest pain 
Syncope 
Hypotension
Some are symptomatic
139
Q

Investigations to carry out in someone with an arrhythmia?

A

Blood - FBC, U&E
ECG
Echocardiogram
Provocation tests

140
Q

What are the two types of bradycardia?

A

Sinus - failure of impulse formation

AV block - failure of impulse conduction

141
Q

What are the causes of sinus bradycardia?

A

Hypothyroidism
Hypothermia
Drugs - beta blockers, digoxin
Acute ischaemia to SAN

142
Q

What is first degree heart block?

A

PR interval >0.22s

Every atrial depolarisation followed by ventricular depolarisation (just with delay)

143
Q

What is second degree heart block?

A

Occurs when some atrial depolarisation trigger ventricle depolarisation but not all.

144
Q

What scale are the various forms of second degree heart block judged on?

A

Mobitz scale

145
Q

What is Mobitz type I?

A

Progressive increase in PR interval until a missed ventricular depolarisation and it is ‘reset.’

146
Q

What is Mobitz type II?

A

A dropped ventricular depolarisation is not followed by a prolongation of PR again.

147
Q

What is third degree heart block?

A

All atrial activity fails to conduct to the ventricles.

148
Q

What is bundle branch block?

A

Delay/blockage of signal from one of the bundles to stimulate ventricular contraction.

149
Q

What is the overarching ECG sign of a bundle branch block?

A

QRS >0.12s

150
Q

What is the ECG finding in right BBB?

A

M in V1 and W in V6 - MaRRoW

151
Q

What is the ECG finding in left BBB?

A

W in V1 and M in V6 - WiLLiaM

152
Q

What two groups can tachycardias be split into?

A

Ventricular and supraventricular

153
Q

What are examples of supraventricular tachycardias?

A

Atrial fibrillation
Atrial flutter
AV nodal re-entry tachycardia

154
Q

What is atrial fibrillation?

A

Irregular, continuous, rapid activation of the atria with irregular ventricular conduction. 300-600 bpm.

155
Q

What are the causes of AF?

A
Hypertension 
Heart failure
Rheumatic heart disease 
Caffeine 
Alcohol
156
Q

What are the signs of AF?

A

Irregularly irregular pulse

157
Q

What are the symptoms of AF?

A

Asymptomatic
Chest pain
Palpitations
Dyspnoea

158
Q

What does an ECG show in AF?

A

Absent P waves

Irregular QRS complexes

159
Q

What is the risk with AF?

A

The formation of emboli

160
Q

What is the treatment for acute AF?

A

Cardioversion - drugs (amiodarone) or electrical.
Rate control with beta blockers/CCB of digoxin.
Anticoagulation with LMWH

161
Q

What are the drugs used for rate control?

A

First line - beta blockers/CCB
Second line - Digoxin
Third line - amiodarone

162
Q

What is the method for rhythm control?

A

Cardioversion

163
Q

What is atrial flutter?

A

Regular, rapid atrial depolarisation (approx 300bpm).

164
Q

What are the ECG changes in normal tachycardia?

A

Normal P wave followed by normal QRS

165
Q

What rate is required for a sinus tachycardia?

A

> 100bpm

166
Q

What are the causes of sinus tachycardia?

A

Anaemia, anxiety, exercise, pain, heart failure.

167
Q

What is ventricular tachycardia?

A

Wide QRS complexes independent of P waves.

168
Q

What are the effects of ventricular tachycardia?

A

Syncope, arrest.

169
Q

What is ventricular fibrillation?

A

Rapid, irregular QRS complexes.

170
Q

What is present in Wolff-Parkinson-White Syndrome?

A

Accessory pathways between atria and ventricles.

171
Q

What are the risk factors for hypertension?

A
Family history 
Male 
Sedentary lifestyle 
Unhealthy diet 
Obesity
172
Q

What are the causes of hypertension?

A
Unknown primary cause
Conn's syndrome - hyperalderosteonism
Renal failure 
Drugs 
Pregnancy
173
Q

What are the symptoms of hypertension?

A

None usually.

174
Q

What is malignant hypertension?

A

An acute rise in BP leading to vascular damage. Systolic >200, diastolic <130.

175
Q

What are the symptoms of malignant hypertension?

A

Headache

Visual disturbances

176
Q

What blood pressure measurement is classed as stage 1 hypertension?

A

> 140/90

177
Q

What tests can be carried out to confirm a diagnosis of hypertension?

A

24 hour ambulatory BP monitor

Multiple home BP measurements

178
Q

What measurement is classed as stage 2 hypertension?

A

> 160/100

179
Q

What measurement is classes as stage 3 hypertension?

A

> 180 and/or >110

180
Q

What other investigation should be carried out in a person with hypertension?

A

Eye exam - hypertensive retinopathy
Urine tests - kidney damage
ECG
Cardiovascular risk test - QRISK

181
Q

At what ABPM do you treat?

A

> 135/85 with a QRISK >20%

>150/95

182
Q

What lifestyle changes are recommended is a hypertensive patient?

A
Smoking cessation 
Low fat diet 
Reduce alcohol and salt intake 
Weight loss 
Exercise
183
Q

What is the treatment pathway for <55 year old with hypertension?

A
ACE inhibitor (or ARB if intolerant) 
ACE inhibitor + calcium channel blocker 
ACE inhibitor + calcium channel blocker + thiazide diuretic 
ACE inhibitor + calcium channel blocker + thiazide diuretic + diuretic/alpha/beta blocker.
184
Q

Give an example of a ACE inhibitor.

A

Lisinopril

185
Q

Give an example of a ARB.

A

Candesartan

186
Q

Give an example of a CCB.

A

Amlodipine

187
Q

Give an example of a thiazide diuretic?

A

Chlortalidone

188
Q

What is the treatment pathway for a patient >55 or afro-caribbean with hypertension.

A

Start with a CCB first

Then add ACEi and follow pathway as normal.

189
Q

What is the BP treatment goal for a standard hypertensive patient?

A

<140/90 (or ABPM 135/85)

190
Q

What is the BP treatment goal for a diabetic hypertensive patient?

A

<130/80

191
Q

What is the BP treatment goal for a >80 year old hypertensive patient?

A

<150/90

192
Q

What are the risks associated with hypertension?

A

Stroke
Ischaemic heart disease
Renal failure
Heart failure

193
Q

What are the three main subsets of cardiomyopathy?

A

Hypertrophic, dilated and arrhythmogenic.

194
Q

What is the physiological effect of hypertrophic cardiomyopathy?

A

Muscle hypertrophy -> decreased chamber volume.
Myocyte disarray - arrhythmias
Fibrosis - arrhythmias
Arterial hypertrophy - blocks arteries and causes ischaemia

195
Q

What are the symptoms of hypertrophic cardiomyopathy?

A
Mostly asymptomatic 
Chest pain 
Dyspnoea
Syncope 
Arrhythmias 
Sudden arrhythmic death syndrome
196
Q

What investigations should be carried out in the case of cardiomyopathies?

A

ECG
Echocardiography
Chest X-Ray

197
Q

What is seen on ECG in hypertrophic cardiomyopathy?

A

Very large voltages

198
Q

What is seen on echocardiography in hypertrophic cardiomyopathy?

A

asymmetric LV hypertrophy

199
Q

What is dilated cardiomyopathy?

A

Dilation of the heart chamber with preserved wall thickness.

200
Q

What is the physiological effects of dilated cardiomyopathy?

A

Blood cannot be pumped out of the heart effectively –> heart failure

201
Q

What is the cause of arrhythmogenic cardiomyopathy?

A

Desmosome gene mutations - cause cells to separate and myocytes are replaced by fat or fibrous tissue.

202
Q

What disease is associated with arrhythmogenic cardiomyopathy?

A

Naxos Disease

203
Q

What are the other features of naxos disease?

A

Woolly hair Palmar and plantar keratoderma.

204
Q

What is a channelopathy?

A

Inherited arrhythmia caused by a channel protein gene mutation.

205
Q

What is an example of a channelopathy?

A

Long QT syndrome

206
Q

What is the cause of Marfan’s disease?

A

Autosomal dominant mutation of the fibrillin gene.

207
Q

What is the effect of Marfan’s disease on the heart?

A

Lots of fibrillin at the base of the aorta so - enlargeed root with aneurysm/rupture.

208
Q

What are the skeletal effects of Marfan’s disease?

A

High arch palette
Tall
Long limbs.

209
Q

What is the primary cause of peripheral vascular disease?

A

Atherosclerosis

210
Q

What is the first symptom felt in peripheral vascular disease?

A

Intermittent claudication

211
Q

What is intermittent claudication?

A

On exercise the demand for oxygen of the tissues rises and this cannot be met my the blood supply - ischaemia occurs.

212
Q

What are the symptoms of intermittent claudication?

A

Cramping and pain on movement

Relieved by rest

213
Q

What is critical limb ischaemia?

A

The oxygen supply to tissues is barely met at rest.

214
Q

What are the symptoms of critical limb ishcaemia?

A

Rest pain, can be relieved on movement ‘hanging leg out the bed.’ Ulceration can occur.

215
Q

What are the differences between intermittent claudication and critical limb ischaemia?

A

In intermittent claudication the oxygen demand is met at rest in CLI it is not.
In IC pain is relieved by rest in CLI it is relieved by movement.

216
Q

What are the causes of acute limb ischaemia?

A

Thrombi

Emboli

217
Q

What are the symptoms of acute limb ischaemia?

A
Pain 
Palor 
Perishing cold 
Pulseless 
Paralysis 
Paraesthesia - 6 Ps.
218
Q

What are the investigations that can be carried out in peripheral vascular disease?

A

Ankle-brachial pressure index - 0.5-0.9
Ultrasound scan
Angiography

219
Q

What are lifestyle changes that can be made in peripheral vascular disease?

A
Smoking cessation 
Blood pressure control 
Weight loss
Exercise
Lower fat diet
220
Q

What is the treatment option in acute limb ischaemia?

A

Revascularisation

Amputation

221
Q

What are the causes of shock?

A
Blood loss
Myocardial failure 
Pulmonary embolus 
Vasodilation 
AV shunt
222
Q

What are the types of shock?

A
Anaphylactic 
Neurogenic 
Hypovolaemic 
Haemorrhagic
Septic
223
Q

What is the mechanism of anaphylactic shock?

A

Type 1 IgE mediated hypersensitivity causes profound vasodilation

224
Q

What are the causes of hypovoleimic shock?

A

Bleeding
Trauma
Rupture

225
Q

What is shock?

A

Circulatory failure resulting in inadequate organ perfusion.

226
Q

What is an aneurysm?

A

Permanent dilation of an artery to twice its normal diameter

227
Q

What are the possible causes of aneurysm?

A

Atheroma - inflammation weakens the wall
Infection
Trauma
Genetic

228
Q

Name two locations of aneurysm.

A

Abdominal aortic

Berry aneurysm - circle of Willis

229
Q

What are the symptoms of an abdominal aortic aneurysm?

A

Asymptomatic

Epigastric/back pain

230
Q

What are the signs of an abdominal aortic aneurysm?

A

Pulsatile mass

231
Q

What as the signs of a ruptured AAA?

A

Hypotension
Tachycardia
Profound anaemia
Sudden death

232
Q

What is an aortic dissection?

A

A tear in the intima of the aorta leads to blood moving in and splitting the vessel wall in two.

233
Q

What is pericarditis?

A

Inflammation of the pericardium

234
Q

What is the anatomy of the pericardium?

A

Visceral layer sits on the surface of the heart
Parietal is a fibrous layer
Between the two is 50ml of serous fluid.

235
Q

What are the causes of pericarditis?

A

Infection
Malignancy
Trauma

236
Q

What is the presentation of pericarditis

A
Severe and sharp chest pain 
worse on inspiration/lying flat 
Relieved sitting forwards 
Dyspnoea 
Cough
237
Q

What are the investigations for pericarditis?

A

ECG

Blood

238
Q

What are the signs of pericarditis?

A

Pericardial friction rub

239
Q

What are the ECG signs of pericarditis?

A

Saddle shaped ST elevation

PR depression

240
Q

What is the management of pericarditis?

A

Treat cause
Analgesia - NSAIDs
Colchicine - reduces chance of recurrence.

241
Q

What are the complications of pericarditis?

A

Recurrence
Pericardial effusion
Tamponade
Constrictive pericarditis

242
Q

What is the effect of a pericardial effusion?

A

If it is slow then the pericardium has time to expand and adapt.
If it rapid then there is no time to adapt, pressure increases and cardiac tamponade occurs.

243
Q

What is cardiac tamponade?

A

Compression of the heart caused by pericardial effusion.

244
Q

What is constrictive pericarditis?

A

Thick, fibrous, calcified pericardium restricts diastolic filling.

245
Q

What is the most common organism to cause endocarditis?

A

Staphylococcus aureus

246
Q

What are the symptoms of endocarditis?

A

Fever
Night sweats
Malaise
Weight loss

247
Q

What are the signs of endocarditis?

A
Any new murmur/change in pre-existing murmur 
Pyrexia 
Splinter haemorrhages (in nails)
Effect of emboli elsewhere
Clubbing
248
Q

What criteria is used to diagnose endocarditis?

A

Duke criteria

249
Q

What tests should be carried out in suspected endocarditis?

A

Blood cultures (3+!!) - can still be culture negative
Blood tests - neutrophillia, raised ESR and CRP
CXR
ECG
Echocardiogram

250
Q

What are possible complications of infective endocarditis?

A

Heart failure
Valvular obstruction
Emboli formation

251
Q

What are the major Duke criteria?

A
Positive blood culture 
Endocardium involved (on echo or new regurgitation)
252
Q

What are the minor Duke criteria?

A

Predisposition
Fever
Vascular/immunological signs
Positive blood culture but doe not fulfil major criteria
Positive echo but does not fulfil major criteria

253
Q

What are the risk factors for endocarditis?

A

Cardiac lesion
IC drug use
Open wounds
Organ transplant