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Phase 2a > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Define angina, and the difference between stable and unstable angina

A

Angina is the mismatch of oxygen demand an supply to the heart muscle, causing chest pain
- Stable angina is described as a chronic coronary syndrome, when the associated chest pain occurs predictably, for a short time, and is relieved with rest/GTN spray
- Unstable angina is described as new onset angina, or abrupt deterioration of stable angina, often occurring at rest, and is an acute coronary syndrome requiring emergency admission

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2
Q

Define acute coronary syndrome

A
  • unstable angina
  • STEMI = ST-elevation myocardial infarction
  • NSTEMI = non-ST-elevation myocardial infarction
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3
Q

Describe the epidemiology of acute and chronic coronary syndromes

A

More common in men, and in older ages

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4
Q

What are the causes of stable angina?

A

Atherosclerosis (IHD)
Also triggered by exercise, cold weather, heavy meals, emotional stress

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5
Q

What are the causes of acute coronary syndromes?

A

Atherosclerosis (IHD)

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6
Q

What are the risk factors for IHD (causing chronic/acute coronary syndromes)?

A

Age
Cigarette smoking
Family history
Diabetes mellitus
Hyperlipidaemia
Hypertension
Kidney disease
Obesity
Physical inactivity
Stress
Male

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7
Q

What are the associations of acute and chronic coronary syndromes?

A

Atherosclerosis
Hypertension
Hyperthyroidism
Valvular heart disease
Hypertrophic cardiomyopathy
Polycythaemia
Diabetes
CKD

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8
Q

Describe the pathophysiology of IHD

A
  • impairment of blood flow by proximal arterial stenosis
  • increased distal resistance e.g. left ventricular hypertrophy
  • reduced oxygen carrying capacity of blood e.g. anaemia
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9
Q

What are the signs/symptoms of stable angina?

A

Chest pain/tightness/discomfort (induced by exertion, relieved by rest/GTN spray)
Breathlessness
Sweating and pale
Gastrointestinal discomfort and nausea
*no fluid retention (unlike heart failure)
*palpitations and syncope are rare

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10
Q

What are the signs/symptoms of acute coronary syndromes?

A

Chest pain/tightness/discomfort (prolonged, new-onset, occurring at rest, not relieved by GTN spray, can be atypical in women or diabetics)
Sweating and pale
Nausea and vomiting
Fatigue and syncope
Palpitations
Shortness of breath

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11
Q

What are the investigations needed for stable angina?

A

ECG = abnormalities can’t confirm confirm diagnosis
Exercise testing (continuous ECG while walking on treadmill, relies on patient’s ability)
Stress echo (pharmacological stressor, needs highly skilled operator)
GOLDSTANDARD but invasive: coronary angiography

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12
Q

What investigations are needed for acute coronary syndromes?

A

ECG = STEMI will show ST elevation and pathological Q waves after a few days, unstable angina may show T wave inversion or ST depression, but normal ECG can’t exclude unstable angina or NSTEMI
Troponin = raised levels become detectable 3-6 hours after MI and stays elevated for several days, may be slightly elevated in unstable angina showing risk of cardiac events/death (not raised in stable angina)
GOLDSTANDARD = coronary angiography (shows presence and severity of coronary artery disease)

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13
Q

What are the treatments for stable angina?

A

Lifestyle changes (stop smoking, weight loss, exercise, diet)
Medication:
- nitrates (GTN spray for rapid-relief and long acting tablet - vasodilation to reduce BP which can be side effect)
- beta-blocker (first line treatment, reduce oxygen demand of the heart)
- calcium channel blockers
- aspirin (secondary prevention, cyclo-oxygenase inhibitor to reduce platelet aggregation), or clopidogrel if intolerant
- statin (HMG CoA reductase inhibitor to reduce LDL cholesterol production)
- ACE inhibitor (consider for patient who also have diabetes, less vasoconstriction to lower BP)
Revascularisation if becomes unstable angina:
- PCI (coronary angioplasty/stenting)
- CBAG (internal mammary artery/saphenous vein used for coronary bypass)

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14
Q

What is the treatment for acute coronary syndromes?

A
  1. Arrange hospital admission for any suspected ACS
  2. Resuscitation if required
  3. Pain relief = GTN spray, opiate
  4. Immediate 300mg of aspirin (or clopidogrel is intolerant) if ST elevation on ECG
  5. Oxygen if hypoxic
  6. Revascularisation = immediate PCI in STEMI, consider angiography with follow-on PCI in NSTEMI (if troponin elevated)/unstable angina
  7. Fibrinolysis (if PCI is not possible within 2 hours, high risk of bleeding)
  8. Consider: nitrates, beta-blockers, calcium channel blockers, ACEi
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15
Q

What are the complications of IHD?

A

Cardiovascular complications caused by coronary artery disease…
- stroke
- MI
- unstable angina
- sudden cardiac death
Other complications…
- anxiety and depression
- reduced quality of life

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16
Q

Define pericarditis

A

Acute pericarditis is inflammation of the pericardium (with or without effusion)

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17
Q

Describe the epidemiology of pericarditis

A

Difficult to quantify
80-90% of all pericarditis are idiopathic

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18
Q

What are the causes of pericarditis?

A

Viral = enteroviruses, herpesviruses, adenoviruses
Bacterial = TB (common cause worldwide)
Autoimmune = e.g. rheumatoid arthritis
Neoplastic = secondary tumours (e.g. breast)
Traumatic and iatrogenic = oesophageal perforation, radiation injury, post-myocardial infarction syndrome, PCI, pacemaker lead insertions

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19
Q

What are the signs/symptoms of pericarditis?

A

Chest pain - severe, pleuritic (worse on inspiration), rapid onset, left anterior chest/epigastrium, relieved by sitting forwards, exacerbated by lying down
Breathlessness
Cough
Fever
Pericardial rub may be heard
Signs of effusion or cardiac tamponade

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20
Q

What are the investigations needed for pericarditis?

A

ECG - saddle-shaped ST elevation, PR depression (but may be normal)
Bloods - FBC, ESR to determine cause, troponin (to rule out STEMI)
Chest X-ray - shows associated pneumonia and pericardial effusion
Echocardiogram - shows pericardial effusion

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21
Q

What is the treatment for pericarditis?

A

Sedentary activity until resolution of symptoms and ECG/CRP
NSAIDs or aspirin (high doses)
Colchicine (reduces recurrence)
Treat underlying cause

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22
Q

What are the complications of pericarditis?

A

Pericardial effusion
Cardiac tamponade

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23
Q

Define pericardial effusion

A

Accumulation of fluid in the pericardial sac

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24
Q

What are the causes of pericardial effusion?

A

Pericarditis
Malignancy
Post-MI
Idiopathic

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25
Q

What are the signs/symptoms of pericardial effusion?

A

Chest pain/pressure/discomfort (relieving by sitting forwards, exacerbated by lying down)
Dyspnoea
Muffled heart sounds
Palpitations and tachycardia
Pulsus paradox (exaggeration of normal respiratory variation in systemic blood pressure - >10mmHg decrease with inspiration)
Signs of cardiac tamponade

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26
Q

What investigations are needed for pleural effusion?

A

ECG (low voltage QRS)
Bloods = FBC, U+Es, cardiac enzymes
Chest X-ray = shows enlarged, globular heart if effusion present
MRI/CT/echocardiogram = detect effusion and inflammation

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27
Q

What is the treatment for pericardial effusion?

A

Oxygen therapy to relieve symptoms
Treat underlying conditions
Surgical removal of fluid

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28
Q

What are the complications of pericardial effusion?

A

Cardiac tamponade (haemodynamic comprise and death)
Chronic pericardial effusion

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29
Q

Define cardiac tamponade

A

A pericardial effusion that raises intrapericardial pressure, compressing the heart chambers, decreasing venous return and filling of the heart, so reducing cardiac output

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30
Q

What are the signs/symptoms of a cardiac tamponade?

A

Beck’s triad…
- falling BP
- rising JVP (jugular venous pulse)
- muffled heart sounds
Pulsus paradox due to reduced stroke volume (exaggeration of normal respiratory variation in systemic blood pressure - >10mmHg decrease with inspiration)

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31
Q

What investigations are needed for cardiac tamponade?

A

ECG
Echocardiogram (diagnostic)

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32
Q

What is the treatment for cardiac tamponade?

A

Remove fluid (pericardiocentesis)

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33
Q

What are the complications of cardiac tamponade?

A

Sudden cardiac arrest -> death

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34
Q

Define tetralogy of Fallot

A

A congenital heart disease characterised by…
- Ventricular septal defect
- Pulmonary stenosis
- Hypertrophy of the right ventricle
- Overriding aorta

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35
Q

Describe the pathophysiology of tetralogy of Fallot

A
  • stenosis of RV outflow leads to RV being at higher pressure than the left
  • deoxygenated blood passes from the RV to the LV through the ventral septal defect, leading to cyanosis
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36
Q

What are the sings/symptoms of tetralogy of Fallot?

A

Symptoms and severity of illness vary depending on the degree of pulmonary stenosis
- Infants may gradually become cyanotic after the ductus arteriosus closes causing increasing right to left flow through the VSD, hypoxic spell symptoms include restlessness and agitation
- In unoperated adults, cyanosis is very common
- In repaired adults, late symptoms include exertional dyspnoea, palpitations, clubbing, RV failure, syncope

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37
Q

What are the investigations needed for tetralogy of Fallot?

A

Echocardiogram to show anatomy and degree of stenosis
Cardiac CT/MRI useful in surgery planning

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38
Q

What are the treatments of tetralogy of Fallot?

A

Surgery (usually before the age of 1) to close ventricular septal defect and correct pulmonary stenosis

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39
Q

Define ventricular septal defect

A

A congenital heart defect characterised by an abnormal connection between the two ventricles, meaning that blood flows from the high pressure LV to the low pressure RV causing increased blood flow to the lungs

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40
Q

What are the sings/symptoms of ventricular septal defect?

A

Small defect: only small increase to pulmonary blood flow, asymptomatic, loud systolic murmur, some endocarditis risk, need no intervention
Large defect: very high increase in pulmonary flow, causing breathlessness, tachycardia, poor feeding, failure to thrive, large heart on CXR requires intervention in infancy, may lead to Eisenmenger’s syndrome

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41
Q

Define Eisenmenger’s syndrome

A

Pulmonary artery hypertension, causing damage to the pulmonary vasculature and increase in resistance of the blood flowing to the lungs, increasing the RV/A pressure and shunting deoxygenated blood to the LV/A through the A/VSD, causing cyanosis and clubbing

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42
Q

Define atrial septal defect

A

A congenital heart defect characterised by an abnormal connection between the two atrium, with the slightly higher pressure in the LA causing blood to shunt into the RA, increasing flow into the right heart and lungs

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43
Q

What are the clinical features of atrial septal defect?

A

Small defect: only small increase in flow, no right heart dilatation, often asymptomatic, but shunt can increase with age
Large defect: significant increase in flow, right heart dilatation, requires surgical closure, may present with chest pain, arrhythmias, dyspnoea, fixed split 2nd heart sound, big heart and pulmonary arteries on CXR, may lead to Eisenmenger’s syndrome

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44
Q

Define patent ductus arteriosus

A

A congenital heart disease characterised by the ductus arteriosus not closing after birth, causing blood to flow from the aorta into the pulmonary arteries

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45
Q

What are the signs/symptoms of patent ductus arteriosus?

A

Small defect: Little flow from aorta to pulmonary arteries, usually asymptomatic, some endocarditis risk
Large defect: Torrential flow from aorta to pulmonary arteries, continuous ‘machinery’ murmur, breathless, poor feeding, and failure to thrive, big heart on CXR, requires surgical closure, can lead to Eisenmenger’s syndrome

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46
Q

Define coarctation of the aorta

A

A congenital heart disease characterised by narrowing of the aorta at the sites of insertion of the ductus arteriosus

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47
Q

What are the signs/symptoms of coarctation of the aorta?

A

Mild: presents with hypertension (often right arm), incidental murmur, should be repaired to prevent problems in the long term
Severe: complete/almost complete obstruction of the aortic flow, presents with collapse and heart failure, bruits (buzzes) over the scapulae, systolic murmur, needs urgent repair (surgical or stenting)

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48
Q

What are the complications of coarctation of the aorta?

A

Hypertension (causing early IHD, strokes, etc.)
Re-coarctation requiring repeat intervention
Aneurysm formation at the site of repair

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49
Q

Define bicuspid aortic valve disease and the problems it can cause

A

A congenital heart disease characterised by an abnormally bicuspid valve (should be tricuspid), which will degenerate and become regurgitant faster than normal valves
Associated with coarctation and dilation of the aorta

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50
Q

Define pulmonary stenosis

A

A congenital heart disease characterised by narrowing of the right outflow tract of the heart, which can be valvular, sub-valvar, supra-valvar, or branch

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51
Q

What are the clinical features of pulmonary stenosis?

A

Mild: well tolerated for many years, seen as right ventricular hypertrophy
Severe: Right ventricular failure as neonate, poor pulmonary blood flow, tricuspid regurgitation

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52
Q

Define cardiomyopathy, and list the types

A

Cardiomyopathies are inherited cardiac conditions relating to disease of the heart muscle, including…
- hypertrophic cardiomyopathy
- dilated cardiomyopathy
- restricted cardiomyopathy
- arrhythmogenic cardiomyopathy

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53
Q

Describe the pathophysiology of each type of cardiomyopathy

A

Hypertrophic cardiomyopathy = caused by increased size/thickness of the heart muscle, leading reduced ventricular volume and less effective pumping of the blood
Dilated cardiomyopathy = caused the heart muscle walls to become thin and stretched, leading to decreased force of contraction
Restrictive cardiomyopathy = caused by stiffening of the muscle walls, affecting the relaxation and pumping
Arrhythmogenic cardiomyopathy = caused by fibro-fatty replacement of the myocytes

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54
Q

What are the signs/symptoms of the cardiomyopathies?

A

Present with symptoms of heart failure

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55
Q

Describe the P wave on an ECG

A

Represents atrial depolarisation
Upright in leads I, II, V2 to V6
Monophasic in lead II, biphasic in V1
Normal duration < 0.12s (3 small squares)
Normal amplitude < 2.5mm (2.5 small squares) in limb leads, < 1.5mm (1.5 small squares) in chest leads
Absent = AF
Tall = right atrial enlargement
Wide = left atrial enlargement

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56
Q

Describe the PR interval on an ECG

A

Represents the times between atrial and ventricular contraction (conduction through AV node)
From the onset of the P wave to the start of the QRS complex
Normal duration is between 0.12 and 0.2s (3-5 small squares)
Too long = AV block (delayed contraction)
Too short = pre-excitation syndromes

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57
Q

Describe the PR segment on an ECG

A

Between the end of the P wave and the start of the QRS complex
Usually isoelectric (flat)
PR segment depression = pericarditis, atrial ischemia/infarction (MI)

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58
Q

Describe the QRS complex on an ECG

A

Represents ventricular depolarisation
Dominantly upright in leads I and II
Normal duration = 0.06-0.1s (1.5-2.5 small boxes), can be up to 0.12 in healthy patients
Narrow complexes = supraventricular origin
Broad complexes = ventricular origin/aberrant conduction (e.g. bundle branch block)
Normal amplitude > 0.5mV (1 large box) in at least one limb lead, and > 1.0mV (2 large boxes)
High voltage (tall) QRS = left ventricular hypertrophy

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59
Q

Describe the QT interval on an ECG

A

Represents the time taken for ventricular depolarisation and repolarisation (ventricular systole)
From the start of the Q wave to the end of the T wave
Normal duration = 0.35-0.45s
Shortens in faster heart rates, lengthens in slower heart rates
Prolonged QT interval is associated with increased risk of ventricular arrythmias (caused by congenital long QT syndrome, drugs, low K, Mg, Ca)

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60
Q

Describe the ST segment on an ECG

A

Represents the time between ventricular depolarisation and repolarisation
From the end of the S wave (J point) to the beginning of the T wave
Should be isoelectric (flat)
Most common abnormality is STEMI
Saddle-shaped ST elevation = pericarditis

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61
Q

Describe the T wave on an ECG

A

Represents ventricular repolarisation
Upright in I, II, V2 to V6 (same orientation as QRS complex)
Duration relates to QT interval
Normal amplitude < 5mm in limb leads, < 10mm in chest leads
Peaked/flattened T waves = hyper/hypokalaemia
Inverted T waves = normal in children, sign of myocardial ischemia/infarction

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62
Q

What should happen to the R and S waves in the limb leads

A

The R wave should grow from V1 to at least V4
The S wave should grow from V1 to at least V3 and disappear in V6

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63
Q

What orientation are all the waves in aVR?

A

Negative

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64
Q

What is the RR interval used for

A

Rate = duration between each heart beat
- 300/number of large boxes between each R
- or number of R waves in 10s x 6
Rhythm =
- a regular rhythm has a constant RR interval
- regularly irregular rhythm has variable RR interval but with a pattern
- irregularly irregular rhythm has variable RR interval with no pattern

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65
Q

Which ECG leads examine the lateral surface of the heart?

A

I, aVL, V5, V6

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66
Q

Which ECG leads examine the inferior surface of the heart?

A

II, III, aVF

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67
Q

Which ECG leads examine the septal surface of the heart?

A

V1, V2

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68
Q

Which ECG leads examine the anterior surface of the heart?

A

V3, V4

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69
Q

Which leads show ST elevation if the left anterior descending artery is occluded?

A

Anterior: V1-V4
Lateral: V5-V6, I, aVL

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70
Q

Which leads show ST elevation if the right coronary artery is occluded?

A

Inferior: II, III, aVF

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71
Q

Which leads show ST elevation if the left circumflex artery is occluded?

A

Lateral: V5-V6, I, aVL
Inferior: II, III, aVF

72
Q

Define aortic stenosis

A

The narrowing of the aortic valve, with symptoms occurring when the valve area is 1/4th of the normal (3-4cm^2)
Can be supravalvular, subvalvular, or valvular

73
Q

What are the causes of aortic stenosis?

A

Congenital: aortic stenosis, or bicuspid valve
Acquired: degenerative calcification (aging) - most common, rheumatic heart disease

74
Q

Describe the pathological effects of aortic stenosis

A

The narrowed aortic valve decreases stroke volume, meaning that the LV pressure increases (due to increased afterload)
LV function in initially maintained by compensating with hypertrophy, but will eventually decline (due to ischemia)

75
Q

What are the signs/symptoms of aortic stenosis?

A

Syncope (on exertion)
Angina (increased myocardial oxygen demand)
Dyspnoea (on exertion, due to heart failure)
Late and weak pulse (relative to heart contraction)
Soft or absent second heart sound in severe cases
Ejection systolic murmur (due to blood flowing through the narrowed valve in systole)
* first presentation can be sudden death

76
Q

What are the investigations needed for aortic stenosis?

A

ECG: may show LV hypertrophy
CXR: LV hypertrophy, calcified aortic valve
Echocardiography: measure….
- LV size and function
- Doppler derived gradient and valve area

77
Q

What is the treatment of aortic stenosis?

A

Infective endocarditis prophylaxis for dental care/hygiene
Medical: limited role as aortic stenosis is not a medical problem (can use anti-arrhythmic drugs, but vasodilators are contraindicated)
Aortic valve replacement (surgical or transcatheter aortic valve implantation = TAVI)

78
Q

Define mitral regurgitation

A

Backflow of blood from the LV to the LA during systole

79
Q

What are the causes of mitral regurgitation?

A

Myxomatous (connective tissue) degeneration (causes mitral valve prolapse)
Annular (ring-shaped) calcification - in the elderly
Coronary artery disease (causes ischemia, ruptures/dysfunction of chordae tendinae and papillary muscles)
LV dysfunction due to dilatation
Rheumatic heart disease
Infective Endocarditis
Congenital - associated with atrial septal defects

80
Q

Describe the pathological effects of mitral regurgitation

A

Volume overload on the left atrium, leading the LA dilatation and enlargement, LV hypertrophy because more effort is needed to pump blood out of aorta, leading to progressive heart failure

81
Q

What are the signs/symptoms of mitral regurgitation?

A

Pansystolic (throughout systole) murmur at the apex radiating to the axilla
Exertion dyspnoea (exercise intolerance)
Fatigue
Palpitations (AF)

82
Q

What are the investigations needed for mitral regurgitation?

A

ECG = may show LA enlargement, AF, LV hypertrophy
CXR: LA enlargement, central pulmonary enlargement, pulmonary oedema, mitral valve calcification
ECHO = diagnostic, measure LA and LV size and function, and valve structure assessment

83
Q

What are the treatments of mitral regurgitation?

A

Medications: rate-control, anticoagulation in AF
*but no medication to treat mitral regurgitation itself
Infectious endocarditis prophylaxis
Surgical repair of valve (can replace with mechanical valve if repair is not possible)

84
Q

Define aortic regurgitation

A

Leakage of blood into LV during diastole due to ineffective closing of the aortic cusps

85
Q

What are the causes of aortic regurgitation

A

Bicuspid aortic valve (usually in combination of aortic stenosis)
Rheumatic heart disease
Infective endocarditis

86
Q

What are the pathological effects of aortic regurgitation?

A

The combined affects of the overload in pressure and volume, leading to LV dilation and hypertrophy, progressively leading to heart failure

87
Q

What are the signs/symptoms of aortic regurgitation?

A

Dyspnoea: exertional, orthopnoea (when lying down)
Palpitations
Angina
Syncope
Wide pulse pressure (high systolic, low diastolic)
Early diastolic murmur (blowing, decrescendo)
Systolic ejection murmur

88
Q

What investigations are needed for aortic regurgitation?

A

ECG: LVH
CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: diagnostic, evaluation of the AV and aortic root, measurements of LV dimensions and function

89
Q

What are the treatments for aortic regurgitation?

A

Infectious endocarditis prophylaxis
Medical: vasodilators (reduce systolic hypertension)
Surgical valve replacement

90
Q

What is the definition of mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole (normally 4-6cm^2, symptoms begin > 2cm^2)

91
Q

What are the causes of mitral stenosis?

A

Rheumatic heart disease (most common)
Infective endocarditis
Mitral annular (ring-shaped) calcification (commonly with calcification of other valves and in the elderly)
Congenital

92
Q

Describe the pathological effects of mitral stenosis

A

Increased pressure in the LA and pulmonary artery causes pulmonary hypertension, which leads to right ventricular failure

93
Q

What are the sings/symptoms of mitral stenosis?

A

Progressive dyspnoea (worse with exercise, fever, tachycardia, and pregnancy)
Palpitations (caused by AF)
Right heart failure symptoms (hepatomegaly, ascites, peripheral oedema)
Haemoptysis (rupture of bronchial vessels with increased pulmonary pressure)
Raised jugular venous pressure (JVP)
Diastolic murmur (low pitched, rumbling)

94
Q

What investigations are needed in mitral stenosis?

A

ECG: may show atrial fibrillation, LA enlargement, and RV hypertrophy
CXR: LA enlargement and pulmonary oedema, occasionally calcified mitral valve
ECHO: diagnostic, asses mitral valve mobility, gradient and mitral valve area

95
Q

What are the treatments for mitral stenosis?

A

Medications: heart-rate control for AF (e.g. beta-blockers, digoxin), diuretics for fluid overload in heart failure
Infective endocarditis prophylaxis
Surgical: restore valve opening (balloon valvotomy), or replacement if valve not pliable

96
Q

What are the complications of valvular heart diseases (aortic/mitral stenosis/regurgitation)?

A

Pulmonary hypertension
AF
Heart failure
Thromboembolic events

97
Q

Define infective endocarditis

A

Infection of heart valve(s) or other endocardial lined structures within the heart (such as septal defects, pacemaker leads, surgical patches, etc), with infectious material travelling around the bloodstream, and damage caused to the heart tissues leading to heart failure
Types divided into left/right, native/prosthetic/device related, early/late post-op (if prosthetic), assessed with Duke’s criteria

98
Q

Describe the epidemiology of endocarditis

A

Used to be because of rheumatic disease in younger people
Now more common in…
- the elderly
- IV drug users
- the young with congenital heart disease
- anyone with prosthetic heart valves
- men

99
Q

What are the causes of infective endocarditis?

A

Staph. aureus (most common overall)
Strep. viridans (most common in subacute)
Fungi (e.g. candida, aspergillus) - usually in IV drug users, immunocompromised, or those with prosthetic valves

100
Q

What are the risk factors for infective endocarditis?

A

Having an abnormal valve, or other structural defect (regurgitant or prosthetic valves are most likely to get infected)
Introduction of infectious material (IV drug users, tattoos, IV lines, wounds heart surgery)
Poor dental hygiene (in developing countries)
Have previously had infective endocarditis

101
Q

What are the signs/symptoms of infective endocarditis?

A

Signs of systemic infection (fever, sweats)
Embolic events (stroke, PE, MI)
Valve dysfunction (causing heart failure, arrythmia)
New heart murmur
Peripheral stigma (petechiae, splinter haemorrhages, Osler’s nodes, Janeway’s lesion, Roth spots on fundoscopy)

102
Q

What are the investigations needed for infective endocarditis?

A

Blood cultures = detect pathogens (diagnosed with 2 positive findings from 3 different sites, before antibiotics)
Blood tests = raised CRP
ECG = may show ischemia/infarction, new appearance of heart block
Echocardiogram = transthoracic/transoesophageal to detect vegetation

103
Q

What are the treatments of endocarditis?

A

FIRST = antibiotics/antimicrobials (IV)
Surgery: if not cured with antimicrobials, remove the infectious material, repair the damage (e.g. drain abscesses), or to remove large vegetations before the embolise
Treatment of other complications (emboli, arrythmia, heart failure, etc)

104
Q

What are the complications of infective endocarditis?

A

MI, stroke
Pericarditis
Cardiac arrhythmias
Congestive heart failure
Glomerulonephritis, acute kidney injury

105
Q

Define heart failure

A

An inability of the heart to deliver blood (and oxygen) at a rate proportionate with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures
Defined as heart failure with reduced (<40%) or preserved (>50%) ejection fraction
Also defined with NYHA: class I - IV = no limitation/symptoms - severe limitation/symptoms

106
Q

What is the difference between right and left sided heart failure?

A

Left-sided heart failure (LV failure) is when the left ventricle is unable to pump blood to the body efficiently, due to conditions which weaken the heart (IHD, MI, cardiomyopathy), usually presenting with shortness of breath and fluid in the lungs
Right-sided heart failure (RV failure) can be caused by issues like lung disease, but usually occurs due to left-sided heart failure, and presents with fluid in the abdomen, legs, and ankles
These can occur independently or together as congestive cardiac failure

107
Q

Define cor pulmonale

A

Right-sided heart failure caused by chronic pulmonary arterial hypertension, due to chronic lung disease (e.g. COPD), pulmonary vascular diseases (e.g. PE), thoracic cage abnormalities, or neuromuscular diseases

108
Q

Describe the epidemiology of heart failure

A

Incidence increases with age
Men are more at risk
Patients will be younger men but older women

109
Q

What are the causes of heart failure?

A

Myocardial dysfunction resulting from IHD (most common)
Hypertension
Alcohol excess
Cardiomyopathy
Valvular
Pericardial

110
Q

What are the signs/symptoms of heart failure?

A

Breathlessness (exertion, rest, lying flat)
Specific for heart failure = paroxysmal nocturnal dyspnoea (shortness of breath when waking from sleeping)
Tiredness + exercise intolerance
Cold peripheries
Leg swelling
Tachycardia
Raised JVP
Added heart sounds and murmurs

111
Q

What are the investigations needed for heart failure?

A

N-terminal pro-B-type natriuretic (BNP) = raised (with myocardial stress)
ECG = may show cause (ischemia, MI, LVH)
Echocardiogram (identifies ventricular dysfunction, valve disease, shunts)
CXR = shows ABCDE: alveolar oedema, Kerley B lines, cardiomegaly, dilated upper lobe vessels, pleural effusion

112
Q

What are the treatments for heart failure

A

Treat underlying cause and comorbidities
Lifestyle modifications
Medications for HFrEF
- 1st line: beta blockers (bisoprolol) most effective, but won’t decrease mortality (CCB if CI)
- loop diuretics, relieve symptoms of fluid overload
- ACEi: less response in Afro-Caribbeans (or ARBs if ACEi contraindicated)
- SGLT2 inhibitors
- consider antiplatelets and statin
Medications for HFpEF
- diuretics (loop) to relieve symptoms of fluid overload
- consider antiplatelets and statin
Cardioversion therapy
Revascularisation (in patients with angina/MI)
Transplant (rare)

113
Q

What are the complications of heart failure?

A

Cardiac arrhythmias
CKD/AKI
Anaemia
Depression
Sudden cardiac death

114
Q

Define hypertension

A

Persistently raised arterial blood pressure (clinic readings above 140/90, and ambulatory/home readings above 135/85)

115
Q

Describe the epidemiology of hypertension

A

Estimated that 1 in 4 adults have hypertension
Slightly higher in men
Prevalence increases with age (over 60% in over 60s)

116
Q

What are the causes of hypertension?

A

Primary hypertension (90%) has no identifiable cause
Secondary hypertension (10%) has a known underlying cause, such as renal, endocrine, or vascular disorder, or the use of certain drugs

117
Q

What are the risk factors for hypertension?

A

Older age
Sex (more likely to be higher in men, but opposite when older)
Diet (high salt)
Lack of exercise
Excessive alcohol
Ethnicity
Emotional stress

118
Q

What are the associations of hypertension?

A

Diabetes
Kidney disease
Family history

119
Q

What are the signs/symptoms of hypertension?

A

Usually asymptomatic
Headaches are more common than in the general public
Signs of end organ damage in kidneys (AKI, proteinuria), heart (ACS, LVH), eyes (papilledema, retinopathy)

120
Q

What are the investigations needed for hypertension?

A

Ambulatory blood pressure monitoring (24hr reading) or structured home blood pressure monitory
ECG/echo to asses cardiac function and look for end organ damage
Fundoscopy: check retinopathy
Bloods: HbA1C, electrolytes, kidney function (eGFR), cholesterol (CVD risk)
Urinalysis: haematuria, proteinuria

121
Q

What is the treatment for hypertension?

A

Lifestyle modifications
If patient has T2DM, or is under 55…
- ACEi or ARB if not tolerated
- add CCB or thiazide diuretic
If patient is over 55, or of Black African or Afro-Caribbean ethnicity…
- CCB
- add ACEi/ARB or thiazide diuretic
If hypertension still persists in either group…
- add third option
- if still high, consider spironolactone, alpha/beta blocker

122
Q

What are the complications of hypertension?

A

IHD
MI
Heart failure
Stroke (haemorrhagic is most closely linked)
Renal failure (CKD)
Dementia (vascular)
Peripheral vascular disease

123
Q

Define arterial thrombosis

A

Blood coagulation in the high pressure arteries, driven by platelets, occurring in the coronary, cerebral, and peripheral circulations

124
Q

What are the causes of arterial thrombosis?

A

Atherosclerosis
Inflammatory
Infective
Trauma
Tumours

125
Q

How does arterial thrombosis present?

A

Angina/MI
Cerebrovascular accident (stroke)
Peripheral vascular disease

126
Q

What are the treatments for arterial thrombosis?

A

Aspirin - COX inhibitor, stopping thromboxane formation and platelet aggregation
Clopidogrel - inhibits ADP induced platelet aggregation by irreversibly binding to p2y12 receptors
LMWH (high risk of bleeding) or Fondaparinux (indirect Xa inhibitor, anti-coagulant)
Thrombolytic therapy (streptokinase)
Reperfusion (catheter directed treatments)

127
Q

Define venous thrombosis

A

Blood coagulation in the low pressure veins, driven by fibrin, commonly occurring in the peripheral veins (iliofemoral, femoropopliteal), and also the cerebral and visceral circulation

128
Q

What are the causes of venous thrombosis?

A

Virchow’s triad:
- endothelial damage (smoking, trauma, chemicals)
- change in blood flow (immobilisation in long haul flights, surgery, trauma)
- change in blood constituents (increased coagulation due to genetic deficiencies, or acquired syndromes e.g. anti-phospholipid)

129
Q

What are the treatments for venous thrombosis?

A

Heparin - binds to antithrombin and increases its activity, short half life so needs continuous infusion and monitoring
LMWH - longer half life so given once/twice daily s/c, dose adjusted for weight and renal function
Warfarin - oral, vitamin K antagonist prevents synthesis of active factors II, VII, IX, X, needs monitoring
DOAC - (e.g. apixaban) oral, act of factors II and X, doesn’t need monitoring, not used in pregnancy or after metal heart valves surgery
Surgical repair (if high chance of long term complications)

130
Q

How is venous thrombosis prevented?

A

Thromboprophylaxis medication (LMWH-delteparin/fondaparinux)
Early mobilisation
Good hydration
Compression stocking (can also improve symptoms of DVT)

131
Q

What are the complications of venous thrombosis?

A

Ischemia (leading to loss of limb)
Long-term swelling
Venous ulceration
Pulmonary embolism

132
Q

Define DVT and PE

A

Deep vein thrombosis = thrombosis occurring in the small veins of the leg
Pulmonary embolism = thrombosis occurring in the small vessels of the lungs (complication of DVT)

133
Q

Describe the epidemiology of DVT and PE

A

25,000 deaths per year in the UK
50% are preventable

134
Q

What are the risk factors for DVT?

A

Surgery
Immobility
Leg fracture
Oral contraceptive pill and HRT (oestrogen)
Pregnancy
Long haul flights
Genetic predisposition
* think Virchow’s triad

135
Q

What are the signs/symptoms of DVT?

A

Leg pain
Swelling (pitting oedema)
Tenderness
Warmth
Discoloration

136
Q

What are the investigations needed for DVT?

A

D-dimer = normal excludes diagnosis, positive doesn’t confirm diagnosis
Ultrasound = GOLD STANDARD

137
Q

What is the treatment of DVT?

A

LMWH or fondaparinux
DOAC (apixaban)
IVC filters
Compression stockings to relieve symptoms

138
Q

What are the signs/symptoms of PE?

A

Breathlessness
Pleuritic chest pain
Haemoptysis
Syncope/hypotension
Signs/symptoms of DVT
Tachycardia
Tachypnoea
Pleural rub

139
Q

What are the investigations needed for PE?

A

CXR (usually normal)
ECG = sinus tachycardia
Blood gases = type 1 respiratory failure, decrease O2 and CO2
D-dimer (normal excludes diagnosis)
CT = GOLD STANDARD

140
Q

What is the treatment for PE?

A

LMWH or fondaparinux
Thrombolysis (if haemodynamic instability)
Long -term anticoagulation (DOAC/warfarin)
Treat underlying cause

141
Q

Define peripheral vascular disease

A

A slow and progressive disorder caused by narrowing, blockage or spasms of the peripheral arteries, veins, or lymphatics

142
Q

What are the causes of peripheral vascular disease?

A

Atherosclerosis
Inflammatory
Vasospastic (Raynaud’s syndrome)
Compression (e.g. from malignancy)
Traumatic (open wounds, sheer forces)
Pro-thrombotic conditions
Poor venous return (valves/muscle pump)

143
Q

What are the risk factors for peripheral vascular disease?

A

Modifiable:
- smoking
- hypertension
- uncontrolled diabetes
- hypercholesterolaemia
Non modifiable:
- age
- sex

144
Q

What are the signs/symptoms of peripheral vascular disease?

A

Acute ischemia…
- pain
- paraesthesia
- pulseless
- pallor
- perishingly cold
- paralysis
- acute emboli (AF, MI)
Chronic ischemia…
- intermittent claudication (pain when walking, relieved by rest)
- rest pain (often at night)
- tissue loss (ulceration, gangrene)
- Burger’s test (angle that leg goes pale when raised and capillary filling time)

145
Q

What are the investigations needed for peripheral vascular disease?

A

Bloods: lipids, glucose, renal function, vasculitis screen, clotting, FBC
ABPI (ankle-brachial pressure index) - ration of blood pressure in upper and lower limb
Duplex scan (ultrasound doppler) - shows flow velocity, and vessel dimensions
Cross sectional imaging - CT/MR angiogram

146
Q

What are the treatments for peripheral vascular disease?

A

Risk factor modifications:
- antiplatelets (clopidogrel)
- statin
- stop smoking
- control of BP and DM
- exercise programmes
Invasive treatments:
- endovascular (stents)
- endovenous laser treatments
- bypass
- amputation

147
Q

Define aortic aneurysm

A

Weakening of the arterial wall leading to dilation to 2x the normal size and involving all three layers of the artery, with the commonest location being the infra-renal aorta (AAA = abdominal aortic aneurysm)

148
Q

What are the causes of an abdominal aortic aneurysm?

A

Atheroma
Trauma
Infection
Connective tissue disorder

149
Q

What are the signs/symptoms of an abdominal aortic aneurysm?

A

Unruptured: often asymptomatic, may cause abdominal/back pain
Ruptured: Intermittent/continuous pain (radiates to back, iliac fossae or groin), collapse, expansile abdominal mass, shock

150
Q

What are the treatments for AAA?

A

Monitoring for risk of rupture
Endovascular (stent)
Open surgery (higher initial morbidity/mortality, but lower long-term morbidity/mortality) - if expanding or symptomatic
If ruptured: immediate vascular surgery

151
Q

Define aortic dissection

A

A tear in the inner layer of the aorta and splitting the aortic wall layers which allows blood to run into the space

152
Q

What are the risk factors of aortic dissection?

A

Hypertension
Smoking
High cholesterol
Personal or family history of aortic disease
Cardiac surgery
Blunt trauma to the chest
IV drugs

153
Q

What are the signs/symptoms of aortic dissection?

A

Chest pain (tearing/sharp) - maximal at time of onset, migrates with dissection
Hypertension
Paraplegia (paralysis of legs)
Hemiplegia (one-sided paralysis)
Pulse difference between left and right

154
Q

What investigations are needed for aortic dissection?

A

ECG: check for infarction/ischemia
Transoesophageal/transthoracic ultrasound: show site and extent of dissection
MRI: confirms diagnosis

155
Q

What is the treatment needed for aortic dissection?

A

Analgesia
Replace blood loss
Manage hypertension
Beta-blockers (reduces force of ventricular contraction)

156
Q

What are the causes of cardiac arrhythmias?

A

Ischemic heart disease
Structural changes
Cardiomyopathy
Pericarditis
Aberrant conduction pathways
Non cardiac: caffeine, smoking, alcohol, drugs (B2 agonists), metabolic imbalances, infection

157
Q

What are the signs/symptoms of arrythmias?

A

Palpitations
Chest pain
Syncope
Hypotension
Pulmonary oedema
*some may be asymptomatic

158
Q

What are the investigations needed for arrhythmias?

A

Bloods: FBC, U&Es, TSH
ECG (simple 12 lead, 24hr, continuous monitoring)
Echocardiogram (look at structural heart disease)

159
Q

Describe the different types of tachycardias

A

Supraventricular tachycardias:
- problem occurs in atria
- ventricles are depolarised via normal conduction pathways
- narrow QRS complex <120ms
- can be atrial fibrillation (irregular and fast atria beats), flutter (regularly fast atrial beats, more often than the ventricles)
Ventricular tachycardias:
- problem occurs in ventricles, they do not depolarise via normal conduction pathway
- broad QRS complex >120ms
- can be ventricular fibrillation (chaotic contraction with no pattern) or ventricular tachycardia (rapid contraction, regular pattern)

160
Q

What does an ECG show in atrial fibrillation?

A

Irregularly irregular rhythm
No P waves
Usually narrow QRS complex (unless pre-existing bundle branch block, or accessory pathway)
Variable ventricular rate

161
Q

What does an ECG show in atrial flutter?

A

Narrow complex tachycardia
Regular atrial activity at ~300bpm
“Saw-tooth” pattern of inverted flutter waves in leads II, III, a VF
Ventricular rate depending on AV conduction ratio (e.g. 2:1 block = 150bpm)

162
Q

What is the treatment for atrial fibrillation?

A

Acute AF:
- ABC
- cardioversion +/- amiodarone
- heparin
- if stable, rate or rhythm control
- correct electrolyte imbalances
Chronic AF:
- rate control (B-blockers, CCB, digoxin, amiodarone)
- rhythm control (cardioversion, flecainide)
- anticoagulation (risk assessed using CHA2DS2VASc score, give DOAC or warfarin)

163
Q

Describe the ECG changes in the different types of heart block

A

1st degree heart block:
- PR interval is prolonged (>200ms) but unchanging, no missing beats
2nd degree heart block:
- Mobitz I = progressive prolongation of PR interval, then an non-conducting P wave (missing beat)
- Mobitz II = sudden unpredictable non-conducting P wave and missing beat, may be with a fixed ratio (constant PR interval)
3rd degree heart block:
- complete AV dissociation, independent atrial and ventricular rates

164
Q

Define bundle branch block

A

When the conduction impulses don’t travel down the left and right bundle equally
In left bundle branch block (LBBB), impulses travel via the right bundle branch to the RV, then across the septum to the LV, so the overall depolarisation is towards the lateral leads
In right bundle branch block (RBBB), impulses travel via the left bundle branch to the LV, then across the septum to the RV, forming small Q waves in the lateral leads

165
Q

What are the ECG changes seen in RBBB?

A

M-shaped QRS complex in V1
W-shaped QRS complex in V6
*MaRRoW

166
Q

What are the ECG changes seen in LBBB?

A

W-shaped QRS complex in V1
M-shaped QRS complex in V6
*WiLLiaM

167
Q

Define the different types of axis deviation

A

Normal axis = sum of QRS between -30 and +90 (positive in I and aVF)
Right axis deviation = sum of QRS greater than +90 (positive in aVF, negative in I)
Left axis deviation = sum of QRS less than -30 (positive in I, negative in aVF)
Extreme axis deviation = sum of QRS between -90 and +180, northwest axis (negative in I and aVF)

168
Q

What are the causes of left axis deviation on an ECG?

A

Left bundle branch block
Left ventricular hypertrophy
Left anterior fascicular block

169
Q

What are the causes of right axis deviation?

A

Right ventricular hypertrophy/strain (from acute/chronic lung disease)
Left posterior fascicular block

170
Q

Define shock

A

Circulatory failure resulting in inadequate organ perfusion, often defined as systolic blood pressure <90 or mean arterial pressure <65, with evidence of tissue hypoperfusion

171
Q

What is the equations for mean arterial pressure, and how does this affect the causes of shock?

A

Mean arterial pressure = cardiac output x systemic vascular resistance
Cardiac output = stroke volume x heart rate
Shock can result from inadequate cardiac output, or a loss of systemic vascular resistance, or both

172
Q

List the 5 types of shock and the basic pathophysiology

A

Hypovolaemic:
- inadequate cardiac output
- e.g. bleeding (trauma, ruptured AAA, GI bleed) or fluid loss (vomiting, burns, pancreatitis)
Cardiogenic:
- inadequate cardiac output
- e.g. acute coronary syndrome, arrhythmias, acute valve failure
Septic:
- loss of systemic vascular resistance
- infection causing acute vasodilation from inflammatory cytokines
Anaphylaxis:
- loss of systemic vascular resistance
- type 1 IgE-medicated hypersensitivity reaction resulting in the release of histamine which causes vasodilation
Neurogenic:
- loss of systemic vascular resistance
- e.g. spinal cord injury, epidural or spinal anaesthesia

173
Q

What are the signs/symptoms of shock?

A

Tachycardia
Tachypnoea
Low systolic blood pressure/narrow pulse pressure (systolic-diastolic)
Slow/absent capillary refill
Pallor
Cold and clammy - cardiogenic shock/fluid loss
Warm and well perfused - septic shock
Rash, wheeze - anaphylactic shock
Reduced GCS (agitation, confusion, unresponsive)
Signs of tissue hypoperfusion (mottled skin, urine output <0.5ml/kg/h, serum lactate >2mmol/L)
Signs of dehydration (skin turgor, postural hypotension)

174
Q

What is the treatment for hypovolaemic shock?

A

ABCDE
Identify and treat underlying cause
Raise the legs
Give oxygen
IV crystalloid fluid
For haemorrhage: give blood products
IV analgesia if needed

175
Q

What is the treatment for septic shock?

A

ABCDE
Antibiotics (IV, broad spectrum) +/- antivirals/antifungals
IV crystalloid fluids
Oxygen
Noradrenaline (vasopressor)
Management of other acute complications

176
Q

What is the treatment for cardiogenic shock?

A

ABCDE
Oxygen
IV analgesia
Fluids if needed
Correct arrhythmias and electrolyte abnormalities

177
Q

What is the treatment for anaphylactic shock?

A

ABCDE
Remove the cause, raise legs
Oxygen
IM adrenaline (repeat as needed)
Fluids
IV chlorphenamine (antihistamine) + IV hydrocortisone
Treat asthma for wheeze (beta-blocker e.g. salbutamol)

Phase 2a (14 decks)

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