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Phase 2a > Cardiovascular Diseases > Flashcards

Cardiovascular Diseases Flashcards

1
Q

What is the normal presentation of atherosclerosis?

A

Normally asymptomatic until complications. If severe, can cause angina or neurological problems.

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2
Q

In which arteries can atherosclerosis occur?

A

Aorta, cerebral, common iliac/femoral, coronary, carotid

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3
Q

What is the normal pathology of atherosclerosis?

A

Endothelial damage causes LDLs to be attracted to the wall. Chemoattractants are released from the endothelium. Neutrophils are attracted and phagocytose LDLs to form foam cells. These are inflammatory and cause an accumulation. Fibrous cap forms. This can then occlude flow or rupture.

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4
Q

How is atherosclerosis normally diagnosed?

A

Patients over 40 should be assessed for their risk during their NHS health check every 5 years

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5
Q

What is a fatty streak?

A

The earliest lesion of atherosclerosis. Aggregation of lipid-laden macrophages (foam cells), and T lymphocytes within the intima

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6
Q

What are the risk factors for atherosclerosis?

A

Hypercholesterolaemia, Hyperlipidaemia, hypertension, smoking, poorly controlled diabetes, males, older age, social deprivation, family history, south Asian African or Caribbean descent

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7
Q

What are some natural preventative measures for atherosclerosis?

A

Smoking cessation, controlling blood pressure, weight reduction, lower alcohol consumption, exercise, managing diabetes

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8
Q

What medications can be used to prevent progression of atherosclerosis?

A

Statins (satorvastatin, fluvastatin),
Blood pressure medications= CCB, ARBs, ACE
Low dose aspirin

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9
Q

What surgical interventions can be used for atherosclerosis?

A

Coronary angioplasty, coronary artery bypass

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10
Q

What are some possible complications of atherosclerosis?

A

Coronary artery disease, angina, myocardial infarction, stroke, TIA, peripheral artery disease

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11
Q

What is the normal presentation of hypertension?

A

Usually asymptomatic

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12
Q

What are the risk factors for hypertension?

A

Obesity, high salt, caffeine, alcohol, low exercise, over 65s, family history, black African or Caribbean descent, some medications such as the pill, steroids, Eclampsia, renal disease

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13
Q

What are the types of hypertension?

A 
Primary= Unknown cause
Secondary= Caused by another condition
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14
Q

What is the aetiology for secondary hypertension?

A

Kidney disease, diabetes, hormonal problems

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15
Q

What is CBP?

A

Clinic blood pressure

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16
Q

What is ABPM?

A

Ambulatory blood pressure monitoring

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17
Q

What is HBPM?

A

Home blood pressure monitoring

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18
Q

What CBP would imply stage 1 hypertension?

A

> 140/90

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19
Q

How is a diagnosis of hypertension made?

A

CBP of over 140/90 on two separate readings, then offered ABPM or HBPM to confirm

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20
Q

What CBP would imply stage 2 hypertension?

A

> 160/100

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21
Q

What CBP would imply stage 3 hypertension?

A

> 180/120

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22
Q

What extra investigations would be offered to someone with hypertension?

A

Urinalysis= for haematuria and proteinuria (Renal disease)
Urine albumin creatinine ratio (End organ damage)
ECG for cardiac arrhythmias
Blood U&E for renal impairment
HbA1c for diabetes

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23
Q

What preventative measures can be taken for hypertension?

A

Exercise, smoking cessation, lower salt intake, lower alcohol and caffeine, healthy BMI

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24
Q

What would be the first line of treatment for someone with type II diabetes or is under 55 and non-black, who has hypertension?

A

ACE inhibitor or angiotensin II inhibitor (ARB)

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25
Q

What would be the second line of treatment for someone with type II diabetes or is under 55 and non-black, who has hypertension?

A

Ace inhibitor or angiotensin II inhibitor

+ Calcium channel blocker or thiazide-like diuretic

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26
Q

What is the third line of treatment for anyone with hypertension?

A

ACE inhibitor or angiotensin II inhibitor
Calcium channel blocker
Thiazide diuretic

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27
Q

What is the first line of treatment for someone over 55 or black African/Caribbean with hypertension?

A

Calcium channel blocker

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28
Q

What is the second line of treatment for someone over 55 or black African/Caribbean with hypertension?

A

Calcium channel blocker

ACE inhibitor or Angiotensin II inhibitor or Thiazide diuretic

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29
Q

What are some complications of hypertension?

A

Myocardial infarction, stroke, heart failure, aortic aneurysm, kidney disease, vascular dementia

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30
Q

What is the epidemiology of patent ductus arteriosus?

A

Affects girls more than boys

0.02% of live births

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31
Q

Briefly explain the pathophysiology of patent ductus arteriosus

A

If the baby is premature or in cases of maternal rubella etc. the ductus ( between the proximal left pulmonary artery and descending aorta) does not close. This leads to an abnormal shunt from the aorta to the pulmonary artery, and eventually leads to pulmonary hypertension and right side cardiac failure.

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32
Q

What is the clinical presentation of patent ductus arteriosus?

A
  • Continuous machinery murmurs
  • Bounding pulse
  • If large- large heart and breathlessness
  • Tachycardia
  • Eisenmenger’s syndrome
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33
Q

How is patent ductus arteriosus diagnosed?

A
  • CXR: With large shunt, the aorta and pulmonary arterial system may be prominent
  • ECG: May demonstrate left atrial abnormality and left ventricular hypertrophy
  • Echocardiogram: May show dilated left atrium and left ventricle
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34
Q

How is patent ductus arteriosus treated?

A
  • Can be closed surgically or percutaneously
  • Low risk of complications
  • Venous approach may require an AV loop
  • Indometacin (prostaglandin inhibitor) can be given to stimulate duct exposure
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35
Q

What is the epidemiology of ventricular septal defect?

A

Common, 20% of all congenital heart defects

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36
Q

What is the aetiology of ventricular septal defect?

A

Unknown, some genetic factors

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37
Q

Briefly explain the pathophysiology of ventricular septal defect?

A

A hole connects the ventricles, leading to a higher pressure in the left ventricle than the right ventricle. Thus left to right shunt. Increased blood flow through the lung

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38
Q

What is the clinical presentation of a large ventricular septal defect?

A
  • Pulmonary hypertension and eventual Eisenmenger’s complex
  • Small breathlessness baby
  • Increased respiratory rate
  • Tachycardia
  • CRX: Big heart
  • Murmur varies in intensity
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39
Q

What is the clinical presentation of small ventricular septal defect?

A
  • Large systolic murmer
  • Thrill (buzzing sensation)
  • Well grown
  • Normal heart rate
  • Normal heart size
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40
Q

How is ventricular septal defect diagnosed?

A

EchoCG: Normal (small), LAD and LVH (Medium), LVH and RVH (Large)
CXR: Pulmonary plethora and cardiomegaly, large pulmonary arteries

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41
Q

How is ventricular septal defect treated?

A
  • Surgical closure
  • Medical initially since many will spontaneously close
  • If small, no intervention required
  • Prophylatic antibiotics
  • If moderately sized lesion; ACE inhibitor, Furosemide
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42
Q

What are some possible complications of ventricular septal defect?

A
  • Aortic regurgitation
  • Cardiac Failure
  • Infundibular stenosis
  • Infective endocarditis
  • Subacute bacterial endocarditis
  • Pulmonary hypertension
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43
Q

What is the epidemiology of abdominal aortic aneurysm?

A
  • Present in 5% of population over 60

- More common in men

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44
Q

What is abdominal aortic aneurysm?

A
  • A diametre of over 3cm

- Most occur below renal arteries

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45
Q

What are the causes/ risk factors of abdominal aortic aneurysm?

A
  • Normally no identifiable cause
  • Severe atherosclerotic damage
  • Family history
  • Tobacco
  • Male
  • Increasing age
  • Hypertension
  • COPD
  • Trauma
  • Hyperlipidaemia
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46
Q

Briefly explain the pathophysiology of abdominal aortic aneurysm

A
  • Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss
  • The dilation affects all 3 layers of the vascular tunic
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47
Q

What are the clinical features of unruptured abdominal aortic aneurysm?

A
  • Often asymptomatic- only picked up via abdominal examination/ x ray
  • Pain in abdomen, back, loin or groin
  • Pulsatile abdominal swelling
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48
Q

What are the clinical features of ruptured abdominal aortic aneurysm?

A
  • Intermittent or continuous abdominal pain (radiates to back, iliac fossa or groin)
  • Pulsatile abdominal swelling
  • Collapse, hypotension, tachycardia, profound anaemia, sudden death
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49
Q

How is abdominal aortic aneurysm diagnosed?

A
  • Abdominal ultrasound- Can assess aorta to 3mm degree

- CT and/or MRI angiography scans

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50
Q

How is abdominal aortic aneurysm treated?

A
  • Small aneurysms are generally just monitored
  • Treat underlying cause
  • Modify risk factors (diet, smoking)
  • Vigorous BP control
  • Lowering of lipid in blood
  • Surgery; open surgical repair, endovascular repair= stent inserted via femoral or iliac arteries
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51
Q

What is the epidemiology of aortic dissection?

A
  • Affects men more than women

- Most common between 50-70 yrs

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52
Q

What are the causes of aortic dissection?

A
  • Inherited
  • Degenerative
  • Atherosclerotic
  • Inflammatory
  • Trauma
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53
Q

Briefly explain the pathophysiology of aortic dissection

A
  • A tear in the intima of the aorta allows a column of blood to enter the aortic wall, creating a false lumne
  • This extends for a variable distance in either direction; anterograde (Towards bifurcations) or retrograde (towards aortic root)
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54
Q

What are the clinical features of aortic dissection?

A
  • Sudden onset of severe, central chest pain that radiates to back and down the arms
  • Patients may be shocked and have neurological symptoms
  • May develop aortic regurgitation, coronary ischaemia, cardiac tamponade
  • Absent peripheral pulses
  • Hypertension
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55
Q

How is aortic dissection diagnosed?

A
  • CXR= Widened mediastinum

- Urgent CT, Transoesophageal endocardiography or MRI will confirm

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56
Q

How is aortic dissection treated?

A
  • Urgent antihypertensives to reduce blood pressure to less than 120 mmHg= IV beta blockers or vasodilators
  • Adequate analgesia
  • Surgery to replace aortic arch
  • Endovascular intervention with stents
  • Long term follow up with CT or MRI
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57
Q

What are the 3 acute coronary syndromes?

A
  • ST-elevation myocardial infarction (STEMI)
  • Non-ST-Elevation myocardial infarction (NSTEMI)
  • Unstable angina
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58
Q

What causes a STEMI?

A
  • A complete occlusion of a major coronary artery previously affected by atherosclerosis
  • Causes a full thickness damage of heart muscle
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59
Q

What causes a NSTEMI?

A
  • A complete occlusion of a minor or a partial occlusion of a major coronary artery affected by atherosclerosis
  • Partial thickness damage of heart muscle
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60
Q

What is the difference between a UA and a NSTEMI?

A

In a NSTEMI, there is occluding thrombus which leads to myocardial necrosis and a rise in serum troponin or creatinine kinase- MB

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61
Q

What are the clinical features of mitral stenosis?

A
  • Pulmonary hypertension leading to dyspnoea and pink frothy sputum
  • Left atrial dilation and AF
  • RV hypertrophy and palpitations
  • Malar flush due to low CO
  • Mid diastolic low rumbling murmer
  • Haemoptysis
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62
Q

What causes mitral stenosis?

A

Rheumatic valvular disease (usually strep pyogenes) causes thickening of the mitral valve, obstructing normal flow. This raises the left atrium pressure, causing left atrium hypertrophy and dilation, causing palpitations. Raised left atrial pressure also leads to pulmonary hypertension thus RV failure.

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63
Q

How is mitral stenosis diagnosed?

A
  • ECG= AF, LA enlargement, RV hypertrophy

- Echocardiography= Definitive diagnosis, measure mitral orifice

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64
Q

How is mitral stenosis treated?

A
  • Diuretics (furosemide)= rate control and anticoagulation
  • Valvotomy
  • Excise segments of valve, or valve replacement
  • Infective endocarditis prophylaxis
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65
Q

What are the clinical features of mitral regurgitation?

A
  • Variable haemodynamic effects
  • Pansystolic murmer
  • Mid-systolic click and late systolic murmer in mitral prolapse
  • Deviated apex beat- towards the axilla
  • AF and palpitations
  • Haemoptysis
  • Progressive dyspnoea and fatigue
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66
Q

What causes mitral regurgitation?

A

Mitral valve fails to prevent blood pressure reflux due to dilation of mitral valve annulus, valve prolapse, infective endocarditis or rheumatic valvular disease. Regurgitation into the left atria, causes a raise in LA pressure. This increases the pulmonary pressure, causing pulmonary oedema.

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67
Q

How is mitral regurgitation diagnosed?

A
  • Echocardiography
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68
Q

How is mitral regurgitation treated?

A
  • Repair preferred over replacement
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69
Q

What is the epidemiology of atrial flutter?

A
  • More common in men

- Prevelance increases with age

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70
Q

What is atrial flutter?

A

An organised atrial rhythm with an atrial rate typically between 250-350 bpm

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71
Q

What are the causes of atrial flutter?

A
  • Idiopathic
  • Coronary heart disease
  • Obesity
  • Hypertension
  • Heart failure
  • COPD
  • Pericarditis
  • Acute excess alcohol
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72
Q

What are the clinical features of atrial flutter?

A
  • Palpitations
  • Breathlessness and dyspnoea
  • Chest pain
  • Dizziness
  • Syncope
  • Fatigue
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73
Q

How is atrial flutter diagnosed?

A
  • ECG: Regular sawtooth-like atrial flutter waves (F waves) between QRS complexes due to continuous atrial depolarisation
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74
Q

How is atrial flutter treated?

A
  • Electrical cardioversion but anticoagulate beforehand
  • Catheter ablation
  • IV amiodarone and beta blockers
75
Q

What is sinus tachycardia?

A
  • Heart rate greater than 100bpm
76
Q

What causes sinus tachycardia?

A
  • Anaemia
  • Anxiety
  • Exercise
  • Pain
  • Heart failure
  • Pulmonary embolism
77
Q

How is sinus tachycardia treated?

A
  • Treat causes. If necessary, beta blockers can be used.
78
Q

Briefly explain the pathophysiology of supraventricular tachycardia?

A
  • The gating mechanism of the AV node is being bypassed
  • In reentrant, a bypass tract exists to go around the node, and in automatic, an impulse is created that never encounters the AV node
79
Q

What are the clinical features of supraventricular tachycardia?

A
  • Paroxysmal attacks
  • May be minimal
  • Syncope and palpitations
  • Tachycardia
80
Q

How is supraventricular tachycardia treated?

A
  • Haemodynamically unstable= Cardioversion

- Haemodynamically stable= Carotid massage

81
Q

What are the risk factors for supraventricular tachycardia?

A
  • Previous MI
  • Mitral valve prolapse
  • Rheumatic heart disease
  • Pericarditis
82
Q

How is supraventricular tachycardia diagnosed?

A
  • ECG= P waves may not be visible. Pre-excitation on resting ECG, and rapid and paroxysmal regular palpitations. Short PR interval
83
Q

What causes supraventricular tachycardia?

A
  • Drugs
  • Alcohol
  • Caffeine
  • Congenital
  • Stress
  • Smoking
84
Q

What are the general clinical features of bundle branch block?

A
  • Asymptomatic usually

- Possible syncope

85
Q

What causes a right bundle branch block?

A
  • Pulmonary embolism
  • IHD
  • Ventricular/ Atral defect
86
Q

How is right bundle branch block diagnosed?

A
  • ECG= maRRow
    QRS looks like a M in lead V1
    QRS looks like a W in leads V5 and V6
87
Q

How is right bundle branch block treated?

A
  • May require pacemaker
88
Q

What causes a left bundle branch block?

A
  • IHD
  • Left ventricular hypertrophy
  • Aortic valve stenosis
89
Q

How is left bundle branch block diagnosed?

A
  • ECG= wiLLiam
    W= QRS looks like a W in leads V1 and V2
    M= QRS looks like an M in leads V4-V6
    Also abnormal Q waves
90
Q

How is left bundle branch block treated?

A
  • Treat underlying cause
91
Q

What are the two types of acute myocardial infarction?

A

STEMI

NSTEMI

92
Q

What are the clinical features of acute myocardial infarction?

A
  • Chest pain= severe ongoing pain which may radiate into the left arm, jaw or neck
  • Nausea, vomitting, dyspnoea, fatigue and/or palpitations
  • Distress and anxiety
  • Pale, clammy and marked swelling
  • Significant hypotension
93
Q

How is a STEMI diagnosed?

A

Can be diagnosed on presentation by ECG

  • ST elevation
  • Tall T waves
  • L bundle branch block
  • T wave inversion and pathological Q waves follow
  • After afew days, the ST segment returns to normal, but the Q wave remains
94
Q

How is a NSTEMI diagnosed?

A

Diagnosed retrospectively by ECG
- ST depression
- T wave inversion
Also troponin I or T increased

95
Q

What is ventricular ectopics?

A

Premature ventricular contraction

96
Q

What are the clinical features of ventricular ectopics?

A
  • May be uncomfortable especially when frequent
  • Pulse is irregular owing to the premature beats
  • Usually asymptomatic
  • Can feel faint or dizzy
97
Q

How are ventricular ectopics diagnosed?

A

ECG= Widened QRS complex (greater than 0.12 seconds)

98
Q

How are ventricular ectopics treated?

A
  • Reassure patient

- Give beta blockers e.g. bisoprolol if symptomatic

99
Q

What is ventricular tachycardia?

A

Pulse of more than 100bpm with at least 3 irregular heart beats in a row

100
Q

Briefly explain the pathophysiology of ventricular tachycardia?

A
  • Rapid ventricular beating so inadequate blood filling between beats
  • Therefore decreased cardiac output, and thus a decrease in the amount of oxygenated blood circulating
101
Q

What are the clinical features of ventricular tachycardia?

A
  • Breathlessness
  • Chest pain
  • Palpitations
  • Light headed/ dizzy
102
Q

How is ventricular tachycardia treated?

A

Beta blockers e.g. bisoprolol

103
Q

What is sustained ventricular tachycardia?

A

Ventricular tachycardia for longer than 30 seconds

104
Q

What is intermittent claudication?

A
  • Ischaemic leg pain

- When exercising, there is lactic acid build up, causing pain

105
Q

What is the epidemiology of aortic stenosis?

A
  • Primarily a disease of the old
  • Congenital= 2nd most common cause
  • Most common valvular disease
106
Q

What are the causes of aortic stenosis?

A
  • Calcific aortic valvular disease
  • Calcification of the congenital bicuspid aortic valve
  • Rheumatic heart disease
107
Q

What are the types of aortic stenosis?

A
  • Supravalvular
  • Subvalvular
  • Valvular
108
Q

Briefly explain the pathophysiology of aortic stenosis?

A
  • Obstructed left ventricular emptying
  • Results in increased afterload
  • This causes increased left ventricular pressure
  • In turn, this results in relative ischaemia of the LV myocardium, and consequent angina, arrythmias and LV failure
109
Q

What are the clinical features of aortic stenosis?

A
  • Syncope
  • Angina
  • Heart failure
  • Dyspnoea on exertion
  • Sudden death
  • Slow rising carotid pulse
  • Heart sounds= soft or absent 2nd heart sound, prominent 4th heart sound, ejection systolic murmer-crescendo-decrescendo character
110
Q

How is aortic stenosis diagnosed?

A
  • Echocardiogram= LV hypertrophy, dilation and ejection fraction. Doppler derived gradient and valve area. Doppler ultrasound to assess pressure gradient across the valve during systole
  • ECG= LV hypertrophy, left atrial delay, LV strain pattern due to pressure overload= ST depression, T wave invesion
  • CXR= LV hypertrophy, calcified aortic valve
111
Q

How is aortic stenosis treated?

A

Surgery

  • Valve replacement
  • Balloon valvuloplasty
  • Transcatheter aortic valve replacement
  • Surgical valvuloplasty

TAVI= Transcathater aortic valve implantation

112
Q

What are the 2 causes of acute lower limb ischaemia?

A
  • Embolitic or thrombotic disease
113
Q

What are the symptoms of acute lower limb ischaemia?

A
  • Pain
  • Pallor
  • Perishing cold
  • Pulseless
  • Paralysis
  • Paraestesia
114
Q

What is critical limb ischaemia?

A
  • Blood supply is barely adequate to allow basal metabolism
  • Rest pain that is typically nocturnal
  • Risk of gangrene and/or infection
  • Critical condition, and most severe clinical manifestation of peripheral vascular disease
115
Q

What are the clinical features of severe chronic lower limb ischaemia?

A
  • Infarction
  • Gangrene
  • General symptoms= Absent femoral, popliteal or foot pulses, cold white legs
116
Q

What is the most common cause of peripheral vascular disease?

A
  • Atherosclerosis
117
Q

What are the risk factors for peripheral vascular disease?

A
  • Smoking
  • Diabetes
  • Hypercholesterolaemia
  • Hypertension
  • Physical inactivity
  • Obesity
118
Q

What are the signs of peripheral vascular disease?

A
  • Absent femoral, popliteal or foot pulses

- Cold, white legs

119
Q

How is peripheral vascular disease diagnosed?

A
  • ECG: 60% of claudication patients have evidence of coronary artery disease.
  • Doppler ultrasonography: Confirm diagnosis. Site, degree and length.
  • ABPI
120
Q

How is peripheral vascular disease treated?

A

Modify risk factors

  • Revascularisation for critical ischaemia
  • Surgical treatment for acute ischaemia
121
Q

What are the 4 types of angina?

A
  • Stable
  • Unstable
  • Decubitus
  • Prinzmetals-vasopastic
122
Q

What is stable angina?

A
  • Angina that is induced by effort and relieved by rest
  • An attack lasts less than 20 mins
  • Subendocardium is most commonly affected
123
Q

What is unstable angina?

A
  • Continuous pain of increasing severity/ frequency
  • Minimal exertion
  • Can also happen at rest
124
Q

What is decubitus angina?

A
  • Pain when lying flat
125
Q

What is Prinzmetals-Vasopastic angina?

A
  • Pain during rest

- Likely involves vasoconstriction factors like platelet thromboxane A2. All layers are affected

126
Q

What causes stable, unstable or decubitus angina?

A

Atheroma obstructing or narrowing coronary vessels. Due to aortic stenosis, atheroma or hypertension

127
Q

What causes Prinzmetals-Vasopastic angina?

A

Coronary artery spasm. Doesn’t correlate with exertion

128
Q

What are the clinical features of angina?

A
  • Tightness or heaviness in chest or exertion/rest/cold/emotion
  • May radiate to one or both arms/jaw/neck or teeth
  • Dyspnoea
  • Nausea
  • Sweatiness
  • Faintness
129
Q

What are the complications of angina?

A

Increased risk of MI

130
Q

How is angina diagnosed?

A

ECG= Normally normal, flat or inverted T waves

  • ST depression for stable and unstable angina
  • ST elevation in Prinzmetals-Vasopastic
131
Q

How is Angina treated?

A
  • Modify risk factors
  • Aspirin
  • Beta blockers
  • Nitrates
  • Long acting calcium channel blockers
  • K+ channel activators
  • Nitroglycerine
  • Calcium channel blockers
132
Q

What is the epidemiology of atrial fibrillation?

A
  • Most common sustained cardiac arrythmia
  • Males more than females
  • Affects around 5-15% of patients over age 75
133
Q

What are the risk factors for atrial fibrillation?

A
  • Over 60
  • Diabetes
  • Prior MI
134
Q

Briefly explain the pathophysiology of atrial fibrillation?

A
  • Atrial activity is chaotic and mechanically ineffective and stagnation of blood in the atria causes thrombus formation
  • Reduction in cardiac output causes heart failure
  • Higher risk of thromboembolic events
135
Q

What are the causes of atrial fibrillation?

A
  • Idiopathic
  • Any condition that results in increased atrial pressure
  • Hypertension
  • Heart failure
  • Coronary artery disease
  • Valvular heart disease
  • Cardiac surgery
  • Cardiomyopathy
  • Rheumatic heart disease
  • Acute excess alcohol intake
136
Q

What are the clinical features of atrial fibrillation?

A
  • Variable symptoms
  • May be asymptomatic
  • Palpitations
  • Dyspnoea and chest pains
  • Fatigue
  • Apical pulse is greater than radial rate
  • 1st heart sound is of variable intensity
137
Q

How is atrial fibrillation diagnosed?

A

ECG

  • Absent P waves
  • Irregular and rapid QRS complex
138
Q

How is atrial fibrillation treated?

A
  • Treat underlying cause
  • Drugs for rate control (calcium channel blocker, beta blockers, digoxin, anti arrhythmic)
  • AV nodal slowing agents
  • Cardioversion
  • Anticoagulation
139
Q

What causes long QT syndrome?

A
  • Jervell-Lange-Nielsen syndrome
  • Romano-Ward syndrome
  • Hypokalaemia
  • Hypocalcaemia
  • Certain drugs
  • Bradycardia
  • Acute MI
  • Diabetes
140
Q

What are the clinical features of long QT syndrome?

A
  • Syncope

- Palpitations

141
Q

How is long QT syndrome diagnosed?

A

ECG

142
Q

How is long QT syndrome treated?

A
  • Treat underlying cause

- IV isoprenaline

143
Q

What causes acute pericarditis ?

A
  • Viral= Enteroviruses, adenoviruses
  • Bacterial= Myocardium TB
  • Neoplastic
  • Autoimmune conditions
  • Pericardial injury syndromes
  • Iatrogenic trauma
144
Q

What are the clinical features of acute pericarditis?

A
  • Chest pain: severe, sharp and pleuritic. Rapid onset. Worse on inspiration or lying flat. Pain may radiate to arm
  • Fever or lymphocytosis if due to infection
  • Pericardial friction rub present on ausiculation
  • Tachycardia
  • Dyspnoea, cough, hiccups
145
Q

How is acute pericarditis treated?

A
  • Restrict physical activity until resolution of symptoms
  • NSAIDs for 2 weeks
  • Colchicine for 3 weeks
146
Q

How is acute pericarditis diagnosed?

A
  • ECG: Saddle shaped ST elevation, PR depression
  • CXR: Cardiomegaly, pneumonia is common
  • FBC: Slight increase in WCC, anti neutrophil antibody in young females, SLE
  • ESR/CRP= increased ESR if autoimmune
147
Q

What are the differentials for acute pericarditis?

A
  • Angina
  • MI (most important to rule out)
  • Pleural pain
  • GI reflux
148
Q

What are the two types of second degree AV block?

A

Mobitz I and Mobitz II

149
Q

What is first degree AV block?

A

Prolongation of the PR interval to greater than 0.22s.

150
Q

What is second degree AV block?

A

Occurs when some P waves conduct and others do not

151
Q

What is third degree AV block?

A

Complete heart block. When all atrial activity fails to conduct to the ventricles

152
Q

What are the 4 types of cardiomyopathy?

A
  • Restrictive
  • Dilated
  • Hypertrophic
  • Arrhythmogenic right ventricular
153
Q

What are the most common organisms that cause infective endocarditis?

A
  • Staph. Aureus (Most common)
  • P. Aeruginosa
  • Strep. Viridans
154
Q

What are the risk factors for infective endocarditis?

A
  • IV Drug use
  • Poor dental hygiene
  • Skin and soft tissue infection
  • Dental treatment
  • IV cannula
  • Cardiac surgery
  • Pacemaker
155
Q

What are the clinical features of infective endocarditis?

A
  • Fever plus prosthetic material inside the heart, RF for infective endocarditis, newly developed ventricular arrhythmias or conduction disturbances
  • Headache, fever, malaise, confusion and night sweats
  • Heart failure
  • Splinter hemorrhages on nail beds, embolic skin lesions, osler nodes, Janeway lesions, roth spots
156
Q

How is infective endocarditis diagnosed?

A
  • Blood cultures
  • Blood test: CRP&ESR raised. Normochromic normocytic anaemia. Neutrophilia
  • Urinalysis- look for haematuria
  • CXR: Cardiomegaly
  • ECG: Long PR interval at regular intervals
  • Echo (normally transoesophageal echo)
157
Q

How is infective endocarditis treated?

A
  • Antibiotic treatment for 4-6 weeks
  • If not staph. then use penicillin
  • If staph then use vancomycin and rifampicin
  • Surgery= removing valve and replacing with prosthetic
158
Q

How is shock recognised?

A
  • Skin is pale, sweaty and vasoconstricted
  • Pulse is weak and rapid
  • Pulse pressure is reduced
  • Reduced urine output
  • Confusion, weakness, collapse and coma
159
Q

What are the causes of shock?

A
  • Hypovolaemic shock
  • Cardiogenic shock
  • Distributive shock
  • Anaemic shock
  • Cytotoxic shock
160
Q

How is shock treated?

A

ABC

161
Q

What are the 4 features of tetralogy of fallot?

A
  • A large, maligned ventricular septal defect
  • An overriding aorta
  • RV outflow obstruction
  • RV hypertrophy
162
Q

What are the clinical features of tetralogy of fallot? -

A
  • Central cyanosis
  • Low birthweight and growth
  • Dyspnoea on exertion
  • Delayed puberty
  • Systolic ejection murmers
  • CXR: boot shaped heart
163
Q

How is tetralogy of fallot treated?

A
  • Full surgical treatment during first 2 years of life due to progressive cardiac debility and cerebral thrombosis risk
  • Often get pulmonary valve regurg in adulthood and require redo surgery
164
Q

What is Cor Pulmonale?

A

Right sided heart failure due to chronic pulmonary arterial hypertension

165
Q

What are the causes of Cor Pulmonale?

A
  • Chronic lung disease
  • Pulmonary vascular disorders
  • Neuromuscular and skeletal disease
166
Q

What are the clinical features of Cor Pulmonale?

A
  • Dyspnoea
  • Fatigue
  • Syncope
  • Cyanosis
  • Tachycardia
  • Raised JVP
  • Pan systolic murmur due to tricuspid regurg
  • RV heave
  • Hepatomegaly
  • Oedema
167
Q

How is Cor Pulmonale diagnosed?

A

ABG- Hypoxia +/- hypercapnia

168
Q

How is Cor Pulmonale treated?

A
  • Treat underlying cause
  • Give oxygen to treat resp failure
  • Treat cardiac failure
  • Consider venesection if haemocrit >55
  • Consider heart-lung transplant in young patients
169
Q

What are the causes of Wolff-Parkinson-White syndrome?

A
  • Congenital
  • Hypokalaemia
  • Hypocalcaemia
  • Drugs; amiodarone, tricyclic antidepressants
  • Bradycardia
  • Acute MI
  • Diabetes
170
Q

What are the clinical features of Wolff-Parkinson-White syndrome?

A
  • Usually benign but can make some arrythmias more severe
  • Palpitations
  • Severe dizziness
  • Dyspnoea
171
Q

How is Wolff-Parkinson-White syndrome diagnosed?

A

ECG= Pre-excitation, short PR interval, Wide QRS complex that begins slurred (Delta wave)

172
Q

How is Wolff-Parkinson-White syndrome treated?

A
  • Vagal manoeuvre= Breath holding, carotid massage, valsalva manoeuvre
  • IV adenosine
  • Surgery
173
Q

What are the causes of aortic regurgitation?

A
  • Congenital bicuspid valves
  • Rheumatic fever
  • Infective endocarditis
174
Q

What are the risk factors for aortic regurgitation?

A
  • SLE
  • Marfan’s and Ehler’s-Danlos syndrome
  • Aortic dilation
  • IE or aortic dissection
175
Q

What are the clinical features of aortic regurgitation?

A
  • In chronic regurg, patients remain symptomatic for many years
  • Exertional dyspnoea and syncope
  • Palpitations, angina
  • Apex beat displaced laterally
  • Heart sounds; Early diastolic low pitched rumbling murmer, and Austin Flint murmer
176
Q

How is aortic regurgitation diagnosed?

A
  • Echo: evaluation of the aortic valve and valve root. Measurement of left ventricle dimensions and function
  • CXR: Enlarged cardiac silhouette and aortic root enlargement. LV enlargement
  • ECG: Signs of LV hypertrophy, tall R waves and deeply inverted T waves
177
Q

How is aortic regurgitation treated?

A
  • Infective endocarditis prophylaxis
  • Vasodilators such as ACE-I will improve stroke vol and reduce regurgitation
  • Serial echos for monitoring
  • Surgery for valve replacement
178
Q

What is the immediate management of acute coronary syndrome?

A 
MONAC
Morphine
Oxygen
Nitrate
Aspirin 300mg stat
Clopidogrel
179
Q

How is STEMI treated?

A
  • PCI (clopidogrel and aspirin) if treated in 120 mins
  • Fibrinolysis (alteplase)
  • Prevention
180
Q

How is NSTEMI/ Unstable angina treated?

A
  • GRACE score for risk of NSTEMI
  • Fondaparinux
  • Prevention
181
Q

How is acute coronary syndrome prevented?

A

ACAAB

  • ACE I
  • Clopidogrel
  • Aspirin
  • Atorvastatin
  • Beta blocker
182
Q

What are the complications of acute coronary syndrome?

A

DREAD

  • Death
  • Rupture of myocardium
  • Edema (Heart failure)
  • Arrhythmia
  • Dressler’s syndrome
183
Q

What is a common side effect of calcium channel blockers?

A

Ankle swelling

184
Q

What is a common side effect of ACE-I?

A

Cough

Phase 2a (31 decks)

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