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My 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 vessels can atherosclerosis occur?

A
  • central and peripheral arteries [cerebral too]
  • coronary arteries
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3
Q

What is the normal pathology of atherosclerosis?

A
  1. Fatty streaks.
    • consist of lipid-laden macrophages [foam cells] + T-lymphocytes within the intima layer
  2. Intermediate lesions.
    • made of layers of foam cells, vascular smooth muscles cells + T-lymphocytes
  3. Fibrous plaque.
    • covered by fibrous cap that is made of collagen and elastin for strength and flexibility.
  4. Plaque rupture.
    • the fibrous cap is resorbed and redeposited in order to be maintained
  5. Plaque erosion.
    • Second most prevalent cause of coronary thrombosis
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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
  • 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
  • weight reduction
  • lower alcohol consumption
  • exercise
  • managing diabetes, controlling blood pressure
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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

PCI, 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
extremely high BP can cause:
- severe headaches.
- chest pain.
- dizziness.
- difficulty breathing
- Visual changes

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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, smoking

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13
Q

What are the types of hypertension?

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

What is the aetiology for secondary hypertension?

A

R – Renal disease
O – Obesity
P – Pregnancy-induced hypertension or pre-eclampsia
E – Endocrine
D – Drugs (e.g., alcohol, steroids, NSAIDs, oestrogen and liquorice)

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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.
  • NICE recommend measuring blood pressure in both arms, and if the difference is more than 15 mmHg, using the reading from the arm with the higher pressure.
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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
  • Urine albumin:creatinine ratio for proteinuria and
  • dipstick for microscopic haematuria to assess for kidney damage
  • Bloods for HbA1c and lipids
  • Blood U&E for renal impairment
  • Fundus examination for hypertensive retinopathy
  • ECG for cardiac abnormalities, including left ventricular hypertrophy
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23
Q

What preventative measures can be taken for hypertension?

A
  • lifestyle changes: Exercise, smoking cessation, lower salt intake, lower alcohol and caffeine, healthy BMI
  • QRISK measurement and early statins if >10%
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24
Q

What would be the first line of treatment for someone with T2DM 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 ACEi/ARB + 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
  • CAD, malignant hypertension, cerebrovascular event [ACS/stroke], CKD, retinopathy, heart failure, LVH, aortic dissection, peripheral arterial disease
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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 pulmonary artery and aorta) does not close.
  • The pressure in the aorta is higher than that in the pulmonary vessels, so blood flows from the aorta to the pulmonary artery.
  • This creates a left to right shunt where blood from the left side of the heart crosses to the circulation from the right side.
  • This increases the pressure in the pulmonary vessels causing pulmonary hypertension, leading to right sided heart strain as the right ventricle struggles to contract against the increased resistance.
  • Pulmonary hypertension and right sided heart strain lead to right ventricular hypertrophy.
  • The increased blood flowing through the pulmonary vessels and returning to the left side of the heart leads to left ventricular hypertrophy
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32
Q

What is the clinical presentation of patent ductus arteriosus?

A
  • Continuous machine-whirring murmurs
  • Bounding pulse
  • If large- large heart and breathlessness
  • Tachycardia
  • Eisenmenger’s syndrome
    Shortness of breath
    Difficulty feeding
    Poor weight gain
    Lower respiratory tract infections
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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: shows left to right shunt and May show right +/or left ventricle hypertrophy
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34
Q

How is patent ductus arteriosus treated?

A
  • Duct closure surgically or trans-catheter
  • Low risk of complications
  • Venous approach may require an AV loop
  • Indometacin [NSAID] (prostaglandin inhibitor) can be given to stimulate duct closure as PGs keep the duct open
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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,
- increased pressure in the left ventricle compared to the right
- Thus left to right shunt created.
- Increased blood flow through the lung –> right sided overload, right heart failure and pulmonary hypertension.
- pt is NOT cyanotic as blood is passing through the lungs before the body
- Over time, the pressure in the right side of the heart may surpass that of the left –> right to left shunt and cyanosis and the lungs are bypassed and deoxygenated blood is circulated around the body. = Eisenmenger Syndrome

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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
  • dilation of the vessel wall >50% -> a diameter of >3cm
  • 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
  • Men are affected significantly more often and at a younger age than women
  • Increased age
  • Smoking
  • Hypertension
  • Family history
  • Existing cardiovascular disease
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46
Q

Briefly explain the pathophysiology of abdominal aortic aneurysm

A
  • The collagen and elastin within the tunica media and adventitia are destroyed and smooth muscle cells lost
  • The dilation affects all 3 layers of the vascular tunic

Degradation of the elastic lamellae resulting in leukocyte infiltrate causing enhanced proteolysis and smooth muscle cell loss

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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, expansile 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
  • Shock:hypotension + tachycardia,
  • profound anaemia,
  • sudden death
  • Grey-Turner’s sign: Flank bruising secondary to retroperitoneal haemorrhage
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49
Q

How is abdominal aortic aneurysm diagnosed?

A
  • Abdominal ultrasound

- CT angiogram gives a more detailed picture of the aneurysm and helps guide elective surgery to repair the aneurysm.

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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
  • Atherosclerosis
  • uncontrolled hypertension
  • Trauma
  • Connective tissue disorders - Ehlers-Danlos Syndrome + Marfan’s Syndrome
  • Bicuspid aortic valve
  • Coarctation of the aorta
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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 lumen
  • This extends for a variable distance in either direction; anterograde (Towards bifurcations) or retrograde (towards aortic root)
  • narrows the true lumen
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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
  • Differences in blood pressure between the arms (more than a 20mmHg difference is significant)
  • Patients may be shocked and have neurological symptoms
  • Chest and abdominal pain
  • Radial pulse deficit (the radial pulse in one arm is decreased or absent and does not match the apex beat)
  • Absent peripheral pulses
  • Hypertension
  • Complications: May develop aortic regurgitation, coronary ischaemia, cardiac tamponade
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55
Q

How is aortic dissection diagnosed?

A
  • CT angiography = GS
    • confirms the diagnosis and can generally be performed very quickly

- MRI angiography will confirm
- Chest X-ray + ECG: may demonstrate a widened mediastinum and rule out other potential causes
- Ultrasound - Indicates site/extent

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56
Q

How is aortic dissection treated?

A
  • Blood pressure and heart rate need to be well controlled to reduce the stress on the aortic walls. This usually involves beta-blockers
  • Adequate analgesia - MORPHINE
  • Surgery to replace aortic arch OR repair the tear depending on type A or B
  • 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 due to infarction
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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 Unstable Angina 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
  • Left atrial dilation and AF
  • RV hypertrophy and palpitations
  • Malar flush due to low CO
  • diastolic murmer
  • Haemoptysis
  • Pulmonary hypertension leading to dyspnoea and pink frothy sputum
    tapping apex beat
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62
Q

What causes mitral stenosis?

A
  • infections: esp Rheumatic valvular disease (usually strep pyogenes) causes thickening of the mitral valve, obstructing normal flow.
    age via annular calcification
  • 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
  • BB for rate control
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65
Q

What are the clinical features of mitral regurgitation?

A
  • Dyspnoea
  • AF
  • Oedema
  • Malar flush
  • Haemoptysis
  • Diastolic murmur
  • Tapping apex beat – palpable with a prominent S1.
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66
Q

What causes mitral regurgitation?

A
  • Mitral valve fails to prevent blood pressure reflux due to inability to shut properly, caused by infective endocarditis or rheumatic valvular disease.
    • IHD + HTN also
  • 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
  • treat underlying AF + HF
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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 = tachycardia
  • caused by a re-entrant circuit that allows propagation of the signal repeatedly through the right atrium.
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71
Q

What are the causes of atrial flutter?

A
  • causes are often pulmonary: COPD, PE, pulmonary hypertension.
    • Also: IHD, sepsis and alcohol
  • Atrial flutter is caused by a re-entrant rhythm in either atrium.
  • The electrical signal re-circulates in a self-perpetuating loop due to an extra electrical pathway in the atria without interruption
  • each signal doesn’t enter the AV node due to the refractory period -> a conduction ratio of 2:1 or 3:1 etc.
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72
Q

What are the clinical features of atrial flutter?

A
  • asymptomatic
  • Palpitations
  • Breathlessness
  • Chest pain
  • Dizziness
  • Syncope
  • Fatigue
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73
Q

How is atrial flutter diagnosed?

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

How is atrial flutter treated?

A
  • Rate control - beta blockers, CCB and digoxin.
  • Rhythm control - electrical cardioversion or pharmacological cardioversion using flecainide.
  • Electrical cardioversion but anticoagulate beforehand
  • Catheter ablation
75
Q

What is sinus tachycardia?

A
  • Heart rate greater than 100bpm
76
Q

What causes sinus tachycardia?

A
  • Anaemia
  • Anxiety
  • Exercise
  • Pain
  • Infection
  • 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
  • Supraventricular tachycardia is caused by the electrical signal re-entering the atria from the ventricles.
    3 types of SVT
  • The gating mechanism of the AV node is being bypassed.
    • 1) In re-entrant, a bypass tract exists to go around the node (Wolff-Parkinson-White syndrome)
    • 2) In automatic, an impulse is created that never encounters the AV node
  • 3) The signal passes back through the AV node into the atria in AV-node re-entrant tachycardia
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/ Valsalva manoeuvre
81
Q

What are the risk factors for supraventricular tachycardia?

A
  • Previous MI
  • Mitral valve prolapse
  • Rheumatic heart disease
  • Pericarditis
    Heart disease.
    Heart failure.
    Other heart conditions, such as Wolff-Parkinson-White syndrome.
    Chronic lung disease.
    A lot of caffeine.
    Drinking too much alcohol.
    Drug misuse, including cocaine and methamphetamine.
82
Q

How is supraventricular tachycardia diagnosed?

what are the results

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
  • Right ventricular hypertrophy
  • Pulmonary embolism
  • Ischaemic heart disease
  • Congenital heart disease (ASD)
  • Normal variant
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
  • Aortic valve stenosis
  • MI
  • Hyperkalaemia
  • Left ventricular hypertrophy
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

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