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Core Conditions > Cardio > Flashcards

Cardio Flashcards

0
Q

How many patients per year are admitted due to acute coronary syndromes in the UK .?

A

114,000

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1
Q

What conditions are included under ‘acute coronary syndromes’

A

NSTEMI
STEMI
unstable angina

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2
Q

What is the annual Incidence of non ST elevated acute coronary syndromes ?

A

3 per 1000

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3
Q

What percentage of artery narrowing is required to produce downstream Ischaemia and chest pain ?

A

70% = unstable angina and NSTEMI

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4
Q

What percentage of artery narrowing is required to cause an infarction ?

A

100% = STEMI

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5
Q

What are the modifiable risk factors for atherosclerosis which contribute to ACS ?

A

Smoking, obesity, inactivity

Hypertension, diabetes, dyslipidaemia

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6
Q

What are the non modifiable risk factors for atherosclerosis contributing to risk of ACS ?

A
  • Increasing age
  • male
  • family history of premature heart disease
  • premature menopause
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7
Q

What are the non-atherosclerotic risk factors that may cause ACS in younger patients ?

A
  • coronary emboli e.g. Due to infected heart valve

- coronary occlusion secondary to: vasculitis, coronary artery spasm, cocaine use, congenital, trauma

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8
Q

What things should be checked for in the initial assessment for ACS?

A
  • Chest pain (and radiation) >15 mins
  • associated nausea/vomiting/sweating/SOB with chest pain
  • New onset chest pain, or abrupt deterioration in stable angina, with recurrent pain frequently with little exertion often lasting longer than 15 mins
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9
Q

What is the immediate management of ACS ?

A

ROMANCE:

  • Reassure
  • Oxygen - sats < 94%
  • Morphine (IV Opioids)
  • Aspirin - loading dose 300mg ASAP
  • Nitrates - (GTN- pain relief, still offer morphine)
  • Clopidogrel - (offer in hospital antiplatlet)
  • ECG - resting 12 lead ASAP /enoxaparin antithrombin
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10
Q

What oxygen sats should be aimed for in people with COPD ?

A

88-92%

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11
Q

What drug should be given when having percutaneous coronary intervention to reduce risk of immediate vascular occlusion ?

A

Glycoprotein IIb/IIIa inhibitor

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12
Q

Which patients are rate limiting calcium channel blockers contraindicated in and why ?

A

Those with left ventricular dysfunction as May precipitate heart failure

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13
Q

What is the long term management of NSTEMI and unstable angina ?

A

Beta blocker
LMWH
Nitrates
PCI if high risk

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14
Q

What is the longterm management of STEMI ?

A
  • PCI/Thrombolysis
  • Beta blocker
  • ACE inhibitor
  • Aspirin (+/- clopidogrel!/ warfarin)
  • query statin
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15
Q

Which conditions present similarly to ACS ?

A
  • stable angina
  • pericarditis
  • myocarditis
  • aortic dissection
  • PE
  • oesophageal reflux/spasm
  • cholecystitis/ acute pancreatitis
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16
Q

What are the complications of ACS ?

A

Arrhythmias
Mitral regurgitation (due to Ischaemia to papillary muscles)
Cardiogenic shock
Acute MI
Conduction disturbances e.g. AV or bundle branch block

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17
Q

In which acute coronary syndromes is troponin raised in ?

A

STEMI and NSTEMI

NOT unstable angina

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18
Q

How is the history of unstable angina differentiated from that of an MI ?

A

Chest pain lasts less than 15/20 mins

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19
Q

What ECG changes would be Seen in a STEMI ?

A

ST elevation >2mm in 2 consecutive chest leads
OR
>1mm in 2 limb leads
Tall T waves

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20
Q

What ECG changes are seen in NSTE-ACS ?

A

ST depression or T wave inversion

In unstable angina may be normal. Some time has passed since episode

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21
Q

What is the typical presentation of ACS ?

A

-Central chest pain radiating to left arm/jaw
Associates with :
- nausea, vomiting, sweating, SOB,
- increased pulse, decreased blood pressure

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22
Q

When is cardiac troponin usually tested ?

A

6-12 hrs after onset of pain

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23
Q

What does the global registry of acute coronary events (GRACE) predict ?

A

6 month mortality

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24
Q

What are the classic radiological signs of heart failure on a CXR ?

A
  • cardiomegaly (>50% cardio thoracic ratio)
  • Classical perihilar bat wings (diffuse interstitial/alveolar shadowing)
  • prominent upper lobe veins
  • Pleural effusion

apart from pulmonary congestion CXR findings are only predictive for HF where there is coexisting typical signs and symptoms

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25
Q

What percentage of the population have atrial fibrillation ?

A

1%

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26
Q

What percentage of the over 85s have atrial fibrillation ?

A

18%

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27
Q

What is the pathogenesis of atrial fibrillation ?

A
  • The regular Impulses produced by the SA are overwhelmed by rapid electrical discharges produced by the atria (and adj. pul veins)
  • atria respond to this rapid rate by uncoordinated mechanical action
  • small proportion of impulses conducted to ventricles
  • causes irregularly irregular rhythm
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28
Q

What is paroxysmal AF ?

A

AF which spontaneously terminates within 7 days (usually 2)

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29
Q

What is recurrent AF ?

A

2 or more episodes which can be paroxysmal or persistent

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30
Q

What is persistent AF ?

A

AF lasting > 7days which is not self limiting and unlikely to revert without treatment

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31
Q

What is permanent AF ?

A

Long term (>1yr) which isn’t successfully terminated by cardio version or if it is relapses soon after

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32
Q

What are the main risk factors for AF ?

A
  • Hypertension
  • thyrotoxicosis
  • coronary artery disease
  • alcohol
  • rheumatic fever

any condition that increases atrial pressure e.g. Atrial fibrosis, mitral stenosis

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33
Q

What is the typical presentation of AF ?

A
  • Irregularly irregular pulse on palpation
  • palpitations
  • SOB
  • syncope/dizziness
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34
Q

What is the characteristic findings on an ECG in AF ?

A
  • Variable R-R intervals
  • absent p waves
  • QRS rapid and irregular
  • tachycardia
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35
Q

Which blood tests should be used to investigate AF ?

A
  • TFTs - hyperthyroidism
  • U&Es - abn. k+ can potentiate arrhythmias
  • FBC - anaemia can potentiate HF
  • LFTs and coag screen if pre warfarin
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36
Q

What are the main aims of management of AF ?

A
  • control arrhythmia
  • thromboprophylaxis
  • treat any underlying cause
  • treat any associated HF
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37
Q

What are the complications of AF ?

A
  • stagnation of atrial blood leading to thrombus and embolism risk
  • decreased cardiac output (esp. In exercise) > HF
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38
Q

Which other conditions present similarly to AF ?

A
  • atrial flutter
  • Supraventricular tachycardias
  • Wolff-Parkinson-White syndrome
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39
Q

When would an urgent referral be needed in AF ?

A
  • pulse > 150
  • loss of consciousness/severe dizziness/chest pain
  • stroke/TIA/acute HF
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40
Q

What is first line strategy for treatment of AF ?

A

Rate control

41
Q

When might monotherapy digoxin be appropriate to treat AF ?

A

In relatively sedentary patients as is only effective at rate control during rest

43
Q

When is rhythm control preferred as first line treatment for AF ?

A

In paroxysmal AF

44
Q

What is the long term drug treatment for rhythm controls?

A

Beta blockers

45
Q

What is the short term option for rhythm control ?

A

IV Antiarrythmics e.g. Amiodarone

46
Q

What is cardio version ?

A

Rhythm control by drugs or electricity

47
Q

What is the treatment option for AF if drug treatment had failed ?

A

Left atrial ablation - removal of some tissue in atria to block trigger points of fibrillation usually near entrance of pulmonary vein

48
Q

What is the most common underlying cause of congestive heart failure ?

A

Coronary artery disease

49
Q

What percentage of the population has essential hypertension ?

A

20-30%

50
Q

Which ethnic group is predisposed to essential hypertension ?

A

Black Africans (40-45%)

51
Q

What are the risk factors for essential hypertension ?

A 
Genetic
Low birth weight
Obesity
Alcohol
Diet/exercise
Stress
Diabetes
52
Q

What is second line strategy for treatment of AF ?

A

Rhythm control

53
Q

What is the rare endocrinopathy causing hypertension that present characteristically with: sweating, headache, palpitations and episodes of feeling like ‘about to die’

A

Phaechromocytoma (tumour of adrenal glands)

54
Q

How does hypertension usually present ?

A 
Usually asymptomatic 
May present with:
- headaches
- epistaxis
- nocturia
- end organ damage
55
Q

3 areas to be investigated with hypertension ?

A
  • end organ damage
  • CV disease prevention
  • specific investigations
56
Q

How would you investigate for end organ damage ?

A
  • urinalysis - protein and blood
  • U&Es and e GFR
  • renal ultrasound
  • ECG
  • echo
57
Q

What constitutes stage 1 hypertension ?

A

Average > 135/85

58
Q

What constitutes stage 2 hypertension ?

A

Average >150/95

59
Q

When do you treat stage 1 hypertension with medication ?

A
  • > 80 yrs
  • end organ damage
  • diabetes
  • CVD risk > 20%
60
Q

What is the initial drug treatment for hypertension in those <55 and not Afro Caribbean ?

A
  • ace inhibitor

Beta blocker if not tolerated

61
Q

Initial treatment for those aged over 55 or Afro Caribbean ?

A

Calcium channel blocker

62
Q

Second line treatment for hypertension ?

A

Ace inhibitor and calcium channel blocker

  • A2RA + CCB in black
63
Q

Third line treatment for hypertension ?

A
  • ACEi
  • CCB
  • thiazide diuretic
64
Q

What is the prevalence of stable angina in those aged 65-74?

A

14% men

8% women

65
Q

What are the risk factors for stable angina ?

A
  • diabetes
  • hypertension
  • family history
  • anaemia
  • cardiac outflow abnormalities
66
Q

What is prinzmetals (variant) angina ?

A
  • Angina occurring unprovoked, usually at rest
  • due to coronary spasm
  • more common in women
67
Q

What is the classical presentation of angina ?

A
  • constricting chest discomfort
  • radiation to left arm and jaw
  • lasting
68
Q

What examinations should be carried out on some one with suspected angina ? (5)

A
  • BMI
  • BP
  • pulse
  • auscultation for heart murmurs
  • look for signs of PVD
69
Q

What blood tests should be done in suspected angina ? (6)

A
  • FBC - anaemia
  • U&ES - renal function
  • cholesterol
  • fasting glucose - if diabetes status not confirmed
  • cardiac enzymes - if MI. Suspected
  • TFTs - hyper makes heart work harder, hypo associated with increased cholesterol
70
Q

What ECG changes are typical of CAD ? (3)

A
  • pathological T waves
  • LBBB
  • ST and T Wave abnormalities (flattening or inversion)
71
Q

What are the complications of stable angina ? (4)

A
  • unstable angina
  • MI
  • Anxiety and depression
  • decreased health and quality of life
72
Q

What is the likelyhood of having an MI within one year of being diagnosed with stable angina ?

A

1/10

73
Q

What is the first line drug treatment of stable angina (besides GTN) ?

A

Beta blockers or calcium channel blockers

  • aspirin and statins
74
Q

What drug treatment should be considered for diabetic patients with stable angina ?

A

ACEi

75
Q

Which conditions present similarly to stable angina ?

A
  • MI - pain > 5 mins
  • GORD - burning pain aggravated by exercise/eating
  • acute pericarditis - more constant, worse lying flat and on inspiration, swallowing and movement
  • MSK
  • acute cholecystitis - not related to exercise
  • PE/pleuritic pain - sharp on deep inspiration
76
Q

What should be the initial investigation in patients with suspected DVT ?

A

Duplex ultrasound

77
Q

What is the gold standard for investigating DVT ?

A

Contrast venography

78
Q

What is the annual incidence of DVT ?

A

1/1000

79
Q

What is thrombosis ?

A

Solidification of blood contents, causing aggregation of platelets on teh side of vessels (due to coagulation cascade)

80
Q

What is Virchow’s triad?

A

Essential things for thrombosis to form:

  1. Change in blood flow e.g. Atheroma, immobility
  2. Endothelial damage e.g. Inflammation, hypertension
  3. Change in blood constituents e.g. Drugs, malignancy, pregnancy
81
Q

What are the major risk factors for DVT ?

A
  • prior history of venous thromboembolism
  • > 60 yrs
  • surgery
  • obesity
  • prolonged travel
  • immobility
  • pregnancy
82
Q

How does a DVT present?

A

pain in calf, often associated with:

  • swelling
  • redness
  • warmth
  • engorged superficial veins
  • ankle oedema
  • tenderness along line of deep veins

-65% asymptomatic or features of PE

83
Q

Bilateral leg oedema due to DVT would involve a clot forming where ?

A
  • iliac bifurcation
  • pelvic veins
  • vena cava
84
Q

What is Homan’s sign ?

A

Pain in calf on dorsiflexion of foot while knee fully extended

*not specific for DVT and so not helpful in diagnosis *

85
Q

A DVT forming where is most likely to cause a PE ?

A

Ileofemoral thrombosis

86
Q

What are the long term complications of DVT ?

A
  • Venous eczema
  • swollen limb
  • oedema

Due to damaged venous valves

87
Q

What investigations should be carried out on a suspected DVT case ?

A
  • D-dimer
  • Duplex Ultrasound
  • wells score
88
Q

What is a D-dimer ?

A

Crossed linked products of fibrin degradation - high sensitivity, poor specificity

89
Q

What is the Well’s score ?

A

DVT probability score, affects how quickly get ultrasound

+1 for:

  • active cancer
  • calf swelling >3cm
  • swollen unilateral superficial veins
  • unilateral pitting oedema
  • previous DVT
  • tenderness along line of deep vein
  • paralysis, paresis, recent immobility
  • recently bed ridden

-2 points if another diagnosis is likely

90
Q

If someone has an unprovoked DVT what is it important to check for ?

A

Cancer

91
Q

If someone has an unprovoked DVT and has a 1st degree relative who has also had an unprovoked DVT, what should be investigated for ?

A

Hereditary thrombophilia

92
Q

Management of DVT (drug)

A

LMWH (UFH in renal impairment)

  • heparin stopped when warfarin in right INR ~ 1-3 months
  • if recurrent long term anticoagulant
93
Q

Lifestyle changes for the management of DVT

A
  • pressure stockings (on affected leg only) - for 2yrs
  • weight loss
  • smoking cessation
  • increase mobility
94
Q

What are the 9 main question to screen someone presenting with a swollen leg ?

A
  1. Both legs
  2. Pregnant
  3. Mobile
  4. Trauma
  5. Pitting oedema
  6. Past disease/medications
  7. Pain
  8. Skin changes
  9. Oedema anywhere else
95
Q

Differential diagnosis in someone with swollen leg

A
  • trauma
  • superficial thrombophlebitis
  • cellulitis
  • vasculitis
96
Q

What causes a bounding pulse ?

A
  • CO2 retention
  • liver failure
  • sepsis
97
Q

What causes a small volume pulse?.

A
  • aortic stenosis
  • shock
  • pericardial effusion
98
Q

Causes of collapsing pulse ?

A
  • aortic incompetence
  • AV malformation
  • patent ductus arteriosus
99
Q

What causes a bounding pulse ?

A
  • CO2 retention
  • liver failure
  • sepsis
100
Q

What causes a small volume pulse?.

A
  • aortic stenosis
  • shock
  • pericardial effusion
101
Q

Causes of collapsing pulse ?

A
  • aortic incompetence
  • AV malformation
  • patent ductus arteriosus

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