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FINALS REVISION > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the difference between a true and false aneurysm?

A

True: involves all three layers of artery - intima, media, and adventitia
False: only involves a single layer of fibrous tissue

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2
Q

What is the screening program for AAA?

A

65+ men, abdominal ultrasound

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3
Q

What causes AAA?

A
  1. Same risk factors as arterial disease: HTN, smoking, diabetes
  2. Connective tissue disease: Marfan’s
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4
Q

How does connective tissue disease increase the risk of AAA?

A

Disruption of extracellular matrix - change in balance of collagen and elastin fibres

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5
Q

How is AAA managed?

A

If symptomatic, or between 5.5-6cm, surgical

If asymptomatic, monitor for growth

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6
Q

How is Laplace’s law relevant in AAA?

A

Increase in size correlates with increase in pressure

As size of aneurysm increases, greater likelihood of rupture.

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7
Q

Which part of the heart do leads V1-4 correspond to?

A

Anterior

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8
Q

Which artery do leads V1-4 correspond to?

A

Left anterior descending artery

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9
Q

Which part of the heart do leads II, III, and aVF correspond to?

A

Inferior

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10
Q

Which artery do leads II, III, and aVF correspond to?

A

Right coronary artery

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11
Q

Which part of the heart do leads I, V5, and V6 correspond to?

A

Lateral

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12
Q

Which artery do leads I, V5, and V6 correspond to?

A

Left circumflex

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13
Q

What is the initial treatment for ACS?

A

300mg aspirin

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14
Q

How does MONAT link to ACS?

A 
Morphine only if in severe pain
Oxygen only if sats <94%
Nitrates with caution if hypotensive
Aspirin 300mg
Ticagrelor
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15
Q

How are nitrates administered in ACS?

A

Sublingually, or IV

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16
Q

How are STEMIs managed?

A

Asprin 300mg
If patient has presented within 12 hours, and PCI possible in 120 minutes, PCI

If more than 12 hours, but patient still has symptoms of ongoing MI, consider PCI

If PCI not possible in 120 minutes, fibrinolysis. If ECG changes still present >90 minutes after fibrinolysis, offer PCI

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17
Q

If a patient is a candidate for PCI, how would you anticoagulate prior to PCI?

A

Dual antiplatelet therapy with aspirin and prasugrel if the patient is not already on an anticoagulant

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18
Q

If a patient is a candidate for PCI, and is already on an oral anticoagulant, how would you anticoagulate prior to PCI?

A

Dual antiplatelet therapy with aspirin and clopidogrel

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19
Q

What drug therapy would you give for patients during a PCI procedure using radial access?

A

Unfractionated heparin + bailout glycoprotein IIb/IIIa inhibitor (GPI)

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20
Q

What drug therapy would you give for patients during a PCI procedure using femoral access?

A

Bivalirudin without glycoprotein inhibtiors

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21
Q

What drugs should be given to patients undergoing fibrinolysis?

A

Antithrombin drugs

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22
Q

When should an ECG be repeated following fibrinolysis?

A

60-90 minutes - if persisting myocardial ischaemia, consider PCI

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23
Q

How should NSTEMI/unstable angina be managed?

A

Aspirin 300mg and fondaparinux if no immediate PCI planned

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24
Q

What are the risk factors for ACS?

A
  1. Age
  2. Male
  3. Family history
  4. Smoking
  5. Obesity
  6. Hypertension
  7. Hypercholesterolaemia
  8. Diabetes
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25
Q

Describe in 5 steps the pathophysiology behind ACS.

A
  1. Initial endothelial dysfunction triggered by smoking, hypertension, hyperglycaemia
  2. Pro-inflammatory changes to endothelium - pro-oxidant state, proliferative, reduced NO bioavailability.
  3. Fatty infiltration of the subendothelial space by LDLs
  4. Monocytes migrate and differentiate into macrophages. Macrophages phagocytose LDLs and become foam cells. As macrophages die, this can propagate the inflammatory process.
  5. Smooth muscle proliferation and migration from the media into the intima results in formation of a fibrous capsule covering the fatty plaque.
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26
Q

which risk stratification scoring system is used for NSTEMI to decide whether coronary angiogram?

A

GRACE score

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27
Q

what are the risk factors for AAA?

A
  1. Age (screening in 65+)
  2. Male
  3. Diabetes
  4. Smoking
  5. HTN
  6. Connective tissue diseases e.g. Marfan’s
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28
Q

What is the screening program for AAA?

A

men aged 65 or more - ultrasound measurement of the aneurysm

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29
Q

when is CT offered for AAA?

A

when size reaches 5cm - CT CAP with a view to manage surgically

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30
Q

When is surgery offered for AAA?

A

5.5-6cm

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31
Q

what symptoms of AAA

A

central tearing abdo pain, radiating to back

pulsatile, expansile mass in abdomen

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32
Q

what is the management of AAA

A

EVAR - endovascular repair

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33
Q

what complication of AAA repair using EVAR?

A

endo-leak - blood still collects in the aneurysm

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34
Q

what is the pathophysiology of aortic dissection?

A

tear in the tunica intima causes blood to pool in the tunica media

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35
Q

how is aortic dissection classified?

A

Type A - ascending aorta - 67% cases

Type B - descending aorta

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36
Q

what are the RFs of aortic dissection

A
  1. HTN
  2. Connective tissue disorders - EDS, Marfan’s
  3. Trauma
  4. Bicuspid aortic valve
  5. Noonan’s/Turner’s syndrome
  6. Pregnancy
  7. Syphilis
  8. Cocaine
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37
Q

What are the symptoms of aortic dissection

A

Central sharp, tearing chest pain.
Upper back pain if type B
some overlap between site of pain

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38
Q

What are the signs of aortic dissection

A
  • HTN
  • pulse deficit - weakness in pulse, absent brachial/femoral/carotid pulse
  • variation (>20mmHg) in systolic BP between two arms
  • aortic regurgitation
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39
Q

What are the complications of aortic dissection?

A
  1. Aortic regurgitation
  2. False lumen puts pressure on subclavian and renal arteries - renal failure
  3. Paraplegia
  4. Cardiac tamponade
  5. Stroke
  6. Myocardial Infarction
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40
Q

what murmur might be heard with aortic dissection?

A

diastolic murmur

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41
Q

which branch of coronary arteries is usually affected by aortic dissection and how would this present on ECG

A

right coronary arteries - inferior ST elevation (II, III, aVF)

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42
Q

how is aortic dissection managed

A

Type A - surgical

Type B - medical, occasionally surgical repair, but labetalol to prevent further progression

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43
Q

what surgical procedure for type b aortic dissection?

A

thoracic endovascular aortic repair (TEVAR)

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44
Q

What are the shockable cardiac arrest rhythms?

A

VT

VF

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45
Q

what are the non-shockable cardiac arrest rhythms

A

PEA

Asystole

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46
Q

how is tachycardia treated in an unstable patient?

A
  • 3 synchronised shocks

- consider amiodarone infusion

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47
Q

how is tachycardia classified in a stable patient?

A

narrow (QRS <0.12s) and broad complex (>012s)

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48
Q

what are the three narrow-complex tachycardias

A
  1. AF
  2. Atrial flutter
  3. SVT
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49
Q

Give an example of broad-complex tachycardias

A

Ventricular tachycardia

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50
Q

How is AF rate control achieved

A

Beta blocker or diltiazem

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51
Q

how is atrial flutter rate control achieved

A

beta blocker

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52
Q

how is rate control achieved in SVT

A

vagal manoeuvres
IV bolus 6mg adenosine (verapamil in asthmatics)
electrical cardioversion

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53
Q

give examples of vagal manoeuvres

A

valsalva

carotid sinus massage

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54
Q

how is ventricular tachy treated

A

amiodarone infusion

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55
Q

what is the pathophysiology of atrial flutter

A

re-entrant electrical signal from atria loops back on itself and overrides normal sinus rhythm.
This establishes an endless loop of stimulation - tachycardia

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56
Q

what are the risk factors for atrial flutter

A
  1. Previous MI
  2. Ischaemia
  3. HTN
  4. Fibrosis
  5. Valvular heart disease
  6. obstructive sleep apnoea
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57
Q

what signs symptoms of atrial flutter

A

palpitations, chest tightness, heart failure

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58
Q

what investigations for atrial flutter

A

ECG
Echo for valvular disease, HF
TSH levels for hyperthyroidism

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59
Q

how is atrial flutter treated

A
  1. if hypertension/hyperthyroidism, treat underlying cause
  2. beta blocker for rate control
  3. anticoagulate based on chadsvasc
  4. radiofrequency catheter ablation
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60
Q

explain the pathophys of supraventricular tachy

A
  1. Electrical signal re-enters atria from ventricles
  2. Signal travels to AVN, stimulating another ventricular contraction
  3. Causes a self-perpetuating electrical loop
  4. Results in a narrow complex tachycardia (QRS <0.12s)
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61
Q

what is paroxysmal SVT?

A

remits and recurrs in same patient over time

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62
Q

give three causes of svt

A
  1. AV node re-entry tachycardia (re-entry through the AVN)
  2. Atrioventricular re-entrant tachycardia - re-entry to ventricles through an accessory pathway (eg WPW syndrome)
  3. Atrial tachycardia - ectopic electrical activity generated in the atria, but not from the SAN
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63
Q

how is svt treated

A
  1. Vagal manoeuvres (valsalva, carotid massage)
  2. IV adenosine, verapamil in asthmatics
  3. electrical DC cardioversion
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64
Q

what is the long term management of patients with paroxysmal SVT

A

beta blockers, rate limiting CCB, amiodarone

radiofrequency catheter ablation

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65
Q

explain the pathophysiology of wolff-parkinson white

A

Congenital accessory pathway connecting atria and ventricles, leading to AVRT.

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66
Q

how does wpw present on ecg

A
  1. delta waves (slurred upstroke to qrs)
  2. broad qrs
  3. short pr
  4. associated with left-axis deviation
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67
Q

how does WPW affect axis-deviation

A

if accessory pathway is in right atrium, left-axis deviation

if accessory pathway is in left atrium, right-axis deviation

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68
Q

how is WPW treated

A

radiofrequency ablation

sotalol, amiodarone, flecainide

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69
Q

when would you avoid giving sotalol/beta blockers/antiarrhythmics in WPW

A

if concurrent AF or atrial fibrillation

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70
Q

what conditions are associated with WPW

A
  1. HOCM
  2. Ebstein’s anomaly
  3. Secundum ASD
  4. Thyrotoxicosis
  5. Mitral valve prolapse
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71
Q

what ECG abnormality causes torsades de pointes

A

long QT

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72
Q

which electrolyte abnormalities cause long QT

A

hypocalcaemia
hypomagnesemia
hypokalaemia

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73
Q

how does hypothermia affect QT interval

A

hypothermia prolongs QT interval

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74
Q

list 6 drug groups that commonly cause QT prolongation

A
  1. Erythromycin and macrolides
  2. Antiarrhythmics - sotalol, amiodarone, flecainide
  3. Tricyclic antidepressants (amitriptyline)
  4. Antipsychotics
  5. Chloroquine
  6. Citalopram
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75
Q

What is the management of torsades de pointes acutely

A

Treat underlying cause
IV mag sulf
defibrillation if VT occurs

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76
Q

what is the difference between normal VT and torsades de pointes

A

normal VT is monomorphic

Torsades is polymorphic ventricular tachycardia

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77
Q

what is the long term management of torsades

A
  1. Beta blockers, but not sotalol

2. Pacemaker or implantable defibrillator

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78
Q

what are ventricular ectopics

A

random electrical impulse originating from outside the atria

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79
Q

how do ventricular ectopics present on ecg

A

individual random broad QRS on a background of normal ECG

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80
Q

what is bigeminy

A

ventricular ectopics happen so frequently that there is one for every normal sinus beat

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81
Q

what is first degree heart block

A

Delayed conduction of atrial impulse through AVN. Despite this, every atrial impulse results in a ventricular contraction.

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82
Q

How does first degree heart block present on ECG

A

prolonged PR interval (>0.2s) - 5 small squares/1 big square

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83
Q

What is second degree heart block mobitz type 1?

A

progressively prolonging PR interval until a dropped QRS occurs and the cycle restarts

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84
Q

what is second degree heart block mobitz type 2?

A

PR interval constant, but some atrial impulses fail to conduct, therefore occasional dropped beats occur, with no QRS.
There is usually a set ratio of impulses conducted to those not conducted, e.g. 3:1

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85
Q

how do you calculate the ratio for mobitz type 2?

A

how many P waves for every QRS. so if three p waves for every qrs, ratio of 3:1

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86
Q

which mobitz is associated with risk of asystole?

A

mobitz type 2

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87
Q

what is third degree heart block

A

no relationship between P and QRS - highest risk of asystole

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88
Q

which heart blocks are at risk of asystole

A

mobitz 2, third degree (complete)

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89
Q

what treatment for heart blocks at risk of asystole

A

atropine 500mcg IV

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90
Q

how would heart block present?

A

syncope
heart failure
regular bradycardia

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91
Q

what long term treatment for heart block

A

permanent pacemaker

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92
Q

what class of drug is atropine and how does it work

A

anti-muscarinic - inhibits the parasympathetic nervous system

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93
Q

what side effects of atropine (anti-muscarinic)

A

pupil dilatation
dry eyes
constipation
urinary retention

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94
Q

what causes arterial ulcers

A

insufficient blood supply to the skin due to peripheral artery disease

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95
Q

where do arterial ulcers usually occur

A

distal - toes, dorsum of foot, heel

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96
Q

what do arterial ulcers look and feel like?

A

small, punched out, may be necrotic/gangrenous, pale due to reduced blood supply
painful

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97
Q

describe surrounding limb in arterial ulcers

A

cold, hairless, pulseless

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98
Q

what is abpi in arterial ulcers

A

low ABPI

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99
Q

how are arterial ulcers treated

A

surgical revascularisation

no beta blockers and no compression

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100
Q

how do venous ulcers present

A

shallow, wide area, poorly defined borders, haemosiderin staining
occur in gaiter area
more likely to bleed than arterial
less painful than arterial

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101
Q

how is pain relieved in venous ulcers

A

pain relieved by elevating the leg

this is the opposite to arterial ulcers, where pain is relieved by lowering the leg

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102
Q

how are venous ulcers treated

A

compression therapy, analgesia - avoid NSAIDs

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103
Q

what ABPI measurement indicates PAD?

A

ABPI is ratio of systolic in legs to systolic in arms. ratio <1 indicates

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104
Q

what swabs if suspecting infection in foot ulcers

A

charcoal swabs

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105
Q

what analgesics must be avoided in venous ulcers

A

nsaids - can worsen condition

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106
Q

what are the three classifications of peripheral artery disease

A

intermittent claudication
critical limb ischaemia
acute limb-threatening ischaemia

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107
Q

what are the the risk factors for peripheral artery disease?

A

same as atherosclerosis - age, FH, male, smoking, HTN, hyperlipidaemia, alcohol, hyperglycaemia, obesity, sedentary lifestyle

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108
Q

how does intermittent claudication present?

A

leg (particularly calves) cramps when walking
predictably occurs after a certain distance of walking
better at rest

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109
Q

how does acute limb ischaemia present (6Ps)

A

Trophic changes - shiny, hairless shins

  • Pain
  • Pallour
  • Pulseless
  • Paraesthesia
  • Paralysis
  • Perishing cold
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110
Q

What sort of pain in critical limb ischaemia, and what symptoms?

A

Pain at rest
Ulceration
Gangrene

Burning pain, worse at night in bed with legs raised when gravity no longer helps to pull blood into lower limbs.
Pain better when dangling legs off bed

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111
Q

what assessments would you do for someone with intermittent claudication

A
  • assess for pulses:
    femoral, popliteal, posterior tibialis, dorsalis pedis
  • ABPI measurement
  • FIRST LINE INVESTIGATION: duplex ultrasound
  • MR angiography prior to any interventions
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112
Q

What is the first line investigation of intermittent claudication

A

duplex ultrasound

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113
Q

what ABPI value suggests critical limb ischaemia?

A

<0.6

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114
Q

what ABPI value suggests intermittent claudication

A

<0.9

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115
Q

what does a high ABPI (>1.3) indicate

A

calcification of arteries, making them difficult to compress

more common in diabetic patients

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116
Q

what is the management of intermittent claudication

A
  • lifestyle changes - stop smoking, lose weight, exercise
  • exercise training
  • pharmacological: statin, clopidogrel, naftidrofuryl oxalate
  • endovascular angioplasty + stenting
  • endarterectomy
  • bypass graft surgery
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117
Q

what is the management of critical limb ischaemia

A

Urgent referral to vascular team for revascularisation

  • endovascular angioplasty + stenting
  • endarterectomy
  • bypass graft surgery
  • limb amputation if irreversible ischaemia
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118
Q

what is the management of acute limb-threatening ischaemia

A

urgent referral to on-call vascular team

  • endovascular thrombolysis
  • endovascular thrombectomy
  • surgical thrombectomy
  • endovascular angioplasty
  • endarterectomy
  • bypass graft surgery
  • limb amputation if irreversible ischaemia
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119
Q

what are the two causes of acute limb threatening ischaemia. explain the pathophys of each

A

thrombus: rupture of atherosclerotic plaque in previously atherosclerotic peripheral artery
embolus: originating from elsewhere eg AF

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120
Q

what factors would suggest thrombus causing acute limb ischaemia

A
  • pre-existing claudication with sudden deterioration
  • no obvious source for emboli (AF, recent MI)
  • reduced/absent pulses in contralateral limb
  • evidence of widespread vascular disease (MI, stroke, TIA, previous vascular surgery)
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121
Q

what factors would suggest embolus causing acute limb ischaemia

A
  • sudden onset painful leg
  • no pre-existing claudication/PAD
  • present pulses in contralateral limb
  • source of embolus identified - AF, recent MI
  • evidence of proximal aneurysm - abdominal/popliteal
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122
Q

what analgesic for acute limb ischaemia pain

A

IV opiates

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123
Q

what pharmacological management for PAD

A

statin - atorvastatin 80
clopidogrel
naftidrofuryl oxalate - vasodilator

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124
Q

what causes leriche syndrome

A

occlusion of distal aorta or proximal common iliac artery

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125
Q

what is leriche syndrome triad

A
  • buttock/thigh claudication
  • absent femoral pulse
  • male impotence
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126
Q

what is aortic stenosis caused by

A
  • degenerative calcification
  • bicuspid aortic valve
  • william’s syndrome - postvalvular aortic stenosis
  • post-rheumatic disease
  • subvalvular: HOCM
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127
Q

what are the symptoms of aortic stenosis

A

chest pain
dyspnoea
syncope/presyncope (exertional dizziness)
murmur - Ejection systolic murmur

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128
Q

what are the signs of aortic stenosis

A 
narrow pulse pressure
absent S2
slow rising pulse
thrill
S4 heart sound?
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129
Q

what complication of aortic stenosis

A

left ventricular hypertrophy/failure

130
Q

how is aortic stenosis managed

A

if asymptomatic, observe
if symptomatic - valve replacement
if asymptomatic with valve pressure >40mmHg - consider for surgery

131
Q

how is aortic stenosis investigated

A

echocardiogram

132
Q

where does ejection systolic murmur from aortic stenosis radiate

133
Q

what are the two branches of causes of aortic regurgitation

A

aortic valve disease

aortic root disease

134
Q

what are the aortic valve disease causes of aortic regurgitation

A

rheumatic fever
infective endocarditis
connective tissue disease (SLE/RA)
bicuspid aortic valve

135
Q

what are the aortic root disease causes of aortic regurgitation

A 
aortic dissection
spondyloarthritidies (ank spond)
HTN
syphilis
Marfan's
Ehler Danlos syndrome
136
Q

what are the symptoms of aortic regurg

A 
exertional dyspnoea
orthopnoea
paroxysmal nocturnal dyspnoea
palpitations
angina
cyanosis if acute
137
Q

what are the signs of aortic regurg

A 
early diastolic murmur
collapsing pulse
wide pulse pressure
Quincke's sign (nailbed pulsation)
De Mussett's sign (headbobbing)
138
Q

what is arterial thrombosis

A

formation of thrombus in an artery, often due to atherosclerotic plaque rupture causing thrombus formation

can also occur as a result of thrombus formation in heart, e.g. in AF

139
Q

what is arterial embolism

A

when arterial thrombus travels downstream and causes blockage of artery

140
Q

what are the complications of arterial thrombosis

A 
MI
stroke
acute limb ischaemia
acute mesenteric ischaemia
hepatic artery thrombosis
141
Q

what investigation for mesenteric ischaemia

A

bloods may show raised lactate, WCC
CT scan
angiography

142
Q

what treatment for mesenteric ischaemia

A

revascularisation - thrombectomy

if necrotic, remove dead bowel

143
Q

explain the pathophys of heart failure briefly

A

impaired left ventricular contraction or left ventricular relaxation causes chronic backpressure of blood in the left ventricles
blood backs up in the left ventricle, left atrium, and pulmonary veins

144
Q

what symptoms of HF

A 
dyspnoea
cough productive of frothy white/pink sputum
orthopnoea
paroxysmal nocturnal dyspnoea
peripheral oedema
cardiac wheeze
cardiac cachexia
145
Q

what signs of right sided HF

A

raised JVP
ankle oedema
hepatomegaly

146
Q

what are the mechanisms behind paroxysmal nocturnal dyspnoea

A
  1. lying flat at night - fluid settles across large surface of lungs
  2. respiratory centre less responsive to hypoxia at night
  3. less circulating adrenaline overnight, decreased cardiac function overnight, worse heart failure
147
Q

what are the causes of heart failure

A 
ischaemic heart disease
cardiomyopathies
valvular heart disease (aortic stenosis)
hypertension
arrhythmias (AF)
anaemia
alcohol
thyrotoxicosis
pulmonary hypertension
148
Q

what is first line treatment of heart failure

A

ACEi and beta blocker

ramipril and bisoprolol

149
Q

what is second line treatment of heart failure

A

spironolactone/eplerenone
monitor K, esp as in conjunction with ACEi (first line HF treatment)

consider ARB in afro-caribbean

150
Q

what is third line treatment of HF

A

cardiac resynchronisation therapy

digoxin

151
Q

what NT-proBNP level warrants urgent referral to cardiology

152
Q

what alternative loop diuretic to furosemide

A

bumetanide

153
Q

which medication for HF should be avoided in valvular heart disease until seen by a specialist?

154
Q

briefly describe the nyha classification

A

class 1: no symptoms, no interference with daily activities

class 2: mild symptoms, ordinary activity results in fatigue, palpitations, dyspnoea

class 3: marked limitation in physical activity, less than ordinary activity results in symptoms

class 4: symptoms present at rest, unable to carry out any physical activity without discomfort

155
Q

what is first line investigation of heart failure?

156
Q

dysfunction of which organ can cause raised BNP

A

kidney, eGFR <60 causes raised

157
Q

what are the actions of BNP?

A

vasodilator
diuretic and natriuretic
suppresses RAAS and sympathetic tone

158
Q

explain the pathophys of cor pulmonale

A
  1. Respiratory disease causes pulmonary hypertension.
  2. Right ventricle unable to pump blood effectively to the pulmonary arteries
  3. This leads to a back pressure of blood in the right atrium, the vena cava, and the systemic venous system
159
Q

what are the most common resp causes of cor pulmonale

A
  1. COPD
  2. Interstitial lung disease
  3. Cystic fibrosis
  4. Pulmonary embolism
  5. Primary pulmonary hypertension
160
Q

what are the symptoms of cor pulmonale

A
  1. breathlessness
  2. peripheral oedema
  3. syncope
  4. chest pain
161
Q

what signs of cor pulmonale

A

cyanosis
raised JVP
peripheral oedema
hepatomegaly (pulsatile if tricuspid regurg)
third heart sound
pansystolic murmur due to tricuspid regurgitation

162
Q

what causes pulsatile hepatomegaly

A

tricuspid regurg

163
Q

what type of murmur is tricuspid regurg

A

pansystolic

164
Q

how is cor pulmonale treated

A

LTOT, poor prognosis unless reversible underlying cause

165
Q

how does cor pulmonale present on CXR

A

right ventricular hypertrophy
prominent pulmonary arteries
right atrial dilation

166
Q

what might you see on ECG of cor pulmonale

A

P pulmonale - characteristic peaked P wave

167
Q

briefly explain pathophys of VTE

A

thrombosis formation in venous system secondary to stagnation of blood and a hypercoagulable state

168
Q

what are the major risk factors for VTE

A 
immobility
long haul flights
recent surgery
pregnancy
HRT, COCP
malignancy
polycythaemia
SLE
thrombophilia
169
Q

what are the two main causes of thrombophilia

A

anti phospholipid syndrome

factor V leiden

170
Q

how does antiphospholipid present and how is it investigated

A

recurrent VTE, recurrent miscarriages

anti-phospholipid antibodies

171
Q

what is used for VTE prophylaxis

A

LMWH eg enoxaparin

compression stockings

172
Q

when is VTE prophylaxis contraindicated

A

active bleeding
existing anticoag with warfarin/DOAC

compression stocking contraindicated in PAD

173
Q

how does DVT present

A
  • calf/leg swelling
  • oedema
  • dilated superficial veins
  • colour changes
  • calf tenderness
174
Q

where should calf circumference be measured, what difference is significant

A

10 cm below tibial tuberosity

> 3 cm is significant

175
Q

what symptoms of PE?

A

shortness of breath
pleuritic chest pain
palpitations

176
Q

how is DVT investigated

A
  • D-Dimer to exclude (positive in preg)

- Doppler ultrasound, if negative, repeat in 6-8 days

177
Q

how is PE diagnosed

A

CTPA or V/Q scan

178
Q

when would V/Q scan be used instead of CTPA

A

contrast allergy

renal impairment

179
Q

what treatment for DVT

A

rivarox/apixaban

catheter directed thrombolysis if ileofemoral

180
Q

what treatment for DVT if clinical suspicion but unable to get scan

A

treat as if DVT with rivarox/apix. treatment may be stopped once ruled out with scan

181
Q

what long term anticoagulation for DVT/PE

A

DOAC
Warfarin
LMWH

182
Q

which form of long term anticoagulation for antiphospholipid syndrome

A

Warfarin and initially LMWH

183
Q

what is first line anticoagulant for DVT/PE in pregnancy

184
Q

how long is long term anticoagulation in provoked DVT/PE

185
Q

how long is long term anticoagulation in unprovoked DVT/PE

A

6 months, same for in active cancer

186
Q

what investigations for patients with unprovoked DVT?

A

cancer screen
- physical examination for evidence of cancer, baseline bloods
CT CAP if over 40
Mammogram in women >40

187
Q

what is budd chiari syndrome

A

thrombosis of hepatic vein usually due to hypercoagulable states

188
Q

what causes of budd-chiari syndrome

A

polycythaemia
thrombophilia
pregnancy
COCP

189
Q

what symptoms of budd chiari

A

sudden onset abdo pain
tender hepatomegaly
ascites

190
Q

how is budd chiari investigated

A

ultrasound with doppler flow studies

191
Q

what are some causes of secondary HTN

A 
CROP
Conn's disease (primary hyperaldosteronism)
Renal disease
Obesity
Pregnancy, pre-eclampsia
192
Q

What are the complications of HTN

A
  • IHD
  • stroke
  • hypertensive retinopathy
  • hypertensive nephropathy
  • heart failure
193
Q

what investigations for newly diagnosed HTN

A
  • urine albumin: creatinine ratio for proteinuria and urine dipstick for microscopic haematuria
  • bloods for HbA1C, renal function, lipids
  • fundus examination for retinopathy
  • ECG
194
Q

what treatment for HTN if under 55/diabetic of any age

A
  1. ACEi
  2. ACEi + CCB
  3. ACEi + CCB + Diuretic
  4. Add either alpha/BB or spiro depending on K levels
195
Q

what treatment for HTN if afro-caribbean/over 55

A
  1. CCB
  2. CCB + ARB
  3. CCB + ARB + diuretic
  4. Add either alpha/BB or spiro depending on K levels
196
Q

what symptoms of very raised HTN (>200/120)?

A

headache
seizures
visual disturbance

197
Q

what lifestyle modifications for HTN

A
  • low salt diet <6g/day
  • reduce caffeine intake
  • stop smoking, drink less alcohol, lose weight, exercise, balanced diet
198
Q

what is HTN based on ABPM

199
Q

what is HTN based on clinic BP readings

200
Q

what BP target for >80

A

<150/90 - abpm less

201
Q

what BP target for <80

A

<140/90 - abpm less

202
Q

what drugs can cause secondary hyperlipidaemia

A

thiazides
beta blockers
oestrogens

203
Q

what conditions can lead to hyperlipidaemia

A

hypothyroidism
renal failure
alcohol consumption
nephrotic syndrome

204
Q

what risk factors for hyperlipidaemia

A
  • diet
  • age
  • obesity
  • physical inactivity
  • genetic influence
  • liver disease
  • unopposed oestrogen
205
Q

what are some complications of hyperlipidaemia

A

atherosclerosis - IHD, PAD
stroke
pancreatitis
cholelithiasis

206
Q

what symptoms of hyperlipidaemia

A

xanthomata

corneal arcus

207
Q

how is hyperlipidaemia managed primary vs secondary prevention

A 
primary = atorva 20mg
second = atorva 80mg
208
Q

what causes of hyperCholesterolaemia

A

nephrotic syndrome
cholestasis
hypothyroidism

209
Q

what are the RFs of infective endocarditis

A
  • previous infective endocarditis
  • prosthetic valves
  • rheumatic heart disease
  • congenital heart defects
  • IVDU
  • recent piercings
  • poor dentition
210
Q

what is most common microorganism implicated in infective endocarditis

A

staph aureus, also most common in IVDU

211
Q

which microorganisms are implicated in poor dentition in IE

A

streptococcus mitis
streptococcus sanguinis

both are strep viridans

212
Q

what microorganism most commonly causes IE in prosthetic valves

A

staph epidermidis (particularly <2 months)

213
Q

which microorganism most commonly associated with colorectal cancer in IE

A

strep. bovis

strep gallolyticus

214
Q

what symptoms of infective endocarditis

A

fever
new heart murmur
septic emboli cause:

  • splinter haemorrhages
  • janeway lesions
  • osler nodes
  • roth spots
  • glomerulonephritis
215
Q

how is infective endocarditis investigated

A

blood cultures to find causative organism

echo to visualise infected heart valves

216
Q

how is infective endocarditis managed

A

antibiotics

surgery, esp if congestive heart failure/abscess

217
Q

how would aortic abscess present on ECG in IE

A

lengthening PR interval

218
Q

what criteria for infective endocarditis

A

modified Duke criteria

219
Q

what are the complications of infective endocarditis

A

aortic abscess formation
congestive heart failure
septic emboli
valvular incompetence

220
Q

what is gold standard investigation for angina

A

CT coronary angiogram

221
Q

what management for angina attack

A

GTN spray. repeat in 5 minutes

if after 5 minutes pain still there, call an ambulance

222
Q

what long term meds for angina

A

beta blocker or calcium channel blocker
statin
aspirin
ACEi

223
Q

what second line treatment for angina

A

add both BB+CCB

224
Q

what third line treatment for angina

A

isosorbide mononitrate
ivabradine
nicorandil
ranolazine

225
Q

what surgical interventions for angina

A

PCI with coronary angioplasty

CABG

226
Q

how to differentiate between NSTEMI and unstable angina

A

unstable angina - no raised troponins, may show ST depression
NSTEMI - troponins raised + ST depressionram

227
Q

what investigation for aortic dissection

A

CT aortic angiogram

228
Q

what is third heart sound associated with

A

dilated cardiomyopathy

229
Q

what murmur associated with dilated cardiomyopathy

A

third heart sound

230
Q

if patient has AF with low CHADSVasc, what investigation must be performed before deciding not to anticoagulate

A

echo to exclude valvular heart disease - if valvular - anticoag must be given regardless of chadsvasc score

231
Q

what grace score in nstemi indicates PCI within 72 hrs of hospital admission

232
Q

what ecg abnormality can be caused by macrolides

A

long QT syndrome and torsades de pointes

233
Q

what side effects of GTN spray

A

hypotension
tachycardia
headache

234
Q

what treatment for torsades de pointes

A

IV magsulf

235
Q

what drug has visual disturbance as side effect and what is it used for

A

ivabradine - angina third line?

236
Q

which beta blocker causes long QT syndrome

237
Q

what medication must be stopped 36 hours before starting sacubitril valsartan

A

ACEi due to bradykinin

ARB due to valsartan also ARB

238
Q

if patient unable to undergo CT aortic angiography for aortic dissection what investigation

A

transoesophageal echo

239
Q

which anti-anginal causes ulceration in GI tract

A

nicorandil

240
Q

what arrest rhythm can be caused by tension pneumothorax

A

pulseless electrical activity

241
Q

what is kussmaul’s sign and what has it to do with constrictive pericarditis

A

JVP rises on inspiration

242
Q

where does furosemide work

A

ascending loop of henle

243
Q

what murmur is associated with heart failure (left sided)

A

third heart sound

244
Q

why are CCBs contraindicated in HF, and which is the only CCB licensed for used in HF

A

CCBs exacerbate heart failure symptoms

Amlodipine is licensed for use in HF

245
Q

if someone has stage 4 ckd, what investigation for PE

246
Q

what is the most common mitral valve disease?

A

mitral regurgitation

247
Q

explain the pathophysiology behind mitral regurgitation

A

blood leaks back to left atrium through mitral valve during systole. this means that less blood is pumped to the body with each contraction.

over time, this can lead to left ventricular myocardial thickening. eventually, the left ventricle become less efficient, and heart failure develops

248
Q

what are the RFs for mitral regurg

A
  • mitral stenosis/prolapse
  • female sex
  • connective tissue disease
  • previous MI
  • infective endocarditis
  • rheumatic fever
  • age
  • renal dysfunction
  • low BMI
249
Q

how does MI cause mitral regurg

A

if papillary muscles/cordae tendiniae are affected in an MI, this causes mitral valve disease as a result of damage to its supporting structures

250
Q

how does infective endocarditis cause mitral regurg

A

vegetations growing on the valve prevent valve from closing fully

251
Q

how does rheumatic fever cause mitral regurg

A

inflammation of valve

252
Q

what symptoms of mitral regurg

A

asymptomatic until heart failure develops, then HF symptoms:

  • dyspnoea
  • oedema
  • fatigue
253
Q

what murmur for mitral regurg. describe s1 and s2 in mitral regurg

A

pansystolic blowing murmur heard at apex and radiating to axilla
quiet S1 and widely split S2

254
Q

What ecg findings for mitral regurg

A

broad P wave due to atrial enlargement

255
Q

what CXR findings for mitral regurg

A

cardiomegaly as enlarged L atrium and L ventricle

256
Q

what gold standard investigation for mitral regurg

257
Q

what is medical management of mitral regurg in acute cases

A

nitrates
diuretics
positive inotropes
intra-aortic balloon pump

258
Q

what treatment of HF associated with MRegurg

A

same as normal HF

ACEi, BB, spironolactone

259
Q

what treatment if acute severe MRegurg

A

surgery - repair or replacement with prosthetic/pig

260
Q

explain the pathophys of mitral stenosis

A

obstruction of blood flow across the mitral valve from left atrium to left ventricle

increased pressure in left atria, pulmonary vasculature, and right side of the heart

261
Q

what is the most common cause of mitral stenosis and what are some other causes

A

rheumatic fever is most common cause

  • mucopolysaccharidoses
  • endocardial fibroelastoses
  • carcinoid
262
Q

what would you hear on auscultation of mitral stenosis

A

mid-late diastolic murmur

loud s1 opening snap

263
Q

what signs of mitral stenosis

A

malar flush
atrial fibrillation
low volume pulse

264
Q

what are the features of severe mitral stenosis

A

length of murmur increases

opening snap becomes closer to S2

265
Q

what investigations of mitral stenosis

A

CXR - atrial enlargement

echo

266
Q

what management of mitral stenosis for:

AF
asymptomatic
symptomatic

A

if AF - requires anticoag regardless of chadsvasc, wafarin

asymptomatic - monitor

symptomatic - percutaneous balloon mitral valvotomy, mitral valve surgery

267
Q

What are the complications of MI darth vader

A

DARTH VADER

Death
Arrhythmia
Rupture - free ventricular wall, septum, pap muscles
Tamponade
Heart failure (both acute and chronic)
Valve disease
Aneurysm of ventricle
Dressler's syndrome
Embolism (thrombo)
Recurrence / Mitral Regurgitation
268
Q

what are the other complications of MI (not darthvader)

A
  • cardiac arrest due to ventricular fibrillation
  • cardiogenic shock
  • AVN block following inferior MI
  • pericarditis
269
Q

what is beck’s triad of acute cardiac tamponade NOT PERICARDITIS

A
  • hypotension
  • raised JVP
  • muffled heart sounds

other signs:

pulsus paradoxus
kussmaul’s sign

270
Q

what ecg finding in tamponade

A

electrical alternans - variable QRS amplitude

271
Q

how does dressler syndrome present

A

fever

pericarditis pain

272
Q

list some causes of myocarditis

A

viral: coxsackie, HIV
bacterial: diphtheria, clostridia
autoimmune
spirochaetes - lyme disease
protozoa - chagas disease, toxoplasmosis
drugs - doxorubicin

273
Q

how does myocarditis present

A

chest pain - acute history
dyspnoea
palpitations
arrhythmias

274
Q

what investigations for myocarditis

A

RAISED:

inflammatory markers
cardiac enzymes
BNP

ECG:
tachycardia
arrhythmia
ST elevation, T wave inversion

275
Q

how is myocarditis managed

A

treat underlying cause - Abx if bacterial

supportive - treat arrhythmias, HF

276
Q

what are the complications of myocarditis

A

arrhythmias - lead to sudden death
heart failure
dilated cardiomyopathy

277
Q

how does pericarditis present?

A
  • chest pain relieved on sitting forward, may be pleuritic
  • dyspnoea, non-productive cough
  • pericardial friction rub
  • tachypnoea
  • tachycardia
278
Q

list some causes of pericarditis

A 
viral - coxsackie
TB
uraemia
trauma
post-MI
connective tissue disease
hypothyroidism
malignancy
279
Q

what are the ECG changes for pericarditis

A

PR depression

saddle shaped ST elevation

280
Q

What investigation aside from ECG should all patients with pericarditis get?

A

Transthoracic echo

281
Q

how is pericarditis managed

A

NSAIDs and colchicine

treat underlying cause

282
Q

what can cause constrictive pericarditis

A

any cause of pericarditis, but especially TB

283
Q

how does constrictive pericarditis present

A
  • dyspnoea
  • right heart failure
    • raised JVP
    • oedema
    • hepatomegaly
  • kussmaul’s sign
  • pericardial knock - S3 loud
284
Q

how would constrictive pericarditis appear on cxr

A

pericardial calcification

285
Q

how does cardiac tamponade typically present - triad

A

beck’s triad

  • muffled heart sounds
  • hypotension
  • raised JVP
286
Q

what are some other features of cardiac tamponade aside from beck’s triad

A

kussmaul’s sign
pulsus paradoxus
dyspnoea
tachycardia

287
Q

what ECG finding of cardiac tamponade

A

electrical alternans

288
Q

how is cardiac tamponade managed

A

urgent pericardiocentesis

289
Q

which valve is most commonly affected with infective endocarditis in IVDU

290
Q

AF and heart failure. what do you do

A

synchronised DC cardioversion

291
Q

what effect may beta blockers have on peripheries

A

cold peripheries. especially bisoprolol NOT atenolol

292
Q

what is most common cause of death following MI

A

ventricular fibrillation

293
Q

what is the difference between aortic sclerosis and stenosis

A

sclerosis is thickening and calcification of valve without actually affecting function

ejection systolic murmur would be present but not radiate to carotids

294
Q

how would left ventricular aneurysm present after an MI

A

blood stagnates in left ventricle - clotting - embolus forms - can present as stroke

295
Q

which valve problem is associated with narrow pulse pressure

A

aortic stenosis

296
Q

what cardioversion in AF

A

amiodarone if structural abnormality

flecainide if no structural abnormality

297
Q

how long must patient be anticoagulated for to receive cardioversion in AF

298
Q

how to decide between electrical or pharma cardioversion for AF

A

if AF has persisted for more than 48 hours - electrical cardioversion

299
Q

how to differentiate between constrictive pericarditis and cardiac tamponade

A

kussmaul’s sign - constrictive pericarditis (JVP rises on inspiration)

300
Q

what drugs should be avoided in HOCM with left ventricular outflow obstruction

A

ACEi - they can reduce afterload and thus reduce the LVOT gradient idk

301
Q

what target INR for VTE despite taking warfarin

302
Q

how would atrial myxoma present

A

benign tumour commonly in left atrium
presents with triad:

  • mitral valve obstruction
  • systemic embolisation
  • constitutional symptoms - weight loss, fever, dyspnoea
303
Q

what would you see on echo of atrial myxoma

A

pedunculated heterogeneous mass in left atrium

304
Q

how would posterior MI present

A

tall R waves in V1 and V2

305
Q

what is mechanism of action of fondaparinux

A

activates antithrombin III

306
Q

when to discontinue treatment with statin if hepatic dysfunction

A

if enzymes over 3x upper limit of normal

307
Q

what condition would result in an absent limb pulse

A

takayasu arteritis - large vessel vasculitis

308
Q

what class of drug are statins and how do they work?

A

HMG-CoA reductase inhibitor

inhibit intrinsic cholesterol synthesis

309
Q

what to do if acute heart failure not responding to treatment with IV furosemide

310
Q

what heart sounds are associated with HOCM and DCM

A

DCM - S3

HOCM - S4

311
Q

what is mechanism of action of alteplase

A

activates plasminogen to form plasmin

312
Q

what condition would cause severe worsening of renal function when starting an ACEi

A

bilateral renal artery stenosis

313
Q

which murmurs are louder on inspiration/exhalation

A

RILE

Right sided louder on Inspiration
Left sided louder on Expiration

314
Q

what side effect of indapamide

A

erectile dysfunction

315
Q

what drugs are contraindicated in hypotension in ACS

316
Q

what antiplatelets for conservative management of NSTEMI

A

aspirin + either

clopidogrel if high risk
ticagrelor if low risk

317
Q

how is amiodaron administered

A

into a central vein to reduce the risk of thrombophlebitis

318
Q

when should warfarin be stopped before surgery

319
Q

when should heparin be stopped before surgery

A

6-12 hours before

320
Q

what sort of sputum can mitral stenosis cause and why

A

haemoptysis - rupture of bronchial veins caused by left atrial pressure

321
Q

what are the CXR findings of HF

A 
ABCDE
Alveolar oedema
Kerley B lines
Cardiomegaly
Dilated upper lobe vessels
Pleural Effusion

FINALS REVISION (17 decks)

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