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Module 2 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is stage 1 hypertension?

A

BP > 140/90 < 159/99 on two separate occasions

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2
Q

What is stage 2 hypertension?

A

BP > 160/100 < 180/120 mmHg on two separate occasions

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3
Q

What is severe/malignant/accelerated hypertension?

A

BP > 180/120 mmHg with possibility of end-organ damage (retinal haemorrhage, papilloedema, kidney failure)

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4
Q

General lifestyle advice for a patient with hypertension

A
  1. Diet - Lower salt, low-fat diet, increase fibre
  2. Reduce caffeine
  3. Stop smoking
  4. Cut back on alcohol
  5. Weight loss and exercise
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5
Q

What 2 classes of drugs may be offered alongside normal antihypertensive drugs?

A

Statins and anticoagulants to reduce overall CVD risk

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6
Q

What is the 1st line antihypertensive for a white 54 year old lady with T2DM?

A

ACEi or ARB

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7
Q

What is the 2nd line antihypertensives for a white 54 year old lady with T2DM?

A
  1. ACEi or ARB

2. ACEi/ARB + CCB or thiazide-like diuretic

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8
Q

What is the 1st line antihypertensive for a black 30 year old man without T2DM?

A

CCB

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9
Q

What is the 2nd line antihypertensive for a black 30 year old man without T2DM?

A
  1. CCB

2. ACEi or ARB or thiazide-like diuretic

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10
Q

A patient with uncontrolled hypertension presents with hypokalaemia. What drug can be offered?

A

Low dose spironolactone

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11
Q

A patient with uncontrolled hypertension presents with hyperkalaemia. What drug can be offered?

A

Alpha or beta blocker

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12
Q

MOA for ACEi

A

Block conversion of angiotensin I to II

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13
Q

Side effects of ACEi

A

Hypotension, impaired kidney function, dry cough, hyperkalaemia

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14
Q

What should be regularly checked for someone on ACEi?

A

Renal function

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15
Q

MOA for ARBs

A

Blocks action of angiotensin II

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16
Q

Side effects of ARBs

A

Hyperkalaemia, hypotension

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17
Q

MOA of thiazide-like diuretics

A

Reduce Na/K resorption and promote diuresis to reduce circulating volume on the distal convoluted tubule

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18
Q

Side effects of thiazide-like diuretics

A

Hypotension, hyponatraemia, hypercalcaemia, gout, sunlight sensitivity

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19
Q

What class of CCB are used for hypertension?

A

Group 1 - dihydropyridines

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20
Q

2 examples of CCBs used for hypertension

A

Nifedipine

Amlodipine

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21
Q

Common side effects of CCBs

A

Vasodilatory flushing/headaches/oedema, bradycardia

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22
Q

What two dietary items can affect the efficacy of antihypertensives?

A

Alcohol and glycerine - liquorice

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23
Q

Name 5 causes of secondary hypertension

A
  1. Renal disease - PKD
  2. Sleep apnoea
  3. Conn’s Syndrome - adrenal cortex tumour secreting aldosterone
  4. Obesity
  5. Hyperthyroidism
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24
Q

Management of hypertensive emergency

A

A&E/ITU referral

IV labetalol

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25
Q

Common causes of hypertensive emergencies

A

Poor medication compliance/sudden withdrawal of antihypertensive, pre-eclampsia, older age

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26
Q

Define postural hypotension

A

Drop in BP upon standing sitting of < 20 mmHg systolic (< 30 mmHg in hypertensive patients) and/or fall in diastolic of < 10 mmHg within 3 minutes of standing.

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27
Q

Pathophysiology behind postural hypotension

A

Delayed/absent constriction of blood vessels in lower body leads to blood pooling in extremities instead of returning to the heart - reduced cardiac output, cerebral hypo perfusion. Can be caused by reduced cardiac output alone.

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28
Q

5 drugs that can cause hypotension

A
  1. Beta blockers
  2. Alpha-blockers (BPH - tamsulosin)
  3. Thiazide diuretics/excess antihypertensives
  4. 5-Phosphodiesterase inhibitors (Sildenafil - Viagra)
  5. Tricyclic antidepressants
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29
Q

Risk factors for hypotension

A

PD, DM, Lewy Body dementia, frailty, dehydration (esp. if on diuretics), alcohol

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30
Q

Investigations for hypotension

A
  • Postural/lying and sitting blood pressure
  • Tilt-table test
  • FBC to rule out anaemia
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31
Q

Management for hypotension

A
  1. Careful elimination of drugs that trigger orthostatic hypotension
  2. Safe moving to improve orthostatic tolerance
  3. Increase dietary salt and drink 2 l of water a day
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32
Q

What does S1 represent?

A

Lub: Closing of AV valves (tricuspid and mitral valves) at the start of systolic ventricular contraction

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33
Q

What does S2 represent?

A

Closing of the semilunar valves (pulmonary and aortic valves) once systolic contraction is complete.

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34
Q

What does S3 represent?

A

Rapid ventricular filling as the chord tendinae pull to their full length. Normal in younger people but can indicate heart failure in older people as the ventricles and chord are weakened/stiffened.

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35
Q

What does S4 represent?

A

Heard before S1. Abnormal - indicates a stiff/hypertrophic ventricle and is caused by turbulent flow from an atria contracting against a non-compliant, stiff ventricle.

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36
Q

Where are each of the valves located?

A

Aortic - 2nd ICS R sternal edge
Pulmonary - 2nd ICS L sternal edge
Tricuspid - 5th ICS L sternal edge
Mitral - 5th ICS MCL

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37
Q

Murmur assessment - SCRIPT

A 
Site - Where is it loudest?
Character - Harsh/soft/crescendo or decrescendo, crescendo-decrenscendo
Radiation
Intensity - How easy it is to hear? 
Pitch - High or low (velocity)
Timing - Systolic or diastolic
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38
Q

What are the semilunar valves?

A

Aortic and pulmonary valves - 3 crescent shape cusps that close to create the DUB sound

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39
Q

What are the atrioventricular valves?

A

Mitral and tricuspid valves - Bicuspid valves with chordae tendinae that close to create the LUB sound

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40
Q

Role of aortic valve

A

Oxygenated blood from the lung passes through the left ventricle to the aorta

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41
Q

Role of pulmonary valve

A

Deoxygenated blood from the body passes through the right ventricle to the pulmonary artery

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42
Q

Role of the tricuspid valve

A

Deoxygenated blood from the vena cava passes through the right atrium to the right ventricle

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43
Q

Role of the mitral valve

A

Oxygenated blood from the pulmonary vein passes through the left atrium into the left ventricle

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44
Q

Order of blood flow via the valves

A

T P M A

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45
Q

What valves are open in systole?

A

Aortic and pulmonary valves

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46
Q

What valves are closed in systole?

A

Tricuspid and mitral valves

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47
Q

What valves are closed in diastole?

A

Aortic and pulmonary valves

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48
Q

Causes of valvular heart disease

A
  1. Infective endocarditis - Tricuspid valves
  2. Old age - Leaky valves or calcified valves (atherosclerotic risk factors)
  3. Congenital disorders - Marfan’s, EDS, cardiac congenital abnormalities
  4. Rheumatic fever - Post untreated Streptococcal throat infection
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49
Q

Characteristics of aortic valve disease

A
  1. Angina, dyspnoea, syncope as oxygenated blood flow is reduced
  2. Loud on expiration (blood forced to left side of heart as intrathoracic pressure increases)
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50
Q

Differences between AS and AR

A

AS: Ejection systolic, carotid artery radiation, radio-radial delay
AR: Early diastolic, whoosh, collapsing pulse, De Musset’s nodding

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51
Q

Characteristics of mitral valve disease

A
  1. Dyspnoea, fatigue, AF as cardiac output is reduced

2. Loud on expiration

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52
Q

Differences between MS and MR

A

MS: Malar flush, palpable apex beat, diastolic murmur
MR: Pansystolic, axillar radiation
MVP: Mid-systolic or late-systolic, low BMI, pacts excavatum

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53
Q

Characteristics of tricuspid valve disease

A
  1. Oedema, JVP, ascites as blood backs up to the body

2. Loud on inspiration as blood enters right heart

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54
Q

Characteristics of pulmonary valve disease

A
  1. Dyspnoea, cyanosis, JVP as reduced blood flow to lungs
  2. Almost always secondary to underlying cause (RHF)
  3. Loud on inspiration
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55
Q

What is a common complication of valve disease?

A

I.E

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56
Q

Main con of mechanical heart valve

A

Lifelong anticoagulation - Warfarin

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57
Q

What is a risk factor for pulmonic regurgitation?

A

Previous pulmonary valve surgery (often for stenosis)

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58
Q

What is a congenital cause of tricuspid regurgitation?

A

Ebstein’s anomaly - Leaflets are abnormally formed and placed downwards

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59
Q

What is a risk factor for tricuspid stenosis?

A

I.E

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60
Q

What is a risk factor for mitral regurgitation?

A

MVP

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61
Q

Pathophysiology of mitral regurgitation

A

Blood leaks back from the left ventricle into the left atrium, due to rupture of chord tendineae/papillary muscles

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62
Q

What is a pulmonary complication of mitral stenosis?

A

Increased left atrial pressure results in pulmonary hypertension

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63
Q

Where does blood leak in aortic regurgitation?

A

Aorta blood leaks back into left ventricle

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64
Q

10 RF for DVT

A
  1. Age
  2. Obesity
  3. Pregnancy (particularly 6 weeks post-birth)
  4. Thrombophilia - Antiphospholipid syndrome, sickle cell disease
  5. Family history
  6. Oestrogen containing medication
  7. Major surgery
  8. Frequent flying
  9. Malignancy
  10. Chronic or inflammatory conditions such as HF
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65
Q

What does the Wells score predict?

A

Probability of a patient with DVT/PE symptoms having a DVT/PE

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66
Q

What bloods should you request in unprovoked DVT?

A

FBC, serum calcium, liver function, anti phospholipid antibodies

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67
Q

What investigations should a patient with unprovoked DVT undergo?

A

Chest/abdo/pelvis CT scan
Prostate check
Mammogram

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68
Q

What arteries are affected in PAD?

A

Large peripheral arteries

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69
Q

Pain on exercise that is relieved by rest could suggest

A

PAD

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70
Q

Name 5 signs/symptoms of PAD

A
  1. Pain in legs whilst exercising that is relieved by rest
  2. Hair loss on legs/feet
  3. Brittle, slow-growing toenails
  4. Erectile dysfunction
  5. Shiny skin
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71
Q

Signs/symptoms and management of critical limb ischaemia?

A

6 Ps: Pain, pulselessness, pallor, paralysis, paraesthesia, poilkothermic.

Referral to vascular immediately, angioplasty, stenting or bypass surgery.

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72
Q

What ABPI measurement suggests PAD?

A

< 0.9

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73
Q

Describe the difference between embolic and thrombotic critical limb ischaemia?

A

Embolic CLI is acute onset and the leg appears white; thrombotic CLI is a progressive onset with increased pain whilst exercising.

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74
Q

3 main pharmacotherapies for PAD

A
  1. Reduce CVD risk with statins and anti platelets
  2. Nafitdrofuryl Oxalate: Peripheral vasodilator, avoid in those with gout/renal stones
  3. Cilostazol: Phosphodiestase III inhibitor that has a vasoldilatory anti-platelet role
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75
Q

What valves become incompetent in varicose veins?

A

Perforator valves found between deep veins and superficial veins

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76
Q

What leads to the brown discolouration of legs in those with varicose veins?

A

The engorged superficial veins leak and Hb is broken down into haemosiderin. This over time turns the skin brown and gives varicose eczema.

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77
Q

What 2 tests can be done to determine if someone has incompetent valves in varicose veins?

A
  1. Trendelburg’s

2. Perthes Manoeuvre

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78
Q

What is the inner-most layer of the aorta called?

A

Tunica intima

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79
Q

What are 5 RF for aortic dissection?

A
  1. Male gender
  2. HTN
  3. Smoking
  4. Aortic valve disease
  5. Cocaine use
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80
Q

What ECG changes might you see in aortic dissection?

A

ST segment elevation in inferior lead

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81
Q

Management for aortic dissection

A

Stenting/grafting

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82
Q

What layers of the aorta are affected in aortic aneurysm?

A

All 3 layers

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83
Q

What is the management of a 3-5.4 cm AAA?

A
  1. Stop smoking
  2. Screening appointments for men > 65 years
  3. Surveillance
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84
Q

Who is a AAA surgical candidate?

A

Aneurysm > 5.5 cm or > 4.5 cm and increased by > 0.5 cm in 6 months

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85
Q

Rheumatic fever is a hypersensitivity reaction to what bacteria?

A

Group A beta haemolytic streptococcus

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86
Q

What are the 3 main areas affected in rheumatic fever?

A
  1. Heart - Murmurs, tachycardia, cardiomegaly
  2. Joints - Migrating polyarticular arthritis
  3. Skin - Erythema marginatum and subcutaneous nodules
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87
Q

What valve is most commonly damaged in rheumatic fever?

A

Mitral valve - mitral stenosis

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88
Q

What type of ulcer affects the tips of toes/between toes/lateral side of leg/bony prominences?

A

Arterial

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89
Q

What type of ulcer affects the gaiter area of the leg?

A

Venous

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90
Q

5 characteristics of arterial ulcers

A
  1. Pain that worsens at night and occurs at rest
  2. Symmetrical
  3. Well defined borders
  4. Minimal bleeding
  5. < 0.8 ABPI
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91
Q

5 characteristics of venous ulcers

A
  1. Discrete borders
  2. Irregular and sloping
  3. Surrounding oedema
  4. Fibrous and granulomatous tissue
  5. > 0.9 ABPI
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92
Q

Management for arterial ulcers

A
  1. Lifestyle changes
  2. Vascular bypass/angioplasty
  3. Skin grafting
93
Q

Management of venous ulcers

A
  1. Clean, compressive bandages
  2. Corticosteroid cream for varicose eczema
  3. Lifestyle changes
  4. Referral to vascular surgeons
94
Q

Criteria (4 points) for vascular surgeon referral for venous leg ulcer

A
  1. Has not healed in 2 weeks despite active treatment
  2. Recurrent venous ulcers
  3. ABPI < 0.8 or > 1.2
  4. Patients who cannot have compression
95
Q

ECG appearance for RBBB

A

Prolonged QRS shifted to the right

96
Q

ECG appearance for LBBB

A

Prolonged QRS shifted to the left

97
Q

Irregular atrial beating and a HR > 140 bpm suggests

A

AF

98
Q

AF that lasts > 30 seconds < 7 days is described as

A

Paroxysmal AF

99
Q

Persistent AF is described as

A

Episodes > 7 days or < 7 days with medical intervention

100
Q

Permanent AF is defined as

A

AF that fails to stop after cardioversion or relapses within 24 hours

101
Q

Common complications of AF

A

Stroke and acute HF

102
Q

What bloods should be ordered in AF?

A

FBC, U&Es, cardiac enzymes, TFTs

103
Q

Management of AF in a haemodynamically unstable patient

A

DC cardioversion

104
Q

2 risk tests to calculate for newly-diagnosed AF

A

CHA2DS2VASc - Stroke risk = CHF, HTN, Age, DM, Stroke, Vascular Disease, Age, Sex

HAS-BLED - Bleed risk = HTN, LFT, Renal function, Stroke, Bleeding, Labile INRs, Elderly, Drugs (antiplatelets/NSAIDs), alcohol

105
Q

Pharmacological intervention for AF

A
  1. Rate control: Beta blockers and/or CCB (verapamil, diltiazem)
  2. Anticoagulation
  3. Rhythm control: Sotalol, flecainide (avoid in IHD/valvular HD), amiodarone.
106
Q

Pathophysiology for atrial flutter

A

Atria beat regularly at a much faster rate

107
Q

RF for atrial flutter

A

Valvular disease, atrial surgery, atrial defects, HF, hyperthyroidism, COPD, pneumonia, asthma.

108
Q

ECG findings in atrial flutter

A
  • Sawtooth P waves
  • -ve P waves in leads II, III, aVF
  • Narrow QRS
  • P:QRS 2:1
109
Q

Definite treatment of atrial flutter

A

Catheter ablation

110
Q

Supraventricular tachycardia is caused by

A

Short circuits between the atria and ventricles, increasing the heart rate

111
Q

Supraventricular tachycardia is commonly seen in

A

Children/young adults

112
Q

Persistent SVT is treated with

A

Cardioversion and IV-antiarrythmics such as adenosine or verapamil

113
Q

What 2 techniques are taught to those with SVT?

A

Valsalva manoeuvre - Blow into syringe for 15 seconds
Carotid sinus massage
(also reduce caffeine/smoking/alcohol)

114
Q

1st degree heart block is characterised by

A

Prolonged PR > 0.2 seconds - athletes, post-MI, beta-blockers, increased risk of AF

115
Q

Type I 2nd degree heart block/Wenkebach is characterised by

A

Dropped QRS and increasing PR in AV node

116
Q

Type II 2nd degree heart block/ Mobitz is characterised by

A

Dropped QRS and constant PR in bundle of His or Purkinje fibres

117
Q

3rd degree heart block/complete is characterised by

A

No association between P waves and QRS, bradycardia, irregular pulse, cardiac arrest.

118
Q

Management for AV block

A

Pacemaker

119
Q

3 fascicles of the heart

A
  1. Right bundle branch
  2. Left anterior fascicle
  3. Left posterior fascicle
120
Q

3 RF for trifascucular block

A
  1. IHD
  2. Cardiomyopathy
  3. Hypertension
121
Q

What type of BBB is common in healthy patients?

A

RBBB

122
Q

What type of BBB is common in patients with underlying cardiac pathology?

A

LBBB

123
Q

ECG findings of BBB

A

Broad QRS and shifted in direction of block

124
Q

Ventricular tachycardia is characterised by

A

Broad QRS and tachycardia

125
Q

Pathophysiology of ventricular tachycardia and 4 causes/aetiology

A

Re-entry electrical circuit in the ventricles initiates its own contractions alongside the normal contractions.

Commonly post-MI (bypass scar tissue) but other RF include FH of Long-QT syndrome, hypokalaemia (low K), hypomagnesaemia (low Mg).

126
Q

Management of ventricular tachycardia in a haemodynamically unstable patient

A

IV anti-arrhythmics, cardioversion, treat electrolyte imbalances

127
Q

Management of ventricular tachycardia in a haemodynamically stable patient

A

Catheter ablation, implantable cardioverter defibrillator (ICD), anti-arrhythmics

128
Q

What 2 drugs are pro-arrhythmic and promote QT prolongation?

A

Sotalol and amiodarone

129
Q

Ventricular fibrillation can lead to

A

Cardiac arrest

130
Q

Pathophysiology of ventricular fibrillation

A

Ventricles quiver preventing efficient heart contraction

131
Q

Prolonged QT is a sign of

A

Torsades de Pointes

132
Q

Dilated cardiomyopathy predominantly affects

A

Left ventricle

133
Q

Systolic dysfunction is secondary to what cardiomyopathy?

A

Dilated cardiomyopathy

134
Q

RF for dilated cardiomyopathy

A

Idiopathic, myocarditis/viral infection, familial, cocaine, alcohol, hypothyroidism, chemotherapy

135
Q

Signs/symptoms of dilated cardiomyopathy

A
  1. Congestive HF symptoms

2. Mitral regurgitation murmur due to LV dilation

136
Q

Hypertrophic cardiomyopathy is what type of genetic condition?

A

Autosomal dominant

137
Q

Diastolic dysfunction is secondary to what cardiomyopathy?

A

Hypertrophic cardiopathy

138
Q

What should be avoided in a patient with hypertrophic cardiomyopathy?

A

Contact sport

139
Q

Restrictive cardiomyopathy is caused by

A

Myocardial fibrosis

140
Q

Myocarditis is caused by (3 points)

A
  • Infection: Viral coxsackie
  • Autoimmune: Giant cell myocarditis, sarcoidosis
  • Toxins: Alcohol, radiation, chemotherapy (anthracyclines)
141
Q

Flu-like symptoms and raised troponin could indicate

A

Myocarditis

142
Q

What ECG leads show an inferior MI?

A

II, III, aVF (right coronary artery)

143
Q

What ECG leads show an anterior MI?

A

V1-V4 (left anterior descending)

144
Q

What ECG leads show a lateral MI?

A

V5-V6, left circumflex

145
Q

NSTEMI management

A

MONA - Morphine, oxygen, nitrates, aspirin

146
Q

STEMI (occluded artery) management

A

OH BATMAN: Oxygen, heparin, beta-blockers, aspirin, clopidogrel, ACEi, nitrates

and then PCI

147
Q

Secondary ACS prevention (AABCs)

A

Aspirin, clopidogrel, beta-blocker, ACEi, statin

148
Q

8 complications of a MI

A
  1. Cardiac arrest
  2. Cardiogenic shock (decreased ejection fraction due to v. damage)
  3. Chronic heart failure
  4. Arrhythmia
  5. Pericarditis
  6. Dressler’s Syndrome
  7. Left ventricular aneurysm
  8. Ventricular septal defect
149
Q

Pericarditis secondary to an MI presents with

A
  1. Pain that worsens when lying flat

2. 48 hours post-MI

150
Q

Dressler’s Syndrome presents with

A
  1. Fever
  2. Pleuritic pain
  3. Pericardial effusion
  4. Raised ESR
  5. 4 weeks post MI
151
Q

Management for Dressler’s Syndrome

A

NSAIDs

152
Q

Persistent ST elevation post-MI is suggestive of

A

Left ventricular aneurysm

153
Q

Acute HF and a pan-systolic murmur post-MI suggests

A

Ventricular septal defect

154
Q

Unstable angina is exacerbated by

A

Nothing - will occur randomly, even at rest

155
Q

Decubitus angina is triggered by

A

Lying flat

156
Q

Prinzmetals angina is caused by

A

Coronary artery spasm

157
Q

What drug is prescribed to reduce frequency of angina attacks?

A

Isosorbide mononitrate

158
Q

3 angina red flags

A
  1. Continuous pain
  2. Pain at rest
  3. Other symptoms - dizziness, nausea, palpitations
159
Q

Gold-standard for angina diagnosis

A

CT-Coronary Angiography

160
Q

ECG findings in someone with angina

A
  1. Pathological Q waves (ischaemia/previous MI)
  2. LBBB
  3. T wave elevation
161
Q

GTN spray recommendations

A

Take spray when symptoms begin, wait 5 minutes, if pain persists take 1 more spray, then call 999

162
Q

LHF causes the backup of blood to the

A

Lungs

163
Q

RHF causes the backup of blood to the

A

Body

164
Q

5 causes of HF

A
  1. Sepsis
  2. CVD
  3. Hypertension
  4. Valvular heart disease
  5. AF
165
Q

A 70 year old man with a AKI develops sudden dyspnoea that worsens when lying down. He has coughed up white/pink frothy sputum. What’s the diagnosis and what’s the management?

A

Acute heart failure

  • Stop IV fluids
  • Oxygen
  • Diuretics: Furosemide
  • Monitor fluid balance
166
Q

A patient with acute heart failure does not respond to usual treatment. What is the next recommendation?

A

Non-invasive ventilation using CPAP and ITU admission

167
Q

What investigations must be ordered in acute heart failure (5 points)?

A 
ECG: Rule out MI/arrythmmias
ABG: Type I resp failure
CXR: Cardiomegaly, pleural effusions, Kerley lines
Bloods: BNP, troponin 
Echo
168
Q

ABAL management plan in chronic heart failure

A

ACei
Beta blocker
Aldosterone antagonist - If reduced ejection fraction and symptomatic with A+B
Loop diuretics

169
Q

What must all patients with heart failure get yearly?

A

Flu and pneumococcal vaccine

170
Q

Subacute IE is caused by bacteria invading a

A

Thrombus

171
Q

Acute IE is caused by

A

A thrombus

172
Q

Most common IE cause in someone with poor dental health

A

Strep. Viridans

173
Q

Most common IE cause in someone post-valve surgery

A

Staph. Epidermidis

174
Q

5 causes of pericarditis

A
  1. Infection: Coxsackie, TB
  2. Post-MI/Dressler’s
  3. Autoimmune: SLE/RA/sarcoidosis
  4. Mediastinal malignancy
  5. Renal failure
175
Q

Constant chest pain that improves leaning forward alongside a fever is a sign of

A

Pericarditis

176
Q

2 ECG findings in pericarditis

A
  1. Saddle-shaped ST elevation

2. PR depression

177
Q

Treatment for pericarditis in someone unable to tolerate NSAIDs

A

Colchicine

178
Q

Constrictive pericarditis is caused by

A

Pericardial fibrosis

179
Q

3 signs/symptoms of constrictive pericarditis

A
  1. RHF symptoms
  2. Pericardial knock on S3
  3. Muffled heart sounds
180
Q

T inversion, AF and P-mitrale are signs of

A

Constrctive pericarditis

181
Q

Pericardial effusions are commonly caused by what 2 conditions

A

Pericarditis and cancer

182
Q

An untreated pericardial effusion can cause

A

Cardiac tamponade

183
Q

4 causes of cardiac tamponade (TAMP)

A

Trauma
Aortic dissection
Medical cardiac catheter or biopsy
Pericardial effusion - cancer/infection/pericarditis

184
Q

5 signs/symptoms of cardiac tamponade

A 
Hypotension
Raised JVP
Tachycardia
Pulsus paoradoxus
Reduced heart sounds
185
Q

2 ECG findings in pericardial effusion/cardiac tamponade

A

Low voltage QRS and tachycardia

186
Q

Management for cardiac tamponade

A

Pericardiocentesis 90 degrees into 5th-6th intercostal space at left sternal border at cardiac notch of left lung

187
Q

Most common atrial septal defect

A

Ostrium secondum

188
Q

Eisenmenger’s Syndrome is caused by

A

Pulmonary hypertension

189
Q

Atrial septal defect causes what type of shunt?

A

Right to left

190
Q

People with atrial septal defects are at an increased risk of what

A

Stroke if they have a DVT

191
Q

2 causes of ventricular septal defect

A

Down’s and Turner’s

192
Q

Most common cause of aortic coarctation

A

Turner’s

193
Q

When should the ductus arteriosus close?

A

2-3 weeks after birth, after this is patent ductus arterioles

194
Q

A boot-shaped heart is a sign of

A

Tetralogy of Fallot

195
Q

4 pathologies in tetralogy of fallot

A
  1. Ventricular septal defect
  2. Overriding aorta
  3. Pulmonary stenosis
  4. RVH
196
Q

Example of a B1 receptor beta-blockers and what conditions is it used in?

A

Bisoprolol

HTN, arrhythmia, secondary ACS prevention

197
Q

Where do B2 receptor beta-blockers target?

A

Lungs/kidneys - can trigger asthma and promotes renin release

198
Q

Side effect of atenolol

A

Increased risk of diabetes

199
Q

Contraindications for beta blockers (3 points)

A
  1. Bradycardia
  2. Heart failure
  3. Asthma
200
Q

What are Group 1 CCBs termed and give an example?

A

Dihydropyridine - Amlodipine

201
Q

What are Group 2 CCBs termed and give an example?

A

Non-dihydropyridine - Verapamil

202
Q

Group 3 CCBs such as Diltiazem are most useful for

A

Angina and arrhythmia

203
Q

Dihydropyridines work best for

A

Hypertension

204
Q

Group 2 CCBS work best for

A

Tachyarryhythmias

205
Q

What CCB should be avoided when a patient is already on a beta blocker?

A

Verapamil - Asystole

206
Q

Diltiazem can worsen

A

Heart failure

207
Q

Nicorandil is a

A

Potassium channel activator (vasodilator)

208
Q

Nicorandil can promote

A

Coronary artery blood flow - HTN/angina

209
Q

Side effects of nitrates (3)

A
  1. Sudden hypotension
  2. Headaches
  3. Flushing
210
Q

Amiodarone is used for

A

Supraventricular tachycardias

211
Q

A patient is on amiodarone. What must they be careful of and what must be checked regularly?

A

Sunlight and check TFT

212
Q

Statins prevent the conversion of HmG-CoA into what?

A

Mevalonic acid

213
Q

Side effects of statins (5)

A
  1. Headache
  2. Myalgia (check CK)
  3. Resp. symptoms (ILD)
  4. T2DM
  5. GI complaints
214
Q

What 3 must be checked before starting a statin?

A
  1. LFT
  2. CK
  3. HbA1c
215
Q

What are 2 cautions/red-flags in statin use?

A
  1. Development of respiratory symptoms i.e. ILD

2. Unexplained myalgia

216
Q

4 key pieces of advice for a patient starting on an anticoagulant

A
  1. Seek medical advice for bleeding that does not stop/recurs
  2. Seek medical advice for sudden back pain (retroperitoneal bleed)
  3. Avoid NSAIDs
  4. Carry an alert card
217
Q

Advice for a patient starting warfarin (5 points)

A
  1. Take warfarin at the same time each day
  2. Do not miss doses/take extra doses
  3. Do not become pregnant
  4. Limit alcohol
  5. Avoid vitamin K foods (spinach, broccoli)
218
Q

3 contraindications for warfarin

A
  1. Haemorrhagic stroke
  2. Renal failure
  3. Liver failure
219
Q

Cautions for warfarin use (5)

A
  1. Age increases risk of bleeds
  2. Previous bleeds/ischaemic stroke
  3. HTN
  4. Excessive alcohol/falls
220
Q

Warfarin can induce what protein deficiency and how does this affect the skin?

A

C or S - causes localised painful skin lesions that thrombolyse

221
Q

5 drugs that interact with warfarin

A
  1. Amiodarone
  2. Metronidazole/rifampicin
  3. SSRIs/SNRIs (antiplatelet effect)
  4. Tricyclic antidepressants increase anticoagulation effect
  5. NSAIDs/aspirin
222
Q

A vaccine that interacts with warfarin

A

Influenza

223
Q

3 food/drinks that interact with warfarin

A
  1. Grapefruit juice
  2. Vitamin K containing food (spinach)
  3. Alcohol
224
Q

What DOAC can not be used to prevent VTE in surgery?

A

Edoxaban

225
Q

What DOAC has an antidote?

A

Dabigatran

226
Q

5 contraindications for DOACs

A
  1. Bleeding/RF for bleeds
  2. Poor renal function: creat clearance < 30
  3. Prosthetic heart valves
  4. Liver disease
  5. Pregnancy
227
Q

What has a quicker onset of action - DOAC or warfarin?

A

DOACs

228
Q

What autoimmune condition pre-disposes someone to recurrent VTEs when on a DOAC?

A

Anti-phospholipid syndrome

229
Q

5 things to check at a DOAC 3 monthly check

A
  1. Compliance
  2. Any new medications/OTC
  3. Bleeding/bruising/haematuria/melana
  4. Symptoms of VTE
  5. Renal and liver function

Module 2 (7 decks)

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