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FCM Matrix > CVS > Flashcards

CVS Flashcards

1
Q

How is hypertension diagnosed?

A

24 hour ABPM

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2
Q

What are the values for stage 1 HTN?

A

Clinic reading: 140/90 – 159/99

ABPM: 135/85 – 149/94

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3
Q

Stage 2 HTN values

A

Clinic reading: 160/100 -180/120

ABPM: (>150/95)

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4
Q

Stage 3 HTN values

A

Clinic reading: >180/120

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5
Q

What are the next steps if clinic reading is >140/90 mmg?

A

Offer ABPM or HBPM then:

  1. if > 135/85 mmg - Diagnose stage 1 HTN + treat if:
    - < 80 years
    - target organ damage
    - established cardiovascular disease
    - renal disease
    - diabetes
    - a 10-year cardiovascular risk equivalent to 10% or greater
  2. if > 150/95 mmHg - Stage 2 HTN + treat all ages
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6
Q

What are the next steps if BP is >180/120?

A

admit for specialist assessment if:
signs of retinal haemorrhage or papilloedema (accelerated hypertension)
- life-threatening symptoms such as: new-onset confusion, chest pain, signs of heart failure, or acute kidney injury

If none of the above:
- Arrange urgent investigations for end-organ damage

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7
Q

What do you do if pt < 40 years old had HTN?

A

Exclude secondary causes

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8
Q

1st line management for HTN

A

Patients < 55 or T2DM:
ACEi or ARB

Patient > 55 or Black:
CCB

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9
Q

2nd line for HTN

A

If already on ACEi or ARB
- Add CCB or thiazide like diuretic

If already on CCB:
ACEi or ARB or thiazide like diuretic

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10
Q

3rd line for HTN

A

ACEi or ARB + CCB + thiazide-like diuretic

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11
Q

4th line for HTN

A

Resistant HTN:
K+ < 4.5 = add low-dose spironolactone

K+ > 4.5 = add alpa or beta blocker

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12
Q

BP target for < and > 80 years old

A

< 80 year = 135/85

> 80 year = 145/85

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13
Q

What is isolated systolic HTN?

A

Systolic blood pressure rises, but your diastolic blood pressure stays normal - 160 mmHg or more.

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14
Q

1st line for isolated systolic HTN

A

thiazides

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15
Q

Secondary causes of HTN

A

Renal diseases:

  • glomerulonephritis
  • pyelonephritis
  • Renal artery stenosis

Endocrine:

  • phaechromocytoma
  • Cushing’s syndrome

Drugs:

  • steroid
  • COCP

Other:
- pregnancy

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16
Q

What is malignant HTN?

A

EMERGENCY

>180/120 w/ signs of retinal haemorrhage, papilledema – target organ damage

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17
Q

Orthostatic/postural hypotension

A

a drop in BP (usually >20/10 mm Hg) within three minutes of standing

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18
Q

Treatment for Orthostatic/postural hypotension

A
  • fludrocortisone (increases blood volume)

- Midodrine (causes vasocontriction)

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19
Q

How is end organ damage assessed?

A

Fundoscopy: check for retinopathy

Urine dipstick: renal disease as a cause or consequence of HTN

ECG: left ventricular hypertrophy or ischaemic heart disease

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20
Q

What might you see in an ECG in someone who has postural hypotension?

A

prolonged QT, bundle branch block

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21
Q

Sx with severe HTN

A
  • headaches
  • visual disturbances
  • seizures
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22
Q

What tests do patients typically have following a diagnosis of hypertension?

A
  • U&Es
  • HbA1c
  • Lipids
  • ECG
  • Urine dipstick
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23
Q

Treatment algorithm for HTN

A

1) <55yo/T2DM : ACEi/ARB
>=55yo or AfroCarribean : CCB

2) ACEi/ARB + CCB
3) ACEi/ARB + CCB + Thiazide-like diuretic

4) K+ <= 4.5 : low-dose spironolactone
K+ >4.5 : alpha/beta blocker

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24
Q

When is an ARB preferred over an ACEi?

A

patients of black African or African–Caribbean origin taking a CCB, if they require a second agent consider an ARB in preference to an ACEi

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25
Q

Which symptoms are life threatening in severe HTN?

A
  • new-onset confusion - chest pain
  • signs of heart failure
  • AKI
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26
Q

Which algorithm can be used to estimate the risk of developing cardiovascular risk of the next 10 years and what is considered as high risk?

A

QRISK

> = 20% is considered high risk

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27
Q

Lifestyle advice for managing Hypertension?

A
  • low salt diet
  • reduced caffeine intake
  • smoking cessation
  • less alcohol
  • weight loss and exercise
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28
Q

Signs of hypovolaemic shock

A
  • Tachycardia/tachypnoea
  • Reduced CRT
  • Cold peripheries
  • Hypotension
  • End organ dysfunction:
  • -> Oliguria/anuria
  • -> Confusion
  • -> irritability
  • -> Chest pain/ SOB
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29
Q

Management of hypovolaemic shock

A
  1. Look for treat and cause
  2. High flow oxygen
  3. Control haemorrhage if present – maintain adequate perfusion of vital organs
  4. Blood should be given
  5. IV fluid resuscitation – crystalloid: normal saline or
    Hartmann’s solution.
  6. Central venous pressure (CVP) line – more sensitive to the balance between loss & replacement than pulse or BP.
  7. Prevent over-replacement - prevents tissues ischaemia
  8. Monitor urine output
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30
Q

What can cause cardiogenic shock?

A

Intrinsic:

  • MI
  • Arrhythmia

Extrinsic:

  • PE
  • Pneumothorax
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31
Q

Why do symptoms occur in cadiogenic shock?

What are the symptoms?

A

Due to hypoperfusion or fluid overload

  • Chest pain
  • SOB
  • Palpitations
  • Syncope
  • Confusion
  • Sweating
  • Pale skin
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32
Q

What are the signs of cardiogenic shock?

A
  • Tachycardia
  • Raised JVP
  • Cold peripheries
  • Hypotension
  • Peripheral oedema
  • Weak pulse
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33
Q

What is a complication of arterial occlusion?

A

Gangrene

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34
Q

What are varicose veins?

A

Dilated, tortuous, superficial veins that occur due to incompetent venous valves.

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35
Q

Sx of varicose veins

A
  • aching, throbbing
  • itching

Complications:

  1. a variety of skin changes may be seen:
    - varicose eczema (also known as venous stasis)
    - haemosiderin deposition → hyperpigmentation
    - lipodermatosclerosis → hard/tight skin
    - atrophie blanche → hypopigmentation
  2. bleeding
  3. superficial thrombophlebitis
  4. venous ulceration
  5. deep vein thrombosis
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36
Q

Ix for varicose veins

A

Diagnosis is mainly clinical

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37
Q

Management of varicose veins

A 
1. If veins are not bleeding:
Conservation advice:
- Weight loss if overweight or obese
- Elevation of legs
- Avoid prolonged sitting or standing
- Compression stockings
  1. Referral to vascular service if:
    - Pt is symptomatic, veins bleeding
    - skin changes secondary to chronic venous insufficiency (e.g. pigmentation and eczema)
    - Hard painful veins (Superficial vein thrombosis)
    - Venous leg ulcer (break in skin below the knee )which hasn’t healed within two weeks- 2WW referral!
    - A healed venous leg ulcer
  2. Possible tx:
    - Surgery: Ligation and stripping
    - Endothermal ablation
    - Foam sclerotherapy
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38
Q

What is acute rheumatic fever?

A

Inflammation in the heart, joints, skin or CNS.

- can develop after strep throat

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39
Q

How does rheumatic fever develop?

A

Following an immunological reaction to recent (2-6 weeks ago) streptococcus pyogenes infection (strep throat/scarlet fever)

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40
Q

What is the diagnostic criteria for rheumatic fever?

A

Jones:
Evidence of recent streptococcal infection accompanied by:
–> 2 major criteria
–> 1 major with 2 minor criteria

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41
Q

What is the evidence of recent streptococcal infection in rheumatic fever?

A
  1. raised or rising streptococci antibodies,
  2. positive throat swab
  3. positive rapid group A streptococcal antigen test
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42
Q

What is the major criteria in rheumatic fever?

A
  1. erythema marginatum
  2. Sydenham’s chorea: this is often a late feature
  3. polyarthritis
  4. carditis and valvulitis (eg, pancarditis)
  5. subcutaneous nodules
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43
Q

What is the minor criteria in rheumatic fever?

A
  1. raised ESR or CRP
  2. pyrexia
  3. arthralgia (not if arthritis a major criteria)
  4. prolonged PR interval
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44
Q

What is the management of acute rheumatic fever?

A
  1. antibiotics: oral penicillin V (10 day course)
  2. anti-inflammatories: NSAIDs = 1st line (e.g. aspirin or naproxen) till CRP normalised
  3. Treatment of any complications e.g. heart failure
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45
Q

Define phlebitis and thrombophlebitis

A

Phlebitis means inflammation of a vein. Thrombophlebitis refers to a blood clot causing the inflammation.

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46
Q

Patients with clinical signs of superficial thrombophlebitis affecting the proximal long saphenous vein should have which investigation?

A

Ultrasound scan to exclude concurrent DVT

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47
Q

Management of superficial thrombophlebitis

A

Oral NSAIDs more effective than topical NSAID

Compression stockings - measure before ABPI

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48
Q

What are the types of arterial occlusion?

A

Acute limb ischaemia: sudden onset of leg pain pr sudden deterioration in claudication- loss of pulse & pallor

Chronic acute limb ischaemia: progressive development of a cramp-like pain in the calf, thigh or buttock – relieved by resting, unexplained leg pain or non-healing wounds., distal pro proximal extremity., absent foot pulses.

Intermittent claudication

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49
Q

Features of intermittent claudication

A
  1. Intermittent claudication: aching or burning in the leg muscles following walking
  2. patients can typically walk for a predictable distance before the symptoms start
  3. usually relieved within minutes of stopping
  4. not present at rest
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50
Q

Ix for intermittent claudication

A
  1. check the femoral, popliteal, posterior tibialis and dorsalis pedis pulses
  2. check ankle brachial pressure index (ABPI)
  3. 1st line = duplex ultrasound
  4. magnetic resonance angiography (MRA) should be performed prior to any intervention
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51
Q

ABPI for intermittent claudication

A

0.6-0.9

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52
Q

Features of acute limb-threatening ischaemia

A

6 P’s:

  • pale
  • pulseless
  • painful
  • paralysed
  • paraesthetic
  • ‘perishing with cold’
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53
Q

1st line Ix for acute limb-threatening ischaemia

A
  • handheld arterial Doppler examination

- Then ABPI

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54
Q

Management of acute limb-threatening ischaemia

A

Initial management:

  1. ABC approach
  2. analgesia: IV opioids are often used
  3. IV unfractionated heparin is usually given to prevent thrombus propagation, particularly if the patient is not suitable for immediate surgery
  4. vascular review

Definitive management:

  1. intra-arterial thrombolysis
  2. surgical embolectomy
  3. angioplasty
  4. bypass surgery
  5. amputation: for patients with irreversible ischaemia
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55
Q

Sx for Critical limb ischaemia

A

Features should include 1 or more of:

  • rest pain in foot for more than 2 weeks
  • ulceration
  • gangrene

Patients often report hanging their legs out of bed at night to ease the pain.

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56
Q

ABPI indicative of Critical limb ischaemia

A

< 0.5 is suggestive of critical limb ischaemia.

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57
Q

Management of Critical limb ischaemia

A

endovascular revascularization:

  1. percutaenous transluminal angioplasty +/- stent placement
  2. endovascular techniques are typically used for short segment stenosis (e.g. < 10 cm), aortic iliac disease and high-risk patients

surgical revascularization:

  1. surgical bypass with an autologous vein or prosthetic material
  2. endarterectomy
  3. open surgical techniques are typically used for long segment lesions (> 10 cm), multifocal lesions, lesions of the common femoral artery and purely infrapopliteal disease

Amputation

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58
Q

Sx of peripheral vascular disease

A

may be sx free

  • sx of intermittent claudication (cramping with exercise, relieved by rest)
  • ulcers
  • hair loss
  • skin changes (thinning, brittle, shiny)
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59
Q

Which investigations may be used in suspected PVD?

A
  • Doppler US
  • Angiogram
  • Ankle-brachial index
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60
Q

Treatment options for PVD

A
  • antiplatelets
  • vascular surgery to reroute the blood flow if blocked
  • angioplasty
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61
Q

Complications of PVD

A
  • stroke
  • restricted mobility
  • reduced wound healing
  • amputation
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62
Q

Which valvular disease is associated with rheumatic fever?

A

mitral stenosis

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63
Q

investigations for arterial occlusion

A

ABPI <0.5 is critical (refer to vascular MDT)
ABPI 0.6-0.9 is intermittent claudication (exercise management, angio or bypass)

Ultrasound of blood flow in peripheries

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64
Q

How to treat cardiogenic shock?

A
  • ACS protocol: MONA
  • Norepinephrine: improve heart function
  • antiplatelets as preventative measures
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65
Q

Management of arterial occlusion

A

Clopidogrel

Embelectomy or bypass if severe

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66
Q

What is venous thrombosis?

A

Formation of a thrombus (blood clot) in a deep vein which partially or completely obstructs blood flow.

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67
Q

Types of DVT

A

Provoked DVT: associated with transient risk factor – significant immobility, surgery, trauma, pregnancy, the pill, HRT.

Unprovoked DVT: occurs in the absence of a transient factor.

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68
Q

Sx of DVT

A
  • Unilateral localised pain – throbbing, pain when walking , bearing weight
  • Calf swelling
  • Tenderness
  • Skin change – oedema, redness & warmth
  • Vein distension
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69
Q

Ix for DVT

A

Measure leg circumference

Proximal leg vein USSS scan

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70
Q

What score is used to manage DVT?

What is the criteria?

A

Well’s score:
DVT likely: 2 points or more
DVT unlikely: 1 point or less

Criteria:
1. Active cancer (treatment ongoing, within 6 months, or palliative)

  1. Paralysis, paresis or recent plaster immobilisation of the lower extremities
  2. Recently bedridden for 3 days or more or major surgery within 12 weeks requiring general or regional anaesthesia
  3. Localised tenderness along the distribution of the deep venous system
  4. Entire leg swollen
  5. Calf swelling at least 3 cm larger than asymptomatic side
  6. Pitting oedema confined to the symptomatic leg
  7. Collateral superficial veins (non-varicose)
  8. Previously documented DVT
  9. An alternative diagnosis is at least as likely as DVT (-2)
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71
Q

What are the next steps if DVT is likely using Well’s score (> 2)?

A
  1. Offer proximal leg vein ultrasound scan within 4 hours if possible.
  2. If not possible, offer – D-Dimer test, interim therapeutic anticoagulation , USS scan within 24 hours.
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72
Q

What are the next steps if DVT is unlikely using Well’s score (< 2)?

A
  1. Offer a D-dimer test with results available within 4 hours.
  2. If not available: offer interim therapeutic anticoagulation .
  3. If D-dimer is positive – offer proximal leg vein USS, offer interim therapeutic anticoagulation
  4. If D-dimer is negative: stop anticoagulation.
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73
Q

What is the interim anticoagulation?

A

1st line: apixaban or rivaroxaban (DOAC) continued if diagnosis is confirmed

2nd line: LMWH for 5 days followed by dabigatran or edoxaban or LMWH with a vitamin K antagonist for 5 days.

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74
Q

If patient has renal impairment and DVT, what medication is given?

A

LMWH, unfractionated heparin or LMWH followed by a VKA

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75
Q

Ix for DVT in pregnancy

A

Compression duplex ultrasound

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76
Q

Length of anticoagulation in DVT

A

3 months for all pt then:

  1. provoked: stop after 3 months
  2. unprovoked: continue till 6 months
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77
Q

What is an aortic aneurysm?

A

It is an abnormal bulge that occurs in the wall of the major blood vessel – aorta.

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78
Q

What is aortic dissection?

A

Occurs when a tear develops in the inner layer of the aorta.

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79
Q

Sx of aortic aneurysm

A

Usually asymptomatic

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80
Q

When do you screen for AAA?

A

single abdominal ultrasound for males aged 65.

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81
Q

Management of AAA

A

1) < 3 cm= No further action
2) 3 - 4.4 cm = Small aneurysm, Rescan every 12 months
3) 4.5 - 5.4 cm = Medium aneurysm, Rescan every 3 months
4) >= 5.5cm = Large aneurysm, Refer within 2 weeks to vascular surgery for probable intervention

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82
Q

What is the surgery for AAA > 5.5cm?

A

Treat with elective endovascular repair (EVAR) or open repair if unsuitable.

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83
Q

Sx of ruptured AAA

A
  1. severe, central abdominal pain radiating to the back
  2. pulsatile, expansile mass in the abdomen
  3. patients may be shocked (hypotension, tachycardic) or may have collapsed
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84
Q

Management of ruptured AAA

A

Surgical repair

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85
Q

Features of aortic dissection

A
  1. chest/back pain
    - severe and ‘sharp’, ‘tearing’ in nature
    - pain is typically maximal at onset
    - chest pain is more common in type A dissection
    - upper back pain is more common in type B dissection.
  2. pulse deficit
    weak or absent carotid, brachial, or femoral pulse
    variation (>20 mmHg) in systolic blood pressure between the arms
  3. aortic regurgitation
  4. hypertension
  5. some pt may have ST-elevation in inferior leads
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86
Q

Types of aortic dissection

A 
Type A (ascending aorta) 
Type B (descending aorta)
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87
Q

Ix for aortic dissection

A
  1. Chest x-ray
    - widened mediastinum
  2. CT angiography of the chest, abdomen and pelvis = investigation of choice
    - suitable for stable patients and for planning surgery
    - a false lumen is a key finding in diagnosing aortic dissection
  3. Transoesophageal echocardiography (TOE) = more suitable for unstable patients who are too risky to take to CT scanner
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88
Q

Management of aortic dissection

A

Type A:
surgical management, but BP should be controlled to a target systolic of 100-120 mmHg whilst awaiting intervention

Type B:
conservative management
bed rest
reduce blood pressure IV labetalol to prevent progression

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89
Q

What is giant cell arteritis?

A

It is a type of chronic vasculitis characterized by granulomatous inflammation in the walls of medium and large arteries.

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90
Q

What condition is commonly associated with giant cell arteritis?

A

Polymyalgia rheumatica

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91
Q

Sx of giant cell arteritis

A
  1. Headache – new onset, localised, unilateral, temporal, temporal abnormality – (tenderness, thickening or nodularity)
  2. Systemic features – fever, fatigues, anorexia, weight loss, depression
  3. Polymyalgia rheumatics – bilateral upper arm stiffness, ache & tenderness, pelvic girdle pain)
  4. Scalp tenderness
  5. Intermittent jaw claudication
  6. Visual disturbance
92
Q

Ix for giant cell arteritis

A

Diagnostic = temperol artery biospy

Other: elevated ESR

93
Q

Management of giant cell arteritis

A
  1. Refer using the local GCA pathway for specialist evaluation (rheumatologist) – same working day
  2. Immediately treat with oral prednisolone : visual symptoms (60-100 mg), no visual symptoms (40-60mg)
94
Q

What is bundle branch block?

A

Condition in which there is a delay or blockage along the pathway that electrical impulses travel to make your heart beat.

The delay or blockage can occur on the pathway that send impulses either to the left or right ride of the ventricles of the heart.

95
Q

Sx for BBB

A

usually asymptomatic

96
Q

ECG findings for BBB

A

ECG: QRS complex widened >0.12 secs

  1. RBBB: QRS complex changed- M shape V1 & W shape in V6 (MarroW)
  2. LBBB: W shape in V1 & M shape in V6 (WiliaM)
97
Q

Causes of RBBB and LBBB

A

Right - PE

Left - MI

98
Q

Management of BBB

A

Not treated but the patient’s symptoms or underlying heart conditions are:

  1. Medication to reduce HTN or symptoms of HF.
  2. May need pacemaker.
  3. BBB with low heart-pumping function – may need cardiac resynchronisation therapy (biventricular pacing)
99
Q

What is premature beat?

A

Premature Atrial/Ventricle Contractions (PA/VCs) – extra heartbeats that begin in the atria or ventricles.

The extra beats disrupt the regular heart rhythm – patient describe fluttering or skipped beat in their chest.

100
Q

Sx for premature beats

A 
Palpitations
Fluttering 
Pounding or jumping
Skipped beats or missed beats
Increased awareness of heartbeat

(Syncope, Chest pain, Fatigue)

101
Q

Ix for premature beats

A

ECG - extra beats originating outside the sinus rhythm

102
Q

Management of premature beats

A

Conservative:
Lifestyles changes: eliminating common triggers such as caffeine or tobacco

Medical:

  1. Beta-blockers – supress premature contractions
  2. Calcium channel blockers
  3. Antiarrhythmic drugs e.g. amiodarone or flecainide

Surgical:
1. Radiofrequency catheter ablation

103
Q

What is atrial fibrillation?

A

It is supraventricular tachyarrhythmia resulting from irregular, disorganised electrical activity & ineffective contraction of the atria.

104
Q

What is atrial flutter?

A

Usually a fast heart rhythm where the atria contract at a very fast rate compared to ventricles, can cause the atria to beat extremely fast ( upto 300bpm)

105
Q

Types of AF

A
  1. Paroxysmal:
    >30 secs but < 7 days
    Self-termination
    Recurrent
  2. Persistent
    > 7 days
    Requires Pharmacological or electrical cardioversion
  3. Permanent
    > 1 year
    Fails to terminate using cardioversion.
    Terminated AF but relapses within 24 hours
106
Q

Sx + signs for AF

A

Symptoms:
palpitations
dyspnoea
chest pain

Signs:
an irregularly irregular pulse

107
Q

Ix for AF

A

ECG needed for diagnosis

108
Q

1st line management for AF

A

Rate control with BB (bisoprolol) or rate-limiting CCB (diltiazem)

109
Q

When is rhythm control 1st line in AF?

A

Pt with coexistent heart failure
First onset AF
Where there is an obvious reversible cause.

110
Q

When you rhythm control in AF what should be considered in regards to stroke risk?

A

Only rhythm control if:

Either have had a short duration of symptoms (less than 48 hours)

or

be anticoagulated for a period of time prior to attempting cardioversion.

111
Q

What score do you use when using anticoagulant in AF?

A

CHA2DS2-VASc:
Congestive heart failure

Hypertension (or treated hypertension)

Age >= 75 years (2)

Age 65-74 years

Diabetes

Prior Stroke, TIA or thromboembolism (2)

Vascular disease (including ischaemic heart disease and peripheral arterial disease)

Sex (female)

1 = Treat in male
2 or more= treat with anticoag

112
Q

Contraindication for BB

A

Asthma

113
Q

Example of rhythm control drugs for AF

A

Beta-blockers

Dronedarone: second-line in patients following cardioversion

Amiodarone: particularly if coexisting heart failure

114
Q

Types of rhythm control

A

Pharmacological cardioversion: Drugs (amiodarone)

Electrical cardioversion: Synchronised DC electrical shocks

115
Q

What is the 1st line anticoagulant in AF?

A

DOAC = apixaban, dabigatran

2nd line = warfarin

116
Q

If pt had AF > 48 hours, what needs to be done before electrical cardioversion?

A

Anticoagulation should be given for at least 3 weeks prior to cardioversion

117
Q

ECG findings of atrial fibrillation

A

Will have no P-waves, a chaotic baseline, and an irregular irregular rate

118
Q

ECG findings for atrial flutter

A

‘sawtooth’ appearance

119
Q

Management of atrial flutter

A
  1. cardioversion

2. radiofrequency ablation

120
Q

What is atrioventricular block?

A

Impaired electrical conduction between the atria and ventricles.

121
Q

Types of AV block + ECG findings

A

1st degree heart block

  • PR interval > 0.2 seconds
  • asymptomatic first-degree
  • No treatment

2nd degree heart block

  • type 1 (Mobitz I, Wenckebach): progressive prolongation of the PR interval until a dropped beat occurs
  • type 2 (Mobitz II): PR interval is constant but the P wave is often not followed by a QRS complex
3rd degree (complete) heart block
- no association between the P waves and QRS complexes
122
Q

Management of AV block

A

Asymptomatic: monitor ECG
Symptomatic:
1st line : Stop all AV-nodal blocking medications

2nd line: PPM or cardiac resynchronisation therapy +/- ICD placement

123
Q

What is paroxysmal SVT?

A

any tachycardia that is not ventricular in origin

124
Q

Sx of paroxysmal SVT

A 
No symptoms  usually but can have:
Palpitations
Dizziness
Sweating 
SOB
Chest pain
125
Q

Acute management of SVT

A
  1. vagal manoeuvres:
    - Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
    - carotid sinus massage
  2. IV adenosine
    - rapid IV bolus of 6mg
    - contraindicated in asthmatics - verapamil is a preferable option
  3. electrical cardioversion
126
Q

What is VT?

A

broad-complex tachycardia originating from a ventricular ectopic focus.

127
Q

Types of VT

A
  1. monomorphic VT: most commonly caused by MI
  2. polymorphic VT: A subtype of polymorphic VT is torsades de pointes which is precipitated by prolongation of the QT interval.
128
Q

Sx of VT

A 
Light-headedness
Palpitation
Chest Pain
Dyspnoea
Syncope
Symptoms of HF
129
Q

Management of VT

A
  1. If the Pt has adverse signs (systolic BP < 90 mmHg, chest pain, heart failure) then immediate cardioversion is indicated.
  2. No adverse signs : antiarrhythmics,
    - if these fail = electrical cardioversion may be needed with synchronised DC shocks
130
Q

Management of torsades de pointes

A

IV magnesium sulfate

131
Q

Example of antiarrhythmics in VT

A
  1. amiodarone: ideally administered through a central line
    (2. lidocaine: use with caution in severe left ventricular impairment
  2. procainamide)
132
Q

What drug is contraindicated in VT?

A

Verapamil

133
Q

What is Ventricular fibrillation?

A

Disorganised electrical impulses causing the heart to quiver rather than contract

134
Q

What is ventricular flutter?

A

tachycardic arrhythmia affects the ventricles, considered as transition between VT & VF.

135
Q

Management of ventricular fibrillation

A

Pulseless ventricular tachycardia or ventricular fibrillation should be treated with immediate defibrillation + CPR

Long term: anti-arhytmic , Beta blockers, ICD,

Surgical:
Angioplasty, CABG, Cardioverter Defibrillator

136
Q

Common causes of endocarditis

A

Staph aureus
Strep

Risk factors such as bacteraemia/IVDU or invasive procedures

137
Q

Sx for infective endocarditis

A 
Fever
chest pain (due to local effect or septic emboli to lungs), 
Dizziness, weakness. 
Arthralgia
Night sweats
138
Q

Signs for infective endocarditis

A 
Pyrexia
Tachycardia
Red spots on palms/soles
Janeway lesions
Osler nodes
Murmurs in lung fields and heart
139
Q

Diagnostic criteria for infective endocarditis

A 
Modified Duke criteria:
pathological criteria positive, or
2 major criteria, or
1 major and 3 minor criteria, or
5 minor criteria
140
Q

What is the pathological criteria in Duke’s

A

Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery

141
Q

What is the major criteria in Duke’s?

A

Positive blood cultures

Evidence of endocardial involvement:
- positive echocardiogram (oscillating structures, abscess formation, new valvular regurgitation or dehiscence of prosthetic valves)
or
-new valvular regurgitation

142
Q

What is the minor criteria in Duke’s?

A
  1. predisposing heart condition or intravenous drug use
  2. microbiological evidence does not meet major criteria
  3. fever > 38ºC
  4. vascular phenomena: major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechiae or purpura
  5. immunological phenomena: glomerulonephritis, Osler’s nodes, Roth spots
143
Q

Management of infective endocarditis

A

amoxicillin or vancomycin with low dose gentamicin

flucloxacillin if Staph

144
Q

Features of acute pericarditis

A
  1. chest pain: may be pleuritic. Is often relieved by sitting forwards
  2. other symptoms include non-productive cough, dyspnoea and flu-like symptoms
  3. pericardial rub
  4. tachypnoea
  5. tachycardia
145
Q

Ix for acute pericarditis

A
  1. ECG changes
    - widespread ‘saddle-shaped’ ST elevation
    - PR depression: most specific ECG marker for pericarditis
  2. all patients with suspected acute pericarditis = transthoracic echocardiography
146
Q

Management of acute pericarditis

A

1st line = NSAIDs and colchicine

acute idiopathic or viral pericarditis

147
Q

which valve is associated with endocarditis

A

mitral

148
Q

What is cardiac tamponade?

A

characterized by the accumulation of pericardial fluid under pressure.

149
Q

Classic features of cardiac tamponade

A

Beck’s triad:
hypotension
raised JVP
muffled heart sounds

150
Q

Other features of cardiac tamponade

A
  1. dyspnoea
  2. tachycardia
  3. an absent Y descent on the JVP - this is due to the limited right ventricular filling
  4. pulsus paradoxus - an abnormally large drop in BP during inspiration
151
Q

What ECG findings will you have in cardiac tamponade?

A

electrical alternans

152
Q

Management of cardiac tamponade

A

urgent pericardiocentesis

153
Q

Features of pericardial effusion

A

Can cause cardiac tamponade:

  • Classic triad: hypotension, muffled heart sounds, jugular venous distention
  • Pulsus paradoxus
  • Pericardial friction rub
  • Tachycardia
  • “swinging heart” – heart moves within the pericardial cavity.
154
Q

Ix for pericardial effusion

A

CXR (effusion/cardiomegaly)

Pericardial fluid analysis

155
Q

Management of pericardial effusion

A
  1. Treat underlying cause & signs/symptoms
  2. Pharmacological :
    Oxygen therapy – to relieve symptoms
    IV fluids – to improve ventricular filliing (dehydration & hypovolaemia)
  3. Surgical :
    Pericardiocentesis
156
Q

What is heart failure?

A

Heart failure is clinical syndrome in which the ability of the heart to maintain the circulation of blood is impaired as a result of structural or functional impairment of ventricular filling or ejection fraction.

157
Q

Sx of HF

A

SOB – on exertion, rest, orthopnoea, PND, nocturnal cough
Fatigue
Ankle swelling, bloated, abdo swelling
Light-headedness, syncope

158
Q

Signs of HF

A 
Signs
Tachycardia (rhythm)
Displaced apex beat 
Heart murmurs
3rd or 4th heart sounds
Raised JVP
Enlarged liver
Tachypnoea, basal crepitation, PE
159
Q

Signs for left-sided HF

A

Pulmonary oedema:

  1. dyspnoea
  2. orthopnoea
  3. paroxysmal nocturnal dyspnoea
  4. bibasal fine crackles
160
Q

Signs for right-sided HF

A
  1. peripheral oedema
    - ankle/sacral oedema
  2. raised JVP
  3. hepatomegaly
  4. weight gain due to fluid retention
  5. anorexia (‘cardiac cachexia’)
161
Q

Ix for HF

A

1st line = BNP

Diagnostic = Transthoracic echocardiogram

162
Q

Management of acute HF

A
  1. IV loop diuretics (furosemide)

Possible additional treatments:
1. oxygen

  1. Patients with respiratory failure: CPAP
  2. Patients with hypotension (e.g. < 85 mmHg)/cardiogenic shock:
    - inotropic agents
    e. g. dobutamine
    - vasopressor agents
    e. g. norepinephrine
163
Q

Long term drug treatment for chronic HF

A

1st line = ACEi & BB (bisoprolol)

2nd line = aldosterone antagonist (spironolactone)

164
Q

What murmur is associated with Aortic stenosis?

A

ESM

- radiates to carotid

165
Q

Features of aortic stenosis

A

narrow pulse pressure

slow rising pulse

166
Q

Management of valvular disorders

A

Valve replacement

167
Q

What murmur is associated with Aortic Regurgitation?

A

early diastolic murmur

168
Q

Features of Aortic Regurgitation

A

collapsing pulse
wide pulse pressure
Quincke’s sign (nailbed pulsation)
De Musset’s sign (head bobbing)

169
Q

What murmur is associated with Mitral stenosis?

A

mid-late diastolic murmur (best heard in expiration)

170
Q

Features of mitral stenosis

A

loud S1, opening snap
low volume pulse
malar flush

171
Q

What murmur is associated with Mitral regurgitation?

A

a pansystolic murmur described as “blowing”.

- heard best at the apex and radiating into the axilla.

172
Q

What murmur is associated with Tricuspid regurgitation?

A

pan-systolic murmur

173
Q

Features of Tricuspid regurgitation

A

prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave

174
Q

Murmur associated with pulmonary stenosis

A

Ejection systolic louder on inspiration

175
Q

Murmur associated with pulmonary regurgitation

A

Early diastolic - Graham-steel murmur

176
Q

Murmur associated with mitral valve prolapse

A

late systolic murmur

177
Q

Features of mitral valve prolapse

A
  1. patients may complain of atypical chest pain or palpitations
  2. mid-systolic click (occurs later if patient squatting)
  3. late systolic murmur (longer if patient standing)
178
Q

What is dilated cardiomyopathy?

A

Characterised by ventricular chamber enlargement and contractile dysfunction with normal left ventricular wall thickness

179
Q

Features of dilated cardiomyopathy

A
  1. classic findings of heart failure
  2. systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
  3. S3
  4. ‘balloon’ appearance of the heart on the chest x-ray
180
Q

Diagnosis of dilated cardiomyopathy

A

Diagnosis of exclusion

181
Q

Management of dilated cardiomyopathy

A

Treat symptoms

182
Q

What is hypertrophic obstructive cardiomyopathy (HCOM)?

A

Autosomal dominant disorder of muscle tissue caused by defects in the genes encoding contractile proteins.

183
Q

Features of HCOM

A

often asymptomatic

  • exertional dyspnoea
  • angina
  • syncope
  • sudden death (most commonly due to ventricular arrhythmias),
  • jerky pulse, large ‘a’ waves,
  • double apex beat
  • ejection systolic murmur
184
Q

Ix for HCOM

A

Echo

ECG : LVH, non-specific ST abnormalities

185
Q

Management of HCOM

A 
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*
186
Q

What is restrictive cardiomyopathy?

A

Characterised by normal left ventricular cavity size and systolic function but with increased myocardial stiffness.

187
Q

Sx for restrictive cardiomyopathy

A

HF symptoms

188
Q

Ix for restrictive cardiomyopathy

A

Diagnostic: right ventricular biopsy for positivity for congo red staining

MRI – distinguish from constrictive pericarditis

189
Q

Management of restrictive cardiomyopathy

A

Treat symptoms

Implantable cardioverter defibrillator

190
Q

What is atrial septal defect?

A

congenital heart defect

191
Q

Features of ASD

A
  1. ejection systolic murmur

2. fixed splitting of S2

192
Q

Ix for ASD

A

ECG - RBBB with RAD

Diagnostic - Echo

193
Q

Sx for ASD

A
  1. Dyspnoea, heart failure or stroke

2. Child – SOB, difficulty feeding, poor weight gain, LRTI

194
Q

Management of ASD

A
  1. ASD – small & symptomatic – watching & waiting
  2. Referral to cardiologist
  3. Surgery – transvenous catheter closure via femoral vein or open-heart surgery
  4. Medication – anticoagulant e.g., aspirin, warfarin & NOACs
195
Q

What is VSD?

A

Congenital hole in the septum (wall) between the two ventricles.

196
Q

Features of VSD

A
  • Poor feeding
  • Dyspnoea
  • Tachypnoea
  • Poor feeding
  • Failure to thrive
  • Features of HF – tachypnoea, hepatomegaly, tachycardia, pallor
197
Q

Signs of VSD

A
  • Pan-systolic murmur – more prominent on left lower sternal boarder in the 3rd & 4th ICS
  • Systolic thrill on palpation
198
Q

Ix for VSD

A

VSD may be picked up on antenatal scans or when murmur is heard during newborrn baby check

199
Q

Management of VSD

A
  1. Refer to (paediatric) cardiologist – high specialised management
  2. Small VSD with no symptoms – watchful waiting
  3. Surgery – transvenous catheter closure or open-heart surgery
200
Q

What is Coarctation of Aorta?

A

congenital narrowing of the descending aorta usually around the ductus arteriosus.

201
Q

Sx for Coarctation of Aorta

A
  1. neonate – weak femoral pulses
  2. Tachypnoea and increased work of breathing
  3. Poor feeding
  4. Grey and floppy baby
  5. HTN at a young age (resistant to treatment)
202
Q

Ix for Coarctation of Aorta

A

ECG, CXR, Echo

203
Q

Management of Coarctation of Aorta

A
  1. In mild cases patients can live symptom free until adulthood without requiring surgical input
  2. In severe cases patients will require emergency surgery shortly after birth.
204
Q

What is Patent Ductus Arteriosus?

A

The ductus arteriosus normally stops functioning within 1-3 days of birth and closes completely within the first 2-3 weeks of life.

When it fails to close, this is called a “patent ductus arteriosus” (PDA).

205
Q

Sx for Patent Ductus Arteriosus

A
  • Shortness of breath
  • Difficulty feeding
  • Poor weight gain
  • Lower respiratory tract infections
206
Q

Examination findings for Patent Ductus Arteriosus

A
  1. continuous crescendo-decrescendo “machinery” murmur that may continue during the second heart sound
  2. left subclavicular thrill
  3. large volume, bounding, collapsing pulse
  4. wide pulse pressure
  5. heaving apex beat
207
Q

Diagnosis of Patent Ductus Arteriosus

A

Echo

208
Q

Management of Patent Ductus Arteriosus

A
  • Typically monitored until 1 year of age using echo

- After 1 year – trans-catheter or surgical closure (ligation)

209
Q

What is tetralogy of fallot + its features?

A

TOF is a result of anterior malalignment of the aorticopulmonary septum.

The four characteristic features are:

  1. ventricular septal defect (VSD)
  2. right ventricular hypertrophy
  3. pulmonary stenosis, right ventricular outflow tract obstruction
  4. overriding aorta
210
Q

Sx of tetralogy of fallot

A
  1. Cyanosis
  2. Clubbing
  3. Poor feeding
  4. Poor weight gain
  5. Ejection systolic murmur heard loudest in the pulmonary area
  6. “Tet spells” – cyanotic episode
  7. Older children may squat when a tet spell occurs.
    - Younger children can be positioned with their knees to their chest.
211
Q

Management of tetralogy of fallot

A

Surgical repair is often undertaken in two parts

Cyanotic episodes may be helped by beta-blockers to reduce infundibular spasm

212
Q

What are the shockable rhythms?

A

VF

pulseless VT

213
Q

In ALS, when can (1mg) adrenaline be administered?

A

After chest compression have started ( 30:2)

214
Q

What ESM is heard louder on expiration?

A

1) aortic stenosis

2) hypertrophic obstructive cardiomyopathy

215
Q

What ESM is heard louder on inspiration?

A

1) pulmonary stenosis

2) atrial septal defect

216
Q

What ECG abnormality is associated with hypercalcaemia?

A

Shortened QT interval

217
Q

When a patient in cardiac arrest has organised electrical activity but there is still no pulse and there are no signs of life, what do you do?

A

1) continuing CPR at a rate of 30:2

2) IV adrenaline

218
Q

Which ECG changes would you see in hyperkalaemia?

A

Tall Tented T waves

219
Q

Side effects of ARB

A

hyperkalaemia, hypotension, renal failure

220
Q

When are loop diuretics given to HF patients?

A

in acute HF, presenting symptomatic

221
Q

How can you distinguish which class of meds to give a patient with an arterial or venous blood disorder?

A

Arterial: antiplatelets (aspirin, clopidogrel)
Venous: anticoagulants

222
Q

Endocarditis which causes HF requires…

A

emergency valve replacement surgery

223
Q

which ECG finding is seen in cardiac tamponade

A

electric alternans

224
Q

ECG findings in an NSTEMI

A

pathological P waves

225
Q

what is Prinzemtal angina

A

sometimes relieved by medication but not by rest

226
Q

What is the most common complication of Hypertrophic obstructive cardiomyopathy?

A

Sudden death due to ventricular arrhythmia

227
Q

What is the gold-standard for ST-elevation MI?

A

PCI

FCM Matrix (17 decks)

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