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2A > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Where can thrombosis occur?

A

Thrombosis can occur in:
Arterial circulation: high pressure - platelet rich
Venous circulation: low pressure - fibrin rich

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2
Q

What is the normal bleeding time?

A

2-7 minutes

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3
Q

List a symptom that could occur due to an arterial thrombosis in the coronary circulation?

A
  • Angina
  • Shoulder pain
  • Sudden death
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4
Q

List a symptom that could occur due to an arterial thrombosis in the cerebral circulation?

A
  • Headache
  • Slurred speech
  • Unilateral weakness
  • CVA cerebral vascular accident
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5
Q

List a symptom that could occur due to an arterial thrombosis in the peripheral circulation?

A
  • Pain in leg
  • Stomach-ache
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6
Q

What is the underlying cause of arterial thrombosis in majority of cases?

A

When an artery is damaged by atherosclerosis

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7
Q

List some examples of Arterial thrombosis Aetiology

A

Atherosclerosis
Inflammatory
Infective
Trauma
Tumours

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8
Q

What is the treatment for coronary arterial thrombosis?

A
  1. Aspirin.
  2. LMWH or Fondaparinux or UFH
  3. Thrombolytic therapy
  4. Reperfusion
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9
Q

What is the treatment for cerebral arterial thrombosis?

A
  1. Aspirin, other anti-platelets
  2. Thrombolysis
  3. Catheter directed treatments
    Reperfusion
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10
Q

Why is heparin not used in patients who have had a CVA (cerebral vascular accident)

A

Increased risk of bleeding complications

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11
Q

What is the treatment for arterial thrombosis in other sites?

A
  1. Antiplatelets, statins
  2. Role of anticoagulants evolving
  3. Endovascular vs Surgical
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12
Q

Why is Fondaparinux used instead of heparin?

A

Much higher risk of bleeding when using heparin.
Fondaparinux also has a longer half life.

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13
Q

Where does venous thrombosis occur?

A

*Peripheral - such as the ileofemoral, femoro-popliteal

  • Other sites such as cerebral and visceral
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14
Q

What are the symptoms of DVT?

A

Usually non-specific symptoms, pain and swelling, groin strain. Calf pain, chest pain, and breathlessness is a common clinical scenario however.

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15
Q

Briefly describe the investigations might be done in order to diagnose a DVT.

A
  1. D-dimer; looks for fibrin breakdown products. If normal, you can exclude DVT. Abnormal does not confirm diagnosis however.
  2. Ultrasound compression scan; if you can’t squash the vein = clot.
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16
Q

What is the treatment for DVT?

A
  1. Heparin or LMWH.
  2. Oral warfarin or DOAC.
  3. Endo-vascular treatment
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17
Q

Give 5 risk factors for DVT.

A
  1. Surgery, immobility, leg fracture.
  2. OCP, HRT.
  3. Long haul flights.
  4. Genetic predisposition: Factor 5 Leiden
  5. Pregnancy.
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18
Q

Causes of thrombosis (Virchow’s triangle, typically 2 out of these 3)

A
  1. Hypercoagulability
  2. Venous stasis
  3. Endothelial damage
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19
Q

When would the treatment of DVT be more aggressive?

A

when the DVT are really long ie right to the IVC from the leg, and when patients are really symptomatic.

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20
Q

Prevention of DVT

A
  • Mechanical or chemical thromboprophylaxis
  • Compression socks
  • Also early mobilisation and good hydration
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21
Q

What is heparin?

A
  • Heparin is an anticoagulant
  • It activates antithrombin which then inhibits thrombin and factor Xa.
  • It has a short half-life
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22
Q

How is unfractionated heparin administered? (UFH)

A

Intravenously, continuous infusion

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23
Q

How is low molecular weight heparin administered? (LMWH). What is it used for?

A

Once daily, weight-adjusted dose given subcutaneously. Used for treatment and prophylaxsis

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24
Q

Is HIT (Heparin induced thrombocytopenia) more common after LMWH or UFH?

A

UFH

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25
Q

Why might you use UFH over LMWH?

A

UFH has a short half life and its effects are easier to reverse. UFH might also be more effective.

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26
Q

What is Warfarin?

A

Warfarin is an anticoagulant.
- It produces NON-functional clotting factors 2, 7, 9 and 10.
- Orally active
- Long half life (36 hours)
- Prolongs the prothrombin time

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27
Q

What is warfarin the antagonist of?

A

Vitamin K.

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28
Q

Why is warfarin difficult to use?

A
  1. Lots of interactions!
  2. Teratogenic.
  3. Needs almost constant monitoring.
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29
Q

What are DOAC/NOAC?

A

Direct oral anticoagulants/ new oral anticoagulants.

Directly acts on factor II or X

Eg: apixaban

No monitoring needed

Shorter half lives

Used for extended thromboprophylasis and treatment of AF and DVT/PE

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30
Q

Why are DOACs not used in pregnancy or in metal heart valves?

A

Pregnancy: Potential for reproductive toxicity

MHV:
It is associated with an increased risk of thromboembolic events and increase in clots and strokes

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31
Q

What is Fondaparinux?

A

It is an anticoagulant that indirectly inhibits factor Xa.

Preferred in patients more prone to HIT.

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32
Q

What is aspirin?

A

It is an antiplatelet that Inhibits cyclo-oxygenase irreversibly. Inhibits thromboxane formation and hence platelet aggregation

Act for lifetime of platelet, 7-10 days

Used in arterial thrombosis, 75-300 mg od

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33
Q

Drug for antiplatelet therapy in angina if aspirin intolerant?

A

Clopidogrel, prasugrel, ticagrelor

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34
Q

How does Clopidogrel work?

A

When platelets are activated they release dense granules which release ADP and can bind to P2Y12. P2Y12 can then amplify platelet activation. Clopidogrel inhibits P2Y12 receptor and reduces platelet activation

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35
Q

What is dual antiplatelet therapy?

A

Management of ACS using a combination of aspirin and a P2Y12 inhibitor

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36
Q

Clopidogrel vs prasugrel which is better?

A

Prasugrel is much more reliable and useful because it is a more efficient prodrug and has a direct liver breakdown pathway while clopidogrel effectiveness relies on genetics alongside other factors

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37
Q

Adverse effects of P2Y12 inhibitors

A

Common to all:
*Bleeding eg epistaxis, GI bleeds, haematuria
*Rash
*GI disturbance

Ticagrelor:
*Dyspnoea (shortness of breath)
*Ventricular pauses

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38
Q

Why are GPIIb//IIa antagonists used selectively? (antiplatelet drugs)

A

*Only IV drugs available
*Increase risk of major bleeding
*But still used in combination with aspirin and oral P2Y12 inhibitors in management of patients undergoing PCI for ACS

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39
Q

DVT signs

A

tenderness, swelling, warmth, discolouration

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40
Q

DVT complications

A

Phlegmasia Alba Dolens and Phlegmasia Cerulae Dolens, PE

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41
Q

How can DVT cause ischaemia?

A

An acute significant widespread venous embolism in a leg causes so much swelling that it blocks the blood flow through the leg. The leg becomes pale or blue and extremely painful. Gangrene (dead tissue) can develop if the blood flow is not restored.

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42
Q

In standard treatment of DVT, why is heparin used initially before switching to warfarin?

A

Heparin displays an anticoagulant effect within 1 day, while the anticoagulant effects of warfarin are not evident until the third day of therapy. If rapid anticoagulant effects are needed, heparin should be initiated first, and warfarin should be started later on.

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43
Q

Pulmonary Embolism symptoms

A

breathlessness, pleuritic chest pain, pain in leg

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44
Q

Pulmonary embolism signs

A

tachycardia, tachypnoea, pleural rub

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45
Q

Pulmonary Embolism Differential diagnosis

A

Musculoskeletal, Infection, Malignancy, Pneumothorax, Cardiac, GI causes

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46
Q

Pulmonary embolism initial investigations

A

CXR usually normal
ECG sinus tachy, (QI,SI,TIII)
Blood gases: type 1 resp failure, decreased O2 and CO2
Mainly done to exclude alternative causes

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47
Q

Pulmonary embolism: further investigations

A

Further investigations include D-dimer: normal excludes diagnosis
CTPA spiral CT with contrast, visualise major segmental thrombi
Ventilation/ Perfusion scan: mismatch defects

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48
Q

Pulmonary embolism treatment

A

Supportive treatment
LMW Heparin
Oral warfarin (INR 2-3)for 6 months
DOAC/NOAC
Treat underlying cause

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49
Q

Pulmonary embolism prevention

A

Anticoagulation
IVC filters - (can be used to catch clots)

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50
Q

How are massive pulmonary embolisms treated?

A

Thrombolytic therapy
Streptokinase and tPA

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51
Q

Complications of a massive pulmonary embolism

A

Haemodynamic instability
Hypotension, cyanosis, severe dyspnoea, right heart strain/ failure

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52
Q

What is peripheral vascular disease (or peripheral arterial disease)? PVD/PAD

A

Peripheral vascular disease is essentially reduced blood supply and ischaemia in the lower limbs due to atherosclerosis and thrombosis in the arteries

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53
Q

What is the most potent risk factor in PAD?

A

Using tobacco products

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54
Q

Risk factors for PAD. Modifiable and non-modifiable

A

Modifiable:
Smoking
Hypertension
Diabetes
Hypercholesterolaemia

Non-modifiable:
Sex
Age

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55
Q

Three main patterns of presentation of PVD?

A
  1. Intermittent claudication (least severe)
  2. Critical limb ischaemia
  3. Acute limb-threatening ischaemia (most severe)
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56
Q

Name the classification system for peripheral vascular disease (PVD).
Brief description.

A

Fontaine classification.
4 stages:
1. Asymptomatic
2. Intermittent claudication
>200m pain free walking
<200m pain free walking
3. Chronic limb ischaemia (pain at rest)
4. Ischaemic ulcers → gangrene

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57
Q

Features of of acute limb-threatening ischaemia

A

6Ps
* Pulselessness
* Pallor
* Pain
* Perishingly cold
* Paralysis
* Paresthesia
Acute-embolus (AF, MI)
Acute on chronic-thrombus

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58
Q

Features of chronic limb-threatening ischaemia

A

*IC (intermittent claudication)
*Rest pain
*Tissue loss
*Burger’s test

6Ps present in chronic limb ischemia too but more you have=more limb threatening

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59
Q

Management of peripheral vascular disease?

A
  1. Intermittent claudication
    Manage risk factors… decrease BMI, cease smoking, control BP, statins and antiplatelets and T2DM control
  2. Chronic limb ischaemia
    Revascularisation surgery… PCI if small, bypass if larger
    Amputation if severe
  3. Acute limb threatening ischaemia
    Surgical emergency → revascularisation within 4-6 hours… otherwise very high amputation risk
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60
Q

What is the name of the circle consisting the arterial supply to brain?

A

Circle of Willis

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61
Q

Are the majority of TIA/strokes ischaemic or haemorrhagic?

A

Ischaemic! 60%

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62
Q

In TIA/stroke is it embolization or thrombosis which is aetiologically important?

A

Thrombosis

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63
Q

What is an aneurysm?

A

Weakening of the arterial wall leading to dilatation and bulging of the wall

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64
Q

Most common location of an aneurysm?

A

Commonest location is the infra-renal aorta

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65
Q

What are false aneurysms/pseudo aneurysms caused by?

A

Damage to wall of artery (ie by cardiologists)
Usually doesn’t involve damage to all 3 walls.

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66
Q

What are mycotic aneurysms caused by?

A

Weaknesses in the wall related to infection.

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67
Q

Initial investigations for in PVD?

A
  • Bloods – Lipids, Glucose, Renal function, Vasculitic screen, Clotting, FBC
  • ABPI
  • Duplex
  • Cross sectional Imaging
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68
Q

What is the diagnosis of peripheral vascular disease?

A

*ABPI → comparing blood in post+ant tibial artery, to the brachial artery with a doppler ultrasound

0.9-1.3 is normal
0.5-0.9 = intermittent claudication
<0.5 = critical limb ischaemia
When ABPI is VERY low… there is a risk of acute life threatening ischaemia

*Colour duplex ultrasound → assess the degree of stenosis

*CT Angiography if surgery is considered

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69
Q

What information does duplex give you?

A

Gives information about the flow of blood ie whether there is backflow etc.
Assess location and severity of stenosis.

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70
Q

CTA vs MRA vs Catheter angiography

A

CTA and MRA are both non-invasive while a Catheter angiography requires insertion of a catheter into the area.

All CTAs require the use of an IV contrast agent, but not all MRAs do.

CTAs require just a few minutes to complete; MRAs may require 20-30 minutes.

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71
Q

What are the advantages of MRA over CTA?

A

CTAs involve exposure to radiation (see below), MRAs do not.
The contrast dyes in CTAs are also more toxic on the kidneys.

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72
Q

Give 4 treatments for peripheral vascular disease.

A
  1. Risk factor modification.
  2. Bypass surgery for critical leg ischaemia.
  3. Balloon angioplasty.
  4. Stenting of occlusion.
  5. Amuptation.
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73
Q

What are the advantages and disadvantages of bypass surgery for peripheral vascular disease?

A

Advantages:
Better patency and limb salvage rates
Disadvantages:
Higher morbidity and mortality

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74
Q

Should a patient with IC (intermittent claudication) have exercise or angioplasty or surgery?

A

Exercise! Graded exercise therapy is officially recommended.

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75
Q

Define abdominal aortic aneurysm? (AAA)

A

Permanent aortic dilation exceeding 50% where diameter >3cm

Typically infrarenal (below renal arteries), in elderly men

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76
Q

A negative risk factor for AAA?

A

Diabetes but unknown reason

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77
Q

Risk factors for AAAs?

A

Smoking = biggest risk factor
Increasing age
Hypertension
Connective tissue disorders - Ehlers Danos and Marfan syndrome (changes in balance of collagen and elastic fibres)
Family history

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78
Q

AAA Treatment

A

Elective surgery
Either:
1) EVAR (Endovascular aortic repair) - stent inserted through femoral/iliac artery
-Less invasive but more post op complications

2) open surgery
-more invasive but fewer complications

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79
Q

What is the current NICE recommendation for AAA repair open surgery or EVAR?

A

Open surgery is preferred by current NICE guidelines.

EVAR can be considered under medical or anaesthetic risks.

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80
Q

Carotid artery disease treatment

A
  1. Carotid Endarterectomy (standard treatment)
    * opens the artery and removes the plaque.
  2. Endovascular stenting
    * fine catheter tube is passed through the skin and into the narrowed blood vessel. A metal tube (stent) is placed inside the vessel to prevent it narrowing again.
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81
Q

How would you treat incompetent deep veins that don’t return blood back to the heart?

A

Compression

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82
Q

What is the current NICE recommendation for treatment of varicose veins?

A

Surgical stripping - Endovenous laser varicose vein surgery

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83
Q

What prevents blood flowing distally?

A

Venous valves

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84
Q

Where is the saphenofemoral junction located?

A

4 fingers breadths lateral and inferior to the pubic tubercle on that common side

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85
Q

What does acute coronary syndromes cover?

A

Term covers a spectrum of acute cardiac conditions including unstable angina, NSTEMI and STEMI

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86
Q

How to define different acute coronary syndromes?

A

Unstable angina- severe ischaemia (no ECG changes)

NSTEMI- partial infarction + non-Q wave infarction

STEMI- transmural infarct and ST elevation in local ECG leads + Q wave infarction

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87
Q

Give 3 signs of unstable angina.

A
  1. Cardiac chest pain at rest.
  2. Cardiac chest pain with crescendo patterns; pain becomes more frequent and easier provoked.
  3. No significant rise in troponin.
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88
Q

Making a diagnosis of ACS? (Step by step) (primary investigations)

A

1) when patient presents with symptoms (eg chest pain) perform ECG

2) ST elevation or new left bundle branch block = STEMI

3) no ST elevation—-> troponin blood tests:

  • increased troponin + changes (ST depression, t wave inversion or path Q waves) = NSTEMI

-normal troponin + no ECG changes then unstable angina or another cause (musculoskeletal chest pain)

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89
Q

What’s the difference between a stable and unstable angina?

A

Unstable angina:
* chest pain that occurs at rest
* not relieved by GTN
* occurs more frequently and lasts for longer.

Stable angina:
* Can be relieved by GTN
* Pain relieved at rest

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90
Q

What is Prinzmetal’s angina? ECG too…

A

Angina caused by coronary vasospasm (not due to cv vessel atherogenesis)

Seen increasingly in cocaine users

ECG shows ST elevation

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91
Q

Causes of ACS

A

Majority of cases: Rupture of an atherosclerotic plaque and subsequent arterial thrombosis.

Myocardial infarction due to atherothrombosis is known as type 1 myocardial infarction

Other causes of myocardial infarction usually fall under the umbrella of type 2 myocardial infarction:
- Drug abuse
- Oxygen demand/supply mismatch caused by sepsis, anaemia, haemorrhage etc
- coronary vasospasm without plaque rupture

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92
Q

What is Tako-Tsubo cardiomyopathy?

A
  • Stress induced cardiomyopathy, may masquerade as myocardial infarction
  • Often precipitated by acute stress such as extreme emotional distress in susceptible individuals
  • Causes transient left ventricular systolic dysfunction, typically ballooning of the left ventricular apex during systole that recovers over days or a few weeks with limited or no permanent damage.
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93
Q

What does an ECG after MI look like?

A
  • pathologically deep q waves
  • ST segment elevation
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94
Q

Symptoms of myocardial infarction?

A

*Cardiac chest pain

  • unremitting
  • usually severe but may be mild or absent
  • occurs at rest
  • associated with sweating, breathlessness, nausea and/or vomiting
  • 1/3 occur in bed at night
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95
Q

Aftermath of a myocardial infarction?

A

Usually causes permanent heart muscle damage although this may not be detectable in small MIs.

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96
Q

Management of a myocardial infarction?

A

*Initial management
- get in hospital quickly
- paramedics - if ST elevation, contact primary PCI centre for transfer for emergency coronary angiography
- Take aspirin 300 mg immediately
- Pain relief

*Hospital management
- make diagnosis
- oxygen therapy only if hypoxic
- pain relief - opiates/nitrates
- aspirin +/- platelet P2Y12 inhibitor
- consider beta-blockers
- consider other antianginal therapy
- consider urgent coronary angiography eg if troponin elevated or unstable angina refractory to medical therapy

MONAC!!
- M - morphine + anti-emetic (metoclopramide)
- O - O2 (if stats <94% or 88-92% if COPD)
- N - nitrates (GTN spray)
- A - aspirin 300 mg
- C - Clopidogrel/Ticagrelor (75mg dual antiplatelet_ or prasugrel if undergoing PCI
- Anticoagulant: fondaparinux or heparin

*Note not all patients require oxygen

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97
Q

What is troponin?

A

A protein complex consisting of troponin C, troponin I, and troponin T that regulates actin:myosin contraction

Cardiac specific isoforms of troponin T and troponin I are highly sensitive markers for cardiac muscle injury

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98
Q

When is platelet adhesion and secretion bad?

A

When it’s reacting to an atherosclerotic plaque rupture. As it causes a thrombus to form inside the artery and potentially occlude it.

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99
Q

Which part of the heart does the P wave represent?

A

The atrium

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100
Q

Which part of the ECG represents the ventricle?

A

The QRS wave

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101
Q

What is a patent foramen ovale?

A

A hole between the left and right atria of the heart that fails to close naturally after birth.

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102
Q

What is a paradoxical embolism?

A

This is when the patent foramen ovale allows venous thrombi to cross into the arterial system causing an ischemic stroke

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103
Q

Which conditions/syndromes is coarctation of the aorta associated with?

A

Turner’s syndrome and Berry aneurysms of the brain

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104
Q

Cardiac output equation

A

Cardiac output = heart rate x stroke volume

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105
Q

Mean arterial blood pressure equation

A

Mean arterial blood pressure = cardiac output x systemic vascular resistance

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106
Q

Normal physiology of heart

A

Normally- increased preload= increased afterload= increased cardiac output (frank starling law)

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107
Q

Overall pathophysiology of a failing heart! (heart failure)

A

Normally… an increased preload = increased afterload = increased CO…

But in heart failure, the cardiac myocytes are messed → frank starling law ineffective → decreased cardiac output…

RAAS+SNS tries to compensate this temporarily, to get BP high. This is why aldosterone and ADH are high as are Adrenaline and Norad

However, the compensation fails and the heart undergoes cardiac remodelling → decreased CO

This normally happens in 1 side of the heart. If it happens in both, this is known as congestive heart failure.

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108
Q

What causes cardiac ischaemia?

A
  • Vessel occlusion
  • coronary artery disease
  • thrombosis and thromboembolism
  • Arterial spasm/compression
  • drugs (eg cocaine)
  • stress (takotsubo)
  • anomalous arteries
  • myocardial bridging
  • Oxygen demand/supply mismatch
  • anaemia
  • CO
  • bleeding
  • decreased cardiac output/bradycardia
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109
Q

Give 5 potential complications of MI.

A

D - Death
A - Arrhythmia
R - Rupture
T - Tamponade
H - Heart failure
V - Valve disease
A - Aneurysm
D - Dressler’s syndrome
E - Embolism
R - Recurrent regurgitation

DARTHVADER

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110
Q

What is atrial fibrillation

A
  • 300-600bpm
  • Irregularly regular atrial firing rhythm → causes irregularly irregular ventricular contraction
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111
Q

What is the most common cardiac arrhythmia?

A

Atrial fibrillation

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112
Q

Which is the most common artery involved in a stroke?

A

The middle cerebral artery (MCA)

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113
Q

A 60 year old retired school teacher is an ex smoker who has shortness of breath and heart murmur - ejection systolic, heard over aortic area, pitting oedema ankles. What is the likely diagnosis?

A

Heart failure - aortic stenosis

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114
Q

What is heart failure

A

Complex clinical syndrome - heart’s inability to effectively fill and/or eject blood

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115
Q

How is heart failure ejection fraction classified?

A

Normal = 50–70%

> 50% = preserved
Diastolic failure (filling issues)

< 40% = reduced
Systolic failure (pump issues)

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116
Q

Describe the NYHA classification for heart failure.

A
  1. Class 1: heart disease is present but there is no limitation.
  2. Class 2: comfortable at rest but slight limitation on activity - mild HF.
  3. Class 3: marked limitation - moderate HF.
  4. Class 4: SOB at rest, all activity causes discomfort (severe HF).
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117
Q

What is arrhythmogenic cardiomyopathy?

A

It is associated with genetic mutations that leads to myocytes to die and be replaced with fat and scar tissues.

It leads to arrhythmia and can lead to sudden cardiac death in young adults

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118
Q

What is angina?

A

Mismatch of oxygen demand and supply

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119
Q

What is the most common cause of angina?

A

Narrowing of the coronary arteries due to atherosclerosis.

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120
Q

Predisposing factors for ischaemic heart disease IHD (list 4)

A
  • Age
  • Cigarette smoking
  • Family history
  • Diabetes mellitus
  • Hyperlipidemia
  • Hypertension
  • Kidney disease
  • Obesity
  • Physical inactivity
  • Stress
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121
Q

Exacerbating factors for ischaemic heart disease IHD

A

Supply:
-Anemia
-hypoxemia

Demand:
-hypertension
-tachycardia
-valvular heart disease

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122
Q

Environmental factors for IHD

A
  • cold weather
  • heavy meals
  • emotional stress
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123
Q

Briefly describe the pathophysiology of angina that results from atherosclerosis.

A

On exertion there is increased O2 demand. Coronary blood flow is obstructed by an atherosclerotic plaque -> myocardial ischaemia -> angina.

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124
Q

Briefly describe the pathophysiology of angina that results from anaemia.

A

On exertion there is increased O2 demand. In someone with anaemia there is reduced O2 transport -> myocardial ischaemia -> angina.

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125
Q

How do blood vessels try and compensate for increased myocardial demand during exercise.

A

When myocardial demand increases e.g. during exercise, microvascular resistance drops and flow increases!

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126
Q

Physiology of ischaemic heart disease

A

Myocardial ischemia occurs when there is an imbalance between heart’a oxygen demand and supply, usually from an increase in demand accompanied by limitation of supply:

1) impairment of blood flow by proximal arterial stenosis
2) increased distal resistance eg. Left ventricular hypertrophy
3) reduced oxygen-carrying capacity of blood eg. Anaemia

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127
Q

How to assess chest pain?

A

OPQRST
O - Onset
P - Position (site)
Q - Quality (nature/character)
R - Relationship (with exertion, posture, meals, breathing and with other symptoms)
R - Radiation
R - Relieving or aggravating factors
S - Severity
T- Timing
T - Treatment

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128
Q

At what point does the coronary flow fall off in stenosis and cause a rapid decline?

A

When the diameter stenosis reaches 70%

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129
Q

How can angina be reversed?

A

Resting - reducing myocardial demand.

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130
Q

How would you describe the chest pain in angina?

A
  • Chest pain (tightness/ discomfort) ***
  • Breathlessness **
  • Fluid retention
  • Palpitation
  • Syncope or pre-syncope
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131
Q

Differential diagnosis for myocardial ischemia

A
  • Pericarditis/myocarditis
  • Pulmonary embolism/pleurisy
  • Chest infection/ pleurisy
  • Dissection of the aorta
  • Gastro-oesophageal (reflux/spasm/ulceration)
  • Musculoskeletal
  • Psychological
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132
Q

Treatment for myocardial ischemia

A
  • Reassure
  • Lifestyle
  • smoking
  • Weight
  • Exercise
  • Diet
  • Advice for emergency
  • Medication
  • Revascularisation
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133
Q

What tool can you use to determine the best investigations and treatment in someone you suspect to have angina?

A

Pre-test probability of CAD. It takes into account gender, age and typicality of pain.

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134
Q

What investigations might you do in someone you suspect to have angina?

A
  1. ECG - usually normal, there are no markers of angina.
  2. Echocardiography.
  3. CT angiography - has a high NPV and is good at excluding the disease.
  4. Exercise tolerance test - induces ischaemia.
  5. Invasive angiogram - tells you FFR (pressure gradient across stenosis).
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135
Q

A young, healthy, female patient presents to you with what appears to be the signs and symptoms of angina. Would it be good to do CT angiography on this patient?

A

Yes. CT angiography has a high NPV and so is ideal for excluding CAD in
younger, low risk individuals.

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136
Q

Treatment for angina

A

At the GP:
- Aspirin
- Nitrates - GTN - Ca++ CB
- β Blocker
- Statin

At hospital:
CTCA/functional test of ischaemia
- ACE inhibitor
- Long acting nitrate

If still no improvement:
- Revascularisation: PCI/CABG: MDT meeting

  • Ca++ channel blocker
  • Potassium channel opener
  • Ivabradine
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137
Q

Effects of β blockers on the heart

A

Beta blockers are beta 1 specific. They antagonise sympathetic activation and so are negatively chronotropic and inotropic.

Myocardial work is reduced and so is myocardial demand = symptom relief.

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138
Q

Give 3 side effects of beta blockers.

A
  • Bradycardia.
  • Tiredness.
  • Erectile dysfunction.
  • Cold peripheries.
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139
Q

When might beta blockers be contraindicated?

A

They might be contraindicated in someone with asthma or in someone who is bradycardic.

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140
Q

Describe the action of nitrates.
i.e GTN sprays

A

Nitrates e.g. GTN spray are arterial and venous dilators -> reduction of preload and afterload -> reduced myocardial work and myocardial demand -> lower BP

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141
Q

Describe the action of Ca2+ channel blockers.

A

Ca2+ blockers are arterodilators -> reduced BP -> reduced afterload -> reduced myocardial demand.

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142
Q

Name 2 drugs that might be used in someone with angina or in someone at risk of angina to improve prognosis.

A
  1. Aspirin.
  2. Statins.
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143
Q

How does aspirin work?

A

Aspirin irreversibly inhibits (cyclooxygenase 1) COX. You get reduced TXA2 synthesis and so platelet aggregation is reduced.

Caution: Gastric ulcers!

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144
Q

What are statins used for?

A

They reduce the amount of LDL in the blood.

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145
Q

What do ACE inhibitors do?

A

Reduces blood pressure.

Angiotensinogen is converted to angiotensin 1 via renin. Angiotensin 1 is then converted to angiotensin 2 via ACE. ACE inhibitors prevents angiotensin 1 binding and so you don’t get angiotensin 2 formation. (Angiotensin 2 is a vasoconstrictor and so ACE can be used in the treatment of hypertension).

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146
Q

What is revascularisation?

A

Revascularisation might be used in someone with angina. It restores the patent coronary artery and increases blood flow.

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147
Q

Name 2 types of revascularisation.

A
  1. PCI.
  2. CABG.
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148
Q

Give 2 advantages and 1 disadvantage of PCI.

A
  1. Less invasive.
  2. Convenient and acceptable.
  3. High risk of restenosis.
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149
Q

Give 1 advantage and 2 disadvantages of CABG.

A
  1. Good prognosis after surgery.
  2. Very invasive.
  3. Long recovery time
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150
Q

When is PCI and CABG preferred?

A

STEMI - PCI preferred
NSTEMI - PCI preferred, CABG may be used
Stable angina - both PCI and CABG used

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151
Q

Briefly describe the electrical conduction pathway in the heart.

A
  1. The SAN generates an electrical impulse.
  2. This generates a wave of contraction in the atria.
  3. Impulse reaches AVN.
  4. There is a brief delay to ensure the atria have fully emptied.
  5. The impulse then rapidly spreads down the Bundle of His and Purkinje fibres.
  6. The purkinje fibres then trigger coordinated ventricular contraction.
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152
Q

What is an ECG?

A

The electrocardiogram is a representation of the electrical events of the cardiac cycle

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153
Q

How does an ECG work?

A

Contraction of any muscle is associated with electrical charges called depolarisation. These changes can be detected by electrodes attached to the surface of the body

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154
Q

What are the three basic laws of electrocardiography?

A

Electrical activity towards a lead causes an upward deflection.

Electrical activity away from a lead causes a downward deflection.

If the lead is 90 degrees to the wave of depolarisation then you get a biphasic wave form.

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155
Q

ECG electrodes: what are bipolar and unipolar leads?

A

*Bipolar leads measure 2 different points on the body

*Unipolar leads measure 1 point on the body and a virtual reference point with zero electrical potential located in the centre of the heart

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156
Q

Standard ECG has 12 leads. What do these include?

A
  • 3 bipolar limb leads, I II III
  • 3 augmented unipolar limb leads - AVR, AVL, AVF
  • 6 unipolar precordial leads
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157
Q

What is the direction of the bipolar limb leads?

A

Lead I
Right to left wrist
- on right wrist
+ on left wrist

Lead II
Right wrist to left leg
- on right wrist
+ on left leg

Lead III
Left wrist to left leg
- on left wrist
+ on left leg

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158
Q

What is the position of the unipolar augmented limb leads?

A

aVR - right shoulder
aVL - left shoulder
aVF - symphysis pubis

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159
Q

What are the pacemakers of the heart?

A

SA node - dominant pacemaker
60 - 100 beats/min

AV node - back-up pacemaker
45 - 50 beats/min

Bundle of His - back-up pacemaker
40 - 45 beats/min

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160
Q

ECG: what is the J point?

A

Where the QRS complex becomes the ST segment.

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161
Q

ECG: what is the normal axis of the QRS complex?

A

-30° -> +90°

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162
Q

ECG: what does the P wave represent?

A

Atrial depolarisation.

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163
Q

ECG: what does the PR interval represent?

A

AV node conduction delay

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164
Q

ECG: how long should the PR interval be?

A

120 - 200ms.
3 - 5 little squares

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165
Q

ECG: what might a long PR interval indicate?

A

Heart block.

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166
Q

ECG: how long should the QT interval be?

A

0.35 - 0.45s.

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167
Q

ECG: what does the QRS complex represent?

A

Ventricular depolarisation.

168
Q

ECG: what does the T wave represent?

A

Ventricular repolarisation.

169
Q

In which leads would you expect the QRS complex to be upright in?

A

Leads 1 and 2.

170
Q

ECG: where would you place the 12 leads?

A

Lead 1: From the right arm to the left arm with the positive electrode being at the left arm. At 0°.

Lead 2: From the right arm to the left leg with the positive electrode being at the left leg. At 60°.

Lead 3: From the left arm to the left leg with the positive electrode being at the left leg. At 120°.

avF: From halfway between the left arm and right arm to the left leg with the positive electrode being at the left leg. At 90°.

avL: From halfway between the right arm and left leg to the left arm with the positive electrode being at the left arm. At -30°.

avR: From halfway between the left arm and left leg to the right arm with the positive electrode being at the right arm. At -150°.

171
Q

Where are the precordial leads placed?

A

V1: 4th intercostal space (ICS), RIGHT margin of the sternum.
V2: 4th ICS along the LEFT margin of the sternum.
V4: 5th ICS, mid-clavicular line.
V3: midway between V2 and V4.
V5: 5th ICS, anterior axillary line (same level as V4)
V6: 5th ICS, mid-axillary line (same level as V4)

172
Q

Which part of the heart do each of the precordial leads look at?

A

V1: right ventricle and septum
V2: septum
V3+V4: anterior wall of the left ventricle
V5+V6: lateral wall of the left ventricle

173
Q

How many seconds do the following represent on ECG paper?

a) small squares.
b) large squares.

A

a) 0.04s.

b) 0.2s.

174
Q

How long should the QRS complex be?

A

Less than 120 ms.
Less than 3 little squares

175
Q

What do ECG leads measure?

A

The difference in electrical potential between two points

176
Q

In which lead are all waves negative?

A

aVR

177
Q

In which leads must the R wave grow?

A

From chest leads V1 to V4.

178
Q

In a normal ECG where should the P waves be upright?

A

In I, II, and V2 - V6

179
Q

What do the waves look like in lead aVR?

A

All waves are negative

180
Q

True or False: The QRS and T waves tend to have the same direction in the limb leads?

A

True

181
Q

What do the R and S waves looks like from V1 to V6

A

The R wave must grow from V1 to at least V4
The S wave must grow from V1 to at least V3 and disappear in V6

182
Q

What should the Q wave look like in leads I, II, V2 - V6?

A

There should be no Q wave or only a small q less than 0.04 seconds in width

183
Q

What should the ST segment look like?

A

The ST segment should start isoelectric except in V1 and V2 where it may be elevated

184
Q

Where should the T wave be upright?

A

The T wave must be upright in I, II, V2 - V6

185
Q

How would you be able to spot right atrial enlargement in an ecg? (P pulmonale)

A

Tall >2.5 mm, pointed P waves (best seen in lead II)

186
Q

How would you spot left atrial enlargement on an ecg? (P mitrale)

A

Notched/bifid (M shaped) P wave (P mitrale) in limb leads

187
Q

What condition might a short PR interval be indicative of?

A

Wolff-Parkinson White Syndrome
* Short PR interval (<120ms) - accessory pathway

ecg should show:
1) slurred delta waves
2) short PR interval
3) wide QRS

188
Q

What condition might a long PR interval be indicative of?

A

First degree heart block

189
Q

How to work out heart rate when rhythm is regular (from ECG)

A

Rule of 300
Count the number of “big boxes” between two QRS complexes.
300 divide by the number of big boxes

190
Q

ECG: what is the normal axis of the QRS complex?

A

-30° -> +90°

191
Q

How to work out heart rate when rhythm is irregular (from ECG)

A

ECGs record 10 seconds of rhythm per page. Count the number of beats present on the ECG and multiply by 6

192
Q

If the QRS axis is between -30° to -90° what does this person have?

A

Left axis deviation (LAD)

193
Q

What can cause a left axis deviation?

A

Left anterior fascicular block
Left bundle branch block
Left ventricular hypertrophy

194
Q

If the QRS axis is between +90° to +180° what does this person have?

A

Right axis deviation (RAD)

195
Q

What can cause a right axis deviation?

A

Left posterior fascicular block
Right heart hypertrophy/strain

196
Q

What method could you use to determine the QRS axis?

A

Quadrant approach:
- Look at the QRS complex of lead I (which is at 0°)
- Look at QRS complex of lead avF (which is at +90°)
- Determine if they are predominantly positive or negative
- The combination should then be placed it into a quadrant

Equiphasic approach:
- Locate a lead that has the smallest total QRS complex and/or is equiphasic. The QRS axis should be at 90 degrees to this lead.
- Now look at the lead that (on the vector diagram) is 90 degrees from the equiphasic lead.
- If this lead’s QRS complex is positive, the QRS axis is in the direction of that lead. If negative, the QRS axis is 180 degrees opposite.

197
Q

Name four things that hypertension is a major risk factor for.

A
  1. Stroke – ischaemic and haemorrhagic
  2. Myocardial infarction
  3. Heart failure
  4. Chronic renal disease
  5. Cognitive decline
  6. Premature death
198
Q

What is the clinical diagnosis of hypertension?

A

BP ≥ 140/90mmHg.

199
Q

What is the clinical diagnosis of stage 2 hypertension?

A

BP ≥ 160/100 mmHg.

200
Q

How can hypertension be treated?

A
  1. Lifestyle modification e.g. reduce salt intake.
  2. Anti-hypertensive drugs.
201
Q

Who would you offer antihypertensive drug treatments to in those with stage 1 hypertension?

A

People aged under 80 years with stage 1 hypertension who have one or more of the following:

  1. Target organ damage
  2. Established cardiovascular disease
  3. Renal disease
  4. Diabetes
  5. A 10-year cardiovascular risk of 20% or greater.
202
Q

Who would you offer antihypertensive drug treatments to in those with stage 2 hypertension?

A

Offer antihypertensive drug treatment to people of any age with stage 2 hypertension.

203
Q

Name 2 systems that are targeted pharmacologically in the treatment of hypertension.

A
  1. Renin-Angiotensin-Aldosterone system (RAAS)
  2. Sympathetic nervous system (noradrenaline)
204
Q

Three types of cardiomyopathy?

A

1) Hypertrophic
2) Restrictive
3) Dilated

205
Q

Causes of hypertrophic cardiomyopathy

A

Familial
- inherited mutation of sarcomere proteins
— troponin T and Myosin B

206
Q

Pathophysiology of of hypertrophic cardiomyopathy

A

Thick non compliant heart
= impaired diastolic filling
=> decrease in cardiac output

207
Q

Investigations to diagnose hypertrophic cardiomyopathy

A

Confirm with abnormal ECG
ECHO (diagnostic)
Genetic testing

208
Q

Cause of dilated cardiomyopathy

A

-Autosomal dominant familial inheritance (cytoskeleton gene mutation)
-IHD
-Alcohol

209
Q

Pathophysiology of dilated cardiomyopathy

A

Thin cardiac walls poorly contract leading to a decrease in CO
LV/RV or 4 chamber dilation and dysfunction

210
Q

Cause of arrhythmogenic hypertrophy

A

Desmosome gene mutations

211
Q

Pathophysiology of arrhythmogenic hypertrophy

A

Replacement of myocardium with fibro-fatty tissue leading to arrhythmia

212
Q

What is the cause of inherited arrhythmia? (Channelopothy)

A

Caused by ion channel protein gene mutations

213
Q

What is long QT syndrome?

A

Ventricular tachyarrhythmia

Typically an inherited congenital order where the mutation affects the cardia ion channels… and therefore heart conduction.

214
Q

What is Brugada syndrome?

A

A channelopathy caused by a mutation in sodium channels.

215
Q

Name 4 channelopathies.

A
  1. Long QT syndrome.2. Short QT syndrome.3. Brugada.4. CPVT.
216
Q

What is marfans syndrome?

A

Marfan syndrome is an autosomal dominant condition affecting the gene responsible for creating fibrillin
Fibrillin is an important component of connective tissue
This means people with Marfan syndrome have features resulting from abnormal connective tissue

217
Q

What are the symptoms of marfans syndrome?

A

1) “Marfans body habitus”:
- tall + thin
- long fingers (arachnodactyly)
- pectus excavatum/carinatum (sternum pressed in/puffed out)

2) Aortic complications:
- aortic regurgitation murmur
- AAA - aortic dissection

218
Q

What is Familial hypercholesterolaemia (FH)?

A

Inherited abnormality of cholesterol metabolism
Can lead to serious premature coronary and other vascular diseases

219
Q

When are ACE inhibitors used?

A
  • Hypertension
  • Heart failure
  • Diabetic nephropathy
220
Q

List 4 ACE inhibitor drugs

A

Ramipril
Perindopril
Enalapril
Trandolapril

221
Q

Adverse effects of ACE inhibitors

A

Due to reduced angiotensin II formation:
- hypotension
- acute renal failure
- hyperkalemia
- teratogenic effects in pregnancy

Due to increased kinins:
- cough
- rash
- anaphylactoid reactions

222
Q

When are ARBs used?

A
  • Hypertension
  • Diabetic nephropathy
  • Heart failure (when ACE-I contraindicated)
223
Q

Name 3 ARBs?

A
  1. Candesartan.
  2. Valsartan.
  3. Losartan.
  4. Telmisartan.
224
Q

Main side effects of ARBs?

A

Generally very well tolerated but can cause:
- Symptomatic hypotension
- Hyperkalaemia
- Potential for renal function
- Rash
- Angioedema

  • Contraindicated in pregnancy
225
Q

At which receptor do ARB’s work?

A

AT-1 receptor.

226
Q

When are calcium channel blockers used?

A
  • Hypertension
  • Ischaemic heart disease - angina
  • Arrrhythmia (tachycardia)
227
Q

Name 3 examples of Calcium Channel Blockers?

A

Amlodipine
Lacidipine
Nifedipine
Diltiazem
Verapamil
Felodipine

228
Q

Dihydropyridines CCBs?

A

Amlodipine
Nifedipine
Felodipine
Lacidipine

Preferentially affect vascular smooth muscle
= peripheral arterial vasodilators

229
Q

Phenylalkylamines CCBs?

A

Verapamil

Main effects on the heart
= negatively chronotropic and inotropic

230
Q

Benzothiazepines CCBs?

A

Diltiazem

= immediate heart/peripheral vascular effects

231
Q

Would you use Amlodipine for tachiarrythmia?

A

No. dihydropyridines are more suitable for treating hypertension while verapamil and diltiazem are more suitable as they affect the heart directly

232
Q

Main side effects of peripheral vasodilation? (CCBs) mainly dihydropyridines

A

Flushing
Headache
Oedema
Palpitations

233
Q

Main side effects due to negatively chronotropic effects? (CCBs) mainly verapamil/diltiazem

A

Bradycardia
Atrioventricular block

234
Q

Main side effects due to negatively ionotropic effects? (CCBs) mainly verapamil

A

Worsening of cardiac failure

235
Q

When are beta-adrenoceptor blockers used?

A

Ischameic heart disease - angina
Heart failure
Arrhythmia
Hypertension

236
Q

Examples of B1 selective beta-blockers?

A

Bisoprolol
Metoprolol

237
Q

An example of a less selective B1 beta-blocker

A

Atenolol

238
Q

B1/B2 (non-selective) Bb examples?

A

Propranolol
Nadolol
Carvedilol

239
Q

What percentage of beta adrenoreceptors in the heart are actually B1?

A

Only 60%
40% are B2
=hence you can’t use the term cardioselective to describe B1 selective beta blockers

240
Q

Main side effects of Bb?

A

Fatigue
Headache
Sleep disturbance/ nightmares

Bradycardia
Hypotension
Cold peripheries
Erectile dysfunction

Worsening of:
Asthma (may be severe) or COPD
Peripheral vascular disease - Claudification or Raynaud’s
Heart failure - if given in standard dose or acutely

241
Q

When would you use Diuretics?

A

Hypertension
Heart failure

242
Q

4 classes of diuretics?

A

1) thiazides and related drugs (distal tubule)
2) loop diuretics (loop of henle)
3) potassium-sparing diuretics
4) aldosterone antagonists

243
Q

Examples of thiazide and related diuretics?

A

Bendroflumethiazide
Hydrochlorothiazide
Chlorthalidone

244
Q

Examples of loop diuretics?

A

Furosemide
Bumetanide

245
Q

Examples of potassium-sparing diuretics

A

Spironolactone - (also an aldosterone antagonist)
Eplerenone
Amiloride
Triamterine

246
Q

Main side effects of loop diuretics

A

Hypovolemia
Hypotension

247
Q

General side effects of diuretics?

A

Hypokalemia
Hyponatremia
Hypomagnesaemia
Hypocalcemia

Hyperuricaemia- gout
Impaired glucose tolerance (mainly thiazides)

Erectile dysfunction (mainly thiazides)

248
Q

Other anti hypertensives?

A

A-1 adrenoceptor blockers
(Doxazosin)

Centrally acting anti-hypersensitive
(Moxonidine + methyldopa)

Direct renin inhibitor
(Aliskeren)

249
Q

Which drug is used as an antihypertensive for during pregnancy?

A

Methyldopa

250
Q

Treatment guidelines for hypertension if under 55 and diabetic?

A

ACE inhibitor or angiotensin II receptor Blocker

251
Q

Treatment guidelines for hypertension if over 55 years or Afro-Caribbean any age?

A

Calcium channel blockers
- People over 55 or Afro-Caribbean tend to have low renin hypertension, so hypertension not caused by RAAS system

252
Q

If first treatment steps using ACE-i/ARBs or CCBs not enough to control hypertension, what should step 2 be?

A

ACE-i/ARB + CCB or thiazide like diuretic

253
Q

If second treatment steps using ACE-i/ARB + CCB or thiazide like diuretic is still not enough to control hypertension what should you do next?

A

ACE-i/ARB + CCB + thiazide like diuretic

254
Q

If hypertension remains uncontrolled after step 3 treatment, what condition is the patient considered to have? And what treatment should be added?

A

Patient has resistant hypertension
- Consider addition of Spironolactone, alpha blocker, beta blocker, (others)

255
Q

What are the two types of heart failure?

A

Heart failure due to left ventricular systolic dysfunction - LVSD

Heart failure with preserved ejection fraction (diastolic failure) - HFPEF

This impaired left ventricular function results in a chronic back-pressure of blood trying to flow into and through the left side of the heart.

256
Q

What is heart failure caused by?

A

The commonest cause is myocardial dysfunction.
This usually results from IHD.
Other causes include:
- Hypertension,
- alcohol excess,
- cardiomyopathy,
- valvular,
- endocardial,
- pericardial causes.

257
Q

What type of chronic heart failure does most of the evidence for pharmacology come from?

A

LVSD (left ventricular systolic dysfunction))

258
Q

When treating heart failure, can you use LV stimulants to try and repair heart function?

A

No. Vasodilator therapy via neurohumoral blockade (RAAS - SNS) should be carried out since VL stimulants will only increase work of heart and oxygen requirements of heart.

259
Q

If ACE-i and ARB intolerant, what should you take for heart failure?

A

Hydralazine/nitrate combination

260
Q

Name 2 ARNIs - Aldosterone receptor antagonist and Neprilysin inhibitor

A

Sacubitril - neprilysin inhibitor
Valsartan - angiotensin II blocker

261
Q

How do ARNI’s work?

A

Neprilysin inhibition increases levels of natriuretic peptides in the heart. These will travel and act on kidneys causing sodium excretion along with water. They are also vasodilators and antagonists of angiotensin II.

262
Q

What are SGLT2 inhibitors?

A

sodium glucose transport 2 inhibitors
They are diabetic drugs that have been found to effectively treat heart failure.
Have mostly become standard treatment

263
Q

How would you treat chronic stable angina?

A
  1. Antiplatelet therapy
    - Aspirin
    - Clopidogrel if aspirin intolerant
  2. Lipid lowering therapy
    - Statins (simvastatin, atorvastatin, rosuvastatin, pravastatin)
  3. Short acting nitrate: GTN spray for acute attack
  4. First line treatment: beta blocker or calcium channel blocker

if intolerant switch
if not controlled combine

If still not controlled consider monotherapy or combinations with long acting nitrate, Ivabradine, Nicorandil, Ranolazine

264
Q

What medication to give to patients with NSTEMI and STEMI for pain relief

A

GTN spray and opiates - diamorphine

265
Q

What medication to give to patients with NSTEMI and STEMI for treatment?

A
  1. Dual antiplatelet therapy: aspirin + ticagrelor/prasugrel/clopidogrel
  2. Antithrombin therapy: Fondaparinux
  3. Consider Glycoprotein IIb IIa inhibitor (high risk cases): tirofiban, eptifibatide, abciximab
  4. Background angina therapy: beta blocker, long acting nitrate, calcium channel blocker
  5. Lipid lowering therapy: statins
  6. Therapy for LVSD/heart failure as required: ACE-i, beta blocker, aldosterone antagonist
266
Q

What to give to patients with arrhythmia?

A

Antiarrhythmic drugs:
Class I: sodium channel blockers Ia - disopyramide, Ib - lidocaine, Ic - flecainide

Class II: beta blockers - bisoprolol

Class III: prolong the action potential - amiodarone

Class IV: calcium channel blocker - verapamil

Digoxin: cardiac glycoside - inhibits Na/K pump

267
Q

Digoxin main effects on heart

A
  1. bradycardia
  2. slows atrioventricular conduction
  3. increased ectopic activity
  4. increased force of contraction
268
Q

Amiodarone adverse effects?

A

Prolongs QT
Polymorphic ventricular tachycardia

Interstitial pneumonitis
Abnormal liver function
Hyperthyroidism/Hypothyroidism
Sun sensitivity

Multiple drug interactions

269
Q

Main examples of nitrates

A

Isorbide mononitrate
GTN spray
GTN infusion

270
Q

Function of the pericardium

A

Restrains the volume of the heart
* Becomes rigid at higher stresses
* Pericardial sac has small reserve volume
* If volume exceeded pressure are transferred to cardiac chamber

271
Q

During normal inspiration, the systemic (left) systolic pressure lowers by less than 10 mmHg. Why?

A

Inspiration lower intrathoracic pressure allows more venous return to right heart
Pulmonary vessels usually compliant so increase blood volume held in these vessels
Reduced blood returned to the left heart = reduced LV preload = reduced cardiac output

272
Q

What is tamponade

A

Accumulation of a large vol of fluid in the pericardial space (pericardial effusion) that begins to impair ventricle filling

273
Q

What is acute pericarditis (Dressler syndrome)?

A

An inflammatory pericardial syndrome with or without effusion.

274
Q

How can acute pericarditis be clinically diagnosed?

A

Clinical diagnosis made with 2 from:
1. Chest pain.
2. Friction rub.
3. ECG changes.
4. Pericardial effusion.

275
Q

Aetiology of pericarditis

A

Infectious:
1. Viral (common): coxsackie virus, Enteroviruses, herpesviruses, adenoviruses, parvovirus B19.

  1. Bacterial: Mycobacterium tuberculosis (other bacterial rare).

Non-infectious:
1. Autoimmune (common): Sjogren syndrome, rheumatoid arthritis, scleroderma

  1. Neoplastic: secondary metastatic tumours (common above all lung and breast cancer, lymphoma)
  2. Metabolic: uraemia, myxoedema
  3. Traumatic and iatrogenic
276
Q

Clinical presentation of someone with pericarditis

A
  1. Chest pain
    * Severe
    * Sharp and pleuritic
    * Rapid onset
    * Left anterior chest or epigastrium
    * Radiates to arm
    * Relieved by sitting forward, exacerbated by lying down
  2. Other symptoms:
    * Dyspnoea
    * Cough
    * Hiccups
277
Q

Pericarditis: Clinical examination findings

A
  1. Pericardial rub - pathognomonic
  2. sinus tachycardia
  3. May have signs of right sided heart failure… constrictive pericarditis
278
Q

Investigations for pericarditis?

A

ECG
Bloods
CXR
Echocardiogram

279
Q

Pericarditis ECG

A

Widespread saddle shaped ST Elevation
PR depression

280
Q

Pericarditis Blood test

A

FBC
- modest increase in WCC

ESR & CRP
- High ESR
- ANA in young females

Troponin
- elevations suggest myopericarditis

CXR
- often normal in idiopathic
- pneumonia common with bacterial pericardial effusion
- modest enlargement of cardiac silhouette

281
Q

What are signs of tamponade?

A

Beck’s triad:
- hypotension (reduced cardiac output)
- raised JVP (heart failure)
- muffled heart sounds

Pulses paradoxes: systolic bp reduction of >10mmHg on inspiration

282
Q

Why does chronic pericardial effusion rarely cause tamponade?

A

The parietal pericardium is able to adapt when effusions accumulate slowly and so tamponade is prevented.

283
Q

Management of percarditis

A
  • Sedentary activity until resolution of symptoms and ECG/CRP
  • NSAID (Ibuprofen 600 mg TDS PO 2/52) or Aspirin (750-1000 mg BD PO 2/52)
  • Colchicine (0.5 mg BD PO 3/12) limited by nausea and diarrhoea, reduces recurrence
284
Q

Complications of pericarditis

A

1) Pericardial effusion—> cardiac tamponade
2) Myocarditis
3) Constrictive pericarditis

285
Q

What is Aortic Stenosis

A

Pathological narrowing or aortic valve -decrease in flow
Normal area 3-4cm
Symptoms occur when valve area is at 1/4 normal size

286
Q
A
287
Q

Types of aortic stenosis

A

Valvular (degenerative, rheumatic)
Supravalvular
Subvalvular

288
Q

Describe the aetiology of aortic stenosis.

A
  1. Acquired e.g. age related degenerative calcification (most common) and rheumatic heart disease.
  2. Congenital bicuspid valve.
289
Q

Pathophysiology of Aortic Stenosis

A
  • A pressure gradient develops between the left ventricle and the aorta. (increased afterload)
  • LV function initially maintained by compensatory pressure hypertrophy
  • When compensatory mechanisms exhausted, LV function declines.
290
Q

Give 3 symptoms of aortic stenosis.

A
  • Syncope: (exertional) 15%
  • Angina: (increased myocardial oxygen demand; demand/supply mismatch) 35%
  • Dyspnoea: on exertion due to heart failure (systolic and diastolic) 50%
  • Sudden death <2%
291
Q

Give 3 signs of aortic stenosis.

A

Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus)

Heart sounds - soft or absent second heart sound, S4 gallop due to LVH.

Ejection systolic murmur- crescendo-decrescendo character.

“Loudness” does NOT tell you anything about severity

292
Q

Investigation for aortic stenosis?

A

Echocardiography

Two measurements obtained are:
1. Left ventricular size and function: LVH, Dilation, and EF
2. Doppler derived gradient and valve area (AVA)

293
Q

How would you grade aortic stenosis?

A

Mild: Aortic valve area >1.5 cm^2
Moderate: AVA 1.0-1.5 cm^2
Severe: AVA <1.0 cm^2

294
Q

How would you manage aortic stenosis?

A

General:
Fastidious dental hygiene / care
Consider (infective endocarditis )IE prophylaxis in dental procedures

Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS

Aortic Valve Replacement:
Surgical
TAVI – Transcatheter Aortic Valve Implantation

295
Q

TAVI (transcutaneous aortic valve implant) how does it work

A
  • Pass a catheter from femoral artery to heart
  • Blow balloon across damaged valve to stent and relief the damaged valve
  • Placed across the damaged aortic valve transcatheter aortic valve that is left and acts like the aortic valve
296
Q

Indications for intervention for patients with aortic stenosis

A
  • Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
  • Any patient with decreasing ejection fraction
  • Any patient undergoing CABG with moderate or severe AS
  • Consider intervention if adverse features on exercise testing in asymptomatic patients with severe AS
297
Q

What is mitral regurgitation?

A

Backflow of blood from the LV to the LA during systole. It is caused by volume overload

Mild MR is seen in 80% of normal individuals

298
Q

What causes chronic mitral regurgitation?

A

Primary (disease of leaflets)
1. Myxomatous degeneration (MVP)
Ischemic MR
2. Rheumatic heart disease
3. Infective Endocarditis

Secondary (normal valve architecture but impaired closure due to abnormal LV/LA geometry)
1. Dilated cardiomyopathy

299
Q

Signs and symptoms of chronic mitral regurgitation

A

Auscultation: pansystolic murmur at the apex radiating to the axilla
* S3 (CHF/LA overload)
* In chronic MR, the intensity of the murmur does correlate with the severity.
* Displaced hyperdynamic apex beat

Exertion Dyspnoea: ( exercise intolerance)

Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

300
Q

Mitral regurgitation investigations

A

ECHO (most helpful): Estimation of LA, LV size and function. Valve structure assessment
TOE v helpful

ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR

CXR: LA enlargement, central pulmonary artery enlargement.

301
Q

Management of mitral regurgitation?

A

Medications
- Rate control for atrial fibrillation with -blockers, CCB, digoxin
- Anticoagulation in atrial fibrillation and flutter
- Nitrates / Diuretics in acute MR
- Chronic HF Rx if chronic MR with CCF
- No indication for ‘prophylactic’ vasodilators such as ACEI, hydralazine

If asymptomatic - no medication given

Serial Echocardiography:
Mild: 2-3 years
Moderate: 1-2 years
Severe: 6-12 months

IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

Surgical valve replacement

302
Q

Indications for surgery in those with mitral regurgitation?

A

severe MR
- ANY Symptoms at rest or exercise (repair if feasible)

Asymptomatic:
1. If EF <60%, LVESD >40mm
2. If new onset atrial fibrillation/raised PAP >50 mmHg

303
Q

What is aortic regurgitation?

A

Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps

304
Q

What can lead to chronic aortic regurgitation?

A

Bicuspid aortic valve
Rheumatic
Infective endocarditis

305
Q

Pathophysiology of aortic regurgitation

A

Combined pressure AND volume overload

Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

306
Q

Signs and symptoms of aortic regurgitation

A

Wide pulse pressure: most sensitive
Hyperdynamic and displaced apical impulse

Auscultation-
Diastolic blowing murmur at the left sternal border
Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
Systolic ejection murmur: due to increased flow across the aortic valve

307
Q

Investigations to diagnose aortic regurgitation

A
  • ECHO gold standard, evaluates aortic valve, root, dimensions
  • CXR
308
Q

Management for aortic regurgitation

A

Consider IE prophylaxysis (consider as differential diagnosis)

Medical: Vasodilators (ACEI’s potentially improve stroke volume and reduce regurgitation but indicated only in CCF or HTN

Serial Echocardiograms: to monitor progression.

Surgical valve replacement if symptoms

309
Q

Indications for Surgery for aortic valve replacement

A

ANY Symptoms at rest or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated > 50mm at end systole

310
Q

What is mitral stenosis?

A

Obstruction of LV inflow that prevents proper filling during diastole. Normal MV area: 4-6 cm^2. Symptoms begin at areas less than 2cm^

311
Q

What is the predominant cause of mitral stenosis?

A

Rheumatic carditis

312
Q

mitral stenosis pathophysiology

A

Progressive Dyspnea (70%): LA dilation -> pulmonary congestion (reduced emptying)
worse with exercise, fever, tachycardia, and pregnancy
Increased Transmitral

Pressures: Leads to left atrial enlargement and atrial fibrillation.

Right heart failure symptoms: due to Pulmonary venous HTN

Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

313
Q

Heart sounds in mitral stenosis

A

Diastolic murmur:
Low-pitched diastolic rumble most prominent at the apex.
Heard best with the patient lying on the left side in held expiration
Intensity of the diastolic murmur does not correlate with the severity of the stenosis

Loud Opening S1 snap: heard at the apex when leaflets are still mobile
Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips.
A shorter S2 to opening snap interval indicates more severe disease.

314
Q

signs and symptoms of mitral stenosis

A

prominent “a” wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy

Signs of right-sided heart failure: in advanced disease

Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks

315
Q

Evaluation of mitral stenosis

A

ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

ECG: may show atrial fibrillation and LA enlargement

CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV

316
Q

Management of mitral stenosis

A

Serial echocardiography:
Mild: 3-5 years
Moderate:1-2 years
Severe: yearly

Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression
beta blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
Duiretics for fluid overload

Identify patient early who might benefit from percutaneous mitral balloon valvotomy.

IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

317
Q

Indications for Mitral valve replacement in patients with mitral stenosis

A

ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms

Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV

318
Q

Eric attended surgery last month because he had been suffering from persistent headaches and fatigue for the previous three weeks. Your colleague found his blood pressure to be high and started him on Bendroflumethiazide. Eric is otherwise well apart from being overweight and requiring treatment (venlafaxine) for depression. He has attended for blood tests and is coming to see you to get the results which are normal apart from borderline low potassium.

What might be the cause of Eric’s high blood pressure?

A
  1. Him being overweight
  2. Venlafaxine - side effect

For the vast majority of patients no underlying cause is found
- early onset <30 years and no risk factors
- Hypertension resistant to 3 drugs
- Malignant hypertension
- Specific feature

319
Q

Eric attended surgery last month because he had been suffering from persistent headaches and fatigue for the previous three weeks. Your colleague found his blood pressure to be high and started him on Bendroflumethiazide. Eric is otherwise well apart from being overweight and requiring treatment (venlafaxine) for depression. He has attended for blood tests and is coming to see you to get the results which are normal apart from borderline low potassium.

In Eric’s case might the hypokalaemia give you a clue?

A

Spontaneous hypokalaemia or in response to thiazides might suggest hyperaldosteronism

320
Q

Patient Eric comes in and you measure his blood pressure and it’s again high at 215/115 mmHg but apparently he stopped his treatment after the tablets ran out. Given his particularly high blood pressure is there any specific part of Eric you want to examine?

A

His eyes!
Is this malignant hypertension
- High blood pressure (even at this level) is not an emergency unless
There is evidence of immediate damage
- Papilloedema
- Acute kidney injury
- Acute stroke
- Acute coronary syndrome
- Aortic dissection

321
Q

Examination including fundoscopy is normal so you start him on treatment with atenolol 50 mg od. A week later he noted some dizziness and so measured his own BP and found it to be only 148/64 mmHg. Is this the size of response you might expect from the full 50mg dose of atenolol?

A

BP response depends in part on starting pressure but in moderate expected reductions with full dose of any single drug are
- systolic 8-10 mmHg
- diastolic 4-6 mmHg

322
Q

Eric asks whether he might have “white coat” high blood pressure only when he sees the doctor. How might you investigate Eric’s home blood pressure further?

A
  • Clinic/surgery measures
  • Unattended automated office BP
  • Home self-assessment
  • Ambulatory blood pressure measurement
323
Q

Eric’s blood pressure was 150/101 mmHg. What threshold would you consider Eric needing drug treatment?

A

For patients:
at low CVD risk 160/100 mmHg
at high CVD risk 140/90 mmHg

324
Q

Eric is started on atenolol. At review his BP is lower at 138/92 mmHg but he complains that he is not feeling any better. Will blood pressure lowering drugs make Eric feel better?

A

Hypertension symptom relief:
By and large hypertension is symptom free
The only symptomatic benefit of treatment is a reduction in headache
- This is of importance if a patient has, or perceives that they have side-effects

325
Q

Eric is started on atenolol. At review his BP is lower at 138/92 mmHg how far do you want to lower Eric’s blood pressure?

A

Target (average clinic)
Routine - <140/90 mmHg
Previous stroke <130/80 mmHg
Heavy proteinuria <130/80 mmHg
CKD AND diabetes <130/80 mmHg
Older patients <150/90 mmHg

326
Q

What types of illness is high blood pressure likely to cause?

A
  1. stroke
  2. dementia
  3. myocardial infarction
  4. heart failure
  5. renal failure
  6. peripheral vascular disease
327
Q

On average how much might high blood pressure shorten someone’s life?

A

With untreated hypertension

50 year old male
- 5 years loss of life
- 7 years loss of disease free life

50 year old female
- 5 years of loss of life
- 6.5 years loss of disease free life

328
Q

Are there any changes in lifestyle by which Eric might lower his blood pressure without drug treatment?

A

Weight loss
Salt restriction
Exercise
Alcohol

329
Q

Are there any circumstances in which blood pressure lowering should be withheld?

A

During general anaesthetic hypotension can be a problem and some antihypertensives block attempts to increase BP
ACE inhibitors and ARBs temporarily stopped

330
Q

Most common congenital cyanotic heart disease

A

Tetralogy of Fallot
10% of all congenital birth defects

331
Q

What is tetralogy of fallot

A

Cyanotic!
Ventricular septal defect with right ventricular outflow obstruction
- therefore O2 deficient blood is systemically shunted
= blue blood passes from RV to LV

332
Q

Most common congenital heart defect?

A

Bicuspid aortic valve
1-2% of the population
M>F

333
Q

Pathology of tetralogy of fallot?

A
  1. Ventricular Septal Defect
    Overriding aorta (over the top of VSD)
  2. Right ventricular hypertrophy
  3. Right ventricular outflow obstruction (due to pulmonary stenosis)
334
Q

Treatment of tetralogy of fallot

A

Full surgical repair within 2y of life and good prognosis if done
Normally at 3-6months👩🏻‍🍼

335
Q

What is ventricular septal defect?

A

Abnormal connection between the two ventricles

336
Q

How common is ventricular septal defect?

A

Common – 20% of all congenital heart
Many close spontaneously during childhood

337
Q

Physiology of ventricular septal defect?

A

L->R non cyanotic shunt (not blue)
Blood flows from high pressure to low pressure chamber
Increased blood flow through the lungs (more in larger defects)
Risk of Eisenmengers syndrome and RVH later

338
Q

What is Eisenmenger syndrome?

A

High pressure pulmonary flow
Damages to delicate pulmonary vasculature
The resistance to blood flow through lungs increases
RV pressure increases
Shunt direction reverses
Patient becomes BLUE

339
Q

How would you treat ventricular septal defect?

A

Large:
Requires fixing in infancy PA band, complete repair

Small:
No intervention needed

340
Q

What is atrial septal defect?

A

Abnormal connection between the two atria (primum, secundum, sinus venosus)
Common
Often present in adulthood

341
Q

Pathophysiology of atrial septal defect

A

Slightly higher pressure in the LA than the RA
Shunt is left to right
Therefore NOT blue
Increased flow into right heart and lungs

342
Q

Clinical signs of atrial septal defects

A

Pulmonary flow murmur
Fixed split second heart sound (delayed closure of PV because more blood has to get out)
Big pulmonary arteries on CXR
Big heart on chest X ray

343
Q

How can you close atrial septal defects?

A

Surgical
Percutaneous (key hole technique)

344
Q

What condition is atrioventricular septal defects linked to commonly?

A

Often linked with trisomy 21 Downs syndrome

345
Q

What part of the heart does the atrioventricular septal defect involve?

A

Involves the ventricular septum, the atrial septum, the mitral and tricuspid valves. Can be complete or partial

346
Q

What do atrioventricular valves in atrioventricular septal defect look like?

A

Instead of two separate AV valves there is one big malformed one. It usually leaks to a greater or lesser degree

347
Q

What is patent ductus arteriosus?

A

When ductus arteriosus fails to close post birth = unusual

348
Q

What is the pathology of patent ductus arteriosus?

A

Ductus arteriosus (shunt between pulmonary artery and aorta) remains patent, rather than turning into ligamentum arteriosum
This causes blood to shunt from the aorta → pulmonary trunk…
Risk of pulmonary overload and eisenmenger syndrome

349
Q

What is coarctation of the aorta?

A

Narrowing of the aorta at the site of insertion of the ductus arteriosus

350
Q

Treatment of coarction of aorta

A

Surgical - Subclavian flap repair or end to end repair
Percutaneous repair - stenting even when mild to prevent long term problems

351
Q

Coarctation of aorta – clinical signs

A

Right arm hypertension
Bruits (buzzes) over the scapulae and back from collateral vessels
Murmur

352
Q

Coarctation of aorta - long term problems

A

Hypertension
Early coronary artery disease
Early strokes
Sub arachnoid haemorrhage
Re-coarctation requiring repeat intervention
Aneurysm formation at the site of repair

353
Q

Is the aortic valve bicuspid or tricuspid?

A

Typically tricuspid
1-2% of population have bicuspid

354
Q

What are the problems with having bicuspid aortic valves over tricuspid?

A

Degenerate quicker than normal valves
Can be severely stenotic in infancy or childhood
Become regurgitant earlier than normal valves
60% lifetime chance of need for surgery

355
Q

What is a pulmonary stenosis?

A

Narrowing of the outflow of the right ventricle
can occur in different locations:
- Valvar
- Sub valvar
- Supra valvar
- in branches

356
Q

Severe pulmonary stenosis?

A

-Right ventricular failure as a neonate
-Collapse
-Poor pulmonary blood flow
-RV hypertrophy
-Tricuspid regurgitation

357
Q

Moderate/mild pulmonary stenosis?

A

-well tolerated for many years
-right ventricular hypertrophy

358
Q

Treatment of pulmonary stenosis

A

Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass the blockage)

359
Q

What procedure is conducted in univentricular hearts (for hearts with only one usable ventricle)?

A

Fontan procedure.
1. Passive connection of great veins to the pulmonary artery

360
Q

What is infective endocarditis?

A

Treatment
Balloon valvuloplasty
Open valvotomy
Open trans-annular patch
Shunt (to bypass the blockage)

361
Q

Treatment of infective endocarditis

A
  1. Mainstay is antibiotics/antimicrobials
  2. May require cardiac surgery to remove the infectious material and/or repair the damage
  3. Treatment of other complications (emboli, arrythmia, heart failure, etc)
362
Q

Types of infective endocarditis

A

Each type can have different presentations, pathogens and outcomes
1. Left sided native IE (mitral or aortic)
2. Left sided prosthetic IE
3. Right sided IE (rarely prosthetic as rare to have PV or TV replaced)
4. Device related IE (pacemakers, defibrillators, with or without valve IE
5. Prosthetic; can be Early (within year) or Late (after a year) post op

363
Q

How do you catch infective endocarditis?

A
  • Have an abnormal valve; regurgitant or prosthetic valves are most likely to get infected.
  • Introduce infectious material into the blood stream or directly onto the heart during surgery
  • Have had IE previously
364
Q

Epidemiology of endocarditis: Who is more likely to have endocarditis?

A

Used to be a disease of the young affected by rheumatic heart disease.

Now it is a disease of:
- the elderly (in an ageing population)
- the young i.v. drug abusers
- the young with congenital heart disease.
- Anyone with prosthetic heart valves

365
Q

How does endocarditis present?

A

Anything at all!
- Depends on site, organism etc
- Signs of systemic infection (fever, sweats, etc)
- Embolisation: stroke, pulmonary embolus, bone infections, kidney dysfunction, myocardial infarction
- Valve dysfunction; heart failure, arrythmia

366
Q

What is the modified Duke Criteria

A

Criteria for diagnosis of infective endocarditis

Requires 2 major criteria, or 1 major and 3 minor, or 5 minor

367
Q

Major Duke Criteria for infective endocarditis

A
  • Pathogen grown from blood cultures
  • evidence of endocarditis on echo, or new valve leak
368
Q

Minor Duke criteria for infective endocarditis

A

Predisposing factors
Fever
Vascular phenomena
Immune phenomena
Equivocal blood cultures

369
Q

Primary investigation for diagnosis of infective endocarditis

A

Echocardiography : TOE more invasive than TTE but much more sensitive and specific = gold standard

Inflammatory markers (CRP) - eg raised ESR\CRP + neutrophillia

-ECG (prolonged PR interval=aortic root abscess)

-Blood cultures - 3 sets in 24 hours BEFORE ANTIBIOTICS

370
Q

Signs of infective endocarditis

A

1) Osler nodes (painful nodules on fingers\toes)
2) Janeway lesions (painless placques on palms and soles)
3) splinter haemmorrhages (red plum lines under nails)
4) Roth’s spots: white centred retinal haemorrhages

heart murmer +- signs of heart failure

371
Q

What is the most common cause for negative blood cultures in patients with infective endocarditis?

A

prior antimicrobial therapy

372
Q

First line treatment for infective endocarditis

A

Antimicrobials: IV for around 6 weeks with choice of agents based on culture sensitivities

Treat complications; arrhythmia, heart failure, heart block, embolisation, stroke rehab, abscess drainage etc

373
Q

Second line treatment for infective endocarditis

A

Surgery: aim to remove infected tissue and repair it replace affected valves

374
Q

When would you operate in someone with infective endocarditis?

A
  1. the infection cannot be cured with antibiotics (ie recurs after treatment, or CRP doesn’t fall)
  2. complications (aortic root abscess, severe valve damage
    to remove infected devices (always needed)
  3. to replace valve after infection cured (may be weeks/months/years later
  4. To remove large vegetations before they embolise
375
Q

How to prevent infective endocarditis?

A

For years, patients with valve disease were given antibiotic prophylaxis during interventions (esp dental)

NICE guidance in 2008 recommended not to give prophylaxis to anyone (and remains current)

ESC guidance is to consider prophylaxis in high risk patients (prosthetic valves, previous IE, cyanotic heart disease)

Talk to the patient and the dentist!

376
Q

Low amplitude p wave possible causes?

A

Atrial fibrosis, obesity, hyperkalaemia

377
Q

High amplitude ‘Tall’ P wave causes?

A

Right atrial enlargement

378
Q

Broad notched ‘Bifid’ P wave causes?

A

Left atrial enlargement

379
Q

Broad QRS causes?

A

Ventricular conduction delay / bundle branch block
Pre-excitation

380
Q

Small QRS complexes causes?

A

Obese patient
Pericardial effusion
Infiltrative cardiac disease

381
Q

Tall QRS complexes causes?

A

Left ventricular hypertrophy
(S wave in V1 and R wave in V5/V6 >35mm)
Thin patient

382
Q

T wave inversion causes?

A

T wave changes (inversion) are non-specific but can indicate:
Ischaemia/infarction
Myocardial strain (hypertrophy)
Myocardial disease (cardiomyopathy)

383
Q

Give 3 causes of long QT syndrome.

A

Congenital.
Electrolyte disturbances e.g. hypokalaemia and hypocalcaemia.
A variety of drugs.

384
Q

Give 2 signs of long QT syndrome.

A
  1. Palpitations.
  2. Syncope.
385
Q

Give 4 causes of sinus bradycardia.

A

Ischaemia.
Fibrosis of the atrium.
Inflammation.
Drugs.

386
Q

Give 3 causes of heart block.

A

CAD.
Cardiomyopathy.
Fibrosis.

387
Q

What kind of heart block is associated with wide QRS complexes with an abnormal pattern?

A

RBBB or LBBB.

388
Q

Describe first degree AV block.

A

Fixed prolongation of the PR interval due to delayed conduction to the ventricles.

389
Q

Describe second degree AV block.

A

There are more P waves to QRS complexes because some atrial impulses fail to reach the ventricles and so you don’t get a QRS complex.

390
Q

Types of second degree AV block: describe Mobitz type 1.

A

PR interval gradually increases until AV node fails and no QRS is seen.

391
Q

Types of second degree AV block: describe Mobitz type 2.

A

There is a sudden unpredictable loss of AV conduction and so loss of QRS. PR interval is constant but every nth QRS complex is missing.

392
Q

Describe third degree AV block.

A

Atrial activity fails to conduct to the ventricles. P waves and QRS complexes therefore occur independently.

393
Q

LBBB: what would you see in lead V1 and V6?

A

A ‘W’ shape would be seen in the QRS complex of lead V1 and a ‘M’ shape in V6.

WiLLiaM.

394
Q

RBBB: what would you see in lead V1 and V6?

A

A ‘M’ shape would be seen in the QRS complex of lead V1 and a ‘W’ shape in V6.

MaRRoW.

395
Q

50 y man presents with 2 hours of central crushing chest pain, sweaty, nauseated
He has a past history of hypertension and smokes 20/d

What might the patient have?

A

Myocardial infarction

396
Q

A 20y female presents with a history of sharp central chest pain, worse on inspiration and worse on lying flat
She is otherwise fit and well but has had a recent bad cold.

What might she have?

A

Pericarditis

397
Q

What might the ECG look like in someone with acute pericarditis?

A
  1. PR depression seen in most leads.
  2. ‘Saddle shaped’ concave ST elevation.
398
Q

50y man
No prior medical history

Palpitations
Missed beat
‘Thud’ or strong beat

Brief racing/fluttering

What might the patient have?

A

Ectopic beats

399
Q

What are ectopic beats?

A

Very common, generally benign arrhythmias caused by premature discharge. The patient may complain of symptoms of ‘skipped beats’.

400
Q

In what situation would you refer a patient with ectopic beats?

A

Who to refer
High burden ectopy (>5%, though risk prob not increased till >20%)
Refractory to BB
Structural heart disease
Syncope

401
Q

A patient comes in complaining of breathlessness and palpitations. What is the most likely diagnosis?

A

Atrial fibrillation!
Commonest sustained arrhythmia

402
Q

26y female PMH of ‘anxiety’
Recurrent episodes of heart racing
Sudden onset
Breathless/panicky

Upon doing an ECG her heart rate was 150 bpm
There were no P waves and she had narrow QRS complexes.

What might she have?

A

Supraventricular tachycardia

403
Q

16y male
Came to UK 3 y ago.
Told he had abnormal ECG in childhood, no further details

Complains of heart racing intermittently, sudden onset for up to an hour

Upon doing an ECG he had no clear PR interval and slurred delta waves.

What might he have?

A

Accessory pathway arrhythmia - Wolff-Parkinson White Syndrome

404
Q

93 year old female

Recently admitted with fall and fracture NOF

On further questioning has been feeling intermittently dizzy while seated

Upon doing an ECG she was shown to have a slow heart rate and a RBBB

How would you treat her?

A

Pacemaker

405
Q

66y male
PMH: type 2 DM

1 hour history of sweating and breathlessness, also felt dizzy. Called ambulance and then blacked out briefly.

ECG showed a slow heart rate 30 bpm and ST elevation in leads II, III and avF. How might you treat him?

A

Pacemaker
More importantly - ST elevation -> Myocardial infarction -> emergency coronary angiography

406
Q

33y female
Recent long haul flight from SE asia

Breathless with sharp right sided chest pain, haemoptysis

ECG shows that she has a sinus tachycardia, T wave inversion in the right ventricle
What might she have?

A

Pulmonary embolism

407
Q

Main phenotypes of heart failure

A

HF with reduced ejection fraction (HFrEF)
HF with preserved ejection fraction (HFpEF)

HF due to severe valvular heart disease (HF-VHD)
HF with pulmonary hypertension (HF-PH)
HF due to right ventricular systolic dysfunction (HF-RVSD)

408
Q

What are the symptoms of heart failure?

A

Breathlessness
Tiredness
Cold peripheries
Leg swelling
Increased weight

409
Q

What are the signs of heart failure?

A

Tachycardia
Displaced apex beat
Raised JVP
Added heart sounds and murmurs
Hepatomegaly, especially if pulsatile and tender
Peripheral and sacral oedema
Ascites

410
Q

How would you treat heart failure?

A

ABAL

  • ACE inhibitor (e.g. ramipril)
  • Beta Blocker (e.g. bisoprolol)
  • Aldosterone antagonist when symptoms not controlled with A and B (spironolactone or eplerenone)
  • Loop diuretics improves symptoms (e.g. furosemide 40mg once daily)

Consider ARNI and SGLT2 inhibitors

411
Q

Use of ACE-i therapy in black as compared with white patients with heart failure?

A

T2DM takes precedence and they should take ACEi
BUT ARBs are preferred for black patients so that might be preferable

412
Q

Do beta blockers work better in black or white patients?

A

No differences with beta blockers

413
Q

What is ivabradine?

A

Blocker of the If current in the SA node
Slows the sinus node rate
Agent for treating angina
Found to effectively treat heart failure

414
Q

What could you give someone with dyssynchronous heart failure?

A

CRT devices

415
Q

What can be used to treat HFpEF?

A

SGLT2 inhibitors

416
Q

What is atypical MI?

A

When they have all the risk factors that point towards an MI, but they don’t have the symptoms ie central crushing pain.

2A (7 decks)

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