Cardiology Flashcards

1
Q

central, pleuritic chest pain and fever 4 weeks following a myocardial infarction suggests what?

A

Dresslers - Pericarditis following MI

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2
Q

traumatic accident with respiratory distress, hypotension, jugular venous distension, and absent lung sounds suggests what?

A

Tension pneumothorax

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3
Q

A third heart sound is considered normal
in patients under what age?

A

<30 years old

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4
Q

What are the common causative organisms of infective endocarditis?

A

Most common/IVDU - Staph aureus
Those with poor dental hygiene/post dental proceudure - Strep viridans
Following prosthetic valve surgery - Staph epidermidis

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5
Q

Widened mediastinum on CXR with severe chest pain suggests what?

A

Aortic dissection

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6
Q

In ALS, if IV drugs cannot be given, how should they be given?

A

Intraosseous

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7
Q

What is the most specific ECG finding in acute pericarditis?

A

PR depression

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8
Q

Type A (ascending) vs Type B (descending) aortic dissection?

A

A - chest pain
B - upper back pain

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9
Q

tall R waves in leads V1-3 are a classic finding for what?

A

Posterior MI

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10
Q

What score should be used to assess the risk of bleeding when starting someone on anticoagulation in AF?

A

Orbit

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11
Q

What are reversible causes of cardiac arrest?

A

Hypoxia
Hypovolaemia
Hyperkalaemia, hypokalaemia, hypoglycaemia, hypocalcaemia, acidaemia and other metabolic disorders
Hypothermia
Thrombosis (coronary or pulmonary)
Tension pneumothorax
Tamponade – cardiac
Toxins

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12
Q

When should warfarin be stopped prior to surgery?

A

5 days before

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13
Q

What is the key diagnostic finding of aortic dissection on CT?

A

False lumen

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14
Q

What are C/I to thrombolysis?

A

active internal bleeding
recent haemorrhage, trauma or surgery (including dental extraction)
coagulation and bleeding disorders
intracranial neoplasm
stroke < 3 months
aortic dissection
recent head injury
severe hypertension

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15
Q

weak or absent carotid, brachial, or femoral pulse
variation in arm BP suggests what?

A

Aortic dissection

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16
Q

When can electrical cardioversion be considered for patients with AF?

A

If presenting within 48 hours

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17
Q

What medication should be stopped when patients are given a course of macrolides e.g. clarithromycin?

A

Statins

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18
Q

Thiazide-like diuretics should not be used in patients with what?

A

Gout

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19
Q

ST elevation and acute pulmonary oedema in a young patient with a recent flu-like illness suggests what?

A

Myocarditis

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20
Q

When should rhythm control be used for AF instead of rate control?

A

coexistent heart failure, first onset AF or an obvious reversible cause

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21
Q

Which medication can reduce hypoglycaemia awareness?

A

Beta blockers

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22
Q

Which medication can impair glucose tolerance?

A

Thiazides

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23
Q

Widespread ST elevation in V1-4 suggests what?

A

100% occlusion of the LAD

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24
Q

Erythromycin can cause which cardiac abnormality?

A

QT prolongation

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25
Q

What kind of bacteria is staph aureus?

A

Gram positive cocci

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26
Q

How should a patient with minor bleeding with INR > 8 be managed?

A

Stop warfarin and give IV Vitamin K with repeat dose of Vit K after 24 hours if INR still high

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27
Q

What drugs can cause hypokalaemia?

A

Loop diuretics e.g. furosemide

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28
Q

A new left bundle branch block should raise alarms for what?

A

ACS

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29
Q

What scoring system should be used to identify patients with a pulmonary embolism that can be managed as outpatients?

A

Pulmonary Embolism Severity Index (PESI)

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30
Q

How does fondaparinux work?

A

Activates antithrombin III

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31
Q

What is the management of AF if ChadsVasc is 0?

A

Echo to rule out valvular causes

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32
Q

What are ecg findings of hypokalaemia?

A

small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
U waves

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33
Q

What is the second-line therapy in patients with HFrEF?

A

SGLT-2 inhibitors e.g Empagliflozin

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34
Q

inferior myocardial infarction and AR murmur suggests what?

A

Proximal aortic dissection

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35
Q

High dose statins should be commenced in stroke patients when?

A

48 hours after stroke

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36
Q

What criteria should be used for infective endocarditis?

A

Duke criteria

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37
Q

What criteria should be used for rheumatic fever?

A

Jones criteria

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38
Q

What drugs should be used for anticoagulation in those with mechanical heart valves?

A

Warfarin/LMWH

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39
Q

Complete heart block following an MI suggests the lesion is where?

A

Right coronary

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40
Q

Investigation of choice for aortic dissection?

A

CT Angio

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41
Q

Management of aortic dissection

A

Control BP with IV Labetalol and surgery

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42
Q

Most common ECG change of PE?

A

Sinus tachycardia

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43
Q

CP of pericarditis?

A
  • pleuritic chest pain: worsen lying flat and relieved by sitting forward
  • fever
  • pericardial rub
  • tachycardia and tachypnea
  • non-productive cough
  • dyspnoea
  • flu-like symptoms
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44
Q

What may a pericardial rub indicate? (friction of heart against pericardium, sounds like sandpaper rubbed on wood)

A

pericarditis

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45
Q

Ix for pericarditis?

A
  • all pts with suspected= TRANSTHORACIC ECHO
  • ECG
  • bloods: inflam markers, only 30% have elevated troponin
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46
Q

Pericarditis is associated with what?

A

pericardial effusion that can sometimes worsen to cardiac tamponade

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46
Q

ECG findings for pericarditis?

A
  • PR depression
  • ‘saddle-shaped’ ST elevation

PeRicardiTiS

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47
Q

Management of pericarditis?

A

NSAIDs plus colchicine

Until CP resolution and normal inflam markers (usually 1-2w) followed by tapering of dose recommended

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48
Q

PR Depression on ECG is indicative of what?

A

Pericarditis

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49
Q

Medical management of NSTEMI?

A

dual antiplatelet therapy, an ace inhibitor, a beta-blocker, and a statin

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50
Q

What is Beck’s triad?

A
  • Raised JVP
  • Muffled heart sounds
  • Falling BP
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51
Q

What is Beck’s triad a sign of?

A

Cardiac tamponade

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52
Q

Management of major bleed with someone on warfarin?

A

stop warfarin, give intravenous vitamin K 5mg, prothrombin complex concentrate

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53
Q

How should episodic palpitations be investigated?

A

Holter monitoring

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54
Q

notching of the inferior border of the ribs suggests what?

A

Aortic coarctation

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55
Q

Management of PE with low PESI score?

A

Can be managed as an outpatient with DOAC

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56
Q

Nitrates for MI are contraindicated when?

A

Patients with hypotension

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57
Q

What is the treatment for torsades de pointes?

A

IV Mag Sulph

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58
Q

What is a normal cardiac variant in athletes?

A

First degree heart block

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59
Q

Investigation of choice for someone with PE and renal impairment?

A

V/Q scan

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60
Q

What is normal in an athlete and does not require any intervention?

A

First degree heart block

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61
Q

If angina is not controlled by a beta blocker, what should be added?

A

Amlodipine

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62
Q

What should be used if atropine if not helping with bradycardia?

A
  • transcutaenous pacing
  • transvenous pacing
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63
Q

Sydenham’s chorea is a complication of what?

A

Rheumatic fever

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64
Q

Management of persistent myocardial ischaemia following fibrinolysis

A

PCI even if time elapsed

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65
Q

What on echo is used to determine the severity of aortic stenosis?

A

Trans-valvular pressure gradient

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66
Q

What is Buerger’s disease?

A

aka thromboangiitis obliterans

  • A small/medium vasculitis which is associated with smoking
  • CP: intermittent claudication, Raynaud’s, ischaemic ulcers, superficial thrombophelbitis
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67
Q

What is the mode of action of statins?

A

Decrease intrinsic cholesterol synthesis by inhibiting HMG-CoA reductase enzyme

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68
Q

How to manage a strong suspicion of PE whilst waiting for scan?

A

Start treatment dose anticoagulant

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69
Q

Electrical alternans is a sign of what?

A

Cardiac tamponade

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70
Q

J waves are associated with what?

A

Hypothermia

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71
Q

Hypertrophic obstructive cardiomyopathy is associated with what?

A

Wolf-Parkinson-White

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72
Q

Management of acute heart failure not responding to furosemide?

A

Consider CPAP

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73
Q

What is a complication of MI?

A

Pulmonary oedema

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74
Q

SVT Management?

A
  1. Valsalva
  2. IV Adenosine upto 3 doses
  3. Electrical cardioversion
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75
Q

Criteria for rate control vs anticoag/cardioversion?

A
  • Under 65
  • No Hx of IHD
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76
Q

Thrombus in aVL, which artery?

A

Left circumflex

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77
Q

What is Framingham risk score?

A

estimate the 10-year risk of heart attack

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78
Q

severe hypertension and bilateral retinal hemorrhages and exudates

A

Malignant HTN

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79
Q

Endocarditis - which valves are affected?

A

Mitral - most common
Aortic
Tricuspid - IVDU

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80
Q

A patient develops acute heart failure 5 days after a myocardial infarction. A new pan-systolic murmur is noted on examination

A

VSD

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81
Q

Treatment for cardiac tamponade?

A

Urgent pericardiocentesis: Pericardial needle aspiration

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82
Q

What is Kussmaul sign?

A
  • JVP rises on inspiration
  • Sign of constrictive pericarditis
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83
Q

holosystolic murmur, high-pitched and ‘blowing’ in character

A

Mitral regurg

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84
Q

Tachycardia and tachypnoea with no signs

A

Think PE

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85
Q

Can warfarin be used when breast feeding?

A

Yes

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86
Q

What electrolyte abnormality do thiazide diuretics cause?

A
  • Hypokalaemia
  • Hyponatraemia
  • Hypercalcaemia
  • Gout
  • Impaired glucose tolerance
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87
Q

Management of irregular broad complex tachycardia

A

Seek cardiology input

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88
Q

What is Takayasu’s arteritis?

A
  • Systemic features of vasculitis
  • Unequal BP in upper limbs
  • Carotid tenderness
  • Absent/weak peripheral pulses
  • Associated with renal artery stenosis
  • MRA/CTA to treat with steroids
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89
Q

Low pitched diastolic murmur?

A

Mitral stenosis

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90
Q

Acute mitral valve regurg + pulmonary oedema

A

Think MI

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91
Q

What is the dose of adrenaline used in cardiac arrest?

A

1mg of IV adrenaline

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92
Q

Breathing problems with clear chest

A

PE

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93
Q

What is Brugada syndrome?

A
  • AD disorder which can cause sudden death
  • autosomal dominant; more common in Asians
  • can be caused by mutation in SCN5A gene (encodes for myocardial sodium ion channel protein)
  • ECG shows ST elevation and T wave inversion (may become clearer after giving flecainide- Ix of choice)
  • Mx is implantable cardioverter-defib
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94
Q

Most common place of inhaled foreign body?

A

Right inferior bronchus

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95
Q

Findings for aortic stenosis?

A

narrow pulse pressure
slow rising pulse
a thrill palpable over the cardiac apex
a fourth heart sound (S4) indicative of left ventricular hypertrophy
a soft/absent S2

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96
Q

Which medications can cause torsades de pointes?

A

Macrolides e.g. azithromycin

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97
Q

What condition are ACE inhibitors C/I with?

A

Renovascular disease

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98
Q

What causes the acute mitral regurg following MI?

A

Rupture of the papillary muscle/ischaemia

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99
Q

When can you commence spironolactone for HTN?

A

When already taking ACE, CCB and thiazide-like diuretic + K is below 4.5

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100
Q

When should adrenaline be given for shockable rhythms?

A

After 3 unsuccessful shocks

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101
Q

Pericarditis vs Myocarditis?

A

Myocarditis -> elevated troponin

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102
Q

Which markers can you test for STEMI?

A

Troponin, CK, AST, LDH

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103
Q

What ECG changes might be seen following STEMI?

A

T wave inversion, pathological Q waves

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104
Q

Driving rules post MI

A
  • No need to inform DVLA
  • Can drive after1 week if successful angioplasty
  • Can drive after 4 weeks if no angio/unsuccessful angio
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105
Q

Complication of coronary angio

A

Bleeding, haemorrhage, infection, MI, stroke, damage to coronary vessels, death

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106
Q

What triggers are there for angina?

A

Exertion, cold weather, emotions such as anger, vivid dreams

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107
Q

How does aspirin work?

A

Inhibits COX which inhibit thromboxane which inhibits platelets aggregation

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108
Q

Abnormally large drop in BP during inspiration?

A

Pulsus paradoxus -> Cardiac tamponade

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109
Q

How should diabetes be managed following MI?

A

Use IV insulin infusion and stop the oral diabetes meds

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110
Q

patients with a GRACE score > 3% should have what?

A

Coronary angio within 72 hours

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111
Q

Management of persistent MI following fibrinolysis

A

PCI

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112
Q

What is the treatment of broad complex tachycardias?

A
  • Amiodarone
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113
Q

Single episode of paroxysmal AF?

A

ChadsVasc and consider DOAC

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114
Q

Management of IE causing congestive cardiac failure

A

Emergency valve replacement

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115
Q

What is the alternative to 3 weeks of anticoagulation for someone having cardioversion with AF?

A

Transoeseophageal echo to exclude left atrial appendage thrombus

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116
Q

What are warfarin INR targets for mechanical valves?

A

Aortic - 3.0
Mitral - 3.5

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117
Q

What is the NYHA heart failure classification?

A

Class 1 - no symptoms and no limitations
Class 2 - mild symptoms with slight limitation (some fatigue, dyspnoea)
Class 3 - moderate symptoms with marked reduction in activity (symptoms anytime except rest)
Class 4 - severe symptoms and symptoms of HF present even at rest

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118
Q

When is AAA screening done?

A

Men aged 65

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119
Q

How is AAA screening managed?

A

< 3 cm - normal
3 - 4.44cm - rescan every 12 months
4.45 - 5.4cm - rescan every 3 months
>5.5 - refer to vascular surgery within 2 weeks

Other referral criteria
- Rapidly growing (>1cm per year)

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120
Q

What is the biggest indicator of a poor prognosis in someone with MI?

A

Cardiogenic shock

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121
Q

What would an ABG for pulmonary embolism show?

A

Respiratory alkalosis -> hyperventilation

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122
Q

When is staph epidermidis the most common organism causing endocarditis?

A

If <2 months post valve surgery

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123
Q

Why is verapamil C/I in heart failure + VT?

A

It can slow down contractility of the heart even further

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124
Q

What is the most common cause of death in patients post MI?

A

V Fib

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125
Q

Haemoptysis can be a symptom of what?

A

Mitral stenosis

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126
Q

mid-diastolic low-pitched rumbling murmur

A

mitral stenosis

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127
Q

Management of BP > 180/120 in GP

A

If unstable/signs of papilloedema/retinal haemorrhages -> refer to specialist
If stable then arrange urgent investigations for organ damage eg. bloods, urine ACR, ECG

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128
Q

What is the normal QRS value?

A

<0.12s / 3 small squares

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129
Q

What are signs of left ventricular failure?

A

Dyspnoea, reduced exercise tolerance, fatigue, paroxysmal nocturnal dyspnoea, orthopnoea, wheeze, cough (worse at night), pink, frothy sputum

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130
Q

What are signs of right ventricular failure?

A

Peripheral oedema, facial engorgement and abdominal distension

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131
Q

What are causes of AF?

A

Pneumonia, MI, PE, Alcohol excess, HF, Endocarditis

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132
Q

What are signs of aortic regurg?

A
  • Collapsing pulse
  • Early diastolic murmur
  • Wide pulse pressure
  • Displaced apex
  • Carotid pulsation: Corrigans sign
  • pulsation of nail bed: Quincke’s sign
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133
Q

Absent arm pulses in a young woman?

A

Think Takayasu’s arteritis

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134
Q

AF + mass in left atrium

A

Cardiac myxoma - bengin tumour of the heart

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135
Q

Patients with aortic valve IE are at risk of what?

A

Developing aortic valve abscess (prolongation of PR can be first sign)

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136
Q

What pulse can you get with heart failure?

A

Pulsus alternans - strong and weak beats due to varying systolic pressure

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137
Q

When is rhythm control used in AF treatment over rate control?

A
  • Coexistent HF
  • First onset AF
  • Obvious reversible cause
  • Use amiodarone/flecainide
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138
Q

What is the inheritance of HOCM?

A

AD

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139
Q

What is the pathophysiology of HOCM?

A
  • Diastolic dysfunction as LVH causes decreases compliance and decreased CO
  • Biopsy shows myofibrillar hypertrophy with disarrayed myocytes
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140
Q

ECG findings for hypercalcaemia?

A

Short QT

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141
Q

What are the components for JONES criteria?

A

Joint involvement
<3 - Myocarditis
Nodules
Erythema marginatum
Sydnehams chorea

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142
Q

Post MI patient develops pulmonary oedema and has pansystolic murmur?

A

Think acute mitral regurg

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143
Q

What can cause orthostatic hypotension?

A
  • Excercise induced
  • After meals
  • After prolonged bed rest
  • Drugs such as CBB, Levodopa
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144
Q

QT prolongation with no electrolyte abnormalities?

A

Think hereditary long QT syndrome -> caused by loss of function/blockage of K+ channels

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145
Q

When should LFTs be checked with statins?

A

Baseline, 3 months and 12 months

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146
Q

What murmur do you get with VSD?

A

Pansystolic murmur - entire systolic period

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147
Q

Which drug when used alongside clopidogrel can make it less effective?

A

Omeprazole/Esomeprazole

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148
Q

What dose of amiodarone is given in ALS?

A

Initially 300mg
After 5th shock, an additional 150mg can be given alongside 1mg of adrenaline

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149
Q

What will type A aortic dissection cause?

A

Acute aortic regurg

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150
Q

What is the treatment for rheumatic fever?

A

IM BenPen or Oral PenV with NSAIDs

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151
Q

Patients taking isosorbide mononitrate should use what dosing regime?

A

Asymmetric dosing interval to prevent nitrate tolerance

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152
Q

NSTEMI in an unstable patient?

A

Immediate coronary angio

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153
Q

Which antihypertensive cause hyperkalaemia?

A

ACE

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154
Q

What is tongue and facial swelling?

A

Angioedema -> ACE inhibitor

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155
Q

What are examination signs of pericarditis?

A

-Pericardial rub
- Quiet heart sounds
- Raised JVP

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156
Q

What are causes of pericarditis?

A
  • Infective: coxsackie, TB
  • Trauma
  • Malignancy eg. lung/breast
  • MI complication
  • SLE
  • RA
  • hypothyroidism
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157
Q

3 main investigations for IE?

A
  • Blood cultures
  • Echo
  • ECG
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158
Q

What are some triggers for worsening pulmonary oedema?

A
  • Arrhythmia
  • MI
  • Sepsis
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159
Q

What is the most common cardiomyopathy?

A

Dilated

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160
Q

management of mitral stenosis?

A

Asymptomatic - Monitor with regular echo
Symptomatic - Percutaneous mitral commissurotomy

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161
Q

When fibrinolysis is done for ACS, when should ECG be repeated?

A

60-90 minutes

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162
Q

What are the ChadsVasc categories?

A

Congestive HF
HTN
Age >75 (2), >65 (1)
Diabetes
Stroke/TIA/VTE
Vascular disease
Sex (Female)

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163
Q

Where is access preferred for PCI?

A

Radial artery

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164
Q

Which medications can worsen glucose tolerance?

A

Thiazides

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165
Q

widespread pansystolic murmur, hypotension, pulmonary oedema post MI?

A

Acute mitral regurg

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166
Q

Management of suspected HF in GP?

A

Measure BNP and refer for TTE if elevated

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167
Q

What does a loud opening snap indicate?

A

The mitral valve leaflets are still mobile in mitral stenosis

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168
Q

What can indicate the severity of the mitral stenosis?

A

Length of murmur increases

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169
Q

What are components of orbit score?

A
  • Haemoglobin
  • Age
  • Bleeding history
  • Renal impairment
  • Treatment with anti platelets
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170
Q

Nailed pulsation?

A

Quincke’s sign -> aortic regurgitation

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171
Q

Rate control for AF?

A

Beta blocker
CCB
Digoxin

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172
Q

Management of continued pain post PCI for MI?

A

Urgent CABG

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173
Q

Reverse nike sign?

A

Digoxin

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174
Q

Persistent ST elevation post MI?

A

Left ventricular aneurysm

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175
Q

What are signs of aortic coarctation?

A
  • radio-femoral delay
  • mid systolic murmur
  • weak peripheral pulses in legs
  • Left ventricular heave
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176
Q

Investigations to confirm aortic coarctation?

A
  • Echo
  • CT aorta
  • Cardiac catheterisation
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177
Q

Management options for aortic coarctation?

A
  • Open surgery
  • Balloon angioplasty and stent insertion
  • Mild cases can be controlled with antihypertensives
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178
Q

What carries the worst prognosis in symptomatic aortic stenosis?

A

Exertional syncope

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179
Q

What medication should be avoided in someone with aortic stenosis?

A

Nitrates

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180
Q

When should adenosine be avoided?

A

Asthmatics

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181
Q

What is the definitive management of bradycardia?

A

Permanent pacemaker

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182
Q

Which organisms often cause rheumatic fever?

A

Strep pyogenes

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183
Q

Stroke + AF?

A

2 weeks of aspirin then warfarin/DOAC

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184
Q

ADPKD is associated with what?

A

Mitral valve prolapse

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185
Q

S3 vs S4 sounds

A

CCF - 3 letters - S3
HOCM - 4 letters - S4

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186
Q

What does aortic dissection cause?

A

Weak/absent carotid, brachial or femoral pulses

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187
Q

HF with rEF vs HF with pEF?

A

rEF - systolic dysfunction e.g. IHD, arrythmias
pER - diastolc dysfunction e.g. HOCM, cardiac tamponade

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188
Q

What can be done for patients not responding to medications for HF?

A

Cardiac resynchronisation therapy if wide QRS

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189
Q

Raised JVP, ankle oedema, hepatomegaly

A

Right sided HF

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190
Q

What are causes of torsades de pointes?

A
  • Congenital
  • Macrolides
  • Subarachnoid haemorrhage
  • Hypothermia
  • Electrolyte disturbances
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191
Q

What is torsades de pointes?

A

Polymorphic VT

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192
Q

Heart failure management

A
  1. ACE + BB
  2. Spironolactone/Eplerenone

3rd lines
- Ivabradine if HR > 75 and reduced EF
- Hydralazine with nitrate for Afro-Caribbean patients
- Sacubitrtil-valsartan for patients with reduced EF after ACE/ARB wash out period
- Digoxin if sinus rhythm

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193
Q

What vaccines should be given to HF patients?

A

Annual flu
One off PCV

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194
Q

Sudden heart failure, raised JVP, pulsus parodoxus post MI?

A

Left ventricular free wall rupture

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195
Q

What ABG picture will hyperaldosteronism cause?

A

Metabolic alkalosis with hypokalaemia

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196
Q

What can cause high output heart failure?

A

Anaemia

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197
Q

When is DC cardioversion done for arrhythmias?

A

Systolic < 90

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198
Q

How to manage HTN when patient is on ACE/CCB/Thiazide and K+ > 4.5?

A

Add alpha/beta blocker

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199
Q

AF with sudden onset abdo pain?

A

Think acute mesenteric ischaemia -> treat with immediate laparotomy

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200
Q

Management of ruptured AAA?

A

Crossmatch 6 units of blood

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201
Q

When is amiodarone preferred for pharmacological cardioversion?

A

Evidence of structural heart disease

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202
Q

Chest pain + neurology?

A

Think aortic dissection

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203
Q

new BP >= 180/120 mmHg + new-onset confusion, chest pain, signs of heart failure, or acute kidney injury

A

Refer for assessment

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204
Q

CCB side effects

A

headache, flushing, ankle oedema

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205
Q

Amlodipine can cause what?

A

Gingival hyperplasia

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206
Q

What is the cut off for aortic valve surgery if no symptoms?

A

Valvular gradient > 40 with features of left systolic dysfunction

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207
Q

pre-excitation syndrome that occurs due to the presence of an accessory electrical pathway between the atria and ventricles

A

Wolf-Parkinson-White

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208
Q

Gallop rhythm is a sign of what?

A

Left sided heart failure

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209
Q

Prosthetic vs mechanical valve?

A

Mechanical last longer so are given to younger patients

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210
Q

What can be considered in CPR if a PE is supected?

A

Thrombolytic drugs such as alteplase

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211
Q

How should 80+ year olds with raised BP be managed?

A

Lifestyle advice

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212
Q

Nifedipine can cause what?

A

Peripheral vasodilation which can cause reflex tachycardia

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213
Q

What is an alternative to amiodarone in arrest?

A

Lidocaine

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214
Q

What drugs are an alternative to atropine?

A

Isoprenaline/adrenaline infusion

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215
Q

How long should CPR be continued when thrombolytic drugs are being given?

A

60-90 minutes

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216
Q

Tension pneumothorax can cause what?

A

Pulseless electrical activity

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217
Q

Clinically unstable aortic dissection?

A

Transoesophageal echo

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218
Q

What is the most common cause of aortic stenosis in young patients?

A

Congenitally bicuspid valve

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219
Q

Hyperlipidaemia can cause what?

A

Pseudohyponatremia -> serum osmolality will be normal

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220
Q

Premature supraventircular beats vs premature ventricular betas on ECG?

A

Supraventricular - narrowed QRS complexes
Ventricular - widened QRS complexes

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221
Q

What is cardiac tamponade?

A

Accumulation of pericardial fluid causing increased pericardial pressure which compromises ventricular filling, resulting in a
reduced cardiac output.

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222
Q

cardiomyopathy + diabetes + joint pain + hepatomegaly

A

Think haemochromatosis

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223
Q

What antibiotic is recommended in COPD patients who continue to have exacerbations?

A

Azithromycin

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224
Q

Chronic infection with Pseudomonas and Bulkholderia in CF

A

Increased risk of morbidity or mortality

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225
Q

Pericarditis vs STEMI ECG?

A

STEMI will have ST elevation greater in lead III than lead II

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226
Q

Aortic dissection can cause what?

A

Neuro deficits

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227
Q

Persistent ST elevation with fatigue

A

Left ventricular aneurysm

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228
Q

When do CK levels normalise after an MI?

A

48-72 hours -> good to check if suspecting a reinfarction

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229
Q

When should sacubitril-valsartan be initiated?

A

Following an ACE/ARB wash out period

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230
Q

What part of the QRS is electrical cardioversion synchronised to?

A

R wave

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231
Q

Mitral regurg is associated with which conditions?

A
  • Marfans
  • Ehlers-Danlos
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232
Q

DC cardioversion vs unsynchronised cardioversion?

A

DC- Tachyarrhythmias
Unsynchronised - Cardiac arrest (VT, VF)

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233
Q

What is the management of atrial flutter?

A
  1. Beta blocker/CCB
  2. Consider cardioversion
  3. Catheter ablation curative
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234
Q

Sudden increase in BP associated with ACS?

A

Treat with IV GTN

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235
Q

Elderly patient with ECG with periods of sinus bradycardia + atrial tachycardia?

A

Sick sinus syndrome

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236
Q

What is a normal PR interval?

A

0.12-0.20s
3-5 small squares

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237
Q

Absent P waves + regular rhythm of QRS

A

SVT

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238
Q

What stroke is most likely during cardiac catheterisation?

A

Embolic -> debris can be scraped from aortic wall

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239
Q

Most common cause of left ventricular hypertrophy in a healthy person?

A

Hypertrophic cardiomyopathy

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240
Q

Heart failure + wide QRS?

A

Consider resynchronisation pacemaker device

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241
Q

2nd line investigation for endocarditis if echo is negative but high suspicion?

A

PET CT

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242
Q

What is the PR interval?

A

Start of P wave to start of QRS complex

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243
Q

Indications for DC cardioversion in tachyarrhythmias except shock?

A
  • Syncope
  • MI
  • Heart failure
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244
Q

What are the 2 options for aortic valve replacement?

A

Surgical - low risk patients
Transcatheter - high risk patients

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245
Q

When to do 1 shock vs 3 shocks in shockable rhythms?

A

3 shocks - if witness cardiac arrest
1 shock - if not witnessed

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246
Q

What is a common cause of tricuspid regurg?

A

Pulmonary HTN e.g. COPD

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247
Q

Investigation of choice for cardiac tamponade?

A

Echo

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248
Q

When in CABG indicated?

A

More significant coronary artery disease e.g. triple vessel

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249
Q

Abx for MRSA resistant endocarditis?

A

Prosthetic valve - Vancomycin, Rifampicin and Gentamicin
Normal valve - Vancomycin and Rifampicin

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250
Q

Thiazides can precipitate what?

A

Digoxin toxicity

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251
Q

De Musset sign is a sign of what?

A

Aortic regurgitation

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252
Q

What is acute coronary syndrome? (ACS)

A

umbrella term covering number of acute presentations of ischaemic heart disease

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253
Q

Presentations of acute coronary syndrome?

A

1) STEMI
2) NSTEMI
3) unstable angina

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254
Q

As a rise in troponins may take hrs, it may be hard to distinguish between unstable angina and NSTEMI initally so what do you do?

A

Treat like NSTEMI until troponin result is known

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255
Q

When is unstable angina considered to be present in patients? (an acute coronary syndrome)

A

pts with ischaemic symptoms suggestive of ACS and NO elevation in troponins, with or without ECG changes indicative of ischaemia

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256
Q

ACS generally develops in what patients?

A

Those with known or unknown ischaemic heart disease

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257
Q

What are other terms for ischaemic heart disease (all have the SAME meaning)?

A

coronary heart disease, coronary artery disease, IHD all mean same thing

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258
Q

What causes IHD?

A

gradual build up of fatty plaques within walls of coronary arteries

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259
Q

What does IHD lead to?

A

1) gradual narrowing of coronary arteries therefore less oxygen reaching myocardium at times of increased demand -> angina

2) risk of sudden plaque rupture -> sudden occlusion of coronary artery -> no oxygen reaching area of myocardium

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260
Q

Unmodifiable RFs for IHD

A

increasing age, male, FHx

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261
Q

Modifiable RFs for IHD

A

smoking, DM, HTN, obesity, hypercholesterolaemia

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262
Q

IDH pathophysiology: inital endothelial dysfunction is triggered by what?

A

factors eg. smoking, HTN, hyperglycaemia

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263
Q

Inital endothelial dysfucntion results in what changes to the endothelium in IHD?

A

pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability

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264
Q

IHD pathophysiology: endothelial dysfunction is triggered and there are a number of changes to the endothelium; fatty infiltration of the subendothelial space by what then occurs?

A

Low-density lipoprotein (LDL) particles

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265
Q

IHD pathophysiology: role of monocytes in the progagation of the inflammatory process?

A

monocytes migrate from the blood and differentiate into macrophages; these then phagocytose oxidised LDL, slowly turning into large ‘foam cells’. As these macrophages die, the result can further propagate the inflamm process

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266
Q

IHD pathophysiology: what forms the fibrous capsule covering the fatty plaque?

A

smooth muscle proliferation and migration from tunica media into intima results in formation of fibrous capsule covering fatty plaque

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267
Q

What pathophysiological changes can be seen in IHD over number of years?

A
  • intial endothelial dysfunction
  • results in a number of changes to endothelium
  • fatty infitration of subendothelial space by LDL
  • formation of ‘foam cells’ and inflammatory process
  • smooth muscle proliferation and migration to form fibrous capsule covering fatty plaque
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268
Q

Cx of atherosclerosis?

A

angina
MI

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269
Q

How does atherosclerosis cause angina?

A

plaque forms physical blockage in lumen of coronary artery; may cause reduced blood flow (and so oxygen) to myocardium, partically at times of increased demand

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270
Q

How can atherosclerosis cause myocardial infarction?

A

plaque may rupture, potentially causing a complete occlusion of coronary artery

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271
Q

Function of endothelium of arteries?

A

protects vessel wall and prevents clotting

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272
Q

Pathophysiology of atherosclerosis?

A
  • damage to endothelium wall allows LDL to enter
  • monocytes enter and break LDL down by oxidation, causes macrophage to die
  • then deposits under damaged endothelium: called foam cells
  • when macrophages die, also release cytokines that causes more monocytes to enter endothelium and break down more LDL
  • foam cells build up to form a lesion called a fatty streak
  • fatty streak is thrombogenic meaning blood can clot on it
  • platelets gather at damaged endothelium and release platelet dervived growth factor which encourages growth of smooth muscle cells
  • smooth muscle meant to stay in middle layer (tunica media) but starts to growth in tunica intima where they multiply
  • smooth muscle cells secrete collagen, proteoglycans, elastin fibrous cells that form a wall around fatty streak preventing blood clotting= extracellular matrix wall of fibrous cap
  • fibrous cap + fatty streak = plaque
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273
Q

Why in atherosclerosis do the walls of the arteries become stiff?

A
  • smooth muscle also starts depositing calcium into the plaque creating crystals
  • Ca crystals normally deposited by LDL and removed by HDL, but plaque stops HDL removing Ca
  • causes build up of Ca in vessel wall and crystallises= stiffens walls of arteries
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274
Q

Why might a high CRP indicate atherosclerosis?

A

atherosclerosis is an inflamm disease as immune sysytem invl (macrophages). Therefore high CRP

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275
Q

CPS of acute coronary syndrome?

A
  • left-sided/central chest pain
  • may radiate to jaw or L arm
  • ‘crushing’ ‘heavy’
  • dyspnoea
  • sweating
  • nausea
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276
Q

What pts with ACS may not experience any chest pain?

A

Diabetics; elderly

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277
Q

Physical signs of ACS

A
  • BP, HR, T, O2 often normal or mild eg. tachy
  • unless HF
  • pale, clammy
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278
Q

Most important Ix when assessing pt with chest pain

A
  • ECG
  • cardiac markers eg. troponin
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279
Q

Deep and widespread ST depression is associated with what?

A

very high mortality because it signifies severe ischaemia usually of LAD or left main stem

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280
Q

Aims of treatment of ACS?

A

1) prevent worsening (further occlusion)
2) revascularise (unblock) vessel if occluded (STEMI)
3) Mx pain

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281
Q

Acute Mx of ACS

A

M.orphine (IV)
O.xygen (if <94%)
N.itrates (IV or subling)
A.spirin (300mg)

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282
Q

When should oxygen be given in Mx of ACS?

A

if sats <94%

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283
Q

Secondary prevention for pts who have had an ACS?

A

Aspirin
Antiplatelet eg. clopidogrel
BB
ACE inhibitor
Statin

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284
Q

STEMI?

A

ST-elevation MI= ST-segment elevation + elevated biomarkers of myocardial damage

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285
Q

NSTEMI?

A

non ST-elevation MI= ECG change but no ST-segment elevation + elevated biomarkers of myocardial damage

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286
Q

Groups of Mx for acute coronary syndromes?

A
  • STEMI
  • NSTEMI/unstable angina
  • Secondary prevention
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287
Q

Dose of aspirin to give in acute Mx?

A

300mg

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288
Q

Acute Mx of ACS: nitrates should be used in caution if the pt is…

A

Hypotensive

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289
Q

Overview of Mx in pt with suspected ACS?

A

1) acute Mx
2) ECG findings- ?STEMI
3) STEMI confirmed= eligability for coronary reperfusion therapy

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290
Q

STEMI criteria?

A

CP consistent with ACS ≥ 20mins with persistent >20mins ECG features in ≥ 2 contiguous leads

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291
Q

STEMI ECG criteria in men?

A

ECG features in ≥ 2 contiguous leads of….

Men <40yrs=
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3

Men >40yrs= ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3

PLUS 1 mm ST elevation in other leads & new LBBB (LBBB should be considered new unless there is evidence otherwise)

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292
Q

STEMI ECG criteria in women?

A

ECG features in ≥ 2 contiguous leads of…

1.5 mm ST elevation in V2-3

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293
Q
A
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294
Q

STEMI Mx?

A

1) 300mg aspirin (+other acute Mx)

2) PCI OR Fibrinolysis

3) dual antiplatelet therapy: Clopidogrel + aspirin (if high bleeding risk) or tricagrelor + aspirin (low risk)

4) stenting indicated? Cardiac rehab and secondary prevention

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295
Q

2 types of coronary reperfusion therapy in STEMI?

A

1) PCI: dual antiplatelet therapy before; then during give either unfractionated heparin with bailout GPI if radial access or bivalirudin with bailout GPI if femoral access

2) Fibrinolysis + antithrombin drug

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296
Q

In STEMI Mx when should pt get PCI?

A

<12hrs of symptoms and can be delivered in 120mins. Consider >12hrs if CG shock or continue ischaemia.

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297
Q

PCI for Mx of STEMI?

A

1) dual antiplatelet therapy before PCI:
aspirin + prasugrel or clopidogrel

2) PCI with radial access: + unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI)

OR

2) PCI with femoral access: bivalirudin with bailout GPI

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298
Q

Dual antiplatelet therapy to give pt with STEMI prior to PCI?

A

Aspirin +
clopidogrel if taking oral anticoag
or
prasugrel if not taking oral anticoag

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299
Q

In STEMI Mx when should pt get fibrinolysis?

A

if <12hrs and PCI not possible in 120mins

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300
Q

Patients undergoing fibrinolysis should also be given what?

A

Antithrombin drug eg. fondaparinux or LMWH

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301
Q

When should ECG be done after fibrinolysis?

A

60-90mins after

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302
Q

STEMI Mx: is radial or femoral access preferred?

A

Radial

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303
Q

What if pt with STEMI gets ECG 90mins after fibrinolysis and it fails to show resolution of ST elevation?

A

PCI

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304
Q

Mx of NSTEMI/unstable angina overview?

A

1) 300mg aspirin + fondaparinux or unfractionated heparin

2) GRACE score

3) low risk= dual antiplatelt therapy (aspirin + ticagrelor or clopidogrel)

3) intermediate/high risk= PCI immediately/within 72hrs; give aspirin + prasugrel or ticagrelor (if pt on oral anticoag give clopidogrel); give unfractioned heparin; use drug-eluting stents

4) assess LV function and consider angiography (eg. if develop ischaemia)

5) cardiac rehab and secondary prevention

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305
Q

What is dual antiplatelet therapy (DAPT)?

A

aspirin + P2Y12 inhibitor eg. clopidogrel, prasugrel or ticagrelor

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306
Q

How to know what drugs to use for DAPT?

A

Apirin +

prasugrel (during PCI) if not taking anticoag

clopidgorel (during PCI) if taking anticoag

ticagrelor if low bleeding risk

clopidogrel if high bleeding risk

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307
Q

How do you decide if you use fonaparinux or unfractionated heparin initally in the Mx of NSTEMI/unstable angina?

A
  • fondaparinux= low risk of bleeding and no immediate angiography
  • unfractionated heparin= immediate angiography planned or creatinine is > 265 µmol/L
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308
Q

What does GRACE score stand for?

A

The Global Registry of Acute Coronary Events

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309
Q

What is the GRACE score?

A

Predicts 6m mortality and risk of cardiovascular events

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310
Q

In Mx for NSTEMI/unstable angina, as well as the GRACE risk score what else needs to be included in the risk assessment?

A

history, examination; ECG; bloods (troponin I or T, creatinine, glucose, Hb); balance possible benefits of Mx against bleeding risk

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311
Q

What factors does the GRACE score account for?

A

age
HR, BP
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

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312
Q

GRACE score: what is low risk?

A

predicted 6m mortality ≤ 3%

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313
Q

GRACE score: what is intermediate or higher risk?

A

predicted 6-month mortality > 3%

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314
Q

Which patients with NSTEMI/unstable angina should have coronary angiography (with follow on PCI if necessary) immediateley?

A

clinically unstable eg. hypotensive

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315
Q

Which patients with NSTEMI/unstable angina should have coronary angiography (with follow on PCI if necessary) within 72hrs?

A

pts with GRACE score >3%

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316
Q

When should coronary angiography be considered for pts with NSTEMI/unstable angina?

A

if ischaemia is experienced after admission

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317
Q

What is cardiac rehabilitation used as the final Mx for ACS?

A

before discharge; assessment 10days after discharge

physical activity, lifestyle advice, stress management and health education

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318
Q

Drug therapy for secondary prevention for ACS (STEMI, NSTEMI, unstable angina)?

A
  • ACE inhibitor
  • DAPT
  • Beta-blocker
  • Statin
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319
Q

DAPT for secondary prevention of ACS?

A

Aspirin + second antiplatelet for up to 12m

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320
Q

Drug titration of beta-blockers for secondary prevention of ACS?

A

titrate to max tolerated or target dose

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321
Q

Drug titration for ACE inhibitors for secondary prevention of ACS?

A

titrate up (with monitoring) every 12-24hrs; complete titration in 4-6w of hospital discharge.

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322
Q

What should you monitor in pts before starting and 1-2w after starting an ACE inhibitor?

A

renal function, electrolytes and BP

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323
Q

Secondary prevention for ACS: if pt already on anticoag, offer clopidogrel for how long?

A

Up to 12m if had PCI

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324
Q

Poor prognostic factors of ACS?

A

age; Hx or development of HF; PVD; reduced systolic blood pressure; Killip class; inital serum creatinine conc; elevated initial cardiac markers; cardiac arrest on admission; ST segment deviation

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325
Q

What is the name of the system used to stratify risk post MI?

A

Killip class

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326
Q

Killip class features and 30 day mortality?

A

I= no signs HF (6%)
II= lung crackes, S3 (17%)
III= frank pulmonary oedema (38%)
IV= cardiogenic shock (81%)

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327
Q

Cx of myocardial infarction?

A

Cardiac arrest
Cardiogenic shock
Chronic heart failure
Tachyarrhythmias
Bradyarrhythmias
Pericarditis
Left ventricular aneurysm
LV free wall rupture
Ventricular septal defect
Acute mitral regurgitation

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328
Q

Most common cause of death following MI

A

Cardiac arrest

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329
Q

Why can cardiac arrest occur after MI?

A

pt develops ventricular fibrillation

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330
Q

Cardiac arrest Mx

A

ALS with defibrillation

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331
Q

Why may pt develop cardiogenic shock after MI?

A

if large part of V myocardium damaged by infarction the EF may decrease to the point the pt develops CG shock

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332
Q

Causes of cardiogenic shock?

A

post MI; mechanical Cx (LV free wall rupture)

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333
Q

Pt with cardiogenic shock may require what?

A

Inotropic support and/or intra-aortic balloon pump

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334
Q

Cardiogenic shock?

A

Heart suddenly can’t pump enough blood to meet body’s needs as it has been damaged so much. Life-threatening- can lead to organ failure.

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335
Q

Why may MI lead to chronic HF?

A

ventricular myocardium may be damaged and dysfunctional

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336
Q

Arrhythmias that may develop post MI?

A

Ventricular fibrillation (most common cause of death following MI); ventricular tachy; bradyarrhythmias

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337
Q

Atrioventricular block is more common following what type of MI?

A

Inferior

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338
Q

What is common (10%) in first 48hrs following a transmural MI?

A

Pericarditis

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339
Q

Pain worse lying flat and better leaning forward; pericardial rub may be heard; may see pericardial effusion on echo

A

Pericarditis

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340
Q

Dressler’s syndrome?

A

Pericarditis that can occur 2-6w following an MI.

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341
Q

Fever, pleuritic pain, pericardial effusion and raised ESR?

A

Dressler’s

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342
Q

Pathophysiology of Dressler’s?

A

autoimmune reaction against antigenic proteins formed as myocardium recovers

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343
Q

Mx of dressler’s?

A

NSAIDs

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344
Q

Ischaemic damage following MI may weaken the myocardium and result in LV aneurysm forming. What is this associated with?

A

Persistent ST elevation and LV failure.

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345
Q

Why may LV aneurysm increase risk of stroke?

A

thrombus may form within the aneurysm

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346
Q

Pts with LV aneurysm are what?

A

Anticoagulated

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347
Q

When could a LV free wall rupture occur after MI?

A

1-2w after (3% of MIs)

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348
Q

Acute HF secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)?

A

LV free wall rupture

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349
Q

Mx for LV free wall rupture?

A

urgent pericardiocentesis and thoracotomy

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350
Q

Pulsus paradoxus?

A

When BP decreases with inhalation eg. in cardiac tamponade

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351
Q

When would rupture of interventricular septum occur post MI (1-2% pts)?

A

in 1st week

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352
Q

Features of ventricular septal defect post MI?

A

Acute HF associated with pan-systolic murmur

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353
Q

Diagnosis of ventricular septal defect post MI?

A

ECHO diagnostic and will exclude acute mitral regurg (presents similar)

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354
Q

Mx of ventricular septal defect post MI?

A

Urgent surgical correction

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355
Q

What may cause acute mitral regurgitation post MI?

A

infero-posterior infarction and may be due to ischaemia or rupture of papillary muscle

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356
Q

CP of mitral regurg post MI?

A

acute hypotension, pulmonary oedema; early-mid systolic murmur

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357
Q

Mx for pt with mitral regurg post MI?

A

vasodilator therapy but often require emergency surgical repair.

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358
Q

Secondary prevention of ACS: dietary advice?

A

Mediterranean style diet; switch butter and cheese for plant oil based products; do NOT recommend eating oily fish

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359
Q

Secondary prevention of ACS: exercise advice?

A

20-30mins a day until pt slightly breathless

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360
Q

When can sexual activity resume after an uncomplicated MI?

A

4w after. Sex does not increase likelihood of further MI

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361
Q

When can PDE5 inhibitors eg. sildenafil be used in pts post MI?

A

6m after MI but avoid in pts prescribed nitrates or nicorandil

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362
Q

DAPT post ACS?

A

aspirin + ticagrelor (stop T after 12m)

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363
Q

DAPT post PCI?

A

aspirin + prasugrel or ticagrelor (stop P or T after 12m)

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364
Q

When might the 12m period for DAPT be altered in patients?

A

If at high risk of bleeding or high risk of further ischaemic events

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365
Q

What should be initiated after ACE inhibitor theraoy in pts who had an acute MI and have symptoms/signs of HF and LV systolic dysfunction for secondary prevention?

A

Aldosterone antagonists eg. eplerenone 3-14days post-MI

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366
Q

Abdominal aortic aneurysm (AAA)?

A

Permanent pathological dilation of abdominal aorta with diameter >1.5 times the expected anteroposterior diameter of the segment given the person’s sex and body size

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367
Q

Threshold for diagnosis of AAA?

A

abdo aortic diameter of 3cm or more

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368
Q

RFs for AAA?

A

male, age, smoking, HTN, FHx, DM, COPD, hyperlipidaemia

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369
Q

When is screening for AAA offered?

A

All men the yr they become 65yrs

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370
Q

AAA screening test?

A

abdo USS to detect any bulging or swelling of aorta

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371
Q

AAA screening: no aneurysm found?

A

<3cm- no further scans requried

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372
Q

AAA screening: small AAA?

A

3-4.4cm. Placed under surveillance and repeat scan in 12m (repeat every 12m)

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373
Q

AAA screening: medium AAA?

A

4.5-5.4cm. Under surveillance and repeat scan in 3m (repeat every 3m)

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374
Q

AAA screening: large AAA?

A

5.5cm+. Referred to vascular surgeon within 2w for probable intervention.

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375
Q

How long does AAA screening take?

A

15mins; told results at appointment

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376
Q

Why is there screening for AAA?

A

majority asymptomatic and if rupture then high mortality.

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377
Q

What AAA have a low rupture risk?

A

asymptomatic, diameter <5.5cm (small and medium)

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378
Q

High rupture risk AAA?

A

Symptomatic, diameter >=5.5cm or rapidly enlarging (>1cm/yr)

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379
Q

How are large high risk AAA surgically managed?

A

Elective endovascular repair (EVAR) or open repair. EVAR stent placed into abdo aorta via femoral artery to prevent blood from collecting in aneurysm

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380
Q

Cx of EVAR for AAA?

A

endo-leak: stent fails to exclude blood from aneurysm; asymptomatic on routine follow up

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381
Q

Why do AAA occur?

A

As result of the failure of elastic proteins in the matrix.

Loss of intima with loss of elastic fibres from the media, associated with increased proteolytic activity and lymphocytic infiltration.

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382
Q

Normal diameter abdo aorta in men and women >50yrs?

A

F: 1.5cm
M: 1.7cm

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383
Q

Aneurysms typically represent dilation of…

A

all layers of the arterial wall; most caused by degenerative disease

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384
Q

Rare causes of AAA?

A

Syphilis; connective tissue disorders eg. Ehlers Danlos type 1 and Marfan’s

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385
Q

Peripheral arterial disease (PAD)?

A

narrowing or occlusion of peripheral arteries affecting blood supply to lower limbs

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386
Q

Types (symptoms) of peripheral arterial disease?

A

Acute limb ischaemia
Intermittent claudication
Chronic limb-threatening ischaemia
Asymptomatic

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387
Q

PAD: acute limb ischaemia?

A

sudden decrease in limb perfusion that threatens limb viability- CP <2w

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388
Q

PAD: intermittent claudication?

A

diminished circulation leads to pain in lower limb on walking or exercise, relieved on rest

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389
Q

Most common symptom of PAD?

A

Intermittent claudication

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390
Q

PAD: chronic limb-threatening ischaemia?

A

chronic, inadequate tissue perfusion at rest and is defined by ischaemic rest pain, with or without tissue loss

391
Q

Asymptomatic PAD?

A

early stage in the condition and may progress with symptoms of intermittent claudication or chronic limb-threatening ischaemia

392
Q

PAD of the lower limbs is most commonly caused by?

A

Atherosclerosis

393
Q

Cause of acute limb ischaemia (PAD)?

A

thrombosis within diseased artery when plaque ruptures

394
Q

RFs for PAD?

A

smoking, DM, HTN, hypercholesterolaemia

395
Q

CP of acute limb ischaemia (PAD)?

A

pain, pallor, pulseless, perishing with cold, paraesthesia and power loss

396
Q

CP of chronic limb ischaemia (PAD)?

A

progressive development of cramp-like pain in calf, thigh or buttock on walking; not relieved by rest; unexplained foot or leg pain; non-healing wounds on lower limb. ?absent foot pulses.

397
Q

Pt with pain in leg worse at night, sleep with leg hanging out of bed or sleep in a chair?

A

Chronic limb-threatening ischaemia

398
Q

Why do pts with chronic limb-threatening ischaemia report pain worse at night?

A

decrease of BP when asleep and no gravity when lying down

399
Q

CP of intermittent claudication (PAD)?

A

pain in lower limb on walking or exercise, relieved by rest (within 10mins), aching, burning, distal extremity before proximal. Uni or bilateral

400
Q

Ix for PAD?

A

ankle brachial pressure index (ABPI)

401
Q

What reading of an ABPI suggests the presence of PAD?

A

0.9 or less

402
Q

Mx of acute limb ischaemia?

A

ABC, IV opioids, IV unfractionated heparin then:

Urgent assessment by vascular specialist: endovascular therapies (eg. percutaneous catheter-directed thrombolytic therapy) or surgical interventions (eg. surgical thromboembolectomy)

403
Q

Mx of chronic limb-threatening ischaemia?

A
  • urgent referral to vascular
  • pain Mx: paracetamol, weak/strong opioids
  • advice
404
Q

Mx of intermittent claudication?

A
  • supervised exercise programme (2hrs per w for 3m)
  • lifestyle advice
  • referral for consideration of angioplasty or bypass surgery
  • if don’t want surgery= naftidrofurl oxalate
405
Q

What if supervised exercise programme is not available in pts with intermittent claudication?

A

30mins exercise 3-5 times per week; walking until onset of symptoms then rest

406
Q

All people with PAD should be given what?

A

Advice and treatment for secondary prevention of CVD

407
Q

Physical signs in someone with PAD?

A

dry shiny skin; elevation pallor; hair loss over dorsum of foot; muscle atrophy; thickened toenails; ulceration on heel

408
Q

Ruptured AAA?

A

catastrophic (sudden collapse) or sub-acute (persistent severe central abdo pain with developing shock). 80% mortality

409
Q

CP of ruptured AAA?

A

severe central abdo pain radiating to back; pulsatile expansile mass in abdo; may be shocked (hypoten, tachy) or collapsed

410
Q

Severe central abdo pain radiating to back?

A

ruptured AAA

411
Q

Ruptured AAA Mx?

A

immediate vascular review for emergency surgical repair.

if stable may get CT angiogram to confirm

412
Q

Tear in the tunica intima of the wall of the aorta

A

aortic dissection

413
Q

Associations with aortic dissection?

A

HTN
trama; bicuspif aortic valve; marfans; turner’s and noonan’s; pregnancy; syphillis

414
Q

Severe and sharp tearing cheat and upper back pain

A

aortic dissection

415
Q

Aortic dissection CP

A

tearing sharp chest and upper back pain; weak or absent pulse; variation (>20) in SBP between arms; aortic regurg; HTN

416
Q

Aortic dissection if involves cornonary/spinal arteries/distal aorta?

A

1) anginga
2) paraplegia
3) limb ischaemia

417
Q

Are there ECG changes in aortic dissection?

A

non-specific or no ECG changes. Some: ST-elevation in inferior leads

418
Q

Stanford classification of aortic dissection?

A
  • Type A (2/3)= ascending aorta
  • Type B (1/3)= descending aorta, distal to L subclavian origin
419
Q

Ix for aortic dissection?

A
  • CT angiography of chest, abdo and pelvis GOLD (if stable)
  • Tranoesophageal echo (if unstable)
  • CXR: widened mediastinum
420
Q

Finding on CT angiography of chest, abdo and pelvis for aortic dissection?

A

False lumen

421
Q

Mx for Type A aortic dissection?

A
  • surgery but BP must be controlled of S target of 100-120 whilst awaiting
422
Q

Mx for Type B aortic dissection?

A

conservative, bed res, reduce BP IV labetalol to prevent progression

423
Q

Complications of a backward tear in aortic dissection?

A

aortic incompetence/regurg
MI: inferior due to right cornonary invol.

424
Q

Complications of a forward tear in aortic dissection?

A

unequal arm pulses and BP; stroke; renal failure

425
Q

Aortic regrurg is the leaking of the aortic valve of heart that causes….

A

blood to flow in reverse direction during ventricular diastole

426
Q

What can cause aortic regurg?

A

disease of aortic valve or dilation of aortic root and ascending aorta

427
Q

Causes of aortic regurg due to valve disease?

A

Chronic= RF, calcific valve disease, connective tissue diseases (RA, SLE), bicuspid aortic valve

Acute= infective endocarditis

428
Q

Causes of aortic regurg due to aortic root disease?

A

Chronic= bicuspid aortic valve, spondylarthropathies, HTN, syphilis, Marfan’s

Acute= aortic dissection

429
Q

What type of murmur is aortic regurgitation?

A

Early diastolic murmur

430
Q

Where is aortic regurg best heard?

A

loudest at the left sternal edge

431
Q

Features of aortic regurg?

A
  • collapsing pulse
  • wide pulse pressure
  • early diastolic murmur
432
Q

Signs in aortic regurg?

A

Quincke’s sign (nailbed pulsation) and De Musset’s sign (head bobbing)

433
Q

What can you get in severe aortic regurg?

A

mid-diastolic Austin-Flint murmur: due to partial closure of anterior mitral valve cusps caused by regurg streams

434
Q

Ix for aortic regurg?

A

echo

435
Q

Mx for aortic regurg?

A
  • medical Mx for any HF
  • surgery if indicated
436
Q

Indications for surgery in aortic regurg?

A

symptomatic patients with severe AR
or
asymptomatic patients with severe AR who have LV systolic dysfunction

437
Q

What type of murmur is aortic stenosis?

A

Ejection systolic murmur; has crescendo-decrescendo quality.

438
Q

Where is aortic stenosis heard loudest?

A

over aortic valve (2nd R ICP) and commonly radiates to carotid arteries. Loudest on espiration and when pt is sitting forward

439
Q

CP of aortic stenosis

A
  • slow rising pulse with narrow pulse pressure
  • non-displaced heaving apex beat (LV hypertrophy)
  • reduced or absent S2
  • reverse splitting of S2
440
Q

Causes of aortic stenosis?

A
  • degenerative calcification (>65yrs)
  • bicuspid valve disease (<65yrs)
  • RF
  • William’s syndrome (supravalvular aortic stenosis)
441
Q

Crescendo vs decrescendo vs crescendo-decrescendo murmur?

A

C= murmur increases in intensity
D= decrease in intensity
C-D= increase in intensity followed by decrease in intensity

442
Q

Is aortic stenosis C, D or C-D?

A

Crescendo-decresendo

443
Q

Is aortic regurg C, D or C-D?

A

Decrescendo

444
Q

Is mitral regurg C, D or C-D?

A

Crescendo-decrescendo

445
Q

Is mitral regurg C, D or C-D?

A

Decrescendo

446
Q

Mx for aortic stenosis

A
  • asymptomatic= observe
  • symptomatic= valave replacement
  • asymptomatic but valvular gradient >40mmHg and features eg. LV systolic dysfunction= valve replacement
447
Q

Mitral regurg occurs when blood leaks…

A

back through mitral valve on systole

448
Q

Where is mitral valve located?

A

between LA and V so regurg leads to less efficient heart as less blood pumped through body with each contraction

449
Q

What can happen as the degree of mitral regurg becomes more severe?

A

oxygen demand > heart can supply; leads to thicker myocardium; then fatigued when comes less efficient -> irreversible HF

450
Q

RFs for mitral regurg?

A

female, lower BMI, age, renal dysfunction, prior MI, prior mitral stenosis, collagen disorders

451
Q

Causes of mitral regurg?

A

post MI, mitral valve prolapse, infective endocarditis, RF, congenital

452
Q

What type of murmur is mitral regurg?

A

Pansystolic murmur heard loudest over apex and radiating to axilla. Severe may cause widely split S2.

453
Q

Where to listen for mitral regurg?

A

L 5th ICP mid-clav line; then left axilla.

454
Q

CP of mitral regurg?

A

most asymptomatic; symptoms due to failure of LV, arrythmias or pulmonary HTN so SOB, fatigue, oedema

455
Q

Ix for mitral regurg?

A

ECHO

  • ECG: broad p
  • CXR: cardiomegaly (enlarged LV and LA)
456
Q

What does mitral regurg sound like?

A

Like a high-pitched blowing, constant whoosh

457
Q

What can sometimes be felt with aortic stenosis?

A

palpable thrill

458
Q

What does aortic stenosis sound like?

A

Whoosh (starts soft, then loud, then soft again)

459
Q

Mx for mitral regurg?

A

Acute: nitrates, diuretics, +ve iontropes and intra-aortic balloon pump to increase cardiac output

Acute severe: surgical repair/replacement

460
Q

Mitral stenosis is when there is an obstruction of blood flow across…

A

the mitral valve from LA to LV; leads to high P in LA, pulmonary vessles and R heart

461
Q

Causes of mitral stenosis?

A

RHEUMATIC FEVER

462
Q

What type of murmur is mitral stenosis?

A

mid-late diastolic murmur best heard in expiration and loud in S1

463
Q

CP of mitral stenosis?

A

dyspnoea; haemoptysis (pink frothy or sudden haemorrhage); opening snap; low volume pulse; malar flush; AF

464
Q

What does an opening snap indicate in mitral stenosis?

A

mitral valve leaflets are still mobile

465
Q

Ix for mitral stenosis?

A
  • echo: cross section of mitral valve <1sqcm (normal 4-6)
  • cxr: may see LA enlargement
466
Q

Mx for mitral stenosis?

A
  • asymptomatic= monitor regular with echo
  • symptomatic= percutaneous mitral balloon valvotomy or mitral valve surgery
  • if AF: warfarin
467
Q

Bicuspid aortic valve?

A

1-2% of population; asymptomatic in childhood

468
Q

The majority of pts with bicuspid aortic valve eventually develop what?

A

aortic stenosis or regurg; higher risk of aortic dissection and aneurysm formation (on ascending aorta)

469
Q

What is bicuspid aortic valve associated with?

A

a left dominant coronary circulation (posterior descending artery arises from circumflex not right coronary) and Turner’s

470
Q

Around 5% of patients with what also have coarctation of the aorta?

A

bicuspid aortic valve

471
Q

What are biological heart valves usually made from?

A

Bovine or porcine

472
Q

Disadvantage of biological heart valves?

A

structural deterioration and calcification over time; so >65/70yrs receive

473
Q

Is long-term anticoag needed for biological heart valves?

A

No; may give warfarin for first 3m; low-dose aspirin long term

474
Q

Most common type of mechanical heart valve?

A

Bileaflet valve

475
Q

Pro and con of mechanical heart valve?

A

low failure rate but increased risk of thrombosis so long term anticoag needed

476
Q

Is long term anticoag needed for mechanical heart valve?

A

Yes, warfarin

477
Q

Target INR for mechanical heart valve anticoag?

A

Aortic: 3.0
Mitral: 3.5

478
Q

Why do you manage pts with AF?

A

reduce the increased risk of stroke

479
Q

What is atrial fibrillation (a supraventricular tachyarrhythmia)?

A

uncoordinated atrial electrical activation and so ineffective atrial contraction, causing an irregular and abnormally rapid vetricular rhythm

480
Q

How would you describe the rhythm of AF?

A

Irregularly irregular

481
Q

Example of regularly irregular rhythm?

A

Ventricular ectopics

482
Q

Classification of AF?

A
  • paraoxysmal (episodes terminate <7days of onset)
  • persistent (>7d)
  • longstanding persistent (>12m)
  • permanent (no more attempts to restore sinus rhythm)
483
Q

RFs for AF and its maintenance?

A

HTN, IHD, HF, valvular disease, intercurrent illness, electrolyte disturbances, thyrotoxicosis, alcohol XS

484
Q

CP of AF

A

usually asymptomatic, undetected and undiagnosed

485
Q

Cx of AF?

A

stroke, HF, mortality, tachycardia-induced cardiomyopathy

486
Q

When should you suspect a diagnosis of AF?

A

irregular pulse with or without symptoms eg. SOB, palpitation, chest pain, dizziness, syncope

487
Q

Ix for AF?

A
  • exam: pulse, auscultate heart and lungs
  • ECG
  • consider bloods, cxr, echo, ambulatory ecg monitoring (if paroxysmal AF)
488
Q

Routine review of someone with AF?

A

managing Cx; lifestyle modification; stroke and bleeding risk; monitor meds. Review symptoms, HR & rhythm, BP, adherence and adverse effects

489
Q

When should you arrange a prompt cardio referral in someone with AF?

A

recurrent or persistent symptoms despite rate and/or rhythm control treatment

490
Q

When to urgently admit someone to hospital with AF?

A

severe CP, haemodynamically unstable, decompensated HF

491
Q

When should you seek urgent cardio advice in someone with AF?

A

new onset within 48hrs, associated with structural disease or uncertainty about Mx

492
Q

Mx for pt with AF?

A
  • assess stroke and bleeding risk
  • lifestyle advice
  • consider DOAC for stroke prevention eg. apixaban (or wafarin 2nd line)
  • consider meds for rate control (BB or CCB)
493
Q

Signs of haemodynamic instability?

A

tachycardia (>150bpm); hypotension (S<90); severe dizziness, syncope, loss of consciousness; ischaemic chest pain or acute pulmonary oedema

494
Q

ECG for AF

A

absence of p waves, iregguarly-irregular R-R intervals,narrow QRS, ventricular rate 90-170bpm

495
Q

When should you arrange a transthoracic echo in someone with AF?

A
  • high risk/suspicion of underlying functional or structural heart disease and this will influence Mx
  • cardioversion (electrical or drug) is being considered
496
Q

Risk score for stroke?

A

CHA2DS2-VASc

497
Q

Assess pts bleeding risk?

A

ORBIT bleeding risk score

498
Q

When to offer a DOAC for pt with AF?

A
  • chadvasc score 2 or more
  • or if man and score of 1
499
Q

DOAC stands for and example?

A

direct-acting oral anticoag
apixaban, rivaroxaban

500
Q

What is warfarin?

A

vit KK antagonist; anticoag

501
Q

When to not offer rate control drug for pt with AF?

A

reversible cause; HF caused by AF; newonset AF <48hrs

502
Q

How to monitor pt on vit K antagonists eg. warfarin?

A

International normalised ratio (INR) until in therapeutic range

503
Q

What indicates that a pt on warfarin has sub-optimal anticoag control?

A
  • TTR <65%
  • 2 INR higher than 5, or one higher than 8 within 6m
  • 2 IRN <1.5 within 6m
504
Q

What factors may cause sub-optimal anticoag control for pt on warfarin?

A

impaired cognitive function, poor adherence, acute illness, lifestyle eg. XS alcohol; medications

505
Q

What meds may interact with warfarn?

A

antiplatelets, SSRIs, NSAIDs

506
Q

When should you review someone who has just started rate control drugs eg. BB?

A

within 1 week of starting or each dose titration

507
Q

Ventricular rate targets for someone on rate control drugs eg. BB?

A

<80bom at rest and <110bpm during moderate exercise.
<100bpm at rest may be appropriate

508
Q

When is the highest risk for embolism leading to stroke in AF?

A

During cardioversion- thrombus in fibrillating atrium suddenly pushed out when sinus rhythm restored. SO make sure pt anticoag before (at least 3w prior)

509
Q

What is electrical cardioversion synchronised to?

A

R wave to prevent delivery of a shock during the vulnerable period of cardiac repolarisation when V fib can be induced

510
Q

Types of cardioversioN?

A

Electrical (DC cardioversion) or pharmacological eg. amiodarone, flecainide

511
Q

Following a TIA, when should anticoag for AF be started?

A

immediately once excluded haemorrhage

512
Q

In acute stroke pts, in absence of haemorrhage, when should anticoag for AF be started?

A

after 2w. In the intervening period give antiplatelet

513
Q

When should pt be electrically cardioverted if have AF?

A

if haemodynamically unstable

514
Q

Form of supraventricular tachy characterised by succession of rapid atrial depolarisation waves?

A

Atrial flutter

515
Q

Flutter waves in atrial flutter may be more visible following what?

A

carotid sinus massage or adenosine

516
Q

What features suggest VT rather than SVT?

A

AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms

517
Q

What does the Mx of bradycardia depend on?

A

1) presence of signs indicating haemodynamic compromise
2) potenial risk of asystole

518
Q

what factors indicate haemodynamic compromise and so the need for Mx in bradycardia?

A
  • shock
  • syncope
  • MI
  • HF
519
Q

Signs of shock?

A

hypotension (SBP <90), pallor, sweating, cold, clammy extremities, confusion, impaired consciousness

520
Q

Mx of bradycardia and tachycardia

A
  • asssess with A-E
  • give O2 if appropriate and gain IV access
  • monitor ECG, BP, Sp02
  • Treat any reversible causes eg. electrolyte abnorm
  • any life threatening signs? (follow the different pathways)
521
Q

Life-threatening signs in someone with brady/tachy?

A

haemodynamically unstable; shock; syncope; MI; HF

522
Q

What may be signs that indicate risk of asystole (flat-line)?

A
  • recent asystole
  • Mobitz II AV block
  • complete heart block with broad QRD
  • V pause >3secs
523
Q

Mx for bradycardia with life threatening features?

A

Atropine 500mcg IV

524
Q

Mx if haemodynamically unstable with bradycardia and no response to atropine 500mcg IV or if there is a risk of asystole?

A
  • repeat atropine up to 3mg
  • isoprenaline 5mcg min-1 IV
  • adrenaline 2-10mcg min-1 IV
  • OR transcutaneuous pacing
525
Q

Mx for tachycardia if there are life threatening features?

A

Synchronised DC shock up to 3 attempts
- if unsuccessful: amiodarone 300mg IV over 10-30mins and repeat shock

526
Q

Mx for tachycardia with no life-threatening signs and broad QRS (>0.12s) that is irregular?

A

could be:
1) AF with BBB: same Mx as irregular narrow QRS tachy

2) polymorphic VT (eg. torsades)= gve Mg 2g over 10mins

527
Q

Mx for tachycardia with no life-threatening signs and broad QRS (>0.12s) that is regular?

A

1) VT (or uncertain)= amiodarone 300mg IV for 10-60min

2) previous diagnosis of SVT with BBB= Mx same as regular narrow QRS tachy

528
Q

Mx for tachycardia with no life-threatening signs and narrow QRs (<0.12s) that is irregular?

A

1) ?AF= BB, anticaog if >48hrs and amiodarone if evidence of HF

529
Q

Mx for tachycardia with no life-threatening signs and narrow QRs (<0.12s) that is regular?

A

1) vagal manoeuvre/fluids (normally decrease HR if sinus tachy)

if uneffective (usually SVT)

2) amiodarone 6mg rapid IV bolus, if unsuccessful give 12mg then if successful give 18mg AND monitor ECG
if uneffective
3) verapamil or BB

530
Q

What does supraventricular tachycardia (SVT) refer to?

A

any tachycardia that is not ventricular in origin

531
Q

SVT?

A

high HR, regular rhythm, narrow QRS.

532
Q

Acute Mx of SVT?

A
  • vagal manoeuvres eg. valsalva manoeuvre (eg. flow into empty syringe) or carotid sinus massage.
  • fluids (both fluids and vagal normally work for sinus tachy)
  • IV adenosine (usually needed)
  • electrical cardioversion
533
Q

Dose of adenosine in SVT?

A

rapid IV bolus of 6mg → if unsuccessful give 12 mg → if unsuccessful give further 18 mg

534
Q

Who is adenosine for SVT contraindicated in?

A

asthmatics- use veramil

535
Q

Prevention of SVT?

A

BB
radio-frequency ablation

536
Q

Torsades de pointes (rhythm strip can look like ribon- ‘twisting of the points’) is what?

A

Form of polymorphic ventricular tachy associated with long QT interval

537
Q

Why can torsades de pointes lead to sudden death?

A

can deteriorate into V Fib

538
Q

Causes of long QT interval?

A
  • congenital
  • drugs
  • electrolyte: hypocal; hypokal; hypomag
  • myocarditis
  • hypothermia
  • subarachnoid haemorrhage
539
Q

Drugs that can cause long QT interval?

A
  • antiarryhtmics eg. amiodarone
  • tricyclic antidep
  • antipyschotics
  • chloroquine
  • terfenadine
  • erythromycin (macrolides)
540
Q

Mx of torsades de pointes?

A

IV magnesium sulphate

541
Q

Ventricular tachycardia?

A

broad complex tachy originating from ventricular ectopic focus

542
Q

V tach can deteriorate to what?

A

V fib so need urgent Mx

543
Q

2 types of V tach?

A
  • monomorphic: commonly caused by MI. QRS complexes look same.
  • polymorphic: eg. torsades de pointes. QRS complexes look different
544
Q

Mx of V tach?

A

1) pulse? if no then ALS + defib +/- epi & amio
2) if pulse= adenosine
3) if doesn’t work then try other antiarrythmics: procainomide, amiodarone, lidocaine
4) prepare for synchronised electrical cardioversion

545
Q

What drug should not be used in V tach?

A

Verapamil

546
Q

Shockable rhythms?

A

Ventricular fibrillation and pulseless ventricular
tachycardia

547
Q

Non-shockable rhythms?

A

pulseless electrical activity and asystole

548
Q

Most dangerous rhythms?

A

V tach and V fib

549
Q

Adult advanced life support?

A

1) CPR 30:2 (100-120/min), attach defib
2) assess rhythm

3) shockable: 1 shock, immediately resume CPR for 2mins
3) non-shockable: continue CPR

4) whilst doing this obtain IV or intraosseous access
5) give adrenaline 1mg every 3-5mins and amiodarone 300mg after 3 shocks and then 150mg after 5 shocks

550
Q

Reversible causes of cardiac arrest?

A

H.ypoxia
H.ypovolaemia
H.yperkal, hypokal, hypogly, hypocal
H.+ (acidaemia)
H.ypothermia

T.hrombosis (coronary or pulmomary
T.ension pneumothorax
T.amponade (cardiac)
T.oxins

551
Q

How old is an infant vs a child?

A

Infant= <1yr
Child= 1yr-puberty

552
Q

Child advanced life support?

A

1) 5 rescue breaths
2) check femoral pulse
3) 15:2 (chest compressions 100-120/min)

553
Q

Depth for chest compressions?

A

Lower half of sternum by at least 1/3 of anterior-posterior dimension of chest (4cm for infant, 5cm for child/adult)

554
Q

Position for chest compressions in adults & children and infants?

A
  • adults & children= lower half of sternum
  • infants: 2 thumb encircling technique (on lower 1/3 of sternum)
555
Q

Features of pulmonary oedema/HF on CXR?

A

A.lveolar and interstitial oedema (bat’s wing appearance)
B. Kerley B-lines
C.ardiomegaly
D.ilated upper lobe vessels (increased blood flow to superior part of lung)
E.ffusion (pulmonary)

556
Q

What do Kerley B lines represent?

A

Expansion of interstitial space by fluid

557
Q

Symptoms of heart failure?

A

S.hortness of breath
O.rthopnea
F.atigue
A.nkle swelling

P.ulmonary oedema
C.old peripheries

cough worse at night, pink/frothy sputum; cardiac wheeze; cardiac cachexia

558
Q

Signs of heart failure?

A

elevated jugular venous pressure, bibasal crepitations and peripheral oedema.

559
Q

What causes heart failure?

A

structural and/or functional abnormality that produces raised intracardiac pressures and/or inadequate cardiac ouput at rest and/or at exercise

560
Q

CP of right sided HF

A

raised JVP, peripheral oedema (ankle/sacral), hepatomegaly, weight gain due to fluid retention, anorexia (cardiac cachexia)

561
Q

CP of left sided HF

A

pulmonary oedema: dyspnoea, cough, orthopnoea, paraoxysmal nocturnal dyspnoea, bibasal fine crackles

562
Q

Heart failure is classified into what 3 main categories?

A

1) reduced ejection fraction
2) midly reduced EF
3) preserved EF

563
Q

What is the New York Heart Association functional classification?

A

symptoms of heart failure are classified according to severity

564
Q

HF is usually caused by what?

A

myocardial dyfunction, systolic or diastolic or move

most common underlying pathophysiology= coronary artery disease

565
Q

Cx of HF?

A

arrhythmias, depression, cachexia, CKD, sexual dysfunction, sudden cardiac death

566
Q

Steps to follow if HF is suspected clinically? (Ix)

A
  • N-terminal pro b-type natriuretic peptide (NT-proBNP)
  • if normal then HF unlikely, if raised then refer for specialist assessment and echo
567
Q

What levels should NT-pro-BNP be to be referred for specialist assessment and transthoracic echo if suspected HF?

A

> 2000ng/L then urgent within 2w

400-2000 then refer within 6w

568
Q

Ix for all people with suspected HF

A
  • NT-pro-BNP (?may need transthoracic echo)
  • 12 lead ECG
  • Loop diuretic for symptom relief whilst waiting for assessment
    -? CXR, bloods, urine dip (protein and blood), peak flow
569
Q

Mx for HF with reduced ejection fraction?

A
  • diuretic if fluid overload
  • ACE inhibitor AND BB
    • mineralcorticoid receptor antagonist (MRA eg. spironolactone) if still symptomatic
  • specialist advice if still symptomatic
570
Q

Mx for HF with mildly reduced EF?

A
  • loop diuretic if fluid overload
  • consider ACE, BB and maybe MRA eg. spirinolactone
571
Q

Mx for HF with preserved ejection fraction?

A

low-medium dose loop diuretic if needed and refer if no response. Manage cormorbities eg. HTN, AF, IHD, DM

572
Q

What to give all pts with confirmed HF?

A
  • consider antiplatelet and statin
  • offer personalised exercise based cardiac rehab programme
  • lifestyle advice
  • assess nutritional status
  • screen for depression and anxiety
  • offer appropriate vaccinations (influenza and pneumococcol)
573
Q

RFs for HF?

A

Coronary artery disease, previous MI, HTN, AF, DM, drugs & alcohol, FHx sudden cardiac death <40yrs or HF

574
Q

What should you examine for in pt with suspected HF?

A

1) tachy (>100bpm) and pulse rhythm
2) laterally displaced apex beat, murmurs, added heart sounds (gallop rhythm)
3) HTN
4) increased JVP
5) enlarged liver
6) resp signs: tachypnoea, basal crep, pleural effusions
7) leg or sacrum oedema, ascites
8) obesity

575
Q

What is a common this for pts with HF to do?

A

sleep with lots of pillows (orthopnea)

576
Q

Dose of loop diuretic for symptomatic relief for pts with HF?

A

furosemide 20-40mg daily

577
Q

Natriuretic peptide levels may be reduced by what?

A

BMI >35
African-Caribbean origin
Drugs eg. diuretics, ACE, BB, ARB, mineralcortioid receptor antagonists eg. spironolactone

578
Q

Natriuretic peptide levels may be elevated by what?

A

> 70yrs; LV hypertrophy, MI, tachy; RV overload; hypoxia; pulmonary HTN; pulmonary embolism; CKD; sepsis; COPD; DM; liver cirrhosis

579
Q

Advice to give pt who has HF and is acutely unwell?

A

Maintain fluid intake and stop ACE, BB, MRA until eating and drinking normally

580
Q

Specialist Mx of HF of reduced EF and ACE+BB+MRA not worked?

A

Either of….
1) <35% EF replace ACI (or ARB) with sacubitril
2) + ivabradine for sinus rhythm with HR >75 and EF <35%
3) + hydralazine and nitrate (esp if African-C descent)
4) digoxin for HF with sinus rhythm to improve symptoms

5) may need cardiac resynchronisation therapy or insertion of ICD (implantable cardioverter defib)

581
Q

Ramipril initial and target dose for HF?

A

2.5mg once a day
then target of 5mg twice a day or 10mg once

582
Q

Initial and target dose of bisoprolol for HF?

A

1.25mg once a day
then target 10mg once a day

(1.25-2.5 to 3.75-5 week 1; 5mg od 4w then 7.5 od for 4w then 10mg)

583
Q

Dose of furosemide for HF?

A

20-40mg

584
Q

When is b-type natriuretic peptide (BNP) or NTproBNP produced by the heart?

A

in response to strain

585
Q

Why is exercise training good for HF?

A

improves symptoms but not hospital/mortality

586
Q

When is cardiac resynchronisation therapy used for pts with HF?

A
  • HF and wide QRS
  • biventricular pacing
  • improved CP and reduces hospitalisation in NYHA class III pts
587
Q

How many classes in NYHA classication?

A

4

588
Q

NYHA Class I

A

no symptoms
no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations

589
Q

NYHA Class II

A

mild symptoms
slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea

590
Q

NYHA Class III

A

moderate symptoms
marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms

591
Q

NYHA Class IV

A

severe symptoms
unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity

592
Q

What is acute heart failure (AHF)?

A

sudden onset or worsening of the symptoms of HF

may be present with or without Hx of pre-existing HF

593
Q

What is de-novo AHF?

A

acute HF without a past history of HF

594
Q

What is decompensated AHF?

A

background history of HF

595
Q

AHF is usually caused by a reduced…

A

cardiac output that results from functional or structural abnormality

596
Q

Causes of de-novo AHF?

A
  • increased cardiac filling pressures and myocardial dysfunction as a result of ischaemia -> reduced cardiac output and so hypoperfusion -> pulmonary oedema
  • less common: viral myopathy, toxins, valve dysfunction
597
Q

Causes of decompensated HF?

A
  • acute coronary syndrome
  • HTN crisis
  • acute arrhythmia
  • valvular disease
598
Q

Patients with HF are broadly characterised into what groups based on what they present with?

A
  • with or without hypoperfusion
  • with or without fluid congestion
599
Q

Symptoms of AHF?

A

breathlessness, reduced exercise tolerance, oedema, fatigue

600
Q

Signs of AHF?

A

cyanosis, tachy, elevated JVP, displaced apex beat, bibasal crackles (maybe a wheeze), S3 heart sound

601
Q
A
602
Q

over 90% pts with AHF have a normal or increased…

A

BP

603
Q

Ix for AHF

A
  • BNP/NT-pro-BNO
  • CXR
  • bloods (?infection, electrolyte, anaemia)
  • echo
604
Q

Acute Mx for HF

A

1) IV loop diuretic eg. furosemide
2) O2
3) Do not routinely offer nitrates, opiates, inotropes or vasopressors
4) CPAP if resp failure

605
Q

When to offer nitrates in acute Mx of HF?

A

pt with concomitant MI, severe HTN or regurgitant aortic/mitral valve

606
Q

When to offer inotropes or vasopressors in the acute Mx of HF?

A

pts who have potentially reversible cardiogenic shock
eg. dobutamine (inotrope) and norepinephrine (vasopressor)

607
Q

When should BB only be stopped in the acute Mx of HF?

A

if HR <50, second or third degree AV block or shock

608
Q

HF with reduced ejection fraction level?

A

<35-40% (measured with echo)

609
Q

HF with rEF typically has what type of dysfunction?

A

systolic (impaired myocardial contraction during systole)

610
Q

HF with pEF typically has what type of dysfunction?

A

diastolic (impaired V filling during diastole)

611
Q

Causes of systolic dysfunction (as so HF-rEF)?

A

IHD
Dilated cardiomyopathy
Myocarditis
Arrhythmias

612
Q

Causes of diastolic dysfunction (as so HF-pEF)?

A

Hypertrophic obstructive cardiomyopathy
Restrictive cardiomyopathy
Cardiac tamponade
Constrictive pericarditis

613
Q

Most urgent symptom of acute HF?

A

LV failure causing pulmonary oedema

614
Q

HR-rEF and HR-pEF typically develop what sided HF?

A

Left

615
Q

Why may HR-rEF and HR-pEF develop left-sided HF?

A

increased LV afterload eg. arterial HTN or aortic stenosis; or increased LV preload eg. aortic regurg resulting in backflow to LV

616
Q

What causes right sided HF?

A

increased RV afterload (eg. pulmonary HTN) or increased RV preload (eg. tricuspid regurg)

617
Q

Left and right sided HF can be used to describe the consequences of HF ie. the backward failure of output of…

A

either RV or LV

618
Q

What is high-output HF?

A

‘normal’ heart is unable to pump enough blood to meet metabolic needs of body

619
Q

Causes of high-output HF?

A

anaemia, AV malformation, Paget’s, pregnancy, thyrotoxicosis, thiamine def

620
Q

Angina?

A

chest pain/constricting discomfort caused by insufficient blood supply to myocardium

621
Q

causes of angina?

A

CAD, valvular disease, hypertrophic obstructive cardiomyopathy or HTN heart disease

622
Q

Stable angina?

A

occurs predictably with physical exertion or emotional stress and is relieved within mins of rest or with a dose of sublingual glyceryl trinitrate

623
Q

Unstable angina?

A

New (usually <24hrs) onset angina or abrupt deterioration in previously stable angina, often occurring at rest. Requires immediate admission/referral to hospital.

624
Q

Mx of stable angina?

A
  • lifestyle advice
  • Sublingual glyceryl trinitrate (GTN) for rapid relief
    + a BB or CCB (first line)
  • 2nd: long-acting nitrate eg. isosorbide mononitrate
  • poor control then add another drug from different class, if still poor then referral to cardio
625
Q

Drugs for secondary prevention of CV events for pts with angina?

A

low dose aspirin 75mg daily
ACE inhibitor
- Mx for lipid modification and HTN if appropriate

626
Q

Hospital admission is recommended for people with possible unstable angina presenting with what symptoms?

A
  • pain at rest (may be at night)
  • pain on minimal exertion
  • angina rapidly progressing despite medical Mx
627
Q

Typical stable angina CP?

A

constricting discomfort in chest, neck, shoulders, jaw or arms + precipitated by exercise + relieved by rest or GTN within 5 mins

628
Q

Atypical angina?

A

2/3 stable angina symptoms + GI discomfort +/or SOB +/or nausea

629
Q

Factors that make diagnosis of stable angina more likely?

A

age, male, CVD RFs, Hx of coronary artery disease eg. previous MI, coronary revascularisation

630
Q

Factors that make diagnosis of stable angina less likely?

A

continuous or prolonged pain, unrelated to activity; brought on my breathing; associated with dizziness, palpitations, tingling or diff swallowing

631
Q

Ix for angina?

A

Clinical
Resting ECG

632
Q

Hypertension?

A

Persistently raised arterial BP

633
Q

Hypertension increases the risk of what conditions?

A

HF, CAD, stroke, CKD, peripheral arterial disease, vascular dementia

634
Q

2 types of HTN?

A

primary and secondary

635
Q

Primary HTN (essential HTN)?

A

90% of pts.
NO identifiable cause.

636
Q

Secondary HTN?

A

has known underlying cause eg. renal, endocrine, or vascular disorder or use of certain drugs

637
Q

When should HTN be suspected?

A

Clinic SBP >=140mmHg or DBP >=90

638
Q

Ix for HTN?

A
  • Clinic BP: if 140/90 to 179/119 offer ambulatory BP monitoring (ABPM) to confirm diagnosis. If unable offer home blood pressure monitoring (HBPM).
  • If clinic 180/120 or higher= same day referral if indicated or Ix for target organ damage. Start antihypertensive Mx immediately.
639
Q

What should be done whilst waiting for confirmation of diagnosis of HTN?

A

Ix for target organ damage and 2 causes of HTN.
Assess CV risk.

640
Q

Classification of HTN (according to severity)?

A
  • Stage 1= clinic BP 140/90 to 159/99 AND ABPM or HBPM average 135/85 to 149/94
  • Stage 2= clinic 160/100 to 179/119 AND ABPM/HBPM 150/95 or higher
  • Stage 3= clinic SBP 180+ OR clinic DBP 120+
641
Q

Accelerated/malignant HTN?

A

severe increase in BP to 180/120 or higher (ofter >220/120) with signs of retinal haemorrhage and/or papilloedema (swelling of optic nerve)

642
Q

White-coat HTN?

A

BP unusually raised when measured during clinic but normal in other ‘non-threatening’ situations eg. home. Suspect if discrepancy of more than 20/10mmHg between clinic and avergae ABPM/HBPM readings.

643
Q

HTN referral for same day specialist assessment should be arranged when?

A
  • clinic BP 180/120+ with signs of retinal haemorrhage/papilloedema OR life-threatening symptoms
  • suspected phaeochromocytoma
644
Q

Life-threatening symptoms for pt with HTN?

A

new onset confusion, chest pain, signs of HF, AKI

645
Q

CP for suspected phaeochromocytoma?

A

labile or postural hypotension, headache, palpitations, pallor, abdo pain or diaphoresis

646
Q

Overall things the Mx of HTN includes?

A
  • lifestyle advice
  • antihypertensive drug Mx
  • ?statin
  • monitor
647
Q

When should pts with HTN be reviewed?

A

Annually= BP, review meds, discuss lifestyle, symptoms

648
Q

Target BP for <80yrs?

A

clinic= <140/90
ABPM/HBPM= <135/85

649
Q

Target BP for 80yrs+?

A

clinic= <150/90
ABPM/HBPM= <145/85

650
Q

BP target for someone with postural hypertension?

A

Base on standing BP

651
Q

How to measure BP in suspected HTN?

A

Relaxed setting, person quiet and seated with arm outstretched and supported.
Both arms.
If diff in reading between arms >15 then repeat. If still different use higher reading/

652
Q

When might automated BP devices not be accurate?

A

If pulse irregularity eg. AF so measure BP manually using direct auscultation over brachial artery if pulse irregular

653
Q

Measure BP for pt with suspected hypotension?

A

Measure seated/supine then again when standing for >1min before measurement. If SBP falls by 20+ when standing, measure subsequent BP with person standing

654
Q

What if BP measured in clinic 140/90 or higher?

A

Take second measurement and record the lower of the 2

655
Q

How to use HBPM?

A

For each BP reading: take 2, 1 min apart whilst seated. Record twice daily (morning and evening) for >4days (ideally 7). Discard first day measurements and use average of all values to confirm HTN.

656
Q

When to confirm diagnosis of HTN?

A

Clinic BP 140/90 or higher AND ABPM/HBPM average of 135/85 or higher

657
Q

When to suspect masked HTN?

A

If clinic BP normal (<140/90) but BP are higher using ABPM or HBPM

658
Q

When to suspect secondary HTN?

A

Pts <40yrs or those with accelerated HTN or if suspicious of underlying cause eg. meds

659
Q

What if HTN is not diagnosed?

A
  • ?evidence of target organ damage
  • if not then measure clinic BP every 5yrs after or more frequently if clinic BP close to 140/90
660
Q

How to Ix for target organ damage in pt with HTN?

A
  • haematuria
  • urine albumin:creatinine ratio (?protein in urine)
  • HbA1c
  • electrolytes, creatine and eGFR (?CKD)
  • examine fundi (HTN retinopathy)
  • ECG

specialist Ix if target organ damage or 2 cause of HTN

661
Q

Assess CV risk in pt with HTN?

A
  • serum total cholesterol and HDL cholesterol
  • QRISK
662
Q

HTN Mx if <55yrs, with or without DMT2?

A

1) ACEi or ARB
2) ACEi or ARB + CCB or diuretic
3) ACEI or ARB + CCB + thiazide-like diuretic
4) if K+ <=4.5 then + spirinolactone. If K+ >4.5 then + BB
5) uncontrolled on 4 drugs= specialist advice

663
Q

HTN Mx if 55yrs or over, Black-African or African-Caribbean origin, without DMT2?

A

1) CCB
2) CCB + ACEi (or ARB) OR diuretic
3) ACEi/ARB + CCB + thiazide like diuretic
4) if K+ <=4.5 then + spirinolactone. If K+ >4.5 then + BB
5) uncontrolled on 4 drugs= specialist advice

664
Q

When should you use an ARB over an ACEi in HTN MX?

A

If ACEi side effects eg. cough not tolerated

665
Q

When to use thiazide like diuretic over CCB in HTN Mx?

A

If not tolerated eg. because of oedema

666
Q

When to use CCB first line in HTN Mx over ACEi/ARB?

A

if 55 yrs or over and DO NOT have DMT2
or
black African or African-Caribbean origin and don’t have DMT2

667
Q

What to do in HTN Mx if have diabetes and are black African?

A

use ARB in perference to ACE

668
Q

What to do in HTN Mx before offering another drug in addition to others?

A

review and ensure taking optimal tolerated doses; discuss adherence

669
Q

ACEi example and dose for HTN Mx?

A

Ramipril

staring dose= 1.25-2.5mg OD
maintenance= 2.5-10mg OD
max= 10mg OD

670
Q

ARB example and dose of HTN Mx?

A

Candesartan

starting= 8mg OD
maintenance= 8mg OD
max= 32mg OD

671
Q

Thiazide-like diuretic example and dose for HTN Mx?

A

Indapamide

2.5mg in morning (immediate release) or 1.5mg (modified)

672
Q

CCB example and dose for HTN Mx?

A

Amlodipine

start= 5mg OD
maintenance= 5-10mg OD
max= 10mg OD

673
Q

Spironolactone dose for HTN Mx?

A

25mg OD with food

674
Q

BB example and dose for HTN Mx (last line)?

A

Bisoprolol

start= 5mg OD in morning
maintenance= 10mg OD
max= 20mg OD

675
Q

If pt BP is very high eg. >200/120mmHg what symptoms might they get? (HTN typically asymptomatic)

A

headaches, visual disturbance, seizures

676
Q

Why do you go ECG, fundoscopy and urine dip on pt with newly diagnosed HTN?

A

ensure don’t have end-organ damage.
eg. F= HTN retinopathy
UD= renal disease (cause or consequence of HTN)
ECG= LV hypertrophy or IHD

677
Q

How to measure BP in children?

A
  • correct cuff size is 2/3 length of upper arm
  • 4th Korotkoff sound used to measure DBP until adolescence, then 5th Korotkoff sound can be used
  • compare results with graph of normal values for age
678
Q

What is the most common cause of HTN in younger children?

A

secondary HTN eg. renal parenchymal disease

679
Q

Causes of HTN in children?

A
  • renal parenchymal disease
  • renal vascular disease
  • coarctation of aorta
  • phaeochromocytoma
  • congenital adrenal hyperplasia
  • as child is older: essential/primary HTN
680
Q

What drugs can cause HTN?

A

steroids, NSAIDs, COCP, monoamine oxidase inhibitors

681
Q

Most common cause of secondary HTN?

A

Primary hyperaldosteronism (incl. Conn’s)

682
Q

Renal causes of HTN?

A

glomerulonephritis
pyelonephritis
adult polycystic kidney disease
renal artery stenosis

683
Q

Endocrine causes of HTN?

A
  • primary hyperaldosteronism
  • phaeochromocytoma
  • Cushing’s syndrome
  • Liddle’s syndrome
  • congenital adrenal hyperplasia (11-beta hydroxylase deficiency)
  • acromegaly
684
Q

Other causes of HTN?

A

pregnancy
coarctaation of aorta

685
Q

Strongest RF for developing infective endocarditis?

A

previous episode of endocarditis

686
Q

What valve is most commonly affected in endocarditis?

A

mitral

687
Q

What types of pts are typically affected by endocarditis?

A
  • prev normal valves
  • rheumatic valve disease
  • prosthetic valves
  • IVDUs
  • congenital heart defects
  • recent piercings
688
Q

Fever and new murmur

A

infective endocarditis likely

689
Q

Causes of infective endocarditis?

A

staph aureus (most common)
strep viridans
staph epidermidis

690
Q

poor oral hygiene/recent dental surgery- cause of IE?

A

strep viridans

691
Q

Murmur in IE caused by strep viridans?

A

mitral/aortic regurg

692
Q

Infective endocarditis in IVDU or acute presentation

A

staph aureus

693
Q

Murmur in IE caused by staph aureus

A

Tricuspid (splitting of 2nd heart sound)

694
Q

Infective endocarditis following prosthetic valve surgery

A

staph epidermidis

695
Q

Streptococcus bovis (s. gallolyticus) that can cause infective endocarditis is associated with what?

A

colorectal cancer

696
Q

Non-infective causes of endocarditis?

A

SLE
malignancy (marantic endo)

697
Q

Culture negative causes of infective endocarditis?

A

prior Abx therapy
Coxiella burnetii
Bartonella
HACEK: haemophilus, actinobacillus, cardiobacterium, eikenella, kingella

698
Q

Infective endocarditis?

A

inflam of endocardium (inner lining of heart) and valves primarily caused by bacteria

699
Q

Criteria to diagnose infective endocarditis?

A

Modified Duke Criteria

700
Q

When is infective endocarditis diagnosed using the Modified Duke criteria? (4)

A

1) pathological criteria positive, or

2) 2 major criteria, or

3) 1 major and 3 minor, or

4) 5 minor

701
Q

Infective endocarditis: what is a positive pathological criteria on Modified Duke?

A

1) microorganisms in a vegetation on histology (autopsy or surgery)
OR
2) Pathologic legions on histology of vegetation or intracardiac abscess

702
Q

Duke Modified Criteria for infective endocarditis: what is included in the major criteria?

A

1) Typical microorganisms consistent of IE from 2 separate blood cultures taken >12hrs apart

2) Evidence of endocardial involv. on ECHO

703
Q

Duke Modified Criteria for infective endocarditis: what is included in the minor criteria?

A

1) Predisposing heart condition or IVDU

2) Fever >38

3) Vascular phenomena: conjunctival haemorrhages, Janeway’s lesions, intracranial haemorrhage, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, splinter H

4) Immunologic phenomena: Osler’s nodes, Roth’s spots, Glomerulonephritis, rheumatoid factor

5) Microbio evidence: +ve blood culture that doesn’t meet major criteria or serological evidence of active infection consistent with IE

704
Q

Ix for infective endocarditis?

A
  • Blood cultures (1st)
  • Trans-oesphageal ECHO (vegetation)
  • ECG: prolonged PR
705
Q

Infective endocarditis CP?

A

F.ever >38
R.oth spots
O.cler’s nodes= fingertips, painful
M.urmur

J.aneway lesions: palm, painless
A.naemia
N.ail bed splinter haemorrhages
E.mboli

Predisposing heart condition, IVDU, recent dental surgery

706
Q

Poor prognostic factors of infective endocarditis?

A
  • staph aureus
  • prosthetic valve
  • culture -ve endocarditis
  • low complement levels
707
Q

Mortality of infective endocarditis according to organism?

A

staphylococci - 30%
bowel organisms - 15%
streptococci - 5%

708
Q

Summary of Mx of infective endocarditis?

A
  • inital blind Abx therapy
  • then specific Abx therapy
  • ?surgery
709
Q

Mx of infective endocarditis: inital blind Abx therapy (empirical)? What is allergic/MRSA/sepsis? What if prosthetic valve?

A
  • Amoxicillin, consider + low dose gentamicin
  • MRSA, severe sepsis or penicillin allergic: vancomycin + low dose gentamicin
  • If prosthetic valve: vancomycin + rifampicin + low dose gentamicin
710
Q

Specific Abx therapy for infective endocarditis if native valve (normal) caused by staphlococci? Allergic/MRSA?

A

Flucloxacillin

Allergic/MRSA= vancomycin + rifampicin

711
Q

Specific Abx therapy for infective endocarditis if prosthetic valve caused by staphlococci? Allergic/MRSA?

A

Flucloxacillin + rifampicin + low-dose gentamicin

Allergic/MRSA=
vancomycin + rifampicin + low-dose gentamicin

712
Q

Specific Abx therapy for infective endocarditis if caused by fully-sensitive strep (eg. viridans)? Allergic?

A

Benzylpenicillin

Allergic= vancomycin + low-dose gentamicin

713
Q

Specific Abx therapy for infective endocarditis if caused by less sensitive strep? Allergic?

A

Benzylpenicillin + low-dose gentamicin

Allergic= vancomycin + low-dose gentamicin

714
Q

Typical Abx if allergic to penicillin or MRSA (eg. if use flucloxacillin)?

A

vancomycin

715
Q

Indications for surgery in infective endocarditis?

A
  • severe valvular incompetence
  • aortic abscess
  • infections resistant to Abx
  • funal infections
  • recurrent emboli after Abx
716
Q

Pts with what cardiac conditions are at incresed risk of developing infective endocarditis?

A
  • acquired valvular heart disease with stenosis or regurg
  • hypertrophic cardiomyopathy
  • previous IE
  • structural congential heart disease
  • valve replacement
717
Q

Advice to give pts who are at increased risk of IE?

A
  • benefits and risks of Abx prophylaxis and why it’s no longer recommeneded
  • importance of good oral health
  • CP of IE
  • risks of invasive procedures incl. non medical eg. piercing or tattoos
718
Q

Is Abx prophylaxis for IE routinely recommended?

A

No

719
Q

What should pts who take standard release isosorbide mononitrate for stable angina Mx do to prevent development of nitrate tolerance and reduced efficacy?

A

use asymmetric dosing interval to maintain a daily nitrate-free time of 10-14hrs.

(not seen in pts who take modified release)

720
Q

Another name for stable angina?

A

Angina pectoris

721
Q

Causes of mitral valve prolapse?

A

usually idiopathic but can be associated with other conditions and CVD

722
Q

Mitral valve prolapse? (Barlow syndrome)

A

the cusps of the mitral valve become enlarged or strecth and these bulge (prolapse) into LA as heart contracts

Usually doesn’t require Mx unless causes severe regurg

723
Q

Mitral valve prolapse associations?

A

congenital heart disease: PDA, ASD
cardiomyopathy
Turner’s syndrome
Marfan’s syndrome, Fragile X
osteogenesis imperfecta
pseudoxanthoma elasticum
Wolff-Parkinson White syndrome
long-QT syndrome
Ehlers-Danlos Syndrome
polycystic kidney disease

724
Q

Features of mitral valve prolapse?

A
  • atypical chest pain/palpitations
  • mid-systolic click (later if pt squatting)
  • late systolic murmur (longer if pt standing)
725
Q

Cx of mitral valve prolapse?

A

mitral regurg, arrhythmias (long QT), emboli, sudden death

726
Q

Myocarditis?

A

Inflamm of myocardium

727
Q

Consider what is a young pt with acute chest pain?

A

myocarditis

728
Q

Causes of myocarditis?

A
  • viral: coxsackie B, HIV
  • bacteria: diptheria, clostridia
  • spirochaetes: Lyme disease
  • protozoa: Chagas’ disease, toxoplasmosis
  • autoimmune
  • drugs: doxorubicin
729
Q

CP of myocarditis?

A
  • usually young pt with acute Hx
  • chest pain
  • dyspnoea
  • arrhythmias
730
Q

Ix for myocarditis?

A
  • Bloods= Increased: CRP & ESR, cardiac enzymes and BNP, elevated troponin
  • ECG
731
Q

ECG findings in myocarditis?

A
  • tachycardia
  • arrhythmias
  • ST/T wave changes incl ST elevation and T wave inversion
732
Q

Mx for myocarditis?

A
  • TUC eg. Abx if bacterial causes
  • supportive treatment eg. of HF or arrhythmias
733
Q

Cx of myocarditis?

A
  • HF
  • arrhythmia, possibly leading to sudden death
  • dilated cardiomyopathy: usually a late complication
734
Q

Classic features of cardiac tamponade?

A

Beck’s triad: hypotension, muffled heart sounds, raised JVP

735
Q

CP of cardiac tamponade?

A
  • Beck’s triad
  • dyspnoea
  • tachycardia
  • absent Y descent on JVP (due to limited RV filling)
  • pulsus paradoxus
  • Kussmaul’s sign rare
736
Q

ECG feature of cardiac tamponade?

A

electrical alternans (alternating QRS amplitude seen in any or all leads with no other changes to conduction pathways)

737
Q

Pulsus paradoxus?

A

abnormally large drop in BP during inspiration

738
Q

Kussmaul’s sign?

A

Paradoxical increase in JVP that occurs during inspiration. Seen in cardiac tamponade, constrictive pericarditis, restrictive cardiomyopathy

739
Q

What does an absent Y descent mean?

A

when filling of RV is impaired following opening of tricuspid valve

eg. in cardiac tamponade:
TAMponade=TAMpaX (no Y)

740
Q

Ix for cardiac tamponade?

A

transthoracic echo and ECG

741
Q

What does X and Y mean in JVP?

A

X descent= RA relaxation
Y descent= RV filling (tricuspid opens)

742
Q

Difference in features between cardiac tamponade and constrictive pericarditis?

A

CT= JVP absent Y descent; pulsus paradoxus present; Kussmaul’s sign rare

CP= X + Y present; absent pulsus paradoxus; present Kussmaul’s sign; pericardial calfication on CXR

743
Q

Causes of constrictive pericarditis?

A

any cause of pericarditis, particularly TB

744
Q

Constrictive pericarditis?

A

Granulation tissue formation in pericardium results in loss of pericardial elasticity leading to restriction in V filling

745
Q

CP of constrictive pericarditis?

A
  • dyspnoea
  • RHF: elevated JVP, ascites, oedema, hepatomegaly
  • JVP shows X and Y descent
  • pericardial knock (loud S3)
  • Positive Kussmaul’s sign
746
Q

Ix for constrictive pericarditis?

A

CXR: pericardial calcification

747
Q

Mx for constrictive pericarditis?

A

NSAIDs, diuretics
Only definitive Mx= pericardiectomy but use in caution if mild disease as high mortality

748
Q

Causes of pericardial effusion?

A

infectious pericarditis: viral, tuberculosis, pyogenic spread from septicaemia and pneumonia
uraemia
idiopathic
post myocardial infarction (including Dressler’s syndrome)
malignancy
heart failure
nephrotic syndrome
hypothyroidism
trauma

749
Q

Pericardial effusion can be made of what?

A

Transudates (low protein content)
Exudates (associated with inflammation)
Blood
Pus
Gas (associated with bacterial infections)

750
Q

Pericardial effusion?

A

XS fluid collects within pericardial sac; can be cute or chronic; can fill entire pericardial cavity or only a localised section

751
Q

Pericardial effusion: transudative effusion?

A

Results from increased venous pressure that can reduce drainage from pericardial cavity. May occur in congestive HF and pulmonary HTN.

752
Q

Pericardial effusion: exudative effusion?

A

after any inflam process affecting pericardium (pericarditis) eg. infection, autoimmune, trauma, malignancy, methotrexate

753
Q

Rupture of heart or aorta can cause bleeding into the pericardial cavity, resulting in rapid onset cardiac tamponade- rupture may be due to what?

A

MI, trauma or aortic dissection type A

754
Q

CP of pericardial effusion?

A

chronic ones may be asymptomatic until pressure rises.

  • chest pain, SOB, fullness in chest, orthopnoea
  • quiet HS, pulsus paradoxus, hypotension, raised JVP, fever & pericardial rub (with pericarditis)
755
Q

Pericardial effusion may compress surrounding structures causing other symptoms like….

A
  • Phrenic nerve compression= hiccups
  • Oseophageal= dysphagia
  • Recurrent laryngeal nerve= hoarse voice
756
Q

Ix for pericardial effusion?

A
  • ECHO (gold & 1st)
  • fluid analysis: underlying cause eg. protein content, bacterial culture, viral PCR, cytology & tumour markers
757
Q

Mx for pericardial effusion?

A
  • TUC eg. inflamm: NSAIDs and colchicine
  • Draining: needle pericardiocentesis
758
Q

Pericardial window?

A

surgical procedure where portion of pericardium removed creating a ‘window’/fistula to allow fluid to drain from pericardial cavity to pleural carvity/peritoneal cavity

759
Q

Membrane that surrounds the heart?

A

Pericardium/pericardial sac

760
Q

What is the pericardium made from?

A

2 layers with small amount of fluid in between (<50ml) providing lubrication to allow heart to beat without friction. These layers separate heart from rest of contents of mediastinum.

761
Q

What is between the 2 layers of the pericardium?

A

‘potenital space’ called pericardial cavity, layers usually touch eachother which is my it is only a potential space. Small amount of fluid.

762
Q

Potential space of pericardial cavity fills with fluid?

A

Pericardial effusion. Creates inward pressure on heart making it more difficult to expand during diastole (filling of heart).

763
Q

What is it called when the pericardial effusion is large enough to raise intra-pericardial pressure?

A

Cardiac tamponade. Leads to reduced filling of heart during diastole resulting in decreased cardiac output during systole.

764
Q

Transudate?

A

Fluid buildup caused by systemic conditions that alter the pressure in blood vessels, causing fluid to leave the vascular system. Eg. due to increased hydrostatic pressure or decreased oncotic pressure

765
Q

Exudate?

A

Fluid buildup caused by tissue leakage due to inflammation or local cellular damage.

766
Q

Transudate vs exudate?

A

Transudate:
- Protein <30g/L
- Clear
- Low cell & protein content
- Causes: HF, liver cirrhosis, nephrotic syndrome

Exudate:
- Protein >30g/L
- Cloudy, yellow or bloody
- High cellular & protein content
- Causes: inflam eg. infections (eg. pneumonia), RA, malginancy

767
Q

Are transudate and exudate both extracellular?

A

Yes they both accumulate in extracellular space eg. tissues or body cavities outside of cells.

768
Q

Exudate diagnostic criteria?

A

High protein content (>3 g/dL).
High specific gravity (>1.020).
High LDH (lactate dehydrogenase) levels.

769
Q

Transudate diagnostic criteria?

A

Low protein content (<3 g/dL).
Low specific gravity (<1.012).
Low LDH levels.

770
Q

Reflex syncope?

A

Transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.

771
Q

Most common cause of syncope?

A

Reflex syncope

772
Q

Subtypes of reflex syncope subtypes?

A
  • vasovagal (faiting)
  • situational: cough, micturition, GI
  • carotid sinus syncope
773
Q

Vasovagal (reflex) syncope?

A
  • ‘fainting’
  • Typically in sitting or standing position & can be triggered by emotion pain or stress.
  • CP: warm/hot or light headed prior
  • <1-2mins
  • prolonged fatigue/amnesia is usual after regaining consciousness
774
Q

What can occur during uncomplicated vasovagal syncope?

A

brief myoclonic jerks

775
Q

Carotid sinus syncope?

A

Type of fainting caused by exaggerated response to stimulation of carotid sinus located in neck. Leads to sudden drop in HR & BP -> reduced blood flow to brain and fainting.
Triggers= tight collars, neck pressure, head movements.
- Diagnosis= carotid sinus massage or tilt table test
- Mx: avoid triggers; severe- pacemaker to regulate HR

776
Q

Signs of tricuspid regurg?

A
  • pan-systolic murmur
  • prominent/giant V waves in JVP
  • pulsatile hepatomegaly
  • left parasternal heave
777
Q

Where is loin pain located?

A

Between lower ribs and buttocks on either side of the spine

778
Q

Where can loin pain originate?

A

Kidneys, adrenal glands, parts of colon, MSK components, referred from abdo or pelvic organs

779
Q

Renal capsule, ureter and muscles are supplied with what that transmit pain signals to the CNS?

A

nociceptors

780
Q

Differential diagnosis for loin pain

A
  • ruptured AAA
  • renal colic
  • pyleonephritis
  • MSK pain
  • radiculopathy (compression or inflam of spinal nerve roots may cause referred pain)
781
Q

Ix for loin pain?

A

identifty life-threatening conditions eg. ruptured AAA; history; physical abdo renal and neuro exam; bloods (FBC, renal function); urinalysis; USS/CT; pain Mx

782
Q

What may make atypical presentation of ACS more likely?

A

female, elderly, diabetic

783
Q

Differential diagnosis for chest pain?

A

MI
pneumothorax
PE
pericarditis
dissecting aortic aneurysm
GORD
MSK chest pain
perforated peptic ulcer
shingles
Boerhaaves syndrome

784
Q

Referral criteria for chest pain?

A
  • current or <12hrs AND abnormal ECG= emergency admission
  • chest pain 12-72hrs ago= refer for same day hospital assessment
  • chest pain >72hrs ago= ECG and toponin then decide
785
Q

Mx for pts in whom stable angina can’t be excluded by clinical assessment alone (eg. symptoms consistent with typical/atypical angina OR ECG changes)?

A

1st line: CT coronary angiography
2nd line: non-invasive functional imaging (?reversible mycardial ischaemia)
3rd: invasive coronary angiography

786
Q

Examples of non-invasive functional imaging?

A
  • myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) or
  • stress echocardiography or
  • first-pass contrast-enhanced magnetic resonance (MR) perfusion or
  • MR imaging for stress-induced wall motion abnormalities
787
Q

You can characterise congenital heart disease into what?

A

Cyanotic and acyanotic

788
Q

Most common causes of acyanotic congential heart disease?

A
  • Ventricular septal defects (VSD) (most common, 30%)
  • atrial septal defect (ASD)
  • patent ductus arteriosus (PDA)
  • coarctation of aorta
  • aortic valve stenosis
789
Q

What are more common- VSDs or ASDs?

A

VSDs but in adults ASDs more common new diagnosis as generally present later

790
Q

Most common causes of cyanotic congenital heart disease?

A
  • tetralogy of Fallot
  • transposition of great arteries (TGA)
  • tricuspid atresia
791
Q

What is more common- tetralogy of Fallot or TGA?

A

Fallot but at birth TGA is more common lesion as pts with Fallot’s generally present at around 1-2m

792
Q

The presence of cyanosis in pulmonary valve stenosis depends on what?

A

the severity and any other coexistent defects

793
Q

When is peripheral cyanosis eg. in hands and feet very common?

A

1st 24hrs of life and may occur when child is crying or unwell

794
Q

Central cyanosis clinical diagnosis?

A

conc of reduced Hb in blood >5g/dl

795
Q

What can be used to differentiate cardiac from non-cardiac causes of cyanosis in neonatal period?

A

Nitrogen washout test (hyperoxia test): infant given 100% O2 for 10mins then ABG taken. A pO2 of <15kPa= cyanotic congenital heart disease

796
Q

Initial Mx of suspected cyanotic congenital heart disease?

A

supportive care + prostaglandin E1 eg. alprostadil

797
Q

Why is prostaglandin E1 eg. alprostadil used in the inital Mx of suspected cyanotic congenital heart disease?

A

Used to maintain a patent ductus arteriosus in ductal-dependent congenital heart defect.
Acts as a holding measure until a definite diagnosis is made and surgical correction performed.

798
Q

Acrocyanosis?

A

seen in healthy newborns and refers to cyanosis around the mouth and extremities (eg. hands & feet)

799
Q

How is acrocyanosis differentiated from other causes of peripheral cyanosis with signif pathology?

A

occurs immediately after birth in health infants; common finding as may persist for 24-48hrs

800
Q

Tetralogy of Fallot (TOF)?

A

most common cause of cyanotic congenital heart disease

801
Q

When does TOF typically present?

A

1-2m old, may not be picked up until 6m

802
Q

TOF is a result of what?

A

anterior malalignment of the aorticopulmonary septum

803
Q

4 characteristic features of TOF?

A
  • ventricular septal defect (VSD)
  • RV hypertrophy
  • overriding aorta
  • pulmonary stenosis
804
Q

what can cause RV outflow tract obstruction?

A

pulmonary stenosis

805
Q

What is the heart defect- overriding aorta?

A

where aorta is positioned over both the LV & RV (not just the LV); causes it to override the VSD so that it receives blood from both the LV and RV (oxygen rich AND oxygen poor blood); so reduces amount of O2 body receives

806
Q

What determines the degree of cyanosis and clinical severity in TOF?

A

severity of pulmonary stenosis (and so RV outflow tract obstruction)

807
Q

CP of TOF?

A
  • cyanosis
  • ‘tet’ spells
  • tachypnoea
  • loss of consciousness
808
Q

what are tet spells in TOF?

A

infants may develop episodic hypercyanotic tet spells due to near occulasion of RV outflow tract.
may become pale/blue (esp fingers and lips); diff breathing; irritable; loss of consciousness

809
Q

Other features of TOF (shunt? murmur?)?

A
  • causes R-to-L shunt
  • ejection systolic murmur due to pulmonary stenosis (VSD doesn’t usually cause murmur)
  • right-sided aortic arch in 25% pts
810
Q

In TOF what does CXR and ECG show?

A
  • cxr= boot-shaped heart
  • ECG= RV hypertrophy
811
Q

Mx of TOF?

A
  • surgical repair often in 2 parts
  • beta-blockers for cyanotic episodes to reduce infundibular spasm
812
Q

Transposition of the great arteries (TGA)?

A

form of cyanotic congenital heart disease caused by the failure of the aorticopulmonary septum to spiral during septation (aorta and pulmonary artery swap places)

813
Q

Who are at increased risk of TGA?

A

children of diabetic mothers

814
Q

Basic anatomical changes in TGA?

A
  • aorta leaves RV
  • pulmonary trunk leaves LV
815
Q

Clinical features of TGA?

A
  • cyanosis
  • tachypnoea
  • loud single S2
  • prominent RV impulse
  • ‘egg-on-side’ appearance on CXR
816
Q

Mx for TGA?

A
  • maintenance of ductus arteriosis with prostaglandins
  • definitive Mx= surgical correction
817
Q

Coarctation of the aorta?

A

congenital narrowing of the descending aorta

818
Q

Association of coarctation of aorta?

A

Turner’s syndrome.

But is more common in males.

819
Q

Coarctation of aorta associations?

A

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

820
Q

Features of coarctation of the aorta?

A
  • infancy: HF
  • adult: HTN
821
Q

Signs of coarctation of aorta on examination?

A
  • radio-femoral delay
  • mid systolic murmur, maximal over the back
  • apical click from the aortic valve
  • notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
822
Q

What causes the first heart sound (S1)?

A

Closure of mitral and tricuspid valves

823
Q

What causes the second heart sound (S2)?

A

aortic and pulmonary valve closure

824
Q

S1?

A

closure of mitral and tricuspid valves

825
Q

What causes soft S1?

A

if long PR or mitral regurg

826
Q

What causes loud S1?

A

mitral stenosis

827
Q

S2?

A

closure of aortic and pulmonary valves

828
Q

What causes a soft S2?

A

aortic stenosis

829
Q

Is splitting of S2 during inspiration normal?

A

Yes

830
Q

What is a third heart sound (S3) caused by?

A

diastolic filling of the ventricle

831
Q

When is a S3 normal?

A

If <30yrs old (may persistent in women up to 50yrs)

832
Q

What is a gallop rhythm?

A

when S1 and S2 followed by pathological S3 and/or S4. commonly associated with LV failure

833
Q

When may S3 be heard?

A

LV failure (eg. dilated cardiomyopathy), constrictive pericarditis and in mitral regurg

834
Q

What is S3 called in constrictive pericarditis?

A

pericardial knock

835
Q

When may a S4 (fourth heart sound) be heard?

A

in aortic stenosis, HOCM, HTN

836
Q

What causes S4?

A

Atrial contraction against stiff ventricle; therefore coincides with P wave on ECG

837
Q

In HOCM a double apical impulse may be felt as a result of a…

A

palpable S4

838
Q

Site of auscultation for pulmonary valve?

A

Left 2nd ICP at upper sternal border

839
Q

Site of auscultation for mitral valve?

A

Left 5th ICP just medical to mid clavicular line

839
Q

Site of auscultation for aortic valve?

A

Right 2nd ICP at upper sternal border

840
Q

Site of auscultation for tricuspid valve?

A

Left 4th ICS and lower left sternal border

841
Q

Causes of loud S2?

A
  • HTN: systemic (loud A2) or pulmonary (loud P2)
  • hyper dynamic states
  • ASD without pulmonary HTN
842
Q

Causes of a soft S2?

A

Aortic stenosis

843
Q

Causes of a fixed (in the middle) split of S2?

A

atrial septal defect

844
Q

Causes of a widely split S2?

A
  • deep inspiration
  • RBBB
  • pulmonary stenosis
  • severe mitral regurg
845
Q

Causes of a reversed (paradoxical) split S2 (P2 occurs before A2)?

A
  • LBBB
  • severe aortic stenosis
  • RV pacing
  • WPW type B (causes early P2)
  • patent ductus arteriosus
846
Q

What does S2 sound like?

A

Higher pitched and shorter duration than S1. ‘dub’ section of ‘lub-dub’

847
Q

What is S2 split into?

A

Closure of aortic (A2) and pulmonary (P2) valves at end of V systole

848
Q

When do you hear the components of S2?

A
  • A2 normally slightly before P2, P2 softer except in certain conditions it is more pronounced.
  • Normal S2: ‘dub’
  • Split S2: NORMAL during INSPIRATION where you can hear A2 and P2 distinctively (lub-d-dub’)
849
Q

What does a split S2 mean?

A

In normal physiology, occurs during inspiration. The 2 components of S2 can be heard separately due to the delay in P2 (resulting in a split sound ‘d-dub’ A2-P2)

850
Q

When is S2 split normal?

A

During inspiration- corresponds to A2 and P2. (d-dub)

NOT during expiration- sound be heard as a single sound (dub) and not a split

851
Q

Types of split S2?

A
  • physiological (normal in children and young adults, widens with inspiration and narrows with expiration)
  • fixed split S2
  • wide split S2
  • paradoxical split S2
852
Q

Fixed split of S2?

A

The split (between A2 and P2) remains constant during both inspiration and expiration.

853
Q

What is associated with a fixed split of S2?

A

ASD

854
Q

Wide split S2?

A

the split (sounds of A2 and P2) is wider than normal and persists during inspiration and expiration.

855
Q

What is associated with wide split S2?

A

RBBB or pulmonary HTN

856
Q

What is a paradoxical split s2?

A

Split (sounds of A2 and P2) occur during expiration and narrows or disappears during inspiration.

857
Q

What is a paradoxical split S2 associated with?

A

conditions that delay the closure of aortic valve eg. LBBB, patent ductus arteriosus, severe aortic stenosis

858
Q

Way to remember the type of S2 split that occurs in different conditions?

A
  • normal during inspiration
  • Reversed/paradoxical split (left): LBBB
  • Widely split (right): RBBB
  • Fixed split: ASD
  • Loud S2: HTN
  • Soft S2: aortic stenosis
859
Q

Innocent murmurs heard in children?

A
  • Ejection murmurs
  • Venous hums
  • Still/s murmur
860
Q

Innocent murmurs in children: ejection murmurs due to?

A

Turbulent blood flow at outflow tract of the heart

861
Q

Innocent murmurs in children: venous hums?

A

due to turbulent blood flow in great veins returning to the heart, heard as a continuous blowing noise just below the clavicles

862
Q

Innocent murmurs in children: Still’s murmur?

A

low-pitched sound heard at the lower left sternal edge

863
Q

Characteristics of an innocent ejection murmur ?

A
  • soft-blowing murmur in the pulmonary area or short buzzing murmur in the aortic area
  • may vary with posture
  • localised with no radiation
  • no diastolic component
  • no thrill
  • no added sounds (e.g. clicks)
  • asymptomatic child
  • no other abnormality
864
Q

Types of murmurs? (6)

A
  • ejection sytolic
  • pansystolic (holosystolic)
  • late systolic
  • early diastolic
  • mid-late diastolic
  • continuous machine-like murmur
865
Q

Causes ff ejection systolic murmur heard louder on expiration?

A

aortic stenosis and hypertropic obstructive cardiomyopathy

866
Q

Causes of ejection systolic murmur heard louder on inspiration?

A

pulmonary stenosis and atrial septal defect

867
Q

Causes of ejection systolic murmurs? (5)

A
  • TOF
  • aortic stenosis
  • hypertrophic obstructive cardiomyopathy
  • pulmonary stenosis
  • ASD
868
Q

Causes of holosystolic (pansystolic) murmurs? (3)

A
  • mitral regurg (high pitched and blowing)
  • tricuspid regurg (high and blowing)
  • VSD (harsh)
869
Q

Why does tricuspid regurg become louder during inspiration, unlike mitral regurg?

A

during inspiration, venous blood blow to RA and V are increased -> increases stroke volume of RV during systole

870
Q

Causes of late systolic murmur? (2)

A

mitral valve prolapse and coarctation of aorta

871
Q

Causes of early diastolic murmur?

A
  • aortic regurg
  • pulmonary regurg (Graham-Steel murmur)
872
Q

Causes of mid-late diastolic murmur?

A
  • mitral stenosis
  • severe aortic regurg (Austin-Flint murmur)
873
Q

Causes of continuous machine-like murmur?

A

Patent ductus arteriosus

874
Q

What does mitral, tricuspid, aortic and pulmonary regurgitation sound like?

A

high pitched and blowing

875
Q

What does a pansystolic murmur from VSD sound like?

A

harsh in character

876
Q

What does mitral stenosis and severe aortic regurg sound like?

A

rumbling in character

877
Q

What does RILE mean in regards to heart murmurs?

A

R.ight sided murmur -> heard best on I.nspiration

L.eft sided murmur -> heard best on E.xpiration

878
Q

What does aortic stenosis sound like?

A

Harsh in character

879
Q

Aortic vs mitral stenosis murmur sound?

A

Aortic: harsh systolic
Mitral: rumbling diastolic with opening snap

880
Q

What is a leg ulcer?

A

break in the skin below the knee which has not healed within 2w

881
Q

Venous leg ulcer?

A

Leg ulcer that occurs in the presence of venous disease (most common type of leg ulcer-60-80%)

882
Q

Where do venous leg ulcers occur typically?

A

in the gaiter area of the leg (from ankle to mid calf)

883
Q

Causes of leg ulceration?

A

venous disease; arterial disease; DM; RA; vasculitis; sickle cell; malignancy; drugs

884
Q

What drugs can cause leg ulcers?

A

NSAIDs, corticosteroids, nicorandil

885
Q

What is venous leg ulceration caused by?

A

sustained venous HTN resulting from chronic venous insufficiency due to venous valve incompetence or impaired calf muscle pump

886
Q

RFs for venous leg ulcer?

A

obesity, immobility, increasing age, varicose veins, Hx of DVT

887
Q

Healing and recurrence rates of venous leg ulcers?

A

Repeat cycles of ulceration, healing and recurrence common.
12m recurrence: 26-69%.
6m healing rates= ommunity 45% and specialist 70%

888
Q

How to examine venous leg ulcer?

A
  • wound= site, edge, size, depth, wound bed, infection
  • leg= oedema, varicose veins, venous skin changes, reduced ankle mobility
889
Q

Ix for venous leg ulcers?

A
  • examination
  • Doppler assessment of both legs to determine ankle-brachial pressure index in both legs to exclude arterial insufficiency
  • consider bloods
890
Q

Primary care Mx of venous leg ulcer?

A
  • cleaning and dressing wound
  • compression therapy if appropritate (4 layer compression banding after excluding arterial disease)
  • consider pentoxifylline improve healing
  • advice
  • follow up to assess
  • Mx of Cx and associated conditions
  • recurrent: refer to vascular specialist ?superficial venous surgery
891
Q

Why may pentoxifylline be prescribed for venous leg ulcers?

A

to improve microcirculatory blood flow and improve ulcer healing (a peripheral vasodilator)

892
Q

Lifestyle advice to promote leg ulcer healing and reduce recurrence?

A

compression therapy; keep mobile with walking regular (exercise calf muscle pump function); elevate legs when immobile; emollient frequently

893
Q

When to arrange specialist referral for venous leg ulcer?

A

Delayed or no healing >2w of adequate Mx or uncertain diagnosis/cause.
For superficial venous surgery.

894
Q

How to reduce risk of recurrence after leg ulcer has healed?

A
  • long-term below-knee graduated compression hosiery
  • lifestyle measures
  • review and follow up
895
Q

When should bacteriological swabs be taken for leg ulcer?

A

only if evidence of infection

896
Q

In venous leg ulcers, after ABPI is done, may consider bloods- why?

A

-FBC: anaemia may delay healing; raised WBC & platelts- infection
- ESR & CRP
- urea and creatinine= high urea- ?dehyrdation which impair healing
- albumin= low may be associated wioth protein loss and malnutrition, may delay healing
- HbA1c: ?DM

897
Q

What is the ankle brachial pressure index (ABPI)?

A

provides index of vessel competency by measuring ratio of SBP at ankle to that of the arm, valve of 1=normal.

always interpret in context of CP

898
Q

ABPI ratio <0.5

A

severe arterial disease- compression treatment contraindicated and urgent referral for specialist vascular assessment

899
Q

ABPI ratio >0.5 and <0.8?

A

arterial disease or mixed arterial/venous disease; refer and generally avoid compression

900
Q

ABPI ratio 0.8-1.3?

A

no evidence of signif arterial disease and compression safe

901
Q

ABPI >1.3?

A

may suggest presence of arterial calcification eg. in DM, RA, atherosclerosis, CKD.

may be misleadingly high so refer

902
Q

Features of venous insufficency?

A

brown pigmentation, oedema, lipodermatosclerosis, eczema

903
Q

Mx for infected leg ulcer?

A

500mg flucloxacillin 4 times a day for 7 days
or 500mg clarithromycin twice a day

904
Q

Marjolin’s ulcer?

A

Squamous cell carcinoma
Occurring at sites of chronic inflammation e.g; burns, osteomyelitis after 10-20 years
Mainly occur on the lower limb

905
Q

Arterial ulcers?

A
  • Occur on the toes and heel
  • Typically have a ‘deep, punched-out’ appearance
  • Painful
  • There may be areas of gangrene
  • Cold with no palpable pulses
  • Low ABPI measurements
906
Q

Neuropathic ulcers?

A
  • Commonly over plantar surface of metatarsal head and plantar surface of hallux
  • The plantar neuropathic ulcer is the condition that most commonly leads to amputation in diabetic patients
  • Due to pressure
  • Management includes cushioned shoes to reduce callous formation
907
Q

Pyoderma gangrenosum?

A
  • Associated with inflammatory bowel disease/RA
  • Can occur at stoma sites
  • Erythematous nodules or pustules which ulcerate
908
Q

Why can’t you use compression for arterial ulcers?

A

will reduce blood supply further, surgery may be needed to clear out blocked artery (angioplasty)

909
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC)?

A

form of inherited CVD that may present with syncope or sudden death; 2nd most common cause of sudden cardiac death in young after hypertrophic cardiomyopathy

910
Q

Pathophysiology of ARVC?

A
  • autosomal dominant
  • RV myocardium is replaced by fatty and fibrofatty tissue
911
Q

CP of ARVC?

A

palpitations, syncope, sudden cardiac death

912
Q

Ix for ARVC?

A
  • ECG= T wave inversion; 50% have epsilon wave (terminal notch in QRS complex)
  • echo= subtle; enlarged hypokinetic RV with thin free wall
  • MRI can show fibrofatty tissue
913
Q

Mx of ARVC?

A
  • sotalol (antiarrhythmic)
  • catheter ablation to prevent V tach
  • implantable cardio-verter defib
914
Q

Naxos disease?

A

autosomal recessive variant of ARVC

triad= ARVC, palmoplantar keratosis and woolly hair

915
Q

Atrial myxoma?

A

Most common primary cardiac tumour.
Females
75% in LA; commonly attached to fossa ovalis

916
Q

Features of atrial myoxoma?

A
  • systemic= dysponea, fatigue, weight loss, pyrexia of unknown origin, clubbing
  • emboli
  • AF
  • mid-diastolic murmur, ‘tumour plop’
  • echo= pedunculated heterogenous mass typically attached to fossa ovalis region of interatrial septum
917
Q

Effects of BNP?

A

vasodilator
diuretic and natriuretic
suppressess both sympathetic tone and renin-angiotensin-aldosterone system

918
Q

What may cause raised BNP?

A

produced by LV myocardium in response to strain

HF, MI, LV dysfunction, valvular disease
CKD

919
Q

How to reduce BNP?

A

ACEinhh
ARB
and diuretics

920
Q

<100pg/ml BNP makes what unlikely?

A

HF

921
Q

Oxygenation of the blood in the heart?

A
  • deoxygenated blood -> R side of heart via SVC and IVC, oxygen sat 70%; RA, RV, PA have oxyegn sat of around 70%.
  • lungs oxygenate blood to around 98-100%; LA, LV and aorta should therefore have oxygen sat 98-100%
922
Q

Oxygen sats you would expect if normal?

A

RA= 70%
RV= 70%
PA= 70%

LA= 100%
LV=100%
Aorta= 100%

923
Q

Oxygen sats you would expect if ASD?

A

RA= 85%
RV= 85%
PA= 85%

LA= 100%
LV=100%
Aorta= 100%

924
Q

Oxygen sats you would expect if VSD?

A

RA= 70%
RV= 85%
PA= 85%

LA= 100%
LV=100%
Aorta= 100%

925
Q

Oxygen levels you would expect in PDA?

A

RA= 70%
RV= 70%
PA= 85%

LA= 100%
LV=100%
Aorta= 100%

926
Q

Oxygen levels you would expect in VSD with Eisenmenger’s?

A

RA= 70%
RV= 70%
PA= 70%

LA= 100%
LV=85%
Aorta= 85%

927
Q

Oxygen levels you would expect in PDA with Eisenmenger’s?

A

RA= 70%
RV= 70%
PA= 70%

LA= 100%
LV=100%
Aorta= 85%

928
Q

Oxygen levels you would expect in ASD with Eisenmenger’s?

A

RA= 70%
RV= 70%
PA= 70%

LA= 85%
LV=85%
Aorta= 85%

929
Q

What cardiac enzyme/protein marker is used to look for reinfarction?

A

CK-MB

930
Q

Troponin T and Troponin I?

A

proteins found in cardiomyocytes; released into blood when heart muscle in damaged eg. MI.

Troponin T= binds the troponin complex to tropomyosin (another protein invl in muscle contraction)

Troponin I= inhibits the interaction between actin and myosin (proteins that cause muscle contraction) when the heart is at rest

931
Q

How is Troponin T and Troponin I used to detect heart muscle damage eg. following MI?

A

troponins rise in the blood within 3-6hrs after heart muscle damage occurs; peak after 12-24hrs and can remain elevated for up to 1-2w

932
Q

Troponin vs NT-proBNP?

A

T= diagnose MI; indicates heart muscle damage; highly specific to heart muscle injury

NT-proBNP= diagnose and manage HF (released by heart in response to increased pressure and vol overload eg. in HF); indicates heart strain or overload; reflects HF but can be elevated in other conditions eg. kidney disease, PE, old age

933
Q

BNP vs NT-proBNP?

A

Both released by ventricles in response to increased pressure and vol overload eg. HF.
BNP is the active hormone and NT-proBNP is the inactive fragment.
NT-proBNP is more stable in the blood and has a longer half-life- 1-2hrs (BNP 20mins) so preferred marker for diagnosing & monitoring of HF.

934
Q

Eisenmenger’s syndrome?

A

the reversal of a left to right shunt in a congenital heart defect due to pulmonary HTN; occurs when an uncorrected L-to-R shunt leads to copulmonale (pulmonary HTN and obstruction of pulmonary blood due to remodeling of pulmonary microvasculature).

935
Q

What is Eisenmenger’s associated with?

A

VSD
ASD
PDA

936
Q

Features of Eisenmenger’s?

A
  • original murmur may disappear
  • cyanosis
  • clubbing
  • RV failure
  • haemoptysis, embolism
937
Q

Mx of Eisenmenger’s?

A

heart-lung transplant required

938
Q

Hypothermia?

A

unintentional reduction of core body temp:
mild= 32-35C
moderate/severe= <32C

939
Q

What happens in the initial stages of hypothermia?

A

thermoreceptors in skin and subcut tissues sense low temp and cause regional vasocontriction; causes hypothalamus to stimulate release of TSH and ACTH; also stimulates heat production by promoting shivering

940
Q

Causes/RFs of hypothermia?

A
  • elderly and newborn babies
  • exposure to cold environment
  • inadequate insulation in operating room/general anaesthesia
  • hypothyroidism
  • impaired mental status
  • homelessness
  • cardiopulmonary bypass
941
Q

Signs of hypothermia?

A
  • shivering
  • cold pale skin
  • frostbite
  • slurred speech
  • Mild= tachypnoea, tachy, HTN
  • moderate= resp dep, bradycardia, hypotension
  • confusion/impaired mental state
942
Q

Frostbite in hypothermia?

A

when skin and subcut tissue freeze, causing damage to cells

943
Q

Hypothermia in babies?

A

can look healthy
may be limp; unusually quiet and refuse to feed.
Extremely common in newborns= hat and blanket soon after birth.

944
Q

Ix for hypothermia?

A
  • temp= tracked over time; low-reading rectal thermometers or thermistor probs
  • ECG= acute ST-elevation and J waves or Osborn waes
  • FBC + U&Es= Hb elevated, platelets & WBCs low (sequestration in spleen)
  • Blood glucose= stress hormones increased so more resistance to insulin
  • ABG
  • Coag factors
  • CXR
945
Q

What should be monitored in hypothermia?

A

temp
potassium as can be hypokalaemic due to shift of potassium into intracellular space

946
Q

Mx for hypothermia?

A
  • remove from cold & any wet clothing
  • warm with blankets
  • secure airway and monitor breathing
  • not responding to warming then maintain circulation using warm IV fluids or apply forced warm air directly onto body
  • RAPID REWARMING can lead to PERIPHERAL VASODILATION AND SHOCK= so if severe prepare for CPR; avoid IV drugs if possible as likely to have drastic response to the drug
947
Q

Advice for pubic on what NOT to do if pt has hypothermia (due to risk of cardiac arrest)?

A
  • don’t put in hot bath
  • don’t massage limbs
  • don’t use heating lamps
  • don’t give alcohol to drink
948
Q

Mx for choking?

A

1) “are you talking”= if respond yes or able to speak, cough or breath then mild airway obstruction. If unable to speak/they nod, unable to breathe, wheezy, silent cough, unconscious then severe.

2) Mild= encourage pt to cough

2) Severe and conscious=
- 5 back-blows
- unsuccessful then 5 abdo thrusts
- if unsuccessful then repeat

2) if unconscious= call ambulance and start CPR

949
Q

Isolated systolic HTN (ISH)?

A

Common in elderly; 50% of >70yrs.
Mx in same way as standard HTN.

950
Q

Where is a non-pulsatile JVP seen?

A

superior vena caval obstruction

951
Q

Kussmaul’s sign: paradoxical rise in JVP during respiration?

A

seen in constrictive pericarditis

952
Q

JVP: jugular vein waveform= ‘a’ wave?

A

atrial contaction
- large if atrial pressure eg. tricuspid stenosis, pulmonary stenosis, pulmonary HTN
- absent in AF

953
Q

JVP: jugular vein waveform= cannon ‘a’ waves?

A
  • caused by atrial contractions against a closed tricuspid valve
  • seen in complete heart block, V tachy/ectopics, nodal rhythm, single chamber ventricular pacing
954
Q

JVP: jugular vein waveform= ‘c’ wave?

A

closure of tricuspid valve
- not normally visible

955
Q

JVP: jugular vein waveform= ‘v’ wave?

A
  • due to passive filling of blood into atrium against closed tricuspid
  • giant v waves in tricuspid regurg
956
Q

JVP: jugular vein waveform= ‘x’ descent?

A

fall in atrial pressure during V systole

957
Q

JVP: jugular vein waveform= ‘y’ descent?

A

opening of tricuspid valve

958
Q

Long saphenous vein?

A

may be harvested for bypass surgery or removed as Mx for varicose veins with saphenofemoral junction incompetence

959
Q

Path of the long saphenous vein?

A
  • Originates at the 1st digit where the dorsal vein merges with the dorsal venous arch of the foot
  • Passes anterior to the medial malleolus and runs up the medial side of the leg
  • At the knee, it runs over the posterior border of the medial epicondyle of the femur bone
  • Then passes laterally to lie on the anterior surface of the thigh before entering an opening in the fascia lata called the saphenous opening
  • It joins with the femoral vein in the region of the femoral triangle at the saphenofemoral junction
960
Q

Long saphenous vein tributaries?

A
  • Medial marginal
  • Superficial epigastric
  • Superficial iliac circumflex
  • Superficial external pudendal veins
961
Q

Short saphenous vein path?

A
  • Originates at the 5th digit where the dorsal vein merges with the dorsal venous arch of the foot, which attaches to the great saphenous vein.
  • It passes around the lateral aspect of the foot (inferior and posterior to the lateral malleolus) and runs along the posterior aspect of the leg (with the sural nerve)
  • Passes between the heads of the gastrocnemius muscle, and drains into the popliteal vein, approximately at or above the level of the knee joint.
962
Q

Path of the subclavian artery?

A
  • The left subclavian comes directly off the arch of aorta
  • The right subclavian arises from the brachiocephalic artery (trunk) when it bifurcates into the subclavian and the right common carotid artery.
  • From its origin, the subclavian artery travels laterally, passing between anterior and middle scalene muscles, deep to scalenus anterior and anterior to scalenus medius. As the subclavian artery crosses the lateral border of the first rib, it becomes the axillary artery. At this point it is superficial and within the subclavian triangle.
963
Q

Branches of the subclavian artery?

A
  • Vertebral artery
  • Internal thoracic artery
  • Thyrocervical trunk
  • Costocervical trunk
  • Dorsal scapular artery
964
Q

Takotsubo cardiomyopathy?

A

type of non-ischaemic cardiomyopahty associated with a transient, apical ballooning of the myocardium.

may be triggered by stress

965
Q

Pathophysiology of Takotsubo cardiomyopathy?

A

Takotsubo= Japanese word that for octopus trap

  • apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments. In simple terms, the bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap)
966
Q

Features of Takotsubo cardiomyopathy?

A
  • chest pain
  • features of HF
  • ECG= ST elevation
  • normal coronary angiogram
967
Q

Mx and prognosis of Takotsubo cardiomyopathy?

A

Mx is supportive.
Prognosis= most improve with supportive treatment.

968
Q

Wolf-Parkinson White?

A

caused by congenital accessory conducting pathway between A & Vs leading to atrioventricular re-entry tachy (AVRT). As the accessory pathway doesn’t slow conduction, AF can degenerate rapidly to VF.

969
Q

Possible ECG features of Wolf-Parkinson White?

A
  • short PR interval
  • wide QRS with slurred upstroke- delta wave
  • left axis deviation if right-sided accessory pathway; right axis D if left sided A P (majority have left axis deviation)
970
Q

Differentiate between type A and B of WPW syndrome?

A

type A (left-sided pathway): dominant R wave in V1

type B (right-sided pathway): no dominant R wave in V1

971
Q

Associations of WPW syndrome?

A

HOCM
mitral valve prolapse
Ebstein’s anomaly
thyrotoxicosis
secundum ASD

972
Q

Mx of WPW syndrome?

A

definitive treatment= radiofrequency ablation of the accessory pathway

medical therapy= sotalol***, amiodarone, flecainide

sotalol should be avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation

973
Q
A