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Junior Medicine > Chest Pain And Palpitations > Flashcards

Chest Pain And Palpitations Flashcards

1
Q

Characteristic presentation of myocardial ischaemia

A

Crushing, gripping or heavy pain focussed centrally on the chest
Can radiate to neck, shoulder or jaw (usually left sided)
Associated with heaviness in one or both arms
Associated with dyspnoea, nausea and sweating
Quick onset (mins)

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2
Q

Characteristic presentation of aortic dissection

A

Severe, central chest pain radiating to the back and down the arms
Patients may be shocked and can have neurological symptoms secondary to blood supply to spinal cord
There may be signs of distal ischaemia or absent peripheral pulses
Rapid onset (seconds)

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3
Q

Characteristic presentation of pleural disease

A

Localised sharp pain, worse on deep breathing and coughing
Associated with costo-chondral tenderness
Pain in the shoulder tip is suggestive of diaphragmatic pleural irritation

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4
Q

Characteristic presentation of oesophageal disease

A

Retrosternal chest pain, can be difficult to separate from cardiac pain
Worse on bending over or lying down, relieved by antacids

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5
Q

Characteristic presentation of MSK disease

A

Can cause very severe pain, importantly associated with local tenderness
Worse with certain movements often a history of trauma or causative event

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6
Q

How to correctly set up the ECG machine

A

Skin must be clean and dry

V1/2 are positioned in the 4th intercostal space either side of sternum
V4 in 5th intercostal space, mid-clavicular line
V3 is placed between V2 and V4
V6 is in 5th intercostal space mid axillary line
V5 between v4 and V6

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7
Q

What is bundle branch block

A

A deficit in the conduction pathways of the bundles of his
- depolarisation wave reaches the septum normally so PR interval is normal, yet there is abnormal conduction through the left / right bundle branches of his

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8
Q

What causes a wide QRS (>120ms)

A

Delayed depolarisation of the ventricles
- right bundle branch block is seen in V1
- ‘M’ shaped in V1 and ‘W’ shaped in V6

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9
Q

How does left bundle branch block present on an ECG

A

Best seen in V6 with a broad M complex and the W pattern in V1 is often not fully developed

If LBBB is present with recent chest pain consider acute MI
If asymptomatic consider aortic stenosis

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10
Q

What is heart block

A

Abnormal conduction from the SAN to the ventricles
Thus creating abnormalities from the PR interval

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11
Q

What is first degree heart block

A

PR interval >0.22 seconds
Each wave of SAN depolarisation is spread to the ventricles but there is a delay somewhere along this path usually at the AVN

Is not pathological itself but can indicate
- coronary artery disease
- electrolyte disturbances
- digoxin toxicity

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12
Q

What is second degree heart block

A

Excitation intermittently fails to pass through the AVN or bundle of His
1. Wenckebach: progressive PR lengthening until an atrial beat is not conducted and then this cycle repeats
2. Mobitz type 2: constant PR interval yet there is sometimes atrial contraction without ventricular contraction
3. 2:1/3:1/4:1- 2-3x more P waves than QRS complex - indicates heart disease

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13
Q

What is complete (3rd degree heart block)

A

Atrial contraction is normal but no beats are conducted to the ventricles
P waves happen regularly but will be completely dissociated from the QRS complexes
Wide QRS complex
Pacing will generally always be required

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14
Q

What is sinus arrhythmia

A

Occurs in young people where heart rate changes with respiration so the R-R interval changes progressively on a beat-beat basis
Sinus bradycardia (<60) can be associated with athletic training, fainting attacks, hypothermia or hypothyroidism and also can occur immediately after a heart attack

Sinus tachycardia (>100) can be associated with exercise, fear, pain, haemorrhage or thyrotoxicosis

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15
Q

What is non sinus rhythm arrhythmias

A

Abnormal rhythms begin in one of three places: atrial muscle, ventricular muscle or the AVN. These are known as supraventricular and the QRS complex is narrow

Ventricular rhythms give wide, abnormal QRS complexes

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16
Q

How does bradycardia initiate

A

Rhythm is controlled by SAN at around 70bpm.
If the SAN fails control will be assumed by an atrial focus or the AVN (50/min)
If these fail, conduction is blocked and a ventricular focus will give a rhythm of about 30/min

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17
Q

What are escape rhythms and escape beats

A

Slow, protective rhythms are escape rhythms

If singular and then normal rhythm returns they are termed escape beats

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18
Q

Management of bradycardia

A

A-E assessment
Assess for adverse features such as shock, syncope, heart failure, MI
Assess for risk of asystole: recent asystole, mobitz II or complete heart block
If any of these features are present initiate atropine 500mcg IV repeated up to max 3mg

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19
Q

How does tachycardia initiate

A

Any foci in the myocardium can depolarise repeatedly causing sustained tachycardia
Finding P waves is important to deciding the origin of the tachycardia

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20
Q

What is supraventricular tachycardia

A

In atrial tachycardia, the atria depolarise faster than 150/min
P waves are often superimposed on the previous T waves
The AV node can only conduct atrial discharge rates up to 200/min so AV block occurs and some P waves are not followed by QRS complexes

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21
Q

Management of supraventricular tachycardia

A

A-E resuscitation
If irregular rhythm treat as AF
If regular attempt vagal manoeuvre
- carotid sinus massage - leads to vagal stimulation
If unsuccessful IV adenosine
Secondary prevention with B blockers

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22
Q

What is ventricular tachycardia

A

Wide, abnormal QRS seen in all 12 leads
Potential to transform to VF so requires urgent treatment

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23
Q

Management of ventricular tachycardia

A

If systolic BP <90mmHg, chest pain, heart failure or rate >150; immediate electrical cardioversion

In the absence of such signs amiodarone may be used (with electrical cardioversion)
- 300mg IV loading dose over 60mins

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24
Q

What is ventricular fibrillation

A

No QRS can be identified and the ECG is disorganised
The patient will have lost consciousness
Manage as per the ALS cardiac arrest protocol

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25
Q

What is atrial fibrillation

A

Fibrillation of the atria gives an irregular ECG baseline with no P waves
The AVN is bombarded and thus will depolarise irregularly leading to ventricular contraction at an irregular rate

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26
Q

Presentation of AF

A

Can be asymptomatic or present with dyspnoea, palpitations, syncope, chest pain or stroke / TIA

  • if no abnormalities are seen on ECG, 24 hour ambulatory ECG monitoring or an event recorder to detect paroxysmal AF
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27
Q

Management of AF

A

If haemodynamic instability carry out emergency electrical cardioversion (don’t delay for anticoagulation)

If haemodynamically stable, manage of AF can involve rate control or rhythm control as well as anticoagulation and investigation for an underlying cause

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28
Q

What is rate control in AF

A

Often first line aiming to slow the ventricular rate
- a B blocker or rate limiting calcium channel blocker

Calcium channel blockers contraindicated in heart failure, B blockers contraindicated in asthma
Digoxin or amiodarone are second line agents

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29
Q

What is rhythm control in AF (cardioversion)

A

Aims to restore sinus rhythm to the heart
Indicated in younger patients with new onset AF or if the AF is causing heart failure

Can be electrical (defibrillator) or pharmacological (flecainide and amiodarone)

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30
Q

Why should all patients with AF be considered for systemic anticoagulation

A

AF is associated with risk of stroke as disorganised contraction of the atria can lead to stasis of blood and formation of blood clots within the atrium
These clots can pass into the ventricles and then the systemic circulation causing emboli vascular occlusions

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31
Q

What is the CHA2DS2VS tool for assessing stroke risk

A

C: congestive heart failure (1 point)
H: hypertension (1 point)
A2: age >75 2 points or age 65-74 1 point
D: diabetes (1 point)
S2: prior stroke or TIA (1 point)
V: vascular disease (1 point)
S: sex - female (1 point)

Anticoagulation should be considered in anybody with a score of 2 or men with score 1

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32
Q

MOA of DOACs (1st line anticoagulant)

A

Direct inhibition of specific proteins within the coagulation cascade
(Preferred to warfarin as more consistent pharmacodynamics, and thus less need for therapeutic monitoring)

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33
Q

What are the underlying cardiac, respiratory or systemic causes of AF

A

Cardiac: hypertension, valvular heart disease, heart failure and IHD
Resp: chest infection, PE and lung cancer
Systemic: excessive alcohol intake, thyrotoxicosis, electrolyte depletion, infections

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34
Q

What is atrial flutter

A

Atrial rate is above 250/min and no flat baseline between P waves exist = atrial flutter
300-450 contraction per min
Similar to AF in that co-ordination of the atria is lost but some element of synchronicity still exists
Treated as per AF

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35
Q

Electrolyte abnormalities on ECG

A

Hyperkalaemia: tall, tented T waves, widened QRS complex, prolonged PR interval
Hypokalaemia: T wave flattening and a U wave on the end of the T wave
Hypocalcaemia: QT prolongation
Hypercalcaemia: QT shortening

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36
Q

What is ischaemic heart disease

A

(AKA coronary heart disease)
Spectrum of disease caused by atheromatous plaque build up in coronary arteries leading to a lack of blood supply to the heart
Encompasses stable angina and the acute coronary syndrome

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37
Q

Pathology of atheroma formation ( 7 steps)

A
  1. Damage to the endothelium due to a variety of risk factors allows entry of LDLs into the intima
  2. LDLs are taken up by macrophages in the intima and accumulate excessively as they bypass normal receptor mediated uptake forming a fatty streak
  3. As the macrophages take up more lipid they release free lipid into the intima
  4. The macrophages stimulate cytokines which leads to collagen deposition by inflammatory cells, and the intimal lipid plaque becomes fibrotic
  5. At this stage it appears raised and yellow, and leads to pressure atrophy of the media and disruption of the elastic lamina
  6. Increased secretion of collagen forms a dense fibrous cap to the plaque which is now hard and white
  7. The endothelium is fragile and can ulcerate, allowing platelet aggregation and acute vessel blockage
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38
Q

Risk factors for ischaemic heart disease

A

Age
Gender: higher in men than pre-menopausal women
Family history: higher rates if first degree relative had IHD before 50
Smoking: stopping reduces immediate risk by 25%
Diet: high fat, low fresh fruit and veg implicated
Obesity: primarily abdo obesity
Hypertension: both systolic and diastolic
Hyperlipidaemia: high serum cholesterol
Diabetes mellitus

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39
Q

What is stable angina

A
  • episodic pain that occurs when there is increased myocardial demand, usually upon exercise in the presence of impaired myocardial perfusion
  • mostly due to low flow in atherosclerotic coronary arteries
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40
Q

Presentation of stable angina

A

Classical ischemic pain of the myocardium from mild ache to severe pain that provokes sweating and fear
- pain is provoked by exercise, especially after meals in the cold and if the patient is angry / excited

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41
Q

What is decubitus angina

A

Angina precipitated by lying down as there is increased venous return to the heart - is associated with LVF

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42
Q

What is variant / prinzmetal angina

A

Occurs without provocation at rest as a result of coronary artery spasm
There is ST elevation during the episode so consider if ST elevation but no troponin rise

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43
Q

Investigations for stable angina

A

Exclude other causes of chest pain
- CXR
- bloods including FBC, HbA1c, lipids, TFTs, troponin
(troponin should not be raised in stable angina)
- resting 12 lead ECG
- CT coronary arteries

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44
Q

Why is CT coronary arteries a good investigation for stable angina

A

A non invasive test with a very good negative predictive value however remains less sensitive than invasive coronary angiography

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45
Q

Management of stable angina

A

Manage cardiovascular risk factors
GTN spray PRN + B blocker or CCI
Statin / low dose aspirin
Refer to cardiology

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46
Q

Counselling for nitrates

A

Sit down, rest and spray once beneath the tongue, wait for 5 mins spray again if there is still pain
If there is still pain at 10min call 999 and unlock the door

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47
Q

Pathophysiology of nitrates

A

Cause marked ve no relaxation thus reducing pre load on the heart
This can cause venous pooling on standing thus can cause postural hypotension and dizziness

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48
Q

MOA of B blockers

A

B1 adrenoceptors are found mainly on the heart acting to increase HR and SV
B2 adrenoceptors act to cause SM relaxation in many organs eg trachea

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49
Q

Side effects of B blockers

A

Bronchoconstriction: contraindicated in asthma, caution in COPD
Cardiac depression / bradycardia: can be critical if combined with other rate limiting agents
Hypoglycaemia: impair the sympathetic warning signs of hypo’s

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50
Q

MOA of calcium channel blockers

A

Prevent SM contraction, reducing afterload and causing coronary vasodilation
Rate limiting agents also act on cardiac calcium channels in the AVN to control heart rate

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51
Q

Side effects of calcium channel blockers

A

Flushing
Headache
Ankle swelling
Constipation

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52
Q

MOA of nicorandil

A

Causes marked vasodilation
It is a combined NO donor and also an activator of ATP sensitive K channels on vascular smooth muscle cells leading to hyperpolarisation

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53
Q

What is the ACS

A

Made up of unstable angina, non ST elevation MI and ST elevation MI

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54
Q

Pathology of ACS

A

Fissuring, ulceration of atheromatous plaques leading to thrombosis within coronary arteries and myocardial ischaemia
This can occur in areas of low grade stenosis which have not previously caused anginal symptoms

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55
Q

What is unstable angina

A

Angina occurring at rest or sudden increased frequency
There is no rise in cardiac enzymes (troponin)
Caused by fissuring of plaques thus there is a risk of subsequent total vessel occlusion and progression to AMI

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56
Q

What is acute myocardial infarction

A

Elevation of serum cardiac troponin levels with additional categorisation based on the ECG
ST elevation / new LBBB = STEMI
No ST elevation / LBBB = NSTEMI

The area of infarction depends on the artery occluded,, and the size of infarction depends on how proximal / distal the blockage is

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57
Q

Involvement of the right coronary artery in ACS

A

Supplied RA, RV, posterior septum
Blockage gives posterior / inferior MI
Also supplies the AVN in 80% and SAN in 60%

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58
Q

Involvement of left coronary artery in ACS

A

Splits into the circumflex and left anterior descending artery
Blockage gives a massive antero-lateral MI
Leads I, aVL, V1-V6

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59
Q

Involvement of the circumflex artery in ACS

A

Mainly supplies LA and LV
Blockage gives a lateral MI
Leads I, aVL, V5/6

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60
Q

Involvement of the left anterior descending artery in ACS

A

Mainly supplies the LV and anterior septum
Blockage gives an antero-septal MI
Leads V1-V4

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61
Q

Symptoms of ACS

A

Severe crushing, gripping or heavy chest pain lasting longer than 20mins
Not relieved by 3x GTN sprays at 5 min intervals
Radiates to left arm, neck or jaw
Associated dyspnoea, nausea and sweating with distress and a feeling of impending death
May present without chest pain

62
Q

OE of ACS

A

Sympathetic activation: tachycardia, hypertension, pallor, sweatiness
Vagal stimulation: bradycardia, vomiting
Myocardial impairment: hypotension, narrow pulse pressure, raised JVP, basal crepitations
Tissue damage: low grade Pyrexia

63
Q

Differential diagnoses of central chest pain

A

Cardiac: coronary artery spasm, pericarditis, myocarditis, aortic dissection
Non cardiac: PE, pneumothorax, oesophageal disease, mediastinitis, costochondritis, trauma

64
Q

ACS investigations

A

ECG
Bloods: FBC and U&E, troponin,
CXR
Echocardiogram

65
Q

Differnece between STEMI and NSTEMI

A

STEMI generally correlates with full thickness myocardial infarct whereas NSTEMI is partial thickness

66
Q

ACS early management

A

A-E resuscitation
300mg aspirin
IV morphine
GTN spray / IV nitrates
If there is ST elevation on ECG immediate referral to cardiology
If there is no ST elevation assess mortality risk and continue regular ECG
Add 2nd antiplatelet agent
Add anticoagulant

67
Q

What is the GRACE score for assessing ACS

A

Takes into account age, heart rate, blood pressure, class of CHF, renal function, ST segment changes, troponin elevations and whether there was an arrest at admission to give a mortality risk at various time intervals

68
Q

STEMI management

A

PCI: invasive angioplasty +/- stenting is gold standard
In STEMI should have a stent in less than 9pm is aimed for

69
Q

Management of NSTEMI

A

High risk: if GRACE mortality >3% in 6m: organise semi elective PCI as an inpatient
Low risk: ie resolved unstable angina or grace <3%: potentially can be discharged with outpatient angiogram and cardiology follow up

70
Q

ACS long term management

A

48h bed rest and continuous ECG
Daily U&Es and cardiac enzymes
- dual antiplatelet therapy: aspirin 75mg OD continued for life + another for a year
- ACE inhibitor
- high intensity statin
- beta blocker
- modifiable risk factors

71
Q

Immediate complications of ACS

A

Arrhythmias
VT and VF
AF
Bradycardia or AV block

72
Q

Short term complications of ACS

A

Pulmonary oedema

Cardiogenic shock

Thromboembolism

Ventricular septal defect

Ruptured chordae tendinae

Rupture of ventricular wall

73
Q

Long term complications of ACS

A

Heart failure

Dressler’s syndrome

Ventricular aneurysm formation

74
Q

What is Dressler’s syndrome

A

Immune mediated pericarditis

75
Q

Driving limitations of angina

A

DVLA do not need to be notified
Driving can continue unless it occurs at rest, whilst driving or with emotion
Recommence when adequate symptom control gained

76
Q

Driving limitations with ACS

A

Patients may return to office work after 2 months but pilots / drivers should not return and heavy manual labourers should seek lighter work

DVLA do not need to be notified. If treated with PCI can continue after 1 week otherwise after 4 weeks

77
Q

Driving limitations for HGV drivers with cardiovascular diagnoses

A

Cardiovascular diagnoses can lead to revocation of licences for 6 weeks
Re-licensing can then be permitted if exercise / other functional requirements are met

78
Q

Causes of hypertension

A
  • adrenal cortical diseases
  • renal artery stenosis
  • chronic kidney disease
  • pheochromocytoma
  • coarction of the aorta
  • neurogenic causes (raised ICP)
  • pregnancy
79
Q

What is benign hypertension

A

Gradual elevation of blood pressure over years
This leads to gradual hypertrophy of the muscular media in artery walls reducing their capacity to expand, and increasing fragility

80
Q

What is malignant hypertension

A

Rapid sustained increase in blood pressure
Leads to intimal proliferation reducing the luminal size and leading to cessation of blood flow through the small vessels
Causes tissue necrosis
Untreated 1yr mortality risk of 20%

81
Q

Diagnosis threshold for malignant hypertension

A

SBP >200 or DBP >120
+
Bilateral retinal haemorrhages / exudates

82
Q

Widespread Pathological consequences of hypertension

A

Heart: LVH with dilation and eventual failure
Aorta: predisposes to AAA and aortic dissection
Brain: intracerebral haemorrhages due to vessel rupture
Kidney: CKD due to progressive nephron ischaemia and glomerular destruction
Eyes: hypertensive retinopathy

83
Q

Diagnosis of hypertension

A

Offer ambulatory BP monitoring at home if clinical measurement is >140/90

84
Q

Measurements of stage 1 HTN

A

Clinic BP >140/90 and ABPM / HBPM >135/85

85
Q

Measurements of stage 2 HTN

A

Clinic BP >160/100 and ABPM / HBPM >150/95

86
Q

Severe HTN measurements

A

Clinic SBP >180 or DBP >110

87
Q

When do you start drug treatment in HTN

A

All those with stage 2 + those under 80 with stage 1 with one of:
- 10 yr CV risk >20%
- renal disease, known CV disease, end organ damage

88
Q

What is the target BP for patients with HTN

A

Clinic: 140/90
Over 80s = 150/90

ABPM / HBPM: <135/85
145/85 if aged >80

89
Q

First line treatment for HTN

A

ACEi for <55 and those with T2DM
CCB for those >55 and Afro Caribbean

If monotherapy ineffective then combine ACEi and CCI
If still not effective then add diuretic therapy

90
Q

MOA of ACEi

A

Act by RAAS system antagonism

91
Q

Side effects of ACEi

A

Cough
Hyperkalaemia
First dose hypotension (should be given at night)
Worsened renal function

92
Q

MOA of CCI

A

Peripheral vasodilation

93
Q

Side effects of CCIs

A

Peripheral oedema
Postural hypotension
Reflex tachycardia

94
Q

What is primary hyperlipidaemia

A

Genetic predisposition to abnormal lipid metabolism

95
Q

What is secondary hyperlipidaemia

A

Systemic metabolic disturbance eg obesity, alcoholism, diabetes

96
Q

Hyperlipidaemia management

A

Lifestyle changes
1st line: statins
2nd line: fibrates
Ezetimibe can be added for those with unsatisfactory lipid control

97
Q

MOA of statins

A

HMG-CoA reductase inhibitors so stop the first line in the cholesterol synthesis pathway
Increases LDL receptor expression by hepatocytes leading to decreased LDL in circulation

98
Q

Side effects of statins

A

Nausea
Headache
Muscle pains

99
Q

MOA of fibrates

A

PPAR alpha activators with the main effect of reducing triglycerides
Also cause small increases in HDL and decreases in LDL

Caution in combination with statins as can cause higher rates of rhabdomyolysis

100
Q

MOA of ezetimibe

A

Inhibits intestinal absorption of cholesterol to reduce serum LDL

101
Q

Pathophysiology of aortic dissection

A

A tear in the arterial intima leads to blood tracking into the arterial media
Arterial media splits forming a false channel
Most commonly occurs in the aorta

102
Q

Possible outcomes of aortic dissection

A

External rupture: massive fatal haemorrhage
Internal rupture: rare, blood tracks back into the lumen to produce a double channel
Cardiac tamponade: retrograde spread into the pericardial cavity

103
Q

Causes of aortic dissection

A

Hypertension
Atheroma
Congenital disease

104
Q

Subtypes of aortic dissection

A

Type A (70%): involve the ascending aorta
Type B (30%) do not involve the ascending aorta

105
Q

Presentation of aortic dissection

A

Severe, sudden onset central chest pain described as tearing
- may radiate down the arm / to the back
- patient is shocked
- signs of blockage of distal arterial trunks

On auscultation: high pitched blowing early diastolic murmur at 2nd intercostal space

106
Q

Aortic dissection investigations

A

CT aortogram
CXR: widened mediastinum
ECG: similar to MI

107
Q

Complications of aortic dissection

A

Retrograde spread can lead to cardiac tamponade
Distal spread = blocked main arterial branches

108
Q

What symptoms would be correlated with different arterial branches being blocked

A

Coronary arteries: MI
Brachiocephalic trunk: unequal arm pulses and central neurological symptoms
Renal arteries: acute kidney injury
SMA / IMA: acute mesenteric ischemia
Iliac arteries: lower limb ischaemia

109
Q

Management of aortic dissection

A

A-E resus with urgent cardiothoracic advice
- ITU admission
Keep SBP around 100 with IV beta blockers

Type A: consider for surgery due to risk of tamponade - grafting of the aortic root - high risk
Type B: manage medically unless complications

110
Q

Next step in poorly controlled hypertension, already taking ACEi, CCI and thiazide diuretic
K+ <4.5mmol/l

A

Add spironolactone

111
Q

Next step in poorly controlled hypertension, already taking ACEi, CCI and standard dose thiazide diuretic, K+ >4,5

A

Add an alpha or beta blocker

112
Q

First degree heart block on ECG

A

PR interval >0.2s

113
Q

Second degree heart block on ECG

A

Type 1: progressive prolongation of the PR interval until a dropped beat occurs

Type 2: PR interval is constant but the P wave is often not followed by a QRS complex

114
Q

Third degree heart block on ECG

A

There is no association between the P waves and the QRS complexes

115
Q

Management of second degree heart block type 1

A

If they are an athlete then no treatment as it is normal
If asymptomatic, no treatment required

116
Q

How to differentiate between unstable angina and an NSTEMI

A

Elevation in troponin indicated NSTEMI

117
Q

Presentation of acute mitral regurgitation

A

Sudden SOB
New onset widespread systolic murmur
Likely ruptured papillary muscle which leads to acute mitral regurgitation

Can present with pulmonary oedema - crackles
Decreased O2 sats
Drop in BP

118
Q

What site does infective endocarditis in IVDU most commonly affect

A

Tricuspid valve

119
Q

Most common cause of endocarditis in post valve surgery

A

Staphylococcus epidermidis

120
Q

What medication should be given for patients undergoing fibrinolytic for a STEMI

A

Altepase and fondaparinux (antithrombin)

121
Q

When should DC cardioversion be used

A

Tachyarrhythmia and a systolic BP <()

122
Q

When is thrombolysis indicated in PE

A

If there is presence of hypotension
Drop of SBP of at least 40 for more than 15 mins

123
Q

How do STEMI’s cause 1st degree AV block

A

Inferior MI’s are typically due to occlusion of the R coronary artery
The R coronary artery supplies the AV node so so a R coronary infarct can cause arrhythmias including sinus bradycardia and AV block

124
Q

Medications used to control rate in patients with AF

A

Beta blockers
Calcium Chanel blockers
Digoxin

125
Q

Medications used to control sinus rhythm in AF

A

Beta blockers
Dronedarone: 2nd line in patients following cardioversion
Amiodarone : esp if existing heart failure

126
Q

Treatment of symptomatic bradycardia

A

Atropine

127
Q

Treatment for broad complex tachycardia

A

IV amiodarone

128
Q

Hypokalaemia ECG features

A

Small or absent T waves
Prolonged PR interval
ST depression
Long QT

129
Q

How to treat symptomatic bradycardia if atropine fails

A

External pacing

130
Q

Features of bacterial endocarditis (FROM JANE)

A

Fever
Roth spots
Osler nodes
Murmur

Janeway lesions
Anaemia
Nail bed haemorrhages
Emboli

131
Q

2 signs of infective endocarditis

A

Fever
New murmur

132
Q

What is unstable angina

A

Chest pain that occurs at rest
Or sudden increased frequency / severity of existing angina

133
Q

Symptoms of ACS

A

Severe, crushing, gripping, heavy chest pain lasting longer than 20 mins

Not relieved by GTN sprays

Radiates to left arm, neck and jaw

134
Q

Pathophysiology of ACS

A

Atherosclerotic plaque rupture or erosion

135
Q

What is takotsubo cardiomyopathy (broken heart syndrome)

A

Left ventricular contractile disorder

Follows extreme psychological stress

The apex balloons and resembles a takotsubo

136
Q

How to differentiate between unstable angina and NSTEMI

A

No troponin rise and no MI in unstable angina

137
Q

Differnece between a STEMI and NSTEMI

A

NSTEMI is partial occlusion - partial thickness infarct

STEMI is complete occlusion - full thickness infarct

138
Q

When do troponin levels peak in MI

A

24 hours

139
Q

Early management for ACS (MONAA)

A

Morphine
Oxygen
Nitrates
Antiplatelet (300mg aspirin)
Anticoagulant

140
Q

Signs of ACS on ECG

A

New left bundle branch block: widening QRS complex
ST segment elevation or depression
T wave inversion

141
Q

What is a supraventricular tachycardia

A

Tachycardia that is not ventricular in origin
Characterised by sudden onset narrow complex tachycardia

142
Q

Management of supraventricular tachycardia

A

Vagal manoeuvres: Valsalva and carotid sinus massage

IV adenosine (verapamil in asthmatics)

Electrical cardioversion

143
Q

What should be given for prevention of supraventricular tachycardias

A

B blockers
Radio frequency ablation

144
Q

Medication for prevention of angina attacks

A

GTN spray
B blocker or CCI

145
Q

Investigation of choice in suspected aortic dissection

A

CT angiography thorax, abdo, pelvis

146
Q

When is a PE treated with oral anticoagulation for 3 months vs 6 months

A

3 months if provoked eg recent surgery, pregnancy, immobility, hormonal contraception

6 months if unprovoked

147
Q

When is synchronised cardioversion indicated

A

Acute presentation of AF
Signs of haemodynamic instability eg hypotension, HF

148
Q

PE CXR findings

A

Normal

149
Q

When are nitrates contraindicated

A

In patient with hypotension

150
Q

ECG changes in digoxin toxicity

A

Prolonged PR interval
Short QT interval
Inverted T waves
ST depression

151
Q

ECG changes in myocardial ischaemia

A

Inverted T waves
Peaked T waves
ST elevation
Long QT interval
Prolonged PR interval
R BBB
L BBB
ST depression

Junior Medicine (6 decks)

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