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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
What is atrial fibrillation
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
26
Presentation of AF
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
27
Management of AF
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
28
What is rate control in AF
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
29
What is rhythm control in AF (cardioversion)
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)
30
Why should all patients with AF be considered for systemic anticoagulation
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
31
What is the CHA2DS2VS tool for assessing stroke risk
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
32
MOA of DOACs (1st line anticoagulant)
Direct inhibition of specific proteins within the coagulation cascade (Preferred to warfarin as more consistent pharmacodynamics, and thus less need for therapeutic monitoring)
33
What are the underlying cardiac, respiratory or systemic causes of AF
Cardiac: hypertension, valvular heart disease, heart failure and IHD Resp: chest infection, PE and lung cancer Systemic: excessive alcohol intake, thyrotoxicosis, electrolyte depletion, infections
34
What is atrial flutter
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
35
Electrolyte abnormalities on ECG
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
36
What is ischaemic heart disease
(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
37
Pathology of atheroma formation ( 7 steps)
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
38
Risk factors for ischaemic heart disease
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
39
What is stable angina
- 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
40
Presentation of stable angina
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
41
What is decubitus angina
Angina precipitated by lying down as there is increased venous return to the heart - is associated with LVF
42
What is variant / prinzmetal angina
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
43
Investigations for stable angina
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
44
Why is CT coronary arteries a good investigation for stable angina
A non invasive test with a very good negative predictive value however remains less sensitive than invasive coronary angiography
45
Management of stable angina
Manage cardiovascular risk factors GTN spray PRN + B blocker or CCI Statin / low dose aspirin Refer to cardiology
46
Counselling for nitrates
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
47
Pathophysiology of nitrates
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
48
MOA of B blockers
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
49
Side effects of B blockers
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
50
MOA of calcium channel blockers
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
51
Side effects of calcium channel blockers
Flushing Headache Ankle swelling Constipation
52
MOA of nicorandil
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
53
What is the ACS
Made up of unstable angina, non ST elevation MI and ST elevation MI
54
Pathology of ACS
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
55
What is unstable angina
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
56
What is acute myocardial infarction
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
57
Involvement of the right coronary artery in ACS
Supplied RA, RV, posterior septum Blockage gives posterior / inferior MI Also supplies the AVN in 80% and SAN in 60%
58
Involvement of left coronary artery in ACS
Splits into the circumflex and left anterior descending artery Blockage gives a massive antero-lateral MI Leads I, aVL, V1-V6
59
Involvement of the circumflex artery in ACS
Mainly supplies LA and LV Blockage gives a lateral MI Leads I, aVL, V5/6
60
Involvement of the left anterior descending artery in ACS
Mainly supplies the LV and anterior septum Blockage gives an antero-septal MI Leads V1-V4
61
Symptoms of ACS
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
OE of ACS
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
Differential diagnoses of central chest pain
Cardiac: coronary artery spasm, pericarditis, myocarditis, aortic dissection Non cardiac: PE, pneumothorax, oesophageal disease, mediastinitis, costochondritis, trauma
64
ACS investigations
ECG Bloods: FBC and U&E, troponin, CXR Echocardiogram
65
Differnece between STEMI and NSTEMI
STEMI generally correlates with full thickness myocardial infarct whereas NSTEMI is partial thickness
66
ACS early management
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
What is the GRACE score for assessing ACS
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
STEMI management
PCI: invasive angioplasty +/- stenting is gold standard In STEMI should have a stent in less than 9pm is aimed for
69
Management of NSTEMI
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
ACS long term management
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
Immediate complications of ACS
Arrhythmias VT and VF AF Bradycardia or AV block
72
Short term complications of ACS
Pulmonary oedema Cardiogenic shock Thromboembolism Ventricular septal defect Ruptured chordae tendinae Rupture of ventricular wall
73
Long term complications of ACS
Heart failure Dressler’s syndrome Ventricular aneurysm formation
74
What is Dressler’s syndrome
Immune mediated pericarditis
75
Driving limitations of angina
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
Driving limitations with ACS
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
Driving limitations for HGV drivers with cardiovascular diagnoses
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
Causes of hypertension
- adrenal cortical diseases - renal artery stenosis - chronic kidney disease - pheochromocytoma - coarction of the aorta - neurogenic causes (raised ICP) - pregnancy
79
What is benign hypertension
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
What is malignant hypertension
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
Diagnosis threshold for malignant hypertension
SBP >200 or DBP >120 + Bilateral retinal haemorrhages / exudates
82
Widespread Pathological consequences of hypertension
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
Diagnosis of hypertension
Offer ambulatory BP monitoring at home if clinical measurement is >140/90
84
Measurements of stage 1 HTN
Clinic BP >140/90 and ABPM / HBPM >135/85
85
Measurements of stage 2 HTN
Clinic BP >160/100 and ABPM / HBPM >150/95
86
Severe HTN measurements
Clinic SBP >180 or DBP >110
87
When do you start drug treatment in HTN
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
What is the target BP for patients with HTN
Clinic: 140/90 Over 80s = 150/90 ABPM / HBPM: <135/85 145/85 if aged >80
89
First line treatment for HTN
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
MOA of ACEi
Act by RAAS system antagonism
91
Side effects of ACEi
Cough Hyperkalaemia First dose hypotension (should be given at night) Worsened renal function
92
MOA of CCI
Peripheral vasodilation
93
Side effects of CCIs
Peripheral oedema Postural hypotension Reflex tachycardia
94
What is primary hyperlipidaemia
Genetic predisposition to abnormal lipid metabolism
95
What is secondary hyperlipidaemia
Systemic metabolic disturbance eg obesity, alcoholism, diabetes
96
Hyperlipidaemia management
Lifestyle changes 1st line: statins 2nd line: fibrates Ezetimibe can be added for those with unsatisfactory lipid control
97
MOA of statins
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
Side effects of statins
Nausea Headache Muscle pains
99
MOA of fibrates
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
MOA of ezetimibe
Inhibits intestinal absorption of cholesterol to reduce serum LDL
101
Pathophysiology of aortic dissection
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
Possible outcomes of aortic dissection
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
Causes of aortic dissection
Hypertension Atheroma Congenital disease
104
Subtypes of aortic dissection
Type A (70%): involve the ascending aorta Type B (30%) do not involve the ascending aorta
105
Presentation of aortic dissection
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
Aortic dissection investigations
CT aortogram CXR: widened mediastinum ECG: similar to MI
107
Complications of aortic dissection
Retrograde spread can lead to cardiac tamponade Distal spread = blocked main arterial branches
108
What symptoms would be correlated with different arterial branches being blocked
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
Management of aortic dissection
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
Next step in poorly controlled hypertension, already taking ACEi, CCI and thiazide diuretic K+ <4.5mmol/l
Add spironolactone
111
Next step in poorly controlled hypertension, already taking ACEi, CCI and standard dose thiazide diuretic, K+ >4,5
Add an alpha or beta blocker
112
First degree heart block on ECG
PR interval >0.2s
113
Second degree heart block on ECG
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
Third degree heart block on ECG
There is no association between the P waves and the QRS complexes
115
Management of second degree heart block type 1
If they are an athlete then no treatment as it is normal If asymptomatic, no treatment required
116
How to differentiate between unstable angina and an NSTEMI
Elevation in troponin indicated NSTEMI
117
Presentation of acute mitral regurgitation
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
What site does infective endocarditis in IVDU most commonly affect
Tricuspid valve
119
Most common cause of endocarditis in post valve surgery
Staphylococcus epidermidis
120
What medication should be given for patients undergoing fibrinolytic for a STEMI
Altepase and fondaparinux (antithrombin)
121
When should DC cardioversion be used
Tachyarrhythmia and a systolic BP <()
122
When is thrombolysis indicated in PE
If there is presence of hypotension Drop of SBP of at least 40 for more than 15 mins
123
How do STEMI’s cause 1st degree AV block
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
Medications used to control rate in patients with AF
Beta blockers Calcium Chanel blockers Digoxin
125
Medications used to control sinus rhythm in AF
Beta blockers Dronedarone: 2nd line in patients following cardioversion Amiodarone : esp if existing heart failure
126
Treatment of symptomatic bradycardia
Atropine
127
Treatment for broad complex tachycardia
IV amiodarone
128
Hypokalaemia ECG features
Small or absent T waves Prolonged PR interval ST depression Long QT
129
How to treat symptomatic bradycardia if atropine fails
External pacing
130
Features of bacterial endocarditis (FROM JANE)
Fever Roth spots Osler nodes Murmur Janeway lesions Anaemia Nail bed haemorrhages Emboli
131
2 signs of infective endocarditis
Fever New murmur
132
What is unstable angina
Chest pain that occurs at rest Or sudden increased frequency / severity of existing angina
133
Symptoms of ACS
Severe, crushing, gripping, heavy chest pain lasting longer than 20 mins Not relieved by GTN sprays Radiates to left arm, neck and jaw
134
Pathophysiology of ACS
Atherosclerotic plaque rupture or erosion
135
What is takotsubo cardiomyopathy (broken heart syndrome)
Left ventricular contractile disorder Follows extreme psychological stress The apex balloons and resembles a takotsubo
136
How to differentiate between unstable angina and NSTEMI
No troponin rise and no MI in unstable angina
137
Differnece between a STEMI and NSTEMI
NSTEMI is partial occlusion - partial thickness infarct STEMI is complete occlusion - full thickness infarct
138
When do troponin levels peak in MI
24 hours
139
Early management for ACS (MONAA)
Morphine Oxygen Nitrates Antiplatelet (300mg aspirin) Anticoagulant
140
Signs of ACS on ECG
New left bundle branch block: widening QRS complex ST segment elevation or depression T wave inversion
141
What is a supraventricular tachycardia
Tachycardia that is not ventricular in origin Characterised by sudden onset narrow complex tachycardia
142
Management of supraventricular tachycardia
Vagal manoeuvres: Valsalva and carotid sinus massage IV adenosine (verapamil in asthmatics) Electrical cardioversion
143
What should be given for prevention of supraventricular tachycardias
B blockers Radio frequency ablation
144
Medication for prevention of angina attacks
GTN spray B blocker or CCI
145
Investigation of choice in suspected aortic dissection
CT angiography thorax, abdo, pelvis
146
When is a PE treated with oral anticoagulation for 3 months vs 6 months
3 months if provoked eg recent surgery, pregnancy, immobility, hormonal contraception 6 months if unprovoked
147
When is synchronised cardioversion indicated
Acute presentation of AF Signs of haemodynamic instability eg hypotension, HF
148
PE CXR findings
Normal
149
When are nitrates contraindicated
In patient with hypotension
150
ECG changes in digoxin toxicity
Prolonged PR interval Short QT interval Inverted T waves ST depression
151
ECG changes in myocardial ischaemia
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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