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IMT interview > Cardiology > Flashcards

Cardiology Flashcards

1
Q

How to calculate heart rate on ECG?

A

Regular
Count the number of large squares present within one R-R interval.
Divide 300 by this number to calculate heart rate.

Irregular
Count the number of complexes on the rhythm strip (each rhythm strip is typically 10 seconds long).
Multiply the number of complexes by 6 (giving you the average number of complexes in 1 minute).

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2
Q

How to interpret ECG

A

Rate
Rhythm
Cardiac axis
P waves
PR interval
QRS complex
ST segment

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3
Q

Right axis deviation?

A

Lead III has the most positive deflection, and lead I should be negative.
Right axis deviation is associated with right ventricular hypertrophy.

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4
Q

Left axis deviation?

A

Lead I has the most positive deflection.
Leads II and III are negative.
Left axis deviation is associated with heart conduction abnormalities.

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5
Q

What is a normal PR interval?

A

120-200ms (3-5 small squares)

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6
Q

what is considered first degree heart block?

A

> 0.2 seconds

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7
Q

what is second degree heart block type 1?

A

Second-degree AV block (type 1) is also known as Mobitz type 1 AV block or Wenckebach phenomenon.

Typical ECG findings in Mobitz type 1 AV block include progressive prolongation of the PR interval until eventually the atrial impulse is not conducted and the QRS complex is dropped.

AV nodal conduction resumes with the next beat, and the sequence of progressive PR interval prolongation and the eventual dropping of a QRS complex repeats itself.

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8
Q

What is second degree heart block type 2?

A

Second-degree AV block (type 2) is also known as Mobitz type 2 AV block.

Typical ECG findings in Mobitz type 2 AV block include a consistent PR interval duration with intermittently dropped QRS complexes due to a failure of conduction.

The intermittent dropping of the QRS complexes typically follows a repeating cycle of every 3rd (3:1 block) or 4th (4:1 block) P wav

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9
Q

What is 3rd degree heart block?

A

Third-degree (complete) AV block occurs when there is no electrical communication between the atria and ventricles due to a complete failure of conduction.

Typical ECG findings include the presence of P waves and QRS complexes that have no association with each other, due to the atria and ventricles functioning independently.

Cardiac function is maintained by a junctional or ventricular pacemaker.

Narrow-complex escape rhythms (QRS complexes of <0.12 seconds duration) originate above the bifurcation of the bundle of His.

Broad-complex escape rhythms (QRS complexes >0.12 seconds duration) originate from below the bifurcation of the bundle of His.

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10
Q

what can cause a shortened PR interval?

A

Simply, the P wave originates from somewhere closer to the AV node, so the conduction takes less time (the SA node is not in a fixed place, and some people’s atria are smaller than others).
The atrial impulse is getting to the ventricle by a faster shortcut instead of conducting slowly across the atrial wall. This accessory pathway can be associated with a delta wave (see below)

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11
Q

what is considered a narrow and broad QRS?

A

Narrow < 0.12 seconds
Broad > 0.12 seconds

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12
Q

LBBB and RBBB

A

Left - W in V1 and M in V6

Right M in V1 and W in V6

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13
Q

what can lead to tall QRS complexes?

A

Tall complexes imply ventricular hypertrophy (although can be due to body habitus e.g. tall slim people). There are numerous algorithms for measuring LVH, such as the Sokolow-Lyon index or the Cornell index.

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14
Q

what is a delta wave?

A

delta wave‘ indicates that the ventricles are being activated earlier than normal from a point distant from the AV node. The early activation then spreads slowly across the myocardium, causing the QRS complex’s slurred upstroke.

The presence of a delta wave does NOT diagnose Wolff-Parkinson-White syndrome. This requires evidence of tachyarrhythmias AND a delta wave.

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15
Q

What is a Q wave?

A

Isolated Q waves can be normal.

A pathological Q wave is > 25% the size of the R wave that follows it or > 2mm in height and > 40ms in width.

A single Q wave is not a cause for concern – look for Q waves in an entire territory (e.g. anterior/inferior) for evidence of previous myocardial infarction.

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16
Q

what may poor r wave progression indicate?

A

can be sign of previous MI

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17
Q

What is the J point segment?

A

The J point is where the S wave joins the ST segment.

This point can be elevated, resulting in the ST segment that follows it being raised (this is known as “high take-off”).

High take-off (or benign early repolarisation) is a normal variant that causes a lot of angst and confusion as it LOOKS like ST elevation.

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18
Q

what is considered ST elevation?

A

ST-elevation is significant when it is greater than 1 mm (1 small square) in 2 or more contiguous limb leads or >2mm in 2 or more chest leads.

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19
Q

What is considered ST depression?

A

ST depression ≥ 0.5 mm in ≥ 2 contiguous leads indicates myocardial ischaemia.

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20
Q

What do t waves represent?

A

depolarisation of the ventricles

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21
Q

what is considered tall t waves and what can they be associated with?

A

> 5mm in the limb leads AND
10mm in the chest leads (the same criteria as ‘small’ QRS complexes)
Tall T waves can be associated with:

Hyperkalaemia (“tall tented T waves”)
Hyperacute STEMI

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22
Q

in which leads are t waves usually inverted?

A

V1
lead III

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23
Q

what may lead to pathological t waves?

A

Ischaemia
Bundle branch blocks (V4-6 in LBBB and V1-V3 in RBBB)
Pulmonary embolism
Left ventricular hypertrophy (in the lateral leads)
Hypertrophic cardiomyopathy (widespread)
General illness

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24
Q

what can cause biphasic t waves?

A

biphasic t waves have two peaks - can indicate ischaemia and hypokalaemia

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25
Q

what can cause flattened t waves?

A

may be non-specific
may represent ischaemia or electrolyte imbalance

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26
Q

U waves?

A

U waves are not a common finding.

The U wave is a > 0.5mm deflection after the T wave best seen in V2 or V3.

These become larger the slower the bradycardia – classically U waves are seen in various electrolyte imbalances, hypothermia and secondary to antiarrhythmic therapy (such as digoxin, procainamide or amiodarone).

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27
Q

AF risk factors?

A

HTN
IHD
HF
Cardiomyopathy
DM
Obesity
Pneumonia
OSA
SMoking
Thyrotoxicosis
caffeine
Alcohol excess
CKD

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28
Q

Triggers for AF

A

The most common trigger for AF is rapid firing from the pulmonary veins (PVs).
Other sites:
- SVC, coronary sinus, vein of Marshall and atrial appendages.

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29
Q

mechanisms which AF is initiated ?

A

Automaticity: This refers to spontaneous depolarisation of myocardial cells in the absence of an external stimulus. In this context, it’s often due to enhanced automaticity where cells outside the sinoatrial node begin firing at a rate faster than the node itself.
Triggered Activity: This involves afterdepolarisations that are caused by influx of calcium ions during phase 4 of the action potential. These can be early (occurring during phase 2 or 3) or delayed (occurring after completion of phase 3).
Micro-reentry: This occurs when there is a small circuit that allows for re-entry within an anatomical or functional obstacle.

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30
Q

what does the substrate refer to in AF ?

A

The substrate refers to structural and electrophysiological changes that facilitate maintenance of AF once it has been initiated. There’s evidence suggesting that atrial fibrosis plays a major role in creating this substrate by causing electrical and structural remodelling.
Electrical Remodelling: This includes shortening of the action potential duration, decrease in wavelength and refractory period heterogeneity leading to multiple wavelet re-entry circuits.
Structural Remodelling: This involves changes in atrial size, shape and fibrosis. Fibrosis disrupts the normal myocardial architecture leading to slow conduction and re-entry circuits.

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31
Q

what are perpetuators in AF?

A

AF itself can lead to further remodelling (termed ‘AF begets AF’) which then perpetuates the arrhythmia. This includes progressive atrial dilatation and fibrosis, as well as alterations in calcium handling proteins and ion channels.
Atrial Dilatation: AF leads to atrial stretch which can increase the dispersion of refractoriness and promote re-entry. It also upregulates angiotensin II, promoting fibroblast proliferation and fibrosis.
Fibrosis: Further fibrosis due to AF creates a more heterogeneous substrate that promotes maintenance of the arrhythmia.
Ionic Remodelling: Changes in ion channel expression (e.g., downregulation of L-type calcium channels) can alter action potential characteristics further promoting AF.

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32
Q

How to manage AF?

A

If haemodynamically unstable - electrically cardioversion

If stable
< 48 hours onset rate or rhythm control
> 48 hours onset - rate control

Rate control
- beta blocker
- calcium channel blocker
- dioxin

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33
Q

when should rate control in AF not be first line management ?

A

whose atrial fibrillation has a reversible cause
who have heart failure thought to be primarily caused by atrial fibrillation
with new-onset atrial fibrillation (< 48 hours)
with atrial flutter whose condition is considered suitable for an ablation strategy to restore sinus rhythm
for whom a rhythm-control strategy would be more suitable based on clinical judgement

Rhythm control
- bet blockers
- dronedarone
- amiodarone - if co-existing heart failure

Catheter ablation

Anticoagulation

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34
Q

what is included in the Chadsvasc score?

A

CCF
HTN
Age > 75 =2
Age 65-74 = 1
Diabetes
previous stroke/TIA = 2
Vascular disease
sex female

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35
Q

what is included in the ORBIT ?

A

Hb
Age > 74
Bleeding history
renal impairment
treatment with antiplatelet agents

36
Q

what is SVT>

A

supraventricular tachycardia (SVT) refers to any tachycardia that is not ventricular in origin the term is generally used in the context of paroxysmal SVT. Episodes are characterised by the sudden onset of a narrow complex tachycardia, typically an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

36
Q

complications of AF

A

Stroke
Acute limb ischaemia
Mesenteric ischaemia

37
Q

what are the mechanisms that lead to SVT?

A

Re-entry

Increased automaticity

Triggered activity

38
Q

what happens in re-entry SVT?

A

This mechanism occurs most notably in AVRT, AVNRT and some forms of atrial tachycardia
In this mechanism, there is normal electrical conduction from the atria to the ventricles in the normal pathway
However, after this, retrograde conduction occurs via an accessory pathway from the ventricles back up to the atria
This leads to repetitive impulse propagation and subsequent tachycardia

39
Q

what happens in increased automaticity SVT?

A

his mechanism is responsible for greater than 70% of cases of focal atrial tachycardia
Normally, the SA node is responsible for generating the spontaneous action potentials to trigger myocardial contraction
However, due to increased automaticity, a group of cardiac cells gain the ability to generate a spontaneous action potential which takes over from the normal SA node functioning
The occurs due to pathological changes in the normal membrane resting potential of these cells
This leads to rapid and spontaneous depolarisation of cells, which become the dominant rhythm and therefore result in episodes of tachycardia
Alternatively, the SA node itself may exhibit enhanced automaticity and therefore trigger action potentials more frequently, leading to tachyarrhythmias

40
Q

what happens in trigger activity SVT?

A

This mechanism is largely responsible for atrial fibrillation and atrial flutter, as well as approximately 30% of focal atrial tachycardias
SVT as a result of triggered activity occurs due to extra depolarisations which occur immediately after cell re-polarisation, termed ‘after-depolarisations’
If the after-depolarisations reach a sufficient amplitude to bring the membrane to the electrical threshold for depolarisation, a spontaneous action potential occurs
These spontaneous action potentials, called a triggered response, lead to extra-systoles, which have the potential to trigger subsequent tachyarrhythmias

41
Q

what is Atrio ventricular nodal re-entrant tachycardia?

A

Most common form of paroxysmal SVT
Originates from a re-entrant retrograde electrical circuit involving the AV node, resulting in initiation and propagation of a cardiac tachyarrhythmia

42
Q

what is trio ventricular re-entrant tachycardia?

A

The second most common form of paroxysmal SVT
Similar to AVNRT, it originates via a re-entrant retrograde electrical circuit, however it involves an accessory pathway between the atria and the ventricles, rather than the AV node
Some forms of AVRT may exhibit a Wolff-Parkinson-White pattern, whereby an accessory pathway capable of anterograde conduction leads to pre-excitation of the ventricles
This accessory pathway is a bypass tract, therefore avoiding the AV node and therefore the normal delay which occurs at this point
Leads to the characteristic ‘delta wave’ on ECG, whereby there is up-sloping at the start of the QRS complex due to the early ventricular excitation

43
Q

Atrial tachycardia?

A

May be either focal or multi-focal
Focal: due to a single focus of atrial tissue generating more rapid action potentials, leading to a rapid tachyarrhythmia
Multi-focal: this is synonymous with atrial flutter, whereby there is a re-entrant electrical circuit in the atria (usually around the tri-cuspid annulus and cavo-tricuspid isthmus) leading to rapid and recurrent de-polarisation without normal SA node functioning and conduction

44
Q

when would SVT be broad complex?

A

SVT with aberrant conduction or anti-dromic AVRT,

45
Q

Management of SVT?

A

unstable - synchronised DCCV

Regular Narrow complex tachycardia - stable
- start with vagal manoeuvres

Adenosine - rapid IV bolus using large cannula
start at 6mg, then if unsuccessful 12mg and then 18mg

If adenosine is contraindicated or fails - trial of verapamil - give over two minute period

46
Q

what are examples of vagal manoeuvres?

A

valsalva manoeuvre, applying a cold stimulus to the face, and carotid sinus massage

47
Q

what is the valsalva manoeuvre?

A

Valsalva manoeuvres commonly used include forceful exhalation against a closed airway for approximately 15-20 seconds, blowing into an occluded straw, or adopting a head-down position for approximately 15-20 seconds (approximately 25% success rate for terminating SVT episodes)

48
Q

when is long term management of SVT required?

A

only indicated if the frequency and severity of SVT episodes significantly impacts on the patients quality of life and functioning

ndications for definitive or long-term treatment include:
Recurrent symptomatic SVT episodes affecting quality of life
Evidence of Wolff-Parkinson-White on ECG and symptoms of SVT episodes
Infrequent SVT episodes but in a profession or sport which puts themselves or others at risk (e.g. drivers, pilots, surgeons)

49
Q

what are the options for long term management of SVT?

A

radio-frequency ablation

If this is contraindicated
beta blocker of CCB

2nd line - medication options include flecainide and sotalol

50
Q

Cardiac causes of bradycardia?

A

Sinus node dysfunction: This intrinsic cardiac disorder often presents with fatigue, light-headedness or syncope. Patients may also experience palpitations.
Atrioventricular (AV) block: Depending on the degree of the block, patients might be asymptomatic or present with symptoms similar to sinus node dysfunction. High-degree AV blocks can lead to Stokes-Adams attacks.
Infective endocarditis: A high index of suspicion should be maintained in patients presenting with new-onset bradycardia and associated fever, night sweats or weight loss. The causative pathogen is often Staphylococcus aureus.
Myocardial infarction (MI): Inferior wall MIs are commonly associated with bradycardia due to vagal stimulation. These patients typically complain of chest pain radiating to the left arm or jaw.

51
Q

Non-cardiac causes of Bradycardia?

A

Hypothermia
Sleep apnoea
Increased intracranial pressure

52
Q

Drugs which induce bradycardia?

A

beta blockers
calcium channel blockers
digoxin

53
Q

How to manage bradycardia?

A

Atropine 500mcg IV

If there is an unsatisfactory response the following interventions may be used:
atropine, up to a maximum of 3mg
transcutaneous pacing
isoprenaline/adrenaline infusion titrated to response

54
Q

what leads are effected in inferior MI

A

II
III
AVF

(supplied by the right coronary)

55
Q

Lateral MI leads and supply?

A

I
AVL
V5
V6

Left circumflex artery (lead I and aVL)

Distal LAD, left circumflex artery or right coronary artery (V5&V6)

56
Q

anterior MI leads and leads?

A

V3 and V4

distal LAD

57
Q

septal MI - leads and supply?

A

V1 and V2
proximal LAD

58
Q

pathophysiology of ACS?

A

nitial endothelial dysfunction is triggered by a number of factors such as smoking, hypertension and hyperglycaemia
this results in a number of changes to the endothelium including pro-inflammatory, pro-oxidant, proliferative and reduced nitric oxide bioavailability
fatty infiltration of the subendothelial space by low-density lipoprotein (LDL) particles
monocytes migrate from the blood and differentiate into macrophages. These macrophages then phagocytose oxidized LDL, slowly turning into large ‘foam cells’. As these macrophages die the result can further propagate the inflammatory process.
smooth muscle proliferation and migration from the tunica media into the intima results in formation of a fibrous capsule covering the fatty plaque.

59
Q

complications of atherosclerosis?

A

the plaque forms a physical blockage in the lumen of the coronary artery. This may cause reduced blood flow and hence oxygen to the myocardium, particularly at times of increased demand, resulting clinically in angina
the plaque may rupture, potentially causing a complete occlusion of the coronary artery. This may result in a myocardial infarction

60
Q

ECG changes in MI?

A

hyperacute T waves are often the first sign of MI but often only persists for a few minutes
ST elevation may then develop
the T waves typically become inverted within the first 24 hours. The inversion of the T waves can last for days to months
pathological Q waves develop after several hours to days. This change usually persists indefinitely

61
Q

STEMI criteira?

A

clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years
1.5 mm ST elevation in V2-3 in women
1 mm ST elevation in other leads
new LBBB (LBBB should be considered new unless there is evidence otherwise)

62
Q

Aortic dissection?

A

Aortic dissection typically presents with severe, tearing chest pain that radiates to the back. It may be associated with symptoms related to end-organ ischaemia such as syncope or stroke.
Unlike ACS, aortic dissection may show wide pulse pressure or asymmetric blood pressure in both arms.
The electrocardiogram (ECG) changes in aortic dissection are non-specific and can mimic those seen in ACS. However, imaging studies such as computed tomography angiography (CTA) or magnetic resonance angiography (MRA) can help confirm the diagnosis.

63
Q

Management of all patients with ACS?

A

aspirin 300mg
oxygen if saturations < 94% in keeping with

morphine should only be given for patients with severe pain

nitrates
can be given either sublingually or intravenously
useful if the patient has ongoing chest or hypertension
should be used in caution if patient hypotensive

64
Q

management of SREMI?

A

PCI if within 12 hours of symptom onset and PCI can be delivered within 120 minutes of the time when thrombolysis could have been given

if patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered

drug-eluting stents are now used

Radial access is preferred to femoral

Thrombolysis - offered within 12 hours of onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when thrombolysis could have been given

DAPT prior to PCI
aspirin + either prasugrel or clopidogrel

65
Q

management on NSTEMI?

A

DAPT

Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately
if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given

66
Q

what risk assessment can be used in ACS?

A

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It can be calculated using online tools and takes into account the following factors:
age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

67
Q

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

A

immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at immediate, high or highest risk
coronary angiography should also be considered for patients is ischaemia is subsequently experienced after admission

68
Q

How to manage high INR?

A

> 8 + minor bleeding - stop warfarin and give phytomenadione by slow intravenous injection. The dose of phytomenadione may be repeated after 24 hours if the INR is still too high.

> 8 with no bleeding - stop warfarin and give vitamin K orally

between 5-8 minor bleeding - stop warfarin and give IV Vk

between 5-8 withhols 1 or 2 doses of warfarin and reduce subsequent maintenance doses

69
Q

What is included in the DVT wells score?

A

Active cancer
recent immobilisation
recent bedridden
Localised tenderness along the distribution of the deep venous system
entire leg swollen
calf swelling at least 3 cm larger than symptomatic side
Pitting oedema
collateral supeficial veins
previous DVT
alternative diagnosis at least as likely = 2 points

70
Q

Invesitgations for DVT ?

A

if wells score >2
carry out USS within 4 hours

If can’t be done within 4 hours then send d-dimer and start anticoagulation

if the scan is negative but the D-dimer is positive:
stop interim therapeutic anticoagulation
offer a repeat proximal leg vein ultrasound scan 6 to 8 days later

If wells =1 pont
perform a d-dimer

71
Q

management of DVT?

A

apixaban or rivaroxaban (both DOACs) should be offered first-line following the diagnosis of a DVT

if renal impairment is severe (e.g. < 15/min) then LMWH, unfractionated heparin or LMWH followed by a VKA

if the patient has antiphospholipid syndrome (specifically ‘triple positive’ in the guidance) then LMWH followed by a VKA should be used

for at least 3 months for provoked
3-6 months for active cancer
Unprovoked - 6 months

72
Q

risk factors for DVT

A

male
> 60
immobilisation
Long haul flights
inflammatory state - vasculitis, sepsis
Malignancy
medication (COCP, chemo)
Obesity
Pregnancy
Previous VTE
surgery or trauma
smoking
varicose veins

73
Q

what is Virchow’s triad?

A

Hypercoagulability: Blood that clots too easily
Endothelial injury: Damage to the lining of a blood vessel
Hemodynamic changes: Abnormal blood flow

74
Q

Clinical features of DVT?

A

pain
swelling
skin changed - Discolouration of the affected leg ranging from pallor (uncommon) to cyanosis and diffuse erythema.
Superficial veins become distended and more prominent in approximately 17% of patients (it is worth noting that up to 20% of patients without DVT will have dilated superficial leg veins).

Increased temp
calf tenderness upon palpation of the deep veins of the leg
difference in size of calves

75
Q

what is the Wells score for DVT?

A

The Wells’ criteria for DVT is a score that predicts the likelihood of DVT. It should be used as a clinical aid rather than for management. It uses a mixture of measures including history and examination to give a score, which identifies probability. Its benefit is it allows the clinician to make a decision on blood testing with D-dimer against US doppler which is more expensive and may be more difficult to arrange.

76
Q

other investigations for unprovoked DVT?

A

Patients diagnosed with an unprovoked DVT, who are not known to have cancer, should have their medical history reviewed and baseline blood test results, including full blood count, renal and hepatic function, PT and APTT, and should be physically examined to rule out any obvious signs of cancer.

Further examinations, such as a CT-TAP should not be routinely ordered for patients with unprovoked DVT unless there is a clinical indication for this test.

hrombophilia testing is also not routinely offered, but may be considered in people with unprovoked DVT

77
Q

Differential Diagnosis for DVT?

A

Cellulitis

Superficial thrombophlebitis - oedema and erythema are localised to the area around the affected part of the vein rather than causing changes in the whole leg; the thrombus may be palpable as feel along the course of the affected vein

Depednant oedema

Trauma

78
Q

Complications of DVT

A

PE

Post thrombotic syndrome - PTS develops in approximately 20% to 50% of patients within two years following a DVT. This syndrome results from chronic venous insufficiency due to damaged valves in the veins, leading to blood pooling and increased venous pressure.
Clinical Presentation: Common manifestations include persistent leg pain, swelling, and heaviness. Chronic venous insufficiency may also lead to skin changes such as hyperpigmentation, eczema, and, ultimately, venous ulcers.
Diagnosis: PTS is primarily diagnosed based on clinical evaluation and history of DVT. Duplex ultrasonography is crucial for confirming venous reflux and valve dysfunction.

79
Q

risk factors for PE?

A

Immobility
surgery
malignancy
trauma
pregnancy and post party
Genetic predisposition - Factor V Leiden, prothrombin gene mutation, deficiencies in protein C, protein S, or antithrombin
Hormone therapy
co-morbidities

80
Q

Investigations for PE?

A

Pulmonary embolism rule out criteria - age > 50, HR > 100, O2 sats < 94%, previous DVT/PE, reset surgery/trauma in the last 4 weeks, haemoptysis, unilateral leg swelling, oestrogen use - if all negative - probability of PE < 2%

Wells score
PE likely - more than 4 points
PE unlikely - 4 points or less

If > 4 points - arrange a CTPA
If delay in CTPA commence DOAC

If <4 ponts - arrange a d-dimer

ECG
the classic ECG changes seen in PE are a large S wave in lead I, a large Q wave in lead III and an inverted T wave in lead III - ‘S1Q3T3’. However, this change is seen in no more than 20% of patients
right bundle branch block and right axis deviation are also associated with PE
sinus tachycardia may also be seen

81
Q

Is d-dimer a good test ?

A

ensitivity = 95-98%, but poor specificity
age-adjusted D-dimer levels should be considered for patients > 50 years

82
Q

what is PE wells?

A

Clinical signs of DVT
PE most likely diagnosis
HR > 100
Recent immobilisation or surgery
previous DVT/PE
Haemoptysis
malignancy

83
Q

when is thrombolysis indicated in PE?

A

Thrombolysis
thrombolysis is now recommended as the first-line treatment for massive PE where there is circulatory failure (e.g. hypotension)
other invasive approaches should be considered where appropriate facilities exist

84
Q

what can be done for patients with recurrent PE despite adequate anticoagulation?

A

Patients who have repeat pulmonary embolisms, despite adequate anticoagulation, may be considered for inferior vena cava (IVC) filters. These work by stopping clots formed in the deep veins of the leg from moving to the pulmonary arteries.

85
Q

Complications of PE?

A

Right ventricular failure
cardiogenic shock
Arrhythmias
Respiratory failure

subacute complications
Infarction and lung necrosis
Pleural effusion
Pneumothorax

Chronic complications - pulmonary hypertension

IMT interview (12 decks)

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