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Supporting Life > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Myocardial infarction definition

A

Necrosis of the myocardium as a result of ischaemia

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2
Q

MI/acute coronary syndrome classifications/DDx

A

Unstable angina - partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG

NSTEMI - severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation

STEMI - complete occlusion of coronary artery, ST elevation of 2mm in >=2 chest leads or 1mm in >=2 limb leads or left bundle branch block plus troponin positive chest pain

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3
Q

Angina definition and types

A

Myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise

stable = only during exertion, unstable = at rest

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4
Q

Type 2 myocardial infarction definition

A

MI due to cardiac hypoperfusion for other reasons such as severe sepsis, hypotension, or coronary artery spasm

may not require conventional MI treatments

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5
Q

Typical MI/ACS presentation

A

Chest pain
Can use SOCRATES mnemonic:

Site - central/left-sided
Onset - sudden
Character - crushing/someone sitting on your chest
Radiation - left arm, neck and jaw
Associated symptoms - nausea, sweating, clamminess, SoB, vomiting, syncope
Timing - constant
Exacerbating/relieving factors - worsened by exercise
Severity - often severe

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6
Q

Atypical MI/ACS presentation

A

Epigastric pain
No pain (more commonly in elderly and diabetics)
Acute breathlessness
Palpitations
Syncope
Acute confusion
Diabetic hyperglycaemic crises

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7
Q

MI/ACS investigations

A

ECG - look for ST elevation, left bundle branch block or other ST abnormalities (if shows STEMI then troponin is irrelevant -> it’s a STEMI)

Bloods:
Troponin - at least 3 hours after onset of pain, repeated after 6 hours
Renal function
HbA1c and lipid profile
FBC
CRP
D-dimer if needed to rule out PE

Chest X-ray

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8
Q

NSTEMI/unstable angina ECG changes

A

ST depressions
T wave inversions
Pathological Q waves not typical

T wave inversions with ST changes = ongoing ischaemia
isolated T wave inversions = post-ischaemic

Do not necessarily represent the vessel location

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9
Q

STEMI management

A

A-E for emergencies

  1. Targeted O2 therapy
  2. Loading dose of aspirin 300 mg
  3. GTN spray
  4. IV morphine/diamorphine
  5. Primary percutaneous coronary intervention for pts who present within 12hrs of onset of pain AND are <2hrs since first medical contact
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10
Q

NSTEMI/unstable angina management

A
  1. Targeted O2 therapy
  2. Loading dose of aspirin 300 mg and fondaparinux
  3. GTN spray
  4. IV morphine/diamorphine
  5. Antithrombin therapy such as low mol weight heparin
  6. Pts with high 6 month mortality offered angiogram
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11
Q

Post-MI management

A
  1. Aspirin 75mg + second anti-platelet (clopidogrel 75mg OD or ticagrelor 90mg OD)
  2. Beta blocker (normally bisoprolol)
  3. ACE-inhibitor (normally ramipril)
  4. High dose statin (e.g. Atorvastatin 80mg ON)

All patients should have an ECHO performed to assess systolic function and any evidence of heart failure should be treated
All patients should be referred to cardiac rehabilitation
Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia

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12
Q

MI/ACS complications

A

Ventricular arrhythmia - usually self-resolve
Recurrent ischaemia/infarction/angina - inserted stends can thrombose, new infarcts can occur, and angina can continue for some time
Acute mitral regurgitation - due to papillary muscle rupture, presents with pansystolic murmur and severe & sudden heart failure
Congestive heart failure - due to impairment of heart muscle function secondary to the ischaemia
2nd, 3rd degree heart block
Cardiogenic shock
Cardiac tamponade
Ventricular septal defects
Left ventricular thrombus/aneurysm - post-anterior MI the myocardium can be susceptible to wall stress; can present as persisting ST elevation
Left/right ventricular free wall rupture - necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space, causing a rapid tamponade
Dressler’s Syndrome - fever and pleuritic chest pain 2-3 weeks or up to a few weeks after an MI
Acute pericarditis

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13
Q

Stable angina definition/presentation

A

Troponin negative chest pain triggered by myocardial ischaemia

  1. Constriction/heavy discomfort to chest (may radiate to jaw/neck/arm)
  2. Brought on by exertion
  3. Alleviated by 5 mins rest or GTN spray

3/3 = typical angina
2/3 = atypical
0-1/3 = non-anginal

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14
Q

Stable angina classes

A

Class I - no angina with normal physical activity, may be triggered by strenuous activity
Class II - angina pain causes slight limitation on normal physical activity
Class III: angina causes marked limitation on normal physical activity
Class IV: angina occurs with any physical activity and may occur at rest (unstable angina)

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15
Q

Stable angina symptoms

A

Central, constricting chest pain that radiates to neck/jaw/arm
Exertional chest pain that is relieved on rest/GTN
Associated symptoms: nausea, vomiting, clamminess or sweating

Stable angina may have no clinical signs on examination at rest

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16
Q

Stable angina investigations

A

ECG
Bloods - FBC and TFTs to exclude anaemia and hyperthyroidism which can exacerbate symptoms

CT coronary angiogram (indicated if typical/atypical angina pain or if ECG shows ischaemic changes in chest pain with <2 angina features)

If inconclusive, functional imaging to be used

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17
Q

Stable angina management

A

optimise cardiovascular risk factors to reduce atherosclerotic processes

Secondary prevention: aspirin 75mg OD and statin 80mg ON
GTN spray for symptom relief: inform patient of side-effects (headache, flushing, dizziness) and to repeat dose if pain not stopped after 5 minutes

1st line = beta-blocker (bisoprolol) OR calcium channel blocker (verapamil or diltiazem). Do not combine due to risk of heart block

If neither can be tolerated to consider a long-acting nitrate (ISMN), ivabradine, nicorandil or ranolazine

2nd line = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker (amlodipine or nifedipine)

3rd line = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker AND long-acting nitrate

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18
Q

Scale on ECG paper

A

Small square = 0.04s
Large square = 0.2s
5 large squares = 1s
300 large squares = 1 min

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19
Q

Limb electrodes colour/placement

A

(ride your green bike)

Red - right arm
Yellow - left arm
Green - left leg
Black - right leg

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20
Q

Views of the heart by lead

A

V1-2 = septal
V3-4 = anterior
V5-6 = lateral

Lead I = lateral
Lead II = inferior
Lead III = inferior
aVR = lateral
aVL = lateral
aVF = inferior

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21
Q

Normal cardiac axis ECG

A

Usually ~30 degrees

Leads I, II and III positive
Lead II most positive, then lead I, then lead III
aVR shows most negative deflection

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22
Q

Right axis deviation ECG

A

Axis distorted to the right (90-180 degrees)

Lead III most positive, then lead II
Lead II deflected
Lead aVF more positive

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23
Q

ECG leads angles

A

Lead I = 0 degrees
Lead II = 60 degrees
aVF = 90 degres
Lead III = 120 degrees
aVR = -150 degrees
aVL = -30 degrees

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24
Q

Left axis deviation ECG

A

Depolarisation between -30 and -90

aVL then lead I most positive
Lead II negative
Lead III most negative

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25
Q

Atrial fibrillation ECG features

A

Lack of P wave
Narrow QRS complex
Fibrillating baseline
Irregularly irregular rhythm

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26
Q

Atrial fibrillation presentation

A

Palpitations
Chest pain
Shortness of breath
Lightheadedness
Syncope

On auscultation, variable intensity heart sound
Apical to radial pulse deficit
Irregularly irregular variable volume pulse

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27
Q

Distinguishing between a fib and atrial flutter

A

Afib shows no p waves
Atrial flutter has a characteristic sawtooth baseline

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28
Q

Afib investigations

A

ECG is definitive
Bloods to look for reversible causes such as infection, hyperthyroidism or alcohol use
Echocardiogram to look for cardiac causes

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29
Q

Acute afib management

A

A-E in emergency

1st line = synchronised DC cardioversion +/- amiodarone

If the patient is stable and onset of AF <48 hours:

Rate or rhythmn control
Rhythm control with DC cardioversion (+ sedation) or pharmacological anti-arrhythmics (fleicanide if no structural heart disease, amiodarone if history of structural heart disease).
If DC cardioversion is delayed then heparin will be required to anticoagulate the patient

If the patient is stable and onset of AF >48 hours/unclear time of onset:

Rate control only
Rate control with beta-blockers or diltiazem
Need to anticoagulate for 3/52 prior to attempting cardioversion due to the risk of throwing off a clot
Also perform a TOE to exclude a mural thrombus

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30
Q

Afib complications

A

Heart failure
Systemic emboli leading to ischaemic stroke, mesenteric ischaemia or acute limb ischaemia
Bleeding

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31
Q

Management of chronic AF -rate control

A

Aims to reduce heart rate to reduce symptoms; first line approach

1st line = beta-blocker (bisoprolol; NOT sotalol) or rate-limiting calcium channel blocker (diltiazem; contraindicated in heart failure)
2nd line medications: dual therapy (under specialist guidance)

Digoxin monotherapy may be considered in those with non-paroxysmal AF who are sedentary

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32
Q

Management of chronic AF -rhythm control

A

The aims to revert a patient back into sinus rhythm

Should be offered to patients who have:

AF secondary to a reversible cause
Heart failure thought to be caused by AF
New-onset AF
Or those for whom a rhythm control strategy would be more suitable based on clinical judgement

Rhythm control can be achieved via two methods:

Electrical cardioversion
Pharmacological cardioversion: amiodarone (only for older, sedentary patients due to side effects), flecainide (can take PRN, preferred in young patients with normal hearts) or sotalol (for patients not meeting demographics for amiodarone and flecainide

Moment of return to sinus rhythm poses the highest stroke risk. Therefore, rhythm control should only be attempted if the onset of AF <48 hours, a patient has undergone 3/52 of anticoagulation or has had a TOE to exclude a mural thrombus

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33
Q

CHA2DS2VASc Score

A

C: 1 point for congestive cardiac failure
H: 1 point for hypertension
A2: 2 points if the patient is aged 75 or over
D: 1 point if the patient has diabetes mellitus
S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA)
V: 1 point if the patient has known vascular disease
A: 1 point if the patient is aged 65-74
Sc: 1 point if the patient is female

Males scoring 1 or more and females scoring 2 or more should be anti-coagulated

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34
Q

Anti-coagulation options in afib

A

Direct oral anticoagulants (DOACs):

Considered first line for anticoagulation in AF
Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran
Do not require monitoring
Generally associated with fewer bleeding risks compared to warfarin
Most have approximately 12 hour half-lives therefore if a patient misses a dose they are not covered

Warfarin:

Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially prothrombotic)
Requires regular INR monitoring
INR can be affected by a whole host of drugs and foods
Has 40 hour half-life therefore anticoagulant effect lasts days
Is the only oral anticoagulant licenced for valvular AF

Low Molecular Weight Heparin (LMWH):

eg enoxaparin
A rare option in patients who cannot tolerate oral treatment.
Involves daily treatment dose injections

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35
Q

Heart failure definition

A

Failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body

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36
Q

Low-output heart failure definition and causes

A

When cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body’s needs

AAPPTT

Anaemia
Arteriovenous malformation
Paget’s disease
Pregnancy
Thyrotoxicosis
Thiamine deficiency (wet Beri-Beri)

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37
Q

High-output HF definition

A

a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet

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38
Q

Systolic vs diastolic heart failure definition

A

Systolic dysfunction = an impairment of ventricular contraction despite adequate ventricular filling e.g. ischaemic heart disease, dilated cardiomyopathy, myocarditis

Diastolic dysfunction =the inability of the ventricles to relax and fill normally; the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling e.g. uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypetrophic cardiomyopathy, cardiac tamponade, constrictive pericarditis

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39
Q

Acute vs chronic heart failure definition

A

Acute HF = new-onset of HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known chronic HF

Chronic HF progresses more slowly and may take many years to develop

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40
Q

Presentation of left heart failure

A

Causes pulmonary congestion

Shortness of breath on exertion
Orthopnoea
Paroxysmal nocturnal dyspnoea
Nocturnal cough (± pink frothy sputum)
fatigue

Tachypnoea
Bibasal fine crackles on auscultation of the lungs
Cyanosis
Prolonged capillary refill time
Hypotension

Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation

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41
Q

Presentation of right heart failure

A

Causes venous congestion

Ankle swelling
Weight gain
Abdominal swelling and discomfort
Anorexia and nausea

Raised JVP
Pitting peripheral oedema (ankle to thighs to sacrum)
Tender smooth hepatomegaly
Ascites
Transudative pleural effusions (typically bilaterally)

42
Q

Heart failure investigations

A

For stable patient in GP

  1. NT-pro-BNP level (released by centricles in response to myocardial stretch), high negative predicted value (2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks; 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks)
  2. 12-lead ECG
  3. Transthoracic echo, look at ejection fraction (if <40% = HFrEF, systolic dysfunction; >40% with raised BNP HFpEF, diastolic dysfunction)
  4. Bloods (U&E), LFTs, FTF, glucose, lipid profile
  5. CXR - ABCDE signs

A: Alveolar oedema (with ‘batwing’ perihilar shadowing)
B: Kerley B lines (caused by interstitial oedema)
C: Cardiomegaly (cardiothoracic ratio >0.5)
D: upper lobe blood diversion
E: Pleural effusions (typically bilateral transudates)
F: Fluid in the horizontal fissure

43
Q

Heart failure conservative management

A

Weight loss if BMI >30
Smoking cessation
Salt and fluid restriction - improves mortality
Supervised exercise-based group rehabilitation programme for people with heart failure

44
Q

Heart failure medical management

A

Symptomatic relief for fluid overload = loop diuretics

1st line = ACE-I and beta blocker

ARB if ACE-I intolerant, hydralazine if ARB and ACE-I intolerant

2nd line = aldosterone antagonist (spironolactone or eplerenone)

If symptoms persist consider:
Hydralazine and a nitrate for Afro-Caribbean patients
Ivabradine if in sinus rhythm and impaired EF
Digoxin = useful in those with AF. This worsens mortality but improves morbidity

Also SGLT2 if needed as add on

(BASH for systolic - beta blocker, ACE-I, spironolactone, hydralazine)

45
Q

Heart sounds

A

S1- tricuspid valve closure
S2 - aortic + pulmonary valve closure
S3 - ventricular filling aka diastole - this would correspond to the T wave
S4 - atria contract against a stiff ventricle - this would correspond to the p wave

46
Q

Atrial flutter symptoms

A

asymptomatic
palpitations
lightheadedness
syncope
chest pain

47
Q

Atrial flutter ECG features

A

Regular rhythm
Saw-tooth baseline with repetition at 300bpm (these are atrial flutter waves)
Narrow QRS complexes
Ventricular rate which depends on the level of AV block:
150bpm if 2:1
100bpm if 3:1
75bpm if 4:1
60bpm if 5:1

48
Q

Atrial flutter management - hemodynamically unstable patients

A

Signs of haemodynamic instability:

Shock: suggests end-organ hypoperfusion.
Syncope: cerebral hypoperfusion.
Chest pain: myocardial ischaemia.
Pulmonary oedema: evidence of heart failure.
If signs of haemodynamic instability:

1st line = direct current synchronised cardioversion +/- amiodarone

49
Q

Atrial flutter management - hemodynamically stable patients

A

Treat reversible causes: fluid rehydration (in septic/dehydrated patients) can revert atrial flutter into sinus rhythm.

Rate and rhythmn control

1st line = beta-blocker (bisoprolol) OR calcium channel blocker (diltiazem, verapamil)
2nd line = if rate control fails to control flutter than consider cardioversion.
3rd line = recurrent or refractory flutter managed with ablation of arrhythmogenic foci at cavotricuspid isthmus. Success rate high at 90%.
Suitable for those symptomatic despite rate control and those in which cardioversion has failed

50
Q

Ventricular fibrillation definition

A

Irregular broad complex tachycardia
Always a pulseless rhythm
Polymorphic and irregular QRS complexes

51
Q

Ventricular fibrillation management

A

Follow ALS algorithm

VF is a shockable rhythm so a 200J bi-phasice unsynchronised shock should be administered
IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock
Adrenaline should be administered every 3-5 minutes thereafter

52
Q

Heart block definition

A

Obstruction in electrical conduction system of the heart

Can occur anywhere from the SA node, to the AV node to the bundle of His or bundle branches themselves

53
Q

First degree heart block definition/causes/management

A

Prolonged conduction of electrical activity via AV node
PR interval >200ms on ECG

Causes
High vagal tone: e.g. athletes
Acute inferior MI
Electrolyte abnormalities: e.g. hyperkalaemia
Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors

Management
First degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed

54
Q

Second degree heart block Mobitz type I/Wenkebach definition/causes/management

A

second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS

Causes
MI (mainly inferior)
Drugs such as beta/calcium channel blockers, digoxin
Professional athletes due to high vagal tone
Myocarditis
Cardiac surgery

Management
It is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine

55
Q

Second degree heart block Mobitz type II definition

A

second degree AV block where there are intermittent non-conducted P waves. The PR interval is constant (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.

In most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block

56
Q

Second degree heart block Mobitz type II causes

A

Infarction: particularly anterior MI which damages the bundle branches
Surgery: mitral valve repair or septal ablation
Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis
Fibrosis: Lenegre’s disease
Infiltration: sarcoidosis, haemochromatosis, amyloidosis
Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone

57
Q

Second degree heart block Mobitz type II management

A

Definitive management is with a permanent pacemaker as these patients are at risk of complete heart block and at risk of becoming haemodynamically unstable

58
Q

Third degree heart block definition

A

atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.

ECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. patients are at high risk of asystole, ventricular tachycardia and cardiac arrest

59
Q

Third degree heart block causes

A

Myocardial infarction: especially inferior
Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine
Idiopathic fibrosis

60
Q

Third degree heart block management

A

Permanent pacemaker requires insertion due to the risk of sudden death

61
Q

Primary hypertension definition

A

primary hypertension is characterised by persistently elevated blood pressure due to age-related pathophysiological changes

accounts for approximately 90-95% of cases of hypertension

62
Q

Hypertension definition

A

a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg

63
Q

Hypertension classification

A

Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg
Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg
Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg

64
Q

Hypertension investigations

A

ABPM or home blood pressure monitoring if ABPM is not tolerated or declined

Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores)

Urine dip and albumin:creatinine level
Blood glucose, lipids and renal function
Fundoscopy for evidence of hypertensive retinopathy
ECG: look for evidence of LV hypertrophy

Referral for same-day specialist assessment should be arranged for people with:

Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI)

65
Q

Hypertension medical management - when to start treatment

A

Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR
Anyone with stage 2 hypertension

66
Q

Hypertension treatment NICE guidelines

A

Step 1:
ACE-inhibitor (e.g. Ramipril) if <=55 years old or has T2D
DHP-Calcium Channel Blocker (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity
If unable to tolerate ACE-inhibitor then switch to Angiotensin Receptor Blocker (e.g. Candesartan)

Step 2:
(If maximal dose of Step 1 has failed or not tolerated)
Combine CCB and ACE-I/ARB

Step 3:
(If maximal doses of Step 2 has failed or not tolerated)
Add thiazide-like diuretic (e.g. Indapamide)

Step 4: Resistant Hypertension
If blood potassium <4.5mmol/L then add spironolactone
If >4.5mmol/L increase thiazide-like diuretic dose

Other options at this point if the potassium is >4.5mmol/L include:
Alpha blocker (e.g. Doxazosin)
Beta blocker (e.g. Atenolol)
Referral to cardiology for further advice

67
Q

Hypertension ABPM targets

A

Age <80 ABPM target <135/85
Age >80 ABPM target <145/85 (due to risk of postural drop and falls)
T1DM with end-organ damage <130/80

68
Q

ACEI side effects

A

persistent dry cough
headaches
dizziness
rash
hyperkalaemia

69
Q

Asbestosis definition

A

chronic lung condition characterized by diffuse interstitial fibrosis

It occurs in patients who have a history of exposure to asbestos and have developed pleural plaque disease

typically manifests ≥10 years following exposure

70
Q

Asbestosis signs/symptoms

A

Dyspnoea
Chronic cough
Crepitations on auscultation
Finger clubbing
Cyanosis
Reduced chest expansion

71
Q

Asbestosis investigations

A

Detailed patient history focusing on occupational asbestos exposure
Chest x-ray: May reveal linear interstitial fibrosis, pleural plaques, pleural thickening, or atelectasis
Pulmonary function tests: May be normal or show a restrictive pattern (reduced FVC and TLC with a normal FEV1/FVC ratio) or obstructive pattern (reduced FEV1)
High resolution CT: May demonstrate pleural thickening and pleural plaques
Bronchoscopy + biopsy: Has limited use as it normally cannot sample enough tissue for a diagnosis
Open lung biopsy: May be considered for a definitive diagnosis if cancer is suspected

72
Q

Asbestosis management

A

Smoking cessation: Essential to slow down disease progression
Pulmonary rehabilitation: Helps to improve lung function and quality of life
Oxygen therapy: Recommended if SpO2 ≤89%
Lung transplant: May be considered in severe cases
Reporting to coroner: Deaths due to asbestosis must be reported

73
Q

Jobs with high risk of asbestos exposure

A

Construction Workers
Shipbuilders and Navy Personnel
Power Plant Workers
Automobile Mechanics
Railroad Workers
Electricians
Plumbers and Pipefitters
HVAC Workers
Demolition Workers
Firefighters
Textile Workers
Miners

74
Q

Sarcoidosis definition

A

multi-system disease that is characterised by the formation of granulomas, leading to widespread inflammatory changes and complications across multiple body systems

(Granulomas are small, organized collections of immune cells that form in response to chronic inflammation or the presence of foreign substances in the body. typically composed of macrophages)

75
Q

Acute sarcoidosis presentation

A

aka Löfgren syndrome

Fever
Polyarthralgia (painful joints)
Erythema nodosum (skin inflammation)
Bilateral hilar lymphadenopathy (bilateral enlargement of the lymph nodes of pulmonary hila)

76
Q

Chronic sarcoidosis presentation

A

Pulmonary: Dry cough, dyspnoea, reduced exercise tolerance, and crepitations on examination
Constitutional: Fatigue, weight loss, arthralgia, low-grade fever, lymphadenopathy, and enlarged parotid glands
Neurological: Meningitis, peripheral neuropathy, bilateral Bell’s palsy
Ocular: Uveitis, keratoconjunctivitis sicca
Cardiac: Arrhythmias, restrictive cardiomyopathy
Abdominal: Hepatomegaly, splenomegaly, renal stones
Dermatological: Erythema nodosum, lupus pernio

77
Q

Sarcoidosis investigations

A

definitive diagnosis of sarcoidosis is made through tissue biopsy (e.g., lung, lymph nodes), which typically reveals non-caseating granulomas

other investigations can also suggest a diagnosis of sarcoidosis:

Blood tests: May show raised ESR, ACE (not specific or diagnostic), and calcium levels; lymphocytes may be reduced

Chest x-ray or CT: May reveal stages of disease progression
Stage 1 - Bilateral hilar lymphadenopathy (BHL)
Stage 2 - BHL with peripheral infiltrates
Stage 3 - Peripheral infiltrates alone
Stage 4 - Pulmonary fibrosis

78
Q

Sarcoidosis management

A

Bilateral hilar lymphadenopathy alone: Usually self-limiting and often does not require treatment
Acute sarcoidosis: Bed rest and NSAIDs for symptom control
Steroid treatment: Oral or intravenous, depending on the severity of the disease
Immunosuppressants: Used in severe disease

79
Q

Measuring rate on an ECG

A

Count the number of QRSs on one line of the ECG (usually lead II – running along the bottom) and multiply by six

OR

Count the number of large squares between R waves and divide 300 by this number (if the patient is in atrial fibrillation report a rate range rather than a single value)

80
Q

Assessing axis deflection on ECG

A

As a general rule if the net deflections in leads I and aVF are positive then the axis is normal

If lead I has a net negative deflection whilst aVF is positive then there is right axis deviation

If lead I has a positive deflection and aVF has a negative deflection then there is left axis deviation

81
Q

Causes of left axis deviation

A

Can be normal if the diaphragms are raised e.g. Ascites, pregnancy
Left ventricular hypertrophy (LVH)
Left anterior hemiblock (see notes on heart block)
Inferior myocardial infaction
Hyperkalaemia
Vertricular tachycardia (VT)
Paced rhythm

82
Q

Causes of right axis deviation

A

Normal in children or young thin adults
Right ventricular hypertrophy (RVH)
Often due to respiratory disease
Pulmonary embolism (PE)
Anterolateral myocardial infarction
Left posterior hemiblock (rare)
Septal defect

83
Q

Features of PR interval on ECG

A

Prolonged in first degree heart block
Shortened in rapid conduction via accessory pathway eg WPW
Depression in pericarditis

84
Q

Features of P wave on ECG

A

Absent in afib
Dissociated from QRS in heart block
Notched (p mitrale) in left atrial hypertrophy
Peaked p waves (p pulmonale) in right atrial hypertrophy and hypokalaemia

85
Q

Normal Q wave leads

A

initial downward deflection in the QRS complex
normal in left sided leads (V5, V6, lead I, aVL)

if >1 small square long and >2mm deep or in other leads = pathological

86
Q

Wide QRS complex

A

> 3 small squares/0.12 seconds

Bundle branch blocks (LBBB or RBBB)
Hyperkalaemia
Paced rhythm
Ventricular pre-excitation (e.g. Wolf Parkinson White)
Ventricular rhythm
Tricyclic antidepressant (TCA) poisoning

87
Q

Small QRS complex

A

pericardial effusion
high BMI
emphysema, cardiomyopathy

88
Q

Tall QRS complex

A

left ventricular hypertrophy
young, tall, thin people

89
Q

Hyperkalaemia ECG

A

Small p-wave
Tall, tented (peaked) t-wave
Wide QRS

90
Q

Infective endocarditis in intravenous drug users most commonly affects the _________ valve

A

tricuspid

91
Q

Beta-blockers should be stopped in acute heart failure if…

A

patient has heart rate < 50/min, second or third degree AV block, or shock

92
Q

STEMI management for patient receiving PCI

A

prasugrel is given in addition to aspirin. If patient is on an anticoagulant then clopidogrel used instead

93
Q

NSTEMI/unstable angina management

A

Aspirin 300 mg
Fondaparinux if no immediate PCI planned

If GRACE <3, give ticagrelor unless on oral anticoagulants, in which case give clopodigrel

If GRACE >3, offer PCI within 72 hours unless unstable, give unfractionated heparin and prasugrel/ticagrelor (swap for clopodigrel if on oral anticoagulants)

94
Q

Interpreting NT-proBNP results

A

if levels are >400 pg/ml arrange specialist assessment (including transthoracic echocardiography) within 2 weeks

if levels are 100-400 pg/ml arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks

95
Q

myocarditis vs endocarditis vs pericarditis definition

A

endocarditis = inflammation of lining in the heart chambers and the valves

Myocarditis = inflammation of the muscle

Pericarditis = inflammation of pericardium (sac around heart)

96
Q

Infective endocarditis - staph aureus

A

now the most common cause of infective endocarditis
particularly common in acute presentation and IVDUs

97
Q

Infective endocarditis - strep viridans

A

historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries
technically

Streptococcus viridans refers to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are Streptococcus mitis and Streptococcus sanguinis

they are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure

98
Q

Infective endocarditis - coagulase-negative Staphylococci

A

eg Staphylococcus epidermidis

commonly colonize indwelling lines and are the most common cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination

after 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)

99
Q

Infective endocarditis - streptococcus bovis

A

associated with colorectal cancer
the subtype Streptococcus gallolyticus is most linked with colorectal cancer

100
Q

Managing STEMI/NSTEMI if patient is hypotensive…

A

be careful with nitrates

101
Q

Drugs causing long QT syndrome

A

amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron

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