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Finals Revision > Cardio > Flashcards

Cardio Flashcards

1
Q

Broad complex tachycardia, BP 88/59, Rx?

A

DC cardioversion

If systolic BP <90 in tachyarrhythmia then DC cardioversion

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2
Q

When is a patient classified as stable or unstable in the context of tachyarrhythmia?

A

Unstable if any of the following adverse signs:

  • Shock (systolic BP <90, pallor, clammy, confusion, impaired consciousness)
  • Syncope
  • Myocardial ischaemia
  • Heart failure

If any of the above are present then give synchronised DC cardioversion. Rx following this is dependent on if it was broad or narrow complex, and if it was regular or irregular

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3
Q

What are potential causes of a broad complex tachycardia with regular and irregular rhythms?
What are their treatments (if stable)?

A

Regular:

  • Assume VT - amiodarone (300mg loading dose then 900mg over 24 hours)
  • SVT with BBB - treat as per SVT

Irregular:

  • AF with BBB - treat as per narrow complex tachycardia
  • Polymorphic VT (torsades de pointes) - IV Magnesium
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4
Q

Potential causes of narrow complex tachycardia with regular and irregular rhythms?
Treatments?

A

Regular:

  • SVT - vagal manoeuvres then IV adenosine
  • If unsuccessful, consider atrial flutter and control rate

Irregular:

  • Probably AF
  • If onset <48 hrs consider electrical/chemical cardioversion
  • Rate control (B blocker/Digoxin) and anticoagulation required
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5
Q

Treatment of acute native valve endocarditis?

A

IV Flucloxacillin 2g 6 hourly

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6
Q

Treatment of subacute (indolent) native valve endocarditis?

A

IV Amoxicillin + Gentamicin

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7
Q

Treatment of prosthetic valve endocarditis or suspected MRSA?

A

IV Vancomycin + Gentamicin + PO Rifampicin

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8
Q

4 common bacterial causes of endocarditis and their associations?

A

Staph Aureus - most common, IVDU

Staph epidermis - peri-operative, <2 months post-op

Strep Viridans - dental procedures

Strep Bovis - colorectal cancer

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9
Q

5 causes of culture negative endocarditis?

A 
Previous antibiotic therapy
Coxiella burnetti
Bartonella
Brucella
HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella)
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10
Q

common drugs which prolong QT interval?

A 
Antipsychotics (mainly typical)
Type 1a, 1c and 3 arrhytmatics
Tricyclics
Other antidepressants (citalopram, moclobemide etc)
Loratadine
Hydroxychloroquine
Macrolides (clarithromycin)
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11
Q

How to tell between aortic stenosis and sclerosis?

A

Aortic sclerosis doesn’t radiate to carotids and has normal ECG

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12
Q

What 2 scenarios is cardioversion used in AF?

When should you offer rate/rhythm control?

A

Haemodynamically unstable - electrical

Electively where rhythm control strategy preferred - electrical or chemical

Offer rate/rhythm control if onset <48 hours
Offer rate control if >48 hours

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13
Q

Management of haemodynamically stable AF onset <48 hours?

A

Heparinise patient, then cardiovert

Electrical - synchronised DC
OR
Pharmacological:
- Amiodarone if structural heart disease
- Amiodarone/Flecainide without

If no other risk factors for ischaemic stroke, further anticoagulation unnecessary. If present, oral anticoagulation for life

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14
Q

Management of haemodynamically stable AF onset >48 hours?

A

Rate control and anticoagulation for at least 3 weeks.

If recurrent AF or previous cardioversion failure, amiodarone/sotalol for 4 weeks.

Electrical cardioversion

Anticoagulation continued for at least 4 weeks after - decision on continuation based on risk factors

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15
Q

Drugs to control rate in AF?

A

Bisoprolol
Verapamil/Diltiazem
Digoxin - normally not preferred, but 1st choice if co-existing heart failure as positive inotropic effect

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16
Q

Drugs to maintain sinus rhythm in Hx of AF?

A

Amiodarone
Sotalol
Flecainide

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17
Q

Factors favouring rate (2)/rhythm (4) control strategy in AF?

A

Rate - age >65, Hx of IHD

Rhythm - age <65, symptomatic, first presentation, CCF

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18
Q

Stroke risk score in AF?

A

CHA2DS2VascS

C - congestive HF
H - hypertension 
A - age 75 or above = 2
     age 65-74 = 1
D - diabetes
S - stroke or TIA (previous) = 2
V - vascular disease (IHD/PVD) 
S - sex (female)

0 = no anticoagulation
1 = males consider anticoagulation
females don’t (they got this score from their sex)
2 = offer anticoagulation

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19
Q

When is catheter ablation used in AF?
What medication must the patient take beforehand?
What does it do to stroke risk?
3 complications?

A

Failure to respond to cardioversion, or wish to avoid antiarrhythmatics

Anticoagulants for 4 weeks minimum beforehand

Whilst ablation might restore to sinus rhythm, it doesn’t reduce stroke risk

tamponade, stroke, pulmonary valve stenosis

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20
Q

How do thiazides cause hypokalaemia?

A

They block Na/Cl co-transporter in DCT, so more Na reaches collecting duct

More K lost in collecting duct as a result

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21
Q

Side effects of thiazide-like diuretics, such as indapamide and chlortalidone?

A

Same as thiazides

Hypokalaemia/Hyponatraemia
Hypercalcaemia
Gout
Postural hypotension 
Impaired glucose tolerance
Impotence

Rarely: agranulocytosis, pancreatitis, thrombocytopenia, photosensitive rash

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22
Q

Hypertension ladder?

A

1:
<55 OR T2DM - A
55+ or black, no T2DM - C

2: A+C or A+D
3: A+C+D

4: If K+ 4.5 or less - spironolactone
If K+ >4.5 B-blocker or A-blocker

5: Specialist

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23
Q

What tests should be done before starting amiodarone?

Monitoring after this?

A

TFT, LFT, U&E, baseline CXR

TFT and LFT every 6 months

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24
Q

Blood pressure targets for clinic and ABPM for someone:
<80 y/o?
>80 y/o?

A

<80:
clinic - <140/90
ABPM - <135/85

> 80:
clinic - <150/90
ABPM - <145/85

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25
Q

7 causes of ST elevation?

A

STEMI
Pericarditis/myocarditis
Normal variant (high take off)
LV aneurysm
Coronary artery spasm (prinzmetal’s angina)
Takotsubo cardiomyopathy (octopus pot, floppy apical LV)
Subarachnoid haemorrhage (rare)

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26
Q

Pathognomic ECG finding in cardiac tamponade?

A

Electrical alternans

Waves are of alternating amplitude, 1st and 3rd will be same height, 2nd and 4th will be etc

Amplitude may be small as well depending on how bad the tamponade is

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27
Q

Which antihypertensive can cause constipation and abdominal pain as a side effect?

A

Thiazides - hypercalcaemia

Bones - bone pain
Stones - kidney stones
Groans - abdo pain
Thrones - constipation/urinary frequency
Tones - muscle weakness and hyporeflexia
Psychiatric moans - depression, anxiety, confusion
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28
Q

What is eisenmenger’s syndrome?
How can it present?
Management?

A

Pulmonary hypertension as a result of an uncorrected VSD
The RV hypertrophies until it overcomes the LV - this causes chronic pulmonary microvascular changes

It causes R to L shunt and chronic cyanosis. This may be seen as:

  • blue tinge to nails/lips
  • clubbing/loss of nail fold
  • RV failure
  • original murmur may disappear
  • haemoptysis (from pul microvasc changes)

Rx: heart and lung transplant needed eventually

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29
Q

VT without haemodynamic instability:

  • What is treatment?
  • What should be avoided?
A

Amiodarone - 1st line option
Procainamide
Lidocaine (use with caution, esp with severe LV impairment)

NEVER use Verapamil

(if drug therapy fails then synchronised DC cardioversion)

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30
Q

What symptom do most patients get following administration of adenosine?

A

Chest pain

due to increased coronary sinus blood flow

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31
Q

ECG of digoxin toxicity? (4)

A
  • Downsloping ST depression widespread (like a reversed nike tick)
  • inverted/flattened T waves
  • Shortened QT interval
  • Can cause AV block/bradycardia
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32
Q

Course of action for patients presenting with acute chest pain:

  • <12 hours ago?
  • 12-72 hours ago?
  • > 72 hours ago?
A
  • take ECG and emergency admission to hospital
  • refer to hospital for same-day assessment
  • Full workup including ECG and troponin - use this to guide your judgement
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33
Q

Immediate management of suspected ACS?

A
  • Morphine (if in pain)
  • Oxygen**
  • GTN spray
  • Aspirin - 300mg (high dose)
  • Clopidogrel or Ticagrelor once in hospital
      • if sats <94% and not at risk of T2 resp failure
      • if at risk of T2 resp failure, aim for 88-92%
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34
Q

3 criteria for angina?

What is unstable angina?

A
  1. Constricting discomfort in chest, neck, shoulders, jaw or arms
  2. Brought on by physical exertion
  3. Relieved within 5 mins by GTN spray

Atypical angina - 2/3 of these - e.g. if pain is ‘stabbing’ instead of ‘constricting’ (more common in women and diabetics)

If only 1/3 - non-anginal chest pain

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35
Q

Investigations for angina if it cannot be diagnosed clinically alone?

A
  1. CT coronary angiography
  2. non-invasive functional imaging
    (e. g. perfusion scintigraphy, SPECT, stress echo, MR perfusion scan)
  3. invasive coronary imaging
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36
Q

Angina pectoris treatment ladder?

A

All patients should receive aspirin 75mg, a statin and GTN (unless CI)

  1. B-blocker or rate-limiting CCB
  2. Once at max dose, add second drug:
    B-blocker + dihydropyridine CCB
  3. If still symptomatic, refer for assessment for PCI/CABG and add a 3rd drug:
    - ivabradine (funny current HCN channel blocker)
    - long-acting nitrate
    - nicorandil (K channel opener/NO activity)
    - minoxidil (K channel opener/NO activity)
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37
Q

Usual 4 medications for pulmonary hypertension?

Other drug options (class + example)?

A

Warfarin/DOAC
Diuretic
High % oxygen
Digoxin

  • CCB’s - nifedipine, amlodipine, diltiazem
  • Endothelin ETa receptor antagonists - bosentan, ambrisentan
  • PDE5 inhibitors - sildenafil
  • Prostaglandins - iloprost
  • guanylate cyclase inhibitors - riocugat
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38
Q

What must you be careful of with nitrates?

Other SE? (4)

A

Tolerance - take second nitrate after 8 hours, not 12, leaving 4 hours nitrate free in body
Effect not seen as much with modified release isosorbide mononitrate

Headache
Postural hypotension
Tachycardia
Flushing

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39
Q 
2 methods of ACS developement?
What is ACS spectrum?
Symptoms?
Often mistaken for? Who gets silent MI?
Signs?
A
  • Gradual narrowing of lumen until occluded by atherosclerotic plaque (angina)
  • Rupture of plaque causing thrombosis

Unstable angina
NSTEMI
STEMI

Central, crushing, heavy chest pain - to neck, jaw, shoulder, arm
Stomach pain, nausea, vomiting
Pale, clammy
Sense of impending doom 
SOB

Often mistaken for dyspepsia
Esp in diabetics/elderly, who may not get chest pain

Often very little signs - BP, temp etc all normal
May be tachycardia/tachypnoeic
Signs of heart failure may begin to develop after a while

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40
Q

Criteria for a STEMI?

A
  • Clinical symptoms consistent with ACS for >20 mins
  • ST elevation of 2 small squares (2mm) in at least 2 contiguous leads

Can also have :

  • ST elevation of 1 small square (1mm) in other leads
  • New onset LBBB
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41
Q

Management of STEMI?

A

If presenting within 12 hours of symptom onset:

If PCI can be accessed within 2 hours:

  • Aspirin + prasugrel (clopidogrel if already on oral anticoagulant)
  • PCI with heparin + abciximab cover
  • Place drug-eluting stent

If PCI cannot be accessed within 2 hours:

  • Thrombolysis + LMWH/Fondaparinux
  • Repeat ECG 90 mins after delivery - if no improvement, organise transfer for PCI
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42
Q

NSTEMI/Unstable angina management?

A

Give aspirin
Give Fondaparinux if no immediate PCI planned and no increased bleeding risk

Calculate GRACE score (6 month mortality)

If >3%:

  • Offer PCI within 72 hours
  • Prasugrel/Ticagrelor + heparin + drug-eluting stent

If <3%:
- Give Ticagrelor

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43
Q

Why does cardiac arrest occur after MI?

A

Most commonly VF

Also VT

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44
Q

Why does cardiogenic shock occur with MI?

A

If a large part of the LV myocardium is damaged, ejection fraction of heart may decrease massively

May occur because of mechanical reasons such as LV free wall rupture

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45
Q

What chronic condition occurs commonly after MI?

A

Heart failure

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46
Q

Which type of MI does AV block occur with?

A

Most commonly inferior

Can cause bradyarrhythmias

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47
Q

2 types of pericarditis following MI?

A

<48 hours - due to transmural MI, occurs in 10%.
Typical pericarditis features - worse on lying flat, pericardial rub, pericardial effusion

2-6 weeks - Dressler’s Syndrome - autoimmune reaction against antigenic proteins.
Fever, pleuritic pain, pericardial effusion, raised ESR.
Rx: NSAIDs

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48
Q

Why might LV aneurysm form after MI?
ECG and signs?
What might it put patients at risk of?

A

Sustained weakness of myocardium

Persistent ST elevation
Signs of LV failure (pul oed)

Thrombus forming and stroke - patients must be anticoagulated

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49
Q

When does LV free wall rupture occur following MI?
Presentation?
Treatment?

A

1-2 weeks
(occurs in 3%)

Acute heart failure secondary to tamponade

  • Raised JVP
  • Pulsus paradoxus
  • diminished heart sounds

Urgent pericardiocentesis and thoracotomy

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50
Q

What type of MI does acute mitral regurg occur with?
Why does it happen?
Symptoms/signs?
Treatment?

A

Infero-posterior MI

Ischaemia/rupture of papillary muscle

Acute hypotension and pulmonary oedema
Early-mid diastolic murmur

Vasodilator therapy and emergency surgical repair

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51
Q

What is plusus paradoxus?

2 causes?

A

Greater than normal (>10mmHg) drop in systolic BP during inspiration
(faint/absent pulse during inspiration)

Cardiac tamponade
Severe asthma

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52
Q

What causes a slow-rising/plateau pulse? (1)

A

Aortic stenosis

also narrow pulse pressure

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53
Q

What is a collapsing/water-hammer pulse?

Causes? (3)

A

Pulse which can be felt rapidly increasing in force through the bulk of the muscle in the forearm when the arm is raised above the head, and subsequently collapses

Aortic regurgitation
PDA
Hyperkinetic states (anaemia, thyrotoxicosis, fever, exercise, pregnancy)

Explanation: if hyperaemic/aortic regurg etc sluggish blood flow through artery in arm. Raising arm above head causes it to rapidly flow back towards the LV, increasing the EDV for the next cycle (valve regurgitates it) - increased stretch from increased volume increases the force of the next contraction via Frank-Starling mechanism

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54
Q

What is plusus alternans?

Cause?

A

Regular alternation of the force of arterial pulse

Severe LVF

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55
Q

What is a bisferiens pulse?

What causes it? (2)

A

‘double pulse’ - 2 systolic peaks

Mixed aortic valve disease
Occasionally HOCM

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56
Q

What is a jerky pulse?

What causes it?

A

Seen in HOCM

Pulse which has a rapid upstroke due to vigorous contraction of hypertrophic LV
As volume of LV decreases there is abrupt blockage of outflow
This causes a rapid fall in arterial pressure

(HOCM may also sometimes be assoc w bisferiens pulse)

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57
Q

Causes of pericarditis? (8)

A 
Viral (often coxsackie)
Uraemia (causes fibrinous pericarditis)
TB
Trauma
MI
SLE
Hypothyroidism
Malignancy
58
Q

ECG changes in pericarditis?
What other investigation should all with suspected acute pericarditis get?
Management?

A

Widespread:

  • ‘Saddle-shaped’ ST-elevation
  • PR depression (most specific)

Transthoracic echo

NSAID + Colchicine
Treat underlying cause

59
Q

Causes of constrictive pericarditis?
Symptoms/Signs?
Specific Ix?
How to differentiate from tamponade?

A

Any cause of acute, particularly TB

Dyspnoea
Pericardial knock (S3)
Elevated JVP with x+y descent
Kussmaul sign is positive (rise in JVP during inspiration)
RV failure:
  - Elevated JVP
  - Ascites
  - Oedema 
  - Hepatomegaly

CXR - shows pericardial calcification

Pulsus paradoxus is ABSENT
(present in tamponade)

60
Q

Who should myocarditis be suspected in?
Causes? (6)
Presentation?

A

Esp young people with acute chest pain

Viral - coxsackie, HIV
Bacteria - diphtheria, clostridia
Spirochaetes: Lyme disease
Protozoa: Chagas disease, toxoplasmosis
Autoimmune
Doxorubicin (chemo drug)

Typical presentation:

  • young person
  • acute chest pain
  • dyspnoea
  • arrhythmia
61
Q

Ix for myocarditis? (2)
Management?
Complications? (3)

A

Bloods:

  • Inflam markers
  • cardiac enzymes
  • bnp

ECG:

  • tachycardia
  • arrhythmia
  • ST elevation
  • T wave inversion

Rx:
- Supportive, treat cause

Comp:

  • HF
  • Sudden death from arrhythmia
  • Dilated cardiomyopathy (late)
62
Q

Underlying cause of VT?
2 types and what causes of each?
Why is it important to treat?

A

Ventricular ectopic focus, leading to broad complex tachycardia

Monomorphic - usually MI

Polymorphic (Torsades de pointes) - Long QT interval

Can lead to VF

63
Q

Apart from drugs, what can cause long QT interval?

A

Congenital (random things including deafness)

Electrolytes:

  • hypocalcaemia
  • hypokalaemia
  • hypomagnesaemia

MI
Myocarditis
Hypothermia
Subarachnoid haemorrhage

64
Q

What is WPW syndrome?
What can it cause?
ECG features? (3)
Management? (2)

A

Congenital accessory pathway between the atria and ventricles leading to AV re-entry tachycardia

(current spreads up through ventricles and rather than stopping at top of ventricles it goes back into atrium)

  1. Short PR interval
  2. Wide QRS with slurred upstroke - delta wave
  3. Axis deviation towards side of pathway (usually left)

Definitive: ablation
Medical: Sotalol/Amiodarone or Flecainide

(avoid sotalol if concurrent AF as prolonging AV refractory encourages transmission through accessory)

65
Q

What therapy should be initiated after MI?
What if they have HF as well?
Is this just for STEMI or for NSTEMI as well?
When can sexual activity resume?
When could sildenafil (viagra) be used?

A 
Statin
ACEI
B blocker
Aspirin
Ticagrelor for 12 months (can extend if high risk)

Add aldosterone antagonist (eplerenone) within 2 weeks

Both

Sex after 4 weeks
Sildenafil after 6 months - NOT if also taking nitrates or nicorandil

66
Q

Timeline of ECG changes in MI?

A

Acutely:
ST elevation/depression

Within 24 hours:
Q wave formation
T wave inversion
ST changes remain

After week(s):
ST back to normal
Q waves and T wave inversion remain

67
Q

Contraindications for thrombolysis? (8)

Potential SE?

A
  • Active internal bleeding
  • Recent haemorrhage/trauma/surgery (including dental extraction)
  • Coagulation/bleeding disorders
  • Intracranial neoplasm
  • Stroke <3 months ago
  • Aortic dissection
  • Recent head injury
  • Severe hypertension

SE:

  • Haemorrhage
  • Allergic reaction - esp streptokinase
68
Q

Diagnosis of chronic heart failure?
What causes release of BNP?
What is its physiological effect? (4)
What to do if raised/high levels?

A

BNP and NT-proBNP

BNP:
Normal <100
Raised 100-400
High >400

NT-proBNP:
Normal <400
Raised 400-2000
High >2000

Released by LV myocardium in response to strain
- causes vasodilation, diuresis, natriuresis, and suppresses RAAS

Raised: specialist assessment within 6 weeks

High: specialist assessment within 2 weeks

69
Q

Treatment ladder of chronic heart failure?

Other treatments these patients should get?

A

All patients start on:
ACEI + B1-blocker

2nd line: aldosterone antagonist
(careful as these + ACEI can cause hyperkalaemia)

3rd line options - to be started by specialist:

  • Ivabradine
  • Digoxin
  • Hydralazine
  • Sacubitril-Valsartan
  • Cardiac resynchronisation therapy

Other things:
- annual influenza vaccine
- One off pneumococcal vaccine
(asplenic or CKD patients need booster every 5 years)

70
Q

What is a preserved (normal) ejection fraction?
What is a mildly reduced ejection fraction?
What is a reduced ejection fraction?

A

Preserved: >50%

Mildly reduced: 40-49%

Reduced: <40%

71
Q

NYHA classification?

A

1 - no symptoms/limitation

2 - mild - fatigue, palpitations or dyspnoea with activity

3 - mod - less than ordinary activities result in marked symptoms

4 - sev - symptoms at rest, unable to carry out any physical activity

72
Q

When should someone receive statins for primary prevention?
What dose and drug for primary and secondary prevention?
What are the CI/interactions of statins?

A

QRISK 10% or more

Primary prevention:
Atorvastatin 20mg

Secondary prevention:
Atorvastatin 80mg

CI: pregnancy
Inter: macrocodes - choose other antibiotic if possible or stop statins during course

73
Q

HOCM:

  • inheritance?
  • gene?
  • Echo abnormalities? (3)
A

AD

beta-myosin heavy chain protein

MR SAM ASH

  • Mitral regurgitation
  • Systolic anterior motion of anterior mitral valve
  • Asymmetrical septal hypertrophy
74
Q

Arrhythmogenic RV dysplasia:

  • what is it?
  • ECG abnormalities?
A

RV myocardium replaced by fatty and fibrofatty tissue

In V1-V3:

  • T-wave inversion
  • Epsilon wave (terminal notch in QRS)
75
Q

7 common causes of dilated cardiomyopathy?
Signs? (3)
What is seen on echo and cxr?

A 
Alcohol
IHD
Muscle disease e.g. DMD
Coxsackie B virus
Wet beri beri
Doxorubicin (chemo drug)
Infiltrative disease (e.g. haemochromatosis, sarcoidosis)

Dilated = most common, 90% of cardiomyopathies

Signs:

  • Signs of HF
  • Systolic murmur (mitral/tricuspid regurg)
  • S3

Echo: all 4 chambers dilated
CXR: ‘balloon’ shape of heart

76
Q

2 most common causes of restrictive cardiomyopathy?

A

Amyloidosis

Radiotherapy

77
Q

When does peripartum cardiomyopathy develop?

Who is it more common in?

A

Between last month of pregnancy and 5 months postpartum (dilated cardiomyopathy)

Older women, greater parity

78
Q

What causes takotsubo cardiomyopathy?
Features? (2)
Rx? (1)

A

‘stress induced’ e.g. bereavement then develop chest pain and heart failure

Transient, apical ballooning of myocardium
LV ‘octopus pot’ shape

Rx: supportive

79
Q

What is subclavian steal syndrome?
Presentation? (2)
Rx? (1)

A

Subclavian stenosis proximal to the origin of the vertebral arteries - resulting in retrograde blood flow from the vertebral arteries to the arm during exercise

Presentation:

  • Dizziness/vertigo during exercise
  • Concurrent arm pain

(typically posterior circulation symptoms)

Rx: stent

80
Q

What are the 3 types neurally-mediated syncope?

What occurs before it?

A
  • Vasovagal episode - usually brought on by emotion, pain or stress
    (‘fainting’)
  • Situational - in response to coughing, micturition
  • Carotid sinus syncope - exaggerated response to pressure applied to carotid sinus

Before: sweating, pallor, nausea/vomiting
Then transient loss of consciousness
Quick recovery, no post-ictal state

81
Q

What can cause cardiac syncope? (3)

A

Arrhythmias (brady or tachy)

Structural: valvular, MI, HOCM

PE

82
Q

Causes of orthostatic syncope?

A

Due to autonomic failure

Primary: Parkinson’s, LBD

Secondary: diabetes, amyloid, uraemia

Drug-induced: diuretics, alcohol, vasodilators

Volume depletion: haemorrhage, diarrhoea

83
Q

Definition of Syncope?

3 broad types?

A

Transient LOC due to global cerebral hypo perfusion - rapid onset, short duration, quick and spontaneous recovery

Reflex (neurally mediated)
Orthostatic
Cardiac

84
Q

What is coarctation of aorta?
How may it present in infancy?
When to suspect coarctation of aorta in an adult?
What is seen on CXR that is not seen in young children?
4 associations?

A

Congenital narrowing of descending aorta (most commonly post-ductal)

Heart failure

Young person with hypertension
Radio-femoral delay
BP difference between left arm and other limbs

Notching of inferior rib borders (due to collaterals)

Turner's syndrome
Bicuspid aortic valve
Berry aneurysms
NF
(more common in males)
85
Q

Warfarin reversal:

  • major bleeding?
  • INR >8 (minor+no bleeding)?
  • INR 5-8 + minor bleeding?
  • INR 5-8, no bleeding?
  • When to restart warfarin?
A

1:

  • IV VitK
  • Prothrombin complex concentrate (or FFP)

2:

  • VitK - IV if minor bleeding, PO if no bleeding
  • Repeat INR after 24 hours

3:
- IV warfarin

4:
- Withhold 1-2 doses, then reduce maintenance dose

5:
- Restart warfarin once INR <5

86
Q

What is Buerger’s disease?

Features? (4)

A

Small-medium vessel vasculitis, strongly assoc w smoking
(young male, smoker, limb ischaemia)

Limb ischaemia
Ischaemic ulcers
Superficial thrombophlebitis
Raynaud’s

87
Q

What is Buerger’s test for?

How is it performed?

A

Limb arterial insufficiency

  • Lying down, raise both patents’ legs to 45 degrees for 1 minute
  • They will become pale due to poor blood flow
  • Then ask patient to sit off edge of bed with legs hanging down
  • Skin first turns blue as deoxygenated blood returns to tissue, then red due to reactive hyperaemia from post-hypoxic dilation
88
Q

Treatment of bradyarrhythmia (e.g. complete heart block) post-MI if:

  • anterior MI?
  • inferior MI?
A

Anterior - external pacing

Inferior - atropine

(because bradyarrhythmias post-inferior MI are normally transient and resolve in hours-days, so treat conservatively)

89
Q

Indications for temporary external pacing? (3)

A
  • symptomatic/haemodynamically unstable bradycardia not responding to atropine
  • post-ANTERIOR MI - if develop type 2 or complete heart block
  • trifascicular block prior to surgery
90
Q

Anticoagulation after mechanical valve insertion?
Target INR?
Who is still given bioprosthetic valves (e.g. pig or cow)?
Problems with these?

A

Warfarin

Aortic 3.0
Mitral 3.5

Older people: >65 if aortic and >70 if mitral
Long-term anticoagulation not needed, just 75mg aspirin
Problems: deterioration & calcification over time

91
Q

What to do if patient starts experiencing increasing chest pain or haemodynamic instability following PCI for STEMI?

A

Arrange urgent CABG

Give nitrates and morphine in meantime

92
Q

P wave changes - what causes:

  • increased amplitude?
  • broad, notched (bifid) p wave?
A

Cor pulmonale (P pulmonale)

LA enlargement classically in mitral stenosis (P mitrale)
Most commonly in lead II

93
Q

5 acyanotic heart defects?

A 
VSD (most common, 30%)
ASD
PDA
Coarctation
Aortic stenosis

VSD more common than ASD but ASD more common as a new diagnosis in adulthood

94
Q

3 cyanotic heart defects?

A

Tetralogy of Fallot
Transposition of Great Arteries
Tricuspid atresia

TOF more common but usually present at 1-2 months
TGA more commonly recognised at birth

(Pulmonary stenosis - presence of cyanosis depends on severity of stenosis and presence of coexistent defects)

95
Q

How to determine if neonatal cyanosis is of cardiac origin?

What to do as initial supportive management if it is ductal dependent?

A

Nitrogen washout test - give 100% O2 for 10 mins then do ABG, pO2 <15kPa indicates cardiac cause

If duct-dependent give PGE2

96
Q

What is acrocyanosis?

A

Blue discolouration of mouth, hands and feet in a newborn caused by vasospasm.

Benign, normal finding in healthy newborns. Lasts 24-48 hours

Differentiated from other causes of neonatal cyanosis (e.g. sepsis) as it occurs straight after birth

97
Q

PDA:

  • connection between what?
  • can it lead to cyanosis?
  • what is seen on praecordial exam?
  • pulse type?
  • murmur?
  • Rx?
A
  • pulmonary trunk and descending aorta
  • yes, eventually, cyanosis of lower extremities (termed differential cyanosis, as upper limbs normal)
  • subclavicular thrill, heaving apex beat
  • large volume, bounding, collapsing pulse
  • continuous machine-like murmur
  • indomethacin/ibuprofen
98
Q

TOF:

  • what are the 4 deformities?
  • when is it picked up?
  • what are tet spells?
  • murmur?
  • cxr/ecg?
  • management?
A

4 deformities:

  • VSD
  • RV hypertrophy
  • pulmonary stenosis/RV outflow tract obstruction
  • overriding aorta
  • 1-2 months
  • When baby becomes cyanotic when it cries/becomes agitated due to rapid decrease in blood oxygenation
  • ejection systolic murmur (due to pulmonary stenosis - VSD doesn’t usually cause murmur)

CXR: boot-shaped heart
ECG: RV hypertrophy

Management - surgical repair in 2 parts. B-blockers to reduce infundibular spasm

99
Q 
What is Ebstein's anomaly?
What causes it?
What is seen in 80% if patients with this?
Clinical features? (5)
Conductive problem?
A

Low insertion of the tricuspid valve resulting in a large atrium and small ventricle (‘atrialisation of RV)

Lithium

PFO/ASD

Features:

  • cyanosis
  • prominent ‘a’ woven JVP
  • hepatomegaly
  • tricuspid regurg (pan systolic murmur, worse on inspiration)
  • splitting of S1 & S2

RBBB (hence splitting of S1&S2)

100
Q

HOCM:

  • what is the physical issue?
  • clinical features?
  • pulse?
  • murmur?
  • ECG?
A

LV hypertrophy, and sub aortic hypertrophy of ventricular septum, resulting in functional aortic stenosis

Features:

  • syncope (following exercise)
  • angina-like pain
  • exertion dyspnoea
  • Often asymptomatic, until sudden death due to ventricular arrhythmia

Pulse: jerky

Murmur: ejection systolic

ECG:

  • LV hypertrophy
  • Non-specific ST and T-wave changes, progressive T-wave inversion may be seen
  • deep Q waves
101
Q

3 drugs to avoid in HOCM?

A

ACEI
Nitrates
Inotropes

102
Q 
What is brugada syndrome? 
Inheritance?
Who is it most commonly seen in?
ECG changes?
What makes ECG changes more apparent?
Rx?
A

Defect in sodium ion channel
AD
Asians

ST elevation followed by negative T wave in V1-V3
Partial RBBB

ECG changes more apparent with flecainide

ICD

103
Q

Pathophysiology of Rheumatic Fever?
Major and minor diagnostic criteria?
Management? (3)

A

Type II hypersensitivity reaction 2-6 weeks after strep pyogenes infection

Diagnosis:
Evidence of recent streptococcal infection by raised/rising streptococcal antibodies or positive throat swab, accompanied by 2 major diagnostic criteria or 1 major and 2 minor

Major:

  • pancarditis (myocarditis + endocarditis)
  • erythema marginatum
  • polyarthritis
  • subcutaneous nodules
  • sydenham’s chorea (late feature)

Minor:

  • raised ESR/CRP
  • pyrexia
  • prolonged PR

Rx:

  • Penicillin V
  • NSAIDs
  • Treat any complications e.g. heart failure
104
Q

2 congenital causes of LQTS?
What is LQTS 1, 2 and 3?
What arrhythmia may arise?

A

Jarvell-Lange-Nielsen syndrome (deafness)
Romano-Ward syndrome (no deafness)

1 - syncope after swimming
2 - syncope after emotional stress
3 - events occur at night or at rest

Torsades de Pointes

105
Q

Management of hyperglycaemia in STEMI?

A

Dose-adjusted insulin to ensure glucose <11

106
Q

Immediate management of a STEMI?

A

Ticagrelor
Aspirin (even if already taking aspirin)
Heparin if going for PCI <2 hours after arrival at hospital

tPA if PCI not available - perform ECG 90 mins after thrombolysis - if <50% improvement arrange transfer to PCI centre

107
Q

What antihypertensive to avoid with hyperglycaemia?

A

Thiazides or thiazide-likes - can worsen glucose tolerance

108
Q

Ix for PE in renal impairment?

A

V/Q scan

109
Q

Presentation of LV free wall rupture post-MI?

A

Signs of L and R HF due to tamponade

  • lung crackles
  • pulsus paradoxus
  • ankle oedema
  • raised JVP
  • diminished heart sounds

Usually 1-2 weeks later
urgent pericardiocentesis required

110
Q

Dissection:

  • features?
  • Ix?
  • types and management?
A
  • tearing chest pain
  • BP variation >20mmHg between arms
  • aortic regurg
  • hypertension
  • may have other features depending on site and branching arteries
  • non-specific ECG changes, may have STE inferior leads

Ix: CT angiography CAP
Trans-oesophageal echo if unsuitable

Type A - ascending aorta
- surgical management but reduce BP to 100-120 systolic before

Type B - descending
- conservative, IV labetalol

111
Q

Which drug is assoc w GI ulcers and can cause perforation?

A

Nicorandil

112
Q

Heart failure treatment ladder?

A
  1. ACEI or B blocker
  2. Second of these
  3. Spironolactone
113
Q

ECG changes and arteries for MI:

  • Anteroseptal?
  • inferior?
  • anterolateral?
  • lateral?
  • posterior?
A

anterolateral:
- V1-V4
- LAD

inferior:

  • II, III, aVF
  • RCA

anterolateral:

  • V4-V6, I, aVL
  • LAD or Left Circumflex

Lateral:

  • I, aVL +/- V5-V6
  • Left circumflex

Posterior:

  • Tall R waves V1-V2
  • May cause ST depression
  • Circumflex or Right Coronary

Isolated new onset LBBB may also point to MI

114
Q

Apart from HF, what causes raised BNP?

What can reduce it?

A

CKD (even with eGFR <60) due to reduced renal excretion
ACEI and ARBs can also raise it

Diuretics can reduce it

115
Q

What to do with warfarin after successful treatment of AF with catheter ablation?

A

Continue treatment

116
Q

2 main indications for loop diuretics?

SE?

A
  • Heart failure - acute IV, chronic orally
  • resistant HTN, especially in those with renal impairment

SE:
Hypotension
Low everything (Na, K, Mg, Cl, H, Ca)
Ototoxicity
Renal impairment (dehydration and direct toxicity)
Hyperglycaemia (less common than thiazides)
Gout

117
Q 
Management of acute HF for all pts?
If hypoxic?
If ischaemia?
If no response to initial hypoxia treatment?
If hypotensive?
What to do with regular meds?
Opiates?
A

IV loop diuretics

Oxygen if sats <94%

GTN if due to ischaemia or HTN

If sats still low after O2 and Furosemide, CPAP

If hypotension/cardiogenic shock:

  • inotrope e.g. dobutamine
  • vasopressor e.g. NA

Continue regular medications such as B blocker/ACEI

Do not give opiates

118
Q

In VF/VT arrest, what is the shock:CPR ratio?
When is it changed?
When should adrenaline and amiodarone be given?
What is an alternative if amiodarone not available?
When should adrenaline be given for non-shockable rhythm?

A

Single shock followed by 2 mins CPR

If witnessed on a monitor e.g. in CCU - 3 quick shocks can be given in succession followed by 1 min CPR

Adrenaline: after the 3rd shock (not stacked) then every 3-5 mins after

Amiodarone also after 3 shocks and after 5 shocks

Lidocaine is alternative to amiodarone

In non-shockable rhythm, give adrenaline ASAP and every 3-5 mins after

119
Q

Adenosine:

  • who should it be avoided in?
  • what drugs can affect it?
  • what adverse cardiac effect can it have?
A

Asthmatics - can cause bronchospasm

Theophylline - blocks its effects
Dipyramidole - enhances its effects

Enhance conduction along accessory pathways causing increased ventricular rate (e.g. WPW)

120
Q

Can ECG changes occur in unstable angina?

A

Yes, can have T wave inversion or ST depression - but lack of troponin being raised or any changes in troponin at 3 and 6 hours differentiates from NSTEMI

121
Q

What is Prinzmetal angina?

What drugs can cause it?

A

Angina due to coronary artery spasm

Usually in younger people who smoke/take cocaine, occurs early in morning or during sleep, and can cause ST elevation. No pain during exercise

Cocaine, Triptans and 5-FU can cause it

122
Q

If ACEI causes hyperkalaemia when should it be stopped?

A

If K >6 switch to another drug, especially if CKD

123
Q

3 main SE of GTN?

A

Hypotension
Headache
HR increase

124
Q

Cause of hypertension in aortic dissection?

A

Catecholamine surge

125
Q

Management of orthostatic hypotension?

A

Initially:
- education - ensure adequate water and salt intake

After that:
- discontinue drugs such as nitrates, antihypertensives, neuroleptic agents, dopaminergic drugs

Then:

  • Fludricortisone or midodrine
  • compression garments, counter-pressure manoeuvres, head tilt-up sleeping

(fludricortisone increases renal Na and water reabsorption, midodrine;
midodrine is an alpha agonist causing vasoconstriction)

126
Q

Monitoring when commencing treatment with a statin?

A

LFT’s at baseline, 3 months and 12 months

Fasting lipid profile may tested at these points also to assess response to treatment

127
Q

What is the only CCB licensed for use to manage hypertension with concurrent heart failure?

A

Amlodipine

128
Q

Signs on examination of acute HF?

A 
Bibasal crackles and wheeze
Cyanosis
Tachycardia
Elevated JVP
Displaced apex beat
S3 heart sound
129
Q

What causes S3?

A

It is caused by diastolic filling of the ventricle, considered normal if <30 y/o

Occurs in:

  • Left ventricular failure (e.g. dilated)
  • Constrictive pericarditis (called pericardial knock)
  • mitral regurg
130
Q

What causes S3?

A

It is caused by diastolic filling of the ventricle, considered normal if <30 y/o

Occurs in:

  • Left ventricular failure (e.g. dilated)
  • Constrictive pericarditis (called pericardial knock)
  • mitral regurg
131
Q

What causes S4?

A

Atrium contracting against a stiff, non-compliant ventricle (coincides with P wave on ECG)

Occurs in aortic stenosis, HOCM, hypertension

(HOCM may have a double apical beat caused by palpable S4)

132
Q

How often is digoxin level monitored in blood?

How long after dose?

A

Not routinely monitored unless toxicity suspected

8-12 hours after dose

133
Q

Dose of adrenaline for cardiac arrest?

A

10ml 1:10,000
OR
1ml 1:1000

(0.5ml 1:1000 in anaphylaxis)

134
Q

Glycaemic control if admitted to hospital with ACS?

A

Stop oral glycaemics, start sliding scale insulin

135
Q

Causes of long QT:

  • electrolytes?
  • drugs?
A

Electrolytes:
Low Ca, Mg or K

Drugs

  • amiodarone/sotalol
  • macrolides, ciprofloxacin
  • Citalopram, TCS’s, neuroleptics (esp Haloperidol)
136
Q

What drugs should be AVOIDED in people with HOCM?

A

ACEI
Nitrates
inotropes

(ACEI and nitrates decrease preload making it worse)

137
Q

4 week old infant presents with poor feeding, on exam tachycardia, tachypnoea, hypertension and weak femoral pulses, no cyanosis. Systolic murmur best heard at left sternal edge?

A

Coarctation of aorta

138
Q

Valves most commonly affected in infective endocarditis in order?

A
  1. Mitral
  2. Aortic
  3. Tricuspid
  4. Pulmonary

Tricuspid most commonly affected in IVDU
Apart from that it’s left side because bacteria generally need damage to latch on, and that is more common in left side due to higher pressure

139
Q

What is stage 1, stage 2 and severe HTN?
When to start medication?
What are BP targets?

A

Stage 1 - ABPM >135/85
Stage 2 - ABPM >150/95
Severe - clinic BP >180/110

Stage 1 - treat only if <80 y/o and Q-RISK >10%, or evidence of organ damage
Stage 2 - start medication for all

Targets: 135/85 if <80, 145/85 if >80

140
Q

BP 1st line treatment in diabetes?

A

ACEI no matter what age

ARB if black

141
Q

If a patient has a BP >180/110?

A 
Check for end-organ damage
If none present, ambulatory/home and recheck after 7 days
If evidence (e.g. blood/protein in urine, papilloedema, retinal haemorrhage) admit for specialist assessment

Finals Revision (29 decks)

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