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Cardiovascular Flashcards

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1
Q

What 3 conditions make up ACS?

A
  1. ST elevation myocardial infarction (STEMI)
  2. Non-ST elevation myocardial infarction (NSTEMI)
  3. Unstable angina- no elevated troponin differentiates from NSTEMI
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2
Q

How to differentiate unstable angina from NSTEMI?

A

No elevated troponin in NSTEMI

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3
Q

Signs and symptoms of ACS?

A

Chest pain- central/left sided, radiate to jaw or left arm, heavy
Diabetics, elderly or female may not experience chest pain

Dyspnoea
Sweating
Nausea and vomiting
Palpitations
Pale and clammy

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4
Q

ACS investigations?

A

ECG

Cardiac markers- troponin

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5
Q

ECG and coronary territories?

A

Anterior- leads V1-V4, left anterior descending artery

Inferior- leads II, III, aVF, right coronary artery

Lateral- I, V5-6, left circumflex artery

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6
Q

ACS treatment?

A

Morphine
Oxygen- if under 94%
Nitrates- caution if hypotensive
Aspirin

For STEMI further management:
Clopidogrel or ticagrelor as well as aspirin
Percutaneous coronary intervention (PCI)- catheter in radial or femoral artery

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7
Q

ACS secondary prevention?

A

Aspirin
Second anti-platelet- clopidogrel, ticagrelor
Beta blocker
ACEi
Statin

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8
Q

STEMI criteria on an ECG?

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)

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9
Q

What are the two types of coronary reperfusion therapy?

A

Percutaneous coronary intervention (PCI)

Fibrinolysis

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10
Q

Criteria for PCI?

A

Should be offered if the presentation is within 12 hours of the onset of symptoms and PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given

If present after 12 hours PCI still to be considered

Radial access preferred using a drug eluting stent

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11
Q

Criteria for fibrinolysis?

A

Should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 mins of the time when fibrinolysis could have been given

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12
Q

Further drugs PCI?

A

Dual therapy- aspirin + another drug

No oral anticoagulant- prasugrel

Oral anticoagulant- clopidogrel

PCI through radial- unfractionated heparin with bailout GPI

PCI through femoral- bivalirudin with bailout GPI

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13
Q

Fibrinolysis further drugs?

A

Patients undergoing fibrinolysis should be given an antithrombin drug

ECG to be repeated after 60-90 mins to see if ECG changes resolved. If persistent myocardial ischemia following fibrinolysis then PCI should be consisdered

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14
Q

NSTEMI further management?

A

Further drug therapy (after aspirin)-
Fondaparinux offered to patients not high bleeding risk or having angiography immediately
If immediate angiography planned unfractionated heparin given

Risk assessment (GRACE)
Low risk- ticagrelor
High risk- PCI, prasugrel or ticagrelor, unfractionated heparin

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15
Q

NSTEMI risk assessment score example?

A

GRACE

age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels

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16
Q

Reasons for coronary angiography in NSTEMI?

A

Clinically unstable (hypotensive)
Within 72 hours GRACE score above 3%

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17
Q

Myocardial infarction complications?

A

Cardiac arrest
Cardiogenic shock
Chronic heart failure
Tachyarrythmias- ventricular fibrillation most common cause of death
Bradyarrythmias- AV block following inferior MI
Pericarditis- in first 48 hours, Dressler’s syndrome 2-4 weeks after MI.
Left ventricular aneurysm
Acute mitral regurgitiation
**Left ventricular free wall rupture
Ventricular septal defect

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18
Q

Dressler’s syndrome?

A

2-6 weeks after MI, autoimmune reaction to proteins formed from myocardium recovery.

Fever, pleuritic pain, pericardial effusion and raised ESR. Treated with NSAIDs.

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19
Q

Secondary prevention after MI?

A

All patients offered:
Dual antiplatelet therapy (aspirin + 1)
ACEi
Beta blocker
Statin

Lifestyle:
Diet
Exercise
Sexual activity 4 weeks after MI

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20
Q

What is the screening for AAA?

A

A single abdominal ultrasound for males at 65 years old
<3cm- normal
3-4.4cm Small aneurysm- rescan in 12 months
4.5-5.4cm medium aneurysm- rescan every 3 months
>5.5cm large- refer within 2 weeks for surgical intervention

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21
Q

Management after AAA screening?

A

Low rupture risk- <5.5cm:
US surveillance and manage risk factors

High rupture risk:
Symptomatic, aortic diameter >5.5cm or rapidly enlarging >1cm per year
Refer within 2 week to vascular surgery
Treat with elective EVAR or open repair.

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22
Q

Risk factors for AAA?

A

Male
Age
Smoking
Hypertension

Rare:
Marfan’s
Ehlers Danlos
Syphillis

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23
Q

Ruptured aortic aneurysm?

A

Very high mortality of 80%

Features:
Severe, central abdominal pain radiating to the back
Pulsatile, expansile mass in the abdomen
Patients may be shocked (hypotension, tachycardia) or may have collapsed

Management:

Surgical emergency- immediate vascular review with a view to emergency repair
Clinical diagnosis in haemodynamically unstable
Haemodynamically stable can havev CT angiogram if diagnosis in doubt

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24
Q

6 P’s of critical limb ischaemia?

A

Pain
Pallor
Pulseless
Paralysis
Paraesthesia
Perishingly cold

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25
Leriche syndrome?
Thick buttock pain Absent femoral pulses Male impotence Blockage of distal aorta
26
What are the three main patterns of presentation seen in peripheral arterial disease?
Intermittent claudication Critical limb ischaemia Acute limb-threatening ischaemia
27
Investigations for acute limb-threatening ischaemia?
Handheld arterial doppler If signals are present ankle-brachial pressure index (ABI) calculated
28
Management of acute limb-threatening ischaemia?
Initial management: ABC approach Analgesia- IV opioids IV unfractionated heparin Vascular review Definitive management: Intra-arterial thrombolysis Surgical embolectomy Angioplasty Bypass surgery Amputation
29
What is an aortic dissection?
Tear in the tunica intima of the wall of the aorta
30
What are he risk factors for aortic dissection?
Hypertension- the most significant risk factor Trauma Bicuspid aortic valve Marfan's, Ehlers-Danlos syndrome Turner's and Noonan's Pregnancy Syphillis
31
Features of aortic dissection?
Chest/back pain- sharp and tearing in nature- chest more common in type A, back more common in type B Pulse deficit- weak puulses with variation >20 between arms Aortic regurgitation Hypotension Angina, paraplegia, limb ischemia No ECG changes
32
Classification of aortic dissection?
Stanford- Type A- asending aorta Type B- descending aorta DeBakey
33
Investigation of aortic dissection?
Chest x-ray- widened mediastinum CT angiography chest, abdomen, pelvis- investigation of choice- stable patients planning for surgery- false lumen is key finding Transoesophageal echocardiography (TOE)- more suitable for unstable patients too risky to take to CT scanner
34
Management for aortic dissection?
Type A- surgical management but BP controlled while awaiting management Type B- conservative management, bed rest, reduce blood pressure
35
What is aortic regurgitation?
The leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole Caused by disease of aortic valve or dilation of the aortic root
36
Causes of AR due to valve disease?
Rheumatic fever Calcific valve disease RA, SLE Bicuspid aortic valve Acute: infective endocarditis
37
Causes of AR due to aortic root disease
Biscuspid aortic valve Spondylarthropathies Hypertension Syphillis Marfan's, Ehler-danlos Acute: aortic dissection
38
Features of AR?
Early diastolic murmur- increased by the handgrip manoevre Collapsing pulse Wide pulse pressure Quincke's sign (nailbed pulsation) De Musset's sign (head bobbing)
39
AR investigations?
Echocardiography
40
AR management?
Medical management of associated heart failure Surgery- aortic valve replacement if severe
41
Aortic stenosis features?
Ejection systolic murmur- radiates to carotids Chest pain Dyspnoea Syncope/ presyncope
42
Features of severe aortic stenosis?
Narrow pulse pressure Slow rising pulse Delayed ESM Soft/absent S2 S4 Thrill LVH or failure
43
Causes of aortic stenosis?
Degenerative calcification (older patients) Bicuspid aortic valve (younger patients) William's syndrome Post-rheumatic disease
44
Management aortic stenosis?
If asymptomatic- observe If symptomatic- valve replacement If asymptomatic but valvular gradient >40 with left ventricular dysfunction consider surgery Can do surgical aortic valvular repair for young, low risk. Transcathetar AVR (TAVR) for high risk. Balloon valvuloplasty.
45
Prosthetic heart valves?
Biological- bovine. Structural deterioration over time- older patients revieve. Don't need long term anticoag. Mechanical valve- bileaflet valve. Low failure rate. Increased risk of thrombosis so long term anticoag used. Warfarin preference.
46
AF classifications?
First detected episode Paroxysmal- recurrent episodes of 2 or more. Self terminating last < 7 days. Persistent- recurrent episodes of 2 or more. Not self-terminating, usually last longer than 7 days Permanent- continuous AF that cannot be cardioverted or inappropriate to do so. Rate control and anticoagulation.
47
Signs and symptoms of AF?
Symptoms: Palpitations Dyspnoea Chest pain Signs: Iregularly irregular pulse
48
AF investigations?
ECG
49
AF management?
Two key aspects: Rate/rhythm control Reducing stroke risk Rate control- slow the rate down to avoid negative effects Rhythm control- try to get patient back into and maintain sinus rhythm. Called cardioversion- using drugs or electric shocks NICE advocate rate control in specific situations such as coexistant heart failure, first onset AF or where there is a reversible cause
50
AF rate control?
Beta blocker or rate limiting CCB (diltiazem) If one drug does not control then add either: Betablocker Diltiazem Digoxin Other one or digoxin
51
AF rhythm control?
As cardioversion is attempted a clot can be pushed out on return to sinus rhythm. Therefore patient must have had symptoms less than 48 hours or be anticoagulated for a period of time prior to attempting cardioversion Can be used as electrical cardioversion emergency if the patient is haemodynamically unstable Electrical cardioversion is synced to the R wave Medical cardioversion is with amiodarone If >48 hours AF then patient should recieve anticoagulation for at least 3 weeks before cardioversion After electrical cardioversion patients should be anticoagulated for 4 weeks
52
AF reducing stroke risk?
CHA2DS2-VASc used to determine if anticoagulation needed Choice of warfarin or DOACs Should be on DOAC and discuss with patient about changing if on warfarin, warfarin second line NICE warn not to withhold anticoagulation based on solely age or falls risk. Use ORBIT system (look up).
53
Components of CHA2DS2-VASc?
Congestive heart failure- 1 Hypertension- 1 Age >75- 2 Age 65-74- 1 Diabetes- 1 Prior stroke, TIA, thromboembolism- 2 Vascular disease (ischaemic heart disease or peripheral arterial disease)- 1 Sex female- 1 Outcome- 0- no treatment 1- Males consider anticoagulation, females no treatment as only due to gender 2- Offer anticoagulation Choice of warfarin and NOACs If no need for anticoagulation make sure transthoracic echocardiogram has been done to exclude valvular heart disease which in combination with AF is an absolute indication for anticoagulation.
54
Features of AF?
Palpitations, dyspnoea, dizziness/syncope Irregularly irregular pulse DIagnosis: ECG- absent P waves 24 hour ECG useful where paroxysmal AF suspected
55
AF Cardioversion?
Can use: Amiodarone Flecainide (if no structural heart disease)
56
AF after stroke anticoagulation?
Following a TIA, anticoagulation should start immediately once imaging has excluded haemorrhage In acute stroke, anticoagulation should be commenced after 2 weeks, in the absence of haemorrhage. Antiplatelet therapy in the intervening period.
57
Atrial flutter features?
Supraventricular tachycardia characterised by succession of rapid atrial depolarisation waves ECG findings: Sawtooth appearance Atrial rate often around 300/min, HR is dependent on AV block 2:1 will be 150 ventricular rate Management: Similar to atrial fibrillation Atrial flutter more sensitive to cardioversion
58
What signs indicate the need for treatment in peri arrest bradycardia?
Shock- hypotension, pallor, sweating, cold, clammy, confusion, impaired conciousness Syncope Myocardial infarction Heart failure First line treatment: atropine If response is unsatisfactory: Atropine up to 3mg Transcutaneous pacing Isoprenaline/adrenaline infustion titrated to response Specialist transvenous pacing if there is no response to above
59
Risk factors for asystole in peri arrest bradycardia?
Complete heart block with broad complex QRS Recent asystole Mobitz type II AV block Ventricular pause > 3 seconds
60
Peri arrest tachycarda signs for unstable?
Shock- hypotension, pallor, sweating, cold, clammy, confusion, impaired conciousness Syncope Myocardial ischaemia Heart failure If any of the above adverse signs are present then synchronised DC shocks given. Up to 3 shocks can be given.
61
Treatment of tachycardia if no life threatening features?
Broad complex tachycardia: Regular: assume ventricular tachycardia- loading dose of amiodarone followed by 24 hour infusion Irregular- expert help- could be atrial fibrillation with bundle branch block, Afib with vent pre-excitation or torsade de pointes Narrow-complex tachycardia: Regular- vagal manouveres followed by IV adenosine If unsuccessful consider A flutter and rate control Irregular- probable A fib, if onset <48 hours consider electrical or chemical cardioversion, rate control first line BB
62
Management of SVT?
Acute management: Vagal manoeuvres: valsalva manoeuvre and carotid sinus manoeuvre IV adenosine- rapid IV bolus of 6mg- then 12mg- then 18mg Electrical cardioversion Prevention of episodes: beta-blockers, radio-frequency ablation
63
What is torsades de pointes?
Polymorphic ventricular tachycardia associated with a long QT interval. Causes of long QT: Congenital, anipsychotics, hypothermia, SAH, erythromycin Management: IV magnesium sulphate
64
What is ventricular tachycardia?
Broad complex tachycardia originating from a ventricular ectopic focus. Potential to precipitate ventricular fibrillation- urgent treatment needed Two types of VT: monomorphic- caused my MI Polymorphic- (torsades de pointes precipitated by prolonged QT. Causes prolonged QT- congenital, drugs- amiodarone, antipsychotics, erythromycin, tricyclic antidepressants, electrolyte imbalances (hypokalaemia, hypomagnesaemia),acute MI, myocarditis, hypothermia, SAH
65

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