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Phase 4 Question Knowledge > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Which conditions are considered to be ACS?

A

STEMI (ST elevated myocardial infarction)

NSTEMI (non-ST elevated myocardial infarction)

Unstable angina- symptoms of ACS without raised troponins or ECG changes

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2
Q

Why treat unstable angina as NSTEMI in first instance?

A

Troponins may take a while to rise so treated as NSTEMI until troponins known

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3
Q

RFs for cardiovascular disease?

A

Male
FH
Age

Smoking
Hypertension
DM
Hypercholesterolemia
Obesity

ABCDEF- Age, BP, cholesterol, diabetes, exercise, fags, fat, family

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4
Q

Signs/symptoms of ACS?

A

Chest pain:
Central/ left sided
Radiates to jaw/left arm
Heavy or constricting

Dyspnoea
Sweating
Nausea and vomiting
Palpitations

Can present with normal BP, HR, temp, oxygen (unless in cardiac failure)

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5
Q

Which patients may not experience chest pain in ACS?

A

Diabetics/ elderly

Female

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6
Q

Investigations for ACS?

A

ECG

Troponin

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7
Q

ECG and correlating region?

A

Anterior- V1-V4- Left anterior descending

Inferior- II, III, aVF- Right coronary

Lateral- I, V5-6- Left circumflex

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8
Q

Management of ACS?

A

Aims of treatment: prevent worsening, revascularise if occluded, treat pain

MONA

Morphine- only for patients in pain
Oxygen- only if less than 94%
Nitrates- sublingual or IV- use with caution if patient hypotensive
Aspirin 300mg

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9
Q

Specific STEMI management?

A

If onset within last 12 hours and PCI can be delivered within 120 minutes of when fibrinolysis could have been given- give PCI

Consider PCI if it has been longer than 12 hours but evidence ongoing ischemia

Give dual-antiplatelet therapy (DAPT) (aspirin + another drug) before PCI
Add prasugrel, ticagrelor if not taking oral anticoagulant orhigh bleeding risk, clopidogrel if already
anticoagulated

Radial (right) access prefered to femoral access

During PCI- unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) if radial

If femoral bivalirudin with bailout GPI

Drug-eluting stents are now used

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10
Q

STEMI fibrinolysis?

A

Eg Alteplase

Give within 12 hours if PCI no possible in 120 mins

Give an antithrombin drug such as unfractionated heparin, fondaparinux

Repeat ECG after 60-90 mins to see if ECG changes have resolved – transfer to
PCI if not

Give ticagrelor post-procedure

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11
Q

Specific NSTEMI management?

A

Fondaparinux should be offered to patients who are not at a high risk of bleeding and who are not having angiography immediately

If immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given

GRACE score used to assess risk and decide further management

PCI- if clinically unstable or within 72 hours if medium or high risk, also if ischemia subsequently experienced after admission
Unfractionated heparin then given regardless of if they have had fondaparinux, dual antiplatelet therapy prior to PCI- Aspirin + another drug- prausgrel or ticagrelor if not taking another oral anticoagulant, clopidogrel if they are taking another oral antigcoagulant

Conservative management- dual antiplatelet therapy- aspirin +
ticagrelor if not at high risk of bleeding
clopidogrel if at high risk of bleeding

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12
Q

ACS secondary prevention?

A

Aspirin

Second antiplatelet if appropriate (clopidogrel)

Beta blocker

ACEi

Statin

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13
Q

ECG STEMI criteria?

A
  • Sx of ACS (>20mins) + ECG features in 2+ contiguous leads:
  • > 2.5mm (small squares) ST elevation V2-3 in M<40yo (>2mm M>40yo)
  • > 1.5mm ST elevation V2-3 women
  • > 1mm ST elevation in other leads
  • New LBBB
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14
Q

What is angina?

A

Chest pain caused by insufficient blood supply to the myocardium

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15
Q

Angina features?

A

Chest pain may radiate to neck, jaw, arm

Symptoms on exertion

Relieved by rest/ GTN spray

Sweaty, clammy
SOB
N+V
Faint

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16
Q

Angina management?

A

Refer to cardiology

Immediate symptom relief- GTN spray

Long term symptom relief-
Beta blocker- bisoprolol CCB- Diltiazem/ verapamil

Then both BB/CCB used- use amlodipine in that case

If cannot tolerate both use either
a long-acting nitrate
Ivabradine
Nicorandil
Ranolazine

Secondary prevention:
All patients receive a statin and aspirin
ACEi- if DM, DTN, CKD or HF also present
BB

REMEMBER no BB with verapamil

If patient taking both and only add a third drug if waiting for PCI or CABG

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17
Q

Nitrate tolerance?

A

Patients who consistently take nitrates can develop a tolerance

NICE advises that patients who take standard-release isosorbide mononitrate should use an asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours to minimise the development of nitrate tolerance

This effect is not seen in patients who take modified-release isosorbide mononitrate

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18
Q

In angina, if a patient is on a CCB and BB contraindicated due to asthma, what is the next drug to add as a second therapy?

A

A long-acting nitrate

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19
Q

What is variant (Prinzmetal angina)?

A

Coronary artery spasms causing angina

Avoid BBs

Use CCBs- amlodipine, verapamil, diltiazem

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20
Q

Most common cause of death following an MI?

A

Ventricular fibrillation

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21
Q

What is Dressler’s syndrome?

A

Occurs 2-4 weeks after an MI. Thought to be autoimmune reaction against antigenic proteins formed as myocardium recovers.

Characterised by a combination of fever, pleuritic pain, pericardial effusion and a raised ESR.

Treated with NSAIDs.

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22
Q

Is pericarditis common after MI?

A

Yes more common in the first 48 hours after MI

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23
Q

Secondary prevention for MI?

A

All patients should be offered:

Dual antiplatelet therapy- aspirin + a second antiplatelet drug

ACEi

Beta blocker

Statin

Diet
Exercise
Sexual activity can resume 4 weeks after MI. If on nitrates should avoid sildenafil

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24
Q

Dual antiplatelet therapy in MI secondary prevention?

A

Aspirin +

Post ACS medically managed- ticagrelor, stop after 12 months

Post PCI- prausgrel or ticagrelor, stop after 12 monhts

12 months may be altered for people at high risk of bleeding or further cardiac events

Aldosterone agonists- after acute MI for patients who have symptoms of HF, should be initiated 3-14 days after MI after ACEi therapy

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25
Q

RFs for AAA?

A

Smoking, hypertension

Syphilis, Ehlers Danlos type 1 and Marfan’s syndrome

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26
Q

AAA screening?

A

Majority of AAA are asymptomatic

Screening for AAA consists of a single abdominal ultrasound for males over 65

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27
Q

AAA screening outcomes?

A

<3cm- Normal- No further action

3-4.4cm- small aneurysm- rescan every 12 months

4.5 - 5.4 cm- Medium aneurysm- rescan every 3 months

> 5.5cm- Large aneurysm- refer within 2 weeks to vascular surgery for probable intervention

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28
Q

AAA further management?

A

Low rupture risk- asymptomatic, aortic diameter < 5.5cm (i.e. small and medium aneurysms)- abdominal US surveillance and optimise RFs.

High rupture risk- symptomatic, aortic diameter >=5.5cm or rapidly enlarging (>1cm/year)- refer within 2 weeks to vascular surgery for probable intervention
Treat with elective endovascular repair (EVAR)

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29
Q

Ruptured AAA features?

A

Severe, central abdominal pain radiating to the back

Pulsatile, expansile mass in the abdomen

Patients may be shocked- hypotension, tachycardia or may have collapsed

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30
Q

Management ruptured AAA?

A

Surgical emergency- immediate vascular review with a view to emergency surgical repair

Haemodynamically unstable patients diagnosis is clinical- straight to theatre. Frail patients- potential for palliative therapy

Patients who are haemodynamically stable may go for CT angiography when diagnosis in doubt

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31
Q

What are the main patterns of presentation seen in patients with peripheral arterial disease?

A

Intermittent claudication- cramping/burning after walking. Relieved by rest.

Critical limb ischaemia- claudication pain at rest, typically nocturnal, relieved by hanging foot out of bed- rink of gangrene, infection, ulcers

Acute limb-threatening ischaemia- sudden decrease in arterial perfusion

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32
Q

Features of acute limb threatening ischaemia?

A

One or more of 6P’s

Pale
Pulseless
Painful
Paralysed
Paraesthetic
Perishingly cold

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33
Q

Initial investigation for acute limb-threatening ischemia?

A

Handheld arterial Doppler examination. If Doppler signals are present, an ankle-brachial pressure index (ABI) should also be obtained.

Attempt usually made to determine if due to thrombus (due to rupture of atherosclerotic plaque) or embolus (secondary to atrial fibrillation)

Buerger’s Test

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34
Q

How to distinguish between thrombus and embolus in acute-limb threatening ischaemia?

A

Factors suggestive of thrombus:
pre-existing claudication with sudden deterioration
no obvious source for emboli
reduced or absent pulses in contralateral limb
evidence of widespread vascular disease (e.g. myocardial infarction, stroke, TIA, previous vascular surgery)

Factors suggestive of embolus:
sudden onset of painful leg (< 24 hour)
no history of claudication
clinically obvious source of embolus (e.g. atrial fibrillation, recent myocardial infarction)
no evidence of peripheral vascular disease (normal pulses in contralateral limb)
evidence of proximal aneurysm (e.g. abdominal or popliteal)

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35
Q

Management of acute limb-threatening ischaemia?

A

ABC approach

Analgesia: IV opioids

IV unfractionated heparin

Vascular review

Definitive management:

Intra-arterial thrombolysis

Surgical embolectomy

Angioplasty

Bypass surgery

Amputation: for patients with irreversible ischaemia

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36
Q

Features of critical limb ischaemia?

A

1 or more of:

Rest pain in foot for more than 2 weeks

Ulceration

Gangrene

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37
Q

Ankle-brachial pressure index (ABPI) for critical limb ischaemia?

A

< 0.5 is suggestive of critical limb ischaemia

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38
Q

What is aortic dissection?

A

Tear in the tunica intima of the wall of the aorta

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39
Q

What is aortic dissection associated with?

A

Hypertension- most important factor

Trauma

Bicuspid aortic valve

Collagens- Marfan’s syndrome, Elhers-Danlos syndrome

Turner’s and Noonan’s syndrome

Pregnancy

Syphilis

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40
Q

What are the features of aortic dissection?

A

Chest/back pain- severe, sharp, tearing in nature, pain maximal at onset
Chest pain more common in type A dissection and back pain in type B dissection but there is overlap

Pulse defecit- weak or absent pulses, over 20 difference between the arms

Aortic regurgitation

Hypertension

Other features may result from the involvement of specific arteries. For example:
coronary arteries → angina
spinal arteries → paraplegia
distal aorta → limb ischaemia

Majority no ECG changes, some ST elevation

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41
Q

Classification of aortic dissections?

A

Stanford-
Type A - ascending aorta, 2/3 of cases
Type B - descending aorta, distal to left subclavian origin, 1/3 of cases

DeBakey classification
type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally
type II - originates in and is confined to the ascending aorta
type III - originates in descending aorta, rarely extends proximally but will extend distally

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42
Q

Aortic dissection investigations?

A

Patients can present acutely and be clinically unstable so use appropriate investigation

CXR- widened mediastinum

CT angiography of the chest, abdomen and pelvis- investigation of choice- suitable for stable patients and planning surgery- false lumen is a key finding in aortic dissection

Transoesophageal echocardiography (TOE)- more suitable for patients too high risk for CT scanner

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43
Q

Aortic dissection management?

A

Type A- surgical management, BP controlled 100-120 while waiting

Type B- conservative, bed rest, IV labetalol to to prevent progression, surgery if complicated

44
Q

What causes aortic regurgitation?

A

Incompetent aortic valve leading to blood leaking back into ventricle from aorta during diastole

45
Q

Causes of AR due to valvular disease?

A

Rheumatic fever

Calcified valve

RA/SLE

Bicuspid aortic valve

IE

46
Q

Causes of AR due to aortic root disease?

A

Bicuspid aortic valve

Ankylosing spondylitis

HTN

Syphilis

Marfan’s, Ehler-Danlos

Aortic dissection

47
Q

Features of aortic dissection?

A

Early diastolic murmur

Collapsing pulse

Wide pulse pressure

Quinke’s sign (nailbed pulsation)

De Musset’s sign (head bobbing)

(SOBOE, oedema, fatigue, angina, syncope)

48
Q

Investigation of AR?

A

Echocardiogram

49
Q

Management of AR?

A

Medical management of HF

Surgery- aortic valve replacement- symptomatic or LV systolic dysfunction

50
Q

Aortic stenosis cause?

A

Narrowing of the aortic valve- most common valvular heart disease

Calcification of aortic valve
Congenital bicuspid valve
Rheumatic heart disease – rare
HOCM

51
Q

Aortic stenosis features?

A

Ejection systolic (crescendo-decrescendo) murmur ESM- radiates to the carotids

Chest pain, dyspnoea, syncope/presyncope

52
Q

Features of severe aortic stenosis?

A

Narrow pulse pressure

Slow rising pulse

Delayed ESM

Soft/absent S2

S4

53
Q

Management of aortic stenosis?

A

Investigation: echo

If asymptomatic observe

If symptomatic then valve replacement

If asymptomatic, but valvular gradient >40mmHg + LVF, consider surgery

Surgical options for aortic valve replacement:
Surgical AVR (open)- low risk patients
TAVI – transcatheter aortic valve implantation –
for higher risk pts

Balloon valvuloplasty- children or adults not fit for valve replacement

54
Q

Bicuspid aortic valve?

A

1-2% of population, asymptomatic in childhood, majority develop aortic stenosis or regurgitation

Associated with left dominant coronary circulation and Turner’s syndrome

Higher risk of dissection/aneurysm

55
Q

Prosthetic heart valves?

A

Most commonly replaced are the aortic and mitral

Options for replacement: biological or prosthetic

Biological- usually bovine. Major disadvantage is structural deterioration or calcification over time. Given to patients >65 for aortic and >70 for mechanical. Long term anticoagulation not needed. Warfarin may be given first 3 months, low dose aspirin long term.

Most common mechanical valve is bileaflet valve. Mechanical valves have low failure rate. Major disadvantage is increased risk of thrombosis meaning long term anticoagulation needed. WARFARIN still used in preference to doacs in mechanical heart valves.
Only add aspirin if there is another indication.

56
Q

What is mitral reguritation?

A

Blood leaking back through the mitral valve during systole

Second most common valve disease after aortic stenosis

Mitral valve between left atrium and ventricle

You get left atrial enlargement and LVH

57
Q

MR causes?

A

Mitral valve prolapse

Post MI

Infective endocarditis

Rheumatic fever

Congenital

Connective tissue disorders – Ehlers-Danlos, Marfan

58
Q

MR presentation?

A

Pansystolic murmur- radiates to axilla

SOBOE, palpitaitons, fatigue, signs of HF

59
Q

MR investigations?

A

Echocardiogram

CXR- cardiomegaly

ECG- LA enlargement- broad P wave- LVH in severe

60
Q

MR treatment?

A

In acute cases, nitrates, diuretics, inotropes, intra-aortic balloon pump – to
increase CO

HF – ACEi, BBs, spironolactone etc

Surgery
Repair / replacement

61
Q

What is mitral stenosis?

A

Obstruction of blood flow from LA to LV, inreased pressure in LA

62
Q

Mitral Stenosis causes?

A

RHEUMATIC fever- most common cause

also infective endocarditis

63
Q

Presentation of mitral stenosis?

A

Mid-diastolic murmur

SOBOE, oedema, angina

Haemoptysis from rupture of pulmonary vessels

Loud S1

Opening snap

Low volume pulse

Malar flush

AF

64
Q

Mitral stenosis investigations?

A

Echo

CXR

ECG

65
Q

Mitral stenosis management?

A

Asymptomatic- regular monitoring with ECHO

If sx
Balloon valvuloplasty
Mitral valve replacement

66
Q

What is atrial fibrillation?

A

Disorganised electrical activity of the atria leading to fibrillation- irregularly irregular rhythm

Type of supraventricular tachycardia

67
Q

Types of atrial fibrillation?

A

First detected episode

Recurrent episodes- 2 or more episodes of AF either:
Paroxysmal AF – terminates spontaneously – tend to be <7d, typically <24hrs
Persistent AF – not self-terminating – >7d

Permanent AF – continuous AF, tx goals are rate control / anticoagulation

68
Q

AF symptoms and signs?

A

Palpitations
SOB
Chest pain
Syncope
Sx of associated conditions- stroke, infection

Irregularly irregular pulse

69
Q

AF investigations?

A

ECG-
Absent P waves
Irregularly irregular pulse

ECHO

For paroxysmal AF:
24 hour ECG

CHA2DS2VASc / ORBIT

70
Q

AF management?

A

Two key aspects:
Rate/rhythm control
Reducing stroke risk

Rate control- slow the rate down to avoid negative effects on cardiac function

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

71
Q

AF rate control?

A

Beta blocker or rate limiting CCB (diltiazem)

If one drug does not control then add either:
Betablocker
Diltiazem
Digoxin

Other one or digoxin

72
Q

AF rhythm control?

A

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

73
Q

AF reducing stroke risk?

A

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).

74
Q

Components of CHA2DS2-VASc?

A

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.

75
Q

AF rate control?

A

Offer as first line tx apart from the following pts:
* AF has reversible cause
* Have HF primarily caused by AF
* New onset AF <48hrs
* AFl suitable for ablation
* Clinical judgement to say rhythm-control would be more suitable
▪ Beta-blocker – eg bisoprolol, metoprolol
▪ Calcium channel blocker – eg diltiazem (is a rate-limiting CCB) – not preferred in HF
▪ Digoxin

76
Q

AF rhythm control?

A

Offer to pts with:
* Reversible cause for AF
* New onset AF <48hrs
* HF caused by AF
* Sx despite effective rate control
Aim is to induce normal sinus rhythm

Elective cardioversion – electrical / pharmacological

<48hrs onset AF → immediate cardioversion
o Give heparin
o Electrical – synchronised DC cardioversion
o Pharm – flecainide / amiodarone – amiodarone if structural heart disease

> 48hrs onset AF → delayed cardioversion
o Give >3wks anticoagulation before cardioversion
o Or use trans-oesophageal echo to exclude left atrial appendage (LAA)
thrombus – then can heparinise + cardiovert immediately
o Electrical cardioversion preferred
o Can give 4wks amiodarone / sotalol prior – esp if high risk of
cardioversion failure
o Anticoagulate >4wks after this

77
Q

ORBIT AF?

A

ORBIT score to assess risk of bleeding
* 0-2 – low risk
* 3 – medium risk
* 4-7 – high risk

78
Q

Anticoag in AF?

A

First line – DOAC
* Apixaban, dabigatran,
edoxaban, rivaroxaban

Second line – warfarin – if DOAC CI’d
or not tolerated

79
Q

Catheter ablation in AF?

A

Catheter ablation
▪ If no response to antiarrhythmics
▪ Can ablate LA, or AVN + insert permanent pacemaker
▪ Ablate faulty electrical pathways
▪ Radiofrequency / cryotherapy can be used
▪ Anticoagulate 4wks before and during procedure

80
Q

What is atrial flutter?

A

Abnormal atrial rhythm with atrial rate up to 300/min- if the block is 2:1 HR would be 150

81
Q

ECG findings in atrial flutter?

A

Sawtooth appearance

82
Q

Atrial flutter management?

A

Similar to AF althought medication not as effective

More sensitive to cardioversion so lower energy can be used

Radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

83
Q

What is broad complex tachycardia?

A

QRS over 120ms

Electrical activity not following the usual conduction system

Ventricular tachycardia

SVT with BBB

Ventricular fibrillation

84
Q

Ventricular tachycardia?

A

Monomorphic VT- caused by MI

Polymorphic VT- subtype of polymorphic VT is torsades de pointes

Management-

ALS guidelines

Unstable – synchronised DC cardioversion, up to 3x, IV amiodarone infusion if
unsuccessful

Stable – IV amiodarone, loading dose, then infusion

Torsades de Pointes – Mg

NO verapamil in VT

85
Q

Torsades de pointes?

A

A polymorphic ventricular tachycardia associated with long QT

86
Q

Causes of a long QT interval?

A

Congenital

Antiarrythmics- amiodarone

Tricyclic antidepressants

Antipsychotics

Erythromycin

Electrolytes- hypocalcaemia, hypokalaemia, hypomagnesemua

Hypothermia

SAH

87
Q

Torsades de pointes management?

A

IV magnesium sulphate

88
Q

What are examples of narrow complex tachycardia?

A

Sinus tachycardia

Atrial fibrillation- technically SVT

Atrial flutter- technically SVt

Supraventricular tachycardia

89
Q

Supraventricular tachycardia management?

A

Acute management-
Vagal manoeuvres- valsalva manoevre, carotid sinus massage

IV adenosine- rapid IV bolus of 6mg if unsuccessful 12mg if unsuccessful further 18mg
Contraindicated in asthmatics with verapamil preferable

Electrical carioversion

Prevention of episodes:
Beta-blockers

Radio-frequency ablation

90
Q

Bradycardia- peri arrest rhythms?

A

A-E approach

Assess for adverse signs-
Shock- hypotension systolic <90, pallor, sweating, cold, clammy, confusion, impaired conciousness
Syncope
Myocardial ischemia
HF

No risk- observe

If risk-

Atropine 500mcg IV

Further-
Atropine up to 3mg (6x)
Transcutaneous pacing
Isoprenaline/adrenaline infusion

Specialist help sought for transvenous pacing

91
Q

Risk factors for asystole in bradycardia?

A

Complete heart block with broad QRS

Recent asystole

Mobitz type II AV block

Ventricular pause > 3 seconds

92
Q

Tachycardia peri arrest rhythm- unstable?

A

A-E approach

Assess for life threatening features (unstable):

Shock- hypotension (systolic BP less than 90), pallor, sweating, cold, clammy, confusion, impaired conciousness
Syncope
Myocardial ischaemia
Heart failure

If present give synchronised DC shocks- up to 3

If unsuccessful amiodarone 300mg IV over 10-20 minutes

Repeat synchronised DC shock

93
Q

Tachycardia peri-arrest- broad complex- stable?

A

Assume VT unlcess confirmed SVT with BBB

Regular- Loading dose of amiodarone followed by 24 hour infusion

Irregular- expert help
Possibly:
AF with BBB
Torsades de pointes- magnesium

94
Q

Tachycardia peri-arrest- broad complex- stable?

A

Likely SVT of atrial flutter

Regular- vagal manouvres followed by IV adenosine
If unsucessful consider atrial flutter and control rate (BBs)

Irregular
Probable AF
if onset <48hours electrical or chemical cardioverrsion
Rate control: BB first line unless CI

95
Q

Adult advanced life support?

A

Shockable- VF, pulseless VT

Non-shockable- asystole, pulseless electrical activity

Chest compressions- 30:2

Defibrillation- single shock for VF/pulseless VT followed by 2 mins CPR
If cardiac arrest witnessed in monitored patient then up to 3 successive rather than 1 followed by CPR

Drug delivery- IV access attempted first line
If IV access not possible drugs given via intraosseous route (IO), no longer tracheal tube

Adrenaline- asap for non shocable rhythms
VF/VT- adrenaline 1mg given after compressions restart after 3rd shock
Repeat adrenaline 1mg every 3-5 mins while ALS continues

Amiodarone 300mg given to patients who are in VF after 3 shocks
Further 150mg given to VD after 5 shocks
Lidocaine is an alternative if amiodarone not available

Thrombolytic drugs- should be considered if PE suspected, if given CPR continuted for extended period of 60-90 minutes

96
Q

Paediatric basic life support?

A

Compressions- 15:2 if more than two people, 30:2 if alone

Shout for help
Feel for breathing
5 rescue breaths
Check for signs of circulation- brachial or femoral in infants, femoral in children

15:2 compression- carried out at 100-120/min
One-third of the chest-
In children- compress the lower half of the sternum
In infants- two-thumb encircling technique for chest compression

97
Q

What is chronic heart failure?

A

Heart unable to to pump enough blood to meet the metabolic needs of the body

Cor pulmonale is the abnormal enlargement of the right side of the heart due to disease of the lungs

98
Q

Heart failure investigations?

A

1st- N-terminal pro-B-type natriuretic peptide (NT-proBNP) blood test

If levels are high- arrange a specialist assessment (including transthoracic echocardiography) within 2 weeks

If raised arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks

Secreted by LV in response to strain

May also rise with ischaemia, valvular
disease, CKD (reduced excretion)

ECG

CXR- ABCDE- pulmonary oedema
▪ Alveolar oedema – ‘bat’s wing shadowing’
▪ Kerley B lines – interstitial oedema
▪ Cardiomegaly – cardiothoracic ratio >50%
▪ Dilated prominent upper lobe veins (upper lobe
diversion)
▪ Pleural Effusions
▪ Also exclude lung pathology

ECHO

99
Q

Chronic heart failure drug management?

A

1st line is ACEi and BB

2nd Aldosterone antagoist (spironolactone)

3rd- by specialist
Ivabradine- sinus rhythm > 75/min and a left ventricular fraction < 35%

Sacubitril-valsartan- initiated after ACEi/ARB washout period

Digoxin

Hydralazine- Afro-Caribbean patients

Cardiac resynchronisation therapy

Offer all patients:

Diuretics- furosemide

Flu vaccine

Pneumococcal vaccine

Lifestyle advice

100
Q

NYHA classification heart failure?

A

New York Heart Association (NYHA) classification
▪ Class I – no symptoms on ordinary physical activity
▪ Class II – mild sx, slight limitation of physical activity

▪ Class III – moderate sx, comfortable at rest but less than ordinary activity leads to sx
▪ Class IV – severe sx, inability to carry out any activity without sx

101
Q

Features of chronic heart failure?

A

SOB
Cough- worse at night- pink/frothy sputum
Orthopnoea
PND
Wheeze
Weight loss- cachexia
Bibasal crackles
Signs of RHF- raised JVP, ankle oedema and hepatomegaly

102
Q

What is acute heart failure without a PMH of HF?

A

De-novo HF

103
Q

Acute HF causes?

A

Cardiac
▪ Acute LVF, ACS, arrhythmias, valvular heart disease, HTN, cardiomyopathy, tamponade
o Non-cardiac
▪ Fluid overload, high-output HF, ARDS, renal artery stenosis

104
Q

Acute HF presentation?`

A

SOB
Tachycardia
Cyanosis
Increased RR
Fatigue
Displaced apex beat
Raised SVP
Crackles/Wheeze
S3- heart sound

105
Q

Acute heart failure investigations?

A

A-E

ECG

Bloods

CXR
▪ Alveolar oedema
▪ Kerley B lines
▪ Cardiomegaly
▪ Dilated upper lobe vessels
▪ Pleural effusions

ECHO

106
Q

Acute heart failure management?

A

IV loop diuretics- furosemide

Oxygen

Vasodilators- nitrates but not to everyone- if severe, but not if BP low

CPAP for resp failure

Hypotension/ cardiogenic shock-
Inotropic agents- dobutamine

Vasopressor agents- noradrenaline

Regular medications for HF continued- BB only stopped if patient HR less than 50

Phase 4 Question Knowledge (30 decks)

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