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
RFs for AAA?
Smoking, hypertension Syphilis, Ehlers Danlos type 1 and Marfan's syndrome
26
AAA screening?
Majority of AAA are asymptomatic Screening for AAA consists of a single abdominal ultrasound for males over 65
27
AAA screening outcomes?
<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
28
AAA further management?
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)
29
Ruptured AAA 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
30
Management ruptured AAA?
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
31
What are the main patterns of presentation seen in patients with peripheral arterial disease?
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
32
Features of acute limb threatening ischaemia?
One or more of 6P's Pale Pulseless Painful Paralysed Paraesthetic Perishingly cold
33
Initial investigation for acute limb-threatening ischemia?
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
34
How to distinguish between thrombus and embolus in acute-limb threatening ischaemia?
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)
35
Management of acute limb-threatening ischaemia?
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
36
Features of critical limb ischaemia?
1 or more of: Rest pain in foot for more than 2 weeks Ulceration Gangrene
37
Ankle-brachial pressure index (ABPI) for critical limb ischaemia?
< 0.5 is suggestive of critical limb ischaemia
38
What is aortic dissection?
Tear in the tunica intima of the wall of the aorta
39
What is aortic dissection associated with?
Hypertension- most important factor Trauma Bicuspid aortic valve Collagens- Marfan's syndrome, Elhers-Danlos syndrome Turner's and Noonan's syndrome Pregnancy Syphilis
40
What are the features of aortic dissection?
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
41
Classification of aortic dissections?
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
42
Aortic dissection investigations?
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
43
Aortic dissection management?
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
What causes aortic regurgitation?
Incompetent aortic valve leading to blood leaking back into ventricle from aorta during diastole
45
Causes of AR due to valvular disease?
Rheumatic fever Calcified valve RA/SLE Bicuspid aortic valve IE
46
Causes of AR due to aortic root disease?
Bicuspid aortic valve Ankylosing spondylitis HTN Syphilis Marfan's, Ehler-Danlos Aortic dissection
47
Features of aortic dissection?
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
Investigation of AR?
Echocardiogram
49
Management of AR?
Medical management of HF Surgery- aortic valve replacement- symptomatic or LV systolic dysfunction
50
Aortic stenosis cause?
Narrowing of the aortic valve- most common valvular heart disease Calcification of aortic valve Congenital bicuspid valve Rheumatic heart disease – rare HOCM
51
Aortic stenosis features?
Ejection systolic (crescendo-decrescendo) murmur ESM- radiates to the carotids Chest pain, dyspnoea, syncope/presyncope
52
Features of severe aortic stenosis?
Narrow pulse pressure Slow rising pulse Delayed ESM Soft/absent S2 S4
53
Management of aortic stenosis?
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
Bicuspid aortic valve?
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
Prosthetic heart valves?
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
What is mitral reguritation?
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
MR causes?
Mitral valve prolapse Post MI Infective endocarditis Rheumatic fever Congenital Connective tissue disorders – Ehlers-Danlos, Marfan
58
MR presentation?
Pansystolic murmur- radiates to axilla SOBOE, palpitaitons, fatigue, signs of HF
59
MR investigations?
Echocardiogram CXR- cardiomegaly ECG- LA enlargement- broad P wave- LVH in severe
60
MR treatment?
In acute cases, nitrates, diuretics, inotropes, intra-aortic balloon pump – to increase CO HF – ACEi, BBs, spironolactone etc Surgery Repair / replacement
61
What is mitral stenosis?
Obstruction of blood flow from LA to LV, inreased pressure in LA
62
Mitral Stenosis causes?
RHEUMATIC fever- most common cause also infective endocarditis
63
Presentation of mitral stenosis?
Mid-diastolic murmur SOBOE, oedema, angina Haemoptysis from rupture of pulmonary vessels Loud S1 Opening snap Low volume pulse Malar flush AF
64
Mitral stenosis investigations?
Echo CXR ECG
65
Mitral stenosis management?
Asymptomatic- regular monitoring with ECHO If sx Balloon valvuloplasty Mitral valve replacement
66
What is atrial fibrillation?
Disorganised electrical activity of the atria leading to fibrillation- irregularly irregular rhythm Type of supraventricular tachycardia
67
Types of atrial fibrillation?
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
AF symptoms and signs?
Palpitations SOB Chest pain Syncope Sx of associated conditions- stroke, infection Irregularly irregular pulse
69
AF investigations?
ECG- Absent P waves Irregularly irregular pulse ECHO For paroxysmal AF: 24 hour ECG CHA2DS2VASc / ORBIT
70
AF management?
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
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
72
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
73
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).
74
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.
75
AF rate control?
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
AF rhythm control?
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
ORBIT AF?
ORBIT score to assess risk of bleeding * 0-2 – low risk * 3 – medium risk * 4-7 – high risk
78
Anticoag in AF?
First line – DOAC * Apixaban, dabigatran, edoxaban, rivaroxaban Second line – warfarin – if DOAC CI’d or not tolerated
79
Catheter ablation in AF?
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
What is atrial flutter?
Abnormal atrial rhythm with atrial rate up to 300/min- if the block is 2:1 HR would be 150
81
ECG findings in atrial flutter?
Sawtooth appearance
82
Atrial flutter management?
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
What is broad complex tachycardia?
QRS over 120ms Electrical activity not following the usual conduction system Ventricular tachycardia SVT with BBB Ventricular fibrillation
84
Ventricular tachycardia?
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
Torsades de pointes?
A polymorphic ventricular tachycardia associated with long QT
86
Causes of a long QT interval?
Congenital Antiarrythmics- amiodarone Tricyclic antidepressants Antipsychotics Erythromycin Electrolytes- hypocalcaemia, hypokalaemia, hypomagnesemua Hypothermia SAH
87
Torsades de pointes management?
IV magnesium sulphate
88
What are examples of narrow complex tachycardia?
Sinus tachycardia Atrial fibrillation- technically SVT Atrial flutter- technically SVt Supraventricular tachycardia
89
Supraventricular tachycardia management?
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
Bradycardia- peri arrest rhythms?
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
Risk factors for asystole in bradycardia?
Complete heart block with broad QRS Recent asystole Mobitz type II AV block Ventricular pause > 3 seconds
92
Tachycardia peri arrest rhythm- unstable?
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
Tachycardia peri-arrest- broad complex- stable?
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
Tachycardia peri-arrest- broad complex- stable?
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
Adult advanced life support?
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
Paediatric basic life support?
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
What is chronic heart failure?
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
Heart failure investigations?
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
Chronic heart failure drug management?
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
NYHA classification heart failure?
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
Features of chronic heart failure?
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
What is acute heart failure without a PMH of HF?
De-novo HF
103
Acute HF causes?
Cardiac ▪ Acute LVF, ACS, arrhythmias, valvular heart disease, HTN, cardiomyopathy, tamponade o Non-cardiac ▪ Fluid overload, high-output HF, ARDS, renal artery stenosis
104
Acute HF presentation?`
SOB Tachycardia Cyanosis Increased RR Fatigue Displaced apex beat Raised SVP Crackles/Wheeze S3- heart sound
105
Acute heart failure investigations?
A-E ECG Bloods CXR ▪ Alveolar oedema ▪ Kerley B lines ▪ Cardiomegaly ▪ Dilated upper lobe vessels ▪ Pleural effusions ECHO
106
Acute heart failure management?
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