Cardiology Flashcards
Which conditions are considered to be ACS?
STEMI (ST elevated myocardial infarction)
NSTEMI (non-ST elevated myocardial infarction)
Unstable angina- symptoms of ACS without raised troponins or ECG changes
Why treat unstable angina as NSTEMI in first instance?
Troponins may take a while to rise so treated as NSTEMI until troponins known
RFs for cardiovascular disease?
Male
FH
Age
Smoking
Hypertension
DM
Hypercholesterolemia
Obesity
ABCDEF- Age, BP, cholesterol, diabetes, exercise, fags, fat, family
Signs/symptoms of ACS?
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)
Which patients may not experience chest pain in ACS?
Diabetics/ elderly
Female
Investigations for ACS?
ECG
Troponin
ECG and correlating region?
Anterior- V1-V4- Left anterior descending
Inferior- II, III, aVF- Right coronary
Lateral- I, V5-6- Left circumflex
Management of ACS?
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
Specific STEMI management?
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
STEMI fibrinolysis?
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
Specific NSTEMI management?
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
ACS secondary prevention?
Aspirin
Second antiplatelet if appropriate (clopidogrel)
Beta blocker
ACEi
Statin
ECG STEMI criteria?
- 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
What is angina?
Chest pain caused by insufficient blood supply to the myocardium
Angina features?
Chest pain may radiate to neck, jaw, arm
Symptoms on exertion
Relieved by rest/ GTN spray
Sweaty, clammy
SOB
N+V
Faint
Angina management?
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
Nitrate tolerance?
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
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 long-acting nitrate
What is variant (Prinzmetal angina)?
Coronary artery spasms causing angina
Avoid BBs
Use CCBs- amlodipine, verapamil, diltiazem
Most common cause of death following an MI?
Ventricular fibrillation
What is Dressler’s syndrome?
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.
Is pericarditis common after MI?
Yes more common in the first 48 hours after MI
Secondary prevention for MI?
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
Dual antiplatelet therapy in MI secondary prevention?
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
RFs for AAA?
Smoking, hypertension
Syphilis, Ehlers Danlos type 1 and Marfan’s syndrome
AAA screening?
Majority of AAA are asymptomatic
Screening for AAA consists of a single abdominal ultrasound for males over 65
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
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)
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
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
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
Features of acute limb threatening ischaemia?
One or more of 6P’s
Pale
Pulseless
Painful
Paralysed
Paraesthetic
Perishingly cold
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
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)
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
Features of critical limb ischaemia?
1 or more of:
Rest pain in foot for more than 2 weeks
Ulceration
Gangrene
Ankle-brachial pressure index (ABPI) for critical limb ischaemia?
< 0.5 is suggestive of critical limb ischaemia
What is aortic dissection?
Tear in the tunica intima of the wall of the aorta
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
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
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
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
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
What causes aortic regurgitation?
Incompetent aortic valve leading to blood leaking back into ventricle from aorta during diastole
Causes of AR due to valvular disease?
Rheumatic fever
Calcified valve
RA/SLE
Bicuspid aortic valve
IE
Causes of AR due to aortic root disease?
Bicuspid aortic valve
Ankylosing spondylitis
HTN
Syphilis
Marfan’s, Ehler-Danlos
Aortic dissection
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)
Investigation of AR?
Echocardiogram
Management of AR?
Medical management of HF
Surgery- aortic valve replacement- symptomatic or LV systolic dysfunction
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
Aortic stenosis features?
Ejection systolic (crescendo-decrescendo) murmur ESM- radiates to the carotids
Chest pain, dyspnoea, syncope/presyncope
Features of severe aortic stenosis?
Narrow pulse pressure
Slow rising pulse
Delayed ESM
Soft/absent S2
S4
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
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
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.
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
MR causes?
Mitral valve prolapse
Post MI
Infective endocarditis
Rheumatic fever
Congenital
Connective tissue disorders – Ehlers-Danlos, Marfan
MR presentation?
Pansystolic murmur- radiates to axilla
SOBOE, palpitaitons, fatigue, signs of HF
MR investigations?
Echocardiogram
CXR- cardiomegaly
ECG- LA enlargement- broad P wave- LVH in severe
MR treatment?
In acute cases, nitrates, diuretics, inotropes, intra-aortic balloon pump – to
increase CO
HF – ACEi, BBs, spironolactone etc
Surgery
Repair / replacement
What is mitral stenosis?
Obstruction of blood flow from LA to LV, inreased pressure in LA
Mitral Stenosis causes?
RHEUMATIC fever- most common cause
also infective endocarditis
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
Mitral stenosis investigations?
Echo
CXR
ECG
Mitral stenosis management?
Asymptomatic- regular monitoring with ECHO
If sx
Balloon valvuloplasty
Mitral valve replacement
What is atrial fibrillation?
Disorganised electrical activity of the atria leading to fibrillation- irregularly irregular rhythm
Type of supraventricular tachycardia
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
AF symptoms and signs?
Palpitations
SOB
Chest pain
Syncope
Sx of associated conditions- stroke, infection
Irregularly irregular pulse
AF investigations?
ECG-
Absent P waves
Irregularly irregular pulse
ECHO
For paroxysmal AF:
24 hour ECG
CHA2DS2VASc / ORBIT
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
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
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
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).
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.
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
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
ORBIT AF?
ORBIT score to assess risk of bleeding
* 0-2 – low risk
* 3 – medium risk
* 4-7 – high risk
Anticoag in AF?
First line – DOAC
* Apixaban, dabigatran,
edoxaban, rivaroxaban
Second line – warfarin – if DOAC CI’d
or not tolerated
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
What is atrial flutter?
Abnormal atrial rhythm with atrial rate up to 300/min- if the block is 2:1 HR would be 150
ECG findings in atrial flutter?
Sawtooth appearance
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
What is broad complex tachycardia?
QRS over 120ms
Electrical activity not following the usual conduction system
Ventricular tachycardia
SVT with BBB
Ventricular fibrillation
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
Torsades de pointes?
A polymorphic ventricular tachycardia associated with long QT
Causes of a long QT interval?
Congenital
Antiarrythmics- amiodarone
Tricyclic antidepressants
Antipsychotics
Erythromycin
Electrolytes- hypocalcaemia, hypokalaemia, hypomagnesemua
Hypothermia
SAH
Torsades de pointes management?
IV magnesium sulphate
What are examples of narrow complex tachycardia?
Sinus tachycardia
Atrial fibrillation- technically SVT
Atrial flutter- technically SVt
Supraventricular tachycardia
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
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
Risk factors for asystole in bradycardia?
Complete heart block with broad QRS
Recent asystole
Mobitz type II AV block
Ventricular pause > 3 seconds
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
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
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
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
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
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
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
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
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
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
What is acute heart failure without a PMH of HF?
De-novo HF
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
Acute HF presentation?`
SOB
Tachycardia
Cyanosis
Increased RR
Fatigue
Displaced apex beat
Raised SVP
Crackles/Wheeze
S3- heart sound
Acute heart failure investigations?
A-E
ECG
Bloods
CXR
▪ Alveolar oedema
▪ Kerley B lines
▪ Cardiomegaly
▪ Dilated upper lobe vessels
▪ Pleural effusions
ECHO
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
