cardiovascular Flashcards
CXR in aortic dissection
Widened mediastinum
Double aortic contour
Irregular aortic contour
Inward displacement of atherosclerotic calcification
CT angiography aortic dissection
False lumen
ix for aortic dissection
CXR
CT angiography is the initial ix - diagnostic
Transoesophageal echocardiography (TOE) - espesh if unstable
types of aortic dissection
type A - ascending aorta, 2/3 of cases - worse prog
type B - descending aorta, distal to left subclavian origin, 1/3 of cases
mx aortic dissection for type A + B
Type A
surgical management - control BP to a target systolic of 100-120 mmHg whilst waiting
Type B
conservative management
- bed rest
reduce blood pressure IV labetalol
murmur for aortic stenosis
ejection systolic
(louder on expiration)
murmur for mitral regurgitation
pan-systolic
presentation of aortic dissection
50+ men
sudden onset tearing chest pain radiating to the back
radio-radial delay
radio-femoral delay
BP diff between arms
RF aortic dissection
Hypertension
Connective tissue disease e.g. Marfan’s syndrome
Valvular heart disease
Cocaine/amphetamine use
who is at risk of having a silent MI
px w DM
ECG changes for hypercalcaemia
shorted QT interval
J waves if severe
what is Wellen’s syndrome and what are the signs of it
characterised by biphasic or deeply inverted T waves in V2-3
history of recent chest pain now resolved (cardiac ischaemia in the setting of unstable angina)
highly specific for critical stenosis of the left anterior descending artery (LAD)
- high risk needing further ix
Troponin normal at this stage
immediate ACS drug therapy
- aspirin 300mg
- oxygen should only be given if the patient has oxygen saturations < 94%
- morphine should only be given for patients with severe pain
- nitrates,useful if the patient has ongoing chest pain or hypertension, should be used in caution if patient hypotensive
mx of STEMI
PCI - if the presentation is within 12 hours of the onset of symptoms AND can be delivered within 120 minutes of the time when fibrinolysis could have been given (i.e. consider fibrinolysis if there is a significant delay in being able to provide PCI)
fibrinolysis (w/ eg alteplase) - should be offered within 12 hours of the onset of symptoms if primary PCI cannot be delivered within 120 minutes of the time when fibrinolysis could have been given
further drug therapy before PCI
or if not taking an anticoag
if taking an anticoag
‘dual antiplatelet therapy’, i.e. aspirin + another drug
if the patient is not taking an oral anticoagulant: prasugrel
if taking an oral anticoagulant: clopidogrel
fibrinolysis/thrombolysis what to do before and after
give another antithrombin drug
An ECG should be repeated after 60-90 minutes to see if the ECG changes have resolved. If patients have persistent myocardial ischaemia following fibrinolysis then PCI should be considered.
when to give heparin in NSTEMI/unstable angina
if immediate angiography is planned or a patients creatinine is > 265 µmol/L then unfractionated heparin should be given
which px w NSTEMI get angiography? (w follow on PCI if needed)
immediate: patient who are clinically unstable (e.g. hypotensive)
within 72 hours: patients with a GRACE score > 3% i.e. those at intermediate, high or highest risk
coronary angiography should also be considered for patients if ischaemia is subsequently experienced after admission
Risk assessment tool for ACS
GRACE
age
heart rate, blood pressure
cardiac (Killip class) and renal function (serum creatinine)
cardiac arrest on presentation
ECG findings
troponin levels
how to terminate supraventricular tachycardias
vasovagal maneuvers if haemodynamically stable
12mg adenosine via large bore cannula (as they are narrow complex)
what are the ECG changes in a posterior MI?
reciprocal changes to STEMI
changes in V1-3
- horizontal ST depression
- tall, broad R waves
- upright T waves
- dominant R wave in V2
see tall R waves? Right behind you!
what artery is affected in posterior MI?
left circumflex
(sometimes right coronary)
where is the lesion if someone gets complete heart block after an MI
right coronary artery (as it supplies the AV node)
triad for cardiac tamponade (pericardial tamponade)
Beck’s triad
- hypotension
- muffled/distant heart sounds
- elevated JVP
tx of cardiac tamponade
urgent pericardiocentesis (pericardial needle aspiration)
classic presentation of myocarditis
Patients are usually <50
hx of recent viral illness
chest pain and features of pulmonary oedema
inflammatory markers and troponin will be raised, and ECG will show non-specific ST segment and T wave changes
Myocarditis can manifest as new-onset congestive heart failure
6 ps of acute limb ischaemia
Pulseless
Painful
Pale
Paralysis
Paraesthesia
Perishingly cold
what blood test indicates right ventricular failure
Raised NT‑proBNP
causes of pericarditis
idiopathic
infection - TB, HIV, coxsacki, EBV etc
AI + inflam conditions - SLE, RA
injury - after MI, surgery, trauma
uraemia 2ndary to renal impairment
cancer
meds - methotrexate
what is pericarditis
inflam of the pericardium (membrane surrounding heart)
what is pericardial effusion
when the potential space of the pericardial cavity fills w fluid - creates an inward pressure on the heart making it harder to expand during diastole
pericarditis presentation
chest pain - sharp, central/anterior, pleuritic, worse when lying down, better when sitting forward
low grade fever
on auscultation w pericarditis
pericardial friction rub - rubbing scratching sound occurring alongside heart sounds
ix for pericarditis
Raised inflam markers -WBCs, CRP, ESR
ECG
- saddle shaped ST-elevation
- PR depression (more specific)
Echo to dx pericardial effusion
mx pericarditis
NSAIDs - aspirin / ibuprofen
colchicine (longer term to reduce recurrence)
what is cardiac tamponade (pericardial tamponade)
when the pericardial effusion is large enough to raise the intra-pericardial pressure squeezing the heart. Decreases CO. Emergency needing prompt drainage (pericardiocentesis)
what is infective endocarditis
infection of the endocardium (inner surface of the heart). Most commonly affecting heart valves
acute, subacute or chronic
RFs for endocarditis
IV drug use
CKD
Immunocompromised
Hx of it
Structural heart pathology
- valvular HD
- congenital HD
- hypertrophic cardiomyopathy
- prosthetic valves
- implantable devices
most common cause of endocarditis
most common is staph aureus
presentation of endocarditis
F fever
R roth spots (haemorrhages on retina in fundoscopy)
O osler nodes (tender red/purple nodules on pads of fingers + toes)
M murmur (new or changing)
J janeway lesions (painless red flat macules on palms or soles)
A anaemia
N nail-bed haemorrhages
E emboli
endocarditis ix
blood cultures - needed b4 abx
3 blood samples separated by 6 hrs + taken at diff sites
ECHO (TOE) - vegetations on valves
Dukes criteria for dx endocarditis
A diagnosis requires either:
- One major plus three minor criteria
- Five minor criteria
Major criteria are:
- Persistently positive blood cultures (typical bacteria on multiple cultures)
- Specific imaging findings (e.g., a vegetation seen on the echocardiogram)
Minor criteria are:
- Predisposition (e.g., IV drug use or heart valve pathology)
- Fever above 38°C
- Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions)
- Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis)
- Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
endocarditis abx + how long
Initial IV broad spectrum abx - amoxicillin (vancomycin if penicillin allergic) + optional gentamicin
Ctu
- 4 weeks (6 wks if prosthetic heart valves)
If prosthetic valve
vancomycin + rifampicin + low-dose gentamicin
common cause of sudden cardiac death in young ppl
hypertrophic obstructive cardiomyopathy (HOCM) / left ventricular outflow tract obstruction
HOCM inheritance
AD
defect in the genes for sarcomere proteins
HOCM presentation
mostly asx
Non-specific sx
- SOB, fatigue, dizzy, syncope, chest pain, palp
Severe: sx of HF
ix for HOCM
ECG - left ventricular hypertrophy (large R waves in L sided leads, v5 v6 avL I, deep S waves in R sided chest leads, v1 v2)
- maybe T wave inversion
CXR - normal / pulmonary oedema
echo for dx
genetic testing
mx HOCM
- Beta blockers
- Surgical myectomy (removing part of the heart muscle to relieve the obstruction)
- Alcohol septal ablation (a catheter-based, minimally invasive procedure to shrink the obstructive tissue)
- Implantable cardioverter defibrillator (for those at risk of sudden cardiac death or ventricular arrhythmias)
- Heart transplant
what sld be avoided in HOCM
activities
and meds
Patients are advised to avoid intense exercise, heavy lifting and dehydration.
ACE inhibitors and nitrates are avoided as they can worsen the LVOT obstruction.
which meds can reduce BNP levels
tx w ACEis
ARBs
diuretics
what can raise BNP
heart failure (high sensitivity varied specificity)
+ any cause of left ventricular dysfunction such as myocardial ischaemia or valvular disease
due to reduced excretion in px w CKD
PE
sepsis
COPD
tachycardia
ix results in left ventricular aneurysm
persistent ST elevation after MI
3rd + 4th heart sound
common finding in takayusu’s arteritis (a large vessel vasculitis)
absent limb pulse
more common in younger females + asian ppl
what is first degree heart block
delayed conduction through to the AVN.
But every atrial impulse leads to a ventricular contraction (each P wave followed by QRS complex)
PR interval > 0.2 secs
what is second degree heart block
some atrial impulses do not make it through the AVN to the ventricles. Instances where P waves not followed by QRS.
2 types: Mobitz type 1 (Wenckebach phenomenon)
Mobitz type 2
what is mobitz type 1 (wenckebach phenomenon)
the conduction through the AVN takes progressively longer till it fails + then resets
Increasing PR interval until one is not followed by QRS
what is mobitz type 2
failure of conduction through AVN
absence of QRS following P
Usually a set ratio of P waves to QRS complexes. eg 3 P waves for each QRS = 3:1 block
risk of asystole
what is third degree heart block
complete heart block.
no observable relationship between P + QRS
signif risk of asystole
can get dizziness, palpitations, syncope
what needs transvenous pacing
complete heart block w broad complex QRS
recent asystole
mobitz type 2 block
ventricular pause > 3 secs (PR)
mx of high INR w major bleeding (variceal / IC haemorrhage)
stop warfarin
IV VK 5mg AND
Prothrombin complex concentrate
mx of INR>8 w minor bleeding
stop warfarin
IV VK 1-3mg
repeat dose VK if still too high after 24 hrs
restart warfarin when INR <5
mx INR > 8 no bleeding
stop warfarin
oral VK 1-5mg (IV prep)
Repeat dose of vitamin K if INR still too high after 24 hours
Restart when INR < 5.0
INR 5-8 minor bleeding
stop warfarin
IV VK 1-3mg
Restart when INR < 5.0
INR 5-8 no bleeding
Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose
what anticoag to use w mechanical heart valves
warfarin
Examples of fibrinolytic agents (used in thrombolysis in MI)
Streptokinase
Alteplase
Tenecteplase
what is dressler’s syndrome
also called post-myocardial infarction syndrome.
occurs around 2 – 3 weeks after an acute MI. It is caused by a localised immune response that results in inflammation of the pericardium (pericarditis).
how to dx dressler’s syndrome
ECG (global ST elevation and T wave inversion)
echocardiogram (pericardial effusion)
raised inflammatory markers (CRP and ESR).
dressler’s syndrome mx
NSAIDs - aspirin/ibuprofen
steroids if severe
Pericardiocentesis?
what do you see on a ECG for LBBB
QRS > 120ms
look at v1 - pointing down
W in V1
M in V6
what could new LBBB indicate
a new LBBB is always pathological
MI (most likely anterior)
hypertension
aortic stenosis
cardiomyopathy
how to prevent further episodes of supraventricular tachy
beta-blockers
radio-frequency ablation
what to do when a cardiac arrest is witnessed in a monitored patient
up to three quick successive (stacked) shocks’, rather than 1 shock followed by CPR
medication for stable angina
ASPIRIN
STATIN
sublingual GTN to abort attacks
BB or CCB (if in monotherapy use verapamil (CAN’T PRESCRIBE W BB AS HEART BLOCK RISK) / diltiazem)
if poor response increase med to max tolerated dose
if still sx - ADD the one you didn’t use first (CCBs in combo w BB use longer acting like amlodipine, nifedipine)
if can’t tolerate CCB+BB - consider adding:
a long-acting nitrate
ivabradine
nicorandil
ranolazine
what drug for wide complex tachycardia
amiodarone - loading dose followed by 24 hr infusion
what drug for narrow complex tachycardia
adenosine
what drug for bradycardia
atropine
when to do an emergency admission for chest pain
current chest pain or chest pain in the last 12 hours with an abnormal ECG
when to refer for chest pain 12-72 hrs ago
refer to hosp for same day assessment
when to refer for chest pain > 72 hrs ago
perform full assessment w ECG + troponin before deciding on further action
most common valve affected in endocarditis
in general
in IVDU
in general it is the mitral valve
in IVDU it is the tricuspid valve (first spot blood comes to after general circ)
which type of MI may lead to AVN block
inferior (occlusion to RCA supplying AVN)
what is Wolff-Parkinson White (WPW) syndrome caused by
congenital accessory conducting pathway between the atria and ventricles leading to atrioventricular re-entry tachycardia (AVRT)
ecg features of Wolff-Parkinson White (WPW)
short PR interval (<120 ms)
wide QRS complexes with a slurred upstroke - ‘DELTA WAVE’
LAD if right-sided accessory pathway
in the majority of cases, or in a question without qualification, Wolff-Parkinson-White syndrome is associated with left axis deviation
RAD if left-sided accessory pathway
mx of WPW
definitive treatment: radiofrequency ablation of the accessory pathway
medical therapy: sotalol*, amiodarone, flecainide
*avoided if there is coexistent atrial fibrillation as prolonging the refractory period at the AV node - may increase the rate of transmission through the accessory pathway, increasing the ventricular rate and potentially deteriorating into ventricular fibrillation
what is the most common valvular defect of rheumatic heart disease
mitral stenosis
most common cause of mitral stenosis
rheumatic fever
what is rheumatic fever caused by
group A Streptococcus
heart sounds in mitral stenosis
mid-late diastolic murmur (heard best on expiration)
loud opening snap
then low pitched rumble
aortic regurgitation murmur
early diastolic murmur
‘austin-flint’ murmur - apex, rumbling
collapsing pulse
what is Pulmonary capillary wedge pressure (PCWP)
used to assess left ventricular filling, represent left atrial pressure, and assess mitral valve function.
used to differentiate between cardiogenic pulmonary edema and noncardiogenic pulmonary edema
- in cardiac it will be raised
what is a pseudoaneurysm
the inner two layers (intima + media) rupture and there is dilation of the vessel, with the blood only being contained within the outer (adventitia) layer of the aorta
usually after trauma / surgery
RF aortic aneurysm
Men are affected significantly more often and at a younger age than women
Increased age
Smoking
Hypertension
Family history
Existing cardiovascular disease
Marfan syndrome and other connective tissue disorders
aortic aneurysm presentation
Dilation of the thoracic aorta is often asymptomatic
May cause sx due to taking up space within the mediastinum:
Chest/back pain
Trachea/left bronchus compression may cause cough, SOB + stridor
Phrenic nerve compression may cause hiccups
Oesophageal compression may cause dysphagia (difficulty swallowing food)
Recurrent laryngeal nerve compression may cause a hoarse voice
ix for aortic aneurysm
Echocardiogram
CT or MRI angiogram
ma aortic aneurysm
treating modifiable risk factors
Surveillance with regular imaging to monitor the size
Thoracic endovascular aortic repair (TEVAR), with a catheter inserted via the femoral artery inserting a stent graft into the affected section of the aorta
Open surgery (midline sternotomy) to remove the section of the aorta with the defect in the wall and replace it with a synthetic graft
ruptured aortic aneurysm presentation
Severe chest pain or back pain
Haemodynamic instability (hypotension and tachycardia)
Collapse
Death (often patients do not reach hospital)
screening for aortic aneurysms
single abdominal ultrasound for males aged 65
<3cm nothing
3-4.4cm scan every 12 mths
4.5-5.4cm scan every 3 mths
surgery if >/= 5.5cm
Poorly controlled HTN
already taking an ACEi, CCB and a thiazide diuretic
K+ < 4.5
K+ > 4.5
add spironolactone
consider bisoprolol
HTN patients < 55-years-old or a background of type 2 diabetes mellitus
ACE inhibitor or a Angiotensin receptor blocker
patients >= 55-years-old or of black African or African–Caribbean origin
Calcium channel blocker
HTN step 2 tx
if already taking an ACE-i/ARB add a CCB or a thiazide-like Diuretic (indapamide)
if already taking a CCB add an ACE-i/ARB or a thiazide-like Diuretic
for patients of black African or African–Caribbean origin taking a calcium channel blocker for hypertension, if they require a second agent consider an angiotensin receptor blocker in preference to an ACE inhibitor
adv + disadv biological (bioprosthetic) valves
Major disadvantage is structural deterioration + calcification over time. Most older patients ( > 65 years for aortic valves and > 70 years for mitral valves) receive a bioprosthetic valve
Long-term anticoagulation not usually needed. Warfarin may be given for the first 3 months depending on patient factors. Low-dose aspirin is given long-term.
3rd heart sound
dilated cardiomyopathy
4th heart sound
HOCM
pulmonary stenosis murmur
ejection systolic murmur louder during inspiration
murmur in PDA
continuous machinery murmur
cardiac output equation
CO = SV x HR
triggers of acute LEFT ventricular failure
often the result of decompensated chronic HF
potential triggers:
iatrogenic (aggressive IV fluids in frail elderly px w impaired LV func)
MI
arrhythmias
sepsis
hypertensive emergency (acute, severe increase in BP)
sx acute left ventricular failure
acute SOB - exacerbated by lying flat + improves sitting up
will look + feel unwell
cough w frothy white/pink sputum
examination acute left ventricular failure
raised RR
reduced O2 sats
tachycardia
3rd heart sound
bilateral basal crackles
hypotension in severe cases (cardiogenic shock)
what type of resp failure does acute left ventricular failure cause
type 1 - low o2 w no raised co2
examination findings in right sided HF
raised JVP
peripheral oedema
assessment in px w acute left ventricular failure
ABCDE if acutely unwell
clinical assessment - hx + exam
ECG - ischaemia / arrythmias?
Bloods - anaemia, infection, kidney func, BNP, consider troponin if MI suspected
ABG
CXR
Echo
what is the action of BNP
released from the heart ventricles when myocardium is stretched beyond normal range
relax the smooth muscle in BVs reducing systemic vascular resistance
also acts as a diuretic to promote water excretion in urine reducing circ vol
what is ejection fraction
percentage of blood in the left ventricle that is squeezed out with each ventricular contraction. An ejection fraction above 50% is considered normal.
how to define cardiomegaly on CXR
cardiothoracic ration of > 0.5
CXR in acute left ventricular failure
upper lobe venous diversion
bilateral pleural effusions
fluid in interlobar fissures (between the lung lobes)
fluid in septal lines (Kerley lines)
mx acute left ventricular failure
hx admission
if severe pulmonary oedema / cardiogenic shock -> HDU/ICU
S - sit up
O - oxygen
D - diuretics - IV furosemide
I – Intravenous fluids should be stopped
U – Underlying causes need to be identified and treated (e.g. MI)
M – Monitor fluid balance - oral + IV intake monitor, UO, U&Es, body weight
what are inotropes
meds that alter contractility of the heart
positive inotropes - increase contractility -> increase CO + MAP
what are vasopressors
meds that cause vasoconstriction increasing systemic vascular resistance + so MAP
can be used to improve BP
when would you get HF w preserved ejection fraction
ie clinical features of HF but ejection fraction > 50%
it is a result of diastolic dysfunc - issue w LV filling up w blood when relaxing
causes of chronic HF
ischaemic heart disease
valvular heart disease - commonly aortic stenosis
HTN
arrhythmias - commonly AF
cardiomyopathy
presentation of chronic HF
breathlessness - worse on exertion
cough - frothy white/pink sputum
orthopnoea
paroxysma nocturnal dyspnoea
peripheral oedema
fatigue
examination signs in chronic HF
tachycardia
tachypnoea
HTN
murmurs?
3rd heart sound
bilateral basal crackles
raised JVP
peripheral oedema
what is paroxysmal nocturnal dyspnoea
the experience that px have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.
establishing dx of chronic HF
Clinical assessment (history and examination)
N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test
ECG
Echocardiogram
Other ix include:
Bloods for anaemia, renal function, thyroid function, liver function, lipids and diabetes
Chest x-ray and lung function tests to exclude lung pathology
New York Heart Association (NYHA) classification
Class I: No limitation on activity
Class II: Comfortable at rest but symptomatic with ordinary activities
Class III: Comfortable at rest but symptomatic with any activity
Class IV: Symptomatic at rest
mx chronic HF
R – Refer to cardiology
A – Advise them about the condition
M – Medical treatment
P – Procedural or surgical interventions
S – Specialist heart failure MDT input, such as the heart failure specialist nurses, for advice and support
Additional management:
Flu, covid and pneumococcal vaccines
Stop smoking
Optimise treatment of co-morbidities
Written care plan
Cardiac rehabilitation (a personalised exercise programme)
what NT-proBNP results mean in regards to referral
From 400 – 2000 ng/litre should be seen and have an echocardiogram within 6 weeks
Above 2000 ng/litre should be seen and have an echocardiogram within 2 weeks
medical tx for chronic HF
A – ACE inhibitor (e.g., ramipril) titrated as high as tolerated (avoid in px w valvular heart dis) (or ARB)
B – Beta blocker (e.g., bisoprolol) titrated as high as tolerated
A – Aldosterone antagonist when symptoms are not controlled with A and B (e.g., spironolactone or eplerenone) (+when there is reduced ejection fraction)
L – Loop diuretics (e.g., furosemide or bumetanide)
what murmur can you get with AF
mitral stenosis
features of severe aortic stenosis
narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
left ventricular hypertrophy or failure
causes of aortic stenosis
degenerative calcification (most common cause in older patients > 65 years)
bicuspid aortic valve (most common cause in younger patients < 65 years)
William’s syndrome (supravalvular aortic stenosis)
post-rheumatic disease
subvalvular: HOCM
mx aortic stenosis
if asymptomatic then observe the patient is a general rule
if symptomatic then valve replacement
if asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction then consider surgery
what is AF
where the electrical activity in the atria of the heart becomes disorganised, leading to fibrillation (random muscle twitching) of the atria and an irregularly irregular pulse.
overall effects of AF
Irregularly irregular ventricular contractions
Tachycardia (fast heart rate)
Heart failure due to impaired filling of the ventricles during diastole
Increased risk of stroke
common causes of AF
S – Sepsis
M – Mitral valve pathology (stenosis or regurgitation)
I – Ischaemic heart disease
T – Thyrotoxicosis
H – Hypertension
Alcohol and caffeine are lifestyle causes
AF presentation
Palpitations
Shortness of breath
Dizziness or syncope (loss of consciousness)
Symptoms of associated conditions (e.g., stroke, sepsis or thyrotoxicosis)
diff dx for irregularly irregular pulse
Atrial fibrillation
Ventricular ectopics
how to differentiate between AF + ventricular ectopics
Ventricular ectopics disappear when the heart rate gets above a certain threshold. Therefore, a regular heart rate during exercise suggests a diagnosis of ventricular ectopics.
AF will have no P waves on ECG. Ventricular ectopics will
what is paroxysmal atrial fibrillation
episodes of atrial fibrillation that reoccur and spontaneously resolve back to sinus rhythm. These episodes can last between 30 seconds and 48 hours.
when might you need an echo if you find AF on ECG
Valvular heart disease
Heart failure
Planned cardioversion
when not to do rate control first line in AF
A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled
rate control options for AF
Beta blocker first-line (e.g., atenolol or bisoprolol)
Calcium-channel blocker (e.g., diltiazem or verapamil) (not preferable in heart failure)
Digoxin (only in sedentary people with persistent atrial fibrillation, requires monitoring and has a risk of toxicity)
when to offer rhythm control to px w AF
A reversible cause for their AF
New onset atrial fibrillation (within the last 48 hours)
Heart failure caused by atrial fibrillation
Symptoms despite being effectively rate controlled
rhythm control options for AF
pharm: flecainide, amiodarone (use in structural heart disease)
electrical: cardiac defib
when to do immediate cardioversion for AF + how
Present for less than 48 hours
Causing life-threatening haemodynamic instability
Can do pharmacological or electrical
when to do delayed cardioversion + how
present for more than 48 hours and they are stable.
electrical cardioversion is recommended
px should be anticoagulated for at least 3 weeks before delayed cardioversion.
long-term rhythm control for AF
Beta blockers first-line
Dronedarone second-line for maintaining normal rhythm where patients have had successful cardioversion
Amiodarone is useful in patients with heart failure or left ventricular dysfunction
mx paroxysmal atrial fibrillation
pill in pocket approach using
FLECAINIDE
use same score for anticoag
score to predict risk of stroke in AF + what does that mean for anticoag
CHA2DS2-VASc
C = Congestive heart failure 1
H = Hypertension 1
A2 = Age ≥75 years 2
D = Diabetes Mellitus 1
S2 = Prior Stroke/TIA/thromboembolism 2
V = Vascular disease 1
A = Age 65–74 years 1
Sc = Sex category (i.e. female sex) 1
0 = no anticoag
1= consider in men (women automatically score 1)
2+ = offer anticoag
score to assess risk of bleeding on anticoag
ORBIT
O = Older age ≥75 years
R = Renal impairment (GFR<60)
B = Bleeding previously
I = Iron (low haemoglobin/haematocrit)
T = Taking antiplatelet medication
1st line anticoag in AF
DOACs - apixaban, endoxaban, rivaroxaban (direct factor Xa inhibitors), Dabigatran (direct thrombin inhibitor).
2nd line anticoag in AF
warfarin (VK antagonist)
give if advanced CKD
criteria for PCI in STEMI
ST elevation of >2mm in 2 contiguous chest leads or >1mm in 2 contiguous limb leads
~Chest pain or other evidence of ischaemia
New or presumed new LBBB was an indication for thrombolysis and is
often considered an indication for PPCI in the right clinical context
when to measure troponin
depends on type of assay
If High-Sensitivity Cardiac Troponin (hs-TnT)
- measure asap
- if raised measure again in 3h - significant rise or fall suggests MI
- if not raised, can rule out MI, unless pain was <6 hrs ago, in which case obtain
further measurement at that point – significant rise suggests MI
- Does NOT rule out ACS (could still be unstable angina)
- signif fall after 2 days also dx
(along w clinical features)
what happens to troponin levels in MI
goes up 3-6 hrs following infarct + peaks at 2 days
what is the HEART score
Predicts 6-week risk of major adverse cardiac event.
Use when deciding to discharge from ED / admit
0-3 = low risk, dis
4-6 = med risk, obs
7-10 = high risk, obs, tx, CAG
mx NSTEMI in ED
Aspirin 300mg
Anticoagulation e.g. Fondaparinux 2.5 mg SC - for px who are not at a high risk of bleeding and who are not having angiography/PCI immediately
GRACE score
If for conservative mx:
* Load with P2Y12 inhibitor – TICAGRELOR 180 mg
If for angio(/PCI)
* TICAGRELOR or PRASUGREL 60 mg (not pras if >75, used if having angio)
* Clopidogrel use in ACS 2nd line (if high bleeding risk or already taking oral anticoagulants )
- Unfractionated heparin
- Do NOT give beta blocker, ACEi etc. at this stage without specialist supervision (can precipitate cardiogenic shock)
- IV GTN infusion if ongoing pain
continuous
* Cardiac monitoring >=24 hours
* Mx of comps such as arrhythmia, acute heart failure
inpx mx NSTEMI
- Cardiac monitoring >=24 hours
- Medical vs invasive management
- PCI vs CABG
- Commence on secondary prevention
- Length of stay about 72 hours
- Monitor for complications
- Physiotherapy
- Optimisation of risk factors
drugs on TTO for MI
Drugs -Big 5
* Aspirin 75 mg OD for life
* Potent P2Y12 inhibitor – ticagrelor 90 mg BD or prasugrel 5-10 mg OD for >=1 year. Can consider a PPI alongside.
* Cardioselective beta blocker (caution if asthmatic, bradycardic, conduction disease) e.g. bisoprolol 2.5 mg OD
* ACEi (/ARB) (caution if hypotensive, severe CKD) e.g. ramipril 2.5 mg OD
* High intensity statin e.g. Atorvastatin 80 mg OD for life
* (PRN GTN)
* Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone) - be v careful if taking w ACEi as both cause hyperkalaemia
follow up for MI
Follow up
* Clinic 1 month – can consider device therapy if significant LVSD
* Transthoracic echo if not had as inpx
* Cardiac rehabilitation programme
* Smoking cessation
* GP – uptitrate secondary prevention e.g. ramipril and bisoprolol towards 10 mg OD
Advice
* Don’t drive for 1 week if PCI, 4 weeks if no PCI (we advise all px 4 weeks)
* Gradual return to usual activity levels
* Typically 6 weeks off work
* Stop smoking
types of MI
Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with procedures such as PCI, coronary stenting and CABG
i.e, “ACDC” mnemonic:
Type 1: A – ACS-type MI
Type 2: C – Can’t cope MI
Type 3: D – Dead by MI
Type 4: C – Caused by us MI
ix in anyone with angina
Physical examination (e.g., heart sounds, signs of heart failure, blood pressure and BMI)
ECG (a normal ECG does not exclude stable angina)
FBC (anaemia)
U&Es (required before starting an ACE inhibitor and other medications)
LFTs (required before starting statins)
Lipid profile
Thyroid function tests (hypothyroidism or hyperthyroidism)
HbA1C and fasting glucose (diabetes)
Cardiac stress testing
CT coronary angiography GS
Invasive coronary angiography
principles of mx for stable angina
R – Refer to cardiology
A – Advise them about the diagnosis, management and when to call an ambulance
M – Medical treatment
P – Procedural or surgical interventions
S – Secondary prevention
Referrals are usually sent to the rapid access chest pain clinic (RACPC).
non pharm causes for long QT
genetic (long QT syndrome)
hypocalcaemia
hypokalaemia
hypomagnesemia
normal PR interval
120 – 200 ms (0.12-0.20s)
causes of RBBB
normal variant - more common with increasing age
right ventricular hypertrophy
chronically increased right ventricular pressure - e.g. cor pulmonale
pulmonary embolism
myocardial infarction
atrial septal defect (ostium secundum)
cardiomyopathy or myocarditis
drugs that cause long QT
Antibiotics: macrolides
Antipsychotics: haloperidol, clozapine
Antidepressants: TCAs
Antiemetics: ondansetron
antiarrhythmics: amiodarone, sotalol, class 1a antiarrhythmic drugs
heart sound in HOCM
S4 hit the floor
most common cause of S3
HF
can be incidental + not signif in young ppl
hypothermia ECG
j waves
mechanism of action of alteplase
Activates plasminogen to form plasmin
Plasmin then degrades fibrin, leading to clot dissolution and restoration of blood flow
cushing’s triad + when might you get it
widening pulse pressure
bradycardia
irregular breathing
a late sign indicating impending brain herniation
Systolic hypertension occurs as a reflex to maintain cerebral perfusion pressure in the presence of raised ICP
