Cardio Flashcards
Broad complex tachycardia, BP 88/59, Rx?
DC cardioversion
If systolic BP <90 in tachyarrhythmia then DC cardioversion
When is a patient classified as stable or unstable in the context of tachyarrhythmia?
Unstable if any of the following adverse signs:
- Shock (systolic BP <90, pallor, clammy, confusion, impaired consciousness)
- Syncope
- Myocardial ischaemia
- Heart failure
If any of the above are present then give synchronised DC cardioversion. Rx following this is dependent on if it was broad or narrow complex, and if it was regular or irregular
What are potential causes of a broad complex tachycardia with regular and irregular rhythms?
What are their treatments (if stable)?
Regular:
- Assume VT - amiodarone (300mg loading dose then 900mg over 24 hours)
- SVT with BBB - treat as per SVT
Irregular:
- AF with BBB - treat as per narrow complex tachycardia
- Polymorphic VT (torsades de pointes) - IV Magnesium
Potential causes of narrow complex tachycardia with regular and irregular rhythms?
Treatments?
Regular:
- SVT - vagal manoeuvres then IV adenosine
- If unsuccessful, consider atrial flutter and control rate
Irregular:
- Probably AF
- If onset <48 hrs consider electrical/chemical cardioversion
- Rate control (B blocker/Digoxin) and anticoagulation required
Treatment of acute native valve endocarditis?
IV Flucloxacillin 2g 6 hourly
Treatment of subacute (indolent) native valve endocarditis?
IV Amoxicillin + Gentamicin
Treatment of prosthetic valve endocarditis or suspected MRSA?
IV Vancomycin + Gentamicin + PO Rifampicin
4 common bacterial causes of endocarditis and their associations?
Staph Aureus - most common, IVDU
Staph epidermis - peri-operative, <2 months post-op
Strep Viridans - dental procedures
Strep Bovis - colorectal cancer
5 causes of culture negative endocarditis?
Previous antibiotic therapy Coxiella burnetti Bartonella Brucella HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella)
common drugs which prolong QT interval?
Antipsychotics (mainly typical) Type 1a, 1c and 3 arrhytmatics Tricyclics Other antidepressants (citalopram, moclobemide etc) Loratadine Hydroxychloroquine Macrolides (clarithromycin)
How to tell between aortic stenosis and sclerosis?
Aortic sclerosis doesn’t radiate to carotids and has normal ECG
What 2 scenarios is cardioversion used in AF?
When should you offer rate/rhythm control?
Haemodynamically unstable - electrical
Electively where rhythm control strategy preferred - electrical or chemical
Offer rate/rhythm control if onset <48 hours
Offer rate control if >48 hours
Management of haemodynamically stable AF onset <48 hours?
Heparinise patient, then cardiovert
Electrical - synchronised DC OR Pharmacological: - Amiodarone if structural heart disease - Amiodarone/Flecainide without
If no other risk factors for ischaemic stroke, further anticoagulation unnecessary. If present, oral anticoagulation for life
Management of haemodynamically stable AF onset >48 hours?
Rate control and anticoagulation for at least 3 weeks.
If recurrent AF or previous cardioversion failure, amiodarone/sotalol for 4 weeks.
Electrical cardioversion
Anticoagulation continued for at least 4 weeks after - decision on continuation based on risk factors
Drugs to control rate in AF?
Bisoprolol
Verapamil/Diltiazem
Digoxin - normally not preferred, but 1st choice if co-existing heart failure as positive inotropic effect
Drugs to maintain sinus rhythm in Hx of AF?
Amiodarone
Sotalol
Flecainide
Factors favouring rate (2)/rhythm (4) control strategy in AF?
Rate - age >65, Hx of IHD
Rhythm - age <65, symptomatic, first presentation, CCF
Stroke risk score in AF?
CHA2DS2VascS
C - congestive HF
H - hypertension
A - age 75 or above = 2
age 65-74 = 1
D - diabetes
S - stroke or TIA (previous) = 2
V - vascular disease (IHD/PVD)
S - sex (female)
0 = no anticoagulation
1 = males consider anticoagulation
females don’t (they got this score from their sex)
2 = offer anticoagulation
When is catheter ablation used in AF?
What medication must the patient take beforehand?
What does it do to stroke risk?
3 complications?
Failure to respond to cardioversion, or wish to avoid antiarrhythmatics
Anticoagulants for 4 weeks minimum beforehand
Whilst ablation might restore to sinus rhythm, it doesn’t reduce stroke risk
tamponade, stroke, pulmonary valve stenosis
How do thiazides cause hypokalaemia?
They block Na/Cl co-transporter in DCT, so more Na reaches collecting duct
More K lost in collecting duct as a result
Side effects of thiazide-like diuretics, such as indapamide and chlortalidone?
Same as thiazides
Hypokalaemia/Hyponatraemia Hypercalcaemia Gout Postural hypotension Impaired glucose tolerance Impotence
Rarely: agranulocytosis, pancreatitis, thrombocytopenia, photosensitive rash
Hypertension ladder?
1:
<55 OR T2DM - A
55+ or black, no T2DM - C
2: A+C or A+D
3: A+C+D
4: If K+ 4.5 or less - spironolactone
If K+ >4.5 B-blocker or A-blocker
5: Specialist
What tests should be done before starting amiodarone?
Monitoring after this?
TFT, LFT, U&E, baseline CXR
TFT and LFT every 6 months
Blood pressure targets for clinic and ABPM for someone:
<80 y/o?
>80 y/o?
<80:
clinic - <140/90
ABPM - <135/85
> 80:
clinic - <150/90
ABPM - <145/85
7 causes of ST elevation?
STEMI
Pericarditis/myocarditis
Normal variant (high take off)
LV aneurysm
Coronary artery spasm (prinzmetal’s angina)
Takotsubo cardiomyopathy (octopus pot, floppy apical LV)
Subarachnoid haemorrhage (rare)
Pathognomic ECG finding in cardiac tamponade?
Electrical alternans
Waves are of alternating amplitude, 1st and 3rd will be same height, 2nd and 4th will be etc
Amplitude may be small as well depending on how bad the tamponade is
Which antihypertensive can cause constipation and abdominal pain as a side effect?
Thiazides - hypercalcaemia
Bones - bone pain Stones - kidney stones Groans - abdo pain Thrones - constipation/urinary frequency Tones - muscle weakness and hyporeflexia Psychiatric moans - depression, anxiety, confusion
What is eisenmenger’s syndrome?
How can it present?
Management?
Pulmonary hypertension as a result of an uncorrected VSD
The RV hypertrophies until it overcomes the LV - this causes chronic pulmonary microvascular changes
It causes R to L shunt and chronic cyanosis. This may be seen as:
- blue tinge to nails/lips
- clubbing/loss of nail fold
- RV failure
- original murmur may disappear
- haemoptysis (from pul microvasc changes)
Rx: heart and lung transplant needed eventually
VT without haemodynamic instability:
- What is treatment?
- What should be avoided?
Amiodarone - 1st line option
Procainamide
Lidocaine (use with caution, esp with severe LV impairment)
NEVER use Verapamil
(if drug therapy fails then synchronised DC cardioversion)
What symptom do most patients get following administration of adenosine?
Chest pain
due to increased coronary sinus blood flow
ECG of digoxin toxicity? (4)
- Downsloping ST depression widespread (like a reversed nike tick)
- inverted/flattened T waves
- Shortened QT interval
- Can cause AV block/bradycardia
Course of action for patients presenting with acute chest pain:
- <12 hours ago?
- 12-72 hours ago?
- > 72 hours ago?
- take ECG and emergency admission to hospital
- refer to hospital for same-day assessment
- Full workup including ECG and troponin - use this to guide your judgement
Immediate management of suspected ACS?
- Morphine (if in pain)
- Oxygen**
- GTN spray
- Aspirin - 300mg (high dose)
- Clopidogrel or Ticagrelor once in hospital
- if sats <94% and not at risk of T2 resp failure
- if at risk of T2 resp failure, aim for 88-92%
3 criteria for angina?
What is unstable angina?
- Constricting discomfort in chest, neck, shoulders, jaw or arms
- Brought on by physical exertion
- Relieved within 5 mins by GTN spray
Atypical angina - 2/3 of these - e.g. if pain is ‘stabbing’ instead of ‘constricting’ (more common in women and diabetics)
If only 1/3 - non-anginal chest pain
Investigations for angina if it cannot be diagnosed clinically alone?
- CT coronary angiography
- non-invasive functional imaging
(e. g. perfusion scintigraphy, SPECT, stress echo, MR perfusion scan) - invasive coronary imaging
Angina pectoris treatment ladder?
All patients should receive aspirin 75mg, a statin and GTN (unless CI)
- B-blocker or rate-limiting CCB
- Once at max dose, add second drug:
B-blocker + dihydropyridine CCB - If still symptomatic, refer for assessment for PCI/CABG and add a 3rd drug:
- ivabradine (funny current HCN channel blocker)
- long-acting nitrate
- nicorandil (K channel opener/NO activity)
- minoxidil (K channel opener/NO activity)
Usual 4 medications for pulmonary hypertension?
Other drug options (class + example)?
Warfarin/DOAC
Diuretic
High % oxygen
Digoxin
- CCB’s - nifedipine, amlodipine, diltiazem
- Endothelin ETa receptor antagonists - bosentan, ambrisentan
- PDE5 inhibitors - sildenafil
- Prostaglandins - iloprost
- guanylate cyclase inhibitors - riocugat
What must you be careful of with nitrates?
Other SE? (4)
Tolerance - take second nitrate after 8 hours, not 12, leaving 4 hours nitrate free in body
Effect not seen as much with modified release isosorbide mononitrate
Headache
Postural hypotension
Tachycardia
Flushing
2 methods of ACS developement? What is ACS spectrum? Symptoms? Often mistaken for? Who gets silent MI? Signs?
- Gradual narrowing of lumen until occluded by atherosclerotic plaque (angina)
- Rupture of plaque causing thrombosis
Unstable angina
NSTEMI
STEMI
Central, crushing, heavy chest pain - to neck, jaw, shoulder, arm Stomach pain, nausea, vomiting Pale, clammy Sense of impending doom SOB
Often mistaken for dyspepsia
Esp in diabetics/elderly, who may not get chest pain
Often very little signs - BP, temp etc all normal
May be tachycardia/tachypnoeic
Signs of heart failure may begin to develop after a while
Criteria for a STEMI?
- Clinical symptoms consistent with ACS for >20 mins
- ST elevation of 2 small squares (2mm) in at least 2 contiguous leads
Can also have :
- ST elevation of 1 small square (1mm) in other leads
- New onset LBBB
Management of STEMI?
If presenting within 12 hours of symptom onset:
If PCI can be accessed within 2 hours:
- Aspirin + prasugrel (clopidogrel if already on oral anticoagulant)
- PCI with heparin + abciximab cover
- Place drug-eluting stent
If PCI cannot be accessed within 2 hours:
- Thrombolysis + LMWH/Fondaparinux
- Repeat ECG 90 mins after delivery - if no improvement, organise transfer for PCI
NSTEMI/Unstable angina management?
Give aspirin
Give Fondaparinux if no immediate PCI planned and no increased bleeding risk
Calculate GRACE score (6 month mortality)
If >3%:
- Offer PCI within 72 hours
- Prasugrel/Ticagrelor + heparin + drug-eluting stent
If <3%:
- Give Ticagrelor
Why does cardiac arrest occur after MI?
Most commonly VF
Also VT
Why does cardiogenic shock occur with MI?
If a large part of the LV myocardium is damaged, ejection fraction of heart may decrease massively
May occur because of mechanical reasons such as LV free wall rupture
What chronic condition occurs commonly after MI?
Heart failure
Which type of MI does AV block occur with?
Most commonly inferior
Can cause bradyarrhythmias
2 types of pericarditis following MI?
<48 hours - due to transmural MI, occurs in 10%.
Typical pericarditis features - worse on lying flat, pericardial rub, pericardial effusion
2-6 weeks - Dressler’s Syndrome - autoimmune reaction against antigenic proteins.
Fever, pleuritic pain, pericardial effusion, raised ESR.
Rx: NSAIDs
Why might LV aneurysm form after MI?
ECG and signs?
What might it put patients at risk of?
Sustained weakness of myocardium
Persistent ST elevation
Signs of LV failure (pul oed)
Thrombus forming and stroke - patients must be anticoagulated
When does LV free wall rupture occur following MI?
Presentation?
Treatment?
1-2 weeks
(occurs in 3%)
Acute heart failure secondary to tamponade
- Raised JVP
- Pulsus paradoxus
- diminished heart sounds
Urgent pericardiocentesis and thoracotomy
What type of MI does acute mitral regurg occur with?
Why does it happen?
Symptoms/signs?
Treatment?
Infero-posterior MI
Ischaemia/rupture of papillary muscle
Acute hypotension and pulmonary oedema
Early-mid diastolic murmur
Vasodilator therapy and emergency surgical repair
What is plusus paradoxus?
2 causes?
Greater than normal (>10mmHg) drop in systolic BP during inspiration
(faint/absent pulse during inspiration)
Cardiac tamponade
Severe asthma
What causes a slow-rising/plateau pulse? (1)
Aortic stenosis
also narrow pulse pressure
What is a collapsing/water-hammer pulse?
Causes? (3)
Pulse which can be felt rapidly increasing in force through the bulk of the muscle in the forearm when the arm is raised above the head, and subsequently collapses
Aortic regurgitation
PDA
Hyperkinetic states (anaemia, thyrotoxicosis, fever, exercise, pregnancy)
Explanation: if hyperaemic/aortic regurg etc sluggish blood flow through artery in arm. Raising arm above head causes it to rapidly flow back towards the LV, increasing the EDV for the next cycle (valve regurgitates it) - increased stretch from increased volume increases the force of the next contraction via Frank-Starling mechanism
What is plusus alternans?
Cause?
Regular alternation of the force of arterial pulse
Severe LVF
What is a bisferiens pulse?
What causes it? (2)
‘double pulse’ - 2 systolic peaks
Mixed aortic valve disease
Occasionally HOCM
What is a jerky pulse?
What causes it?
Seen in HOCM
Pulse which has a rapid upstroke due to vigorous contraction of hypertrophic LV
As volume of LV decreases there is abrupt blockage of outflow
This causes a rapid fall in arterial pressure
(HOCM may also sometimes be assoc w bisferiens pulse)
Causes of pericarditis? (8)
Viral (often coxsackie) Uraemia (causes fibrinous pericarditis) TB Trauma MI SLE Hypothyroidism Malignancy
ECG changes in pericarditis?
What other investigation should all with suspected acute pericarditis get?
Management?
Widespread:
- ‘Saddle-shaped’ ST-elevation
- PR depression (most specific)
Transthoracic echo
NSAID + Colchicine
Treat underlying cause
Causes of constrictive pericarditis?
Symptoms/Signs?
Specific Ix?
How to differentiate from tamponade?
Any cause of acute, particularly TB
Dyspnoea Pericardial knock (S3) Elevated JVP with x+y descent Kussmaul sign is positive (rise in JVP during inspiration) RV failure: - Elevated JVP - Ascites - Oedema - Hepatomegaly
CXR - shows pericardial calcification
Pulsus paradoxus is ABSENT
(present in tamponade)
Who should myocarditis be suspected in?
Causes? (6)
Presentation?
Esp young people with acute chest pain
Viral - coxsackie, HIV Bacteria - diphtheria, clostridia Spirochaetes: Lyme disease Protozoa: Chagas disease, toxoplasmosis Autoimmune Doxorubicin (chemo drug)
Typical presentation:
- young person
- acute chest pain
- dyspnoea
- arrhythmia
Ix for myocarditis? (2)
Management?
Complications? (3)
Bloods:
- Inflam markers
- cardiac enzymes
- bnp
ECG:
- tachycardia
- arrhythmia
- ST elevation
- T wave inversion
Rx:
- Supportive, treat cause
Comp:
- HF
- Sudden death from arrhythmia
- Dilated cardiomyopathy (late)
Underlying cause of VT?
2 types and what causes of each?
Why is it important to treat?
Ventricular ectopic focus, leading to broad complex tachycardia
Monomorphic - usually MI
Polymorphic (Torsades de pointes) - Long QT interval
Can lead to VF
Apart from drugs, what can cause long QT interval?
Congenital (random things including deafness)
Electrolytes:
- hypocalcaemia
- hypokalaemia
- hypomagnesaemia
MI
Myocarditis
Hypothermia
Subarachnoid haemorrhage
What is WPW syndrome?
What can it cause?
ECG features? (3)
Management? (2)
Congenital accessory pathway between the atria and ventricles leading to AV re-entry tachycardia
(current spreads up through ventricles and rather than stopping at top of ventricles it goes back into atrium)
- Short PR interval
- Wide QRS with slurred upstroke - delta wave
- Axis deviation towards side of pathway (usually left)
Definitive: ablation
Medical: Sotalol/Amiodarone or Flecainide
(avoid sotalol if concurrent AF as prolonging AV refractory encourages transmission through accessory)
What therapy should be initiated after MI?
What if they have HF as well?
Is this just for STEMI or for NSTEMI as well?
When can sexual activity resume?
When could sildenafil (viagra) be used?
Statin ACEI B blocker Aspirin Ticagrelor for 12 months (can extend if high risk)
Add aldosterone antagonist (eplerenone) within 2 weeks
Both
Sex after 4 weeks
Sildenafil after 6 months - NOT if also taking nitrates or nicorandil
Timeline of ECG changes in MI?
Acutely:
ST elevation/depression
Within 24 hours:
Q wave formation
T wave inversion
ST changes remain
After week(s):
ST back to normal
Q waves and T wave inversion remain
Contraindications for thrombolysis? (8)
Potential SE?
- Active internal bleeding
- Recent haemorrhage/trauma/surgery (including dental extraction)
- Coagulation/bleeding disorders
- Intracranial neoplasm
- Stroke <3 months ago
- Aortic dissection
- Recent head injury
- Severe hypertension
SE:
- Haemorrhage
- Allergic reaction - esp streptokinase
Diagnosis of chronic heart failure?
What causes release of BNP?
What is its physiological effect? (4)
What to do if raised/high levels?
BNP and NT-proBNP
BNP:
Normal <100
Raised 100-400
High >400
NT-proBNP:
Normal <400
Raised 400-2000
High >2000
Released by LV myocardium in response to strain
- causes vasodilation, diuresis, natriuresis, and suppresses RAAS
Raised: specialist assessment within 6 weeks
High: specialist assessment within 2 weeks
Treatment ladder of chronic heart failure?
Other treatments these patients should get?
All patients start on:
ACEI + B1-blocker
2nd line: aldosterone antagonist
(careful as these + ACEI can cause hyperkalaemia)
3rd line options - to be started by specialist:
- Ivabradine
- Digoxin
- Hydralazine
- Sacubitril-Valsartan
- Cardiac resynchronisation therapy
Other things:
- annual influenza vaccine
- One off pneumococcal vaccine
(asplenic or CKD patients need booster every 5 years)
What is a preserved (normal) ejection fraction?
What is a mildly reduced ejection fraction?
What is a reduced ejection fraction?
Preserved: >50%
Mildly reduced: 40-49%
Reduced: <40%
NYHA classification?
1 - no symptoms/limitation
2 - mild - fatigue, palpitations or dyspnoea with activity
3 - mod - less than ordinary activities result in marked symptoms
4 - sev - symptoms at rest, unable to carry out any physical activity
When should someone receive statins for primary prevention?
What dose and drug for primary and secondary prevention?
What are the CI/interactions of statins?
QRISK 10% or more
Primary prevention:
Atorvastatin 20mg
Secondary prevention:
Atorvastatin 80mg
CI: pregnancy
Inter: macrocodes - choose other antibiotic if possible or stop statins during course
HOCM:
- inheritance?
- gene?
- Echo abnormalities? (3)
AD
beta-myosin heavy chain protein
MR SAM ASH
- Mitral regurgitation
- Systolic anterior motion of anterior mitral valve
- Asymmetrical septal hypertrophy
Arrhythmogenic RV dysplasia:
- what is it?
- ECG abnormalities?
RV myocardium replaced by fatty and fibrofatty tissue
In V1-V3:
- T-wave inversion
- Epsilon wave (terminal notch in QRS)
7 common causes of dilated cardiomyopathy?
Signs? (3)
What is seen on echo and cxr?
Alcohol IHD Muscle disease e.g. DMD Coxsackie B virus Wet beri beri Doxorubicin (chemo drug) Infiltrative disease (e.g. haemochromatosis, sarcoidosis)
Dilated = most common, 90% of cardiomyopathies
Signs:
- Signs of HF
- Systolic murmur (mitral/tricuspid regurg)
- S3
Echo: all 4 chambers dilated
CXR: ‘balloon’ shape of heart
2 most common causes of restrictive cardiomyopathy?
Amyloidosis
Radiotherapy
When does peripartum cardiomyopathy develop?
Who is it more common in?
Between last month of pregnancy and 5 months postpartum (dilated cardiomyopathy)
Older women, greater parity
What causes takotsubo cardiomyopathy?
Features? (2)
Rx? (1)
‘stress induced’ e.g. bereavement then develop chest pain and heart failure
Transient, apical ballooning of myocardium
LV ‘octopus pot’ shape
Rx: supportive
What is subclavian steal syndrome?
Presentation? (2)
Rx? (1)
Subclavian stenosis proximal to the origin of the vertebral arteries - resulting in retrograde blood flow from the vertebral arteries to the arm during exercise
Presentation:
- Dizziness/vertigo during exercise
- Concurrent arm pain
(typically posterior circulation symptoms)
Rx: stent
What are the 3 types neurally-mediated syncope?
What occurs before it?
- Vasovagal episode - usually brought on by emotion, pain or stress
(‘fainting’) - Situational - in response to coughing, micturition
- Carotid sinus syncope - exaggerated response to pressure applied to carotid sinus
Before: sweating, pallor, nausea/vomiting
Then transient loss of consciousness
Quick recovery, no post-ictal state
What can cause cardiac syncope? (3)
Arrhythmias (brady or tachy)
Structural: valvular, MI, HOCM
PE
Causes of orthostatic syncope?
Due to autonomic failure
Primary: Parkinson’s, LBD
Secondary: diabetes, amyloid, uraemia
Drug-induced: diuretics, alcohol, vasodilators
Volume depletion: haemorrhage, diarrhoea
Definition of Syncope?
3 broad types?
Transient LOC due to global cerebral hypo perfusion - rapid onset, short duration, quick and spontaneous recovery
Reflex (neurally mediated)
Orthostatic
Cardiac
What is coarctation of aorta?
How may it present in infancy?
When to suspect coarctation of aorta in an adult?
What is seen on CXR that is not seen in young children?
4 associations?
Congenital narrowing of descending aorta (most commonly post-ductal)
Heart failure
Young person with hypertension
Radio-femoral delay
BP difference between left arm and other limbs
Notching of inferior rib borders (due to collaterals)
Turner's syndrome Bicuspid aortic valve Berry aneurysms NF (more common in males)
Warfarin reversal:
- major bleeding?
- INR >8 (minor+no bleeding)?
- INR 5-8 + minor bleeding?
- INR 5-8, no bleeding?
- When to restart warfarin?
1:
- IV VitK
- Prothrombin complex concentrate (or FFP)
2:
- VitK - IV if minor bleeding, PO if no bleeding
- Repeat INR after 24 hours
3:
- IV warfarin
4:
- Withhold 1-2 doses, then reduce maintenance dose
5:
- Restart warfarin once INR <5
What is Buerger’s disease?
Features? (4)
Small-medium vessel vasculitis, strongly assoc w smoking
(young male, smoker, limb ischaemia)
Limb ischaemia
Ischaemic ulcers
Superficial thrombophlebitis
Raynaud’s
What is Buerger’s test for?
How is it performed?
Limb arterial insufficiency
- Lying down, raise both patents’ legs to 45 degrees for 1 minute
- They will become pale due to poor blood flow
- Then ask patient to sit off edge of bed with legs hanging down
- Skin first turns blue as deoxygenated blood returns to tissue, then red due to reactive hyperaemia from post-hypoxic dilation
Treatment of bradyarrhythmia (e.g. complete heart block) post-MI if:
- anterior MI?
- inferior MI?
Anterior - external pacing
Inferior - atropine
(because bradyarrhythmias post-inferior MI are normally transient and resolve in hours-days, so treat conservatively)
Indications for temporary external pacing? (3)
- symptomatic/haemodynamically unstable bradycardia not responding to atropine
- post-ANTERIOR MI - if develop type 2 or complete heart block
- trifascicular block prior to surgery
Anticoagulation after mechanical valve insertion?
Target INR?
Who is still given bioprosthetic valves (e.g. pig or cow)?
Problems with these?
Warfarin
Aortic 3.0
Mitral 3.5
Older people: >65 if aortic and >70 if mitral
Long-term anticoagulation not needed, just 75mg aspirin
Problems: deterioration & calcification over time
What to do if patient starts experiencing increasing chest pain or haemodynamic instability following PCI for STEMI?
Arrange urgent CABG
Give nitrates and morphine in meantime
P wave changes - what causes:
- increased amplitude?
- broad, notched (bifid) p wave?
Cor pulmonale (P pulmonale)
LA enlargement classically in mitral stenosis (P mitrale)
Most commonly in lead II
5 acyanotic heart defects?
VSD (most common, 30%) ASD PDA Coarctation Aortic stenosis
VSD more common than ASD but ASD more common as a new diagnosis in adulthood
3 cyanotic heart defects?
Tetralogy of Fallot
Transposition of Great Arteries
Tricuspid atresia
TOF more common but usually present at 1-2 months
TGA more commonly recognised at birth
(Pulmonary stenosis - presence of cyanosis depends on severity of stenosis and presence of coexistent defects)
How to determine if neonatal cyanosis is of cardiac origin?
What to do as initial supportive management if it is ductal dependent?
Nitrogen washout test - give 100% O2 for 10 mins then do ABG, pO2 <15kPa indicates cardiac cause
If duct-dependent give PGE2
What is acrocyanosis?
Blue discolouration of mouth, hands and feet in a newborn caused by vasospasm.
Benign, normal finding in healthy newborns. Lasts 24-48 hours
Differentiated from other causes of neonatal cyanosis (e.g. sepsis) as it occurs straight after birth
PDA:
- connection between what?
- can it lead to cyanosis?
- what is seen on praecordial exam?
- pulse type?
- murmur?
- Rx?
- pulmonary trunk and descending aorta
- yes, eventually, cyanosis of lower extremities (termed differential cyanosis, as upper limbs normal)
- subclavicular thrill, heaving apex beat
- large volume, bounding, collapsing pulse
- continuous machine-like murmur
- indomethacin/ibuprofen
TOF:
- what are the 4 deformities?
- when is it picked up?
- what are tet spells?
- murmur?
- cxr/ecg?
- management?
4 deformities:
- VSD
- RV hypertrophy
- pulmonary stenosis/RV outflow tract obstruction
- overriding aorta
- 1-2 months
- When baby becomes cyanotic when it cries/becomes agitated due to rapid decrease in blood oxygenation
- ejection systolic murmur (due to pulmonary stenosis - VSD doesn’t usually cause murmur)
CXR: boot-shaped heart
ECG: RV hypertrophy
Management - surgical repair in 2 parts. B-blockers to reduce infundibular spasm
What is Ebstein's anomaly? What causes it? What is seen in 80% if patients with this? Clinical features? (5) Conductive problem?
Low insertion of the tricuspid valve resulting in a large atrium and small ventricle (‘atrialisation of RV)
Lithium
PFO/ASD
Features:
- cyanosis
- prominent ‘a’ woven JVP
- hepatomegaly
- tricuspid regurg (pan systolic murmur, worse on inspiration)
- splitting of S1 & S2
RBBB (hence splitting of S1&S2)
HOCM:
- what is the physical issue?
- clinical features?
- pulse?
- murmur?
- ECG?
LV hypertrophy, and sub aortic hypertrophy of ventricular septum, resulting in functional aortic stenosis
Features:
- syncope (following exercise)
- angina-like pain
- exertion dyspnoea
- Often asymptomatic, until sudden death due to ventricular arrhythmia
Pulse: jerky
Murmur: ejection systolic
ECG:
- LV hypertrophy
- Non-specific ST and T-wave changes, progressive T-wave inversion may be seen
- deep Q waves
3 drugs to avoid in HOCM?
ACEI
Nitrates
Inotropes
What is brugada syndrome? Inheritance? Who is it most commonly seen in? ECG changes? What makes ECG changes more apparent? Rx?
Defect in sodium ion channel
AD
Asians
ST elevation followed by negative T wave in V1-V3
Partial RBBB
ECG changes more apparent with flecainide
ICD
Pathophysiology of Rheumatic Fever?
Major and minor diagnostic criteria?
Management? (3)
Type II hypersensitivity reaction 2-6 weeks after strep pyogenes infection
Diagnosis:
Evidence of recent streptococcal infection by raised/rising streptococcal antibodies or positive throat swab, accompanied by 2 major diagnostic criteria or 1 major and 2 minor
Major:
- pancarditis (myocarditis + endocarditis)
- erythema marginatum
- polyarthritis
- subcutaneous nodules
- sydenham’s chorea (late feature)
Minor:
- raised ESR/CRP
- pyrexia
- prolonged PR
Rx:
- Penicillin V
- NSAIDs
- Treat any complications e.g. heart failure
2 congenital causes of LQTS?
What is LQTS 1, 2 and 3?
What arrhythmia may arise?
Jarvell-Lange-Nielsen syndrome (deafness)
Romano-Ward syndrome (no deafness)
1 - syncope after swimming
2 - syncope after emotional stress
3 - events occur at night or at rest
Torsades de Pointes
Management of hyperglycaemia in STEMI?
Dose-adjusted insulin to ensure glucose <11
Immediate management of a STEMI?
Ticagrelor
Aspirin (even if already taking aspirin)
Heparin if going for PCI <2 hours after arrival at hospital
tPA if PCI not available - perform ECG 90 mins after thrombolysis - if <50% improvement arrange transfer to PCI centre
What antihypertensive to avoid with hyperglycaemia?
Thiazides or thiazide-likes - can worsen glucose tolerance
Ix for PE in renal impairment?
V/Q scan
Presentation of LV free wall rupture post-MI?
Signs of L and R HF due to tamponade
- lung crackles
- pulsus paradoxus
- ankle oedema
- raised JVP
- diminished heart sounds
Usually 1-2 weeks later
urgent pericardiocentesis required
Dissection:
- features?
- Ix?
- types and management?
- tearing chest pain
- BP variation >20mmHg between arms
- aortic regurg
- hypertension
- may have other features depending on site and branching arteries
- non-specific ECG changes, may have STE inferior leads
Ix: CT angiography CAP
Trans-oesophageal echo if unsuitable
Type A - ascending aorta
- surgical management but reduce BP to 100-120 systolic before
Type B - descending
- conservative, IV labetalol
Which drug is assoc w GI ulcers and can cause perforation?
Nicorandil
Heart failure treatment ladder?
- ACEI or B blocker
- Second of these
- Spironolactone
ECG changes and arteries for MI:
- Anteroseptal?
- inferior?
- anterolateral?
- lateral?
- posterior?
anterolateral:
- V1-V4
- LAD
inferior:
- II, III, aVF
- RCA
anterolateral:
- V4-V6, I, aVL
- LAD or Left Circumflex
Lateral:
- I, aVL +/- V5-V6
- Left circumflex
Posterior:
- Tall R waves V1-V2
- May cause ST depression
- Circumflex or Right Coronary
Isolated new onset LBBB may also point to MI
Apart from HF, what causes raised BNP?
What can reduce it?
CKD (even with eGFR <60) due to reduced renal excretion
ACEI and ARBs can also raise it
Diuretics can reduce it
What to do with warfarin after successful treatment of AF with catheter ablation?
Continue treatment
2 main indications for loop diuretics?
SE?
- Heart failure - acute IV, chronic orally
- resistant HTN, especially in those with renal impairment
SE:
Hypotension
Low everything (Na, K, Mg, Cl, H, Ca)
Ototoxicity
Renal impairment (dehydration and direct toxicity)
Hyperglycaemia (less common than thiazides)
Gout
Management of acute HF for all pts? If hypoxic? If ischaemia? If no response to initial hypoxia treatment? If hypotensive? What to do with regular meds? Opiates?
IV loop diuretics
Oxygen if sats <94%
GTN if due to ischaemia or HTN
If sats still low after O2 and Furosemide, CPAP
If hypotension/cardiogenic shock:
- inotrope e.g. dobutamine
- vasopressor e.g. NA
Continue regular medications such as B blocker/ACEI
Do not give opiates
In VF/VT arrest, what is the shock:CPR ratio?
When is it changed?
When should adrenaline and amiodarone be given?
What is an alternative if amiodarone not available?
When should adrenaline be given for non-shockable rhythm?
Single shock followed by 2 mins CPR
If witnessed on a monitor e.g. in CCU - 3 quick shocks can be given in succession followed by 1 min CPR
Adrenaline: after the 3rd shock (not stacked) then every 3-5 mins after
Amiodarone also after 3 shocks and after 5 shocks
Lidocaine is alternative to amiodarone
In non-shockable rhythm, give adrenaline ASAP and every 3-5 mins after
Adenosine:
- who should it be avoided in?
- what drugs can affect it?
- what adverse cardiac effect can it have?
Asthmatics - can cause bronchospasm
Theophylline - blocks its effects
Dipyramidole - enhances its effects
Enhance conduction along accessory pathways causing increased ventricular rate (e.g. WPW)
Can ECG changes occur in unstable angina?
Yes, can have T wave inversion or ST depression - but lack of troponin being raised or any changes in troponin at 3 and 6 hours differentiates from NSTEMI
What is Prinzmetal angina?
What drugs can cause it?
Angina due to coronary artery spasm
Usually in younger people who smoke/take cocaine, occurs early in morning or during sleep, and can cause ST elevation. No pain during exercise
Cocaine, Triptans and 5-FU can cause it
If ACEI causes hyperkalaemia when should it be stopped?
If K >6 switch to another drug, especially if CKD
3 main SE of GTN?
Hypotension
Headache
HR increase
Cause of hypertension in aortic dissection?
Catecholamine surge
Management of orthostatic hypotension?
Initially:
- education - ensure adequate water and salt intake
After that:
- discontinue drugs such as nitrates, antihypertensives, neuroleptic agents, dopaminergic drugs
Then:
- Fludricortisone or midodrine
- compression garments, counter-pressure manoeuvres, head tilt-up sleeping
(fludricortisone increases renal Na and water reabsorption, midodrine;
midodrine is an alpha agonist causing vasoconstriction)
Monitoring when commencing treatment with a statin?
LFT’s at baseline, 3 months and 12 months
Fasting lipid profile may tested at these points also to assess response to treatment
What is the only CCB licensed for use to manage hypertension with concurrent heart failure?
Amlodipine
Signs on examination of acute HF?
Bibasal crackles and wheeze Cyanosis Tachycardia Elevated JVP Displaced apex beat S3 heart sound
What causes S3?
It is caused by diastolic filling of the ventricle, considered normal if <30 y/o
Occurs in:
- Left ventricular failure (e.g. dilated)
- Constrictive pericarditis (called pericardial knock)
- mitral regurg
What causes S3?
It is caused by diastolic filling of the ventricle, considered normal if <30 y/o
Occurs in:
- Left ventricular failure (e.g. dilated)
- Constrictive pericarditis (called pericardial knock)
- mitral regurg
What causes S4?
Atrium contracting against a stiff, non-compliant ventricle (coincides with P wave on ECG)
Occurs in aortic stenosis, HOCM, hypertension
(HOCM may have a double apical beat caused by palpable S4)
How often is digoxin level monitored in blood?
How long after dose?
Not routinely monitored unless toxicity suspected
8-12 hours after dose
Dose of adrenaline for cardiac arrest?
10ml 1:10,000
OR
1ml 1:1000
(0.5ml 1:1000 in anaphylaxis)
Glycaemic control if admitted to hospital with ACS?
Stop oral glycaemics, start sliding scale insulin
Causes of long QT:
- electrolytes?
- drugs?
Electrolytes:
Low Ca, Mg or K
Drugs
- amiodarone/sotalol
- macrolides, ciprofloxacin
- Citalopram, TCS’s, neuroleptics (esp Haloperidol)
What drugs should be AVOIDED in people with HOCM?
ACEI
Nitrates
inotropes
(ACEI and nitrates decrease preload making it worse)
4 week old infant presents with poor feeding, on exam tachycardia, tachypnoea, hypertension and weak femoral pulses, no cyanosis. Systolic murmur best heard at left sternal edge?
Coarctation of aorta
Valves most commonly affected in infective endocarditis in order?
- Mitral
- Aortic
- Tricuspid
- Pulmonary
Tricuspid most commonly affected in IVDU
Apart from that it’s left side because bacteria generally need damage to latch on, and that is more common in left side due to higher pressure
What is stage 1, stage 2 and severe HTN?
When to start medication?
What are BP targets?
Stage 1 - ABPM >135/85
Stage 2 - ABPM >150/95
Severe - clinic BP >180/110
Stage 1 - treat only if <80 y/o and Q-RISK >10%, or evidence of organ damage
Stage 2 - start medication for all
Targets: 135/85 if <80, 145/85 if >80
BP 1st line treatment in diabetes?
ACEI no matter what age
ARB if black
If a patient has a BP >180/110?
Check for end-organ damage If none present, ambulatory/home and recheck after 7 days If evidence (e.g. blood/protein in urine, papilloedema, retinal haemorrhage) admit for specialist assessment
