Cardiology Flashcards
Helpful mnemonics for acute and longer term management of MI?
MONA:
Morphine and anti-emetic
O2 if hypoxic
Nitrates (GTN spray)
Aspirin
DABS:
Dual antiplatelet therapy
ACEi
BB
Statin
When can PCI be carried out?
If the MI presents within 12 hours of onset AND PCI can be delivered within 120 minutes of the time when fibrinolysis could have been given
If PCI cannot be delivered in 120 mins give immediate fibrinolysis
Poor prognostic factor in ACS?
Cardiogenic shock
ECG changes in pericarditis? Tx?
‘saddle-shaped’ ST elevation (concave)
PR depression: most specific ECG marker for pericarditis
Tx is NSAIDs
How should suspected aortic dissection be investigated?
What is the key finding?
CT angiography of the chest, abdomen and pelvis is the investigation of choice
TOE for unstable patients who are too risky to take to the scanner
the key finding suggestive of aortic dissection on CT angiography is a false lumen
Will also see widening of the mediastinum on CXR
How do you treat acute onset AF?
If haemodynamically stable you do not need to cardiovert immediately
If the patient is stable and onset ≥ 48 hours - rate control initially (e.g. bisoprolol) and delay cardioversion until they have been maintained on therapeutic anticoagulation (e.g. apixaban) for a minimum of 3 weeks
If very unstable with acute onset AF- can do TOE to look for left atrial thrombi before urgent cardioversion
Tx for angina where BB contraindicated?
Nicorandil - can cause ulcers along the GI tract
What protein marker is most useful for determining reinfarction in the weeks following MI?
Creatine kinase (CK-MB)
- it remains elevated for only 3 to 4 days following infarction. Troponin remains elevated for 10 days.
Main ECG change in hypercalcaemia?
shortening of the QT interval
How do you manage HOCM (hypertrophic obstructive cardiomyopathy)?
ABCDE:
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator (If they have arrested once, implant a cardioverter defibrillator to prevent recurrence)
Dual chamber pacemaker
Endocarditis prophylaxis
Outline the acute management of key peri-arrest rhythms : unstable VT, stable VT, and SVT
Unstable VT (dropping bp)= cardioversion, then maybe IV amiodarone
Stable VT = IV amiodarone
Supraventricular tachy= IV adenosine
How do you determine the cause of orthostatic htn?
How do you treat?
Orthostatic hypotension (A fall in SBP of >20mmHg on standing) accompanied by an exaggerated increase in HR = due to anaemia or hypovolemia
Orthostatic hypotension with minimal/no change in heart rate = neurogenic (e.g. due to diabetes)
Tx= Fludrocortisone and midodrine
Outline the key points of PE investigation
- Wells score
Wells score 4 or less = D-dimer to exclude PE
Wells score- over 4 = likely PE
- Do an ECG - sinus tachy commonest finding in PE (S1Q3T3 characteristic but rare)
- Do a CXR - clear/ wedge shaped opacification in PE
- Do a CTPA (unless contraindicated e.g. allergy to contrast/renal impairment in which case VQ scan used as an alternative)
Strong suspicion of PE but delay in the scan - start tx dose anticoagulant and monitor closely in the meantime
If CTPA +ve proceed with treatment (thrombolyse or give DOAC)
If CTPA -ve but DVT strongly suspected then consider a proximal leg vein ultrasound scan
Outline the key points of PE management
What is the target INR for pts with recurrent PEs?
Tx:
If there is massive PE + hypotension - thrombolyse immediately
For haemodynamically stable PE (not hypotensive/tachycardic):
3 months DOAC for provoked PE (obvious temporary risk factor)
6 months DOAC for people with active cancer and confirmed proximal DVT/PE
Lifelong tx for patients with unprovoked PE or persistent risk factors such as antiphospholipid syndrome, active cancer or thrombophilia
Target INR for patients with recurrent PEs is 3.5
If the patient has a PESI class 1 or 2 (very low risk PE) and do not want to be admitted, they can be managed as an outpatient with rivaroxaban.
Key contraindications to thrombolysis?
Contraindications to thrombolysis:
active internal bleeding
recent haemorrhage, trauma or surgery (including dental extraction)
bleeding disorders
intracranial neoplasm
recent head injury
stroke < 3 months
aortic dissection
severe hypertension
What is Takayasu’s arteritis? Give features, association and tx
Common in young Asian women - fibrous thickening of aortic branches
Features:
systemic features of a vasculitis e.g. malaise, headache
carotid bruit and tenderness
unequal blood pressure in the upper limbs
limb claudication on exertion
absent/ weak peripheral pulses
Associations: renal artery stenosis
Management: steroids
1st and 2nd line tx for patients with stable impaired LV function? Vaccinations offered?
1st: ACE inhibitor + beta-blocker
2nd: aldosterone antagonist
Yearly flu jab and one off pneumococcal
Posterior MIs cause reciprocal changes in V1-3 - describe them
Remember- ‘ugh don’t STRRT”
horizontal ST depression
tall, broad R waves
dominant R wave in V2
upright T waves
Outline the tx for the 2 types of aortic dissection
type A - ascending aorta - control BP (IV labetalol) + surgery*
type B - descending aorta - control BP(IV labetalol)
*Proximal aortic dissections are generally managed with surgical aortic root replacement as opposed to stenting
What do p mitrale (bifid p wave) and p pulmonale (tall p wave) represent ?
P mitrale- left atrial hypertrophy/strain e.g. in mitral stenosis (seen more in lead 2)
P pulmonale- right atrial hypertrophy e.g. tricuspid regurgitation and pulmonary hypertension
What part of the ECG is DC cardioversion synchronised with? Why?
the R wave to minimise the risk of inducing ventricular fibrillation
A patient develops acute heart failure 10 days following a myocardial infarction.
On examination he has a raised JVP, pulsus paradoxus (dramatic drop in bp on inspiration) and diminished heart sounds- what is the diagnosis?
left ventricular free wall ruputure- Urgent pericardiocentesis and thoracotomy are required.
ECG features in hypokalaemia?
“In Hypokalaemia, U have no T, but a long PR and a long QT”
U waves
Small/absent T waves
prolonged PR and QT intervals
What is a CHA2DS2-VASc score?
Used to determine need for anticoagulation in AF
one point would be allocated for each of the following:
Congestive heart failure
Hypertension (controlled or uncontrolled)
Age of 65-74 years
Diabetes
Vascular disease
Sex (female)
2 points for:
An age of 75 years or over
Prior stroke or thromboembolism.
How do you differentiate between cardiac tamponade and constrictive pericarditis? (both present with dyspnoea and signs of HF)
Kussmaul’s sign positive in c. pericarditis - JVP that raises/ doesn’t drop on inspiration
What drugs are given to someone receiving PCI?
prasugrel + unfractionated heparin + bailout glycoprotein IIb/IIIa inhibitor
When should statins be taken to improve efficacy?
at night as this is when the majority of cholesterol synthesis takes place
What is Dressler’s syndrome?
Dressler’s syndrome (postmyocardial pericarditis) is secondary pericarditis
If a pt presents with central, pleuritic chest pain and fever 2-6 weeks following a myocardial infarction and the ESR is elevated - think Dressler’s syndrome!!
Describe Beck’s triad for cardiac tamponade
How is cardiac tamponade investigated?
muffled heart sounds, hypotension and a raised jugular venous pressure
an echocardiogram. It can show an enlarged pericardium or collapsed ventricles.
Give causes of ejection systolic murmur that are louder on inspiration and louder on expiration
Ejection systolic
louder on inspiration:
- pulmonary stenosis
- atrial septal defect
also: tetralogy of Fallot
louder on expiration:
- aortic stenosis
- hypertrophic obstructive cardiomyopathy
Sign of hypothermia on ECG? On bloods?
J waves
Bloods can show high haemoglobin due to haemoconcentration, and low platelets and WCC due to splenic sequestration
First line management of acute pericarditis?
combination of NSAID and colchicine
What is Torsades de points? risk factors? tx?
a form of polymorphic ventricular tachycardia associated with a long QT interval- can lead to v fib and death
presents with dizziness, shortness of breath, palpitations
increased risk with macrolides e.g. azithromycin
tx with IV magnesium sulphate
Give 3 causes of pansystolic murmur and differentiate between them
mitral/tricuspid regurgitation (high-pitched and ‘blowing’ in character)
- tricuspid regurgitation becomes louder during inspiration, unlike mitral regurgitation (bc during inspiration, the venous blood flow into the right atrium and ventricle are increased)
ventricular septal defect (‘harsh’ in character)
What can cause a late systolic murmur?
mitral valve prolapse
coarctation of aorta
Outline the referral criteria for people presenting to the GP with chest pain
current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission
chest pain 12-72 hours ago: refer to hospital the same-day for assessment
chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action
How do you categorise angina as typical or atypical?
NICE define anginal pain as the following:
- constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
- precipitated by physical exertion
- relieved by rest or GTN in about 5 minutes
patients with all 3 features have typical angina
patients with 2 of the above features have atypical angina
patients with 1 or none of the above features have non-anginal chest pain
How should you manage angina ?
Medication:
all patients should receive aspirin and a statin in the absence of any contraindication
NICE recommend using either a beta-blocker or a calcium channel blocker first-line
sublingual glyceryl trinitrate to abort attacks
How can you treat Pulseless electrical activity and asystole?
They are non-shockable rhythms and therefore are unresponsive to defibrillation.
The patient should immediately receive 1mg of IV adrenaline whilst continuing high-quality CPR.
For a person < 80, with stage 1 hypertension, only treat medically if:
diabetic, renal disease, QRISK2 >10%, established coronary vascular disease, or end organ damage
Otherwise patients with stage 1 are given lifestyle advice
What is Eisenmenger’s syndrome?
reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension
Give 5 key features of aortic regurgitation
- early diastolic murmur: intensity of the murmur is increased by the handgrip manoeuvre
- collapsing pulse
- wide pulse pressure
- Quincke’s sign (nailbed pulsation)
- De Musset’s sign (head bobbing)
Outline the acute management of SVT
vagal manoeuvres:
- Valsalva manoeuvre: e.g. trying to blow into an empty plastic syringe
- carotid sinus massage
intravenous adenosine
- rapid IV bolus
- 6mg → 12mg → 18 mg escalation if rhythm isn’t terminated
Broad complex tachycardia following a myocardial infarction is almost always due to…
ventricular tachycardia
Who should be prescribed a statin?
How should patients be monitored after this prescription?
When should it be discontinued?
all people with established cardiovascular disease
anyone with a Q-risk >= 10%
patients with T1DM who were diagnosed > 10 years ago OR are > 40 OR have established nephropathy
Monitoring:
LFTs at baseline, 3 months and 12 months
Treatment should be discontinued if serum transaminase concentrations rise to and persist at 3 times the upper limit of the reference range
Patient presents with poorly controlled hypertension, already taking an ACE inhibitor, calcium channel blocker and a standard-dose thiazide diuretic. K+ > 4.5mmol/l (in normal range). What is the next step?
What about if the potassium is low (< 4.5)?
add an alpha- or beta-blocker
K+ < 4.5mmol/l - add spironolactone
How should you manage patients on warfarin with an INR over 5 and minor bleeding?
Stop warfarin
Give intravenous vitamin K 1-3mg
Restart warfarin when INR < 5.0
How should you manage patients on warfarin with an INR of 5.0 - 8.0 but no bleeding?
Withhold 1 or 2 doses of warfarin
Reduce subsequent maintenance dose
How do you manage patients on warfarin who have a major bleed?
Stop warfarin
Give intravenous vitamin K 5mg
Prothrombin complex concentrate
The ORBIT score is now the recommended scoring tool to assess bleeding risk in patients with AF who are being considered for anticoagulation. What are its five parameters?
- age (75+ years)
- anaemia (haemoglobin <130 g/L in males, <120 g/L in females)
- bleeding history
- renal impairment (eGFR <60 mL/min)
- tx with antiplatelets
Acute heart failure not responding to treatment -
CPAP
What is the treatment for acute onset heart failure?
IV loop diuretics
e.g. furosemide or bumetanide
May add O2
May add vasodilators (not if hypotensive)
How should you treat complete heart block following an inferior MI ?
How would this be different if it was following anterior MI?
Atropine - AV block and bradyarrhythmias are usually transient (hours to days) when caused by inferior MI so external pacing is not usually required
Anterior MI is more likely to cause prolonged or permanent arrhythmia so more likely to need external pacing
What is NSTEMI management for patients with a GRACE score > 3% ?
coronary angiography within 72 hours of admission, NOT emergency PCI as this is reserved for STEMIs
What type of heart failure can occur with HOCM?
HFpEF- Hypertrophic obstructive cardiomyopathy typically causes diastolic dysfunction
Tx for hypertensive emergencies?
IV:
1. Sodium nitroprusside
2. Labetalol
3. GTN (1 - 10 mg/hr)
4. Esmolol
Give the major causes of heart failure
- Ischaemic heart Disease (most common)
- Hypertension
- Valvular heart disease (Rheumatic fever in elderly)
- Atrial fibrillation
- Chronic lung disease
- Cardiomyopathy (Hypertrophic, dilated and right ventricular, post viral, post-partum)
- Previous cancer chemo drugs
- HIV
How is infective endocarditis treated?
Endocarditis caused by streptococci eg. Viridans streptococci: benzylpenicillin IV (or vancomycin if penicillin-allergic) plus low dose gentamicin
Endocarditis caused by enterococci eg. Enterococcus faecalis: amoxicillin IV (or vancomycin if penicillin-allergic) plus low-dose gentamicin IV
Endocarditis caused by staphylococci eg. Staph. aureus, Staph. Epidermidis: flucloxacillin (or vancomycin if penicillin allergic or MRSA) plus gentamicin
What underlying pathology is indicated by a sawtooth appearance on ECG? What is the most common aetiology?
Atrial flutter - a form of supraventricular tachycardia characterised by a succession of rapid atrial depolarisation waves
The most common aetiology for this is re-entry circuits around the tricuspid annulus
What is Brugada syndrome?
How does it appear on ECG? What clinical criterion must it be associated with?
A sodium channelopathy which is a cause of sudden death in patients with structurally normal hearts
On ECG: ‘coved’ (concave) ST-segment elevation in V1-V3, followed by T wave inversion
must be associated with one clinical criterion:
- documented v fib or polymorphic ventricular tachycardia
- family history of sudden cardiac death at <45 years old 3. coved-type ECGs in family members
- inducibility of VT with programmed electrical stimulation
- syncope
- nocturnal agonal respiration
High-output heart failure refers to a situation where a ‘normal’ heart is unable to pump enough blood to meet the metabolic needs of the body.
What can cause this? (AAPPTT)
Causes
anaemia (severe)
arteriovenous malformation
Paget’s disease
Pregnancy
thyrotoxicosis
thiamine deficiency (wet Beri-Beri)
How is aortic stenosis managed?
If symptomatic, automatically qualifies for AVR surgery
If asymptomatic, the cut-off for surgery is an aortic valve gradient of 40 mmHg
surgical AVR for low/medium operative risk patients
transcatheter AVR for high operative risk patients
Infective endocarditis in intravenous drug users most commonly affects…
the tricuspid valve
Why is Hypertrophic obstructive cardiomyopathy associated with sudden death in young athletes?
Causes ventricular arrhythmia
How should you treat pulseless VT?
a single shock ASAP followed by 2 minutes of CPR