Professional Documents
Culture Documents
Hx of ISCHEMIC pain:
o Duration --> Minutes to Hours (typically >20-30min; NOT seconds or days)
o Quality --> Sore, dull, squeezing, crushing (NOT sharp or point-like; cannot point at it)
o Location --> 90% substernal (uncommon to left; very rare to right)
o Radiation --> Neck, arm
o Precipitating Factors --> Exertional
o Alleviating Factors --> Rest, nitroglycerine
GORD can worsen with nitroglycerine
o Associated Symptoms
SOB
Vagal symptoms
Inferior wall sits on diaphragm and is in contact with vagus
Inferior wall MI cause vagal stimulation
o N+V
o Bradycardia (also due to 3rd degree AV block in inferior MI)
o Sweating
o Light headedness
o NON-associated symptoms
Positional --> Change with position (? pericarditis)
Pleuritic --> Changes with respiration (? PPPPP)
PE, Pneumonia, Pericarditis, Pneumothorax, Pleuritis
Tender --> Pain reproduced on palpation (? costochondritis)
Examination of ISCHEMIC pain: Not very useful as signs often non-specific or absent
o Vitals: RR, HR (if , ?inferior wall), BP or (>20mmHg difference between arms
present in 70% of aortic dissections)
o Heart sounds: Mostly normal, but sometimes...
Widely split S2 (caused by anything delaying right sided conduction)
Pulmonary HTN
Pulmonary stenosis
RVH
RBBB
Paradoxical S2 (caused by anything delaying left sided conduction)
HTN
Aortic stenosis
LVH
LBBB
S3 Gallop
S4 Gallop
Aortic regurgitation
Mitral regurgitation (papillary muscle dysfunction from posterior wall infarction)
Mx of ISCHEMIC pain:
o First: ECG
ST elevation --> Infarction (STEMI)
Non-ST elevation (i.e. normal or ST depression [ t-wave inversion])
o 4th heart sound Tennessee Early systolic extra sound (imagine split S1)
What is it Atrial systole splashing blood into stiff LV
Causes LVH, AS, HOCM, HTN
Mx Nil (benign), but treat underlying heart failure (and causative condition)
o Murmurs:
AS ejection systolic radiating to clavicle + carotids
MS mid-diastolic
AR early diastolic
MR pan-systolic radiating to axilla
PS ejection systolic radiating to back
Blood Pressure
o BP = CO x SVR
CO = SV x HR
o Normal systolic = 100-160
o Mean arterial pressure (MAP) = ([2xdiastolic] + systolic)/3
E.g. 120/80 = MAP of 93.3
~60 MAP needed for adequate organ perfusion (e.g. 80/50 = minimum)
If hypertensive body used to high pressure and organ perfusion needs ~75 MAP (e.g.
145/80)
Anaesthetists use MAP more than systolic BP as is better estimator of perfusion
ECG
Enzymes:
o Myoglobin Most sensitive EARLY marker (<6hr) for MI (non-specific though)
o CKMB:
Rises: 4-6 hours
Peaks: 12-24 hours
Normalizes: 3-4 days
Hence best biomarker for early re-infarction as 4 days later CK-MB should
be normal, but troponin will still be elevated as it takes 2 wks to normalize
o E.g. Chest pain again 5 days later, troponin useless but CK-MB
helpful
*In these cases, take troponin and TREND IT (you MUST see rise and fall as
this indicates acute condition such as MI; stable trop = artificially raised)
o hsTrop
Allows detection of smaller changes in troponin
Useful as no need for admission + 12hr trop, can measure admission + 6hr trops
Allows quicker decision to be made on diagnosis and quicker intervention
o hsCRP
Detects smaller levels of CRP (i.e. the ones normally reported at <1, this will find)
Clinically significant as some patients may benefit from STATIN therapy if hsCRP
raised (JUPITER trial), but trial done later found no association between hsCRP and
statin therapy benefit (Lancet study Heart Protection Study Collab Grp)
o Echo
TTE
Easier to do
Better tolerated
Better visualisation of ventricles (esp ventricular apex)
TOE
Better visualisation of:
o Posterior structures (e.g. atria, pulmonary veins)
o Left atrial appendage (since transducer positioned against LA)
o Prosthetic valve assessment
Notes
Do not perform echo when patient has pH <7.3 LV does NOT contract
well in acidotic conditions and this will misrepresent their LV function
Indications:
Screening asymptomatic w/ one or more cardiac risk factors
Screening with Framingham risk over 10yr @ 10-20%
Strong FH of pre-mature CAD
How:
Scan for atherosclerotic plaque calcium
Amount of calcium mathematically converted to calcium score
Known correlation between calcium + risk of future ischaemic events
Add in contrast visualise lumen of coronary arteries
Benefits: High negative predictive value for IHD (esp if contrast also used)
Interpretation:
Non-viability on STRESS images, but same area viable on REST images =
likely succeed w/ PCI at recovering function and reducing symptoms
Indications: Medium risk in angina, but ?why this over e.g. echo
Notes: Shows very similar information to echocardiography for the most part, but
has some further specific information (as does Echo)
How:
MR images provide structure AND functional assessment
Add in Gadolinium Some information on myocardial perfusion
o Not in CKD 4/5 risk of nephrogenic sclerosing fibrosis w/ eGFR
<30
Benefits:
Defines anatomy
Can visualise wall motion
With contrast, can visualise infarcted areas
Drawbacks:
Lack of resources and training precludes the use of CMR
Does not tell too much about CAD (CT + MPI + angiography better)
Angiography/Percutaneous Coronary Intervention
o Use: For stent insertion (balloon angioplasty is NOT performed alone anymore)
o Complications of Stents:
Stent thrombosis
1-2% (biggest risk = compliance with anti-platelet Rx, esp clopidogrel),
poor prognosis
First month biggest risk, but any time in first 12mo (esp if stops
clopidogrel)
Presents like acute MI (rapid onset; will not be relieved by GTN)
Higher risk in drug-eluting stent (due to slow endothelialisation)
Rx: GP 2b/3a inhibitor + immediate PCI
o GP 2b/3a reduces morbidity and mortality if used pre-PCI in stent
thrombosis (PasTest)
Restenosis
15%, good prognosis
First 6mo (due to excessive tissue proliferation around stent), but can
occur at any point in lifetime; Also has high risk thrombosis in first month
(just like DES but after 1mo BMS is lower risk and DES still high risk to
12mo)
Presents like recurrence of angina (slow onset; exertional; may be relieved
by GTN)
Higher risk in bare metal stent
Rx: Angina medications + angiogram (+/- angioplasty)
o Types of stents:
Bare metal stent (BMS)
Drug-eluting stent (DES)
Coated with paclitaxel OR sirolimus (AKA rapamycin; inhibit local tissue
growth)
Reduces re-stenosis rates
Increases stent thrombosis rates as slower rate of stent endothelisation
hence why clopidogrel so important
Variations:
o 4% of people have third main stem posterior coronary artery
o Artery dominance:
The artery which supplies the posterior descending artery is dominant
70% right dominant (supplied by right coronary artery)
20% co-dominant (both RCA + circumflex)
10% left dominant (supplied by circumflex)
NB: RCA supplies SA node (60%; also LCX) and AV node (90%; minimally supplied
also by LCX)
Cardiac Action Potential
Common Drugs Used in Cardiology
ACE-I
o Monitoring U+E (prior to Rx, within 2wk of initiation, after increasing dose [as ACE-I gets
titrated up], at least annually)
o S/E Cough, AKI, hyperkalaemia, angioedema (can even be MANY YEARS after initiation!)
Stop if K+ >6
If K+ still >6 post-stopping, advise low K+ diet
B-Blockers
o Selective Bisoprolol, atenolol, Metoprolol (shorter acting, good for rate control in lung
disease where may want to ensure patient does not have SOB related to B-blockade
bronchoconstriction)
o Overdose Rx: First = Atropine; Second = Glucagon (activates adenyl cyclase promoting
formation of cyclic AMP [from cyclic ATP], which causes direct stimulation to heart), also by
increasing BMs (but less imp)
CCBs
o Non-rate controlling (dihydropyridines)
Ideal for >55 w/ systolic HTN
Especially good in angina and PVD
Poor in CCF due to fluid retention (except amlodipine is okay in CCF)
o Rate controlling (non-dihydropyridines)
Types:
Verapamil
Diltiazem
How they work:
SA + AV node rely mainly on slow calcium channels for depolarisation
Ca channel blockade = even slower depolarisation = reduced HR
I.e. reduce frequency of impulse (whereas e.g. flecainide slows Na channels
used for conduction, so flecainide slows velocity of impulse)
Diuretics
o Furosemide For fluid off-loading
Can cause ototoxicity if given in high doses (e.g. >2 GRAMS/day)
o Thiazides (e.g. HCTZ) Previously used for HTN, but now thiaz-like preferred (indapamide +
chlorthalidone; still later options)
S/E Gout, impaired glu tol, hypokalaemia, hyponatraemia, hypercalcaemia
Hypokalaemia caused by:
o 1) Increased sodium in tubules makes the Na/K exchangers more
active (resorb Na, excrete K)
o 2) Increased flow in distal tubule + collecting duct = K+ washes
away
Spironolactone
o Use: CCF, cirrhosis (large doses), hyperaldosteronaemia (i.e. Conns), HTN (4 th line)
o Mechanism: Aldosterone antagonist acting at the DCT (and partly CDs)
o S/E: HyperK, gynaecomastia
o Notes: RALES trial NYHA 3+4 and already on ACE-I would benefit from low dose spiro
Digoxin**
o How does it work:
Blocks Na/K ATPase (by preventing hydrolysis of the ATP)
The increased intracellular sodium consequently causes intracellular calcium (by
way of the Na/Ca exchange) Positively inotropic
AV blockage Negatively chronotropic
o Indications: AF (1st if CCF present), CCF (late, but 1st line if also has AF), SVT (children)
Amiodarone
o Indications: Atrial, nodal or ventricular tachycardias
o SEs: Hepatitis, pulm fibrosis, skin discolouration in sun (slate grey appearance), thyroid,
peripheral neuropathy, bradycardia, thrombophlebitis, corneal deposits, LQTS (anything that
blocks K+ channels will do this)
o Monitoring:
Monitor TFT, LFT, U+E, CXR prior to Rx
Check U+E prior as ?hypokalaemia (if present, increased risk arrhythmia)
Monitor TFT + LFT 6-monthly
o Notes:
Do NOT give with TCAs (risk of long QT, VT, VF, TdP); half the dose of digoxin (as
both affect K+)
Long half-life (up to 3mo) hence need for carbimazole in AIT type 1, also drugs can
interact even up to 3mo after stopping amiodarone!
Give in central vein (otherwise risk of thrombophlebitis)
Sotalol (class III anti-arrhyth NB: B-blockers are class II; this is class III along with K+ recept blockers)
o Increase refractory period hence slowing heart rate (like amiodarone as same mechanism)
o Used in AF when standard beta-blockers not effective
o The only anti-arrhythmic (perhaps also amiodarone) which may cause LQTS + TdP
Flecainide
o Blocks sodium channels so slows conduction velocity
o Indications AF (rhythm control), SVT w/ accessory pathway (e.g. WPW)
Do NOT use flecainide in WPW if there is any doubt of ?WPW ?VT (also do NOT use
any AV node blocking drugs esp verapamil)
o S/Es Neg inotropy, neg chronotropy (bradycardia), proarrhythmic, oral paraesthesia,
visual disturbances
o CI Post MI, structural heart defects
Clopidogrel Blocks platelet ADP receptors (P2Y12 ADP receptor) inactivates platelets
o Use: MI, Stroke, TIA (RCP favours this over A+D), PVD (1 st line now)
o Other similar drugs: Prasugrel, ticagrelor, ticlopidine
o Interactions: PPI (omeprazole, but lansoprazole is OKAY)
Adenosine
o Use: SVTs (if asthma, use IV verapamil)
o Dose: 6mg, 12mg, 12mg
o Mechanism: Transient AV node block via A1 receptor agonism (leads to hyperpolarisation by
creating outward potassium flux); but has short half life (8-10s)
o S/E: Chest pain (+feeling impending doom), bronchospasm, worsens WPW + access pathways
o Interactions: Dipyridamole enhances effect (inhibits the uptake of adenosine into platelets,
hence increasing extracellular concentration; caused prolonged arrest of rhythm!),
aminophylline reduces effect (will have minimal effect at AV node)
Nicorandil
o Mechanism: Nitrate + potassium channel activator
Ivabradine
o Effect: Reduce HR
o Use: Angina (once BB/CCB failed)
o Mechanism: If (funny current) inhibition
Funny current seen in SA + AV nodes
They help regulate the cardiac pacemaker activity
o S/E: Visual symptoms (e.g. luminuous phenomenon), bradycardia
Cholesterol lowering drugs
Physiology
o Cholesterol
Production: Made from steroids + fat in complex process starting w/ HMG-CoA Redu
Aim (total cholesterol): <5mmol/L (only have targets in SECONDARY prevention)
Average in UK: 5.9mmol/L (80% >50 = higher than 5)
Target when on therapy: TChol <4mmol/L, LDL <2mmol/L
o Triglycerides
Production: Ester + 3 fatty acids (both attained from e.g. oil + all sources of fat)
Transport: From intestine to liver + muscle + adipose tissue via chylomicrons
>6 = Risk of pancreatitis, retinal vein thrombosis
>10 = Use fibrates ONLY if isolated (i.e. no hypercholesterolaemia, otherwise statin)
o Lipoproteins (transferring cholesterol and triglycerides in blood)
HDL Collect cholesterol from body tissues + return to liver (good cholesterol)
LDL Carry cholesterol from liver to cells of body (bad cholesterol)
IDL Between LDL and VLDL, not detectable in blood
VLDL Carry newly synthesised cholest + triglycerides from liver to adipose tissues
Chylomicrons Carry triglycerides from intestines to liver + muscle + adipose tissue
NB: Pts will be heterozygotes; homozygote is rare and usually die of MIs in teens
Statins
o Mechanism Reduce hepatic cholesterol synthesis by blocking HMG-CoA reductase =
increased uptake of LDL from blood to the liver = less delivery of cholesterol to body cells =
less atheroma
HMG CoA Formed from acetyl CoA + acetoacetyl CoA; converted to mevalonate
by HMG-CoA reductase (target for statins)
TChol:HDL >6
o Initiation
First Simvastatin 40mg OD (20mg if increased risk myopathy) OR start with
Atorvastatin immediately (NICE 2014 Lipid Modification Guidelines)
TChol >4 or LDL >2 despite Simva 40 Simva 80mg
o MHRA risk myopathy with Simva 80mg
Failure of Simva 80mg Atorva +/- ezetimibe
Intolerant Pravastatin 40mg OD
*Take at night as they have slightly greater effect then as most cholesterol synthesis
occurs at night
Hepatitis Discont if LFTs 3x norm range, otherwise continue + rpt LFT in 1mo
Nicotinic Acid Best for raising HDL (use when statin working but HDL still too low); limited
by its side effects (flushing, impaired glucose tolerance, myositis) so often not used
Orlistat Block pancreatic + gastric lipase (causes lack of fat digestion) may cause steat
(can get OTC)
Indications BMI >28 + risk factors CVD, BMI >30 alone, Wt loss on Rx 5% at 3mo,
use for <1yr
JVP
Definition: Indirect measure of central venous pressure (CVP) using the internal jugular vein (IJV)
Waveforms:
o A Pre-systolic; Produced by right atrial contraction
o C Early systole; Closure of tricuspid valve (not normally visible)
o X Descent Atrial relaxation (occurs whilst ventricles contraction)
Atria opens so negative pressure sucks blood in causing descent of JVP
o V Late systole; Increased blood in right atrium from venous return
o Y Descent Opening of tricuspid valve
Blood exits atrium into ventricle allowing JVP blood to descend and fill atrium
Diseases:
o A Wave
Absent A waves AF
Large A waves Tricuspid stenosis (RA contraction against a partially closed valve)
Cannon A waves CHB + VT (RA contraction against a fully closed valve, occur randomly)
o Prominent/Giant V Waves TR
Notes:
o The double waveform seen is a result of the A + V waves
A occurs before pulse
V occurs toward end of pulse
Definition: Indirect estimate of LA pressure to determine if heart is being adequately filled with blood
Method:
o Swan-Ganz catheter (two ports, one balloon)
o Insert into peripheral vein
o Advance catheter to RA RV Pulm art Branch of pulm art
o Pressure tranducers record pressures in:
Branch of pulm art (distal port) ~25/10mmHg
RA (proximal port) ~0-3mmHg
o Balloon is then inflated to STOP pulmonary flow, and after few seconds atrial backflow
(which has the same pressure as the LA) reaches the distal port (ahead of the balloon) and
that pressure can be recorded to identify LA pressure ~8-10mmHg
This LA pressure = PCWP
It will have arterial saturations
It should be close to the same pressure as the LV diastolic pressure
Uses:
o Severity of (all give LA pressure and therefore PCWP)
LVH
AS, AR, MS. MR
*Normal = 8-10mmHg
*Can guide the use of therapy e.g. nitrates, frusemide; more fluids
Background: Cardiac output is not the same for all individuals, it is based on body size
Pathogenesis of MI:
o Atherosclerosis breaks off to expose inside of plaque
o Platelets adhere to exposed plaque and block artery
o Platelets stabilised by fibrin (made from fibrinogen)
Fibrin lysed by plasmin (made from plaminogen which is activated by Tissue
plasminogen activator [TPA]) unless F13 (clot stabilising factor) acts on clot
Fibrin = Creator (Brahma); Plasmin = Destroyer (Shiva); F13 = Preserver (Vishnu)
o Drugs used:
Aspirin + Clopidogrel Prevents further aggregation of platelets (pre-fibrin)
TPA Breaks the fibrin meshwork to bust clot (pre-factor 13)
Angioplasty Compresses clot (post-factor 13)
o Diagnose:
First:
ECG (normal, unless in episode... ?q-waves, ?LBBB, ?LVH, ?ST depression)
Bloods (cardiac risk, anaemia, TFTs, troponins)
o Cardiac MRI
*NB: Note exercise ECG is NEVER used anymore for investigating new chest pain (NICE guidelines)
o Treat: ALL PATIENTS GET CARDIAC REHAB
o Medical: Prior to angiography (in many cases)
Acute chest pain: GTN x3 doses spaced 5min apart after 3x/15min seek help
Chronic disease management:
Risk factor modification: Aspirin, Statins, ACE-I (if diabetic)
NB: ACE-I provide benefit in ANY coronary artery disease, irrespective of LVH,
beyond just BP control (HOPE study)
NB: Aspirin is the single most important intervention for stable angina
FOR ANGINA
First line: B-blocker/atenolol 50mg OD (most important) + GTN (PRN)
o If B-blocker CId: Rate limiting CCB (e.g. dilt/verap monoRx)
Second refractory to low-dose BB: Increase BB/atenolol 100mg OD
Third refractory to high-dose BB: Add CCB (e.g. nifedipine MR)
Fourth if still refractory: Add one of the following (sometimes 2)
o Long-acting nitrate (e.g. ISMN + ISDN)
Tolerance builds easily, may need to take more regularly if
this occurs (i.e. instead of 12 hours apart, take two doses 8hr
apart) not seen in ISMN MR, just the non-MR version
o Ivabradine (Funny current inhibitor in sinoatrial node)
o Nicorandil (coronary artery dilation via NO + K+ ATP agonism)
o Ranolazine (reduced myocardial ischemia)
o Definitive: Angiography (if medical failure [refractory to CCB stage], stress test pos [e.g. 30-60%
risk w/ MPS/Echo] OR high risk CAD [60-90% Framingham risk])
Aim Reduce angina (NOT to reduce mortality or future MI)
Complications:
o Neurology (due to CardioPulm bypass)
o Cardiac tamponade
Features: As per tamponade
Ix: TOE
Pericardial effusions may be loculated to posterior
aspect of heart, therefore TTE cannot reliably
exclude diagnosis as only TOE can see posteriorly
Rx: As per tamponade
o Haemolysis (sheer stress due to bypass system)
Features: As per anaemia
Ix: Raised unconj bilirubin, NORMAL other LFTs,
schistocytes
NB: Right heart failure gives you only direct
hyperbili and raised ALP
o Notes:
Exercise stress test w/ ECG:
Should not be done on b-blockers as cannot reach target heart rate
Should not be done on digoxin as normally causes -sloping ST segment
A down or horizontal sloping ST segment is WORSE than an up-sloping ST
segment
ST elevation or depression should be measured 80ms AFTER the J-point, as
tachycardia induced J-point depression and this is NORMAL
o E.g. young man with strong FHx, exercise test, ECG shows 1-2mm
J-point depression at 120bpm NORMAL test.
Considerations for stenting:
Distal vessels must be adequate
LV EF% must be intact (or else no improvement will be seen)
ECG EXERCISE TESTING HAS POOR SENSITIVITY AND SPECIFICITY AND NUMEROUS LIMITATIONS... CENTRES
NOW ARE PREFERRING TO DO CT Ca SPECT/Echo/MRI Angiography
Acute Coronary Syndrome (ACS)***
Symptoms of ALL: Substernal chest pain (enough to consider ACS) for >15min anytime in last 9hr
o See first section (above) for further symptoms + signs
Signs:
o S3 or S4
o Pan-systolic murmur (new)
MR Posterior MI causing chordae rupture
VSD LAD MI causing septal infarct
o N+V+Sweating+Bradycardia Inferior MI causing vagal stimulation/CHB
o All STEMIs
Diagnose: ABCDE + ECG + O2 (if <95%) + Fluid... then begin Rx (as below)
o First: ECG (NB: Arrival-to-ECG time = 10min)
UA + NSTEMI:
ST depression >1mm
T wave inversion >2mm in 2 adjacent leads
Normal ECG
STEMI 1mm in 2 adjacent limb leads (2mm in chest leads)
Notes
Pure lateral infarcts often only affect the limb/augmented leads (I, aVL,
sometimes also II); likely anterolateral if any of V4-6 affected
o Second: Troponin T/I (UA from others) If ST-elevation, troponin does not guide initial Mx
Detectable at 3-6hr (take on admission and at 12hr post-onset)
Peak 12-24hr (6-12hr with hsTrop)
Remain raised up to 10-14d
Since can be artificially raised, if this is thought then you should TREND the troponin
and expect to see a rise and drop (indicated acute rise of trop e.g. MI)
Released most often in response to ISCHAEMIA, but INFARCTION will raise it highest
Troponin CAN be elevated in 30% of UNSTABLE ANGINA (poorer prognosis, this is
basically NSTEMI though)
Troponin levels are PROGNOSTIC higher = worse prognosis = higher chance death
o Other Full bloods inc random glucose, random lipids, CXR, Echo, Angiography stenting
TO DIAGNOSE STEMI, NEED 2/3 (Cardiac Chest Pain, ECG findings, Troponin rise) [WHO Guidelines]
BEFORE STARTING TREATMENT IN UA/NSTEMI, ASSESS RISK: GRACE score (NICE recom)
o Factors assessed Age, HR, SBP, Degree of CCF (if any), Creat, Arrest on admission?, ST
changes?, Trop raised?
o Interpretation
Depends on whether STE or NSTE
Predicts in-hospital mortality AND post-discharge mortality
NSTEMI 6mo mortality of 3% = high risk = needs angiography in <96hr
Aspirin 300mg
o Start whilst history being taken! Do NOT wait for ECG
o Followed by 75mg Aspirin maintenance dose (continue lifelong)
o Do NOT use if aspirin allergy, use clopidogrel alone; beware of dissection
Clopidogrel 300mg not for angio [UA, some NSTEMI], 600mg for angio [STEMI,
some NSTEMI] (cont 12mo in ALL patients with DES; 1mo BMS; stop before major
surgery but contact cardiologist first [risk stent thrombosis])
o Followed by 75mg Clopidogrel maintenance dose (continue for 12mo)
o NB: PPIs, particularly omeprazole, interact with clopidogrel
Stop and replace with PO Ranitidine 300mg BD (e.g. if GORD)
Use lansoprazole if treating gastric ulcer
o Relevant trials CLARITY (proved 300mg effective), COMMIT (proved
75mg also effective, but less so than 300mg)
o May be soon replaced by Ticagrelor
Heparin
o If no thrombolysis planned <24hr LMWH (Fondaparinux 2.5mg OD
x8d)
Not if eGFR <20 or creat >265
If Trop neg at 12hr + pain free + no ECG changes STOP
NB: Enoxaparin also improves morbidity + mortality
o If thrombolysis likely in 24hr:
UFH (can reverse with PS)
Abciximab or Eptafibitide (GP 2b/3a inhibs)
Omega-3-acid ethyl esters (Omacor) All post-MI patients who do NOT eat 2-4
portions of oily fish/wk
o Reduce risk of ventricular arrhythmias, especially after anterior MI
(Eplenerone if CCF post-MI; start within 3-14d post-MI ideally after ACE-I started,
?convert to spiro after 14d post-MI)
(No driving for 4 weeks post-MI)
If intermediate/high risk (GRACE Score >3% 6mo mortality) OR ongoing chest pain: If in DGH
call primary centre as per STEMI protocol
<96hr: Angioplasty (NB: if GRACE 6mo <3% then angio can be done after 96hr!)
o NB: Even NSTEMI needs inpatient angiogram (+/- angioplasty) prior to
discharge EVEN if low risk and often within 5d
STEMI:
o Acute:
Immediate: Should take aspirin, ADP-receptor blocker (e.g. clopidogrel, prasugrel, ticragelor),
injectable anticoagulant (ideally bivaludin, NOT LMWH), and if being transferred GP 2b/3a
inhibitor (e.g. tirofiban, Abciximab) ESC guidelines
Definitive: TPA (not as good) or Angioplasty (better) But SAME efficacy if <2hr, PCI better
if >2hr despite extra time needed for transport from DGH to PCI centre
*TPA <12hr from onset + <30min from door, PCI <90min from door
Prognosis: 10% risk of death in next 12mo following an MI, and there is a 5% chance of death for any given
person in each year thereafter (use GRACE score for mortality in 6mo post-discharge)
Ways to get angioplasty
Stable angina with very high Framingham risk
Stable angina with positive exercise test who get angiogram with 1-2 vessel disease (3+ vessel = CABG)
UA/NSTEMI with low risk who then get follow up with exercise test (positive), angiography (2 vessel)
UA/NSTEMI with med-high risk (3% 6mo mortality on GRACE score)
STEMI
Complications of ACS: DIM PTT
o Dysrhythmia NB: RCA supplies both SA and AV node! Occur within first 48hr
Slowing:
SA node dysfunction Bradycardia; SSS (RCA 75%, LCX 25%)
Quickening
Supraventricular tachys (Rx: Adenosine IV Verapamil if asthma)
o NB: Do NOT treat asymptomatic heart failure (i.e. low EF, no symptoms)
except with ACE-I (only one which shows mortality benefit)
E.g. patient has MI, then echo shows low EF but asymptomatic
do NOT give frusemide
Cardiac rupture
Septal rupture (O sats from RA to RV [as RV+LV communicating], pulm oedema)
Valve rupture (MR in posterior leads to pulm oedema)
o Pericarditis
Pericarditis; <48hr post-MI (often after transmural MI 10% of these patients)
Dressler Syndrome; 2-12wk after MI NSAIDs, aspirin, steroids
Can lead to cardiac tamponade
o Psychosocial
Depression
ED (1. Psychosocial, 2. B-blocker therapy)
o Thromboembolic (mural thrombus clot forms in weak heart wall outpocket) LMWH
Low BP post-MI
+JVP, +pulm oedema Acute CCF/LV dysfunction, Acute VSD, Acute MR, tamponade
+JVP, -pulm oedema 3rd deg AV block (cannon A-waves), Tamponade, PE, RV infarct
-JVP, -pulm oedema Bleeding, dehydration
Posterior MI
Pathology: RCA branches (70%), or sometimes LCX (if left dominant [20%] or co-dominant [10%])
ECG changes: Look at leads V1-V3... V2 is the most important
o Dominant and slightly wide R waves (also seen in RVH, WPW)
o ST segment depression
o Upright T wave in V2 If inverted ?RVH
Notes: There is no such thing as a pure posterior MI you MUST have either an inferior MI with
posterior extension, or lateral MI with posterior extension (depending on which forms the dominant
circulation the right heart with RCA or left heart with LCX posterior MI is a distal occlusion of these
vessels)
o The ST elevation seen in a posterior MI e.g. in the inferior leads is truly an inferior STEMI, not
just reciprocal changes
o Reciprocal changes themselves represent ischaemia (even in e.g. anterior MI getting
reciprocal inferior changes) and signify worse MI reciprocal changes are NOT just an ECG
phenomenon (they signify ischaemia in a different territory)
Anterior (LAD)
o LVOT Obstruction
o LV mural thrombus
o LV aneurysm (which may cause persistent anterior ST elevation)
o Ventricular septal rupture
o Pericarditis (Dressler = 2-12wk post-MI)
o Heart block (less common than inferior, but if HB associated with ant MI = much worse as
more extensive area of myocardium damaged; hence MUST pace [inc temporary pacing]
even if asymptomatic + stable)
Inferior (RCA)
o RV infarction (1/3 of inferior MI = RV infarction = RVHF = pre-load = shock)
o MR (RCA supplies chordae tendinae + papillary muscles)
o Heart block (all degrees; RCA supplies AV node via AV nodal branch)
More common than anterior MI CHB, can also occur if LCX supplies AV node (some
patients)
Do NOT need to temporary pace if asymptomatic + stable
o Bradycardia (vagus stimulation, sick sinus syndrome [RCA supplies SA node also], CHB)
o N+V (vagus stimulation)
Prinzmetal Angina Coronary vasospasm, occurs at rest (usually smoker from sleeping)
o Risk: Age, smoking
o Features: Rest chest pain usually occurring during sleep, often in smoker
o Diagnose:
First: ECG (ST!)
Best: Angiogram (clean coronaries)
Can use ERGONOVINE or intracoronary ACh to stimulate spasm (should not
happen in normal patients)
o If no vasospasm ?cardiac syndrome X
If stress test was done, would be normal too
Takotsubo Cardiomyopathy AKA Stress Cardiomyopathy AKA Apical Ballooning Syndrome AKA
Broken Heart Syndrome
o Definition: Transient systolic dysfunction of the apical and/or mid-segments of the LV that
mimics MI, but in the absence of CAD
NB: Takotsubo = Octopus trap (has a similar shape to the apical ballooning)
o Epidemiology: Women account for at least 90% of cases (possibly 100%), mostly post-
menopausal
o Triggers:
Significant illness
Physical stress
Emotional stress (e.g. death of relative, shocking news, domestic abuse, arguments,
financial losses, etc)
o Ix:
ECG ST elevation which often does NOT mimic single vascular territory, but many
Echo
Regional wall motion abnormalities (RWMA) extending beyond a single
vascular territory, which is likely to be transient
May see apical mid-segment ballooning, but not always as may have
disappeared
Angiogram Clean coronary arteries (smooth, no occlusions, little-to-no CAD)
o Theories:
Ischaemic: Abnormal coronary microvasculature
Non-ischaemic: Altered cardiac pain perception + hypersensitivity
Pathology: Tear in intima hematoma within aortic wall which extend in either direction
o Commonly 2cm from aortic valve, or distal to L subclavian in descending aorta
o Most prevalent in 50-70
Worrying Affects aortic root can track blood into the pericardial space leading to cardiac
tamponade and death
o Type B (AKA Debakey III) Does NOT affect ascending aorta at all (distal to L subclavian; 30%)
Risk factors: Cardiac risk (esp poorly controlled HTN, biscuspid aortic valve), connective tissue disorders
o Many begin with an aneurismal aorta
Features: Sudden, severe ripping/tearing/sharp chest pain radiating to back in a 60yr old, AR murmur
o NB: Pain is maximal at time of onset, MI gradually gets worse (and is dull)
o NB: Pain migrates as dissection progresses
o May get (proximal to distal): Aortic regurgitation, Cardiac tamponade, Angina (coronaries involvement),
Stroke-like symptoms, Distal limb ischemia (back pain, mesenteric ischemia, AKI, claudication...)
o May get Horners syndrome (mass effect of dissection causing sympathetic nerve blockage)
Ix:
o ECG (MI or ST-depression changes) May lead wrongfully to thrombolytic therapy!!
o CXR (widened mediastinum in 80%)
o TOE (very good and may be done in anaesthetic room/ITU [rather than in radiology])
o Best: CT/MRI Confirms diagnosis and vessels involved
Must be done in radiology where support is poor patient MUST be stable!
CT scanner = Tube of Death ONLY for stable patients
NB: Lumen of dissection can extend from aortic arch to iliacs!
o Third definitive: Surgery endovascular repair, graft stenting, inc stenting of branch vessels
Grafting performed via median sternotomy + cardiopulmonary bypass
Defective aorta removed and replaced with graft
Aortic valve spared if possible
NB: Type A vs Type B Type A always requires surgery, type B often medical (BP control)
Surgery in type B has risk of paraplegia, so medical Rx first
Surgery for type B if aortic RUPTURE, limb ischaemia, unrelenting pain
Symptoms:
o Left sided SOB, cough (pink frothy), PND + Orthop
o Right sided Ankle swelling, nocturia
Signs:
o Left sided:
Cardiomegaly
End inspiratory crackles
Dull lung bases
Pulsus alternans (varying strong/weak beats; a sign of LV systolic dysfunction and poor
prognosis, usually associated with 3rd heart sound) do not confuse with electrical alternans
of cardiac tamponade
o Right sided:
JVP
Dependent oedema
Hepatomegaly ascites
Ix:
o Acutely:
First: ECG Rule out arrhythmias
If in arrhythmia, correction of this = fastest correction of cardiac output
Second: CXR
Alveolar oedema (extending from hila)
B lines (Kerley) Horizontal lines @ bases = fluid btwn lobules (not lobes)
Cardiomegaly
Diversion of blood to upper lobe vessels (prominent upper lobe vessels)
Effusions (pleural) Meniscus sign
*Lateral/decubitus X-ray = more sensitive than CXR for effusion
Third: Echo (as inpatient)
Third: PCWP (will guide whether fluid can be given and how to give diuretics)
o Chronically: All patients get ECG first, and baseline bloods + CXR can be done
If previous MI: Echo in 2wk LV syst + diast func, LV thickness, valve disease
Normal (BNP <100): Heart failure unlikely, consider other diagnoses (NICE
recommends BNP as a test to rule out CCF i.e. good NPV)
*BNP/NT-ProBNP aids diagnosis AND risk stratification, but mainly used in primary
care (funded there, but not in hosp costs 15 in hosp)
*Released in response to LV strain
*Very good marker of prognosis
*Very good NEGATIVE PREDICTIVE VALUE (but poor PPV)
*Raised levels also seen in AKI/CKD, MI; reduced with ACE-I/ARB
*Effects Vasodilate, diuretic + natriuretic, suppress RAAS + sympathetic tone
***Must ALWAYS ask... what precipitated this episode of decompensated heart failure?***
Common things are Worsening ischemia/MI, additional valvular dysfunction, infection, arrhythmia
Complications:
Asymptomatic hypotension = Do NOT change drug
Symptomatic bradycardia = Half dose
2nd or 3rd deg HB = STOP
*NB: Beta-blocker therapy usually comes AFTER ACE-I initiation (usually
when ACE-I are beginning to be titrated up in dose CBIS-III trial)
o Hydralazine + Nitrate (symptomatic control for Type III and IV, but of
PROGNOSTIC benefit in black people!)
NB: All calcium channel blockers (except amlodipine) and NSAIDs + COX-2 inhibitors are contraindicated in CCF
NB: Ideal to increase all medications to maximum dose, but this may be limited by S/Es (most importantly hypotension and
bradycardia) and hence cannot achieve maximum doses
If still refractory, Type III + IV:
Digoxin 125mcg (62.5mcg for elderly) (however, strongly indicated if also in AF but
still NOT before B-blockers [as B-blocker have MORTALITY benefit]! )
o K+ = Dig activity; K+ = Dig toxicity
o Dig very effective at slowing HR, but NOT during exercise (however B-
blockers ARE good even during exercise)
o Works via reduced AV conduction, increased LV contraction (inhibition of
Na/K ATPase), vagal stimulation
o Rx:
First: Stop drug, K+ replacement
If CNS/ECG change: Digibind (Antibods)
Ivabradine (inhibits funny current and slows down heart through different
mechanism than B-Blockers)
o Definitive/Surgical:
Biventricular pacing/Cardiac resynchronisaton therapy ICD
Indication: All must be met
o Maximal medical Rx in NYHC Stage 3/4
o EF <35%
o Prolonged QRS (>120; particularly with LBBB) or observed dyssynchrony
Notes:
o Bivent pacing/CRT-P for dyssynchrony (one lead in RV, one lead in
coronary sinus to pace LV)
o ICD for poor EF
o Can combine CRT + ICD (CRT-D) if suitable for both, but if only suitable for
one then ONLY do that one (rather than prophylactically putting in CRT-D)
PCI, CABG
Valvular correction
Mitral Stenosis** mid-to-late diastolic rumbling murmur best heard with bell in left lateral position
o Cause:
Rheumatic fever (most common; usually in immigrants see below)
SPECTRUM: Strep pyo pharyngitis Scarlet Fever Rheumatic fever
Degenerative calcification
o Ix:
First: ECG
LA enlargement; + RV + RA enlargement due to pulmonary HTN
A-Fib
Second: CXR
LA enlargement Straightening of right heart border + lifting up of left
main stem bronchus
Third: Echo
Diastolic mitral flow murmur, thickened mitral valve leaflets, LA dilatation
If asymptomatic but significant murmur, follow-up every 2-3yr
Fourth: Cardiac MRI (rarely needed)
Best: Angiography (rarely done)
o Rx:
Conservative: Salt restriction Pre-load
Medical:
Diuretics OR long acting nitrates Pre-load, relieve SOB
B-blocker OR rate-limiting CCBs Improve exercise tolerance
Anticoagulation (based on CHADSVASC) if A-Fib
Surgical:
First: Percutaneous Mitral Commissurotomy (PMC AKA valvuloplasty)
o Insert catheter into vein RA Puncture septum Enter LA
Balloon valvuloplasty of MS
o Contraindicated in LAA clot (risk of breaking off embolism)
If not candidate for PMC: Valve Replacement
o Notes:
Swan-Ganz right heart catheter can suggest mitral stenosis
Normally PCWP = LV diastolic pressure; if PCWP is
higher (i.e. >5mmHg different) then indicates
mitral stenosis
Results also show pulmonary HTN (RV-to-pulm art
pressure rises, and pulm art pressure more than
20% of SBP), and aortic stenosis (LV-to-aortic
pressure has gradient >25 [it is 75 = very severe])
Mitral Regurgitation** Pan-systolic murmur + radiation to axilla; soft S1, wide split S2, S3 present
o Types:
Primary Intrinsic lesions affecting the valve
Degenerative (most common)
Ischemia (i.e. posterior MI causing chordae rupture)
Infective endocarditis (mitral = most common valve affected in non-IVDU)
Secondary Secondary to left ventricular defects
LV enlargement
o Pres:
Acute MR (e.g. posterior MI) SOB, cough
Rapid pulmonary oedema life threatening, needs emergency valve repair
o Ix:
First: ECG
LVH + LA enlargement
Second: CXR
Cardiomegaly
Third: Echo
Systolic mitral flow murmur, LA and/or LV dilation
Fourth: Cardiac MRI
Best: Angiography (rarely done)
Other: On examination, isometric exercise tests (e.g. handgrip exercises) make the
MR murmur WORSE but make the AS, MVP and HOCM murmurs BETTER! Standing
makes the MR murmur better.
o Rx:
Medical: Can use nitrates, diuretics, sodium nitroprusside
First: ACE-I if CCF present (pulmonary congestion, pre-load = CO)
o Beta-blockers, spironolactone also appropriate
o Epidemiology: Very common (3% of population, more in females) risk for developing MR
Risk factors for developing MR >50, HTN, obese, thick mitral leaflet, AF, big LA...
o Cause: Dilated mitral annulus; often leaflets are thickened; associated diseases are:
Marfans (NB: dilation of aortic sinuses/AR is the most common defect in Marfans)
Ehlers-Danlos
Osteogenesis imperfecta
PCKD
o Ix: ECG, CXR, Echo (systolic displacement of mitral leaflets), Cardiac MRI, Angiogram (rarely)
o Rx:
Low risk of developing MR: Symptomatic treatment (e.g. b-blocker for panic)
High risk of developing MR: Surgery Valve repair annuloplasty
Valve repair involved leaflet resection
Annuloplasty makes annulus SMALLER, leaflets re-join
This procedure is NOT percutaneous
o Complication:
Endocarditis (3-8x relative risk)
Stroke (rare)
Arrhythmia + Sudden death
Aortic Stenosis** Ejection systolic murmur + radiation to carotids/clavicle; S2 single or paradox; S4
o Cause:
Young <65:
Bicuspid valve (present in 1% of population)
Williams syndrome (supravalvular aortic stenosis)
HOCM (subvalvular aortic stenosis)
Rheum fever (mitral more common)
o Pres - SAD: Syncope, Angina (most common), Dyspnea, CHF (worst prognosis)
Asymptomatic <5% incidence of death per year
Angina 5 year median survival
Syncope 3 year median survival
CCF 2 year median survival
*Once symptoms appear, the prognosis is POOR; When asymptomatic, good prog
o Examination findings:
Slow-rising (small + late) pulse... AKA pulsus parvus et tardus
Narrow pulse pressure (syst + diast BP close together)
Diminished S2 = severe AS... A2 is normal/loud in aortic sclerosis
BOTH stenosis and sclerosis radiate to carotids!
Aortic sclerosis is MORE COMMON in population than stenosis!
Presence of S4 (marker of severity)
o Ix:
First: ECG LV Hypertrophy
o Method
Peripheral access e.g. via femoral artery
Bring new valve into centre of existing stenotic aortic
valve
Blow up balloon with new valve around it so native valve
gets compressed against endothelial walls
New valve now expanded (and native valve compressed)
and new valve functional
Severity: Loss of S2, slow rising pulse, narrow pulse pressure, BP, radiating murmur
Aortic Regurgitation** Early diastolic murmur (at LLSB)
o Cause:
Cardiac enlargement HTN, IHD
Congenital bicuspid aortic valve (commonest congenital)
Infective Tertiary syphilis, infective endocarditis
Rheumatological AnkSpon, ReA, SLE
Aortic dissection
o Ix:
First: ECG LV Hypertrophy
Second: CXR LV or Aortic dilatation
Third: Echo Dilated LV and/or aorta, LV volume overload
Fourth: Cardiac MRI
Best: Angiogram
o Rx:
Conservative: Salt restriction
Medical:
ACE-I (if hypertensive, LVH present, or cannot tolerate surgery)
B-blocker (only if Marfans as it slows aortic root dilation)
Surgical: Valve replacement
Indications:
o Acute AR (esp w/ poor LV function - Sx should be done urgently)
o Symptomatic despite medical therapy
o Asymptomatic with LV dysfunction (EF <55%)
AR should have EF; EF = decompensation
MS AS MR AR MVP
Cause Rheumatic Young: Bicuspid Ischemia Ischemia Congential
Fever valve (dilation) (connect tissue)
HTN
Old:
Calcification
Key Findings Mid-Diastolic Ejection systolic Pan-systolic + Early diastolic Pain,
+ radiation to radiation to Palpitations,
Emboli/stroke carotids axilla S3 in Panic attacks,
decompensation SyncoP
Hoarseness S4 gallop; S2 S3 w/ soft S1
single or and widely split Wide pulse Mid-systolic
Dysphagia paradoxical S2 pressure click
No
cardiomegaly
Rx Salt restriction Valve Salt restriction Salt restriction B-blocker
+ Replacement + +
Diuretics TAVI First: ACE-I First: ACE-I NO DIURETICS!
(if symptoms)
Surgical: If refractory: If refractory:
Balloon If unsuitable for ARB then other ARB then other
Valvuloplasty or surgery vasodilator vasodilator
Valve balloon therapy therapy
Replacement valvuloplasty
(re-stenosis in Surgical: Valve Surgical: Valve
6-12mo ) repair or replacement
replacement
Bioprosthetic Valve (Bovine or Porcine) = For older people = WARFARIN x3mo, then ASPIRIN ONLY
Mechanical = For younger people = WARFARIN + ASPIRIN LONG-TERM
Tricuspid Valve Disease
Epidemiology:
o Less common than aortic and mitral
o TR > TS
o TR usually associated with pulmonary HTN secondary to MS or MR
o Features: General signs of right and left sided heart failure (esp right)
LARGE A wave (JVP upstroke due to contraction against relatively closed tricuspid)
NB: NOT Cannon A waves (this is seen in complete heart block)
o Rx:
Medical: Treat symptoms (e.g. of endocarditis, heart failure, arrhythmias)
Surgical: Valve replacement (cannot repair as leaflet tissues not compliable)
o Features: Often asymptomatic unless with pulmonary HTN Signs of right/left heart failure
Giant V wave (more blood in venous system following systole, but cannot fill atrium
as already filled with regurgitant blood hence prominent V wave)
cV = cardiovascular wave
V = ventricular wave
*Same thing
Rapid y-descent (blood rushing into ventricle from previously high pressure V wave
causes rapid Y-descent)
Pulsatile liver in systole
o Rx:
Medical: Treat symptoms (e.g. of endocarditis, heart failure, arrhythmias)
Surgical: Valve Annuloplasty (preferred) or Valve replacement (if severe, rare)
Pulmonary Valve Disease
Epidemiology:
o Rare
o Congenital defects most common cause of PS or PR
o Features: In neonates
SOB, syncope, heart failure (right and left)
Cyanosis dependent on degree of PS
Parasternal heave
Sometimes prominent/cannon A waves (due to severe backlogging)
o Rx:
Medical:
ABCDE resus + knees to chest (increase pulm circ in ToF)
Prostaglandin E1 (keep PDA open)
Surgical: Balloon valvotomy
Pulmonary Regurgitation: Early diastolic murmur with loud P2, without a collapsing pulse (?AR)
o Cause: Rare congenital anomaly, OR after valvotomy of PS (e.g. in ToF)
Others Dilated annulus due to RVH, Pulmonary HTN, Marfans
NB: Severe stenosis of ANY valve is considered high risk for pregnancy (not as bad if tricuspid)
Myocardial + Pericardial Diseases
o General Points
Definition: Conditions where heart muscle is structurally or functionally abnormal in
the ABSENCE of CAD, HTN, valve disease and congenital heart disease severe
enough (if present at all) to cause the degree of dysfunction observed
Epidemiology: Can all occur at young ages must have high suspicion (except for
restrictive)
Cause:
Idiopathic (most common)
Genetic (25%, auto-dom; family will have it)
Alcohol
Ischaemia
Valvular
Infective Post-viral [e.g. adenovirus, myocarditis leading to DCM], HIV
Tachycardia-induced DCM (e.g. AF, A-Flut, hyperthyroid, any chronic tachy)
Sarcoid, Hemochromatosis
Connective tissue disorders
Chemotherapy
Definitive:
o Biventricular pacing (wide QRS [esp LBBB] w/ NYHC 3/4)
o Implantable defibrillator
o Valvular repair/replacement
o Heart transplant (esp if young)
o Hypertrophic Obstructive Cardiomyopathy/HOCM*** = EF (can contract, but not relax)
Epidemiology:
Second most common CM (1/500 = 0.2% of population)
Often presents 20-30y/o
Most com cause sudden cardiac death in young people + athletes (inc female)
Pres: Syncope, Angina, Dyspnea, YOUNG, athlete, FH sudden cardiac death (SCD)
Ejection systolic OR mid-systolic murmur which does NOT radiate to carotids
o DECREASES on squatting + leg elevation
o INCREASES on Val Salva
I.e. INCREASED murmur when pre-load DECREASED
Classically JERKY pulse (vs AS = slow rising pulse)
Large A waves
Double apex beat
Mid-to-late systolic precordial impulse
Rx: ABCD Amiodarone, Beta-blockers OR verapamil, Cardioverter defib, Dual chamber pace
Conservative: Avoid strenuous activity
First: B-Blocker
o Can also use verapamil if B-blockers CId
o Amiodarone can be used for arrhythmias
DDx: LQTS (this does NOT have FH; this will have STRUCTUALLY NORMAL heart)
Complications: Sudden death due to spontaneous ARRHYTHMIA
Occurs secondary to ischemia of hypertrophied segment
1% risk of SCD per year
Risk of sudden death (1 = possibly significant; two or more = very significant)
o Unexplained syncope
o FH sudden death (<45y/o + history syncope)
o Episodes of VT (non-sustained OR sustained)
o LVOT obstruction (gradient >30mmHg)
o Septal thickening >30mm
o Exercise-induced hypotension (highly important risk factor)
Causes: Amyloid (most com), Haemochromotosis, Sarcoid, Cancer (inc myeloma), Fibrosis
(e.g. endomyocardial fibrosis = most common cause of RCM; scleroderm)
Pres:
Pure diastolic heart failure (i.e. normal systolic function - normal EF)
o Kussmaul Sign Inspiration = JVP (should normally JVP)
Positive = Restrictive Cardiomyopathy, Constrictive Pericarditis,
or Cardiac Tamponade
Often right sided heart failure symptoms (>> left)
Ix: As above
ECG (voltage key sign)
o Also seen in fat, muscle, air (emphysema)
CXR/CT (norm/mildly enlarged heart size, N pericardium [calcified = e.g.
constrictive pericarditis])
Echo (rigid myocard, small thick vents, thick interatrial septum [amyloid deposits],
granular sparkling/global speckled/echogenic appearance [amyloid], mild
pericardial effusion [e.g. 5mm] but not enough to be tamponade)
Rx:
Medical: Manage heart failure
Definitive:
o Pacing or implantable defibs
o Heart transplant
Notes: Do NOT use digoxin in amyloid heart disease amyloid can cause 2nd or 3rd deg HB,
and digoxin will exacerbate this (i.e. digoxin is CONTRAINDICATED)
Notes: Naxos disease Auto recessive ARVC, + palmoplantar keratosis + woolly hair
o Other considerations:
Catecholaminergic polymorphic VT
Definition: Inherited disorder of VT episodes
Epidemiology: 1/10,000; 15% of SCD
Features: Exercise-induced VT (presents w/ collapse), sometimes emotional
Ix:
o ECG Normal
o Echo Normal (hence not cardiomyopathy)
o MRI Normal (hence not cardiomyopathy)
o Acute Pericarditis***
Cause:
Viral (most common) Coxsackie virus
Rheum SLE, RA, Sarcoid
Renal Uraemia
Cardiac Post-MI (Dresslers syndrome if 2-12wk)
Drugs Hydralazine
Bacterial or Fungal
Post-radiotherapy
Pres:
Pain Classic cardiac pain and...
o Pleuritic
o Positional (better on sitting forward, worse on lying back)
Pericardial friction rub (70%; pathognomonic)
o Best heard with patient sitting up and leaning forward
Previous URTI (1wk ago)
Pyrexia
Long term:
o If first attack: Nil
o Following recurrence to prevent attacks: Colchicine
o Constrictive Pericarditis
Cause: Idiopathic, post-heart surgery, thoracic radiation, post-viral
Pres:
R+L sided failure symptoms (e.g. lung symptoms/SOB, fluid retention)
Fatigue
Kussmaul sign ( in JVP during inspiration [normally should reduce])
o RARELY seen in tamponade
Pericardial knock (confused w/ S3)
Rapid Y descent of JVP (as most ventricular filling occurs in early diastole)
o NB: In tamponade, the Y-descent is absent or blunted
Ix:
ECG (volt) Same as restrictive cardiomyopathy
CXR/CT/MRI (calcified pericard) KEY DIFFERENCE to restrictive CM
Cardiac catheterisation for pressures Equal pressures in ALL chambers
in diastole, matching of RV + LV pressures in respiration
Pres:
Becks Triad JVP, BP/shock, Distant heart sounds
Pulsus paradoxus 10mmHg BP on inhalation
Absent or Blunted Y descent due to limited RV filling (differentiates from
constrict pericard)
Ix: Full bloods (inc U+E for urea, ANA, HIV testing, TB testing)
First: ECG (electrical alternans QRS alternates from - volts = severe!)
Second: Water bottle heart enlarged (acutely)
Third: Echo (pericardial effusion, diastolic collapse of RA + RV)
Definition: Acute or chronic inflammation of the myocardium which may present like MI and may
progress to dilated cardiomyopathy
Causes:
o Infection
Viral (most common) Coxsackievirus, others (adenovirus, parvovirus, HIV, EBV)
Bacterial (much less common) Diphtheria (most common bacterial)
Protozoa Chagas (trypanosomiasis [cruzi = American, Gambia [west Africa])
o Drugs
Hypersensitivities Various medications
Toxins Alcohol, chemotherapy (esp anthracyclines e.g. doxorubicin), cocaine,
trastuzumab
o Other
Metal poisoining
Electrical shock
Radiotherapy/radiation
Ix:
o ECG ST elevation OR depression, TWI (diffuse), atrial arrhythmias, transient AV block
o Bloods FBC (leucocytosis 25%), CK/Trop (often elevated), CRP/ESR (elevated in 60%)
o CXR Signs of CCF
o Echo
o Cardiac MRI (can differentiate transient [myocarditis] from permanent [MI] tissue damage)
VERY good test
o Endomyocardial biopsy (gold standard)
Definition: Extracellular and intracellular deposition of insoluble amyloid fibrils, which arise from
various proteins, causing parenchymal dysfunction
Classification: Commonly affect cardio + renal, but can affect either one alone
o A Amyloidosis (AA) Acute phase reactant amyloid, therefore seen in patients with chronic
inflammation
Causes: e.g. RA, chronic microbial infections like TB, sometimes neoplasia like RCC
Features: Renal most common, 10% cardaic
o Light Chain Amyloidosis (AL) Monoclonal plasma cell disorder similar to multiple myeloma
OR from multiple myeloma itself
Causes: Mult myel (BJ deposition), MGUS, Waldenstroms
Features: Cardiac in 50% + neuro most common
Fatal in 80% of cases
o CNS Amyloidosis
Beta-protein amyloid Alzheimers
Prion protein amyloid CJD
Cause: Unknown, but risk factors = chronic inflammation (e.g. RA), hereditary
Features: Depends on organs affected, multiple systems often involved
o Hepatic Hepatomegaly
Rarely jaundice + cirrhosis
LFTs normal, possibly raised ALP
*Note the absence of hyperpigmentation, bronze diabetes (haemochromotosis) when considering the cause of
cardiomyopathy (and for amyloid cardiomyopathy, chronic inflammatory states are NOT needed)
Ix:
o ECG Low voltage DESPITE LVH (LVH should have large voltage big clue to diagnosis)
o Urinalysis
Proteinuria
Light chains (on electrophoresis essentially this is low levels of Bence Jones
protein which are immunoglobulin light chains)
o Blood
FBC (anaemia)
U+E (raised creatinine)
LFT (raised ALP, low albumin)
Inflammatory markers (raised ESR, normal CRP)
Clotting (abnormal in 50% - INR or Factor X deficiency [PT/APTT])
Blood film Howell-Jolly bodies (splenic dysfunction)
o Renal USS LARGE kidneys despite CKD (if renal failure is present)
Only other large kidneys in advanced renal disease = Hydronephrosis, Diabetic
nephropathy, Acromegaly, Renal vein thrombosis
o Echo
Ventricular thickening with reduced ventricle size
Thickened intra-atrial septum
Thickened valvular leaflets
Speckled/granular myocardial appearance
Renal biopsy Mesangial amyloid light chain protein deposition (lambda + kappa
chains) light green staining in mesangium
NB: Multiple myeloma = lambda + kappa light chains EXCRETED, not
deposited (but chains may block up tubules causing obstructive disease)
Types:
o Cardiac myxoma (usually in left atrium, hence Atrial Myxoma) 50% of cardiac tumours
What is it:
Polyp-like mass on pedicle usually coated in layer of thrombus
Often in the left atrium, and often on the interatrial septum
Ix: ECG, CXR, Echo (pedunculated heterogenous mass typically attached to fossa
ovalis region of interatrial septum), Endocardial biopsy
Dextrocardia
Definition: Major visceral organs are on opposite side in mirror image to normal
Types:
o Situs inversus with dextrocardia (i.e. totalis)
o Situs inversus with levocardia (i.e. incompletes) heart on normal side, other organs not
*Associated with Kartageners syndrome Dextrocardia + bronchiectasis + sinusitis
Rate and Rhythm Disturbances
Disorder of SA Node
Rx:
Asymptomatic: Do not treat
o Sinus Tachy (P wave present) Cause: Everything and anything! Rx: Treat underlying cause
AV Block/Heart Block**
o Causes for all:
1st degree Normal aging (common), athletes (common)
All Ischemia/Post-MI, drugs, structural abnormalities (e.g. valve disease)
o 1st Degree
Definition: PR >0.2s, no dropped beats
Rx: NO treatment avoid AV node inhibiting drugs (e.g. b-blocker, CCBs, digoxin)
o 2nd Degree
Types:
Mobitz 1 (Wenckebach) AV nodal hence normal QRS complexes
o Definition: PR elongating then drop
o Rx: NO treatment (unless post-MI and causing symptoms)
Mobitz 2 Infranodal (His/Purkinje) hence usually wide QRS complexes
o Definition: PR stable then drop
o Rx: PACE (progresses to 3rd degree)
Treat:
Symptomatic, Adverse signs (HR <40, BP <90, CCF), Risk of asystole (broad
QRS, ventricular pause >3s whilst awake/>5s whilst sleeping)
Isoprenaline (then urgent pace) beta agonist
o If hypotensive Adrenaline
Asymptomatic + none of other things above Elective pacing
o NB: 3rd deg AV block associated with inferior MI often transient,
but may still requires pacing if HR remains slow after some time
o NB: 3rd deg AV block associated with anterior MI needs urgent
pacing irrespective of symptomatic/asymptomatic
o NB: Stable 3rd degree AV nodal block (HR 45-60) does not need
urgent pacing if asymptomatic, can DISCHARGE for ELECTIVE PPM
insertion (still need PPM as can progress unpredictably)
o Specific indications for pacing 2nd degree (Mobitz II) and 3rd degree AV block
Symptomatic bradycardia
Documented periods of asystole >3s when awake (this would make the HR at that
point 20BPM) or 5s when sleeping
Any escape rate <40bpm in AWAKE patients (doesnt count if asleep)
Tachycardia Resus Council UK Algorithm
o First: Assess using ABCDE (in full)
o Are there adverse features? Shock, Syncope, Myocardial ischemia, Heart failure
Narrow
o Irregular AF, AF with accessory pathway (irregular SVT-like)
o Regular SVT or A-Flut
1) Vagal manoeuvres
2) Adenosine 6mg rapid IV
3) Adenosine 12mg rapid IV
4) Adenosine 12mg rapid IV (again)
Restored rhythm?
Yes SVT
No A-Flut
Supraventricular Tachycardia/SVT*** Definition: HR>100, QRS <0.120
o Paroxysmal Supraventricular Tachy A type of AVNRT - (technically includes AF + A-Flut, but these
are generally considered on their own)
Definition: Sudden onset ectopic tachy followed by abrupt cessation
Cause: Re-entry @ AV node (hence why adenosine works for AVNRT + AVRT)
Pres: HR 130-200, narrow QRS, asymptomatic or syncope
Key factors: No flutter wave, no fibrillatory wave, tachy (p-waves absent though)
o Fourth: Digoxin
o Types:
Type 1 (typical)
Baseline atrial rate ~300
Subsequent 2:1 5:1 AV block (most commonly 2:1)
o The length of the circuit corresponds with size of RA, hence creating
predictable atrial rate at 300bpm (can be 200-400 though)
o 2:1 block is most common, giving ventricular rate of 150
1:1 block is rare, often only seen in WPW when AV nodal
blocking drugs given this leads to severe haemodynamic
instability and VT/VF
Variable block AV block may alternate between
2:1/3:1/4:1/5:1 giving an appearance like atrial fibrillation/AF,
but flutter waves present
Anticlockwise re-entry in 90%
o Retrograde atrial conduction leading to:
Inverted flutter waves in inferior leads (II, III, aVF)
Positive flutter in V1 (may resemble upright P-waves)
(NB: the opposite is true in 10% of cases)
o Pathology:
Atrial impulse occurs
Some of atrial impulse travels down AV node to create QRS
Some of atrial impulse travels back around the atria to then quickly meet again at
AV node
o AV node blocks
o Cycling of electricity continues
AV node blocks at 2:1, 3:1, 4:1 (e.g. 4 re-entrant cycles AKA 4 p-
waves = 1 QRS)
o Ix:
ECG (Ps present + saw-tooth, regular, 2/3/4:1 AV block [often 2:1 = 150bpm], narrow QRS)
Can get VARIABLE BLOCK swapping between e.g. 2:1, 3:1 and 4:1 blocks
TOE (R/O LAA clot prior to DC cardioversion if flutter present for >48hr)
o Rx:
Stable:
First: B-Blocker or CCB (verapamil or diltiazem) or Digoxin
Second: DC Cardioversion (MUST do TOE first if >48hr rule out LAA clot)
o More effective than in AF so often less Joules can be used
o Followed by 6wk warfarin
Recurrent A-Flut: Catheter radiofrequency ablate (of tricuspid valve isthmus)
o Note:
AV blocking meds + chemical cardioversion often unsuccessful
DC Cardioversion is followed by 6 weeks of warfarinisation
Atrial Fibrillation/A-Fib/A Fib/AF*** (An atrial SVT)
o Def: Uncoordinated atrial activity leading to an irregularly irregular beat with disassociation
between the cardiax apex and radial pulse
Source of ectopic electrical activity often pulmonary veins (whereas A-Flut =
tricuspid isthmus)
o Terminology/types:
If LA size <5cm, more likely to be:
Acute <48hr onset
Paroxysmal Spontaneous termination within 7d, usually <48hr
o Recurrent 2+ episodes
o May degenerate into sustained forms
If LA size >5cm, more likely to be:
Persistent Lasting >7d, or if does not self terminate (i.e. required rhythm
control)
o E.g. if DC cardioversion needed on D5 and successfully reverts, this
is still PERSISTENT
o May degenerate into permanent AF
Permanent >1yr and not terminated by cardioversion (if failed
cardioversion at 3mo, this is still PERSISTENT until it reaches 1yr)
Other classification
Recurrent 2 or more episodes of AF (usually paroxysmal, possibly
persistent [esp if needed cardioversion])
o This will require anticoagulation (whereas single episode will not)
o Ix: ECG Holter monitor/Event recorder (if paroxysmal suspected) No p-wave, irreg irreg
CXR
Echo (?LAA thrombus prior to cardioversion, ?LV function, ?LA size ?suitability for
cardioversion, ?valvular disease)
CT/MRI if stroke...
Rx: Paroxysmal = Always RHYTHM control, if persistent/permanent use below criteria
o Acute Rate and Rhythm control:
o Can give repeated doses of each to achieve max dose if not controlled as
long as BP syst >100
o CCB in asthma or if there is another B-Blocker CI
Second: Digoxin (1st line in CCF ONLY; NOT for paroxysmal AF exacerbates!)
o Loading: 500mcg PO, then 500mcg PO 6-8hr later, then 250mcg PO 6-8hr
later
Maintenance: 62.5mcg to 250mcg oD
*If one medication doesnt work alone, ADD the other (e.g.
bisoprolol/verapamil AND digoxin together)
Third: Amiodarone
Consider: Consider swapping b-blocker to sotalol?
If fails: IV amiodarone 300mg in 10-20min, then 900mg in 24hr (as per ALS)
>48hr + stable:
Option 1: Get TOE if no clot, then heparin + DC cardioversion
o Continue warfarin for AT LEAST 4wk
Option 2:
o Warfarin 3wk minimum
Give Warfarin + bridge with Rx dose LMWH
Continue until 3 consecutive weeks of INR therapeutic (2-3)
o DC cardioversion (100J then 200J then 360J then 360J with pads in AP
*Initial DC cardioversion has 80% success rate, but 40% relapse by 1 month and
80% by 1 year
*Sustained sinus rhythm most likely if AF <6mo (if >12mo = unlikely sustained sinus
will revert back to AF eventually); young; small LA size
*Consider chemical agents PRIOR to DC cardioversion if cardioversion likely to fail
o Chemical:
Alternative: Ablate AV node and insert pacemaker (sense atrial depol, pace ventricle)
Makes people pacemaker dependent though
Electrical of chemical first? Can give chemical first, and if non-responder then DC cardioversion
For AF <48hr in young, chemical first (e.g. flecainide; no anti-coagulation needed) then if fails DC cardioversion
(with anticoag)
Chronic - thromboprophylax: Warfarin or Dabigatran (better!) SADCHAVS
Oral anticoagulants
o Dabigatran (direct thrombin/F2 inhibitor 110 or 150mg BD)
o Rivaroxaban (Factor Xa inhibitor 15 or 20mg OD)
Used more often for prophylactic and Rx DVT Rx
o Apixaban (Factor Xa inhibitor 2.5mg or 5mg BD)
Notes:
o If paroxysmal AF with risk factor (e.g. alcohol, infection) spontaneously resolves discharge with no Rx
o If paroxysmal AF with no risk factors spontaneously resolves ?Rx only if recurrent
NB: New guidelines state that if NO risk factors with AF (i.e. score = 0), then NO Rx preferred to aspirin
NB: New guidelines state that if ONE risk factor with AF (i.e. score = 1) then Warfarin/Dabigatran preferred to
aspirin! (preferred to means can still use aspirin, but most evidence says it is not as good)
Wolff-Parkinson-White (WPW)** An SVT which fits the category AVRT
o Def: Re-entrant rhythm where signal passes through AV node + Bundle of Kent:
Orthodromic Down AV node, back up BoK (10x more common)
Antidromic From atria to ventricle through the BoK, thereby bypassing the AV
node (hence short PR), but then back up AV node
o Epidemiology:
Can occur from any age >20 (also affects older
people!)
Most common ventricular pre-excitation syndrome
o Risk factors:
MVP
Cardiomyopathy (e.g. HOCM)
Ebsteins anomaly (see picture)
o Symptoms
Pre-Excitation WPW ECG but NO symptoms and NO tachycardia
Occurs when impulse AV node reaches ventricles before impulse travelling
through the BoK (despite the AV delay at AV node)
The impulse travelling through the BoK still creates the delta wave + wide
QRS as some early depolarisation occurs, but the impulse through AV node
predominates the cardiac depolarisation hence, asymptomatic
Since normal pathway dominates and refractory period sets in, merely get:
o SINUS RHYTHM
o Short PR interval
o Delta wave
o Slightly wide QRS
Unstable: Cardioversion
o Chronic
Medical: Flecainide (esp good for WPW with AF), amiodarone + verapamil, sotalol
(avoid if co-existing AF as prolongs refractory time at AV node, hence increases
transmission through accessory pathway, increased ventricular rate + risk of VT)
Slow conduction rate
Slow down refractory time of bypass tract
Chronic medical Rx at reducing WPW episodes is unpredictable
Definitive: RF catheter ablation of BoK (ALL symptomatic patients need this, and
some asymptomatic even [esp young]! 95% success rate)
Young, No AF: Minimal risk, done early
Concomitant AF: Inpatient RFA as HIGH risk of death due to VF
*These are all indications to DC Cardiovert a tachycardia rhythm in the FIRST instance (inc AF) WITHOUT
exceptions!
*Patients should be given IV UFH prior to emergency DC cardioversion to reduce risk of thromboembolism
*All SVTs can be differentiated by their P-wave presence + morphology (except WPW which has other classical
findings)
Ventricular Arrhythmias***
o Ventricular Tachycardia/V-Tach/VT/Monomorphic VT
Definition:
Broad complex tachycardia originating from ventricular ectopic focus with potential
to RAPIDLY decompensate into VF + asystole (i.e. even if patient haemodynamically
stable, this is an extremely time-sensitive emergency)
Must be at least 3 ventricular extrasystoles in a row @ >120bpm
o If 100-120BPM, termed accelerated idioventricular rhythm
Cause:
Ischemia (esp post-MI) if patient in VT, MI = top differential
Cardiomyopathy
Metabolic/electrolyte deranged (K+, Mg, Ca)
May see:
o Capture beats (ectopic focus stimulates SA node to make a normal beat,
and if ventricles are not refractory this will conduct through AV node and
cause narrow QRS beat)
o Fusion beats (where capture beat/normally conducted beat meets
ventricular conduction to create a superimposed beat)
o *see below for more on this*
Sustained >30s
Run <30s
Types:
Monomorphic Constant QRS morphology (all look the same), 90% are >0.12s
width, regular aside from where fusion or capture beats seen
Fascicular Similar to monomorphic, but slightly narrower QRS (0.11-0.14s)
RVOT origin VT RAD + LBBB + VT pattern
Polymorphic AKA Torsades Risk factor is long QTc, and risk for this is:
o Congenital Jervell-Lange-Neilsen OR Romano-Ward Syndromes
o Electrolytes HypoCa, HypoMg, HypoK
o Drugs Amiodarone, TCAs, dopaminergic drugs, methadone
o Other IHD, SAH, Hypothermia
Catecholeminergic VT VT on exercise of emotional stress (e.g. fright, shock)
Rx:
o Pulseless: Adult ALS http://www.resus.org.uk/pages/alsalgo.pdf
CPR + Emergency Cardioversion (exactly same as VF)
Start at 150-200J biphasic, then subsequent shocks work-up to max 360J
Give 3 shocks (1 immediately, then 2min apart), and if still in VT:
o Adrenaline 1mL of 1:1000 IV, AND
o Amiodarone 300mg IV, THEN
o Pulse: http://www.resus.org.uk/pages/tachalgo.pdf
Unstable: Cardioversion x3 SYNCHRONISED shocks (then IV amiod as above)
NB: SYNCHRONISED shocks (shock aligned with peak of QRS) are used for ANY
unstable tachyarrhythmia WITH a pulse
Stable:
IV Amiodorone 300mg in 250mL D5W over 20-60min
THEN
900mg further in 500mL D5W over next 24hr
IF STILL REFRACTORY after 24hr
IV Lidocaine bolus then infusion over 6.5hr (with caution in severe LVF)
Function:
o Anti-bradycardia pacing (like a normal pacemaker)
o Cardioversion shocks (to end VT low energy feels like a jolt)
o Defib shocks (to end VF high energy feels like kick to chest)
NB: Presence of BBB can be rate related, so not seeing BBB on previous patient ECG
does not rule out SVT w/ aberrant conduction
o Torsades de Pointes (TdP) AKA Polymorphic VT V-Tach which gets larger and smaller
Risk: LQTS, Drugs (anything dopaminergic or anti-arrhythmic)
Congenital Jervell-Lange-Neilsen (deaf) OR Romano-Ward Syndromes (not deaf)
Electrolytes HypoCa, HypoMg, HypoK
Drugs Amiodarone, TCAs, SSRIs, dopaminergic drugs, methadone, macrolides
Other IHD, SAH
o Ventricular Fibrillation/V-Fib/VF (always going to be pulseless basically i.e. follow ALS pathway)
Definition: Random ventricle contraction = poor CO cardiac arrest/sudden death
Risk: Post-MI, LQTS, Brugada
Features: Heart failure symptoms
Ix: ECG, blood (myoglobin, CK-MB, troponin, electrolytes inc K+ Mg Ca), etc
Advanced Life Support (ALS)
Background
o Whats the point of an algorithm?
Allow for rapid decisions in time sensitive emergency
All cardiac arrest team members work from same
guideline, hence management is standardised and team members can predict next actions
o Chain of survival
Early recognition + call for help
Agonal breathing Slow, sighing respirations
o Occurs early AFTER initiation of cardiac arrest (i.e. patient may be
arresting whilst agonal breathing present)
Early CPR
Technique for compressions Good quality compressions related to outcome
o Centre of chest (middle of the lower half of the sternum)
o 5-6cm depth
o Allow full chest recoil before next compression
o 2/s (i.e. 100-120/min)
o 30 compressions 2 breaths
Once airway secured, continuous chest compressions and
asynchronous ventilation
o Swap compression provider every 2min to avoid fatigue
Other things
o Get IV access
Cant attain: IO access
NB: Do NOT use central line unless patient ALREADY has a
patent one in situ
Early defibrillation (in VF + VT)
Attach ASAP (but do NOT interrupt chest compressions to attach)
Once attached, pause chest compressions to assess rhythm
o Shockable Shock + get medications ready
VF coarse or fine?
Coarse responds well to shock
Fine responds poorly to shock, progresses into
asystole (and often confused with asystole as chest
wall movement may give fine VF picture also in this
case treat as asystole [as would be poor response to
shock anyway]) high quality chest compressions in
fine VF may precipitate larger amplitude VF (good
thing) and hence increased response to shocking
o Non-shockable Continue compressions + get medications ready
Charge defibrillator WHILST compressions still occurring (i.e. you ONLY stop to
analyse rhythm if for shock, continue compressions until charged then hands-off
again for shock delivery) once charged, do NOT pause to re-check rhythm
Deliver shock at appropriate energy (different for every machine)
o Use 150-200J biphasic starting, work up to 360J biphasic (or start 360J
monophasic)
o If unsure use HIGHEST available energy; DO NOT delay shock deciding
what energy to use
Post-shock IMMEDIATELY re-start CPR for 2 min
ONLY check pulse when an organised rhythm compatible with life is present
After third shock, give adrenaline (1mg IV) AND amiodarone (300mg IV) whilst
compressions occurring
o MUST flush with 20mL fluid
o Drugs are LESS important than good quality chest compressions and early
shocks (perhaps more importance in PEA/Asystole)
Continuing resuscitation:
o VT/VF attempt as long as patient remains in VT/VF do NOT stop
attempting resuscitation
o PEA/Asystole continue for 20min at least, always looking for reversible
causes (after 20min without identification of reversible cause, unlikely to
survive and reasonable to stop)
Must reduce pre- and post-shock hands-off time as the longer spent not doing
CPR = reduced shock efficacy
Post-resuscitation care
Goals
o Normal cerebral function
o Stable cardiac rhythm
o Adequate organ perfusion
o Quality of life
Tasks
o Get all obs
Constantly monitor (including urine output)
Consider arterial line for continuous BP monitoring (should
ALWAYS be present if patient transferred to ITU)
o A+B
Controlled oxygen and ventilation (maintain 94-98% sats NOT
higher)
Ventilation ONLY if patient has low GCS post-arrest
AVOID hyperventilation
Monitor capnography aiming for normocarbia
Check respiratory function via examination (broken ribs may
cause pneumothorax, or pneumothorax may be initial cause;
etc)
Insert NG tube for decompression
Following BVM ventilation or mouth-to-mouth some
air may go into stomach
Decompression also improves lung compliance
Portable CXR
IV sedation (most will need this to maintain
intubation/mechanical ventilation will also help with shivering
if therapeutic hypothermia to be conducted)
o C
ECG monitor + 12-lead ECG (?MI)
Assess cap refill
Check for signs of CCF
Get bloods (if not already taken during arrest)
ABG gives quick information on many reversible
causes (hypoxia, hyper/hypokalaemia, acid/base
status ?toxins)
Venous bloods FBC, U+E, CRP, Glucose, Troponin
Echo
Quantifies degree of post-arrest myocardial
dysfunction (i.e. weak heart despite optimal filling due
to reperfusion injury)
Echo may help determine need for inotropes OR IABP
A blood pressure should be attained to achieve urine
output of 1mL/kg/hr and normalising lactate
o D
Therapeutic hypothermia (especially AVOID hyperthermia)
Situations to use
o VF arrest ROSC but unconscious still (most useful here cool to 32-34
deg)
o Non-shockables after ROSC (may benefit)
Contraindications
o Severe sepsis
o Coagulopathy
How to use
o Induce 30mL/kg 4deg C IV fluid and/or external cooling
o Maintain (for 24hr)
External cooling (ice packs, wet towels, cooling blankets or
pads, water-circulating gel-coated pads)
Internal cooling (intravascular heat exchanger, cardiopulmonary
bypass)
o Rewarm slowly by 1 degree every 4hr
Complications
o Shivering (which raises body temp) Rx = sedate + neuromusc blocking
drugs
o Bradycardia + cardiovascular instability
o Infection
o Hyperglycaemia
o Impaired coagulation
o Reduced drug clearance
Assess neurology (NB: successful CPR leaves patient without neurological compromise)
GCS
Pupils
Limb tone and movement
Posture
o E
Look for and treat all possible underlying causes
o Further history
Health before cardiac arrest
Time delay before resuscitation
Duration of resuscitation
Cause of cardiac arrest
o Further tasks
Discuss with relevant team/on call consultant; discuss with ITU
Secure cannulae, tubes, etc
Suction as necessary
Regular monitoring by nursing staff
Document
Call family
Re-assess yourself before leaving
Tamponade
Think of risk factors Chest trauma, cardiac surgery
Get urgent echo
Rx with needle pericardiocentesis OR resuscitative thoracotomy
Toxins
Rare unless OD
Check drug chart
Tension pneumothorax
Check tube position if intubated
Resp examination (reduced breath sounds, hyper-resonant, tracheal deviation)
Needle decompress to start (or thoracostomy [create incision] if chest wall is too
big for a cannula), then drain
Thrombosis (PE, coronary thrombosis/ACS)
If high risk PE, give thrombolysis
If thrombolysis given, you MUST continue CPR for 60-90min before discontinuing
CPR (unless patient comes back before)
o Case reports demonstrating patients can come back from cardiac arrest
due to PE after this long without significant neurological damage
Notes
o Predicting cardiac arrest
50-80% deteriorate prior to cardiac arrest hypoxia and hypotension are COMMON, and all
obs may start to worsen (high RR, tachycardia)
Agonal breathing (patient may already be arresting)
o If someone can do USS at the arrest, reversible causes can be more readily identified
What can be identified
Tamponade
PE
Ischaemia (via RWMA)
Hypovolaemia (IVC compression)
Pneumothorax
When to probe
Place probe just before rhythm assessment
Start scanning during rhythm assessment (only have 10s hence need well-trained
operator; can take Focused Echo Extended Life-support [FEEL] course)
DNAR
Most common reason for DNAR = futility patient will have unacceptable QoL
following CPR
Do NOT need to discuss DNAR with patients who are highly unlikely to have a
cardiac arrest OR patients who are at end of life (final stage of irreversible illness)
and CPR would be futile
Aim to involve relatives, but if patient has capacity must respect if they refuse to
tell relatives
If patient doesnt have capacity use next of kin, and if not available then use IMCA
(Independent Mental Capacity Advocate) if not emergency and doctors belief of
best interest in emergency (it is accepted that there is a subjective element, but
discussion with other healthcare providers is essential to confirm decisions)
o Relatives CANNOT force CPR if doctor believes it will be futile
DNAR (better/new term = DNACPR) is ONLY for withholding CPR, not other
treatments (otherwise this is palliative)
o Public places
In UK there is NO legal obligation to offer medical assistance in public place
If you stop to help, the legal situation changes and you assume duty of care
There have been NO successful litigations against good Samaritan acts by doctors
in the UK
This is NOT the case in Europe where it is MANDATORY to help
o Special circumstances
Types
Anaphylaxis
Asthma
Electrolyte disorders (e.g. hyperkalaemia)
o If cardiac arrest Rx hyperkalaemia DURING arrest (inc calcium
gluconate), consider haemodialysis DURING arrest if refractory to medical
Rx; give sodium bicarbonate (for hyperkalaemia and TCA OD)
Hypovolaemia
Poisoning
o E.g tricyclic give sodium bicarbonate
Pregnancy
o PEA + Asystole
Background
These are NOT shockable
WORSE outcomes than VT + VF
MORE common in hospital (VT+VF in community)
UNLIKELY to recover from PEA/asystole unless reversible cause is found and treated
PEA rarely a perfectly straight line trace (if this occurs check lead placement)
Management
CPR 30:2
IV Adrenaline 1mg immediately (continue every 3-5min) this is the drug of choice
Continue CPR without pausing during ventilation
Consider reversible causes of PEA/Asystole (see below H4 T4)
o E.g. if hypovolaemia present Rx with fluids during arrest
Class 1 Na+ channel blockers (avoid in CAD/struc heart defect/CCF risk death; esp flecainide)
o 1A (fast channel blockers which affect QRS complex, lengthen cardiac action potential):
Examples: Procainamide, quinidine
Mechanism: Increases AP
Uses: Ventricular arrhythmias, WPW
Notes:
Procainamide causes drug-induced lupus
Quinidine (and quinine) causes cinchonism (headache, tinnitus, low plates)
Class 2 Beta-blockers:
o Examples: Propranalol, metoprolol, atenolol, bisoprolol (NB: sotalol is Class 3)
o Mechanism:
Beta-blockade (selective + non-selective [propranalol])
Sinoatrial node blockade (mostly)
o Uses: Post-MI, prevent recurrence of tachyarrhythmias
Class 3 K+ Channel:
o Examples: Amiodarone, sotalol (also beta blocker), dofetilide
o Mechanism:
K+ channel blockers; amiodarone has class 1,2,3,4 activity
Widen cardiac action potential
o Uses: WPW (if with structural heart defects)
o S/E: Can prolong QT as they widen AP (as per all K+ channel blockers)
Types:
o AV Nodal Re-Entrant Tachy (AVNRT) Electrical signal MUST pass through AV node (e.g.
Paroxysmal SVT)
o AV Re-Entrant Tachy (AVRT) Alternative pathways are made between the atria and
ventricles (e.g. WPW)
Orthodromic Atrial impulse passes through AV node, toward ventricles, back up
the atria, then toward AV node again (narrow QRS complex)
Antidromic Atrial impulse passes down accessory pathway, down ventricles
(wide QRS), up toward AV node, then around again to accessory pathway
Notes:
o It can be EXTREMELY difficult to tell the difference between AVNRT (e.g. Paroxysmal SVT)
and Orthodromic AVRT (e.g. orthodromic WPW [most common form])
Definition: Collection of conditions with sinus node dysfunction with inappropriate atrial rate
Cause: Idiopathic fibrosis (most common), fatty infiltration of SA node/AV node/His bundles/fascicles,
post-MI (RCA in 70%, LCX in 30%)
Definition: Transient LoC caused by global cerebral hypoperfusion characterised by rapid onset, short
duration, and spontaneous recovery (i.e. excluding seizures, coma, shock)
Causes:
o Neural mediated (AKA reflex syncope):
Vasovagal (i.e. common faint)
Situational (e.g. cough, sneeze, defecation, micturation)
Carotid sinus hypersensitivity
o Cardiac (often during exercise)
Arrhythmia
Subclavian-steal
Any cardiac disease (e.g. LVOT obstruction/HOCM/AS)
o Orthostatic hypotension (AKA postural hypotension)
o Autonomic problems:
Diseases Multiple system atrophy, PD, Diabetes
Medication Anti-HT
o Psychogenic Factitious, anxiety, panic attack
Ix: Score using the European Guidelines in Syncope score BP + ECG + Bloods always
o Neural mediated/Reflex: Carotid sinus massage, tilt test, implantable loop recorder
Do NOT carotid massage anyone with prior TIA or stroke (listen for bruits first)
o Cardiac:
ECG ambulatory monitoring (e.g. Holter monitor, event recorder [e.g. Holter where
can press button to record when symptoms felt], external OR implantable loop
recorder, home telemetry)
Implantable Loop Recorder e.g. Reveal device
o Indications: REGULAR Syncope OR light headedness/dizziness OR
palpitations thought to be cardiac but not diagnosed on 24-hour
ECG or 30-day external monitor (i.e. so longer recording is needed
ILRs can last 2-3yr)
Especially indicated where ECG findings show risk factors
for arrhythmias (e.g. bifascicular block, long QT)
Rx:
o Neural mediated Reassure these are benign
o Cardiac Treat underlying defect
o Orthostatic
Conservative: Stop offending drugs, raise bed head, hydration, support stockings
Medical: Low dose fludrocortisone
Brugada Syndrome
Cause: 20% due to SNC5A gene defect (codes for sodium channel;
most common abnormality)
Epidemiology:
o More common in Asians
o 10x more common in MEN
But genetic defects same in M/F
Men have much higher penetrance (unknown why)
Features:
o Syncope (most common presentation, due to runs of VT)
o Sudden cardiac death (often in sleep!)
o FH sudden cardiac death
o AF (20%)
o Nightmares + thrashing at night
o Classic ECG findings (ST elevation leads V1-3) this is key to differentiate from ?HOCM
o Often unmasked by sodium channel blockers (e.g. flecainide)
Ix:
o First: ECG (3 types, mainly ST elevation in V1-3, ?but may have completely normal ECG)
Type 1: Raised J point with ST elevation, T-wave inversion V1 + V2
Type 2: Saddle-backed ST segments with elevation
Type 3: ST elevation only
o Second: Bloods (K+, Ca2+, Trop, SNC5A gene)
o Third: Echo (?Arrhythmogenic RVCM [must rule this out, can have similar ECG], ?HOCM)
o Fourth: Flecainide challenge/provocation (for ANY syncope w/o obvious cause, test for
channelopathies)
This will unmask the classic ECG findings of Brugada syndrome or other channelops
o Fifth: Electrophysiology (test for inducible arrhythmias)
Rx:
o Asymptomatic + No FH: Close monitoring
o Symptomatic OR FH sudden death: Implantable cardiac defibrillator (ICD)
Methods:
o Percussive/Percussion AKA Transthoracic mechanical
Closed fist on left lower edge of sternum
Strike this area (overlies the RV + IVC) at 10cm swing lengths
Only use for interim in bradycardic cardiac arrest where electrical pacemaker is
being brought to patient
Best if bradycardia with some output as saves patient trauma of CPR
Should see a QRS complex if not then move fist around precordium until
QRS generated
If no QRS generated within a few seconds, start CPR
o Transcutaneous
Give sedation + analgesia
Apply defib pads to either under right clavicle and axilla (less preferred) or antero-
posterior over heart (more preferred, better success)
Select pacing current (measured in mA) and increase until electrical capture is seen
(wide QRS, tall broad T-wave)
Once capture seen, assess pulse to ensure electrical capture is associated with
mechanical capture
Only use in emergencies (i.e. haemodynamically unstable) awaiting transvenous
o Transvenous
This is a temporary measure
Done for haemodynamically unstable patients
Insert wire through vein into RA or RV wire connected to pacer pace
Remove once:
Permanent subclavicular pacemaker inserted
There is no longer a need for pacing
o Epicardial
During open heart surgery if patient enters AV block
Place electrodes directly on epicardium
Temporary measure until transvenous pacing achieved
o Subclavicular
Permanent pacing measure
Electrode wires pass through veins and connect to pacer which is inserted under the
skin below the clavicle
Types:
Single-Chamber
o One pacing lead
o One chamber of heart (atria or ventricle)
Dual-Chamber (NB: different to bivent pacing)
o Two pacing leads
o One in atria, one in ventricles mimics natural contraction
Rate-Responsive
o Detects physical activity and automatically adjusts HR to fulfil
bodily metabolic needs
o Intracardial New, wireless pacing inserted directly into myocardium (not available yet)
o Biventricular (AKA Cardiac Resynchronization Therapy) For severe heart failure with lack
of RV and LV synchronization (e.g. bundle branch blocks) leading to worsening of CCF
Indications:
Clinical Refractory heart failure (NYHC III or IV) i.e. medications maxed
AND
ECG
o QRS >120ms (e.g. LBBB) especially if coupled with 1st deg AV block
OR
o Noticeable ventricular dysychrony on ECG
AND
Other (more minor criteria) EF <35%
BUT
Cannot have arrhythmia (e.g. AF) must be in sinus rhythm
Why: Improves outcomes (mortality, morbidity CARE-HF + COMPANION studies)
How: Two leads, one through right side paces septum, left side lead paces LV,
coordinates with RV, sometimes has lead which senses RA also
Other: Can be combined with ICD to protect against arrhythmia (known as CRT-D)
Indications:
o Emergency/Acute Start transcutaneous if dire emergency, then change to transvenous
Asystole
3s when awake
5s when sleeping
Symptomatic bradycardia
Bilateral bundle branch block (i.e. bifascicular block) + trifascicular block
Heart block Mobitz 2 or 3rd degree HB w/:
o Symptoms (inc syncopal episode)
o Haemodynamic compromise
o BBB
o Following MI
o Elective:
Refractory heart failure with LBBB (Bivent AKA CRT)
Nomenclature: Four letters
o 1st: Chambers paced Which chambers can receive an impulse to contract
A = atrium can receive an impulse/contraction
V = ventricle can receive an impulse/contraction
D = both A+V
o 2nd: Chambers sensed Which chambers are monitored for abnormal electrical activity
A
V
D
o 3rd: Response to sensing When the pacer detects electricity, what will it do?
T = trigger an impulse
I = inhibit an impulse
D = have the capability for both T + I
o 4th: Rate modulation If undergoing physical activity, can pacer respond by HR?
O = No
R = Rate modulation pacer CAN increase HR based on physical activity (detects
vibrations and increases HR (problems in Parkinsons and shivering!)
*Cannon A waves can occur as a result of VVIR pacing Ventricles may be paced, but since atria not sensed
the ventricles and atria may beat with disassociation, so if a A + V beat occur at same time then tricuspid will
be closed (due to overpowering pressure in RV to close tricuspid) causing a cannon A wave in JVP
*All pacemakers are now DDDR except for AF with (long pauses OR 3rd degree HB) which are VVIR
Other Pacing Notes
o VVI
Atria is not sensed nor paced, but ventricle is sensed and paced
Will create pacing spikes before each QRS, and likely no P-waves present (unless
CHB)
o DDD
Both right atria and right ventricle sensed and paced
For when SA node not creating P-waves
Will see pacing spikes before P-wave, and assuming normal AV node conduction will
have normal QRS without pacing spike OR may have packing spike also before QRS
(double pacing spike = definitive way of knowing dual chamber pacing)
The ECG would be similar with an AAI pacemaker
Implantable cardiodefibrillator** Restoration to sinus rhythm during arrhythmias (not constantly going)
Indications:
o Episode of sustained VT causing syncope or EF <35%
o Previous MI due to VT/VF
o MI complicated by non-sustained VT (or sustained, but this is indication with or without MI)
o Familial conditions (e.g. LQTS, Brugada)
o HOCM with syncope
Notes: Also known as anti-tachycardia pacing (though is not a pacemaker in the conventional sense)
Anderson-Fabry Disease
Marfans Syndrome**
Definition: Inherited (auto dom) connective tissue disorder characterised by skeletal, dermatological, cardiac +
aortic, ocular and dural malformations
Cause: Mis-sense mutation in chromo 15q21 gene encoding for fibrillin-1 (elastin-matrix glycoprotein)
o Inherited
o Sporadic (associated with increasing paternal age)
Epidemiology: 2-3/100,000, affects all sexes + regions + ethnicity equally; prognosis 70yr old
Features: Tall, thin, long arms + legs (arm span to height ratio >1.05), arachnodactyly
o Skin Striae
o Heart + vessels Aortic sinus dilation (90%) + AR (80%), MVP (75%), MR, AAA
o Eyes Lens dislocation (superotemporal ectopia lentis; 75%), closed angle glaucoma
o Joints Hypermobile
o Skeleton
Pectus excavatum + pes planus
Kyphoscoliosis
Arachnodacytly
Walkers wrist sign (sounds rubbish!)
Steinbergs thumb sign (sounds rubbish!)
o Lung Repeated pneumothorax
o Face High arched palate, retrognathia
Ix:
o ECG Aortic root dilation (?1st deg HB)
o Pelvic XR Protrusio acetabula (50%!)
o Echo Aortic root dilation (best for monitoring condition)
o MRI
Spinal column Dural ectasia
Aorta Measure dilation
DDx:
o Ehlers-Danlos
o Fragile X
o Acromegaly
o Homocystinuria
Fx: Learning difficulty, clots, no FH (recessive, Marfans =
Dom), epilepsy in 30%, inferior lens dislocation
Ix=cyanide-nitroprusside test, homocysteine levels
Rx=Vit B6/pryidoxine
o MEN 2b (Marfanoid phenotype + Follicular thyroid + Pheo)
Rx: MDT geneticist, ophthal, cardio, ortho
o Non-drug:
Counselling
Avoid vigorous activity + contact sports
o Drug:
B-blockers (reduce MAP Reduced aortic root dilation/rupture)
ACE-I have emerging evidence
Prognosis: Much better now with BB + ACE-I therapy, and echo monitoring; death by aortic dissection + other
CVS disease
ECG Abnormalities
o Causes:
Aortic stenosis, HTN
DCM
Acute MI, IHD
Extensive CAD
o Rx:
New LBBB in context of chest pain warrants PCI!
RBBB
o Criteria:
Rhythm must be supraventricular
QRS >0.12 (or >0.10 for incomplete block)
Terminal R wave in V1 (e.g. R, rR, rsR, qR)
T-wave inversion relative to QRS in V1
NB: if T-wave same direction, ?ischemia or MI
Slurred S wave in lead I + V6
o Causes:
RVH
Pulmonary HTN (e.g. PE)
*NB: Whenever a fascicle is blocked, conduction occurs to that area via the myocardium (e.g. in RBBB,
conduction and subsequent contraction of the RV occurs via trans-septal conduction of the LV
impulse through the myocardium to the RV) hence why conduction is significantly slowed
Epsilon potential Seen in ARV Cardiomyopathy, RV
dysplasia
o Seen in V1 + V2 (RV leads)
o Due to fat displacing myocytes
U-wave Hypokalaemia
J-wave Hypothermia
Bigeminy
o Normal QRS followed by ventricular ectopic
o Benign in structurally normal hearts and people without CAD
o Pathological (increased risk arrhythmia and sudden death) in
those with CAD or structurally abnormal hearts
Trigeminy
o Two normal QRS followed by ventricular ectopic
o Same significance as bigeminy (see above)
Electrical alternans Cardiac tamponade
o NB: Not to be confused with pulsus
anternans seen in heart failure
(alternating strong and weak beats
felt at the pulse)
Capture beat
o In a ventricular arrhythmia (often VT), the ectopic focus causes a retrograde depolarisation
of the ventricles
o This can then stimulate the SA node to fire, causing synchronised atrial contraction and a p-
wave
o If the ventricles are not refractory at this point, then this beat will travel through the AV
node to cause a normal, narrow-complex QRS complex
o VT may continue afterwards
Fusion beat
o Electricity from an ectopic focus and the normal cardiac pacemaker (i.e. sinoatrial node)
reach a particular area at the same time causing a bigger contraction (i.e. an ectopic beat
meets a capture beat in VT, or an ectopic beat meets a normal beat in someone who has
random ectopic beats)
o The resulting ECG change is a mix of both the ectopic will be predominantly negative but
the capture/SA-originating beat will be positive, so the resultants will be a small wave
(usually slightly negative with a not-wide-but-not-narrow QRS complex)
If in ventricles Ventricular fusion beat
If in atria Atrial fusion beat
*Notice fusion beat still looks like a mini-VT complex as the VT wave will me the majority of the fusion
*Notice the capture beats look exactly like a normal QRS complex, and much different to that of the
VT complex
Wave lengths:
o P-wave 0.12-0.2s
o PR interval (<0.2s)
Prolonged Idiopathic, athletes, IHD, Dig tox, hypoK+ and hyperK+ [rare], aortic
root pathology (e.g. abscess in endocarditis), Lyme, sarcoid
Short WPW, LGL
Depressed Pericarditis
LQT9-12
o Rx:
Collapse with QTc <500: Beta-blockers (but NOT sotalol as this prolongs QT)
Collapse with QTc >500 (i.e. high risk): ICD
Pulsus bisferiens Double peak in the pulse per cardiac cycle; mixed AR + AS
Pulsus paradoxus Decrease >10 in BP during inspiration; Tamponade (NOT constrictive pericard)
Kussmaul sign Rise in JVP on inspiration; constrictive pericarditis (NOT tamponade), restrictive CM
Endocarditis**
Risk: DPIGS
o Structural heart Prosthetic valve, Rheum valves (one of the biggest risk factors),
Congenital heart defect (repaired or not), HOCM
o IVDU
o GI Colonic malignancy, chronic cholecystitis
o Pneumonia
o Dental surgery, poor oral hygiene
o (Previous endocarditis biggest risk factor!)
Organisms:
o Staph
Aureus (2nd most com; G+ coccus in grape-like clusters) Risk: IVDU, Prosthet valve
Most com when skin infection, abscess, or vascular access site (e.g. IVDU)
Poor prognosis (30% mortality)
Epidermidis (uncommon [1-3%] but most com 1st year post-valve surg [esp 2mo] +
may have delayed pres [e.g. 6mo post-surg but infection derived from events peri-
surgery) e.g. without surgery, even Haemophilus is more prevalent than S epid
o Strep:
Viridans (most com 50%) Risk: Oral surgery, poor dental hygiene
Most com overall
Better prognosis (5% mortality) than S aureus + neg-culture endocard
E.g. S milleri (but this is a LARGE group of organisms)
Other streps (e.g. mitis part of viridans group, after dental surgery)
o Others Pseudomonas, HACEK organisms (culture negative), Fungi (Candida seen in IVDU
mostly), Non-infective Libman-Sacks endocarditis AKA non-bacterial thrombotic
endocarditis AKA marantic endocarditis (e.g. SLE, cancer)
Features: Fever (?few weeks), Murmur ONLY! Feel slightly off and under the weather
o Systemic signs:
Sore throat initially
Weight loss + night sweats + loss of appetite
Diagnostic criteria Modified Dukes Criteria: Pathological Criteria OR 2 major OR 1 major + 3 minor
OR 5 minor
o MAJOR criteria:
Positive blood cultures
Blood cultures x2 with TYPICAL organism (S viridans and HACEK)
OR
Persistent bacteraemia from x2 cultures taken >12hr apart
OR
X3 cultures (not 12hr apart each) where pathogen is less specific
OR
Positive serology for Coxiella burnetii, Bartonella spp, or Chlamydia psittaci
OR
Positive molecular assays for specific gene target
o MINOR criteria:
Risk factor (e.g. predisposing heart condition or IVDU)
Positive blood culture which does not meet major criteria
Cultures x1
OR
Atypical organism
Fever >38
Vascular phenomenon Major emboli, splenomegaly, clubbing, splinter
haemorrhage, Janeway lesions, petechiae, purpura
Immunological phenomenon Oslers nodes, Roth spots, glomerulonephritis
Ix:
o First:
Urine dip + MCS (haematuria proteinuria)
Blood culture x3 taken >6hr apart each (i.e. need 18hr to collect) >90% sensitive
(but cannot culture after ABx started)
DO NOT do echocardiogram first
Start empiric therapy AFTER culture taken, and if negative but positive
echocardiogram (vegetation seen) use FEVER, 1 RISK AND EMBOLIC
PHENOMENON to make diagnosis
Cultures may not be useful if a patient has received empiric antibiotics prior
to culturing
Cultures taken 6hr apart demonstrate CONSTANT bacteraemia an
important feature of endocarditis
Cultures DO NOT need to be taken from 3 separate sites (there is NO
evidence for this PassMedicine)
If antibiotics started already, patient not improving after some days, high
risk endocarditis: STOP antibiotics for 1 week, re-culture x3 taken 6hr apart
each (British Society for Antimicrobial Chemotherapy and European Society
for Cardiology)
Other:
ECG (1st degree HB = aortic root abscess Must be Rx with valve replace)
CXR
o Second: Trans-thoracic echo (TTE) not as good as culture or TOE, but easy
o Best: Trans-oesophageal echo (TOE) 95% sensitive, not dependent on ABx use
Treat:
o Empiric (waiting for culture): **Gentamicin mainly used to PREVENT penicillin resistance**!
o After culture:
MSSA: Penicillins (Flucloxacillin)
o Surgery?
CONGESTIVE FAILURE FROM VALVE RUPTURE
Uncontrolled infection
Recurrent embolic phenomenon
Large vegetations
Aortic root abscess/vegetation causing 1st deg HB (i.e. presence of 1degHB = surg)
Prosthetic valve endocarditis
First: Treat any pulmonary oedema/major complications
Second: Operate (metallic valve if young, bioprosthetic if old [as only has
10-15yr lifespan, therefore if young will need further high risk operation])
Third: After operation, 4-6wk antibiotics
Complications:
o Complete heart block
o TIA
o AKI
o CCF
o Painful swellings of fingers
o Bowel infarction
o Haematuria
Presentation:
o Acute pharyngitis in recent past
o Febrile
o Symmetrical polyarthritis subcutaneous extensor surface nodules (e.g. elbows)
o MR (acute, then progresses to MS)
Ix:
o ECG 1st degree HB (long PR)
o Throat swab
o Blood
Raised WBC, CRP, ESR
Anti-streptolysin O (ASO) titre Peaks at 4-5wk post-pharyngitis
Cultures
o CXR
o Echo
Rx: Admit
o All cases: IM BenPen 1.2g
o If arthritis OR carditis present: Aspirin OR Naproxen
o If CCF: As per CCF
Complications:
o Pregnancy may precipitate recurrence
o Higher risk endocarditis
o CCF
Other
Driving/DVLA in Cardiology
o HTN can drive unless medication side effects
o Angioplasty (elective) 1 wk
o Pacemaker insertion 1wk
o CABG 4wk
o ACS 4wk (1wk only if successfully treated with angioplasty)
o Angina Indefinite ONLY if episodes occur whilst driving
o ICD
For sustained VT/VF 6mo
Prophylactically 1mo
o Successful catheter ablation for arrhythmia 2 days
o Aortic aneurysm >6cm Still drive, need annual R/V
o Aortic aneurysm >6.5cm Cannot drive
Paediatric Cardiology**
Common presentations in paediatric cardiology are:
Cyanosis Must disting btwn resp and cardiac (NB: cardiac usually LACK of subcost/intercost
recession)
Heart failure
Heart murmur
Cause:
o L-to-R cardiac shunt (e.g. large VSD)
o Left sided obstruction (e.g. stenotic disease, coarctation, hypoplastic left heart)
o HOCM
Features:
o Infant Respiratory, hepatomegaly, failure to thrive
General Poor feeding, failure to thrive (fluid overload may put weight falsely
high)
Left sided RR, cough/creps
Right sided Hepatomegaly
o Child More similar to adult
Ix: ECG, CXR, Echo (three tests for ALL congenital heart disease)
Rx: O2, Diuretics, ACE-I
*LVH occurs from CoA, PDA, VSD but NOT ToF (RVH) or ASD (RA enlargement)
*ECG characteristic findings with AVSD, Tricuspid Atresia but NOT mild PS, PDA, VSD
Murmurs
Acyanotic Cyanotic
PDA Tetralogy of Fallot
ASD Transposition of Great Arteries
VSD (without Eisenmengers) Tricuspid Atresia
HOCM Total Anomalous Pulmonary Venous Drainage
Aortic Stenosis Hypoplastic Left Heart Syndrome
Coarctation of Aorta
Circulatory Adaptations at Birth
Before birth
o Oxy blood from placenta Placental vein Bypass liver via ductus venosus RA
RA Foramen ovale LA LV Ascending aorta
RA RV Pulmonary artery Ductus arteriosus Descending aorta
RA RV Pulmonary artery Pulmonary system (small amount)
After birth
o O2 inhalation closure of ductus arteriosus (ligamentum arteriosum now)
o O2 inhalation pulmonary artery vasodilation pulmonary blood flow pulmonary
vein return to LA closure of foramen ovale (fossa ovalis now)
NB: Only functional closure occurs now, TRUE closure of ductus arteriosus occurs by 3wk
NB: COMPLICATIONS OF ALL CONGENITAL HEART DISEASE IS: Poor growth, heart failure, endocarditis
Acyanotic Congenital Heart Disease: Patent Ductus Arteriosus
Definition: Failure of DA to close in 24hr post-birth (normally closes by 24hr, fully shuts at 3wk)
Presentation:
o Small patency: Asymptomatic
o Large patency:
Machinery murmur (continuous sounds like a train with regular gushes)
Heard at upper left sternal border
Continuous murmur heard because aortic pressure > pulmonary pressure
in both systole + diastole hence blood travels BACKWARD across PDA
As RVH ensues due to pulm HTN, RV > LV pressure, diastolic component of
murmur lost, then murmur completely lost when pressures equal (severe
disease and may now progress to cyanosis/low sats)
Bounding pulses distal to the PDA with collapsing element
SOB, poor leg perfusion (as deoxygenated blood is being sent there)
Ix: ECG, CXR, Echo
Rx:
o Asymptomatic: Observe
o Symptomatic:
Conservative: Fluid restriction + O2 + Diuretics
Medical: NSAID Indomethacin, ibuprofen
USE FOR <1yr (best for pre-term)
Surgical Best for term: Ligation Cardiac cath + insertion of SPRING OCCLUDING
COIL
USE FOR >1yr (as indomethacin will not be effective)
Acyanotic Congenital Heart Disease: Atrial Septal Defect (ASD) (Surgery in all cases)
Features: Asymp until 3-5th decade (?early heart failure, paradoxical stroke from DVT), wide
fixed split S2, eject systolic + mid-diastolic (for secundum only), triphalageal thumbs (Holt-
Oram syndrome)
o Ostium Primum Less common (30%), more serious, located at BOTTOM of atria (hence can also
interfere with AV node)
Features: Asymptomatic (small) Heart failure (large); wide fixed split S2, eject systole
Presents at 10-20yr
Ix:
ECG In adulthood
o RBBB with RAD = Secundum (more benign)
o RBBB with LAD = Primum (more worrying; DDx Trifascicular block)
CXR
Echo
Definition: Constriction of the aorta distal to the left subclavian (98% of cases)
Types:
o Infantile pre-ductal PDA supplies blood to volume + O2; when closes leg cyanosis
NB: even though PDA blood deoxygenated, some O2 is still carried
o Child onset juxta-ductal Less severe as heart grown properly
Risk: Turner syndrome (45X) 90% of child onset coarctation
Features: Asymptomatic Heart failure in adulthood
o Hypertension in the upper body, hypoperfusion in the lower body BP Arm > BP Leg
BP R-Arm > BP L-Arm (if pre-left subclavian)
o Commonly has aortic regurgitation due to common association with bicuspid aortic valve
o Continuous murmur over thoracic spine if VERY stenotic coarctation (<2mm)
o May go unnoticed, collateral supply develops to leg and becomes asymptomatic!
o Radiofemoral delay (esp if coarctation distal to L subclavian [i.e. most of time]), but can get radio-radial
delay if pre-left subclavian
Ix: ECG, CXR, Echo CXR may show rib notching (often seen in ADULTHOOD)+ 3 sign
Rx:
o Neonates:
First: Maintain PDA w/ Prostaglandin E1
Second: Surgery
o Child:
First: Treat HTN
Second: Surgery in ALL cases, no exceptions! (NB: Surg may NOT
cure HTN)
Balloon dilation
Resect affected area + graft
Complications:
o High risk for endocarditis
Acyanotic Congenital Heart Disease: Aortic Stenosis
Types:
o Supra-aortic (least common e.g. William syndrome)
o Aortic
o Sub-aortic (IHSS/HOCM)
Features: Most have bicuspid aortic valve; EJECTION SYSTOLIC
o Infant Heart failure, collapse
o Child Syncope, chest pain on exertion
Ix: ECG, CXR, Echo
Rx: Balloon dilatation if symptomatic or severe, sometimes valve replacement
4 Cardinal Features:
o Pulmonary stenosis
o RV hypertrophy
o Large VSD
o Overriding aorta
Features: E.g. Cyanotic spell in 3mo old after feeding, was sweaty, worsened w/ crying
o Cyanosis usually NOT present @ birth, usually at ~3mo or so
Pulmonary stenosis is the most important factor
Age of presentation is dependent upon degree of pulmonary stenosis (often worsens with
age)
CAN present @ birth if PS severe; RVH will make PS worse hence some present later
o Paroxysmal hypercyanotic spells, especially during exertion (feeding, crying)
o Sweating
o SOBOE (resp signs WITHOUT chest recession), Heart failure, Fail-to-thrive, murmur
Ix: Hyperoxic test (O, sats do not improve but should with resp disease) ECG, CXR (for resp disease; may show
boot shaped heart), Echo (not always readily available)
o NB: With hyperoxic test must cease test ASAP if sats do not rise or else PDA will close
Rx: Consider Abx for ALL blue babies (pneumonia, Mec Asp Synd, etc)
o First: Place child w/ knees to chest (SVR therefore pulmonary circulation )
o Second Medical
In neonates: Maintain PDA w/ IV Prostaglandin E1 (if at birth will not work later)
NB: PDA is aortic pulmonary = more oxygenation
In >1mo: Propranalol + refer for surgery
o Third Surgery:
Immediately: Blalock-Taussig shunt to delivery more blood to pulmonary circulation
At 6mo+: Corrective surgery
Cyanotic Congenital Heart Disease: Transposition of the Great Arteries (ToGA)
*Second most common cyanotic heart disease, but most common cause of cyanosis at birth
Features:
o Cyanosis in first few hours days (@closure of PDA/FO)
o Hypoxia (PaO2 VERY low)
o Murmur, CXR egg-on-string appearance
Wide cardiac silhouette, thin pedicle
Ix: Hyperoxic test, ECG, CXR, Echo
Rx:
o First - Supportive:
Keep warm
Correct acidosis + hypoglycemia
o Second - Medical: Maintain PDA + PFO w/ IV
Prostaglandin E1 (ALPROSTADIL)
NB: PDA is pulmonary aortic! (different) = more oxygenation
o Third Surgery:
Immediately:
Balloon atrial septotomy (i.e. make big ASD)
Subclavian Artery Pulmonary artery SHUNT (Blalock-Taussig Shunt)
o This puts MORE blood into lungs which then passes through FO
>2wk old: Corrective switch
Cyanotic Congenital Heart Disease: Hypoplastic Left Heart Syndrome (HLHS)
Definition: Underdevelopment of left heart forcing right heart to supply both pulmonary + systemic
circs
Mechanism:
o RV Pulmonary vessels LA (nearly fully blocked mitral valve)
o LA PFO/ASD RA RV Pulmonary vessels PDA Systemic perfusion
Features:
o Cyanosis in first few days
o Heart failure + collapse in first couple weeks of life
o Weak peripheral pulses
Rx:
o First: Maintain PDA + FO w/ Prostaglandin E1
NB: PDA goes FORWARDS as no aortic pressure
o Second: Surgery
Reconstruction: 2-3 steps which correct the heart
Definitive: Transplantation
Cyanotic Congenital Heart Disease: Tricuspid Atresia
Mechanism:
o RA PFO LA LV
LV Aorta
LV VSD Pulmonary system
Rx:
o First: Maintain PDA w/ Prostaglandin E1
o Second: Surgery
Cyanotic Congenital Heart Disease: Total Anomalous Pulmonary Venous Drainage (TAPVD)
Definition: Pulmonary veins drain into RA, so only blood through PFO enters left heart
Features: Cyanosis in the first few days of life
Ix: Hyperoxic test, ECG, CXR, Echo
Rx:
o First: Maintain PDA w/ Prostaglandin E1
o Second: Surgery (insert PVs into LA)